Orthopedic Final

‫ﺑﺴﻢ اﷲ اﻟﺮﺣﻤﻦ اﻟﺮﺣﻴﻢ‬
Ain Shams University
Pediatric Orthopedics
Mohamed Sobhy
Quick Guide
• Dysplasias
• Gait
• Deformities
• Regional pediatric problems

[Pediatric Orthopedics] Page | 3
Arthrogryposis
Definition
• Congenital, non progressive stiffness ð due to soft tissue contracture affect 2 or more joints.
• 1st described by Stern as ARTHROGRYPOSIS MULTIPEX CONGENITA
Aetiology
Pathology:
• Fibrofatty tissue Î doughy feeling of the tissues
• z Elasticity & Contractures Î Difficult correction & relapse of deformities
Clinically
1. Amyoplasia: 40%
• No special inheritance & normal mentality
• Tubular appearance of the limbs
• Absent skin creases
• Dimples over the joints
• Deformities:
o Spine: ..................... Scoliosis
o Shoulder: .............. Adduction, IR
o Elbow: ................... flexion or extention
o Wrist: ..................... flexion adduction or extension abduction
o Thumb: ................. In palm
o IP joints: ............... Rigid
o Hip:......................... F Ab ER or Dislocation
o Knee:...................... Flexion or extension + patella alta
o Ankle: .................... Pes calcaneo-cavo-valgus or PPV
TEV or CVT or MTAD
2. Distal Arthrogryposis:
• Distal joint affection (hands & feet) & Normal proximal ms
• AD DISTAL ARTHROGRYPOSIS
TYPE I TYPE II
- 98% Hand affected - Involve other body systems

• Overlapped fingers - 5 Subtypes
• Simian Crease
• Absent DIP
- 87.5% Foot deformities:
• Calcaneo-Valgus
• TEV
• Vertical talus
• Plano-Valgus
4 | Page [Pediatric Orthopedics]
Evaluation:
• History & Clinical picture
• Genetic consultation
• Neurologic consultation
• US in 2nd trimester is helpful
Treatment:
• Aim: is to reach the optimal possible independent fuction
• Tools:
o Casting
o Bracing
o Physical, Occupational & Neurologic consultation to evaluate intellectual function
and predict the response
• Options:
1]. Fractures
o Birth related & infantile traumas are frequent
o Standard techniques in fr. ttt is followed with modification according to limb function
o Usually in the form of CRUGA + casting
2]. Spine:
o 30% of amyoplasia develop scoliosis
o Starts early but manifest in adolescence
o It is a neuromuscular scoliosis (Rigid Curve)
Amyoplasic scoliosis
Early Late
Bracing PSD
(Does not prevent the ±
disease progression) Ant.release
3]. Upper Limb:

o Ranging – stretching – splinting – Bracing – Surgery
o Patient usually develop compensatory mechanisms
o Shoulder IR: ................................. humeral rotational osteotomy

o Elbow extension ........................ Posterior capsulotomy
{
Tenotomy
± Triceps Lengthening
Transfer
o Wrist: ............................................. Mennen operation

• Proximal row carpectomy
• Wrist flexor transfer to extensor
• Triceps transfer to radial neck
• Posterior capsulotomy of elbow
4]. Hip:
o Dislocation .................................. as CP
o Flexion ......................................... as CP
o Flexion ER ................................... as polio
5]. Knee: .................................................... as polio
6]. Foot & ankle: Most commonly affected

o TEV ................................................ as polio
o Calcaneo-Cavo-Valgus ............ as polio
o Metatarsus adductus ............... see later
o Congenital vertical talus ........ see later
Vertical Talus
Early Late (>24 mo) Resistant cases Old
Initial Subtalar Talectomy Triple fusion

manipulation distraction
arthrodesis
+ STR
Anterolateral
+ posterior
STR (at 9m) AFO for a long time
•
Spina bifida
Congenital disorder in which the 2 posterior vertebral arches (or several arches) fail to fuse
• Occur in 1st 6 wk of gestation
• Associated with mal development of neural tube
• Subsequent mal development of the overlying skin
• Dysraphism refers to be the sum of; Bony, Neural, skin defects
• Site: Lumbar or Lumbosacral
• If neural element: -Paralysis
-Hyposthesia
-Incontinence
Pathology:
1- Spina Bifida Occulta (Mildest form)
Midline defect between 2 laminae
If multisegment Î skin (tuft of hair ± Naevus)
Sometimes: -Conus tethering
-Caudal lipoma
-Caudal cysts
-Diastematomyelia (Cord splitting)
2- Spina Bifida Cystica (severe)
Missed lamina
Vertebral prolapse
2 Sub forms:
A. Meningocele:
5%
Cord & root in the canal
Dura is open posteriorly
CSF filled sac protrude
No CNS manifestations
B. Meningomyelocele:
Commonest
Cord & roots prolapse into the meningeal sac
Neurological deficit below the level
If neural tissue is exposed to air Î ulceration Î infection Î
Meningomyelocele
Closed Open
- Neural tube is fully formed - Primitive cord
- Covered by membrane and skin - Unfolded neural tube Î form
the sac roof
Hydrocephalus as sequelae:
cord tethering Î cerebellar and brain stem herniation through
foramen magnum Î obstruction of CSF Î hydrocephalus Î y ICT Î
cerebral atrophy + MR
Epidemiology:
Meningocele 5%
Spina bifida cystica ⎯⎯ ⎯⎯→ 2:100
Secondchild 2:1000
Folic acid administration in 1st trimester Æ z
incidence
Neural tube defect Æ y α Fetoprotein in amniotic fluid after 1st
trimester
Clinically:
1- SB Occulta:
discovered incidentally in X ray
Tuft of hair
Pigmented nevus
Sometimes neurological manifestation:
• Paresis
• Hyposthesia
• Enuresis
• Incontinence
2- SB Cystica:
Hydrocephalus:
• Starts even at birth
• No y ICT ⎯⎯ ⎯⎯→ ICT y
Afterclosure
Paralysis:
• Level vary according to the lesion level
• Increase if the case was neglected (y root traction)
SB Cystica Paralysis
33%
33% 33%
Preserved distal cord
Complete LMNL Incomplete lesion
segment
Paralysis + - Segmental intact Some moves and

Hyposthesia + reflexes sensation are
Bladder - Spastic ms group preserved
Saccular lesion over Lumbosacral region:
Skin & Saccular lesion
Meningocele MeningoMyeloCele
Closed Open
Normal Skin
Tuft of hair Covered by skin & Neural tube form the roof
Nevus membrane of the sac
Deformities: (ð ms imbalance, IU position, independent)

• Hip: Dislocation (5%)
• Knee: Genu recurvatum
• Ankle: TEV + claw toes
8 | Page [Pediatric Orthop
pedics]
Tre
eatment:
1- Defect closure
Ms chaart at time of
o closure is mandato ory for asse essment
Within 48 hr
Neurall tissue is preserved, Dura
D is clossed, Skin iss undermin
ned and
closed
Asse
ess Hydrocepha
alus
VentricculoAtrial drainage
d via
v 1 valve shunt
s
orm z)
Till 6 y (tendency to fo
Removval of shunt
2- Tethere
ed cord is inevitable;
i release if:
y pain
Neurollogical defficit
mities:
3- Deform
Optima al ttt calls for
f team workw (ortho, neuro, ph hysical therrapy, … etcc)
Repeatt ms chart aftera defecct closure and
a healing g
Start é stretch and strap Æ ⎯⎯ ⎯ ⎯ ⎯⎯→ Sugery
AssessAtFourYea
ars
y Orthoticcs
Child never
n becoome indepe endent
UL & mental
m skillss are moree importantt than walkking
Childreen é below w L4 lesionss have qua ads. Æ can walk
Avoid prolonged
p d immobilizzation Æ frracture
Avoid urinary
u pro oblems
Kyphoscoliosis:
1. Common in MMC C
2. ð ms. weakness,
w imbalance
e, vertebral anomaly, or tethered
d cord
Kypho
oscoliosis
Visceral com
mpression
No compression
c
Skin breaakdown
Early localize
ed vertebral
Bracce till 12 year
resction++ Fusion
Progressive Not pro

ogressive
Scoliosis Sco
oliosis + tetherred cord No Sugery
S
Fusion (P
Posterior + Anterior)
F
Fusion + cord release
r
±
Pelvic
P fusion
Hip:
[Pedia
atric Orthopedics] e|9
Page
Hip
A
Above L1 In
n-between (co
ommon) Be
elow S1
Flail hip Dislocatio

on Flexion defromity
Splintage & wheel cha

air O
OR + Add. Tenootomy + Psoas lengthening
l
moodification Sh
harrard +/-oste
eotomies + Soutter (flexor ms slide)
pedics]
Knee:
Knee
Earrly Recurvatum
m Fixed
d extension Late flexion
Qua
ad lengthening Soft tissue release Stretch
h & splint
Ham
mstring
(release, length
hening, transffer)
Foot:
3. Aim: Pllantigrade foot
Foott
Floppy foot Fixxed TEV V

Vertical talus Claw Toes
No ttt (balance
N ed E
Electric Reduction
n Outer four
Talecctomy Hallu
ux
paralysis) AFO
O Stimu
ulation test (3y) toes
Paralysed Actiive Flexo

or
contracted unopp
posed Flexor to
tenodessis to
ms exxtensor transfe
er
prox.p
phx.
Extensive PM
E
release
Transfer
Late Triple
fu
usion 6-12 mo o
Muscle dystrophies are genetically determined progressive disease of the skeletal muscles in
which pathologic changes occur within the ms fibers
Duchenne
Progressive muscle weakness
XR ( X p21) Î abscent dystrophine Î leak of CPK
Male child or adolescent
70% +ve
1:3300
2nd lethal genetic disorder
Clinically:
Progressive ms weakness (Proximal)
Delayed milestones
Loss of some already acquired skills
Deformities:
• Knee flexion
• Hip flexion abduction
• Lordosis ð hip deformity
Calf pseudo hypertrophy (sometimes the shoulder)
Wide based gait
+ve Gowers sign (pt. climbs on his legs to stand up)
Recurrent chest infection
Cardiomyopathy } Cause of death at 2n decade
Investigations:
y CPK very high from the 1st year
DNA testing is conclusive (blood and amniotic fluid)
Dystrophin testing (differentiate from Backer)
Ms. Biopsy:
• Necrosis
• Phagosytosis
• CT infiltration
• Type 3 collagen
• Type IIc fibers
• Multisegmented hypertrophied ms fibers
• Lateral sarcoplasmic masses
• Signet ring like structures (Annulets)
EMG:
• Necrosis
• Fibrillation
• Low amplitude polyphasic potential
Treatment:
hip flexion Î souter
knee flexion Î hamstring release
Equinus Î TAL
TEV Î TPL
UL flexion Î physiotherapy
Spinal collapse Î fusion (zpelvic obliquity; but same longevity)
Prerequisites:
forced vital capacity > 40% of normal
Intact cardiac function
pedics]
Baackerr Musscle D
Dystro
ophy
y
XR (XXp21 Î inssufficient or
o dysfunction of dysttrophine)
Clin
nically:
delayed milestonnes
+ve fam
mily historyy
Giveupp walking by
b 30y
ound 4th de
Die aro ecade
Less de
eformities & contractures than Duchenne
D e
DD
D
LGD Bu
ut:
• yy CPK
• Pseudohyp pertrophy
• Degeneration of ms Biopsy
DMD:
• But dystro
ophin testin
ng
FSSHD Facio-S
F Scapullo-Hum
meral Dystro
D ophy
AD
Clin
nical:
1st: weaak facial ms
m :
• zeyelid clo osure
• zblowing and whisttling
• Pursing off the lips
Worst: weak shou ulder abduuction + wiinging of sscapula
Pt. doees substitutte motions
Lower limb: Drop p foot + Pro
oximal weaakness
Norma al life span
Tre
eatment:
Stabilizze the scap
pula to thorrax (Lotern
nel)
LG
GMD Limb Girdle
G Muscle Dystophyy
AR
♂=♀
e 1st till the 4th decade
Onset is from the e
Clin
nical:
Proxim
mal weakne ess
+ve go
ower sign
Normaal life span
DD: Becker
PK y
Mild CP - +ve channges in biopsy
No pseeudohyperrtrophy - dyystrophin testing
CPK level Diagnosis

K X20 to X200 DMD BMD
(but falls in
late adolescence)
K x10 LGD
K X mildly elevated FSHD EDMD
Muscle biopsy Frozen In liquid nitrogen within minutes
Light microscopy
H&E General morphology (atrophy? hypertrophy? degeneration?
fibrosis? inflammation?
infiltration?)
ATPase Fiber type (grouping? disproportion?)
Nicotinamide adenine Fiber type, cellular architecture (e.g., central core)
dinucleotide—tetrazolium
reductase
Gomori trichrome Connective tissue elements (e.g., nemaline rods)
Periodic acid—Schiff Glycogen
Oil red 0 Lipid
Electron microscopy Fixed in the operating room In 4% gluteraldehyde; Selected
patients to confirm a structural myopathy and assess lipid or
glycogen storage and mitochondria
Emery Dreifoss MD
XR
Clinically:
Extension contracture of the neck
Rigid paraspinal ms Î limited scoliosis
Non progressive ms weakness
Deformities: equinus, TEV
Fatal cardiac diseases
Investigations:
Mild y CPK
Dystrophin testing
DNA testing
Treatment:
TAL
TPL
No need for treatment of scolosis
Clinical Features of Principal Types of Muscular Dystrophy
Features Duchenne’s Becker’s Emery-Dreifuss Limb-Girdle FSHD

Incidence Most common Less common but not Uncommon Less common Not common
rare
Age at onset Usually before 3 yr; Usually after 7 yr Variable (usually 2nd Variable (usually in between 3 and 6 yr
some decade, occasional later) second decade)
Sex Male Male Either sex Either sex Male
Inheritance XR AR AD
Responsible Xp2l region of X CH Xq28 region of X Ch. 15 4q35 region of ch. 4
gene chromosome
Pattern of Proximal (pelvic and shoulder girdle affected Humeroperoneal Proximal: shoulder & Face and shoulder
muscle early Æ distal limbs late) distribution pelvic girdle Æ periph girdle; later spreads to
pelvic girdle
Muscles spared Gastroc, FDL, TP, In upper extremity, Back extensors,
until late hamstrings, hand brachioradialis and iliopsoas, hip
muscles, upper trape- hand; in lower ex- abductors, quadriceps
zius, biceps, triceps, tremity, calf muscles
face, jaw, pharynx,
larynx, and ocular
Pseudohypertro 80% of cases (calf Same as Duchenne’s <30% of cases Rare
phy muscles)
Contractural Common Common in severe Common Develop late in course; Mild, occur late
deformities cases; less common in less severe than in
milder cases Duchenne
Scoliosis and Common in late stage More common in Se- Does occur but may Mild in late stage Mild, occur late
kyphoscoliosis vere cases self-stabilize
Cardiac Hypertrophy and ECG abnormalities Cardiomyopathy, most Very rare
involvement tachycardia common; common; dilated commonly presenting
in late stages,cardiomyopathy in high as heart block
widespread percentage of patients;
degeneration, fibrosis,mitral regurgitation and
and fatty infiltration heart failure seen in
late stages
Intellectual Commonly L Normal
level
Myotubular Myopathy
Different forms of inheritance
Clinical Picture:
Non progressive weakness
Investigations:
Myotubular appearance of the ms fibers
ATPase stain Î Donut appearance
[Pedia
atric Orthopedics] Page | 15
Co
onge
enita
al MD
M
Rare hereditary ms disorder
d du
ue specific pathologicc ultra stru
uctural changes; usuaally require
e
bracing
g and follow
w up and rarely
r need
ds surgery (e.g. spina al fusion)
Ce
Central C e Disease
Core Di AD
D
Ms. Fib
ber devoid of enzyme
e activity
Clin
nical Picture
e:
Scoliossis
TEV
CDH
Malign
nant Hypo
othermia
a
S
Succinyle c
choline Ha
alothan
y HR , Temprature,
T Contracturees
Death
Investigattion Treatment
Caffe
eine tested Ms biopsy - sto
op anesthetiic
- NaHCo3
- Dantrolene So odium
- Clo
ose the incission
- Cool the pt.
Most se he malignant hypothe
erious is th ermia (AD))
Inve
estigation:
Ms fibe
ers are not stained
(No ennzymatic acctivity)
Prominnent type I fibers
Caffein
ne tested ms
m biopsy
Nem
malinee MD AD
D
Clin
nically:
Mild lim
mited weakkness
Scloiossis
Chest wall
w deform mity
TEV
Die Earrly
Inv
vestigatio
ons
Rod likke structure
es by "Gom
mori tr me"
richrom stain
n
Mitoochonddrial Myop
M athy
Inv
vestigatio
ons: − Ragged d red fibers é "Gom
mori tricchrom me" stain
on Mic. Î Abnormal
Electro A Mitochond
dria in shap
pe & size
DD
D:
Cardiomyopathyy & Lipid sto
orage Carn
nitine deficciency
pedics]
C
Congeni
ital Myopath
M hy
AR
Clin
nically:
Severe neonatal hypotoniaa
Little progression
n
Contra actures:
• CDH
• TEV V
• Sco oliosis
Inv
vestigatio
on:
Abscen
nt type II fib
bers
EMG: motor
m unit potential (MUP)Î
( z amplitude & time < 15 ms
C al Fibber Tyype Diisproporrtion

Congenita
Clin
nically
Hypoto onia - CDH
Scoliossis - Torticcollis
Contraactures
Inv
vestigatio
ons:
Ms biopsy: Disprooportion of the ms fib
bers in no a
and size
Type I z in size & number
Type II y
M nia Coongenitta
Myoton
(THOMPSON'S DISEASE) ≠ congenital myotonic Dystroph hy
AD disorder characterize
c ed by abno ormal calciium perme eability
Clin
nically:
Early childhood
Marked d initial mu ability Î z with repe
uscle excita etition
Difficullt relaxing
Hypotrrophy
Painfull stiffness Î y with rest
r & cold - z é repettition
Norma al life span
Inv
vestigatioon:
Biopsy: abscent IIIB fibers
EMG: - Hyper exxcitability
- y with re
est and cold
- z with re
epetition
Paraa My
yotoniaa Conggenita
(Eulenburg disease) AD
Clin
nically:
Episodes of myottonic paralyysis predisposed by ccold
Mainlyy in face an
nd hand Hyypertrophyy
[Pedia
Steeinert's My
yotonic dy
ystropphy
AD (cchromosom
me 19)
Clin
nically:
Two form
ms
Congenittal Adult form

-Severe & progressive -Moderate picture
p
-Hypotonnic Baby -Myotonia
-Maternally inherited -Paternally inherited
i
-Marked deformities
d -Less deform
mities
Frontal baldness
Mentall retardatio
on
Cataract
Infertiliity
Distal weakness
w
Deform mities
• CDH
• Scoliosis
• TEV: Î Trriple Fusion
n
• Hallux valggus: Î Surrgery
Inv
vestigatio
on:
y CPK mild
EMG: hyper
h excittability
DNA teesting
Biopsy:
• CT infiltrattion
• Central nu uclei
• More invo olvement of type I fibe
ers
• Fibers are variable inn size
Myasthenia Gravis
Humoral mediated hypersensitivity Î Acetyle choline receptor AB
No single inheritance
1:5000
♀:♂ = 3:1 (z with age)
Clinically:
Adult type (classic y fatigability of all muscles)
• Ocular Î Diplopia & ptosis
• Dysarthria
• Dysphagia
• 20% limbs
Transient neonatal myasthenia:
• 15% in children for myasthenic mothers
• ð transfer of Acetyle Choline receptor IgG
• Resolve in 2-4 weeks
Juvenile Myasthenia:
• 10 y of age
• Usually facial
• Rarely proximal UL
Infantile Myasthenia:
• AR
• Ptosis
• ophthalmoplegia
• RDS
• General weakness
Thymoma 10%
Investigations:
Neostigmine test
Biopsy: Type II atrophy
EMG: early fatigability by repetitive stimulation (Jolly)
Treatment:
Thymectomy if any
Neostigmine (pyridostigmine)
Plasmapharesis
Steroids
Immunosuppressive drugs
Spinal Muscle Atrophy

AR
Classification
Infantile Juvenile
- Severe - Mild
- WERDING HOFFMAN - KUGELBURG WALENDER
Clinically:
- Poor head control - Unable to walk
- Sitting imbalance - Sit unaided
- Severe prog. Weakness - Progressive weakness
- Hypotonia - +ve Gowers
- Hyporeflexia - ± hyporeflexia
- Fasciculation - ± fasciculation
- Start early - Starts few mo after birth
- Die in the 1st year - Survive
- Achieve 1st mile stones
- Scoliosis
- Contractures
Investigation
- Normal CPK - Mild yCPK
- Biopsy: -Hypertrophy - Biopsy: -fiber type grouping
-type I fr. Clumping -type II predominance
- EMG: -difficult to interpret - EMG: -Denervation
reinnervation pattern
Treatment:
- Body jacket with neck extension - ttt of contractures
- Diaphragmatic Breathing - scoliosis Î PSF
- Exercises
- ttt osteoporosis
- Wheel chair & Vehicle Modification
pedics]
C cot Ma
Charc Marie To
Tooth
Pe
eroneal Muscle
e Atrop
phy
• = Type I & II Here
editary Mottor & Senso
ory Neurop
pathy (HMSN)
• AD
• 1:25000
• +ve fam
mily historyy
Patthology:
• Hyperttrophic dem myelinating g neuropa athy
• Ms imb balance Î dynamic deformity d Î fixed de eformity
Clin
nically:
1]. Weakn ness:
o Distal
o Atrophy
o Hypotonia a
o Hyporeflex xia
2 Hypostthesia
2].
3 Deform
3]. mities:
o Hands = in ntrinsic mu uscle wastin ng
o STORK LEG G = INVERTE ED CHAMPA AGNE BOTTL LE legs.
o Pes cavo-v varus (COLE EMAN BLOC CK test; varrus heel corrects with
h a block un
nder the
lateral edg ge of the fo oot)
o TEV ± claw w toe
o kyphoscoliosis
Tre
eatment:
• Kyphosscoliosis ........................................... Î PSF if pu ulmonary fu unction peermits
• Toe waalking .............................................. Î Casting – AFO – TA AL
• Pes Cavvus ................................................... Î Transfer
• TEV + claw
c toe .......................................... Î PT transffer + TAL
If fixxed
Î Dwyer osteotomy
o
Î Calcanea al valgus wedge
w oste
eotomy
Î Triple fussion
Hereditary Sensory & Motor Neuropathies (HSMN)
4 Hallmarks
1]. EMG: neuropathic pattern
2]. NCS: z conduction velocity
3]. Muscle biopsy: neuropathic pattern (uniformly small diameter fibres)
4]. Nerve biopsy shows Demyelination.
HMSN Types (HEREDITARY MOTOR & SENSORY NEUROPATHY = DEGENERATION OF PERIPHERAL NERVES)
• HMSN type 1A and B ......................(hypertrophic Charot Marie Tooth $)
• HMSN type 2 ......................................(neuronal Charcot Marie Tooth $)
• HMSN type 3 ......................................(Dejerine-Sottas = hypertrophic neuropathy of infancy)
• HMSN type 4 ......................................(Refsum $ hypertrophic neuropatht ð phytanic excess)
• HMSN type 5 ......................................(+ spatic paraplegia)
• HMSN type 6 ......................................(+ optic atrophy)
• HMSN type 7 ......................................(+ retinitis pigmentosa)
HSAN (HEREDITARY SENSORY & AUTONOMIC NEUROPATHY) = DEGENERATION OF DRG & AUTONOMIC GANGLIA
• HSAN type 1 .......................................AD + distal sensory involvement
• HSAN type II .......................................AD + distal and proximal sensory loss
• HSAN type III ......................................Riley Day dysautonomia $
• HSAN type IV .....................................insensitivity to pain, MR, charcot joints.
• HSAN type V ......................................selective loss of pain & intact touch &vibratory sensation
ggggggbiiiiii

Charcot Marie Tooth Disease (HSMN I & II) AD
• motor & sensory demyelinating neuropathy. (motor > sensory defects)
• CMT HYPERTROPHIC form (HMSN 1) - onset 2nd decade of life.
• CMT AXONAL form (HSMN 2) - Onset 3rd or 4th decade
Dejerine Sottas Disease (HSMN III) AR
• HYPERTROPHIC NEUROPATHY of infancy CMT3
• CP - Delayed ambulation, hypotonia, areflexia, pes cavus, glove & stocking dysaesthesia
• Confined to wheelchair by 3rd/4th decade
Refsum disease (HMNS IV) AR
• HEREDOPATHIA ATACTICA POLYNEURITIFORMIS)
Inborn error of phytanic acid metabolism (H
• Demyelinating hypertrophic neuropathy
• CP: distal weakness, hyporeflexia, ataxia, nyctalopia, retinitis pigmentosa, anosmia
Riley Day Syndrome (HASN III) AR
• Sensory + AUTONOMIC neuropathies.
• Only in Ashkenazic Jews
• Clinically - Dysphagia, alacrima, hyperhidrosis, postural hypotension, hyposthesia
Friedrich's Ataxia AR (9q13)
• Hereditary ataxia (Cerebellar + DRG + PN degeneration)
• Onset before age 10 & death by 40-50 yrs
• CP: Staggering broad based gait, nystagmus, ataxia, cardiomyopathy, nystagmus, cavus
foot, scoliosis, motor and sensory deficits.

Guillain‐Barré syndrome
Definition
• Acute inflammatory demyelinating polyradiculoneuropathy characterized by
albuminocytologic dissociation (ie, elevation of CSF protein with normal CSF cell count)
Epidemiology
• With the eradication of poliomyelitis, GBS is the commonest cause of acute paralysis in
children
• Death occurs ð respiratory failure & cardiomyopathies
• Males >40y
Etiology:
1]. Epstein-Barr virus
2]. Cytomegalovirus
3]. Hepatitis virus
4]. Varicella,
5]. Mycoplasma pneumonia
6]. Campylobacter jejuni
Pathology
1]. Demyelinating form: segmental demyelination of PN + cell mediated immune reaction
2]. Axonal form: degeneration + antiglycolipid antibodies (no demyelination or inflammation)
Clinical
• Motor:
o Ascending weakness from lower to upper exterimities
o Unsteadiness
o Areflexia
• Sensory:
o Pain
o Dysthesia
• Autonomic manifestations: arrhythmia, orthostatic hypotension
Investigations
• Lumbar puncture: yyy proteins (>45gm/dl) & no cells (no infection)
• MRI with gadolinium: y signal at cauda equina nerve roots
• EMG:
o Absent F response
o y distal latencies
o z conduction velocity
• Muscle biopsy: Demyelination + Infiltration é mononuclear, lymphocytes, & macrophages
Treatment
• Steroids
• Immunoglobulins
• Plasmapharesis
[Pedia
M iple Neur
Multi N rofibroomatossis
Types NF-1 - Von
V Recklinnhausen's Disease
D NF-2
Site Peripherral NF Central NNF
Incidence 1/4000 1/100 00 00
Inheritence AD (Ch 17); 50% ne ew mutationss AD (ch 2 22)
Nature Multi-sysstem disease
e affecting grrowth of neu
ural tissue bilateral acoustic sch
hwannomas
CLINICAL DIAGNOSTIC CRITERIA (Conse ensus Development Conferencce, 1987)

1]. > 6 cafe
e-au-lait sp
pots of at le
east 15mm m in adult & 5mm in child.
2 Multiplle axillary or
2]. o inguinal freckling (C (CROWE'S SIGN)
3 Two orr more neu
3]. urofibroma as of any tyype or one plexifrom neurofibro
oma
4 Two orr more Lisc
4]. ch nodules (Iris hama artomas)
5 Optic Glioma
5]. G
6 Distinctive bony lesion
6]. l
7 First de
7]. egree relative affected
CLINICAL FINDINGS:
1. Café-au-lait
C spots
Mellanotic piggmentation n in the bassal layer off the epidermis
In areas
a of skin not expo osed to the e sun
Smo ooth borde ers (''COAST OF CALIFORNIA')
DDx: cafe-au-lait spots of o fibrous dysplasia
d Æ jagged bo orders = 'COAST OF MAINE'
2. Axillary
A & in
nguinal fre eckles = CROWE'S sign (40%)
3. Fibroma
F mo olluscum
Sma all NF (schwwann cellss + fibrobla asts + endoothelium + glandular element)
Slig
ghtly bluish
h colour
4. Plexiform
P neurofibrom ma
Largge NF é pu urplish pigm mentation
Roppey 'BAG OF WORMS'
Verry sensitivee
Hass potential to become e malignan nt
5. Elephantias
E sis
Skin
n thickenin ng é rough h, villous surface
Dyssplasia of underlying
u bone
6. Verrucous
V h
hyperplasia a
Marrked skin overgrowth
o h é velvetyy soft
pappillary surfa
ace
Creevices form which bre eak down &
wee ep
Cann become superficiall
s ly infected..
7. Lisch
L nodulles (90%)
Raissed well-cirrcumscribe ed hamarto omas in the iris
8. Optic
O gliommas
Astrocytoma of o the optic nerve
Cann cause exo ophthalmo os & visual impairmen nt
9. Orthopedic
O c affection:
Kyppho-scoliossis
Tibiial pseudo--arthrosis
Maccromelia
Sarccomatous change
pedics]
1. Spinall Defor rmities s

General:
1. Widened spinal
s canaal
2. Widened neural
n fora
amina
3. Scallopingg of posterior vertebraal margins
4. Defective pedicles
p
5. Spindling of transverrse processs
6. Severe rotation of ap pical verteb
bra
o ribs - 'TWISTED RIBBON'
7. Rotation of
8. Paraspinall mass
Cervical Sp
pine
1. Kyphosis
2. C1-C2 disloocation
Scoliosis
• Dystrop phic curvees:
1. Short segmmented - in ncludes < 6 spinal seg
gments
2. Sharply anngulated
3. Tends to progress
p
4. Left conveex thoracic curve mosst common n
• Non-dy ystrophic curves:
c
1. Similar to idiopathic
i curves
2. More common than dystrophicc
• Aetiolo ogy:
1. Dural ectaasia (circum
mferential dilatation
d of
o dura)
2. Primary bo one dyspla asia
3. NF tumou urs
4. DUMBELL LESIONS - enlarged fora amen in obblique XR ð NF exitin
ng spinal ca
anal.
5. Meningocceles
Management:
NF Scoliosis
< 20ºº
2
20‐40º >40º
Observe 6
6 mo PSF é insstrumentation
n ASF + PSF
2. Congenittal Tibial Pseudoarrthrosis(se

ee later)
3. Disorderss of Bone e Growth

1]. segmen ntal hyperttrophy 2ryy to hypertrrophy of
the roo
ots of the brachial
b or lumbosacrral plexus
2 subperriosteal hyp
2]. pertrophy 2ry2 to mino or # é
subperriosteal bleeding
-Periostteum in NFF-1 is less adherent
a
-Elephaantoid overlying hypertrophy
-Dough hnut sign on
o Tc
4. Tumours Risk of sarrcomatous change = 3.6%
1]. Neuroffibrosarcom ma
2 rhabdo
2]. omyosarco oma of urog genital tracct
3 Wilms tumour
3].
4 childho
4]. ood leukaeemia
Dysplasias
Heterogeneous group of developmental disorders occur due to structural abnormalities in the
bone itself leading to disturbances in growth
CLASSIFICATION OF GROWTH DISTURBANCE
1 Disorders of cartilage and bone growth
I. Epiphyseal Dysplasias V. Combined and mixed Dysplasias
A. Hypoplasias o Fibrous dysplasia (McCune Albright)
o Spondyloepiphyseal Dysplasia o Chondrodystrophica myotonia (Schwartz-Jampel)
o Multiple Epiphyseal Dysplasia o Kniest Dysplasia
B. Hyperplasia o Diastrophic Dysplasia
o Dysplasia Epiphysealis Hemimelica (Trevor's) o Chondro-Ectodermal dysplasia
o Chondrodysplasia punctata (Stippled Epiphysis) o Camptomelic dysplasia
II. Physeal Dysplasias o AcroCephalySyndactyly (Apert)
A. Hypoplasias o Cleidocranial dysplasia
o Achondroplasia o Nail—patella syndrome
o Hypochondroplasia o Infantile cortical hyperostosis (Caffey’s)
o Pseudoachondroplasia o Pyknodysostosis
B. Hyperplasias o Thanatophoric Dysplasia
o Dyschondroplasia (Enchondromatosis, Olier's) o Jeune's Dysplasia
III. Metaphyseal Dysplasias o Short rib Polydactyly dysplasia
A. Hypoplasias
o Metaphyseal Dysplasia (Pyle's Disease) 2 Connective tissue disorders
o SpondyloMetaphyseal Dysplasia (Kozlowski) o Marfan $
o Metaphyseal chondrodysplasia (Schmid, Jansen) o Ehlers—Danlos $
o Hypophosphatasia o Larsen’s $
o Osteopetrosis (Marble Bone) o Fibrodysplasia Ossifcans Progressiva
o Spotted bones (Osteopoikilosis)
o Striped bone (Osteopathia striata) 3 Storage and metabolic defects
o Candle bone (Melorrheostosis) o Mucopolysaccharidoses
B. Hyperplasia o Gaucher’s disease
o Hereditary Multiple Exostoses (Diaph.Aclasis) o Homocystinuria
IV. Diaphyseal Dysplasias o Alkaptonuria
A. Hypoplasias o Congenital hyperuricaemia
o Diaphyseal Dysplasia (Camurati's)
o Osteogenesis Imperfecta (Brittle Bone)
Idiopathic Osteoporosis 4 Chromosome disorders
B. Hyperplasia o Down’s syndrome
o Progressive diaphyseal dysplasia o Limb anomalies
dddddddddfffffffff
DYSPLASIA Generalised intrinsic bone abnormality.
• comes from Latin roots dys and plasia, meaning "bad growth”
• It is the preferred term for dwarfism
DYSOSTOSIS Segmental bone abnormality ð mesodermal defect
DYSTROPHY Metabolic bone or soft tissue abnormality
DWARFISM Pathological diminution of stature.
• Is broadly divided into:
o Proportionate (midget):
Endocrinopathy, e.g. cretinism, pituitary dwarfism
Chromosomal: e.g. Trisomy 21
Metabolic: e.g. rickets
o Disproportionate
Limb Dwarfism
RHIZOMELIC (proximal) Achondroplasia, Diastrophic dysplasia
MESONELIC (middle) Léri-Weill madelung $
ACROMELIC (distal) Ellis-Van-Creveld $
Trunk Dwarfism Kniest dysplasia, Morquio’s, vertebral anomalies
Combined Dwarfism OI, SED, SMD
Head/epiphysis Thorax /metaphysis Spine /diaphysis Limb Elbow Hand Hip Knee Foot
Achondroplasia Platybasia y kyphosis Stenosis Rhizomelic Short Square Varus
PHYSEAL
Macrocephaly V‐lower femoral Trident

AD
Maxilla hypoplasia metaphysis
Hypochondroplsia Squaring Flaring Long fibula TEV
Pseudo‐achond Same as Hypochondroplasia + OA Platyspondyly
Olier’s Enchondromatosis LLD Sled Runner tracks
Malignancy Deformity
MED Delayed 2ry ossific Dwarf Short OA Valgus Valgus
centers Broad Waddling
EPIPHYSEAL
AD
SED Delayed 2ry ossific Pectus carinatum Platyspondyly Dwarf Coxa vara Varus

Cleft lip y kyphosis Odontoid hypoplasia Coxaplana
y lordosis OA
Stenosis Waddling
Trevor’s (dysplasia Half over growth LLD
epiphysealis hemimelica) Half of the body Deformity
Conradi Hunerman Delayed 2ry ossific Scoliosis LLD
AD
(chondrodysplasia punctatal Punctate epiphysis Deformity

Pyle (MMD)
METAPHYSEAL
Erlyenmyer falsk Cortical thinning Flexion Valgus

AR
Osteoporosis
Kozlowski (SMD) Pectus carinatum Platyspondyly OA
AD
Kyphosis Odontoid hypoplasia Waddling

Schmid (CMD) Normal Wide Scalloping Mild Dwarf Varus
Osteopetrosis Blindness Sclerotic brittle bone No medulla (osteoclast
AR/AD
Palsies (marble like) Pancytopenia defect)

Bat shaped skull Pathological #
HME Multiple exostoses LLD
AD
Malignancy Deformity
Camurati Wide Sclerotic Fusiform Waddling Pain
D
AD
(Diaphysieal dysplasia) Narrow medulla

Fibrous dysplasia Wide Ground Glass LLD Shepherd
Nail Patella $ Deformity Valg & Flex Ө nails Iliac horns Valg & F Pes
Radial disloc DDH ө patellaplanus
MIXED DYSPLASIAS
Schwartz Jampel $ Myopia & Flat facies Platyspondyly Myotonia Coxaplana

Apert’s $ Coronal synostosis Syndactyly
AD
(Acrocephaly syndactyly) Flat occiput & face Broad DIP

Cleido-Cranial $ Plagio‐cephaly Absent clavicle (intramemb Delayed
ossif defect) symphysis
Kniest $ Delayed 2ry ossific Short trunk Platyspondyly Trunk dwarf Large
Flat facies Kypho‐scoliosis AARI PG defect OA
Camptomelic Dspl Delayed 2ry ossific Tibia, femur, fibula LLD TEV
(Bent limb) CNS deficit Deformity
Diastrophic Dspl Calcified kyphosis Rhizomelic Flexion Hich‐hicker Flexion Flexion TEV
cauliflower ear Symphalanx
Pyknodysostosis Rachitic skull
AR
Blue sclera
Ellis Van Cerveled Ө hair, teeth, nails Acromelic Polydactyly
Chondro-ectodermal D Short DIP
Thanatophoric D Shrot rib Æ Narrow Short bow
Jeune Thorcic D Irregular epiphysis thorax Æ die Short Polydactyly ٓiliac DDH
[Pedia
Achondropplasia
Dyssplasia cha
aracterized by disprop portionate e short statture with rhizpmelic (proximal) shortening of
long
g bones
Most common Dyysplasia
1:10.00 00
AD, Bu ut 80% starrts as new mutation (where
( inh
heritance < 1%)
Gene 4 p16.3
Mutatio ons occur at "fibrobla ast growthh factor recceptor3" FG
GFR3 (whicch
has an importantt role in en ndochondral growth))
Clin
nically:
1. Norma al life span
2. Norma al mentalityy
3. Psycho ological trooubles
4. Rhizom melic dwarffism: 130 cmc ♂/ 125 cm in ♀
5. Face:
• Macrocephaly
• Frontal bo ossing
• Saddle nose
• Maxillary hypoplasia
h s
• Prognathia
6. Hands:
• Short & brroad
• Wedged gap g between 3rd & 4th 4
fingers (triident handds)
7. Spine:
• Cervical co onstriction ð narrowiing of foramen magn num
• Lumbar lo ordosis
8. Knee: Genu
G varum
X-R
Ray
Skull:
• Large Calvvarium
• Short skulll base
Pelvis:
• Square sha aped
• Small sacro osciatic no
otch
Spine:
• Short pediicle
• Short interrpedicular distance
long bines (Femu ur)
• short & broad
• V-shaped distal femo oral epiphyysis
Tre
eatment:
• Human n Growth Hormone:
H 1st year heeight gain isi maximum m (7.5cm) Æ effect z by time
• Surgica
al limb leng
gthening
• Cord decompresssion
pedics]
H chondrroplassia
Hypoc
− AD; buut more muutations are
e found
− Mild fo
orm of acho
ondroplasia
Clin
nically:
− Late prresentation
n (mild pictture)
− Norma al head & fa
ace
− Norma al neurologgy
− MR
− Norma al hand
− Mild lo
ordosis
− Mild vaarus
− Talipess Varus
X- Ray
R
− Flaring
g metaphyssio-epiphysseal junctio
on of long bone
− Squarin
ng of epiphhysis
− Norma al physis
− Less na
arrowing of
o interpedicularr disttance
− Long dista
d fibula Æ TV
P o Achondroplassia
Pseudo
(Pseu
udo achond
droplastic form of spondyloepipphyseal Dyysplasia)
− Rhizom melic dwarffism
− AD & AR A
Clin
nically:
− Normaal initial devvelopmentt
− 2-3y staart growthh retardatio
on
− Disproportionatee growth reetardation
− Lordossis
− Degen nerative join
nts
PXRR:
− platysp pondyly
− Epiphyyseal chang ges
− Metaph hyseal cha
anges
− Joint inncongruityy
− Prematture degen neration
Tre
eatment:
− Reconsstructive su urgery
[Pedia
M
Multiple E
Enchond
dromatoosis
Olier'ss
Sporaddic Metaph hyseal & diaphyseal pathologic
p cal replacem
ment by areas
of hyalline cartilag
ge
Clin
nically:
Unilate
eral or bilatteral asymmmetrical
Asymmmetrical gro owth
Angulaar deformitty and sho ortening of affected b
bone
Low malignancy
m
Patholo
ogical fr
PXR
R:
Cartilag
ginous encchondromas
Cartilag
genous strreaking
Tre
eatment:
Corrective osteottomies
ttt path
hological frr
M
Maffuci's
s$
Olier's + heamangiomata:
• Capillary
• Cavernouss
• Phlebectassic
Clin
nically:
Hemanngioma
y Fractures
y Malig
gnancy
Tre
eatment:
Fixation
Excision
Amputtation is the last choicce if all fail
Spondyloepiphyseal Dysplasia
Congenita AD
• + Also mutations affect type II collaged gene (vitreous & carilage)
Clinically
• Trunk:
o Trunk Dwarfism ○ Pectus carinatum (barrel chest)
o lumbar Lordosis ○ Thoracic kyphosis
o Cord compression
• Limbs:
o Coxa Plana & Vara ○ Waddling gait
o short limbs ○ Genu Valgum & varum
o Normal hands & feet ○ Hypotonia
• Head:
o Cleft palate
o Myopia
o Retinal degeneration & detachment
Investigations
1- Prenatal US (2nd&3rd trimester):
o Short long bone
o Flat hypoplastic vertebrae
o Small thorax
2- PXR
o Delayed ossification at pubis & upper and lower femoral epiphysis
o Pear shaped vertebra (childhood) Æ Platyspondyly (adulthood)
o Flat ossific centers e.g. femoral head Æ incongruous Æ sublux Æ OA
o Coxa Plana & Vara (neck shaft angle < 100°)
o Odontoid hypoplasias Æ cervical instability (AARI) Æ cord compression
Treatment
• cervical instability: Æ progressive loss of motor power
o cervical fusion
• LLD
o Osteotomies
• Hip:
o Valgus osteotomy
o THR
Tarda XR
Clinically: (late presentation)
• short trunk
• Coxa vara
• Platyspondyly é dorsal kyphosis & lumbar Lordosis
• z ROM in hip & back
Treatment: THR
[Pedia
Multtiple Eppiphyseall Dysplaasia AD

D
• Two tyypes:
1]. Se
evere Fairba ank
2]. Mild
M Ribbing g type: more e hip involvvement
• Chromosome 1 & 19
Clin
nically:
• Late prresentationn 5 – 10 y
• Mild sh
hort staturee
• Short broad
b handds
• Waddliing gait
• Valgus knee
• Double e layered patella
p (trip
partite)
• Valgus ankles
PXRR:
• Norma al at birth
• 2ry ossific centre::
o Delayed apppearance
o Patchy
o Irregular
o Symmetricaal
• OA hip
p (early 20 y)
y
• OA sho
oulder (hattchet head
d)
pedics]
D lasia Epiphyse
Dyspla Ep p ealis Hemime
H melica
(Treevor's Dissease(
(
• more inn♂
Clin
nically:
• Distal femur,
f proxximal tibia, talus.
• Osteocchondral over growth h of ½ of one
o or mo ore epiphyssis of one half of the
e body (me
edial
½ or la
ateral)
• z é ma aturity
• Angula ar deformitty
• Limb leength discrrepancy
PXRR:
• Pathog gnomonic over
o grow wth of one ½ of an ep
piphysis
C honndro
d ysplasia
P uncttata
AD
D
Connradi Hunnerman
• Group of diseases
• Small fo
ocal calcificcation in ca
artilage (arrticular, ep
piphysis, ..)
• This wiill lead to Epiphyseal
E dysplasia
• AD + High
H mutattions
• Severe forms are lethal
Clin
nically:
• Scoliosis (early)
• Limb le
ength discrrepancy
• Limb deformities
PXRR:
• Delayeed appearance of 2ry ossific cen ntre
• Focal calcification
c n of cartilag
ge
[Pedia
Meetaphyyseal Dyspl
D lasia AR
R
Py
yle Diseasse
Clin
nically:
Genu valgum
Elbow
w flexion contractur
c e
PXR
R:
Erlenmmyer flask k like flare of distal fe
emur & pro
oximal tibia
a
Cortica
al thinning
Osteopporosis
Sponndylo Meta
M aphyseeal Dyysplassia AD
D
Kozlowsk
(K ki)
Clin
nically:
Thoraccic kyphosis - Pectu
us carinatum
m
OA - Wadddling
z ROMM
PXR
R:
Platysp
pondyly - Odontoid d hypoplassias
Thoraccic kyphosis - Rachitic like mettaphysis
Metaaphyseaal Chonndrodyysplasiia
Schmid Jansen McKusick
-comm
monest -Fresh
h mutations -Cartilage
e Hair Hypopla
asia
-AD -AD -AR (ch9)) ± Fresh muta
ations
-Mild sho
ort stature -Progresssive shortening
g of long
-Hip & kn
nee flexion deff. bones (htt ~ 120 cm)
-Genu vaarum
-Waddlinng gait -z cell meediated immunity
n z é developm
-Leg pain ment
-y malignnancy
-Fine sparrce hair
-At birth: -Intestina
al malabsorptio
on
-Wide scalloping of lon ng bone
metaphyysis (LBM) o diffuse irregular radio
olucency
-Normal epiphysis -childhood d: -Widee scalloping of LBM
-DD: Vit D resistant rickets ometphyyseal cupping -Shortt long bone
owide zo one of calcifica
ation -Mild scoliosis
s
-Adult: -Hypooplastic anemiaa
oLarge osssific metaph. mass -macro ocytosis
oBulbouss bowed & sho ort bones
pedics]
OSTEO
OPET
TROSIS
S
= Marb
bel Bone Disease
D
Severe Mild
R
-AR AD
-A
-Letthal -Acccidental disccovery
-Resorption rem
modeling defe
ect -Noormal life spa
an
Resorp
ption remod deling defe
ect
Osteoccalstic defe
ect
No meedullary can nal
• z bone marrow cell
• Pancytope enia
nically:
Clin
z cranial foramena remode
eling:
• Blindness
• Palsies
Patholo
ogical fracttures
PXR
R:
Dense but brittle bone
Bat sha
ape skull
Tre
eatment:
Bone marrow
m ansplantation
tra
Os
steop
poikilosis AD
D
(spo
otted bo
one)
Numerrous white
e spots all over
o the ske
eleton
Clin
nically:
White skin spots as well
Dissem nticular derrmatofibrosis
minated len
Ossteop
path
hia Stria
S ata a AD
D
(Str
riped bo
one)
Scatterred lines off increased

d density:
• Parallel to shaft of long bone
• Fan like in n pelvis
No ttt
[Pedia
Meelorrrheo
osto
osis
(Leri's ca
andle bone
e disease)
Rare no
on familial condition
Clin
nically:
Usuallyy 9y is the age
a of pressentation
actures Æ deformities
Soft tisssue contra d s Æ recurre
ent
Usuallyy one limb (but be alll 4)
Limb Length Disccrepancy iss common
Thick & puckering g of skin over (Wood
dy)
PXR
R:
Hyperoostosis & scelrosis resembles
r molten w
wax runnin
ng down the
cortex::
• Periosteal in adults
• Endosteal in childrenn
Patthology:
Thick bone
b
Over la
aying fibrosis
Tre
eatment:
Soft tisssue release
e of contra
actures 00>> bracing
Corrective osteottomy for de eformities
Amputtation if sevvere & recuurrent defo ormities
OsteeoCho
ondroD
Dysplaasia AD
D
(Hereditarry Multiple Exostoses))
Most common dyysplasia

CP::
Multiplle osteocarrtilagenouss exostosess
Grow from
f Juxta
a epiphysea alregion
Away form
f joint
Stalk off bone
Cartilag
ge cap
Growth h related too bear phyysis so stop
ps at skeleta
al maturityy
Malignnant transfo ormation Æ chondro osarcoma:
- Pain
- Growth affter maturity
Tre
eatment:
Excision:
• Pain.
• Impinge a structure.
• Mechanicaal problem
m.
• Associated
d angular deformity.
d
Diaphyseal dysplasia AD
Camurati-Engelmann $
Rare
AD + sporadic mutation
Clinically:
Present in the first decade Æ lead a normal life span
Femur & tibia mainly
Painful limb
Waddling gait
Difficult walk & running
z ms & sc mass (ms weakness)
Decrease é age
PXR:
Wide diaphysis (mid shaft)
Sclerosis & thickening on both endosteal & Periosteal surfaces
Progressive narrowing of medulla
Fusiform diaphysis
z remodeling
DD:
Osteopetrosis
Melorrheostosis
Paget's
Fibrous dysplasia
Hyper phosphatasia
Myopathy
Investigations:
y ESR
ttt:
Steroids: only z pain
[Pedia
Os
Osteogen
nesis Imper
I rfecta
(Lob
bstein Vro
olik)
CT gennetic disord der with bo one fragilitty ð defect in type I coollagen

Gennetics and
d pathog
genesis:
Collage Helix (two α1 & one α2 polypep
en is a TriH ptide chain
ns)
Ch.17 isi responsible for α1 synthesis
s & ch.7 for α2
In OI there
t is a defect
d in gene
g COL1A1 ch.17 long arm that enco odes
either mutant
m α1, or only 50% of the amount
a α1 chains
The ressult is eitheer:
• 50% only of o the collaagen amou unt (OI typ pe I)
• Mutant de efective colllagen (OI types II, III,, IV)
Inh
heritance (and Shap
piro classiffication):
OI congenita A (llethal): is AR Still birrth
OI congenita B (ssevere): is AR Birth frr.
OI tard
da A (mode erate): is AD Fracture before walking
w
OI tard
da B (mild):: is AD Fracture after wa alking
Mutations can occurr also, as a dominant negative ttrait; leadin ng to the sa
ame
gene defeect
Inc
cidence:
OI I & IV
I ~ 1:35,0 000
Clin
nically (an
nd Sillence classifica
ation):
Type I A: mild éo out dentino ogenesis immperfecta
B: mild é dentinogen
d nesis imperrfecta
Type II : lethal; baby
b born SB é multip ple fracture
es (crumpled)
Type III : severe; Neonatal fractures
f
Type IVV A: Moderate
M éout
é dentin
nogenesis imperfecta a
B: Modera ate é dentinnogenesis imperfecta a
Features:
Growth h retardatiion
Blue Sclera
S (In Types I, II, III)
Condu uctive hear loss
Genera alized osteoporosis + Pathologiical fractures
Genera alized lig. la
axity
Skin: Eaasy bruisab bility, Exesssive sweatiing (hyper metabolicc state)
Skeletaal deformitiies after fraactures hea aling
Kypho oscoliosiss 40%
Basila ar Impression (fora amen mag gnum inva agination into poste
erior
cranial fossa):
• Headache e
• Facial spassm
• Bulbar sym mptoms
• Long tractts compresssion Æ paresis & hyp posthesia
Pathology (defective collagen and disturbed bone formation)

y woven bone
y bone turn over
Trabeculae are thin and disorganized
y osteocytes
Normal osteoclasts
z spongiosa
PXR:
Multiple fractures & healing with hyperplastic callus Æ deformed long
bones
Pop corn calcification in metaphysis & epiphysis Æ Whorls of
radiodensities
Mushroom shape skull
Osteoporosis
Laboratory:
Normal Ca, P
y AKP
Biochemical analysis of type I collagen (from fibroblast culture) to
diagnose mild forms
DD:
Hypophosphatasia: z AKP, y urinary phosphoryl Ethanolamine
Achondroplasia (large skull, short limbs): PXR
Idiopathic Juvenile Osteoporosis: self limiting
Child abuse: biochemical collagen testing
Treatment:
Physiotherapy to improve ms power
}
Medical ttt to improve bone quality:
1]. Sex and growth hormones
2]. Sodium floride & magnesium oxide
Doubtful effect
3]. Calcitonin
4]. Vit. D and C
5]. Bisphosphonates: may have an effect
Gene therapy is not well established
Orthopedic management:
• Protective bracing
• Closed osteoclasis & bracing
• Closed osteoclasis & percutaneous intramedullary nails
o Steinmann pins
o K- wires
o Rush pins
• Open shish kebab osteotomies & IM nailing
o Fixed length nails: rush and Steinmann
o Extensible nails: (Baily & Dubow/Nancy)
• Kyphoscoliosis: spinal fusion + auto and allograft
• Basilar impression: Anterior transoral decompression + Posterior
occiput to lower cervical fusion
[Pedia
Fib s Dysp
brous plasi
ia
Sporad
dic congennital anommaly ccc by
b malfun
nction of bone
b form
ming
mesenchyme
McCunne Albrightt $:
• Fibrous dyysplasia
• Café au lait patches
• Precociouss puberty
Clin
nically:
Progre
essive deforrmities
Café auu lait patch
hes: irregullar borderss
Recurreent pathological fracctures
Precoccious puberrty
PXR
R:
Ground glass app pearance
Cortica
al expansioon
Deficie
ent remode eling
Bowing g deformitties & fractu
ures
Shephe erd's crookk deformities of proximal femurr
Tre
eatment:
Very difficult to tttt by curettte & BG Æ usually resorb
Wide lo
ocal excisio on or radiccal excision
n
ogical # Æ ORIF
Patholo
Young children respond lesss satisfacto ory é BG
Schwarttz-Jaampell $ AD
D
(Ch
hondroDy
ystrophic
caMyoton
nia)
Clin
nically:
Myoton nia + delayyed motor function
Slow lin
near growwth Blepharrophimosiss
Myopia a
Sad flat facies
PXR
R:
Fragmentation & flattening
g of femora
al epiphysiss
Platysp
pondyly
pedics]
Kniesst Dysplasi
y ia AD
D
AD, bu
ut mainly mutations
m
Clin
nically:
Disproportionate e dwarfism
Short trunk
Flat faccies
Joints:
• Enlarged
• Stiff
• Contractures
• Early OA
Kyphosscoliosis
Atlanto o-axial insta
ability
PXR
R:
Platysp
pondyly
Delayeed ossificatiion of femo
oral head
Patthology:
Defective proteog
glycan syn
nthesis in growth
g platte
Tre
eatment:
Aggresssive
Diast
trophiic Dys
splasia
a AR
R
me Rhizom
Extrem melic dwarrfism
Clin
nically:
Marked d short statture
Several deformities
{
• Kyphosis
- Proximally sset
• Rigid TEV
- Abducted
A
• Hitch Hickker thumb - Hypermobiile
• Symphalan ngism PIP - Short 1st me
etacarpal
• Joint flexio on deformity: Elbow, hips, knee es
Cauliflo
ower ear (ccalcification of ear pin
nna)
Respiraatory RDS Æ lethal (o other wise the child survive)
Chondro Ecctodermaal Dyssplasia

(Ellis-Va
an Creveld
d $)
Ecto
odermal Dysplasia
D
-Hairs: fine
f sparce & scanty bro
ows -Chonndrodysplasiia
-Teeth: peg like rud
dimentary -Shortt limbs, long
g trunk (éin normal
n ht)
-Nails: Small
S dystrop
phic -Polyactyly (post-axial)
-Morbbus Cordis
PXR
R:
Short and
a thick lo
ong bones
Poorly developed
d distal pha
alanges
[Pedia
C
Camptom
melic Dyysplasia AR
R
(Bent limb
b)
Clin
nically:
Usuallyy die in neo
onatal deaath
Ant. Boowing of tiibia (With dimpling
d o overlying
of g skin)
Femora al bowing
Fibularr shortenin
ng
TEV
Abnorm mal: scapuula, vertebrrae, ribs
CNS de eficits
PXR
R:
Absencce of 2ry ossific
o cente
ers of:
• Distal femur
• Proximal tibia
• Talus
CCC de
eformities
A s Synndrome
Apert’ AD
D
Acrocepphalic Syn
ndactyly
Mainlyy mutationss
Clin
nically:
Skull:
• Short AP deameter
d of
o skull (corronal craniiosynostossis)
• Flat occipu ut • High
H foreh
head
Face:
• Flat • Small
S nose
e
• Hypertolerism • Strabismus
S s
• Hypoplasttic maxilla
Syndacctyly & broad distal phx. of thum
mb and G.ttoe
Visceraal organ afffection
Tre
eatment:
Craniosynostosis
Hand and
a facial plastic
p surg
gery
CleiddoCra
anial Dysp
D lasia
AD
Defect in gene CFBA1 Æ defective
d In
ntramembranous Ossificati
O ion
Clin
nically:
Hypop plasia even aplasia of clavicle
y transsverse diam meter of skkull
z fonta anelles osssification
Dental abnormallity
Delayeed or absen nt symphyssis ossificattion
Scoliossis & Syring gomyelia a
Nail Patella Syndrome AD

OsteoOnychoDysostosis
Genetically linked to ABO Blood Grouping Locus on Ch.9p
Involved family members have the same bl.group
No bl. Group predilection found
Clinically:
Delayed presentation (unless +ve family history)
Post. projectios
Pt. remain ambulatory from post. ilium
Deformities:
• Hip: Sublux, dislocation, iliac horns
• Knee:
o Genu valgum
o Flexion contracture
o Patella: Absence, hypoplasias, sublux
• Foot: Pes planus Æ TEV
• Elbow:
o Cubitus valgum
o Flexion contracture
o Radial head lateral dislocation
• Spine deformities
Hypoplastic nails more in hands
Treatment:
Mainly directed to deformities and contractures correction
Infantile cortical hyperostosis ??

Caffey's Disease
There is an inconclusive evidence for genetic transmission
3:1000
Clinically:
2-6mo is the time of presentation
Attacks in remissions and exacerbation of:
• Irritable
• Fever
• Tender bone
Investigations:
yESR & yAKP
PyknoDysostosis AR
Clinically:
Short
Frontal bossing + Triangular facies
Small mandible
Prone to fracture + Blue sclera + abnormal teeth (= Osteogenesis I)
PXR
Large skull + Open fontanelles
Dense bone (≠ OI)
Hypoplastic mandible
DD:
Osteogenesis Imperfecta
[Pedia
Thannatophoric Dyspplasia Mu
ut
(Death bringing
b Dysplasia)
D )
Clin
nically:
− severe growth re etardation
− short, bowed
b ling
g bones
− short ribs Æ narrow thoraxx Æ pulmon
nary insuffficiency
− Die shoortly after birth
b
Tre
eatment:
− supporrtive
Jeunne Tho
oracicc Dyspplasiaa AR
R
(Asphyx
xiating Dy
ysplasia)
Clin
nically:
− Short ribs
r & narro ow thorax Æ RDS of newborn Æ death
− Some ssurvive (aftter thoracicc growth)
− Ploydactyly
PXR
R:
− Thoraxx: short ribss, narrow thorax,
t irre
egular costoochondral junc
− Pelvis: Hypoplastiic iliac wing, Horizonntal acetabular roof
− Long bone:
b irregular epiphyysis & meta aph., shortt ulna & fib
bula
ort Ribb Polyydactyyly

Sho AR
R
(Majewski)
Clin
nically:
− Dwarfiism
− Polydactyly
− Narrow
w thorax Æ Pulmona
ary insufficiency Æ die
e shortly
PXR
R:
− Pre & post
p axial syyndactyly
− Short tibia, MC, & MT
− Narroww thorax & Short horizontal ribss
Connective Tissue Disorders
1- Marfan $ AD
Definition
• It is a generalized disorder in which there is hyperlaxity of the joints and ligaments
Aetiology
• Ch.15 defect; on Fibrillin gene FBN1 Æ defective Collagen & Elastin Cross Linkage
Clincally:
• Tall: Span > height; i.e. disproportionate tall limbs
• Upward lens dislocation
• High arched palate
• CVS: Aortic aneurysm, AR, MR
• Spine:
o Spondylolithesis
o Scoliosis
• LL: SCFE, Pes Planus
• UL: dislocations & arachnodactyly = spider fingers
PXR: Excessive lengthy limbs, Pes planus, SCFE, Spondylithesis, Scoliosis
DDx:
• Homocystinuria: Tall AR, MR, ms weakness, lower lens dislocation; ttt vit B 6 since birth
• Alkaptonuria: dark urine, accumulation in tissues Æ OA, disc calcification
Treatment
• Ttt of complications; Pes planus, SCFE, Spondylithesis, Scoliosis
2- Ehler Danlos AD
Definition
• Group of inherited disorders characterized by lax joints and skin ð defective collagen
Pathogenesis
• Type III: has z collagen III production
• Type VI: has z lysine hydroxylase Æ z cross linkage
• Type VII: has ch. 7 mutantation Æ α2 chain defect
Clinically:
• Ocular lens octopy
• Skin:
o Extreme laxity even in palm & sole o Wound dehiscence
o Delayed relaxation o Hyper pigmentation
o Thin & easily bruise o Pseudo tumors at pressure areas
• Periodontal Bleeding gums
• Joints:
o Hypermobility o Joint distactability if severe
o Recurrent dislocations o Effusion and hemarthrosis
• Spine: Scoliosis, Spondylolithesis
Classifications:
• Type I ............. Gravis (severe) AD
• Type II............ Mitis (Mild) AD
• Type III .......... Benign hypermobile joints AD
• Type IV .......... Ecchymotic AD & AR
• Type V ........... Skin & Joint XR
• Type VI ......... Ocular Scoiliotic AR
• Type VII......... Arthrochalasia multiples congenita AD
• Type VIII ....... Progressive periodontal AD
[Pedia
3- La
arsen
n$ AD
D
M
Multiple congenital dislocation
Clin
nically:
Facial chan
F nges:
• Hyp pertelorismm (promineent forehea ad)
• Spa aced eyes
• Dep pressed na asal bridge
e
E
Elbow, knee, hip disloocations
F
Foot: TEV, TE
T valgus
C
Cylindrical f
fingers (no
ot tapered)
A
Abnormal s
spine segmmentation & cervical kyphosis
k
y no of osssification ce
enters in wrist
w & calca
aneus
A
Abnormal p
palate
Rad
diologicallly:
U
Unusual ad
dditional osssification centre
c of calcaneus
c & wrist
Tre
eatment:
Reduction of
R o dislocatiions
• Kne ee: may ne
eed ITB & vastus
v relea
ase
• Hip p: CRUGA
• Elbbow: may need
n radiall head exciision if sym
mptomatic
F
Foot deform
mities
• Serrial manipu
ulation andd casting Æ PM releasse + orthossis
4- Myocit
M tis Osssificanns Proogresssiva AD
D
FIBROD A OSSIFICA
DYSPLASIA ANS PROGR
RESSIVA
Clin
nically: (ea
arly childho
ood)
PAINFUL ERYTHEMATOUS SUBFASCIA ALL NODULES (neck and back):
• Usu ually resolvve
• May progresss into heterrotopic bone Æ z RO OM
P
Pain, fever
S
Short big to
oe
H
Hallux valgus
Patthology:
D
Develops in
n:
• Aponeurosis
• Fassciae
• Ten ndons of neck
• Dorsal trunk
• Sterno Cleido o Mastoid
C
Cellular atyypia, and po otential maalignant ap
ppearance
e
D
Death ð pu
ulmonary complicatio ons in 3rd decade
d
Tre
eatment:
E
Early ns Æ steroid
lesion ds + pisphoosphonate e
Maroteau Morquio Sanfilippo Hunter MPS Hurler Scheie $ Hurler $
lamy MPS IV MPS III II Scheie $ MPS I
heparan
MPS VI
sulfaturia
keratan &
46 | Page
1:25,000
C
A
Glucuronidase
Name
AR AR Genetic
XR
N ac‐
sulfatase
N acetyl‐
aminidase
α-L iduronidase Enzyme
sulfamidase
Aryl sulfatase B
β‐galactosidase
glucosamine‐6‐
glucosamine‐6‐
β‐glucuronidase
sulfate sulfatase
sulfate sulfatase
N‐ acetyltransferase
N‐ac‐gal‐ 6 sulfate
α N acetyl‐glucos‐
iduronate sulfatase
Ac‐CoA glucosaminide
Heparan Urine
keratan
Heparan
Dermatan Keratan Heparan Dermatan
Dermatan excretion
chondrotine
Presentat
4y 2-4 y 1-3 y 6-12 mo 2y 5y 1y
ion time
-
Mild Severe Moderate Normal Severest MR
+
+
+ Lucoma
+
+
+
+ + Deafness
[Pediatric Orthopedics]
Inborn Errors of Metabolism
-
-
±
+
+
+
+
HSM
-
+
+
mild AR - CVS
AR
MR
1-MucoPolySaccharedosis
Gargoyle
Severe Severe Mild Moderate Late
severest Facies
&
Platyspondyly Platyspondyly Wide medial clavicle / Joint Kyphoscoliosis
Spatulated rib CFE flat Become wheel chair limitation Peaked vertebra Dwarfism
Kyphosis Coxa vara dependant Spatulated ribs &
Genu valgum genu valgum Shallow acetab Deformity
Defective glycosaminoglycans (gags) metabolism Æ accumulation Æ manifestation & urine excretion
Flared iliac wing
Tapered fingers
Is the largest lysosomal storage diseases leading to storage of intracellular degradation components
Die at 30y Normal die at 30 Normal die at 10 Prognosis

2- GAUCHER'S DISEASE AR
Definition
• Genetic lysosomal storage disorder in z glucocerebrosidase Æ y glucocerebroside in RES
cells (HSM, medullary bone)
• AR (ch 1q21)
• Commonly seen in children of Jewish descent.
Pathology: lipid-laden Histiocytes.
Classification:
• Type I: (Adult form = chronic non neuropathic form)
o CNS is spared
o Slowly progressive visceral and osseous involvement (huge splenomegaly)
o Pancytopenia Æ splenectomy is done for thrombocytopenia
o Bone pain is a common complaint, resolves after 1-2 d (ð fr/osteomyelitis/ DJD)
• Type II:
o Acute neuropathic form; fatal in 9 months;
• Type III:
o Sub acute neuronopathic; convulsions are frequent;
Clinically
• AVN femoral head (μß bilateral).................................. 'BONE WITHIN BONE' appearance
• Bone erosion of the cortices of bone ........................ 'MOTH EATEN'
• Crisis similar to Sickle Cell Anaemia ........................... Intractable pain & fever
• Dwarfism & discriasis (pancytopenia)
• Expansion of metaphyses ð z remodeling .............. 'ERLENMEYER FLASK' distal femur
• Fractures
MRI: z T2 signal in BM of long bones, vertebrae, & hips (marrow infiltrated by Gaucher's lipids)
Treatment:
• pathologic frx:
o Fr. related to pathologic weakening of skeleton, common in young children
o Frx proximal end of femur may occur in children & adults
o Best treated conservatively although there may be with some varus deformity
• bone crisis:
o Bed rest and analgesics, which is followed by crutches as tolerated
• AVN:
o no effective treatment or preventative measures
o Bed rest and analgesics Æ crutches as tolerated
o THR Æ K infection, bleeding, loosening
• enzyme replacement: is now available
3- NIEMANNPICK DISEASE AR
• Caused by accumulation of phospholipid in RES cells.
• Seen commonly in Eastern European Jews.
• Niemann Pick = Gaucher's + severe MR
4- HOMOCYSTINURIA AR
Rare disorder ð L cystathionine-synthetase Æ accumulation of homocysteine & methionine
Clinically:
Tall and thin + Features like Marfan’s
MR
Downward lens octopy
Ms weakness ≠ marfan laxity
Marked osteoporosis
Thromboembolic disease is common and may be fatal
Investigations
y Flomocysteine in the blood and urine
z enzyme in fibroblast cultures
Treatment:
Pyridoxine (vitamin B6) administered from early childhood
Others may be helped by a low methionine, cysteine-supplemented diet.
5- ALKAPTONURIA = Ochronosis AR
L Homogentisic acid oxidase Æ K homogentisic Æ K in connective tissue and urine
On standing the urine turns dark (hence the name, alkaptonuria)
Cartilage and other connective tissues are stained GREY (hence the name ochronosis)
OA
Calcification of the intervertebral discs.
6- CONGENITAL HYPERURICAEMIA XR
The LESCH—NYHAN syndrome is a rare
L hypoxantbine-guanine phosphoribosyltransferase (HGPRT) of purine metabolism
K uric acid formation and gout
Clinically:
MR
prone to SELF-MUTILATION (biting their fingers tips)
Severe early-onset gout
y HGPRT in red cell preparations
SICKLE CELL DISEASE
Discussion:
• Most common genetic blood disease
• More in blacks
• Is more severe but less common than sickle cell trait (8% prevalence)
• Crises usually begin at age 2-3 years and may lead to bone infarctions
Clinically
• AVN femoral head (μß bilateral).................................. collapsed head (DDx Perthes)
• Bone Infections:
o Osteomyelitis: often in diaphysis
o Septic Arthritis:
best treated é 3rd generation cephalosporin
Staph and salmonella are probably the commonest
o Dactylitis (acute hand/foot swelling):
Self limiting after few days or weeks
Swelling of hands and feet +z ROM + fever (ð vascular occlusion)
PXR: Small osteolytic lesions in MC & MT + Periostitis in phalanges
o Pneumococcal infections:
septicemia & meningitis Æ death; ttt: pneumococcal vaccine + penicillin
• Crisis when sickle cells Æ clogs BV +z O2 ................ Intractable pain & fever
• Dwarfism & discriasis (sickle anemia)
• Fractures
Bone Scan:
• y uptake (DDx osteomyelitis)
• Differentiate by Tc sulfur colloid instead of Tc MDP; the former has affinity to bone marrow
cells instead of HA of osteoblastic activity
Treatment
• Packed RBC transfusion to z haemoglobin S (fetal-haemoglobin) Æ < 45%
• Exchange transfusion + Erythropoietin + Expanders + adequate hydration + O2
• Avoidance of intraopeative hypothermia & hypoxia
• Tourniquet use:
o No contraindication to use of tourniquets, No complications
o ttt: varus osteotomy, Chiari osteotomy, THR.
THALASSAEMIA
• Patients are usually of Mediterranean descent
• Bone pain, leg ulceration
• PXR:
o Osteoporosis
o Distorted trabeculae
o Hair on end appearance of the skull PXR (all hemolytic anemias)
pedics]
C omo
Chro osom
me Disord
ders
s
Chro
omosome disorders
d are
e common but usually result in fe
etal abortion
n. Of the no
on-lethal co
onditions, sevveral
prod
duce bone or
o joint abno
ormalities.
1 Down’s Syndrom
me (Triso
omy 21)
This condition results from having
g an extra coopy of chrom
mosome 21
It is more common
c thaan any dysp
plasias (1:800
0) & (1:250 iff the motherr > 37y)
Clinically;
Eyes: slantt upwards, with
w promine ent epicanth hic folds
Nose is fla
attened
Abnormal palmar crea ases “Comp plete Simian n Crease”, clinodactyly
c
spreading g of the first and
a second toes
The babie es are unusually floppy (h hypotonic)
MR
Joint laxityy Æ sprains or
o subluxatioon (e.g. of th
he patella)
Adults Æ atlanto-axiall instability
Treatment:
Atlanto-axxial fusion is occasionallyy needed forr patients witth neurological symptom
ms
2 Turner’s Syndrrome
Congenita
al female hyp
pogonadism
m is a rare ab
bnormality ð a defect in one
o X chrom
mosome
Clinically;
Patient is phenotypica
p ally female Æ normal vag
gina & uteruus (but ovarie
es are hypop
plastic)
short, withh webbing ofo the neck
K carryingg angle of the elbows
1ry ameno orrhoea, andd hypogona adism Æ early-onset oste
eoporosis
Treatment
Oestrogen
n replaceme
ent from pub
berty onward
ds
3 Klinefelter’s Sy
yndrome
e
Klinefelterr’s syndrome
e, a form of male
m hypogo onadism
1:1000 ma ales
Those affeected have more
m than on
ne X chromo
osome (as well
w as the ussual Y chrom
mosome)
Clinically;
Patient is phenotypica
p ally male, bu
ut
they havve gynaeccomastia &
eunuchoid d proportionns
underdevveloped testiccles
Osteoporo osis in men
Treatment
Androgen
ns may imp
prove bone
e
mass.
Localized Malformations
Vertebral Anomalies
(1) Agenesis, with total absence of vertebrae
(2) Dysgenesis, é hemivertebrae, or fused vertebrae (sometimes called errors of segmentation)
(3) Dysraphism, with deficiencies of the neural arch e.g. spina bifida.
Klippel—Feil $: .............................................................. see spine
Limb Anomaly
Amelia ........................................................................................ Complete absence of a limb is called,
Phocomelia .............................................................................. almost complete absence (a mere stub remaining)
Ectromelia ................................................................................. Partial absence
o The embryonal limb buds appear ................ 26th day of gestation
o Segmentation into arm, forearm, hand...... 30th day
o Embryo has a recognizable form ................. 6th week
o UL & LL are fully formed ................................... 12 - 14 week
o Nerve & ms are fully formed ........................... 20th week & joint movement is possible
o Most of the malformations involving limb reductions are ð embryonal insults between 4-6 wk
o Some are genetically determined ................ AD
CLINICAL FEATURES
Sprengel’s Deformity ............................................ See Shoulder

Pseudarthrosis of The Clavicle .................... See Shoulder
Transverse Deficiency of The Arm
Transverse deficiency of the distal part of the arm will leave a simple stump below a normal
elbow. This can be ttt by fitting a prosthesis é a mechanical facility for grasp.
RADIAL DEFICIENCY
Absence Or Hypoplasia of the radius may occur alone or in association with visceral anomalies or
(more rarely) certain blood dyscrasias. Sometimes the thumb is missing too, and the elbow is often
abnormal. In about half the cases the condition is bilateral.
The forearm is short and bowed; the hand is underdeveloped and markedly deviated towards the radial
side (radial club hand). In some cases the thumb is absent. Usually the function requires no surgery
Madelung’s Deformity .................................. see hand and wrist
ULNAR DERCIENCY
Hypoplasia of the distal end of the ulna is usually seen as part of a generalized dysplasia, but
occasionally it occurs alone. Radius is medially bowed (as if growth is tethered on the ulnar side) and the
radial head may dislocate; the wrist is deviated medially.
Only if function is severely disturbed should wrist stabilization be advised
Congenital Absence of the ulna is extremely rare. The forearm deformity is not as marked as in radial
deficiency but overall function is severely restricted. Operative reconstruction may improve ! Condition
Digital anomalies .............................................. see hand and wrist
Proximal Focal Femoral Deficiency: .......... see later
Congenital Tibial Pseudarthrosls ............... see later
Tibial & fibular hemimelias .............................. see later
pedics]
Syn
nostosis
Thee various tyypes of inteerosseous fusion
f (rad
dioulnar, tib
biofibular, carpal or ttarsal) are discussed
d in
the relevant chapters.
c Thhey rarely cause sign nificant disa
ability, exce
epting tarssal synosto osis (which
mayy be associiated with spastic flatt foot) or raadioulnar fusion
f which limits foorearm sup pination (a
con
nsiderable disability
d iff both foreaarms are affected). Inn spastic fla
at foot, diviision or rem
moval of thhe
bonny bridge may
m improvve symptoms. Radiou ulnar fusionn resists anny form of operative mobilizatio on,
beccause of the associate ed soft-tissu
ue involvemment. How wever, the bones can n be osteotomized an nd
rota
ated to leavve the han nd in a morre function nal positionn.

Sw
wanson Classifi fication of Congenital Anoma alies
1]. Failure
e of formatiion
a.Traansverse arrrest
b. Lo ongitudina al arrest
2 Failure
2]. e of differen ntiation (se
eparation) of parts
c. Sofft tissue invvolvement
d. Skkeletal invo olvement
3 Duplica
3]. ation
4 Overgrrowth
4].
5 Underg
5]. growth
6 Constriiction ring syndrome
6]. e
7 Genera
7]. alized abno ormalities and
a syndro omes
A
Anomal
ly
Transverse Lo
ongitudinal
Terminal Terminal
- Amelia - Paraxial
P hemim
melia (absent leg element +
- Hemimelia
a hand part)
- Apodia/A
Archeiria
Intercalary: Inteercalary:
- Phocomellia (hand is attached to
o - Paraxial
P hemim
melia (one leg
g or FA bone
trunk) is ab
bsent)
- PFFD
[Pedia
G
Gait Abn
nor
rmalitie
es
Abnorm
mal Gait
Osteopath
hic Neuropathiic
Con
ngenital Devvelopmental Traumatic Infection Congenital Traumatic Inflammtorry Degenerative Endocrinal
Myopathic Hystrical
Con
ngenital Trraumatic Infflammatory Idiopathic
1]. Osteop
pathic:
o Congenita al: dysplasia as, malformmations
o Developm mental:
DDH H
Miseerable mala alignment $
o Traumatic:
nful spains, strains Æ antalgic giat
Pain
Nonn united fracture neck femur
Malunited fracttures & defo ormities & limb
l length discrepenccies
o Infections::
Pain
nful
Postt infection stiffness
s
2 Neurop
2]. pathic:
o Congenita al:
CP
Atax xia: Friedricch’s, Refsum
m (HMSN IV))
Spin
nal ms atrop phy
o Traumatic nerve inju uries:
Commmon peroneal n. injury
Scia
atic n.
o Inflammattory:
Poliomyelitis
Tabbes dorsalis
SLE neuritis
o Degenrative
Guiallan Barre $
Amy ytrophic Lateral Sclerosis
o Endocrina al DM
3 Myopa
3]. athic:
o Congenita al myopath hy:
Ducchenne, Beccker
Limb Girdle dysstrophy
o Traumatic
e.g. Tendoacille es avulsion
o Inflammattory:
Myaasthenia Gra avis
o Ideopathic c:
Afte
er arthropla asty ð muscle excessive manipulatiion ± n. inju
ury
Myoocitis ossifica ans
Approach to a limping child
• Assess LLD
• Check foot for injury , infection, arthritis
• Check knee for swelling, tenderness, instability
• Check hip for arthritis, dislocation, Transient synovitis, Perthes’, tumour
• General assessment for non accidental injury
Causes of a Limping Child:
1. Short Leg Limp
o Difficult to discern at maturity If discrepancy is less than 2cm
o There is pelvic tilt, short leg ankle equinus; and hip & knee of long leg in flexion
2. Antalgic Limp
o Stance phase shortened
o More gentle heel-strike in painful limb
3. Trendelenburg Gait (Unstable Hip Limp)
[1]. Fulcrum - DDH
[2]. Lever - short neck
[3]. Motor - gluteus medius weakness e.g. polio, OP
4. Stiff Hip Gait
o Increased motion of pelvis on lumbar spine during swing
o N.B.- limp minimal if hip stiff (fused) in 25o flexion
5. Stiff Knee Gait
o Pelvis raised during swing phase so heel will clear floor
6. Gluteus Maximus Weakness
o Hip In hyperextension so centre of gravity behind joint
7. Quadriceps Weakness
o ‘Back Knee’ gait - knee locked in hypertension during stance phase
o Lurching more marked if also weakness of glut max.
o May place hand on thigh to assist
o Difficulty with stairs
8. Calf Weakness - Calcaneus Gait
o Poor push-off due to calf weakness
o ‘Hitch’ at each step
9. Tibialis Weakness – High steppage gait (drop foot gait)
o Weakness of pre - tibial muscles
o Increased flexion of hip and knee to allow ground clearance Æ y heel rise
10. Spastic Gait - Cerebral Palsy
o Many patterns - hemiplegia, diplegia
o Value of gait analysis; short step, unsteady, failure of foot clearnce at swing
11. Shuffling Gait
o In parkinsonism; gait is short, é out lifting one’s feet
12. Stamping Gait (Double Tap)
Proprioception or dorsal column affection; DM & tabes dorsalis
o
Patient does not feel the ground Æ y heel rise & strike + wide base + looks at the ground
o
+ve Rombergism
o
13. Ataxic Gait (Cerebellar Ataxia)
o Wide base (Feet apart)
o Tremors and nystagmus
o –ve Rombergism
14. Hysterical Gait
o Diagnosis by exclusion & history of emotional upset
o Bizarre and inconsistent é CP
Pediatric Hip Problems

DDH
• The term “CCONGENITAL HIP DYSPLASIA” was introduced by HILGENREINER IN 1925. It is a term
denoting delayed or defective development of the hip joint.
• HIP DISLOCATION” refers to non contact of the acetabular and femoral cartilages
The term “H
• The modern term DDH “D DEVELOPMENTAL DYSPLASIA OF THE HIP” realistically indicates a wide
spectrum of pathologic conditions, ranging from subtle acetabular dysplasia to irreducible
hip dislocation .There is a spectrum of disease severity from mild dysplasia with slight
acetabular sloping, to the most severe form of congenital hip dislocation.
Epidemiology
• The incidence DDH ~ 1:1000 live births.
• The most common is left hip > bilateral involvement > right hip alone
• More with +ve family history 10%.
• Breech delivery.
• ♀:♂ Î 8:1.
• 2/3 are 1st born.
• More with congenital torticollis, metatarsus adductus, and TEV.
• Racial more in white race.
• u in cultures that place infants in swaddling clothes with ! hip in constant ext.
• Most dislocations occur during the first 2 weeks of life. Occasionally, DDH is diagnosed as
late as 1 y in a child é prior documented normal hip
Anatomy of Normal Hip Joint
• Synovial joint of the ball and socket variety.
• Stability is due to adaptation of the acetabulum and femoral head.
• Wide range of movement is due to a relatively narrow neck is the.
• The triradiate (Y) cartilage is located at the acetabular center
• The three components of the acetabulum are:
o Superior two-fifths composed of ilium
o Inferolateral two-fifths of ischium
o Medial one-fifth of pubis.
• The labrum & transverse lig. Æ complete ring deepening the acetabulum.
• The cavity is filled by cartilage and a Haversian pad of fibro-fatty overgrowth.
• Normal acetabular growth and development occur through balanced growth of the
proximal femur, the acetabular and triradiate cartilage, and the adjacent bones.
• Implanced growth Î DDH.
• Femoral head growth rate is more rapid in early life Î then growth decline occures in the
head & acetabulum. This decline explains the failure to achieve femoral head coverage by
shallow acetabulum often over 18 months age.
Development of the Hip Joint:
4 weeks:
: Mesenchymal limb buds (from blastoma central mass) begin on anterolateral body wall at
lumber & sacral segmentsÎ differentiate to cartilage, bone, synovium …etc
6 weeks:
: blastoma condenses to form the cartilage hip model. The primitive chondroblasts Î
differentiate & secretes matrix material.
In older embryos:
: The joint space forms along the femoral head periphery, gradually extending centrally Î
acetabulum separates from the femoral head.
: Head coverage is max. at 12 wks.
: Acetabular depth , but its coverage to the femoral head ↓.
: Femoral head represents 80% of sphere.
At birth:
: The acetabulum represents of a sphere.
: Femoral head represents 50% of sphere
: head coverage = the minimum of 65% Î y gradually until development ceases.
Later:
: The femoral head Î relatively uncovered during the early years of growth.
: CE (center-edge) angle Î y with time from 22º to > 30º at maturity.
: Roof slope z é time ð ossification of roof & change of acetabular orientation
Ossification around the hip joint
• At birth both the acetabulum and the proximal end of the femur are cartilagenous.
• yorz femoral head pressure as in DDH Î delayed 2ry center ossification Æ more dysplasia
• Intact ossific nucleus may protect the head from compressive ischaemia during reduction
• Delayed ttt Î z acetabular remodeling necessitating reconstructive procedures.
PRIMARY OSSIFICATION:
Ossification of pelvic bones occurs by 3 1ry centers for ilium, ischium and pubis
• the iliac appears ..............................2 mo above the greater sciatic notch.
• the ischial appears ...........................4 mo in its body.
• the pubic appears............................6 mo in superior ramus.
SECONDARY OSSIFICATION
Hip centers appear about puberty and join between the 15th & 25th y.
• iliac crest ............................................2 centres fuse at 21y
• triradiate cartilage ..........................5 centers fuse at 14y
• articular acetabular surface .........3 centers
Proximal femur has 3 centers of ossification:

• head ....................................................3 mo.
• greater trochanter ...........................3 y
• lesser trochanter .............................13y
Factors affects normal concentric reduction
T
he capital femur needs a certain degree of congruency with the acetabular articular surface
to develop the normal spherical state. The concentric disposition of the femoral head in the
acetabulum is important for normal growth of the hip joint of the newborn or dysplasia of
the hip occurs.
1. Acetabulum:
• z Depth.............................................. y DDH
• y Inclination .................................... y DDH
• y Anteversion ................................. y DDH
2. Femoral neck:
• y neck shaft angle ......................... y DDH
• y anteversion .................................. y DDH
3. Stability Index:
• femoral anteversion + acetabular anteversion > 60º (! upper level of ! normal).
• If stability index > 60º .................... y DDH
4. Morphology & consistency of the Peri & intraarticular soft tissue:
• Intact labrum ................................... z DDH
• The ligamentum teres ................... z DDH
• Intact capsule .................................. z DDH
• Intact pelvifemoral ligaments ...... z DDH
Etiology of DDH:
A. Simple Ligament laxity:
• Generalized joint laxity of familial or hereditary type is present in a high proportion of
children suffering from DDH.
B. Hormonal Factors:
1]. 2nd trimester MATERNAL estrogens+progesteron u
2]. 3rd trimester FETAL ADRENALS estrogens+progesteron u
3]. estrogens+progesteron ⊕ FETAL FEMALE UTERUS Î relaxin.(DDH is > in ♀)
4]. ESTROGENS+PROGESTERON+RELAXIN Î u fetal ligaments laxity.
C. Mechanical factors
1]. BREACH presentation
The gluteal musculature is often damaged by hge during delivery and

this may be an additional factor in the causation of dislocation
2]. OLIGO-HYDRAMNIOS
3]. PRIMIGRAVIDA tight uterine and abdominal wall (56% of DDH are PG).
4]. LOA position .................................................. y pelvic obliquity & lt. hip adduction Æ u left. DDH.
5]. y ANTEVERSION Of Neck & Acetabulum.
6]. SHALLOW ACETABULUM
7]. SHORT ILIOPSOAS Tendon.
8]. EXTEREME positions and motions:
a. Extreme flexion ................... sublux over the posterior acetabular rim.
b. Extreme ER ........................... sublux anteriorly.
c. Extreme add. + flexion...... lateralization of head vs. posterolateral rim
D. Genetic & Familial Factors:
• More with +ve family history 10%.
• 2nd child chance to develop DDH is 10 times more
N.B. gestational periods during which DDH occur:

- 12 wk during the limbus formation
- last 4 wk of fetal development: (mutifactorial)
• Hormonal
• Breach
• Mechanical
Pathogenesis of DDH:
• Genetic message + biomechanical stress Î affect growth cells Î Changes in the contour of
the upper femoral growth plate.
Laxity and other PDF
Subluxation
If laxity permits
+ Tight Iliopsoas Altered Biomechanics of hip
z head stressed z congruency over the acetabulum

Altered superior physeal stresses
more
Short Neck z cup remodeling
Coxa Valga
Dysplasia
• In utero: The sequence of events goes on in the way of production of dislocation where a
primary laxity of the capsule permits the flexed hip to subluxate. Once the head is
subluxated a degree of dysplasia will be present at birth.
• At birth: Spontaneous tendency occur for the capsular laxity to diminish and for the hip to
become stable. This tendency is opposed by a variety of additional factors of which the
most potent is the LEVERING ACTION OF THE SHORT ILIOPSOAS muscle. This mechanism is
potentiated by the acetabular or femoral anteversion & by any dysplasia which may
develop. Upon the balance of all these factors the fate of the hip depends.
Pathological Changes in DDH:
1. Bony Changes:
A. Changes In The Acetabulum:
I. The lateral acetabular epiphysis:
1- At first the limbus is flattened antero-superiorly
2- Inverted limbus once the dislocation occur
3- Degenerative tears ð abnormal movement across the limbus
4- Delayed acetabular ossification ð destruction Æ more dysplasia
II. Acetabular anteversion

• y In DDH ......................................................... 23º (N ≈ 17º)
III. Acetabular Index (Hilgenreiner Angle):

• y In DDH ........................................................ >30º (N; <30º)
• Also, y acetabular angle (inclination) .... >60° (N; <60°)
IV. Coverage and congruence:

• COVERAGE = extent of the WB area of the acetabulum.
o z head coverage Î ↓ load-bearing areaÎ u OA.
• CONGRUENCE describes fit of the femoral head to the acetabulum.
1. SPHERIC CONGRUITY Is ! normal relationship in DDH Î
Redirectional osteotomy.
2. SPHERIC INCONGRUITY In CP dysplastic hip (uacetabular curvature radius) Î Periarticular
osteotomy (Pemberton), or later é shelf.
3. ASPHERIC CONGRUITY After head shape change e.g. AVN complicating DDH Î Shelf or
Chiari.
4. ASPHERIC INCONGRUITY Is the worst relationship in which the head flattens and the
acetabulum, with less remodeling capability, remains more or
less spheric
B. Changes In The Upper End Of The Femur:
1. The femoral head:
• Small
• Flattened
2. Neck and upper femur
• Short neck.
• Posterior displacement of the greater trochanter.
• Tight isthmus.
• y NECK SHAFT ANGLE ..................................... valga or vara (normally 145º-150º at birth)
• y ANTEVERSION ANGLE .................................. 35-85º (N; at birth 35º-40º & z till reach 15º)
3. Changes in the bones of the leg:
• The bones of the leg may be either shorter or longer than the other limb ≈ ½" - ¾"
2. Soft Tissue Changes:
A. Changes In The Capsule:
• LAXITY at first
• THICKENED
• ELONGATION and migration with dislocated head
• ADHERE TO THE ACETABULUM and may obliterate it in long standing cases
• hip capsule may have an HOURGLASS configuration
B. Changes In The Muscles:
• The iliopsoas tendon is directed posterolaterally on the capsule (instead of passing
downwards with a slight inclination backwards)
• The hamstring, adductor, and quadriceps muscles Î shortened.
• The abductor mass with proximal migration Î horizontal orientation & shortening.
• The horizontal group of muscles Æ are directed up and backwards to reach GT
C. Changes In The Nerves And Vessels:
• SCIATIC n. is shortened and vulnerable to injury if limb-lengthening is attempted.
• The FEMORAL N. & PROFUNDA FEMORIS A. Are at u risk of injury (their course is altered)
D. Changes In The Ligamentum Teres & Transverse:
• LIGAMENTUM TERES .................................. hypertrophied and sometimes absent.
• LIGAMENTUM TRANSVERSE ....................... ossified.
• The ACETABULUM cavity ........................ filled é fibro-fatty overgrowth of HAVERSIAN pad
Dunn Classification of pathological changes:
Type I: positional instability (subluxatable)
Marginal acetabular changes
Measurements beyond its standard deviation
Joint laxity
If not detected
Type II: Sublimed (subluxation)
Everted limbus
Progressive loss of head spherity
TypeIII: Dislocated If not treated

Postero-superior dislocation
Everted limbus
Elongated lig.teres
Hour glass capsule
False acetabulum
Flexion & add.contractures
Dysplasia of anterior acetabulum
y FAV (ð incongruity and dislocation)
pedics]
DIAGNOSIS
A. Clinical P
Preseentatiion
1. I
In newb
borns (u
up to 3 m
months)):
Orrtolani te
est and Barlow maneuv
ver:
• BARLOW’S PROVOCATIVE MANEUVER of is a test for dislocatable
d e
hip; whilee the hip is flexed 90°9 in add duction the e examine er
gently sta
abilizes infa
ant’s left hip and places left ha and around d
right thigh and inde ex and mid ddle fingerrs over gre eater troch h.
Back ward d pressure and outw ward thumb b pushh Æ palpable and a audible clunck
• ORTOLANI test is a teest for dislo
ocated hip p; again wh hile the hip is flexed
d 90° gentle abductioon +
press on GT
G anterio orly by the middle fin nger to red duce the head
h Æpallpable &auudible clun
nk of
reductionn of head innto true accetabulum.
• Less than 2% of infaants will haave a +ve Barlow
B test;
o 60% will normalize
n é
éout ttt afte
er 1 mo.
o 88% will normalize
n é
éout ttt afte
er 2 mo.
• After 3 months Î z abductio on is the most
m reliable
e clinical (B
Barlow andd Ortolani are not do
one;
as they tu
urn negativve any wayy) & US is th he most re eliable test ever done
• DUNN thre ee Stages of
o Subluxattion:
o I Subluxxatable (Ba arlow sugg gestive)
o II Disloca atable (+ve e Barlow)
o III Disloca ated (+ve e Ortolani)
2. C
Child 3 to 8 mo
onths of age:
1- z ABDUCTION Off The Disloc
cated Hip
2- ASYMMETRICAL SKIN FOLDS (N
Not Alwayss).
3- The G
Galeazzi Sign:
S The Femoral Head Beccomes Displaced
Proximmally Î Ap hortening ( Bilateral Dislocation
pparent Sh ns May
Appea ar Symmettrically Abn
normal).
4- KLISIC Test: Plaace The Middle Finger Ove er The Greater
G
Trochanter, And The Ind dex Finger On The e ASIS. No ormally
Imaginnary Line Drawn
D Bettween The
e Two Fing gers Pointss To The
Umbillicus. In DDH,
D The Trochante
T r Is Elevatted And TheT Line
Projeccts Halfwayy Between The Umbiilicus And The
T Pubis.
3. C
Child off walkin
ng age:
1- z ABDUCTION the e hip during diaper changes.
2- WADD DLLING type of
o gait.
3- TRENDELENBURG GAIT + TRENDELENBURG sign.
4- Slight SHOTENING of the affeected side.
B. Imaging
1. Conventional Radiology
• The femoral head is not ossified at birth Îit is not visible on standard films.
• DELAYED APPEARANCE OF THE HEAD OSSIFIC CENTER (N; 3-6mo) Î indication of DDH
• Femoral neck is used ascertaining this relationship.
a. Anteroposterior (AP) View:
• Although roentgenograms are not always reliable in making the diagnosis of DDH in newborns,
screening roentgenograms may reveal any acetabular dysplasia or a teratological dislocation. By
time the soft tissues become contracted, & the roentgenograms become more reliable and
helpful in the diagnosis and treatment.
Figure Roentgenographic signs of DDH:

1]. HILGENREINER line.
2]. PERKINS line.
3]. Quadrants (formed by lines 1 and 2).
4]. Acetabular index (KLEINBERG&LIEBERMAN).
5]. Broken Shenton line & Calve’s line
6]. Upward displacement of femoral head.
7]. Lateral displacement of femoral head.
8]. U figure of tear-drip shadow (Kohler).
9]. Y coordinate (Ponseti).
10]. Capital epiphyseal dysplasia:
a. Delay of ! head ossification center.
b. Irregular maturation of ossification center.
c. Acc. Ossification centre 60%
11]. Bifurcation: (furrowing of acet.roof-Ponseti).
12]. Hypoplasia of pelvis (ilium).
13]. Delayed fusion (ischiopubic juncture).
14]. Absence of shapely, defined, well-ossified acetabular
margin, caused by delayed ossification of cartilage of
roof of socket.
15]. Femoral shaft-neck angle.
16]. Adduction attitude of extremity.
17]. Development of epiphyses of other joints.
18]. Radiolucent acetabular roof, limbus, joint capsule (arthrographic studies).
19]. Pseudo acetabulum.
20]. Bilateral DDH.
1.Delayed appearnce of head occific centre
2. The Hilgenreiner line (Y-line)

• Line through the superior part of the triradiate cartilage
3. The Perkins-Ombredanne line
• Perpendicular line to the Y-line at ! most lateral edge of ! ossified acetabular cart.
• Intersection of this line é the Y-line Æfour quadrants.
• Normal medial aspect of ! neck or the ossified head falls in the lower medial quadrant.
• Subluxed if they fall in the lower lateral quadrant
• Dislocated if they fall in upper lateral quadrant
4. The acetabular index (Hilgenreiner angle)
• angle formed by a line tangent to the acetabular roof & the Y-line.
• cannot alone be diagnostic of dysplasia
• values > 30º Î impending dislocation.
• There is reference graph with mean and standard deviation for each age group.
o 1y: 30°
o 1-3y: 25°
o >3y: 20°
5- The Andrén-Von Rosen line
• Drawn on PXR in abduction 45º & internally rotated, describes
the relationship of the longitudinal axis of the femoral shaft to
the acetabulum.
6- The Shenton-Menard line
• smooth arc through ! medial aspect of the neck & ! superior
border of ! obturator foremen.
• subluxation or dislocation of the hip Î interrupted line.
7- The Calve’s line:
• It is the counter part of the shenton’s line but it is drawn on the superior neck and the iliac
bone
8- The Center Edge Angle of Wilberg (CE Angle)
• Determination of this angle is most useful after full ossification of ! head, since its
relationship to the acetabulum is then fully established.
• It is the angel between the line from the head centre (C) and the acetabular edge (E) and
the vertical line
• Normally ...................................................... 35º (25º-45º).
• In DDH ........................................................ 7º.
9. Teardrop Configuration
• This configuration outlines the shape of the medial wall of the acetabulum.
• Normally ..................................................... biconcave.
• In dysplasia with subluxation .............. triangular, small, or may be absent
10. Lateralization of the head
• The shortest distance between the medial edge of the head & the ilioischial line (y
acetab.thickness, y head size, soft tissue obstruction)
11. Cranialization of the head
• Cranialization is distance of the inferior edge of ! head & acetabulum.
• Preoperatively Lateralization and cranialization are compared é the opposite side
• Postoperatively are compared with the measurements obtained previously
12. Degenerative arthritis (in neglected cases)
Presence of OA before surgery and at regular follow up is graded according to the following
criteria:
: G 0: Absence of osteoarthritis.
: G I: y sclerosis zone + minimal osteophytes + slight narrowing (< 1 mm).
: G II: < 50% loss of joint space + cyst formation.
: G III: >50% (<1 mm) + additional finding of progressive OA.
ry
´ Earliest sign of 2 OA in DDH ..................... laterally based U sclerosis at acetabular roof (NBF)
´ u Pressure Æ reinforcement trabeculae fail ........ microfracture & bone cysts.
´ uu pressure localized to lateral margin ..... acetabular rim fr.
´ uuu pressure ..................................................... OA + joint narrowing.
b. Lateral View (False-profile view):

• Is taken with the patient standing and 65º oblique
• ANTERIOR CENTER-EDGE ANGLE provides useful information about
anterior cover .The angle is composed of a vertical line through
the center of the head (line VC) and a second line through the
center of ! hip & ! foremost aspect of the acetabulum (line CA).
o anterior C-E angle ..............................> 25º as normal
o 20º - 25º ................................................borderline
o < 20º .......................................................DDH
c. Abduction-Internal Rotation View:

• This is an AP with Abduction-Internal Rotation maneauver.
• expect the coverage and congruence of the hip after redirectional osteotomy.
• If the congruous hip becomes incongruous in the AIR view Î redirectional osteotomy is
contraindicated.
Race & Herring Criteria

FOR SATISFACTORY REDUCTION:
1.Shenton's line ............................................Intact
2.Von-Rosen line ..........................................directed to centre of triradiate cart.
3.Lateralization difference ........................<2mm from the other side
4.Clinically stable ..........................................does not need extreme positions for reduction
5.z Acetabular index ..................................< 25° (1.6° / month)
6.y CE angle ..................................................>20°
7.No AVN
Last three means that the ttt is satisfactory and hip is considered cured
2. Arthrography:
Advantages
1- D IAG NO SIS
2- Assess the LIMBUS size and if it is inverted or not
3- Assess the acetabular CARTILAGINOUS COVER of the head.
4- Detect the soft tissue OBSTACLES FOR REDUCTION
5- HOUR-GLASS APPEARANCE (stretched capsule + inverted limbus +constrecting iliopsoas)
6- When performed UNDER FLUOROSCOPY, it becomes a dynamic study
Disadvantages
• Its invasive nature
• Requirement for anaesthesia
Technique
: Insertion of 22-gauge spinal needle one fingerbreadth lat to femoral a.& inferior to ASIS
Normal arthrogram of the neutral Arthrogram of ! right hip in a 1 y girl é cong. subluxation of !
position right hip 5 mo old boy. hip shows ! typical displacement of the hip lateral to but below
the acetabular labrum.
3. Computed Tomography
• Useful in the POSTOPERATIVE ASSESSMENT OF REDUCTION. In contrast to routine roentgenography,
a cast does not alter the image of an axial CT scan
4. Magnetic Resonance Imaging (MRI):
Advantages:
1- It is non-invasive, high resolution, and multiplaner images
2- Assess the SOFT TISSUE condition; the cartilage, the limbus, the capsule, the tendons
3- Assess the DETAILS OF ACETABULUM (cartilage thickness, shape, limbus)
4- detect OBSTACLES FOR REDUCTION
5- MRI can demonstrate areas of AVN.
6- GADOLINIUM ENHANCED MRI may give better images to assess the cartilge & Pulvinar
7- OPEN CONFIGURATION MRI SYSTEM:
o Achieves dynamic imaging Î analysis of bone & soft tissue
o MRI guided reduction
o MRI-guided surgical procedures. ÎAdductor tenotomies & psoas tenotomy &
limited open reduction.
5. Ultrasonography:
• Child is put in LATERAL DECUBITUS to get the CORONAL PLANE FOR EXAMINATION
Advantages:
1]. US is the best early Diagnostic & Prognostic tool
2]. Best Screening test
3]. Real-Time techniques
4]. Multiplanar evaluation
5]. Non invasive
6]. Non Irradiating
7]. Assess Development & Stability & Relationship of the hip components.
8]. Evaluate soft-tissue Obstacles for reduction (inverted limbus)
9]. Assess the Cartilagenous Head Coverage
10]. Assess PAVLIK success even during it is worn; if > 7-14 d <20% coverage = eventually will fail
11]. The GRAF α & ß angles:
¾ α angle is made between a the vertical iliac line & the acetabular roof line
¾ ß angle is made between the vertical iliac line & the abductors line (= reflect the labrum)
¾ y α & z ß = y coverage = z dysplasia.
Graf Classification α β
I >60º <55º
II 43-60º 55-77º
III <43º >77º
IV Dislocation (Unmeasurable)
12]. SUZUKI Classification:

¾ Type I: .............................................. lateralized head
¾ Type II:............................................. rests on post. rim
¾ Type III: ........................................... Behind acetabulum
13]. MORIN INDEX: depend on the head coverage

¾ Covered (d)/Total (D) >58% .... Normal
¾ Covered (d)/Total (D) < 33% .. Abnormal
TREATMENT OF DDH
T he treatment of congenital or developmental dysplasia of the hip is age related and five
treatment groups related to age have been designated:
(1) Newborn Î 0-6 mo of age.

(2) Infant Î 6-18 mo of age.
(3) Toddler Î 18-36 mo of age.
(4) Juvenile Î 3-8 y of age.
(5) Adolescent Î 8-12y of age.
(6) Teenage Î 13-19y of age.
DDH
Diagnosed Untreated
Early
ORIF +
capsulorrhaphy +
Abduction Pavlik Pelvic osteotomy
Spica 6wk Harness +
ORIF/GRUGA Residual <3y >3y

± Tenotomy
<2y Congruent Incongruent ± VDO ± VDO

shortening
osteotomy
2-8 y 8-14 y >14 y < 8y >8y
(Acet can remodel) (Open triradiate) (closed triradiate)
Salter / Steel / Steel / Salter Chiari /

Dega/ Dega/ Ganz Shelf /
Pemberton Pemberton ± Fusion /
±VDO / ± VDO VDO THR
Nonoperative Treatment:
1. Newborn (birth to 6 months of age):
TYPES:
Harnesses
Secure Restraints Simple positioning
Freyka pillow / triple diapers / Craig splint
PAVLIK HARENESS:
Consists of:
1]. 2 Abdomen strap + 2 shoulder harness + 2 leg stirrup + 2 posterior straps + 2 ant.straps
2]. Posterior strap limits the adduction (dislocation)
3]. Anterior strap adjusts flexion > 90° so the head moves form a sup. to postero-inferior
position éin acet.
Indications:
1]. +ve Ortolani or Barlow test 0-6 mo.
2]. Mild-moderate adduction contracture.
Contraindications:
1]. -ve Ortolani test.
2]. If a teratological dislocation is present
3]. After 9mo of age.
Advantages:
1]. Success rate of 85-95%.
2]. Allow motion during wearing(zAVN)
3]. Hip remains reduced é motion
4]. Hip remains éin safe zone of reduction
Disadvantages:
1]. ¾ Pavlik success rate é ½ age + ½ contracture + ½ 2ry acetabular changes.
2]. AVN head if posterior straps used for abduction
Prerequisites & follow up:
o Good abduction range is required (may need add.tenotomy; usually in babies > 3m)
o The Barlow test should be performed in Pavlik to ensure stability
o Child is then placed prone & palpate GTs; if asymmetry Æ persistent dislocation
o Clinical or PXR assessment is essential to evaluate carefully before ttt:
Reducibility of the hip.
Stability of the hip.
o If dislocation persist > 3-6 wkÎ Pavlik is discontinued & consider other ttt modality
Duration of treatment:
o Pavlik is worn full-time till stability is attained (-ve Barlow & Ortolani tests).
o Remove Pavlik for 1-2hr/day; this time is doubled/2wks until it is worn only at night
o Follow up 1-2/week:
Adjust the straps to accommodate growth.
PXR or US assessment for the success of the treatmnet
o Mean time for pavlik use (including the weaning time) depend on age of presentation:
3mo duration: <1mo age
6mo duration: 1-3mo age
9mo duration: 3-6mo of age
Operative treatment:
2. Infant (6 to 18 months of age):
• Once a child reaches crawling age (approximately 4-6 mo), success with the Pavlik harness
significantly ¾Î Treatment in this age should follow a standard regimen:
A. Preoperative Traction:
• The aim is to bring the head down to the level of the true acetabulum for more gentle
reduction
• The role of preliminary traction:
o ¾AVN.
o improve reduction.
o Whether home or in-hospital traction.
o The amount of weight that should be used. Controversial.
o The most beneficial direction of pull.
o The duration of traction.
B. Adductor Tenotomy:
• Percutaneous adductor tenotomy: for mild adduction contracture
• Open adductor tenotomy: if adduction contracture of long duration
C. Closed reduction:
• AIM is concentric reduction Æ normal hip development and resolution of the dysplasia
• Gentle CRUGA followed by clinical & radiographic assessment for stability if not Î OR
• OBSTACLES include: ilio-psoas tendon, Pulvinar, contracted inferomedial capsule, lig. transverse
• PXR or arthrograms to ensure anatomical reduction
• FOLLOW-UP : Clinical & PXR is essential till cure
• CT is useful in the postoperative assessment as cast does not alter its image
D. Open reduction:
• INDICATION: Failed CRUGA and not related to a certain age
• APPROACHES: Anterior, Anteromedial, Medial.
• During OR:
• Test of stability during OR can help to decide further osteotomy (pelvic, femoral or both)
• Reconstructive surgery should be done at the time of OR or 2-4 wks later
• If stable reduction in ! position of wt-bearing at ! time of OR Î No immobilization, no orthosis,
early mobilization once ! tissues & osteotomies heals.
E. After Treatment for either which

9]. Hip Spica In The RAMSEY SAFE ZONE Of Abduction 6wk-6mo followed by
10]. Pavlik for 3weeks
“ S af e Z o n e ” C o n c e pt O f R am s e y
To determine the zone of abduction in which
! head gonna be immobilized, determine the
extreme limits for dislocation & reduction and
stay 10-15º less than these degrees
• A wide safe zone (20-45˚) is desirable.
• Narrow safe zone = unstable CR.
3. Toddler (18 to 36 months of age):
• For these children with well-established hip dysplasia, OPEN REDUCTION + OSTEOTOMY (femoral
/pelvic/both), often is required. Persistent dysplasia can be corrected by a redirectional
proximal femoral osteotomy in very young children. If the primary dysplasia is acetabular,
pelvic redirectional osteotomy alone is more appropriate.
• Many older children require both femoral and pelvic osteotomies if significant deformity is
present on both sides of the joint.
Femoral Osteotomy:
Aim:
1- Concentric reduction
2- VDRO performed to correct either anteversion / valgus deformity of femoral neck in
patients é dysplasia that reduces é abduction and medial rotation.
Indications:
1- 1ry femoral deformity.
2- Mild acetabular dyspasia.
3- < 4-5 y of age; (benefits ¾ after 4-8 yrs of age as the acetabulum loses its ability to
develop satisfactorily over concentrically located femoral head).
4- In chidren > 4 years + pelvic osteotomy.
5- In severe dysplasia + pelvic osteotomy.
Pre-Requities for Osteotomy:
1- Hip should be reducible on AIR view
2- Osteotomy should leave neck shaft angle < 115º
Complications:
h LLD if > 15º correction
Concomitant pelvic osteotomy after VDRO Indications:
1]. Old baby > 4 y with low potential for remodeling

2]. Severe acetabular changes
3]. Unsatisfactory acetabular development
4]. Unsatisfactory reduction
4. Juvenile or child (38 y of age):
R atio n al e :
• The management of untreated DDH in a child > 3 y is difficult:
1]. Soft tissue contractures
2]. Head structural changes
3]. Acetabular structural changes
• Preoperative SKELETAL TRACTION SHOULD NOT BE USED
• NO PLACE FOR CLOSED REDUCTION
• ONLY OR + COMBINED VDO + PELVIC OSTEOTOMY
A d v an tag e s o f C o m bin e d appr o ac h :

1]. It facilitates reduction in children >3 y old.
1]. Avoids expensive in-hospital traction
2]. Obtains predictable reduction
3]. ¾ AVN.
Untreated DDH
• Persistent dysplasia can be corrected by a VDO in

very young children Soft tissue contracture
• If the primary dysplasia is acetabular, pelvic +
redirectional osteotomy alone is appropriate. Persistent hip dysplasia
• Many older children, however, require both
femoral and pelvic osteotomies if significant
deformity is present on both sides of the joint. Early OA
FEMORAL OSTEOTOMY
±
PELVIC OSTEOTOMY
5. Adolescent & young adults > 8 y of age:
1]. > 8-10 y or in young adults + difficult reduction Æ palliative SALVAGING OPERATIONS
2]. If OA + pain + z ROM Æ THR may be indicated at the appropriate age.
Pelvic Osteotomies
Rational
1- z load by ½ the contact area.
2- Relaxing the capsule and muscles about the hip.
3- Improving the lever arm of the abductors.
4- Normalizing the forces of weight bearing
Pelvic osteotomy
Reconstrutive Salvage
Redirectional Reshaping
• Salter • Pemperton
• Sutherland • Dega
• Steel • Lance
• Ganz • Wagner
RECOSTRUCTIVE PROCEDURES
(A) REDIRECTIONAL (COMPLETE) OSTEOTOMIES
: These procedures rotate ! hyaline cartilage of ! acetabulum into a more desirable
position over ! head.
: Redirectional osteotomies are the most useful of the acetabular procedures.
: They have application over a wide range of ages.
: Do not alter the shape of the acetabulum.
: PREREQUISITS:They require spheric congruence head.
: TYPES: 1- Single innominate osteotomy (Salter, Hall,& Kalamchi procedures).
2- Double innominate osteotomy (Sutherland procedure).
3- Triple innominate osteotomies (Steel procedure and Tonnis procedure).
4- Ganz quadrible osteotomy.
1. SALTER’S INNOMINATE OSTEOTOMY
I
n 1961, Salter reported that the acetabulum in congenital dislocation of the hip was often
deficient in anterior and lateral coverage of the femoral head. So he adevised an osteotomy
in ώ the acetabulum is rotated anteriorly and laterally over the femoral head.
Idea:
• The osteotomy is performed by a transverse linear cut above the acetabulum at the level of
AIIS. The entire acetabulum together with the pubis and ischium is rotated as a unit
(anteriorly and laterally), the symphysis pubis acting as a hinge. The osteotomy is held open
anterolaterally by a wedge of bone, and thus the roof of the acetabulum is shifted more
anteriorly and laterally.
Indications:
1]. Mild to moderate DDH éout significant incongruity
2]. DDH of 6-8 y old
3]. residual subluxation In adult é reasonable mobile and congruous hip (up to fifth decade)
Contrandication:
1]. NONCONCENTRIC hip.
2]. NON CONGRUENT
3]. SEVERE dysplasia
4]. STIFF hip
5]. OLD cases (relative as there is no upper limit for Salter especially the residual deformity)
PREREQUISITES
1]. CONCENTRICALLY reduced
2]. CONGRUENT
3]. MOBILE
4]. MILDLY dysplastic (Salter can not y the depth)
5]. Head must be at ! level of acetabulum Î traction/femoral shortening/contracture release
Advantages
1]. PHYSIOLOGIC head coverage é the hyaline acetabular roof (best for remodeling & WB)
2]. It does not z the ACETABULAR CAPACITY
3]. It doesn’t disturb ! ACETETABULAR GROWTH
4]. SIMPLE single osteotomy
5]. RAPID CONSOLIDATION Î early mobilization & loading.
Disadvantages
1]. Inherently unstable, so IF by pin is needed é the hazards for other operation
2]. Does not y the acetabular depth
3]. It is not suitable for cases é postero-superior uncoverage (e.g. CP uncoverage)
Complications
1]. Transitory STIFFNESS: ð joint penetration by a K-wire ..................................................11.6%.
2]. SEPTIC problems .....................................................................................................................9.4%.
3]. RESUBLUXATION or redislocation ........................................................................................4.4%.
4]. AVN ...........................................................................................................................................3.3%.
5]. osteotomy Medial DISPLACEMENT (ð poor fixation or osteotomy openning ........3.3%
6]. PREMATURE CLOSURE of ! triradiate cart: ð extensive inner periosteal exposure
7]. GREENSTICK FRACTURES around ! knee ð delay WB .................................................................3.3%
Technique:
• Incision from the middle of the iliac crest to just inferior to the ASIS continuing to about the
middle of the inguinal ligament.
• Splitting of ! the iliac apophysis longitudinally and reflects the apophysis and soft tissues
subperiosteally down to the superior rim of the acetabulum and posteriorly to the sciatic
notch.
• Pass a Gigli Saw from medial to lateral by the aid of a nylon tape attatched to its loop &
divide ! bone in a straight line from ! sciatic notch to just above AIIS.
• A triangular full-thickness bone graft is taken from ! crest as a wedge.
• Salter uses a large towel clip to grasp ! ant. part of ! roof & pull it ant. Lat.& inf. + putting the
leg in a figure of four and applying a down pressure on the knee simultaneously
• During this maneuver the osteotomy should open anteriorly & remain closed posteriorly.
• A wedge of bone graft is inserted anteriorly into the osteotomy, so that it press the distal
fragment and acetabular roof forward & laterally over the head.
• Salter transfixes ! osteotomy by a stout K-wire from proximal frag. through the graft and into
! distal fragment, & drilling a 2nd K-wire post. into the roof.
• Spica is put on 6 wks after the wound is closed.
Results
• It is best in the FIRST 6 YEARS of life é 80-90% statisfactory results
• The older ! child the less outcome would be expected form Salter osteotomy:
[i]. ¾ progress of remodeling
[ii]. ¾ ! rotation that can be obtained.
[iii]. ½ degree of 2ry acetabular dysplasia
[iv]. ½ the incongruity of hip.
[v]. ½ shortening of associated muscles.
[vi]. Difficult to obtain necessary reduction of the hip.
• For subluxation, there is no such upper age limit, as reduction is obtained by simple
abduction, internal rotation and flexion of the hip.
• SALTER used SEVERIN’S OUTCOME CLASSIFICATION for assessment of his results:
Severin Outcome Classification CE Wilberg angle <13y PXR Subluxation

I a >19º Normal -
b 15º-19º Normal -
II 15º-19º Mild deformity -
III <15º Moderate dysplasia -
IV a 0º Moderate subluxation +
b <0º Severe subluxation ++
V Immeasurable Pseudoacetabulum +++
IV Immeasurable Redislocation +++
CE angle values for > 14y patients are higher by 5º
Modifications of Salter’s osteotomy:
• Salter’s osteotomy by its nature, adds length to the ipsilateral limb w' mb advantageous if
the ipsilateral limb is shorter. The effect of limb length can be altered by 2 modifications of
the operation:
Hall modification, trapezoidal graft is placed Î add length to the limb.
Kalamchi modification,
Idea:
• opening-closing wedge procedureÎ avoid limb lengthening.
Indications:
• If ipsilateral limb is the longer.
Disadvantages:
1]. Less stable Î fixation more critical
2]. Distortion of ! sciatic notch may place the sciatic n. at greater risk
Technique of Kalamchi modification:
• Using the same exposure described by Salter.
• The original Salter’s osteotomy is performed.
• Then a triangular far posterior bone wedge from the proximal part of the ilium, whose base
being along the osteotomy line is removed, e’out disturbing the posterior cortex of the
innominate bone.
• Then the distal fragment is pulled forward and distally.
• Then posterior corner of the distal segment is engaged into the triangular slot created in the
proximal portion of the ilium.
• One or two steinmann pins are used to further stabilize the osteotomy.
3. COMBINATION PELVIC OSTEOTOMY (PEMBERSAL)

Idea
• It is a combination of Pemberton & Salter osteotomies. The Pemberton osteotomy is carried
through ! triradiate cart. deep into the body of the ischium.
• When the osteotomy is opened, a green-stick fracture forms through the rest of the ischial
body. The distal pelvic fragment rotates about an axis through the symphysis & the ischial
green-stick fracture. Also, the acetabular roof is rotated downward & laterally, wrapping
around ! head, hinging through ! triradiate cart.
Advantages:
1]. Large correction
2]. Less acetabular distortion than Pemberton’s osteotomy.
3]. Internal fixation is not required
4]. It combines the advantages of the Pemberton and Salter pelvic osteotomies
Indication:
1]. Persistent dysplasia
2]. Severe dysplasia
3]. Failure of coverage after successful OR or CR
4]. Excellent procedure for older children é less acetabular remodeling
Technique of Pembersal combination osteotomy:
1]. An anterior iliofemoral approach exposes the ilium subperiosteally.
2]. The osteotomy is begun as for the Pemberton’s procedure, approximately 10mm above
AIIS. It parallels ! acetabular dome & extends downward toward ! ischium. In contrast to the
Pemberton’s osteotomy, the osteotomy continues through ! ilioischial limb of ! Y cartilage,
deep into ! body of ! ischium.
3]. Opening the osteotomy creates a green-stick fracture through ischeal body.
4]. Hinging occurs through ! ischium & triradiate cartilage Î acetabulum is reoriented as in the
Salter’s & deepened as in the Pemberton procedure.
Results:
• Based on clinical & radiographic grounds.
• Clinical:
65% Î unchanged.
25% Î improved in terms of a Ç ROM, È in gluteal limb, and È pain.
10% Î deterioration e’ slight È ROM, mild Ç pain & limp.
• Radiographic:
90% Î improvements.
90% Î acet. index z≈14.4º.
95% Î CE angle of Wilberg y ≈ 36º
85% Î improved Shenton’s line.
1. DOUBLE INNOMINATE OSTEOTOMY

(Sutherland procedure).
Idea:
• It’s simply a SALTER OSTEOTOMY + PUBIC OSTEOTOMY medial to the obturator foramen, in the
interval between the symphysis pubis and pubic tubercle. So, a 3rd osteotomy through the
ischial ramus becomes unnecessary.
Advantages:
1]. When compared with triple innominate osteotomy, it has no advantage over triple
osteotomy as regard the degree of acetabular rotation. But, it needs simpler preparation, & !
op can be performed through 2 simple incisions.
2]. The procedure is indicated in pts. > 6y. It can be performed in adolescents & adults. ! hip must be
reducible e’out advanced deg. changes particularly at ! acetabulum.
Disadvantages
1]. The fixation is uncomfortably close to vital components of ! urogenital system.
2]. The axis of rotation of the inferior fragment (near the symphysis) is rather distant from the
major site requiring correction (the acetabulum). Thus, any substantial and lateral rotation
of the acetabulum requires some degree of elevation of the superior pubic ramus at the site
of the osteotomy leading to superior and anterior prominence of the ramus at the site of
the osteotomy.
3]. The versatility of correction of the acetabular defect (when abnormal direction or abnormal
configuration) is < that e’ a Pemberton’s osteotomy or triple osteotomy.
Complications
1]. Inward rotation of the acetabular fragment and non-union at the site of innominate
osteotomy due to unsecured pin fixation of the graft.
2]. Extraperitoneal tear of the bladder.
3]. Temporary scrotal or labial swelling in all patients.
4]. Narrowing of the bi-ischial diameter of the pelvic, due to the planned medial displacement
of the acetabular fragment.
2. TRIPLE INNOMINATE OSTEOTOMY

(Steel procedure and Tonnis procedure)
Idea:
• In the triple innominate osteotomy (Steel), the ischium, the superior pubic ramus, and the
ilium superior to the acetabulum are all divided, and the acetabulum is repositioned and
stabilized by a bone graft and metal pins .
Indication:
1]. Skeletally MATURE (poor remodeling of the acetabulum)
2]. SEVERE dysplasia
3]. RESIDUAL SUBLUXATION
Advantages:
1]. PHYSIOLOGIC Reduction (Hyaline Acetabulum)
2]. LARGE CORRECTION
3]. NO DISTORTION Of The Acetabulum
4]. LESS AVN
5]. Allows Some MEDIALIZATION Of The Acetabulum
6]. NO AGE LIMIT (done after closure of the triradiate cartilage)
Prerequisites
1]. CONCENTRIC reduction
2]. CONGRUENT
3]. MOBILE é range of abduction (éout it is not possible at operation to rotate the acetabulum)
4]. Avoid advanced OA (M MODERATE OA is accepted)
Technique
• The patient is placed on the operating table. The first incision is made, with the hip and
knee flexed, just proximal to ! gluteal crease over ! ischial tuberosity.
• Osteotomy around ! ischium is directed lateromed. and should be as long as possible to
afford sufficient bony contact after rotation of ! acetabulum.
• Transverse osteotomy Î Ç ! chance of pseudoarthrosis.
• It is absolutely essential that the sharp inner rim of the obturator foramen is divided completely Î
otherwise rotation of the acetabulum will be prevented.
• Osteotomy of the sup. pubic bone is made vertically via ant.approach, osteotomy is
performed close to the hip joint in a vertical direction to obtain sufficient contact even after
rotation of the acetabulum.
• ilium is then osteotomized with a Gigli saw exactly as for Salter osteotomy.
• The acetabular fragment now is free Î rotated to cover the head.
• Osteotomy of the iliac wing bone to be used as a graft.
• Graft is kept in place by two divergent Kirschner wires & spica 6 wks.
• Partial wt. bearing is permitted at 10-12 wks & FWB at 14-16 wks.
Complications
1]. NON UNION of one of the osteotomies (if excessive acetabular rotation)
2]. INADEQUATE COVER of the femoral head
3]. FAULTY PIN PLACEMENT Î loss of reduction.
[Pedia
5. PERIACETABULAR (GANZ) OSTEOTOMY:

I ntroduuced in 198
reorien
88 by Ganzz ! periacettabular osteotomy alllows exten
ntation, inccluding me
ed. & lat. displacemen nt.
nsive acetabular
I de
eaa:
• Osteotomies are performed d in ! pubis,, ilium, andd ischium.
• A verticcal post.-coolumn osteo otomy con nnects ! posst. extremes of iliac & ischial oste
eotomies 1 cm
ant. to ! sciatic nottch (the possterior column is split vertically).
v
Indications:
• DDH after skeleta al maturity,, because it i crosses ! Y cartilage e
Advantages:
1]. Very STABLE as no o complete e cut is mad de into thee sciatic notch.
2]. NO CAST is require ed & Imme ediate crutcch weight bearing
3]. NO AVN (Preserva ation of the blood su upply to the e acetabula ar fragmen
nt)
4]. SINGLE APPROACH.
5]. o the pelvvis Æ norm
PRESERVATION OF THE SHAPE of mal vaginal delivery.
Disadvantag
gee.
1]. DIFFICULT to learn.
2]. HETEROTROPIC bon ne formatio
on
3]. DVT
4]. Pubic NONUNION.
Results:
• The HARRIS HIP SCORE Ç from
m of 62 pooints preop. Î 86 poiints postop
p.
• The anterior edgee angle Ç from 1º prreop. Î 27
7º postop.
(B) Reshaping (Periarticular) Osteotomies

• In periarticular osteotomies the osteotomy parallels the joint surface and allows
repositioning, and sometimes reshaping of the acetabulum.
1. LANCE PROCEDURE
(Marginal periarticular osteotomy)
• It has been described as a lip osteotomy that extends a variable distance from ! acetabular
margin over ! sup. dome of ! socket. It Å ! retention capability of the acetabulum.
2. DEGA OSTEOTOMY:
• The Dega osteotomy is an acetabuloplasty that also changes acetabular configuration and
shape. It Å posterolateral coverage by means of an osteotomy of ! iliac lat.cortex only,
hinging through the open Y cartilage. The 1ry indication for this osteotomy is the presence
of a capacious acetabulum with POSTEROLAT.DEFICIENCY, as is often found in CHILDREN WITH
CP. Some authors also use it for persistent acetabular dysplasia in DDH.
Figure ■ Periarticular osteotomies. A, The Lance procedure is the “lip” osteotomy. B, The
Pemberton osteotomy extends into the triradiate cartilage. C, The Westin osteotomy extends
beyond the triradiate cartilage into the ischium. D, the Eppright procedure frees the acetabular
fragment so that it can be rotated E, Dega osteotomy.
3. PEMBERTON’S ACETABULOPLASTY
(Intermediate periarticular osteotomy)
O riginally described by PEMBERTON IN 1965 pericapsular osteotomy of the ilium in which the
osteotomy is made through ! full thickness of ! bone.
Idea:
• Done from just sup. to ! AIIS ant.to !Y cartilage post.
• It relies on the plasticity of the horizontal arms of the Y cartilage to hinge the rotation of the
acetabulum anterolaterally.
• It Æ the capacity of the acetabulum & Æ the roof inclination (incongruity).
• It requires the remodeling capability of the acetabulum.
• Older children have less statisfactory results:
• z remodeling of ! acetabulum & ! head
• less flexible Y cartilage
Indications:
1]. Concentric DDH with severe dysplasia and low CE angle
2]. Only for anterolateral uncoverage (as Salter)
3]. 14y ♂~12y in ♀ DDH cases
Contraindications:
1]. NON CONCENTRIC
2]. NON CONGRUENT
3]. MARKED z ROM
4]. >14Y
Prerequisites
1]. CONCENTRIC reduction
2]. Near-NORMAL ROM.
3]. CONGRUITY (e’ PXR F Abd IR).
4]. OPEN TRIRADIATE CARTILAGE.
Advantages:
1]. GREAT CORRECTION (because the hinge is close to the site of desired correction)
2]. STABLE é internal fixation
3]. Posterior acetabulum is not disturbed
Disadvantages:
1]. Technically DIFFICULT
2]. demanding a very careful placement of specially CURVED OSTEOTOMS
3]. zTHE SIZE of acetabulum (not for old children)
4]. Not for POSTERIOR COVERAGE
Complications:
1]. REDISLOCATION: as the posterior acetabulum in this procedure is not altered
2]. SCIATIC paralysis: ð excessive force for reduction in high dislocations
3]. AVN: ð compression of ! head by the loss of acetabular volume.
4]. Excessive STIFFNESS
5]. GRAFT RESORPTION ð soft iliac bone (y ambulation for months prior to osteotomy)
6]. PREMATURE CLOSURE OF THE Y CARTILAGE:
7]. Crossing the growth plate by the osteotome
8]. Pressure induced by hinging
Technique
• Anterior iliofemoral approach.
• Subperiosteal dissection of both inner and outer walls of the ilium.
• Retractors are inserted into the sciatic notch, exposing the entire anterior third of the ilium,
both inside and outside the pelvis.
• Osteotomies through both tables by a narrow curved osteotome starting e’ ! outer table
just above ! AIIS Î backwards to the ilioischial limb of the Y cartilage.
• A corresponding cut is made through the inner table. The cancellous bone between these
two cuts is then osteotomized with a wider osteotome. This portion of the acetabulum can
now be rotated forward and downward around the femoral head.
• Wedge of BG is then fashioned & inserted into ! defect. IF is usually not necessary.
• Pemberton (1974) added few changes:
o The capsule is now opened routinely.
o In high dislocation, traction is applied before ! op. for a maximum of 3 wks.
o In dislocations that are not pulled down readily to the level of the acetabulum prior
to the operation, the iliopsoas tendon is sectioned at the operation.
Results
• Best results in children < 4y
• Good results in children < 7 y.
• > 7y e’ higher complications
Salter Pemperton
Indications Mild concentric congruent cases Severe concentric congruent cases
<8y <14y
Contraindications Severe
Stiff Stiff
Non concentric Non concentric
Non congruent Non congruent
>8y >14y
Advantages Simple Great correction
Rapid consolidation Greater age
Physiologic Greater stability
Does not z acetabular size Does not distrub posterior acetabulum
Disadvantages Not for posterior coverage Not for posterior coverage
Does not y acetabular depth z size of the acetabulum
Inherently unstable Difficult & demanding
Complications: … Complications: …
4. WESTIN PROCEDURE
(EXTENDED PERIARTICULAR OSTEOTOMY)
• It is a procedure in ώ the osteotomy extends beyond the Y cartilage into the ischium
5. EPPRIGHT PROCEDURE
(DIAL OSTEOTOMY)
Idea:
• The entire acetabulum superiorly, posteriorly, inferiorly, and anteriorly is freed by osteotomy
and redirected like the dial of a telephone to appropriately cover ! head.
Indications:
• Skeletally mature residual DDH (No growth potential)
Advantages:
1]. More mobilization than other procedures
2]. Greater correction
Disadvantages:
• Technically more difficult to perform.
Prerequisites:
1]. Concentric
2]. Normal Thickness Of The Cartilage
3]. Normal ROM (except some limitation of external rotation)
6. WAGNER PROCEDURE:
W agner (1978), described the procedure as a spherical osteotomy when it parallels the
articular surfaces in all planes. He modified the procedure to provide distal or medial
displacement of the acetabular fragment to improve hip mechanics
Wagner typeI osteotomy:
• fluoroscopic guided HEMISPHERICAL SOPHISTICATED OSTEOTOMY till the obturator foramen and
the teardrop // to the articular space using a special spoon-shaped chisel
• leaving a layer of bone at least 10 to 15 mm thick
• The loosened acetabulum is then redirected
anterolaterally over the femoral head
Wagner typeII osteotomy:
• CORTICOCANCELLOUS WEDGE is inserted into the lat. part
of the osteotomy to move the acetabulum caudally
• In DDH é LLD ð varus osteotomy
Wagner typeIII osteotomy:
• WAGNER I + CHIARI
• In severe DDH > 10 y & adults & subluxation
Indications
1]. The best age is 14-18 years
2]. Norma head & joint line (C/I in deformed head &
narrow joint space)
3]. Presence of sufficiently large articular cartilage surface in the acetabulum
Advantage
• Hip is put into normal position with complete coverage of the femoral head.
Disadvantages:
• Can not be performed é insufficient cartilage
• The osteotomy is not suitable for deformed joints (deformit will persist)
• yrisk of acetabular necrosis & chondrolysis
• technically demanding
SALVAGE PROCEDURES
A. SHELF PROCEDURE (Staheli)
Idea:
• Moving an anterolateral bony shelf at or near the outer edge of the acetabulum to
construct a bony buttress, y acetabular volume, and prevent head migration. No alteration
of the shape of the acetabulum.
• The fibrocapsule change to fibrocartilage.
Indication:
1]. DEFICIENT ACETABULUM that cannot be corrected by redirectional osteotomy
2]. DEFORMED HEAD
Contraindication
1]. Spherical congruity suitable for redirectional osteotomy
2]. Hips requiring OR that must have supplementary stability
3]. Patients unsuited for spica cast immobilization.
Technique:
• Acetabular roof is extended laterally, posteriorly, or anteriorly, either by a graft or by turning
the part of the lateral cortex of the ilium distally over the femoral head
Advantages:
1]. Extra-Articular
2]. Minimal Stiffness
3]. It does not alter the pelvic ring
4]. It does not affect the head viability
5]. Easy THR following this method
Walker technique of Slotted acetabular augmentation (Modified Staheli)
• Elevate the entire iliac crest/hip-abductor mechanism as a single unit

• A slot is fashioned over the acetabular margin with a high-speed burr
• Bone graft will be placed in the slot prepaired
• No hip spica and early motion is an advantage of Walker protocol
B. CHIARI OSTEOTOMY
Idea:
• Innominate osteotomy with medial displacement of the acetabulum, to create a lateral
extension for the acetabulum so the head would be beneath a surface of bone and capsule
• Chiari at first designed the osteotomy in a horzontal or slightly arched fashion, some
authors prefer to perform it in a DOME SHAPED fashion for quick remodeling
Technique:
• Bone is cut close to and in conformity é superior capsule
• Femur and the acetabulum are displaced medially
• Inferior surface of the proximal fragment forms a roof over the head for later molding
Indications
1]. SEVERE and Residual DDH
2]. INCONGRUENT DDH
3]. DDH with OA
4]. DEFICIENT acetabulum that can not be corrected by redirectional osteotomies
5]. DEFORMED HEAD
6]. PARALYTIC dislocations
7]. PERTHE'S Coxa magna
8]. Contraindication for any reconstructive osteotomy
Contraindications: An absence of any of the indication
1]. No Incongruence
2]. No (Or Severe) OA
3]. Markedly zROM (at least 90 degrees of flexion)
4]. Upward Subluxated Hip (difficult to perform)
5]. Broken Shenton (>1.5mm)
Advantages
1]. Postpones the need for THR &improved roof cover for THR
2]. The SHELF IS A VASCULARIZED iliac bone, not prone to absorption
3]. STABLE
4]. NO UPPER AGE LIMIT for this procedure
Disadvantages
1]. Superior joint capsule is replaced é FIBROCARTILAGE
2]. y OBLIQUITY of the true acetabulum.
3]. z PELVIC DIAMETER Æ may affect childbirth
4]. Slight SHORTENING of the limb.
Complication of Chiari osteotomy:
1]. Sciatic palsy: ð angulation at the osteotomy level & z sciatic notch.
2]. Too low osteotomy Æ insufficient space for capsule to develop a cartilage
3]. GREENSTICK FRACTURE of the ilium.
4]. INADEQUATE DISPLACEMENT: y or z (z abduction or less correction)
5]. CHONDROLYSIS: 3mo after surgery, pain, and z ROM
6]. DAMAGE OF THE CAPSULE Æ z ROM
Results of Chiari osteotomy:
• 66% have good results and no degenerative changes for about 25 years.
DDH
Diagnosed Untreated
Early
ORIF +
capsulorrhaphy +
Abduction Pavlik Pelvic osteotomy
Spica 6wk Harness +
ORIF/GRUGA Residual <3y >3y

± Tenotomy
<2y Congruent Incongruent ± VDO ± VDO

shortening
osteotomy
2-8 y 8-14 y >14 y
(Acet can remodel) (Open triradiate) (closed triradiate)
Chiari /
Shelf /
Salter / Steel / Steel / Fusion /
Dega/ Dega/ Ganz THR
Pemberton Pemberton ±
±VDO / ± VDO VDO
Coxa vara
Development of upper femur:
• At birth proximal femur is a composite chondroepiphysis
• Neck shaft angle is 150° & depend on medial & lateral contribution of capital growth physis
• 4-6m two 2ry ossific foci starts in the head Æ coalesce. Then the neck elongate and
separate the head form GT
• 1y there is a postero-superior continuity between neck & GT
• 3y Ossific foci for GT coalesce and ossify
• 5-8y final contour is formed, neck shaft angle = 142° & z till adulthood
Aetiology:
Coxa Vara
Early onset Aquired
Developmental Congenital 2ry to SCFE AVN bone disease

- Renal osteodys
- Hyper parath
Limb anomaly Dysplasia DDH Trauma & infection

Isolated Perthes - Fr. Neck
Infantile
PFFD - SED postreduction
- Pyle - Hip dislocation
Coxa Vara - OI - Septic necrosis
- FD
Infantile Coxa Vara
Incidence:
• 1:25,000
Etiology:
• Vascular abnormality
• Endochondral ossification defect at inferomedial portion
• Perinatal trauma
Pathoanatomy:
• Progressive z neck shaft angle
• Triangular Metaphyseal bone fragment is noted at the inferomedial aspect of the neck =
FAIRBANK’S Δ
• This Δ is separated from normal metaphysis by a radiolucent line (resembles pseudoarthrosis
in microscopic ex)
• This line runs supero-laterally till it meets the physeal line, then the defect continues along
the physeal line laterally.
• The smaller the Δ Æ y distance of the defect is through the physeal line Æ y deformity
• HOFFA found large amount of fibrous tissue at this line that makes it weak point
• Body wt. stresses cause the capital physis to migrate inferiorly through this weak point
• Higher GT to an extent that may articulate é ilium
• Acetabulum at late stage is dysplastic Æ disturbed tear drop
Biomechanics:
• Greater Trochanter is higher than normal Æ y abd. lever arm
• Compressive forces come in a shearing direction across the capital physis
Clinically:
• Cases may be discovered early during DDH US screening
• Limping & waddling gait
• +ve trendelenburg sign
• Weak abduction and IR
• Some times pain and LLD <2cm
Radiography
1]. Head:
o At a lower level Æ mb at lesser trochanter
2]. Neck:
o Coxa vara
o Short
o Fairbank U enclosed in an inverted V or Y radiolucency
3]. GT:
o Above Nelaton’s line
o Elongated and curved inward
4]. Bone survey to exclude dysplasia
5]. Measurements:
o zNeck shaft angle
o Hilgenreiner Epiphyseal angle HE° (Wenestein)
Between Hilgenreiner & metaphyseal side of the defect
Normally: upto 25° but the average is 16°
CT scanogram for LLD
MRI: wide growth plate
Treatment:
• Aim:
o Correct the deformity
o Promote ossification of the pseudoarthrosis
• Indications
o HE angle:
> 60° Î surgery
< 45° Î spontaneous recovery
46-59Î observe: gait training & abd.ms. strengthen
• Timing of surgery:
o Too early Æ recurrence
o Too late Æ acetabular dysplasia
o Best when enough bone stalk is there to stand fixation
• Fixation by
o Pins o Bifurcate plates o Fixators
o Blade plates o DHS o Wire loop
• Types of valgus osteotomies:
1]. Pauwels' Y osteotomy
2]. MacEwen Shands
3]. Borden valgus osteotomy
Pauwels' Y osteotomy:
• Satisfactory results are:

o HE° < 35°
o Neck shaft angle > 130°
• Lines drawn: axes of shaft, physis, Hilgenreiner’s

• The HE° - 16° (normal HE°) = wedge to be resected
• Superior limb of the closing wedge osteotomy is taken from base of GT to the lower portion
of the Δ fragment
• Distal limb of the dosing wedge osteotomy is cut with the appropriate angle; till it meats the
other limb at a distance from the medial cortex equals the height of the Δ fragment
• Adduction of the proximal fragment till the osteotomy is closed then fixation is done
• May add GT epiphysiodesis to z recurrence

• NWB 8-12 wks
Borden osteotomy:
• Angled blade plate is used to close the osteotomy and fix it
• The blade is inserted parallel to the superior neck
• Cut subtrochanteric by 2.5 cm below the blade entry point (≈ femoral shaft diameter at this point)
• Roughen the lateral cortex of the proximal fragment
• Adduction of proximal fragment till its lateral cortex lie on the distal osteotomy end (and the
plate on the distal shaft)
• Fix the plate
MacEwen Shands (Bowen)
• It is an inter trochanteric osteotomy to correct the varus and the retroversion
simultaneously
Other Surgeries:
• Coxa Magna Æ trochanteric epiphysiodesis
• Coxa Brevis Æ transplantation
• Measure the Articular Trochanteric Distance

Femoral Head Vascular anatomy:
IArterial supply Trueta (1957)
Phase "1" At birth:
• Vessels coming from lateral side of head proceed horizontally to medial side
• Other vessels emerge almost vertically from the top of the ossified shaft
• Vessels of the round ligament are not constant.
Phase "2” Infantile: 4mo-4y
• Main bl.supply comes from metaphyseal vvs. Crossing the area of future physis
• The lateral epiphyseal vv are also important, but no penetrating vv coming from lig.teres
Phase “3" Intermediate : 4-7y
• The physis has established a firm barrier bet. Epiphysis & metaphysis
• The metaphyseal blood flow L to become negligible, or nearly so
• The round ligament has not yet provided vessels penetrating the epiphysis
• During this period the only source of blood to the head comes from the lateral epiphyseal
vessels ώ may become obstructed by trauma or inflammation.
• This might explain the occurrence of Legg-Calvé- Perthes’ disease at this age
Phase "4" pre-adolescent 9-10y
• Arteries from the ligamentum teres finally reach depth of the epiphysis and anastmose é
lateral Epiphyseal arteries.
• So, epiphysis receives blood from 2 sources at the greatest possible distance from each other
Phase "5" Adolescence
• The barrier of the epiphyseal plate begins to break down
• Vascular anastomosis crosses over, being the adult stage of circulation, where the
epiphyseal & round ligament vessels are joined again to metaphyseal vv
Blood supply of femoral head
1]. Medial Circumflex Femoral A (MCF) ......... most important supply, (from profunda a.)
• It run posteriorly bet Pectineus and iliopsoas, above LT and posterior to the neck, to find the
obturator externus, run below it and deep to quadratus, where it gives some branches to GT.
• Then it forms the medial, posterior, & lateral portions of the EXTRA-CAPSULAR ART RING that gives
the ascending cervical aa. (R RETINACULAR VESSELS OF WEITBRECHT), posteriorly they pass beneath
the orbicular fibers of capsule (= Artery of Brodetti)
• There are Four Groups of the ascending cervical vessels; anterior, medial, posterior, & lateral. The
Lateral provides most of the blood to femoral head.
• As they traverse the neck they give metaphyseal vessels that entres the neck at regular intervals
• When they reach physeal junction, they form the SUBSYNOVIAL INTRA-ARTICULAR ARTERIAL RING,
that gives many epiphyseal arteries the most important are TRUETA'S LATERAL EPIPHYSEAL aa that
enter the head postero-superiorly, and gives the major supply to the head
2]. Lateral Circumflex artery (LCF) ................... (branch of profunda femoris artery)
• Passes anterior to iliopsoas tendon till it reaches the Intertrochanteric line running over it
supplying the capsule and muscles and form the anterior portion of the extra-capsular ring
• This portion gives the ant retinacular v v., pierce the capsule at the intertrochanteric line
• 1st it supplies the anterior head portion, while in adult its role is
mainly to supply the metaphysis
3]. Artery of the ligamentum teres ................ minor in adult (from
post branch of obturator or from Medial Circuflex Femoral)
• When it enters the head it gives the MEDIAL EPIPHYSEAL
ARTERIES that only supplies a small area under fovea centralis
4]. Intraosseous cervical crossing the neck from below
94 | Page pedics]
[Pediatric Orthop
NON-UNION OC
CCURS DUE TO:
1]. No cambiu um layer ovver the intra

acapsular pa art of the neck
n
2]. Synovial flu
uid hinders blood clottting and fraacture hematoma form mation
3]. Close proximity of thee retinacular vessels to the neck
4]. Fracture neeck femur disrupts
d moost of the blood supplyy at time of fracture
5]. Inadequate e remaining g supply, an
nd variablee anastmosis bet med & lat epiphyyseal vessells
IIV
Venous Drainag
ge
• Venous drainage e normally flows through the medial
m circu
umflex vein
n
• hes’ diseasse Æ K ven
In Perth nous presssure in the neck Æ metaphysea
m nÆ
al venous congestion
outflow
w has been n found to exit more distally thrrough diap
physeal veins
Legg-Calvé-Perthes Disease
Coxa Plana
Definition:
• Non inflammatory pathological condition in ώ the immature head undergoes varying
degree of ischemia and subsequent necrosis of the femoral head.
Ætiology:
P DF :
}
1]. Trauma
2]. Inflammation • Hypofibrinolysis Thrombotic
3]. Endocrinopathy • z ptn. C. Venous
4]. Malnutrition • z ptn. S. occlusion
5]. Vascular: venous hypertension & arterial • y lipoptn. A.
insufficiency • Hemophilia pt. D Joint tamponade
• Attention Deficit Hyperactivity Disorder
Incidence:
• 1 : 10,000
• White Boys 4-8 y .................................... (≠ Black 12y in SCFE)
• >8y .............................................................. poor prognosis
• ♂:♀ ............................................................. 4:1
• family history ............................................ +ve
• Bilateral ...................................................... 12% (é diff. stages).
• Rare in black race
• y é Low birth wt. & breach
• y é previous Irritable hip $ (10%)
• y é some cong.malformation: Pyloric obst. & UT anomalies & cong.HD
• y é high IgG & IgM & low IGF I & somatomedin C
Pathogenesis
• The precipitating cause is unknown but the cardinal step is ischemia of the head.
• Up to the age of 4 months, the femoral head is supplied by:
1]. Metaphyseal vessels which penetrate the growth disc.
2]. Lateral epiphyseal vessels running in the retinacula.
3]. Scanty vessels in the ligamentum teres.
• Metaphyseal Bl.supply gradually z between 4&7y, as the ligamentum teres vv. have
developed. Between 4-7 y the femoral head may depend for its blood supply and venous
rainage almost on the lateral epiphyseal vessels whose situation in the retinacula makes
them susceptible to stretching and to pressure from an effusion (by trauma or synovitis) Æ
block off the venous drainage Æ VENOUS STASIS Æ y intraosseous pressure Æ ischaemia.
Pathology: (it takes 2-4 years to complete)

I Stage of Ischemia:
Earliest:
• Bulging of the capsule (rarely seen)
Early
• Medial metaphyseal osteopenia
• DELAYED OSSIFIC NUC (AVN of the head nucleus (epiphysis) Î stays small)
• WALDENSTRÖM'S SIGN (subtle subluxation): as articular cart is nourished by synovial fluid Î
continues thickening & growing Î false impression as if the head is subluxed
Late:
• SCLEROSIS of AVN Bone ð:
o Relative osteopenia of the surrounding viable bone
o Calcification of the dead bone
o Creeping substitution of dead bone
Later:
• CRESCENT SIGN Subchondral bone fracture ð z head support (best in lateral PXR)
II Stage of Fragmentation
Head
• FRAGMENTATION ð creeping substitution replaces necrotic trabeculae by NBF
• Head FLATTEN, and extrude antero-laterally
• LATERAL CALCIFICATION when Extruded part calcify
• LATERAL SUBLUXATION (hing sublux) as head abuts on superolateral acet in Abd
Metaphysis:
• CYSTIC METAPHYSIS hyperemic/widened/abnormal enchondral ossification
• GAGE SIGN: superolateral neck lysis
III Stage of revascularization & reossification:
• Revascularization from periphery (paraphyseal), rather than (transphyseal) Î resorption
via creeping substitution Î cartilage columns become distorted Î abnormal
endochondral ossification
• yBONE DENSITY ð calcification of necrotic trabeculae + NBF + relative osteopenia around
• SUBCHONDRAL COLLAPSE occur if there is weak support as bone resorption > NBF
• RESOLUTION occur if NBF > bone resorption
IV Stage of deformity and remodeling
• REMODELING continues till maturity
• DEFROMITY:
o MUSHROOM shaped: distorted head
o SAGGED ROPE sign: distorted metaphysis
• Hip joint adaptive changes continues through out pt. life
Extensive Necrosis
AL collapse
with Add.
Uncoverage of Head Flat or Mushroom Head Lateral subluxation
Limited or Hinged Abduction
Premature closure of neck physis + persistence of greater troch. physis

Î Short neck.
Î Short femur.
Î Coxa vara & magna Î gluteal insufficiency Î limited abduction in extension.
Clinical Picture:
C/O: insidious onset of
o Pain in the hip or knee.
o Limping.
O/E:
o Early:
• The hip is irritable Î ↓ all movements + painful extremes
• Antalgic gait (limb dips on the bad side)
o Late:
•limb is held in Flexion Add ER
•z IR (early sign)
•z Abd
• Flexion deformity (+VE THOMAS TEST)
• Trendelenburg gait (+VE TRENDELENBURG)
Stage Timing X-Ray clinically

Infarction & Subch# (1-14m) Av 6m Lateralization. Pain and limping on & off.
yDensity.
Subchondral #.
Fragmentation (2-35m) Av 6m Fragmentation. Pain & limp more evident.
Collapse. z ROM.
Lat.calcification.
Cystic neck.
Reossification (2-122m)Av 18-36m Subchondral NBF Resolve gradually till disappear
Head reossification
Remodeling till maturity Normal density. Some limitation of ROM.
Deformed. Incongruity.
pedics]
D
Diifferential diagnosis
U
Unilateral P
Perthes Bilaterral Perthess
- KESR, CRP
Septic arthritis (K P) - Hypo othyroidism
m (rather symmetrical)
- Transieent synovvitis - MED (ra
ather symm metrical).
- SED taarda - SED tarda
t (Oth
her joint a
affection)
- Sickle cell
c - Sickle
e cell
- Gauch her's diseaase
- Eosinoophilic graanuloma
Radiographic findings
he antero--lateral part of the head).

- At firrst: (At thiss stage: Tcc shows a void in th h
• Wideening of th he joint sp
pace.
• ASYMMETRY OF THE OSSIFIC CENTRES.
ntigraphy shows y activity)
- Laterr: (At this stage scin a
• Incre
eased den nsity of the
e ossific nu
ucleus.
• FRAGMENTATION.
• CRESCENTIC sub
barticular fracture
f best
b in the lateral vie
ew
- Latesst:
• Flatte
ening and d lateral displaceme ent of the epiphysis.
• Obviious increa ase in the
e joint spacce.
• Rareffaction annd widening of the metaphyssis
• SAGGING ROPE SIGN: a sclerotic line curvving acrooss the feemoral neck,
probbably due to distortiion and re emodeling g of metapphysis
• Withh healing the femo oral head may rega ormal for near-norm
ain its no mal)
shappe; howevver, in le ess fortun
nate case es the fem moral heead becommes
MUSHROOM sh haped, larrger than n normal and latterally dissplaced inn a
dyspplastic acettabular so
ocket
• HINGE SUBLUXATION
• Head
d at risk sig
gns: (at rissk of more
e deforma ation)
1- GAGE’S SIGN: Radiolu ucent lat ed
dge of epipphysis
2- LATERAL CALCIFICATION: calcific cation of exxtruded tisssue
3- LATERAL SUBLUXATION
4- SEVERE METAPHYSEAL RESORPTION
5- HORIZONTAL GROWTTHH PLATE
Classifications
1- CATTERALL: described four groups, based on both AP standing & lateral views
Group Extent sequestrum Collapse ttt X-ray

I <50% no No No
II 50% Y No No
III 75% Y Y Y
IV 100% Y Y Y
(Flat
head)
2- SALTER-THOMPSON: based on the percentage of the subchondral fracture

• STAGE A: <50% involvement of the head ........................... good prognosis
• STAGE B: >50% involvement of the head ........................... poor prognosis
3- HERRING’S LATERAL PILLAR CLASSIFICATION: In the AP x-ray, the head is divided into 3
pillars by lines at the medial & lateral edges of central sequestrum.
• GROUP A: Minimal density changes in the lateral pillar and no loss of height
• GROUP B: partial collapse (< 50% of height) of the lateral pillar
o < 9y Æ good prognosis
o > 9y Æ likely to develop flattening of the femoral head.
• GROUP C: severe collapse of the lateral pillar (> 50% of normal height)
o Take time to heal & end é significant head distortion
4- MOSE CLASSIFICATION (for prognosis): a template of concentric circles are applied to

the femoral head in the AP & lat. Views and compared:
A) Identical ................................good prognosis
B) < 2mm deviation...................fair prognosis
C) > 2mm deviation ..................poor prognosis
5- STULBERG CLASSIFICATION: applied for the patients at the skeletal maturity; based on
the AP view:
C lass size of the head acetabular angle T roch. H t. H ead C overage N eck
I N
II N ? C oxa M agna Short
III ovoid
IV Flat Flat
V Flat N
• Class I & II .........................Spherical congruity ................No arthrosis.
• Class III & IV .....................Aspherical congruity ............Mild arthrosis >50y
• Class V ...............................Aspherical incongruity .........Severe OA <50y
Scintigraphy:
Early cases may show a void in the anterolateral part.
Early revascularisation :
• Pathway A = Lat column appears early = revascularization = good prog
• Pathway B = -------------not ------------- = slow revascularization =Poor prog
US: may reveal thickened synovium (rather than the effusion as in irritable hip $)
MRI: superior in evaluation of the extent of necrosis & revascularization & everted limbus
Arthrography: • Assess the head.
• Delineate hinge subluxation.
• Plan for treatment.
Prognosis:
• CLINICALLY:
Age: is the most important prognostic factor:
i. Under 6 y Î good prognosis.
ii. Above 6 y Î poor prognosis.
Sex: poorer prognosis for ♀>♂ (reach sk.maturity early Æ less remodeling)
• RADIOGRAPHIC:
A. Caterall classification.
B. Salter-Thompson classification.
C. Herring’s lateral pillar classification
D. Mose classification
E. Head at risk signs: (at risk of more deformation)
1- GAGE’S SIGN: Radiolucent lat edge of epiphysis i.e. more weak
2- LATERAL CALCIFICATION of extruded tissue (will not remodel)
3- LATERAL SUBLUXATION: soft head abut acetabular margin Æ K deformity
4- SEVERE METAPH RESORPTION: = weak neck ώ is liable for deformation
5- HORIZONTAL GROWTH PLATE: make physis vulnerable to shear forces
Treatment
PERTHES
During Necrosis &

During Reossification
fragmentation
<6 y >6 y Reconstructive

Motion Containment Operation
-Caterall 1,2 - Herring C Bony Soft tissue

-Herring A,B - Head at risk
-Herring A,B
• Symp. ttt • Brace • Osteotomy Femoral Pelvic • Add. tenotomy

• Motion ttt • Cast • Garceau • Shelf • Psoas tenotomy
• Traction • Valgus osteotomy
• Chiari • Arthrotomy
• GT advancement
VDO
Salter
110º & 15º
I- EARLY MANAGEMENT (During necrosis & fragmentation)

1- Irritable Hip:
Skin traction applied to the affected leg and the hip in a little flexion and external rotation
⎯⎯→ irritability subside Æ movement is encouraged (particularly abduction)
3 wk
Clinical / radiographic features / bone age are then reassessed. The choice of further
management is between (a) Motion treatment and (b) containment
2- Motion treatment:
ROM physiotherapy program + pain control
Avoid strenuous activities
If fails:
o Abduction traction
o Abduction cast or brace
o Adductor tenotomy
3- Containment Treatment:
Idea:
Means that the physeal plat is medial to acetabular border
Acetabulum acts as a mold for head remodeling
L stress on the head Î protect the head from further subchondral #
Prerequisites:
>6y
>50% head affection
Minimal collapse
Good ROM
No irritability
Types:
Brace
Add tenotomy +Abd cast 3 M
operative containment
A) Abduction cast:(Petrie & Bitenc)

Bilateral long leg cast (LLC)
Idea: provide continuous abduction & z subluxation
Position: Abduction & IR
Child ambulate é crutches
Change cast /6-8wk for a year
Disadvantages:
o Cumbersome
o Difficult regaining knee & ankle ROM
B) Abduction Brace:
Position: Abduction ER (some é IR as Birmingham) Types:
Tachdjian abduction brace
Advantages: less cumbersome
Salter stirrup crutch
Disadvantages: Atlanta Scottish Rite Orthosis
Less satisfactory results Birmingham splint
Less lateral coverage of the head
C) Femoral varus osteotomy:

Aim:
Redirect the head into the acetabulum, by varus angulation + IR
Varus angulation < 110° Æ epiphysis is contained within acetabulum
IR 10-15° Æ K coverage of anterior portion of the femoral head
Spica cast until adequate union has occurred
Indications:
1- Head at-risk
Contraindications:
1- Catterall I
2- Deformed head or acetabulum
3- The epiphysis is group I Catterall’s classification.
4- The epiphysis is not “ at risk”
Prerequisites:
Adductor tenotomy may be necessary in some cases
Preoperative arthrography in abduction IR & anteversion views
preliminary traction to K ROM
Advantages:
1- The degree of containmnet which can be achieved and the required angles of
varus and internal rotation can be measured exactly by radiography
2- Femoral osteomtomy is easy to perform and stabilize
3- The operation is done on the affected bone
4- It decreases the force across the joint ( Axer et al, 1980) .
5- It provides better lateral coverage than does innominate osteotomy
Disadvantages:
1- The requirment of a second operation to remove the implant.
2- Loss of position due to failure of internal fixation .
3- Development of the limp due to leg shortening , abductor insufficency
D) Salter innominate osteotomy
Advantages:
1- It gives better anteior and lateral coverage of the femoral head.
2- It does not result in further shortining of the femoral neck
3- Does not y fucnctional LLD (actually it lengthens about 1 cm).
4- It improve Trendelenburg gait.
5- Metal removal is easier.
6- There is no risk for fracture through screw holes in the proximal femur .
Disadvantages:
1- The degree of containment can not be judged exactly
2- Technically more difficult to perform satisfactory than the femoral osteotomy unless
the surgeon has been adequately trained in its performance.
3- It may y the transarticular pressure
Complications :
1- Infection, which may lead to joint stiffness.
2- Migration of the pins inside the joint
3- Heterotropic bone formation which may compromise joint motion.
II - Late Surgical Management Of Deformity

A) Muscle release and arthrotomy followed by abduction cast:
Indications:
1- Moderately flattend healing head
2- Hinge abduction (in AP X-ray)
Types:
1- Adductor tenotomy
2- Iliopsoas release
3- Arthrotomy
Idea:
Is to gain sufficient abduction Æ flattend head will be contained éin acet.
After ttt:
Abduction weight bearing cast 3-4mo for completion of remodeling
B) Combined innominate and femoral osteotomy
Indications:
1- Severe Perthes’ é lateral subluxation
2- Catterall III and IV / Sallter – Thompson B involvement
3- Moderately deformed extruded femoral heads
Advantages:
1- Maximal femoral head containment may be achieved
2- Avoid some of the complications of either procedure alone
3- The converge gained by Salter L the correction required by PFVO
4- Less LLD
5- Less neck shaft varus angulation, and associated abductor weakness
6- L any increase in joint pressure or stiffness after pelvic osteotomy
7- Progressive spherical remodeling
C) Garceau Cheilectomy:
Indication:
1- Extruded anterolateral rim of the flattened
2- Saddle – shaped femoral head can not be contained within the acetabulum
3- It could be concomitantly used é soft tissue release and arthrotomy
Disadvantage:
1- K the load per unit area through the femoral head.
2- Raw cancellous bone Æ K stiffness & OA
3- SCFE (it is better to delay Gareau till physeal closure)
D) Proximal femoral valgus osteotomy .
Catteral recommended this procedure as:
1- Alternative to peripheral cheilectomy for a hinged abduction
2- When the hip joint is more congruous in adduction
Advantages:
1- Improves the LLD, gait, ROM (abduction)
2- Maintains load bearing without hinging effect
3- Improve hip biomechanics (GT moves distally & laterally) Æ y abduction
E) Greater trochanteric advancement:

Idea:
Correction of functional coxa vara secondary to premature physeal closure
Transfer the greater trochanter both distally and laterally
Advantages:
Effective in relieving muscle pain
L Trendelenburg limp
L joint pressure Æ L OA
F) Lateral shelf acetabuloplasty.
Indications:
Lateral subluxation of the femoral head.
Hinge abduction of the hip.
After failure of other non operative treatment
Some surgeons, consider it as 1ry containment &do it éin 6mo of the disease
Advantages:
It does not alter the neck shaft angle.
Decrease the tendency to stiffness of the hip joint.
Disadvantages:
Possibility of damage of the lateral acetabular epiphysis
G) Chiari osteotomy .
As shelf osteotomy but:
The shelf is vascularized iliac bone
Not prone to absorption
Inherently stable
The ilium above becomes weight–bearing even if there is a radiological gap
Idea:
Displace the whole hip joint medially Æ iliac bone completley covers the head
It is placed as close as possible to the joint capsule
Effectiveness of the new roof depend on three factors:
- The closeness of the iliac graft to the capsule.
- The angle of the osteotomy.
- The degree of displacement
Indications :
1- When other operations are not technically feasible
2- Large Deformed head or deformed acetabulum
3- Older patients (difficult rotation of the acetabulum)
4- K head cover will relieve pain
Contraindications
1- Severe L ROM or contractures (should be at least 90° flexion present)
2- Marked distortion of the head outside the hip + Advanced OA
Disadvantage:
The procedure does not place hyaline articular cartilage over the femoral head
Injury to the sciatic n.: may occur during serving the posterior cortex of ilium
Too high osteotomy Æ ineffective biomechanically
Too low osteotomy Æ injury the hip joint it self
Over displacement Æ Central dislocation of the hip
Precaution:
Success of Chiari depends on preservation of the capsule beneath the shelf
It should not be regarded as a replacement for the salter osteotomy
After treatment
Hip spica for 6 wk
OR: 2 wk spica then 3 weeks balanced traction to K ROM
III- Late surgical treatment for secondary degenerative arthritis

Many alternatives were discussed:
Intertrochantric femoral osteotomy
Arthrodesis
Arthroplasty
IV-Recent Trends In ttt of Perthes’ disease

Ilizarov distraction diastasis: introduction of 3 pins in the iliac crest and connected to
another 2-3 pins at the subtrochanteric area or crossing wires at the condylar area;
aiming at distraction of the hip joint thus prevent further mechanical compression and
ischemic insult and abort the pathological process; and at the same time maintain a
concentric reduction of the head in the acetabulum
Advantages:
o Allow wt bearing
o Allow for physiotherapy
o Abort the pathological process
o Prevent further head collapse
Other Protocol
Grade & age of onset
Group A Group B > 6y

Group B& C > 9y
Group B < 6y Group C < 9y
Pelvic + Femoral
Symptomatic Salter
osteotomy
Q :Criteria of unfavourable prognosis in Perthe`s disease
Answer
Points
1 Age at onset: patients older than 6 years at onset 20
2 Sex :females have less favorurable prognosis 3
3 Obesity: Obese patients have less favorurable prognosis 2
4 Salter & Thompson classification: Group B (Subchondral fracture extends 10
throughout more than half the femoral head in X-ray)
5 Lateral pillar classification of Herring ,etal :Group C= Loss of more than 10
50% of epiphyseal height on AP X-ray
6 Catterall classification 10
• Grade III ( involvement of most of the head with loss of
epiphseal height due to collapse)
• Grade IV ( total head involvement with total collapse)
7 Head at risk signs : 15
• Gage`s sign :Lytic area in lateral part of epiphysis &/or adjacent
metaphysis
• Calcification lateral to femoral epiphysis
• Lateral subluxation of the femoral head ( uncoverage of the
femoral head more than 20%)
• Diffuse metaphyseal neck changes
• Horizontal growth plate.
8 Tc 99 bone scan : pathway B Lateral column does not appear early during 5
revascularisation stage which means slow revascularisation
9 Degree of head deformity at end of healing process: 15
Mose sphericity scale : More than 3 mm deviation from sphericity
Stulberg classification :
Group III & IV hips (Aspherical congruency between the femoral
head & the acetabulum) develop osteoarthritis after age of 50 years
Group V hips (Aspherical incongruency between the femoral head &
the acetabulum ) develop osteoarthritis before age of 50 years
10 Stiffness of the hip 5
11 Affection of proximal growth causing coax vara & short neck 5
Total score of 100% 100
PERTHES
During fragmentation During Reossification
<6 y >6 y Reconstructive

Motion Containment Operation
-Caterall 1,2 - Herring C Bony Soft tissue

-Herring A,B
-Herring A,B - Head at risk
• Symp. ttt • Brace • Osteotomy Femoral Pelvic • Add. tenotomy

• Motion ttt • Cast • Garceau • Shelf • Psoas tenotomy
• Valgus osteotomy
• Traction • GT advancement • Chiari • Arthrotomy
VDO
Salter 110º & 15º
Epiphyseal Growth Plate / Physis
Vascular supply
• 2ry ossific centre is supplied by epiphyseal artery, branches of ώ end in proliferating zone
• The metaphysis is supplied mainly by the nutrient artery, with the periphery having an additional
supply from metaphyseal vessels
• Terminal branches of these arteries end in capillary loops below intact cartilage septae that
delineate the end of the cartilage zone
• These capillaries drain into the large central vein of the diaphysis.
• Hypertrophic zone of the growth plate is avascular.
• Only the proliferative zone has an abundant blood supply.
Physis (RPM DCOR = Resting, Proliferative, Maturation, Degeneration, Calcification,

Ossification, Remodeling)
Resting zone
• Columnar cells exist singly or in pairs separated by an abundant matrix
• Differentiate Æ chondrocytes
• Have low proliferation
• Ca free
• Store for later requirements
Proliferative zone
• Matrix synthesis & cell division Æ longitudinal
growth
• Chondrocytes are flattened & in columns
• The true germinal layer of ! Physis; é active dividing
cells
• K collagen II & mRNA
• Ca free
Hypertrophic zone -
• Cells mature: ysize & less regular columns
• y Vacuolation of the cells Æ swell & die
• Matrix synthesis 3-folds of prolif zone
• Type II, X collagen & aggrecan
• Divided into 3 zones:
1. Maturation zone: prepare matrix for
calcification
2. Degeneration zone: deg & death (glycogen
from anaerobic glycolysis)
3. Zone of Provisional Calcification: chondroid
matrix becomes impreg-nated é ca salt from
mitochondria of destroyed cartilage cells
• Widened in: Rickets & SUFE
• Physeal fractures occur through the zone of
provisional calcification.
Ossification Zone:
• Osteoblasts secrete collagen ⎯⎯ ⎯ ⎯⎯→ minerals deposite Æ bone lamellae é osteocytes in lacunae
Alk. Phosphatase
Periphery of the Physis

• Groove of Ranvier - supplies chondrocytes to the periphery for lateral growth (width)
• Perichondrial ring of LaCroix - dense fibrous tissue which anchors & supports the physis
Metaphysis
• Primary Spongiosa - vascular invasion; osteoblasts from osteoprogenitor cells line up on calcified
cartilage bars; mineralised to form woven bone
• Secondary Spongiosa - from remodeled primary spongiosa; removal of cartilage bars; replacement of
woven bone with lamellar bone
[Pedia
S
Slipped Capital Femoral Epiphy
E ysis
• It is a condition in
n which dissruption of the uppe
er femoral physis
p occu
urs so the upper fem
moral
epiphyysis will acq
quire an infferior, postterior, and varus posiition in rela
ation to ne
eck
• Actua ally The Epiphysis
E Keep Itss Relation n Within The Acettabulum, and the neckn
and shaft displaces anteriorr and upwa ard on thee epiphysis..
• Rarely: anterior and lateral slips
s may occur.
o
I n c id e n c e :
• 1:30,00 00
• 12-14y y
• Black, ♂
• Left hips are morre than right hips.
• Bilatera al 25%.
• Endocrrinopathiess 70%.
Aeetiolo
ogy:
Predispossiing factors:
1]. Obesit ty
2]. Childre
en with Rap pid growthh Spurts
3 Hypot
3]. thyroidism m
4 Renal Rickets
4].
Mechanicca al factors:
1]. y stressses over th
he physeal line:
o Over Weig ght
o Taller attittudes of SC CFE patients
o z Anteve ersion
o z α Angle e of physea al inclinatio
on (= comp
plementary to
t HE angle
e of Infantile
e coxa vara))
2
2]. z Physseal streng gth (load to
o failure ≈ 15% less th
han norma al)
o Thin Perich ng of LaCro
hordial Rin oix
Fibrou
us band con nsist of verticcal, circumfferential, & o
oblique collagen fr
Spans bet ossifyin
ng epiphysiss & metaphyyseal
Gives mechanical
m l support to physis
o Thin Tran nsphyseal Collagen bundles: ru un across the
t growth h plate
o Shallow Mammillary
M y processe es of the ph
hysis (their depth y é aage Æ y sh hear resistan
nce)
Endocrine factors:
• Physis maturation
m n depends on balancce between n GH & sexx hormone es
o GH respon nsible for hypertroph
h hy
o Sex H respon nsible for maturation
m n and closu ure
• Norma al balance betb both Æ normal developme
d nt éout slip
ppage
• yGH & zSex horrmones Æ y zone of hypertrophy + irregu ular arrang
ged collage en fibrils
• Endocttinopathiess associate ed é SCFE:
1]. Hypothyro oidism
2]. Pan-Hypo o-Pituitarism
m
3]. Hyper PTH H
4]. Hypogona adism (Froolich)
5]. Acromega aly
Maturation factors:
• SCFE occurs
o while the pericchondrial ring
r z in sizze while th
he physis iss still thick
• SCFE physis
p is thicck and lesss resistant to
t shear:
o y hypertrophic zone o z collagen in matrix
o Disorganize
ed cell colum
mns o Cellular degenerationn and death
h
Pathology:
Mic:
o EPIPHYSIS acquire a postero-inferior position
o P HY S I S :
THICK (hypertrophic & proliferative layers), z cells, y matrix
Main displacement occur through the HYPERTROPHIC zone
o M E TA PHY S I S :
Antero-superior portion Æ "HUMPY"
Impinge on acetabular rim é F AB IR; but eventually remodel
o P E R I O S TE U M :
Stripped from postero-inferior neck Æ callus Æ ossify

Stretched antero-superiorly Æ resorption of sup.neck

In acute slips: anterior periosteum tears Æ hemarthrosis

o SYNOVIUM, periosteum, and capsule are edematous
o CHONDROCYTES: not arranged in columns Æ clumpy
o ACETABULUM: Antero-superior erosion + postero-lateral labral tear
Electron Microscopy:
o z collagen and irregularly arranged
o D E GE N E R A TI V E C HO N DR O CY TE S
Classifications:
1. Clinical classification Preslip / Acute / Chronic / Acute on chronic
2. US classification (KALLIO): stable, unstable, acute on chronic
3. Functional (LODER): Stable / Unstable
4. Morphological (KLIEN / SOUTHWICK): Mild / Moderate / Severe
Clinically:
o 12-14y kid
o Pain
Anterior groin
Anterior thigh
Medial knee pain
o Flexed hip
o In chronic cases: hip flexion is associated é ER
CP Preslip Acute Chronic Acute on chronic

Percent 10% 10% 60% 20%
Trauma - Trivial - ± Trivial
Pain Vague < 3wk Sharp acute # pain Vague > 3wk Sharp after vague > 3wk
Gait Mild limp Unable to WB Antalgic Severe Antalgic
ROM z IR Marked limitaion z F Ab IR Marked Tender
Flexion Æ ER
Chronicity - - +ve (ms atrophy & shortening & F Ab ER)
PXR - Slip Slip + round superior As chronic but the slip is
neck + NBF inf beyond the remodeling
US - Effusion No effusion Mild Effusion
Unstable Stable Mild Instability
Manipulation - Improve Contraindicated Contraindicated
Prognosis Best AVN Good AVN
Fu n c tio n al c l as s if ic atio n :
Stability (Loder)
Unstable Stable
- Acute - Chronic
- Unable to bear wt. - Can bear wt.
- Considerable joint effusion - No joint effusion
- US no remodeling - Evident remodeling
- May improve é traction & gentle - Manipulation is contraindicated
manipulation - Good prognosis
- High incidence of AVN - Low incidence of AVN
Radiological:
• Both hips should be evaluated
• Views:
1]. AP
2]. True lateral
3]. Frog lateral: easy, both hips; but position variability is not accurate for severity & penetration
4]. Modified Billing's: 90° flexion, 60° abd + AP projection
5]. Modified Dunlap
• Findings:
1]. y physeal width
2]. y Physeal Inclination (z α Angle)
3]. z Epiphyseal height
4]. METAPHYSEAL BLANCH SIGN: overlapped epiphysis over metaphysis
5]. Scham sign: in AP normally inferomedial neck has a dense Δ of overlap over the posterior wall
of acetabulum; in SCFE Æ head neck is laterally displaced Æ this Δ disappear
6]. Trethowan sign: when KLIEN'S lines are drawn along anterior or superior neck normally
intersect the epiphysis; if not Æ +ve
7]. AVN: y density and collapse … etc
8]. Chondrolysis:
o z joint space by 2mm than sound side
o If bilateral: joint space < 3mm
• Degree of slip: is measured by two methods:
o Klien
o South Wick
• Classifications:
Using Klien Lines
Mild Moderate Severe

<1/3 metaph. uncover 1/3-2/3 uncover >2/3 metaph. uncover
• Another classification method:

o Measure the angle between the ⊥ line on epiphyseal margins; and the line along the
femoral shaft axis
o The difference between the normal & the slip side is calculated
o According to this difference the slip severity is determined
o If Bilateral case: subtract form the normal values
o Normally: 145° in AP; 10° in lateral
South Wick method
Mild Moderate Severe

<30° 30-60° >60°
CT:
• Accurate measurement for retroversion
• Accurate measurement for severity
• Accurate assessment of hard ware penetration
• Accurate assessment of physeal closure
MRI:
• For early marrow changes and AVN
Tc99:
• y in preslip stage
• z uptake in AVN
• y uptake in chondrolysis (hot joint space)
Serial sonography:
• Sensitive and accurate
• Assess:
1]. Epiphyseal displacement
2]. Joint effusion
3]. Metaphyseal remodling
4]. KALLIO classification: Stable, Unstable, Acute on chronic
[Pedia
5]. Treatment:
Immeddiate NWB isi instructedd
Hospita
al admission as soon asa possible
Assessm
ment for enndocrinopa athy and coontralateral slips
Assessm
ment for th
he stability of
o the slip
Stabillity
Unstabble
Stab
ble
- pt. unable to bear wt.
- pt. is ambullatory
- there is jointt effusion
- No joint efffusion
Tractioon No traction nor

manipuulation
Gentle Manippulation
Assess the contraa-lateral
A
hiip by the oxfoord bone
sccore
Surgical coorrection
Mild to modeerate Mod. to

t severe
Pinning in situ
s BG epipphysiodesis Corrective osteotomies
o
Intracapsular Neck Ost.

