Q&A on common orthopaedic practical exam cases

13th Calicut Ortho Course 2015

Patron
Prof. T. S. Gopakumar

Organising Chairman
Dr. Kumarsn Chettiar

Organising Secretary
Dr. Subramanian V

Organising Treasurer
Dr V Ravikumar

Edited by

Dr. Rajesh Purushothaman, MS, D.Ortho, DNB

Dr. Ravikumar V., MS, D.Ortho

Dr. Jacob Mathew, MS, D.Ortho

Dr. Aneen N. Kutty, MS, D.Ortho

Dr.Balaji Zacharia,MS Ortho

Dr. Jojo Inassi, MS Ortho

Dr. Sibin Surendran, MS, D.Ortho, DNB, MRCS (Ed), fellow knee

Dr. Jeejeshkumar T. K., D.Ortho, DNB

Department of Orthopaedics
Govt. Medical College, Kozhikode
CONTRIBUTORS

Prof. T. S. Gopakumar Professor And HOD

Prof. K. S. Jyodish Professor
Dr. Raveendran MK Associate Professor
Dr. Gopinathan P Calicut
Dr. Rajesh Purushothaman Associate Professor
Dr. Ravikumar V Associate Professor
Dr. Ravikumar R Associate Professor
Dr. Kumaran Chettiar Associate Professor
Dr. Balaji zacharia Assistant Professor
Dr. Raju K Associate Professor
Dr. Aneen N. Kutty Assistant Professor
Dr. Jojo inassi Assistant Professor
Dr. Sibin surendran Assistant Professor
Dr. Thanveerudin Sherule Assistant Professor
Dr. Jijesh Kumar Assistant Professor
Dr. Subramanian V Assistant Professor
Dr. Harvey George United Kingdom
Dr. Biju Kiliyanpilakkal United Kingdom
Dr. Rejith Valsalan
Dr. Sameer Ali Paravath
Dr. Rahul Mohan
Dr. Asif Kassim
Dr. Nijith Govindan
 Preface

Calicut Ortho Course is being conducted for the 13th successive year. Over the years the
program has gained immense popularity due to the wealth of clinical material, best of faculty
members and whole hearted and enthusiastic participation of the entire department. Our
institution have become a DNB Orthopedics examination centre as well.

Over the years we noticed a pattern in the common questions asked during the past courses and
have gleaned the best of questions and answers. This is a humble attempt to compile these
questions along with the answers. We sincerely hope that this will help you become better
clinicians, guide you to provide scientific and evidence based treatment to your patients and
above all will help you to meet the expectations of your examiners; who can unpredictable and
hard to please.

We thank all the contributors which includes our staff members, residents and alumni. We
specially thank Dr. Gopinathan P our former faculty for his articles. We thank Dr Harvey George
and Dr Biju Kiliyanpilakkil; both working in United Kingdom for their articles.

Best wishes from Calicut Medical College

Prof T S Gopakumar
Dr Rajesh Purushothaman
Dr. Ravikumar V.
Dr.Jacob Mathew
Dr. Aneen N. Kutty
Dr. Balaji zacharia
Dr Jojo Inassi
Dr. Sibin Surendran
Dr. Jeejeshkumar T. K.

Q&A on common orthopaedic practical exam cases

First Edition: 2011
© 2011 HOD, Department of Orthopaedics, Governement Medical College, Kozhikode
Second Edition: 2012
Third Edition:2013,
Fourth Edition:2014 Published on the occasion of 12th Calicut Ortho Course.
Fifth Edition 2015 Published on the occasion of 13th Calicut Ortho Course
All rights reserved
CONTENTS
SECTION I THE HIP

1. EXAMINATION OF A HIP CASE -Dr Rajesh Purushothaman 5

2. GENERAL EXAMINATION - Dr Raju K 21
3. SLIPPED CAPITAL FEMORAL EPIPHYSIS 27
4. SUFE - Dr Harvey George 33
5. TUBERCULOSIS OF THE HIP - Dr Thanveer Sherule 35
6. DEVELOPMENTAL DYSPLASIAS OF THE HIP 40
7. DDH - Dr Harvey George 45
8. OSTEOTOMIES AROUND THE HIP- Dr Ravikumar R 48
9. SEQUELAE OF HIP SEPSIS - Dr Jojo Inassi 54
10. NON UNION NECK OF FEMUR 59
11. PERTHES DISEASE - Dr Harvey George, Dr Rajesh Purushothaman 63
12. BILATERAL HIP CASE WITH OSTEONECROSIS 68
13. THR - Dr Gopinathan P 75
14. TKR - Dr Gopinathan P 78

SECTION II THE SPINE

15. EXAMINATION OF THE SPINE 80
16. INTERVERTEBRAL DISC PROLAPSE- Dr K Kumaran Chettiar 83
17. SCOLIOSIS - Dr Balaji Zakaria 86
18. TUBERCULOSIS SPINE 89
19. SPONDYLOLISTHESIS - Dr Biju Kilaiyanpilakkil 92

SECTION III SHORT CASES

20. EXAMINATION OF SHOULDER- Dr Rajesh Purushothaman 101
21. UNSTABLE SHOULDER– Dr Sameer Ali Paravath, Dr Rejith Valsalan 111
22. EXAMINATION OF ELBOW- Dr Jojo Inassi 117
23. ANGULAR DEFORMITIES OF ELBOW- Dr Jojo Inassi, Dr Sameer Ali Paravath 119
24. EXAMINATION OF A PERIPHERAL NERVE- Dr Sibin Surendran 128
25. BRACHIAL PLEXUS INJURYDr Sameer Ali Paravath 130
26. PERIPHERAL NERVE LESIONS- Dr Sibin Surendran 135
27. NEUROMUSCLAR DISORDERS EXAMINATION 141
28. CEREBRAL PALSY-Dr Raju K 143
29. EXAMINATION OF LOWER LIMB DEFORMITY - Dr Rajesh P 148
30. EXAMINATION OF A KNEE DEFORMITY 156
31. GENU VARUS AND VALGUS DEFORMITY- Dr Jijesh Kumar 157
32. EXAMINATION OF THE ANKLE AND FOOT 164
33. CONGENITAL TALIPES EQUINO VARUS 165
34. EXAMINATION OF A SWELLING 171
35. MUSCULOSKELETAL NEOPLASMS 172
36. OSTEOMYELITIS 176
37. EXAMINATION OF THE KNEE JOINT 180
38. INTERNAL DERANGEMENT KNEE- Dr Sibin Surendran 182
39. EXAMINATION OF HAND AND WRIST 191
40. MALUNITED LOWER END OF RADIUS 192
41. KIENBOCK’S DISEASE- Dr MK Ravindran 195
42. PERIPHERAL NERVE INJURIES 197
43. FOOT DROP Dr. Nijith Govindan 201
SECTION IV EXAM CASES 204
SECTION V IMPORTANT THEORY TOPICS 211
SECTION VI PATH FINDER - PREVIOUS YEARS QUESTION PAPERS OF KUHS,
CALICUT AND KERALA UNIVERSITIES FOR ORTHOPAEDICS
Dr. ASIF KASSIM & Dr. RAHUL MOHAN
 SECTION I
THE HIP JOINT

1. EXAMINATION OF A HIP CASE

Prepared by Dr Rajesh Purushothaman http://www.learningorthopedics.com

Examination of the Hip Joint

Introduction

 Introduce yourself and get the consent of the patient EXAMINATION CHECKLIST or the
parent of the child for examination.
 Note down the name, age, sex, race and occupation Clean coat with ID card of the
patient. Admit card
 The patient should be adequately exposed while Measuring tape
making sure that external genitalia are covered and Goniometer with scale the
Torch
patient is comfortable and relaxed. Explaining why you
Skin marking pencil
need to expose and the steps of examination will CNS kit
help in
relaxing the patient and in establishing a good Knee Hammer
rapport. Tuning fork
 When examining a female patient make sure that T bandage you
have a female nurse or assistant. Tourniquet
 Examine the child with the parents by the side. Very Scoliometer & plumbline young
children may be examined in the parent’s lap. Writing pad and pencil
 First examine the normal or less symptomatic side first to
establish the normal range of movement for the particular patient and to make the patient
understand what is going to be done on the painful side.
 Steps of all procedures should be explained to the patient to ensure patient comfort and
cooperation.

Patients with hip joint disease may present with pain, alteration of gait, instability, functional
limitation or limb length discrepancy as their presenting complaint. Hip symptoms may be due to
intra-articular, extra-articular or referred causes. Intra-articular conditions usually will cause
deformity, limitation of range of movement and worsening of symptoms on joint activity. Extra-
articular conditions usually will not cause restriction of range of movement, pain will be present
mainly in one particular movement or position of joint and tenderness will be localized to a
specific area. Always rule out referred pain from spine, pelvis, and sacroiliac joint or vascular
causes. Rarely hip disease may present as pain referred to the knee.

Examine the patient in standing, sitting, walking and lying down. When the patient is lying in the
supine position, always examine the patient from the right side. Make sure that the patient lies on
a hard surface to ensure that deformities are not concealed by a soft mattres.

HISTORY

Presenting complaints – Give the presenting complaints in the chronological order.

History of presenting complaints

Pain

 Duration – How long the pain is present?

 Onset – How it started?
 Progress – What has happened to the pain after it started? Has it increased, decreased or
remain in the same intensity. Is it constant or intermittent?
 Site- Ask the patient to pinpoint the site of pain with a single finger. Note down
whether in the groin, trochanteric area, buttocks etc. and don’t use vague terms like pain
in the hip. Remember that a patient with hip disease may present with knee pain.
 Severity- How disabling is the pain? What is its effect on routine activities, self care,
locomotion, occupation and recreational activities?
 Character – What is the nature of pain? Throbbing pain is due to inflammatory causes,
burning pain is due to neuropathic causes.
 Radiation- Pain of hip may radiate to knee or thigh. Pain radiating to the testes is
suggestive of ureteric calculi. Pain radiating below knee is due to sciatica.
 Aggravating and relieving factors- Mechanical pain due to osteoarthritis or impingement
is aggravated by activity and relieved by rest. Pain due to inflammatory arthritis is
aggravated by rest and partially relieved by activity.
 Diurnal variation- Pain of osteoarthritis is more towards the evening and less when
patient gets up in the morning. Pain of inflammatory arthritis like ankylosing spondylitis
is more in the morning and less in the evening. Nocturnal pain that interferes with sleep
is an ominous sign of malignancy or infection.
 Associated symptoms

Deformity

 How long the deformity is present?

 How did it start?
 How is it progressing?
 Any associated symptoms?
 Is there any history of trauma or infection?

Limb length discrepancy

 How long it is present?

 Is it static or progressive?
 Associated symptoms?
 Any history of infection or trauma?

History to assess function

 Walking ability
o Normal or altered
o Restricted or unrestricted
o Aided or unaided
o If aided; which aid is used
 Ability to squat
  Ability to sit cross legged
 Ability to drive car
 Ability to tie shoes

Fever – Whether associated with chills and rigor, severity, continued or intermittent and the
treatment taken.

Past history

 Hypertension
 Diabetes mellitus
 Inflammatory arthropathy
 Septic arthritis
 Tuberculosis
 Umbilical sepsis
 H/o prolonged IV infusion in childhood
 Blood Dyscriasis
 Frequent episodes of bleeding
 Frequent episodes of infection
 H/o Childhood limping
 Previous hospital admission
 Previous surgery
 Previous trauma

Personal history

 Prolonged drug intake

 Alcohol abuse
 Smoking
 Diet
 Menstrual history
 Occupational history
 Recreational activities

Treatment History

Family history

 Any family history of dwarfism

 Any family history of angular deformities
 Metabolic disorders
 Similar illness
 Tuberculosis

GENERAL EXAMINATION

Head to foot examination

Eyes- Blue sclera, irirtis ,uveitis, squint, microophtalmos, cornea, pigmentation of sclera.

Pinna- Low set, blackish discoloration.

Cheeks- Malar rash.

Mouth – Normal dental hygiene, arch of palate.

Hair Line- Normal or low

Neck – Webbing , thyroid swelling.

Nipples- Normal level or not.

Shape of chest wall- Pectus carinatum/ excavatum.

Abdomen- Protuberant , undescended testis , hernias.

Nails- Pitting.

Palms and soles- Hyperkeratosis.

Thickening of lower end radius, malleoli and costochondral junctions.

Ligamentous laxity (Wynne-Davis Criteria- 3 out of 5 needed for diagnosing generalized laxity)

 Apposition of thumb to flexor aspect of forearm

 Passive extension of fingers so that they lie parallel to the forearm.
 Hyperextension of elbow at least 10 degrees
 Hyperextension of knee at least 10 degrees
 Excessive passive dorsiflexion of ankle (45 degree) with eversion of foot.

Neurocutaneous markers-

LOCAL EXAMINATION

The steps of local examination are inspection, palpation, movements, measurements, gait
analysis, special tests and examination of spine and other joints and other system.

Inspection

Inspection should be done with the patient standing, walking, sitting and lying down. Look from
the front, sides and back. Look for any asymmetry when compared to the normal side.

Look for the following.

 Attitude
 Deformity
 Bony contours
  Soft tissue contours
 Swelling
 Wasting
 Limb length discrepancy
 Skin over the joint

Attitude and Deformity

Attitude is the position of joint which is most comfortable to the patient. Position of comfort for
the hip joint is flexion, abduction & external rotation; as it allows maximum distension of the
capsule. If the joint is moved it can be brought to neutral position. In deformity; there is a fixed
contracture of the joint which will prevent the joint from being placed in the neutral position. A
flexed attitude of the hip joint can be corrected but a fixed flexion deformity cannot be corrected.

Normally when a person lies supine on a firm surface the lumbar spine lies flat on the table and
there will not be any gap between the lumbar spine and the couch; if there is a gap then lumbar
lordosis is exaggerated. In the case of flexion deformity of the hip (FFD) it is usually masked by
forward tilting of the pelvis, which in turn is masked by increased lumbar lordosis. Hence
exaggerated lumbar lordosis is a sign of fixed flexion deformity of the hip. Unmasking of the
fixed flexion deformity of hip can be done by the Thomas well leg raising test.

A coronal plane deformity such as abduction or adduction is masked by compensatory coronal

tilting of the pelvis, which can be identified by looking at the level of both anterior superior iliac
spines (ASIS). In case of an adduction deformity; the ASIS of the deformed side will be at a
higher level, the affected limb will appear to be shortened and there will lumbar scoliosis with
convexity to the opposite side. In case of abduction deformity; the ASIS of the deformed side
will be at a lower level, the affected limb will appear to be lengthened and there will lumbar
scoliosis with convexity to the same side.

Anteriorly from proximal to distal;

 Level of ASIS
 Normal hollowing of iliac fossa
 Inguinal orifices
 Widened perineum
 Femoral artery pulsations
 Abnormal fullness in the Scarpa’s triangle
 Contour and level of the greater trochanter
 Contour and bulk of the thigh muscles looking for abnormal contour and wasting
 Scars, discolorations, swellings and sinuses

Laterally:

 Exaggerated lumbar lordosis

 Position and bulk of the trochanter- Look for any superior migration and more posterior
position when compared to opposite side. Superior migration may be due to
dislocation/subluxation, joint space destruction, fracture of neck /trochanter and coxa
vara. Excessive lateral prominence is seen in subluxation/dislocation. Reduced
prominence seen with protrusio acetabuli.
  Scars sinuses or any abnormal prominences

Posteriorly:

 Scoliosis
 Level of posterior superior iliac spine and iliac crests
 Symmetry of the gluteal folds
 Wasting of gluteal muscles
 Scars, sinus or abnormal masses

Palpation

Palpate for any local rise in temperature, tenderness, bony thickening or swelling, soft tissue
mass or defect.

Anteriorly:

 Local rise of temperature

 Anterior joint line tenderness- Anterior joint line is 2-3 cm below and lateral to mid-
inguinal point. Mid-inguinal point is the centre of a line connecting ASIS and the
symphysis pubis.
 Confirm level of ASIS.
 Feel the resistance over the Scarpa’s triangle. It will be reduced if the hip is dislocated
and it will be more in case of cold abscess.
 Femoral pulsations- The volume of pulse when compared to opposite side will be reduced
if the head is dislocated (Vascular sign of Narath).

Laterally:

 Greater trochanter
 Level in both supero-inferior as well as antero-posterior directions.
 Surface – Smooth or irregular or is it thickened.
 Tenderness both local and on thrust

Posteriorly:

 Any mass- Globular bony mass that moves with the femur is suggestive of dislocated
femoral head in presence of an unstable hip.
 Posterior joint line tenderness- Located at the junction of the lateral one third and the
medial two third of a line connecting the posterior superior iliac spine (PSIS) and
greater trochanter.

Movements

Look for active and passive movements in all three axes. Look for flexion & extension,
abduction & adduction and the external & internal rotation. Look for any fixed rotation
deformities in both hip flexion as well as extension.
A deformity almost always occurs in all three planes, but it will be predominantly in one or two
planes. It may occur in the sagittal plane (Flexion-Extension), coronal plane (Abduction-
Adduction) or in the axial plane (Internal rotation-External rotation). In the case of flexion
deformity of the hip (FFD) it is usually masked by forward tilting of the pelvis, which in turn is
masked by increased lumbar lordosis. Hence exaggerated lumbar lordosis is a sign of fixed
flexion deformity of the hip. Normally when a person lies supine on a firm surface the lumbar
spine lies flat on the table and there will not be any gap between the lumbar spine and the couch;
if there is a gap then lumbar lordosis is exaggerated. Unmasking of the fixed flexion deformity of
hip can be done by the Thomas well leg raising test.

A coronal plane deformity such as abduction or adduction is masked by compensatory coronal

tilting of the pelvis, which can be identified by looking at the level of both anterior superior iliac
spines (ASIS). In case of an adduction deformity; the ASIS of the deformed side will be at a
higher level, the affected limb will appear to be shortened and there will lumbar scoliosis with
convexity to the opposite side. In case of abduction deformity; the ASIS of the deformed side
will be at a lower level, the affected limb will appear to be lengthened and there will lumbar
scoliosis with convexity to the same side.

In order to assess the deformity, the coronal plane deformity is made manifest by correcting the
coronal compensatory tilting of the pelvis. This is called squaring of the pelvis.

Squaring of the pelvis is done by making both the ASIS at the same level. This is done by further
adducting the affected hip in presence of an adduction deformity till both ASIS are at the same
level. If there is some degree of free adduction present then the hip has to move through that free
range before the pelvis starts tilting. Hence before measuring the degree of adduction deformity,
gently abduct the limb till the free range of movement is over and pelvis just starts to tilt again.
Now measure the degree of adduction deformity by using a goniometer. The goniometer is place
with the hinge over the centre of hip and one arm is parallel to the midline of trunk and the other
arm is parallel to the lower limb. Abduction deformity is measured by further abducting the
affected hip using the same principles.

Normal ROM in Hip in adults

Flexion 1200

Extension 100

Abduction 400

Internal rotation in flexion 350

Internal rotation in Extension 300

External rotation in flexion 450

External rotation in Extension 400

Range of movement depends largely on the age, gender and race. Children and women have
greater range of movement. Elderly will have lesser range of motion. Asian populations have
greater range of movement.

Movements should be tested both actively and passively.

The important points to be noted are the following.

1. Is the range of movements normal?

The range of movement in all three axes should be measured using a goniometer. The hinge of
the goniometer should be at the centre of rotation of hip. The proximal arm of the goniometer
should be in the long axis of the body and the distal arm should be in the long axis of the lower
limb.
2. If restricted; which movement is restricted?

Global limitation of all movements is seen with arthritis and differential limitation of abduction
and external rotation is seen with coxa vara.
3. If restricted; what is the severity?

Compare with the opposite side. If the opposite side is also abnormal then compare with the
normal range for the age, gender and race
4. Is the movements painless, painful?
5. If painful; during which movement and during which part of the arc of movement?
In patients with synovitis, the range of movements is normal but the terminal part of the arc is
painful. In case of arthritis all movements are restricted to some degree and painful. Pain on one
particular movement alone with normal range of movement is suggestive of extra-articular cause
of pain.
6. Is the limitation of movement due to mechanical causes or due to pain and spasm?
7. Is the axis of movement normal?
Normally when the hip is flexed the lower limb flexes towards the opposite shoulder. Axis
deviation during flexion can be seen in patients with slipped capital femoral epiphysis.
8. Was there any exaggeration of the normal movements?
In presence of childhood septic arthritis (Tom Smith arthritis), dysplastic hip or post polio
residual paralysis the range of movements is exaggerated in all directions. In SCFE there will
be exaggerated extension, adduction and external rotation and limitation of flexion, abduction
and internal rotation.

Measurement

One should measure the length and circumference of the limb. Longitudinal measurement
includes measurement of the length of the entire lower extremity and measurement of segments.
The segements to measure are the leg segment, infratrochanteric segment and the
supratrochanteric segment. Longitudinal measurement of lower extremity involves measurement
of apparent length and true length.

Apparent length:
Keep both lower limbs parallel to each other in line with the trunk and measure from the
xiphisternum to the medial malleolus tip.

True length:

Square the pelvis in the method described earlier. Further adduct if there is an adduction
deformity and vice versa. True length of the affected limb is measured from the inferior edge of
ASIS to the tip of medial malleolus. Place the normal limb in exactly the same position as the
affected limb and then measure from ASIS to medial malleolus.

Segmental measurements

If there is limb length discrepancy then one should identify the anatomic region of discrepancy.

Supratrochanteric region is assessed by drawing the Bryant’s triangle, Nelaton’s line and
Shoemakers’ line. Infratrochanteric region is measured from the tip of greater trochanter to
lateral knee joint line. Leg segment is measured from medial malleolus tip to medial knee joint
line.

Bryant’s triangle is drawn by placing the patient in the supine position. Mark the tip of greater
trochanter and the inferior edge of ASIS with a skin pencil. Draw a line from the inferior edge of
ASIS vertically to the couch. Draw another line from the tip of trochanter to the first line and
measure. Normally the greater trochanter lies about 2-3 cm below the first line. Compare with
the opposite side. In case of severe shortening the greater trochanter may lie above the first line;
in such cases shortening will be the measured length of the line with 3 cm or normal side
measurement added to it.

Nelaton’s line is drawn by placing the patient in the lateral position with affected side up. Flex
the hip and knee to 900. Draw a line connecting the inferior edge of ASIS to the most prominent
portion of ischial tuberosity. In the normal hip the tip of greater trochanter will be just touching
the line. In patients with supratrochanteric shortening it will be above the line.

Shoemaker’s line is drawn on both sides from the tip of trochanter to the inferior edge of ASIS
and extended further on to the abdomen. Normally the lines will cross in the midline. In case of
supratrochanteric shortening the lines will cross on the opposite side.

Girth measurement is done at the bulkiest part of thigh and calf to look for wasting of muscles.
Wasting of muscles is usually found in long standing disease.

Special tests

Special tests are done as required depending on the clinical diagnosis. They can be divided into
the following.
1. Tests for deformity assessment
2. Tests for stability
3. Tests to assess limb length discrepancy
4. Tests for impingement
5. Tests for muscle contracture

Tests for deformity assessment

Thomas well leg raising test

Patient position- Supine

Procedure – Stand on the right side of the patient with one hand under the lumbar spine of the
patient. With the other hand hold the unaffected side. Flex the unaffected knee fully, then flex
the unaffected hip till the excessive lumbar lordosis disappears. Measure the angle between the
thigh of the affected side and the couch to assess the angle of fixed flexion deformity of the hip.

Interpretation- Normally the limb will lie flat on the examination table. But if there is a fixed
flexion deformity the affected side will be off the couch. The angle between the long axis of
thigh and the examination table gives the angle of flexion deformity.

Staheli prone extension test

Patient position- Prone with hip and knees dangling beyond the end of the examination table

Procedure- Place one hand over the sacrum to stabilise the patient and to detect pelvic motion.
Gently extend the tested lower limb till the pelvis starts to move. Measure the angle between the
long axis of thigh and long axis of the examination couch.

Interpretation- The angle between the thigh and the table is the fixed flexion deformity.

Craig’s test

Patient position – Prone

Procedure- One hand of the examiner is placed flat on the greater trochanter. Knee flexed to 900.
Hold the leg and gently rotate the hip in both directions till the greater trochanter is maximally
prominent.

Interpretation- The amount of internal rotation needed to make the greater trochanter maximally
prominent is the degree of anteversion.

Tests for stability

Trendelenberg test

Described by Freidreich Trendelenberg in 1894.

Patient position – Standing.

Examiner position- Standing behind the patient.

Procedure- Ask the patient to do a one legged stance on the affected limb for one minute. Note
the level of gluteal fold and PSIS.

Interpretation- Normally the pelvis on the opposite side will move up to shift the centre of
gravity due to contraction of gluteus medius of weight bearing side. Up to 50drop is considered
normal. If more than 2cm or 50then it is abnormal and suggests abductor insufficiency.
Insufficiency may be due to abnormal fulcrum, lever or power of the abductor mechanism.

Fallacies- False positive in adduction deformity of hip, quadratus lumborum paralysis and
painful lesions of sacroiliac joint. False negative in abduction deformity.

Don’t do if hip has fixed adduction or abduction deformity.

Telescopy test (Piston or Dupuytren’s test)

Patient position – Supine

Procedure- Flex the knee and hip to 900 and 100 adduction. Stabilise the pelvis with one hand.
Hold the knee and thigh with the other hand. Push and in a to and fro motion.

Interpretation- Relative movement of the hip is suggestive of instability.

Ortolani test

Described by Prof Marino Ortolani in 1936.

Patient position – Infant should be relaxed and in supine position.

Procedure- Flex the hip to 900 and fully flex the knees. Hold both the proximal thigh with the
thumb over the medial aspect of thigh and other fingers over the greater trochanter region. Apply
pressure over the greater trochanter and gentle longitudinal traction. Move the hip into abduction
gently.

Interpretation- If the hip is dislocated; resistance to abduction will be felt at 30-400 of abduction,
then a clink will be felt as the femoral head reduces into the acetabulum slipping over the
acetabular rim. Once the hip is reduced further abduction will be possible up to normal.

Barlow test

Has two parts. First step is similar to Ortolani test, but each hip is separately tested.

Patient position – Infant should be relaxed and in supine position.

Procedure- Flex the hip to 900 and fully flex the knees. Hold both the proximal thigh with the
thumb over the medial aspect of thigh and other fingers over the greater trochanter region. Apply
pressure over the greater trochanter and gentle longitudinal traction. Move the hip into abduction
gently.

Interpretation- If the hip is dislocated; resistance to abduction will be felt at 30-400 of abduction,
then a clink will be felt as the femoral head reduces into the acetabulum slipping over the
acetabular rim. Once the hip is reduced further abduction will be possible up to normal.

Second Part is as follows

Apply backward and outward pressure over the medial aspect of proximal femur with the thumb.

Interpretation- If the hip is unstable the head will be felt to dislocate with a clunk. Once the
pressure is removed, the head relocates.

Gouvain’s test

Patient position- Supine or lateral position

Procedure- Hold the femur with one hand, stabilise the pelvis. Adduct and internally rotate the
hip. Look for spasmodic contraction of muscles

Interpretation- Seen in Tuberculous hip with fibrous ankylosis

Tests to assess limb length discrepancy

Galeazzi’s test

Patient position – Supine

Procedure- Flex the hip and knee to 900. Note the relative level of knees.

Interpretation- If the knee of the affected side is at a lower level there is limb length discrepancy.

Allis test

Patient position – Supine

Procedure- Flex the knee to 900, flex the hip and place the foot flat on the couch. Note the
relative level of knees.

Interpretation- If the knee of the affected side is at a lower level there is limb length discrepancy.
If it is lower towards the hip side; the femoral side is shortened. If it is lower towards the leg
side; the tibial segment is shortened.

Tests to assess impingement

FABERE (Flexion-Abduction-External rotation-Extension) test

Patient position – Supine

Procedure- Put the affected limb on the opposite limb in the Flexion-Abduction-External rotation
(FABER) position or Figure 4 position. Apply hand over the medial aspect of knee and force the
hip into full abduction and extension.

Interpretation- If the hip cannot be fully abducted and extended to the level of opposite limb or if
there is catching type of pain then test is positive.

Scour test

Patient position- Supine

Procedure- Done by moving the hip in an arc involving flexion-adduction and extension-
abduction. During this movement apply axial load and rotate into external and internal rotation.

Interpretation- Pain and limitation of movement suggest intra-articular pathology.

Stinchfield test (Resisted SLR test)

Patient position- Supine

Procedure- Ask the patient to actively flex the hip to 30 degrees while keeping the knee in
extension and to hold the position. Apply resistance just proximal to the knee.

Interpretation- Pain felt in the groin is suggestive of intra articular pathology.

Posterior impingement test (Hyperextension-Abduction-External rotation (HEABER test)

Patient position – Prone

Procedure- Passively place the affected hip in the Hyperextension-Abduction-External rotation

(HEABER) position.

Interpretation- If there is catching type of pain then test is positive.

FADDIR (Flexion-Adduction-Internal rotation) test or Anterior impingement test

Patient position – Supine

Procedure- Put the affected limb in the Flexion-Adduction-Internal rotation (FADDIR) position.
Apply hand over the anterolateral aspect of knee and force the hip into full adduction and
internal rotation.

Interpretation- If there is catching type of pain then test is positive.

McCarthy test

Patient position- Supine on the couch.

Procedure- Flex both hips fully. Extend the affected hip.

Interpretation- If patient complains of catching pain the test is positive.

Tests to assess muscle contracture

Piriformis test (FAIR (Flexion-Adduction-Internal Rotation test)

Patient position – Lateral position with the affected side up.

Procedure- Flex the hip to 600 and flex the knee. Stabilise the pelvis with one hand. Hold the leg
with other hand. Move the hip into adduction and internal rotation with gentle force.

Interpretation- If there is pain in the buttocks or sciatica then test is positive.

Obers test

Patient position – Lateral position with the affected side up. Opposite hip and knee flexed to 900.

Procedure- Flex the hip and the knee to 900. Stabilise the pelvis with one hand. Hold the leg with
other hand. Move the hip into full abduction and external rotation. Extend the knee and hip and
let the limb drop down due to gravity.

Interpretation- Normally the limb should drop down and rest on the couch. If the limb is held
high in abduction, there is contracture of the iliotibial band.

Ely’s test

Patient position – Prone

Procedure- Flex the knee fully. Observe for flexion of hip.

Interpretation- If the hip flexes, there is rectus femoris contracture.

Examination of Gait:

Front : Look at trunk , pelvis and swinging of hand (contralateral to the hand)

Back : Look at shoulder and pelvis:

Side : Excessive Lordosis, ankle plantar flexion and knee flexion, hip and knee extension.

Examination of the opposite hip, knee and spine

Examination of the sacroiliac joint

Examination of the distal neurovascular deficit

Per rectal examination

SUMMARY

DIAGNOSIS

Anatomical : Synovitis/Arthritis/Coxa vara/Unstable hip/ Ankylosis of hip

Pathological : Traumatic/Inflammatory/Neoplastic/Infective/Degenerative

2. General Examination
Dr Raju K, Associate Professor, Calicut Medical College

1. What are the Genearl Examination Features of Rickets ?

Skull - Frontal bossing , Cranio tabes and Scaphocephali

Delayed closure of sutures and wide fontanellae
Face- Triangular Facies
Teeth- Delayed teeth erruption and caries teeth
Chest- Pigeon chest or pectus carinatum, Rachitic rosary and Harrison's sulcus
Abdomen - Protuberant and hepatomegaly
Widening of metaphyseal region (widening of wrist, double malleoli sign)
Deformities
Lower limb - Coxa vara, anterolateral bowing of femur, genu varum or valgum,
anterolateral bowing of lower tibia. rachitic dwarfism (Renal rickets)

2. How do you classify dwarfism?

Dwarfism is a medical disorder with the sole requirement being an adult height under 147 cm (4
ft 10 in).Two main categories of dwarfism depending on the upper segment:lower segment ratio

Disproportionate and Proportionate.

a. Proportionate Dwarfism (Eg; Nutritional Primordial dwarfism, Seckel syndrome and
growth hormone deficiency).
b. Disproportionate Dwarfism
Short Limb Dwarfism- Eg: Achondroplsia (70%)
Short trunk Dwrfism – Eg: SED, Muchopoly sacharidosis

As per the location

Rhizomelic = root, proximal bones or bones of the upper arm or thigh- Achondroplsia
 Mesomelic = middle, e.g., bones of the forearm or lower leg
Acromelic = end or distal bones, e.g., bones of hands and feet.
Micromelic = entire limbs are shortened

As per the source

Chondro = of cartilage
Osteo = of bone
Spondylo = of the vertebrae

3. What are the neurocutaneous markers of Spinal Dysraphism?

Spinal dysraphism refers to a spectrum of congenital anomalies characterized by an
incomplete fusion of the midline mesenchymal, bony, or neural elements of the spine.
Congenital midline paraspinal lesions, mostly localized in the lumbosacral area, are widely
recognized as cutaneous markers. They include
a. Subcutaneous lipomas
b. Dermal sinuses, tails, and localized hypertrichosis
c. Hyperpigmented lesions and aplasia cutis congenita
d. Gluteal furrow

3. What are the hand deformities in Rheumatoidn arthritis?

Hand deformity is a typical feature of RA. Due to disease manifestations in structures of the
hand, e.g. tendons, capsules, bone and ligaments, different deformities can occur
Most prevalent deformities are
I. Ulnar deviation of the MCP joints
II. Button hole deformity
III. Swan neck deformity
IV. Mallet finger deformity
V. Z thumb deformity
VI. Finger drop or thumb drop due to tendon repture
VII. Anterior subluxation or dislocation
VIII. Rotation of the Thumb.-This is a complex process, taking place in both the carpo-
metacarpal and metacarpo-phalangeal joints.

4. What are the general examination findings of Primary OA?

Primary OA usually feel better with gentle use but worse with excessive or prolonged use, thus
distinguishing it from rheumatoid arthritis.
In smaller joints, such as at the fingers, hard bony enlargements, called Heberden's nodes (on the
distal interphalangeal joints) Bouchard's nodes (on the proximal interphalangeal joints) can be
seen. OA at the toes leads to the formation of bunions

5. How do you diagnose Ligament Laxity?

Criteria (Wynne Davies Ligamentous Laxity JBJS 1970)

If 3 of the 5 pairs of joints examined in any one individual showed this degree of laxity it is
taken as positive
1. Thumb touching forearm on flexing wrist
2. Fingers parallel to forearm with wrist extension
3. Elbows extend past 180°
4. Knees extend past 180°
5. Ankle dorsiflexion past 45°

6. What are the general features of Morquio's disease?

Moderate kyphosis or scoliosis
Mild pectus carinatum ("pigeon chest")
Dysplastic hips, large unstable knees, large elbows and wrists, and flat feet
The combined abnormalities usually result in a duck-waddling gait
Hypermobile joints (Stiff in other types of mucopolysaccharadosis)
Large fingers
Knock-knees
Widely spaced teeth
Bell-shaped chest (flared ribs)
Short stature and short neck (caused by flat vertebrae)
Mid-face hypoplasia and mandibular protrusion
Thin tooth enamel
Corneal clouding
Mild hepatosplenomegaly

7. What are the general features of Osteogenesis Imperfecta?

The disorder charectorised by a generalised connective tissue disor
Skull - Vault of skull is broad
Face- Triangular facies
Eye - Blue sclera due to abnormality of collagen
Teeth- May be small. Failure or Delayed teeth erruption and Carries teeth.
Greyish brown or yellowish dentine. Enamel is defective so that breaks
and peel off easily.
Joint- Excessive joint laxity,sometimes being associated with joint dislocation
and hernias
Skin - Bruising following minimal trauma
Poor wound healing and thin scar tissue due to abnormal skin collagen
Deafness due to otsclerosis
Deformities - Coxa vara and Bowing of lower limb bones. Sabre tibia

8. What are the general features of Neurofibromatosis(Von Recklinghausen's diseases)?

Skin- Cafe-au-lait patches is the most constant feature
Cutaneous neuromas in association with any nerve
Axillary or inguinal frekling
Plexiform neurofibromata
Diffuse soft tissue hypertrophy
Hemangioma and lymphangiomas
Local Overgrowth(gigantism)- Macrodactyly or enlargement of entire limb
Mental status - retardation sometimes with epilepsy
Limbs - Bowing and pseudarthrosis of lower tibia. Rarely fibula and ulna
Axial skeletan - scoliosis (short and sharp curve) or kypho scoliosis
9. What are the cutaneous markers of Neurofibromatosis?
Cafe-au-lait spots – Most common clinical features( More than 6 spots. Each of 15
mm in diameter in adult And 5 mm in children)
Axillary and inguinal freckling
 Cutaneous neurofibroma- also called fibroma molluscum
Plexiform neurofibroma – very sensitive subcutaneous neurofibroma
Verrucous hyperplasia- Thickened overgrowth of skin with velvety soft feel

10. Causes of nerve thickening?

Hansens disease
Rufsums disease
Amyloidosis
Neurofibromatosis
Diabetes mellitus
Sarcoidosis
Nerve abscess
Charcot Marie Tooth disease

11. What is the typical Achondroplasia patient’s posture?

Short Stature consequent on short limb- Proximal segment( Trunk is of normal
length)
Finger tips may only reach the iliac crest
Bulging cranium with scooped out glabella
Low nasal bridge
Small maxilla with prominent mandible
Upper limb short with flexion contracture of elbow
Hands: short and broad, Trident hand, All digits being of equal length(starfish hand)
Lower limbs re also short with varus tibia
Muscular development of limbs is accentuated

12. What are the general features of Psoriatic arthritis?

Oligo to poly arthritis
Predominently affects small joint of hands and feet
Psoriatic skin lesions
Pitting of nail

13. What are the types of obesity?

Obesity is a state where BMI is greater than 30 kg/m2
BMI Classification
< 18.5 underweight
18.5–24.9 normal weight
25.0–29.9 overweight
30.0–34.9 class I obesity
35.0–39.9 class II obesity
≥ 40.0 class III obesity

Any BMI ≥ 35 or 40 is severe obesity

A BMI of ≥ 35 or 40–44.9 or 49.9 is morbid obesity
A BMI of ≥ 45 or 50 is super obesity
 14. What is the physical appearance of spondylolisthesis?
Exagerrated lumbar lordosis
Flattening of buttocks
Step-off at lower lumbar spine
Lower portion of abdomen appears thrust forward
Transverse crease at the level of umbilicus

15. What are the signs of DVT?

Unilateral leg oedema
Warmth and erythema
Engorged superficial veins
Pitting oedema
Pain and tenderness along the course of veins
Palpable cords along the course of veins

16. Features of Reflex sympathetic Dystrophy?

Pain and altered sensation

(1) Severe and very unpleasant pain often graphically described as `knife-life’ or `burning’
(2) Altered sensation with
Numbness
Paraesthesia (pins and needles)
Hyperalgesia (increased sensitivity to painful stimuli)
Allodynia (normal stimuli perceived as pain)
Vasomotor/autonomic changes
Variable skin colour changes from pallor to redness or purple, blotchy discoloration
Temperature changeÐmay be either warmer or colder than the unaffected limb
Swelling and oedema
Sweating changeÐeither decrease or increase
Trophic changes (shiny skin with hair loss)

17. What are the general features of Osteoporosis?

Thoracic Kyphosis – Dowager’s or widow’s hump

Deformities of appendicular skeleton

18. What are the general examination findings in Musculo skeletal Malignancy?

As a general rule hair to foot examination

Cachexia and anaemia in long standing case
Generalized or localized lymphadenopathy

19. What are the general features of Marfan’s syndrome?

Tall stature- Distal bones of the limb is longer is most striking

Skull – High arched palate, Long narrow face,Prognathism
Eyes – Strabismus and cataract( Ectopia lentis)
Skin – Elastic with stria
Skeletal – Pectus excavatum and Pectus carinatum
 Kyphosis and kyphoscoliosis, spondylolisthesis
Joint laxity
Deformities- Pes planovalgus, genu recurvatum
Hernias- Inguinal, femoral diaphragmatic etc
 3. SLIPPED CAPITAL FEMORAL EPIPHYSIS

CASE DESCRIPTION
HISTORY
12 year old male presenting with
Pain left hip – 1month
Limping left side – 1 month
Apparently normal child gives history of insignificant trauma to left hip 1 month ago when he
tripped and fell down. Even though he was able to walk after the incident, he had significant pain
over the left groin which subsided with analgesics over 2 days. He continued to have dull aching
pain over the groin and medial aspect of thigh aggravated by activity and relieved by rest which
was accompanied by limping over the same side, which was noticed by his parents. There is no
radiation of the pain, rest or night pain. He had no fever or other constitutional symptoms over
the same period. He gave no history suggestive of involvement of other hip or other joints of the
body. No h/o childhood limp. He is currently able to squat in an Indian toilet with difficulty and
unable to sit cross legged.
Past history is insignificant with no history of major surgery, trauma, prolonged hospitalization
or any chronic intake of medication. Developmental milestones are comparable to siblings.
He is the 2nd child of a non-consanguineous marriage with no similar complaints in his sibling or
parents.

GENERAL EXAMINATION
(Anthropometry)- height 120 cm weight -60 kg us:ls ratio – 1 . arm span – 125 cm.
(Head to foot) – no craniofacial dysmorphism, thyroid swelling, rachitic features or features of
generalized ligamentous laxity. Genitalia normally developed for age with presence of axillary
and pubic hair.

LOCAL EXAMINATION
Inspection
Patient lying supine on a hard couch with hip and knee extended and left limb in external
rotation as evidenced by patella and left foot facing outward with apparent shortening on the left
side.
ASIS on the left side is at a higher level. Thigh muscle atrophy on lt side. No scars , sinuses,
dilated veins or abnormal swellings anteriorly. Greater trochanter is posteriorly placed and
elevated as compared to opposite side with no scars or sinuses. Posteriorly no scars , sinuses or
swellings or muscle atrophy.
Palpation
No anterior or posterior joint tenderness. Normal resistance in Scarpa’s triangle. Femoral pulses
palpable equally and normally on both sides. Trochanter shows no irregularity, is non tender ,
smooth, elevated and posteriorly placed. No abnormal masses palpable posteriorly.

Movements
Patient has no fixed flexion deformity with 0 -120 flexion accompanied by axis deviation
evidenced by knee moving to same shoulder past 90 degrees of flexion . Flexion is terminally
limited by pain. Arc of motion is not associated with pain or crepitus. Fixed adduction deformity
of 10 degrees with free adduction of 20 degrees limited by pain and spasm. External rotation
deformity of 30 degree with further ER of 20 degrees limited by pain and spasm. No difference
of rotations in extension. Extension of 10 degree.
Measurements
Patient has an apparent shortening of 2 cm on the left side with true shortening of 1 cm on
squaring the pelvis, which is accommodated in the supra trochanteric area on drawing the
Bryant’s triangle. No discrepancy of circumferential measurements on both side.
Lines and special tests
On drawing the Nelaton’s line, GT is above the line on the left side. Shoemaker’s lines
converges on the opposite side, line on the left side pass below the umblilicus. Chiene’s lines
converge on the left side.
Trendelenberg not done. Telescopy negative.
Sacroiliac stress tests, opp hip, spine and i/l knee – NAD
No distal neurovascular deficit, no inguinal lymphadenopathy
GAIT
Trendelenberg
DIAGNOSIS
Unilateral hip disease left sided probably due to Slipped capital femoral epiphysis

Q&A

Q1. Why do you say it is a SCFE?

A. Male, obese, hypogonadal features
History of insignificant trauma followed by painless limp
Restriction of flexion , abduction and internal rotation
Maintained or increased extension, adduction and external rotation
Exaggeration of ER on hip flexion
No FFD
 Axis deviation on flexion

Q2. You said there is restricted FABIR. is there an actual loss of motion?
A. No. It probably represents a change in the arc of motion because of the displaced
epiphysis, with restricted FABIR and relatively increased EXADER.

Q3. Would you expect a hip flexion deformity in

this case?
A. Not in an uncomplicated SCFE. FFD only
occurs in SCFE with chondrolysis, osteonecrosis,
degenerative joint disease or an anterior slip(rare)

Q4. What do you want to do?

A. Anteroposterior and frog leg lateral views(if not
severely painful)

Q5. Read the XRay. Does it confirm your

diagnosis (What are the radiographic signs in
SCFE)?
A. Anteroposterior and frog leg lateral views.
Yes. Xray pelvis with both hips AP view of an immature skeleton.There is widening and
blurring of the physis with decreased height of the epiphysis. Mild, periarticular osteoporosis
with maintained joint space. Klein’s line does not intersect the lateral epiphysis.
Chronic stages- Herndon hump – reactive bone over superolateral aspect of femoral neck.

Q6. What is the relevance of a frog leg lateral

view in scfe?
A. Since the slip is usually posterior, subtle
stable slipping is best appreciated in frog leg lateral
comparison views. This should not be attempted in
unstable slips.

Q7. What is the relevance of other imaging modalities in scfe?

A. Bone scan and magnetic resonance imaging scan allow earlier diagnosis of avascular
necrosis and chondrolysis.
Ultrasonography - visualization of an effusion in the hip (a sign of an unstable slipped
capital femoral epiphysis) and remodelling of the femoral neck (a sign of a stable slipped capital
femoral epiphysis).
Computerized tomography scanning provides three-dimensional imaging of a slipped
capital femoral epiphysis

Q8. What type of slip is this? What are the different types?
A. Chronic slip as the duration is more than 3 weeks.
I. Onset of symptoms :
Acute (< 3 weeks)/ chronic(> 3 weeks) / acute-on-chronic
II. Functional (patients ability to bear weight)
Stable(able to bear weight +/- crutches)1 / unstable2
III. Morphologic (Southwick – head-shaft angle on frog-leg lateral view
Mild – differs by less than 30º from the normal contralateral side
 Moderate – angle difference between 30º and 60º
Severe - > 60⁰

Q9. What would you do in this case?

A. Stable SCFE – percutaneous in- situ single screw fixation under fluoroscopic control.

Q10. Explain in situ pinning?

A. A 6 or 7 mm cannulated screw, either partially or fully threaded , is inserted into the
center of the epiphysis. Because the epiphysis is posterior, screw insertion begins on the anterior
aspect of femoral neck( more severe the SCFE , more anterior the screw insertion)
Goals of fixation are – prevent further slipping and incite closure of physis.

Q11. Would you do anything for the opposite hip?

A. Prophylactic fixation is indicated in unilateral SCFE only –
-If there is significant remaining growth( age < 10 years)
-SCFE associated with endocrine disorders.
Otherwise, unilateral SCFE after fixation should be followed up to complete physeal
closure with 3- 4 monthly radiographs. Scfe in opposite hip, if it develops, develops within 18
months.

Q12. What are the complications of your technique and how will you avoid it?
A. Incorrect screw placement with screw penetration into the joint is the most common
complication.
To avoid this – tip of the screw must be in the center of the epiphysis both in AP and
lateral views. Advance the screw tip to no more than 8mm or one third of the femoral head
radius from subchondral bone.

Q13. Are there any other methods of treatment? What are the advantages and
disadvantages of each?
A.Immobilization in a hip spica cast
Advantages- Avoids surgery
Prophylactic immobilisation of opp. Hip
Disadvantages- No proper immobilisation given. Progression of slip frequent.
B. Open epiphyseodesis with iliac bone graft
Advantages – avoids complications of internal fixation
Disadvantage – fixation not stable as with screws or pins
C. Open reduction with corrective osteotomy through physis and internal fixation with use of
multiple pins( Dunn, Fish cuneiform subcapital osteotomy)
Advantage – epiphysis is anatomically repositioned on the metaphysis without creating tension
on the epiphyseal vasculature
Disadvantage – high risk of AVN
D. Compensating base – of – neck osteotomy with in situ stabilization of SCFE with use of
multiple pin fixation(Kramer – intracapsular BON ; Barmada – extracapsular BON)
Advantage – less chance for AVN
Disadvantage – only 35 – 55 degree correction possible. ; shortens femoral neck leading to
femoroacetabular impingement
E. Intertrochanteric osteotomy with internal fixation ( southwick – through lesser trochanter;
Correction possible only upto 45 degrees . less chance for AVN. Currently not recommended as
primary treatment of SCFE

Q14. I agree with treatment for a moderate to severe slip. But can’t you leave a mild
degree SCFE alone?
A. A mild slip should also be treated with pinning because of –
Risk of progression of slip
Future risk of degenerative joint disease

Q15. What is a preslip?

A. It is a radiographic finding of irregularity, widening and fuzziness of the physis . There
may be pain in the hip or knee with minimal limitation of IR.

Q16. Is there any difference in the treatment for an unstable slip?

A. Usual treatment is gentle closed reduction under anaesthesia, fixation with two screws,
with decompressive arthrotomy.
Controversial topics – closed/open; need for arthrotomy ; one vs. Two screws

Q17. What are the complications of treatment?

A. Avascular necrosis –most common ; as high as 50 % cases.
Chondrolysis – less frequent ; 1-2%
Further slipping after pinning.

Q18. How can you diagnose chondrolysis radiologically/clinically?

A. Narrowing of the joint space to at least one-half of that in the contralateral hip in
unilateral cases and as narrowing of the joint space to less than 3 mm in bilateral cases.
On examination, the affected hip is held in an externally rotated position at rest, with
flexion contracture and global restriction of hip motion. The patient usually complains of pain
throughout the arc of motion rather than just at its extremes.

Q19. You mentioned that FFD can occur with an anterior slip. Are there any other types?
A. Valgus slip – superior and posterior displacement - restriction of flexion and adduction.
Anterior slip – anterior displacement. Restriction of extension and external rotation.
 4. Slipped upper femoral epiphysis (SUFE)
Dr Harvey George, United Kingdom

What is SUFE and were does it occur?

A disorder of the proximal femoral physis where a dehiscence occurs through the growth plate of
the immature hip. The slip occurs through hypertrophic zone of the physis. Bilateral in 30% of
cases.

Aetiology of SUFE?

Most cases are idiopathic. It may be associated with endocrine and metabolic disorders.
Imbalance between oestrogen and growth hormone increases the thickness of the physis while
reducing its resistance to shear forces. Complication of treatment with chemotherapy and
radiotherapy or occur with administration of growth hormone for short stature.
Associated Factors include obesity (single greatest risk factor), femoral retroversion and
puberty

How would you classify SUFE ?

The most useful classification system is the one by Loder. This outcome-related classification of
slips is based on epiphyseal stability. This classification system is useful as it correlates with
outcome and predicts the likelihood of AVN.
Stable slip. The child is able to weight bear with or without crutches.
Unstable slip. Child is unable to tolerate any kind of weight bearing on the affected hip
Unstable hips have a 47% satisfactory prognosis compared to a 96% satisfactory prognosis in the
stable-hip group. The incidence of AVN in the stable group is nil, whereas 50% in the unstable-
hip group will develop AVN. Joint effusion is absent and the severity of slip is less in the stable-
hip group.

What are the six radiographic features of SUFE ?

1. Kline’s line (Perkin’s sign). A line drawn on the superior border of the femoral neck transects
the femoral head and does not pass through the
femoral head = Trethowan’s sign
2. Metaphyseal blanch sign of Steel. A crescent shaped, dense area in the metaphysis on AP view
represents superimposition of the posteriorly displaced epiphysis
3. Joint space increased inferiorly
4. Widening and irregularity of physis (appears woolly, earliest sign)
5. Decreased epiphysis height (slipped posteriorly)
6. Remodelling changes of the neck (in chronic slips): smooth superior anterior portion and
callus formation on inferior posterior portions

How would you treat SUFE?

The aim of treatment is to stabilise the slip to prevent further progression, and to promote
physeal closure.
Operative options include:
• Pinning in situ: with a single cannulated AO screw (for grade I and II slips)
• Bone graft epiphysiodesis (high complication rates: AVN, chondrolysis, HO bone formation)
• Primary osteotomy by experienced paediatric hip surgeon (for severe slip)

Osteotomies
The more distally chosen the site, the lower the rate of AVN and chondrolysis. In severe SUFE,
the following osteotomies can be carried out at four levels:
• Subcapital osteotomy
• Dunn procedure. A relatively high degree of deformity can be corrected by subcapital
osteotomy but the growth plate must still be open. This is a cuneiform subcapital wedge
resection with trimming posterior beak. This remains controversial due to the high reported rates
of AVN (37%)
• Fish and Cuneiform. Similar to Dunn with modification
• Basal cervical osteotomy. Offers a less precise correction but gives good results. Avoids
dissection of the adjacent growth plate
• Intertrochanteric osteotomy (Kramer)
• Subtrochanteric osteotomies
• Southwick triplanar osteotomy at the level of the lesser trochanter. Reasonably safe but
technically difficult

How do you check your screw is not in the joint?

Screening the hip with the image intensifier (moving the image intensifier around, near near far
far method)
Radiographic contrast medium injection through the cannulated screw.
Serial radiographs during follow up.

Complications of SUFE ?

AVN. Most common complication. Related to unstable (50%) or severe (25%) slip.
Chondrolysis. Rapid progressive loss of articular cartilage associated with pin penetration of the
joint and multiple screw fixation. Diagnosis indicated by virtually nil range of hip movement,
hip pain and a narrowed joint space. Confirm with MRI
Subtrochanteric fracture. Due to low screw placement at insertion or removal
Degenerative joint disease. Can develop in welltreated moderate slips with no complications.
Approximately 10% of patients with SUFE develop OA
Residual leg length inequality and rotational deformity (severe slips that may require late
corrective osteotomy
5. TUBERCULOSIS OF HIP
Q&A
Q1. Why do you say that this case is tuberculous arthritis of the hip?
A. History
Age and Sex: First four decades (though any age is not an exception, this is the most
common age group affected).
Pain of few weeks or months duration
Night Cry
 Fever, loss of body weight
Previous history of Pulmonary TB (If present)
H/o Pulmonary TB in the family contacts etc. (if present)
On Examination:
Antalgic Gait
Characteristic deformity of Flexion, Adduction, Internal Rotation with apparent
shortening with or without true shortening (depending upon the stage of arthritis)
Wasting of muscles out of proportion to the symptoms
Palpable cold abscess (If present)
Sinus (If present)
Hip Movement is painful and restricted in all direction throughout the range of movement
associated with spasm of adductors and lower abdominal muscles
On measurement there is apparent shortening with or without true shortening depending
on the stage

Q2. What is the clinical Staging of tuberculosis? Why are you specifically saying that
this is arthritis?
A. Clinically Tuberculosis of the hip has four stages.
Stage of synovitis
Stage of early arthritis
Stage of advanced arthritis
Stage of dislocation/subluxation
In the synovitis stage, limb has got characteristic attitude of flexion, abduction and
external rotation with apparent lengthening. There will not be much restriction to the hip
movement and pain is felt at the extremes of the movement. This position is seen because this is
the position which allows maximum capsular distention.
In early arthritis stage, the attitude is that of flexion, adduction and internal rotation with
apparent shortening. This deformity develops because patient prefers to lie in the lateral position
with the affected hip up, and also because of muscle spasm. In early arthritis, there will be only
apparent shortening whereas in advanced arthritis, there will be apparent as well as true
shortening. Shortening will be in the range of 2-3 cm.
In the stage of dislocation, attitude will be flexion, adduction, and internal rotation with
true shortening. Shortening will be more than 3cm. Femoral head is usually palpable in the
gluteal region

Q3. Whether patient can get the attitude of flexion abduction and external rotation in
the stage of arthritis?
A. Yes. This occurs if the patient habitually keeps her limb in this attitude for pain relief.
This may also occur if ligament of Bigelow (iliofemoral ligament) is destroyed in the
tuberculous process. In this situation patient may have true shortening with no apparent
shortening (or may even have apparent lengthening of the limb) due to abduction deformity.

Q4. What is cold abscess? What all locations will you look for cold abscess in a case of
tuberculosis of hip?
A. Cold abscess is the combined result of tuberculous infection as well as due to reactive
exudative process. It usually composed of serum, leucocytes, caseous material, bone debris,
tubercle bacilli etc.
In hip tuberculosis, usual sites of cold abscess are in the front of hip in the femoral
triangle, in the medial side of thigh, posteriorly in the gluteal area, laterally in the trochanteric
region, ischiorectal fossa etc. It may even track down to the knee or even ankle along with
neurovascular bundle. From hip joint it may track medially to reach the pelvis. From here it may
travel above the levator ani and point above the inguinal ligament or it may track below the
levator ani to track into the ischiorectal fossa. (So, do not forget to do a per rectal examination of
the patient)

Q5. What are the boundaries of femoral triangle?

A. It is bounded by:
Superiorly the inguinal ligament
Medially the medial border of the adductor longus muscle
Laterally medial border of the sartorius muscle
Its floor is formed laterally by iliopsoas, medially by pectineus and adductor longus. Its roof is
formed by the fascia lata.

Q6. What are the areas around hip where TB commonly starts?
A. Roof of the acetabulum (commonest), Head of the femur, Babcock’s triangle, greater
trochanter. Rarely it can be synovial type of tuberculosis.
Q7. What is the boundary of Babcock’s triangle
A. It is a radiological triangle seen at the neck of femur. Its boundaries are
Medially physis of head of femur
Inferiorly inferior border of neck of femur
Laterally primary compressive trabeculae.
Its significance is that it is a common focus of origin of tuberculosis on the femoral side.

Q8. How will you proceed further in this case?

A. I will take X-ray pelvis with both hips AP and frog leg lateral views. Also will do blood
routine examination and Mantoux test. I will also take chest X-ray and sputum examination for
AFB. ESR will be elevated. X-ray will show reduced joint space, destruction of acetabulum or
femoral head, proximal migration of head, or even frank dislocation. In active stage of the
disease the entire hip will be severely osteoporotic.
A negative Mantoux test practically rules out tuberculosis. A negative Mantoux is also
seen in miliary tuberculosis, immunocompromised state, steroid therapy etc.

Q9. What is the TK Shanmughasundaram’s radiological classifications of TB hip?

A. In Adult
Atrophic type
Protrusio acetabuli type
Wandering acetabulum type
Mortar and pestle type
In Children
Normal type
Perthoid type
Dislocated hip type
Protrusio acetabulum type
Wandering acetabulum type
Mortar and pestle type.
Good functional outcome is usually seen in normal type and Perthoid type where as wandering
acetabulum and mortar and pestle type usually gives a poorer outcome.
Q10. What is the role of MRI in TB hip?
A. If a lesion has to be seen in X-ray at least 40% demineralization has to occur. So pre-
destructive lesions are best seen in MRI. MRI also shows abscess and extent of lesion more
clearly.

Q11. Now clinically and radiologically we are suspecting tuberculous arthritis of hip, how
will you proceed further?
A. I would like to confirm the diagnosis. I will aspirate the joint and send the specimen for
AFB staining as well as for tuberculous culture. I will also send the aspirate for RT PCR
(Reverse transcriptase PCR). Culture can be done either by LJ medium or by Bactec radiometric
method. I will also try to get a tissue diagnosis either by a Tru-Cut biopsy or open biopsy.

Q12. Why do you want to do all of these tests?

A. If patient is diagnosed to have active tuberculosis he will have to take the ATT for a
prolonged period. All the ATT drugs are potentially toxic drugs. So I would like to confirm the
diagnosis before starting the treatment.
LJ medium culture usually takes an average of 6 weeks to get a positive result. BACTEC
radiometric method will usually give a positive result in 3-4 week. But unfortunately culture will
be positive only in 30%-60% of the patients. Direct smear examination for AFB will be positive
only in less than 10%.
Next Option is RT PCR of the specimen. This will enable us to say whether patient is
having active tuberculosis.
Many a times HPE will be reported as granulomatous disease. This can be tuberculosis,
mycotic infection, brucellosis, sarcoidosis etc.
So it is better to do all these tests to get a better chance of diagnostic yield.
BACTEC is a radiometric culture method. Here a culture medium containing palmitic
acid labeled with radioactive carbon 14(C14) is used. Mycobacterium will utilize the palmitic
acid and in the process radioactive 14CO2 is released which is detected by an ionic chamber.
PCR is polymerase chain reaction. Here DNA of mycobacterium is amplified many fold
enzymatically and detected using various methods. Problem here is it cannot differentiate
between live bacteria and dead bacteria. To circumvent this we use bacterial mRNA which has a
half life of a few minutes. Using this mRNA we create a complementary DNA strand and
amplify this. This is the principle behind reverse transcriptase PCR. So if RT PCR is positive it
means pt is having active tuberculosis.
Do not get confused between RT PCR and Real Time PCR. Latter is a faster method of
doing PCR where you get result within 30 to 120 minutes.

Q13. What is the usual end result of osteoarticular tuberculosis?

