Short Cases in Orthopaedics For PG Practical Examination

Prelims.
pdf
Chapter-01_Short Cases.pdf
Chapter-02_Things to be Taken.pdf
Chapter-03_Cases Seen in Ward Rounds.pdf
Short Cases in
ORTHOPAEDICS
Short Cases in
ORTHOPAEDICS
for PG Practical Examination
S Kumaravel
MS (Ortho) D (Ortho) DNB (Ortho) (PhD) MNAMS
Associate Professor
Department of Orthopaedics
Government Thanjavur Medical College and Hospital
Thanjavur, Tamil Nadu, India
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Short Cases in Orthopaedics for PG Practical Examination
First Edition : 2013
ISBN: 978-93-5090-083-3
Printed at
Preface
The thought that why to write such a book when lots of

clinical orthopaedics books are available is normal. In fact,
this is not a regular clinical orthopaedics book. It is
conceived and written with the only intention to make
passing the practical examination so easy, so that there is
no need to panic.
After the theory examination, the candidate faces the
practical examination. It is a different ball game. Here, the
confrontation occurs. The tips for examination given in this
book will make you to clear the paper with much ease.
This approach when put to use for others, for example,
my postgraduate students at two Medical Colleges, worked
wonders. Even a few students who had some difficulties in
presenting cases found later that they can confidently
answer the questions.
This unique approach is a variety of methods to tackle
the examinations, including a range of hypothetical
questionnaire, ways to elicit present complaints and past
history, correct methods to palpate, how to examine and
how to diagnose cases, etc. Not a single candidate who
followed this approach has been unsuccessful. The
external examiners were also happy to have examined a
good set of postgraduates. One of the students became the
best outgoing MS Orthopaedics student of the Tamil Nadu
Dr MGR Medical University, Chennai, Tamil Nadu, India.
vi SHORT CASES IN ORTHOPAEDICS
However, this book is not an alternative for your

teacher’s direct guidance—as orthopaedics is a surgical
speciality—it is learned mainly by apprenticeship.
WHY THIS BOOK

Any amount of work you do in the wards, any number of
hours you work, toil with textbooks, the ultimate fruit of
all this is achieved only, if you pass the examination.
When it comes to postgraduate examinations, either it
is diploma, degree or DNB examination, the day’s
performance holds the key.
When you are writing a theory examination then the
“confrontation factor” is not there, because you have a
question paper and questions set to be answered. You can
select, which questions to be answered first. This is not so
in practical examinations. You cannot choose which
question you will answer first. This will obviously irritate
the examiner. So only, I decided to write something useful
for the students which will help to confront the examiner
and sail smoothly to pass the examination.
Very useful words for the young minds are:
1. “Don’t beg for a pass—you should demand it”.
2. Any student enters the hall with 100% marks and, by his
misdeeds and unforced errors, he loses marks slowly.
So, if, at all, a postgraduate fails, it is he who fails and
not the examiner. Having gone through 3 such
postgraduate examinations: Diploma in Orthopaedics, MS
Orthopaedics, and DNB Orthopaedics, I decided to expose
the weak areas in our mind, which need to be strengthened
to clear the examination with ease.
S Kumaravel
Acknowledgements
I thank—all my professors, assistant professors, tutors,

senior postgraduates, junior postgraduates and orthotist
who have gave ideas and new insight.
I acknowledge all my teachers while doing my
undergraduation at Coimbatore Medical College, especially
Dr Muthu Meenakshi Ramanathan, Dr Perumal Rajan,
Dr Kesavalu, Dr Sadasivam, Dr Chandra and also my
Postgraduate teachers at Madras Medical College my alma
mater, Professor K Sriram, Professor Mayilvahanan
Natarajan, Professor K Annamalai, Professor CT Alagappan,
Professor RH Govardan, Professor K Chandran, Professor
M Subramanian, Professor R Dhanapal, Professor Nalli R
Uvaraj, Professor R Selvaraj, Professor Sudheer, Professor
Gopinath Menon, Professor S Najimudeen.
I acknowledge Professor SP Mohanty, Professor
Benjamin Joseph and Professor Bhaskar Anand Kumar of
Mahe Manipal for enriching my knowledge while, I was
a visiting fellow there.
I sincerely acknowledge Professor DK Taneja our past
IOA president and my DNB examiner, who has
enlightened me during his COE lectures.
I acknowledge professors, Professor V Shanmugam,
Professor KJ Mathiazhagan, Professor A Navaneethan,
Professor R Rathinasabapathy and Professor M
Gulammohideen for their encouragement.
viii SHORT CASES IN ORTHOPAEDICS
I acknowledge Mr Pandian, Orthotist, Institute of

Physically Handicapped, New Delhi.
I sincerely acknowledge all my patients who kept their
patience till all my demonstrations of test were being
photographed.
I thank my Postgraduate Dr Gopi Shankar Balaji now
a full-fledged orthosurgeon, who helped in proofreading
and preparation of the text. I thank my postgraduates
Dr R Vijayakumar, Dr Manogaran, Dr Sivaraj for their help.
I thank Shri Jitendar P Vij (Group Chairman), Mr Ankit
Vij (Managing Director) and Mr Tarun Duneja (Director-
Publishing) of M/s Jaypee Brothers Medical Publishers (P)
Ltd, New Delhi, India and Mr Jayanandan of Chennai
Branch for the encouragement and support for this book.
I thank my parents Sri G Shanmugasundaram and
Smt Jayalaxmi for their sincere blessings.
My work is not possible but for silent cooperation from
my better half Dr Mangaleswari MDS and my son Vishva.
Contents
Short Cases ..................................................... 1

1. Congenital Talipes Equinovarus (CTEV) 2
• List of Findings above Downwards 4
2. Osteosarcoma 6
• Questions on Local Staging 6
• Biopsy 8
3. Erb’s Palsy 19
4. Exostosis 20
5. Osteomyelitis 24
6. Winging of Scapula 31
7. Cubitus Varus 33
8. Cubitus Valgus 36
9. Tardy Ulnar Nerve Palsy 37
10. Lateral Condyle Nonunion 40
11. Malunited Intercondylar Fracture 41
12. Unreduced Dislocation of Elbow 42
13. Post-traumatic Stiffness of Elbow 43
14. Arthritis of Elbow 46
15. Congenital Radioulnar Synostosis 47
16. Fracture Medial Epicondyle 48
17. Malunion of Both Bones Forearm 50
18. Galeazzi Fracture Dislocation 52
19. Sudeck’s Osteodystrophy (RSD) 53
20. Volkmann’s Ischaemic Contracture 55
21. Osteoclastoma 58
22. Neglected Shoulder Dislocation 62
x SHORT CASES IN ORTHOPAEDICS
23. Fresh Dislocated Elbow 64

24. Nonunion of Both Bone Forearm 66
25. Brachial Plexus Injury 67
26. Torticollis 74
27. Cerebral Palsy 75
28. Wrist Drop 84
29. Claw Hand 87
30. Radial Club Hand 91
31. Compound Palmar Ganglion 92
32. Neuropathic Joint 93
33. Carpal Tunnel Syndrome 94
34. Dupuytren’s Contracture 95
35. Spina Ventosa 96
36. Mallet Finger (Base Ball Finger) 97
37. Foot Drop 98
38. Baker’s Cyst 101
39. Maduromycosis 103
40. Genu Valgum 104
41. Genu Varum 105
42. Residual Poliomyelitis 109
• History of the Patient 109
• General Examination 109
• Measurements 109
• Special Tests 110
43. Nonunion Fracture Both Bone Leg 113
44. Nonunion Patella 118
45. Congenital Pseudarthrosis of Tibia 120
46. Osgood-Schlatter’s Disease 122
CONTENTS xi
Things to be Taken .................................. 123

Things to be Taken to the Clinical Examination Hall 124
Cases Seen in Ward Rounds ................. 125

1. Cases and Appliances You may be Asked in Ward
Rounds in DNB and Notes for Them 126
Ward Procedures 126
Region with Condition 128
• Shoulder (Rotator Cuff Tear) 128
• Arm 130
• Elbow 132
• Wrist and Hand 135
• Hip 142
• Thigh 143
• Knee 145
Foot and Ankle 151
• Retrocalcaneal Bursitis 154
• Localised Gigantism 157
2. Paediatric Cases 165
• Birth Fractures in a 3-day-old Child 169
3. Complications of Injuries and Treatment 170
4. Metabolic Bone Disorders 174
• Osteomalacia 179
5. Spine 180
How to Use this Book
We would start with the common cases in postgraduate

examinations—their presentations, history/examination
and viva.
Firstly let us see Pearls, which provides essential items
needed and expected of you in the examinations. Later in
the cases section we would be presenting a case, then start
questioning,
1. during the history
2. during the examination
3. after the diagnosis and
4. discuss the management.
This volume is about the common short cases. Some will
be heavily “theory” filled, some not. I have even included
few cases which may be of some use in ward rounds, in
DNB examination, in objectively structured clinical
examinations and also in day-to-day practice.
I like to suggest you to sit with one of your batchmates
and ask these questions to each other, where one playing
the role of the examiner. Thus, you can familiarise with
the usual questions and startlers.
I have tried to be exhaustive but firmly believe that there
is always scope for improvement and so, I look forward
towards your suggestions for further enriching the quality
of this book.
Pearls
READ ONE BY ONE CAREFULLY

• Do not ignore any problem of patient.
For example, patient has no cause of right hip but has
some findings for right hip, you may be caught
napping.
• Do not avoid presenting any finding.
• The present history starts from the time of onset of the
complaint.
You may think a mild restriction of movement in the
contralateral hip is of no use but this will definitely change
the diagnosis.
• Do not irritate the examiner.
• Talk confidently, not arrogantly.
• See the external examiner’s eyes and talk.
Do not see the internal examiner (if any). Its a sign of
weakness.
• Dress neatly.
• Impress the examiner at the first instance, either it a
short or a long case.
• Training is at ward, itself.
For example, any question from patients or the attendant
of the patient may be an examination question.
For example, in a tumor case a patient’s attendant will ask:
 Doctor can you cure it?
 Can you remove it fully?
 Can you burn the tumor (irradiation)?
xvi SHORT CASES IN ORTHOPAEDICS
 Can you give chemotherapy?

 How long will he/she live?
 Can she marry and have children?
• In the examinations, answer in a broad based
manner.
• While presenting, do not go for a diagnosis.
• Real case does not matter—diagnosis does not
matter. Its how you fight for your case.
• Do not avoid presenting or alter any finding. Just tell
what the patient has.
• If you are given a chance to go back and see, go and
see the case, and after all, which doctor will you prefer?
• The one who will make sure one more time his findings
or the one who bluntly tell his findings are correct, if
you are the patient?
• While thinking about a treatment tell what is the
treatment if you have the problem, i.e. what would you
like to have as treatment if you were at the patient’s
end?
• Do not see X-rays at any of your clinical presentation.
If your eyes see the X-rays, it freezes your brain and it
runs in the same orbit and never thinks further; X-rays
come last.
• Try to stand and present rather sit—sitting is
psychologically cramps you to the chair.
• Once you finish off taking history and clinical
examination, sit and think.
1. What will be the discussion if X-ray is normal?
2. If the X-ray is arthritic with joint narrowing?
3. If the X-ray is a tumorous condition?
PEARLS xvii
• Keep your mind open till the entire question is asked.