O Exttracap.Basal neeck ost. Inntertrochantericc osteotomy
(Dunn) (Kramer) (South W
Wick)
1- Manipula
ation:
Forcefuul manipula ation is con
ntraindicateed absolute
ely
Manipu ulation in stable casess is forbidde
en
In acutte on top of chronic Æ partia al reductio
on may occcur (comp
plete
reductiion lead to AVN)
Mere putting
p thee patient in orthope edic table with no much inteernal
n Æ may do
rotation d the job.
2- Pinning in situ:
Indicationss:
1- Preslip
ps
2- Mild to
o moderate e slips
Technique e:
Pt is puut in orthoppedic table in extensio
on and neu utral or even
n mild IR
In chro onic slips pt could be put
p on any table
Skin inc cision is maade at the intersectio
on between n two liness overlying
g the
neck inn both AP and
a lateral views
v
1 cannulated scre ew is inserte
ed in AP direction tow
wards the head
h centree
Usually y the screww inters at th
he base of the
t neck
Stop th he screw when the threads enga age into thee physis
Ensure e the positio
on of the sccrew using fluoroscoppy
Precautionns:
Avoid enthusiastic
e c manipula ation
Avoid supero-late
s eral corner of
o the epip
physis
Complicatiions:
Chond drolysis
Acetab bular injury
3- Bone Graft Epiphysiodesis:

Indications:
Moderate to severe
Advantages:
1- Avoid pinning complications
2- Promote physeal fusion
3- Remove metaphyseal humps ώ impinge labrum in IR in chronic slips
Disadvantages:
1- Graft fixation problems
2- Heterotopic ossifications
Technique:
Bony tunnel is made into the neck
Starts from metaphysis till epiphysis using a burr
Autogenous cortico cancellous BG is used
4- Intracapsular femoral neck osteotomy (Dunn):
Indications:
Moderate to severe slips
Technique:
T-shape incision of the capsule ώ base at acetabulum
Trapezoidal bone of femoral neck is removed Æ Pinning fixation
Disadvantages:
25% AVN
5- Extracapsular Basal femoral neck osteotomy (Kramer):
Indications:
Moderate to severe slips
Advantages:
1- Safer than intracapsular osteotomy
2- Less AVN
Technique:
Preoperative planning based on AP and Lat. views to calculate the 3D
osteotomy accurately
Antero-lateral approach
Anteriorly based wedge is removed < 2cm & < 55°
Internal rotation to close the sedge
Pin fixation by 3 screws with one screw reaching the epiphysis
P R E CA U TI O N S :
1- Avoid removal of >2cm wedge Æ compromise femoral neck length
2- Correction > 55° of the deformity (very difficult)
3- Avoid screws into the superolateral corner of the head
Add:
Contralateral distal femoral epiphysiodesis to avoid LLD if > 15 mm
Contralateral DHS in endocrinopathies
6- Intertrochanteric osteotomy (Southwick)

Indications:
Severe slips up to 60-70°
Advantages:
Avoid AVN
Disadvantages:
Shortening
Difficulty of later THR
Chondrolysis
Technique:
Preoperative planning and recreation of the decided wedge is
mandatory
Flexion, valgus, IR osteotomy is done
It is an anterolateral based wedge with double angles measured in
both AP and lateral views
Precaution:
Avoid > 60-70°
Contralateral in situ fixation

Indications:
In SCFE with endocrinopathy
If oxford bone score is < 16
Triradiate
cartilage
Lesser
Trochanter
Ilium
Greater
trochanter
Femoral
head
No child ώ Oxford Bone Score >22 and develop a contralateral slip

C o m pl ic atio n s :
1. Chondrolysis:
Rapid progressive narrowing of joint space 2ry to articular cartilage loss
E TI O L O GY :
1- Multiple pin fixation
2- May occur spontaneous ð disuse
3- May be autoimmune reaction to chondrocytes
Incidence:
More in black children (so; SCFE in blacks Æ pinning in situ)
Pathology:
Cartilage: thin, fissured, collagen aleration
Capsule & synovium: inflamed, fibrotic, contractured
Then fibrous adhesions cross the joint space
C L I N I CA L L Y :
z ROM
FIXED FLEXED hip in ER
PAIN IS ALLOVER THE ARC of motion not only in extremes
Pain is then z ð ankylosis
Investigations:
MRI
TC99 y UPTA K E
CT to role out hard ware penetration
Aspiration & Culture to role out infection

Treatment:
TRACTION to relief spasm
Gentle physiotherapy to regain ROM
C PM
Antiinflammatories
THR or ARTHRODESIS: If severe continuous pain and z ROM
2. AVN
Incidence:
47% of unstable slips Æ AVN (more risk to injure bl.supply)
Seldom in chronic
y with:
1. Delayed ttt
2. Neck osteotomies especially the intracapsular
3. Enthusiastic manipulations
z ώ:
limitation of manipulations for SCFE (i.e. very gentle
manipulations for acute unstable cases only)
Traction
Diagnosis: by MRI
Treatment:
NWB
Remove hard ware to prevent further protrusion into the hip
If poor functional position Æ intertrochanteric osteotomy
If progressive pain and deformity Æ arthroplasty
DDH Infantile Coxa Vara Perthes SCFE

Aet 1].Generalized laxity Endochondral 1].Vascular ischemia 1].PF:
2].+ve Family history ossification defect 2].Trauma: LBW, Breach a. Rapid Growth spurt
st b. Renal failure
3].1 baby DDH Vascular defect 3].Endocrinopathy
4].Hormonal y E Perinatal trauma 4].Inflammatory 2].Mechanical:
5].Oligohydramnios 5].Hypofibrinolysis: c. Tall
d. Obese
6].Primigravida Other coxa vara: a. z ptn C
e. Thin perichordial ring
7].LOA postion -Congenital: SED, MED b. z ptn S
f. y physeal inclination (α)
8].anteversion -Acquired: SCFE, AVN, c. y lipoprotein A g. z anteversion
9].Shallow acetabular depth DDH, OI, Trauma, RF d. Hemophilia h. Shallow mamillary proce
10].z iliopsoas length 3].Endocrinal:
i. Hypothyroidism
j. Hypogonadism
k. hypopituitarism
Epidem 1:1000 1:20,000 1:10,000 1:30,000
Neonate Infant 4-8y 12y
White White Black
female:♂ = 8:1 Male male
Left hip Bilateral 12% Left hip (or bilateral)
Breech Breach, LBW Endocrinopathy
Path 1].Acetabulum: • Fairbank’s ∆ 1].Stage of ischemia: Metaphysis slip on physis
a. y Anteversion....... >17º • Progressive z neck shaft o Capsular bulge (early) Æ humpy antero-sup
b. y Acet. Index ........ >30º • Pseudoarthrosis like bet o Delayed ossific nucleus portion
c. z Depth &filled é the ∆ & physis o Waldenström sing
o Crescent subch #
fibrofatty tissue • High GT Æ z abd tension
d. Limbus is deg & inverted • y abd lever arm
2].Stage of Fragmentation: Epiphysis acquires
o Mottling (y density + Varus
2].Head: Joint reaction force o
creeping substitution) Retroversion
a. Small & flattened becomes a shearing force o Head extrude, Hinge, Ca
o
b. z antero-lateral coverage o Recurvatum
o Cystic metaphysis
o Gage sign (neck lysis)
3].Neck: 3].Stage of reossification: Physis: thick hypertrophic
a. y Neck shaft ......... >130º o Calcification & proliferative layers
b. y anteversion........ >35º o NBF
o y bone density
o Collapse or healing Acetabulum: antero-sup
4].Soft tissues: 4].Deformity & remodelling erosion
a. Thick lig.teres o Till maturity
b. Thick lig.transverse o Mushroom head
c. Hourglass, thick capsule o Sagging rope sign
d. Short, thick Iliopsoas
e. Short sciatic
Class DUNN ........... (Subluxation) • CATTERAL PXR AP CLINICAL
GRAF ............ (α & β angles) • SALTER % of cresent KALLIO (US)
SUZUKI ......... (Head position) • HERRING’S Lateral pillar LODDER (function)
MORIN ......... (Coverage) • MOSE Sphericity SOUTHWICK (PXR)
RACE & HERRING • STULBERG Congruity KLEIN (PXR)
CP 1].Neonate: 1].Preslip:
• Barlow = dislocatable o Vague pain 3wk
• Ortolani = dislocated 2].Acute
• z abduction o Acute pain
2].Infant o Marked z ROM
o Unstable
• Galeazzi
3].Chronic:
• Klisic test
o Vague pain > 3wk
• Asymmetric skin folds
o z FAbIR
• z abduction
o shortening
3].Toddler and later • Pain o Stable
• Waddling gait • Waddling gait • Antalgic Gait 4].Acute on chronic
• Trendelenburg • TRENDELENBURG • Trendelenberg o Acute after vague
• LLD • LLD • +ve Thomas o Marked limitation
• z abduction • z abduction • z IR, Abduction o Shortening
DDH Infantile Coxa Vara Perthes SCFE

PXR 1].HILGENREINER (Y) + PERKIN 1]. Coxa vara: z neck . All the five classifications 1]. Bilaterality
• Lower medial ........... Normal shaft angle . Head at risk signs: 2]. yphyseal inclinationº
• Lower Lateral .......... Subluxatn 2]. FAIRBANK’S U a. Gage lateral radiolucency 3]. yphyseal width
• Upper Lateral ........... Dislocation 3]. yHILGENREINER b. Lateral calcification 4]. z epiphyseal height
. HILGENREINER Acet Index > 30º EPIPHYSEAL angle ≈ 60º
c. Lateral subluxation
5]. BLANCH sign
. VON-ROSEN line out of acet. d. Horizontal growth plate
4]. High GT on NELATON 6]. SHAM sign
. WIBERG CE angle .... z 7º e. Severe metaphyseal
5]. Low Head at LT resorption 7]. TRETHOWAN=Klien uncut sign
. Broken SHENTON line 8]. AVN
. Broken CALVE’S line 9]. Chondrolysis
. Altered Tear drop 0]. Slip Degree:
. Lateralization & cranealization o KLIEN method
. z anterior CEº in false profile o SOUTH WICK method
US • Early, accurate, practical • Thick synovium KALLIO
• Best in prognosis • DD: irritable hip Æ • Stable, Unstable, & acute
• Graf, Suzuki, Morin effusion on chronic
MRI • For soft tissue assessment • Extent of AVN & • To assess AVN early
revascularization
CT • For post reduction assess • To assess penetration &
closure of physis
Tc • Assess prognosis (A&B) • z uptake in AVN
• y uptake in chondrolysis
TTT 1].NEONATE: • Indications: . <6y & Herring A&B: 1]. Acute: 1 gentle manipulation
oPavlik till 1-6 mo o Correct the deformity o MOTION TTT 2]. Chronic proceed to surgery:
Congruent Residue: o Ossification of the o Mild-mod.... Pinning
o <8y Salter pseudoarthrosis o Severe .......... BG
. >6y or C
o 8-14y Steel o >60º ............. Operate epiphysiodesis or
o CONTAINMENT TTT:
o 46-59º ......... Observe
o > 14y Ganz o <45º ............. Recovers a. Herring A&B Æ Brace osteotomies:
Incongruent Residue: b. Herring C Æ Osteotomy a. DUNN
• Aim:
o <8y Salter b. KRAMER
o Neck shaft ... >130º . >8y (during reossification):
o >8y Chiari or Shelf c. SOUTH WICK
o HE angle ..... <35º o RECONSTRUCTIVE TTT:
o OA Arthroplasty • Osteotomy types: a. Bony:
2].INFANT: ......... 6-18m
o PAUWEL’S i.Valgus osteotomy
o Traction
o BORDEN ii.Garceau
o Adductor tenotomy
o BOWEN iii.GT advancement
o CRUGA or ORIF
z iv.Shelf
o Spica in Ramsey safe zone 3m v.Chiari
o Pavlik Harness 3wk b. Soft tissue
3].TODDLER....... 18m-3y vi.Adductor tenotomy
o VDO vii.Psoas tenotomy
4].JUVENILE....... 3-8y viii.Arthrotomy
5].ADOLESCENT 8-12y
o ORIF
o Capsulorrhaphy
o Pelvic osteotomy
o VDO ± shortening
6].TEENAGE ........13-19y
o Salvage operation
7].ADULT: ...........>20y
o Fusion or THR
[Pedia
P mal Femo
Proxim
D e f in itio n
F oral Foca
F al D
Deficiency
• Congenital termin nal interca alary failure e of femora
al formation
Em
mb br y o l o g y :
• Limb buds appea ar ................................... 4wk
4
• Femur & acetab. differentiate ............ 6 wk; head is part of acetab a
• Diaphyysis ossify & joint cavitation ..... 6-8 6 wk
• Ossif. re eaches the
e metaphysses ........... 12 wk
• Ossifica ation reach
h the neck ................ 15-40 wk
Clinically:
• Child born
b with ....................................... Short Limb
• Hip: .............................................................. F Ab ER
• Knee: ........................................................... Flexion
F Conntracture
• Short Tibia
T
• Fibularr Hemimelia
• Talipes Equinovalgus & Abssent Latera al Ray of the foot
Cllassifficatio
ons
1]. PAPPAS Classification
2]. ATKIN Classificatio
C on
3]. HAMANASHI classiffication
4]. FIXIN & LLOYD
5]. GILLESPIE & TORODE classify patients
p sim
mply into 2 main grou
ups:
Gillesp
pie & Torrode
Type I Type II
-Short femur -Tru
ue proximal femoral defiiciency
oot at mid tib
-Fo bia -Fooot at knee le
evel or even above
-Radiolucent up pper femur -Fixed flexion of hip and kn
nee
p is stable
-Hip
-= Pappas
P 5-9 Æ lengtheniing -= Pappas
P 4 Æ amputation
a rotation
R ad io l o g ic al l y :
• When acetabulum
a m is normaal = head iss normal
• ump is bulbous Æ co
When prox. End of distal stu ontinuity off head and
d neck & GT follows
• Recenttly MRI mayy be used for
f exact diagnosis
Fiixen & Lloyd
Type I Type III Type

e III
-There is continuity
c be
etween -Blunt ossificatiion tuft -Irre
egular or tape
ered ossified
head, necck, & GT separated from sha aft proxximal end of the shaft
-Subtrochh. pseudo artthrosis -Unstable hip Æ ne eed -Unsstable hip Æ need
-Stable hip stabilizzation stabbilization
Class I II III IV V VI VII VIII IX
Shortening 100% 80% 70% 60% 50% 40% 30% 20% 10%
Defect Absent Absent head Both present fibrocart hypoplastic, Short Distal Coxa vara Coxa valga Hypoplastic
Femur & no connection irregular femur, & Hypoplasti Hypoplastic femur
connection Femur hypoplastic c femur femur
Acetabulum Acetabular delayed may be Developed
deficiency ossiftcation absent
Distal Tapered irregular tuft Pseudo- Hypoplastic
femur arthrosis
Condyles Mal- abnormal Irregular LFC deficiency &
developed mid-shaft Valgus
Leg Absent short tibia short tibia and fibula Single bone short tibia and fibula short tibia
fibula and fibula Unstable knee lateral and fibula
Patella Absent patella Absent patella High riding patella
Foot Foot malform Foot malform Foot malform

Treatment Iliofemoral fusion + Metaphysio- Knee Lengthening ± Realignment osteotomies
Van Nes + Prosthesis Ephiphyseal fusion + fusion +
prosthesis Prosthesis
Pappas classification of PFFD (pathological)
Fixen Lloyd Roberts (radiographic)
Atkin Classification (Clinical)

Hamanashi classification
(Comprehensive)
Treatment:
1- L I M B L E N G T H E N I N G :
• Indications: Class VII, VIII, IX (proportionate growth)
• Limit: 20 cm lengthening
• Procedure: Lengthening / Contralateral epiphysiodesis
2- E Q U I N U S P R O S T H E S I S ± A N K L E D I S A R T I C U L A T I O N ± K N E E F U S I O N
3- ILIOFEMORAL FUSION + ankle disarticulationÆ prosthesis (for hip stabilization)

• Indications: Class: I, II
• Procedure:
o Femur is shortened till the knee is at the triradiate cartilage (to act as a hip)
o Fused femur é iliac bone
o Later Van Nes, Syme's, and orthosis
• Adverse effects: Trendlenburg gait + Stiff joint Æ difficult rehab
4- METAPHYSIO EPIPHYSEAL FUSION (same as previous & for hip stabilization)

• Indications: Only in unstable III, IV
• Excision of fibrous (pseudo arthrosis) segment to enhance the synostosis
5- V A N N E S R O T A T I O N O P L A S T Y :
• Aim: convert a non functioning limb into a below knee
amputee
• Prerequisits:
o Normal bundle
o Normal foot & ankle
• Advantages: Good function
• Disadvantages: Cosmesis & Psychological troubles
• Procedure
o Mobilize popliteal a. form adductor canal
o Mobilize common peroneal n
o Cut gastrocnemius heads at the knee
o Proximal tibial osteotomy
o Rotate proximal segment 140°
o Rotate distal tibia 40°
o Additional procedure
o Knee fusion or Iliofemoral fusion
6- FEMORAL OSTEOTOMIES for valgus deformities

[Peediatric Orth
hopedic] Page | 123
D form
De mities
Rota
ational
In‐ttoeing
A
Angular
Out‐‐toeing
Coronal
Sagittal
Linear
LLD
on
Translatio
Defform
mity
124 | Page [Pediatric Orthopedic]
Definition
Rotational Deformities
• Are the deformities that result in in toeing or toeing out
• Toeing-in is the inward rotation of the lower limb
• Toeing-out is the outward rotation of the lower limb
Anatomical considerations
Development :
Femur Tibia:
• Fetus: ............................ -25° retroversion • Fetus:......................................-40° (IR)
• Birth ............................. +35° anteversion • Birth .......................................-15° (IR)
• 10 y ............................... +25° anteversion • 1 y............................................+ 5° (ER)
• 15 y: .............................. +15° anteversion • 15y ..........................................+ 20°
Tibial torsion
• = Angle between posterior plateau axis & transmaleolar axis
Anteversion (Femral torsion)
• It is the angle between neck axis & post-condylar axis in the horizontal plane
Functions of anteversion:
Aids propulsion as it y hip posteior offset Æ y G.Maximus lever arm
Aids the normal foot progression angle is important for toe off
y ROM of the hip
Make the sagittal mechanical axis passes anterior to knee in stance Æ keep it extended
Toeing in
Incidence
• Is much more common than toeing out
• Up to 25° is tolerated
• If acquired, there is no remodling (unlike angular deformity)
Aetiology:
1]. Idiopathic (commonest)
2]. Developmental: DDH
3]. Traumatic: Fracture malunion
4]. Neuromuscular disorders: CP
Pathogenesis of Idiopathic Toeing in
Internal TT y FAV Metatarsus Hallux varus
Incidence Toddler Juvenile Infantile Neonate
Degree 8° till 8y 8° till 8y Few degrees Few degrees
Age limit 16y 8y 3-4y Must be corrected
Correction usually corrects spontaneously with age Needs surgery
Complications of toeing-in:
• y FAV Æ y PF & knee OA
• y ITT Æ OA knee
• z FAV Æ OA hip
[Pediatric Orthopedic] Page | 125
Toeing out
Inidence
• Normally foot is in 30° ER in relation to tibia
• Less common than toeing-in
• At 3y ~ 3° and at 12y ~ 12°
• Up to 60° ER is tolerated by the foot
• More on right side & in over weight
Aetiology:
1]. External tibial torsion (compensatory to yFAV)
2]. z anteversion (less common)
3]. Developmental hip problem: SCFE
4]. Traumatic: Fracture malunion
5]. Neuromuscular: CP
Clinical Evaluation of Rotational deformity
History
Complaints: Clumsiness, difficulties, cosmetic, emotional
Prenatal History
• Oligohydramnios
• Preterm Æ ETT
• Neuromuscular disorder
Family history
• Torsional deformities run in families
Examination:
• Inspection:
• Standing .............................. Q angle y in y FAV
• Sitting ................................... W-position / Grass-hopper patellae (cong patellar dislocation)
• Gait analysis
• Running .............................. exaggerate gait abnormality
• ROM:
o y FAV in extension y IR & z ER in extension
o y FAV in flexion regain ER (ant capsule relax)
• Staheli's Rotational Profile:
1]. Foot progression angle (N:30°)
2]. Hip rotation (IR/ER) (N:45°/30°)
3]. Hip anteversion Craig test = Ryder's method
4]. Foot thigh angle (N:30°)
5]. Transmaleolar thigh (N:30°)
•
nd
• N.B. hind foot axis normally projects to the space between 2
& 3rd toes if displaced lateral Æ adductus
Imging:
PXR: two methods
1]. Conventional method: repeated views at different
degrees of internal rotation, 0-10-15-20° then determine
the longer neck length at degree of rotation = FAV
2]. Trigonometric method: AP & trans-table Lateral views
are taken with the patella facing upward, then measure
the angle between the shaft axis and the neck ( & ß)
then draw them on a graf to get the true neck version
CT:
• Assess present pathology; e.g. physeal injury, bars
• Scanograms for associated angular deformity
US: Accurate and sensitive
MRI: good results but expensive
Treatment:
1. Observation & Reassurance
• Most cases correct at 8y
• <1% require surgery
• Instruction of not setting in W may be of some value
• Mild in toeing gives athletic advantages
2. Conservative: Braces & splints are of value Only for uncorrected Metatarsus adductus
3. Surgery:
Time
• After 8y ............................... if idiopathic
• Early ....................................... if neuromuscular to improve gait & z energy expendature
Types:
1 Femoral osteotomies:
Indications:
1]. y FAV
2]. > 80° IR
Types:
1]. Ilizarov technique
2]. Supracondylar osteotomy: if associated y Q angle
3]. Intertrochanteric osteotomy: less complications, less immobilization, more accurate
4]. Closed femoral intramedullary osteotomy: good results, > 12y
2 Tibial osteotomies:
Indications:
1]. <10° ITT
2]. >40° ETT
Types:
1]. Proximal (if with angular deformity)
2]. Distal + pin fixation & LLC
3]. Fixation is by pin fixation, ext.fix, Ilizarov
Limb Length Discrepancy

• complex problem characterized by LL inequality, and involve the neuromuscular bundle as well
Aetiology:
LLD
Congenital Acquired
Idiopathic
Anomaly Diseases
Developmental
- DDH
- Coxa vara
Transverse Longitudinal Dysplasia - Blount's
Terminal Terminal - Fibrous Dysplasia
- Neurofibromatosis Traumatic
- Amelia - Paraxial hemimelia - Physeal injury & #
- Hemimelia (absent leg element + - Oliers
- Diaphyseal acalasis - SCFE
- Apodia/Archeiria hand part)
Infectious
Intercalary: Intercalary: Vascular disease - Septic AVN
- Phocomelia (hand is - Paraxial hemimelia - Klipple trenaunay
attached to trunk) (one leg or FA bone is Tumours
- PFFD absent) - And their ttt
Neurological
- Polio
- CP
Pathogenesis
Patterns of LLD progression (Shapiro)
A. Type I Upward slope pattern

• The discrepancy y continually é time at the same rate.
• Examples: PFFD, Epiph.inj., Olliers
B. Type II upward slope deceleration pattern

• The discrepancy yprogressively then decelerate
• Examples: # femur, Septic arthritis hip
C. Type III Upward slope plateau pattern

• over growth of the femur after anatomical reduction
• Examples: some Polio, congenital short femur
D. Type IV Upward slope plateau upward slope pattern:

• The discrepancy ysteadily, stabilize, then yagain.
• Examples : Hip diseases in children e.g. Perthes’
E. Type V upward slope downward slope pattern

• The discrepancy undergoes spontaneous correction
• with growth and correction of the pathology
• Examples: JRA
128 | Page [Peddiatric Orthopedic]
Ev
valuaation
Hisstory: Anyy clue to the cause
Exaamination n:
• Generall:
o Mentality ............. CP
o Built ....................... Stuntted growth
o Endocrine ........... SCFE
• Inspectio
on:
o Standing.............. Q-ang gle, squintin
ng patellae e
o Sitting.................... W-sig gn, grass-ho opper patellae, Tripod sign (hamss tightness)
o Walking ............... Dyna amic thrust, stiff gait, Trrendelenbe erg gait, sho
ort limb gaiit
o Supine .................. ER in SCFE
• ROM:
o z ROM ................. (zabd duction in DDH
D & coxxa vara, z FIR
F in Perthe es, zFAbIR in SCFE)
o Fixed def ............. Abdu uction, addu uction, flexiion (Thom mas test), (Ely’s test), (O
Ober’s testt)
• LLD
o Tape metho od........ from tip of mediial malleolu us to ASIS & compare
o Block meth hod .... child stands on serial s blockss é different heights tilll the pelvis is leveled
o Galleazi ............. deterrmine the sh hortening tibial
t or fem
moral or botth
o Bryant’s Δ ...... Meassure from GT G to line from ASIS (supratroch
( h. Shortenin ng unilat)
o Nelaton ............Line from f ischial tuberosityy to ASIS sho
ouldn’t inteersect GT (iff bilat)
o Klisic test ........... line frrom GT to ASIS A should d pass into umilicus no ot below it (apparent
( sho
ort)
• Angularr deformity........... Interc condylar disstance
• Rotation
n deformityy .......... Stahe eli's approacch
Raddiography y:
• AP, and Lateral + Wrist films (bone age e)
• Ortho-ro
oentgenogrram (Telera adiograph hy): 1 expossure for a whole
w limb, h
has magnification errorr
• CT Scannograms / 6m 6
Groowth Cha arts:
A
Advantag ges:
1]. Record & predict growth
g patte
ern
2]. Anticipa
ate time forr epiphysiod
desis
3]. Accuratte objective
e method
T
Types:
1]. Green Anderson
A Table Calculate the
t remaining growth
2]. Moseleey chart Predict the
e future gro
owth
3]. Moseleey Compute ed Prog Computerr program analyze da ata & sugge
ests the time
e of ttt
4]. Greulic
ch-Pyle atlas Wrist Xrayys used as a reference for
f bone age
Trreatm
ment
Amou
unt of LDD
D
< 2 cm 2-3 cm 3 cm
3-5 > 5 cm
Obseervatio
Shoe lifts Bridge Sh
hortening Epiphysiodeesis Lengtheening
n
Amp
putatio 1
1 cm Restt Temp Metaphhysea
Removal Open Closed Diaphysseal Phyyseal
n? in
nside outsid
de staples l
chon
ndrodiastasis O
Open Phemister CODILLLA ORTHO
OFIX Chon
ndro‐
WAGN
NER ILIZAR
ROV diastasis
1- Observati
O ion:
P
Percuteaneous
• Usually spontaneo
s ous correctio
on occur <2
2cm
2- Physeal bridges removal + soft tissue interposition:
• Usually ð inf. & trauma Æ sclerotic bone bridge Æ traverse physis Æ restrict growth & deformity
• Types:
o Peripheral: from edge of metaphysis inward
o Linear: from metaphysis to another metaph. point
o Central: conical & surrounded by physeal tissue
• Preoperative 3D CT for accurate Dx of size, site & contour (if >40% shift to other ttt)
• Resect the overlying periosteum & the sclerotic bone till the physis is exposed all around
• Central type: is removed via metaphseal window
• Fat or Methylmethacrylate Æ interposition
• Draw Backs: reformation & phseal closure
3- Chondrodiastasis:
• Progressive distraction across the physis till the bridge breaks
• Aim:
o Bridge breakage if used at a high rate
o Lengthening if used at a low rate
• Disadvantages: Reformation and premature closure
4- Epiphysiodesis:
• Iatrogenic destruction of the physis Î fuse and arrest growth of the long bone & equalize the
limb length discrepancy
• Preparation, prediction and timing for surgey are the same as discussed
Techniques:
• Staple: temporary Epiphysiodesis and could be removed to resume growth; but some times
fusion, angular deformity reversal occur
• Phemister & white: 2 bone blocks are removed from each side of physis, rotated, and reinserted
to creat bone bridges Æ 6wk cast Æ consolidate in 2-3 mo
• Percutaneous fluoroscopy guided epiphysiodesis: physis is drilled on each side via medial lateral
small incisions and under image control, destroy the physis to stimulate bridge formation; care
must be taken for the undulant nature of the physis Æ PWB & ROM and close follow up
5- Shortening procedures:
• Done near growth arrest
Types:
• Open: remove segment Î plate fixation e.g. Wagner’s osteotomy
• Closed: IM osteotomy & fixation by IMN (less invasive, less morbidity, but
techniqually demanding)
6- Limb Lengthening
Prerequisits:
• >5 cm LLD
• Fully understand (biology, techniques, complications)
• Psychological preparation of the patient
Techniques:
• Codilla technique (Single stage diaphyseal cut & stretch ):
High rate of complications
• Wagner Technique:
o Diaphyseal osteotomy
o After day 7 start daily distraction 1mm/day
o Use unipolar fixators till desired length Æ plate &
BG
o After consolidation remove the plate
o Pitfalls:
• Diaphyseal
• Single daily lengthening
• Necessity of plating
• Orthofix:
o Metaphyseal cortecotomy (Compactotomy): better callus formation
o After desired length Æ dynamization of the device
o After callus maturation Æ removal of the device
o Can correct angular deformity
• Ilizarov
o Ring fixator method that its stability depends on -- frame stability / wires tension
o Distraction osteogenesis: distraction NBF along the long axis of bone
o 1mm/d lengthening (0.25mm/6h)
o Advantages:
Stable
Correct angular deformity
Correct rotation malalignment
Correct LLD up to 20cm
Can be used for LL & UL & foot
Pt. can bear wt. with the frame on
o Disadvantages
Pin tract infection Muscle tether
Cyst formation Fixator failure
Bone fractures Frequent adjustment
Joint stiffness Techniqually demanding
Nerve injury Need close follow up
o After Care
ROM
Orthosis
Physiotherapy: for ms. strengthening
• Taylor spatial frame (Six-axis deformity correction)

o Actually any deformity occurs as a compined defomities in 6 axes.
o It is difficult to correct 6- axis deformity by single axis hinge
o Charles Taylor modified ilizarov fixator into six telescopic struts free to rotate at proximal
and distal rings
o Soft ware computor program is used to correct and give an idea about the frame to be
used
o Another software for residual deformity.
7- Amputation:
• Fibular Hemimelia
• Congenital insensitivity to pain
Coronal, and Sagittal, Deformities

Mechanical axis
• It is the static weight bearing axis
Frontal mechanical axis:
o From femoral head centre to ankle centre
o Normally passes medial to the centre of the knee
Sagittal mechanical axis:
o From centre of gravity (infront S2) to the centre of ankle
o Runs behind the anatomical axis of hip Æ extension in stance
o Runs just ant. to knee Æ extension in stance
Anatomical axis
• It is the central axis of the bone
• It is represented by a line drawn between the middle points at different levels of the bone
• There is frontal and sagittal anatomical axes as well
Bony axes
• Tibia:
o Coronal anatomical axis & mechanical axis are almost the same
o Sagittal anatomical axis is the line between a point 1/5 way from ant end of proximal tibial
orientaion line to the centre of the ankle, passing through the mid diaphyseal points
o Sagittal mechanical axis is the line between the mid points of the knee & ankle
• Femur:
o Coronal anatomical axis runs from pyriformis fossa to centre of knee (COK)
o Coronal mechanical axis from the centre of hip (COH) to COK
o Sagittal anatomical axis from pyriformis fossa to COK passing the mid—diaphyseal points
o Sagittal mechanical axis from the centre of hip (COH) to COK
o There is an angle of 6° between the 2 axes
• Mechanical axes of femur & tibia form an angle of 1.3°; so mechanical axis of the one bone can be
extrapolated to represent the near-by segment mechanical axis
Meechanical Axis
A Deviation
• Is the disstance betw ween the COKC and thee mechaniccal axis =
the mom mentary arrm of defo ormity forcee around the
t knee
(N:8mm m or at the medial
m tib.sp
pine)
• MAD y as the defo ormity apprroach the knee
k
• Soft tissu
ue laxity & contracture
c es Æ dynam mic MAD
Joint Fronta al orienta ation liness:
• Joint aliggnment: re elation of joint to mech hanical axis
• Joint oriientation: re elation of jo
oint surface
e to the bon
ne axis
• Distal feemoral OL and PTOL are almost // to the ground
(converg gence anglle is 1.5°) exxcept if NWWB and stresss films
Sag
gittal Orie entation lines:
l
• Proxima al tibial OL: 10° posterior slope
• Distal tib
bial OL: 5-10 0° anterior slope
Hip D
Distal Femu ur Proximal Tib
P bia Ank kle
Line
e From head centre Across
A lowesst points of A
Across the two Acrooss the domee of
Sagittal Frontal
to tip off GT ffemoral cond

dyles p
plateaus the talus
t
Anaatomical axis 84° 8
81° 8
87° 89°
Mecchanical axis 90° 8
88° 8
87° 89°
Line
e From head centre Meeting
M poinnts of the L
Line along tthe flat Linee bet ant & post
p
to tip off GT c
condyle é me
etaphysis p
plateau lips of
o joint
Ana
atomical axis 90° 8
83° 8
81° 80°
Mecchanical axis 90° 90° 9
90° 90°
Deform
mity
• Deformity occurs as
a a mixture
e of deform
mities in the different pllanes &theiir magnitud
de is more than
t
it looks in
i AP & late
eral views
• Uniapic
cal deform
mity is a defoormity that occur at sin
ngle point
• Multiap
pical deforrmity is a de
eformity tha
at occur at more
m than 1 point
Defformity described
d by:
1]. Magniitude of th he deformitty
2]. Directiion of dista
al segmentt (e.g. varu
us) or
3]. CORA (centre off rotation of
o angulatio on) = Defo
ormity apexx (e.g. 30° lateral apexx)
4]. Plane of
o deformiity
Rotational malalignment
• Not appreciated in XRay
• Alter the appearance of angular deformity e.g. recurvatum + IR Æ false varus
• It can be assessed clinically by staheli approach
1‐ Malalignment test: Dror Paley
• Deformity description: CORA, Magnitude, Apex, Direction, Plane
Step 1:
• Standing AP & true lateral with patellae facing forward
• Draw mechanical axis of the limb in AP & lat ….
• Draw all axes in coronal & sagittal planes
Step 2:
• Draw all joints orientation lines in AP & lat. (hip, knee, ankle)
Step 3: if there is a deformity
• Draw segmental mechanical axis by extrapolation of the near by bone mech axis
• Another alternative method is to use normal referrence angles between JOLs & bone axes
• You can use the anatomical axis as an alternative
• Proximal femur: line 84° to hip OL from the piriformis fossa

• Distal femur: extrapolate the tibial mechanical axis
• (or line 88° on distal femoral orientaion line)
• Proximal tibia: extrapolate the femoral mechanical axis
• (or 87° line on prox tibial orientaion line)
• Distal tibia: line 89° to ankle OL from centre of ankle
Step 4:
• Apex of deformity is where the segmental axes intersect =CORA
• If CORA is not opposite the maximum deformity Æ there is another apex
(multiapical deformity)
rd st
• Then draw 3 mechanical axis of the middle segment; starts from the 1 angulation point passing
through the mechnical of anatomical axis of that segment till it meets the other mechanical axis
Step 5: recreation of the plane and magnitude of deformity
• Axis of correction is to the plane of deformity
• Draw a graph and draw an epsilateral foot in the centre of that graph (i.e. if you are dealing with
a rt. Limb draw a rt. foot)
• Name the axes of the graph in relation to the
foot (medial, lateral, anterior,…) é a scale 1mm/1°
• If the deformity is measured 25° anterior apex
and 20 lateral apex plot that point on the graph
• And measure its distance form the centre and its
angle on the horizontal plane
• The distance = magnitude in degrees
• The angle = plane of deformity from horiz. plane
• In our example: Magnitude 32° with Apex 51°
in the anterolateral Plane
Step 6:
• Translation is determined in the same way
• Rotational malalignment is measured by Staheli approach or scanograms
• LLD is measured clinically by tape or block technique
•
•
2‐ Jackson and Waugh old technique
• Osteotomy made distal to the tibial tuberosity to correct varus or valgus deformities
• Disadvantages:
1]. Inaccurate
2]. Non union
3‐ Coventry conventional technique
• High tibial osteotomy is done to correct the deformity
• Over correction is advised by 8° valgus
• Indications:
1]. Osteoarthritis that significantly interfere with recreation especially in < 60y
2]. Unicompartmental OA seen on WB PXR especially in good ROM ≈ 90° flexion
3]. Varus or valgus deformity especially in ligamentous instability
4]. Good vascular status
• Contraindications:
• Lateral space narrowing < 2 mm
• Lateral tibial subluxation >1 cm
• Medial tibial bone loss .. >2-3 mm
• Flexion contracture ....... >15°
• z flexion ROM ................. <90°
• If correction needed ...... >20°
• Rheumatoid Arthritis.
• Disadvantages:
1]. Recurrence of deformity
2]. Inferior results é over weight patients
• Technique:
• Simply by measuring the tibio-femoral angle (between the 2 anatomical axes)
• Wedge = tibiofemoral angle + 6-7° normal valgus + 3-5° overcorrection (≈ 10° net valgus)
• Methods of measuring the size of the wedge base to be removed
• Insall method ................. W = 1mm for each 1° (true for 57mm tibiae)
• Coventry method ........ W = tibial diameter × 0.02 × angle
• Pt supine & knee flexed 90° throughout the operation to protect popliteal & peroneal bundle
• Curved lateral incision starts at the fibular neck, till reaches it proximal to LFC
• Expose the fibular head / ITB / LCL / biceps femoris tendon (usually, peroneal n is not exposed)
• Manage the fibula by one of the following methods:
• Excise the fibular head after freeing of its attachments
• Open superior tibio-fibular joint the resect the infero-medial part only
• Osteotomize the fibula by a seprate incision
• Divide posterior 2.5 cm of ITB to expose the lateral tibial plateau
• Cauterize the lateral inferior genicular v v. & protect the peroneal n
• Elevate the periosteum from medline till posteior as much as possible é protection of popliteal v v.
• Begin the proximal cut at least 2 cm distal to the articular surface
• Distal cut is done as calculated. Stop both cuts at the medial cortex without cutting it
• Remove the wedge & close the osteotomy site
• Fix the osteotomy é one or two staples / or é a contoured T-pate

4‐ Maquet dome shaped osteotomy
Advantages
1]. Curved shaped osteotomy allowed more accurte correction
2]. Easy adjustability even postoperatively if no internal fixation used by
modification of the cast
3]. Inherently stable, extensive internal fixation is not required
Disadvantages:
1]. Technical difficulty
2]. Intraarticular fracture
3]. Scarring about the patellofemoral extensor mechanism.
5‐ Hernigou Medial HTO
• Medial opening wedge tibial osteotomy above the tibial tubercle
• Claimed more precise correction > lateral osteotomy
6‐ Jig Techniques
• Hoffman technique for lateral closing HTO using a special jig
• Turi technique: Medial opening tibial osteotomy below tibial tubercle
using an orthofix jig
Complications of tibial osteotomies:

1]. Under correction: commonest
2]. Recurrence of deformity
3]. Intraarticular fracture
4]. Nonunion
5]. Patella baja ð fibrosis of the patellar tendon & NBF
6]. Peroneal nerve palsy: related to fibular osteotomy
7]. Muscle stiffness
8]. DVT
9]. Compartment syndrome
10]. Infection
Compensatory mechanisms in varus

1]. Pt. sways side to side to unload medial compartment
2]. Foot is externally rotated so the heel approach the mid line and the
GRF and the knee as well Æ z deformity momentary arm around
the knee
Different joint adaptive reservoir for deformities
• Ankle and hip adapt frontal deformities
• Subtalar joint also adapt mild frontal deformities
• Stiff subtalar joint Æ y ankle loads Æ ankle OA
• Hip fusion in abduction Æ knee OA
Pediatric Knee Problems

Congenital Knee Dislocation
Definition:
• congenital displacement of tibia over the femur
Incidence:
• 2:100,000 (1:100 DDH)
• Female > Male ................ 10:3 ratio
• Bilateral ................................ 30%
Aetiology:
1]. Extrinsic: Fetal position, y in Breech
2]. Intrinsic:
o Absent ACL
o Quadriceps fibrosis acquired
Associated deformities:
1]. DDH
2]. TEV
3]. Spina bifida
4]. Arthrogryposis/Down's/Larson
Pathology:
1]. Contracture of: quadriceps, ITB, lateral intermuscular septum
2]. Anterior subluxed tibia
3]. Underdeveloped or absent patella & laterally displaced
4]. Hamstrings and ilio-tibial band anterior
5]. Absence suprapatellar pouch
6]. Hypoplastic or absent cruciates
Classification:
• G I (mild) .............................. knee 20º hyperextended
• GII (moderate)................... knee 25-45º hyperextended
• GIII (total)............................. no contact, hip flexed, foot at mandible
Diagnosis:
• Neonate born é a strikingly hyperextended knee, limited flexion
• Tibia Dislocated Anterior to femur
• Tight quadriceps
TREATMENT:
• The knee is usually Too Stiff for Splintage or manipulation
[i]. Gentle manipulation to flexion Æ ant splint
[ii]. change splint every day é y flexion degree
st
[iii]. If + DDH: correct dislocation 1 till reach 45º flexion Æ correct both by pavlik
• Surgical treatment usually at 3-6 Mo of age:
[i]. Perform before weight bearing via ant-medial approach
[ii]. Inverted V in rectus femoris + quad release
[iii]. Release anterior knee capsule & ITB
[iv]. Hip spica x 6 weeks, then night splint
[Peediatric Orth
hopedic] Page | 137
Patellar Dislocation
Congeenital Devellopmental Traumatic
Co
ongen
nital Patellla Diislocaation
Deffinition
• Permanent laterally y displacedd patella ass a part of a congenital
abnorm mality of the quad mech hanism
• Present at birth & diagnosed
d t
then or witthin first deccade.
Aettiology
• Failure of the my yotome con ntaining th he quadrice eps & pate ella
from intternally rota
ating in thee first trimester.
Patthology
• Extensoor mech. is short
s & inse
erted antero olaterally
• Patellar ligament iss displaced laterally
l 45º
• Valgus knee
k
• Hypopla astic LFC
• Shalloww trochlea (bbold end fe emur)
• External rotation of tibia
• Contraccture of late
erals: ITB, VLL & lateral capsule
c
• Loose medials:
m VMO / medial retinaculum m / medial capsule / medial
m pateello-femoral ligament
• 2 types:
o Persistent: contractu ure of lat.re
etinaculum / patella is tethered
t latteral to LFC
C
o Obligator ry: contractture is less severe
s / pattella displacces é flexionn & replace e in extensio
on
• May be associated é: Achondroplasia / Down’s D
Clin
nically:
Perrsistent Obligatory
Age of presentatio
p on Todd
dler (may be at
a birth) laterr
Position
n of patella
a tethe
ered laterally dislo
ocate & relocatte
C/O flexio
on contracture
e knee
e instability
compliccations Dela
ayed & difficultt walking OA & delayed wallking esp. if billat.
an to be pallpated Æ difficult
• May be smaller tha d diag
gnosis
Rad
diologically:
• Patella ossify
o at 3-5 y
• MRI is diiagnostic
Tre
eatment
• Treat < 1y
1 of age Congenittal
patellarr
dislocatio
on
Lateeral
Quadriceps Reinsertion of
retinaacular M
Medial plication
ning
lengthen don
patellar tend
± rele
ease
• Consideer Roux-Golldthwaite
• Posterio
or release if flexion defo
ormity is present
• McEwin n varus osteeotomy or modified
m in skeletally im
mmature ptt. é G.valgu
um
• Galeazzi & Dewar ifi there is medial
m quad driceps deficciency
Recurrent Patellar Dislocation
Incidence
• Adolescent
• Female >male
• There is familial tendency
Predisposing Factors
• Generalized laxity • Patella alta
• Weak vastus medialis obliquus • Hypoplasias of LFC
• Tight lateral retinacula • y Q angle Æ lateral vector ms force
• Tight lateral patello-femoral lig • Twisting Æ damage medial capsule
History:
• Teenager girl
• Ant. Knee Pain K é activity
• Instability:
o Impingement of patella against LFC during flexion
o Recurrent giving way
o Popping
o Locking
• May be there is a History of acute episode of complete lat.displacement of patella
O/E
• Patella Alta points more towards ceiling rather than strait ahead é 90º flexion
• Apprehension é medial pressure Î patella over hang the LFC
• +ve J Sign (during extension patellar tracking moves medial with a path like letter J
• Palpable deficiency of V.Medialis Obliquus (by vigorous quad contraction)
• Q Angle: > 20º Æ valgus force predispose to subluxation
PXR Skyline view
o Patellar tilt
o Incongruence between patella & trochlear sulcus
o It is a static tool and not dynamic
o The best is dynamic patellar testing
Treatment:
Chronic and Habitual patellar dislocation
• Vigorous exercise program to balance forces around knee
• Braces are helpful
• Lat.retinacular release if L lateral patellar excursion
• Prerequisite: Preoperative strengthening
• Indication: resistant cases
Patellar dislocation
• Lateral retinacular release
+
• Medial placation / or medial augmentation by semimembranosus (Galeazzi & Dewar)
OCD knee .................................. see knee

[Peediatric Orth
hopedic] Page | 139
Os
sgoo
od-Schlatt
ters Disea
ase
Intro
oduction
• Described simultaneouusly by Osgoood and Schlatteer in 1903
• Lesion afffects adolescent apophysiss of proximal tiibia (young athletes)
• ♂>♀ = 3::1; but boys arre older at preesentation
• Bilateral 25-50%
2
Anattomy
• Tibial tubberosity apophhysis developss from few osssif.centers
• Calcificattion begins disstally (averagee age 9 ♀, 11 ♂)
• They fusee & coalesce é proximal tibiial epiphysis (12♀/13♂)
• Blood supply
o Anterior, laterral & medial suurfaces of tubeerosity
o Communicatioon é metaphysis via traverssing canals across physis (m may still be
open at 10-12 2 years)
Etiollogy (controve
ersial)
• Most com mmonly accepted: microavulsions caused d by repeated traction
• Recent MRI/CT:
M revealed tendonitis ώ is importan nt as apophysiitis
• Often refeerred to as ossteochondrosiss, but no AVN nor remodelin ng unlike Pertthes
Signns and Sympttoms
• Pain ώ K é resisted knee extension
• Local sweelling, heat, teenderness at tibial
t tuberosityy
• Prominennt tibial tuberoosity
Radiiography Limited role. Cliniical diagnosis.
• Soft tissuue swelling antterior to tuberoosity is most common
c findinng
• XRay: maay see ossiclee. (NB: Fragmeentation of tubberosity is norrmal variation in ossification)
• CT/MRI: changes at insertion of pateellar tendon. Distended
D infra
apatellar bursaa.
• U/S: Thicckening of tenddon (more echhogenic). Hypoechoic soft tissue swellingg. fragments
Diffe
erential Diagnnosis
• Infection ● Malignancy
M
• Tibial tubbercle fracture ● Patellar
P tendonitis (Jumper'ss Knee)
• Sinding-LLarsen-Johanssson Disease (analogous coondition at infe erior pole pate
ella)
Treaatment:
• symptom ms often recur - makes treatm ment difficult
• Natural history
h of untre
eated disease::
o most recover spontaneouslly with no limittation of activity with closuree of physis
o many are unaable to kneel without
w pain
o if fragmentatioon on X-Ray = chronic symptoms
Conservative Treatment
• Withdraw wal from active e sports that caause pain
• Ice, NSA AIDs, pad to prrotect tuberosiity or Infrapateellar strap during activity
• Cast imm mobilization forr 6 weeks if seevere symptom ms
• Steroid innjection NOT recommended
r d (risks; very questionable
q efficacy)
e
Surgical Treatment
• Indicationns:
o Rarely indicatted (Conservaative treatmentt works >90%/no differencee in results connservative vs. surgery)
o after ossification of tuberossity
o symptomatic separated osssicles
• Types of surgeries:
o Thompson-F Ferciot tubercle thinning proocedure: (excission of ossiclees ± excision oof prominent tu ubercle)
o Drilling of tubeercle
o Bosworth Bone Pigs operaation: (drill 2 drrill holes in the e tuberosity wide enough too insert an auto
ogenous pre-
tailored bone pigs taken froom the antero--medial tibial cortex)
c
• Complicaations:
o Continued pain with kneelinng
o Increased tibial tuberosity fracture
f
o Genu Recurvatum ð careleess removal beefore apophyssis fused Æ recurvatum
ACL INJURIES IN CHILDREN
Incidence
• Very uncommon injury in children with open physis
• Occurs much less commonly in children than adults (~1.5% of all ACL ruptures)
• Distal femoral and proximal tibial physeal fractures are commonly associated with ACL injuries
• Increasing incidence likely related to increased participation in vigorous sports, increased
incidence of multiple trauma, increased awareness among physicians
Anatomy
• Ligaments are stronger than physis
• In children, collagen fibers of ACL are continuous with perichondrium of epiphyseal cartilage
• In adults, ligament inserts directly into bone by way of Sharpey's fibers
• Ligamentous laxity may offer some protection to children (decreases as approach skeletal
maturity)
• Physeal fractures/anterior tibial spine avulsions more common than ACL injury
Mechanism
• Hyperextension, direct blow, sudden twisting in open field
• In younger children, injury associated with multi-trauma (5/9 struck by motor vehicle)
• As with tibial eminence fracture, bicycle accidents are relatively common cause
• Adolescents are more likely to sustain during contact sports or sports where cutting maneuvers
while running
Imaging
• MRI : 97% accurate compared to arthroscopy in diagnosing ACL tears (ages 14-69, average age
33)
• Less accurate in diagnosing tears in children
Treatment
Conservative
• No better in children than adults
• Kannus, et al : 8 year f/u. Children with complete ACL tears had poor results with chronic
instability, continuous symptoms, post-traumatic osteoarthritis
• McCarroll and Shelbourne : 40 patients less than 14 years. old with midsubstance tears. Most
patients that were treated conservatively (bracing, rehab, activity modification) were unable to
return to sports. All experienced recurrent episodes of giving way, effusions, pain.
Operative Treatment
• Why operate?
o High incidence of meniscal injury in ACL-deficient knee
o Protect repaired meniscus
o Prevent Degenerative Joint Disease
• Repair does not work
• 1ry concern about reconstruction is injury to growth plate and resultant growth arrest
• Intraarticular vs. extraarticular procedure - Greater potential risk of growth arrest with intraarticular
so some prefer extraarticular in younger patients.
• Good results with early reconstruction (McCarroll and Shelbourne; Lipscomb and Anderson;
Parker and Drez)
Baker’s Cyst
• Tumour like gelatinous filled swelling occur at the back of knee
Incidence
• ♂:♀ = 2:1
• 5-8 yrs & resolve é in 2 y
• Usually unilateral, from the gastrocnemius-semimembranosus bursa
• 70% communicate with the knee joint
Clinically:
• Usually asymp
• Mass in the back of knee
o Under the medial head gastroc
o y é extension & z é flexion
o +ve transillumination
• ± Stiffness & pain
• ± PHMM (in adults)
• Recover spontaneously (in children)
• It may reach a big extent as in rheumatoid synovitis
Radiologic
• US is difficult to differentiate it if it is a cyst or not
• MRI delineate the lesion & PHMM
Treatment
• Transillumination if +ve Æ aspirate é a wide bore cannula Æ if gelatinous aspirate Æ
• Reassurance:
o Lesion is benign
o Resolve spontaneously 85%
o Recur after surgery 50%
Discoid Meniscus
• Incidence is 1.5-5% in the West , but 15% in Japan
• Lateral more common than medial
Aetiology
• Smillie suggested it was failure of the fetal discoid form
of the meniscus to involute. The meniscus is derived from mesenchyme, is initially a disc & then
forms as a semilunar structure.
Classification
• Stable, Complete
• Stable, Incomplete
• Wrisberg Unstable type, ð congenital absence of the meniscotibial ligament
Diagnosis
• Symptoms of snapping and popping usually at 6-12 years.
• Patients with type III discoid menisci Æ instability.
• MRI
Treatment
• Preserve the meniscus
• Aim to refashion the meniscus
• If type III will require refashioning & stabilisation, using a capsular suture
Peddiatric Leg
L Prooblemss
Geenu V
Varum
m
Ge
enu Varu
um
Physio ologic Path

hologic
Tibial, <1
15°, <2y Femorall, >15°, >2yy
Phyysiologica al varus
• Present at birth ................. up to o 15° varus
• z till 2y ................................ 0° Æ then startss in the othher way Æ Physiologic
P c valgum
• y till 4y ................................ 8° Æ slow return n to norma al
• 11y ......................................... Norm
mal alignmeent
Patthologic GenuG Varum
1- Congenital:
Lim mb anomalyy: tibial hem mimelia
Dyssplasia: SED D, Schmid, Olier’s
2- Develo opmental:
Tibiia vara: Blo ount, Juven nile, adolesscent
3- Physea al destructio on by (trau uma, infecttion, Trumo ours)
4- Metabo olic:
Rickkets
Hyp pophospha atasia
5- Neurom muscular disorders d
T bia Va
Tib ara
• it is a rarre disorder involving physis,
p meta
aphysis, and
d epiphysis
Cla
assificatio
ons
• Blount t classificatio
on: (infantile and adole escent)
• Thomp pson classiffication (infa antile, Juve
enile, and ad
dolescent)
Tibia Vara
a (Thompso
on)
Infantile (Blount’’s) Juv

venile Adolesscent
-<3y -3-10 y ->10y
-Common n -recurrent -N
No recurrence
e
-60% Bila
ateral -M
Mild & rare
Inc
cidence off Blount’ss:
• more in:
Afriican Ameriicans ▪ Fema ales
Obese ▪ Earlyy walkers
• 60% bila
ateral
[Peediatric Orth
hopedic] Page | 143
Ætiiology mu ultifactoriall
1]. Early re
epetitive wtw bearing
2]. Physiollogical varu us
3]. Ligame entous laxity
4]. geneticc predispossition: but no actual mandelian n inheritancce
Patthology:
• Disorganized cells
• Islands of
o fibrosis alternating é Islands of hypertroph
hic cartilage
e
• Transph hyseal Bl.v.
Clin
nically: Obese, blackk, female
1]. Progre essive defo ormity
2]. >12° vaarus
3 Interna
3]. al tibial torssion
4 Lateral thrust durring stance
4]. e
DD
Dx
• Adolesce a Ù femoral varus ≠ Blou
ent tibia vara unt Ù femo
oral valgus
• SED • Achondroplasiia
• Schmid • Oliier’s
Cla
assificatio
on: Langen
nskiöld & Riska acccording to age and X-ray
X
I Peeking of the
P t medial metaphysis
m
Resolve
II M depression of the medial mettaphysis
Mild
III S
Stepping-off
ff of the med dial metaphhysis Neeed simple
IV S
Stepping-doown of the medial
m epip
physis on th he metaphyyseal step ossteotomy
V y slope of medial
m articu
ular surface
e + cleft bet med & lat epicondyle
e Poor prognosis &
VI Bony bridge across the e physis recur
PXR
R
• Langensskiöld +
• Sharp vaarus angulaation
• Lateral subluxation
s n of prox tib
bia
• Metaph-diaph ang gle is prognoostic measu
ure
Tre
eatment
• Wait Tiill Unequiivocal Rad diographic c Diagnossis Is Estab
blished
Blo
ount’s
< 3y Aftter 3-4 y

V & VI
I & II III & IV
Bracing for 1y Oste

eotomies Ilizarrov
z Q angle Normal Q angle
RAB for ro
otation
Wedge Dome Che
evron
too
NG HKAFO: for 1y, Effective

1]. BRACIN E 80
0%
2]. Rab Osteotomy:
o Oblique osteotomy
o é an infeero-superiorr Inclinatio
on calculate
ed
according to how mu uch ITT & va arus should
d be correctted
Single laterral screw fixxation allow
o w post-operrative manippulation
Close wound and che
o eck PXR Æ fine
f tuning g of the corrrection
Single Hip Spica 6wk Æ LLC
o
3 Ilizaro
3]. ov for type V & VI Lan ngenskiöld: medial pla ateau eleva ation + HTO
O + bridge
e excision
• NB Som
me times in blount’s
b the
ere is MFC hypertroph
h hy making treatment q
quite proble
ematic
Genu valgum
• Pathologic binding of the knee to out side causing knock knees
• Physiologic valgus: Usually bilateral
1st there is a varus and z ............................till 2y
Then it is reversed to valgus and y .........till 10-15º at 4y
then it starts to z .............................................over 2y till it reaches adult level (7ºvalgus)
Ætiology (pathological genu valgum)
1]. Idiopathic:
• Unresolved genu valgum
2]. Traumatic (commonest):
• Incomplete fracture of proximal tibia (green stick)
• Distal femoral physeal injuries
• Usually occur 2y post traumatic
3]. Congenital:
• MED, MMD (Pyle’s), Nail patella $
• Pseudo Achondroplasia
• Renal rickets
4]. Neuromuscular: CP. Polio
Biomechanics:
• z Tibio-Femoral angle
• y Q angle
• Patellar malalignment
• Abnormal forces with over wt. Æ physeal growth retardation
Clinically: Obese
1]. PesPlanus
2]. Lax ligaments
3]. Chondromalicia
4]. y Q angle
5]. +ve Ober’s test = contracted ITB especially in paralytic patients
PXR
1]. z LDFA (lateral distal femoral angle)
2]. Sky line view: Æ patella subluxation
3]. Femoral hypoplasias
Treatment
1- Prevention
Post traumatic:
• Unaccept any degree of valgus
• Cast in extension (Flexion in cast isn’t sufficient to avoid malreduction)
Idiopathic
• Physeal stapling Æ gradual temporary epipysiodesis
• Osteotomy may Æ neurovascular complications
2- Osteotomy:
Indications:
• Skeletally mature patients
• Osteodystrophies
Prerequisites:
• Avoid medialization
• Assess ankle for possible associated varus or valgus
3- Ilizarov in hemimelia
Congenital Tibial Bowing

Postero-Medial Antero-Medial Antero-Lateral
Aetiology Physiological Fibular Hemimelia ð Congenital pseudoarthrosis: (misnomer)
mutation during fetal 1]. Neurofibromatosis
development 2]. Fibrous Dysplasia
Incidence Unilateral Uni or bilateral Unilateral
Associated é: PFFD, Lat. Rare
foot ray, pubic anomaly
Pathology Apex at distal 1/3 MIC: thickened periosteum + Fibrous
Soft tissue is involved proliferation + metaplasia into
disorganized weak bone ± NF
TWO TYPES:
1]. Infantile: Deformity then #: Poor
2]. Adolescent: # Æ deformity: good
Classification LETT Classification BOYD’S Classification:
A].<6cm 1]. Tibial defeciency + bowing
B].6-10 cm 2]. Tibial hour-glass (in NF)
C].>10 cm + foot def 3]. Tibial Cystic lesion
D].Bilateral 4]. Tibial sclerosis
5]. + Fibular dysplasia
6]. + Intraosseous neuroma
CP o Bow + LLD o Bow + LLD o Bow + LLD
o Till 18m then recover o Neonatal o Infantile or adolescent
o Posterior bow 1st o TEVLgm o Obese
o Flexible Pes calcaneo- o Absent ray
valgus o GenuValgum
PXR o Posteromedial bowing o Anteromedial bow o Antero-Lateral bow
o Post bow may recover o Tarsal coalition o Cortical tapering
earlier o Absent lat. foot ray o Sclerotic edges
o Hypoplastic LFC o Cystic formation
Treatment Observation Aim: normal foot & gait Aim: Axis restoration + y radius of healing
Foot: Manipulation A & B = good foot Æ Prophylaxis: ......... BG, orthosis, IM rods
LLD: plot and correct osteotomy or counter Non union:
stapling + LLD 1]. IM Rods é temporary ankle fixation
C & D = Poor foot Æ 2]. Free vascularized fibular graft
amputation 3]. Ilizarov: better union & alignment
Failed union........ Amputatn (Syme’s, Boyd)
PEMF ..................... Enhance wider healing
Postero‐medial Bowing
Unknown ætiology; may be mal-positioning in-utero
•
Bone, ms, sc tissues are involved in this disorder
•
Spontaneous radiographic recovery of posterior bow by 6mo & medial bow by 18mo
•
There is LLD
•
Foot:
•
o Hyperdorsiflexed Æ Rests on anterolateral aspect of tibia
o In newborn it can be manipulated into normal position
o Progressively z even after osseous recovery of the bow
Treatment:
1- Mainly observation
2- Manipulation of foot Æ cast or splint
3- LLD:
o Plot the growth curve to anticipate the final out come
o <2 cm observe or shoe lift
o 2-5 cm contralateral timed epiphysiodesis
o >5 cm lengthening
Congenital Anterolateral Bow

Congenital Pseudoarthrosis
Infantile tibial non union
• Congenital pseudoarthrosis is a misnomer; fracture is not at birth & it is not a pseudoarthrosis
(it is not a synovial filled space) but it is filled é hamartomatous fibrosis
Incidence:
• Rare 1:140,000
• Present in childhood
• Poor prognosis for healing even é long immobilization
• LLD is present ð abnormal tibial growth
Ætiology:
• Is unknown but it’s common é:
1]. Neurofibromatosis
2]. Fibrous dysplasia
Histologically:
1]. Thickened periosteum
2]. Fibrous proliferation
3]. Metaplasia occurs into disorganized poorly formed bone
4]. Rare neurofibroma
Clinically:
• Antero-lateral bowing of distal 1/3 tibia
• Obese infant
• Two presentations
1]. Infant é# though clinically angulated abnormal tibia Æ poor prog.
2]. Child é # after minor trauma even before deformity:
Good prognosis
Before deformity
But X-ray may be +ve (scelerosis, tapered cotex, cystic formation)
PXR
1]. Anterolateral bowing of the tibia
2]. Sclerotic edges
3]. Cortical tapering
4]. Cyst formation
Classification: BOYD’S CLASSIFICATION:

1]. Tibial defect + bowing
2]. Hourglass constriction at mid lower 1/3 tibia
-associated é neurofibromatosis
-# <2y
3]. Diaphyseal Cystic lesion Æ fr. through it
-Bow occurs before or after that fracture
4]. Sclerotic lesion Æ fr.
-No diaphyseal narrowing
5]. Associated dysplastic fibula
6]. Associated intraosseous (neurofibroma or schwannoma): rare
[Peediatric Orth
hopedic] Page | 147
Treatment:
Concepts::
• Mec chanical axiss restoration is a gold standard too z refractu
ure and non nunion
• Strenngth of tubbular objectt ∝ radius4 ; so K of dia
ameter by:
BG
Side to side healin ng
Insertio on of spindle end to distal
• LLD K at surgerry as the afffected segment is to be b resectedd; but theree is associatted accelera
ated
rate of growth
• Noww success ra ate is 75%
• Amp putations may
m be bette er functionally than re
epeated tria
als for limb ssalvage
Options:
1- Propphylaxis: (a
all are a failu
ure)
• BG from con ntralateral tibia + cyst curette
c + BG
G
• Orthosis
O
• Fllexible IM roods
2- Esta
ablished no on union:
E
Established
d Non Unio
on
<3cm: Re
esection + IM
M + BG
3-5cm: Ressection + fibu
ula >5cm: Ilizarov
(William)
IM roddin
ng:
• Reesection off the dysplastic portion
n till bleedin
ng & patentt medulla oon both end ds
• William
W femaale rod is paassed throu
ugh distal tibia, talus, calcaneus
c
• Advance
A the
e rod back into
i the pro
oximal tibia a
• With
W growth h nail is dragged é thee proximal fragment
f & disengagee the talus
Free vascu ularized fiibular trannsfer:

• In
ndications:
Defectss > 3cm
Shorten ning > 5 cm
m
• Can
C achieve e 2cm acutee lengthening
• Fiixation by IM
M rod + Addd BG ± PEM MF
Ilizarov:
• Good
G rate of union & le
ess rate of refracture
r
• Correct
C anguulation and
d LLD
• Wide
W union
3- Failed ttt or complicated cases

c Am
mputation (SSyme’s or Boyd)
4- Pulssed Electro Magnetic Field
F
CONGENITAL PSEUDOARTHROSIS OF FIBULA

- Veery rare cond dition
- Late presentattion as the fib bula bears 1/6 of the bo ody wt.
- Pt.. usually pressent at the scchool age
Clinicallyy:
- Vaalgus ankle + Pain ± tibia al involvemen nt
Treatme ent
1]. Pain
P relief
2]. Excision
E IM BG
B (iliac)
3]. Tibio
T fibular synostosis
s é 2 mo immobilization ± syndesmotic
s c screw
4]. Medial
M distal epiphysiode esis of the tib
bia (stapling or malleolarr screw)
5]. Wiltse
W ∆ osteeotomy is do one when th he patient is skeletally
s ma
ature
F ar Hemimel
Fibula He lia
• The co
ommonest longitudina
l al intercalarry limb deficciency
Ætiology:
1 Unknow
1]. wn
2 Chemic
2]. cal & irradiation during g fetal deve
elopment
Associated é
• Pubic anomalies
a
• PFFD
• ACL inssufficiency
• Lat.foott ray
Incidence:
1 Sporadiic
1].
2 May occ
2]. cur as a parrt of pseudo othalidomidde $ or Vollkmann’s $
Clinically:
1 Pt. prese
1]. ent in neonnatal period d
2 Unilaterral ANTEROMEDIAL BOW + skin dim
2]. mple on tibiia Æ correcct over time
e
3 LLD:
3].
a. If fibular hyypoplasias Æ Less LLD D
b. If fibular ap
plasia Æ high
h LLD
4 Genu va
4]. algum:
c. Hypoplastic LFC
d. Tibia valgu us
5 Foot & ankle:
5]. a
e. Equinovalg gus
f. Absent late eral foot rayy
g. Tarsal coaliition (X-ray Æ ball & so ocket appeaarance)
Classification of Lett
SHORTENING UNILATERAL FOOT DEFORMITY F E MU R

A <6cm Unni minimaal minimal
B 6-10 cm Unni minimaal minimal
C >10 Unni Major ± major
D Billat.
Treatment:
A
Aim:
• Norma al gait
• Norma al foot funcction
Consideraations:
• LLD
• Foot & ankle defo ormity
Options:
Fibula
ar Hemimelia
LLD < 20 cm Expected LLD > 20 cm

Go
ood foot condition (A&B) Poor foot funcction (C&D)
LLD Angular deformity Syme’s or Boyd
Osteotommy or
Lengthen
ning
Counter stapling
Tibial Hemimelia
• Longitudinal intercalary limb deficiency of the medial portion of the leg.
• 1:1000,000
• Limb buds start at 4wk Æ continue till 8 wk so concurrent insult Æ hemimelia
Aetiology:
• Unknown
• Chemical & mechanical insult during development
• AD & AR inheritance had been proposed for tibial hemimelia
Associated anomaly:
• Scoliosis
• DDH
• TEV
• Femoral bifurcation
• Talocalcaneal coalition ± Foot polydactyly
Clinically: usually present in the neonatal period
• LLD
• Knee flexion deformity
• TEV
• Lateral skin dimple
Classification: (Jones Barnes Lloyd)

• Avoid above and below knee amputations to avoid residual over growth
Defect Tibia Fibula Knee ttt

Ia Complete absence Total proximal 45° Knee disarticulation
migration Hypoplastic
femur
Ib proximal Moderate proximal 45° 1]. Proximal fibula centralize

cartilagenous migration 2]. Distal fibula to talus
anlage 3]. Late Syme’s
II Proximal bony Moderate proximal 25°-45° 1]. Proximal synostosis

anlage migration 2]. Disal fibula to talus
3]. Late Syme’s
III Distal tibial Upward dislocated N 1]. Proximal fibula central

dysplasia 2]. Distal TF synostosis
3]. Late Syme’s
IV Short tibia Upward dislocated Boyd or Syme’s amputations

Distal TF diastasis
Pediatric Foot Problems

Club Foot (Talipes EQUinovarus )
Definition:
• Congenital complex 3 dimensional deformity of the joints, ligaments, soft tissue, and tendons of
foot and ankle that is present at birth Î the ankle is in equinus, and the heel is inverted, and the
mid & fore foot are inverted and adducted i.e. varus
• It is the commonest congenital anomaly; and may be severe enough that the baby walks on the
lateral aspect of the foot
Incidence:
• The commonest congenital abnormality of the foot.
• Bilateral in up to 50%.
• Occurs in about 1/1000 births in Caucasians (7/1000 in polynesian).
• ♂:♀ Î 2:1 (ð unknown X- linked factor that modifies its manifestation).
• Rt. > lt.
Aetiology: TEV is Multifactorial. Theories of the pathogenesis of clubfeet are as follows:
1]. Genetic Theory:
oPolygenic pattern of inheritance is proposed
oA normal parents ώ affected ♂ child Î next ♂child risk is 2% (v.low for ♀).
oA normal parents ώ affected ♀ child Î next ♂child risk is 6% (2% for ♀).
oOne affected parent ώ affected child Î next child risk is 10-25%.
oIncidence in 1st degree relations Î 2-5%.
oIncidence in 2nd degree relations Î 0.6%.
oOne affected monozygotic twin Î second twin risk is 32%.
oIn AR inherited $ as: diastrophic dwarfism, camtomelic dysplasia
oIn AD inherited $ as: Larsen$
oIn XR inherited $ as: Pierre Robin $
2]. Germplast defect Teorry:
o Defective cartilaginous anlage of the anterior talus. (may be vascular defect)
3]. Developmental Arrest theory (teratogenic theory):
o If fetus is subjected to a teratogen in the 1st half of tibial phase of foot development Æ severe TEV
o And if occur in the 2nd half of tibial phase Æ mild TEV
4]. Vascular theory
o 1ry defect in ant.tibial a. Æ fibrosis and medial tethering & defective talar anlage
5]. Neurogenic theory:
o 1ry defect in the nerve supply to the muscles
o z in the number of motor units in common peroneal N. is found
6]. Myofibrosis:
o TEV was found to have yType I Fibrous tissue in muscles and y in Arthrogryposis.
o Zimny found myofibroblasts in medial fascia Æ medial contracture
7]. Anomalous Tendon insertion theory:
o Inclan proposed that anomalous tendon insertions result in clubfeet.
o However, others said “This is due to distorted TEV anatomy”
8]. Mechanical theory: TEV occurs ð extrinsic pressure from outside e.g. oligohydramnios
9]. Others
o Congenital constriction rings.
o Tibial hemimelia.
[Peediatric Orth
hopedic] Page | 151
Pathoana atomy:
I. Affectted limb: − may be shortened.
− Calf musclle is atrophicc.
− Foot is sho
ort compared d to opposite
e side.
II. Bony
1- Talus: − Equinus
− Small, ante
ero-laterally eccentric
e osssific centre (isschemic).
− Neck (1ry pathology)
p
o Short
o 50° med & down nward tilt (n=25°) (yobliquity angle & &z inclinatio
on)
o Unccovered and palpable at the t sinus tarssi.
− Head:
o Tilte ed medially & downward (in the ankle e mortise).
o Acq quires cart. onn medial & planter surfacce (in untreatted case-UTC C)
− Body:
o Rota ated laterallyy (Caroll deppate?) Î Horrizontal brea ach
2- Calcaneus:
− Equinus + Varus + IR (ffollow the talus)
− Medial: boowing + Sustentacalum ta alai is small & close to meed.maleolus.
− Ant. Part .......................................................IR around talo-calcane
eal interos. lig
g
− Post. part ....................................................ER & tethe ered to fibula
a by:
1- Calccaneo-fib. Lig g
2- Delttoid lig
3- Pero oneal tendon n sheath
4- Pero oneal retinacculum
3- Navicular:
− Rotated ve
ertically & meedially leavin
ng the antero o-lateral talarr head unopp posed.
− Abut the m
med mal ÎT Tibio-Navicula ar interval Ð Î may form m articular facet.
4- Cuboid:
− Medially displaced
d in relation to the calcaneus under cunifo
orms.
5- Metatarsals
− Adductus
− Foot is in extreme
e supiination
− forefoot is pronated re elatively to th
he hindfoot
− Cavus ώ planter
p flexed
d 1st metatarrsal
− Medial ang gulation.
6- lat. malleolus: posterior displacement
d t Æ horizonttal breach
7- medial tibial rotation (deebatable)
III. Joints changes:

1- Ankle: − Equinus
− anterior talus is denuded from cartilage (in UTC)
− Medial articular facet is obliterated by the deltoid lig.
2- Subtalar: − Equinus, varus.
− Only 2 articular facets instead of 3
− Anterior facet Is tilted medially & downward Î talus articulate é antero-medial surface
of calcaneum Î varus & lateral displacement of calcaneus Æ tethering to fibula
3- TNJ: − moved to medio-planter surface of the talus (ð navicular displacement).
4- CCJ: − Is not fully articulating (ð cuboid displacement)
IV. Skin:
1- Posterior crease
2- Medial crease (indicates severe deformity sometimes deep farrow).
3- Curved lateral foot border + lateral callosities
o N.B. the whole fulcrum of rotation of the foot is around the interosseuos ligament & you should cut its 3
components.
V. Soft tissue contractures:

Tendons
1. Achillis tendon contracture ..................... antero-medially inserted.
2. Tibialis posterior tendon ..................... displaced anteriorly.
3. FHL, FDL. Î cavus
4. Abductor hallucis.
5. MASTER KNOT OF HENRY: binds FHL & FDL to navicular undersurface Î preventing its mobility.
Ligaments
}
6. Talo-navicular (sup., med & plantar parts)
7. Tibio-navicular ligament. Navicular Displacement
8. spring ligament (calcaneo-navicular lig)
9. Bifurcate lig. (dorsal CC & Calcaneo-navicular).
}
10. Deltoid ligament (5parts?)
11. Calcaneo-Fibular ligament
Calcaneal Displacement
Membranes & retinaculae
12. Superior peroneal retinaculum.
13. Posterior ankle capsule.
14. Interosseous ligament.
VI. Vascular:
o Dorsalis pedis is 85% absentÎ avoid injury to the posterior tibial a. during a posteromedial release
[Peediatric Orth
hopedic] Page | 153
The os calciss is rotated medially

T m
T talus is rotated
The r laterally
T talar hea
The ad is diveatted mediallyy
T cuboid is
The i displaced d medially
T navicula
The ar is subluxe ed to MM
Clinical:
• Family hist: − cllubfoot or neuromuscular disorrders.
• General exam. − Any
A other abnormaliti
a ies in hip, spine,
s and other limb b.
− Complete neuro-musccular examination esp pecially in older casess.
• Local exam:
e − Exxamine the e feet in prrone, supin ne, and standing & w walking if old enough h.
− Normally
N neewborn fee et can be dorsiflexed
d & everted till it touch
hes ant. tib
bia.
− Ankle & hind foot Î equinus
e & varus.
v
− Mid
M & forefo oot Î add ducted & su upinated.
− Degree
D of th
he deformity is determ mined:
ostural type:
1. Mild po
− Uncommon n.
− No
N Family history.
h − Easily corrigible
c m
manually at a birth.
− No
N sole & po osterior creeases. −The heel is prominent.
− Adequate Nav-malleo
N lar intervall. − Nil calff atrophy.
− Active dorsiflexors and d evertors. − Simple e manipulation is nee eded
− ± contralat. foot valgu us, CDH…ettc. ð intrauterine malp position.
− Reesolve withhin 6 wks.
2. Moderate resolving type (exxtrinsic ð intrauterin
i ne pressure e):
− Coommonestt, 60% bilateral, 63% affect females.
− No
N family hiistory. − Partiallly corrigible manuallyy at birth..
− No
N deep solle and back creases. − Well defined hee el.
− Ð Navicularr-malleolarr interval. − Minimal calf atro ophy.
− Fo
orefoot sup pination is 56°. − Respon nd to manipulation and a casting g.
3. Severe rigid type (intrinsic type):
ty
− Le
ess commo on, 45% billateral (mo ore severe),, 67% affecct males.
st
− +vve family hist.
h (10% in n 1 ° relattives).
− Little manua al correctio
on at birth.
− Deep
D sole & back anklle furrow. − Ill-defin ned heel.
− No
N navicula ar-malleolarr interval. − Marked d calf atropphy.
− Su
upination reaches
r 900°. − Poorly respond to manipula ation.
− 2 Palpable bones:
b Tala
ar head at thet foot do orsum & Cu uboid at thhe outer eddge.
− In
n UTC big callosities
c p
present on the outer foot edge ð walking.
− Su
urgery alwways neede ed.
• Even fo ollowing coorrection, the
t foot offten remain ns short an nd the calf thin
Classifications:
1. Catterall Classification (clinical)
Mild Postural Flexible Fixed

(tendon contracture) (Joint contracture)
Occurrence Uncommon Commonest Less common
Bilaterality usually unilateral 60% 45%
Family History - - +ve (10%)
Deformity No fixed deformity Tight post structures Fixed foot deformity
Talar neck N Ð ÐÐ 115-135°
Subluxation N Mild Marked
*Heel N well defined ill-defined
*Calf atrophy N Minimal Marked
*Lateral malleolus N N Posteriorly displaced.
*Sole & back creases - Not deep Furrows
*Dorsolateral crease well defined Present Absent
*Foot lateral border straight straight Curved
*Cavus - ± ±
*Fixed Equinus - + +
*Naviculo-malleolar interval N z zzz
*Mid tarsal mobility N N zzz
*Foot Supination mild & correctable 55º 90° and fixed.
Response to ttt Excellent to manipulation Good to serial casting Poor & needs surgery
*every one of the criteria are given 1 score and an overall score is taken for follow up
2. Dimeglio Classification (reducibility)

1. Stiff (Irreducible)
2. Severe (slightly reducible)
3. Mild (partially reducible)
4. Postural (totally reducible)
3. Simon Classification (radiological)

• On AP view the centre of the cuboid
ossification is in line é mid axis of calcaneus
+1: the centre of cuboid is medial to the

calcaneal axis
+2: the centre of the cuboid is medial to the
medial tangent
+3: it become more proximal than the
calcaneal nucleus
It is useful as the ossific centers may take a
while to appear
Radiographic Assessment of Club Foot
• Aim:
o Helps diagnosis, severity, results and prognosis of ttt.
o Intra-op fluoroscopy confirmation of reduction.
o Define the relation between tarsal bones.
o Ossification centers of the talus, calcaneus, and cuboid are present (navicular at 3 yr).
• Method of Beatson and Pearson; 1966
1- AP:
∂ Position: 30º plantar flexion.(dorsiflexion&external rot)
∂ Projection: x-ray tube directed 30º from the perpendicular.
∂ Lines: -Talar long axis parallel to its medial border
-Calcaneus long axis parallel to its lateral border
-1st metatarsal axis
-Simon grade
∂ Normal -talocalcaneal angle = 20-40º (talus points to MT1, and calcaneus to MT5).
-Talo-1st metatarsal angle (T-MT1) = 0-15°
∂ TEV: -z TC ANGLE < 20º even may reach 0º or reverse (both points to MT5).
-zT-MT1 Î more negative
2- Lateral of Foot (fibula at the post. Half of the tibia):
∂ Position: 30º plantar flexion.
∂ Projection: x-ray beam should be perpendicular to both malleoli.
∂ Lines: -Talar long axis.
-Tibial long axis
-Calcaneus lower border
-MT1 axis
∂ Normal -Talocalcaneal Angle = 20º-40º
-Tibio-Talar & tibio-calcaneal angles are < 90º
-T-MT1 angle = 0-15º
∂ TEV: -zTALO-CALCANEAL <20º even Æ 0º or reverse (// of the 2 bones is key)
-this does not increase on max dorsiflexion view
-yTIBIO-TALAR and CALCANEAL ANGLES (equinus)
-yT-MT1 ANGLE (1st ray equinus)
3- Forced dorsiflexion & evertion lateral:
∂ Position: maximal dorsiflexion & eversion of foot & int.rot. of leg.
∂ Projection, and lines are the same as plantigrade lateral.
∂ Normally -the angle increases than in plantigrade view.
∂ TEV: -axes of talus & calcaneus becomes more PARALLEL (angle more decrease).
-the calcaneus is fixed and the talus dorsiflex.
-tibiocalcaneal relationship reveals EQUINUS.
4- Kite's angles from AP and Lateral views are added together to form talocalcaneal index;
Talocalcaneonavicular subluxation is present if:
1- TC index < 40°.
2- T-MT1 is >20° & TC° <15°.
• Prenatal Sonography (16-20 wk):

o Very high specificity & sensitivity
Diff dx:
Talipes varus or metatarsus adductus. arthrogryposis multiplex congenita
Myelomeningocele club foot. Poliomyelitis.
Cerebral palsy. Proneal type of progressive muscle atrophy.
Diastematomyelia. Guillain-Barré $.
Myotonic muscular dystrophy. Diastrophic dwarfism.
Freeman-sheldon $. Streeter’s dysplasia (constriction rings).
Larsen’s $. Mobius $ (long arm 18 deletion $.
Tibial deficiency. Congenital ankle dislocation.
Diastrophic dwarfism:
− Short stature. − Cystic ear penna Î hypertrophic cartilage.
− Short 1st metacarpal. − cleft palate.
− Flexion contracture. − progressive webbing of joints.
− Severe bilateral TEV. − progressive kyphoscoliosis.
Freeman-sheldon $ (cranio-carpal dysplasia):
− Flat face, deep set eyes. − Small mouth ώ protuberant lip Î whistling facies
− H shaped chin crease. − High arched palate & Ð movement Î nasal tone
− Fingers are deviated upward. − TEV ώ flexion deformity of the toes.
Larsen $:
− Multi joint dislocation. − prominent fore head.
− Flat facies, spaced eyes. − depressed nasal bridge.
− Short metacarpal, spatulated thumb. − kyphoscoliosis.
− Multi carpal ossific centers. − TEV.
Möbius $:
− Absent pectoralis major. − Mask facies, eyes lost abduction.
− Facial n. palsy. − Syndactyly & Microdactyly.
− Anklylosed prox.interphalangeal joints. − Absent lat. 3 foot rays, or absent all phalanges.
− TEV 30%.
Treatment Options:
o Manipulation, casting, taping, physiotherapy, splinting, CPM, and surgery.
o Aim: painless, functional, plantigrade foot with good mobility.
I. Clubfoot Casting:
• Value: − Method of definitive ttt.
− Decrease the severity for less invasive surgery.
• Timing:
o Casting begins in the first days of life to take advantage of the initial elasticity.
o Every cast for 5-10 days; ώ in the first 2-3 months (5-6 manipulations).
o Children who present for treatment > 4-5 mo old may require operative correction.
• Sequence of Correction: (Ponsetti)
o correction of cavus deformity first to unlock the talo-navicular joint:
∂ Forefoot is supinated and 1st metatarsal is dorsiflexed Î
∂ This reverses the forefoot relative pronation & puts MT, cuneiforms, & Nav. On the same plane.
∂ The lever arm necessary for the forefoot abduction then is formed.
∂ Avoid foot Pronation Î 1st metatarsal is further plantarflexed Î Ï the cavus & mid foot break.
o correction of adduction and heel varus:
∂ Abduct the fore foot & evert the hind foot while counter pressure is applied with the thumb against
the head of the talus.
∂ Foot is abducted in dorsiflexion and slight supination to stretch the medial tarsal ligaments.
∂ this spontaneously Î calcaneus abduct & rotate under talus Î correction of varus heel.
∂ Note: − calcaneus cannot evert unless it is abducted.
− navicular cannot be fully reduced; but partial reduction puts the foot into place.
− X-ray may be taken at this point to confirm that the TNJ joint is reduced.
o Correction of equinus:
∂ equinus is corrected last, by dorsiflexion of midfoot after forefoot in abduction & heel in valgus.
∂ if foot is dorsiflexed prior to correction of the hindfoot varus, rocker bottom foot may be created;
∂ Lateral x-ray are helpful in assessing quality of cast correction;
∂ percutaneous TAL may be necessary in order to avoid rocker bottom deformity.
∂ dorsiflexion of ankle to > 10-15° is rarely possible ð talar malformations and tight ligaments.
∂ Posterior capsulotomy may relapse due to retraction of the scar tissue.
o Correction of the supination:
∂ In the last few casts; metatarsals are positioned in neutral ┴ plane on the leg.
∂ Never overpronated.
o Correction of the deformity is only achieved when the foot is held in severe abduction & external rotation in
a cast for a several weeks Î Denis Brown Splint for long period.
• Casting:
∂ Gradual correction of the deformity can be achieved with toe-to-groin casts.
∂ 90° knee flexion.
∂ Foot is at max abduction and lateral rotartion 50-60° as the thigh part is hardening.
∂ 15°dorsiflexion.
∂ 6-8 casts 7-10 days apart.
∂ Last on is applied after TAL for 3 weeks.
• Evaluation:
∂ Completely normal foot should not be expected.
∂ Clinical: − Navicular position to the talar head.
− Cuboid position to the calcaneal anterior tuberosity.
− Position of the heal.
− Position of the hindfoot to the fore foot.
− Ankle ROM.
∂ Radiological: Calcaneo-navicular index.
∂ Relapse in 50% could be expected till 7y old.
• Maintenance :
∂ Denid-brown splints:
− High top, 60° ER, & padded heal shoes for a long time.
− Shoes are attached to a bar in ER; but allow for some ankle motion
− Full time 3m Æ Night time till 3y Æ discontinue when plantigrade foot
• Cautions:
∂ Never pronate the forefoot Î Ï cavus & rocker bottom foot.
∂ forced foot ER to correct adduction (ώ the calcaneus is in varus) Î ER of talus Î posterior
displacement of the LM
∂ Rocker-bottom deformity: ώ dorsiflexion of forefoot to correct the equinus
ώ abduction of pronated forefoot to correct the adductus
∂ avoid abducting the foot against pressure at CCJ Î block calcaneal abduction.
• Complications:
∂ Increased cavus deformity;
∂ Rocker-bottom deformity;
∂ Longitudinal breach
∂ Flattening of the proximal surface of the talus
∂ Lateral rotation of the ankle.
∂ K stiffness of the ligaments and joints;
• Relapse:
∂ 50% with careful parents.
∂ Detected when slight equinus & varus occurs.
∂ ttt: manipulation Î toe-to-groin cast/7-10d Î 4-8w Î recovery Î TAL & Denis Brown at night
∂ Prevent more relapses with Tibialis anterior transfer to the 3rd cuneiform.
• Residuals:
∂ Equinus Î TAL.
∂ Cavus Î plantar fasciotomy + EHL recession to the MT1 neck.
∂ Varus Î tibialis anterior transfere.
∂ Adductus: does not recur
II. Surgical Options:
• Aim: − Complete ttt after manipulation.
− ttt of replapse.
− ttt of rigid & neglected cases.
• Varieties:
Soft tissue procedures:
1. TAL.
2. Turco one stage posteromedial release.
3. McKay-Simmon complete subtaloid release
4. Codivilla postero-medial release.
Bony procedures:
5. Calcaneal osteotomy.
6. Calcaneo-cuboid fusion.
7. Metatarsal osteotomy & Tarso-metatarsal release.
8. Triple arthrodesis.
Tendon transfere.
• Timing:
∂ best when extensive PM release is delayed till 1 y (walking age)
∂ Although some believe in 4inches foot length & 4-6 mo..
• Anesthesia: GA + caudal anesthesia for postoperative analgesia
• Position:
∂ Supine: if Turco
∂ Prone: if Cincinnati, or 2 incisions
• Tourniquet is put and raised above systolic by 100mmgh
• Skin Incisions:
∂ Turco postero-medial incision:
o Start at base MT1 Æ below MM Æ TA
o A/E: − Cross skin crease at the medial side of the ankle
− Difficult exposure of plantar fascia
− Difficult to address posterolateral pathology
∂ Cincinnati:
o Starts at nav.cuneiform Æ below MM Æ TA Æ lat.malleolus Æ ant. to sinus tarsi
o A/E: − Heal flap sloughing
− Calcaneal infection
− Difficult TAL
− Difficult plantar release
∂ 2 separate incisions (medial & posterolateral incisions)
o Medial: over a base of Δ made by MM, centre of calcaneus, Base of MT1 Æ anteriorly is
curved dorsally and posteriorly is curved plantar ward
o Post.: oblique incision from midline down and lateral bet. TA & lat.malleolus
o 3rd incision: may be needed to address the CC pathology well
∂ Caroll posterolat. & med. plantar incision.
∂ Zig-zag incision.
• Structure
es to be invoolved:
∂ Posteriorly:
1. Achillis tendon.
t
2. Tibialis posterior.
p
3. Post. cap psule of ankle & subtalar..
4. Calcaneo-fibular lig.
5. Posterior talo-fibular.
6. Posterior superficial deltoid.
d
∂ Medially:
7. Tibio-navicular capsu ule.
8. Anteriorr tibio-nav. Lig.
9. Medial capsule
c of subtalar.
10. Master Knot
K of Henrry
11. Abducto or hallucis.
∂ Plantar:
12. Plantar fascia.
f
13. FDB.
14. Plantar calcaneo
c navv. & calcane-ccuboid lig.
∂ Laterally:
15. Calcaneo-cuboid cap psule.
∂ Subtalar:
16. Talo-calccaneal interoosseous lig.
• Clinical and
a radiolog gical approacch for plannin
ng
∂ Bensahel ma atch the exte
ent of surgeryy to the defo
ormity complexity “a la ca
arte” approacch
∂ Posterolatera a the basicc elements for TEV surgica
al elements are al correction if needed
∂ Other elemeents are deteermined preooperatively byy thorough clinical
c & radiological asse
essment
TEV
- Straight lateral fo
oot - Nav.Malleolar in
nterval is spare
ed
No 1st ray equinus
CJ is aligned
- CC orrectable sup
- Co pination (midta arsal mobility)
No plantar
p release
e No CCJ release No
o medial releasse
Modified McKay procedure using Cincinnati incision:

• Discussion:
∂ In severe cases é marked IR of the calcaneus.
∂ Posteromedial & posterolateral release can be done.
∂ Position is kept ώ a single K-wire that transfixes TNJ
• Timing:
∂ best age: 1-2y, and the upper age limit is 6y.
• Prerequisites:
∂ Forefoot adductus is passively correctable to neutral (to avoid would healing problems).
• Sequential Strategy for Release:
∂ Preserve as possible the lat. Veins and the sural nerve.
C Posteriorly: Sc tissue dissection over achillis for 1” for Z-lengthening; ώ the distal cut is medial.
∂ Incise the superior peroneal retinaculum as it blends ώ the achillis.
∂ Incise the thickened peroneal sheath, care to the tendon.
C Plantar release:
∂ Elevate the AHL muscle from it origin and retract it distally (some excise it).
∂ insert a blunt dissector between medial & lateral plantar n (under lat. Plantar n.)
∂ Release fascial slip between the medial and lateral br. of the plantar nerve.
∂ Slide a scissor blade between the n and fascia & the other blade superficial to the pascia
∂ Cut plantar fascia & Abd.digiti quinti & remainents AHL & FDB & long plantar lig. Î Talus roll back
∂ If not Î cut posterior talo-fibular lig. If not Î cut posterior portion of the deep deltoid.
C Medailly:
Follow the FDL tendon at the MM till the Master knot of Henry (MKH)
∂ Dissect FDL & FHL tendons from MKN till the ankle joint. (free them from Sustentacalum tali).
Lengthen FDL & FHL (behind the ankle) if in dorsiflexion toes can not be straightened
Release the master knot of Henry
Identify the TA & follow Æ peroneus longus Æ retaract then cut the long & short plantar lig.
∂ Enter the TP sheath above the MM and incise it all along its length.
Lengthen the TP tendon 2.5 cm by Z-plasty at the ankle joint
∂ Neurovascular bundle is dissected carefully through out the arch of the foot; especially the
medial calcaneal branch of the lateral plantar n.
Open TNJ by pulling TP tendon & cut dorsal TNL, plantar TNL, and the capsule all around.
∂ Release both ends of bifurcate ligament.
Follow ! FHL till sustentacalum tali Î cut superficial deltoid, med. & posteromed. TCJ capsule.
C Laterally:
Cut the calcaneo-fibular ligament close to the calcaneus
Cut the posterior talo-fibular ligament
∂ Cut the posterior & lateral talocalcaneal ligament and capsule.
∂ In severe cases cut EDB, inferior extensor retinaculum, dorsal CCL & oblique CuNL.
Cut TC interosseous ligaments if the correction is not complete especially if the child is 1y.
• Fixation:
Put the foot in corrected position.
∂ Pass K-wire into the talus via posterior incision to lateral aspect of the head & used to rotate !
talus IR then advance Î TNJ Î naviculo-cuneiform Î MT1 Î out of the foot.
∂ Place the chuck into the anterior tip of the K-wire and drag it till it is buried into the talus.
Rotate calcaneus by pushing CCJ laterally, and the post. calcaneus medial & down & valgus
∂ Hold the hind foot in corrected position (Foot axis ┴ Bimalleolar axis).
∂ Pass a K-wire from calcaneus to talus.
3rd wire may be put across CCJ after cuboid is pushed laterally on the calcaneus
• Closure:
∂ Put the foot in 20° plantar flexion and suture all the tendons after their lengthening
∂ Cover the EDL & EHL & TP tendons by their sheathes.
∂ Cover the peroneal tendons by the soft tissue anterior to achillis.
∂ Deflate the tourniquet & hemostasis & put a hemovac medially
∂ Close skin by interrupted sutures.
∂ Toe-to-groin cast is applied with 90° knee flexion, and fully corrected foot or slightly plantar
flexed.
• Cautions:
∂ Lateral veins and sural nerve during lateral exposure.
∂ Plantar bundle during medial and plantar release.
∂ Don’t open the FDL & FHL sheathes or lengthen the tendons at the medial foot Î hammer toe
∂ Preserve the deep deltoid.
∂ Extensor tendons and dorsal bundle during TNJ opening.
∂ Preserve the 3 TC interosseous lig.
∂ Not to penetrate the ankle joint during the last K-wire.
• After care:
∂ Cast is put & changed/3-4 wks in fully corrected foot position.
∂ At 4-6 wks cast is changed and pins are removed Æ ± Denis Brown orthosis till walking started
∂ Stop ttt when the foot is plantigrade clinically & Radiologically & pt can actively dorsiflex ! foot
Tendo Achillis Lengthening:
C Skin incision: 2” incision on the medial aspect of the tendon.
∂ Open the paratenon medially.
∂ Tenotomy of the plantaris tendon if present.
∂ Secure the tendons and neurovascular bundle.
∂ Achillis Z-plasty is done ώ distal medial cut & proximal lateral cut.
C Plantarflexion and gentle dissection to show the posterior ankle capsule.
∂ Make sure by small vertical snip of the post. ankle capsule Î synovial fluid.
∂ Capsulotomy is done for the medial part stopping at the TP tendon.
C Subtalar capsulotomy is done if needed; By following the FHL tendon proximally till enter the joint Î
extend the capsulotomy medial and lateral as needed.
C 1st Suture of the achillis is done ώ foot in 15° dorsiflexion.
∂ Put the foot in plantigrade position and complete the suture of the tendon.
∂ Deflate tourniquet, hemostasis, & closure in layers.
∂ Long leg cast is applied in 90° flexion & 10° dorsiflexion.
C After care: cast removed at 6 wks Î AFO or short leg Phelps brace 6m
Resistant Clubfoot
• Residual or resistant TEV is one of the most difficult problems in pediatric orthopaedics.
• The deformity may take many forms.
• Incomplete correction may not be obvious at the time of surgery, but it becomes apparent with growth as the
persistent deformities become more evident.
• Clubfoot that appears by clinical and x-ray to be uncorrected may not always require surgery.
• Each child must be carefully evaluated to determine what treatment will best correct his problem.
• Etiology:
o Inadequate prior surgery ð failure to release the CCJ & plantar fascia.
o failure to recognize residual adductus on intra-operative x-ray.
o Inadequate follow up
o Persistent pathology:
underlying neuropathy.
abnormal growth of the bones.
muscle imbalance.
• Thorough physical examination:
o careful assessment of the forefoot and hindfoot.
o Dynamic (with a flexible forefoot) or rigid.
o Calcaneal inversion and eversion should be determined.
o Ankle dorsiflexion and plantar.
o Any prior surgery Î significant scarring about the foot or loss of motion should be noted.
• Radiologic evaluation:
o Standing AP and lateral X-ray should be obtained to assess the angles.
o if TEV is unilateral, the opposite foot can be used as a control for measurements.
• Previously the most common persistent deformities were forefoot adduction and supination.
• With evolution of Ponsitti technique recently the commonest are Equinus & varus.
• The functional ability of the child, the severity of symptoms, and the likelihood of progression if the deformity
is left untreated must be considered when treatment decisions are being made.
Hind foot varus <3y Tibialis anterior transfere or McKay

3-10y (isolated varus) Modified Dwyer lat. closing osteotomy.
3-10y + short med.column Dillwyn-Evans procedure.
3-10y (long lat.column) Lichtblau operation
>10y Triple fusion.
Equinus Mild-Moderate TAL + Posterior capsulotomy.
Severe Lambrinudi procedure.
Cavus plantar fasciotomy + EHL recession to the MT1 neck
Adductus <3y & dynamic TA transposition
>5y (long lat.col) Metatarsal Osteotomy
Cuboid decancellation after reduction
Evans CCJ exision fusion
Lichtblau anterior calcaneal resection
>5y (short medial col) Talar neck lengthening osteotomy (Æ AVN)
Hoffman cuneiform osteotomy
>10y Wedge tarsectomy
All >10y Triple fusion, or Ilizarov
• In general, the older the child Æ need combined procedures

• Children 2-3 y Æ modified McKay, but if previous release + stiffness&talus AVN Æ osteotomies
• Children > 5 y Æ osteotomies for correction of resistant deformity
• Children 1-5y Æ gray area in which ttt guidelines are unclear and careful judgment is required
• The separate components of the residual deformity must be assessed accurately
• Common components of resistant clubfoot deformity are:
o Fore foot: adduction / supination, or both Æ metatarsal or tarsal osteotomies or TA transfer
o Midfoot: short medial column or long lateral column of the foot
o Hind foot: IR & varus & equinus: (determine if isolated heel varus/long lat.foot column/short medial
column):
2-3y é varus Æ extensive subtalar release
3-10y Æ combined procedures.
N.B. Ankle valgus ≠ hindfoot valgus and is ttt by percutaneous medial malleolar epiphysiodesis (N:5-20º)
Heel varus + mild forefoot supination Æ Dwyer + lat.calcaneal closing wedge
Opening calcaneus wedge osteotomy is followed by sloughing of tight skin
heel varus + IR + long lat.column of the foot Æ Lichtblau procedure; but may complicate the
condition and a "skew"-foot develops
Osteotomy of Calcaneus for Persistent Varus Deformity of Heel

C Dwyer reported osteotomy of the calcaneus for relapsed TEV é an opening wedge osteotomy medially to y
the length and height of the calcaneus.
C TECHNIQUE (Dwyer, Modified)
• Lateral skin incision over the calcaneus, cuboid, and base of MT5.
• Strip the lateral surface of the bone subperiosteally.
• Resect a bony wedge based laterally large enough, when removed, to correct the heel varus.
• Take care not to injure the peroneal tendons.
• Place the heel into the corrected position, and close the incision with interrupted sutures.
• If necessary, fix the osteotomy with a K-wire.
• Apply a short leg cast with the foot in the corrected position.
C AFTERTREATMENT: remove K-wire Î6wks & casting Î 12wks.
Medial Release with Osteotomy of Distal Calcaneus (Lichtblau Procedure)

C An alternative to calcaneocuboid arthrodesis is lateral closing wedge (LCW) osteotomy of the calcaneus
(Lichtblau); that lacks long-term hindfoot stiffness seen with the Dillwyn-Evans procedure.
TECHNIQUE (Lichtblau):
C Medial incision: begin 1 cm below the MM, cross the nav.tuberosity, and slope downward to MT1 base.
• Identify and free superior border of AHL ms. & reflect it plantarward.
• Identify TP tendon at navicular insertion & free it from its sheath.
• perform TP Z-plasty about 1 cm from its insertion.
• Resect the tendon sheath overlying the joint and open it on its medial, dorsal, &plantar aspects.
• Open the flexor tendon sheaths & lengthen them by Z-plasty.
C Lateral incision: 4 cm long centered over the CCJ.
• Dissect the origin of EDB and reflect it distally to open CCJ.
• Identify the distal end of the calcaneus.
• Take distal wedge osteotomy; é 1cm lateral &2mm medial border.
• Take care to leave the articular surface of the calcaneus intact.
• Bring cuboid into contact é the distal calcaneus; & check correction
• If cuboid cannot be approximated to the calcaneus, resect more.
C A smooth K-wire can be inserted across CCJ to fix the osteotomy.
• Repair all soft tissues and close the sc tissue and skin.
• Apply a long leg cast with the foot in the corrected position.
C AFTERTREATMENT: 3wks Î change cast to short leg cast.
9wks Î remove cast & pin.
Triple Arthrodesis, Talectomy, and Ilizarov for Uncorrected Clubfoot

• Triple fusion & talectomy are salvage operations in children (10y) é severe hindfoot deformity Triple
arthrodesis corrects severely deformed feet by LCW through the subtalar &midtarsal joints.
• Triple arthrodesis is functionally and cosmetically superior to talectomy.
• Talectomy is reserved for severe, neglected, or previously treated TEV & neuromuscular TEV
• Ilizarov also is considered a good alternative for ttt of severe cases
Triple Arthrodesis
C TECHNIQUE
• Medial foot incision // to the inferior border of the calcaneus.
• Free the plantar fascia & short toe flexors from the plantar aspect of the calcaneus.
• Manipulate the cavus deformity as much as possible.
• Through an oblique antero-lateral approach, expose the midtarsal and subtalar joints.
• Resect enough LCW (including the midtarsal joints) to correct the forefoot varus and adduction.
• Also; resect enough LCW (including subtalar joint) to correct the varus deformity of the calcaneus.
• If necessary during these LCW:
¾ Include enough parts of; navicular, cuboid, lateral cuneiform, & the anterior talus & calcaneus.
¾ Include much of the superior calcaneus & the inferior talus.
• Finally, do Z- TAL & posterior ankle capsulotomy.
• Manipulate the ankle to correct the equinus deformity.
• Fix the correct position ώ a staples or K-wires inserted across the CCJ & TNJ.
• Cast applied toe-to-groin ώ the foot in the corrected position & knee flexed 30°.
C AFTERTREATMENT: 3wks Î change cast
6wks Î remove K-wires & change cast to short leg walking cast.
10wks Î remove cast.
[Peediatric Orth
hopedic] Page | 165
Talectomy:
• First wass described forf TEV é mye elomeningoccele, but ! tecchnique can be modified d for severe cases.
c
C TECHNIQQUE (TRUMBLE)
• Skin incision // to the e inferior borrder of the ca alcaneus.
• Expose lateral
l articullar margin off the navicula ar in the inte
erval between the EDL & peroneus te ertius.
• Invert & plantar
p flex thee forefoot. Plaace a towel clip
p around the talar
t neck & deliver it into thhe wound.
• Dissect all
a talus ligam ments & excisse it; as retain ned cartilagee may interfere ώ proper foot position ning.
• Also; theese remnantss also may grrow and cau use later defoormity and loss of correctiion.
• Derotate e the forefoott and displace e the calcaneeus posteriorlyy, until the na
avicular abutss the ant. plaffond
• The expo osed articular surface of the e plafond shoould be oppossite the middle e articular faccet of the calca
aneus.
• In propeer plantigrade position; th he foot axis ┴ bimalleolarr axis; that ne eeds 20-30° ffoot ER.
• If necesssary:
¾ If ad
dditional soft tissue releasse is required d Î talecttomy is done after
a circumfe erential release.
¾ To obtain
o adequ uate posterior displaceme ent Î excise tarsal naviccular. Section n deltoid & LCL.
¾ To correct
c hind foot
f equinuss Î cut th he achillis so its proximal end will retrract
¾ In se
evere TEV tala ar dome extru udes anteriorrly Î relea ase of ant. & post. tibiofibular ligaments off the
synddesmosis to allow
a properr posterior po ositioning of the calcaneu us (widen the e mortis).
• Fix one or
o two Steinm mann pins frrom the heel through the e calcaneus anda into the distal tibia.
• Cast is applied long leg l cast with h the knee 60 0°.
C AFTERTRREATMENT: 6wks Î remove Stteinmann pin ns & short leg walking ca ast applied.
18wk Î remove cast. c
- Complications:
• recurren nt deformity or
o partial reccurrence
• Excessivve heel valgus (which mayy follow com
mplete subtalar release)
Goldner four quadrant approach:

a
• Plantar, medial,
m posteerior, & latera
al, modifying the extent off release acco ording to the deformity severity
• Plantar quadrant includ
des the plantaar fascia, the sh
hort toe flexorrs, & the long & short plantaar ligaments
• Medial quadrant
q involves TNJ & subtalar
s release - lengthe ening of TP, FHL,
F FDL – AAHL recession n
• Rarely necessary
n to cut interosse eous ligamen nt of subtalaar joint Æ ovvercorrection n of clubfoott (other causes of
overcorrrection over lengthening g and excessivve lateral pla acement of navicular)
n
• Lengthe ening of the deltoid
d ligam
ment may imp prove ankle ROMR
• Posterior quadrant: ankle
a & subta alar capsulottomy + releasse of post.tallofibular & calcaneofibu ular
• Lateral quadrant
q invvolves CCJ capsulotomyy, completion of talonavvicular and subtalar rele ease, and, often,
o
sectionin
ng of perone eal tendon sh heath
• Foot is maintained
m m
most reliably in a reduced d position by pinning TNJJ; many also p pin TCJ
• Postoperative casting g is continue ed for 12 wee eks, & pins arre removed by b 6wk
TEV
Earrly
Untreated
diagn
nosis
Manipulatio
on & serial 8y till After
<8y
casting /2w
wk for 3mo maturity maturity
m
Denis-Bro
own 3mo Caavus
Soft tissue / Equinus Varus Adductu
us
full time Ilizarov (Planta
aris MT1)
TF +
Distractionn ap
ppropriate
Stiff Ligamentotta Stein
ndler
Re
esponding TAL Tohen Tohenn wedge
xis Jones
C
Continue di
Lambribud Dwyer MT osteottmy
pas
Jap
w Denis
with PM releasee
t 3years
till ((McKay via Turcco) Or
(active (Bensaheli))
do
orsiflexion)
Cast for 6-8 wk

w
ffollowed by Den nis till
walking
IF Relapse
ttt as neglectted
Co
ongen
nital Vertiical T
Talus
=CCongen nital Flat foot
= Congen
C nital con nvex pe es valgu us
• Itt is a conge der in ώ the
enital disord ere are FIXE
ED:
1]. Vertic
cal talus
2]. Dorsaal navicular dislocation
n
3]. Equinnus
Pathology:
1]. Vertic
cal talus
2]. Dorsaal dislocatio
on of TNJ & CCJ
3]. Poste
erior 1/3 only of talar dome
d articu
ulate é ! plaffond
4]. Calcaneus Æ pla antarflexed
5]. Hypooplastic susttantaculum tali
6]. Contrracted dorssal ligamentts
7]. Atten
nuated plan ntar ligamennts
8]. Contrracted:
Triceps surae
TA
EDL & EHL
E
9]. Sublu
uxed anterio orly:
TP
Perone eal They be }
ecome dorrsiflexors tendon
ns
May associated é:
• Menningemyelo ocele
• Sacraal agenesiss
• Lipo
oma of caud da equine
Classifications:
• COLEMAN classiffication:
I
: TN
N dislocation
n
II
: CC
C dislocation
n
• L IC HTBLAU class
HT sification:
Cong. Ve
eritcal Ta
alus
T
Teratogenic Acquirred
Neu
urogenic
-+ve familyy history -Intrauterine malp
position
-Meningomyelocele
-Bilat. -Unilateral
-Neurofibroma a
-DDH -Mod derate
-Less rigid
-Tight TAchhillis & extenso
ors -Corrrectable
Clinically:
• Fixed d EQUINUS + ROCKER BOTTOM DEFORMITY
• Conv vex Medial column
c of foot
f = Abducted foreffoot
• Talar head is palpable in so ole
PXR:
1]. Persisstent vertica
al talus ......................................................................... é max dorsi & plantar flexion
2]. Persisstent equinuus
3]. Fixed navicular dislocation
d
4]. y CAAMBA (Calccaneal Axiss Metatarsal Base Anglle) ............ >2 20º
5]. y PFT TCA (Planttar Flexion Talo-Calcan
T neal Angle) ................. >3 30º
6]. y TAAMBA (Tala ar Axis Meta atarsal Base e Angle) ........................ >6 60º
Treatment:
1. Two staged operation:
a.Stage one:
• Open reduction of TN & CC joints
• Dorsiflexors lengthening
• Forefoot should realign é hind foot
b. stage two: after 6 wk
• correct equinus
Drawbacks:
• after stage 2 the lengthened dorsiflexors are too long that hinder the foot from ground
clearance during the swing phase
2. One stage operation:
Timing:
• At 6 mo of age
Approach:
• Combined approach: medial for TN, lateral for CC & vertical for TAL
• Cincinnati approach
Technique:
• Follow TP to reach TNJ
• Release TNJ completely
• Capsulotomy of CC
• Release tight dorsal capsules & ligaments
• Z plasty of the TAL é distal lateral limb
• Peroneal lengthening
• Posterior capsulotomy of ankle & subtalar
• Correct equinus & valgus of calcaneus
• Correct talar position using K wire
• Reduce forefoot on hind foot & TN & CC are pinned
• ± TA & TP lengthening
Metatarsus Adductus
• Adduction of forefoot é convexity of lateral foot border ± spreading of the toes
Classification:
• HEEL BISECTOR method of Bleck: The weight bearing surface of heel forms an ellipse ; the axis
of this ellipse is the heel bisector and it act as a reference line:
Mild adductus: Æ bisect the 3rd toe
Moderate : Æ between 3rd & 4th
Severe: Æ between 4th & 5th
• STAHELI STABILITY CLASSIFICATION:

Flexible: abduction is possible beyond the heel bisector
Partial: abduction to heel bisector
Inflexible: no abduction at all
Pathology:
• Medial cuneiform shape is altered é medial deviation of its articular surface
• 2nd to 5th metatarsals are adducted
Clinically:
• KITE FEATURES of adductus:
The foot is turned inward (especially when viewed from dorsal aspect)
Bean shaped sole
Prominent base of 5th metatarsal
Wide space bet. 1st & 2nd toes
Higher arch
Fixed adductus when heel is held in neutral position
LICHTBLAU TEST: forefoot abd Æ big toe abd é apparent tight abductor hallucis
PXR
• Medial deviation at TMJ
• In old cases medial deviation of metatarsal shafts
• ± mild valgus heel
Treatment:
Metatarsus adductus
Flexible or partly Rigid
Stretch exercises Manipulation & serial casting
If not responding
Abductor Hallucis release Metatarsal osteotomies

Tarsometatarsal capsulotomy
Skew Foot
S or Z foot
• Rare deformity
• Like metatarsus adductus but + hind foot valgus & both are rigid
• Lat. Subluxation of navicular on talus
PXR
• K Talocalcaneal angle in AP & lat
• TN subluxation
• Line drawn along 1st metatarsal to talar head to talar body axis from a Z line
ttt
• Same as adductus Æ convert it to flat foot ( valgus heel is not correctable é cast)
• ± EVAN’S calcaneal lengthening é Fowler medial cuneiform open wedge
TEV Vertical Talus MT Adductus Skew Foot

Aetiology Equinus Equinus
Varus Heel Valgus heel Valgus Heel
MT adductus MT abductus MT adductus MT Adductus
First Ray Cavus Navicular dislocation
Incidence Rare
Path 1].Talus: short, tilt medial & down 1]. Vertical talus 1]. MT2 – MT5 adducted Same as MT adductus
2].Calc: equinus, varus, IR 2]. Equinus 2]. Med cuneiform is altered 4]. Hind foot vagus
3].Nav: rotatates medial & vertical 3]. Dorsal dislocated TN & CC 3]. Medial deviation of its 5]. Lat subluxed TNJ
4].MT: adductus, supination 4]. Hypoplastic sustantaculum articular surface
5].MT1: Cavus 5]. Tight Dorsal lig. & tendons
6].Lat.Malleoli: post displacement 6]. Slender plantar lig & tendons
7].Limb, joints, skin, tendons,
ligaments, vessles
Class CATTERALL ...... (Clinical) • COLEMAN: I; TN & II; CC • BLECK Heel Bisector
DIMEGLIO ........ (Reducibility) • LICHTBLAU: • STAHELI Stability
SIMON .............. (Radiologic) A]. Teratogenic
B]. Neurogenic
C]. Acquired
CP 1].Fixed or Flexible TEV • Fixed Equinus • KITE features … • Valgus ankle
2].Foot adductus • Fixed Abducted forefoot o Fixed add forefoot • Fixed Add forefoot
3].Foot supination • Talus in sole o Bean sole
4].Pes Cavus • Rocker Bottom Foot o Higher arch
5].z nav-malleolar interval • Persian Slipper Foot o Wide spaced toes 1& 2
6].Med, Post & Lat Creases (TE.Valgus + abductus • LICHTBLAU test AHL
7].Lateral Callosities
8].Heel Prominence
9].Calf atrophy
PXR • AP: z TC & T-MT1 < 20º 1]. To 4]. as pathology 1].Med deviation at T-MT J 1]. Same
• Lat: -z TC < 20º 5]. y CAMBA 2].Med deviation of MT shaft 2]. Same
-yT-MT1 angle 6]. y PFTCA 3]. y TC angle in AP
-y Tibio-Talar angle 7]. y TAMBA & Lateral views
-y Tibio-Calc angle 4]. TNJ subluxation
• Angles z more é dorsiflex 5]. TAFML is Z shape
• KITE’S ANGLE: TC in both
views > 40º = subluxation
TTT • Serial casting Æ Denis • One Stage operation 1].Flexible.............Stretches • 1]. & 2]. to convert
• 3y Æ PM release via TURCO • Two Stage operation 2].Rigid .................CastingÆAHL it to flat foot Æ
• Neglected Æ release + release Æ MT osteotomy EVAN’S + FOWLER’S
osteotomy
• Fixed Æ TF + wedge
F at Foo
Fla F ot
• LLoss of the normal
n medial longitu udinal arch
• T calcane
The eus is in valg
gus ER in reelation to th
he talus; an
nd the nav iss subluxed on the talu
us
• S
Staheli: flat foot
f is usua
ally in infantts, common n in children
n, normal in
n adults
• G
Gould: longgitudinal arrch develop p spontane eously durin ng infancy & does no ot depend ono type of foot
w
wear
Flat foott
Fle
exible Riigid
Conge
enital A
Acquired Congen
nital Acquired
A
Id
diopathic RA acccessory nav Osteochondral #
V
Valgus heel inn CP plantar fascia rupturre Veertical talus Juvenile RA
H
Hyper-pronattion TP ruptu
ure: unoppossed tarsal coalitionn Reactive peroneal sp pasm
A
Accessory navvic PBrevis (fr./chron
nic joint d)
M
Marfan's $
frragile X $
♂/child/flatfee
(♂/ et/MR)
C
Calcaneovalgus
Ætiology:
CONGENITAL TYPE
1].Flexible
Asympttomatic flexxible flatfoo ot
Sympto omatic, flexiible, or sem
miflexible flattfoot
Genera alized dysplasia (e.g., Marfan,
M Ehleers-Danlos, Fragile-X)
2 Rigid
2].
Tarsal coalition
c ± peroneal
p sp
pasm
Residua als of conge enital deforrmity (e.g. TEV,
T congenital verticaal talus)
3 Flatfoot with
3]. w an acccessory navvicular
Acq
quired typ pe (See foo ot & Ankle e)
1].Traumatiic
Residua al of a calca
aneal fractuure
Talonavvicular fractture
Lisfrancc’s fracture
Ide
eal child shoe:
Posterioor tibial tendon laceration 1].Proper
P length
Spring ligament ru upture 2].Proper
P width
2 Arthrosess & RA
2]. 3].Flexible
F
4].Flat
F
Talonavvicular jointt 5].Porous
P upper
Tarsommetatarsal jo oints 6].Rough
R sole
3 Tumor off the foot
3]. 7].Extend
E above tthe ankle
8].Good
G price
4 Neuromu
4]. uscular diso order 9].Good
G looking
CP 10].Shock
S absorbinng
Nerve injury
Charco ot foot secon ndary to DM M or PN
Polio
5 Posterior tibial tendo
5]. on dysfuncction
Anatomical consideration Foot Arches

Medial Arch Lateral Arch Transverse Arch
Shape High Arch Low Arch ½ arch
Formation Apex: talus Apex: Talus middle & lat cuneiforms
Ant Pillar: nav, 3cuns, 3MT Ant Pillar: cub + 2 MT Metatarsal bases
Post Pillar: Calcaneus Same
Function Propulsion Wt support Protection
Ligaments 1- Plantar aponeurosis 1- Plantar aponeurosis • Deep trans metatarsal
2- Spring 2- Short plantar
3- Deltoid 3- Interosseous
4- Long plantar
5- Interosseous
Tendons 1- FHL 1- PL 1- Proneus Longus
2- TA 2- Short ms of little 2- TP
3- TP toe 3- Transverse head of Add Hal
4- Short ms of big toe
Bones Negligible Negligible Most important; the congruent
wedge shape of the mid & lateral
cuneiforms & the metatarsal bases
Congenital Flexible flatfoot

1- Asymptomatic Pes Planus
• Most infants, Many children, and 15% of adults
Classification:
1- DEVELOPMENTAL: as a stage of normal child development
2- PERSISTENT HYPERMOBILE FLATFOOT ώ can be inherited
Clinically:
• Foot appear normal if NWB
• With standing :
1]. Mid foot sags down
2]. Heel valgus
3]. Foot appear ER in relation to leg
4]. Wt. bearing axis falls medial to the foot med axis
• Tiptoe walking (or big toe hyper extension)
Heel goes to varus
Longitudinal arch reconstitutes: “WINDLESS ACTION” plantar fascia originates from
calcaneus & inserts into the base of big toe; é dorsiflexion Æ calcaneus is pulled
• Exclude neuromuscular disorders & tight tendoachillis (extend the knee + forefoot supination (fix
hind foot) Æ absence of the normal 10-15º dorsiflexion available)
2-Flexible Flat Foot +Tight Tendoachillis

Clinically:
• When stand:
1]. The heel goes in valhus
2]. Forefoot evert
3]. 1st ray become incontact with the ground
4]. Later Æ forefoot supinate Æ wt.bearing drop on metatarsal heads
• Pain as the foot is flexible and the TA is tight so there is a mid foot break
• Dorsiflexion is gone with neutral heel
Treatment:
• Stretching exercises: with a block under MT1 to keep foot supinated Æ supination cast
• TAL & lat.column lengthening
172 | Page
Congeenital Rigid
R Flatt Foott
3- TARSAL COALITION
(RIGID PERONE
EAL SPAST T FOOT)
TIC FLAT
It is a congenital multifacctorial disorrder characcterized by presence of
o connectio on betwee
en two or more
of thhe tarsal bo
ones (bony,, cartilagenous, or fibrous)
Aetiology:
• AD Failure
F of se
egmentatio on of 1ry mesenchyme e during fettal development
• May be e associated é PFFD and fibular hemimelia
h
Incidence:
• <1%
• ♂>♀
• Bilatera
al 50%
• Talocaalcaneal mid
ddle facet & calcaneon navicular arre the comm monest
• Both may
m occur in the
t same foo ot; If you see CN coalition
n, check for coexisting
c TC
C coalition
Pathogenesis:
• It startss as fibrous Æ cartilagenous Æ ossify o
• If not ossified
o this will allow joint
j motion n & preven nt symptoms
• Ossification time:
Talonavvicular .........................................3-5y
Calcane eonavicular .............................8-12y
Talocalccaneal ........................................12-16yy
HARRIS Classification (For middle facet f coalitio on)
I]. Continuous bon ny bridge
II]. Incom
mplete: med dial talus an nd sustantaculum tali are a separated é fibrou
us tissue
III]. Rudim
mentary é bony b projecction from medial m taluss
IV]. Rudim mentary é bony b projecction from medial m calcaaneus
Biomechanics:
3]. Subta
4]. Durin
alar
ng walking:
{ Rotaryy
Gilding motion ns
Initial sta
ance: calcan neus is in va algus ER
Terminal stance: calcaneus is in n varus IR
5]. Tarsal coalition restrict
r these e motions Æ peronea al spasm
6]. Calcaneus Æ vallgus
7]. Navic cular Æ ove er ride talar head Æ TN N capsule & dorsal TN ligament trraction
Clinically:
• 1st it iss asymptom matic
• Pain inn 2nd deca ade (bar osssification):
CN bar Æ pain at siinus tarsi an nd lat. Foott
TC bar Æ pain is de eep below the t ankle
• O/E:
Flat long gitudinal arcch
Valgus heel
h
Tiptoe walking
w Æ heel
h does no ot go to varus
Unable to t walk on lateral side of foot
Forced varus
v Æ mo ore pain & peroneal p sp
pasm
PXR
• Standing AP / latteral / Harriis Axial view w of hindfoot / Borden n Oblique vview
• Radiographic parameters fo or flat foot are: a
Talar inclination
Talometa atarsal angle
CT & MRI: are e the best
DD peroneal spastic flatfoot

• Inflammation
RA
Posttraumatic
Septic arthritis
Tuberculosis
• Tumor
Osteoid osteoma (talus)
Aneurysmal bone cyst (calcaneus)
Treatment:
1- Conservative:
Orthosis or Casting
Activity limitation If fail
2- Calcaneo-navicular bar resection:
Add fat interposition
Cast in inversion 2-3 wk NWB till subtalar motion is normal
3- TC bar resection (controversial):
Bar size & post.facet

cartilage thicknessSagittal
Large bar & thin cartilage Small bar-Recurvatum

-Procurvatum (kyphus)
Sliding osteotomy OR Triple fusion excision
Peroneal lengthening
CalcaneoValgus
Ætiology: Intrauterine pressure
Pathology:
• Dorsiflexors & peronei are short, to the level that foot dorsum is in contact with the anterior leg
• Normal functioning muscles
• Recover spontaneously
Treatment:
• Stretch exercises may speed recovery
174 | Page
A
Accesso
ory Navicul
N lar
= Os
O Tibiale Exxtermum = Navicular Secundum
S = Accessoryy Scaphoid
d = Prehalluxx
• Commo on 25%
Patthology:
• Syncho ondrosis
• Chronic c inflammation
• Partially
y separated
d
Cla
assificatioon
A
Accessory N
Navicular
T
Type I Typee II Type III
--Small -Larrge (1cm) -Curnuate navicular
-
-within TP tendon -Con nnect by cart. bridge -After fusion
f
Clin
nically:
• May be e asymp
• Pain
• Promin nence of thee normal na avicular (larrge size) Æ pain & tenderness
• Callosity
ty may be se een over th his promine ence
PXR
• Best on n oblique views
• Navicular ossifies at
a 3-5 y
• Accesso ory naviculaar ossify later
Treatment
• Observ ve
• If symptomatic
A]. Sooft pad & sidde shoes
B]. Sh
hort leg casst
C]. Lo
ocal injectio
ons
• Excision n (after exp
ploration of TP)
OTHER ACCESSORY FOOT BONES
Os Trigonum (Att the tip of th
he posterior malleolus)
m
• In 6-8% of peo
ople
• To
o be aware of
o so as not to
o confuse with
w fracturess
Os Ve
esalianum (A
At the base of the 5th metatarsal)
m
• To
o be aware of
o so as not to
o confuse with
w fracturess
Otherr Pediattric Fooot Abnorm

rmalities
1 BALL & SOCKET ANKLE = sphe
1]. erical talus + cupped
d tibia. Usua
ally no ttt but may be
b associate
ed é
fibular deficiency,
d t
tarsal coalittion, absentt lat ray, and d LLD
2
2]. BIPARTITE NAVICULAR is a comma shap ped separatted segme ent of naviccular that has
h a sepa arate
articulattion with th he talus
3
3]. ATAVISTIC GREAT TOE (Congen nital Hallux Varus): defformity occcurs at MP + short thickk MT1 + Fibrotic
Abd Ha allucis Long gus tendon ώ is release ed at surgerry
th th
h
4].
4 OVERLAPPING TOE (5 ( over 4 ): is treated d by; stretch hing, tenoto
omy, syndaactylization to 4th
5
5]. UNDERLAPPING TO OE E (Curly to oe): usually at the late eral 3 toes,, and usually asymptoomatic, if need
n
treatmeent flexor te enotomy is done d
6].
6 OCD TALUS: ..............................................................see foot and
a ankle
7
7]. FOOT & ANKLE OSTEOCHONDROSIS: ................see foot & ankle
[Peediatric Orth
hopedic] Page | 175
P Caavus
Pes
Definition:
• It is a fixed equinus fore foo ot on hind foot, é y lo
ongitudina
al arch heig
ght.
Anatomy: of the foot arcches ........se
ee Pes Planu
us.
Ætiology
1 PHYSIOLOGICAL PES CAVUS is a familial co
1]. ondition.
2]. PATHOLOGIC PES CAVUS.
A]. Ms imbalan
nce; Polio, CP, Menin
ngioMyeloccoele, Arth
hrogryposiss.
B]. CHARCOT MARIE TOOTH is a commmon cause e.
C]. Post-Traum
matic: e.g. compartme
c ontracture..
ental $, VOLKMAN’S co
Pathology:
• Degeneration of interossei Æ atrophy y Æ fibrosiss Æ shorte ening Æ co ontracture
RANG TRIPOD ANALOGY of pes ca avus: Archiitecturally, Foot
F is a trripod é its sspokes are; 1st ray, 5th ray,
and calcanneus & acco ording to th heir relation
n together; 4 cavus defformities ma ay occur:
1]. Plantaris: .................................... MT
M 1 & MT5 both
b are dra awn back to o heel.
2 Cavo-V
2]. Varus: .............................MT M 1 is drawn n back + Vaarus heel.
3 Calcane
3]. eus: ................................HeelH is draw wn downwa ard.
4 Calcane
4]. eo-carus: ......................MT M 1 is drawn n back + doown heel.
Clinically: usu
ually asymp ptomatic.
1 Pain & callosities under MT heads.
1].
2 Atroph
2]. hy of intrinssic ms of th
he foot.
3 Claw To
3]. oes.
4 ± Varuss heel Æ COLEMAN TEST (Lateral block test), to check fo
4]. or correctab
bility.
5 ± Calca
5]. aneus ankle e.
6 ± neuro
6]. ological ma anifestation of the ca
ause.
Radiologically:
• Standin ng: AP, lat, axial, obliq
que:
a.. MEARY’S ANGLE: TAF FMA (Talar Axis
A First MT
T Angle).
b.. y CALCAANNEAL PITCH: Normally y 10º-30º.
• X-ray sp pine, EMG, Ms. biopssy, Gait ana alysis.
Treatment:
D
Deformity Immature Mature
Wedgee Fusionn Tendon tra ansfer No
o Tendon
1].Cavu us (Plantaris) Steindler + Jones or Hib bbus Japas Dorsa al V-shaped osteotomy
o off the tarsus
2].Calccaneo-Cavus Steindler + Banta + Sam milson Elmsli or TF Banta Panta
alar
3].Cavo o-Varus Steindler + BILSLA + Tohen Dwyer or la ateral calcane
eal displacemment osteotom my
4].Claww Toes Big .............. Jones
J Same If there is OA Æ
Toes ........... Hibbus
H + IP fusion DuVries M MP excision arthroplasty
a
Or ............... Taylor
T FDL to
o EDL + MP capsulootomy or Fusion
5].Ham
mmer Toe FDL tenotom my DuVries PIP P Excision arthroplasty or Fusion
6].Mallet Toe FDL tenotom my DuVries DIP P Excision artthroplasty or Fusion

Trauma
Review
Dr M OHAMED S OBHY

[Fractures, Union & Biomechanics] Page | 179
Trauma Review
Region Classification
Clavicale Allman:
Gp I: Middle third .............................................
Gp II: Lateral third:
Type I: undisplaced inter-ligamentous
Type II: displaced medial to lig
A: intact conoid ............................
B: Torn conoid ...............................
TypeIII: undisplaced lat to lig
Gp III: Medial third (nondisplaced, displaced,
intraarticular, transphyseal, comminuted)
AC Joint Dameron & Rockwood
Dislocation GI: Sprained joint
GII: Torn AC lig
GIII: Torn AC + CC lig
GIV: Posterior dislocation
GV: Superior dislocation > 100%
GVI: inferior dislocation
Sterno- Anterior dislocation
Clavicular Posterior dislocation
Dislocation
Scapula Damholt classification:
GI: Body #
GII: Process #
GIII: Glenoid #
Coracoid Ogawa Classification:
GI: Base #
GII: Tip #
Acromion Khan classification:
GI: Undisplaced
GII: displaced é no subacromial narrow
GIII: displaced é subacromial narrowing
Glenoid Ideburg classification:
GI: anterior rim
GII: transverse to inferior #
GIII: transverse to superior #
GIV: transverse to medial border #
GV: = II + IV
Humerus AO classification
Supracondylar Flexion type
Humerus Extension type
Intercondylar Riseborough & Raden:
Humerus GI: non-displaced
GII: displaced
GIII: rotated
GIV: intra-articular comminution
Condylar Milch:
humerus GI: intact lateral trochlear edge
GII: # lateral trochlear edge
Capitellum GI: Hahn Steinthal (Osteochondral #)
GII: Kocher Lorenz (uncapping)
GIII: Comminuted
180 | Page [Fractures, Union & Biomechanics]
Shoulder I- Anterior:
dislocation -Subglenoid
-Subcoracoid
-subclavicular
-intrathoracic
-Retroperitoneal
II- Posterior
III- Luxatio erecta
IV- Superior
Elbow I- Anterior
dislocation II- Posterior (postero-lat & postero-medial)
III- Medial
IV- Lateral
V- Divergent (AP & medio-lateral)
Forearm shaft AO classification:
A1: simple ulna
A2: simple radius
A3: both simple
B1: wedge ulna
B2: wedge radius
B3: wedge both
C1: comminuted ulna
C2: comminuted radius
C3: comminuted both
Olecranon Schatzker classification:
GI: Transverse
GII: Transverse impacted
GIII: Oblique
GIV: Comminuted
GV: Oblique distal to coronoid
GIV: fracture dislocation elbow
Ulna Bado:
1- Night stick
2- Monteggia: (# unla + radial head (RH) disloc)
I: anterior angulation + ant RH disloc
II: post angulation + post RH disloc
III: lat angularion + lat RH dislocation
IV: ant angulation + ant radial # disloc
Radius -Radial head: Mason classification
-Radial shaft: AO
-Distal radius: Frykman
Radial head Mason Classification:
GI: non displaced
GII: displaced
GIII: comminuted
GIV: # dislocation
Distal radius GI: extra-articular GII: + Ulnar styloid
GIII: RC intra-artic GIV: + Ulnar styloid
GV: RU intra-artic GVI: + Ulnar styloid
GVII: RU & RC intraart GVIII: + Ulnar styloid
Scaphoid Russe:
GI: tubercle
GII: distal 1/3 horizontal
GIII: waist transverse
GIV: waist vertical oblique
GV: proximal
[F
Fractures, Union
U & Biiomechanics] Page | 181
Reg
gion Classiification
Basse of first GI: E
Extra-articul ar:
mettacarpal -T
Transverse
-O
Oblique
GII: In
ntra-articula
ar
-B
Bennett vola
ar ulnar lip
-R
Rolando vola
ar & dorsal lip
p
MP1Joint MCL Spprain
a- Gamekeeper
G r’s thumb: <3 35º open ................. Thum mb spica
b- Stener lesion n: >35º op pen é addu uctor
aponeurosis opening ................................................ Open n repair
ury: rare ........................................................................... Thum
LCL inju mb spica
Dorsal dislocation:
d
a- Simple: no interposition of o volar plate e ..... CRUG GA & immob
bilization 3w
wk
b- Complex:
C é in nterposition of volar platte;
MP1 angle > 90º) ................................................ Open
(M n repair
Spine Fracture Classification
Atlas # Levine
GI- Apophysis fracture.
GII- Post arch #.
GIII- Ant arch #.
GIV- Lat mass #.
GV- Burst #.
AARI (Atlanto- Fielding
Axial Rotary GI- Odontoid # & ADI < 3mm.
Instability) GII- Dens facet # & ADI < 5mm.
GIII- Subluxed anteriorly & ADI > 5mm.
GIV- Subluxed posteriorly
GV- Dislocation.
Odontoid # Anderson & D’Alonzo
GI- Apex #.
GII- Neck #.
GIIa- Waist & extends to body.
GIII- # extends to lat mass.
Hangman’s # Levine-Edwards-Effendi
(C2 spondylolithesis) GI- Non displaced ..................................................... Orthosis.
GII- Displaced one pars # ....................................... Halo traction.
GIII- Displaced pars # + disco-ligamentous # . Immobilization.
GIV- Displaced pars # + C2-3 facetal joint # ....... Halo 3wk Æ OR + posterior fusion.
C3-C7 # Allen Ferguson
GI- Flexion compression (tear drop).
GII- Vertical compression.
GIII- Flexion distraction.
GIV- Extension compression.
GV- Extension distraction.
GVI- Lateral flexion.
GVII- Miscellaneous.
Thoraco- McAfee
Lumbar # GI- Wedged compression #.
GII- Stable burst #.
GIII- Unstable burst #.
GIV- Chance # (seat belt = flexion distraction).
GV- Flexion distraction #.
GVI- Translation #.
Gain’s ....................................................... (see spine).
White & Punjabi ............................... (see spine).
Posterior Hip Thompson & Epstein:
dislocation GI: dislocation
GII: posterior wall # dislocation
GIII: comminuted post wall # dislocation
GIV: posterior column # dislocation
GV: head # dislocation
Anterior hip Epstein:
dislocation GI: Iliac:
-no #
-#head
-#acetabulum
GII: obturator:
-no #
-#head
-#acetabulum
Femoral Head Pipkin:
GI: caudad to fovea
GII: cephalad to fovea
GIII: head & neck #
GIV: head & acetabulum #
Femoral neck Garden:
GI: incomplete impaction in valgus
GII: complete non displaced
GIII: partially displaced & trabeculae are not
in line é acetabular trabeculae
GIV: completely displaced & trabeculae in line
Trochanteric Boyd:
GI: intertroch
GII: intertroch + coronal #
GIII: reversed obliquity
GIV: subtrochanteric extension
Evans:
GI: Inter-trochanteric #
a-undisplaced
b-displaced reduced
c-displaced unreduced
d-comminuted
GII: reversed obliquity
Subtrochanteric Fielding:
GI: at lesser trochanter
GII: 1 inch below LT
GIII: 2 inches below LT
Seinsheimer:
GI: non displace
GII: 2parts
a-trasverse
b-oblique é LT proximal
c-oblique é LT distal
GIII: 3 parts:
a-LT wedge
b-Lateral wedge
GIV: 4 parts
GV: inter-subtrochanteric
Russell & Taylor:
I: intact pyriformis:
-intact LT
-# LT
II: # Pyriformis:
-intact LT
-#LT
Femoral shaft AO classification
Pelvis Young & Burgess:
GI: Lateral Compression (LC)
-Rami #
-Rami + posterior liac #
-Any + contralateral lig disruption
GII: Anterior compression (AP)
-<2.5cm symphysis diastasis
->2.5cm diastasis + ant SI disruption
-complete disruption (rotation + translation)
GIII: vertical shear
GIV: combined
Tile
GI: Stable # (avulsion #, Wing, Tr sacral#)
GII: Partially Stable:
a- Rotationally unstable
b- Vertically unstable
GIII: Unstable
a- Rotationally unstable
b- Vertically unstable
Acetabulum Judet & Letournel:
I-Elementary:
1-anterior wall
2-anterior column
3-posteior wall
4-posterior column
5-transverse
II-Associated
1-posterior wall posterior column
2-posterior wall trasverse
3-anterior column trasverse
4-T
5-both columns (floating acetabulum)
Sacrum Denis
GI: Lateral to formina
GII: Transforminal
GIII: medial to formina
Distal femur Seinsheimer:
GI: non displaced
GII: displaced supracondylar:
a-2parts
b-comminuted
GIII: intercondylar:
a-medial condyle
b-lateral condyle
c-both
GIV: intraarticular:
a-medial condyle
b-lateral condyle
c-both
Tibial plateau Schatzker:
GI: lateral split #
GII: lateral split depressed #
GIII: lateral depressed #
GIV: medial plateau #
GV: bicondylar #
GVI: V+metaphyseal comminution
Tibial shaft AO
Pilon Rudi & Allgower:
GI: congruent non displaced
GII: incongruent 3-4 parts
GIII: incongruent comminuted
Ankle Lauge Hansen:
SA: supination adduction
SER: supinartion external rotation
PA: pronation adduction
PER: pronation external rotation
Talus Hawkin:
GI: fracture non displaced #
GII: fracture + subtalar dislocation
GIII: fracture + ankle & subtalar dislocation
GIV: fracture + TN, ankle & subtalar disloc
Calcaneus Extra-articular:
I: anterior process
II: medial process
III: posterior tuberosity
IV: sustentaculum
V: body
Essex Lopresti Intra-articular:
1ry: 1ry line anterior to posterior facet
2ry: joint depression: 2ry line post to post facet
Tongue #: 2ry line pass to post tuberosity
Sanders CT classification (depends on 3
lines; A: Lat 1/3, B: lat 2/3, C: lat to
sustentaculum)
GI: non displaced
GII: 2 parts displaced # IIA, IIB, IIC
GIII: 3 parts displaced # IIIAB, IIIAC, IIIBC
GIV: 4 parts fracture
Navicular GI: transverse
GII: vertical
GIII: comminuted
Lisfranc joint Ouenu & Kuss:
GI: Homo-lateral
GII: isolated medial
GIII: divergent
Sesamoid Jahss
GI: avulsed from MT1
GII: intersesamoid
GIII: intrasesamoid
Pediatric Classification Treatment
C1-C2 Grisel’s: laxity 2ry to local inflammation ...... Traction immobilization 6-8wk
dissociation Rotary:
GI- No C1 shift ................................................... Soft collar
GII- < 5 cm anterior shift ................................. Traction immobilization 4-6 wk, if
GIII- > 5cm anterior shift .................................. recurrence, neglected >4wk, or neurologic
GIV- Posterior shift ............................................. deficit Æ C1-C2 fusion
SCIWORA Spinal Cord Injury With Out Radiologic MRI evaluation + supportive ttt
Abnormality
Epiphyseal Salter-Harris classification:
Injury GI- Complete transphyseal #.
GII- Transphyseal + metaph. Fragment.
GIII- Transphyseal + ephiph. articular #.
GIV- # across & epiphysis & metaphysis.
GV- Physeal crushing.
Ogden modification
GVI- Perichondrial ring injury.
GVII- Epiphyseal # only.
GVIII- Metaph. # affecting physis bl. Supply
GIX- Diaphyseal # affecting periosteal
appositional growth
SCJ, ACJ, & As adults.
scapula
Clavicle As adults. <2y sling for 2wks.
>2y sling for 4wks.
ORIF if neurovascular & skin complication
Proximal Salter-Harris 1-4 y <70º is acceptable.
humerus 5-12y <40º & 50% displaced is acceptable.
>12y <20º & 30% displaced is acceptable.
Otherwise OR & pin fixation is needed.
Supracondylar Gartland
fracture Extension type
humerus GI- Non displaced .............................................. LAC (long arm cast) at 90º for 3 wks.
GII- Displaced with intact post cortex. ......... CRUGA ± Pin fixation Æ LAC at 90º X 3wk.
if fail
GIII- Completely displaced. ................................ CRUGA ORIF.
Flexion type:
GI- Non displaced. ............................................ LAC (long arm cast) at 90º for 3 wks.
GII- Displaced with intact anterior cortex .. CRUGA ± Pin fixation Æ LAC at 90º X 3wk.
GIII- Completely displaced ................................ CRUGA
if fail
ORIF.
Lateral Condyle Milch
fracture GI- # line passes lateral to trochlea. If non displaced <2mm Æ LAC 90º X 3wks.
GII- # line passes across the trochlea. If displaced Æ ORIF + LAC 90º X 3wks.
Medial condyle Milch
fracture GI- # line passes across the trochlea. Same.
GII- # line passes lateral to trochlea.
Transphyseal Delee
fracture GA- <6m (no ossific centre). S&H type I. <5 d Æ CRUGA Æ LAC 90º & pronation.
GB- 7mo-3y (ossified lat. Centre) S&H II. >5 d or GC Æ ORIF Æ LAC 90º X 3wks.
GC- 3-7y with large metaphyseal fragment.
Capitellum As adults.
fracture
Radial head O’Brien
fracture GI- <30º angulation .......................................... LAC 90º X 1 wk.
GII- 30º-60º angulation ................................... CRUGA in extension, supination, varus Æ
flex & pronation with thumb pressure over
radial head Æ LAC 90º X 2 wks.
GIII- >60º angulation ......................................... ORIF (also if >3mm displaced, or failed GII).
Pulled elbow CRUGA in supination from ext to flexion.
CRUGA in hyperpronation also.
Pediatric Classification Treatment
Elbow As adults.
dislocation
Olecranon GI- Flexion injuries. Tension band.
fracture GII- Extension injuries: Cancellous screw.
a. Valgus.
b. Varus.
GIII- Shear injuries.
(MUS) Bado
Monteggia GI- Ant SRU dislocation + Ant ulna #.
Ulna # GII- Post. SRUJ dislocation +Post Ulna #.
Sup radio-ulnar
GIII- Lat. SRUJ dislocation + Lat ulna #.
GIV- Ant SRU disloc + Prox ulna & radius #s.
Monteggia Variants
I. Isolated radial head dislocation.
II. Prox ulna & radius #s.
III. Isolated radial neck #.
IV. Elbow dislocation.
(GRI) Galeazzi
Galeazzi. GI- Dorsal displacement by supination. ORIF
Radius #. GII- Volar displacement by pronation.
Inf radio-ulnar
Fracture neck Delbert
femur GI- Trans-epiphyseal. If non displaced pin fixation in place.
GII- Trans-cervical. If displaced & irreducible Æ ORIF.
GIII- Cervico-trochanteric.
GIV- Inter-trochanteric.
Tibial spine Meyer & McKeever
fracture GI- Minimally displaced .................................. LLC in extension.
GII- Ant part only is displaced up ................. LLC in extension.
GIII- Complete displacement .......................... ORIF + LLC 4-6 wk.
GIV- Comminuted ............................................... ORIF + LLC 4=6 wk.
Tibial tubercle Watson Jones
fracture GI- Tubercle avulsion. CRUGA + LLC (long leg cast) for 4-6wk.
GII- Tubercle + part of tibial epiphysis. ORIF + LLC 4-6wk.
GIII- Same and reaching the joint.
Toddler’s # = spiral fracture of the tibia. LLC 3wks Æ SLC 3wks.
Ankle # Dias & Tachdjian (as Lauge-Hansen)
GI- SA.
GII- SER. ORIF
GIII- Supination plantar flexion.
GIV- PER.
Tillaux # S&H III of the antero-lateral tibial epiphysis.
Foot #s. As adults.
Radiological Views
Exam View Finding Significance
Shoulder
1]. Out let View Acromial morphology (type I-Ill) Type Ill acromion in impingement
2]. 30º Caudal Tilt Standing + 30° caudal beam Subacromial spurring Subacromial impingement area
3]. Zanca Standing & 10º cephalic tilt AC joint pathology AC DJD, distal clavide osteolysis
4]. West Point Prone & overhang elbow Anteroinferior bony bankart Bony Bankart lesion seen with
rays inward & cephalad 25° instability
5]. Garth view Anteroinferior glenoid evaluation Bony Bankart
6]. Stryker Notch Hand over head + rays 30° Hill-Sachs defect & coracoid # Hill-Sachs impression fracture &
cephalad coracoids fractures
7]. Shoulder AP IR Standing + max IR & rays AP Hill-Sachs defect Hill-Sachs defect
8]. Hobbs view Sitting + hands over head & Sternoclavicular dislocation Sterno –clavicular AP dislocations
rays from above down
9]. Serendipity view Supine + cephalad rays Sternoclavicular dislocation AP dislocations
10]. Axillay view Standing abduction & beam Shoulder Posterior dislocation & glenoid rim
cephalocaudal # & AC Grade IV dislocation
11]. Velpeau axillary Standing + leaning backward Shoulder if axillary is difficult Same as axillay
12]. Heinig view Standing + lat rays Sternoclavicular dislocation AP dislocations
13]. 45º abd true AP Glenohumeral space OA Subtle DJD
14]. Heinig view Standing + lat rays Sternoclavicular dislocation AP dislocations
15]. Alexandar View Standing trans-scapular + AC joint AC dislocation
forward shrug
Elbow
1]. Tuberosity view Elbow 90° é ulna on cassette Assess radial tuberosity rotation Radial # location in relation to
& beam 20° to olecranon To olecranon = supination & vv pronator ms insertion
2]. Jones view Arm on cassette + flexed Baumann’s angle (upper border of >20º Æ cubitus valgus.
elbow & beam via forearm lat.condylar nucleus to vert. axis)
Hand & Wrist
1]. PA wrist Palm down Carpal instability SL & LT dissociations
2]. AP clinched fist SL space SL dissociation
3]. AP supinated 30° LT space LT dissociation
4]. PA pronated 20° Dorsum of triquetrium Triquetral #
5]. Zieter view PA wrist in slight extension Scaphoid fracture
6]. Tunnel view Extension axial Hamate Hook fracture
7]. Roberts view FA full pronation + arm full IR Trapezio-MCJ TM osteoarthritis (rhizarthrosis)
8]. TMC dynamic stress AP é pressing both thumbs Trapezio-MC OA
radial tips together
Hip
1]. Faux Profile Standing + rays 60° outward Antero-lateral head coverage Assessment of DDH
2]. Von Rosen Supine AP é abduction & IR DDH hip congruity
3]. Modified Billing’s 90° flexion + 60° abduction / Modified lateral view é constant Assessment of SCFE
rays direct AP parameters (≠ frog view)
4]. Iliac oblique Judet Supine & beam 45° external Ant acet lip & Kohler’s line Anterior wall & posterior column
5]. Obturator oblique Supine & beam 45° internal Posterior lip & ilio-pectineal line Posterior wall & anterior column
Judet view direction + 15° cephalad
6]. Pelvic Inlet Supine & beam 60° caudad Pelvic brim AP & rotational displacement of SI
7]. Pelvic outlet Supine & beam 45° cephalad Sacroiliac anterior view Vertical shear of SIJ
Foot & Ankle
1]. Sesamoid axial Sitting & foot is vertical + Sesamoid fracture, subluxation, Hallux Valgus
hyper extension of MPj OA, metatarsal bisector
2]. Blackburn series Harris view Subtalar Valgus TPPD
Standing Lateral Meary’s angle Pescavus & planovalgus
Standing AP foot & ankle Kite, CAMPA, TAMPA TEV, vertical talus
3]. Harris view Supine + max DF & beam 45° Alignment, bars Tarsal Coalition
cephalad
4]. Broden Views knee 90º , Ankle 0º, IR 40º Subtalar joint & sinus tarsi
Beam 10,20,30.40º cephalad
5]. Canale view Foot pronated 15° & beam Talar neck & sinus tarsi
15° cephalad
Fracture Biomechanics
• Bone can be considered as a biphasic composite material, mineral as one phase, and
collagen and ground substance as the other
• The combined substances are stronger for their weight than either substance alone
• Cortical bone is stiffer than cancellous bone and more brittle, withstanding less strain before
failure than cancellous bone
o Fracture occurs in cortical bone in vitro at strains of only 2%
o Fracture occurs in cancellous bone in vitro at strains of > 75%
• Bone is VISCOELASTIC (= time dependent property where the deformation of the material is
related to the rate of loading, hysteresis, creep, stress relaxation)
• Load deformation curve for bone compared to other materials = the elastic portion of the graph
has a slight curve in bone.
• Bone stiffness compared to other materials:
Bone behaviour under various loading modes

• Bone is ANISOTROPIC (i.e it has different mechanical properties when loaded along different
axes). This is ð structure of bone is dissimilar in the transverse and longitudinal directions
• Adult cortical bone is stronger in compression than tension and weakest in shear.
• Most fractures occur as a result of several loading modes
1- Tension
• At the microscopic level, the failure mechanism for bone loaded in tension is mainly
debonding at the cement lines and pulling out of the osteons
• The type of fracture occurring in tension is a transverse fracture
• Tension #s tend to occur in areas with a large proportion of cancellous bone eg calcaneum,
5th metatarsal
2- Compression
• At the microscopic level the failure mechanism for bone tissue in compression is mainly
oblique cracking of the osteons
• The type of fracture that occurs in compression is an oblique fracture at an angle of 30
degrees as shear forces at this angle are responsible for the failure.
• There are few fractures which occur purely due to compression
• These fractures tend to occur in the metaphyses of bones where there is more cancellous
bone which is weaker.
3- Bending
• In bending there is a combination of
compression and tension. Tensile stresses and
strains on one side of the neutral axis and
compressive stresses and strains on the other
side. Because bone is assymmetrical, the
compressive and tensile stresses may not be
equal
• Bending causes transverse fractures as failure
on the tension side progresses transversely
across the bone and the neutral axis shifts.
Three point bending- three forces act on a structure produce 2 equal moments, each being the
product of one of the two peripheral forces and the distance to the axis of rotation (the point at
which the middle force is applied. If loading continues to yield point assuming the structure is
homogenous and symmetrical, it will break at the point of application of the middle force. Fracture
begins on the tension side in adult bone as bone is weaker in tension than compression. Examples
include skiboot fractures of the tibia. In immature bone it may fail by compression causing buckling
on the compression side
Four point bending- Two force couples acting on a structure produce two equal moments. The
magnitude of the bending moment is the same throughout the area between the two force
couples. The structure will break at its weakest point between them. Eg a previous unhealed
fracture.
4- Compression and bending combined

• A combination of fracture type occurs. Bending produces a transverse crack on the tensile
side of the bone, compression causes an oblique fracture on the other side. Where they
meet a butterfly segment results
5- Torsion
• A load is placed on a structure so that twisting occurs about an axis. A torque or moment is
produced within the structure.
• Maximal shear stresses act in planes parallel and perpendicular to the neutral axis
• Maximal tensile and compressive forces act on planes diagonal to the neutral axis
• The fracture for a bone loaded in torsion is a spiral fracture.
• It begins é failure in shear, with the formation of a crack parallel to neutral axis of the bone
• Followed by failure in tension along the line of maximal tensile stress at a diagonal to the axis
6- Shear
• A structure subjected to shear loading deforms internally in an angular manner, right
angles on a plane surface within the structure become obtuse or acute.
• Whenever a structure is subject to compressive or tensile loading, shear stress is also
produced
• The value for the stiffness of a material under shear loading is known as the shear modulus,
not elastic modulus
• Shear fractures tend to occur in cancellous bone eg. Femoral condyles, tibial plateau.
Bone strength
Compression Strongest
Tension Weak
Shear Weakest
Bone type Load type Elastic modulus (109 N/m2) Ultimate stress (106 N/m2 )
Cortical Compression 15.1 - 19.7 156 - 212
Tension 11.4 - 19.1 107 - 146
Shear 73 - 82
Cancellous Compression 0.1 - 3 1.5 - 50
Tension 0.2 - 5 3 - 20
Shear 6.6
Influence of muscle activity & loading on stress distribution in bone

1- When bone is loaded in vivo, simultaneous contraction of surrounding muscles act to oppose
these loads, so that it can withstand higher loads.
Wolff's Law (Julius Wolff, 1884)
• 'form follows function'.
• Bone has the ability to adapt, by changing its size, shape, and structure, to the mechanical
demands placed on it.
• Bone is laid down where needed and resorbed where not needed.
• The remodelling may be either external (a change in the external shape of the bone) or
internal (a change in the porosity, mineral content, and density of bone).
Rate dependency in bone

• Because bone is viscoelastic, its biomechanical behaviour varies with the rate of application
of forces
• Bone is stiffer and more brittle and can sustain a higher load to failure when loads are
applied at higher rates [Graph]
• Bone also stores more energy to failure before failure at high loading rates. When a bone
fractures the stored energy is released. At a low loading rate the energy can dissipate
through formation of a single crack. At a high loading rate, the greater energy stored
cannot be dissipated rapidly enough through a single crack and comminution and
extensive soft tissue damage result
Fatigue fracture of bone
• Caused by repeated applications of a load below the ultimate strength/stress of the bone
• The fatigue process in living bone is affected by the amount of load, the number of
repetitions and the frequency of loading. Fatigue fracture only occurs when the rate of
remodelling is outpaced by the fatigue process.
• Fatigue fractures tend to occur during continuous strenuous physical activity causing the
muscles to fatigue and reduces their ability to contract and counteract the imposed loading.
Influence of bone geometry on biomechanical behaviour

In tension and compression,
• The load to failure and stiffness are proportional to the cross sectional area of the bone
In bending,
• The load to failure and the stiffness are proportional to the ‘area moment of inertia.’ This is a
figure which takes into account the cross sectional area and the distribution of bone about
the neutral axis.
• The area moment of inertia for a rectangular block= BxH3/ 12 (B = width H = height)
• Block III is more resistant to bend than block I and II.

• Bones increase their area moment of inertia by distributing most of the bone tissue in the
periphery, away from the neutral axis
• In bending, the load to failure and stiffness is also inversely proportional to the length of the
bone. The longer the bone is, the bigger the bending moment produced for the same force.
• For a tubular structure / cylinder the further the material is from the neutral axis, the stiffer
the construct under a given loads = Second Moment of Area (I)
4
o Circle: I = [pi.r ] /4 (hollow: r= outer radius-inner rad.)
o Bending Stiffness = E.I (where E is Youngs Modulus)
o The region of a bone/nail with the smallest I is subjected to the largest deformation
under load & will fail first
o Indirect bone healing (thick periosteum) -> incr. I -> incr. stiffness & strength.
In Torsion:
• The load to failure and stiffness are proportional to the Polar Moment of Inertia(J)
• This takes into account the cross sectional area and the distribution of bone tissue around
the neutral axis
• J = [pi/2]x[Ro4-Ri4] = 2.I; T/ø = JG/L (T/ø= torsional stiffness, T= torque, ø= angle of twist, G=
shear modulus, L= length of shaft)
In bone healing:
• Callus formation around the periphery of a fracture increases the Second Moment of Area
(I) and the Polar Moment of Inertia(J) of a bone, thus maximising the strength and stiffness
of the bone in bending and torsion during healing.
Bone remodelling
• Wolff’s law – Bone is laid down where needed and resorbed where not needed
• Thus disuse leads to supperiosteal and periosteal bone resorption, reducing its stiffness and
strength.
• Stress protection of bone- is a phenomenon whereby an implant, by sharing the imposed
load can cause resorption of the underlying/surrounding bone as this bone carries less load
than normal.
• Bone hypertrophy can also occur at implant attachment sites, eg. Around screws.
• Laying down of bone can occur as a result of strenuous exercise, or resorption can occur in
prolonged weightlessness or inactivity.
Strain Theory of Fracture Healing
• The theory of interfragmentary strain hypothesis is that the type of tissue formed in a
healing gap depends on the strain that it experiences
• If the strain is between:
o 10%-100% granulation tissue can be expected to form
o 2%-10% fibrocartilage will form
o < 2% bone will form
Effect of movement on bone healing

Kenwright et al studied osteotomies with a gap of 3mm and subjected them to movement. They
showed that when compared to a rigidly held osteotomy there was:
• Increased bone mineral content in the gap with movement of 0.5mm (16% strain)
• Decreased bone mineral content in the gap with movement of 2.0mm (66% strain)
It is important to note that it is not compressive load but strain, whether compressive or tensile that
increases bone mineralisation
Other Factors Affecting Bone Strength

Effects of use and disuse
Rubin and Laynon in an avian model (turkey ulna):
Disuse
• 42 days without functional load decreased bone mineral content to 88% of normal
• Bone is lost from the endosteal surface
Use
• Controlled cyclical loading (as low as 36 cycles per day) produced a hypertrophic response
with an increase of between 140%-150% of normal bone mineral content
• Bone is deposited on the periosteal surface
Effects of holes on bone strength

• The strength of bone is effected by the size and shape of holes
• Holes with sharp corners will reduce the torsional strength of bone to a greater extent than
those with smooth edges due to the stress riser effect associated with sharp corners
• 4 point bending strength decreased to 80% of normal for a hole diameter of 10% of the
diameter of the bone
• Torsional strength is affected when the hole size is greater than 10% of the diameter of the
bone
• 20% size hole would reduce the torsional strength to 67% of normal
Changes in bone associated with aging

• Progressive loss of bone density occurs with age
• Young bone is more ductile /less brittle than older bone, so more strain before breakage is
allowed in young bone.
Fracture Healing
1- HEMATOMA FORMATION
2- INFLAMMATORY RESPONSE ........................... WITHIN 24-72 hours
• Injured tissues and platelets release vasoactive mediators,
growth factors and other cytokines.
• These cytokines influence cell migration, proliferation,
differentiation and matrix synthesis.
• Growth factors recruit fibroblasts, mesenchymal cells &
osteoprogenitor cells to the fracture site.
• Macrophages, PMNs & mast cells (48hr) arrive at the fracture
site to begin the process of removing the tissue debris.
Important cytokines in bone healing:

BMP Osteoinductive, induces metaplasia of mesenchymal cells into osteoblasts
Target cell for BMP is the undifferentiated perivascular mesenchymal cell
TGFβ ⊕ UMC to produce type II collagen and proteoglycans
⊕ osteoblasts to produce collagen
PDGF Attracts inflammatory cells to the fracture site
FGF ⊕ fibroblast proliferation
IGF-II Stimulates type I collagen production, cartilage matrix synthesis and cellular proliferation
IL-1 Attracts inflammatory cells to the fracture site
IL-6 Attracts inflammatory cells to the fracture site
3- REPARATIVE RESPONSE ................................. WITHIN 2 weeks

a. Vasoactive substances (Nitric Oxide & Endothelial Stimulating Angiogenesis Factor) cause
neovascularisation & local vasodilation
b. Undifferentiated mesenchymal cells migrate to the fracture site and have the ability to form cells
which in turn form cartilage, bone or fibrous tissue.
c. The fracture haematoma is organised and fibroblasts and chondroblasts appear between the bone
ends and cartilage + Type II collagen are formed (SOFT CALLUS)
d. Endochondral ossification takes place and the soft callus is turned Into (HARD CALLUS)
e. The amount of callus formed is inversely ∝ to the amount of immobilisation of the fracture.
• In fractures that are fixed with rigid compression plates there can be primary bone healing with little
or no visible callus formation.
Types of callus:
External (bridging) callus From the # haematoma Æ endochondral ossification Æ woven bone
Periosteal callus from inner cambium layer Æ intramembranous ossification Æ woven bone
Internal (medullary) callus Forms more slowly and occurs later
4- REMODELLING:
– Middle of repair phase up to 7 years
• Remodelling of woven bone depends on mechanical forces applied (W
WOLFF’S LAW - 'form follows function')
• Fracture healing is complete when there is repopulation of the medullary canal
• Cortical bone
o Remodelling occurs by invasion of an osteoclast “cutting cone” which is then followed by
osteoblasts which lay down new lamellar bone (osteon)
• Cancellous bone
o Remodelling occurs on the surface of the trabeculae ώ causes trabeculae to become thicker
Bone Remodeling
The BMU remodeling sequence
Phase Factors Description
1- Origination (+) PTH, IGF, IL-1, IL-6, After microdamage to the bone, following
PGE, calcitriol, TNF, mechanical stress, following exposure to some
NO cytokines, or at random, a BMU will originate. The
(-) estrogen lining cells become active and change from a
pancake-like to a cuboidal shape.
2- Osteoclast (+) RANK-ligand, M- Lining cells that have been activated by IL-1, PTH,
recruitment CSF calcitriol, etc (but not IL-6) will then secrete RANK-
(-) osteoprotegerin ligand, which may remain bound to the cell surface.
(OPG), GM-CSF Osteoblast precursors also secrete RANK-ligand. Pre-
osteoclasts have membrane receptors called RANK.
When RANK-ligand activates these receptors the cells
fuse and differentiate into mature multinucleared
osteoclasts which develop a ruffled border and resorb
bone. Meanwhile, OPG is a free-floating decoy
receptor, related to the TNF family, which can bind
the RANK-ligand and prevent it from activating the
RANK.
3- Resorption (+) Integrins, some The mature osteoclasts resorb bone. As the BMU
interleukins, acidosis, wanders, new osteoclasts are continuously activated
vitamin A and then start resorption. At any one spot on the
(-) estrogen, surface the resorption lasts about two weeks. The
calcitonin, interferon, osteoclasts then undergo programmed cell death or
TGF, other apoptosis, which is delayed by estrogen deficiency.
interleukins, sFRP-1
4- Osteoblast (+) Wnt, BMPs, IGF, Osteoblasts are derived from marrow stromal cells,
recruitment FGFs, PDGFs, CSF, which can differentiate into either adipocytes or
PTH, calcitriol, Runx2, osteoblasts; the transcription factor Runx2 (previously
GST-RANK-Ligand, named Cbfa1) is necessary for osteoblastic
TGF-beta differentiation. Osteoblasts are probably attracted by
(-) ? leptin bone-derived growth factors. Wnt-signalling and
bone morphogenic proteins are important.
5- Osteoid (+) TGF-beta, BMPs, The active, secreting osteoblasts then make layers of
formation IGF osteoid and slowly refil the cavity. They also secrete
(-) FGFs, PDGFs, growth factors, osteopontin, osteocalcin, and other
glucocorticoids proteins.
6- Mineralization (+) calcium, When the osteoid is about 6 microns thick, it begins
phosphate to mineralize. This process, also, is regulated by the
(-) pyrophosphate osteoblasts.
7- Mineral Other ions For months after the cavity has been filled with bone,
maturation the crystals of mineral are packed more closely and
the density of the new bone increases.
8- Quiescence The final osteoblasts turn into lining cells which

participate in the minute-to-minute release of calcium
from the bones. Some of the osteoblasts also turn into
osteocytes which remain in the bone, connected by
long cell processes which can sense mechanical
stresses to the bones.
Factors influencing bone healing
Systemic Local
Age Degree of local trauma &vascular injury
Hormones Degree of bone loss
Functional activity Local pathological condition
Nerve function Type of bone fractured
Nutrition Immobilization
Drugs (NSAID) Infection
Hormonal influences on bone healing

Hormone Effect Mechanism
Cortisone z Decreased callus production
Calcitonin y Unknown
TH/PTH y Bone remodelling
GH y Increased callus volume
Androgens y Increased callus volume
Type of immobilization and Healing

Implant Type of Healing
Cast Periosteal bridging callus + endochond ossification
DCP Primary cortical healing (cutting cone)
IMN Early ......... as cast
Late .......... Medullary callus
External Fixator z rigid ..... Periosteal Callus
y rigid ..... Primary cortical healing
Inadequate immobilization + Hypertrophic non union (ytype II collagen)
adequate blood supply
Inadequate immobilization + Atrophic non union
Inadequate blood supply
Fracture displacement Oligotrophic nonunion
Electricity and fracture healing

• Stress generated potentials serve as signals that modulate cellular activity. Piezoelectric effect and
streaming potentials are examples of stress generated potentials
1. Piezoelectric effect: charges in tissues are changed secondary to mechanical forces
2. Streaming potentials: occur when electrically charged fluid is forced over a tissue (cell
membrane) with a fixed charge
• Transmembrane potentials: generated by cellular metabolism
• Fracture Healing
1. Direct current inflammatory response
2. Alternating current repair phase collagen synthesis and calcification
3. Pulsed Electro Magnetic Field remodeling & calcification of fibrocartilage
Ultrasound
• Can decrease the time to clinical healing and radiological union
Implants for Fracture Surgery
1. BONE SCREWS
There are two types of screws = Machine screws & Wood screws.
Bone screws are machine screws.
1. A wood screw is inserted into a small pilot hole. The screw threads compress the wood,
which is less stiff than the screw, resulting in an elastic force.
2. A machine screw is inserted into a pre-drilled & pre-tapped hole. The screw itself deforms
plastically when inserted into metal.
Screw Head
• = attachment for screwdriver
• Countersink = conical area under head
• Hexagonal head recess design is most popular because:
1. it avoids slippage of screwdriver & thus head distortion
2. it allows for better directional control during screw insertion
3. the torque is spread between 6 points of contact
Screw Shaft
• = smooth link betw. head & thread.
• The 'Run out' is the transitional area between shaft & thread. This is the area screws break.
Screw Thread
• The standard orthopaedic screw has a single thread (more threads increase the rate of advancement,
but produces less compression for the same energy)
• Core/root diameter = the narrowest diameter.
o The cube of the root diameter is proportional to the torsional strength of the screw.
• Outer/thread diameter = across the maximum thread width.
o The larger the outer diameter the greater the resistance to screw pullout.
• Pitch= the distance between adjacent threads.
o Cortical screws have small pitch & cancellous screws have large pitch
o The stronger the bone the smaller the pitch
• Lead= the distance the screw advances with each turn.
o The smaller the lead the greater the mechanical advantage of the screw.
o Cortical screws have a smaller lead than cancellous screws
• Pitch & lead = incline of a ramp. A barrel travels a shorter distance on a steeper incline before it gets
to the top, but it is harder to push it up the ramp.
• Thread design:
o 'V' profile - produces shear + compression forces
o Buttress profile - produces compression forces only
o shear forces promote bone resorption, reducing pullout strength.
• Thread length:
o Partially threaded screws are designed for lagging cancellous bone.
o 80% of the screw's grip is determined by the thread on the near cortex & 20% on the
purchase at the far cortex.
Screw Tip
1. Blunt tip of self-tapping screw - cortical
• Fluted to act as a cutting edge & transport bone
chips away.
• The sharpness, number & geometry of flutes
determine its effectiveness.
2. Blunt tip of non-self-tapping screw - cortical
• The rounded tip allows for more accuracy &
direction into a pre-tapped hole.
• More 'effective torque' is obtained from pre-
tapping -> increased inter-fragmentary
compression.
3. Corkscrew tip - cancellous screw
• Compresses trabecular bone & produces
compression by overshooting the pre-drilled hole.
4. Trocar tip -
• Doesn’t have a flute, thus displaces bone as it advances.
SCREW INSERTION
Drilling:
Heat Generation:
1. Bone heated to >45ºC leads to osteocyte necrosis, deactivation of alkaline phosphatase &
degradation of collagen hydroxyl-apatite bone. This results in permanent alterations in the
mechanical properties.
2. Causes:
1. Dull drill bit - also causes crushing of bone & small local fractures.
2. Time
3. Thick bone
4. Excessive thrust & speed
5. Dry bone
6. No drill sleeve -> drill wandering
3. Good drilling practice:
1. straight, sharp drill bit with 3 flutes & cutting angle of >70o
2. Clean the tip frequently
3. start slowly & maintain the drilling angle
4. Use a drill sleeve
5. Simultaneous saline irrigation
Tapping:
1. Allows precision placement when placing screw obliquely (lag)
2. Less torque lost in overcoming friction at the bone-screw interface.
3. Less force required. = less likelihood of losing # position.
Self-Tapping Screws => quicker, less instruments, tight fit, same holding power as pre-tapped screw.
Lag Screws:
• = involves placement of one or more screws across a fracture or osteotomy site to produce inter-
fragmentary compression.
• ِAchieved by over-drilling the near cortex.
• The ideal position is perpendicular to line of fracture, but this does not provide axial or rotational
stability. Therefore, should try & use more than one screw with the other screw perpendicular to the
long axis of the shaft.
• LAG SCREW EXERTS 3000 N INTER-FRAGMENTARY EVEN COMPRESSIVE FORCE FROM WITHIN THE
FRACTURE
2. PLATES:
Benefits:
• Anatomical reduction of the fracture with open techniques
• Stability for early function of muscle-tendon units and joints
Disadvantages:
• Risk of bone refracture after their removal
• Stress protection and osteoporosis beneath a plate
• Plate irritation
Types/ Techniques of Plates:
1) Compression Plate(DCP):
• Applied to the tensile surface; under compression Æ tension within plate & compression on bone.
• Compression produced by the DCP = 600 N, and not even (either on the compression side in prestressed
plates, or one the tension side in the contoured plates)
• Fracture edges resorb after 72hrs Æ z stresses in plate & bone -> improved apposition.
• Plate resists bending moment by its tension.
2) Neutralisation Plate (semitubular plate usually):
• applied at right angles to the above.
• If apposition is poor this arrangement is more rigid.
• But screws are subject to bending & torsional forces.
• Plate is centred at the neutral axis rather than the extreme fibre.
3) Buttress
4) Bridging
5) Tension-band
6) Double plates
• y torsional rigidity.
7) LC-DCP (Titanium)
• less disturbance of periosteal blood supply, reduces bone resorption under plate
• Prebending plates -> prevents gapping of cortex opp. to plate -> more uniform compression.
8) LCP locked Compression Plate:
• Best for osteoporotic patients
AO PLATES & SCREWS SIZES
BASIC LAG DCP CANCELLOUS
Drill 3.2 & 4.5 3.2 3.2/4.5
Tap 4.5 4.5 6.5
Screw 4.5 4.5 cort. 6.5 spong.
SMALL LAG DCP/Tub. CANCELLOUS
Drill 2.5 & 3.5 2.5 2.5
Tap 3.5 3.5 4.0
Screw 3.5 3.5 4.0
MINI LAG
Drill 1.5 & 2.0 OR 2.0 & 2.7
Tap 2.0 OR 2.7
Screw 2.0 OR 2.7
Max. Screw-Plate Angle:

• DCP = 25º in horizontal plane & 7º in transverse plane
• Third Tubular = 50º
• DCP EXERTS 600 N AXIAL UNEVEN COMPRESSIVE FORCE
LAG COMPRESSION DCP COMPRESSION

FORCE 3000 N 600 N (prestressing & eccentric fix)
DISTRIBUTION EVEN FROM WITHIN # UNEVEN
DIRECTION INTER-FRAGMENTARY AXIAL
BEST SUIT SMALL POROUS BONE LARGE DENSE BONE
[F
Fractures, Union
U & Biiomechanics] Page | 201
3. INTRAMEDULLARY NAILS
Nail Length:
• The working len ngth is deffined as th he length of a nail bet the
most proximal
p point of fixxation in th he distal fragment anda the
most distal
d poin
nt of fixation in the e proximall fragmentt = the
unsupp ported porrtion of nail between n the bone e fragmentts. More
important than actual lengtth
• Torsionnal stiffnesss 1/workking length h
• Bendin ng stiffnesss 1/workking length h2
• Femora al bow forrces the na ail to contaact the me edullary waall Æ z
working length Æ y torsiona al & bendinng stiffness
Nail Diammeter & Area
A mom ment of ine ertia:
• = The principal factor that alters BENDING stifffness (and d shape
also)
• Distribuution of material
m in cross secction (SECOND MOMENT OF AREEA A) is a cru
ucial facto
or to
bendinng
• Wider diameter hollow tu ube is stiffeer than so olid smaller dr tube é the sam me amoun nt of
materiaal.
• This is why
w boness have a medullary
m ca
anal
• Tubes with a wa all thickness/radius < 1/8 Æ behave b as curved sh heets ratheer than tuubes.
These thin-walled
t d tubes are e subject too buckling.. (Bone is th
hick-walledd).
S
Slot:
• = The principal
p fa
actor that alters
a TORSIONAL stiffnness (POLAR MOMENT OF INERTIA)
• Non-slo otted nail is
i 40 times stiffer in Torsion.
• A slot reduces
r torrsional stifffness by 988% -> quickker healing
g with calluus.
• Disadv vantages: y torsional stress duriing insertio on Æ z ma aterial arou
und the scrrew holes
Locking:
Dynamic Staticc
Deform
mation conttrol Bending & rotational Axial, bending, & rotational
Load Sharing Bearin
ng
Used in
n Axially stab
ble # Comm minuted unsstable #
Reaming Effects on
R o Blood flow f & un nion:
Normally bone
b has centrifugal
c blood flow
w, from cenntre (endo
osteal) outwwards.
Callus is largely indeppendent ofo endostea al blood supply.
1. Reamin ng y periosteal bl floww. (not dependent ono nutrientt artery), -> z endoste eal bl flow.
2. 2wk: re eaming ma arkedly y blood
b flow
w.
3. 6wks fllow in corttical bone recovers
r to
o normal & periosteal blood flow w is still hig
gh.
Reason n= centrifugal flow is reversed. (law of com mpensation, Treute)
4. y Ream ming produ ucts = fibrooblasts, bone, mesenchymal cells Æ NB BF.
5. union is i quicker in reamed fractures (Hooper, 19 991)
Reamed vs v Unream med:
Reeamed Unrea amed
Larrger, stiffer nail Suitable
e for contam
minated fracctures
y area
a of bon
ne-nail conta
act
y stability
s of lo
ocking boltss Does no ot disturb th
he endosteaal blood vesssels
inittial bone deevasculariza
ation delayed d union (due to excessiive motion at
a # site).
y local
l pressuure less pre
essure
miccrothrombi Æ PE less miccrothrombi
the
ermal necro osis nil
Compartm
C ment Presssures:
• Comparrtment pressures: yin bone
b (up to 300mmHg)), but no change in com
mpartmentaal pressure
Intramedullary Nails vs. Plates
IM NAIL PLATE & SCREWS
Load sharing Load Bearing
zendosteal circ. z periosteal circ.
Indirect reduction Direct reduction
Preserves soft tissue Destroys soft tissue
Allows # motion Rigid fixation
Early union-callus Slow union- no callus
Rare anat. Reduction Frequent anat. Red.
Failure at crossbolts Failure at plate
For segmental #'s For intraarticular #'s
For shaft #'s For juxtaarticular #'s
Removal of Internal Fixation Devices:

Usually remove 12 to 18 months following insertion.
There is a very high incidence of refracture and of neurological complication following removal
of forearm plates.
4. EXTERNAL FIXATION:
Advantages:
• Apply quickly
• Technically easy to perform
• Adjust later
• Soft tissues not disturbed
• Access to wounds
• Joints can be mobilized
• Can dynamize
• Easy removal
• Reconstruction surgery
Disadvantages:
1- Pin tract infection
2- Malunion
3- Patient compliance required
Types:
• Rod
1- Uniplanar
2- Biplanar
• Circular
• Hybrid Frames
• Six axes spacial frames.
Factors affecting construct stiffness
Useful for:
1- Any fracture
2- Bone transport
3- Limb lengthening
4- Angular correction
5- Soft tissue reconstruction
6- Contractures
ILIZAROV EXTERNAL FIXATOR
1- wires= 1.5mm in adults & children; 1.8mm in adult femur.
2- wire types= smooth & olives (for stability/translation)
3- Insertion= Push-Drill-Tap
4- Aim for wires at 90deg. to each other & 4-5 wires per segment
5- Bring the ring to the wire- Not the wire to ring -Tether through muscles in joint extension
6- Wire Tension= 1.2mm-90kg; 1.5mm-110kg; 1.8mm-150kg
7- Focus = fracture / non-union site
8- Segments = bone fragments
Taylor spatial frame (Six-axis deformity correction)
o Actually any deformity occurs as a compined defomities in 6 axes.
o Modified ilizarov fixator into six telescopic struts free to rotate at proximal and distal rings.
o Software program is used to correct the deformity & to deal é residual deformity.
204 | Page [Fractures, Union
U omechanics]
& Bio
Im
mplan
nt Faiilure
Deffinition:
• It is fa
ailure of an
n implant (Standard
d alloy) to satisfy the
e specific function for
f which it is
implan nted or inse
erted.
• In the past, the
ere were different
d im
mproper im
mplants not of a quality goo
od enough
h to
withsta
and bone stresses.
s
days, due to the evo
• Nowad olution in metallurgyy & biome
echanics, w
we have (standard alloy)
which is a meta w mostly achieve th
al , if inserrted accurrately & properly, will he aims of
o its
applica
ation
Typ
pes:
Faiilure
Biological Mechanical
Bone Implant Struuctur Mateerial

related related al Faailure failu
ure
Se
eptic Aseeptic Creap &
ossteo‐ Ossteo‐ corro
osio
loossenin loossenin Fatigue Fraccutre Buckkling wear deform
matio
maalacia po
orosis n
n n
g g
This depends on Two factors:

1- Implan
nt material choice
o Implant material
o Implant de esign
o Implant biochemical activity (in
nert or not)
2- Implan
nt applicatiion:
o Implant tyype size sha
ape
o Application techniqu ue.
Types of implant.
1) Implaants for fracture fixatiion e.g. Pla
ating.
2) Arthrroplasty.
3) Artificcial ligame
ents.
4) Silastic implantss e.g. Bead sadius & MPM Joints.
Biomechanics of implant
YOUNG’S MODULUS OF ELASTICITY : (measure
e of stiffnesss) = stress / strain.
MODULUS OF RESILIENCE: energyy/vol. a maaterial cann absorb éout
é yieldin
ng (=area below
b the elastic
curve)
MODULUS OF TOUGHN ESS: energy
NE y/vol. a maaterial can absorb till breakage (=area below w the curve)
AMOUNT OF DEFLECTION = measu ure of rigid
dity or stiffn
ness of imp
plant.
YIELD STRESS: the max
x stress a metal
m éstand d éout plasstic deformmation
ULTIMATE TENSILE STRENGTH = th he max stre ess a metall éstand éo out # é a sin
ngle peek load
RENGTH = the maximu
FATIGUE STTR um cyclic lo
oad a meta al éstand éout
é # é 1007 cyclic loa
ads.
ENDURANCE (Fatigue Limit) = the cyclic loa ad limit below fatig gue will noot occur
FATIGUE: fa
ailure 2ry to
t cyclic loa ading
FRACTURE: failure 2ryy to bendin ng stresses into > 2 pa arts
BUCKLING: failure 2ryy to compre ession of a thin walleed tube
CORROSION: failure 2ry to electrrochemical action
WEAR: failu
ure 2ry to mechanica al deteriora
ation of solid surface
CREEP & deeformation n
LOOSENING: failure 2ry to
t a biologicc response of
o colonizing
g bacteria orr wear particcles (septic or
o aseptic)
Implant Failure
1. CORROSION
• MATERIAL DETERIORATION ð ELECTROCHEMICAL ACTION
• It requires a GALVANIC CELL = 2 diff electrically conducting solids + conducting pathway +
electrolytes in-between
• PASSIVATION is the formation of an oxide layer on the surface to prevent corrosion
• Types:
1)GALVANIC: between metals é different electrochemical potentials
2)FRETTING: surface breakdown 2ry to motion & loads between metal surfaces
3)CREVICE: motion bet metals depassivate their surfaces
4)PITTING: surface abrasion galvanic corrosion
5)STRESS: load generated crack galvanic corrosion Æ y the crack, and so on
6)MICRO-BIOLOGIC: micro-org secrete corrosive metabolite
7)INTERGRANULAR: corrosion at weld points & not the metal Æ structure failure (weld decay)
• Corrosion can be minimised by
o Choosing a corrosion resistant material
o Treating the surface with a passivating layer prior to use
o Not using combinations of metals in close proximity
o Careful operating technique to reduce surface scratching
o Using non modular implants.
2. FATIGUE-
• PROGRESSIVE MATERIAL DETERIORATION 2RY TO CYCLIC STRESSES BELOW THE ULTIMATE TENSILE STRESS CAUSING
CRACK PROPAGATION.
• Crack usually starts at a STRESS RISER:
o Scratch
o Hole
o Corner
o Change in cross section
o Fretting
• The stress concentration factor (ratio of maximum stress at the surface irregularity to the
average stress in the same direction depends on the geometry of the surface. Stress at a
large distal interlocking hole of an IM nail is < small hole, but the stress concentration factor
is higher é the large hole because the surface area of the metal left in that plane will be less.
• S-N CURVE relates stress applied to number of cycles to failure
• ENDURANCE, FATIGUE LIMIT is the maximum cyclic loads below fatigue will not occur. However,
it is best to consider all orthopaedic implants as having no fatigue limit as there is the
potential for damage during insertion, and the corrosive environment of the human body
and the variability of the stresses applied are difficult to control.
• Reduction of fatigue failure can be achieved by
o Appropriate design of implants, avoiding sudden changes in geometry
o Surface treatments of implant, e.g. peening, polishing
o zfretting corrosion
o Correct insertion of implants, e.g. avoiding distraction of fractures, so that bone heals
and can share the loads with the implant.
o z early WB until fracture is healing.
3- BUCKLING:
• sudden material deterioration 2ry to compression of a thin walled tube (diameter < 1/8 its length)
4. WEAR
• MECHANICAL DETERIORATION OF SOLID SURFACE
• Types: (the main are the 1st two types)
1]. ABRASIVE: the harder grooves the softer material
2]. ADHESIVE: the softer material adheres on the harder surface
3]. FATIGUE, in which repetitive loading Æ subsurface delaminate Æ lost from the surface
4]. THIRD-BODY WEAR implies the retention of debris bet. sliding surfaces Æ abrasive wear.
5]. BACK SIDE WEAR: bet PE & the metal backing
6]. RUN IN WEAR: is the accelerated wear that occur in the 1st few millions of cycling
• Effects of wear most predominant in joint prostheses. Particles produced by wear
(metal/PE/PMMA) are phagocytosed by osteoclasts Æ osteolysis Æ loosening + material loss
5. SEPTIC LOOSENING
RACE FOR SURFACE THEORY
When a total joint prosthesis is placed into the
human body, the body's cells & bacteria (usually
skin bacteria) hurry to get hold on the
prosthesis surface &colonize.
If bacteria win, thet evolve the capability to adhere
to surfaces for their survival, by secretion of a
surface glycoprotien called GLYCOCALYX:
i. Very strong adhesive
ii. Mask the bacterial antigens
iii. Colonize inside this biofilm away from
immune system
iv. Invite other types of bacteriae to trick the immune system
v. When they adhere to the inert implant surface, bacteria are protected by the
antiphagocytic effect of biomaterial. All these Æ powerful resistance 100-1000 times
against AB & immune system.
MATERIALS USED IN FRACTURE FIXATION

Stainless steel
1]. Stiff
2]. Cheap
3]. Ductile; so it is useful in contouring of plates and wires during operative procedures.
4]. Relatively inert
5]. Chromium passivate when dipped in nitric acid Æ z corrosion
6]. Can still undergo corrosion if carbon gets to the surface.
7]. y Young’s modulus - 200 Pascals (10x that of bone) Æ y stress shielding Æ bone resorption
• Used in plates, screws, external fixators, I.M. nails.
• Stainless Steel Composed of:
o Iron ................................................. 60% (cold forged or annealed to y strength)
o Chromium .................................... 20% (major corrosion protection after passivation)
o Nickel ............................................. 15% (corrosion resistance)
o Molybdenum ............................... 3% (protects against pitting corrosion)
o Carbon .......................................... 0.03% (y stiffness)
o Mg, Si, P, S .................................... 2%
Titanium and its alloys
1]. Inert
2]. Less stiff: less stress shielding & stress risers at the tip of the implant (modulus ≈ ½ of SS)
3]. More expensive than stainless steels
4]. More wear (not good for bearing surfaces)
5]. Less ductile < stainless steel, but ductile titanium alloys being produced
• Used in plates, screws, I.M. nails, external fixators, & halos.
Adhesives
• Not common in orthopaedics but potentially useful in small fragment fixation, controversial
• Prerequisits:
i. Sufficient bond strength
ii. Able to bond to moist surfaces
iii. Permit healing across the bond line
iv. Sterilizable.
Bone cement does not count as an adhesive.
CYANOACRYLATE: has poor results
FIBRIN: is the only suitable adhesive for fracture provided that it has an inherent stability or NWB
Biodegradable polymers
• Potential advantages
o Hardware removal not necessary, reducing morbidity and cost.
o Stiffness of polymer decreases as stiffness of fracture callus increases.
o Can be used in future for controlled release of antibiotics or stimulants to healing
• Requirements
o Adequate mechanical stability
o Sufficient strength over a sufficient period of time
o Degradability into products those are not harmful.
• Examples
o Polyglycolic acid
o Polylactic acid
o Copolymers
• Only about 1/20 the stiffness and strength of stainless steel
• Used in ankle fractures with poor results
• Used in phalangeal fractures with better results
Summary Of Implant Properties
Steel Titanium alloy Ceramic Composite

Stiffness ++ + +++ +
Hardness ++ + +++ +
Corrosion Resistance + ++ +++ ++
Wear Resistance + - +++ +
Ultimate Strength ++ + ++ ++
Yield Strength + +++ - +
Ductility + ++ - +
Cost ++ - -- +
Perfect Material =
1]. Stiff .................................................... resist deformation
2]. Hard ................................................. resist surface abrasion
3]. Inert .................................................. resist corrosion
4]. Tough .............................................. resist breakage
5]. Ductile ............................................. able to deform before breakage
6]. Adapt to loading
7]. Regenerate (reduce failure) = a composite = Bone (a ceramic phase (calcium
hydroxyapatite), dispersed in a collagen-based matrix).
Fracture Non-Union
Pseudoarthrosis
Definition:
• Arrest of bony fracture repair process, Short of osseous bridging of the defect between the
fracture fragments, where fibrous or cartilaginous tissue will interpose.
• Pseudoarthrosis is the final status of non-union é formation of a synovial lining & joint fluid.
Causes of non union:
General factors:
Age. Nutrition. Radiation
Burns Hyperpara Drugs: anticoagulants, steroids
Local:
1- Biological:
[1]. Individual bone succeptibility:
Scaphoid.
Neck femur
Lower 1/3 tibia. (no surrounding ms & depend on vessels)
[2]. Injury to:
Soft tissue
Vascular inj: severe injury, periosteal stripping, reaming Æ poor revascularization
[3]. Infection
Necrosis & bone devitalization bl. Supply.
Osteolysis gaps
Motion instability.
2- Mechanical:
[4]. Improper fracture coaption (gap):
Loss of bone substance
Soft tissue interposition
Distraction, Displacement, or overriding
[5]. Insufficient immobilization:
Moving fracture fragments.
[6]. Abnormal mechanics:
Shearing, torsional & bending stresses counteract the biological repair process,
e.g. Vertical fr. Neck femur Æ Shearing stresses.
Pathology non union:
Stage I ..................................................................... ( 3-6 months)
• Bone ends are covered by fibrocartilage & enclosed in a fibrous capsule
• The centre of the callus shows:
1- Amorphous fibrinoid degeneration
2- Hyaline degeneration.
Stage II ....................................................................... (2 Years)
• Bone ends become highly sclerotic
• Mechanical disturbance of the fracture Æ Cleavage of the amorphous area & formation of
extra-cellular fluid containing mucin.
Stage III ...................................................................... (2-5 years):
• Mature pseudo-arthrosis is formed:
1- Cavity filled with highly viscous fluid.
2- Lining synovial like membrane
• Callus osteogenesis never ceases, but never bridges the gap
• Proximally it is saucered concave cavity to receive the rounded distal end
• Over growth of bone around the bone ends.
• Continued fibrinoid degeneration of callus
Classification non union:
I. ACCORDING TO CALLUS FORMATION (WEBER)
A. Hypervascular (Hypertrophic)
1- ELEPHANT FOOT:
i) Rich in callus
ii) Caused by:
• insecure fixation.
• Premature W.B.
2- HORSE HOOF:
i) Poor in callus.
ii) Caused by moderately unstable
plate & screw fixation.
3- OLIGOTROPHIC:
i) Absent callus
ii) Caused by:
• Fracture displacement
• Fragment distraction
B. Avascular (Atrophic).
1- TORSION WEDGE: z Intermediate fragment
vascularity Æ unites to one end
2- COMMINUTED:
• One fragment, became necrotic
• No callus formation
• Usually complicated by plate break
3- DEFECT non-union: lost diaph fragment
4- ATROPHIC non-union:
• Lost diaphyseal fragment + atrophic ends
• After sequestrectomy, tumor excision
II. ACCORDING TO TIME OR DEGREE :
A. Delayed union: healing has not advanced at the
average rate for the site & type of fracture (usually 3-6
mo). It needs immobilization, osteoinduction, PEMF,….
B. Non-union: either é mobile gap or immobile gap
C. Synovial pseudo-arthrosis.
III. ACCORDING LOCATION:
A. Diaphyseal.
B. Metaphyseal
C. Intra-articular
IV. ACCORDING TO INFECTIONS.
A. Non-infected (felsitic).
B. Infected (static)
1. Draining.
2. Non-draining (Dry) 3 months
V. CLINICAL & RADIOGRAPHIC PALY CLASSIFICATION.
A. Type A (with bone loss < 1 cm)
1. A1 : mobile deformity.
2. A2 : stiff .
- A2.1 eout deformity
- A2.2 é fixed deformity
B. Type B (with bone loss > 1 cm).
1. B1 : with bony defect.
2. B2 : with loss of bone length.
3. B3 : with both
Diagnosis of non union:

A) History:
1. Mechanism of inj 4. Excessive traction. 7. Other # & their healing
(high or low energy) 5. Long immobilization. 8. Skin grafts or muscle
2. History of infection 6. Implant removal. transfers.
3. History of operation
B) Clinical examination, (S.&S.):
1. Pain 6. Sinus 10. joint pain, contraction.
2. Swelling 7. Limb vascularity. 11. Skin condition.
3. ROM 8. Limp. 12. Limb sensations
4. Tenderness 9. ms. Weakness. 13. Malrotation
5. Colour charges.
C) Investigations :
1. X-rays (for both sides): AP, Lateral, Obliques (rt & lt according to type of non.)
o The entire bone in diaphyseal non-union.
o Leg-length film in L.L. frs (shortening, rotation).
2. CT & Tomogram (AP, lat) , esp in metaph non- unions.
3. Arthrography or arthroscopy (to check state of cartilage in metaph non-unions).
4. Siniogram (M.blue)
5. Culture & Sensitivity test.
6. MRI.
7. EMG & nerve conduction test.
8. Arteriogram if limb circulation is doulotfull.
9. Tc99, Ga67, In111: hot zone = biologically active non-union. Cold zone = pseudoarthrosis.
1- Non-Operative Treatment
Objectives
1. Union of the bone in a reasonable time.
2. Correction of shortening, angulation or notation.
3. Mobilization of the adjacent stiff joint(s).
4. Eradication of infection.
Modalities:
1- Functional cast bracing with weight-bearing (tibia).
2- Functional cast bracing after osteotomy of intact or united fibula.
3- Electric stimulation by: invasive, semi-invasive, non-invasive
Indications:
1- Gaps > 1 cm
2- Synovial pseudoarthrosis
3- Metaphyseal non-union
4- Difficult control of # motion; e.g. proximal femur & proximal humerus
Disadvantages
1. Does not correct shortening or malposition
2. Requires long POP NWB immobilize. Æ stiffness, porosis & loss of function.
3. Usually does not suffice alone, so used as an adjuvant to operative treatment.
Principle:
Cathodal electrodes convert fibrous union to fibrocartilage endochondral ossification
[Biomechanics & Union] Page | 211
2- Operative
Principles
1. REDUCTION OF THE FRAGMENTS : (provides axial compression with mechanical stability) .
• When in good position, do not dissect the fibrous tissue surrounding the periosteum
• Callus and fibrous tissue preserves the fragment's circulation Æ they ossify ofter a
bridging graft unites with the fracture fragments .
• Necrotic bone acts as a scaffold for union.
2. GRAFTING BONE Æ Induction of ostergenesi cortical .
• Bridge gaps with bone graft:
o cancellous.
o cortico-cancellous.
• Types:
A. Onlay, sliding , inlay.
B. Autogemnous, allograft.
C. Vascularized, non – vascularized.
• Also, bone covering by skin of flaps is essential.
3. CORRECTION OF BIOMECHANICAL FACTORS e.g. By osteotomy: Shearing , torsion or bending
stresses should be eliminated by e.g. McMurray medial osteotomy & Schanz Osteotomy.
4. STABILIZING THE FRAGMENTS , by a compressive device: e.g. plate & screws or Ilizarov
• External support should be for many months to guard against fatigue failure.
5. ERADICATION OF INFECTION:
• Excision of non-union site.
• Sequestrectomy.
6. EXCISION OF SYNOVIAL PSEUDOARTHROSIS.
7. PROSTHETIC REPLACEMENT : in Old patients .
8. AMPUTATION: When the anticipated results of ttt are inferior to that after amputation.
NOTES
Operative rationale:
The rationale for treatment of non-unions is to reverse the causative factors:
1]. If excess motion Æ stable internal or external fixation.
2]. If there is a gap Æ obliterating or diminishing the space by compression or bone grafting.
3]. IF there is poor blood supply.
• start early active exercise of adjacent joints.
• Shingling & cancellous bone gr Æ bone stim, induct. & revasc.
• Drilling or petalling avasc. Cortices Æ revascularization them.
N.B: SHINGLING: both sides of non union, by using sharp chisel to decorticate bone with fine asteopertosteal
fragments attached to peritoneum and muscle , assuring their vascularity, and increasing surface area of
fracture. This is usually followed by cancellous bone grating of the pocket between shingles and bone.
Principles of treatment:
1]. Know the local pathology; non-union vs delayed–union, by history, examination, PXR & Tc
2]. Correct biomechanical factors e.g. Transposition osteotomy
3]. Provide stability: by internal or external fixation.
4]. BG
5]. Excessive synovial pseudoarthrosis "When Tc shows hot zone, with central cold zone".
6]. Bridge gaps
7]. Decortications "SSHINGLING" procedure of Dunn, to elevate periosteum & ⊕ periosteal NBF
8]. Eradicate infection by
• Excision of non-unions
• Antibiotics
• Sequestrectomy
9]. Plan surgical approach to ensure skin covering.
212 | Page [Biomechanics & Union]
N.B:
When large gaps are present.
OR
When a shortened extremity requires lengthening prior to the above proc.
⇓
• Vascularized fibular, iliac or rib graft. (By microvasc. Anast.)
• Continue with the external fixator till healing occurs. Encourage early joint motion.
• Don't accept mal position or shortening. It is mandatory to achieve a final mechanically neutral
position of the limb. Unacceptable major shortening is corrected by preliminary lengthening
with the Wagner apparatus before definitive fixation
• Lengthening of lesser degrees (up to l inch) is usually done as are procedure with the müller
distractor, Wagner apparatus or external fixator rods in bilateral frame configuration, at the
time of internal fixation.
Treatment of specific types of Non-union:
1- Hypertrophic vital non-union (Elephant's foot callus):
1]. Non – displaced diaphyseal
2]. Corectable diaph. Non –unions.
⇓
a]. External fixators.
b]. Closed I.M.N. (é reaming) + I.M. BG (through chest tube) ILN (if not Instability)
c]. Open I.M.N.
d]. Tension band plating.
• BG is not necessary, as hypertrophic callus provides > enough BG for healing.
• Some prefer removing excess callus Æ small fragments & use it as BG Æ y heal. Potent.
• Some prefer shingling :
a]. y surface area.
b]. Induce local bone formation
• To control rotational instability either by: Lag screw fixation, Cerclage wire.
• Before correction of deformity, insert k- wires in the proximal & distal fragments at the
exact angle & rotation to be corrected.
3]. Open displaced diaphyseal non-union
a]. Shingling
b]. Excise pseudarthrosis.
c]. Mobilize the non-union.
d]. Correct the deformity.
e]. ORIF either by: Plate, T.band, I.M.N.
2- Atrophic Non-unions:
1]. Stable fixation (plates, lag screws, I.M.N…)
2]. Shingling (or decortications).
3]. Bone graft inserted between the shingled osteoperiosteal fragments & the cortex.
1,2,3 Æ to reactivate the dormant bone healing" switch.
When the cortex is osteoporotic:

1]. With plate & screws Æ petalling instead of shingling.
2]. With IMN Æ no much reaming.
• Reinforce the screws with liquid PMMA bone cement, injected with a syringe into
the loose screw holes. Tighten! Screws only after setting cement.
• Avoid cement entesing into the fracture site.
• Use cancellous bane graft liberally.
• External hinged plaster post – operative is recommended.
3- Metaphyseal articular Non-unions : (The most difficult).
1]. Arthrotomy Æ see articular surface, realign fragments, lyse adhesions, release contractures,
remove loose bodies or fragments, gently manipulate the joint.
2]. Reconstruct the articular surface (k.wires, screws, ).
3]. Attach the reconstructed articular Block to the metaph. Or. Shaft Æ straight, blade, T,L,
spoon. Plates, with compr.
4]. Start early active motion after prelimin splinting, depend on ligam. Repair or release, or
immediately, via a C.P.M. machine.
5]. Weight bearing is late, with brace or hinged cast brace, when fr. Is uniting.
4- Synovial pseudarthrosis: (PXR, Clinical: motion at fr. Site, Tc: cold cleft)
1]. Reaming the medullary Cavity.
2]. Excision of pseudarthrosis tissue.
3]. Opening the medullary Canal.
4]. Fracture reduction.
5]. Internal fix Æ plates, IMN.
6]. Shingling.
7]. Bone grafting in atrophic types or in presence of gaps.
5- Infected non- draining non-unions:

1]. If dry for at least months Æ as non-infected, but they should be debrided of any potent
infected fibrous as granulation tissue.
2]. Shingling & bone grafting Æ if avascular bone is present.
3]. Excision of Sequestra.
4]. Internal fixation: Plates & screws / IMN with reaming.
5]. Proper antibiotics & triple antibiotics for irrig. Intra-oper.
6- Infected draining non-union:

1]. If hardware is still holding and giving stability to the fracture, leave it in situ.
2]. If hardware is loose and ineffective Æ Remove it + :
a]. Incision & drainage.
b]. Debridement.
c]. Sequestrectomy.
d]. Open packing or closed suction irrigatioin.
e]. Antibiotic- Impregnated PMMA. Beads may be used to fill the dead space till healthy
granulation tissue develops (usually 1-3 wks.)
f]. Healing the non-union:
• Tibia bypass fibula pro-tibia operatio, through posterolat app. At fr. Level or by a
proximal & distal tibial. Bl. Synastosis using cancel bonegralf & screw fix.
• Ext fixation frames Æ Unit or bil.
g]. Following successful bypass. Bridging (usually months. Etadicate the infection.
a. Saucerization sequestrectomy.
b. Radjcal cxcistion of infected sinuses.
c. Excl of fibrurs & granul tissue with the addution of another bone PMMA
anthbiotic beads.
MANAGEMENT OF INFECTED NONUNION

1. Conventional treatment:
• The object is to convert an infected draining nonunion to one that has not drained for
several months and then promote healing of the nonunion by bone grafting.
• Disadvantage: needs a long time (one or more years) and may lead to joint stiffness.
• The skin requires three operations:
1]. Wound saucarization and debridement to provide a vascular bed.
• Correct major overlap or displacement and attempt to fix the fracture:
• Plates and screws usually lead to persistent drainage.
• Pins in prox & distal fragments are incorporated in a cast may be used (less secure)
• After 4-7 days when the granulation tissue covers the wound
2]. Split thickness skin graft. After 4 wks.
3]. Full thickness pedicled graft. .
• BG is delayed until the skin graft is stabilized.
• Reconstructive operations are delayed until at least 6 mo till infection is gone
2. Active treatment:
• The object is to obtain early bone union and thus shorten the period of convalescence and
preserve motion in the adjacent joints.
• This is done in the following steps:
1]. Restore bone continuity. This takes absolute priority over treatment of infection.
Expose the nonunion through the old scar and sinuses decorticate the ends of the
bones forming small osteoperiosteal grafts (detached grafts are discarded).
2]. Remove all devitalized infected bone and soft tissue.
3]. Align the fragment and stabillze by an external fixator while applying compression
across the nonunion if possible. A plate may be used when drainage have stopped.
4]. Apply cancellous bone graft.
5]. Close as much of the wound as possible and apply suction. Give AB.
3. Ilizaroy method:
4. PEMF
ELECTRO-STIMULATION OSTEOGENESIS
Electricity and fracture healing
1]. PIEZOELECTRIC EFFECT: charges in tissues are changed secondary to mechanical forces, so the
compression side has the negatively charged potentials & the tension side has he positively charges
2]. STREAMING POTENTIALS: occur as electrically charged fluid is forced over a cell membrane
3]. TRANSMEMBRANE POTENTIALS: generated by cellular metabolism
Fracture Healing
1]. DC (Direct Current) ...................................... inflammatory response (constant better than pulsed)
2]. AC (Alternating current) ............................ repair phase collagen synthesis and calcification
3]. PEMF (Pulsed Electro Magnetic Field) ........ remodeling & calcification of fibrocartilage
RESPONSE OF BONE TO DIRECT CURRENT:
1]. Bone forms at the cathode, whereas cell necrosis occurs around the anode.
2]. Resistance rapidly y between the electrodes Æ z in current; and so further increase in the
voltage is required to keep the amperage at the optimum level.
3]. Electrically induced osteogenesis exhibits a dose –response curve:
A) Current < 5 μAmp .................... do not produce ostegenesis.
B) Current = 5-20 μAmp ............... Produce y amount of bone formation and.
C) Current levels > 20 μAmp ....... Show NBF giving way to cell necrosis.
4]. Electricity # healing & NBF, but the cathodes must be at the fracture site.
5]. Reaction at cathode Æ consumption of O2 Æ hydroxyl radicals: 2 H2O + 4e - + O2 = 4 OH-.
RESPONSE OF BONE TO ELECTROMAGNETIC FIELDS:
• Pulsed electromagnetic fields (PEMF) induce electric potentials, The polarity of these potentials
changes as the magnetic field y & z Æ alternating current in the tissue.
• The PEMF – induced currents modify cell behavior in bone, cartilage and other tissues, Thus,
by properly programming the electrical events about the mesenchymal cells, a sequence of
histologic changes can be induced. For example, the calcium contont of chondrocytes can be
y or z, cAMP, collagen & proteoglycans can be modified & DNA synthesis can be changed.
MECHANISM OF ELECTRICALLY INDUCED OSTEOGENESIS:
1]. Cathode y local O2 consumption Æ relative hypoxia Æ NBF. It is known that bone
follows a predominantly anaerobic metabolic pathway.
2]. The electric impulses realign the collagen molecules Æ initiating calcification.
3]. cAMP by electrical stimulation has also been suggested.
Methods Used For Application Of Electricity:

Invasive Semi-Invasive Non Invasive
Idea • Totally implantable electrical • Insertion of cathodes • PEMF induce electric
stimulator of three parts: indirectly into nonunion potentials ώ change
polarity as the magnetic
1. Power unit Æ DC of 20 1. The power source. field y and z, ώ Æ AC in
μamp regardless of bone the tissues.
tissue resistance Changes.
Some use a pulsed direct
current freq of 20 Hz. • Pair of coils mounted on
2. 1-4 titanium cathodes to be 2. The cathode is a Teflon the surface of the cast.
implanted in the nonunion coated stainless steel k- They should be // to each
site whether it is a single or wires percutaneously. other & centered over the
multiple fracture sites. # site
3. One anode that is placed in 3. The anode.
the soft tissues adjacent to
the generator.
Results >85% within 12-36 weeks

Cons 1. It is portable é minimal 1- High success rate, 1- Can be used in OM.
postop discomfort. 2- No need for operations. 2- No surgery needed
2. Short hospital stay. 3- z infection 3- No risk of infection
3. No pt coop needed 4- z postop pain.
5- Portable
Pros 1. Need minor op for insert & 1- Patient remains NWB for 3 1- It is not portable.
removal mo to z cathode break 2- Should be used daily for
2. Not é acute OM. 2- Not é acute OM. at least 10 hours,
3- Not é motion at # site 3- Prolonged NWB POP.
4- Pin tract infection,
5- cathodes breaking
6- Recurrence of the OM.
7- Cathode dislodgement.
216 | Page [Biomeechanics & Union
U ]
Bone Graft
Deffinition
• Replacing missing bo
one, addin ng to existin
ng bone, or
o stimulation of the e
existing bo
one to
produce adequate sttructural and functional supporrt
Cla
assificatio
on:
BONE
E GRAFTS (Accoording to)
Structure Function Source
Osteo-
Cortico- Osteo- BM
M& Osteo- Osteo- Xenograft
Cortical Cancellou
us inductiv Human Substitutes
S
cancellous chondral BM
MP genic cconductive
e
Osteo-
Osteo- Ossteo-
Autograft Isograft Allograftt inductiv
genic cond
ductive
e
Indications
e structural stability (ccortical bone best)
1. To provide
2. To provide
e linkage, i.e. replace missing bo one:
Congen nital deficienncies
Trauma atic deficiencies: best to
o be applied
d at the com
mpression side
Infectio
ons after deb bridement: e.g. ca sulpphate granuules
Tumorss after excisiions
3. To stimula
ate osteogeenesis and bone healling
Non un nited fracturres
Osteoporotic fractu ures
Revision n surgeries
Spine fuusions (TCP) & Kyphoplasty (ceram mic cement)
Conntraindica ations:
1. Infections:: (can use ca
c sulphate
e bone sub
bstitutes)
Woundd infection
Open frractures
2. Non-viable
e surround ding bone Æ not cap pable of suppporting and anchorring the im
mplant
3. Bone disorrders that hinders BGG incorpora ation
Inflamm matory bone e disease.
Metabo olic bone dissease é altered calcium
m metabolismm.
Immunologic abno ormalities.
Systemiic disorders é poor wou und healing
g over the im
mplant site..
Types according to structure

1. Cortica al:
• Strong im
mmediate structural su upport
• Slow inc
corporation Æ initially weakens
w the graft
• ~ 50% weaker
w than n normal boone from 6 wksw - 6 mo Æ returns to normal 1--2 y after
2. Cancellous:
• Revascularised morre quickly
• Osteoblaasts lay NBF F down on oldo trabecu ulae which iss later remo
odelled
• Only surrface cells re
emain viable e by diffusio
on.
3. Cortico o-cance ellous:
• Producee both structtural stabilitty & quick in
ncorporatio
on
4. Osteoc chondra al
• For tumoour surgeryy
• Osteochhondral grafft survival en nhanced byy immersion n in glycerol
5. Bone marrow
m w & bioactivve inductivve substancces:
• BMAT; has
h osteopro ogenitor cells
• BMP; impregnated ceramics
[Biome
echanics & Union] Page | 217
Typ
pes Accorrding to Source
S
1. Autogr
rafts
• From thhe same pe erson, most still dies
• No immmunogenicity
• Highestt osteogen nic and osteeoinductivve capacity
• Revascu ularized moore quicklyy than alloggraft
• Donor site
s morbid dity (20%) with
w hema atoma, pain n, fracture,, wound in
nfection
• Limited supply
• Best resserved for area
a of larg
ge bone lo oss or irradiiated tissuees
• No resoorption at either
e endss of BG, seg gment hea als as a fraccture
2. Isografft:
• Same ass allograft but from genetically
g win Æ nott immunog
identical tw genic
3. Allogra
aft
• Donor bone
b from another person
p
• No don nor site morbidity
• Large amounts avvailable
• Not osteeogenic
• Incorpooration:
o Qualitative ely similar to
t that for autograftss
o Delayed (μ μß ð collag gen alteratiion after irrradiation)
o Less exten nsive
o Biologicallly inferior
• Immuno ological response and less reliable incorporation
• Infection 10% Æ 80%8 clinica
al failure
• Transmission of HIV, Hep B, Hep C
4. Xenograft
• From a different species i.e. porcine,
p bo
ovine
• Similar tto allograftt bone afte
er freezing and irradia
ation.
eramics (see later)

etic Grafts / Ce
5. Synthe
1]. Allograaft matrix
2
2]. Polylacctic & Polyg
glycolic ma
atrix
3
3]. Hyaluronic acid
4
4]. Collageen
5
5]. Ceramics
Types according to fuction
1- OSTEOINDUCTIVE: = BIO-ACTIVE POLY-PEPTIDES THAT BONE FORMATION
I. Bone Morphogenetic Proteins (BMP.s):
• Recruit & progenitor cells of osteoblast lineage
• bone collagen synthesis.
II. Insulin-Like Growth Factor (IGF):
• It plays a critical role in growth, whether it plays a role in bone healing is less certain.
III. Platelet-Derived Growth Factor (PDGF):
• Potent mitogen for UMC
• DNA synthesis, cell replication, and production of collagen
IV. Transforming Growth Factor-ß (TGF-ß):
• Mesenchymal cell growth and differentiation
• Collagen synthesis
• y fibroblasts and macrophages chemotaxis
• TGF-ß y osteoinductive activities of BMP.s.
V. Fibroblast Growth Factors (FGF.s):
• Mesenchymal cell growth and differentiation
• The most studied members are aFGF and bFGF
2- OSTEOGENIC: = ACTIVE CELLS CAPABLE OF BONE PRODUCTION

I. Unfractionated Fresh Bone Marrow: BMAT
• Harvested from the iliac crest and immediately transplanted to skeletal repair
• Simple procedure that is inexpensive and can be done on an outpatient basis.
• Limited source of osteoprogenitor cells
• Complications of harvesting
II. Connective Tissue Progenitors:
• Able to replication without differentiation, & has multilineage developmental
potential.
• C.T. progenitors are expanded in number without undergoing differentiation.
III. Differentiated Osteoblasts & Chondrocytes
• Difficult to obtain > osteoprogenitor cells & has limited capacity for proliferation
• Mature osteoblasts could be generated from culture expanded progenitor cells
IV. Genetically Modified Cells:
• In this new technique, gene therapy is used for treatment of bone cells, using a
delivery vehicle to transmit the genetic material coding for osteoinductive stimuli
3- OSTEOCONDUCTIVE (scaffolds) = materials that attachment, migration, and distribution

of cells responsible for bone-healing
I. ALLOGRAFT BONE MATRICES:
• Although allograft bone lacks any viable cells that might contribute to NBF
• Allograft matrix is highly OSTEOCONDUCTIVE é some osteoinductive properties.
• Drawbacks; less satisfactory results < autograft, disease transfer, & immunogenic reaction
II. COLLAGEN: (delivery system)
• Collagen is conductive to bone formation
• Surface contains sites for deposition of mineral
• Binds the non-collagen proteins, which provides sites for cell attachment
III. HYALURONAN:
• Hyaluronan is not osteoconductive, but it is useful tissue engineering substrate
IV. POLYLACTIC AND POLYGLYCOLIC POLYMERS:
• Degradable polymers have little osteoconductive potential
• Highly biocompatible so it is used also a successful substrate in tissue engineering
V. CERAMIC MATRICES:
A. HA from corals: = HYDROXYAPATITE:
• Derived from coral ca carbonate, PORITES as cortical bone & GENIPORA as cancellous
• Slowly resorbed & low porosity
B. Calcium Sulfate Matrices:
• Can be used in presence of infection, & is the cheapest
• Two forms, with or without AB.
C. Tricalcium phosphate:
• The porosity ≈ 35%, with pores ranging from 100-300 μM.
• Greater solubility >HA, and as a result implants are reabsorbed more rapidly.
D. Injectable Ceramic Cements : These Injectable cements are usually composed of α-TCP,
dicalcium and tetra calcium phosphate monoxide.
• Cements can be injected into # sites or bone defects
E. Ultraporous β-tricalcium Phosphate:
• A newly developed β-TCP é higher porosity & faster resorption.
• Larger surface area is exposed to cells and nutrients.
• Ultraporous β-TCP seeded é autologous BM could act as autograft
COLLECTION OF DONOR BONE (Femoral Heads)

• Blood tests (HIV, Hep B, VDRL, Rhesus)
• Swabs are taken form cut site & acetabulum
• Head placed in 2 sterile bags, sterile container & un-sterile bag
• 2.5 MRad of γ radiation
• Stored in (-70°C) ultra cold freezer
Preservation & transplantation:
1- FRESH - requires no preservation. No test for disease or sterility. There is y immune response.
The application of fresh allograft is limited to joint resurfacing.
2- FROZEN < (-60°C) Æ enzyme degradation Æ z immunogenicity + intact mech. Properties
3- LYOPHILIZED (Freeze-Dried):
• Removing water + vacuum packing + freezing + storage up to 5y
• z antigenicity
• Osteoconductive only
• Biomechanical alteration on rehydration.
4- IRRADIATED:
• Powerful sterilizing method
• z antigenicity
• Biomechanical alteration
Graft Healing
STAGE DESCRIPTION
1- Haemorrhage
2- Inflammation Chemotaxis stimulated by necrotic debris
3- Revascularisation
4- Creeping Substitution Replacement of necrotic host tissue by donor NBF
along the invasive host Bl. v v.
1]. Osteoblast differentiation ................ From Precursors
2]. Osteoinduction ................................... Osteoblast and clast function
3]. Osteoconduction .............................. New bone formation over a scaffold
5- Remodelling Continues for years
Factors adversely affecting healing
1- General:
o Mal nutrition
o Debility
o Extreme ages
o Drugs: NSAID’s, diphosphonates
2- Local:
o Severe soft tissue laceration & devitalization
o z Vascularity
o Infection
o Foreign Material
Immunogenicity
In general bone and cartilage ................. weakly immunogenic
Fresh allografts .............................................. most immunogenic
Freeze dried (lyophilized) ................................... least immunogenic; but BMP is depleted + low structural
integrity
Irradiation ....................................................... alter its structural strength
Advantages of grafts:
1]. Decrease cost: by seeking new definitive treatments (e.g. Osteoarthritis).
2]. Solve many reconstructive problems
3]. Good results as regard management of delayed and non union
4]. Multiple & variable sources
5]. Allo & synthetic grafts avoid autograft harvesting & donor site morbidity
Disadvantages:
1]. Disease transmission e.g. xeno & allografts
2]. Unavailable technology for the recombinant and genetically modified options
3]. Decreased osteogenic efficacy as compared é autografts
4]. Cell expansion & differentiation still under trials
5]. Osteoconductive matrices are still expensive
Properties of Bone Graft Materials

Material Osteoinductive Osteogenic Osteoconductive Integrity
AUTOGENOUS CANCELLOUS BONE ++ +++ +++ -
AUTOGENOUS CORTICAL BONE + + + ++
VASCULARIZED AUTOGRAFT + + + +++
ALLOGRAFT "+/-" - + +
BONE MARROW + + + -
DBM + - ++ -
COLLAGEN - - + +
CERAMICS - - + +
BMP "++" - - -
"+ = Moderate" " ++ = Marked " " - = None" " +/- = Some "
Cartilage Substitutes
• No consistently reliable means to regenerate joint cartilage currently exists.
• As with bone tissue engineering we have three basic elements for cartilage:
1- Growth Factors.
2- Chondorogenic cells.
3- Matrices ( Scaffolds).
1- GROWTH FACTORS
a. INSULIN-LIKE GROWTH FACTOR (IGF) :

• IGF.s, beside their effect on osteoblasts, known to be differentiative and mitogenic for
cartilage tissue. Their importance lies with their role in osteoarthritis.
b. BONE MORPHOGENETIC PROTEINS (BMP.S):
• BMP.s based on their variable functional expression, are able to modulate
chondrogenesis
• Theoretically, BMP.s are optimal growth factors to recruit undifferentiated stem cells
for the repair of full-thickness articular cartilage defects as they are unique in that they
can initiate the formation of cartilage by a process similar to the endochondral
ossification that occurs in the growth plate..
c. HEPATOCYTES GROWTH FACTOR (HGF):
• HGF has been reported to have mitogenic effects on chondrocytes, meniscal cells, and
ligament cells.
d. BASIC FIBROBLAST GROWTH FACTOR (BFGF):
• Several reports have shown that bFGF is capable of inducing repair of superficial or
partial thickness articular cartilage defects when injected intraarticularly..
e. TRANSFORMING GROWTH FACTOR-β (TGF-β):
• TGF-β is produced by articular chondrocytes and remains in the cartilage in a latent
form. It has been reported to influence the proliferation of human articular
chondrocytes.
2- CHONDROCYTES AND UNDIFFERENTIATED MESENCHYMAL CELLS
• Produce a new cartilage matrix.
• Selective transfer of gene expression to chondrocytes or chondroprogenitor cells may
be preferable to synovial cell transfer. These studies are encouraging for the future use
of ex vivo gene transfer to chondrocytes to treat cartilaginous defects.
3- ARTIFICIAL MATRICES
• y ingrowth of new cells
• y matrix formation
• Protective
• Different methods for holding matrices and cells in articular cartilage lesions may
include GLUES, FLAPS, PINS….etc.
• Intra-Articular Inj of Hyaluronan is an example of matrices in cartilage tissue engineering
Medically appropriate administration
1- Osteoarthritis of knee is documented with radiographic evidence: and
2- Osteoarthritic knee pain that interferes with functional activities such as; ambulation,
prolonged standing , etc.; and
3- Lack of functional improvement following a trial of at least three months of conservative
therapy; and/or Inability to tolerate NSAID therapy
4- Failure of at least one injection of a steroid product into the knee resulting in unsatisfactory
relief or relief that lasted less than three months.
• Repetition of a cycle (3 to 5 injections) every 6mo, if symptomatic relief from the previous
course of ttt has been confirmed and documented, is considered MEDICALLY APPROPRIATE.
Medically Inappropriate administration

1- Active inflammatory joint disease or synovitis affecting the knee (e.g., crystal synovitis,
rheumatoid arthritis)
2- Presence of infection of the target joint or skin surrounding the proposed site of injection
3- Allergy to birds, feather, eggs etc
4- Pregnancy.
• Repetition of treatment cycles (3 to 5 injections), more frequently than every six months, is
considered NOT MEDICALLY APPROPRIATE.
Terminology:
1- AUTOGRAFT: is tissue transplanted from one area to another in the same individual.
2- ALLOGRAFT: is tissue transplanted from one individual to another.
3- XENOGRAFT: is tissue transplanted between animals of different species.
4- ORTHOPTIC: anatomically appropriate graft.
5- HETEROTOPIC: anatomically inappropriate graft.
6- OSTEOGENESIS: bone formation with no indication of cellular origin. This may be graft or host
origin (i.e. osteogenesis refers to augmentation of bone formation).
7- OSTEOINDUCTION: refers to recruitment from the surrounding bed of mesenchymal-type cells,
which then differentiate into cartilage forming and bone forming cells. Osteoinduction is
mediated by graft-derived factors.
8- OSTEOCONDUCTION: refers to the three-dimensional process of ingrowth of sprouting capillaries,
perivascular tissue and osteoprogenitor cells from the recipient bed into the structure of the
graft. Simply, the graft functions as a scaffold, for the ingrowth of new host bone.
9- BIOMATERIAL: A non-viable material used in a medical device, intended to interact with
biological systems.
10- BIOCOMPATIBILITY: The ability of a material to perform with an appropriate host response in a
specific application.
11- BIOINERT: No host response to the material.
12- IMPLANT: An object made from non living material that is inserted into the human body where
it is intended to remain for a significant period of time in order to perform a specific function.
13- POLYMER BONE GRAFT: nonviable engineered materials formed from polylactic acid and/or
polyglycolic acid, nylon, animal derived collagen and other materials. Depending on the
material it degrades through inflammatory or metabolic processes. In some formulations its
mechanical properties allow it to be used as a resorpable plate or screw.
14- CERAMIC BONE GRAFT: nonviable brittle dense engineered material, solid or with formed or
natural porosity, generally available in powders, granules or standard geometric shapes such
as blocks and wedges. Most formulations degrade very slowly with some newer formulations
being reported to degrade more rapidly.
Biomechanics
Topic: Definition Notes
Load Is the force applied (newton)
Stress(ð) (nominal, F/A= N/m²= Pa= the force applied True stress (ðt) uses true csa instead of original csa (as
engineering) over a surface unit area. (measure with nominal stress).; ðt= [F/original csa] x [1+ nominal
of the force on an object) strain].; ðt>>ðn because of lower csa ('Necking')
Strain (ε) L-Lo/Lo = a ratio between the true strain= ln(1+ nominal strain).
change of length : original length
= how far atoms are displaced apart
Strain types 1]. Bending:
o 3 points bending
o 4 points bending
o Cantilever bending
2]. Compressive buckling
3]. Shearing
4]. Torsion
Stress Shielding Is the stress by pass from the less stiff material to the more stiff one when they are fixed
together
HOOKE’S Law Stress is directly proportionate to strain till the yield point (Robert Hooke, 1678)
Yield stress Is the stress beyond which the material will express plastic deformation (yield point= elastic
limit)
Tensile Strength Max stress the material can resist without breaking when exposed to a single load, beyond ώ
continuous deformation occur even with decrease of the stress
Failure Strength Max stress beyond which the material eventually fail
Fatigue strength Max cyclic loads the material can resist without breakage when exposed to 107 cyclic loads
Endurance Max cyclic loads below fatigue will not occur (theoretical for ortho implants)
(Fatigue Limit)) Polished steel endurance = ½ the tensile strength
YOUNGS Modulus measure of STIFFNESS of a material. =stress/strain. Usually the same in tension & compression
of elasticity (E)
Strain Energy(U) The increase in energy associated with the deformation of a structure, as a result of the
(Joules) application of a slowly increasing load. = Area under load-extension curve.
Strain Energy Energy associated é deformation of Strain energy density obtained by loading to rupture
Density (u) (J/m³) a structure, eliminating the effects MODULUS OF RESILIENCE= energy per unit volume that
of the structures size. =area under the material can absorb without yielding (= area under
stress-strain curve. u= stress²/2x elastic portion of stress-strain curve).
Modulus.
Strain y yield strength, z ductility & toughness, unchanged modulus(stiffness).
Hardening
Toughness Ability of a material to resist Toughness measurements:;
breaking (i.e. absorb energy & deform a. MODULUS OF TOUGHNESS =The area under the
plastically) = energy/unit volume a curve up to the breaking point
material can absorb before failure. b. Impact Tests- Charpy
Tough material has yductility & yyield
stress & withstands ystresses & c. Fracture toughness: ability to resist crack propogation
ystrains.
Stiffness Ability of a material to resist 1]. Axial Stiffness(A) = [pi/4]x [Do-Di];
deformation. Measured as Elastic 2]. Bending Stiffness= Area Moment of Inertia(I)
Modulus. 3]. Torsional Stiffnes= Polar Moment of Inertia(J)
Hardness Measure of a materials resistance to Hardness Tests: ; 1. Brinell- 10mm steel ball,
abrasion or indentation. Hardness is HB=F/½piD[D-sq.rt(D²-d²)]; 2. Vickers- pyramid-shaped
proportional to Tensile Strength. diamond, HD=1.854F/d²; 3. Rockwell
Ductility/ Is the ability of a materials to deform Measures of Ductility
Brittleness before they break (elastic & plastic) / 1. Percentage Elongation
2. Percentage Reduction in cross-sectional area
Is the resistance to plastic 3. Bend tests;
deformation before breakage 4. Cupping tests(Erichson);
5. Impact test(Charpy) - ductile absorb yenergy till #
SOURCIL Subchondral bone condensation at superomedial acetabulum (R is maximum at this point)
GOTHIC ARCH Remodeled bone at the acetabular roof above the sourcil
Euler's Column Determines critical load for scoliosis. Pcrit = C.(E.I/L²); Pcrit = critical load, C=end conditions, E
Law = modulus, I = moment of inertia, L =column length.