A. Usual sequela of osteo articular tuberculosis is fibrous ankylosis. Here there will be a jog
of movement at the affected joint and it is extremely painful.

Q14. If this patient is diagnosed to have active tuberculous arthritis, how will u manage
the patient?
A. Nutrition: Improve the nutrition of the patient
ATT: Do a LFT, ophthalmology evaluation and start antituberculous treatment as per
DOTS regimen. In the intensive phase give four drugs for 2 months (Rifampicin 450 mg, INH
600 mg, Pyrazinamide 1500 mg and Ethambutol 1200 mg all given thrice weekly) and in
continuation phase only INH and Rifampicin is given in the above dosage for 4 more months.
 HIP: I will put the patient on traction and will start active mobilization of the hip joint as
tolerated by the patient. Usually by 6 months patient may be able to do a partial weight bearing
crutch walking and by 12-18 months patient may be able to fully weight bear. If patient is not
responding for this nonoperative treatment I will do a joint debridement surgery and then
continue traction and ATT as usual. In spite of this treatment if it is felt that the joint is going for
fibrous ankylosis I will offer either a stable but immobile painless hip or a mobile but unstable
painless hip, and treat depending on the patient’s preference. Depending on that I will do an
excision arthroplasty or an arthrodesis of the hip.

Q15. What are the prerequisites before doing the hip arthrodesis? What position you will
do arthrodesis?
A. Lumbo sacral spine, ipsilateral knee and contralateral hip should be normal. So never say
arthrodesis as an option of treatment in a bilateral hip disease patient.
Hip is arthrodesed in 300 flexion, neutral abduction-adducion and 150 external rotation.

Q16. What are the structures removed in girdle stones excision arthroplasty?
A. Head of femur, neck, proximal part of greater trochanter and acetabular margin.

Q17. Will you do total hip replacement arthroplasty in tuberculosis hip?

A. If there are no signs of active infection or drainage for the last 2 years then THR is a well
accepted treatment now. Usually preoperatively ATT is given for 3-4 weeks and post operatively
ATT is continued for 6-9 months. Warn the patient of recurrence.
With the knowledge that mycobacteria is not forming biofilm on the implant and is still
susceptible to the antibiotics and body’s immune response, THR is nowadays done in active
tuberculous arthritis of hip. In these cases ATT is frequently given for 2-3 months prior to the
surgery and continued for 12-18 months post surgery.

Q18. If you are doing THR whether you will do a cemented or uncemented in a case of
tuberculous arthritis.
A. There is no difference whether you do a cemented or uncemented regarding disease flare
up, functional results etc as far as tuberculosis is concerned.
The decision to do a cemented or uncemented is based on the patient’s age, bone stock,
affordability etc. If the patient is young and has good bone stock it is better to go for uncemented
hip.

Q19. What are the drugs used for tuberculosis?

A. First line: Rifampicin, INH, Pyrazinamide, Ethambutol, Streptomycin
Second line: Aminoglycosides (Amikacin, Kanamycin)
Quinolones (Ciprofloxacin, Levofloxacin, Moxifloxacin)
Ethionamide
Cycloserine
PAS
Combination drugs are given to prevent drug resistance. INH, Rifampicin and ethambutol
are bacteriocidal and PZA is weakly bacteriocidal. INH and Rifampicin are very active against
rapid growers, where as all the four are active against slow growers. PZA alone can act at acidic
media (at the site of abscess and inflammation).
Q20. What is DOTS?
A. DOTS Stands for Directly Observed Treatment Short course. This is a WHO initiative. It
is implemented in india as part of RNTCP(Revised National Tuberculosis Control Programme).
It consists of 5 principles which include
Government commitment to control TB
Diagnosis based on sputum-smear microscopy tests done on patients who actively
report TB symptoms
Direct observation short-course chemotherapy treatments, where a person actively
watches the pt swallowing the drug.
A definite supply of drugs
Standardized reporting and recording of cases and treatment outcomes
DOTS uses thrice weekly regimen of R3H3Z3E3 for the initial two months and then
R3H3 for next 4months. In RNTCP, tuberculosis categorized into two categories. CAT 1 is all
newly diagnosed cases. CAT 2 is defaulters, relapse and failure cases.
Previous CAT 3 group is abandoned now

6. DEVELOPMENTAL DYSPLASIA OF THE HIP

Q&A

Q1. What are the examination findings in CDH ?

Trendelenburg Gait (Waddling gait in B/L)

Increased Lumbar lordosis
Higher buttock fold on affected side
Buttocks are broad & flat (B/L)
Perineal space is widened (B/L)
Greater trochanters are elevated & more prominent than normal
Positive Vascular sign of Narath
Head of femur palpable in the gluteal region
Adduction contracture
Movements – restricted abduction & increased internal rotation
Supratrochanteric shortening
Positive Galeazzi sign
Positive Barlow’s & Ortolani’s sign
Telescopy Positive
Positive Trendelenburg’s sign

Q2. What is Barlow's Test ?

A. This test has got 2 Parts- Thumb on the medial side of thigh and fingers on the back of
hip.
First part- Hip is flexed, & adducted, while pushing posteriorly in line of the shaft of
femur, causing femoral head to dislocate posteriorly from acetabulum.
Second part- Similar to Ortolani's test. Dislocation is palpable as femoral head slips out
of acetabulum.
Barlow's test identifies unstable hip that lies in the reduced position but can be passively
dislocated (and hence unstable). Less than 2% of infants will have a positive Barlow test

Q3. What is Ortolani's Test ?

A. Hips are examined one at a time.
Flex infant's hips & knees to 90 deg.
Thigh is gently abducted & bringing femoral head from its dislocated posterior position
to opposite the acetabulum, hence reducing femoral head into acetabulum.
In positive finding, there is a palpable & audible clunk as hip reduces.

Q4. What are the differential diagnosis of DDH ?

A. Septic arthritis sequelae
Coxa vara
Pathological dislocation
Paralytic dislocation of Polio
Cerebral Palsy

Q5. The incidence of DDH is higher in ?

A. Breech position –
A double breech position is associated with a low incidence of DDH.
A single footling breech is associated with a 2% risk of DDH.
A frank breech, especially with the knee(s) extended, is associated with a 20%
risk of DDH.
First-born children
Females: 80% of cases
Pregnancies complicated by oligohydramnios
Left hip is more often involved than the right. Because the most common intrauterine
position has the left hip adducted against the maternal sacrum which places the left hip at greater
risk for dislocation than the right hip.
Down's syndrome

Q6. What are the congenital associations of DDH ?

A. Torticollis (15%-20%)
Metatarsus adductus (1.5%-10%)
(Clubfoot has not been shown to have a significant relationship to DDH)

Q7. Clinical classification of DDH ?

A. Crowe classification
Crowe I - Least severe; the femur and acetabulum are almost normally
developed,<50% subluxation. Crowe II - 75%?dislocation
Crowe III - Acetabulum lacks a roof and there is formation of "false acetabulum"
Crowe IV - Acetabulum is completely underdeveloped and there is high
dislocation
Klisic classification
DDH at risk
DDH I - Hypoplastic with limited abduction
DDH II- Reducible displacement with a click on entry
DDH III- Reducible displacement with a click on exit
DDH IV- Subluxation & limited abduction
DDH V- Dislocation with limited abduction, femoral shortening & telescoping

Q8. What is the reason for valgus deformity of upper femur in DDH ?
A. Normally when a child is born there is coax valga and increased femoral anteversion. As
the child grows older and starts weight bearing the anteversion and neck shaft angle decreases.
Due to abnormal pattern of weight transmission excessive valgus and anteversion persists in
children with DDH. Muscle imbalance can also significantly affect the growth and morphology
of the upper femur. Excessive adductor pull or inadequate abductor muscle function results in a
valgus deformity of the upper femur.
Q9. What is C E angle and its importance ?
A. Center edge angle of Wiberg
Provides useful information after the age of 5 years (may be used in adults);
AP radiograph should be made standing in neutral rotation
Mark the centre of femoral head
Angle formed by a line drawn from the center of the femoral head to the outer
edge of the acetabular roof, and a vertical line drawn through the center of the femoral
head;
Angles greater than 25 deg are considered normal
Less than 20 deg indicates severe dysplasia
Q10. What is Von Rosen View & its significance?
A. Used to evaluate femoral head reduction in child with suspected congenital hip
dislocation/subluxation
Patient is supine with hips abducted 45 deg & maximally internally rotated
AP projection of the pelvis is then obtained
Normally an imaginary line extended up the femoral shaft intersects the acetabulam
If hip is dislocated the line crosses above the acetabulam

Q11. What is Hilgenreiner's Line & Perkin's Line and its importance ?
A. Hilgenreiner's Line: horizontal line along inferior aspect of triradiate cartilage
Perkin's Line: vertical line along lateral edge of acetabulum
Perkin's quadrant’s Lower inner – Normal
Upper inner – Subluxation
Lower outer – Dislocation
Upper outer – High dislocation

Q12. Role of Arthrogram in DDH ?

A. Note size of the limbus, capsular distension, medial pooling of dye
Two directional arthrography:- allows evaluation of the anterior, superior, and posterior
portions of the limbus;
The lateral arthrogram - allows visualization of the anterior/ posteror limbus & iliopsoas
muscle

Q13. What are the obstacles for reduction of hip in DDH?

A. Femoral head and neck remain anteverted and in the valgus position
Muscles crossing the hip jont (hamstring, hip adductors, & psoas) become shortened and
contracted
Psoas cross acetabulum, blocking reduction
Arthrogram may show hour glass configuration of joint space
Hip joint filled with fibrofatty tissue known as pulvinar
Acetabular labrum
-becomes enlarged along the superior, posterior, and inferior rim
- may infold into joint (inverted limbus)
 - limbus blocks reduction of femoral head acetabulum
- becomes flattened (dysplastic) becuase it is not stimulated to develop around the absent femoral
head;
Ligamentum teres becomes lengthened, hypertrophic & redundant;
Transverse acetabular ligament - pulled superiorly with capsule which blocks lower
portion of acetabulum;
Capsule of hip joint – expanded, pericephalic insertion & adhesions

Q14. What is the MRI classification of DDH ?

A. Kashiwagi classification
-Group 1 hips had a sharp acetabular rim, and all were reducible with a Pavlik
harness.
-Group 2 hips had a rounded acetabular rim, and almost all could be reduced with
a Pavlik harness.
-Group 3 hips had an inverted acetabular rim, and none was reducible with the
harness.

Q15. Treatment Goals of DDH

A. Goal is to achieve and maintain a concentric reduction of hip joint
Concave acetabulum cannot develop without concentric force exerted by the reduced
femoral head
Upto age 1 yrs, concentric reduction generally results in normal hip
Upto age 4 yrs, reduction along w/ operative correction of acetabular dysplasia or
correction of femoral anteversion can lead to normalization of the hip

Q16. Age-Based Guidelines for Treatment of DDH ?

A. Neonate: Place in Pavlik harness for 6 weeks
1 to 6 months: Place in Pavlik harness for 6 weeks after hip reduces
6 to 18 months: Traction; closed reduction. If closed reduction is successful, place in cast
for 3 months. If closed reduction is unsuccessful, perform open reduction. Open reduction is
performed by a medial approach in children younger than 12 months of age and by an
anterolateral approach in children older than 12 months of age.
18 to 24 months: Trial of closed reduction, or primary open reduction (anterolateral
approach). A Salter osteotomy may or may not be part of the procedure
24 months to 6 years: Perform primary open reduction (anterolateral approach) and
femoral shortening, with or without a Salter osteotomy

Q17. What are the indications of Pavlik harness ?

A. Infants with DDH who are younger than six months

Q18. What are the contra-indications of Pavlik harness ?

A. Infants with a "hip click" but a normal physical exam (Barlow's test and Ortolani's test)
Teratologic dislocation
Child is in walking age
Q19. What are the indications of open reduction in DDH ?
A. Femoral head lying persistently above triradiate cartilage
Femoral head lying laterally > 6weeks
Previous fail reduction
Q20. What is the complication of open reduction in DDH ?
A. Avascular necrosis
Traction & Femoral shortening prevent excessive compression of femoral epiphysis &
will prevent AVN

Type of Osteotomy Comments

With Concentric Reduction
Younger than 8 yr of age
Salter Redirects acetabulum
Pemberton Restructures acetabulum, decreases volume
8-15 yr of age (triradiate open)
Triple innominate (Steel) Greater redirection of acetabulum
Double innominate (Sutherland) Greater redirection of acetabulum
Dega Restructures acetabulum
Older than 15 yr of age (triradiate
closed)
Triple innominate Greater redirection of acetabulum
Ganz (Bernese) Maximum acetabular redirection; achieves stable pelvis;
difficult
Spherical (Wagner, Eppright) Maximum acetabular redirection; difficult
Without Concentric Reduction
Shelf (Staheli)
Chiari
 7. Developmental dysplasia of the hip (DDH)
Dr Harvey George, United Kingdom

1. Define DDH?

DDH comprises a wide spectrum of hip abnormalities ranging from mild acetabular dysplasia to
complete dislocation of the hip.

2. What are the other “packaging” disorders associated with DDH?

Torticollis, plagiocephaly, metatarsus adductus, congenital recurvatum or dislocation of the

knee, calcaneovalgus feet and clubfoot deformities.

3. Explain Graf’s method of assessing DDH?

Graf used ultrasound for assessing DDH. Graf’S Hip angle measurements are based on three
lines and two angles
1. Baseline is drawn on the ilium to the junction of the cartilaginous roof and bony acetabular
roof 2. Bony acetabular roofline 3. Cartilaginous roofline.
The alpha (a) angle is formed by the bony acetabular roofline and the iliac line
The beta (b) angle is between the baseline and the cartilaginous roofline
In the normal hip a>60°, and the smaller the angle the greater the dysplasia. When b>77° the hip
is subluxed and the labrum is everted. The hip ratio measurement calculates the percentage of
femoral head coverage under the bony roof.

4. What is Graf ultrasound classification?

Based on the depth and shape of the acetabulum as seen on coronal image. Four types of hip are
described:
Type I: Normal hip.
Type II: Shallow acetabulum with a rounded rim. Immature or somewhat abnormal.
Immature(physiological) hip spontaneously resolves in infants <3 months old. Mildly dysplastic
in infants >3 months old persists without treatment.
Type III: Subluxated or low dislocation. Bony roof deficient, labrum everted.
Type IV: High dislocation. Flat bony acetabulum. Labrum interposed between femoral head and
lateral wall of the ilium.

5. Describe the natural history of untreated DDH ?

Muscles about the hip contract and become shortened. Iliopsoas tendon becomes interposed
between the femoral head and acetabulum blocking reduction
The hip joint becomes more dysplastic and filled with fibrofatty tissue (pulvinar)
The capsule becomes redundant and expanded. An arthrogram may show an hourglass
constriction of the joint capsule caused by the contracted iliopsoas, which blocks hip reduction
Ligamentum teres becomes lengthened, hypertrophied and redundant. The femoral head and
neck remain anteverted and in valgus position. Head becomes misshapen and flattened with
delayed ossification of the epiphysis
Acetabulum labrum becomes elongated and hypertrophied and may infold into the joint (inverted
limbus) blocking reduction of the femoral head.
Abnormal femoral head and false acetabulum develop in the ilium wing Transverse acetabular
ligament contracts and is a major block to a deep concentric hip reduction

6. Describe five radiological features of DDH?

Break in Shenton’s line

Increased acetabular index (normal is <25°; >30° indicates dysplasia, significant if >40°)
Delay in appearance of the ossific nucleus of the femoral head
Lateral and superior migration of the femoral neck
Delayed ossification: U figure or teardrop of Koehler

7. How do you perform an arthrogram ?

Place patient in supine position, usually with GA, aseptic technique. Use fluoroscopic control
with careful placement of the needle through the adductor approach into the empty acetabulum.
Check the position of the needle using fluoroscopy and inject a small amount of diluted contrast
medium. Image in the position of dislocation and reduction. Note any obstacles to reduction and
determine the stability of reduction. Dangers include scoring of the femoral head cartilage with
the needle, injection into the growth plate or the piercing of femoral blood vessels.

8. What do you look for in an arthrogram?

Whether the acetabulum is dysplastic

Is the hip subluxed or dislocated? Can the hip be reduced?
Is there soft-tissue interposition (pulvinar fat)?
Is there pooling of the dye medially (normal ≤7 mm)?
Is the ligamentum teres hypertrophic and redundant?
If the labrum is normal or inverted (limbus), look for a rose thorn sign of an inverted labrum
between the femoral head and acetabulum
Is there an hourglass constriction of the capsule (by psoas tendon)?

9. What is Pavlik harness?

It is a dynamic flexion/abduction orthosis used to treat DDH in children up to 6 months of age.

It maintains the affectedhip in 90°–100° of flexion and abduction (usually halfway between full
abduction and dislocation,approximately 60°) and restricts extension and adduction. The harness
allows for motion within the range of reduced stability.

10. What are the complications of Pavlik harness?

Femoral nerve palsy secondary to excessive hip flexion. Brachial plexopathy due to compression
from high-riding shoulder strap and knee subluxations from improperly positioned straps. AVN
occurs in as many as 2.4% of cases splinted in the safe zone. Failure of hip reduction. Fixed
posterior dislocation with damage to the posterior acetabulum due to failure to detect persistent
dislocation (Pavlik harness disease) and skin maceration

11. Describe medial open reduction of hip in DDH?

(Advantage, disadvantage, indication, procedure)
The true medial approach described by Ludloff utilizes the interval between pectineus and
adductor longus and brevis. Ferguson modified it to pass between adductor longus and brevis
anteriorly and adductor magnus and gracilis posteriorly. Indication - Before walking age (6–9
months).
Advantages include small groin incision, minimal soft tissue dissection, avoids splitting the iliac
apophysis and it approaches the hip joint over the site of the obstacles to reduction
Disadvantages include poor exposure, poor visualization of joint interior, unable to reef
redundant capsule, concerns regarding the completeness of removal of obstacles to reduction,
risk of re-dislocation and it increased rates of AVN.

12. What are the complications you are worried about following DDH treatment?
Osteonecrosis seen following all forms of treatment
Increased rates associated with excessive or forceful abduction, previous failed closed treatment
and repeat surgery
Diagnosis based on radiographic findings that include failure of appearance or growth of the
ossific nucleus 1 year after reduction, broadening of femoral neck, increased density and
fragmentation of ossified femoral head and residual deformity of proximal femur after
ossification
Recurrence approximately 10% with appropriate treatment; requires radiographic follow-up until
skeletal maturity
 8. OSTEOTOMIES AROUND HIP
Q1. Name few osteotomies around hip ?
A. Name any few osteotomies given in this section which you are sure of answering
properly.

Q2. What are the osteotomies done for CDH and unstable hip ?
A. Femoral osteotomies : Varus derotation
Primary femoral shortening
Acetabular : Salter innominate osteotomy
Pemberton osteotomy
Steel or Ganz osteotomy
Chiari shelf osteotomy
Dial osteotomy
Spherical acetabular osteotomy

Q3. What are the osteotomies done for SCFE ?

A. Triplanes osteotomy
Biplane osteotomy of Southwick
FISH, DUNN, Abraham, Kromer

Q4. What are the osteotomies done for Perthes disease?

A. Axer’s Open Wedge Varus Derotation osteotomy
Salter's innominate osteotomy

Q5. What are the osteotomies done for osteonecrosis of femoral head ?
A. Transtrochanteric rotational osteotomy of Sugioka

Q6. What are the osteotomies done for coxa vara ?

A. a) Inter trochanteric valgus osteotomy of Borden
b) Cuneform “Y” shaped intertrochanteric osteotomy of Pauwel

Q7. What are the osteotomies done for osteoarthritis hip ?

A. Pauwels type I varus osteotomy hip
Pauwels type II valgus osteotomy
Blount’s osteotomy
Milch Bachelor osteotomy
McMurray’s osteotomy
Periacetabular osteotomy of Ganz

Q8. What are the indications for varus derotation osteotomy in CDH?
A. Stable hip in internal rotation and abduction

Q9. What are the indications for innominate osteotomy in hip?

A. Stable hip in flexion and Abduction

Q10. What are the indication for Pemberton’s osteotomy?

A. Double diameter acetabulum and Anterolateral deficiency
Q11. What is Salters osteotomy ?
A. Ilium is osteotomised from the greater sciatic notch to anterior inferior iliac spine.
Grasp the inferior fragment pull anteriorly, inferiorly and laterally to open anterolaterally
using pubic symphysis as hinge. Keep the gap open with iliac crest graft. Fix it with k wire.

Q12. What are the prerequisites for Salter osteotomy?

A. Age 18 months to 6 years, Concentric hip reduction.No contractures. Full range of
movements.

Q13. What is the other name for Pemberton's osteotomy ?

A. Acetabuloplasty or Pericapsular osteotomy of ilium

Q14. What is the hinge for rotation in Pemberton's osteotomy ?

A. Triradiate cartilage
Q15. What is the pelvic osteotomy done in adolescent / adult CDH with degenerative
changes ?
A. Ganz (Bernese) Periacetabular osteotomy

Q16. What is Staheli procedure ?

A. Shelf osteotomy to augment acetabulum where hip cannot be contained by a
redirectional procedure due to deficient acetabulum

Q17. What is Chiari osteotomy?

A. This is a capsular interposition arthroplasty done in situations where other reconstructive
procedures are not possible. Osteotomy is done at the superior margin of the acetabulum just
above the attachment of hip joint capsule and the pelvis inferior to the osteotomy with the femur
is shifted medially.

Q18. What is the level of Dunn osteotomy done for SCFE?

A. Cuneform osteotomy just proximal to the epiphysis

Q19. What is the principle of Dunn osteotomy ?

A. Slip of the femoral head strips the periosteum from the back of femoral neck and a beak
of new bone is laid beneath it.
The main retinacular blood supply runs up the back of femoral neck
Laterally approach allows stripping of the periosteum and its contained blood vessels under
direct vision to avoid damage of the blood vessels to the femoral head.

Q20. What is the advantage of Dunn osteotomy ?

A. It corrects the deformity at the level of the deformity
Q21. What is the disadvantage of Dunn osteotomy ?
A. AVN
Chondrolysis

Q22. What is Southwick osteotomy ?

A. Extra capsular, intertrochanteric “Biplanar” osteotomy, to create in opposite deformity
taking a measured wedge from the anterolateral aspect of intertrochanteric region.

Q23. What is the principle behind the Axer's osteotomy

A. To obtain maximal coverage of the femoral head (containment)
To decrease the excessive femoral anteversion

Q24. What are the prerequisites for doing a VDO:

A. 1. Age above 5 years
2. Free abduction, adduction and internal rotation
3. No hinge abduction

Q25. What is the osteotomy done for hinged abduction

A. Valgus extension osteotomy

Q26. What is the principle behind Sugioka’s osteotomy

A. To reposition the necrotic anterosuperior portion of the femoral head to a non weight
bearing posterior location.

Q27. What are the objectives of the cuneiform Y shaped valgus osteotomy of the Pauwel
in congenital coxa vara ?
A. To keep the capital femoral epiphysis perpendicular to the compressive force
and to decrease the bending stress in femoral neck.
Medial displacement of the upper femoral shaft widens the femoral neck, and eliminate
the tension stress caused by the bending.

Q28. What are the aims in doing on osteotomy in osteoarthritis hip ?

A. 1. Relieve pain
2. Restore motion
3. Correct deformity
4. Restoration of stability
5. Reversal of degenerative process

Q29. How pain is relieved by osteotomy in OA hip ?

A. Haemodynamic by decreasing the intra-osseous pressure
Biomechanic Reducing the muscle force
Displacing the fulcrum
Relaxing capsule
Restoring the acetabula to femoral congruency

Q30. What are the indications for varus osteotomy ?

A. 1. Antalgic gait
2. Abduction deformity
3. Free abduction beyond abduction deformity
4. Pain full adduction

Q31. What are the indications for valgus osteotomy ?

A. 1. Trendelenberg limp
2. Adduction deformity
3. Adduction beyond adduction deformity
4. Extension may be obtained by taking the wedge posteriorly

Q32. What are the features of Pauwels type I varus osteotomy ?

A. Medially based wedge
Abductor lever arm is increased
Relaxes abductors, psoas and adductors
Extension may be obtained by taking the wedge posteriorly

Q33. What is the disadvantage of Pauwel’s Type I osteotomy ?

A. Shortening
Trendelenberg gait
Prominence of greater trochanter

Q34. What is the Muller’s modification of the varus osteotomy ?

A. A short wedge taken from the medial side and is placed laterally

Q35. What are the features of Pauwel’s valgus osteotomy ?

A. Done for acetabular dysplasia with uncovered femur head anterolaterally
required

Q36. What is Milch - Batchelor osteotomy ?

A. This is a salvage osteotomy.
Resection angulation osteotomy

Q37. What is McMurrays osteotomy ?

A. This is an oblique osteotomy from the lower border of a trochanter at the lateral aspect of
the shaft below the level of the lesser trochanter to a level above the level of lesser trochanter
medially. Shaft is displaced medially.

Q38. What are the indications for McMurray’s osteotomy ?

A. 1. Severe OA hip for pain relief
2. Ununited fracture neck of femor in young adults

Q39. What is the principle of doing McMurray’s osteotomy in ununited fracture neck of
femur ?
A. Valgus lifting of the proximal fragment occurs due to the pull of psoas major on the
medially displaced distal fragment, making the fracture line more horizontal
Arm chair effect the distal fragment is placed directly under the head of femur. The
weight transmission occurs from the head to the distal shaft fragment by passing the fracture site.
Hence even if the fracture does not unite, painless weight bearing is possible.
McMurrays osteotomy allows painless weight bearing even in the presence of persistent
non union, which is it’s advantage over angulation osteotomies.

Q40. What is the disadvantage of McMurray’s osteotomy ? How it can be countered ?

A. A future THR is difficult
The medial displacement is reduced to not more than 50% of the width of the shaft, so
that a future THR is possible, when McMurray’s osteotomy is done for OA hip.

Q41. What is disadvantage of doing a valgus osteotomy in ununited fracture neck of

femur ?
A. - The abductor lever arm is decreased
- This increases the joint reaction force(JRF)
 - More the valgus, more the JRF
- This leads to early OA or AVN of the Head of femur
- The limb following the valgus osteotomy is unacceptable.

Q42. What are the angulation osteotomies done for ununited # neck of femur
A. 1. Pauwels valgus osteotomy
2. Dickson’s high geometric osteotomy

Q43. What are the displacement osteotomies done for the ununited fracture neck of
femur :
A. 1. McMurray’s osteotomy (oblique)
2. Putti's osteotomy (horizontal)

Q44. What are the osteotomies done for the ankylosed hip as a sequelae of septic arthritis
in unsound position ?
A. 1. Open wedge osteotomy (Gant)
2. Closing wedge osteotomy (Whitman)
3. Brackett Ball and Socket osteotomy

Q45. What are the pelvic support osteotomies in unstable hip:

A. - Shanz osteotomy
- Mitch Batchelor osteotomy – resection arthroplasty with pelvic support

Q46. What is Shanz osteotomy ?

A. This is an abduction osteotomy done at the level of the Ischial tuberosity to get pelvic
support.

Q47. What are the complications of doing a Shanz osteotomy ?

A. 1. Increased valgus -The osteotomy apex may contact the acetabulum and may produce
pain
2. Genu valgum and external rotation may develop as compensatory deformities
 9. SEQUELAE OF HIP SEPSIS

Q&A

Q1. What are the points in favour of your diagnosis?

A. 1. Obstetrical and nursing history suggestive of umbilical cord sepsis,intramuscular
injections,intravenous access for treating any infections,dermatitis and any aspiration/surgical
drainage around the hip.
2. Limb length discrepancy (true shortening)
3. Wasting of muscles
4. Abductor lurch
5. Absent femoral pulses
6. Trochanter shifted high up

Q2. What is the most common differential diagnosis?

A. DDH

Q3. What are the complications and sequelae of septic arthritis of hip?
A. Sepsis may result in both direct and indirect consequences to one or both sides of the
joint.
Direct damage to the articular cartilage is common, and if severe, partial or complete
joint destruction may culminate in ankylosis (fibrous or bony) or instability from
subluxation/dislocation .
Indirect consequences result from physeal damage and avascular necrosis.
In addition to joint destruction, consequences of neglected hip sepsis include joint
instability, abductor insufficiency, and leg length discrepancy. Leg length discrepancy results
from physeal arrest, joint subluxation/dislocation, and/or malpositioning of the extremity from
contracture or ankylosis.
Complications
Destruction of articular cartilage
Destruction of the physis
AVN
Subluxation or dislocation
Long term sequelae
Deformity
Stiffness
Instability
LLD
Growth disturbances
Arthritis
Ankylosis
Osteomyelitis

Q4. What are the poor prognostic factors?

A. Infection occurring before 22 weeks of age because the head of femur is mostly is
cartilaginous and may be completely destroyed by infection
Prematurity
 Delay in treatment more than 4 days
Associated osteomyelitis of proximal femur

Q5. How will you classify the late sequelae?

A. Choi et al classification
Hunka classification

Q6. What are the salient features of Choi et al classification?

A. It is a radiological classification
4 major types- 8 subtypes
Type I
I A - Normal radiographic appearance - Needs no treatment
I B - Those with evidence of avascular necrosis
(Some patients with type Ib with flattened and subluxed head will require
containment treatment, similar to Perthes disease)
Type II(involvement of epiphysis, physis and metaphysis)
Results from avascular necrosis, with or without significant damage to the capital
femoral physis. Asymmetric physeal arrest within the femoral neck may result in alterations in
the neck-shaft angle
II A – Coxa breva with deformed head
(During the early stages, the avascular necrosis is treated by containment, and a
greater trochanteric apophysiodesis may help to manage abductor insufficiency. A pelvic
osteotomy is recommended for coverage if necessary, and leg length discrepancy may require
epiphysiodesis later in life.)
II B - Either coxa vara or coxa valga from asymmetric closure of the proximal
femoral physis.
Managed by realigning the neck shaft angle by osteotomy, and also completing
the growth arrest of the proximal femoral physis to prevent recurrence. Leg length discrepancy
may be managed by epiphysiodesis later on.
Type III (Damage to femoral neck)
III A – Coxa vara /coxa valga with or without excessive femoral anteversion or
retroversion.
( treatment is by proximal femoral osteotomy.)
III B – Pseudarthrosis of femoral neck
(treatment is valgus osteotomy with bone grafting )
Type IV (loss of femoral head /neck)
IV A- a segment of the neck is preserved
In younger patients (< 6 years) with a femoral neck remnant and a cartilage cap,
treatment by open reduction can be considered. A modified Harmon operation and distal transfer
of the greater trochanter may be preformed at the same time. If this fails, then a pelvic support
osteotomy may be the best choice.
IVB- complete resorption of head and neck
(In patients less than 6 years of age who have no femoral neck (or a remnant that
cannot be salvaged), greater trochanteric arthroplasty can be considered.(modified to include
proximal varus osteeotomy) with or without a pelvic osteotomy)
For those older than 6 years of age (Type IVa or IVb), or those in whom a greater
trochanteric arthroplasty has failed, a pelvic support osteotomy is recommended.

Q7. What is Hunka classification?

A. Type I:
There is minimal collapse of the femoral head, which is later followed by
reossification. Radiographic course is comparable to that seen in Perthes disease.
Type II:
Deformity of the femoral head.
IIA - No evidence of physeal damage
IIB - Premature physeal closure, resulting in deformity of the femoral neck as
well.
Type III:
A pseudarthrosis of the femoral neck is observed.
If the femoral head is viable, bone grafting and a valgus osteotomy may promote
healing by increasing compressive forces across the site of nonunion.
If the femoral head is nonviable, resection of the head and neck, followed by
greater trochanteric arthroplasty
Type IV:
Destruction of the femoral head, with retention of a variable portion of the
femoral neck.
IVA- There is sufficient femoral neck present to maintain a stable articulation(
the recommended treatment is to maximize hip joint motion by soft tissue release (adductors
and/or psoas).
IV B - Only a small portion of the femoral neck is retained, and the articulation is
unstable. Consider resection of the residual femoral neck and conversion to a greater trochanteric
arthroplasty
Type V:
Destruction of both the femoral head and the femoral neck is seen( the
recommended treatment is greater trochanteric arthroplasty with or without femoral and pelvic
osteotomies)

Q8. What are the surgical options available and what needs to be considered while
deciding on the surgical option.
A. A. Painful Joint Degeneration
1. Resection Arthroplasty
2. Hip Arthrodesis
3. Greater Trochanteric Arthroplasty
4. Pelvic Support Osteotomy
5. Total Hip Replacement
B. Abductor Insufficiency
1.Greater Trochanteric Growth Arrest(in <7yrs old with near normal hip
articulation)
2. Greater Trochanteric Transfer Distal, Lateral, Or Both
3. Pelvic Support Osteotomy
C. Leg Length Discrepancy
1. Soft Tissue Release
2. Osteotomy
3. Epiphysiodesis
4.Lengthening
5. Pelvic Support Osteotomy
D. Instability (Pistoning)
1. Open Reduction
 2. Greater Trochanteric Arthroplasty(The greater trochanter is surgically placed
into the acetabulum in order to restore stability at the articulation).
3. Pelvic Support Osteotomy
4.Arthrodesis Or Total Hip Replacement
E. Loss of Motion
1. Soft Tissue Release
F. Malpositioned Extremity
1. Realignment Osteotomy

Q9. What do you know about Ilizarov hip reconstruction?

A. It’s a treatment option for the more severe sequelae of hip sepsis. This treatment method
addresses all of the major clinical problems encountered, including instability, abductor
insufficiency, and leg length discrepancy
The procedure involves two osteotomies, one for pelvic support (proximal) , and one for
lengthening and realignment of the mechanical axis (distal). An external fixator is employed,
either an Ilizarov ring fixator , or a hybrid construct with an articulated fixator proximally (to
stabilize the proximal osteotomy) and a lengthening rail distally.
The proximal, abduction osteotomy is performed in the subtrochanteric region, at the
level of the ischial tuberosity. This component of the procedure provides pelvic support for the
proximal femur (eliminates pistoning), and also lengthens the abductor moment arm by
lateralizing the greater trochanter (improves abductor insufficiency). Pain from an incongruous
articulation or breakdown of cartilage is relieved by joint distraction.
The distal osteotomy is performed at the diaphyseal level, and is used for lengthening and
restoration of the mechanical axis of the limb .

Q10. What is L Episcopo or Harmon reconstruction?

A. It’s a sagittal bifurcation trochanteroplasty to fashion a “new head”in cases where head
and neck have been absorbed.
Proximal femur is osteotomised longitudinally (in the anteroposterior direction) and the
medial fragment is bent medially to create a greenstick fracture medially. cortical grafts from
opposite tibia is placed inbetween the osteotomy to keep the fragment angulated medially.the
limb is then manipulated to place this medial fragment in the acetabulum.one and a half hip spica
is applied with limb in neutral rotation and slight abduction.after 3 months gradual weight
bearing is begun

Q11. What do you mean by a trochanteric arthroplasty?

A. The greater trochanter is surgically placed into the acetabulum in order to restore stability
at the articulation (prevent pistoning). The cartilagenous apophysis of the uninvolved greater
trochanter does have the potential to remodel and is thought to mould towards the shape of
femoral head.
Femur is osteotomised below the lesser trochanter and a medial based wedge is removed.
Trochanter is placed within the acetabulum.hip abductors are transferred distally. Vastus lateralis
is reefed over the new insertion of the glutei. The patient is placed in a spica with the hip in
extension and 20 degrees abduction

Q12. If you have a relatively intact neck which is articulating with the acetabulum,what
are the different proximal femoral osteotomies you can do?
A. i) Gantz - Open wedge osteotomy
ii) Whitman – Closed wedge osteotomy
 iii) Brackett – Ball and Socket osteotomy

Q13. Why do you say that the treatment of sequelae of septic hips should be delayed?
A. i) Because of risk of reactivation of infection
ii) The status of femoral head and neck will be understood better only if sufficient time is
given for remodelling

Q14. When will you do an limb length equalisation procedure in case of shortening?
A. It should be done only after the reconstruction surgery

10. NONUNION NECK OF FEMUR FRACTURE

Q&A

Q1. What makes you think this is an old #NOF ?

A. Definite h/o trauma &inability to bear weight
Tenderness over mid inguinal point
Telescopy +ve
Trendelenberg test +ve
Shortening &external rotation
Trochanter is normal

Q2. Why do you think it is not an intertrochanteric fracture?

A. There should be irregular broad thickened trochanter
Tenderness at trochanter

Q3. Why it is not dislocation hip?

A. Flexion, adduction and internal rotation deformity with shortening seen with posterior
dislocation.
B. Head of femur is palpable in the gluteal region.
C. Extention, abduction and external rotation deformity with lengthening may be seen
with anterior dislocation.
D. Narath sign will be +ve in dislocation

Q4. When do you call a #NOF a non union?

A. > 3 months following the fracture.

Q5. What are the causes for nonunion # NOF?

A. Predominantly mechanical
High #angle(more than 60)
Displaced #(garden 3&4)
#comminution
Inadequate reduction &stability of fixation
 Poor bone quality
Injury to vascularity
Absence of cambium layer of periosteum
Lack of hematoma formation
Washing away and dilution of osteogenic factors

Q6. How does delay in treatment affect planning of treatment ?

A. Resorption of #ends
Soft tissue contractures prevent adequate lengthening &reduction
Up riding of trochanter
Acetabular cartilage damage

Q7. What are your D/D?

A. Old ununited #I/T
Old #head of femur(telescopy may be absent)
Malunited # acetabulam
Old treated TBhip (wandering acetabulam mortar & pestle type)

Q8. What are the treatment options available?

A. ORIF with cancellous BG
ORIF with fibular graft
ORIF with vascularised BG(FREE vascularised fibular or muscle pedicle BG
Neck reconstruction
Osteotomies
Arthroplasty
Arthrodesis
Resection arthroplasty

Q9. What all factors will you consider for planning surgery?
A. Age
Presence of AVN
Resorption of fracture ends
Posterior comminution
Amount of osteoporosis
Previous surgery
Presence of infection
Condition of acetabulum
Prior hip symptoms(OA)
Comorbidities
Duration of injury
Fracture variability(site and angulation)

Q10. What are the various muscle pedicle grafts described?

A. Quadrates femoris based(Meyers, Judet)
Gluteus medius based(Hibbs)
Sartorias based
TFLbased(Bakshi)
Gluteus maximus based(Onosun)
Vastus lateralis based(Stuck&Hinckey)
 Myoperiosteal quadratus femoris graft

Q11. What are the advantages of muscle pedicle bone grafts?

A. There is no substitute for original biological joint
Gives a chance to save salvageable joint
Additionally take care of AVN

Q12. What is the role of osteotomies in # NOF

A. Osteotomy alters biological and mechanical environment around #
Alters mechanics-medial shift of line of weight bearing
Correction of deformity
Re alignment of limb during movement
Relaxed joint capsule
Increased vascularity
Increased leverage and stability
Redistribution of tensile forces in to compressive forces

Q13. Which are various osteotomies described?

A. Displacement osteotomies described by has revised by McMurray and Leadbetter
Angulation osteotomy described by Shanz with modification by Pauwel

Q14. What is McMurrays osteotomy?

A. Medial displacement oblique I/T pelvic support osteotomy
Put the shaft beneath the head
Line of wt bearing shifted medially
Makes #line horizontal
Shortens lever arm between trochanter and hip
No longer popular now as it makes futureTHR difficult

Q15. Which are other osteotomies described?

A. Pauwels osteotomy
-Abduction osteotomy at I/T LEVEL
-Converts shearing force in to compressive force
Shanz angulation osteotomy
-Made distal to lesser trochanter at the level just below the level of ischial
tuberosity.
-Angulated so as to gain length
-Line of wt bearing shifted medially
-Not popular now
Dicksons geometric osteotomy

Q16. What is the blood supply of femoral head?

A. Primary sources as described by Crock includes metaphyseal system,retinacular
system,foveolar system
EXTRACAPSULAR ARTERIAL RING
Located at base of femoral neck ,formed by
-Medial circumflex femoral artery(posteriorly)
-Lateral circumflex femoral artery(anteriorly)
 ASCENDING CERVICAL BRANCHES arrives from ECA(Also knows as epiphyseal
artery of TRUETA)
Divided in to anterior ,posterior,medial,lateral group
Lateral group (main group)gives rise to lateral ascending cervical vessels
SUBSYNOVIAL ARTERIAL RING OF CHUNG(circulus articuli vasculosus of Hunter)
Formed from lateral ascending cervical vessels located at base of head
ARTERY OF LIGAMENTUM TERES-BRANCH OF OBTURATOR ARTERY

Q17. What are the various closed reduction maneuvers described for #NOF
A. Maneuvers in extension-
-Whitman
-Deyerle
-Swiontkowsi
Maneuvers in flexion
-Leadbetter-flexion-IR-circumduction to abduction and extension- reduction
checked by resting heel on palm if it rests with out ER then there is secure reduction
-Flynn

Q18. How will you classify #NOF

A. Anatomical classification- Basicervical, transcervical, subcapital
Garden’s classification- Based on the alignment and displacement of the trabeculae
Pauwels classification- Based on the angle of the fracture line from horizontal
Perlingtons classification- Based on the angle of fracture line from vertical

Q19. Which are the tests for stability of hip joint?

A. Active SLR(STINCHFIELD”S test)
Trendelenbergs test
Telescopy test
Ortolanis and Barlows maneuver

Q20. What are the causes for a telescoping hip

A. Girdlestone arthroplasty
Old unreduced dislocations
DDH
Pathological dislocations –TB
Charcots joint
Sequel of septic arthritis
TB HIP (Mortar and pestle type,destroyed head,wandering acetabulam,)
Non-union #NOF
Non-union #trochanter
 11. Legg–Calve–Perthes disease
Q1. Define Perthes disease ?

Non-inflammatory idiopathic AVN of the femoral head in a growing child produced by

interruption of blood supply to the proximal femoral epiphysis.

Q2. Aetiology of Perthes disease ?

Aetiology of Perthes disease is poorly understood, there are several theories.

Hydrostatic pressure theory. Epiphyseal arteries transverse the neck between bone and an
inelastic capsule. This makes them vulnerable to pressure rise, e.g. reactive synovitis. The
femoral neck venous drainage is disturbed with increased interosseous venous pressure. This
leads to arterial or venous thrombosis.

Fibrinolytic disorders.There is evidence to support the association between thrombophilic and

hypofibrinolytic disorders like Protein S and C abnormalities, Leiden factor 5 mutation,
Anticardiolipin antibodies, Micro-trauma or passive smoking etc

It is thought that repeated ischaemic episodes at the femoral epiphysis rather than a single event
cause the disease syndrome.

Q3. What are the differential diagnosis of of Perthes disease ?

Unilateral Perthes disease

1. Transient synovitis
2. Infection (septic arthritis, tuberculosis and osteomyelitis)
3. Blood dyscrasias (lymphoma, leukaemia)
4. Juvenile chronic arthritis
5. Rheumatic fever
6. Sickle cell disease
Bilateral in 10 to 12%. Both hips are never at the same stage of disease (metachronous) unlike
in skeletal dysplasia were both hips looks similar (synchronous).

Bilateral Perthes disease

1. Slipped capital femoral epiphysis

2. Develepmental dysplasia of hip
3. Hypothyroidism
4. Multiple epiphyseal dysplasia
5. Spondyloepiphyseal dysplasia
6. Gaucher’s disease
7. Morquio’s disease
8. Trichorhinophalangeal syndrome

Q4. Describe Waldenstrom staging for Perthes disease ?

Waldenstrom described four radiographic stages.

Necrotic stage - infarction produces a smaller, sclerotic epiphysis with medial joint space
widening

Fragmentation stage - process of ongoing necrotic bone resorption and new bone formation. This
repair process produces the appearance of lateral fragmentation of the femoral epiphysis.

Re-ossification - ossific nucleus undergoes reossification as new

bone appears as necrotic bone is resorbed.

Remodelling stage - femoral head remodels until skeletal maturity

Residue deformity may be coxa magna, coxa plana or coxa breva.

Q5. Describe Catterall’s staging for Perthes disease ?

Catterall’s staging for Perthes disease is based on amount of femoral head involvement on AP
and lateral radiographs. It is determined during the fragmentation stage. The group may appear
to change during the disease process. Hence has little prognostic value. Catterall’s classification
has large inter- and intra-observer errors, inter-observer agreement 85%.

Group I: Central anterior head involvement

Group II: More than 25% head involvement but medial and lateral columns intact

Group III: 75% femoral head involvement but intact medial column

Group IV: Whole head involvement

Q6. Describe Salter–Thompson classification for Perthes disease ?

Salter–Thompson classification for Perthes disease is based on extent of subchondral fracture

(crescent sign). The advantage over theCatterall’s classification is that it provides you with an
early means of predicting what is going to happen to the femoral head.

Group A: Less than half the femoral head is involved and intact lateral pillar

Group B: More than half of the head is involved and involved lateral pillar

Q7. Describe Herring lateral pillar classification for Perthes disease ?

Herring lateral pillar classification for Perthes disease is evaluated in the early fragmentation
stage using AP radiographs of the pelvis. It has less inter- and intra-observer error. The height of
the lateral epiphyseal pillar is compared with the height of the normal contralateral epiphysis.

Group A: Lateral pillar intact

Group B: Lateral pillar collapsed but less than 50% of the normal side

Group B/C: Lateral pillar narrowed 2-3mm or poorly ossified with about 50% height

Group C: Lateral pillar collapsed more than 50% of normal height.

Q8. What are the early radiological findings in Perthes disease ?

Early radiological findings in Perthes disease are medial joint space widening (earliest) ,
irregularity of femoral head ossification and cresent sign (represents a subchondral fracture)

Q9. What are Catterall’s head-at-risk signs?

These are radiographic findings associated with poor prognosis in Perthes disease.

1. Lateral subluxation (most important)

2. Calcification lateral to the epiphysis
3. Gage’s sign: V-shaped defect laterally
4. Diffuse metaphyseal reaction
5. Horizontal growth plate

Q10. Why head at risk signs indicate poor prognosis?

Lateral subluxation and calcification lateral to the head suggest that head is already deformed.
Gage sign suggests that physeal and epiphyseal ossification is severely affected; such growth
arrest leads to head deformity in future. Diffuse metaphyseal reaction suggests that entire
proximal femoral physis is affected and ossification is defective. Horizontal growth plate
suggests that the lateral part of physis is not growing while the medial part continues to grow;
points to future head deformity

Q11. What is Waldenstrom sign?

Widening of medial joint space is called Waldenstrom sign. It is due to lateral subluxation of
head, effusion into the hip, swelling of soft tissue within the fovea and continued growth of
articular cartilage which draws nutrition from synovial fluid.

Q12. What is the earlist sign of Perthes disease on X-ray?

Decreased size of capital epiphysis when compared to other side and Waldensrom sign are the
earliest sign of Perthes disase.

13. What is the role of bone scan and MRI in Perthes disease ?

Bone scan can confirm suspected case of LCP . Decreased uptake (cold lesion) can predate
changes on radiographs

MRI can provide early diagnosis revealing alterations in the capital femoral epiphysis and physis
Q14. What is the role of arthrogram in Perthes disease ?

A dynamic arthrogram can demonstrate coverage and containment of the femoral head .

It is also used to assess suitability for surgery by assessing hinging or point loading at
acetabulum, area of contact and containment.

Q15. Treatment of Perthes disease ?

Key principals in treatment of Perthes disease is containment and maintainance of range of

motion

Conservative treatmrnt includes NSAIDs, painkillers, physiotherapy and crutches, traction,

hospital admission for acute exacerbations and regular outpatient follow-up.

Ambulation abduction brace . This is a difficult type of treatment and there are concerns about
when to start and when to finish bracing.

Surgical treatment includes femoral and / or pelvic osteotomy

Femoral osteotomy - proximal femoral varus osteotomy to provide containment . It can be

combined with de-rotation to reduce anteversion and extension.

Pelvic osteotomy - Salter, triple innominate, Dega or Pemberton osteotomy.

Salvage procedures includes

Shelf arthroplasty. Indicated in the older child to prevent subluxation and increase acetabular
coverage

Chiari osteotomy. Performed in the older child with little remodelling potential to increase the
load-bearing area. May buy several years of painfree hip function before further surgery is
required

Valgus osteotomy. For hinge abduction when an enlarged head is laterally extruded and
impinges against the lateral acetabular rim on abduction, causing pain.

Epiphysiodesis of the greater trochanter. To prevent trochantric over growth.

Q16. Describe Stulberg classification for Perthes disease ?

Stulberg classification is gold standard for rating residual femoral head deformity and joint
congruence. Done at maturity.

Class I: Completely normal spherical head

Class II: Spherical femoral head with either coax magna, short femoral neck or abnormally steep
acetabulum

Class III: Non-spherical (ovoid, mushroom or umbrella shaped)

Class IV: Flat femoral head, flat acetabulum

Class V: Flat femoral head but normal acetabulum

Three types of congruency were recognized:

1. Spherical congruency (Class I and II hips): arthritis does not develop

2. Aspherical congruency (Class III and IV hips): mild to moderate OA develops in late
adulthood

3. Aspherical incongruency (Class V hips): severe arthritis develops before the age of 50 in these
hips.

Stulberg’s results showed that a lack of sphericity alone was not the only predictor of a poor
outcome(congruency was more important).

Q18. Why is the greater trochanter thickened in Perthes disease?

1. Lateral subluxation
2. Muscle wasting and adduction deformity making palpation easier
3. Coxa vara making the greater trochanter more prominent
4. Overgrowth off greater trochanter as its growth is unaffected
And because of increased pull of abductors on the greater trochanter in coxa vara.
 12. BILATERAL HIP CASE

CASE PRESENTATION
HISTORY
42 year old female with pain left hip since the past 5 years and right hip since the past 2 years.
History of limping for the past 2 years. Pain is dull aching in nature, which is aggravated on
walking and relieved on taking rest. There is no radiation of pain and no diurnal variation. She is
unable to sit cross legged or squat. She has difficulty in climbing stairs and can manage to walk
to the toilet and back. She has been taking occasional analgesics with which pain was relieved
initially, but not now.
She has been suffering from bronchial asthma for which she has been on medication since the
past 20 years. She was on traditional medicines initially for 5 years following which she was on
allopathic treatment with oral and inhalational drugs. There has been a weight gain and puffiness
of face for the past 4 years. She is also taking drugs for hypertension. There is no past history of
seizures, diabetes, CAD or tuberculosis.
There is no family history of similar illness or tuberculosis in the family.
There is no history of childhood limping, no history of fever and hospitalization during
childhood. There is no early morning stiffness, involvement of small joints, evening rise of
temperature, no history of any significant trauma, no waxing or waning of symptoms, no history
of rashes, conjunctivitis, or any other features of seronegative arthritis.

GENERAL EXAMINATION
Ht.155 cm
Wt. 68 kg
Upper segment lower segment ratio 1:1
Arm Span normal
No ligamentous laxity or neuro cutaneous markers or pigmentation.
Puffiness of face, hirsuitism, obese, stria over the abdomen present.
There is no craniofacial dysmorphism, subcutaneous nodules, skin rashes.

GAIT is antalgic

LOCAL EXAMINATION
Inspection
Patient is lying comfortably on a hard couch. There is exaggerated lumbar lordosis, hip and knee
extended, patella facing upwards and left foot is more externally rotated than right. ASIS on the
left side is at a higher level. There are no scars, sinuses or swellings, visible. Iliac fossa, inguinal
ligament and Scarpa's triangle appears normal. There are no visible pulsations. Trochanter
cannot be made out. There is no anterior thigh muscle or gluteal wasting.
Palpation
On palpation there is no local rise of temperature, the left ASIS is at a higher level. Normal
resistance is felt over the Scarpa's triangle. There is anterior joint line tenderness on both sides.
The femoral pulsations are felt normally on both sides. Trochanter on the left side is elevated and
more posteriorly placed and is tender on thrust palpation. Posterior joint line tenderness present
on both sides. No mass palpable in the gluteal region.
Movements
On doing the modified Thomas test, there is a fixed flexion deformity of 20 degrees on the left
side with further flexion possible up to 100 degrees, which is limited by pain and spasm, the
range of movement is painful and crepitus is present. On the right side there is a fixed flexion
deformity of 10 degree with further flexion possible unto 120 degree, which is limited by pain
and spasm, the range of movement is painless and there is no associated crepitus. There is no any
axis deviation.
There is an adduction deformity of 20 degrees on the left side with jog of further adduction.
There is an abduction of 20 degrees and adduction of 30 degree on the right side. On flexing the
hip, There is a fixed external rotation deformity of 20 degree on the left side with further external
rotation possible up to 40 degrees. On the right side there is no fixed rotational deformity with
internal rotation of 10 degree and external rotation of 40 degree. On examining the hip in
extension, there is a fixed external rotation deformity of 20 degrees on the left side with further
external rotation possible up to 30 degrees. On the right side there is 10 degree of internal
rotation and 35 degrees of external rotation.
Measurements
There is a limb length discrepancy of 2 cm with left side being shorter. The segmental
measurements are equal on both sides. The circumferential measurements on both sides are
comparable.
On drawing the Shoemakers line the lines converge below the umbilicus towards the left side.
On drawing the Nelaton's line, the tip of the trochanter is above the line on both sides.On
drawing the Chiene's line, the lines converge on the left side.
Trendelenberg test was done on the the right side and is found to be positive. Telescopy test is
negative on both sides.
Sacroiliac joint, spine both knee joint is within normal limits. There is no distal neurovascular
deficit.

SUMMARY
42 year old female with 5 year history of left hip pain and limping and 2 year history of right hip
pain with history of treatment of bronchial asthma for the past 20 years who is functionally
limited to a few steps with inability to squat or sit cross-legged. On examination there is flexion
adduction and external rotation deformity of the left side and flexion deformity of right side with
limitation of internal rotation and abduction.

DIAGNOSIS
Bilateral hip disease with left more affected than the right. Due to secondary osteoarthritis,
probably due to avascular necrosis of both hips.

DIFFERENTIAL DIAGNOSIS
Old perthes
DDH
Q&A

Q1. What are the conditions you should think of when you get a case of bilateral hip
disease?
A. Rheumatoid arthritis
Ankylosing spondylitis
Seronegative Spondyloarthropathy
Bilateral DDH
Bilateral Slip/ Perthes
Osteonecrosis
 MED/SED/Trichorhinophalangeal syndrome
Hypothyroidism
Metabolic disorders eg. Morquio

Q2. What is meant by Sectoral sign?

A. Difference in range of rotation of hip in extension and flexion is called Sectoral sign.

Q3. How did you assess flexion deformity in this case?

A. Supine. Flex both legs till Lumbar lordosis obliterated. Then extend one hip at a time till
pelvis just starts tilting or till lumbar lordosis just begins to reappear. Also called Modified
Thomas test.

Another method is prone extension test or the Staheli' method.

Recently described method is Hamstring shift test, which measures the difference in
popliteal angle of the unaffected side with the affected side in extension and flexion. If there is
exaggerated lumbar lordosis due to fixed flexion deformity of hip, the popliteal angle of the
normal side is more when the affected side is kept straight on the couch.

Q4. What are the methods to assess coronal plane deformities(abduction/adduction

deformities)
A. Kotharis’s method – limbs brought parallel
Perkin’s method – limbs not parallel

Q5. Can you use the Kothari’s parallelogram to find out coronal plane deformity in a
bilateral hip case?
A. No. As the limbs in a bilateral hip case with bilateral abduction/adduction deformity
cannot be made parallel, the Kothari’s method cannot be used here.

Q6. What are the problems in measuring limb length in this case?
A. True length should be measured with both the lower limbs in as nearly the same position
with respect to the pelvis after squaring the pelvis. This is not possible in case of bilateral
abduction/adduction deformity.
Apparent length is measured keeping the limbs parallel to each other, which is also not
possible here.
Q7. What is the dose of corticosteroids thought to be associated with AVN?
A. >2 gram of prednisolone, or its equivalent within a period of two to three months.

Q8. You have taken Anteroposterior and lateral x-ray views in this case which shows
collapse of the femoral head. Don't you want to take an MRI to confirm your diagnosis?
A. No.MRI in a case with established collapse on x-ray is unnecessary.
But MRI is the best diagnostic method(99%sensitive and 98% specific) for cases that are
radiographically occult or not obvious on x-ray.

Q9. Would you prefer a bone scan over an MRI?

A. No. Bone scanning has reported to be insensitive for the diagnosis of AVN of the femoral
head)

Q10. Is there any role for drugs in treatment of AVN?

A. For prophylaxis in at risk patients and in cases diagnosed in the pre collapse stage.
Drugs counteract specific physiological risk factors for AVN such as lipid emboli,
adipocyte hypertrophy, venous thrombosis, increased intraosseous pressure and resorption of
bone.
LOVASTATIN – patients with SLE on high dose corticosteroids and high serum
cholesterol levels.
STANOZOLOL – anabolic steroid in patients with high level of plasminogen activator
activity.
ILOPROST – prostacyclin derivative used as vasodilator in AVN and bone marrow
edema syndrome.
Bisphosphonates- ALENDRONATE prevents bone resorption.

Q10. How can you classify osteonecrosis?

Method for grading size of lesion- Combined necrotic angle described by Kerboul
Small - < 160
Medium – 160 – 200
Large - >200
A major disadvantage of the Ficat and Arlet system is that it has no measurement of lesion size.

Q11. When will you do core decompression?

A. Core decompression is done in cases in precollapse stage with small or medium sized
lesions irrespective of other risk factors.

Q12. What are the surgical options in the management of AVN?

Q13. What osteotomies can you do in AVN?
A. Rotational osteotomies and Angular osteotomies.
Rotational osteotomy – allows translation of the necrotic segment employing a rotational femoral
bone flap based on a vascular pedicle( the medial femoral circumflex artery)
Disadvantages- difficult to perform, high morbidity, future THR is difficult.
Angular osteotomies( varus and valgus)- best results in
young active patients not taking corticosteroids, who had
unilateral hip disease with a good preoperative range of
hip motion, and had a small lesion without femoral head
collapse.

Q14. Is there any role for bone grafting these

lesions?
A. In the precollapse stage , both non vascularised
and vascularised BG can be done.
Non vascularised BG is done in 3 ways-
Placement of cortical graft through a core track
made in the femoral neck and head
Grafting performed through a so-called trapdoor
made through the articular cartilage of the femoral head
(the trapdoor exposes the underlying lesion, necrotic bone is removed, and the cavity is filled
with cancellous and/or cortical bone graft)
Grafting through a window made in the femoral neck at the base of the head (the necrotic
area is removed, and bone graft is placed in the defect)

Q15. What is Bryant's triangle and what is it's significance in a bilateral hip case?
A. A triangle drawn in order to determine the upward displacement of the trochanter in
fracture of the neck of the femur. A line is drawn around the body at the level of the anterior
superior iliac spines, another line is drawn perpendicular to it as far as the great trochanter of the
femur, and the third line is drawn from the trochanter to the iliac spine. Also called iliofemoral
triangle.

Q16. Why wasn't Trendelenberg test done on the left side?

A. Patient has no free abduction on the left side which is needed to perform the test.

Q17. What is assisted Trendelenberg test?

A. It is done where the patient is unable to stand on the affected side for 30 secs on his own.
The examiner stands in front of the patient with palms facing upward to support the palms of the
patient. When the patient stands on the affected side, patient exerts pressure on the examiners
hand on the opposite side
.
Q18. What are the prerequisites of doing a Trendelenberg test?
A. Patient should be able to stand on the affected side for at least 30 seconds.
He should have free abduction and adduction.
He should be able to comprehend the test.

Q19. Conditions in which Trendenlenberg test is positive? What is pseudo

Trendenlenberg?
A. Problems related to fulcrum – osteoarthritis hip
Problems related to lever – Coxa vara
Problems related to muscle power – polio
Psedo-Trendelenberg-- it will always be positive if done in presence of adduction
deformity and always be negative in presence of abduction deformity. This is why it should be
down in presence of fixed adduction or abduction deformity.

Q20. What are the causes of avascular necrosis of the femur?

A. Idiopathic, corticosteroids(h/o asthma), alcoholism, smoking, connective tissue
disease(SLE), sickle cell anemia, Gaucher’s disease, caissons disease, radiation necrosis, oral
contraceptive pills, immunosuppressants.

13.Total Hip Replacement

Frequently Asked Questions
1. What is the principle behind Charnley’s low friction ?
Ans: A) 22mm head to reduce torsional friction B) Metal on polyethylene design C)
Medialization of acetabulum and lateralization of greater trochanter to increase abductor lever
arm, resulting in low friction at the interface.