• While asked to demonstrate a clinical sign, try to stand
always on the right side of the patient.
• Demonstrate the signs you are asked to do in the most
classical way and not the cursory way because this
½ hour (or) 1 hour assessment will reflect your entire
(3/2 years) training.
• Postgraduate presentation and discussion of clinical
cases should involve facts and not controversies.
• It is usual and expected that a question is asked
previous answer. Examination is not a war but a plot—
by you.
You have to pull the examiner to your fold rather than
otherwise.
Short
Cases
2 SHORT CASES IN ORTHOPAEDICS
1. CONGENITAL TALIPES
EQUINOVARUS (CTEV)
A B
Figs 1A and B: Unilateral club foot (Right side)
Fig. 2: Same patient after surgery

SHORT CASES 3
A B
Figs 3A and B: (A) Recurrent club foot following surgery;

(B) Bilateral club foot neglected for 10 months
A B
Figs 4A and B: Another such deformity since birth

LIST OF FINDINGS IN CLUB

FOOT ABOVE DOWNWARDS
 Internal tibial torsion
 Calf atrophy
 Lateral malleolus prominent
 Medial malleolus less prominent
 Inner border of foot shorter/outer border of foot longer
 Abnormal creases posterior and medial
 Tendo calcaneus taut
 Adduction of forefoot
 Callosity present on lateral side foot
 Inversion at subtalar joint
 Heel small and elevated
 Cavus
 Inward curling of toes
 Bilateral in 50%
 Examine hips and spine always.
1. What is the etiology of this condition?
• Abnormal uterine position (most accepted)
• Primary germ plasm-talar defect
• Primary soft tissue abnormality.
2. Pathological anatomy of this condition?
• Talus—plantar flexed, neck elongated and rotated
• Calcaneus—inverted
• Navicula—rotated
• Soft tissue contractures
• Tendo Achilles, tibialis posterior, Flexor hallucis
longus (FHL), Flexor digitorum longus (FDL),
Abductor hallucis
SHORT CASES 5
• Ligaments—spring ligament, plantar fascia

• Capsules—subtalar/midtarsal joints.
3. What are the differential diagnoses?
• Myelomeningocele
• Arthrogryposis
• Poliomyelitis
• Cerebral palsy
• Constriction bands
• Tibial hemimelia.
4. What is the most common associated anomaly?
• Urogenital.
5. What is the management?
• Depends on the age of the child and type of the
CTEV
• Ponsetti’s method of serial cast correction, every
week
(sequence of manipulation→ fore foot cavus→
adduction→ varus-equinus).
6. What are the surgical options?
• Posteromedial soft tissue release
• Extensile release
• Corrective osteotomy of the calcaneum
• Triple arthrodesis
• JESS/Ilizarov apparatus application.
7. What is the single most important tendon to release
in posteromedial soft tissue release?
• Tibialis posterior.
2. OSTEOSARCOMA
 Age group—younger age usually (sometimes middle
age—parosteal)
 Swelling, pain (pain starts first)
 Region—around the knee
 Step by step approach. Clinical examination, local
staging, systemic staging, Histopathology
 Usually soft in consistency/fast growing/vascular
 Clinically candidate can only tell it is a malignant bone
tumor most probably it may be osteosarcoma.
8. What is the common presentation of osteosarcoma?
• 100% cases—swelling
• 75%—pain.
Questions on local staging

9. How will you start investigating?
• X-ray
a. Periosteal reaction (elevation)
b. Bone destruction
c. Cortical erosion
d. Pathological fracture
e. Soft tissue involvement.
10. Elevation of periosteum is specifically called in this
case?
• Codman’s triangle (not pathognomonic of
osteosarcoma).
11. Sunray spicules—how it is formed?
a. They are formed along the blood vessels of
periosteum as it is elevated from the bone by the
tumor
SHORT CASES 7
b. It is also hypothesized to be formed by the

Sharpey’s fibres of the periosteum.
12. What is the best investigation for local staging?
• Magnetic resonance imaging (MRI).
13. How is osteosarcoma staged?
• Low grade
A—Intracompartmental
B—Extracompartmental
• High grade
A—Intracompartmental
B—Extracompartmental
• Metastasis.
14. What is a satellite lesion?
• It is a small nodule separate from primary foci-
embedded in medullary sinusoids with no
reaction—not even detected by Tc 99 scan
differentiated from secondary as there are no
metastasis.
• 50% picked by MRI, 50% at autopsy only.
• Associated with poor prognosis. Recurrence can
follow after amputation also.
15. What is the best investigation of choice to pick up
satellite, lesions?
• Magnetic resonance imaging (MRI).
16. How many percent of satellite nodules picked by
MRI?
• About 50%.
17. What is the importance of satellite nodules?
• To plan the level of resection.
18. What is the commonest secondary of osteosarcoma?

• Lungs.
19. What are the characteristics of lung secondaries?
• These are multiple, basal, bilateral, subpleural
(mnemonic → MBBS).
20. What is the use of chest computed tomography?
• Chest computed tomography more specific to pick
up during secondaries.
21. If the chest X-ray is normal, still will you order
computed tomography chest?
• Yes, computed tomography scan can pick up
micrometastasis.
BIOPSY
22. What are types of biopsy?
a. Fine needle aspiration cytology (FNAC)
b. Core needle biopsy—Ideal
c. Open biopsy.
23. Why core needle biopsy is ideal?
• You get a bit of tissue for diagnosis with minimum
contamination of track
• There is less bleeding and less seeding.
24. In open biopsy, what is the precaution you will take?
1. Avoid crossing compartments
2. Incision placed in such a way that it is included
in the final surgery incision
3. Cut the window in an oval shaped not in a stress
increasing manner
4. Achieve perfect hemostasis in the form of bone wax
5. No drain.
SHORT CASES 9
25. What is the diagnostic histopathological appearance

of osteosarcoma
• Presence of malignant osteoid.
26. What are the histological types of osteosarcoma?
Types of osteosarcoma
a. Osteoblastic
b. Fibroblastic
c. Chondroblastic
d. Telangiectatic
e. Small cell type.
27. What are the treatment options?
• Stage IA—Intracompartmental low grade → Limb
salvage
• Stage IB—Extracompartmental low grade
→ Ablation
• Stage IIA—Intracompartmental high grade
→ Limb salvage
• Stage IIB—Extracompartmental high grade
→ Ablation
• Stage III—Metastasis → Palliative ablation/
chemo/radiotherapy.
28. What is a compartment?
• Bone is a compartment.
• Each muscle group is a compartment.
29. If you plan for limb salvage, how will you proceed?
• If the case is planned for limb salvage, patient is
put on chemotherapeutic drugs before any
surgical procedure is undertaken. This is called
Neoadjuvant chemotherapy.
30. What are the advantages of neoadjuvant chemo-

therapy?
1. Controls micrometastasis and metastasis during
surgery
2. Tumor regression
3. Decrease vascularity
4. Tumor becomes more firm and easy to dissect
5. It gives time to fabricate a custom prosthesis
6. When chemotherapy is given before surgery, the
resected specimen can be sent for study of necrotic
material and chemotherapeutic drugs can be
changed if no necrosis, i.e. the tumor has not
responded.
31. What are the common chemotherapeutic agents
used in osteosarcoma?
• Cisplatin, adriamycin and ifosphamide.
32. What is adjuvant chemotherapy?
• Given after surgical ablation.
33. What stage of cycle of tumor tissue is amenable for
chemotherapy?
• G2 multiplying mitotic stage.
34. How to suspect osteosarcoma clinically?
• Young age → 1st and 2nd decade
• No joint involvement (may have extra-articular
restriction)
• No constitutional symptoms.
35. How to differentiate Ewing’s from osteosarcoma?
Osteosarcoma Ewing’s sarcoma
Site—appendicular skeleton 50% axial
50% appendicular
Constitutional symptoms absent Present (++)
SHORT CASES 11
36. Can we get osteosarcoma at old age?

• Yes/usually secondary osteosarcoma
• Classical osteosarcoma in old age due to irradi-
ation, Paget’s, consisting congenital conditions
like hereditary, multiple exostosis and fibrous
displasia
• They are typically highly malignant.
37. Having diagnosed osteosarcoma clinically, what
investigation you will order next?
• Plain X-ray of bone with joint above and below
• We see permeative lesion with cortical destruction.
38. What are the differences between multicentric
origin and multiple secondaries?
• Multicentric origin—multiple areas with lesions
similar to primary (Codman’s, etc.) with no lung
lesions
• Multiple secondaries—osteolytic lesions only.
39. Where will be the bone secondaries seen commonly?
• To the vertebra.
40. What is the role of trauma in incidence?
• Trauma history is only incidental and have no
etiological importance in this condition.
41. What is the common stage of presentation of
osteosarcoma?
• Stage II B (Enneking)—70%
• Stage III—20%.
42. What is the prognosis of osteosarcoma?
• Prognosis has improved dramatically with
adjuvant chemotherapy.
• 5 years survival in case of limb salvage is 85%
with adjuvant chemotherapy.
43. Any other important factor other than stage and

adequacy of resection?
• Yes
• Tumor size; smaller the tumor—better is the
prognosis.
• Response to chemotherapy is better.
• Tumor necrosis after chemotherapy is the only
significant variable.
44. What is MDR 1 and P-Glycoprotein?
• MDR 1 is Multidrug Resistant 1 gene.
• It codes for 170 KDA Membrane protein called P-
Glycoprotein. This decreases the intracellular
concentration of many cytotoxic drugs by energy
efflux pump.
• This is of significance in osteosarcoma and other
tumors.
45. What is the natural course of osteosarcoma after
diagnosis if left untreated?
• It breaches the cortex and the soft tissues interior
of muscles, nerves, vascular structures and
distant metastasis and not by lymphatics. This is
because bone has no lymphatics.
46. What are the investigations possible?
• X-ray
• CT (Computed tomography)
• MRI
• Angiography
• Thallium study.
47. What is Micrometastasis?
• When X-ray chest and CT scan are normal with
no other demonstrable secondaries in isotope
SHORT CASES 13
scan, patient is suspected to have micrometa-

stasis.
• 35% normal X-rays will have CT chest positive
for secondaries.
48. X-ray shows single lobe of lung involved. Why you
need CT?
• Other lung micrometastasis.
49. Open biopsy. How is it dangerous?
• Contamination
• Hemostasis is must
• Bone cement for bone
• Gel for soft tissue.
50. What bearing the biopsy site have over treatment?
• Since osteosarcoma patient should be approached
positively, i.e. with chemotherapy they live longer,
we should not hamper the chance of limb salvage.
• It is better to do a core needle biopsy where
dissemination chance is less and if needle
specimen is inadequate, open incisional biopsy
is planned so that the scan with margin is
removed in definitive surgery.
51. How to diagnose and subtype osteosarcoma?
• Demonstration of malignant osteoid.
• There are 5 types histologically:
– Osteoblastic
– Chondroblastic
– Fibroblastic
– Telangiectatic
– Small cell.
52. What are the types of medullary lesion in osteo-

sarcoma?
• Three types: Sclerotic, Lytic, Mixed.
53. What is classical picture of osteosarcoma?
• Site—Metaphysis, Codman’s triangle, sunray
spicules, usually no pathological fracture.
54. Is Codman’s triangle pathognomonic?
• No. It can occur in other conditions also where
periosteum is elevated.
55. What is the cause of Sunray spicules?
Two theories
1. Calcifications along the attachment of Sharpey’s
fibres from periosteum to the cortex
2. Calcifications along the periosteal blood vessels.
56. Why osteosarcoma is more common in meta-
physis?
• Growth based on Johnson’s theory of field
selection, proliferative primitive spindle cells
lodged in metaphysis
• Proliferative primitive round cells are lodged in
diaphysis
• It is not just due to the blood supply of the
metaphysis.
57. How will you confirm?
• Core needle biopsy—diagnostic.
58. What are the components of limb salvage?
• Wide excision of the tumor
• Followed by reconstruction
SHORT CASES 15
• In adults, knee joint fusion, endoprosthesis,

allograft, ilizarov, rotation plasty
• In children expandable prosthesis.
59. When secondary osteosarcoma occurs?
• In premalignant diseases like Paget’s, irradiated
bone, diaphyseal achalasia, enchondromatosis,
secondary OS can occur
• Skeletal—secondaries.
60. When will you do biopsy?
• When the primary not detected.
61. When will you do prophylactic fixation?
• Mirel’s scoring system 4 variables-1, 2, 3 points
in that order
Veriable Score 1 Score 2 Score 3

1. Location of the upper lower peritrochanter........
lesion ................ limb limb
2. Degree of pain mild moderate severe

caused by the
lesion
3. Type of lesion lytic blastic mixed
.......................
4. Size of the lesion < 1/3 1/3 = 2/3 > 2/3
............................
8/12 = 15% risk of fracture 9 or above indication

for prophylactic fixation.
Figs 5A and B: A case of osteosarcoma of distal tibia

SHORT CASES 17
A B
Figs 6A and B: X-ray of the above patient with sunray appearance
Fig. 7: A girl with osteosarcoma of lower femur