Definitions Kinematics= Analysis of motion w/out reference to forces.;
Kinetics= Analysis of motion under the action of given forces or moments. (= static /
dynamic); Statics= study of forces & moments acting on a body in equilibrium (at rest or
constant speed)
Dynamics= study of forces & moments acting on a body (accelerating/ decelerating)
Failure When a material lost its ability to Types(7):
satisfy the original design function. 1].FFATIGUE: failure 2ry to cyclic loading
FRACTURE: failure 2ry to bending stresses into > 2 parts
2].F
3].BBUCKLING: 2ry to compression of a thin walled tube
4].CCORROSION: 2ry to electrochemical action
5].WWEAR: mechanical deterioration of solid surface
6].CCREEP & deformation
7].LLOOSENING: septic & aseptic
Failure Ductile metals may fail in a brittle manner at; low temps, thick sections, at high strain rates or
where there are flaws.
Fatigue The z of strength by the application Low cycle fatigue = max. stress in a cycle > yield stress.
of cyclic loads below the tensile High cycle fatigue = max. stress in a cycle < yield stress.
strength of the material. This z by surface scratches.; PEENING= light hammering of
the surface with a round-nosed hammer Æ y Fatigue Life by
inducing residual compressive stresses in material
Fatigue Fracture Occurs in 3 steps:;
1]. Nucleation of a crack- occurs at locations of highest stress & lowest local strength. These are
usually at or near the surface & include surface defects, such as scratches or pits, sharp
corners, inclusions, grain boundaries or dislocation concentrations.;
2]. Propagation of a crack- towards lower stress regions. The crack propagates a little bit
further each cycle, until the load-carrying capacity of the metal is approached
3]. Catastrophic failure- in a brittle manner; implant buckles into 2 or more parts when the load
is changed during service.
Endurance Is the cyclic load limit below fatigue will not occur (theoretical for ortho implants)
(Fatigue Limit)) Polished steel endurance = ½ the tensile strength
Corrosion Destruction of metal by electrochemical action
Corrosion 1) GALVANIC: between metals é different electrochemical potentials
Mechanism 2) FRETTING: surface breakdown 2ry to motion & loads between metal surfaces
3) CREVICE: motion bet metals depassivate their surfaces
4) PITTING: surface abrasion galvanic corrosion
5) STRESS: load generated crack galvanic corrosion
6) MICRO-BIOLOGIC: micro-org secrete corrosive metabolite
7) INTERGRANULAR: corrosion at welding points &not the metal Æ structure failure (weld decay)
Corrosion z by o PASSIVATION (surface oxidation) ○ Implants é one metal type
o PEENING (light surface hammering) ○ Implants é non modular components
o POLISHING ○ Implants é inert metal
o Heat treatment
o Good surgical treatment technique to z abrasions
Types of Material 1]. ISOTROPIC= has same properties in all directions.;

2]. ANISOTROPIC= different properties in diff. directions.;
3]. ORTHOTROPIC= has same properties in a particular direction throughout the material
4]. BRITTLE = has linear stress strain curve till failure; i.e. zaffinity for plastic deformation
5]. DUCTILE = has great affinity for plastic deformation before failure
6]. VISCOELASTIC = has time-rate dependant stress strain curve (e.g. bone and ligament)
Creep Continuous deformation under constant stress.
It is stress, time & temp. dependent (fatigue is stress & time dependent only).
Stress Relaxation Decrease stress under constant strain over time.
Hysteresis Viscoelastic phenomenon that exhibits a different loading & unloading patterns of stress-strain
curve when subjected to cyclic loading,
ENERGY (JOULES) The ability to do work. Potential E=MGH (static energy);
Kinetic E=½mw² (motion energy)a, w=angular velocity
Energy cannot be created or destroyed.
Tribology concept 1]. Wear
2]. Friction
3]. Lubrication
1]. Wear Material shedding from solid surfaces as a consequent of the mechanical action.
1. ABRASIVE: the harder grooves the softer material
2. ADHESIVE: the softer material adheres on the harder surface
3. FATIGUE, in which repetitive loading Æ subsurface delaminate Æ lost from the surface
4. THIRD-BODY WEAR implies the retention of debris bet. sliding surfaces Æ abrasive wear.
5. BACK SIDE WEAR: bet PE & the metal backing.
6. RUN IN WEAR: is the accelerated wear that occur in the 1st few millions of cycling
2]. Friction The undesirable effect when two F=μR (μ= coefficient of friction) (frictional force, F, is
surfaces move in contact with each proportional to the normal component of the reaction
other. force, R); μ=tanø (ø is the critical angle on an incline
when motion starts to occur= 'angle of friction')
Coefficient of the resistance encountered in Normal joints= 0.008-0.02; metal-on-metal= 0.8; metal-
Friction moving one object over another. UHMWPE= 0.02; metal-bone= 0.1-0.2; ceramic-ceramic=
v. low; ceramic-UHMWPE= v. low; metal-ceramic= v. high
Coulombs Law of The shear stress is always parallel to the relative velocity & equal to the product of the contact
Friction pressure & the dynamic friction coefficient as determined from measurements on particular
combinations of materials. [Shear Stress= Compressive stress × Coefficient of Friction]
Torque Rotational Force [Newton X T= I x α; [I = Mass Moment of Inertia (Nm.sec²); α = angular
Meters(Nm)] acceleration (radian/sec²)]
Frictional Torque Is the force transmitted from head-PE interface to bone interface through out the motion arc
3]. Lubrication 1]. ELASTOHYDRODYNAMIC = the bearing materials deform elastically; friction is determined
by the complete lubricant film that separate the bearing surfaces
2]. BOUNDARY LUBRICATION = the bearing surfaces come much closer together & friction is
determined by the coefficient of friction of the non-deformable material surface (lubricant
partially separate the surfaces)
3]. BOOSTED LUBRICATION = the bearing surfaces are partially separated by pools of lubricant
ώ is trapped by areas of bearing surfaces
4]. HYDRODYNAMIC LUBRICATION = the load & motion influence the lubricant film between
the bearing surfaces.;
5]. WEEPING LUBRICATION = in which fluid shifts from cartilage to loaded areas
Wetability Is the affinity of a material to a Depends on the surface tension of the material = the
lubricant material angle of contact bet the material and a lubricant drop
Velocity the rate of change of the position of = a Vector (has magnitude, direction & sense). Speed is
the body. scalar (only has direction).
0.1% Proof Stress the stress which results in a 0.1% Line drawn on force-elongation/ stress-strain graph
plastic strain. For materials where parallel to the linear part of graph & passing through the
the yield stress is not easily 0.1% strain value(=0.1% gauge length).
identified (aluminium). (proof stress
not usually quoted for polymers)
Annealing Process involving heating to & Results in a softened state (more ductile), to facilitate
holding at a temp. high enough for cold-working, improved machine-ability and mechanical
recrystallization to occur and then properties.; eg. Orthop. wires (stainless steel 316L,
cooling slowly. annealed)
BOYLE'S Law Pressure= Force/Area
BARBA'S Law Takes into consideration the effect % Elong.= {[a x sq.rt.(csa)/gauge length] + b} x100
of csa on % elongation in Tensile
testing.
Bone Fracture Bone fails in TENSION. Shear failure is a tension failure, but crack propagates in spiral because of
the ANISOTROPY of bone.; *Haversion canals help to prevent crack propagation.
Brittle Fracture Break a material, & the broken ends fit together perfectly (i.e. no reduction in csa).

Solid 1]. METALS: High tensile strength & modulus of elasticity, medium hardness, can be ductile, poor
materials resistance to corrosion, high electrical & thermal conductivity.
ALLOYS-
• Mild steel= iron & carbon;
• Stainless steel- Fe, chromium, carbon & manganese (C y strength, Cr y R to corrosion)
• Vitallium= chromium, cobalt & molybdenum alloy (historical).
2]. POLYMERS:
1]. Thermosets= decompose when heated. Bakelite.
2]. Thermoplastics= soften when heated.
POLY-ETHYLENE. Low modulus of elasticity; low hardness; medium tensile strengths; ductile;
low densities; high corrosion resistance; low electrical & thermal conductivities; tend to creep;
properties depend on temp. Can withstand high strains, not high stresses.;
3]. CERAMICS:
1]. Brittle (Can withstand high stresses, not high strains)
2]. Hard
3]. High modulus of elasticity
4]. Stronger in compression than in tension
5]. Low electrical conductivity.
4]. COMPOSITES: two different materials bonded together. More expensive to produce.
Alloy A substance containing two or more metals mixed in ! liquid phase.
Ceramics A substance chemically comprised Properties determined by ionic bonds, stronger than
of metallic and non-metal covalent bonds of polymers & metallic bonds of metal.;
elements/molecules (eg. ZnO, SiO, 1]. High chemical resistance.
TiO2)) 2]. High Elastic Modulus.
3]. Highly Crystalline -> Brittle.
4]. Hard -> High wear resistance.
5]. Inert (eg. calcium hydroxyapatite).
6]. Can éstand high stresses, but cannot produce
high strain
NB- because of high melting point large ceramics are
prepared by compressing small powder particles Æ this
always has small defects Æ stress risers + Brittle Æ WEAK.
Composites = a multiphase material. The Types:;
constituents must be chemically 1]. PARTICLE REINFORCED:
dissimilar & seperated by a distinct a. Large particle (concrete)
interface. (matrix & dispersed b. Dispersion strenthened (atomic);
phases). It should provide distinctive 2]. FIBER REINFORCED: whisker, fiber, wire; continuous,
properties that cannot be obtained by discontinuous; aligned(anisotropic),random(isotropic);
the individual components alone.
High strength to weight ratio.
3]. S TRUCTURAL:
a. Laminar(wood)
b. Sandwich panels.
Finite = The ability to model structures of The main requirement is to have, for a range of elements of
Element complex geometry as an assemblage varying shapes, solutions of the governing differential
Modelling/An of simple elements. equations for arbitrary boundary conditions.
alysis (FEM)
Instant centre It is the point about which the joint rotates
of rotation
Free Body The segment of the body of interest. The segment is assumed to be in equilibrium.
Diagram
IM Nails *Tubes é a wall thickness:radius ratio of < 1/8 tend to behave as curved sheets rather than tubes.
These thin- tubes are subject to buckling. (Bone is thick-walled).; *A wider diameter hollow tube is stiffer than a
solid smaller diameter tube with the same amount of material. A slot/slit Æ z torsional stiffness by 98% ->
quicker healing with callus.
Topic: Def: Notes:
PE - Glossary • BASE RESIN - The PE granules or powder; the raw source polymer.
• MEDICAL-GRADE PE is a very small percentage of the worldwide production of PE. Only ultra-
high molecular weight material is used in the manufacturing of components for total joint
replacement.
• CALCIUM STEARATE - A compound mixed with the PE powder (in some grades of the
material) before it is formed into a solid. The calcium stearate serves as a scavenger of residual
acid. In ram extrusion, it also acts as a lubricant, and has been shown to help prolong the life
of the manufacturing equipment. It also results in the poly ethylene having a whiter color.
However, some reports have indicated that fusion defects are more common in PE that
contains calcium stearate. Fusion defects may make the component more susceptible to crack
initiation and propagation. Consequently, many manufacturers now use grades of PE that do
not contain calcium stearate. However, the quantitative effects of calcium stearate on the
wear properties of PE components are a subject of ongoing debate. ; In several retrieval
studies, components manufactured from 1900 PE resin have shown significantly lower levels
of oxidation following sterilization by gamma irradiation in air. The reason(s) for this have not
been clearly identified.
• CHAIN SCISSION - Breakage of the long chains of PE into shorter molecules. Extensive chain
scission can substantially increase the crystallinity, density, stiffness and brittleness of the PE,
weakening the material. Oxidation is a primary cause of chain scission in PE.
• COMPRESSION MOLDING - A consolidation method that subjects the PE powder to high
temperature and pressure, fusing it into a solid form, either into bulk stock for subsequent
machining, or into net-shape components.
• CONSOLIDATION - The fusing of PE powder into a solid form by application of heat and
pressure. The two principal methods of consolidation are compression molding and ram
extrusion.
• CROSS SHEAR - The particular type of stress applied to the surface of the PE component due to
the crossing-path motion of the femoral ball. Crossing-path motion is also present, albeit to a
lesser extent, in some designs of knee prostheses. Studies have shown that PE wear is 10 to
100 times greater with crossing path motion than with simple linear reciprocating motion.
• CROSSLINKING - The process by which chemical bonds link carbon atoms in adjacent PE
molecules by combining two free radicals. Cross linking has been shown in laboratory wear
simulators (both hip and knee) to markedly y the wear resistance of PE.
• ELECTRON BEAM IRRADIATION - Also known as E-beam, the PE is bombarded with high-
energy electrons which induce crosslinking. Because there is more attenuation of an electron
beam than gamma rays, a high beam energy (e.g., 10 MeV) is used to produce crosslinking in
the PE. Residual free radicals generated by the electron beam can be extinguished by an
appropriate post-crosslinking thermal treatment to avoid long-term oxidative degradation; EtO
sterilization - A sterilization method that utilizes ethylene oxide gas (EtO). EtO does not induce
free radicals or oxidation; it also does not induce crosslinking. To eliminate the toxic gas,
components must be outgassed for a sufficient period prior to being implanted.
• FREE RADICAL - An electron on an atom that is a potential reaction site for oxidation or cross-
linking.
• GAMMA IRRADIATION - Irradiation by exposure to a radioactive cobalt source, which emits
gamma rays. Gamma radiation (in air) has been the predominant method used to sterilize
prosthetic joint components for more than two decades, with free radical production,
oxidation and crosslinking being unintentional by-products. Only recently has gamma
radiation been used to intentionally crosslink PE to improve its wear resistance.
• GAS PLASMA STERILIZATION - A non-irradiation sterilization method in which a device is
exposed to energized O2, nitrogen and argon gas particles and a peracetic acid gas in
alternating cycles. The plasma sterilizes the product by inactivating microorganisms. As with
EtO sterilization, gas plasma does not generate free radicals, induce oxidation or crosslinking.
• INERT GAS PACKAGING - Sealing the PE component in a package flushed with an inert gas,
such as argon or nitrogen, to remove the O2 present during sterilization and subsequent shelf
storage.
• ISOSTATIC MOLDING - A multi-step process that begins é manufacture of a cylindrical compact
of UHMWPE powder from ώ most of the air is expelled. Subsequently, the compacted rods are
sintered in a hot isostatic pressure (HIP) in an argon-filled pouch to z oxidative degradation of
the UHMWPE. Finished implants are then made by either turning or milling operations.
Topic: Def: Notes:

PE (cont.) • O2 LESS PACKAGING - PE components are sealed in a package in an atmosphere é minimal O2
during sterilization and subsequent shelf storage. Current versions include combinations of
inert gases partial vacuum, and enclosing a packet containing an O2 scavenger.
• OXIDATION - Reaction of an O2 molecule with a free radical on the PE molecule. This typically
leads to chain scission, indirectly increasing the crystallinity, density and stiffness of the
polymer and reducing its resistance to fracture and wear.
• RAM EXTRUSION - A consolidation process in which a ram is used to force the PE powder
through a heated nozzle, resulting in a fused bar as large as six inches in diameter. Careful
control of the processing variables (principally, the extrusion rate and the nozzle temperature)
is required to produce a fully and uniformly consolidated material (e.g., containing minimal
fusion defects).
• THERMAL STABILIZATION - Heating the PE to neutralize residual free radicals and, thereby,
stabilize it against long-term oxidation. Bulk PE (molded blocks or extruded bars) can be
heated above the melting temperature (about 150° C), held there for a number of hours, and
then cooled ("remelting") to extinguish the free radicals before being machined into a final
component. ; In contrast, if radiation crosslinking is applied to the finished components, they
cannot be remelted, but they can be heated to below the melt temperature and held at that
temperature for a number of days ("annealing") to substantially reduce the residual free
radicals. Because annealing occurs with the PE still in a semi-crystalline state (i.e., below the
melting temperature), it is not as effective as remelting in eliminating the residual free radicals.
• VACUUM PACKAGING - Typically, the PE components are placed in a barrier package, flushed
with an inert gas (i.e., nitrogen) and then evacuated to minimize the O2 present during
radiation, sterilization and subsequent shelf storage.
Polymers (Plastics) made up of long-chain molecules *viscoelastic (deformation time & stress dependent);
based on carbon & hydrogen. *Hysteresis
Power (watts) The rate of doing work. P=W/t
Slip =plastic deformation in metals, one Dislocations are faults or distorted regions. (types of
layer or plane of atoms gliding over dislocations= edge & screw dislocations); Material
another. Slip occurs step by step with deformation occurs by slip or 'twinning'.
the movement of 'dislocations' within
the crystal.
Mechanical = a form of Deformation where atoms in each succesive plane within a block will move different
Twinning distances, with the effect of altering the direction of the lattice so that each half of the crystal
becomes a mirror image of the other half. As compared to 'slip' where all atoms in one block
move the same distance.
Moment of Represents the resistance a structure 1]. MASS MOMENT OF INERTIA= R to angular acceleration
Inertia has to acceleration 2]. AREA MOMENT OF INERTIA= resistance to Bending.
3]. POLAR MOMENT OF INERTIA= resistance to Torsion.
Polar Moment of Measure of the Torsional Stiffness of a J = [pi/2]x[Ro4-Ri4] = 2.I; T/ø = JG/L (T/ø= torsional
Inertia (J) column/ shaft stiffness, T= torque, ø= angle of twist, G= shear modulus,
L= length of shaft)
Second Moment A property which measures the The further the material is from the neutral axis, the
of Area/ Area distribution of the material around stiffer the construct under a given load.; Circle: I = [pi.r4]
Moment of the cross section. (a measure of /4 (hollow: r= outer radius-inner rad.);
Inertia (I). bending stiffness) Bending Stiffness = E.I (where E is Youngs Modulus)
Rectangle: I= w×h³ ÷12;
The region of a bone/nail with the smallest I is subjected
to the largest deformation under load & will fail first.;
Indirect bone healing (thick periosteum) -> incr. I -> incr.
stiffness & strength.
Momentum Linear momentum= m.v
Angular momentum= I.w (I=mass moment of inertia)
Newton's Laws of 1]. A body will remain at rest or continue moving with a constant velocity along a straight line,
Motion unless a resultant external force acts on it.;
2]. The acceleration of a body is proportional to the resultant force acting on it and is in the
direction of this force. (F=ma);
3]. To every action there is an equal but opposite reaction.
Passivity Conditions existing on a metal Methods:;
surface because of the presence of a 1]. Surface Treatment- with a highly oxidizing solution
protective film that markedly lowers (nitric acid).;
the rate of corrosion. 2]. Some alloys & metals spontaneously form a passive film
(Type 316 stainless steel, Titanium).;
3]. Altered environment by incr. passivating/ oxidizing
agents (chromate, nitric acid);
4]. Applying a current (anodic protection)
Poiseuille's Law Rate of flow of fluid through a pipe/vessel is proportional to the fourth power of the radius, &
inversely proportional to the length.
Poisson's Ratio The lateral/transverse compressive v(mu)= lat. strain/longit. strain.; It may take on values
strain is proportional to the betw. 0(a fully compressible material) and 0.5(a material
longitudinal tensile strain, within the which maintains a constant volume during deformation).
elastic range of a material. Values >0.5 imply expansion of vol during deformation.
Titanium vs. Ultimate Strength(failure): Stainless Steel > Titanium; Yield Strength(permanent deformation):
Stainless Steel Titanium > Stainless Steel
Implant fixation 1].Interference Fit: (Press fit): depends on formation of fibrous tissue interface
2].Interlocking fit (PMMA): Grout that allow for gradual transfer of stresses to bone = Microinterlock
3].Biological Fit (Porous coating): bone ingrowth into the implant
Work Work is done by a force when the W=Fs ; W=Frø=Mø (for angular motion)
(Joules=N.m) point of application of the force
moves in the line of action of that
force.
Perfect Material =
1]. Stiff ............................................................. resist deformation
2]. Hard ........................................................... resist surface abrasion
3]. Inert ........................................................... resist corrosion
4]. Tough ....................................................... resist breakage
5]. Ductile ....................................................... able to deform before breakage
6]. Adapt to loading
7]. Regenerate (reduce failure) = a composite = Bone (a ceramic phase (calcium
hydroxyapatite), dispersed in a collagen-based matrix).

INFECTIONS
Dr Mohamed H Sobhy
Ain-Shams University

[Infections] Page | 233
Synovium
• = inner lining of synovial joints
• Synovial membrane is not a true membrane since it does not have cells joined to their neighbours
by tight junctions (desmosomes) and has no basement membrane of collagen.
• Instead the cells are loosely arranged on a matrix of hyluronate (secreted by the synovial B cells).
• It is one or two layers thick
• Supported by capillaries & thin fibrous stroma
• Richly supplied with blood vessels, lymphatics, and nerves; richness of blood capillaries and their
proximity to inner surface account for hemorrhage into joints that may follow minor injuries
Cells:
• A Cells = macrophages
• B Cells
o exocrine / synthetic cells
o synthesize hyaluronic & glycosaminoglycan (GAG)
• C Cells May exist as an intermediate cell type.
• Arranged into villi resulting in a large surface area (knee = 100m2; whole body = 1000m2)
Functions of Synovium
1- Controls diffusion
2- Ingest debris
3- secrete immunoglobulins
4- secrete lysosomal enzymes
5- secrete hyaluronate
6- secrete lubricating glycoproteins
7- reduce friction in joint
Regenerative Capacity
• synovial cells may transform into chondrocytes at attachment site of Synovium to articular cartilage
• synovial cells are capable of rapid and complete repair or regeneration
Response to Infection:
• Acute inflammatory response with accumulation of PMN's & monocytes
• Complement activation produces chemotactic factors and other inflammatory mediators
• Lysosomal enzymes attack hyaluronate leading to loss of the diffusion barrier
• Inflamed synovium contains large clefts which probably permit passage of molecules of almost any size
• Synovium acts as a 'leaky sieve'
• If infection is not ttt Æ synovium necroses éin 24H Æ chondrocytes necrosis & failure of GAG production
• Acute inflammatory response along with cellular disintegration (with release of lysosomal enzymes &
proteases) will further injure chondrocytes
• Antibiotics can also easily get into the joint
• Lysosomal enzymes (collagenase, protease, galactosidase) damage the joint Æ joint toilette required
• Hydrocortisone blocks the release of lysosomal enzymes
Synovial Fluid = an ultrafiltrate of plasma (by molecular sieving) plus hyaluronic & glycoproteins
• The viscosity depends on amount of hyaluronate. Does not contain fibrinogen - thus no clotting
• Exhibits non-newtonian fluid characteristics - viscosity yé y shear rate.
Functions:
• Nourishes articular cartilage through diffusion
• Lubricates via the following mechanisms:
1.Hydrodynamic (fluid separates the surfaces under load)
2.Boundary (slippery surfaces)
3.Weeping (fluid shifted to loaded areas)
4.Boosted (fluid entrapment)
Lubricin (a glycoprotein) is a key lubricating component. [See Joint Lubrication]
DISEASES OF SYNOVIUM
• Pigmented Villonodular Synovitis (PVNS)
• Rheumatoid Arthritis
• Synovial Chondromatosis
234 | Page [Infection
ns]
Bacterial
F
Fungal TB
In
nfection
ns
Parasite
e sp
pirochaettal
Accute Osteo
omyeelitis
Inc
cidence:
• 5%
Ætiiology:
B
Bacterioloogy
• Low viruulent organnisms:
Staph epid
dermidis (m
methicillin sensitive,
s non
n glycoca alyx forminng)
Staph aure
eus (methicillin sensittive, non glycocalyx
g f
forming)
ß hemolytic strept
Anerobic strept
s
• High virrulent orga
anisms:
Staph aure
eus & epidermidis methicillin n resistant & glycocalyyx forming g
Gram negative organisms E. coli, Pse
eudomonas, Proteus, & Entero-ccocci
Haemophilus influen nzae especially in children n <4y
Samonellaa especially in sickle ceell desease)
• Mixed oraganism
o ms: usuallyy in postoperative infe ections (sta
aph, E.coli,, proteus, pseudomon
p nas)
• Others: Coryneba acterium, Group
G B strep, Strep fa aecalis
PDF
P Hemattogenous
• Endoge
enous
Elderly Obese
DM Sickle dissease
Gaucher’s Steroids & malnutrrition
Leukemia Multiple operation
ns
• Exogen
nous: in thee surgical technique
t Accute
Soft tissue damage Osteommyelitis
Hematoma
Bone deatth Post-
Po
ostoperative
Foreign immplant. Traumattic
Route of infection
R i
• Indirectt: hematoggenous from a distan nt focus; bo
oils, omphillitis, cathetter, IV cann
nula…etc
• Direct: from ou
utside, instrruments, or
o surgeonss
Rac
ce For Surrface The eory of Gristina
When a to otal joint prosthesis
p is placed into the human
h bod dy,
the body'ss cells & bacteria
b (ussually skin bacteria) hurry to get
g
hold on th he prosthessis surface &colonize.
If bacteria win, that evolves the e capabilityy to adherre to surfacces
for their suurvival, by secretion of a surfa ace glycop
protien called
GLYCOCALYX:
i. Very strong adhe esive
ii. Mask th
he bacteria al antigenss
iii. Colonizze inside th
his biofilm away from m immune system
s
iv. Invite other
o typess of bacteriiae to trick the immun ne system
v. When they adhe ere to the in nert implant surface,, bacteria are
a
protectted by the e antiphag gocytic efffect of bioomaterial. All
these Æ powerrful resista ance 100-1000 time es to AB &
immun nity.
ns]
Clin
nically:
Early Interrmediate late
Tim
me within 1 m 1m- 1y > 1y
CP Frank History of wound problem -Asymp. foor long perio od
in the early posto
operative -insidious pain & not acute
period -low grade e inflammattion
Lab
b y ESR -PXR ass asepticc loosen
ning
y CRP (resorptionn)
y WBC -may y pe eriosteal rea
action
+ve C/S -MRI: high
h signal inten nsity of puss
+ve blood culture -persistentt y ESR > 6mmo
-may yy y Tc99 acttivity in both b
blood and d bone phasses
-+ve culturre of aspiratte is diagnoostic
Cla
assificatioon
Stage 1= im
mmedialte postoperati
p ive:
o Staph-aure eus /ß hemo olytic streptt
o Usually nee eds irrigatio
on, unless glycocalyx
g forming
f org
ganism is id
dentified
Stage 2 = 6-24
6 mo
o Methicillin resistant sta
aph epidermidis
o Usually nee eds staged operation
Stage 3: aftter 2y
o Hematoge enous sprea ad from oth her septic fo
ocus
New
w Classifiication
Type I Early < 6wk
6
Type II Late > 6wwk
Type III Hemato ogenous
Type IV Incidenttal +ve cultu
ure
Nattural Histtory
Inflam
mmation
-Cell infiltration
-Exudatio on of purulent / seropurulent discharge
d
-Cartilage e erosion
Erosion & Necrosis

-In
n Infants Æ entire epiphysis may be severely
s damage ed
-In
n children Æ vascular occlusion
o Æ epip physeal necrosis
-In
n adults Æ confines to
t articular cartilage
Progresss Healing
Outside Com
mplete erosion
n
Complete Parrtial erosion an
nd & bony ankylosis
Bone z
resoultion a
arthrofibrosis ne destruction
bon
Sinus & absce
ess & deformity
Patthology:
• Sites:
Metaphyysis of long g bones (prrox.tibia& femur)
f
Kinked blood vv
Vasscular stasis
More liable to o trauma
Epiphysiss in infantss: still free an
nastmosis bet.
b epiphyyseal & mettaphyseal vv
v
Vertebrae in adults
Patthogenessis
Inflam
mmation Suppuraiion Necrosis
N New bone
b resolution
n
1]. Inflammatiion:
Vasscular cong gestion
Exuudation
PNLL infiltration
n Reenter
the
y intraosseus
i s pressure Æ pain, z blood bone
flow
w, Thrombo otic ischem
mia
Whole Near by
shaft muscles
Subperiosteal
S
abscess
2]. Suppuratio
on: Joint
Epiphysis
Puss is formed and sneakk out via Voolkmann in infants (hip,
shoulder)
chaannels to fo
orm a subpe
eriosteal ab
bscess
Medullary
abscess in
adults
3]. Necrosis:
Isschemia Nec
crosis Sequestra
ation
⇑ Intra-osseo
•⇑ ous •B
Bone •Ingrowth h of granulattion
prressure •P
Physis •Macropha ages &
•In
nfective thro
ombosis •E
Epiphysis lymphocyytes resorb smmall
•B
Bacterial toxiins dead spicuules
•B
Bacterial enzzymes •Large spiccules remain
n
inaccessib
be
4]. New bonee formation n:

Strippped perioosteum Æ new
n bone formation
f Æ thickens to form the involucrrum
ώ iss interrupte
ed by perfo
orations tha
at continue
e to discharrge pus & tiny
t dead bone
b
via the cloaca a and skin sinus
s
5]. Resolution:
If in
ntraosseus pressure
p is released th
he process is
i aborted
hyp peremia Æ fibrosis
App positional new
n bone formation
f + periosteal new bonee formation
n
Thicckening & remodeling
r g occur to restore
r the bone into the normaal contour
Som metimes the ere is perm
manent defo ormity
238 | Page [Infections]
Clinically:
1. Hematogenous:
a. Children:
i. C/O: General Fever, anorexia, headache, malaise.
Local Pain, Redness, Hotness, Swelling, Tenderness.
History Septic focus.
ii. O/E General Fever, Tachycardia.
Local Severe tenderness to touch and movement.
Limb is held still é out any movement.
LN.
b. Infants: (less immune response)
History of birth difficulty.
General Drowsy, irritable, mild constitutional signs.
Local Tenderness to pressure and movement.
c. Adults: History of urological procedure.
General mild fever.
Local Mild backaches and tenderness. Æ after 1 wk. Æ +ve PXR
(thoraco-lumbar is the commonest)
2. Post-operative & post-traumatic:
History of wound problems after implantation of a hardware or open
fracture
General ± Mild fever.
Local ± Pain, Redness, Hotness, Swelling, Tenderness.
Diagnosis YOU MUST SUSPECT INFECTION ALL THE TIME & USE EVERY TOOL TO REACH THE FINAL DIAGNOSIS
Radiological
1- PXR:
• Need serial radiographs (get original post-op films)
• Hematogenous EARLY Soft tissue shadow; but usually NORMAL PXR.
> 10d Periosteal New Bone Formation (NBF).
Late Mottling = osteopenia (reactive bone) + osteosclerosis (dead bone).
Chronic Sequestrum, Involucrum, cloaca.
• Post-traumatic OM As chronic hematogenous + delayed or non-union.
• Postoperative OM Osteolysis around the components
Loosening, breaking, or change the position of an implant.
2- Bones scans
99m
• Tc-HDP (Hydroxymethylene Di Phosphonate) y uptake in perfusion & bone phases.
111
• Indium & 67Ga may be helpful as a sequential scanning é 99mTc scans. Both are specific only.
• usually unable to differentiate septic from aseptic loosening
3- US:
• Detects subperiosteal fluid collection.
4- CT:
• Detects sequestrum separation.
5- MRI: (gadolinium inhanced):
• z T1 & y T2 signal intensity.
• Detects early marrow edema.
Laboratory
6- Blood: usually not helpful (usually –ve or irrelevant) except if strongly suggestive
• WBC ....................................... y
• ESR ....................................... >30 mm (late to rise & late to return)
• CRP ....................................... > 6 IU (1st to rise & 1st to return)
• ASOT ....................................... y
• RBC ....................................... z (anemia)
• Blood culture .................... +ve
7- Aspirates:
3
• Cell Count ............................ >25.000/mm (May be helpful 85%)
• Differential Count ........... >75% PNL
• Gram stain............................... +ve 25% especially in septic arthroplasty.
• Glucose..................................... z
• Protein....................................... y
• PCR ....................................... Newly introduced to diagnostic tools
• IL6 serum level ...................... Newly introduced to diagnostic tools
8- Open biopsy:
• Often identifies organism & sensitivities.
Morrey & Peterson’s diagnostic criteria for osteomyelitis:

• Pathogen isolated .................... Definite osteomyelitis.
• +ve blood culture & CP .......... Probable osteomyelitis.
• +ve CP & PXR .............................. Likely osteomyelitis.
& therapeutic test
Peltola and Vahvanen’s diagnostic criteria for osteomyelitis:
• Pus aspirated form bone
• Positive blood culture diagnosis is established é 2 criteria are present of these 4 criteria.
• Positive clinical picture
• Positive PXR findings
Prevention
Pre-operative:
[1]. All septic lesions must be identified & treated (feet, dental, urinary, prostate)
[2]. Admit patient as late as possible & into a clean ward
[3]. Shave in the anaesthetic room
Intra-operative:
[1]. Surgical Technique:
1. Careful tissue handling & Haemostasis
2. Length of procedure
3. Wound lavage - mechanical effect more important than type of fluid used.
[2]. Antibiotic prophylaxis: IV MRSA resistant AB & AB Loaded Cement (z infection risk 11 fold)
[3]. The team: few number é less motion (shed up to 10 000 skin scales/min).
[4]. Theatre gowns.
• Standard Gowns are permeable to organisms when wet “moist bacterial strike through”
• Weaved Gortex & disposable non-woven 'paper' gowns are preferred
• Body Exhaust Suit (for arthroplasty): maintain –ve pressure, cool surrounding (zshedding)
[5]. Footwear: no evidence that outdoor shoes are a source of infection.
[6]. Overhead, face masks, sterile & water proof drapes.
[7]. Gloves and hands: scrub in a separate area, wear 2 gloves, change the outer after prepping.
[8]. Drainage of wound has y risk of becoming infected than closed wound (only when sure)
[9]. Transporting the patient to operating theatre on a separate clean trolleys in the induction zone.
[10]. Theatre equipment & instruments.
[11]. Ventilation System: Vertical Laminalr Air Flow is recommended for arthroplasties.
[12]. Ultra-violet Light: bacteriocidal; but not commonly used, ð potential dangers to staff.
Post-operative:
[1]. In the early post-op phase - antibiotic cover for urethral catheterisation (Gentamycin IM)
[2]. AB cover for all GI & UTI & skin & Dental lesions é antistaphylococcal agent.
ns]
Tre
eatment
1- General supportiv
s ve ttt: sup
pportive
• Bed resst. y Fluidds.
• Analge esics. y Anti--inflammattory.
2- Splintage e:
Splintage OM
O D
Drain
• Skin tra
action, slab
bs, or half cylinders.
c
t z pain, contractur
• Helps to c res,
3- Antibioti
A ic suppresssion
• AB will not eradicaate deep seepsis & septtic arthropla asty if indica
ated alone.. AB
• Duratioon: 8 weekks (2 IV + 6 PO); till CR RP is lowerred:
• Type: AB
A is given according
a t C/S, but start
to s imme ediate broa ad-spectrum
m AB.
o Flucloxacilllin + Fucidinn for sta
aph infectio ons
o Flucloxacilllin + Benzyll penicillin for strrept infectio
ons
o Cefotaxime e or augme entine for Ha aemophilus influenzae e (<4y)
o Chloramph henicol or co-trimoxaz
c zole for sa almonella in nfections w
with sickle ceell disease
o New cepha alosporin for im
mmune-com mpromized patients
o Flucloxacilllin + Gentamycin for im
mmune-com mpromized patients
• In posto
operative & post-arthrroplasty infe ections usually of a lim mited stan nd-alone tttt except in n:
o Elderly. { Unfit t for surgeryy.
o Early infecttion. { Single, Gram +v ve, and (or) low virulennt organism m.
4- Drainage e & Debrid dement alone:
Signs off Pus
Ope
en
sub-perio
osteal absce
ess If no absscess if me
edullary absscess
Drain
nage only Drill few holes Co
otical windo
ow
• In postooperative OM,
O debride e & leave th A till # healing Æ rem
he fixation implant + AB move.
• In post--arthroplastty OM it has only 20%
% success ratte and usua ally needs rrevision.
5- Resection
n arthrop
plasty:
• For posstoperative infections; but it is nott good for infected
i TK
KR.
• for the unfit or unw
willing to have
h revision surgery & severe RA A
6- Revision Arthroplasty: > 75% success is achievable.
One Stage Two Sttage
Advanntages: 1. Single operation n probablly safer & mo
ore successfu
ul
2. quickker return to
o normal fun nction
Disadv
vantages: onged proce
1. Prolo edure 1. two p
procedures
2. AB seensitivity mu
ust be known n pre-op 2. prolon
nged bed re
est betw. stag
ges
3. Can'tt use cem mentless pro osthesis (losse
benefitt of antibioticc in cement))
Contraindicated
d: 1. If AB
B sensitivities not kno own pre-op
2. Mixeed infection
3. Gramm –ve organ nism
4. bone e loss requiriing allograft
5. Doubt about debridement adequacy
a
6. Failu
ure of previou us one stagee revision
7- Arthrode
A esis:
• For posstoperative infections, remains a last
l resort especially
e fo
or young acctive patients
8- Amputat
A tion:
• If recurrrent intracttable cases é hopeless non functio
oning limbs.
• If highe
er functiona al status cou
uld be achieved é prosthetics.
Differential diagnosis:
[1]. Acute cellulitis ..................... no PXR findings.
[2]. Suppurative arthritis ......... same CP, and clinical distinction is theoritical.
[3]. Necrotizing myocitis ........ acute streptococcal infection é MRI signal of muscle envolvement
[4]. Acute rheumatic fever .... Arthritis, Carditis, Nodules, Erythema.
99m
[5]. Sickle crisis ............................ Tc-Sc (sulpher colloid) scan shows z uptake (unlike infections)
[6]. Gaucher’s crisis ................... hepato-splenomegaly & other criteria of the disease.
Complications:
[1]. Septicemia: is rare é the evolution of the AB industry.
[2]. Suppurative arthritis: especially for intra-capsular metaphysis and infants.
[3]. Spread of infections to near by joints, bones, and soft tissue.
[4]. Chronicity.
[5]. Physeal damage & leg length discrepency.
Post operative care:
• Once signs of infection subside, movements are encouraged and the pt. is allowed to walk.
• Start PWB é crutches.
• FWB is usually possible after 4 weeks.
ns]
Su
ubacu
ute Osteom
myeliitis
Epiidemiolog gy:
Incidence e:
• In some e countries it has as high incidence as acute e hematoge enous OM.
• More in n children or
o adolescen nts.
A
Aetiology y:
• Presummably it is caaused by a lowl virulen
nt organism; almost alwways staph aureus if isolated.
• More to o occur in highly
h resisttant patientts.
Patthology
S
Site
• Distal fe
emur.
• Proxima al tibia.
• Distal tiibia.
• Calcane eus.
M
Macroscop pic:
• Well de efined cavityy.
• Surroun nded by thick trabeculae.
• Filled with
w sero-pu urulent fluidd.
• Lined by
b a membrrane of granulation.
M
Microscop pic:
• 50% sta aph aureuss could be issolated.
G
Gledhill’s Classificaation
[1]. Type 1 is a centra al metaphysseal lesion
2]. Type 2 is an ecce
[2 entric metap physeal lesion é cortica
al erosion.
3]. Type 3 is a cortica
[3 al diaphyseeal lesion.
4]. Type 4 is a diaphy
[4 yseal periossteal NBF é out a defin nite bone leesion
5]. Type 5 is a primary subacute
[5 e epiphysea al osteomyeelitis.
6]. Type 6 is a lesion that crosse
[6 es the physis involvingg both the metaphysis
m and epiphyysis.
R
Roberts a
and assoc
ciates classsification n of subac cute OM
Type IA
T Metaphyse eal lesion
T
Type IB Metaphyse eal lesion é sclerosis
s
T
Type II Metaphyse eal lesion é cortical
c erossion
T
Type III Localized diaphyseal
d é periosteal reaction
T
Type IV Diaphyseaal new bone e formation éout
é an actu
ual lesion
T
Type V Epiphyseaal lesion
T
Type VI Vertebral lesion
l
Varriants of subacute
s OM:
Hema atogenouss Garre's SRMO S
SCCH Cafffey
Diaphysis, metaphyysis, Long d
diaphysis & Long metaphysis & Stternum & vertebbrae Long
g bones & mandiible
Pathology
calcaneus mandible clavicle & verteebrae Reecurrent multifoccal OM Some

etimes flat boness
Well defined cavity Cortical th
hick & sclerosis Small lytic lesio
ons
Surroundinng sclerosis No abscesss Some are surrrounded by
sclerosis
Vertebral colla apse
Subacute Subacute and attacks Attacks of fever and 40 é recurrent Infannt
Mild pain & tenderness pains Paain and swellingg No loocal inflammation
CP
Wasting & limping Sometimes sym mmetrical Skkin pustiolosis Refusse to move the limb
Feveer & irritable
Normal WBC
W Cortical th
hickening and Lytic lesions Hyperostosis,
H ssclerosis, Perioosteal new bone b
Investigation
y ESR sclerosis yESR ossified ligamentss formation Æ b

bone
y Tc on of medulla
Obliteratio yTc y ESR thickkening
Sure Æ AB
B Thorough
h biopsy Palliative (AB
B has no N effective ttt
No No effective
e ttt
ttt
Doubt Æ biopsy
b effect)
SRMO: Suba ent Multifocal OM; SCCH: Sterno-Costo--Clavicular Hyyperostosis.

acute Recurre
Clin
nically:
• Child with
w pain around one of o the big jooints for we
eeks or mon
nthes.
• Limping g.
• Mild swwelling.
• Muscle wasting.
• Tenderrness.
• Normal temperatu ure (no feve er)
Inv
vestigatioons
L
Laborator ry
• y ESR
• Normal WBCs.
P
PXR
• 1-2 cm lucent caviity at the tibbial or femooral metaph hysic.
• Surroun nded by scllerosis “Bro odies Abb bsess”.
• Usuallyy no periostteal reactionn unless dia aphyseal.
9
99m
Tc
• Very ho ot spot.
B
Biopsy:
• Culturee and sensittivity is posittive in 50%
% only.
Diffferential diagnosis
[1]]. Osteoid
d osteoma: there is fluiid instead of
o nidus.
[2]]. Acute OM.
O
Tre
eatment:
Diiagnosis
Su
ure Do
oubtful orr failed
conservative
conse
ervative biopsy + curette
AB 6
Im
mmobilization AB for 6 wk
w
(fucid
dic + flucloxxacillin)
Chronic Osteomyelitis
Aetiology:
• Usually mixed infection
• Usually occurs as a sequel to acute hematogenous, postoperative, post-traumatic OM.
• Organisms:
o Staph. aureus.
o E. coli.
o Strept. pyogenes.
o Proteus.
o Pseudomonas.
o Staph. epidermidis is commonest after metal implant is applied.
Pathology:
Macroscopic
• Bone dies at the area of infection or at the surface of the implant.
• Cavities containing dead bone specules (Sequestra) that may act as a substrate - as implants -
for bacterial adhesion Æ persistence of infection.
• Surrounded by a vascular granulation & pus that may tickle outside via bone openings (Cloaca).
• Peripherally there is an area of sclerosis & reactive new bone formation (Involucrum).
• Pus & sequestra may drain to skin via sinuses.
Microscopic
• Chronic inflammatory cell infiltration.
• A cellular dead bone.
Clinically:
• Recurrent Flares of FAHM (fever, anorexia, headache, & Malaise) + local pain, & redness.
• Draining sinuses that may seal for weeks or months and reopen or sneak into another sinus.
• Sero-purulent discharge and excoriate the surrounding skin.
• Thickened puckered tissues which anchor to the underlying bone.
• Mal-united or non-united fractures after post-traumatic OM.
• Pathological fracture.
Cierney & Mader Classification and Treatment
Type Site Picture Treatment
Type I Medullary cortical de-roofing and medullary debridement
Type II Superficial shallow decortication back to bleeding bone
Type Localized saucerization and debridement
Type Diffuse infected area excised en-bloc and stabilised with ex-fix
Physiological subtypes:
• A Normal.
• B local and/or systemic compromization.
• C Surgically compromised.
Inv
vestigatio ons
R
Radiologi cal
1]. PXR:
[1
o Patchy bon ne density.
o Cavites & excavations
e s around immplants.
o Sequestra, involucra & cloacae.
o Deformed or non united bone.
2]. Sinogra
[2 am: it is a tra
aditional method
m to delineate the e sinus & alll its tracks ((rarely done
e nowadayys).
3]. CT: sho
[3 ows the exte ent of the sequestra
s & their full se
eparation.
4]. MRI: shows the ex
[4 xtent of the soft tissue involvemen nt.
99m
[5
5]. Tc HDP
H scans are a +ve in blood b and bone
b phase es.
67
[6
6]. Ga & 111In scans are useful to delineate the hidde en infection
n sites.
L
Laborator ry
7]. y ESR & WBC are important prognostic parameterrs.
[7
8]. y ASOT
[8 T.
9]. Pus C/S
[9 S.
Tre
eatment:
1. AB
A
• Bacteric cidal.
• Good bioavailabili
b ity to bone..
• Broad spectrum;
s a
although it seldom com mbat the in nfection aloone.
• Fucidic,, cephalosp porins, & clindamycin are a good exxamples.
2. Local trea atment
• Sinus dressing.
• Abscess draining.
• Colosto omy paste forf skin exco oriation.
3. Surgical debridem
d ment:
Indication ns:
• Sequestrum separration.
• Clear picture.
Techniqu ue:
[1]. Irrigatio
on sucktion n:
o Sulphan blue stains th he living tisssue.
o Methylene e blue stainss the dead tissue.
t
o Application n of double e lumen tub be.
o AB solution n is instilledd in /4hr & drained
d outt before the e next instilllation.
o Continue till t the effluxx is sterile (3 3-6 wk)
[2]. Debride ement + se eptopal bea ads to be drrawn out affter 2wks (o or solmycin sheat)
[3]. Papinea au excision n & packing technique e.
[4]. Excisionn + closure of dead space by:
o Ilizarov seg gment transsfer.
o Cancellouss graft.
o Fibular gra aft.
o Vascularize ed graft.
o Flaps.
4. A
Amputattion
• For helpless functiionless prob
blematic recurrent infe
ections.
• For Cierney-Made er type C hoosts.
Closure of dead spaces:
1. Local flaps
2. Free flap transfer
• Up to 40 % failure when these are used for chronic osteomyelitis
3. Open cancellous grafting – Papineau technique
• Useful for bone deficiencies of less than 4cm
• Labour intensive
4. Vascularised bone graft
• Heals as a segmental fracture.
• Indicated when defect is > 6cm.
• Iliac crest for defects > 8cm.
• Fibula 6-35cm can be bridged.
5. Bypass graft
• Involves the establishment of a cross union between the fibula and tibia proximally and
distally to the defect which has been debrided and bone grafted
6. Ilizarov technique
• Acute shortening of the area debrided and the stabilised with ring fixator
• Coticotomies then performed either above or below Æ distraction to correct length
7. Amputation: should always be considered especially early in the type "C" host
Seeptic arthrritis
Aettiology:
O
Organism m:
• Staph aureus
a common nest.
• H influeenza infants.
• Gonoco occi adults.
• Strept
• E. coli sometime es
• Proteuss
R
Route:
• Hemato ogenous sppread is thee usual wayy to settle th
he organism
m in the syn
novial mem
mbrane.
• Direct inoculation via penetra ating wounnd.
• Direct spread
s from
m nearby infection.
P
Predispos sing Facto ors:
• RA.
• Drug abuse.
• Mal nuttrition.
• Debilitaating diseasses.
• Immun ne suppression (AIDS, drugs).
d
Patthology:
Inflamm
mation S
Suppuraion
n Ne
ecrosis Spread
d Healing
1. Inflamma ation
• Usually y the organism settles ini the synovium by he ematogeno ous spread
• Acute inflammatio on, swellingg, and exud dation of the synovium m.
2. Suppurattion
• Second dary to immmune reactio on and dea ath of the innflammatorry cells.
• Purulen nt or sero-p
purulent disccharge.
• Increases the toxa aemia & pre essure inside e the joint.
3. Necrosis
• Articulaar cartilage necrosis du ue to (toxaeemia, throm mbosis, y pressure, bacct. & synovvial enzymess).
• Articulaar cartilage erosion.
• Massive e epiphysea al damage:
o In infants with
w entire cartilaginou
c us epiphysiss.
No
o In toddlers 2ry to vasc cular occlussion. d
destruction
o In adults 2rry to severe e & extensivve affectionn of the bon ne. =
Resolution
4. Spread
• If the in
nfection is not
n treated it will sprea ad to:
o Nearby tisssues.
o Skin (absce esses or sinuuses). Bone & Joint Minimal
destructtion H
Healing destruction
5. Healing = Deformmity = Fibrosis
• May en nd into:
o Complete resolution.
r
o Partial loss of articularr cartilage Æ fibroosis.
o Destruction n of articula
ar cartilage Æ ankyylosis. Marked
cartilage
o Destruction n of the bone Æ jointt deformity.. d
destruction
=
Ankylosis
A
ns]
Clin
nically: acccording to o age
Infants:
• Irritabiliity & refusal of feedingg.
• Some tiimes: fever & tachycarrdia.
• Locally:: warm & te ender.
• Exclude e omphalitiis & phlebitis 2ry to IV infusion.
C
Children:
• Acute pain
p in a larrge joint (ussually the hip).
h
• Genera al illness (FA
AHM): Feve er, Anorexia
a, Headache e, Malaise.
• Local: (P SHIRT): Pa ain, Swellinng, Hotness,, Inability to
o move, Red dness, Tend
derness (tre
emendous)..
• Pseudo o-paresis (coompletely abolished
a m
movement).
• Exclude e septic toee, boil, or otiitis.
A
Adult
• Acute pain
p in a su uperficial joint (knee, wrist,
w ankle).
• P SHIRT T.
• Exclude e gonococccal infection n, drug abu
use, steroid intake, or immmune-sup ppression.
Moorrey criteeria for dx x of septic c arthritiss: (PEUGOT).
[1]. Pain y with motio on.
2]. Edema
[2 a & swelling g.
3]. Unexpllainable by other causses.
[3
4]. Good AB
[4 A response.
5]. Other generalized
[5 g d picture.
6]. Tempra
[6 ature > 38.5 5°C.
Inv
vestigatio ons
[1]. PXR:
o Soft tissue shadow.
s
o ± subluxatiion.
o Joint space e:
y early.
e
z Late.
L
2]. US: sho
[2 ows fluid co
ollection inside the joinnt.
3]. y WBC
[3 C & ESR & CRP.
C
4]. +ve blo
[4 ood culture..
5]. Aspiration of the jo
[5 oint fluid & examinatio on:
o Bacteriolog gy / Culture e & sensitiviity.
o Chemical.
o Cytologic: WBC
W & malignant cellls.
Tre
eatment:
[1]. Supportiv ve:
• Analge esics.
su
upportive
• Fluids.
[2]. Splintagee:
• Splint.
• POP. Septic
S
Splintage Drain
• Traction n. A
Arthritis
[3]. AB:
• Infant acillin + Fusiidic IV 1wk. Æ PO 3 wks.
Flucloxa w
• Child Ampicillin or new cephalospo
c orin. AB
[4]. Drainage e:
1- Earlyy aspiration
(éin 3dayys may be of a
v
value
ponse Æ ope
If no resp en
dra
ainage
2-Ope
en drainage
Irrigation suction 3 days

ecially in
espe
Infant Hip Thick pus
3-Knee arthhroscopic waash

is of the
e same value
e
Articular carrtilage is Articu e is not

ular cartilage
rescue ed rescued
Immo
obilization till
t bony
ehabilitation and ROM
Re
ankylosis
Tuberculosis
Organism:
• Red acid-alcohol fast obligatory INTRACELLULAR Mycobacterium tuberculosis bacilli.
Pathology:
1- 1ry lesion:
Site:
Lung ▪ Pharynx ▪ Gut
Changes:
Local inflammatory focus Æ Lymphangitis Æ Lymphadenitis
Seculae:
TB bacilli remain dormant in LN
Body is sensitized to toxins
2- 2ry lesion: spread to
a. Lung Æ military TB
b. Meninges: Æ TB meningitis
c. Other tissues
3- 3ry lesions (10% affect the musculoskeletal system)
a. Tuberculoma formation:
Central caseation necrosis
Surrounded by epithelioid cells, Langerhans giant cells, lymphocytes
They tend to coalesce to form a wide area of caseation necrosis
Dead bone and caseation is retained in the centre
Spread to cartilage Æ destruction and spread to joint space
b. Synovitis
Synovium is thickened
Marked effusion rich in cells
Granulomatous pannus may form & creaps on the cartilage & bone
Cartilage erosion (gradually)
Bone erosion peripherally at the synovial reflection
Juxta articular osteopenia ð hyperaemia
If secondary infection occurs Æ rapid destruction
c. Cold abscess formation:
Caseation spread via soft tissue planes.
May burst to skin to form a sinus.
May collect at a distant site far from the original pathology e.g lumbar TB Æ
groin.
4- Healing:
a. Resolution.
b. Ankylosis.
c. Dormant bacilli.
Clinically:
• General:
Night sweat, night fever.
Loss of weight, loss of appetite.
• Local:
Night Cries: joint is splinted at day time by spastic ms ⎯⎯⎯→ spasm is relieved Æ
AtNight
stretch or compression of the damaged tissue Æ pain.

Marked muscle wasting.
Marked synovial thickening.
z ROM & stiffness.
Joint deformity.
Spine: pain, abscess kyphosis, neurological manifestation.
PXR
R:
}
Juxta Articcular Osteeopenia Æ washed out o bone ends.
e
Narrow jo en epiphysiis y 2ry to hyperaem
oint space (in childre mia). Pheemister Tria
ad
Peripheral bone ero osion and cystic
c subcchondral le esions.
No periostteal reactio
on.
Spine erossion, collap
pse, parasppinal absceess calcifica
ation & kyp
phosis é cro
owded relaated
ribs Æ Sunn Ray Appe earance.
Hip erosio
ons occur in 3 areas (Babcock k’s Δ); erosion of the superior acetabulum
a mÆ
Wanderin ng Acetabulum.
y Knosta am angle in n kyphotic pott’s dise
ease of the spine.
Inv
vestigatio
on
B
Blood:
1. yESR
2. Leucopenia é relative e lymphoccytosis
3. z Lympho ocyte/monocyte ratio o≈1
Immunolo ogical:
1- +ve PCR
2- +ve Manto oux test
A
Aspirate f
fluid:
1- Physical: ......................... z viscosity
2- Chemical: ..................... y ptn / zglucose / poor mucin clot
3- Bacteriolog gical: ........... Red acid-alcohol fast INTRACELLULAR bacilli é ZEAL NELSEN . 20%
4- n: ................... LOWENSTEIN JENSEN media or Dorset egg .................................... 80%
Cultivation
Con ncentrated centrifuged c d decontaminated samp
ple (Petroff method)
Kee ep 35º for 6 wk
5- Organismss also FLUORESCE WITH AURAMINE staining
6- Guinea pig g inoculation
B
Biopsy:
• Granulo
omatous rea action (case
eation + Lan
ngerhans + epitheliod + lymphocyytes)
• Charactteristic evide
ence of a de
elayed hypeersensitivityy reaction
• TB tend
d to give ne egative resu ults
S
Skin tests
• Delayed d hypersen nsitivity reacction used to t diagnose e tuberculo osis
• The two common nest tests are e the Mantoux and He eaf test
• Manto oux test:
• 0.1 ml of purified
p pro otein deriva ative is inje
ected intrad dermally
• +ve if ..................................................... > 5 mm papule
p at 72
7 hours
• Heaf test
• PPD is inoc culated intto the skin using a gu un to produ uce multip
ple puncturres
• +ve if ..................................................... > 4 papu
ules at puncture sites at 72 hours
• Positive
e skin test arre indicativve of active infection i orr previous BCG
B vaccin
nation
Treatment
• Rest ................................................................... (in Acute stage):
Bed rest + Splintage and traction to prevent ms spasm and deformity.
Maintained till:
1- Clinically: No fever, no wt loss, no spasm.
2- PXR: y calcification.
3- Lab: z ESR, y lymph/monocyte ratio >5.
Then motion is encouraged é the orthosis on 18mo ⎯⎯⎯→ gradual weaning
Then

& if pain & spasm return Æ resume orthosis.
• Chemotherapy:
RIPES - Rifampicin, Isoniazid, Pyrazinamide, Ethambutol, Spectinomycin.
Rifampicin + Isoniazid 6-8 mo.
Ethambutol (or pyrazinamide) for the initial 8wk.
Streptomycin is toxic.
• Operative:
Drainge of a TB focus is seldom done nowadays.
Cold abscess calls for urgent drainage.
Painful destroyed joint arthrodesis.
Painful destroyed joint arthroplasty.
Spinal TB open drainage, debridement, PSF, and BG.

Brucellosis
Epidemiology
• Although non usual infection, but it is very important to keep in mind as it occurs every now and
then.
• Common in Mediterranean countries.
Aetiology
• Gram –ve intra-cellular cocco-bacilli; 3 types can affect humans:
[1]. Brucella melitensis ............. from humans.
[2]. Brucella abortus ................ from cattle.
[3]. Brucella suis ......................... from pigs.
• Route of infection:
[1]. Drinking unpasteurized milk.
[2]. Contact with infected meat.
Pathology
• Organism enters the body with infected milk or through skin or mucosal surfaces.
• It travels via lymphatics Æ then blood to infect distant organs.
Sites:
• Vertebral bodies.
• Synovium of big joints.
Macroscopic:
• Chronic granulomatous lesions
• Destruction of bone and cartilage.
• Abscess formation.
Microscopic:
• Round cell infiltration.
• Giant cells.
• Central necrosis & caseation.
Clinically
General:
• FAHM.
• Undulant Fever may occur (fluctuating).
Local:
• Back aches & joint pains.
• P SHIRT.
Investigations
• PXR:
o z Joint space.
o Bone erosion.
o Juxta-articular osteopenia.
o Vertebral destruction of adjacent bodies, with stepping appearance of the body.
• IHAT (Indirect Hemo-Agglutinin Test).
• Brucellin skin test.
DDx:
• TB by serology & biopsy.
Treatment
• Tetracycline and streptomycin for 3-4 wks.
• Rifampicin.
• New cephalosporins.
• Surgical drainage and debridement of abscesses and infected tissues.
• Arthrodesis & arthroplasty may be necessary some times.
ns]
Sy
yphiliis
Epiidemiolog gy
• Once was
w a comm mon disease e.
• Now sp pirochaetal infections area rare.
• But, syp
philitic bone e affection still could be
b found in some partss of the wo orld.
Aettiology
• Trepon nema pallidu um is a frag
gile spiral ba acterium.
• Survivee only brieflyy outside off the body
• Transmmission almo ost always requires
r dirrect contactt with the in
nfectious le
esions.
• Route of
o infection:
o Direct conttact with in nfectious lession.
o Sexually tra ansmitted disease.
d
o Vertical tra ansmission (via
( the placcental bloo od barrier).
Patthology
• Penetraates abrade ed skin or in ntact muco ous membra anes easily Æ bl. vesse els
and lym
mphatics.
• Acute immune ressponse Æ endarteritis
e and periarteritis.
• Chronic c infection Æ granulomatous lesiions called gummas.
Congenitaal syphilis
• Child is ill and irrita
able.
• HSM.
• Pseudo oparalysis due to pain & swelling.
• +ve serrological tessts.
• PXR:
o Periostitis with
w onion peel.
o Metaphysittis with trabbecular erosions.
o Bone destrruction.
Primary S
Syphilis
• 2-6 wk usually afte er sexual coontact with an infectedd person.
Chancre” appears
• Painlesss infectiouss red sore “C a on the genita als
• May apppear on mouth or recctal area acccording to the contactt type.
• y LN.
• Withouut treatmen nt, the channcre heals affter 4-6 wkss, leaving a thin scar.
Secondary y Syphilis
• 2-10 wk ks after the
e chancre heals.
• T pallidum spread d via blood Æ rash “Grreat Pox”..
• Gray orr white warrt-like patch hes of skin called
c “Con ndylomata a Lata”.
• FAHM.
• In this stage,
s syphiilis may affe
ect the liverr, kidneys, eyes
e or men ninges.
• With tttt syphilis wiill go away.. But without treatmen nt Æ 3ry syyphilis.
Late (Terttiary) Syphhilis
• Multiplee granulommatous desttructive punnched out lesions
l “Guumma”.
• Affect the
t eyes, larrge blood vessels,
v heart, bones, CNS.
C
• Bone gummata
g are surrounded by NB BF (New bo one formatiion) & sclerrosis
Æ mayy affect the entire
e tibia Æ “Sabre Tibia”
• Neurossyphilis (CNNS infection n): memoryy loss, tabe
es dorsalis, blindness, and
impote
ence.
Investigations:
• T pallidum cannot be cultivated in vitro and is too small to be seen under the light microscope.
• Therefore, direct visualization of the organism by:
o Darkfield microscopy (difficult but specific).
o Immunofluorescent staining:
TPIT (T Pallidum Immobilization Test).
o Serologic tests (sensitive but not specific):
VDRL (Venerial Disease Research Laboratory).
RPR (Rapid plasma reagent).
TPHA (T Pallidum HemAgglutination).
FTA-ABS (Fluorescent Treponemal Antibody ABSorption) .
MHA-TP (Micro-Hemo-Agglutination assay for T pallidum).
• The last two tests are specific T pallidum tests (not done for screening).
• False-positive results may result, and no one test alone should be relied upon.
Treatment
• Penicillin G benzathine synthesis of cell wall:
o Adult Dose:
Disease for <1 year: 2.4 million U IM once in 2 injection sites
Disease for >1 year: 2.4 million U in 2 injection sites weekly for 3 doses
o Pediatric Dose:
Disease for <1 year: 50,000 U/kg IM once (max. 2.4 million U/dose).
Disease for >1 year: 50,000 U/kg IM weekly for 3 doses (max. 2.4 million U/dose).
• Doxycycline (Vibramycin) – binds 30S ribosomal subunit protein synthesis Æ growth.
o Adult Dose300 mg/d PO in divided doses for 10 d
• Tetracyclin.
• Erythromycin.
ns]
Hydatiid dissease
Epiidemiolog gy
• Commo on among sheep farm mers.
• Bone le esions are ra are.
• Live cyc cle is comp plicated as shown; and the man n act as an intermedia ate host if he
h ingests food
f
contamminated by the t worm ova o or segm ments.
• When reach
r the GIT
G it hatche es and larva
ae travels via
v portal cirrculation.
• When reach
r the liver or otheer organs thhey grow an nd produce e cysts with
h scolices.
• When these
t organ ns are eaten n by caninees (dogs) th
hey give another gene eration of ta
ape worm.
Aettiology
• Cause byb a Cestod de worm (ta ape worm) Echinococccus granulosus.
• Route ofo infestatio on: faeco-orral.
Patthology
S
Sites:
• Vertebrrae. • Femurr.
• Pelvis. • Ribs.
M
Macroscop pic:
• Bone cy ystic lesion..
• May cause patholo ogical fractture.
• Hydatic c cyst with scolices
s are
e seen.
Clin
nically
• Farmerr with cattle e contact.
• Pain & swelling.
s
• Patholo ogical fractu ure.
• Spinal compressio
c on.
Inv
vestigatio ons:
• PXR:
o Cystic lesion with mod derate expa ansion of th
he cortices.
o Vertebral destruction
d may involvves adjacen nt vertebrae
e.
• Casoni’s complem ment fixatio on test.
Tre
eatment
• Albend dazole 6 cou urses (wks each)
e + Pra
aziquantel.
• Curette e + hypertonic saline irrrigation + BG.B
• ORIF if pathologic cal fracture.
Fungal Infections
Epidemiology
• More common in North Africa and India.
• Usually bone and joint infections are uncommon except in immunocompromized patients.
Aetiology
• Superficial mycoses:
o Maduromycoses.
o Candida albicans.
o Actinomyces israelii (actually are anaerobic bacilli with fungus like appearance)
• Deep mycoses:
o Blastomyces.
o Histoplasma.
o Coccidiodes.
o Cryptococcus.
o Aspergillus.
• Occur mainly in immune-compromized.
Different Fungal infections
Maduromycosis Candidiasis Actinomycosis Deep Mycosis

Etiology Maduromucoses. Candida albicans. Actinomyces Israelii -Histoplasmosis.
Enters via foot cut. Immunocompromized anerobic gram –ve -Blastomycosis.
bacilli. -Coccidioidomycosis.
Epidemiology Invade via sc tissue & Normal commensal ώ Rare Rare.
tendons to reach bone. rarely causes deep Mandible More in immune
infections in HIV Pelvis & vertebrae. compromized patients.
Pathology Organism invade via sc Direct contamination. Infection occurs by -Large joint arthritis.
tissue & tendon Æ sc direct infection. -Unusual site
nodule Æ discharging 1st affect soft tissues osteomyelitis.
sinus. then bone.
CP Early: nodule. Osteomyelitis or -Firm Tender abscess. -AIDS
Late: discharging sinus. arthritis. -Discharging sinuses. -Arthritis & OM.
PXR -bone cavities. -Periosteal reaction. -Cystic bone lesion.
-bone destruction. -Bone destruction.
Investigation Organism is isolated Sampling & culture. -Anaerobic cultivation -Special biological
from the discharge. from sinus discharge. investigations.
ttt -IV amphotericin B. Same -Penicillin G. -IV amphotericin B.
-Debridement. -Tetracycline. -Debridement.
-Erythromycin.
For several months.

ϢϴΣήϟ΍ ϦϤΣήϟ΍ Ϳ΍ ϢδΑ
AIN SHAMS UNIVERSITY
Bone Tumors
Dr Mohamed Sobhy
Quick Guide
• Bone Tumor Diagnosis
• Different Bone Tumors
• Tumor Like Conditions
• Soft Tissue Tumors

[Orthopedic Onchology] Page | 261
Tumour Principles
ENNEKING CLASSIFICATION FOR MALIGNANT TUMORS: based on
STAGE GRADE (G) SITE (T) METASTASES (M)
I A Low(G1) Intracompartmental(T1) None(M0)
B Low(G1) Extracompartmental(T2) None(M0)
II A High(G2) Intracompartmental(T1) None(M0)
B High(G2) Extracompartmental(T2) None(M0)
III Any Any Yes(M1)
G0 Histologically benign (well differentiated and z cell / matrix ratio)

1 LG malignant (zmitoses, moderate differentiation, local spread & z metasases
2 HG malignancy (frequent mitoses, poorly differentiated); High risk of metasases
T0 Intracapsular
1 Intracompartmental (eg cortical bone, joint capsule or fascia)
2 Extracompartmental (spreads beyond fascial plane éout longitudinal containment)
M0 No evidence of regional or distant metastases
1 Regional or distant metastases evident
STAGING SYSTEM OF MUSCULOSKELETAL TUMOR SOCIETY (MTS) for benign tumors:

STAGE DESCRIPTION CRITERIA
I Inactive (latent) no pain no active growth Æ observation only
2 Active pain, disability, grow
3 Aggressive large, recurrent, actively growing, #
Features of aggressive tumours:

1]. Cellular atypia
2]. Frequent mitoses
3]. Hyperchromasia
4]. Extensive necrosis, vascularity, and hge
5]. Small amounts of immature matrix
LOW (G1) HIGH (G2)

Parosteal osteosarcoma classic osteosarcoma
LG medullary osteosarcoma radiation osteosarcoma
Giant Cell Tumour Paget's osteosarcoma
Secondary Chondrosarcoma Primary Chondrosarcoma
Fibrosarcoma Malignant Fibrous Histiocytoma
Myxoid Liposarcoma Pleomorphic Liposarcoma
Clear cell tumour of tendon sheath Neurofibrosarcoma (Shwannoma)
Chordoma Rhabdomyosarcoma
Adamantinoma Synovioma
Broder’s classification into

G 0...................................................................................... benign
G 1 .................................................................................... low malignant
G2 ...................................................................................... highly malignant
262 | Page [Orthopedic Onchology]
Site (T): anatomic setting of the lesion

Intracompartmental Extracompartmental
intraosseous soft tissue extension
intra-articular deep fascial extension
Intra-fascial compartments: Extra-fascial planes/spaces: (neurovascular
• ray of hand or foot containing spaces)
• posterior or anterior leg • mid & hind foot / mid hand
• ant, med, post thigh • popliteal fossa
• buttocks • Femoral triangle
• volar or dorsal forearm • intra-pelvic
• anterior or posterior arm • axilla
Tumour Workup
1. Thorough history taking: course, duration, pain, y in size, past tumors, surgeries
2. Clinical examination (age, sex, site and past history)
o Thyroid o Liver
o Breasts o Kidney
o Chest o Rectal (prostate & rectal tumours)
3. Bloods
o CBC & differential count
o ESR (often elevated)
o Biochemistry (Ca++, PO4, liver enzymes and Alkaline Phosphatase)
o Acid Phosphatase (prostate and increased with metastatic deposits)
o Thyroid function tests
o PSA
o Serum Protein Electrophoresis (Myeloma)
4. Urinalysis: e.g. Bence-Jones (myeloma), VMA neuroblastoma
5. Abdominal ultrasound
6. MRI Æ soft tissue extent and association with nerves and vessels
7. CXR
8. CT of lesion and chest (Æ staging)
9. Bone scan Æ other sites
10. Angiography Æ tumour blood supply and relationship to major vessels
11. PET: positron emission tomography unlike other modalities it utilizes radiation emitted from the
patient to develop images. Patient is given either 9F18 or 2 9F18 - deoxy-D-glucose (FDG), which
is similar to a natural glucose (+ radioactive 9F18 atom); so it is readily taken by active tissues
(tumors) for their metabolism. 9F18 emits positrons (+ve charged, electron counterpart)
produce γ rays when meet with electons. Gamma rays are detected by PET scanner
12. Biopsy
Diagnosis
1. AGE PREDILECTION
Benign Malignant Other
0 - 5yr 1. Eosinophilic Granuloma (EG) 1. laeukaemia 1. Osteomyelitis
2. (Unicameral bone cyst- rare) 2. Metast.Neuroblastoma 2. healing/ stress fracture
6-18yr 1. UBC 2. ABC 1. Ewings Sarcoma 1. Osteomyelitis
3. Chondroma 4. Blastomas 2. Osteosarcoma 2. Fibrous Dysplasia
5. Nonossifying fibroma 3. Osteofibrous Dysplasia
6. Chondromyxoidfibroma 7.EG
19-40y 1. Giant Cell Tumour 2.EG 1. Ewings Sarcoma
40+yrs 1. Metastases 1. Hyperparathyroidism
2. MM & Lymphoma 2. Osteomyelitis
3. osteo,chondro,fibrosarcoma 3. Paget's
2. NUMBER
Monostotic or polyostotic?
Skip & satellite lesions
3. SITE
VERTICAL: Metaphyseal – diaphyseal – epiphyseal
HORIZONTAL: central, eccentric, cortical, & juxta-cortical:
o Parosteal OS - no space bet lesion & cortex
o Exostoses - shares cortex é bone
4. TUMOR DESTRUCTION: Lytic, Sclerotic, Mixed
5. TUMOUR GROWTH (LODWICK CLASSIFICATION)
GI geographic: a-é well defined border & sclerosis
b-é well defined border
c-ill defined border & cortex penetration
GII moth-eaten: 2-5mm radiolucency =intermediate growth
GIII permeative: <1mm radiolucency =rapid growth é long or ill defined zone of transition
6. TUMOR MATRIX
Cartilage producing lesions ..... stippled calcification: POPCORN / RINGS & ARCS / FLOCCULENT
Osteoid mineralization ............. CLOUD Like Matrix 'SMOKE UP A CHIMNEY' / IVORY
Fibrous dysplasia ........................... Ground Glass appearance of fine spicules of dysplastic bone
7. EFFECT ON BONE: (Erosion, Expansion, Penetration, Trabeculation)
NB - describe lesion as AGGRESSIVE/NON-AGGRESSIVE NOT malignant/benign
Non aggressive:
1. Lobulated erosion ............. “S SCALLOPED Margin” e.g. Enchondromas
2. Trabeculation: ð................. 1- Displacement of residual trabeculae
2- Reactive NBF evoked by the near by tumor
Aggressive growth:
1. Progressive endosteal erosion ± periosteal reaction Æ Cortical Expansion
2. Cortex penetration Æ elevate periosteum Æ codman/sunray/hair on end/ onion peel
8. RESPONSE OF BONE = ZONE OF TRANSITION
HG spread too rapidly for the bone to respond Æ wide zone of transition
LG Æ bone has the time to react:
1. Sclerosis: é narrow zone of transition
2. thickened periosteal response
264 | Page [Orthoped ogy]
dic Oncholo
9. PERIOSTEAL REACTION:
• Continuous:
1- Solid osteoid
o ostteoma
2- Single lamella ABBC, GCT
3- Onion n Skin (Lam
mellated)
4- Spiculaated
• Interrupted
1- Buttress
2- Codma an angle
3- Lamelllated
4- Spiculaated
• Comple ex
• Divergent speculated: Sunb burst and Hair
H on end
d
10. SOFT TISSUE MASS: ussually deno

otes primarry lesions
Site Predilection
Behavior Grading
Grade Tyypical exam
mple
Bo
one Soft T
Tissue
Grade 1 NOOF Lipo
oma
Grade 2 (grow
w é capsule) AB
BC Anggiolipoma
Grade 3 (no ca
apsule) Gia
ant-cell tum
mor Agggressive fibro
omatosis
Malignant/low
w-grade Parosteal oste
eosarcoma Myxoid liposarccoma
Malignant/highh-grade Cla
assic osteosarcoma MFHH
Trabeculations
Lesiion Trabeccular Patterrn
Gian Cell Tummor Delicatte
ABCC Delicatte & horizoontal
Hemmangioma a Delicatte & vertica
al
Choondromyxo oid fibroma
a Coarsee
Nonn ossifying
g fibroma Lobulaated
RADIOLOGICAL FEATURES
PHEMISTER'S LAW = COMMONEST SITE OF INFECTION & TUMOURS IS ! FASTEST GROWING SITE OF ! LONG
BONE
To see a lucent lesion in bone, an estimated 30 - 50 % of the bone must first be lost
Features of Malignancy: Metaphyseal: Expand bone: Spinal Lesion:
1. size of lesion (small is • Simple (central) • Giant cell tumour - adults Î metastases /
good, big is bad) • FCD (eccentric) • ABC myeloma / hemangiomas
2. cortical destruction - young:
• Simple bone cyst
3. No sclerosis margin ▪ body: histiocytosis
4. Soft tissue mass ▪ arch: ABC /O.blastoma
osteoid osteoma.
-sacrum Î chordoma
osteoid osteoma Enchondroma- speckled Fibrous Dysplasia = a long Giant cell tumours nearly
looks as Brodie's abscess cyst, small bones lesion in a long bone always occur near a joint
Enchondroma, simple bone surface (in mature bone)
cyst & fibrous dysplasia
can look very similar
Cartilage tumours - have speckled calcification Lytic infection- mimics any Histiocytosis X (Eosinophilic
Chondroblastoma= Giant cell tumour of children. Only tr bone lesion. granuloma)- flat bones
arising in the epiphysis usually, commonest is skull
Chondromyxoid fibroma- older Pt., eccentric, speckled Hydatid- rural
Hyperparathyroidism- brown tumour, phalangeal erosions, sclerosis, subperiosteal bone resorption, osteitis fibrosa cystica
Certain bones in the body can be considered "epiphyseal equivalents" for purposes of differential diagnosis. These include the
patella, the calcaneus, and most apophyses. Therefore, for lucent lesions in these areas, one should include the classic
epiphyseal entities such as chondroblastoma (children), giant cell tumors (adults) and aneurysmal bone cysts.
Buzzwords:
Onion Peel .................................. Ewing Sarcoma
Popcorn balls .......................... Cartilage tumours
Smoke up a chimney ............ Medullary infarct
Scallops from without ............. Neurofibromatosis
Scallops from within ............. FD, NOF, SBC, enchond, CMF & chondrosarc
Fallen leaf .................................... SBC
Pencil in cup ............................... ABC
Blow-out ................................... ABC
Punched-out lesion ............... MM, EG
Permeative pattern ................ Round cell tumours
Moth-eaten .............................. Round cell tumours
Rat bite ....................................... Congenital syphilis
Bear bite ................................... Fibrosarcoma
Soap bubble ............................ GCT
Nidus .......................................... Osteoid osteoma
Sunburst spiculation ............. Osteosarcoma
Ground glass ........................... Fibrous dysplasia, enchondromas
Chinese letters ........................... Fibrous dysplasia
Sled runner tracks .................. Ollier's & Mafucci's
Gracile bones .......................... Osteogenesis imperfecta
Erlenmeyer flask ..................... Gaucher's disease
Salt &pepper skull .................. Paget's disease
Stress lines ................................ Paget's disease (on convex tension side of bone)
Looser's lines ........................... Rickets / osteomalacia (on compression side)
MRI FEATURES:
• Most tumours ............................................................ dark on T1 & bright on T2
• Desmoids, scars, fibrous & cortex....................... dark on both
• Lipomas, liposarcomas & haemangiomas are bright on T1 & T2
TUMOUR AGE ORIGIN ♂:♀ REMARKS

MM 5-6th decade Plasma cells 2:1 (black) COMMONEST 1RY MALIG
Ewing’s Sarcoma 2nd decade Endothelial element of BM Æ PNET 3rd common 1ry malignancy
RCS 5 -6th decade BM lymphoid cells ♂
Hodgkin 20-30 Lymphoid reticulum ♂
Lymphosarcoma 40-60 Lymphocytes ♂
Osteosarcoma 10-30 Bone forming mesenchyme 2nd Common 1ry malignancy
Osteoid Osteoma 10-30 Unknown Reactive lesion 2:1
Osteoblastoma 10-30 Unknown 2:1
Osteochondroma <20y Physeal herniation 3:1 Commonest Benign
MHE 3-12y AD & EXT 1&2 genes
Chondrosarcoma 30-60 Cartilage forming cells 2:1 4th common 1ry malignancy
Enchondroma 10-50 chondroblasts - Olier’s & Maffucci
Chondroblastoma 10-20 chondroblast=young GCT image 2:1
Chondromyxoid 10-30 Physeal remnants - Eccentric metaph
Fibrous dysplasia 10-30 GNAS 1 mutation Æ abnormal osteoblasts Chinese letters + shepherd
EG (BFH) Histiocytes
MFH Fibroblasts
Fibrosarcoma Fibroblasts
Desmoid <30y 2ry to add.magnus stress ♂ Rare
Giant cell Tumor Supporting cells of bone CT
ABC Aneurysmal malformation
Adamantinoma 10-40 Epithelial origin ♂ Rare & usually tibial
Chordoma 40-70 Remnants of notochord 2:1 5th common 1ry malignancy
CHRORNOSOMAL ABNORMALITIES
RB I GENE ........................................................ retinoblastoma and osteosarcoma
P53 tumour suppression gene .............. 50% of human tumours and nearly all types of sarcomas
NFL GENE .......................................................... neurofibrosarcomas neurofibromatosis, schwannoma
T(11;22):(q24:q12) translocation ..... Ewing’s sarcoma and PNETs
HAMARTOMA: Non-neoplastic disorganized proliferation of a tissue, could normally occur in that
place; e.g. hemangioma
CHORISTOMA: Non-neoplastic proliferation of a tissue, does not normally occur in that anatomical
place; submucosal osseous choristoma of the tongue
TERATOMA: Neoplastic proliferation of germ cells differentiate to form elements of all the 3
embryological layers - ectoderm. endoderm, and mesoderm; and may be benign or malignant
Giant Cells Are Found In: ABC NOF

1]. Giant Cell Tumor
2]. ABC
3]. Brown Tumors
4]. Chondroblastoma
5]. NOF
6]. Osteoblastoma
7]. Fibrous Dysplasia
LUCENT BONE LESIONS = FOG MACHINES
Fibrous Dysplasia
Osteoblastoma
Giant Cell Tumour
Metastasis/ Myeloma
Aneurysmal Bone Cyst
Chondroblastoma/ Chondromyxoid Fibroma
Hyperparathyroidism (brown tumour)
Infection
NOF
Eosinophilic Granuloma/ Enchondroma
Simple Bone Cyst
SCLEROTIC BONE LESIONS

• CONGENITAL
o Bone islands
o Osteopoikilosis
o Osteopetrosis
o Pyknodysostosis
• INFECTION
o chronic osteomyelitis
• TUMOR
o primary
osteoma
osteosarcoma
o metastatic: (prostate, breast, Oat cell lung carcinoma)
• ENDOCRINE/METABOLIC
o hyperparathyroidism
o Paget's disease
• VASCULAR
o hemangiomas
o infarct
• DRUGS
o Vitamin D
o fluoride
Radiological Investigations
Bone Scan
• Tc99m -HDP (Diphosphonates labelled é Technetium 99) has affinity for HA crystals layed down by
osteoblasts, i.e. it is a good indicator for the osteoblastic activity
• Tc99m -Sc (sulpher colloid labelled é Tc99) has affinity for phagocytes in the RAS in BM; i.e. it is a good
indicator for the vascularity of the BM
• Phases:
1]. Flow phase: .................................. immediately after injection, assess the vascular spread of Tc
2]. Blood pool phase: ...................... 30min, delineates the perfusion of Tc into the lesion
3]. Delayed static phase: ................ 3hr, delineates the accumulation of the Tc into the lesion
• Tc99m -HDP Pool phase is +ve for #, osteogenic tumors, infections, and sickle infarctions
• Tc99m -HDP Delayed phase is +ve for osteogenic tumors, sickle infarctions, OCD, & SONK
• Tc99m -Sc is +ve for infections & -ve for sickle infarctions (also SONK, OCD)
• Ga67 &WBC labelled by In111 & radiolabelled monoclonal antibody; all have affinity for inflammatory
reactions
CT Scans
1- For diagnosis:
o Size, site, extent
o Effect on bone & reaction of bone
o CT guided biopsy
2- For Staging
3- For treatment:
o CT guided interventional ablation and other procedures
o Assessment of therapy
Angiography
1- Preoperative:
i. Feeding vessels
ii. proximity to major vessels
iii. Displacement of vessels by tumour -> access for excision of the tumour
2- Treatment:
i. Embolisation of vascular tumour prior to surgery
ii. Intra-arterial chemotherapy
MRI
1- Intra-osseous extension ............................ T2
2- BM evaluation .............................................. T1
3- Skip metastasis ....................................... T2
4- Soft tissue extension .................................. T2
5- Neuro-vascular involvement .................. T2
6- Joint (epiphyseal) involvement ............. T2
7- Best technique to identify haemorrhage/oedema/inflammation- eg prior biopsy
8- Oedema ................................................... surrounds malignant & is unusual é benign tumours
PET: (Positron Emission Tomography)

• Unlike other modalities it utilizes radiation emitted from the patient to develop images.
• Positron is an elementary atomic structure; similar to electorns but é +ve charge, and tend to collide é
electron producing γ rays, and unlike the protons that they have no measurable size
9
• O15, C11, Br75, F18 all can emit positron, but F18 have the longest half life (2hours)
9 9
• 2 F18 - 2deoxy-D-glucose (FDG) is similar to a natural glucose (+ RA F18 atom); so it has affinity for
METABOLICALLY ACTIVE TISSUES (tumors) for their metabolism. 9F18 emits positrons produce γ rays
when collide with electons. Gamma rays are detected by PET scanner
Biopsy of Bone Tumours

Principles:
1. Should know probable diagnosis & stage before biopsy (it is the last step in pt staging)
2. Performed by the surgeon who will perform the definitive surgery (? biopsy -> frozen section ->
definitive surgery during the same anaesthetic)
3. Biopsy tract orientation & location is critical Æ included in the definitive surgery if malignant
4. Meticulous haemostasis to avoid tracking haematomas
5. Send samples for microbiological analysis
Open Biopsy
• Aim for excisional biopsy when possible esp. in benign lesions
• Incisional biopsy preferable in malignant lesions
• After consultation with the pathologist and radiologist
1. Longitudinal incision
2. Sharp dissection should proceed directly to the tr (via muscle not between muscle planes)
3. Uninvolved anatomic compartments should not be exposed
4. Avoid all major neurovascular structures to prevent contamination
5. Excise block of reactive tissue, pseudo capsule, capsule & tr block Æ formalin +/- frozen
6. Windows in bone should be as small as possible and oval to avoid stress risers and pathological
fracture
7. Release tourniquet prior to closure Æ haemostasis
8. Close with a subcut. stitch
9. Drains should come out through the wound
10. If proceed following biopsy Æ new instruments and drapes to stop seeding
Needle Biopsy
1. As for open biopsy
2. Place the biopsy tract where it can be excised
3. FINE NEEDLE BIOPSY:
o relies on cytological interpretation by an experienced pathologist
o accuracy = 65 to 95% (determined by the adequacy of the collected tissue sample)
o does not allow for immunohistochemical analysis
4. CORE NEEDLE BIOPSY:
o uses trocar cannula system, é outer sleeve closes over the trocar to grap ! tissue
o provides more tissue than FNAC and allows for immuno-histochemical analysis
o accuracy = 75 to 95%
o A/E of needle biopsy = tissue may be from necrotic part Æ not suitable for dx, or tissue
may be reactive Æ not representative of tumor Æ Frozen may be beneficial.
Frozen Section
1. Able to determine if specimen is adequate or representative
2. Can decide if lesion is inflammatory and needs culturing / need further investigations
3. Immediate diagnosis possible- can proceed to definitive surgery
SURGICAL PROCEDURES (Aim: remove the lesion é
minimal risk of local recurrence)
Limb Salvage
• Types of osseous resection
1. Inter calary (between joints)
2. Intra articular (one side of joint)
3. Extra articular (both sides of the joint)
• For details see later
Surgical Margins:
1. INTRA-LESIONAL
o Through the tumour & leaves
macroscopic tumour
o Not therapeutic
2. MARGINAL
o Via pseudo-capsule = reactive zone
(contains inflammatory cells, oedema,
satellites of tr)
o Controls non-invasive benign tr
o Recurrence of malignant tumours = 25-
50%
3. WIDE
o Around reactive zone, leaving a cuff of
normal tissue
o Skip lesions left
o 3-5 cm in low grade
o 5-7 cm in high grade
o Recurrence of malig tr < 10%
4. RADICAL
o Removal of entire compartment or
compartments
o Distant metastases left
5. AMPUTATION
o Should be thought of as a form of
reconstruction when function
outweighs preservation
ADJUVANT CHEMOTHERAPY
Nomenclature:
ADJUVANT" = chemotherapy given to ttt micrometastases
"A
NEOADJUVANT" = preoperative chemotherapy before resection of 1ry tumor.
"N
Neo-adjuvant chemotherapy
• = Staging Æ Chemotherapy Æ Restaging Æ Surgery Æ Tr kill rate Æ Further treatment
(change chemo or introduce radiotherapy as indicated)
• The aim is 90% kill rate and if < 90% Æ change agents
• Commence adjuvant treatment once the wound has healed
• May persist for 2 months to 2 years depending on the response
• Localized disease = 60-70% long-term disease-free survival
ADVANTAGES:
1].z tumor mass
2].z tumor vascularity prior to definitive surgery
3].Enables time for operative planning
4].Prognostic value; ≥ 90% kill rate good prognosis
ADVERSE EFFECTS:
1. Stunting of growth (catch up later)
2. Osteoporosis
3. AVN
4. Cisplatinum .......................... nephro & ototoxicity
5. Adriamycin .......................... cardiotoxicity
6. Vincristine ......................... Neurotoxicity
7. Chemotherapeutic induced malignancy usually blood forming eg leukaemias; also
cyclophosphamide Æ Ca bladder
Methotrexate
• Binds to dihydrofolate reductase and therefore blocks purine synthesis.
• Potentiates the effects of radiotherapy
• Citravorum factor "rescue" replenishes the folate pool
Adriamycin
• Cytotoxic antibiotic
• Also potentiates radiotherapy
RADIOTHERAPY
Mechanism Of Radiation
1]. Direct = absorption by complex molecules Æ RUPTURE OF CHEMICAL BONDS Æ lethal effects
2]. Indirect :
o IONISATION Æ y intracellular free radicals Æ DNA changes Æ z cell division & function. This
effect on cancer cells not ð rapid growth, but ð z capacity for recovery and repair as
normal tissues
o END ARTERITIS OBLITERANS of small blood vessels, on which tumor growth depends
o INDUCED INFLAMMATORY RESPONSE Æ destroy weakened cells by radiation
Factors affecting radiotherapy
1]. O2 .............................................................................. y sensitivity of cells up to a level (≈ atmospheric pressure);
above this level sensitivity does not increase appreciably (hypoxic tissue has decreased radio
sensitivity)
2]. MITOTIC ACTIVITY ................................................... y radiosensitivity
3]. UNDIFFERENTIATION ....................................... y radiosensitivity
Types:
1]. Extra-corporeal irradiation.
2]. Intraoperative irradiation.
3]. Brachi-radiation: iridium rods are passed into a previously inserted, plastic tubes into the
surgery field.
Advantages:
1]. z size of the tumour pre-operatively.
2]. z chance of seeding at the time of resection.
3]. If seeding Æz chance of viability of the shed cells.
Adverse effects:
1]. Erythema of skin and hyper pigmentation.
2]. Lymphoedema.
3]. Hair loss and skin flaking.
4]. Subcutaneous fibrosis.
5]. Muscle atrophy and fibrosis.
6]. Scoliosis may develop therefore include both sides of vertebrae.

7]. Joint stiffness and loss of function Æ physio.
8]. Children: premature fusion of growth plates.
9]. Irradiation induced sarcoma.
10]. Enteritis, diarrhoea, obstruction and bleeding.

11]. Cystitis and hepatitis.
Definitions
• Rad (radiation absorbed dose) is a measure of the energy imparted to the matter by ionising
radiation per unit mass (1 Rad = 100 erg/gram (0.01j/kg).
• Grays (Gr) = 1 joule of energy absorbed by a mass of 1kg (equivalent to 100rad).
[Myelogenic Tumors] Page | 273
`çxÄÉzxÇ|v gâÅÉÜá
(1) Ewing Sarcoma.
(2) Multiple Myeloma.
(3) Lymphosarcoma.
(4) Choloroma.
(5) Leukaemia.
Ewings Tumour
• It is a peripheral primitive neuroectodermal tumour
Incidence
• 5% of all primary malignant bone tumours
• 90% occur between 10 - 30 years old (reported 5/12 - 70 y)
• 2/3 less than 20 years
• Male : Female 3:2
Clinically
• 60% occur in long tubular bones (also pelvis ribs and
scapula)
• Considered a systemic disease
• Present with pain + limp. Pain is throbbing, worse at night
and often severe
• Patient may be ill and sometimes pyrexial
• May have a palpable lump, which is tender with an ill
defined edge
• Pathological fracture is rare
• 30% have metastatic deposits at presentation - Lung &
Lymph Nodes most common
Serology
• Anaemia
• Increased ESR & WCC
• Increased serum Alkaline Phosphatase
X-Rays
• "onion skin" periosteal reaction
• Rarefied area in medulla, but bone marrow infiltration is
often not obvious on plain x-ray
• Often the cortex is perforated
• Appearance varies widely
MRI
• MRI is essential to elucidate the soft tissue involvement
T1 - z intensity compared to the high intensity of BM
T2 - tumour is hyper intense compared to muscle
Bone Scan
• increased uptake
Pathology
• poorly demarcated and soft tissue extension common
• Macroscopically tissue is grey and brain like or red like red currant jelly if haemorrhagic
• Microscopically - homogenous population of densely packed small, round, neoplastic cells
with large oval hyperchromatic nuclei
• Cells may form a ring of 7-8 cells around a central area of necrosis= "rosette"
• Haemorrhage and necrosis are typically present
• Spread to distant sites via the blood and lymphatics (? multi centric from the onset)
Differential Diagnosis:
1]. Osteomyelitis is often the first diagnosis made
2]. Lymphoma (Reticulum cell sarcoma)
3]. Osteosarcoma
4]. Chondrosarcoma
5]. Neuroblastoma
6]. Metastatic Ca
Treatment
• Best results with combined therapy
• Relatively radio sensitive
• 12 wks induction chemotherapy with VAC (vincristine, actinomycin D & cyclo-
phosphamide) are used preoperatively Æ re-evaluate and restage -> surgical resection
• Wide surgical excision & limb salvage, usually.
• Radiotherapy Æ whole of bone
• Usually stop 2 - 4 weeks prior to surgery
Prognosis
• 50% 5 year survival (30-60% depending on the presence of metastatic disease at
presentation)
• 14% of long term survivors -> secondary tumours and 1 - 2% are malignant (eg leukaemia
or osteosarcoma)
• Young males and pelvic lesions -> worse prognosis.
• If less than 10% viable tumour after chemotherapy =80% cure ;If not =20-30% cure
Multiple Myeloma
Definition:
• MM is a malignant tumor of PLASMA CELLS that causes widespread osteolytic bone damage
• =plasma cell myeloma = plasmacytic myeloma = plasmacytoma = myelomatosis
• Cytogenetic: recently common ch.abnormality at Ig heavy chain switch region was found
Ætiology theoretical
• Chronic inflammatory diseases
• Herpes Virus 8 (HPV8)
• PDF: Asbestos, Benzene, Pesticides, Radiation of atomic bomb
Epidemiology:
• Commonest 1ry malignancy of bone > 40y (~ 40% of bone – 10% of blood – 1% of cancer)
• May affect any bone with haematopoietic red marrow (spine, skull, ribs, sternum and pelvis)
• Age 40-60 year
• ♂:♀=2:1
• Black:white people also 2:1
Pathogenesis:
• Plasma cells are the most mature form of B-lymphocytes i.e. they secrete mature IgGs
• That’s why the tr is characterized by overproduction of: Monoclonal IgG, IgA, and/or
light chains
• Sequelae depend on the site involved:
1. Skeletal:
MM produce osteoclastic activating factor
bone is destroyed and replaced by tr Æ pain & spinal cord compression & path#
2. Hematologic
BM infitraltion by tr Î neutopenia, anemia, thrombocytopenia (Pancytopenia)
Myeloid components interact é clotting factors Æ defective aggregation Æ
bleeding
3. Renal
Renal infiltration by plasma cells Æ myeloma, light chain nephropathy,
amyloidosis, glumerulosclerosis Æ hypercalcemia & hypercalcuria
4. Nervous:
Amyloid infiltration of nerves Æ radiculopathy, cord compression, skeletal
destruction
5. General
Hyper viscosity ð sludging of the myeloid infiltrates in capillaries
Purpura, retinal he, papilledema, coronary ischemia, CNS confusion or vertigo
Pathology:
SITE:
• flat bones are the commonest (site of red bone marrow) Æ skull/spine/sternum/ scapula/ribs
• rare below the level of elbow and knee
MACROSCOPIC
• Red-grey color é the appearance & consistency of “RASPBERRY CUSTARD”
• Surrounded by thin layer of cortical bone that show MULTIPLE INFARCTIONS
• No reactive bone formation
• Hge & cyst formation is common
• Path# is frequent
HISTOLOGY
• Biopsy reveals sheets of densely packed plasma cells
• Round or ovoid cells
• Nuclei are eccentric, é typical “CART WHEEL” appearance = CLOCK FACE nuclei
• The nuclear chromatin is sometimes broken and clumped beneath the nuclear membrane
• Basophilic cytoplasm é ccc clear area “HALO”
• The degree of cytological atypia of these cells has no prognostic value
• Osteolysis occurs ð y cytokines released by the plasma cells Æ ⊕ osteoclastic resorption
• Histological classification of MM:
1]. Plasma myeloma ......................................... Æ plasma cells
2]. Myelocytoma ................................................ Æ myeloblasts
3]. erythroblastoma .......................................... Æ Erythroblast
4]. lymphoctoma ............................................... Æ lympoblasts
TYPES:
1]. Multiple myeloma
2]. Solitary myeloma
3]. Diffuse myeloma (myelomatosis)
4]. chloroma: are type occurs in the skull; its cut section shows
green color ð pigment production that rapidly fades
Presentations
1- Those ð mass destroying bones and replace BM
2- Those ð excessive proteins
3- Those ð impaired kidney function
1- Due to Mass:
1]. Pain
insidious bone pain starts in back, thorax, pelvis & precedes PXR findings
Duration of symptoms before dx ~ 9 mo
ð lytic effect on bone: Cortex is eroded from inside & Cancellous bone is melted away
2]. Pathological fractures
The tumor may remain silent till this event
ð thining and weakness of cortical bone
3]. Neurological manifestation:
Compression fracture of a vertebra Æ nerve root injury
Sciatica is a common & sometimes initial symptom
4]. Anemia: ð extensive BM replacement
5]. Bleeding tendency: ð thrombocytopenia + interaction é clotting factors by m proteins
6]. Constitutional symptoms related to anaemia, thombocytopenia and renal failure
7]. Hypercalcemia: nausea, fatigue, thirst
2- Due to excess proteins:
• Total serum protein may reach 10 gm/dl or more
• Bacterial infections are common because of a lack of normal Ig production.
• Hyperviscosity: FAHM, bruising, presthesia, sluggish mentation
3- Due to Renal failure: 2ry to
1]. Toxic Bence Jones ptn 4]. BJ ptn deposition in DCT Æ internal hydronephrosis
2]. Nephrocalcinosis 5]. Renal ischemia ð y viscosity
3]. Amyloidosis
Investigations
• CBC:
Pancytopenia (normocytic normochromic anemia)
Bleeding tendency (thrombocytopenia-abnormal coagulation)
y ESR (>100 mm/hr)
y Reticulocytes & Rouleaux formation
• Chemistry:
y Ca, AlkPh
y creatinine
y s.uric
y LDH & β2microglobulins
y serum proteins: >10gm/dl é reversed A/G ratio (mainly in the globulin fraction)
• S.Protein Electro-Phoresis (SPEP)& high resolution SPEP Æ MONOCLONAL GAMMOPATHY
N/z alb
N α1 & α2 & β
y γGlobulin in monoclonal pattern (M-component > 30g/L is the minimal dx ccc)
Accumulation of light chain proteins found in 20% and execreted in urine BJP
• Immune fixation to determine the type of Ig:
60% IgG
20% IgA
1% IgD (IgM & IgE are rare)
• Urine:
y ca
z sp.gravity (RF)
Amyloid cast
BENCE JONES PROTEINS:
1]. Light chain subunits of γ globulins
2]. Detected by heating urine ⎯⎯→ ⎯ precipitate ⎯⎯→ ⎯ cleared (or HCL)
50º C 100 C
3]. If not detected Æ collect 24hr urine Æ UPEP or Immunoelectrophoresis

4]. It is not diagnostic and found in leukaemia and secondaries
Radiology
PXR Skeletal survey is the most sensitive; as Tc scan fail to show y uptake in 25%
• The characteristic appearance of MM:
Multiple, round, lytic, lesions
Lesions are “Punched Out”, well defined, variable in size, é no periosteal reaction
Generalized demineralization
• The characteristic appearance of single plasmacytoma:
Bubbly expansion of a single bone (rib or spine posterior arch)
Associated é soft tissue mass
MRI
• is useful for delineating spinal lesions & early cord compression
• low T1 & high T2 (related to muscle); and it is enhanced é the use of gadolinium
CT: Usually not needed in most of the patients; but it shows the extent of bony affection
Tc99m: Lesions are osteoclastic and not osteoblastic Æ COLD SPOTS
BM aspiration (sternal puncture)

• BM biopsy (CT guided) accounts for more accurate dx than BM aspiration
• y plasma cells: > 5% is suspicious Æ 10% is established diagnosis
Treatment Chemo + Radio ± Operation ± Drugs
• Radiotherapy
MM is Radio & chemosensitive, and reossification of tr defects may occur in months
Radiotherapy is recommended for intractable bone pain & <50% affection of bone
Initially there might be additional bone loss ð inflammation Æ NWB for 4-6 weeks
• Drugs: although MM is incurable many drugs were proposed to have a good effect
Interferon α2b + prednisolone Æ prolong disease free interval
Bisphosphonates: z pain, recurrence, hypercalcaemia.
• Chemotherapy
Melphalan/Prednisone (MP) is the standard ttt for MM since 60s
MP 4days Æ 4wks Æ MP these courses are repeated for a yearPalliative only
Recent combination Vincristine, Adriamycin, Dexamthazone (VAD) especially for relapse
Response to ttt & tumor burden are measured by M-component in serum or urine
(50% reduction is a good response)
• Surgery
Prophylactic IM nails for femoral, humeral deposits
ORIF of other pathological fractures IM nails ± MMA
spinal decompression for root compression or fracture
if joint is affected arthroplasty is thought about
Prognosis
• 3% only show complete cure
• Untreated, a patient will only survive an average of 6-12 mo usually from infection or hge
• Keys for prognosis:
Tumor burden
Proliferation rate
• Follow up of the treatment is by:
Monoclonal Ig
LDH & β2microglobulins z é ttt
• Poor prognosis é:
Tumor mass
Hypercalcemia
Bince Jones Proteins
Renal failure
• Multiple lesions - 5% 5YSR
MM Secondaries
distribution Symmetric Asymmetrical
common sites Skull, mandible, spine body These sites are rare
(≠arch)
predominant pattern Osteolytic Osteolytic or sclerotic
Morphology Will defines Ill defined
uniform Variable sizes
Bone Lymphoma
(Non-Hodgkin's) reticulum cell sarcoma
=osteolymphoma = histiocytic lymphoma of bone
Definition
• It is the 1ry malignancy of BM lymphoid cells. Although, 1ry lymphoma is potentially
curable & 2ries are fatal, both have the same cell type; but they are completely different in
behavior & also in ttt. Disseminated reticulum cell sarcoma is a generalized disease
affecting bone & other lymphoid tissues
• Criteria for diagnosis (definition):
Histologically proved to be Lymphoma
No other Lymphoid affection
Solitary or multi bone lesion ± regional LN
Ætiology
• viral agents and immunosuppressives are accused
• In immunosuppressed pt after transplantations and é AIDS
Epidemiology
• 3% of primary bone malignancy 5% of lymphomas
• 40-60 ♂ are common
• Most intraosseous lesions are non-Hodgkin's lymphoma
Pathology:
SITES:
• Long bones: femur / tibia / fibula / radius / ulna / metacarpals
• Flat bones: scapula (acromion) / ilium
• Irregular bones: patella / vertebrae / tarsal bones
LOCALIZATION:
• Metaphysio-Diaphyseal lesion
• Take at least ¼ the shaft of the bone
MACROSCOPIC
• Nothing characteristic; Pinkish grey mass
• Begins IM and erodes bone from éin to extend to soft tissues
• Sometimes erosion is slow giving the chance of periosteum to
lay down shell of bone Î cortical expansion
• Less necrosis than Ewing; but more pathological fracture
MICROSCOPIC:
• Larger pleomorphic cells (≠ small uniform cells in Ewing)
arranged in syncytial bands that are supported by primitive
reticulum
• Cell membrane is usually not seen or irregular é Pseudopods
• Cytoplasm:
smooth / granular / or basophilic
é a ratio to nuclear volume > 1:1
• Nucleus:
Large / hyperchromtic / reniform in mature tumor forms
frankly lobulated in younger cells (may appear as a
cluster of nuclei)
High mitotic figures (> Ewing)
Coarse irregular chromatin (may look like Ewing=fine and regular)
Nucleoli are evident
• No intracellular glycogen (≠ Ewing)
• +ve Argenophilia (+ve Special Silver Stain ≠ Ewing) ð reticulin fibrils
METASTASIS:
• Late metastasis unlike Ewing
• Mainly metastasize to LN > bone the opposite of the situation in Ewing
• Both kill by lung metastasis
STAGING:
• SI ....................................................................... one bone lesion ± soft tissue mass
• SII ...................................................................... Two lesions of the same side of the diaphragm
Or ................................................................. One lesion + regional LN
• SIII ............................................................................. Two lesions on both sides of the diaphragm
• SIV ..................................................................... BM or CNS affection
Clinically (slower than Ewing)
• 40-60 ♂
• 40 -50% occur around the knee
• Good General condition (wt loss and night fever < 10%)
• Pain: 60-100%
Gradual onset more at night
Dull aching
Precedes the swelling
• Swelling:
Tender swelling, hard in consistency
Smooth surface, and illdefined border
LN enlargement of and affected region
• Pathological fracture
More common and insidious than Ewing
• Hypercalcemia: especially in pediatric age group and associated é poor prognosis
X-Rays
• Reticulum Cell Sarcoma (RCS) does not affect less than ¼ of the bone (extensive erosion)
• Plain radiographs often underestimate the extent of the lesion
• Bone Destruction:
Irregular, small, multiple foci
Medullary origin and eventually erodes the cortex in an irregular manner
Tumor behavior:
1. Lytic: Moth-eaten or Permeative 65%
2. Mixed: 30%
3. Pure sclerotic: 5% (may be more common é Hodgkin)
Matrix has patchy opacifications ð reactive bone formation (indicate slow growth)
MOTTLED APPEARANCE: ð alternating areas of normal bone, lytic tumor, & new bone formation
Little periosteal reaction except late when cortex is eroded
• Soft tissue mass:
Early in flat bones; but late in long bones
Large shadow éout calcification
• Pathological fractures: not uncommon and occurs early in the disease
• Hodgkins disease Æ typical appearance of IVORY VERTEBRAE
DDx
Ewing’s MM
Osteosarcoma MFH or fibrosarcoma: arise from the fibrous elements of the
2ry endosteum, mainly IM extension, and saucerize the cortex late
Difference Ewing’s sarcoma Reticulum cell sarcoma
1- Incidence: More common Less than 1/2 as common as Ewing’s
2- Age: 5-15 40 - 60 y
3- Pathology:
A/ Site: Diaphyseal M&D. at least ¼ the bone is involved
B/ Macro. : Like brain matter, cheese or inspisated Not ccc: malig.destructive mass involving shaft &
pus (always mistaken é osteomyelitis) destroy cortex & extending to soft tissue
Necrotic lamellae Less necrosis.
Cl Micro.:
1) Cells Medium size Large
Uniform Pleomorphic
Contain glycogen glycogen
2) Cytoplasm / nuc vol 1 : 1 or 1 : 2 y
3) Mitotic figures z y
4) Special silver stain Rosette arrang. & éin center by sss, Reticulin fibrils by special silver stain (sss)
collagen fibrils are demonstrated
4- Clinically:
A) G. condit: BAD GOOD
B) Pain: severe Less severe
C) Path. Fr. z yy
5- X-ray; Much periosteal reaction Little periosteal react. But destructive &
some bone destruction expanding lesion
6- Prognosis: It is ! most lethal malign. Bone tumor About 30% can be cured by adequate radio
Mortality rate 95% even é early Dx & é correct early Dx
ttt Excellent results even after LN metastasis
It arises from BM very rapidly spreads It grows more slowly, metastasizes later
giving metast. by all means Radiosensitive more than other BM tumours
Investigations
• CBC & blood smears to rule out leukaemia
• y s.Ca
• y ESR
• y LDH
• Flow Cytometry studies: to detect CD markers of different lymphoma e.g. CD20 (Cluster of
Differentiation). It is simply a Ag-AB reaction (Ag is the CD marker in blood & the AB is
Fluorescent labeled) and the fluorescence is automatically detected by the flow device
• Cytogenetic studies: to detect ch.abnormalities (common in lymphomas)
BIOPSY:
• Is mandatory for definite diagnosis & taken By:
Open biopsy
Core biopsy
FNAC only to retrieve cells and do Flowcytometric and cytogenetic studies
• Studies to be done:
Histopathology
Immunohistochemistry
Immunophenotyping
Cytogenetic study
• Bone marrow aspirates
• CT
• Abdominal exploration -> splenectomy -> staging
Treatment (mainly medical)
• Chemo & radiotherapy are used in conjunction in most cases
• VAC-P (Vincristine, Adriamycin, Cyclophosphamide, Prednisone) for severalcycles
• Radiotherapy 40-60 Gy divided over several weeks (not used in children Æ Growth R)
• Other drugs as anti-CD20 AB is used for B-cell lymphomas
• BM transplantation is reserved for refractory cases
• Surgery: ORIF for pathological fractures; amputations are not done now after modern
trends in ttt
Prognosis
• Lymphoma of bone has the best prognosis of all primary malignant bone tumors
• 30% cure é correct early Dx
• 60% 5ysr é ttt
• Excellent results even after LN metastasis
• It grows more slowly, metastasizes later
• Radiosensitive more than other BM tumours
Other Lymphomas
• Hodgkin
• Lymphosarcoma
• Follicular lymphoma
• Lymphatic Leukemia
These tumors arise from

LN
Spleen
Intestinal Follicles
Liver
Skin
Thymus
In that order, and affect the BM reticulum as a part of generalized lymphoma, or may be 1ry
Hodgkin
Malignant granuloma of lymphoid reticulum
Affect bone as a part of generalized disease & boney lesions are the same as visceral ones
Pathology:
Commonest Boney sites to be affected:
Lumbar spine Skull
Pelvis ⎯⎯ ⎯ ⎯⎯→
TheSecondCommon Upper tibia
Upper femur Lower femur
Complex variety of cells: mainly inflammatory origin + reticulum hyperplasia
Epithelioid cells, histiocytes, lymphocytes, primitive reticulum cells.
Reed Sternberg cells:
Large, double nucleated cells
Chromatin is condensed on the nuclear membrane Æ penciled delineation of
nucleus
Nucleolus is large & pink staining
6 Histological types (The commonest is the granulomatous type)
y eosinophilic granulocytes
Plasma cells, lymphocytes, fibrosis
Survival is closely related to the type of the tumor:
1-2 Æ 8-16 y
3-4 Æ 5-10
5-6 Æ 1-8
Clinically:
20-30 y ♂
LN:
The earliest manifestation
Discrete, smooth, soft rubbery
Painless, mobile
Late they become hard
General:
Anemia
z wt
Bel Ebstein intermittent fever 15 d on & 15 d off
Abdomenal examination
HSM LN
Ascites
Boney affection:
Late to occur after the disease is manifested in other tissues
Dull aching pain & tenderness
Cord compression
PXR
1. Lumbar spine: body collapse (one or more bodies)
2. Pelvis & Skull: lytic areas surrounded by sclerosis
3. Ribs: Lytic areas é pathological # is pathognomonic
4. Long bones: -Destruction + marked NBF (look like COM or unicameral bone cyst)
-Pure destruction as lymphosarcoma
Investigations:
1. CBC:
a. Anemia
b. Leucocytosis or leucopenia + relative lymphocytosis
2. CXR:
a. Hilar LN
b. Pulmonary Hodgkins
3. Biopsy: is the main parameter for accurate diagnosis
Treatment
Radiosensitive: Deep X Ray therapy Æ z Pain & kill tumor
Amputation if failure to control the tumor
Lymphosarcoma
Very rare tumor of bone characterized by multiple bone affection if occur
Pathology:
• Site: vertebrae
• Extend diffusely in the medulla Æ erode the cortex
• Extend via Haversian canals subperiosteally to infiltrate soft tissues
• No NBF
Microscopic:
• Diffuse lymphocytic growth
• Reticular stroma
• No multinucleated cells
Clinically:
• Early pain
• Vertebrae are commonly affected Æ referred chest pain & LL pain
PXR:
• Lytic permeative lesions éout NBF
• Vertebral wedging
Treatment:
• Irradiation Æ z pain
• Death éin 3y
•
chloroma
It is a form of leukemia in ώ tissues contain green pigment ώ appear in cut sections
• Children near puberty are the commonly affected
• Rapidly fatal éin 5mo
• Affects LN, spleen & bones; skull Æ invade its structures esp.orbit Æ exophthalmos & lid edema
• Bones é red BM also invaded by the tumor ώ may extend to involve surrounding muscles &
tendons
Clinically, PXR, Microscopically: are the same as leukemia but:
Large atypical monocytes Mitotic figures
Primitive myeloblasts Hyperchromatic nuclei
Treatment: DXT
Leumkemia
• Is a condition characterized by malignant production of immature lymphocytes
(lymphoblastic) or polymorphs (myeloblastic); é resultant replacement of hemopoietic &
lymphoid tissues
• It occurs as acute or chronic forms ; the acute being common & predominantly in children
Clinically:
1]. Fever
2]. Anemia
3]. z wt
4]. HSM LN
5]. Bone affection (50%): pain & palpable masses in superficial bones (e.g. Ulna)
6]. Painful joints (synovial involvement)
7]. Rib pathological fracture
Pathologically:
• Diffuse replacement of BM by leukemic infiltrate
• Later erode cortex Æ periosteal NBF
• Types:
Lymphoblastic: commonly produce bone changes
Myeloblastic: short acute course Æ less boney changes
Aleukemic: commonest around the knee, shoulder; despite its very rapid course
Investigations:
• CBC:
Anemia
Thrombocytopenia
Lymphopenia or lymphocytosis
Immature WBC
PXR
1]. Diffuse osteoporosis
2]. punctuate rarefied cortical lesions Æ Ragged Appearance
3]. Transverse radiolucent line on the metaphyseal side of the physis (zendochondral
ossification)
4]. Lamellar periosteal NBF
5]. In chronic leukemia Æ osteosclerosis (otherwise Æ osteolysis)
Treatment:
• Irradiation is effective for pain relief (eventually loses its effect)
• Multiagent chemotherapy is the main ttt
Prognosis
• Chronic leukemia have longer survival
• Chronic leukemia in elders may remain inactive éout ttt for years
[Fibrous Tumors] Page | 287
Y|uÜÉâá gâÅÉÜá
o Fibrous Dysplasia
o Fibrous cortical defect & Non ossifying fibroma
o Fibrosarcoma
o MFH
o BFH (Eosinophilic Granuloma)
o Desmoplastic Fibroma
288 | Page [Fibrous Tumors]
Fibrous Dysplasia
Definition
• Non hereditary developmental disorder of bone forming mesenchyme (≠ actual tumor) é a
defective osteoblastic differentiation & maturation; é abnormal growth. Unknown ætiology
Incidence:
• EQUAL sex and racial occurrence
• REMAIN ASYMPTOMATIC: till 10y in Polyostotic & till 30y in Monostotic (10-30y)
Genetics & pathogensis:

• FD is caused by a MUTATION IN (GNAS 1) gene Æ abnormal Gsα (a protein ԅ enables hormones to
act on all cells) Æ cell acts as if the hormone is always present
• The mutation effect depends on:
o Type of embryonic cell affected
o № of tissues affected
o Time of occurrence during development; if early Æ Affect bones ± endocrinal glands
• Normally bone UMC (fibroblastic type) Æ preosteogenic Æ osteoblasts. In fibrous dysplasia Æ y
PREOSTEOGENIC cells & z osteoblasts ώ are abnormal:
o Immature rounded osteoblasts Æ immature bone trabeculae
o Less adherent ð: y versican, z osteopontin, z sialoprotein
o Does not respond to stresses Æ deformity
o Secretes more IL6 ώ Æ ْ osteoclasts Æ osteolysis
Pathology:
NEA:
Medulla is replaced by FIBROUS Tissue (PXR radiolucent é ground glass appearance)
Scattered TRABECULAE of woven bone
There are fluid filled CYSTS embedded in fibrous matrix
Microscopic::
WOVEN TRABECULAE: é CHINESE LITTERS appearance ԅ lack osteoblastic rimming (when
path # Æ reactive NBF é osteoblastic rimming + periosteal reaction)
CARTILAGENOUS small foci
FIBROUS stroma é spindle cells é oval nuclei & ill defined border
OSTEOCLASTIC GIANT CELLS
• 5 Types: (Monostotic, Polyostotic, Cheburism, Cranio-Facial, McCune-Albright)

1]. Monostotic: ............................................. 70%
o Sites: rib (30%)/ femur (25%)/tibia, craniofacial (20%)/humerus
o CP:
Pain
Pathological #
Less severe deformity than polyostotic
2]. Polyostotic: ............................................. 30%
o Sites: femur (90%), tibia (80%), pelvis (70%), ribs (60%), skull (50%), UL, spine, clavicle
o May be Monomelic, Unilateral, Bilateral
o CP:
Pain, limp, Pathological #, usually before age of 10
Femoral coxa vara + upper femoral bowing Æ Shepherd’s Crook Deformity
3]. Cherubism:
o AD
o Regress after adolescence
o Broad protruded jaws; both maxilla & mandible are symmetrically affected
4]. Craniofacial:
o May be part of monostotic, or polyostotic, or occur as an isolated form as in here
o In isolated form no other skeletal affection
o Commonest sites: FrontalÎ sphenoid Æ maxilla Æ ethmoid
o Less common: occiput and temporal
o CP:
Cranial asymmetry ............ facial deformity
Orbital affection: .................exophthalmos & blindness
Sphenoid & temporal: ......vestibular manifestation, vertigo, tinnitus, hearing loss
Cribriform plate: .............. anosmia, hyposmia
5]. McCune Albright $

o Polyostotic FD
o Precocious Puberty
o Endocrinopathy: ............................hyperparathyroidism, hypothyroidism
o Café au-lait patches .................. é jagged borders as Coast Of Maine
Clinically:
1]. Wide spectrum; from monostotic asymptomatic cases to polyostotic markedly deformed pts.
2]. Pain .....................................................................70%
3]. Deformities ......................................................by the age of 10y
4]. Pathological fractures
5]. Special presentation ............................... e.g. blindness, hearing loss…etc
PXR
1]. Long bones:
o Metaphyseal or diaphyseal LUCENT LESIONS (may extend to epiphysis after closure)
o Homogenous matrix é GROUND GLASS APPEARANCE
o Endosteal SCALLOPING
o Bone EXPANSION
o Femoral COXA VARA + upper femoral bowing Æ SHEPHERD’S CROOK
o ± Calcifications & endochondral NBF
o ± Premature closure of physis Æ ADULT DWARFISM
o Absent periosteal reaction
2]. Skull and facial bones:

a. Frontal bone > sphenoid and both are affected Æ sclerotic base
b. Obliteration of sphenoid and frontal sinuses
c. Lucent or sclerotic lesions in skull or facial bones may be seen
3]. Pelvis and ribs:

o Lytic lesions é Ground Glass appearance
o Cystic lesions are common
o Protrusio acetabuli is common Æ Kohler’s line, tear drop, Ranawat ∆
DDx
1]. Olier’s 5]. Hemangioma
2]. EG 6]. Osteitis fibrosa cystica (PTH)
3]. GCT 7]. NF: café au lait é smooth borders as Coast of California
4]. SBC 8]. Paget’s
MRI Æ fluid (≠ fibrous)
Tc Æ rim lesion (hot lesion all over)
Complications:
1. Malignant transformation:
0.4-1%
May take several years to develop
Commonest are: skull & facial lesions in monostotic / femur & facial in polyostotic
Osteosarcoma, fibrosarcoma are the commonest (chondrosarcoma is less)
PXR:
• Rapid y in size
• Change of the sclerotic lesion to be lytic
Clinically:
• y pain
• y size of soft tissue mass
2. Metabolic changes:
HYPOPHOSPHATEMIC RICKETS
OSTEOMALACIA
May be because FD secretes phophaturic hormone
T r ea t m en t:
Monostotic lesions are usually asymptomatic and needs no treatment
Indications for excision:
1. Severe or progressive deformity
2. Nonunion of a fracture
3. Femoral shaft fracture in an adult
4. Persistent pain
INTRALESIONAL EXCISION + BG (don’t use cancellous only; use STRUCTURAL BG)
Internal fixation has no effect on the disease but fix the weak bone
Multiple osteotomies to correct the deformities + IF
In expendable bones Æ enbloc excision
TUMOUR AGE ORIGIN ♂:♀ REMARKS

th
MM 5-6 decade Plasma cells 2:1 (black) COMMONEST 1RY MALIG
Ewing’s Sarcoma 2nd decade Endothelial element of BM Æ PNET 3rd common 1ry malignancy
RCS 5 -6th decade BM lymphoid cells ♂ Pleomorphic cells, large tr
Osteosarcoma 10-30 Bone forming mesenchyme 2nd Common 1ry malignancy
Osteoid Osteoma 10-30 Unknown Reactive lesion 2:1
Osteoblastoma 10-30 Unknown 2:1
Osteochondroma <20y Physeal herniation 3:1 Commonest Benign
MHE 3-12y AD & EXT 1&2 genes
Chondrosarcoma 30-60 Cartilage forming cells 2:1 4th common 1ry malignancy
Enchondroma 10-50 chondroblasts - Olier’s & Maffucci
Chondroblastoma 10-20 chondroblast=young GCT image 2:1
Chondromyxoid 10-30 Physeal remnants - Eccentric metaph
Fibrous dysplasia 10-30 GNAS 1 mutation Æ abnormal osteoblasts Chinese letters + shepherd
EG (BFH) Histiocytes
MFH Fibroblasts
Fibrosarcoma Fibroblasts
Desmoid <30y 2ry to add.magnus stress ♂ Rare
Giant cell Tumor Supporting cells of bone CT
ABC Aneurysmal malformation
Adamantinoma 10-40 Epithelial origin ♂ Rare & usually tibial
Chordoma 40-70 Remnants of notochord 2:1 5th common 1ry malignancy
Fibrous Cortical Defect

&Non-Ossifying Fibroma
Definition
Small painless cortical lesion with well defined festooned edge
Incidence
20% of benign bone tumours
♂>♀
Histology:
Small purely INTRA-CORTICAL lesion
Sometimes multiple
WHORLED fibrous tissue
Foam cells é cholesterol
GIANT CELLS
Clinically
Usually an incidental finding in children
PAINLESS
Most heal spontaneously
Larger ones may Æ pathological # (common presentation)
X-Rays
Intra-cortical lucent lesion in a long bone
Metaphyseal
Eccentric
SCALLOPED margin well defined and often sclerosed
1. MFH
2. EG
3. Osteosarcoma
4. Histiocytic lymphoma
5. Pyogenic osteomyelitis
Treatment
Most spontaneously resolve or move to the diaphysis of the bone with growth
Pathological fractures:
Usually heal with a normal amount of callus, but resolution of the fibroma may or
may not occur
Intracapsular curettage is usually sufficient to promote healing of lesion, however,
the defect may be supplemented with bone grafts +/- stabilisation
Jaffe-Campanacci syndrome:
Multiple FCDs
Cafe-au-lait spots
Mental retardation
Hypogonadism
Ocular & cardiovascular abnormalities.
Fibrosarcoma
• Rare tumor that may arise éin the medulla (central), or on
surface (periosteal)
• Differentiation is difficult bet. LG fibrosarcoma & the aggressive
benign tumors (desmoplastic fibroma & periosteal desmoid)
• Also the diff. bet. HG fibrosarcoma and osteosarcoma & MFH
Incidence
• 2% primary malignant bone tumours
• Middle age ♂
• But it occurs in any age and sex
Ætiology
• no definite cause
• Mutations and translocations are suspected
• 2ry fibrosarcomas (on top of other pathologies):
1]. VonRecklinghausen $
2]. FD
3]. Infarcts
4]. Paget’s
5]. Radiated bone
6]. OM
7]. Osteosynthis
Types:
Central (medullary)
Peripheral (periosteal)
Difference Central Peripheral
1- Incidence: 10% of 1ry bone malignancy Less frequent
2- Behavior Early destructive May encircle the whole bone (éout NBF)
3- Pathology:
A/ Site: Metaphyseal Origin from the fibrous layer of periosteum
Extracortical & firmly anchored to bone
B/ Macro. : Whitish grey (predominant collagen) Pale color (sometimes white and glistening)
LG is more white
HG is fast invader
Early cortical invasion Saucer shaped excavations ð pressure
Vascular necrosis
Some NBF Less vascular
No capsule No NBF (if bone formation Æ Parosteal)
Pseudo-capsule ð compressed surroundings
Both show areas of hge, necrosis, and cystic formation
Cl Micro.: Same as than of fibrosarcoma of the skin
1) Cells Fusiform cells or spindle cells Same
2) Whorly appearance Very evident fibrous whorls Less evident
3) Bone Trabeculae Wave through the tr substance Less bone formation
4- Clinically:
A) Principle complaint Pain Mass: mobile, lower femoral, steadily y size
B) Pain: severe Late after mass by years
C) Path. Fr. Common Less common
D) Metastasis Late Late
5- X-ray: Central lytic lesion Faintly outlined soft tissue shadow éout NBF
Cortex is penetrated Saucer shape depression
Periosteal NBF is evident Periosteal reaction at the periphery
Soft tissue mass after cortical invasion Soft tissue shadow is very important
Histopathological Grading:
Grade I: Grade II:
Collagen Abundant (Thinner Than Desmoid Tumor) Thin Collagen
Spindle Fibroblasts
Nucleus Hyperchromatic Nuclei Large Plump Irregular
Chromatin Coarse Uneven Clumped
Mitosis Few Many
Nucleoli May Be Prominent Large And Evident
Neoplasm Non Neoplasm
Metastatic carcinoma paget
multiple myeloma FCD NOF
MFH Reticulo-endotheliosis
Prognosis:
Fibrosarcoma recur rather than metastasize
Like parosteal OS & chondrosarcoma; tend to change their cytological ccc after surgery
10 YSR is 30% in primary FS; and < 10% in secondary FS
Treatment
LG Stage I Æ limb salvaging excision with wide margin
HG StageII Æ radical or wide margin é adjuvant chemoradiotherapy
Classically considered radio-resistant
May however be useful as adjuvant to surgery and chemotherapy
Useful for irradiation of lung secondary deposits not accessible to surgery
Malignant Fibrous Histiocytoma

Definition: malignant neoplasm of uncertain origin that arises both in soft tissue and bone
Incidence
• 5% of 1ry bone sarcomas
• Age: > 30 (often > 50)
• Male > Female
Ætiology and histiognesis:
• Cell of origin (controversial): histiocytic cell; fibroblasts; UMC
• 1ry .......................................................................80%
• 2ry .............................................................. 20% (FIPRO)
Pathology:
SITE:
• Around the knee .................................... 40%
• Metaphyseal
MACROSCOPICALLY:
• Discrete Greyish Rubbery tumour
• Irregular bony margins
MICROSCOPICALLY:
• Composed of a fibroblasts, myofibroblasts
• Large plump foamy histiocytes
• Storeiform pattern" (radiating)
The fibrous component is in a "S
SPREAD:
• To lung and bone ......................................via blood
CLASSIFICATION
1. Myxoid
2. Non Myxoid
Clinically
• Pain
• Swelling
• Path #
X-Rays
• Metaphyseal lytic lesion é MOTH EATEN appearance
• y SOFT TISSUE SHADOW
• Reactive NBF
• Little periosteal reaction
• Metastatic carcinoma
Treatment
• Surgery is the corner stone for almost all sarcomas
• Radical excision / Amputation or
• Radiotherapy
o if not amenable to resection
o adjuvant to z recurrence and survival
• y survival with neo adjuvant chemotherapy (doxorubicin, vincristine, methotrexate, T10)
Prognosis
• Better in young & initial procedure a wide or radical excision = more than 80% 4yr survival
Benign Fibrous Histiocytosis

Definition
It is the benign spectrum of Langerhan's cell histiocytosis,
characterized by single or multiple skeletal lesions in young age
Terminology:
Eosinophilic Granuloma (EG)
Histiocytosis X (the old name) = Langerhans cells histiocytosis
Xanthofibroma = Fibroxanthoma
Aetiology
Solitary EG is non-neoplastic reaction of RES histiocytes to
unknown stimulus
Accumulation of lipid metabolites in RES ⎯stored
⎯⎯ ⎯ in
→ histiocytes Æ
rupture Æ inflammatory granulomatous reaction Æ fibrosis.
Incidence
1 - 5% benign bone tumours, usually solitary
5-10 y ......................................................................80%
♂:♀ = 3:2
Pathology
SITES: ...................................................................... Any bone
Skull (common), spine, ribs, pelvis
Femur is the commonest long bone ... not below elbow & knee
Diaphyseal (≠ NOF)
NEA
Glistening reddish tissue with flecks of yellow
M IC
HISTIOCYTES: Pale / foamy / cholesterol filled
Langerhan's Cells: (Langerhans histiocytes)
Grooved or Coffee Bean shaped nucleus
Abundant pale cytoplasm
Well defined cytoplasmic borders
EM: Birbeck granule = Racquet-Shaped cytoplasmic inclusions /
Eosinophils, plasma cells, PNL & giant cells
Spindle Fibroblasts at the back ground
Bone Spicules at the periphery
No evidence of cartilage or bone matrix
SUB-TYPES:
1. Hand Schüller Christian disease
>3 y
Triad of Skull Lesion & Exophthalmos & Diabetes Insipidus ± visceral involvement
2. Letterer-Siwe disease
<3y
Characterized by more lymphomatous proliferation
liver, spleen, skin, CNS involvement
Rapidly fatal
look for recurrent bacteremia, diffuse LN & skin lesions
Clinically
Mostly asymptomatic
Pain
Mass
Pathological # (Rarely)
Special:
Pelvic lesion .....................................subtle hip pain ԅ y by movement
Spinal lesion ............................... dorsal scoliosis
X-Rays
DIAPHYSEAL ............................................... (≠ NOF metaphyseal)
Oval Mottled Lytic intramedullary defect
No Sclerotic rim ........................ (≠FD & NOF)
Erodes The Endosteum + bone expansion as it enlarges
Trabeculation: May appear loculated ð sparing of large trabeculae
Periosteal NBF ± Soft Tissue Mass
Skull, flat bones, and ribs
lesions appear PUNCHED OUT
Cortical SCALLOPING may occur
Spinal lesions:
Vertebra Plana
Dorsal Scoliosis
Sometimes appears as generalized OSTEOPOROSIS é no localized bone lesion
Tc99m Usually hot (but sometimes cold)

1. Ewing’s: .................................................... soft tissue mass, bad general condition, onion peel
2. NOF ........................................................... metaph, sclerosed scalloping, few foam, no eosinophills
3. FD ............................................................... large deforming, sclerosed rim, expansion, ground glass
4. ABC ............................................................ metaphyseal, expansion, MRI
5. Osteomyelitis .......................................... bad general condition, FAHM, y ESR, CRP
6. Lymphoma & Leukaemia
Treatment
Usually heal spontaneously and need no ttt
When large and symptomatic:
i. Intralesional excision + BG Æ disappointing Æ recurrence é more extensive lesion
ii. Wide excision + BG is recommended
iii. Steroids is another option and tends to result in rapid resolution
iv. Radiotherapy for aggressive or inaccessible lesions (500-1000 rads)
Prognosis
1]. Skeletal lesions only .....................................good prognosis
2]. Hand schuller christian ..............................excellent prognosis if there is no extra-osseous disease
3]. Letterer Siwe disease .................................worst prognosis often fatal in infancy
4]. Other prognostic factors:
o Soft tissue involvement ............. worse prognosis
o Rapid course .............................. worse prognosis
o Young age .................................. worse prognosis
o Liver involvement .................... 50% die
o Lung involvement ................... not fatal
o Anaemia ..................................... poor prognosis
Desmoplastic Fibroma
Definition
• Rare locally aggressive tumor that involve bone or soft tissue; but does not metastasize
• In femur it may be a reaction to muscle stress exerted by the adductor magnus
Epidemiology
• Extremely rare (less than 200 cases )
• <30y adults (≠ fibrosarcoma)
• ♂ = ♀ (Noted to be associated é pregnancy)
Pathology: Aggressive stage 3 lesion Æ aggressive local infiltration
SITE:
• Soft tissue involvement: abdomen, shoulder, and axilla (rare distally)
• Mandible, Femur, pelvis, tibia & fibula ........................ (in femur occur at the insertion of add magus)
• Metaphyseal or diaphyseal
MACROSCOPICALLY:
• Grayish white Whorled Rubbery tumor
• Cystic foci with clear fluid
MICROSCOPICALLY:
• Interlacing Thick Collagen bundles ........................ >10 μm (≠ FD & Fibrosarc)
• Fibroblasts é oval nuclei é no atypia .................... (≠ fibrosarc)
• No multinucleated giant cells nor foam cells ........... (≠ FD & NOF & fibrosrc)
Diagnosis:
Clinically::
o Pain is late
o Mass
o Path #
o Effusion in nearby joint
PXR::
• Central Metaphyseal lesion aligned é the long axis of bone
• Trabeculae Æ lobulated "SSoap-Bubbly" appearance
• Erodes the cortex + Sclerotic Margin + thin NBF
• Wide zone of transition
CT Demonstrate cortical breakthrough
DD :
FD NOF LG FIBROSARC MFH EG DESMOID
Age 10-30 Young 40-50y >30y 5-10y <30y
Site M-D (cortical) M-D M or peripheral M D M-D (central)
Cellularity z z y y z z
Mitotic z z y y z z
Pleomorphism y y y y y z
Polarized mic -Thin -Few foam -Thin -Storiform -Foam Thick Lamellar
-Chinese letter -GC -Atypia -Langerhan’s
-Eosinophils
PXR -Sclerosed -Sclerosed -Periosteal NBF -Moth eaten -Nonsclerosed -Sclerotic
-Ground glass -Scalloping -Saucer -Soft shadow -Scalloping -Soap bubbly
Treatment ±curette + strut ±curette + BG Wide or radical Wide ±Wide Wide
Treatment:
1]. Enneking recommended Wide Excision as the method of choice
2]. Intralesional Curettage + BG ± adjuvants (Phenol/Cryotherapy) if care for function
NB: GARDNER SYNDROME: Desmoid tumors + osteomas + epidermal cysts + colonic polypi

[Osteogenic Tumors] Page | 299
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o Osteosarcoma
o Osteoid Osteoma
o Osteoblastoma
300 | Page [Osteogenic Tumors]
Osteosarcoma
Definition:
1ry sarcoma of bone é Malignant Osteoid Formation arising from Bone Forming Mesenchyme
Onchogenesis
• Oncogenes: Retinoblastoma gene (RB I) and P53
• Cell of origin: UMC
Classification:
I- Intra-Medullary Osteosarcomas
1- Conventional Osteosarcoma
Incidence:
• 2ND MOST COMMON PRIMARY malignancy of bone behind MM
• ~ 20% of primary malignancies of bone
• ~ 1-3/million/Y
• Adolescence; if occur > 40y it is usually 2ry to:
1]. Paget's disease
2]. Radiation
• No significant racial differences
Clinically:
• Pain is the most common complaint:
o HG OS Æ progressive pain
o LG OS Æ painless swelling
o initially z with conservative measures and activity modifications
o eventually y if the diagnosis is delayed
o Night pain is very important clue (only 25% of patients)
• Mass
• Patients frequently are MISDIAGNOSED with a more common problem at the initial visit
• The average DELAY from onset of symptoms to the correct Dx ≈ 4mo ð:
1]. failure to obtain PXR at the initial visit
2]. failure to repeat the PXR when a patient's symptoms persisted or worsened
Pathological features
Site:
• Metaphyseal (90%)
• Commonest sites: Distal Femur, Prox Tibia & Prox Humerus
NEA
• GRAYISH FLESHY mass eroding the cortex & the periosteum.
• Areas of HEMORRHAGE, NECROSIS & CYSTIC degeneration
• FUNGATE outside the bone & involve the soft tissues
• NEVER PERFORATE the skin if reached it; only stretches it
• As the neoplasm permeates the cortex, the periosteum may be elevated
Æ ⊕ NBF Æ "CODMAN'S U ". Codman's U is a bit of a misnomer, it is not
a complete U (growth is too fast for the periosteum, so it responds é
thin shells of NBF) Æ only the edges will lay down NBF Æ ossification is seen tangentially on PXR
as a small angle é bone surface, but not a complete U
• As growth continue Æ the (SHARPEY'S FIBERS) that connect the periosteum to bone are stretched
out ⊥ to bone Æ when NBF is laid down around these fibers and ossify Æ "S SUNBURST" or "H
HAIR-
ON-END" patterns of periosteal reaction
• SKIP LESIONS within the medullary canal is seen
Microscopic: Key ward = “Malignant Osteoblasts Lay Down Malignant Osteoid
Matrix”
• SPINDLE Cells:
o Haphazardly arranged
o Pleomorphic
o Hyperchromatic and irregular nuclei
o Mitotic figures, often atypical, but usually numerous
• MALIGNANT OSTEOID MATRIX: lace-like eosinophilic matrix deposited among these cells
• HISTOLOGIC SUBCLASSIFICATION: according to the predominance of one tissue type
1]. Osteoblastic Osteosarcoma:
o Malignant osteoid (mo) prevails
o Arranged as a delicate meshwork or broader confluent masses
2]. Chondroblastic osteosarcoma:
o Malignant cartilage production
o Still there must be malignant osteoid matrix present to dx
3]. Fibroblastic osteosarcoma
o Large areas of fibroblasts arranged in intersecting fascicles.
o Such areas are indistinguishable from fibrosarcomas
4]. Giant cell variant
o Abundant giant cells (confuse é GCT)
Radiological features
• METAPHYSEAL lesion (~ 10% are primarily diaphyseal & < 1 % epiphyseal)
• MEDULLARY lesion é radiodensity & radiolucency
• PERMEATIVE invasion é poorly defined borders & wide zone of transition
• Cortical DESTRUCTION
• Periosteal elevation & reaction Æ SUNRAY , HAIR-ON-END, CODMAN’S
• Extra-osseous EXTENSION, and soft-tissue CALCIFICATION
RADIOLOGICAL CLASSIFICATION:
1]. Sclerotic osteosarcomas .....................(30%)
2]. Osteolytic osteosarcomas .................(25%)
3]. Mixed pattern ........................................(45%)
• There is no prognostic value for the radiographic matrix
• Errors in Dx often occur é pure osteolytic osteosarcoma.
Mixed Matrix Pattern
2- Telangiectatic osteosarcoma
Incidence
• RARE - 5% of all osteosarcomas
• AGGRESSIVE
Pathology
site: same
Gross
• Multi-cystic "BAG OF BLOOD"
• May look like ABC
Mic
• Large Blood Filled Spaces ............ (DDx ABC)
• Within the septa there is MO + pleomorphic malignant cells; é high power
Clinical
• Presents with PATHOLOGICAL FRACTURE
Radiology
• Often PERMEATIVE osteolytic é cortex erosion
• Sometimes has BALLOONED appearance é expansion
• PERIOSTEAL reaction & Codman's U
MRI
• T1 - high intensity with Fluid-Fluid Levels.
Prognosis
• Poor
3- Small-Cell Osteosarcoma
• Small cell osteosarcoma, another RARE variant
• It is HG LESION that consists of small blue cells that may resemble Ewing or lymphoma.
• ∴ Cytogenetic and immunohistochemistry studies sometimes are needed to differentiate
Histologically:
• In small-cell osteosarcoma the neoplastic cells are round rather than spindle-shaped
• Consists of NESTS & SHEETS of blue cells separated by fibrous septa (similar to Ewing)
• Cells:
1]. Small round blue cells
2]. Well defined border
3]. Distinct rim of cytoplasm
4]. Round nuclei é Fine chromatin
• Occasionally, transition to spindle cells is noted
• LACE-LIKE OSTEOID MATRIX often surrounds small nests of cells Æ confirms the diagnosis if present. It
may present in only a small quantity, can be difficult to differentiate from the fibrin-like material
that may be present in Ewing sarcoma.
4- Low-Grade Intramedullary Osteosarcoma

• RARE type characterized by an INDOLENT course é relatively BENIGN features on PXR
• Mistaken histologically & on PXR for an osteoblastoma or fibrous dysplasia
Pathology:
• As the name implies, it is located in an intramedullary location
• Only erodes through the cortex very late
Mi c
• Slightly atypical spindle cells producing slightly irregular MO trabeculae
II- Juxta-Cortical Osteosarcomas

1‐Parosteal Osteosarcoma
• It is a distinct variant of osteosarcoma that arises from the cortical bone characterized by SLOW
growth and LATE METASTASIS
Incidence:
• ~ 4%
• Older age group
• Has a Better Overall Prognosis than osteosarcoma (long-term survival rate ~ 75-85%)
Pathology:
Site:
• Arise form the CORTEX of DISTAL FEMUR (most common location)
• Characteristically, ATTACHED TO POSTERIOR FEMORAL ASPECT
• Prox humerus & tibia ..... (next most frequent sites)
NEA
• Tends to form a PROTUBERANT LOBULATED ossified mass
• Other areas may INFILTRATE into the adjacent soft tissues
• The tumour usually ENCIRCLES (partially or completely) the bone
• μβ covered in part by a CARTILAGINOUS CAP (DD. Osteochondroma Æ bone medulla is not
continuous é that of the neoplasm)
Microscopically:
• It is regarded as a Mesenchymoma i.e. it contains all mesenchymal tissues:
1]. Bone
2]. Cartilage (bluish white)
3]. Fibrous tissue
4]. Even muscles μβ present in peripheral parts (after it invades the surroundings)
• Classically LG lesion:
1]. irregular MO trabeculae surrounded by a FIBROBLASTIC spindle cell
2]. There may be foci of ATYPICAL CHONDROID differentiation
• HG lesions: y the chance for IM involvement
Clinically:
• Usually present as a mass ± pain.
Radiological features
• Large. Dense. Lobulated mass
• Broadly Attached to the underlying bone Without Involvement Of The Medullary Canal
• The tumour may Encircle the entire bone.
• IM Extension is difficult to determine on PXR & accurately detected é CT
DD: Commonly mistaken as osteochondroma, myositis ossificans, or conventional OS

2‐Periosteal Osteosarcoma
• Periosteal osteosarcoma is a rare INTERMEDIATE-grade malignancy that arises on bone SURFACE
• It occurs in a slightly OLDER and broader age group.
Pathology:
Site:
• DIAPHYSES of the femur and tibia
NEA
• It projects into the adjacent soft tissues as a well-CIRCUMSCRIBED LOBULATED mass
Histologically:
• Intermediate-grade chondroblastic OS
• The tumour reveals a DOMINANT CHONDROID LOBULES
• May contain markedly ATYPICAL CHONDROCYTES.
• At the periphery of the lobule the SPINDLE-CELL component produced intercellular MO
• Areas of MO and chondroid matrix can be seen to INFILTRATE the cortex
Radiologically
• Small. RADIOLUCENT lesion with some evidence of BONE SPICULATION
• The cortex is characteristically INTACT with SCOOPED-OUT appearance and a CODMAN'S U
3‐High‐Grade Surface Osteosarcoma
• High-grade surface osteosarcoma is THE LEAST COMMON TYPE of osteosarcoma
• As the name implies, it is an AGGRESSIVE tumour arising on the outer aspect of the cortex.
Histologically:
• Like conventional OS: HG tumour é y cellularity, mitosis & nuclear pleomorphism
• Medullary invasion is common at the time of presentation (≠ Parosteal OS)
Radiologically
• invasive lesion with ill-defined borders
III- Secondary Osteosarcomas

• Secondary osteosarcomas occur at the site of another disease process.
• They rarely occur in young age & ≈ 50% of the 2ry osteosarcomas > 50 y
• The most common factors associated é2ry osteosarcomas include Paget &previous radiation
PAGET’S SARCOMA
Incidence
• Age: 50-70y
• Male : Female 2:1
• Occurs in advanced POLYOSTOTIC disease 10%
• Affects 1% of all patients with Paget’s
Pathology
• PELVIS is the most common site
• 50% ....................................... osteosarcomas
• 25% ....................................... fibrosarcomas
• 25% ........................................ chondrosarcomas or anaplastic tumours
Prognosis
• Poor - < 50% 1 year survival
RADIATION SARCOMA
• Occurs ~ 1 % of patients who have been treated with > 2500 cGy
• Can occur in unusual sites e.g. skull / spine / clavicle / ribs / scapula / pelvis
• Criteria for diagnosis:
1]. Evident BENIGN INITIAL lesion (both histologically & radiologically)
2]. Must be identified HISTOLOGICALLY & DIFFER from original pathology
3]. 2ry OS must arise in RADIATION ZONE
4]. LATENT PERIOD must pass (at least 5 y) before appearance of the 2ry lesion
• Earlier appearance in younger patients
• Prognosis: Cumulative: 5YSR = 15%.
IV- Multifocal Osteosarcoma

• = Osteosarcomatosis is HG OS characterized by multiple foci of osteosarcoma at presentation
• Previously osteosarcomatosis was considered to be MULTICENTRIC PRIMARY NEOPLASIA
Incidence:
• UNCOMMON ~ 3-4% of osteosarcoma
• More common in SKELETALLY IMMATURE patients (but it occurs also in the old age group)
Pathology
• In young pts: SPEEDY, SYMMETRIC, SCLEROTIC lesions
• In old pts: it is fewer, asymmetric sclerotic lesions
Radiologically
1]. The dominant lesion:
PERMEATIVE aggressive behavior é ill-defined margins
Usually contain Cloud-Like Osteoid, but also, purely LYTIC lesions may be seen
Cortical DISRUPTION, aggressive periosteal REACTION, & soft-tissue EXTENSION
2]. The secondary foci:
Smaller, more SCLEROTIC, and better DEFINED
Lack cortical destruction or periosteal reaction
Prognosis
• Very poor even é intensive chemotherapy. Patients die éin 1y
V- Intra-CorticalOsteosarcoma
• This is the RAREST osteosarcoma, and the term applies to the lesion ώ arises éin the cortex
st
• It was 1 described by Jaffee in 1960 in a report of 2 cases, & through 1991 only 9 cases
Pathology:
S i te
• Intracortical in the femur or tibia
• Measures <4 cm in diameter
Mic
• Sclerosing variant of osteosarcoma (M
Mineralized Mo)
• May contain small Foci of Chondrosarcoma or Fibrosarcoma.
PXR
• Although it is difficult to make generalizations on the basis of such a small № of cases;
• Lesion shows GEOGRAPHIC bone lysis + dense areas of osteoid formation (G IA Ludwick)
• Well DEFINED edge é THICKENING of the surrounding cortex
• Medullary invasion is only rarely reported.
Prognosis
• High rate of METASTASIS (29%) may be sufficient to justify adjuvant chemotherapy
VI- Extra-SkeletalOsteosarcoma
• =Soft-tissue OS is RARE ≈ 1.2% of all soft-tissue sarcomas & 4% of all osteosarcomas
• ♂>♀
Pathology:
Sites:
• Deep soft tissues of the THIGH (45%)
• UPPER extremity ................. (20%)
• RETROPERITONEAL ................. (15%)
• Osteosarcomas are usually large (~10cm)
Histologically:
• Variable amounts of Mo
• Cartilage, fibrosarcoma, MFH, and Schwannoma all are seen (Mesenchymoma)
Clinically:
• Slowly growing PAINFUL MASS
• History of trauma ............. (15%)
PXR
• Large soft-tissue masses é focal to massive areas of mineralization & z osseous involvement
• Pseudo capsule may also be apparent
Tc
• y uptake in both primary and metastatic foci
Treatment:
• Amputation or wide surgical resection with neoadjuvant chemotherapy or radiation therapy
Prognosis:
• Tumour size is the most important prognostic factor (> 5 cm having a bad outcome)
• Despite aggressive therapy, overall prognosis is poor (Death >60%)
• Metastases are frequent to Lung, LN, bone
308 | Page [Osteogenic Tu
umors]
D
Differential Diagno
D osis
Ra
adiologicall
Osteosarccoma
Osteolytic Osteoscle
erotic Mixed
Fibrosarcom
ma
Osteoid osteom ma Osteoid d osteoma
MFH
Stre
ess fracture Stress fracture
f
ABC
Osteoblastoma a Osteob blastoma
GCT
Ew
wing OM
Brodies absscess
Pa
athological
Osteogenic Low grade Intramed

duullary
3]. Osteo oid osteomaa 1]. NOOF
4]. Osteo oblastoma 2]. Fibrrous dyspla
asia
5]. Stresss fracture 3]. Ostteoblastoma
6]. Healinng callus 4]. Choondomyxoid fibroma
Chondrogenic Small cell OS
1]. Chon
ndrosarcom
ma 1]. Ew
wing sarcom ma
2]. Encho
ondroma 2]. Plassma cell tum
mour
3]. Chon
ndroblastom
ma ParostealOS
Fibrogenic 1]. Myo ositis ossificcans
1]. Fibrossacoma 2]. Ostteochondro oma
2]. MFH Periosteal OS:
3]. Fibrous dysplasia
a • Myo
ositis ossificcans
4]. Chonndomyxoid fibroma Giant cell type
• Giant cell tumo
our
Prognosis of Osteosarcoma
• When osteosarcoma affects one limb, the LONG-TERM SURVIVAL RATE (LTSR) is 60 - 75%
• The prognosis will depend on :
1]. Surgery 5]. Size
2]. Response to chemo 6]. Type of osteosarcoma
3]. Spread 7]. Serum markers
4]. Site 8]. General health
1- Surgery
• Resectability of the tumor is the MOST IMPORTANT Prognostic factor as OS is very radio-resistant
• Complete ablation of 1ry &2ries + neoadj. ................... good LTSR
• Unilateral lung metastases & fewer LN is better than bilateral, and many LN
2- Response to chemotherapy:
• The only feature that PREDICTS outcome
Huvos Grading system Degree of necrosis Prognosis
Grade I <10% Necrosis Bad
Grade II <90% Necrosis Bad
Grade III >90% Necrosis Good
Grade IV 100% Necrosis Excellent
3- Spread
• Patients é localized disease Æ better prognosis.......... 5YSR ≈ 70%
• 20% of pts have lung metastases at diagnosis ............ 5YSR ≈ 40%
• The prognosis for metastatic disease depends on:
o Site ○ №
o Surgical resectability of the metastatic disease.
4- Site
• Axial skeleton primary ........................................................... y risk of progression & death
• Pelvic osteosarcomas ~ 10% of all osteosarcomas .... 5 YSR ≈ 20-40%
5- Type of osteosarcoma in relation to conventional OS
• Multifocal sclerosing OS ......................................................... Very bad
• 2ry OS ............................................................................................ Poor prognosis.
• Small-cell OS ................................................................................ Poor
• Telangiectatic OS ..................................................................... was worse & now the same
• HG surface OS ............................................................................ AS conventional OS
• Periosteal osteosarcoma ........................................................ Intermediate
• Intramedullary LG OS ............................................................. Good prognosis.
• Parosteal osteosarcoma ......................................................... Best prognosis
• Intracortical OS prognosis..................................................... Unclear because of its rarity
• Multicentric osteosarcoma prognosis is dire:
o Synchronous multi focal:
o In childhood .................................. always fatal éin 6-8 months
o Adult form ...................................... always fatal éin 2 y
o Asynchronous multifocal Not as uniformly fatal as synchronous type
6- Serum markers
• A number of potential prognostic factors were identified and not validated yet; include:
1]. Human epidermal growth factor.
2]. Tumor cell ploidy.
3]. Specific chromosome gains or losses.
4]. Loss of heterozygosity of RB gene.
5]. Loss of heterozygosity of p53 locus.
6]. y expression of p-glycoprotein
• y AlkPh. at diagnosis are more likely to have lung metastases
• y LDH is bad prognostic value
Treatment of osteosarcoma
• It is a combination of all of the following:
1. Adjuvant therapy: Preoperative & Postoperative CHEMOTHERAPY
2. Operative: Which will be tailored according to the stage & extension of the tumour
3. Radiotherapy
1. Adjuvant therapy (Chemotherapy)

• Chemotherapy administered preoperatively is referred to as induction (NEOADJUVANT)
1]. Induce TUMOUR NECROSIS, particularly in the reactive zone (pseudocapsular region), where
microscopic satellite nodules reside
2]. ∴ FACILITATING LIMB-SPARING resection with a wide margin.
3]. INITIATES early treatment of microscopic and overt metastatic disease
• Postoperatively Chemotherapy, when tumour burden is lowest, is called Adjuvant Chemotherapy
CHEMOTHERAPEUTIC Agents used in the treatment of osteosarcoma

Agent Mechanism of action Side effects
Doxorubicin Doxorubicin intercalates at point of local Cardimyopathy, trasnient ECG changes,
(Adriamycin) uncoiling of DNA double helix, emesis, alopecia, mucositis,
Also DNA & RNA synthesis BM supression
Cisplatin (platinol) Cisplatin DNA synthesis via formation of RF, PN, otoxicity, emsis, BM depression,
DNA cross-links; it binds to tumour DNA alopecia, z Mg
Ifosfamide (Ifex) with Ifosfamide causes cross link defect Æ Hemorrhagic cystitis, RF, emsis, BM
mesna (mesnex) DNA synthesis depression, alopecia, encephalopathy
Methotrexate Methotrexate is a folate antimetabolite; it RF, mucositis, BM depression, CNS
(Rheumatrex) + purine synthesis & thymidine by
leucovorin ca binding dihydrofolate
Mesna is a prophylactic agent used to prevent hemorrhagic cystitis; it has no intrinsic cytotoxicity. Mesna binds é urotoxic
metabolite of ifosfamide Æ inactivating it
Leucovorin is a tetrahydrofolic acid derivative that acts as a biochemical co-factor for carbon transfer reactions in the
synthesis of purines and pyrimidines. Leucovorin does not require the enzyme dihydrofolate reductase; therefore, it is able
to rescue normal cells and prevent severe myelosuppression and mucositis
2. Qperative Treatment:
• Enneking Stage I A & II A (Intra-Compartmental Lesions):
LIMB SPARING SURGERY
• Enneking stage I B & II B (Extra-compartmental lesion):
LIMB SALVAGE VS AMPUTATION
Radical excision = Amputation OR Disarticulation
• Enneking stage III (Lesion with metastasis): (Osteosarcoma with pulmonary metastasis)
I. RESECTABLE METASTASIS:
Resection of all macroscopic tumour e.g. by median sternotomy
Amputation or resection of the tumour
Intensive adjuvant chemotherapy
II.INOPERABLE METASTASIS
Chemotherapy
Palliative procedures
Limb Salvage
Definition:
• Wide tumour resection & reconstruction by common modalities of reconstructive options
Guidelines
1]. BONE is resected 4 cm beyond abnormal uptake as determined by Tc. MRI is useful
2]. En bloc resection of normal MUSCLE cuff in all directions
3]. Enbloc resection of all previous BIOPSY SITES & potentially contaminated tissues
4]. Adjacent JOINT & capsule should be resected
5]. There must be enough MUSCLE REMAINING for a functional limb to be reconstructed
6]. There must be FREE NEUROVASCULAR bundle of tumour
7]. There must be adequate soft tissue COVERAGE
Relative contraindications
1. Major neurovascular Or Muscle involvement
2. Pathological fractures
3. Inappropriate biopsy sites
4. Infection
5. Skeletally immature patients Æ LLD
Types:
I. LIMB SALVAGE IN SKELETALLY MATURE PATIENT:
1. Biological Reconstruction
A. Bone grafting
I. Autograft:
1]. Vascularized: Fibula, Rib, Iliac crest, Scapular lateral border
2]. Nonvascularized:
1]. Cancellous
2]. Cortico-cancellous
3]. Cortical: free fibular graft is a well-recognized source of bone &has
important advantages over other donor sites:
i. Easy harvesting
ii. Its size and shape allow intramedullary insertion
iii. Donor site morbidity is minimal
II. Allograft:
Allograft is a commonly used for reconstruction of large bone defect after tumour
resection & good results have been achieved because of its biological nature
Disadvantages:
1]. Immunological reaction.
2]. Transmission of diseases.
3]. Religious and social dissatisfaction.
4]. Infection or non union esp. é chemotherapy.
Types:
1]. Nonstructural allograft
2]. Structural allograft
Osteochondral allograft: Hemicondylar / Total candylar
Intercalary allograft.
3]. Resection arthrodesis
4]. Allograft prosthesis composite (APC)
III. BG substitutes:
Osteoinductive Stimuli (Bioactive factors, GF): biochemical substances that
stimulate bone production and healing
1]. Bone Morphogenetic Proteins (BMP.s):
2]. Transforming Growth Factor-β (TGF-β):
3]. Platelet-Derived Growth Factor (PDGF):
4]. Insulin-Like Growth Factor (IGF):
5]. Fibroblast Growth Factors (FGF.s)
Osteogenic Cells (Osteoprogenitors):
1]. Unfractionated Fresh Bone Marrow
2]. Connective Tissue Progenitors
3]. Differentiated Osteoblasts & Chondrocytes
4]. Genetically Modified Cells
Osteoconductive Matrices (Scaffolds):
1]. ALLOGRAFT BONE MATRICES
2]. COLLAGEN
3]. HYALURONAN
4]. POLYLACTIC AND POLYGLYCOLIC POLYMERS
5]. CERAMICS: HA, TRI CA PH, CERAMIC CEMENT, ULTRAPOROUS β-tri ca-ph, Calcium
sulfate.
B. Distraction osteogenesis:
• It has been employed in the reconstruction of diaphyseal defects after excision of
tumours and for arthrodesis after joint resection. Five types based on the location
of the defect after resection of the tumour.
• The best is by using Ilizarov frames for a period ranging around 12 months;
which is sufficient of regenerate a length about 20 cm
• Distraction has many types according to the site of application:
I. Type 1: diaphyseal
II. Type 2. Methaphyseal reconstruction
III. Type 3. Epiphyseal reconstruction
IV. Type 4. Subarticular reconstruction
V. Type 5. Arthrodesis
C. Reimplantation: for ostegenic tumors only; by devitalization of the tumour cells by:
I. Heat:
Autoclaving: Reimplantation of the resected segment after
devitalization of the tumour cells by autoclaving at 134ºC / 15 min and
after debridement of all the soft tissue
Pasteurization 60ºC / 30min: keep the bone architecture
Microwave induced hyperthermia: probes are inserted at a
measured distances from the tumors, then electro-magnetic waves are
concentrated over the tumor; while the soft tissues are cooled by a
special irrigation system
II. Freezing (Liquid nitrogen)
III. Extra-corporial irradiation:60-90 gray
2. Metallurgic reconstruction
• Modular arthroplasty systems
3. Composite reconstruction:
A- Auto-prosthetic composite:
i. Extracorporeally irradiated autograft-prosthetic composite arthroplasty
ii. Autoclaved autograft-prosthetic composite arthroplasty
iii. Pasteurized autograft-prosthetic composite arthroplasty
B- Allo-prosthetic composite.
4. Soft tissue coverage:
• Is a very important entity in the biological reconstruction of tumors:
1]. Important for proper healing of the construct
2]. Viable non infected tissues are important for nutrition of the bone
3]. It should be not involved by the tumor
• Types:
1]. Skin: full thickness, partial thickness, tirsh graft
2]. Muscles: rotational flabs, V-Y flabs, vascularized flabs
3]. Nerve, tendon, and vascular grafts
II. LIMB SALVAGE IN SKELETALLY IMMATURE PATIENTS

The options for limb salvage in immature patient include:
1- Rotationplasty
2- Expandable endoprosthesis
3- Distraction osteogenesis
3- Radiotherapy:
Relatively radio-resistant tumour; but can be used for:
i. Palliation of local pain
ii. Treat surgically inaccessible lesions
iii. Treat painful metastatic deposits
iv. Pre-operative to z the size and vascularity of the tumour
Osteoid Osteoma
Introduction
• Benign skeletal neoplasm of unknown etiology ώ is Composed Of OSTEOID & WOVEN bone
• The lesion initially appears as a small sclerotic island éin a circular lucent defect. (N
NIDUS)
• OO may REGRESS spontaneously. The mechanism of involution is not known (μβ infarction)
Aetiology
• It is a REACTIVE BONE lesion, of unknown cause (not a neoplasm)
Theories of etiology of osteoid osteoma
1. Congenital.
2. Neoplastic: Jaffe “Very slowly growing tumor”
3. Rheumatic.
4. Reactive bone lesion (Now) ð localized reaction to infection
5. Inflammatory (Lymphocytes) sclerosing osteomyelitis ð:
a. Its SELF LIMITING nature
b. Its SHELL OF BONY SCLEROSIS
c. Its characteristic SITE
d. In some cases STAPHYLOCOCCI has been cultured
Classification
1. Cortical 3. Subperiosteal
2. Cancellous 4. Intra-articular
Cortical Osteoid Osteoma
• Most common.
• The radiolucent nidus is within the cortical bone
• Fusiform cortical thickening + laminated periosteal NBF
Cancellous osteoid osteoma
• Intramedullary location.
• LITTLE SCLEROSIS occurs around the nidus
• Sites:
o Juxta-articular region of the Femoral Neck
o Posterior elements of the Spine
o Small bones of the Hands And Feet
Intra-articular osteoid osteomas
• Intra-articular osteoid osteomas are DIFFICULT to identify
• DELAY of 4 mo- 5 years before diagnosis is not unusual.
• JOINT-SPACE WIDENING due to joint effusion or synovitis
• DD:
o inflammatory or infective arthritis
o Nonspecific synovitis
o Legg-Calve-Perthes disease
Subperiosteal osteoid osteoma
• RARE form of the disease
• ROUNDED SOFT-TISSUE MASS adjacent to a bony cortex & excavates
• LITTLE SCLEROSIS occurs around the nidus
• Sites:
o Medial Femoral Neck (Juxta- or intra-articular)
o Hands and Feet, in particular, the neck of the talus.
Incidence
• 12 % of benign tumors & 3% of all tumors.
• ♂:♀= 2:1
• 10-30 y .................................. 75% (range from 5-55 y)
• It is uncommon ................ <5y or > 50 y
Pathology
Site:
METAPHYSIS or DIAPHYSIS ......... 75%
Appendicular skeleton........... 65% (FEMUR &Tibia & Humerus; but occur in any bone)
Spine: .................................... 12% (Posterior arch)
Hands: ................................... 8%
Feet: ....................................... 4%
The skull and facial bones are involved exceptionally
80% of cases involve the cortical bone; 20% are intramedullary
Gross Pathology
Aggregate of RED, brown, purple or grey tissue (according to vv), é GRITTY consistency
Encased in a dense cortical SCLEROSIS
Size of surrounding sclerosis may exceed the size of the principle lesion many times
Nidus does not exceed 2 cm (0.5-2 cm)
Described as a Cherry Piece inside the bone.
Microscopic
Nidus of OSTEOID TISSUE + WOVEN BONE TRABECULAE
HIGHLY VASCULAR CT matrix é large dilated vascular channels.
GIANT CELLS and OSTEOCLASTS are frequently observed.
Jaffe described it microscopically to be formed of 3 characteristic regions:
Inner region .............. vascular GRANULATION + OSTEOBLASTS.
Intermediate ............. CALCIFICATION & OSTEOID formation
Outer region ............. Bone TRABECULAE in various stages of ossification
Clinical picture
• The most important clinical characteristic of osteoid osteoma is PAIN
• The site of involvement may be TENDER to touch or pressure.
Pain of osteoid osteoma ............................ 95%
Characters:
y é activity & at night with congesion & z by salicylates.
Not relieved by rest.
At 1st it is vague & later y in severity & becomes aching in character
Some times, severe enough to waken the patient.
In a few instances pain becomes severe & persistent (6y) Æ threats of suicide
Site:
Usually the pain is at the site of the lesion
Femoral upper end; esp. the neck, Æ may be referred into the leg as a LDP.
Cause:
Result from the lesion being very vascular é numerous nerve fibers.
Œdema & increased tension result in ⊕ of these nerve endings
Osteoid Osteoma Of The Spine

PAINFUL SCOLIOSIS ð ms spasms Æ abnormal alignment (+ kyphosis, torticollis & lordosis)
A may be CONCAVE TOWARD the Lesion.
May be ACUTE and is frequently initiated by PHYSICAL EXERTION.
Osteoid osteoma has been called the most common cause of painful scoliosis.
Osteoid osteoma affecting the hip
• May cause pain simulating as that pain caused by LDP
• Intracapsular lesion often Æ considerable intra-articular inflammation Æ look like arthritis
• Marked weakness & muscular atrophy é long-standing tumor may occur
X rays:
• A circular or OVOID LUCENT defect is seen in 75% of patients.
• Size is usually smaller than 1.5 CM in diameter
• Variable degree of cortical & endosteal SCLEROSIS; according to the site:
Cortical and subperiosteal Æ considerable sclerosis.
In medullary tumors Æ sclerosis is minimal or absent.
Subarticular & intracap ..................Æ sclerosis is minimal & distant to the lesion.
Long-standing cases ........................Æ more sclerosis.
Children also ......................................Æ more sclerotic response than adults
• Intra-articular tumors .......................................EFFUSION é premature loss of cartilage.
• intra-articular osteoid osteoma ....................OA (50% of intraarticular OO)
• Spinal osteoid osteoma ...................................SCOLIOSIS, kyphosis, or hyperlordosis.
• children with a long-standing tumor........OVERGROWTH of the involved bone
• Regional OSTEOPOROSIS ð disuse.
CT:
• CT is BEST diagnostic tool for nidus localization
MRI
• The nidus signal is ISOECHOIC to muscle on T1 & HIGH on T2
• BM edema around the nidus .......................60%
• Soft tissue edema ...............................................50%
Bone scan:
99m
• Tc shows INTENSE ACTIVITY at the site of the tumor.
• Occasionally, DOUBLE-DENSITY sign (Nidus of y uptake on top of a larger area of radioactivity)
Differential diagnosis
1]. Osteoblastoma
2]. Sclerosing osteomyelitis
3]. Sclerotic metastases
4]. Osteosarcoma
5]. Ewing tumor
6]. Subperiosteal ABC
7]. Stress fracture
8]. Bone Infarct
Prognosis:
• Good & if the patient withstand the pain for 5 y, it will disappear (self limiting disease)
• Malignancy has not been reported after surgical treatment.
Treatment:
• Complete Excision é the Whole Nidus will provide cure
• Partial removal of Æ only symptomatic improvement but not cure & will recur
• To avoid incomplete removal:
PRE-operative Good x-ray
INTRA-operative x-ray for the removed specimen (more clear than the whole bone)
Remove nidus ENBLOC + Prophylactic ORIF + BG (esp. in neck femur & long bones)
• Techniques of osteoid osteoma ablation:
Percutaneously ablated by using radiofrequency (RF)
Ethanol
Laser
Thermo coagulation therapy under CT guidance
• If sclerotic bone is removed and not the nidus Æ pain will continue
• Metaphyseal lesions ð its rapid healing; prophylactic ORIF is usually not necessary
• Spinal lesions sometimes complete ablation & resection are not feasible
Intraoperative procedure for localizing the lesion.

1. X-rays
2. Multiplanar fluoroscopy
3. The use of a radioisotope probe
4. Intraoperative tetracycline fluorescence
5. The specimen should be radiographed in two planes intraoperative
6. Pathologist should examine the specimen carefully é 5mm cuts to detect the nidus
Ivory Osteoma
= Compact osteoma = Ivory exostosis
Rare benign tr. arise as a localized thickening on the outer or inner surface of bone
Sites:
usually in skull and medial tibia
Clinically:
Painless, hard lump, on the outer surface of the skull
If occur on the inner surface Æ epilepsy
P X R:
Sessile dense bone é well circumscribed edge
TTT:
Only when symptomatic
Osteoblastoma
Introduction
• Osteoblastoma (OB) is an UNCOMMON primary neoplasm of the bone. It has clinical and histologic
manifestations similar to osteoid osteoma (producing osteoid, primitive woven bone & fibro-
vascular CT); therefore, some consider the two lesions to be variants of the same disease, with
osteoblastoma representing a giant osteoid osteoma. However, an aggressive type of
osteoblastoma has been recognized, making the relationship less clear
Ætiology
• Unknown.
• Tumour is usually considered Benign
• Aggressive Variant has been described in literature, é histologic features as osteosarcomas
Incidence
• 4% of benign bone tumors.
• 1% of all primary bone tumors
Pathology
S i te
• 40% in SPINE (17% of spine OB are in the SACRUM)
• Posterior element
• DIAPHYSES is another common site (LL more affected)
• Sometimes Metaphyses are affected
• Rarely epiphyses are affected
• Pelvis, hands, feet, skull, clavicle, scapula, ribs, and talus are also
documented
Macroscopically
• Irregular Osteoid mass
• More Vascular, More Gritty, but Less Sclerotic than osteoid
osteoma
Microscopic
• Most important: IMMATURE BONY TRABECULAE & primitive WOVEN bone± ossification
• Lined é OSTEOBLASTS
• HIGHLY VASCULARIZED CT: The stroma has dilated capillaries & blood sinusoids
• NIL MITOTIC ACTIVITY
It may simulates osteoid osteoma & osteosarcoma but:
1]. larger than 2cm; but does not permeate the bone
2]. y № of osteoblasts hence its name.
3]. Very low mitosis and cytologic atypia
4]. Intercellular matrix varies in amount & maturation (from osteoid up to lamellae peripherally)
5]. Rarely has a cartilaginous matrix (≠ osteosarcoma)
Clinical picture
• Usually present with PAIN of several months duration:
Less intense
not worse at night
not relieved readily é aspirin
• If the lesion is superficial Æ localized SWELLING and TENDERNESS.
• Spinal lesions can cause PAINFUL SCOLIOSIS (this feature is more é osteoid osteoma)
• NEUROLOGIC deficits
X-RAY
• Spine Osteoblastomas:
In the Posterior Elements
Well-Defined expansile lesion
50% contain Matrix Mineralization.
• Long bones lesions:
66% éin the cortex & 33% éin medullary canal.
>2 cm unlike osteoid osteoma
Well-circumscribed radiolucent lesion
Thin shell of peripheral NBF & reactive zone of bone
Computed tomography (CT):
Tumor delineation when the lesion is within the cortex
Extent of the lesion
Size of the lesion
Identify spine lesions clearly Æ smaller and more accurate surgical resections.
Magnetic resonance imaging (MRI)
• Provides information about the extent (NB. MRI findings alone are not diagnostic)
• Detects soft tissue changes
• Detects BM extension
Bone scintigraphy
99m
• y Tc is sensitive but not specific.
• Many bone tumors, for example osteoid osteoma show the same type of focal activity
ABC GCT
Chondromyxoid Fibroma Osteoid Osteoma
Enchondroma and Enchondromatosis Osteomyelitis
EG Osteosarcoma
Osteoid Osteoma Osteoblastoma

Pain More Less
Size <2 cm whatever the duration Increase with long standing up to 7 cm
Grossly Only sclerosis of neighboring bone Some destruction & expansion of neighbor bone
Mic Less osteoblasts More osteoblasts
Treatment
• The treatment goal is complete surgical excision of the lesion.
• The type of excision depends on the location of the tumor.
• For non aggressive lesions:
Extensive intralesional excision, using a high-speed burr (remove tr + normal margin)
• For aggressive lesions:
Wide resection is needed to remove all tumour-bearing tissue
This type of complete excision is usually curative for osteoblastoma.
Prognosis
• Recurrence ~ 10-20% ð inadequate resection especially in spine lesions
[Chondrogenic Tumors] Page | 321
V{ÉÇwÜÉzxÇ|v gâÅÉÜá
o OSTEOCHONDROMA
o MULTIPLE HEREDITARY EXOSTOSIS
o ENCHONDROMA
o CHONDROBLASTOMA
o CHONDROMYXOID FIBROMA
o CHONDROSARCOMA
322 | Page [Chondrogenic Tumors]
Osteochondroma‫اﻟﺰواﺋﺪ اﻟﻌﻈﻤﻴﺔ‬
• Osteochondroma is the MOST COMMON BENIGN BONE TUMOR. Mostly
asymptomatic, but they can cause mechanical symptoms
• CARTILAGE CAP histology has the same defined zones in physis, namely
zone of proliferation, hypertrophy, calcification, and ossification
Incidence:
• 35% of benign bone tumors
• 10% of all bone tumors
• <20 years
• ♂:♀=3:1.
Etiology:
• UNKNOWN; although, it was thought to be a PHYSEAL HERNIATION
(Idiopathic, traumatic or perichondrial ring deficiency)
• It is a REACTIVE METAPLASTIC CARTILAGE that responds to the factors
that stimulate the growth plate and thus results in exostosis growth.
• Recently, genetic karyotyping suggested that it is a TRUE NEOPLASTIC
process, not a reactive one. These findings and conclusions are in
the early stages of research
Pathology:
Site
• Any bone that undergoes endochondral bone formation.
• FEMUR .......................................................... 30% / distal: proximal=3:1
• Tibial .......................................................... 20%
• Proximal Humerus ................................. 20%
• Hands and feet (10% of cases), scapula (4%), pelvis (5%)
Location:
• Osteochondromas develop Metaphyseal Adjacent To Physis
• Then, grow Away From Physis ð (as if isolated physis):
Rate of epiphyseal cartilage growth > osteochondroma
The muscle pull (even if not attached to it)
• Growth of the osteochondroma STOP AT SKELETAL MATURITY
Macroscopic
• May have a stalk Æ PEDUNCULATED, or a broad base Æ SESSILE
• The stalk is made up of mature bone.
• By definition, medullary canals of the bone and the stalk are
CONNECTED
• CARTILAGE CAP -ώ is thick in children- is replaced by endochondral
bone at maturity
Microscopic:
• Lesion is topped with a cartilage cap é VARIABLE CELLULARITY.
• The cap has an overlying fibrous layer é MESENCHYMAL CELLS responsible for its growth
• Cap cells are VERTICALLY oriented as in physis
Staging: Musculo-Skeletal Tumor Society (MSTS) staging for all benign lesions:
Stage I ...................................... Inactive or static lesions (Latent)
Stage II .................................... Actively growing lesions (Active)
Stage III ................................... Actively growing & locally destructive (aggressive)
Clinical picture:
• most commonly diagnosed INCIDENTALLY when PXR obtained for some other reason.
• The second most common presentation is a MASS (± pain)
Causes Of Pain In Osteochondroma:

Pressure on the overlying nerve or soft tissue.
1].
Bursitis over the exostosis.
2].
Stalk fracture
3].
Cap infarction
4].
Malignant transformation
5].
Complications:
1]. Fracture
2]. Neurologic Sequelae
3]. Bursa Formation
4]. Malignant Transformation
Fracture
• Site: typically involves the stalk base esp. around the knee
• Subsequently, callus formation causing band like sclerosis on PXR occurs é healing.
• No significant incidence of nonunion has been reported.
• Interestingly, REGRESSION of solitary osteochondroma occur spontaneously and following #
Neurologic Sequelae
• Peripheral lesions may compress nerves nerve palsy
• PERONEAL affection é foot-drop & RADIAL nerve Palsies are reported
• Also central neurological manifestations are reported also é central lesions
Bursa Formation
• The commonest locations: (sites é motion & friction):
o SCAPULA ....................................... 50% of shoulder cases
o LESSER TROCHANTER
• Lined by synovium ................................ may become inflamed, infected, or hemorrhagic.
• ± chondral or fibrin bodies .................. 2RY SYNOVIAL CHONDROMATOSIS.
Malignant Transformation
• Malignant transformation .................. 1% of solitary lesions.
PXR
• Metaphyseal cartilage capped protuberance é variable cap Calcification
• There is Continuity between the mass and the bone:
o Broad ............................................ Sessile osteochondroma
o Narrow with a bulbous tip .... Pedunculated osteochondroma
• Characteristically there is CONTINUITY bet.the cortex and medulla of the parent & son
• However, this contiuity is not apparent in:
o Osteochondromas of flat bones with complex anatomy (i.e., pelvis, spine, scapula)
o Sessile lesions
• Pedunculated lesions usually Point Away from the nearest joint
CT scanning:
• 1n certain bones, such as the pelvis and scapula Æ useful to localize the lesion
MRI
• Is only needed in cases in which malignancy is suspected
• MRI is the modality of choice to assess the cartilage cap thickness.
• Thick cartilage caps (>4 cm) + pain ⎯⎯ ⎯ ⎯→ of malignant degeneration
Suggestive
Treatment:
• INIDICATIONS FOR EXCISION
1]. Painful bursae
2]. Location é recurrent injury
3]. Significant deformity
4]. Suspicion of malignant change
• Guide lines:
o Ideally, line of resection should be through ! Base of ! Stalk
o Ensure that none of the cartilage cap or perichondrium is left Æ otherwise recurrence
o Ensure removal é fibrous cover
o Investigate very large lesions to exclude malign (MRI of choice in cartilage thickness)
o Avoid damage to the physis
o Avoid deep dissection Æ violate normal tissue
o Avoid superficial dissection Æ leave a pathology
o The resected surface of the host bone can be rasped smooth
o Bone wax can be packed on the cut surface to stop bleeding
Prognosis:
• For solitary osteochondromas Æ excellent (local recurrence rate <2%)
• Poorer outcomes are associated with:
o Surgical exposure
o Secondary bone deformity due to lesion location (in the multiple hereditary)
Recurrence:
• The local recurrence ~ 1.8%
• Causes of recurrence after excision:
1]. 1f you left the cartilage cap
2]. If malignant
Multiple Hereditary Exostoses

Diaphyseal Aclasis
Introduction
• Multiple Hereditary Exostoses is an inherited disorder of bone growth characterized by growth of
multiple exostoses (benign cartilage-capped tumors) that grow out of metaphyses.
Inheritance & Incidence
• AD
• 65-75% have Mutations at Ext1 gene & ~ 21-30% at Ext2 gene
• Peak at 3y (nearly all patients are diagnosed by 12y)
• HME Findings y with:
AGE: at birthÆ5% & 12 YÆ96% & adultÆ75% have an evident deformity
MALES > females.
• HME Malignant risk y é age
Pathology
• Sites: Any bone can be affected
o KNEE ............................................. (70%)
o Humerus .................................... (50%)
o Forearm ...................................... (50%)
o Ankle & scapula ....................... (50%)
o Pelvis, shoulder, ribs
o Face and skull are generally unaffected
• Location
o Multiple &Usually bilateral &symmetrical
o JUXTA PHYSEAL METAPHYSES (distance to epiphysis y é growth)
o From the SURFACE OF FLAT bones
• Gross:
o EXOSTOSES bony growths &by definition they must have:
Cartilage-cap ± small punctate calcifications
Their own cortex, medulla, and physis but continue é those of mother bone
Grow away from physis Æ OSSIFY and STOP GROWING by maturity
o An exostosis may be SESSILE or PEDUNCULATED
o ABNORMAL BONE REMODELING Æ short, bowed bone é wide metaphysis
Clinical picture:
• The affected individual has 6 EXOSTOSES; typically BILATERAL, SYMMETRICAL.
• DEFORMITY:
o ð ABNORMAL REMODELING Æ shortening, bowing, widening of metaphyses
Radius&Tibia
o BOWING of the forearm or leg, is the commonest ð y Ulma& Fibula Æ deformities
oHand deformity ð shortened metacarpals is common
oLLD ð marked interference with growth in length of the affected bones
• MASS ώ may cause:
o Compress or stretch peripheral nerves pain, sensory, motor
o Displace nerves and vessels .. complicating attempts at surgery
o Irritate overlying ms & tendons pain and loss of motion
o Large exostosis impinging a joint mechanical blocks to motion
o Large pelvic exostosis ............. urinary or intestinal obstruction
• COMPLICATIONS: e.g. rapid y in size and pain Æ malignant change …
326 | Page [Chondrrogenic Tum
mors]
MHHE triad
oses
1]. ≥ 6 Exosto
2]. Barrel meetaphysis ð failure of
o remodeling (Tubulation,
funnelizatio
on or cylinde
erization)
3]. Short statture (or eve
en Dwarfissm)
PXR
R
• Multiplle EXOSTOSES (descripttion as tho
ose of solita
ary ones)
• ~ 70%% have a clinically appparent exxostosis ab bout the knnee, sugge esting that PXR knee e to
detect non-palpa able exostooses may be b a sensitive screen ning test tto detect mildly
m affeccted
individuals.
Com
mplicatioons
1]. Deform
mity
2]. Fracturre
3 Neurollogic Seque
3]. elae
4 Bursa Formation
4]. F
5]. Malign
nant Transfformation
6 Vascula
6]. ar
Co
osmetic and
a Osseo ous Deforrmity
• Wrist: ............................................................ Ulnar
U tilt of radial articcular surfacce, Ulnar deviation
d
• Forearm m: .................................................... Ulnar
U shortening, radial bowing g
• Elbow:: ........................................................ ra adial head dislocation n
• Hip: .............................................................. coxa valguss
• Knee: ........................................................... genu
g valgus
• Ankle: ......................................................... tiibiotalar tiltt (valgus deformity)
• Signific
cant LLD &short & statu ure
• Other skeletal
s abnormalities may occu ur:
o Shortening g of 4th an nd 5th mettacarpals
o Supernum merary finge ers and/orr toes
o Madelung g / reversed d Madelung deformitty
Vascular Compromi
V C ise
• Vessel displacemment is common é la arge lesions but asym
mptomatic
• Stenos sis
• Throm mbosis: eitther arteria
al or venou
us. Most fre
equently se
een in POPLITEAL vv
• Pseudoo aneuryssm formation.
• Clinically:
o Pain, swellling
o Rarely clau
udication
o Palpable pulsatile
p m
mass usuallyy affecting
g
a young patient.
p
Malignant Transformation (most serious)
• Usually occurs in adulthood
• The loci on chromosome 8 & 11 é loss of heterozygosity Æ associated é malignant change
• Symptoms suggesting of malignant change:
o Rapid y in SIZE
o Rapid y in PAIN
o Any pain and growth AFTER skeletal maturity
• Sign of malignant change:
o Suspected more in PELVIS and shoulder
o BULKY CARTILAGE CAP (best visualized é MRI or CT) >3cm
99m
o y Tc UPTAKE after skeletal maturity
• Types:
o CHONDROSARCOMA arise from the cartilage cap
o Rarely osteosarcoma arise from the base of the stalk
o Usually solitary and LG ........... 85% (multifocal & dedifferentiated may occur)
• Incidence
o 8% of all chondrosarcomas
o Change rate is .......................... 0.5-20%
o Sites more prone: ..................... pelvis, hips, and shoulders lesions are
o Age: (unusual before 20y)
HME ............................... 25y
Solitary osteoch ........... 50y (usually)
Prognosis
o Exostosis begins in childhood
o Stops growing when nearest epiphyseal center fuses
Enchondroma
Benign tumour of cartilage originating within the medullary cavity
Periosteal form originates in the periosteum and erodes into the cortex
Incidence
• 10% of benign bone tumours
• Peak incidence ....................................... 10-50Y
• Long bone chondromas ..................... > 30 years
• May be SOLITARY or MULTIPLE (Olliers, Mafuccis)
Pathology
• Site:
o HANDS AND FEET ........................ >50% occur in
o Femur & humerus .................... 15% each
o METAPHYSEAL
Solitary swelling ........................ 75%
o
• Macroscopically - BLUISH white well DEMARCATED, ENCAPSULATED
and often LOBULATED gritty tissue
• Microscopically - HYPOCELLULAR; NESTS of mature cartilage cells,
nuclei are small and uniform, no atypia ± calcification

• Sarcomatous change may occur in a benign lesion (section all lesion)
• Periosteal Form less common
o Similar pathology but more cellular
o Proximal humerus near deltoid insertion
o Never turn malignant
• OLLIER'S more cellular............................ 50% malignant transform
• MAFFUCCI'S é haemangiomata ............ 100% malignant change
Clinically
• Present as FRACTURES ............................ 60%
• LUMP, or as INCIDENTAL finding
• Cortex remains intact unless fracture
Radiology
• SCALLOPED EROSION of endosteal surface
• Flecks of calcification .................................. 'GROUND GLASS'
• Periosteal form (juxtacortical)................... SHALLOW
CRATER lined é rim of reactive bone, elevate
periosteum; the lesion itself may not show on PXR
• Olier’s & Maffucci........................................... SLED RUNNER TRACKS
Treatment
• Observe x-ray 6mo & 1y after presentation
• Latent ........................................................ CURETTAGE + BG
• Active .......................................................... Recurrence may be better than morbidity of en block
• Periosteal form......................................... MARGINAL EN BLOC excision
Prognosis
• Risk of malignant change in Olliers is 50% &
in Maffucci is 100%
• Recurrence is higher é active lesions (GII)
and é periosteal form
Chondroblastoma
Incidence
• ♂:♀ ≈ 2:1
• Peak age 10 - 20 Y ................................... (rare over 30 years)
• the adult counterpart of chondroblastoma is giant cell tumour
Pathology
• Arises from Chondroblasts
• Usually Active Benign lesion (Stage 2)
• Sites:
o Upper Humerus ...................... 15%
o Upper Tibia .............................. 15%
o Upper femur .......................... 15%
o Lower femur .......................... 15%
o Epiphyseal but may expand into metaphysis
• Mac: PINKISH grey LOBULATED tissue, may be haemorrhagic
• Mic: Richly cellular MNGC + CHONDROBLASTS (polyclonal or round)
Clinically
• Present with PAIN of increasing severity
X-Rays
• Open Physis
• Eccentric, Epiphyseal, Well Defined, Lytic area placed in the or across the physis
• No reaction in surrounding bone
• 50% ............................................................. central Calcification
• 50% ............................................................. Linear Periosteal Reaction
Tc99
• y uptake at margins
• GCT (adults)
• ABC (histology similar)
• clear cell chondrosarcoma
• epiphyseal osteomyelitis
Treatment
• Curettage & bone grafting (15% recurrence)
• AVOID JOINT PENETRATION because chondroblastoma cells will grow in joint fluid
• Use cryotherapy if extension intra capsular to avoid excision of joint
Prognosis
• Probably no chance of malignant change
• Recurrence 15%
Chondromyxoid Fibroma
• Benign tumor of bone characterized by formation of variable amounts of chondroid,
fibromatoid & myxoid elements
Incidence
• Peak age 10-30Y ...................................... (75%)
Pathology
• May develop from a Remnant Of The Growth Plate?
Sites:
lower extremity ............................... 75%
Tibia...................................................... 50%
Forearm.............................................. 10%
Usually Eccentric Metaphyseal lesions
Macroscopic:
firm LOBULATED JELLY like areas of MUCOID masses
areas of CHONDROID and MYXOMATOUS tissue
Microscopic:
MnGC
Macrophages
Monocytes with condensations of cells on the periphery
Usually No Bone Osteoid
Clinically
• Present with a CHRONIC PAIN
X-Rays
• Rounded or oval LYTIC area
• Usually ECCENTRIC METAPHYSEAL ; but may cross the growth plate
• SHARP outline
• Sclerotic rim
• SCALLOPED margin and thin cortex
Treatment
• Extra Capsular Marginal Excision ... almost no recurrence
• If skeletally immature ............................. WAIT until maturity
Prognosis
• Malignant change is reported ............ should be excised
Chondrosarcoma
• Primary malignant tumour whose CELLS PRODUCE CARTILAGE MATRIX
• May arise DE NOVO (usually IM) or 2RY to an existing benign tumour
Incidence
th
• 10% of primary bone sarcoma (4 common sarcoma)
• AGE: ............................................................ 30 - 60 years
• Male : Female .......................................... 2:1
Pathology
Sites:
1]. PELVIS .................................... 30%
2]. Prox Femur .......................... 20%
3]. Prox Humerus ...................... 10%
4]. Ribs ...................................... 10%
5]. Rare in hand but it is the commonest sarcoma there
6]. Often metaphyseal
Conventional Macroscopic appearance:
• EXPANDING lesion é cortical DESTRUCTION, soft tissue extension
• Grayish HYALINE FUSED NODULES é areas of CALCIFICATION
Conventional Microscopic appearance:
• Cellular PLEOMORPHISM + focally CALCIFIED matrix
Histological Classification:
Clinical Behavior Chondrocytes Matrix
Grade I SLOW GROWING Small, dark nuclei, scant cytoplasm, in clones Low cellularity
(30-35%) Occupy lacunae with odd number of cells Abundant matrix
No mitoses Calcification
Grade II LOCALLY AGGRESSIVE Larger and paler nuclei, y cytoplasm More cellular
(40-50%) Metastasis in 20% Mild pleomorphism Less Matrix
Very rare mitoses Focal myxoid change
Grade III METASTASIZING Large and vesicular nuclei, yy cytoplasm Intense hypercellularity
(15-30%) Metastasis in 70% Marked Pleomorphism Sparse matrix
Mitoses: 2 /10 HPF
Topographic Classification:
1. INTRAMEDULLARY either DENOVO or 2RY to enchondroma:
Olier's & Maffucci's are at much higher risk
2. SURFACE usually 2RY to osteochondroma:
y SIZE, FUZZY, CAP > 4cm, BASE > 6cm diameter
Pathological Classification:
1. CONVENTIONAL
2. LOW GRADE:
1. CLEAR CELL (MALIGNANT CHONDROBLASTOMA)
2. JUXTA-CORTICAL
3. HIGH GRADE:
1. MESENCHYMAL CS
2. DEDIFFERENTIATED CS
Metastasize: to lung
Clinically
• Presents with CONSTANT PAIN or increased size of a pre-existing lump
• Most common malignant tumour of the hands and face in middle aged patients
• Metastatic deposits are infrequent and usually go to lung
X-Rays
• Variable appearance with 60 - 70% have calcification and 50% have sub periosteal NBF
• Large CYSTIC lesion é cortical DESTRUCTION + SCALLOPING & EXPANSION
• CENTRAL CALCIFICATION
Treatment
• These tumours tend to METASTASIZE LATE therefore attempt wide local excision initially
• Radiotherapy useful for the treatment of surgically inaccessible sites however are relatively
CHEMO & RADIO-RESISTANT
• Treatment protocol as those of malignant osteosarcoma = LIMB SALVAGE
Prognosis
• Dependant on grade:
• Low grade................................................. 80% 5YSR
• High grade ............................................... 20% 5YSR
DEDIFFERENTIATED CHONDROSARCOMA
• HG chondrosarcoma + areas of osteosarcoma, fibrosarcoma, or MFH (in this frequency)
• PXR: aggressive lucent area on previous classic chondrosarcoma
CLEAR CELL CHONDROSARCOMA

• LG variant of chondroblastoma
• Affects epiphysis of long bones, usually UPPER FEMUR
• Pathology
Numerous cells é abundant CLEAR VACUOLATED CYTOPLASM
Scattered MNGC
Scant CHONDROID matrix
May be confused with GCT, Chondroblastoma, or renal clear cell tumour
• PXR:
Well CIRCUMSCRIBED LUCENT defects often with thin SCLEROTIC border
MESENCHYMAL CHONDROSARCOMA
• Rare HG
• Usually occurs in the RIBS or JAW
• Age usually 10 - 30 years
• Sheets of small undifferentiated cells resemble HG EWINGS + focal LG CHONDROID matrix
• Metastasis usually to lung
[Cystic Lesions] Page | 333
Vçáà|v _xá|ÉÇá
(1) Simple Bone Cyst
(2) Aneurysmal Bone Cyst
(3) Giant Cell Tumor
Unicameral Bone Cyst

(Simple Bone Cyst)
Definition:
• The simple bone cyst is a common benign lesion, ώ is characterized by fluid-containing cyst
at the metaphysis of long bones, and usually of unknown cause
• The unicameral bone cyst is probably not a true neoplasm.
• Cysts that abut a physis have in the past been termed active & have tended to recur with
greater frequency than those separated from the plate by normal bone i.e.: inactive.
Epidemiology
• AGE: .................................................................. 5- 15 years.
• After 10y .......................................................... z recurrence rate
• SEX: ♂:♀........................................................... 2 : 1
The pathogenesis: (unknown)
VENOUS OBSTRUCTION AND BLOCKAGE

• Venous obstruction and blockage of interstitial fluid drainage, in an area of rapidly growing
and remodeling cancellous bone lead to the development SBC
TRAUMATI C THEORY :
• Because the lesion occurs in a growing bone, it is probably the result of mechanical trauma
to an area of bone growth in the physeal line Æ creating a defect at that point Æ failure of
endochondral bone formation Æ resulting in a hiatus Æ present as a unicameral bone cyst.
• In favor of this theory .................................. age group affected.
• Against this theory ....................................... cysts that cross the mid-diaphyseal point
HEMORRHAGIC T HEORY
• Some suggest that solitary cyst is the result of a hæmorrhage into the metaphysis Æ organizes by
fibrous wall formation; while the blood volume clots then liquefies
• The surrounding fibrous capsule acts as a semi-permeable membrane & if the osmotic pressure
of the intra-cystic content is higher than that of the surrounding tissue, water is drawn into the
cyst Æ y intra-cystic pressure and the cyst expands Æ pressure erosion on the surrounding
cancellous tissue & then cortex.
• Extra & intra cystic densities...................... eventually stabilizes Æ latent stage
• Against this theory........................................ pts é hemophilia do not show a y incidence of SBC
FAILURE OF BONE FORMATION :

• If the cyst is a defect resulting from failure of bone formation by an aberrant part of the
physis Æ defect involves the diaphyseal portion supposed to be formed by that part
• The cartilage growth is no longer converted to bone; while the surrounding bone is
remodeling normally Æ false appearance of expansion that never been wider than the
epiphyseal line & this is a diagnostic feature.
• NBF laid down as the child matures & the cyst then occupies an area towards diaphysis
• In adult state many cysts are obliterated radiographically by NBF on the overlying cortex.
• It becomes smaller than the width of the adult bone
336 | Page [Cystic Lesions]
Pathology
SITE
• Tubular bones .............................................. 90-95% of patients.
• Location ........................................................... PROXIMAL METAPHYSEAL
• Diaphyseal in only ....................................... 4-12% of patients
• Commonest site ............................................ PROXIMAL HUMERUS & UPPER FEMUR.
MACROSCOPIC:
• There is always .............................................. ZONE OF NORMAL BONE bet the cyst & physis ώ
represents the amount of longitudinal bone growth since the establishment of the lesion.
• It has been stated that cysts that appear very near the line are still actively growing & that
therapy at this time ..................................... result in a RECURRENCE
• As the bone continues to grow ............... CYST DRIFT to mid-diaphysis (never cross it)
• The outer cortical shell................................ covered by an intact periosteum
• The cyst contains ......................................... CLEAR SEROUS FLUID (Occasionally, blood if #)
• The cyst is lined by ...................................... PALE BROWN MEMBRANE of few mm thickness
• After a fracture ............................................. Fibrous septa form Æ MULTILOCULAR APPEARANCE.
MICROSCOPIC:
• There are no pathognomonic features about the tissue that is curetted from the bony walls
• Lining membrane is formed of .....................young fibrocytes + deeply stained fibrin + collagen
• Hemosiderin pigments
• Xanthoid cells
• Mngc
Clinical picture:
• Usually ASYMPTOMATIC SBC develops very slowly
• Rarely causes mild PAIN
• Pain occurs when the overlying cortex is thinned to the point of pathologic fracture.
• INCIDENTALLY, a bone cyst is discovered in radiographic surveys done for another reason.
• 50% of patients have PATHOLOGICAL FRACTURE
X rays
• WELL-DEFINED, GEOGRAPHIC, LYTIC lesion with narrow transition zones
• A thin SCLEROTIC MARGIN is a typical finding.
• INTRAMEDULLARY METAPHYSEAL immediately JUXTA-PHYSEAL (occasionally diaphyseal)
• The distance to physis varies .................... depending on the duration
• Although EXPANSION & THINNING ............ cortex usually not wider than metaphysis
• The long axis of the lesion ......................... parallels that of the bone
• Pathologic fracture lead to the migration of a fragment of bone to a dependent portion of
the fluid-filled cyst ........................................ pathognomonic ”FALLEN FRAGMENT” SIGN
• Some may have ............................................. multilocular appearance
1]. Fibrous dysplasia.