2. What is the current concept regarding cementation in THA?

Ans: It is a controversy. Cemented THA was the rule to start with. Failure of cemented THA was
attributed to the bone cement and called “cement disease” leading to increasing popularity of
uncemented THA. Later it was established that the cause of failure was not bone cement but
polyethylene debris. Then Hybrid and reverse Hybrid studies became a matter of interest. Now
the concept is to invest on bearing surface and not merely on whether cemented or uncemented.

3. What is the difference between level of neck resection in coxa vara and coxa valga?
Ans: Always do keep maximum neck length possible in coxa valga, means high neck cut in
coxa valga and low neck cut in coxa vara.

4. What is the principle behind restoration of center of rotation of hip?

Ans: Try reproduce the normal anatomy where ever possible bilaterally. Keep the center of
rotation of the hip at the level of the tip of the trochanter. One must remember that just bring
down the centre of roration to the normal level and one must not destroy the abductor
mechanism.

5. What is the correct orientation of the acetabulum?

Anz: 450 inferior inclination and 100 of anteversion.

6. What is cement disease?

Ans: Aseptic loosening of the components was thought to be due to the problems with the
cement and was erroneously named as cement disease. Now the concept is that is the wear
particle from the bearing surface which causes the aseptic loosening and it is now correctly
named as particle disease.

7. What are the common approaches in THA?

Ans: Posterlateral, original anterolateral Charnleys and true lateral Hardinge approaches..

8. What is the best guide to orient the acetabulum?

Ans:Transverse acetabular ligament. The component should be parallel and just proud of TAL.

9. What is best method getting the correct anteversion of the stem?

Ans: Lesser trochanter, adductor tubercle and then the stem should be parallel to the posterior
cortex of the cut neck.

10. What do you mean by the term tribology in THA?

Ans: Study of frictional resistance at the bearing surface in articulating surfaces like metal on
metal, metal of poly, ceramic on ceramic, ceramic on poly etc is called tribology

11. What is the advantage of bigger heads in THA?

Ans: Reduced dislocation rate better functional performance. The distance the head has to travel
before it gets dislocated (Jump distance) is higher. Increased head neck ratio hence better range
of motion and chances of early impingement is less.

12. What is the disadvantage of bigger heads?

Ans: Increased volumetric wear.

13. What about smaller heads?

Ans: Disadvantage is increased dislocation rate and lesser functional performance. Advantage is
reduced volumetric wear but increased point wear. Head neck ratio is less hence reduced range
of motion and early impingement.

14. What is the principle of soft balancing in THA?

Ans. It starts with the perfect neck cut and final ending up with correct abductor tensioning
obtained by the horizontal and partly by the vertical offset.

15. What is horizontal offset?

Ans: The distance from the tip of trochanter to the centre of the femoral head which decides the
correct abductor lever and abductor tension. Vertical offset mainly decides the limb length.

16. In dysplastic hips what is the special precaution one must take?
Ans: Restore the correct center of rotation of the hip. Reconstruct the acetabulum for the best
support to the cup do high neck cut as there may be coxa valga.

17. What are the common causes of failure of THA?

Ans: Malalignment ,infection, wear ,aseptic loosening.

18. What is the major disadvantage of metal on metal implants?

Ans: Metallosis and increased serum and urinary metal ions. Metallosis occurs usually occurs
when there is edge loading which means malalignment of the acetabular cup which results in the
edge of the acetabulum rubbing against the femoral head producing wear particles.

19. What is the biggest disadvantage of postero- lateral approach?

Ans. Dislocation and sciatic nerve damage. The rate of dislocation was 7% and reduced to 2%
with perfect soft tissue repair at the time of closure.
 20. What is ALVAL?
Ans.Aseptic Lymphocyte dominated Vasculitis Associated Lesion. It is seen in failed metal-on-
metal (MOM) total hip arthroplasty.

21. What is the current status of metal on metal articulations?

Ans. It is not advisable to use MOM articulations due to the growing concerns about ALVAL. It
is contraindicated in females of child bearing age due to teratologic risk of increased metal ion
levels if they conceive a child.

14. Total Knee Replacement

1. What is total condylar concept in TKA?
Anz: Recreate the shape of normal condylar shape of the knee in the prosthesis. Other shapes of
prosthesis like ball and socket has failed.

2. What is the current concept regarding cementation in TKA?

Anz: Uncommented TKA is under trial and selected centers follow that concept. The most
widely accepted one is cemented TKA.

3. What all x-rays will you ask for preoperative evaluation?

Anz: Weight bearing AP view of both knees, lateral view to assess size of femur, Skyline/
Merchant view to assess patellofemoral joint and 3-Joint standing view showing both hips, knees
and ankles to assess alignment and to rule out extra-articular deformities of femur and tibia.

4. What is the concept of soft tissue release in varus knee?

Anz: Always release it from the tibia only not from the femur that too by perfect subperiosteal
techniques only.

5. What is the technique of soft tissue release in valgus knees?

Anz: Always release from femur never from tibia.

6. What Is the best guide in the tibia for tibial cut?

Anz: Commonly Extra medullary guide as the tibial canal may not always bee straight.
Intramedullary guide can also be used if one is very particular.

7. What is the common guide for Femur?

Anz: Intramedullary as the femur canal accepts the intramedullary rod much easily.
Extramedullary guide can also be used if one is very particular.

8. Femoral cut is in varus or valgus?

Anz: Always in valgus as to mimic the normal anatomical Valgus in the femur.

9. Tibial cut is varus or valgus?

Anz: Always at 90 degrees to the Mechanical axis of Tibia.
 10. PCL to be retained or not?
Anz: A controversy. As a beginner it is better to sacrifice PCL but as one get experience PCL
can retained. Current concept is towards PCL retaining knee but technical little more demanding.
In knees without much deformity, cruciate retaining prosthesis may be an option, but with
significant deformity sacrifice the PCL.

11. What is safe sleeve technique?

Anz: Elevating the medial soft tissues exactly subperiosteally in continuity with the medial
periosteal sleeve on the tibia.

12. Resurfacing the patella or not?

Anz: A controversy but in Indian situations where the patellae are very small non resurfacing
patellae is good option

13. If the flexion gap is little loose and extension gap is tight what to do?
Anz: Try to avoid further femoral resection. Up size the femoral component to match the
extension gap. If not balanced go for little more constraint one. Try further tibial resection only
as last option as it will lead to further laxity in flexion.

14. If further distal femoral cut is made what is the problem?

Ans: It leads to upward joint line migration?

15. If the joint line is migrated what is the problem?

Anz: It leads to patellar maltracking. It also leads to global instability IN TKA

16. If flexion gap is tight and extension gap is loose what will you do?
Anz: Down size the femur and go for thicker poly. Augment the distal femur.

17. Why do you give 3 degrees external rotation in the femoral cut?
Anz: to make the flexion extension gap rectangular?

18. How does the 3 degrees femoral component external rotation make the flexion
extension gap rectangular?
Anz: The upper tibia is in 3degrees varus anatomically but the cut is made at 90 degrees. The
distal femoral is made parallel to the tbial cut so the extension gap is rectangular. when the
femoral component is external rotated it affects only the flexion gap. So more bone is removed
from the posterior condyle on the medial side. So the flexion gap also become rectangular.

19. Why does one wants to cut the tibia at 90 degrees when the original upper tibia is in
3 degrees varus?
Anz: All varus and valgus positioned tibial components will fail eventually.

20. Will you go for mobile bearing or fixed bearing tibial platform?
Anz: It is a controversy. Start with fixed bearing and go for mobile bearing as one get more
experience.

21. What are the usual reasons for failure of TKA?

Anz: Malalignment of components, infection, soft tissue instability.
.
SECTION II
THE SPINE

15. EXAMINATION OF THE SPINE

History
Vertigo, blackouts, drop attacks (s/o cervical spine involvement)
Upper respiratory tract infection (s/o cervical spine involvement)
H/o rheumatoid arthritis, steroids or anti coagulants.
H/o pain and sciatica: Mode of onset
Site of pain - Is there below knee radiation of pain?
Aggravating and relieving factors.
Is it aggravated by walking and standing forcing the patient to sit or stoop forwards?
(Neurogenic claudication)
Diurnal variation
H/o pelvic Inflammatory disease
H/o adolescent backpain (spondylolisthesis) and occupation
H/o dyspnoea, cyanosis or palpitation (s/o thoracic component)
H/o trauma
H/o weakness: Onset Red flag signs in LBA
 Loss of weight and appetite
Progression  Fever
Severity  Nocturnal pain
Diurnal variation  Rest pain
Assoc. with involvement of other joints  Bilateral sciatica
H/o fasciculations  Sphincter disturbance
 Age less than 15 or
Abnormal movements More than 50
H/o Numbness:  H/o trauma, malignancy
Onset  Gross motor weakness
Progression
Site
Dermatomal distribution
Difficulty in walking
Difficulty in washing face in darkness (s/o ataxia)
Perianal sensory loss
H/o Bowel and bladder involvement:
Retention
Overflow incontinence
Bladder sensation present or no
Associated h/o renal, cardiac or GIT complaints
Associated constitutional symptoms
If there is presence of deformity:
Onset,
Progression
Onset of menarche
H/o Polio,
Immunization history.
Full Developmental history (Antenatal, natal and postnatal)
R/o any neuromuscular cause of the deformity.
 Any family History
R/o Any h/o infection Tuberculosis
General Examination
Height
Weight
US/LS ratio
Arm span
Gait and Posture
Abnormal movements
Neurocutaneous markers like ash leaf macule/ neurofibromas
Local examination
Inspection
From behind the patient
Head tilt and neck tilt
Hairline and level of shoulders
Level of scapulae and any rib hump
Alignment of the spine coronally
Level of the iliac crest
Any swellings or cold abscess
Any features of spina bifida occulta (hairy nevus/ mole/dimple/lipoma)
Any step
From the side
Exaggerated lumbar lordosis
Shape of the chest wall
Rib hump
From Front
Level of nipples and breast folds
Level of the ASIS
Pot belly
Palpation
Tenderness over the spinous process
Point tenderness
Twist tenderness
Thrust tenderness
Feel for any cold abscesses per abdomen as well as superficial
Any step deformity as in spondylolisthesis
Movements
All movements of the cervical spine, dorsal and lumbar spine
Schober’s test
Measurements
Chest expansion
Limb length discrepancy
From occipital protuberance to tip of coccyx
12th rib to iliac crest
Modified schoebers test
Special tests
SLRT/Lasegue test for lumbar spine
Spurling test for cervical spine
Adson test or Roos test for thoracic outlet syndrome
 Forward bending test for rib hump
Neurological examination
Higher mental functions
Cranial nerves
Motor system- Bulk, Tone, Power, Reflexes, Abnormal movements/ Fasciculations
Sensory system- Fine touch, crude touch, vibration, temperature sense, position sense, 2-point
discrimination, stereognosis
Reflexes- Under motor system
Autonomic system
Coordination
Muscle charting- Under motor system

16. INTERVERTEBRAL DISC PROLAPSE

Q&A

Q1. What is the pathognomonic sign of the lumbar IVDP?

A. A positive cross Straight leg raising test (SLR).

Q2. How do you diagnose or what are the signs of upper lumbar disc herniation?
A. A positive femoral nerve stretch test (FNST)
Patient in prone position keeping hand on popliteal fossa, a sudden flexion of the knee
produces pain along ant aspect of thigh.

Q3. What are the indications for surgical intervention?

A. -Failure of conservative treatment for more than 10 to 12 wk and difficulty in attending
the normal daily routine activities
-developing a neurological deficit or worsening of the already existing deficit
-“the indication” is cauda equine syndrome

Q4. Which disc can produce a false positive finding in MRI? Which is the largest disc?
What percentage of the disc contains water?

A. L4 L5disc is the largest disc (so it can produce a false positive test)
60-65% of the disc contains water

Q5. What is the difference btw prolapse/extrusions/sequestra

A.Prolapse: bulge of the nucleus pulposes with intact post annulus
Extrusion: prolapsed disc materials cones beyond annulus with post long ligament intact
Sequestrum: a piece of disc material separating from disc and lying in the corner reaching post
long ligament

Q6. What are root tension and root irritating signs?

A. SLR and bowstring sign - root tension signs
Calf tenderness is root irritating sign
Q7. How to differentiate between axillary and shoulder disc?
A. In case of axillary disc, lateral bending to the same side increases the pain. Reverse will
happen if it is a shoulder disc.

Q8. What portion of the root lies in the canal?

A. Normal extension of root in the canal-3mm

Q9. What are the signs of L5 root compression?

A. Sensory -loss anterior, lateral leg and dorsum of foot.
Motor- EHL, Gluteus medius weakness.

Q10. Which disc is prolapsed for L5 root involvement?

A. Disc between L4&L5 vertebrae. The nerve root that passes in between L4 and L5 is L4.
But the root involved is L5 as the L4 root would have already exited above the prolapsed disc.

Q11. Differentiate btw neurologic and vascular claudication pain.

A. Neurogenic: pain relieves with rest, sitting, squatting and bending forwards (to produce
slight flexion relieves vertebrae
Vascular: improves once the patientstops walking

Q13. What are the contra indications of epidural steroids?

A. Local infection, systemic infection, uncontrolled diabetes, congestive cardiac failure

Q14. How do you differentiate between referred pain and radicular pain?
A. Radicular pain always extend distal to knee along the course of nerve
Referred pain is felt in low back, sacroiliac region or posterior aspect of thigh.

Q15. What is the most consistent triad in cauda equina syndrome?

A. Saddle anaesthesia
B/L ankle areflexia
Bladder symptoms

Q16. What is the role of xray in a case of suspected IVDP?

A. To rule out infection, tumor and other unsuspected anomalies

Q17. What is a positive bowsting sign?

A. After a positive SLR, slightly flex the knee to relieve pain. Now pressing at popliteal
fossa produces pain either proximally or distally along the course of nerve.

Q18. How to differentiate between piriformis syndrome and IVDP?

A. External rotation of leg reduces the pain in piriformis syndrome as piriformis muscle
relaxes in external rotation as IVDP pain persist inspite of rotation.

Q19. What is failed back syndrome?

A. Persistence of back pain after surgical procedure for backpain. The causes are
Inproper selection of patient
Failure to identify the proper disc
 Nerve root anomalies
Prolapse of disc above or below
Instability
Infection
Arachinoiditis

Q20. What are the complications of dural tear?

A. Psuedomeningocele, CSF leak through persistent fistula, meningitis

Q21. What is fenestration?

A. Surgical procedure which removes the ligamentum flavum of one side with undercutting
lamina to increase the space for removing the disc.

17. SCOLIOSIS

Aim of Examination of scoliosis:

Anatomical site of curvature (extent of curvature ie. Apex & End vertebra)
Identify the apex vertebra.
Direction of curvature
Cause of the scoliosis
Identify the major and the minor curve
Identify the Primary curve and the secondary curve
Identify the structural curve and which is not .ie the flexibility
Presence of neurological deficit
Whether the curve is balanced

Q&A

Q1. What is scoliosis? What are the common types of scoliosis?

A. It is defined as a lateral deviation of the spine greater than 10° with a rotational
deformity. The most common type of scoliosis is idiopathic scoliosis, comprising nearly 80% of
cases, congenital scoliosis (15%), neuromuscular scoliosis and syndromic-related scoliosis.

Q2. What is Adams forward bending test?

A. This is to differentiate between postural and structural scoliosis. The patient is asked to
bend forward while observing the deformity .If deformity disappears it is a postural deformity
and persist it is structural.

Q3. What are the associations to be looked in a case of scoliosis?

A. Vertebral anomalies, Anal atresia,Cardiac anomalies, Tracheosophageal fistula, renal and
Limb anomalies (VACTERL association), plagiocephaly, torticollis, spina bifida as evidenced by
a dimple, hairy patch, lipoma, or hemangioma ,Klippel- feil syndrome (Congenital scoliosis)
Q4. What are the factors related to progression of AIS ?
A. Girls > boys
Premenarchal age
Risser sign of 0
Double curves > single curves
Thoracic curves > Lumbar curves
More severe curves

Q5. What are the problems of untreated scoliosis?

A. Back pain, pulmonary compromise, psychosocial effects due to cosmesis, mortality and
curve progression.

Q6. What are the types of idiopathic scoliosis?

A. Infantile idiopathic scoliosis –Birth to 3 yrs. Common in boys, left thoracic curve.
Juvenile – 4-10 yrs, common in girls, right thoracic curve.
Adolescent idiopathic curve-common in girls, right thoracic.

Q7. Which types of scoliosis are most frequently pathological?

A. Left thoracic curve and right lumbar curve

Q8. What are the types of congenital scoliosis?

A. Failure of formation- (a) Partial –Wedge vertebrae
(b) Complete- Hemivertibrae
Failure of segmentation- (a) unilateral unsegmented bar
(b) Bilateral- Block vertebrae
Mixed type

Q9. Which congenital curve is having worst prognosis?

A. Unilateral unsegmented bar with contralateral hemivertibra is the most severe and rapidly
progressive of all types of congenital scoliosis.

Q10. What are the types of scoliosis in neurofibromatosis?

A. Nondystrophic – It is like idiopathic scoliosis
Dystrophic – short segmented, sharply angulated curve with severe wedging and rotation
of vertebrae.

Q11. What are the important points in history to be noted in scoliosis?

A. Time of onset, progression, h/o trauma, infection, surgery, whether pre/post menarchal,
gait abnormalities, neurological deficit, developmental delay? h/o metabolic disease, family h/o
deformities.

Q12. What are the important physical examination points in scoliosis?

A. Sitting and standing height
Level of shoulder /iliac crest /scapula/ head
Positions and prominence of breast
Flexibility of curve
Major and minor curves
Number, level, convexity of the curves
Fixed pelvic obliquity
 Limb length discrepancy
Neurological deficits
Plumb line
Scoliometer measurement

Q13. How are apical vertebrae and end vertebrae determined?

A. Apical vertebra is the vertebra which is maximally rotated and most deviated from the
vertical axis.
Upper end vertebra is the upper most in the curve which is maximally into the concavity
of the curve and lower one is the lowermost which is maximally into the concavity of the curve.

Q14. What are neutral and stable vertebrae?

A. Neutral vertebrae are the first non rotated vertebrae at the caudal and cranial ends of the
curve.
Stable vertebra is the vertebra that is bisected by the midsacral line.

Q15. What is Cobb method of radiographic measurement of scoliosis?

A. Perpendicular lines are are constructed from the superior endplate of superior end
vertebra and inferior endplate of inferior end vertebra. The angle subtended by the intersection of
these two lines is the magnitude of the curve- Cobb angle.

Q16. What is mehta”s rib vertebral angle difference?

A. RVAD measures the intersection of a line perpendicular to the apical vertebral end plate
and a line drawn from the midneck to midhead of the right and left corresponding ribs. If RVAD
is >20 the infantile idiopathic curve is likely to progress.

Q17. Which are the 2 common classification used for scoliosis?

A. King”s classification and Lenke”s classification.

Q18. What is the use of Nash-Moe classification and Risser sign?

A. Nash-Moe classification is used to assess vertebral rotation and Risser sign for skeletal
maturity.

Q19. What are the treatment options for idiopathic scoliosis?

A. Observation - curve less than 25 degree
Orthosis - curves between 25-45 degree
Surgery - curves more than 45 degrees, curves progress despite bracing,
adult scoliosis more than 50 degrees.

Q20. What are the surgical methods of treating AIS?

A. There are two main types of surgery: Anterior fusion: This surgical approach is through
an incision at the side of the chest wall. Posterior fusion: This surgical approach is through an
incision on the back and involves the use of metal instrumentation to correct the curve. One or
both of these surgical procedures may be needed.
 18. TUBERCULOSIS SPINE

Q&A
Q1. What are the common levels of involvement of spinal tuberculosis?
A. Thoracic spine -35- 40 %
Thoracolumbar spine – 25 – 30 %
Lumbosacral spine- 25- 30 %
Cervical spine – 4- 5 %

Q2. What are the sites of lesion in the vertebrae?

A. Paradiscal
Anterior
Posterior
Central
Spinal tumour syndrome

Q3. What are the problems associated spinal tuberculosis?

A. Abscess formation
Deformity
Neurological deficits

Q4. Why paradiscal lesions are the commonest type of lesion?

A. Common blood supply to the adjacent metaphyseal regions of the nearby vertebrae.

Q5. Why kyphus deformity is common in children?

A. Because vertebrae are mostly cartilaginous and destruction occurs anteriorly with normal
growth of the posterior aspect of vertebrae.

Q6. Which are the common sites of tracking of tuberculous pus?

A. Cervical spine - Retropharyngeal region
Posterior triangle of neck
Along the axillary sheath into upper limb into the mediastinum
Thoracic spine - Laterally bird nest abscess, anterolateral chest wall
Into the renal angle, Petit’s triangle, rectus sheath
Inguinal region, Scarpa's triangle
Lumbar spine - Psoas abscess.

Q7. What are the causes of early onset paraplegia?

A. Abscess, inflammatory oedema, granulation tissue, sequestrum, thrombosis of anterior
spinal artery.

Q8. What are the causes of late onset paraplegia?

A. Stretching of cord over the internal gibbus deformity.

Q9. What is spinal tumour syndrome?

A. Tuberculous extradural granuloma producing neurological deficit without radiological
evidence of vertebral involvement.
Q10. What are the deformities seen in tuberculosis of spine?
A. Knuckle - single vertebra
Gibbus - 2 vertebral involvement
Kyphosis - >3 vertebral involvement

Q11. What are the radiological signs of spinal tuberculosis?

A. Osteopenia of vertebral bodies
Disc space narrowing with destruction of end plate
Concertina collapse of body
Serrated appearance of anterior vertebral body
Ivory vertebra
Bird nest and V shaped abscess
Widening of psoas shadow

Q12. What are the indications for CT scan?

A. Posterior spinal disease, craniovertebral involvement, sacroiliac joint involvement

Q13. What are the indications for MRI scan?

A. To better delineate the soft tissues, abscess, skip lesions, spinal tumour syndrome.

Q14. What are the investigations in a case of spinal tuberculosis?

A. Blood routine investigations
Chest xray
Mantoux test
X ray of the spine
MRI of spine
Open biopsy / CT guided aspiration and RT PCR

Q15. What are the radiological “spine at risk” signs?

A. Facet joint separation at the apex of the curve
Posterior retropulsion of the diseased segment
Lateral translation
Toppling sign

Q16. What are the regimens used for treating spinal tuberculosis?
A. Hong Kong regimen - Radical surgery
Kenyan regimen - Only ATT
BMRC regimen - Middle path regimen

Q17. What is Middle path regimen?

A. Initial treatment with ATT and surgery in certain indications

Q18. What are the indications for surgery in Middle path regimen?
A. Not responding to ATT after 4-8 weeks of treatment for debridement and biopsy
Progressive neurological deficit
Neurological deficit developing while on treatment
Worsening of neurological deficit during treatment
Kyphosis more than 30 degree
Spinal tumour syndrome
Q19. What are the surgical options for treating D/L tuberculosis?
A. Anterior decompression and fusion
Anterolateral decompression
Costotransvesectomy
Transpedicular decompression and posterior fusion
Rarely laminectomy - in posterior type

Q20. Why is pseudoflexion deformity of hip in spinal tuberculosis?

A. Due to irritation of psoas muscle by abscess.

19. Spondylolisthesis
1: What is spondylolisthesis?
Spondylolisthesis is a condition of the spine whereby one of the vertebra slips forward or
backward compared to the next vertebra. Forward slippage of one vertebra on another is referred
to as anterolisthesis, while backward slippage is referred to as retrolisthesis. Spondylolisthesis
can lead to a deformity of the spine as well as a narrowing of the spinal canal (central spinal
stenosis) or compression of the exiting nerve roots (foraminal stenosis).

2: What are the types of spondylolisthesis?

The Modified Wiltse Classification of Lumbar Spondylolisthesis

Type Name Description

I Dysplastic Congenital abnormalities in the
posterior arch of L5 or S1
II Isthmic Also referred to as
spondylolytic; a lesion in the
pars interarticularis
III Degenerative Osteoarthritis of the facet joints
and degenerative disk disease
IV Traumatic Acute fractures of the bony arch
V Pathological Weakening or absence of the
normal bony restraints to
motion.[metabolic/metastatic]
Paget's disease of
bone, tuberculosis, giant-
cell tumors, and
tumor metastases.
VI Iatrogenic Resection of the facet joints or
disk material causing instability

3: What are the symptoms of spondylolisthesis?

The most common symptom of spondylolisthesis is lower back pain. This is often worse
after exercise especially with extension of the lumbar spine. Other symptoms include tightness of
the hamstrings and decreased range of motion of the lower back and muscle spasms. Some
patients can develop pain, numbness, tingling or weakness in the legs due to nerve compression.
Severe compression of the nerves can cause loss of control of bowel or bladder function,
or cauda equina syndrome.

4: How do you diagnosis spondylolisthesis?

Spondylolisthesis is easily identified using plain radiographs. A lateral X-ray (from the side) will
show if one of the vertebra has slipped forward compared to the adjacent vertebrae.
Spondylolisthesis is graded according the percentage of slip of the vertebra compared to the
neighbouring vertebra. If the patient has complaints of pain, numbness, tingling or weakness in
the legs, additional studies may be ordered

5: How do you grade the severity of slip

The most common grading system for spondylolisthesis is the Meyerding grading system for
severity of slip. The system categorizes severity based upon measurements on lateral X-ray of
the distance from the posterior edge of the superior vertebral body to the posterior edge of the
adjacent inferior vertebral body. This distance is then reported as a percentage of the total
superior vertebral body length.
Grade 1 is 0–25%
Grade 2 is 25–50%
Grade 3 is 50–75%
Grade 4 is 75–100%
Over 100% is Spondyloptosis, when the vertebra completely falls off the supporting vertebra

6: What are the radiographic features of spondylolisthesis?

Anteroposterior and lateral projection plain radiographs of the lumbar spine. The lateral view is
especially useful in detecting and grading spondylolisthesis.. The pars defect may or may not be
visualized on the lateral view.

Spondylolisthesis. Lateral lumbar spinal radiograph in a pediatric patient shows spondylolysis

with grade 1 spondylolisthesis.
Spondylolisthesis. Grade 4 traumatic spondylolisthesis.
Bilateral oblique views may be obtained to visualize the pars defect, which has the appearance of
a Scottie dog with a collar (as demonstrated in the radiographs below). An elongated pars also
may be seen. Note that oblique views increase the specificity, but not the sensitivity, for pars
defects.

Spondylolisthesis. Oblique projection radiograph shows the presence of bilateral pars defects
(arrows), with an appearance resembling a Scottie dog with a collar. (The collar is the pars
defect.)

Spondylolisthesis. Diagram in the oblique projection shows the components of the vertebrae that
result in the appearance of a Scottie dog with a collar.

7: What is pelvic incidence?

Pelvic incidence = pelvic tilt + sacral slope

A line is drawn from the center of the S1 endplate to the center of the femoral head
A second line is drawn perpendicular to a line drawn along the S1 endplate, intersecting the point
in the center of the S1 endplate
The angle between these two lines is the pelvic incidence (see angle X in figure above) correlates
with severity of disease

8: What is pelvic tilt?

Sacral slope = pelvic incidence - pelvic tilt

A line is drawn from the center of the S1 endplate to the center of the femoral head
A second vertical line (parallel with side margin of radiograph) line is drawn intersecting the the
center of the femoral head
The angle between these two lines is the pelvic tilt (see angle Z in figure above)

9: What is Sacral slope?

Pelvic tilt = pelvic incidence - sacral slope

A line is drawn parallel to the S1 end plate
A second horizontal line (parallel to the inferior margin of the radiograph) is drawn
The angle between these two lines is the sacral slope (see angle Y in the figure above)

10: What are the indications for Computed Tomography

To get more information regarding spondylolisthesis and its cause, along with other possible
conditions, such as disk disease, disk herniations, spondylosis, and spinal canal stenosis. Other
associations, such as spina bifida, may be seen.
In patients with radiculopathy, CT myelography can yield information regarding nerve-root
impingement and its etiology, such as disk herniation, abscess, or neoplasm.

Spondylolisthesis. Sagittal CT reconstruction image shows the pars defect along with grade 1
spondylolisthesis (arrow).
With spondylolysis, CT is performed as close as possible to an angle that is 90° to the level of
interest. CT scans typically demonstrate a horizontally oriented defect in the pars, which
interrupts the normally complete bony ring of the posterior elements.
Spondylolisthesis is evaluated best on lateral tomogram, but it can be suggested in patients with
spinal stenosis in the absence of disk pathology, posterior hypertrophic changes, or a
congenitally narrow spinal canal. One typically looks for an elongated spinal canal (as seen in
the images below).

Spondylolisthesis. Axial CT image shows bilateral spondylolysis (arrows). Note elongation of

the spinal canal at this level.

Spondylolisthesis. Axial CT image shows bilateral spondylolysis (arrows). Note elongation of

the spinal canal at this level.
CT scans can also demonstrate findings of congenital/dysplastic and degenerative types of
spondylolisthesis. Abnormalities of the vertebral body or articular processes may be present.
Changes of spondylosis deformans (degenerative changes) are apparent on CT scans.
Degenerative disease of the spine has a characteristic appearance involving a loss of disk space
height with or without the presence of vacuum phenomenon, narrowing of the facet joint space,
subchondral sclerosis, osteophyte formation, and subchondral cysts. Some or all of the changes
may be present and cause altered alignment of the facet-joint articular surface, leading to
slippage. Spinal canal and/or intervertebral neural foraminal stenosis may be present.
In traumatic spondylolisthesis, findings may include jumped facets and fractures of the articular
processes and/or lamina that result in spondylolisthesis.

11: Indications for Magnetic Resonance Imaging in Spondylolisthesis

Abnormality of the pars interarticularis, pedicles, or facet joints.
Abnormality pf nerve structures, including those exiting neural foramina.
To evaluate spinal canal.
Degenerative disease, narrowed disk space, with disk desiccation . This disk narrowing causes
superoinferior subluxation at the facet joint at the level of disease, resulting in anterolisthesis or
retrolisthesis.
Neoplastic disease involving the pars interarticularis or other parts of the vertebra
Infection
Other diseases causing a sclerotic response (eg, Paget disease)

12: What are the indication for Nuclear Imaging?

Nuclear medicine has no role as a primary imaging modality in spondylolisthesis. Spondylolysis
can be detected as areas of increased activity on bone scans, but the appearance is nonspecific,
and such findings may be seen in other disorders (eg, neoplasms and infections). Usually,
correlation with clinical and plain radiographic findings is helpful in narrowing the differential
diagnosis.
Indications:
To rule out another lesion, such as osteoid osteoma, infection or malignant disease;
Clinically suspected spondylolysis that but cannot be confirmed w/ x-rays;
For detection of small or partial fractures & areas of increased bone turnover at site of a healing
fracture. Bone scans will be positive in patients who have had symptoms for only five to seven
days.
There is a stress-reaction stage before fracture which may be detected initially by radioactive
bone-scanning;
To distinguish between patients with established non-union versus patients with slowly healing
frx (who would benefit from immobilization);
To assess recovery from frx and to determine when athlete can return to competition;
Bone scans allow an assessment of the acuity of the lesion, with increased uptake seen with
acute lesions.

Contra-indications:
- Patients who have had symptoms for > 1 year or those who are asymptomatic;
- Bone scans are not indicated once the lesion has become established

13: Risk factors for progression

Young age at presentation
Female gender
Slip angle of greater than 10 degrees
High-grade slip and a dome-shaped or significantly inclined sacrum (> 30 degrees beyond
vertical position).
Dysplastic spondylolisthesis are at a higher risk for slip progression and the development of
cauda equina dysfunction because the neural arch is intact. Patients with a greater than 25% slip,
or with L4-L5 or L3-L4 spondylolisthesis, have a higher risk of low-back pain than the general
population

14: What is the significance of Slip angle?

Angle that is formed by extending a line along anterior border of body of L5 until it intersects
line that has been drawn along the posterior border of the body of first sacral vertebra. Slip angle
is measured by drawing a line perpendicular to line drawn along posterior aspect of first sacral
vertebral body and measuring angle between that and a line parallel to inferior end plate of L5

14: What is the conservative treatment?

The initial treatment for spondylolisthesis is conservative and based on the symptoms.
A short period of rest or avoiding activities such as lifting and bending and athletics may help
reduce symptoms.
Physical therapy can help to increase range of motion of the lumbar spine and hamstrings as well
as strengthen the core abdominal muscles .
Physical modalities such as thermal treatment, electrical stimulation and lumbar traction can help
with reactive muscle spasm
Anti-inflammatory medications can help reduce pain by decreasing the inflammation of the
muscles and nerves.
Patients with pain, numbness and tingling in the legs may benefit from an epidural steroid
injection. Patients with isthmic spondylolisthesis may benefit from a hyperextension brace. This
extends the lumbar spine bringing the two portions of the bone at the defect closer together and
may allow for healing to occur.

15: What are the indications for surgery?

Persistent or recurrent leg pain despite conservative treatment

Progressive neurological deficit
Pain with significant reduction in the quality of life, and confirmatory imaging studies consistent
with the clinical findings.7 It is important to give the patient a long trial of conservative care,
including the use of epidural steroids, before surgical intervention. If all reasonable methods fail,
surgical options can be discussed
16: What are the various surgical options?
Include pedicle-to-pedicle decompression, decompression and posterolateral fusion, and
decompression with interbody fusion. The role of instrumentation is controversial.
Posterior decompression and posterolateral fusion (+/- instrumentation)
Indications
Fusion indicated in most cases due to instability
May consider fusion alone in patient with slip progression but no evidence or symptoms of
neurologic compression
Decompression technique
Usually done with laminectomy, wide decompression, and foraminotomy
Fusion technique
Posterolateral fusion with instrumentation most common
Use of instrumentation decreases pseudarthrosis rate
TLIF/PLIF growing in popularity and may increase fusion rates and decrease risk of
postoperative slip progression
Reduction of listhesis has limited role in adults
Complications
Postsurgical infection
Treat with irrigation and debridement (usually hardware can be retained)
Posterior Decompression (laminectomy)
Indications
Usually not indicated due to instability associated with spondylolithesis
Only indicated in medically frail patients who cannot tolerate the increased surgical time of
performing a fusion
Anterior Lumbar Interbody Fusion (ALIF)
Reserved for revision cases with pseudoarthrosis
 SECTION III
SHORT CASES

20. EXAMINATION OF THE SHOULDER JOINT

Examination of shoulder
By Dr Rajesh Purushothaman

Shoulder symptoms may be due intrinsic causes or referred causes due to spine, thorax or
abdomen pathology. Hence it is important to rule out referred causes for shoulder pain.

History

Should include age, handedness, occupational and recreational activities and the shoulder
symptoms. In patients with pain; ask for the exact site, duration, onset, progress, character,
radiation, associated symptoms, aggravating factors and relieving factors. In case of left sided
shoulder pain ask for cardiac symptoms. Patient should be asked to point out the site of pain with
a single finger. If site is over the lateral arm especially during overhead activity, the cause is
likely to be rotator cuff pathology or impingement. Superior pain especially on adduction is
suggestive of acromioclavicular pathology. Anterior shoulder pain may be due to long head of
biceps pathology. Deep shoulder pain is likely to be due to glenohumeral pathology or labral
lesions.
In patients with instability; ask for the duration, onset, frequency, precipitating posture or
activity, position of shoulder after the dislocation, and how it gets corrected after an episode.
Also ask for history of epilepsy as posterior instability is more likely in such patients. Also look
for history suggestive of voluntary dislocation.

Glenohumeral instability has been classified according to the cause and direction. Cause can be
classified into traumatic and atraumatic. Atraumatic instability develops either due to laxity or
overuse. Direction of instability can be classified into anterior, posterior, inferior and
multidirectional. If history of trauma is not present then careful history of occupational and
recreational activities must be made to identify overuse. Position of arm at the moment of
instability is very helpful in the identification of the direction of instability. In anterior
instability, the shoulder will be abducted, externally rotated and extended. In posterior
instability, the shoulder is adducted, internally rotated and flexed. In inferior instability, the arm
is abducted and the hand is supported over the head.
Anterior instability causes pain during late cocking phase of throwing due to anteroinferior
capsule laxity. Posterior instability causes pain during follow through phase. Patients with
anterior instability may present with dead arm syndrome; paralysing pain in the maximally
externally rotated, abducted and extended position.

Different age groups have different causes for their presentation. Patients <25 years present due
to traumatic dislocations, recurrent instability or acromioclavicular pathology. Adults below 40
years present due to impingement, frozen shoulder or ACJ arthritis; and those over 40 years
present due to rotator cuff impingement or tear and osteoarthritis of glenohumeral or
acromioclavicular joint. The steps of physical examination of shoulder is determined by patient's
presenting complaints and history. The entire region from the cervical spine to the hand should
be examined.
Inspection

Patient should be dressed in such a manner that shoulder can be assessed fully. Observe the
posture and the bony and soft tissue contour of both shoulders and look for any asymmetry.
Observe whether the pelvis is level and the spine is straight as their malalignment may cause
secondary shoulder abnormality.

Drooping of shoulder may be caused by trapezius palsy. Winging of scapula is abnormal

prominence of vertebral border of scapula. Winging can be produced by injury, dysfunction of
muscles and nerve palsy. It may be dynamic or static. Dynamic winging may be due to trapezius
palsy or serratus anterior palsy. True winging is due to serratus anterior palsy. Serratus anterior
supplied by long thoracic nerve, and it’s action is protraction of the scapula. It’s function is
tested by asking the patient to stand at an arm length from wall and push against it.
Pseudowinging is produced by trapezius palsy, acromioclavicular dislocation and scapular
dysrrhythmia. In trapezius palsy, winging is more during abduction of shoulder, the inferior
angle of shoulder is rotated laterally and it is more obvious when the patient stoops forward so
that the body so parallel to the floor and then tries to abduct the shoulder. In serratus anterior
palsy, winging is more pronounced during forward flexion of the shoulder and the inferior angle
of scapula is rotated medially. Winging may also occur due to scapular muscle dysrrhythmia due
to shoulder instability or rotator cuff tear. It may also occur acromioclavicular joint dislocation
with ruptured coracoclavicular ligaments or fracture of outer third of clavicle.

A step deformity may be seen at the ACJ in dislocations of the ACJ. Contour of clavicle may be
altered in case of clavicle malunion or nonunion. Popeye sign of abnormal prominence of biceps
is seen in patients with long head of biceps rupture. Abnormal contour of anterior auxiliary fold
and pectoralis major is seen patients with pectoralis major tendon rupture and Poland syndrome.
Wasting of supraspinatus and infraspinatus may be seen.

Palpation

Feel for local rise of temperature. Stand on the back of the patient and palpate the structures of
the shoulder using the Kochers method of palpation starting at the sternoclavicular joint and
moving laterally over the clavicle, ACJ, coracoid, spine of scapula and down the humerus. Look
for tenderness, irregularity, thickening, defect, abnormal mobility etc. Biceps tendon should be
palpated in its groove anteriorly.

The tenderness over the glenohumeral joint is elicited anteriorly over a point 1cm inferior and
lateral to the coracoid process and posteriorly over the point 2cm medial and inferior to the angle
of acromion. Diffuse tenderness over the trapezius and interscapular area may be seen in patients
with shoulder instability and scapular dysrrhythmia due to abnormal shoulder biomechanics.

Movements

Assess range of motion using the recommendations of the American Shoulder and Elbow
Surgeons Research Committee 1. Abduction is tested in the scapular plane (30 degree-
anteriorly)and not in the coronal axis of the body. Ideally patient should be stripped to the waist
and examiner should stand behind the patient and both shoulders are abducted simultaneously. In
the resting position the vertebral border of both scapula should be equidistant from the vertebral
column. Both scapula should move symmetrically when the arm is abducted, asymmetrical
movement is noted as scapular dyskinesis. Normally the ratio of glenohumeral to scapulothoracic
movement on abduction is 2:1.

Shrug sign is seen in patients with supraspinatus dysfunction, the patient shrugs at the beginning
of abduction to substitute glenohumeral abduction by supraspinatus with scapulothoracic motion.
If there is abnormal prominence of vertebral border then there is dynamic scapular winging.
Maximum achievable angle between the humerus and thorax is recorded as shoulder elevation.
Internal and external rotation are measured in 90 flexion of elbow and with arm by the side of
body and in 90 abduction of shoulder. Rotations are better tested in the supine position after
applying pressure over the anterior shoulder to fix the scapula.

Strength testing

Strength of rotator cuff muscles are measured. Supraspinatus is assessed in the empty can
position; 90 abduction of shoulder with elbow straight and shoulder in the fully internally rotated
position with the thumb pointing downwards and the patient is asked to abduct further against
resistance. Strength of infraspinatus is measured with the arm in 90º abduction, elbow at 90º
flexion and the patient is asked to externally rotate against resistance.

Special tests

May be classified into

Tests for impingement
Tests for laxity
Tests for instability
Tests for rotator cuff disease
Tests for SLAP
Tests for biceps tendon
Tests for ACJ
Tests for cervical disc disease

1. Tests for impingement

Neer impingement sign- (Forced forward elevation test)

Examiner position- Stand next to the patient with one hand over the top of shoulder and other
hand holding the patient’s arm.
Patient position- Standing.
Joint position- Arm by the side of body
Procedure- Stabilise the scapula with one hand, passively flex the shoulder fully and then push
further.
Interpretation- Pain is due to rotator cuff impingement. Test is 79% sensitive and 53% specific.

Hawkins-Kennedy test(Forced internal rotation test)

Examiner position- Stand in front of the patient.

Patient position- Standing.
Procedure- Flex the arm and elbow to 90 degrees and then internally rotate the shoulder using
the flexed forearm as a lever.
Interpretation- Test is positive if pain is reported. Test is 79% sensitive and 59% specific.

Neer impingement test

Inject 10 ml of 1% lidocaine into the subacromial space using a sterile technique. Then ask the
patient to actively abduct. Relief of pain for the duration of the anesthetic effect is confirmatory
of impingement.

2. Tests for laxity

Anterior drawer test

Described by Gerber and Ganz.

Examiner position- Stand on the affected side
Patient position- Supine. Patient’s hand is stabilised in the axilla of examiner.
Joint position- Shoulder in 80-120 abduction, 0-20 forward flexion, 0-30 external rotation.
Procedure- Stabilise the shoulder with one hand, grasp the proximal humerus with the other
hand. Apply anterior translation force.
Interpretation – Click and abnormal laxity indicate anterior instability. Grade the degree of
translation.
0- None or minimal when compared to contralateral shoulder.
1+ – Up to glenoid rim.
2+- Beyond glenoid rim and spontaneously relocates.
3+- Dislocates and doesn’t reduce spontaneously.

Posterior drawer test

Described by Gerber and Ganz.

Patient position- Supine.
Joint position- Shoulder in 80-120 abduction, 20 forward flexion, 60-80 internal rotation.
Procedure- Stabilise the shoulder, grasp the proximal humerus. Apply posterior translation force.
Interpretation- Click and abnormal laxity indicate posterior instability. Grade the degree of
translation.

Load and shift test

Described by Silliman and Hawkins

Patient position- Sitting
Joint position- Arm by the side and hand resting in the lap of patient
Procedure- Stabilise the shoulder with one hand, grasp the proximal humerus with the other
hand. Load the humeral head against the glenoid and then slide the head anteriorly and
posteriorly
Interpretation- Look for abnormal anterior translation, which suggest anterior instability. Grade
the translation.

Sulcus sign
Described by Neer and Foster.
Patient position- Sitting
Joint position- Arm by the side and hand resting in the lap of patient
Procedure- Hold the elbow of the patient with one hand and then stabilise the shoulder with other
hand and then apply longitudinal traction.
Interpretation- Appearance of a gap more than the other side below the acromion suggest inferior
capsular laxity. It is indicative of multidirectional instability. Grading – 1+ -0-1cm, 2+- 1-2cm,
3+- >2cm.
Recent modification- Now externally rotate the shoulder, if the gap persists then rotator interval
is likely to be defective.

Gagey hyperabduction test

Principle – Tests inferior glenohumeral ligament complex.

Patient position – Sitting
Examiner position – Behind seated patient
Joint position – Arm by the side of body.
Procedure – Place the forearm of examiner on the top of shoulder to stabilise the scapula. Abduct
the shoulder of patient maximally and note the range of abduction till the scapula start moving.
Interpretation – Normal range of passive abduction is 105 degrees. If it is more then there is IGL
laxity.

3. Tests for Instability

Glenohumeral laxity is the ability to translate the humeral head to glenoid rim and glenohumeral
instability is the unwanted translation of humeral head on the glenoid that compromises patient
comfort and shoulder function. Multidirectional instability is instability in two or more directions
and the hallmark of inferior instability is positive sulcus sign.

Apprehension test

Patient position- Supine,

Joint position- Shoulder in 90 abduction, elbow in 90 flexion.
Procedure- Maximally externally rotate shoulder while applying anteriorly directed pressure.
Interpretation- Look for apprehension.

Jobe apprehension relocation test

If apprehension is present with previous test, repeat the test with posteriorly directed pressure.
Absence of apprehension is confirmatory of anterior instability. This test is the gold standard for
the diagnosis of anterior instability. With apprehension as the criteria for diagnosis; it shows
85% accuracy, 68% specificity, 100% sensitivity, 100% positive predictive value and 78%
negative predictive value.

Jerk test
Patient position- Supine
Joint position- Shoulder abducted to 90, elbow flexed to 90.
Procedure- Grasp elbow. Axially load the shoulder. Adduct the shoulder horizontally across the
body
Interpretation- Clunk and pain in presence of posterior instability. Return to abducted position
may produce another jerk due to relocation of joint.
Reliability – 90% sensitivity, 85% specificity, 72% positive predictive value and 94% negative
predictive value. 10

4. Tests for rotator cuff disease

Jobe empty can test

Ask the patient to actively abduct the shoulder in the scapular plane with the elbow in extension
with the shoulder in full internal rotation and the thumb pointing down.4 Reinard identified by
electrical studies that more fibres of supraspinatus are active if the test is done with the thumb
pointing up (Full can test) and may be more useful.5. Jobs test has 75% accuracy in detection of
supraspinatus tear. 6
Integrity of subscapularis is assessed separately for the upper fibres and lower fibres.

Lift off test

Lower fibres are tested by the lift-off test; ask the patient to place the dorsum of the hand against
the small of back and then lift the hand posteriorly away from the body against resistance.
Inability to lift the hand indicate subscapularis tear.

Belly press test

Upper fibres are tested by the belly press test; patient is asked to place his palm against the
umbilicus and push against the abdomen. Inability to do this indicate subscapularis tear.

Drop sign

Done to detect infraspinatus tear. Patient is asked to lie in the lateral decubitus position with the
affected side up. Flex the shoulder and elbow to 90 degrees. Hold the wrist and externally rotate
to the maximum. Now release the wrist and ask the patient to hold the limb in external rotation.
In presence of infraspinatus tear, he will not be able to do this.

5. Tests for Superior labrum Anterior Posterior (SLAP) lesion

Numerous tests are available, but they are of 2 types; active tests which try to recreate the
torsional traction force that caused the injury or passive tests that exert compressive stress on the
labrum. O’Brien test is an active test and crank test is a passive test.

O’Brien’s test (Active compression test)

Patient position- Standing.

Examiner position – By the side with one hand on shoulder and other hand on the distal forearm.
Joint position- Forward flexion of shoulder to 90, adduction of 10-15, fully internally rotated.
Elbow straight. Thumb pointing down.
Procedure- Elevate against resistance. Repeat with shoulder in external rotation.
Interpretation – Pain in internal rotated position and absence of pain in external rotation
suggestive of SLAP lesion. Ask about the location of pain, if it is over the acromioclavicular
joint then the test is negative.
Sensitivity- 90%
Specificity- 98%

Crank test(Compression rotation test)

Patient position – Supine

Joint position- Shoulder in 160 abduction, 30 forward flexion. Elbow flexed
Procedure- Stabilise scapula with one hand, grasp the elbow with the other hand. Axially load
and rotate externally and internally.
Interpretation- Pain and reproduction of patient’s symptoms indicate labral pathology
Reliability – 91% sensitive, 93% specific, 94% positive predictive value, 90% negative
predictive value.

Resisted supination external rotation test

Patient position- Supine.

Joint position- Shoulder 90 abducted, elbow 70 flexed, forearm semipronated.
Procedure- Externally rotate the shoulder and ask the patient to supinate the forearm against
resistance.
Interpretation- Pain indicative of SLAP lesion.

Anterior slide test

Patient position – Standing.

Joint position – Hand on hips with thumb pointing posteriorly.
Procedure – Apply forward and axial pressure over the elbow and ask the patient to resist.
Interpretation – Pain indicate superior labral pathology.
Reliability – 78% sensitive and 90% sensitive for type II SLAP lesion.

6. Test for Biceps long head

Pathology may be tendinitis, tear, instability of the long head of biceps or synovitis of its sheath.

Speed test

Patient position- Standing.

Examiner position- By the side of patient with one hand over shoulder and other hand over the
anterior aspect of distal forearm.
Joint position – Shoulder forward flexed by 60. Elbow extended. Forearm supinated.
Procedure- Flex the shoulder against resistance with elbow kept straight.
Interpretation – Anterior shoulder pain indicate long head of biceps pathology.
Sensitivity- 90%
Specificity – 14%
Reference – Bennet WF. Arthroscopy. 1998 Nov‐Dec;14(8):789‐96

Yergason test
7. Tests for acromioclavicular joint

Horizontal adduction test- The shoulder is passively elevated to horizontal and the arm is
adducted across the body beyond the full range. Ask the patient if there is pain and the site of
pain. If pain is located over the ACJ then the test is positive for ACJ pathology. Test is 77%
sensitive and 79% specific with an accuracy of 79%

8. Test for cervical spine

Spurling test
Patient position – Sitting
Joint position – Neck flexed forward and tilted laterally.
Procedure – Apply axial load over the head.
Interpretation- Reproduction of patient’s symptom of radiating pain indicate cervical root
pathology.

Further Reading

Richards RR, An KN, Bigiliani LU et al: A standardized method for the assessment of shoulder
function. J Shoulder Elbow Surg 1994; 3:347-52

Chronopoulos E, Kim TK, Park HB, et al. Diagnostic value of physical tests for isolated chronic
acromioclavicular lesions. Am J Sports Med . 2004;32(3):655-661

Hegedus EJ, Goode A, Campbell S, et al. Physical examination tests of the shoulder: a
systematic review with meta-analysis of individual tests. Br J Sports Med . 2008;42(2):80-92

Jobe FW, Jobe CM. Painful athletic injuries of the shoulder. Clin Orthop Relat Res . 1983;(173):
117-124.

Reinold MM, Macrina LC, Wilk KE, et al. Electromyographic analysis of the supraspinatus and
deltoid muscles during 3 common rehabilitation exercises. J Athl Train . 2007;42(4):464-469.

Itoi E, Kido T, Sano A, et al. Which is more useful, the “full can test” or the “empty can test,” in
detecting the torn supraspinatus tendon? Am J Sports Med . 1999;27(1):65-68.

Gerber C, Krushell RJ. Isolated rupture of the tendon of the subscapularis muscle: clinical
features in 16 cases. J Bone Joint Surg Br . 1991;73(3):389-394.

Harryman DT 2nd, Sidles JA, Harris SL, Matsen FA 3rd. The role of the rotator interval capsule
in passive motion and stability of the shoulder. J Bone Joint Surg Am . 1992;74(1):53-66

Speer KP, Hannafi n JA, Altchek DW, Warren RF. An evaluation of the shoulder relocation test.
Am J Sports Med . 1994;22(2):177-183
Kim SH, Park JC, Park JS, Oh I. Painful jerk test: a predictor of success in nonoperative
treatment of posteroinferior instability of the shoulder. Am J Sports Med . 2004;32(8):1849-1855

O’Brien SJ, Pagnani MJ, Fealy S, et al: The active compression test: A new and effective test for
diagnosing labral tears and acromio-clavicular joint abnormality. Am J Sports Med 26: 610–613,
1998

Parentis MA, Mohr KJ, ElAttrache NS: Disorders of the superior labrum: Review andtreatment
guidelines. Clin Orthop 400: 77–87, 2002

Written by

Dr Rajesh Purushothaman,

Associate Professor,

Government Medical College, Kozhikode,

Kerala, India.

http://www.learningorthopaedics.com

[email protected]
 21. UNSTABLE SHOULDER
Q&A

Q1. What are the important points in history taking in a case of RDS?

A. Amount of initial trauma

Position in which dislocation occurs
What is the position when dislocated?
Ease with which relocation occurs
Reduced by the patient/ doctor
H/o of recurrent subluxation of shoulder

Q2. Tell me about the glenohumoral ligaments?

A. Superior
Primary restraint to inferior humeral subluxation in 0 degree of abduction.
Primary stabilizer in anterior & posterior direction at 0 degree of abduction
Middle
Limits external rotation in lower &middle range of abduction.
Inferior
O’Brien discussed this ligament as a hammock type of model.
External rotation, hammock slides anteriorly&superiorly and anterior band tightens.
Restraints at extremes of motion& hence assists in the roll back of humeral head
Main stabilizer in anterior & posterior stress when the shoulder is abducted 45degree or
more.

Q3. What are the physical findings to demonstrate RDS?

A. Physical examination
Atrophy or asymmetry of the shoulder
Amount of tenderness in anterior and posterior capsule, rotator cuff and AC joint
Active and passive ROM in all direction
Strength of deltoid and rotator cuff muscles
Strength of scapular stabilizers
Test for scapular winging

Stability tests
Shift and load test (Drawer test) –one hand along the edge of the scapula, grasp
the humeral head with the other hand, apply compression and shift anteriorly and posteriorly

Sulcus test -- The limb is pulled distally and observing for a sulcus between the
humerus and acromion
0 degree --- indicates rotator cuff laxity
45 degree—indicates ligament laxity
Grade 0 to 3
1+ <1cm subluxation
2+ 1-2 cm subluxation
3+ >2 cm subluxation
 Anterior apprehension test (Crank test) -- Done with the patient supine. Abduct
the arm to 90 and externally rotate. If the patient has anterior instability, he will resist placement
into this position. If positive do, Jobe relocation test.

Posterior clunk test – shoulder 90 degree abduction, forward flexed and internally
rotated and posterior stress is given along the humerus.

Shoulder lachman test – Left hand grasps the proximal humerus and right hand
lightly holds the elbow. Forward pressure is given from the posterior aspect of shoulder and the
amount of translation is graded.

Relocation test Jobe – Patient supine, shoulder 90degree, in various levels of

external rotation and anterior stress is given. At the level at which apprehension or pain appears,
posterior directed force is applied to relocate the humerus.

Andrews’s test – This test is similar to anterior apprehension test but the patient is
examined in prone position and hence eliminates the learned response to apprehension test

Fulcrum test – Examiners’ hand is under the glenohumeral joint and downward
pressure is given at the elbow. The test is positive when the patient becomes apprehensive (i.e.
when the head is about to dislocate)

Q4. What is mean by TUBS and AMBRI

A. TUBS: Traumatic Unidirectional with Bankart lesion, frequently require Surgery.
AMBRI: Atraumatic Multidirectional Bilateral, treatment mainly Rehabilitation, although
an Inferior capsular shift procedure may be performed.

Q5. What is the importance of patient age at initial presentation?

A. <20 year at first dislocation: up to 80% chance for RDS
>30 year: up to 20%

Q6. What are the pathological conditions that may predispose to RDS?
A. Bankart lesion, Hill- Sachs lesion, SLAP lesion and Glenoid rim fracture.

Q7. What is the role of X-ray?

A. Roentgenographic evaluation
AP, lateral in the plane of the scapula
Other views
Recurrent GH Instability
2 approaches
Stress views
Seeking underlying pathology

STRESS VIEWS
Amount of glenohumeral translation with loading
Inferior translation- AP with sulcus test
Anterior: Axillary with fulcrum test
Posterior: Axillary with push pull test
Views seeking underlying pathology
Direction of instability
Contributing factors
AP in plane of scapula & Axillary view
Ant & post lip #
New bone formation
Glenoid rim changes
Bony lesion in ant glenoid rim (ax lat view)
# post glenoid rim( ax lat view)
WEST POINT VIEW
Patient prone
Involved shoulder raised by 7.5cm
Cassette :sup aspect of shoulder
Beam : 25 downward & 25 medial : centered at axilla
Apical oblique view (Garth)
Scapula flat on cassette
Beam : perpendicular to cassette 45 to coronal plane & 45 caudally centering
coracoid
HILL SACH`S VIEW
Marked IR
STRYKER NOTCH VIEW
Patient supine
Cassette : under shoulder
Palm on top of head: elbow upward
X ray :10 cephalad centering coracoid
Best view for #Coracoid
+ assesses posterolateral defect

Q8. What is the gold standard procedure to treat anterior instability?

A. Bankart’s procedure.

Q9. What are the alternative procedures?

Putti Platt procedure
Magnuson Stack procedure
Bristow procedure
Boytchow procedure
Latarjet procedure

Q10. How do you manage a Hill Sachs lesion?

Hill Sachs lesion is the most common bony defect in a case of anterior dislocation of the
shoulder and occurs in about 70 % of dislocators. It is considered significant only if more than
25 % of the head is involved. The options available are
Boyd Sick procedure - Transfer of long head of biceps to fill the defect of Hill Sachs lesion.
Remplissage procedure: attaching posterior cuff to the defect so that the defect is exteriorized
and do not engage
Structural bone grafting
If the defect is more than 40% humeral head arthroplasty may be required.

Q11. What is the pathognomonic clinical sign in multidirectional instability?

A. Sulcus sign
Q12. What is the clinical sign to demonstrate posterior dislocation?
A. Loss of external rotation.

Q13. What is the radiological sign to demonstrate posterior dislocation?

A. Light bulb sign.

Q14. What is meant by Perthes lesion in shoulder?

A. Soft tissue Bankart lesion is otherwise called Perthes lesion.

Q15. What are the causes of recurrrence?

A. 1. Failure to immobilize for 3 to 4 weeks
2. Site&nature of initial damage (McLaughlin&cavellaro)
3. Greater the initial trauma, lower the recurrence. (Rowe)
4. Age of patient during primary insult.

Q16. Narrate the treatment of RDS?

TUBS- With plastic ligamentous deformation with glenolabral damage – Modified Bankarts’
Procedure

For Microtraumatic lesions with subtle anterior instability and with no significant labral damage
--- Altchek procedure (capsular reefing )

Recurrent Posterior dislocation with large reverse Hill Sach lesion – Modified McLaughlin
Procedure.

Glenoid deficiency and poor capsular tissue – Bristow with Bankart

Elderly patient with recurrent seizures and dislocation – medical management + Bankarts’+
Puttiplatt

Large Hillsach lesion – Weber osteotomy

Severe Glenoid dysplasia – Scott-type osteotomy.

For AMBRI – Rehabilitation is the main treatment option. Neer and Foster lateral capsular shift
may be resorted to in selected cases.
To eliminate inferior laxity, closure of rotator cuff interval is indicated.
Posterior instability with inferior instability is treated with posterior shift of the
capsuloligamentous complex.
Q17. How does posterior dislocation differ from anterior dislocation?
A. Association with seizures and shock
Associated with lesser tuberosity fractures unlike GT in anterior dislocation
Much less common
Lesser risk of recurrence
Immobiled with gunslinger type brace rather than sling and swathe.

Q18. What are the issues with Elderly (>40yrs) dislocation?

A. Patients older than 40 years have a higher risk of rotator cuff tears associated with
anterior dislocation of the shoulder. Awareness, of this risk is critical, because patients with
anterior dislocation and Rotator cuff tear will not do well without rotator cuff repair. Delay in
diagnosis will result in retraction and atrophy of the rotator cuff tendons.

Q19. An 18 year old female swimmer reports shoulder instability. On physical examination,
she has systemic, hyperlaxity, positive responses on anterior and posterior drawer tests, and a
positive sulcus sign. What would be the ideal initial line of management?
A. This patient has multidirectional instability and atraumatic instability. She needs
aggressive rehabilitation for atleast 3-6 months before ever considering surgery. Rotator cuff
strengthening is the mainstay of physical therapy efforts.thermal capsuloraphy has been shown to
have a high risk of recurrent instability in this population. These patients rarely have a Bankart
lesion. Ultrasonography and other imaging modalities have a limited role in patients with
multidirectional instability.

Q20. How would you manage glenoid bone loss?

A. Defects less than 20 % are usually managed arthroscopically by a bankarts procedure.
Defects more than 20% are managed by structural bone grafting or Latarjet procedure.

Q21. What is Latarjet procedure?

