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Acute haematogenous osteomyelitis

- Aetiology & pathogenesis


a) Mainly d/s of children
b) Lowered resistance adult (immunocompromised adults) usually affected
c) Site of infection in pts with concurrent bacteraemia: trauma causing blood (small
haematoma)/fluid collection in bone
d) Incidence higher in less affluent popn; decreasing in western European children d/t
improving social condn (Glasgow, Scotland: <3 per 1,00,000 per yr)
e) Causative organism
1) Both children & adults: Staphylococcus aureus (>70% cases); Streptococcus
pyogenes (in chronic skin infections; Group A beta-hemolytic streptococcus; Gm+ve
cocci); S. pneumonia (alpha haemolytic diplococcus)
2) Newborn: group B streptoccus
3) 1-4 yr children: Gm-ve Haemophilus influenza (for OM & SA; decreased d/t H.
influenzae type B vaccn); Kingella kingae (following URTI in young children)
4) Occasional mico-org causing acute bone infection: Gm-ve (Escherichia coli,
Pseudomonas aeruginosa, Proteus mirabilis & anaerobic Bacteroides fragilis)
5) pts with sickle-cell d/s: prone to Salmonella typhi
6) mixed infection with anaerobes: particularly Peptococcus magnus
7) unusual org: heroin addicts
8) opportunistic pathogens: compromised immune defence mechanism
(immunocompromised)
f) Source of infection
1) Newborn: infected umbilical cord
2) Invaded blood stream from a minor skin abrasion, treading on a sharp object, an
injection point, a boil, a septic tooth
3) Adults: a urethral catheter, an indwelling arterial line, a dirty needle & syringe
g) Predilection for vascular metaphysis of long bone (pr tibia or pr/distal ends of femur) d/t to
peculiar blood vessel arrangement (non-anastomosing terminal brs of nutrient artery twist
back in hairpin loops before entering large network of sinusoidal veins) in that area; relative
vascular stasis; consequent lower O2 tension favouring bacterial colonization
h) Structure of fine vessels in hypertrophic zone of physis allows bacteria to easily pass thru &
adhere to type I collagen in that area
i) Infants: anastomoses between metaphyseal & epiphyseal vessels; infection can reach
epiphysis
j) Adults: staphylococcus aureus (commonest); pseudomonas aeruginosa (iv drug users);
diabetes (prone to soft-t/s infection of foot with contiguous bone infection from variety of
org) ; haematogenous route (20% cases of OM ; only vertebrae)