2]. Non-ossifying fibroma.
3]. Giant cell tumour.
4]. Enchondroma.
5]. Osteitis fibrosa cystica.
6]. Neurofibroma.
Treatment:
• Surgery is indicated primarily:

o Younger age group
o Impending #
o Coxa vara deformity or any deformity (z bone strength)
• Modalities:
1. Currently successful healing is reported by Methyl-Prednisolone Acetate (200 mg)
injection into the cavity
• The mechanism of action:
o Unclear, μß reparative response to the injection process
• Advantages:
o Shorter operating time
o less bleeding
o Minimum hospital stay
o Minimum rehabilitation time
• Disadvantages:
o unpredictable healing
o Incomplete healing even after multiple injections
o Failure rate in WB bones ........ high
• Radiographic evidence of a good response:
o z cavity size
o y radio-opacification of the cyst
o Cortical thickening
o Osseous remodeling
2. Traditionally ............................................... Curettage + BG
• Recurrence that require redo ............ 25%.
• Recurrence z with ............................... high-speed burr on the cyst walls after curettage
• Cauterization with phenol following curettage has not reduced the recurrence.
Complications::
• Pathological fracture:
o Common...................................... 50%
o Callus of repair .......................... exerts healing influence SBC
o Considered as ........................... diagnostic & curative -5-15y male
-Upper Humerus & Femur
• Malignant transformation .................. very rare
Juxtaphyseal Metaphyseal
-Clear fluid filled cyst
-Fibrous Wall
-Asymptomatic
-50% pathological #
-PXR: Fallen Leaf
-Sclerotic edge
-Treat é Curette BG or
steroid injection
Aneurysmal Bone Cyst

Introduction
• WHO definition “ABC is a benign expanding cystic osteolytic tumor lesion consisting of
blood-filled spaces separated by CT septa containing trabeculae or osteoid tissue and
osteoclast giant cells” & occurs ð vascular malformation ð unknown cause
• Although benign, the ABC can be a rapidly growing and destructive
Incidence
• True incidence is difficult to calculate ð spontaneous regression & silent cases
• Considered .................................................... rare especially in very young age
• SEX .................................................................... SLIGHT ♀>♂
• AGE: ................................................................... 2nd decade 15Y (70%); but it occurs at any age
Etiology:
• Vascular malformation within the bone ð unclear cause
• Three commonly proposed theories are as follows:
1.ABC may arise de novo = Primary ABC associated é gene 17p13
2.ABC may arise in an area of prior trauma
3.ABCs caused by a reaction 2ry to another bony lesion = Secondary ABC:
This theory was proposed ð y incidence of associated tumors in 30 %
Giant cell tumors are the most commonly present
Other benign and malignant tumors are found:
Giant Cell Tumor FD
SBC NOF & EG
Osteoblastoma Telangiectatic Osteosarcoma
Chondroblastoma Chondrosarcoma
Chondromyxoid Metastatic carcinoma
Pathogenesis
• The true pathogenesis is unknown
• Different theories:
o Vascular malformations
o AV fistulas
o Venous blockage
o Altered hemodynamics
• Local hge Æ reactive osteolytic tissue y pressure / expansion / erosion / bone resorption
Pathology
Site:
• ABCs may affect any bone in the body
• ABCs most common ................................... 80%LONG BONES Æ spine Æ flat bones (pelvis)
• Mainly ............................................................... ECCENTRICALLY METAPHYSEAL
MACROSCOPIC APPEARANCE:
• Cystic blood-filled cavity é charcteristic BLOOD-SOAKED SPONGE appearance
• marked expansion or ballooning of the bone
• The cavity is divided into cavernous spaces by intertwining fibrous mesenchymal septa
• Thin subperiosteal shell of NBF surrounds the lesion
• Intra-op.: when blood is sucked Æ refill quickly (WELLING UP) = (POURING OF BLOOD)
• It has no connection é systemic circulation; but its blood comes from septal capillaries
MICROSCOPIC APPEARANCE:
• Large vascular spaces
Fibrous septa: same as SBC (fibrous tissue, fibroblasts, mngc, hemosiderin macroph)
o
+ Osteoid areas
o
• Mitotic figures are common, but no atypia
Clinical picture:
• Patients usually present with PAIN ......... 90%
• A MASS ώ may ................................................ Rapidly enlarged
• PATHOLOGIC # ................................................. 10-20% (y in spinal lesions)
• GROWTH DISPROPORTION ............................... ð disruption of the physis
PXR
• Eccentric (μß central or subperiosteal), cystic lytic lesion
• Expansion of bone ...................................... BLOWN-OUT, BALLOONED
• Compressed trabeculae ............................... SOAP-BUBBLE & PENCIL IN CUP
• Periosteal NBF rim .......................................... EGG-SHELL appearance
• Spine:
o Loss of pedicle of involved vertebrae
o Posterior elements is preferred location
• CAPANNA RADIOLOGICAL CLASSIFICATION:

Type Site Cortical Expansion Cortical Erosion
Type I Central metaphyseal Min -
Type II Entire segment of a bone Marked +/-
Type III Eccentric metaphyseal Min -
Type IV Subperiosteal diaphyseal Min +
Type V Metadiaphyseal Marked & push periosteum +
to soft tissue
Q: Malignant ABC is a term used for multiple recurrent aggressive ABC

Rarely present é malignant change or pathological #
CT
• Same PXR finding; trabeculation
• Fluid-fluid levels; these are most often found in the ABC, but they are not exclusive to it.
MRI
• As CT scan, but they can more specifically reveal Æ blood & expansion into soft tissues
• The appearance on imaging studies has been divided into 4 PHASES OF PROGRESSION:
Phase Progression Cortical Expansion Cortical Erosion Trabeculation
I- Initial (incipient) -Starts slow -Little & saucer shape -Little -Min
II- Growth -Rapid -Severe & blown out -Massive destruction -Destruction outpace
-Minimal periosteal reac. & bone lysis trabeculation & NBF
III- Stable -Plateau -Classic Soap-Bubble -Classic -Numerous
-Egg-shell surround
IV- Healing -Progressive calcifn -Diminished -Healing -Coarse irregular
DDx
ABC Giant Cell tumour
Age Young Adult
Site Metaphyseal Eccentric Epiphyseal central may extend to metaph.
PXR Ballooning Lacks expansion
Macroscopic Blood-soaked sponge Liver piece
ABC SBC
Age young younger
Site Eccentric Metaphyseal Central Metaphyseal then diaphyseal é growth
Macroscopic Blood-soaked sponge Clear yellow fluid
Ballooning & Egg shell Cortical endosteal erosion & expansion
• Telangiectatic osteosarcoma Difficult to distinguish radiographically from an aggressive ABC
• FD
• Osteoblastoma; may have also soap bubble appearance on PXR but no fluid fluid level
Treatment:
• Stage 1 (latent ABC) intralesional Curettage +BG
• Stage 2 (Active ABC) Extended (roof burring) Intralesional Excision + BG +
adjuvant (see later)
• Stage 3 (Progressive) En Bloc or Wide Excision
• Expendable bone En Bloc
• Huge pelvic or spine ABC Megavoltage 30Grays (exception for the rule of irradiation to
malignant tumors only)
• Reconstructive options after wide excision include:
1]. Structural allografting
2]. Autografting
3]. Reconstruction with either endoprosthesis or APC.
• Selective arterial embolization:
o By using angiography, an embolic agent is placed at a feeding artery to the ABC
o Various materials, such as springs and foam, have been used to create the emboli:
o Selective arterial embolization is indicated in:
1]. Difficult locations
2]. May be performed within 48 hours prior to surgery to z hemorrhage
Prognosis:
• The prognosis for an ABC ......................... generally EXCELLENT but recurs
• The overall cure rate ................................... 90-95%.
Recurrence
• Usually happens within .............................. 1st y after surgery ABC
• All episodes occur within .......................... 2 y -15y female
• Patients should be monitored till ............ 5y till maturity to -Unknown cause
-Eccentric Metaphyseal long bone
detect early recurrence -Blood soaked sponge
• Recurrence y é: -Welling of Blood
Capanna I , II .................................... 24% -CP: Pain, Pathological #, Mass
-PXR: Soap Bubble, Egg-shell,
Capanna III, IV, V ............................ <5% Pencil in cup, Ballooning
younger age & open growth plate -Capanna PXR classification
Metaphyseal lesion -MRI Fluid-fluid level, classification
-ttt: Excision (accordingly) + BG
Stage 3 aggressive lesions
Ganglion cyst of bone
• Occur typically in middle-aged men at the ends of long bones, particularly the distal tibia.
• Considered intra-osseous extensions of soft tissues ganglia
• Subperiosteal ganglia have also been reported .
• Treatment: soft tissues excision + bone curettage (Recurrences is unusual)
Giant Cell Tumor of Bone

= Myeloid sarcoma = tumor of myeloplaxus = osteo-blasto-clastoma = osteoclastoma
• GCT of bone has been described as the most challenging benign bone tumor. Although
benign, GCT shows a tendency for significant destruction, recurrence, and metastasis
Cell Of Origin
• Supporting cells of bone CT & not osteoclasts (both originate from mesenchymal cells)
Theories Of The Etiology:
1]. Traumatic theory
2]. Neoplastic theory
3]. Chronic inflammation
4]. Localized form of parathyroid osteodystrophy
Incidence
• 5% of all tumors
• 20 % of all benign bone tumors
• Race: Affects all races esp. ........................ China & southern India
• Sex:
o ♀>♂ (Unlike the majority of osseous neoplasms)
o In contrast, malignant GCT is more in men (3:1)
• Age:
o The vast majority ............................ SKELETALLY MATURES
rd
o 80% ..................................................... 3 Decade (20-50y)
o < 14y ................................................... rare (1-3%)
o >50y ..................................................... 10%
ggggggbiiiiiii
Pathologic Features
• Site: ABOUT THE KNEE (50-65%)
o The single commonest site:
Distal femur.......................... (30%)
Proximal tibia ...................... (25%)
Distal radius ........................ (10%), sacrum (5%), prox.humerus (5%)
o GCT also occur in:
Sesamoid bones ...................... patella
Apophyses ............................... eg, G.trochanter ώ is considered epiphyseal equivalents
• Location
o Eccentric meta-epiphyseal
o 85-99% of lesions reach ................... 1 cm sub articular (most important diagnostic feature)
o Site of origin is controversial ........... metaphyseal side of the epiphyseal plate.
o Macroscopic
Relatively large lesions extending to the articular surface.
Cortex is expanded / periosteum is not breached / soft-tissue extension is not uncommon
Grossly Æ soft, friable, fleshy, chocolate brown, yellowish-orange ð hemosiderin
Areas of:
Fibrosis..................................... (white)
Hge &blood........................... (red to brown depending on chronicity)
Xanthomatous .................... (yellow).
Blood filled cystic cavities
• Microscopic
o GCT = large № of GIANT CELLS IN A BACKGROUND OF MONONUCLEAR & SPINDLE CELLS
o MULTINUCLEATED GIANT CELLS (MnGC):
There are ................................. 30 Giant cell/HPF (but sometimes vary with the spindles)

Cell contains ........................... 30 nuclei

Cell diameter .......................... 30 μm

MnGC invade vessels ..............3%

MnGC Concentration ........... not related to recurrence or metastasis

o MONONUCLEAR CELLS:
Round, oval, or polygonal & may Resemble Histiocytes
Fusion of mononuclears ... giant cell formation
Mitotic figures may be abundant
o STROMA:
Spindle cells NUCLEI ARE INDISTINGUISHABLE from MnGC (helpful in DDx)
VASCULAR é numerous thin-walled capillaries
o OSTEOID FOCI small osteoid foci (never chondroid) produced by stromal cells
o ASSOCIATED:
2RY ABC but é solid areas of classic GCT
Extensive hemorrhage
Pathologic fracture, or previous surgery can alter significantly the usual
histologic picture of GCT Æ resemble a 1ry sarcoma
According To the Predominant Growth Character 5 Types Are Present:

Maroon color type
1].
Cystic type
2].
Telangiectatic type
3].
Fibrous or white (Myeloid)Type ÆLower radius
4].
Yellow (Xanthometaous ) type
5].
• Spread
Metastasize to the lung ................ 3%
o
The metastases appear................. clusters of GCT located within the lung
o
Metastasis appears ........................ 3-5 y after detection (detection may take 10y)
o
The natural history of lung metastases is unpredictable; may regress, remain stable,
o
continuously grow slowly, or rapidly progress have been reported
• Staging,
Jaffe Histologic Staging:

Grade Behavior % MnGC Mononuclear Mitotic Figures
GI Benign PXR 15 y z Absent
G II Aggressive PXR 70 Numerous Moderate + Atypia
G III Metastasis 15 z & small y Marked atypia + pleomorphism
Campanacci Radiographic Grading System

Grade Behavior Margin Cortex
GI Latent Well defined Intact
G II Active Relatively well defined, Not sclerotic Thin expanded
G III Aggressive Ill defined Eroded
• No correlation exists bet. grading systems and the incidence of recurrence or metastases
• DNA analysis has shown only limited value in prediction the behavior of GCT
ggggggbiiiiiii
Clinically:
• Nonspecific and include (in order of decreasing frequency) pain, swelling, z ROM
• PAIN is usually of several months duration / z by rest.
• Related to associated PATHOLOGIC # Æ acute onset of pain (10%)
• NEUROLOGIC symptoms may be associated with spine lesions
• DDx of GCT is extensive, including (but not limited to):
o Brown tumor ○ Osteoblastoma
o Chondroblastoma ○ ABC
o NOF ○ Osteosarcoma é giant cells.
• These lesions can be difficult to distinguish from one another, particularly é FNAC or with
frozen section specimens Æ careful clinical, pathologic, and PXR correlation. This is
particularly true of brown tumor of hyper PTH, which can be indistinguishable from GCT.
Laboratory analysis (Ca, ph, & PTH levels) should be performed to exclude this possibility
ggggggbiiiiiii
PXR
• 80% Geographic Lysis + narrow zone of transition + z surrounding sclerosis
• 20% Geographic aggressive growth + wide zone of transition
• ECCENTRIC EPIPHYSEAL ......................................... (90%); but large lesions appear central at presentation
• Cortex THINNING, EXPANSILE remodeling ....... (60%)
• Cortical PENETRATION .................................. (50%) often é an associated soft-tissue mass
• OPERCULUM on metaphyseal end ........... is a medullary plug of compressed bone
• Prominent TRABECULATION ........................ (50%) Æ MULTILOCULATED = SOAP BUBBLE appearance
ð pseudo-trabeculation from osseous ridges created by endosteal scalloping.
• This PSEUDO-TRABECULATION is well seen by comparing PXR é CT
• Pathologic fracture .................................... (30%)
• Periosteal reaction ...................................... (20%)
• Sclerotic rim .................................................. (2%)
• Multicentric locations ................................ (< %) = involve both joint sides:
o More common in atypical sites.
o More common among young patients (80% < 25 years old).
Bone Scan
99m
• y Tc static uptake in the vast majority of GCT
• y uptake peripherally é photopenia centrally DONUT SIGN (60%)
Angiography
• Angiography of GCT is only infrequently performed since the advent
of CT and MRI:
o Hyper vascular ..................................... (60%)
o Hypo vascular ....................................... (30%)
o Avascular ............................................... (10%)
• Preop transcatheter arterial embolization can be used to z blood loss during surgery
CT NB
• CT improves detection of ................................ cortical thinning, • ABC is well seen é CT & MRI
expansion, path #, periosteal reaction (better); as multiple fluid level in
sagittal & axial cuts
• ABC component detection............................. FLUID-FLUID LEVEL • Wait 10 min before taking graphs
MRI allowing fluid to sediment
• ABC components in GCT .......................... 14% (common)
• GCT + 2ry ABC ............................................. 40% (the commonest lesion to have 2ry ABC)
• GCT + ABC .................................................... more aggressive PXR; ð expansile cystic component
• ABC component detection....................... Fluid-Fluid Level
• CT is superior to MRI in periosteal reaction, pathologic #, and absence mineralization.
• MRI superior to CT in delineating soft-tissue tumor extent
344 | Page [C
Cystic Lesions]
Tre
eatment
1- BENIGN GCT
• Depends on:
1]. Locatioon of the tuumour.
2
2]. Size of the tumorr.
3
3]. Tumor grading.
4
4]. Soft tisssue extenssion & articcular involvvement Æ Joint prese
ervation is impossible
e
Benign GC
CT
Excision Curettage
Alon
ne Reconstrucction Bone Graftt Bone Cement
Prosthetic Biological
Disstraction oste
eogenesis BG
Currettage
• Intralessional EXTENDED CURETTE is a limb-sparing option that offfers good ffunctional outcomes o
• Simple curettage ± BG ................................... RECURRENCE rates of 30-50%
• A largee CORTICAL WINDOW ............................. necessary to t expose the
t entire tu umour
• The intrraosseous tumour
t bullk is remove ed with a la
arge curettee till normall-appearing
g bone
• The cav vity is then enlarged........................... HIGH-SPEED BURR (5mm m) in all dire
ections + ADJUVANT
High spee
H ed burr
• Not onnly MECHANICALLY REMOVE remna ants; but allso adds a THERMAL NECROSIS forr the tumour
g of the cavvity then ⎯⎯ ⎯⎯→ chemicall or physica
• Burring
FollowedBy
al ADJUVANT + PMMA oro BG
Local adju
L uvant age ents
al adjuvantt Æ Liqu
1. Physica uid Nitroge en (LN)
2. Chemiccal adjuvan nt Æ Phenol
• z locall recurrenc ce rate (Fro om 50% Æ 10%).
L
Liquid Nitrogen
• Cryotherapy is th he therapeu utic use of cold (LN) to t induce tissue
t necrrosis.
• Mechanism of ne ecrosis via:
1]. Form mation of intracellula
i ar ice crysta
als
2]. Mem mbrane dissruption
3]. Elec ctrolyte cha anges
4]. Den naturation of cellular proteins
5]. Microvascularr failure.
• After curettage N2 is poured d through a stainlesss steel funn nel Æ left till evaporates
• Irrigate
ed the surrounding é warm saliine to prevvent therma al injury Æ repeat 2-33 times
• Cellular death de epth ................................. 1-2 cm
• Recurre ence rates ....................................... 2-12%
• Fracturre is the mo ost commo only reportted complication.
P
Phenol
• Mechanism: Phen nol (5%) ca auses:
o Protein coagulation
o DNA damage and tisssue necro osis.
• Technique: Phenol is simply y applied by b using so oaked swaabs Æ rema enol is suck
aining phe ked
Æ cavity is filled é absolute alcohol Æ irrigate with w isoton nic saline
• Advanttage: less penetration
p n power < LN2 Æ1-1 1.5 mm off bone necrosis Æ z fracture.
f
Reconstruction of defects after curettage and adjuvant treatment is done using either:
1]. Autologus bone graft with or without allograft
2]. Bone cement
3]. Combined (bone Graft + bone cement)
Curettage and bone grafting:

• After intralesional curettage Æ high speed burr Æ adjuvant Æ pack the lesion é autograft ±
allograft to fill the defect completely
• When necessary, ORIF is used to buttress the bone
• Advantages:
o Restoring normal biomechanics to the joint surface to z OA
o Restoring bone stock, which may help if future procedures
• Disadvantages:
o The limb must be protected for along time to prevent a pathologic #.
o Tumor recurrence is difficult or impossible to distinguish from graft resorption.
Curettage and bone cement:

• Intralesional curettage followed by packing é cement z recurrence than that é BG.
• Mechanism of action:
o Direct cytotoxic effect on the tumour cells
o The thermal effect of the polymerization reaction Æ 2 - 3 mm of necrosis
o Can é stand high stresses so it is preferred more than BG. In knee lesions because
defects in these areas usually too large to be filled é BG & to heal é out collapse
• Advantages:
o Lack of donor-site morbidity.
o An unlimited supply.
o Immediate structural stability.
o Low cost.
o Ease of use
o Radiopaque cement sharply contrasts é bone, so recurrence is more readily detected
• Disadvantages:
o Difficulty in removing it when revision is needed.
o Subchondral cement may predispose to early OA.
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Excision:
• Indicated only for
o Grade III tumours.
o Displaced Pathologic # + poor bone stock not allowing for ORIF é cement
o Joint Destruction
• Biological reconstruction using bone graft can achieve:
1. Joint mobility as by using osteochondral proximal fibular autograft or allograft in
cases of GCT of the distal radius and proximal humerus.
2. Joint fusion as by using iliac crest, fibular graft or rotational graft
ggggggbiiiiiii
2- RECURRENT BENIGN GCT
• The most important factor for prognosis is the Adequacy Of Tumour Resection.
• Recurrence after curettage > wide excision.
• Jaffe & Campanacci grading are unreliable
• Time: most recurrences are expected in 2y (some pts remain at risk up to 30y)
• Pathology: Recurrent GCT usually has malignant biological behavior.
• Treatment:
o Repeat curette: If benign behavior & no soft tissue extension &no articular damage
o Wide excision. If pathological # / soft tissue extension / articular damage
o Radiotherapy is recommended when:
Complete excision or curettage is impractical surgically (spine and sacrum)
Medical contraindication for surgery
Aggressive multiply recurrent GCT of bone
o Amputation is indicated in massive local recurrence beyond reconstruction.
3- BENIGN GCT WITH PULMONARY METASTASIS

• Although GCT is typically benign, lung metastases occur in 2 - 6 % of cases.
• Primary lesion & metastasis usually have the Same Histological Features of a benign tr
• Pulmonary metastases may be Multiple.
• High risk for development of metastasis:
o Recurrent lesions
o Radiologically stage III lesions
o Vascular invasion by tumour growth or surgical manipulations
• Pulmonary metastases are divided into 3 types:
1. The spontaneous regression type
2. The continuously slow-growing type
3. The rapid-growing type.
• About 20% of the patients with continuously slow-growing type and rapid-growing type
die of the disease.
• Survival of the remaining 80% suggests that benign GCT of bone with pulmonary
metastasis has a relatively good prognosis
• Solitary metastasis Æ resection + ttt of the primary lesion
• When pulmonary metastases cannot be surgically excised Æ local DXT + chemo
4- MALIGNANT GCT
• Malignant giant cell tumour is a term used to describe a heterogeneous group of giant cell-
containing lesions that are capable of MALIGNANT BEHAVIOR and PULMONARY METASTASES.
• Prevalence: .................................................... 5%-10% of all GCT
• Site: .................................................................... distal tibia and sacrum.
• Types:
oPrimary malignant GCT (De Novo lesions)
Extremely rare
Occur most frequently in recurrent cases.
o Secondary malignant GCT: (Radiation sarcoma)
Are sarcomas that occur at the sites of
previously treated GCT by DXT
• Treatment:
o Surgery alone
o Surgery And Chemotherapy.
o Radiotherapy alone
[Miscellaneous Lesions] Page | 347
`|ávxÄÄtÇxÉâá
o ADAMANTINOMA
o CHORDOMA
o HEMANGIOMA
o GORHAM MORBUS STOUT
348 | Page [Miscellaneous Lesions]
Adamantinoma
• An EXTREMELY RARE, locally aggressive, osteolytic, LG malignant tumour of epithelial origin of long
bones. It is not related to adamantinoma or ameloblastoma of the mandible and maxilla which is
derived from Rathke's pouch
Incidence
• Age ...................................................................... 10-40 Y
• M>F
Pathology
• Osteofibrous dysplasia (OSSIFYING FIBROMA) has a striking predilection for the tibia and has well
documented association with adamantinoma and may be a benign precursor to it
Site:
• tibia ......................................................................(90%)
Gross:
• GRAYISH white RUBBERY mass é areas of HGE and necrosis
• Bone SPICULES and CYSTS filled é blood or straw-colored fluid
Microscopic
• Biphasic tumor .................................................epithelioid islands + surrounding reactive fibrous stroma
• The stroma consists of spindle cells producing collagen
Presentation
• History of TRAUMA usually associated with adamantinoma (remains unclear role)
• The patient usually has SWELLING that may be painful of 3WK-3Y duration
Radiology
• Eccentric, well-circumscribed, lytic lesion + cortical thinning + Little Periosteal Reaction
• Several lytic defects separated by sclerotic bone é "Soap-Bubble" appearance.
• The lesion may break through the cortex and extend into soft tissue
• MRI helps demonstrate the intraosseous and extraosseous involvement.
Differential diagnosis (radiologically)

• Osteofibrous dysplasia
• fibrous dysplasia
• ABC
• chondromyxoid fibroma
• chondrosarcoma.
Treatment
• WIDE SURGICAL EXCISION
• RADIO & CHEMO-RESISTANT
Prognosis
• May METASTASIZE to Lungs, LN, Liver by both haematogenous and lymphatic routes
• Survival é metastasis ...................................... 12 Y
• Local recurrence.............................................. 20%
[Miscellaneous ] Page | 349
Chordoma
• RARE malignant tumor arises from remnants of notochord!!
Incidence:
• Age ...................................................................... 40-70y
• M:F ........................................................................ 2:1
Aetiology:
• At 4-6 wk of fetal development, mesenchymal cells from sclerotomes
merge to surround the notochord & form vertebral bodies.
• The notochord normally degenerates ⎯⎯ ⎯ ⎯ ⎯→ nucleus pulposus
Re mnantsForm
• The prevailing theory is that in chordomas the notochord fails to

degenerate and then undergoes malignant transformation.
• Against this; normal notochord remnants have never been observed!
Pathology
Sites:
• Sacrococcygeal region ......................... 50%
• Skull Base .................................................... 30%
• Transverse processes of vertebrae
• Paranasal sinuses.
Gross
• Soft, blue-gray, lobulated, Encapsulated tumor
• Gelatinous translucent areas
• Tumor Tracks Along Nerve root at sacral plexus or sciatic
notch in planes of least resistance
Microscopically:
• Lobules + Fibrous Septa.
• "PHYSALIPHOROUS" cells: EOSINOPHILIC CYTOPLASM + MUCIN VACUOLES push the nuclei to the side
resulting (=greek word for bubble)
Clincal
• Sacrococcygeal tumours:
o Low back PAIN (no characteristic pattern or course)
o Bowel and bladder DYSFUNCTION
o Often large at presentation & can be palpated on PR
• Other sites:
o DYSPHAGIA ...................... Anterior cervical tumours
o NEUROLOGICAL DEFICITS Posterior cervical tumors
o HEADACHE ....................... Base of the skull
Radiology:
• PXR: solitary mid-line LYTIC lesion + bony DESTRUCTION + soft tissue MASS + focal CALCIFICATION
• CT & MRI: demonstrate soft tissue + epidural extension + calcification + identify recurrence
• Chordomas have reduced uptake on bone scan.
Treatment
• WIDE EXCISION ................................................. (rarely feasible ð the anatomic location of the tumor)
• Sacrococcygeal tumor ............................... sexual & sphincter dysfunction after surgery
• RADIATION ....................................................... if complete resection is impossible
• CHEMOTHERAPY .............................................. for late stage disease.
Prognosis:
• Chordomas METASTASIZE to lymph nodes, lungs, liver and bone.
Haemangioma Of Bone
Features
• Haemangiomas are hamartomas characterised by vascular spaces lined with endothelial cells
• Common, é ~ 10% of autopsy cases having vertebral haemangiomas
• M:F ........................................................................ 1:2
• Age........................................................................ 30 - 50 Y
Site
• VERTEBRAL BODIES (thoracic) ........................50%
• Calvarium ...........................................................20%
• Also tibia, femur and humerus
Pathology
• GROSS: Vascular HAMARTOMA with CYSTIC, DARK RED CAVITIES (DDx: ABC, telangiectatic OS)
• 4 types:
o Capillary
o Cavernous
Most Common
o Arteriovenous: remnants of foetal capillary beds
o Venous
• MICROSCOPY : Non-vascular components: fat, smooth ms, fibrous, bone, haemosiderin & thrombus
Presentation
• Usually asymptomatic and solitary..........discovered on x-ray or at post mortem
• Vertebral haemangiomas ...........................chronic back ACHE + neurological symptoms
• Pathological ..................................................... FRACTURE
• Long bones may ............................................ OVER GROW ð y blood supply
Radiology
PXR
• Vertebral lesions ..............................................coarse, thickened vertebral trabeculae ð erosion of the
horizontal trabeculae Æ CORDUROY appearance
• Vertical striations without bone expansion (DD Paget's)
CT
• Body lesions ..................................................... POLKA DOT as the vessels are seen in cross section
• Calvarial lesions ...............................................lytic é radiating WHEEL SPOKES
• Metaphyseal or epiphyseal.........................lytic lesions é spiculated pattern of "IRISH LACE"
MRI
• T1 vary from low to high intensity depending on fat content
• T2 sequences demonstrate lesions with high signal due to the vascularity
Treatment
• Asymptomatic ..................................................No ttt
• calvarium Lesions............................................resected é thin margin of normal bone
• Vertebral lesions ..............................................radiation or excision preceded by embolisation
• Metaphyseal lesions .....................................excision + BG
[Miscellaneous ] Page | 351
High Grade Angiosarcoma of Bone

• Seems to have two distinct clinical presentations:
o First, the lesion can present as multiple lesions in a single bone, two or more
adjacent bones, or perhaps all the bones of a limb. These lesions seem to have an
indolent course and the prognosis remains good.
o The second presentation is that of single or multiple rapidly progressive lesions that
metastasize to other bones or to the lung this form of the disease has a very poor
prognosis.
Gorham Morbus Stout Syndrome

Hajdu-Cheney Syndrome
Phantom or Vanishing bone disease
Definition:
• It is a rare idiopathic non neoplastic massive acro-osteolysis of unknown aetiology that can affect
almost any bone.
Epidemiology
• Any age and gender, but
nd rd
• Slightly more in ♂ 2 – 3 decades
Pathogenesis Theories:
• Unknown loss of the coupling between the osteoblastic and osteoclastic activities, with resultant
uncontrolled bone resorption without NBF
• Traumatic theory: after # episode; clot neo vascularization takes place in a defective way that
trigger the uncontrolled angiomatous proliferation which leads to the uncoupling
Pathology:
SITE:
• Affect ANY BONE, and spread to ADJACENT BONE, or MULTIFOCAL
• Pelvis, spine, & skull are common
MACROSCOPICALLY:
• Bone is replaced by angiomatous engorged capillaries.
• Eventually the bone is replaced by dense fibrous tissue
• Pathological # triggers more angiomatous formations
MICROSCOPICALLY:
• Non neoplastic angiomatous proliferation; that fill the medullary canal
• Histochemical studies: shows y acid phosphatase, yIL6, and y leucine
aminopeptidase activities
Diagnosis:
Clinically:
• Pathological #, at time of presentation
• Swelling
• Pain
• Deformity
PXR:
• Massive osteolysis of one bone or of adjacent bones
• Tapered bone ends appearance
DD :
• HEREDITARY MULTICENTRIC OSTEOLYSIS: AD or AR dysplasia, ccc by osteolysis of the hands & feet
during the 1st decade of life
• KASABACH-MERRITT SYNDROME: is a potentially life-threatening coagulopathy that is related to
platelets being trapped in a large cavernous hemangioma. Some times pt die from hemorrhage
or infection.
• GAUCHER’S
Treatment: there is no consensus about an effective treatment
1]. ORIF + PEMF
2]. Radiotherapy
3]. Bisphophonate
4]. Steroids
5]. Interferon α2b
[
[Miscellane
eous ] Page | 353
T or likee con
Tumo nditions
Definition
• Any non-neoplas
n stic patholoogical cond
dition that causes a soft
s tissue m
mass or a bone
b lesion
n that
could be mistake en for a tum mor
Classification
Bony Lesion
• Conge enital
1]. Fibrous dy ysplasia
2]. Caffy’s synd drome
3]. Osteopetro osis
4]. Osteopoikiilosis
• Traum matic
1]. Myositis osssificans
2]. reactive lessions of thee bone surfaace
3]. Extuberantt healing ca allus
4]. Stress fracttures
• Infections:
1]. pyogenic osteomyelit
o tis
2]. Subacute sclerosing
s o
osteomyelit is
3]. T.B arthritiss/osteomye elitis
4]. hydatid cysst of bone
• Prolifeerative cond ditions
1]. Nora’s lesiion
2]. Tarlov cystt: cord cysttic lesion thhat may en nchroach on
o the cord t vertebra
d & erode the
3]. Elasto-fibroma dorsi::
4]. Intraosseo ous ganglio on
5]. Turret exo ostosis: calccifies traum
matic hand subperiostteal haemo
orrhage onn dorsum
• Inflammmatory con nditions
1]. Gout & pse eudo-gout
2]. Tumoral ca alcinosis
3]. Giant cell reactions
r
4]. Neuropath hic joint
5]. Radiation o osteitis
• Metab bolic disorde ers:
1]. Osteitis fibrrosa cysticaa
2]. Paget’s dise ease
• Vascu ular:
1]. AVN
2]. OCD
3]. Bone infarc cts
Soft tissue & synovial lesions:
• Gangllion cyst
• Synov vial lesions:
1]. PVNS
2]. Synovial ch hondromattosis
3]. Rheumato oid synovitiss
4]. Hemophilic and hemorrhagic sy ynovitis
• Mecha anical and irritation
i lessions
• Soft tisssue infectioons
• Amylo oidosis
Nora’s lesion
Definition
• Bizarre Parosteal Osteochondromatous Proliferation (BPOP) is a rare lesion probably represents an
immature lesion that over time will mature to solid cortical attachment.
Epidemiololgy
• ♂=♀
• 20-30y
Pathology
Site:
• Hands & feet
Mac
• Nodular surface covered with glistening cartilage
• Wrap extensively around bone
• Cut surface of the lesion bleeds freely.
Mic
• Hypercellular basophilic cartilage e calcification, but No Columnation (≠ osteochondroma)
• Disorganized Cancellous bone undergoing maturation
• Bizzare fibroblasts, no atypia, hyperchromasia, nor pleomorphism
Clinically
• Pain
• Mass
• Hand joints stiffness
Radiologically
PXR
• Well defined margins
• Projects into the surface of the bone
• Lacks the characteristic picture of osteochondromas as related to the physis
• Starts on the dorsolateral surface of the bone and then grew towards the palmar surface
CT
• Cortex and medullary cavity of the bone are Not Continuous with their counter part in BPOP
• Absent well formed cartilage cap
MRI
• Dark on TJ and bright on T2 (≠ osteochondroma)
Ttt
• Complete excision with the best possible margin
• Recurrence is 50% within 2years
[Soft Tissue Sarcomas] Page | 355
fÉyà g|ááâx ftÜvÉÅtá

o PERIPHERAL NERVE TUMORS
o SYNOVIAL TUMORS
o FIBROUS TUMORS
o MUSCLE TUMORS
o VASCULAR TUMORS
o FATTY TUMORS
o RARE SARCOMAS
o BONE METASTASIS
356 | Page [Soft Tissue Tumors]
Soft Tissue Tumours

Incidence Staging Diagnostic Clues Diagnostic Steps
Peripheral Nerve Tumours Synovial Tumours Fibrous Tumours Muscle Tumours
Vascular Tumours Fatty Tumours Rare Sarcomas
INCIDENCE
Benign soft tissue tumours common
Malignant soft tissue tumours rare
Pathological Classification:
1. Benign
2. Malignant
3. Reactive tumour like lesions
Tissue of origin Benign Malignant Reactive lesions
Fibrous Fibroma Fibrosarcoma Palmar & plantar fibromatoses
Nodular fasciitis Extraabdominal fibromatoses
Proliferative fasciitis
Fibrohistiocytic Fibrous histiocytoma MFH Intermed dermatofibrosarcoma
Atypical fibroxanthoma protruberans
Fat Lipoma Liposarcoma
Pleomorphic lipoma
Lipoblastoma
Angiolipoma
Hibernoma
Striated muscle Rhabdomyoma Rhabdomyosarcoma
Smooth Muscle Leiomyoma Leiomyosarcoma
Blood vessels Haemangioma Haemangiosarcoma Interm. hemangioendothelioma

Glomus tumour Mgn hemangiopericytoma
Lymph vessels Lymphangioma Lymphangiosarcoma
Synovial tissue GCT of tendon sheath Synovial sarcoma PVNS

Malignant GCT Ganglia
Synovial osteochondromatosis
Peripheral nerves Traumatic neuroma Malignant schwannoma
Morton’s neuroma Peripheral tumours PNET
Benign schwannoma
Neurofibroma
Extraosseous Myositis ossificans Extraskeletal
Fibrodysplasia chondrosarcoma
Bone and Panniculitis ossificans Extraskeletal osteosarcoma
cartilage Extraskeletal chondroma
Extraskeletal osteoma
Uncertain Tumoral calcinosis Alveolar soft part sarcoma
Myxoma Epithelioid sarcoma
Clear cell sarcoma
Extra-skeletal Ewings
STAGING
Benign
Enneking Stage Behavior
1 Inactive
2 Growing and symptomatic
3 aggressive
Malignant
Enneking Classification
[Soft Tissue Tumors ] Page | 357
DIAGNOSTIC CLUES
Size
• A small mass < 5 CM in its greatest dr ............ unlikely to be malignant
• Mass that is > 5 cm ........................................ 20% chance of being a soft tissue sarcoma
• The size of the lesion can be determined by physical examination if the lesion is
subcutaneous and easily palpable, or by ultrasound, computed tomography (CT) or magnetic
resonance imaging (MRI).
Site: Superficial or deep?
• Superficial lesions are more likely.................. benign or malignant é better prognosis than deep
• The depth is best determined by .................... physical exam, ultrasound or MRI.
• The THIGH and BUTTOCKS are the two most common sites for soft tissue sarcomas. Any large
deep mass in the thigh or buttocks should be considered at high risk for being a sarcoma
Consistency
• Soft tissue sarcomas tend to be ...................... FIRM and NOT VERY PAINFUL until they get very
large and compromise their vascular supply or adjacent neural structures.
• Lipomas are usually ....................................... SOFT and NON TENDER
• Infectious and inflammatory .......................... WARM and TENDER
• Pseudoaneurysm ............................................. PULSATILE é AUDIBLE BRUIT on auscultation.
Cystic or solid
• Most cystic lesions are .................................... INFLAMMATORY or BENIGN, as ganglion & abscess
• Solid lesions is either ...................................... benign or malignant neoplasm.
• Attempt Transillumination
• If deep ultrasound or MR scan will determine this
Duration
• A mass that has rapidly increased in size over two months is more likely to be a sarcoma
than the lesion that has slowly enlarged over a 20-year period.
• A mass that increases and decreases in size is usually a cystic lesion.
• However, caution should be taken with masses that have been present for a long time. Soft
tissue sarcomas occasionally present with a history of many years duration up to 30 years.
PXR
• Every soft tissue mass that is going to undergo intervention should have a plain radiograph
• Fat density lesion ............................................. lipoma
• Punctate calcifications ..................................... synovioma, chondrosarcoma, hemangioma
• Ossification ...................................................... osteosarcoma or myositis ossificans
• skeletal abnormalities ...................................... osteomyelitis, primary bone lesion or periosteal
reaction from the soft tissue tumor
MRI
• The MRI gives the most information of any radiographic study but should be reserved for
large lesions or those that are ill defined.
• It will clearly delineate whether the lesion is a bone lesion with a very large soft tissue
component (bone malignancy) or whether the lesion is a primary soft tissue lesion.
• z Tl & T2 ..................................................... either an extra-abdominal desmoid tumor,
extensive scar tissue, cortical or dense bone or a foreign material such as bone cement or air.
• y T1 & T2 ..................................................... likely a lipoma.
• z T1 & yT2 ................................................. low-grade liposarcoma & any neoplastic lesion;
benign or malignant.
DIAGNOSTIC STEPS
• History
• Examination +/- transillumination
• Ultrasound and plain radiography
• If lesion< 5cm, cystic and subcutaneous ........... observe
• (If patient keen on removal use a longitudinal incision with good haemostasis, ensure the
incision can be encorporated in any later excision and perform an excisional biopsy)
• If lesion >5cm, not cystic, or painful .................. MRI, then incisional biopsy / trucut needle
biopsy / fine needle aspiration (see principles of biopsy)
99m
• If a possibility of malignancy ............................. Tc , CXR, Chest CT, Abd CT, CBC, ESR
TREATMENT
• Soft tissue sarcoma treatment ............................ resection, amputation, DXRT or a combined
• Systemic control includes ................................... chemotherapy is controversial because it has
not been very effective in improving survival & has significant patient morbidity & cost.
PROGNOSTIC FACTORS
1. Stage of the patient (Ennekings stage)
o Metastasis is most frequently identified in the lungs Æ LN Æ skeleton.
o The standard staging studies include a physical examination of LN, CXR, CCT, Tc,
and gallium scan.
o A patient é non-metastatic disease at presentation has a far better prognosis
2. Histologic grade.
o Patients é HG lesions have a worse prognosis than patients é LG lesions.
3. Size of the lesion
o Although small lesions (< 5 cm) are rarely malignant, when they are, they have a
better prognosis than larger lesions.
4. Depth of the lesion
o Superficial (subcutaneous) soft tissue sarcomas have a better prognosis than deep
(below the muscle fascia) lesions.
ÆTIOLOGY:
1. Genetic: e.g. mutations, translocations, deletions, monosomy, trisomy as in NF1
2. Radiation: induce mutations
3. Carcinogenic: e.g. thorium, vinyl chloride
4. Lymphedema: predispose to lymphangiosarcoma
5. Infection: HPV 8, Epstein-Barr virus
6. Trauma
[So
oft Tissue Tumors ] Page | 359
Benign Peripheral Nerve Tumours

1. Neurilem
mmoma (beenign schw wannoma)
• BENIGN nerve sh heath tumo our
• YOUNG to middlle aged pattients
• Usuaally ASYMPTOMATIC apaart from the mass
• MR scan
s showss eccentric MASS arisinng from a peripheral
p nerve
• Histoologically:
o ANTONI A- compactt spindle ce ells, twisted nuclei, inndistinct cyytoplasm, clear
c vacuooles
o ANTONI B-less cellu ular
• TREAT .......................... exccision leaviing the nervve intact
2. Neurofibrroma & Neurofibrom
Ne matosis (seee neurofibbromatosis))
• CP: ............................ Mo ost are SUPERFICIAL, groow SLOWLY and are PAINLESS
• Gross s: .........................Exppand the neerve in a FUSIFORM fasshion
• Mic: ........................... inte
erlacing buundles of ELONGATED cellsc with WAVY DARK nuclei
• Treattment ................... exc cision with a marginal margin
• maliggnant changge .......In neurofibrom
n matosis (55-30%)
3.MORTON’S NEUROMA
Innterdigital neuroma
n waas first desccribed in 18845 by Durrlacher, chirropodist to the Queen of England d, as a
"fform of neu uralgic affeection" invoolving the plantar n. between 3rd & 4th M MT bones. In 1876 Morton
M
exxpanded thee clinical deescription anda postulatted that thee neuroma resulted
r froom pinching
g of the com
mmon
diigital branchh of lateral plantar
p n. too 4th web sppace between the mobille 4th & 5th MT heads. Other theorries:
Anatomy
th
• 4 dig gital br. of medial
m planntar n. emerrges from beneath the medial
m sidee of FDB annd while couursing
obliquuely acrosss the plantaar surface of the musscle receivees a comm municating branch from m the
comm mon digital br. of lat.pplantar n. The T "neurooma" (morre preciselyy degeneraative & fibbrotic
changges) occurss in the com
mmon digiital n. near its bifurcaation.
Aetiology A number off causative factors have been sugggested:
1. Tetheringg of the 3rd space n. byy the ANASTTO
OMOTIC BR. between medial
m and laateral plantaar nn.
2. Tetheringg of the n. by FORCED TOE DOSIFLEXION in higgh-heel shoee/hindfoot VALGUS/inteerdigital BURSITIS
3. LAXITY off transverse MT lig. → plantar dissplacement ofo MT headds → presssure on adjaacent digital n.
4. Relative NARROW 3RD INTER MT space
5. Relative HYPERMOBILITY of laterral 2rays (jooined to cuboid), on meed. 3rays (jooined to MTT cuneiform
m)
6. INSTABILITY of the 4thh MTP joint
7. Pressure on
o the nervee during BW W Æ PRESSURE NEURALGIA
8. TUMOR innvolving thee lateral most branch off the mediall plantar n.
9. LUMEN OCCLUSION inn the comm mon digital A.
A adjacent tto the n.
10. DEGENRATION OF MTP3 Æ deviaation of thee 3rd toe med dially pushiing the MTT3 laterally impenging
i the
t n.
11. Pathological Findings
HISTOLOGICALLY:
1. Perineural fibrosis
2. Thickened vasanervosa é hyalinized walls
3. Neuronal edema
4. Neuronal demyelinization and degeneration
5. No inflammatory changes
6. Frequent presence of bursal tissue
ELECTRON MICROSCOPY:
y in the normal Amorphous deposition & y eosinophilic tubular filaments
In a strict sense the term neuroma is not correct because the haphazard proliferation of axons seen in
a traumatic neuroma is not found, and the deposition of hyaline and collagen filaments accounts for
the enlargement is probably degenerative rather than proliferative, with repetitive trauma against the
deep transverse intermetatarsal ligament being the most likely cause. Repetitive microtrauma,
perineural fibrosis, vasa nervorum occlusion, and endoneural edema probably are causations
Clinically:
• Neuralgic PAIN:
rd nd th
o Plantar pain at 3 interdigital space (some times 2 but 4 is rare)
o y é walking
o y at night sometimes
o z on removing shoes
• TINGLING, NUMB, BURNING, or "DEAD" toe
• Vague FOREFOOT tingling
• COLOUR changes
• The condition may remain undiagnosed for many years.
Clinical assessment
The diagnosis is often strongly suspected within the first minute of the consultation.
Ask about:
• PN .................................................... DM and chronic inflammatory disorders
• Foot Trauma
• Ankle Discomfort ............................ may suggest tarsal tunnel syndrome
• Spinal problems ............................... history of root entrapment symptoms.
Examination
Any nerve entrapment in spine, proximal limb or tarsal tunnel.
On local examination look for:
o Local TENDERNESS
o SWELLING in the intermetatarsal space
o MULDER'S CLICK or crunching sensation + pain
o LOCAL ANAESTHETIC injection into the affected space
o whole foot should be examined for any cause of METATARSALGIA
A, Squeezing forefoot just proximal to metatarsal heads between index finger and thumb
B, Simultaneous compression of the suspected web space é two fingers of opposite hand
Imaging
US & MRI have been described for imaging a neuroma, but we have not had any success
If there is a suggestion of other forefoot pathology Æ PXR should be obtained.
Treatment:
NON OPERATIVE TREATMENT:
1. Metatarsal bars or pads
2. Local injection of a steroid preparation into the affected web space,
3. wide toe-box shoes
4. Avoid high heel
5. No place for orthosis
OPERATIVE TREATMENT:
The mainstay of treatment, of course, is surgery é 90% satisfaction
Division of deep transverse inter MT lig is controversial may lead to dropped MT, but is
needed in the dorsal approach
Painful scar may result from plantar incision despite its better visualization éout MT lig cut
Never do a transverse plantar incision
Plantar approach is better in the case of recurrent cases; but avoid superficial dissection for
fear of fat pad necrosis and painful scar
The nerve is divided 2-3cm proximal to the bifurcation and excised
Decompression of the interdigital space with excision of the bursa
Warn patients that it may take several months to reach full benefit & that they may develop a
new neuroma on the severed nerve end which may be more painful than the original one
DORSAL APPROACH
The dorsal approach is the most common and widely used surgical treatment for interdigital
neuroma. Overall, one can expect 90% good and excellent results with this approach
Under tourniquet, make 3 cm incision starting in the involved web space (usually 3rd)
Place the incision between the metatarsals to avoid injury to a small dorsal sensory nerve
Carry out blunt dissection with a thumb or small scissors down between the MTs
Place a retractor or a small lamina spreader into the wound between the metatarsal heads, and open
it, placing the transverse metatarsal ligament under tension
Use a Freer elevator to bluntly dissect in line with the incision to identify the transverse metatarsal
ligament and the normal interdigital nerve proximally. The nerve occasionally courses close to the
metatarsal and is not always in the center of the interspace .
Plantar pressure under the web space should reveal the enlarged neuroma protruding distal to the
transverse metatarsal ligament . Then sharply divide the metatarsal ligament.
Identify the nerve in the proximal part of the wound and trace it distally into the irregular mass.
Look for any accessory branches coming from either metatarsal to join the common digital nerve. If
one is identified, dissect it and clearly define it. This prevents the nerve end from retracting &
forming a potential painful neuroma stump directly under metatarsal head .
Trace the common digital n. and transect it in the most proximal aspect of the wound so the cut end
does not end up bet metatarsal heads. Then dissect neuroma out distally and excise
PLANTAR APPROACH
Palpate the metatarsal heads on each side of the involved interspace and draw them
Place a small-gauge needle (25-27 gauge) from a dorsal to plantar direction in the interspace,
piercing the plantar aspect of the foot. This identifies the interspace plantarward so the incision can
be made accurately. Draw the incision in line é interspace, but proximal
Carry the incision through the subcutaneous tissue. Place a Weitlander retractor. Carryout dissection
with a blunt scissors in line with the skin incision. Retract slips of the plantar fascia, exposing the
interdigital nerve and neuroma. Transect. the nerve proximally and continue dissection distal to the
neuroma. Excise the neuroma as in thedorsal approach
Malignant Peripheral Nerve Tumours

1. Neurofibrosarcoma
• Rare
• Can arise de novo or in neurofibromatosis
• Tend to be high grade, therefore treated with wide surgical resection +/- radiotherapy
Benign Tumors of Muscles

• Leiomyoma, Rhabdomyoma (glycogen tumor)
• Seldom occur in the extremities
Malignant Tumors of Muscles

1. Leiomyosarcoma
• HG or LG tumor arising from the smooth ms of blood vessels
• Gross: Appear encapsulated but avoid mere enucleation of the tumor
• Mic: Tumor cells é elongated nuclei é mitotic figures & sometimes arrange in palisades
• Wide/radical surgical excision and radiotherapy
2. Rhabdomyosarcoma
• The MOST COMMON sarcoma in young patients
• Among the MOST MALIGNANT sarcomas; grows rapidly, yyy metastasis to LN
• Microscopically:
Type Age Site Principle cell MnGC Special feature
Embryonal: Adolescent Limb & head spindle cells + y Myxoid areas
(ycytoplasm)
Boytroid Embryonal type but occur in UT beneath epithelium
Alveolar: Adolescent Limb & head round cells + Rhabdomyoblasts
(zcytoplasm) (é striations)
Pleomorphic Adult UL & LL Spindle cells + Racquet cells
• sensitive to multiagent chemotherapy
• Treat with preop chemo, followed by wide surgical excision and radiotherapy
Synovial Tumours
A. Benign tumors
l. Tenosynovial giant cell tumor
a. Localized tenosynovial giant cell tumor
b. Diffuse tenosynovial GCT (extraarticular PVN synovitis, florid tenosynovitis)
2. Ganglion
3. Synovial chondromatosis
4. Tumoral calcinosis
B. Malignant tumors Synovial sarcoma
1. Biphasic (fibrous and epithelial) synovial sarcoma
2. Monophasic (fibrous or epithelial) synovial sarcoma
Ganglion Cyst
Ganglia are the most common cause of focal masses in the hand and characteristically arise either
from synovium of joints or tendon sheaths or from tendons, where they may cause trigger fingers.
Incidence:
Ganglion cysts are the most common soft tissue tumors of the hand and wrist.
2ND & 4TH decade ...................................... 70% (Any age, including children)
♀:♂ ............................................................. 3:1
No relation to side or occupation
Etiology theories
1- MUCOID DEGENERATION:
The most accepted explanation ............ MUCOID DEGENERATION of collagen and CT.
2- TRAUMA AND TISSUE IRRETATION:
A more recent theory ............................ TRAUMA or IRRITATION Æ ⊕ Synovial cells to produce
mucin ώ sneak its way out across capsule Æ form a duct ώ function as valve like producing
lakes. Mucin ducts and lakes eventually coalesce to form a solitary cyst
3-DEFECT IN CAPSULE OR TENDON SHEATH:
Such defect allow protrusion of synovial tissue
Pathology:
Site:
Dorsal wrist ganglions ................... 70% (scapho-lunate lig bet 2nd & 4th ext tendon comp)
Volar wrist ganglions ................. 20% (scapho-trapezial joint just radial to FCR tendon)
Flexor tendon sheath ..................... 10% (at the level of the A1 pulley)
Gross:
Well CIRCUMSCRIBED, SMOOTH-walled, WHITE and TRANSLUCENT mucin filled cysts
Ganglion cysts may be single or multilobulated (communicate via duct network)
Ganglions are usually CONNECTED by a stalk to an underlying joint capsule or ligament.
Ultrastructure:
Highly viscous mucin................. HYALURONIC + ALBUMIN + GLOBULIN + GLUCOSAMINE
Wall is made up of ..................... COLLAGEN éout epithelium, synovium, nor necrosis
Clinical Picture: ............................................ASYMPTOMATIC
Presenting symptoms................................. PAIN, z MOTION, PARESTHESIAS, and weakness .
Ganglions are usually ................................ SOLITARY & < 2 CM in diameter.
Ganglia occasionally.................................. disappear spontaneously
Sometimes RECUR when treated by ........... rupture or aspiration
DIP GANGLION = mucous cyst
Arise dorsally bet DIP JOINT crease and eponychium (on either sides of the extensor tendon) occur
in OA of DIP & may lead to longitudinal grooving of the nail plate ð long pressure on the
germinal matrix
OCCULT DORSAL GANGLION:
SCAPHOLUNATE tenderness é extreme wrist motion, especially in extension. Radiographic findings
are often normal, and MRI is useful in confirming the diagnosis. Surgical excision of the occult
ganglion is successful for alleviating pain and symptoms in the majority of cases.
Investigations
PXR (cyst is not seen) ............................... evaluate any bone or joint abnormality
MRI ............................................................ confirm atypical presentation e.g. occult ganglia
ALLEN TEST ................................................. evaluate the blood flow to the hand
TREATMENT
NON SURGICAL THERAPY
Aspiration ± steroid injection. This is especially successful for tendon sheath ganglions in the hand
and digits. Avoid multiple steroid injections to avoid skin and fat atrophy & hypopigmentation.
SURGICAL THERAPY:
Generally .................................................... Total ganglionectomy + portion of the capsule
Dorsal wrist ganglion:
GANGLIONECTOMY + attachment to SCAPHOLUNATE ligament
Usually approached through a transverse incision
Volar carpal ganglion:
GANGLIONECTOMY + attachment to radio-carpal capsule of the SCAPHO-TRAPEZIAL joint
Longitudinal incision
Volar retinacular ganglion (A1 pulley)
Transverse incision near the distal palmar crease.
Other ganglia of the volar digits:
GANGLIONECTOMY + small portion TENOSYNOVECTOMY
Via Bruner or mid-lateral incision Æ identify the bundle
Mucous cyst:
Curved oblique incision, or an H-shaped incision, on dorsal DIP
If the overlying skin is adherent Æ it is excised in an elliptical fashion
Cyst is dissected proximally to the DIP Æ GANGLIONECTOMY + PARTIAL DIP CAPSULECTOMY
Surgical excision of a ganglion should include the removal of a generous capsular margin about
the cyst base, and no attempt should be made to close the joint capsule
Recurrence after complete excision is rare
Arthroscopic resection of dorsal wrist ganglions is currently being investigated.
Pigmented Villo-Nodular Synovitis

Benign Synovioma = GCT of Tendon Sheath
Introduction:
xanthomatous non neoplastic lesion affecting synovium of joints and tendons, characterized by
deposition of hemosidrin and cholesterol. It occurs due to idiopathic synovitis.
Epidemiology
2/106/y
Age ......................................................... 20-45 y (range 11-70)
♂=♀ ........................................................ equal
No environmental, genetic, ethnic or occupational predilection .
Since bursae & tendon sheaths are related to synovium, they may have xanthomatous growths
Commonest presentation ....................... monoarticular swelling; sometimes polyarticular
Pathogensis Theories:
1. PROLIFERATIVE REACTION ......................... ð unknown inflammatory or antigenic agent
2. NEOPLASTIC TRANSITION ............................ from the inflammatory to proliferative "tumour"
3. REACTION TO INTER-CELLULAR HGE ............ attractive hypothesis as MnGC / xanthoid cell /
hemosiderin are often a prominent feature, all of which factors are caused by extravasated
blood. But the lesion is not common in hemophilics who commonly bleed into their joints &
also the lesion can't be produced by injecting blood into the joint cavity.
4. Recently; ALLERGIC INFLAMMATORY REACTION to hemosiderin or its metabolites
Pathology:
SITE:
1. Related to tendons: (Giant cell tumour of tendon sheath).
Common ...................................... FLEXOR TENDONS SHEATH of the hand
Less common .............................. EXTENSOR ASPECT OF IP joint (often the P.I.P joint).
Rarely .......................................... ankle & the toes are involved.
2. Within joints: Pigmented Villo-Nodular Synovitis (PVNS)
most commonly ........................... KNEE (80%)
Other joints .................................. hip, ankle, shoulder, wrist
3. Rare in bursae
4. Recently described in cancellous bone (Intra-osseous PVNS) that occur after a long standing
articular PVNS that followed by erosion of the bone, and the synovial tissue penetrates into the
underlying cancellous tissue & continues to proliferate there.
MACROSCOPICALLY:
1. PIGMENTED VILLO-NODULAR SYNOVITIS:
Localized or diffuse form.
The localized form ...................... identical histologically AS GCT
The diffuse form.......................... same but involve the ENTIRE KNEE SYNOVIUM
May produce a BULKY mass ......... Gives false impression as if it is a sarcoma
Tumor may cause BONE EROSION Gives false impression as if it is a sarcoma
Tumor may break through the articular plate & invade the metaphysis & in rare
instances no perforation can be found, as if the metaphysis has the same pathology
2. GIANT CELL TUMOUR OF TENDON SHEATH:
PEA-SIZED, bright YELLOW, LOBULATED, ENCAPSULATED, firmly ATTACHED to its origin
STREAKS of yellow & brown of hemosiderin & cholesterol ester
Sometimes PROJECTIONS arise from the mass & dissect between tendons Æ recurrence
MICROSCOPICALLY:
1. IN THE EARLY STAGE:
Non-specific inflammation ......... thick edematous synovium
HEMOSIDERIN deposition............... RED-BROWN colour.
SHAGGY or BEARD appearance ...... ð fibroblastic reaction & villous reaction
LYMPHOCYTIC infiltration
2. DOMINANT PROLIFERATIVE REACTION BECOMES MORE:
Nodules of solid tissue are produced.
3. EVENTUALLY:
Very cellular sheets of ................ SPINDLE, cylindrical, or POLYHEDRAL cells
Fibroblastic & synovial .............. HYPERPLASIA
SYNOVIAL LINED CLEFTS .................. suggesting the synovial origin of its cells.
MNGC formed by ......................... fusion of contiguous lining cells.
LIPID-BEARING HISTIOCYTES ............ are found scattered in FIBROUS STROMA.
XANTHOID CELLS ........................... are found scattered in FIBROUS STROMA
Stromal cells may appear ........... undifferentiated ⎯ConfuseWit
⎯ ⎯⎯h → sarcoma & GCT
Cellularity Fibrosis Pigment Cholesterol Vascularity

PVN ++ ++ ++
GCT ++ ++
Diagnosis:
Two types: PVN
1- Diffuse
A- Pigmented Villo-Nodular Synovitis 2- Localized
Age: .... 20 in diffuse
Hist: ............ 30 in localized
Gradual onset, intermittent course of moderate PAIN Male & knee are the most common
Associated with ........................... SWELLING & LIMP
Mechanical interference ............. STIFFNESS, locking, snapping & limitation of extension
Exam:
1- Large BOGGY swelling................ in diffuse form
Small palpable JOINT MOUSE ..... in localized form
2- Effusion may be pronounced .... FLOATING PATELLA
3- Generalized TENDERNESS
Aspiration:
In diffuse form............................. BLOOD-TINGED fluid é y bilirubin & cholesterol
In localized form ......................... effusion is NOT ABUNDANT, STRAW coloured & sterile.
Lab: y S.CHOLESTEROL .............................. High normal é normal chol/ester ratio (not diagnostic)
PXR:
NARROW JOINT space
SOFT TISSUE SHADOW .................... thickened synovium
CORTEX EROSION from without ..... Superficial or extensive ± margin of sclerosis
Double contrast arthrogram reveals:
Diffuse form .................. BUBBLY FLOCCULENT effect within the synovial cavity
Localized form............... Soft CREEPING shadow on suprapatellar synovium
CT ............................................................... Best to demonstrate bone involvement
MRI ........................................................... Best to demonstrate soft tissue masses
Arthroscopy: ................................... characteristic gross pathological picture of PVN
B- Giant Cell Tumour of Tendon Sheath

Clinical picture:
Discrete mass(s) fixed to the tendons of the hands & feet & Achilles (and move é them)
At first they are PAINFUL .............. later they are PAINLESS
Spontaneous TENDON RUPTURE IS RARE
BILATERAL involvement is usual
DISCRETE, SOFT TO FIRM, PEA-SIZED
Some times ................................. large, bulbous & disfiguraing & they are fixed to &
Overlying skin ............................. normal & freely movable over the tumours
Growth is very slow .................... Take years
Yellow plaques around the eye ... Part of familial hypercholesterolemic xanthomatosis
Lab:
y s.cholesterol is often associated.
PXR:
Pressure erosion of the adjacent phalanx. The articular surfaces are never involved.
Treatment:
1. PVN
Localized form ............................ MARGINAL EXCISION
Diffuse form ................................ TOTAL SYNOVECTOMY ± Radiotherapy if surgery fail
If significant bony erosion .......... ARTHROPLASTIC RECONSTRUCTION
2. Giant cell tumour of tendon sheath:
EXCISION, which may be technically difficult in large lesions
Recurrence
Recurrences are not infrequent if the excision is incomplete .
Even after meticulous excision ... 27% recurrence rate
Risk factors for recurrence:
Adjacent OA
DIP location
Thumb IP
+ve osseous pressure erosion on PXR
Presence of the dissecting projections if left behind during surgery
Tumoral Calcinosis
Definition:
• A rare condition, characterized by fine non-tender tumour-like masses Resume
around joints, é Ca sallts deposition -Child
-Shoulder swelling
Epidemiology -Encapsulated cyst
• Children -Ca salts
-Amorphous & crystals
• Once occurred other lesions are common to follow!! -MnGC + lymphocytes
-
• Genetic back ground had been proposed
Pathology:
SITE:
• Soft tissue around large joints ................. Shoulder 60%
• Other joints .............................................. elbow and hip
MACROSCOPICALLY:
• Encapsulated cystic mass ...................... embedded in the collagenous tissues
• The cavity of the cyst contain a fluid or semi-f1uid é Ca salts.
MICROSCOPICALLY:
• Amorphous masses of powdery Ca salts
• Mineral crystals
• Giant cell reaction about these deposits forming a scalloped & convoluted border
• Lymphocytic infiltration & fibrous proliferation
Clinically:
• Masses are usually painless
• Interfere with function only .................. if develop to a large size
• May reach ............................................ 20cm
DD :
1- Calcinosis universalis:
Generalized calcification of skin, s.c. tissues & muscles in children.
2- Calcinosis circumscripta:
Localized deposits of Ca associated with Raynaud's or scleroderma in adults.
Treatment:
• Excise lesions that ................................ cause disfigurement or limitation of function
Prognosis And Recurrence
• If a solitary lesion of tumoral calcinosis is discovered one can expect that other lesions will
develop in other joints as the patient ages
• They are quite apt to recur
.
Synovial Chondromatosis
SYNOVIAL CHONDROMETAPLASIA Chondromatosis
Definition: -Rare middle aged male
-Metaplasia of
RARE lesion resulting from cartilaginous or osteocartilaginous embryonal rests at the
metaplasia in the synovium of joints, bursae or tendon sheaths. villi top
-Joint Rice
In synovial chondromatosis multiple cartilaginous nodules develop & -Snow Storm
grow éin the synovium of a joint & may become loose bodies. -Monoarticular (Knee)
Epidemiology -Locking & Pain (OA)
-+ve PXR only if ossify
Age: ..................................................... 30-50 Y -Total synovectomy +
Sex: ......................................................... MALES predominate Loose body removal
Considered to arise from ........................ Embryonal rests (origin of synovium & cartilage)
1. May represent ........................................ detached OCD or traumatic cartilage detachments
2. May represent ........................................ detached cap of an INFLAMMATORY SPUR
3. Frequently they result from ................... METAPLASTIC ERROR of synovial cells.
Pathology:
SITE:
KNEE, elbow, ankle, hip & shoulder are involved in this order of frequency.
The condition is usually........................ MONOARTICULAR but both knees may be affected.
MACROSCOPICALLY:
HUNDREDS OF SPHEROID CARTILAGINOUS NODULES protrude into the joint cavity
JOINT MICE or RICE BODIES may be formed
Arthroscopically it has a characteristic SNOW STORM appearance
MICROSCOPICALLY:
Hyaline cartilage forms in .................... stratum synoviale at the synovial reflection
Chondroid masses ................................ begin to appear at the tips of the synovial villi
Surrounding cells are altered ................ resemble chondroblasts
Cartilage mass grow & form ................ spheroid body, the villous process being its pedicle
Eventually it becomes detached ........... falls free into the joint space
Chondroblasts continue ........................ Proliferation & production of spheroid cartilage
Chondroblasts may metaplase to .......... osteoblasts Æ nidus of bone surrounded by cartilage
The story ends by.................................. joint distended by uniform glistening white bodies
They cause repeated trauma to the articular surface Æ multiple erosions Æ OA
In the past, this condition had been given a misnomer “osteochondromatosis”
Diagnosis:
Clinically:
Usually mild, duration long & coarse intermittent.
Pain............................................. dull ache.
Swelling
Stiffness.
Transient locking episodes
Giving way ................................ in case of the knee joint
Signs:
Generalized joint tenderness.
Thickened synovial membrane
Marked audible & palpable crepitus.
Loose bodies may be palpable.
Tenosynovial chondrometap1asia:
Sometimes the tendon sheath or bursal synovia may assume the same picture
DDX: .............................................................. CHONDROSARCOMA.
Cartilage SIZES VARY ............................... from microscopic to over a centimeter in diameter.
As they age ............................................ their CENTERS MINERALIZE Æ radiopaque.
Sometimes they .................................... LIE éin the sheath wall
Other times are found ............................ as FREE BODIES éin the sheath lumen
WRITS & hand .........................................most involved in tenosynovial chondrometaplsia
PXR:
Usually show MULTIPLE LOOSE BODIES (Only when calcify or ossify)
№ is always much more than seen on PXR
When all are chondromatous ................ air or DOUBLE CONTRAST ARTHROGRAPHY may be
needed
DD :
Monoarticular swelling…
Rheumatic arthritis ............................... fragments of articular cartilage detach & incorporate
in the synovium or become free in the joint
Severe OA as multiple osteophytes........ may detach
Treatment:
TOTAL SYNOVECTOMY + REMOVAL OF LOOSE BODIES
Joint mice removed immediately.......... to z damage to articular surfaces
Patient is forewarned ............................ OA is already present Æ residual symptoms
Total synovectomy + All communicating bursae are also excised.
As a general rule the menisci are damaged, requiring removal. The outlook for permanent
cure is excellent.
Prognosis And Recurrence

RECURRENCE is not unusual.
Malignant change very rare.
Malignant Synovial Disorders

Synovial Sarcoma Synovioma
-32y
Definition: -Male
-Lower limb swelling
• Malignant sarcoma occurs in close proximity to joints but rarely from -Long History
an intra-articular lesion. It has adenomatous & fibrous elements -Small size
Epidemiology -Adenomtous + Fibrous
-Gray + Ca + pseudocap
• 10% of sarcomas -PXR spot calcification
• Age: ....................................................... 32y
• ♂:♀ ....................................................... 3:2
• 90% translocation ................................. t(X;18)(p11;q11)
• Genes affected SSX on Xp & SYT on ch.18 (they are transcription modulators)
• Synovial origin is controversial but it is indicated by:
1. Formation of clefts
2. Formation of villous projections
3. Formation of gland like spaces lined by cuboidal cells & filled é mucin
4. Formation of cell tufts
Pathology:
SITE:
•
•
Most common ...................................... Ankle & foot 80%
Second common .................................... knee }
• Rarely .................................................... Shoulder, Chest, Abdomen, neck
• Usually arise from ................................. Tendon sheath & capsule
• Only 10% are intra-articular
MACROSCOPICALLY:
• Circumscribed, rounded, lobulated, Grayish pink mass
• Areas of Ca, cyst, hge, necrosis ........... Brownish color
• Compress surroundings......................... pseudo-capsule
• Difficult to find synovial attachment
MICROSCOPICALLY:
• Difficult ð cell variations; mainly 3 types
Incidence Slits Cells Stroma
Monophasic Commonest ++ Spindle ++
Biphasic + Spindle & epithelioid Pseudoacinar
Endothelial Least - Pleomorphic & round -
Diagnosis:
Clinically:
• Slowly growing over years before seeking an advice & misdiagnosed as benign (small size)
• Usually male 32y é a painful swelling below the mid-thigh
• as it turns severely painful
• Soft to firm, nodular, tender 1- Hyperintense fluid ± level
PXR: 2- Intemediat muscle signal
3- Hypointense fibrous signal
•Soft tissue mass é spot calcifications .... 30%
•z joint space
MRI .......................................................... 30% Triple signal pattern on T2
Treatment:
• Aggressive LIMB SALVAGE PROTOCOL wide resection + chemo + Radio vs AMPUTATION
Fibrous Benign
1. Calcifying aponeurotic fibroma
• Slow Growing, painless mass ,ages 3-30
• Xrays show faint mass with stippling
• Histology shows fibrous tumour with some calcification and cartilage formation
• 50 % recurrence after excision
• Resolves with maturity
2. Nodular fasciitis
• Painful reactive rapidly enlarging lesion in a young person
• 50% in upper limbs
• Histology- short irregular bundles and fascicles, only small amounts of mature collagen
• Treat with excision with marginal resection
3. Palmar (Dupuytrens) and plantar (Ledderhosen) fibromatoses
4. Extraabdominal Desmoid tumour
• Most locally invasive of the benign soft tissue tumours
• Most common in adolescents and young adults
• Rock hard on palpation
• May be multiple lesions
• Histologically well differentiated fibroblasts and abundant collagen
• Infiltrates surrounding tissues
• Surgery aims at excision with a wide margin
• Local recurrence common
Fibrous Malignant
1. Fibrosarcoma
• Enlarging painless mass
• Age group 30-80
• Usually 10cm in size before symptoms
• Plain Xray usually normal unless encroaching on bone
• MRI deepseated inhomogenous mass
• Histology- fasciculated growth pattern with fusiform or spindle shaped cells, scanty
cytoplasm, indistinct borders separated by interwoven collagen, or herringbbone appearance
• Treatment- Wide local excision. If > 5cm add radiation therapy, preop/postop/periop
2. Fibrohistiocytic
• Dermatofibrosarcoma protruberans
• Rare, nodular cutaneous tumour
• Occurs in early adult life
• Intermediate in grade
• Recurs locally but only rarely metastasises
• Treat with wide resection
3. Malignant fibrohistiocytoma
• Similar to malignant fibrosarcoma
• Histology slightly different with cartwheel pattern to the spindle and histiocytic cells
• Treat as for fibrosarcoma
Benign Vascular Tumours

1. Haemangioma
• Seen in children and adults
• Can be cutaneous, subcutaneous, intramuscular
• If large, patients complain due to symptoms of venous engorgement (aching)
• Plain Xray can show small pleboliths
• MR scan shows a heterogenous lesion with many small blood vessels
• Treat nonoperatively if possible
• Wide surgical resection if symptomatic, local recurrence rate high
Malignant Vascular Tumours

1. Haemangiopericytoma
• Rare tumour of the pericytes of blood vessels
• Can be benign or malignant and from intermediate to high grade
• Slowly enlarging painless mass
• Treatment based on grade of lesion
2. Angiosarcoma
• Rare tumour resembles the endothelium of blood vessels
• Treatment depends on grade and location of lesion
Benign Fatty Tumours

1. Lipomas
• Subcutaneous/intramuscular or intermuscular tumours of mature fat
• Most are not painful
• Plain xrays may show a radioluscent region in the soft tissues
• MR or CT scan show a well demarcated lesion with exactly the same signal as fat
• If no symptoms and definite radiological diagnosis, leave alone
• If mass growing or causing symptoms excise with a marginal line of resection
• Recurrence uncommon
• Subgroups are spindle cell cell lipoma and pleomorphic lipoma
Malignant Fatty Tumours

1. Liposarcomas
• Malignant tumours with differentiation towards fatty tissue
• Heterogenous group of tumours with the presence of signet ring type cells(lipoblasts) in
common
• Lipoma like, Sclerosing, Inflammatory, Dedifferentiated, myxoid, round cell, pleomorphic
• Range from low grade to high grade
• LG liposarcomas - can be difficult to differentiate from benign lipoma
• Low grade liposarcomas treated with wide local excision +/- radiotherapy
• High grade liposarcomas treated with wide local excision + radiotherapy
Other Rare Sarcomas

1. Epithelioid Sarcoma
• Nodular tumour occuring in the hands of young adults, buttock thigh, knee or foot
• May ulcerate and mimic a granuloma or rheumatoid nodule
• Lymph node metastases may occur
• Histologically ovoid to polygonal with eosinophilic cytoplasm
• Wide surgical excision required
2. Clear cell sarcoma

• Slow growing painless mass in young adults
• In region of tendons or aponeuroses
• Treat with wide surgical resecion with adjuvant radiotherapy
3. Alveolar Cell Sarcoma

• Most common in the anterior thigh
• Treat with wide surgical excision and radiotherapy
Bone Metastases
Bone is the third most common site of metastatic disease
Cancers most likely to metastasise to bone:
1. Breast
2. Lung
3. Prostate
4. Thyroid
5. Kidney
6. Bowel
Carcinomas are much more likely to metastasise to bone than sarcomas
The axial skeleton is seeded more than the appendicular skeleton, partly due to the persistence
of red bone marrow in the former
The ribs, pelvis and spine are usually first affected
Batson's vertebral venous plexus allows cells to enter the vertebral circulation without first
passing through the lungs. The sluggish blood flow in this plexus is more conducive to tumour
survival, accounting for the high rate of prostate cancer metastasis to the spine.
CLINICALLY:
Pain, pathological fractures and hypercalcemia are the major sources of morbidity with bone
metastasis
Pain is the most common symptom found in 70% of patients with bone metastases. Pain is
caused by stretching of the periosteum by the tumour as well as nerve stimulation in the
endosteum
Pathological fractures are most common in breast cancer due to the lytic nature of the lesions.
They are uncommon in lung cancer due to short life span and rare in prostate cancer which
tend to be osteoblastic lesions
PXR
Lytic bone metastases must be greater than 1 cm and have destroyed 30-50% of the bone
density in order to be seen by x-ray
Metastatic bone lesions can be described as osteolytic, osteoblastic and mixed
The osteolytic lesions are most common where the destructive processes outstrip the laying
down of new bone
Osteoblastic lesions result from new bone growth that is stimulated by the tumour
WORKUP
Known Primary:
• Bone Scan - Galasko reported that a period of two to eighteen months was necessary before a
lesion identified on bone scanning could be visualised on plain x-rays
• FBC, Bone Biochemistry, LFT, Coagulation screen, G&S
• Biopsy not necessary
Unknown Primary:
• FBC, Bone Biochemistry, LFT, Coagulation screen, G&S
• SPEP, TFT, PSA, Tumour markers, ESR, CRP
• Bone Scan
• CXR
• CT chest & abdomen (or USS)
• Biopsy lesion(s) for histology & microbiology (incl. TB)
TREATMENT
NORMALLY PALLIATIVE
RADIOTHERAPY:
o useful for reducing bone pain and progression of tumour growth
o 90% will receive some relief, and 50% will receive near complete relief with between
20 to 40.5 gray of radiation
o Complications: radiation induced osteonecrosis & y rate of stress # or nonunion
o Lesions that do not represent a risk for fracture may be treated with radiation or by
appropriate chemotherapy directed at the tumour
o Patients who have recurrence of pain because of biomechanical weakness should be
managed with operative stabilisation
BIPHOSPHONATES
o Because of their down-regulation of bone resorption, bisphosphonates have become
attractive adjuvants for the reduction of the risk of pathological fracture stemming
from osteolytic lesions and for the treatment of bone pain
o Studies of patients being managed for hypercalcemia have demonstrated a decrease in
bone pain with attainment of normal levels of calcium
o Clodronate can be administered intravenously or orally, and although it affects bone
resorption it does not alter bone mineralization
o Clodronate was found to reduce bone pain after a few months of therapy
o The need for palliative DXT; and, potentially, the risk of pathological # z
o Although bisphosphonates act quickly to reduce hypercalcemia, long-term
administration is necessary to treat widespread osteolytic disease.
PATHOLOGICAL FRACTURE:
• Pathological fractures have been reported to occur in 9-29% of patients who have bone
metastases, depending on the location of the lesion
• High risk of pathological fracture =
1. > 50% loss of the cortex / shaft diameter on any view
2. Avulsion of the lesser trochanter is an indication of imminent hip fracture
3. (>2.5cm lesion)
4. MIRELS SCORING SYSTEM (CORR 1989) - a numerical score according to 4 variables:
location of the lesion
the degree of pain
PXR appearance
the size of the lesion
Mirels recommended: < 7 Æ irradiation; > 7 Æ operative treatment
• Goals of surgery:
1. relief of pain
2. restoration of the ability to walk
3. preserve stability and function
4. an increased duration of survival
5. improved fracture-healing
• Options:
o IM Nails + DXT entire bone
o Prosthesis - Epiphyseal fractures
o Endoprosthesis 4 extensive lesions
o major bone defects use PMMA
o Emergency surgery is done for spinal metastasis in the hope of preserving
neurological function.
o Postop radiotherapy should be considered in all cases, once wound healing has
occurred.
378 | Page [Metastasis]
Multidisciplinary approach in the
management of metastatic bone disease
Managing MBD requires the collaboration of:
• Orthopaedic surgeon
• General surgeon
• Clinical oncologist
• Radiotherapist
• Radiologist
• Pathologist
• Physiotherapist
Role of the orthopaedic surgeon
• Diagnosis and staging of MBD.
• Management of pathological fractures.
• Management of impending fractures.
Patients could present to the orthopaedic patients by:
• Pathological fracture.
• Impending fracture
• Pain only.
Pathological fracture
• Definition of pathological fracture
• How do you suspect a pathological fracture?
• How do you diagnose the cause of the pathological fracture?
• How do you treat the patient who sustained a pathological fracture?
Definition
• It is a fracture occurring in an abnormally weak bone.
• The cause of this weakness may be neoplastic, inflamatory, metabolic, etc..
Diagnosis
History
1]. Trivial trauma
2]. Pain (or limp) before the fracture
3]. Known history of cancer
4]. Symptoms suggestive of cancer (weight loss, heamoptysis, heamatemesis, bleeding PR, urinary ..)
5]. History of previous irradiation
Xray
1]. abnormal bone quality
2]. underlying lytic, blastic or mixed lesion
3]. other lesions in the same or adjacent bone
4]. abnormal fracture pattern
[Bo asis]
one Metasta Page | 379
Dia
agnose & stage
1]. If it is a primary neoplasm, what
w type and what stage?
2]. If it is a secondaryy, where iss the prima
ary and are
e there other seconda
aries?
3 If it is a non neop
3]. plastic causse, what is it?
General exam:
G e
• LN, scarrs of previouus operatioons, abnorm
mal pigmentations or deformities.
d
• Breast, thyroid,
t pro al examination.
ostate, recta
L
Laborato ory
• CBC, ES SR, kidneyy and liver functions, calcium,, phospho orus, alkalinne phosph
hatase, +/--acid
phospha atase, plasm
ma protien electrophe eresis, CEA, PSA, alpha feto protie
en, PTH.
R
Radiolog ical
• Chest & pelviabdom minal CT.
• Bone sc can.(false -vve in myelo oma, lymph homa, histiocytosis. Extensive
E prostate me
ets .. Supersscan
looks noormal but re enal stealin
ng)
• Local MRI (includess the whole e affected bone).
b
Then Look for th

he Cause
Not revea
aled Revealed
d
• Biopsy (core
( is pre
eferable) dia
agnoses typ
pe of prima
ary sarcoma and mayy give a clu
ue to the sitte of
primary carcinoma a
Hen nce, you reach
r a diagnosis:
• Non neo oplastic cau
use
• Primary sarcoma an nd its stage
e
• Myelom ma (solitary or
o multiple))
• Seconda ary
he fracture is due to second
If th dary carciinoma
In addition
a to fracture manageme
m nt:
• Is it solita
ary or multiple? Assesss other lesioons for imp
pending fraccture.
• Known primary or unknown? ? Repeat invvestigationss after 6 we
eeks.
• Primary tumour tre eated or no ot yet treated? Treat the primary
Exppectation ns
• Level 1: normal unsupporte
u ed ambulattion
• Level 2:
2 supporte ed ambulattion.
• Level 3:
3 ambulation outside e the bed.
• Level 4:
4 comforta able mobilizzation in bed.
b
Thiss goal is determined
d d according to the underlying
u g cause, ge
eneral con
ndition, fra
acture patttern,
tech
hnical skillss, economiics…)
Tre
eatment options
o
• Non operative trea atment
• Operativ ve treatmen nt
• Is surgerry associate
ed with high risk morta ality ?
• Will surrgery achie eve the prooposed goa al (bearing
g in mind the availab
ble implantts, instrume
ents,
operativve setting and technicaal skills) ?
NON OPERATIVE TREATMENT
1]. Biphosphonates:
o blocks osteoclastic activity
o decreases the incidence of fracture
o decreases hypercalcaemia
o decreases pain
o reports on decreasing incidence of mets.
o Zoladronic acid (Zometa): 4 -8mg short infusion saline every 4 weeks.
2]. Radiotherapy:
o partial pain relief in 80%
o complete pain relief in 20%
o it has a temporary effect.
o It has no effect on renal cell carcinoma mets, or sarcoma mets
3]. Hormonal therapy: eg tamoxifen in breast cancer and LHRH agonist in prostate cancer.
4]. Chemotherapy: Radioactive iodine in thyroid mets after thyroidectomy.
5]. Pain control:
o NSAID, neuroleptics, ms relaxants, antidepressants
o mild then strong opiods
o Patient controlled analgesia (PCA)
o biphosphonates
o Radiotherapy
6]. DVT control:
o used cautiously as there are circumstances of increased bleeding tendency
7]. Ambulatory aids:
o crutches, walker, wheelchairs
o splints, braces, slings
8]. Vocational therapy
o Is surgery associated with high risk mortality ?
o Will surgery achieve the proposed goal (bearing in mind the available implants,
instruments, operative setting and technical skills) ?
Operative Treatment
Perioperative considerations:
1]. multidisciplinary anaesthesia, oncologist, orthopaedist to assess risk
2]. Cardiopulmonary high risk: recent MI, +ve stress, severe heart failure, uncontrolled BP,
pulm functions <35%.
3]. 10/30 rule, minimum platelets 50000, INR <1.5, serum albumin >2g/dl, normal Ca, P, Na, K.
Adjunct procedures:
1]. Preoperative embolization:
o effective in 60 -90%
o gel foam, polyvinyl alcohol beads, coils..)
o Operation should be within 24 hrs if gel foam is used & 24 -36 hrs if alcohol is used.
o Complications (rare): muscle and skin necrosis, paresis, arrest.
o Added value: decreases pain in inoperable cases !
2]. IVC filters
[Bone Metastasis] Page | 381
Internal fixation (open reduction / minimally invasive / Replacement
o after wide, marginal or intralesional resection
1]. Internal fixation of fractures
o preferablly intramedullary fixation or else a long plate.
o use PMMA in metastatic lesions
o be prepared é a whole array of sizes, different modalities and possible replacement
2]. Resection and replacement

Indications
1]. solitary lesions
2]. lesions that are expected not to respond to non operative treatment (RCC mets).
3]. Lesions close to a joint so that ORIF is not possible
4]. expendable bones which are problematic
5]. salvage of failed ORIF
General principles in decision making:
o The first procedure has the best prognosis so do more rather than less to eliminate
the need for a second procedure.
o Replace as much of the destroyed bone.
o Do a procedure that will allow maximum functional restoration.
o Perform a wide surgical margin in resecting solitary metastases aiming at cure.
o Impending pathological fracture or Pain …. Staging ….Impending fracture
Treatment of impending fractures Indications for prophylactic fixation (Mirels):
1 2 3
Site Upper Lower Peritrochanteric
Pain Mild Moderate Functional
Lesion Blastic Mixed Lytic
Size <1/3 1/3 -2/3 > 2/3
<6 = 0%, 12 = 100% incidence of fracture

Radiotherapy
1]. If surgery is planned, radiotherapy should always be postop and not preop
2]. It has no effect on renal cell carcinoma mets, or sarcoma mets
3]. Some lesions (eg breast mets) may reconstitute after radiotherapy
Relationship of fracture healing and irradiation
1]. Irradiation affects chondrogenic phase of callus and not osteogenic phase.
2]. Higher incidence of healing with rigid internal fixation.
3]. Healing depends on type of tumour and expected survival (67% healing in myeloma,
37% in breast mets ..)
ggggggbiiiiiii
Algorithm for management of metastatic bone disease

Diagnosis
Non neoplastic Primary bone tumour Myeloma Secondary

Manage fracture
+
Treat cause Splint Fixation Multiple lesions Unknown primary Untreated primary
Treat accordingly chemo & radiotherapy
Assess impending fractures Repeat investigations after Treat primary

Mirels score 6 weeks

Management of pathological fractures due to
secondaries
Expectations
General condition
Facilities, technical skills, economics
Favourable Not favourable
Assess: Non operative treatment

Location
Fracture pattern
Radiosensitivity
ORIF Replacement
Radiotherapy Radiotherapy
Managing MBD requires the collaboration of:

1]. Orthopaedic surgeon
2]. General surgeon
3]. Clinical oncologist
4]. Radiotherapist
5]. Radiologist
6]. Pathologist
7]. Physiotherapist
[Gene Therapy] Page | 383
Gene Therapy
Gene therapy is performed either to replace a harmful genes or to modify the action of
harmful genes
Approach:
1- Transfer of a well type of gene
2- Delivery to a specific tissue
3- Qualitative or quantitative replacement of a defective tissue
4- Suppression of a mutant gene
o Anti sense RNA
o Ribosomes
o Interfering RNA
Requirements
1- Gene map
2- Analytic equipment
3- Polymorphic markers
4- Mapping agent
Vectors
1- SUPPLEMENTATION: Either viral non-viral
a. VIRAL: z infectivity & replace the gene or genes from the virus with the required
gene (s) as retrovirus, adenovirus & herpes simplex virus
b. NON-VIRAL: Plasmids, peptides, liposomes & ligands (surface receptors)
2- GENE GUN
3- REPLACEMENT: Either replacement with introduction of repair or only replacement of
the hannful gene
Methods of delivery:
1. IN VIVO is less invasive but less safe and uncontrollable
2. EX VIVO is more invasive as the affected part is removed and treated by genes and re-
inserted thus technically more complex, however it is more safe and well controllable
Expression-regulation:
This achieved by either:
1- Enhancers
2- Silencers: are parts of DNA that regulate RNA activity é no relation to disease process
3- Promoters: These are either viral, acaryotic cell and hybrids. These are disease
dependent stimuli that are affected by the diseas process.
Safety of gene therapy:
• There are several problemsthat are associated with gene therapy that include:
transmission of diseases, infection, neoplastic potential and initiation of a
hypersensitivity reaction.
Clinical application: Gene therapy is applied in either:
I. Inherited disorders as:
• Achondroplasia: fibroblast growth factor receptor 3
• Pseudochondroplasia and MED: Cartilage Oligomeric Matrix Protein COMP
• SED: type II collagen disorder I o . Gusher's disease: glucocerbrodase enzyme
• Duschene and .f?acker's muscle dystrophies: dystrophein
• Mucopolysacchridosis
II. Acquired disorders
384 | Page [Gene Therapy]
1. Repair of:
• Cartilage
• Ligaments
• Tendons
• Bone union and spinal fusion
2. Treatment of certain diseases:
• Osteoarthritis Rheumatoid arthritis Osteoporosis
3. Management of certain tumors: Osetosarcoma, Ewing's sarcoma
4. Bone repair:
• It is best achieved by Bone morphogenetic protein and usmg , adenovimses.
Factors transmitted are:
1- Bone morphogenetic protein
2- Transforming growth factor
3- Fibroblast growth factor
4- Platelet derived growth factor
5- Insulin like growth factor
5. DeQenerative arthritis:
• In this condition gene therapy can be applied either systemically or directly into
certain target cells as synovial lining cells or chondrocytes. Factors transmitted
are:
• Tumor necrosis factor α
• Tissue inhibitors of metalloproteinases
• Growth factors for growth of cartilage as:
1- Transforming growth factor β
2- Fibroblast growth factor
3- Platelet derived growth factor
4- Insulin like growth factor
6. Ligaments and tendons:
• Also either systemic or direct introduction of the repair factors which are:
1- Decorin
2- Transforming growth factor β
7. Articular and meniscal repair:
• This performed by harvesting a part of periosteum with mesenchymal cells that
are injected with the vector carrying factors: Transforming growth factor β2,
BMP type II and Insulin like growth factor. The best combination is BMP IX and
Interleukein -11, then, the cells are re-injected into the site of meniscal repair or
degenerated cartilage
8. Tumors:
• Tumor control can be achieved by using factors:
1- z vascularity of the tumor by: Anti-angiogenesis factor
2- y surface expression of tumor cells by: yadhesion molecules'
3- ө tumor cell adhesion to other tissues in the process of metastasis by: y
anti adhescence factor
4- ө anti-inflammatory cell reaction by InterJeukein -6
5- ө of osteoclast activation
I
Meta
bolic
Disor
ders
Dr Mohamed
Sobhy rs i ty
Un ive
am s
n S h
Ai

[Metabolic Disorders] Page | 387
Bone
BONE ULTRASTRUCTURE
Bone is a specialized form of dense connective tissue.
Bone function =
1. Mechanical - gives the skeleton the necessary rigidity for support, attachment, and lever
2. Chemical - Calcium homeostasis & metabolism
3. Hematological
Three types of bone can be distinguished macroscopically:
1. Trabecular bone - (also called cancellous or spongy bone)
consists of delicate bars and sheets of bone, trabeculae,
which branch and intersect to form a sponge like network.
The ends of long bones (or epiphyses) consist mainly of
spongy bone.
2. Compact bone - does not have any spaces in the bone
matrix that are visible to the eye.
3. Woven bone - immature, disorganised bone.
Compact Bone (Cortical = lamellar bone)

• Compact bone consists almost entirely of MATRIX.
• OSTEOBLASTS deposit the matrix as thin sheets ώ are called
LAMELLAE (microscopic structures)
• Osteoblasts deposit ! matrix ⎯⎯⎯→ in hollows éin the matrix (LACUNAE) Æ osteocytes
Trapped
• COLLAGEN fibers within each lamella run parallel to each other. Collagen fibers which belong to
adjacent lamellae run at oblique angles to each other.
• Fiber density seems lower between adjacent lamellae, which gives the lamellar appearance
• Lamellae form concentric rings (CONCENTRIC LAMELLAE) around longitudinal canals ≈50μm
(HAVERSIAN CANALS) ώ run parallel to the surface & along the long axis of bone.
• The canals and the surrounding lamellae are called a HAVERSIAN system or an OSTEON.
• CEMENT LINES surround the outer border of each osteon & appear as the demarcation between
finished bone resorption, and begun bone formation; - collagen fibers and canaliculi do not cross
cement lines; - these lines do not bind adjacent lamellae but rather separate them.
• HAVERSIAN CANAL generally contains one or two capillaries and some nerve fibers.
• Immediately beneath the periosteum and endosteum a lamellae run parallel to bone surfaces.
These are the CIRCUMFERENTIAL LAMELLAE and ENDOSTEAL LAMELLAE. (vs. concentric lamellae)
• A second system of canals (VOLKMANN'S CANALS), penetrates bone ⊥ to its surface & connect inner
and outer surfaces of the bone with the vessels in the Haversian canals.
Trabecular Bone (Cancellous)

• Lamellae in trabecular bone do not form Haversian systems
•Lamellae of trabecular bone are deposited on preexisting trabeculae depending on the
mechanical forces on the bone (WOLFF'S LAW).
• Osteocytes, lacunae and canaliculi in trabecular bone resemble those in compact bone.
• Lamellar bone forms both trabecular bone and compact bone, which are the two
macroscopically recognizable bone forms.
Woven Bone (primary bone)
• forms embryonic skeleton, and is largely absent from normal bone after age 4 yrs
• is seen in fracture callus in both children and adults
• does not contain lamellae, and rather has a relatively disorganized array of collagen and irregular
mineralization pattern;
388 | Page [Meetabolic Disorders]
Bone Matrix Cellls

Bonne Cells
1. Osteoblasts
• Derived from messenchymal precursor cells in BM M ώ can differentiate into fat ce ells, fibrobllasts,
chondro ocytes or muscle
m cells
• 20μm cu uboidal cells arranged d in rows on
n the surfacce of bone lamellae
l
• Rich in alkaline
a phoosphatase ώ hydrolyse es phospho orylethanollamine liberrating phossphateÆ the
Ca x P product
p (solubility prodduct) Æ min neralizationn
• Responssible for:
1]. Formation n, organizattion, and mineralizat
m tion of EC matrix
m
2]. Synthesis
S o collagen
of n & other bone
b proteins
3]. Involved in n the initiattion and acctivation ofo osteoclasstic activityy
4]. When
W trap
pped becom me osteocyyte
• Produce e matrix, wh hich comprrises:
1]. Type
T 1 colla
agen (90% of the prottein in bone e)
2]. MPS
3]. osteocalcin
o n (indicatorr for osteobblastic activity)
4]. osteoponti
o n
5]. osteonectin
o n
6]. proteoglyc
p ans
7]. alkaline
a phosphatase
• They de eposit osteooid on pre-e existing min
neralised suurfaces onlyy (= the min
neralisation front).
• Some ossteoblasts become
b trapped in laccunae Æ ossteocytes, co onnected b by canaliculi.
2. Osteocytes
• Similar to nerve cel
ells; and can be regarde ed as spentt osteoblastts lying in th
heir lacunae
e
• osteocyttes have se everal thin processes
p ώ run in smaall canalicu
uli éin the b bone
• canalicuuli are respo
onsible for intercellularr communiccation
• Theorettical functioons:
1]. reggulate the e response e of bone e to the mechaniccal
envvironment & transm mit stress informattion to th he
ostteoblasts
2]. Reg gulate the Ca homeo ostasis undder PTH con ntrol
3. Resting su urrface cells (Bone Lining cells)

• flat cell ly
ying on thee surface off bone
• develop ps from ostteoblasts, once
o they have com
mpleted the
eir
work
• may ded differentiate
e back into osteoblastss
4. Osteoclasts
• Structure
o Large motile, MULTINUCLEATED cell located on bone surfaces é some features of
macrophages
o Formed by the fusion of mononuclear cells derived from haematopoetic stem cells in
marrow
o [The theory that osteoclasts and osteoblasts are derived from different precursors has
been challenged by a recent report proposing that stromal cells and haemopoetic cells
have a common ancestry: a single multi-potential stem cell in marrow]
o Osteoclasts have a RUFFLED BORDER ώ is surrounded by an organelle-free, or 'clear zone'
• Histochemistry
o Rich in Acid Phosphatase Æ resorption of previously formed bone (wear and tear)
o Osteoblasts express RANK Legend that binds pre-osteoclasts so they coalse and form the
active osteoclasts (OPG “osteorotegrin” is a competitive inhibitor of the RANK)
o Active osteoclasts adhere to the bone surface via specialized receptors ”INTEGRINS”
o After doing its function it is left in shallow excavations on the surface (HOWSHIP’S LACUNAE)
• Functions: Osteoclastic resorption (mineral dissolution ⎯⎯ ⎯⎯ ⎯→ organic degradation)
Followed By
1]. Mineral Dissolution

Osteoclasts lower the pH gradient across the ruffled border, by active
transport mechanisms: Na+/H+ pump, ATP- proton pumps, and carbonic
anhydrase Æ pH Æ HA solubility Æ demineralization
2]. Collagen degradation
Synthesize lysosomal enzymes and release them at the ruffled border:
Tartrate resistant isoenzyme of acid phosphatase (T TRAP)
Cysteine-proteinases such as the Cathepsins that degrade collagen.
• Regulators of Osteoclast activity:
1]. PTH ................................................................. ? ADP pump .........................................bone resorption
2]. Glucocorticoids ........................................... osteoblastic .........................................bone resorption
3]. Prostaglandins ............................................ ADP pump ...........................................bone resorption
4]. IL-1, IL-6 .......................................................... clast precursor proliferation ..........bone resorption
5]. IL 10 ................................................................ osteoclastic activity ...........................bone forming
6]. 1,25(OH)2D3 ..................................................................... Alk Ph, Osteocalcin ............................bone forming
7]. Calcitonin .............................................................................................................. bone forming
o PTH and 1,25(OH)2D3 are unable to osteoclastic resorption in vitro éout
osteoblasts. Both ⊕ osteoclasts to resorb bone via a 'Coupling' Factor.
o Osteoclasts do not have receptors for 1,25(OH)2D3; and until recently were not
believed to have PTH receptors
o Osteoclast have calcitonin receptor Æ resorption directly by cellular motility,
retract cytoplasmic extensions and ruffled border size.
8]. Biphosphonates (pyrophosphate analogs) osteoclastic .........................bone forming
9]. TNF & TGF α Æ osteoblasts ......................................................................................bone forming
10]. Oestrogens TGF α & Alk Ph / IL6 & ADP pump .........................................bone forming
11]. ? Androgens
12]. ? Thyroid hormones
390 | Page [Metabolic Disorders]
ORGANIC MATRIX ....................................................... (40%)
1. Collagen ........................................................................... (90% of organic matrix)

• Mainly Type 1
• Synthesized by fibroblast as Collagen Location
procollagen ⎯Converted
⎯⎯⎯→ collagen 1 Bone, Tendon, Meniscus, Annulus of Discs, Skin
2 Articular Cartilage, Nucleus Pulposus of Discs
• Collagen molecule consists of 3 Skin, Blood Vessels
two a1 & one a2 PP chains each 4 Basement Membrane (basal lamina)
coiled in a left handed helix 5&6 Articular Cartilage (small amounts)
• Mole.wt 340,000 daltons 7 & 8 Basement Membrane (epithelial)
9 Articular Cartilage (small amounts)
• The three chains coil together in 10 Hypertrophic Cartilage & é cartilage calcification
a right handed triple helix to 11 Articular Cartilage (small amounts)
form a molecule of collagen 12 Tendon
• Crosslinks between the chains 13 Endothelial cells
and the molecules of collagen give collagen its TENSILE STRENGTH
2. Proteoglycans see previous cartilage

•functions:
1. Responsible for the COMPRESSIVE STRENGTH
2. Organizes collagen fibers
3. mineralisation
4. binds growth factors
3. Matrix Proteins (non-collagenous)
1. osteocalcin
o binds calcium
o attracts osteoclasts
o levels in urine in Pagets, hyperparathyroidism & renal osteodystrophy
2. osteopontin
o cell-binding protein
o anchors osteoclasts to mineralised matrix
3. osteonectin
o binds calcium
o regulation of mineralisation
4. Sialoprotein
o important in cell attachment
5. Thrombospondin
o binds calcium & important in cell attachment
6. Serum proteins
o in same concentrations as in serum except albumin, which is increased
4. Cytokines
• have autocrine, paracrine & endocrine functions
• important in growth , differentiation & remodeling of skeleton
• IL-1, TGF, TNF, IGF1 & 2, FGF, PDGF, prostaglandins
INORGANIC MATRIX ................................................... (60%)
1. Calcium Hydroxyapatite - Ca10(PO4)6(OH)2 = (ca + P + HCo3)

• responsible for the COMPRESSIVE STRENGTH of bone
2. Osteocalcium Phosphate (Brushite)
BONE FUNCTION
Remodelling = osteoclasts resorb bone & the resulting hole is filled by osteoblasts with
new bone & osteocytes. (e.g. cutting cone of compact bone)
Modelling = osteoclasts remove bone from one area while osteoblasts add bone
elsewhere. Occurs in trabecular bone in response to load changes (WOLFF'S LAW).
Remodelling Cycle:
• osteoclasts resorb bone surfaces to form an erosion cavity
• Mononuclear cells then fill in the cavity ⎯⎯⎯ ⎯→ osteoblasts and begin to lay down matrix
differentiate
• This process can take 3mo & with mature osteoblasts secreting matrix for up to 100 days.
• This balanced process is described as coupling (uncoupling of formation from resorption
that leads to skeletal diseases such as osteoporosis where net resorption > formation.)
Cortical / Compact bone:
• Remodels by osteoclast tunneling (Cutting Cone), followed by layering of osteoblasts &
successive deposition of lamellae, forming a Haversian canal.
• The head of the cutting cone is the osteoclasts, followed by capillaries, then osteoblasts.
PERIOSTEUM (CT membrane covering bone)

• Well developed in children ð its role in cortical bone deposition (growth in diameter)
• 2 layers:
o Inner Cambium Layer:
loose & vascular
osteogenic
o Outer Fibrous Layer:
less cellular
contiguous with joint capsules
BONE CIRCULATION (5-10% of cardiac output)

1. Nutrient artery system (High pressure system )
o supplies the inner 2/3 of cortex from within (endosteal)
o Divides after reaching the medullary cavity, sending arteriole branches in proximal
and distal directions to join with metaphyseal arteries
o In children, they end on metaphyseal side of ! physis & contribute to endoch. ossification.
2. Periosteal system (low pressure system)
o forms an extensive network of vessels covers ! entire shaft
o supplies outer 1/3 of cortex
o v. important in children, for appositional bone growth (circumferential)
3. Metaphyseal system
o supplies the zone of provisional calcification in the physis
o anastomoses with the nutrient artery system
4. Epiphyseal system
o supplies physis by diffusion: resting, germinal, proliferating, & upper hypertrophic
o In femoral & radial heads (almost covered by cartilage), vessels enter in region bet.
articular cartilage & growth-plate cartilage, and hence, the blood supply is tenuous
o Arterial supply of the cortex is centrifugal (inside to out). The direction is reversed in
displaced fractures, é disruption of the endosteal (nutrient) system.
o Venous flow is centripetal é cortical capillaries draining to venous sinusoids to
emissary venous system.
EMBRYOLOGY
The appendicular skeleton develop from limb buds, which are mesoderm covered by
ectoderm.
The first visible outline of the embryonic limb follows a condensation of MESENCHYMAL CELLS
which subsequently differentiate into cartilage cells, the CHONDROCYTES.
These cells secrete matrix Æ CARTILAGINOUS MODELS of the future bones & surrounded by the
perichondrium; the outer layer ⎯⎯⎯→ CT sheath & the inner cells remain pluripotential.
Becomes
PRIMARY DIAPHYSEAL OSSIFIC CENTRE,

develops as the inner layer starts to
lay down bone trabeculae to
surround the inner hypertrophied
chondrocytes and calcifying matrix
Irruptive vasculomesenchymal canals
appear & pass into the calcified
matrix Æ Primordial BM
Irruptive canal osteoblasts lay down
bone on the on the calcified matrix
Æ bone trabeculae Æ haversian
In long bones, another SECONDARY
CENTRE of ossification appears at the
growing cartilaginous ends, the
EPIPHYSEAL OSSIFICATION CENTRE.
A transverse plate of cartilage form to
separate epiphyseal from diaphyseal
PHYSIS)
ossific centre (P
Interstitial growth
Physeal growth continues, but it
does not thicken because on its
diaphyseal side the cartilage
matures, calcified, resorbed and
replaced by bone.
This is ENDOCHONDRAL OSSIFICATION,
the mechanism responsible for
bone length
Appositional growth
As ht Æ bone diameter ; by new
bone laid down by cambium layer
This is INTRAMEMBRANOUS OSSIFICATION
that does not involve prior cartilage
formation –mesenchymal cells produce collagen and MPS directly upon ώ ca hydroxapatite
ossification.
[Metabolic
M Disorders] Page | 393
Bo
one rremod
delin
ng
B neG
Bon Growtth
Bon
ne Growth
h Occurs Through:
T
Typ
pe M
Mechanism Norma
al exampless Path. examples
e
Intramembrannous UMC differentiate
d into 1]. Em
mbryonic flat bone
b formatiion Cleidocrania
al dysostosis
bone forming
f 2]. Disstraction oste
eogenesis
osteob blasts 3]. Bla
astema bone
Enddochondrall Bone replaces
r 1]. Phyyseal growth h................... (le
ength) Achondrop
plasia
cartilag
ge model 2]. Em
mbryonic long g bone forma ation
3]. Fra
acture callus
4]. NBBF é the demiineralized bo one matrix
Ap
ppositional NBF on existing bo
one 1]. Perriosteal bone enlargement (width) Paget’s
by Ostteoblasts 2]. Bonne formation in remodeling Caffey’s
ers: see beefore RPM DC

Phyysis Laye D
Vitamin D
It is a fat soluble vitamin Absorbed in the upper part of the small intestine utilizing bile
Daily needs:
• In full term = 400-800 IU/day starting from the 4th month
• ln Preterm =1000-1200 supplied from the 2nd month
Sources:
1. Endogenous D3 (cholecalciferol): Formed in the skin from 7 dehydrocholesterol
by UVR
2. Animal source:
o Fish liver oil and egg yolk (Cow & breast milk are poor sources)
3. Plant source :
o Vit D2- ergocalciferol: irradiated green Plants & vegetables oils
Preparations
1. oral preparations:
o cod liver oil, Halibut liver oil
o Other new preparations: Decal B12 (1000IU/5ml)
2. Parentral preparations: therapeutic (e.g. Devarol 600,000 IU/1ml)
Actions:
Active vit D is considered as a hormone bec it is a secreted from kidney and circulate in the blood
and act on a remote tissue namely the bone to perform an action é a feed back mechanism same
as any hormone; if –ve feed back Æ 24,25 (OH)2D is formed
1) Intestine: ca & p absorption
2) Kidney: tubular reabsorption of ca
3) Bone: - if ca X p product is high Æ mineralization
- if Ca X P product is low Æ demineralization (resorption)
Alk. phospatase
- Organic phosphates ⎯⎯ ⎯ ⎯ ⎯ ⎯⎯→ INORGANIC ph (mineralization)
CALCIUM: 99% in bone / 1% in serum

Calcium
Function:
muscle /nerve function
clotting
Bone structure
Daily needs:
Kids: 600mg/day
Adult-750mg/day
Preg & adolescent & fr: 1500mg/day
Breastfeeding-2g/day
Metabolism:
Absorbed in duodenum (active transport) & jejunum (diffusion)
98% reabsorbed in kidney PCT, may be excreted in stool.
Calcium balance- positive first 3 decades then neg
Normal serum level: 9-11 mg%
1) Non diffusible = protein bound (45%)
bound to albumin, prealbumin, & globulin
in case of hypoalbuminaemia e.g. nephritic $
2) Diffusable
1. Non-ionized= 5% in the form of citrate, phosphates & carbonates
2. Ionized (active form) 50 %
o by acidosis ○ By alkalosis (even é N level) Æ tetany
[Metabolic
Phoosphoorus
y Normal
N um level: 4.5
seru 4 - 6.5 mg%
m mainlyy unbound
d y Phosp
phate 85% in bone
y Daily
D requirrements: 1-1.5g/day
Me
etabolism::
Reg
gulation Of
O Ca & P Metabolis
M sm:
Facctor Zone
e eratn Matu
Prolife uration Co
ollagen GA
AG Calcification
PTH
H All Physiss y - - y
yy z (yca bby resorption & reabsorption
r & ⊕
Vit D hyd
droxylation)
GHH PZ y (IGF) - y y y (+ve caalcium balance)
Sommatomedinn PZ y - y y -
Inssulin PZ y (IGF) - - - -
PG HZ + MTP Ph y - z y z (Resorrption)
Thy yroxine HZ + PZ y (IGF) y (T3) - - -
Callcitonin HZ + MTP Ph - y - - y (z ca bby Θ Osteoclasts & reabsorptioon)
1,2
25 (OH)2D3 HZ - y - - y (y abssorption)
IL-1
1 All Physiss - yy ( ⊕ metallo- z z -
protien
nases)
Ste
eroids All physiss z z z z -
Oeestrogen All physiss - Clo
osure - - y ( Θ Boone Loss)
PTH: Hypercalcemic & hypopho osphatemic effect

y Rennal Ca reabssorption & z P reabsorrption
Vit D: y ca a & Po4 intesstinal absorrption
Calcitonin: .......... bone sparing hormone: (seccreted from parafollicular cells of tthyroid)
GH: +ve Ca balance (y mineralization)
Thyroid Ho ormone: imp portant for normal
n bonne developm ment in norm
mal levels
Steroids: ............... y bon ne loss: Cata
abolic effect on bones + Antivitammin D: z Ca absor. & reabsorption
Growth facctors
IGF I (Somatome
( edin C): prodduced by ossteoblast &liver
Transforming Growth factorrs (TGF): Æ osteobla asts
IL1 & PGs: produ uced by bon ne cells; regu
ulate osteob
blasts & classts
BMP found
f in maatrix Æ o
osteoblasts & chondrog genesis
Mechanical Stress: (Wolff’s law)
Bones are adjusted to withstand normal and
abnormal forces; so more bone form on the
compressive side & thins out on tension side
Electric stimulation: load generate small
Piezo-electric potential
-ve on compressive side
+ve on tension side
PEMF is used to y bone union and
in AVN but not yet FDA approved
US: Low intensity ⊕ Healing
Irradiation: ............. Θ Healing
Environmental Factors
y temperature Æ y Bone form
y PO2 Æ y bone formation
Acidosis Æ y bone formation
Phosphates Æ z resorption
Bisphosphonates Æ z resorption
Fluoride:
⊕ osteoblasts & y mineral density
form fluoroapatite (resist
osteoclast)
Ca2+ retention
2ry PTH++
Rickets
Definition
• It is a developmental disorder in ώ there is a disturbance in of ca & ph metabolism é failure of
mineralization of growing bone
• NB. Failure of mineralization of grown bone is termed osteomalacia
Classification:
1) Vit D deficiency Rickets (Vit D sensitive rickets)
it is the commonest in our country
2) Vit D resistant rickets (not responsive to ordinary doses of oral vitamin D)
Renal Rickets:
Glomerular dysfunction
o Renal osteodystrophy
o Vit D dependant rickets type I
Tubular dysfunction:
o Genetic primary hypophosphatemia
o Fanconi $, Lowe $, Lignac $
o Renal tubular acidosis (Lightwood $)
Hepatic Rickets (Coeliac rickets)
Malabsorption rickets
Condition simulating rickets
Hypophophatasia
Hyper parathyroidism
Infantile Rickets
= Vit D deficiency rickets
•
Aetiology:
1- Rachitogenic diet
i. Cow milk
ii. Prolonged breast feeding without vit D supplementation
iii. Cereals rich in phytates and phosphate
iv. z acidity (poor intake of vit C)
v. y alkalinity (e.g. excess beverages
2- In adequate exposure to sun light
i. Glass windows, cloudy weather, industrialized countries (polution)
ii. Over rapped infants
iii. Dark skinned infants
Contributing factors
1- Age most seen between 6-24 mo
in severe osteomalacic mothers & premature + LBW it can be seen as early as 2
mo
2- Rate of growth
Rickets is a disease of growth
Rapidly growing infants as preterms and LBW are more susceptible than those é
z growth rate (as cretins and marasmic pt)
Season: more common in winter because of escessive wrapping Æ lack of
exposure to UVR
Pathology:
∂ Active rickets:
Cartilage cells fail to complete their normal cycle of proliferationand degeneration
with continuous division & with subsequent accumulation of non rigid osteoid
tissue at the growing parts
Osteoid tissue is uncalcified, vascular and irregular
The epiphyseal line is invaded by the osteoid tissue and capillary penetration Æ
zone of provisional calcification disappears
The non rigid osteoid tissue becomes compressed and bulges Æ Broadening,
cupping, Fraying
The epiphysis shows the following changes:
Bone resorption ð 2ry hyperparathyroidism
Deposition of osteoid tissue at diaphysis under raised periosteum
The diaphysis loses rigidity Æ deformaities & green stick fr
∂ Healing rickets:
Calcium deposition takes place in the accumulating tissue
ZPC reappear (line if calcification)
∂ Healed rickets
Mineralization of osteoid tissue is completed
ZPC appear thick and
Normal bone density is regained
Deformities may be not corrected if severe
Chemical pathology
∂ Vit D deficiency Æ less ca absorption from the intestine and kidneys Æ slight lowering of
serum ca level
∂ PTH secretion y to maintain normal s.ca level (PTH mobilize ca from bone)
∂ Serum P level z (ð 2ry hyperparathyroidism)
∂ Seum alk.ph. y (ð y osteoclastic activity)
So in active rickets
∂ S.ca Æ normal (9-10 mg%)
∂ S.ph Æ z (N= 4.5 - 6.5 mg%) earliest to return normal é ttt
∂ S.alk.ph.:y
The first to y, and the last to return to normal
Normal value in adult = 3-13 KAU
Normal value in children =3-25 KAU (higher rate of growth)
NB Hypocalcaemia and tetany may occur if

Parathyroid gland fail to respond to hypocalcaemia (exhaustion)
Bone stores f Ca are exhausted
Vit D shock therapy is given withour Ca supplementation
Severe Chest infection Î hyper ventilation Æ washes O2 Æ alkalosis
CAUSES OF ALK PH (= causes of stimulated osteoblasts)

Rickets
Osteomalacia
Hyperparathyroidism
CAUSES OF ALK PH
Hypophosphatasia
Cretinism
PTH
1,25 (OH)2D3
Howland formula Ca x Ph < 30 normally is 50
Urine Ca is absent
Urine P
Generalized amino aciduria
Clinically:
Earliest: Irritability, anorexia & sweating ( p autonomic disturbance)

Commonest: Recurrent chest infections * GIT disturbances
Delayed motor milestones (Hypotonia & deformities)
Delayed teething
Skeletal deformities
Late: Tetany (most dangerous)
Examination
Early stage
• Disturbed autonomic NS
• Craniotabes: abnormal skull softness Æ ping pong ball sensation on firm pressure over occipital
Endof 1stYear
bones (ð thining of the outer skull plate) ⎯⎯ ⎯ ⎯ ⎯ ⎯ ⎯→ the skull becomes slowly growing Æ
disappear
• Rachitic rosary: palpable enlargement of the costochondral junction
• Thickening of the wrists and ankles = Broadening
• +ve Marfan sign may be considered as an early sign
• Biochemical and radiological manifestation occur in early rickets
Advanced Stage:
1. Skeletal manifestation:
Head:
Caput quadratum (frontal and parietal bossing)
occipito-frontal circumference (macrocephaly)
Craniotabes
Delayed closure of ! fontanelles (never > 5 cm ≠ hydrocephalus)
Delayed teeth eruption and dental caries (defective enamel)
Thorax:
Rachitic rosary: enlarged costochondral junction (rib metaphysis)
Harison sulcus: horizontal along the lower border of the chest cage opposite the
costal insertion of the diaphragm
Protruded sternum: pigeon shaped chest (pectus carinatum)
Pectus excavatum
Longitudinal sulcus lateral to the rosaries at midaxillary
Spine:
Smooth, rounded correctable kyphosis
Scoliosis, Kyphoscoliosis
Exaggerated lumbar lordosis (ð weak muscles & lax ligaments)
Pelvis
Inlet contraction ð ant displacement of sacral promontory
Outlet contraction ð ant bending of coccyx Æ may need cesarian during delivery
later on
Rachitic dwarfism
Limbs
Epiphyseal enlargement of the wrists and ankles Æ broadening
Marfan’s sign: transverse groove on both malleoli (more on medial) ð abnormal
proliferation of osteoid tissue at the 2 ossific centers of the malleoli;
PATHOGNOMONIC
Deformities:
- Bending of soft diaphysis by body wt. & ms traction
- UL: in crawling infants Æ convex ext.surface of radius & ulna
- LL: - Genu varum
- Genu valgum
- Genu recurvatum
- Coxa vara
Green stick fractures
2. laxity due to:

Hypotonia: Due to hypophosphatemia
Lax ligaments
These explain
Delayed motor milestones
Abdominal manifestations
Spine deformities
Visceroptosis
3. Neurogenic manifestation
Early: Hypotonia
Late: tetany
4. susceptibility to infections
5. Abdomen:
Pot Belly abdomen (protruded abd)
Hypotonia of abdominal ms
Intestinal Hypotonia Æ distension
Exaggerated lumber lordosis
Organomegaly & visceroptosis
Narrow chest and pelvis
Umbilical hernia and divercation of recti
Palpable liver & spleen due to:
Ptosis (weak ms & lax lig)
True enlargement:
o RES hyperplasia (infections)
o Von Jack’s anemia
o Hepatic Rickets &associated hepatomegaly
o Cystinosis
Investigations:
∂ Biochemical changes: see before
∂ Radiological changes:
○ Active: best seen at lower ends of long bones (e.g radius & ulna) in AP
Epiphyseal: broadening, cupping, fraying (vascularity) of epi.line
Diaphyseal:
Rarefaction
Double periosteal lines
Green stick fracture
Deformities
radiological joint space (large epiphysis)
○ Healing Stage:
Appearance of line of provisional calcificn ώ is dense concave line at the
region of metaphysis é less dense area between it and the shaft
○ Healed stage:
Ossification becomes continuous é ZPC Æ thick dense epiphyseal
Normal cortical density is regained & periosteal changes disappear
Normal joint space
Fractures healed
Complications:
1- Bones:
Persistent deformities
Fractures
Short stature
Obstructed labor
2- RTI: Bronchitis, Lobar pneumonia, bronchopneumonia, asthmatic bronchitis (ms
hypotonia & immunity & hypocalcemic spasm)
3- GIT:
Constipation (hypotonia)
GE (swallowed infected sputum)
4- Anemia
ð repeated infections / malnutrition é Fe & folic acid
Von Jacks Anemia: Anemia + LN + HSM (pseudoleukemia Infantum; leukocytosis
up to 25,000/mm3)
5- Tetany if alkalosis 2ry to O2 wash in severe infections
Differential Diagnosis
1- Other causes of inability to walk
2- Craniotabes:
OI
Hydrocephalus
Premature
3- Other causes of rickety rosary:
Scurvy
Achondroplasia
4- Other causes of spine deformity
5- Other causes of dwarfism
Treatment
Prevention
Health education
Dietary instructions
Exposure to sun light
Vit D supplementations
Prevention of deformity
Active treatment
Vitamin D
Oral: 2000-6000 IU daily till complete recovery
Injection: shock therapy (600,000 IU / 2wk for 3 doses)
Maintenance therapy: 400-800 IU/d
Adjuvant therapy:
Adequate ca , P
Exposure to sun light
Treatment of complications:
Treatment of deformities:
Osteoclasis
Open osteotomy osteoclasis
Late deformities: HTO
Treatment of infections
Treatment of tetany: correct alkalosis & ca
[Metabolic
Pr
rognos sis
Morrbidity:
t healing starts ώin
With ttt n days (2-4 4 wk and progress slowly till normal bone
b
structuure is restorred 6-8 wkk)
Epiphyyseal enlarg mity, & rosaries may p
gement, skkull deform persist yearss
In adva anced neg glected case es; perman nent deform
mities mayy occur
Morrtality:
It is not a fatal dissease; but its compliccations mayy be fatal e
e.g. pneummonia
Cr
riteria for improvement:
geeneral con nditions
Biocchemical normal ALP P
Radiological siigns for he ealing
NB;; Hypervita
aminosis D occur é administrration of high h dose ng periodss Æ
es of vit D for a lon
hyp
percalcemiaa, metastattic calcificaation, hypeercalcuria
Clinically the pt
p has:
Anorexxia
Constip pation, vom miting, wt loss
Polyuriia, polydep psia, dehyd
dration
Renal colics
c
Anemia
Calcificc aortic stenosis
Rena
al Ricke
ets
Glomeru
ular Tubu
ular
Renal
R 1ry Mu
ultiple Ren
nal tubula
ar
osteod
dystrophy
y hyp
pophospha
atamia de
efects acidosis
a
Vit D dependan
d nt
Fanconi Lo
owe Lignac
T
Type I
Renal Osteodystrophy
Renal Glomerular rickets / Uremic rickets
Definition: It is alteration of skeletal growth in children with chronic renal failure CRF or chronic
renal insufficiency
Ætiology:
Chronic glomerulonephritis
Ch.pyelonephritis
CRF of any other cause
Polycyctic kidney
Mechanism
Failure of renal hydroxylation of vit D Æ active form Æ s.Ca
Defective Glomerular filtration Æ s.Ph
Both Æ 2ry hyperparathyroidism Æ bone resorption Æ osteitis fibrosa cystica
Metabolic acidosis Æ solubilization of ca salts of bone
NB: Tetany is rare

Clinically:
Of the original disease: HTN, oliguria, hematuria …
Marked growth failure and dwarfism ð:
Under nutrition
Osteodystrophy
Hormonal abnormality
Medications esp.steroids
Rickets …
Investigations
For renal dysfunction: urea, creatinine, acidosis
For Rickets:
Chemical (as before but é s.P)
S.Ca: N/slight
S.Ph: (the only rickets with hyperphosphatemia)
Ca x P:
ALP:
Radiological:
As rickets +
osteitis fibrosa cystica (osteopenia + cystic changes)
Treatment:
Treatment of renal dysfunction: hemodialysis, transplantation
Large doses of Vit D:
Oral high dose 10,000-25,000 IU/d
Calcitriol 1,25 (OH)2D recently 0.1-1.2 μg/kg/d
1 α (OH) D
Any of them is taken till healing or toxicity occurs
High ca intake
Low ph intake
Phosphate Chelators
Aluminum hydroxide (chelates Ph)
better Ca Co3 (chelates Ph, give Ca. no Al toxicity)
correct metabolic acidosis
Vitamin D dependant rickets
Type I Type II
Genetics AR AR
defect in renal hydroxylation of vit D into
Mechanism Target organ resistance to vitamin D
1-25 (OH)2D: renal 1α hydrloxylase
Serum Ca
serum P
ALP
1,25 (OH)2D
treatment 1,25 (OH)2D Æ 1-2 μg/d No ttt

1-α (OH)D is also effective Or very high doses of 1-25 (OH)2D
Some of the cases of type 2 are associated with alopecia totalis and short stature
CELI C RICK
IAC KET
TS
Malabsorption rickets
Ætiiology: Ma alabsorptio
on $
Patthogenessis:
vit D absorpption
Caa absorptio
on
Clin
nically
Man nifestation of malabso orption
Man nifestationss of rickets
Inv
vestigatioons:
For malabsorp ption: stooll analysis , fecal
f fat, an
nd intestin
nal biopsy
For rickets … etc
Tre
eatment
Pareentral Vit D
Ttt of
o the causse if possiblle
HEPA C RIC
E ATIC CKET
TS
Ætiiology:
Seve ere hepaticc diseases e.g.
e Biliary atresia , ch h.Hepatitis
Patthogenessis:
Failuure of 25 hydroxylati
h on of vit D in liver
ab bsorption of o vit D due to bile de eficiency
Clin
nically
Man nifestation of hepatic dysfunctio on (jaundicce, ascites,…
…)
Man nifestation of rickets
Inv
vestigatio ons
Liveer function tests
sGPT T, sGOT, billirubin
bumin Æ Reversed A//G ratio
s alb
Inve estigations for rickets:: as infantille rickets
Tre
eatment:
ttt livver disorde er
ttt ricke
ets: Better by injectio
on ð defective absorp ption
25 (OH H) D Æ 1-2 μg//kg/d
1,25 (O OH)2D Æ 0.1 - 0.22 μg/kg/d
Dose iss adjusted till criteria for healing
g appear
Adju uvant thera apy
Rickeets Witth Antiiconvvulsaant

Thiss occur esp
pecially witth the com
mbination of
o phenoba arbitone + phenytoinn
Meechanism::
Enzyyme induccer
Tre
eatment
Follo
ow up by clinical
c exa
am and estimation off serum Ca,, P, ALP
Highh Vit D intaake by 5000-1000 IU/d
d
CongenitalHypophosphatasia
AR marked deficiency of alk.ph
Clinically
Congenital lethal form:
Born é soft skull, and ribs, fractures , and deformities
Either still born or dies shortly after birth
Hypophosphatasia tarda
Rickets, deformities, and short stature
Investigations
Normal ca & p
ALP
phophoryl-ethanolamine
PXR: ccc radiolucent areas extended from physis into the metaphysis
Treatment
Genetic engineering may be helpful
CongenitalH yper
p hosphatasia
AR disorder é alk.ph
Pathology
Subperiosteal proliferation of osteoid tissue Æ periosteal elevation
Thick deformed diaphysis + osteopenia
Clinically
Painful deformed limbs
Limping
Pectus carinatum + large skull
Kyphoscoliosis + rib fraying
Investigations
PXR: Bone halos, osteopenia, with intermingled cotton wool dense areas
Normal ca & p
ALP
Leucine aminoacid peptidase
Treatment
Calcitonin
Primary hypophosphatemic Rickets

1ry Vit D resistant Rickets
Genetics:
XD (More common in females)
Pathogenesis:
Isolated tubular defect
Defect in renal reabsorption of P by proximal convoluted tubules PCT Æ s.Ph
Defective renal hydroxylation of Vit D
NB; normal PTH Æ normal intracellular P Æ no autonomic disturbance
Clinically:
Pt present in 2nd year of life (late presentation)
Minimal involvement of skull and chest (ð late onset)
Retarded linear growth Æ dwarfism & deformities
General condition and tone are good (Normal Intracellular Ph)
Tetany is rare (ca is normal)
Investigation
Normal or low normal ca
S.Ph (Normal intracellular p)
Urine Po4
ALP
PXR rachitic manifestation
Treatment
Oral phosphate 0.5-1 gm/d (for infants) / 1-4 gm/d (for children)
1,25 (OH)2D (enhance p absorption)
Fanconi Syndrome
It is a multiple renal tubular defect é resultant loss of p, glucose, AA in urine
Ætiology:
Idiopathic: inherited as AD or AR (most common)
Associated é IEM
Cystinosis (Lignac $)
Tyrosinosis
Galactosemia
Associated é lowe $
Acquired as in
Lead poisoning and Hg poisoning
Outdated tetracycline
Pathogenesis:
Essential
Ph Æ hypophosphatemia
Glucose Æ glucosuria (no hypoglycemia)
Generalized aminoaciduria
Non essential:
K Æ hypokalemia
Na Æ hyponatremia
HCo3 Æ metabolic acidosis and alkaline urine
Clinically:
Rickets ð hypophosphatemia and acidosis
Anorexia, nausea, vomiting ( Na, P Æ GI upset)
Polyuria, polydepsia, dehydration (osmotic diuresis)
Failure to thrive and short stature
Investigations
Urine: Po4, glucose, AA, PH
Blood:
S.Ca: N
S.Ph:
K & Na
PH (metabolic acidosis)
ALP:
PXR
Rachitic manifestation
Treatment:
Correction of:
Hypophosphatemia Æ oral phosphate see before
Hypokalemia Æ oral potassium
Acidosis Æ Na HCo3
Fluid therapy if dehydrated
Vit D high doses (1,25 (OH)2D is the best)
Stoppage of the cause in acquired forms
Lignac $ Lowe $
Cystinosis Occulo-cerebro-renal disease
AR Inborn error of metabolism of cytine AA Rare XR disorder é MR & rickets
Pathogenesis: Clinically
Abnormal accumulation of cystine crystals Eye: cong.cataract &
Clinically: glaucoma
Skeletal: rachitic manifestation Cerebral: MR + hypotonia
Eye: photophobia (corneal affection) Renal: Fanconi
Renal: Fanconi and CRF Investigation and ttt
RES: HSM and LDN As Fanconi
Blond hair & fair skin (melanocytes affection)
BM: pancytopenia
Investigations
As Fanconi
Slit lamp Æ corneal cystine crystals
cystine content in WBCs or fibroblasts
Treatment
As Fanconi + ttt of CRF
possible chelation by cystiamine or D-penicillamine
Lightwood Syndrome
Rickets with Renal Tubular Acidosis
Ætiology:
AR or sporadic
Renal tubular acidosis is a clinical state of systemic acidosis resulting from impaired
renal ability to acidify urine
Types: 3 types
Distal type I: deficiency of hydrogen ion secretion by DCT
Proximal Type II: PCT reabsorption of HCO3
Mineralocorticoids Æ H+ secretion
Clinically:
Severe form (fatal):
Failure to thrive
Vomit & dehyd
Acidotic breath
Mild from
Rachitic & frs
Renal calculi
Investigations:
Blood:
Normal S.Ca
s.Po4
s.K
PH
Urine:
K, Ca, Po4,PH
PXR:
Rachitic
manifestation
Treatment:
Oral NaHCo3 , K, Po4
High doses of Vit D (or 1,25 (OH)2D is the best)
NB; Rickets + dwarfism occurs in:
Renal osteodystrophy
Familial hypophophatemic rickets
Fanconi, Lignac, Lowe
Severe neglected infantile rickets
Infantile Uremic phosphatesia phosphatemia Fanconi RTA PTH

Ca N/ N/ N N/ N/ N
P N
Blood ALP
PTH N N/
PH N N N N
Ca - - - - -
P -
Urine PH N N N
Glu - - - - -
AA - - Po4Eth.Amn. - -
Tetany
Definition:
A state of hyper excitability of peripheral and CNS resulting from Ca, Mg, or Alkalosis
Ca is important for neurotransmission in synapses; when Æ unstable synapse
Mg is important for synthesis and release of PTH
Aetiology:
Hypocalcemia
Hypoparathyrodism
Familial
Aplasia or hypoplasias of the glands (DiGeorge or VATER)
Post-thyroidectomy
Autoimmune
Early neonatal hypocalcemia ....... (1st 72 hrs)
▪ Infant of diabetic mother & PT & IUGR
Late neonatal .................................... (5-10 days)
▪ High Po4 food e.g. cow milk Æ ca deposition in bone (due to still
immature PTH & will not respond to ca)
Tetany of Vit D deficiency (rickets)
Hypomagnesemia (<1.2 mg%)
Chronic diarrhea
TPN éout sufficient Mg
Bl.transfusion é citrated blood
Alkalosis
Hyperventilation
Excessive vomiting
Clinically:
Latent Tetany (ca is 7-9 mg%)
It becomes evident by the following tests:
Chvostick sign: tapping the facial n. anterior to the tragus Æ contraction of the
facial ms
Trousseau sign: occluding the arterial flow to the forearm Æ ischemia Æ carpal
spasm
Peroneal sign: Tapping the peroneal m. over the neck of the fibula Æ
dorsiflexion and eversion of the foot
Prolonged QT interval
Manifest Tetany (Ca level is <7mg%)
Carpal spasm: painful flexion of wrist & metacarpophalangeal joints but interphalangeal
joints are extended & thumb is adducted over the palm
Pedal spasm: plantar flexion and adduction and toes are plantar flexed
Laryngismus stridulous: inspiratory obstruction, cyanosism croup
Convulsions & Paraethesia: the commonest
Investigations:
Ca (N = 9-11 mg%)
Mg (N = 1.5-1.8 mg%)
PH (N = 7.35 – 7.45 in arterial heparinized sample)
Treatment:
Immediate ttt
Ca gluconate 10% solution 100 cc/kg SLOWLY IV é monitoring of the HR
Mg sulphate 50% solution 0.2 cc/kg DEEPLY IM (IV Æ arrest)
If convulsing:
Ensure patent airway & ventilation ± O2 if needed
Anticonvulsant drugs as barbitone
If laryngeal spasm Æ Tracheostomy + O2
Psychogenic hyperventilation Æ rebreathing into a bag
Maintenance ttt: the cause + Ca oral supplementation
[Metabolic
Disorders of Bone Min

neeralisation (rickets, ossteomalacia, hypocalcem
mia)
Hy caemia
Hypocalca
It iss a conditio
on in ώ ion n serum Æ neuromuscular instab
nized ca is lowered in bility, catara
act, fungal nail
infe
ections, Proloonged QT on
o ECG
1-O
Osteom
malacia in
i adultts (Failure of bone mineralizationn)
Cau
uses;
1. Nutritio
onal deficien
ncy-
• Vit D
• chelators of calcium- phytates,
p chelates, phossphorous
• Antacid abuse, causing g reduced dietary
d phosphate bind
ding
2. GI Absoorption defeects
• Post gastrectomy, Sma all bowel dissease
• Biliary diseaase (reduced absorptio
on of Vitamiins ADEK)
3. Renal tuubular defects
4. Renal osteodystrop
o phy
5. Miscella
aneous causses
Cliinical feattures;
• aches and pains
p
• muscle wea akness
• loss of heig
ght
• stress #s
X-ra
ay:
• LOOSERS ZONES - incomplete stress # on com mpression side of long b
bones.
• MILKMAN’S FRACTURE (pseudofrac
( cture of the proximal ulna)
• Codfish veertebrae du ue to pressu
ure of discs
• Trefoil peellvis, due to
o indentatio
on of acetab bulae stress #s
• + the Xray changes
c of 2ndary hypperparathyrroidism
Blo
ood tests;
• Ca, Ph, urin on of calcium (ALL DECREASE
nary excretio )
• alk. Phos.
• CALCIUM PHOSPHATE PRODUCT (= ( serum [C
Ca] x serum
m [PO4]) n
normally 3. In rickets and
osteomalaccia is < 2.4
2. Primarry hypoparathyyroidism
m
• Causes: cann be iatroge enic after thhyroidectom
my
• Clinical Fea
atures: fungal infections of nails, haair loss, vitiligo
• Xrays: skull Xrays, calciification of basal
b ganglia
• Blood resullts: ca p
3- Pseudoo hypop
parathyrroidism
m eg. Albright hered
ditary osteo
odystrophyy
• Incidence: rare
r
• Pathology: genetic XD D. lack of effe
ect of PTH at
a target celll.
• Clinical fea
atures: obeesity, dimin nished intelligence, shhort 1st 4th, 5th metacarpals and
metatarsalss, exostoses,, brachydacctyly.
• Blood tests: N/ PTH, Ca, pho osphate
NB Ideopathic Juvenile osteopo
orosis
• Incidence: rare
r
• Age: 8-14
• Pathology: Osteopenia a, growth arrest
• Blood tests: normal calcium and phosphate
p
• Prognosis: spontaneou
s us resolution
Disorder of Bone Density
Osteoporosis
Definition
WHO Definition 1994:
A skeletal disease characterised by low bone mass and deterioration of the
microarchitecture of bone tissue é a consequent in bone fragility and susceptibility to
low trauma fractures.
• Bone density measured relative to the population mean in young adults
• Normal- bone mineral density above 1 standard deviation below the mean
• Osteopenia- 1- 2.5 standard deviations below the mean for a young adult
• Osteoporosis- > 2.5 standard deviations below the mean for a young adult
• T score is № of SDs away from ! mean for a sex & race matched young population
• Z score is № of SDs away from ! mean for an age & sex & race matched population
• Z score should not be used to define osteoporosis.
Incidence
Incidence is difficult to measure, as most cases are not recorded until a fracture has
occurred.
The National Osteoporosis Society: state that at least 1:3 ♀ & 1:12 ♂ will develop
osteoporosis.
Ætiologic Classification
I. Primary: (i.e. no cause; but occurs as an exaggeration of physiological bone depletion that
accompany aging and gonadal activity). More in:
1. Caucasian or Asian, Females é Low body mass index < 19KG/M2
2. Blond hair, red hair, hypermobility & adolescent scoliosis have genetic predisposition.
3. Family history of fracture
II. Secondary:
1. Lifestyle and nutritional: Smoking, alcohol, Sedentary
2.Medical Condition:
1. Anorexia nervosa 7. Early menopause <45y
2. RA 8. 1ry hypogonadism
3. MM 9. 2ry Amenorrhea
4. CRF 10. Hyperthyroidism
5. Chronic RT or GI disease 11. Hyperparathyroidism
6. Transplantation 12. Cushing
3.Drugs
4. steroids 1. L-thyroxin
5. chemotherapy 2. anticoagulants
6. GnRH agonist or antagonist 3. anticonvulsants
4.Other Factors:
1. Previous history of fragility fracture
2. Loss of height suggesting a kyphosis
3. Osteopenia or loss of vertebral morphology on PXR
PATHOPHYSIOLOGY
• There is an UNCOUPLING of osteoblastic bone formation & osteoclastic resorption
• It is a QUANTITATIVE not qualitative defect in bone.
• Normally, ♂ & ♀ bone mass until age 30 y (3% /y rate) to a peak bone mass.
• After 30y, bone is lost slowly (0.3% /y)
• Women have a sudden in bone loss at menopause (3% /y).
• After 70 y, the rate of bone loss for ♀=♂ ≈ (0.5% /y)
• With aging the body expands the cortical bone to further away from the centre of bone
• This compensate for loss of
bone strength in torque
and bending, but not for
compression.
HISTOLOGY
• diameter of trabeculae
• size of osteons
• Haversian & marrow
spaces; and being more
peripherally located
• Normal mineralization
Classification Riggs And Melton

Type Cause Pathology F:M Bone affected Sites
I Post menopausal High Turn over 6:1 Cancellous Spine & wrist
II Age Related; ca absorption Low Turn over 2:1 Cortical & Cancellous Hip & pelvis
• HIGH TURNOVER: № & depth of osteoclast resorption sites; and the normal osteoblast effort
cannot repair the defect
• LOW TURNOVER: ð gradual slow down of osteoblastic activity (N/ osteoclast resorption)
CLINICAL FINDINGS
• Asymptomatic until # occurs, causing kyphosis due to vertebral #, radius #, hip #
PXR
• Wedging of the spine; and kyphosis
• Osteopenia; occurs é loss of > 30% of bone mass
Singh’s Index
G6 ..... Normal
G5 ..... Trochanteric
G4 ..... 2ry compression
G3 .... 2ry tensile
G2 .... 1ry tensile
G1 .... 1ry compression
INVESTIGATIONS
Routine diagnostic procedures

1. History for risk factors
2. Physical examination, including ruling out causes of falling, eyesight etc
3. PXR spine. Although >30% bone loss required to be visible, there may be silent wedges
4. Bone mineral Density measurement
5. Blood tests, CBC, ESR, serum biochemistry, TFT to rule out causes of bone weakness
6. Testosterone and Gonadotrophin levels in men
Optional
1. Serum CA2+, PHOSPHATE (fasting)/also urinary excretion is measured
2. Serum PTH (assay of the COOH terminal; not in CRF)
3. Serum 25-OH D (plasma electrophoresis)
4. Markers for bone formation- Bone specific ALKPH & OSTEOCALCIN
5. Markers for resorption: urine PYRIDINIUM & TELOPEPTIDES (Collagen cross-link breakdown)
6. Less accurate is the urinary HYDROXYL-PROLINE e.g. in Paget’s
7. Urinary free CORTISOL
8. BM BIOPSY after tetracyline labelling, can rule out osteomalacia ( bone turn over)
The GOLD STANDARD TEST is measurement of BMD (g/cm3) of the spine and hip
Only vertebral measurements can be used to assess effectiveness of treatment at present.
Bone measurement techniques:
1. DEXA SCANS (Dual Energy Xray Absorptiometry)

• Simultaneous measurement of the passage of Xrays through the body é 2 diff.energies.
• Low Radiation, accurate, Can be performed on hip, spine, whole body, or any where
• The National Osteoporosis society has guidelines on the use of wrist DEXA scans.
• Wrist scans are less predictive of hip and vertebral #s than hip and vertebra scans.
• If T score is > -1........................................ reassure patient
• If Tscore between (-1)&(-2) ................. request DEXA of hip/spine
• If Tscore < -2 (more -ve) ....................... treat, If monitoring required, refer for DEXA
2. RADIOGRAPHIC ABSORPTIOMETRY
• The 1st quantitative technique. Standard hand Xrays are taken beside aluminium wedge
• BMD is measured by comparison to the density of the aluminium
• Only suitable for phalanges & metacarpals are surrounded by little soft tissue.
3. SINGLE PHOTON XRAY ABSORPTIOMETRY (SPA)

• Still only useful in the peripheral skeleton eg wrist as the body part needs to be placed within
water, waterbags or a water equivalent material to correct for overlying soft tissue
4. QUANTITATIVE COMPUTER TOMOGRAPHY

• An external bone mineral reference phantom is scanned é patient to calibrate the CT values
• More sensitive in vertebra than DEXA (measure BMD/cm3)
• However, radiation, cost, precision
• Used for assessment of vertebral # risk, and follow up.
5. QUANTITATIVE ULTRASOUND
• Inexpensive, small, portable, does not involve radiation
• Different instruments Æ different readings, ð different calibration, analysis software used
• Can be used for screening; But, NOS recommended referral of +ve QUS pts for DEXA
DDx
Osteoporosis Osteomalacia
Definition Bone mass Mineralisation
Age at onset Generally elderly and postmenopausal Any age
Aetiology Idiopathic Vitamin D deficiency
Endocrine abn., inactivity Abnormal of vit D pathway
Disuse Hypophosphatasia
Alcoholism Renal tubular acidosis
calcium
Symptoms Pain referable to # site Generalised bone pain
Signs Tenderness at # site Tenderness at # site and generalised tenderness
PXR Mainly axial skeleton #s Looser stress line #s in appendicular skeleton
Lab tests
S.Calcium N /N ( high in hypophosphatasia)
S.phosphate N /N
Alk.Ph N (even within 5 days of a new #) unless hypophosphatasia
Urine Ca /N /N (high in hypophosphatasia)
Bone biopsy Tetracycline labels normal Tetracycline labels abnormal
Prevention
1. load bearing exercise in young women
2. intake of calcium & vit D
3. smoking & alcohol intake
4. drug abuse
5. House held falls.
6. Evaluate post menopausal women (PMW) for HRT
7. Evaluate high risk group e.g. those on steroid, considering DEXA and treatment
Treatment
1]. Calcium + Vit. D supplements

• Minimum daily intake of ca should be met (prescribed if this is not achieved by diet)
• People > 65yrs
• Adding 500mg calcium & 700IU Vit. D Æ # by 50% over 3yrs of taking supplements
2]. Calcitriol (1,25 dihydroxycholecalciferol)

• The active metabolite of vit D. 0.25 μg/d
• risk of VERTEBRAL #.
• Need monitoring of plasma calcium
3]. HRT (OESTROGEN)

• Dose: 0.625mg/d (Premarin) Æ bone density by 2% /y
• Advantages:
o Prevent osteoporosis and osteoporosis progression in PMW
o Also has a role in steroid induced osteoporosis
o bone density by 2% /y
o If given for 5-10 y from the menopause Æ risk of Pm # 50%
o Other benefits: loss of menopausal symptoms, cardiovascular protection
• Disadvantage:
o Bone loss may happen again if HRT discontinued (2% /y)
o Risk of endometrial carcinoma, Br.cancer, undx vaginal bleeding
4]. Bisphosphonates
• Synthetic analogues of inorganic pyrophosphate. Inhibit bone resorption by osteoclasts
• Disodium Etidronate (Didronel®)
o Dose: 400mg/d for 2wk ⎯⎯ ⎯⎯→ Ca2+ 500mg 2.5 mo & NPO 2h before & after intake
FollowedBy
o Adv.:
effective in VERTEBRAL # .........................(statistically significantly)
NON-VERTEBRAL # ......................................(Not Statistically Significantly)
Useful in PMW & steroid induced osteoporosis
o Disadv:
Dyspepsia, diarrhoea, abd.pain, flatulence, constipation
Hypersensitivity, headache
Parasthesia, PN, mild cramps
o Contraindications: renal impairment
• Pamidronate (Aredia®): IV infusion
• Alendronate (Fosamax®)
o Dose:10mg/d 35 mg/wk; before breakfast & sit upright for at least 30 mins
o Adv.; HIP, WRIST AND VERTEBRAL # in PMW
o Disadvantages: Oesophagitis, abd pain, constipation, rash, skeletal pain
o Contraindications: gastric and oesophageal troubles, renal problems
• Residronate (Actonel®): less reflux oseophagitis
• Ibandronate (Boniva®):
o No gastric upset
o Tablets, 2.5mg/d 150 Mg/Mo IV 3 mg/3 ml (should be taken on empty
stomach, remain upright é not food or drinks for 1 hour)
• Zoledronic (Zometa®): IV injection used for hypercalcemia of malignancy & not for CRF
5]. Strontium Ranelate (Protelos®)
• New class of drugs that act by osteoblasts & osteoclasts
• Sachet 2g/d
• No GI upset
6]. Teriparatide (Forteo®) is a recombinant parathyroid hormone, used in the treatment of
advanced cases, very effective, expensive.
• osteoblasts Æ NBF right away
• Dose: 20 μg/d for 2 years
• Not for paget’s
7]. Selective Oestrogen Receptor Modulators Raloxifene (Evista®)
• Advantage
o Work like oestrogen at bone without other harmful effects
• Disadvantage: PMW symptoms Æ not to be given within 5 y of menopause
8]. Calcitonin (Miaclacic®)
• Dose: Nasal form at dosages of 200 IU/d
• Advantages:
o Non sex, non steroid hormone
o of osteoclasts & bone mass
o Can be used for analgesia in osteoporotic #s without inhibiting healing
9]. Nafl (sodium fluoride)
• Given in low dose (slow release) é Ca supplements
• osteoblasts
• bone density (but bone quality would be affected in high doses)
Scurvy
Definition
• Defective intracellular biosynthesis of collagen ð Vit C deficiency Æ chondroitin sulphate
synthesis & defective collagen Æ weak bl.v. & bone (defective endochondral ossification)
• Rickets + Scurvy = Barton’s disease
Epidemiology
st
• Vit C deficient diet: In the 1 year / elderly / sailors
Pathology:
• NBF: Trabeculae are replaced é granulation Æ brittle
• Collagen fibrils swollen & polysaccharides
• Physis widening of the zone of provisional calcification
• Metaphysis Collateral collapse under the physis
• Diaphysis sub-periosteal hge & calcification
CP
1]. Irritable, anemic
2]. Skin ecchymosis , nail splinter hge, hematuria, hematemesis
3]. Old scars & wounds .................................................... rupture more easily
4]. Gum ................................................................................... Bluish Spongy Bleeding
1]. Sub-periosteal hemorrhage
2]. Limb is swollen, painful é ms spasm ........... Pseudo Paralysis
3]. Slipped epiphysis ................................................. lower femur, upper tibia, upper humerus
4]. Costochondral separation .............................. Scorbotic Rosary
PXR
1]. Epiphysis:
o Calcification around epiphysis ................. Ring Sign
o Dense line éin the epiphysis ..................... Whimberger’s line
2]. Physis: dense wide calcification zone ........... Fränkel White line
3]. Metaphysis:
o Rarifaction below white line .............. lateral ∆ defect (C Corner Sign Of Park)
o When the ∆ collapse into shaft ......... Pelkan Spur (projection of lat metaphysis)
4]. Diaphysis ................................................................... Rarefaction, Thin Cortex, Ground Glass appearance
5]. Subperiosteal Hge &calcification ................... (DDx hyperphosphatasia)
Lab
1]. Ascorbic acid level (serum <0.1 mg/dl & WBC <10 mg/ dl)
2]. alk ph
3]. phosphoryl ethanolamine
Treatment: Vitamin C: 30-50 mg/day
Disease Aetiology CP Radiological

Hyper Calcemia
Hyperparathyroidism Adenoma Bone, groans, moan, stone Osteopenia, Osteiitis fibrosa cystica
Hypo Calcemia
Hypo PTH Idiopathic Neurological irritability Calcified basal ganglia
Renal osteodystrophy CRF Renal abnormality Rugger Jersey spine
Rickets
Vit D def Vit D Bone deformity, hypotonia Rosary, Wide physis, deformity, #
Vit D dep AR Alopecia Totalis
Vit D Res (hypophosph) PCT defect Bone deformity Poor mineralization
Hypophosphatasia AR Hypotonia
Osteopenia
Osteoporosis bone mass Kyphosis & fractures Compression vertebral #
Scurvy vit C Fatigue, bleeding, effusion Thin cortex, corner, Pelkan, Park, ...
Osteodense
Paget’s Osteoclastic ab Deformity, pain, CHF, # Coarse trab, deformity, candle flame
Osteopetrosis Osteoclastic ab HSM, anemia Bone éin bone, double iliac wing
Hypercalcaemia
Symptoms- ‘Bones, Moans, Stones and Abdominal Groans’; polyuria, constipation, lethargy,
disorientation, bony resorption +/- fibrous replacement (Osteitis Fibrosa Cystica), weakness, CNS
effects.
1. Primary Hyperparathyroidism
• Age: 40-65 , ♀:♂= 2:1
Pathology
• Adenoma/hyperplasia
Clinical
• Often Asymptomatic
• Moans, bones, stones & abdominal groans
Xrays
1]. OSTEOPENIA (bone resorption + phosphate)
2]. OSTEITIS FIBROSA CYSTICA (fibrous replacement of BM)
3]. BROWN TUMOUR (RBC extra-vasation, & hemosiderin)
4]. LAMINA DURA RESORPTION (teeth socket)
5]. PHALANGEAL SUBPERIOSTEAL EROSION
6]. SHAGGY TRABECULAE
7]. pathological frs
8]. soft tissue CALCIFICATION
9]. NEPHROCALCINOSIS
Blood results:
a. PTH
b. Ca
c. Po4 ( renal excretion)
d. N/ ALP ( é OSTEITIS FIBROSA CYSTICA)
Treatment
• Parathyroidectomy
• Beware Hungry Bone Syndrome post op,
(hypocalcaemia ð rebound NBF)
2. Secondary Hyperparathyroidism
• Parathyoid over secretion is a predictable response to chronic hypocalcaemia.
• found in rickets and osteomalacia, accounting for some of radiological findings
• Renal osteodystrophy
3. Other causes of Hypercalcaemia
1. MEN
2. Malignancy
3. Hyperthyroidism
4. Addisons (Hypoadrenocorticism)
5. steroids
6. peptic ulcers
7. kidney disease
8. sarcoidosis
Paget’s Disease
(OSTEITIS DEFORMANS)
Definition:
• Bone thickening disease; although the bones are brittle & have an abnormal internal architecture
Aetiology
• Unknown but thought to be virus (PARAMYXOVIRUSES & CANINE VIRUS found in osteoclasts)
• It is thought to be related to a viral infection in a GENETICALLY PREDISPOSED individuals
Epidemiology
• AGE: 50-70Y ............................................................ 85% (Rare<40 y & 10%> 80y )
• +ve Family history ................................................ 25%
• SEX: little preference ............................................. ♂
• GEOGRAPHICAL distribution: common in NORTHERN EUROPE, USA and Australasia
Pathology
SITE:
• Polyostotic ............................................................... 85%
• Monostotic ............................................................. 15%
• Tibia & Pelvis commonest ................................ then femur, skull, spine, clavicle
MACROSCOPIC: Bone is thick, wide, and deformed; though brittle
MICROSCOPIC
• Primary abnormality is a focal in Osteoclastic Bone Resorption Æ compensatory new
bone formation (nbf) ð accelerated bone remodelling (up to 40 times normal)
• NBF is coarse fibred é Disorganized architecture, Mosaic pattern & mechanically Weak
• Fibrous BM é scanty haematopoetic cells
• This abnormal bone is rapidly resorbed by osteoclasts and bone turnover is greatly
• Pathological phases
Phase Characteristics Type of cells
Osteolytic (vascular) Intense resorption & excavations filled é fibrosis Osteoclastic
Mixed Compensatory osteoblastic bone production Both
Irregular cement lines Æ Mosaic pattern
Sclerotic Intense osteoblastic activity Æ irregular sclerotic brittle bone Osteoblasts
Clinical Features
• Asymptomatic ............................................. (95%) ; Incidental Finding on PXR or AlkPh
• Pain
o Chronic constant aching pain related to OA (common); at night, not to activity
o Acute pain .....................................................fracture (common in the femoral neck)
o If severe in previously asymp sarcomatous change
o Lesions detected on Tc Æ painful; whereas many lesions seen on x-ray are not
• Symptoms ð bone distortion or enlargement:
1]. DEFORMITY: bowing of long bones across high stress areas (ant. tibia/anterolat.femur)
2]. SPINAL STENOSIS & ISCHEMIA .................. spinal claudication
3]. DEAFNESS (30-50%) ð otoscelerosis + foraminal size Æ CN encroachment
4]. SKULL SIZE "My hats don't fit anymore!"
• Metabolic complications
1]. GOUT related to the increased nucleic acid turnover
2]. HYPERCALCIURIA and Hypercalcaemia (both rare)
3]. HIGH COP Failure (steal syndrome)
4]. HYPERPARATHYROIDISM, if present, is usually coincidental
Investigations
• Alkph ( osteoblastic activity) can be used as a index of disease activity
• urinary Pyridinium, Telopeptides, Hydroxyproline (marker of collagen turnover)
• Ca & P usually éin normal ranges
[Metabolic
X-rays
1]. Osteop porosis Ciircumscrip pta: discrette area of osteolysis
o is an early fea
ature
2]. Candle e Flame: in n vascular stage
s flame like poroticc areas in thhe cortex (aarrow or fla
ame sign)
3]. Diseasee involveme ent usually seen
s at onee end of the e bone (generally PROXIMAL)
4]. Fine cra
acks may ap ppear (STRESS FRACTURES) on tension side (un nlike Looserr zones)
5]. Widen ned Deform med bone es
6]. Coarse e Wide Tra abeculae
7]. OA: atro
ophic é little
e remodelinng
8]. Kypho osis
9]. Platybbasia: remo t skull base Æits inva
odelling of the agination byb the cx ve ertebrae
10
0]. Only 65% of the lesions
l see
en on bone e scan will be seen on n X-Rays
DD
Dxx
1. Osteitiss Fibrosa cyystica
2. Fibrouss Dysplasiaa
3. Osteobblastic secoondaries
4. Osteoppetrosis
5. Lymphhoma
Treatment
re
• Most reequire no treatment
t (asymptom
matic)
A Æ NSAID
• Pain ussually ð OA Ds
I- DRUGS:
• bone turnover as calcitonin
n & diphosp
phonates
• Course of
o therapy continues
c 6
6mo, and 60%
6 achieve
e remission
n éout relap
pse for 5y
• Indicatio
ons:
1. Persistent bone painn
2. 3mo Beforre and afteer major boone surgeryy where th
here is risk of excessivve hge
3. Repeated fractures
4. Neurological complications
5. High COP failure
6. Hypercalca aemia due
e to immobbilisation
• If relapse
e occurs -> recommennce therapyy
1-CALCITONIN
• Osteocla
asts have reeceptor for calcitonin bone resorption by their a d№
activity and
• Pain of
o Paget's inn up to 80%% of cases
• When tttt is stopped
d levels quickly return to normal but relief off pain may persist for mo
• A/E: ana
aphylactic reaction,
r GII upset, itch
hing, hypoccalcaemia (limit the use
e)
2-MITHRAMYCIN
• A cytotooxic antibiootic and prooduces imprressive clinical responsses
• Specific effect on osteoclasts Æ plasma a calcium
• Side effe
ects: BM, livver, kidney toxicity
t (No
ot currently used)
• Useful in
n patients é resistant se evere disea
ase & neuro ological com
mplications
3-DIPHOSPHONATES
• Exact mechanism
m m of action remains unclear
• Bind to
o HA crystaals Æ the eir dissolution & aggrregation in
nto large crrystals by osteoclasts
o
• They bone turn n over Æ production
p n of lamella
ar bone rather than w
woven
• pendant Æ 60% relief of pain in
Effect is dose dep n 6 mo Æ prolonged
p remission
• Disadvvantage:
o on at high dose Æ bone pain
bone mineralizatio n and fractures
o Narrow th herapeutic range bet resorption n & mineralizatio on used é caution
c
Drug Administration Special Characteristics
Calcitonin (Salmon) SC injection daily Anti-salmon AB develop in 60%
Calcitonin (Human) SC injection daily Useful in salmon calcitonin resistant cases
Pamidronate (new) IV single daily dose or weekly infusion for a 5-10 May impair osteoblast function
dose course Transient fever common
Alendronate (new) Orally for 6 months Oesophageal irritation
Etidronate (old) IV or oral for 6 months Osteomalacia, diarrhoea, nausea, gastric irritation
II- SURGERY
1-ORIF
• For fractures & useful to straighten the bone if possible
2-CORRECTIVE OSTEOTOMY
• Occasionally required for intractable pain or impending pathological #
3-THR
• Assess Protrusio or proximal femoral Deformity need to be assessed
• 6wk pre-operative medical ttt may be required to intra-op.bleeding & hypercalcaemia
• Both cemented and uncemented designs have been used
• incidence of heterotopic calcification ........ (50%)
• incidence of aseptic loosening OA ............ (15 %)
4-TKR
• May need to use extramedullary alignment jigs because of deformity
• Results of both cemented and uncemented designs are satisfactory at 12 years
5-SPINAL DECOMPRESSION: for spinal stenosis
6-TUMOR EXCISION
MALIGNANCY
• Patients with Paget's disease have a 30 fold in the incidence of bone sarcoma
• Said to occur in less than 1% of all Paget's patients
• Sarcomatous change usually in diffuse, polyostotic, long standing disease
• Sarcoma commonest in femur, humerus, pelvis, tibia
• 50% are osteosarcoma, but also - fibrosarcoma, chondrosarcoma, and giant cell tumour
• Treatment: Palliative resection ± chemotherapy
• Prognosis is grave, with survival beyond 2 years a rarity
Cartilage
• Cartilage is avascular, aneural, alymphatic.
• Hyaline cartilage is the most common & found in:
1]. Bone apophyses
2]. Bone epiphysis Articular (Hyaline) Joint surfaces
3]. Articular cartilage Fibrocartilage Tendon & ligament insertion
4]. Costal cartilages Elastic Trachea, earlobe
5]. majority of the fetal skeleton Fibroelastic Meniscus
Cartilage Growth
1]. Appositional Growth:
• new cartilage is formed at cartilage surface by cells derived from chondroblasts of perichondrium
(surface of hyaline cartilage)
• with maturation, majority of cartilage growth is primarily appositional
2]. Interstitial Growth:
• increase in internal mass of cartilage
• by activity of chondrocytes that multiply within their lacunae
• in mature cartilage, cellular turnover rate is exceedingly low
Articular Cartilage Comprises:

1. Chondrocytes (5%)
2. Extracellular matrix (95%)
1. Water (75%)
2. Collagen (5%)
3. Proteoglycans (20%)
4. Enzymes
5. Lipids
6. Adhesives (fibronectin, chondronectin)
7. Growth Factors (PDGF, TGF beta, IGF-1)
Zones
[1]. Surface
[2]. Superficial Tangential zone
o collagen II fibers orientated tangential
o Greatest ability to resist shear stress
[3]. Transitional / middle zone
o Transition between the shearing forces of surface layer to compression forces in the
cartilage layer
o Collagen arranged obliquely
o Composed almost entirely of proteoglycans
[4]. Radial / deep zone
o Collagen fibers attached radially (vertical) into the tidemark
o Distributes loads and resists compression
[5]. Calcified zone
o Containing the Tidemark Layer (basophilic line which straddles the boundary between
calcified and uncalcified cartilage)
o Contains Type 10 collagen
[6]. Subchondral bone
Chondrocytes (5% wet weight)
• Chondroblasts which are derived from mesenchymal cells become trapped in lacunae and
develop into chondrocytes. Chondrocytes are important in the control of matrix turnover through
production of:
1]. collagen
2]. proteoglycans
3]. enzymes for cartilage metabolism
Organic matrix:
1]. Water 75%
2]. Collagen Type II 20%
3]. Proteoglycans 5%
4]. Proteins
Proteoglycan(PG) :
• 10%-15% of wet weight
• Produced by chondrocytes and secreted into the matrix
• Half life of 3 months”
• Functions:
1]. Responsible for the Compressive strength of cartilage
2]. Serve to trap and hold water to regulate matrix hydration
3]. Binds growth factors
• Formed of :
1]. Polysaccharides Chondroitin & Keratan sulfate (GAGs). Sulfate + carboxyl ends Æ -ve
charge Æ Donnan Osmotic Pressure Æ hydrophilic
2]. GAGs binds (é covalent sugar bond) protein core molecule monomer to form a
Proteoglycan Subunit (PGS) = Aggrecan molecule
3]. Link proteins stabilise aggrecans (é non covalent bonds) to Hyaluronic acid (another
non sulfated GAG ώ act as a major aggregating factor) to form a Proteoglycan
Aggregate
4]. Other small proteoglycans: Diglycan & Decorin & Fibromodulin are also present (may have
function in fibrillogenesis regulation (some of them contain dermatan sulfate)
• Glycosaminoglycans (GAG’s) include:
1]. Chondriotin-4-sulphate (decreases with age)
2]. Chondriotin-6-sulphate (increases with age)
3]. Keratan sulphate (increases with age)
• The aggregated proteoglycans & water are strongly electronegative. This generates a resistance
to compressive force & contributes to the elasticity of cartilage.
• Mucopolysaccharidoses are a group of disorders characterized by inability to degrade GAGs
Collagen:
• 20% wet weight: >50% dry weight
• Mainly type 2 (other types = 5, 6, 9 & 11)
• Type 9 lies on the surface of type 2, acting as interfibrillary glue.
• Type 10 is associated with calcification of cartilage
• Forms the cartilaginous framework and is responsible for the TENSILE strength of cartilage
• Collagen tension prevent excess PG aggregate hydrophilic power ( excess H2O adsorption)
• Disruption of the collagen network is a key factor in the development of OA
Proteins:
• Anchorin II anchors the chondrocytes to collagen
• COMP collagen oligomeric protein ( é cartilage destruction in OA
Water
• 75% of wet weight
• Allows for deformation of the surface by shifting in and out in response to stress
• H2O content Æ permeability, strength & Young’s modulus (less stiff)
• Water content increases in osteoarthritis
Functions
• Decreasing friction in joints
• Load distribution in joints
• Mature articular cartilage is avascular, aneural and alymphatic
• Chondrocytes receive nutrition and oxygen via diffusion from synovial fluid through the cartilage
matrix
Mechanics
• Creep occurs when a viscoelastic tissue shows deformation when subjected to a constant load.
• Stress Relaxation occurs when a viscoelastic tissue with constant deformation shows stress.
• In both when the load is removed the tissue regain its length
• In contrast to bone, articular cartilage tends to stiffen w/ increasing strain.
• In contrast to viscoelastic materials; linear materials shows elastic and plastic deformation
Changes with Ageing

• With ageing cartilage becomes hypocellular and has decreased elasticity.
Chondrocytes
• in size
• in №
• lysosomal enzymes
Matrix
• Proteoglycans
o in mass and size - decreased length of chondroitin sulfate chains
o change in proportion - keratin sulfate
o hyaluronic acid
• Water content (increases in OA)
• Protein content (decr. carbohydrate: protein ratio)
Calcification
• Much of hyaline cartilage of the body ultimately calcifies with aging.
• When calcification occurs, chondrocytes die & matrix disintegrates
• The superficial zones do not calcify, except in pathologic states such as pseudogout
Healing of Articular Cartilage

Deep lacerations
• extend below the tidemark
• heal with Fibrocartilage
• blunt trauma may cause osteoarthritic changes
Superficial lacerations
• Above the tidemark
• Chondrocytes proliferate but do not heal
• Immobilisation leads to atrophy
• Continuous Passive Motion is beneficial to healing
Gout
• Disorder of purine metabolism ccc by hyperuricaemia & recurrent attacks of acute synovitis
Epidemiology:
• 2:1000 (Only a small number of people with hyperuricaemia develop gout)
• M:F = 20:1 / Obese / Caucasian / Rubicund / alcoholic / NSAIDs / Duretics
• 2 Types:
1]. Primary (95%): inherited disorder é overproduction or under excretion of uric acid
2]. Secondary (5%): myeloproliferative disorders, renal disease
Pathology:
• Hyperuricaemia: uric acid is the final product of purine metabolism; if there is a defect in the purine
metabolism e.g. HGPRT deficiency Æ accumulation of Urate, it becomes poorly soluble if serum
conc. > 7mg/Dl; and starts to precipitate in tissues. Although, this level is usually exceeded in
normal individuals é no pathological consequences.
• Gout: MSUMH crystals deposit in the tissue especially the cartilage of small joints of the hands
and feet ⎯⎯ ⎯ ⎯→ remain inert till minor trauma Æ Crystals Disperse Æ inflammatory
Months& years
reaction Æ phagocytozed or float free in the joint Æ Destruction of the articular cartilage
• Similar changes may occur in the tendons, skin, ear pinnae, kidney stones
Clinical:
• Male (or female menopause) 30y / Obese / Caucasian / Rubicund / Alcoholic / NSAIDs /
Duretics / +ve family history
• Acute Attack: Sudden onset of red, hot, swollen, tender, and shiny joints of:
1. Forefoot
o podagara: - classic presentation of acute attack of first MTP joint
o Hyperuricaemia is present at some stage of the disease but not necessarily during
the acute attack
o Undoubtful diagnosis is established by finding the –Vely Birefringent crystals
in the synovial fluid of the affected joint
2. Elbows, ankles, and hands
o unlike RA hand & wrist joints Æ preserved joint spaces and mineralization
3. Large Joints (hips, knees, and shoulders) are infrequently involved
4. Spine very rarely affected.
Chronic Gout: Joint die, Tophi (may ulcerate), Calculi
Nephrolithiasis is major extraart.manifestation; - only small % of pts get tophi, but many
get stones; - pure uric stones = 80%, & is probably nidus for Ca-Phos & oxalate calculi
Radiology:
• The radiographic changes occur late; usually é chronic tophaceous stage.
• Chronic changes are of two main types:
1. Joints show signs of OA (narrowing, osteophyte, sclerosis, cysts) Æ tophaceous
material Erode the joint Æ fibrous Ankylosis.
2. Well circumscribed, cortical "Punched Out" cystic lesions ≠ other arthritides:
Little bit Away from the joint margin
cyst size > 5mm
Tophaceous material eventually breech the cortex Æ extensive bone
destruction Æ "Vanishing Bones".
Laboratory:
• Hyperuricemia > 7mg/Dl
o biochemical hallmark of gout, but not by itself diagnostic for gout
• Leukocytosis
• ESR
• Synovial Fluid
o leukocyte counts = septic arthritis
o viscosity is < septic or inflammatory arthritis
o MSU needle-like intracellular & extracellular crystals
o Negatively Birefringent Crystals under polarized light microscopy = Diagnostic for
Gout
Treatment:
Acute Attacks:
1]. Inomethacin 75mg stat. then 25mg BD
2]. Colchicine intravenous - 0.6 mg 2 hours until pain decreases
3]. Effusion Aspiration ± local cortisone
Chronic: PDF (alcohol, duretics, aspirins, wt)
1]. Allopurinol for hyperuricaemia & tophi ( XO, never used in acute attacks, it precipitates
acute attacks)
2]. Anti-Inflammatory
3]. Curettage of ulcerated tophi & repeated dressings
CPPD Deposition
Comprises 3 pathologies:
2+
1]. Chondrocalcinosis: appearance of ca in cartilage
2]. Pseudo-gout: crystal induced arthropathy
3]. Chronic pyrophosphate arthropathy
Pathology:
2+
• Pyrophosphate generate from an abnormal cartilage + Ca from matrix Æ crystals
• Crystals grow into tophi on collagen fibers (Often fibrocartilage) Æ amorphous nests
• Extrusion of the crystals into the joint will excite inflammatory synovitis
• Recurrent attacks precipitate OA (Hypertrophic reaction + marked osteophyte formation)
• Some times there is severe joint destruction
Clinically:
> 60 female (recurrence é age)
Three presentations:
1. Asymptomatic chondrocalcinosis:
Elder Female >50 (if < 50y suspect metabolic or familial predisposition)
calcified menisci (concomitant OA is common)
2. Acute synovitis (pseudogout):
Middle aged Female
Attack of acute pain in a Large Joint for few weeks
Precipitated by minor illness or operation
Positively Birefringent crystals are diagnostic
3. Chronic Pyrophosphate arthropathy:
Elder woman
Polyarticular OA affecting the large joints (hips and knees)
Marked Joint Destruction (as neuropathic joint disease)
Radiology:
• Calcification hyaline or fibrocartilage, found in knee
menisci, labrum, & TFCC
• OA Changes: even seen in non wt bearing joints /
isolated Patellofemoral, talonavicular
• Later Advanced Joint Destruction and loose bodies
Laboratory:
• Fluid analysis:
o CPPD crystals are visualized under
compensated polarized light microscopy
o squared or Rhomboidal shaped ends
o Smaller size
o Intralysosomal location
o Less brilliant colors
o CPPD crystals show weak Positive Birefringency
o Alizarin red stain, can confirm that these clumps are masses of calcium crystals
DDx:
Acute attacks:
o Gout: crystal type
o Traumatic effusion: CPPD usually ppt by trauma; aspiration is the clue
o Septic arthritis: constitutional symptoms, age, fluid aspiration
o Reiter’s: conjunctivitis, urethritis
Chronic CPPD
o OA: non wt bearing involvement, marked destruction
o Hemochromatosis: middle aged male, chronic Fe2+ overload, cirrhosis, DM, bronze
skin, MP chondrocalcinosis and destruction
o Alkaptonuria: painful chondrocalcinosis of large joint, dark pigmentation of ear pinna,
dark urine with time or alkali, narrowed calcified intervertebral discs
o Hyperparathyroidism: pathological calcifications + osteopenia
Treatment:
• Aspiration of the involved joint and steroid injection, once diagnosis of infection has been
excluded, will usually control symptoms
• Rest
• NSAIDs are dangerous in elders
• Chronic case Æ ttt of OA
Calcium Hydroxy‐Apatite Crystal deposition
• Calcium HA is a normal constituent of the bone mineral; but it is deposited abnormally in dead or
damaged tissue (torn ligament, tendon attrition, degenerated cartilage, HA deposition in joints
can cause:
o Acute synovitis
o Chronic destructive arthropathy
Pathology:
Sites:
o Knee, Shoulder
o Around Chondrocytes, Torn Ligaments, Damaged Tissues
o Posterior Longitudinal Ligament Of The Spine
HA Crystals Are Minute < 1μm ; but they deposit and grow till it becomes evident on the
PXR
HA Deposits Starts Creamy In Consistency Æ Then Become Chalky Æ Crystal Shedding
into the joint space Æ Synovitis or Erosive arthritis
Clinically
1. Acute: 30-50 years
o Pain close to one of the large joints (knee, shoulder) rather than in the joint
o Swelling, warmth, tender
o Onset is acute and sometimes gradual Æ subsides within weeks.
o Commonest in Rotator Cuff
2. Chronic destructive arthropathy: (either denovo, or crystals modify the preexisting OA)
o Milwaukee shoulder is a more dramatic form of arthritis in association é HA
o It may occur in hips and knees
PXR:
Periarticular Calcification
Loose Bodies (but never meniscal and disc calcification)
Erosive Arthritis: loss of joint space with little or no sclerosis nor osteophytes
Laboratory
Fluid analysis: HA Crystals can be identified using the ELECTRON PROBE OR THE TRANSMISSION
ELECTRON MICROSCOPY
Treatment:
Acute periarthritis:
o Rest + NSAIDs
o Aspiration of the involved joint and steroid injection in acute prodromas
o Persistent pain Æ operative Removal of the calcific deposits or decompression
Chronic case Æ Ttt Of OA; but early operative intervention is usually needed
bÜà{ÉÑxw|v
axâÜÉÄÉzç
Dr Mohamed Sobhy
Ain Shams University Date

[Orthopedic Neurology] Page | 439
Neuro-Anatomy
Neuron:
• Is the specialized cell of the nervous system that capable of electrical exciation (action
potential) along their axons
440 | Page [Orthopedic Neurology]
• Peripheral nerve has a mixture of neurons:
1]. Motor
2]. Sensory
3]. Reflex
4]. Sympathetic
5]. Parasympathetic
• Types of fibers: A (α, β, γ, δ), B, C
Motor Sensory Ms reflex sympathetic Parasymp
Neuron AHC Dorsal root ganglia AHC IHC relay at organ
Root Anterior Dorsal root Ant Ant Ant
Tract 1- Direct pyramidal 1- Spinothalamic (Pain, temp, Stretch reflex
crude) arc from ms
2- Indirect pyramid 2- Lemniscal (DC) spindle
(proprioception, fine touch)
Fibre α Motor (12-20 μm) α Propriocep (12-20 μm) γ fibers B preganglionic B fibres
β Touch, vib (5-12 μm) C Postganglionic
δ fast pain, temp (2-5μm)
C Slow pain, crude (0.2-2μm)
• A fibers are most affected by pressure
• C fibers are most affected by anesthesia and are the principle fibers in the dorsal root
• Neurons are surrounded by endoneurium ⎯ ⎯ ⎯ ⎯⎯→ fascicles surrounded by
GroupToFor m
perineurium ⎯⎯ ⎯ ⎯⎯→ nerve surrounded by epineurium

GroupToFor m
Muscle:
• Motor unit is the unit responsible for motion and formed of the group of ms fibers and
neuromuscular junction and feeding neuron
• Ms fibers types:
1- Smooth ms fibers
2- Cardiac ms fibers
3- Skeletal ms fibers:
Type I: slow twitching, slow fatiguability, posture
TypeII: fast twitiching, fast fatigue
• MS CONTRACTION: is the active state of a ms, in which
there is response to the neuron action potential either
by isometric or iso tonic contraction
• ISOMETRIC CONTRACTION: is the contraction in ώ there is
y tension ώ out change in the ms length
• ISOTONIC CONTRACTION: is the contraction in ώ here is a
change in the length of the ms éout change in the tone
• MS TONE: is the resting state of tension
• MS CONTRACTURE: is the adaptive structural changes in a
ms ð prolonged immobilization in a shortened position,
in the form of shortening and fibrosis
• MS WASTING: is the adaptive structural changes in a ms ð prolonged disuse of denervation,
in the form of hypoplasias and hypotrophy, and eventually shortening and fibrosis
• SPASTICITY: Abnormal y contraction of a ms in response to stretch. Growth of ms is
impaired
• RIGIDITY: Involuntary sustained contraction of a ms not stretch-dependent. Growth of ms is
fair
[Orth
hopedic Ne
eurology] Page | 441
Saarcomere
A band ......................................Actin + myocin (= H + ove
erlap zone)
H band .....................................Myocin
M line ........................................Myocin Interconnnect
I band
b ........................................Actin
Z line
l .........................................Actin Anchors
Contraction Deffinition Phasses

Isoto
onic Connstant ms teension & z Conccentric: ms shortens du
uring contra
action
length (dynam mic) Eccentric: ms len
ngthens duuring contraction
Isom
metric Connstant ms le
ength (staticc)
Isok
kinetic Max contractioon é constan nt Conccentric
velo
ocity over a full ROM Eccentric
Aero
obic In the
t presence e of O2 Reple
enishes 34 ATPA via Kreb b’s
Ane
erobic In the
t absence e of O2 Glyco
olysis into la
actic and 2 A
ATP
ATP
P hydrolysiss éouut O2 ATP hydrolysis
h to
o produce ddirect, fast en
nergy

Derrmatome:
o Is th
he area of skin suppliied by a sp
pecific nervve root
My
yotome
o Is th
he group of
o muscles supplied by
b a specificc nerve roo
ot
Scle
erotome
o Is th
he area of bone and fascia supp
plied by a specific
s nerve root
Sprrain:
o Tea
aring or inju
ury of a no
on contracttile motion
n unit, e.g. Ligament
Stra
ain
o Tea
aring or inju
ury of a co
ontractile motion
m unitt, e.g. Musccle
Muscle injuries:
1]. Muscle Strain:
• Occurs at Musculo-tendinous junction of the ms that cross 2 joint (e.g. gastroc,
hamstring)
• First there is inflammation then ends by fibrosis
2]. Muscle tears:
• Occurs at the Musculo-tendinous junction
• During the higher eccentric contractions & Heal by dense scarring
3]. Muscle soreness: During the higher eccentric contractions
4]. Muscle denervation: Causes atrophy and y sensitivity to acetyl-choline and fibrillation in
2wk
Tendons
• COMPOSED OF:
1]. Collagen I .........................................80%
2]. Fibroblasts synthesis tropocollagens Æ micro-fibrils Æ sub-fibril Æ fibril Æ fascicle
3]. Loose areolar CT ..........................Endotenon Æ epitenon Æ paratenon
• TYPES OF TENDONS:
a. PARATENON covered tendons rich capillary supply = better healing
b. Sheathed tendons .......................segmental bl.supply via mesotenon (VINCULA)
• MUSCULO-TENDINOUS JUNCTION:
1]. Tendon
2]. Fibro-cartilage
3]. Mineralized fibrocartilage (SHARPEY’S fibers)
4]. Bone
• HEALING STARTS by fibroblasts and macrophages of the epitenon in 3 phases:
1]. ................................................................Initial fibroblastic phase: 10 days (weak)
2]. ................................................................Intermediate Collagen phase 30 days (most of
the strength is regained)
3]. ................................................................Late remodeling phase 6 month (maximal
strength is regained)
• Collagen tends to arrange along stress lines; so immobilization causes weak healing
Ligaments
• COMPOSED OF:
1]. Collagen I (same ultrasturcture) ........ 70%
2]. Elastin
3]. Fibroblasts + Loose areolar CT
• BL SUPPLY is uniformly arranged via the ligament insertion at bone
• Types of ligamentous insertions:
1]. Indirect: .............................................superficial fr insert to periosteum @ acute angle
2]. Direct .................................................Deep fr insert to bone @ 90º
• BONY LIGAMENTOUS JUNCTION:
1]. Ligament
2]. Fibro-cartilage
3]. Mineralized fibrocartilage (SHARPEY’S fibers)
4]. Bone
• HEALING starts by fibroblasts and macrophages of the epitenon
Phase Time Process Strength
1].Hemostasis 10 min platelet plug Æ fibrin clot Weak
2].Inflammatory 10 days macrophages debride granulation tissue Weak
3].Fibrogenesis 30 days UMC Æ fibroblasts Æ strong type I collagen most strength regained
4].Remodeling 6-18 mo Realignment & cross linking of collagen bundles Max strength
• LIGAMENTS GRAFTING:
1]. Autografts: .....................................................Faster healing, no disease transmission
2]. Allograft: .........................................................no donor morbidity but may transmit diseases
3] . Synthetic: (Gortex, Leeds Keio) ................no initial weakness, but cause sterile effusion
Tendon Transfers
Definition
• A tendon transfer is a procedure in which the tendon of insertion or of origin of the functioning
muscle is mobilized, detached or divided and reinserted into a bony part or onto another tendon,
to supplement or substitute for the action of the recipient tendon, in order to correct muscle
imbalance and keep the corrected position rather than to correct a deformity
Indications
1]. Irreparable nerve damage
2]. Loss of function of a musculotendinous unit due to trauma or disease
3]. In some nonprogressive or slowly progressive neurological disorders
Contraindications
1]. Unstable joint
2]. Stiff joint
3]. Fixed deformity
4]. Advanced arthritis
5]. If affection of all muscles at the same degree
6]. If no suitable tendon or muscle is available for transfer
Principles
Preoperative
1]. Age:
• It is better to delay operations >5y so you can get cooperation in physiotherapy:
o If the patient is skeletally immature do tendon transfers (TT)
o If the patient is skeletally mature do fusion + removal of appropriate wege ± TT
o If the patient is has talipes valgus add stabilizing bony op. e.g. Grice Green or Evans
2]. Timing:
• Early tendon transfers – within 12 weeks of injury: If no chance of functional recovery, transfers
should be performed ASAP
• Late tendon transfers -- If reasonable return of function not present for 3m after the expected
• Following nerve injury repair, the date of expected recovery can be calculated by measuring the
distance between the injury to the most proximal muscle supplied, assuming a rate of
regeneration of 1mm/day
3]. Planning
• Make a list of deficient functions
• Make a list of available donor muscles
• Availability of tendon for transfer:
o If many tendons are available do tendon transfers for all deficient muscles
o If 2 tendons are available do TT for the most crucial functional muscle
o If one agonist tendon is available do TT to the middle line e.g. Tohen transfer
o If one antagonist tendon do split TT & suture under equal tension
Operative
Joint:
1]. Should be stable
2]. Should be a freely mobile joint (free ROM)
3]. Should not have fixed deformity
4]. Should not have advanced arthritis
Muscles:
1]. Adequate donor muscle Strength (G IV, V)
2]. Adequate recipient muscle Excursion:
o Wrist flexors ........................................... 33cm
o Finger extensor ..................................... 50cm
o Finger flexor ........................................... 70cm
3]. Adequate neurologic & blood supply
4]. Agonists better than antagonists
5]. Synergestic better than non synergestic
6]. Start Proximal then distal
Tendon
1]. Should be of an adequate Length
2]. Should pass in a Straight line
3]. Should pass through a Gliding Medium (the best is fat or superficial fascia)
4]. Should be sutured under Moderate Tension
5]. Should be Covered
6]. Better to suture tendon To Bone (pull-out technique)
Techniques
1]. Multiple short transverse incisions rather than long longitudinal incisions
2]. Careful tendon handling
3]. Joining the tendons
o End to end anastomoses
o End to side anastomoses
o Side to side anastomoses
o Tendon weave procedures can all be used
4]. Achieving proper tension - No general rule, but reasonable to place limb in the position of
maximal function of the tendon transfer and suture without tension
Postoperative:
1]. Protect the transferred tendon to avoid stretching
2]. Physiotherapy & training
Famous Transfers
• Pronator teres to ECR
• FCU to EDL
• Palmaris longus to EPL (or split FCU)
• ECRL to sublimis or profundus
• Tibialis anterior & Peroneus brevis are preferred in the transfer as Tibialis posterior & Peroneus
longus are important for foot arch Skeletally immature with Varus (alone or with other
deformities)
• In Drop foot (NO deformity) + skeletally immature Æ Tibialis posterior is the ONLY tendon
available for transfer
Cerebral Palsy
Definition
• Disorder of movement and posturing
• Caused by static non progressive brain UMNL lesion
• Acquired during the stage of rapid brain development (perinatal)
Classification
1- Spastic ............................................................................. (60%)
o MOST AMENABLE TO SURGERY
o UMNL involvement - mild to severe motor impairment
o Contractures:
% Walking limb № UL:LL Associated problems
1- Hemiplegia 40 3mo later than N 2 UL>LL • Mild learning
• Seizures
2- Diplegia 30 4y 4 LL>UL • Delayed develop milestones
• Strabismus
3- Quadriplagia 25 25% at 7y 4 UL=LL • Floppy baby
• pseudobulbar palsy Æ fail to thrive
• IQ, hearing, vision
4- Monoplagia 4 as hemi 1
5- Double hemi <1 4 UL>LL • As hemi
6- Total body <1 4 • Severe trunk, neck, limb affection
7- Triplagia ? 3
2- Hypotonic Usually a stage through which an infant passes.
3- Hemiballistic Sudden movements . As if throwing ball.
4- Ataxic ..........................................................................................................10
%
o Involvement of the cerebellum or its pathways
o Weakness, incoordination, and intention tremor Æ unsteadiness, wide based gait
POORLY AMENABLE TO SURGICAL CORRECTION
o
5- Combination
6- Athetoid / Dyskinetic .......................................................................20%
o Writhing involuntary movements: y é excited, wriggle as if tickled. z é sleep
o ð basal ganglia involvement (deposition of bilirubin or erythroblastosis fetalis)
o Hips & knees ext+ stepping gait + Lean backward, shouler & trunk extension.
o Intelligence normal (often above average)
o MOST DIFFICULT TO CORRECT - results are unpredictable & POP hazardous ð friction
o Types:
1- TENSION ATHETOSIS:
Child is hypertonic but not hyperreflexive (no clonus or Spasticity)
Deafness and absence of an upward gaze.
2- DYSTONIC ATHETOSIS:
Continuous, tortuous, slow, twisting type of motion.