A. Latarjet procedure involves transfer of the coracoid process osteotomised at the base to
the anterior glenoid neck. The coracoclavicular ligament and base of the coracoid process are left
intact. A remnant of the coracoaacromial ligament remains attached to the transferred coracoid
process and is imbricated into the anteroinferior glenohumeral capsule for further stability. The
triple blocking effect attributes to the success of latarjet procedure.
1. The structural bone graft that the coracoid process provides effectively
increasing the glenoid diameter
2. Hammock effect of the inferior subscapularis preventing excess humeral
translation in abducted and external rotated position
3. The ligamentous augmentation of the anterior band of IGHL to coracoacromial
ligament

Q22. What does suprasinatus and infraspinatus wasting signify?

It could mean a chronic tear of the rotator cuff, brachial plexus injury, suprascapular
nerve impingement or as a part of muscular dystrophies

Q23. What is Popeye sign?

A. Rupture of the biceps tendon presenting as a prominence at the middle of the arm

Q24. Name the tests for rotator cuff muscles

A. Empty can test- Supraspinatus
Horn blower test- infraspinatus
Napoleon or belly press test – Sub scapularis

Q25. Describe O’briens test for SLAP tear

A. With the arm in 900 forward flexion and abduction at the shoulder, ask the patient to flex
the arm against resistance. If the arm drops down with pain at the shoulder joint, it is considered
a positive O’Brien test. However conditions such as full thickness rotator cuff tear, Bankarts tear
and florid AC joint arthritis may present as false positive.
 22. EXAMINATION OF THE ELBOW JOINT

History:
General points regarding the trauma (especially note mode of trauma, treatment, h/o massage,
complications)
Any h/o septic arthritis, haemophilia, tuberculosis, Hansen’s disease, morning stiffness
Symptoms of ulnar neuritis.
Mention the handedness of the patient.

Local Examination: (from cervical spine to the finger tips)

Pre requisites
Both elbows examined in identical position
Patient stands / sits on a stool
Proper exposure

Inspection
Examine from the front, back and the sides
Attitude & deformity
Abnormal prominences
Swellings (localised – olecranon bursa/rheumatoid nodule, diffuse - extra and intra articular
swellings)
Scars or sinuses, previous surgery, steroid injections
Wasting of the muscles
Paraolecranon fossae
Palpation
Palpate the following and look for thickening, irregularity, stepping or tenderness
Medial and lateral supracondylar ridges
Medial and lateral condyle
Radial head
Mass in the cubital fossa - to r/o myositis ossificans
Three point bony relationship (compare with opposite side)
Supratrochlear/epitrochlear lymph nodes
Ulnar nerve in the cubital tunnel
Anconeus triangle (b/w the olecranon , radial head and the lateral epicondyle)
Collateral ligaments
Movements
Flexion & Extension
Supination & Pronation (remember to keep arms adducted by the trunk)
One must have good idea about the muscles primarily responsible for the particular
movement, their nerve supply, root value etc

Measurements to be taken in case of an elbow case:

Medial and Lateral ‘Column’ measurements of the arm
Length of radius and ulna
Carrying angle
Three point bony relation
Circumferential measurement of arm and forearm
ROM of shoulder
 ROM of wrist joint.
ROM of elbow joint
Special tests
Posterolateral Instability test
Valgus and varus instability
Look for DRUJ Instability
Look for DNVD especially ulnar nerve

23. ANGULAR DEFORMITIES OF THE ELBOW

CASE PRESENTATION
History
10 year old female admitted with complaints of deformity of right elbow of 2 years duration.
There is no history of pain and there is no limitation of daily activities. There was a history of
fall from a tree 2 years back and she sustained an injury to the right elbow which was treated by
a traditional bone setter with bandaging and massage for 1 month. One month after the treatment,
parents noticed the deformity of the right elbow which is not progressing. There is no history of
any other joint involvement or any difficulty in using the hand for her daily activities. She is
attending fifth standard.
General Examination
There is no ligamentous laxity, no deformities on any other joint. She is moderately built
and nourished.
Local examination
On inspection there is an inward deviation of the forearm at the elbow and hyper
extension at the elbow joint. There no scars or sinuses. There is no muscle wasting. There is an
abnormal prominence seen on the lateral aspect of the elbow and medial condyle appears less
prominent. Olecranon appears normal and the attachment of the triceps appears to be more
medial. Paraolecranon fossae appear normal.
On palpation there is no local rise of temperature. There is no joint line tenderness. There is
thickening of the medial and lateral supracondylar ridges. Medial and lateral condyle, radial
head, olecranon is felt normally. The three point bony relationship is maintained. Ulnar nerve is
felt in the cubital tunnel and does not subluxate on flexion.
On taking segmental measurements the arm and forearm segments are comparable with the left
side. Intercondylar distance is comparable on both sides.
There is hyper extension of 20 degrees with limitation of flexion up to120 degrees. Carrying
angle is 10 degree varus. Supination and pronation at the elbow is within normal limits. There is
no varus or valgus instability.
On examining the right shoulder there is a limitation of external rotation of 10 degrees and
exaggerated internal rotation of 10 degrees compared to the left side. Wrist is normal.
Examination of the ulnar, median and radial nerve is within normal limits.
Diagnosis
Cubits varus deformity of the right elbow most probably due to a malunited supracondylar
fracture of the humerus.
Q&A
Q1. What is cubitus varus?
A. A deformity of the elbow resulting in a decreased carrying angle (so that, with the arm
extended at the side and the palm facing forward,there is deviation of the forearm toward the
midline of the body. Cubitus is the Latin word for elbow and varus means angled inward.
Q2. What are the components of elbow joint
Humeroulnar joint , it is a simple hinge-joint, and allows of movements of flexion and
extension only.
Humeroradial joint, it is a hinge-joint.
Proximal radioulnar joint
Q3. What is carrying angle?
A. It is the angle formed by the long axis of the arm and long axis of forearm with the elbow
extended and forearm supinated. It is because the medial column of the humerus is longer than
the lateral column. This angle permits the forearms to clear the hips in swinging movements
during walking, and is important when carrying objects
In males normal carrying angle is 5-10°and in females it is 10-15°
If carrying angle is exaggerated, it is called cubitus valgus
Reduction, neutralisation or reversal of carrying angle is cubitus varus

Q4. What is the age of appearance of ossification centers around elbow?

A.
Capitellum: 6 months to 2 years; includes the lateral crista of
the trochlea
Radial head: 4 years
Internal/Medial 6 to 7 years
epicondyle:
Trochlea: 8 years
Olecranon: 8 to 10 years; often multiple centers, which
ultimately fuse
External/Lateral 12 years
epicondyle:
CRITOE (2, 4, 6, 8, 10, 12): mnemonic for the appearance of the ossification centers
around the elbow

Q5. Why do you say this is malunited supracondylar fracture?

A. There is history of significant trauma in the past
Cubitus varus deformity is the most common cause of malunited supracondylar fracture
O/E
Thickening and irregularity of medial and lateral supracondylar ridge
Maintained three point relationship
Hyperextension at the elbow
Internal rotation increased with restricted external rotation of the shoulder

Q6. What are the associated deformities of cubitus varus?

A. Internal rotation
Extension of distal fragment
Medial tilt

Q7. What type of a deformity is this?

A. Static deformity
Q8. Will there be progressive cubitus varus deformity after supracondylar fracture?
A. Growth disturbance in the distal humerus, especially overgrowth of the lateral condyle,
can occur and sometimes osteonecrosis and delayed growth of the trochlea, with relative
overgrowth of the normal lateral side of the distal humeral epiphysis, is seen. These are rare
cause of progressive cubitus varus deformity after supracondylar fracture

Q9. What are the other causes for cubitus varus deformity?
A. Congenital
Malunited intercondylar fracture
Malunited medial condyle fracture
Trochlear osteonecrosis
Malunited fracture lateral condyle

Q10. What do you call if the angulation at elbow is lost?

A. Cubitus rectus
In this condition the alignment is neutral. (No varus/valgus angulation). It is still a
deformity

Q11. What are the deformities in supracondylar fracture?

A. Medial displacement
Medial tilt
Internal rotation
Posterior displacement
Posterior tilt
Proximal migration

Q12. What neurovascular structures are particularly in risk in a supracondylar fracture?

A. Radial nerve – posteromedial type # displacement
Median nerve – posterolateral type # displacement
Ulnar nerve – flexion type of # displacement
Brachial artery - posterolateral type # displacement

Q13. What is three point relationship?

A. At 90° of elbow flexion olecranon process of ulna and the medial and lateral epicondyles
of the humerus normally form an NEAR isosceles triangle (Some examiners insist on saying
neither isosceles nor equilateral but a triangle congruent with the opposite elbow). When the arm
is fully extended the three points normally form a straight line.
The isosceles triangle is sometimes called the triangle sign.
You should also be prepared to explain what an isosceles or equilateral triangle is!!!

Q14. What are the interpretations of three point relationship?

A.Decreased length of medial limb
Posteromedial dislocation
Medial rotation of fractured fragment
Decreased length of lateral limb
Posterolateral dislocation
Lateral rotation of fractured fragment
Increased length of medial limb
Fractured medial epicondyle/condyle
Increased length of lateral limb
Fractured lateral condyle
Increased length of base
Malunited intercondylar fracture

Q15. What are the fallacies of three point relationship?

A. Displaced fractures of medial and lateral epicondyle
Surgical intervention leading to altered morphology
Excision arthroplasty of elbow
Lateral spur formation
Charcot’s arthropathy

Q16. What are the complications of supracondylar fracture?

A. Early
Compartment syndrome (Volkmanns ischemia)
Nerve injury
Vascular injury
Late
Malunion
VIC
Myositis ossificans
Cubitus varus
Cubitus valgus
Tardy ulnar nerve palsy
C/C nerve entrapment in healed callus

Q17. Which muscle is most commonly involved in myositis ossificans?

A. Brachialis, other involved muscles are pronator teres and brachioradialis

Q18. How will you classify supracondylar fracture?

A. Gartland classification for supracondylar fractures:
Type I- undisplaced
Type II- displaced with intact posterior cortex
Type III- displaced with no cortical contact (III A – posteromedial and III B –
posterolateral)

Q19. What is fat pad sign?

A. The soft tissues shadow seen both anteriorly and posteriorly in the lateral view of an
elbow xray in type 1 supracondylar fractures due to the displacement of the fat pad by the
hematoma is known as fat pad sign. The posterior fat pad is of more significant than the anterior
fat pad.

Q20. How will you manage acute supra condylar fracture?

A. Type I – POP slab with 90 degree flexion of elbow
Type II - Closed reduction and immobilization with elbow in 120 degrees of flexion
Type III - unstable hence treated by closed or open reduction and percutaneous pinning
Q21. Why supracondylar humerus fractures are reduced in hyperflexion?
A. Splinting is obtained by tightening of triceps posteriorly, in type 1 & 2 extension type
supracondylar fractures posterior periosteum also acts as splint.

Q22. What are the treatment options available for supracondylar fractures?
A. Dameron listed, depending on the type of fracture, four basic types of treatment:
(1) Side-arm skin traction,
(2) Overhead skeletal traction,
(3) Closed reduction and casting with or without percutaneous pinning, and
(4) Open reduction and internal fixation

Q23. How do you assess the adequacy of reduction?

Baumann angle
A. Angle subtended between the tangent to lateral physeal line
and long axis of diaphysis of humerus
Normal - 64-81° (mean - 72°)
The common formula is that a change of 5 degrees in the
Baumann angle corresponds to a 2-degree change in the clinical
carrying angle
Metaphyseal diaphyseal angle
On anteroposterior radiograph, transverse line is drawn through metaphysis at its widest
point, and longitudinal line is drawn through axis of diaphysis; angle is measured between lateral
portion of metaphyseal line and proximal portion of diaphyseal line
Normal angle is 90 degrees. Angle greater than 90 degrees indicates varus angulation and
angle lessthan 90 degrees indicates valgus angulation
Humeral- ulnar- wrist angle
Most consistent and accurate method of approximating the true carrying angle
The crescent sign and the fishtail sign
Assessed in lateral radiograph presence of this imply angulation and rotation
Q24. How is ulnar nerve involved in cubitus varus?
A. In cubitus varus triceps insertion is medially shifted which leads to narrowing of cubital
tunnel or fibrous band across the heads of flexor carpi ulnaris, leading to ulnar nerve
compression
Q25. How will manage this patient?
A. Confirm the diagnosis radiologically and do modified French osteotomy

Q26. How will you assess correction required for osteotomy?

A. Preoperatively assess the humeroulnar angle of the normal side and involved side.
Assess how much correction is required . eg in a case with 13° of varus angle it has to be
corrected to normal 10° valgus.The total correction required is 23°. A template has to be made
with angle of 23°. During surgery laterally based based wedge is taken using this template.

Q27. How will you correct rotation during French osteotomy?

In French osteotomy the proximal lateral screw is put posterior to coronal plane and
distal screw is put anterior to coronal plane. This disposition leads to external rotation of distal
fragment when wires are tightened.
Remember- proximal screw is posterior

Q28. What are the types of osteotomy for correction of cubitus varus?
A. Lateral closing wedge osteotomy
Medial opening wedge osteotomy with a bone graft - King and Secor
Oblique osteotomy with derotation
Step-cut osteotomy - Derosa and Graziano
Step-cut translation osteotomy and fixation with a y-shaped humeral plate - Kim
If a more extensive osteotomy is needed
Dome osteotomy
Q29. When will you plan for osteotomy?
A. At least one year after fracture, this provides adequate time for remodeling of bone and
regaining of tissue equilibrium.
Q30. What are the complications of osteotomy?
A. Stiffness of joint
Nerve injury
Persistent deformity
Non union
Malunion

Q31. What are the differences between French osteotomy and Modified French
osteotomy (Bellemore?)

French osteotomy Modified French osteotomy

Posterior longitudinal incision Posterolateral incision
Ulnar nerve explored Ulnar nerve not explored
Medial periosteal hinge Medial periosteal and bony hinge
Q32. What are the causes of restriction of flexion and extension in elbow?
A. Myositis ossificans
Olecronon # malunited
Coronoid # malunited
Elbow Dislocation
Malunited Intercondylar #

Q33. How do you confirm medial tilt clinically in case of cubitus varus due to malunited
supracondylar fracture?
Ask the patient to bring both the elbows flexed to 90 degrees towards MIDLINE.note the
position of epicondylar tips – the one with medial tilt will be located HIGHER up

Q 34.In the above case, how will you confirm medial (internal) rotation?
Keep both elbows flexed at 90 degrees with arms by the side of the chest. Ask the patient to
externally rotate both the shoulders. The external rotation of the shoulder on the affected side
will be limited more or less by the same degree as the medial (internal) rotation at the elbow
Yamamoto method - "With the subject bending slightly forward, the upper limb is held at the
side and then positioned behind the back with the elbow at 90 degree flexion and the shoulder
held at the maximum extension position. In this position the midline of the forearm gets exposed
for inspection by the examiner, who stands behind the subject, applying maximum internal
rotation to the subject's upper limb around the long axis of the humerus. When no internal
rotation deformity of the humerus is present, there is no change in the forearm position. The
horizontal plane of the back is parallel with the midline of the forearm. Conversely, in children
with the internal rotation deformity of cubitus varus, a certain abnormal angle is formed between
the horizontal plane of the back and the midline of the forearm. The angle is designated the
internal rotation angle."

CASE PRESENTATION 2

18 year old female admitted with complaints of deformity of right elbow of 3 years duration.
There is no history of pain and there is no limitation of daily activities. There was a history of
fall 3 years back and she sustained an injury to the right elbow which was treated by a traditional
bone setter with bandaging and massage for 1 month. One month after the treatment, parents
noticed the deformity of the right elbow which is not progressing. There is no history of any
other joint involvement or any difficulty in using the hand for her daily activities.
On examination
There is no ligamentous laxity,no deformities on any other joint. She is moderately built and
nourished.
Local examination
On inspection there is a cubitus valgus deformity of the forearm at the elbow. There is a flexion
deformity of 10 degrees.There are no scars or sinuses. There is no muscle wasting. There is an
abnormal prominence seen on the medial aspect of the elbow.
On palpation there is no local rise of temperature. There is no joint line tenderness. The lateral
lateral condyle is thickened and irregular.Medial and lateral supracondylar ridges, Medial
condyle, radial head, olecranon is felt normally. The three bony relationship is altered with
lateral epicondyle lying at a higher level. Ulnar nerve is felt in the cubital tunnel and does not
subluxate on flexion. There is painless abnormality with crepitus over the lateral condyle.
The acromion to lateral condyle distance is decreased by 2 cm on the right side. The inter
condylar distance is increased by 1 cm. There is a fixed flexion deformity of 10 degrees with
further flexion possible upto 140 degrees.Varus stress test is positive. Supination and pronation
at the elbow is within normal limits. There is no distal vascular deficit.
Wrist is normal. Examination of the ulnar, median and radial nerve is within normal limits.

Q&A

Q1. What are the common D/D of cubitus valgus

A. Neglected Pulled Elbow
Congenital Dislocation of radial head
Non-Union of Lateral Condyle
Monteggia fracture dislocation
Malunited radial neck #
Septic arthritis of radio-capital joint

Q2. What are the causes for cubitus valgus at birth?

A. Noonan syndrome
Turner syndrome
Nail patella syndrome

Q3. Why do you say this is a case of non union of fracture lateral condyle?
A. Three bony point relationship is disturbed
Thickening of lateral supracondylar ridge
 Flexion deformity of elbow
Abnormal mobility of lateral condyle
Varus stress test positive

Q4. Why is non union common in lateral condyle?

A. Poor vascularity of metaphyseal fragment
Fragment bathed in synovial fluid
Pull of muscles arising from lateral condyle
Displacement of the fragment with opposition of articular cartilage to proximal fracture
surface

Q5. How will you classify lateral condyle fracture?

A. Milch classification
Type I fracture, which is Salter-Harris type IV epiphyseal fracture
Type II fracture, which is Salter-Harris type II epiphyseal fracture
Jackob’s classification
Undisplaced
Moderately displaced
Completely displaced and rotated
Finnbogason, Karlsson & Lindberg classification
Fracture through lateral humeral condyle with minimal lateral gap
Fracture through lateral humeral condyle to epiphyseal cartilage with lateral gapFracture
through lateral humeral condyle with fracture gap as wide laterally as medially, fracture with
high risk of later displacement

Q6. What type of a deformity is this?

A. Cubitus valgus due to non union of lateral condyle is a progressive deformity.This can
lead to change in elbow mechanics and cause neurological complications.

Q7. What is the cause for tardy ulnar nerve palsy in cubitus valgus?
A. Stretching of nerve due to progressive medial angulation
Perineuritis due to friction
Adhesion due to entrapment of nerve in cubital tunnel

Q8. How will you manage this case?

A. Confirm the diagnosis by getting radiograph of elbow in AP and lateral projections

Q9. What is the absolute indication for surgery in cubitus valgus?

A. Progressive deformity
Tardy ulnar nerve palsy
Elbow instability

Q10. How will you treat this case?

A. Patients with established non union of lateral condyle
Open reduction + in situ fixation in compression with screws and bone grafting
Patients concerned about cosmetic deformity (>20°)
Supracondylar corrective osteotomy
Non progressive cubitus valgus in adult with tardy ulnar nerve palsy
Transposition of ulnar nerve
 24. EXAMINATION OF A PERIPHERAL NERVE INJURY

History
Handedness
Occupation eg. Industrial worker
Vascular Ischaemia:
Infection :Hansen/Polio.
Compressive myelopathy:
Metabolic : Diabetes, gaucher, lead poisoning (purely motor)
Amylodosis:
Alcoholism,
Trauma – open/closed.
Drug induced.
Any improvement in symptoms.
Rheumatoid arthritis: Mononeuritis multiplex
Inability to wear slippers in case of lower limb lesions
General Examination:
Nerve swelling, beading, thickening,
Position of the distal aspect of the extremity.
Site of scar, Ulcers, smoothness or dryness of the skin.
Absence of callus.
Temperature changes.
Hypopigmented patches (Hansen’s disease)
Examination Pattern:
Differentiate between UMN and LMN
UMN LMN
Plantar: Upgoing Absent
Tone Increased Absent
Reflexes: Initially absent, later increases Absent
Power : Group of muscles inv. Individual muscles
Wasting Mild or seen very late. Gross Wasting.

Rule out compressive myelopathy / radiculopathy.

Find out the nerve involved: use of autonomous zones.
Find out whether it is high or low lesion.
Any evidence of injury (Non union ,malunion stiffness),
Inspection
Attitude and deformity
Brittle nails, shiny skin, pin point ulcers
Scars/ sinuses
Muscle fasciculations
Any bony swellings or deformities
Palpation
Thickening of nerves
Parasthesia/anaesthesia
Motor system
Bulk
Tone
Reflex
 Power of the affected muscles
Sensory system
Pain/ touch/ vibration especially in the autonomous area
Autonomic system
Causalgia
Trophic changes
Shiny edematous skin
Movements
Both active and passive
Look for tendons that can be used for tendon transfers eg. Palmaris longus
Tinel’s sign: (never forget)
Extent of injury: Neuropraxia/ axonotemisis/ neurotemsis
Muscles neede for transfer
Joints are supple.

25. BRACHIAL PLEXUS INJURY

History:
History similar to plexus injuries
History of # scapula ribs, clavicle.
Rate of progression of deformity.
Any improvement in symptoms,
Difficulty in vision in the evenings (s/o Horner’s)
In Obstetric palsy, antenatal / natal / and post natal history.

Examination findings
Similar to examination of peripheral nerves,
Palpate along clavicle, scapula and along first rib.

Examination Pattern:
Check for plantar reflex, long tract signs and serratus anterior (Root lesion) and/or horners sign
and paraesthesia along the paraspinal muscles:
If positive : then Preganglionic;
If negative : then check Supraspinatus (ie integrity of the Trunk via the suprascapular nerve)
If negative then check:
a) Musculocutaneous nerve: lateral cord
b) Ulnar nerve :Medial Cord
c) Radial nerve : Posterior nerve

Document recovering/ non recovering

Upper arm lesion C5 C6
Lower arm lesion C7C8T1,
PanPlexus.
Preganglionic or postganglionic

Diagnosis
a) Post traumatic/ obstetric
b) pre/ post ganglionic
c) Recovering/ non recovering
d) Upper plexus/ lower plexus / pan Plexus
e) Deformity if any

Autonomous zones ( To r/o root lesion)

Muscle Reflex Sensation

C5 Deltoid Biceps along the deltoid border.

C6 Wrist extensors Brachioradialis Lateral forearm,thumb,index

C7 Finger Extensor
Wrist Flexor Triceps Middle finger

C8 Finger Flexion Medial forearm, ring small finger

T1 Finger Abduction Medial Arm

Finger Adduction

CASE PRESENTATION

This 35 year old right handed manual laborer presented with weakness of right hand for 8
months following fall from bike, at that time his right shoulder hit on the ground. He was on
ayurvedic treatment for the last 8months, with no improvement in his condition. Now the patient
is not able to do his day today activities like eating, combing hair, buttoning the shirt etc.
Well cooperative patient, right arm kept on side of the body, elbow extended, forearm pronated
and wrist is semiflexed, with appreciable wasting of supraspinatous, deltoid, biceps, triceps and
forearm muscles. Ther is no facial dismorphism, pupil equal and reacting to light,
supraclavicular fossa and posterior triangle of neck normal, clavicle shape is normal.
Bulk and tone of the shoulder, arm and forearm muscles reduced. Rhomboids and Serratous
anterior and has grade zero power. Supraspinatous, Deltoid, Biceps, Brachialis, Dorsiflexors of
wrist has a power of grade zero. Triceps, wrist palmar flexors has grade 3 power. Hand grip and
intrinsic have grade 5 power. Biceps reflex and supinator reflex is absent, Triceps reflex is
diminished, plantar is downgoing.sensation over the lateral aspect of arm forearm and middle
finger is absent.
Trapezius and lattismusdorsi has grade 5 power (required for reconstructive procedures)
Shoulder, elbow and wrist has full range of passive movement.
DIAGNOSIS: RIGHT SIDED , POST TRAUMATIC, CLOSED , UNRECOVERED
PREGANGLIONIC ,BRACHIAL PLEXUS INJURY WITH COMPLETE INVOLVEMENT
OF C5 AND C6 ROOTS AND PARTIAL INVOLVEMENT OF C7 ROOTS.
Q&A

Q1. Describe the supply of components of brachial plexus.

A. Dorsal scapular: Rhomboids, levator scapulae
Long thoracic: serratous anterior
Supra scapular: supraspinatous and infraspinatous
 Nerve to subclavius: subclavius
Lateral pectoral: clavicular head of pectoralis major
Medial pectoral: sternocostal head of pectoralis major
Muscuolocutaneous: biceps, brachialis and brachioradialis
Upper and lower subscapular: subscapularis and teres major
Thoracodorsal: latismus dorsi
Axillary: Deltoid, teres minor
Lateral root of median: pronator teres, flexor carpi radialis
Medial root of median: FDS, FDP lateral half, Lateral two lumricals, all thenar muscles
except adductor pollicis
Ulnar: FCU, FDP medial half, hypothenar muscles, adductor pollicis
Radial: Triceps, all dorsal compartment muscles of forearm.

Q2. What are the features of preganglionic lesion?

A. Involvement of dorsal scapular and long thoracic nerve
Long tract signs
Cervical spine fractures
Denervation potential in paraspinal musculature
Cutaneous axon reflex test by Bonney (flare response will be absent in post ganglionic
lesion)
Cold vasodilatation test
Sensory nerve root velocity test
MRI- pseudomeningocele or complete absence of root shadows (recommended after 6-12
weeks)
Horner’s syndrome.

Q3. Describe the representation of C5 to T1 nerve roots.

A. C5- Shoulder abduction, elbow flexion + sensation lateral aspect of arm.
C6-wrist extension + sensation lateral aspect of forearm and hand.
C7-Elbow extension, wrist flexion and MCP joint extension + sensation middle phalanx.
C8-finger flexion + sensation medial aspect of forearm and hand.
T1- finger abduction and adduction + sensation medial aspect of arm.

Q4. What is the deformity that seen in Erb’s palsy and Klumpky’s palsy.
A. Erbs- police man tip deformity
Klumpky- claw hand

Q5. What are the components of Erb’s palsy?

A. Loss of shoulder abduction (weak supraspinatus and deltoid)
Loss of shoulder external rotation (weak infraspinatus and teres minor)
Loss of elbow flexion (weak biceps brachials and brachioradialis)
Loss of supination (weak supinator)

Q6. What is mean by Erb’s point?

A. It is the meeting point of following six nerves: C5 and C6 root, suprascapular nerve,
nerve to subclavius, anterior and posterior division of upper trunk.
Q7. How will you classify brachial plexus injury?
A. LEFFERT classification:
Open
 Closed : A-supraclavicular, B-infraclaivicular, C-post anaesthetic
Radiation
Obstetric: A- Erbs’s, B-Klumpke, C-mixed.

Q8. How will you classify obstetric brachial plexus injury?

A. NAGARO’S classification
C5, C6
C5,C6,C7
C5 to T1
C5 to T1 with temporary Horner’s syndrome
C5 to T1 with permanent Horner’s syndrome.

Q9. How will you grade the shoulder deformity in Erb’s palsy?
A. WATTER’S classification
Normal glenohumeral joint
Minimal hypoplasia
Posterior subluxation
Presence of false glenoid
Flattening of head of humerus
Infantile dislocation
Proximal humeral growth arrest.

Q10. How will you treat erb’s palsy?

A. Give rest for 1 week to subside hemorrhage and edema.
Start passive ROM exercise after 1 week
Maximum recovery expect by 3 months.
Possible full recovery obtained by 1 year.

Q11. What are the indications for surgical treatment?

A. Absence of biceps recovery by 3 months
Toronto scale score < 3.5
Total palsy with horner’s syndrome.

Q12. What is the ideal time for surgery?

A. 1-6 months

Q13. When will you do reconstructive surgeries?

A. Usually after 4 years unless it is rapidly progressive

Q14. What is meant by TORONTO scale?

A. Used to predict the outcome, if microsurgical repair is not done.
Grade A: Elbow flexion
B: Elbow extension
C: Wrist extension
D: Finger extension
E: Thumb extension
Scale: 0: No movement
1: Limited movement
2: Normal movement.
Q16. What are the aims of reconstructive surgery?
A. Shoulder abduction
Elbow flexion
Sensation of medial side of hand.

Q17. How will you treat shoulder internal rotation contracture?

A. Mild to moderate: SEVER’S anterior subscapular release.
Severe: ROGER’S derotational osteotomy.

Q18. What are the options to regain shoulder abduction?

A. BATEMAN Procedure: Trapezius along with spine of scapula transferred to proximal
humerus.
SAHA procedure: Trapezius transferred to proximal humerus.

Q19. How will you restore Elbow flexion?

A. STIENDLER’S FLEXUROPLASTY: Common flexor origin transferred to distal
humerus (5cm proximal to elbow joint) disadvantage: pronation deformity.
Carrol and Gartland modification: transferred to anteriorly and proximally.
Bunnel’s modification: Transfer more laterally.

Q20. What is meant by neurotisation?

A. The less important nerve like intercostals nerve is transferred to musculocutaneous nerve,
which is useful in root avulsion.

Q21. What are the late radiological features of Erbs palsy?

A. 1.Thick and elongated coracoids.
2. Beak like acromion
3. Small, retroverted and flattened humeral head.

Q22. What is SOMSAK procedure?

A. Transfer of nerve to long head of triceps to Axillary nerve.

Q23. What is Oberlin transfer?

A. Transfer of ulnar nerve to musculocutaneous nerve

26.Peripheral Neve Lesions

Ulnar Nerve Injury :

1. Describe relevant anatomy of ulnar nerve
Ulnar nerve arises from the medial cord of the brachial plexus (C8, T1), pierces the
medial intermuscular septum in the middle third of the arm, passing thro the ulnar groove behind
the medial epicondyle. Then it enters the forearm between two heads of FCU thro the cubital
tunnel. Enters the hand through the Guyons canal. Both palmar and dorsal cutaneous branches
are given in the forearm. The motor branch in the hand ends by supplying the first dorsal
interossei.
2. List the muscles supplied by the ulnar nerve.
Axilla and arm – no motor branches
Forearm – flexor carpi ulnaris, medial half of Flexor digitorum profundus
Hand – all hypothenar muscles (abductor, opponens, flexor, digiti minimi)
Two thenar muscles (adductor pollicis, flexor pollicis brevis one head)
Medial two lumbricals
All interossei
Muscles to be tested: Flexor carpi ulnaris (first muscle supplied)
(Can be palpated, power tested) Abductor digiti minimi
First dorsal interossei (last muscle supplied)

3. What do you mean by high and low ulnar nerve palsy?

Involvement of FCU and medial two halfs of FDP with distal palsy – high ulnar nerve palsy
Sparing of FCUand FDP with distal palsy – low ulnar nerve palsy

4. Define ulnar paradox?

Higher ulnar lesion produces lesser clawing and low ulnar nerve palsy produces classical
clawing. Happens due to the involvement of FDP in higher lesions.

5. How will you localize the level of ulnar nerve palsy?

High ulnar palsy – lesion above elbow. Paralysis of FCU, FDP medial two heads,
hypothenar muscles, all interossei, medial two lumbricals with sensory loss on both the volar and
dorsal aspect , medial side of hand.
Low ulnar palsy – lesion below elbow, usually below wrist with sparing of FCU and
FDU.

6. What are the tests for ulnar nerve palsy?

A. Test FCU – differentiate high and low nerve palsy

Test abductor digiti minimi, and test 1st dorsal interossei – all three are palpable and
power can be assessed.

Egawa test / Pitres-Testut sign – test 2nd and 3rd dorsal interossei
Card test – tests palmar interossei

Froment’s sign / Book test/ Newspaper sign/ Bunnell’s “O”sign – tests adductor
pollicis

Duchenne’s sign –clawing of ring and little fingers

Jeanne’s sign – hyperextension of the MP joint of thumb on performing key pinch

Masse’s sign – loss of hypothenar elevation

Pollock’s sign – inability to flex the distal phalanges of ring and little fingers

Wartenberg’s sign – inability to adduct the extended little finger to the extended ring
finger
 Inspection findings – ulnar claw hand, guttering of intermetacarpal spaces, loss of metacarpal
arch, loss of hypothenar eminence, trophic changes tip of little finger, wasting of medial aspect
of forearm

7. What are the basic hand functions lost in ulnar nerve palsy?
Loss of lateral or key pinch of the thumb
Loss of grasp – as the sequence of finger flexion is reversed (normally MP joint of the
fingers flex followed by the IP joints which gets reversed in Ulnar nerve palsy – hence the
objects are pushed away instead of being grasped)

8. List few causes of tardy ulnar nerve palsy?

Development of late onset ulnar nerve palsy (usually takes years) is seen in nonunion
lateral condyle of humerus with cubitus valgus deformity
Recurrent subluxation of ulnar nerve
Malunited medial epicondyle humerus – usually results in high ulnar nerve palsy

9. What is cyclist’s palsy or handlebar palsy?

Ulnar nerve paralysis, resulting from pressure over the nerve in the Guyons canal ,with the
handle of the cycle. Results in low ulnar nerve palsy.

10. List the anomalous innervation patterns seen in ulnar nerve lesions?
Martin –Gruber anastomosis: seen in proximal forearm. Between median nerve or its
anterior interosseous branch and ulnar nerve. 15% occurrence.
Riche-Cannieu anastomosis: seen in the hand. Between the motor branch of ulnar nerve
and recurrent branch of the median nerve.

Radial Nerve Palsy :

1. Briefly describe relevant anatomy of radial nerve?
Radial nerve is the largest of all branches of the brachial plexus, arising from the posterior cord
(C5-T1), posterior to the third part of axillary artery. Largest contribution from C7. Then it
accompanies profunda brachii vessels and enters the radial groove on the posterior aspect of the
humerus through the lower triangular space. It pierces the lateral intermuscular septum about 10
cm proximal to the lateral epicondyle. . In the spiral groove, the nerve is separated from the
underlying bone by a layer of muscle. The nerve is in direct contact with humerus only in the
distal arm where it pierces the lateral intermuscular septum. At or just below the elbow, it
divides into superficial and deep branches. Posterior cutaneous nerve of the arm is the first
branch of radial nerve. First motor branch goes to the long head of triceps. Just above the elbow,
it gives branches to the brachioradialis and extensor carpi radialis longus (main wrist extensor)
muscle.

2. Describe the anatomy of posterior interossseous nerve?

PIN passes from the proximal anterior forearm to posterior forearm thro’supinator muscle
winding around the radial neck. It supplies the supinator, entering thro’ the arcade of Frohse
which is the fibrous arch in the proximal margin of supinator. It exits supinator approx. 8 cm
distal to the elbow joint dividing into multiple branches described by Spinner as Cauda equine.
The branches are arranged into two major groups – a superficial branch (supplying the ext
digitorum, ext digiti minimi, ext carpi ulnaris ) and a deep branch dividing into medial branch
(supplying APL & EPB) and a lateral branch (supplying EPL & E indicis). PIN is purely motor
except for several branches to the wrist joint in its termination, which are sensory.

3. What are the common causes of radial nerve palsy?

Axilla - aneurysm axillary vessels, crutch palsy
Spiral groove – humerus shaft # (Holstein –Lewis #), Saturday night palsy, tourniquet
palsy, surgical positions
Elbow – elbow dislocation, # radius neck ,Monteggia # dislocation (PIN palsy)

4. How will you localize radial nerve palsy?

VERY HIGH RADIAL NERVE PALSY
– lesion in axilla
- weak elbow extension (triceps palsy)
- wrist drop ( ECRL palsy )
- finger/thumb drop (Ext digitorum, EPL, APL palsy)
- sensory loss below mid arm
HIGH RADIAL NERVE PALSY (LOW TYPE 1)
- mid arm lesion
- normal elbow extension
- wrist drop ( ECRL palsy )
- finger/thumb drop (Ext digitorum, EPL, APL palsy)
- sensory loss below mid arm
LOW RADIAL NERVE PALSY (LOW TYPE 2)
- below elbow lesion
- normal wrist extension (ECRL spared)
- finger/thumb drop (Ext digitorum, EPL, APL palsy)
- sensory loss autonomous area (first web space dorsally)

Key muscles to be tested to localize the level: triceps, ECRL, Ext digitorum, EPL

5. What is Wartenberg syndrome?

Compression of superficial branch radial nerve by ECRB / BR
Symptoms
Cheiralgia paresthetica - Paresthesia first dorsal webspace

6. What is intrinsic plus deformity?

Flexion at MCP joints and extension at IP joints. Seen in overcorrected Bunnels
procedure, rheumatoid hand etc

Median Nerve Palsy :

1. Describe briefly the anatomy of median nerve?

Arises from medial & lateral cord C5 – T1. Runs medial to axillary and brachial
artery.Enters forearm between two pronator heads. Gives off Anterior Interosseous Nerve 2-8 cm
below medial epicondyle. Palmar cutaneous branch given above wrist. Passes deep to carpal
tunnel to the hand. Median nerve has no branches in the axilla and arm segment.
2. How would you localize the level of median nerve lesion?
High median palsy
- lesion above elbow
- all forearm flexors(except FCU and ulnar half of FDP)
- all pronators
- thenar muscles
- 1st,2nd lumbricals

Low median nerve palsy

- lesion below elbow
- forearm flexors & pronators spared
- sensation over thenar eminence spared

Key muscles to be tested to localize lesion – FCR, Pronator teres, APB

3. What are the clinical features of median nerve palsy?

Wasting of the flexor prominence radial aspect
Thenar wasting
Ape thumb deformity (thumb in plane of palm)
Sensory loss in autonomous area ,trophic changes
Pen Test – test APB
Pointing index finger sign / Benediction sign / Oschner’s clasping test – tests FDP
Kiloh Nevin Sign – test FPL, FDP index finger ( sign of AIN palsy)
4. List few compression neuropathies of median nerve?
Carpal tunnel syndrome
Anterior interosseous syndrome
Pronator syndrome

5. What are the main functional deficits with high median nerve palsy?
Loss of active pronation, loss of opposition of thumb and loss of digital flexion of thumb,
index and middle fingers, resulting in weak grip.

6. Describe Tinel sign?

It’s the transient tingling sensation felt at the site of distribution of the nerve
Percuss along the course of nerve from distal to proximal
Distally advancing tinel sign occurs in axontemesis, not seen with neuropraxia and neurotemesis
It’s a cortical sensation , similar to phantom limb sensation.
At the site of repair, axons take one month to enter distal endoneural tubules (duration for
wallerian degeneration) .After 2 months – Tinel elicited 1 inch beyond repair. Advancing Tinel
can be separated from static Tinel after 6-8 weeks.

Interpretation of Tinel sign

Strong static Tinel at injury site+ no advancing Tinel distally = no chance of recovery
Reducing static Tinel at injury+ distally advancing Tinel=good chance of recovery
Strong static Tinel at injury+ distally advancing Tinel=poor chance of useful recovery

Limitations of Tinel sign:

Qualitative not quantitative test
Deep seated nerves can’t be tested eg – Sciatic nerve
Less useful for purely motor nerves eg – PIN

Some commonly missed points in nerve examination:

Look for features of

Hansen’s (hypopigmented patches, thickened nerves)
Syringomyelia when bilateral features (dissociative anaesthesia)
Diabetes and Rheumatoid arthritis (polyneuropathy)
Look for tendons available for transfer (eg Palmaris longus in radial nerve palsy)
Babinski sign (to r/o myeloradiculopathy)
Reflexes (UMN/LMN)
Tinel sign
Active and passive movts (to r/o contractures)

7. How will you express the diagnosis in a peripheral nerve injury case?
Nerve with side of lesion
Age of patient with duration of injury
Etiology
Level of injury
Complete /incomplete
Recovering / not recovering
Type of nerve injury
Associated bony and soft tissue injury
Complications

8. What is Hilton’s law?

A joint is supplied by the same nerves which supply the muscles crossing the joint and
the skin over the joint. In joint disease, therefore, the irritation of the nerves causes a reflex
spasm of the muscles which fixes the joint in the position of maximum comfort and may cause
pain referred to the overlying skin.

9. What are the boundaries of Guyon’s canal?

Floor – transverse carpal ligament
Roof - pisohamate ligament
Wall - proximally by pisiform, distally by hook of hamate
 27. EXAMINATION OF NEUROMUSCULAR DISORDERS

History
UMN Cortical Lesions:
H/o seizures, auditory or visual abnormality.
Whether the child is mentally retarded.
H/o any basal ganglia lesions
H/o jaundice (neonatal Jaundice causes basal ganglia lesions)
H/o Incoordination
H/o Bulbar involvement: Change of voice, dysphagia.
Spinal Cord Involvement:
Extramedullary: More radicular pain
March of paralysis
Intramedullary: More dense lesions
Bladder Involvement.
b/l symmetric involvement of lower limb
Dissociative anaesthesia: loss of spinothalamic sensation with preservation of the dorsal
column sensation. There will also be loss of motor power and reflexes with upgoing plantar.
Enquire about the order of paralysis

Anterior Horn Cells:

Demyelinating Disorders:
Guillian Barre: Postinfectious disorder with sudden onset of weakness, with NO sensory
involement.
Transverse Myelitis: Myelopathy with variable spectrum of involvement of the motor and
sensory systems.to functional transecttion of the spinal cord.
Degenerative Disorders:
Motor Neuron Disease (in Children Spinal Muscular atrophy and Madras Motor neuropathy.
Thus history wise enquire about post infectious palsy, sensory involvement and bulbar
involvement.
Peripheral Nerve involvement:
History of Diabetes, uraemia
Lead toxicity, Vit B12 Def.
C/C Liver d/s, Malabsorption
Antimalignancy drug intake
Isoniazid intake
Phenytoin intake
Neuralgic amyotrophy
Charcot Marie Tooth d/s
Amylodosis
Friedrich’s Ataxia
NeuroMuscular Junction Involvement:
Myaesthenia gravis
Use of pencillamine
Paraneoplastic disorders (Lambert Eaton)
History of diplopia, ptosis in the evening, weakness on repeated activity, which is relieved by
rest
Muscular Dystrophy:
These children will usually be normal at birth, but later at around 3-5 years, they develop
weakness of walking, hopping etc. eg Duchene

General Examination (specific to neuromuscular disorders)

Squinting with visual field abnormalities
Micro-ophthalmos with inc. size of head (hydrocephalus)
Down’s syndrome, Trisomies, Chromosomal anomalies
Ptosis
Nerve thickening
Speech
Nystagmus

28. CEREBRAL PALSY

Q&A

Cerebral palsy was first described by English surgeon William John LIttle in 1862. It was then
known as Little's Disease for decades. The term was originated by Freud.

Q1. Define cerebral palsy?

A. Cerebral palsy is the term used for a group of nonprogressive disorders of movement and
posture caused by abnormal development of, or damage to, motor control centers of the brain.
In the cerebral palsy following must be true:
Is the result of brain lesion, there for the spinal cord and the muscles are structurally and
biochemically normal
The brain lesion must be fix and non progressive
The abnormality of the brain result in motor impairment

Q2. What is the aetiology of cerebral palsy?

A. It will be divided in to three time periods
Prenatal
TORCHES groups of infection
Fetal exposure to drugs and alcohol
Congenital malformation of brain
Rh incompatibility
Maternal health problems like renal failure or infection
Perinatal
Anoxia as a result of perinatal complications like, tight nuchal cord (umbilical
cord around the baby's neck) and prolapsed cord (cord delivered before the baby) placental
abruption and placenta previa .
Severe congenital heart disease
Premature delivery
Sepsis in neonatal period
Postnatal
Infection such as meningitis in early child hood
Any episodes of hypoxia such as cardiopulmonary arrest, near drowning and
suffocation
Trauma producing head injury
Q3. Classify cerebral palsy?
A. Two ways
Physiological which describe the type of movement disorder present
Spastic type – Clasped knife tone (the most common type)
Hypotonia type
Dystonia type- Lead pipe tone
Athetosis type- abnormal writhing movement
Ataxic type- cerebellar lesion
Geographic which describe the part of the body is affected
Hemiplegic CP
Diplegic CP
Triplegic CP
Quadreplegic CP

Q4. What are the histopathological findings of the brain in CP children?

A. Periventricular leukomalasia
Intraventricular and periventricular hemorrhage

Q5. Can severity of spasticity be measured?

A. There is no clear best test. Modified Ashworth Scale is the most widely used method for
the clinical assessment.

Grade Description Q6.

0 No increase in muscle tone Ho

w
Slight increase in muscle tone, manifested by a catch and release, or by do
1 minimal resistance at the end of the range of motion when the affected part(s) you
is moved in flexion or extension eval
Slight increase in muscle tone, manifested by a catch, followed by minimal uat
2 resistance throughout the remainder (less than half) of the range of movement e a
(ROM) CP
chil
More marked increase in muscle tone through most of ROM, but affected d?
3
part(s) easily moved A.
4 Considerable increase in muscle tone, passive movement difficult
A
5 Affected part(s) rigid in flexion and extension det
aile
d complete History
Documentation of motor milestone
Ask about any preferential use of one hand or leg
Physical examination:
Tone,
Deep tendon reflexes,
Infantile reflexes persisting
Balance, sitting and gait
 Other assessment includes imaging rarely

Q7. How can you predict the prognosis for ambulation?

A. Molnar and Gordens primary criteria for walking is the ability to sit by the age of 2 years
Bleck proposed that persistant of two or more infantile reflexes beyond 12 to 15 months
implies a poor prognosis.
Presence or absence of mental retardation does not affect the ability to walk
If a child nonambulatiry by 7 years, the child will probably never become ambulatory

Q8. What is the prognosis for hand function?

A. If there is no early dominance offhand use and if the hands are not crossing the midline
the prognosis is poor

Q9. What are the non surgical treatments of cerebral palsy?

A. Physical therapy – Often the first treatment offered to CP
Casting- Inhibitive casting has waxed and waned in popularity
Orthosis- Helpful in improving the gait (AFO)

Q10. Mention the indications for bracing?

A. Dynamic equines, to obtain a plantigrade foot position and reduce genu recurvatum
In foot drop to support the foot in swing phase
Post operatively, while weakness is being addressed through physical therapy
When mild crouch- can be improved with AFO

Q11. Describe the medical treatments of cerebral palsy?

A. Oral medications to reduce the tone (Valium and Baclofen)
Intrathecal Baclofen – The inability to adequately reduce the tone with oral medications
Botulinum toxin- become a popular form of treatment.Muscle that produce dynamic
deformities in absence of fixed contracture are the site of injection.

Q12. Mention the common indications for Botulinum toxin injection?

A. In a child with a dynamic equines deformity in absence of fixed plantar flexion
contracture
In a child with equines gait without multilevel crouch
In a child less than 4 years old who cannot tolerate AFO orthosis because of dynamic
equines
If parents refuses surgery and desires injections

Q13. What are the general considerations for Surgery?

A. Speak clearly and frankly to the family about the goals of surgery and the expected
postoperative course
Weakness is a frequent short term sequela of lower extremity surgery in cerebral palsy
Better to follow Single Event Multi- Level Surgery or SEMLS
Better to perform the surgeries when the child began to walk
Aneasthetic concern- Cerebral palsy patients experiences latex allergy frequently. Hence
to better do the allergy testing for latex products.

Q14. What is the role of surgery to prevent hip subluxation in CP?

A. Hip subluxation or dislocation is exclusively seen in non walking patients.
 Surgery can prevent the dislocation if done early preferably before 4 years (Iliopsoas
tenotomy and adductor myotomy)
If the child has a flexion or adduction deformity, the Reimers migration index can be
measured on a neutral rotation hip X-ray to make the diagnosis of subluxation.In children with
established subluxation a subtrochanteric derotation osteotomy to correct the excessive
anteversion with or without a pelvic osteotomy.

Q15. What is the surgery for scissoring gait?

A. Scissoring gait could be due to adductor spasticity which can be
treated with adductor longus myotomy. Obturator neurectomy in
ambulatory patients should be avoided because it also innervates the
adductor brevis which is a major hip stabilizer in stance phase of gait.
Scissoring gait can also be due to the spasm of the medial hamstrings, where the
fractional release would be indicated.

Q16. What is the surgery for the flexed knee gait?

A. Fractional lengthening of medial hamstrings should be tried first and assess the popliteal
angle on the table. Aim of the surgery is to achieve atleast 30 degrees of popliteal angle.
If the angle is more than 30 degrees the biceps apneurosis fractional lengthening should
be tried

Q17. What are the current operations for the valgus foot in skeletally immature child?
A. Mosca procedure ( open wedge interfacet calcaneal osteotomy)
Grice green procedure (Sub talar extra articular arthrodesis)

Q18. How do you decide to do gastrocnemius recession or tendo achillis lengthening in

equines foot?
A. Assessment with Silverskioled test.
If the equines persist in knee flexion and extension- TA lengthening
If equines get corrected from knee extension to flexion – Gastrocnemius recession alone

Q19. Mention the techniques of gastrocnemius recession?

A. Strayer - Aponeurosis of the gastrocnemius is cut intransverse fashion
Baker- Aponeurosis of the gastrocnemius is cut in tongue in groove
Volpius- Aponeurosis of the gastrocnemius is devided in a chevron fashion

Q20. What is the role of hand surgery in CP?

A. Only in spastic CP. While the results can look good but function is compromised by the
common lack of steriognosis in the child with hemiplegia.

Q21. When should the surgery of Lower limb be done?

A. Generally surgery is done in spastic diplegia and hemiplegia once the gait pattern is
established and child is walking. It is usually between 5 to 7 years.

Q22. What are the indications for the triple arthrodesis?

A. Fixed varus or valgus deformity in a skeletaly mature patient

Q23. What is the most common type of hand deformity and how can it be corrected?
A. Thumb in palm deformity.
 Correction entails the release of adductor pollisis at its insertion, release of first dorsal
interosseous muscles, fixation or fusion of the hypermobile MCP jointand rerouting of the EPL
tendon

Q24. How and when should scoliosis be treated in CP?

A. Scoliosis is common in non walking patients. Orthosis is not at all useful in the correction
or prevention of the progression of the curve. Correction should be in the early adolescent period
when there is not much potential for additional major growth of the spine.
When the curve is 40 degrees or more and approximately 50% passively correctable
fusion with instrumentation is the choice.
If the Curve resists passive preoperative correction, anterior disc excision and fusion
without interval fixation is required.

Q25. What is Single Event Multi-Level Surgery?

A. Single Event Multi- Level Surgery or SEMLS is when a number of orthopaedic
procedures are performed at one time. This means children only need one anaesthetic followed
by one block of rehabilitation therapy. Orthopaedic surgery means surgery to either bones and/or
muscles. Multi-level means the surgeries performed usually occur around the hip, knee and ankle
joints

29.Clinical Examination of Lower Limb Deformity

When a child is born, it has 10-15 degrees of physiological genu varum, 5 degree internal
tibial torsion and external rotation contracture of the hip. It reaches the maximum by about 9-
12 months. This usually gets corrected to neutral by the age of 18-24 months then the limb
develops a valgus angulation, which reaches the maximum of about 12 degrees by the age of
3-4 years. This physiologic valgus usually gets corrected to the adult value of 7 degrees of
valgus by the age of 8 years. Physiologic valgus is bilateral and symmetrical; less than 15
degrees and the inter-malleolar distance doesn’t exceed 8 centimetres

Tibial torsion is the angle between the transverse axis of the knee and the transmalleolar axis.
The tibia is internally rotated at birth. Internal tibial torsion is 5 degrees at birth and gets
corrected to neutral by 4-5 years of age. The tibia then gradually becomes externally rotated and
reach the adult value of 20-25 degrees of external rotation by the age of 8 years.

Femoral anteversion is the angle between the transcondylar axis and the longitudinal axis of
the femoral neck in the horizontal plane. Femoral anteversion is 40 degrees at birth and
reaches the adult value of less than 15 degrees by the age of 8 years. It produces intoeing gait
which gradually increases during the first five years of life due to summation of deformities.
It gets corrected by 8 years of age

Deformity is defined as a deviation from normal structure or function which may be

symptomatic or has the potential to produce symptoms
Goals of deformity assessment

The goal of deformity assessment is to answer the following questions.

1. Is there a deformity?

One should be able to differentiate between physiological and pathologic malalignment.

2. What is the deformity?

Identify the name of the deformity.

3. Where is the deformity?

Identify the site of deformity whether it is at the joint level or in the bone. If in the bone, then it
is in the epiphysis, metaphysis or diaphysis. Deformities due to tilting of the joint line becomes
less when the joint is flexed. This is because the area of contact between the articular surfaces is
altered during flexion.

4. Which is the plane of deformity?

Identify the alteration produced by the deformity in all three planes and any associated limb
length discrepancy as well. Thus a deformity may have a component of flexion or extension in
the sagittal plane, varus or valgus in the coronal plane, internal or external rotation in the axial
plane; in addition there may be shortening or lengthening as well.

5. How severe is the deformity?

Identify the severity of deformity in each plane and also the severity of limb length discrepancy.
Assess how much of passive correction of the deformity is possible.

6. Why there is a deformity?

Identify the cause of deformity. Identify whether it is a localised problem or part of a systemic
disease. Try to detect whether it is due to soft tissue contracture, muscle paralysis or spasm or
rupture, joint dislocation or subluxation or malformation and lastly bony malunion or nonunion
or deformation.

7. Are there any consequences of the deformity?

Identify whether there are any compensatory malposition of neighbouring joints and secondary
effects such as osteoarthritis on the concave side or laxity of ligaments on the convex side.
Assess whether it is associated with any secondary joint instability such as patellofemoral
instability in genu valgum. Identify how it is affecting the gait or joint function.

8. When does the deformity occur?

Identify whether it is a static or dynamic deformity.

History

From the history try to understand the relevant details about the deformity, look hints that help
identify the cause and understand the secondary effects of the deformity and its impact on
function. History should start with the following questions.
• How long the deformity is present?
• How did it start?
• How is it progressing?
• Any associated symptoms?
• Is there any history of trauma or infection?
In children get perinatal history
• Did the mother take any drugs during pregnancy especially in the first trimester?
• Did the mother have any infections especially in the first trimester?
• Did the mother have any history of substance abuse?
• Is there any maternal health problems?
• Did prenatal ultrasounds show any abnormality?
• Was there any abnormality in previous pregnancies?
Get a natal history in appropriate case.
• Was it a full term delivery?
• What was the type of delivery?
• What was the type of presentation at birth?
• What was the birth weight?
• Was there any delay in first cry?
• Were there any complications during delivery?
Get details of nutrition to assess the chance of nutritional deficiencies like rickets.
• Vegetarian or non-vegetarian
• Calorie intake
• Food fads
• Exposure to sunlight
• Whether diet is balanced or not
Family history
• H/o similar or other deformities

Developmental history
• When did social smile appear?
• When did the child achieve
• Neck steadiness
• Sitting
• Standing
• Crawling
• Walking
• Stair climbing and descending
• Hand to hand transfer

General Examination

In general examination look for features of generalised ligamentous laxity, general

manifestations of rickets or known dysplasias.

Inspection

Inspect the patient in standing, sitting, walking and in the supine position. Inspect from the front,
back and both sides. Look for any asymmetry in size, shape and function.
Look at
• Head tilt and rotation
• Level of shoulders, scapula and iliac crests
• Look for spinal deformity such as scoliosis or kyphosis
• Look for lumbar lordosis suggestive of flexion deformity of hip when the patient is supine on a
hard surface
• Look for knee deformity in all three planes
• Look for ankle equinus or calcaneus deformity from the side
• Look for any hindfoot varus or valgus from the back
• Look for any forefoot or toe deformity

Palpation

Palpate the bone, soft tissues and joint. Look for change in temperature; limb with post-polio
residual contracture is cold. Look for any tenderness and note the site of tenderness. When
palpating bony and soft tissues; look for any asymmetry, thickening, swelling or defect.

Movements

Assess the active and passive movements of spine, hip, knee and the foot and ankle. Record the
range of movement. Look for restriction of range of movement, pain during joint movement,
ligamentous laxity, joint instability and any abnormal sounds during joint movement. While
moving the joint passively, watch out for muscle spasm. Movement should be assessed in all
three planes depending on the normal movement for that particular joint.

Measurements

Measurement is done to detect any limb length discrepancy, to assess degree of muscle wasting.
Limb length discrepancy may be true or functional. True LLD is due to real shortening or
lengthening. Functional LLD is due to abnormal joint positioning such as adduction contracture
of hip. Girth of the thigh is measured 15 cm above the knee joint line and girth of the calf is
measured at the bulkiest area.

In addition measure intercondylar distance between medial femoral condyles in the standing
position for genu varum. In cases of genu valgum measure the intermalleolar distance in the
standing position.

Torsional profile of the lower limb

Torsional abnormalities may be in the femur, tibia or foot. Torsional abnormalities lead to either
in-toeing or out-toeing. Intoeing is more common. Commonest cause of intoeing in children
below one year is metatarsus adductus, commonest cause from 1-3 years is internal tibial torsion;
and after 3 years of age excessive femoral anteversion is the commonest cause. It is identified by
assessment of foot progression angle. Foot progression angle is the angular difference between
the direction of walking and the long axis of the foot. If the foot is externally rotated then the
angle is positive and if internally rotated then the angle is negative. Normal value for children
and adolescents is 10 degrees.
Femoral anteversion is assessed by doing the Craig’s test. It is done in the following method.

Patient position – Prone

Joint position – Knee flexed to 90 degrees.
Procedure- One hand of the examiner is placed flat on the greater trochanter. Hold the leg and
gently rotate the hip in both directions till the greater trochanter is maximally prominent. The
amount of internal rotation needed to make the greater trochanter maximally prominent is the
degree of anteversion.

In addition the range of rotational movement of the hip is also recorded. The patient is made
prone and the pelvis is made level. Then rotate the hip internally and externally to the
maximum

point to which it is maintained by gravity alone. In patients with excessive femoral anteversion,
the range of internal rotation is increased and external rotation is diminished. In femoral
retroversion, the external rotation is increased and internal rotation diminished.

Tibial torsion is assessed by the thigh foot angle or angle of the transmalleolar axis.

Thigh foot angle is assessed by the following method.

Patient position – Prone

Joint position – Knee flexed to 90 degrees, ankle in neutral position.
Procedure – Measure the angle between the thigh axis and the foot axis. Angle is negative if
internally rotated and positive if externally rotated. Normally the angle is 10 degrees in adults. In
the newborn, there is 5 degrees internal tibial torsion normally.

If the foot is not normal, then measure the angle of the transmalleolar axis.

Patient position – The patient is asked lie prone on a couch with the knee flexed to 90 degrees.
Procedure – The centre of each malleoli are marked. Connect these points by a line across the
plantar surface of the sole. Draw a line perpendicular to it.
Interpretation – The angle between the thigh axis and a line perpendicular to the transmalleolar
axis is measured, which is equal to the tibial torsion.

Torsional deformity of the foot is assessed by heel bisector line. Heel bisector line divides the
heel into two equal halves in the longitudinal axis. In the normal foot it passes through the
second toe. If it passes medial to the second toe, forefoot is abducted and if it passes lateral to the
second toe, the forefoot is adducted. If it passes through the third metatarsal, adduction deformity
is mild, through fourth metatarsal is considered moderate and through fifth metatarsal is
considered to be severe metatarsus adductus.

In newborn feet, V- finger test is done to assess the forefoot adduction. The heel of the child is
placed in the second interdigital cleft of the examiner. Normally the lateral border of foot is
straight and will be in contact with the examiners finger. If the lateral border of the foot beyond
the fifth metatarsal base is not in contact with the examiner’s finger due to medial deviation, then
there is metatarsus adductus deformity.

Angular profile of the lower limb

Angular deformities may be physiological or pathological. It is more likely to be pathological if
it is unilateral; asymmetrical; painful or if progressive.

Ask the patient to stand with his feet and knee touching each other while the patella is facing
forwards. When inspected from the front, there will be a gap between the knees in patients with
genu varum. In patients with genu valgum, the ankles will be kept apart. Inspect from the side,
specifically looking for equinus or calcaneus deformity of ankle, flexion deformity or
hyperextension deformity of knee.

Ask the patient to lie supine on a hard couch and look for any lumbar lordosis suggestive of
fixed flexion contracture of hip. If present do the Thomas test to assess the severity of flexion
deformity.

Thomas well leg raising test

Patient position- Supine

Examiner position – Stand on the right side of the patient with one hand under the lumbar spine
of the patient. With the other hand hold the unaffected side.
Procedure- Flex the unaffected knee fully, then flex the unaffected hip till the excessive lumbar
lordosis disappears. Measure the angle between the thigh of the affected side and the couch to
assess the angle of fixed flexion deformity of the hip.