- Pathology
a) Characteristic progression marked by
1) Inflammation
2) Suppuration
3) Bone necrosis
4) Reactive new bone formation
5) Ultimate consequence: - resolution & healing OR intractable chronicity
b) Depends upon pts age, site of infection, virulence of org, host response
c) Acute OM in children: classical 2-6 yrs; earliest metaphysis change: acute inflammatory
reaction with vascular congestion, exudation of fluid, infiltration by polymorphonuclear
leucocytes-------------------increased IOP-----------cause intense pain, blood flow obstruction &
IV thrombosis-------------------early stage threatening to bone t/s: impending ischaemia &
resorption d/t phagocytes, local accm of cytokines, growth factors, prostaglandin & bacterial
enzymes----------------2nd /3rd day: pus within bone-----force along Volkmann canal to surface-
------subperiosteal abscess (esp in children d/t loosely attached peiosteum)---spread along
shaft----re-enter bone at another level/burst into surr soft-t/s; developing physis: barrier for
direct spread towards epiphysis; partly inracapsular metaphysis (hip, shoulder, elbow) pus
may discharge thru periosteum into jt
d) End of 1st week: rising IOP, vascular stasis, small-vessel thrombosis, periosteal stripping-------
increasingly compromised blood supply --------microscopic evidence of bone death
e) Advancing t/s destr----------d/t bacterial toxins & lecocytic enzymes
f) Defined boundary bet living & devitalized t/s by gradual ingrowth of granulation t/s
g) Separated pieces of dead bone: sequestra (vary in size: mere spicules---------------large
necrotic segments of cortex in neglected cases)
h) Increasing nos of macrophages & lymphocytes ; debris removed slowly by phagocytosis &
osteoclastic resorption
i) Small cancellous bone focus ------completely resorbed leaving atiny cavity------------a large
cortical or cortico-cancellous sequestrum remain entombed (inaccessible to final destrn or
repair)
j) Advancing acute OM: new bone formn; initial area around infection: porotic d/t hyperaemia
& osteoclastic activity; not released pus spontaneously or by sx decompression: new bone
formn in viable bone surface & deep stripped priosteum layer
k) End of 2nd wk x-ray: fine streaks of subperiosteal new bone (typical of pyogenic infection)----
with time ----------thickened bone in a casement or involucrum (enclosing sequestrum &
infected t/s)
l) Persistent infection: pus & tiny sequestrated bone spicules discharge thru perforations
(cloacae) in involucrum & track by sinuses to skin surface
m) Halted dire progression if infection controlled & IOP released at an early stage
n) Increasingly dense bone around zone of infection + periosteal rxn: thickening of bone
o) Reconstituted normal anatomy; or sound healing with permn deformed bone or no healing
with nidus of infection locked inside causing pus & bone debris to be discharged
intermittently thru a persistent sinus or several sinuses : infection lapsed into chr OM
p) Acute OM in infants: early features similar to older children; 1st yr life: freq metaphyseal
infection spreading to epiphysis & from there into adjacent jt; irreparably damaged physeal
anlage ---------severely retarded further growth --------perm deformed jt; 1st 6-9 months:
metaphyseal vessels penetrate physeal cartilage permits infection to spread into
cartilaginous epiphysis; acute OM & SA often together during infancy; unusually exuberant
periosteal rxn resulting in bizarre new bone formn along diaphysis; gradually restored
diaphysis anatomy with longitudinal growth & remodelling
q) Acute OM in adults: bone infection following open injury, operation or spread from
contiguous focus of infection (neuropathic ulcer or an infected diabetic foot); true
haematogeneous OM uncommon: but if occurs affects one vertebrae (following pelvic
infection) or a small cuboidal bone; vertebral infection spread thru end-plate & IVD into an
adjacent VB
r) Infected long bone: abscess spread within medullary cavity; erode cortex; extend into surr
soft-t/s; less periosteal new bone form than in childhood; # of weakened cortex; involved
bone end: risk of infection spreading to adj jt ; outcome: subacute & chr OM
- C/Fs:
a) Children: >4yr child; severe pain; malaise; fever; marked toxaemia if neglected; child refuses
to use one limb or dont allow it to be handled or even touched; recent h/o of infection (a
septic toe, boil, sore throat, ear discharge); looks ill & feverish; pulse rate >100; raised temp;
limb held still; acute tenderness near one of the large jts (above or below knee; in popliteal
fossa; in groin); gentlest manipulation: painful; restricted jt movement (pseudoparalysis);
local redness, swelling, warmth , oedema: later signs signifyin pus escape from bone
interior; non-specific common lymphadenopathy; attenuated features if antibiotics
administered
b) Infants: <1yr & esp in newborn: mild misleading constitutional disturbance; baby simply fails
to thrive; drowsy but irritable; suspicion: h/o of birth difficulties; umbilical artery
catheterization; mild site of infection (an inflamed IV infusion point; heel pucture);
metaphyseal tenderness & resistance to jt movement: OM or SA (botn +nt in infant; no
distinction required); multiple infection in hospital; radionuclide bone scans: to detect other
sites
c) Adults: commonest site for haematogenous infection: thoracolumbar spine; urological
procedure H/o followed by mild fever & backache; tenderness: not very marked; may take
weeks before X-ray signs appear: confirm diagnosis by fine-needle aspiration &
bacteriological culture; other bones involved: diabetes, malnutrition, drug addiction,
leukaemia, immunosuppressive therapy or debility; very elderly & those with immune
deficiency: mild systemic features, missed diagnosis

Diagnostic imaging:

Plain x-ray

1st wk after symp onset: no bone abnormality seen on xray


Displacement of fat planes: soft-t/s swelling/infection or haematoma

2nd week: faint extra-cortical d/t periosteal new bone formn (classic xray sign of early pyogenic OM);
dont delay t/t

More obvious periosteal thickening later; patchy rarefaction of metaphysis; later ragged features of
bone destruction

An imp late sign: combination of regional OP + localized segment of apparently increased density; OP:
feature of metabolically active & living; the segment that fails to become OP: metabolically inactive &
dead

USG: detect a subperiosteal collection of fluid in early stages of OM;; cant distinguish between
haematoma & pus

Radionuclide scanning: 99mTc-HDP increased activity in both perfusion & bone phase; highly sensitive
investigation in very early stages; low specificity: other inflammatory lesions can show similar changes;
doubtful cases: scanning with 67 Ga- citrate or 111 In-labelled lecocytes is more revealing