A B
Figs 8A and B: X-ray of the above patient
Fig. 9: MRI of the above patient

SHORT CASES 19
3. ERB’S PALSY
1. Deformity is present since birth
2. History of difficulty in 2nd stage of labor.
Child unable to flex the elbow, supinate the forearm.
Flexion of finger is possible with attitude of waiter’s tip
receiving position (see Fig. 10A).
62. What is prognostic indicator in Erb’s?
• Biceps recovery within 3–6 months of delivery is
of good prognosis.
63. What is the position of limb to be kept in infants?
• Abduction and external rotation of upper limb, this
will relaxed brachial plexus.
64. What is the typical finding in adult X-ray?
• Beaking of acromion.
65. What are the reconstruction procedures available?
1. Shoulder arthrodesis in functional position.
2. Muscle transfer to augment elbow flexion.
A B
Figs 10A and B: A lady with a left side Erb’s palsy and her X-ray
4. EXOSTOSIS
66. How to tell any mass as exostosis?
• Site—Bony swelling around the joint
• Age group—Skeletally immature age group
• Abnormality of the host bone, e.g. shortening,
dysplasia
(Theories of exostosis—periosteal defect theory
and others).
67. Is Exostosis a tumor?
• It is not a tumor. It is a developmental anomaly.
68. Why clinically exostosis appears larger than
X-ray?
• Because of the cartilage cap.
69. What are the complications of exostosis?
1. Mechanical block for joint movement with
adjoining joint
2. Adventitious bursa and pain
3. Fracture of exostosis stalk and pain
4. Malignant transformation.
70. What are the causes of pain in exostosis?
1. Adventitious bursa
2. Fracture of stalk
3. Malignancy.
71. What is the malignancy that usually arises from
exostosis?
• Chondrosarcoma (secondary).
SHORT CASES 21
72. How to identify the malignany of cartilaginous

origin?
• It is difficult even for an experienced pathologist.
73. The cytological features suggesting malignancy are:
1. Water and calcium content > 85%
2. DNA > 5.5 microgram
3. Protein > 350 microgram
4. Keratin sulphate decreased
5. Hexosamine < 75 microgram.
74. What are the other causes of secondary chondro-
sarcoma?
• Fibrous dysplasia.
75. Which has more predilection for malignancy—
solitary or multiple?
• Multiple.
76. What is the importance of the thickness of the
cartilaginous cap?
• Thickness > 6 mm will have more changes of
malignancy.
77. What are the other indicators of malignancy?
1. Haziness of outer cortex
2. Irregular matrix inside the tumor
3. Cartilage cap thickness.
78. How the upper fibular exostosis exposure is done?
1. Exposure is for the common peroneal nerve
2. Nerve is first protected. Then exostosis is resected.
A B C
Figs 11A to C: (A) Exostosis lower femur; (B) X-ray; (C) Exposure
A B
Figs 12A and B: (A) An X-Ray of the leg seen on the side shows
an exostosis arising from the tibia pressing on the fibula;
(B) Exostosis from posterolateral side of leg clinical diagnosed
arise from fibula, if you tell this swelling arises from the tibia
then you have already seen the X-ray shows it actually arise
from the tibia pressing on the fibula
SHORT CASES 23
A B C
D E F
Figs 13A to F: Another case multiple exostosis of right
upper arm, right femur and right tibia
Fig. 14: An exostosis from left clavicle

5. OSTEOMYELITIS
Clinical Findings
Fig. 15: Osteomyelitis of femur
Fig. 16: Another similar case of osteomyelitis

SHORT CASES 25
Fig. 17: Osteomyelitis of tibia
Clinical Findings
 Sinus with discharge
 Warmth in the region around the sinus
 Thickening of bone
 Tenderness
 Growth disturbance—shortening/lengthening
 Pathological fracture
 Deformity.
79. Definition of osteomyelitis?
• Osteomyelitis is inflammation of bone and
marrow (usually blood borne).
80. Why in metaphysis?
1. Vascularity and hairpin loop of capillaries
2. Macrophage activity
3. Slowing of blood.
81. What are the stages of osteomyelitis?

1. Intramedullary abscess
2. Subperiosteal abscess from erosion of cortex
3. Stripping of the periosteum
4. Diaphyseal sequestrum
5. Periosteum forming new bone called involucrum.
82. How to identify sequestrum?
Sequestrum is identified by
1. Ivory white color
2. Smooth side (on the pus)
3. Rough side (Granulation side)
4. Dull note on dropping down
5. Sinks in water whereas a normal bone will float.
A B
Figs 18A and B: Patient femur infected plate and screws

removed with sequestrum the right osteomyelitis
83. What are types of osteomyelitis in adult (Cierny-

Madder)?
Types of osteomyelitis in adult
A. Medullary
B. Superficial cortex
SHORT CASES 27
C. Localized cortical and medullary

D. Diffuse cortical and medullary (unstable)
Host classified as
A—Healthy
BS—Compromise due to systemic factors
BL—Compromise due to local factors
BLS—Compromise due to both local and
systemic factors
C—Treatment worst than disease.
84. Any specific osteomyelitis you know?
1. Tuberculous OM
2. Salmonella OM.
85. What are the areas in which metaphysis is intra-
articular?
• Shoulder, hip and elbow.
86. What are the usual investigations of osteomyelitis?
1. X-ray to see the cavity and sequestrum and to see
formation of mature involucrum
2. Sinogram in chronic osteomyelitis.
87. What is the importance of involucrum from
management perspective?
• It is important to wait for maturation of the
involucrum. Premature opening of window to
remove the sequestrum will end in pathological
fracture.
88. What is the importance of sinogram?
• To curette or remove a sequestrum it is better to
open the window at the site of the sinus rather
than normal bone to not to weaken the cortex in
the already diseased bone.
89. What are the causes of persisting sinus?

1. Nondependant drainage
2. Epithelialization of tract
3. Low grade infection of tract
4. Resistant bacteria
5. Immunocompromised host
6. Presence of foreign body
7. Specific infection like tuberculosis.
90. What is MOTT?
• Mycobacteria other than tuberculosis.
91. What is the investigation of choice in acute
osteomyelitis?
• Three phase bone scan—it differentiates acute
osteomyelitis and cellulitis. Former will have
activity in delayed images and latter has normal
activity in delayed images.
Osteomyelitis of Humerus in a Girl
Fig. 19: Now the disease is quiescent. It is better

to leave her alone
SHORT CASES 29
Fig. 20: Same patient
A B
Figs 21A and B: X-ray for the above patient

Fig. 22: Sinus of thigh—osteomyelitis of right femur
A B
Figs 23A and B: Osteomyelitis of distal tibia with deformity

SHORT CASES 31
6. WINGING OF SCAPULA
92. Differential diagnosis?
1. Weakness of serratus anterior—Involvement of
long thoracic nerve of bell
2. Sprengel’s shoulder
3. Deltoid fibrosis.
• Serratus anterior holds the medial border of
scapula on to the chestwall. So when it is weak,
the medial border becomes more prominent or
winged-long thoracic nerve of bell involvement.
• Sprengel’s—Scapula is smaller and elevated
(Appears to be winged).
• Deltoid fibrosis—There is a fixed abduction
deformity of the shoulder. So when the arm is
brought to the side of chestwall, scapula appears
winged (abduction reduces winging).
A B
Figs 24A and B: (A) Pushing the wall → winging; (B) No

winging on adduction rules out deltoid fibrosis. This is a case
of weakness of right serratus anterior due to viral infection of
the long thoracic nerve of Bell
A B
Figs 25A and B: Abduction causes

prominence of scapula even from front
A B
Figs 26A and B: Abduction does not reduce winging
All the above photographs are of one gentleman with right

side long thoracic nerve palsy.
SHORT CASES 33
7. CUBITUS VARUS
 History of injury to the elbow

 History of massage/splinting
 Patient usually brought for cosmetic purpose.
On Examination
 Deformity (Gunstock)
 Thickening of supracondylar region of humerus
 Range of motion (ROM)—Flexion is restricted usually.
Clinically diagnosed as cubitus varus due to malunited
supracondylar fracture with or without myositis ossificans.
93. What are the areas to be seen for myositis
ossificans?
• Brachialis and triceps.
94. Other joints involved in myositis ossificans?
• Hip.
95. What are the investigations and treatment you will
order?
• X-ray of both elbows—AP in extension—to
compare the carrying angle.
96. What is cubitus rectus?
• When correction of the varus to valgus is
attempted if the lateral wedge of bone is taken
less then it results in neutral and not valgus.
97. What is the cause of the varus?
1. Medial tilt of the distal fragment of the
fracture.
2. Increased bone formation on the lateral side

probably due to the weight of the limb.
Plan: Corrective osteotomy and internal fixation
• French osteotomy
• Step cut osteotomy.
99. The patient is in skeletally immature age group.
Will you not allow for remodelling?
• This deformity is in the coronal plane.
Remodelling can only occur in the plane of
movement of the joint, i.e. flexion and extension.
In elbow, there is no movement in the coronal
plane. Hence remodelling is not possible and
hence the osteotomy.
Fig. 27A: Gunstock deformity on the left side

SHORT CASES 35
Fig. 27B: On flexion the deformity disappears
Fig. 28: The gunstock deformity on the left side in another case
8. CUBITUS VALGUS
Fig. 29: Cubitus valgus
 History of injury
 History of massage.
On examination: Deformity of valgus > normal side
 Irregularity over lateral condyle
 Abnormal mobility may or may not be present
 Patient may have ulnar neuritis
 ROM—Reasonablly maintained.
Plan:
100. What will you see in the X-ray?

• Confirm the mal/nonunion
• Usually it is difficult to identify the fracture.
SHORT CASES 37
9. TARDY ULNAR NERVE PALSY

101. How will you prevent tardy ulnar nerve palsy?
• Anterior transposition of ulnar nerve.
Fig. 30: Tardy ulnar nerve palsy
102. When will you do bony correction?

• Osteotomy at second stage.
• Bone grafting to unite the lateral condyles with
minimal fixation.
103. Why do you need an osteotomy?
• To reduce undue loading of medial side of joint.
104. What is the type of osteotomy?
• Step cut osteotomy.
105. What is the cause of this condition?

• Associated with progressive cubitus valgus due
to epiphyseal arrest of the lateral condyle and
progressive growth of medical epiphysis.
Commonly after epiphyseal injury involving
lateral condyle, or humerus.
106. What will the patient complain?
• The patient complain numbness of medial one
and half fingers and weakness of fingers
(intrinsic weakness).
107. Before attempting any treatment what will you
order or do?
• Nerve conduction studies.
108. What is the treatment?
• Early cases—anterior transposition of ulnar nerve
physiotherapy to the finger should be decided not
later than three months of injury.
• Later cases—as for ulnar claw hand—tendon
transfers.
109. What is cubital tunnel syndrome?
• The groove behind the medial epicondyle may be
shallow in some individuals. So after a trauma
may not be related to this region but a
supracondylar fracture, etc. the patient may
experience numbness and weakness of the region
of the ulnar nerve.
SHORT CASES 39
110. What is the treatment for this syndrome?

• Extension splint—neurovitamins—for a period of
three months from injury. Nerve conduction
studies are done and the slowing or no
conduction is confirmed and anterior trans-
position of ulnar nerve is done.
111. What is the complication of this surgery?
• Temporary to permanent loss of ulnar nerve
function is a known complication.
10. LATERAL CONDYLE NONUNION
Fig. 31: Lateral condyle fracture of left elbow

 History of injury/indigenous treatment and massage
 Deformity of elbow in the form of cubitus valgus
 Bony irregularity/abnormal mass of the elbow over the
lateral condyle
 Relative mobility of the mass to be tested against the
humerus.
Treatment: Same as for cubitus valgus.
112. If you have lateral condyle fracture with no
abnormal mobility but X-ray shows no callus.
How will you explain?
• Patient is having fibrous union.
113. Why should this fracture have so common to
undergo process of nonunion?
• The fracture ends are not opposed to each other.
In fact the distal fragment rotates 180° and both
fracture surfaces are facing laterally.
SHORT CASES 41
11. MALUNITED INTERCONDYLAR

FRACTURE
Patient presents with stiffness of elbow, History of injury/
indigenous treatment.
114. What will be the usual violence?
Fall on the point of elbow.
On examination:
• Intercondylar distance widened
• Range of movements restricted
• Fixed flexion deformity present
• May or may not be myositis.
115. What is the treatment of choice?
• The bony union is assessed and confirmed with
radiographs.
• Arthrolysis can be done to improve the range of
movement.
12. UNREDUCED DISLOCATION OF ELBOW

History of injury.
 Indigenous treatment usually in extension
 Difficulty in movement of elbow.
On examination:
 Fracture disease + over entire upper limb
 Skin shiny/loss of hair +
 Triceps standing out (Tendo Achilles sign of triceps).
Fig. 32: Look for ulnar nerve palsy

• Open reduction of the dislocation and
mobilization.
117. Any other procedures to reduce instability?
• Anterior bone block-surgery
• Anterior transposition of triceps.
SHORT CASES 43
13. POST-TRAUMATIC
STIFFNESS OF ELBOW
• History of injury/indigenous massage
A B
Figs 33A and B: Reaching the mouth;

(B) Available extension
Fig. 34: Another case attempting to reach the mouth

Fig. 35: X-ray of the above patient
118. Should they always have a bony injury?