Intercondylar distance is measured to assess the severity of genu varum deformity. Ask the
patient to stand with his medial malleoli touching each other and then measure the distance
between the medial femoral condyles. Intermalleolar distance is measured in patients with genu
valgum deformity. Ask the patient to stand with his medial femoral condyles touching each other
and the foot should be in neutral rotation, measure the distance between the medial malleoli.
Both these measurements have the disadvantage of being influenced by the size of the patient. In
this situation, measurement of the tibiofemoral angle using a goniometer is essential. This is
measured in the standing position. Lateral thigh leg angle is measured by keeping the arms of the
goniometer on the lateral surface of thigh and leg and the hinge of the goniometer at the level of
knee. Other method is by keeping the arms of goniometer on the anterior surface of the thigh and
leg and the hinge of goniometer over the centre of patella.

In patients with genu valgum one should do the Ober’s test to rule out ITB contracture and assess
the patient for patellofemoral instability. Measure the standing height, sitting height and arm
span of the patient.

Assessment of lower limb length discrepancy

Limb length discrepancy(LLD) may be true or functional. True limb length discrepancy is due to
shortening or lengthening of bone or joint dislocation. Functional LLD is due to abnormal joint
positioning such as pelvic obliquity due to adduction contracture or flexion deformity of knee.

LLD may be due to abnormal pelvic height, femoral length, tibial length or foot height. LLD
may lead to abnormal gait, cosmetic problem, osteoarthritis due to abnormal weight transmission
or low backache. LLD up to 2 cm at skeletal maturity is considered physiological as only about
25-30% of normal population have equal limb length. Left lower limb is longer than the right in
a ratio of 3.5:1.
When the patient is standing; assess whether the shoulder, iliac crest and the popliteal and the
gluteal creases are at the same level. Look for compensatory scoliosis, which will disappear if
the patient is made to sit. LLD may be masked by flexion of opposite knee and plantar flexion of
ankle.

LLD is best measured using blocks of known height under the foot of the affected side; till the
pelvis is level and the compensatory lordosis disappears. Lower limb length measurement
includes measurement of the whole lower limb and measurement of length of individual limb
segments. Whole length measurement is done either by placing blocks of known thickness under
the shorter limb till the pelvis is level or by measuring using a measuring tape.

With measuring tape; measure both the true length and apparent length. Apparent length is
measured from the xiphisternum or umbilicus to the inferior tip of the medial malleolus when the
limbs are kept parallel. To measure the true length, both the limbs should be kept in an identical
position. Hence if there is a fixed adduction deformity of hip; first make the pelvis level by
adducting the affected hip till both the anterior superior iliac spines (ASIS) are at the same level.
Measure the true length if the affected limb from the inferior edge of ASIS to the inferior edge of
medial malleolus. Now keep the opposite hip also in an identical degree of adduction and then
measure the other side as well.

The lower limb has 4 segments; supratrochanteric (pelvic), infratrochanteric (femur), tibial and
foot segments. Infratrochanteric segment is measured from the tip of greater trochanter to the
lateral joint line of knee. Tibial segment is measured from the medial joint line of knee to the tip
of medial malleolus.

Supratrochanteric segment is measured by drawing the Bryant’s triangle, Nelaton’s line or

Shoemaker’s line. Bryant’s triangle is drawn by drawing three lines in the supine position. First
line from the inferior edge ASIS vertically down towards the examination table. Second line is
drawn from the ASIS to the tip of greater trochanter. Third line is from tip of trochanter to the
first line. Measure each sides of the triangle and compare with the other lower limb. Difference
in the length of third line suggests supratrochanteric shortening. Supratrochanteric shortening
may be due to hip arthritis, hip dislocation, fracture neck of femur or coxa vara.

Galeazzi test or Allis test

Patient is supine on the table. Flex both the hip and knees and place both the feet together. Note
the level of knee. In case of LLD the levels will be different. Now look from the side. If the
shortening is in the femoral segment; the level of knee will be proximal to the other knee and if
shortening is in the tibial segment, knee will be distal to other knee.

Cover-up test

Done between the ages of 1-3 years. The child is either standing or lying supine. The part of tibia
distal to the proximal third is covered by a hand and observe the angular relationship between the
thigh and proximal tibia. If in neutral or valgus, no need to observe for tibia vara. If in varus then
observe to rule out tibia vara.
Suggested reading

1. Pauwels F. Biomechanics of the locomotor apparatus. New York: Springer Verlag, 1980.
2. Chao EYS, Neluheni EVD, Hsu RWW, Paley D. Biomechanics of malalignment. Orth
Clin N.A. 25: 379-386, 1994.
3. Moreland JR, Bassett LW, Hanker GJ. Radiographic analysis of the axial alignment of the
lower extremity. J. Bone Joint Surg, 69A: 745-749, 1987.
4. Andriacchi TP. Dynamics of knee malalignment. Orth Clin N.A., 25: 395 406, 1984.
5. Paley D, Tetsworth K. Malalignment and realignment of the lower extremity. Orth Clin N.
A., 25:355-367, 1994.
6. Paley D,Herzenberg JE,Tetsworth K et al. Deformity planning for frontal and sagittal
plane corrective osteotomies. Orthop Clin North Am. 1994;25:425-465
7. Salenius P, Vankka E. The development of the tibiofemoral angle in children. J Bone Joint
Surg Am 1975;57:259-61
8. Bruce RW Jr. Torsional and angular deformities. Pediatric Clinics of North America
1996:43:867-81.
9. Staheli LT, Corbett M, Wyss G, King H. Lower extremity rotational problems in children.
Normal values to guide management. J Bone Joint Surg Am 1985;67:39-47

30. EXAMINATION OF A KNEE DEFORMITY

History:
Trauma
Renal diseases (failure to thrive, acidotic breathing)
Family history
Infection
GIT diseases - oily stools, failure to thrive, diffuse abdominal pains)
Muscle weakness: esp proximal muscle weakness:
Tumors
Nutritional disease
General Examination: To r/o Dysplasias
Examination:
Intermalleolar /Intercondylar Distance: on standing and sitting
Thigh leg angle
Anteversion of hip
Thigh –foot angle
Transmalleolar axis
Knee flexion to find the component of the varum / valgum
Q angle:
ITB contracture;
Fibular Hemimelia/ Tibial Hememelia:
Metatarsus varus:
Calcaneo Valgus,
Equinus:
Examination of foot and ankle:
Examination of hip: to r/o coxa vara.
Intermalleolar dist: Normal : 2.5 cm.
Mild : 2.5 – 5 cm.
Moderate : 5 –10 cm.
Severe : >10 cm.

31. GENU VARUS AND VALGUS DEFORMITY

Q1. What are the angular deformities of knee?

A. Genu varum, Genu valgus, Genu recurvatum and procurvatum of knee

Q2. How do you define genu varus /valgus?

A. These are angular deformities in coronal plane of lower limb. In a normal person standing
with heels/knees touching each other ,ASIS centre of patella –centre of malleoli-second toe /web
are in a straight line, deviation of this line to inside of knee is varus at knee and vice versa

Q3. What are the causes of Genu varum?

A. a) Unilateral causes
Growth abnormalities of upper tibial epiphysis, trauma, infections, tumor
b) Bilateral causes
Physiological (get corrected by 4 years)
Pathological:-
congenital,postural,developmental,metabolic(rickets),endocrine,degenerative(MCOA)idi
opathic, blount’s disease(tibia vara), pagets disease

Q4. What are the causes of Genu valgus?

A. a) Unilateral causes
Trauma, infection, tumors
b) Bilateral causes
Physiological
Pathological;-congenital,idiopathic( most common), developmental(epiphysial
dysplasia, endocrine disorders(thyroid disorders),metabolic disorders (rickets),traumatic,
paralytic, infective, degenerative, inflammatory disorders(rheumatoid arthritis)

Q5. What is genu valgum complex?

A. Primary and secondary deformities together are called genu valgum complex. Primary
deformity is a medial angulation of the knee. Secondary deformities are external rotation
deformity of distal end of femur and tibia because of pull of tensor fascia lata and biceps,
internal rotation of tibia, lateral subluxation of patella, shortening of lateral structures and
elongation of medial structures.

Q6. What are the components of genu varum complex?

A. Internal torsion of the distal tibia, in toeing of both feet, tight medial structures and lax
Lateral structures, patella face outward while walking.

Q7. What is apparent genu varum?

A. Due to anteversion of the femoral neck, there is medial rotation of the femur and the child
looks bow-legged

Q8. What is physiological malalignment?

A. Child is born with genu varum which is due to persistence of tight posterior capsule of
hip (external rotation) and internal tibial torsion.This over corrects to physiologic valgus by 24-
36 months of ambulation .Valgus should correct to adult levels by 7 years of age.So varus should
be pathological after 2-3 years of age and valgus after 11 years of age (> 2SD of normal
physiologic alignment)

Q9. What is idiopathic genu valgum?

A. It is the commonest variety of valgus deformity occurs at the age of 2-3 years and
recovers by the age of 6 years. It is seen invariably bilateral.

Q10. How will you asses a valgus and varus deformity?

A. History: - Nutritional deficiency, renal diseases, muscle weakness, gastrointestinal
problems, family history, trauma, infection
Examinations: Stature, upper segment lower segment ratio, facies , teeth, metaphyseal
thickening, hand, nails, features of rickets, proximal muscle weakness
a. inter malleolar distance is measured in genu valgus deformity to assess the severity
of deformity. The acceptable normal limit is 8 to 10 cm. In valgus deformity it will be more than
10 cm.
b. intercondylar distance is measured in varus deformity . If it is more than 3 cm and it
is unilateral it should be investigated
c. plumb line test - Draw a line from ASIS through the centre of the patella to medial
malleolus, normally all the structures are in the same line but in varus deformity medial
malleolus is medial to this line and in valgus it will be in opposite way.
d.Knee flexion test - This is to find if the deformity is arising from femur or tibia. If the
deformity disappears with flexion of the knee, the cause lies in the femur and if it persists on
flexion the cause lies in the upper end of tibia. This is because anterior part of the articulating
surface of the femur articulates with the tibia in extension whereas on flexion the posterior part
articulate which is not involved usually. This is not true always
e. Lateral tibiofemoral angle
f. Q angle- Q angle represents the mean vector angle of quadriceps pull on patella. It
represents the dynamic instability of patella –the greater it is the more unstable patella will be. It
is clinically measured by intersection of the line formed between center of patella and ASIS and
that between patellar center and tibial tuberosity (in standing position).
Prerequisite - patella should be centered in trochlea otherwise in an already dislocated patella
angle will be falsely reduced.
g. Patellar stability
h. Tibial torsion
i. Flat foot

Q11. What is j sign?

A. Denotes one of the forms of abnormal dynamic patellar tracking ( maltracking). Normally
patella glides in a straight line with minimal sideways shift at the end of extension in trochlear
groove, however, due to various reasons patella may have excessive lateral shift at the end
describing an inverted J trajectory. Dynamic patellar tracking is judged in sitting position while
patient extends knee from 90 degree flexion to full extension .Active patellar tracking is checked
in full extension asking the patient to contract quadriceps and observing patellar shift which
should be more superior than lateral.

Q12. What are the investigations you will do?

A. Full length X ray of both limbs - AP and Lateral view. Stress X rays - varus and valgus
stress views.
Laboratory tests - Serum and urinary calcium , phosphate, alkaline phosphatase.

Q13. What are the precautions you have to take while taking X ray?
A. Both patellae should face forward.
B. If there is any LLD that has to be corrected by keeping wooden block under the short
limb so that both ASIS should be at the same level. Hip, knee and ankle should be
visible in a single film.

Q14. How will you take full length X ray?

First you keep the patient in position. The
radiograph tube is 10 feet away from the film.
The cassette should be of 51 inch
(magnification is 4 – 5 %).For children 3 feet
film is enough. If single film is not available 3
cassettes can be stacked.

Q15. What is the difference between full length x ray and scanogram?
A. In scanogram standard size of film is used with 3 separate exposures of the hip, knee &
ankle in recumbent position. Beam is centre on joint with a radio-opaque ruler.
Full length x ray is taken in weight bearing, so that you will get real deformity and you
can draw the mechanical axis and further planning.

Q16. What is the normal alignment of a limb?

A. Normally if you draw the mechanical axis line in the femur and tibia the angle formed is
2 degree varus. Whereas if you draw anatomical axis the
angle formed is 7 degree valgus. Any deviation from this
value will produce undue force on the respective side of
the joints.

Q17. What is MAD?

A. If you draw a mechanical axis of the whole limb it
will pass 8 mm medial to the centre of the knee
joint.MAD is described as either medial or lateral i.e.
varus or valgus mal alignment. Our final aim in deformity
correction is to get a normal MAD.

Q18. What would you do to confirm the location of disease?

A. Draw CORA after taking the full length X ray. Then measure CORA (center of rotation
of angulation).This reveals site of deformity, magnitude of the deformity and planning for
osteotomy.

Q19. What is the normal change of the angle during development of the limb?
A. 6-12 months - moderate genu varum
18 – 24 months – leg straight
4 years – pjysiological genu valgus
6 years – leg straight

Q20. What are volkman law and wolf law?

A. Hueter volkman law-Pressure inhibit growth and decreased pressure accelerate the
growth of the physis
Wolf law- every change in the form and function of the bones or function alone is
followed by certain definite changes in the external configurations in accordance with
mathematical laws.

Q21. What is miserable malalignment syndrome?

A. A combination of malalignments of the leg that include excess femoral anteversion with
internal rotation of the hip, genu valgus, squinting patellae, external tibial torsion, and flat feet.
Athletes with miserable malalignment syndrome are predisposed to overuse injuries and are
often advised not to take part in certain sports, for example, long distance running.

Q22. What are the x ray findings in Physiological genu varum?

A. Tibia angulated medially at the junction of proximal and middle third, femur angulated in
the distal third, medial cortex of tibia and femur thickened and sclerosed , epiphysis,physis and
metaphysis have normal appearance, symmetrical involvement, Metaphyseo diaphyseal angle <
11 degrees

Q23. What are the findings in Blount’s disease?

A. Growth defect in the proximal medial tibial epiphysis
Infantile <3 year
Juvenile 3 – 10 years
Adolescent > 10 years
 Obese children, often assymetrical, progressive varus deformity, lateral thrust on
standing, Siffert Katz sign
RADIOGRAPHIC FEATURES
Varus angulation at epiphseo metaphyseal junction, Widened and irregular
physeal line medially, Medially sloping and irregularly ossified epiphysis, Prominent beaking of
medial metaphysis , Lateral subluxation of proximal tibia. Normal knee radiograph in a toddler
does not exclude Blount’s

Q24. What are the angles in the tibia vara?

A. Tibiofemoral angle, Metaphyseo diaphyseal angle, Epiphyseo metaphyseal angle

Q25. Difference between the physiological varus and tibia vara?

Physiological genu varum Blounts disease
Invovement Symmetrical Often assymetrical
Site of angulation prox &middle third Proximal metphysis
Femur Bowed medially Normal except late
Lateral thrust Absent Often present
Meta Dia angle < 11 Greater than 11
Upper tib Metaphysis Normal Irregular rarifaction
Upper tib Epiphysis Normal Sloping
Upper tib Physis Normal Narrowed medially
Lateral Tib Cortex Gentle curve Straight
Med Tib Cortex Gentle curve Sharp angulation

Q26. What are components of Rotational Profile (Staheli)?

A. This is to find the tibial torsion
1. Foot progression angle
Normal average + 10-15 degrees .Compensatory tibial torsion may make FPA
normal even with excessive femoral torsion
2. Medial hip rotation in extension
3. Lateral hip rotation in extension
Medial 40 –60 - 50 more in females
Lateral 25- 65 - 45 equal in both sexes
4. Thigh foot angle
Patient prone, Knee flexed 90 degrees, Ankle neutral, Angle between the long
axis of foot and long axis of the thigh. This is for assessment of tibial torsion. Normal is +10
degree
5. Angle of the trans malleolar axis
Patient prone, Knee flexed 90 degrees, Ankle neutral, Line joining the center
point of medial and lateral malleolus are marked on sole of foot. Draw Perpendicular to trans
malleolar axis and Thigh axis line. Mean is +15 degree
6. Configuration of the foot

Q27. What are the features of femoral torsion?

A. Clinical features:- In toeing gait,exaggerated IR in extension of the hip, limitation of ER,
ER of hip increased in 90 degree flexion of the hip . Adaptive changes are hind foot valgus and
external tibial torsion

Q28. How will you assess the femoral torsion?

A. Ryder method
Patient is prone,GT palpated, leg is laterally rotated till GT is most prominent. The
degree of rotation from neutral is the degree of anteversion.

Q29. What are the effects of lower limb deformity?

A. Altered joint orientation and joint alignment. Consequences on: Gait, weight bearing
loads, energy expenditure

Q30. What are the indications for deformity correction in a symptomatic patient?
A. Pain & inflammation in joints, restriction of motion, gait dysfunction or alteration and
aesthetic & psychosocial

Q31. What are the indications for deformity correction in a non symptomatic patient?
A. Femoral mechanical valgus > 5 deg, Tibial mechanical varus > 5 deg, MAD > 15 deg,
XRay evidence of degenerative joint disease and clinical signs (trendelenburg, lateral thrust)
Q32. What are the treatment methods available for these deformities?
A. Conservative method is bracing. Surgeries includes epiphysiodesis, 8 plate application,
osteotomy and fixation by internal plates or by external by iliizarov

Q33. What do you mean by guided growth?

A. These are some internal fixation systems which guides growth while allowing natural,
safe and gradual correction of limb alignment. 8 plates is one of the implant which has got so
many advantages in deformity management in children without doing any major surgery.

Q34. What is the difference between hemiepiphysiodesis and hemiepiphyseal stapling?

A. Hemiepiphysiodesis is a permanent method whereas other is a temporary measure for the
deformity correction.

Q35. What are the different types of osteotomies?

A. Open wedge, closed wedge and dome osteotomy.

a)focal dome b) Maquet osteotomy

Q36. What are the concepts in deformity management?

A. Braces have no role in the management now a days. Braces work on the concept of three
point fixation with knee locked in extension. It is very un physiological situation to the patient
Current concept is do intervention early so that you can prevent the secondary deformity
formation. If the patient is child you can do the guided growth systems like the 8 plate. Whereas
in adults you can do corrective osteotomy . The correction should be done at the CORA whether
it is femur or tibia. Better option in deformity correction is Ilizarov Hexapod systems with which
you can do correction more precisely.
 32. EXAMINATION OF THE ANKLE AND FOOT

History
Rule out symptoms s/o peroneal tenosynovitis / Peroneal subluxation/
Peroneal impingement. (in malunited calcaneal #)
r/o septic arthritis and sequelae of tuberculosis.
Adult with flat foot - enquire about a similar family history and r/o presence of subtalar arthritis.

Measurements to be taken in foot and ankle cases:

Circumferential measurement of the ankle

Circumferential measurement of the calf
Oblique circumferential measurement (Decreased in equinus and increased in calcaneus)
Forefoot circumferential measurement
MidFoot circumferential measurement (Increased in Congenital vertical talus)
Hind foot circumferential measurement (Increased in malunited calcaneum)
Distance from lateral malleolus to ground (Useful for Varus/valgus deformity)
Distance from medial malleolus to ground ( Useful for Varus/valgus deformity)
Length of medial column (CTEV)
Length of lateral column
Segmental measurement of tibia and fibula.

Paediatric foot deformities : CTEV

Congenital Vertical Talus
Tarsal Coalition
Flat Foot
Adult foot deformities : Hallux Valgus
Malunited Bimalleolar #
Malunited# Intra-articula Calcaneal #
AVN talus
Neglected Lisfranc’s
Tendo-Achilles injury
Synovitis of ankle joint.
 33. CONGENITAL TALIPES EQUINOVARUS

Q&A

Q1. What is club foot? What are the deformities in clubfoot?

The term clubfoot refers to congenital foot deformity, characterized by equinus of the
hind foot, adduction of the midfoot and forefoot with varus through the subtalar joint complex.
There is also cavus deformity.
The deformities in clubfoot are equinus, Hindfoot varus, forefoot adductus, and cavus.

Q2. Why do you call it congenital talipes equinovarus?

A. Deformity since birth. Deep medial crease with small and wider foot, small heel, and
atrophied calf muscle with cylindrical leg. Other congenital abnormalities may be present.
Neurological examination is normal.

Q3. What is the incidence of clubfoot?

A. The incidence is one in every 1000 live births. The incidence is 6.8% in Hawaiians and
Polynesian population.

Q4. What do you know about the etiology?

A. Clubfoot is an isolated birth defect and considered idiopathic. It is not an embryonic
malformation. The various factors attributed are in utero positioning, oligohydramnios, genetic,
environmental, vascular deficiencies, abnormal muscle insertions and smoking.
Q5. What are the types of clubfoot?
A. Primary (Idiopathic)
Secondary (Associated with other syndromes or diseases)
Type 1 (extrinsic, non-rigid)
Type 2 (intrinsic, rigid)

Q6. What is rigid clubfoot?

A. The foot is smaller with marked varus and small elevated heel that cannot be brought
down with ease. There are deep medial, posterior and plantar creases.

Q7. What syndromes are associated with CTEV ?

A. Arthrogryposis
Streeter dysplasia
Prune belly syndrome
Tibial Hemimelia
Mobius syndrome
Freeman Sheldon syndrome
Diastrophic dwarfism
Down syndrome
Larsen syndrome
Opitz syndrome
Pierre Robin syndrome
Fetal alcohol syndrome

Q8. What are the scoring systems you know of?

A. Pirani scoring system
 Dimeglio scoring system

Q9. Can you elaborate the Pirani scoring system?

A. Mid foot score: curved lateral border
Medial crease
Talar head coverage
Hind foot score: posterior crease
Rigid equinus
Empty heel
Mild- 0 moderate- 0.5 severe- 1
The most severe deformity has a score of 6.

Q10. What are the aims of treatment?

A. Aim is to obtain a supple, plantigrade foot with good function
.
Q11. When to start treatment for CTEV?
A. Started on day 1 by the mother, who is taught the manipulation.Thumb rests on Talus
and press fore foot in to abduction, repeated at least six times in a day.

Q12. What are the various treatment options available?

A. Manipulation and serial casting
Soft tissue procedures
Bony procedures
Differential distraction with JESS and Ilizarov fixator

Q13. What are the manipulative correction techniques you know of?
A. Kite and Lovell’s
Ponseti’s

Q14. What is Kite’s method?

A. It is a sequential correction of deformities, using calcaneocuboid joint as the fulcrum,
in the order of adduction of forefoot- invertion at subtalar joint- varus at heel- equinus at ankle.

Q15. What is Ponseti method of correction of clubfoot?

A. Ponseti technique simultaneously corrects the deformities beginning from pronation and
correcting equinus in end. Simultaneous correction is achieved at talonavicular, calcaneocuboid,
and talocalcaneal joints.Fulcrum is the talar head. The pronation twist is corrected by supinating
the forefoot to bring it in alignment with hindfoot. The tarsal bones distal to the talus are then
abducted in supinated foot so that navicular comes in front of talus and cuboid in front of
calcaneous and calcaneous glides below the talus into corrected position. Above knee casts are
applied every 5-7 days. About 70 degree of abduction is achieved before last cast is applied.
Equinus is corrected at the end. Percutaneous Achilles tenotomy is done just before the
application of last cast that heals in about 3 weeks. After that cast is removed and brace is
applied immediately. The brace should be worn full time (day and night) for the first 3 months
after the last cast is removed. After that, the child should wear the brace for 12 hrs at night and
whenever he/she is sleeping (night time and nap time).This protocol continues until the child is 3
to 4 years of age.

Q16. What are the indications for soft tissue release in clubfoot?
A. Neglected clubfoot
Resistant clubfoot
Relapse /Residual deformities

Q17. What are the various releases described for clubfoot?

A. Posterior release
Posteromedial release
Lateral release
Combined posteromedial and posterolateral release
Extensile posteromedial release

Q18. What are the incisions used for posteromedial release.

A. Turco’s: Hockey stick posteromedial incision
Cincinnati: circumferential incision
Caroll’s two incision technique
Q19. What is the role of tendon transfer in clubfoot?
A. Commonly done either to correct everter insufficiency or triceps surae insufficiency, both
of which are associated with poor foot positioning during walking. Minimum age for tendon
transfer is 5 years.

Q20. What are the complications of operative treatment?

A. Neurovascular damage
Undercorrection
Overcorrection
Skew foot
AVN Talus/Navicular
Sinus tarsi syndrome
Dorsal navicular subluxation
Dorsal bunion

Q21. What are the bony procedures you know?

A. Dwyer osteotomy
Dillwyn-Evans osteotomy
Litchblau procedure
Triple arthrodesis

Q22. Which are the joints fused in triple arthrodesis?

A. Talonavicular joint
Calcaneocuboid joint
Subtalar joint

Q23. What is JESS fixator?

A. Joshi External Stabilisation system. Controlled fractional differential distraction is used
to sequentially correct deformities.

Q24. What is Kite’s error?

A. Kite corrected forefoot adduction by putting pressure on the calcaneo-cuboid joint
,abducting and pronating the forefoot. Ponseti used talar head as the fulcrum of force, never
pronating the foot.
Q25. What are the associated problems seen with club foot ?

Hand anomalies, diastrophic dwarfism, arthrogryposis, tibial hemimelia, myelomeningocele

Q26. What is the aetiology of club foot ?

The exact pathogenesis and aetiology is unknown. There are numerous theories which include:
Primary germ plasm defect
Mechanical moulding theory
Neurogenic theory: histochemical abnormalities secondary to denervation changes in various
muscle groups of the foot
Myogenic theory: primary muscle defect. Predominance in type I muscle fibres, fibre type IIB
deficiency and abnormal fibre grouping
Arrest of normal development of the growing limb bud
Congenital constriction annular bands
Retracting fibrosis: increased fibrous tissue and localised soft tissue contractures found in the
muscles and ligaments of the clubfoot
Familial incidence but precise genetics are unknown (25% of patients with CTEV have a
positive family history)
Viral causes

Q27. How would you clinically assess a patient with club foot?

Examine the whole child to exclude associated abnormalities like myelomeningocele, intra-
spinal tumour, diastematomyelia, polio, CP. Also look for any associated developmental
syndromes like arthrogryposis, diastrophic dysplasia. Look for other moulding conditions.
Examine the spine to exclude neurological causes. Pulses: usually present but vascular dysgenesis is
possible. Dorsalis pedis artery may be absent. Look for creases: medial, plantar, posterior. The affected
limb may be shortened, calf muscle is atrophic, and foot is short compared to opposite side

Q28. What are the muscles contractures that lead to the characteristic deformities in
CTEV?

Midfoot Cavus (tight intrinsics, FHL, FDL)

Forefoot Adductus (tight tibialis posterior)

Hindfoot Varus (tight tendoachilles, tibialis posterior)

Hindfoot Equinus (tight tendoachilles)

Q29. What are the bony deformity seen in CTEV ?

Talar neck is medially and plantarly deviated

The calcaneus is in varus and rotated medially around talus

The navicular and cuboid are displaced medially

Q30. What are the radiological findings in CTEV?

Lateral xray shows hindfoot parallelism between talus and calcaneus

Dorsiflexion lateral view or Turco's view shows talocalcaneal angle of < 35° and flat talar head
(normal is talocalcaneal angles of > 35°)

AP xray shows talocalcaneal angle or Kite's angle of < 20° (normal is 20-40°) and talus-first
metatarsal angle will be negative (normal is 0-20°)

Q31. Describe Dimeglio classification for club foot?

Dimeglio classified club foot in to 4 types - Stiff: Irreducible, Severe: Slightly reducible, Mild:
Partially reducible and Postural: Totally reducible

Q32. Describe the sequence of correction of deformities in Ponseti casting technique?

First is correction of cavus, followed by correction of adduction and heel varus
and finally correction of equinus followed by achilles tenotomy in 90% of cases
 34. EXAMINATION OF A SWELLING

History
Duration
How it was first noticed
What exactly is the present problem?
The swelling itself
Cosmetic
Pain
Compression of nearby structures
Has the swelling increased in size? If so
Was it gradual?
Or was it sudden?
Has it changed shape?
Or has it remained of the same size
Pain
Did pain occur before the swelling or after?
What is the character of the pain?
Presence of fever and other constitutional symptoms
Has there been any impairment of function distal to the swelling
How has the swelling limited his/her daily activity?
Similar swellings elsewhere
Loss of weight/ loss of appetite
Family history of similar swellings or malignancy

General examination
Features of malignancy
Cachexia
Pallor/ jaundice/ LNE/HSM
Local examination
Other than routine Site/size/Shape/Surface/Surrounding area/Consistency/Pulsation/Plane of the
swelling/Engorged veins/ …. One must look for
Attitude of the limb
Compression of the distal structures.
Continuity with that of the parent bone
What type of bone and which part of bone eg. Upper metaphyseal region of the tibia
Presence of other swellings in the same bone as well as in the other bones
Change in consistency/ prominence on flexing or extending a joint.
Restriction of movements of the nearby joints. If present, mention if its due to mechanical block
or pain and spasm
Examine regional lymph nodes and distal neurovascular deficits
Examine for pressure effects
 35. MUSCULOSKELETAL NEOPLASMS

Q&A
Q1. Why do you say it is a neoplasm?
A. It is a swelling that is likely to be due to abnormal proliferation of cells.

Q2. What are the differential diagnoses you have?

A. Possibilities vary in individual patients. It may be infections, tumour like conditions,
bursae, hematoma, fracture callus etc.

Q3. What is the plane of swelling? How will you identify it?
A. Fixed to bone if intraosseous or attached to bone. Not affected by muscle contraction
Intramuscular swellings are mobile when muscle is relaxed and fixed when muscle is
contracted
Mobile deep lesions not affected by muscle contraction are deep to deep fascia and
extramuscular
Superficial mobile swellings with pinchable skin are superficial to deep fascia but deep to
skin
Intradermal swellings are attached to skin

Q4. What all neoplasms arise from the epiphysis?

A. Chondroblastoma, Eosinophilic granuloma, subacute osteomyelitis and Giant cell tumour
in skeletally mature

Q5. What all neoplasms arise from the diaphysis?

A. Adamantinoma, fibrous dysplasia, Ewings sarcoma

Q6. What is ledge sign or sulcus sign?

A. Smooth transition when palpated from epiphysis to metaphysis and ledge like sudden
resistance when palpated from diaphysis to epiphysis is called Ledge sign. Seen in
osteochondroma.

Q7. What is the hallmark of giant cell tumour radiologically?

A. A geographic type of osteolysis that extends up to the subchondral bone is the hallmark
of GCT.

Q8. Is it benign or malignant clinically?

A. Signs of malignancy are
Short duration
Pain preceding swelling
Nocturnal pain
Rest pain
Loss of weight and appetite
Emaciated appearance
Engorged veins
Warmth
Tenderness
Variable consistency or large hard lesions
Infiltration into adjacent tissue
 Neurovascular deficits due to infiltration
Lymph node metastasis
Metastasis
Any soft tissue mass > 5cm in size deep to deep fascia

Q9. What are the principles of doing a biopsy?

A. If possible do it under tourniquet
Should be done by the longitudinal incision along the line of incision for second definitive
procedure
No flaps
Do not retract vigorously
Do not expose nerves and vessels
Use internervous approach or through the muscle approach
Make oval or round window in the bone to prevent stress risers
Biopsy should contain normal, reactive and pathologic zones
Avoid necrotic areas
Close bone window with wax
Achieve complete hemostasis
Close the layers
Subcuticular sutures for skin
Drain if put should be put into the superficial layers only and never into the vicinity of lesion. It
should be brought out in the line of incision so that track can be easily excised during definitive
surgery

Q10. What all tests will you send the specimen for?
A. All specimens should be sent for both culture and histopathologic study.

Q11. How will you send the specimen?

A. Culture to be send in sterile moist swabs or culture bottle.
B. Histologic sample to be send in formaldehyde.
C. If electron microscopy is required send the specimen in glutaraldehyde.

Q12. What other areas/systems should you examine?

A. Palpate the neck for thyroid swelling and left supraclavicular lymph node enlargement
(Virchow’s nodes
Palpate the skull, breast and testes for mass
Look at the skin for abnormal naevi
Auscultate and percuss the chest for abnormal breath sounds and pleural effusion
Examine the abdomen for mass, hepatosplenomegaly and ascites
Do a per rectal and vaginal examination

Q13. How benign musculoskeletal tumours classified?

A. They are classified into latent, active and aggressive stages. Latent tumours are
intracapsular and asymptomatic. Active tumours are intracapsular, but actively growing.
Aggressive tumours have extracapsular extension into the adjacent tissue.

Q14. How are malignant tumours classified?

A. They are classified by Enneking depending on their histologic grade into low grade and
high grade, depending on location into intracompartmental and extracompartmental and
depending on the presence or absence of metastasis.
Enneking W, Spanier S, Goodman M: A system for the surgical staging of
musculoskeletal sarcoma. Clin Orthop Relat Res 1980;153:106

Q15. What is a compartment? Give examples

A. Compartment is an anatomical region surrounded by natural anatomic barriers that resist
spread of neoplasm. Examples are intraosseous lesions, subperiosteal space, muscle
compartments etc.

Q16. What neoplasms are extracompartmental from the beginning itself?

A. Lesions that arise from popliteal fossa, sole of foot, palm of hand, cubital fossa, axilla,
inguinal region etc. are considered extracompartmental from the beginning.

Q17. Is there any complication?

A. Look for pathologic fracture, neurovascular deficit, lymph node and distal metastasis.

Q18. What are the most important clinical evidences of malignancy?

A. Signs of infiltration and metastasis are the most important evidence of malignancy

Q19. What is neo-adjuvant chemotherapy? Why is it needed?

A. High grade malignancies have micrometastasis at the time of presentation, hence they
require early chemotherapy. Chemotherapy given before the surgery is called neo-adjuvant
chemotherapy. It makes the prognosis better; it makes the tumour less vascular, allows limb
salvage and also helps in assessment of sensitivity to chemotherapy possible.

Q20. When will you do the surgery after neo-adjuvant chemotherapy?

A. Usually after 2 cycles of chemotherapy.

Q21. How will you stage a primary bone malignancy?

A. Needs CT of chest to look for lung metastasis
Ultrasound of abdomen for liver metastasis
Bone scan to assess skeletal secondaries
MRI of the part to assess soft tissue extension
CT of the part to assess bony extent.

Q22. When will you do the staging?

A. Should be done before biopsy and after chemotherapy before definitive surgery

Q23. What are the contraindications for limb salvage?

A. Infection
Metastasis
Poor general condition
More than 6 cm of shortening at skeletal maturity

Q24. What are the options available for filling the skeletal defect after limb salvage?
A. Resection arthrodesis
Bone graft
 Massive allograft
Rotationplasty
Megaprosthesis
Distraction osteogenesis

Q25. What are the various surgical margins that can be achieved?
A. Intralesional- Resection within the capsule
Marginal excision- Just outside the capsule/psuedocapsule
Wide excision- Through the normal tissue within the compartment of origin
Radical excision- Excision includes the entire compartment of tumour origin

Q26. What is the difference between wide amputation and radical amputation?
A. Wide amputation- Done through the compartment of origin
Radical amputation- Compartment of tumour origin excised completely

Q27. How can you increase the margin of clearance in intra-lesional curettage?
A. Chemical cauterization using phenol or bone cement
Cryo-cauterization using liquid nitrogen

36. OSTEOMYELITIS

Q&A

Q1. Clinical features suggestive of chronic osteo myelitis.

A. H/o pain, swelling, discharge, , trauma, surgery, discharging bone pieces sinus fixed to
bone, puckered scar exposed necrotic bone, soft tissue contracture, bony tenderness, fixed sinus,
irregular surface, thickened bone.

Q2. Describe the Xray findings

A. Sequestrum
Involucrum
Ill defined bone destruction
Local irregular thickening
Loss of corticomedullary differentiation

Q3. What is a Sequestrum

A. It is a dead piece of bone separated from living bone by a layer of unhealthy granulation
tissue or pus, and lying freely in the cavity.

Q4. What are the types of sequestrum?

A. Tubular sequestrum-pyogenic infection in children
Feathery-pyogenic infection
Coarse sandy –tuberculosis
Dense ivory-syphilis
Ring –pin tract infection
 Bombay sequestrum (black)-calcaneal OM
Kissing sequestrum-TB spine
Conical sequestrum-amputation stump

Q5. What are the gross charecteristics of sequestra?

A. White, brittle bone piece with smooth pus facing and rough granulation facing surface
lying free from parent bone
No punctuate bleeding
Sinks in water
Dull note on percussion
Closed haversian canal

Q6. What is involucrum?

A. Immature, subperiosteal, reactive, living new bone formation around a dead bone

Q7. What is the common sites of OM and why?

A. Metaphysis because
Hairpin bend arrangement of arterioles
Less number phagocytes
More prone for trauma
Sluggish flow
Torturous blood vessels and skimming of bacteria
Dead and degenerating cartilage cells from physeal plate serving as a medium for
bacterial growth

Q8. What are causes of diaphyseal OM?

A. Long standing OM in children
Post traumatic
Implant related
Tubercular OM
Drug abusers
Immunocompromised
Salmonella OM, [often b/l and may be symmetrical]
Sickle cell anaemia

Q9. What is Ciery and Mader classification for chronic OM

A. Based on anatomical and physiological criteria
To determine stage of infection

Anatomical Type
I Medullary Endosteal disease
II Superficial Cortical surface infected because of coverage defect
III Localized Cortical sequestrum that can be excised without compromising stability
IV Diffuse Features of I, II, and III plus mechanical instability before or after
debridement
 Physiological Class
A host Normal Immunocompetent with good local vascularity
B host Compromise Local (L) or systemic (S) factors that compromise immunity or healing
d
C host Prohibitive Minimal disability, prohibitive morbidity anticipated, or poor prognosis
for cure
Cierny and Mader Staging System for Chronic Osteomyelitis

Q10. What is the cause of chronicity of infection?

A. Unabsorbed and retained sequestra
Unobliterated cavities
Microbiological shift
Mixed infections
Q11. How would you explain the role of bone scan?
A. Tc bone scan
Triphasic scan
Phase 1 -arterial flow
Phase 2-venous flow
Phase 3-focal bone uptake
1&2 phases positive &phase3 negative in soft tissue infections
1,2 & 3 phases positive in chronic osteomyelitis
Gallium scans show increased uptake in areas of increased leucocytes and bacteria
Indium-111 labelled leucocytes are more sensitive than gallium and Tc and are
especially used in differentiating chronic OM and neuropathic joint.

Q12. What are the principles of treatment of chronic osteomyelitis?

A. Identify the organism and sensitivity
Locate the sequestrum
Thorough debridement of necrotic tissue and bone, sinus tract, infected granulation, and
saucerisation done through a wide window
Stabilization of bone
Obtaining intra operative cultures
Dead space management
Soft tissue coverage
Limb reconstruction
Systemic antibiotic treatment

Q13. What are the surgical treatment options in osteomyelitis?

A. Sequestrectomy and curettage
Open bone grafting [Papineau technique]
Debridement, muscle flap followed by bone graft (Belfast technique)
Grafting
Wound coverage
PMMA antibiotic beaded chains
Biodegradable antibiotic delivering system
Closed irrigation & suction
Soft tissue transfer
 Illizarov technique
Hyperbaric oxygen therapy
Silver iontophoresis
Amputation

Q14. What are the complications of osteomyelitis?

A. Growth disturbances-
Increased rate of growth
Decreased rate of growth
Pathological #
Muscle contracture
Septic arthritis
Secondary septicaemia
Epithelioma
Joint stiffness
Amyloidosis
Recurrances & relapses

Q15. What is bead pouch technique?

A. Used as an interim method between wound excision and definitive coverage
Cavity filled with antibiotic impregnated beads and covered by sterile transparent
adhesive covering.

Q16. What is biofilm?

A. A biofilm is an aggregate of microorganisms in which cells adhere to each other on a
surface. These adherent cells are frequently embedded within a self-produced matrix of
extracellular polymeric substance (EPS) polymeric conglomeration generally composed of
extracellular DNA, proteins, and polysaccharides. It protects bacteria from phagocytosis,
recognition, & helps to cling to inert implant material and form numerous colonies. It inhibits T
lymphocyte proliferation, B lymphocyte blastogenesis, immunoglobulin production, interferes
with cell chemotaxis and white cell degranulation.

Q17. What is pulse lavage?

A. Iriigation with 10-14 litres of saline
Fluid pressure 50-70 pounds/sq inch
800 pulses /minute

Q18. What is Garres OM?

A. Also known as idiopathic cortical sclerosis
Sclerotic thickening of cortex of long bones
Infants and children affected mostly
Tibia is the most common site
Thought to be caused by low grade anaerobic bacteria
Dull aching pain, worse at night, diffuse tenderness and swelling over affected bone
Treatment – fenestration of sclerotic bone and antibiotics

Q19. What are the specific types of OM

A. Tuberculous OM- metaphysis in children and epiphysis in adults
Syphilitic OM - caused by treponema pallidum - shaft involved more frequently
 Typhoid OM-Subacute OM of hematogenous origin, Diaphysis affected, Symmetrical
involvement - Common in sickle cell anemia patients
Brucella OM- brucella abortis most common, more common in vertebrae

37. EXAMINATION OF THE KNEE JOINT

History
H/o any previous trauma
What was the mechanism of trauma
Position of knee at time of trauma
After trauma, was the patient able to continue playing
post trauma - weight bearing possible or not, what treatment taken, how long
immobilised
pain – aggravated by sqautting, stairs, running, sudden twisting episodes
giving way – aggravating factors
recurrent swelling of knee – recurrent synovitis
paresthesia, loss of sensation foot, distal weakness
subluxating patellae
When did the effusion occur after the trauma (if immediate .. think of # intraarticular if delayed,
think of meniscal injury)
What was the treatment used?
Any h/o Clicks, thuds, giving away?
Any h/o locking / unlocking
Difficulty in climbing stairs, squatting
Any history of recurrent fever
How far it has affected his present job.
Examination
Gait
Inspection
Attitude and deformity eg. locked knee, triple deformity
Position of the patella
Any bruises, scars or sinuses
Wasting of the muscles
Any obliteration of the parapatellar fossae or any other swellings elsewhere
Never forget the POPLITEAL FOSSA
Palpation
Local rise of temperature
Anterior, medial and lateral joint line tenderness
Tests for effusion
Severe effusion: Fluid thrill, cross fluctuation
Moderate effusion: Patellar tap test
Mild effusion: Squeeze test or the wipe test
Look for synovial hypertrophy ( at the superomedial region of the knee)
Popliteal artery pulsations
Change in the prominence of the swelling on movements of the knee
Palpation of the bones for any irregularities/ tenderness
Movements
Flexion/Extension of the knee
Tracking of the patella
Measurements
Limb length
Q angle
Intermalleolar distance
Inter condylar distance
Lateral thigh leg angle
Circumferential measurements
Special test
Anterior and posterior drawer test
Lachmans test
Pivot shift test
Mcmurray test
Sag sign
Varus and valgus stress test
Wilsons test for osteochondritis dissecans
Dial test for PLC
Patellar tilt
Patellar apprehension test
Patellar glide test

Always assess the distal neurology

Always r/o injury to the common peroneal nerve
Always feel for pulsation of the popliteal artery
Always do muscle charting.. esp if ACL reconstruction is needed
R/o ligamentous laxity
Mention the presence of Chondromalacia patella or PatelloFemoral arthritis
Compare the ROM with the opposite Knee
 38. INTERNAL DERANGEMENT KNEE

CASE DISCUSSION
A 32 year old male patient presents with h/o injury to right knee sustained while playing football
two years back. Now c/o of recurrent episodes of pain and instability of right knee. There is no
history of locking.

Q&A

Q1. What are four common causes of hemarthrosis?

A. Cruciate ligament injury
Peripheral meniscal injury
Osteochondral injury/ fractures
Capsular tear

Q2. What are the causes of “giving way”?

A. Cruciate injury
Recurrent patellar dislocation
Collateral ligament injury
Extensor mechanism injury

Q3. What are causes of locking?

A. Bucket handle tears of menisci (true locking)
Loose bodies
Recurrent subluxating patella
Cystic lesions arising from the cruciates

Q6. What are the common DDs when you find recurvatum in a posttraumatic knee?
A. Injury to PCL/PLC/Posterior capsule injury
Malunited fractures of L/3rd femur or U/3rd tibia.

Q7. What is the difference between locking and extensor lag?

A. Locking – inability to extend the knee (both actively & passively)
Extensor lag – inability to extend the knee terminally actively but passively full extension
possible eg: quadriceps/ extensor mechanism weakness/ rupture

Q8. What are the structures in the lateral three layers of the knee joint?
A. I Superficial ( by Seebacher et al)
Iliotibial tract
Biceps femoris
Lateral deep fascia
II Middle
Quadriceps retinaculum
Patellofemoral ligaments
III Deep
Lateral collateral ligament
Popliteofibular ligament
Popliteus tendon
Fabellofibular ligament
 Arcuate ligament
Capsule

Q9. What are the structures in the medial three layers of the knee joint?
A. I Superficial layer (Warren & Marshall et al)
Deep fascia of thigh
Medial patellar retinaculum
In middle splits to enclose sartorius
II Middle layer
Superficial medial collateral ligament
Medial patellofemoral ligament
III Deep layer
Joint capsule
Thickened medially by deep medial collateral ligament
Posterior thickening called posterior oblique ligament
## Pes Anserinus lies between superficial and middle layer

Q10. What are radiologic features suggestive of ligamentous injury?

A. Avulsion fractures of tibial spine suggesting ACL injury
Avulsion fracture of lateral tibial condyle (Segund fracture/ lateral capsular sign) suggesting
ACL injury
Fracture of the fibular styloid process (arcuate sign) suggesting Posterolateral corner injury
Capsular avulsion fracture of medial tibial condyle (reverse Segund #) suggesting PCL injury
Avulsion of medial epicondyle of femur suggesting MCL injury ( pellagrini steida’s in late
cases)
Stress radiography to demonstrate collateral ligament injury
Look for associated osteochondral fractures

Q11. What are the tests for knee joint effusion?

A. Mild effusion (5-15ml) : bulge test
Moderate effusion (15-30ml) : patellar tap
Severe effusion (> 30 ml) : cross fluctuation

Q12. How do you examine for synovial thickening?

A. Palpate the superolateral aspect of the knee joint and try to roll the thickened edge of
synovium underneath…doughy feel.
Q13. Why superolateral aspect?
A. VMO is wasted first among quads (as it developed later in the evolution of quadriceps)

Q14. What is the significance of positive valgus test in 30 deg and 0 deg?
A. Positive valgus in 30 deg only: medial strs injured – MCL
Positive valgus in 30 & 0 deg: medial strs injured along with cruciates (ACL and / or
PCL) and posteromedial capsule

Q15. What are the tests for ACL injury?

A. Lachman test
Anterior drawer test
Pivot shift test of Hughston
Q16. Whats is unhappy triad of O’Donoghue?
A. Injury to ACL , MCL and medial meniscus

Q17. QWhats the most sensitive test for ACL injury?

A. Lachman test.
Can be performed in emergency set up.
Look for
Excessive anterior translation
Soft end point

Q18. What are the drawbacks of anterior drawer test?

A. Cannot be done in acute set up (knee flexion not possible)
Hamstring spasm may prevent anterior translation
Door stopper effect of meniscus
Always look for posterior sag before ant. drawer test (look for the 10mm anterior step of medial
tibial plateau to R/O PCL injury)

Q19. What are the requisites for a positive pivot shift test?
A. A non functioning ACL
An intact medial complex
An intact iliotibial tract

Q20. What is the treatment of ACL injury in skeletally immature patients?

A. Conservative treatment - muscle strenghtening exercises esp. hamstrings
Avoid any procedure involving bony tunnelling until skeletal maturity
If indicated extra-articular reconstruction (eg: McIntosh repair)

Q21. What are tests of PCL injury?

A. Quadriceps active test
Godfrey’s 90-90 test
Posterior drawer test
## PCL prevents hyperextension of the knee joint. So injured knees shows recurvatum.
## PCL is twice stronger than ACL, so injuries are rare

Q22. Describe the various rotary instabilities and tests used to diagnose it?
A. Anteromedial rotary instability(AMRI) :
injury to medial strs like MCL, posterior oblique ligament (POL) & ACL.
Anterior drawer test
Slocum in ER
Valgus stress in 30deg
Anterolateral rotary instability(ALRI):
injury to ACL and lateral capsular ligament
Slocum in internal rotation
Pivot shift test of Macintosh
Jerk test of Hughston
Flexion rotation drawer test
Posterolateral rotary instability(PLRI):
Injury includes posterolateral structures like popiteus tendon, arcuate ligament
complex,lateral capsular ligament, posterolateral capsule with or without PCL.
 External rotation recurvatum test
Reverse pivot shift test
Posterolateral drawer test
Tibial external rotation test or Dial test
Posteromedial rotary instability(PLRI):
Injury to MCL, posteromedial capsule, posterior oblique ligament, semimembranosus
insertion with or without PCL

Q23. Which meniscus is commonly injured, why ?

A. Medial meniscus because;
Excursion of medial meniscus (5mm) is less than lateral meniscus (11mm)
Attachment of lateral meniscus to popliteus makes it more mobile

Q24. Which meniscus commonly injured in acute ACL injury and chronic ACL injury?
A. Acute ACL – lateral meniscus
Chronic ACL – medial meniscus

Q25. What are the signs and tests for meniscal injury?
A. Signs:
Joint line tenderness (high sensitivity, low specificity)
Locked knee (short of terminal extension)
Recurrent effusions ( look for synovial thickening)
positive McMurray’s ( high specificity, low sensitivity)
Bounce-home test ( painful terminal extension)
Thessaly test
Quadriceps wasting

Q26. What are the functions of meniscus?

A. 1. Load bearing: at least 50% of the commpressive load of the knee is transmitted
through the meniscus in extension, and approx 85% of the load is transmitted in 90° flexion.
In the meniscectomised knee the contact area is reduced approx 50%
2. Shock absorption
3. Knee jt stability
4. Lubrication
5. Proprioception

Q27. What is McMurray Test?

A. Thomas Porter McMurray , a British orthopaedician described as
“ internal rotation of the leg produces pain in injury to the external ligament (lateral
meniscus) and external rotation of leg produces pain with injury to the internal ligament (medial
meniscus)”
No varus or valgus stress was applied
Knee was flexed beyond 90 degs and extended
McMurray described it to detect tears in the posterior segment of meniscus
A positive test was described as a click or thud that can sometimes be heard but always
felt on palpation
McMurray TP. The semilunar cartilages. Br J Surg 1942; 29:407-14.
 Modifications of McMurray’s test..
Varus or valgus stress application
Reproduction of pain during test is also considered positive ( not just click or thud)
McMurray more sensitive for MM & more specific for LM
Associated pathologies reduce the diagnostic accuracy of McMurray’s test
Both posterior and middle segments of menisci are tested
Circumduct the limb while doing flexion extension - Sensitivity (58%) specificity (93%)
positive predictive value (82%)

Q28. What is Thessaly Test

A. Patient stands on affected leg
Knee bent at 20 degrees
Examiner holds pt’s hands and rotates pt to both sides
Meniscal grind and loading
Positive test: pain, painful click.
High diagnostic accuracy (94%)
JBJS Am. 2005 May;87(5):955-62

Q29. What exercises are preferred in post ACL reconstructed knee

rehabillitation?
A. Closed chain exercises as open chain exercises stresses the reconstructed ACL by
quadriceps pull esp. in terminal extension

Q30. List the autograft options for ACL reconstructon?

A. Bone patellar tendon bone
Quadrupled hamstring (semitendinosus & gracilis)
Central quadriceps tendon
Iliotibial band

Q31. How to treat a case of PCL injury?

A. Acute PCL avulsion – arthroscopic /open fixation
Acute PCL injury in young – reconstruction after attaining full ROM
Chronic PCL injury – quadriceps strenghtening, correct varus deformity, reconstruct PCL
if still symptomatic

Q32. What are the components of posterolateral complex of knee?

A. Iliotibial band
Biceps femoris
Lateral collateral ligament
Popliteofibular ligament
Arcuate complex
Posterolateral capsule

Q33. Whats the significance of identifying PLC injury?

A. Often associated with cruciate ligament injuries , if diagnosis missed, may lead to early
failure of reconstructed ligaments.
Often associted with common peroneal nerve injury
Hughston Laxity Classification
 Grade I – 1-4 mm laxity
Grade II – 5-9 mm laxity
Grade III – >10 mm laxity (soft endpoint)
Hughston JC, Andrews JR, Cross MJ, Moschi A: Classification of knee ligament instabilities.
Part I. The medial compartment and cruciate ligaments. J Bone Joint Surg Am 58:159-172, 197

Q34. How to palpate for the knee joint line

A. Flex the knee to 90 deg. Then palpate upwards along the tibial flares, on either side of the
lig patellae. The first depression felt is the knee joint line. Confirm by moving the knee joint.
Q35. Give some examples of overuse knee pain syndromes?
A. Iliotibial Band Friction Syndrome
Popliteus Tendinitis
Pes Anserinus Bursitis
Patellofemoral Synovial Plica
Infrapatellar Fat Pad Syndrome
Patellar Tendinitis(jumper’s Knee)
Patellofemoral Joint Pain Syndrome

Q36. What are the Ottawa knee rules (i.e; when to order
Xrays after acute knee trauma)?
A. Unable to walk
tenderness on patella
Age > 55 or < 18
tenderness on fibular head
Unable to flex 90 deg

Q37. What are the treatment options for meniscal injury?

A. Meniscal balancing- tears in the inner 2/3rd of the meniscus
meniscal repair – longitudinal tears in the outer 3rd of meniscus in young patients. Radial tears
(current concept, previously balancing)
subtotal menisectomy – complex tears beyond repair or balancing
meniscal transplantation – under experimental stage
small peripheral tears (< 5mm) may be treated non surgically. H/O recurrent locking episodes
favours surgical management. Arthroscopic procedures are favoured over open procedures.

Q38. How will you treat ACL injured knee ?

A. ACL injury requires surgical treatment only if the patient gives C/O recurrent instability
& giving way. Treatment is based on the history & clinical examination rather than MRI
findings. If associated with meniscal injuries, ACL reconstruction has to be done along with
meniscal procedures.
In skeletally immature : nonsurgical options preferred. If surgery required, avoid bone drilling
procedures- extraarticular procedures preferred
In active young adults: ACL reconstruction once the knee is cold ( post inflammatory stage)
and ROM is regained. Usually 4-6 wks after trauma.
In old patients with degenerative changes in knee and sedentary lifestyle : non surgical
option preferred. Strenghtening of hamstrings, ROM exercises.

Q39. What are the treatment options in combined ligamentous injury?

A. Meniscal injury + ACL injury : meniscal procedure with ACL reconstruction
Meniscal injury + ACL injury + MCL injury: meniscal procedure with ACL reconstruction
and MCL repair / reconstruction in grade III MCL injury. In grade I & II MCL injuries, non
surgical treatment for MCL is preferred.
ACL + PCL + meniscal injury: PCL reconstruction + meniscal procedure in first stage
followed by ACL reconstruction or if possible all three procedures can be done simultaneously.
Always PCL reconstruction has to be done before ACL reconstruction. #### ACL / PCL
+ meniscal injury + PLC injury (posterolateral corner): always combine the ACL/PCL
reconstruction with PLC reconstruction, otherwise high chances of ACL/PCL failure.

Q40. Why is arthroscopic ligament surgery not preferred in acute stage?

A. High chances of arthrofibrosis postoperatively.
Associated capsular tear may lead to leakage of the irrigation fluid peroperatively and may cause
compartment syndrome.
Clinical assessment of injured knee ligaments better done once the acute stage is over.

Q41. What are the anatomical components of posterolateral corner of the knee joint?
A. 1. tibia, fibula, lateral femur (bony)
2. iliotibial band (IT band)
3. biceps femoris tendon
4. fibular (lateral) collateral ligament (FCL)
5. popliteus tendon
6. popliteofibular ligament
7. Arcuate ligament
8. lateral gastrocnemius tendon
9. fabellofibular ligament
10. Posterolateral capsule
4/5/6 are the most important structures

Q42. What are the tests to diagnose posterolateral corner injury

knee?
A. Tibial external rotation test (Dial test)
External Rotation Recurvatum test (Hughston)
Reverse Pivot test ( valgus & ER )
Posterolateral drawer test
Varus stress test (0&30 deg)

Q43. What is the importance of recognizing posterolateral corner injury?

A. PLC injuries commonly are associated with PCL or ACL injuries and are seldom
isolated.
A missed PLC injury is a cause of failure of ACL or PCL reconstructions
Look for common peroneal nerve injury in PLC injury

Q44. What is the treatment of PLC injury?

A. In Acute stage,
Gr I & II – brace in extension X 3weeks
Gr III – anatomical repair within 3 weeks, may or maynot be combined with other
ligament reconstruction.
In chronic stage,
Varus aligned knee – valgus osteotomy , reassess, reconstruction if needed
 normal aligned but unstable – reconstruction eg: Larsen technique

Q45. Describe the anatomy of posterior oblique ligament and oblique posterior ligament?
A. Posterior oblique ligament (POL): thickening of the medial capsular ligament attached
proximally to adductor tubercle of femur and distally to tibia & posterior aspect of the capsule;
anatomically this is the third (deep) layer of the medial compartment, provides resistance to
valgus loads
Oblique posterior ligament : a slip from the insertion of the semimembranosus on
posteromedial aspect of tibia that runs obliquely & laterally upward crossing popliteal fossa
toward the lateral femoral condyle.
Anatomically in the middle layer . Tightens the posteromedial capsule of knee

Q46. What are the tests for patella instability?

A. Apprehension test
Tracking
Quadrant test
Tilt
check retropatellar tenderness
defect in quadriceps / patellar ligament

Q47. What is your diagnosis?

A. Do not give diagnosis as Internal derangement of Knee (IDK). Just mentioning IDK
means you are unable to come to proper diagnosis. Better to mention which all structures are
damaged.
Also, better not to mention as rotatory instability (eg AMRI). Be specific regarding which
all structures are damaged.
Look for injury to cruciates, menisci, collaterals, patella & extensor mechanism .
Mention the grade of injury of each structure as it determines the management. Always
examine the ipsilateral hip and ankle with foot.
 39. EXAMINATION OF THE WRIST JOINT AND HAND

History
Always r/o the presence of R.S.D.
Always determine the dominance of the hand
Examination
Inspection
Attitude and deformity
Swelling at the wrist joint
Trophic changes
Wasting
Orientation of the fingers towards the scaphoid.
Palpation
Local rise of temperature
Joint line tenderness ( at individual joints as well as anatomical snuff box)
Always palpate for thickness of wrist or any step sign
Volkmanns sign
Movements
Look for wrist Palmar flexion and extension/ radial and ulnar deviation/ pronation and
supination
Examine for stiffness of the fingers, elbow and the shoulders
Malunited Colles # : dorsiflexion increased with alteration of styloid process
Malunited Smith# : Volar flexion increased with alteration of styloid process
Malunited Barton# : Movement will be restricted with normal styloid relation
CIADER : Movement will be absent or grossly restricted with altered styloid
Madelung’s deformity: Restriction of dorsiflexion, supination and radial deviation
Examination of the hand functions
Grip
Grasp
Pinch
Special tests
Piano Key sign: DRUJ instability
Allens test for assessing vascularity
Tests for ulnar impingement:
Scapholunate instability: Scapholunate ballotment
Watson’s shift test
Lunotriquetral instability: Reagen test
Lunotriquetral ballotment
Klienman shear test
Tests for nerves and vascularity

40. MALUNITED LOWER END OF RADIUS

 Q&A
Q1. Why do you say this is a malunited fracture)
A. There is history of significant trauma with POP immobilization for 1 month, after which
patient noticed a non progressive deformity. On ex. there is manus valgus, shortening of the
radius by 1 cm with restricted palmar flexion, preserved dorsiflexion and terminal restriction of
pronation.

Q2. Why do you say that there is DRUJ involvement?