Magnetic resonance imaging: helpful in cases of doubtful diagnosis; particularly suspected infection of
axial sk; best method of demonstrating bone marrow inflammation; extremely sensitive even in early
phase of bone infection; assist in differentiating a soft-t/s infection & OM; too low specificity to exclude
other local inflammatory lesions

Laboratory investigations

- Confirm clinical diagnosis: aspirate pus or fluid from metaphyseal subperiosteal abscess,
extraosseous soft t/s or an adjacent jt using 16- or 18-gauge trocar needle
- Even if no pus: a smear of aspirate examined immediately for cells & organisms; a simple gram
stain: identify type of infection & assist with intial antibiotic choice
- A sample: also sent for detailed microbiological examination, tests for antibiotic sensitivity
- t/s aspiration: +ve result >60%cases;
- blood cultures: +ve <50% cases of proven infection
- CRP (C-reactive protein): usually elevated within 12-24 hrs after onset of symptoms
- WBC count: rises
- Haemoglobin concentration: diminished
- Very young & very old: these tests are less reliable; may show normal range values
- Antistaphylococcal antibody titres: raised; useful in atypical cases w doubtful diagnosis
- OM in an unusual site or with an unusual org: possibility of heroin addiction; sickle-cell d/s
(salmonella cultured from faeces); deficient host defence mechanism (HIV)

DD
- Cellulitis: often mistaken for OM; widespread sup redness, lymphangitis, source of skin
infection: not obvious & should be searched for (on sole or between toes); MRI if doubt: helps
to diff bone & soft-t/s infection; org: staph or strep; mild cases: high dose oral antibiotics; severe
cases: IV antibiotics t/t
- Acute suppurative arthritis (septic arthritis): diffuse tenderness; complete movement at jt
abolished by m/s spasm; infants: both co-exist OM & SA& diff to distinguish metaphyseal OM &
SA of jt; a progressive rise in CRP values over 24-48 hrs : suggestive of concurrent SA
- Streptococcal necrotizing myositis: GABH streptcocci (org resp for sore throat); early stage:
mistaken for cellulitis or OM; rare condn; rapidly spiral out control towards m/s necrosis,
septicemia, death; warning signs of a medical emergency: intense pain, board-like swelling o f
limb in apt with fever, general feeling of illness; MRI: reveal m/s swelling, possibly signs of t/s
breakdown; essential imm IV antibiotics t/t; sx debridement of necrotic t/s & sometimes even
amputation to save a life
- Acute rheumatism: less severe pain; tends to flit from one jt to another; signs of carditis,
rheumatic nodules or erythema marginatum
- Sickle-cell crisis: similar features of acute OM; Salmonella endemic areas: treat with sutable
antibiotics until infection definitely excluded
- Gauchers d/s: pseudo-osteitis features closely resemble OM; diagnosis: by finding other
stigmata of d/s (spleen & liver enlargement)
- Cardinal features of acute OM in children: pain, fever, refusal to bear wt, elevated white cell
count, elevated ESR, elevated CRP

T/t

- OM suspicion on clinical grounds: send blood & fluid for lab inv; immediate t/t w/o final reports;
4 imp aspects of pt MX:
- Supportive t/t for pain & dehydration
- Splintage of affected part
- Appropriate antimicrobial therapy
- Surgical drainage

- General supportive t/t: comfort distressed child; treat pain (analgesics at repeated interval w/o
waiting pt asking for them);severe dehydration d/t septicemia & fever should be t/t with IV
fluids

- Splintage: desirable; partly for comfort & to prevent jt contractures; simple skin traction (may
suffice; if hip involved: helps to prevent dislocations); a plaster slab; half-cylinder; w/o obscuring
affected site