• May or may not have bony injury.
119. What are the common findings?
• Range of movement of elbow restricted.
• Irregularity of any of the bony prominence.
(Lateral supracondylar ridge, lateral condyle,
radial head, olecranon, medial epicondyle,
medial supracondylar ridge in that order is
palpated).
SHORT CASES 45

Conservative treatment:
• Indomethacin
• Low dose radiation
• Active mobilization.
121. If no improvement with this conservative treatment,
what is your plan?
Adhesiolysis.
14. ARTHRITIS OF ELBOW
 Pain and swelling

 History of injury (May or may not be)
 History of fever/Morning stiffness.
On examination:
 Tenderness and diffuse swelling on either side of
olecranon (Common site to look for synovial swelling).
 Tenderness over radial head, lateral condyle, on either
side of olecranon.
 To see axillary and supraclavicular nodes
 To see other joint movements.
122. What is your clinical diagnosis?
• Tuberculosis/Rheumatoid arthritis
123. How will you proceed?
• Investigation for above two diseases. The X-ray
and blood investigation.
• Synovectomy or excision elbow and anti-
tubercular therapy (ATT)—for tuberculosis
• Synovectomy and antirheumatic drugs and joint
replacement—for rheumatoid arthritis (RA).
125. Joint replacement should not be done in?
• Main contraindication is active infection.
SHORT CASES 47
15. CONGENITAL RADIOULNAR

SYNOSTOSIS
Child brought with complaints of inability to receive
objects (supinate)—usually bilateral.
On examination:
 Restricted supination (Rotation)
 Hypermobility of wrist joint
 Forearm fixed in pronation.
126. What are the types of congenital radioulnar
synostosis?
Three types:
1. Upper radius imperfectly formed no head and
fused with ulna
2. Ill formed head/radius attached by a thick
introsseous ligament near the coronoid
3. Head is present malformed—fused with upper
ulna 80% bilateral.
127. What is the differential diagnosis?
• Differential diagnosis: Pulled elbow.
• Leave alone the child if the child is comfortable.
Usually they have hypermobility of the wrist joint
and can adjust to all movements except the
supination.
• If the parents prefers a surgery to correct deformity
only—inspite of thorough explanation regarding
a poor outcome—only a corrective osteotomy and
fixation with forearm in supination can be done.
16. FRACTURE MEDIAL EPICONDYLE
On examination:
 Look for any irregularity of medial epicondyle
 Carefully see for any involvement of ulnar nerve.
• Non-union → small fragment → excision
• Non-union → large fragment → fixation.
130. What will the patient complain in an ulnar nerve
involvement?
• The patient complain numbness of medial one
and half fingers and weakness of fingers
(intrinsic weakness).
131. Before attempting any treatment what will you
order or do?
• Nerve conduction studies.
• Early cases—wait for 3 months treating with
conservative methods anterior transposition of
ulnar nerve physiotherapy to the finger should be
decided not later than 3 months of injury.
• Later cases—as for ulnar claw hand—tendon
transfers.
133. What is cubital tunnel syndrome?
• The groove behind the medial epicondyle may be
shallow in some individuals. So, after a trauma
may not be related to this region but a
SHORT CASES 49
supracondylar fracture, etc. The patient may

experience numbness and weakness of the region
of the ulnar nerve.
134. What is the treatment for this syndrome?
• Extension splint and neurovitamins—for a period
of 3 months from injury. Nerve conduction studies
are done and the slowing or no conduction if
confirmed, anterior transposition of ulnar nerve
is done.
135. What is the complication of this surgery?
• Temporary to permanent loss of ulnar nerve
function is a known complication.
17. MALUNION OF BOTH BONES FOREARM

 History of native treatment and massage
 Angulation present
 Rotations restricted
 Patient will have stiffness of fingers
 Patient may have Volkmann’s ischemic contracture
(VIC)—should look for Volkmann’s sign.
A B
Figs 36A and B: Malunion with still acceptable function
A B C
Figs 37A to C: Malunion with still acceptable function

SHORT CASES 51

• Corrective osteotomy, realignment, bone grafting
and fixation are indicated if the patient has
functional disability, e.g. reaching his mouth.
A B C
Figs 38A to C: Malunion with poor function, he needed

corrective osteotomy and fixation
18. GALEAZZI FRACTURE DISLOCATION

 Deformity of radius
 Prominence of ulna
 May or may not be transmitted mobility according to
union.
Pathology
 Shortening and angulation of radius
 Disruption of distal radioulnar joint (DRUJ).
136a. What are the treatment options?
• Open reduction internal fixation
• If necessary transfixation of distal ulna with
radius
• Stabilization of DRUJ with K wire.
SHORT CASES 53
19. SUDECK’S OSTEODYSTROPHY (RSD)

 Radiological term extended to a clinical condition
 Spotty decalcification is distinguished from generalized
osteoporosis
 Shoulder hand syndrome its another for this condition
 Reflex sympathetic dystrophy (RSD) is a group of
conditions occurring after trauma classified into minor
causalgia, major causalgia, minor traumatic injury,
major post-traumatic injury
 This is caused by exaggerated response to post-
traumatic conditions
 Pain, hyperesthesia and tenderness out of proportion
to the physical findings and in non anatomic sites not
connected to original injures
 Early stages—There is redness and warmth
 Later stage—Pallor, dry shining skin and coolness.
137. What are the stages of RSD?
There are 3 stages
• Stage 1: Burning, aching and pain.
• Stage 2: Edema, cold glossy skin and joint
stiffness.
• Stage 3: Progressive atrophy of skin and muscle
and significant joint contracture.
From 2nd stage Sudeck’s is prominent.
Shoulder hand syndrome is a variety of this
condition.
• Initially physiotherapy, calcium, calcitonin can be
tried along with analgesics.
• Later on sympathetic block.
• Progressive loading of extremity and progressive

resistant exercises.
139. What is the cause of the symptoms?
• Short circuiting of nerves
• Hence the nonanatomic pain.
A B
Figs 39A and B: Sudeck’s osteodystrophy
140. What is the X-ray finding?

• Speckled decalcification.
SHORT CASES 55
20. VOLKMANN’S ISCHAEMIC

CONTRACTURE
 History of trauma
 Native treatment and massage
 Difficulty in using the limb.
A B
Figs 40A and B: During acute ischemia
Fig. 41: Volkmann’s ischemic contracture (VIC)

On examination:
 Wrist and fingers in flexion
 Look for sensations ulna/median nerve
 Dorsiflexion of wrist increases the deformity
 Skin will have atrophic changes, dry and scaly
 In the case of forearm VIC, fingers can be atleast
partially extended when the wrist is flexed
(Volkmann’s sign). (This is because when the wrist is
extended, the shortened muscle tendon unit stretches
over the fingers causing extension.)
 Atrophy of forearm muscles, nail atrophic.
141. What is the pathology?
• Sequel to Volkmann’s ischemia, muscle undergoes
ischemic necrosis and replaced by fibrous tissue
which causes flexion-contracture of wrist and
fingers. There may be peripheral nerve involve-
ment with sensory loss and motor paralysis of
hand and forearm.
142. What is Volkmann’s sign?
• The flexion deformities of the fingers is becoming
partially correctable with a flexed wrist
• The deformities become more pronounced when
the wrist is dorsiflexed.
• Passive stretching and splinting
• Soft tissue (muscle) sliding operation (Max page)
• Shortening of forearm bones—Garre’s procedure
• Carpal bone excision
• Neurolysis of nerves.
SHORT CASES 57
144. What nerve is commonly involved in VIC of

forearm?
• Median nerve.
145. Why?
• It runs in the centre of the maximum infarcted
zone of muscle supplied by anterior interosseous
artery.
• This muscle can sometimes called as ‘muscle
sequestrum’ as it is separated by fibrous tissue from
the normal muscle.
146. What is Volkmann’s sign?
• On flexing the wrist passive extension of fingers
is possible.
21. OSTEOCLASTOMA
Cause of pain, difficulty in walking or using the upper limb
or presents with abnormal mobility (pathological fracture).
 Difficulty in using limb after trivial fall (pathological
fracture).
 Age : Middle age group (20–40).
 Incidence more in females.
147. What is the common presentation of osteoclastoma?
• Swelling arising from the bone near a joint
especially around the knee or distal end of radius
(End of long bone) may be painless to startwith.
148. Can we diagnose osteoclastoma clinically?
• Clinically it should not be diagnosed as
osteoclastoma.
• It is better to say as benign bone tumor most
probably giant cell variant osteoclastoma.
149. How will you diagnose osteoclastoma?
• In X-ray we can see expansile eccentric lesion, in
the end of long bone.
150. What are the types of osteoclastoma?
• Aggressive—No sclerosis between tumor and host
bone (Surrounding bone has no time to react).
• Nonaggressive—Sclerosis present.
Intralesional
• Curettage
• Adjuvant cryotherapy/cautery
SHORT CASES 59
• In packing with bone cement—heat produced

during the setting of cement kills residual cells
• Packing the defect with bone graft or substitute
• Excision if the bone is expendable. If the lesion
is too big-excision and reconstruction.
Reconstruction includes arthrodesis, arthro-
plasty.
• Radiotherapy for inaccessible lesions.
152. What is significant bone defect?
• A defect in bone > 1.5 times the diameter of bone
never heals by itself (JA Key).
153. What is the appearance of an aggressive tumor in
X-ray?
• Doesn’t have sclerosis of margin because it
doesn’t allow time for the surrounding bone to
react.
154. What are the X-ray findings in GCT?
• Eccentric expansile lesion with typical soap
bubble appearance
• Thinning of cortex with/without sclerosis of
margin
• Tumor doesn’t enter the joint
• Usually no calcification.
155. What are the giant cell variants?
• Osteoclastoma
• Fibrous cortical defect
• Nonossifying fibroma
• Chondromyxoid fibroma
• Brown’s tumor of hyperparathyroidism
• Osteoblastoma
• Solitary bone cyst
• Aneurysmal bone cyst
• Recently, giant cell rich osteosarcoma.
156. How will you diagnose gaint cell tumor (GCT)?
• Presence of giant cells.
157. What is the tumor cell of giant cell tumor?
• Fibrous stromal cell (undifferentiated spindle
cells).
158. What is egg shell crackling?
• It is due to fracturing of osteoclastoma by deep
palpation.
159. What is the cell of origin of GCT?
• Unknown.
A B
Figs 42A and B: Osteoclastoma of right lower tumor

SHORT CASES 61
Fig. 43: GCT of distal femur same patient in Figure 42
A B C
Figs 44A to C: X-ray and CT Scan of the above case
A B C
Figs 45A to C: Recurrent GCT after distal radius

excision and fibular grafting
22. NEGLECTED SHOULDER DISLOCATION

160. What is the nature of injury?
• Fall on out stretched hand.
A B
Figs 46A and B: (A) Loss of contour of shoulder;

(B) Cannot touch opposite shoulder
Fig. 47: Flattening of shoulder (Patient should

sit with both shoulders bare)
SHORT CASES 63
161. What are the clinical findings?