A. There is tenderness over the distal radioulnar area with pain and crepitus during
pronation - supination

Q3. What are the fracture characteristics contributing to the development of malunion
A. severe communition
severe osteoporosis
disruption of the distal radioulnar ligaments

Q4. What are the radiographic criteria for acceptable healing of distal radial#
Radiographic
Criterion Acceptable Measurement
Radioulnar length Radial shortening of <5 mm at distal radioulnar joint compared with
contralateral wrist
Radial inclination Inclination on posteroanterior film ≥15 degrees
Radial tilt Sagittal tilt on lateral projection between 15-degree dorsal tilt and 20-
degree volar tilt
Articular incongruity Incongruity of intraarticular fracture ≤2 mm at radiocarpal joint

A.radial inclination 22-23 degree of

radial inclination
B.volar tilt =11 to 12 degrees
C.radial height =11 to 12mm
D.ulnar variance=2mm(difference
compared to opposite wrist)

Q6. Which all joints may be involved in a

case of malunited lower end radius?
A. radialcarpal joint
mid carpal joint
radioulnar joint
Q7. Why are you concerned about a malunited LER as this patient does not have
significant loss of function?
A. loss of palmar tilt shifts the carpus distally on the radius ,there by increasing contact
stress on the dorsal tip of radius
loss of radial inclination results in increased stress at the radiolunate articulation,the increased
contact stresses result in a higher likelihood for degenerative changes

Q8. Which abnormality of radius in malunion mainly causes loss of grip stength of
hand?
A. Shortening of radius

Q9. What are the clinical features expected in a case of malunited lower end radius?
A. Pain, stiffness, weakness, cosmetic deformity
impaired ulnar deviation and increased radial deviation
decreased pronation and supination –malunited smith fracture and incongruity at the
distal radioulnar joint
impaired grip strength
s/o median nerve compression ---from a dorsally tilted malunion that increased pressure
within the carpal tunnel

Q10. Absolute CI for surgical correction of malunited #l LER?

A. Patients with active reflex sympathetic dystrophy syndrome crps

Q11. What are theSurgical procedures of Rx of malnunited # LER

A. 1. Corrective osteotomies for deformity of the distal radius intraarticular and
extraarticular osteotomies
2. Procedures that treat the pathology of the distal radio ulnar jt. Ulnar shortening,
hemiresection arthroplasty, Sauve-Kapandji procedure
Darrach resection of distal ulna
3. Salvage procedures
- limited or total wrist arthrodesis
- arthroplasty
- proximal row carpectomy
These procedures can be used alone or in combination, depending on the specific
deformity, functional demands and degree of arthritic changes present in a particular patient.

Q12. What are the Primary indications for resection of the distal ulna ?
A. Malunion in older patients with significant ulnar variance, arthritis of the distal RUJ or as
a salvage procedure after failed reconstruction of the distal RU jt.

Q13. What are the Indication for salvage procedures (wrist fusion)?
A. symptomatic fractures with marked intra articular comminution or severe radiocarpal or
intercarpal degenerative changes for which conservative Rx has failed.

Q14. What is the procedure for extra articular malunion with dorsal angulation
A. Osteotomy – dorsal open wedge metaphyseal osteotomy
With grafting of the radius
With internal fixation with plate and screw
Q15. What are the contraindication for radial osteotomy?
A. 1) Active reflex sympathetic dystrophy
2) Acceptable function despite deformity
3) Poor soft-tissue envelope
4) Severe osteopenia
5) Advanced radiocarpal or intercarpal arthritis

Q16. What is the procedure for extra articular malunion with volar angulation
A. Volar opening wedge osteotomy for distal radius bone grafting and Plating

Q17. Indications for intra articular osteotomies

A. Young, active patients with high functional demands, more than 2mm of articular step off
and no c/o post traumatic arthritis.

Q18. Surgical procedures to correct distal RU jt dysfunction – 2 major categories

A. 1. Joint preserving procedures offered a more anatomized reconstruction and better
preservation of jt kinematics.
2. Procedures that ablate the joint

Q19. The preserving procedures

A. 1. Radial and ulnar osteotomies alone or in combination
2. Ulnar shortening osteotomy alone is indicated
a) If the radial deformity is not severe <10o of abnormal angulation in the frontal
and sagittal planes.
b) Unacceptable positive ulnar variance
c) Distal RU Jt. Is reducible

Q20. Ablative procedure

A. If pain in the distal RU Jt persists after joint preserving procedures
Algorithms in DRUJ management

41. KIENBOCK'S DISEASE

Q1. Why do you say this is a case of kienbock's disease?

A. Age 15-40 years
\Profession of the patient. Seen in patient in which there are repeated small trauma to the wrist
like mason, blacksmith, roti maker.
Restriction of wrist movements mostly dorsiflexion and palmar flexion
Pinch strength and grip strength is reduced.
Tenderness over lunate.
Q2. What are the differential diagnosis.
A. Arthritis of the wrist- All wrist movements are grossly restricted and painful in this case
Drillers disease- tenderness all over the wrist and also over the carpal bones.

Q3. How would you proceed with this case.

A. I would like to get an xray of the wrist both AP and lateral

Q4. How do you classify kienbock's disease?

A. Lichtmann classification
Stage 1-
Clinically tenderness over the lunate
Xray maybe within normal limits
Can be detected in CT
Stage 2
Sclerosis present
Fracture seen along the long axis of the bone
No collapse
Stage 3a
Collapse and fragmentation of the lunate and sclerosis
Scapholunate angle maintained
Stage 3 b
Collapse and fragmentation of the lunate and sclerosis
Scapholunate angle changed
Stage 4
Perilunate arthritis

Q5. What is the treatment of kienbock's disease?

A. Stage 1- POP immobilization
Stage 2 radial shortening
Stage 3a- radial shortening
Stage 3b- radial shortening by lateral closing wedge osteotomy
Stage 4- radial shortening gives only some relief. Proximal row carpectomy gives good
relief.

Q6. What is the rationale in radial shortening.

A. Around 70 percent of the patient having kienbocks disease is having negative ulnar
variance, which is corrected by radial shortening. This changes the force acting at the lunate.
 42. PERIPHERAL NERVE INJURIES

Q1. What is a claw hand?

A. It is a dformity of hand with hyperextension at the mcp and flexion at interphalangeal
joint.

Q2. What is the diff between ulnar and total clawing?

A. Ulnar clawing is predominantly seen in little and ring fingers where as total clawing
involves all the fingers. It is due to combined median and ulnar nerve palsy.

Q3. What is ulnar paradox?

A. Due to paralysis of fdp of ring and little finger in high ulnar nerve palsy clawing will be
less evident.

Q4. What are the common causes of ulnar nerve palsy in india?
A. Hansens disease, diabetes mellitus, rheumatoid arthritis.

Q5. Why ulnar nerve is commonly involved in Hansens disease?

A. It is more superficial in the elbow region and the medial side is colder than lateral side as
it is over the medial epicondyle.

Q6. What is Guyons canal?

A. It is an osteofibrous canal between the hook of hamate and the pisiform bone through
which the ulnar nerve enters through the hand.

Q7. What are the clinical signs of ulnar nerve lesion/

A. Card test , Froments sign, Egawas sign, Wartenberg sign, Groove sign.

Q8. How will you differentiate between high and low ulnar nerve palsy?
A Ulnar paradox will be present in high ulnar nerve palsy and FCU will be weak in high
ulnar nerve palsy.

Q9. What is bouvier - beevors phenomenon?

A. In claw hand on flexing the mcp joint the patient will be able to extend the IP joint.

Q10. What is in intrinsic minus sign?

A. It is claw hand due to ulnar nerve palsy.

Q11. What are the prerequisites for tendon trannfers in hand?

A. 1. Tendons muat be having adeqate strength atleast grade 4 power.
2. Transfereed tendon must be acting in the same line of action of previous muscle.
3. Joints must be supple.
4. It must be transferred through a smooth tunnel.

Q12. Name a few tendon graft materials ?

A. Palmaris longus, extensor tendons of the toes, fascia lata.

Q13. Name the tendon teansfers for tratment of claw hand?

A. Bunnel
 Modified Bunnel
Riordan
Fowler

Q14. What is the critical time perod of ulnar nerve

A. 12 months

15. What is finger drop?

A. Inability to extend the fingers due to pin palsy.

Q16. How will you differentiate between high and low radial nerve palsy?
A. In high radial nerve palsy brachioradialis will be affected.

Q17. What is crutch palsy?

A. High radial nerve palsy due to usage of axillary crutches.

Q18. What is the autonomous zone of radial median and ulnar nerve?
A. Radial-dorsum of first interdigital web.
Ulnar-palmar aspect of distal phalynx.
Median-palmar and dorsal aspect of index fingers distal phalynx,

Q1. . Describe the tendon for high radial nerve palsy?

A. Modifeid Jones transfer
1. FCR--------ECRB--wrist extension
2. Pronator Teres----------extensor digitorum---for finger extension
3. PL----------APL &EPB-------for extension and abduction of thumb

Q20. What is the clinical sign of AIN injury?

A. Poinitng index deformity.

Q21. What is foot drop?

A. Inability to extend the ankle.

Q22. How will you differentate between finger drop of polio and leprosy?
A. Sensory involvement in leprosy.
Equinus will be more prominent in polio.
Trophic changes will be present in leprosy.

Q23. What is established foot drop?

A. Foot drop persisting more than 1 year.

Q24. What are the tendon transfers for foot drop?

Ober and Barr transfers

Q25. What is dermatome and myotome?

A. Dermatome –exclusive sensory supply of nerve roots
Myotome exclusive motor supply

Q26. What is Seddons classification?

A Neuropraxia,axontemesis, and neurontmesis

Q27. What is Sunderland’s classification

In

first-degree injury, conduction along the axon is physiologically interrupted at the site of injury,
but the axon is not disrupted. No wallerian degeneration occurs, and recovery is spontaneous and
usually complete within a few days or weeks
In second-degree injury, disruption of the axon is evident, with wallerian degeneration distal to
the point of injury and degeneration proximal for one or more nodal segments. The integrity of
the endoneurial tube (schwann cell basal lamina) is maintained,
In third-degree injury, the axons and endoneurial tubes are disrupted, but the perineurium is
reserved. The result is disorganization resulting from disruption of the endoneurial tubes
regeneration
In fourth-degree injury, the axon and endoneurium are disrupted, but some of the epineurium
and possibly some of the perineurium are preserved, so complete severance of the entire trunk
does not occur.
In fifth-degree injury, the nerve is completely transected, resulting in a variable distance between
the neural stumps. These injuries occur only in open wounds and usually are identified at the
time of early surgical exploration.
Sixth-degree (mackinnon) or mixed injuries occur in which a nerve trunk is partially severed, and
the remaining part of the trunk sustains fourth-degree, third-degree, second-degree, or rarely
even first-degree injury.

Q28. What is motor march?

A. In recovering phase there is a proximal to distal recovery of muscles.

Q29. Define autonomous intermediate and maximus zone?

A. After severance of a peripheral nerve, only a small area of complete sensory loss is
found. This area is supplied exclusively by the severed nerve and is called the autonomous or
isolated zone of supply for that nerve.
A larger area of tactile and thermal anesthesia is readily delineated and corresponds more
closely to the gross anatomical distribution of the nerve this larger area is known as the
intermediate zone.
When a nerve is intact, and the adjacent nerves are blocked or sectioned, an area of
sensibility exceeds the gross anatomical distribution of the nerve; this area is known as the
maximal zone

Q30. Which is the first returning sensation after nerve repair?

A. 2 point discrimination
Q31. What are the methods by which you close the gap between nerve endings?
A. 1. Mobilisation
2. Joint positioning
3. Bone shortening
4. Transposition
5. Nerve grafting
6. Pedicle grafting
7. Nerve stretching

Q32. Types of nerve repair?

A. Endoneurolysis
Neurorraphy- Epiperineurorraphy
Epineurorraphy
Partial neurorraphy

Q33. What is Erbs point?

A. Also called punctum nervosum formed by the union of c5 and c6 nreve roots which later
converge.at the nerve trunk,branches of suprascapular nerves and the nerve to the subclavus also
merge.the merged nerve then divides into ant and post divisions of c5 and c6,it is located at the
lateral root of brachial plexus located 2-3 cm above the clavicle.altogether 6 types of nerves
merga at this point.

Q34. How will you differentiate between preganglion and postganglion lesions?
A. Post ganglionic lesions will not give a positive flare with histamine that is axon reflex is
absent.
Long tracts,dorsal scapular nerve and long thoracic nerve of bell are involved in
preganglionic lesions.

43…Footdrop
Clinical Approach

 Bilateral
 LMN
 Peripheral neuropathy
 UMN
 Cord lesion
 Unilateral
 Once dorsiflexion impaired
 Check eversion (dorsiflexion + eversion = Common peroneal nerve)
 Check inversion and plantarflexion (= posterior tibial nerve)
 If foot drop and inversion + eversion is lost with normal plantarflexion = L5 nerve root
 If all gone = posterior tibial + common peroneal, sciatic nerve or plexus/roots
 Knee flexion intact
  Go to sensory
 Peripheral neuropathy
 Common peroneal nerve palsy (sensory loss over dorsum of the foot)
 Determine if common peroneal nerve or
 Deep branch only or
 The superficial branch only
 If knee flexion weak, test hip abduction and internal rotation and intact
 Go to sensory
 Sciatic nerve
 If hip abduction and internal rotation is weak
 Go to sensory
 Nil = anterior horn cell
 L4 and L5 dermatome = plexus or root
 Sciatic nerve (L4 L5 S1 S2 S3)
 Weakness of the knee flexion also
 Knee jerk is intact but ankle jerk is affected and plantar response absent (for common
peroneal nerve, all reflexes intact)
 L5 nerve root
 Weakness of hip abduction and internal rotation as well as loss of foot inversion

 Once site is located, go for the cause (see later)

Anatomy
 Sciatic nerve (L4, L5, S1, S2, S3) divides at the popliteal fossa into the Tibial (L4, L5, S1, S2, S3
) and Common Peroneal nerves (L4, L5, S1 & S2)
 The posterior tibial nerves supplies plantar flexors and invertors of the foot
 The common peroneal nerves winds round the neck of the fibula; is covered by s/c tissue
and skin only; and prone to extrinsic compression
 It then divides into the
 Superficial branch: foot everters and sensation to lateral calves and dorsum of the foot
 Deep branch : toe dorsiflexors and dorsiflexion of the ankle and sensation to the first
interdigital web space
 Therefore wasting of the peroneous and anterior tibialis muscles; weakness of
dorsiflexion of the foot and eversion; foot drop and high steppage gait and loss of
sensory over the lateral aspect of the calf and dorsum of the foot

 Causes
 Trauma - # lateral condyle of tibia, fibular neck fracture
 Surgical – post THR, TKR (patients with spinal canal stenosis are more prone ~ “Double
Crush hypothesis”; proximal insult diminishes axoplasmic flow)
 Compression at the neck of the fibula (habitual leg crossing, cast, brace)
  Infection – Leprosy (cooler parts of the body, attacks schwann cells), poliomyelitis
(muscles supplied by shorter column are more subjected to permanent paralysis; Tibialis
anterior is commonly affected in polio)
 Inflammatory – CIDP
 Ischaemic - Vasculitis
 As a part of mononeuritis multiplex (Endocrine, Autoimmune, infection, infiltrative and
cancer)
 Exogenous toxins (lead, mercury, arsenic)

At the end of history taking, the examiner should be able to identify whether foot drop is due
to trauma, post surgical, infective or inflammatory origin.

 Key muscle testing

 Tibialis anterior – dorsiflexion of the ankle joint and inversion of the foot without
extension of great toe
 Tibialis posterior – inversion of foot with plantar flexion of ankle joint
 Peroneus longus – eversion of foot with plantar flexion of ankle joint
 Biceps femoris – flexion of knee between 500 – 700 with thigh in slight lateral rotation
and leg in slight lateral rotation on the thigh.
 Semimembranosus – flexion of knee between 500 – 700 with thigh in medial rotation
and leg medially rotated on the thigh

 Investigations- NCS and EMG

 Mgmt-
 Conservative – static or dynamic splint
 Surgery – If joint supple, tendon transfer.
If joint not supple, arthrodesis

 Named tendon transfers

 Barr’s technique of anterior transfer of Tibialis posterior
 Ober’s technique of anterior transfer of Tibialis posterior
 Kaufer – split transfer of Tibialis posterior tendon
 Srinivasan’s technique – two tailed transfer of Tibialis posterior
 Appendix

EXAM CASES
HIP CASES
Non union neck of femur
Malunited trochanteric fracture
Neglected dislocation hip (traumatic, paralytic )
Unstable hip
Post traumatic protrusion acetabulum ( central fracture dislocation hip)
Post traumatic Myositis ossificans
Perthes disease
SCFE
Avascular necrosis femoral head
DDH /CDH
Chondrolysis hip
Congenital coxa vara
Sequelae septic arthritis hip / infectious sequelae
TB hip
Synovitis hip
Osteoarthritis hip ( secondary common, primary rare)
Rheumatiod arthritis / juvenile RA
Ankylosis spondylitis
Fibrous ankylosis
Bony ankylosis
Multiple epiphyseal dysplasia
Spondyloepiphyseal dysplasia
Proximal focal femur deficiency
Benign and malignant tumours ( osteochondroma, aneurysmal bone cyst, secondaries,
osteosarcoma, chondrosarcoma…)

SPINE CASES:
TB spine/ infection with neurological deficit
IVDP with neurological deficit (foot drop, bowel bladder deficit, abductor weakness)
Scoliosis (congenital, idiopathic), kyphoscoliosis

SHOULDER CASES:
Neglected dislocation shoulder
Recurrent / habitual dislocation shoulder
TB shoulder / post infectious sequelae
Brachial plexus palsy
Deltoid contracture
Nonunion humerus with nerve palsy
Postpolio residual palsy (PPRP)
Tumours (benign- bone cysts/ osteochondroma/ GCT….. malignant – osteosarcoma/
chondrosarcoma/ secondaries/ GCT)
Syringomyelia

ELBOW CASES:
Cubitus varus /valgus
Malunited supracondylar fracture / intercondylar fracture
Post traumatic stiff elbow
Malunited Monteggia
Nonunion lateral condyle
Neglected dislocation elbow
Unreduced radial head
Myositis ossificans
Radioulnar synostosis
TB elbow / post infectious sequelae
Sequelae side sweep injury
Tardy ulnar palsy
Volkman ischemic contracture
Tumours

WRIST & HAND:

Compound palmar ganglion
Synovitis /arthritis wrist
Keinbock’s disease
Scaphoid nonunion
Madelung’s deformity
Dupuytren’s contracture
TB wrist / spina ventosa
DRUJ instability/ carpal instability
Claw hand
Malunited # lower end radius
Rheumatoid hand
Carpal tunnel syndrome
Wrist drop
Radial club hand
Pseudo madelungs deformity ( multiple ostoechondromatosis)
Post traumatic stiff/ deformed hand with multiple tendon / nerve injury
Tumours ( GCT lower end radius, enchondroma)

KNEE & LEG CASES:

Ligament/menisci injuries
Recurrent/ habitual /congenital patellar dislocation
Genu varum/valgum / recurvatum
Blount’s disease
Anterolateral bowing leg ( congenital pseudoarthrosis tibia)
Postero medial bowing leg
Chronic synovitis knee
Pigmented villonodular synovitis
Meniscal cyst
Discoid meniscus
TB knee
Neuropathic joint
Quadriceps contracture
Cystic lesions around knee – Baker’s, bursae, ganglion
Synovial chondromatosis
Post traumatic stiff /ankylosed knee
Malunited upper tibia/ lower femur with unstable knee
Chronic osteomyelitis tibia /femur
Infected nonunion leg
Malunited both bones leg
Post polio sequlae
Volkman’s Ischemic Contracture leg
Tumours (osteochondroma, osteosarcoma, GCT,chondrosarcoma, synovial sarcoma,
fibrosarcoma)
FOOT & ANKLE :
AVN talus
Neuropathic ankle
Neglected CTEV
Chronic osteomyelitis calcaneum
Post polio ankle foot
Malunited ankle fracture with ankle arthritis
Chronic synovitis (TB ankle)
Unstable ankle
Flat foot
Cavus / cavovarus foot
Tarsal tunnel syndrome
Foot drop
Sequelae compartment syndrome

GENERAL TOPICS
Nerve injuries ( radial, median, ulnar, sciatic, common peroneal nerve, brachial plexus, leprosy)
Pseudoarthrosis
ITB contracture
Chronic osteomyelitis
Epiphyseal / Metaphyseal dysplasias
Dwarfism
Cerebral palsy
Polio
Osteogenensis imperfecta
Sickle cell disease

SOME WARD ROUND TIT BITS

Dressing materials are of two types
BASIC
Gauze, Gamgee
Bandages
Elastic Bandages
Elastic Adhesive
Silastic Gauze:
Transparent
Does not get wet
Autoclavable
Porous
SPECIALIZED
Vaseline Gauze
Framycetin medicated gauze(Sofratulle)

TOPICAL AGENTS USED FOR DRESSING

ANTISEPTIC AGENTS
1. Spirit
2. Savlon
3. Dettol
4. Chlorhexidine

ANTIBIOTIC AGENTS
1. Silver sulphadiazine
2. Povidone-iodine ointment( betadine)
3. Nitrofurazone ointment( furacin)
4. Framycin sulphate cream ( soframycin)
5. Neomycin, polymyxin and bacitracin combination ( neosporin)
6. Gentamycin

DESLOUGING AGENTS
1. Eusol
2. Salutyl ointment:
3 Alum
4. Magnesium sulfate
5. Debrisan granules
7. 1% zinc sulfate solution

GRANULATING AGENTS
1. Oxeferrin
2. Placentrex
HYGROSCOPIC AGENTS
To reduce surrounding edema
( eg: Glycerine, Magsulf)
CLEANSING AGENTS
Hydrogen peroxide

POVIDONE-IODINE ( BETADINE)
Products available: POVIDONE-IODINE ( 5% & 10 %), Surgical scrub ( 7.5% w/v), ointment
Properties & Effects:
-Iodine useful germicide- effective against bacteria, viruses, fungi, protozoa and yeast.
- Disadv: insolubility, instability, irritant & staining properties.
- these undesirable qualities eliminated by combining with polyvinyl pyrrolidone (
povidone)- organic polymer which is water-soluble
- combination leads to complex formation- Polyvinyl Pyrrolidone Iodine
( Povidone- Iodine) having bactericidal activity of iodine without its toxic effects

SAVLON
Composition:
 Chlorhexidine Gluconate 7.5 % V/V
Cetrimide 16%
Isopropyl alcohol 6.8 % v/v
Colour: Tartrazine ( yellow)
Properties and effects: Germicide & Detergent
Dilution: 1: 30 aqueous solution- 35 ml savlon in 1 ltr. of water- used for orthopaedic purposes
Uses: Cleaning and disinfection of dirty wounds where extra detergents are required.

HYDROGEN PEROXIDE
COMPOSITION: 20 VOL. H2O2 ( one vol. 20-vol. h2o2 releases 20 vol. of nascent oxygen)
EFFECTS: Not an antiseptic but a cleansing agent
MECHANISMS AND USES:
1. Destroys Anaerobic Organisms- Thus used for wounds infected or contaminated
with anaerobes.
2. Produces frothing and thus brings out debris from depth of wound.
3. Produces heat on tissue contact and thus prevents capillary oozing- hence used as
haemostatic agents sometimes eg: after I & D
4. Used in removing blood stains from clothings.

EUSOL ( Edinburg University Solution) B.P

COMPOSITION:
1.25 gm Boric Acid
1.25 gm Bleaching Powder (Chlorinated Lime)
Sterile water upto 100ml
# EUSOL should be prepared & used fresh everyday.
MECHANISM: release of nascent chlorine
Uses:
1. To separate slough from infected wounds, bed-sores and ulcers and burns.
2. Acidic in pH and thus useful for drtessing of wounds infected with Pseudomonas

SPIRIT
COMPOSITION: Alcohol. ( Optimum Conc. Of 70 % alcohol highly effective)
USES:
1. Removal of Iodine in preparation of skin in operatiopn
2. Cleaning the stitched wound.
3. Cleaning the surrounding skin of ulcer or open wounds
4. Used along with other disinfectants like savlon and betadine for painting parts
before surgery.

DRY/ WET DRESSING

DRY DRESSING: Wound without granulation
WET DRESSING: Ulcer with granulation eg. Eusol, Betadine

DRESSING BAG
Blue in colour
Contents
i.Plain forceps
ii. Cotton swabs
iii.Gauze pieces
iv. Pad
v. Bandage
vi. Artery forceps
Sterilization- autoclaving

STITCH REMOVAL BAG

Green in colour
Contents
i. Tooth forceps
ii. Stitch removal scissors
iii.Blade
iv. Sinus forceps
Sterilization- Autoclaving
INSTRUCTIONS FOR WOUND DRESSING
Wash hands thoroughly before & after use
Instruments used for dressing should be sterilized
Use instruments for one dressing only
Clean wound from centre to periphery
Take utmost care for preventing cross-infection
Isolate wound by spreading sterile towels
Wound and drain area should be dressed separately
If dressing is stuck to wound, it should be made wet by pouring savlon/ normal saline.
 IMPORTANT THEORY TOPICS
CONGENITAL

1. KRUKENBERG’S operation
2. Congenital absence of thumb
3. Congenital coxa vara
4. Proximal femoral focal deficiency
5. Pathological anatomy in CDH at birth, 5yrs, methods of assessing these
abnormalities.
6. Cong club foot pathological anatomy at 7 days, 4yrs, 14yrs .How would you
manage?
7. Sprengels shoulder.
8. Congenital Pseudo arthrosis oftibia.
9. Neglected CTEV
10.Radial Hemimelia
11.Osteogenesis imperfect-clinical features, Inv, Rx
12.Components of deformity in CTEV-discuss Mx of this condition up to the
age of 7 yrs. Diagnostic features of CDH at birth and during first year of life.
Role of Saltesis osteotomy.
13.Rigid club foot.
14.Pes cavus.
15.Congenital vertical talus.
16.Congenital pseudo arthrosis of tibia- Newer methods of Mx
17.Klippal Feil ssyndrome.
18.Madelungs deformity.
19.Fibular hemi Melia.
20.Pes Planus.
 BASICS, METABOLISM, GENERAL ORTHO

1. Renal rickets.
2. Osteomalacia.
3. Prophylactic antibiotic in orthopedic surgery.
4. Bacteraemia, Septicaemia, Pyemia, Toxicemia with illustration.
5. Osteopetrosis.
6. Electrical properties of bone.
7. SCURVY.
8. Crystal Synovitis.
9. Disturbances of uric acid metabolism.
10.NSAIDS in RA Disorder.
11.Myositis Ossificans Traumatica.
12.Hyper parathyroidism.
13.BRODIES ABSCESS.
14.MRI in Orthopaedics.
15.Autosomal dominant inheritance -10 common disorders.
16.Role of parathormore in mineral metabolism.
17.Changes that occur in the Morphology of articular cartilage in degenerative
joint diseases.
18.Role of PYRAZINAMIDE in Orthopaedic practice.
19.Role of bone scan in orthopaedic practice.
20.What is bone mass- How it is affected in senile osteoporosis and in
osteomalacia.
21.Traumatic myositis ossifications pathogenesis.

TUMORS

1. Recent advances in the Mx of EWINGS sarcoma

2. Osteoid osteoma
3. Osteochondroma
4. Histological grading in giant cell tumor & its merits & demerits in Mx.
5. Aggressive fibromatosis
6. Chondroblastoma
7. Secondary Tumours of bone.
8. Osteochondromatosis
9. Eosinoptritic granuloma
10.Glomus tumour
11.Neuro fibromatosis in orthopaedics
12.Classify bone tm & discuss the technique of limb conservation malignant
bone tumour.
13.Discuss the tumour for primaries in a patient having secondary metastasis
in the lower dorsal vertebrae
14.What is a giant cell. What are its characteristics in common orthopaedics
condition.
15.Causes of pathological # & their management
16.Aneurismal bone cyst.
17.Cl. Features, Inv, treatment of multiple myeloma
18.Parosteal ossteosarcoma
19.Describe Rx of giant cell tumour.
20.FIBROMATOSIS
21.Diagnostic aids in myelomatosis
22.Chondromyxoid fibroma
23.Giant cell variants
24.Pigmental villonodular synovitis
25.Diagnosis and Mx of Osteoid osteoma
26.Metastatic lesions of bone its inv & Mx
27.Myositis ossificans progressive

28.CHORDOMA

1. Mx of post operative wound sepsis, modern drugs in orthopaedics fracture.

2. Postoperative anesthesia.
3. Volkmanns Ischaemic contracture Eliopathology.
4. Vitamin D resistant rickets.
5. Microscopic pathological fracture in tubercle in TB.
6. Modular prosthesis.
 7. Etiopath anatomy and Mx of INFANTILE rickets.
8. SUDECKS Osteodystrophy.
9. Discuss in detail the characteristics of synovial fluid and the role it plays in
the diagnosis of common joint disordes.
10.Vitamin D
11.Reflex sympathetic dystrophy syndrome.
12.Osteogenesis Imperfecta.
13.Pathophysiology and Mx of gram negative septicaema in a patient with poly
trauma.
14.Clinical features, Epidemiology, radiological features, Investigations,
medical management of crystal induced arthritis.
15.Actiology clinical features, investigations, management including
antimicrobial therapy in adult SEPTIC ARTHRITIS.
16.Myositis ossificans progressiva.
1. Crush syndrome.
2. Management of severe RTA with emphasis on priority of Rx.
3. Pathology of pyogenic chronic osteomyeltis.
4. Implant failure- causes and management.
5. Role of an orthopaedic surgeon as the team leader during a major train
accident.
6. Measures to prevent infections in open fracture.
7. Types of skin grafting.
8. Structure to PERIOSTEUM and what is its role in health, injury and diseases
of bone.
9. Fat Embolism, etio, pathjological, clinical features and management.
10.Endotoxic shock.
11.Compartment syndrome.
12.Non specific synovitis.
13.Interferone Therapy.
14.Blood salvage techniques.
15.Role of radionucleotide scanning in Orthopaedics.
 SPINE

1. Idiopathic scoliosis.
2. Cervical spondylosis.
3. Pressure sores.
4. Describe mechanism of injury to the dorsal spine junction, current concepts
in the stabilization of spinal injuries- discuss.
5. AUTOMATIC urinary bladder.
6. Thoracic outlet syndrome.
7. Caudaequina syndrome.
8. Classification and Mx of the injuries of the ATLAS & AXIS.
9. Anatomy of atlanto axial joint. Principal of Mx of fracture of adontoid
process.
10.Types of fracture healing.
11.Reflex bladder in paraplegia.
12.C.F, pathological anatomy of spine Bifida
13.Basic care of paraplegia
14.Neurological findings- transaction of cord at D6
15.Neurogenic bladder
16.Enumerate the causes of failed lumbar Disc Surgery and Rx.
17.Describe the biomechanics of dorsolumbar spine & classification of injuries
at this region
18.Conservative Mx of cervical spondylosis
19.Fracture ATLAS
20.Innervations of urinary bladder.
21.Etio, Patho, Mx of spinal canal stenosis
22. Cord bladder
23.Psoas abscess
24.IDIOPATHIC SCOLIOSIS Mx.
25.Halopelvic traction
26.Halotraction device
27.Lumbar canal stenosis.
28.Automatic bladder
GENERAL SURGERY
1.Pathogenesis,management o f the lower limbs in diabetes mellitus

2.management of diseases of the lower limb in diabetes mellitus

3.abdominal complications of orthopaedic procedure

4.symes amputation

5.effects of thyroid on bone

6.peripheral vascular disease

7.thoracic outlet syndrome

8.madura foot

9.stove in chest

10.etio pathogenesis management of gas gangrene

11.dd,management of lump in riht iliac fossa

12.ARDS

13.ideal amputation stump

14.management of DVT,what is its basic pathology

15.pathology,clinical factors,etiology and management of TAO

16.what is paralytic ileus,treatment

17.what is thrombophlebitis and phlebothrombosis.how will you prevent and treat these conditions in
orthopaedics

18.central venous pressure

19.tension pneumothorax

20.phantom limb

21.claassify acute vascular occlusion of lower limb.discuss its clinical features including management
FRACTURES

1.osteochondral fractures

2.classification of ankle injuries

3.bartons fracture

5.non union of fracture

6.classification of tibial condyl fractures and their management

7.callotasis,bone transplant

8.montaggia fracture dislocation

9.external fixation of pelvic fractures

10.locked IM nail-principles

11.tension band principle and its application

12.distraction osteosynthesis

13.fracture of neck of talus

14.traction as a method in treatment of fractures

15.management of fracture NOF 3 month old in 35 year old man

16.fracture scaphoid

17.bennets fracture.

18.types of fracture healing

19.biomechanical principles of ring fixators and their application in orthopaedic trauma care

20.complications of fracture calcaneum and their management

21.biology of natural healing at cellular level of fracture of tubular bone in wound

22.biomechinics of lag screws and its application in trauma

23.tendo Achilles rupture

24.tarso metatarsal dislocation

25.non union fracture scaphoid

26.describe in detail the process of healing of fracture under stable condition in a cortical bone
27.discuss carpal instability and management

28.use of external fixator in fracture management

29.jones fracture

30.fracture acetabulum

31.classify fracture of pelvis,discuss the mechanism of injuries of pelvis and their management

32.lisfrancs fracture dislocation

33.classify dislocation of the hip joint

34.classify fracture of os callus

35.dislocation of MPJ of thumb

36.acromioclavicular dislocation

37.fracture lateral condyl of humerus

38.stress fracture

39.cause of non union in intra capsular fractures of NOF,how could you manage a case of subcapital
fracture NOF in 35 year old patients

40.biological fixation

41.classify fracture around ankle,describe the mode of such injuries and discuss their managemnt

42.intra articular fracture

Paediatric injuries and infection

1.epiphyseal injuries

2.lower tibial epiphyseal injuries type V

3.histology of PHYSIS and mention the factors that cause derangements of its growth

4.aseptic necrosis following fracture neck of children in children

5.battered child syndrome

6.Clinical ,investigation methods in early diagnosis of septic arthritis of the hip in infancy

7.problem of femoral neck fracture in children

8.fracture neck of femor in children

9.transient synovitis of the hip

10.classification of epiphyseal plate injuries

FOOT AND ANKLE

1.hallux valgus

2.calcaniovalgus deformity

3.arches of foot_anatomy of normal,give rationale of pathological condition resulting from their

abnormalities

4.clinical features,treatment of hallux valgus in adult patient

5.talo calcaneal bar

KNEE,PATELLA

1.anterolateral rotational instability of the knee

2.chandromalacia patella

3.pigmented villo nodular synovitis

4.ACL injury

5.clinical features,treatment of osteoarthritis knee

6.rotatory instability of the knee

7.Discoid meniscus

8. Osgood-Schlatter Disease
9.management of triple deformity of the knee in TB

10.osteochondritis dessicans

11.total condylar knee

12.genu recurvatum

13.biomechanics of malalignment of the knee joint and its role in regenerative arthropathy

14.blounts disease

HIPS

1.AVN of the femoral head in adults

2.old unreduced dislocation of the hip

3.pathogenesis clinical features and managenment of perthes disease

4.biomechanics of the normal hip joint and its role in total hip replacement

5. trendlenbergs gait

6.etiopathology of SCFE diagnosis and management

7.osteonecrosis of the femoral head

8.trendlenbergs test

9.anatomical basis of trendlenbergs gait

10.pathology and treatment of AVN of head of femur

11transient synovitis of the hip

12. perthes disease-pathological changes

13.blood supply of femoral head

14.abductor mechanism of the hip

15.TOM SMITH’S ARTHRITIS

16.discuss failure factos in implant surgery.write in short the management of failed austin moore
athroplasty

17.head within head phenomenon

18.ideal implants for THR

SHOULDER AND ELBOW

1.rotator cuff injuries

2.posterior dislocation of the shoulder

3.FROZEN shoulder

4.pathological antomy and treatment of anterior dislocation of shoulder

5.role of physiotherapy in the management of FROZEN SHOULDER

6.what is BANKARTS lesion?describe different steps of bankarts operation for recurrent dislocation of
shoulder

7.discuss pathological anatomy and management of rec. dislocation of shoulder

8.rotator cuff tendinitis

9.painful arc syndrome

10.cubitus varus

11.sprengel shoulder

12.klipper feil synovitis

13.cubitus valgus

14.cubital tunnel syndrome

HAND

1.trans scapulo peri lunate dislocation of the wrist

2.free tendon grafting

3.dupuytrens contracture
4.pathogenesis of rheumatois hand

5.intrinsic plus finger

6.ulnar claw hand

7.placement of incision in hand surgery

8.tendon transfer opponens palsy of thumb

9.compound palmar ganglion

10. Boutonniere deformity …and management

11.intrinsic minus hand

12.opponens palsy

13.trigger thumb deformit

14.trigger finger

PROSTHESIS

1functional bracing of factures

2.ROLE of CPM in joints and their pathological basis

3.SACH FOOT

4.above knee prosthesis

5.various kind of exercises forn an adult with LBA resulting from prolapsed disc syndrome including their
rationale

6.orthosis fo foot drop

7.orthosis for calcanio valgus

8.vo frozen splint

9.russel traction

10.cock up splint

11.jaipoor foot
12.electrical stimulation of ms

13.radial nerve injury various orthosis

14.cast bracing

15.microwave diathermy

16.newer concepts in orthopaedic braces

17.pavliks harness

MISCELLANEOUS TOPICS
1. Cementing techniques
2. Limb salvage in Osteosarcoma
3. Biological agent in Rheumatoid arthritis
4. Total shoulder replacement
5. Double bundle ACL reconstruction
6. Local antibiotic delivery system
7. Safe surgical dislocation of hip
8. Custom mega prosthesis
9. Ceramics in orthopaedics
10. Stem cells in orthopaedics
11. Joint lubrication
12. Isotope bone scan
13. Zolendronic acid
14. Bone cement
15. Proximal femoral nail
16. Bearing surfaces in THR
17. Image intensifier in orthopaedics
18. Lasso procedure
19. Immuno assay in skeletal infections
20. Aseptic loosening of prosthesis
21. Femeroacetabular impingement
22. Bioabsorbable implants
23. Neoadjuvant chemotherapy
24. Bone substitutes
25. Bone bank
26. Floor reaction orthosis
27. Guided growth
28. Biological fixation
29. Damage control orthopaedics
30. Viscosuplimentation
31. Evidence based orthopaedics
32. Cement disease
33. Biofilm
34. Total elbow replacement
35. Single event multilevel surgery in CP
36. Continuous passive motion
37. Vertebroplasty
38. Disc replacement
39. High tibial osteotomy
40. Piezoelectricity in orthopaedics
41. Ligamentotaxis
42. Somatosensory evoked potential
43. Low temperature thermoplastics
44. Hoopstress
45. Slap lesion
46. Computer navigated arthroplasty
47. Percutaneous discectomy
48. Unicompartmental knee replacement
49. Extracorporeal irradiation
50. Tissue expanders
51. Hydroxyapetite coating
52. Laser in orthopaedics
53. Glycocalyx
54. Ulnar drift
55. Endoscopic CTS release
56. ILN in humerus
57. Bone marrow edema syndrome
58. Osteitis condensans ilii
59. Discography
60. Autologous chondrocyte implantation
61. Far out syndrome
62. Laser discectomy
63. Stress shielding
64. Bone morphogenic protein
65. Articular cartilage replacement
66. Nerve conduction study
67. Ulnar drift
68. Nano technology in tumour treatment
69. Clean air system in OT
70. Text message injury
71. Artificial disc
72. Liss plate
73. Hybrid total hip arthroplasty
 PATH FINDER
PREVIOUS YEARS QUESTION PAPERS OF KUHS, CALICUT AND KERALA
UNIVERSITIES FOR ORTHOPAEDICS
 PREFACE

While we were doing our post graduation we had always wondered how we were
going to get through the initial step to success --theory exams. It was after a bit of scare after
seeing how much we had to study in such a short time towards the end of our pg that we got
our hands on some previous years question papers.

We noticed that there was repetitions and decided to study them well. But the one
thing we felt the lack of was a book that was in an orderly manner and with some tip from
where we could find the answers from. We are not claiming this book has all that, but it is the
closest to our dream book which we felt was missing in the pg students armamentarium.

We hope "PATH FINDER" will help you get an idea of the questions oft repeated and
the pattern of the examiners when preparing theory questions.

This book has been divided into sections for different question papers so that
revision is quite easy towards the last precious days. Some questions have tips from where it
can be read from best, although they may be present in books that may have missed us.
Various books have been followed while making those tips (refer section 10). Kindly do let us
know of corrections and suggestions so that later editions can be made better.

We are of the opinion that this book should be used only in the last few weeks of
exam preparation and that wide knowledge of Orthopedics is necessary for a better future. It
is this thought that helped both of us get the top marks in last year's KUHS exam rather than
studying only question papers for theory papers. Having said so we also agree that going
through the question papers of the last 5 years will surely fetch you enough marks to make it
comfortably through the KUHS theory exams.

This book would not have seen the light of the day had it not been for our friend
Dr. Thomas Angelo who provided us with the bulk of the question papers.

Our deepest appreciation goes to our supportive spouses and kids, who endured our struggles
with grace and humor.

We are greatly indebted to our teachers, colleagues and juniors of three great institutions who
provided us the motivation and support for coming out with such a venture- Calicut govt
medical college , Trivandrum govt medical college and Jubilee mission medical college,
Thrissur.

Dr. ASIF KASSIM

Dr. RAHUL MOHAN

 SECTION 1

KUHS QUESTIONS (2012-2014)

MS ORTHO PAPERS (1-4)

 JUNE 2012 ( MS ) JUNE 2012 ( MS )

PAPER I PAPER II

ESSAY 20 MARKS ESSAY 20 MARKS

1. DESCRIBE THE EXTENSOR MECHANISM OF 1. EXPLAIN THE BIOMECHANICS OF THORACO

KNEE JOINT. LUMBAR SPINE.

DISCUSS THE AETIOLOGY, DIAGNOSIS AND CLASSIFY AND DISCUSS ABOUT MANAGEMENT

MANAGEMENT OF RECURRENT DISLOCATION OF THORACO SPINE INJURIES.

OF PATELLA.

SHORT ESSAYS (8 X 10=80 MARKS)

SHORT ESSAYS (8 X 10=80 MARKS)

2. GROWTH PLATE ANATOMY AND ITS

2. RECURRENT DISLOCATION OF SHOULDER
FUNCTIONS ( DAV PART 1 GENERAL L/3RD )
3. PUBIC DIASTASIS
3. DIFFERENTIATE BETWEEN OSTEOPENIA AND
OSTEOPOROSIS 4. DUNLOP TRACTION-STEWART

4. GLASGOW COMA SCALE-ZUKERMAN 5. MC MURRAY’S OSTEOTOMY

5. METHOTREXATE 6. LOCKED COMPRESSION PLATE

6. ADULT RESPIRATORY DISTRESS SYNDROME 7. NEGLECTED TENDOCALCANEUS INJURY

7. TRANSFUSION REACTIONS 8. ODONTOID FRACTURE

8. TYPES OF BIOPSY 9. CRUTCH GAIT

 JUNE 2012 ( MS ) JUNE 2012 ( MS )

PAPER 3 PAPER 4

ESSAY 20 MARKS ESSAY 20 MARKS

1. DEFINE OSTEOPOROSIS, DISCUSS ABOUT 1. WHAT IS OSTEOSYNTHESIS

CLINICAL FEATURES, CAUSES AND
DESCRIBE WAYS TO ACHIEVE OSTEOSYNTHESIS
MANAGEMENT OF GENERALIZED
IN TREATMENT OF FRACTURE WITH RECENT
OSTEOPOROSIS
ADVANCES

SHORT ESSAYS (8 X 10=80 MARKS)

SHORT ESSAYS (8 X 10=80 MARKS)

2. CHORDOMA ( CAMPBELL - MALIGNANT

2. BEARING SURFACES IN TOTAL HIP
BONE TUMOURS)
REPLACEMENT KULKARNI 3702
3. ARTHROGRYPOSIS MULTIPLEX CONGENITA
3. ZOLENDRONIC ACID
(CAMPBELL VOL2; NEURVOUS SYSTEM
DISORDERS IN CHILDREN) 4. TUMOUR MARKERS

4. CONGENITAL PSEUDOARTHROSIS OF TIBIA 5. FEMERO ACETABULAR IMPINGMENT

5. HALLUX VALGUS, CAMPBELL FOOT AND 6. BONE CEMENT GOPALAN 672

ANKLE, DISORDERS OF HALLUX
7. DEXA SCAN GOPALAN PG 282
6. DOTS REGIME FOR TUBERCULOSIS
8. PROXIMAL FEMORAL NAIL
7. SOLID ANKLE CUSHION HEEL FOOT
9. POST OPERATIVE DVT- PREVENTION ,
KULKARNI 3941
CLINICAL FEATURES AND MANAGEMENT.
8. VERTEBRA PLANA

9. ULNAR CLAW HAND

 MAY 2013 ( MS ) MAY 2013 ( MS )

PAPER 1 PAPER 2

ESSAY 20 MARKS ESSAY 20 MARKS

1. DISCUSS BRIEFLY THE BLOOD SUPPLY OF 1. EXPLAIN THE ANATOMY OF BRACHIA!

TALUS. (CAMPBELL, FRACTURES AND PLEXUS.
DISLOCATION OF FOOT)
CLASSIFY AND DISCUSS IN DETAIL THE
DESCRIBE IN DETAIL CLINICAL FEATURES, MANAGEMENT OF BRACHIA! PLEXUS INJURY.
CLASSIFICATION AND MANAGEMENT OF TALUS
FRACTURE
SHORT ESSAYS (8 X 10=80 MARKS)
SHORT ESSAYS (8 X 10=80 MARKS)

2. SCAPULAR FRACTURE
2. VITAMIN D RESISTANT RICKETS.
3. PCL DEFICIENT KNEE
TACHDJIAN CH 32 (METABOLIC&ENDOCRINE
DISEASES) 4. SCAPHOID NON UNION

3. HYALINE CARTILAGE TUREK 5. DAMAGE CONTROL IN ORTHOPAEDICS

4. JOINT LUBRICATION TUREK CH 7 6. CHANCE'S FRACTURE

PHYSIOLOGY OF CARTILAGE
7. AUTOMATIC BLADDER
5. DVT PROPHYLAXIS
8. JUMPER'S KNEE
6. DUCHENNE MUSCULAR DYSTROPHY
9. MALGAIGNE FRACTURE
7. DISCOID MENISCUS (CAMPBELL ; CH-
ARTHROSCOPY OF LOWER EXTREMITIES)

8. HAMILTON RUSSEL TRACTION - STEWART

9. MYOSITIS OSSIFICANS
 MAY 2013 ( MS ) MAY 2013 ( MS )

PAPER 3 PAPER 4

ESSAY 20 MARKS ESSAY 20 MARKS

1. DISCUSS THE PATHOGENESIS , CLINICAL 1. DESCRIBE THE ETIOLOGY, MODERN

FEATURES AND MANAGEMENT OF DIAGNOSTIC METHODS, PREVENTION AND THE
TUBERCULOSIS OF SPINE WITH PARAPLEGIA. VARIOUS MANAGEMENT METHODS FOR
OSTEOPOROSIS

SHORT ESSAYS (8 X 10=80 MARKS)

SHORT ESSAYS (8 X 10=80 MARKS)

2. RADIOLOGICAL FEATURES OF PERTHES

DISEASE 2. POSITRON EMISSION TOMOGRAPHY

3. SPINA VENTOSA- TULI 3. BONE BANKING KULKARNI 1137

4. FOOT DROP 4. METHICILLIN - RESISTANT STAPHYLOCOCCUS

AUREUS
5. CHONDROCALCINOSIS
5. FLOOR REACTION ORTHOSIS
6. MENISCAL CYST (CAMPBELL ; CH-
ARTHROSCOPY OF LOWER EXTREMITIES) 6. ENDOSCOPIC DISC SURGERY

7. MULTIPLE MYELOMA 7. LMMUNO MODULATORS IN RHEUMATOID

ARTHRITIS
8. SEVER'S DISEASE
8. BIO ABSORBABLE IMPLANTS (CAMPBELL
9. MYOSITIS OSSSIFICANS PROGRESSIVA
,GENERAL PRINCIPLES OF FRACTURE
TREATMENT; BIOMECHANICS)

9. CHEMOTHERAPY FOR OSTEOSARCOMA

 MAY 2014 ( MS ) MAY 2014 ( MS )

PAPER 1 PAPER 2

ESSAY 20 MARKS ESSAY 20 MARKS

1. DISCUSS THE HEALING OF FRACTURES. HOW 1. CLASSIFY THE LATERAL CONDYLE FRACTURES
WILL YOU MANAGE INFECTED NON UNION OF OF HUMERUS IN A CHILD.

FRACTURE SHAFT OF FEMUR IN A 20 YEARS OLD DISCUSS THE CLINICAL FEATURES,

MALE. MANAGEMENT AND COMPLICATIONS OF THIS
FRACTURE IN A FIVE YEAR OLD CHILD
SHORT ESSAYS (8 X 10=80 MARKS)
SHORT ESSAYS (8 X 10=80 MARKS)

2. ISOTOPE SCAN IN DIAGNOSIS OF BONE

INFECTIONS (KUL 1 - 155),CAMPBELL, 2. FRACTURE NECK OF TALUS
INFECTIONS ; OSTEOMYELITIS
3. TENSION BAND WIRING
3. LOOSER’S ZONE
4. MONTEGGIA FRACTURES (CAMPBELL VOL2;
4. ANATOMY OF ROTATOR CUFF (CAMPBELL FRACTURES AND DISLOCATION IN CHILDREN)
SPORTS MEDICINE-SHOULDER INJURIES)
5. DESCRIBE NO-MAN’S LAND IN THE HAND
5. NEUROGENIC CLAUDICATION AND ITS RELEVANCE (CAMPBELLS, CH- THE
HAND)
6. SYME’S AMPUTATION
6. CHANCE FRACTURE
7. PTB PROSTHESIS
7. FRACTURE DISEASE
8. COMPARTMENT SYNDROME ( DAV PART 1
GENERAL L/3RD ) 8. WOUND DEBRIDEMENT

9. NORMAL GAIT 9. THOMAS SPLINT

 MAY 2014 ( MS ) MAY 2014 ( MS )

PAPER 3 PAPER 4

ESSAY 20 MARKS ESSAY 20 MARKS

1. DISCUSS THE CAUSES OF PAIN AROUND THE 1. WHAT IS DISTRACTION OSTEOGENESIS.

SHOULDER WITH PARTIAL RESTRICTION OF ENUMERATE THE INDICATIONS FOR IT AND
MOVEMENTS. DISCUSS

HOW WILL YOU MANAGE A CASE OF CHRONIC DIFFERENT METHODS OF DISTRACTION

ROTATOR CUFF INJURY. (CAMPBELL SPORTS OSTEOGENESIS KULKARNI PG 1519
MEDICINE-SHOULDER INJURIES)

SHORT ESSAYS (8 X 10=80 MARKS)

SHORT ESSAYS (8 X 10=80 MARKS)
2. BONE GRAFT SUBSTITUTES CAMPBELL,
2. TENNIS ELBOW (CAMPBELL SPORTS GENERAL PRINCIPLES, SURGICAL TECHNIQUES;
MEDICINE-ELBOW INJURIES) KULKARNI 1312

3. TARSAL COALITION (CAMPBELL ,FOOT AND 3. BIODEGRADABLE IMPLANTS (CAMPBELL

ANKLE; PES PLANUS) ,GENERAL PRINCIPLES OF FRACTURE
TREATMENT; BIOMECHANICS)
4. DISCOID MENISCUS (CAMPBELL ; CH-
ARTHROSCOPY OF LOWER EXTREMITIES) 4. CERAMICS IN ORTHOPAEDICS

5. CHONDROMALACIA PATELLA (CAMPBELL 5. TRAUMA SCORING SYSTEMS

SPORTS MEDICINE-KNEE INJURIES, CAMPBELL
6. LIMB SALVAGE IN TUMOURS
ARTHROSCOPY OF LOWER EXTREMITIES)
7. TENS
6. BLOUNT’S DISEASE (GOPALAN PG324)
8. GALLIUM BONE SCAN
7. JONES TRANSFER IN RADIAL NERVE PALSY
9. NOSOCOMIAL INFECTIONS
8. OSTEOBLASTOMA (TACHDJIAN ; BENIGN
MUSCULOSKELETAL TUMOUR)

9. ADHESIVE CAPSULITIS
 SECTION 2

MS ORTHO

PAPER 1

-- CALICUT UNIVERSITY (2012-2002)

-- KERALA UNIVERSITY (2012-2004)

 MAY 2012 JUNE 2012

PAPER 1- BASIC SCIENCES PAPER 1- BASIC SCIENCES

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE BLOOD SUPPLY OF TALUS. 1. DESCRIBE THE EXTENSOR MECHANISM OF

DISCUSS THE MECHANISM OF INJURY, KNEE JOINT. DISCUSS THE ETIOLOGY,DIAGNOSIS
CLASSIFICATION, MANAGEMENT AND AND
COMPLICATIONS OF FRACTURE NECK OF TALUS
MANAGEMENT OF RECURRENT DISLOCATION
(DAV-KNEE ANKLE TRAUMA; F/3RD, M/3RD) OF PATELLA

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.ISOTOPE BONE SCAN (KUL 1 - 155) 2.GROWTH PLATE ANATOMY AND ITS
FUNCTION( DAV PART 1 GENERAL L/3RD )
3.OSTEOPETROSIS (TACHDJIAN, ORTHOPEDIC
DISORDERS) 3.DIFFERENTIATE BETWEEN OSTEOPENIA AND
OSTEOPOROSIS
4.SERONEGATIVE SPONDYLOARTHROPATHY
(KUL 1- 886) 4.GLASGOW COMA SCALE

5.MID PALMAR SPACE INFECTION 5.METHOTREXATE

6.ARDS 6.ADULT RESPIRATORY DISTRESS SYNDROME

7.SYNOVECTOMY OF KNEE 7.PATHOLOGY OF COLD ABSCESS - DAV --

INFECTION; F/3RD.
8.RENAL TUBULAR ACIDOSIS
8.TRANSFUSION REACTIONS
9. SOMATO SENSORY EVOKED
POTENTIAL(CAMPBELL CH- 9.TYPES OF BIOPSY
SCOLIOSIS&KYPHOSIS)
 NOVEMBER 2011 MAY 2011

PAPER 1- BASIC SCIENCES PAPER 1- BASIC SCIENCES

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE BLOOD SUPPLY OF FEMORAL 1. DISCUSS THE ETIOPATHOGENESIS,

HEAD. DISCUSS THE CLINICAL FEATURES, DIAGNOSIS AND MANAGEMENT OF
DIAGNOSIS OSTEOPOROSIS.

AND MANAGEMENT OF AVASCULAR NECROSIS DISCUSS THE PRINCIPLES IN MANAGEMENT OF

OF FEMORAL HEAD IN A 35 YR OLD MALE OSTEOPOROTIC FRACTURES

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.COMPOUND PALMAR GANGLION 2.GROWTH FACTORS IN FRACTURE HEALING -

KUL (I)- PG27
3.VASCULARIZED BONE GRAFT
3.ISOTOPE BONE SCAN (KUL 1 - 155)
4.FIBROUS DYSPLASIA (TACHDJIAN ; BENIGN
MUSCULOSKELETAL TUMOUR) 4.PSEUDO GOUT

5.NEURITIS IN HANSENS DISEASE (KUL 1 - 658) 5.SALMONELLA OSTEOMYELITIS

6.FAT EMBOLISM GOPALAN PG 68 7.TRIPLE 6.SURGICAL SITE INFECTION

DEFORMITY OF KNEE
7.SPINA VENTOSA
8.NERVE CONDUCTION STUDY(TUREK CH 14
8.FOOT DROP
ORTHOPEDIC NEUROLOGY) 9.INDIRECT
REDUCTION OF FRACTURES 9. NERVE LESIONS IN HANSENS DISEASE (KUL 1
- 658)
 MAY 2010 NOV 2009

PAPER 1- BASIC SCIENCES PAPER 1- BASIC SCIENCES

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE FACTORS THAT INFLUENCE 1. DISCUSS THE SURGICAL ANATOMY OF

HEALING OF FRACTURES. SHOULDER JOINT.

MENTION THE DISORDERS OF FRACTURE BRIEFLY DESCRIBE SHOULDER INSTABILITY

HEALING.

DISCUSS THE ROLE OF GROWTH FACTORS IN

SHORT ESSAYS (8X10=80 MARKS)
FRACTURE HEALING KUL (I)- PG27
2. THORACIC OUTLET

3.LISFRANC JOINT
SHORT ESSAYS (8X10=80 MARKS)
4.OSTEOPOROSIS
2.ISOTOPE BONE SCAN (KUL 1 - 155)
5.MID PALMAR SPACE
3.LOCKING COMPRESSION PLATE KULKARNI
PG1433 6.RADIOULNAR JOINT

4.VERTEBROPLASTY (KUL 1 - 190) 7.ARTERIAL SUPPLY OF CAPITAL FEMORAL

EPIPHYSIS
5.RENAL TUBULAR ACIDOSIS
8.DELTA PHALANX
6.BIOABSORBABLE IMPLANTS (CAMPBELL
,GENERAL PRINCIPLES OF FRACTURE 9.RENAL RICKETS
TREATMENT; BIOMECHANICS)
TACHDJIAN CH 32 (METABOLIC&ENDOCRINE
7.VISCO SUPPLEMENTATION DISEASES)

8.SPINAL MOTION SEGMENT

9. TARSAL TUNNEL SYNDROME

 MAY 2009 MAY 2008 (RPT OF NOV 2009)

PAPER 1- BASIC SCIENCES JANUARY 2008

PAPER 1- BASIC SCIENCES

ESSAY (20 MARKS)

1. DISCUSS THE FACTORS THAT INFLUENCE ESSAY (20 MARKS)

HEALING OF FRACTURES. MENTION THE
1. WITH THE HELP OF A DIAGRAM DESCRIBE
DISORDERS OF
THE ANASTOMOSIS AROUND THE ELBOW.
FRACTURE HEALING.DISCUSS THE ROLE OF
WHAT IS ITS RELEVANCE TO VIC?DISCUSS THE
GROWTH FACTORS IN FRACTURE HEALING KUL
CLINICAL FINDINGS AND MANAGEMENT OF VIC.
(I)- PG27

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.ARCHES OF FOOT (DAV-LOCAL
2.ISOTOPE BONE SCAN (KUL 1 - 155)
COMPLICATIONS OF#; M/3RD)
3.LOCKING COMPRESSION PLATE KULKARNI
3.DISEASE MODIFYING DRUGS IN RHEUMATOID
PG1433
ARTHRITIS
4.VERTEBROPLASTY (KUL 1 - 190)
4.TUBERCLE
5.RENAL TUBULAR ACIDOSIS
5.HORNERS SYNDROME
6.BIOABSORBABLE IMPLANTS CAMPBELL
6.PES ANSERINUS
,GENERAL PRINCIPLES OF FRACTURE
TREATMENT; BIOMECHANICS) 7.GUYONS CANAL

7.VISCO SUPPLEMENTATION 8.Q ANGLE

8.SPINAL MOTION SEGMENT 9. CHONDROCALCINOSIS

9. TARSAL TUNNEL SYNDROME

 MAY 2007 SEPTEMBER 2006

PAPER 1- BASIC SCIENCES PAPER 1- BASIC SCIENCES

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE BIOMECHANICS OF HIP JOINT. 1. DISCUSS THE SURGICAL ANATOMY OF

INTERVERTEBRAL DISC AND INTERVERTEBRAL
DESCRIBE THE DISORDERS OF ABDUCTOR
FORAMEN
MECHANISM OF HIP
DISCUSS DIFFERENCES IN CERVICAL AND
LUMBAR SPINES WITH REFERENCE TO DISC
SHORT ESSAYS (8X10=80 MARKS) PROLAPSE (CAMPBELL CH- LOWER BACK PAIN)

2.CARPAL TUNNEL CAMPBELL ; CH - THE HAND

3.TRIANGULAR FIBROCARTILAGE COMPLEX SHORT ESSAYS (8X10=80 MARKS)

4.BISPHOSPHONATES 2.ERBS PALSY

5.SINGHS INDEX 3.LIGAMENT LAXITY

6.MEDIAL MENISCUS OF KNEE (CAMPBELL ; 4.SYNOVIAL FLUID(TUREK CH13 DISEASES OF

SPORTS MEDICINE CH-KNEE JOINT)
INJURIES)(CAMPBELL ; CH-ARTHROSCOPY OF
5.PERIOSTEAL NEW BONE FORMATION - (DAV-
LOWER EXTREMITIES)
TUMOURS; M/3RD)
7.BONE MORPHOGENIC PROTEIN
6.SCURVY
8. BIGELOWS LIGAMENT
7.BACTERIAL RESISTANCE
9. METATARSUS ADDUCTUS
8.TIBIAL CLUB FOOT

9. BMD- BONE MINERAL DENSITY

 MAY 2006 MAY 2005

PAPER 1- BASIC SCIENCES PAPER 1- BASIC SCIENCES

ESSAY (20 MARKS) ESSAY (2 X 35 =70 MARKS)

1. DISCUSS VITAMIN D METABOLISM AND DISO 1. DECSRIBE WITH THE HELP OF A DIAGRAM
THE ANATOMY OF THE BRACHIAL PLEXUS.
RDERS OF PARATHYROID GLAND AND ITS
EFFECT ON SKELETON. BRIEFLY DESCRIBE THE MECHANISM OF
BRACHIAL PLEXUS INJURY.