All extremities, as well as the neck and trunk, tend to be involved.

3- CHOREIFORM ATHETOSIS.
More common than dystonic athetosis
Continual movement of the patient's wrist, fingers, ankles, toes, and
tongue.
4- DRAMATIC BALLISMUS ATHETOSIS.
Continuous dramatic movement of the trunk and proximal extremities
These patients can injure themselves or their caregivers by this
5- RIGID ATHETOSIS
The most hypertonic & stiff of all CP (Yet no spasticity or clonus)
446 | Page [Ortho
opedic Neurrology]
Epiidemiolog gy
• 1-5 in 1000 live birrths. More common in n advanced d countries (ð Advanced perinata al care)
Aettiology
1- Prena
atal ...............................................................(30%)
o Maternal in nfection - To oxoplasmosis . Rubella a . Cytomeg
galovirus . H
Herpes . Syp philis
o Maternal exposuree - Alcohol
A . Drrugs
o Congenital brain malfformations
2-Perina
atal
o Difficult pro olonged lab bour ð y Birth wt >2.5 5kg (25-40%)
o Anoxia ........................................................(10-20%))
3-Postn
natal ..............................................................(10%)
o Encephalittis
o Head injury y
o Carbon Mo ono Oxide poisoning p
Patthogenessis
1- Braain Damag ge: accordin ng to the siite of involvvement:
• Area 6 precentral gyru us:.....................SPASTIC UMNL
• Area 4 precentral gyru us: ................ FLACCID UMNL
• Combined: ...................................... RIGIDITY
• Basal gang glia: ................................. ASTHETOSIS
• Cerebellum m: .................................... ATAXIA
• Mid brain: ................................................. TREMORS
2- We eakness
• Loss of volu untary movvement & Weakness W (ð
ð co contra
action of aggonist & anttagonist)
3- Spa asticity
• Feature of all lesions of o pyramida al system: Cerebral,
C cappsular, pon
ntine, midbrrain lesions
• Related to DISINHIBITED STRETCH REFLEX ώ is regulated by b descend ding tracts
• SPASTICITY, HYPER-REFLEXIA, CLONUS may ap ppear
• CLASP-KNIFE PHENOMENON: Attem mpt to chan nge position Æ initial rresistance + quickly yie
eld
4- Con ntracture.
• Normally ms m adds sa arcomeres at muscullotendinous junction in response to consstant
stretch
• When mu uscles spasttic, this me echanism cannot
c occcur Æ relative shorte ening of msm in
contrast to o bone Æ prolonged shortening and a contracture
5- Defformity ð unopposed
u ontracture.
d muscle co
Hip Adductiion Flexion
n Flexio
on + IR Disloccation
Knee Flexion Recurvaatum Genu valgum
v Patella
a alta
Ankle Eqinovarus Equinovvalgus calcaneus Claw & metatarsu
us
UL shoulder add IR Elbow flex
f Wrist & finger flexx Thummb in palm
st
1. Hip
p dislocatio
on: (usuallyy correct 1rry 1 )
• 1ry: ð paralyzed abduuctors & exttensors (anttigravity mss) + good antagonists
• 2ry: ð adap
ptive changges:
o Coxa va alga: ð abse
ent gluteal pull
o Shallow w acetabulu um
o Lax cap psule
2. Kne
ee Flexion
n deformitty
• 1ry: ð tightt hamstring
g Or tight Gracilis
G
• 2ry: compe ensation to hip flexion deformity or equinus
• Prolonged flexion defformity Æ le engtheningg of patellarr tendon & tight latera
al retinaculu
um
Clinical Feature
History
• Abnormal birth history & Prematurity
• Neonatal nursery
• Delayed Developmental milestones (brackets are 95th percentile)
o Head control ..................................3 mo ........................ (6 mo)
o Sitting independently ................. 6 mo ........................ (9 mo)
o Crawling ...........................................8 mo ........................ (never)
o Pulling to stand .............................. 9 mo ........................ (12 mo)
o Walking .............................................12 mo....................... (18 mo)
Examination
• General:
1. Mentality 3- Speech
2. hearing 4- Vision
• Gait:
1- Trunk leans forward, SCISSORING, STIFF-LEGGED, TIP-TOE GAIT, CROUCHED
2- z Stride length, Narrow walking base
3- Lordosis . Co-ordination in turning.
• Hip deformities:
1- Adduction: ..................................... ð adductor spasm (GRAB TEST +VE z Hip Abduction)
2- Flexion: ............................................ ð rectus spasm ....... (ELY & THOMAS & STAHELI +VE)
3- Flexion internal rotation: ........... ð psoas spasm (true scissoring ≠ pseudo scissoring ð
flexion + yanteversion Æ +VE W SIGN)
4- Hip dislocation ............................... ð 1ry & 2ry...............(GALEAZZI TEST +VE)
WINDSWEPT POSTURE - one hip adducted & other side abducted
SCISSORED GAIT if bilateral
Apparent LLD if unilateral
STAHELI TEST is better than Thomas as it is not affected by the other side
y lumbar lordosis + prominent bottom é standing / z sacrofemoral angle
z SLR because of flexed pelvis from FFD.
• Knee deformities:
1- Knee flexion contracture (tight hamstring): ........+VE TRIPOD SIGN & TOE TOUCH
2- Knee recurvatum .................... ....................................REVERSED POPLITEAL ANGLE
3- Genu valgum
4- Patella alta (BLUEMANSAAT, INSALL-SALVATI RATIO<1) ð flexed knee & quad spasm
Flexion deformity angle is best assessed by the popliteal angle
Flexion contracture lead to CROUCHED GAIT (also ð hip flexion & calcaneus)
Tight rectus femoris Æ stiff legged gait (prolonged stance & diff. foot clearance)
Sitting - Legs forward
• Ankle deformities:
1- Ankle EQUINUS (NB, False equinus = flexed knee lifts heel from ground)
2- CALCANEUS
3- VARUS
4- VALGUS
5- CLAW TOES
6- METATARSUS ADDUCTUS
TIPTOE GAIT
SILFVERSKIÖLD TEST: equinus z é knee flexion = gastroc tight > soleus
Equinus y knee recurvatum in stance phase
Calcaneus y crouch gait
Kneeling eliminates contracture effect
• Upper limbs
Shoulder adduction internal rotation
1-
Elbow flexion
2-
Forearm pronation
3-
Wrist & finger flexion
4-
Thumb in palm
5-
o Hand placement. Ask patient to place hand on knee and then head.
o Stereognosis. Test ability to recognise shape in palm
• Spine
o Scoliosis usually present at age 5. Reaches 50º. by age 15
o Treated initially with chair that fits the curve.
o Braces of little benefit. Only 15% respond.
o If curve reaches 60º Æ segmental fusion indicated.
o Indications for Surgery = curves > 50º. or progression > 10º.
o Scoliosis curves are divided into Group 1 (ambulators) or 2 (non-ambulators):
Group 1 Double small curves- thoracic & lumbar Posterior fusion Luque rods & sublaminar wires
Group 2 large thoracolumbar or lumbar curve pelvic Ant + Post Fusion Luque rods & sublaminar wires &
obliquity Galveston pelvic fixation
• Neurology
o CLASP-KNIFE phenomenon
o Primitive reflexes:
A, ASYMMETRICAL TONIC NECK: as head

is turned to one side, contralateral
arm and knee flex.
B, MORO REFLEX: Hold child at 45o.
Allow head to drop back, UL extend
away from body and then come
together in embracing pattern.
C, EXTENSOR THRUST: as child is held
upright by armpits, lower extremities
stiffen out straight.
D, NECK-RIGHTING REFLEX: as head is
turned, shoulders, trunk, pelvis, and
lower limbs follow turned head.
E, PARACHUTE REACTION: as child is
suspended at waist and suddenly
lowered forward toward table, arms
and hands extend to table in
protective manner.
F, SYMMETRICAL TONIC NECK: as neck is
flexed, arms flex and legs extend.
Opposite occurs as neck is extended.
G, FOOT PLACEMENT REACTION: when
top of foot is stroked by underside of
flat surface, child places foot on
surface.
[Orth
hopedic Ne
Potentia
al for
walking
Assesss (midbrain
n & perinatal)
If mid
m brain re
eflexes appear Perina
atal reflexess persist >1y
y
(norm
mally disappe
ear at 4-6m)
(early balan
nce reaction) •Moro
•Parach
hutte reflex
x •Tonic neck (symmetric & asymm)
a
•Neck righting (body follow
w head turn)
•Steppiing •Extensor th
hrust on vertica
al susp
Can walk
Will not walk
w
• If any 2 of 7 are ina

appropriate
e by 1y it is highly
h unlikkely to walkk independently
Rad
diography y:
Hip:
• WIBERG CE angle
• MP of REIMER (migrration perce
entage = he ead coverage %)
• Sacrofemmoral angle n top of sacrrum and femoral shaftt (N 40-60º)) z in FFD
e: between
• Acetabuular dysplassia
• Dislocattion
Knee:
• Flexion Deformity
• Recurva atum
• Insall-Salvati Ratio <1
<
• Blumansaat Line Below The Patella
P Alta
Prin
nciple Dia
agnostic Features:
F :
• UMNL
• Delayed mile estones
• Peersistent Priimitive refle
exes
• Abnormal po osture & mo ovement
Treatment of CP
Aphorisms.
Priorities Patient priorities are • A little equinus better than calcaneus.
1]. Communication • A little valgus better than varus.
2]. Activities of daily living • A little varus better than a lot of valgus.
3]. Mobility & Walking • A little knee flexion better than recurvatum.
Objectives
1]. Maintain straight spine and level pelvis
2]. Maintain located, mobile, painless hips
3]. Maintain mobile knees for sitting and bracing for transfer
4]. Maintain plantigrade feet
5]. Provide maximal functional positions for sitting, feeding, and hygiene
6]. Provide appropriate adaptive equipment, incl. Wheelchairs
7]. Avoid hip dislocation.
o Painful
o Make nursing difficult
o y pelvic obliquity & scoliosis Æ difficult wheelchair ambulation
o zquality of life.
8]. Strategy
o 0-3 y .................................... physiotherapy
o 4-6 y .................................... surgery
o 7-18 y .................................. schooling and psychosocial development
o 18 yrs + ............................... work, residence and marriage.
ggggggbiiiiiii
LOWER LIMBS
1- PHYSIOTHERAPY - physiotherapy approaches z contractures or y development, y ROM:
o Neurodevelopmental approach ( Θ exaggerated reflexes by certain positions)
o Sensorimotor approach ( Θ exaggerated reflexes by sensory ⊕ )
o Proprioceptive approach (proprioception used to improve posture)
o Neuromuscular reflex approach (graduated pattern of movement learning)
2- CAST CORRECTION - Inhibitive casting. Stimulation of sole can cause muscles to contract
was basis of inhibitive casting. Not used much now.
3- CORRECTIVE CASTING - for mild fixed equinus. Well-padded POP é max dorsiflexion
4- BRACING - Useless for treating fixed deformity AFO's useful for Dynamic equinus
5- NEUROSURGERY - Selective posterior RHIZOTOMY of rootlets used. Via laminectomy. 30-70%
of posterior rootlets cut. Decreases feedback from stretch receptors. Can ⊕ rootlets to find
which mediate spinal reflex. If only these cut, sensation unchanged. Results promising.
6- CHEMONEURECTOMY: selective neurectomy is done using certain chemical substances:
a. ALCOHOL 45% gives improvement for 6 wks
b. PHENOL 5% 2ml gives permanent effect
c. BOTULINUM TOXIN gives 6m improvement ( Θ acetyle choline)
d. BACLOFEN intrathecal implanted pump (GABA agonistÆ Θ excitatory
transmitters)
7- Orthopaedic operations
Indications:
1]. Postural contractures
2]. Correction of fixed deformities
3]. Stabilizing unstable joints
4]. Spastic CP: Quadri Æ hip release at 3y / hemi Æ TAL at 4y / Diplegics Æ 5y hip release
5]. Rigidity signify marked brain damage so Æ only correct severe deformities
6]. Tendon transfers: remove the dynamic force and serve as motorized tenodesis (unlike
polio and nerve injury where it act as coordinated functional solution):
1- Impaired & slow voluntary control
2- Spasticity &sensory problems
3- Dysphasic contractions i.e. antagonistic activity unrelated to the action
4- Skilled coordinated learning of movement after transfer is difficult

7]. Athetosis will not benefit from transfer as this shift the problem to another region not ttt
A. Hip Procedures:
1. Hip at risk :
<50% REIMER’S MIGRATION PERCENTAGE
Abduction < 25º
Broken Shenton
Treated by psoas, adductor and hamstring LENGTHENING.
2. Subluxed hip é RMP > 50%.
VARUS DEROTATION OSTEOTOMY
3. Adducted hip:
COMPLETE ADDUCTOR TENOTOMY ± obturator neurectomy
All the Add longus, brevis, most of magnus, & gracilis

Still the patient can adduct with pectineus

4. Adducted subluxed hip:
ADDUCTED SUBLUXED HIP

Assess RMP
<50% >50%
<5y
<50% MP
No dislocation
Soft tissue Bony
operations operations
>45° flexion <30°Abd Subluxed >50% MP Hip Dysplasia Dislocated
VDO OR+VDO+
Total Add Adductor Ant. Chiari
tenotomy ± Brevis Obturator
Psoas lengthen nurectomy
Acetabulo-plasty
452 | Page [Ortho
opedic Neurrology]
5. Flexxtion defo
ormity (<20 0º may corrrect by tracction)
1]. SOUTTER’S sartorius,
s re
ectus, & tensor fascia la
ata (flexor release) via Smith Peterrson
2]. MUSTARD: iliopsoas
i tendon transsfer to GT
3]. SHARRARD: iliopsoas transfer
t + iliacus inserrtion transffer
from anterior to posterior iliacc wing, th he latter caan
compensatte for Glut maximus
m
4]. All followed by hip sppica in neutrral rotation and sagitta
al
5]. Other alternative: OBER’S op peration (sacrospina
( alis
transfer to act as hip extensor
e
6. Flex
xion + inte
ernal rota
ation
F
Flexion
Fle
exion Pure
S
Soutter’s
Flexiibl
Then do
d Thomas test
t
So
out
Still there is FFD
D No FFD
Ilio
Mustard
d Sharrard Neutral spica rece
ess
ca
Late
era
ham
mst
7. Dislocation:
Dislocation
n
Painless Painless
Reducible Irreduciblee
Correct Correct
C Correct Adductorr
M
Muscle valgus
v dysplasia release ±
neurectom my
Sh
harrar + traction
n
d or VDO Salter Chiari
Mustard When head d
at acetab
do OR &
proceed ass
painless
reducible Ad
ddress ipsilaateral
kne
ee deformitty & lig
8. Pelv
vic obliqu
uity beffore hip fussion
}
Fixed
d obliquity Dyn
namic obliqquity
z z
P
PSF Abd
d release off opposite sside
[Orth
hopedic Ne
B. Knee Procedurrees
I. Flexion deeformity:
• Due to:
A. 1ry hamstring Spasticity
B. 2ry to hip FFD
D or equinuss
ent:
• Treatme
K
Knee Flexion
Prolonged
Correctable Fixed = Pateellar
malalign
nment
+ Hip adduction
a
Check Hip & Egge er’s
Testt abd in Egger’s + Egger’s +
E
ankle forr + IR P
Pure Flexion +
flex
xion & H
Hauser
deformityy Insall lat ret
exte
ension release Patelllar
plicatiion
Same y in flexio
on Egg
ger’s Egger’s
= Gracilis = Hamstrin
ng + Gage
G Release
Adductor
tenotomy ± Egger’s release
neurectomy
1. EGGER’S Ha amstring tra ansfer:

• Transfer the hamstrring from th he back of the
t tibia to the back off the femurr
• Some ad dvocated th he lengthen ning of memmbranosus to prevent recurvatum m
• Followed d by a long leg cast forr 6 wk
• Disadvan ntages:
A].. Genu rec curvatum: contraindica
c ated in equuinus
B].. lumbar lo ordosis
C]. weak kne ee flexion
2. TACHDJIAN Fractional Lengthenin ng of Hamsstring Tend dons:
• Z-plasty of gracilis and
a semiten ndinosus ± biceps + re ecession of semimemb branosus
3. SUTHERLAND TRANSFER
• Lateral Transfer
T of Medial
M Ham
mstrings forr Internal Rootational D
Deformity off Hip
4. GAGE DISTAL RECTUS TRANSFER + hamstring release
r
• Gives ann advantag ge of enhan ncing the kn
nee flexion in the swin ng phase
5. Ischeal tub
berosity trannsfer to bacck of femur
6. EVAN’S lenggthening plasty
p
7. Selective neeurectomyy of hamstrin ng
8. all may be added ITB division ± Extension
E osteotomy
o (better in po
olio)
II. Knee Recurvatum:
• Recurvatum may be:
1]. 1ry: quadriceps spasticity or quadriceps spasticity > hamstrings & gastroc spasticity
2]. 2ry to Egger’s or Equinus (to detect equinus causation apply POP in dorsiflexion
and see if the recurvatum is corrected or not)
• Treatment:
1- Sage proximal rectus femoris Z plasty lengthening
2- Equinus Æ TAL
3- Neurectomy of femoral nerve
4- Irwin femoral flexion osteotomy
III. Genu valgum:
• Usually ð:
1- hip adduction and coupled é Flexion IR
2- Tight ITB
• Treatment:
1- Correct the hip via Adductor and iliopsoas release
2- Yount ITB resection
3- Supracondylar varus osteotomy
IV. Patella alta:
• ð quad spasm or long knee FFD
• ttt as in prolonged knee FFD
V. Patellar subluxation and dislocation:
1]. In valgus knee
2]. Flexion adduction and IR of the hip Æ y Q angle
• Treatment: ttt the cause + Insall release of Fulkerson osteotomy
C. Ankle deformities:
• Any calcaneus must have cavus as the pt can not walk on the heal only
• Calcaneocavus = calcaneus started 1st. Pes cavus means that the cavus started 1st.
• In skeletally immature; stabilizing operations are done only in valgus. In varus Æ soft tissue op.
• When tendon transfer is considered if there is only one tendon then transfer it to the mid foot.
If many tendons then transfer one to the affected side.
I. Equinus:
• Pathology (5types according to Triceps surae vs Dorsiflexors):
1- Spastic vs spastic
2- Spastic vs normal
3- Spastic vs flaccid
4- Normal vs flaccid
5- Flaccid vs flaccid
• The exact offending ms (gastroc or soleus) can be done by Silfverskiöld Test
• The muscle nature must be determined - spastic or contractured - by procain injection
Non Operative Ttt in the form of manual stretching, bracing, casting
Operative Ttt: if failed non operative ttt:
1- Neurectomy: for spastic equinus (not contractures) & for clonus é WB cut it from
origin or at insertion
2- Triceps surae release:
a. Silfverskiöld Gastroc recession (spasm): distal recession of gastroc origin
b. Gastroc slide (contracture): lengthening of gastroc tendon
c. TAL (this is for gastroc and soleus after Silfverskiöld testing):
Strayer transverse release
Vulpius V-shaped release
Baker tongue shaped release
Semi open (lateral distal release if equinovalgus)
Percutaneus (medial distal release if equinovarus)
3- MURPHY Heel cord advancement:
• In spastic vs spastic dorsiflexors replacing TA more ant in front of FHL
II. Varus:
• Due to:
TP spasm
TA or Tendoachillis tightness & evertor
weakness may assist
• Treatment (according to rule no bony

operation):
SKELETALLY IMMATURE:
1- TP Lengthening (MAJESTRO)
2- TP Rerouting in front of med malleolus (BAKER)
3- TP transfer via Interosseous membrane to dorsum of Foot (BISLA)
4- TP split transfer to the proneus Brevis (KAUFER)
5- TA split transfer to the cuboid (HOFFER)
6- FDL & FHL transfer to Dorsum (ONO)
7- TA & EHL transfer to the mid dorsum or lateral Dorsum (TOHEN)
SKELETALLY MATURE:
• Triple fusion + Laterally based wedge (DWYER) + tendon transfer
456 | Page [Ortho
opedic Neurrology]
s: more com
III. Valgus mmon than n varus
o Pathology::
Usu ually it is asssociated witth equinus
More ð tight trriceps surae e (less ð eve
ertor inverto
or imbalancce)
Dorrsiflexion oc ccur at the mid tarsal + eversion ofo the calca
aneus + MT abduction
Susttentaculum ownward Æ talar head
m tali is shifted lat & do d sublux me
edially
o Treatment::
Ta
alipes
Equin
noValgus
Imma
ature Mature
TAL + post P.Brev

vis to Grice Green or Rem
move Med Other softt
Triple fussion
capsulotomyy cunieform D
Dillwyn Evan W
Wedge tissue
GRICE GREEN extra-articula

e ar lateral su
ubtalar arth
hrodesis
DENNYSON AN D FULFORD MODIFICATION uses screw
ND s betw
ween talus and
a calcan
neus.
Iliacc crest graftt in sinus tarrsi. Walking 2 weeks.
g cast for 12
DILLWYN-EVAN’S transversse calcanea al osteotommy + fibular BG (lateral lengthenin
ng)
Medial sliding g calcanea al osteotom my may be done in nstead of medial
m closing
wed dge
IV. Calcan
neocavus:
o Due to:
2ry to excessiv ve TAL
1ry to spastic dorsiflexors
d (EDL & TA) in relation Triceps surae
n to weak T
SKELETALLY IMMATURE:
2ry ..................Taalectomy but Æ painfu ul pseudoarthrosis, LLD, deforminng, one waay
1ry ..................▪ Partial
P EDL denervatio
on
TA shorteningg & transfer to Tendo A
Achilles
Cavvus Steindle
er ± Samilso
on calcaneaal crescent osteotomyy
Valggus Grice or Dillwyn
D
SKELETALLY MATURE:
1- Theere is tendo
on to transffer:
(1) ELMSLI 2 stage op peration:
Stage 1 Stage 2
Osteotommy Dorsal Weedge Posterior W
Wedge
Fusion TNJ subtalar
Cut Steindler TA + PL trannsfer to tendoo-achilles
POP Full dorsi-fflexion to corrrect cavus In plantar fle
exion to aid healing
h
(2) Triple fusion
f + Ten
ndon transfer
2- No tendon forr transfer:
Pantala
ar fusion
V. Claw toes:
o Neurectomy of the motor br of the lateral pantar nerve
o Release of the insertion of the FDB
VI. Metatarsus adductus
o Resection of the abductor hallucis & its tendon
Four Stages of Winter: Treatment
Stage I Weak TA No tightness of triceps surae . AFO.
Stage II Above + tight triceps surae + TP TA lengthening + split TP transfer.
Stage III Above + quad & hams spasticity. + hams lengthening + rectus transfer
Stage IV Above + hip flexor & add spasticity + psoas + adductor release.
D. Upper Limb deformity:

I. Shoulder adduction internal rotation
1- SEVER’S release: subscap, pec major, coracobrachialis, short head biceps, coraco-
humeral lig.
2- L’EPISCOPO ZACHARY: Sever’s + Teres & latissimus transfer to post-lat aspect of prox
humerus
3- ROTATIONAL HUMERAL OSTEOTOMY
II. Elbow flexion
1. Flexor tenotomy
2. Biceps transfer to triceps
III. Forearm pronation
1. Pronator tenotomy
2. FCU to ECR
Gershwind & Tonkin Classification TREATMENT
Group 1 Active supination beyond neutral No surgery
Group 2 Active supination to neutral or less Pron quad release ± flexor aponeurotic release
Group 3 No active sup, loose passive sup Pronator teres transfer
Group 4 No active sup, tight passive sup Pron quad release ± flexor aponeurotic release
IV. Wrist & finger flexion

1. Arthrodesis wrist
2. Release common flexor origin
3. FDP high cut & FDS low cut; then suture the tendons together
ZANCOLLI CLASSIFICATION TREATMENT
1 finger ext é wrist <20º flex Flexor Aponeurotic Release (FAR) ± FCU tenotomy
2A Finger ext é wrist > 20º flexion + active ext FAR + FCU tenotomy
2B same + No active wrist extensor FAR + FCU to ECRB
3 No Finger extension FCU to EDL or Prox row carpectomy or Wrist Fusion
or FDS to FDP.
V. Thumb in palm
1. Cut pollicis (adductor, flexor, opponense) & 1st interossei
2. Tendon transfer to restore the thumb abduction: Pronator teres transfer
Poliomyelitis
• It is a neuromuscular disorder 2ry to viral infection é subsequent development of deformities
Epidemiology
• It is considered to be eradicated from all the developed countries
• Our county is declared to be eradicated from endemic polio especially after free vaccination
programs (SABIN live attenuated vaccine oral drops, SALK IM killed vaccine)
Ætiology::
• Organism:
o Polio virus: small RNA virus (3 types; BRÜNHILDE, LANSING, LEON)
• Route of infection:
o The virus enters the body via feco-oral route
o 10 Incubation period during which the virus reaches the peripheral circulation
o Viraemia then occurs till the virus reaches the CNS
Pathogenesis::
• Subclinical infection: no manifestation even of viraemia (local immunity)
• Minor illness
• Abortive infection: no paralysis
• Major illness
Pathology::
• CNS: (AHC, Dorsal root ganglia, Internuclear cells)
• Affect the AHC:
1- Irritative: temporary paralysis
2- Reversible toxic changes: cloudy swelling and chromatolysis Æ reversible paralysis
éin 2y
3- Irreversible damage
• Motor cranial nerve nuclei (bulbar palsy)
• Brain stem and cerebellar nuclei may lead to sympathetic and extrapyramidal manif
• Meningitis
• Dorsal root ganglia & internuclear cells Æ pain & spasm of ms Æ continuous contraction that
may end with a contracture as well
• Peripheral nerves: Axonal degeneration and replacement by fibrofatty tissue
• Muscle
1]. Fibrofatty degeneration and atrophy
2]. Fibrosis and shortening
• Bone:
1]. Disuse atrophy ð z ms stresses
2]. Short limbs
• Joints: Unbalanced and instability
Polio In The Upper Limb

1- Shoulder: Deltoid, subscapularis, supraspinatus, infraspinatus, and serratus paralysis
• Skeletally immature (SAHA TENDON TRANSFERS)
1]. Deltoid ...................................................................... trapezius to humerus transfer
2]. Subscapularis .......................................................... superior 2 digits of serratus to subscap transfer
3]. Suraspinatus .......................................................... levator scapulae or sterno-mastoid transfer
4]. Infraspinatus .......................................................... latissimus or teres transfer
5]. Serratus .................................................................... pec minor transfer
• Skeletally mature:
1]. Shoulder fusion .................................................... 45º abd, 30º IR, 15º flexion (hand to face)
2- Elbow:
• Flexor paralysis: (MUST HAVE GOOD HAND FUNCTION)
1]. BROOKS-SEDDON ................................................ all pec major to biceps
2]. CLARK’S .................................................................... sternal pec major to biceps
3]. HOVNAN ................................................................. Latissimus origin to biceps
4]. Pec mior to biceps
5]. Sterno-mastoid to biceps (fascial graft to give more length Æ webbing of neck)
6]. Triceps to biceps
7]. STEINDLER FLEXORPLASTY................................ advancement of the common flexor origin to lower humerus; before op
assess flexors, doing elbow flexion 90º hand clench test, if he can not do, cancel the operation
8]. BUNNEL modification ......................................... augment the transfer by fascia and attach it to the lat border of
humerus for better pronation
9]. MAYER-GREEN ...................................................... flexor palsty to the anterior aspect of humerus (better pronation)
• Extensor paralysis:
1]. Latissimus transfer
2]. Brachio-radialis transfer
3- Forearm
1]. Pronation deformity (supinator weak):
2]. Pronator teres + FCR ........................................... around ulna to radius
3]. Supination deformity (pronation paralysis)
4]. ZANCOLLI ................................................................. biceps rerouting around radial neck
4- Wrist:
1]. Extensor paralysis ................................................ Pronator to ECR
2]. Flex paralysis (wrist & hand) ............................ ECRL to sublimis
3]. Wrist Drop: ............................................................. wrist fusion
5- Fingers:
1]. Flexor paralysis....................................................... ECRL to sublimis or profundus
2]. Extensor paralysis ................................................ FCU to EDL + palmaris longus to EPL (or split FCU)
6- Thumb: Loss of pinch:
o Loss of adduction (as in Ulnar) ...................... 1] Brachioradialis............................. (B BOYES)
BRAND)
2] ECRL ............................................... (B
3] Sublimis ......................................... (R ROYLE THOMPSON)
o Loss of opposition (as in median) ................. 1] Ring sublimis ................................ (R RIORDAN)
(= Abd & rotation at CMCJ + flex IP) BURKHALTER)
2] EIP .................................................... (B
3] Riordan + FCU
7- Intrinsic Minus hand
o Claw hand as low ulnar & median ............ 1] ECRL ................................................ (B BRAND)
2] Sublimis .......................................... (B BUNELL)
RIORDAN)
3] EIP ..................................................... (R
8- Index:
o Loss of abduction (Ulnar): ............................... EIP or Abd Pollicis ........................... (N NAVIASER)
THUMB ADDUCTION
THUMB OPPOSITION
CLAW HAND
Polio in Lower Limb

1- Hip
1]. FLEXION DEFORMITY .......................................... As CP
2]. PARALYTIC DISLOCATION ................................. As CP
3]. FLAIL HIP : (according to the condition of spine, epsilateral knee, contralateral hip)
a. Free ................................................................ Fusion
b. Abnormal .................................................... Orthosis
4]. FLEXION ABDUCTION
c. Mild.................................................................. YOUNT’S ITB & lateral IM septum release
d. Severe ............................................................ CAMPBELL Iliac crest transfer above the acetabulum
e. Alternative ................................................... IRWIN COMBINATIONS:
i. Mild ................................................... Yount’s + Soutter’s
ii. Severe ............................................... Yount’s + Campbell
2- Knee:
1]. FLEXION DEFORMITY:
a. Mild ................................................................ POP wedging
b. Moderate (30-40º) .................................... Supracondylar extension osteotomy (REVERSED IRWIN)
c. Severe (90º) ...................................................... Post capsulotomy + hamstring lengthen/transfer to patella
2]. RECURVATUM :
a. Type I ................................................................. (Quad =0 / Hamstring =5)
i. IRWIN Supracondylar flexion osteotomy
ii. Biceps to patella
b. Type II ................................................................ (Quad = 5 / Hamstring = 0)
iii. Long Leg Brace
iv. Soft operation:
HEYMAN ......................... Collateral ligaments reconstruction
PERRY ............................... Triple tenodesis (ITB, ST, Biceps)
v. Bony operations:
MÜLLER ........................... Tibilaization of patella
Fusion
3]. GENU VALGUM: .................................................... MODIFIED MCEWIN’S osteotomy (¾ osteotomy/ ¼ clasis)
4]. FLAIL KNEE: ............................................................ Long Leg Brace or Fusion
3- Foot & Ankle
Deformity Immature Mature
Wedge Fusion Tendon transfer No Tendon
1].Varus Mild ............ Hoffer, Kaufer, Tohen Lateral (Dwyer) TF Same TF + Dwyer
Severe ........ Drennan TA Post transfer
2].Valgus P. Brevis to cuneiform + GG or EV GG or EV TF P.B to C TF + GG or EV
3].Equinus TAL + Bisla ± Ankle fusion Lambrinudi TF TAL + Bisla Ankle Fusion
4].TEV TAL + Bisla ± Steindler AnteroLateral TF TAL + Bisla Ankle or Pantalar
5].TE valgus TAL + PB to Cuneiform + GG or EV Anteromedial TF TAL + PB to C Ankle or Pantalar
6].TC Valgus Banta + PL & PB relocation + GG or EV Posteromedial TF Banta Pantalar
7].Cavus (Plantaris) Steindler + Jones or Hibbus Japas Dorsal V-shaped osteotomy of the tarsus
8].Calcaneo Cavus Steindler + Banta + Samilson Elmsli or TF Banta Pantalar
9].Pes cavovarus Steindler + BISLA + Tohen Dwyer or lateral calcaneal displacement osteotomy
10].Claw Toes Big .............. Jones Same If there is OA Æ
Toes ............ Hibbus + IP fusion DuVries MP excision arthroplasty
Or ................ Taylor FDL to EDL + MP capsulotomy or Fusion
11].Hammer Toe FDL tenotomy DuVries PIP Excision arthroplasty or Fusion
12].Mallet Toe FDL tenotomy DuVries DIP Excision arthroplasty or Fusion
13].Dorsal Bunnion Lapidus (TA to Nav + FHL to P.Phx base + Nav-Cuneiform fusion + Cuno-MT fusion + plantar IP capsulotomy)
GG= Grice Green (Tibial graft) / EV= Evans (Fibular Graft) / PB= Proneus Brevis / PL= Proneus Longus / C = Cuneiform
• Proneus Translocation must be done before age of 1 year:
1]. Eliminates the calcaneus and valgus force early before 2ry bone changes
2]. No orthosis can control the calcaneus deformity at the walking age
462 | Page [Ortho
opedic Neurrology]
B chial Plex
Brac P us Injuries
I s
Introduction
• It is nott a common
nly encountered thoug
gh grave in
njury
Brachial plexus anatomy

• 5 roots: C5,6,7,8,T1
1
• 3 Trunkss: Upper, Middle,
M Low
wer
• 6 divisio
ons: 3 anterior, 3 poste
eior
• 3 cords: lateral, me
edial, posterrior
• Nerves from
f the ro
oots: Long thoracic
t (C55,6, 7), Phre
enic (C5), Dorsal scapu
ular (C5)
• Nerves from
f the tru
unks: Supraascapular nerve, n to subclavius (fform upperr)
• Nerves from
f cords::
• Lateral cord:
c LL Muusculocutan neous
• Medial cord:
c MMM MM Ulnar
• Posterioor cord: ULN
NAR
Ætiology:
1- Open Plexus injury: sharp knif & glass (usually associated é vascular and visceral injuries)
2- Closed Brachial plexus injury:
1- Obstetric birth plasy:
High birth wt > 4 kg
Shoulder dystocia
Breach
2- Traumatic:
Traction injury: mostly due to motor cycle accidents & sport injury ð sudden fall on tip of
the shoulder Æ sudden traction injury
Compression by:
(1) Direct blunt trauma to the side of the neck
(2) Fractures: transverse process, rib, clavicale, scapula
(3) Dislocations: shoulder, AC, Sternoclavicular
3- Inflammatory: Radiation plexopathy: pain after radiation DXT
4- Tumors:
Neural: neurolemmoma, plexiform neurofibromatosis
Non neural: Pancoast tumor
5- Compression neuropathy:
Thoracic outlet syndrome: thoracic rib,…
6- Vascular ischemia
7- Iatrogenic: ð mal position of a patient on the operative table (usually neuropraxia)
Pathology:
1]. Preganglionic injury:
o Avulsions form the spinal cord Æ herniation of the dura
o Injury proximal to the DRG i.e. intact axons Æ the DRG cells does not degenerate but there is
loss of sensation
o Back muscles are denervated
o Usually + phrenic + long thoracic + dorsal thoracic + Horner
o All nerves that emerges from the roots are injured
2]. Postganglionic:
o Ruptures distal to the DRG Æ they degenerate + loss of sensation
o Back muscles only are intact
o No herniation of dura
3]. Trunks
o Intact nerves: long thoracic and pectoral nerves
o Suprascapular nerve is affected
o Upper trunk (deltoid & biceps)
o Middle trunk (radial n)
o Lower trunk (ulnar + median)
4]. Cords
o All the 3 nerves are intact
o Medial (UMMMM)
o Lateral (LLM)
o Posterior (ULNAR)
Microscopically:
SEDDON’S CLASSIFICATION:
1]. Neuroparaxia (conduction block that recover = 1 Sunderland)
2]. Axonotemesis (cutting of axons but intact peri and epineurium = 2.3)
3]. Neurotemesis (all are cut = 4,5)
SUNDERLAND CLASSIFICATION
1]. Type 1 : neuraparaxia
2]. Type 2 : axonotemesis with intact endoneurium
3]. Type 3 : severe axontemesis with only intact peri & epineurium
4]. Type 4 : neurotemesis é only intact epineurium
5]. Type 5 : neurotemesis is complete with fibrosis
1-NEURAPARAXIA:
1]. Physiological Conduction block
2]. No degeneration reaction occur
3]. Due to myelin disintegration
4]. Regeneration of myelin occur with schwann cells with regain of the full function
2- WALLERIAN DEGENERATION FOR AXONO & NEUROTEMESIS

• Proximal to axonotemesis or neurotemesis
1]. Perikaryon: swell then retract, nucleus becomes more peripheral, chromatolysis (Niessers
granules desintigrate)
2]. Adjacent cells show similar changes
3]. Retrograde degeneration of the axon till the next NODE OF RANVIER
• Distal to the cut:

1]. Axon maintain activity for 4 days then degeneration starts
2]. Axonal Degenration and disintegration down till the end of the nerve fiber
3]. Myelin disintegrate
4]. Schwann cells and macrophages clean the debris
5]. Schwann cells multiply and form Bunger tubes for future axon sprouts to come in
6]. Muscle atrophy, fasciculations, polyphasia
• Regeneration:
1]. 30-40 days latency occurs till the beginning of the regeneration
2]. Axon sprouts starts to bridge the gap till it finds the way in the distal end
3]. Axons travel 1mm/d till reach the distal organ
4]. MUSCLE: y № of motor end plate, y sensitivity, then starts to respond &z fasciculation
5]. SENSORY IS BETTER THAN MOTOR: and can wait for longer periods till start to regenerate
Clinically:
1- Motor: Flaccid paralysis or weakness (LMNL):
1- ERB’S DUCHENNE: Upper roots C5,6 (30%) + C7 (50%) :
Arm adducted, elbow flexed, forearm pronated, fingers flexed (C7)
Winging of scapula + lost protraction = preganglionic injury
2- DEJERINE KLUMPKE PALSY: Lower roots (C8,T1) avulsion + upper roots rupture (20%)
Complete flail paralysis
Phrenic
3- COMPLETE + Horner Æ marble skin
2- Sensory:
o Diminished spinothalamic sensations:
Pain, Temp, Crude touch
o Diminished Lemniscal sensation:
Fine touch (tactile discrimination, 2 point discrimination, moving discrimination,
depth discrimination, streognosis)
Proprioception: sense of position, sense of movement
Sense of vibration
3- Autonomic:
Vasomotor: VD followed by VC
Sodomotor: anhydorsis (in complete) hypohydrosis (in incomplete) using the
Guttman quinizarine test + coffee and aspirin powder turns purple
Atrophy
4- Reflexes: Lost deep and superficial reflexes
5- Causalgia: pain due to injury of a sensory nerve (e.g. median)
466 | Page [Ortho
opedic Neurrology]
Electodiagnosis:
1- Reaction of
o degenrattion:
lost resp ponse to faaradic curre ent (sustaine ed contracttion)
Slow re esponse to galvanic
g cuurrent
Polar re eversal: ano odal closing g current > cathodal c clo
osing curreent
2- y CHRONAXIE (time needed for DOUBLE RHEOBASE = th he minimal current can n cause a coontraction))
3- SD (strenggth duration n) curve:
Normally: 100 mssec voltage threshold is i < double 10 msec th hreshold
Denerv vation: the curve is ste eep and th he 100 mse ec voltage tthreshold iss > 2x 10 msec
m
threshoold ώ is slow
wer than no ormal
4- EMG:
1- No ormal patterrn
Insertio onal potential; normally ly immediatte and brieff
Resting g potential: normally no fibrillation n nor fascicculation
Motor unitu firing: bizarre,
b gian nt, dublette e, polyphasia are abno ormal
Recruitment patte ern (normallly complete e interferen nce pattern = disapp ofo baseline)
2- Can n detect thee level
3- Can n detect thee acute and d chronic
4- Can n detect thee regeneration pattern n: polyphassia, and giant waves
5- Sev verity
Butt purely motor, does no ot evaluate e the motorr root functiion, does not measure e pain
5- Nerve con nduction:
1- Nerve conduc ction velociity: by ⊕ of a nerve at a point & record r the stimulus att another point
p
in the
t course of o the same e nerve the en measure the velocity ty of conduction
a. If slow conduction
c n .... Myelin problems & compresssion
b. If motoor is absent + intact sen nsory ........................prega anglionic in
njury
c. If both are intact despite
d the injury ......................neura apraxia
d. If both are absent ...... .................................................neurootemesis
2- Roo ot assessme ent by delayyed respon nses:
H-REFLEX (electric c ankle jerkk) by subm maximal nerrve Æ ⊕ γ fibers Æ dorsal roo ot Æ
monosyynaptic ⊕ of o AHC Æ ms m contracttion
F RESPPO ONSE: (anttidromic motor m nerve e conductiion) stimullation of a motor nerve
producce normal orthodromi
o c propagattion of actio on potentia al to the mu
uscle and in
n the
same tiime there is i an antidromic volle ey that travvel to the p perikaryon Æ ⊕ Rensh haw
cells Æ till ⊕ the ce
ell itself Æ another
a ressponse F ressponse
Still botth are moto or, not for muscles th hat are inne ervated by multiple ro oots or you can
not diffferentiate, and
a can not differentia ate bet acutte and chro onic
6- Bulbocave ernosus reflex Æ perin neal contracction
7- SEP: Stimuulation of neerve Æ elecctrodes at sp pine & corttex
1- Can n purely me easure the root functio on
2- Can n measure the conducction velosity
3- Do oes not depe end on mo otor function
4- Can n detect deelays due too CNS delayys e.g. MS
5- Can n detect thee root avulssions in Erb b’s plasy
PXR
• Detect
D phreenic paralyssis
• Detect
D fracttures of 1st rib
r or tumo
ors
• Cervical
C myyelography Æ diverticu e preganglionic injury
ulosis of the
Treatment:
Non operative:
• Literature indicates that the spontaneous recovery is the rule in 80%
• Usually if closed injury é early biceps twitches
• Physiotherapy is mandatory to maintain normal ROM
• Ms ⊕ is important to keep active ms
Operative:
1- INDICATIONS AND TIMING:
1]. If the point of 3mo passed without evidence of biceps regeneration
2]. Reconstructive surgery for late sequelae
2- FINDINGS:
1]. Root avulsion
2]. Continuous root and trunk (traction injury)
3]. Neuroma formation
3- TECHNIQUE:
1]. Neurolysis if the lesion is in continuity
2]. Direct repair (not in root avulsions; but in peripheral nerves):

o Timing:
Acute repair if clean cut and every thing is ready
2 weaks: is the rule for the oedema to subside & the soma is fully active
Delayed if (6wk) if contaminated or é vascular and tendon injury to avoid fibrosis
o Methods:
a. Perineural
b. Fascicular
c. Group Fascicular
d. Perineural and fascicular
o Avoid:
Gaps
Infection
Tension:
(1) <5cm: transposition, limb position, neurolysis, cut of unnecessary branche
(2) >5 cm: nerve grafting:
o Fibrin & plasma glue: may be used to z operative time and z the use of suture Æ z fibrosis
o Postoperative:
Immobilization: 2-6 wk
Physiotherapy
3]. Nerve Grafting
o Nerves to be used: sural, medial cut n of fore arm, superficial radial
o Technique:
a. Interfascicular
b. Inlay: in neuroma
c. Cable grafting
d. Pedical rotational intergrafting (bet ulnar and median)
4]. Homografts are immunogenic

5]. Neurotization: two types:
1]. Internal Plexo-Plexus:
C7 to upper trunk
C3,4 to upper trunk
2]. External: (to upper trunk, musculocutaneous, axillary, suprascapular, radial, median)
Pectoral nerves
Intercostal n
Spinal accessory
Long thoracic, thoraco-dorsal, subscapular
6]. Late Reconstructive surgery to shoulder:
1]. FAIRBANK release of the subscapularis + pec major + ant capsule
2]. SEVER’S release of the subscapularis + Pec major lengthening
3]. L’EPISCOPO: transfer of Latissimus & teres major to the back of the humerus Æ ER (Z ZACHARY,
TACHIDJIAN modifications)
4]. HOFFER transfer of latissimus and teres into the rotator cuff Æ ER + abduction
5]. OBER long head triceps + short head biceps transfer to acromion
6]. GILBERT & MAYER trapezius transfer to humerus
7]. SAHA acromion with the attached trapezius advancement to humerus as distal as possible
8]. Humerus derotation osteotomy
9]. Arthrodesis is the last resort
Lesion procedure as recommended by AAOS

Adduction + IR Subscapularis Release
Supra or infraspinatus Dysfunction Latissimus to greater tuberosity
Deltoid Dysfunction Saha or Hoffer
IR or ER + incongruent shoulder joint Humeral derotation osteotomy
Severe dysfunction of shoulder Glenohumeral arthrodesis
7]. Elbow reconstruction:

Flexor paralysis: (MUST HAVE GOOD HAND FUNCTION)
BROOKS-SEDDON .................... all pec major to biceps
CLARK’S ...................................... sternal pec major to biceps
HOVNAN .................................... Latissimus origin to biceps
Pec mior to biceps
Sternomastoid to biceps ..... using a fascia to give more length Æ webbing of neck
Triceps to biceps
STEINDLER FLEXORPLASTY...... advancement of common flexor origin to lower humerus;
assess 1st flexors condition by doing elbow flexion 90º hand clench test
BUNNEL modification............ augment by fascia &fix to lat humerus (better pronation)
MAYER-GREEN .......................... flexor palsty to the anterior humerus (better pronation)
Extensor paralysis:
Latissimus transfer
Brachio-radialis transfer
8]. Forearm
Pronation deformity (supinator weak): Pronator teres + FCR around ulna to radius
Supination deformity ........... ZANCOLLI biceps rerouting around the radial neck
9]. Wrist:
Wrist Drop ............................... FCU to ECRB
Prognosis
A]. Preoperative:
1]. Level of injury: the distal the better
2]. Delay of injury: the more acute the better
3]. Type of injury: the apraxia the better
4]. Type of nerve: the pure the better & the small the better
5]. Type of pt: the younger the better
B]. Operative:
6]. Huge gaps
7]. Huge tension
8]. Huge suture (we use 8-0 or 9-0)
C]. Postoperative
9]. Hematoma
10]. Infection
11]. Inadequate physiotherapy
RECENT TRENDS IN NERVE REPAIR
1. Phamacoloical agents
1- Gangliosides
2- Polyamines
2. Immune system modulators
1- Azathioprine
2- Corticosteroids
3- Cyclosporin A
4- Cvclophosphamides
3. Enhancing factors
1- Nerve growth factor
2- Fibronectin
3- Insulin-like growth factor
4- Ciliarv neurotrophic factor
4 Entubulation chambers
1- Autogenous vein
2- Silicone Polvglycolic acid G
3- Gore-tex
THUMB ADDUCTION
THUMB OPPOSITION
CLAW HAND
Carpal Tunnel Syndrome

Commonest middle aged F:M = 3-5:1
Anatomy Of Carpal Tunnel
• floor and walls bony carpus
• roof flexor retinaculum /transverse carpal ligt
• radial attachment tubercle of scaphoid + ridge of trapezium
• ulnar attachment hook of hamate + pisiform
• Contents FPL / FCR (deep to FPL) / FDS - middle & ring lie superficial / FDP
Median Nerve
Flexor tendons run deep to nerve
Causes (ICRAMPS)
• Idiopathic
• Colles, Cushings
• Rheumatoid
• Acromegaly, amyloid
• Myxoedeoma, mass, (diabetes) mellitus
• Pregnancy, Persistent median a.
• Sarcoidosis, SLE
Symptoms not always classical

1- Aching and parasthesia in thumb , index middle and 1/2 of ring finger
2- worse at night
3- forearm pain
4- dropping things
Signs
1]. Hand normal looking
2]. If severe, thenar wasting, trophic ulcers
3]. weakness of thumb abduction
4]. Semmes Weinstein monofilament test & Vibration test are more sensitive than 2 point
discrimination test in assessment of the slowly progressive sensory compression change
5]. Tinels Sign -74% sensitivity, 91 % specificity: Gentle tapping over median nerve at the wrist
in a neutral position. Positive if this produces paraesthesia or dysaesthesia in the distribution
of the median nerve
6]. Phalens Sign –61% sensitivity, 83% specificity: Elbows on the table allowing the wrists to
passively flex. If symptoms provoked within 60 secs then positive
7]. Median Compression Test – 86% sensitivity, 95% specificity* : Elbow ext, forearm
supination, wrist flex 60º, one thumb pressure over the carpal tunnel. Test positive if
parasthesia or numbness within 30 secs
Differential diagnoses
• Cervical radiculopathy
• Spinal cord lesions - tumour, MS, syrinx
• Peripheral neuropathy- toxic, alcoholic, ureamic, diabetic
Investigations
Nerve conduction studies :
• sensory conduction prolongation ......... >3.5ms (more sensitive)
• distal motor latency .................................... >4.0 ms
• accuracy = 85-90%
• 10-15% false negative
Reminder of how nerve conduction studies are performed:
• Motor
1]. stimulus to skin over nerve, Motor Action Potential recorded in muscle supplied
2]. Latency = time between stimulus and MAP
3]. Conduction velocity, normal = 40-60 m/s
4]. compression causes z CV in a segment
5]. If very severe MAP also reduced
• Sensory
1]. SNAP recorded in proximal nerve after distal stimulation
2]. sensation often affected before motor function
3]. SEP (Somato sensory evoked potential) record response in brain or spinal cord, used to
diagnose brachial plexus injuries
Management
Conservative-
• Night splint, injection, NSAIDs, correct any cause (75-81% relief short term)
Surgical-
1]. open /endoscopic decompression
1]. Need to bear in mind anatomical variations
2]. Beware palmar cutaneous branch of median nerve, and motor branch
3]. Apply volar splint to hold the wrist in extension Æ z bowstring & RDS
Complications of surgery
1]. Complex Regional Pain Syndrome
2]. Tender hypertrophic scar pillar pain
3]. neuroma in palmar branch
4]. tenosynovitis / tendon adhesions
5]. bowstringing of tendons
Endoscopic release Okutso&Agee
1]. one or two incisions
2]. less scarring
3]. less pillar pain
4]. quicker return of strength and to work
5]. but:
6]. Anecdotal reports of disasters
7]. Big learning curve
8]. Time consuming, expensive
Pronator Teres Syndrome

Compression at
• Lacertus Fibrosus = biceps aponeurosis
• pronator teres muscle
• fibrous arcade of FDS
• Ligamentum Struthers (present in 1.5 % of people)
Causes
1]. Repeated minor trauma/ repetitive use of elbow
2]. fracture / fracture dislocation of elbow
3]. Tight/scarred lacertus fibrosus
4]. Tendinous bands in pronator teres
5]. Tight fibrous arch at prox FDS
Symptoms
1]. Aching / fatigue of forearm after heavy use
2]. Clumsiness
3]. Vague, intermittent parasthesia, but rarely numbness
Signs
1]. local tenderness to deep pressure and reproduction of symptoms
2]. TINELS TEST
3]. pain on resisted pronation of forearm with elbow extended = Pronator teres
4]. pain on resisted elbow flexion and supination= lacertus fibrosus
5]. pain on resisted flexion of PIP joint middle finger = FDS arch
Investigations
1]. NCS not much use, intermittent symptoms
2]. EMG z innervation of muscles & differentiate from CTS
Management
1]. Conservative-avoidance of repetitive elbow movements, NSAIDS, Splintage with elbow
flexed with pronation
2]. Surgical- Decompress all the structures
Anterior Interosseous Syndrome

• Compression under humeral part of pronator teres
• Anterior interosseous nerve motor to FPL, radial side of FDP and pronator quadratus
• Does not supply skin sensation
• Afferent sensory fibres from capsular ligament structures of wrist and DRUJ
Clinical diagnosis
• spontaneous vague forearm pain
• reduced dexterity
• weakness of pinch
• unable to make 'OK Sign' due to weakness of FPL & FDP index finger (makes square
instead of circle)
• weak pronation with elbow in full extension (isolates PQ)
• direct pressure over nerve can elicit symptoms
• Tinels sign usually negative
Investigations
• EMG + NC unhelpful
Management
• Conservative- NSAIDS, avoiding aggravating movements
• Surgical exploration- most common compressing structure deep head of pronator teres
Cubital Tunnel Syndrome

• Ulnar nerve entrapment about the level of the elbow
Aetiology:
1]. At elbow:
o Cubitus Valgus ○ Trauma
o Bony spurs ○ Tumours
2]. Proximal 8cm by ‘Arcade Of Struthers’ ≠ ligament of Struthers’. It is a
thin aponeurotic band extending From Medial Head Of Triceps To The
Medial Intermuscular Septum; it is 8 cm proximal to the medial
epicondyle; it may look like triceps fibers crossing superficial to the ulnar n.
& usually it is not site for entrapment under ordinary circumstances, but it
do é anterior transposition of ulnar nerve is performed
3]. Distal by hypertrophied FCU
Symptoms
• Vague dull aching forearm, intermittent parasthesia, ulnar side of hand
Signs
1]. Hypoesthesia ulnar side of hand + 1½ fingers
2]. Tinels TEST, behind medial epicondyle
3]. Wartenburg’s sign weakness of abduction of little finger
4]. Froment’s Sign pinch grip and grasping, both of which are impaired by a low ulnar nerve
palsy due to weakness of adductor pollicis
5]. Ulnar clawing if severe (Note - Ulnar Paradox - no clawing if FDP & intrinsics weak)
6]. Wasting: 1st dorsal Interosseus + hypothenars + ulnar FA (FDP & FCU)
Differential Diagnosis
• Cervical radiculopathy
• Thoracic outlet $
• Amyotrophic lateral sclerosis (MND)
• Localized peripheral neuropathy
Investigation
1]. NCS reduced nerve conduction velocity
2]. EMG evidence of denervation of muscles
Management
Conservative
1]. Avoidance of repetitive bending of elbow; Extension Block night splint.
1]. injection contraindicated
Surgical -controversy
1]. Decompression- ‘Cubital Tunnel $ Does Not require transposition of the ulnar n’
2]. Transposition: - subcutaneously/ Submuscularly (better)
3]. +/- medial epicondylectomy
Results
• Sensation improves better than motor function over 3-5 y period
Complications
1]. Recurrence ð inadequate decompression or irritation or redislocation or neuoma
2]. CRPS
Ulnar Tunnel Syndrome

Guyons Canal
Anatomy Of Guyons Canal
• Floor transverse carpal ligt to pisiform
• Ulnar wall pisiform
• Radial distal wall hook of hamate
• Roof volar carpal ligt
• Contains Ulnar nerve + art
Causes
• Repetitive indirect trauma most common
• Tumours- ganglion, lipoma
• Pisiform instability
• Pisotriquetral arthritis
• Fractured hook of hamate / pisiform
• Ulnar artery thrombosis
Symptoms
• Weakness atrophy para / hypoasthesia ulnar side of hand motor sensory or both
• Dorsoulnar sensory branch spared
Signs
• Local tenderness, tinels test, phalens sign, local swelling, negative allens test, severe ulnar
clawing (remember Ulnar Paradox)
Investigations
• Ncs, show delayed motor latency from wrist to 1st dorsal interosseous
Management
• Conservative
1]. Splinting
2]. Avoidance of repetitive trauma
• Surgical
1]. Decompression of motor and sensory branches
2]. +/- excision of pisiform/ hook of hamate
476 | Page [Ortho
opedic Neurrology]
P or Intterrosseoous Syndrom
Posterio S me
(Pain And Pa
aresis)
Cau
uses (FREAAS & Montteggia)
1]. Fibrous tendinouus band at origin of supinator (330% of peo ople)
2 Radial recurrent vessels
2]. v (the Leash Of O Henry) (less convincing evid
dence)
3 Extensor carpi radialis brevis
3].
4 Arcade
4]. e of Frohse
5 Supina
5]. ator (the distal borderr).
6 Monte
6]. eggia fractture especiaally types ! & III
7]. R.A of elbow
7 e
8 surgical resection of
8]. o radial hea
ad
9 mass lessions
9].
Sym
mptoms
• pain inn 50%
• weakness of exte ension of wrist
w and MCP
M joints
Sig
gns
• Radial deviation of
o wrist witth dorsiflexxion (ECRLL supplied by
b Radial n
nerve)
• If partia
al, pseudo clawed haand
• Able too extend IP
P joints due
e to interro
ossei
• no losss of sensation
Investigations
• NCS -decreased la atency across arcade e of Frohse
e
• EMG denervation
d n fibrillation
ns of affectted muscle
es
Treatment
• Conserrvative obsserve for 8--12 wks if no
n evidencce of mass lesion
• Surgica al decomprression
Im
mportantt tests
• Jeannne's Sign Thuumb MP hyyperextenssion 10° -15° é key pin nch or grooss grip.
• Fromeent's Sign Thuumb IP hyp perflexion é key puncch by FPL iin ulnar ne erve palsiess.
• Warteenberg's Sign
S Inability to addduct the extended
e liittle finger ð ulnar neerve palsy
• Ducheenne's Siggn Clawing of th he ring and
d small fing
gers ð ulnar nerve palsy
• Polloc
ck's Sign Inability to fle
ex the DIP of
o the ring and small fingers in high palsie es
• Phalenns Sign Elb
bows on the table allo owing the wrists to p passively fle
ex. If media
an
nerrve sympto oms provokked within 60 secs = positive
Radial Tunnel Syndrome

(Pain & No Paresis)
• Mild compression of post interosseous nerve without paresis
Causes
• As for posterior interosseus syndrome but not usually any mass lesions
Diagnosis
Symptoms
• dull aching in extensor muscle mass
• worse at end of day
Signs
• local tenderness 5cm distal to lat epicondyle
• pain elicited by resisted active supination
• Middle Finger Test.
o Each finger is tested under resisted extension. Testing the middle finger increases the
pain. Due to ECRB inserting into base of 3rd metacarpal.
o Performed with the elbow and middle finger completely extended with the wrist in
neutral position.
o Firm pressure is applied by the examiner to the dorsum of the proximal phalanx of
the middle finger.
o The test is positive if it produces Pain At The Edge Of The ECRB in the proximal
forearm.
Investigation
• NCS
• Increased motor latency in active forceful supination
• Injection of local anaesthetic into radial tunnel
• Tennis elbow
Management
• Conservative, anti inflammatories, avoidance of repetitive provoking activities
• Surgical, decompression. Internervous plane between ECRB and E Digitorum developed.
PIN found just proximal to arcade of Frohse.
Wartenberg Syndrome
• Described in 1932- isolated neuritis of superficial sensory branch of radial nerve
• As it winds out from deep fascia beneath brachio-radialis, to be superficial to ECRL
• Both tendons may act as scissors entrapping the n
• Pain & parasthesia over the distribution of RSN; y with hyperpronation + Tinel’s sign
• Treatment- local steroid injection, surgical exploration and release.
Nerve Entrapments in Lower Limb

NE R V E SITE CAUSE SYMPTOM
ILIO-INGUINAL Hypertrophied abdominal ms Intense training Pain & parasthesia
OBTURATOR Hip adductor Skaters Medial thigh pain
FEMORAL LAT. CUT. ASIS Tight belt Lateral thigh pain
Meralgia paresthetica
SCIATIC Ischial tuberosity, pyriformis ms Pyriformis Sciatica
SAPHENOUS Hunter’s canal Quad or sartorius Infero-medial knee pain
COMMON PERONEAL Fibular head Direct blow Foot drop
SUPERF PERONEAL 12 cm above Lat.Maleolus, as it Inversion injury Dorsal foot pain &
pierce the deep fascia paresthesia
SURAL 12 cm distal to Lat Malleolus Jone’s fr Lat. foot parasthesia
DEEP PERONEAL Inf. extensor retinaculum Inversion injury Sole pain & parasthesia
(anterior tarsal tunnel $)
POSTERIOR TIBIAL Flexor retinaculum FDL accessorius, RA, Sole pain & paresthesia
(Tarsal tunnel $) tumors, ganglion
1ST LAT.PLANTAR Bet AHL fascia, quadratus plantae High heels Plantar fasciitis
MEDIAL PLANTAR Henry Knot (cross of FDL & FHL) Orthotics Big toe pain & parasthesia
INTERDIGITAL Bet MT3-4 plantar to deep MT lig Push phase in runners Digital pain, parasthesia,
(Morton’s Neuroma) dead toe
Thoracic Outlet Syndrome

• Impingement of subclavian v v, and lower trunk (C8 /T1) of
brachial plexus
• Boundries: scalenus anterior and medius, and the 1st rib
• Age 18-40 (never before puberty rare after 50yr)
Aetiology:
1]. Neck:
o Cervical Rib ......... 10 % will have TOS
o Fibrous bands
o Scaleneus anterior constriction
2]. Shouder
o G VI Acromio-clavicular dislocations & Clavicular fractures
o In some cases, y by recurrent anterior shoulder instability, μß Æ Dead Arm $
3]. Pancoast tumour
Examination::
1]. Tenderness or mass in supra-clavicular fossa
2]. Lower trunk C8/T1 manifestation:
3]. Sensory changes in the Ring and Little finger
4]. Intrinsic weakness
5]. Vascular Examination
o Radial pulse obliteration + Reproduction Of Symptoms is specific (radial alone is not)
Provocative Tests
1. Adson’s TEST
o Arm of the affected side adducted with forearm supinated
o Turn head toward the affected side
o Extend neck and hold breath
o Positive test is obliteration of the radial pulse
2. Reverse Adson’s TEST
o As above but head turned away from the affected side
3. Wright’s test (Hyperabduction stress test)
o Axillary vessels and plexus bent 90º at the junction of the glenoid and humeral head
o Place extremity in full abduction, external rotation and reach back as far possible. Turn
head away and check for decrease or loss of radial pulse
o Creation of a bruit in the supraclavicular area is further evidence
4. Roos overhead exercise test
o Above head repeated forearm exercise may reproduce symptoms
Investigations:
1- X-ray -Cervical ribs may be seen but more commonly the cause is a fibrous band (not seen)
2- CXR to rule out pancoast tumour
3- MR scan to exclude cervical disc disease
Treatment
1- Non-Operative (for At Least 4 Months)
o Postural re-education
o Activity modification
o Weight loss
2- Operative (rarely required)
o Excision of first rib with fibrous band and anterior scalene muscle via supra-clavicular,
subclavicular or axillary approach

The Shoulder
Dr Mohamed Sobhy
Quick Guide
•Anatomy
•Examination
•Radiological views
•Rotator Cuff
•Instability
•SLAP
•Frozen Shoulder

[The Shoulder] Page | 483
Applied Anatomy
BONES
Scapula
• Body is formed by intramembranous ossification
• Glenoid has 2 ossific centers ................... Failure of inf centre formation Æ 1ry glenoid dysplasia
• Glenoid has thicker cartilage to the periphery & thin in centre - making it congruent
• It has a smaller surface than head ........ y mobility.
Acromion
• Acromion has 2 ossific centers ................ Failure of fusion Æ os acromiale.
• Humans & chimpanzees are the only animals with an acromion
• Acromion provides a platform for a powerful deltoid but impedes repeated overhead activities
Proximal Humerus
• Epiphysis has 3 ossific centers ................ head, greater & lesser tuberosities.
• The centre of head rotation .................... medial & posterior to shaft
LIGAMENTS
1]. Coracohumeral ligament (CHL)
• Very strong thickened fold of the shoulder capsule
• From lat border of coracoid base, as a continuation of
pec minor tendon & divides into 2 bands:
a) One band inserts into GT
b) One band inserts into LT
• Primary restraint to inferior translation &ER
• Equivalent to Y ligament of bigelow at hip joint
2]. Superior Glenohumeral ligament

• Arises from glenoid labrum at 1 o' clock.
• Joins CHL & form the internal reflection of the pulley for LHB
3]. Middle Glenohumeral ligament

• Courses obliquely from 2 o' clock to attach to LT
• Outpouching of capsule above this lig. Forms the subscapular recess
4]. Inferior Glenohumeral ligament Complex

• MOST IMPORTANT ligament in preventing anterior dislocation; it acts as a Hammock
• Arises at 4 to 8 o' clock on glenoid
• In ER, IGHL moves anteriorly .................. z anterior humeral head translation; and vice versa
• In the abducted neutral position ........... IGHL tightens inferior to the joint
• In IR, IGHL moves posteriorly .................. z posterior translations of the humeral head
5]. Coraco-Acromial Ligament

• Pec minor tendon separate it into 2 bands from tip and base of coracoid to the acromion tip
• Any shoulder movement dysfunction causes strain of CAL causing it to hypertrophy, leading to

spur formation, leading to impingement.
Articulations (5 articulations)
1]. Gleno-humeral
2]. Acromio-clavicular
3]. Sterno-clavicular
4]. Pseudo joint between the head and coraco-acromial ligament
5]. Scapulo-thoracic articulartion
484 | Page [The Shoulder]
Glenoid inclination and retroversion
o Retroverted ..................................6º
o Inclined superiorly ....................6º
o Scapula anteversion .................30º
NERVES
1]. Axillary n. passes into quadrilateral space with post. circumflex humeral a & v and if compressed
there (Quadrilateral $)................................ axillary palsy
2]. Musculocutaneous n. ................................ enters the conjoined tendon 2cm distal to coracoid
3]. Suprascapular n. ........................................... passes below the transverse ligament & the art. above it.
• Gives 2 branches to supraspinatus
• Passes around the spine of scapula at the spinoglenoid notch to supply infraspinatus
BLOOD SUPPLY (of Humeral Head)

1]. Ascending br of ant circumflex artery (main blood supply); passes lat to long head of biceps &
forms ARCUATE A as it penetrates bone & gives branches to lesser and greater tuberosities
2]. Posterior circumflex artery supplies only a small area in posteroinf aspect of the humeral head
Rotator cuff muscles are:

• Supraspinatus...............................................Bipennate (supra-scapular n.)
• Infraspinatus ................................................Bipennate (supra-scapular n.)
• Subscapularis ...............................................Multipennate (upper & lower subscapular n.)
• Teres minor ..................................................Bipennate (axillary n.)
• Some add biceps tendon (LHB)
Kinematics
• First 30º abduction:
o Mainly at gleno-humeral joint
o Little motion at sterno-clavicular joint
• 30-90º abduction:
o 2/3 of motion comes from gleno-humeral joint
o 1/3 comes from scapulo-thoracic motion
• 90-180º elevation
o Mainly scapulo-thoracic
o Associated gleno-humeral ER so the greater tuberosity clears from the acromion
o ACJ moves during the last 60º of abduction
o SCJ moves during shrugging & protraction
Codman's Paradox:
• Complete elevation in coronal plane ... ER
• Complete elevation in sagittal plane .... IR
INDIVIDUAL JOINT MOTION

1]. Gleno-humeral joint
1. Rotation
2. Translation (gliding)
3. Rolling (combination of rotation & translation)
2]. Acromio-clavicular joint (plane, synovial joint with meniscus
1. Forward rotation........................................ constrained by conoid ligament
2. Backward rotation .................................... constrained by the trapezoid lig.
3. Axial rotation .............................................. constrained by both lig
3]. Sterno-clavicular joint (synovial joint, meniscus)
1. protraction/retraction ............................. constrained by CCL & SCL
2. elevation/depression ............................... constrained by subcalvius muscle
3. rotation .......................................................... constrained by both
4]. Scapulothoracic articulation
1. protraction/retraction
2. elevation/depression
3. rotation
• The lack of true joint allows for the wide range of shoulder motion
• The range of glenohumeral to scapulothoracic motion is 2:1
• scapula twists at maximal arm elevation (coracoid moves up)
Shoulder Examination Special Tests

TEST TECHNIQUE SIGNIFICANCE
IMPINGEMENT
1]. Impingement sign Passive FF >90 degrees Pain = impingement syndrome
2]. Impingement test Same after subacromial injection Relief of pain = impingement syndrome
3]. Hawkin test Passive FF 90 degrees and IR Pain = impingement syndrome
4]. Jobe test Resisted pronationlFF 90 degrees Pain = supraspinatus lesion
5]. Drop arm test Maintain FF in plane of scapula Inability = supraspinatus lesion
6]. Hornblower segn Resisted max ERJabd 90 degrees Pain = infraspinatus/(post) supraspinatus lesion
7]. Rubber band sign Resisted max ER/slight abd Pain = infraspinatus lesion
8]. Lift off test Arm lR behind back Inability to elevate from back = subscapularis lesion
9]. Modified lift off Resisted arm held off back Inability to keep elevated off back = subscapularis lesion
10]. Belly push Elbow held ant with abd pressure Inability to hold elbow forward = subscapularis lesion
INSTABILITY
11]. Apprehension Supine abd 90 degrees and ER Apprehension = ant instability
12]. Relocation test Apprehension é posterior force Relief of apprehension = ant instability
13]. Load & shift Ant/post force on humeral head degree of translation = laxity vs. instability (see grading)
14]. Modified load & shift Supine load /shift with elbow bending degree of translation = laxity vs. instability (see grading)
15]. Jerk test Post force é arm addr and FF “clunk” = posterior subluxation
16]. Sulcus Inferior force é arm at side increased acromiohumeral interval = inferior laxity vs.
instability (see sulcus grading)
LABRUM / BICEPS
17]. Active compression 10º add. 90º FF max pronation pain with resistance = SLAP lesion
18]. Anterior slide test Hand on hip, joint loading pain with resistance = SLAP lesion
19]. Crank test Full abd, humeral loading, rotation pain = SLAP lesion
20]. Speed test Resisted FF in scapular plane pain = bicipital tendonitis
21]. Yerguson test Resisted supination pain = bicipital tendonitis
MISCELLANEOUS
22]. Spurling test Lat. flexion, rotation. cervical loading Cervical spine pathology
23]. Wright’s test Ext-abd-ER arm é neck rotated away Loss of pulse and reproduction of sx = thoracic outlet $
Radiological Views
EXAM FINDING SIGNIFICANCE
1].Out let View Acromial morphology (type I-Ill) Type Ill acromion associated with impingement
2].30º Caudal Tilt Subacromial spurring Area below level of clavicle = impingement area
3].Zanca 10º cphalic tilt AC joint pathology AC DJD, distal clavide osteolysis
4].West Point Anteroinferior glenoid evaluation Bony Bankart lesion seen with instability
5].Garth view Anteroinferior glenoid evaluation Bony Bankart
6].Stryker Notch Humeral head evaluation Hill-Sachs impression fracture
7].AP IR Humeral head evaluation Hill-Sachs defect
8].Hobbs view Sternoclavicular injury AP dislocations
9].Serendipity view Sternoclavicular injury Ant-post dislocation
10].45º abd true AP Glenohumeral space Subtle DJD
11].Arthrography Rotator cuff injuries Dye above cuff = tear
12].CT Fractures Classification easier
13].MRI Soft-tissue evaluation Labral, cuff, muscle tears
Sprengel’s Deformity
Definition:
• Failure of scapular descent. It is the most common pediatric shoulder deformity
Pathology:
• Scapula is small, wide, high, and medially rotated
• Clavicle sometimes affected
Associated With
1]. Omovertebral bar: fibrous or cartilagenous bar that connects scapula to spine
2]. Klipple Feil $
3]. Scoliosis
4]. Diastematomyelia
Diagnosis:
1]. Lennie’s test (See later)Æ shoulder asymmetry .......... sometimes bilateral
2]. Scapula: small, high, winged ............................................. sometimes the clavicle is affected
3]. L ROM & on abduction or elevation, scapula moves very little or not at all
Treatment:
Rational
• Best performed 3-6y
• Avoid injury to the accessory nerve or the brachial plexus.
• Indications:
a. Severe limitation of motion
b. Cosmetic
Operations
1]. SCHROCK GREEN: entire scapular dissection + supraspinous and bar excision + move down the
scapula and INF. POLE IS ANCHORED TO A RIB
2]. OBER’S STAGED OPERATION: Release Æ SKELETAL TRACTION Æ soft tissue anchor to bone; gradual
correction gives chance for less axillary traction
3]. WITTEK’S SCAPULOTOMY: cut ½ inch lat. to med.border, and move the scapula down, so the inf.
pole is inserted into a LATTISSMUS DORSI POCKET, and cut the excess supero-medial angle
4]. GREEN: entire sub-periosteal dissection + omovertebral bar & supraspinous excision. Move the
scapula down, reattach the muscles into inferiorizing positions + skeletal traction
5]. WOODWARD: subperiosteal dissection of ms attached to the spinous process. Excise the bar,
enlarged supraspinous part, and periosteum. Trapezius and rhomboids are reattached into a
lower spinous processes.
Congenital Clavicular Pseudoarthrosis

• Thought to be ð pressure by the subclavian artery on the developing bone
• Mid shaft painless lump
• Right sided usually except with dextro cardia
• ttt: Heals after excision and BG
Supraspinatus Tendinitis
Definition:
Non infectious inflammation of one or more of the rotator cuff tendons, secondary to
•
abnormal contact and compression of the rotator cuff under the coracoacromial arch
Epidemiology
• More over 40 y
• More in overhead athlete
• More in overhead workers
Anatomical consideration:
• Rotator cuff muscles are:
1. Supraspinatus (SS)
2. Infraspinatus (IS)
3. Teres minor (TM)
4. Subscapularis
• Types of the acromion:
According to shape (Bigliani) According to thickness
Type I ............................Flat Type A ......................... < 8 mm
Type II ..........................Curved Type B ......................... 8-12 mm
Type III .........................Hooked Type C .......................... > 12 mm
• Os-Acromiale is non-united acromial ossific centre Æ hypermobile Æ impingement
• Supraspinatus outlet is bounded by:
1. Coracoacromial arch superiorly: formed by the acromion, coracoid, and the CA ligament
2. Acromio-clavicular joint anteriorly
• Vascular supply of the rotator cuff:
1. Suprascapular artery.
2. Anterior circumflex humeral artery.
3. Posterior circumflex humeral artery.
4. Thoraco-acromial artery.
5. Subscapular artery.
• The critical zone = hypovascular zone of the rotator cuff
• 1cm medial to bony attachment
• Area of anastomosis and limited potentiality for healing
• Vascularity of this part depends on arm movement; elevation squeeze the vv Æ z filling
Biomechanics
• Normally during abduction the rotator cuff slides under the coracoacromial arch
• Beyond 90º abd there is added ER Æ allow RC to occupy widest part of subacromial space.
Aetiology:
Pathogenesis:
• When the arm is held persistently in abduction and then moved to and fro in IR and ER, the rotator
cuff is compressed against the anterior edge of the acromion
• Abduction, flexion, and internal rotation impose the maximum stress on the rotator cuff and this
position is called the impingement position
• Mainly the impingement occurs at the critical zone of vascularity; i.e. 1cm prox to tendon insertion
• INTERNAL IMPINGEMENT = dynamic compression occur between the postero-superior labrum and the
HH (humeral head) especially in ABER athletes
• ROTATOR INTERVAL TEAR = Tear or laxity of the interval between the Supraspinatus and
subscapularis tendons
• SUBCORACOID IMPINGEMENT = overhang coracoid impinge anteriorly on head during flexion IR. Dx
by CT in cross chest position. Ttt by coracoid recession and reattachment of conjoint tendon
Pathology:
1]. TENDONOPATHY STAGE: ...................................................(WEAR)
• It is the mildest type of injury and occurs in the form of swelling, oedema, and frictional bursitis
• y cell apoptosis, degeneration
• y glycosaminoglycans
• Usually self limiting
2]. TEARS ..................................................................................(TEAR)
• Occurs as a result of prolonged insult to the rotators
• In young age: Acute micro tears heal by scarring & fibrocartilaginous metaplasia or calcification
• In older age: Chronic partial or complete tears
3]. HEALING .............................................................................(REPAIR)
• Vascular reaction and granulation followed by fibrosis
• y collagen III
• Local congestion of the healing process may contribute to the further impingement
4]. SECONDARY ARTHROPATHY:
• Neglected large tears eventually leads to mechanical disturbance with upward migration of the
humeral head and abutting against the acromion
• Abduction is severely restricted
• OA of the glenohumeral joint is inevitable
• Occasionally it is rapidly distructive “M MILLWAUKEE SHOULDER”
Young Middle Old

Wear & pain +++ + Painless
Tear Acute micro tears Chronic +++ (Partial or complete)
Repair Rapid and Painful Less painful Never Heal
Classifications:
ROSSI Classification for partial tears & Impingement:

1]. Bursal Tear
2]. Interstitial Tear
3]. Articular = PASTA (Partial Articular SS Tendon Avulsion)
4]. PSGI = Internal impingement = Postero-Superior
Glenoid Impingement
5]. Subcoracoid impingement $ (ð overhang coracoid)
ELLMAN Classification of Rotator cuff Tears
1]. Transverse
2]. Crescent
3]. L-Shaped
4]. Reverse L
5]. Trapezoid
6]. Massive irreparable
Diagnosis:
Clinically: .................................................................................... See Page 4 for Special Tests
1].STAGE OF ACUTE TENDINOPATHY
1]. PAIN:
Antero-lateral shoulder pain
o
Insidious onset, progressive course
o
o More at night
o y with over head activity
2]. PAINFUL ARC between 60º-120º abduction
3]. TENDERNESS over the anterior edge of the acromion
4]. +VE IMPINGEMENT SIGN: pain with F AB IR
5]. +VE IMPINGEMENT TEST: 10 ml Lidocaine injection into the subacromial space and repeat the
previous test it becomes -ve
2].STAGE OF CHRONIC TENDINOPATHY Rotator Interval Tear
1]. PAIN: • Torn capsule between SST &
1. Recurrent attacks of anterior shoulder pain subscapularis ð forced IR force
2. worse at night • Clinically:
3. z by lying upright 1]. z ER
2]. STIFFNESS 2]. Instability
3]. CREPITATION and snapping while moving the shoulder 3]. Biceps tendinopathy
4]. z ADL • PXR: ± lesser tuberosity cyst
5]. -VE ARM DROP sign • MRI: Torn RI, corcoid bursitis, SGHL
3].STAGE OF CUFF TEAR or CHL tears, LHB tendinitis
1]. PAIN: Refractory chronic pain • MRI Arthrography: leak of dye
2]. STIFFNESS
3]. WASTING of supra & infraspinatus
4]. -VE ARM DROP ......................................................................................partial tear (DDx chronic tendonitis)
5]. +VE ARM DROP =abduction paradox ........................................complete tear
6]. LOST ABDUCTION even after subacromial injection ..............Complete tear
7]. Biceps tendonitis
8]. AC tenderness
9]. Severe gleno-humeral OA and painful restricted ROM
PXR:
• Early: No changes
• Later: sclerosis and cyst formation
• Late:
Humeral head migration ..................<7mm subacromial space is risky
1.
AC OA
2.
Gleno-humeral OA
3.
Os Acromiale, Hooked acromion
4.
Calcification of Supraspinatus tendon
5.
Arthrography
• Reveal full thickness tear
• Reveal partial thickness humeral tear
US
• Reveal tears but it is operator dependant
MRI
• The most effective method to detect:
1. Cuff tendonopathy
2. Cuff tears
3. AC pathology
4. Biceps tendonopathy
5. Coraco-Acromial arch anatomy
DDx
1]. Adhesive capsulitis .............................................Frozen shoulder, MRI thick capsule
2]. AC OA ......................................................................Anterior pain, local injection relief test, PXR
3]. SLAP lesions vs PSGI lesion ..............................+ve speed test
4]. Bennet lesion (post extra articular ossification adjacent to labrum) secondary to labral or capsular
tears ..........................................................................Painful F Add IR, MRI & MRI arthrography
5]. POLPSA lesion (posterior ALPSA) .................Posterior pain & instability, MRI
Treatment:
• Conservative
1. Activity Modification
2. Resting sling
3. Physiotherapy
4. NSAIDs
5. Local steroid inj
• Surgical:
o Indications:
i]. Young active pt
ii]. Failed conservative ttt for 3 mo
iii]. Signs of cuff tear
iv]. Recurrence
o Rationale:
i]. Decompression (acromio-plasty & bursectomy)
ii]. Recession of the coraco-acromial lig
iii]. Repair of the cuff tear
iv]. AC joint recession
o Techniques:
i]. Open: via anterior approach and deltoid split,
Expose the coracoacromial lig, then excesie the ant acromion
Corcaoacromial recession
Inspect the cuff and repair any tears
AC resection of protrusions, and if severe OA Æ distal clavicular resection
Reattachment of the deltoid is mandatory by any mean
ii]. Arthroscopic follow the same objectives, but no deltoid is split
o After care: ................................................Sling for 4-6 wk

st
i]. Passive pendulum ..................... 1 wk
nd
ii]. Passive supine flexion .............. 2 wk
rd
iii]. Passive over head motion ..... 3 wk
th
iv]. Active assisted (wall walk) ...... 4 wk
th
v]. Passive behind back T8 ........... 5 wk
th
vi]. y abduction & IR to 60º ......... 6 wk
th
vii]. Active abd & flex ....................... 7 wk
th
viii]. Isometric strengthening ......... 8 wk
th
ix]. Isotonic strengthening ........... >8 wk
Shoulder Instability
Definition
• Loss of the normal joint relationship among any of its parts; or in relation to the surrounding.
Anatomical Considerations: (Shoulder stabilizers)
1]. Passive:
a. JOINT CONFORMITY: articular surfaces match
b. JOINT GEOMETRY: Head retroversion + scapular inclination + glenoid retroversion
c. FINITE JOINT VOL: minute + closed joint space + minimal fluid Æ difficult distraction
d. SYNOVIAL ADHESION: high surface tension Æ y molecular & intermolecular attraction Æ
difficult separation between glenoid and humeral head
e. SYNOVIAL COHESION: molecular attraction makes synovial fluid molecules remain together
f. LABRUM: deepens the joint ~ 5-10mm, & gives GHL attachment
g. LIGAMENTS: SGHL, MGHL, IGHL, CHL PF FOR RECURRENCE
h. CAPSULE 1].Flat, mal positioned glenoid
2]. Active: 2].Thin lax capacious capsule
a. Rotator cuff: pull the head back into the glenoid 3].y Labral compliance
4].Weak rotator cuff
LHB: • IR Æ y tension of LHB Æ z ant translation
b.
5].Poor neuromuscular control
• ER Æ z posterior translation 6].Voluntary malpositioning
c. Proprioception: guards against extremes of motion
d. Scapular Rotators tone i.e. trapezius, lattissmus, serratus, rhomboids, & levator
Ætiology:
MATSON CLASS TUBS AMBRI
Aet Traumatic Atraumatic joint laxity
Path Uni-directional Multi-directional
Unilateral Bilateral
Bankart Recurrent
Treat Surgical Rehabilitation = Inferior cap shift & Interval closure
Pathology: (Anterior Dislocation)
MACROSCOPICALLY:
• Labral tear according to the pre-mentioned type ................................................usually antero-inferior
• Glenoid osteo-chondral fracture Æ inverted pear shaped glenoid .............in bony Bankart
• Hill Sachs Lesion: Postero-lateral superior humeral impaction # ....................anterior dislocation
• Reversed Hill Sachs: same but in ..................................................................................posterior dislocation
• ± soft tissue inj e.g. RC, RI, LHB, or axillary n, or any axillary plexus injury
CLASSIFICATION OF LABRAL TEARS:
LESION DESCRIPTION TRAUMA
1]. Bony Bankart Anterior Glenoid rim # + its capsular & lig attachments Anterior Dislocation
2]. Bankart Lesion Anterior labral + IGHL avulsion + periosteal disruption Anterior dislocation
3]. Perthes Lesion Same but with intact periosteum Anterior dislocation
4]. ALPSA Anterior Labro-ligamentous Periosteal Sleeve Avulsion Anterior dislocation
5]. POLPSA Posterior Labro-ligamentous Periosteal Sleeve Avulsion Posterior dislocation
6]. HAGL Humeral Avulsion of Gleno-Humeral ligament Anterior dislocation
7]. BHAGL Bone Humeral Avulsion of Gleno-Humeral ligament Anterior dislocation
8]. Reverse HAGL Same injury occurs to the posterior stabilizers Posterior dislocation
9]. SLAP Superior Labrum anterior to posterior tear Fall on stretched hand
10]. GLAD Glenoid Labrum Articular Disruption (labrum in place) Anterior subluxation
COMPLICATIONS:
1]. Recurrence .......20%
2]. Vascular .............subclavian a & v
3]. Axillary plasy .... DDX QUADRILAT SPACE $
Diagnosis:
Epidemiology (young active male)
Symptoms
• History of dislocation,
If not ask about: seizure or electric shock ........ especially in posterior dislocation
• Pain and catch é ABER (over head activity) .... DEAD ARM syndrome
• Recurrence 20% .......................................................... Hill Sachs or bony Bankart
• Complications .............................................................. vascular, axillary palsy
Signs ................................................................................. See Page 4 for special tests
1]. +ve apprehension test
2]. Jobe relocation test
3]. Jerk test
4]. Load & shift - Modified load & shift
5]. Sulcus sign
Grading
ANTERO-POSTERIOR GRADING SCHEME
Go Normal amount of translation
G1 Translation to glenoid rim
G2 Translation over glenoid rim
G3 Translation + Locking over glenoid rim
SULCUS GRADING SCHEME
G1 Acromio-Humeral interval <1cm
G2 Acromio-Humeral interval 1-2 cm
G3 Acromio-Humeral interval > 2 cm
PXR:
• Views: West Point/Garth/Stryker/AP IR ........... See Page 4 for the PXR views
• Axillary or Y views for missed posterior dislocations
• Associated Hill Sachs, Reversed Hill Sachs, or glenoid fractures
CT For associated fractures & Posterior dislocations, Hill Sachs, Reversed Hill Sachs
MRI Most sensitive & specific
DD:
• Adhesive capsulitis .................................................... painful restriction, 3 stages, limited ER
• RCT & RIT (rotator cuff & rotator interval) ....... no dislocation event, older age, impingement
Treatment:
OPEN PROCEDURES FEATURE REMARKS
1].Bankart Reattachment of labrum & IGHL to glenoid Gold Standard
2].Putti Platt Subscap advancement z ER & OA
3].Capsular shift Inf capsule shifts superior “Pant over vest” Over tightening, Gold st for MDI
4].Magnuson Stack Subscapularis transfer to greater tuberosity z ER
5].Boyd-Sisk Transfer of biceps lat & posterior Non anatomic Æ recurrence
6].Staple capsulorraphy Capsular reattachment and tightening Staple migration
7].Bristow-Latterjet Tip of coracoid transfer to inf glenoid Nonunion, migration, labral tears
8].Trillat All coracoid transfer to inferior glenoid Non union
9].Bone Block osteotomy Anterior bone block Nonunion, migration, articular injury
ARTHROSCOPIC PROCEDURES
10].Knotted anchors Reattach labrum & capsule to glenoid Gold standard
11].Knotless Anchors Same é strong hold without knots Difficult
12].Capsular shrinkage Anterior capsule radiofrequency shrinkage Heat induced necrosis
Posterior Instability
Ætiology:
1]. Violent jerk in abnormal position
2]. Epileptic fit
3]. Electric shock
Pathology:
• Posterior capsule ......................................... stripped or stretched
• Humeral head .............................................. indentation anteriorly = reversed Hill-Sachs
• ± proximal humeral .................................... fracture
• Recurrent subluxation .............................. 50% in flexion IR positions Æ +ve drawer, apprehension
Clinically
• Rare and often missed
• Pain in external rotation
1]. Arm held in IR and maneuvers to ER are painful
2]. +ve posterior drawer ................................. 1 hand hold spine & coracoid, & 1 hand holds the head
3]. +ve apprehension test .............................. flexion, IR + axial loading on elbow Æ pain
PXR
• LIGHT BULB = end on appearance of the proximal humerus ð IR
• Axillary view in abduction is ideal for diagnosis
• Lateral scapular Y view also is diagnostic
CT is diagnostic, assess glenoid inclination and retroversion
MRI is sensitive for labral, capsular, ligamentous assessment
Treatment
1]. Muscle strengthening
2]. Activity modification to avoid the vulnerable positions
3]. Surgery if:
o Uncontrollable laxity
o Disabling condition
o Emotionally stable patients only
• Modalities:
a. Post bone block ............................ with capsular repair
b. Reversed Putti-Platt ...................... TM & IS advancement
c. Humeral or glenoid osteotomies if glenoid retroversion is seen on CT
• After care: arm is held in spica in abduction ER for 6wk
Multidirectional Instability
Ætiology: AMBRI ..................................................... see before
Pathology:
• Capsule ............................................................ thin & lax
• RC ....................................................................... weak
• Labrum ............................................................ y compliance
• Glenoid ............................................................ shallow
Clinically
1]. Little force is required for displacement, even with little stressful activities
2]. Generalized laxity may be notices
3]. +ve anterior & posterior drawer ........... 1 hand hold spine & coracoid, & 1 hand holds the head
4]. +ve apprehension test .............................. flexion, IR + axial loading on elbow Æ pain
Treatment
1]. Muscle strengthening
2]. Activity modification
3]. Inf capsular shift + interval closure ...... rarely indicated
Slap Lesion
Definition:
• Superior Labral Anterior to Posterior lesion
Epidemiology
• Usually following fall on out stretched hand
• Young male
Pathologic Classification
PATHOLOGY TREATMENT
GI Degenerative fraying Debridement
G II Detached superior labrum + biceps anchor Stabilization
G III Bucket handle sup labrum + intact biceps Debridement
G IV Bucket handle sup labrum + biceps anchor Stabilization ± biceps tenodesis
GV SLAP extends to ant labrum Stabilization
G VI SLAP extends as superior flap tear debridement
G VII SLAP extends to MGHL Stabilization
G VIII SLAP extends to posterior labrum Stabilization
G IX SLAP extends circumferentially Stabilization
Diagnosis:
Clinically: Buford Complex:
• Bicepital groove tenderness o Antero-sup labrum is absent + cord like MGHL
• +ve Speed’s test Sublabral Hole:
• +ve Yerguson’s test o Antero-sup labrum exists without osseous attachement
• +ve Crank test Biceps Subluxation:
• +ve O’Brien’s test o Usually associated é subscap tears, or transverse humeral lig tear
PXR: o Palpable click felt é abd ER
• For associated lesions o ttt: strengthening, release, groove deepening, or tenodesis
MRI Bicepital tendinitis and tears
• Diagnostic o Usually secondary to RC disease
Treatment: o Tender bicipital groove é IR & ER + speed & Yerguson
• NSAIDs o ttt: tenodesis (trans-osseous, Key-hole technique, anchors)
• Activity modification
• Physiotherapy & ms
strengthening
• Surgical stabilization & reattachment of the detached labrum
Snapping Scapula
• Is painful scapulo-thoracic crepitus associated with arm elevation
• Many causes:
1]. Traumatic non & mal united scapular fractures
2]. Inflammatory subacromial bursitis
3]. Tumors: osteochondroma of subscapular fossa
4]. Scapulo-thoracic dyskinesia
• Pain is relieved by manual stabilization of the scapula
• PXR: scapular tangential Y view to exclude osteochondroma
• Treatment:
o Scapular strengthening
o NSAIDs
o Local injections
o Arthroscopic bursectomy
o Medial border excision
Adhesive Capsulitis
Frozen Shoulder
Definition
• Must be reserved for a condition é progressive idiopathic painful restriction of shoulder
movements ð fibrovascular proliferation and subsequent fibrosis, which resolve spontaneously
Epidemiology
• 40-60y
• More in females
Aetiology:
1]. DM 2]. Hyper lipidaemia
3]. Trauma 4]. Chest or breast surgery
5]. Neurosurgeries 6]. Prolonged immobilization
7]. Thyroid disease 8]. Dupuytren’s disease
Pathology: ..........................................................................3 phases (6-9 mo each)
• Fibrovascular infiltration followed by wide spread fibrosis at:
o Rotator interval .....................................RI
o Coraco-Humeral ligament ............... CHL
o Anterior capsule ...................................AC
• PHASE PATHOLOGIC FEATURES CLINICALLY

1]. Active phase Inflammatory fibrovascular infiltration of RI, CHL, AC Painful
2]. Freeze phase Wide spread fibrosis at RI, AC, CHL Marked stiffness
3]. Thaw phase Fibrosis cease and fibrovascular tissue production z Regain ROM & pain z
Diagnosis:
Clinically:
• Symptoms:
1. Progressive pain after trivial trauma, usually more at night
2. z ROM as the pain ameliorates
3. When pain disappears Æ ROM is regained Frozen Shoulder Triad
• Signs: 1]. Painful restricted motion
1. Wasting of shoulder ms 2]. Triphasic history
2. Mild tenderness 3]. Normal PXR
3. Marked limitation of passive and active movements
PXR:
• Late disuse osteopenia and exclude other causes
MRI
• Thickened anterior capsule and RI
DD: other conditions must be excluded first before diagnosis of frozen shoulder
1]. Infection ..................................................................at first 2 days may be not evident
2]. Trauma ....................................................................Pain starts maximum then decrease
3]. Disuse stiffness .....................................................prolonged immobilization, pain with motion only
4]. RSD ............................................................................ Trophic and vasomotor changes
Treatment:
1]. NSAIDs + Reassurance
2]. Regular pendulum exercises
3]. Steroid injection
1 2 3 4 5
4]. Manipulation UGA: Flexion Æ ER Æ Abd ER Æ Abd IR Æ Cross Chest Æ inj Æ early ROM
5]. Distension therapy: 200ml saline inj under pressure (both methods rupture the capsule)
6]. Open or arthroscopic release of RI, CHL, AC
Complex Regional Pain Syndrome (CRPS)

• An abnormal sympathetic firing 2ry to minor injury
• Synonyms: Reflex Sympathetic Dystrophy (RDS)= Sudeck's Atrophy = Causalgia
Aetiology:
1]. Minor trauma out of proportion 4]. Brain & cord lesions
2]. Surgery 5]. Infections
3]. Myocardial infarction 6]. Repetitive trauma e.g. carpal tunnel.
Pathology:
1]. ACUTE STAGE Swollen, red, warm, and dry skin
AGGEEE
G
2]. DYSTROPHIC STAGE Allodyna & trophic changes & cool cyanotic skin
A
STTTA
3]. ATROPHIC STAGE Wasting, Osteopenia; Glossy, pale, cool skin

1]. MINOR CAUSALGIA Purely sensory nerve to distal portion of limb
D
ASSSSS
D
RD
S
2]. MINOR TRAMATIC DYSTROPHY Most common type

ORR
D CLLA A
O
GFFFO
L
3]. MAJOR CAUSALGIA Partial injury to a major proximal mixed nerve

C
NGG
OLLDD
ANN
4]. MAJOR TRAUMA DYSTROPHY Trauma produces swelling, redness, pain; eg crush inj & colles
L
A
LA
O
5]. SHOULDER HAND $ Prox trauma or painful lesion (shoulder injury, cx disc)
CRPS TYPE I (RSD) Classic CRPS after a noxious event
ASSSSSS
W
NEEEWW
A
CRPS TYPE II (CAUSALGIA) Features of peripheral nerve lesion

CLLA
C L
Diagnosis ............................................................. weeks to years é remission and exacerbation

I. Pain – The hallmark is pain and z ROM
1]. Severe, constant, burning or deep aching pain.
2]. ALLODYNIA: All tactile ⊕ of the skin are painful even a light breeze
3]. HYPERPATHIA: repetitive tactile stimulation e.g. tapping y pain + prolonged after-sense
4]. MS TRIGGER POINTS = MYOFASCIAL PAIN $ = point-tender spots in the ms ð ms spasms
5]. PAROXYSMAL LANCINATING PAINS & sharp pain jabs in the affected region
6]. DYSESTHESIAS: either warm or cold perception of touch or even without touch
II. Skin: All may y é changes in the room temperature, especially cold environments
1]. SHINY, ŒDEMATOUS: pitting brawny, y é tying bands around the limb (done for comfort)
2]. VASOMOTOR Changes: chromatic changes; white mottled, red, or blue appearance
3]. SUDOMOTOR Changes: y sweating or chilling of the skin
4]. PILOMOTOR Changes: GOOSE FLESH
st
5]. HAIR & NAILS initially grows coarse and then thins out Æ brittle (1 fast growth= RDS)
6]. RASHES, scales, ulcers and pustules μβ life-threatening recurring infections Æ amputation
III. z ROM ð:
1]. Associated pain 4]. TREMORS and jerking
2]. DISUSE ATROPHY 5]. CRAMPS: sudden incapacitating
3]. DIRECT of CRPS on ms 6]. DYSTONIA: y ms tone Æ ms relaxation
IV. SPREADING Symptoms:
MMA AALLLEEEKKIII
K CONTINUITY TYPE Spread upward e.g. from hand to shoulder
SSPPPRRREEEAAD
A D
D MIRROR-IMAGE TYPE Spread to the contralateral limb
PPAATTTTTTEEER
A RRN
NNSSS INDEPENDENT TYPE Spread to a distant region of the body.
Investigations:
• PATCHY OSTEOPOROSIS on PXR
• Triphasic Tc is specific Æ diffuse tracer uptake
• Sympathetic stellate ganglion block
Treatment
1]. Sympathetic Block (stellate ganglion)
2]. Active ROM exercises 3]. Vasodilators
4]. Steroids. 5]. Treatment of the cause
Winging Scapula
Causes:
1]. Bony abnormality: (scapula, ribs, spine)
a. Osteochondroma
b. Malunited fracture
2]. Muscle:
a. Contracture
b. Dystrophy (FSHD)
c. Elasto-fibroma-dorsi (female, 50y, may be bilateral)
3]. Intra-articular pathology
4]. Nerve injuries:
NERVE AFFECTED MS WINGING DIRECTION TREATMENT
Long thoracic Serratus Medial ( protraction) Transfer of sternal pec major to inf pole
Spinal accessory Trapezius Lateral ( retraction) Lateral transfer of rhomboid & levator
Dorsal scapular Rhomboideus Infero-lat
Types:
1]. Classic winging: the medial border moves away from the posterior chest wall
2]. Rotary winging: the inferior angle moves away from the midline as compared to the other side
3]. Dynamic winging: usually nervous and occurs with movement
4]. Static winging: usually bony structural causes
5]. Scapular tilting: superior or inferior border moves out from the ches wall
Little Leaguer’s Shoulder

• Salter Harris I slipped epiphysis of the humeral head
• PXR: wide proximal humeral physis
• Ttt:
a. Rest
b. Activity modification
Shoulder Arthroplasty
Anatomical considerations:
• Humeral head is a 140º arc of a sphere with a radius of ~ 25mm (radius of TSA is 44mm)
• Head:
1]. Thickness (BC) .................................... 15-23 mm (determined by either we need to y RC
lever arm, or z tension on the RC if needs a repair)
2]. Retroversion ........................................ 30º
3]. Neck shaft º inclination ( ) ............. 45º to the horizontal plane
4]. Offset:
• Lateral offset (FH) ..................... ≈ 50mm (y é head thickness)
• Vertical offset (ED) .................. ≈10mm (y é head thickness)
• Posterior offset: y é rotation of a modular head over the stem in some designs
• Glenoid (curvature radius ~ 2-3 mm larger than the head)
1]. Retroversion on scapula ................. 6º
2]. Inclined superiorly ............................ 6º
3]. Scapula anteversion ......................... 30º
Indications:
1]. Unremitting pain
2]. Uncontrolled loss of function
3]. Traumatic:
o Four part fracture
o Three part fracture é GT involvement in elderly
o Head split fracture
o Dislocation + OA
4]. Inflammatory: if failed conservative ttt in OA & RA
5]. Tumors of the proximal humerus
6]. AVN
Contra-indications:
1]. Active infection
2]. Severe bone loss
3]. Mild symptoms and pathologies
4]. Functional loss of RC
5]. Paralyzed RC or deltoid
Alternatives:
1]. Open debridement ....................................................... young mild OA
2]. Arthroscopic debridement ........................................ Poor candidate for arthroplasty
3]. Soft tissue balance ......................................................... IR contracture
4]. Humeral head resection ............................................. good salvage in infection, failed arthroplasty
5]. Arthrodesis ....................................................................... Paralytic conditions
Types
1]. Humeral head replacement
2]. Total shoulder arthroplasty
a. Unconstrained: NeerII, isoelastic, bipolar, …
b. Semiconstrained
c. Constrained ............................................... y failure rate
i. Ball and Socket
ii. Reversed ball and socket ....... for cuff arthropathy; e.g. NeerIII, DeltaIII
Head replacement vs Total replacement
Total Arthroplasty Is Done For:
1]. Glenoid incongruity
2]. Good RC, or small tears
3]. Good bone stalk
C/I
1]. RC insufficiency Æ y Sup Glenoid Stresses Æ failure
2]. Glenoid insufficiency (Eroded by OA, #)
Head Replacement is done for
1]. Intact glenoid
2]. Large RC tears
Operative Techique
Approach
• Semi-setting position é shoulder out of the table to allow for extension
• GA + interscalene block
• Delto-pectoral approach is done
• Avoid coracoid osteotomy Æ avoid Musculo-cutaneous nerve injury
• Free subacromial space from bursal adhesion
• Preserve coraco-acromial arch except if severe impingement)
• Preserve LHB
• Release pec major insertion if needed
• Identify the axillary nerve by TUG TEST
• Release subscapularis & capsule together; starting from most lateral aspect of LT
Humeral prepartion
• Excise all osteophytes & loose bodies is far beneficial in:
a. y excursion of the soft tissue
b. Give an exact idea about the normal head
c. Prevent over resection of the head; not to jeopardize the axillary n, and RC
• Dislocate the shoulder by ER + Ext; this is facilitated by release of inferior & post-inf capsule
• Determine the precise location of post RC insertion to avoid its inj during head resection
• Note superior head is eroded i.e. head centre is lower than normal
• Head cut is done & avoid excessive removal by 30º-40º ER & cut is done parallel (or by using
epicondyles as a reference to horizontal)
• Lat fin of stem must be 5-10mm post to post edge of bicipital groove
• Superior end of osteotomy must exit above the insertion of post cuff
• z cut retroversion ....................................... for post instability
• y cut retroversion ....................................... for anterior instability
• Do the canal reaming & make a Slot by narrow ronguer for lat fin (zincidence of GT#)
Stem application
• Trial is done; keeping the fin in the made slot, to adjust the retroversion
• Height is adjusted éin ≈ 8-10mm (if less .... GT impingement)
• Posterior offset is adjusted in some modular implants
• Soft tissue balance is adjusted to be within:
o 50% translation of humeral head
o 40º ER with arm at side
• Trial removed, 2 drill holes are done at ant. humeral neck; and pass non absorbable suture
within these holes for subscapularis repair
• Cementation without pressurization (to avoid cement extrusion into the weak humerus)
• Introduce the stem with its fin in the slot as mentioned
Glenoid if needed only
• Humeral head retractor is applied and head is retracted posteriorly
• Excise all the labrum and soft tissue around the glenoid
• According to the prosthesis technique preparation of the glenoid is done

• Apply cement first and pressurized by an edge of a gauze ball, into the holes or keel bed
• Another cement pulse is applied by a syringe; followed by the PE and hold it till it set
• Apply the stem into the medulla, & test for stability and soft tissue balance as mentioned
Rehabilitation Three Phases:
1]. Phase I: local heat, PROM, AAROM............................(0-6wk)
o Sling
o Passive elevation & rotation
o AAROM elevation & ER (IR is postponed to protect the subscap till 6wk)
o Pendulum
o Pulley exercises
o Stick excercises
o Wrist and hand exercises, is begun on the first day after surgery.
o Avoid pushing up from bed or chair
2]. Phase II: starts AROM & exercises ..............................(6-10wk)
o Remove the sling
o Start AROM elevation & rotation
3]. Phase III: ms stretching + resistive exercises ...........(10wk)
o Isometric elbow
o Unrestricted activity is permitted
o Avoid participation in contact sports till 6mo
o Exercises ~ five times a day for 10 min
Complications
INTRAOPERATIVE COMPLICATIONS
1]. Humeral shaft fracture ...................................... 1%
2]. Axillary nerve inj
3]. Malpositioning of components.
POSTOPERATIVE COMPLICATIONS
1]. Glenoid loosening
2]. Tuberosity nonunion or malunion
3]. Instability
o Anterior instability ................................ ð too small humeral head
o Posterior instability ............................... ð malpositioning of the components.
o Inferior instability .................................. ð loss of humeral height after prox humeral fractures.
4]. Rotator Cuff Tear (2%)
5]. Infection (< 0.5%). Staphylococcus aureus or gram-positive organisms Implant
6]. Loosening Dx by a change in implant position or progression of radiolucent lines.
7]. Heterotopic Ossification
8]. Stiffness
9]. Periprosthetic Fracture

The
Elbow
Dr Mohamed Sobhy

• Anatomy
• Congenital Deformities
• Acquired Deformities
• OCD
• Arthritides
• Stiffness
• Operative

Ain‐Shams University

[The Elbow] Page | 505
Applied Anatomy
Type: .................................................. Trochoginglymus Hinge joint
Ossific Centres around the elbow: CRITOE

1]. Capitulum.......................... 6mo
2]. Radial Head ..................... 5y
3]. Internal condyle ............ 7y
4]. Trochlea ............................ 9y
5]. Olecranon ........................ 11y
6]. External condyle ........... 13y
Stabilizing factors:
1]. Joint conformity of the olecranon to the trochlea
2]. MCL especially the anterior band
3]. LCL especially the medial band
4]. Radial head is a 2ry restraint to the valgus thrust
Carrying angle
• The complex geometry of the elbow joint has a special orientation of the trochlea that allow
valgus attitude in extension; while in flexion the forearm comes to the same line of the arm
• This valgus angle is called the carrying angle
• = 15º in ♀ / = 10° in ♂ (this to accommodate for wider pelvis in females)
Kinematics:
• Trochoginglymus the elbow is, premits flexion, extension & pronation supination
• The actual needed range of motion at most activities: 30º-130º & 45º-45º
506 | Page [The Elbow]
Congenital Deformities
1]. Congenital Dislocation:
• Usually bilateral
• Could be anterior or posterior
• Function is surprisingly excellent
• PXR: the radial head .................. dislocated and dome shaped
• ttt: only if lump limits elbow flexion
2]. Congenital Synostosis
• Rare condition
1]. Humerus is fused to ulna or radius + FA deficiencies
• ttt: osteotomy
2]. Proximal radio-ulnar synostosis
• Causes loss of rotation only, and usually the limitation is mild
Acquired Deformities
[
[The Elbow
w] Page | 507
O
OCD Capittulum
m
Definition
• NON INFLAMMATORY path hologic coondition ofo the carrtilage é IMPENDING OR ACTUAL
separation of a seegment of cartilage é underlyinng subchonndral bone
e
• Tends to t heal spoontaneous in skeletallly immature personss
Ætiology:
1- Repeated TRAUMATA (over head & WB W activitiess)
2- Could be AVN
Pathogenesis:
1]. Intraossseous edema Æ cap pillary compression Æ ischemia
2 Subcho
2]. apse Æ artteriolar com
ondral colla mpression Æ necrosiis
3 Fragme
3]. entation Æ NBF
Diagnosis:
Clinically:
• Aching g pain; y é activity, z by rest
• Swellinng &Effusioon
• Tenderrness
• ROM
PXR:
1]. Fragme entation ± Flattening
g of capitullum
2 Loose body
2]. b
TC
• y uptakke
MRI
• MRI T1 ...............................z signa
al lines
• MRI T2 ...............................Doublee line =z Sig n & y signa
gnal Margin al inner bord
der
DD
Dxx: Panner’s disease: <12y
< pitellar phyysis Æ painful flattening
pitchers, disruption of cap
Treatment:
1]. NON OPERATIVE TREATMENT: - NWB SYMPTTOMATIC TTTT USUALLY THE RULE

2 OPERATIVE TREATMENT: if the Lesion disssects and became
2]. b loo
ose boy
DIFFERENT TYPES OF CHONDROSES

OSTEOCHONDROSIS DISEASE SITE
AVVN 1]. Legg g –Clave-Pertthes’ disease. Uppper Femoral Epiphysis
Crrushing 2]. Kienbock’s diseasse Lunate
3]. Preisser’s disease Scaaphoid
4]. Pann ner’s disease Ca
apitulum
5]. Sche euermann’s disease
d Veertebral Bodiees
6]. Kohller’s disease Tarsal Naviculaar
7]. Freibberg’s diseasse 2ndd Or 3rd Meta
atarsal Head
8]. Blouunt’s Kn
nee ?
9]. Theimann’s disea ase Muultiple Phalan
nges
10]. Frieddrich’s diseasse Ste
ernal End Of The Clavicle
e
OC
CD 11]. OCD D Kn
nee
12]. OCD D Talus
13]. OCD D Patella
14]. OCD D 1st MT Head
15]. OCD D Ca
apitulum
16]. Buscchke’s diseasse Meedial Cuniforrm
Trraction apoph
hysitis 17]. Osgo ood –Schlattter’s disease Tib
bial Tuberositty
18]. Joha ansson-Larsen syndrome Patella
19]. seveers disease Ca
alcanius
20]. Iselin
n’s disease Tuberosity Of 5th MT
21]. Man ndl’s disease Grreater Trochaanter
Strain Syndromes
1]. Tennis elbow
• Definition: painful lat humeral condyle 2ry to forceful repetitive wrist extension
• Etiology: repetitive forceful extension Æ ECRB Tendinopathy
• Pathology:
o Attritional changes to ERCB origin ± ECRL, ECU
o Small tears
o Microscopic calcifications
o Angio-fibroblastic hyperplasia
o Fibrocartilaginous metaplasia
• CP:
o 30-40y é unaccustomed forceful gripping or wrist extension activity
o Progressive dull aching pain, localized to LHC
o y é “TENNIS BACK HAND”, pouring tea, opening a door handle, lifting é pronated FA
1]. PAINLESS elbow flexion & extension
2]. PAINFUL passive elbow extension + pronation + wrist flexion (max stretch of ECRB)
3]. PAINFUL resisted active wrist extension
4]. TENDER LHC
• PXR: usually normal except for rare calcification
• DDx: Radial tunnel syndrome
• ttt:
1. Activity modification, physiotherapy, US waves
2. Local steroids inj
3. Surgery: detachment of the CEO (common extensor origin)
4. ± synovial fringe & orbicular ligament excision
2]. Golfer’s elbow
• Same, but affects..................................... CFO (flexor origin) & pronator origin
• Pain y by .................................................. resisted pronation & wrist flexion
3]. Pitcher’s elbow:
1]. Repetitive strong throwing ................ damage bone, soft tissue
1]. Lower humerus hypertrophy ............. Incongruity
2]. OA & Loose intra-articular bodies
4]. Little Leaguers’ elbow:
• Partial avulsion of the medial humeral epicondyle
• ttt: ............................................................... Stay away from pitching
5]. Javelin throwers’ elbow
• Over arm vigorous activity
• ð Olecranon tip avulsion ± MCL avulsion
• ttt: activity modification + rest
6]. Students’ elbow
1]. Frictional olecranon bursitis
2]. Gout
3]. RA
7]. MCL injury:
• ð repetitive vigorous valgus stresses (late cocking and acceleration phases)
• Tender medial elbow aspect ............. ± ulnar n palsy
• Valgus instability (only 50%) .............. é Arm is held in ER + supination; apply valgus thrust
• ttt: rest + motion .................................... Docking procedure (MCL recon by Palmaris tendon)
8]. LCL injury
• The 1st ligament to rupture in elbow dislocation
• Pain / clicking / locking / postero-lateral instability; all during extension
• Varus instability ...................................... é Arm is held in IR + pronation; apply varus thrust
• ttt: same as MCL
[The Elbow] Page | 509
Arthritidies

Treatment:
1]. Prevention: early ACTIVE ROM, serial splinting (avoid passive forced manipulation)
2]. Surgery:
o Rationale:
a) Wait 1y of conservative ttt
b) Choose compliant emotionally stable pt
c) Heterotopic ossification & synostosis should be in the fully formed stage
d) Exclude neuropathic cause
o Options:
a) Capsular release
b) Heterotopic bone excision
c) Corrective osteotomies of a non or mal united fractures
d) Proximal radio-ulnar synostosis excision
e) Outerbridge-Kashiwagi olecranon fossa fenestration
Operat
ative
Arthroscopy
Portals:
Po
1]. Antero
o-lateral: 1ccm antero-iinferior to LEC
2 Antero
2]. o-medial: 2ccm antero--inferior to MEC
1]. Postero
o-lateral: 2ccm prox to
o olecranon n and just lat to tricep
ps
Indications:
1]. Debrid
dement
2 Capsular release
2].
3 Synove
3]. ectomy
4 Osteop
4]. phytes and d loose boddy removall
5 OCD drilling
5]. d

Arthroplasty
T
Tyypes:
1]. Resectiion: lower humerus, olecranon notch, rad dial head excised
e
2 Interpo
2]. osition: sam
me é a tissu ue in-bet to o y motion n & z ankyylosis; e.g. fa
fat, muscle,, fascia lata
a
3 Implan
3]. nt arthropla asty:
o Constraine ed ............................y faailure rate ð loosening
o Unconstra ained ......................unsttable
o Semiconsttrained ...................bettter results (Coonrad-M
( Morrey pro o)
Indications:
1]. Incapacitating pa ain 4]. Bilateral
B ankylosis
2 Rheum
2]. matoid 5]. z ROM & sttability
3 OA
3]. 6]. Non
N united fracture
f humerus
Contraindications:
1]. Infectio
on
2 Severe laxity
2].
3 Previou
3]. us radial heead resectiion (if unco onstrained d prosthesiss is used)
4 > 2 cm of distal humeral bo
4]. one loss (may require customize ed prosthessis)
T
Teechnique: (usin ng the Coo onrad-Morrrey prosthe esis - semicconstrainedd);
1]. Approa ach: POSTERIOR TRICEPS REFLECTING APPROACH
o Ulnar n is identified and a is tran nsposed ant
o Medial hallf of tricepss is reflecte ed é post caapsule
o The extenssor mechanism is reflected laterally
o Tip of the olecranon + portion of the MCL are remo oved for beetter expossure
o MCL & LCLL are releassed if a sem miconstrain ned is used d (their rep
pair is not necessary)
n
o Pitfalls: avo
oid ant capsulotomyy 4 correction of flexio on contracctures
2 HUMERAL PREPARATION:
2].
o Only the diaphysis
d iss needed fo
or fixation; i.e. absentt epicondyyle INBD (is not a big deaal)
o Medullary reaming iss done Æ alignment
a stem is pu
ut é a cuttin
ng block
o Cutting bloock: set to remove an n appropria ate amoun nt of distal humerus
o Best is press fit fixatioon with a circumferen
c ntial plasm
ma spray
3 ULNAR PREPARATION:
3].
o Medulla is entered é a high speeed drill via
a the previously remo
oved olecranon tip
o Sequential rasping iss performed (care not to # proxx ulna)
o Best is PE cemented
c ulnar com
mponent;
4 CEMENT &COMPONENTS INSERTION:
4].
o Use a cemment gun to o insert cemment
o Humeral & Ulnar com mponents are inserte ed
o Ulnar commponent is articulated d é humera al component before e seating
o Allow cemment to sea at in extenssion; (even post op 3d days to allo
ow healing
g)
o BG is place
ed behind the anterio or flange to prevent posterior & rotationaal instabilityy
o Maximal sttresses are anterior, at
a the inserrtion site of humeral componen nt. After BGG
incorporattes, the thickened cortex will re esist these forces
f
[
[The Elbow
w] Page | 511
Complications
1]. Instability; posterior elbow dislocation d n ~ 10% é unconstrai
u ined arthro
oplasty
2 Ulnar nerve
2]. n dislocation & in njury
3 proxim
3]. mal ulna fracture
4 fracture
4]. e of ulnar componen
c nt
5 imping
5]. gement of the t radial head h
6 hardwa
6]. are failure
7 Loosen
7]. ning
8 Wound
8]. d dehiscen nce & tricep ps rupture
9 Infectio
9]. on ........................................................... (1-10%)
All bush hing need to t be remo oved
Staged removal Æ debride ement Æ re-implanta
r ation of thhe
same co omponentss (unless sttaph epide ermidis infe
ection)
Resectio on arthrop plasty Æ errradication n of infection, but haas
poor fun nction
Arthrodesis
Positions
Po
1]. 100 ................................................................... Feeding
2 45 ....................................................................... perineal hygiene
2].
Fixation
• Usuallyy by comprression plate

‫ اﻟﺮﺣﻴﻢ‬Sobhy
Mohamed ‫اﻟﺮﺣﻤﻦ‬ ‫ﺑﺴﻢ اﷲ‬
Dr Mohamed Sobhy
HAND
Quick Guide
• CARPAL INSTABILITY
• DISTAL RADIO-ULNAR INSTABILITY
• KEINBOCK DISEASE
• FRACTURE SCAPHOID
• RHIZARTHROSIS
• FLEXOR TENDON INJURIES
• RHEUMATOID HAND
• DEQUERVAIN’S SYNDROME
• ULNAR IMPACTION SYNDROME
• DUPUYTREN'S CONTRACTURE

[The Hand] Page | 515
Applied Anatomy
WRIST Consists of 3 Columns:
1]. Central column (Flex-ext ) Distal row & lunate Centre of rotation = capitate
2]. Second mobile column Scaphoid Abduction – adduction & Axial loading
3]. Rotation column Triquetrum Carpus rotates around triquetrum independent of FA rotation
2 Rows:
A. Proximal row:
[1]. SCAPHOID (boat): articulates é distal radius and distally é trapezium and trapezoid.
[2]. LUNATE (crescent): articulates with the LUNATE FOSSA of the distal radius & é capitate
[3]. TRIQUETRUM (pyramidal): articulates prox é TFC & ant é pisiform and hamate.
[4]. PISIFORM (pea-shaped): articulates é the palmar surface of triquetrum (FCU sesamoid)
B. Distal row:
[5]. TRAPEZIUM (quadrangular): articulates é scaphoid, and distally with the base of MC1. Its
palmar surface is grooved for FCU tendon é a crest lateral to the groove.
[6]. TRAPEZOID (irregular): articulates é scaphoid, and distally with the base of MC2.
[7]. CAPITATE (headed): articulates with the Scaphoid, lunate & MT3
[8]. HAMATE (hooked): articulates é triquetrum, capitate and distally with the base of MC4,5.
Hook of hamate # may encroach on Ulnar N medial To It
Bipartite Hook = HAMULI PROPRIUM
Anatomy of carpal ligaments:

516 | Page [The Hand]
Extensor Compartments
COMP TENDONS NOTES PATHOLOGY
1 EPB, APL Both in separate synovial sheaths De Quervains
2 ECRL, ECRB Radial to Lister's tubercle Carpal boss
3 EPL Ulnar to Lister's tubercle Rupture over Lister's tubercle
4 EDC, EIP Common synovial sheath Tenosynovitis & ruptures
5 EDM Double tendon, over DRUJ Tenosynovitis & ruptures
6 ECU Lies over distal ulna Subluxing at ulnar styloid
Flexor retinaculum (Transverse Carpal Ligament)

• Radial attachment ................................ tubercle of scaphoid + ridge of trapezium
• Ulnar attachment ................................. hook of hamate + pisiform
Carpal Tunnel
• Floor and walls = ................................... bony carpus
• Roof = ....................................................... flexor retinaculum /TRANSVERSE CARPAL LIGAMENT (TCL)
• Contents:
1]. Median nerve ............................... most superficial (just beneath the retinaculum)
2]. FPL / FCR (deep to FPL)
3]. FDS - middle & ring lie superficial
4]. FDP
Guyon’s Canal
• Roof = ...................... volar carpal &pisohamate lig
• Floor = ..................... TCL to pisiform
• Ulnar wall = ........... pisiform
• Radial wall = .......... hamate hook
• Contains ................. ulnar n & a
• Compression occurs by:
1]. Zone1 .............. Hamate hook # (trunk)
2]. Zone2 .............. ganglion cyst (deep br)
3]. Zone3 .............. ulnar a aneurysm (superficial br)
Ossific Centres around the wrist: C H T L STRAP

1]. Capitate ......................6m
2]. Hamate........................1y
3]. Triquetrum ................3y
4]. Lunate .........................4y
5]. Scaphoid ....................5y
6]. Trapezium .................6y
7]. Trapezoid ...................7y
8]. Pisiform .......................12y
Muscles
MUSCLE ORIGIN INSERTION 1RY & 2RY ACTION DESCRIPTION INNERVATION
Brachialis Mid 1/3 Humerus Ulna coronoid Elbow: Flexion The main flexor of FA Musculocutaneous
Coraco- Coracoid Process Middle 3rd of Elbow: Flexion CORACOBRACHIALIS SYNDROME -- Musculocutaneous
brachialis humerus has Musculocut N. N. (lateral cord)
Biceps Short Head: Tuberosity of Elbow: Flexion Head is the lateral border of rotator Musculocutaneous
Coracoid Radius supination cuff N. (lateral cord)
Long Head:
Supraglenoid
Triceps Infraglen tubercle Olecranon of Elbow: Extension Triangular Interval and Radial N.
Brachii Above & below Ulna Quadrangular Space are between
spiral groove the two heads of the Triceps
MUSCLE ORIGIN INSERTION 1RY & 2RY ACTION DESCRIPTION INNERVATION

Palmaris Common Flexor NONE | Wrist: Flexion Does not pass via tunnel Median N.
Longus Tendon Used in transfers
Sublimis Common Flexor Middle phx of 2- Digits: Flexion of SPACE OF PARONA is directly deep Median N.
Tendon (CFT) 5 digits. fingers to it.
FCR Base of index Wrist: Flexion, Median N. Radial A., Ulnar A.
finger MC Abduction
FCU CFT and proximal The Pisiform Wrist: Flexion and CUBITAL TUNNEL $: Ulnar N. Ulnar N.
ulna Bone adduction Entrapment bet 2 heads;
FDP CFT & Radius Distal phx of the Digits: Flexion of SPACE OF PARONA is directly Lateral Half: Ant
2-5 digits fingers superficial to it. Interosseus N., Med
Half: Ulnar N.
FPL 1st distal phx Digits: thumb Flex Ant Interosseus A.
Pronator The distal ulna The distal radius Forearm: Pronation + Anterior Interosseus
Quad elbow ext A.
Pronator Humeral Head: Distal third of Forearm: Pronation PRONATOR TERES SYNDROME -- Median N.
Teres Med Epicondyle; radius (Radius over Ulna) Median N. Entrapment between the
Ulnar Head: two heads
Proximal Ulna
APL MC1 base Abduction of thumb Radial N.: Deep Branch Posterior Interosseus
A.
Radius, Ulna, &
Interosseus
Membrane
EIP Prox phx of the Digits: Extension of Radial N.: Deep Branch Posterior Interosseus
2nd digit index finger A.
EPB Prox phx of the Digits: Extension of DeQuervain's Disease in Radial Bursa Radial N.: Deep
1st digit thumb Branch
EPL Distal phalanx of Digits: Extension of DeQuervain's Disease in Radial Bursa Radial N.: Deep
the 1st digit thumb Branch
Supinator Proximal ulna and Proximal radius Forearm: Supination Deep br of Radial N. pierces the Radial N.: Deep
lateral epicondyle supinator to go to post forearm -- Branch
of humerus SUPINATOR CHANNEL SYNDROME
Anconeus Common Elbow: Ext | Abduction It gets the ulna out of the way Radial N.: Deep
Extensor Tendon of ulna during during pronation of the forearm Branch
pronation
Brachiorad Common Styloid process Elbow: Power flexion MOBILE-WAD: part of lateral Radial N.
ialis Extensor Tendon of the radius compartment. May become
damaged with radial fractures near
the wrist
ECRB Common Base of the meta Wrist: Extension and Radial N.: Deep Branch Posterior Interosseus
Extensor Tendon carpal bones Radial deviation A.
(abduction)
ECRL Common Ext Base of MC Wrist: Ext & abd MOBILE-WAD: Part of lateral Radial N.
Tendon bones compartment
ECU Common Ext The base of the Wrist: Ext & add Radial N.: Deep Branch Posterior Interosseus
Tendon MC bones A.
EDM Common The prox phx of Digits: Ext of little finger Radial N.: Deep Branch Posterior Interosseus
Extensor Tendon the 5th digit A.
ED Common Ext All med 3 phx Digits: Extension of The tendons split & reunite to insert Radial N.: Deep
Tendon fingers on the distal 2 phx Branch
Abductor Digits: Abduction of
Digiti Little Finger
Minimi
Ulnar N.
FD minimi Digits: Flexion of the

little finger
Opponens Digits: Opposition of
Digiti M little finger
Dorsal int Abduction of Fingers
Palmar Int Adduction of fingers
Lumbrical Tendons of the Post aspect of Digits: Flexion of MCP Ant to MCP joints & post to PIP and 1st & 2nd Me dian N.,
FDP prox & distal phx joints; Ext of PIP & DIP DIP joints; proprioception 3rd & 4th: Ulnar N.
APB Abduction of thumb Median N. Princeps Pollicis A.
(from Radial A.)
Adductor Digits: Adduction of Ulnar N. Princeps Pollicis A.
Pollicis thumb (from Radial A.)
FPB Flexion of thumb Median N.
Opponens Digits: Opposition of Median N.
Pollicis thumb
Congenital Malformation
EMBRYOLOGY of the Upper Limb at Weeks 4 to 6
• The critical APICAL ECTODERMAL RIDGE the limb mesenchyme for growth & development of the
limbs. Factors play a vital role in this process.
• The upper extremity, with pronated forearms begins to rotate externally.
• Developmental disturbances during this period give rise to major congenital malformations. Early
suppresion of limb development causes AMELIA (complete abscence of a limb); Late suppression
causes MEROMELIA (partial abscence).
Weeks 7 to Birth
• By wk 7 the ten finger rays appear & continue to differentiate till 12 wk when the hands appear.
• The fingers develop as a result of cell death in tissue bet.digits (failure of this causes syndactyly).
INTERNATIONAL CLASSIFICATION (FDD.OUC)

1]. Failure of Formation
o Transverse Arrest / Aplasia
Amputations: arm, forearm, wrist, hand, digits
o Longitudinal Arrest
Phocomelia: complete, proximal, distal
Radial deficiencies (radial club hand)
Central deficiencies (cleft hand)
Ulnar deficiencies (ulnar club hand)
Hypoplastic digits
2]. Failure of Differentiation
o A. Synostosis: elbow, forearm, wrist, metacarpals, phalanges
o B. Radial head dislocation
o C. Symphalangism
o D. Syndactyly
Simple
Complex
Associated syndrome
o E. Contracture
i. Soft tissue
• Arthrogryposis • Pterygium cubitaIe
• Trigger digit • Absent extensor tendons
• Hypoplastic thumb • Thumb-clutched hand
• Camptodactyly • Windblown Hand
ii. Skeletal
Cleinodactyly
Kirner's deformity
Delta bone
3]. Duplication (polydactyly)
o A. Thumb (preaxial) polydactyly
o B. Triphalangism/hyperphalangism
o C. Finger polydactyly
Central polydactyly (polysyndactyly)
Postaxial polydactyly
4]. Overgrowth
o Macrodactyly
5]. Undergrowth
o Brachidactyly
6]. Constriction bands
[The Han
nd] Page | 519
Am
Arm
• These in
nclude extra a bones, ab
bsent bones, hypoplastic bones an
nd fusions.
• Failure of Differenttiation
• Failure of Formatioon - transveerse (Aplasia
a) or axial
• Most off the defectss are non-geenetic but some
s are AD
D
1]. Amelia:
A com
mplete absen
nce of a limb
2]. Phocomelia
P : almost com
mplete abse
ence (stub remaining)
r
3]. Ectromelia:
E p
partial abse
ence
4]. C
Congenital radio-ulnar
r synostosis
• Union ofo the forearm bones usually pro
oximally pla
acing
the armm in a pron nated position. Associa ated with DDH,
D
CTEV, chromosom
c mal abnorma alities and fooetal alcoho
ol $
T
Two types
1. Medulla ary canals are
a linked creating
c arge radius with
a la
anteriorr bowing
2. Proxima al radial dislocation with
w less extensive
e fusion
(usuallyy unilateral)
• Both types are diffiicult to treat. Osteotom mies for disa
abling
pronation but if bilateral
b leave the dom minant armm and
osteotoomize the otther to 20-330° supinatio on.
5]. C
Congenital dislocation
d of the radia
al head
• Abnorm mally formed d radial heaad + bowedd ulna.
• Capitelllum shape abnormal
a ≠ traumatic dislocation.
d
• Radial head
h excisio
on if pain de
evelops otherwise leavve alone.
6]. C
Congenital pseudoarth
p hrosis of the
e forearm
• Rare dissorder assoc
ciated é Neurofibromaatosis. Refracctory to ttt but
b vascularized BG ma
ay be usefu
ul.
7]. C
Congenital webbing
w off the elbow
w (Pterygium
m cubitale)
• Broad skin
s web crossing the elbow caussing a flexioon deformitty and a pro
onated fore
earm. Surge
ery is
difficultt because it sometimes requires ve
essel and ne
erve lengthe
ening.
8]. Madeelung’s Deform

D mity
Definition: it is a develop
pmental dissorder ð premature fu usion of uln
nar half of distal radia
al physis
Pathology
1]. Dorsal + lateral boowing + shoortening off the distal radius
r
2 Dorsal DRUJ sublu
2]. uxation (uln
na dorsal)
3 Wedge
3]. ed carpal boones
4 Atroph
4]. hic radial he
ead + Hyperrtrophic cap pitulum
5 Associa
5]. ated with: Dysplasias,
D Turner, Lang
ger syndrom
me
Dx
• Adolesc
cence; median nerve irrritation; wrrist pain.
PXR:
y widtth between
1]. n the distall radius and ulna.
Positive
2]. e ulnar varriance
3 triangu
3]. ularization of the distal radial ep piphysis.
4 wedgin
4]. ng of the carpus c bet radius and d ulna, with
h the lunatte at the ap
pex of the wedge.
Treatment:
1]. Child ........................................... Co
orrective ossteotomy + Milch ulna
ar resection
2]. Adult .......................................... Coorrective ossteotomy + Darrach ullnar resectio
on
520 | Page [The Hand
d]
9]. R
Radial Hemiimelia / defiiciency (Rad
dial club han
nd)
• Absenc ce or hypoplasia of pre--axial structures:
a. radius
b. radial ca
arpus (scap phoid, trapezium, trape ezoid)
c. Thumb - may be flo oppy (P e Flottante) or absent
Poucce
• May oc ccur in asso ociation wiith visceral anomalies (CVS/GI/G GU), VATER R or blood dyscrasias e.g.
Fancon ni’s syndrom me.
• Most co ommon in th he right hannd
• Bilateraal in 50% of cases.
• Classifie
ed I-IV based d on how much
m radiuss is present
Type Featuress Treatme ent
I Short addresss thumb
II hypopla astic individuualized
III partiallyy absent centralization
IV totally absent
a centralization
• Treatme ent is difficcult - mild cases
c - strap
pping & manipulation
m n;
severe cases
c - corre ection of wrist deformiity (Centralization) by fusing
f ulna to carpus or
o circular frrame
& provision of a th humb (Polliccisation) using Buck-Grramko meth hod (transfeer, shortenin
ng & rotatio
on of
index finger).
• Abnorm mal distributtion of nervves & arterie es must be appreciated
a d prior to surrgery.
10]. U
Ulnar Hemim
melia / deficciency (postt-axial)
• This is not
n associatted with syystemic diso orders as is the
t radial club
c hand b
but can be associated
a with
other musculoskele
m etal deform
mities, especiially hand deformities.
d
• Only if function
f is severely
s disturbed shou uld wrist sta
abilization be
b performe
ed.
11]. R
Reduplicatio na (Mirror hand)
on of the uln
• The rad dius and pre
e-axial
• Ulna an nd carpus are
a redupliccated leavin
ng 7/8 digits and no thumb.
t Trea
atment inclludes remo
oving
most ab
bnormal dig
gits and polllicization to
o create a 5--digit hand.
12]. C
Central Deficiency (clefft hand / lob
bster claw hand
h / ectro
odactyly)
• Central abscense of o at least onne digit
• other digits may fu use (syndacttyly)
• Typical Deformity = AD; often bilateral; more
m commo on in boys & may invollve the feet
• Atypicaal Deformityy = sporadic; associated d with cardia
ac & GIT ab
bnormalitiess
Hand Deformities
• Goals of surgery are to preserve or improve hand function and appearance.
• Timing of surgery should be:
o Iimmediate if limb/digit threatening e.g. constriction bands
o Within the first year if disorder has a tethering growth effect e.g. club hand
o Before 3 if development patterns are affected e.g. pollicisation
o Delayed until past 4 years if co-operation is required e.g. tendon transfers.
Digits
1]. Syndactyly (joined phalanges)
• Can be Simple (skin only) or Complex (bone involvement).
• may be Complete or Incomplete: (complete= entire length of digit is affected)
• Incidence = 1:2000 births (commonest congenital abnormality of the hand)
• Can be associated with many anomalies.
• Apert Syndrome = acrocephalosyndactyly
• Release performed 18 months-5years.
• PreOp Planning:
o Individual Allen's tests to each involved digit
o Radiographs to rule out tethering of digits
o One side of digit should be operated on at a time, in order to avoid vascular insufficiency
o With multiple syndactyly attention is first directed to border digits
o The usual strategy is to preserve as much regional skin as possible on the radial side of the
involved digits (z pinch sensation) and saving FTSG for ulnar side of the affected digit
2]. Polydactyly (duplicated digits) Of three types
• Extra soft tissue only
• Bone, tendon and cartilage
• Completely developed with its own metacarpal (rare)
3]. Thumb Duplication (pre-axial polydactyly)
• Incidence = 1:1000 births
• Look for Cardiac anomilies & Fanconi anaemia.
• Wassel classification: seven subgroups depending on level of bifurcation.
1. Bifid distal phalanx
2. Duplicated distal phalanx
3. Bifid prox phalanx
4. Duplicated prox phalanx
5. Bifid metacarpal
6. Duplicated metacarpal
7. Triphalangism (single MC, dublicated PP & DP + additional phalanx at end of one)
4]. Brachydactyly (short digits) / undergrowth
5]. Macrodactyly / overgrowth

• Enlargement of all structures, especially nerves of one or more
digits. Can be associated é Neurofibromatosis.
6]. Deviated digits

Clinodactyly
• Skeletal abnormality causes deviation in the lateral plane. Usually involves the little finger and is
caused by a trapezoidal middle phalanx. Surgical correction for cosmesis only.
Camptodactyly
• Familial soft tissue abnormality with deviation in the sagittal plane. Commonly involves the little
finger causing a flexion contracture at the PIPJ.
• May be ass. with Dupuytren's, Marfan's, arthrogryposis or other genetic syndromes.
• Few good surgical procedures exist.
• 2 stage correction (with ex-fix applied at the time of FDS – extensor transfer has good results.
Kirner’s Deformity
• In-curling of little finger DIPJ in prepubertal girls. Usually requires no treatment
Symphalangism (Stiff PIPJ’s)
• Secondary to congenital ankylosis of the joint. Associated with Apert Syndrome. Observe only.
Delta phalanx
• Triangular phalanx and physis, usually of the thumb and little finger. A delta bone results in a
sideways curve of the finger. Surgery only if significant deformity.
Thumb anomalies (Hypoplastic thumb)
BLAUTH GRADE DESCRIPTION TREATMENT

I Short thumb, hypoplastic thenar muscles Augment intrinsics
II Grade I + Adducted MPJ Soft tissue Z-plasty
III Deficient MC + Abducted thumb Augment/ BG /pollicisation
IV Floating thumb Pollicisation
V Absent thumb Pollicisation
Congenital trigger thumb
• Congenital stenosis at A1 pulley. Often bilateral. 30% may resolve spontaneously by 1 year. Attempt
splinting but aim to correct surgically by 3 years.
Constriction band/ring (Streeter’s Dysplasia)
• Commonly involves digits or toes (especially centrally) but can occur more proximally
• Associated with syndactyly, club feet and neurological abnormalities. Treatment is by Z-plasty.
Congenital amputation
• ð either constriction bands or failure of development, commonest short below elbow amputation.
Carpal Instability
Definition: is the state of loss of normal relation ship of different parts of wrist joint through motion arc
Anatomy of carpal bones & ligamens: ..............................see before
Wrist kinematics
• LICHET proposed the carpal ring analogy “The distal carpal row is moving as 1 unit & scapoid,
lunate, triquetrium are moving as independent units:. WEBER later on proposed that the carpus
is composed of 2 columns: the scaphoid, lunate, capitate, trapezoid are the column for load
transfer; and the triquetrum & hamate are the column ώ control pronation supination moves
• Wrist flexion Æ abduction + pronation
• Wrist extension Æ adduction + supination
Pathomechanics of carpal instability
• Normally forces affecting scaphoid push it into flexion,
and those of triquetrum are extension forces, the lunate
is connected to both and in a state of equilibrium
between them that keeps it in neutral position
• If the lunate is dissociated from any of the two bones; it
will follow the other
• If SL lig is disrupted scaphoid will flex, & lunate will
extend é triquetrum Æ y SL angle (DISI).
• In the same way, disruption of LT lig Æ VISI = flexed scaphoid & lunate + extended triquetrm
Classification:
I. According to Chronicity
A. Acute
B. Sub-acute > 1w
C. Chronic > 6w
II. According to Pattern
I. Carpal instability dissociative (CID)
A. Dorsiflexion DISI
B. Palmar flexion VISI
II. Carpal instability non-dissociative (CIND)
A. Radiocarpal
B. Midcarpal
C. Ulnar Translocation
III. Carpal instability complex (CIC)
A. Perilunate Dislocation (Dorsal / volar)
B. Trans-scaphoid Perilunate
IV. Carpal instability longitudinal (Axial)
A. Axial Ulnar: Capitate-Hamate diastasis
B. Axial Radial
C. Axial Ulnar-Radial – Combined
III. According to Constancy
I. Dynamic instability (Normal PXR; +ve cinerdiographs)
II. Static (fixed) Instability (seen on plain x-rays)
III. Predynamic
IV. According to Direction
I. DISI
II. VISI
III. Ulnar translocation
IV. Radial translocation
V. Volar translocation
VI. Dorsal Translocation
d]
Diagnosis:
Mechanim off injury:
1]. Commo onest FOOSH:
A. Dorsiflexioon + abducction Æ VISSI, scaphoid #
B. Dorsiflexioon Æ capittate or luna ate fracturre
C. Dorsiflexioon + adducction Æ DISSI, Periluna ar dislocatio
on
2 Fall on flexed wrist Æ dorsal lunate dislo
2]. ocation
3 Rarely a direct trau
3]. uma may ca ause fracture hook of hamate
4 RA: cau
4]. use radiocarrpal disrupttion Æ ulna ar transloca
ation and raadial tilt
Clin
nically
1]. History
y of trauma even if veryy old
2 Pain, sw
2]. welling and d limitation of
o wrist mootion are the main pressentations.
3 Palpatio
3]. on of the sp
pecific carpal bones an nd ligaments
4 Point te
4]. enderness over
o the do orsal scaphoolunate and d lunotriquetral spacess
5 Grip strrength; gra
5]. abbing exa aminer fingers, specificc mech pre essure gauge,
sphignoomanometter
6 WATSO
6]. ONN’S SL INCOMPETENCE: press on the t distal sccaphoid tubercle vola arly,
then paassive add & abd in this position Æ the proxximal pole sublux dorsa ally (SL dissociation)
7 LUNO-TRIQUETRAL BALLOTTEMENT test: pinch
7]. p the luunate betwween the thumb and d index of one
hand & the triquetrium in the e other han
nd and try tot shear them apart Æ pain
8 PIVOT SHIFT: the hand is grasped
8]. g an
nd apply axial
a comppression + alternating g adductio on &
abducttion Æ Pain nful clunk = mid carpal instability (CIND)
(
PXRR
A- The
T PA -palm m down- or AP full sup pination vieews are exa amined for::
• Disturbeed GILULA’S LINES
• Wide sca apholunate e distance (TERRY THOMAS SIGN)
• Fracturee scaphoid
• Scaphoiid ring sign n (flexed atttitude give the scapho oid the end d
on appeearance)
B- The
T lateral view
v
• Capito lu
unate angle e ....... (normmally = 0º)
• Scaphollunate anglle ...... (norm mally = 60º)
• Capito-lu
unate-radia al alignmen nt is disturbe
ed: the capitate axis is dorsally dissplaced in DISI
D
• Lunate attitude:
a fleexed in VISI & extended d in DISI
C- Oblique
O view
ws
• 20º pronnation .................... back of triquetriuum
• 30º supiination .................. luno-triquetrium m space
• Tunnel view
v ...................... Hookk of hamate e
• Scaphoiid view .................. fractu ure scaphoiid (wrist abduction)
D- AP
A clenched d fist view: ........... view the SL disso ociation better
E- Motion
M serie
es: for dynamic instabilities
Measuremen nts of carp pal angles::
1- Capitattolunate an ngle: 0º-15ºº is normal
2- Scapho olunate ang gle: Nomallly 30-60º; y in DISI, an nd z VISI
3- Carpal height Rattio: distance e bet MC3b base - distal radius / len
ngth of MC C3 = 0.53 ± 0.03
4- The revvised carpa al height rattio = carpal height / ca apitate lenggth.
Cin
neradiogra aphy: to de elineate th
he dynamicc carpal insstability
CT scan: orien nted along the scapho oid axis Æ collapse
c (hu
umpback) & union in ffusion
Tc99: for occult fractures as a scaphoidd
MRRI: best to asssess soft tisssue
Artthrograph hy: has been n replaced by MRI
Artthroscopy: visualize & treat some e condition
ns
CARPAL INSTABILITY DISSOCIATIVE (CID)

I. Scapholunate dissociation:
• = (Dorsal Intercalated Segmental Instability) DISI
• Mechanism of injury: FOOSH in adduction
• Pathology: injury of RSL or inter SL ligaments.
• O/E
1. Tenderness over SL joint & anatomical snuff box.
2. z ROM by pain.
3. WATSON TEST: the examiner's four fingers of the same hand as that to be
examined are placed behind the radius, the thumb is volarly pushing on the
distal pole. The other hand moves the hand from ulnar to radial deviation. In
ulnar deviation the scaphoid is dorsiflexed, while in radial deviation the scaphoid become palmar
flexed and assumes a position more perpendicular; pressure on the scaphoid will prevent it from
palmar flexing and the proximal pole will displace dorsally out of its radial fossa if there is sufficient
ligamentous laxity. Compare é opposite side
4. SCAPHOID LIFT test: painful dorso-palmar translation of the scphiod
5. SCAPHOID SHIFT test: the same as Watson but in # scaphoid; the distal fragment subluxes on
the proximal one
• Radiographic diagnosis:
AP full supination view:
1. y SL Gap, > 3 mm Æ diagnostic = "TERRY THOMAS" sign, after the comedian diastema.
2. Shortened scaphoid é Ring Pole sign = z distance from the ring to the proximal pole ≈ 3mm
3. TALEISNIK "V" sign, in normal wrist the volar aspect of the radius and the scaphoid make a C-shape
pattern, but when the scaphoid is rotated it changes into V-shaped.
Lateral View:
4. y SL Angle = DISI.
5. Radio-Luno-Capitate Malalignment
6. Palmar flexion Æ scaphoid lies more Perpendicular.
• Treatment:
I. Acute:
1. CLOSED REDUCTION + POP alone: is impossible to consistently maintain a reduction.
"WINE WAITER POSITION" is recommended = full supination, mid dorsiflex & adduction,
however cineradiographic studies have shown that no single position will reduce all
2. CLOSED REDUCTION + K WIRE: Under image intensifier the scaphoid is reduced first in
dorsiflexion Æ K-wires between scaphoid and lunate
3. ORIF AND REPAIR OR AUGMENTATION OF LIGAMENTS: Open
reduction is done through a palmar approach in acute cases. If
the ligament is badly damaged capsular reinforcement can be
done.
II. Subacute:
4. DORSAL TENODESIS USING ECRB OR FCR: to reconstruct the Dorsal SL ligament
5. BONE TENDON BONE ALLOGRAFT RECONSTRUCTION
III. Chronic irreducible:
6. BLATT technique of capsulodesis
7. SL OR SCAPHO-CAPITATE ARTHRODESIS
IV. SL advanced collapse (SLAC):
8. PROXIMAL ROW CARPECTOMY
9. WRIST ARTHRODESIS In Manual Worker
10. FOUR CORNER FUSION is the best (SLAC operation):
scaphoid excision + triquetro-luno-capito-hamate
fusion
NB SNAC = Scaphoid Non-union Advanced Collapse
II. Lunato-Triquetral dissociation: VISI (Volar Intercalated Segmental Instability)

• Mechanism of injury:
▪ FOOSH in abduction + pronation:
o Stage I: partial or complete tear of the lunato-triquetral (LT) interosseous ligament
o Stage II: complete disruption of the interosseous and volar LT ligaments
o Stage III: as II + injury of the dorsal RC lig (either scaphoid or lunate portions)
• Pathology:
▪ The underlying pathology is injury of the volar, dorsal, & Interosseous LT ligaments
• Physical examination:
1- The most important is Point Tenderness directly over the LT joint
2- +ve Reagan Ballottement test: lunate is firmly stabilized é the thumb and index finger of
one hand, while the triquetrum and pisiform are displaced dorsally and palmarly with the
other hand Æ pain, crepitus, and excessive laxity
3- Modification is the “KLEINMAN SHEAR” test: with the patient's elbow resting on the table +
palm down Æ examiner's contralateral thumb is placed over the dorsal aspect of the
lunate (just beyond the medial edge of the distal radius); then, the examiner's other thumb
directly loads the piso-triquetral joint in a dorso-volar direction (shear the LT joint) Æ pain
• Radiographic diagnosis:
▪ z LT Angle; normally (+14°) to (–16°)
▪ z SL angle; < 60°
CARPAL INSTABILITY NON-DISSOCIATIVE (CIND)

Aetiology:
1]. Congenital:
o Hyperlaxity
o Marphan
o Ehlar Danlos
2]. Traumatic
3]. Inflammatory:
o Rheumatoid arthritis
Pathology
• The key feature:
1]. Absence of dissociation within the proximal carpal row
2]. DESTABILIZATION between either:
I. Distal & Prox rows (scaphotrapezial, capitolunate, & triquetrohamate)
II. Distal forearm & Proximal row
III. Carpus & Metacarpals
• Locating the level of the instability is critical and often difficult.
C l i n i ca l l y
1- +VE PIVOT SHIFT: the hand is grasped and apply axial compression + alternating adduction &
abduction Æ Painful clunk
PXR
2- This shift is seen also on CINERADIOGRAPHS
3- Absence of SL or LT dissociation on x-ray, or surgical exploration.
Treatm en t
• Since this entity has only recently been described, it is difficult to offer firm recommendation.
• Midcarpal (capitolunate and triquetrohamate) arthrodesis will obviously solve the problem, but
that may be more than is needed.
• Soft tissue reconstruction is under trials
[The Han
nd] Page | 527
CARPAL INSTABILITY COMPLEX (CLIP WRIST)

Definition
It is a com
mmon carp pal instability form inn which th he force prropagate ffrom radia
al side causing
progressivve disruptioon of carp pal ligameents and/o or bones around
a thee lunate, with
w resultant
dislocation
n of the disstal row in a dorsal diirection on
n the lunate
e
Pathology
I. Lesser Arc: through
h the perilu
unar ligame
ents
II. Greater Arc: throug gh carpal bones
b around (4stagees)
1- Trans-SScapho Pe erilunar fr dislocatio
on
2- Luno-ccapitate diissociationn
3- Luno-ttriquetral dissociatio
d on
4- Perilun
nate Disloccation
• Taveernier’s Red
duction ma aneuver:
o axial tracction then in extensio
1]. 5-10 min of on
2]. Lock the capitate
c in
nto the lunnate conca avity
by gradua al palmar flexion é the lunatte is
f
fixed from the volar side
s
3]. Reduce the e capito-lu
unate unit into
i the radius
by extensioon, then chheck by PX
XR
4]. ± K wire fix
xation (SL & SC); remove at 8wkk
5]. Scaphoid
S c in 30° flexion 12wk
cast
• Ope en Reductio on
1]. If closed re
eduction faail: Scaphoiid # fixation é Herberrt screw & supplemen
ntal K-wire
e
2]. If lost redu w hump back scaphoid Æ OR
uction afterr CRUGA with RIF + BG
o As early ass possible
o Both dorsa al &volar approachess
CARPAL INSTABILITY LONGITUDINAL (AXIAL)

Cap
pitate –ham
mate dissociation and d others
• Mechanism
M m of injury y: high-ene ergy traumma (either a dorsopalm mar crush or blast force).
• Pathology
P y: Injury of the intrinsic ligaments
• Treatment
T t:
o The
T earlierr the treatm ment the better
b
o Debrideme ent of dam maged musscle ,early skeletal
s stabilization
o Address
A co
oncomitan nt neuro-vaascular or teendon inju uries
o Both dorsa al approachh to visualizze the carp
pal disruptio
on + extended palma ar approach
h
t assess th
to he associatted soft tisssue damag ge are usua ally require
ed .
ISOLATED CARPAL DISLOCATIONS

• All
A are rare
e but the ra
arest is the capitate one case reported
1- Scaphoo-trapeziall dislocatio
on
2- Trique
etro-hamate dissociattion
3- Volar /dorsal
/ perrilunate disslocation
o Forced hyp perflexion from a fall on the back of the hand.
h
o Fall on the
e hyper-exttended wriist with suppination off the forearrm
o Easily madde on the la
ateral view
w
o “CROWDED CARPAL SIGN “i.e., oveerlap of the
e proximal &distal row ws on AP view
v
NB Gymnasticc wrist = prremature distal

d radia
al physeal closure
c growth Æ rest
+ ulnar overg r for 6mo
Distal Radio-Ulnar Instability

Definition
• Instability is the loss of the normal joint relationship throughout the whole arc of motion
Anatomy
• DRUJ is a pivot joint, in ώ the radius rotates around the ulna
• Triangular fibro-cartilage complex (TFCC) = Ulno-carpal meniscal homologue is formed of:
1]. TFC
2]. Dorsal & volar radio-ulnar ligament
3]. MCL
4]. ECU sheath
5]. Some add UL, UC, UT ligaments
• All stabilizers inserts into the ulnar styloid fovea ∴ Isolated DRUJ dislocation éout styloid # is rare
• Extensor retinacula does not insert into distal ulna Æ pisiform & triquetrum
Ætiology
1]. Acute instability:
o Dorsal DRUJ dislocation ....................... pronation inj Æ starts é dorsal capsule & volar RU lig inj
o Volar DRUJ dislocation .......................... supination inj Æ starts é volar cap & dorsal RU lig injury
2]. Chronic instability:
o Simple after residual acute
o Complex after mal-united fracture BBFA
o Resection arthroplasty
Pathology:
1]. Rupture of the whole UCMH (TFCC)
2]. Styloid ulna #
3]. Fracture BB forearm ....................................... 60%
4]. Essex Lopresti injury ....................................... DRUJ + Interosseous membrane + radial head #
5]. Galeazzi fracture dislocation ...................... DRUJ + radial shaft # (fall on OSH + hyper pronation)
6]. Coles’ fracture ................................................... with TFCC insertion avulsion or ulnar styloid avulsion
Diagnosis:
Clinically ACUTE CHRONIC
Pain Acute pain y by pressure and supination pronation Chronic mild pain
Swelling Severe Mild
Deformity - in dorsal DRUJ dorsal prominence (More common) Same parameters
- in volar DRUJ wrist appears narrow ± sigmoid depression
Elbow Normal motion
Piano & Clunk May be +ve Usually +ve
PXR 1].Lat view shows subluxed or dislocated ulna Same
2].AP in dorsal DRUJ ..........yRU distance
3].AP in volar DRUJ .............RU overlap
CT Diagnostic Same
Ulna must fall within the confines of Mino’s lines
Treatment:
1]. Acute instability:
a. Simple Dorsal ..................................... reduction + supination cast
b. Simple Volar ....................................... reduction + pronation cast 6wk
c. Complex = (unstable) ..................... same but add wire fixation
2]. Chronic:
d. Simple subluxation .......................... TFCC reattachment ± styloid ORIF
e. Simple dislocation ............................ ECU sling operation
f. Complex dislocation ....................... Corrective osteotomy + ECU sling
g. After resection arthroplasty ......... ECU sling / Pronator Quad advancement / radius to ulna
transposition (One bone forearm operation)
Keinbock Disease
Definition
• Collapse of the lunate ð vascular insufficiency & AVN
Epidemiology
• Male aged 20-40 y
• Dominant wrists
• 75% ulna minus
• Manual laborers & recreational activities
Pathogenesis Theories: (Uncertain aetiology)
I]. Intrinsic factors:
1]. PATTERN I of the Lunate bl supply: ................. 30%
Single extraosseous vessels running in the dorsal
and volar radiocarpal ligaments
Less intraosseous vessels Æ y risk of losing vascular supply.
2]. Lunate architecture: some authors found TYPE I LUNATE é ulna minus has weaker architecture
3]. z RADIAL INCLINATION
II]. Extrinsic factors:
4]. Single forgotten WRIST TRAUMA
5]. REPETITIVE MICROFRACTURES Æ vascular compromise Æ z blood supply to lunate
6]. Recurrent compression of lunate bet capitate & radius Æ disrupts the intraosseous
structure. Associated é ULNA MINUS (there is no report of Kienbock's after Darrach's)
Diagnosis:
Clinically:
• Symptoms:
o Young adults
o Wrist pain that radiates to forearm
o Wrist stiffness
• Signs:
o Tenderness over lunate dorsally
o Weakness of grip
PXR:
• Ulnar variance is measured on PA views with wrist in neutral rotation
• LICHTMAN STAGING
STAGE 1 Ischemia Normal architecture & density ± linear compression # (TC & MRI)
STAGE 2 Necrosis Increased density, normal architecture & outline; cysts
STAGE 3 Fragmentation
3A Collapse No instability
3B Instability (prox. migration of capitate)
STAGE 4 OA OA
CT
• Determining the true extent of disease.
• Demonstrate collapse more clearly
• Demonstrate coronal fractures that split the lunate into volar and dorsal halves
TC
• z uptake (not specific, but exclude other causes of a hot lunate)
MRI
• MRI is most helpful in stage I Æ focal z T1 + y T2 = early involvement
• Other stages have both z T1 and T2
• MRI is an extremely sensitive and specific to detect marrow changes in osteonecrosis.
• Demonstrate revascularization following operation
Treatment:
• Remember:
1]. Keinbock's often causes little disability
2]. The radiological findings & symptoms do not correlate well.
3]. No surgical procedure has been conclusively shown to prevent progression.
4]. Excision of lunate alone Æ migration of other carpal bones Æ joint incongruity, limited wrist
motion and grip strength, and OA
• Surgery:
o Stage 1 & 2:
Indication: when pain & disability cannot be managed by splint, NSAIDs & reassurance
Aim: prevent lunate collapse
Results: 70% success rate in pain relief
Modalities:
1]. Joint Leveling:
a. Radial shortening
b. Ulnar lengthening - high non-union rate.
2]. Lunate Revascularization
a. Vascularized Pedicle graft from distal radius + pronator quadratus
b. Dorsal digital artery placed into drill hole on lunate
o Stage 3:
1]. Limited carpal fusion ± lunate excision (STT or scapho-capitate)
2]. Four corner fusion: triquetro-luno-capito-hamate fusion
3]. Wrist denervation
4]. Proximal row carpectomy
5]. Total wrist arthrodesis - in heavy laborers + severe OA
6]. Titanium lunate implants ± limited fusion
o Stage 4:
1]. Wrist denervation
2]. Total wrist fusion.
Blood Supply of the scaphoid:

• The bone is completely covered by cartilage except at two areas
1]. Volar insertion of the radio-scapho-capitate lig (Sling lig) that cross the waist of the scaphoid
2]. Dorsal spiral groove = waist of scaphoid through ώ blood supply to proximal 2/3 enters
• Radial artery gives:
1]. Dorsal branch ............... (~80% of supply via waist)
2]. Latero-volar branch .... (~20% via tuberosity)
3]. Distal branch ..................(variable presence)
• 65% ............................................ have scattered arterial foramena
• 20% ............................................. foramena at waist only
• 15% ............................................ foramena at distal 1/3 only
• This means that 35% of # scaphoids at proximal 2/3 would
have inadequate blood supply.
Fracture Scaphoid
Aetiology:
• FOOSH = fall on out stretched hand
Anatomy:
• Blood supply ......................................................... See before
Pathology:
• 5 fracture configurations are defined .........See picture
CLASSIFICATION (HERBERT)
A]. Stable acute
B]. Unstable acute
C]. Delayed union
D]. Established non-union
CLINICAL
History
• Forcible dorsiflexion of the wrist
• Palmarflexion in 3% of cases
Examination
1]. Fullness in the ASB = wrist effusion
2]. Tenderness in the ASB and scaphoid tubercle
3]. Pronation followed ulnar deviation will cause pain
Special tests
4]. Scaphoid compression test – longitudinal force along the 1st metacarpal
5]. KIRK-WATSON’S test
6]. Resisted pronation
X-ray
1]. PA in ulnar deviation
2]. Lateral with wrist in neutral
3]. Scaphoid view 1: PA 45deg. pronation & ulnar deviation; + shows STT joint
4]. Scaphoid view 2: AP with 30deg supination & ulnar deviation; + shows radioscaphoid joint
5]. Others:
o PA with wrist in slight extension (ZITER VIEW)
o AP with clenched fist to detect a ligamentous injury
OCCULT FRACTURES
Tc
• Sensitive but not very specific
CT
• Can still miss fractures
MRI
• Excellent sensitivity and specificity
• Fracture line will be visible on T2 (after 12 hours) as line of y signal = BM oedema
TREATMENT
1]. Stable non-displaced fractures
o POP cast: Below elbow cast ....................8wk (Moulded palm & neutral in AP)
o No need to include thumb & excessive ulnar deviation Æ distract the fracture
o Re-examine + PXR Æ If still ......................4 weeks cast more Æ then remove what ever the result
o Re-X-ray at 6 months
2]. Operative treatment
o Indications
a. Trans-scaphoid perilunate dislocations
b. Displacement of more than 1mm in any direction
o Approach
a. Volar through bed of FCR ................Good for waist & distal # (JOE DIAS)
b. Dorsal bet EPLIII and EDCIV................Good for proximal 1/3 fractures
o Types of internal fixation
a. Herbert screw
b. Herbert-Whipple screw
c. AO low profile compression screw
d. Acutrack screw
e. K-wires
SEQUELAE OF SCAPHOID FRACTURES

1. Delayed union ..................................................>4 months
2. Non-union .......................................................................5-10%
3. Malunion .......................................................... "HUMP BACK" deformity
4. Avascular necrosis - See eHand Images
5. DISI
6. Scaphoid non-union advanced collapse (SNAC) = loss of carpal height. It takes 5-10 years to develop
STAGE PATHOLOGY MANAGEMENT
SNAC I RS OA • Radial styloidectomy & preserve the radiocarpal ligaments
SNAC II SC + RS OA • Partial scaphoid excision (distal pole)
• Proximal row carpectomy
• Prox pole excision or prosthesis are abandoned Æ instability
SNAC III LC + SC + RS OA • Scaphoidectomy plus 4-corner fusion
Luno-capitate (LC), scapho-capitate (SC), Radioscaphoid (RS).
What is the aim of treating non-union?

1]. Correct carpal kinematics
2]. To achieve union
3]. Reduce pain
4]. Increase function
5]. z OA
Flexor Tendon Injuries Of The Hand

ACUTE FLEXOR TENDON REPAIR
Anatomy
• Annular & Cruciate pulleys prevent bow stringing of flexor tendons

• Thumb - Oblique pulley over proximal phalanx.
Tendon Nutrition
• The vinculae are remnants of mesotenon & provide the blood supply
& nutrition to the flexor tendons.
• The vincular system is supplied by the transverse communicating
branches of the common digital artery.
• Nutrition of the tendons is also derived from the synovial sheaths -
thus early mobilisation post-op is important.
Types of Injury
• The position of hand at injury determines the tendon retraction:
1- Flexed fingers - distal tendon retracts
2- Extended fingers - proximal tendon retracts
Treatment
Aim:
1- Regain of normal anatomy
2- Provide functional results
3- Avoid complications
Contraindications to Repair
1. Wounds liable to infection
2. Inability of patient to cooperate with rehabilitation
• Failed primary repair is worse than no repair! If only one tendon is cut the functional result will
be better than a poor repair.
Zones
Zone 1 FDS insertion to FDP The tight A4 pulley makes repair difficult. Aim to advance FDP stump
insertion to reattach to terminal phalanx.
Zone 2 Zone 1 to proximal part two slips of FDS; Vincula
of A1 pulley
Zone 3 Zone 2 to distal edge of easily repaired with good results. Don't suture lumbrical muscle
flexor retinaculum around tendon repair.
Zone 4 within carpal tunnel
Zone 5 proximal to carpal Can use mattress sutures if many tendons need repair.
tunnel
Thumb T1 FPL insertion to A2 FPL tendon lacerations often retract into the thenar area or wrist; -
pulley unlike the fingers, the FPL often lacks a vinculum and does not have a
Thumb T2 Zone 1 to distal part A1 lumbrical, and therefore the tendon is free to retract; Repair requires
pulley an incision prox. to carpal tunnel & 'pull-through'
Thumb T3 Zone 2 to carpal tunnel also damage thenar muscles & recc. br. median nerve.
Incisions
Safe Volar Hand Incisions
For retracted tendons:
• Try milk the tendon with the wrist flexed.
• Small incision a the distal palmar crease just proximal to A1
pulley. Pass a silastic cannula from the distal wound
through the sheath to the proximal wound. Attach the
proximal tendon to the cannula & pull through to distal
wound.
Technique
Core Non-absorbable 4/0 suture - Modified Kessler technique.
6/0 monofilament running epitenon suture.
Close sheath, if possible.
Multiple Flexor Tendons at the Wrist (Zone 5)

Order of Repair:
1. FPL
2. FDP tendons
3. FDS to middle & ring fingers
4. FDS to index & little fingers
5. Ulnar nerve
6. Ulnar artery
7. Median nerve
8. FCU
9. FCR
10. Radial artery - ligated.
Post-operative program
BELFAST REGIMEN:
1- 48hrs post-op remove dressings & put splint
o Thermoplastic splint: wrist 20º., MCP
70º, 2/3 up forearm, straps on palmar
crease, wrist & forearm.
2- First 6 weeks:
o Fingers- Every 2hrs:
a. Passive flex (2x/ individual finger)
b. Active extension (2x/ mass action)
c. Active flexion (2x/ mass).
o Thumb- Every 3hrs.- as above.
3- After 6 weeks:
o Remove splint & progress to active
flexion of individual joints.
4- 6-8 weeks: use hand, no heavy liting.
5- 8-10 weeks: slowly incr. activity, stretches into extension, fine work.
6- 10-12 weeks: Driving, heavier work.
7- >12 weeks: Full funtion (60% strength back at 16 weeks).
Complications
1. Rupture
2. Infection
3. Adhesions - prevented by early passive ROM
4. Joint contractures - too tight repair or from prolonged splintage
5. Bow stringing - from damaged pulleys
SECONDARY FLEXOR TENDON REPAIR & RECONSTRUCTION

Defined as delayed primary repair performed > 3wks after injury.
Contracture of the muscle-tendon unit has usually occurred & tendon graft often required.
Prerequisites for tendon reconstruction:

1. Adequate skin & soft tissue cover
2. Skeletal alignment
3. Good passive ROM of joints
4. Adequate sensation & circulation of finger
Methods: JEANNE'S sign identifies thumb metaphalangeal joint

1. Delayed direct repair hyperextension of 10° to 15° with key pinch or gross grip.
FROMENT'S sign refers to the exaggeration of thumb
2. single stage flexor tendon grafting interphalangeal joint flexion during key punch by the flexor pollicis
3. two-stage grafting longus in ulnar nerve palsies.
WARTENBERG'S sign is the inability to adduct the extended small
4. tenodesis or arthrodesis finger due to an ulnar nerve palsy.
5. tendon transfer DUCHENNE'S sign refers to clawing of the ring and small fingers.
Pollock's sign is the inability to flex the distal interphalangeal joints of
6. Amputation the ring and small fingers in high palsies
Two-stage Flexor Tendon Reconstruction

Contraindications:
1. Infection
2. Too much damage to support an implant or allow decent tendon gliding
3. Motivated patient
4. Experienced surgeon
5. Experienced Hand Therapist
First Stage:
Aims:
1. Joint contractures must be released
2. Tenolysis of scarred tendons
3. Finger must have free & full passive ROM
4. Digital nerve repair or grafting
5. Provide healthy skin (may require a flap)
6. Full flexion on traction of the silastic rod at the wrist
7. Preserve A1, A2 & A4 pulleys
Second Stage:
2 - 3 months after first stage.
Tendon Graft options:
1. Palmaris Longus
2. Plantaris - best for multiple tendon grafts
3. Long toe extensors - 2nd, 3rd or 4th toes
4. EIP
5. Fascia Lata
Trapezio-Metacarpal OA (Rhizarthrosis)
ANATOMY
• Key joint of the thumb
• Saddle-shaped joint: Biconcavo-convex shape
• Joint compression force = 12kg (120kg for strong grip)
• 3 Main ligamentous stabilisers:
1. VOLAR OR BEAK LIGAMENT (volar oblique lig., anterior oblique lig.(AOL), volar CMC lig., deep ulnar lig.)
• Very strong - primary static stabiliser
• Prevents dorsal translation of the MC in key pinch
• Allows rotational motion
• Important in bennett's fractures
2. DORSAL LIGAMENT
• thin & reinforced by APL
3. LATERAL LIGAMENT
• broad band running from lateral surface of trapezium to 1st MC base
PATHOPHYSIOLOGY
• Described by Pelligrini (1991) as attritional changes in the beak lig. Æ destabilisation of the TMJ
• These changes initially occur in the palmar contact areas of the joint.
CLINICAL
History
1- Female:male .............................................. 10:1
2- Enquire about history of injury.
3- Pain y by- forceful pinch grip such as turning door key, holding tea cup or sewing.
Signs
1- ADDUCTION-FLEXION deformity of the thumb reducing the thumb index web angle.
2- 'SHOULDER SIGN' = radial prominence at base of thumb, from dorsal sublux. of MC on
trapezium
3- CRANK TEST = axial loading + passive flexion & extension of 1st MC
4- GRIND TEST = axial loading + rotation of 1st MC on trapezium
5- TORQUE TEST = Distract MC & rotate. - differentiates CMCJ OA from de Quervain's disease.
6- Look for Trigger fingers & CTS.............. 45%
RADIOGRAPHS
• AP, oblique & lateral views are usually adequate.
• ROBERT PRONATED view = fully pronate forearm & internally rotate shoulder.
• Dynamic stress views
o Indicated where instability suspected & standard x-rays are –ve
o = AP views of both 1st CMJ whilst pressing the radial aspects of thumb tips together.
d]
TRE
EATMENT T
Alw
ways non-o
operative initially
• Splinting
• Strengthening thenar muscless
• Steroid injections
Surrgery: Wheen non-operrative treatm ment fails.