On examination:
• Loss of contour of shoulder/flattening
• Anterior axillary fold is at lower level (Bryant’s
sign)
• Patient is not able to touch opposite shoulder
(Dugas test)
• Vertical circumference at axilla is increased
(Callaway sign)
• Hamilton ruler test positive, i.e. ruler kept on lateral
condyle will not touch the acromion normally
because of resistance of head of humerus. In a
dislocated case, the ruler touches the acromion.
Fig. 48: A case of fracture-dislocation shoulder

• Depends on age
• Open reduction (if patient is young)
• Mobilization (if old patient).
23. FRESH DISLOCATED ELBOW

History of injury and deformity
Difficulty in moving the limb.
On examination:
 Triceps is taut and standing out (Tendo-Achilles sign
of triceps)
 Three bony points altered relationship between
olecranon, medial epicondyle and lateral condyle of
humerus.
 Flexion of elbow restricted
 Olecranon protrudes abnormally out
 Test other bony point like the entire lower humerus,
medial epicondyle, lateral condyle, radial head and
look for ulnar nerve involvement.
163. What is the treatment in fresh and neglected
dislocated elbow?
• For fresh dislocation → closed reduction
• Above elbow slab in 90° flexion for 3 weeks.
164. What are the treatment options for neglected
dislocated elbow?
• Open reduction—Posterior approach—protecting
the ulnar nerve
• Transposition of triceps anteriorly
• Bone block surgery.
SHORT CASES 65
A B
Figs 49A and B: (A) Case of dislocated elbow (neglected);

(B) Another case of fresh dislocated elbow
24. NONUNION OF BOTH BONE FOREARM

 History of injury to forearm
 History of immobilisation
 Cause of difficulty in using forearm especially rotation
 Stiffness of hand and wrist
 May or may not have VIC/atrophic changes of hand.
On examination:
 Deformity of forearm more obvious if fracture is in ulna
(subcutaneous)
 Loss of transmitted mobility on radial head on
supination/pronation
 Defect or abnormal mobility in ulna
 Look for scars over site of fracture (May have loss of
bone or primarily open fracture).
Plan: ORIF with plate and screws, square nail and bone
grafting
Square nail is otherwise called ‘Talwalkar‘s nail’
165. How will you identify rotation in nonunion?
• In nonunion there is no spikes to interdigitate.
• Ends are sclerosed so rotation is matched by
interosseous border.
166. In fresh cases which is the first bone you will fix—
radius or ulna?
• Less comminuted bone first.
167. What is the common complication of a both bone
fracture surgery?
• Posterior interosseous nerve palsy
• Tourniquet palsy.
SHORT CASES 67
25. BRACHIAL PLEXUS INJURY
Fig. 50: Cut injury involving shoulder—injuring

the brachial plexus
History of Road Traffic Accident.

 Head separated violently from shoulder resulting in
stretching of nerve or deep cut in the shoulder region
 Thrown from two wheeler or fall from height
 Handedness of individual is important
History of pre-existing pain neck
 Should ask if weakness was static/worsening/improving
 Occupation—manual labour or clerical
 Activities done at present
 Past history of hospitalization, epilepsy, congenital

disorders.
On examination: patient will not be able to move his entire
upper limb.
Attitude: Waiter’s tip receiving position in Erb’s palsy
totally flail upper limb in total brachial plexus injury.
 Wasting of deltoid supraspinatus, infraspinatus and
Pectoralis major
 Atrophic changes of hand
 Hair loss
 Dermatomal pattern
 C1—purely motor
 Examine for motor power of upper limb—shoulder,
elbow, wrist and hand (Should not be examined for
separate nerves)
 Sensation tested according to the dermatome
 Reflexes elicited—Biceps, triceps, supinator
 Autonomous—Ciliospinary reflex, Horner’s syndrome
 Muscle power—Muscles of scapula—Serratus anterior,
rhomboids.
Power of the above Case

 Shoulder abduction—weak
 Elbow flexion—0
 Supination—0.
168. What is wrinkle test?
• Put the hand in water for five minutes, appea-
rance of wrinkles show intact of nerves.
SHORT CASES 69
A B
Figs 51A and B: A case of partial brachial plexus
169. What is axonal reflex?

• The skin is scratched through a drop of
histamine. A sequence of vasodilatation, wheel
and flare are noted.
• If the nerve is injured proximal to ganglion with
anesthesia in the region the above reflex is noted.
• If the nerve is injured distal to the ganglion
with anesthesia the flare is absent in the sequence.
170. What is sweat test?
• Presence of sweating after testing with Quinizarin
dye indicates nerve intact.
171. How will you diagnose a case?
• Complete, incomplete brachial plexus
• Open, closed
• Recovered, not recovered
• Preganglionic and postganglionic lesions.
172. What are the investigation you will order?

• X-ray cervical spine—Anteroposterior, Lateral-
Look for fracture of transverse process
• Myelogram after 6 weeks (Pseudomeningocele
effect)
• MRI
• Electroneuromyography (ENMG).
173. What are the poor prognostic indicators in brachial
plexus?
• All the five nerves involved (C5 – T1)
• First nerves involved (Nerve to levator scapula,
rhomboids)
• Supraclavicular anesthesia
• Pain in anesthetic limb
• Horner’s syndrome
• Avulsion of transverse process in X-ray.
174. How to test supinator?
• I will extend the shoulder and elbow—so that only
supinator not biceps longus will act.
175. How to differentiate peripheral nerve and plexus
injuries?
• Peripheral nerve injury pattern follows
innervation of nerve.
• Plexus injury involves root or trunk dermatomal
pattern.
For example consider—C5C6 injury and muscul-
ocutaneous nerve injury.
In C5C6 root injury, patient will have sensory loss
over outer aspect of arm and shoulder and lateral
aspect of forearm and hand. Patient will also have
SHORT CASES 71
loss of abduction of shoulder, flexion of elbow.

Weakness of dorsiflexion of hand, supination of
forearm.
But in musculocutaneous nerve injury which has
C5C6 root value patient will have only sensory loss
over lateral aspect of forearm and weakness of elbow
flexion only.
176. How to test autonomous nervous system?
• Alizarine test
• Looking for skin changes loss of hair
• Wrinkle test.
177. Can you test subclavius?
• It is difficult to test subclavius. It is one of the
accessory inspiratory muscles.
• It is a shoulder girdle muscle arising from the
undersurface of clavicle going on to first rib and
cartilage.
• Innervated by C5, C6 roots.
178. What are the components of Horner’s syndrome?
• Ptosis, Miosis, enophthalmos, anhidrosis, no
ciliospinal reflex.
179. How to classify?
• Leffert’s classification.
180. What else will you examine?
• Examine passive movements of joints of the same
side, cervical spine and opposite upper limb.
181. What are the other causes of plexus injuries?
• Lathyrism, irradiation, neurotoxins.
182. What are the contractures in plexus injuries?

• Shoulder—Adduction, internal rotation
• Elbow—Flexion, pronation
• Fingers—Flexion.
183. What is the relationship between prognosis and
recovery time?
• In infants, good prognosis—if biceps recovers in
less than 3 months—good recovery.
• If it occurs 3–6 months partial recovery.
• If not recovered even after 6 months— difficult.
184. In Erb’s palsy, good recovery in what lesion?
• Post ganglionic C5C6.
185. What is the EMG in 1st hour after injury?
• Normal.
186. When will you do nerve procedures?
• Nerve procedures—Nerve suturing/grafting/
repair within 2 years.
187. Why so?
• Neuromuscular junction degenerates within 2
years
• After 2 years—Tendon transfer and muscle
transfer can be done
• Joint fusion of joints like shoulder.
188. What are the ways of nerve repair?
• Mobilization, nerve grafting, joint positioning.
189. What is the classification of brachial plexus injury?
Leffert’s classification
1. Open
SHORT CASES 73
2. Closed
• Supraclavicular—supraganglionic, infra-
ganglionic
• Infraclavicular
• Postanesthetic palsy
3. Radiation injury
4. Obstetric palsy.
190. When is Tinel’s sign not useful?
• Neuropraxia, cut injuries without any nerve
repair.
191. When will you interfere in Tinel’s?
• No progression of Tinel’s
• Nonanatomical progression
• Slow progression.
192. Imaging of choice to identify suspect lesion of
brachial plexus?
• MRI.
• Initial phases—Splinting, pain control, prevention
of contractures
• Late phase—Muscle strengthening, reeducation of
muscles, modication of splints TENS to control
pain.
Acute phase—
1. Preganglionic—no surgery
2. Postganglionic—nerve suturing
• Late phase—muscle/tendon transfer
• Shoulder—transfer of trapezius/arthrodesis
• Elbow—latissimus dorsi
• Reeducation of transferred muscles.
26. TORTICOLLIS
 Contracture of sternocleidomastoid
 Occiput turned to same side and chin to opposite side
 Later—facial asymmetry and visual disturbance
 Child—congenital, infection, muscle, primary visual
problem, trauma to spine are the causes to be ruled out.
• Splinting with collar passive gentle stretching
• In resistant cases unipolar or bipolar release —
before visual area fixation in brain (early
childhood).
Fig. 52: A child with left side sternomastoid contracture

seen from front and back
SHORT CASES 75
27. CEREBRAL PALSY

Cerebral palsy is a nonprogressive neurological disorder.
Types
 Prenatal
 Natal
 Postnatal.
Patient will have variable degree of mental retardation,
difficult in muscle coordination.
Difficulty in walking and doing activities of daily living.
Fig. 53: Cerebral palsy

195. What questions will you ask in the birth history?

• Antenatal history
– Drugs
– Antiemetics
– Anticonvulsant
– Diabetic mother
• Birth at
– Hospital or home
– Delayed 2nd stage of labor.
196. What is the importance of the first cry?
• The pulmonary circulation—pressure (Pulmonary
resistance) is reduced as the solid lung becomes
aerated.
197. What are the detailed milestones?
• Social smile, lying prone, crawling, sitting,
standing, walking normal, hearing, speeching
bowel or bladder control.
198. What are the types of patient/children with CP?
• Various types are shown in Figures 54 to 56.
Fig. 54: Group A—Can do activities of daily living by themselves

SHORT CASES 77
Fig. 55: Group B—Can do activities of

daily living with help
Fig. 56: Group C—Completely depend on others

for daily living, bed ridden
199. What is the diagnostic typing for treatment?

• Normal independent child
• Mild MR needs help for many of her activities
• Totally bed ridden
On examination:
• General attitude
• Whether cooperating for examination
• IQ of the child
• Spine examination, stability in sitting and standing
• Deformities of spine
• Scoliosis in sitting position is significant
• Scoliosis exists with lordosis
• Power of all limb muscles and contractures of
joints.
A B
Figs 57A and B: Patients with cerebral palsy require

help for their activities
SHORT CASES 79
200. What is the precaution during muscle testing?

• Do not allow the child to recruit other muscles.
201. Spastic muscle is not a strong muscle why?
• Because power involves voluntary act of the
muscle not spastic contractions (MRC grading).
202. What is the maximum power you can give in case
of a fixed deformity?
• For fixed deformities, power for reverse movement
is given at grade 1 MRC grading only. For example,
in equines ankle dorsiflexor power is assessed by
palpating the contraction of tibialis anterior.
203. How will you assess equinus?
• Equinus or Forefoot drop.
204. How to Dorsiflex?
• Dorsiflex holding up the talar head with thumb.
205. What are the invertors of ankle?
• Tibialis anterior is the invertor in dorsiflexion of
ankle
• Tibialis posterior is the invertor in plantar flexion
of ankle.
206. Why to test hip abduction in knee flexion/knee
extension?
• The hamstrings are relaxed in flexion of knee and
hence you get more abduction of hip in knee
flexion.
207. Gait in Cerebral palsy?
• Scissoring.
208. What are the main points in a cerebral palsy (CP)

child examination?
• Higher function
• Muscle group spasticity
• Deformities
• Sitting balance
• Gait.
209. How will you assess the power of muscles in a CP
a child?
• Spastic muscle is not a strong muscle. Strength is
measured as power and spasticity is involuntary.
Hence spasm is not power. Only when the child
understands and does the movements voluntarily
then we can assess the power of the muscles in
a CP child.
210. What is the maximum power given to the muscle
which has a reverse deformity?
• In fixed flexion deformity maximum power of
extensor is only 1/5.
211. What is birthday syndrome?
• If child is not assessed properly by the team of
spastic care, then the child will spend each
birthday in hospital for some surgery. Hence it is
better to assess the child and do all surgeries in
a single stage.
212. What is reciprocating gait?
• As the child is made to walk with support
then he can alternately bring one lower limb in
front of other.
SHORT CASES 81
213. What is the role of tendon lengthening in deformity

correction?
• Open tendon lengthening is not advised now-
adays
• Closed tendon lengthening, fractional lengthening
is the in thing in CP.
Fig. 58: Tendon lengthening
214. What is the measure of equinus?