HOW WOULD YOU DIFFERENTIATE A

PREGANGLIONIC AND POSTGANGLIONIC
SHORT ESSAYS (8X10=80 MARKS) INJURY?

2.ULNAR NERVE ENTRAPMENT DAV--NEUROLOGY; F/3RD; CAMPBELL VOL2;

NEURVOUS SYSTEM DISORDERS IN CHILDREN
3.RADIOULNAR JOINTS
2.DESCRIBE THE MICROSCOPIC PICTURE OF GCT
4.FAT EMBOLISM GOPALAN PG 68
OF BONE.
5.BONE SUBSTITUTES
BRIEFLY DESCRIBE GCT VARIANTS.
6.ROTATOR CUFF (CAMPBELL SPORTS
DISCUSS THE DIAGNOSIS AND MANAGEMENT
MEDICINE-SHOULDER INJURIES)
OF LYTIC LESION IN THE LOWER END OF RADIUS
7.LUMBO SACRAL INSTABILITY IN A 30 YR OLD MAN (DAV- TUMOURS; GCT)

8.CAMPTODACTYLY SHORT ESSAYS (3X10=30 MARKS)

9. CORROSION OF IMPLANTS 3.HYPERCALCEMIA

4.ULNAR PARADOX

5.NON OSSIFYING FIBROMA

 JUNE 2004 NOVEMBER 2003

PAPER 1- BASIC SCIENCES PAPER 1- BASIC SCIENCES

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE PATHOGENESIS, CLINICAL 1. DESCRIBE THE BLOOD SUPPLY TO THE HEAD
FEATURES AND MANAGEMENT OF ULNAR OF FEMUR.
DRIFT OF FINGERS.
DISCUSS THE MANAGEMENT OF A CASE OF
AVN OF THE HEAD OF FEMUR IN A 30 YR OLD
MALE ( DAV- GENERAL; M/3RD)
SHORT ESSAYS (8X10=80 MARKS)

2.BIOLOGIC FIXATION OF FRACTURES

SHORT ESSAYS (8X10=80 MARKS)
3.CHONDROITIN SULFATE
2.VASCULARISED BONE GRAFT
4.HIGH MEDIAN NERVE PARALYSIS
3.BONE MORPHOGENIC PROTEIN
5.BONE GRAFT SUBSTITUTES CAMPBELL,
GENERAL PRINCIPLES, SURGICAL TECHNIQUES; 4.BONE BANK KULKARNI 1137
KULKARNI 1312
5.NEOADJUVANT CHEMOTHERAPY (DAV -
6.DEEP VEIN THROMBOSIS TUMOURS; M/3RD) CAMPBELL- GENERAL
PRINCIPLES TUMOURS 6.ARDS
7.BMD - BONE MINERAL DENSITY
7.OSTEOPOROSIS
8.ANEURYSMAL BONE CYST (TACHDJIAN ;
BENIGN MUSCULOSKELETAL TUMOUR) 8.MULTIFOCAL TUBERCULOSIS

9. HALLUX VALGUS (DAV-LOCAL 9. RADIOLOGICAL EVALUATION FOR

COMPLICATIONS OF#; M/3RD) CAMPBELL FOOT RECURRENT DISLOCATION OF PATELLA
AND ANKLE, DISORDERS OF HALLUX
 MAY 2002

PAPER 1- BASIC SCIENCES

ESSAY (2 X 35= 70 MARKS)

1. DESCRIBE THE FACTORS CONTRIBUTING TO

THE STABILITY OF THE SHOULDER JOINT.

HOW WILL YOU CLASSIFY SHOULDER

INSTABILITY.

DISCUSS THE PRINCIPLES OF MANAGEMENT OF

RECURRENT ANTERO-INFERO INSTABILITY

2. DISCUSS THE AETIOPATHOGENESIS OF

RHEUMATOID ARTHRITIS.

DESCRIBE THE VARIOUS HAND DEFORMITIES

AND THE BIOMECHANICS.

BRIEFLY DISCUSS THE MANAGEMENT OF

BUTTON HOLE DEFORMITY.

SHORT ESSAYS (3X10=30 MARKS)

3.CERVICAL RIB.

4.PNEUMATIC TOURNIQUET (STEWART-

TOURNIQUET)

5.TECHNIQUES OF BIOPSY IN SKELETAL

NEOPLASMS
 JUNE 2012 NOV 2011

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE ANATOMY OF BRACHIAL 1. DISCUSS VITAMIN D METABOLISM

PLEXUS AND CLINICAL FEATURES OF PROXIMAL
DESCRIBE THE PARATHYROID GLAND AND ITS
PLEXUS INJURY.
EFFECT ON SKELETON
HOW WILL YOU DIFFERENTIATE BETWEEN
POST AND PREGANGLIONIC LESIONS AND HOW
WILL YOU MANAGE THEM? DAV-- SHORT ESSAYS (8X10=80 MARKS)
NEUROLOGY; F/3RD , CAMPBELL VOL2;
2.ARCHES OF FOOT (DAV-LOCAL
NEURVOUS SYSTEM DISORDERS IN CHILDREN
COMPLICATIONS OF#; M/3RD)

SHORT ESSAYS (8X10=80 MARKS)

3.TECHNIQUE OF BIOPSY IN SKELETAL

2.TFCC NEOPLASMS

3.NEUROGENIC CLAUDICATION 4.CERVICAL RIB

4.RENAL RICKETS 5.BONE MORPHOGENETIC PROTEIN

TACHDJIAN CH 32 (METABOLIC&ENDOCRINE 6.DEEP VEIN THROMBOSIS

DISEASES)
7.CHONDROITIN SULFATE
5.ROTATOR CUFF (CAMPBELL SPORTS
8.HIGH MEDIAN NERVE PALSY
MEDICINE-SHOULDER INJURIES)
9.SINGHS INDEX
6.BONE BANK KULKARNI 1137

7.CAMPTODACTYLY

8.FAT EMBOLISM GOPALAN PG 68

9.PLASTIC DEFORMITY
 MAY 2011 JUNE 2010

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE ANATOMY OF FLEXOR 1. DESCRIBE THE ANATOMY OF THE GROWTH

TENDON IN THE FINGER. PLATE.

DESCRIBE THE DIFFERENT METHODS OF DISCUSS THE CHANGES IN THE GROWTH PLATE
TENDON SUTURING. HOW WILL YOU MANAGE IN RICKETS. ( DAV PART 1 GENERAL L/3RD )
A CASE OF FLEXOR TENDON INJURY IN ZONE 2
WHICH IS 2 DAYS OLD.
SHORT ESSAYS (8X10=80 MARKS)
SHORT ESSAYS (8X10=80 MARKS)
2.BRYANTS TRIANGLE
2.PATHOPHYSIOLOGY OF COMPARTMENT
SYNDROME ( DAV PART 1 GENERAL L/3RD ) 3.SPRENGELS SHOULDER CAMPBELL
(CONGENITAL ANOMALIES OF TRUNK AND
3.FUNCTIONAL CAST BRACING STEWART-
UPPER EXTREMITY)
PG215
4.QUADRICEPS GAIT
4.STRUCTURE OF ARTICULAR CARTILAGE AND
HISTOPATHOLOGICAL CHANGES IN OA (TUREK 5.BIOCHEMICAL AND RADIOLOGICAL
CH2) DIAGNOSIS OF MULTIPLE MYELOMA

5.BONE BANK KULKARNI 1137 6.DIAGNOSIS OF CARPAL TUNNEL SYNDROME

CAMPBELL ; CH - THE HAND
6.TRANSCUTANEOUS ELECTRICAL NERVE
STIMULATION 7.NEUROPRAXIA

7.BLOOD SUPPLY OF PROXIMAL FEMUR AND 8.OSSIFICATION OF POSTERIOR LONGITUDINAL

ITS CLINICAL RELEVANCE LIGAMENT

8.ARDS AND ITS MANAGEMENT 9.LOOSE BODY OF KNEE KULKARNI

PG 1818
9.THOMAS TEST AND ITS SIGNIFICANCE
 NOV 2010 DEC 2008

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE STRUCTURE OF EPIPHYSEAL 1. OUTLINE DEVELOPMENT OF HIP JOINT.

PLATE. PATHOLOGICAL CHANGES SEEN IN
DESCRIBE THE BLOOD SUPPLY OF UPPER FEMUR
EPIPHYSEAL PLATE IN METABOLIC DISORDERS.
IN A CHILD AND
CORRELATE WITH CLINICAL&RADIOLOGICAL
FEATURES. DISCUSS ITS RELEVANCE IN PEDIATRIC HIP
PATHOLOGY
SHORT ESSAYS (8X10=80 MARKS)
SHORT ESSAYS (8X10=80 MARKS)
2.CALCIUM METABOLISM (TUREK CH6
PHYSIOLOGY OF BONE) 2.LOCAL STEROIDS

3.INDICATION AND COMPLICATIONS OF 3.ENDOCHONDRAL OSSIFICATION TUREK CH 3

AMPUTATION HISTOLOGY OF BONE

4.ULTRASOUND IN ORTHOPAEDICS 4.COX-2 INHIBITORS

5.ANATOMY OF ANKLE JOINT IN RELATION TO 5.BONE REMODELLING TUREK CH 3 HISTOLOGY

THEIR INJURIES OF BONE

6.ANATOMY &C/F OF ROTATOR CUFF INJURY 6.NEOADJUVANT CHEMOTHERAPY (DAV -

(CAMPBELL SPORTS MEDICINE-SHOULDER TUMOURS; M/3RD) CAMPBELL- GENERAL
INJURIES) PRINCIPLES TUMOURS

7.ANATOMY,STRUCTURE OF LUMBAR I.V DISC. 7.ILIOTIBIAL TRACT

CHANGES SEEN IN IVDP
8.ALKALINE PHOSPHATASE
8.PERTHES -PATHOPHYSIOLOGY TACHDJIAN
9.FANCONIS SYNDROME
9.WHAT IS A GIANT CELL? WHAT ARE THE
DIFFERENT TYPES OF GIANT CELLS? DRAW A
NEAT DIAGRAM OF GIANT CELL. (DAV-
TUMOURS; GCT)
 MAY 2008 MAY 2007

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE ANATOMICAL BASIS RELATED 1. DESCRIBE THE ARTERIAL ANASTOMOSIS

TO THE VARIOUS SURGICAL EXPOSURES TO HIP AROUND THE ELBOW
JOINT.
DISCUSS ITS RELEVANCE IN SUPRACONDYLAR
FRACTURES OF THE HUMERUS IN CHILDREN

SHORT ESSAYS (8X10=80 MARKS)

2.TINELS SIGN SHORT ESSAY (8X10=80 MARKS)

3.PHYSEAL INJURY (CAMPBELL VOL2; 2.CALCIUM HOMEOSTASIS (TUREK CH 6

FRACTURES AND DISLOCATION IN CHILDREN) PHYSIOLOGY OF BONE)

4.ANKYLOSIS 3.DISCOID MENISCUS (CAMPBELL ; CH-

ARTHROSCOPY OF LOWER EXTREMITIES)
5.DISLOCATION
4.TRENDELENBURG GAIT
6.CALLUS
5.COMMON PERONEAL NERVE
7.PLASTER OF PARIS
6.MRSA
8.LOCKING OF KNEE
7.EXTENSOR EXPANSION OF THE FINGERS
9.BREATHING TIME IN TOURNIQUET
APPLICATION (STEWART- 8.CRYSTAL ARTHROPATHY
TOURNIQUET)
9.MOTOR END PLATES
 NOV 2007 NOV 2006

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE ANATOMY OF BRACHIAL 1. DESCRIBE EXTENSOR MECHANISM OF THE

PLEXUS. INTERPHALANGEAL JOINTS OF THE FINGERS.

DESCRIBE THE CLINICAL FEATURES AND MENTION THE DEFORMITIES OF HAND IN

MANAGEMENT OF NEGLECTED CASE OF ERBS RHEUMATOID ARTHRITIS .BRIEFLY MENTION
PALSY. THE KINETO MECHANISM OF THE DEFORMITIES.

DAV--NEUROLOGY; F/3RD, CAMPBELL VOL2; SHORT ESSAYS (8X10=80 MARKS)

NEURVOUS SYSTEM DISORDERS IN CHILDREN
2.ECTRODACTYLY
SHORT ESSAYS (8X10=80 MARKS)
3.MALLET FINGER CAMPBELL,
2.DEQUERVAINS DISEASE (FRACTURE,DISLOC OF HAND CH 64)

3.PHALENS TEST 4.CAUSES OF HALLUX VALGUS

4.BUCKET HANDLE TEAR OF MENISCUS (DAV-LOCAL COMPLICATIONS OF#; M/3RD)

(CAMPBELL ; SPORTS MEDICINE CH-KNEE CAMPBELL FOOT AND ANKLE, DISORDERS OF
INJURIES)(CAMPBELL ; CH-ARTHROSCOPY OF HALLUX
LOWER EXTREMITIES)
5.ARCHES OF FOOT (DAV-LOCAL
5.CALCITONIN COMPLICATIONS OF#; M/3RD)

6.NON UNION 6.COBB ANGLE

7.MANNUS VALGUS 7.DISTRACTION OSTEOGENESIS KULKARNI PG

1519
8.TENDON TRANSFERS
8.MYOSITIS OSSIFICANS PROGRESSIVA
9.BAUMANS ANGLE
9.SYNOVIAL FLUID ANALYSIS(TUREK CH13
DISEASES OF JOINT)
 JUNE 2006 JUNE 2005

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DECSRIBE THE ANATOMY OF THE DEEP 1. DESCRIBE THE HISTOLOGICAL FEATURES OF

PALMAR SPACE. EPIPHYSIS,PHYSIS AND METAPHYSIS.

DISCUSS THE AETIOPATHOGENESIS OF DESCRIBE THE DISEASES AFFECTING THE

INFECTIONS IN THIS SPACE. GROWTH PLATE. ( DAV PART 1 GENERAL L/3RD
)
GIVE THE TREATMENT FOR INFECTIONS OF THE
MIDDLE PALMAR AND THENAR SPACE

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.ANATOMIC CONSIDERATIONS OF 2.PULLEYS OF THE HAND

RADIOCARPAL AND INTERCARPAL LIGAMENTS
3.GROWTH HORMONE
3.POLIO VIRUSES AND POLIO VACCINES
4.PRINCIPLES OF FRACTURE HEALING
4.MYCETOMA FOOT
5.BONE GRAFT SUBSTITUTES CAMPBELL,
5.BONE MORPHOGENETIC PROTEIN GENERAL PRINCIPLES, SURGICAL TECHNIQUES;
KULKARNI 1312
6.HISTOPATHOLOGICAL APPEARANCE OF
OSTEOSARCOMA 6.FRENKEL CLASSIFICATION OF NEUROLOGICAL
INJURY IN D-L FRACTURES
7.RADIOLOGICAL FEATURES OF
HYPERPARATHYROIDISM 7.BONE MINERAL DENSITY

8.SECOND LINE ANTITUBERCULOUS DRUGS 8.RADIO ISOTOPE DENSITY (KUL 1 -

155)
9.RADIO ISOTOPE BONE SCANNING (KUL 1 -
155) 9.DRUGS USED FOR TREATING OSTEOPOROSIS
 NOV 2004

PAPER 1 JUNE 2004

PAPER 1

ESSAY (20 MARKS)

1. DESCRIBE THE STRUCTURE OF PERIOSTEUM. ESSAY (20 MARKS)

(DAV - TUMOURS; M/3RD)
1. DISCUSS THE PATHOGENESIS, CLINICAL
DISCUSS THE FUNCTION AND ROLE OF FEATURES AND MANAGEMENT OF ULNAR
PERIOSTEUM IN FRACTURE HEALING, TUMOURS DRIFT OF FINGERS
AND INFECTIONS OF BONE

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.BIOLOGICAL FIXATION OF FRACTURES
2.ACCESORY BONE OF FOOT
3.CHONDROITIN SULFATE
3.PATELLA ALTA
4.HIGH MEDIAN NERVE PARALYSIS
4.MECHANISM OF CLAW HAND
5.BONE GRAFT SUBSTITUTES CAMPBELL,
5.BOHLERS ANGLE GENERAL PRINCIPLES, SURGICAL TECHNIQUES;
KULKARNI 1312
6.ANTEVERSION OF FEMORAL NECK
6.DEEP VEIN THROMBOSIS
7.SENSORY EVOKED POTENTIALS
7.BONE MINERAL DENSITOMETRY
8.STRUCTURE OF EPIPHYSIS
8.ANEURYSMAL BONE CYST (TACHDJIAN ;
9.DIAGNOSIS OF STRESS FRACTURES KULKARNI
BENIGN MUSCULOSKELETAL TUMOUR)
1218
9.HALLUX VALGUS (DAV-LOCAL
COMPLICATIONS OF#; F/3RD)
 SECTION 3

MS ORTHO

PAPER 2

-- CALICUT UNIVERSITY (2012-2002)

-- KERALA UNIVERSITY (2012-2004)

 JUNE 2012 MAY 2012

PAPER 2-TRAUMATOLOGY PAPER 2- TRAUMATOLOGY

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. EXPLAIN THE BIOMECHANICS OF THORACO 1. CLASSIFY FRACTURES OF THE ACETABULUM.

LUMBAR SPINE.
DISCUSS THE EVALUATION AND MANAGEMENT
CLASSIFY AND DISCUSS ABOUT MANAGEMENT OF ACETABULAR FRACTURES.
OF THORACO LUMBAR SPINE INJURIES.

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.SIDE SWIPE INJURY KULKARNI 1956
2. RECURRENT DISLOCATION OF SHOULDER
3.DAMAGE CONTROL ORTHOPAEDICS
3. PUBIC DIASTASIS
4.FLOATING KNEE
4. DUNLOP TRACTION
5.SCAPHOLUNATE DISSOCIATION
5. MCMURRAYS OSTEOTOMY
6.ACROMIOCLAVICULAR SUBLUXATION
6. LCP
7.MEDIAL EPICONDYLE FRACTURE OF ELBOW
7.NEGLECTED TENDOCALCANEUS INJURY
8.UNSTABLE PELVIC RING FRACTURE
8.ODONTOID FRACTURES
9.MALUNITED FRACTURE CALCANEUM
9.CRUTCH GAIT
 NOVEMBER 2011 MAY 2011

PAPER 2- TRAUMATOLOGY PAPER 2- TRAUMATOLOGY

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. CLASSIFY PROXIMAL HUMERUS FRACTURES. 1. CLASSIFY CALCANEAL FRACTURES.

DISCUSS THE CLINICAL EVALUATION,
DISCUSS THE CLINICAL FEATURES,
DIAGNOSIS AND MANAGEMENT OF PROXIMAL
MANAGEMENT AND COMPLICATIONS OF
HUMERAL FRACTURES
INTRAARTICULAR FRACTURE OF CALCANEUM.
SHORT ESSAYS (8X10=80 MARKS)
SHORT ESSAYS (8X10=80 MARKS)
2.HANGMANS FRACTURE- ZUKERMAN
2.GAMEKEEPERS THUMB CAMPBELL,
3.ACROMIOCLAVICULAR SUBLUXATION (FRACTURE,DISLOC OF HAND CH 64)
3.FRACTURE SCAPHOID
4.LATERAL CONDYLE FRACTURE IN CHILDREN
4.SHOULDER IMPINGEMENT SYNDROME
5.KAPLAN LESION
(CAMPBELL SPORTS MEDICINE-SHOULDER
6.ACL DEFICIENT KNEE (CAMPBELL ; SPORTS INJURIES)
MEDICINE CH-KNEE INJURIES)(CAMPBELL ; CH-
5.PATHOLOGICAL FRACTURES
ARTHROSCOPY OF LOWER EXTREMITIES)
7.FRACTURE HEAD OF FEMUR 6.CHRONIC COMPARTMENT SYNDROME OF
LEG ( DAV PART 1 GENERAL L/3RD )
8.LISFRANC DISLOCATION
7.POSTERIOR CRUCIATE LIGAMENT INJURY
9.DUPUYTRENS FRACTURE
8.FRACTURE FEMORAL HEAD

9.CUBITUS VARUS
 MAY 2010 MAY 2008

PAPER 2- TRAUMATOLOGY PAPER 2- TRAUMATOLOGY

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. CLASSIFY THE FRACTURES OF LOWER END OF 1. CLASSIFY FRACTURES OF ACETABULUM.

RADIUS.
DISCUSS RELEVANT INVESTIGATIONS AND ITS
DISCUSS THE MANAGEMENT OF TFCC INJURIES
MANAGEMENT

SHORT ESSAY (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.FRACTURES OF CALCANEUM
2.PFN
3.CARPAL INSTABILITY
3.FLOATING KNEE
4.MEDIAL MENISCAL TEAR (CAMPBELL ;
4.TRAUMATIC SPONDYLOLISTHESIS OF AXIS
SPORTS MEDICINE CH-KNEE
INJURIES)(CAMPBELL ; CH-ARTHROSCOPY OF 5.DISTRACTION OSTEOGENESIS KULKARNI PG
LOWER EXTREMITIES) 5.FRACTURE DISEASE 1519

6.ZERO HOUR FIXATION 6.DIE PUNCH LESION

7.PRINCIPLE OF LOCKING HEAD SCREWS 7.SLAP LESION - KULKARNI PG 1868

KULKARNI PG1433
8.GAMEKEEPERS THUMB CAMPBELL,
8.REPETITIVE STRAIN INJURIES (FRACTURE,DISLOC OF HAND CH 64)

9.FRACTURE SCAPULA 9.CUBITUS VALGUS

NOVEMBER 200 (RPT - MAY 2010)

MAY 2009 (RPT OF MAY 2008)

 JANUARY 2008 MAY 2007

PAPER 2 TRAUMATOLOGY PAPER 2 - TRAUMATOLOGY

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE CLASSIFICATION OF VALGUS 1. DESCRIBE THE CLASSIFICATION,

INJURY OF THE ELBOW IN A CHILD. INVESTIGATIONS AND MANAGEMENT OF
CERVICAL SPINE INJURIES
BRIEFLY DESCRIBE THE MANAGEMENT OF EACH
TYPE

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS) 2.FRACTURE HEAD OF FEMUR

2.HIDDEN FLEXION INJURY OF CERVICAL SPINE 3.CRUSH SYNDROME

3.ATLANTO AXIAL DISLOCATION 4.TENDON RUPTURE

4.ESSEX LOPRESTI FRACTURE 5.HOFFAS FRACTURE

5.FAT EMBOLISM GOPALAN PG 68 6.WOUND DEBRIDEMENT

6.LISFRANC DISLOCATION 7.DISTAL RADIUS FRACTURE

7.ACUTE ACL INJURY(CAMPBELL ; SPORTS 8.TENNIS ELBOW (CAMPBELL SPORTS

MEDICINE CH-KNEE INJURIES)(CAMPBELL ; CH- MEDICINE-ELBOW INJURIES)
ARTHROSCOPY OF LOWER EXTREMITIES)
9.PATHOLOGICAL FRACTURES
8.ACROMIOCLAVICULAR DISLOCATION

9.TENSION PNEUMOTHORAX
 OCTOBER 2006 MAY 2006

PAPER 2 - TRAUMATOLOGY PAPER 2 - TRAUMATOLOGY

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE CLASSIFICATION , CLINICAL 1. DESCRIBE THE CLASSIFICATION, RADIOLOGY

FEATURES, INVESTIGATIONS AND AND MANAGEMENT OF CALCANEAL FRACTURES
MANAGEMENT OF BRACHIAL PLEXUS
INJURIES.
SHORT ESSAYS (8X10=80 MARKS)
(DAV--NEUROLOGY; F/3RD), CAMPBELL VOL2;
NEURVOUS SYSTEM DISORDERS IN CHILDREN 2.GALLEAZI FRACTURES

3.SPINE BOARD

SHORT ESSAYS (8X10=80 MARKS) 4.LIGAMENT INJURIES OF ANKLE

2.GAS GANGRENE 5.UNSTABLE STRESS FRACTURE KULKARNI 1218

3.ACUTE DISC PROLAPSE 6.EXTERNAL FIXATOR

4.EPIPHYSEAL INJURIES OF HIP 7.LAG SCREW

5.POST TRAUMATIC STIFF KNEE 8.PROXIMAL FEMORAL NAIL

6.INTERLOCKING NAILS FOR FEMUR 9.TENDON REPAIR

7.VOLKMANNS ISCHEMIC CONTRACTURE

8.FRACTURE OF ATLAS

9.CAST BRACE
 MAY 2005 MAY 2004

PAPER 2 - TRAUMATOLOGY PAPER 2 - TRAUMATOLOGY

ESSAY (35 X 2 = 70) ESSAY (20 MARKS)

1. WHAT DO YOU MEAN BY THE TERM 1.HOW WILL YOU EVALUATE AND TREAT
POLYTRAUMA PATIENT (5) PATHOLOGICAL FRACTURE OF SHAFT OF FEMUR
BRIEFLY DISCUSS THE PRIORITIES IN IN 60 YR OLD MAN
ASSESSMENT OF A POLYTRAUMA PATIENT (10)
LIST THE STEPS IN RESUSCITATION AND EARLY
MANAGEMENT OF A POLYTRAUMA PATIENT SHORT ESSAY (8X10=80 MARKS)
(20)
2.INTERCARPAL INSTABILITY
2.DISCUSS THE BIOCHEMICAL ABNORMALITIES
3.SUPRACONDYLAR NAIL
IN MULTIPLE MYELOMA (10)
DESCRIBE THE RADIOLOGICAL 4.LIGAMENTOTAXIS
MANIFESTATIONS (10)
5.ERBS PALSY
BRIEFLY DESCRIBE THE CHEMOTHERAPY OF
MULTIPLE MYELOMA (15) 6.STRESS FRACTURES KULKARNI 1218

SHORT ESSAYS (3X10=30 MARKS) 7.OLD UNREDUCED POSTERIOR DISLOCATION

ELBOW
3. ANTIBIOTIC PROPHYLAXIS IN ORTHOPAEDIC
SURGERY 8.OSTEOCHONDRITIS DESSICANS (DAV-LOCAL
COMPLICATIONS OF#; F/3RD) CAMPBELL
4.PSEUDO GOUT
SPORTS MEDICINE-KNEE INJURIES)
5.NEOADJUVANT CHEMOTHERAPY (DAV -
9.FLOATING HIP
TUMOURS; M/3RD) CAMPBELL- GENERAL
PRINCIPLES TUMOURS
 NOVEMBER 2003 NOVEMBER 2002

PAPER 2 - TRAUMATOLOGY PAPER 2 TRAUMATOLOGY

ESSAY (20 MARKS) ESSAY (20 MARKS)

1.WHAT ARE PILON FRACTURES. DISCUSS THE 1.DISCUSS THE CLINICAL FEATURES,
GOALS OF TREATMENT AND THE VARIOUS PATHOLOGICAL ANATOMY AND MANAGEMENT
TREATMENT OPTIONS IN AN ACUTE PILON OF RECURRENT DISLOCATION OF THE
FRACTURE OF THE TIBIA IN A 20 YR OLD ADULT. SHOULDER

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.GLASCOW COMA SCALE 2.WHIPLASH INJURY

3.GAMMA NAIL 3.MALGAIGNE FRACTURE

4.4-PART FRACTURE OF THE HUMERUS 4.LAG SCREW

5.CANNULATED SCREWS 5.BAUMANNS ANGLE

6.EPIPHYSEAL INJURY (CAMPBELL VOL2; 6.BRYANTS TRACTION (STEWART PG42)

FRACTURES AND DISLOCATION IN CHILDREN)
7.PULLED ELBOW
7.JEFFERSON FRACTURE.
8.DUPUYTRENS FRACTURE
8.PAPINEAU TECHNIQUE OF BONE GRAFTING
9.FUNCTIONAL CAST BRACING STEWART-
9.SOFT TISSUE COVERAGE IN FRACTURE PG215
MANAGEMENT.
 JUNE 2012 NOVEMEBER 2011

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DEFINE CERVICAL SPINE INJURY, ITS 1. DESCRIBE THE CLASSIFICATION, RADIOLOGY

ETIOLOGY, CLINICAL FEATURES AND AND MANAGEMENT OF FRACTURE
MANAGEMENT. CALCANEUM (2006,2005)

ROCKWOOD 7TH EDITION CH 42

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS) 2. FLOOR REACTION ORTHOSIS (2007)

2. CRUSH SYNDROME (2008) 3.TENDON RUPTURE

3. LAG SCREW 4. LIGAMENT INJURIES OF ANKLE

4. SHOULDER HAND SYNDROME 5. PROXIMAL FEMORAL NAIL

5. FUNCTIONAL CAST BRACING STEWART- 6. COMPARTMENT SYNDROME (DAV

PG215 PART 1 GENERAL L/3RD )

6. HOFFAS FRACTURE 7. BARTONS FRACTURE (2008)

7. PATHOLOGICAL FRACTURE (JUNE 2004) 8. EPIPHYSEAL INJURY (CAMPBELL VOL2;

FRACTURES AND DISLOCATION IN CHILDREN)
8. FRACTURE DISEASE

9. JEFFERSON FRACTURE
9. LOW TEMP THERMOPLASTICS STEWART PG
201
 MAY 2011 NOVEMBER 2010

PAPER 2 PAPER 2

ESSAY (20 MARKS)

ESSAY (20 MARKS) 1. DISCUSS MECHANISM OF INJURY, C/F

&RECENT TRENDS IN A/C ACL INJURY (2006)
1. DEFINE LATERAL CONDYLE OF THE
(CAMPBELL ; SPORTS MEDCINE -KNEE
HUMERUS.
INJURIES)(CAMPBELL ; CH-ARTHROSCOPY OF
DISCUSS THE MANAGEMENT OF LATERAL LOWER EXTREMITIES)
CONDYLE FRACTURES. ENUMERATE ITS
SHORT ESSAYS (8X10=80 MARKS)
COMPLICATIONS. (2010,2008)
2. CLASSIFICATION OF FRACTURE TALUS
SHORT ESSAYS (8X10=80 MARKS) ,MANAGEMENT (2005,2004) (DAV-KNEE ANKLE
TRAUMA; F/3RD)
2. NEUROLOGICAL EVALUATION IN SPINAL
INJURY 3. POSTERIOR DISLN OF HIP.

4. ERBS PALSY -MANAGEMENT (2004)

3. CLASSIFY FRACTURE NECK OF FEMUR IN
CHILDREN AND RELEVANCE IN MANAGEMENT 5. ROLE OF ISOTOPE SCAN IN TRAUMA
PATIENTS (KUL 1 - 155)
4. DISCUSS THE PRINCIPLE OF TENSION BAND
6. MANAGEMENT OF IPSILATERAL CLOSED
WIRING AND ITS INDICATION (2006) FRACTURE NECK OF FEMUR WITH OPEN
FRACTURE SHAFT OF FEMUR
5. MYOSITIS OSSIFICANS
7. NEGLECTED MONTEGGIA FRACTURE
6. HOLSTEIN LEWIS LESION,SIGNIFICANCE DISLOCATION (2006) (CAMPBELL VOL2;
FRACTURES AND DISLOCATION IN CHILDREN)
(2007)
8. INCOMPLETE CORD INJURY WITH
7. BENNETS FRACTURE PARAPLEGIA

8. HANGMANS FRACTURE 9. ACUTE SCAPHOID FRACTURE-MANAGEMENT

(2010, 2006)
9. MARCH FRACTURE AND MANAGEMENT
 JUNE 2010 DEC 2008

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE CLASSIFICATION OF 1. CLASSIFY DISTAL FEMORAL FRACTURES.

FRACTURES OF THE PELVIS.
DISCUSS THE MANAGEMENT OF
DISCUSS IN BRIEF THE VARIOUS INTERCONDYLAR FRACTURE OF FEMUR IN 60 YR
COMPLICATIONS OF FRACTURES OF PELVIS OLD MAN
(2005)

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2. BARTONS FRACTURE
2. MANAGEMENT OF FRACTURE SCAPHOID
3. NERVE CONDUCTION STUDY(TUREK CH 14
(2006)
ORTHOPEDIC NEUROLOGY) 4. BIOLOGICAL
3. CLASSIFICATION OF ACETABULAR OSTEOSYNTHESIS
FRACTURES (2008,2006)
5. REFLEX SYMPATHETIC DYSTROPHY
4. COMPLICATIONS OF FRACTURES OF UPPER
6. JAIPUR FOOT KULKARNI 3941
END OF HUMERUS
7. ANTEROMEDIAL INSTABILITY OF KNEE
5. ELBOW CRUTCHES
8. CRUSH SYNDROME
6. MILWAUKEE BRACE
9. LATERAL CONDYLE FRACTURE OF HUMERUS
7. CLASSIFICATION OF FRACTURES OF NECK OF
FEMUR IN CHILDREN

8. SCHANZ OSTEOTOMY

9. MANAGEMENT OF FRACTURES OF LATERAL

CONDYLE OF HUMERUS IN CHILDREN (2008)
 MAY 2008 MAY 2007

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. CLASSIFY ACETABULAR FRACTURES. 1. CLASSIFY FRACTURES OF THE

DESCRIBE THE CLINICAL FEATURES AND THORACOLUMBAR SPINE AND DISCUSS THE
MANAGEMENT OF FRACTURE OF ACETABULUM MANAGEMENT OF UNSTABLE, ACUTE T 12
FRACTURE WITH PARTIAL PARAPARESIS.

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2. WHIPLASH INJURY
2. AVIATORS FRACTURE
3. COTTON FRACTURE
3. SELF INTERMITTENT CLEAN
4. SPHERICAL GLIDING PRINCIPLE
CATHETERISATION
5. HYDROTHERAPY
4. FLOOR REACTION ORTHOSIS
6. GAIT CYCLE
5. TRANS SCAPHOID PERILUNATE FRACTURE
7. BABY CAR FRACTURE DISLOCATION

8. LIVELY SPLINT 6. HOLSTEIN LEWIS INJURY

9. CLOVER LEAF NAIL 7. ULNAR DRIFT IN RHEUMATOID ARTHRITIS

8. LCP

9. ELECTROMYOGRAPHY (KUL 1- 900) (TUREK

CH 14 ORTHOPEDIC NEUROLOGY)
 JUNE 2006 NOV 2006

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. CLASSIFY FRACTURES OF THE UPPER END OF 1. DESCRIBE THE CLASSIFICATION OF

HUMERUS. ACETABULAR FRACTURES AND BRIEFLY
OUTLINE THE VARIOUS OPTIONS IN THE
DISCUSS TREATMENT OPTIONS FOR A 3 PART
MANAGEMENT OF ACETABULAR FRACTURES.
AND 4 PART FRACTURES.

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2. MONTEGGIA VARIANTS (ZUKERMAN PG 653)
2. TENSION BAND WIRING.
; ROCKWOOD; RADIUS AND ULNA SHAFT
3. FRACTURES OF THE ATLAS FRACTURES; GOPALAN 381

4. INTERLOCKING NAILS 3. CLASSIFICATION OF FRACTURES OF THE

CALCANEUM
5. ARDS
4. ARDS
6. MANAGEMENT OF DIFFERENT TYPES OF
NONUNION IN MIDDLE THIRD SHAFT OF FEMUR 5. FRACTURES OF SACRUM

7. ACL DEFICIENT KNEE(CAMPBELL ; SPORTS 6. RETROGRADE FEMORAL NAILING

MEDICINE CH-KNEE INJURIES)(CAMPBELL ; CH-
7. CLASSIFICATION OF TIBIAL PLATEAU
ARTHROSCOPY OF LOWER EXTREMITIES) 8.
FRACTURES
SULCUS SIGN
8. FRACTURE SCAPHOID
9. CLASSIFICATION OF MONTEGIA FRACTURES.
9. CHANCE FRACTURE
 JUNE 2005 NOVEMBER 2004

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. CLASSIFY TROCHANTERIC FRACTURES. 1. DESCRIBE THECLASSIFICATION OF DISTAL

FEMORAL FRACTURES.
GIVE TREATMENT OPTIONS FOR THEM
MENTION THE VARIOUS OPTIONS IN THE
MANAGEMENT OF DISTAL FEMORAL
SHORT ESSAYS (8X10=80 MARKS) FRACTURES IN ADULT AND THE
COMPLICATIONS OF DISTAL FEMORAL
2. 4-PART FRACTURES OF PROXIMAL HUMERUS
FRACTURES.
3. FRACTURE NECK OF TALUS (DAV-KNEE ANKLE
SHORT ESSAYS (8X10=80 MARKS)
TRAUMA; F/3RD)
2. PERILUNAR DISLOCATION
4. TITANIUM IMPLANTS
3. CLASSIFICATION OF TALUS FRACTURES AND
5. BONE MARROW INJECTIONS
THEIR COMPLICATIONS (DAV-KNEE ANKLE
6. TREATMENT OPTIONS FOR VARIOUS TRAUMA; F/3RD)
FRACTURES OF CALCANEUM
4. TARDY ULNAR NERVE PALSY
7. GAMMA NAIL
5. ODONTOID FRACTURE
8. TRIAGE
6. COMPLICATION OF PELVIS FRACTURES
9. ANTERO MEDIAL INSTABILITY KNEE
7. CLASSIFICATIONS OF FRACTURE NECK OF
FEMUR IN CHILDREN

8. DYNAMISATION

9. CLASSIFICATION OF SUBTROCHANTERIC
FRACTURES
 JUNE 2004

PAPER 2

ESSAY (20 MARKS)

1. HOW WILL YOU EVALUATE AND TREAT A

PATHOLOGICAL FRACTURE OF THE SHAFT OF
FEMUR IN A 60 YR OLD MAN

SHORT ESSAYS (8X10=80 MARKS)

2. INTERCARPAL INSTABILITY

3. SUPRACONDYLAR NAIL

4. LIGAMENTOTAXIS

5. ERBS PARALYSIS

6. STRESS FRACTURE KULKARNI 1218

7. OLD UNREDUCED DISLOCATION OF ELBOW

8. OSTEOCHONDRITIS DESSICANS (DAV-LOCAL

COMPLICATIONS OF#; F/3RD) CAMPBELL
SPORTS MEDICINE-KNEE INJURIES)

9. FLOATING HIP
 SECTION 4

MS ORTHO

PAPER 3

-- CALICUT UNIVERSITY (2012-2002)

-- KERALA UNIVERSITY (2012-2004)

 JUNE 2012 MAY 2012

PAPER 3-ORTHOPAEDIC DISEASES PAPER 3 - COLD ORTHOPAEDICS

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DEFINE OSTEOPOROSIS. 1. DISCUSS THE PATHOLOGICAL ANATOMY OF

DDH.
DISCUSS CLINICAL FEATURES, CAUSES AND
MANAGEMENT OF GENERALISED DISCUSS THE EVALUATION AND MANAGEMENT
OSTEOPOROSIS OF NEGLECTED DDH IN A 2 YR OLD CHILD

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.CHORDOMA ( CAMPBELL - MALIGNANT BONE 2.TUBERCULOSIS OF SHOULDER

TUMOURS)
3.HALLUX VALGUS(DAV-LOCAL
3.ARTHROGRYPOSIS MULTIPLEX CONGENITA COMPLICATIONS OF#; M/3RD)
CAMPBELL VOL2; NEURVOUS SYSTEM
4.TIBIALIS POSTERIOR DYSFUNCTION
DISORDERS IN CHILDREN
5.CHORDOMA ( CAMPBELL - MALIGNANT BONE
4.CONGENITAL PSEUDARTHROSIS TIBIA
TUMOURS)
CAMPBELL (CONGENITAL ANOMALIES OF
LOWER EXTREMITY) 6.MADELUNG DEFORMITY

5. HALLUX VALGUS (DAV-LOCAL 7.OSTEOCHONDRITIS DESSICANS OF KNEE

COMPLICATIONS OF#; M/3RD) (DAV-LOCAL COMPL OF#; F/3RD) CAMPBELL
SPORTS MEDICINE-KNEE INJURIES)
6. DOTS REGIME FOR TUBERCULOSIS
8.CROUCH GAIT
7.SOLID ANKLE CUSHION HEEL FOOT (SACH
FOOT) KULKARNI 3941 9.SCHUERMANNS DISEASE (CAMPBELL CH-
SCOLIOSIS&KYPHOSIS)
8.VERTEBRA PLANA

9.ULNAR CLAW HAND

 NOVEMBER 2011 MAY 2011

PAPER 3- COLD ORTHOPAEDICS PAPER 3- COLD ORTHOPAEDICS

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE MECHANISM OF TUMOUR 1. CLASSIFY ADOLESCENT IDIOPATHIC

METASTASIS TO BONE. SCOLIOSIS.

DISCUSS THE CLINICAL FEATURES, DIAGNOSIS DISCUSS EVALUATION AND MANAGEMENT OF

AND MANAGEMENT OF METASTATIC BONE A 15 YR OLD GIRL WITH RIGHT THORACIC
DISEASE CURVE (CAMPBELL CH- SCOLIOSIS&KYPHOSIS)

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.TOTAL CLAW HAND 2.RENAL TUBULAR ACIDOSIS

3.SYNOVIAL CHONDRAMATOSIS 3.CONGENITAL COXA VARA

4.OSTEOBLASTOMA(TACHDJIAN ; BENIGN 4.SUBACUTE OSTEOMYELITIS

MUSCULOSKELETAL TUMOUR)
5.TOURNIQUET PALSY(STEWART-TOURNIQUET)
5.IDIOPATHIC CHONDROLYSIS OF HIP
6.ORTHOPAEDIC MANIFESTATION OF
6.CARIES SPINE HEMOPHILIA

7.NEUROPATHIC PLANTAR ULCER 7.TARSAL COALITION(CAMPBELL , FOOT AND

ANKLE; PES PLANUS)
8.POST POLIO SYNDROME
8.MID PALMAR SPACE INFECTION
9.HYPER PARATHYROIDISM
9.BLOUNTS DISEASE (CAMPBELL VOL 2 ;
OSTEOCHONDROSIS), GOPALAN PG 324
 MAY 2010 NOVEMBER 2009

PAPER 3- COLD ORTHOPAEDICS PAPER 3- COLD ORTHOPAEDICS

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE PATHOLOGY AND 1. DISCUSS THE PATHOLOGY AND

MANAGEMENT OF DDH MANAGEMENT OF DDH

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.RHEUMATOID ELBOW 2.RHEUMATOID ELBOW

3.TARSAL COALITION(CAMPBELL ,FOOT AND 3.TARSAL COALITION(CAMPBELL , FOOT AND

ANKLE; PES PLANUS) ANKLE; PES PLANUS) 4.CHONDROLYSIS

4.CHONDROLYSIS 5.XANTHOMA TENDINOSUM

5.XANTHOMA TENDINOSUM 6.GIANT CELL VARIANTS (DAV- TUMOURS;

GCT)
6.GIANT CELL VARIANTS (DAV- TUMOURS;
GCT) 7.OSTEOCHONDRITIS DESSICANS CAMPBELL
SPORTS MEDICINE-KNEE INJURIES)
7.OSTEOCHONDRITIS DESSICANS (DAV-LOCAL
COMPLICATIONS OF#; F/3RD) 8.RISSERS SIGN (CAMPBELL CH-
SCOLIOSIS&KYPHOSIS)
8.RISSERS SIGN (CAMPBELL CH-
SCOLIOSIS&KYPHOSIS) 9.AVN FEMORAL HEAD (DAV- GENERAL;
M/3RD)
9.AVN FEMORAL HEAD( DAV- GENERAL;
M/3RD)
 MAY 2009 MAY 2008

PAPER 3 - COLD ORTHOPAEDICS (RPT OF MAY 2009)

JANUARY 2008

ESSAY (20 MARKS) PAPER 3 - COLD ORTHOPAEDICS

1. DISCUSS THE ETIOPATHOGENESIS AND

MANAGEMENT OF PERTHES DISEASE
ESSAY (20 MARKS)

1. DESCRIBE THE CLASSIFICATION OF SCFE.

SHORT ESSAYS (8X10=80 MARKS)
DESCRIBE THE MANAGEMENT OF EACH TYPE.
2.SCIWORA
LIST THE MAJOR COMPLICATIONS
3.TARSAL COALITION (CAMPBELL , FOOT AND
ANKLE; PES PLANUS)

SHORT ESSAYS (8X10=80 MARKS)

4.SINGLE EVENT MULTI LEVEL SURGERY IN CP

2.MARFANS SYNDROME , GOPALAN PG 392

5.TENNIS ELBOW (CAMPBELL SPORTS
MEDICINE-ELBOW INJURIES) 3.RUGGER JERSEY SPINE

6.TRIPLE ARTHRODESIS 4.MALIGNANT FIBRO HISTIOCYTOMA

7.DOTS REGIMEN IN SKELETAL TUBERCULOSIS 5.TINELS SIGN

8.BARLOWS TEST 6.NEGLECTED CLUBFOOT

9.HALLUX RIGIDUS 7.PSEUDOSPONDYLOLISTHESIS (CAMPBELL CH-

SCOLIOSIS&KYPHOSIS)

8.CONGENITAL POSTERIOR BOWING OF TIBIA

9.SCHMORLS NODES
 MAY 2007 OCTOBER 2006

PAPER 3 - COLD ORTHOPAEDICS PAPER 3 - COLD ORTHOPAEDICS

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE CLASSIFIFCATION OF BONE 1. DESCRIBE THE PATHOLOGY, CLINICAL

TUMOURS. FEATURES, INVESTIGATIONS AND
MANAGEMENT OF PERTHES DISEASE
DISCUSS THE MANAGEMENT OF
OSTEOSARCOMA

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS) 2.OLLIERS DISEASE

2.VERTICAL TALUS CAMPBELL (CONGENITAL 3.SEQUESTRUM

ANOMALIES OF LOWER EXTREMITY)
4.CHONDRO OSTEDYSTROPHY
3.SYNOVITIS KNEE
5.BURSITIS AROUND KNEE
4.TRIGGER FINGER
6.DUPUYTRENS CONTRACTURE CAMPBELL ; CH
5.COXA VARA - THE HAND

6.PES EQUINO VARUS 7.SPINAL TUMOUR SYNDROME

7.ROUND KYPHUS 8.GIANT CELL VARIANTS (DAV- TUMOURS;

GCT)
8.OSTEPETROSIS
9.BRUCELLOSIS (DAV -- INFECTION; L/3RD.)
9.SABRE TIBIA
 MAY 2006 MAY 2005

PAPER 3 - COLD ORTHOPAEDICS PAPER 3 - COLD ORTHOPAEDICS

ESSAY (20 MARKS) ESSAY (35 X 2 = 70)

1. DESCRIBE THE PATHOLOGY, CLINICAL 1. DESCRIBE THE TERM "GOLDEN HOUR" IN

FEATURES, INVESTIGATIONS AND TRAUMA CARE.(5)
MANAGEMENT OF POTTS PARAPLEGIA WHAT ARE THE REQUIREMENTS FOR SETTING
UP A GTRAUMA CARE UNIT.(15)
DISCUSS BRIEFLY THE DUTIES AND
SHORT ESSAYS (8X10=80 MARKS) RESPONSIBILITIES OF THE TEAM MEMBERS.(15)

2.HETEROTROPIC OSSIFICATION- GOPALAN 2.DEFINE CEREBRAL PALSY.(5)

PG211 WHAT ARE THE CLINICAL TYPES OF CP.DESCRIBE
CLINICAL FEATURES OF EACH TYPE.(15)
3.GARRES OSTEOMYELITIS
HOW WOULD YOU EVALUATE A 4 YR OLD CHILD
4.MADURA FOOT WITH CP WHO HAS NOT YET WALKED (15)

5.NEURALGIC AMYOTROPHY

6.SECONDARY OSTEOSARCOMA (CAMPBELL VOL 2 ; NERVOUS SYSTEM

DISORDERS IN CHILDREN)
7.KEINBOCKS DIESEASE
SHORT ESSAYS (3X10=30 MARKS)
8.KNEE IN HEMOPHILIA
3.EVALUATION OF DDH IN NEONATE
9.SUBUNGAL EXOSTOSIS(CAMPBELL ,
DISORDERS OF NAIL) 4.COMPLICATIONS OF THR

5.SINGHS INDEX
 MAY 2004 NOVEMBER 2003

PAPER 3 - COLD ORTHOPAEDICS PAPER 3 - COLD ORTHOPAEDICS

ESSAY (20 MARKS) ESSAY (20 MARKS)

1.DISCUSS THE CAUSES AND MANAGEMENT 1.DESCRIBE THE RADIOLOGICAL FEATURES OF

(OPERATIVE AND NON OPERATIVE) OF EQUINUS TUBERCULOSIS OF THE HIP.
DEFORMITY OF ANKLE IN A 20 YR OLD MALE
HOW WILL YOU MANAGE A BURNT OUT CASE
SHORT ESSAYS (8X10=80 MARKS) OF TB HIP PRESENTING AS A PAINFUL LIMP IN A
30 YR OLD MALE--TULI
2.ABRASION CHONDROPLASTY
SHORT ESSAYS (8X10=80 MARKS)
3.OVERUSE INJURIES IN ATHLETES
2.TRANSIENT SYNOVITIS OF HIP
4.TURN GRAFT
3.SURGICAL MANAGEMENT OF CONTAINED
5.POSTERIOR LUMBAR INTERBODY FUSION
CHONDRAL DEFECTS OF THE FEMORAL
6.FROZEN SHOULDER CONDYLE

7.GARRES SCLEROSING OSTEOMYELITIS 4.SWAN NECK DEFORMITY

8.HYALURONIC ACID 5.PROTRUSIO ACETABULI

9.CERAMICS IN ORTHOPAEDICS 6.SPINAL TUMOUR SYNDROME

7.EXTENDED TROCHANTERIC OSTEOTOMY

8.CHONDROBLASTOMA(TACHDJIAN ; BENIGN
MUSCULOSKELETAL TUMOUR)

9.EXCESSIVE LATERAL PRESSURE SYNDROME OF

PATELLA
 NOVEMBER 2002

PAPER 3 COLD ORTHOPAEDICS

ESSAY (20 MARKS)

1.DISCUSS THE PATHOLOGICAL ANATOMY OF

CTEV.

DISCUSS ITS MANAGEMENT WITH MODERN

TRENDS IN TREATMENT. CAMPBELL
(CONGENITAL ANOMALIES OF LOWER
EXTREMITY)

SHORT ESSAYS (8X10=80 MARKS)

2.OLLIERS DISEASE

3.TOM SMITH ARTHRITIS

4.BRODIES ABSCESS

5.FROZEN SHOULDER

6.CHARCOTS JOINT

7.DUPUYTRENS CONTRACTURE CAMPBELL ; CH

- THE HAND

8.CODMANS TRIANGLE

9.SHENTONS LINE
 JUNE 2012 NOV 2011

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE GCT VARIANTS, CLINICAL 1. DISCUSS THE PATHOLOGICAL ANATOMY OF

FEATURES AND MANAGEMENT. (DAV- CTEV.
TUMOURS; GCT)
DISCUSS ITS MANAGEMENT WITH MODERN
TRENDS. CAMPBELL (CONGENITAL ANOMALIES
OF LOWER EXTREMITY)
SHORT ESSAYS (8X10=80 MARKS)

2.CHONDROBLASTOMA (TACHDJIAN ; BENIGN

MUSCULOSKELETAL TUMOUR) SHORT ESSAYS (8X10=80 MARKS)

3.TIBIA VARA 2.SEQUELAE OF SEPTIC ARTHRITIS OF HIP IN

CHILDREN
4.DOTS IN SKELETAL TB-TULI
3.CHARCOTS JOINT
5.CHEMONUCLEOLYSIS
4.DUPUYTRENS CONTRACTURE CAMPBELL ; CH
6.TARSAL COALITION(CAMPBELL , FOOT AND
- THE HAND
ANKLE; PES PLANUS)
5.CODMANS TRIANGLE
7.NEUROPATHIC JOINT
6.CONGENITAL VERTICAL TALUS CAMPBELL
8.PLIF
(CONGENITAL ANOMALIES OF LOWER
9.SPINAL TUMOUR SYNDROME EXTREMITY)

7.OSTEOPETROSIS (TACHDJIAN, ORTHOPEDIC

DISORDERS)

8.CLASSIFICATION OF BONE TUMOURS

9.KEINBOCKS DISEASE
MAY 2011 NOV 2010

PAPER 3 PAPER 3
ESSAY (20 MARKS)
ESSAY (20 MARKS)
1. DESCRIBE FACTORS CONTRIBUTING TO
STABILITY OF SHOULDER JOINT. WHAT ARE THE 1. WHAT DO YOU MEAN BY SERONEGATIVE
PATHOLOGICAL CHANGES IN RECURRENT ARTHROPATHIES? (KUL 1- 886)
ANTERIOR SHOULDER DISLOCATION. DISCUSS
THE RECENT TRENDS IN MANAGEMENT OF ENUMERATE THE DISEASES WHICH ARE
RECURRENT SHOULDER DISLOCATION
INCLUDED IN THIS ENTITY. DISCUSS THE ROLE
SHORT ESSAYS (8X10=80 MARKS) OF SURGERY IN ANY ONE OF THEM.

2.MANAGEMENT OF SPASMODIC FLAT FOOT

SHORT ESSAYS (8X10=80 MARKS)
3.DESCRIBE MEHTAS R-V ANGLE (CAMPBELL CH-
SCOLIOSIS&KYPHOSIS) 2.COMPOUND PALMAR GANGLION

4.MANAGEMENT- OSTEOGENESIS 3.INDICATIONS AND COMPLICATIONS OF TRIPLE

IMPERFECTA (DAV-LOCAL COMPLICATIONS
ARTHRODESIS
OF#; M/3RD) TACHDJIAN Ch 32 (METABOLIC)

5.CLINICO RADIOLOGICAL FEATURES OF 4.CAUSES OF NEUROLOGICAL COMLPICATIONS

OSTEOCHONDRITIS DESSICANS (DAV-LOCAL IN SPINAL TUBERCULOSIS
COMPLICNS OF#; F/3RD)
5.MADELUNG DEFORMITY AND ITS
6.SYNOVIAL CHONDRAMATOSIS AND
RADIOLOGICAL FEATURES
MANAGEMENT

7.CONG.PSEUDARTHROSIS TIBIA CAMPBELL 6.CLINICO RADIOLOGICAL FEATURES OF

(CONGENITAL ANOMALIES OF LOWER BRODIES ABSCESS
EXTREMITY)
7.SURGICAL STAGING OF BONE TUMOURS,
8. DUPUYTRENS CONTRACTURE AND ITS
MANAGEMENT CAMPBELL ; CH - THE HAND IMPORTANCE IN Mx

9.C/F AND MANAGEMENT OF DEQUERVAINS 8.BLOUNTS DISEASE(CAMPBELL VL 2 ;

DISEASE.
OSTEOCHONDROSIS), GOPALN PG 324

9.BIOMECHANICS OF DEFORMITIES OF THE

HAND IN RA
 JUNE 2010 MAY 2009

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE CLASSIFICATIONS, 1. DISCUSS THE ETIOPATHOLOGY AND

EVALUATION AND MANAGEMENT OF PERTHES MANAGEMENT OF IDIOPATHIC AVASCULAR
DISEASE OF HIP. NECROSIS OF FEMORAL HEAD

SHORT ESSAYS (8X10=80 MARKS)

2.TOM SMITH ARTHRITIS SHORT ESSAYS (8X10=80 MARKS)

3.MULTIPLE ENCHONDROMATOSIS (DAV- 2.NEUROPATHIC JOINT

TUMOURS; M/3RD)
3.RENAL OSTEODYSTROPHY
4.DIAGNOSIS AND COMPLICATIONS OF PAGETS
4.CONGENITAL VERTICAL TALUS CAMPBELL
DISEASE
(CONGENITAL ANOMALIES OF LOWER
5.PAEDIOLOGICAL EVALUATION OF EXTREMITY)
SCOLIOSIS(CAMPBELL CH-
5.OSTEOBLASTOMA(TACHDJIAN ; BENIGN
SCOLIOSIS&KYPHOSIS)
MUSCULOSKELETAL TUMOUR) 6.BRUCELLOSIS -
DAV -- INFECTION; L/3RD.

6.DIAGNOSIS OF GOUT(TUREK CH 9 7.SWAN NECK DEFORMITY

METABOLIC BONE DISEASE)
8.HALLUX VALGUS (DAV-LOCAL
7.PULLED ELBOW COMPLICATIONS OF#; M/3RD), CAMPBELL
FOOT AND ANKLE, DISORDERS OF HALLUX
8.MANAGEMENT OF CARPAL TUNNEL
SYNDROME CAMPBELL ; CH - THE HAND 9.SPONDYLOEPIPHYSEAL DYSPLASIA

9.CAUSES OF PARAPLEGIA IN TB SPINE-TULI

 DEC 2008 MAY 2008

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE PATHOLOGY OF 1. CLASSIFY SPONDYLOLISTHESIS. DESCRIBE THE

OSTEOARTICULAR TB. CLINICAL FEATURES, ROENTGENOGRAPHIC
FEATURES AND MANAGEMENT OF ISTHMIC
OUTLINE THE MANAGEMENT OF CARIES SPINE
SPONDYLOLISTHESIS. (CAMPBELL CH-
AT D10 LEVEL WITH PARAPARESIS -- TULI
SCOLIOSIS&KYPHOSIS)

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.CRYSTAL ARTHROPATHY
2.FRAGILITIS OSSIUM
3.BLOUNTS DISEASE(CAMPBELL VOL 2 ;
3.ENDOSCOPIC RELEASE OF CARPAL TUNNEL
OSTEOCHONDROSIS), GOPALAN PG 324
CAMPBELL ; CH - THE HAND
4.OSTEOMALACIA
4.JOINT MOUSE
5.RADIAL CLUB HAND
5.SANDY SEQUESTRUM
6.DUPUYTRENS CONTRACTURE CAMPBELL ; CH
6.CONGENITAL RADIOULNAR SYNOSTOSIS
- THE HAND
7.FNAC
7.CHONDROBLASTOMA(TACHDJIAN ; BENIGN
MUSCULOSKELETAL TUMOUR) 8.ENZYMES IN OSTEOMYELITIS

8.THORACIC OUTLET SYNDROME 9.INTERVERTEBRAL DISC (CAMPBELL CH-

LOWER BACK PAIN)
9.SYNOVIAL CHONDRAMATOSIS
 MAY 2007 JUNE 2006

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DEFINE AND DESCRIBE SCFE AND DISCUSS ITS 1. DISCUSS IN DETAIL PRIMARY
MANAGEMENT. HYPERPARATHYROIDISM.

HOW WILL YOU DIFFERENTIATE BETWEEN

PRIMARY AND SECONDARY
SHORT ESSAYS (8X10=80 MARKS)
HYPERPARATHYROIDISM.
2.HEMOPHILIC ARTHROPATHY

3.IDIOPATHIC AVASCULAR NECROSIS OF

SHORT ESSAYS (8X10=80 MARKS)
FEMORAL HEAD
2.PAROSTEAL OSTEOSARCOMA
4.AIDS IN ORTHOPAEDIC SURGERY
3.GROWTH HORMONE
5.CARIES SICCA
4.PRINCIPLES OF FRACTURE HEALING
6.ACTINOMYCOSIS
5.GIANT CELL TUMOUR OF TENDON SHEATH
7.MORQUOI SYNDROME
6.OTTO PELVIS
8.TENNIS ELBOW (CAMPBELL SPORTS
MEDICINE-ELBOW INJURIES) 7.HAMMER TOE DEFORMITY

9.TARSAL TUNNEL SYNDROME 8.INTERPOSITIONAL ARTHROPLASTY

9.WINGING OF SCAPULA
 NOV 2006 JUNE 2005

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. CLASSIFY SPONDYLOLISTEHSIS. DISCUSS IN 1. DISCUSS THE AETIOPATHOGENESIS OF POTTS

BRIEF THE MANAGEMENT OF ISTHMIC TYPE OF DISEASE OF THE SPINE.
SPONDYLOLISTHESIS IN ADULT (CAMPBELL CH-
DISCUSS THE TREATMENT OPTIONS FOR POTTS
SCOLIOSIS&KYPHOSIS)
PARAPLEGIA.