1. Soft tissue reconstruct
r tion alone
• for insttability with h no articu ular change es
• FCR to reconstruc ct the beakk lig.
2. Osteotomy
O y
• abducttion-extenssion osteottomy to offf-load the palmar p surrface of thee joint.
• For hig gh demand d young ad dults with early
e disease.
3. Arthrodesis
A s
• for you ung high demand
d paatients
• 20% failure rate
4. GERVIS EXCISION ARTHROPLASTY (Trrapeziectomy) alone
• Causess weaknesss, instability y, prox. miggration of MC
5. SWANSON INTERPOSITIONAL ARTHROPLASTY (sillicone prossthesis)
• Problem ms:
1]. imp plant sublu uxation & dislocation
d
2]. rapid wear
3]. siliccone synovvitis
6. Total
T joint arthroplast
a ty
• Constra ained ball & socket design
d
• Wear ratesr of 34%% at 5yrs.
• Less co onstrained designs in developm ment.
7. Excision
E Artthroplasty & soft tissu ue reconstrruction
• = TRAPIEZECTOMY & LIGAMENT RECONSTRUCTION & SOFT TISSUE INTE ERRPOSITION (LRSTI)
• Theore etically dea als with artiicular dege eneration + instabilityy + length
• Technique (N NOTTINGHAM}:
• Incision n: inverted 'Y', centred over bon ny promine ent base off 1st MC. (oover ASB)
• Dissectt down to joint j avoid ding radial artery (at proximal
p en nd of wound) & term minal brancches
of radia al nerve (laarge)
• Trapeziectomy: Divide D Trappezium into o halves or quarters w/
w osteotome or saw w, & remove e it
piecem meal. Avoid d cutting FC CR.
• + LRSTII:
[1]. Make
M hole in
n MC1 base e ⊥ to plane of thum mbnail, fromm radial coortex to basse
[2]. Harvest half of FCR R tendon: thro a series of oblique iincisions. (Split tendon
ongitudinallly to inserttion on MC
lo C2). Detach h a 10-12 cm strip.
[3]. To o suspend MC base: pass p free end
e of FCR through hole h in base
e of 1st MCC & out raddial
ho ole. Suture e it to the sooft tissues on the MC C & then to
o itself.
[4]. Make
M spacer: put long gidudinal weaving
w suture in FCRR remnant & Anchovvy tendon on o
itsself. Insert it into trappezium fosssa.
• Close: Can C put K--wire acrosss trapezium m fossa if not
n doing LRTI
L + vola
ar slab, é th
humb IPJ frree.
• Post-op p: Mobilise at 3-6wks (Davis: rem move k-wirre at 3wks, mobilise a at 6wks)
• Compliications: Damage to
1]. su uperficial branch
b of ra
adial nervee
2]. Ra adial arteryy
3]. Pa almar cutaneous branch of median nerve e.
Rheumatoid Hand
Clinical Assesment
• Wrist radial shift • DIP mallet
• MCP ulnar drift • Rheumatoid Thumb
• PIP swan & boutonniere’s & intrinsic + • Tenosynovitis
HISTORY:
1. Pain - due to synovitis or secondary OA
2. Loss of Function: Using toothbrush, hairbrush, knife, fork
3. Cosmesis - may be extremely imp to patient.
EXAMINATION: Quick elbow, shoulder & neck
LOOK (MOST NB):
1- Exensor surface
2- Flexor surface
1- swelling
2- Nodules
3- wasting
4- Deformity:
zig-zag - coronal / sagittal

MCPJs - dropped fingers, ulnar drift

finger deformities

5- Piano sign of DRUJ when wrist supinated
6- Features of SLE, Psoriasis, scleroderma (see below)
FEEL :
1- Tender areas
2- Correctability of joints é MP flexion (tight lig) = soft tissue procedures indicated
3- Stability of the joints (e.g. MCL of thumb)
4- Sensibility
MOVE:
1- Actively EXTEND & FLEX joints fully & OPPOSE thumb Æ ext lag or subluxation
2- Passive movement
3- Intrinsic Tightness:
1- Bunnel Test: (DDx tight capsule)
Ask the pt to flex the PIPs é extended MPJ (taught intrinsics)
•
If it doesn't flex ......................tight intrinsics or PIP capsule contracture.
•
• Flex MP (relax intrinsics) .....If it doesn't flex = tight capsule.
2- DDx Long flexor tightness
• Ask the pt to flex the IPs if tight, Relax FDS & FDP (by wrist flexion)
• If pt can flex the IPJ's ..........intrinsic tightness
• If can not ................................Volkmann's contracture.
3- Bouvier's Test (DDx PIPJ capsule & ext expansion tightness)
• Block MPJ hyper-extension & ask the pt to extend IPJ:
• If he can ..................................PIPJ capsule & ext. mech are normal
• If he can not ..........................= abnormal (central slip adherent / volar sublux of lateral bands)
4- DDx Lumbrical Plus
• = MPJ flexion lead to IP extension; because FDP becomes an extensor of the PIP
• Ask pt to flex fingers ............PIP extension
• Relax FDP (wrist flexion) .....sublimis work without antagonism ÆPIP flex
GENERAL MEDICAL ASSESMENT:

1. cervical spine
2. TMJ
3. Pulmonary
4. General
Investigations:
1. Hb (anaemia of chronic disorders)

2. ESR
3. WBC (z in Felty's syndrome)
4. platelet count (z with NSAIDs)
5. Rh factor
6. Anti CCP
7. LFT (z é methotrexate)
Treatment
Lumbrical plus: (lumbrical tighter than FDP)
Causes: -
Aims of Treatment: 1- Fdp laceration or rupture distal to the
1- Pain relief lumbrical origin
2- Improve function 2- Amputation of the distal phalanx
3- Prevent further damage (distal to central slip insertion)
4- Cosmesis 3- Excessively long tendon graft.
Treatment: division of the lumbrical
Principles:
• Operate on proximal joints then distal
• Tendons before joints
• Alternate fusions with motion-sparing procedures
• Staged procedures: according to SOUTER Staging
Souter Stage Clinical Treatment

1 Acute synovitis medical Mx & splinting
2 Chronic synovitis Synovectomy
3 Specific deformation Reconstructive
4 Severe crippling Salvage
METACARPOPHALANGEAL JOINTS
ULNAR DRIFT
Pathogenesis of the deformity:
Early
1- Radial deviation of wrist
2- Synovitis push the extensor mechanism ulnar ward
3- Destabilization of volar plate, LCL, & A2 pulley Æ flexor tendon slips ulnar ward
4- Erosion of metacarpal heads.
Late
5- Contracture of MCL
6- Contracture of the interossei on ulnar side (At this stage passive correction is impossible)
Clinical, Investigations:
• as before (look, feel,…)
• + main problem is INABILITY TO HOLD LARGE OBJECTS (loss of MPJ ext)
Treatment
• as before (Principles, aim, staging)
• + RECONSTRUCTIVE PROCEDURES:
1. SOFT TISSUE BALANCING: Vital to ascertain which structures are tight
1. FLATT radial ext mech reefing & double-breasting & LCL reconstruction
2. Ulnar release; extensor mechanism, MCL …
3. Combined ulnar & radial procedures:
[i]. Ulnar ext mech is passed via radial capsule to prox phx base
[ii]. Crossed intrinsic transfer - ulnar IOM transfer to the next radial finger (LCL)
2. MP ARTHROPLASTY:
1- Excision arthroplasty - causes unstable joint, shortening of ray
2- Excision arthroplasy & soft tissue interposition - poor ROM
3. MCPJ REPLACEMENT (SWANSON'S):

• Simply a spacer + some stabilising features Æ Good results
• Complications:
[i]. Silicone synovitis (very rare)
[ii]. recurrent ulnar drift
[iii]. implant failure
[iv]. infection
Proximal Inter Phalangeal Joints

A. Swan-neck deformity:
• Causes:
Failure of PIPJ stabilizers 2ry to:
[1]. Generalized joint laxity
[2]. Volar synovitis Æ FDS insufficiency (failed CHIASMA OF CAMPER bet the 2 FDS slips)
[3]. Volar plate insufficiency (2ry to synovitis)
Intrinsic over activity 2ry to:
[4]. intrinsic spasticity
[5]. intrinsic tightness 2ry to MCPJ disease
Long extensor over activity 2ry to
[6]. Extrinsic spasticity
[7]. Tight posterior PIP capsule
[8]. DIP mallet
Nalebuff Swan Neck type Pathology Diagnosis Treatment

[1]. PIPJ flexible -FDS insufficient -Can Extend DIPJ é flexed PIP -FDS tenodesis (FDST)
-DIP mallet -Cannot -DIP Fusion
[2]. zPIP flexion é ext MP -Tight Intrinsics -Bunnell Test -Intrinsic Release
= locked swan -Weak volar plate -Advance volar plate
[3]. PIP stiff even é flexed MP -Tight post PIP cap -Bunnell (PXR NAD) -MUA ± Dorsal release
[4]. PIP stiff + OA -Sublux + OA -PXR Articular/ bony changes -Arthrodesis
B. Boutonniere deformity
• Causes:
1- PIP Dorsal synovitis Æ tighten the extensor tendons
2- Rupture of CENTRAL SLIP of extensor tendon 2ry to this synovitis
3- Volar dislocation of LATERAL BANDS, being converted from extensors to flexors.
4- HYPER EXTENSION OF DIP & MP occurs ð tightening of the extensor tendon
Deformity Clinically PXR Treatment
Mild (10-15º) PIP is actively correctable N Reposition the lat bands+ synovectomy ± extensor tenotomy
Mod (30-40º) PIP is passively correctable N Central band reconstruction é the lateral band
Severe (fixed) Stiff OA Arthrodesis - from 20º (index) – 45º (little finger)
C. Intrinsic Plus Deformity

• Due to intrinsic tightness. Pathology. CP as previous
• Treatment:
1- Intrinsic release
2- Synovectomy
3- Total arthroplasty
Rheumatoid Thumb
Nalebuff Deformity Initiating feature CMJ MPJ IPJ Treatment

1 Boutonniere MP synovitis Abd. Flex. Hyperext. Arthroplasty MP ±
extensor realignment
2 1+3 MP & CM synovitis Add. Flex. Hyperext. 1± 3
3 Swan-neck CM synovitis Add. Hyperext Flex. CM arthroplasty
MP volar plate tight
4 Gamekeepers MP MCL destruction Add. Abd. - Lig. recon ± MPJ fusion
5 3 + Normal CM MP volar plate tight N Hyperext Flex. MP fusion
6 Arthritis mutilans Bone destruction Short Unstable Unstable Fusion
OTHER FORMS OF ARTHRITIS OF THE HAND
Systemic Lupus Erythematosus (SLE) Littler intrinsic release

A, Extensor aponeurosis at
• Ligamentous laxity of the MCPJs level of
• Joint surfaces often unaffected metacarpophalangeal joint
consists of long extensor
tendon, transverse fibers (ώ
Psoriasis flex MP joint), and oblique
• DIPJ involvement fibers (ώ extend IP joint).
• Gross joint changes Crosshatched part is
resected from each side of
• No tendon involvement hood.
• nail changes B, Appearance of
aponeurosis after release
Scleroderma
• calcinosis causing fingertip ulceration
• CREST syndrome - Calcinosis, Raynaud's syndrome, Eosophageal strictures, Sclerodactyly,
Telangectasia.
FLEXOR TENOSYNOVITIS
Pathogenesis:
• Tendons are affected by either the synovitis or ð attrition on a bony irregularity
[I]. Trigger fingers: synovium is thickened hypertrophied & has fibrinoid rice bodies
1- Type I: ....................... A1 pulley
2- Type II: ...................... Proximal to A1 pulley
3- Type III: ..................... A2 Pulley
4- Type IV: .................... Generalized
[II]. Tendon Ruptures: The most commonly affected are:
1- EPL on prominent LISTER tubercle
2- EDC to ring and little ð prominent ulna VAUGHN-JACKSON $
3- FPL ð attrition on spike from scaphoid = MANNERFELT $
4- FDP to index finger
Clinical, Investigations:
1- As before (look, feel,…) +
2- Trigger finger
3- CT$, Cubital tunnel $, Posterior Interosseous $
4- PUFFY thick feeling palm
5- PINCH TEST – thickened tenosynovium can be 'pinched' thro defects in fibrous sheath
6- Test function of FDP index & FPL by asking patient to pinch:
o Normal = tip-to-tip
o AbN = pulp-to-pulp (also occurs with AIN palsy) [also called PINCH TEST by some]
Management:
I. Acute synovitis = splinting & drugs (NSAIDs, steroids)
II. Chronic synovitis:
• If conservative Rx has failed after 4 months should consider surgery.
• SYNOVECTOMY at three sites:
1. Carpal tunnel
2. Palm at level of mouth of A1 pulley
3. Just distal to A2 pulley
III. Tendon Rupture:
• Same as secondary tendon reconstruction in flexor tendon injury; see before
Vaughn-Jackson Syndrome
• Rupture of EDC of ring & little fingers
• ð prominent ulna (CAPUT ULNA) &DRUJ synovitis
• Clinically: 'TUCK SIGN' = synovitis tucks under the skin with movement.
• DD= subluxation, PIN palsy, locked trigger finger
• Treatment:
1- DARRACH for pre-rupture
2- TENDON TRANSFER (EIP to EDM) for rupture.
Mannerfelt Syndrome
• FPL rupture due to Scaphoid spike or volar synovitis
• Treatment:
1- IPJ arthrodesis
Zones of extensor tendons

De Quervain’s Syndrome
Definition
st
• It is an entrapment tendinitis of the 1 dorsal compartment tendons at the wrist, resulting in pain
é thumb motion
Anatomical Considerations:
st
• APL & EPB tendons pass through 1 dorsal compartment (DC1), & anchored by ext retinaculum
• APL tendon usually is multistrand
• EPB tendon is single slim and μβ congenitally absent
• A septum separating DC1 into 2 subcompartments often is noted at surgery Æ move the thumb;
if a tendon glides with MCP ..................................... EPB
Aetiology:
1]. Acute trauma ⊕ thickening of the tendon sheathes
2]. Repetitive trauma
3]. Efforts at thumb motion + radial or ulnar deviation of the wrist y inflammation
Epidemiology
• The most common entrapment tendinitis in the wrist
• Trigger digit is the most common in hand and wrist (20 times more common)
• Mothers of infants aged 6-12 mo; repetitive lifting of the baby
Diagnosis:
Clinically:
• Symptoms:
o Usually bilateral
o Pain with thumb and wrist motion
o Thickening at the radial styloid.
o Crepitation or actual triggering rarely is noted.
• Signs:
o Fusiform thickened over DC1
o Tenderness
o +VE FINKELSTEIN TEST: thumb flex across palm + ulnar deviation Æ sharp pain at DC1
o Tenderness is absent over the muscle bellies proximal to the first dorsal compartment.
o Tenderness is absent on axial loading at CMCJ unless the patient has arthritis
PXR
• It is not done for routine diagnosis of DeQuervain
• It is used to exclude cases of rhizarthrosis
DD:
1]. RHIZARTHROSIS ................................................................ PXR
2]. INTERSECTION SYNDROME ............................................. Friction tenosynovitis of DC2 tendons
o ð friction between ECRL, ECRB & APL, EPB (DC2 & DC1 Tendons)
o It is more common than DeQuervain especially in athletes and heavy lifters
o Clinically: ............................................................ more prox tenderness + WET LEATHER crepitus
o ttt: .......................................................................... usually by activity modification
3]. WARTENBERG syndrome: ............................................ radial sensory n irritation
o As it winds out from deep fascia beneath brachio-radialis, to be superficial to ECRL
o Both tendons may act as scissors entrapping the n
o Pain & parasthesia over the distribution of RSN; y with hyperpronation + Tinel’s sign
o ttt: treated by surgical release
Treatment:
Medical therapy:
1]. Splinting of the thumb
2]. Steroid Injection ............................................................. 50% permanently relieves symptoms
Surgical therapy: ............................................ If injection therapy fails

• Under local or regional anesthesia + tourniquet
• A 3-cm transverse incision is preferred ................ better appearance of the scar
• Longitudinal blunt dissection is used ................... until the first dorsal compartment is exposed.
• Care should be carried not to injure the superficial radial nerve
• DC1 is sharply opened longitudinally.................... for 2 cm to release APL & EPB.
• If a septum is found in DC1 bet APL & EPB ........ release it
• Tendon sheath; could be excised, even partially for the thickened part, or step cut reconstruction
may be done for loose roof reconstruction, to prevent subluxation
COMPLICATIONS
1]. Superficial radial nerve injury is the most irksome complication.
2]. Persistent entrapment ...............................if APL slip is mistaken for EPB ώ will remain entrapped.
3]. Subluxation of released tendons is possible.
ULNAR IMPACTION SYNDROME

Anatomy: ulnar variance
• Normally distal surfaces of radius & ulna are leveled & share in lunate support = neutral variance
• 80% of loads .................................................. transmitted through radius
• 20% of loads .................................................. transmitted through TFCC to ulnar head
• Short ulna is called ulna minus & long ulna is called ulna plus
• Pronation and power grip y the variance (2mm y variance Æ 40% y loads)
Ætiology:
1]. Congenital
a. Ulna plus Chronic DRUJ disorders
b. Madelung’s deformity 1]. DRUJ chronic instability
2]. Traumatic: 2]. Ulnocarpal impingement $
a. Ulnar styloid fractures 3]. DRUJ arthritis
b. Radial mal union: e.g. Galiazzi #
c. Distal radial physeal arrest
d. Longitudinal Radio-Ulnar Dissociation LRUD:
i. Essex-Lopresti lesion
ii. Radial head Fracture & excision
3]. Wrist arthrodesis
Pathologic types
1]. Ulnar impaction syndrome ..................... +ve variance
2]. Ulnar impingement syndrome ............. -ve variance
3]. Impaction $ 2ry ulnar styloid process nonunion
4]. Ulnar styloid impaction $ ........................ long ulnar styloid
5]. Hamato-lunate impingement $ ........ Type II lunate é hamate articulation Æ hamate malacia
STAGES:
1]. Central TFCC wear
2]. Ulno-lunate chondromalacia
3]. Perforated TFCC
4]. Perforated luno-triquetral lig
5]. Ulno-carpal OA
Diagnosis:
Clinically:
• Symptoms: Ulnar sided pain y é pronation & gripping
• Signs: Tenderness y é ulnar deviation & pronation
PXR:
• Detect cause; ulnar variance, mal-union, …
• Detect complication, e.g. OA
Treatment:
1]. Conservative: ................................................ activity modification, NSAIDs, spints
2]. Surgical: ................................................... a]. Corrective osteotomies
................................................... b]. Ulnar shortening
................................................... c]. Arthroscopic Wafer: debride central TFCC perforation
................................................... d]. Excision arthroplasty for terminal stage 5
Dupuytren's Contracture
INCIDENCE
1. Anglo-Saxon, Males > 65yrs ....................... 25%
2. Family history - AD; 1st º relatives............... 70%
3. Alcoholic liver, DM, IHD, COAD, HT
Other related fibromatoses
1. GARRODS KNUCKLE pads: MP or PIP dorsal plaques
2. LEDDERHOSE $ (plantar fibromatosis)....... 5%
3. PEYRONIE'S disease (penis) ........................... 3%
AETIOLOGY
• Two Theories:
[1]. Intrinsic Theory = METAPLASIA of deep fascia
[2]. Extrinsic Theory = arise in the SUBDERMAL FIBROFATTY tissue &attach to deep fascia
• Either of which the basic initial event is Oxygen free radicals:
[1]. y PDGF-β
[2]. y type III collagen
[3]. y myofibroblast: derived from skin, fibrilar bundles & y ATPase & y Fibronectin Æ contractility
PATHOANATOMY
• Superficial palmar fascia consists 3 parts:
1. Medial part covering hypothenar muscles
2. Mid-palmar fascia
3. Lateral part covering thenar muscles
Bands = healthy fascia
o GRAYSON'S LIG. converts to the spiral cord
o CLELAND'S LIG. Is not involved in Dupuytren's.
o SUPERFICIAL TRANSVERSE LIG is not involved in the process. It overlies superficial palmar arterial arch
o SAGITTAL FIBRES run from mid-palmar to deep palmar fascia. They are not involved in the disease.
Cords = diseased fascia:
1. PRETENDINOUS CORD causes MP4-5 contractures
2. CENTRAL & LATERAL CORDS cause PIP4-5 contractures.
3. SPIRAL CORD cause PIPJ contractures + push the NVB towards the skin & midline of the finger.
4. NATATORY CORDS causes:
[1]. Web space contractures
[2]. Envelopes ADM & NVB on the ring & little fingers
[3]. Forms the DISTAL COMMISURAL lig. Between index & thumb &causes contracture.
Stages:
[1]. Proliferative stage: ......................... y cellularity of the palmar fascia
[2]. Involution stage: ............................ dense myofibroblast network + less collagen
[3]. Residual stage: ................................ few fibroblasts + dense collagen
CLINICAL
HISTORY:
1. Fingers get in the way with:
• washing face
• combing hair
• putting hand in pocket
• putting hand in glove
• racquet sports & golf
2. Palmar THICK NODULE that progress to the little and ring fingers
3. PROGRESSIVE DEFORMITY &palmar puckering
4. Dominance, Family history, DM, IHD, COAD, Epilepsy, Alcohol, …
5. Other involvement
EXAMINATION: same +
1. Sites of nodules & cords
2. Sensibility & RSD
3.MP ANGLE - measure
4. PIP ANGLE - measure
5. TABLE TOP TEST OF HUESTON - place the hand & fingers prone on a table. Positive = hand won't go
flat. If negative surgery is not indicated.
6. KNUCKLE PAD (GARROD) - well-circumscribed firm dermal papules, nodules, or plaques approximately
0.5 - 3.0 cm in size, located on the extensor aspect of the PIP or MCP joints
7. Other fibromatoses; Peyronie, and Ledderhose
STAGING - Woodruff
STAGE DESCRIPTION MANAGEMENT
1 No contracture Leave alone
2 One finger MP contracture Surgery
3 One finger MP + PIP contracture Surgery not easy
4 > one finger MP + PIP Surgery prolonged & only partly succesful
5 Finger-in-palm deformity consider amputation
SURGERY
INDICATIONS
1- No absolute indications
2- Patient is incapacitated by the contracture.
3- Tabletop test of Hueston = Patient unable to place hand flat on table due to contractures.
4- Patient is understanding that it:
o Recurs DUPUYTREN'S DIATHESIS = y recurrence
o Complications; CRPS, stiffness 1. young
o May leave painful scar 2. male
o <30° contractures needs no surgery 3. family history
o MP are better than PIP 4. bilateral
o Needs rehabilitation 5. fibromatosis elsewhere
AIMS
1. Excise the diseased fascia
2. Release digital contractures
3. Retain full flexion of the digits
4. Preserve neurovascular structures
d]
T
Teechnique
INCISION ADVANTAGES DISADVANTAG ES
GE
1- Transversse midpalm
m for preetendinous band Req
quires frequ
uent dressin
ngs &
- Left open
o MCCASH techniqu
(M ue) coo
operation ppost-op.
- Full th
hickness gra HUESTON)
aft (H
2- Bruner's zig-zag
z Good exposure Diff
fficult to raisse flaps if thin skin
y NVB
N damag ge
y scarring
s at ssides & basee
3- Longit., Z-plasties
Z Good exposure,
e zd
damaging NVB
N Diffficult to matcch incision in
n 2 finger dissease
PROCEDURE ADVANTAGES DISADVANTAGES

1- Fasciotom
my Elderlyy é MCP con
ntracture ma
ainly
Severe contracture é bad skin
n
2- Partial Fa
asciectomy Removves the nodu ules only
SKOOG)
(S Most commonly performed
p
3- Total Fascciectomy Removves most of the fascia Imppossible to rremove all fascia,
f
MCINDOE)
(M Reccurrence,
Sw
welling & joinnt stiffness.
4- Dermofasciectomy For Du
upuytren's & recurrence
e
HUGSTO
(H N)
ON
5- External Fixator Gentlee correction for 2wks. Then
T
MESSINA)
(M surgica
al release; under distracction
the disease seemss to regress!
6- Amputattion 4 finge
er-in-palm é macerated
m skin
s neu
uromas, bio
omechanica
al
PO
OST-OPERATIVE CARE
• Splint hand
h with coomfortably extended
e wrrist & fingers
• Check wounds
w at 48
8hrs. & applyy Thermoplaastic splint essp for McCa
ash open pallm.
• Hand thherapy &sca ar care contiinue for 3 months
• Night sp
plint for 6 moonths.
PIIP
P STABILIZEER
RS
CO
OMPLICAT
TIONS
1. Digital nerve
n divisio
on
2. Ischaemmic digit
3. Haemattoma
4. Infectio
on (early deb bridement)
5. Skin neccrosis
6. Scar con ntracture
7. Joint stiiffness
8. CRPS
9. 2ry CT$$ & trigger finger
f
10. Recurreent disease
PIP Joint
J Releasse:
• Never perform
p vola
ar plate cap
psulectomy, since it can n cause stiffn
ness
• Preferreed method =
1. Release Cle
eland's ligam
ments
2. Release the
e fibrous flexxor sheath
3. Release the
e check-reinn ligaments of the volarr plate
4. Release the
e lateral bannds of the exxtensor mechanism (so o it shifts do
orsally)
5. Can use a percut.
p transsarticular K--wire for 7-1
10days.
6. For a severe flexion co
ontracture consider arth hrodesis with digital sh hortening.
Chronic Wrist Pain
DIFFERENTIAL DIAGNOSIS:
Location Cause
Radial 1]. De Quervain's tenosynovitis
2]. Rhizarthrosis
3]. Intersection $
4]. Wartenberg $
5]. Scaphoid non-union
6]. ganglion
Dorsal/ Central 1]. SL dissociation

2]. SLAC
3]. SNAC
4]. Intra-osseous ganglion
5]. Ganglion
6]. Keinbock's disease
Ulnar Dorsal Zone

1]. Traumatic:
a. Fractures: hook of hamate
b. Carpal instability: CID, CIA
c. DRUJ instability
d. TFCC tears
e. ECU subluxation
2]. Inflammatory:
a. DRUJ OA
b. Ulno-carpal OA
a. CMC OA
3]. Tumors:
b. Ganglion
c. Intraosseous ganglion
4]. Vascular:
f. Kienböck
g. AVN capitate
5]. Miscellanous:
h. Ulnar abutment syndromes
Volar zone
1]. Traumatic:
a. Fractures: piso-triquetral
b. DRUJ volar dislocation
2]. Inflammtory:
c. Piso-triquetral OA
d. FCU tendinitis
3]. Tumors: Ganglion
4]. Miscellaneous:
e. Guyon’s Canal $
Tourniquets
‘The use of a bloodless field is an integral part of much limb surgery, but may have become a ritual’.
Application
• Application of a pneumatic tourniquet should be performed by experienced personnel who possess a
good knowledge of its use and potential complications.
• Relative contraindications are sickle cell disease, peripheral vascular disease, prosthetic vascular graft or
extensive soft tissue injury.
• The tourniquet should be tested by inflation, and then completely deflated, prior to limb application. To
apply the tourniquet, the limb is exsanguinated, either by elevation for 3 to 5 minutes, or by applying a
soft rubber compression bandage.
• The tourniquet should be padded with a soft dressing to prevent the wrinkles and blisters that may
occur when the skin is pinched. It should be applied to the upper arm or thigh where there are
adequate muscle envelopes to protect invested nerves from compression.
• Following tourniquet application, inflation should be rapid to prevent filling of the superficial veins
before arterial occlusion.
• Deflation prior to wound closure allows identification and coagulation of major bleeding vessels.
Inflation pressure
• The ideal pressure to which the tourniquet should be inflated is unknown. It depends on the patient’s
age, blood pressure and extremity size.
• On conical extremities, for example in very muscular or obese individuals, curved cuffs are ideal because
they require significantly lower arterial occlusion pressures than straight (rectangular) cuffs
• In addition, wider cuffs are more effective at lower inflation pressures than are narrower ones
• Several methods are proposed for the determination of optimal inflation pressure for extremity surgery
Methods used in determining pneumatic tourniquet inflation pressure
1. Add 50-75 mm Hg above the systolic by Doppler stethoscope, to allow for collateral circulation
2. Add 90-100 mm Hg to the preoperative arm blood pressure for lower limb surgery
3. Add 50-75 mm Hg / 100-150 mm Hg above the systolic pressure for UL / LL surgery, respectively.
Post-tourniquet syndrome pathology

• Interruption of blood supply leads to tissue hypoxia, metabolic derangement and ultimately, cell death.
• Cellular hypoxia results in anaerobic metabolism and lactic acidosis.
• Depletion of high-energy phosphate occurs with subsequent loss of physiological ion gradients cross the
cell membrane due to impaired sodium pump acitivity
• Prolonged tissue ischaemia ultimately leads to cell necrosis.
Pathophysiological consequences of tourniquet ischaemia
1. Tissue hypoxia & acidosis
2. Blood coagulation changes
3. y capillary permeability
4. Depletion of muscle ATP
5. Muscle necrosis
Post-tourniquet syndrome picture:

Features of post-tourniquet syndrome
1. Edema
2. Stiffness
3. Pallor
4. Weakness without paralysis
5. Subjective numbness of extremity without anaesthesia
• The post-tourniquet $ is common but concealed with casts and splints
• Usually resolves within one week, though the recovery period may be prolonged.
Tourniquet-application time
• Two hours is considered safe for human upper limb surgery; other wise sCPK y and damage the ms
• Limiting tourniquet application to one and one-half hours avoids skeletal muscle ischaemic injury.
• Short periods of ischaemia followed by reperfusion (ischaemic preconditioning) renders cardiac muscle
more resistant to a subsequent ischaemic episodes
Complications
Complications of pneumatic tourniquets
Local Systemic
1. Compression neuropraxia 1. Cardiorespiratory decompensation
2. Bone and soft-tissue necrosis 2. Increased CVP
3. Direct vascular injury 3. DVT
4. Postoperative swelling and stiffness 4. Cerebral infarction
5. Delay in recovery of muscle power 5. Alterations in acid-base balance
6. Wound haematoma 6. Rhabdomyolysis
7. Wound infection
Avoiding pneumatic tourniquet complications

Measures to avoid pneumatic tourniquet complications
1 Use of a wide low-pressure tourniquet cuff
2 Anticoagulant prophylaxis
3 Juxtaposition of two tourniquets
4 Ensuring good padding beneath the tourniquet
5 Any solution applied to the skin must not be allowed to run beneath the tourniquet
6 Careful perioperative haemodynamic monitoring of patients with poor cardiopulmonary reserve
7 Regional hypothermia by cooling the extremity

Arthroscopy
Portals:
Indications:
1]. Diagnostic for unexplained pain
2]. TFCC tears
3]. Chondral lesion debriddment
4]. Arthroscopic assisted intra-articular #
5]. Synovectomy
6]. Loose body removal
Wrist Arthorplasty
Rationale:
1]. Improve function till 50% of normal
2]. Best for dominant side
3]. Best for certain recreational jobs as musicians, surgeons, artists
4]. Other laborer jobs are better treated with fusion
5]. 15 y follow up has been reached
Indications:
1]. Severe arthritis; OA, RA
2]. Incapacitating pain
Types:
1]. Capitate resurfacing after proximal row carpectomy OA
2]. Silicon spacers severe reactive synovitis
3]. Total wrist replacement
Total wrist design
1]. Radial component
2]. CMC component: either stemmed or fixed by screws
3]. PE spacer between the two components: either fits on the distal or proximal component
Operative details:
• Dorsal wrist approach is used
• Transect the dorsal carpal lig from its ulnar side
• Proximal row carpectomy + total synovectomy + excision of all the pannus
• Radial cut is done + trim the end of the ulna to the same level
• Capitate cut is done; through reaming of MC3
• If tight ulnar side (z radial deviation); release the FCU & ECU & ulnar capsule
• Insert cement by a syringe
• Insert the distal segment first then the proximal
• Reduce the prosthesis and hold it till the cement sets
Complications: the most frequently encountered are:

1]. Loosening
2]. Infection
3]. Neuro-vascular injury
fÑ|Çx W|áÉÜwxÜá
Dr Mohamed Sobhy

[Spine Disorders] Page | 557
Anatomy
• There are 2 lordotic segments:
o Cervical: .............................................. 25º cervical lordosis
o Lumbar ............................................... 50º
• And 2 kyphotic segments:
o Thoracic ............................................. 35º
o Sacrococcygeal
• These allow for the head to be directly over the pelvis é WB line just anterior to S1
• Cross sectional anatomy of the spine reveal 3 columns
o Anterior column:
Anterior longitudinal lig
Anterior ½ of body
Annulus fibrosus
Disc
o Middle column
Posterior ½ of body
Annulus
Disc
Posterior longitudinal lig
o Posterior column
Facets
Neural arches
Ligamentum flavum
Interspinous lig
• Fracture instability is a big issue in spine surgery as it affects the
plan for treatment
o Compression fractures that affects the anterior and middle columns Æ stable
o Distraction and fracture dislocations are unstable
o Gains Classification scores the degree of comminution, displacement, & kyphosis
o Fractures that score > 7 points are unstable and need anterior and posterior fixation
o Some times the answer for the Q of instability is difficult and need extensive clinical
and dynamic radiologic studies
558 | Page [Spine Disorders]
• Osseous anatomy:
o Cervical spine protect brain stem & sp cord and suppor the head
o 50-60% of flexion-extension occur between base of skull and C1
o 50-60% of axial rotation occurs at the level of C1-C2
o Remaining motion occur between C2 and the CxTh segment
o Cup and ball type of articulation between C0-C1 allows coronal and sagittal rotation
o Horixontal & flattened orientation of C1-C2 allow predominantly axial rotation
o Inspite of theis unstable osseous anatomy that permits wide range of flextion
extension & rotation Æ stability comes from ligamentous structures
o The subaxial spine contributes approximately half of the flexion-extension and
rotation of the cervical spine.
o The orientation of the posterior facet joints (45-degree angle in the coronal plane)
allows for more mobility than is possible in the other spinal regions.
o Motion at the facet joints is also complemented by concomitant motion between
vertebral bodies through the intervertebral disks.
• Biomechanics:
o Four smooth curves causes flexion, extension, bending to occur together in harmony
by the so coupled movements
o The mobile cx & lumbar areas are separated by rigid thoracic vertebral segment; this
creates Æ stress risers at cervico-thoracic & thoraco-lumbar junctions
o Ideally, centre of gravity passes through cx vertebral bodies Æ anterior to Thx
vertebrae Æ intersecting ant corner of sacrum
o So most of spinal column experience compressive forces anteriorly and tensile
posteriorly; except in lumbar lordosis this μβ reversed
o 1ry WB component in compression is cancellous bone Æ adapted for this
o While cortical bone is responsible only for 10% of compressive strength
o Marrow element has viscous property Î hydraulic system provide both strength
and dampening effect (energy absorption)
o Posterior column Æ less massive osseous elements Æ designed to attachment for lig
& tendons are mostly collagenous & extremely strong to tension (most stabilizing
element of posterior column)
o Lig attachment at a distance form instantaneous axis of rotation gibes them excellent
mechanical attachment
o Discs act as force transmission & dampening unit for ant column
o Disc nucleus transmit axial load from body to body& transfer compressive force Î
tension force éin the annulus
o Outer layer of annulus Æ important for rotational stability
o Annulus thick ant & lateral; and thin posterior & postero-lateral corner Æ stress risers
Æ this is a common site for disc herniation
[Sp
pine Disord
ders] Page | 559
• Instantaneous axis of rota
attion:
o Axis aroun nd ώ relativve motion of an objecct occurs frrom one p position to another
a
o It is a geom
metric conccept that lo ocate the line around d ώ vertebrral body rootate
o It is not ne
ecessary to be contain ned in the vertebral body
b
o Its position
n is affectedd by:
Deg generative e changes
Loss of anatom mic stabilizzers
Ana atomic desstruction
o All these causes
c shiftt IAR towarrds uninjurred segme ent (but éin
n certain lim
mits)
o IAR is important to know;
k to put any con nstruct in mechanica
m ally favorabble position
n far
distant froom IAR Æ y momen nt arm of the implant Æ
y mechan nical advanntage
o Atlanto-Occcipital IAR R (lateral bend)
b = 2--3 mm above
the dense apex in th he middle liine
o Atlanto-axxial IAR (flexxion & exte ension) is éin
é the den nse
o Cervical IAAR for flexxion Æ an nterior boody; while for
lateral bennding is cen ntre of thee body
o Lumbar IA AR for rotattion Æ nea ar the postterior annu ulus;
if destroyeed Æ IAR migrates posterior; if posterio or is
destroyed Æ migrate es anteriorr
o Structures far form m the IAR R are ressponsible for
constrainin ng the mo otion; e.g. anterior lo ongitudinal lig
(ALL) & anterior
a a
annulus arre the strructures most
m
important in rotation n control inn intact spine
o If anterior column is injured Æ rotational instability
o Lumbar IA AR for flexio
on is the within
w nucleeus pulpossus
o In flexion if Ant colu umn is desstroyed IAR R moves in nf &
post; if Annt & Midd dle column ns are desttroyed Æ IAR
further back and infe erior
o In extension if Posterior co olumn (faccetal joint) is
destroyed Æ ant & in nferior
Circulation of Spinal Cord
• THREE MAIN TRUNKS:
1- ANTERIOR MEDIAN LONGITUDINAL ARTERIAL TRUNK Æ is the main supply and are responsible
for the more vascularity of the ant part of the body at the ALL
2- Pair of POSTEROLATERAL TRUNKS near the posterior nerve rootlets.
1. The source of these trunks are:
a. In the neck they come from .................. vertebrala, costocervical & thyrocervical trunks (In
60% additional source arises from the ascending pharyngeal of ext.carotid artery)
b. In thoracic and lumbar areas from...... Aorta
c. In sacral area from .................................... lat sacral, mid-sacral, 5th lumbar, & iliolumbar
2. Direction of flow in the blood vessels of the spinal cord. The three longitudinal arterial channels
permit reversal of flow and alterations in the volume of blood flow in response to metabolic
demands. Relative demands of gray matter > white matter and these arterial trunks are largest
in the cervical and lumbar near the girdle plexus.
3. Trunks connect: by mean of segmental vessels
4. SEGMENTAL ARTERIES OF THE SPINE; at every vertebral level
a pair of segmental arteries that run to reach the
intervertebral foramen (External Distribution Point) and
give rise to many branches:
a. Vertebral branch: richly supply the anterior
aspect of the body and ALL (THIS IS THE MOST
VASCULAR POINT OF THE VERTEBRA)
b. Dorsal branch: supply the arch
c. Spinal branch
5. SPINAL BRANCHES enters the intervertebral foramen and
give rise to superior, inferior, transverse branches that anastmose é the above, below, other side
artery Æ transverse arterial rings (VERTEBRAL ARTERIAL PLEXUS):
a. Internal arterial circle of the cord Æ RADICULAR VESSELS to the cord
b. Extradural arterial circle: gives 3-4 VERTEBRAL NUTRIENT aa. enters the body via posterior
nutrient foramen. These are of two types:
o End arterioles that reach the metaphysis
o Anastmotic arterioles that anastmose with there counterpart from segmental a.
6. ARTERY OF ADAMKIEWICZ. Is the main feeder of lumbar cord; arise at T9 to 11 on the left side, the
most important feeder is the anterior longitudinal arterial channel of the cord; but all are
important and must be preserved. Spinal blood supply is very variable
Venous Drainage: Metaphyseal minute tributaries drain into:

1. centre of the body Æ large valveless Basivertebral v. ώ
emerges from nutrient foramen Æ anterior internal plexus
2. Via emissary viens to anterior external plexus
3. From posterior arch tributaries drain into the posterior internal
and external venous plexuses
4. All these plexuses form an extensive network called Batson’s
vertebral plexus that drain into the segmental vein
Embryology
• A typical vertebra is ossified from three primary centres: 9-12 wk
1- 2 at the side of vertebral arch Æ transverse process, lamina, spine, & pedicles
2- One in the centrum. The body's major part, the centrum, ossifies from a primary centre
dorsal to the notochord. (Centra are occasionally ossified from bilateral centres which may
fail to unite.
• During early postnatal years the centrum is connected to each half neural arch by a
synchondrosis or neurocentral joint.
• During the first year the arches unite behind é each other, first in the lumbar Æ thoracic Æ
cervical
• Centra unite with arches about the third year, the lumbar being the last at 6th year
• Until puberty the upper & lower surfaces of bodies + apix of transverse + apix of spinous
processes are cartilaginous = five secondary centres appear:
1- 2 at the apex of each transverse
2- Apix of spinous process
3- 2 annular epiphyseal 'rings' for circumferential parts of upper and lower surfaces of the
body
• Costal articular facets are extensions of the annular epiphyses.
• 2ry centres fuse at ~ 25 years. In bifid cervical spinous processes there are two secondary
centres. The annular 'epiphyses' of vertebrae probably cannot be equated with epiphyses of
long bones. In most mammals they are complete osseous discs.
ALLEN CLASSIFICATION OF
CERVICAL FRACTURES
Back Pain
Prevalence
1. 60-80% of people will have LBP sometime in their lives.
2. 90% LBP resolves in 6w, 75% may experience symptoms & disability 1y after
Types of Back Pain:
1- DISCOGENIC BACK PAIN

o pain from innervated ligamentous layer of the annulous & LDP
o it is midline & worse with lordotic postures, bending & lifting
2- FACETAL JOINT PAIN:
o Each facet is enervated by 2 nerves (non specific and difficult to localize)
o 2 types of pain:
Arthritic pain
Root compression ð lateral recess stenosis
3- SACRO-ILIAC PAIN:
o Also may cause back aches: usually due to inflammatory arthritis e.g. Ank Sp
4- RADICULAR BACK PAIN Ð: has a Dermatomal Pattern
o External Pressure from a facet, hypertrophied LF, NPH, Pseudoarthrosis of lytic
Spondylolithesis
o Ischemia of blood flow
o Inflammation around e.g. TB, pyogenic osteomyelitis, discitis
5- REFERRED BACK PAIN: No dermatomal pattern (sclerotomal distribution)
o Aortic Aneurysm
o Visceral (DU, GB, Pancreatic disease, endometriosis, pleural disease)
o Infection: UTI, PID
o Hip Arthritis
6- MUSCULOGENIC PAIN:
o Inflammatory: myofacial $ or fibromyalgia rheumatica
o Vascular: lumbar paraspinal ms compartmental $
o Exertional
7- IATROGENIC BACK PAIN
o Dural adhesions
o Post surgical instability
o Post operative discitis; arachnoiditis
8- GANGLIONIC PAIN:
o Compression by an abscess or tumor Æ edema Æ ⊕ the release of substance P &
CGRP (calcitonin gene related peptide) Æ ⊕ the nociceptors Æ pain
9- PSYCHOGENIC BACK PAIN
o must exclude organic pathology
o WADDELL'S inappropriate signs often present:
Painful JACKSON’S TEST (axial skull compression)
a.
Painful Pelvic rotation: é Passive rotation of shoulders and pelvis together
b.
Resisted hip flexion
c.
Non-dermatomal sensory loss
d.
COGWHEEL" (give-way) weakness
"C
e.
Inconsistent SLR é a clinical Dx
f.
Widespread tenderness
g.
Overreaction - disproportionate expressions, or tremor during examination
h.
o >3 present = be wary of operating ≈ nonorganic features
Discogenic Pain
• Normal discs have sensory nerve endings of the sinovertebral nerve (recurrent br of the
spinal n ώ supply the dura, PLL, annulus) in the outer 1/3 of the annulus
• Disc stimulation studies (using either hypertonic saline or contrast media) showed normal
discs do not cause pain
• Pain correlate with the degree of disc fissuring & not with disc degeneration
• Discogenic pain can result from infection (discitis), a torsional injury (circumferential tear of
the annulus) and internal disc disruption
• Internal disc disruption cannot be diagnosed clinically but only after post-discography CT
• The correlation between reproduction of pain and a grade 3 tear is very strong
Grade Disruption
Grade 0 No disruption evident
Grade 1 Disruption to inner 1/3
Grade 2 Disruption to middle 1/3
Grade 3 Disruption to outer 1/3
Xeroradiography:
• Still it is an ionizing radiation (electro-magnetic field), but it is
received on a special photoconductor plate that enhances
images
Sprung back
• Pain from upper sacrum to knees
• Due to PLL tear +- posterior annulus
• Tenderness, depression may be felt
• z flexion, otherwise is normal, SLR painful > 100
• ttt: fusion if resistant
Osteitis Condensans Ilii

• Sclerosis of one or both sacro-iliac joints
• Unknown etiology
• More in young females
• PXR is diagnostic
Lumbago (fibromyocitis of lumbar muscles)

• Acute painful spasm and tenderness of lumbar ms
• Uncertain etiology & pathology
• Tender nodules may be felt
• Usually attributed to cold exposure
• ttt: rest, NSAIDS, warmth, local Novocain inj
Fibro-Myalgia
• Regional myofascial pain
• ACR Criteria for diagnosis:
1. Widespread pain
o > 3 months:
o Pain is bilateral
o Pain is above and below the waist
o Pain is axial (neck, mid-back, low back)
2. Pain must be in > 11 of 18 fibromyalgia tender points
o These points must have marked tenderness to palpation
o ± refer pain, and not just "tender"
o Pain is elicited é ≈ 4 kg of pressure
Disc Degeneration
Definition:
• Altered intervertebral disc structure ώ production of pain especially at L4-5, L5-S1
Aetiology
• It is not exactly clear why discs degrade, but it is not related to aging
• Theories put forward include:
1- End plate fracture which then causes disruption of the delicate nuclear homeostasis
2- Autoimmune process
• Intervertebral discs are able to withstand large forces éout herniation ð:
1. y load to failure = 10,000N (vertebral end plate fail first)
2. y Intrinsic cohesiveness; even if é annular tear, herniation occur only to degraded disc
• Predisposing factors for degradation:
1- Smoking (z O2 tension at the annulus)
2- Chronic cough and constipation
3- Bad postural habits in work, office, driving,…
4- Repetitive trauma
5- Obesity
Pathology:
HILL DEGENERATIVE CASCADE:
1. Stage of DYSFUNCTION:
Minor disc tears, Facetal synovitis, & ms sprain
Axial dull aching ms pains é trigger points
2. Stage of DEGENERATION:
Proteoglycans disturbance (z chondroitin sulphate) + z water content
y collagen content of the nucleus bulbosus
Nucleus appear dry and brown & less gelatinous (BLACK DISC $ on T1)
All lead to inelastic nucleus é less stress sharing function
This leads to y stresses over:
1]. Annulus fibrosis Æ fissuring // to end plate Æ herniation
2]. End plate Æ failure
3]. Facetal joints
3. Stage of SPONDYLOSIS:
REACTIVE BONE FORMATION:
(1) Around the end plate herniation Æ Schmorl’s nodes
(2) Around protruded disc ð periosteal elevation Æ marginal osteophytes
(3) Around the facets Æ osteophytes & OA
FLATTENING of the disc
4. Stage of STABILIZATION:
As the reactive bone formation continue é more osteophytes formation Æ
stabilization of the adjacent vertebrae
Acute Disc Prolapse

1. LUMBAR DISC PROLAPSE
Definition::
• Acute disc herniation that produce Neurologic compressive disorders and pain
Epidemiology
3 Ages
• Mostly in MIDDLE AGE; very young and very old seldom have acute disc prolapse
• In adolescents look for infection, benign tumours and spondylolisthesis
• In the elderly look for vertebral compression fracture and malignancy
3 Warnings
• SCIATICA is referred pain ( ⇐ prolapse). It can also come from facet, SI joints or infection
• Maximum two LEVELS; if multiple levels Æ suspect neurological cause
• Severe, UNRELENTING PAIN is not a feature of disc prolapse; suspect tumour or infection
3 Major DDx
• INFLAMMATORY disorders such as infection, ankylosing spondylitis
• VERTEBRAL TUMOURS; cause severe pain and spasm
• NERVE TUMOURS such as neurofibromata of cauda equina Æ sciatica é continuous pain
Pathology:
• The condition occur ð:
a. Physical stress: combination of flexion + compression (mainly on L4,5 or L5,1) where
stress is more severe
b. Disturbance of hydrophilic properties of the nucleus
• At first: there is posterior bulge of the disc é out rupture
• Eventually: the annulus will rupture usually postero-lateral, but may occur central
• Neurological manifestation occur due to:
o Compression of the roots of the level below é posterolateral bulge (90%)
o Compression of the root of the same vert above é far lateral bulge
o Compression of the multiple roots centrally (Cauda Equina) é central bulge
o Compression of the cord (Conus Medullaris) é central bulge at T12L1
Nerve Root Affected

Disc Post lat Motor Sensory Reflex Far Lat root Central
L2/3 L3 knee extension Ant knee L2 (hip flexion) Cauda
Knee jerk
L3/4 L4 Dorsiflexion Medial leg L3
L4/5 L5 Hallux extension Lat leg Medial hams L4
L5/S1 S1 Plantar flexion Lat foot Ankle jerk L5
S1/S2 S2 knee flexion Back leg Lat hams S1
Pain Back & leg Leg Back
Clinically:
• C/O:
1. Sudden Severe BACKACHE é lifting a heavy object ⎯⎯ ⎯⎯→ inability to straighten up
FollowedBy
2. After few days symptoms of nerve irritation (SCIATICA) appear:

1. Referred to buttocks, back of thigh, & leg more to one side
2. y é cough and strain
3. Few days later: symptoms of n compression appear (RADICULOPATHY) more to one side
1. Sensory symptoms; hyposthesia, parasthesia
2. Motor weakness
4. If central compression occur (CAUDA EQUINA) manifestation occurs:
1. Bilateral LMN weakness in the legs
2. Loss of perianal sensation “SADDLE ANAESTHESIA”
3. Insensinate UB, painless retention é overflow: urinary incontinence
4. Fecal incontinence
5. If central compression at a higher level D12L1 (not common) CONUS MEDULLARIS lesion:
1. Bilateral LMN weakness at L1 + Bilateral UMNL motor weakness below
2. L1 SENSORY LEVEL
3. Fecal urinary incontinence (insensinate UB, painless retention é overflow)
• O/E:
1. Standing: .................................(postural changes)
1- Inspection:
[1]. SCIATIC LIST (scoliosis): pt bend to one side ð ms spasm
[2]. FLEXED KNEE: pt bend it to z tension on the sciatic n
1- Palpation: Back TENDERNESS max on lower vertebrae
2- Movements: Limited all back movements +VE SCHOBER TEST 3 points in posterior
midline are marked and the pt is asked to bend & straight up & measure the diff
2. Supine: .....................................(stretch signs)
2- LASÈGUE’S: SLR Æ pain at 70º at buttocks and calf (rather than thigh and back) Æ
slow drop of leg Æ z pain Æ passive dorsiflexion Æ reappearance of pain
3- BRUDZINISKE’S: also passive neck flexion Æ reappearance of pain
4- KERNIG’S sign: Flexion of the knee Æ relief of pain (if persist = +ve BUTTOCK problem test)
5- BOWSTRING sign: SLR + flex the knee 20º + press ! lat popliteal n Æ pain reappear
6- FAJERSZTAJN sign: well leg raise Æ pain on the affected leg (=Cross over sign) and
indicates large axillary disc protrusion of the other side
7- BILATERAL SLR: pain after 70º raising
8- HOOVER test for malingerer: if pt can not do active SLR Æ put 2 hands below each
heels and feel if he is trying (you feel a push over the other palm) or he is not trying
9- PRONE KNEE BENDING sign: max flexion of knee in prone position Æ unilat. Lumbar
pain (femoral stretch test) = L2,3 irritaion
Postive degree Lasegue Bilateral SLR Brudziniske
30º-70º Hip Sacroiliac if (+ve) Lasegue + (-ve)
70º Sciatic stretch Lumbar Brudziniske sign Î
>70º Sacroiliac or facetal Lumbar hamstring tightness
3. Neurological impairment:
L5 impairment S1 impairment
Motor weakness EHL & ST TP & TAch & peronei
Sensory Outer leg & dorsum foot Outer foot & dorsum 5th toe
Reflex Brisk knee (weak ST) z ankle jerk
Radiological
1- PXR:
Narrow disc space
[1].
Traction spur
[2].
Facetal arthropathy
[3].
Straightening of the spine (ms spasm)
[4].
2- CT: More accurate and reliable
3- Myelography: to exclude intrathecal tumor & confirm disc (limited value after MRI)
4- Discography: to delineate disc degeneration.
5- MRI:
[1]. Assess the cord and root condition
[2]. Confirm the disc & its extent & size
[3]. The study of choice
Natural History
• After:
• 1st episode 90% .................................... improve and do not relapse
• 2nd episode 90% .................................. improve and 50% relapse
• 3rd episode 90% ................................... improve and 100% relapse
• Regardless of treatment, impaired motor function had a good prognosis whereas
sensory deficits remained in almost one half of all the patients.
DD:
• Inflammatory condition:
o ystiffness
o y ESR
o Erosive on PXR
• Vertebral tumor
o Severe pain (osteoid osteoma, osteoblastoma)
o Marked spasm
o PXR lesion
• Nerve tumor:
o Sciatica
o Continuous pain
o MRI
Red Flags for Back Pain:

1- Fever
2- Deformity
3- Loss of wt
4- Neurological Acute
5- Past history of malignancy
6- Bladder
[Sp
pine Disord
ders] Page | 569
Treatment (M MAJORITY REQUIRE NO N SURGIC CAL INTER RVENTION)
N
Non-operat tive .............................................................. 90% effecctive
1- Bed re est in Fowle er position é knee flexed ± Tracction for 2w weeks
2- Pelvic corset
3- NSAID D's
4- Physio otherapy: Back B classess helpful
5- Epidurral injection ns of LA ± steroid 80--120mg de epo medro
ol
6- If all fa
ailed chemo onucleolyssis by chem mopapain (dangerous & less efffective than
n surgery)
Operative
O
Indication
1- CAUDA equina sy yndrome is considere ed an emerrgency
2- PERSISTENT leg pain despite adequate conservatiive measurres >3wk
3- Neuro ological DETERIORATION in spite of o conserva ative ttt
Standard d operativve treatme ent
1- INTELAMINAR DISCECTOMY (Fenestratiion of LF + Partial Lam minectomy)): for central discs
2- INTER TRANSVERSE DISCECTOMY for fa ar foramennal disc
3- MICRO-DISCECTOMY: under microscop pic magnifiication
o Shorter sta ay, mini inccision
o Need expe erience + in ntraop PXR R
o More complication (B Bleeding, infection,
i liimited field
d)
o Dural tear: headache e + soaked d wound é brown halo
+vee β 2 transfferin
Sma all ..........................nothing to be done
d Æ be ed rest
Med dium ....................interrrupted water tight su utures
Largge .........................autog genous fatt graft or gel foam orr adcon-L
4- PERCUTANEOUS SUCTION DISCECTOMY (Automatted Percut Lumbar Discectomy)) APLD:
o Rotatory shaver prob be is inserted into the e disc unde er PXR guid
dance
o The probe e cut the diisc and the en sucked viav the sam me probe
5- PERCUTANEOUS LASER DISCECTOMY ussing the YA AG or KTP laser beem m
6- PERCUTANEOUS ENDOSCOPIC DISCECTOMY:
o Series of dilators are introduced d to the boone follow wed by insertion of wide cannulaa
o Special endoscopic in nstrumentts are used to retract, cut, & exccise the discc
7- PERCUTANEOUS DISC RADIO-ABLATION:
o Evaporization of the nucleus n pullposus using g the radio
ofrequency
• Excelleent treatmeent for erad dicating leg g pain but not for ba ack pain
• The ad ddition of spinal
s fusio on at the same time e as discecctomy has not been proven to o be
superio
or to simple
e discectom my and adds conside erable morbidity
8- DISC R EPLACEMENT SURGERY: see laterr
RE
Persistent pain after surgery:

• Residuaal disc mate
erial
• Disc proolapse at another
a leveel
• Root coompression n ð:
o Facetal OA A
o Narrow latteral recess
• Late ð post-lamen
p ectomy Insstability NEVER REMOVE > 1/3 THE FACET
Rational for Disc Prosthesis:
• Replace the degenerative painful disc by a mechanically sound prosthesis
• It restores the height
• It restores the motion
• Regain the physiologic stiffness in all planes of motion plus axial
compression
• With stand the physiologic stress and transmit it to the next level
Types:
[1]. Screw fixation
[2]. Staple fixation
[3]. Teeth fixation
[4]. Porous coated prosthesis
[5]. Macrotexture surface prosthesis
[6]. Hydrogel prostheses: replace of the NP only & retain the AF. Consist of hydrogel core
constrained in a woven polyethylene jacket
Indications:
1- Diagnosis of Degenerative Disc Disease at the L4/L5 or L5/S1 level
2- At least six months of conservative treatment
3- Still under trial for cervical and thoracic disc prolapse
Precautions
1- Should be place centrally not to shift axial load to the facets
2- Avoid the destruction of facets and ligaments.
3- An artificial disc must exhibit tremendous endurance.
4- The intervertebral disc prosthesis ideally would replicate normal range of motion
Contraindications:
1- Previous back surgery (except discectomy, laminotomy or nucleolysis at the same level)
2- Multiple level degeneration, ligamentous laxity, Spondylolisthesis, or Scoliosis
4- Facetal pain
3- Osteoporosis, steroid ttt, metabolic bone disease, or autoimmune disorder
5- Morbid obesity
Advantages:
4- The device maintain the proper intervertebral spacing
5- Provide stability
6- Restore the normal shock absorbing mechanism of the spine
7- Less morbidity than the standard fusion techniques
8- Better functional out come
5- Percutaneous placement could be done é nuclear hyrdogel replacements
Complications:
1- Biomechanical problems:
1- Bone resorption
2- End plate failure
3- Prosthesis failure
4- Facetal over load and degenration
2- Surgical complications:
5- Neurological complications
6- Vascular complications
7- Visceral complications
3- Biological complications:
8- Abnormal bone deposition
9- Infections
2. THORACIC DISC PROLAPSE

• Very rare .............................................0.5% of all prolapsed discs (75% > T8 & very rare < T4)
• Cord compression and thoracic back pain from malignancy more common
• Most common in the 4th decade
• Thoracic back pain radiating round the chest with UMN signs in the lower limbs
• Investigate with MR scan
• Treatment
1. Posterior surgery with laminotomy possible but the cord does not tolerate retraction
2. The disc can be approached via a costotransversectomy, or transthoracic approach
with fusion of the affected level with rib strut graft
Age Related Changes in the Intervertebral Disc

• Proteoglycan synthesis decreases with age thus the concentration of proteoglycans will
diminish with age from 65% in early adult life to 30% by the age of 60 years
• The proteoglycans that persist are smaller in size and the concentration of chondroitin
sulphate falls (keratan sulphate concentrations remain constant)
• This causes a drop in the water content from 88% at birth to 65% by age 75.
• However most of this dehydration occurs in childhood and early adolescence, with a
decrease of only 6% from early adult life to old age.
• Collagen content y in both the nucleus and the annulus but the concentration of elastin z
• This loss of water and increase in collagen content causes the discs to become stiffer and
less resistant to deformation and also less able to recover from creep deformation
• As the nucleus dries out and the becomes more fibrous it is less able to transmit forces to
the annulus and the annulus then has to play a greater role in load transmission therefore
subjecting it to greater stresses
• Disc height does not decrease with age but stays constant, with any loss of disc height
representing a degenerative process as opposed to an age related change
3. CERVICAL DISC
Categorization By Odom
Unilateral soft disc protrusion Nerve root compression /radiculopathy
Osteophytes /hard disc Nerve root compression /radiculopathy
Medial soft disc protrusion Spinal Cord compression / myelopathy
Cervical spondylosis Spinal Cord compression/ myelopathy
Cervical Radiculopathy
Definition
• A condition caused by compression of a nerve root in the cervical spine
Incidence
• <1:1000
• Age: ................................................................. 40s and 50s.
• Cervical degeneration begin 10 years later than lumbar spine degeneration
• Sex – ♂:♀ .................................................. 3:2
Pathology
• Lateral Disc herniation ....................... 50% (soft disc)
• Osteophyte formation in Lushka ...... 50% (hard disc)
• Developmental spinal stenosis .......... 5% also have (AP dr of spinal canal > 13)
• Compression site ..................................... ENTRANCE or MID zones & occasionally at exit
• Frequency of root compressed .......... C7>C6>C8>C5
Symptoms
1- 1st symptom is UNILATERALNECKPAIN: nape, suprascapular, scapular or interscapular regions
2- RADIATING ARM PAIN
3- Finger PARASTHESIA
4- WEAKNESS
Signs
1- Motor + Sensory + Reflexes
2- SPURLINGS NECK COMPRESSION TEST- Downward pressure to head é the neck ext & tilt to the
painful side Æ pain. Usually positive but may be negative in chronic cases
C5 (C4-5) C6 (C5-6) C7(C6-7) C8(C7-T1)

Neck pain Suprascapular Scapular / interscapular
Arm pain lat upper arm Lateral arm Posterior arm Medial arm
Paresis Deltoid (biceps) Biceps (Deltoid) Triceps Intrinsics (triceps)
Sensory none Thumb Index/long little
z Reflexes Biceps Triceps
• DDx is usually achieved by : neck pain < other symptoms, Spurling sign, Radiculopathy
1- Shoulder pathology
2- Thoracic outlet syndrome
3- Cubital tunnel syndrome
4- Tennis elbow
5- De Quervains disease
Investigations
• In contrast to the spinal cord in myelopathy, compressed root can rarely be depicted even
with MRI
Plain Xrays
• Spurs of the superior articular process
• Spurs of the Luschka joint.
• Disc joint spaces at levels of herniation are usually preserved.
CT scanning
1- Most useful for detecting bony spondylitic spurs.
2- The slice just cranial to the to the disc space is the most informative slice
3- CT myelogram with low dose water soluble contrast media
MRI is the most useful for herniated disc.
• However NPH are seen in 20% of asymptomatic pts 45-54yrs old. 57% in those over 64.
Conservative treatment ........................................... up to 90% resolve
• More effective with acute cases
• Collar, NSAIDS, bed rest ± Halter
• Poor man’s traction - with head (5kg) hanging over the end of the bed (prone in flexion/
supine in extension) for several minutes several times a day.
• cervical epidural injection
• direct cervical nerve root block
Indications for Surgery
1]. Failure of conservative treatment
2]. Increasing neurological deficit
3]. Unbearable pain
Surgical Procedures
• Approach should be determined by the position and type of lesion
• Soft lateral discs easily removed by posterior approach
• Spurs and more paramedian discs, via an anterior approach
Approach:
Posterior approach:
• Positioning- Prone with face in a headrest, neck flexed. Shoulders retracted inferiorly é tape
• Incision- midline 2.5 cm lower than the interspace to be explored
• Division of ligamentum nuchae
• Blunt dissection of paraspinal muscles
• Fenestration of ligamentum flavum, identify nerve root, osteophytes, disc excision
• tissue through a cruciate incision in posterior longitudinal ligament
Anterior approach:
• Recurrent laryngeal nerve is the most important structure at risk
• Positioning: Supine 30º elevation (zbleeding) é neck ext & use head ring & NG tube
• Incision: Make a oblique skin crease incision at level of the pathology using landmarks
described in the table. Extend it from the midline to post border of sternocleidomastoid
Landmarks Vertebral level

Hard palate Arch of atlas
Lower border of mandible C2-3
Hyoid bone C3
Thyroid cartilage C5
Cricoid cartilage C6
• Superficial
o Incise fascia over platysma in line with skin incision
o Split platysma with fingers in the line of fibres or cut in line of incision.
o Identify the anterior border of sternocleidomastoidand incise the fascia immediately
anterior to it
• Deep
o Using fingers retract sternocleidomastoid laterally and sternohyoid and sternothyroid
strap muscles, with trachea and oesophagus medially
o Divide omohyoid (Omohyoid lies over carotid sheath + Transverse cervical artery are
landmarks to brachial plexus)
o Palpate the carotid artery, develop a plane between the medial edge of the carotid
sheath and the midline structures (thyroid, trachea and oesophagus), cutting
through pretracheal fascia
• The superior & inferior thyroid aa may limit the exposure but can be divided
• Reccurent laryngeal n between the two forks of the inferior thyroid a (on the right mainly)
• Vertebrae covered by longus colli Æ enter this 'valley' between longus colli muscles.
• ALL is in the midline, cut here, as Sympathetic chain is on longus colli just lateral to body
• Structures at Risk
o Main dangers are recurrent laryngeal nerve and sympathetic chain
o (Thoracic duct on the left)
• Excise the anterior annulus fibrosis & as much disc material as can be seen
• Insert an interspace spreader
• Remove the posterior annulus and the extruded disc and or any associated bone spurs
• PLL can be removed for a better view of the dura and nerve roots
• Interbody grafting then performed using:
Smith Robinson fusion
Cloward fusion
Bailey Badgely fusion
Bloom Raney modification of the Smith Robinson fusion
Moss cage
Moss cage & Plate
Surgical results
• No difference in results reported for anterior or posterior approaches
• No significant differences between the results of surgery for soft disc or for osteophytes
Level Pedicle Dimension Inclination

T1 7 mm 35º medial
T3 6 mm 20º medial
T4,5 5 mm (narrowest) 5-10º medial
T12 7 mm 5-10º medial
L3 13 mm 25º medial
L4 15 mm 30º medial & 10º caudal
L5 17 mm (widest) 35º medial & 20º caudal
S1 35º medial & 30º caudal
Costotransversectomy. A, Straight longitudinal

incision about 2.5 inches (6.3 cm) lateral to spinous
processes, centered over level of vertebral dissection.
B, Resection of costotransverse articulation.
Pedicle Entrance point in spine at

intersection of lines drawn through
middle of inferior articular facet and
middle of insertion of transverse
processes (1 mm below facet joint). A,
Anteroposterior view. B, Lateral view.
Entry points of pedicular screws

Thoracic: base of transverse process near
superior facet.
Lumbar: meeting of tr process é superior

facet lateral to pars.
Sinuvertebral nerve A: The sinuvertebral Sacral: base of S1 facet in line é the neural
nerve shown on a cutaway drawing. B: foramena.
The branches of the invertebral nerve
shown on a lateral view of an intact spine.
a: Dorsal root ganglion. b: Rami
communicantes. c: Autonomic ganglion. d:
Sinuvertebral nerve. e: Terminal branches
of the nerve (may ascend or descend one
or two vertebral levels).
Cervical Myelopathy
Incidence
• 6: 100 000
• Age .................................................................. 50s or 60s
• Sex M:F ........................................................... 2:1
Pathology:
• Compressive Factors:
1]. Anterior cord compression by .............. Disc / Posterior Spur / OPLL (ossification of PLL)
2]. Anterolateral compression by .............. Joints Of Luschka
3]. Lateral compression by ............................ Facets
4]. Posterior compression by ........................ hypertrophied or calcified Ligamentum Flavum
5]. Developmental Stenosis ....................... <12mm
6]. Dynamic Stenosis- PENNING’S JAW DIAMETER: distance from postero-inferior corner of the
body, to the lamina below ...................... <12mm + 2mm of retrolisthesis with extended neck
• Site:
1]. Most commonly affects C5-6 > C4-5 > C3-4 > C6-7 (≠ radiculopathy common at C6-7). As
cervical enlargement of the spinal cord is at C4-5 & C5-6 levels.
2]. Retrolisthesis on extension (dynamic instability) is rare at C7 ð its anterior tilt
3]. Grey matter is more vulnerable to compression than white matter
Symptoms In order of appearance:
1]. Electric shock é neck extension indicating an early stage to the disease 30%
2]. PAIN - characterized by central burning and stinging
3]. PARAESTHESIA of the fingers
4]. PARESIS: clumsiness of the hands and heavy writing
5]. Tightness, hot or cold sensations in the trunk
6]. Tingling in legs
7]. ataxic broad based shuffling gait ð spasticity
8]. Urinary disturbance
Signs:
Upper Extremity: - UMNL & LMNL
1]. Hoffman's Sign: pinching distal phx of middle finger Æ flexion of other fingers IP joints
2]. Finger Escape Sign: small finger spontaneously abducts ð weak intrinsics
3]. Inverted Radial Reflex: (C5 - C6) tapping brachiorad tendon Æ reflex fingers flexion
4]. Biceps Reflex primarily indicates neurologic integrity of C5 ± C6 component
Lower Extremity - UMNL
1]. Decline in ability to walk, APPARENT ATAXIA
2]. HYPER-REFLEXIA and frank CLONUS
3]. z PROPRIOCEPTION
4]. L’hermitte's SIGN: Electric shock of leg é neck flexion
5]. Babinski's SIGN: +ve in severe myelopathy
jaw jerk (trigeminal function) ............................. rules out pathology above the foramen magnum
• Tapping on the slightly opened jaw Æ contraction of the masseter effectively
Crandall Classification of symptomatology -

Central cord syndrome Symptoms and signs in UL > LL
1- Transverse lesion syndrome Symptoms and signs in upper and lower extremities
2- Brown-Sequard syndrome Ipsilat motor & DC loss; contralateral pain & temp loss
3- Motor syndrome éout sensory
4- Brachialgia + cord $ =radiculomyelopathy UL pain + Pyramidal tract involvement
DDx
Spinal cord syndrome

• Complete ...............................................................................Cord transection
• Incomplete:
1- Central: (extension injury é OA) .........................Disc + buckled LF
2- Hemi: Brown Sequard $ ..............................U + DC + contralat sp thalamic
3- SCIWORA ...........................................................sudden traction in a child
• Root:
1- Cauda equina (Lesion below T12L1) ...............LMNL + radiculopathy
2- Conus medullaris (Lesion at T12L1) ................UMNL + saddle + sphincters
• Vascular:
1- Anterior cord syndrome: .............................U + AHC + spinothalamic
2- Posterior cord syndrome: ............................Lemniscal + dorsal horn
• Neurologic
1- Transverse myelitis .........................................All
2- Syringo myelia (central) ...............................Crossing sp. thalamic
3- Tabes dorsalis (dorsal column) .................Lemniscal
4- Friedreich’s Ataxia ........................................ U + Lemniscal + cerebellum
5- Subacute combined degeneration ........U + Lemniscal
6- Amytrophic lateral sclerosis .......................U + AHC
7- Familial spastic paresis ...................................U
8- Poliomyelitis & Peroneal ms atrophy .....AHC
Investigations
• Plain Xray, for stenosis
• MR scan , shows cervical disc prolapse well. Demonstrates spinal cord well. High intensity
signal can be found in spinal cord on T2 weighted images, representing necrosis/cavity
formation. Not able to detect compression of spinal cord on extension.
• CT scan, shows OPLL and bone spurs best
Treatment
Conservative
• In early phases, try NSAIDS, collar, muscle relaxants
Surgical
• Absolute indication: ................................... Progressive Neurological Deficit
1. Anterior Decompression And Fusion:
o If disc herniation or posterior spur causing compression at 1-2 levels
o If there is kyphotic deformity, so that correction can be achieved
2. Posterior Decompression
o If compression > 3 levels
o In developmental stenosis
o Calcification of LF
3. Laminectomy
4. Spinous Process Splitting Laminoplasty.
5. Kirta’s bilateral open door laminotomy (elevated to y spinal canal diameter) ± BG
Prognosis
• Herniation shows ....................................... better improvement after surgery
• Older patients & dynamic stenosis ........ less improvement
• Most get worse ............................................ if not treated
CERVICAL DISC PROSTHESIS
Rationale
• A new technique which has been available in Europe for the past 2 years is replacing the disc é an
artificial disc that has many benefits:
1]. Regain the normal motion is maintained
2]. Regain the physiologic stresses é no adjacent segment disease in the future.
3]. Regain the physiologic stiffness in all planes of motion plus axial compression
4]. Regain the physiologic height é no fear of root compression
5]. Replace the degenerative painful disc by a mechanically sound prosthesis
6]. With stand the physiologic stress and transmit it to the next level
• The idea of spinal disc replacement is not new. It was first attempted 40 years ago when implanted
stainless steel balls were implanted into the disc spaces of over 100 patients.
Indications
1]. Disc Prolapse: one or two levels é anterior compression
2]. Degenerative cervical disease (spondylosis) é persistant pain, radiculopathy or myelopathy.
3]. Focal compressive lesion should be documented by Myelo-CT or MRI.
4]. Above six weeks failed conservative treatment
Contra-Indications
1]. Neck or arm pain of unknown etiology.
2]. Advanced mechanical problems:
o Marked instability (Translation > 3mm)
o Severe spondylosis with absence of movement (e.g. Total loss of disc height)
o Severe facet joint disease.
o Cervical spinal stenosis (AP diameter < 10mm).
o Ossification of PLL
3]. Abnormal bone stalk:
o Post-traumatic affected vertebral bodies.
o Iatrogenic: failed previous decompressive / fusion surgery
o Neoplastic: destroyed vertebral body
o Infectious: destroyed vertebral body
o Metabolic bone disease: Osteoporosis/Osteomalacia/Pagets/Ankylosing Spondylitis
o Drugs interfering with bone or soft tissue healing
4]. Systemic disease
o Infections ○ HIV / AIDS
o Rheumatoid Arthritis ○ Hepatitis - Morbid Obesity (BMI > 35)
5]. Component allergies (Titanium / Cobalt / Polyethylene)
Types:
According To Fixation
[1]. Screw fixation [2]. Keel fixation
[3]. Teeth fixation [4]. Porous coated prosthesis
[5]. Macrotexture surface prosthesis [6]. Combined
According to bearing surfaces

[1]. Metal on Metal
[2]. Metal on polyethylene
[3]. Hydrogel prostheses: replace of the NP only & retain the AF. Consist of hydrogel core constrained
in a woven polyethylene jacket
The Bristol disc Prestige Bryan total disc PCM Centurion Kineflex Cervi-Core
Advantages:
1]. The device maintain the proper intervertebral spacing
2]. Provide stability
3]. Restore the normal shock absorbing mechanism of the spine
4]. Less morbidity than the standard fusion techniques
5]. Better functional outcome
6]. Percutaneous placement could be done é nuclear hyrdogel replacements
Precautions
1]. Should be place centrally not to shift axial load to the facets
2]. Avoid the destruction of facets and ligaments.
3]. An artificial disc must exhibit tremendous endurance.
4]. The intervertebral disc prosthesis ideally would replicate normal range of motion
Operative details
• The table is placed in a slight Reverse Trendelenburg position ± adhesive pull of shoulders
• The skin incision on the right or left side may be transverse or obliquely vertical along the anterior
border of the sterno-mastoid. Transverse incisions are better cosmetically & vertical incision allows
greater exposure
• Platysma is retracted & hemostasis is obtained
• The superficial & deep cervical fascia around sterno-mastoid muscle is sharply divided along its
medial edge
• Divide the omohyoid muscle (runs obliquely across the field at the level of the C6)
• Palpate the carotid artery & retracted laterally with the sternocleidomastoid muscle.
• The short strap muscles, trachea, and esophagus are retracted medially
• Divide the pretracheal fascia é scissors. The anterior longitudinal ligament, however, should not be
disturbed until the operative disc level is positively identified.
• Spinal needle is carefully inserted into the the disc space & checked fluoroscopically
• Once the operative disc space is identified reflect Longus Colli musculature from the anterior lateral
edges of the vertebral body, so the entire anterior surface of the disc space.
• Remove ALL and Anterior Annular fibers are removed with scalpel dissection.
• Remove as much as easily accessible from Disc space & Osteophytes é small curette or rongeur
• Disc space distraction is applied gently using a lamina spreader rather than by halter traction
• Apply the prosthesis & test for its stability under fluoroscopy
• Put a drain, close in layers & apply a cervical collar
Complications:
1- Biomechanical problems:
1- Bone resorption
2- End plate failure
4- Facetal over load and degenration
2- Surgical complications:
5- Neurological complications:
Rt. recurrent laryngeal n.
Superior laryngeal n
Sympathetic chain (3 ganglia; superior at C3, middle at C6, cervicothoracic at C7-T1)
Æ Horner's syndrome
6- Vascular complications
Carotid a
Internal juglar vein
Vertebral artery if anomalously enters into a higher level than C6
Thyroid arteries; inferior & superior
7- Visceral complications:
Trachea
Œsophagus
Thoracic duct in left exposures
3- Biological complications:
8- Abnormal bone deposition
9- Infections
ggggggbiiiiiii
Facetal Joint Dysfunction

Spondylosis & Segmental Instability
Definition::
• Degenerative disease characterized by flattening of the IV disc Æ posterior displacement of
the facet joint Æ disturbed movement of the vertebrae (segmental instability)
Pathology: Hill Degenerative Cascade:
1. Stage of Dysfunction: Minor disc tears, Facetal synovitis, & ms sprain
2. Stage of Degeneration:
Inelastic nucleus bulbosus Æ z stress sharing Æ y stresses over:
1]. Annulus fibrosis Æ fissuring // to end plate Æ herniation
2]. End plate Æ failure
3]. Facetal joints
3. Stage of Spondylosis:
y reactive bone formation Æ End plate Schmorl’s nodes/marginal
osteophytes/facetal hypertrophy
Flattening of the disc Æ posterior displacement of the facet Æ y OA
During flexion & ext Æ disturbed movement Æ segmental instability
4. Stage of Stabilization: Æ y y osteophytes Æ stabilization of the adjacent vertebrae
Clinically::
• Stage of dysfunction: Axial dull aching ms pains é trigger points
• Stage of degeneration Sharp back pain Æ sciatica Æ radiculopathy (disc prolapse)
• Stage of Spondylosis Intermittent back pain referred to buttocks & GT (≠ sciatica)
o y é work, walk, or prolonged sitting & z é lying down
• Stage of Stabilization Constant but less intense back pain
o z by physiotherapy and local warmth
Examination Male 70y
• Inspection: NAD
• Palpation: poorly localized tenderness over the buttocks & lower lumbar spine
• Movements: painful limited ± catching during straightening
• Residual signs: zankle jerk / Spinal stenosis
PXR
Early Late
Narrowing of the disc space Flattening + vacuum sign (black deg disc)
Retrolithesis (L4-5& L5-S1) Degenerative spondylolithesis
Anterior end plate sclerosis (abnormal loading) Marginal osteophytes
White & panjabi ccc of degenerative lumbar instability:
1]. >4.5 mm of translation
2]. >22º relative sagittal angulation
3]. >15°-25° of angular motion bet adjacent segments on flexion–extension PXR
Discography
• Not routinely done as it has Controversial value
Tc
• hot spot at the disc space
MRI:
• Asymmetrical facetal joint
• OA of facetal joint
• Advanced disc degeneration
• MODIC CLASSIFICATION: as the annulus tear into end plate
o GI: oedema y T1 (low T2)
o GII: fatty inf y T2 (T1 turns low)
o GIII: fibrosis both T1and T2 z
DD:
• Forestier’s disease: usually multiple spurs at multiple levels more on rt side
• Ochronosis: intervertebral calcification
Treatment
• Conservative as usually the joint will stabilize itself
1. Physiotherapy strengthening of the back muscles & abdominal muscles
2. Corset: relief pain especially in obese patients
3. Facetal injection: If the lesion is localized to one or two levels
o Position: prone on fluoroscopy under local anaesthesia
o 20 gauge needle introduced ⊥ to skin 2-3 cm from the middle line at spinous process
o Pt rolled into oblique position and the needle is adjusted under image
o 2 ml LA + steroid
4. Modification of activity
5. NSAIDs mild
6. Psycho-therapy
• Surgical SPINAL FUSION
• Exhaust every mean to avoid surgery as the results are usually unsatisfactory
• Indications:
o Failure of conservative measures
o Intractable pain
• Precautions:
o Careful repeated examination to detect any treatable pathology
o There should be some response to medical ttt other wise pt will not benefit from fusion
o There should be unequivocal proof for OA or spondylosis at a specific leve
o Pt should be emotionally stable & entailed that there is failure rate 10-20%
o And that this pathology may occur at a different level after fusion upto 40%
582 | Page [Sp ers]
pine Disorde
Sp lolysiss & Spon

Spondyl S ndylolisthesiss
SPONDYLOLYSIS
• caused by a defecct in the paars interartiicularis
• usuallyy a fatigue fracture froom repetitiive hyperexxtension sttresses (gym
mnasts)
• most coommon cauuse of LBP P in adolescents
• Radioloogy
o plain x-ray ys demonsttrate 80% of o lesions
o oblique viiews - add ditional 15% % picked upu - 'Scotttie
dog' sign (Lachapelle
( e)
• CT - may
m miss fracture
• Tc - y uptake inddicates an acute
a lesionn ώ will prrobably heaal
• Non-unnion is com mmon
SPONDYLOLISTHESIS
Definition
• "sponddy" refers too the vertebbrae and "llisthesis" means
m "to slip"
s
• It is thee forward “anterolithe
“ esis” or baackward “R Retrolithesiis”
• Normaally laminaee & facets have lockiing mechan nism preveenting forw
ward slippag
ge
• usuallyy L4/5 and L5/S1 ð saagittal faceet orientatioon
New
wman Classsification
n
1. Dysplastic
D (20%) S1 Supe
erior articular facets are
a dysplastic ± sp.bifiida occulta
a:
1. Axial malaliignment
2. Coronal maalalignment
2. Issthmic (50%%) Spondy
ylolysis ............................... (L5/S1) neural arch
h still in pla
ace
m
more in chilldren: a. Lytic—fattigue fractu
ure of the pa
ars interarticcularis
-yy lordosis b. Pars Elonngation
-tthin pars c. Pars fracture
3. Degenerativ
D ve (25%) Degene
erate facett joints ............ (L4/L5) more in ♀ < m
menopause ð lig laxity
OA, goutt. Neural arch
h slip back; bu
ut usually <30%
% displaceme
ent
4. Post-trauma
P atic Acute fracture
f of pedicle, faacet that alllows a slip to occur
pars is intact here
e
5. Pathologica
P al Tumou urs, paget's
6. Post-operat
P tive Postlam
menectomy y instability
y
• Effect of
o spondyloolithesis = CAUSES OF NEUROLOGICAL symptooms:
1- Pressure on n the roots ..... Radicuulopathy ð pars
p pseudoarthrosis, L
LF, facet, sp
purs
2- Pressure on n the dura ....... by lamiina above or
o body beloow
3- Pressure on n the cord ...... Cauda equina by NPH
N
4- Lumbar diisc prolapse e
Meyerding Severity of Slip:
1. Percentage
P e of slip disstance to AP A diameteer of the veertebra beloow:
• Grade I ..................................... < 25%
• Grade II
I .................................... 25-50%%
• Grade III
I .................................. 50-75% %
• Grade IV
I .................................. 75-1000%
• Grade V .................................... >100%% (spondylo optosis) = L5
L below tthe promon
ntory line
2. Slip
S Angle
• normall = > 0º ............................ >55º iss progressiv
ve
Clinical
• usually asymptomatic esp in children Æ discovered only incidentally on x-rays
• Begins during the second or third decade & injury may aggravate any symptoms
1- INSIDIOUS BACKACKE ώ y with walking and standing z by rest
2- LEG PAIN (Radiculopathy L5)
3- FLATTENING of the back & LOST WAIST
4- Spinous process STEP-OFF can be felt at L5S1 if significant displacement
5- +VE SCHOBER TEST (limited Lumbosacral mobility)
6- COMPENSATORY LORDOSIS at the segment above
7- HEART SHAPED BUTTOCKS ð sacral prominence & vertical orientation
8- CLAUDICATION may signal the development of lateral stenosis
9- SCOLIOSIS μβ associated: idiopathic, lithetic, sciatic
10- +VE TRIPOD SIGN
PXR
1- NAPLEON HAT .............................. appearance of lamina of severely slipped vertebra in AP view

2- SCOTTY DOG ................................ in spondylolysis before slippage in oblique view only
3- MEYERDING SLIP % ....................... lateral view (slip displacement / AP diameter of vert below)
4- SLIP ANGLE: .................................. between the upper border of L5 and sacral ⊥ line
5- SACRAL INCLINATION: .................. to the vertical on standing lateral view
6- SACRO-HORIZONTAL ANGLE: ....... same but to horizontal line (y in sacral kyphosis = dysplastic)
7- DOME SACRUM & TRAPEZOID L5 .. (ð resorbed ant & post edges of the sacrum)
8- LUMBAR INDEX: ............................ measure the trapezoidal wedging of L5
CT:
• Detect the pars defect in lytic type
• Detect facetal orientation in dysplastic type
Tc:
• y uptake = acute pars lesion ώ will probably heal Signs of Progression:
MRI 1. Clinical:
In degenerative SL é neurologic complications
• 1- Young
May show Modic changes
• 2- ♀
SPECT (Single Photon Emission Tomography) 3- Postural & gait abnormality
4- Episodes of backache
• Done for lytic defects:
2. Radiological
• If hot = recent defect Æ put him in a brace for 6mo 5- Meyerding G III, IV, V
• If cold = old defect Æ physiotherapy till operation 6- >40º Slip angle or progress
7- >30º inclined sacrum
Treatment 8- >25º Angular rotation
Non-operative: (GI – GII) 9- Dome shape sacrum
• reduce sports
• adolescents - x-rays every 6 mo until maturity
Operative:
Indications:
1- slip >50%
2- PROGRESSING in adolescents …. explain
3- PAIN UNRESPONSIVE to non-operative treatment
4- functionally significant neurological DEFICIT
Type of surgery
1. Grade II .............................................. in situ PEDICULAR FIXATION ± DECOMPRESSION
2. Grade III, IV & V .............................. in situ PEDICULAR FIXATION + DECOMPRESSION
3. Elderly degenerative cases ................. DECOMPRESSION without fusion
4. Lytic lesions & children even if low grade:
[1]. POSTERO-LATERAL FUSION without Instrumentation for L1-L4 SL
[2]. PARS REPAIR for L5-S1 defects:
o Buck: screw fixation
o Scott: wire fixation
o Combined: tension wire bet t.process or spinous process & a screw
5. ANTERIOR INTERBODY FUSION - for failed posterior fusions or some times in combination
6. MINI ALIF, PLIF, XLIF can be used as a limited approach in combination é posterior fusion
7. REDUCTION is debatable:
• y stability
• z progression
• Better cosmetically
• But time consuming
• Does not give better clinical result than in situ fusion
DD between degenerative & lytic:

Degenrative Lytic
Age Old Young
Level L4-5 or L3-4 L5-S1
Canal Compromized Not compromised
Progression Stable Progressive
CT Facetal OA Facetal malalignment
Pearl:
• To determine the appropriate surgical procedure to be done first know your pathology:
I. Coronal balance: ........................ (scoliosis) 10º/25º/35º/45º
II. Sagittal balance: .......................... (kyphosis) -60/-40/ -20 / 0
III. Width: ......................................... (Stenosis) 11.5/10/8/6
IV. Translation ................................... (lithesis) 1 mm Æ 10 mm
• 4 groups:
1- Conserve
2- Decompression
3- + fusion ± instrumentation
4- + anterior surgery
Lee Zones of lateral canal
ENTRANCE zone (1) antero-medial to the inferior facet
MID-ZONE (2) between the body anterior and the pars posterior; medial boundary is open to spinal canal.
EXIT ZONE (3) is formed by intervertebral foramen.
Spinal Stenosis
• Is the narrowing of the spinal canal at its central, lateral recess, or lateral foramen é
production of symptoms.
• It is one manifestation of the general process of spinal degeneration that occurs with aging,
and often becomes symptomatic in the 7th & 8th decades of life.
Epidemiology
• The L4-L5 segment is the most commonly affected, followed by the L3-L4.
• Men are more commonly affected, because their canals are narrower at the L3-L5 levels.
Anatomy
• In most individuals, the spinal cord ends by the L1 level; below
this level the remaining n. roots travel as the Cauda Equina.
• The nerve roots are more tolerant of chronic pressure than the
spinal cord, which is why an individual may tolerate a higher
stenosis degree in the lumbar spine than in cx or thx
• The boundaries of the central canal vary with the level:
o At body: (most affected by congenital short pedicle)
Anterior border is formed by the body
Lateral border by the pedicles
Posterior border by the laminae posteriorly.
o At the level disc: (most affected by degenerative)
Anterior border is formed by annulus
Posterolateral borders by the facet joints
Posterior border by ligamentum flavum.
Diameter of spinal canal:

Aetiology – Normal Relative Stenosis
ARNOLDI CLASSIFICATION Midsagittal dr (Lat) >11.5 10 - 11.5 <10mm
Interpedicular (AP) > 20 16-20 <16mm
1. Congenital cross section area 1.45 cm2 1 - 1.45 <1 cm2
[1]. Idiopathic
[2]. Achondroplasia
2. Acquired
[1]. Degenerative
Central
Peripheral (lat recess, foramen)
[2]. Combined degenerative + congenital
[3]. Trauma
[4]. Iatrogenic (laminectomy, fusion, chemonucleolysis)
[5]. Infection (TB)
[6]. Spinal tumour
[7]. Spondylolytic & spondylolithetic
[8]. Metabolic: Paget's & Fluorosis
Pathological Classification by site:
A. Central Stenosis .......................................................... affect the Thecal Sac & Cauda Equina
• caused by:
1- Arthritic facets with medial encroachment
2- Congenitally narrow canal ('Trefoil' shape)
3- Spondylolisthesis
4- Central disc herniation
5- Posttraumatic; Post-surgical Æ fibrosis
B. Lateral Stenosis ........................................................... affect the Root at Lee Zones Of Lat Canal
1- Entrance Zone ........................................... affects the traversing (lower) nerve root
2- Mid & foraminal Zones .......................... affects the exiting (upper) nerve root
3- Extra-foraminal (far-out): ....................... sacral ala, tr. process affect the dorsal root
• Caused by:
o Superior articular facet enlargement
o Lateral disc herniation
o Ligamentum flavum hypertrophy
o Uncinate spurring
Factors affecting the Dimensions of the canal

[1]. Dynamic factors
[2]. Level of the canal: The foramina z size while the nerve roots y in diameter as you move
down the spine. Thus the lumbar spine is most commonly affected.
[3]. Postural factors:
[1]. Axial loads y bulge of the disc Æ y root compression
[2]. when standing y lumbar lordosis Æ y the stenosis Æ subarachnoid obstruction Æ
z diffusion of fluid from endoneurium to subarachnoid Æ y endoneurial pressure
Æ 'COMPARTMENT SYNDROME' in the nerve roots Æ z conduction
Clinical
• Virtually all individuals at 8th decade have some degree of spinal stenosis
1- Central stenosis:
a. NEUROGENIC CLAUDICATION. (ð cauda equina compression = Pseudo-claudication)
b. y IMBALANCE & PARASTHESIA
c. feeling better if they walk STOOPED forward (sitting, bending, squatting)
d. Rarely - urinary incontinence & cauda equina syndrome
2- Foramenal stenosis:
e. RADICULOPATHY from narrowing of the lateral recess or the neural foramen.
f. BROAD-BASED GAIT + FORWARD STOOP posture
g. CHECK HIP
h. CHECK DISTAL PULSES to SCREEN for vascular causes of claudication.
i. Stress Test = walk until symptoms occur then
j. Stoop test = continue walk é stoop Æ pain z (if persist = vascular or hip)
effect of … on Neurogenic Claudication Vascular claudication
Walking Proximal bilateral thigh pain Distal-proximal pain; calf pain
Uphill Walking late pain ++
Rest relief with sitting or bending relief with standing
Bicycling - ++
Lying Flat ++ -
Investigations
I. X-rays:
1- Uncinate spurs
2- z disc height
3- Facet hypertrophy in older patients
4- Calcified ligament
5- Mid sagittal diameter ................ <10mm

6- Interpedicular distance ............ <16mm
7- HARDLEY’S LINE is broken: it is a smooth S line that extend from the inf border of the
transverse process to the lateral contour of superior facet of the vertebra below
II. CT:
1. more accurate than PXR for bony anatomy
2. less accurate than MRI for soft tissue compromise
3. AP Diameter < 10mm ........ Absolute Stenosis
III. MRI: (without gadolinium) is the "gold standard" in the evaluation of central stenosis.
1. T1 ..................................................... absence of the foramenal fat around the root
2. T2 ..................................................... condition of the cord
IV. Epiradicular Nerve root block:

• improvement of radiculopatht after LA injection is suggestive of lateral stenosis.
V. Myelography é water soluble metrizamide: it can be useful in selected cases
Natural History
• Symptoms unchange ................... 60-70%
• Worse ................................................ 15-20%
• Improved .......................................... 15-20%
DD 1- Spinal canal Stenosis LDP

Age & sex >50 ♀ <50 ♂
Onset Chronic Acute
Pain Referred Radicular
Weakness - +
Sensory - +
Lasegue & neuro - +
Provocation Position Walking Sitting
Palliation Position sitting Standing or Lying
2- DIABETIC NEUROPATHY:
o Glove and stocking
o First to vibration
3- FACETAL SYNOVIAL CYST:
o May rupture into the dura and compress the root
4- FORESTIER’S HYPEROSTOSIS
Treatment
Non-Operative:
1- NSAIDs
2- Muscle relaxants
3- Antidepressants for chronic radicular pain
4- Calcitonin in paget’s
5- EPIDURAL ROOT INJECTION: long-term relief in foramenal or lateral recess stenosis
6- Flexion BRACE (Williams brace) - prevents lordosis. Not well tolerated.
7- PHYSIOTHERAPY (with massage, ultrasound, TENS, braces or supports, acupuncture,
biofeedback, hot or cold packs, traction, or manipulation) can offer symptomatic relief of
radicular or low back pain, but not for claudicant symptoms.
Operative
• Indications:
1. Severe neurological symptoms
2. Failed conservative treatment
3. Impaired ADL (activities of daily living)
• Modalities:
1- Cervical anterior decompression
2- Laminaplasty: in which the lamina is cut completely from one side, and partially from the
other side to the level it could be opened like a book while it is in place, then BG is placed to
elevate the lamina, then the lamina is sutured in the new position. This technique is useful
for cervical stenosis where the stenosis is rather central more than lateral recess or foramenal
stenosis
3- Lumbar foramenotomy éout fusion
4- Lumbar lamenectomy + Facetectomy (< 1/3 of medial facet) + Fusion if:
i. Pt < 60 y with 2 facetectomies
ii. Pt < 55y with spondylosis
iii. Pt < 50y with isthmic spondylolithesis
Rheumatoid Arthritis
• Affects 3% of women & 1% of men
• Hand > Knee > hip > cervical spine
Diagnosis:
Ara Criteria (American Rheumatism Association):
1- Morning Stiffness: Lasting at least 1 hour before maximal improvement.
2- Arthritis Of 3 Or More Joint Areas
At least 3 joint areas simultaneously have had soft tissue swelling or fluid (not bony
overgrowth alone) observed by a physician; the 14 possible joint areas are right or left
proximal interphalangeal (PIP) joints, metacarpophalangeal (MCP) joints, wrist, elbow,
knee, ankle, and metatarsophalangeal (MTP) joints.
3- Arthritis Of Hand Joints
At least 1 area swollen (as defined above) in a wrist, MCP or PIP joint.
4- Symmetric Arthritis
5- Rheumatoid Nodules
Over bony prominences, or extensor surfaces, or in juxta-articular regions
6- Rheumatoid Factor +Ve
7- Radiographic Changes
• At Least 4 Of 7 Criteria.
• Criteria 1 Through 4 (At Least 6 Weeks).
• Clinical Staging:
o 7 ccc ............................................. Classic
o 5 ccc ............................................. Definite
o 3 ccc ............................................. Probable
o 2 ccc ............................................. Possible
Aetiology:
• Genetic susceptibility: RA is common in first degree
relatives of RA patients and twins
• Immunological process: HLA-DR4 & DW4 encoded on
chromosome 6; and is found on the surface of APC
(antigen presenting cells); & when interact é the antigen
(some times the antigen with the HLA form the activating
complex) Æ autoimmune response
• When APC and T-cells interact Æ cell proliferation +
cyokines secretion Æ ⊕ phagocytes & B-cells
• Rheumatoid factor: Anti-IgG auto antibodies which is
detected in the serum of the patient
Pathology:
Affected joints:
1. Atlanto axial joint + transverse ligament ................................. Atlanto-Axial Instability
2. Atlanto-occipital Æ dens project into f.magnum ................. Cranial Settling=Basilar Invagination
3. Facetal joints of the mid cervical region .................................. Subaxial Subluxation
Stage 1: Synovitis
• vascular congestion & effusion Æ Osteopenia (also from the steroid ttt)
• synoviocyte proliferation Æ Villous formation
• infiltration of subsynovial layers by PMNs, lymphocytes & plasma cells
Stage 2: Destruction
• a Pannus of granulation tissue creeps over the articular surface eroding cartilage & bone
• cartilage destruction occur partly ð proteolytic enzymes & vascular tissue
• bone destruction occur partly by proteolytic enz, & osteoclastic activity
• direct invasion occurs at the margins of the joint
• similar changes occur in tendon sheaths Æ rupture
Stage 3: Deformity & Complications:
• acute inflammation subsided
• deformities occur ð: articular destruction / capsular stretching / tendon ruptures
• Neurological manifestation occur ð:
o Different Instabilities
o Mechanical compression of the cord by a pannus
o Compression of the vertebral artery
o Peripheral neuritis from the disease itself
o DMAR drugs
Extra-articular Manifestations: FELTY'S, SJORGEN, CAPLAN $, PERICARDITIS,VASCULITIS, NODULES

Clinically: Palendromic, Systemic, Monoarticular, Myalgic
• 40 ♀ may be é positive family history Ranawat Neurologic Classification
• Early: usually no cervical manifestations:
Class I Pain
o Painful swollen Hands + morning stiffness
Class II Parasthesia & hyper-reflexia
o Painful, Swollen, Stiff, Cracking Joints Class IIIa Motor ambulatory
o loss of Weight, weakness Class IIIb Motor non ambulatory
• Late:
o Deformity: F Add ER of the hip
o Path #: from the disease and drugs (usually neck femur)
o Bouchard’s nodules, Swan neck , Boutonniere, Z-thumb, fingers ulnar deviation,
wrist radio-volar deviation, valgus knee, valgus feet, clawed toes
o Atlanto-Axial Subluxation: 20% of patients
1- Headache (C2 nerve compression) & Black out spells
2- Pain, stiffness, rarely parasthesia
3- Severe neck tenderness & z ROM
4- LMNL in UL + UMNL in LL
5- Lhermitte’s sign: sudden shocking leg parasthesia é neck flexion
Laboratory Findings:
• y. ESR, CRP
• RF +ve in 80%, ANA 30%
• ACCP (anti Cyclic Cetrolinated Peptide): 97% early +ve in RA even in seronegative RA
• anemia: ð abnormal erythropoiesis, and chronic blood loss from analgesic gastritis
• WBC: Normal or y (if z suspect Felty)
• z Complement
Synovial Biopsy & Fluid:
• Biopsy: is non specific to RA
• Fluid: zptn, C, glucose / poor clot / y RA cells & PNL
PXR:
LARSEN = DALE RADIOLOGIC INDEX
1- Stage I: juxta-articular Osteopenia
2- Stage II: Narrow joint space (usually bilat, symmetrical, concentric ± protrosio)
3- Stage III: Bone Erosion + bone Cysts
4- Stage IV: Deformity
• Usually no sclerosis nor osteophytes (except if 2ry OA)
White Criteria of basilar invagination on PXR cervical lateral view:

1. PADI (Posterior Atlanto-Dental Interval) ............................. <13mm = BI
2. AADI (Anterior Atlanto-Dental Interval) .............................. >4mm = BI
3. DBI (Dens-Basion Interval) ........................................................ <4mm = BI
4. Wackenheim's clivus tangent line ....................................... should tangent the dens not cut it
5. Chamberlain's line from f.magnum to hard palate ....... <3mm cut to dens
6. McGregor's line from occiput to hard palate .................... <5mm cutting to dens
7. McRae's line bet basion & foramen magnum ................... dens should never pass it
8. Ranawat's from C2 pedicle to transverse plane of C1.... 15-17mm
9. Redlund-Johnell from axis base to McGregor's line ...... 29-34mm
NB The Atlas sublux anteriorly (commonest) on the axis with flexion & reduce é extension (AADI
change > 3mm) this is the old method
DDx:
• Seronegative: SLE, Still’s
• AS: spondarthropathy
• Reiter’s: Conjunctivits, urethritis, Arthritis
• Gout & CPPD: crystals
• OA: DIP affection, osteophytes
• Polymyalgia rheumatica: pelvic, and pectoral weakness, and aching, +ve steroid test
• Sarcoidosis: Erythema nodosum, Hilar LN, +ve Kveim test
[Sp
pine Disord
ders] Page | 593
Management Principles:
• Stop th
he Synovitiss
o Rest
o DMAR Drrugs (Disea ase Modifying Anti-Rh heumatic) - Pyramid A
Approach = NSAID-
Antimalariials - Sulphasalazine – Gold – MTXM – D-peenicillamine
e - Azathioprine –
Leflunomide (Avara) + low dosse steroids
o Synovecto omy - chem mical, irradia
ation, surg
gical
• Prevennt Deformitty
Splintage ⎯⎯ ⎯→ ha ard collar ⎯ ⎯ ⎯ ⎯ ⎯ ⎯ → Trraction ⎯⎯⎯→ surg
Wear If Cranial Settling
S I
IfFail
o gery
o Physiotherrapy
o Tendon re epairs & joint stabilisaation
• Surgica
al (start é knee
k if > 45
5º flexion deformity)
d
o Arthroplassty is the gold standa ard
o Osteotomy y not done e:
i. Doessn’t remove e the cartila
age ώ is a source
s of
inflam
mmation
ii. RA is concentricc & no hea althy cartila
age
o Arthrodesis not to be e done (billateral)
o Cervical fu usion:
Indications:
A. Severe pain
B. Neurollogic signs
C. PADI < 13mm
Pro ocedure:
(1) C0-C2 fusion by BG & wirin ng ± C1 lammenectomyy or odonttoidectomyy
(2) Hartsh hill-Ransford loop + suublaminar wire (if atla
anto-axial + subaxial))
(3) C0-C2 fusion by plating ± BG B
(4) Inter la
aminar clam mps + BG
(5) Posterior atlanto oaxial transarticular sccrews
(6) C0-C2 fusion by BG followe ed by Halo o traction
• Rehabiilitate & keep moving g
o Cervical co ollar for 3-66 mo
o Physiotherrapy
At Onset: NSAID, exercise

Earrly: NSAID, Ste
eroids, DMD, local injjections, ph
hysiotherapy, Rest annd splitage e
Ero
osive: DMD, splin
ntage, opeerative (syn
novectomy,, tendon re epair, jointt stabilizatio
on)
Latte: Reconstructive arthro
oplasty
Drugs Details:
Drug Mechanism A/E
NSAIDs PG synthesis Æ z pain and inflammation Gastric Upset
Antimalaria PG & phagocytic activity of PNL Lucoma
Sulphaslsazine Anti-inflammatory Megaloblastic anemia
Gold Alters the function of macrophages and complement Thrombocytopenia
Methotrexate Immune suppression Liver toxicity
D-Penicillamine Dissolve RF complexes in joints to be excreted Late resp.& nephrotic
Azathioprine Immuno suppression Liver toxicity
Leflunomide DiHydro-Orotate Dehydrogenase Æ z T-cell prolif
Complications:
• Fixed Deformities
• Joint Rupture
• Infection
• Spinal cord compression
• PN compression
• Vasculitis
• Amyloidosis, proteinuria
• progressive RF
Poor Prognostic Signs:
• Very high RF
• Peri-articular erosions
• Nodules
• Muscle wasting
• Joint contractures
• Vasculitis
• PADI < 13mm
Prognosis:
• 10% improve after first attack of synovitis
• 60% have remissions & exacerbations
• 20% have severe joint erosions requiring multiple operations
• 10% become completely disabled

Some Abnormal Gait Patterns
Ankylosing Spondylitis
Aetiology:
• Affects spine & sacroiliac joints primarily
Prevalence
• 0.2%
• Males > females & Familial involvement
• HLA-B27 marker
Pathology:
I. Affected Joints
st nd
1]. Plane synovial joint: 1 SACROILIAC Æ 2 FACET (L, Thx, & Cx) Æ 4th COSTOVERTEBRAL
2]. Syndesmosis & symphyses: IV discs, sacroiliac ligaments, symphysis pubis
3]. Cervical spine:
a. Atlanto-occipital erosion
b. Subaxial subluxation and kyphosis
c. Atlanto-axial subluxation ð:
(1) rigid spine Æ y C1-2 stresses
(2) Transverse ligament dysfuction
II. Stages:
1]. Inflammation & erosion:
• Round cell infiltration, granulation tissue
• Erosion of anterior edge of the vertebra Æ Squaring of the vertebra
• Repair process starts Æ prominence of edges + Osteopenic Midsection
2]. Fibrosis:
• Replacement of granulation tissue with fibrous tissue
3]. Ossification of:
A]. Fibrous tissue
B]. ALL
C]. Annulus Æ vertical marginal osteophytes “Syndesmophytes”
4]. Evolution:
A]. reformation of the anterior concavity of the body
B]. Symmetrical syndesmophytes Æ pathognomonic Bamboo appearance
C]. Kyphosis deformity measured by the chin-brow to vertical angle:
o Acute Type
o Chronic type kyphosis deformity
III. Extraskeletal:
1. Prostatitis
2. Conjunctivitis & uveitis in 20%
3. Carditis, AS, Pulmonary fibrosis
Clinical:
[1]. Insidious Pain & stiffness & ADL limitation
[2]. CHIN TO CHEST deformity
[3]. WALL TEST: pt can not stand with heal, occiput, buttock touching the wall
[4]. ENTHESOPATHY of tendo-achilles
[5]. z spinal motion (+VE SCHOBER’S) Sacroiliac Tests:
[6]. z Chest expansion < 7cm [1]. Baer’s point Tender: med to McBurney = iliacus spasm 2ry to SI
[7]. z Hip motion (+VE THOMAS TEST) [2]. Gapping test: painful down pressure on ASIS (Ant.SI)
[3]. Squish test: painful down & 45º caudal pressure (Post.SI)
[8]. +VE SACROILIAC TESTS [4]. Approximation test: while pt lateral position (post.SI)
[9]. Difficult cervical spine fractures [5]. SI Rocking test: knee to shoulder
Radiology: [6]. Toe to mouth
[1]. EROSIVE arthritis [7]. Resisted Motion: flexion, abduction, and extension stress the SI
[2]. SQUARING of vertebral bodies [8]. Sacral apex pressure: pt prone press on sacrum Æ rotation
[3]. Patchy periarticular OSTEOPENIA [9]. +ve joint play
[4]. SYNDESMOPHYTES [10]. Lasègue é pain >70º
[5]. BAMBOO spine [11]. Bilat SLR é pain < 70º
[6]. CHIN-BROW to vertical angle [12]. Piedallu’s: flexion é sitting Æ hypermobile PSIS comparatively higher
Laboratory: [13]. Gaenslen’s lateral: lower hip held & upper hyperextended Æ pain
[14]. Gaenslen’s supine: sound side held & test side hang free at edge
[1]. ESR ........................... y [15]. Laguere’s test: F Ab ER hip + pelvis stabilizn on ASIS Æ buttock pain
[2]. HLA-B27 .................. +ve 90% [16]. Patrick: foot on knee position + down pressure on knee Æ buttock pain
[3]. RF ............................ -ve [17]. Yeoman’s: patient is prone hip and knee hyperextension Æ pain
Management:
[I]. Early: NSAIDs (phenylbutazone) + Postural management + activity modification
[II]. Later: corrective ttt:
[1]. Acute kyphosis:
• Halo traction in the line of deformity é gradual correction
• Followed by Halo cast brace for 12 mo
[2]. Chronic kyphosis:

• Extension closing wedge under LA setting position (only GA during the osteoclasis
only) at C7-T1; why?

Wide Canal
C8 is flexible and less important
Vertebral artery passes anterior to the C7 Æ less liable to be injured
• Lumbar closing wedge osteotomy at L2: but
Aortic disruption
Superior mesenteric $
[III]. Latest: reconstructive operations
[3]. THR
[4]. Sacroiliac fusion: using screw fixation, transsacral rods
[5]. Atlanto-Axial fusion
DDx:
[1]. OSTEITIS CONDENSANS ILII: pregnant ♀ é sclerotic U medial ilial aspect of the SI joint
[2]. FIBRODYSPLASIA OSSIFICANS PROGRESSIVA: generalized heterotopic ossification & fused SI
[3]. DIFFUSE IDEOPATHIC SKELETAL HYPEROSTOSIS (FORESTIER'S $)
i) Old ♂
ii) Right side
iii) Ossification ALL & sharpee’s fibers at vertebral waist
iv) Non marginal syndesmophytes
v) No erosive arthropathy, squaring, nor narrowing
vi) Normal ESR
Spinal Injury
Spinal cord syndrome
COMPLICATIONS OF SPINAL INJURY

1. Neurological damage
2. Damage to vertebral column causing deformity and pain
Stable injuries
• Vertebral components won’t be displaced by normal movement.
• An undamaged spinal cord is not in danger
• There is no development of incapacitating deformity or pain
Unstable injuries
• Further displacement of the injury may occur
• Loss of 50% of vertebral height
• Angulation of thoracolumbar junction of > 20 degrees
• Failure of at least 2 of Denis’s 3 columns
• Compression # of three sequential vertebrae can lead to posttraumatic kyphosis
• The upper Thx spine (T1-T10) is protected by ribs, sternum and the facet joint orientation
• At thoracolumbar junction there is a fulcrum of increased motion Æ y risk of injury
• The middle thoracic spine is a vascular ’watershed’, vascular insult can cause cord ischaemia
(Artery of Adamkiewitz)
• Cauda equina begins at L1-L2. Lesions below L1 have a better prognosis as nerve roots, not
cord are affected
Mechanisms of injury
1- Hyperextension -common in the neck. Anterior ligaments and disc may be damaged.
2- Flexion- If posterior ligaments intact, wedging of vertebral body occurs. If posterior
ligaments torn, may cause subluxation
3- Axial compression- Causes burst #s. Bony fragments may be pushed into spinal canal
4- Flexion, with posterior distraction- May disrupt middle and posterior columns.
5- Flexion with rotation- Causes dislocation with or without #.
6- Shear.
SPINAL SHOCK
1. Diaphragmatic breathing
2. Flaccid limbs
3. warm periphery
4. decr. pain sensation
5. reduced reflexes
6. erection
7. Urinary retention
8. decr. BP + decr. pulse rate = Neurogenic
9. decr. body temp.
10. Return of bulbocavernosus reflex at 24hrs= end of Spinal Shock
INITIAL MANAGEMENT OF SPINAL INJURY PATIENTS
ABC, Spinal board, hard collar
History
• Strongly suspect spinal injury if any major accident, unconscious patient, fall from a height,
sudden jerk of neck after rear end car collision, facial injuries or head injury
• Ask about neck or back pain, numbness, tingling, weakness, ability to pass urine
Examination
• Logroll- look for bruising, palpate for a step, tenderness
• Repeated neurological examination to determine neurological damage and its
progression/resolution
• Thorough overall examination for fractures etc as patient may not feel pain
Imaging
• Xrays-Cervical spine AP, Lateral including C7/T1, open mouth view of odontoid. Swimmers
view or pull arms down. AP and lateral view of other tender areas of spine
• CT scan shows bony injury
• MR scan shows soft tissue involvement
If neurological damage
1. Catheterise
2. Note reduced BP and bradycardia due to neurogenic shock (temporary generalised
sympathectomy). Rule out hypotension due to haemorrhage elsewhere. May need treatment
with vasopressors, not fluid resuscitation.
3. Invasive monitoring required
4. Give methylprednisolone IV 30mg/kg over 15 mins then 5.4mg/kg/hr for next 23 hours.
Needs to be given within 8 hrs. Discuss with the spinal team.
5. Attend to skin by turning
DEFINITIVE MANAGEMENT
Objectives
• Preserve neurological function
• Relieve reversible nerve or cord compression
• Stabilise the spine
• Rehabilitate patient
With no neurological deficit

• If stable spinal injury- pain relief, collar or brace. Exception can be a burst #, ? operatively
stabilise
• If unstable injury, reduce and hold secure until bone / ligts heal with ORIF or traction in
tongs, halo vest
With complete sensory and motor loss
• Usually an unstable injury
• Only consider conservative management for high thoracic injuries
• Early operative stabilisation- to help with nursing, prevent spinal deformity and pain. Speeds
up rehab
With Incomplete neurological loss
• Stable injury- conservative bed rest, brace. Exception can be burst # ?operatively stabilise
• Unstable injury- early reduction and stabilisation
NEUROLOGICAL ASSESSMENT IN SPINAL INJURIES
Aims
• To determine the level of the lesion- counted as the lowest level at which neurological
function is intact bilaterally
• To determine whether damage is complete/ incomplete
• To determine prognosis
• May be difficult until period of spinal shock (flaccidity, areflexia) is over (24-48 hrs after
injury)
1. Tone
2. Power
Diaphragm C3-4-5
Shrugging shoulders C4
Flex elbows C5,6
Extend elbows C7
Abduct fingers C8
Active chest expansion T1-T12
Hip flexion L2
Knee extension L3-4
Ankle dorsiflexion L5-S1
Ankle plantar flexion S1-S2
Eversion of foot L5
Inversion of foot L4
MRC Power Grading

0 No active contraction
1 Visible contraction without movement
2 Movement with gravity eliminated
3 Movement against gravity
4 Movement against resistance but weak
5 Normal power
3. Reflexes
Biceps C5-6
Triceps C6-7
Supinator C5-6
Knee jerk L3-4
Ankle jerk L5-S1
Plantar response If upgoing = UMN lesion
Abdo cutaneous If lost = UMN lesion
Bulbo cavernosis Pull penis, causes anal sphincter tightening
If returned, period of spinal shock is over
4. Sensation
5. PR
1. Always perform this to assess S2, 3, 4
INCOMPLETE CORD INJURIES
Syndrome injury/pathology Features Prognosis
B.Sequard Penetrating trauma Loss of ipsilateral motor function and vibration and Best
position sense, contralat loss of pain & temp
Ant cord Flex.compression Motor loss , dorsal columns spared Poor
Central cord Age>50 ext.injuries Affects UL > LL, motor and sensory loss Fair
LONG TERM CARE OF NEUROLOGICALLY INJURED SPINAL PATIENTS

Frankel grade- Useful in monitoring functional improvement from spinal cord injury
Frankel grade Function
A Complete paralysis
B Sensory function only below injury level
C Incomplete motor function below injury level (1or 2/5)
D Fair to good motor function (3-4/5) below injury level
E Normal function below injury level
Highest mortality in the first 2 weeks
Most common causes of morbidity and mortality:
1. Respiratory insufficiency- atelectasis and pneumonia. Any deficit proximal to T10 causes
increased reliance on the diaphragm. Treat with IPPV, physio, tracheostomy and suction,
repeated bronchoscopy
2. Paralytic ileus- Keep NBM initially for 24 hours, IV fluids
3. GI bleeds from haemorrhagic gastritis -? Due to unopposed parasympathetic activity. Give
H2 antagonists
4. Urological complications- UMN lesion of bladder, catheterise intermittently to stop urinary
stasis and infection. LMN, may manage with suprapubic pressure to relieve bladder
5. Pressure sores- Turn every 2 hrs, teach to relieve pressure later
6. Joint contractures- Passive movements +/- splintage 2x per day
7. Psychological withdrawal- multi disciplinary approach.
Conus medullaris syndrome

Injury of the sacral cord (conus) and lumbar nerve roots within the spinal canal, usually results in areflexic
bladder, bowel, and lower extremities. Most of these injuries occur between T11 and L2 and result in flaccid
paralysis in the perineum and loss of all bladder and perianal muscle control. The irreversible nature of this
injury to the sacral segments is evidenced by the absence of the bulbocavernosus reflex and the perianal
wink. Motor function in the lower extremities between L1 and L4 may be present if nerve root sparing
occurs.
Cauda equina syndrome

Injury between the conus and the lumbosacral nerve roots within the spinal canal, also results in areflexic
bladder, bowel, and lower limbs. With a complete cauda equina injury, all peripheral nerves to the bowel,
bladder, perianal area, and lower extremities are lost, and the bulbocavernosus reflex, anal wink, and all
reflex activity in the lower extremities are absent, indicating absence of any function in the cauda equina. It
is important to remember that the cauda equina functions as the peripheral nervous system, and there is a
possibility of return of function of the nerve rootlets if they have not been completely transected or
destroyed. Most often the cauda equina syndrome presents as a neurologically incomplete lesion.
Spine Infections
Vertebral Osteomyelitis
Aetiology
Risk factors:
• older debilitated & immunocompromised patient
• IV drug addicts (pseudomonas)
• history of pneumonia, UTI, skin infection
• 70% arise from UTI, chronically ill, elderly adults via Batson's venous plexus
• Sickle cell anemia
Organisms:
• Staph aureus ....................................................... 60% & MRSA is on the increase
• Gram negatives (E coli, Pseudomonas, Proteus) & anaerobes are on the increase
• Strep viridans
• brucellae, candidae, coccidiomycosis (in immunocompromised)
• tuberculosis (commonest site = T10)
• Superinfection on TB may occur during surgery
Route of infection:
1. Hematogenous spread (commonest): can affect any part of the spine; body, arch, facet,
odontoid,…Baston has attributed this to the presence of the large valveless vein in the
anterior body, but Trueta proved the arterial route being the principle way for infection
2. Direct spread from near structure: colon, subphrenic abscess, abdominal abscess
3. Direct inoculation: postop either after open surgery, nucleolysis, or discography, laser
Site of infection:
• lumbar is the commonest ..................................... (60%) éout paralysis
• thoracic & cervical ................................................ higher incidence of paralysis
Pathophysiology
1- Haematogenous spread via arterial route (Trueta) rather than the old theory of (Batson's
venous complex); and goes via the end arterioles where it stop:
A. In children: the disc ................................... (still vascular)
B. In adults: the anterior metaphysis .............. (disc is avascular)
2- toxins cause septic thrombosis, infarct, abscess, blocks nutrition
3- Infection SPREAD locally via:
A. Intermetaphyseal anastmosis by passing the segmental artery
B. Along the ALL
C. posteriorly Æ epidural abscess .................. Early paralysis ð abscess & oedema
D. Anteriorly Æ paravertebral abscess .......... Late paralysis ð kyphosis
4- PARAVERTEBRAL ABSCESS may tickle down:
A. Cervical: ⎯⎯⎯⎯ ⎯→ Retropharyngeal, supraclavicular / ⎯ ⎯

Sternomastoid
⎯ ⎯⎯→ Axilla
BrachialPl exus
B. Dorsal: ⎯⎯⎯⎯→ paraspinal / ⎯⎯⎯⎯⎯ ⎯→ paranephric, or psoas abscess

Intercos tal Pr evertebralFascia
C. Lumbar: ⎯⎯⎯⎯⎯⎯→ psoas, femoral / ⎯⎯⎯ ⎯→ Gluteal, ischiorectal, Petit’s U

Psoas&FemoralArt GlutealArt
5- weakening of the bone may cause vertebral COLLAPSE.

6- PARALYSIS either early or late y by age, level, DM, staph.aureus; and of 2 types:
o Central cord $ .................................................. 66%
o Anterior cord $ ................................................ 33%
Clinical
• Often a significant delay in diagnosis (6-12 weeks)
Symptoms
• Triad = back pain + fever + tenderness (consider bacterial endocarditis)
1- Pain: ................................................ is the hallmark symptom
o Insidious course, developing over 1-3 mo
o y é activity & z rest
o May reach to be pain at rest & even nocturnal pain
2- Fever: .............................................. only 50%
3- Neurology: ..................................... only 10%
Signs:
1- Local tenderness
2- Ms spasm ........................................ z back motion and torticollis é +VE COIN TEST
3- Deformity ........................................GIBBUS
4- z SLR .............................................LASEGUE, Brudziniske, Kernig’s, …
5- Neurological signs ..........................Motor, sensory, reflexes
6- Meningeal signs .............................. LHERMITTE
Radiology DRES OFF
X-Rays: (lateral cervical & AP lumbar, dorsal)
• 2 weeks ........................................... disc space NARROWING (two bodies + disc affected)
• 4 weeks ........................................... RAREFACTION
• 6 weeks ........................................... ENDPLATE EROSION; osteolysis
• 8 weeks ........................................... reactive SCREROSIS ð trabecular collapse
• 12 weeks ......................................... NBF
• 6-12 months .................................... intervertebral FUSION - usually signifies resolution
• Examine paravertebral soft tissue mass - retropharangeal & psoas contours.
• Disc destruction is atypical of neoplasms
CT:
• Can diagnose more early
• Show the signs of rarefaction, erosion, lysis + reactive sclerosis
• Can be combined with myelography:
o More accurate for cord condition
o Can with draw CSF for analysis
MRI
• Very sensitive & specific & accurate (for differentiating from tumour)
1- zT1 (loss of distinction bet disc & body)
2- y T2 é streaky linear appearance + absent nuclear cleft
3- Gadolinium enhances sensitivity
4- STIR (short T1 inversion recovery=Fat suppresion); Æ high contrast bet norm & abnorm
Nuclear studies:
• high sensitivity & fair specificity; but all are less accurate than the MRI
1. TC99 show: ▪ Flow phase z ..................detect perfusion abnormality
▪ Blood Pool phase y .........detect hyperemia
▪ Static bone phase y .........detect osteoblastic activity (absorbed by HA)
2. GA67 is more specific for infection the substance is taken by the leucocytes
3. IN111 labelled WBC accuracy is 66% & can not differentiate bet acute and chronic
4. SPECT (single photon emission CT) simply is a CT + radionuclide (best in osteoid osteoma)
5. Recent: STRONIUM 100% specific
Investigations
1- Leucocytosis ........................................30% increase
2- y ESR ..................................................30% > 100, 70% > 50
3- CRP ......................................................30% positive
4- blood cultures .....................................30% positive
5- CT guided FNAC .................................68-86% +ve; but sacrum are not safe for needle
aspiration; do stains (Gram & AFB & fungi), Cultures, histopathologic examination
6- Specific for organisms:
o ASOT
o anti-staph. titres
o Tuberculin skin tests for TB
o IFAT, IHAT for brucellosis and salmonellosis
Treatment
Goals: (of any ttt):
• ttt the disease
• relief the symptoms
• prevent complications: collapse, deformity, neurological symptoms
Non Operative
• IV AB for 6w ⎯Oral
⎯
⎯→ 6wk.
• LSO / TLSO / CO / CTO / CTLSO (Milwaukee)
• Follow up by: CP, PXR, MRI, ESR an other lab
Operative
• Indications
o failure of response to medical treatment
o Progression of the disease
o severe pain and neurological symptoms
o Complications: instability, deformity, abscess
o need for open biopsy
• Objectives:
1- Debridement
2- Decompression of the cord
3- Realignment
4- Stabilization
• Approaches:
o ANTERIOR APPROACH provides better exposure + draining abscesses
o Ant. decompression & strut GRAFT. (for all levels cervical, thoracic, and lumbar)
o Role of spinal INSTRUMENTATION is controversial - with a large deformity, posterior
instrumentation may be indicated
Tuberculosis
• Tuberculosis is common throughout the world
• Usually due to Mycobacterium tuberculosis or Mycobacterium bovis infection
• Spine is the most common site of skeletal TB
Pathology:
1ry lesion:
• Site:
• Lung usually (sub-pleural Ghon’s Focus + mediastinal lymphadenopathy)
• Pharynx & Gut
• Changes:
• Local inflammatory focus Æ Lymphangitis Æ Lymphadenitis
• Seculae:
• TB bacilli remain dormant in LN (intra macrophage)
• Body is sensitized to toxin (Type IV delayed hypersensitivity)
2ry lesion:
• Due to reactivation, repeat exposure, z immunity (e.g. drugs or HIV infection)
• Results in more significant symptoms as it spreads to:
• Lung .......................................... military TB, TB bronchopeumonia
• Meninges:................................. TB meningitis
3ry lesions (10% affect the musculoskeletal system)
• Tuberculoma formation:
• Central CASEATION necrosis (coagulation necrosis)
• Surrounded by EPITHELIOID cells, LANGERHANS giant cells, LYMPHOCYTES
• They tend to coalesce to form a wide area of caseation necrosis
• TB Arthritis (hip, knee, ankle, shoulder, then wrist)
• Synovium is THICKENED é Cell rich EFFUSION
• Granulomatous PANNUS may form & creaps on the cartilage & bone
• Cartilage & bone EROSION (peripherally at synovial reflection)
• Juxta articular OSTEOPENIA ð hyperaemia
• Appendicular skeleton:
• Metaphyseal bone destruction (no sclerosis, no periosteal reaction)
• TB Dactylitis = Spina Ventosa (middle and distal phalanx)
• Digit is swollen spindle shape é little pain
• Starts diaphyseal é bone rarefaction + PNBF + soft tissue swelling
• PXR: Spina (spindle shaped digit) Ventosa (full of are i.e. rarefied)
• Cold Abscess:
• Infected LN may COALASE together to form big area of caseation
• Caseation spread via soft tissue planes i.e. through skin or along ms fascia or a bundle
• May burst to skin to form a sinus
• TB Spondylitis:
• Blood borne - settles in vertebral body anteriorly
• Thoracic is commonest ± skip lesions & multiple level (lumbar for OM & discitis)
• POTT’S PARAPLEGIA
Healing:
• Resolution
• Fibrous Ankylosis
• Dormant bacilli
TB SPONDYLITIS:
• Sites of vertebral affection respectively:
1-Anterior in the body the most vascular part of the body
2-Paradiscal & Central are less common
3-Synovial affection of the facetal joint is rare
4-Posterior elements are recorded as well
• Thoracic is commonest ± skip lesions (lumbar for OM & discitis)
1. May be MULTIPLE LEVEL form the start
2. may have 'SKIP LESIONS'
3. SPREAD locally:
[A]. Extensive destruction, more sequestra, gaseous pus > pyogenic
[B]. IV DISCS preserved until late when break via the end plate
4. COLD ABSCESS formation more common than pyogenic OM :
[C]. Cervical: ⎯⎯⎯⎯ ⎯→ Retropharyngeal, supraclavicular / ⎯ ⎯
Sternomastoid
⎯ ⎯⎯→ Axilla
BrachialPl exus
[D]. Dorsal: ⎯⎯⎯⎯→ paraspinal / ⎯⎯⎯⎯⎯ ⎯→ paranephric, or psoas abscess

Intercos tal Pr evertebralFascia
[E]. Lumbar: ⎯⎯⎯⎯⎯⎯→ psoas,femoral/ ⎯⎯⎯ ⎯→ Gluteal, ischiorectal, Petit’s U

Psoas&FemoralArt GlutealArt
5. COLLAPSE of anterior vertebral body Æ sharp kyphosis if progressive Æ

6. POTT'S PARAPLEGIA:
1. EARLY Pott’s paraplegia:
[F]. Progress then subside: paraplegia ð abscess & OEDEMA
[G]. Progressive ð mech pressure by SEQUESTRA, disc, or bone bridge
[H]. Acute paraplegia ð THROMBOSIS or concertina collapse of Seddon
[I]. Compression paraplegia ð TB OF LAMINA or encysted TB Æ
2. LATE Pott’s paraplegia:
[A]. Soon after cure: ð REACTIVATION of the disease
[B]. Very late: ð CORDOMALACIA &friction against kyphotic canal
Hodgson Classification of Pott’s Paraplegia:

Group A Active disease
1 External pressure on the cord by an abscess or laminar TB
2 Penetration of dura by infection
Group B Healed Disease
1 Cord Transection by the kyphotic bone
2 Constriction of cord by granulation & fibrosis
Clinically:
• General: Night sweat, night fever, Loss of weight, loss of appetite
• Local:
o NIGHT CRIES: ð z ms spasm Æ stretch of the damaged tissue Æ pain
o Marked MS WASTING
o TB arthritis: SYNOVIAL THICKENING, STIFFNESS, DEFORMITY
o POTT’S PARAPLEGIA: (4 Grades)
Paraplegia Motor Sensory Jerk Clonus & Babinisiki Sphincters

1- Mild Mild Spasticity but the pt can walk Intact Slight increase -ve both Intact
2- In extension Pyramidal weakness of flexors + Brisk extensor +ve both Intact
Extrapyramidal intact extensors
3- In Flexion Complete motor paralysis of both + Brisk flexors -ve clonus Intact
z extensor +ve Babiniski & Mass
4- Complete Same Lost Lost both Same Lost
608 | Page [Sp ers]
pine Disorde
P XR:
}
1. JUXTA ARTICULAR OSTEOPENIA Æ washe
ed out bon
ne ends
2. CONCENTRIC z JOINT SPACE (child epiphysiss y ð PHEMISTER Triad
hyperaaemia)
3. Peripheeral bone e EROSION and CYSTIC subch
hondral lesions
4. NO perriosteal reaction
5. NO SCLEROSIS
6. Erosionns in BABCOCK’S Δ, Sup p. Acetabu ulum Æ WANDERING ACETABULUM
7. POTT’S disease
d of the spine
[1]. Earliest sign
s is OSTEOPENIA of two adjace ent vertebrrae
[2]. EROSION:
o MULTISEGMENTAL
o SKIP lesions
o SCALLOPING of the antterior borde er of the veertebra
o DISC SPARING (≠ pyog gnic)
[3]. SOFT TISSUE MASS ........... Parasp pinal abscesss
[4]. COLLAPSE: ................................KYPHOSIS / RIB SUN RAY APPEARANCE
[5]. Healing: ........................... y BONE DENSITY & paraverte ebral absce
esses may CALCIFY
[6]. KONSTAM angle: pre edict the de evelopmentt of kyphosis é 90% (y = a + bx)
(y) = predicted d angle =5.5 + 30.5 X Konstam att presentation × 1
No of Vertebrae
V 10
a annd b are co onstants = 5.5 & 30.5, re espectively
MRI
• No y off disc space
e signal ð granulatio
g n (≠ pyoge
enic)
• Extent of
o the destruction and soft tissuue mass
• Cord co
ondition e.gg. cordoma alacia, com
mpression …
Bone Scans:
• high fallse -ve rate with Tc & Ga
DD
• Other in
nfections
• Traumaatic paraple
egia
• Tumors Pyogenic
P D
DD:
• Rheuma atoid & AS Pyyogenic TB
• Sheurm
mann accute chronic
Investigation Single vertebrral focus Multisegment
• Blood: Syymmetrical collapse Kyphosis
1. yESR Sp
preads intraoosseously Spread é fasscial planes
2. Leucopenia é relative
e lymphoccytosis Disk
D destroyed d y T2 Disk sequestered z T2
3. z Lympho
ocyte/monocyte ratio o≈1 Ant-column in nvolvement 3 columns innvolvement
Eppidural absceess Paravertebrral abscess
• Immuno
ological:
1- +ve PCR
oux test
2- +ve Manto
• Aspirate
e fluid:
1- Physical: ......................... z viscosity
2- Chemical: ..................... y ptn / zglucose / poor mucin clot
3- Bacteriolog gical: ........... Red acid-alcohol fast INTRACELLULAR bacilli é ZEAL NELSEN ......... 20%
4- n: ................... LOWENSTEIN JENSEN me
Cultivation edia or Dorsset egg ......................................... 80%
Con ncentrated centrifuged c d decontaminated samp ple (Petroff method)
Kee ep 35º for 6 wk
5- Organismss also FLUORESCE WITH AURAMINE sttaining
6- Guinea pig g inoculation
• biopsy:
o Granuloma atous reactioon (caseatio on + Langerrhans + epittheliod + lym
mphocytes))
o Characterisstic evidence e of a delayyed hyperse
ensitivity rea
action
• TB tend to give neg
gative resultts
Skin tests
• Delayed hypersensitivity reaction used to diagnose tuberculosis
• The two commonest tests are the Mantoux and Heaf test
• Mantoux test:
• 0.1 ml of purified protein derivative is injected intradermally
• +ve if ................................................... > 5 mm papule at 72 hours
• Heaf test
• PPD is inoculated into the skin using a gun to produce multiple punctures
• +ve if ................................................... > 4 papules at puncture sites at 72 hours
• Positive skin test are indicative of active infection or previous BCG vaccination
Treatment
1. Rest: ............................................................... (in Acute stage)
• Bed rest + Spinal orthosis (prevent deformity and ms spasm) till:
1- Clinically: .............................. No fever, no wt loss, no spasm
2- PXR: ....................................... y calcification
3- Lab: ....................................... z ESR, y lymph/monocyte ratio >5
• Then motion is encouraged é the orthosis on 18mo ⎯Then
⎯⎯→ gradual weaning & if
pain & spasm return Æ resume orthosis
2. Chemotherapy: ............................... (at lease 9-12mo)
• RIPES - Rifampicin, Isoniazid, Pyrazinamide, Ethambutol, Spectinomycin
• Rifampicin + Isoniazid 6-8 mo give 80% recovery of the infection
• Ethambutol (or pyrazinamide, spectinomycin) for the initial 8wk
• Streptomycin is toxic
3. Operative:
• Indications:
Large abscess
1-
Instability
2-
Neurology
3-
Progressive impairment to pulmonary function
4-
No response to medical therapy
5-
Young pt é Konstam angle > 150º (y risk for kyphosis progression)
6-
• Adjuvant chemotherapy beginning 10 days before surgery is essential
I. Hong Kong Procedure: .............................. (For active infection)
• Radical anterior debridement
• Anterior fusion iliac strut grating (allows better correction of the kyphosis)
• Posterior instrumentation
II. Costotransversectomy:................................ (For tense abscess)
• Excision of the transverse process + medial 4 cm of the rib
• Evacuation of the abscess and closure
III. Lateral Rhachotomy: .................................. (For Paraplegia)
• As costotransversectomy + removal of the ant and side wall of the canal
• Lamenae, pedicles, and facets are preserved
IV. Laminectomy: ............................................... (For TB of the lamina only)
±
• Cold abscess ........................... calls for urgent drainage
• GT bursitis ............................... Bursectomy
• Painful destroyed joint ......... Girdle stone then arthroplasty
Discitis (Juvenile)
Definition
• inflammation of the intervertebral disc or end plate in young children, probably ð
autoimmune condition, no sepsis to be found
Epidemiology:
• 2-6 y ................................................................ ♂=♀
• Self-limiting condition ............................... 30%
• No organism in culture ............................. 75%
• L4,L5 commonest ....................................... 75%
Pathology:
• Inflammation of the IV disc or end plate
• it may represent extension of subacute vertebral endplate osteomyelitis which did not
progress to give vertebral osteomyelitis
Clinical
1- children are typically afebrile or mild fever (≠ osteomyelitis)
2- Back pain
3- Child refuses to stand, walk, or flex the spine
4- may also complain of hip or abdominal pain
5- Tenderness, paravertebral spasm, loss of normal lumbar lordosis, zROM
Investigations
• WBC is usually normal
• ESR elevated > 40
• when a causative organism can be identified, it is most commonly S. aureus.
• Biopsy is indicated if failed response or if an organism is suspected
Radiology
X-rays:
• may appear normal early on
• disc-space NARROWING
• LOSS OF DISTINCTION between adjacent vertebral end-plates (never severe destruction)
• later - in adult disc space usually FUSE, while in child usually is RESTORED
Bone Scan:
• Tc y uptake of isotope in infected disc space - may be useful in early diagnosis of discitis.
MRI:
• MRI is more sensitive than bone scans in early discitis
• z T1 and yT2
Treatment
• Bedrest + TLSO (avoid traction)
• Empirical systemic antibiotics (Probably make no difference)
• Never sugery
Epidural Abscess
• Uncommon devastating condition 2:10000
• Mortality rate = 12%
Aetiology:
1- Same org as pyogenic
2- Same predisposing factors
3- more common in immunocompromised, malignancy, DM, alcohol abuse, invasive
procedures, vertebral fractures
Pathology:
• Level:
o thoracic spine most common
o Followed by lumbar then lastly the cervical as it has little epidural fat
o Epidural abscess tend to span over 2-3 levels; but may spans the whole spine
• Site:
o Dorsal abscess is the most common in thoracic, lumbar & following surgery
o Ventral abscess is the most common in cervical region & é discitis or osteomyelitis
• Severe necrosis, suppuration
Clinically: Triad Of Fever, Leukocytosis, ESR , Neurological Signs
• Early: Unexplainable Axial Pain + Fever
• 3d Later: Rapid Deterioration É RADICULAR PAIN, NEURAL DEFICIT, and MENINGEAL SIGNS
• Must be kept in mind when investigating a patient for spinal infection or tumour
Investigations:
• yyy ESR
• yy leukocytosis
DD
1. Other infection
2. Tumors
3. Epidural hematoma
4. Acute transverse myelitis
5. Meningitis
Treatment:
1- it is a medical & surgical EMERGENCY :
2- Immediate DECOMPRESSION: - laminectomy usually is sufficient as the lesion tend to be
thoracic and dorsal
3- Ventral cervical abscesses require anterior approach
4- Immediate empirical broad spectrum AB that cross the BBB
5- Stabilization + BG
Poor prognostic factors:
• rapidly progressing paralysis
• complete paralysis
• neurological deficits for > 36 hours
• immunocompromised, DM, elderly
Post-Operative Infections
Incidence:
• Discectomy ................................................... 0.5%
• fusion éout instrumentation ................... 2%
• fusion é instrumentation .......................... 5%
Post-op disciitis may be difficult to diagnose - keep in mind.
Clinical
• y Back pain not coinciding with the wound appearance
• May be considered as malingering or hysterical
• Tenderness, paravertebral spasm
• z SLR
• ± neurological signs
Investigations:
• y ESR ± normal leucocytes
• PXR & Tc are not conclusive
• MRI is of choice Æ BODEN TRIAD = z T1 / y T2 at disc / yyy T1 gadolinium or BM & disc
Treatment:
Prevention:
• Prophylactic antibiotic
• Delicate handling of the tissues
• Meticulous hemostasis
• Debridement of jeopardized tissues before closure
Active ttt:
1- Open the woun in toto
2- Debride the necrotic & pus
3- Irrigate with 8-10 L of Ringer’s
4- Remove the instrumentation
5- Closure é suction irrigation for 5 days
6- Dressing UGA is done after the 5 days
COMPARISON TABLE
Osteomyelits Discitis TB Tumour
Age adult child any any
Region lumbar lumbar thoracic lumbar
Site metaphysis end anterior posterior body
plate,disc body
Disc yes yes no no (except lymphoma &
involvement myeloma)
ESR high high high normal
WBC high N N N
Biopsy + - + +
Brucellosis
Ætiology:
Organism:
• Non motile, non spore forming, acid fact, gram –ve coccobacilli
• Route of infection ingestion of milk product of infected cattles
Pathology:
• Usually affect the spine, lumbar spine 15% of all brucella infection
• Granulomatous lesions with giant cell caseating lesions are present
• Spinal cord compromise occur in 12%
Clinically:
• Fever, anorexia, headache, malaise, night sweat
• Polyarthralgia
PXR:
• Step like spinal erosion at the anterior margin of the vertebra
• MRI show a picture like that of TB
Lab:
• Brucella titre: 1:80 or more
Treatment:
• AB: Deoxycyclin, Rifampicin, Vibramycin for 4 mo may be sufficient
• Surgery: is rarely indicated and if so it follows the rules for the pyogenic surgery
Fungal Infection
• Usually it is opportunistic infections that affect patients with bad general condition
• They are slow infections, less painful, é similar PXR and lab finding as pyogenic infection
• DD: TB & tumors
• Dx: is made absolutely by isolation of the organism by biopsy and direct cultivation
• Aspergillus:
o Is an opportunistic infection esp in cardiac and renal transplanted pt
o Spinal affection ......................... 65%
o ttt: amphotericin B ± surgery only if neurologic compression
• Cryptococcal infection:
o In leukemia & sarcoidosis
o ttt: Amphotericin B
• Candidiasis
• Actinomycosis
• Blastomycosis
• Coccidioidomycois
Echinococcus Granulosus
• 1-2% may affect the bone; é the spine being 50% of these cases
• Space occupying lesion that may enlarge Æ weaken the vertebra & collape
• CP: mainly pain, swelling, and deformity
• PXR: large lytic expanding lesion (like gct, or fibrous dysplasia)
• Dx: casoni test
• Ttt: mebendazole + surgery
614 | Page [Sp ers]
pine Disorde
P
Paediat
tric Spina
S al Deformi
D ities
Biomechanics
• Kyphossis= failure in 1 plane, Scoliosis=
S = failure in 3 planes (sa
agittal, rotattion & latera
al wedging
g)
• HEUTER-VOLKMANN LAW = Prressure on epiphysis z rate of growth; w whilst tension y the rate.
r
Thus thhe 'leadingg edge' of a deformitty grows morem rapidly than the e 'trailing edge'
e Æ y the
rate of progressioon.(eg. Scooliosis)
Scoliosis Classification (International Scoliosis Society):

1- Idiopathic: ...................................................... 65%
1- Infantile <3y: < ▪ Reg gressive ........ 85%
Pro ogressive ...... 15% (wo orst)
2- Juvenile 3-8y 3
3- Adolescen nt >8y
2- Conge enital: .................................................... 15%
o Posterior Failed F Form mation: we edge verteb bra, or Hemmivertebra
o Posterior Failed F Segm mentation: Unsegme ented Bar, Block
B verte
ebra, Unfussed Ribs
o Anterior Open: O spina a bifida / AnteriorA Clo
osed: Diasttomato-myyelia
3- Neuro omuscular ............................................ 10%
o Neuropath hic
UM MNL - CP, Sp pinocerebe ellar degen ord tumor,, cord trauma, other
neration, co
LMN NL- polio, trauma, t spinal muscu ular atroph
hy, myelommeningocoe ele
o Myopathic c - dystro ophies (Du uchenne, LGD, FSH HD), Arthrrogryphosiis, Congen nital
hypotonia a, myotonia a, myasthe enia
4- Neuro ofibromatossis (Kyphosscoliosis) ...... 5%
o +ve family y history, 5 cafè au lait patches, pachyderm matocoele,, pseudoarrthrosis
5- Otherss: ............................................................. 5%
1- Dysplasiass - Achond droplasia, SED, diastro ophic dwarrfism, MPS
2- Traumatic c Fracture//dislocation n, irradiatio
on, burns
3- Rheumato oid
4- Tumours
5- Metabolic c - Rickets, OI, O Marfans, homocyystenuria, Ehlers-Danl E los
6- Functiona al - postura al, leg lengtth, ms spassm, Hysteriical it not a structurall scoliosis:
Corrrect by lea aning forw ward or lying down
Coleman bloccks
Scoliiosis
Id
diopathic Conge
enital Neuromuscular
N Neurofibrom
matosis Otther
65% 15%
% 10% 5% 5
5%
oliosis
Kyphosco
Dyspplasia
Infa
antile <3 y JJuvenile Ad
dolescent F
Failed Form Failed seg Neuropatthic Myoopathic
Traum matic
Regre
essive 85% 3-8y >8 We
edge vertebra Unseg bar UMNL: CP
C Dystrrophies
Inflam
mmat
Progressive H
Hemi vertebra Block vertebra LMNL: Po
olio Arthro
ogryposis
ory RA
R
15%
Tumo ors
Meta abolic:
rickets
Congenital Scoliosis
• Congenital scoliosis is a developmental curvature of the spine ð vertebral anomalies
Classification:
[1]. Failure of Formation - Partial Unilat (wedge vertebra), Complete Unilateral (Hemivertebra)
[2]. Failure of Segmentation - Unilat (Unilat. unsegmented bar), Bilateral (Block vertebra)
[3]. Mixed
Assessment:
[1]. Severe spinal deformity
[2]. Overlying skin shows: angioma, tuft of hair, nevus, fat pad
[3]. Radiography: must be extensive to Dx the type of the malformation
a. PA, Lat, lateral bending, Risser Cortel, Ferguson, Stagnara
b. (MRI) or myelography should be performed to see if there are any associated
intraspinal anomalies. Should an anomaly, such as diastematomyelia, be discovered,
it should be resected before correction of the scoliotic curve.
Treatment (staged operation)
• Resection of the curve apex
• Anterior and posterior spinal fusion
ggggggbiiiiiii
NeuroMuscular Scoliosis
• Ætiology: as before
• Pathology:
[1]. long severe curve é convexity to the paralyzed side
[2]. Marked instability
[3]. In severe there is pelvic obliquity, sitting imbalance
[4]. Loss of sensibility
• PXR: in traction to assess the correctability
• Rx:
[1]. Mild: .......................................No ttt
[2]. Moderate: ............................as idiopathic
[3]. Severe: ..................................anterior and posterior fusion
ggggggbiiiiiii
Scoliosis in Neurofibromatosis
• CP:
[1]. +ve family history
[2]. >2 Skin multiple neurofibromatosis
[3]. >6 Café au lait patches
[4]. Optic glioma
[5]. Iris lisch nodules on slit lamp
[6]. Pseudoarthrosis
[7]. Scoliosis ................................(30%)
Short sharp curve
Mild to severe in degree
• Rx:
[1]. Mild: .......................................as idiopathic
[2]. Moderate: ............................Combined anterior and posterior fusion
Idiopathic Scoliosis
Aetiologic theories:
1]. ENDOCRINE THEORY: Patients é idiopathic scoliosis often taller é high SOMATOMEDIN levels
2]. EQUILIBRIUM THEORY- Abnormalities in the VESTIBULAR system, Scoliosis was induced in rats by
destruction of brain stem
3]. NEUROTRANSMITTER: removal of pineal gland in chickens Æ SCL
st
4]. GENETICS: multifactorial mode of inheritance (y é 1 degree relatives having scoliosis)
Epidemiology:
• Overall prevalence is 25:1000
• Small curves are more common
• RIGHT-sided prevalence ð spine asymmetry probably ð descending aorta on left
• Increased incidence in GIRLS explained by normal flattening of thoracic kyphosis at age 12,
which corresponds to female growth spurt
Pathogenesis
• LORDOSIS may be the initiator of deformity as it shifts the normal axis of rotation backward.
• Pt tend to flex the trunk to correct the deformity, and this causes ROTATION of lordotic
section é convexity to one side (usually rt). Vertebral changes occur after the rotation
• SPINOUS PROCESS rotate to concavity & the RIB HUMP to convexity
• At first the deformity is correctable then as it exceeds the limit of stability spine buckle &
rotate into a fixed position. Usually this is accompanied by appearance of a 2ry
compensatory curve ώ is less marked and easily correctable for a while. The process
deformity continue to y é a rate that may reach 1º/y (if the curve >50º); & z at maturity
Pathology
1]. IV DISC: z GAG & y collagen content
2]. BODY: concave side are hypoplastic & convex side hypertrophied (Heuter Volkmann law)
3]. Paravertebral MUSCULATURE- Diff ms fibres on either side of curve
4]. LIGAMENTS and tendons: PLL is thickened
5]. CURVE PATTERNS
Curve Region Start End Apex Prevalence

• Rt Dorsal Dorsal D5 L1 D9 85%
• Lt Lumbar lumbar D12 L4 L2
• Rt Dorsolumbar both D9 L2 D12
• Double major Rt dorsal Lt lumbar
• Double dorsal major Lt upper Rt lower
Classifications:
• Classified according to time of onset (old SRS)
1- Infantile- < 3y
2- Juvenile – 3-8y
3- Adolescent – 8-20y
• According to curve pattern
King Moe Classification: see

later
Assessment
Diagnosis holds 4 parameters:
1. ÆTIOLOGY
2. REGION
3. Convexity towards which SIDE
4. COMPENSATED or not
Complaint:
1- Usually progressive deformity
2- Pain is an unusual symptom and must rule out other causes
3- Neurological or cardiopulmonary complications
General examination:
1- Cardiopulmonary status
2- Skin: café au lait patches
3- Associated congenital malformation: CVS, CNS, GUS
4- Delayed 2ry sexual characters + family history of late menarche (both z the progression)
5- LL examination:
o LLD correctable or not COLEMAN TEST
o Pelvic obliquity corrected or not PILLOW TEST
Local examination
• Complete trunk exposure: and the pt is examined from back, forward, and sides
1- Assess the CURVE region & convexity e.g rt dorsal curve & rib hump
2- Assess if it is COMPENSATED or not:
[1]. PLUMB LINE form C7 vertically down

• and note its distance to the natal cleft
[2]. Shoulder level
[3]. Scapular level
[4]. Arm Torso Distance
[5]. Asymmetrical loin creases
3- Assess CORRECTABILITY:
1- Lean forward Æ z or y the rib hump (ADAM’S TEST)
2- Traction
3- Lt & Rt bending
4- Assess pelvic OBLIQUITY:

1- Block test of COLEMAN
2- PILLOW test: pt is seated on a pillow over the lower pelvis only and see if it corrects
5- NEUROLOGICAL examination is essential
6- ROM
Radiological
1- View:
[1]. First: PELVIS AP & LT WRIST to assess the skeletal maturity
[2]. PA (zradiation to breast & ovary): Supine , standing , Rt & lt bending , in traction
[3]. LATERAL: supine and standing (flexion, extension)
[4]. STAGNARA DEROTATION VIEW: cassette lie // to medial aspect of the rib hump & ! beam ⊥
[5]. FERGUSON VIEW, which is taken perpendicular to the plane of the L5/S1 disc, is used to
look for abnormalities at the lumbosacral junction
2- Changes: Ætiology, Dx of curve, Describe, Complication
[1]. Congenital malformation, dysplasia, tumor, …etc
[2]. Bodies, pedicles & discs narrow to concavity.
[3]. Curve side, region, & Rotation
[4]. End vertebra most tilted
[5]. Apical vertebra ...... at centre of curve
[6]. Stable vertebra ....... bisected by mid-sacral line
[7]. Neutral Vertebra .... see both pedicles equally
[8]. Compensatory changes: e.g. pelvic obliquity
[9]. Completely correctable by bending or not
3- Measurements:
I. COBB ANGLE:
• Line drawn along upper end plate of upper end vertebra and lower end plate of lower end
vertebra. Perpendiculars drawn from these lines. Angle of intersection measured.
• For double curve, one vertebra is lower end vertebra for upper curve and upper end
vertebra for lower curve (transitional curve). Only one line drawn on this vertebra.
• Future, measurement should always be from same vertebrae.
• True size of curve can be measured by Stagnara derotation views that measure both lat
curves of scoliosis & sagittal curves of kyphosis for more accurate figures and isolation of a
particular curve
II. MEHTA RIB-VERTEBRAL ANGLE DIFFERENCE (RVAD):

• Is the difference bet the angle formed by a vertical
line through the apical vertebra & rib lines on either
side
• RVAD > 20º or overlap of the head of the rib over
the vertebra = progressive infantile Æ will y
III. RISSER'S staging - Indicates skeletal maturity and

physiological age. Based on ossification of the iliac
crest apophysis & graded 0-5 from anterior to
posterior. The iliac crest is divided into quarters &
ossification graded according to the number of
quarters with ossified apophysis (from ant to post),
with Stage 5 = fusion of the ossified apophysis.
IV. Moe Method - measures the apical vertebra rotation:

• Draw the Dattum line and divide the area from it to the lateral
border into 3 zones; and grades are according to the position of the
convex side pedicles in relation to these zones:
o Grade I: slight asymmetry but still in zone 1
o Grade II: convex side pedicle entered the 2nd zone
o Grade III: entered the middle zone
o Grade IV: passed the Dattum line
• Traction radiographs é RISSER-COTREL frame are used to assess torso
balance and pelvic leveling, which decides between a one-stage
PSF or 2-stage APSF approach for neuromuscular scoliosis
• ISIS (intergrated shape imaging system) true 3d computerized
image of the spine provide true sagittal profile é no need for
multiple PXR
Other investigations:
• A painful functional scoliosis Æ Tc to exclude tumour or infection
• Pulmonary function test before the operation
• MRI - If intraspinal pathology suspected; e.g. Left-sided, Male, Painful, Rapidly progressive,
Neurological abnormality.
• 20% of right curves have pathology, 80% of left curves have pathology
Progression
• Progression is defined as: > 5º of change on 2 sequential x-rays. Not all curves progress. The
larger the curve at presentation the more likely it is to progress.
• Risk Factors for progression:
1- Female: Incidence is relatively equal; but larger curves are more common in ♀
2- Young age at Diagnosis: < 12y has 3 x greater chance for progression
3- Single thoracic curve
4- Sexually immature (premenarche)
5- Skeletally immature - Risser 3-5 < 20% Risser < 2 ≈ 50% /
6- Nash & Moe ...................................................... GIII, GIV
7- Cobb angle ........................................................ > 50o
8- Mehta RVAD .................................................... > 30o
9- Lonstein Progression factor ............................ > 1.5
Lonstein progression factor [Pf]

• Pf = (Cobbº - 3 x Risser) / chronological age
• Pf 1 = 25% risk / Pf 1.5 = 50% risk / Pf 2 = 75% risk / Pf 2.5 = 100% risk
• Growth potential evaluated by a number of factors- Historical, Age, Menarche, Growth spurt
(outgrowing shoes and clothes), Height, Tanner's sign (breasts and pubic hair), Risser stage,
Hand (Gruber & Pyle)
• Risk factors in thoracic curves = Vertebral rotation (RVAD > 30º, apical rotation > 30º)
• Risk factors in lumbar spine = Vertebral rotation, Direction of curve (right), Position of L5
(not below intercrest line)
• 70% of curves progress after skeletal maturity & progress an average of 20º
• Curves < 30º Æ not progress
• Curves 50º-75º Æ progress; esp. thoracic curves by a rate of 1º/y
Classification - King-Moe
• Type I - lumbar dominant (10%) - S-curve, Both thoracic > lumbar curves cross midline
• Type II - thoracic dominant (33%) - S-curve, Both thoracic > lumbar curves cross midline
• Type III - thoracic (33%) - Thoracic curve, Lumbar curve does not cross midline
• Type IV - long thoracic (10%) - Long thoracic curve, L5 over sacrum, L4 tilted into curve
• Type V - double thoracic (10%) - Double thoracic curve, T1 tilted into upper curve
Treatment
Depends on
1- Cobb angle
2- Growth potential:
o Premenarche (girls) and axillary hair (boys) = ....... Rapid growth
o Risser 2 = ................................................................ Rapid growth
Curve Rapid growth Decreased growth Adult

>40o brace Observation Observation
40-60o surgical Surgical or observation Observation
>60º surgical Surgical Observation
Non-surgical treatment If documented progression

• MILWAUKEE (CTLSO) if apex above T8: Provides Availability of the brace
Compliance of pt
passive correction by pressure on convex side and Young Female
active correction by muscle contraction pulling body
away from pads.
• BOSTON (TLSO) if apex of curve below T8
• Brace worn 23 hours a day. Allowed out to play sport. Patient then seen every 3-6 months till
maturity if curve progresses > 45º Æ surgery indicated.
Surgical treatment
Rationale & Goals
1- CORRECT the deformity (the rotation and the rib hump)
2- Prevent RESPIRATORY insufficiency
3- RIGID FUSION OF STRUCTURAL CURVE only and not compensatory curve (é bending films)
4- Avoid fusion < the measured curve and usually more
5- Avoid fusion to L5 (L4 or sacrum)
6- Avoid fusion above T1
7- Fuse down to NEUTRAL STABLE VERTEBRA
8- Fuse LEVEL ABOVE & LEVEL BELOW measured curve
Plan: Anterior or posterior:
• If correctable (é Risser Cortel) < 50% Æ ANT RELEASE Æ fusion + BG
• If correctable > 50% Æ POST FUSION direct, and be ware of the crankshaft phenomenon
• Costoplasty: may be done for correction of rib hump
Level of Fusion
Treatment according to king Moe classification
King I Fuse both curves to lower vert No lower than L4
King II Selectively fuse thoracic curve only Lower level at stable vert (rather than neutral)
King III Fuse measured thoracic curve Lower level at first stable vertebra
King IV As for king III Usually stop at L4
King V Fuse both thoracic curves Lower level at stable vertebra
Instrumentation:
• Posterior: Complete excision of facet + laminae + transverse processes + BG
• Harrington rod and hook: No longer used
• Winsconsin: instrumentation wires passed through spinous processes. No longer used
• Luque and sublaminar wires: rigid & control some rotation but wires endanger the dura
• Cotrel-Dubousset:
o 2 Rods & multihooks (1rod on convex for compression, 1 on concave for distraction)
o Initial distraction and subsequent rotation.
o Rods cross-linked with transverse linkage bars Æ Rigid fixation so no TLSO needed
o Technically more difficult & very expensive.
• Anterior: release of rigid anterior structures as ALL, disc, PLL then fuse
1- Indications – rigid thoraco-lumbar curve in young pt to avoid CRANKSHAFT PHENOMENON
(posterior fusion Æ y lordosis)
2- Advantages - Less levels instrumented & Better rotational correction
3- Instrumentation - Dwyer system Æ now Zielke system
Early complications
1- Neurological injury during surgery 1% (use intraoperative SEP)
2- Blood loss Æ Hypotensive anaesthesia, Autotransfusion
3- Wound infection - Prophylactic antibiotics indicated
4- Pneumothorax in anterior approach
5- Dural tear - During ligamentum flavum removal or hook or wire insertion
6- Inadvertent 'flat-back' alignment
7- Incorrect fusion levels
8- Inappropriate ADH secretion
Late complications
1- Pseudarthrosis ~ 1-5% with fusion to sacrum. Solid fusion should occur by 6 months
2- Rod or wire breakage - Due to pseudarthrosis or fatigue failure.
3- Back pain - Appears to be due to Fusion below L4 , Loss of lumbar lordosis
Juvenile Idiopathic Scoliosis

• Worse prognosis than the adolescent
• Usually progress
• ttt: brace till 10y then surgery
Infantile Idiopathic Scoliosis
• ♂ left thoracic curve
• 85% regressive
• 15% progressive (worst prognosis): RVDA > 20º & cardiopulmonary complication
• ttt: serial EDF POP (elongation derotation flexion) if progressive (15%) Anterior Zielke
Kyphosis
Ætiology:
1- Postural:
o 2ry to flat foot or 2ry to exaggerated lumbar lordosis
o Disappear é back stretch + shoulder retraction
2- Scheuermann’s disease
3- Congenital
o Defect of segmentation
o Defect of formation
o Mixed é rotary instability
4- Skeletal dysplasias
o Achondroplasia
o Mucopolysaccharidoses
o Other
5- Neuromuscular
6- Myelomeningocele
7- Posttraumatic
o Acute
o Congenital
8- Postsurgical.
o Postlaminectomy
o Following excision of vertebral body
9- Postirradiation
10- Inflammatory
11- Collagen disease: e.g Ankylosing spondylitis
12- Tumor
13- Metabolic
o Osteoporosis Dowager’s Hump
o Osteogenesis imperfecta
o Other
Normal regional alignment:

1- Cervical ....................... -30º
2- Thoracic ...................... 45º
3- Lumbar ........................ -60º
SVA (sagittal vertical axis)

1- Axis from centre of C7 body vertically downward Æ posterior to L5 disc
2- Most children stand in slight –ve balance
[Sp
pine Disord
ders] Page | 623
C nital Kyphos
Congen K sis
• Deformity
D IS characteerized by severe
s angular deform
mity with a promineent gibbus at the apex of
t curve;
the
Ætiology
• DEFECT OF FORMATION (TYPE 1): -failure of formation
f of
o the anteerior elemennts:
o The worst proggnosis
o Sequuelae: - paraplegia
p a commonly results if untreatted; & com mpression of viscerra; -
impaairment of pulmonaryy function; - poor sittting posturee;
• DEFECT OF SEGMENTATION (TYPE 2):
o Slighhtly better prognosis;; - producees a more ro
ounded kypphotic shappe
o Defoormity proggresses moore slowly and parapllegia is unccommon;
Treatment
1- Poster
rior Fusioon: - in children
c <5 yrs witth curves <55 deg, only an situ posteerior
arthroddesis is reequired sinnce some spontaneo ous correcttion of kyyphosis wiill occur with w
continuued growthh; - posteriior fusion may
m have wider
w indiccations witth kyphosiss due to faiilure
of segmmentation (as opposeed to failurre of formation); - poosterior kyyphectomy & arthroddesis
involve meticuloous care off tissues; - resectionn of the noon-functionning cord at a apex off the
deform
mity; - water-tight duural closuree, with care being takken not to occlude teerminal ennd of
normaal spinal coord at site of transecttion of corrd; - bivalvve total-coontact ortho
osis is useed to
supporrt trunk unttil fusion iss solid;
2- Anteriior & Possterior Fu usion: - combined anterior
a & posterior fusion is indicatedd for
childreen >5 yearrs, curves > 55 deg, and
a neurolo ogical deficcits;
Sheuermann’s Disease
Definition = Spontaneous Wedging of 3 adjacent vertebrae of at least 5 degrees.
Atiology: Unknown; although
1. Strong HEREDITARY tendency (may be AD)
2. OSTEOCHONDRITIS of the end plate Apophysis is claimed as an ætiology
3. Primary COLLAGEN DISORDER theory
4. ABNORMAL ENDOCHONDRAL OSSIFICATION
5. Growth deficiency ð mechanical stresses on the anterior column
Epidemiology:
• Most common cause of structural kyphosis of thoracic & thoracolumbar spine
• Skeletally immature ♂
Pathology:
• Most commonly affect the thoracic spine
• Weakness of upper and lower end plates occur Æ with activity IVD are compressed against the
weak end plates Æ vertebral collapse Æ wedging with anterior marginal detachments
• 3 Forms:
1- Thoracic type .................... apex T7-9 (commonest)
2- Thoracolumbar type ....... apex T10-L1
3- Athletic lumbar hypolordosis
• Associated pathologies:
o Spondylolysis: y lordosis strains L5 pars interarticularis
o Scoliosis: ............................ 25%
Clinical Findings:
• Teenage male +ve family history
• Deformity:
1- Progressive till the maturity
2- Rigid: doesn't reverse with hyperextension
3- Rounded thoracic kyphosis
4- Compensatory lumbar lordosis is common & Scoliosis may occur
5- Shoulders are prominent
• Backaches:
o lower lumbar ms sprain (é progressive compensatory lordosis)
o Facetal dysfunction 2ry to chronic lordosis
o Scheuermann’s disease of the lumbar spine itself is painful
o May occur over the apex of kyphosis
• Neurologic manifestations rarely ð Scheuermann’s but 2ry to:
o UMN paresis ..................... by NPH or compression #
o zSLR ð spastic hamstring (+ve Tripod, popliteal angle)
• Thoracic Scheurman's is not usually painful, lumbar Scheurman's is often symptomatic
PXR: SORENSON CRITERIA
a. Thoracic kyphosis ........................ >40º (25º-40º being normal)
b. Thoracolumbar kyphosis ............ > 30 deg (thoracolumbar spine is normally straight)
c. Wedging ........................................ >5º of 3 adjacent vertebrae (clefting & striations are normal)
d. Irregular end plates ...................... (normally in children are straight)
e. Loss of disc space height
• Schmorl’s nodes are constant finding that reflect high pressures at the disc end plate interface
• Angel is measured in the Lateral view (≠ scoliosis)
DD:
• Postural kyphosis: painless, correctable, no PXR changes
• Discitic & OM: severe pain, PXR show erosions, soft tissue mass
• SED: affection of the whole body joints
Non Operative Treatment:

• <60º adolescent the ttt is follow up
• 60-75º bracing (CTLSO) if correctable or hyperextension cast if fixed, for 1-2 y
• pain usually subsides at end of growth unless deformity is severe;
Operative Treatment:
Indications:
1. Thoracic kyphosis ........................ >75º
2. Rigid kyphosis ............................. > 55º
3. persistent back pain that is unresponsive to non operative treatment;
Technique
• Anterior release (leave the PLL intact) + interbody fusion ⎯⎯⎯⎯ ⎯→ PSF é compression
Followed by
instrumentation (in the same setting)

• Cortel-Dubousett is the system of choice
Post-Laminectomy Kyphosis
• Occur when multiply level laminectomy is performed in children
Predisposing factors:
• Young age
• Cervical and upper thoracic laminectomy
Mechanism:
• Lack of posterior support
• Abnormal anterior compressive forces
• Hypermobility of the segment
Prevention:
• Avoid facetectomy
• Surgical fusion by BG or instrumental would prevent kyphosis
• Postoperative bracing
• Laminaplasty: is a technique could be used in children to avoid laminectomy, in ώ the
lamina is removed in toto then replaced and fixed inplace
Active ttt:
• Cervical ........................................... Anterior interbody fusion
• Thoracic .......................................... Anterior release & fusion Æ posterior fusion
• Postoperative bracing
CERVICAL SPINE DISORDERS
Torticollis
Definition:
• It is the head (up) tilt and rotation to one side at or shortly after birth
CONGENITAL
1. Congenital Muscular Torticollis (see below)
2. Odontoid hypoplasia
3. Klippel -Feil syndrome
ACQUIRED:
1- Osseus,
Trauma - Atlantoaxial rotary instability
o
Infections
o
tuberculosis
pyogenic infections
Grisel's syndrome - follows upper respiratory tract infection
o Tumours
Osteoid osteoma
o Inflammatory
ankylosing spondylitis
Rheumatoid arthritis
2- Non-osseus
Neck burn contractures
traumatic: Prolapsed disc
Infections: retropharyngeal abscess
Tumours: intraspinal or intracranial - posterior fossa e.g medulloblastomas
ocular - with a superior oblique muscle paresis Æ compensatory head tilt
1-Congenital Muscular Torticollis

Pathology:
• the sternomastoid on one side is fibrous & fails to elongate Æ progressive deformity
• Head tilt towards the ms affected & chin rotate to the other side
Aetiology: unknown
1. may be due to ISCHAEMIA of the muscle from a distorted position in-utero
2. Local COMPRESSION on the soft tissue of the neck Æ fibrosis of the sternomastoid
• associated with:
o Breech
o DDH
o Difficult labour
Clinical
1- lump may be noticed in first few weeks of life
2- TORTICOLLIS & z ROM
3- sternomastoid feels TIGHT &hard
4- ASYMMETRICAL FACIAL DEVELOPMENT
5- DDH may be associated
PXR
• To exclude other pathology but here it is usually negative
• Hip PXR & US Æ DDH
Treatment
1- Start by STRETCHING excercises & physiotherapy
2- After 1 year:
o Z PLASTY of the sternal end ± division at upper end as well
o immobilise with a collar
o then stretching exercises
2-Odontoid Hypoplasia
Pathology:
• Types:
1- Aplasia
2- Hypoplasia
3- Os Odontoidium: unfused ossicle odontoid tip may confuse é # but sclerotic border
4- Ossiculum terminale (unfused odontoid tip eventually may separate & fuse é C1
• Complication: predisposes to atlantoaxial instability
Clinically:
• discovered INCIDENTALLY usually
• NEUROLOGICAL deficits as cervical disc
• TORTICOLLIS
Associated with:
• Morquio's Disease –
• Down's Syndrome
• Klipple Feil $
• SED
Treatment
• C1-C2 FUSION advised if marked discomfort or neurological symptoms
3-Klippel-Feil Syndrome
PTERYGIUM COLLI
HALLMARKS
I. Short neck
II. Low posterior hair line
III. z neck ROM (fusion of at least two cervical segments)
Etiology is unknown.
• It is a failure of the normal segmentation of cervical during the 3rd & 6th wks of gestation.
Pathology:
• Vertebrae are fused and may encroach on the canal or root Æ neurological symptoms
• CLASSIFICATION:
1]. Type I: C2-C3 fusion with occipitalization of the atlas
2]. Type II: Long fusion below C2
3]. Type III: Single open space between two fused segments
• ASSOCIATED ANOMALIES:
1]. Springle deformity,
2]. Cervical rib & disrafism
3]. Diastematomyelia & syringomyelia
4]. ARNOLD CHIARI I malformation
5]. Cleft palate, Syndactyly, supernumerary digits
6]. VSD, renal, respiratory
CLINICAL FINDINGS:
TRIAD of …
1]. TORTICOLLIS: flexion and extension are better than bending and rotation.
2]. NECK WEBBING (Prominent trapezius)
3]. LOW ANTERIOR HAIR LINE
PL US …
1]. Compensatory HYPERMOBILE at the unfused segments Æ instability and pain
2]. NEUROLOGIC: Root irritation & cord compression may reach paraplegia & death
3]. FACIAL ASYMMETRY.
4]. FACIAL N PALSY
5]. ABDUCENT PALSY (lateral rectus palsy) ± Ptosis of the eye
RADIOGRAPHIC FINDINGS:
1- Flat fused vertebrae
2- hemivertebrae or block vertebrae
3- Intersegment instability
4- WASP-WAIST SIGN- indentation at the site of open space between the fused vertebrae.
MRI access cord compression along with cord anomalies.
TREATMENT:
• Minimally involved patients lead normal lives with only minor restrictions.
• Avoid contact sports that place neck at risk.
1. Cervical COLLAR, NSAIDS, ± traction
2. Posterior FUSION of the irritation segment of root or cord ± Decompression if stenosis
3. Dislocations and basilar invagination Æ traction Æ posterior fusion.
4- Basilar Impression
• It is the malposition of the odontoid being more cephalad than normal
Pathology
• When occur it compresses:
1- Cord
2- Vertebral a
3- CSF flow
4- Cranial Nerve
• It may confuse with:
1- Posterior fossa tumor
2- Polio bulbar palsy
Ætiology:
• Associated é:
1- KLIPPLE FEIL
2- ARNOLD CHIARI $
Odontoid malformation
3-
Bifid posterior atlas arch
4-
• May be 2ry to:
1- OI III, IV
2- RA, Ank Sp, Paget’s
3- NF
4- Osteomalacia, Rickets
Clinically:
1- Pure UMNL
2- In ARNOLD CHIARI $: Dizziness, ataxia, nystagmus
3- Cranial N. affection (CN that come out form the f.magnum); 5, 9, 10, 11
4- Vertebral artery: dizziness & syncopal attacks
PXR
White Criteria of basilar invagination on PXR cervical lateral view:
1- Padi (Posterior Atlanto-Dental Interval) ..................................<13mm = BI
2- AADI (Anterior Atlanto-Dental Interval) ................................>4mm = BI
3- DBI (Dens-Basion Interval) ...........................................................<4mm = BI
4- WACKENHEIM'S clivus tangent line ............................................should tangent the dens not cut it
5- CHAMBERLAIN'S line from f.magnum to hard palate .........<3mm cut to dens
6- MCGREGOR'S line from occiput to hard palate .....................<5mm cutting to dens
7- MCRAE'S line bet basion & foramen magnum ....................dens should never pass it
8- RANAWAT'S from C2 pedicle to transverse plane of C1 ....15-17mm
9- REDLUND-JOHNELL from axis base to McGregor's line .......29-34mm
10- FISCHGOLD & METZGER digastric line in AP at lower edge of mastoid Æ should be tangent to dens
11- POWERS Ratio: ....................................................................................>1 anterior translarion / < 0.55 post
Treatment:
1. Splintage ⎯⎯ ⎯→ hard collar ⎯ ⎯ ⎯ ⎯ ⎯
Wear
⎯ → Traction ⎯⎯⎯→ surgery
If Cranial Settling IfFail
2. Cervical fusion: C0-C2 by Wires, Luque, BG, Plates, Screws

5- Occipitalization of the Atlas

• refers to failure of segmentation between occipital and spinal sclerotome that ranges
between synostosis to syndesmosis
Pathology:
• Axis and occiput are fused together Æ y mobility at the atlanto-axial joint
• Normally movement at C0-1 is flexion extension & at C1-2 is rotation mainly
• When occipitalization occur Æ C1-2 show y abnormal motion Æ degeneration and
instability and pain
• Basilar invagination may occur
• Associated condition:
1- C2-3 fusion
2- Kyphosis & scoliosis
3- C1-2 instability
4- Cervical rib, cleft palate,
Clinically:
• As the abnormal motion segment starts to develop OA & basilar impression
• NEUROLOGICAL symptom ð basilar impression, or irritation of the cord
1- Anteriorly: Æ pyramidal tract
2- Posteriorly: Æ lemniscus system
3- Basilar: Æ nystagmus, vertigo, cranial nerve
• TORTICOLLIS
Radiological:
• PADI <13mm
• MCRAE line
• CT is the best as it shows the coalition segment at C0-1
Treatment:
1- Minor symptoms: Æ conservative
2- Major symptoms:
o Anterior: traction then fusion
o Posterior: Æ MRI and according to the tethering structure
Suboccipital craniotomy ± fusion
Excision of atlas arch ± fusion
6- Atlanto-Axial Rotary Instability

• refers to loss of ligamentous stability between atlas and axis, occurs most often in older
children and adolescents
Pathology: unknown
• The basic pathology is dysfunction of transverse ligament or the one of the alar ligaments
either ð trauma or spontaneous
• This leads to instability at C1-2 Æ Rotation + lateral tilt of the neck Æ compression of the
cord + vertebro-basilar insufficiency
• approx 50 % of cervical rotation takes place between atlas and axis, slightly anterior dens
Æ lateral wall of atlas when rotates it encroach the canal Æ physiologically z canal
diameter
• Spinal canal of the atlas is large compared with that of other segments,
• STEELE'S RULE OF THIRDS: - canal of atlas is about 3 cm in its AP diameter; - spinal cord,
odontoid process, and free space for cord are each about 1 cm in diameter
• CLASSIFICATION:
1- AARI
2- AARI with anterior shift of C1 < 5mm
3- AARI with anterior shift of C1 > 5mm
4- AARI with posterior shift
• ASSOCIATED CONDITIONS
1- Grisel's &: - AARI after torticollis ð pharyngeal infection & hyperemia Æ demi-
neralization of attachment of transverse lig to ant arch of atlas, é subsequent
rotary subluxation of atlas on axis or anterior atlantoaxial subluxation
2- Morquio syndrome
3- Down syndrome (25% of patients)
4- Klippel Feil
5- SED, Achondroplasia, Larsen's syndrome
6- Rheumatiod Arthritis (adults)
Clinically:
1- Torticollis “COCK ROBIN” poition:
oHead tilt to one side and rotate to the other
oSternomastoid of the long side is spastic
oNeck is slightly flexed
2- Occipital neuralgia
3- Occasionally vertebrobasilar artery insufficiency
Radiographs: Lateral View in flexion
• ADI < 3.5mm ........... transverse ligament is intact
• ADI 3-5mm .............. transverse ligament is insufficient = type II injury
• ADI > 5mm .............. failure of the alar ligaments = type III rotatory subluxation
AP open mouth view
• Asymmetrical distance between both facets and the dens
• Cine radiography is a dynamic roentographic imaging technique
Treatment:
1- <1wk ...................... soft collar, NSAIDs
2- >1wk ...................... Halter
3- If failed reduction C1-2 fusion
Diastomatomyelia
•Fibrous, cartilagenous or bony bar creating a longitudinal cleft in the spinal cord.
•usually in lumbar spine
•can cause tethering of the cord with neurological deficits
•X-rays: widened interpedicular distance
•MRI makes the diagnosis
Treatment:
No spinal deformity or neurology ............ observe
Spinal deformity ± neurology ..................... resect bar before correcting deformity.
Sacral Agenesis
• = partial or complete abscence of the sacrum & lower lumbar spine.
• associated with maternal Diabetes
• accompanied with GI, GU & cardiac abnormalities
Clinically:
• prominant lower lumbar spine & atrophic legs; sit in 'Buddha' position
• motor deficit below level of agenesis; sensory spared
Treatment:
• amputation or spinal-pelvic fusion.
Arnold Chiari Malformation

Description:
• Protrusion of the inferior poles of cerebellum + medulla oblongata through foramen
magnum into the spinal canal, without displacing the lower brain stem.
Aetiology:
• Deformity Of Occipital Bone & Upper Cervical Spine.
• ± stenosis of the aqueduct of Sylvius Æ hydrocephalus Æ atrophy of the brain tissue.
Clinical
1]. Hydrocephalus ± Mental dullness
2]. Spina bifida and meningomyelocele
3]. Headache, vomiting
4]. Visual disturbances, diplopia
5]. Paralysis of extremities
6]. Cerebellar ataxia
Chiari's classification:
• Type I: ............................................................. herniation of cerebellum-tonsils
• Type ii: ............................................................ herniation of vermis and pons + dilated 4th ventricle.
• Type iii: ........................................................... high cervical hernia containing cerebellum-tissue.
• Type iv: ........................................................... hypoplasia of cerebellum ± encephalocele.
Spine Tumors
Benign Tumors
Incidence
• They are the 2nd most common cause of pain
• Night pain is exclusively suggestive of osteoid osteoma (OsOs) & osteoblastoma (OB)
• Usually ............................................................ 3rd decade
• Sacral tumors occur in adults; if occur in child it is mostly malignant
Pathology
• Types:
1- Most common ................................ GCT
2- OsOs .................................................. 50%
3- OB
4- Hemangioma
5- Osteochondroma
6- ABC
7- EG
• Sites:
o GCT, Hemangioma, Osteochondroma, ABC, EG in the body
o OsOs & OB ....................................... in the arch
• Classification
o Latent ................................................ Osteochondroma & Hemangioma Æ no ttt
o Active ................................................ OsOs, ABC, EG
o Aggressive ....................................... GCT, OB
Diagnosis
Symptoms
1- Pain:
o y night
o Radicular pain may occur ........... OsOs & OB
o Dull aching pain ............................. GCT, ABC, H, EG
2- Painful scoliosis
3- Myelopathic symptoms ............................ more in thoracic and cervical vertebral tumors
Signs
1- Myelopathic signs: as in cervical …
2- Decompensate curve usually
3- z ROM
PXR
• No rotation (≠ idiopathic)
• No wedging (≠ idiopathic)
• OsOs & OB .................................................... sclerotic pedicle & usually found in the concave side.
And usually interpreted as –ve PXR
• GCT & ABC ................................................... Lytic lesion
• Hemangioma ............................................... vertical striation
• EG .................................................................... Vertebra plana
Tc
• Of choice in painful scoliosis ................... mostly OsOs, OB; Tc scan is very sensitive to them
• False –ve in ................................................... hemangioma
CT
• To detect the bony extent
• CT myelogram may be very beneficial in some cases of cord compression
MRI
• To detect soft tissue shadow and involvement
• Sometimes surrounding edema may be marked to over estimate the tumor size
Treatment
1- Marginal excision for latent, active, or cases é neurological compression
2- Wide excision ............................................... for Grade III aggressive tr:
o Avoid complete laminectomy
o Partial laminectomy
o <50% of the facet to be removed
o If complete laminectomy ............ posterolateral fusion & BG is performed
o Complete facetectomy ................. posterolateral fusion & BG
o Total segmental resection .......... posterolateral fusion & BG + Anterior structural BG
3- Adjuvant ....................................................... Cryotherapy is preferred than, PMMA, or radiation
4- Stabilization + fusion ................................. is necessary esp. after complete laminectomy in
Cx&Thx
5- Orthosis postop. ......................................... Is mandatory as well
6- Reconstruction :
I. Autograft ......................................... Iliac & fibula
II. Allograft
III. Composite ....................................... Hollow titanium cages + BG
Precautions
1- Vertebral a in cervical spine
2- Approach in thorax should be anterior approach not via limited costotransversectomy
3- Sacrum is very vascular and embedded in a dense venous plexus Æ profuse bleeding
4- Sacrum is in close contact to bladder and rectal innervation
5- If dura is adherent to a tumor ................ excise the stuck part and then graft it
Complications::
1- Kyphosis especially after laminectomy in cervical and thoracic
2- Wound problems:
I. Infection: leave a drain, meticulous closure
II. Wound dehiscence
Radiation::
• Role of radiation is mainly in ABC & hemangioma
• ABC .................................................................. 30Gy
• Hemangioma ............................................... 40Gy
• GCT may be sensitive but its use must be limited to:
I. Complicated cases
II. Unresectable
• Complications:
o Scoliosis ............................................ 30%
o Late sarcomatous change ........... after several years
Malignant Tumors
Incidence
• More common in adults
• Metastatic carcinoma is the majority
• Spine metastasis .......................................... 50% of all bone metastasis
Pathology
• Site:
o 75% .................................................... in thoracic
o 75% .................................................... in body
• Secondaries ................................................... is the majority
o Breast, Lung
o Prostate, renal
o GIT, Lymphoma
o Thyroid
• Primary sarcoma ......................................... Less common
o Multiple Myeloma ......................... is the commonest primary
o Chordoma ....................................... in the sacrum
o Osteosarcoma ................................ less common
Diagnosis
Clinically
1- Pain:
o Relentless pain
o Awakening pain
o Night pain
o Radicular pain may occur
o Dull aching pain
2- Myelopathic manifestation ..................... 20%
3- Survival .......................................................... <1y
PXR
• Unfortunately > 50% of the body must be destroyed before the tr being visible
• Osteoporosis may harden the job more
• Unilateral absent pedicle ......................... Awl eye appearance
• Usually confined to 1 vertebra ............... respect the disc
MRI
• Detect spinal canal compromise
• Detect paraspinal extension
• Less helpful incase of pathological # ... yy surrounding edema & confusion
CT
• May be more helpful in case of pathological #
• For CT guided biopsy
Staging investigations
Preoperative investigations
Treatment
• Unfortunately surgery is not the line of choice in ttt of spine malignancy
• Contraindications to surgery:
1- Secondary tumors
2- Multiple Myeloma
3- <2mo survival is expected after surgery
4- Bad general condition
• Other modalities:
1- Radiotherapy
2- Chemotherapy
3- Hormonal therapy
4- Angiographic embolization for thyroid and renal secondaries (very vascular)
• Indications for surgery:
1- Pathological #
2- Neurological compromise é radioresistance
3- Painful kyphosis
• Rational of surgery:
1- ttt of complications
2- regain pt to fair functional status
3- Remove as much tumor as could be
4- Restore stability
5- Improve the quality of remaining life
6- Laminectomy is abandoned
• Approaches: Anterior approaches are better than the posterior approaches
1- Transthoracic
2- Retroperitoneal
3- Thoracolumbar
4- Lumbar exposures
5- Posterior approach:
posterolateral extracavitary decompression
Transpedicular decompression
Total spondylectomy
Laminectomy?
6- Sternal splitting ............................. T1-4
7- Cervical anterior approach......... for cervical tr
8- Posterior approach ...................... for sacral tumors; after coccygectomy, develop the
retrorectal plane and sacrum is excised
• Technique:
1- Anterior corpectomy
2- Total spondylectomy (via anterior fusion + PSF)
3- Excision to the level of structurally sound vertebra above and below
4- Excision up to total vertebrectomy + decompression + fusion + instrumentation
5- Extensive lesion + bad condition Æ Posterior decompression + BG + fusion
6- Laminectomy is done only if the tumor originate from the lamina
• Reconstruction:
1- Steinmann pins (or Harrington) + cement
2- Wide sheet of gel foam to protect the dura
3- Split fibula or double fibula ........ if survivor is expected to be > 2y
4- Combined BG + cement
Postoperative
• Radio & chemotherapy is used but should be delayed 6wk if BG is used
• Postoperative TLSO
Results of surgery
• 70-90% ........................................................... effective in pain and neurological control
• Anterior approach results are too much superior to posterior
• Laminectomy give bad results ................ 40% = the results of the radiation therapy alone
DDx of osteochondroses
Osteochondrosis Disease Site

AVN 1]. Legg –Clave-Perthes’ disease. Upper Femoral Epiphysis
Crushing 2]. Kienbock’s disease Lunate
3]. Preiser’s disease Scaphoid
4]. Panner’s disease Capitulum
5]. Scheuermann’s disease Vertebral Bodies
6]. Kohler’s disease Tarsal Navicular
7]. Freiberg’s disease 2nd Or 3rd Metatarsal Head
8]. Blount’s Knee ?
9]. Theimann’s disease Multiple Phalanges
10]. Friedrich’s disease Sternal End Of The Clavicle
OCD 11]. OCD Knee
12]. OCD Talus
13]. OCD Patella
14]. OCD 1st MT Head
15]. Buschke’s disease Medial Cuniform
Traction apophysitis 16]. Osgood –Schlatter’s disease Tibial Tuberosity
17]. Johansson-Larsen syndrome Patella
18]. severs disease Calcanius
19]. Iselin’s disease Tuberosity Of 5th MT
20]. Mandl’s disease Greater Trochanter
638 | Page [Sp ers]
pine Disorde
M
Mini In
nvasiv
ve Sp
pine SSurgeery
Advantages:
1- z surg gical compllications
2- z surg gical blood loss
3- z use of postop narcotic pa ain medicines
4- z hosp pital stay
5- y spee ed of functtional returrn to daily activities
6- Better exposure
Cla
assificatio on
I. Based ono spine re egions:
1- Minnimal invassive surgerry Cervical
2- Minnimal invassive surgerry Thoracicc spine
3- Minnimal invassive surgerry Lumbar spine
II. Based on
o body plains
1- Anterior
2- Possterior
3- Posstrolateral
III. Based ontechniq
o ue
1- Miccroscopic techniques
t s: e.g.anterrior cervical microforaaminotomyy
2- Enddoscopic te echniques
In Cervical
C s
spine:
1- Anterior:
a. Endoscop pic foramminotomy for cervica al disc hern
niation
b. Percutan neous end doscopic anterior
a cervical disce
ectomy
2- Posterior:
a. Endoscop pic foramminotomy
b. Cervical laaminaplassty
3- Poste erolateral endoscopic approacch for tumo ors
In thoracic:
t
1- Anterior Transthoracic end doscopic su urgery
2- Posterior Transpe edicular en
ndoscopic approach
In lumbar:
l
1- Endoscopic Surg geries:
a. Anterior endoscopic c lumbar ap pproaches
b. Posterior Endoscop
E pic Microfo oraminottomy e.g. Lumbar
L Ste enosis
c. Posterior Micro
M Enddoscopic Discectom
D my
d. Postero-latteral endosscopic lum mbar approaches
2- Mini innvasive lum mbar fusionn approach hes:
a. PLIF: Postterior Lumb bar Interboody Fusion n
b. ALIF:
A Antero-Lumba ar Interboddy Fusion
c. TLIF Transforaminall Lumbar In nterbody; i.e.
i postero o-lateral + ffacetal amp
putation
d. XLIF:
X Extreme Lat Innterbody, i.e. extra-pe eritoneally via
v lat approach und der fluoro
e. Mini ALIF F: reach the disc extraa-peritoneally via lat approach under fluo oroscopy
2- Mini innvasive aiding device es:
a. Laser
b. Motorized d Shaver & Suction
c. Thermal: disc
d ablatio on, also conntrols pain
d. Radiofrequ uency Neu ucloplasty
3- Interve ention spinne radiologgy:
a. Kyphoplassty
e. Vertebrop plasty
Back Pain in a child
• Congenital:
1- Klippel-Feil $: - pain is usually due to hypermobility or instability of adjacent vertebral
segment or to degenerative osteoarthrosis;
2- Diastematomyelia: - frequently associated with a cutaneous malformation overlying
defect, is more likely to present with neurological abnormalities involving lower extremities,
such as unilateral cavus foot or calf atrophy, rather than with back pain;
3- Scheuermann's Kyphosis - is the commonest cause of pain in thoracolumbar regions
• Traumatic:
4- Herniated Disc in the Child
5- Slipped Vertebral Apophysis:
o Posterior displacement of the ring apophysis é adjacent disc into vertebral canal
o ð incomplete or delayed fusion bet vertebral ring apophysis & central cartilage
o Occur in lumbar region mostly
o Cause both discogenic and radicular pain
6- Spondylolisthesis
• Infections:
7- Osteomyelitis of the Spine
8- Tuberculous Spondylitis
9- DISCITIS
• Tumors
10- Spinal Cord Tumors
11- Primary Bone Tumors: EG, OB, OsOs, ABC
12- Secondary tumors: metastatic neuroblastoma
Crankshaft Phenomenon
• in skeletally immature pt, isolated posterior arthrodesis with INSTRUMENTATION OF A LORDOTIC
CURVE MAY ACT AS A POSTERIOR TETHERING BAR, producing lordosis & bending of the fusion
mass as the unfused anterior vertebral bodies continue to grow
Risk Factors:
1. open triradiate cartilages
2. physiologic youth: - girls younger than 11 years; - boys younger than 13 years
3. Risser grade 0 or 1
4. juvenile scoliosis > congenital scoliosis (abnormal anterior growth plates)
Radiographs:
• >10º progression of the Cobb angle or RVAD (assuming that other causes of curve
progression such as pseudoarthrosis is not present)
Prevention:
• Anterior and posterior arthrodesis for risk group
Pseudo-Sciatica
Definition
• Sciatica is a symptom commonly used to describe symptoms of pain radiating downward
from the buttock over the posterior or lateral side of the lower limb. It is usually assumed to
be caused by compression of a nerve roots as they emerge from the spine; LDP, spurs,
fibrosis, …
• Pseudo-sciatica is the same but occurs 2ry non spinal causes
Aetiology
1]. Piriformis S 4]. Gluteus minimus $
2]. Psoas S 5]. ITB S
3]. Hamstring S 6]. Fibromyalgia
Pathogenesis
• Pseudo-sciatica pain arises from:
1- Entrapment of: ...... ▪ Sciatic n.
Posterior cutaneous n. of thigh
2- Trigger points in the soft tissue can be elicited by manual palpation of the
musculature associated with the hip if the pain is not to be misdiagnosed.
• Piriformis syndrome: The piriformis muscle is in such a state of constant tension and irritates
the sciatic nerve.
• Iliopsoas $ (mischief maker): No other muscle has so many functions & cause so much pain
& is so difficult to palpate. Iliacus is active in running & posas is active during the last 60°
while sitting
• Fibromyaglia: chronic lumbar & gluteal fatigue $ Æ sciatic nerve irritation
• ITB $: Runners who run on only one side of a slanted track can irritate ITB Æ sciatic n.
• Sciatic entrapment causes pain to be referred to its autonomous cutaneous areas, back of
thigh, lateral leg, & foot
Clinically
• Pain:
○ Low back radiating into one buttock and down the leg
○ May be severe enough that may lock back motion
○ by sitting, standing, certain positions
○ by cough, sneeze
• Numbness & z Reflexes
• TRIGGER POINTS = area of extreme tenderness & irritability that when compressed nerve
along its pathway, or of an irritated muscle
Differentials
CAUSE PAIN TRIGGERS TTT
Piriformis Fall on butt Back thigh IR (by Morton’s neuroma) Injection
Back knee Long drive é leg on paddle Release
Psoas Psoas tension Front of thigh Long upright standing Physiotherapy
Long steep sitting or flex attitude
Hamstring Pressure on Upper thigh Up from crossed leg sitting Injection
hamstrings Back of knee High seats é firm front edge Release
Glut Minimus Overuse Back pain to calf Sleeping on the affected side Physiotherapy
Too long too fast walks & standing Release
Long sitting on a bulky wallet
ITB Overuse Lat knee & back Long uphill running & cycling US & Release
Fibromyalgia Overuse Back pain Long standing & sitting Rest & injection
• Pain referred from trigger points in gluteus medius less likely to involve the thigh
• Pain referred from trigger points in gluteus maximus flexion
• Pain referred from trigger points in piriformis IR
Coccydynia
Definition:
It is a painful coccyx
Anatomy:
• Triangular piece of bone that originally formed of Four Pieces that fuse at skeletal maturity
• It may fuse as well with the sacrum
• It has 2 upper CORNUAE & 2 lateral TRANSVERSE PROCESSES
• Two intercornual ligaments are attached to the cornu
• 2 lateral coccygeal ligaments are attached to the transverse processes
• The gluteus maximus and the sacrotuberous ligament are attached to the posterior surface
• GANGLION IMPAR (end of the sympathetic chain) is situated at the ventral surface
• ANO-COCCYGEAL BODY situated at the tip where ano-coccygeal lig & coccygius ms attach
Types:
• Type I: .............................................................. slightly curved anterior
• Type II: ............................................................ markedly curved anterior at S5C1
• Type III: ........................................................... markedly curved anterior at C1C2
• Type IV: .......................................................... Subluxed anterior
Ætiology:
1]. Congenital types II, III, IV • Perianal fistulae
2]. Truamatic: 4]. Tumors:
• Fracture (uncommon) • Chordoma of the sacrum
• Sprains • Glomus tumor: middle scaral A-V fistula
• Post-traumatic OA • Tumors of the cauda
3]. Inflammatory: 5]. Degenrative disc
• Adventitious Bursitis 6]. Psychogenic
• Assessment: usually female middle age
• Symptoms:
• Duration of the symptoms ....................... acute (traumatic) or chronic (tumor or bursa)
• Related to certain position ........................ (traumatic)
• Is the pain is continuous............................ (tumors)
• Is there dyschasia, constipation ............. perianal fistulae
• Note the attitude of the pt ...................... hysterical pt
• Examination:
• Tenderness, hotness, warm...................... bursitis & trauma
• Sinuses & fistulae ........................................ perianal fistula
• PR:
Attitude of the coccyx ............. Abnormal types
Mobility ....................................... hypermobile (fractures)
Size ................................................ enlarged if there is a tumor
Tenderness ................................. if not tender the pt hysterical
• PXR:
o Abnormal type & size
o Fractures
o Chordomal of the sacrum
• MRI: May be needed to evaluate the presence of a tumor
Treatment
• Conservative: NSAID, Donut pillow, hot packs, local inj, mobilization UGA
• Surgical coccygectomy:
o Prone & through a curved incision at the lateral border of the coccyx
o Divide the structures attached to the tip first
o Subperiosteal dissection till it is freed totally + local lidocain
o Total coccygectomy may endanger the rectum as it lies just in front the S5C1
GENERAL CLASSIFICATION OF JOINTS

The classification of articulations based on the extent of joint motion:
1- Synarthroses: Fixed or rigid joints.
2- Amphiarthroses: Slightly movable joints.
3- Diarthroses: Freely movable joints.
According To Type Of Tissue That Characterizes The Junctional Area.
1- Fibrous articulations: bony surfaces are fastened by fibrous
2- Cartilaginous articulations: connected by cartilaginous tissue.
3- Synovial articulations: Apposed bony surfaces are separated by an articular cavity
that is lined by synovial membrane.
Fibrous Joints:(Articulationes Fibrosae)
In most instances fibrous joints consist of predominantly collagenous junctions between
bones but in a minority of situations fibro-elastic tissue predominates. Three main groups of
fibrous articulation are generally recognized, namely:
1. SUTURES: limited to the skull where bones ends are separated only by connective
tissue, and covered by a layer of osteogenic cells (the 'cambial' layer), then capsular
lamella of fibrous tissue corresponds to and continues with periosteum. Between the
two layers of sutural periosteum is a central stratum of loose fibrous connective
tissue that contains blood vessels which communicate with diploic vessels,
intracranial venous sinuses and external veins in the scalp. When cranial growth
ends, osteogenic cells starts complete ossification of sutural ligaments, ultimately
leading to obliteration and rigid synostosis.
2. SCHINDYLESIS: is a specialized suture where a ridged bone fits into a groove on a
neighbouring element, e.g. the cleft
between the alae of the vomer that
receives the rostrum of the sphenoid.
3. GOMPHOSES: A peg-and-socket joint
(articulatio dentoalveolaris) is a
specialized fibrous articulation for fixation
of teeth in alveolar sockets in the
mandible and maxillae.
4. SYNDESMOSES: is a fibrous articulation in
which bony surfaces are bound together
by an interosseous ligament as in the
POSTERIOR SACROILIAC JOINT & TIBIO-FIBULAR JOINT
Cartilaginous Joints
Cartilaginous Joints (Articulation Cartilaginaeae), or synarthroses, bone junctions bonded
by solid connective tissue, Cartilaginous joints are classified into two groups:
1- SYNCHONDROSES (primary cartilaginous joints): These articulations occur where originally
separate, but adjacent, centres of ossification appear within a continuous mass of
hyaline cartilage. As ossification spreads it invades the actively GROWING ZONE OF
CARTILAGE occupying the interval between the contiguous osseous surfaces.
Functionally, synchondroses are primarily growth mechanisms and, although
contributing slightly to the more flexible skeleton of youth, their growth potential is
combined with the ability to successfully resist forces, whether of compression,
tension, shear or torsion. Later endochondral ossification ceases and entirely
replaced by complete bony union between the originally separate osseous surfaces,
forming a synostosis, losing its cartilaginous growth potential and mechanical
properties, but acquiring the maximal rigidity of bone.
2- SYMPHYSES (secondary cartilaginous joints): is another variety of cartilaginous

synarthrosis having many features in common with other arthroses,
Topographically, all symphyses are median and, with one exception, are confined to
the axial skeleton; as manubriosternalis, INTERVERTEBRALIS, symphysis menti, and
SYMPHYSIS PUBIS. Symphysis consists of two surface areas of articulating endochondral
bones; the osseous surfaces varying from a few millimetres to over a centimetre
apart being bound together by strong, tightly adherent, solid connective tissues.
Each bony surface is firmly attached to a thin lamina of hyaline cartilage, which in
turn blends with the surface of a thick, strong, but deformable pad (or disc) of
fibrocartilage. Collagenous ligaments extend from the periostea across the
symphysis and blend with the hyaline and fibrocartilaginous perichondria. Usually
unlike synchondroses they are permenant.
Synovial Joints
1. PLANE JOINTS
These are appositions of almost flat surfaces (e.g. INTERMETATARSAL, INTERCARPAL joints,
FACETAL, ANTERIOR SACROILIAC, PATELLO-FEMORAL), movements being considered pure
translations or sliding between bones.
2. GINGLYMI (HINGE JOINTS)
These resemble hinges and are shaped to restrict movement to one plane, i.e. they are
uniaxial. They have strong collateral ligaments; INTERPHALANGEAL and HUMEROULNAR joints
3. TROCHOID (PIVOT) JOINTS
Also uniaxial, they have an osseous pivot in an osteoligamentous ring, allowing rotation
only around the pivot's axis, as the HEAD OF THE RADIUS ROTATES WITHIN THE ANNULAR LIGAMENT,
and the atlas (with its transverse ligament) rotates around the dens of the axis.
4. BICONDYLAR JOINTS
Largely uniaxial, with a main movement in one plane, they also have limited rotation
about a second axis. The rotation is of two varieties:
-Conjunct, with the main movement.
-Adjunct which can occur independently and may or may not accompany the principal
movement. They have two convex condyles (knuckles) articulating with concave surfaces.
Condyles may be almost parallel (e.g. KNEE) with a common fibrous capsule
5. ELLIPSOID JOINTS
These are biaxial, with an oval, convex surface apposed to an elliptical concavity, as in
RADIOCARPAL and METACARPOPHALANGEAL joints. Primary movements are about two orthogonal
axes (e.g. flexion–extension, abduction–adduction), which may be combined as
circumduction; rotation around the third axis is largely prevented by shape.
6. SELLAR (SADDLE) JOINTS
Also biaxial, these have concavoconvex surfaces; each is most convex in a particular
direction but at right angles to this they are maximally concave. The convexity of the larger
is apposed to the concavity of the smaller surface and vice versa. Primary movements occur
in two orthogonal planes but articular shape causes axial rotation of the moving bone.
Such conjunct rotation, as mentioned above, is never independent and is not simply a by-
product of 'imperfect' mechanics but is functionally significant in habitual positioning and
limitation of movement. The most familiar sellar joint is the carpometacarpal joint of the
thumb; others include the ANKLE and CALCANEOCUBOID joints.
7. SPHEROIDAL JOINTS ('BALL-AND-SOCKET')
Formed by reception of a globoid 'head' into an opposing cup, e.g. HIP & SHOULDER joints,
they are multiaxial, with three degrees of freedom. Their surfaces, although resembling
parts of spheres, are not strictly spherical but slightly ovoid. (Articulatio ovoidalis is an
accepted alternative.) Consequently, in most positions congruence is not perfect,
occurring only in one position, at the end of the commonest movement (see below).
Statistics
Incidence = RATE of occurrence of a NEW disease in a population previously free of the
disease.
• = [No. of new cases in study period]/[No. at risk at the beginning of study period]
Prevalence = FREQUENCY at any given time
• = [No. of patients with the disease]/[No. of patients with the disease + those at risk]
Sensitivity
• Ability to exclude false negatives
• = True positive / all with condition (all positives)
Specificity
• Ability to exclude false positives
• = True negatives / all without condition (All negatives)
Positive Predictive Value
• Probability that a subject who tests positive is truly positive
Negative Predictive Value
• Probability that a subject who tests negative is truly negative.
Accuracy
• how often is a test correct?

Ain Shams
University
The Hip
Dr Mohamed Sobhy
Quick Guide
♦ Anatomy and Biomechanics
♦ Osteonecrosis
♦ Arthritis
♦ Miscellaneous conditions
♦ Arthroplasty
[Hip Disorders] Page | 649

Hip Applied Anatomy

Type
• Ball and Socket synovial joint
Os Coxae = the hip bone (Ilium + pubis + Ischium)

Krause's bone: small bone (2ry ossific center) in the triradiate cartilage between ilium, ischium,
and pubis
Acetabulum
• Bony cavity faces obliquely:
o Outward
o Forward ...................................... 12° from sagittal plane
o Downward ................................ 60° from horizontal plane (labrum make it 45-50°)
Femoral Head
• Forms 2/3 of a sphere
• Articular surface is thicker on the mediocentral part and thinnest on the periphery
• The Joint reaction force usually acts on the superior quadrant
Femoral neck
• The angle of anteversion ................................. ≈ 12° in adults
• Neck shaft angle ................................................. ≈ 125° (90-135°)
• >125° = coxa valga ............................................. < 125 ° = coxa vara
650 | Page [Hip Dissorders]

Calcar femorral
• Intra ossseous vertiical plate off dense bon
ne, located postero-meedially at th
he neck shaft junction
• It is nott the inferio
or cortex of the neck
• Functio on: buttresss at the med d neck & prrox shaft to absorb WB
B compresssive & bend ding forces
• It has 3 extensionss (Harty 195 57)
Proxiimally ..................................................................... extends to o postero-infferior neck
Laterrally ......................................................................... extends too posterior GT
G
Dista
ally ............................................................................ extends ant
a to LT & fu use é shaft postero-mediially
Blood supply of femoral head
1]. Medial Circumflex Femoral A (MCF) .......... most im mportant su upply, (fromm profunda a a.)
• It run posteriorly
p bet Pectineeus and ilio opsoas, ab bove LT and d posteriorr to the ne eck, to find
d the
obturattor externuus, run below w it and de eep to quad dratus, whe ere it gives ssome brancches to GT.
• Then itt forms the medial, po osterior, & la ateral portio ons of the EXTRA-CAPSULAR ART RING that gives g
the asccending cerrvical aa. (RRETINACULAR VESSELS OF WEITBRECHT), postteriorly theyy pass bene eath
the orb
bicular fibers of capsulee
a Four Groups of th
• There are he ascendin ng cervical vessels;
v antterior, medial, posterioor, & lateral. The
Lateral provides most
m of the blood to fe emoral head.
• As they y traverse th
he neck the ey give metaphyseal ve essels that entres
e the nneck at regular interva
als
• When they reach h physeal ju unction, the ey form the e SUBSYNOVIAL INTRA-ARTICULAR ARTERIAL RING,
that givves many epiphyseal
e arteries; th he most important are e TRUETA'S LAT EPIPHYSEAL aa (art of
Brodettti) that ennter the hea ad postero-ssuperiorly, and a gives the major blood supplyy to the hea ad
2]. Lateral Circumflex artery (LC CF) .................... (branch of profunda femoriss artery)
• Passes anterior to o iliopsoass tendon till t it reaches the Intertrochante eric line ru
unning ove ver it
supplying the capsule and muscles
m and form the anteriora porrtion of the extra-capsu ular ring
• This poortion gives the ant retinacular v v., v pierce the capsule e at the inteertrochanteeric line
st
• 1 it sup pplies the anterior
a heaad portion, while in ad dult its role is mainly to
o supply the e metaphyssis
3]. Artery of the ligamentum teres ................. minor in n adult (po ost br. of ob bturator orr MCF)
• When it enters the t head iti gives the e Medial Epiphyseal
E
Arteriess that only supplies an n area just beneath the t fovea
centraliis
• Head blood
b supplly comes thhrough thre ee sources:
1]. Reetinacular v v. Æ subsyynovial ring Æ lat epiph
hyseal vv.
2]. In
ntraosseous cervical croossing the neck
n from be
elow
3]. Artery of liga
amnetum te eres Æ medial Epiphyseal.
• Non-un
nion occurss ð:
1]. No cambium m layer over the intracappsular part of the neckk
2]. Syynovial fluid
d hinders clo
otting & # hematoma
h formation
f
3]. Cllose proximmity of the re
etinacular vessels to the
e neck
4]. Frracture neck femur disrrupts most ofo the blood d supply at
tim
me of fractuure
5]. In
nadequate anastmosis
a bet med & lat
l epiphyse eal vessels
KINEMATIC
CSS
Motiion Av
verage ran
nge
Flexio
on 115°
Extennsion 30
0°
Abdu uction 50
0°
Addu uction 30
0°
Intern
nal rotationn 45
5°
Exterrnal rotation
n 45
5°
Kinetics
• Joint Re
eaction forcce (JRF) = fo
orce applied by internal and exte
ernal factorss
• Wt is ap
pplied on le
ever arm pa assing from
m body centtre to head centre
• Abducttors act on a lever armm from the GTG tip to he
ead centre
• The ratio of A:B = 1: 2.5 Ab bductors mu ust work ~ 2.5 BWt
Hip Disorderrs]
[H age | 651
Pa

Statics
Two leg stance
• During a two leg stance
s the line of gravvity of the body
b passess behind the
e pubic sym
mphysis
• As the hip
h joint is a stable join
nt, no musccle forces neeeded in sta
ance
• The forrce on eachh hip = ½ x (bodywt - leegs wt)
Single leg stance
• W is fo orce producced by bod dy weight; M is force produced
p b the abd
by ductors of th
he hip; R iss the
joint rea
action forcee
• Assume e A Band q are known n
• For equ um of moments = a
uilibrium Su
o WxB=M MyxA
o If B andd A are knoown
o My= Wx W BfA
o A value e for My is then found
• For equ uilibrium Su
um of the foorces is a (in
n the Y axis))
o My+W--Ry=O
o Ry can therefore be b found R can now be b found byy using • Ryy=R sin q
• On usin ng elbows and
a heels to t get onto a bed pan unaided
o JRF at hip
h = 4 x bo ody weight
o Much reduced
r wh hen using overhead
o trrapeze
• Using a walking sttick how it reduces
r JRFF:

In equilibrium sum of moments = a
Witho
out Stick Witth stick
Ab x A = W x B (Ab
b x A) + (W
WS x C) = W x B
Ab = W x B / A Ab = (W x B) –(WS
– x C) / A
• So the force
f requirred by the abductors
a A is smalle
Ab er if a stick iss used
• The big
gger C the smaller
s Ab, walking stiick the furth
hest away fromf the hip
p the most effective
• In equillibrium, the
e sum of the
e forces in the
t Y plane = 0
Witho
out Stick Witth stick
Ab x A = W x B (Abb x A) + (W
WS x C) = W x B
Ab = W x B / A Ab = (W x B) –(WS
– x C) / A
• Therefoore JRF is le
ess when a walking stick is used d. Not only is Ab force
e smaller, but
b the upw
ward
force exxerted by th
he stick red
duces the JRRF further.
• Body wt
w tend to push
p the ste
em into Varrus and Rettroversion:
• Torsional stabilitty by:
o Longerr neck cut
o Rounde ed rectangular cross section.
o Cutting g flutes.
o Extensive porous coating.
c

DY
YNNAMICS
On walkiinng
• Paul et al, using a force plate
e and kine
ematic data for the no
ormal hip fo
ound 2 pea
aks in the Joint
J
reaction
n force in th
he hip.
Joinnt reaction
n force afte
er heel strrike JRF just b
before toe
e off
Men 4 x body
b weightt 7 x body w
weight
Women 2.5 x body weig
ght 4 x body w
weight
o
Forces acting on the hip
[1]. Compre essive f
forces:
axial lo
oads on th he axis
of the prosthesis
p
2]. Bendin
[2 ng f
forces:
eccentrric loads parallel
p
to the e axis off the
prostheesis
3]. Shear forces: forces
[3
appliedd é an ang gle to
the axis of the
prostheesis
Hip Disorderrs]
[H age | 653
Pa

Av
vascu
ular n
necrosis off the femo
oral h
head
Definition
• = Death of bone from f ischae emia.
• Osteocy ytes will survive 12 - 48 hours of ischaemia and a marrow
w cells 6 ho
ours
Features
• Age 20 0-50 y ............................................................ (average
e 38 y)
• Sites: in
n descendin ng order
[1]. Fe
emoral headd
[2]. Medial femora
M al condyle 3-- Humeral he
ead
[3]. Ta
alus
[4]. Lu
unate, proxim
mal part of scaphoid
[5]. Ca
apitellum
[6]. M
Metatarsal hea
ads
• Bilatera
al in 50% off idiopathic cases, and 80% of steroid induce
ed cases
• 5% of THR
T perform med as a re esult of OA secondary
s to AVN
Pathogenesis (Theories)
[1]. Direct injjury: injury
y to retinacu
ular vv in fr neck femu
ur
[2]. Intraosse
eous Hype
ertension (Compartm
ment $ of Bone)
• Vascula ar sinusoid (no adven ntitia & éin a hard bon ne) can be
compre essed by su urroundingss
• IOP hav ve been consistently fo ound in casses of ON
• IOP is inversely prroportional to Bl flow w IOP Æ BF Æ
ischaem mia and ON N
[3]. Vascular stasis
• Those sites
s are farr distal, cartiilage enclossed, & supp
plied é end
art é inssufficient coollaterals
• Superse elective ang gio of the medial
m circu
umflex a to study
s femo
oral head AV VN
• Loss of transcortica al blood floow from the e superior retinacular
r h
have been demonstra ated
• Revascu ularization occurs in non n reversib ble osteoneecrosis
[4]. Fat Embo olism
• subcchondral fat fa volume Æ vascullar stasis Æ platelet aggregatio on, hyperccoagulabilityy, &
endoth helial damag ge Æ intravvascular coa agulation Æ local mechanism
m ms of repair.
• Histolog gically: intra
aosseous th hrombosis / periphera al haemorrhhages.
[5]. Fat Cell Hypertrop
H phy
• High-do ose corticossteroid Æ FatF cell hype ertrophy & fatty marroow overload
• Histolog gical chang ges consiste ent with ne ecrosis were frequentlly identified
d and femooral head bllood
flow wa as consisten ntly diminisshed
• Use of lipid
l ng agents Æ improve this
clearin t alteratioon in bloodd flow.
654 | Page [Hip Disorders]

Ætiology:
[1]. Idiopathic ........................................... (40%)
[2]. Arterial insufficiency:
[1]. Fracture & Dislocation fr. neck femur, talus, scaphoid severe ! retinacular a
[2]. Infection
[3]. Arteriolar occlusion
[1]. Sickle cell disease and other haemoglobinopathies
[2]. Caisson disease in divers and compressed air workers (e.g. miners)
[3]. Vasculitis e.g. SLE, irradiation
[4]. Antiphospholipid $ (e.g. in SLE)
[5]. Coagulation disorders: thromobocytopenia, ITP, familial thrombophilia
[4]. Capillary occlusion (by fatty infilterates and swollen adipocytes)
[1]. Systemic steroid treatment ............... (37%)
o > 30 mg prednisolone for > 30 days
[2]. High alcohol intake ............................. (20%)
o > 400 ml/wk or cumulative dose of 150 litres
[3]. Fatty liver ð other drugs e.g. chemotherapy
[4]. Gaucher’s disease
[5]. Hyperlipidaemia
[5]. Venous occlusion
[6]. Other
[1]. Pregnancy ( fibrinolysis, fatty liver)
[2]. Perthes’
[3]. Pancreatitis
[4]. DM
[5]. IBS
[6]. Nephrotic $
[7]. Renal transplant patients (16% will develop ON)
[8]. Haematological malignancies e.g. lymphomas, leukaemias
[9]. Toxic shock & endotoxin reactions
Pathology
• 6h ............................................Marrow cells can with stand iscemia
• 2 - 48 h...................................Osteocytes can withstand iscemia
o Dead bone is grossly and radiologically look as normal bone for weeks
• 2 - 4 d.......................................loss of BM adipocyte, oedema, infiltration, histeocytes
o Necrotic BM is replaced é UM tissue
o Necrotic osteocytes may look normal for wks (Empty lacunae are a late feature)
• 2-4 weeks: ...............................necrotic sector becomes demarcated
o substitution creeps from surviving trabeculae (10mm max) rarefaction
o New bone is laid down on the dead trabeculae }
sclerosis Mottling
o Repair & revascularisation starts at vascular margin Æ appositional growth
• Dead bone may fracture & collapse OR repair maintaining joint congruency
• Shear stress + large + wt bearing lesion + inadequate remodeling Æ tangential subchondral
stress fr & collapse
• This fracture may run into the cartilage surface; that may resist breakage till it yields fragments,
and leads to deformity & destruction of the joint surface
• Necrotic segment never in size; even it may in size.
Hip Disorderrs]
[H age | 655
Pa

Clinically: early stage is asymptomatic and the pt present late

• Hip paiin is comm mon & prese ent for mon nths before X-Ray channges are ma anifest
o Insidiouus pain ώ sttarts é activity or IR Æ at
a rest Æ evventually att night
o Pain ma ay be severre for 6-8 weeks
w and th
hen subsidee
o Night pain
p may be e an early fe
eature
• Clickin ng: due to snapping
s o loose frag
of gment
• Late de eformity andd stiffness
• Mild sym mptoms an nd effusion usually perrsists
• Earliestt examinatio
on finding is i IR
• Late: teenderness, ROM, fixxed deformiity
Investigations
X-ray features
• S 0-I: NORMAL L
• S II: O
Osteopennia (hypera
aemia) & scllerosis (new
w bone)
• S III: S ral COLLAPSE “CRES
Subchondr SCENT sign n” (sclerosiss )
• S IV: 2ry OA Æ joint spa ace (before JS is normaal)
MRI (100% sensitivity, 98% specificity)
• Earliestt finding (be
efore gross and radiolo ogic findinggs)
o T1: Ban ndlike area of
o low signnal intensityy ð ischaemic BM
o T2: 2nd high signa al intensity line éin the n on T1; Æ
e line seen
hyperva
vascular graanulation tisssue “DOU UBLE LINE SIGN”
%
• When ¼ of head diameter
d & 2/3 of WB B area is invo
olved c
collapsed w
within 3y
• Rarely AVN
A may be
b found on n histology with a norrmal MRI
• Small NWB
N lesionss tend not to
t collapse
• Size of ischemic
i se
egment is determined very early anda rarely after thatt
MRI Staging for signals
Classs T1 T2 Definition
D n
A brightt intermedia
ate "ffat" signal.
B brightt bright "b
blood" signa al.
C interm
mediate bright "ffluid" or "edema" signal.
D dark dark "ffibrosis" sign
nal.
Bone scan features 75-80% sensitivity in precollaap pse stage

• Tc99mSu
ulphur collo
oid is taken by BM mye eloid tissue;; in AVN upptake
• Tc99mHDP
H early (2 2-3wk) Co old area in blood
b zation Æ ho
phasse (prior to revasculariz
r ot)
• Usually
y uptake ata time of sttudy
• uptake on bothh sides of joiint suggestss OA ratherr than AVN N
Single Photon Emission Computed Tomography (SPECT) scan
• SPECT is i a 3D isoto ope techniq que useful ini analysis of
o BG healing & early A AVN
• It is able
e to visualizze 3D bone e reactivity Æ identify cold
c spot within
w the arrea of acttivity.
Hemodynamic Tests (bone marrow pressure)
• Metaph hyseal cann nula is inserrted & meassure restingg pressure & after rapid d injection of saline
• Three fold
fo increase is noted (N: 10 mmH Hg rising to
o 15 mmHg g)
• This is also
a demon nstrated by venograph hy
Other investigations to diagnose th he e cause of the A VN
• e.g. Alccohol abuse e: • γOt, uraate, sTG, MCV.
• in non--traumatic and a in Perth hes': coagulopathy pro ofile is recom
mmended.
• SLE & antiphosph
a holipid $: anntibodies arre measured.