• The heel to ground distance.
215. What are the recent advances in CP?
• Recent advances in CP
• Not just lengthening of tendons
• Ability assessment
• Occupational therapy,
• Physiotherapy
• Spasm relieving orthosis spasm relieving brace

(footwear)—given upto tip of toe for lower limb,
initialization of spasm is relieved
• Intrathecal baclofen depot—no sedation, patient
attender can control dose
• Gait analysis before and after surgery
• Selective dorsal rhizotomy
• Fractional lengthening of tendons
• Nerve blockades. Regional nerve blocks can be
tried first before neurectomy
• Block with lignocaine and look whether spasm
is relieved or not, then neurectomy is done.
(Phenol may be used for permanent neurectomy)
• All surgical procedures in one stage
• Helps in rehabilitation of the child
• Avoid birth day syndrome
• Botulinum toxin—costly but useful.
216. What are the procedures in CP, done by orthopedic
surgeons?
• Hip—Adductor tenotomy, obturator neurectomy
• Knee—hamstring release
• Foot → valgus - leave alone
Varus—osteotomy
• Fractional lengthening of tendons.
217. Where tendo- Achilles lengthening should not be
done?
• Equinus correction should not be done when
quadriceps power is less than three.
SHORT CASES 83
218. How will you differentiate the cause of equines

soleus or gastrocnemius?
• Silfverskiold test—The equinus is mainly due to
gastrocnemius only if equines gets corrected in
knee flexion. If there is no correction then it is both
gastrocnemius or soleus causing equines.
219. Importance of the first cry?
• Air enters the erstwhile solid lung.
• The pulmonary oxygenation occurs.
• Pressure on the left side of heart becomes more
than right side.
• Functional closure of foramen ovale occurs.
220. What is APGAR scoring?
• Appearance
• Pulse-Rate
• Grimaces
• Activity
• Respiration.
Fig. 59: Inability to walk in a child with cerebral palsy

28. WRIST DROP
Fig. 60: Clinical sign due to weakness of dorsiflexor

of wrist and extensor of finger
Clinical Findings is as Seen in Figure 60

Anesthesia present over 1st web space over the dorsal
aspect. The entire course of radial nerve is palpated and
to looked for tenderness (Nerve ends at the level of lateral
condyle and continues as posterior interosseous nerve to
midpoint of wrist).
Treatment
 Initial—splinting in volar cock-up splint, electroneuro-
myography
SHORT CASES 85
221. What is Holstein Lewis syndrome?

• Post manipulation radial nerve palsy in humerus
fracture.
• Lower fragment with lateral spike catches the
nerve inside fracture.
222. What is the treatment of Holstein Lewis syndrome?
• Immediate exploration and release of nerve and
reduction and fixation of fracture.
223. What is the treatment of open injury of the nerve
(Neurotmesis)?
• Debridement of the wound.
• Secondary nerve repair in centre of specialis-
ation of peripheral nerve surgery.
224. When will you do nerve repair/grafting?
• Nerve repair/grafting less than 2 years (when
myoneural junction is still viable)
225. When will you do tendon transfer more than 2
years.
• Median nerve muscles are transferred to hand
• Pronator teres to wrist dorsiflexion
• Flexor digitorum superficialis (FDS) of ring finger
to all finger extensors
• Palmaris longus for thumb extension.
226. What is autonomous zone?
• It is that part of skin supplied only by the nerve
in question and not by any other nerve.
227. What is maximal zone?

• If the other nerves, e.g. the median and ulnar are
completely blocked, still some area of these nerves
will retain sensation. This is due to the supply of
radial more than its anatomic area.
228. What is anatomical area of this (radial) nerves?
• This area is described in anatomy books as
supplied by radial nerve that is the dorsum of
hand and fingers.
SHORT CASES 87
29. CLAW HAND
Figs 61A and B: Two different cases of claw hands

Fig. 62: See the flexion of the left thumb of this patient is on the
right side wearing watch. ‘Claw’ is the hyperextension of MCP
and hyperflexion at IP ulnar claw—leprosy, ulnar nerve injury
229. Cause of claw hand.

• Intrinsic minus hand.
230. What is the autonomous region of ulnar nerve?
• Medial side of the distal phalanx of the little
finger.
231. Why claw hand develops? (Intrinsic minus)?
• Intrinsic muscle flex metacarpophalangeal joint
(MCP) and extend the interphalangeal (IP).
• When intrinsic muscles are paralysed there is
unopposed action of long flexors and extensors.
Long flexors cause IP flexion
• Extensors cause MCP extension.
SHORT CASES 89
232. What is the treatment of claw hand?

• Physiotherapy to keep the joints supple
• Paul Brand I—Extensor carpi radialis brevis (ECRB)
• Paul Brand II—Extensor carpi radialis longus
(ECRL)
• Total claw—4 tail transfer.
233. Why in Paul Brand II—ECRL is used?
• Because ECRB was a bulky muscle.
234. Where in India this pioneering work was done and
by whom?
• Work done in CMC Vellore by Professor Paul-
Brand and Professor AJ Selvapandian.
235. What is ulnar paradox?
• When the nerve lesion is proximal the deformity
is less.
• When the nerve lesion is distal the deformity is
more.
RELATED QUESTIONS
236. What is intrinsic plus hand?
• When patient flexes actively his finger, finger goes
for extension-action through lumbricals.
1. Complication of amputation
2. Severance of Flexor digitorum profundus (FDP)
3. Loose graft of FDP
4. Avulsion of FDP.
237. What is quadriga effect?
• Tight-repair or shorter graft—repaired finger goes
for flexion faster than other fingers in the same
musculotendinous group.
Fig. 63: Clawing

• In the other nerves, e.g. the median and radial are
blocked still some of the area of those nerves will
retain sensation. This is due to the supply of
ulnar more than its anatomical area. This is called
the maximal zone of ulnar.
240. What is anatomical area?
• This is described in anatomy books as to medial
1½ fingers and adjoining hand (the volar aspect).
SHORT CASES 91
30. RADIAL CLUB HAND

Congenital—bilateral
Child has extreme radial deviation of wrist, thumb touching
forearm.
Contracture of radial side of wrist.
X-ray: Partial/total absence of radius (Tetralogy of Fallot—
absence of radius).
241. What surgical treatment you will offer?
• Initial splinting, later excision of lunate and wrist
arthrodesis with centralization of ulna.
Fig. 63A: A child with radial club hand

31. COMPOUND PALMAR GANGLION

 Swelling on either side of flexar retinaculum
 Cross fluctuation +
 Not much of tenderness
 Usually TB, osteoporosis of carpal bone
 Crepitus from the “Melon seed bodies “
 ‘TB tenosynovitis of ulnar bursa’—chronic cases hour
glass swelling above and below the carpal ligaments
 Finger tightly flexed.
242. What is Kanavel’s sign?
• Tenderness over the ulnar aspect of palm—in
cases of ulnar bursa inflammation.
• Investigations as for TB.
243. What is the treatment for compound palmar
ganglion?
• Antitubercular treatment.
Fig. 63B: Case of compound palmar ganglion of wrist

SHORT CASES 93
32. NEUROPATHIC JOINT

 Elbow, knee and sometimes ankle
 Acquired in the 4th decade
 Joint is excessively swollen, not much of pain, crepitus,
abnormal mobility
 Patient may have findings of laminectomy, syringo-
myelia, meningocele
 Sensory examination should be thorough.
 Any swollen painless joint should be suspected for
neuropathy
 X-ray—excessive degeneration with loose bodies
 Rule out tabes dorsalis (VDRL), syringomyelia, (MRI)
spine (laminectomy).
Treatment
 Splinting
 More prone for infection—loss of limb.
244. What treatment you will never do or tell in this case?
• Arthroplasty not to be told/fusion may be tried
• Contraindication for arthroplasty or fusion may
also be difficult
• More prone for infection.
Fig. 63C: Case of neuropathic ankle joint

33. CARPAL TUNNEL SYNDROME

 Patient will complaint of paresthesia over palm more
over thenar aspect
 Phalen’s test positive—Flexion of wrist for 30 seconds
reproduces symptoms
 Most common in myxedema, pregnancy.
• Initial—diuretics, control of myxedema.
246. What is the treatment in resistant cases?
• Resistant cases can be subjected to nerve
conduction tests and carpal tunnel release can be
done.
Fig. 63D: Carpal tunnel syndrome with wasting

of left thenar muscles
SHORT CASES 95
34. DUPUYTREN’S CONTRACTURE

 Fibrosis and contracture of MCP joint
 Thickening of palmar fascia—little and ring finger
 Feel of nodularity of affected finger
 Fibrous strand cross the crease into the affected finger
 Grading of Dupuytren’s.
Treatment
 Splinting, open release.
Fig. 64: Dupuytren’s contracture with involvement of PIP

joint of little fingure bilaterally
35. SPINA VENTOSA

 Swelling of phalanges
 Spina—“ache” as produced by spike/thorn
 Ventosa—fusiform.
247. What is the cause and treatment for this?
• TB osteomyelitis and anti-tuberculous treatment
should be started followed by curettage.
248. What differential diagnosis you will think of?
• Enchondromata.
Fig. 64A: A case of spina ventosa

SHORT CASES 97
36. MALLET FINGER (BASE BALL FINGER)
Fig. 65: Mallet finger
Characterized by flexion of DIP joint due to avulsion of long

extensors from the distal insertion/passive extension is
possible in early cases.
249. What would be the X-ray picture?
• Avulsion of distal phalanx.
• Volar splinting with DIP joint extension—6 weeks
in early cases
• Repair and suturing by a transverse elliptical
incision, if presented late.
37. FOOT DROP
Figs 66A and B: Foot drops; (A) In a child on his left side;
(B) An adult on his right foot
 History of injury to leg or spine or surgery knee or tumor
 Cause of difficulty in lifting toes of the ground
 Patient cannot walk with heel strike.
SHORT CASES 99
On examination:
 Foot in equinus
 Tibialis anterior is weak
 Peroneus long as not acting.
Loss of sensation of autonomous area of common peroneal
nerve.
Common peroneal nerve sites are inspected palpated for
scar, nerve thickening and swelling over the area.
Tinel’s sign is tested in injuries.
 With injuries (except in neuropraxia) neurological
recovery can be assessed
 X-rays of ankle and knee are taken
 Muscle and nerve conduction study are done.
• Immediately dynamic foot drop splint is given.
Observation (Neuropraxia)
• Intervention (no improvement, nonanatomical
Tinel’s).
Reconstruction procedures:
• If patient presents after one year, neuromuscular
junction is already damaged—“Srinivasan’s
procedure (transfer of tibialis posterior to dorsum
with TA lengthening).
252. How will you differentiate a musculotendinous
injury or a nerve injury?
• The contractions of the muscle can be palpated
in case of a tendon injury and not in nerve injury,
as the patient attempts to dorsiflex the ankle.

• In the other nerves are blocked still some of the
area of those nerves will retain sensation. This is
due to the supply of nerve in question more than
its anatomical area.
255. What is anatomical area?
• This is described in books as to dorsum, medial
half and lateral ½ of sole.
SHORT CASES 101
38. BAKER’S CYST

 Patient has pain in the knee (anterior and posterior)
 Difficulty in squatting
 Cystic swelling, lesion in popliteal region
 On flexion, less prominent
 On extension, more prominent
 Associated with degenerative joint disease of knee
 Popliteal cyst is the other name.
256. How will you treat if patient is less than 6 years?
• Observe.
257. What is the treatment in rheumatoid arthritis
patient?
• Popliteal cyst excision and synovectomy.
258. What is the treatment if the patient has associated
findings for deep venous thrombosis (DVT)?
OR What is the treatment in suspected DVT
patient?
• Ruptured popliteal cyst may mimic DVT—must
do ultrasound of the region to find if the sac is
ruptured and treat for DVT.
259. What is fluctuation?
• Displacing a fluid inside a sac is called
fluctuation.
260. What is cross fluctuation?
• Fluctuation → In more than one plane is called
cross fluctuation.
261. What is pseudofluctuation?