- Antibiotics: imm examn & culture of blood &aspiration material; prompt IV antibiotics w/o
result; initially choice of antibiotics : based on direct examination findings of pus smear;
clinicians experience of local condn (best guess at most likely pathogen); staphylococcus
aureus: common at all ages & t/t: cover all bacteria encountered in each age group; an
appropriate drug with good bone penetration can be substituted once infecting org identified &
antibiotic sensitivity known; factors: pts age; general state of resistance; renal function; degree
of toxaemia; previous h/o of allergy; recommendation guide:
a) Neonates & infants upto 6 months: antibiotic effective against penicillin-resistant
staphylococcus aureus, group B streptococcus, gm ve org: DOC: flucloxacillin + 3rd-generation
cephalosporin (cefotaxime); alternative effective empirical t/t ( flucloxacillin + benzylpenicillin +
gentamicin for each resp org)
b) Children 6 months to 6yrs of age: empirical t/t covering against Haemophilus influenza unless
child has got anti-haemophilus vaccinnation for sure; IV flucloxacillin + cefotaxime /cefuroxime
c) Older children & previously fit adults: staphylococcal infection in vast majority: IV flucloxacillin +
fusidic acid (preferred over benzylpenicillin d/t highly prevalent penicillin-resistant staphylococci
& well concentrated fusidic acid in bone); known streptococcal infection: benzyl-penicillin
better; pts allergic to penicillin: 2nd-/3rd generation cephalosporins
d) Elderly & previously unfit pts: greater risk of Gm ve than usual d/t respiratory, gastro-intestinal
or urinary d/os & likelihood of pts requiring invasive procedures; AOC: flucloxacillin + 2nd/3rd
generation cephalosporins
e) Pts with sickle-cell d/s: prone to OM d/t salmonella or other gm-ve; or even staphylococcus;
DOC: chloramphenicol (previously; not used d/t rare complication of aplstic anemia); 3rd-
generation cephalosporins or fluoroquinolones like ciprofloxacin
f) Heroin addicts & immunocompromised pts: unusual infections likely (pseudomonas aeruginosa,
proteus mirabilis, anaerobic bacteroides species); HIV infected infants with sexually transmitted
org during birth; empirical t/t with broad spectrum antibiotics: 3rd-generation cephalosporins or
a fluoroquinolone preparation depending on sensitivity test results
g) Pts of AHOM at risk of MRSA infection(MRSA endemic hospital/previous h/o of MRSA): IV
vancomycin/similar antibiotics + 3rd-geneartion cephalosporins
Administer drug IV & adjust as per AST results until pts condn improves, CRP values returm to
normal X 2-4 wks usually depending on virulence of infection & pts general degree of fitness;
oral appropriate antibiotics of AST result for 3-6 wks but for prolonged period If bone
destruction is marked: track serum antibiotic level while on oral antibiotics to ensure MIC is
maintained or exceeded; check CRP, ESR, WBC values at regular intervals with discontinue of t/t
when values return to normal
Continuous collaboration with a microbiologist when treating pts with bone or jt infection
- Drainage: often unnecessary if antibiotics given early (within first 48 hrs of onset of symptoms);
indications for drainage:
a) No improvement in c/fs within 36 hrs of starting t/t
b) Even earlier if signs of deep pus (swelling, oedema, fluctuation)
c) Even if pus aspirated; abscess drained by open operation under GA
d) 1/3rd pts with confirmed AOM need operation; adults seldom with vertebral infection

If pus found & released: little gained by drilling into medullary cavity
If no obvious abscess found: drill few holes into bone in multiple directions; no evidence of widespread
drilling has any advantage: it may do more harm than good

If extensive intramedullary abscess: drainage by cutting a small window in cortex; wound closed w/o
drain; splint (or traction) reapplied

Encourage movements once signs of infection subside; child allowed to walk with aid of crutches; full
wtbearing after 3-4 wks

Complication

- Epiphyseal damage & altered bone growth: in neonates & infants whose epiphysis are entirely
cartilaginous; metaphyseal vessels penetrate physis & carry infection into epiphysis; irrecovably
damaged growth plate; destroyed cartilaginous epiphysis; arrest of growth; shortening of bone;
at hip jt: pr end of femur severely damaged leading to pseudoarthrosis
- Suppurative arthritis: may occur in a) very young infants in whom growth disc is penetrable; b)
intracapsular metaphysis (upper femur) c) metastatic infection; USG: jt effusion demonstrated;
definitive diagnosis: given by jt aspiration (arthrocentesis); supp arthritis common in infants with
OM of femoral neck
- Metastatic infection: sometimes seen; generally in infants; may involve other bones, jts, serous
cavities, brain or lung; some cases multifocal infection from outset; missed sec sites of infection
with attention focused on one particular area; examine child all over & repeatedly to be alert to
this complication
- Pathological #: uncommon; occur if delayed t/t; weakened bone by erosion at site of infection or
by overzealous debridement
- Chronic OM: acute OM fails to resolve despite improved methods of diagnosis & t/t;
wks/months after onset of acute infection a sequestrum appears in F/up X-ray & pt left with
chronic infection & draining sinus; d/t late o rcinadquate t/t; in debilitated pt; those with
compromised defence mechanisms
- Lethal outcome from septicaemia: rare; child recovers with antibiotics; bone may return to
normal; morbidity common if delayed t/t or org insensitive to chosen antibiotic
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