Staging
[1].Ficat & Arlet staging:
Stage Pain Findings X-ray Tc MRI Treatment
0 (Preclinical) None None (FEB +ve) N N +/- None
I (Preradiological) Minimal IR N N +ve Core decomp
II (Precollapse) Moderate ROM Osteopenia +ve +ve Core decomp/
/sclerosis Strut graft
III Moderate ROM Head collapse +ve +ve Strut graft/THR
/Severe /crescent sign
IV Severe Pain 2ry OA +ve +ve THR
• Original Ficat & Arlet 1968, did not include Stage 0.
• Stage 1 was known as the 'Silent Hip'.
[2]. Steinberg modification: same as above for stages 0-3
• Stage IV Flattening of the femoral head
• Stage V Narrow Joint space ± acetabular involvement
• Stage VI OA
• Stages are further divided into:
o A............................................................ Mild.
o B. .......................
o C. .......................................................... Severe.
[3]. Shimizu Predictive Staging (MRI staging): the
likelihood of progression to Collapse depends on the
location and extent of the boundary changes on
MRI. Number of pluses represents the risk of
progression.
[4]. Association Research Classification Osseous


Arlet and Durroux Histoloaical classification

Grade Pathology
GI haemopoietic marrow, odema, hemorrhage, foam cells
GII marrow necrosis, eosinophilic reticular pattern, oil cysts
GIll complete medullary and trabecular necrosis
GVI complete necrosis + dense fibrosis + appositional new bone formation
Functional exploration of bone (FEB):

• Simple and safe method for diagnosis in the early stages (pain / ROM / normal PXR)
[1]. Bone marrow pressure: BLP, ST, P02
• Cannula placed in the intertrochanteric area under local anaesthesia
• "Base line pressure" N:20 mmHg; if lOP is normal Æ 5 ml of isotonic saline is injected
• Pressure recorded 5 min after Æ "stress test" pressure, is normally < 10 mmHg rise.
• If both tests are normal Æ repeated using a cannula placed in the head.
• In AVN:
o Baseline pressure > 30 mmHg.
o Stress test > 10 mmHg rise.
• Blood sample from trochanteric area is taken for P.02; if > 85% uptake = circulation failure =
head anoxia.
[2]. Intramedullary venography:
• 10 ml contrast medium is injected through the same cannula used for the stress test
• N: dye quickly cleared by ischial & circumflex veins, eout diaphyseal reflux or stasis
• In A VN the injection is difficult/painful/diaphyseal reflux/1M stasis for 15 minutes
• A VN diagnosis is probable even if only one of the BLP, ST, or venography is positive
[3]. Core biopsy
RD
• 3 stage of FEB, establishes the diagnosis e certainty.
• A trephine, 6 - 8 mm is introduced into the neck from an opening in GT ~ head
• Stop 5 mm subchondral under fluoroscopy
• Second channel is made with a smaller trephine in a different direction
• forage channels are left open, so providing decompression.
Avascular Necrosis Transient Osteoporosis
Incidence 15,000 cases/yr Rare
Patient
Male : female Equal 3 to 1
Age 20-40 years old ♂: 40 y
♀ during last trimester of pregnancy
In children Equivalent to Legg-Calvé-Perthes disease Extremely rare
Etiology Interruption of circulation to femoral head Unknown; may be RSD or AVN
PDF Known risk factors in 80 % of patients Pregnancy
Laterality Bilateral in more than 50% of patients Unilateral, may be recurrent
Onset Insidious Acute
Symptoms Pain at rest, limp (late finding) Pain é WB, antalgic gait, functional
disability
Imaging
PXR Osteopenia, Sclerosis, mottling, crescent, collapse Osteopenia at 4-6 wks.
Bone scanning Lesion more localized, may present with photopenic area Diffuse, homogeneous lesion;
increased uptake of isotope
MRI Focal lesion, anterosuperior region of femoral head; Diffuse BM-edema pattern.
signal intensity on both T1- T2- double-line sign Low signal on T1
High signal on T2
Prognosis Progressive in 70-80% of patients, usually leading to Spontaneously resolves within 6 to 8
collapse of femoral head and end-stage degenerative joint mo without sequelae, prognosismore
disease guarded in pregnant
patients
Treatment Early operative intervention is recommended Protected weight-bearing & ttt of
symptoms

Treatment Modalities
• alcohol and steroids in high risk patients.
• Regulation of the rules for divers and air workers.
• Arthrocentesis for traumatic hip tamponade.
• Potentially reversible early if corticosteroids or alcohol stopped.
• Antithrombothic medications in thrombophilia and hypofibrinolysis.
• Symptomatic treatment, weight loss and physio.
[1]. Protective Weight bearing .......................... (Stage I & II)

• Relative poor choice; however mb indicated in very limited disease or not fit for surgery.
• Start é NWB Æ progress to FWB as clinically demonstrate that the hip is less irritable.
• Usually it takes 3 - 6 months to return a patient to FWB status.
• Radiographic and clinical follow-up at 6-week intervals until pain has subsided.
• Success 5-20% at 3-5 y (inferior to core decompression in Ficat stage I & II).
[2]. Core Decompression ...............................(Best for stage I & II)

• Aim: demonstrate IOP (venous) Æ remove a central core of bone Æ IOP.
• The biopsy obtained can confirm the disease histologically.
• Patients remain NWB for 6 weeks post op.
• Core decompression + PEMF results - the same as core decompression alone.
• Conclusion: Core decompression delays the need for THR.
• Its reported success rates 45-85% according to the stage.
[3]. Electrical Stimulation ....................................... (Stage I, II, III)
• The use of PEMF's with external coils in a large multicentre study was successful for hips,
irrespective of the aetiology of the condition.
• As effective as core decompression for stages 1 and 2, but is more effective for stage 3.
• Awaiting final FDA approval before it can become widely available.
[4]. Trapdoor Procedure ........................................... (pre-collapse Stage II)

• Anterolateral dislocation of the head is done to expose the area of the collapse.
• The break in the articular cartilage is identified and opened like a trapdoor.
• Necrotic bone is excavated & removed if needed by burr Æ expose bleeding bone.
• This defect is then filled with iliac BG over packed to prevent subsidence.
• May cause subluxation; so it must be combined é acetabuloplasty ± VDO.

Hip Disorderrs]
[H age | 659
Pa

[
[5]. Proxim
mal Femorral Osteottomy ....................... (Stage
e III)
• Aim is preservation
p n of the he ead by strress in the diseased
d heead sector.
• Varus osteotomy
o s
shifts the most
m involve ed portion Æ medially (best for lateral lesions).
• Successs has been reported in n 74% of staage 3 hips in one serie
es
• Rotational osteoto omy (SUGJ JOKA) Æ shift the diseased porrtion med.in nf.posteriorr.
• It is tech
hnically diffficult & asso
ociated é morbidity
m Æ best reservved subcho ondral collap pse
• Its repoorted successs rates 20-6 65% accordding to inta
act WB areaa after transsposition.
• It is technically diffficult, interfferes é THR
R, & associa
ated é morb bidity Æ b best reserveed subchon
ndral
collapse e.
[
[6]. Strut Grafting
G (F
Fibula/tibia//iliac) ................... (Stage
e II pre-collapse)
• Either Bonfiglio
B n
non-vascula arized type
e or using a vascularize ed grafting technique.
• Effectivve if the graft is placed carefully in
n the subchondral regiion.
• Cortical strut graftts e.g. ilium, fibula placced into a coore track in
n the femora
al neck.
• Ineffecttive for stresss-transfer in
i the uppe er femoral regions.
r
• Not wid despread yet.
y
[
[7]. THR
• Both un
ncementedd and ceme ented total hip
h arthrop
plasty have been used in this pop
pulation.
• Reporte
ed success rates are below wh hat appearr to be exp
pected from
m series inn other pattient
populations.
[
[8]. Vascula
arised Pediicle Flaps
• Quadrratus femo oris graft (MMeters) .......... posteriorr.
• Tensor Fascia Lata
a muscle................................. anterior.
[
[9]. Arthrodesis
• Young patient witth unilatera
al disease e.g. trauma.
• Problem
m is that 50
0-80% of casses are bilateral.
• Conclu
usion: bestt to manage
e conservattively until bad
b enoug
gh to perforrm THR.

Osteoarthritis
DEFINITION
• Non-inflammatory degenerative joint disease ccc by progressive softening & disintegration of
articular cartilage é associated new bone formation & capsular fibrosis.
[1]. It is not a simple wear as it is: asymmetrical, localized, & related to abnormal loading.
[2]. It is not purely degenerative (misnomer) as it is accompanied by a healing process in the form
of reactive new bone formation
Epidemiology:
• It is the commonest joint diseases and considered a universal disorder
• > 60y .......................................................................... 50%
• Fingers, hip, knee, and spine are more affected than other sites
• OA hands are more common in females
• ♀:♂ = 2:1 (more DDH in ♀) unlike china & Africa
AETIOLOGY
• Primary - no obvious cause more é aging (effect of aging on cartilage)
• Secondary - occurs following certain predisposing factors:
o Trauma: ............................................. direct injury, deformity, joint instability
o Congenital: ...................................... DDH, Perthes, Blount,…etc
o Infection
o Metabolic: ........................................ ochronosis, hemochromatosis, gout, Paget
o Endocrine disorder: ..................... Acromegaly and hyperparathyroidism
o Occupation: knee (in benders)- UL (vibrating tools) –hands (boxers) –shoulder
(pitchers)
o o Obesity: ................................ loads across the WB joints.
• OA is uncommon in pts é osteoporosis.
• OA is due to failure of chondrocytes to repair damaged cartilage.
• There is a DISPARITY BET.STRESS APPLIED AND CHONDROCYTE RESPONSE. = 'wear vs. repair'.
Mechanical causes of the disparity of the stress and strength:

Abnormal Loads on normal joint:
• Articular cartilage can withstand loads of up to 25MPa without damage.
• Loads exceeding this Æ chondrocyte death & cartilage fissures.
• Single impact loads or less intense multiple impact loads can cause articular damage.
• Impact loading Æ loss of proteoglycans from matrix Æ cartilage stiffness, hydraulic
permeability & disrupt collagen meshwork.
• If repair cannot keep up with damage Æ degeneration.
Normal load on abnormal Joints:

• Instability Æ altered congruence Æ shear & compression forces on regions of cart.
• Partial loss of joint sensory innervation accelerates joint degeneration.
• Forced activity following joint injury or ACL transection Æ joint degeneration, whereas
immobilization after injury prevents degeneration.

PATHOGENESIS
Theory 1
• The initiating event is FATIGUE OF THE COLLAGEN MESHWORK Æ HYDRATION of the articular
cartilage Æ LOSS OF PROTEOGLYCANS from the matrix into the synovial fluid.
• Cartilage SOFTEN Æ CHONDROCYTES DIE Æ release of proteolytic enz Æ further damage.
• Cartilage deformation Æ stresses on collagen network Æ damage.
• Cartilage can’t withstand stresses ώ are concentrated on the subchondral bone Æ subchondral
degeneration, cyst, vascularity, and sclerosis.
• Repair occurs at the joint margin in the form of growth & endochondral ossification Æ
hypertrophic osteophytes (unlike the atrophic diseases e.g. RA).
• Evidence of collagenolytic activity; but collagen loss may be ð mechanical causes.
Theory 2:
• The initial lesions are SUBCHONDRAL MICROFRACTURES following repetitive loading.
• Healing of these microfractures Æ undue subchondral bone & violation of Tide mark.
• A stress gradient develops Æ articular cartilage is lost in areas of maximum stress.
• Underlying bone becomes hardened and eburnated.
• Proliferative changes also occur at the joint margins with formation of osteophytes.
Molecular Pathology:
[1]. WATER content (unlike water content in ageing) – ð weakening of type 2 collagen.
[2]. Proteoglycans ( size, chondroitin 6-sulphate, keratan sulphate, hyaluronic).
[3]. Chondroitin / Keratin ratio (unlike ageing).
[4]. Proteoglycan-Degrading Enzymes (collagenase & stromelysin & plasmin).
[5]. collagen, and proteoglycans synthesis and loss Æ net result level.
[6]. Increased levels of:
o Matrix METALLOPROTEINASES (MMPs) (collagenase, gelatinase, and stromelysin).
o CATHEPSIN B & D (proteases found in synovium, chondrocytes, and PNL)
o IL1 - enhances enzyme synthesis & has a catabolic effect.
o IL6
o TNFα
o TGFβ
o GAGs and polysulfuric acid
PATHOLOGY
• Cartilage Damage: (in pressure areas).
o softening Æ fibrillation (chondromalacia) Æ cracks Æ ulceration.
o eburnation (loss of cartilage é sclerotic 'polished' bone).
o tufts of fibrocartilage on the bone surface.
• OSTEOPHYTES (in non-pressure areas) due to:
o vascularization of subchondral bone.
o develop in the path of least resistance.
o capsule traction & synovial metaplasia.
o proliferation of cartilage adjacent to WB.
o area é endochondral ossification.
• Subchondral SCLEROSIS, congestion, and IOP.
• Subchondral CYSTS:
o In the areas of max damage.
o containing thick gelatinous material.
o ð microfractures that degenerate & accumulate synovial fluid.
• Capsular Thickening and fibrosis deformity F AD IR (antero inferior capsule).
• Mild Synovitis usually (sometimes thick and villous).
• Fragmentation of osteochondral surfaces.
• Loose Bodies: usually ð synovial metaplsia and extrusion and not separation of an osteophyte.

Microscopically:
Early:
• Superficial SPLITS and irregularities.
• Deep METACHROMASIA (depletion of matrix proteoglycans).
• CHONDROCYTES clusters.
• SUBCHONDRAL OSTEOBLASTIC activity, marked vascularity.
• Margin OSTEOPHYTES: ð cartilage hyperplasia and ossification.
Late:
• Extensive CLEFTS.
• CYSTS é amorphous material (squeezed synofluid, disintegrated trabeculae, osteonecrosis).
• Bone NECROSIS and denuding.
Types
[1]. Hypertrophic 75%.
[2]. Atrophic 20%.
[3]. Progressive 5%.
Variants:
[1]. Polyarticular (generalized): commonest, 50y♀, hands painful stiffness, also trapMC OA.
[2]. Monoarticular & Pauciarticular: is the classic form, WB OA or 2ry to a cause (DDH).
[3]. Endemic OA: either environmental factor or genetic dysplasia.
[4]. Unusual site OA: Milwaukee shoulder.
[5]. kashin-Beck disease: generalized OA in hands, elbows, knees + short stature.
[6]. Mseleni joint disease: Polyarticular esp hips crippling deformities ð MED & protrusio.
[7]. Rapid destructive OA: elder ♂ under strong NSAIDs, usually hip ð Ca2+ crystal deposition.
[8]. Charcot’s disease: the most severe form of OA.
CP
• Old age, +ve family history, + PF.
• WB joints (hands in females).
• Insidious onset & Intermittent course é attacks may lasts for few months.
[1]. PAIN:
o The main symptom: ð ms fatigue, capsular stretch, congestion, IOP.
o Site: anterior (sometimes posterior or lateral).
o é exertion, WB, Cold, Ext Abd IR.
o é rest (relief by time).
o Referred to medial side of the knee (via the obturator n.).
o Progress to be even at rest.
[2]. STIFFNESS & loss of function: after periods of inactivity constant.

[3]. DEFORMITY: F Add ER ; ð ms spasm capsular contracture.
[4]. ROM ± crepitus (especially Ext Abd IR).
[5]. Ms WASTING: in acute stage mainly in the abductors.
[6]. TENDERNESS: over the site of capsular inflammation (most accessible bet. GT & ischium).
[7]. SWELLING: intermittent (effusion) or constant (cap/synovial thickening, or osteophytes).
[8]. +VE F AB ER test: abduction Ext.rotation in flexion Æ pain.
• HEBERDEN’S NODES: thickening of the DIP joints (≠ Bouchard’s nodes of RA).

Hip Disorderrs]
[H age | 663
Pa

Radiography
PXR:
}
• Asymm metrical narrrowing off joint space
e.
• Subchoondral sclerrosis.
• Subchoondral cystts. + any
a other 1ry1 patholo
ogy.
• Osteop phytes at the margin ns.
• Late bo oint deformity and insttability.
one destrucction and jo
Tc-HDP scan
• uptake in bone phase ( vascularity
v & new bone formation n).
COMPLICATIONS
[1]. Loose bodies.
b
2]. Backer’’s cyst: capssular hernia
[2 ation.
3]. Spinal deformity
[3 d 2 to pelvicc deformity lordosis & side bend
2ry d.
4]. Ankylosis.
[4
TREATMENT:
• Vary ac ccording to o the site, sta
age, age, seeverity, andd symptomss.
Early: keep moving, prevent overload, relieve pain.
[1]. EXERC CISE of sup pporting mu uscles aroun nd joints to
o avoid wassting and ke eep ROM.
2]. PROTE
[2 ECTION off affected jo oints from overloading
o g: wt, wa alking stick.
3]. Pain rellief by analg
[3 gesics or NSAIDS.
4]. MODIF
[4 FY activity: avoid climb bing stairs, squatting,…… etc.
5]. HYALU
[5 URONIC acid a injectio ons.
6]. GLUCO
[6 OSAMINE E & chondro oitin.
New & Experimental Treatments:
[1]. Doxycy ycline Æ cartilage collagenase
c e activity.
2]. Transfo
[2 orming grow wth factor beta (TGF beta)
b can re
epair partia
al thickness lesions.
3]. Metallo
[3 oproteinase e inhibitors matrix destroying
d enzymes
e & block cytokines.
4]. Gene th
[4 herapy - Ge enes that ha ave either anti-arthritic
a c or synthettic properties can be delivered
d into
the join
nt via non-re eplicating viral
v vectorss; e.g. IL1.


Late Surgical treatment - is indicated for patients é persistent symptoms:

[1]. Cysts curette and BG Æ release the fluid under pressure inside (obsolete).
[2]. BG of AVN (to be effective must be precollapse).
[3]. Arthroscopic debridement, wash, removal of lbs, and removal of osteophytes.
[4]. Realignment osteotomies in young age;
o Advantages:
1]. pain ð:
o Unload the disease part.
o Decompress the congested metaphysis relief pain dramatically.
o Adduction of prox fragment Æ relax the capsule & intraarticular tension.
o Relax the adductors
2]. Joint space
3]. cysts and sclerosis
o Indications of valgus osteotomies:
1]. Fixed adduction deformity.
2]. Painful abduction.
3]. Trendelenberg gait.
4]. Must have adduction range after the osteotomy.
o Indications of varus osteotomies:
1]. Fixed abduction deformity.
2]. Painful adduction.
3]. Antalgic abductor gait.
4]. Must have abduction range after the osteotomy (confirm by PXR).
o Contraindications:
1]. Extensive oa é rom < 50º.
2]. RA.
3]. Extensive AVN é no healthy segment to be utilized for WB.
o Precautions:
1]. Pre PXR in adduction and abduction to determine the osteotomy angle.
2]. Never do varus osteotomy for varus deformity and vice versa.
3]. Stable internal fixation is mandatory.
[5]. Hanging hip operation: muscle release all around the hip via 3 incisions to joint Tension and
regain attachment é elongation after few weeks (obsolete).
[6]. Arthrodesis if young and stiffness is accepted.
o Indications:
1]. Severe unilateral OA.
2]. Severe limitation of movements.
3]. Medical treatment is exhausted.
4]. Epsilateral knee & spine should be sound.
[7]. Girdle stone: may be done after failure or sepsis of arthroplasty as a transition till 2nd op.
[8]. Pelvic support osteotomy: girdle stone + subtrochanteric osteotomy at the level of the
Ischium é angulation beneath the acetabulum for wb support; it provides support, pain relief,
motion especially in chronic infection, oa after infection & unreduced DDH.
[9]. Colonna trochanteric reconstruction: resection of head and neck + implantation of the GT
into the acetabulum.
[10]. Arthroplasties; (total, femoral head, cup).
o Indications:
1]. > 60y.
2]. Severe limitation of movements.
3]. Severe involvement.


Tuberculosis
Organism:
• Red acid-alcohol fast obligatory INTRACELLULAR Mycobacterium tuberculosis bacilli.
Pathology:
1- 1ry lesion:
Site:
Lung. ▪ Pharynx. ▪ Gut.
Changes:
Local inflammatory focus Æ Lymphangitis Æ Lymphadenitis.
Seculae:
TB bacilli remain dormant in LN.
Body is sensitized to toxins.
2- 2ry lesion: spread to:
Lung Æ military TB.
Meninges: Æ TB meningitis.
Other tissues.
3- 3ry lesions (10% affect the musculoskeletal system).
Tuberculoma formation:
Central CASEATION necrosis (coagulation necrosis).
Surrounded by EPITHELIOID cells, LANGERHANS giant cells, LYMPHOCYTES.
They tend to coalesce to form a wide area of caseation necrosis.
TB Arthritis (hip, knee, ankle, shoulder, then wrist).
Synovium is THICKENED é Cell rich EFFUSION.
Granulomatous PANNUS may form & creaps on the cartilage & bone.
Cartilage & bone EROSION (peripherally at synovial reflection).
Juxta articular OSTEOPENIA ð hyperaemia.
Appendicular skeleton:
Metaphyseal bone destruction (no sclerosis, no periosteal reaction).
TB Dactylitis = Spina Ventosa (middle and distal phalanx).
Digit is swollen spindle shape é little pain.
Starts diaphyseal é bone rarefaction + PNBF + soft tissue swelling.
PXR: Spina (spindle shaped digit) Ventosa (full of are i.e. rarefied).
Cold Abscess:
Infected LN may COALASE together to form big area of caseation.
Caseation spread via soft tissue planes i.e. through skin or along ms fascia or a
bundle.
May burst to skin to form a sinus.
TB Spondylitis:
Blood borne - settles in vertebral body anteriorly.
Thoracic is commonest ± skip lesions & multiple level (lumbar for OM & discitis)
POTT’S PARAPLEGIA.
4- Healing:
a. Resolution.
b. Ankylosis.
c. Dormant bacilli.


Clinically:
• Genera al:
Night sweeat, night fe
ever.
Loss of we
eight, loss of
o appetite
e.
• Local:
e by spasticc ms ⎯⎯⎯→⎯ spasm
AtNigght
Night Criies: joint iss splinted at
a day time m is relieved Æ
stretch or compressio on of the damaged
d tissue
t Æ pa ain.
Marked muscle wasting.
Marked syynovial thicckening.
ROM & stiffness & Joint defo ormity.
PXR:
Juxta Articcular Oste
Narrow jo
eopenia Æ washed out
oint space (in childre
Peripheral bone ero
o bone ends.
e
en epiphysiis 2ry to hyperaem
osion and cystic
c subcchondral leesions.
mia). Pheemister Triad
d
}
No periostteal reactio
on.
Spine erossion, collap
pse, parasppinal absce
ess calcifica
ation & kyp
phosis é cro
owded rela ated
ribs Æ Sunn Ray Appe earance.
Hip erosio
ons occur in 3 areas (Babcock k’s Δ); erosion of the superior acetabulum
a mÆ
Wanderin ng Acetabulum.
Investigation
B
Blood:
1. ESR.
2. Leucopenia é relative e lymphoccytosis.
3. Lymphoocyte/monocyte ratio o ≈ 1.
Immunolo ogical:
1- +ve PCR.
2- +ve Manto oux test.
A
Aspirate f
fluid:
1- Physical: ......................... viscosity.
2- Chemical: ..................... ptn / glucose / poor mucin clot.
3- Bacteriolog gical: ........... Red acid-alcohol fast INTRACELLULAR bacilli é ZEAL NELSEN . 20%.
4- n: ................... LOWENSTEIN JENSEN media or Dorset egg .................................... 80%..
Cultivation
Con ncentrated centrifuged c d decontaminated samp
ple (Petroff method).
Kee ep 35º for 6 wk.
5- Organismss also FLUORESCE WITH AURAMINE staining.
6- Guinea pig g inoculation.
B
Biopsy:
• Granulo
omatous rea action (case
eation + Lan
ngerhans + epitheliod + lymphocyytes).
• Charactteristic evide
ence of a de
elayed hypeersensitivityy reaction.
• TB tend
d to give ne egative resu ults.
S
Skin tests
• Delayed d hypersen nsitivity reacction used to t diagnose e tuberculo osis.
• The two common nest tests are e the Mantoux and He eaf test.
• Manto oux test:
0.1 ml of purified
p pro otein deriva ative is inje
ected intrad dermally.
+ve if ..................................................... > 5 mm papule
p at 72
7 hours.
• Heaf test
PPD is inoc culated intto the skin using a gu un to produ uce multipple puncturres.
+ve if ..................................................... > 4 papu
ules at puncture sites at 72 hours
• Positive
e skin test arre indicativve of active infection i orr previous BCG
B vaccin
nation


Treatment
• Rest ................................................................... (in Acute stage):
Bed rest + Splintage and traction to prevent ms spasm and deformity.
Maintained till:
2- PXR: calcification.
3- Lab: ESR, lymph/monocyte ratio >5.
Then motion is encouraged é the orthosis on 18mo ⎯⎯⎯→ gradual weaning
Then

& if pain & spasm return Æ resume orthosis.
• Chemotherapy:
RIPES - Rifampicin, Isoniazid, Pyrazinamide, Ethambutol, Spectinomycin.
Rifampicin + Isoniazid 6-8 mo.
Ethambutol (or pyrazinamide) for the initial 8wk.
Streptomycin is toxic.
• Operative:
Precautions to start:
2- PXR: calcification.
3- Lab: ESR, lymph/monocyte ratio >5.
Drainge of a TB focus is seldom done nowadays.

Cold abscess calls for urgent drainage.
Painful destroyed joint arthrodesis.
Painful destroyed joint arthroplasty.
Spinal TB open drainage, debridement, PSF, and BG.

Rh
heum
matoid
d Artthritiss
• Affects 3% of wom
men & 1% ofo men.
• Hand > Knee > hip
p > cervical spine.
Diagnosis:
• ARA Criteria
C (A
American Rh
heumatism Association
n):
1- Morning
g stiffnesss:
Lasting
g at least 1 hour
h before
e maximal improveme
i ent.
2- Arthritis
s of 3 or more joint areas:
At leasst 3 joint arreas simulta
aneously have had so oft tissue sw
welling or fluid
f (not bony
b
overgrowth alone e) observedd by a physsician; the 14 possible jjoint areas are right or left
proxim
mal interpha alangeal (PIIP) joints, metacarpop
m halangeal (MCP) jointts, wrist, elb
bow,
knee, ankle,
a and metatarsop
m phalangeal (MTP) jointss.
3- Arthritis
s of hand
d joints:
At least 1 area sw
wollen (as de
efined abovve) in a wrisst, MCP or P
PIP joint.
4- Symmet
tric arthrritis.
5- Rheuma
atoid nod dules:
Over bony
b promin
nences, or extensor
e su
urfaces, or in
n juxta-articcular region
ns
6- Rheumaatoid facttor +ve.
7- Radiogr
raphic ch
hanges.
• At leastt 4 of 7 crite
eria.
• Criteria 1 through 4 (at least 6 weeks).
7 ccc ............................................. Classic
C
5 ccc ............................................. Definite
D
3 ccc ............................................. Probable
P
2 ccc ............................................. Possible
P

Aetiology:
• Genetic c susceptibiility: RA is co
ommon in first degreee relatives of
o RA patien
nts and twin
ns.
• Immun nological prrocess: HLA A-DR4 & DW4
D encodded on chromosome e 6; and is found on the
surface
e of APC (anntigen pressenting cellss); & when interact é thet antigenn (some tim
mes the antiigen
with the
t HLA form th he activating comp plex) Æ
autoimmune response.
• When APC and T-cells inte eract Æ cell proliferattion +
cytokin n Æ ⊕ pha
nes secretion agocytes & B-cells.
• Rheum matoid facto or: Anti-IgG G auto antibodies wh hich is
detecte
ed in the serum of the patient.

Pathology:
Stage 1: Synovitis
• Vascular congestion & effusion
• Synoviocyte proliferation Æ VILLOUS formation
• Infiltration of subsynovial layers by PMNs, lymphocytes & plasma cells
• A PANNUS of granulation tissue creeps over the articular surface eroding cartilage & bone
• Cartilage destruction occur partly ð proteolytic enzymes & vascular tissue
• Bone destruction occur partly by proteolytic enz, & osteoclastic activity
• Direct invasion occurs at the margins of the joint
• Similar changes occur in tendon sheaths Æ rupture
Stage 3: Deformity:
• From:
Articular destruction.
Capsular stretching.
Tendon ruptures.
• Acute inflammation subsided.

Extra-articular Manifestations:
• Nodules - in 20% of RA - skin, synovium, tendons, sclera, viscera.
• Lymphadenopathy & Splenomegaly ........ FELTY'S Syndrome (pancytopenia) .
• salivary & lacrimal gland secretion ......... SJORGEN Syndrome.
• Pulmonary (pleurisy & Rh. nodules) ........... CAPLAN $.
• Vasculitis.
• Myopathy & neuropathy, or direct compression from synovitis.
• Visceral: pericarditis, nodules.
Clinically:
• 40 female may be é positive family history.
Early:
Painful swollen HAND joints é morning stiffness.
PAINFUL LIMPING.
ROM ± crepitus.
loss of WEIGHT, weakness.
O/E: symmetrical swelling, tenderness, crepitation, synovial hypertrophy.
Late:
Valgus Deformity.
Instability, tendon rupture.
Path #: from the disease and drugs.
Bouchard’s nodules, Swan neck , Boutonniere, Z-thumb, fingers ulnar
deviation, wrist radio-volar deviation, valgus knee, valgus feet, clawed toes,
atlanto-axial subluxation
Types of presentations:
• Palendromic: starts intermittent episodes of multi joint affection Æ evolve to classic
• Systemic: severe form é visceral affection
• Monoarticular: usually knee. Also, may present as tenosynovitis or CT$
• Myalgic: as fibromyalgia rheumatica but with +ve RF

Blood:
1]. . ESR, CRP
2]. RF +ve in 80%, ANA 30%
3]. ACCP (anti Cyclic Cetrolinated Peptide): 97% early +ve in RA even in seronegative RA
4]. anemia: ð abnormal erythropoiesis, and chronic blood loss from analgesic gastritis
5]. WBC: Normal or (if suspect Felty)
6]. Complement
Synovial biopsy & fluid:

7]. Biopsy: is non specific to RA
8]. Fluid: ptn, C, glucose / poor clot / RA cells & PNL
PXR: LARSEN - DALE RADIOLOGIC INDEX

1- Stage I: juxta-articular osteopenia
2- Stage II: Narrow joint space (usually bilateral, symmetrical, concentric ± protrosio)
3- Stage III: Bone erosion of the head near the neck + bone cysts
4- Stage IV: Deformity (don’t forget the cervical PXR)
• Other complications: AVN, fracture neck
DDx:
9]. Seronegative: SLE, Still’s
10]. AS: spondarthropathy
11]. Reiter’s: Conjunctivits, urethritis, Arthritis
12]. Gout & CPPD: crystals
13]. OA: DIP affection, osteophytes
14]. Polymyalgia rheumatica: pelvic, and pectoral weakness, and aching, +ve steroid test
15]. Sarcoidosis: Erythema nodosum, Hilar LN, +ve Kveim test
Stop the Synovitis:
o Rest.
o DMAR Drugs (Disease Modifying Anti-Rheumatic) - Pyramid Approach = NSAIDs -
antimalarials - sulphasalazine – gold – MTX – D-penicillamine - Azathioprine –
Leflunomide + low dose steroids.
o Synovectomy - chemical, irradiation, surgical.
Prevent Deformity:
o Splintage.
o Physiotherapy.
o Tendon repairs & joint stabilization.
Reconstruct (start é knee if > 45º flexion deformity):
o Arthroplasty is the gold standard.
o Osteotomy not done:
Doesn’t remove the cartilage ώ is a source of
inflammation.
RA is concentric & no healthy cartilage.
o Arthrodesis not to be done (bilateral).
Rehabilitate & keep moving:
o Occupational therapists - aids, support.
o Physiotherapy.

• At Onset: NSAID, exercise.

• Early: NSAID, Steroids, DMD, local injections, physiotherapy, Rest and splitage.
• Erosive: DMD, splintage, operative (synovectomy, tendon repair, joint stabilization).
• Late: Reconstructive arthroplasty.
Problems é surgery:
1- Bilateral knee involvement
2- Ipsilateral hip involvement ..................................start é knee if flexion def >45º start é it
3- UL affection ..............................................................needed for PWB
4- Infections ...................................................................scan for oral, UTI, skin before surgery
5- Bad general condition & systemic disease
6- Cortisone therapy ..................................................need to the dose preop
7- Atlantoaxial subluxation .....................................difficult intubation
8- Femoral #s .................................................................be gentle & ready
9- Loosening .................................................................Cemented or Hybrid are favored
Drugs Details:
Drug Mechanism A/E
NSAIDs PG synthesis Æ pain and inflammation Gastric Upset
Leflunomide DiHydro-Orotate Dehydrogenase Æ T-cell prolif
Complications:
1]. Fixed Deformities.
2]. Joint Rupture.
3]. Infection.
4]. Spinal cord compression.
5]. PN compression.
6]. Vasculitis.
7]. Amyloidosis, proteinuria.
8]. Progressive RF.
Poor prognostic signs:

1]. Very high RF.
2]. Peri-articular erosions.
3]. Nodules.
4]. Muscle wasting.
5]. Joint contractures.
6]. Vasculitis.
Prognosis:
1]. 10% improve after first attack of synovitis.
2]. 60% have remissions & exacerbations.
3]. 20% have severe joint erosions requiring multiple operations.
4]. 10% become completely disabled.

Prutrosio Acetabuli
Ætiology:
[1]. Idiopathic (young female bilateral)= Otto pelvis = Arthrokatadysis
[2]. 2ry:
1]. Congenital: Marfan syndrome.
2]. Tauma.
3]. Infection.
4]. Inflammatory: RA & Ankylosing spondylitis.
5]. Metabolic bone disease:
Osteomalacia & Rickets.
Osteoporosis.
Paget’s disease.
Pathology:
• Probably it results from remodeling of a weak medial wall after repeated stress #s.
• In 1ry cases medial displacement continue till the GT impinge on the acetabular rim Æ the otto
stops and the ossification of the medial wall begins (N.B. healing ώ is rare in 2ry prutrosio)
Clinically: ...................................................Usually asymptomatic
• PAINFUL LIMP as OA develops.
• ROM especially abduction.
• FLEXION DEFORMITY Æ lordosis.
• PR examination Æ lateral globular mass over the rectal wall.
Radiologically:
1]. Medial intrapelvic bluge of the acetabulum ± head erosion.
2]. WIBERG CE angle > 40º.
3]. ALTERED TEAR DROP (formed of medial acet wall & quadrilateral plate).
4]. BROKEN KÖHLER line (ilioischial line); >1-3mm in ♂ / >3-6mm in ♀.
RAMOS ♂mm ♀ CHARNELY & GARZA OVERGAARD (tear drop)
Mild <8 <12 <5mm Closed.
Moderate 8-12 12-18 5-15 Crossed.
Severe >12 >18 >15 Reversed.
5]. BROKEN ILIOPECTINEAL line.
6]. RANAWAT ∆ :
o Pelvic height = the distance bet the 2 parallel horizontal lines drawn at the levels of
the ischial tuberosities and the iliac crests.
o Point (1) located 5 mm med to the intersection between Shenton’s (5) and Kohler’s (4).
o Point (2) is located above point 1, at a distance = 1/5 of the pelvic height.
o Point (3) is located medial to point (2) by the same distance bet 1 & 2.
o The isosceles bet 1, 2, 3 locates the normal acetabulum, é the line 2-3 being the
sourcil.
Treatment
Conservative:
1]. Protective WB
2]. Steroid, NSAIDs, heat
3]. ttt the cause
Surgical: If advanced OA or progressive (1ry)
4]. Valgus trochanteric osteotomy: pain & progression only; but does not ROM.
5]. Cup arthroplasty: temporary and needs thick medial wall.
6]. Arthrodesis: in young unilateral cases.
7]. Bone Transplantation: bone graft is fixed to the floor of the acetabulum till THR.
8]. Wire mesh: placed over the transplanted BG.
9]. THR.

Transient Synovitis of the Hip
• It is the most common cause of hip pain in children 2-12y
• More common in males
Ætiology
1]. Viral infection: (usually preceded by sore throat).
2]. Allergic hypersensitivity to septic focus in the body.
3]. Trauma.
Clinically
• Normal temperature.
• Acute PAIN radiating to the knee and ant thigh.
• LIMPING ± inability to WB.
• ROM especially (Abduction IR).
• Ms SPASM (flexors and adductors).
• Local TENDERNESS.
Investigations
PXR
1]. NAD.
2]. ± joint space .
3]. ± LATERAL HEAD DISPLACEMENT < 2mm (if > 4mm suspect PERTHES’).
US
• Effusion and thick capsule.
• Aspirate the effusion to exclude septic arthritis.
99m
Tc-HDP only to rule out Perthes’.
Lab
• Normal WBC.
• ESR.
• -ve culture.
DDx
• By exclusion of Perthes’, TB, Septic, RA
Treatment
• Bed rest + light traction usually Æ complete recovery in most of the cases.
• If severe symptoms & effusion on US aspirate the effusion for relief and to avoid AVN.
• Once ms spasm disappears Æ AROM & PWB.
• Follow up to 3mo by US & PXR Æ if persistent lateral displacement Abduction splint even if
there is no evidence of Perthes’.
ggggggbiiiiii
CALCIFIED TENDONITIS OF THE HIP
• Amorphous Ca deposition in the tendon of:
o Gluteus medius lateral to the GT.
o Gluteus minimus superior to the capsule of the hip joint.
Clinically:
• Painful Limping.
• Ms spasm.
PXR:
• Cloudy opacity on the soft tissue.
ttt: Heat & rest & NSAID if persists Æ excision.


Coxa Saltans
= SNAPPING HIP
•Audible and felt or even visible snap made when a tense fascial band catches as it slides over
the superior margin of the GT as the hip is flexed add or IR.
Ætiology
1]. External...................................GT é soft tissue around.
2]. Internal....................................Iliopsoas tendon é the structures behind it (e.g. bursa).
3]. Intra articular ........................ Synovial chondromatosis.
o Loose bodies.
o Labral tears or fracture fragments.
Pathology (of external)
• The band consist of the thickened posterior border of the ITB.
• Anterior border of the gluteus maximus near its insertion.
Clinically
• The snap can be produced voluntarily and painless.
• Involuntary, painful, and habitual.
Treatment
1]. External...................................Z-plasty of the ITB é local anaesthesia PWB and wide gait 6wk.
2]. Internal ...................................Z-Plasty of the ilio psoas tendon.
3]. Intraarticular ........................ttt the cause.
ggggggbiiiiii
Hip Bursitis.
Introduction
• 18 bursae are found around the hip.
• Only 3 are important: trochanteric, iliopectineal, ischiogluteal.
• Bursitis are usually due to overuse & excessive pressure & subsides é rest, heat.
Intertrochanteric Bursa
• Between the GT and the gluteus maximus.
• Pain é flexion IR.
• ttt: if septic excision & drainage.
Iliopectineal Bursa
• it is the largest bursa around the hip & 10% communicate é the hip joint.
• between the iliopsoas and the iliopectineal eminence.
1]. Pain & tenderness over the femoral ∆.
2]. Pain may radiate along the femoral n. to the anterior aspect of the thigh.
3]. Coxa saltans.
Ischio-Gluteal bursa
• Over the ischeal tuberosity.
• Inflamed in occupations é prolonged sitting (e.g. tailors).
• May produce sciatica.
• ttt: avoid prolonged sitting or excision.


Proximal Femoral & Pelvic Osteotomies
Definition:
• Osteotomy is an elective surgical procedure in ώ the bone is cut & realigned in a new position to
alter a disease process or to create a new favorable articulating surface, moving the abnormal
area away from the weight bearing axis.
• = reduce point loading & improve congruity.
• This can be achieved by either performing a proximal femoral or pelvic osteotomy (or both).
• Proximal femoral osteotomy blood flow to the femoral head & neck & venous drainage.
• For early disease results of 80-90% relief of pain.
• Success rates = 70% over 11 years follow-up.
• However, conversion to THR can be difficult due to alignment of femur & metalwork which can
Be difficult to remove.
Indications
1]. Reserved for young patients with advanced degenerative changes in whom THR is not wise.
2]. Non-union of a femoral neck fracture.
3]. Dysplasia (varus osteotomy).
4]. Post-Perthes hinge abduction (valgus extension osteotomy).
5]. SCFE (flexion osteotomy).
6]. AVN (flexion osteotomy).
7]. Idiopathic protrusio (valgus extension osteotomy).
Clinical
• Pain in certain hip positions only (e.g. Adduction WBing)
• Arc of Movement - which part of the arc is painful.
• Leg lengths (effect of FFD).
Planning
• Careful pre-operative planning required to find the position of LEAST PAIN & CONGRUENT.
• For varus osteotomy must have >15º ABDUCTION preop.
• For Valgus osteotomy must have >15º ADDUCTION preop.
• AP and lateral X-rays are taken in adduction/abduction.
• BERNE or FAUX PROFILE view (WB + 25º body tilt) - shows anterior uncovering.
• CT or MR can give additional information.
• Best results are in young, non obese patients with a good range of motion (minimum 90º
Flexion, 15º abduction/adduction).
• Femoral osteotomy may distort the anatomy which may jeopardise a future THR.
Need to determine:
• 1. The amount & direction of correction.
• 2. Choice of implant.
Varus Osteotomy
• Generally indicated where lateral subluxation is associated with coxa valga.
• Require good range of abduction prior to surgery.
• Relaxes adductors, abductors & flexors.
Disadv- shortens leg.
• Must have >15deg. Abduction preop.
Valgus Osteotomy
Indic:
1]. 1. Uncovered head made worse by abducting hip.
2]. 2. Deformed head with lateral osteophyte (post Perthes).
3]. 3. Fixed adduction deformity.
• Can add lat displacement of GT to hip joint reaction forces.
• Must have >15deg. Adduction preop.


C
Contraind
dications::
1]. Stiff.
2]. Obese.
3
3]. Atrophiic inflammaatory feature
es.
4
4]. Gross narrowing
n with sclero
osis & no
normal joint surfacce.
Arthroplasty types:
1]. Osteot
[1 tomy arthhroplasty.
2]. Interpo
[2 osition arrthroplasty
ty.
3]. Reconstructive arthropla
[3 a asty.
4]. Head replaceme
[4 r ent arthro
oplasty.
5]. Total hip
[5 h arthro oplasty.
M
McMur
rray O
Osteo
otomy
y
I
n the operration is orriginally de
escribed by MCMURRA AY (1935) the femur
was divide ed just belo
ow the GT and the liimb is held d in a POP spica, the
operation then
t modiffied using medial
m disp
placement ofo the shaftt fragment
med dially not more
m than ¼ of the sha aft diameteer using a na
ail plate it was
w initially
fixed by McMu urray by Jew
wett nail pla
ate.
Upper Femorral
U
Osteo
otomie
es
For
For F
For For For For weight
w
defo
ormity
Containment exp
posure Unloading compression
n redistrribution
corre
ection
V
Varus & Medializati P
Pelvic
D
Derotation Varus F
Flexion Chevron Varus Va
algus Valg
gization
valgus o
on su
upport
LLD:
DDH DDH Dunn Wagner Sugioka Perthes Wagner &
W S
Sarmiento M
McMurray MccMurray
IM
ossteotomy
D
Diamon
Perthes Krammer Protrusio Broden
Hughston
H
Southwick Pauwel's

Arthrodesis
Definition
• Arthrodesis is operative induction of bony Ankylosis.
Indications
1]. To halt disease as in tuberculosis.
2]. To relieve pain: In osteoarthritis and other forms of chronic arthritis, particularly when the painful joint
is already stiff.
3]. To provide stability after poliomyelitis, especially at the shoulder, wrist and foot.
4]. For permanent correction of deformity: As in club foot above the age of 12 y and in scoliosis.
Methods
• Arthrodesis may be intra-articular, extra-articular, or the two methods may be combined.
[1]. INTRA-ARTICULAR: The joint is opened, the articular surfaces excised as in tuberculous arthritis.
[2]. EXTRA-ARTICU1AR: Union between healthy bony surfaces outside the joint is by a BG which
bypasses the joint. PSF between, the arches of the vertebrae is an example of extra-articular
arthrodesis.
[3]. COMBINATION is often done. After excision of the articular cartilage, BG are placed across the
joint.
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Optimum Position For Arthrodesis
JOINT POSITION REMARKS

SHOULDER Abduction ........45° More abduction for children because they have range of
Flexion ................30° scapulothoracic movement. Flexion keeps the humerus in
IR ..........................45°
line é the scapula. Rotation is calculated from the
horizontal plane while the shoulder is in abduction. The
position ensures hand to face position
ELBOW Mid Flexion Position is modified for to the patient’s job e.g.90° for a
clerk, 60° for a laborer. The radio-ulnar joints is in mid
prone or pronated for writing.
WRIST Rt dorsifiexionl5°. Slight dorsiflexion gives a better grip. In ♀ the wrist is
Lt: 0-10° flex arthrodesed straight for better cosmetic appearance.
FINGERS IP Mid fiexion Mid flexion is the position of lunction for the finger joints.
SPINE Normal curves are Flexion and lordosis of the lumbar spine are avoided
maintained. because they predispose to low back pain.
HIP Flexion ............... 25º. Flexion is one degree for each year of age, and little more
Abduction ........ 0º. up to 30º for comfortable sitting. Flexion permits sitting but
Neutral rotation. excessive fiexion strains the lumbar spine. More abduction
up to 2° is allowed when there is shortening. Excessive
abduction strains the knee and spine.
KNEE 0-10º Full extension is the position of stability. Climbing stairs is
easier when there is 10° flexion.
ANKLE ♂: right angle. Plantar-flexion in women is preferred for wearing high
♀: 10 plantar flex heels.
SUBTALAR, & Neutral position Valgus or varus deformity cause pain in the ankle and foot.
MID TARSAL
TOES Straight Straight toes are less likely to cause callositics.

Hip Arthrodesis
• Fusion (ANKYLOSIS) can occur spontaneously following childhood sepsis, following ORIF of
acetabular fractures (secondary to heterotopic bone) and in ankylosing spondylitis
• Unpopular as leads to increased stress on other hip and ipsilateral knee.
• Oxygen consumption 32% greater than normal.
• Average walking speed 84% of normal.
Indication
• Young patient with unilateral hip disease (usually post-traumatic).
• Contra-lateral hip, both knees and spine must all be normal.
Technique
• Anterior or posterior approach inorder to dislocate the hip and to remove the joint surfaces
[1]. AO Cobra Plate: stable but disrupts abductors
[2]. Trans-articular sliding hip screw
• lag screw is inserted across the joint and just superior to the dome of the acetabulum
• disadvantage of this technique includes poor fixation (due to large lever arm and the resulting
torque on the lever arm) and need for postoperative hip spica casting.
• Some authors advocate supra-acetabular osteotomy or subtrochanteric osteotomy for improved
positioning.
Complications
[1]. Non-union.
[2]. Malunion.
[3]. OA of hip, spine, knee.
[4]. Instability of ipsilateral knee.
Prognosis
• All are able to work.
• 78% satisfied with the arthrodesis.
• 57% low back pain to some degree - onset ~ 20 years.
• 45% have ipsilateral knee discomfort.
• 17% complain of pain in the contra-lateral hip.
• 13% required conversion to arthroplasty for relief of back/knee pain.
Revision to THR gives relief of back pain but not relief of knee pain.
• THR for back or knee pain - all had marked relief of back pain and 1/2 had relief of knee pain
• Those with fusion in slight adduction have a better gait, less problems with back pain and with
knee pain than those fused in slight abduction
Optimal position
• 25º FLEXION.
• NEUTRAL – 5º EXTERNAL ROTATION.
• NEUTRAL OR SLIGHT ADDUCTION.
• AVOID ABDUCTION AND INTERNAL ROTATION.

Hip Arthroplasty Basics
•Hip is affected by 3 forces:
[1]. 1. The Body Weight “BW” in front of S2
[2]. 2. The Abductor force = 2 times BW
[3]. 3. The Total Femoral Head force = 3 times BW in stance
• These forces affect the hip joint through 2 lever arms (the abd. & BW lever arms) which meet in
the “HIP CENTRE OF ROTATION” which is nearly the center of the femoral head which is
opposite to the tip of the greater trochanter. It is located by many methods:
[1]. RANAWAT ∆ METHOD (in bilateral affection).
[2]. TEAR DROP METHOD (in unilateral case); tear drop is u-shaped PXR finding & formed of:
Straight medial limb = the antero-inferior margin of the quadrilateral plate.
Curved lateral limb = the medial wall of acetabular fossa.
Floor = acetabular notch.
• “US” line at the lower border of both tear drops.
• “Y” = vertical migration = distance bet “HC” & “US”.
• “X” = horiz migration = bet “HC” & Kohler line.
• Compare with the normal side.
• Stress and strain distribution in intact acetabulum.
The medial wall stresses are mild tensile.
The lateral wall stresses are mild compressive ð the
bending forces of the abductors.
• After THR, peak stresses ð changes in the load transmission from the cortical shell of the
innominate bone and the subchondral bone to the acetabular component and the cement. To
decrease peak stresses:
[1]. Retention of the subchondral bone.
[2]. Keeping the hip center within 5 mm from the true center.
[3]. Stiff components:
Cementless cup.
Cemented cup with metal packing.
Cemented cup with increased polyethylene thickness.
Cement mantle evenly 2:3 mm to avoid “buttoming – out” phenomenon.
Hip Quadrants:
1]. The sciatic n. & superior gluteal n. & v. course opposite the postero-superior quadrant.
2]. The inferior gluteal & internal pudendal are opposite the post inferior quadrant.
•Bone depth in anterior quadrants is shallow.
•Bone depth in posterior quadrants = 25 mm.
•Bone depth in central regions > 25mm.
•Screws & anchoring holes can be placed safely in these zones. In addition, the sciatic n. can be
gently displaced during screw placement Æ its injury.
High Hip Centre:
• HHC quadrants are formed by drawing a line from ASIS through the
new center & the second line drawn to the first.
• The peripheral halves of the posterior superior & posterior inferior
quadrants have the best bone stock = relatively safe for transacetabular
screw placement.
• The ant superior & inferior HHC quadrants & the central half of the
post superior & inferior quadrants, should be avoided, as it has many
negative factors (better avoided):
[1]. Less bone stalk.
[2]. Close to intra-pelvic structures é few protective musculature on the inner wall of the pelvis.
[3]. More lateral = more body wt lever arm.
[4]. Short abductor lever arm.


Hip Arthroplasty
1. Rationale
•Pain relief
•Restoration of normal limb alignment
•Restoration of a functional range of motion.
Before doing THR think about:
1- Osteotomy.
2- Interposition Arthroplasty (ometoplasty).
3- Reconstructive Arthroplasty.
4- Hemi-arthroplasty.
5- Bipolar arthroplasty.
6- Trapdoor procedure for AVN.
Before doing THR:
• wt.
• Try NSAID.
• Try walking aids.
• Try activity modification.
Choosing a type of THR
• Cemented vs uncemented
Acetabulum
• Poor results with cemented acetabulae
• How to get good results with cemented acetabulum:
1]. Preparation reamer skirt.
2]. Containment and bone graft.
3]. Pressurization.
4]. Polyethylene - x link; aging; thickness; low frictional torque
• Types of uncemented - not as bone conserving as you might think
• Screws - safe zone; liner wear and snap fit; risk of backside wear
Head
• size - reasons for small and large
• material steel or ceramic
• consequences of modularity
Stem
• Two types; cemented & cementless.
• Nature of loosening process; loosening and osteolysis macrophages etc wear; size of particles
and source. Third body wear. Nature of scratches etc gruen zones
• Proximal vs distal loading in femoral stems detection of loosening possible definite loosening; rsa
how to institute a follow up system
Cement
• Viscosity; high or low viscosity, according to cementing technique.
• With or without AB.

Hip Disorde
[H ers] Page | 681

2. Cho
oosin
ng Ty
ype O
Of THR
The choice of prosthesis depends on:
1]. Dorr inddex: > 0.75 ......................................... ce emented
2]. Bone sttalk: poor bo one stalk ....................... ce emented
3
3]. Age: oldd age ..................................................... ce
emented
4
4]. Prostheesis type, surrgical experrience é the e prosthesis..
DORR & SPOTORNO INDEX

• The prroximal femmur has a trumpet-likke or cham mpagne-
fluted configurration. B
Because these different
d
configuurations afffect the ability of the porous coa ating of
to be ad
dequately apposed
a to
o subchond dral bone.
• Spotorrno cortica al index can

n give an id dea about femoral
bone sttalk or femo
oral stenosis (2.5 : 3).
• The Doorr index is a ratio of th

he canal diiameter at the
t level
of the lesser troch
hanter to th he canal diameter
d at a point
10 cm distal:
d
Class A
[1]. < 0.5 .........................Invertted champa agne Æ cem menless
Class B
[2]. 0
0.5-0.75 ...................thinn
ning of the posterior
p co
ortex
Class C
[3]. > 0.75 .......................stove epipe Æ cemmented
Clinical findings
1]. Acetabulum:
• The aim
m of the cup
p is to orien
ntate the TH
HR as close to the
anatom
mical as posssible.
• Cemennt on the socket
s doees very we ell for abou
ut a decad de. Then, in ncreasinglyy, there's more
m
looseniing and hig
gher inciden
nce of re-op
peration. (H
Harris)
• UNCEMMENTED CUP P: HAC threeaded cup have
h prove
ed better tha
an press-fit & screw fixxed cup.
2]. Femoral Componen
C nt:
• CEMENNTED FEMOR
RAL stems have
h proved
d more relia
able than uncemented
u d.
Findings:
• Inferiorr results of uncemente
u ed uncoated d press-fit sttems and uncoated
u th
hreaded cup ps
• Good results of hydroxy yapatite(ha))-coated stems s andd cups, a and of ciircumferenttially
porouscoated stem ms and porrous-coated d cups
• Only smmall differen nces were observed
o am
mong cemented prossthesis bran nds
• Inferiorr results for the Bonelooc cement and a the low w-viscosity cement
c CMW3
• A comb bination of antibiotic-ccontaining high viscossity cement and system mic antibiottic, gave
fewer revisions
r du
ue to infection and ase eptic loosen ning than other
o proph hylaxis regim
mens
• Revision n for aseptiic looseningg was more e é HA-coatted cups co ompared to o the cemen nted cups
• 62 diffe
erent THR prosthesis
p b
being Identiified
• There were
w reportts of 5YSR reesults in pe
eer-reviewed d journals for
f only eight implantss.
• For threee implantss (Charnley, y, Stanmore and Mullerr), there we ere ten-yearr survival re
esults
• For two o (Charnleyy and Stanm more) 15-ye ear survival results
• Only on ne (Charnle ey) had 20-y-year resultss
• The gre eatest volum me of evideence is availlable for the e Charnley,, but the Chharnley dessign has
change ed, and it is not clear how
h much ofo the evide ence is relevvant to thee current deesign.
• CONCER RN TO PATIE ENTS, PARTICCULARLY PAIIN AND FUNC CTION, AND NOT SOLELY Y ON REVISIOON
SURGER RY

3. Indications, Preop management
Indications
1]. OA (primary or secondary).
2]. Inflammatory arthritis.
3]. Osteonecrosis.
4]. Fractures.
5]. Failed reconstructions.
6]. Tumors.
7]. Incapacitating pain from the hip with limited ambulation, night pain, severe quality of life limitation
despite conservative therapy.
8]. Conservative ttt tried 1st: wt, NSAIDS, walking stick in contralateral hand.
Contraindications
Absolute:
• Active Infection.
Relative:
[1]. Preexisting medical problems which have not been optimised.
[2]. Skeletally immature.
[3]. Non ambulators.
[4]. Neurotrophic joint.
[5]. Abductor muscle loss.
[6]. Progressive neurological disease.
Preop assessment
• Ensure that pain is from the hip, not referred from the back etc.
• Medical evaluation.
• Dental evaluation.
• FBC, U+Es, MSU.
• Consider preop donation of blood.
• Nasal and perineal swabs for MRSA.
• Preop Xrays, AP pelvis, AP view centred at the hip, with leg internally rotated to 15º (allows
templating by eliminating femoral anteversion). Lateral film.
• Planning of surgical approach and templating.
Prevention of infection
• Shave at the last minute.
• Intravenous antibiotic, 1.5g IV cefuroxime, to be continued for 24-48 hrs post op.
• Wilson and Salvati found reduction of infection from 11% to 1%.
• infection to 0.1% with combination of clean air sytems, body exhaust suits and antibiotics. The
antibiotics decreased the risk of sepsis to the greatest extent.

Surgical approach
• Mainly a matter of personal preference and training
Direct Lateral Approach To The Hip
• In view of the increasing popularity of the direct lateral
approach to the hip joint for hemi- or total hip arthroplasty,
the location of the superior gluteal nerve (SGN) was
studied. This nerve is in danger when using a transgluteal
incision. In 20 embalmed specimens the relation of the SGN
to the tip of the greater trochanter (GT) was studied as well
as the relation to the iliac crest. For this purpose
macroscopy, microscopy and CT were used. In 13 hips a so-
called most inferior branch was found at an average of 1
cm distal to the inferior branch, the main trunk of the nerve.
There was substantial variation in the course of both the
inferior and the most inferior branch of the SGN. In order to
prevent nerve damage, proximal extension of the
transgluteal incision should be limited to 3 cm cranial to GT.
Furthermore the incision has to be confined to the distal
one third of the distance GT-iliac crest. In tall people extra
care should be taken.
Charnley approach
• Patient supine
• Slightly curved skin incision centred over greater trochanter
beginning at level of ASIS
• Fasci lata incised for whole length of incision
• Cholecystectomy forceps placed into joint and pushed
from anterior to posterior
• Gigli saw used to perform trochanteric osteotomy, with
or without a pin to create a chevron
• Trochanteric wiring or Dall Miles cable grip to refix
trochanter
Advantages according to its advocates Disadvantages according to its opponents

Easy to dislocate hip Increased blood loss
Good exposure of acetabulum Longer operating time
Less penetrations in reaming the femoral canal Technical difficulty é fixation of the trochanter
Cement can be inserted easily Trochanteric non union Æ trendelenburg gait
Useful in primary THR when anatomy distorted Wire breakage
Better femoral component alignment
Can be used in primary and revision surgery Trochanteric bursitis
Hardinge direct lateral approach
• Patient supine or in lateral position.
• Slightly curved skin incision centred over greater trochanter.
• Incise fascia lata for whole length of incision.
• Incise gluteus medius from the greater trochanter, leaving posterior ½ to 2/3 attached.
• Split the vastus lateralis distally and extend proximally through the line of fibres of gluteus medius
(not more than 3cm to avoid hitting superior gluteal nerve).
• Detach gluteus minimus from its insertion & open the capsule with a T shaped incision.
• Closure can include sutures between bone and capsule through drill holes.
• Main disadvantage is potential damage to superior gluteal nerve and the abductors.
• Not always suitable for revision surgery.

Dall variation of the Hardinge approach

• Involves taking a sliver of bone of the greater
trochanter with the muscle

Posterolateral approach (Moore or Southern)

• Patient in lateral position
• Slightly curved skin incision centred over posterior
aspect of the greater trochanter from level of anterior
superior iliac spine to 10cm distal to greater trochanter
• Divide the fascia lata in line with the skin incision at the level of the greater trochanter
• Bluntly split the gluteus maximus proximally in the line of its fibres by blunt dissection
• Retract gluteus maximus and fascia lata to expose the
posterior aspect of the hip with overlying external
rotators and sciatic nerve
• Internally rotate the hip to put the external rotators on
stretch and place stay sutures into piriformis and
obturator internus
• Divide the external rotators just before they inset
into the greater trochanter and fold them back
over the sciatic n.
• Quadratus femoris does not normally need to be
divided
• Incise capsule é a Longitudinal or T shaped
incision
• Dislocate hip by IR

Advantages (by advocates) Disadvantages (by opponents)

Avoids cutting the abductors risk of posterior dislocation ? ð difficult orientation
Avoids trochanteric osteotomy Needs to be done in lateral position, so
Can be used for 1ry and revision surgery Anatomic orientation can be difficult


Anterolateral approach of Watson-Jones

• Exploits the internervous plane between tensor fascia lata and gluteus medius (actually both are
supplied by the superior gluteal nerve but the supply to TFL enters very high up)
• Patient supine
• 15cm straight incision centred over tip of greater trochanter
• Divide fascia lata proximally heading anteriorly and distally along the line of the femur

• Dissect the few fibres of glueus medius from the anterior flap of the fascia lata.
• Locate the interval between the TFL and gluteus medius with the fingers.
• Retract gluteus medius and minimus and externally rotate the hip to stretch capsule.
• Incise the origin of vastus lateralis along its insertion ridge.
• Lift off the fat pad overlying the hip capsule.
• Partial resection of gluteus medius tendon posteriorly.
• Detach the reflected head of the rectus femoris from the joint capsule to expose the anterior rim
of the actebulum (with the hip flexed).
• H shaped incision in the capsule.


4. Femoral component
Design (Charnley, Muller, Exeter, Furlong, C-stem)
1- Cemented:
o Polished.
o Textured (Matte): mechanical interlock; by PMMA pressurization into the suface spaces.
o PMMA coated: depend on chemical & mechanical interlock.
2- Cementless:
o Press fit ............................. (for bone macrointerlock):
Surface ridging.
Anatomical bow.
Iso-elastic hip (condemned).
o Porous coated ................ (surface pores for microinterlock):
According to thickness.
According to extent: extensive, circumferential, partial.
According to processing: sintering, diffusion, plasma spray.
According to material; metal, ceramic, carbon, polymers.
o HA Coated: bone ingrowth enhances to the double.
o HA-TCP coated: for osteo-induction & osteo-conduction as well.
3- Modular stems: Calcar replacement, tumor & limb salvage hips.
4- Dysplastic stems: small, straight, with 22mm head.
The Stem has 3 offsets:
7- Medial offset = OFFSET.
8- Vertical offset = height (from the head centre of lesser troch).
9- Anterior offset = version.
Abductor Lever Arm by:
1- The medial offset.
2- Centralization of the femoral head.
3- Lateral displacement trochanteric osteotomy. Now THR are done éout trochanteric osteotomy
(Heterotopic ossification) & minimal reaming (preserve the anatomy).
Offset Medial stem offset is the distance from the head center through the axis of the stem.
• offset:
1- Abductor lever arm Æ abductor force Æ JFR.
2- Stress of medial cement mantle Æ loosening (Charnley offset of his design).
3- Stress & bending moment at neck–stem junction Æ Broken Prosthesis.
4- Stress at the stem tip Æ calcar pivot “Wind Shield” effect and loosening.
5- Rotational micromotion Æ bone in-growth in cementless stems Æ loosening.
• offset:
1- abductor moment arm Æ abductors do more power to perform.
2- JRF Æ acetabular loosening & polyethylene wear.
3- incidence of limp.
4- Laxity in the abductor musculature Æ instability.
5- impingement.
• Offset is altered by:
1- Designs é modular heads 8-12mm.
2- Designs é enhanced offset (127º & medial take off point).
3- High Level of the femoral neck osteotomy (neck take off point) .... offset.
4- Varus insertion of the femoral component ............................................ offset.
5- Depth of implant insertion into the canal .......................................... offset.
• This additional surgical flexibility is not for cementless THR, as depth & orientation is
determined by stem fit éin the femoral metaphysis rather than by the neck osteotomy level.
• A larger-size component may be considered if the offset.
• Adequate cement mantle must be assured (2-mm distal, 4mm proximal mantle)

Height:
• Normally varus hips:
o Has offset & ht
o To normalize the offset, this may lead to lengthening
o This is overcome by enhanced offset designs
• Valgus hips:
o Ht & offset
o The opposite …
Stem length:
• Originally 13 cm
• Long stems:
o varus occurrence
o ttt periprosthetic #
o Tip engage anteriorly
o May Perforate
o Inadequate cement
The neck resection should be planned to utilize a neck length without a “skirt”:
1- Tends to impinge at extremes of motion.
2- ROM
3- PE wear
4- instability.
• Most implant systems offer four or five head choices, of which the first two or three do not have a
skirt or extension. Generally, low neck cuts are unforgiven and necessitates the usage of extra
long neck which is typically comes é a skirt. Alternatively, the neck can be re-cut.
Version:
• Normally there is an angle of 10-15º anteversion; and the aim is to restore this angle
• Retroversion ..................................................... Posterior dislocaion
• Anterversion ..................................................... Anterior dislocaion
Stem geomety:
1]. Triangular to provide rotational stability.
2]. Round edges to avoid stress risers.
3]. Longitudinal taper allow for subsidence to maintain cement mantle compression.
4]. Medial taper = broader lat border to maintain cement mantle compression.
rd
5]. Some designs (C-stem) provide a 3 posterior taper for the same reason.
6]. Polishing the particle load generated by the implant Æ the 3rd body wear.
7]. Textured (matte) stems may provide:
Advantages Disadvantages
large surface for Load transfer But generate particles
Better chance micro-interlock Texture act as stress risers
compression stresses & shear stresses
Cementing of a cementless porous stem
• Usually end with difficult removal, fat embolism, defective cement mantle.
Stress shielding
• Is the stress bypass after fixation from the less stiff bone to the more stiff implant
• Stress shielding by:
1]. Modulus of elasticity (stiffness) e.g. titanium
2]. Stem diameter; as stiffness dr4 diameter > 13.5mm Æ stiffness.
3]. stem length
4]. design stiffness (cementless designs stiffness by ridges & splitting even é large dr)
5]. Extensive porous coating especially é large stems
6]. Collared stems Æ axial loading upon the medial cortex Æ stress shielding
• In cementless stems we need to the press fit, basically by stem diameter é inadvertent in
stiffness & stress shielding; so the solution is to alter the extent of the coating, modulus, design.

Head and Neck diameter:
Small Head 22mm Large Head 32mm

Advantages: • frictional torque • Theoretical more stable
• stresses on acetabulum • ROM
Disadvantages: • linear wear • volumetric wear
• dislocation
• creep
Optimal size for head 26mm (? no clinical proof);
• penetration and volumetric wear
Materials
Stiffness (Lowest-Highest)
1- Bone
2- Titanium (Ti-6Al-4V)
3- Stainless steel
4- Cobalt chrome
5- Ceramic

Material Surface Hardness

1- Titanium (Ti-6Al-4V) 330
2- Cobalt-chrome alloy 400
3- Nitrogen ion-implanted Ti-6Al-4V 770
4- Zirconia 1430
Bearing Surfaces
STAINLESS STEEL
• Cheap, easily machinable to high level of surface finish
COBALT CHROME (VITALLIUM)
• Tough, highest level of surface finish possible with Co-Cr alloys
TITANIUM (TI-6AL-4V)
• Higher adhesive wear releasing Ti ions into the surrounding tissues, relatively "soft"
• Prevention of stress shielding because of closer elastic modulus to bone
NITROGEN ION-IMPLANTED TITANIUM (TI-6AL-4V)
• Superior surface finish available with harder surface to prevent excessive wear
CERAMIC (ZIRCONIA AND ALUMINA)
• Difficult to manufacture, brittle
• Actually less smooth than metal bearings
• Abrasion resistant (hardest bearing surface)
• wear ð frictional characteristics (<50% of metal on PE) and adhesive wear properties
ggggggbiiiiii
Collar
1]. Simply determine the level of the depth of the stem
2]. Pressurize the proximal medial cement while it hardens
But
1]. May prevent the useful cementless subsidance
2]. Collared stems claimed to have almost normal proximal strain Æ medial cortical stress shield
3]. May provide a fulcrum for distal toggling Æ loosening
4]. Radiolucent lines at Gruen Zones 2 & 7
Hip Disorde
[H ers] Page | 689

Centralizer (distal & proximal)

• Allow for
f due cem a around Æ areas of
mentation all o defective cement Æ cement breakage
Surface finish
• In Cemented stem ms texturingg, flutes, ridg
ges, groovees, slots, andd matte are e made to:
o Cementt bonding (cement
( deebonding usually occcur at ICI).
o Rotation nal instability.
o But when debonding strats Æ more debris Æ rapid d loosening g (e.g. mattte exter).
• The surrface finish of cementless designss has been discussed
d e
earlier.
• Data froom the Swe edish hip reegister show ws that the
ere is significcantly higher failure ra ates in stem
ms
with a rough
r surfa
ace finish co
ompared to o polished stems.
s
• The cha ange in the e Exeter stem from pollished to matt finish re esulted in a higher failu ure rate.
• Coating g the stem with
w PMMA A in order tot increase the
t bond between
b the compone ent and thee
cementt has also been
b shown n to be asso ociated with
h a much higher
h earlyy failure rate
e.
Biological bone ingrowth ώ occurs in 3 phases:

1]. In
nflammatoory osteoco onductive .......2wk (C CT invasion
n).
2]. Reparative
R ossificationn phase ...........6mo (W Woven bon ne).
3]. Remodeling
R g phase ..................................2y (lam
mellar bon
ne).
4]. Apposition
A al phase .................................>2y.

5. Cemented vs cementless
Macro-interlock:
• Rationale: Press fit gives immediate stability ð the shape matching.
• Types:
o Press fit using bowed stems.
o Rectangular proximal end.
o Surface ridging for bone macrointerlock.
Micro-Interlock:
1]. Porous coated
• Pre-requisites
o Immediate torsional and axial stability is needed i.e. <40 μm mico-motion
o Micro motion > 40 μm Æ fibrous stable interlock, which is fair result as well
o Intimate implant fit is needed to achieve bony micro-interlock
o Pore size of 100-400 μm is optimum for cellular invasion and calcification
• Types: (according to thickness, extent of coating, material, and manufacturing) see before
o Sintering ........................... Heating both.
o Diffusion bonding ......... Heating and pressurizing both(less heat).
o Plasma spray ................... Beads are heated & sprayed out of nozzle under pressure.
• Disadvantages:
o Titanium is notch sensitive (breaks if pores at the lateral stem).
o Anatomical stems may engage anteriorly Æ postop. thigh pain.
2]. HA Coating
• Many types present according to the manufacturing method:
1]. Plasma spraying. 2]. Sand Blasted. 3]. Ion sputtering.
4]. Electrophoretic deposition. 5]. Biomimetic method. 6]. Hot Isostatic Pressing.
• Plasma spray is prefered ............... doubles the bone ingrowth & surface on growth ~ 60-80%.
o HA particles are injected é high temperature (15,000º C) which solidify on contact
with the metal substrate.
o HA porosity of 150-400 μm is optimal for ingrowth.
o HA thickness of 50-75 μm is optimal (15μm of HA is lost in the 1st year).
o Thicker HA coatings Æ toughness and fatigue resistance.
o In-growth is greatest é cortical bone & UNPREDICTABLE WITH CANCELLOUS bone.
o If motion at the HA/bone interface is >50μm Æ fibrous tissue forms instead of bone.
o The ideal load transfer with cementless stems to prevent proximal stress shielding is
GRADUATED LOAD TRANSFER from proximal to distal, é the highest load is the proximal.
• Extensively coated stems >80% HA coating Æ proximal load transfer Æ proximal
stressshielding & osteolytic induced fractures.
• Proximally coated stems:
o Rely on biological fixation proximally + distal mechanical fixation.
o 1st generation ....................proximal porous coats + smooth distal stems Æ loosening.
o Recent designs ...................proximal third porous coating + grit blasted distal stem.
o Disadvantage is the incomplete seal Æ allows free passage of particulate wear debris.
POROUS COATED HA COATED

Time Slow Rapid
Bonding 6wk Half Double
In-Growth Amount Less More
Compatibility Less More
Hip Disorde
[H ers] Page | 691

Third body wear

• They thhought to arise
a from barium
b or zirconium pa articles relea
ased from tthe cementt.
• These substances
s are added to cement to make it radio-opaq
r ue.
• Cemen n cause 3rd
nt (PMMA) itself does not r
body wear.
• But it was
w proven n to be the PVC particcles released
d from the plastic cup p 2ry to we
ear is the mean
m
source of 3rd bodyy wear.
• Femora al loosening
g plateau at about 5y / when cup p loosening g continuess to .
Bipolar Hip arthroplasty
• was intrroduced as an interme ediate step between

b TH
HR & hemiarthroplasty.
• Consist of :
1- Stem
2- Metal head
h (22 or 32)
3- Metal cup
c
4- Plastic shell
• Advantages:
1- Better longevity
l fo
or the prosthhesis as the
e motion is distributed
d o
on two surffaces:
o Inner bearing: betwee en the head d and the PEE
o Outer bearring: betwee en the meta al cup and the
t acetabu ulum
2- Better longevity
l fo
or the acetabulum
3- Can be e converted to THR
4- The cen ntre of the cup
c rotation n is eccentric Æ when WB Æ rota ate externallly Æ head d
imping
gement on the
t PE & pro oduce bette er coverage e
• Disadva
antages:
1- After im
mplantation n it was foun
nd that afteer a while th
he motion iss mainly is outer
o bearin
ng


6. (UH
HMW
WPE) /
/ (HD
DPE)
Schematicc showing g the arrrangementt of
macromo olecules off polyethyylene and the
crystallitess of:
• HDPE (left).
(
• UHMW WPE (center).

• Cross-liinked UHM MWPE (righ ht).
• Made by
b low pressure O2-ca atalyzed add
dition polym
merization of ethylene
e, producing a low den
nsity
materia
al that is exttremely tou
ugh and duuctile.
Production methods:
1]. RAM EXTRUSION
E N - powder is compactted in a heated cylinder ................... poor qualitty & cheap
2]. SHEET T COMPRES SSION MO OULDING slo ow processiing .................................... better quality & costy
3
3]. ISOSTAATIC MOU ULDING colld compactiion Æ heat consolidation ............... isotropic & homogenous h s.
4
4]. DIRECT T COMPRE ESSION MO OULDING - is similar inn concept to sheet com mpression moulding,
m but
obvioussly on a much smaller scale.
s This enables
e high
her pressure es and quicker heat conduction to o
the cen
ntre of the moulding
m
Ad
dvvantages:
1]. Very loww surface teension Æ id deal for WB articulating
g surfaces.
2]. Low coefficient of friction.
3
3]. Low mo oisture adsoorption.
4
4]. High im
mpact streng gth.
5]. Tough.
6
6]. Ductile..
7]. Chemiccal resistancce.
8
8]. No obse erved toxiciity effects.
Disadvantages:
1]. UNACC CEPTABLE E CREEP ra ate for long term appliccations
2]. WEAR R
3
3]. Polyethhylene WEA AR DEBRIS S appears too play a rolee in implant loosening & osteolysiss
4
4]. DIFFIC CULT TO MACHINE
M b
because of its creep pro
operties.
5]. mall amountts of fluids Æ fatigue
Still mayy absorb sm e failure
6
6]. Inadequ uate contro ocessing Æ incomplete
ol of the pro i consolidatiion and “FU
USION DEFE ECTS” Æ pitting
and dellamination Æ stress rise ers Æ FATIG GUE cracks
Sterilization methods:
1- GAMM MA STERIILIZATION N:
• IMPRO OVES CRO OSS LINKIN NG resultin ng in a nettwork of HM MWPE, witth the pote ential beneffit of
increased strength h, thus incre
eased resisttance to weear.
• Causes CHAIN SC CISSION by b breaking chemical bonds
b Æ crreates reacttive free rad
dicals.
• Oxygen n diffuses into the ma aterial and
d reacts witth free radicals to cau use OXIDA ATION, which
w
leads to
o much sho orter molecular chains
• Air sterilization Æ initiates oxidative proc cess Æ mechanical
m properties Æ vol wear.
• O2 free e or inert (A
Argon or N2 2) Æ oxid dation that occurs durring steriliza
ation
• Raising the temp perature off the mate es the FREE HYDR
erial enable ROGEN RA ADICALS TO
CROSS SLINK WIT TH CARBO ON ATOM MS and crea ates a stronger PE.
• Shelf ag ging Æ oxid dation & fre
ee radical fo
ormation of insert, so VACUUM
V P
PACKING iss needed
2- ETHY YLENE OX XIDE STER RILISATIO ON: Does not
n cause oxidative
o deegradation n.
3- GAS PLASMA:
P Over the e lifetime ofo an impllant, polye ethylene b becomes sttiffer near the
surface
e, and therrefore, con ntact forcess will increaase with timme.
Thermoplassttic Prope errties: -
• Deform mation of po olyethylene e is dependent on tem mperature.
• Heat pressing
p altters the phhysical prop P Æ makkes the devvice more susceptible
perties of PE e for

fracture
e at the subbsurface jun ncture of heeat-press material
m and the bulk po olyethylenee.
Hip Disorde
[H ers] Page | 693

7. Cup
p
T y pe s :
1- Cem
mented UMW WHPE (with h wire marke er to assess th
he position & wear rate).
2- Cem
mented meta al backed & PE (PE liner could be revvised alone; but may disslodge also).
3- Cem
mentless:
o Porous coated:
c
Fixed by: sc crews, pegs, spikes & threading.
Press fit.
o HA coatted.
o Double coating.
4- Cusstom shaped
d:
o Oblong g: for acetabuular deficienccy.
o Deep prrofile: for pro
otrusion.
Metal Back: (m
metal cup é plastic
p liner give
g the adva antage of revvision of the
e liner alone).
Mettal cup need atigue Æ liner thickn
ds thicknesss to avoid fa ness.
If lin
ner < 5mm Æ high stresses Æ linerr failure.
Thee solution off this dilemm ma is to head
h size.
Effeectively doubles the rate of wear.
Provvide the ability to put thet cup in anatomical
a position (55 5º) while puutting a PE liner é an offset
o
(antti-dislocation
n rim).

Wire marker, PMMA spacer, cup flanges

• Wire marker is inserted at the PE rim:
Assessment of linear wear.
Assessment of the position:
(1) Inclination .............. 45º (normally 55º).
(2) Anteversion ........... 0-10º.
PMMA spacers are small knobs on the back surface of the PE:
•
Prevent BOTTOMING OUT (adequate mantle 3mm).
Allow for uniform cement mantle.
• Cup flanges are rim projection that allow for cement pressurization as the cup is inserted.
Cemented vs cementless
• Long term cup survivorship is limited ώ make surgeons use cementless cups.
• Cemented cups:
Best suiting elder, low demanding patients.
Low cost.
Simple application & easier detection of loosening.
More suitable for some tumor management.
In revision THR + acetabular BG (metal ring μβ added).
• Cementless cups:
Young active individual
Screw fixation μβ dangerous; the most secure position is the posterosup.
Stress at CBI by:
1- Thin PE cup is used (> 5mm plastic is recommended)
2- Subchondral bone is removed
3- PE sockets alone (metal backed cups have lower evenly distributed stresses)
4- Cementless inadequate cup coverage (stress concentration & less bone ingrowth)
Tribology
I. WEAR
• It is the Loss Of Material From Prosthesis Surfaces ð Motion Among Them.
• Wear measurement is difficult, as it is Volumetric, so realistically, it is measured as a LINEAR wear
= the smallest radius from the center to acetabular rim.
• Normal wear rate = 0.1mm/Y
Types of wear:
1]. Abrasive: the harder grooves the softer material
2]. Adhesive: the softer material adheres on the harder surface
3]. Fatigue, in which repetitive loading Î subsurface delaminate Î lost from the surface
4]. Third-body wear implies the retention of debris bet. sliding surfaces Î abrasive wear.
5]. Back side wear: bet PE & the metal backing.
6]. In wear: is the accelerated wear that occur in the 1st year of implantation
• In THR, abrasive & adhesive wears are more than fatigue (in contrary to TKR).
Factors that determine wear:
1]. The material Friction coefficient.
2]. The material surface finish & hardness.
3]. The material molecular wt (the higher the better).
4]. The load applied.
5]. The sliding distance/cycle, depending on the head diameter and arc of motion.
6]. The number of cycles that occur over time.
• Metal surfaces form an oxide film, ώ is worn away and reformed ............... gradual roughness.
• Alumina & Zirconia ceramics are oxidized from the start ................................. no oxide roughness.
• Alumina & Zirconia ceramics are harder than metals ........................................ less liable for abrasion.
• PE sterilized by O2 free γ radiation Æ oxidized Æ cross linking Æ molec wt Æ wear.
• Volumetric wear is maximum é head 32mm / linear wear is max é 22mm heads

II. Friction
• Friction coefficient is the resistance encountered while moving one object
over another.
It friction varies according to:
}
•
1- Material used.
2- Finishing.
}
3- Temperature. Friction coefficient
}
4- Lubricants. Frictional Force
5- Load. Torque
6- length of lever arm (affect the contact surface area).
The normal joints coefficient ≈ 0.008-0.02.
Metal-on-metal joints tested in vivo ≈ 0.8.
Metal on HDPE ≈ 0.02 (ceramic-on-ceramic/ceramic-on-PE also is low).
Metal-on-ceramic produces a high coefficient of friction Î metal wear.
• Frictional torque: is the force transmitted from head-cup interface to BCI along the lever arm
between the head centre and the BCI Î loosening.
III. Lubrication
• Lubrication is the main determinant of the Coefficient of friction in mobile joints.
1- ELASTO-HYDRO-DYNAMIC lubrication ....... is the main dynamic type of lubrication.
o Deformation of the articular cartilage + thin film of fluid lubricant.
2- HYDRO-DYNAMIC lubrication ............................. thin lubricant film separates the surfaces only.
3- BOUNDARY lubrication ......................................... adsorption of lubricant film of on each surface.
o This type of lubrication prevents direct surface to surface contact Æ wear.
o WETABILITY is the affinity of a material for lubricant adsorption = the angle of contact
between the material and a drop of the lubricant.
o Alumina & Zirconia have angles = wetability.
o In synovial joints the “LUBRICAN” glycoprotein is the adsorbed molecule.
4- WEEPING lubrication .............................................. Fluid shifting to loaded areas
5- BOOSTED lubrication ............................................. Fluid Entrapment
• Lubricating fluid is trapped in pools made by bearing surfaces that in contact.
• Friction is higher in boosted > elasto-hydrodynamic lubrication.
ggggggbiiiiii
8. Acetabular ring
• Cement in acetabular revision is not used to attach the component to bone, but rather to attach
modular acetabular components together (e.g., to bond the polyethylene liner into a metal shell).
• Idea:
1]. Provides a painless, stable, and, hopefully, durable construct.
2]. Maintains bone stock.
3]. Restores hip mechanics to near normal.
Types:
1- SCREWS & HOOK:
1]. Ganz Ring.
2]. Link Pelvic Reinforcing Ring.
3]. Graft Augmentation Prosthesis (GAP).
2- SCREWS ON BOTH iliac & ischium:
4]. Mueller Ring.
5]. Burch-Schneider Antiprotrusio Cage.
Indications:
1]. Severe acetavular defects.
2]. Pelvic discontinuity.
3]. Tumors.
4]. Protrusio.

9. PolyMethylMethAcrylate (PMMA = Bone cement)

How it works in arthroplasty
• It is a Space Filling & Load Transferring Material or ‘Grout’.
• It is Not A Glue, as it has no adhesive properties.
• Allows secure fixation of the implant to bone.
• Its success in doing so depends on how it is used.
• It does not bond chemically to bone or to the surface of the metal components.
• Mechanical bonding to cancellous bone is produced by forcing cement into the
interstices. It is important that this bonding is strong to minimize movement at the cement
bone interface which can load transfer and can generate and distribute wear debris.
• A mechanical bond can be achieved between the cement and implant if the implant
surface is textured or porous though this reduces survival clinically.
• It is a classic brittle material i.e. cannot undergo plastic deformation and breaks.
• Brittleness is the resistance to plastic deformation.
• Ductility is the ability for deformation (elastic & plastic).
• Stiffness is the resistance to strain ( modulus).
• Hardness is the resistance to scratch.
Mechanical properties of PMMA
• Brittle, therefore notch sensitive, best not to be used with implants with sharp corners.
• Stronger in compression than in tension and shear.
• It is viscoelastic.
• The fatigue strength is approx 20-25% of the single cycle strength.
Composition
1- Powder POLYMER - Packet of powder containing:
o PMMA Particles .................................................................................................. 90%.
o Radiopaque barium sulphate (or zirconium-O2) .................................... 10%.
o Initiator for polymerisation = benzoyl peroxide ...................................... 1%.
2- Liquid MONOMER - Vial of liquid containing:
o MMA monomer ................................................................................................. 90%.
o Activator = DMP toluidine the cold curing process ......................... 3%.
o Retardant trace to monomer polymerisation during storage ....... 1%.
Other additives include
3- Antibiotics - Only heat stable antibiotics in a powder form can be used eg Gentamycin,
Tobramycin, erythromycin, vancomycin, cephalosporin. Palacos has the best results for
leeching of the contained antibiotic.
4- Colourant - methylene blue or chlorophyll, for easy differentiation from bone during
revision.
Mixing
• Depending on the manufacturer the liquid is added to the powder or vice versa.
• Modern mixing with a vacuum of 500mmHg Æ porosity from 25% to 1%.
• Centrifugation also the porosity of the cement produced.
• Porosity reduction improves the fatigue properties of the cement.
Hip Disorde
[H ers] Page | 697

Curing of PMMA
• This is the
t polymerization pro ocess when n the dry an nd liquid co
omponents are mixed.
• This forrms long-ch
hain polyme ers that are
e essentiallyy linear and relatively frree of crosss linking.
• The curring processs may be characterize ed by the fo ollowing tim
me periods:
1- Dough time sttarts from beginning g of mixin ng and en nds at the e point wh hen the bone
b
cemen nt mixture will not stick to unp powered surgical
s gloves. Occcurs ~ 2-3 min after the
beginnning of mixxing for moost PMMA cements.
2- Work king time is the tim me from th he end of dough tim me until th he cementt is too stifff to
manippulate, usuaally 5-8 min
ns.
3- Settinng time iss from the e beginning of mixin ng till the surface te emperature e is 50% of o its
maximmum value = dough + working time t = 8-10 0 min.
• The polymerization process iss an exoth hermic rea action Æ 12-14 kcal/1
100g
• The hea
at generateed in vivo = ........................ 40º-43º.
• Protein
n Denaturration at ............................. 47º.
• Bone necrosis
n at ............................................... 56º.
Factors affecting cement strength & curing* times:

ec
Uncontro ollable Fac
ctors Effe
ects
1]. Cemen nt aging aftter implanta
ation • Gradual 10%
% loss of stre
ength due to
o chemical ch
hanges
2]. Enviro
onmental teemperature • 10% weakerr at body temmp than at rroom temp
3]. Moistu
ure contentt • Weaker by 3-10%
3 than dry
d cement
Partially Controlla
able Factors
4]. Cemen
nt thicknesss. • Optimum th
hickness bet 2-5mm.
If too thick, stress
s protecction occur in
n the surrouunding bone e.
If too thin th
he cement frractures.
5]. Cemen nt due. • Using centra alizer (distal & proximal)..
6]. Constrraint. • T more constrained the
The t cement is the more e likely it is th
hat
compression n is the resulltant force > tension or shear.
7]. Inclusiion of blood
d or tissue. • Can decreasse strength by b up to 70% % depending g on the
a
amount.
8]. Stress risers (edge
es in implan
nt). • Cement is notch sensitivve.
Controlla
able Facto
ors
9]. Radiop
paque mate erial. • strength 5%.
5
10]. Antibiotic inclusio
on. • strength 5-10%.
5
11]. Mixing
g speed (too o fast, or slo
ow). • strength 20%
2 (If mixin
ng too fast o
or too slow).
12]. In app
propriate steem position. • strength.
13]. Stem motion
m duriing setting. • strength.
14]. Centrifugation/va acuum mixing. • strength 10-25%.
1
15]. Pressu
urization. • strength ( porosity).
16]. Room temperature.* • dough & setting
s timess ~ 5%/1º ( / in eitherr way).
17]. Room humidity.* • setting tim
me.


Cementing techniques
Technique
1st generation 1- Finger packing,
2- Distal vent
3- High viscosity
4- No Femoral canal preparation nor plug
2nd generation 1- Femoral canal preparation + plug
2- Cement gun to allow retrograde filling
3- Low viscosity
4- ± pulsatile lavage ± proximal seal
Has improved femoral revision rates, no effect on acetabular side
3rd generation 1- Pressurization after insertion.
2- Proximal seal is mandatory.
3- Low viscosity.
4- cement porosity (vacuum & centrifugation).
5- Surface changes to the implant to attempt to improve implant cement
bonding (roughening or texturing) or precoating of the implant with bone
cement to form a chemical bond found to be detrimental.
6- More recently, use of spacers to ensure uniformity of the cement mantle
Still awaiting proof that this is an improvement on 2nd generation.
4th generation 1- Cancellous suction using cannulated screw suction.
2- Triple package cementation.

Problems with PMMA

1. Cement reaction
• Hypotension can occur on pressurisation of the cement into the femur, maybe due to
peripheral vasodilatation and direct myocardial depression. This is ð monomer leakage.
• The transient hypotension does not correlate with the level of monomer in the circulation
but with the deficit in blood volume.
• Fat and bone emboli or air emboli have been reported.
2. Local tissue effects of PMMA
• Heat of polymerisation may exceed the coagulation temperature of the tissue proteins (67º).
• Occlusion of the nutrient metaphyseal vessels which may produce bone necrosis.
• Cytotoxic and lipolytic effects of the nonpolymerised monomer.
Willert histological progression

1st 3wk Soft tissue and fibrin up to 3mm thickness becomes necrotic.
3wk-2y Fibrous tissue ingrowth of Implant bed replacing necrotic bone (Repair).
>2y Well established implant bed. Thin membrane of CT 0.5-1.5mm thick.
Spaces containing round fragments of cement have a giant cell response.
Barrack Grading of Cement Technique

Grade A Meduallary canal completely filled ώ cement (white out).
Grade B Slight radiolucency at BCI (Bone Cement Interface).
Grade C > 50% radiolucency at BCI.
Grade D > 100% of BCI + absent of distal femoral cement mantle < 1 mm + defects in the
cement mantle Æ early loosening.


10. Preoperative Planning
1- Careful history taking & examination.
2- Radiological examination:
o Good quality PXR AP 15º IR (pelvis showing both hips) & lateral hip.
o Assess bone stalk & how much reaming is allowed and needed.
o Osteophytes: central Osteophytes shift the hip centre laterally ( abd lever arm).
o Protrusio.
o Femoral bow, offset, canal width.
o Old fractures, osteotomies, dysplasia.
o Deficiencies (femoral, acetabular).
3- Templating:
o Acetabular size; template stops at the tear drop & superior rim.
o Point the centre of the cup.
o Template the stem: select the best match for the contour.
o Determine the most suitable neck length according whether there is LLD or not.
o If LLD the centre of the head should be in a distance away from cup centre = LLD.
o Neck resection level from the lesser troch.
o Offset.
o Neck shaft angle.
o Dorr Index.
o Special situations.
4- Lateral radiographs must be templated to assure fit can be achieved with the planned stem
diameter and length. If stem IMPINGEMENT is predicted:
o Varying the entry point in the AP plane
o switching to an anatomic (bowed) stem
o implanting a cemented stem.
5- Plan the ENTRY POINT. By drawing the neutral axis of the femur and extending it proximally,
this is more crucial in a cementless stem. Typically, this involves a lateral entry site near the
pyriformis fossa and requires removal of any remnants of the lat. aspect of the neck.
• If difficulty is encountered seating reamers below the planned size, often the entry point is
incorrect, usually medial, and reaming and broaching is often being done in a varus
orientation. If difficulties persist, an INTRAOPERATIVE X-RAY with a broach in place will often
confirm the problem. If reaming of the femur is proceeding above the planned size, it may
also be prudent to obtain an intraoperative radiograph with a reamer or broach in place.
6- VERY EASY REAMING: the choice of a cementless stem should probably be reconsidered.
Isthmus diameter is also helpful to know for selecting the appropriate-size canal plug for
cemented stems.
7- COXA VARA: Patients with coxa vara have higher than usual femoral offset. This can be
compensated for by utilizing a component with a lower neck–shaft angle, or by making a
lower neck cut and utilizing a longer neck. Making a standard-length neck cut can
significantly lengthen the leg without restoring offset. The use of high-offset components
or components with a lower neck–shaft angle help preserve bone by minimizing the
necessity of the low neck cut (Fig. 27).
8- COXA VALGA: The opposite situation exists when the patient’s neck–shaft angle significantly
exceeds that of the prosthesis. There is a relatively low offset and more length. To
compensate for this with a component with less valgus, it is necessary to make a higher
neck cut and use a shorter neck to maintain length and offset
9- COXA BREVA: When avascular necrosis of the capital femoral epiphysis occurs early in life, as
in Perthes disease, a short femoral neck (coxa breva) can result. In these cases, length and
offset are usually increased when using a standard acetabular component. If a standard
neck cut and neck length are employed, overlengthening may occur. Often a low neck cut
and short head may be necessary to avoid this

11. Complications
Early Late Not related to time
1- Nerve inj. 7- Anterior thigh pain. 14- Fractures.
2- Vascular inj. 8- Trochanteric non union. 15- Dislocation
3- Hemorrhage. 9- Heterotopic ossification. 16- Infection
4- Urinary Bladder. 10- Loosening 17- Others.
5- LLD 11- Osteolysis
6- Thromboembolism. 12- Stem Failure
13- Cup wear
1. Nerve Injuries
• Incidence of sciatic & femoral palsies:
o 0.7-3.5% in primary THR.
o 7.5% in revision THR.
• Risk Factors:
1]. Revision THR Somatosensory evoked potential (SSEP) to monitor it during revision.
2]. Female gender.
3]. THR for DDH. 2-3.5 cm Æ common peroneal
4]. Significant lengthening of the extremity.
• Nerves injured:
1]. Sciatic n.
2]. Obturator.
3]. Femoral.
4]. Superior & inferior gluteal nerve.
5]. Common peroneal nerve.
• Causes:
1]. Retraction ................................................................................................... (femoral, sciatic, gluteal).
2]. Excessive lengthening causing stretching of nerve .................... (sciatic).
3]. Iatrogenic direct trauma ....................................................................... (any).
4]. Thermal or pressure injury from extruded cement ...................... (femoral, sciatic).
5]. Dislocation .................................................................................................. (sciatic).
6]. Subgluteal hematoma formation ....................................................... (sciatic).
7]. Post-op positioning with abduction pillow .................................... (common peroneal).
• Types of injuries:
1]. Subclinical ................................................................................................... 75% to gluteal n.
2]. Neurpopraxia.
3]. Neurotemesis.
• Management of sciatic palsy:
1]. Foot splint & perform a base line EMG.
2]. At 6wk do another EMG to monitor the nerve regeneration.
3]. At 6mo if no recovery Æ exploration and do cable grafting by sural of Post cut n.
2. Vascular Injuries Rare (0.2% to 0.3%) mostly during revision.

• Retraction & dissection over the front of the acetabulum .................... Femoral a. & v.
• Removal of soft tissue and bone from the inferior aspect .................... obturator vessels.
• Penetration of the medial wall during reaming ........................................ common iliac a or superf.iliac v.
• Cementless cup superolateral screws ............................................................. superior gluteal vessels.
• Antero superior screw .......................................................................................... external iliac a.
• Late vascular problems include thrombosis, AV fistula, and false aneurysms.

3. Haemorrhage & Haematomas

• Risk factors:
1]. Bleeding tendency (liver disease, hemophilia,…).
2]. NSAID & steroids & Anticoaggulants.
3]. Paget’s.
4]. Gaucher.
5]. Revision.
• Common sources of venous and arterial bleeding are:
1]. OBTURATOR vessels during ligamentum teres and transverse lig are removed.
2]. CRUCIAL anastomosis vessels near the attachment of the gluteus maximus tendon.
3]. MEDIAL CIRCUMFLEX vessels distal to the attachment of the psoas tendon to LT.
4]. FEMORAL vessels branches near the anterior capsule.
5]. Inferior and superior GLUTEAL vessels branches.
6]. Bone ooze.
• Control of bleeding:
1]. Hemostasis.
2]. Gel foam soaked in thrombin
3]. Bone wax
4]. Hemostatic collagen derivative
5]. Diluted epinephrine
• ttt:
1]. prophylactic AB against infection
2]. never aspirate or remove stitches in ward Æ in op theatre
4. Urinary Tract Complications
1- Bladder inferior is the most common complication = 7-14% after THR.
o In patients with urinary obstruction caused by prostatic enlargement, transurethral
resection should be advised before hip surgery; otherwise the risk of postoperative
retention and subsequent infection is high.
2- Bladder injuries rare.
3- Acute renal failure ......................................................... rare.
5. Limb Length Discrepancy

• LLD of < 1cm is well tolerated
• Causes:
1]. Insufficient resection of the neck.
2]. Too long neck.
3]. Inadequate stem seating.
4]. Protrusion.
5]. Varus.
6]. Coxa valga.
7]. Coxa breva.
• Effects:
1]. Patient dissatisfaction
2]. lengthening > 2.5cm can cause sciatic nerve palsy
3]. vaulting type gait pattern
4]. low back pain (?)
5]. JRF and premature mechanical failure are not linked to leg length discrepancy
• Prevention:
1]. Preoperative planning and templating.
2]. Intraop measurement: - superior iliac pin to femoral ant cut distance.
- Shuck test 2-4 mm telescoping is acceptable.
- Centre of head opposite the tip of GT.

6- THROM M (MOST COMMON

MBOEMBOLISM O COMPLICATIO
O ON)
Incidence
• 50% poostoperativee mortality if WITHOUUT prophyla axis.
Predisposing factors
• Generaal: Previous DVT , Agin
ng , Use of general
g anaaesthetic.
• Local: VIRCHOW’S TRIAD- stasis, hypercoaagulability and
a intimal damage.
Stasis Hype ercoagulab bility Intiimal injury
y
Immob bility & paressis Maliggnancy Trau
uma
Pregnaancy Birth control pill
Varicosse veins blo
ood viscosityy
Obesityy Smokking
Congesstive cardiacc failure Clotting discriasis eg F V Leiiden
Pathology
1- Stasis:
o Activated factors acccumulate.
o Thrombin formation occurs.
o Platelets aggregate.
o Platelet rellease reacttion.
2- Fibrin formation::
o Thrombin absorbed by fibrin and neutrallized.
3- Clot re
etraction:
o Thrombin release causes platellet aggregation.
4- Propaggation:
o Successive e layers of fibrin
f and platelets.
p

Intrinsic Pathway:
• Monito ored by PTT T.
• Pathwa ay activated
d when Facctor XII makkes contact with collag gen in damaged vesse els.
• Inhibiteed by Hepa arin (activatiing Antithrombin III).
Extrinsic Pathway:
• Monito ored by PT (INR).
(
• Pathwa ay activated
d by releasee of thromb boplastin into the circuulation seco ondary to ce ellular injury
ry.
• Inhibiteed by Warfa arin ( prod duction of Vit
V K dep fa actors from liver = II, VIII, IX, X & Pttn C).
Antithrombin III:
• Is a plassma proteaase inhibitorr that serve
es as a proteease scavennger.
• Inhibitoor of the en
nzymes thro ombin, Xa, IXa;
I is activa ated by hepparin.
Clinical feattu
ures
Of DVT
• Often asymptoma
a atic ± Mild inncrease in temp.
t
• Calf or thigh
t swellling and pa ain.
• Positivee HOMAN’S sign,
s dorsifle
exion of annkle causes pain.
Of P.E.
• Can be e asymptom matic.
• Shortne ess of breatth, pleuritic chest pain,, Pleuritic ru
ub.
• Haemo optysis, , cya
anosis, tach hycardia, & SUDDEN COLLAPSE.
• RBBB and /or T wave w inverssion in lead III on ECG G, Hypoxia on
o art blood
d gases.

Investigations
For D V T
• VENOGRAPHY the gold standard- 97% accurate (70% for iliac veins), expensive invasive.
• DOPPLER US, B mode, 90% accurate for thigh DVT.Not as useful in calf or pelvic thrombi.
Sensitivity of 79%, specificity of 98%.
• RADIO-LABELLED FIBRINOGEN can cause false positives and is expensive and time consuming.
• Impedance PLETHYSMOGRAPHY, noninvasive and allows monitoring, but needs venography.
For P E
• CXR may show hyperlucency.
• VQ scan.
• Gold standard PULMONARY ANGIOGRAPHY.

Prevention
Mechanical Prophylaxis
1]. Early mobilization.
2]. Early physiotherapy.
3]. Thromboembolism stockings: Proven to be useful in abdominal surgery not in ortho.
4]. Calf and foot pumps & sequential pressurizers.
Proven to have a similar effect to chemical prophylaxis.
o
Tend only to be used during the inpatient period and some events happen after this.
o
Chemical Prophylaxis
1]. Unfractionated heparin 5000 units TDS (monitoring is needed).
2]. Low Molecular weight heparin.
Dose and frequency
Certoparin 3000 units O.D
Dalteparin (Fragmin) 5000 units O.D
Enoxeparin(Clexane) 2000 units O.D
o FXa (Heparin- binds to & the activity of Antithrombin III Æ Θ thrombin, F IXa &
Xa. (reversed é Protamine))
o More effective than heparin in orthopaedic prevention of DVT and PE.
o Low bleeding complications with LMWH than with heparin (doesn’t affect PTT).
o Longer halflife therefore able to give only once daily.
o Does not need monitoring.
3]. Oral anticoagulants:
o Warfarin as effective as heparins but requires monitoring.
o Affects F II, VII, IX, X (Vit dependent) Æ take up to 48 hours to become effective.
4]. Antiplatelet drugs e.g. Aspirin.
o Reduces platelet aggregation & inhibits cyclooxygenase (not effective).
Treatment
DVT:
• Compression stocking and analgesia.
• Heparin IV(é monitoring) Æ warfarin 3 mo OR.
• LMWH (éout monitoring) Æ warfarin.
• Dextran may be used but not for old age Æ Pulmonary oedema, HF, RF.
P E:
• Supportive Measures, Oxygen, analgesia.
• Heparin IV(é monitoring) Æ warfarin 3 mo OR.
• LMWH (éout monitoring) Æ warfarin.
• Rarely thrombolysis, vena cava interruption.

7- ANTERIOR THIGH PAIN (more in cementless).

Aetiology:
1]. Stress concentration at bone implant interface ................... activity pain.
2]. Inflammatory response ................................................................. Rest pain.
3]. Failure to achieve stable ingrowth ........................................... start up pain.
4]. Stem up motion ............................................................................... end pain.
5]. Stem subsidence > 2mm .............................................................. progressive pain (bead shedding + distal
periosteal reaction).
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8- TROCHANTERIC NON-UNION & MIGRATION

•3-8% (more in revision).
•Rationale for trochanteric osteotomy involves distal advancement of the GT is done to
enhance or to restore the abductor mech.
• Nowadays trochanteric osteotomy is seldom done except when:
1- Some patients with DDH.
2- Protrusio acetabuli.
3- Conversion arthroplasty from arthrodesis.
Ætiology of non union:
1- Small trochanteric fragment.
2- Poor-quality bone.
3- Inadequate initial fixation.
4- Reattachment under excessive tension.
5- Prior radiation therapy to the hip.
6- Patient noncompliance during the postoperative period.
Pathology variations:
1- Non union ð excessive shear forces during movement Æ fatigue failure of the wires.
2- Stable fibrous union éout proximal migration Æ good function & little pain.
3- Pseudoarthrosis (known by painful resistance to abduction).
4- Migration > 2 cm significantly abductor function (more important than nonunion).
Picture and problems:
1- Patients with nonunions subjected to fatigue more easily.
2- Trendelenburg gait.
3- Higher rate of dislocation.
4- Painful bursitis ð trochanteric wires.
5- Delayed sciatic palsy may result from migrated broken trochanteric wires.
6- Arthrosis also may occur ð metal debris from braided cables (impossible removal).
Treatment:
• Indications: displaced nonunion / pseudarthrosis / abd weakness / Trendelenburg.
• Careful preparation and contouring of the GT is essential to obtain maximal stability
• The trochanter must not be reattached under excessive tension (not > 15º abduction)
• place the trochanter against bone rather than cement
1- Reattachment of the greater trochanter by wire fixation
2- Double cross-over wire with a compression spring.
3- Abductors subperiosteal release from their origin on the iliac wing.
4- Weight-bearing and active abduction exercises are delayed until bony union
5- A period of bracing in abduction or spica cast application tension on the repair.

9- HETEROTOPIC OSSIFICATION
Incidence
• Variable in reports from 3% to 50%.
Causes
• Unknown.
• ? due to intraoperative muscle ischaemia and post op trauma.
• ? due to increased bone debris in cementless hip replacement.
PDF
1- Men.
2- Ankylosing spondilitis & Forestier disease.
3- Previously fused hip.
4- Postraumatic arthritis.
5- Previous heterotopic ossification on other side.
Histologically:
• Zonal pattern with mature bone peripherally and immature tissue at the centre.
Clinically
• Usually painless.
• Can cause STIFFNESS.
• Does not cause limp or loss of strength.
Xray
• Calcification of soft tissues begin at 2nd or 3rd wk post op and maturing fully by 12 mo.
Brooker classification
Appearance on Xray
I Islands of bone within soft tissues
II Bone spurs from femur or pelvis with at least 1cm gap between opposing surfaces
III Bone spurs from prox femur/ pelvis < 1cm between opposing surfaces
IV Ankylosis
Prevention
• Low dose radiation ............................................ 700 cGy immediately post op.
• Indomethacin ....................................................... 75 mg / day for 2-6 weeks.
• Both porous ingrowth in uncemented components, but it can be shielded é lead.
Treatment
• Surgery not usually advocated as can be difficult and cause bleeding, recurrence common.

10. ASEPTIC LOOSENING

• Radiographic changes in the intergrity of the load carrying cement mantle.
• Implant fixation depend on:
1- Implant cement interface: depend on either polished, textured, tapered.
2- Bone cement interface: depend on cement viscosity.
3- Cementless: (A) bone ingrowth, (B) stable fibrous, (C) unstable.
• Not every Radiolucent Line RL mean that it is a cement debonding:
Immediate postoperative RL may occur due to incomplete cancellous removal.
Age related femoral canal widening .............. (0.33 mm/y).
Age related cortical thinning ............................ (0.14mm/y).
It was found that these RL are not surrounded by sclerosis and also there is a
radiologic indistinguishable internal cortex adherent to cement mantle that is
separated from the true cortex by radial cancellous trabecular struts.
• Not every debonding means loosening:
Some designs e.g. polished tapered designs may undergo micro-subsidence.
• Not every loosening means that the patient is complaining.
I- Cemented Stem Loosening

• The hip articulation is a particle generator ώ release UHMWPE particles into the joint.
• Small Irregular phagocytosible particles 0.5-10μm are more active than large or very small.
• Macrophage activation causes release of IL-1, PGE2, TNF, IL-6 Æ ⊕ osteoclastic resorption.
• Irregular shaped particles are more bioactive than spherical particles.
• Particles > 10μm Æ giant cell response but no osteolysis.
• Once the wear particles are generated Æ path of least resistance Æ BCI or ICI in cementless.
Zones of cemented Loosening
• Acetabulum/Cup = DELEE & CHARNLEY:

Considered loose if radiolucency >2
mm in all 3 DeLee zones, or change in
position of cup (Loosening bet the
cement and cup is unusual).
• Femoral = Gruen Modes of Failure


Ætiology of cemented loosening:

1- Failure to remove soft cancellous bone on the calcar Æ cement rests on a weak BCI.
2- Removal of all cancellous bone ώ is the substrate for the BCI (the microinterlock).
3- Thin cement mantle (4mm prox., 2mm stem, 1-2 cm distal).
4- Inadequate cement.
5- Inadequate stem stability during hardening.
6- Inappropriate stem position (varus, not centralized).
7- Inappropriate cementation technique (mixing, pressurization, retrograde inj., plug, seal).
8- Osteolysis.
Harris Cemented Stem Loosening Classification
• Radiolucent lines are commonly found in the lateral and anterior aspects of the proximal
femur, since these areas can be difficult to visualize and difficult to pressurize.
• In the proximal 1 cm of the femur, linear radiolucencies < 2 mm in width ≠ loosening.
• Cement debonding at ICI (Implant Cement Interface) in zone 1 ≠ poor results.
1- Definite loosening
• STEM FRACTURE OR CHANGED POSITION.
• CEMENT FRACTURE.
• Implant/cement interface (ICI) RADIOLUCENCY > 1 MM is a definite sign of loosening.
• NEW RADIOLUCENCY at implant/cement interface (ICI) of any size then suspect loosening.
• GRUEN modes of loosening: Pistoning , Medial stem pivot, Calcar pivot, Cantilever.
2- Probable loosening
• Continuous Radiolucent lines at BCI and typically surrounded by lines of density.
• Endosteal cavitation (linear osteolysis and focal osteolysis) Æ suggestive of loose stem.
3- Possible loosening
• Radiolucent lines at BCI 50-100% of the total bone cement interface.
Barrack Grading of cement technique:

Grade Cementation
Grade A Medullary canal completely filled (white out)
Grade B Slight radiolucency exists at the BCI <50%
Grade C Radiolucency > 50% at BCI.
Grade D Radiolucency 100% of BCI in any projection + absence of cement distal to stem tip
Prevention:
• Complete cement mantle.
• Circumferential proximal HA coated implant.
• To amount of particles Æ VOLUMETRIC WEAR ∴ SMALLER HEADS.
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II- Cemented Cup Loosening
• More common at BCI unlike stem loosening ώ occur more common at ICI.
• More common to be a 3rd body wear than mechanical (unlike the stem loosening).
• Findings:
1- Bone RL: Any progressive or > 2mm RL line ALL AROUND the cement mantle.
2- Cup Migration; medial or superior (protrusion).
3- Cup Change in inclination or anteversion.
4- Cup wear (linear wear).
5- Cement and/or cup fracture.
• Aetiology:
1- Inadequate bone support.
2- Inter position of blood, loose fragments, fibrous tissue, cartilage.
3- Inappropriate cementation technique (mixing, pressurization).
4- Inadequate uniformity of the cement mantle (cement spacers may do the job).
5- Inadequate cup stability during hardening.
6- Inappropriate cup position (neck will impinge early on the rim).

III- Cementless Stem loosening:

1- Bone in
ngrowth:
No subsidence e.
No radio-opaq que line.
SPOT WELDS: endosteal hypertroph
h hy distal to coating.
c
Proxximal stresss shielding.
2- Fibrous Stable:
No progressive e subsidencce (or < 4mmm).
Evid dent sclerottic demarca ation lines separated
s frrom cortex é < 1mm ra
adiolucencyy.
No spot weldss = uniform stress transsfere.
less stress shiellding.
3- Unstab
ble:
Progressive subsidence ± varus tilt of the stem.
Loc cal hypertroophy at calccar & distal to
t stem (P PEDESTAL) = local loadin
ng & stresse
ed.
IV- Cementless Cup Loosening:

• Uncommon é poroous coated cups.
• High é threaded, non poroous, and HA
coated.
Ætiology:
1- Poor cup position.
p
2- Liner poo or fixation
n to me etal
backing.
3- Thin liners..
4- Protrudingg screws into
o the PE.
5- Sharp screw w hole edge
Findings:
1. Cup migrattion.
2. Progressivee radiolucen
ncy.
3. Radiolucenncy > 2mm alla over the BCI.
4. screw breakage
5. fracture of metal shell
6. defoliation of porous surface
s
Diagnosis
• Pain:
o Start up witth WB (≠ cla
audication pain);
p indica
ate loose im
mplant ώ engage betterr é WB.
o Groin.
o Appearancce of Trende elenburg Ga ait or antalggic gait.
o History of prolonged
p p
postop pain
n.
• PXR:
o Progressivee radiolucen ncy (review previous PX
XR).
o Radiolucen nt line >2mm m (possible loosening).
l
o Measure su ubsidence in relation to a fixed point in the
t
patient (tea
ar drop, lessser troch).
• Arthrog
graphy afterr walking maym be of a significance
s e.
• Tc up
ptake after 6mo
6 is sugg
gestive.
Hip Disorde
[H ers] Page | 709

11. OSTEOLYSIS:
• Localized bone re
esorption due
d to a macrophagee mediated
d reaction.
• Pathoggenesis:
o Metal
M & PE & cement particles and debrris
arre generated at the BCI, ICII, and join nt
su
urface by adhesive
a an
nd abrasive e wear.
o Thhese particcles move through the path of o
east resisttance BCI & bon
le ne implan nt
in
nterface “eeffective joint space” = space ofo
co
ontact betw ween impllant and bo one.
o Sm
mall phago ocytosible particles 0
0..5-10μM arre
m
more bioacttive than laarge or verry small.
o IRREGULAR shaped particles are morre
bioactive than regularr round on nes.
o Thhe macrop phages eng gulf these particles Æ
re
elease of IL-1, PGE2, TNF, IL-6.
o Thhese me ediators ⊕ osteocla astic bon ne
re
esorption.

Gggg
gggbi
iiiii
ii
12. STEM FAILURE

1- Usually
y developss several ye
ears after surgery - avverage 3.5 years.
2- The fracture usu
ually begin ns in the MIDDLE 1/3 of the anterolatera al aspect of
o the stem
m &
progre
esses media
ally (due to
o bending & torsiona
al forces).
3- Deform
mation and
d fracture of
o the stem
m occurs in response to cyclic lo
oading.
Increased incidence with:
• Heavy, active patie ents.
• Varus position
p of stem.
s
• Stems with
w small cross-section
c nal area.
• Stem with
w long ne eck or increeased offsett.
• Stainlesss steel - low
w fatigue strength.
• Metalluurgical defects in the sttem.
• Poor suupport in th he proximal third.
Diagnosis
1- Bendin ng and inccomplete frracture of the t stem arre painlesss.
2- AP and d lateral PX XR should be b comparred carefullly with pre evious filmss.
3- Torsionn tends to deflect the e stem med dially and posteriorly
p y.
4- To dettect bendin ng angle: ........ Draw a line throug gh the cennter of the head and neck.
........ Anotherr line tange
ent to the lateral disttal 2/3 of sttem.
5- Also, superimpossition of the x-rays is anothera method.
m
Treatment:
• Revisionn is indicate ed ASAP for bending and a breakin ng a stems; before fraccture comp pletely.


13. CUP WEAR
Wear Increased By:

Normal wear rate = 0.1MM/Y
• debris - third body wear
• metal backing
Linear Wear
• =The measurement of rate and distance the metal component penetrates into PE.
• Wear is measured as smallest radius from the center of femoral head to outer border of the
acetabular cup - ranges from 0.01-0.56 mm/y (≈ 0.29) Æ é time to 0.15 mm/y after 9 years
• Linear wear increases with heavier pts and pts that exercise.
• 22 mm femoral heads have a greater amount of linear wear than do 28 mm heads.
• Excessive wear may be associated with osteolysis.
• It is important to measure the initial amount of "APPARENT LINEAR WEAR".
• Initial postop PXR can show ≈ 1.1 mm ALW ð liner design and PE plastic deformation, and
should not be counted in final assessment of volumetric wear.
• Weight bearing films must be used.
Volumetric Wear
• = The calculation of the volume of lost polyethylene and is proportional to the penetration
rate and the area of contact.
• Related to size of femoral head - lowest rate of volumetric wear can be found with 22 mm
head, and the highest rate of wear is found w/ 32 mm heads (and result increase in
osteolysis).
Backside Wear
• Wear occurring between PE & the metal backing effectively doubles the rate of wear.
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14. FRACTURES
Incidence:
• 1% after primary THA; Cementless > cemented
• 4% after revision THA
Prevention:
• Better than the most succesful treatment option
• Avoid cortical defects
• Avoid malalignment of prosthesis
• Regular radiological follow-up to detect early loosening and osteolysis
RISK FACTORS:
1- Osteoporosis
2- RA
3- Inadequate calcar cancellous bone removal (with subsequent calcar resorption)
4- Varus positioning of the stem
5- Lateral stem nicks produced by drilling for greater trochanteric wires
6- Progressive osteolysis
At what stage:
1- At hip dislocation (if resistance during dislocation Æ ST release or cut the neck before disloc)
2- At reductions (trials and definitive)
Johansson Classification of periprosthetic fracture:
Type Fracture pattern
Type 1 Proximal to the tip of the prosthesis with no distal extension.
Type 2 Extend from the proximal portion of the shaft to a point beyond the tip.
Type 3 Occur entirely distal to the tip of the prosthesis.
Hip Disorde
[H ers] Page | 711

Management
Management Aims:
• Restoree function
• United fracture
• Stable prosthesis
p
• Preservve bone stoock
• 65% Un nsatisfacto
ory results so
s these fra
actures aree better preevented thhan treated
d
• If the prosthesis
p iss well fixed
d + minima
ally displace p treatment is indicate
ed # a triall of non op ed
Duncan & Masri Classification (VANCOUVER CLASSIFICATION)
Fraacture Manag
gement
A. Trochante eric
AG Greateer trochante
er Usually stable and needs consservative ttt and NWB.
AL Lesser trochanter
t Other wise
w cerclage fixation or Dall-Miles cable grip ssystem μβ done.
d
B. Around
A Sttem:
B1 Fixed stem
s Extrame
edullary fixa
ation + BG (beware Varrus stem - h
high risk of failure)
f Æ rT
THR
B2 Loose stem
s 1. LONG STEM REVISION + prox lo
oading IMPACTION BG + CEMENTED STEM
+ goodd bone stocck 2. HA/p
porous coateed CEMENTLESS STEM
consider teemporary CERCLAGE STABILISATION ± strut BG.
B3 prosthe
esis loose 1. Long g stem revisiion + proxim
mal loading
g BG & exten
nsive BG as necessary
+ poorr stock 2. If seve
ere osteolyssis or comm
minution:
Allograft/im mplant commposite
Tumour en ndoprosthessis
Interlocking long stem m.
C. Distal to stem
s ORIF (P
Plate + diverrgent screw
ws / Plate + cables
c / cab
bles / Menen
n plate)
COMPLICATIONS:
1- Reduced function .................................. 30% 3
2- Non-union ................................................ 30%
3
3- Malunion ................................................. 30%
3
4- Plate Failure
F ............................................ 15%
5- Infectio
on .................................................. 8%
8
6- Dislocaation .............................................. 8%
8
7- Aseptic Loosenin ng ................................. 8% 8


15. DISLOCATION:
Incidence
• Average incidence 3%.
SUGGESTED CONTRIBUTING FACTORS
1- Faulty positioning of femoral or acetabular components.
o Safe range for cup is anteversion of 15 +/- 10º and inclination of 40º ±10º.
o Femoral component anteversion is 5-10º. If > 15º ....... anterior dislocation.
o Retroversion .............................................................................. posterior dislocation.
o If both cup & femur anteverted by 15º ........................... dislocation more likely.
o Inclination (Rx 45º) if > 55º .................................................... superior dislocation.
2- Revision:
o Weak ms.
o ST release.
3- Extensive soft tissue release .............................................................. dislocation 20%.
4- Surgical approach.
o Some say that a posterior approach increases the risk for dislocation.
o There is tendency for cup retroversion in posterolat approach jig is forced back.
o Division of short external rotators thought to allow dislocation.
o Very low dislocation rate é posterior approach + ER tendon reattachment.
5- Impingement of femur on the pelvis or residual osteophytes:
o More likely if femoral offset not restored.
o Coxa Magna.
o Large osteophytes.
o Excessive deepening of the acetabulum.
6- Impingement of neck of femoral component on margin of the socket.
o Small head.
o Skirt neck.
o If marked linear wear é medial penetration.
o Cup é anti dislocation rim (if used improperly).
7- Insufficient or weak abductor muscles.
8- Avulsion/nonunion of greater trochanter.
9- Noncompliance or extremes of position in the perioperative period.
10- Infection.
Early And Late Dislocation
1- Most dislocations occur early (3 mo) ð:

1- Malposition before regain of ms strength.
2- Technical error during surgery.
nd
2- Late dislocation usually in 2 decade post op is ð:
1- Impingement and ROM.
2- Wear.
Management
1. Analgesia.
2. Adequate Xrays to determine the underlying cause.
3. Reduction under sedation and analgesia or GA.
4. Longitudinal traction then abduction when head at the level of the acetabulum.
5. Or flexion and traction é image intensifier on the table.
6. Assess stability: -if unstable Æ ttt the cause or revision of a component or Total revision.
-if stable Æ bed rest / light traction / abduction 20-30º (No flexion >60º).
7. Abduction orthosis for 6-12 wks.


Management Of The Recurrent Dislocator

• Rule out infection (see infection), consider revision surgery.
• 45% of late dislocations will require revision for recurrence.
• 60% for success of revision surgery for recurrent dislocators.
• Retained osteophytes and cement causing impingement should be removed.
• Malpositioned implants should be revised and positioned appropriately.
• Cup Malposition of > 10º ..................... revision but may get away é an elevated rim liner.
• If no component malposition ............ distal GT advancement.
• As a last resort ........................................ constrained socket can be used, but loosening.
• Revision to a bipolar .............................. may instability.
• Removal of components ...................... Girdle stone in noncompliant, debilitated, multi revisions.
Ggggggbiiiiii
16. INFECTION (MOST SERIOUS COMPLICATION).

P D F:
• EXOGENOUS: in the surgical technique
• ENDOGENOUS: in the patient e.g. DM, poor nutritional status, steroid, immunocompromized
Bacteriology
• Low virulent organisms:
o Staph epidermidis (methicillin sensitive, non glycocalyx forming)
o Staph aureus (methicillin sensitive, non glycocalyx forming)
o ß hemolytic strept
o Anerobic strept
• High virulent organisms:
o Gram negative organisms E. coli, Pseudomonas, Proteus, & Entero-cocci
o Staph epidermidis (methicillin resistant, glycocalyx forming)
o Staph aureus (methicillin resistant, glycocalyx forming)
• Others: Corynebacterium, Group B strep, Strep faecalis
Sources
Intra-operative:
• Sampling of theatre air identified the same organisms & same proportions
• Contamination with the surgeons gloves, gowns, light handles (75% staph.).
Post-operative:
• Drains left for 48 hours allow ingrowth of organisms (Willett et al. JBJS 1988)
• Haematogenous spread: Most common source is skin(46%), mouth(15%), UTI(13%)
Classification
Stage 1= immedialte postoperative:
o Staph-aureus /ß hemolytic strept
o Usually needs irrigation, unless glycocalyx forming organism is identified
Stage 2 = 6-24 mo
o Methicillin resistant staph epidermidis
o Usually needs staged operation
Stage 3: after 2y
o Hematogenous spread from other septic focus
New Classification
Type I Early < 6wk
Type II Late > 6wk
Type III Hematogenous
Type IV Incidental +ve culture
Organism Virulence
ORGANISM RESISTANCE TO AB:
RACE FOR SURFACE THEORY ..................................... (SEE INFECTIONS)


PREVENTION
Pre-operative:
1. All septic lesions must be identified & treated (feet, dental, urinary, prostate).
2. Admit patient as late as possible & into a clean ward.
3. Shave in the anaesthetic room.
Intra-operative:
1. Careful tissue handling & Haemostasis.
2. Length of procedure.
[2]. Antibiotic prophylaxis
• Systemic antibiotics: methicillin-realated penicillin or cephalosporin
• Antibiotic Loaded Cement: reduces risk of infection by 11 fold
[3]. The team: keep the operating team as small as possible
[4]. Movement: shed up to 10 000 skin scales/min
[5]. Theatre gowns.
• Body Exhaust Suits (Charnley): maintain –ve pressure, cool surrounding ( shedding)
[6]. Footwear: no evidence that outdoor shoes are a source of infection; but overshoes wearing can
result in the contamination of the hands of the clinicians.
[7]. Headgear, Face masks, & sterile drapes.
[9]. Drainage of wound has risk of becoming infected than closed wound (only when sure)
[10]. Transporting the patient to operating theatre on a separate clean trolleys in the induction zone
[11]. Theatre equipment & instruments
[12]. Ventilation System: Vertical Laminalr Air Flow is recommended for arthroplasties
[13]. Ultra-violet Light: bacteriocidal; but not commonly used, ð potential dangers to staff
Post-operative:
• In the early post-op phase - antibiotic cover for urethral catheterisation (Gentamycin IM)
• AB cover for all GI & UTI & skin & Dental lesions é antistaphylococcal agent
DIAGNOSIS
1- Clinically
• History of pain, swelling, erythema, fever problems post-op.
2- Radiology:
• Need serial radiographs (get original post-op films).
• Osteolysis around the components & Periosteal reaction.
3- Blood: WBC, ESR, CRP usually not helpful (usually –ve or irrelevant) except if strongly suggestive
4- Bones scans (incl. white cell scan):
usually unable to differentiate septic from aseptic loosening
•
Indium111 may be helpful
•
5- Aspirates:
•
CELL COUNT .................................. >25.000/MM3 (May be helpful 85%)
•
DIFFERENTIAL COUNT ..................... >75% PNL
•
Gram stain ................................................... +ve 25%
•
Glucose .........................................................
•
Protein ...........................................................
•
PCR ................................................................. Newly introduced to diagnostic tools
•
IL6 serum level .......................................... Newly introduced to diagnostic tools
6- Open biopsy:


TREATMENT
1- Antibiotic suppression
• Antibiotics alone will not eradicate deep sepsis so it is rarely indicated alone
• Considered in:
o Elderly, unfit for surgery.
o Early infection
o Single organism
o Low virulent
o Gram +ve organism
2- Debridement alone:
• 20% success rate in TKR.
• Considered in the same conditions but can combat also virulent organisms
3- Resection arthroplasty:
• for the unfit or unwilling to have revision surgery & severe RA
• not good for knee
4- Arthrodesis:
• Remain a last resort especially for young active patients
5- Amputation:
• for knee - High functional cost - end of line.
6- Revision Arthroplasty:
• 75% success is achievable
• Pre-requisites:
o Healthy individuals who can stand long treatment
o Organism sensitive to AB
o Adequate bone stalk
One Stage Two Stage
Advantages: 1. single operation probably safer & more successful
2. quicker return to normal function
Disadvantages: 1. Prolonged procedure 1. two procedures
2. AB sensitivity must be known pre-op 2. prolonged bed rest betw. stages
3. Can't use cementless prosthesis (lose
benefit of antibiotic in cement)
Contraindicated: 1. If AB sensitivities not known pre-op
2. Mixed infection
3. Gram –ve organism
4. bone loss requiring allograft
6. Failure of previous one stage revision
Two stage Revision:

• First stage:
o Debridement (Capsule, prosthesis, inf tissues, Cement, & cement restrictor) & lavage
o Tissues must be sent for microbiology (even if organism is diagnosed pre-op)
o Insert AB loaded cement beads or a ab cement spacer
• Between stages:
o Continue iv antibiotics
o Traction if beads used (or ext fix)
• Second stage:
o Timing:
Early at 3wk
Late: after 6 wk, more effective (the wound would have healed & -ve CRP); but more tissue
scarring that’s why many surgeons use AB spacers (AB-PMMA)
Continue antibiotics for 3 months.

17. OTHER
1. Gastrointestinal:
o Bleeding gastric ulcer may be caused by a stress reaction.
o Acute cholecystitis.
o Postoperative ileus usually is neurogenic and lasts for only a short period, but when
persistent, it could be a result of intrapelvic extrusion of cement.
2. Myocardial infarction and congestive heart failure.
3. Fat embolism syndrome.
4. Mortality - 1.2%.
Hip Disorde
[H ers] Page | 717

2. Diffficullt situ
12 uatio
ons
I Protrusio A
Acetab
bulae
• Normally medial wall
w of aceta abulum is:
2mm LATERAL to Köhler’’s line in a MALE.
1mm MEDIAL to t that line
e in FEMALES.
• If media
al wall of th
he acetabulum is > 3-5mm medial to the Koh hler’s line = Protrusio.
Aetiology:
• Primaryy idiopathicc form is term
med arthrookatadysis i..e. Otto's disease
d =OOtto pelvis.
• More coommon in women, de evelops sooon after pub
bertyÆ OA A in mid adu ult life.
Pathology
Associated with:
1. bonee density:
1. Osteoporo osis.
2. Osteomala acia & Rickkets.
3. OI.
4. RA.
2. Normaal bone den nsity:
1. OA.
2. Idiopathic (Otto's dissease).
3. denssity:
1. Hypophossphataemia a.
2. X-linked in nherited.
Hirst Classification
Grade Protrusio
P
Grade I 5-10 mm pro
otrusion.
Grade II 10-15 mm prrotrusion.
Grade III > 15 mm pro
otrusion.
Treatment:
1]. Graft th
he floor and
d lateralise th
he cup.
Wire mesh
2]. m appliccation deepp in the acetabulum.
3Metal ring.
3]. r
4Use a protrusio
4]. p p
prosthesis (use of slive
ers of the head
h ood technique).
is a go
Precautionss::
1]. Calculate the norm e Ranawat’ss Δ.
mal acetabulum centre preoperativve using the
2]. Trochaanteric oste
eotomy oftten require ed.
3 Disloca
3]. ation of hip
p is usually difficult.
Prognosis:
• If the cu
up placed in
n the right place ....... 8% 8 Loosenin
ng.
• If not placed right .......................................... 50%
5 Loosen
ning (within
n 10 mm).


II THE DYSPLASTIC HIP
Anatomy:
• A. Acetabulum:
Anteromedial wall ................................................ v. thin & Anteverted
• B. Femur:
Femoral head ......................................................... Small
Neck ........................................................................... Anteverted & small
GT .............................................................................. Post. Displaced
neck-shaft angle ............................................... (looks on AP ð anteversion)
Femor al canal ...................................................... Narrow, straight, tapered
• C. Soft tissues:
Hamstrings, adductors, quadriceps ................ shortened
Abductors ................................................................ orientated horizontally
Psoas tendon .......................................................... thickened
Capsule ..................................................................... HOURGLASS shape & thickened
Sciatic nerve ............................................................ shortened
Femoral n & profunda femoris a....................... forced laterally by the high riding
femur -> vulnerable to injury.
Classification
Crowe Grading Subluxation
Grade 1 < 50% subluxation
Grade 2 50% - 75% subluxation (no LLD or bone loss)
Grade 3 -75% - 100% subluxation
-No superior acetabular roof
-Thin Floor
-Intact Columns
Grade 4 > 100% subluxation (i.e. dislocated)
True acetabulum is deficient but recognisable
• Extent of prox. migration (x)= Vertical distance from bottom of Teardrop to junction of femoral
head & neck. (Normal = at same level)
Femoral component difficulties:
• Anteversion > 40º ....................................... subtroch derotation osteotomy
• Narrow femoral canal ................................ Small stem (DDH stem)
• Short femoral neck
• Distortion of proximal femoral shape from previous osteotomies
• Shortening when needed via:
Subtroch Shortening ............................................ If subtroch derotation(several cm).
Neck shortening .................................................... é Psoas & ER release (few cm).
Neck is sequentially shortened until trial reduction is possible, and may be
shortened down to lesser trochanter.
Trochanteric non union
• If trochanteric osteotomy performed, and the acetabular component placed anatomically, the
trochanter may not reach the trochanteric bed
Acetabulum difficulties:
• Key question is whether to place the cup in:
Anatomic (low hip centre).
Non-anatomic (high hip centre) position.
• Cup placement depends on where is the greatest bone stock Æ optimum bony coverage.
• Most authors recommend placement in ! true acetabulum:
JRF.
Facilitate limb lengthening.
Improvement in abductor function.

Anatomic Positioning: (low hip centre)

• Advantages:
1- More anatomic (resotre the shenton, easier lengthening)
2- Better long term success rate
3- Better bone stalk
• Disadvantage:
Difficult especially following many surgeries & in high dislocations
• Technical considerations:
1- Use the transverse acetabular ligament to locate the true acetabulum
2- Ranawat’s Δ preoperatively is done to locate the true acetabulum
3- femoral head autograft fixed with screws used to augment the acetabulum
Non-Anatomic Positioning: (high hip centre)
• Advantages
Technically easier than anatomical placement
• Disadvantages
1- Poor acetabular bone stock
2- Leg length inequality
3- Higher rate of impingement of GT on iliac wing Æ limited abduction.
4- Higher rate of dislocation.
5- Higher rate of loosening (the higher the more loose).
1- Requires adequate bone stock.
2- Avoid LLD > 3 cm ................................................. use long neck.
3- Avoid lateralization of the acetabular component.
4- Avoid over reaming more then necessary for the superior roof.
5- Adequate coverage (50-60%) by medialization down to the inner table.
6- If hip centre is medialized > 1 cm ..................... use wide femoral offset stem.
Acetabular coverage
• Procedures:
1- BG .....................................................................................
2- Cement .................................................................... 85% success
• When reaming, direct most of the reaming in a superior and posterior direction, and take care not
to fracture the anterior wall.
• Dunn & Hess Cotyloplasty: deliberate # of the floar to place cup éin the iliac bone +/- mesh.
• Small acetabular component [offset bore].
Sciatic nerve palsy
• In DDH, sciatic n. has not reach its normal length & its excursion may not be sufficient
• This is in contrast to an adult with a shortened extremity due to trauma in which case the limb
can often be lengthened to its original position
• Attempts at leg length equalisation may result in sciatic neuropraxia
• Kavanagh Index
LLD < 4 cm ....................................................................... No patients developed palsy.
LLD > 4 cm ....................................................................... 28% of patients developed palsy.
Abductor Function:
• GT lies superior to femoral head d.t. osteonecrosis & trochanteric overgrowth.
• Procedures:
Appropriate femoral component é offset to improve abductor fx.
Psoas release.
Superior Abductor slide (advancement of abductors origin up).
If cannot reattach abductors/ grt. troch. then attach it to fascia lata in wide
abduction & immobilise in abduction for 6w.


III Previous hip arthrodesis
• Indications:
Severe persistent low back pain
Ipsilateral knee pain
Painful pseudarthrosis
Knee has a tendency for valgus deformity when the hip is fused
Poor fusion position (flex > 30º/add >10º/Any abd or IR) Æ consider osteotomy.
Assess abductors function, difficult, but sometimes can be felt on contraction:
If abductors inadequate procedure will be abandoned
• Safer and easier with a trochanteric osteotomy.
• Sciatic nerve can be closer than normal so care needed.
• Divide the femoral neck with a saw.
• Release psoas and capsulotomy, ream acetabulum.
• If abduction < 15º, adductor tenotomy performed.
• Post op treatment routine, except 3 months of crutches whilst abductors are strengthened.
IV Failed proximal femoral osteotomy
• Requires careful reaming.
• May require repeat osteotomy either as a one stage procedure or a two stage procedure.
V Advanced OA:
• May need to removal of some osteophytes before dislocation.
• Hard sclerotic subchondral bone and needs good reaming.
• Curtain osteophytes may obscure the Pulvinar.
• Inferior osteophytes may displace the head out so must be removed to seat the head.
VI Inflammatory Arthritis:
• The risk of infection, fracture, bad skin is high.
• Anesthesia may encounter problems é intubation (atlanto axial subluxation).
• Abnormal blood discriasis.
• Osteoporosis.
• Severe bilateral deformities that may call for Osteotomies.
• If the epsilateral knee has severe flexion deformity operate first on knee.
• Pt is usually satisfied although his higher rate of complication.
VII AVN:
• May be bilateral if ideopathic
• High incidence of complications é cemented
• Thick vascular capsule Æ more bleeding
• Remove previous core graft using high speed burr cause varus placement & undersizing


VIII Revision Hip Arthroplasty
Rational
• Increasing numbers of revision hip replacements are being performed
• Much more difficult than primary surgery.
• Results definitely not as satisfactory as primary surgery.
Complication Incidence
Infection rate 30% aseptic loosening.
Failure rates 30% failure rate at 8 years.
Failure rate with longer stems 10% at 6 yrs.
• Many failed primary arthroplasties can be traced to a technical problem at the time of the primary
surgery. This is often the case when the pain has been present since immediately post op.
• A well done 1ry procedure clearly provides the patient é the best chance of long term success.
Indications
1]. Painful aseptic loosening of one or both components (most common).
Progressive loss of bone.
2].
Fracture or mechanical failure of the implant.
3].
Recurrent or irreducible dislocation.
4].
Infected total hip arthroplasty as a one or two stage procedure.
5].
Treatment of a periprosthetic fracture.
6].
Contraindications
1]. Pain referred from elsewhere.
Very debilitated é complex reconstruction, Girdlestone would probably be better.
2].
Rarely indicated for painless loss of motion.
3].
Not indicated for painless limb length discrepancy.
4].
Be wary of operating for limp éout an obvious cause.
5].
Be wary of operating for pain éout an obvious cause.
6].
When the pain that was present prior to hip replacement persists, the pain was probably
7].
not from hip.
Preoperative planning
• Good quality AP & lat PXR to determine any mismatch bet. femoral bow and the long stem.
• If intrapelvic cement present or markedly protrusion may require IVP and ANGIOGRAPHY.
• Acetabular defects can be accurately assessed é CT even é metal backed acetabular component.
• Ensure access to the original op note and information about the prosthesis to be removed.
• Ensure adequate equipment is present.
• If allograft bone required order it in advance.
Equipment to consider using:
1]. Image intensifier and radioluscent op table.
2]. Stem extraction instrument.
3]. Hand and or motorized cement removal instrumentation.
4]. Flexible medullary reamers.
5]. Flexible thin osteotomes for cementless stem removal.
6]. Fibreopic lighting.
7]. Screws and pelvic reconstruction plates.
8]. Trochanteric fixation device and cerclage wires.
9]. Allograft bone.

Surgical approach
• Previouus skin incisiion should be used if possible
p
• Any ap pproach used for prrimary surg gery can be b used for f revision n, but for most com mplex
procedures the tra anstrochanteric appro oach is best
• The po osterolateral approach h is good foor posteriorr aspect off the acetab bulum and d the femurr but
not goood if the an
nterior aspect of the accetabulum needs
n to bee reconstru
ucted é retained stem
• A reasoonable apprroach men ntioned in Campbells
C iss to begin with
w a postterolateral approach
a and a
trochannteric osteo
otomy can be b performmed at any stage
s if neccessary (stan
ndard or tro
ochanteric slide
or exten
nsive trocha anteric oste
eotomy (see e femoral reevision tech hnique)
Stem Removal
• Loose does
d not alw
ways easily removed
• Use thee designate ed extraction device
• If no de
esignated extraction
e device, use the
t collar ass a platform
m to punch stem out
• If curve
ed proximal stem remo ove lateral proximal
p ement 1st
ce
• If after removal ofo proximal cement the t prostheesis will no
ot come out, perform m an exten nded
trochan nteric osteo
otomy to exxpose more e of the cemment prosth hesis interva
al
• Or makke a windo ow anteriorly not at thhe tip of the
e prosthesiss but just d
distal to the
e level to which
w
cementt has been removed


Removal of cement from femur
THREE STAGES APPROACH:
1]. Metaphyseal Stage ....................................... above lesser trochanter.

2]. Diaphyseal Stage ................................... below lesser trochanter
3]. Distal plug Stage .................................... below the cement.
• Usually performed after revision

of cup because bleeding from
the femoral canal can obstruct
the view of the acetabulum.
• SEGMENTAL CEMENT EXTRACTION APPROACH: although initially

advocated for removal of all cement; currently it is utilized for the
diaphyseal cement stage and the distal cement plug:
A- Special threaded rod is inserted into the canal.
B- New cement is applied over the threaded rod.
C- New cement injected will bond firmly with the preexisting
cement (stronger than BCI).
D- Cement is then removed in steps with an extraction system.
Instruments:
1]. Oscar (high frequency ultrasound probes).
Osteotomes, radial splits Æ wedging BCI.
2].
Pituitary rangeurs.
3].
Fibreoptic lighting.
4].
If difficult, extended trochanteric osteotomy.
5].
All cement should be removed in the presence of infection.
6].
High speed burr but with image intensifier.
7].
Removal of cup and cement from acetabulum
• Loose all polyethylene cup.
• If cup has a flange remove it.
• Remove some peripheral cement.
• Use a thin curved ostetome between the cup and the cement.
• Avoid using the osteotome at BCI ........ fracture of bone may occur.
• If this fails .......................................................... try quartering the implant
with a saw or burr.
• Other types of cup are more difficult to remove (see Campbells).

Reconstruction of acetabular deficiencies

AAOS classification of acetabular deficiency
Type I SEGMENTAL DEFICIENCY Complete loss of bone in supporting rim of acetabulum,
• Peripheral including the medial wall,
Superior
Anterior
Posterior
• Central, medial wall absent
Type II CAVITATORY DEFICIENCY Volumetric loss in the substance of the acetabular cavity.
• Peripheral
Superior
Anterior
Posterior
• Central, medial wall intact Protrusio is an example of cavitatory central defect
Type III COMBINED DEFICIENCY Protrusio with deficient medial wall
Type IV PELVIC DISCONTINUITY Fractures of the anterior and posterior columns with
separation of the superior and inferior portions of the
acetabulum
Type V ARTHRODESIS No deficiency of acetabulum, but difficult
Causes of acetabular deficiency

• Osteolysis caused by wear, loosening or infection
• Excessive bone resection at previous surgery
• Pre existing defect due to dysplasia
• Destruction of bone during removal
Objectives of acetabular reconstruction
• Restore anatomical centre of rotation of the hip
• Restore structural integrity of the acetabulum
• Restore normal joint mechanics & limb length
• Adequate containment of the new prosthesis
• Adequate fixation of the prosthesis & the BG
• If previous component cemented then revise to uncemented; and vice versa
Segmental defects
• Small defects ................................................... can be ignored
• Peripheral defect ........................................... structural auto/allograft (esp. large post & sup deficiency)
• Central defect ................................................ morsellized autograft/allograft; or use mesh
• Femoral head structural BG usually sufficient + fixation (screws superiorly / plate posteriorly)
Cavitatory defects: easiest to deal with
• If small................................................................. ream to a slightly larger size Æ the area of contact
• If larger .............................................................. reaming will breach the rim; ∴ impaction grafting
(morsellized)
• This is only a filler not a structural support, so the intact acetabular rim is used as support
Combination of segmental and cavitatory defects
• Often coexist ................................................... Reconstruct segmental deficiency first to restore the rim
• Any remaining cavitatory .......................... fill é morsellized graft
Pelvic discontinuity
• Requires plate fixation of fracture
• May require entire acetabular structural allograft

Reconstruction of femoral deficiencies
AAOS classification of Femoral deficiency

Type 1 Segmental deficiency Any loss of bone in the supporting shell of
• Proximal partial the femur
Proximal complete
Intercalary (intact bone above and below/ cortical
• Greater trochanter window)
Type 11 Cavitatory deficiency A contained lesion with Excavation of either
• Cancellous cancellous or endosteal cortical bone
• Cortical
• Ectasia (dilatation of the femur with loss
of cancellous bone and cortical thinning)
Type111 Combined deficiency
Type1V Malalignment Eg due to previous osteotomy
• Rotational
• Angular
Type V Femoral stenosis
TypeV1 Femoral discontinuity fracture
Same Objectives
Segmental defects
• The revision prosthesis should extend at least 2 or 3 shaft diameters distal to the defect
• If hole < 30% of shaft diameter .............. particulate graft can be used
• Defects >30% ................................................. onlay cortical strut graft fixed é cerclage wires
• If proximal loss ................................................ structural BG + distal stem fixation or long neck (4 LLD)
• Massive allograft may be necessary, with cement, as bone ingrowth will not occur. Best method
of fixing the allograft to host bone not known yet
Cavitatory defects
• Always present to some degree ............ on revision of femoral prosthesis
• To regain cement interdigitation .......... use morsellized impaction grafting + cemented stem +
distal plug
Deformity of femur
• Correct deformity by osteotomy ............ extensively porous coated stem ± hip spica

13. New Trends
1-Primary Total Hip Arthroplasty

1- Fixation with Cement
• Controversies exist with regard to the most optimal stem surface finish for cement fixation
• White et al. reviewed the two to five-year results of 251 hip replacements that had been
performed by multiple surgeons using stems with four ' different surface finishes (polished,
matte, rough, and 'precoated with methylmethacrylate). There were no differences among
the four groups with regard to the clinical or radiographic outcome.
• Stems with precoated matte finish have a mean duration of follow··up 7.4 years (range, five
to eleven years). The rate of stem survival was 97.8% at ten years, with loosening as the end
point. These data were in contrast to previous reports describing accelerated early
debonding with this particular stem design. Surface finish may be a critical factor in the
durability of fixation with cement, particularly with specific stem geometries.
2- Fixation with Out Cement

• There has been little new information on the clinical outcome of cemehtless hip arthroplasty.
Implants with a coating of hydroxyapatite have been dely used. It is appealing to apply
other chemical or pharmacological additives to the implant surface for the purpose of
improving fixation, preventing loosening or osteolysis, reducing infection, or delivering
analgesia.
• Which a titanium-alloy cylinder with a porous coating with without growth factors (TGF-
beta and IGF-I) was placed in resurfacing arthroplasty.
• There has been a resurgence of interest in resurfacing arthroplasty. Sales of resurfacing
implants have become one of the fastest-growing segments in the worldwide market. The
use of this procedure in the United States is limited at the present time. The clinical outcome
of total surface arthroplasty has been reported to parallel that of stem-type total hip
arthroplasty. Amstutz et a1.l· reported on 400 metal-on-metal hybrid surface arthroplasties.
• One of the complications of surface arthroplasty is femoral neck fracture. Mont et a1.
reported a high prevalence of femoral neck fractures (22%) in their first fifty cases. With more
experience, the fracture rate was reduced to 0.4%.
• However, technical factors, including notching of the lateral cortex, out-of axis reaming, and
excessive removal of marginal osteophytes from the femoral neck, were identified as
contributing risk factors. Limb-length equalization within 1 cm was achieved with both types
of reconstruction. The authors concluded that surface arthroplasty is less ideal in patients
who have a substantial leg-length inequality or a varus neck-shaft angle (large offset)
preoperatively.

2-Revision Total Hip Arthroplasty

• Fortunately, the year-to year revision rate did not increase over this period.
• Moreover, the cause of failure leading to revision surgery has changed. osteolysis The most
common mode of failure leading to revision was osteolysis, followed by loosening and
recurrent dislocation.
1- Acetabulum
• A pelvic reinforcement cage has been used most often in conjunction with structural
allograft to address major acetabular bone deficiencies. surgeons also reported that they
inserted a tantalum shell to bridge major bone deficiencies and supported the shell with a
pelvic reinforcement cage in selected situations. The long-term durability of this device and
technique remains to be validated.
2- Femur
• Allograft-prosthesis composites have been utilized for patients with extreme femoral bone
deficiencies. In patients had Paprosky type-III or IV femoral bone deficiencies. Major
complications included 1 infection necessitating hip disarticulation, 2 recurrent dislocations,
2 wound hematomas, and 8 intraoperative femoral fractures. This technique serves as an
alternative to the use of either large-diameter extensively coated cylindrical stems or modular
tapered stems for these complex reconstructions. Another option for addressing massive
femoral bone loss is to use a megaprosthesis originally designed for reconstruction following
tumor resection.
• Complications included infection and dislocation one of these patients. The high rate of
dislocation may be reduced with use of newer constrained liners and soft tissue
reconstruction around the prostheses. The rate of infection may be reduced with use of
suppressive antibiotic therapy and antibiotic impregnated bone cement.
3-Complications management
1- Thrombo-embolic Disease
• It is agreed that prophylaxis against venous thromboembolism is required following total hip
arthroplasty. Substantial controversies remain with regard to which method is the safest and
most effective. The newest form of prophylaxis is the use of an oral direct thrombin inhibitor.
Extensive phase-3 clinical trials of one such direct thrombin inhibitor (ximelagatran) have
been performed in patients managed with hip or knee arthroplasty. Ximelagatran was more
efficacious than warfarin in patients managed with knee arthroplasty (p = 0.003)25, but it
was not superior to low-molecular-weight heparin in patients managed with hip
arthroplasty. There was no difference between warfarin and low-molecular-weight heparin
with regard to bleeding complications.
2- Dislocation
• Recurrent dislocation has now become the third most frequent\cause of revision surgery,
resulting in an intense focus on surgical technique, large diameter articulations, increased
femoral stem offset, and rehabilitation protocols. One of the most common methods with
which to address dislocation is the use of a constrained acetabular liner.
3- Infection
• Serum interleukin- 6 levels is used as a marker for infection as it has significantly elevated
levels in the patients with infection (p < 0.01). Elevated levels were found to have a sensitivity
of 1000/0, a specificity of 95%, a positive predictive value of 89%, a negative predictive value
of 100%, and an accuracy of 97%. This test may be of value in some cases, particularly for
excluding infection as a cause of a suboptimal clinical result. polymerase chain reaction
analysis on the synovial fluid. A two-stage reimplantation protocol has been used for the
treatment of deep infection around joint replacements for more than two decades.

4-Bearing Surface
• Wear at the bearing surface is one of the most important areas of research related to total hip
arthroplasty. This is reflected by the fact that wear and osteolysis are among the most frequent
causes of revision surgery.
[1]. Highly Cross-Linked Polyethylene
• The principal aim of highly cross-linked PE is to surface wear and oxidation. At the present time,
six different types of HCLPE are commercially available, all differ in radiation dose, radiation
technique, thermal treatment to remove free radicals, and sterilization technique.
• Such differences Æ influence the wear characteristics and mechanical properties of a given
material.
• Greater amount of free radicals found in material made é postirradiation annealing (heating
below the melting temperature) compared with materials that were melted.
• Greater amounts of free radicals also were found in the material following artificial aging (5
atmospheres of oxygen at 70°C to 80°C for two weeks)
• Post-irradiation melting crystallinity of PE ( annealing) Æ modulus of elasticity & yield
strength & ultimate tensile strength
[2]. Ceramic
• Implant fracture is the most feared complication associated with ceramic bearings.
[3]. Metal-on-Metal
• The current generation of metal-on-metal couplings was introduced into clinical application in
1988... This bearing coupling has been used more frequently with the in surface arthroplasty.
• Its success depends on several factors:
1]. Larger-diameter femoral heads to dislocation.
2]. Larger heads allow wider ROM & better rehabilitation.
3]. Surface roughness (Ra); Smooth surface ( easy lubrication .
(Cr-Co = 0.05 μm / Zr = 0.02 μm / UHMWPE = 400 μm).
4]. Radial clearance RC (= cup diameter - head diameter):
-ve RC = Equatorial bearing Æ lubricant ingress & egress Æ fric torque.
RC = Polar bearing + low conformity Æ friction and wear.
RC ~ 150μm = Polar bearing + high conformity Æ allow lubricant ingress.
5]. Carbon content in manufacturing Æ wear.

6]. Sphericity variation is < 10μm Æ high surface points Æ stress points; “Run-In”
phenomenon in hard-to-hard bearings occurs during the first few million cycles of wear, in
there is a high wear rate (ًsphericity variation), after there is a low steady rate of wear.
7]. Studies shows no change in the serum metal ion level of Cr-Co, nor in the urine.


[4]. Surface Arthroplasty

Advantages:
1]. Anatomical.
2]. Near normal biomechanics: the sector removed is exactly replaced.
3]. Large head Æ less dislocation rate.
4]. Better lubrication Æ less friction (metal-on-metal).
5]. Easy revision.
Ideal cases
1]. OA without change of the head shape.
2]. Head/neck ratio > 1.2.
3]. Long neck > 2cm.
4]. Valgus neck.
5]. Below 60y.
High Risk
1]. Head cyst > 1cm.
2]. Abnormal shaped head; e.g. old perthes.
3]. Weak stalk e.g. AVN.
4]. Head/neck ratio <1.2.
5]. Short neck.
6]. Loss of the lateral bone stalk of head & neck.
7]. Shallow acetabulum.
8]. Abnormal biomechanics; e.g. protrusion acetabuli, femoral deformity.
Complications
1]. Fractures.
2]. Capsulitis ossificans.
3]. Implant Failure:
o Fracture neck.
o Osteonecrosis.
o Mechanical failure of implant cement interface.
4]. Cr in blood? carcinogenic?
5]. Others complications of the conventional arthroplasty; e.g. infection, dislocation, DVT.
[5]. Immune Response

• At the present time, there is no conclusive evidence regarding any adverse clinical impact from
metal debris and ion release in patients with metal-on metal articulations. The histological
appearance of periprosthetic tissue obtained from hips with early-generation metal-on-metal
couplings was generally characterized by a mild foreign-body reaction. perivascular lymphocytic
infiltrate with histological features resembling those associated with a type-IV hypersensitivity.

5- Practice Management
1- Wound Drain
• The use of wound-suction drains following total hip arthroplasty is controversial. Parker et
al.28 conducted a meta analysis evaluating the efficacy of using and not using wound drains
following total hip and total knee arthroplasty. The investigators selected eighteen
prospective, randomized studies involving 3495 patients with 3689 wounds. There was no
difference between patients who had been managed with a drain and those who had not
with respect to the occurrence of wound infection, hematoma, or reoperation for wound
complications. There was also no difference with respect to pain, thromboembolism, or
range of motion. The only significant difference was a greater rate of transfusion among
patients who had been managed with a drain (p < 0.02).
2- Blood Transfusion
• Limiting allogeneic blood transfusion is desirable because it would reduce the potential for
viral disease transmission as well as cost. Pierson et al.29, in a study of patients undergoing
total hip and total knee arthroplasty, presented a blood conservation algorithm, based on a
mathematical formula, that was used to calculate the projected lowest hemoglobin level
after surgery. If this level was <7.0 g/dL, the patient was offered preoperative erythropoietin
treatment. No intraoperative or postoperative blood salvage was done.
3- Pharmacological Agents and Bone-Remodeling

• The adverse effects of nonsteroidal anti-inflammatory drugs on fracture repair and bone-
remodeling have been extensively studied .. The revision rate among patients who had been
managed with a cementless replacement and nonsteroidal anti-inflammatory drugs was
higher than that among patients who had not received nonsteroidal anti-inflammatory
drugs (relative risk, 3.09). In contrast, the revision rate among patients who had been
managed é a cemented hip replacement & NSAIDs was < that among pts who had not
received NSAIDs, (possibly ð a protective effect). The investigators recommend avoiding the
use of NSAIDs after surgery if cementless fixation was used. Periprosthetic femoral bone loss
due to stress transfer is generally greater in association é cementless implants and in Gruen
zone 7 (the calcar region) Decreasing peri prosthetic bone loss is important because more
patients are receiving cementless total hip replacements and because the implants remain in
place for longer durations.
• A study was conducted using Biphospdonate to determine its inhibitory effect on bone loss
and follow up with The marker of bone resorption (C-terminal telopeptide of type-l collagen)
for as long as six months in association é bisphosphonate treatment.
• One marker of bone formation (bone-specific alkaline phosphatase) increased, whereas
another (osteocalcin) remained unchanged in association with bisphosphonate treatment.
However the data available should be taken with caution until further studies is available
Hip Disorde
[H ers] Page | 731

4. Miini In
14 nvasiv
ve TH
HR
Definition:
• Mini-invvasive Total Hip Repla acement (M MITHR) surggeons mean a skin incision ≤ 10 0 cm associiated
with red duced tissu ue trauma
Indications
• No absolute indica ation
• Cosmettically bette er
Contraindications
• Problem matic 1ry TH HR; e.g. DDDH, protrusio, femoral deficiency,
d acetabularr deficiency
• Revision n arthropla asty
• Single oro double stage re-imp plantation.
Ad vantages
dv
[1]. Better cosmetic
c apppearance.
2]. Reduce
[2 ed tissue disssection.
3]. Reduce
[3 ed intra and d postopera ative blood loss.
4]. Reduce
[4 ed blood tra ansfusion.
5]. Reduce
[5 ed postoperrative pain and narcottics.
6]. Reduce
[6 ed operative e time.
7]. Reduce
[7 ed hospital stay.
8]. Rapid recovery an
[8 nd early retu urn to everyyday activitties
Disadvantages
[1]. Inadequate expossure (Interm mittent com mplete visualization).
2]. Eccentrric reaming
[2 g and comp ponent malp position.
3]. Difficultt in larger patients
[3 p witth high BMII.
4]. Increased operativ
[4 ve time at fiirst till impro
oving surge
eons skills.
5]. Need sp
[5 pecial instruuments.
6]. Same complication
[6 c ns as stand
dard THR: diislocation, component
c t loosening
g and femorral fracture..
Complications statistically higher than standard THR
1]. Femora al fracture
2 Acetab
2]. bular comp ponent loosening
3 Disloca
3]. ation.
Techniques three main categories:
1.. Modific
cations of Stand
dard Ap
pproach
• Approa aches that are

a used co ommonly fo or THR but performed
p through wwounds 7-100 cm in lenggth
A Modifie
A. ed minima e Posterio
ally invasive or Moore-G Gibson Ap pproach A 7-10 cm skins incisio
on is
done along
a the posterior
p a
aspect of th
he greaterr trochanteer with 70% of the in ncision plaaced
distal to
o tip of the
e greater trrochanter and
a 30% proximal
p to
o it.
B. Modifie ed minimally invasive e Anterolaateral (Wa atson-Jonees) approa ach
C. Modifie ed minimally invasive e Anteriorr (Smith-Pe eterson) approach:
a A 5-8 cm curved
c incision
with itts convexitty placed laterally frrom a point just disstal to the e ASIS exteending to the
anterioor border ofo the greatter trochan nter
D. Modifie ed minimally invasive e Lateral (H
Hardinge) approach h is c entered on
a pointt 2 cm disttal to the tip
t of the greater
g trochanter annd the inciision is
marked d 1.5 inchees on both sides of thhis point, th
he proximaal half anglled 30°
posterior to the loong axis off the femurr and the distal
d half 30°
3 anterior.

2. The TwoIncision Approach:
• Posterior incision for femur + anterior incision for acetabulum.

• Position: supine.
• Skin Incision: lies three fingerbreadths distal to the line connecting anterior–superior iliac spine
and greater trochanter which corresponds to the femoral neck extending form the head-neck
junction to 2 inches distally and its position is confirmed by fluoroscopy using a metal marker.
• Dissection: First between sartorius and tensor fascia lata taking care of lateral circumflex n.
• Then dissection between rectus femoris and gluteus medius retracting rectus femoris medially
exposing lateral circumflex vessels ώ are cauterized and exposing the hip joint.
• The capsule is incised along midline of femoral neck from edge of acetabulum to intertrochanteric
line and retractors are replaced intracapsular
• Two neck osteotomies are done in situ and "hockey puck" section of the neck is removed using a
Schanz pin allowing removal of the femoral head by a Schanz pin or corckscrew.
• Then acetabular reaming is done using specially designed, low profile reamers that are cut out on
the sides and aggressive square cutting teeth, followed by insertion of cup
• To access the femur, the surgeon passes an index finger around the posterior aspect of the
gluteus medius (between it and piriformis muscle) pointing proximally and posteriorly into the
buttock and a 2 cm transverse incision is marked on skin over the surgeon's finger.
• Then an awl is passed through this incision to the piriformis fossa and starts the entry point in the
femoral canal, followed by femoral preparation.
3. Navigation System
•Computer guided Image analysis system that allow for precise planning of the components
alignment before surgery, and to perform mini-invasive THR with the same efficacy as standard
THR.
• Includes 2 components.
Preoperative Planning:
• Data Input: input the data into the navigation computer system.
o 3D CT scan.
o Implant database.
o Patient database.
• Data Processing to detect optimal parameters as regard:
o Components size.
o Components orientation.
o Hip centre.
o Required ROM simulation for selected size & orientation.
• Intraoperative Guidance: depends on insertion of optical probes on specific points directly on
the bone. Optical sensor is mounted to receive data impulses from the probes; these data are
tailored into the previous data on the system about the pt & the implant to give certain angles &
directions during surgery, bony preparation, component choice & position
Special Instruments Needed
• Were designed to overcome inadequate exposure resulting from incision and dissection
• Curved acetabular reamers.
• Notched femoral reamer.
• Curved impactors.
• Flanged retractors supplied by light source for illumination.
• Square reamer (cut out on the sides).
• Femoral elevator.


Fracture Neck Femur
Trochanteric Fracture

Dr Mohamed Sobhy
The Knee

[Knee Disorders] Page | 737
Knee Anatomy
Muscles
Biceps Femoris
• multiple insertions
• 3 layers:
o superficial layer - superficial to LCL
o middle layer - surrounds LCL
o deep layer - attaches to head of fibula & Gerdy's tubercle on tibia
• Function - flex knee & externally rotate tibia
Popliteus
• forms floor of popliteal fossa
• muscle attached to posterior tibia - tendon passes intraarticularly deep to femoral
attachment of LCL to attach to femur
• Functions
o flex & internally rotate tibia when leg is free OR externally rotate femur on tibia
when tibia is fixed.
o dynamic reinforcement of PCL, preventing post. displacement of tibia on femur
Semimembranosis 5 distal attachments:
1]. Oblique Popliteal ligament
2]. Posterior Oblique Ligament
3]. Deep Head - deep to MCL (Pars reflexa)
4]. Direct Head - to post medial tibial condyle
5]. Anterior Expansion - over anterior leg fascia
6]. Popliteal expansion: over the popliteus fascia
Pes Anserinus
1. Sartorius, gracilis & semitendinosis (Say Grace before Tea)
2. sartorius - very broad insertion, forming a sheath over gracilis & semiT
3. Gracilis - smaller & anterior to semiT
4. Semitendinosis - enveloping muscle belly extending more distally
5. Functions - flexor of knee & internal rotator of tibia
Iliotibial Tract
1. inserts into GERDY'S tubercle on the tibia & extends to form the lateral patellar
retinaculum
2. also attaches to the lateral femoral condyle forming a static lateral restraint
3. Function: since it crosses the centre of rotation of the knee moving from flexion to
extension it acts as a flexor in flexion & an extensor in extension
738 | Page [Knee Disorders]
KNEE STABILISERS (ANATOMICAL)
I- EXTRA-ARTICULAR: see later
II- INTRA-ARTICULAR STRUCTURES
1]. Anterior Cruciate Ligament
• Intraarticular extrasynovial
• Anteromedial fibers - tight in flexion - limits anterior
translation of tibia on femur
• Posterolateral fibers - tight in extension - limits anterior
translation plus external rotation
• Bl.supply - middle genicular a. (post) & synovial vv (ant)
• Mechanoceptors with a proprioceptive role
• Acl strength = 50% pcl strength
• Load to failure = 1700n
• STRAIN RATE plays a role in the failure location
1. Midsubstance tears occur at higher rates
2. Avulsions occur at lower rates
2]. Posterior cruciate ligament

• 2 bundles: posteromedial and anterolateral
• Function:
1]. Limits hyperextension
2]. Prevents post translation of tibia on
femur especially during flexion
3]. Meniscofemoral ligaments:

1. Ligament of HUMPHREY - anterior
2. Ligament of WRISBERG - posterior
4]. Meniscii
• Fibrocartilagenous crescent; triangular in cross-section
• Lateral meniscus is more circular; medial meniscus more c-shaped
• Lateral meniscus has twice the excursion of the medial meniscus during knee motion.
• Anterior horn of LM & post horns of both menisci attach to the intercondylar eminence
• Anterior horns attached to each other by the intermeniscal ligament
• Popliteus muscle is attached to lateral meniscus (not the tendon)
• Semimembranosis is attached to medial meniscus
• Blood supply:
o From branches of the lateral, middle & medial genicular arteries
o Vascular synovial tissue from the capsule supplies the peripheral 25% of
meniscus
• Constituents:
1. Type 1 collagen fibers arranged radially & longitudinally (circumferential)
Longitudinal fibers - dissipate hoop stresses in the meniscus
Radial fibers & longit fibers - allows meniscii to expand under
compression
2. Proteoglycans trapped within collagen fibers to absorb energy
• Functions:
o Provision of stability
o Shock absorption
o Provision of increased congruity
o Aids lubrication
o Prevents synovial impingement
o Limits extremes of flexion & extension
o Transmits loads across the joint – 50- 100% of load is transmitted through
menisci
o Reduces contact stresses
• Mechanics:
o The circumferential fibers act in much the same way as metal hoops placed around a
pressurized wooden barrel. The tension in the hoops keeps the wooden staves in
place.
o The compression of the menisci by the tibia and the femur generates outward forces
that push the meniscus out from between the bones.
o The circumferential tension in the menisci counteracts this radial force.
o These hoop forces are transmitted to the tibia through the strong anterior and
posterior attachments of the menisci.
o This hoop tension is lost when a single radial cut or tear extends to the capsular
margin and that in terms of load-bearing, a single radial cut through the meniscus is
equivalent to meniscectomy.
• Following total menisectomy there is a decrease in tibiofemoral contact area and an
increase in the contact stresses
• With only one third of the meniscus removed, as with partial meniscectomy, there has been
shown to be an estimated 65% increase in articular contact stress
• total meniscectomy may increase peak loads up to 235%
• In the ACL-deficient knee the menisci, specifically the posterior margins aid in stabilising the
knee from anterior translation.
NERVE SUPPLY
Motor
• Femoral n. - All 4 Quad muscles and the sartorius [Picture]
• Tibial Component of the Sciatic n. - Semitendinosis, Semirnembranosis, and the LHB
• Common Peroneal Component of the Sciatic N. - Short head of Biceps
• Obturator n. - Gracilis
Sensory
• Saphenous nerve is the largest cutaneous branch of the femoral nerve, and supplies
sensation to the skin over the anteromedial aspect of the leg [Picture]
• The main terminal branch, the sartorial nerve, runs distally with the greater saphenous vein
• The infrapatellar branch of the saphenous n. arises proximal to the knee joint, around or
through the sartorius, and then crosses underneath the patella to innervate the skin over
the proximal anterior tibia
• Free nerve endings are prominent in the peripheral portions of the menisci Æ transmit pain
• Mechanoreceptors have been identified in the anterior and posterior horns
• ACL & PCL receive nerve fibers branches of the tibial n. Æ proprioceptive and sensory
PATELLA
• Largest sesamoid bone in the body (usually 3 - 5cm in length)
• Patella tendon to patella length usually ratio of 1:1 (+/- 20%)
• 10% of patients have complete supra-patella membranes and 75% will have at least one of
the 3 plica's even if only as a remnant (supra-patella, medial patella or infra-patella)
• Ossification centre appears between 2 and 3 years of age but can be as late as 6 years
• Blood supply is via the anastomosis of the genicular vessels via the anterior-middle 1/3 and
is directed mainly upwards, from the inferior pole vessels also enter from the deep surface
• Function:
1]. y quadriceps lever arm Æ y mechanical advantage of the quadriceps
2]. Aid articular cartilage nourishment of the femoral condyles
3]. Provide some protection of the femoral condyles
• Normal function depends on the alignment, stability, articular cartilage and muscle control
Knee Mechanics
KINEMATICS
Instant Center of Rotation
• "If one rigid body rotates about another rigid body, its motion at any instant can be
described by a point or axis of rotation called the instant center of rotation (ICOR).
Surface Joint Motion

• Motion between the tibia and the femur is both rotational and translational. The femoral
condyles both ROLL BACK and glide as they articulate with tibial plateaus. As the knee
moves from full extension into flexion the ICOR moves posteriorly relative to both the
femur and the tibia. This increase the flexion range
Screw home mechanism

• It is the lateral rotation of the medial tibial plateau on femur during stance phase (extension), and
internal rotation during swing phase (flexion).
• 3 factors leads to this mechanism:
1]. The more distal alignment of the MFC
2]. The bigger radius of curvature of the MFC
3]. The cruciates crossing in-between; around which this rotation occur
• Its significance it that it tightens both cruciates and locks the knee in the position of maximal
stability
Patellofemoral Joint
1. 1ry function of the extensor mechanism of the knee is deceleration during the swing phase
2. FUNCTIONS:
1. increases the moment arm of the quadriceps
2. allows wider distribution of compressive stress between the patellar tendon & the
femur
3. from full extension to full flexion the patella glides caudally 7cm on the femoral condyles.
4. by 20 º of knee flexion the patella first begins to articulate with the trochlear groove. Beyond
90º the patella rotates externally & only the medial facet articulates. At extreme flexion the
patella lies in the intercondylar groove.
5. Initially the patella contact occurs distally and with increased flexion the contact areas shift
proximally on the patella
6. patellofemoral contact pressure is 0.5 times body weight with walking, and increases to 2.5
to 3.3 times body weight with stair climbing and descending
Knee Instability
Definition
• It is the loss of normal relationship among the different parts of the joint throughout the
whole arc of motion
Anatomy: (knee stabilizers)
I. Extra-articular
Site Layer Content Importance
Medial Layer 1 Crural fascia investing sartorius & gastroc
WARREN &
(W Sartorius
MARSHALL): Layer 2 Superficial MCL 1ry restraint in 30º
POL 2ry restraint in 0º
Semimembranosus
Layer 3 Deep MCL
Coronary lig
True capsule 2ry restraint in 0º
Lateral Layer 1 ITB
Biceps
Layer 2 Patello-femoral lig 2ry restraint in 0º
Patellar retinacula
Layer 3 LCL 1ry restraint in 30º
Arcuate
Capsule 2ry restraint in 0º
PMC = postero-medial quadruple 1]. MCL
NICHOLAS and MINKOFF
(N 2]. Semi-membranosus & its 5 attacments…
quadruple complexes) 3]. SGS
4]. OPL / POL / PMC
PLC= postero-lateral corner 1]. LCL
2]. ITB
3]. Arcuate
4]. Popliteus Tendon
5]. Biceps Tendon
6]. Popliteo-Fibular Ligament (PFL)
AMC AM capsule
Medial retinacula
Patellofemoral & patellotibial lig
ALC AL capsule 1ry restraint
Lateral retinacula
ITB
Anterior ACL 1ry restraint
Mid med & lat capsule / ITB / Mensci / collatrals 2ry restraints
Posterior PCL 1ry restraint
Internal Rotation ACL 1ry restraint
POL / PMC 2ry restraints in 45º
External Rotation PFL & MCL 1ry restraint
POL / PMC / LCL / PLC 2ry restraints in 45º
Arcuate Complex 1]. LCL 4]. Biceps tendon
2]. Arcuate lig (Y shaped condensation) 5]. Lateral head gastroc
3]. Popliteus tendon
II. Internal structures:

ACL, PCL, Menisci and their ligaments
Knee biomechanics:
• The MECHANICAL AXIS of the femur ≠ anatomical axis = 7º
• This produces greater WB stresses on the LFC > MFC
• The mechanical axis generally passes slightly medial to the center of the normal knee
• Because of the disparity between the lengths of the articular surfaces of the femoral
condyles and the tibial condyles, TWO MOTIONS are produced; ginglymus (hinge) +
trochoid (pivot):
1]. Flexion & extension ............................ sagittal plane
2]. Some degree of IR &ER ...................... Horizontal plane (5º-25º é the IR > ER)
• The complex flexion-extension = ROCKING + GLIDING:
1]. Rolling motion is demonstrable in the first 20º of flexion
2]. Gliding motion predominates after 20º flexion
• The MENISCI MOVE é femoral condyles in flexion and extension & move é tibia in rotation
• LFC IS BROADER in frontal and sagittal planes > medial
• MFC is taller i.e. projects distally to compensate for the 7º valgus
• MFC is prolonged forward > LFC Æ Screwing and unscrewing occurs around an AXIS NEAR
THE MFC & IS INFLUENCED BY PCL
• No rotation is possible when the knee is in full extension.
• In full extension; femur IR until the medial articular surfaces are in contact & LFC rotates
forward Æ "SCREWING HOME" movement, locking the knee in the fully extended position.
• FLEXION AND EXTENSION are from 0-140º
• Normally there is SAGITTAL LAXITY of the tibia over the femur, but not > 3-5 mm
• Also there is a coronal laxity (abduction-adduction) but never > 0-15º (not with full
extension)
• When the MCL is ruptured...................... the vertical axis of rotation shifts lat & vice versa.
• Changes in the "ICOR" are responsible for OA associated é knee instability
KNEE RESTRAINTS - Sectioning Studies
DIRECTION PRIMARY RESTRAINTS SECONDARY RESTRAINTS

Anterior ACL • ITB ...................................... 25%
• mid medial capsule .... 20%
• mid lateral capsule: ... 20%
• MCL ................................... 15%
• LCL: ................................... 15%
• Menisci
Posterior PCL (large anterior bundle more) LCL
Internal rotation ACL POL/PMC has secondary effect éin 0 - 45 º
External rotation PFL (Popliteofibular ligament) POL/PMC
LCL and PLC .......... mainly at 30 º flexion
MCL .......................... at all degrees
Valgus Superficial MCL .... at all deg (least at full ext) POL - especially near or at full extension
PMC ........................... at full extension ACL
Deep MCL .............. little resistance to valgus
Varus LCL ............................ all degrees (more at 30º , PLC (PFL)
least at full extension ) ACL
Palmer Mechanisms Of Injury
1]. flexion, Abd, IR of the femur on the tibia,
2]. flexion, Add, ER of the femur on the tibia,
3]. hyperextension,
4]. AP displacement.
• F ABD IR is the commonest Æ medial side injury, respectively;

1]. MCL then Medial capsule
2]. ACL
3]. MM = “O'DONOGHUE UNHAPPY TRIAD”
• F ADD ER Æ injury of lat ligaments of the knee;

1]. LCL then lateral capsule
2]. ACL
3]. Arcuate complex
4]. Popliteus tendon
5]. ITB
6]. Biceps femoris
7]. Common peroneal nerve,
• HYPEREXTENSION mechanism;
1]. ACL
2]. PCL & posterior capsule
• ANTERO-POSTERIOR DISPLACEMENT; e.g. dashboard accident:

1]. ACL or
2]. PCL
• ISOLATED LIGAMENT DISRUPTION;

1]. Some say all ligaments work in concert especially the ACL, and probably no single
ligament can be disrupted
2]. Isolated PCL disruption can result from a direct blow to the front of the tibia with the
knee flexed.
• AVULSIONS occur either at the femoral, tibial, or mid-substance
Classification of injury
1- PLANES CLASSIFICATION 2- O'DONAGHUE:

• I. One-plane instability (simple or straight)
Degree Pathology
1]. One plane medial
2]. One plane lateral 1st Degree Sprain Lig injury with no instability
3]. One plan posterior 2nd Degree Sprain partial tear with some laxity
4]. One plane anterior 3rd Degree Sprain complete tear é instability
• II. Rotary instability
1]. Anteromedial 3- NOYES
2]. Anterolateral Grade
3]. Posterolateral
Grade 1 <5mm
4]. Posteromedial
Grade 2 6-10mm
• III. Combined instability
1]. Anterolateral-anteromedial rotary
Grade 3 11-15mm
2]. Anterolateral-posterolateral rotary Grade 4 16-20mm
3]. Anteromedial-posteromedial rotary
History
INJURY SIGNIFICANCE SYMPTOM SIGNIFICANCE
Noncontact + Pop ACL Pain at sitting & stairs Patellofemoral pathology
Patellar dislocation Locking Meniscal tear
Contact + pop Collateral injury Loose body
Menical injury Pseudo Locking PF disorder + painful ext
Fracture Hge + hamstring spasm
Anterior dashboard PCL or Patellar # Acute swelling ACL
Ant + Plantar-flexion PCL Peripheral meniscal tear
Ant + dorsi-flexion Patellar # Osteochondral fracture
Hyper-ext + varus + ER PLC corner injury Giving way Ligamentous injury
Patellar dislocation
Pseudo Giving way Anterior knee pain
(Reflex inhibition of quad)
Examination:
LOOK
• Skin- SCARS, redness, swelling ................. Remember to look in popliteal fossa
• Muscle- WASTING of quads ....................... compare diameter of thigh if quads wasted
• Varus Valgus DEFORMITY( measure intermalleolar distance if valgus)
• Q ANGLE
• Bone/joint- EFFUSION
• Walking - look for varus THRUST = dynamic varus collapse in stance loading (ð laxity)
FEEL
• Skin - Temperature, back of hand
• Muscle- Ask patient to contract quads
• Bone/joint- Effusion fluid displacement test, patellar tap test
• Synovial thickening
• Joint line tenderness (with knee bent)
MOVE
• Active then passive- Flexion & extension (0-140º normal)
• Feel for crepitus
SPECIAL TESTS
1]. MCL + LCL
• leg under arm, 2 hands, 10º flexion to relax pos capsule (careful not to rotate knee)
• Valgus stress in flexion ........................... MCL
• Valgus stress in extension ..................... MCL + POL
• Varus stress (taut in full ext) .................. LCL (normally lax in flexion)
2]. Anterior Cruciate Ligament

1- ANTERIOR DRAW at 90º
2- LACHMAN'S TEST - at 15-30º (put patient's knee over your knee) - most sensitive
3- MACINTOSH THE PIVOT SHIFT TEST- Knee extended, valgus strain, foot internally rotated, if
instability present, tibia is subluxed anteriorly. Now flex knee, clunk at 30º is +ve
4- LOSEE PIVOT SHIFT TEST- knee & hip flexed 45º and the other hand thumb behind the
fibula. ER and valgus the tibia + slow extension + push the fibula forward Æ tibial
condyle shifts or subluxes forwards in full extension.
5- MODIFIED PIVOT SHIFT TEST- Grasp foot between arm and chest, valgus IR stress, , then
flex knee, femoral condyle will 'appear' to sublux ant (but tibia is reducing)
6- JERK TEST (HUGHSTON) - patient supine. flex knee 90º & hip 45º. Internally rotate tibia. Let
knee slowly extend while applying a valgus stress. High false -ve rate
7- ALRI TEST (SLOCUM) - Patient lies on unaffected side, with unstable knee up & flexed 10º.
Medial aspect of foot rests on table. Patient maintains ipsilateral pelvis rotated posteriorly
30-50º. Knee pushed into flexion. Easier to do in heavy or tense patients.
3]. Posterior Cruciate Ligament
1- POSTERIOR SAG (in extension)
2- DANIAL DROP-BACK in 90º flexion (active & passive)
3- GODFREY CHAIR TEST: the same but on a chair
4- POSTERIOR DRAW
5- REVERSE PIVOT SHIFT TEST (JAKOB): knee 30º flexed (Subluxed) Æ valgus ER slow
extension Æ reduces anteior
4]. Posteromedial Corner
1- Hold heel, look for foot position
2- HUGHSTON POSTERO-MED DRAWER............. ACL, MCL sup & deep, (possible: POL, PMC)
• knee flexed & IR then post drawer is done; if lax Æ Postero-med instability
5]. Posterolateral Instability
1- DIAL TEST - pt prone & bend knees or perform supine with the knees at 30º (PLC
only) and 90º (PLC + PCL) &assistant holding the knees Æ ER maximally Æ note
the difference between the two sides; > 15º difference = arcuate / PFL tear
2- HUGHSTON POSTEROLATERAL DRAWER
• knee flexed & ER then post drawer is done; if lax Æ Postero-lateral instability
3- EXTERNAL ROTATION RECURVATUM TEST - by holding big toes, lifting feet off table &
watching to see if tibia falls into ER & Recurvatum
6]. Antero-medial rotary instability ...................... MCL, ACL (possible : POL, PMC)
1- SLOCUM TEST: knee flexed & ER then ant drawer is done; if lax Æ Antero-med instability
7]. Anterolateral rotary instability ......................ACL (possible: PLC, AC)
1- SLOCUM TEST: knee flexed & IR then anterior drawer is done; if lax Æ Antero-lat
instability
2- MAC-INTOCH: .......................................... see before
3- LOSEE: ..................................................... see before
4- JERK: ....................................................... see before
8]. Meniscal, muscle flexibility, others: see later
Different Instabilities of the knee

Plane Direction Test Used Deficient Structure
Valgus Valgus (Full Extension)…………….……….. MCL sup & deep, ACL (possible: POL, PMC, PCL)
Valgus (20-30° Flexion)…………….……….. MCL (possible: POL) Æ O’Donoghue or Hughston
One plane
Varus Varus (Full Extension)……………..………… LCL, PCL, AC, PLC, ACL, ITB
Varus (20-30° Flexion) …………..………….. LCL (possible: PLC, AC)
Anterior Lachman (Only)……………………..…………. ACL (PLF)
Anterior Drawer (Only)……………..……… ACL (AMF)
Lachman & Ant. Drawer…………………… ACL complete (possible: POL)
Posterior Posterior Drawer; Daniel; Godfrey …… PCL
AM Slocum ……………………………………………… MCL, ACL (possible : POL, PMC)
planes
AL Slocum; MacIntoch; Losee; Jerk..................... ACL (possible: PLC, AC)

Two
PM Hughston………………………………………….. ACL, MCL sup & deep, (possible: POL, PMC)

PL Hughston; Jakob; Dial; ERR ……………… PCL, AC (possible: PLC, LCL)
8].
Figure : A; Daniel test, B; Godfrey test, C; Slocum AMRI and ALRI test,
D; Slocum ALRI test for unrelaxed patients, E; Losee Test,
F; Lateral Pivot Shift of MacIntosh, G; Noyes test, H&I; Jacob test.
Meniscal Test
1- HELFET TEST é patient sitting mark the midline of the patella and the tibial tuberosity;
normally in 90° flexion, the tibial tuberosity is aligned with the mid-patellar line & in
extension, it moves laterally. This indicates the normal screw-home movement. If
rotation is blocked, possibly by a meniscal fragment this movement is lost
GRIND TESTS
Fig: A; McMurray test, B; Apley compression, C; Jump test, D; Steinmann test.

2- McMurray: acute knee flexion as possible. The leg is then rotated internally and
externally with varus and valgus rotational stresses Æ Trapping of damaged MM is felt
as a clunk
(at 90º= PHMM / at 60º or less = body or AHMM)
3- ANDERSON GRIND TEST (if full flexion is difficult) varus and valgus rotational stresses are
applied to 45º flexed knee as the knee is extending. The maneuver is repeated with
progressive loading Æ a clunk may be felt
4- APLEY COMPRESSION TEST
5- STEINMANN 1ST test is done with the patient sitting the same as Apley
6- STEINMANN 2ND test is done with the pt supine; ER during flexion & extension Æ pain moves
from posterior to anterior with extension
7- JUMP TEST (especially for pt with ACL tears): knee flexed to 130º-140º. The proximal tibia is
grasped as in anterior drawer and pulled anteriorly with a firm, prolonged force Æ jump or
jerk
COMPRESSION TESTS
Fig.: A; Abduction adduction test, B; Dehaven test, C; spring test

8- BRAGARD’S EXTENSION TEST the knee is hyperextended & ER; so the menisci are forced to
move forward so the injured meniscus is stretched producing pain over the joint line.
9- BOHLER’S ABDUCTION ADDUCTIONTEST valgus and varus stresses cause pain over the lateral
or medial joint line respectively.
10- DEHAVEN ABDUCTION GRAVITY TEST may help to demonstrate tears of the anterior or middle
segments of the lateral meniscus. With the patient on his sound side, the affected knee is
flexed and extended from 90°-0°, so the force of gravity apply compression to the lateral joint
space
11- PAYR’S TEST: is the same idea by applying varus stress while the pt is sitting in Buddha position
12- SPRING TEST is done by grasping the heel with the knee flexed as much as possible, and then
extended passively. When a painful “spring block” occur = torn meniscus (fig.2-14; C).
13- THESSALY TEST: é the pt. mono-pedal standing on the affected side at 5º & 20º flexion &
supported by holding his out-stretched hands; he is asked to rotate his body on his knee internally
& externally. Pain, locking, or catching is pathognomonic to meniscal tear (95% accuracy)
14- MERKE’S TEST: is the same but the patient is standing bipedal unsupported
15- DUCK WALK TEST: pain is produced at the corresponding joint line
9]. Patellofemoral joint
1- ALIGNMENT
2- GRASS HOPPER SIGN of lateral subluxation of patella
3- Q ANGLE: between line joining ASIS to mid-patella & line from mid-patella to tibial
tubercle.
4- 'J' SIGN TRACKING - = maltracking due to lateral subluxation.
5- Grinding/crepitus
6- CLARKE'S (SNATCH) test - patella fixed with hand on it's superior border. Patient asked to
contract quads. Reproduction of symptoms = +ve (all patients get some discomfort)
7- PATELLAR APPREHENSION TEST (for instability) - Flex knee whilst trying to push patellar
laterally, if positive patient will react with apprehension or try to push examiner away.
8- PLICA GRIND TEST: flexion 30º then push patella medially Æ pain if medial plica
10]. Othe usually forgotten tests:
Back of the knee
1].
Hip
2].
Muscle flexibility tests: Ely, Tripod, Ober, Silfverskiold
3].
Nerve assessment especially of the common peroneal nerve in PLC injuries
4].
Radiological
1].X-RAY ACUTE INJURY CHRONIC INJURY
AP Lateral capsular sign = SEGOND # ACL deficiency: Central osteophytes + Peaking
of the tibial spines (TETON sign)
Growth plate fracture MCL: PELLEGRINI-STIEDA disease
Avulsed fibular styloid OCD
Torn ligaments. (stress film) FAIRBANK’S joint line changes;
Squaring of MFC
Narrowing of medial joint space
Osteoscelerosis
Marginal and central osteophytes
DISCOID Lateral meniscus :
Squaring of LFC
Widening of Lat. joint space
Cupping of lat tibial plateau
Bipartite patella
Tunnel In addition to above findings: OCD
Loose body
Avulsed ACL, or PCL
Lateral Avulsed ACL at tibial spine Patella alta
Avulsed patellar tendon SINDING-JOHANSSON-LARSEN syndrome
Avulsed quadriceps tendon OSGOOD-SHLUTTER disease
Osteophyte (inf. and sup. patellar border)
Calcified fat pad (HOFFA’S disease)
Calcified prepatellar bürsa
Patellofemoral Avulsed medial capsule Subluxed patella (Merchant 45°&Lauren 20º)
Fractured lateral osteophyte Calcification
2].MRI
• Allows assessement of PLC injury as well as
ACL & PCL
• Assess which structures of the
posterolateral corner are injured and
whether the injuries are mid-substance or
whether they have been avulsed from the
fibula or femur
Non-operative Treatment:
• Good results if:
o thigh circumference is equal or better than opp. side
o stable
• Poor results if:
o thigh atrophy
o meniscectomy performed
o instability
Arthroscopic findings:
• "DRIVE THROUGH SIGN" = >1cm of lateral opening and exceptional posterior visualization of the
lateral meniscus
Rationale:
• ACL & PCL arthroscopic reconstructions are usually delayed for 6wk then reconstruct
• PLC & PMC are best treated in the acute stage
ACL Instability with degenerative changes

• Ligamentous stabilisation alone often fails
• Usually medial compartment OA
• Rx: combined tibial osteotomy plus extra-articular reconstruction
ACL
• Completely intraarticular extrasynovial ligament measures 33mm X 11mm
• ACL max TENSILE STRENGTH = 50% PCL strength = 1700n
• STRAIN RATE plays a role in the location of ligament failure
o Midsubstance tears occurring at higher rates
o Bone ligament complex tears occurring at lower rates
• BLOOD SUPPLY - middle genicular artery (post) & synovial vessels (ant)
Function
1]. Anteromedial fibers - tight in flexion - limits anterior translation of tibia on femur
2]. Posterolateral fibers - tight in extension - limits anterior translation + ER
3]. Mechanoceptors with a proprioceptive role
4]. Important as a secondary restraint to varus and valgus stresses
5]. Screw home motion occurs around its axis
Isometry:
1. Isometric placement of ACL refers to the concept that a full range of knee can be
achieved without causing long-term ligament deformation
2. isometry can not exist because, during ROM, there is no one point on femur that
maintains a fixed distance from a single point on tibia; elongation always will occur
3. placement of graft as closely as possible to centers of tibial & femoral attachments of
anterior medial band results in least amount of strain (least change in the length of
ACL during complete ROM of knee)
Operative Treatment:
1]. ACL TREATMENT
I. Direct Repair
1- Screw fixation or pull out sutures for avulsion fractures
• Not recommended for mid-substance tears due to poor healing potential.
II. Extra-articular reconstruction
2- MACINTOSH PROCEDURE: (historical)
• Pass a mobilised strip of ITB to the posterolateral corner of the knee through a tunnel
deep to the LCL
3- LOSEE MODIFICATION: Loop through bony tunnel & lat. Gastroc.
4- ANDREWS ITB tenodesis
III. Intra-articular Reconstruction
5- CLANCY BTB reconstruction
6- MACINTOCH : distally attched BTB reconstruction
7- ZARICZNYJ hamstring reconstruction - semitendinosis + gracilis
8- LIPSCOMB distally attached ST graft
9- PUDDU proximally unstripped ST graft
10- ALLOGRAFT reconstruction
11- SYNTHETIC grafts
IV. Intra & extra articular Reconstruction
12- ZARIN ITB & ST in the opposite direction
13- LOSEE modification of Zarin ITB &ST in opposite direction
2]. PCL TREATMENT
• Traditionally, most authors have recommended NONOPERATIVE TTT FOR ISOLATED PCL
• Salvage procedures:
1]. MÜLLER OLECRONIZATION of Patella to prevent posterior sag of tibia
• Reconstruction procedures:
2]. O’DONOGHUE transosseous suturing
3]. If avulsed REFIXATION of the avulsed fragment
• Arthroscopic assisted PCL reconstruction:
4]. SINGLE BUNDLE PCL reconstruction
5]. DOUBLE BUNDLE PCL reconstruction
6]. INLAY PCL reconstruction
3]. POSTERO-MEDIAL RECONSTRUCTION:

1- Repair:
1]. Anatomical repair from the deepest structures to the most superficial structures
2]. O’DONOGHUE transosseous suturing method
2- Reconstruction
3]. HUGHSTON reconstruction of POL through trans-osseous suture
4]. SLOCUM Pes Anserinus transplantation + sartorius advancement to reinforce MCL
4]. POSTEROLATERAL RECONSTRUCTION

1- Acute Repair:
1]. Anatomical repair from the deepest to superficial + BUNNEL LCL suturing
2]. O’DONOGHUE transosseous suturing method
2- Chronic reconstruction:
1]. HUGHSTON postero-lateral advancement
2]. MÜLLER LCL reconstruction using biceps slip
3]. CLANCY Biceps tenodesis
4]. WARREN two tailed graft reconstruction (both LCL & popliteo-fibular lig)
5]. NOYES allograft reconstruction
6]. LARSEN semitendinosus for reconstruction
POST-OP CARE:
• CPM range of motion immediate post-op
• Closed chain exercises (foot is maintained on the ground or a platform)
• Running & any activity that involves excessive knee rotation (cutting) is
discouraged for the first several months.
Complications:
1. Loss of knee extension / Arthrofibrosis
o more common with early reconstruction
o incorrect tunnel placement can cause decreased motion and fibrosis
(diagnose with x-rays & MRI)
2. Tibial tunnel syndrome
o y size of tibial tunnel over 1yr following surgery
3. Graft failures:
o Improper placement of graft tunnels
o Impingement of the graft in the femoral notch:
due to improper tunnel placement
due to inadequate notchplasty
o Inadequate graft fixation
o Associated injuries (varus knee, significant osteochondral defects)
o CRPS (0.5%)
o Infection (<1%)
4. Patellofemoral pain
5. Patella fractures
6. CRPS (0.5%)
7. Infection (<1%)
Knee Dislocations
Clinical Findings:
1. Popliteal artery & vein injury is common
1. note that knee dislocations that have spontaneously reduced may look benign but
may lead to thrombosis of the popliteal artery
2. popliteal a. is usually tethered proximal at adductor hiatus & distal by soleus arch
3. injury to popliteal a. may initially manifest as an intimal tear or intraluminal thrombus
2. Peroneal nerve injury:
1. in 20% to 40% (half of these palsies are permanent)
2. w/ peroneal nerve injury, be highly suspect for vascular injury; - even if pulse
returns following reduction, consider need for arteriogram, since incidence of
intimal injury is high w/ concomitant nerve injury
3. Both cruciates and least one collateral ligament are usually disrupted
Classification:
• Anterior (31%)
o hyperextension of knee (may need > 30 º of hyperextension to produce this injury)
o often PCL & ACL torn
o either the MCL or LCL or both will usually be injured
o alternatively, hyper-extension Æ ACL & posterior capsule while the PCL is spared
o Popliteal artery injury
• Posterior (25%)
o disruption of both cruciate ligaments
o possible extensor mechanism disruption
o avulsion of or complete disruption of popliteal artery
• Lateral (13%) & Medial ( 3%)
• Rotatory ( 4% - usually posterolateral)
Investigations:
1. X-Rays:
o Tibial plateau fracture & Proximal fibula fracture & Avulsion of Fibular Head
o Avulsion fracture of Gerdy's Tubercle
o Intercondylar spine fracture
2. Arteriogram - indications unclear
3. MRI - see above
Management:
• Reduction
o may be complicated by interposed soft tissue
o External fixation - it is important that the external fixator pin sites will not interfere
with the ACL/PCL tunnel sites (during future ligament reconstruction)
• Vascular Inuries
o the worst error to make is to underestimate the need to promptly treat these injuries
• Nerve injury:
o the location of the nerve injury may be well above the knee joint
• Assessment of ligament injuries:
o EUA
• Surgical Treatment of Ligament Injuries:
o if vascular injury has been previously repair, get clearance from the vascular
surgeon to utilize a tourniquet
o Deep to superficial (as above)
Patellofemoral Disorders
Anatomy
WIBERG’S CLASSIFICATION of patella shape
Type I 10% Concave facets, symmetrical and equal
Type II 65% Medial is smaller. Lateral is concave
Type III 25% Marked lateral predominance
Type IV <1% Tiny medial facet
Jagerhut Rare No articulating medial facet
Extensor mechanism:
1]. Quad & Quad tendon
2]. Medial and lateral retinaculae
3]. PF ligaments
4]. Patello-tibial lig
5]. Patellar tendon
6]. Tibial tubercle
Patellofemoral kinematics
• Patellofemoral joint reaction force
o 0.5 times body weight with walking
o 3.3 times body weight with stairs
• Patella y the moment arm of the quadriceps Æ y quad strength by 33-50%
• The femur articulates only with a portion of the patella in each position of flexion
CLINICAL
HISTORY: Determine if complaint is instability or pain
EXAMINATION (Also see Torsional Profile Assessment)
• Standing examination
o Varus/ valgus alignment & Q-angle
o Pelvic obliquity and LLD
o MISERABLE MALALIGNMENT $ = femurIR + Tibial ER ± pronated foot ± pes planus
• Sitting examination
o GRASSHOPPER EYES appearance: high and lateral patellas
o Lateral patellar tilt
o Patellar tracking: pain and crepitation, 'J' SIGN
o Position of tibial tubercle é respect to trochlear midline ≈ < 20mm lateral to the midline
• Supine examination
o Quadriceps (Q) angle (Normal M 10° F 15)
o Quadriceps mass (VMO atrophy); hand breadth above patella
o Hamstring tightness (popliteal angle)
o Tenderness on quadriceps or patellar tendon insertion, patellar facets, retinaculum
o Crepitation and patellar compression
o Apprehension test (20-30°flexion)
o Examination for medial plica
o CLARKE'S SNATCH TEST (pain on contraction of the quadriceps with the patella fixed)
o PATELLAR TILT (evaluates tension of the lateral restraint)
o PATELLAR GLIDE TEST (knee flexed 20 to 30°)
z: 1 quadrant or less medial glide is indicative of tight lateral
y: subluxable, or dislocatable patella
• Prone examination
o Hip motion - femoral neck anteversion (abnormal if IR exceeds ER > 30°)
o Quadriceps tightness - ELY TEST (especially rectus femoris)
o Leg-heel alignment (Normal 2-3° of varus)
o Hindfoot-forefoot alignment: (N: long axis of heel ⊥ to transverse axis of forefoot)
INVESTIGATIONS
RADIOGRAPHY • Blumensaats line
• AP • Insall / Salvati Ratio ≈1 • Hughston Prone ..... 55º
• True lateral view • Blackburne Peel ≈ 1 • Merchant view ........ 45º
• Laurin view .............. 30º
• Skyline views:
• Ficat ........... 30º,60º,90º
o Sulcus angle of Brattström: 120º-140º
PatellarWedth
o Patellar index: =17
MedialPFW − LateralPFW
o Congruence angle: between the sulcus line and the patellar vector = -16º to + 4º
o Lateral PF angle: bet. the tangent on femoral condyles & Lat.PFJ line Æ N: +ve
o Lateral PF index: PFJ space ( CentralPFJ space )=1.6
LateralPFJ space
CT
• More accurate assessment of sulcus & congruence angle
• Perform é knee in different flexion degrees ± quad contraction
MAGNETIC RESONANCE IMAGING

• Midpatella transverse images with knee flexed 15°
• Assess other areas of knee: articular cartilage, muscle and supporting retinacular structures
• Dynamic MRI to assess patella tracking
Patellofemoral Trauma
PATELLA FRACTURE
PATELLAR STRESS FRACTURES
• Rare overuse injury reported in endurance runners, volleyball players, and high jumpers
• Two types: longitudinal and transverse (Iwaya 1985)
• In cases with delayed diagnosis operative treatment
• Quadriceps or Patellar tendon rupture
Non-arthritic patellofemoral pain
1. PATELLAR TENDONITIS (JUMPERS KNEE)
• Secondary to repetitive trauma: running, jumping and kicking sports
• Tenderness usually on the inferior pole
Blazina Classification Affect Participation Treatment
I Pain only after activity N Activity modification, warm-up,
II Pain at the start of activity & fatigue N stretching, ice, NSAID's
III Pain during and after participation Y As above Æ Steroid inj Æ debridement
IV Complete tendon disruption Y Primary repair of the tendon
2. PLICA SYNDROME
• Medial patellar (most common), lateral and suprapatellar
• Inflammation and impingement on medial femoral condyle
• Treatment
o NSAID's, quadriceps exercises ± Steroid injection ± Arthroscopic excision
3. OSTEOCHONDRITIS DISSECANS (OCD)
• Knee is most common site
• Typically in teenage athletes
• Location in the patella is rare
• Medial facet (70%), lateral facet (30%)
4. CHONDROMALACIA
• "softening" of the articular cartilage
• Aetiology
o 50% idiopathic
o 15% post traumatic
o 20% secondary to maltracking- lateral patellar compression syndrome
o 15% due to unstable (recurrent dislocaters) patellae
• Treatment is dependent on cause
Outerbridge Classification
I Articular cartilage softening
II Chondral fissures and fibrillation < 1.25mm
III Chondral Fibrillation > 1.25 mm (crabmeat changes)
IV Exposed subchondral bone
5. PATELLOFEMORAL MALALIGNMENT
MEDIAL PATELLAR SUBLUXATION/DISLOCATION
• Usually iatrogenic, secondary to realignment procedures, but has also been described without
previous surgery (Richman 1998)
• When associated with internal tibial torsion
If Tibio-Tubercle distance z: external derotational tibial osteotomy proximal to
tibial tubercle
If Tibio-Tubercle distance is normal: external derotational tibial osteotomy distal
to tibial tubercle
LATERAL PATELLAR SUBLUXATION/DISLOCATION
• 5% are associated with an osteochondral fracture
• Treatment
o First time instability episode with no malalignment and normal radiographs
o immobilisation followed by early range of motion and PT
o If osteochondral loose bodies are present Æ arthroscopic removal or fixation
Fulkerson Clinically Q Angle Lateral Retinaculum Realignment
I Subluxation alone yy Normal Distal
II Subluxation and tilt yy Tight Distal + Proximal
III Tilt alone Normal Tight Proximal
IV No malalignment Normal Normal Physiotherapy ± Proximal
o Subdivided:
A]. Absence of articular lesion
B]. Presence of minimal chondromalacia
C]. Presence of osteoarthritis
6. DORSAL DEFECT OF THE PATELLA
• Benign lesion - Non-specific fibrous tissue
• Located along the superolateral aspect of the articular surface of the patella
• Radiolucency with sclerotic margins and intact overlying articular cartilage
• Frequently heals spontaneously by sclerosis
7. BIPARTITE PATELLA
• 15% of people in childhood & 2% in adulthood
TRIPARTITIE)
• Sometimes a 3rd ossific centre appears (T
• 57% are unilateral with a male: female ratio of 9:1
Saupe Classification
TYPE I 5% Distal pole
TYPE II 20% Lateral
TYPE III 75% Supero-lateral
8. OSGOOD SCHLATTER’S
• Traction injury to the apophysis where patella tendon inserts (some inserts on either side)
• 11-15 y male, usually no history of injury and may be bilateral
• Symptoms are aggravated by running, squatting, jumping, stairs etc
• PXR: May show fragmentation of the apophysis
• Spontaneous recovery is usual but takes time
• Where symptoms are persistent and troublesome excision of a separate ossicle
9. SINDIG-JOHANSSON-LARSEN'S DISEASE: (traction tendinitis at lower pole of patella, w/ calcification)
• Traction apophysitis of the distal pole of the patella Æ traction tendonitis develops
• Similar pathology to Osgood-Schlatter’s disease and usually resolves spontaneously
10. TORN MENISCUS
11. DISCOID MENISCUS
12. PATELLA BURSITIS
13. PATELLA CYSTS OR TUMOURS
14. REFLEX SYMPATHETIC DYSTROPHY
Relationship of patellofemoral malalignment to femoral and tibial torsion

INTERNAL FEMORAL TORSION / FEMORAL NECK ANTEVERSION
1. Toeing-in if it exists alone and external rotation of hip < 30 °
2. Feet straight: if compensatory external tibial torsion, pes planus, or external hip rotation at
least 30°
EXTERNAL TIBIAL TORSION
• Primary or secondary to medial femoral torsion
• Primary deformity responsible for PF malalignment
• Gait with normal foot progression angle (straight ahead) but with kneeing-in medial thrust
with stance phase.
Treatment
CONSERVATIVE
1. Activity modification, rest, NSAID's and rehabilitation are successful in 90%
2. Supervised exercise program should be continued for at least 6 months
3. Patellar taping (Powers et al, 1997):
o Average pain reduction of 78%
o Taping changes the timing of VMO and VL activity in subjects with patellofemoral pain
during step-up and step-down tasks
o When the patellofemoral joint was taped, the VMO was activated earlier.
SURGICAL
A. PROXIMAL REALIGNMENT PROCEDURES:
• LATERAL RELEASE (OPEN OR ARTHROSCOPIC)
o Indication: for patellar tilt < 8 º or lateral retinacular tightness
o Do only when it is tight
o Adequate release should allow inversion of patella to 70-90 º
o The superficial and deep layers of the retinaculum must be divided.
o Best results in patients with pain. Worse in patients with instability and severe DJD.
o 85% good results in pts é pain and PXR evidence of tilt and Outerbridge I
o 92% good & excellent results in patients with minimal articular degeneration and tilt
• LATERAL RELEASE AND MEDIAL PLICATION (PROXIMAL REALIGNMENT)
o Attempt to decrease the valgus quadriceps moment on the patella
o Indication: retinacular tightness and medial laxity
o for recurrent lateral subluxation /dislocation in skeletally immature patients
o 82% good/excellent results in patients with instability (Scuderi 1988)
o Poor results in patients with significant chondromalacia
• GALLEAZI procedure (semitendonosis tenodesis)
o Reconstruction with semitendonosis tendon
o Tensioned at 30° of flexion
B. COMBINED PROXIMAL AND DISTAL REALIGNMENT PROCEDURES
• ELSMLIE-TRILLAT: Lateral release with medialisation of tibial tubercle
o Best candidates have recurrent instability, evidence of increased Q angle and minimal,
if any articular degeneration
• FULKERSON: Lateral release with antero-medialisation of the tibial tubercle
o Biomechanical studies have shown that the patellofemoral joint reaction force
decreases about 50 % after a 2-cm anteriorisation of the tibial tubercle
o Due to the obliquity of the osteotomy, no bone graft is necessary.
o Best for pts é lateral patellar tilt and with Outerbridge grade III-IV chondrosis
o See Later for details of distal osteotomies
C. PATELLOFEMORAL ARTHROPLASTY
• Hemiarthroplasty (PATELLAR RESURFACING) or total patellofemoral arthroplasty
• Indicated for OA of the patella and trochlea
• Great care must be taken to ensure that any malalignment or maltracking is identified and
corrected otherwise the procedure will fail
D. FEMORAL OSTEOTOMY (ALBEE)
• For trochlear dysplasia
• Elevation of the lateral facet of the femoral trochlea with osteotomy and bone graft
E. PATELLECTOMY
• Last resort surgery which may not eliminate pain
• Complicated by loss of quadriceps strength 30 to 50%
760 | Page [Knee Disorderss]
B]. DISTAL REALIGNMENT PROCEDURES:
1]. HAUSER (ABANDONED)
• Tibial tube ercle osteottomy with the t tubercle e moved medial,
m distal and poste
erior
• Complicatted by dev velopment of patelloffemoral DJD D in 70 % of patientts because of
increased PFJ joint re eaction forcces (Hampsson et al, 19 975)
2]. MAQUET
• Elevation (anteriorisa ation) of tib
bial tubercle
e
• Salvage operation in n patellofem moral DJD without
w malalignmentt
• Risk of antterior skin necrosis
n whhen anterio orisation > 2 cm
3]. GOLDTHWAITE-ROUX
a. The pate ella tendon is split & th he lateral haalf is passed
d under the e medial haalf & attached
to the peeriosteum on o the tibia in a mediall position.
4 HEMI-PATELLAR TENDON TRANSFER ± late
4]. eral release/
e/medial ree efing
5]. ELMSLIE-TRILLAT
• Medializattion of tibia al tubercle + lateral rele
ease + med dial capsularr reefing
• Considere ed when th here is min nimal or ab bsent articu ular injury in patientss with late
eral
instability caused by malalignm ment
• Good/exc cellent results in 81% (Brown, 198 84)
• Best resultts when po ostoperative e congruen nce angle < 15° (Shelbo ourne et al,, 1994)
6]. FULKERSON
• Anterome edial tibial tubercle
t ostteotomy
• Malalignm ment and la ateral facet chondrosiss
• Slope of cut
c depende ent on amo ount of sub bluxation an nd DJD
• Not as suc ccessful witth medial fa acet chondromalacia
• 90% good d/excellent results (Fulkerson et al.1990)
a
Anterior Kne
ee Pain
Patellar Patelloffemoral Intraarrticular Patellar tendon

t
Re
eferred
(-ve Clinical & (+ve PXR & patellar (-ve PXR
R + joint (Local tender
t
+ve PXR lesioon) RSD
compression or tilt) line tendderness) ±Swelling±PXR)
Traumatic P
Plica Osggood
Chond
dromalacia OA OCD
overuse Syndrome Schlatter
Congenita
l Malalignment Trau
umatic
Bursitis
Bipartite AHMMM
Paiin & Insall > 1.2 + Conngenita
Tumor norrmal Insall < 1.2 Outerb bridge l Sindiing J
ind
dices IIII $
Disccoid
Lat re
elease Elme
eslie
Jump
per’s
Patello-Femoral Instability
Patello-Femoral Joint Mechanics
1. Patella increases moment ( lever ) arm of extensor muscles
2. Slides 7 cm in trochlear groove
3. Patello-femoral contact minimal until 20 º flexion
4. Contact area moves from proximal -> distal in trochlea & distal to proximal on patella
5. >90º flexion quads tendon is in contact with the trochlea
6. 10º flexion -> lever arm increased 10 %
7. 45º -> 30 % then decreases
8. Patello-femoral joint reaction force determined by quads force and amount of knee flexion
9. Normal walking -> joint compressive forces = half bodyweight
10. Up stairs -> 2.5 - 3.3 times body wt
11. Deep knee bends -> 7-8 x body wt
Presentation
PFJ instability may present as:
• Anterior Knee Pain
• Patello-femoral subluxation
• Patello-femoral Dislocation
Anterior Knee Pain

Other causes of anterior knee pain include:
1. Patello-femoral overload (Chondromalacia)
2. Plica Syndrome
3. 'Jump' knee (enthesitis of patella tendon origin)
4. Sinding-Johansson-Larsen $
5. Torn Meniscus
6. Discoid Meniscus
7. Osteochondritis Dissecans
8. Patella Bursitis
9. Bipartite Patella
10. Patella cysts or tumours
Risk Factors / Causes

A. Bony (Static Stability)
1. Shallow femoral trochlea
2. Hypoplastic LFC Fulkerson Clinically Q retinacula Realignment
3. Patella Shape (Shutzer et al.) I Subluxation alone yy Normal Distal
4. Patella Alta II Subluxation + tilt yy Tight Distal + Proximal
III Tilt alone N Tight Proximal
B. Malalignment IV No malalignment N Normal Physiotherapy ± Prox
• External tibial torsion Subdivided:

A]. Absence of articular lesion
• Incr. femoral anteversion
B]. Chondromalacia
• Incr. genu valgum C]. Osteoarthritis
• Incr. Q angle (unreliable)
C. Soft Tissue (Dynamic stability)

• Ligamentous laxity
• contribution of distal oblique portion of vastus medialis muscle is critical
• (tight hamstring & gastrocnemius w/ pronated feet)
Clinical
• Mechanism of injury, acuity, previous treatment, and status of the opposite knee.
• Q ang gle
• The integrity off the ACL (because
( similar dero
otation, decceleration m
mechanism
ms that cau
use
patelllar instabilitty can cause
e ACL injury
ry)
Radiology
LATERAL X-RAY: (knee at a 30º = Pattella is centtered in trocchlear groo
ove at 30º fllexion)
• BLUMENSAAT'S Line:L The suuperior pattella pole should not be higher than interccondylar ro oof
line
• INSALL-S SALVATI index-
i lenggth of patella to length
h of patella tendon,
t ormal=1. Patella Alta z
no
• BLACKBURNE-P PEEL index- length of patella articular surfa ace to the distance of o its inferior
marg gin from the
e tibial plateeau w/ knee in 30º. fleexion. normmal=0.8-1.1. More accu urate.
SKYLINE VIEW:
• Sulcu us angle of BRATTSTRÖ ÖMM: 120º-140º
• Cong gruence ang gle: betwee en the sulcu
us line and the patellar vector = -16º to + 4º
PatelllarWedth
• Patellar index: =17
M
MedialPFW W − LateralPPFW
CentrralPFJ spacee
• Latera al PF index:: PF joint sp
pace ( )=1.6
LaterralPFJ spacee
• Latera al PF angle: bet. the taangent on femoral
f conndyles & Lat.PFJ line Æ N: +ve
• Troch hlear signs- Crossing sig gn, 'Bump' sign, Dyspllastic condyyles, Trochleear depth < 8mm.
AP & Tunnel views: fo or osteocho ondral fracttures.