• Fluctuation → In only one direction is called
pseudofluctuation (e.g. muscle mass).
A Popliteal cyst
A B
C D
Figs 67A to D: Popliteal cysts

SHORT CASES 103
39. MADUROMYCOSIS
 History of bare foot walking
 Agricultural laborer
 Swelling and pigmentation of foot and ankle
 Multiple sinuses discharging fungal granules.
262. What are the X-ray findings?
• Multiple osteolytic lesions in the tarsals.
• Antifungal Amphotericin B
• Debridement
• Amputation in resistant cases.
264. Why History of bare foot walking?
• Common in farmers and barefoot walkers which
favor inoculation of spore.
A B
Figs 68A and B: (A) X-ray of the patient with mycetoma

foot; (B) Above patient with mycetoma
40. GENU VALGUM

 A condition where the limb distal to the knee is
deviated outwards
 Intermalleolar distance increased to at least 10 cm
 Medial joint laxity present. In children with stunted
growth vitamin D levels, calcium, phosphorus
estimation, USG abdomen for renal and neurological
problem is must.
265. Where is deformity whether in tibia or femur?
• Disappear on flexion → deformity is in femur
• Did not disappear on flexion → deformity is in
tibia.
266. Treatment of choice?
• Vitamin D supplementation if rickets
• Macewan’s—osteotomy to correct deformity.
A B
Figs 69A and B: Two cases of genu valgus

SHORT CASES 105
41. GENU VARUM

 By the nomenclature limb distal to the knee, i.e. legs
moving towards the midline
 Usually bilateral
 Intercondylar distance is measured in standing and
lying down positions
 Used to assess progression
 It is physiological usually—manifested by 1½ years and
corrected by 3 years
 Also seen in rickets, Blount’s, osteoarthrosis of knee.
A B
C D
Figs 70A to D: There can be flexion deformity also

A B
Figs 71A and B: No deformity in flexion →

appears on extension only → deformity is in femur right
Fig. 72: Case of bilateral osteoarthritis

SHORT CASES 107
Fig. 73: X-ray on the above case
267. Where is the deformity?

• If it disappears on flexion → deformity is in femur
• If it did not disappears on flexion → deformity is
in tibia.
268. Treatment options?
• Splinting in children
• Calcium and vitamin D.
269. What is the indication for high tibial osteotomy in
OA knee?
• Unicompartmental disease
• Young patient < 65 years
• Good range of movement.
270. Who is the author of above surgery?
• Coventry.
271. What is the advantage of lateral approach for the
above surgery?
• The problem of laxity of the lateral ligaments is
taken care by reefing.
272. What is the indication for total knee replacement

OA knee?
• Tricompartmental disease
• Older patient > 65 years
• Poor range of movement.
273. Where will you see for synovial thickening?
• Anteromedial aspect of knee joint.
• Also gripping the sides of patella.
274. Why Anteromedial aspect of knee joint?
• Because in any synovial effusion or inflammation
or immobility due to pain vastus medialis obliqus
is the first muscle to get wasted. By rolling over
this site synovial reflection is felt with a craggy
feel.
275. Why should you preserve patella in fracture
patella, what is the necessity of bone, e.g. even
horses do not have patella?
• Patella gives lever arm for the quadriceps to
contract. If there is no patella then the excursion
of quadriceps tendon is reduced and flexion is
reduced.
• Patella is essential for bipeds.
• In this era of total knee arthroplasty (TKA)
preserving patella is a must—though with a
nonanatomical reduction.
276. What is mechanical axis deviation (MAD)?
• Line joining the centre of head of femur to the
centre of ankle joint is the mechanical axis line. Any
deviation is called mechanical axis deviation.
SHORT CASES 109
42. RESIDUAL POLIOMYELITIS

Patient presents complaints—for deformity, weakness.
History of the Patient

 Delivery, vaccination, development, childhood fever—
intramuscular injections during fever
 Splintage previous orthosis
 Present occupation.
General Examination
 Gait—Patient walks alone/support/caliper
 Neurological examination muscle power of upper and
lower limb
 Shoulder—Extension, flexion, abduction, adduction,
internal rotation, external rotation
 Elbow—Flexion, extension
 Wrist—Dorsiflexion, plantarflexion
 Small joints of hand MCP and IP
 Hip level of ASIS/attitude, fixed deformities, Range of
movement—active and passive—Extension, flexion,
abduction, adduction, internal rotation, external
rotation
 Knee—Flexion, extension
 Ankle—Dorsiflexion, plantarflexion
 Toes—Dorsiflexion, plantarflexion, spine deformity—
region and length.
Measurements
 Apparent and true measurements.
SPECIAL TESTS
Abduction contracture of hip—Ober’s test a diagnostic test
that assesses the degree of tautness in the iliotibial band. The
patient in a side lying position with hips at zero degree flexion
and the leg is passively adducted. Tightness and knee not
touching the couch indicates iliotibial band syndrome.
A B
C D
Figs 74A to D: (A) Residual poliomyelitis of right lower limb

standing with quadriceps gait; (B) the same patient trying to
passively extend his knee; (C) his pelvis X-rays; (D) another
patient with left upper limb polio
SHORT CASES 111
277. What are the possible surgical treatment of polio?

• Deformity correction
• Muscle balancing
• To stabilize a flail joints
• To correct limb length discrepancy.
278. What are the causes of deformity in polio?
• Untreated unsplinted positioning of limb
• Muscle imbalance—over action of un affected
muscle.
279. What are the prerequisites and principles of tendon
transfer?
6S
• Supple joints
• Same power donor tendon
• Transfer
• Straight line
• Supply—nerve and muscle intact
• Stable insertion into bone preferable.
280. What a proper tendon transfer is intended to
achieve?
• Remove a strong muscle or strengthen a weak
muscle
• Dynamic correction
• Stabilize a joint
• Make a patient to walk around with a near
normal gait preferably without calipers.
281. Which is the commonest muscle to get paralysed?
• Tibialis anterior.
282. Which is the commonest muscle to get spared?

• Peronei.
283. Why?
• Tibialis anterior—get supplied only from L4
• Peronei—get supplied from more number of roots
L5 S1 S2.
284. Which is the easy muscle to teach after transfer?
• Peroneus brevis.
285. Is arthrodesis an alternative for tendon transfer?
• No it can be considered to be done with a tendon
transfer. Arthrodesis is not an alternative to
tendon transfer.
SHORT CASES 113
43. NONUNION FRACTURE

BOTH BONE LEG
A cause of deformity of the leg/history of injury to patients
leg in a road-accident.
 History of indigenous treatment
 Now after 6 months the patient cannot weight bear on
the limb.
 On examination the leg is deformed there is a valgus
deformity M/3 D/3 junction
 Abnormal mobility present there
 Shortening of 2 cm.
Fig. 75: A gap nonunion (the above patient’s X-ray)


• Ends of the fracture sclerosed.
• No evidence of callus there is a gap.
287. Classification?
• Hypertrophic,
• Atrophic types.
A B
Figs 76A and B: An example of hypertrophic nonunion in

another patient
• Internal fixation with interlocking nail or plating
after freshening of fracture with posterolateral
bone grafting.
289. If this case is an infected nonunion how will you
proceed?
• Debridement of the infected site
• Ilizaro frame application and bone transport.
SHORT CASES 115
Fig. 77: Infected gap nonunion
Fig. 78: Nonunion with deformity

Fig. 79: X-ray of above case
290. Why in the non union of tibia there is difficulty in

eliciting abnormal mobility in both planes?
• As there are two bones in the leg the fibula almost
always unite faster and hence restricts movement
in the form of abnormal mobility.
A B C
Figs 80A to C: Nonunion treated with Ilizaro

SHORT CASES 117
A B
Figs 81A and B: Postoperative
291. What is the advantages of Ilizaro?

• Immediate weight-bearing can be allowed in
infected fracture also. Addresses all issues of
fracture like shortening, bone loss, deformity,
nonunion.
44. NONUNION PATELLA

 Case of difficulty in walking
 History of injury mostly direct on the patella 8 months
back
 Indigenous splintage and over the counter (OTC) drugs.
On examination:
 Extension is weak
 Extensor lag present
 A palpable gap present over the patella.
• Gap seen in the fracture site.
• Whatever time it presents the best treatment is to
retain the patella.
294. What is the difference between extensor lag and
fixed flexion deformity?
• In extensor lag passive extension of final degrees
is possible. It is not possible in fixed flexion
deformity.
SHORT CASES 119
Figs 81C to E: A case of neglected fracture of patella

45. CONGENITAL PSEUDARTHROSIS

OF TIBIA
Fig. 82: Congenital pseudarthrosis
 Cause of deformity of the leg in the form of anterior

bowing
 The deformity may be seen from birth
 History of indigenous treatment
 History of surgery
 Deformity and abnormal mobility m/3 of leg.
SHORT CASES 121
Fig. 83: X-ray of congenital pseudarthrosis

• Tibial shaft is thinned out
• Fibula is thickened.
296. What are the types of this lesion?
Boyd classification
Six types
1. Defect
2. Hourglass
3. Cyst
4. Sclerosis
5. Dysplasia of fibula
6. Intraosseous fibroma.
• Ideal treatment and that gives some hope is
resection and transport with ilizaro
• Other options are vascularised fibular graft
• Bone grafting and internal fixation.
46. OSGOOD SCHLATTER’S DISEASE
Figs 84A and B: Adolescent boy cause of pain

over the tibial tuberosity
 Swelling and prominence over the tibial tuberosity

 Tenderness over the tibial tuberosity
 Flexion almost full except mild restriction in the extreme
flexion.
• Fragmentation of the tibial tuberosity apophysis.
1. Extension splints and non-steroids anti-
inflammatory drugs (NSAIDs)
2. Excision of the fragment, if pain is severe and not
responding to conservation.
Things to
be Taken
THINGS TO BE TAKEN TO THE

CLINICAL EXAMINATION HALL
1. White coat with number written legibly
2. Inch tape (avoid steel)
3. Tuning Fork-128 Hz
4. Tuning Fork-256 Hz
5. Knee hammer
6. Skin marking pencil
7. Goniometer
8. Plumb lime
9. Test tubes
10. Cotton wisp
11. Pins
12. Pad
13. Scale ruler
14. Stethoscope
15. Coins
16. Stopwatch.
Cases Seen
in Ward
Rounds
CASES AND APPLIANCES YOU MAY BE

ASKED IN WARD ROUNDS IN DNB AND
NOTES FOR THEM
WARD PROCEDURES
1. The BB Splint or Bohler–Braun splint
Fig. 85: BB splint
It has a limb rest with a genu corresponding to the knee.

In the above picture the left lower limb is kept in BB splint
with upper tibial pin traction.
CASES SEEN IN WARD ROUNDS 127
2. The Stryker frame
Fig. 86: Stryker frame
It has two boards to rotate the patient. It has a pulley in

the upper end. In the above picture the patient is kept in
the Stryker frame with skull tongs traction.
3. Calcaneal pin traction
Fig. 87: Calcaneal pin applied

4. One and half hip spica
Fig. 88: Hip spica for pediatric femur fracture
REGION WITH CONDITION

SHOULDER (ROTATOR CUFF TEAR)
A B C
Figs 89A to C: (A) Patient attempting active abduction—which

he is not able to do; (B) He can touch the opposite
shoulder; (C) Patient can passively lift his shoulder to abduction
6. Another such patient
Fig. 90: Patient is trying to abduct his shoulder
7. Post shoulder hemiarthroplasty
Fig. 91: Patient with post shoulder hemiarthroplasty

8. An osteotomy done for Erb’s palsy
A B
Figs 92A and B: Erb’s osteotomy
ARM
1. Malunited humerus fracture
A B
Figs 93A and B: Humerus fracture (Malunited)
2. Wounds for nail entry, proximal and distal locking for

humerus fracture fixed with an interlocking nail.
Fig. 94: Humerus fracture (proximal and distal locking)
A B
Figs 95A and B: Immediate—postoperative closed

ILN of humerus of above case
3. Another similar case (2-year follow-up)
Fig. 96: Humerus tracture (after 2-year follow-up)
ELBOW
A B
Figs 97A and B: Dislocated elbow

Fig. 98: Fracture olecranon (see the

olecranon retained in fossa)
A B
Figs 99A and B: Prominent implants under the skin

Fig. 100: Puckering in supracondylar

fracture of humerus type III
A B
Figs 101A and B: A case of flexion type of supracondylar fracture

of humerus—presented late with ankylosed elbow with ulnar
nerve palsy
Fig. 102: Extension osteotomy, arthrolysis and anterior

transposition of ulnar nerve done in one stage (for above case)
WRIST AND HAND
Fig. 103: An extensor tendon injury

A B C
Figs 104A to C: Volar barton fracture—after fixation

degree of volar and dorsiflexion after surgery
A B
Figs 105A and B: Tuberculosis of wrist—lower end of ulna

A B
Figs 106A and B: Carpometacarpal

dislocation of third metacarpal
Fig. 107: Heberden’s nodules osteoarthritis of small joints

Fig. 108: PIP joint dislocation of ring finger neglected
A B
Figs 109A and B: A rheumatoid hand

Fig. 110: The ulnar deviation of PIP of right middle finger
Fig. 111: Trigger finger