CT Scan he
elpful in asse
essing the relationship
r p of the PF joint
j in term
ms of tilt or ttranslation,, or both.
Arthroscopy
• Use a suprapate ella portal to
o watch pattella centre
e in trochleaar groove b betw. 30-60 0º.
Treatment
• Treatment is individualized and is based on the patient's lower extremity alignment, joint
motion, ligamentous laxity, muscle strength, and quadriceps competence.
• The goal of treatment is to prevent recurrence.
Proximal Realignment
• to alter the tension of tissues attached to the patella.(Lat release & med. reefing)
• Lateral retinacular release
• Direct medial retinacular repair in acute dislocations.
• Quadriceps transfers, particularly the vastus medialis obliquus are used to restore medial
vector balance (Medial plication).
• Medial hamstring transfer (G GALEAZZI technique) may be required to provide a tenodesis
effect in troublesome cases.
DISTAL REALIGNMENT = transpose the tibial tubercle
1]. HAUSER PROCEDURE: (HISTORICAL)

• Involves medialization of the tibial tubercle in order to decrease Q angle. due to the anatomy
of the proximal tibia, translating the tibial tubercle medially, will also translate the tubercle
posteriorly. Posterior translation of the tibial tubercle will have the effect of increasing
patellofemoral contact pressures ώ leads to pain & OA. Also can produce a low patella (baja)
2]. ELMSLIE-TRILLAT PROCEDURE:
• medial tibial tubercle transfer which has no posterior displacement
• does not involve anterior / posterior displacement of the tuberosity
3]. MAQUET PROCEDURE: (HISTORICAL)
• Anterior translation of the tibial tubercle which has the effect of decreasing patellofemoral
contact forces. Patients with pain due to early patellofemoral arthrosis may expect pain relief
following the Maquet Procedure. Disadvantages with this procedure include high incidence
of skin necrosis, compartment syndrome and no effect on the Q angle;
• A combination of tibial tubercle transfer, proximal lateral release, medial capsulorrhaphy and
tendon transfer may be required to establish appropriate alignment.
4]. GOLDTHWAITE-ROUX PROCEDURE:
• The patella tendon is split & the lateral half is passed under the medial half & attached to the
periosteum on the tibia in a medial position.
5]. FULKERSON
• Anteromedial tibial tubercle osteotomy
• Malalignment and lateral facet chondrosis
• Slope of cut dependent on amount of subluxation and DJD
• Not as successful with medial facet chondromalacia
Contra-indications to Re-alignment:
1]. Absence of clear physical examination and radiographic findings
2]. Patellofemoral pain which results from "dashboard" car accident injuries; often have significant
patellofemoral pain chondromalacia, but do not improve with surgery
3]. Patellar instability associated with abnormal ligamentous laxity; eg, Down $ & Ehlers-danlos $
Osteochondritis Dissecans
Definition
• NON INFLAMMATORY pathologic condition of the cartilage é IMPENDING OR ACTUAL
separation of a segment of cartilage é underlying subchondral bone
• Tends to heal spontaneous in skeletally immatures
Ætiology:
1- Repeated TRAUMATA
2- May be AVN
Pathogenesis:
1]. Intraosseous odema Æ capillary compression Æ ischemia
2]. Subchondral collapse Æ arteriolar compression Æ necrosis
3]. Fragmentation Æ NBF
Pathology:
SITE:
• Bilateral .........................................................................20-30%
• Poster-lateral MFC (ant to PCL foot print)...........70%
• LFC ..................................................................................20%
• patella ............................................................................10%
MACROSCOPICALLY:
• DEGENERATED cartilage
• Underlying a segment of OSTEONECROSIS
• lesion DISSECTS Æ early OA ....................................25%
• More common Æ Spontaneous healing ............75%
• Healing takes 3-4 mo Æ L pain
CLASSIFICATIONS
GUHL ARTHROSCOPIC CLASSIFICATION
STAGE PATHOLOGY CARTILAGE
A Subchondral # soft and yellowish
B Incomplete separation cracked cartilage
C Complete undetached Cartilage lesion all over
D Complete detached Crater
PAPPAS CLASSIFICATION: Depends on age at presentation:

TYPE PHYSIS PROGNOSIS
Juvenile Open Excellent
Adolescent Partial closure Either way
Adult Closed Poor
Clinically:
• Young male 10-20y ≠ SONK
• No history of major trauma, Usually physically active with multiple minor traumata
• PAIN:
o Insidious onset ≠ SONK
o Dull aching; if sharp = dissection
o Deep Pain ≠ SONK
o yé activity
• If fragmentation: locking, swelling, and sharp pain may occur
INVESTIGATIONS
• PXR TUNNEL VIEWS (60º flexion é the beam // to the plateau)
o May be the only key view in 25% of cases
o shadow of scelerotic fragment of separation and crater
o Anterior to BLUMESAAT’S line and adjacent to PCL femoral foot print
o DD: CAFFEY ISLANDS of ossification defects develop posteriorly on the condyles
(posterior to Blumensaat’s line, painless, and tend to coalase)
• MRI:
o MRI T1, serpiginous z signal lines
o MRI T2, Double line =z signal margin & y signal inner border
o MRI T1Rho sequence can delineate the GAG of the cartilage
TREATMENT (based on Pappas & Ghul)
OCD
<12 y
>12
Usually heal
Usually progress
spontaneously
Usually heal <3cm >3cm

spontaneous
• PWB
• ROM
ARTHROSCOPIC ARTHOROTOMY
Stage A Stage B,C StageDD

Stage
Fragment removal and

Drilling via Fixation reconstruction
single puncture (usually swollen and larger)
Biodegradable Metal Osteochondral Cartilage alone Matrix scaffolds

• Screws • Herbert Screw •OATS • ACI Soft tissue
• Collagen
• pegs • K-wire •Allograft • MACI • Periosteal
• Carbon fiber
• Fascia
• PLA
Other New Treatments for irreparable lesions in WB zone:

1- Electromagnetic pulsed cartilage delivery technique: An idea depends on the injection of Anti
CD44 antibody-magnetic beads labeled mesenchymal cells into the knee after very localized
provocation of the cartilage lesion by a strong magnetic field; this will affect the concentration
of the mesenchymal cells into the cartilage lesion
2- Salu Cartilage implantation
3- Arthro-surface implantation
Patellar OCD
• Uncommon & present as ant. knee pain
• Distal ½ of the patella
• 30% bilateral.
• PROGNOSIS: less clear; but subchondral sclerosis = poor prognosis (as femoral OCD)
• TREATMENT principles are similar to those for femoral OCD.
Knee Bone Infarction
Definition:
• Ischemic death of bone & BM of a portion of the knee = AVN, that usually heals
spontaneously
Ætiology:
1. Steroids
2. Alcohol
3. SLE
4. Renal transplantation
5. Gaucher disease
6. Sickle disease
7. Caisson disease
Pathology:
SITE:
• More metaphyseal than epiphyseal extending to the subchondral plate
MACROSCOPICALLY:
• Pale BM
• 2ry OA & cystic degeneration of the necrotic area
MICROSCOPICALLY:
• Bone death
• Marrow necrosis
• Granulation tissue healing
• NBF
CLASSIFICATION
CLASS SYMPTOMS HISTOLOGICAL RADIOLOGICAL
Stage 0 Asymptomatic Abnormal -ve
Stage I Preclinical Abnormal +ve MRI only
Stage II Pain Precollapse PXR: osteopenia, MRI: double line
Stage III Pain Collapse Collapse
Stage IV Arthrosis OA
Diagnosis:
Clinically:
• Race, age, and gender are according to the cause
• Generalized pain
PXR:
• Lucent lesion surrounded by sclerotic shell
MRI
• T1: serpiginous lines of z signal
• T2: Double line sign: outer z signal line + inner border of y signal
• Chinese letters serpiginous lines
Tc: cold spot
DD:
• OCD ..........................................................................lateral part of the MFC, young, active, and healthy
• SONK ........................................................................WB portions of the knee, elder female
Prognosis
• Usually heals spontaneously
Treatment:
• if not ...........................................................................as OCD
Spontaneous Osteonecrosis Of Knee

SONK = Ahlbäck disease
First reported by Alback et al. in 1968. They described a radioluscent area in the femoral condyle
surrounded by a sclerotic halo and associated with a focally active bone scan.
Aetiology
1]. Unknown
2]. Vascular theory: Thrombotic veno-occlusive disease Æ venous hypertension and ischemia
3]. TRAUMA THEORY: in osteoporotic patients stress fractures may be followed by bone necrosis
(most accepted theory)
Pathology:
SITE:
1]. Wt bearing portion of MFC ≠ OCD
2]. Wt bearing portion of LFC
3]. Tibial plateau
MACROSCOPICALLY:
• Crescentic linear subchondral # line
• Over lying hyaline cartilage: discoloration Æ detach Æ OA
• Marrow œdema
MICROSCOPICALLY:
• Tide mark fibrillation
• Bone necrosis + NBF
Clinical
1. Typically female > 60yrs ≠ OCD
2. SUDDEN onset of severe pain on the medial side of the knee ≠ OCD
3. pain worse at night
4. WELL LOCALISED tenderness over the affected condyle ≠ OCD
Radiology
X-Rays
STAGE PATHOLOGY
Stage-1 Normal (PXR visible lesion never develops, & symptoms resolve spontaneously)
Stage 2 Flattening of the MFC
Stage 3 Radiolucency + sclerotic halo
Stage 4 Sclerosis enlarges + collapse
Stage 5 Secondary OA changes
Bone scans (+ve after 72hr)
• yuptake is necessary to diagnosis
• The osteonecrotic lesion appears
as a focally intense area of
uptake over the affected LFC
MRI
• Extremely Valuable In
Osteonecrosis About The Knee
• T1 - Discrete z Signal In The Femoral Condyle
• T2 - z Signal in the centre + y Signal at the margin
DD:
• OCD ............................................................................. Lateral aspect of MFC (non WB portion) in
teenage
• Subchondral # ......................................................... younger patient
Prognosis
• Prognosis is related to the size of the lesion at presentation:
1]. > 50% of the width of MFC ..................... OA, and collapse
2]. < 50% ................................................................ 90% spontaneous recovery
Treatment
• Usually arthroscopy or meniscectomy are initiated before Dx is established till collapsed
• Initially, most patients should be treated conservatively, as the stage of the lesion and the size
of the osteonecrotic segment are not clearly defined at the onset:
1]. > 50% of the width of MFC:
1. Core decompression
2. Osteochondral Allografting
3. Arthroscopic debridement
4. Mosaicplasty
5. HTO
6. Prosthetic replacement
2]. < 50% ................................................................ 90% spontaneous recovery
OC D SONK AVN
Cause Traumatic Unknown Vascular
Site NWB WB Metaphysio-epiphyseal
Pt Young active Elder female Variable with a PF
Pain Insidious Acute Usually asymptomatic
PXR Demarked Sclerotic fragment Radiolucency + sclerotic halo Mottling + collapse + OA
MRI T1 serpiginous z signal lines z signal z signal + surrounding oedema
MRI T2 Double line =z signal margin & y signal at margin y signal
y signal inner border z signal at centre
TC y uptake y uptake z uptake
Synovial Diseases:
1]. PVN synovitis
2]. Synovial condromatosis
3]. Rheumatoid
4]. Hemophilia
5]. Plicae
6]. HOFFA’S disease (anterior fat pad $): fat pad fibrosis and ca 2ry to trauma
ITB syndrome:
• ITB friction with LFC Æ localized OA especially in hill runners and cyclists
• +ve Noble’s test: Max tenderness at 30º flexion, 3 cm proximal to the joint line
• +ve Ober’s test
• DD:
1]. Lateral meniscal cyst or tear
2]. LCL injury
3]. Chondromalacia of lat patella
4]. Segond #
• Ttt is usually rehabilitation; other wise ellipse ITB excision may be required
Osteoarthritis
DEFINITION
Non-inflammatory degenerative joint disease ccc by progressive softening & disintegration of
articular cartilage é associated new bone formation & capsular fibrosis
1. It is not a simple wear as it is: asymmetrical, localized, & related to abnormal loading
2. It is not purely degenerative (misnomer) as it is accompanied by a healing process in the form
of reactive new bone formation
Epidemiology: it is the commonest joint diseases and considered a universal disorder
1]. > 60y ..........................................................................50%
2]. Fingers, hip, knee, and spine are more affected than other sites
3]. OA hands are more common in females
4]. ♀:♂ = 2:1 (more DDH in ♀) unlike china & Africa
AETIOLOGY
• Primary - no obvious cause more é aging (effect of aging on cartilage)
• Secondary - occurs following certain predisposing factors:
o Trauma: ....................................................direct injury, deformity, joint instability
o Congenital: ..............................................DDH, Perthes, Blount,…etc
o Infection
o Metabolic: ................................................ochronosis, hemochromatosis, gout, Paget
o Endocrine disorder: .............................Acromegaly and hyperparathyroidism
o Occupation: knee (in benders)- UL (vibrating tools) –hands (boxers) –shoulder
(pitchers)
o Obesity: .....................................................y loads across the WB joints
• OA is uncommon in pts é osteoporosis
• OA is due to FAILURE OF CHONDROCYTES TO REPAIR DAMAGED CARTILAGE.
• There is a DISPARITY BET.STRESS APPLIED AND CHONDROCYTE RESPONSE. = 'wear vs. repair'
Mechanical causes of the disparity of the stress and strength:
ABNORMAL LOADS ON NORMAL JOINT:

• articular cartilage can withstand loads of up to 25MPa without damage. Loads exceeding this
Æ chondrocyte death & cartilage fissures.
• single impact loads or less intense multiple impact loads can cause articular damage.
• impact loading Æ loss of proteoglycans from matrix Æ z cartilage stiffness, y hydraulic
permeability & disrupt collagen meshwork.
• if repair cannot keep up with damage Æ degeneration.
NORMAL LOAD ON ABNORMAL JOINTS:

• Instability Æ altered congruence Æ y shear & compression forces on regions of cart.
• Partial loss of joint sensory innervation accelerates joint degeneration
• Forced activity following joint injury or ACL transection Æ joint degeneration, whereas
immobilisation after injury prevents degeneration.
PATHOGENESIS
Theory 1
• The initiating event is FATIGUE OF THE COLLAGEN MESHWORK Æ y HYDRATION of the
articular cartilage Æ LOSS OF PROTEOGLYCANS from the matrix into the synovial fluid
• Cartilage SOFTEN Æ CHONDROCYTES DIE Æ release of proteolytic enz Æ further damage
• Cartilage deformation Æ y stresses on collagen network Æ y damage
• Cartilage can’t withstand stresses ώ are concentrated on the subchondral bone Æ y
subchondral degeneration, cyst, vascularity, sclerosis
• Repair occurs at the joint margin in the form of growth & endochondral ossification Æ
hypertrophic osteophytes (unlike the atrophic diseases e.g. RA)
• Evidence of y collagenolytic activity; but collagen loss may be ð mechanical causes.
Theory 2:
• The initial lesions are SUBCHONDRAL MICROFRACTURES following repetitive loading.
• Healing of these microfractures Æ undue subchondral bone & violation of Tide mark
• A stress gradient develops Æ articular cartilage is lost in areas of maximum stress
• Underlying bone becomes hardened and eburnated
• Proliferative changes also occur at the joint margins with formation of osteophytes.
Molecular Pathology:
1- y WATER content (unlike z water content in ageing) – ð weakening of type 2 collagen
2- PROTEOGLYCANS (z size, z chondroitin 6-sulphate, z keratan sulphate, zhyaluronic)
3- yCCHONDROITIN / KERATIN RATIO (unlike ageing).
4- y PROTEOGLYCAN-DEGRADING ENZYMES (collagenase & stromelysin & plasmin)
5- y collagen, and proteoglycans synthesis and loss Æ net result z level
6- Increased levels of:
o Matrix METALLOPROTEINASES (MMPs) (collagenase, gelatinase, and stromelysin).
o CATHEPSIN B & D (proteases found in synovium, chondrocytes, and PNL)
o IL1 - enhances enzyme synthesis & has a catabolic effect.
o IL6
o TNFα
o TGFβ
o GAGs and polysulfuric acid
PATHOLOGY
• CARTILAGE DAMAGE: (in pressure areas)
softening Æ fibrillation (chondromalacia) Æ cracks Æ ulceration
eburnation (loss of cartilage é sclerotic 'polished' bone)
tufts of fibrocartilage on the bone surface
• OSTEOPHYTES (in non-pressure areas) due to:
vascularization of subchondral bone
develop in the path of least resistance
capsule traction & synovial metaplasia
proliferation of cartilage adjacent to WB area é endochondral ossification
• Subchondral SCLEROSIS, congestion, and y IOP
• Subchondral CYSTS:
In the areas of max damage
containing thick gelatinous material
ð microfractures that degenerate & accumulate synovial fluid
• CAPSULAR THICKENING and fibrosis Æ deformity F AD IR (antero inferior capsule)
• Mild SYNOVITIS usually (sometimes thick and villous)
• FRAGMENTATION of osteochondral surfaces
• LOOSE BODIES: usually ð synovial metaplsia and extrusion and not separation of an osteophyte
Microscopically:
• Early:
Superficial SPLITS and irregularities
Deep METACHROMASIA (depletion of matrix proteoglycans)
y CHONDROCYTES clusters
SUBCHONDRAL OSTEOBLASTIC activity, marked vascularity
Margin OSTEOPHYTES: ð cartilage hyperplasia and ossification
• Late:
Extensive CLEFTS
CYSTS é amorphous material (squeezed synofluid, disintegrated trabeculae, osteonecrosis)
Bone NECROSIS and denuding
Types
1. Hypertrophic 75%
2. Atrophic 20%
3. Progressive 5%
Variants:
1. Polyarticular (generalized): commonest, 50y♀, hands painful stiffness, also trapMC OA
2. Monoarticular & Pauciarticular: is the classic form, WB OA or 2ry to a cause (DDH)
3. Endemic OA: either environmental factor or genetic dysplasia
4. Unusual site OA: Milwaukee shoulder
5. kashin-Beck disease: generalized OA in hands, elbows, knees + short stature
6. Mseleni joint disease: Polyarticular esp hips Æ crippling deformities ð MED & protrusio
7. Rapid destructive OA: elder ♂ under strong NSAIDs, usually hip ð Ca2+ crystal deposition
8. Charcot’s disease: the most severe form of OA
CP
• Old age, +ve family history, + PF
• WB joints (hands in females)
• Insidious onset & Intermittent course é attacks may lasts for few months
1. PAIN:
1-The main symptom: ð ms fatigue, capsular stretch, congestion, y IOP
2-Site: anterior (sometimes posterior or lateral)
3-y é exertion, WB, Cold
4-z é rest (relief z by time)
5-Progress to be even at rest
2. Stiffness &loss of function: after periods of inactivity Æ constant
3. z ROM ± crepitus
4. Ms Wasting
5. Flexion & Varus Deformity ð ms spasm Æ capsular contracture
6. Tenderness
7. Swelling: intermittent (effusion) or constant (cap/synovial thickening, or osteophytes)
8. Heberden’s Nodes: thickening of the DIP joints (≠ BOUCHARD’S nodes of RA)
Radiography
• PXR
}
1- Asymmetrical narrowing of joint space
2- Subchondral sclerosis
3- Subchondral cysts Fairbank’s changes
4- Osteophytes at the margins
5- Late bone destruction and joint deformity and instability
• Tc-HDP Scan
y uptake in bone phase (yvascularity & new bone formation)
• MRI (T1rho):
new MRI sequence that delineates glycosaminoglycans distribution, so it can assess
early degenerative changes in symptomatic osteoarthritic subjects
COMPLICATIONS
1- Loose bodies
2- Backer’s cyst: capsular herniation
3- Spinal deformity 2ry to pelvic deformity Æ lordosis & side bend
4- Ankylosis
TREATMENT: Vary according to the site, stage, age, severity, and symptoms
• Early: keep moving, prevent overload, relieve pain,
1. EXERCISE of supporting muscles around joints to avoid wasting and keep ROM
2. PROTECTION of affected joints from overloading: z wt, walking stick
3. Pain relief by analgesics or NSAIDS.
4. Modify activity: avoid climbing stairs, squatting,… etc
5. HYALURONIC acid injections
6. GLUCOSAMINE &chondroitin
• Late Surgical treatment - is indicated for patients é persistent symptoms:
• Arthroscopic debridement, wash, removal of LBs, and removal of osteophytes
• Realignment osteotomies may be done in younger patients to redistribute WB load,
decompress the congested metaphysis relief pain dramatically
• Arthrodesis if young and stiffness is accepted
• Total joint arthroplasties for older patients (over 60) in advanced cases
• New & Experimental Treatments:
1. Soft tissue grafts - periosteal / perichondral
2. ACI
3. Mosaicplasty
4. Artificial matrix - carbon fibre, collagen, polylactic acid
5. Fresh osteochondral allografts
6. Doxycycline Æ cartilage collagenase activity
7. Transforming growth factor beta (TGF beta) can repair partial thickness lesions
8. Metalloproteinase inhibitors matrix destroying enzymes & block cytokines
9. Gene therapy - Genes that have either anti-arthritic or synthetic properties can be delivered
into the joint via non-replicating viral vectors; e.g. IL1
The potential long-term treatment or cure of OA really lies in the development of agents that
reverse the balance bet. degradative and synthetic processes of the chondrocyte.
Forestier’s Disease
DISH (DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS)
• = a type of OA with significant amount of osteophyte formation
• more common in elderly men
• associated with diabetes & gout
• prevalence of DISH may be as high as 28%
• spine shows calcification of the anterior longitudinal ligament & peripheral disc margins (disc
space height is preserved)
• Marginal osteophytes may be seen in all peripheral joints
• Clinically have spinal stiffnes & heel pain (with spurs)
• Differs from Ankylosing Spondylitis by abscence of inflammatory markers & HLA-B27
• increased risk of heterotopic ossification following THR
Rheumatoid Arthritis
• Affects 3% of women & 1% of men.
• Hand > Knee > hip > cervical spine.
Diagnosis:
• ARA Criteria (American Rheumatism Association):
1- Morning stiffness:
Lasting at least 1 hour before maximal improvement.
2- Arthritis of 3 or more joint areas:
At least 3 joint areas simultaneously have had soft tissue swelling or fluid (not bony
overgrowth alone) observed by a physician; the 14 possible joint areas are right or
left proximal interphalangeal (PIP) joints, metacarpophalangeal (MCP) joints, wrist,
elbow, knee, ankle, and metatarsophalangeal (MTP) joints.
3- Arthritis of hand joints:
At least 1 area swollen (as defined above) in a wrist, MCP or PIP joint.
4- Symmetric arthritis.
5- Rheumatoid nodules:
Over bony prominences, or extensor surfaces, or in juxta-articular regions
6- Rheumatoid factor +ve.
7- Radiographic changes.
• At least 4 of 7 criteria.
• Criteria 1 through 4 (at least 6 weeks).
7 ccc ............................................Classic
5 ccc ............................................Definite
3 ccc ............................................Probable
2 ccc ............................................Possible
Aetiology:
• Genetic susceptibility: RA is common in first degree relatives of
RA patients and twins.
• Immunological process: HLA-DR4 & DW4 encoded on
chromosome 6; and is found on the surface of APC (antigen
presenting cells); & when interact é the antigen (some times
the antigen with the HLA form the activating complex) Æ
autoimmune response.
• When APC and T-cells interact Æ cell proliferation + cyokines
secretion Æ ⊕ phagocytes & B-cells.
• Rheumatoid factor: Anti-IgG auto antibodies which is detected
in the serum of the patient.
Pathology:
Stage 1: Synovitis
• vascular congestion & effusion
• synoviocyte proliferation Æ VILLOUS formation
• infiltration of subsynovial layers by PMNs, lymphocytes & plasma cells
• a PANNUS of granulation tissue creeps over the articular surface eroding cartilage & bone
• cartilage destruction occur partly ð proteolytic enzymes & vascular tissue
• bone destruction occur partly by proteolytic enz, & osteoclastic activity
• direct invasion occurs at the margins of the joint
• similar changes occur in tendon sheaths Æ rupture
Stage 3: Deformity:
• From:
Articular destruction.
Capsular stretching.
Tendon ruptures.
• Acute inflammation subsided.
Extra-articular Manifestations:
• Nodules - in 20% of RA - skin, synovium, tendons, sclera, viscera.
• Lymphadenopathy & Splenomegaly .............FELTY'S Syndrome (pancytopenia) .
• z salivary & lacrimal gland secretion ...............SJORGEN Syndrome.
• Pulmonary (pleurisy & Rh. nodules) .................CAPLAN $.
• Vasculitis.
• Myopathy & neuropathy, or direct compression from synovitis.
• Visceral: pericarditis, nodules.
Clinically:
• 40 female may be é positive family history.
• Early:
Painful swollen HAND joints é morning stiffness.
PAINFUL LIMPING.
z ROM ± crepitus.
loss of WEIGHT, weakness.
O/E: symmetrical swelling, tenderness, crepitation, synovial hypertrophy.
• Late:
Valgus Deformity.
Instability, tendon rupture.
Path #: from the disease and drugs.
Bouchard’s nodules, Swan neck , Boutonniere, Z-thumb, fingers ulnar
deviation, wrist radio-volar deviation, valgus knee, valgus feet, clawed toes,
atlanto-axial subluxation
Types of presentations:
• Palendromic: starts intermittent episodes of multi joint affection Æ evolve to classic
• Systemic: severe form é visceral affection
• Monoarticular: usually knee. Also, may present as tenosynovitis or CT$
• Myalgic: as fibromyalgia rheumatica but with +ve RF
• y. ESR, CRP
• RF +ve in 80%, ANA 30%
• ACCP (anti Cyclic Cetrolinated Peptide): 97% early +ve in RA even in seronegative RA
• anemia: ð abnormal erythropoiesis, and chronic blood loss from analgesic gastritis
• WBC: Normal or y (if z suspect Felty)
• z Complement
Synovial biopsy & fluid:
• Biopsy: is non specific to RA
• Fluid: zptn, C, glucose / poor clot / y RA cells & PNL
PXR: LARSEN - DALE RADIOLOGIC INDEX
1- Stage I: juxta-articular osteopenia
2- Stage II: Narrow joint space (usually bilateral, symmetrical, concentric ± protrosio)
3- Stage III: Bone erosion of the head near the neck + bone cysts
4- Stage IV: Deformity (don’t forget the cervical PXR)
• Other complications: AVN, fracture neck
DDx:
1]. Seronegative: SLE, Still’s
2]. AS: spondarthropathy
3]. Reiter’s: Conjunctivits, urethritis, Arthritis
4]. Gout & CPPD: crystals
5]. OA: DIP affection, osteophytes
6]. Polymyalgia rheumatica: pelvic, and pectoral weakness, and aching, +ve steroid test
7]. Sarcoidosis: Erythema nodosum, Hilar LN, +ve Kveim test
• Stop the Synovitis:
o Rest.
o DMAR Drugs (Disease Modifying Anti-Rheumatic) - Pyramid Approach = NSAIDs -
antimalarials - sulphasalazine – gold – MTX – D-penicillamine - Azathioprine –
Leflunomide + low dose steroids.
o Synovectomy - chemical, irradiation, surgical.
• Prevent Deformity:
o Splintage.
o Physiotherapy.
o Tendon repairs & joint stabilization.
• Reconstruct (start é knee if > 45º flexion deformity):
o Arthroplasty is the gold standard.
o Osteotomy not done:
Doesn’t remove the cartilage ώ is a source
of inflammation.
RA is concentric & no healthy cartilage.
o Arthrodesis not to be done (bilateral).
• Rehabilitate & keep moving:
o Occupational therapists - aids, support.
o Physiotherapy.
• At Onset: NSAID, exercise.
• Early: NSAID, Steroids, DMD, local injections, physiotherapy, Rest and splitage.
• Erosive: DMD, splintage, operative (synovectomy, tendon repair, joint stabilization).
• Late: Reconstructive arthroplasty.
Problems é surgery:
1- Bilateral knee involvement
2- Ipsilateral hip involvement ................................. start é knee if flexion def >45º start é it
3- UL affection .............................................................. needed for PWB
4- Infections ................................................................... scan for oral, UTI, skin before surgery
5- Bad general condition & systemic disease
6- Cortisone therapy ................................................. need to y the dose preop
7- Atlantoaxial subluxation .................................... difficult intubation
8- Femoral #s ................................................................ be gentle & ready
9- Loosening ................................................................. Cemented or Hybrid are favored
Drugs Details:
Drug Mechanism A/E
NSAIDs PG synthesis Æ z pain and inflammation Gastric Upset
Leflunomide DiHydro-Orotate Dehydrogenase Æ z T-cell prolif
Complications:
1]. Fixed Deformities.
2]. Joint Rupture.
3]. Infection.
4]. Spinal cord compression.
5]. PN compression.
6]. Vasculitis.
7]. Amyloidosis, proteinuria.
8]. Progressive RF.
Poor prognostic signs:

1]. Very high RF.
2]. Peri-articular erosions.
3]. Nodules.
4]. Muscle wasting.
5]. Joint contractures.
6]. Vasculitis.
Prognosis:
1]. 10% improve after first attack of synovitis.
2]. 60% have remissions & exacerbations.
3]. 20% have severe joint erosions requiring multiple operations.
4]. 10% become completely disabled.
Sero-negative Inflammatory Arthroses
Common Clinical Features (diff. to rheumatoid arthritis)
1. Enthesopathy (inflammation of ligament & tendon insertions)
2. Axial skeleton involvement
3. Asymmetrical joint involvement
4. Heel pain (Achilles tendinitis, calcaneal bursitis, plantar fasciitis)
5. Extraskeletal involvement = skin, mucous membranes, GUT, GIT
6. HLA-B27
7. Radiological:
1. ankylosis
2. calcification of adventitia
3. No osteopaenia (typical of rheumatoid)
SLE
• young females
• Arthritis in 75% of SLE patients
Clinical:
• fever, anorexia, weight loss, malaise
• skin rashes (butterfly malar rash)
• Raynaud's phenomenon
• splenomegaly
• nephritis, carditis
Laboratory:
• anaemia, leucopenia
• high ESR
• ANA positive
Treatment:
• Corticosteroids for severe disease
Complications:
• AVN hip (? from steroids)
Ankylosing Spondylitis
Aetiology:
• Affects spine & sacroiliac joints primarily
• Prevalence = 0.2%
• Males > females & Familial involvement
• HLA-B27 marker
Pathology:
• Inflammation & erosive destruction of:
1. Diathrodial joints = sacroiliac, vertebral facet, costovertebral
2. Fibro-osseous junctions - intervertebral discs, sacroiliac ligaments, symphysis pubis
• 3 Stages:
1. Inflammation - round cell infiltration, granulation tissue, joint erosion
2. Fibrosis - replacement of granulation tissue with fibrous tissue
3. Ossification - of fibrous tissue (e.g. syndesmophytes)
Clinical:
1. Spinal stiffness (classical posture)
2. WALL TEST.
3. Chest expansion < 7cm
4. Hip involvement with FFD
5. Achilles tendon insertion pain
6. Difficult cervical spine fractures with epidural haemorhage
Extraskeletal:
1. Prostatitis
2. Conjunctivitis & uveitis in 20%
3. Carditis, aortic valve disease
4. Pulmonary fibrosis
Radiology:
• Squaring of vertebral bodies
• Syndesmophytes
• Bamboo spine
• erosive arthritis with progressive ankylosis
Laboratory:
• High ESR
• HLA-B27 in 90%
• RF negative
Management:
• Postural management
• NSAIDs
• Operations to correct deformity & restore mobility
o Lumbar / cervical spine osteotomies
o THR
ANKYLOSING HYPEROSTOSIS (FORESTIER'S DISEASE)
• common disorder in older men
• widespread ossification of tendons & ligaments
• Diff to AS:
o No erosive arthropathy
o Normal ESR
Reiter’s Syndrome
Hans Reiter, 1916
Triad = Urethritis + Arthritis + Conjunctivitis
Aetiology:
• follows dysentery or venereal infection
• Causative organisms:
o Chlamydia trachomatis
o shigella, salmonella, campylobacter, Yersinia
o Lymphogranuloma venereum
Clinical:
1. Acute Phase:
o inflammatory arthritis of: knee or ankle or foot joints
o pustular dermatitis of the feet (keratoderma blennorrhagicum)
o balanitis
o painless buccal ulceration
2. Chronic Phase:
o spondyloarthropathy
o sacroiliitis in 60%
Radiology:
• erosive arthropathy similar to AS
Laboratory:
• HLA-B27 in 80%
• ESR high in acute phase
• organism may be isolated from urethral fluids or faeces
Treatment:
• Supportive
• Tetracycline for persistent urethral infection
Enteropathic Arthritis
Peripheral arthritis - in 15% of people with Crohn's disease & ulcerative colitis
Sacroiliitis & spondylitis - in 10% of people with Crohn's disease & ulcerative colitis
Must exclude the following first:
1. Septic arthritis of the hip from direct spread from bowel
2. Psoas abscess
3. AVN from steroids
4. Osteopenia from malabsorption & steroids
Psoriatic Arthritis
Prevalence of Psoriasis is 1-2%; only 5% of those will develop psoriatic arthritis.
Aetiology:
• Familial
• HLA-B27 in 60%
Pathology:
• similar to rheumatoid arthritis, but destruction usually severe (arthritis mutilans)
• rheumatoid nodules are not present
Clinical:
• IPJs of fingers & toes affected (ARTHRITIS MUTILANS)
• asymmetrical
• 'sausage digits'
• sacroiliac & spine involvement in 30%
• psoriasis of skin & nails usually precedes arthritis - nail pitting
• ocular inflammation in 30%
Radiology:
• 'pencil in cup' deformity
• arthritis mutilans
Laboratory:
• RF negative
• HLA-B27 in 60%
Diagnosis (diff. to RA):
1. RF Negative
2. asymmetrical
3. distal finger joints
4. sacroiliitis & spondylitis
5. No rheumatoid nodules
6. No tendon involvement
Treatment:
• immunosuppresive agents in severe disease
• prevent deformities
arthrodesis of IPJs to improve function
TB Knee
• Tuberculosis is common throughout the world
• Usually due to Mycobacterium tuberculosis or Mycobacterium bovis infection
Pathology:
1- 1ry lesion:
Site:
Lung usually (sub-pleural GHON’S FOCUS and mediastinal lymphadenopathy)
Pharynx ▪ Gut
Changes:
Local inflammatory focus Æ Lymphangitis Æ Lymphadenitis
Seculae:
TB bacilli remain dormant in LN
Body is sensitized to toxins (Type IV cell mediated delayed
hypersensitivity)
2- 2ry lesion:
Due to reactivation, repeat exposure, z immunity (e.g. drugs or HIV infection)
Results in more significant symptoms as it spreads to:
Lung ............................... military TB, TB bronchopeumonia
Meninges: ....................... TB meningitis
3- 3ry lesions (10% affect the musculoskeletal system)
a. Tuberculoma formation:
Central CASEATION necrosis (coagulation necrosis)
Surrounded by EPITHELIOID cells, LANGERHANS giant cells, LYMPHOCYTES
They tend to coalesce to form a wide area of caseation necrosis
Spread to cartilage Æ destruction and spread to joint space
b. TB Spondylitis: (mainly throracic)
Starts ant. in the body at multiple level; destroy bone & respect ! disc except late
POTT’S PARAPLEGIA ð (kyphosis, abscess, z blood supply to the cord)
c. TB Arthritis (hip, knee, ankle, shoulder, then wrist)
Synovium is THICKENED é Cell rich EFFUSION
Granulomatous PANNUS may form & creaps on the cartilage & bone
Cartilage & bone EROSION (peripherally at synovial reflection)
Juxta articular OSTEOPENIA ð hyperaemia
d. Appendicular skeleton:
Metaphyseal bone destruction (no sclerosis, no periosteal reaction)
e. TB Dactylitis = Spina Ventosa (middle and distal phalanx)
Digit is swollen spindle shape é little pain
Starts diaphyseal é bone rarefaction + PNBF + soft tissue swelling
PXR: Spina (spindle shaped digit) Ventosa (full of are i.e. rarefied)
f. Cold Abscess:
Infected LN may COALASE together to form big area of caseation
Caseation spread via soft tissue planes
May burst to skin to form a sinus
May collect at a distant site far from original pathology e.g lumbar TB Æ groin
4- Healing:
a. Resolution
b. Fibrous Ankylosis
c. Dormant bacilli
Clinically:
• General:
Night sweat, night fever
Loss of weight, loss of appetite
• Local:
NIGHT CRIES: joint is splinted at day time by spastic ms ⎯⎯⎯→ spasm is relieved
AtNight
Æ stretch or compression of the damaged tissue Æ pain

Marked MS WASTING
Marked SYNOVIAL THICKENING
z ROM & STIFFNESS
Joint DEFORMITY
Spine: pain, abscess kyphosis, neurological manifestation
PXR:
}
JUXTA ARTICULAR OSTEOPENIA Æ washed out bone ends
z JOINT SPACE (in children epiphysis y 2ry to hyperaemia) PHEMISTER Triad
Peripheral bone EROSION and CYSTIC subchondral lesions
NO PERIOSTEAL reaction
NO SCLEROSIS
Spine erosion, collapse, paraspinal abscess calcification & kyphosis é crowded
related ribs Æ SUN RAY APPEARANCE
In hip erosions occur in 3 areas (BABCOCK’S Δ); erosion of the superior acetabulum
Æ WANDERING ACETABULUM
Investigation
• yESR
• Leucopenia é relative lymphocytosis
• z Lymphocyte/monocyte ratio may reach 1
• +ve Mantoux test (indicate TB infection recent or old)
• +VE PCR
• Synovial fluid:
y ptn, zglucose
z viscosity, poor mucin clot
Red acid-alcohol fast INTRACELLULAR bacilli é ZEAL NELSEN ....20%
Cultivation on LOWENSTEIN JENSEN media or Dorset egg .........80%
• Difficult to culture needs adequate relevant conc. (centrifuged) sample
• Decontaminate & remove other organism (Petroff method)
• Keep 35º for 6 wk
Organisms also FLUORESCE WITH AURAMINE staining
Negative microscopy does not exclude tuberculosis
Guinea pig inoculation
• Synovial biopsy:
Granulomatous reaction (caseation + Langerhans + epitheliod + lymphocytes)
Characteristic evidence of a delayed hypersensitivity reaction
Skin tests
• Delayed hypersensitivity reaction used to diagnose tuberculosis
• The two commonest tests are the Mantoux and Heaf test
• Mantoux test:
0.1 ml of purified protein derivative is injected intradermally
+ve if .................................. > 5 mm papule at 72 hours
• Heaf test
PPD is inoculated into the skin using a gun to produce multiple punctures
+ve if .................................. > 4 papules at puncture sites at 72 hours
• Positive skin test are indicative of active infection or previous BCG vaccination
DDx
• Transient synovitis
• Monarticular RA
• Subacute arthritis
• Old septic arthritis
Treatment
• Rest:
Splintage and traction to prevent ms spasm and deformity
Maintained till pain and inflammation is over
Then motion is encouraged; if pain & spasm return, resume splints
• Chemotherapy:
RIPES - Rifampicin, Isoniazid, Pyrazinamide, Ethambutol, Spectinomycin
Rifampicin + Isoniazid 6-8 mo
Ethambutol (or pyrazinamide, spectinomycin) for the initial 8wk
Streptomycin is toxic
• When to start surgical ttt:
Clinically: ................................................ No fever, no wt loss, no spasm
PXR: ....................................................... y calcification
Lab: ................................................................ z ESR, y lymph/monocyte ratio >5
• Operative:
Drainge of a TB focus is seldom done nowadays
Cold abscess .................................................. calls for urgent drainage
Young age ...................................................... synovectomy
Clearance operation ....................................... debride all infected & dead tissue
Painful fibrous ankylosis in middle age ....... arthrodesis
Painful destroyed joint ...................................spacer then arthroplasty
Charcot’s Osteoarthropathy
NEUROPATHIC JOINT
It is a severe form of Degenerative OA caused by loss of propriosensation to involved joints
Ætiology:
1- DM is the commonest cause ............................. 0.5% will have charcot
2- TABES DORSALIS: ...................................................... 10% will have charcot
• Charcot’s is not a syphilitic infection of the joint, it is 2ry to tabes dorsalis
• Knee & hip are the mostly affected
• Knee jerk is lost
• Argyll Robertson Pupil
3- SYRINGOMYELIA: ........................................................ 50% will have Charcot
• Degenerative condition of the spinal cord (at the shoulder girdle segment)
• Shoulder and elbow are the mostly affected
• Lost of reflexes & thermal sensation
4- Other causes:
• Congenital indifference to pain
• Meningomyelocele & dysraphism
• CPPD
• Multi steroid injections
• Alcoholic & amyloidosis
Pathogenesis:
• Loss of propriosensation Æ repetitive trauma to unprotected joints Æ OA
• Usually extreme movement and harmful strains are prevented by the protective
contraction of the ms evoked by the Proprioceptive reflex arc
• é loss of joint sensibility this function is lost + no pain Æ trauma & strain are not appreciated
• On the long run this leads to severe OA & disorganization of joint
• Alternatively sympathetic reflexes may lead to hyperaemia & bone resorption
Pathology: exaggerated OA
• Articular cartilage ...................................................... Degenerated, destroyed, disorganized
• Metaphysis ................................................................... rarefied & irregular destruction
• Osteophytes & Loose bodies (LB) ........................ is a characteristic feacture
• Intra-articular .............................................................. ACL vanish
• Synovium...................................................................... thick, polypoid, chondromatosis, pannus
• Capsule ......................................................................... stretched & lax
• Joint ............................................................................... Disorganized, Grotesque, dislocated
Clinically: Painless joint + lost reflexes
TYPE INCIDENCE COURSE TYPE OF JOINT LB &OSTEOPHYTES
1-Hypertrophic commonest Chronic WB Marked
2-Atrophic Rare Acute NWB Not evident
PXR:
• Joint is markedly DESTROYED, DISORGANIZED, and DISLOCATED
• Hypertopic NBF
Scans: hot as infection ..................................................... but cold indium scan
Treatment
• Conservative ttt: zwt, orthotics ............................ (no NSAIDs, or steroids)
• Operative ttt: arthrodesis & Ilizarov ..................... (No arthroplasty)
• Aim is to achieve fibrous Ankylosis
• Amputation are rarely indicated ......................... if broken neglected & severely infected
Haemophilia
• Combined incidence is 1 in 10 000 male births
Haemophilia A (Classic haemophilia)
• Deficiency of factor VIII
• Most common of severe disorders
• XR inheritance
• Only affects males. Carried by females. 30% are new mutations
• Severity varies depending on level of clotting factor VIII:
50% ............................................normal
25-50% .....................................seldom have problems
5-25 % ......................................severe bleeding with operations (mild)
1-5 % .........................................severe bleeding after minor injury (moderate)
<1% ...........................................spontaneous bleeding (severe)
• 50% of known haemophiliacs are moderate or severe
• 5% of patients develop antibodies to factor VIII
• Very difficult to treat. Infused factors are destroyed
Christmas disease
• Deficiency of factor IX
• Less common
• Also XR inheritance
• Similar spectrum of severity
Von Willebrand's disease
• Deficiency of von Willebrand factor
• AD inheritance
Clinical Presentation
• Male with positive family history
• May present after circumcision; Otherwise first bruising appears at 3-4 months; Severe
bruising at walking age; May be spontaneous haemarthroses; Milder forms may present
after dental extraction or operative procedure
• Bleeding In the form of:
o Bruises
o Muscle hematomas
o Haemarthroses
o May occur sometime after injury
• Defect is in clot formation (2nd phase) rather than haemostasis (1st phase)
• May be no known trauma
• HIV .......................................................................70% of whom received pooled factor VIIII
Investigations
• Platelet count and bleeding time normal
• APTT prolonged and PT normal ie Intrinsic
• Low factor VIII coagulant activity diagnostic
Treatment
1. Blood products
• Initially fresh frozen plasma used ...............but the volume was too great
• Then cryoprecipitate used ...........................higher level of F VIII; stored at very low temp
• Then factor VIII concentrates ......................Available in convenient dried concentrate form
o Administration: 1 U/KG elevates VIII by 2% (½ life is 6-12 hrs) till 15-30%
Haemophilic Arthropathy
• Recurrent intra-articular bleeding can cause:
1- Chronic synovitis
2- Progressive articular destruction
Pathology:
o HAEMOSIDERIN ACCUMULATION in synovial cells
o SYNOVITIS makes synovium more susceptible to further injury
o Intra-articular clots Æ Organize Æ ADHESIONS Æ may tear Æ bleed
o Cartilage gradually eroded ð LIBERATION OF LYSOSOMAL ENZYMES
o Vascular pannus covers articular surface and further destroys it
o Subchondral bone exposed - Subchondral cysts - Osteoporosis ð disuse
o y blood flow to joint Æ EPIPHYSEAL OVERGROWTH &osteophytes
Muscle
• Recurrent bleeds lead to FIBROSIS AND CONTRACTURE
• May result in deformity
• May be complicated by:
1. Compressive nerve palsy
2. Compartment syndrome
3. Cysts and pseudotumour
4. Cyst from massive ms bleed (before it is absorbed draw in more fluid by osmosis)
5. Erode through skin or viscus and become an abscess
Pseudotumour (From subperiosteal or intraosseous bleed )
1- SUBPERIOSTEAL .........................................shows periosteal stripping + NBF
2- INTRAOSSEOUS ..........................................ill-defined lesion + extensive osteolysis ± NBF
• May be confused with sarcoma, GCT, ABC
• May destroy bone and lead to pathological fracture
Stage
Stage 1 After acute haemarthrosis • Soft tissue swelling
Stage 2 Subacute haemarthropathy • Epiphyseal osteoporosis; overgrowth
Stage 3 Chronic é no narrrowing • Squaring off of patella
• Widened intercondylar notch of knee
• Widened trochlear notch in elbow
Stage 4 Chronic severe • Marked narrowing of joint space
Stage 5 Destructive • Joint disintegration
Clinical
1. ACUTE HAEMARTHROSIS
o Most commonly affects - Knee, Elbow, Ankle, Hip and shoulder
o Joint is Hot red and swollen, Acutely painful, Held in flexion
2. SUBACUTE HAEMARTHROSIS
o After 2 or more acute bleeds
o Synovium is thickened and boggy
o Moderate z ROM
o Pain not prominent
3. CHRONIC DISEASE
o After subacute form present for 6 m or more
o Bleeds less frequent and more difficult to detect
o z ROM due to
Fibrous contracture
Deformity
Muscle wasting
o Muscles most commonly affected = Iliopsoas, Thigh, Calf, Forearm
X-rays ........... Progressive destruction
Treatment
Acute haemarthrosis
• Usually treated at home; Usually single dose sufficient to z pain quickly
• Immediate IV dose of factor VIII to achieve level above 30%
• Adequate analgesia (not aspirin or NSAIDs) + Immobilise limb for first 24 hrs
• Place of aspiration or washout controversial
o Reduces pain and swelling
o Removes blood Æ z degradation with possible toxic effects
o No evidence that it decreases risk of arthropathy
Subacute haemarthropathy
• Further treatment indicated if:
i. Failure to respond to above treatment
ii. Two or three bleeds in short period of time
• Initially:
o Prednisolone 5 days
o 2 or 3 doses of factor VIII for level 30%
• If still not settled: 6-8 wk course of Prophylactic factor replacement + Active
physiotherapy
Chronic haemarthropathy
1- Nonoperative
o 6 months of small dose of prednisone, prophylactic factor replacement, active
physiotherapy
2- Synovectomy
o When nonoperative treatment fails
o Not indicated beyond stage 3
o Open or arthroscopic
o Reduces number of bleeds
o Does not slow cartilage degeneration
3- Corrective surgery
o For stage 4 and 5
o Presence of antibodies is contraindication to elective surgery
o Avoid pins that penetrate skin
o Screen for HIV and hepatitis B preoperatively
o Check factor levels intraoperatively
o METICULOUS HAEMOSTASIS
o Increase factor levels for procedures such as MUA
o OSTEOTOMY
Most common deformity is flexion contracture with valgus of knee. Can be
corrected with supracondylar osteotomy
o ARTHRODESIS
Not often indicated because multiple joints involved
Useful for ankle and subtalar joints
o TOTAL JOINT REPLACEMENT of hip and knee
Higher perioperative complication rate (esp. Haematoma and infection)

Only 50% SURVIVAL AT 10 YRS

Maintain factor VIII LEVELS AT 100-130% for 2 days post-op; 50-60% for 2

wks; 30-50% for 6 wks
o TENDON LENGTHENING of tendo Achilles for equinus deformity
Gaucher’s Disease
Discussion:
• In 1882, Gaucher described idiopathic hypertrophy of spleen w/o leukemia
• AUTOSOMAL RECESSIVE deficiency of lysosomal enzyme GLUCOCEREBROSIDASE. It is the most
common genetic lysosomal storage disorder & results in accumulation of of glucocerebroside
in retinuloendothelia cells
• Commonly seen in children of Jewish descent.
Pathology:
• Bone involvement is common in Gaucher's disease:
• expansion of metaphyses - failure of remodeling Æ 'ERLENMEYER FLASK' distal femur (also
found in Niemann-Pick disease and osteopetrosis).
• erosion of the cortices of bone ('moth eaten')
• AVN femoral head ('Bone within bone' appearance)
• Bone crisis similar to Sickle Cell Anaemia
• Pathologic frx.
Histology: lipid-laden Histiocytes.
Classification:
• TYPE I: (adult form) - chronic noneuronopathic type; - central nervous system is spared &
disease is characterized by slowly progressive visceral and osseous involvement; enlarged
spleen may cause mechanical problems, including abdominal distention and abdominal pain
as well as shortness of breadth, as well as causing pan cytopenia; splenectomy may be
performed for thrombocytopenia; bone pain is a common complaint, which often resolves
after 1-2 days; bone pain may also be due pathologic frx, osteomyelitis, or DJD;
• TYPE II: acute neuropathic form; most patients don't survive more than 9 months;
• TYPE III: - sub acute neuronopathic; convulsions are frequent;
Clinical Presentation:
• BONE CRISES (episodes of pain and swelling), sometimes accompanied by fever but w/o x-ray
changes, are common, recurrent manifestations of the disease. - often the pain cannot be
controlled w/ narcotics; pain may last days or several weeks;
• AVN OF THE FEMORAL HEAD - is the most symptomatic lesion; bilateral disease is comon;
MRI:
• zT2 signal is seen in the marrow of long bones, vertebrae, & hips and is related to the areas
of marrow infiltrated by Gaucher's lipids.
Treatment:
• PATHOLOGIC FRX: - are best treated conservatively; frxs are esp common in yound children. Frx
proximal end of femur may occur in children & adults - these may be treated non operatively
although there may be with some varus deformity
• BONE CRISIS: ...................................................... brief bed rest + NSAIDs Æ crutches as tolerated
• AVN: ............................................................... brief bed rest + NSAIDs Æ crutches as tolerated
THR carry yrisk of infection, bleeding, loosening
• ENZYME REPLACEMENT therapy is now available.
Knee Swelling
Generalized
d Localized
d
Acute e Chronic Anteriior Posterior To one side

•Hemarthrosis •OAA •Prepatella
ar •Ba
aker’s cyst
•Hemophillic •PV
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•Septic arth
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novial •Pes Anserrinus sus cyst Soft
Hard d
•Gout chondromatosis •Deep patellar •Po
opliteal •M
Meniscal
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schlatter •Osteocho ondro
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•MCL
on
calcificatio
Pe
ellegrini Stieda:
Deep p MCL lacerration é hem matoma forrmation
Ossiffication of thhe hematoma Æ pain nful lump deeep to the M
MCL
ttt: re
emoval if sym mptomatic
Se
emimemb branosus Bursa
The bursa
b betw
ween the sem mimembranosus and the medial head gastrroc
CP:
pa ainless lummp behind the knee slightly to the medial side
y é knee fle exion
Flluctuant lu ump and th he fluid cou uld not be pushed into the joint ð ms thatt
obbstruct the e communiication
So ome times painful
ttt: exxcision via transverse
t in
ncision
Recurrence is co ommon
Baker’s cysst
Synovial herniattion of the posterior
p ca
apsule
Occu ur é OA, RA A, TB
CP:
Older
O peoplle
Midline
M at th
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Flluctuant lu ump
So ome times rupture an nd become e painful é release of the synovial contentt
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Arthrrography:
Re eveal the communica
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Excision is not re ecommend ded as the cyst
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[Kn
nee Disord
ders] Page
P | 791
Anterio
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Knee Paain
Patellar Pateellofemoral Intraarticularr Patella

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Congenita al Pain & Insall > 1.2 + Traumatic

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Jumper’s
Knee - Osteotomies
• 60% of the load of the body weight passes through the medial compartment of the knee
Loads up to 4 times body weight are produced on climbing stairs
• Osteotomy redistributes the force
• Valgus osteotomy most commonly performed (varus knee) and is indicated in patients that have uni
compartmental disease, are less than 60 - 70 years old, are of optimal weight, have an active
occupation or lifestyle ώ they want to maintain and have a good range of motion
NB: ROM is not likely to improve with an osteotomy
INDICATIONS
1. AGE: physiologic age < 60 yrs in an athlete, laborer, or anyone who needs to knee down
such as for gardening (TKR will generally not allow the patient to kneel)
2. WEIGHT: > 80 kg are at increased risk for component failure;
3. ANGULAR DEFORMITY:
1. >15º varus deformity (often patients will have varus laxity)
2. > 10º valgus deformity
4. SAGITTAL RANGE OF MOTION:
1. < 15 º flexion contracture
2. > 90 º flexion
5. UNICOMPARTMENTAL INVOLVEMENT
Contraindications:
1. TIBIAL SUBLUXATION > 1 cm
2. Bicompartmental or tricompartmental arthritis
3. OCD lesion of more than 5 mm deep
4. ACL tear
5. RA & inflammatory arthritis
6. Inadequate bone stalk
CLINICAL
• Observe patient WALK (look for varus thrust & foot progression angle)
• Test LIGAMENTOUS STABILITY tests
• Q ANGLE
• COMPENSATORY ARC OF MOTION - to correct a valgus knee deformity - for a 20º varus
osteotomy, 20º of hip abduction is required so pt does not end up é an add deformity
• Examine the FOOT FIXED VARUS DEFORMITIES which may worsen med compartment
loading
• LLD Coventry closing wedge osteotomy might be indicated, where as, if the arthritic side
is shorter (than the other leg), then consider opening wedge osteotomy
• STAHELI ROTATIONAL PROFILE is done to role out rotational malalignment
Preoperative Planning
Radiology
• STANDING LONG-LEG film with patellae facing forward (rather than the patient's feet)
o Mechanical axis = centre of femoral head - medial tibial spine - centre of ankle
joint
o Weight-bearing axis = centre of femoral head - centre of ankle joint
o Anatomical axis = line along axis of the femur to the intercondylar notch and the
line formed by the interspinous region to the centre of the ankle
• SUPINE films
• Perform the ALIGNMENT TEST.
Technique
Medial Compartment Disease
• High Tibial Osteotomy (HTO) above the tibial tubercle:
o Lateral closing wedge & fibular shortening
o Open medial wedge
o Dome shaped osteotomy
o Rap osteotomy in severe degrees and Blount’s
• OVERCORRECTION of the mechanical axis by 3º is ideal (the mechanical axis pass through
the medial 1/3 of the lateral plateau)
• COMPLICATIONS:
1. Undercorrection - most common
2. Overcorrection
3. Penetration of the articular surface
4. AVN of tibial plateau
5. Anterior compartment syndrome
6. Peroneal nerve injury
7. Patella baja
8. TKR may be more difficult
Lateral Compartment Disease
• >12º...............................femoral (as the LFC usually erodes Æ accentuating the valgus)
o Distal femoral medial closing wedge
o Distal femoral lateral opening wedge
• < 12º ............................HTO (if preop. plan shows no joint line obliquity will result)
Other Osteotomies Around The Knee:

• Osteotomies of the patellofemoral malalignment
• Osteotomies of Blount’s
Knee Arthrodesis
Indications:
1. FAILED KNEE REPLACEMENT (most common)
1. better fusion rate following failed condylar components (80%) than failed hinged
prostheses (55%)
2. uncontrollable SEPTIC ARTHRITIS with complete joint destruction
3. young patient with SEVERE ARTICULAR DAMAGE as in joint tumors
4. SEVERE LIGAMENTOUS INSTABILITY that can not be addressed by TKA
5. NEUROPATHIC JOINT disease
Contra-indications:
Ideal position:
1. Contralateral knee disease • 10-15 º FLEXION
2. Contralateral leg amputation • 0-7º VALGUS
3. Ipsilateral ankle or hip disease
4. Ipsilateral severe segmental bone loss
Techniques of Arthrodesis:
1- External Fixation
o Ilizarov technique
o minimal soft tissue dissection
o allows for late adjustment
o allows arthrodesis in the presence of active infection
2- Intramedullary Nailing Arthrodesis
o most reliable for achieving fusion
o 2 stage technique in active infection
o can insert nail antegrade thro the piriform fossa
or thro the knee joint
o complication rates of 20-50%
3- Plate Fixation
o 2 twelve hole plates
Complications:
1- Non-union- 20%
2- Malunion
3- Delayed union
Uni Compartmental Knee replacement

Rational
• Used to treat unicompartmental knee arthroses where it is better than the osteotomies as it
offers less early complications and fast initial success
Indications
1]. Unicompartmental knee arthroses
2]. <60 y
3]. degenerative arthritis
4]. Range of motion at least 15-90º flexion
Contraindications
1]. Bicompartmental arthroses
2]. Crystalline deposition arthroses
3]. ACL & Ligamentous instability
4]. Subluxation > 1 cm
5]. Large intercondylar erosion (sign of subluxation) convert of TKR
6]. Marked coronal malalignment > 10º varus, > 15º valgus
Technique
• Midline, subvastus, or lateral approach
• Protect the ACL and anterior horn meniscus
• Keep moist the contralateral cartilage surface
• Distal femoral cut should be minimal
• Anterior cut should allow the anterior flange to be recessed below the level of the normal cart
• Tibial cut parallel to the femoral cut (8-10 cm)
• Soft tissue balance and gap measurement are done as in TKA
Complications
• Anterior impingement of the patella
• Pes Anserinus bursitis
• Arthritis of the contra lateral compartment
• Loosening, vascular, thromboembolic…
Results
• Controversial, most surgeons stick to the indications only
• Up to 90% success
Arthrodesis Osteotmy Unicompartmental TKR

Age Any <60 >60 Any age
Patient Active Heavy active Light sedentary Light sedentary
Arhtritis Severe uni uni Bi or tri
Pathology Infective degenerative degenrative Any
Range Any range 15º - 90º 15º - 90º Any
P mary Tota
Pri T al Knee
K Arthrop
A plastyy
Ra
ational
1]. Pain relief
2]. Resto
oration of normal
n limb alignmen nt
3]. Resto
oration of a functionaal range off motion
In
ndicationss
1]. The coommonestt indications for TKA are a 1ry & 2ry 2 Osteoa arthritis
nd
2]. The 2 is Rheu umatoid Arthritis
A
3]. Hemo ophilic Arrthritis and d other typ pes of arthrropathy
4]. End-SStage Arrthritis that is nonrespons n sive to th he usual
nonop perative tre
eatment
5]. Sever re Intractaable Pain
6]. Ideally
y indicate ed for old d ages; altthough also done in young
patiennt ώ severee patholog gy
7]. Failedd Alignme ent Osteo otomies
Co
ontradicttions
Absolutte
• Activ ve Infectio on in the knnee, ipsilate
eral extremiity, or elsew
where in thee body
Relative e
1]. Inadeequate bo one stock due to oste eoporosis or other metabolic
m bone diseasse
2]. Afterr arthrode esis ð scarin
ng & muscle e fibrosis th
hat needs highly
h consttrained kne
ee
3]. Markked Recurv vatum in polio
p as the e prosthesiss is unable to addresss the recurvvatum such
ha
deformmity that may
m lead to early
e loosen ning and fa ailure
4]. Neur ropathic Jo oint ώ preclude moto or control of the knee or lead to o a Charcoot knee
5]. Weak k Extenso or Mechan nism
6]. Geneerally Poor Health orr Systemic c Disease
Cllassificatiion
Knee
e Arthro
oplasty
Un
nconstraine
ed
To
otally consttrained
•UCR Se
emi constrained
•Hinge
ed & rotating
g
•Kinemattic Knee (historical)
PCCL Retaininng PC
CL substituting PCL sacrificing
•Difficult balance esp. in •Cam annd spine mech
hanism
•obsolete
severe ma alalignment •Mobile Bearing Knee
•Constra
ained Condylar
Th
hree broad d types off arthroplaasty are ussed in unccomplicate ed primaryy TKR toda ay:: Cruciatte-
Reetaining, Cruciate e-Substitutting, An nd Mobile e-Bearing Knees. For more complex
re
econstructions in wh hich instabbility due to ligament failure iss present, nonlinked constraine ed
arrthroplastie
es have beeen used. (Linked
( connstrained devices
d such as “hingges” are ra
arely used or
evven indicated.) All of
o these arrthroplastiees are desccendants of o the succcessful Total Condylar
kn
nee, the go old standarrd for resurfacing typ
pes of totall knee replacement. IIn the bestt designed of
eaach catego ory, long-te
erm resultts are exceellent in te
erms of fixaation, funcction, pain scores, annd
m
motion.
PCL-Retaining Knees
1]. The theoretical basis for retention of PCL in TKA suggests that with a posterior tether
between the femur and the tibia, STRESS BYPASS the TKA components
2]. Proprioception is maintained, and normal motion (femorotibial rollback) is preserved.
3]. Preservation of QUADRICEPS power and
4]. Preservation physiologic ROLLBACK may theoretically result in a more normal gait in
walking stairs. The demands of balancing the anatomic function of the PCL dictate that
the normal joint line be closely restored, possibly further improving patellofemoral
kinematics. In order to facilitate the femoral rollback, tibial polyethylene components
were historically kept relatively flat in the anteroposterior (AP) direction, with a
physiologic posterior slope. This avoided the “Kinematic Conflict” of a dished
polyethylene, preventing normal rollback. Although some laxity is necessary to preserve
range of motion, more 1anametric posterior cruciate–sparing prostheses depend entirely
on the soft tissues to resist posterior translation. Later iterations of cruciate-retaining
implants have added more congruence to the articular polyethylene to improve stability
and contact stresses.
5]. Restoration of the proper posterior translation of the femoral component Æ y flexion;
this is reproduced by High-Flexion Designs in ώ there is y in the thickness of the
posterior condyle Æ delay of the tibial impingement during flexion
Kinematic conflict occurs if

concepts are mismatched. In
this case, the posterior
cruciate ligament is
preserved using a dished
tibial component.
Impingement occurs
posteriorly with flexion.
Precautions:
1]. LEVEL OF THE JOINT LINE must be near normal height Æ or may cause tight PCL
2]. Avoid TIGHT PCL, ώ will produce:
i. Restricted flexion
ii. Excess femur on tibia rollback = Booking
iii. High posterior polyethylene-bearing load Æ Articular failure.
3]. FLAT TIBIAL INSERT avoids that conflict.
4]. The technical challenge with a PCL-retaining knee design is to realign the limb and
restore full motion while keeping the PCL under proper tension.
• Normal physiologic tension is found in only 1 /10 knees undergoing a PCL-retaining

• Well-functioning PCL-retaining TKAs may have nonphysiologic AP movement.
• Some cases demonstrated “R ROLL FORWARD” rather than “roll back”
PCL-Substituting Knees
• Sacrifice and substitution for the PCL gives predictable femorotibial kinematics and may
facilitate balancing knees with greater angular deformity, especially when secondary
changes in the PCL contribute to the deformity.
• The function of the PCL is partially replaced by:
1]. More CONGRUENT articular surface
2]. Tibial SPINE
3]. Femoral CAM mechanism
• Historically, the most popular designs had a higher rate of patellofemoral complications.
• Patellar pathology may be partially due to:
1]. Relative elevation of joint line
2]. Relative patella baja
3]. Impingement of fibrous tissue proximal to patella Æ “PATELLAR CLUNK”
4]. Boxy femoral profile é no recession of trochlear groove Æ y patellar retinacular tension
• Recently, improved designs replicate patellofemoral anatomy and mechanics.
Mobile-Bearing Knees
• Potential design advantages:
1]. Highly congruent femoral and tibial articular surfaces Æ very low contact stresses
2]. z PE wear
3]. Tibial articular surface “float” by gliding Æ z kinematic conflict by highly congruent surfaces
• Fluoroscopic information suggests that in vivo kinematics may imperfectly replicate design goals
• In USA:
1]. 45%................................... PCL substituting
2]. 45% ................................. PCL retaining
3]. 10% ................................. Mobile bearing
PCL retaining PCL substituting Mobile bearing

1]. Preserve anatomy 1]. y congruence 1]. Ultraconforming
Advantage
2]. Preserve Roll Back 2]. Fixed roll back 2]. Floating tibial insert z conflict
3]. zstress; dissipated to soft tissue 3]. Less sensitive to JL changes 3]. z contact stress
4]. Enhance upstairs activities 4]. Correct moderate deformity 4]. Automatic correction of
rotational deformity
Disadvantage
1]. Less congruent 1]. Patello-femoral clunk 1]. Diff precise flex-ext gap
2]. Paradoxical roll-back 2]. Implant dislocation 2]. Bearing dislocation
3]. Late PCL instability 3]. Loss of PCL proprioception
4]. Diff to correct big deformity 4]. Femoral notch resection

Accurate limb alignment z stresses. The main goal of instrumentation is to provide accurate alignment
• The mechanical axis = line that passes from hip center to ankle center & falls on the med side of knee
center
• Consistent reproduction of a mechanical axis landmarks are difficult intraoperatively
• Anatomic axis landmarks, by contrast, are available, easy to instrument, and approximate mechanical
axis
• Precision is paramount because an asymmetry of only 5% Æ LIFT OFF of the femoral component on
tibia, with compressive forces all on one side and tensile forces on the other.
• Subtle malalignment y by time as soft tissues attenuate under excessive forces
• Fixation is reliably achieved with both cemented and cementless techniques, but PMMA remains the
standard and generally the most widely used technique.
Planning of skin incision:

1- Medial Parapatellar Approach
2- The Subvastus Approach
3- Lateral Parapatellar Approach Kinetics is the study of forces
4- Modified Lateral Capsular Approach Kinematics is the study of motion
5- Mid-Vastus approach
Surgical Procedure
Preoperative Evaluation
7]. TAKE GOOD-QUALITY RADIOGRAPHS on large cassettes in both the AP and lateral planes. AP
weight-bearing films demonstrate better any potentially dynamic instability. They also
accentuate joint space narrowing. A Merchant view (or other similar radiograph) is useful to
evaluate patellofemoral mechanics. A TUNNEL VIEW may be useful to evaluate for
osteonecrosis.
8]. Fixed ANGULAR DEFORMITIES and CONTRACTURES need to be released at the time of surgery
either through soft tissue or bony maneuvers.
9]. LIGAMENTOUS INSTABILITY, particularly in the medial-lateral plane, may need to have specially
stabilized components or ligamentous augmentation for a successful procedure.
10]. VASCULAR DISEASE in LL, may be there is a contraindication for use of a tourniquet
11]. Assess SKIN condition; avoid flaps and undermining of the skin, particularly laterally over the
patella to avoid potentially devastating problems. In general, old incisions performed. Cross
transverse incisions for patellectomy or high tibial osteotomy at 90°. More recent parapatellar
incisions are problematic. In general, include recent parapatellar incisions in the line of the
main incision if practical.
12]. In the absence of long bone and hip deformities,, STANDARD 36-INCH RADIOGRAPHIC films with
the patient standing are adequate for preoperative planning.
13]. TEMPLATE for the size of prosthetic components on the radiographs with acetate overlays that
are compensated for radiographic magnification. Preoperative templating is only an
approximation of the required prosthetic sizing—never use templating to determine the
precise size used at surgery.
SURGICAL PREPARATION
.
• POSITION the patient carefully in the supine position on the operating table.
• Protect the elbows with foam pads and gently flex them approximately 30°.
• Elevate the patient's buttock é soft roll (hard ones Æ sciatic nerve palsy)
• Contralateral leg often lies in external rotation; so pad the lateral side of the knee.
• Position &secure TWO SEPARATE BUMPS to the table as leg positioners:
• When the leg lie on top of both full extension
• When the foot lie on the 1st bump 30° flexion
• When the foot lie on the 2nd bump 100º flexion
• Rotate the table toward the opposite limb z tendency to ER
• Confirm that PREOP AB have been given before tourniquet
inflation; cephalosporin is an appropriate choice.
• TOURNIQUET should have been placed on the thigh as high as
possible and the skin protected with soft webril padding.
• WALK AROUND” the patient just before scrubbing.
Finally, take a “W
Check all peripheral nerve sites for appropriate padding.
• SHAVE the skin around the knee immediately before op to z
compromise of the skin surface. Extended time between shaving
and surgery promotes colonization of small nicks with bacteria.
• Reaffirm that the CORRECT LIMB is being prepared. Although it is
rare, wrong limb side surgery does occur and is disastrous for patient and surgeon. AAOS
recommended confirmation of the side to minimize this complication
• Avoid EXCESSIVELY BULKY DRAPES as precise alignment in total knee replacement depends on
the ability to palpate the bony landmarks
Operative Technique
• Flex the knee to a 30° position and mark the surgical incision. Flexion produces tension on the
anterior tissues, which allows a more precise surgical exposure.
• A midline incision is preferred, extending ~ five fingerbreadths above & below the patella
• Carry the incision through the midpoint of the knee and distally just medial to the tibial
tubercle
• Then carry the incision through the deep fat and the prepatellar bursa.
Preserve the epitenon for later closure
• Perform a medial arthrotomy with a new knife blade. The location of the
quadriceps tendon can be very deceiving proximally, as it may be biased
laterally if only the visual landmarks are used, and this may lead to
transection of the bulk of the quadriceps. Often, feel the tendon
• Use a #10 blade perpendicular to the tendon, longitudinally in a gentle
curve, which curve around the patella.
• In the inferior region of the arthrotomy, split the fat pad with the medial
bulk of fat maintained. This facilitates the lateral exposure, and leave a fair tissues for closure.
• When the incision comes to the tibial tubercle, bring the incision parallel to the shaft of the
tibia and carry it distally for a few more millimeters.
• Place a right angle retractor medially and transect the anterior horn of the medial meniscus,
witht the medial soft tissue from proximal to distal, staying strictly at the subperiosteal level to
maintain the vascularity of the medial flap of tissue.
• If severe varus knee, the medial exposure can be extended into a medial release.
• Once the deep portion of MCL has been elevated, place the Z-type retractor between the
MCL and bone to gain medial exposure.
• Remove large medial osteophytes at this point as part of the medial release.
• Flex the knee to 90° or 100°. The potential for patella tendon avulsion exists in the tight knee.
As the knee is flexed
• Watch the insertion of the patella tendon to avoid any excessive flexion that may avulse the
patella tendon. If the patella cannot be easily everted without the risk of patella tendon
avulsion, obtain more extensile exposure either by:
I. Extending the arthrotomy proximally
II. Doing more distal soft-tissue release
III. Quadriceps release
IV. Tibial tubercle osteotomy: this is mostly prefered
• This situation most often occurs in:
i. Very obese patient
ii. Patient with prior knee surgery, e.g. HTO Æ patella tendon is scarred and tight
• Once patella tendon avulsion occurs, it is very difficult to treat, so this complication is best
avoided.
• Flex the knee 100º, patella is everted; so femoral condyles, and tibial plateau should be at least
partially visualized.
• ACL is resected to enhance exposure.
• Using a 1-inch osteotome, remove medial and lateral osteophytes to expose the PCL
attachment
• If the PCL is being intentionally sacrificed, it is best done at this point. The PCL should not be
sacrificed in a cavalier fashion, but it should be done precisely by electrocautery
subperiosteally off
• Release the lateral periphery of the meniscus with a #15 blade in a precise curvilinear fashion
along to its insertion next to the PCL.
• Branches of the lateral geniculate artery are just outside the insertion of the lateral meniscus
and should be cauterized at this time.
• Once the lateral meniscus is removed, place a Z-type retractor in the corner overlying the
lateral tibial condyle to gain extensile exposure of the flexed knee.
Principles of Balancing:
• At least four directions for spatial relations must be carefully maintained:
1]. CORONAL ANGULATION 3]. SAGITTAL ANGULATION
2]. ROTATION 4]. JOINT LEVEL
• In tibia use IM or extramedullary alignment guides, but in femur only use IM guides
Angulation:
• Femoral medullary hole ≈ 9 mm, just med to notch center & above PCL insertion Æ best
alignment
• Avoid midline drill hole in femur Æ valgus angulation, as it is not aligned é medullary canal.
• Put your opposite hand on the femoral shaft to provide appropriate
directional control
• Once the hole is drilled, aspirate BM to z embolization.
• Distal cut is made in a preset angle from mechanical axis = 5°-6° valgus
• Tibial cut is made to its long axis
Rotation Of The Femoral Component
• Patello-femoral mechanics are altered dramatically by femoral rotation.
• Excessively IR of femoral component Æ y patellar subluxation
• Some ER of femur is desirable to achieve equal flexion gap, as tibial
cut is done to tibial long axis, not in ! normal 3° MEDIAL INCLINATION
• ER of femoral cut is necessary to make flexion gap equal, achieved by;
1]. WHITESIDE'S LINE and draw the transverse axis ⊥ on it
2]. TRANSEPICONDYLAR AXIS gives 3-5° ER to post condylar axis
3]. POSTERIOR CONDYLAR AXIS in cut is made 3° ER to that line
4]. Parallel to the tibial cut (G GAP TECHNIQUE)
• No one landmark is always reliable. Use all three in combination;
o Epicondylar Axis .................. is the most reliable, but difficult to palpate
o Post condylar axis ............. not for valgus knees or RA
o Transepicondylar ................ not for lat condylar hypoplasia
Femoral cut depth and rotation techniques:
1]. GAP TECHNIQUE
• Begins é tibial cut to tibial axis 5-10 mm below the articular surface of
the more normal side, then check ligament balance.
• Measure the WHITESIDE'S LINE (AP axis) is the line between the deepest
After resection of the
part of the patellar groove anteriorly & the center of the intercondylar distal femur and
notch posteriorly; this gives you an idea about the femoral size proximal tibia, the
• Posterior femoral cut is made // to tibial cut extension gap (B)
must equal the flexion
• Disadvantages: gap exactly
o Midrange laxity (only 0° - 90° are checked)
o Possible elevation of JL (in flexion contracture + y flexion gap cut
Æ undersized femoral)
2]. MEASURED RESECTION TECHNIQUE
• Replace resected bone from femur & tibia = thickness of implant
• = Joint Line Technique, as the joint lines are fairly well maintained and
the normal anatomy is essentially resurfaced.
• Femur is usually resected first
• It is very important in PCL retaining; as slight elevation of the joint line in
PCL-retaining designs can have adverse effects on knee kinematics
• Advantages:
o Close matching of the AP dimension of femur
o Preserve femoral rollback without the “booking” phenomenon
o Avoids y post stresses
o Avoids limited flexion associated é tight PCL
o Avoids excessive translation é loose PCL
o Whiteside line ......................... not for big anterior osteophytes
Preparation of Femoral Cut
• The distal level of the femoral implantation is critical to preserve the proper level of JL
• The flexion and extension gap must be equal.
• The coronal alignment and proper ER are critical.
1].Anterior and Posterior Sizing

• After the distal femoral cut is made and the ER has been determined, make the anterior and
posterior femoral cuts. In general, there are two references:
1]. ANTERIOR REFERENCING technique, where the anterior cut is made first by referencing
from the anterior cortex. This approach ensures no femoral notching
2]. CALIPER TECHNIQUE (Jig system technique, mostly used): measure the distance bet post
condyles & ant cortex. If size is bet 2 sizes, take the smaller one to avoid overstuffing
• OVERSTUFFING is a phenomenon that occurs when too large femoral component is placed. If
the component is placed posterior Æ tight flexion gap & z flexion. If an oversized component
is placed too far anterior Æ extensor mechanism impinge on the femoral flange Æ tight knee.
• In the so-called “GGREYHOUND KNEE,” named for its resemblance to canine anatomy, there is
large AP diameter & narrow medial-lateral diameter Æ medio-lateral over hanging femoral
component. Proper implant system selection z this phenomena
• Restoration of the proper posterior translation of the femoral component Æ y flexion; this is
reproduced by High-Flexion Designs in there is y in the thickness of the posterior
condyle Æ delay of the tibial impingement during flexion
• Lastly, check the bone cuts for:
1]. Appropriate rotations.
2]. MATTERHORN SIGN (after a mountain) = longer lateral
condylar ant cut than the medial one
3]. Posterior cuts should show asymmetry, é more medial
> lateral bone in most cases.
2].Removing the Posterior Osteophytes

• Remove posterior osteophytes after the chamfer and other finishing cuts. The posterior
osteophytes do not act as a mechanical block to limit flexion only, but also tent the posterior
capsule and limit full extension.
• With the knee held in extreme flexion, retract the femur superiorly with a blunt bone hook
placed in the notch. Use a 1-inch sharp, curved osteotome to resect posterior osteophytes
• Remove adherent capsular attachments by either curettage or rongeur. A soft sulcus should
result behind the posterior condyles
• This approach will maximize the potential extension and flexion of the knee
Check for pitfalls:

1]. Oversized femoral component
2]. Improper ER
3]. Notching of the femur
4]. Improper axial alignment
5]. Flexion & extension gaps: this can be a guide to
the amount of tibial cut needed
Tibial Resection
• Tibia is resected to its long axis. The anatomic axis is in 3° varus.
• Implant systems initially attempted to replicate this slight varus profile 2°
to 3° varus that produced 5-6° varus cut Æ early component loosening.
• Therefore, attempt a cut with the knowledge that a slight varus cut 2-
3° should not alter clinical results. We prefer extramedullary technique.
Multidirectional orientation of tibial cut:
[1]. ROTATION
• This is best determined by sighting down “bird's-eye view” relying on:
a- Tubercle line (most reliable): keep the profile centred on the
medial third of the tubercle
b- Posterior condylar axis
c- Transcondylar line
[2]. CORONAL ALIGNMENT
• Secure the yoke of the tibia cutting guide at 2/3 of the way down the
tibia above the ankle; not at the ankle joint, as the fibula widens it Æ
produce a lateral offset Æ varus angularion.
• Place the proximal jig of the tibia cutting guide right over the center of
the tibial tubercle. The bulk of the patellar tendon may bias the cutting
jig medially Æ varus angulation, so a smaller cutting block is better
• Distally, place the guide // to the chin of the tibia / its tip over TA tendon
/ pointing to 2nd ray
• Always, place the distal tip of the guide medially (over the anterior tibialis
tendon) Æ z varus risk
[3]. HEIGHT
• Variety of height guides are available:
1]. Curved wing-shaped device
2]. Measuring Jig that measure from the cutting surface to fixed points above the tibial surface
• In general, it is prefered to take 10 MM OFF THE “NORMAL” SIDE Æ slight subchondral resection
on the “abnormal” side.
[4]. POSTERIOR-TIBIAL TILT
• AP Caudal downslope of the tibia ≈ 5º (most systems have it built in i.e. use a neutral cut)
• Avoid putting the tibia in extension Æ tight flexion gap & z motion
[5]. TIBIAL COMPONENT SIZE
• The largest size is used to z force/area unit
• Avoiding overhang of the tibial plateau, particularly posterolaterally.
Resection
• Resect the proximal tibia, protecting the medial collateral ligament on the inside of the knee,
the patellar tendon on the outside of the knee, and the posterior vascular structures.
• Then lift off the plateau one piece after releasing it from soft-tissue
Saving the PCL When to sacrifice PCL
• Make a slot ant to PCL by a saw, then place a 1]. Bowstring tension of PCL
rectangular osteotome into that slot. 2]. Incomplete flexion or forced flexion
• Start to do tibial cut é that osteotome in place 3]. Excess rollback at >90º flexion
4]. Anterior lift off ð tight flexion gap
5]. Femoral sublux ð tight flexion gap
Check for pitfalls
1]. Varus alignment caused by:
o Patellar tendon bias
o Medial ankle offset
2]. Mal-rotation
3]. Over hang tray
4]. Elevation of joint line
5]. Reversed tilt Æ tight flexion
Balance of the Knee
• Perform rigorous medial and lateral ligament balancing, and flexion and extension gap
balancing using appropriately sized blocks.
• If femoral preparation is completed, trial components are inserted & lig balance checked
• In general, balance the knee with soft-tissue releases rather than by bony cuts.
Ligament Balancing
• Lig balancing can be straightforward or complex
• Plan to have more constrained implants available if the deformity is severe e.g. > 15° of varus
or valgus, but remember that constrained knee implants have poor longevity
• There are 7 points of lig balancing Seven points of ligamentous balance
that must be achieved 1]. Achieve full extension of the knee
• At this point, balancing may require 2]. Achieve full flexion é out excessive rollback of femur
conversion from PCL retaining Æ 3]. Achieve good medio-lateral balance at full extension
PCL–substituting, as PCL may 4]. Achieve good medio-lateral balance at full flexion
contribute to the deformity esp if 5]. Track the patella over a full arc of motion é no thumb
6]. Good rotational balance in full extension
severe
7]. Good varus-valgus must be correct
Varus Deformity
• Is the commonest & usually the simplest deformity to correct by cutting the tibial to the axis.
• However, commonly there is still medial tightness in extension, after appropriate cuts.
• Steps To Correct Varus Deformity:

1]. Remove medial OSTEOPHYTES on the femur and tibia
2]. Release the MEDIAL CAPSULE with care to MCL
3]. Release DEEP MCL subperiosteally
4]. Release SUPERFICIAL MCL subperiosteally (é break SHARPEY frs.)
5]. Release PES ANSERINA as a secondary constraint medially.
6]. Release the POSTERIOR CAPSULE and PCL
7]. Release MEDIAL GASTROC
The Valgus Knee
• Technically is more difficult to realign
• The tightest structure is usually the ITB with the knee in full extension. Release this from
inside out to ITB long axis at the joint line.
• Steps To Correct Valgus Deformity:

1]. Release ITB at the joint line .................... *
2]. Release popliteus tendon ...................... ♠
3]. Femoral attachment of the LCL .......... ♠
4]. Release fibular attachment of LCL....... ♠
5]. Release PLC .................................................. *
6]. PCL Is Resected Routinely
7]. Biceps tendon is transected from fibular insertion
8]. Consider other implant system
* If tight in extension only (14%) ♠ If tight in flexion only (1%) If both are tight do both (85%)
• Combined deformity; valgus flexion are the most challenging

• Valgus + flexion deformity = tight in extension
• Bony lateral release (lateral femoral sliding osteotomy) & fibular head decompression could
be done as an alternative to LCL release
1]. Sagittal balance (Fle
exion and Extension Gap)
2]. Coronal balance

ba
VARUS DEFORMITY (mediial release) VALGUS DEFORMITY (lateral rellease)
1]. Osteoophytes 1]. Osteophyte es
2]. MCL deep
d (coron
nary) then superficial
s 2]. Lateral Cappsule
3]. Postero-medial coorner + sem
mi-membran nosus 3]. ITB If Tight In Extension
4]. Pes Anserinus 4]. Popliteus Iff Tight In Fle
exion
5]. PCL in
n rare cases 5]. LCL
Patella (follows femoral

f & tibial co omponentts, & ligamment bala ancing)
• Indica ations:
i. Inflammato ory arthritiss
ii. Severe OA A
iii. Patellar deformity & in nsufficiencyy
iv. Some do itt routinely
• PF artticulation is the source e of the MAJORITY OF COMPLICATIONS IN TKA due to:
i. Boxier femmoral compo onents
ii. Inadaquate e patellar trracking
• PATELLAR CLUNK resultss from fibrosis f on
n
quadriceps tend don that cattches on the anterior
aspecct of the e femoral compone ent. The
offend ding fibroous tissue may be resected
arthro oscopically
Pa
atellar ma
altracking etiology and
a preven
ntion
ISSUE GUIDE LINE PROBLEM SOLUTIIO ON
1]]. Femoral rotation Never IR fe emur beyon nd Laateral patellaar Slight EER of femorral
neutral axis tiltt & lat sublu
ux compo onent
2]]. Femoral position Never med dialize femuur y Q angle Centraalize or evenn lateralize
3]]. Tibial rottation Never IR tibbia past me ed side y ER of TT Tibia iss centered bet
b centre &
of tibial tub
bercle (TT) yQ Q angle med border of TT
4]]. Leg alignnment Never leavve excess valgus y Q angle Revise bone cuts
5]]. Patella position Avoid laterralization y Q angle Centree or slight medialize
m
Avoid inferriorization Paatella baja Centree or slight su
up
6]]. JL positio
on Never raise e joint line le
evel Paatella baja Norma al or lower JL
J if pat bajaa
[Kn
nee Disord
ders] Page
P | 807
• Reflec
ct the fat pad
p & rem
move all ostteophytes til
t you see patellar m
margin all around
a é out
o
comp promizing quadriceps
q t
tendons.
• Cut th he patella fllat to give symmetricsy c & drill th
cut he peg hole es
• Most componen nts are pegg ged
• Checkk PF trackin ng by “NO THUMB” or to ouch-free te ech
• Tracking & latera al retinacula ar tension is controlled d by:
i. Subvastal ap pproach is better b for trracking
ii. Appropriate
A e ER of femo oral & tibiall componen nts
iii. Appropriate
A e alignmentt
iv. Lateralizatio on of femora al and tibial compone ents z retina
acular tensiion & impro
ove tracking
g
v. Never
N latera
alize the pattella usua ally lateralizze every thing except p patella
vi. Iff still there iss mal tracking ............................do la ateral retina
acular release (5%)
vii. Distal
D realig
gnment pro ocedures or o medial capsulorrap phy, μß nee eded in extreme case es
• Pitfallss:
i. Under
U resecction ...........................................overstuuffed PF joinnt
ii. Too
T much re esection ...................................patellarr fracture
iii. Lateralized
L p
patella .......................................maltraccking
iv. Asymmtrica
A l cut ...........................................patellarr tilt
Cementtation
• Remo ove the triall componen nts Æ lavagge the bone e surfaces é normal sa aline Æ Cleaar the debriis
• Drill sclerotic
s bo
one small sh hallow holes, to y ce ement interrdigitation (avoid man ny holes in
n1
line)
• Mix th he cement Æ pressuriize some ce ement into the plateau u 1st Æ add d another 1-mm
1 ceme ent
layer on plateau Æ gives ad dequate cement manttle in spite of o bone irre egularity
• Apply y the tray an nd impact it.
i Vigorouss impaction n improve pressurizatio
p on, but mayy #
• Remo ove excess cement,
c particularly poosterior to thet tibial tra
ay.
nd
• 2 ap pply a donu ut-shaped piece
p of cem
ment to fem mur &pressu urize it into a uniform thickness
t
• Place a small am mount of cem ment on th he posteriorr rails of thee femoral co omponent
• Impac cat the femmoral compo onent neithher in flexio on nor in exxtension.
• Alway ys remove excess
e cem
ment before and after every e comp ponent cem mentation
• Place a trial inserrt and exten nd the knee e fully till the cement sets.
s
• Patella ar cementa ation is donne é a cut in
nsulin syring ge used to pressurize
p tthe cementt into holes
• Apply y the patella ar component onto th he three ho oles &pressuurize é the ppatella clam
mp.
• After the cemen nt has harde ened, verifyy the seven points of lig gament balancing
Wound Closure
• Irrigatte all of the
e soft tissue, and prosthhetic and bony surface es of the kn
nee joint vig
gorously.
• Now close exten nsor mecha anism watertight, with h monofilamment resorb bable suture e.
• Distall seal is diffic
cult but impp (that’s wh
hy distal inccision incoo orprating th he patellar tendon is VIP)
V
• Close the deep fat f layer, pe eritenon, annd the skin withw stapless Æ dress th he wound.
Tibial Tu ubercle Osteotomy
O y
• Indica ations:
i. Difficult exposure
e iv. Prior su urgery
ii. Severe an ngular deforrmity v. Obese e patients
iii. Bone defficiency vi. Associa ated patellaar disorderss
• Place the oscillatting saw // to the tibia a and make a 1cm thicck, 8cm long g cut from medial
m to la
at
• Keep the lateral periosteal hingeh intact laterally.
• Make e a 2nd cut /// to JL and 2 cm distall to it, at a 45°
4 angle to o meet the iinitial osteo
otomy site.
POSTOPERATIVE CARE
• Beginn early motiion according to your preference es and the clinical
c situa
ation
• Early motion can n improve recovery
r annd shorten the
t hospita al stay.
• CPM isi useful forr obtaining early motioon (achieve
e extension early and a advance CP PM by 10°/d
d)
• WB allowed on the t first posstoperativee day
• Disch
harge from thet hospita al at 90° in an
a immobiliizer until su
ufficient quaadriceps control
PITFALLS AND COMPLICATIONS
Long-lasting complications of TKA are rare, and long-term success is generally the rule.
NONMECHANICAL COMPLICATIONS
The most common nonmechanical complications of TKA are thromboembolism and anemia.
1- THROMBOEMBOLISM
o 50% of pts mainly at or below knee; 10% are proximal to the knee; < 2% pulmonary
o Pulmonary emboli may be fatal esp if large
o Dx:
Contrast venography: gold standard, sensitive, specific, nepphrotoxic
B-mode duplex: not for iliac or deep vv, technician dependant
131
Other: clinical (Homann, Hoffman,..), I labeled fibrinogen scan,
plethysmography
No test yet proven to be effective as a postop screening test to pick risky pts
o Prophylxis:
For those reasons; most surgeons favor chemical, mechanical, or both
Mechanical: all may prevent leg DVT but not the serious higher embolism
1- elastic calf
2- thigh hose
3- sequential intermittent pneumatic compression stockings
4- Plantar foot compression pumps
5- Early mobilization
6- CPM
7- Inferior vena caval filters; but invasive, expensive, hazardous contrast
Chemical:
1- Continuous IV heparin
2- LMWt heparin sc
3- Oral warfarin
4- IV dextran
5- Aspirin
6- All predispose to bleeding, hematomas, hemarthrosis, GI & CNS
bleeding
o Treatment:
Immediate IV heparin infusion (keep PTT 1.5-2 times the control)
Discontinue heparin and replace by warfarin (the same level) till 6wk-6mo
Discontinue afterward
Continuously monitor the patient for bleeding (40%)
2- NEUROLOGIC INJURY after knee arthroplasty is

o most common in valgus deformity ± flexion deformity of severe rheumatoid arthritis
o Mainly peroneal nerve (1/3 complete, and 2/3 incomplete)
o Due to:
Traction upon the nerve during surgery after realignment of the deformity
Compression by a tourniquet
Compression by a tight bandage or orthosis
o Prognosis
½ recover and ½ would have partial recovery
o Treatment:
Prophylactic decompression is not recommended
Remove all the tight bandages
Flex the knee
Conservative ttt + rehabilitation
AFO
Surgery after several months of no improvement Æ decompression
3- VASCULAR INJURY:
o Most common vessels to be injured:
Superficial femoral
Popliteal
Genicular
o Type of injuries:
Direct lacerations
Late AV fistulae
Aneurysm
Thrombosis: esp in predisposed pt é peripheral vascular disease
o Dx: diminished pulses (esp é lacerations)
o Treatment:
Prophylaxis: consultation of vascular surgery – non use of tourniquet in risky pt
TTT:
4- FAT EMBOLISM SYNDROME (FES)

o Mainly occur with trauma; but also é joint replacements (3% of TKA)
o Pathogenesis:
Incompletely understood
Introduction of BM elements into the systemic circulation
Eventually deposited in the pulmonary vv Æ liberates inflammatory mediators
Mediators cause compromised gas exchange and respiratory failure
o PDF:
1- Intramedullary drills
2- Guide rod system
3- Stemmed prosthesis
4- Sudden release of the tourniquet
o Clinically: (usually mistaken as narcotic sequelae, or senile sundowning)
Respiratory insufficiency
Mental confusion and agitation
Petechae (trunk, axilla, conjunctiva)
Fever & tachycardia
Retinal changes
o Prophylaxis:
1- Use of fluted IM guides
2- Lavage the IM marrow fat
3- Over drilling of the guide holes
4- Slow advancement of the IM guides and stems
o Treatment: (mainly supportive)
Mechanical ventilation
IV fluids & glucose
Heparin, Aspirin, Dextran, Ethanol (proven to have no effect)
Steroids may be effective if given early
5- WOUND PROBLEMS:
o More in obese, DM, Poor nutritional status, RA, Multiple scars
o y é hematoma formation, clumsy technique, inadequate tight closure of all layers
o No relation to tourniquet deflation time or to CPM usage had been attributed
1- Prolonged Drainage:
o Expected for several days. After 7-10 days considered prolonged
o ð incomplete closure, poor superficial healing
o the problem is that it promotes bacterial contamination of sc tissues
o ttt: immobilization till closure Æ explore Æ irrigation Æ close in layers
2- Superficial necrosis:
o Uncommon
o ttt; do not overlook and do gastroc rotational flap
3- Wound dehiscence:
o Rare
o Usually 2ry to trauma, obesity, patellar instability, premature stitch removal
o ttt: as a surgical emergency, copious lavage, Broad AB, closure é 2ry sutures
MECHANICAL COMPLICATIONS
• The majority of the mechanical complications of TKR can z é careful attention to proper soft-
tissue balance in all planes. Patients é more challenging preop deformity or motion restriction
should be counseled about possible postoperative complications
1- ASEPTIC LOOSENING
• Typically is different from aseptic loosening of the total hip arthroplasty. Polyethylene debris–
induced, macrophage-initiated osteolysis is considerably more rare. This problem is thought to
be due to the different wear environment of the TKA. Threefold larger wear particles are
produced in a shearing, less-conforming environment. These larger particles are less likely to
induce a macrophage response and lead to a lower rate of aseptic loosening. Malalignment,
especially of the tibial component in varus, can lead to mechanical subsidence of tibial
component & loosening.
2- INFECTED TKA:
• Costly complication that occurs in approximately 1% of all knees
PDF:
• EXOGENOUS: in the surgical technique
• ENDOGENOUS: in the patient e.g. DM, poor nutritional status, steroid, immunocompromized
Bacteriology
• Low virulent organisms:
o Staph epidermidis (methicillin sensitive, non glycocalyx forming)
o Staph aureus (methicillin sensitive, non glycocalyx forming)
o ß hemolytic strept
o Anerobic strept
• High virulent organisms:
o Gram negative organisms E. coli, Pseudomonas, Proteus, & Entero-cocci
o Staph epidermidis (methicillin resistant, glycocalyx forming)
o Staph aureus (methicillin resistant, glycocalyx forming)
• Others: Corynebacterium, Group B strep, Strep faecalis
Sources
Intra-operative:
• Sampling of theatre air identified the same organisms & same proportions
• Contamination with the surgeons gloves, gowns, light handles, skin blades and needles
mainly affected. 76% of the organisms grown were coagulase-negative staphylococcus.
Post-operative:
• Drains left for 48 hours allow ingrowth of organisms (Willett et al. JBJS 1988)
• Haematogenous spread: Most common source is skin(46%), mouth(15%), UTI(13%)
Organism Virulence
1]. ORGANISM RESISTANCE TO AB:
[i]. Altered target: altered DNA gyrase (Quinolones)
[ii]. Detoxyfying enzymes: ß lactamase (penicillins)
[iii]. z uptake: membrane transport (erythromycin & tetracyclin)
2]. RACE FOR SURFACE THEORY

• When a total joint prosthesis is placed into the human body, the body's cells hurry to get hold
on the surface of the prosthesis.
• Once the body cells colonize the surface of the total joint prosthesis they can protect this non
living surface against the bacterial colonization.
• If any bacteria (usually skin bacteria) are present in the operation wound, they hurry to get
hold on the prosthesis surface too, racing the body cell to colonize the surface.
• If bacteria win, thet evolve the capability to adhere to surfaces for their survival, by secretion
of a glyco-protien cell wall called GLYCOCALYX:
i. Very strong adhesive
ii. Mask the bacterial antigens
iii. Colonize inside this biofilm away
from immune system
iv. Invite other types of bacteriae to
trick the immune system
v. When they adhere to the inert
implant surface, bacteria are
protected by the antiphagocytic
effect of biomaterial.
• All these factors will create a very
powerful resistance 100 to 1000 times
against AB & immune system.
Classification
1]. Stage 1= immedialte postoperative:
o Staph-aureus /ß hemolytic strept
o Usually needs irrigation, unless glycocalyx forming organism is identified
2]. Stage 2 = 6-24 mo
o Methicillin resistant staph epidermidis
o Usually needs staged operation
3]. Stage 3: after 2y
o Hematogenous spread from other septic focus
New Classification
1]. Type I Early < 6wk
2]. Type II Late > 6wk
3]. Type III Hematogenous
4]. Type IV Incidental +ve culture
PREVENTION
Pre-operative:
1. All septic lesions must be identified & treated (feet, dental, urinary, prostate)
2. Admit patient as late as possible & into a clean ward
3. Shave in the anaesthetic room
Intra-operative:
1. Careful tissue handling & Haemostasis
2. Length of procedure
[2]. Antibiotic prophylaxis
• Systemic antibiotics: methicillin-realated penicillin or cephalosporin
• Antibiotic Loaded Cement: reduces risk of infection by 11 fold
[3]. The team: keep the operating team as small as possible
[4]. Movement: shed up to 10 000 skin scales/min
[5]. Theatre gowns.
• Body Exhaust Suits (Charnley): maintain –ve pressure, cool surrounding (zshedding)
[6]. Footwear: no evidence that outdoor shoes are a source of infection; but overshoes wearing
can result in the contamination of the hands of the clinicians.
[7]. Headgear.
[8]. Face masks.
[10]. Sterile drapes
[11]. Drainage of wound has y risk of becoming infected than closed wound (only when sure)
[12]. Transporting the patient to operating theatre on a separate clean trolleys in the induction zone
[13]. Theatre equipment & instruments
[14]. Ventilation System: Vertical Laminalr Air Flow is recommended for arthroplasties
[15]. Ultra-violet Light: bacteriocidal; but not commonly used, ð potential dangers to staff
Post-operative:
• In the early post-op phase - antibiotic cover for urethral catheterisation (Gentamycin IM)
• AB cover for all GI & UTI & skin & Dental lesions é antistaphylococcal agent
DIAGNOSIS
• You must suspect infection all the time & use every tool to reach the final diagnosis
1- Clinically
• History of pain, swelling, erythema, fever problems post-op
2- Radiology:
• Need serial radiographs (get original post-op films)
• Osteolysis around the components
• Periosteal reaction
3- Blood: WBC, ESR, CRP usually not helpful (usually –ve or irrelevant) except if strongly suggestive
4- Bones scans (incl. white cell scan):
• usually unable to differentiate septic from aseptic loosening
• Indium111 may be helpful
5- Aspirates:
• CELL COUNT .................................. >25.000/MM3 (May be helpful 85%)
• DIFFERENTIAL COUNT..................... >75% PNL
•Gram stain ............................................+ve 25%
•Glucose ..................................................z
•Protein .................................................... y
•PCR .........................................................Newly introduced to diagnostic tools
•IL6 serum level ...................................Newly introduced to diagnostic tools
6- Open biopsy:
TREATMENT
1- Antibiotic suppression
• Antibiotics alone will not eradicate deep sepsis so it is rarely indicated alone
• Considered in:
o Elderly, unfit for surgery.
o Early infection
o Single organism
o Low virulent
o Gram +ve organism
2- Debridement alone:
• 20% success rate in TKR.
• Considered in the same conditions but can combat also virulent organisms
3- Resection arthroplasty:
• for the unfit or unwilling to have revision surgery & severe RA
• not good for knee
4- Arthrodesis:
• Remain a last resort especially for young active patients
5- Amputation:
• for knee - High functional cost - end of line.
6- Revision Arthroplasty:
• 75% success is achievable
• Pre-requisites:
o Healthy individuals who can stand long treatment
o Organism sensitive to AB
o Adequate bone stalk
One Stage Two Stage

Advantages: 1. single operation probably safer & more successful
2. quicker return to normal function
Disadvantages: 1. Prolonged procedure 1. two procedures
2. AB sensitivity must be known pre-op 2. prolonged bed rest betw. stages
3. Can't use cementless prosthesis (lose
benefit of antibiotic in cement)
Contraindicated: 1. If AB sensitivities not known pre-op
2. Mixed infection
3. Gram –ve organism
4. bone loss requiring allograft
6. Failure of previous one stage revision
Two stage Revision:
• First stage:
o Debridement (Capsule, prosthesis, inf tissues, Cement, & cement restrictor) & lavage
o Tissues must be sent for microbiology (even if organism is diagnosed pre-op)
o Insert AB loaded cement beads or a ab cement spacer
• Between stages:
o Continue iv antibiotics
o Traction if beads used (or ext fix)
• Second stage:
o Timing:
Early at 3wk
Late: after 6 wk, more effective (the wound would have healed & -ve CRP); but
more tissue scarring that’s why many surgeons use AB spacers (AB-PMMA)
o Continue antibiotics for 3 months.
3- PERIPROSTHETIC FRACTURE
o Is the fracture that occurs éin 15cm of the prosthesis; or adjacent to prosthesis stem
o 1%, more in femur > in tibia, more in Revision & osteoporosis
o Ætiology:
Traumatic
More in poor bone quality
Intraop during impaction, during trailing
Post op ð anterior femoral notching Æ fatigue fracture
o Treatment:
Conservative as long as the alignment is preserved
Operative ORIF with plate and screws or IMN
4- TIBIAL FRACTURE is associated with malalignment or component loosening. The fracture
may be bypassed with a stemmed prosthesis.
5- PATELLAR FRACTURE:
• Well known complication that may occur with or without resurfacing of the patella
• Ætiology:
o Direct trauma
o Under resection (marked stresses over the patella)
o Over resection (weak patella)
o Patellar pegs create stress risers (some use multiple small rather than one large peg)
6- PROSTHETIC FAILURE
• In contemporary arthroplasties is limited to delamination or fracture of tibial polyethylene
components or failure of metal-backed patellae. In the compromised environment with either
mechanical imbalance or secondary to polyethylene failure, a tibial metal backing may rarely
crack. This type of failure may often lead to particulate-induced synovitis & mechanical
symptoms.
7- PATELLAR INSTABILITY:
• Ætiology:
o Excessive internal rotation of the tibial or femoral components
o Over sized or overhang patellar component
o Lateral placement of the patellar component
o Avoid thick patellar component Æ tight patellar tracking
o More to occur é valgus deformities é tight lat retinaculum ± medial reefing of the VMO
• Treatment:
o Revision arthroplasty
o If sure about the rotation of the major components Æ proximal of distal realignment
o are the most common reason for revision knee arthroplasty. These complications
were addressed in the technique section.
8- AVN PATELLA
• May predispose to patellar fracture
• Ætiology:
o ð sacrifice of the supero-medial genicular and infero-medial genicular vv in medial
parapatellar approach
9- PATELLAR LOOSENING
• Uncommon event
• More é patellar maltracking
• Require revision of the patellar component
• If no bone stalk; retain unsurfaced patella or do the hated patellectomy
10- PREMATURE FAILURE É METAL BACKED PATELLA
• Previously used to improve the stress transfer from the implant of the bone and consequent
decrease in deformation and shear rate on PE. More with patellar maltracking
• Failure modes:
o PE wear
o PE metal dissociation
o Peg failure
• Dx:
o Anterior knee pain and swelling
o PXR: Ficat views metal to metal articulation / AP metal debris
o Aspiration: dark + metallic debris
• Treatment:
o Patellar revision ± total synovectomy
o Sometimes tri-compartmental TKA revision
11- DISRUPTION OF THE EXTENSOR MECHANISM: (rare but distastrous)

• Ætiology:
o After difficult exposures and over release of the tendon
o Tibial tuberosity osteotomy
o After revision TKA
o É limited ROM
o Poor bone stalk
• Prophylaxis:
1- Thorough lateral gutter debridement
2- Cut Patellofemoral ligament
3- Lateral retinacular release
4- Quad snip
5- Quad V-Y turn down
6- Distal tibial osteotomy
• Treatment:
o Immediately postop:
Immediate reattachment ± screw fixation
o Later postop
Autograft or allograft reconstruction of the patellar tendon
• Prognosis:
o persistent extension lag Æ abnormal gait and walking stairs
o Rerupture
12- CATASTROPHIC WEAR: is the premature failure of prosthetic implants
FACTOR PROBLEM SOLUTION

1]. PE thickness PE < 8 mm Æ past the yielding Thinnest PE portion must be >8mm
strength Thicker tibial cut
All PE tibia
2]. Articular design Flat PE Congruent articular surface design
Low contact surface area High contact surface design
High contact stress load Low contact stress load
3]. Kinematics Femoral role back PCL retained design
Posterior slope to improve flexion
4]. Kinematics Diskinetic sagittal motion PCL substituting design
Sliding wear
5]. PE sterilization PE chain session Vacuum PE γ irradiation
Subsurface delamination Vacuum packing
Metal-on-metal / ceramic-on-ceramic
6]. PE machining PE stretching at subsurface Direct compression molding instead of surface
zone Æ delamination machining
CONTROVERSIES IN TKA
Cementless Vs cemented:
• ð the brittle nature of the PMMA and its association é osteolysis sight was aroused towards
cementless TKA
• Porous coating provides biological interlock
• Disadvantages:
o Radiolucent lines
o Tibial subsidence
o Loose beads
o More pain and patellar failure and inadequate bone ingrowth
• Some suggested hybrid cementless femur + cemented tibia
• Till now the cemented TKA remain the gold standard procedure
Retaining vs substituting:
• Retaining Rational:
o Normal knee kinematic
o Preserve proprioception
o Minimal constraint
o Preserve femoral bone stalk
o Normal gait
• Substituting Rationale:
o PCL even if present never normal Æ alter the normal kinematics
o Difficult balance with PCL sparing
• Almost same clinical outcome and scores are noticed for both
Obesity
• Was considered to be a relative contraindication for TKA
• Associated é high rate of complications, PE wear & hospital stay
Age
• Young age has been a relative contraindication for TKA
• But if the conservative ttt fail to control the condition Æ make the pt is candidate for surgery
• Surgery start é arthroscopic debridement Æ realignment osteotomies Æ arthrodesis
• If all fail é pain persistence + functional limitations Æ TKA
• Long term results shown 94% results é PE wear being the major failing factor
Hemophilia
• Recurrent hemarthrosis Æ articular degradation and severe arthritis Æ Ankylosis
• Pathogenesis of arthritis: free radical formation 2ry to hemoglobin breakdown Æ synovitis &
cartilage damage
• Knee is the most common affect joint
• Arthrodesis is an option; but UCR and osteotomies are contraindicated
• Treatment:
o Prevent bleeding: Factor VIII (may secrete anti F VIII make things worse)
o Preserved joint space ................................................. Splintage for rest followed by
physiotherapy
o Narrowed joint space ............................................... TKA
o Synovitis .......................................................................... synovectomy
o Any surgery require F VIII monitoring:
> 100% ............................................................. till 3rd day postop
> 50% ................................................................ till 3rd week
30-50% ............................................................. till 6th week
• Prognosis there is a high level of adverse effects & HIV transmission is common
Paget’s
• Not uncommon disorder in UK and USA; and usually asymptomatic & discovered accidentally
• Most symptomatizing patients are ð DJD of the knee
• TKA results are satisfactory
Revision TKA
• Rationale:
o Done when it is expected to achieve a good function
o Can neutralize minor deficiencies (major bone deficiencies call for arthrodesis)
• Indications:
1- Aseptic loosening
3- Severe pain
1- Active infection
2- Marked bone deficiency
3- Severe ligamentous laxity and subluxation
4- Extensor mechanism insufficiency
5- Bad general condition
• Preoperative Planning:
o Address cause of failure (pt selection, implant failure, malalignment, instability)
Poor pt selection: young, active, heavy wt
Failures are common with the old constrained designs
Alignment, rotation, and soft tissue balance are crutial
• Exposure:
o Through the previous planes
o New incisions Æ hinders the superficial blood supply Æ sloughing
o If previous transverse incision Æ crossed at right angle
o Usually median parapatellar incision is used
o Care should be taking during eversion of the patellar tendon
o Thorough synovectomy, lateral release, and lateral gutter release for better exposure
o Quad snip or turndown may be needed
o Remove the components and the cement anchor
• Implantation:
o Coronal orientation is adjusted ...................... 7º valgus
o Femoral cut is done using IM guide & keep it at minimum (usually augments needed)
o Rotational orientation is difficult ð absent reliable bony land mark; but depend on
epicondyles; the medial being more anterior
o Tibial cut is a straight forward procedure .. ⊥ to the anterior tibial border
o JL should mimic the normal for better flexion extension balance and PF tracking
o Normal joint line is determined by ............... Preop AP view (1.5cm above fibular head)
• Implant size:
o Difficult ð bone loss; so preoperative planning and templating is mandatory
o Intraoperative posterior augments are the key for proper sizing é the best balance
o Tibial size is selected as in primary
o If upper tibial deformity Æ custom tibial component é asymm stem orientation is used
o Usually CEMENTED UNCONSTRAINED STEMMED PCL SUBSTITUTING device is used
Unconstrained ......................................... z stressed across the joints
Stemmed ................................................... stresses distribute away from bone interface
PCL ............................................................... usually scarred and un physiologic
Cemented ................................................. Immediate strong fixation
• Bone deficiency:
o Central........................................................................ cementation or BG (acc to age, size of loss)
o Peripheral.................................................................. bone or metal wedge, custom implant
• Patella:
o Revise only if maltracking + good bone stalk
o Rule of thumb; at least 10mm is needed as a stalk for revision
• Results: up to 75% with semiconstrained & 90% é unconstrained
• Complications:
o PF malalignment
o Slough
o Wound problem
o Sepsis
• The modern TKA has instrumentation that facilitates reproducible alignment and proper
ligament balance, and materials and design that permit functional and durable recovery of
motion. When implanted in closely monitored and maintained surgical and rehabilitation
environments, it has a remarkable and predictable record of success. Most of the mechanical
and some of the nonmechanical complications of knee replacement are preventable by
meticulous surgical technique with careful cross checking of anatomic landmarks and soft-
tissue tensions with appropriate jigs
Dr Mohamed Sobhy
Foot & Ankle

[Foot & Ankle] Page | 821
Gait
• STEP = The advancement of a single foot
• STRIDE = The advancement of both feet (one step by each side of your body.)
• STEP LENGTH = longitudinal distance between 2 feet
• STRIDE LENGTH = distance covered during 1 cycle = 2 step lengths
• VELOCITY = stride length/cycle time (m/s)
• CADENCE = steps /minute
• DOUBLE SUPPORT = both feet on ground
• FLOAT PHASE = neither foot is on the ground
P HASES OF N OR M AL GAIT
• 2 periods of double stance 10% each -at these times the body's centre of gravity is at its lowest.
Start End Knee Ankle Muscles

st
1 Contact Heal strike Start of double supp 0º 0º Knee starts flex to damp impact
Loading Start of double support Contralateral toe off 15º 15º PF Hams, TA exessive PF
STANCE
Quad, glutei stabilize hip/knee

60%
Mid stance Contralateral toe off COG over ref foot 0º 0º Calf propulsion & dorsi
Terminal st COG over ref foot Contralat foot contact 0° 10° DF Subtalar invert & foot locks
Preswing Contralat foot contact Ref toe off 30° 20° PF Toes dorsiflex at MTP
Initial swing Ref Toe off Max knee flex 60° 10° PF Quad forward leg swing &
heal high rise
SWING
40%
Mid swing Max knee flex Tibia is vertical 30° 0° TA Dorsi & subtalar 0°
Terminal sw Tibia is vertical Initial contact 0° 0° Ham forward leg swing Æ
control foot position at strike
Running:
• The two periods of double support are replaced by periods of double float (NWB)
• Heel strikes are more forciful
822 | Page [Foot & Ankle]
FOOT
• The foot contains: 26 bones & 57 joints
ANKLE JOINT
1]. Syndesmosis between the distal tibia and fibula
2]. A diarthrodial mortise between the distal tibia, fibula, and talus.
• Ankle has a larger WB surface area than the hip & knee joints.
• Ankle Mortise is a uniplanar hinge joint é its axis line just distal to the palpated malleolar tips
• In the axial plane, the ankle axis projects antero-medially 25°
• In the coronal plane, ankle axis projects cephalo-medially 10°
• Dorsiflexion Æ eversion of the foot
• Plantarflexion Æ inversion of the foot
Ankle stabilisers
Static
1]. Bony conformity: with the malleoli act as butress for talus
2]. Talar shape: narrows posteriorly i.e. ant width > post width;
in PF together é lig tautness provide most of the stability
3]. Interosseous membrane
4]. Ant. & post. Talofibular ligaments
5]. Calcaneofibular ligament
6]. Deltoid ligament
7]. Ankle joint capsule
Dynamic
8]. Fibular distal movement during FWB
9]. Proprioception
10]. Muscle tone
Subtalar & Chopart’s joint
• The subtalar joint can be modelled as a mitered hinge, &
the Chopard joint as a pivot.
• Chopart’s joint = Mid-tarsal = CCJ + TNJ
• DURING HEAL STRIKE: Leg IR Heel eversion (subtalar valgus) Chopart is // & unlocks foot
pronates to absorb energy
• DURING TERMINAL STANCE & PRESWING: Leg ER Ankle PF Heel inversion (subtalar varus)
Chopart locked in supination (forefoot supination)
Foot motion
• Supination = 1]. Heel inversion +
2]. Ankle plantar flexion +
3]. Forefoot varus
• Pronation = 1]. Heel eversion +

2]. Ankle dorsiflexion +
3]. Forefoot valgus
Compensatory Mechanisms in Initial Contact
• There are 4 shock-absorbing reactions to floor contact:
• free ankle plantar flexion,
before the pretibial muscle
action catches it.
• Leg IR evert the heel &
unlock the midtarsal joint
leading to pronation
1]. Knee flexion restrained by
the quadriceps is the
second.
2]. Contralat pelvic drop
decelerated by the hip abductors. This occurs as weight is rapidly dropped onto the loading limb
(large arrow) as the other limb is being lifted (small arrow).

Distal fibula:
• Fibula bears 1/6 WB transmitted downward from the knee during static weight bearing.
• The distal fibula moves distally ≈ 2.4 mm when changing from NWB to WB; pulled distally by the
contraction of foot flexors. This distal movement Æ y ankle stability by:
• Deepening the mortise
• Tightening the interosseous membrane
• Pulling the fibula medially
Gait Abnormalities
Approach to a limping child
• Assess LLD
• Check foot for injury , infection, arthritis
• Check knee for swelling, tenderness, instability
• Check hip for arthritis, dislocation, Transient synovitis, Perthes’, tumour
• General assessment for non accidental injury
Causes of Limp (abnormal gait) in Childhood:
1. Short Leg Limp
• Difficult to discern at maturity If discrepancy is less than 2cm
• There is pelvic tilt, short leg ankle equinus; and hip & knee of long leg in flexion
2. Antalgic Limp
• Stance phase shortened
• More gentle heel-strike in painful limb
3. Trendelenburg Gait (Unstable Hip Limp)
• Fulcrum - DDH
• Lever - short neck
• Motor - gluteus medius weakness e.g. polio, OP
4. Stiff Hip Gait
• Increased motion of pelvis on lumbar spine during swing
• N.B.- limp minimal if hip stiff (fused) in 25o flexion
5. Stiff Knee Gait
• Pelvis raised during swing phase so heel will clear floor
6. Gluteus Maximus Weakness
• Hip In hyperextension so centre of gravity behind joint
7. Quadriceps Weakness
• ‘Back Knee’ gait - knee locked in hypertension during stance phase
• Lurching more marked if also weakness of glut max.
• May place hand on thigh to assist
• Difficulty with stairs
8. Calf Weakness - Calcaneus Gait
• Poor push-off due to calf weakness
• ‘Hitch’ at each step
9. Tibialis Weakness – High steppage gait (drop foot gait)
• Weakness of pre - tibial muscles
• Increased flexion of hip and knee to allow ground clearance Æ y heel rise
10. Spastic Gait - Cerebral Palsy
• Many patterns - hemiplegia, diplegia
• Value of gait analysis; short step, unsteady, failure of foot clearnce at swing
11. Shuffling Gait
• In parkinsonism; gait is short, é out lifting one’s feet
12. Stamping Gait (Double Tap)
• Proprioception or dorsal column affection; DM & tabes dorsalis
• Patient does not feel the ground Æ y heel rise & strike + wide base + looks at the ground
• +ve Rombergism
13. Ataxic Gait (Cerebellar Ataxia)
• Wide base (Feet apart)
• Tremors and nystagmus
• –ve Rombergism
14. Hysterical Gait
• Diagnosis by exclusion & history of emotional upset
• Bizarre and inconsistent é CP
Tibialis Posterior Insufficiency

• Commonest cause of adult acquired flat foot
Anatomy of the foot arches
Medial Arch Lateral Arch Transverse Arch
Shape High Arch Low Arch ½ arch
Formation Apex: talus Apex: Talus middle & lat cuneiforms
Ant Pillar: nav, 3cuns, 3MT Ant Pillar: cub + 2 MT Metatarsal bases
Post Pillar: Calcaneus Same
Function Propulsion Wt support Protection
Ligaments 1- Plantar aponeurosis 1- Plantar aponeurosis • Deep trans metatarsal
2- Long plantar 2- Short plantar
3- Interosseous 3- Interosseous
4- Spring
5- Deltoid
Tendons 1- FHL 1- PL 1- Proneus Longus
2- TA 2- Short ms of little toe 2- TP
3- TP 3- Transverse head of Add Hal
4- Short ms of big toe
Bones Negligible Negligible Most important; the wedge shape of
the cuneiforms & the metatarsal bases
Causes of flatfoot deformities

CONGENITAL TYPE
1]. Flexible:
Localized: Asymptomatic, Symptomatic, flexible, or semiflexible flatfoot
Generalized laxity: e.g., Marfan, Ehlers-Danlos, Fragile-X
2]. Rigid: Tarsal coalition, residuals of TEV, congenital vertical talus
3]. Flatfoot with an accessory navicular
ACQUIRED TYPE
Flexible:
1]. Traumatic: ........................................... calcaneal #, TNJ #, Lisfranc #, TP & Spring lig rupture
2]. OA & RA: .............................................TNJ, TMTJ
3]. Tumor
Rigid:
4]. Neuromuscular: ................................CP, Polio, Charcot
5]. Posterior tibial tendon dysfunction
Aetiology of Tibialis Posterior Insufficiency

1- Congenital accessory navicular
2- Trauma
3- RA .........................................................middle age
4- Degenerative tendonopathy .......old age
Pathology:
• Normally TP is the most important for push-off & hind foot inversion (a movement that locks
the midtarsal joint this locking is crucial for push off)
• TP vascular supply depends on the synovial diffusion & segmental blood supply
• In PTTD: Tear occur at ! hypovascular zone 3-5 cm prox to insertion (distal to MM 1-2cm)
• TP loses its excursion Æ elongate Æ attenuation Æ rupture
o Weak push off
o Midtarsal collapse
o Unopposed peronei exaggerate the condition
826 | Page [Foot
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& Ankle
Diagnosis
C/O
1 Post-ma
1]. alleolar or arch Pain
2 Progresssive Flat Foot
2]. F
3 Complic
3]. cation: HALLUX VALGUS, metatarsalgia, lesserr toe deform mity, TARSAL TUNNEL $
O/E
• Flat fooot:
1]. To
oo many to oes
2]. Planovalgu us deformity & Achilles lateral deviation
d (
(Helbing’s s sign) from
m behind
3]. Midtarsal
M th
hrust
• Tibialis posterior
4]. Poost-malleollar Tenderness Tenosynovi
T itis
5]. Swwelling
• Insufficiency:
6]. Siingle heell rise (+ve) D
Degenerati on (can’t stand
s on sin
ngle tip toe)
7]. MT
M 1 Rise TEST (+ve) E
Elongation (tibial ER Ù rise of MMT1 even if told not)
8]. Double
D heeel rise A
Attenuation n
9]. Ja
ack wind D
Disruption (DF
( of 1st MP
M fail to correct the planus)
10]. In
ndividual joint
j flexiibility te est for fixed
d deformityy é arthrossis
Imaging
Blackburn n Deformitty Series (allso in pes ca
avus and de eformities)
1 Standin
1]. ng HINDFOOT ALIGNMENT view: sh hows whe ere the valg gus is
2 Standin
2]. ng LATERAL foot show w talonaviccular j & Me eary’s anglle
3 Standin
3]. ng AP foreffoot and ta alometatarrsal alignm ment
4 MRI best techniqu
4]. ue for asse
essing tenddons
Pathology:
Meyyerson claassificatio on
Stage I Stage II Sttage III Stage IV V Staage V
Pa
athology Peritendoonitis Degenerattion Eloongation attenuattion Disruption
Exxcursion Normal Normal Sh
hort Insufficie
ent Insu ufficient
Pa
ain After activity Mild media
al Mod/ severe lateral Ankle
Fo
orefoot Normal Normal Supinated
d (due to m mid tarsal atttenuation)
Hindfoot Normal Normal Fle
exible valgu
us Fixed va algus (subta alar arthrosis)
Ta
alus Normal Normal Noormal Normal Vallgus
1 heel
h rise - painful + + +
MT T1 rise - - + + +
To
oo many toess - - + + +
Co
onservative Cast 6-8 wk
w + Medial arch support Sa
ame + steroid d Rigid AFO
O Rigiid AFO
NSAID the en AFO + Hinged AF FO injj. in sinus
Op
perative Tenosyn novectomy TP debride e DL+calc.osteo
FD ot. TF Pan
ntalar fusio
on
+ FDL trannsfer Or + FDL transffer Or Orr + CCJ bone
calc. osteo
otomy calc. osteoto
omy block fusion
Pe
es Plano
ovalgus
Flexible F
Fixed
Me
edial Pain é MT
T1 La
ateral Pain Ankle pain
-ve MT1 rise + MT1 rise
+ve
rise No
ormal talus gus Talus
Valg
Tenosynovitiss Degeneration
D E
Elongation Attenuation Ru
upture
[F
Foot & Ankkle] Page | 827
T do Achilles
Tend Ac Ten
T ndinitiss
• Tendinosis = tendo on degene eration with hout associa ated inflammation
• Peritendinitis = ten nosynovitis
• Tendinitis = inflam mmation of the
t tendon n
Patthogenessis:
• Tendinitis occurs in n the hypo
ovascular arrea 2-6 cm above a the tendon
t inse
ertion.
• Normally tibia ER in extensio on; if the fo oot is over pronated Æ coupled IR of the tibia;
t so in over
o
pronate ed foot there is stress conflict
c imp
posed on TA A Æ Hypovvascular miccrotears
Aettiology
I
Inseriona al
1]. Ove er loading ofo musculottendeniouss junction:
Ove er-training, hill running
g
Pooor running shoes
s
Runnning on un neven terraain
Insuufficient gasstrosoleus strength
s or flexibility
2]. Infla
ammatory conditions:
c RA, Reiter’ss, AS, Gout
N
Non inserrtional
3]. Funnctional ove er-pronationn (tibia varaa or foot va arus)
4]. Paraa-tendinitis may occurr in associattion é tendiinitis or as a separate e entity
Clin
nical
• History y of change in training habits.
• Tight TA A
• Heel aliignment may m be in varus
• Localise ed tenderness + swelliing in tendo on
Raddiological
• PAVLOV PARALLEL PITCH LINES: a line be etween the e anterior
and me edial calc tuubercles & the
t other lin ne is // to itt from the
posterioor margin of o the posteerior calcan neal facet
• MRI; diistinguish paratenoni
p itis (fluid in
n the shea ath) form
tendon nitis (class c signal oedeema inside the endon)
Insertio
onal Non-inssertiona
al
Pa
athology • Involve posterosup p. Calc. tuberrcle gn 3-5cm ab
1- Hypovascular deg bove insertio
on
(Haglunnd’s) & retro
ocalcaneal bursa
b
• often asssociated é calc.bony
c prrominence 2- Parate
enonitis ± n
nodular TA thickening
t
Cliinically • Heal pa
ain & swellinng • Heal coord pain & sw welling
• ± varus heal or tibia a vara
Co
onserve 1]. Eccenttric calf stre
etch & physsiotherapy 1]. Eccen ntric calf strretch & phy ysiotherapyy
2]. er + z calc 2]. Heal rise
Heal risse (Modify ! heal counte
inclinattion Æ move e bursa awaay from TA) 3]. Rest, Icce
3]. AFO too z overpron nation 4]. Med arch supportt
4]. Avoid steroid
s ment steroid
5]. Brisem d inj into TA sheath???
6]. US
7]. Phono ophoresis
Op
perative • Excise the
t Haglund d’s + bursa + debride • Paraten non debridement
any deggenerated te endon • Excisionn of TA nodules if > 2/3 TA thickness +
• TA reinfforcement transfer
t • FDL transfer +
• Turndown TA flap technique
Tendo Achilles Rupture

AETIOLOGY
1]. middle-aged athletes.
2]. 3rd most frequent tendon rupture
3]. Most commonly:
1- Pushing off with WB forefoot while extending the knee
2- Sudden unexpected dorsiflexion of the ankle
3- Violent dorsiflexion of the plantar flexed foot as in a fall from a height.
PATHOPHYSIOLOGY
1]. Hypovascular area of the tendon 2 to 6 cm above the tendon insertion into the calcaneus.
2]. The major blood supply is via its mesotendon mainly through the anterior mesentery.
3]. With increasing age:
a. z anterior mesenteric supply
b. Changes in collagen cross-linking Æ ystiffness and z viscoelasticity
4]. Repetitive microtrauma Æ reparative process unable to keep pace Æ attrition
5]. Long term use of Ciprofloxacin Æ collagen alterations increasing risk of tendon rupture.
DIAGNOSIS
1]. Dramatic Acute Pain, Swelling
2]. Palpable tendon defect
3]. Inability to do toe-raise on affected side (weak planter flexion is possible by toe flexors)
4]. SIMMONDS squeeze test (= Thompson test in USA)
5]. O'BRIEN'S needle test - A 25-gauge needle is placed percutaneously in the midline of the
proximal tendon. Motion of the proximal tendon indicating continuity is detected by
observing the needle when the foot is put through passive range of motion.
6]. MRI & US in flexion 20 ° to detect tendon gap & interposition
Non-operative Operative
Regain of function 75% 90%
Re-rupture at 1yr 15% 5%
Advantages less minor complications return to sports earlier; less calf atrophy;
better ankle movement
Disadvantages Less function More complications; infection, wound
Non-operative Technique:
1]. Indications:
a. Acute <48hr
b. No tendon diastasis in 20° flexion by US & MRI
c. Non athlete
d. Steroid induced
2]. Technique
a. POP in equinus 4-6wk
b. POP in 3cm raised position 4-6 wk
c. POP in neutral position 4-6wk
d. Shoe raise for 4-6 wk
3]. Success depends on:
1- Time of presentation
2- Tendon diastasis in 20º flexion (plotted by MRI or US)
3- Presence of huge hematoma or soft tissue interposition Æ repair is non tendinous
4]. Alternative Functional Bracing - starting in 45 º of flexion; the functional brace prevents
ankle dorsiflexion but allows ankle plantar flexion.
Primary repair
1- Acute & subacute ruptures <4wk
2- Athletes
3- If not acute enough
4- Tendon diastasis
Techniques:
1]. Direct Repair é nonabsorbable tension suture, using a Modified Kessler stitch through the
stump 2.5 cm from the rupture.
2]. Plantaris reinforcement
3]. Percutaneous Repair Webb & Banister via 3 posterior transverse incisions - the middle one
at the level of the rupture & the other two 5cm prox. & distal. Make the proximal incision
slightly medial (to avoid the sural nerve).
4]. Ma & Griffith: Uses medial & lateral percut. wounds Æ y risk of sural n entrapment.
5]. Post-op: same as in conservative management but é 2wk intervals & return to sport after 8m
Reconstructive operations: for neglected ruptures: (> 4wk)

Options:
1- Tendon diastasis <3cm .......... Lindholm Turndown flap ± Teuffer augment
2- Tendon diastasis 3-8 ............... Abraham V-Y advancement é the v arms being 1½ the
length of tendon gap ± Teuffer
3- Tendon diastasis >8 ............... Bisworth Achilloplasty
Peroneal Tendon Ruptures
Pathogenesis:
• Injury of the etendon Æ swelling proximal to bony fulcrum (LM for PV & cuboid tunnel for PL) Æ
z tendon excursion Æ tendon more susceptible to injury
Sobel Classification
Level Tendon Restraint Pathology Clinically
Zone I LM PB Superior Peroneal 1].Tendinites Mimic ankle sprain
Retinacula 2]. Attritional splits
3]. Dislocation
Zone II Cuboid tunnel PL Bony truph Os Peroneum Lateral foot pain
Lat Calc Wall
Pathology:
ZONE I
1- Dislocation:
Aetiology:
1- Lax SPR Æ may lead to PB sublux
2- Lat. Malleolar geometry:
• 80% stable concave
• 20% narrow sulcus Æ sublux
3- Severe inversion inj Æ SPR avulsion ± fibular rim #
• Clinically may mimic lat. ankle sprain é point tenderness over ATFL or
retromalleolar “usually reports treatment as chronic sprain”
4- Peroneus quartus anomaly Æ y PB entrapment in Zone 1
Clinically:
• Ask the pt to dorsiflex while resist in plantarflexion Æ dislocation
2- Tendinopathy:
• Confuse é lateral ankle instability
• Retromalleolar crepitus
• Rupture
DD
1]. Post ankle impingement
2]. Sinus tarsi $
3]. Subtalar arthrosis
4]. Lat. Ankle instability
Treatment:
1]. Conserve
• RICE: rest, ice, compression, elevation
2]. Operative:
a. SPR:
i. Direct repair
ii. Soft tissue augment (fibular periosteum)
iii. Deepening of fibular groove or Bone block
iv. Rerooting under calcaneo-fibular lig.
b. Tendon nodule excision + debridement + tenodesis to PL
ZONE II
Aetiology:
1]. Acute: inversion injury Æ os peroneum fracture
2]. Chronic: tenosynovitis
CP:
1]. Lat foot pain
2]. Weak MT1 plantar flexion
3]. Chronic: Lateral instability
PXR: Proximal migration of os peroneum #
DD: multipartite os peroneum (Tc)
TTT:
1- Acute repair + os peroneum excision
2- Chronic:
POP 6-8 wk
Debridement
Os peroneum excision + proximal PL tenodesis to PB
• NB: loss of PL function Æ pes cavovarus
Tibialis posterior tendon injury
Tears bet inferior retinaculum & insertion of the tendon into the medial cuneiform & MT1
Aetiology: attritional injury 2ry to exostosis
CP:
1]. Steppage gait
2]. Unable to heel walk
TTT:
1]. Acute: 1ry repair
2]. Chronic: extensor ms transfer

832 | Page [Foot
F e]
& Ankle
Osteocchond
dritiss Disssicanss of th
he Taalus
Aetiology:
• Post-traaumatic or idiopathic
i o
osteonecros sis
Posteromedial lesions: ......................................................(55%)
• Impactiion of talus on tibia, ass plantar-fle exed ankle is
i forced intto inversion
n & ER
• these le esions are deeper
d and cup shape ed
Antterolateral le
esions: .........................................................(45%)
• Impactiion of talus on fibula as a dorsi-flexed ankle is forced into o inversion
• these leesions tend d to be shalllow
Examination
n::
• palpate
e just posterrior to the medial
m mallleolus with the ankle dorsiflexed
d
Radiographs:
• Osteoc chondral # may be e anterior oro posteriorr to dome,, requiring
plantarr or dorsiflexxion of ankkle to be visiible on morrtise view
• if radioggraphs are negative consider rep peat radiographs in 2-4 4 weeks
• Hawkiin’s sign: is the su ubchondrall radioluce ency that appear é
revascuularization
Radiographic Classification:
PXR
R findings may or mayy not correelate ώ arthrroscopic fin
ndings nor prognosis
p
Bernddt & Harty y PXR Staging
I: Subchnod dral Comprression #
II: Partially detached
d fra
agment
III: Complete ely detacheed, non-disp
placed fragm
ment
IV: Detached d and Displaaced fragmment
V Radioluce ent fibrous defect
d LOOMER’S mod
(L dification of
o the same classificatio
on)
Bon
ne Scan: (1
100% sensittive) a Neg
gative TC = No OCD
D
CT for accurate delineattion of bon
ny lesion
R Scan: for Dx & staging (very sensitive & detect bon
MR ne œdema
a)
Hepplle MRI Sta aging

1 Articular damage
d on
nly
2 cartilage injury
i + und derlying fra
acture
a bone œd dema
b No bone œdema
3 detached d & undispla aced
4 detached d & displace ed
5 subchond dral cysts
Treatment:
1 NON OPERATIVE TREATMENT: - no eviden
1]. nce that no
on wt beariing cast offfers improvved results over
o
wt bearing casts; - no evide
ence that patients
p nee
ed to be im
mmobilized
d if they are kept non
n wt
bearing
g
2]. OPERATIVE TREATMENT:
OCD
<12 y >12
Usually heal Usually
spontaneously progress
Usually heal
Anterolat Posteromedial
spontaneous
• PWB
• ROM
ARTHROSCOPIC MALLEOLAR OSTOETOMY
Stage I Stage II, III Stage D
Drilling via Fragment removal and

single puncture Fixation reconstruction
(usually swollen and larger)
Or
Retrograde
transtalar
Biodegradable Osteochondral Cartilage alone
drilling via sinus Metal Soft tissue Matrix scaffolds
tarsi • Herbert Screw •OATS • ACI coverage • Collagen
• K-wire •Allograft • MACI • Periosteal • Carbon fiber
• Fascia • PLA
Different types of chondroses

Osteochondrosis Disease Site
AVN 1]. Legg –Clave-Perthes’ disease. Upper Femoral Epiphysis
Crushing 2]. Kienbock’s disease Lunate
3]. Preiser’s disease Scaphoid
4]. Panner’s disease Capitulum
5]. Scheuermann’s disease Vertebral Bodies
6]. Kohler’s disease Tarsal Navicular
7]. Freiberg’s disease 2nd Or 3rd Metatarsal Head
8]. Blount’s Knee ?
9]. Theimann’s disease Multiple Phalanges
10]. Friedrich’s disease Sternal End Of The Clavicle
OCD 11]. OCD Knee
12]. OCD Talus
13]. OCD Patella
14]. OCD 1st MT Head
15]. OCD Capitulum
16]. Buschke’s disease Medial Cuniform
Traction apophysitis 17]. Osgood –Schlatter’s disease Tibial Tuberosity
18]. Johansson-Larsen syndrome Patella
19]. severs disease Calcanius
20]. Iselin’s disease Tuberosity Of 5th MT
21]. Mandl’s disease Greater Trochanter
Osteochondroses Of The Foot & Ankle
SEVER'S DISEASE
• Pain at Achilles tendon insertion
• usually 8-12 years old
• density + fragmentation of calcaneal apophysis - normal variant
• symptomatic treatment
KOHLERS'S DISEASE
• AVN of navicular
• very rare usually 4-8 years old (Brailsfords disease it is the counterpart that occurs in old ♀)
• DDx: infection
• ttt:
o symptomatic treatment Æ revascularize
o may need cast during initial illness
o long term prognosis good
ISELIN'S DISEASE
• Apophysitis of 5th MT base
FREIBERG'S DISEASE
• Avascular necrosis of a lesser metatarsal head with infraction
• usually in teenagers or young adults
• usually 2nd MT
• possibly caused by trauma
Smillie Classification (1967)
1 # alone
2 surface contour altered
3 central portion depressed
4 loose body separation
5 Flattening
Clinical features
• pain in MTPJ
• stiffness
• swelling
• sometimes large palpable
osteophytes
Treatment
Non-surgical management
• analgesia
• orthosis
• shoe adaptation
• steroid injections into joint
Surgery
• simple debridement and cheilectomy
• metatarsal head osteotomy
• excision arthroplasty
Rheumatoid Foot
Introduction
1]. 70-90% of rheumatoids have foot involvement.
2]. 15% present initially with foot complaints.
STAGES
Stage 1 synovitis
Stage 2 Joint erosion & tendon dysfunction
Stage 3 Progressive deformities
CLINICAL
Present with Pain or Deformity.
1]. Forefoot:
i. Swelling of the MTPJs
ii. Hallux Valgus
iii. Claw toes
iv. Bursae, nodules, dorsal corns, plantar callosities
v. Morton's neuroma
2]. Hind foot & ankle
vi. PTTD
vii. Pes plano valgus (most common) ð PTTD or TNJ or Subtalar arthritis
viii. Tarsal Tunnel Syndrome - 2ry to synovitis of contents.
Look for:
3]. Vascular status - PVD or rheumatoid vasculitis
4]. Neurology - neuropathic process more common in rheumatoids.
5]. Tendonitis or ruptures (tibialis posterior, proneal)
6]. Primary deformity - Forefoot or Hindfoot
7]. Which joint is the cause of pain and/or deformity (may need diagnostic injections)
TREATMENT
Conservative
1]. Medications
2]. Footwear - shoes should not be made to correct the deformity, but rather be adjusted to it.
Surgery
Pre-op precautions:
• Check the positions of the knees & hips (should correct these first for ankle & hindfoot problems).
• Skin condition.
• Medications - methotrexate & corticosteroids may need to be stopped.
SURGERY
Ankle Joint
1- ARTHROSCOPIC SYNOVECTOMY
• useful for cases of marked synovitis & minimal articular damage
2- SUPRAMALLEOLAR OSTEOTOMY
• For stiff hindfoot in equino-varus.
3- ANKLE ARTHRODESIS
• Operation of choice:
1- Arthroscopic arthrodesis if minimal osteoporosis & destruction.
2- Intramedullary nail through heel
3- Dowel arthrodesis Fusion Position
o 0º FLEXION EXTENSION
4- Square cut arthrodesis
o 0 MEDIO-LATERAL
5- Arthroscopic arthrodesis
o HIND FOOT VALGUS 5-10º
6- Mini-open Meyerson arthrodesis o ER 5-10º
7- Charley external fixator if gross deformity o <1CM POST DISPLACEMENT (z
MIDFOOT LOADING)
4- ANKLE ARTHROPLASTY
• Indication = severe destruction with a stiff, non-deformed hindfoot (or triple arthrodesis)
• 2 main types = 1. semi-constrained (Mayo) and 2. LCS prosthesis.
• Failures were awful & complication rates high.
• This may be improving with newer designs (eg. STAR prosthesis).
• Note requirements for a joint replacement prosthesis are:
1- Permit normal motion
2- Eliminate pain
3- Accept a salvage procedure
4- Give stability
5- Have no adverse effects on surrounding joints
6- Good fixation
7- Tolerate repeated loading.
Anklereplacementstar1 Star2 Star3 Star4 star
Hindfoot
• 2 main forms of RA affect the hindfoot:
Type Synovitis Deformity Arthrodesis
Loose mobile ysynovitis Mobile planovalgus Arthrodesis is difficult
Stiff dry less synovitis fixed deformity Responds well to arthrodesis
Treatment
• Talonavicular fusion - operation of choice for early cases since it will stabilize the hindfoot
by reducing subtalar motion by 90%.
• Triple arthrodesis if the deformity is severe - screws are better than staples.
Forefoot
1]. Synovectomy of MTPJs - best synovectomy is excision arthroplasty.
2]. Metatarsal oblique Osteotomies (HELAL)
3]. Claw toes: DuVries excision arthroplasty or PIP fusion + MTP dorsal capsulotomy
4]. Excision of MT heads + proximal 1/3 Proximal phx
5]. Pobble amputation - amputation of all the lesser toes at the MTPJs - only for severe deformity
& pain.
Tendons
1]. Tibialis Posterior tendon rupture Pesplanus
2]. Tendoachilles insertion rupture Hitching gait (calcaneus gait)
3]. Peroneal tendons rupture Peroneal muscle spasm (pes planus)
4]. Tarsal tunnel syndrome
Other Structures
1]. Neuropathic joints
2]. Rheumatoid nodules (indicative of aggressive disease)
3]. Rheumatoid ulcers
4]. Stress fractures
838 | Page [Foot
F e]
& Ankle
Halllux Valgu
V us
Definition: itt is a big to
oe deformitty in ώ there is:
1]. Bunion n: promine ent eminen nce of the MT1 head
2]. Hallux valgus
3 Hallux valgus inte
3]. erphalange eal
4 Metata
4]. arsus primu us varus
5]. Hallux lateral dev viation
6 Hallux pronation
6].
7]. Lateral subluxatio on of sesam moids
8]. Overcrrowded toe es
Aettiology
1. HEREDITARY FACTORS: 60% +V Ve Family History:
H
1]. METATARSUS PRIMUS VARUS
2]. MEDIAL SLANTED MC1 (First Meta atarso Cun neiform Joint)
3]. HYPERMOBILE MC1
4]. HYPER PRONATED 1ST RAY
5]. ATYPICAL MT1 LENGTH
2. ACQUIRED
• Splaye ed Foot seccondary to weak intrin nsics in elde
ers
• Fashio onable Sho oes for wo omen (Narro ow toe boxx & high he eal)
• Hallux valgus
v wass 70 times more
m comm mon among g shoe wearrers
Anatomical Considerrations
A
Angles
1]. InterMe etatarsal Angle
A IMTA
2]. Hallux Valgus An ngle HVVA
3 Distal Metatarsal
3]. M Articular Angle
A DMMAA
4 Interph
4]. halangeal joint
j Anglee
5]. 1st MTP joint Con ngruence
Normal Angle Values

V
IMT <9º.
HVA <15º.
DMAAA <15º.
Stabilizerrs:
S
• Static:
1]. Bonny congrue ence of MTP P & MC
2]. Cappsule
3]. Liga
aments:
i. Collateral
ii. Hoood ligamen nt
4]. Sesa
amoid (intrra FHB) sta abilized by:
i. Thheir bony configurat
c ion
ii. Seesamoid lig gaments
iii. In
ntersesamo oid ligamennts
• Dynam mic:
1]. Abdductor Halluucis
2]. FHBB (Flexor Haallucis Brevvis)
3]. Addductor Halluucis (transvverse & oblique heads))
Classification
HVA IMTA Incongruent MTPJ
Normal <15º <9º No
Mild 15-30º 9-15º No
Moderate 30-40º 15-20º. Yes (unless abnormal DMAA)
Severe >40º > 20º Yes
Management
History
• Age
• What is the chief complaint?
• Medial Pain z é taking off shoe (≠ OA y é WB shod or not)
• Intractable plantar keratosis
Examination
• Observe gait to see if the hallux is used in its normal push-off
function
• See if there is a predisposing factor (liable for recurrence)
Valgus knee & pes planovalgus & pronated hallux are liable for recurrence
Pronated forefoot
lesser toe deformities
OA, RA
HYPERMOBILE MT1 by comparing MC1 motion é contralat side & é MC2 (if IMTA >15º)
• Plantar keratosis:
IP MTP1 MTP2
Excessive Hallux pronation Equinus Short MT1
Cavus Long MT2
Prominent sesamoid Dorsiflexed or hypermobile MT1
Plantar flexed MT1 Hammer 2nd toe
• Is the deformity Correctable without pain
Check ROM of MTP Joint (after realignment to normal); predict postop mobility
Check ROM of IP Joint (Hallux valgus interphalangeus)
Check ROM of Ankle and Subtalar movement - ? TA tightness
• Grinding Pain on passive movement of MTPJ = MTPJ OA.
• Neurovascular assessment
Juvenile Hallux Adult onset
IMTA y yyy
HVA yyy y
DMAA yyy y
Congruence Congruent Incongruent
X-Rays
WEIGHT BEARING AP + LAT + AXIAL SESAMOID VIEWS
1]. Hallux valgus angle
2]. Inter-metatarsal angle
3]. DMAA < 10-15º: between prox articular edge & MT1 axis
4]. Angulation of MCJ1
5]. OA 1st MTPJ and IPJ
6]. JOINT CONGRUENCE
7]. LENGTHS OF THE 1ST & 2ND metatarsals
8]. SESAMOID POSITION & OA & CRESTA EROSION (using the metatarsal bisect
method; positions 4-7 = lateral subluxation + cresta erosion Æ soft tissue
release)
Treatment
Non-operative treatment
• Treatment should always begin conservatively
1]. Wider shoe with a broader toe box
2]. Low soft heel
3]. Orthoses are not helpful
Operative Treatment
• 3 groups:
1]. Congruent joint
2]. Incongruent or subluxed joint
3]. Joint with arthrosis
Ideal Hallux Valgus Surgery

• Correction of the IMT and HV angles
• Creation of a congruent MTP1 é sesamoid realignment
• Bunionectomy is done // and flush é MT1 shaft
• Retention of function and ROM of the 1st MTPJ
• Maintenance of normal weight bearing mechanics
Osteotomies Pro’s and Cons
Precautions and advantages Disadvantages
Akin • Mild • Done é others
• Can correct DMMA
Chevron • Mild/mod deformity • Pt >60 y have less satisfactory outcome ð pain & stiff
• Stable when fixed • Max displacement 30% (5mm=5ºcorrection)
• can correct DMAA (if + med wedge) • AVN 4-20% (does not always mean bad result)
Mitchell • Moderate/severe deformity • Shortens 1st ray
• Can plantar flex/displace distal part • Transfer metatarsalgia
Basal • Moderate/severe deformity • DMAA must be <20º.
Keller’s • Low demand pt • Lots
• No shortening • OA
Fusion • If OA, recurrent, salvage • Non union
• 15º valgus, 10º dorsiflexion
Complications
1- Recurrence:
Juvenile HV (up to 30%)
inadequate soft release and failure to correct alignment
severe ffot pronation
metatarsus adductus
long or short MT1
2- Hallux varus: esp. in soft tissue proc eg McBride with lat soft tissue release +/- excision of
lat sesamoid, overexcision of medial eminence and med reefing
3- Transfer metatarsalgia
4- AVN of MT head - avoid significant distal stripping of both dorso-lateral aspect of MT1
5- Non-union of osteotomy
6- Infection, dehiscence, adherent scar, paresthesia, and slough
Contraindications:
1- Spasticity
2- Equinus contracture
3- Marfan
4- Ehler Danlos
5- Short MT1
Prognosis
• 80/90% of patients will have good or excellent clinical and radiological results
• The operation is only if pre-operative planning, post-operative positioning and immobilisation
CHEVRON:
• Osteotomy distal to articular surface by 1cm
• Angle of osteotomy 50-60º
• Plantar limb is longer (to avoid injury of the metatarso-sesamoid joint)
• Every 1mm lateral displacement = 1º correction of the IMTA
• width of MT at osteotomy = 15mm Q we can displace only 1/3 of the width ∴ max
correction = 5º in IMTA
• It can correct the DMAA if + medial closing wedge
1- >50 y
2- >15º IMTA
3- >30º HVA
• Complications:
1- AVN head (bl.supply is intraosseous & extraosseous from dorsolat surface ∴ avoid
lateral tissue stripping & DSTP distal soft tissue procedure)
2- Under correction if the indication is stretched
Proximal Osteotomies:
1- Crescent osteotomy:
• Approach via dorsal incision over the proximal 1/3
• Concavity must be face proximal and toward heel to avoid overcorrection
• Technically difficult
• May produce dorsally united MT1
2- Proximal chevron:
• Easy
• Avoid the dorsal malunion
• More cancellous bone union & more stable
Distal Soft Tissue Procedures (DSTP)
1- McBride
• Elements:
1- Adductor hallucis release (care must be taken not to injure the lat head of FHB Æ
Hallux varus)
2- Bunionectomy
3- Medial capsular reefing
4- Lateral sesamoid excision
2- Mann modification of mcbride:
• Elements:
1- Adductor hallucis release and reattached to soft tissue between MT1 & MT2
2- Bunionectomy
3- Medial capsular reefing
4- Lateral capsular release
5- Intermetatarsal ligament release
Indications:
• Must be incongruent
• Mild Incongruent cases alone (as chevron correct 5º alone)
• Moderate to severe Incongruent cases + crescent osteotomy
• Passively correctable (not rigid) otherwise DSTP will give no result
• No facet at the lateral aspect of the MT1 base (not rigid)
Akin Proximal Phalangeal Osteotomy
• 8 mm proximal to the articular cartilage
• Medially based osteotomy
• Usually combined é other procedures e.g. Chevron
osteotomy
Mitchell Osteotomy
• Lateral displacement osteotomy of the distal MT
• It is a double step plantar flexion osteotomy (biplaner
osteotomy)
• Can correct congruent HV either mild or severe
Scarf Osteotomy
• Z-shaped distal rotational osteotomy along the MT
shaft
• Angulate and displace
• Big contact area & better healing and stability
• Can correct DMMA in moderate to severe cases
Lapidus
• Fusion of the MT-Cuneiform j
• ± TA tendon to navicular ± FHL to dorsal surface
• The joint is irregular calling for an expert surgeon
• May produce shortening and angulation of the
MT1
Hallux Rigidus
• Hallux rigidus is a degenerative arthritis that affects
MTP joint as a result of wear and tear on the joint
surface over time.
• The condition may follow an injury to the joint or, in
some cases, may arise é no well-defined injury
• CP: limited ROM + tenderness
• Treatment by:
• Shoe modification
• Cheilectomy
• Fusion
•
•
Hallux Extensus: FHL injury or its

•
sesamoids. ttt: Jone’s transfer
• Hallux Saltans: FHL triggers at the

posteior process of the talus
• Pseudo Hallux Rigidus: FHL locked

trigger at the same site
Ankle Instability
Definition
• It is the loss of the normal relationship among all parts of the ankle joint along the normal arc of
motion and usually results when the ankle is twisted, or inverted
• Ankle joint stabilizers: see before
• Ankle motions & subtalar see before
• Normally:
• Deltoid is the 1ry restraint to abduction
• Anterior & posterior capsule are the restrait for AP
• ATFL is the 1ry restraint to anterior drawer & inversion
• CFL is the 1ry restraint to inversion
• PTFL is the 1ry restraint to posterior drawer
Pathophysiology:
• Type I collagen density and orientation depends dynamically on
mechanical stress
• y joint capsule excursion Æy muscle sharing in stress
absorption Æ z sprain rate
• Ankle joint is a ginglymus synovial joint é combined movement in dorsiflexion & plantarflexion
directions > 100° & bone-on-bone abutment occurs beyond this range
• Ankle spurs may occur at any of the bony ligament attachments. An anterior spur observed on
lateral radiograph at the neck of the talus. This occurs ð ossification of organized hematoma
associated with anterior ligament sprains.
• CFL ligament is thicker, cordlike, and stronger than ATFL & the PTFL is the strongest and runs
horizontally from the inner fossa of the lateral malleolus to the posterior talar tubercle
th
• A 4 strong lig. -syndesmotic lig- is rarely sprained ð its great strength, but usually occur as a part
of an ankle #. It has deep and superficial, (ant & post) portions. This tibiofibular ligament holds the
distal tibia and fibula together at the ankle joint and maintains the integrity of the ankle mortice. It
takes a great amount of force to strain this ligament, which normally does not have much
excursion. A tear of this lig necessitates surgery as widened mortice for a short time Æ ankle OA

Aetiology of Traumatic
• The muscle of inversion is slightly stronger than the foot evertors. When the foot lands in an
awkward manner there is a tendency for the heel to invert and create stress on lat ligaments
• The foot is not designed to withstand Inversion Strain as that is not the position of its normal
functions & when occurs forces of WB stresses the lateral ligaments especially the ATFL & CFL
• Severe high energy trauma: causes Ankle Syndesmosis injury, “High Ankle Sprain”
• Predisposing factors:
• Ligamentous laxity • Rigid plantarflexed first ray
• LLD • Poor muscle tone
• Tibial vara & ankle varus • Poor proprioception
• Forefoot valgus • Inadequate training or experience
• Talar & calcaneal torsion • Obesity
• Uncompensated equinus
Diagnosis
Clinically
• History of inversion-type twist of the foot &pt can almost always walk on the foot carefully
• Pain & Tenderness antero-laterally
• Swelling
• Bruising
• Painful ROM
• +ve Anterior Drawer Ù ATFL: (knee flexed
& equinus to relax the gastroc & neutralize any
bony stabilizing factor) then compare Æ >
4mm difference or overall 10mm subluxation is +ve
• Prone Anterior Drawer test is done é the pt in prone position é feet hang over the end of the
examining table. Pushes the heel forward é one hand & note y ant movement & skin dimpling
on both sides of the Achilles tendon.
• +ve Inversion/ Eversion Stress Test
• With plantarflexion Ù ATFL is more vertical and best to be evaluated
• With dorsiflexion Ù CFL is more vertical and best to be evaluated
• Neutral position will confirm a diagnosis of double ligamentous disruption
• Both ankles are also tested for comparison.
• The Kleiger Test for deltoid ligament. The patient sits é the knee 90° flexed & foot must be
relaxed and NWB. The foot is rotated laterally. +ve test Æ pain & talus displace from the medial
malleolus, In high ankle sprains this test elicits pain at the syndesmosis
• Squeeze test: both leg bones are squeezed together at the mid calf Æ pain at lower leg.
• Cotton test: é distal tibia supported é one hand the other try to displace the foot é fibula lat
Investigations
1]. Plain radiography: AP standing, lateral, and ankle mortise in 15º IR
2]. EUA - Stress x-rays under anaesthesia (GA or peroneal block) ± KT-1000 arthrometer
o Anterior drawer 5mm shift
o Inversion talar tilt views 10 º difference (= the angle between the plafond & dome )
3]. Arthrography: 10ml injection into the joint. If > 10ml Ù capsular disruption (not after 5days)
o Dye spil laterally = CFL rupture
o Dye spil antero-lat =ATFL rupture
o Peroneal tenography dye in joint Ù CFL, ATFL, peroneal injury
4]. CT: for associated OCD
5]. MRI: best
6]. US assessment is used by the japannese
7]. Arthroscopy

Treatment
Non-operative: most patients will improve with it
In severe strains, protect ankle with pneumatic brace or taping for sports for 3-6mo
Non-Operative Treatment
Phase 1 RICE (immobilize in POP for 2-3wks) + brace ± taping (controversial)
Phase 2 Peroneal & dorsiflexors strengthening/ TA stretching/Isometric exercise using rubber band
Phase 3 Proprioceptive training. When pain & swelling gone. = Wobble Board exercises. Progress thro
functional activities- walking, running, figure-of-eight running, hopping, jumping & cutting.
Operative Treatment
Prior to considerations for surgery, ensure that Subtalar Instability is not present
Indications:
1]. Failed non-operative management
2]. +ve anterior drawer & talar tilt tests clinically
3]. stress x-rays
o Tibiotalar tilt > 20 deg.
o Anterior translation > 5mm.
Aims
• Restore functional stability.
Techniques
• The methods of reconstruction fall into two general types:
o non-augmented
o Augmented.
Non-Augmented methods:
• Brostrom repaired the free ends of the ligaments é fine continuous sutures.
• Karlsson reinserted the lig into fibula through drill-holes, but this caused shortening of lig
• Gould = Karlsson + repair of lateral talocalcaneal lig
+ suturing of the lateral extensor retinaculum to
fibula. This modification is important in patients é
subtalar laxity.
Advantages:
1. Restore normal anatomy & mechanics
2. Preserve motion of the subtalar joint
3. No associated donor-site morbidity
4. No eversion weakness ð sacrifice of peroneal tendon
5. Single, smaller cosmetic incision
Disadvantages:
1. Inability to achieve stability with only the weak & attenuated local tissues
2. Failure to reconstruct the calcaneofibular ligament adequately
3. Failure to address the relatively frequent problem of subtalar instability.
Augmented methods
Employ the peroneus brevis tendon to limit instability of the ankle.
Evans Watson-Jones Chrisman- Snook (preferred)

Peroneus brevis tendon is Evans tenodesis + the Peroneus brevis graft is brought
anchored to fibula, limiting graft is routed through the fibula from ant. to
inversion of ankle and anterior anteriorly through the post. to reconstruct ATFL. It is then
talar translation indirectly, while talar neck to brought post. & inferiorly to the
also z subtalar motion reconstruct ATFL. calcaneus to reconstruct CFL.
Preferred Operative Technique:
• Longitudinal incision, running just posterior to the prominence of the lateral malleolus. This
incision can be extended to allow harvest of the peroneus brevis tendon if augmentation of the
reconstruction is found to be necessary.
• The anterior talofibular ligament and the calcaneofibular ligament are reconstructed.
• The ligaments are divided just distal to their fibular attachments.
• The joint is inspected and debrided as necessary.
• Occasionally, one or both ligaments are avulsed from the fibula with a piece of bone. This so-
called Os Subfibulare should be excised.
• The bone at the anatomic attachment sites of the
ATFL & CFL is roughened, and the ligaments are
reefed and reattached to the fibula with the use of
drill-holes. The repair is oversewn with the proximal
stump of the lig to reinforce the repair.
• During the repair:
o Ankle in neutral
o Foot in eversion
• Augmented reconstruction é peroneus Brevis if:

• ATFL & CFL are so disrupted and frayed that they
cannot be repaired
• Hypermobility of the subtalar joint
• Previous failed reconstruction of the ankle.
• Expose the peroneus brevis, while maintaining the integrity of the superior peroneal retinaculum
• Anterior third of the tendon is isolated distally and split from the distal position to the
musculoskeletal junction. This tendon portion is transected at its proximal aspect. A drill hole is
made through the distal fibula, and the split portion of the peroneus brevis is passed through this
hole. The tendon is tensioned with the foot in mild plantar flexion and eversion.
• This augmentation procedure results in significant loss of eversion and inversion.
Post-operatively:
1]. 0-2 wk NWB + BK cast é ankle in neutral and the foot in eversion.
2]. 2 weeks WB as tolerated.
3]. 6 weeks ROM + progressive resistance exercises + proprioceptive exercises
4]. 3 mo full sports activities can be resumed with the ankle taped or braced.
• Most athletes should continue to use tape or a brace indefinitely during sports activities, but
bracing is not routine after 3 months for most work-related activities or ADL

Chronic Inversion Injury
Bony Ligamentous Tendon Soft tissue
1]. Osfibulare avulsed # 1].Ankle sprain (ATFL, CFL) 1]. Peronei 1]. Ant-lat Impingement $
2]. Ant calcaneal process 2].High ankle sprain=syndesmosis 2]. FHL 2]. Posterior impingement $
3]. Lateral talar process 3].Lat Talo-Calcaneal lig 3]. Anterior impingement $
4]. Ostrigonum (Shepherd’s #) 4]. Sinus tarsi $
5]. Fibrous TC coalition
ggggggbiiiiiii
Antero-lateral Impingement Lesions

• Related to scarring of the lateral talo-malleolar recess (miniscoid lesion):
1- Scarred superior portion of anterior talofibular lig (ATFL)
2- Scarred distal portion of antero-inferior tibio fibular lig (AITFL)
CP:
1]. Antero-lateral ankle pain
2]. Catching & Giving way
3]. Local injection to exclude sinus tarsi pain
Treatment:
• Arthroscopic debridement: Complete AITFL excision + Partial ATFL excision
Sinus Tarsi Syndrome

Anatomy: (Talus Bl.supply) .........................................................see subtalar instability diagram
A]. Tarsal Canal: lies obliquely between the TCN joint & TC joint; and contains:
1]. Anterior and posterior interosseous TC ligaments
2]. Artery of tarsal canal: from POST TIBIAL a. ........form anastmotic sling with a. of sinus tarsi
3]. Deltoid a.: supply medial 1/3 talar body ..........branch from the a. of tarsal canal
B]. Sinus Tarsi: it consists of the concavity between the talus and the calcaneus at the lateral end of
the tarsal canal, 1 finger antero-inferior to Lat Malleolus; and contain:
1]. Ligamentum Cervicis Tali 1].Ant. Lat malleolar br. ........ 100%
2]. Interosseous TC ligament 2].Prox Lat tarsal br. ................ 100%
3]. Fibroadipose Tissue “HOKE’S TONSIL” 3].Distal lat tarsal br ................ 70%
4].Peroneal artery .................... 30%
4]. Origin of the EDB
5]. Artery of sinus tarsi mainly from DORSALIS PEDIS branches
6]. All covered by the root of the inferior extensor retinaculum
Pathogenesis:
1]. Partial tears interosseous Talocalcaneal lig
2]. Lax TC & cervical lig Æ supination at heel strike Æ stretch lateral lig Æ peroneal ms
3]. Scarring of sinus tarsi fat pad
4]. Synovitis
CP: • Pain similar to antero-lat impingement $
• Local inj. into sinus tarsi completely relief the pain
• Unstable propulsion on uneven surfaces ð
INV:
• Peroneal EMG before and after local injection
TTT: • Steroid inj.
• Immobilization, peroneal training
• Debridement of the scarred fat “HOKE’S TONSIL” &preserve IO ligament
Syndesmotic Injury
(High Ankle Sprains)
Formed of :
1]. AITFL
2]. PITFL
3]. Transverse ligament
4]. IOM (interosseous membrane)
Mechanism of injury;
1]. Pronation ER
2]. Hyper dorsiflexion
CP:
1- Point tenderness over syndesmosis
2- SQUEEZ test: squeeze mid calf Æ pain at AITFL
3- ER stress test: (like Kleiger’s test)
• Knee 90º & foot neutral
• ER torque to foot Æ anterior pain at AITFL, PITFL, IOM
4- COTTON test:
• Neutral ankle & subualar
• Try to displace fibula posterolateral Æ displacement is +ve
PXR:
1]. PXR: AP & mortise + ER stress Æ if negative
2]. Tc99 Æ hot spot
3]. High resolution axial CT: demonstrate TILLAUX CHAPOT occult avulsion #
Complications:
1- Fibular shortening +ER Æ ankle incongruence Æ OA
2- IOM heterotopic ossification Æ pain and limitation of dorsiflexion
Treatment:
1]. Open reduction + cleaning of all soft tissue + syndesmotic screw
2]. IOM heterotopic bar excision
• NB: PITFL may accompant AITFL or syndesmotic inj Æ scarring

• ttt: arthroscopic debridement
Subtalar Instability
• CFL & Interosseous ligament play a very important role in subtalar stability
Anatomy:
• Ætiology: inversion injury

• CP:
o Difficult to differentiate from lateral ankle instability
o Tender sinus tarsi
• PXR: may not differentiate form lateral ankle instability

o AP talar tilt
o Lateral anterior drawer
o 40º stress Broden view: knee 90º , Ankle 0º, IR 40º & Beam 10,20,30.40º cephalad
• Ttt:
o Chrisman Snook
o Broström Gould
Posterior Impingement Syndromes
Mechanism Of Injury:
• full WB in maximum plantar flexion of the ankle
• either Demi pointe or full pointe position
• 7 -10 % of the population & 50’% bilateral
Types:
1 Os Trigonum Syndrome
• = Talar Compression Syndrome
• Occurs In Ballet Dancers
Pathology:
Non-united posterolateral tubercle of posterior process of the talus
United os trigonum is called trigonal process (Stieda’s Process)
When steida is # Æ Shepherd’s # (DD Cedell’s # of postero-medial tubercle of talus)
2 FHL Tendinopathy
= Dancers tendonopathy
Pathology:
FHL tendon passes through fibrocartilagenous retinaculum bet lat and med tubercles of the
posterior process of talus to sustentaculum tali
Tendonopathy of the FHL Æ triggering of FHL at the retinaculum Æ Hallux Saltans
If FHL nodule is locked at the retinaculum Æ Pseudo Hallux Rigidus
CP:
• Posterolateral ankle pain
• Tenderness behind the proneals
• Pain y by passive ankle PFlexion (Plantar Flexion Sign) in OsTrigonum $ ≠ FHL tendinopathy
• Local lidocain injection posterior to the peroneal sheath at site of compression
Treatment:
1]. Activity modification
2]. Steroid injection after +ve lidocain injection test
3]. Os trigonum removal (between the FHL and peronei)
4]. If FHL tendonopathy medial approach to release and debride the tendon
ggggggbiiiiiii
Anterior ankle impingement
• Due to osteophytes
• Pain in dorsi flexion
PXR
Lateral standing to assess the amount to be excised
•
60º regain of anterior tibio talar angle is mandatory
•
Treatment::
• Cheilectomy open or arthroscopic
Painful Foot
Painful Heel
Children:
1. SEVERS DISEASE (apophysitis) usually male aged about 10 years with increased density and
fragmentation of the calcaneal apophysis
Raise heel and avoid strenuous activities, severe cases may require POP
Adolescents:
2. WINTER CALCANEAL KNOBS (bilat.retrocalcaneal bursitis) ♀15-20y, more in winter & high heels
Young Adults:
3. HAGLUND’S BUMP + Retrocalcaneal Bursitis above the Achilles tendon insertion
4. PAINFUL HEEL PAD: young athlete after vigorous fall on the heel Æ inflammation, necrosis,
and detachment of the fat pad
Older Adults:
5. PLANTAR FASCIITIS (enthesopathies) may occur also in young adults .....Most common
6. CALCANEAL LESIONS: Stress#, Brodies, Cysts, Osteoid osteoma, Pagets .chronic ache
7. Entrapment of 1ST BR OF LATERAL PLANTAR N (between AbH fascia & quadratus plantae)
8. Tarsal Tunnel Syndrome
Painful Tarsus (midfoot)

1- KOHLERS DISEASE
(osteochondritis of the navicular) usually children < 5 years old present with a painful limp
and tender warm swelling over the navicular Rest and strap for a few weeks results in relief
and eventually ® normal looking navicular
2- BRAILSFORDS disease similar to Kohlers but in older women ± chopart’s joint degeneration
3- THE "OVERBONE"
In adults with high arches, ridge of bone form between dorsal surfaces of the med
cunieform &MT1: adjust shoes, bevel lump
Painful Forefoot
1- METATARSALGIA: Symptom not a diagnosis = generalized ache of the forefoot. May be 1ry or
2ry to a variety of conditions that cause a mismatched wt distribution
A. Primary metatarsalgia due to chronic imbalance in weight distribution between the toes
and metatarsal heads due to absent or ineffective muscle function
B. Secondary metatarsalgia caused by:
1. Intractable plantar keratoses (most common)
2. OA
3. RA
4. gout
5. Distal plantar fasciitis
6. intermittent claudication
2- LOCALIZED:
1- STRESS FRACTURE
2- FREIBERG'S INFRACTION: OCD of the MT2 head (rarely MT3) mostly young females
3- MORTON’S NEUROMA
4- TARSAL TUNNEL $
5- SESMOIDITIS
Tarsal Tunnel Syndrome

= Compression of the tibial nerve in the tarsal tunnel
ANATOMY:
The tarsal tunnel is formed by the flexor retinaculum behind and distal to the medial malleolus
Contents from ant. to post.: (Tom Dick ANd Harry)
1]. Tibialis Posterior Tendon
2]. Flexor Digitorum Longus tendon
3]. Posterior Tibial artery
4]. Posterior Tibial Nerve
5]. Flexor Hallucis Longus tendon
POSTERIOR TIBIAL NERVE
• Branch of sciatic, enters the deep post leg compartment bet the two gastroc heads
• It passes deep to soleus, and travels distally bet it and the posterior tibialis muscle.
• 3 terminal branches in the tarsal tunnel
o Medial plantar nerve:
sensory to med plantar aspect of foot from big toe to medial ½ of 4th toe
Motor to abd hallucis, FDB & 1st lumbrical
o Lateral plantar nerve:
Sensation to the 4th & 5th rays & toes
Motor to ADQ, the interossei, adductor hallucis, 2nd to 5th lumbricals.
o Calcaneal branch: provides sensation to the heel pad.
AETIOLOGY:
1. Flexor Digitorum Accessorius ms (anatomical variation)
2. Proliferative synovitis - Rheumatoid
3. Ganglia & Lipomas
4. Varicosities
5. Neurilemomas
EXAMINATION:
• Insidious onset of symptoms in the sensory distribution of the involved nerves
• Pain radiates along the plantar side of the foot
• Paresthesias, & atrophy of foot intrinsics
• +ve Tinel sign behind medial malleolus
• Manual compression for 30 sec. may reproduce symptoms
INVESTIGATIONS:
• Nerve Conduction Studies: sensory conduction studies are more sensitive than motor.
• MRI - 88% +ve
DDX
• stress fractures (identified on 45º medial oblique view)
• inflammatory arthritides
• plantar fasciitis
TREATMENT: .....................................................Depends on the aetiology
1]. Rheumatoid synovitis ................................ rest & NSAIDs.
2]. Space occupying lesions .......................... surgical decompression.
3]. Steroid injections are a useful temporizing measure.
4]. Surgery:
a. Curved incision that follows the nerve posterior to the medial malleolus.
b. The flexor retinaculum is divided from proximal to distal, down to the abductor hallucis
fascia. [Picture]
c. The calcaneal branch or branches are protected as they extend posteriorly
d. The medial and lateral plantar nerves are followed and freed beneath the abductor
hallucis.
e. The deep fascia of the abductor hallucis should be divided if it is tight.
DEEP PERONEAL NERVE ENTRAPMENT

ANTERIOR TARSAL TUNNEL SYNDROME
Aetiology:
• Can occur as the nerve passes under the inferior extensor retinaculum.
• Other causes include:
o Compression against dorsal osteophytes on the tarsal bones
o Shoe wear that is tight over the dorsum of the foot.
• Patients complain of aching over the dorsum of the foot with numbness or pain in the first
webspace.
• If the lateral branch of the nerve is involved, the extensor brevis will show signs of atrophy.
• Medial branch entrapment causes a sensory deficit in the first webspace.
• Nonsurgical treatment involves shoe modifications & NSAIDs or steroid injection.
• Surgery is indicated for persistent symptoms and is directed toward decompression of the nerve
by the release of the tight retinaculum and the removal of any osteophytes.
SUPERFICIAL PERONEAL NERVE ENTRAPMENT

• The Superficial Peroneal nerve passes through the fascia about 10 cm above the ankle to become
subcutaneous. It branches into the medial & intermediate dorsal cutaneous nerves just proximal
to the ankle which supply sensation over the dorsum of the foot except for the first webspace.
• Entrapment may occur where the nerve passes through the fascia of the lateral compartment.
SURAL NERVE ENTRAPMENT

• A branch of the tibial nerve that accompanies the small saphenous vein.
• It provides sensation to the calf, lateral heel, and lateral border of the foot.
• Entrapment of the sural nerve is rare, because it is protected over its course by subcutaneous
tissue & does not pass under restraining fascial edges or against bones.
• It can become entrapped against a fracture fragment of the lateral malleolus, tarsal bones, or fifth
metatarsal, or against an adjacent ganglion.
NE R V E SITE CAUSE SYMPTOM

ILIO-INGUINAL Hypertrophied abdominal ms Intense training Pain & parasthesia
OBTURATOR Hip adductor Skaters Medial thigh pain
FEMORAL LAT. CUT.ASIS Tight belt Lateral thigh pain
Meralgia paresthetica
SCIATIC Ischial tuberosity, pyriformis ms Pyriformis Sciatica
SAPHENOUS Hunter’s canal Quad or sartorius Infero-medial knee pain
COMMON PERONEAL Fibular head Direct blow Foot drop
SUPERF PERONEAL 12 cm above Lat.Maleolus, as it Inversion injury Dorsal foot pain &
pierce the deep fascia paresthesia
SURAL 12 cm distal to Lat Maleolus Jone’s fr Lat. foot parasthesia
DEEP PERONEAL Inf. extensor retinaculum Inversion injury Sole pain & parasthesia
(anterior tarsal tunnel $)
POSTERIOR TIBIAL Flexor retinaculum FDL accessorius, RA, Sole pain & paresthesia
(Tarsal tunnel $) tumors, ganglion
1ST LAT.PLANTAR Bet AHL fascia, quadratus plantae High heels Plantar fasciitis
MEDIAL PLANTAR Henry Knot (cross of FDL & FHL) Orthotics Big toe pain & parasthesia
INTERDIGITAL Bet MT3-4 plantar to deep MT lig Push phase in Digital pain, parasthesia,
(Morton’s Neuroma) runners dead toe
Plantar Fasciitis
Clacaneal Spur
Definition:
• It is the most common cause of subcalcaneal heel pain
Epidemiology
• More common in Middle aged males
• More in athletes especially joggers
• More in overwt
1- DEGENERATIVE THEORY: ð repetitive trauma Æ degeneration at the origin of the plantar fascia Æ
micro tears Æ inflammation Æ extend to med calcaneal br of the post tibial n
2- FAT PAD THEORY: degenration of the fat Pad with age and overwt Æ z collagen and water Æ z
elasticity Æ make the underlying structures more liable to microtrauma
3- CALCANEAL SPUR THEORY: calcaneal spur was long attributed to be a cause of the plantar fasciitis,
a relation ship never well established. Now it is accepted that the spur is more likely to be a sequela
to the fasciitis rather than a cause; ð repetitive trauma & inflammation
st
4- NEUROGENIC THEORY: entrapment of the 1 branch of the lateral plantar nerve between abductor
hallucis fascia & quadratus plantae muscle
Pathology:
Anatomy:
• Heel pad is a honey comb like structure that is made of many fibrous compartment
• Inside the fibrous compartments there are fat globules that help shock absorption
• Plantar aponeurosis is divided into 3 slips: medial (over abd Hallucis), lateral (over Abd quinti), &
central ώ is the plantar fascia that originate from medial calcaneal tuberosity
Macroscopically
• Heel pad shows z water content and z collagen & elasticity but y thickness
• Plantar fascia is degenerative, é microtears & inflammatory cells
• Plantar fascia may eventually rupture completely or in a partnother entity of the disease is the
distal plantar fasciitis
Diagnosis:
Clinically:
• Pain:
o Gradual onset
o Dull aching (may be neuritic if lateral plantar n is entrapped)
o Worst at morning Æ fades with first few steps
o y at the end of the day
• Inability to WB if the pain is severe
• Swelling & erythema
Exam:
• Tenderness over the medial tuberosity
• +ve stress test: é hyper extension of the toes tenderness y
• +ve tinel sign if nerve entrapment
• Examination of motor and sensory
PXR AP & Lateral standing
• Spur is found 50% a finding never been fully explained
• y fat pad thickness
Other Radiographic
• Tc to exclude stress # when exhausted conservative ttt does not relieve the condition
• EMG of the abd Digiti quinti
• MRI & US: y heel pad thickness
• HLA-B27: in seronegative arthropathy
Treatment:
Conservative
• 80% effective but take a long time
1- NSAIDs
2- Steroid injections: may produce fat pad atrophy, plantar fascia rupture (avoid to be given in the
fat septa
3- Night splint: seem to give fair good results (prevent contractures of the fascia
4- Heel cushions: z mechanical loading and direct trauma & z stretch of the fascia
5- Walking Othosis: z toes hyperextension Æ z windlass effect & stretch of plantar fascia
6- Calf stretching exercise
7- US & iontophoresis
Surgical
• Patient must be informed that the surgery may not give the desired result
1- Plantar fascial release (releasing the medial half only will give the same result & z the recovery
time):
o Through medial longitudinal incision
o Fascia is identified and release the medial 1/3 and excised 1cm
o Superior elevation of the abd hallucis & release its fascia
o Calcaneal spur is deep to the FHB ώ should be partially released to get it
2- Calcaneal spur excision
3- Spur excision + portion of the medial tuberosity (to broaden the WB area)
4- Release of the deep fascia of abductor Hallucis ms ± neurolysis of the n to abd digiti quinti
5- Endoscopic plantar fascial release (95% effective; but demanding, not in nerve entrapment as the
fascia over the abd hallucis cannot be released)
Sassamoiditis
Misnormer as the inflammation actually is around the sesamoid bones of the MT1 (particularly the
medial sesamoid)
Pathology:
1- Acute sessamoiditis: due to acute trauma or unaccustomed effort
2- Chronic sessamoiditis:
Chronic displacement
AVN
Infection (in DM)
3- Sesamoid chondromalacia: due to undue stresses over the medial sesamoid
4- Bipartite or multipartite sesamoid: malformation that cause chondromalacia and usually
mistaken as a fracture
Clinically:
• Pain:
Under the head of the MT1 head
y by walking & WB
• Tenderness that y by passive dorsiflexion
Treatment:
• Wt reduction
• Pressure pad in the shoe
• Local steroid injection
• Sesamoid shaving
• Sesamoid excision (care must be taken not to injure the FHB tendon)
Turf Toe
Definition:
• Tender stiff big toe after severe dorsiflexion
Epidemiology
• More in footballers and contact sports
METATARSAL FAT PAD
• When the toes extend beyond 50° Æ MT fat pad is
locked under the MT heads
Aetiology
st
• Sprain of the plantar capsule of 1 MTP joint of big toe
• Occurs due to hyper dorsiflexion of big toe
Diagnosis:
Clinically:
• Stiff
• Swollen
• Painful
PXR & Tc
• Rule out stress # of the proximal phx of the big toe
Treatment:
• Motion
• RICE

Orthopedic Final

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‫ﺑﺴﻢ اﷲ اﻟﺮﺣﻤﻦ اﻟﺮﺣﻴﻢ‬

Ain Shams University

- 98% Hand affected - Involve other body systems

3]. Upper Limb:

o Shoulder IR: ................................. humeral rotational osteotomy

o Wrist: ............................................. Mennen operation

5]. Knee: .................................................... as polio

6]. Foot & ankle: Most commonly affected

Early Late (>24 mo) Resistant cases Old

Initial Subtalar Talectomy Triple fusion

Paralysis + - Segmental intact Some moves and

Saccular lesion over Lumbosacral region:

Skin & Saccular lesion

Deformities: (ð ms imbalance, IU position, independent)

Progressive Not pro

Flail hip Dislocatio

Splintage & wheel cha

Floppy foot Fixxed TEV V

Paralysed Actiive Flexo

CPK level Diagnosis

Clinical Features of Principal Types of Muscular Dystrophy

Features Duchenne’s Becker’s Emery-Dreifuss Limb-Girdle FSHD

C al Fibber Tyype Diisproporrtion

Congenittal Adult form

Spinal Muscle Atrophy

CLINICAL DIAGNOSTIC CRITERIA (Conse ensus Development Conferencce, 1987)

1. Spinall Defor rmities s

2. Congenittal Tibial Pseudoarrthrosis(se

3. Disorderss of Bone e Growth

Macrocephaly V‐lower femoral Trident

SED Delayed 2ry ossific Pectus carinatum Platyspondyly Dwarf Coxa vara Varus

(chondrodysplasia punctatal Punctate epiphysis Deformity

Erlyenmyer falsk Cortical thinning Flexion Valgus

Kyphosis Odontoid hypoplasia Waddling

Palsies (marble like) Pancytopenia defect)

(Diaphysieal dysplasia) Narrow medulla

Schwartz Jampel $ Myopia & Flat facies Platyspondyly Myotonia Coxaplana

(Acrocephaly syndactyly) Flat occiput & face Broad DIP

Multtiple Eppiphyseall Dysplaasia AD

Scatterred lines off increased

Most common dyysplasia

CT gennetic disord der with bo one fragilitty ð defect in type I coollagen

Pathology (defective collagen and disturbed bone formation)

Chondro Ecctodermaal Dyssplasia

Nail Patella Syndrome AD

Infantile cortical hyperostosis ??

ort Ribb Polyydactyyly

Die at 30y Normal die at 30 Normal die at 10 Prognosis

Sprengel’s Deformity ............................................ See Shoulder

Pediatric Hip Problems

Proximal femur has 3 centers of ossification:

The gluteal musculature is often damaged by hge during delivery and

N.B. gestational periods during which DDH occur:

Laxity and other PDF

z head stressed z congruency over the acetabulum

Short Neck z cup remodeling

II. Acetabular anteversion

III. Acetabular Index (Hilgenreiner Angle):

IV. Coverage and congruence:

TypeIII: Dislocated If not treated

Figure Roentgenographic signs of DDH:

1.Delayed appearnce of head occific centre

2. The Hilgenreiner line (Y-line)

b. Lateral View (False-profile view):