Fig. 112: Dorsal capsulotomy of MCP joints for a stiff hand
Negative ulnar variance with snapping distal ulnar
A B C
Figs 113A to C: Prominent ulnar head in

supination → Snaps in pronation
A B
C D
Figs 114A to D: Wrist dislocation fusion done for the same
A B
Figs 115A and B: Colles’ fracture

A B C
Figs 116A to C: Level of styloids, stiffness of hand joints

and dinner fork deformity
A B C
Figs 117A to C: Another case of old malunion distal radius
HIP
Fig. 118: Old Perthes disease

Fig. 119: Fracture of acetabulum with fracture femur shaft
THIGH
A B
Figs 120A and B: Infected fracture femur → Antibiotic

Loaded Acrylic Cement laden nail for the same case
A B C D
Figs 121A to D: Infected fracture femur treated with Ilizaro

X-ray of the same case
Fig. 122: Floating knee treated with knee

spanning Ilizaro apparatus
KNEE
A B C
Figs 123A to C: Painful swelling over medial collateral

ligament, X-ray of the same case showing calcification of
ligament
Fig. 124: Patellofemoral arthritis—osteophyte seen on

the lateral aspect of the fibula
Fig. 125: Quadriceps lengthening done for congenital

dislocation of both knees—(now after 50 years)
A B
Figs 126A and B: Bilateral genu varus (more on right side)

A B
Figs 127A and B: The knee deformity patient

also had chest deformity pigeonchest and stunted growth
A B
Figs 128A and B: X-ray of the above case—

possibility of Rickets
Fig. 129: Another patient with bilateral genu valgum (Rickets)
A B C D
Figs 130A to D: Dislocation knee, treated with reduction

and stabilization. Arterial injury is notorious complication
A B
Figs 131A and B: Post-patellectomy status–on

left side, extension is almost full
Fig. 132: Flexion deformity knee treated with Ilizaro

Fig. 133: Soft tissue swelling from upper part of

medial collateral ligament
Figs 134A and B: Hemophilic arthritis (see the wide

intercondylar notch). In AP view X-ray condyles magnified and
distorted due to associated flexion deformity
Poor fixation of upper tibia fracture—causing delayed

mobilization
A B
Figs 135A and B: (A) No plate was used for an upper tibial
fracture; (B) Locking compression plate for a similar fracture
expected to achieve early mobilization
Foot and Ankle
A B
Figs 136A and B: Communited distal tibia fracture

Fig. 137: Pronation abduction injury ankle
See the lateral cortical comminution in fibula and the

avulsion fracture of the medial malleolus
A B C
Figs 138A to C: Post-traumatic equinus contracture
Patient cannot dorsiflex actively or passively

Fig. 139: X-ray of the above patient—see the forefoot—

equinus—a fit case for lambrinudi arthrodesis
A B
Figs 140A and B: Another such patient

with equinus contracture
Fig. 141: Loss of toes after an end arteritis
RETROCALCANEAL BURSITIS
Fig. 142: See the prominent swelling over and near the
attachment of tendocalcaneus-pointed tenderness
*Must rule out—Rheumatoid Artheritis
*Main stay of treatment are Wax bath and NSAIDs
*Excision of the bursa in resistant cases, with trimming
posterior end of calcaneum.
Closed TA rupture
A B
Figs 143A and B: (A) Squeeze test; (B) Palpable gap
300. How to diagnose?

• History of sudden giving way in persons above
50 years of age.
• Palpable gap in the substance of Tendo Achilles.
• Patient can still attempt a plantar flexion by
contracting the long flexors but it is not powerful
at all.
• Patient cannot walk on toes.
• Squeezing the calf will not cause plantar flexion
of the foot.
301. What are the other tests?
• Obrien’s test needle is introduced into the distal
end and then the above test is demonstrated
(squeezing of calf muscles).
302. What is the another diagnosis which may mimic but

is not so devastating?
• Plantaris tendon rupture.
• Posteromedial and the pain and hematoma is less.
• More important there is no gap felt over the Tendo
Achilles.
Fig. 144: Another case of TA
303. What is the tendon that can be of use to augment

the TA?
• Peroneus brevis.
Localised Gigantism
Plexiform neurofibroma of foot involving the second and
third toes. This patient was not able to wear shoes to
school. Both cosmetic and functional problem settled with
ray amputation of the toes. Preoperative assessment
included a search for any other evidence of neurofibromata,
MRI of the part and an arterial doppler.
B
Figs 145A and B: Postoperative
Fig. 146: Hallux varus
A B
Figs 147A and B: Bilateral flat feet with accessory navicula

304. What tendon rupture can cause similar picture?

• Tibialis posterior tendon rupture.
Fig. 148: Bilateral flat feet with accessory navicula
• Pain over the medial part of the foot especially

the navicula area—more on long standing
• Sometimes in extreme cases the pain may be over
the lateral aspect impinging on the lower end of
fibula
• Clinically there is flattening of the medial arch.
• X-ray as you see above will have flat arch and
sometimes an accessory navicula—which can
even be unilateral
• Treatment include Wax bath, intrinsic excercises
to feet
• Medial arch support in foot-wear.
Fig. 149: A case of open ankle dislocation in a diabetic

patient: needs debridement-glycemic control and antibiotics
A B C
Figs 150A to C: Pilon fracture—with open wound—initially

managed with calcaneal pin traction—then treated with fibular
plating
Fig. 151: Avulsion injury of medial malleolus—for the lateral

side the entire fibula should be X-rayed to rule out a fracture
Fig. 152: Rheumatoid feet

Fig. 153: A Marjolin’s ulcer. If a painless ulcer developed

on a healed scar, a biopsy is warranted
A B
Figs 154A and B: Another similar case of Marjolin’s ulcer

A B
Figs 155A and B: Forequarter amputation done for

sarcoma of scapula
Fig. 156: X-ray of the same patient

A B C D
Figs 157A to D: Bone transport done for

tumor of upper tibia
A B
Figs 158A and B: No pain only on deep palpation it was

tender-involvement of medial cortex Campanacci disease
PAEDIATRIC CASES
Fig. 159: Osteomyelites in a child; femur
Fig. 160: Constriction bands with CTEV (constriction goes all

around the limb while crease is on only one side of limb)
A B C
Figs 161A to C: Clinical picture of flat feet in a child—must

R/o congenital vertical talus
Fig. 162: Right side femur fracture in a 2½-year-old girl

A B
Figs 163A and B: Congenital agenesis of right upper limb
Fig. 164: Osteomyelitis of upper humerus

A B
Figs 165A and B: Congenital shortening of femur (left)
A B
Figs 166A and B: Hemimelia

Birth fractures in a 3-day-old child
A B C
Fig. 167A to C: (A) Right clavicle; (B) Right

femur; (C) Left femur
1st and 3rd were intrauterine fractures
Multiple congenital deformities thumb in palm and rocker

bottom feet—like
A B C
Figs 168A to C: Edward patau syndrome

COMPLICATIONS OF INJURIES AND TREATMENT
A B
Figs 169A and B: Operated patient with deformity of his left
shoulder and no useful function of the shoulder. His X-ray
showed a loosened implant with deformity and nonunion
A B
Figs 170A and B: (A) Broken nail—probably due to → leaving
a distal locking hole close to the fracture free which is a stress
raiser which has coupled with premature weight bearing;
(B) Broken plate—probably due to premature weight bearing
Fig. 171: Blisters after a fracture both condyles of tibia
A B
Figs 172A and B: Ulceration in a resin cast

A B
Figs 173A and B: (A) Vein thrombosis in an extravasation of

chemotherapy; (B) Deep vein thrombosis
Fig. 174: A case of loosened and dislocated prosthesis causes

→ uncemented implant → no adductor release was done for
this old neck fracture
Fig. 175: Bone graft taken very close to ASIS
A B
Figs 176A and B: (A) Wrongly applied Thomas splint—ring did

not touch the ischial tuberosity—see also the associated
fracture of right pubis; (B) Paraphimosis—failure to pull the
prepuce forward after catheterization is the reason
Fig. 177: Lymphedema of old flap area. Should rule out a deep
vein thrombosis. Treatment is strict elevation and antiedema
measures
Metabolic Bone Disorders
A B C D
Figs 178A to D: Preoperative X-rays of knee

A B C
Figs 179A to C: Postoperative X-rays of knee
A B
C D
Figs 180A to D: Postoperative X-rays of knee after

osteotomy (The patient is seen in the next picture)
A B
Figs 181A and B: The girl after deformity correction
Fig. 182: A medial gastrocnemius flap for proximal tibial coverage

A B
Figs 183A and B: Abdominal flap for a soft tissue defect of forearm
Fig. 184: Paddy thresher injury

Fig. 185: Stubbies for bilateral above knee

amputation stump
OSTEOMALACIA
A B C
Figs 186A to C: The patient with osteomalacia—
champagne pelvis
A B C
Figs 187A to C: Brother of the above patient also had

same deformities
Fig. 188: Siblings both males with multiple deformities

including this bilateral genu valgus possibility of Multiple
Epiphyseal Dysplasia
SPINE
A B
Figs 189A and B: Cervical spondylosis with

restricted neck movements
A B C
Figs 190A to C: Ankylosing spondylitis—the patient’s

spine fixed in hyposis
Fig. 191: Osteoporosis—cod fish disc space (biconvex)
Fig. 192: Last cervical spine
305. How to identify the last cervical spine in AP view?

• The cervical transverse processes will point
downwards
• The thoracic transverse processes will point
upwards.
Fig. 193: Loss of lordosis of cervical spine—infact kyphosis
Fig. 194: Multiple cysts of nerve sheath—usually need

conservative treatment only
Fig. 195: This is an unintentional work done by our nursing

home watchman which forced me to note and show you. We
had tried to support a weak plant by tying to a wooden stick
(symbol of orthopaedics). Thanks for your patient reading

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Short Cases in Orthopaedics for PG Practical Examination

First Edition : 2013

The thought that why to write such a book when lots of

However, this book is not an alternative for your

WHY THIS BOOK

I thank—all my professors, assistant professors, tutors,

I acknowledge Mr Pandian, Orthotist, Institute of

Short Cases ..................................................... 1

23. Fresh Dislocated Elbow 64

Things to be Taken .................................. 123

Cases Seen in Ward Rounds ................. 125

We would start with the common cases in postgraduate

READ ONE BY ONE CAREFULLY

 Can you give chemotherapy?

• Keep your mind open till the entire question is asked.

Figs 1A and B: Unilateral club foot (Right side)

Fig. 2: Same patient after surgery

Figs 3A and B: (A) Recurrent club foot following surgery;

Figs 4A and B: Another such deformity since birth

LIST OF FINDINGS IN CLUB

• Ligaments—spring ligament, plantar fascia

Questions on local staging

b. It is also hypothesized to be formed by the

18. What is the commonest secondary of osteosarcoma?

25. What is the diagnostic histopathological appearance

30. What are the advantages of neoadjuvant chemo-

36. Can we get osteosarcoma at old age?

43. Any other important factor other than stage and

scan, patient is suspected to have micrometa-

52. What are the types of medullary lesion in osteo-

• In adults, knee joint fusion, endoprosthesis,

Veriable Score 1 Score 2 Score 3

2. Degree of pain mild moderate severe

8/12 = 15% risk of fracture 9 or above indication

Figs 5A and B: A case of osteosarcoma of distal tibia

Figs 6A and B: X-ray of the above patient with sunray appearance

Fig. 7: A girl with osteosarcoma of lower femur

Figs 8A and B: X-ray of the above patient

Fig. 9: MRI of the above patient

72. How to identify the malignany of cartilaginous

Fig. 14: An exostosis from left clavicle

Fig. 15: Osteomyelitis of femur

Fig. 16: Another similar case of osteomyelitis

Fig. 17: Osteomyelitis of tibia

81. What are the stages of osteomyelitis?

Figs 18A and B: Patient femur infected plate and screws

83. What are types of osteomyelitis in adult (Cierny-

C. Localized cortical and medullary

89. What are the causes of persisting sinus?

Osteomyelitis of Humerus in a Girl

Fig. 19: Now the disease is quiescent. It is better

Fig. 20: Same patient

Figs 21A and B: X-ray for the above patient

Fig. 22: Sinus of thigh—osteomyelitis of right femur

Figs 23A and B: Osteomyelitis of distal tibia with deformity

Figs 24A and B: (A) Pushing the wall → winging; (B) No

Figs 25A and B: Abduction causes

Figs 26A and B: Abduction does not reduce winging