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.PAROSTEAL OSTEOSARCOMA
2.WINGING OF SCAPULA
3.BROWNS TUMOUR
3.HISTIOCYTO XANTHO GRANULOMA
4.SPINA VENTOSA
4.HAMMER TOE DEFORMITY
5.CONGENITAL VERTICAL TALUS CAMPBELL
5.HOFFAS DISEASE
(CONGENITAL ANOMALIES OF LOWER
EXTREMITY) 6.HIGH TIBIAL OSTEOTOMY

6.PIGMENTED VILLONODULAR SYNOVITIS(DAV- 7.INTERPOSITIONAL ARTHROPLASTIES

TUMOURS; L/3 RD)
8.RELAPSED CLUB FOOT
7.PRINCIPLES OF TENDON TRANSFER
9.THORACIC OUTLET SYNDROME
8.ULNAR CLAW HAND - TREATMENT OPTIONS

9.CLAW TOE
 NOVEMBER 2004 9.TRIPLE DEFORMITY

PAPER 3

ESSAY (20 MARKS)

1. DESCRIBE THE CLINICAL AND RADIOLOGICAL

DIAGNOSIS OF DDH. DISCUSS THE
MANAGEMENT IN A 3 YR OLD CHILD WITH THE
SAME

SHORT ESSAYS (8X10=80 MARKS)

2.ANEURYSMAL BONE CYST (TACHDJIAN ;

BENIGN MUSCULOSKELETAL TUMOUR)
3.DIAGNOSIS OF GOUT(TUREK CH 9 METABOLIC
BONE DISEASE) 4.RADIOLOGICAL CHANGES IN
GOUT(TUREK CH 9 METABOLIC BONE DISEASE)

5.MANAGEMENT OF HALLUX VALGUS (DAV-

LOCAL COMPLICATIONS OF#; M/3RD),
CAMPBELL FOOT AND ANKLE, DISORDERS OF
HALLUX 6.OSTEOCHONDRITIS DESSICANS (DAV-
LOCAL COMPLICATIONS OF#; F/3RD),
CAMPBELL SPORTS MEDICINE-KNEE INJURIES)

7.BANKARTS LESION

8.DIAGNOSIS OF CARPAL TUNNEL SYNDROME

CAMPBELL ; CH - THE HAND
 SECTION 5

MS ORTHO

PAPER 4

-- CALICUT UNIVERSITY (2012-2002)

-- KERALA UNIVERSITY (2012-2004)

 MAY 2012

PAPER 4 - RECENT TRENDS

JUNE 2012

PAPER 4- RECENT ADVANCES

ESSAY (20 MARKS)

1. CLASSIFY PROXIMAL HUMERAL FRACTURES.

ESSAY (20 MARKS)
DISCUSS THE RECENT ADVANCES IN THE
1. WHAT IS OSTEOSYNTHESIS.
MANAGEMENT OF PROXIMAL HUMERUS

DESCRIBE THE WAYS TO ACHIEVE FRACTURES.

OSTEOSYNTHESIS IN TREATMENT OF
SHORT ESSAYS (8X10=80 MARKS)
FRACTURES WITH RECENT ADVANCES
2.ADVANCES IN CEMENTING TECHNIQUES

3.SAFE SURGICAL DISLCATION OF HIP

SHORT ESSAYS (8X10=80 MARKS)
4.PATHOPHYSIOLOGY OF SPINAL CORD INJURY
2.BEARING SURFACES IN TOTAL HIP
REPLACEMENT KULKARNI 3702 5.MEDICAL MANAGEMENT OF OSTEOPOROSIS

3.ZOLEDRONIC ACID 6.REVERSE SHOULDER PROSTHESIS

4.TUMOUR MARKERS 7.SOFT TISSUE BALANCING IN TKR

5.FEMEROACETABULAR IMPINGEMENT 8.FEMEROACETABULAR IMPINGEMENT

6.BONE CEMENT GOPALAN 672 9.SPASTICITY MANAGEMENT IN CEREBRAL

PALSY (CAMPBELL VOL 2 ; NERVOUS SYSTEM
7.DEXA SCAN GOPALAN PG 282
DISORDERS IN CHILDREN)

8.PFN

9.POSTOPERATIVE DVT --
PREVENTION,CLINICAL
FEATURES,MANAGEMENT.
 NOVEMBER 2011 MAY 2011

PAPER 4 -RECENT ADVANCES PAPER 4 - RECENT ADVANCES

ESSAY (20 MARKS)

1. CLASSIFY DISTAL RADIUS FRACTURES. ESSAY (20 MARKS)

DISCUSS THE RECENT ADVANCES IN THE 1. CLASSIFY PERIPROSTHETIC FRACTURES.

MANAGEMENT OF DISTAL RADIUS FRACTURES DISCUSS THEIR MANAGEMENT
WITH SPECIAL EMPHASIS ON FRAGMENT
SPECIFIC FIXATION
SHORT ESSAYS (8X10=80 MARKS)
SHORT ESSAYS (8X10=80 MARKS)
2.GUIDED GROWTH
2.BEARING SURFACES IN THR KULKARNI 3702
3.BONE BANK KULKARNI 1137
3.PONSETI TECHNIQUE
4.UNICAMERAL BONE CYST (TACHDJIAN ;
4.PATHOPHYSIOLOGY OF SPINAL CORD INJURY
BENIGN MUSCULOSKELETAL TUMOUR)
5. DISEASE MODIFYING DRUGS IN RHEUMATOID
5.BONE SUBSTITUTES
ARTHRITIS
6.MECHANICAL AXIS DEVIATION
6.LOCAL ANTIBIOTIC DELIVERY SYSTEM
7.BONE CEMENT GOPALAN 672 8.FLOOR
7.SURGICAL SITE INFECTION
REACTION ORTHOSIS
8.DOUBLE BUNDLE ACL
9.POSTERIOR STABILISED TKR
RECONSTRUCTION(CAMPBELL ; SPORTS
MEDICINE CH-KNEE INJURIES)(CAMPBELL ; CH-
ARTHROSCOPY OF LOWER EXTREMITIES)

9.SAFE SURGICAL DISLCATION OF HIP

 MAY 2010 NOVEMBER 2009

PAPER 4- RECENT ADVANCES PAPER 4- RECENT ADVANCES

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE RECENT ADVANCES IN THE 1. DISCUSS INTERNAL DERANGEMENT OF KNEE

MANAGEMENT OF OSTEOSARCOMA WITH WITH EMPHASIS ON MANAGEMENT
EMPHASIS ON LIMB SALVAGE - (DAV)

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.LOW TEMPERATURE THERMOPLASTICS
2.DOUBLE BUNDLE ACL STEWART PG 201
RECONSTRUCTION(CAMPBELL ; SPORTS
3.MIPPO
MEDICINE CH-KNEE INJURIES)(CAMPBELL ; CH-
ARTHROSCOPY OF LOWER EXTREMITIES) 4.HOOP STRESS

3.FOOTBALLERS ANKLE 5.DISC REPLACEMENT

4.EVIDENCE BASED ORTHOPAEDICS 6.PREVENTION OF HIV TRANSMISSION IN OT

5.DIAGNOSIS OF OSTEOPOROSIS 7.BONE BANK KULKARNI 1137

6.DUPUYTRENS CONTRACTURE CAMPBELL ; CH 8.HIGH TIBIAL OSTEOTOMY

- THE HAND
9.DMARD
7.COMPLEX REGIONAL PAIN SYNDROME
(CAMPBELL PERIPHERAL NERVE INJURIES;
EFFECTS OF PERIPHERAL NERVE INJURIES)

8.CEMENT DISEASE

9.BONE BANK KULKARNI 1137

 MAY 2009 MAY 2008

PAPER 4 - RECENT ADVANCES PAPER 4- RECENT ADVANCES

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE RECENT ADVANCES IN THE 1. DISCUSS INTERNAL DERANGEMENT OF KNEE

MANAGEMENT OF OSTEOSARCOMA WITH WITH EMPHASIS ON MANAGEMENT
EMPHASIS ON LIMB SALVAGE (DAV)

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.LOW TEMPERATURE THERMOPLASTICS
2.DOUBLE BUNDLE ACL STEWART PG 201
RECONSTRUCTION(CAMPBELL ; SPORTS
3.MIPPO
MEDICINE CH-KNEE INJURIES)(CAMPBELL ; CH-
ARTHROSCOPY OF LOWER EXTREMITIES) 4.HOOP STRESS

3.FOOTBALLERS ANKLE 5.DISC REPLACEMENT

4.EVIDENCE BASED ORTHOPAEDICS 6.PREVENTION OF HIV TRANSMISSION IN OT

5.DIAGNOSIS OF OSTEOPOROSIS 7.BONE BANK KULKARNI 1137

6.DUPUYTRENS CONTRACTURE CAMPBELL ; CH 8.HIGH TIBIAL OSTEOTOMY

- THE HAND
9.DMARD
7.COMPLEX REGIONAL PAIN
SYNDROME(CAMPBELL PERIPHERAL NERVE
INJURIES; EFFECTS OF PERIPHERAL NERVE
INJURIES)

8.CEMENT DISEASE

9.BONE BANK KULKARNI 1137

 JANUARY 2008 MAY 2007

PAPER 4 RECENT ADVANCES PAPER 4 - RECENT ADVANCES

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE POLYTRAUMA PATIENT. 1. DISCUSS THE RECENT ADVANCES IN

MANAGEMENT OF MALIGNANT BONE
DISCUSS THE STEPS IN EVALUATION AND
TUMOURS WITH EMPHASIS ON LIMB SALVAGE
PRINCIPLES OF MANAGEMENT OF A
(DAV)
POLYTRAUMA PATIENT

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.BMP
2.ANTERIOR KNEE PAIN
3.PERCUTANEOUS VERTEBROPLASTY
3.PERCUTANEOUS DISCECTOMY
4.LCP
4.CRUSH SYNDROME
5.ENDOSCOPIC DISCECTOMY
5.RADIAL SHORTENING
6.GENE THERAPY
6.COMPUTER NAVIGATED ARTHROPLASTY
7.BONE BANK KULKARNI 1137
7.FRAGILITY FRACTURES OF ANKLE
8.RADIOFREQUENCY TREATMENT
8.UNICOMPARTMENTAL KNEE REPLACEMENT
9.BIODEGRADABLE IMPLANTS (CAMPBELL
,GENERAL PRINCIPLES OF FRACTURE 9.BMD
TREATMENT; BIOMECHANICS)
 OCTOBER 2006 MAY 2006

PAPER 4 - RECENT ADVANCES PAPER 4 - RECENT ADVANCES

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE RECENT ADVANCES IN THE 1. DISCUSS THE RECENT ADVANCES IN THE
PREVENTION, INVESTIGATIONS AND INVESTIGATIONS AND MANAGEMENT OF
MANAGEMENT OF POST OPERATIVE INFECTION FRACTURE NON UNION .
IN ORTHOPAEDIC IMPLANTS

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.BONE MARROW OEDEMA SYNDROME
2.THROMBOPROPHYLAXIS
3.HIV INFECTION OF PERIPHERAL NERVES
3.EXTRA CORPOREAL IRRADIATION
4.METATARSALGIA
4.COMPUTER ASSISTED SPINAL
5.OSTEITIS CONDENSANS ILLI
INSTRUMENTATION
6.COMPENSATION NEUROSIS
5.TISSUE EXPANDERS
7.DISCOGRAPHY
6.HYDROXY APATITE COATING
8.ANTERIOR KNEE PAIN
7.LASER IN ORTHOPAEDICS
9.AUTOLOGOUS CHONDROCYTE
8.GLYCOCALYX
IMPLANTATION
9.BONE MINERAL DENSITY
 MAY 2005 NOVEMBER 2003

PAPER 4 - RECENT ADVANCES PAPER 4 - RECENT ADVANCES

ESSAY (35 X 2 = 70) ESSAY (20 MARKS)

1. DISCUSS THE CRITERIA FOR SELECTION OF 1. DESCRIBE THE NATURAL HISTORY OF

PATIENTS FOR DIFFERENT TYPES OF TOTAL HIP DEGENERATIVE ARTHRITIS OF THE KNEE.
ARTHROPLASTY.
DISCUSS THE EVALUATION, OPERATIVE AND
BRIEFLY DISCUSS THE IMAGING MODALITIES NON OPERATIVE MANAGEMENT OPTIONS IN A
USED IN INVESTIGATING A SUSPECTED SEPSIS IN CASE OF UNICOMPARTMENTAL
TOTAL ARTHROPLASTY OF HIP. OSTEOARTHRITIS OF KNEE.

2.WHAT ARE THE CAUSES OF ACUTE

HEMARTHROSIS OF KNEE.
SHORT ESSAYS (8X10=80 MARKS)
HOW WOULD YOU EVALUATE AN ACL INJURY.
2.FEMORAL IMPACTION GRAFTING.
DISCUSS THE RECENT ADVANCES IN ANTERIOR
CRUCIATE RECONSTRUCTION(CAMPBELL ; 3.PERIPROSTHETIC FRACTURE.
SPORTS MEDICINE CH-KNEE
4.FLEXIBLE TITANIUM NAILING.
INJURIES)(CAMPBELL ; CH-ARTHROSCOPY OF
LOWER EXTREMITIES) 5.INTERBODY CAGES IN SPINAL SURGERY.

SHORT ESSAYS (3X10=30 MARKS) 6.SLAP LESIONS OF THE SHOULDER.KULKARNI

1868
3.COMPUTER ASSISSTED ORTHOPAEDIC
SURGERY 7.MALIGNANT FIBROUS HISTIOCYTOMA.

4.LC DCP 8.ARTHROSCOPY OF THE ANKLE.

5.BONE BANK KULKARNI 1137 9.SULCUS SIGN IN SHOULDER INSTABILITY.

 NOVEMBER 2002

PAPER 4 RECENT ADVANCES

ESSAY (20 MARKS)

1.DISCUSS THE ROLE OF MICROSURGERY IN

MODERN ORTHOPAEDIC PRACTICE

SHORT ESSAYS (8X10=80 MARKS)

2.CEMENTLESS TOTAL HIP REPLACEMENT

3.ARTHROSCOPIC RECONSTRUCTION OF
ACL(CAMPBELL ; SPORTS MEDICINE CH-KNEE
INJURIES)(CAMPBELL ; CH-ARTHROSCOPY OF
LOWER EXTREMITIES)

4.GAMMA NAIL

5.LC DCP

6.BIOLOGICAL FIXATION

7.BONE TRANSPORT

8.DYNAMIC HIP SCREW

9.MRI IN ORTHOPAEDICS KULKARNI

PG 93
 JUNE 2012 NOV 2011

PAPER 4 PAPER 4

ESSAY (20 MARKS)

ESSAY (20 MARKS) 1. DECSRIBE THE ETIOLOGY OF SHOULDER

INSTABILITY. DISCUSS THE CURRENT TRENDS IN
1. DESCRIBE DISTAL RADIUS FRACTURES.
THE MANAGEMENT OF SHOULDER INSTABILITY
WHAT ARE THE RECENT ADVANCES IN
SHORT ESSAYS (8X10=80 MARKS)
MANAGEMENT
2.FEMOROACETABULAR IMPINGEMENT

3.DOUBLE BUNDLE ACL

SHORT ESSAYS (8X10=80 MARKS)
RECONSTRUCTION(CAMPBELL ; SPORTS
2.CERAMICS IN ORTHOPAEDICS MEDICINE CH-KNEE INJURIES)(CAMPBELL ; CH-
ARTHROSCOPY OF LOWER EXTREMITIES)
3.BIODEGRADABLE IMPLANTS (CAMPBELL
,GENERAL PRINCIPLES OF FRACTURE 4.DEXA SCAN GOPALAN PG 282
TREATMENT; BIOMECHANICS)
5.COMPLEX REGIONAL PAIN
4.MIPPO SYNDROME(CAMPBELL PERIPHERAL NERVE
INJURIES; EFFECTS OF PERIPHERAL NERVE
5.DMARD
INJURIES)
6.HIV IN ORTHOPAEDICS
6.RESURFACING HIP ARTHROPLASTY
7.DISC REPLACEMENT
7.LOCKING COMPRESSION PLATE KULKARNI
8.BMP PG1433

9.SUPRASCAPULAR NEUROPATHY 8.CEMENTLESS TOTAL HIP REPLACEMENT

9.BONE MORPHOGENETIC PROTEIN

 MAY 2011 NOV 2010

PAPER 4 PAPER 4

ESSAY (20 MARKS)

1. WHAT ARE THE VARIOUS INVESTIGATIVE ESSAY (20 MARKS)

MODALITIES IN DIAGNOSING DDH. (TACHDJIAN)
1. WHAT ARE THE DIFFERENT METHODS OF
WHAT ARE THE RECENT TRENDS OF TREATING
FIXATION OF PROSTHESIS TO THE SKELETON?
DEGENERATIVE ARTHRITIS OF THE HIP IN A
YOUNG ADULT DISCUSS THEIR ADVANTAGES AND
LIMITATIONS.
SHORT ESSAYS (8X10=80 MARKS)
WHAT ARE THE RADIOLOGICAL FEATURES OF
2.TERMINAL DEVICES IN PROSTHESIS
ASEPTIC LOOSENING OF A PROTHESIS.
3.RECENT MANAGEMENT GUIDELINES FOR
SHORT ESSAYS (8X10=80 MARKS)
BRACHIAL PLEXUS INJURY, CAMPBELL VOL2;
NEURVOUS SYSTEM DISORDERS IN CHILDREN 2.CERAMICS IN ORTHOPAEDICS

4.BIODEGRADABLE IMPLANTS (CAMPBELL 3.MEGAPROSTHESIS - KULKARNI 1130

,GENERAL PRINCIPLES OF FRAC TREATMENT;
4.ROLE OF CONTINOUS PASSIVE MOBILISATION
BIOMECHANICS)
IN ORTHOPAEDICS
5.FUTURE ROLE OF STEM CELL THERAPY (KUL 1-
5.ROLE OF MINIMALLY INVASIVE SURGERY IN
PG53)
ORTHOPAEDICS
6.VASCULARISED FIBULAR GRAFT AND ITS
6.RECENT INVESTIGATIVE MODALITIES FOR
APPLICATION
BONE TUMOUR
7.ROLE OF BONE LENGTHENING IN UPPER
7.ROLE OF CALCITONIN IN ORTHOPEDIC
LIMBS
PRACTICE
8.ARTICULAR CARTILAGE TRANSPLANTATION
8.SUTURE ANCHORS AND ITS IMPORTANCE
9.SMALL JOINT REPLACEMENT IN HAND
9.PITFALLS OF LCP
JUNE 2010 DECEMBER 2008

PAPER 4 PAPER 4

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE MANAGEMENT OF 1. DISCUSS THE BIOMECHANICS OF SHOULDER

ACETABULAR FRACTURES AND DISCUSS THE JOINT.
ROLE OF MINIMALLY INVASIVE TECHNIQUES
DESCRIBE THE COMPLICATIONS OF SHOULDER
ARTHROPLASTY AND THEIR MANAGEMENT

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.MRI 2.ULNAR DRIFT

3.BIOLOGICAL THERAPY IN RHEUMATOID 3.PATELLAR INSTABILITY

ARTHRITIS
4.POLYETHYLENE WEAR
4.ROLE OF TEMPORALIDE IN MANAGEMENT OF
5.BONE GRAFTING IN TKR
OSTEOPOROSIS
6.COLLEGEN MENISCUS IMPLANT
5.CERAMICS IN ORTHOPEDICS
7.CAPITULUM FRACTURE
6.NERVE CONDUCTION STUDY(TUREK CH 14
ORTHOPEDIC NEUROLOGY) 8.SPONDYLOTIC MYELOPATHY

7.PFN 9.TRANS SCAPHOID PERILUNATE DISLOCATION

8.METAL ON METAL HIP

9.PEDICULAR INSTRUMENTATION
 NOVEMBER 2007 MAY 2008

PAPER 4 PAPER 4

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE IN DETAIL THE ORGANISATION OF 1. DESCRIBE THE CLINICAL FEATURES,

TRAUMA CARE SYSTEM PATHOLOGY AND RECENT ADVANCES IN THE
MANAGEMENT OF OSTEOSARCOMA.

ADD A NOTE ON GENETHERAPY IN TUMOUR

SHORT ESSAYS (8X10=80 MARKS)
MANAGEMENT.
2.ISOTOPE BONE SCAN (KUL 1 - 155)
SHORT ESSAYS (8X10=80 MARKS)
3.SYNTHETIC BONE GRAFT SUBSTITUTE
2.PMMA
CAMPBELL, GENERAL PRINCIPLES, SURGICAL
TECHNIQUES 3.RADIOLOGY OF CLUBFOOT

4.TEXT MESSAGE INJURY 4.NANO TECHNOLOGY IN TUMOUR

TREATMENT
5.SLAP LESION KULKARNI 1868
5.ALLEN TEST
6.HYBRID EXTERNAL FIXATOR
6.THOMAS TEST
7.WRINGER INJURIES
7.POLYGLYCOLIC ACID
8.NANO TECHNOLOGY IN TUMOUR
TREATMENT 8.TEXT MESSAGE INJURY

9.CLEAN AIR SYSTEM IN OPERTAING THEATRES 9.MEYERS MUSCLE PEDICLE GRAFT

 MAY 2007 JUNE 2006

PAPER 4 PAPER 4

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE PATHOLOGY AND THE 1. DEFINE AND CLASSIFY LUMBAR SPINAL
VARIOUS STAGES OF OSTEOARTHRITIS OF THE STENOSIS.

KNEE JOINT. SUMMARISE ROLE OF XRAY, MRI, CT AND CT

MYELOGRAPHY IN THE ASSESSMENT OF
DISCUSS RECENT ADVANCES IN THE NON LUMBAR SPINAL STENOSIS. (CAMPBELL CH-
OPERATIVE MANAGEMENT OF MILD TO OTHER DISORDERS OF SPINE)

MODERATE OSTEOARTHRITIS. DISCUSS THE NON SURGICAL MANAGEMENT

OPTIONS.ALSO EXPLAIN THE BASIC STEPS
SHORT ESSAYS (8X10=80 MARKS) INVOLVED IN DECOMPRESSING THE LATERAL
ZONE STENOSIS BETWEEN L4 AND S1.
2.GENE THERAPY
SHORT ESSAYS (8X10=80 MARKS)
3.INTERLEUKINS
2.PEDICLE SUBTRACTION OSTEOTOMY
4.SERMS AND POST MENOPAUSAL 3.OPERATIVE AND REHABILITATION
OSTEOPOROSIS STRATEGIES TO MINIMISE FLEXOR TENDON
SEARING.
5.ARTICULAR SURFACE REPLACEMENT OF THE
4.CRPS
HIP KULKARNI 3706
5.RISSER SIGN (CAMPBELL CH-
6.BONE GRAFT SUBSTITUTES CAMPBELL, SCOLIOSIS&KYPHOSIS)
GENERAL PRINCIPLES, SURGICAL TECHNIQUES;
6.METAL REACTION
KULKARNI 1312
7.BRIDGE PLATE
7.VERTEBROPLASTY (KUL 1 - 155)
8.ROLE OF METHYL PREDNISOLONE IN SPINAL
CORD INJURY
8.BIOLOGICAL FIXATION OF FRACTURES
9.ACL REPAIR(CAMPBELL ; SPORTS MEDICINE
9.DISTRACTION HISTIOGENESIS KULKARNI PG CH-KNEE INJURIES)(CAMPBELL ; CH-
1519 ARTHROSCOPY OF LOWER EXTREMITIES)
 NOV 2006 JUNE 2005

PAPER 4 PAPER 4

ESSAY (20 MARKS)

ESSAY (20 MARKS) 1. CLASSIFY SPONDYLOLISTHESIS.

1. OUTLINE DIFFERENT TYPES OF NON UNION. WHAT IS THE PROCEDURE OF CHOICE IN

CHILDREN WITH LOW GRADE
DESCRIBE IN BRIEF THE VARIOUS OPTIONS IN
SPONDYLOLISTHESIS.
THE MANAGEMENT OF NON UNION OF TIBIA IN
AN ADULT COMPARE THE POTENTIAL ADVANTAGES OF
SPONDYLOLISTHESIS REDUCTION PROCEDURES
SHORT ESSAYS (8X10=80 MARKS)
WITH IN SITU FUSION (CAMPBELL CH-
2.MENISCAL REPAIR (CAMPBELL ; SPORTS SCOLIOSIS&KYPHOSIS)
MEDICINE CH-KNEE INJURIES)(CAMPBELL ; CH-
SHORT ESSAYS (8X10=80 MARKS)
ARTHROSCOPY OF LOWER EXTREMITIES) 3.LCP
2.FOCAL DOME OSTEOTOMY
4.NOSOCOMIAL INFECTION
3.SURGICAL OPTIONS IN UNICOMPARTMENTAL
5.HANGMANS FRACTURE
OSTEOARTHRITIS KNEE
6.VASCULARISED FIBULAR GRAFT
4.BONE CEMENT GOPALAN 672 5.NERVE
7.WARDS TRIANGLE GRAFT

8.ARTIFICIAL DISC 6.PROTEOGLYCAN

9.LISS PLATE 7.ARTHROFIBROSIS

8."TUBS" "AMBRII"

9.THERAPEUTIC OPTIONS (DIFFERENT

PROTOCOLS AND REGIMENS ) IN TREATING
MULTIPLE MYELOMA
 MAY 2004

PAPER 4

ESSAY (20 MARKS)

1. DISCUSS THE PATHOLOGY, SYMPTOMS ,

SIGNS, INVESTIGATIONS AND MANAGEMENT
OF A ROTATOR CUFF TEAR IN A 50 YR OLD
MALE

(CAMPBELL SPORTS MEDICINE-SHOULDER

INJURIES)

SHORT ESSAYS (8X10=80 MARKS)

2.MENISCAL REPAIR (CAMPBELL ; SPORTS

MEDICINE CH-KNEE INJURIES, CH-
ARTHROSCOPY OF LOWER EXTREMITY)

3.POLYETHYLENE WEAR

4.POSTERIOR STABILISED KNEE PROSTHESIS

5.SURGICAL MANAGEMENT OF OSTEOGENESIS

IMPERFECTA (DAV-LOCAL COMPLICATIONS
OF#; M/3RD) TACHDJIAN CH 32
(METABOLIC&ENDOCRINE DISEASES)

6.TENSION BAND PRINCIPLE

7.MINIMALLY INVASIVE SPINAL SURGERY

8.COMPUTER ASSISSTED ORTHOPAEDIC

SURGERY

9.HYBRID TOTAL HIP ARTHROPLASTY.

 SECTION 6

D ORTHO

KUHS (2012-2014)

PAPERS 1-3
 JUNE 2012 JUNE 2012

PAPER I - BASIC SCIENCES PAPER II

ESSAY 20 MARKS ESSAY 20 MARKS

1. DISCUSS THE ANATOMY OF MENISCUS. 1. DISCUSS THE CLASIFICATION BIOMECHANICS

AND ITS MANAGEMENT OF POTT'S FRACTURE
HOW WILL YOU MANAGE A CASE OF BUCKET
HANDLE TEAR OF MEDIAL MENISCUS IN A SHORT ESSAYS (8 X 10=80 MARKS)
PROFESSIONAL FOOTBALL PLAYER (CAMPBELL ;
2. BLOOD SUPPLY OF SCAPHOID. CLASSIFIC
SPORTS MEDICINE CH-KNEE
ATION AND MANAGEMENT OF SCAPHOID
INJURIES)(CAMPBELL ; CH-ARTHROSCOPY OF
FRACTURE
LOWER EXTREMITIES)
3. BAUMANN'S ANGLE

4. JEFERSON’S FRACTURE
SHORT ESSAYS (8 X 10=80 MARKS)
5. FUNCTIONAL CAST BRACING STEWART-
2. WALLERIAN NERVE DEGENERATION
PG215
CAMPBELL PERIPHERAL NERVE INJURIES
6. FRENCH OSTEOTOMY
3. ARTHROGRAPHY
7. RUPTURE OF EXTENSOR POLLICIS LONGUS
4. CRUSH SYNDROME
8. STRESS FRACTURE KULKARNI 1218
5. BROWN TUMER
9. COMPLICATIONS OF PELVIC FRACTURES
6. THOMAS TEST

7. SYMES AMPUTATION

8. TENDON TRANSFER IN FOOT DROP

9. USG IN ORTHOPAEDICS KULKARNI PG 146

 JUNE 2012 NOVEMBER 2012

PAPER 3 PAPER I

ESSAY 20 MARKS ESSAY 20 MARKS

1. DESCRIBE THE BLOOD SUPPLY OF TIBIA. 1. DESCRIBE THE PATHOLOGICAL ANATOMY OF

CLASSIFY NON-UNION AND DISCUSS THE IDIOPATHIC CONGENITAL TALIPES
MANAGEMENT OF INFECTED GAP NON UNION EQUINOVARUS AND ITS MANAGEMENT IN A SIX
OF TIBIA. MONTH CHILD

SHORT ESSAYS (8 X 10=80 MARKS) SHORT ESSAYS (8 X 10=80 MARKS)

2. FIBROFASCITIS 2. ARDS

3. KRUKENBERG OPERATION 3. WRIST DROP

4. IMAGE INTENSIFIER IN ORTHOPAEDICS 4. BONE GRAFT SUBSTITUTES CAMPBELL,

GENERAL PRINCIPLES, SURGICAL TECHNIQUES
5. LASSO PROCEDURE
5. NUTRITIONAL RICKETS AND ITS EFFECT ON
6. CHONDROBLASTOMA (TACHDJIAN ; BENIGN
EPIPHYSEAL PLATE TACHDJIAN CH 32
MUSCULOSKELETAL TUMOUR)
(METABOLIC&ENDOCRINE DISEASES)
7. IMMUNOASSAY IN SKELETAL INFECTIONS
6. BIGELOW'S LIGAMENT
8. ASEPTIC LOOSENING OF PROSTHESIS
7. NEO-ADJUVANT CHEMOTHERAPY
9. VARUS DE-ROTATION OSTEOTOMY OF
8. SMITH PETERSON APPROACH TO HIP JOINT
FEMUR IN PERTHES DISEASE.
9. ANKLE FOOT ORTHOSES
 NOVEMBER 2012 NOVEMBER 2012

PAPER II PAPER 3 - RECENT ADVANCES

ESSAY 20 MARKS ESSAY 20 MARKS

1. EXPLAIN THE CLASSIFICATION OF SUPRA 1. DISCUSS THE ANATOMY, CLASSIFICATION,

CONDYLAR FRACTURE OF HUMERUS, THE EVALUATION AND MANAGEMENT OF
RADIOLOGICAL FINDINGS AND MANAGEMENT. ACETABULAR FRACTURES

SHORT ESSAYS (8 X 10=80 MARKS) SHORT ESSAYS (8 X 10=80 MARKS)

2. SYNOVIAL CHONDROMATOSIS. 2. TIBIAL PILON FRACTURES.

3. JAIPUR FOOT. KULKARNI 3941 3. ESSEX-LOPRESTI FRACTURE DISLOCATION.

4. LUMBAR DISC PROLAPSE. 4. ADVANTAGES V/S DISADVANTAGES OF

REAMING.
5. GUSTILO AND ANDERSON CLASSIFICATION.
5. ROLE OF CERAMICS IN ORTHOPAEDICS.
6. LUBRICATION MECHANISM OF A JOINT.
TUREK CH 7 PHYSIOLOGY OF CARTILAGE 6. RECENT ADVANCEMENT ON CARTILAGE
REPAIR.
7. PIGMENTED VILLONODULAR SYNOVITIS.
7. WORKING LENGTH OF AN IMPLANT.
8. LEG LENGTH DISCREPANCY.
8. ULTRASOUND-GUIDED REGIONAL
9. HETEROTOPIC OSSIFICATION. GOPALAN
ANESTHESIA.
PG211
9. ROLANDO'S FRACTURE.
 MAY 2013 MAY 2013

PAPER I- BASIC SCIENCES PAPER II

ESSAY 20 MARKS ESSAY 20 MARKS

1. DESCRIBE THE ETIOLOGY, CLINICAL 1. DISCUSS THE CONGENITAL AND

FEATURES, INVESTIGATIONS AND DEVELOPMENTAL DYSPLASIA OF HIP, ITS
MANAGEMENT OF PERTHE'S DISEASE. CLINICAL FEATURES , DIAGNOSIS AND
MANAGEMENT FROM NEWBORN TO
ADOLESCENT. (TACHDJIAN)
SHORT ESSAYS (8 X 10=80 MARKS)

2. OSTEOPOROSIS.
SHORT ESSAYS (8 X 10=80 MARKS)
3. RHEUMATOID ARTHRITIS.
2. BIOFILMS IN BONE AND JOINT INFECTIONS.
4. TORTICOLLIS.
3. FIBROMYALGIA .
5. CRUSH SYNDROME.
4. MYOSITIS OSSIFICANS .
6. THORACIC OUTLET SYNDROME.
5. AVASCULAR NECROSIS HEAD OF FEMUR.
7. DUPUYTREN'S CONTRACTURE. CAMPBELL ;
6. MILWAUKEE BRACE.
CH - THE HAND
7. RECENT ADVANCES IN OSTEOGENIC
8. REGIONAL ANESTHESIA FOR FOOT AND
SARCOMA.
ANKLE.
8. ARTHRODESIS OF THE WRIST JOINT.
9. CORROSION OF METALLIC IMPLANTS.
9. CAUDA EQUINA SYNDROME .
 MAY 2013 NOVEMBER 2013

PAPER 3 PAPER I - BASIC SCIENCES

ESSAY 20 MARKS ESSAY 20 MARKS

1. CLASSIFICATION OF DORSO-LUMBAR 1. DESCRIBE VASCULAR SUPPLY OF SCAPHOID

FRACTURES AND MANAGEMENT OF UNSTABLE
DISCUSS THE CLINICAL FEATURES AND
FRACTURE WITH POSTERIOR PEDICULAR
MANAGEMENT OF SCAPHOID FRACTURES.
IMPLANTS.

SHORT ESSAYS (8 X 10=80 MARKS)

SHORT ESSAYS (8 X 10=80 MARKS)
2. ELECTRO DIAGNOSIS IN NERVE LESIONS
2. TOURNIQUETS. (STEWART-TOURNIQUET)
(TUREK CH 14 ORTHOPEDIC NEUROLOGY)
3. HERBERT SCREW.
3. GAIT ANALYSIS
4. MOORE'S APPROACH.
4. CYSTIC LESIONS OF BONE
5. BONE SCAN.
5. LUMBAR DISC
6. TIBIAL PLATEAU FRACTURES.
6. BONE HEALING
7. HANGMAN'S FRACTURE.
7. HEAT THERAPY
8. LOCKING COMPRESSION PLATE KULKARNI
8. COMPARTMENT SYNDROME ( DAV PART 1
PG1433
GENERAL L/3RD )
9. ROLE OF BIOCHEMICAL AND BONE GRAFT
9. SPRENGEL DEFORMITY (CONGENITAL
SUBSTITUTES. CAMPBELL, GENERAL
ANOMALIES OF TRUNK AND UPPER EXTREMITY)
PRINCIPLES, SURGICAL TECHNIQUES
 NOVEMBER 2013 NOVEMBER 2013

PAPER II PAPER III - RECENT ADVANCES

ESSAY 20 MARKS ESSAY 20 MARKS

1. DESCRIBE THE CLINICAL FEATURES, 1. DISCUSS THE ANATOMY, BLOOD SUPPLY,

CLASSIFICATIONS AND MANAGEMENT OF CLASSIFICATION AND MANAGEMENT OF
TROCHANTERIC FRACTURES. FRACTURE NECK FEMUR.

SHORT ESSAY (8 X 10=80 MARKS) SHORT ESSAYS (8 X 10=80 MARKS)

2. FRACTURE TALUS SHORT ESSAYS: (8X10=80)

3. TRENDELENBERG TEST 2. VERTEBROPLASTY.

4. ANTERIOR CRUCIATE LIGAMENT 3. LOCKING COMPRESSION PLATE. KULKARNI

PG1433
5. CARPAL TUNNEL SYNDROME CAMPBELL ; CH
- THE HAND 4. FLOATING KNEE.

6. COLD ABSCESS 5. PHYSEAL INJURIES. (CAMPBELL VOL2;

FRACTURES AND DISLOCATION IN CHILDREN)
7. RICKETS TACHDJIAN CH 32
(METABOLIC&ENDOCRINE DISEASES) 6.TFCC

8. MONTAGIA FRACTURE 7. PROPHYLACTIC FIXATION IN TUMORS.

9. FLOUROSIS 8. BIO ABSORBABLE MATERIALS.

9. MONTEGGIA FRACTURE DISLOCATION.

(CAMPBELL VOL2; FRACTURES AND
DISLOCATION IN CHILDREN)
 MAY 2014 MAY 2014

PAPER I PAPER II

ESSAY 20 MARKS ESSAY 20 MARKS

1. DESCRIBE A TYPICAL SPINAL NERVE. DISCUSS 1. DESCRIBE THE AETIOLOGY , CLASSIFICATION

THE PATHOPHYSIOLOGY OF PERIPHERAL NERVE AND SURGICAL MANAGEMENT OF SPASTIC
INJURY AND ITS MANAGEMENT CEREBRAL

PALSY. (CAMPBELL VOL 2 ; NERVOUS SYSTEM

DISORDERS IN CHILDREN)
SHORT ESSAYS (8 X 10=80 MARKS)

2. CHRONIC OSTEOMYELITIS
SHORT ESSAYS (8 X 10=80 MARKS)
3. STIFF ELBOW
2. KRUKENBURG OPERATION.
4. SUDECKS OSTEODYSTROPHY
3. SYNOVIAL FLUID ANALYSIS. (TUREK CH13
5. FAT EMBOLISM GOPALAN PG 68
DISEASES OF JOINT)
6. HIP INSTABILITY
4. GIANT CELL TUMOR LOWER END RADIUS.
7. SPONDYLOLISTHESIS (CAMPBELL CH- CAMPBELL - BENIGN BONE TUMOURS
SCOLIOSIS&KYPHOSIS)
5. ARTHROGRYPOSIS MULTIPLEX CONGENITA.
8. GAS GANGRENE
CAMPBELL VOL2; NEURVOUS SYSTEM
9. BONE GRAFT DISORDERS IN CHILDREN

6. SLIPPED CAPITAL FEMORAL EPIPHYSIS.

7. SPINAL SHOCK.

8. BONE HEALING.

9. CLAW HAND.
 MAY 2014

PAPER III - RECENT ADVANCES

ESSAY 20 MARKS

1. DESCRIBE THE INDICATIONS, PROCEDURES

AND COMPLICATIONS OF TOTAL HIP
REPLACEMENT

SHORT ESSAYS (8 X 10=80 MARKS)

2. FLOOR REACTION ORTHOSIS

3. PHARMACOTHERAPY OF GOUT(TUREK CH 9
METABOLIC BONE DISEASE)

4. MRI IN SPINE

5. PERONEAL TENDINITIS

6. OSTEOID OSTEOMA

7. LIGAMENTOTAXIS

8. ANTI OSTEOPOROTIC DRUGS

9. FOOT DROP
 SECTION 7

D ORTHO

PAPER 1

-- CALICUT UNIVERSITY (2012-2001)

-- KERALA UNIVERSITY (2012-2005)

 JUNE 2012 NOVEMBER 2011

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE ANATOMY OF A MENISCUS. 1. DEFINE OSTEOPOROSIS.

HOW WILL YOU MANAGE A CASE OF BUCKET
DISCUSS CLINICAL FEATURES, DIAGNOSIS,
HANDLE TEAR OF MEDIAL MENISCUS IN A
MANAGEMENT AND COMPLICATIONS OF POST
PROFESSIONAL FOOTBALL PLAYER (CAMPBELL ;
MENOPAUSAL OSTEOPOROSIS
SPORTS MEDICINE CH-KNEE
INJURIES)(CAMPBELL ; CH-ARTHROSCOPY OF SHORT ESSAYS (8X10=80 MARKS)
LOWER EXTREMITIES)
2.PRIMARY BONE HEALING

3.NEURITIS IN HANSENS DISEASE (KUL 1 - 658

SHORT ESSAYS (8X10=80 MARKS)
4.CRUSH SYNDROME
2.WALLERIAN NERVE DEGENERATION
5.RENAL TUBULAR ACIDOSIS
3.ARTHROGRAPHY
6.SYNOVIAL CHONDRAMATOSIS
4.CRUSH SYNDROME
7.TARSAL TUNNEL SYNDROME
5.BROWN TUMOUR
8.OSTEOGENESIS IMPERFECTA(DAV-LOCAL
6.THOMAS TEST COMPLICATIONS OF#; M/3RD) TACHDJIAN CH
32 (METABOLIC&ENDOCRINE DISEASES)
7.SYMES AMPUTATION
9. CHORDOMA ( CAMPBELL - MALIGNANT
8.TENDON TRANSFER IN FOOT DROP
BONE TUMOURS)
9. USG IN ORTHOPAEDICS KULKARNI PG 146
 MAY 2011 NOV 2010

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE BLOOD SUPPLY OF FEMORAL 1. DISCUSS THE ANATOMY OF BRACHIAL

HEAD IN CHILDREN. PLEXUS. DISCUSS THE ETIOLOGY, CLINICAL
FEATURES, INVESTIGATIONS AND
DISCUSS THE ETIOLOGY,CLINICAL FEATURES
MANAGEMENT OF UPPER BRACHIAL PLEXUS IN
AND MANAGEMENT OF LEGG CALVE PERTHES
AN YOUNG ADULT
DISEASE
DAV--NEUROLOGY; F/3RD ; CAMPBELL VOL2;
NEURVOUS SYSTEM DISORDERS IN CHILDREN
SHORT ESSAYS (8X10=80 MARKS)
SHORT ESSAYS (8X10=80 MARKS)
2.SYNOVIAL FLUID ANALYSIS (TUREK CH13
2.STEM CELLS (KUL 1- PG53)
DISEASES OF JOINT)
3.DVT PROPHYLAXIS
3.MEDICAL MANAGEMENT OF OSTEOPOROSIS
4.PSEUDOGOUT
4.STEM CELLS IN ORTHOPAEDICS (KUL 1-
PG53) 5.NEUROPATHIC PLANTAR ULCER

5.CLAW HAND 6.ROTATOR CUFF INJURY (CAMPBELL SPORTS

MEDICINE-SHOULDER INJURIES)
6.SALMONELLA OSTEOMYELITIS
7.VITAMIN D RESISTANT RICKETS TACHDJIAN
7.CARIES SICCA
CH 32 (METABOLIC&ENDOCRINE DISEASES)
8.HYPERPARATHYROIDISM
8.FRACTURE SCAPHOID
9. CHONDROBLASTOMA(TACHDJIAN ; BENIGN
9. INFERIOR RADIOULNAR JOINT
MUSCULOSKELETAL TUMOUR)
 MAY 2010 MAY 2009

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE BLOOD SUPPLY OF FEMORAL 1. DISCUSS THE ANATOMY OF ARCHES OF

HEAD IN CHILDREN. FOOT. (DAV-LOCAL COMPLICATIONS OF#;
M/3RD).DISCUSS THE CLINICAL FEATURES AND
DISCUSS THE ETIOLOGY, CLINICAL FEATURES,
MANAGEMENT OF FLAT FOOT
DIAGNOSIS AND MANAGEMENT OF PERTHES
DISEASE

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS) 2.VITAMIN D RESISTANT RICKETS TACHDJIAN

CH 32 (METABOLIC&ENDOCRINE DISEASES)
2.GENE THERAPY
3.FLOOR REACTION ORTHOSIS
3.DMARD IN RA
4.UNICOMPARTMENT KNEE ARTHROPLASTY
4.GOUT(TUREK CH 9 METABOLIC BONE
DISEASE) 5.BONE SUBSTITUTES

5.PRESSURE SORE GOPALAN PG 697 6.LIVELY SPLINT

6.HABITUAL DISLOCATION OF PATELLA 7.SELF LENGTHENING NAIL

7.CENTRAL CORD SYNDROME 8.KYPHOPLASTY

8.RENAL TUBULAR ACIDOSIS 9. RISSER SIGN (CAMPBELL CH-

SCOLIOSIS&KYPHOSIS)
9. KEINBOCKS DISEASE

NOVEMBER 2009 (RPT OF DEC 2008)

 DEC 2008 DEC 2007

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE SURGICAL ANATOMY OF KNEE 1.DISCUSS THE SURGICAL ANATOMY OF THE
JOINT IN RELATION TO INTERNAL KNEE
DERANGEMENT OF KNEE

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.GATE CONTROL THEORY
2.JOINT LUBRICATION TUREK CH 7 PHYSIOLOGY
3.ALKALINE PHOSPHATASE
OF CARTILAGE
4.ARTICULAR CARTILAGE (TUREK CH2)
3.NEUROPATHIC JOINT
5.MRI
4.BISPHSOPHONATES
6.TENDON TRANSFER
5.SELF LENGTHENING NAIL
7.ARCHES OF FOOT (DAV-LOCAL
6.TRIANGULAR FIBRO CARTILAGE COMPLEX
COMPLICATIONS OF#; M/3RD)
(TFCC)
8.BONE
7.ERBS POINT
9.COMPARTMENT PRESSURE( DAV PART 1
8.VITAMIN D METABOLISM
GENERAL L/3RD )
9. TARSAL TUNNEL SYNDROME
 MAY 2007 MAY 2006

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1.DISCUSS THE ANATOMY OF SHOULDER JOINT 1.DISCUSS THE ANATOMY OF KNEE JOINT.
WITH REFERENCE TO INSTABILITIES OF DESCRIBE THE INJURIES OF MENISCI OF KNEE.
SHOULDER (CAMPBELL ; SPORTS MEDICINE CH-KNEE
INJURIES)(CAMPBELL ; CH-ARTHROSCOPY OF
LOWER EXTREMITIES)
SHORT ESSAYS (8X10=80 MARKS)

2.BONE GRAFT
SHORT ESSAYS (8X10=80 MARKS)
3.REFLEX SYMPATHETIC DYSTROPHY
2.SINOGRAM
4.TINELS SIGN
3.BIOLOGICAL PLASTICITY
5.SYNOVIAL FLUID(TUREK CH13 DISEASES OF
4.DISTRACTION HISTIOGENESIS KULKARNI PG
JOINT)
1519
6.MYELOGRAM
5.TOURNIQUET (STEWART-TOURNIQUET)
7.DMARD
6.RADIOLOGICAL FEATURES OF CDH
8.FOOT DROP
7.OSTEOPOROSIS
9.RADIO ULNAR JOINT
8.THORACIC OUTLET

9.VASCULAR SUPPLY OF SCAPHOID

 OCTOBER 2006 MAY 2005

PAPER 1 PAPER 1

ESSAY (2 X 30 =60 MARKS)

ESSAY (20 MARKS) 1.DESCRIBE THE ANATOMY OF CARPAL TUNNEL

(10) --CAUSES OF CARPAL
1.DISCUSS THE ANATOMY OF SPINAL MOTION
TUNNEL COMPRESSION(5) CAMPBELL ; CH -
SEGMENT. DESCRIBE THE PATHOLOGICAL
THE HAND --HOW WOULD YOU DIAGNOSE
ANATOMY OF DISC HERNIATION.
CARPAL TUNNEL SYNDROME(5) --DISCUSS
MANAGEMENT OF CARPAL TUNNEL
COMPRESSION AT VARIOUS STAGES(10)
SHORT ESSAYS (8X10=80 MARKS)
CAMPBELL ; CH - THE HAND
2.JOINT LUBRICATION TUREK CH 7 PHYSIOLOGY
2. DESCRIBE WITH HELP OF A DIAGRAM
OF CARTILAGE
MICROSCOPIC FEATURES OF A "TYPICAL
TUBERCLE" --DIFFERENT
3.PIEZOELECTRICITY
TYPES OF GRANULOMAS?
--DISCUSS MANAGEMENT OF AN
4.DUNLOP TRACTION
UNCOMPLICATED TB T-L SPINE IN ADULT.-TULI
--SECOND LINE DRUGS USED IN TREATMENT OF
5.FRACTURE HEALING
TUBERCULOSIS AND ITS INDICATIONS.

6.RADIOLOGICAL FEATURES OF CTEV CAMPBELL SHORT ESSAYS (4X10=40 MARKS)

(CONGENITAL ANOMALIES OF LOWER
3.HYPERCALCEMIA
EXTREMITY)
4.NEOADJUVANT CHEMOTHERAPY (DAV -
7.NEOADJUVANT CHEMOTHERAPY (DAV - TUMOURS; M/3RD) CAMPBELL- GENERAL
PRINCIPLES TUMOURS
TUMOURS; M/3RD) CAMPBELL- GENERAL
PRINCIPLES TUMOURS 5.MONTEGGIA VARIANTS (ZUKERMAN PG 653)
; ROCKWOOD; RADIUS AND ULNA SHAFT
8.TENDON SHEATHS AROUND THE WRIST FRACTURES, GOPALAN 381

9.MRSA 6.SPRAINED ANKLE

 NOVEMBER 2003 NOVEMBER 2002

PAPER 1 PAPER 1

ESSAY (20 MARKS)

ESSAY (20 MARKS) 1.DISCUSS THE SURGICAL ANATOMY OF

1.DISCUSS THE CHARACTERISTICS OF NORMAL EXTENSOR MECANISM OF KNEE JOINT. DISCUSS
SYNOVIAL FLUID AND CHANGES IN DIFFERENT IN BRIEF THE MANAGEMENT OF RECURRENT
ARTHRITIC CONDITIONS(TUREK CH13 DISEASES
DISLOCATION OF PATELLA.
OF JOINT)

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS) 2.VOLKMANS SIGN

2.MANAGEMENT O FOOT DROP

3.HALLUX VALGUS (DAV-LOCAL
3.MANAGEMENT OF FRACTURE PATELLA COMPLICATIONS OF#; M/3RD) CAMPBELL FOOT

4.LOCKING KULKARNI PG1433 AND ANKLE, DISORDERS OF HALLUX

5.NEUROTEMESIS 4.FIBROUS DYSPLASIA (TACHDJIAN ; BENIGN

6.AVASCULAR NECROSIS MUSCULOSKELETAL TUMOUR)

7.RENAL RICKETS TACHDJIAN 5.CHONDROCALCINOSIS

CH 32 (METABOLIC&ENDOCRINE DISEASES)
6.OSSIFICATION OF DISTAL HUMERUS
8.SPONDYLOLISTHESIS (CAMPBELL CH-
SCOLIOSIS&KYPHOSIS) 7.COSTO TRANSVERSECTOMY
9.ERBS PALSY
8.CLASSIFICATION OF EPIPHYSEAL INJURY.
CAMPBELL VOL2; FRACTURES AND
DISLOCATION IN CHILDREN

9.ETIOPATHOGENESIS OF RICKETS TACHDJIAN

CH 32 (METABOLIC&ENDOCRINE DISEASES)
 OCTOBER 2001

PAPER 1

ESSAY (2X30=60 MARKS)

1.DECSRIBE THE PRINCIPLES OF TENDON

TRANSFER SURGERY. DISCUSS VARIOUS
TENDON TRANSFERS FOR HIGH RADIAL NERVE
INJURY

2. DEFINE PATHOLOGICAL FRACTURE. DISCUSS

ETIOPATHOGENESIS OF METASTATIC BONE
DEPOSITS. HOW WILL YOU MANAGE AN 80 YR
OLD MAN WITH PATHOLOGICAL
INTERTROCHANTERIC FRACTURE.

SHORT ESSAY (4X10=40 MARKS)

3.GAS GANGRENE

4.PNEUMATIC TOURNIQUET (STEWART-

TOURNIQUET)

5.GENU RECURVATUM

6.PLANTAR FASCITIS (DAV-LOCAL

COMPLICATIONS OF#; M/3RD)
 JUNE 2012 MAY 2011

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DEFINE CALCIUM METABOLISM (TUREK CH 6 1. DESCRIBE THE STRUCTURE OF THE GROWTH

PHYSIOLOGY OF BONE) CLINICAL PLATE. DISCUSS THE COMPLICATIONS OF
FEATURE,PATHOLOGY AND MANAGEMENT OF EPIPHYSEAL INJURY. CAMPBELL VOL2;
RENAL RICKETS. TACHDJIAN CH 32 FRACTURES AND DISLOCATION IN CHILDREN
(METABOLIC&ENDOCRINE DISEASES)

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.BONE GRAFTING
2.CORTICOTOMY
3.OSTEOCLAST
3.CODMANS TRIANGLE
4.FAT EMBOLISM GOPALAN PG 68
4.INJURITY SEVERITY SCORE
5.NEUROPRAXIA
5.DEQUERVAINS INJURY
6.GENU RECURVATUM
6.ULNAR CLAW HAND
7.HALLUX VALGUS MANAGEMENT (DAV-
7.CUBITUS VARUS LOCAL COMPLICATIONS OF#; M/3RD)
CAMPBELL FOOT AND ANKLE, DISORDERS OF
8.ALKALINE PHOSPHATASE
HALLUX
9.PES CAVUS
8.CERVICAL RIB

9.SPINA BIFIDA
 NOV 2010 JUNE 2010

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE PATHOANATOMY OF CLUBFOOT 1. DISCUSS THE ANATOMY OF COMMON

IN RELATION TO PONSETI TECHNIQUE. DISCUSS PERONEAL NERVE OUTLINE THE MANAGEMENT
IN DETAIL THE STEPS OF PONSETI METHOD OF OF FOOT DROP.
CORRECTION OF CLUB FOOT.

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.SYNOVIAL FLUID(TUREK CH13 DISEASES OF
2.FROZEN SHOULDER JOINT)

3.CONGENITAL PSEUDARTHROSIS TIBIA 3.RHEUMATOID FACTOR

CAMPBELL (CONGENITAL ANOMALIES OF
4.CEPHALOSPORINS
LOWER EXTREMITY)
5.PRIMARY BONE HEALING
4.CHONDROBLASTOMA(TACHDJIAN ; BENIGN
MUSCULOSKELETAL TUMOUR) 6.SEVERS DISEASE

5.NON UNION FRACTURE SCAPHOID 7.EPIPHYSEAL PLATE

6.SPINAL MOTION SEGMENT 8.NEOADJUVANT CHEMOTHERAPY (DAV -

TUMOURS; M/3RD) CAMPBELL- GENERAL
7.BIOLOGICAL FIXATION
PRINCIPLES TUMOURS
8.RENAL TUBULAR ACIDOSIS
9.GOUT(TUREK CH 9 METABOLIC BONE
9.BOUTONNIERE DEFORMITY DISEASE)
 NOV 2009 DEC 2008

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE VASCULARITY OF FEMORAL 1. DISCUSS THE ANATOMY OF KNEE JOINT

HEAD. DISCUSS THE CLINICAL FEATURES AND MENISCI. CLASSSIFY MENSICAL INJURIES AND
MANAGMENT OF IDIOPATHIC AVASCULAR OUTLINE THE MANAGEMENT. (CAMPBELL ;
NECROSIS OF FEMORAL HEAD. SPORTS MEDICINE CH-KNEE
INJURIES)(CAMPBELL ; CH-ARTHROSCOPY OF
LOWER EXTREMITIES)
SHORT ESSAYS (8X10=80 MARKS)

2.KEINBOCKS DISEASE
SHORT ESSAYS (8X10=80 MARKS)
3.HYPERPARATHYROIDISM
2.FIBROUS ANKYLOSIS
4.OSTEOGENESIS IMPERFECTA (DAV-LOCAL
3.DMARD
COMPLICATIONS OF#; M/3RD) TACHDJIAN CH
32 (METABOLIC&ENDOCRINE DISEASES) 4.POLYMERASE CHAIN REACTION

5.ANEURYSMAL BONE CYST (TACHDJIAN ; 5.OSTEOID

BENIGN MUSCULOSKELETAL TUMOUR)
6.ENDOCHONDRAL OSSIFICATION TUREK CH 3
6.LOCKING COMPRESSION PLATE KULKARNI HISTOLOGY OF BONE
PG1433
7.BONE REMODELLING TUREK CH 3 HISTOLOGY
7.ANTERIOR CRUCIATE LIGAMENT OF BONE

8.REFLEX SYMPATHETIC DYSTROPHY 8.HYALURONIC ACID

9.RECURRENT DISLOCATION OF PATELLA 9.PARATHYROID HORMONE

 MAY 2008 MAY 2007

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE PATHOLOGICAL ANATOMY OF 1. DECSRIBE THE ARTERIAL SUPPLY OF THE

RECURRENT DISLOCATION OFSHOULDER. FEMORAL HEAD. DISCUSS THE MANAGEMENT
OF POST TRAUMATIC FRACTURE NECK OF
DESCRIBE IN DETAIL THE STEPS OF PUTTI PLATT
FEMUR IN A 11 YR OLD BOY.
OPERATION.

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.SENILE OSTEOPOROSIS
2.MALUNION
3.INJURIES TO THE ULNAR NERVE
3.GENU VALGUM
4.CARPAL TUNNEL SYNDROME CAMPBELL ; CH -
4.SPRAIN ANKLE
THE HAND
5.CONGENITAL PSEUDARTHROSIS TIBIA
5.ALKAPTONURIA
CAMPBELL (CONGENITAL ANOMALIES OF
LOWER EXTREMITY) 6.BISPHOSPHONATES

6.CUBITUS VALGUS 7.ANATOMY OF ACL(CAMPBELL ; SPORTS

MEDICINE CH-KNEE INJURIES)(CAMPBELL ; CH-
7.CLINICAL SIGNS OF LONG BONE FRACTURES
ARTHROSCOPY OF LOWER EXTREMITIES)
8.DUPUYTRENS FRACTURE
8.SYNOVIAL FLUID(TUREK CH13 DISEASES OF
9.DISLOCATION JOINT)

9.ACID FAST BACILLUS

 MAY 2007 NOV 2006

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1.DISCUSS THE PATHOLOGICAL ANATOMY AND 1.DESCRIBE THE ANATOMY OF

MANAGEMENT OF DDH IN A 4 YR OLD CHILD. COMPARTMENTS OF LEG. HOW WILLYOU
DIAGNOSE INCREASED COMPARTMENTAL
PRESSURE IN LEG? DISCUSS MANAGEMENT OF
SHORT ESSAYS (8X10=80 MARKS) FRACTURE BOTH BONES LEG UPPER 1/3rd WITH
THREATENED ISCHEMIA. ( DAV PART 1 GENERAL
2.METHOTREXATE
L/3RD )
3.PARATHORMONE
SHORT ESSAYS (8X10=80 MARKS)
4.ELECTROMYOGRAPHY (KUL 1- 900), (TUREK
2.SPRING LIGAMENT
CH 14 ORTHOPEDIC NEUROLOGY)
3.COURSE OF MEDIAN NERVE IN THE ARM AND
5.BLOOD SUPPLY OF SPINAL CORD
FOREARM. NAME THE MUSCLES PARALYSED IN
6.PERIOSTEAL REACTION (DAV-TUMOURS; COMPLETE CUT OF THE NERVE AT ELBOW
M/3RD) LEVEL.

7.HYDROXYAPATITE 4.HISTOLOGICAL APPEARANCE OF

OSTEOSARCOMA
8.ENDOCHONDRAL OSSIFICATION TUREK CH 3
HISTOLOGY OF BONE 5.FRACTURE HEALING IN CORTICAL AND
CANCELLOUS BONE
9.GLENONHUMERAL JOINT INSTABILITY
6.SPINAL SHOCK

7.DMARD

8.PREVENTION OF DVT AFTER ORTHOPAEDIC

PROCEDURES

9.TARSAL TUNNEL SYNDROME

 JUNE 2006 NOVEMBER 2005

PAPER 1 PAPER 1

ESSAY (20 MARKS) ESSAY (20 MARKS)

1.DESCRIBE MECHANISM OF COAGULATION. 1.DISCUSS THE SURGICAL ANATOMY AND

DISCUSS THE DIAGNOSIS AND MANAGEMENT BIOMECHANICS OF THE CRUCIATE LIGAMENTS
OF HEMOPHILIC ARTHROPLASTY. OF THEIR IMPORTANCE IN RECONSTRUCTION
OF THESE LIGAMENTS AFTER INJURY.

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.POST PHLEBITIC SYNDROME.
2.SINGH INDEX
3.SINGHS INDEX
3.ANATOMY OF ROTATOR CUFF (CAMPBELL
4.PAPINEAU GRAFTING.
SPORTS MEDICINE-SHOULDER INJURIES)
5.PES ANSERINUS
4.DEEP VEIN THROMBOSIS
6.LOCKING OF THE KNEE
5.NEUROGENIC BLADDER
7.DEQUERVAINS DISEASE
6.TRIANGULAR FIBRO CARTILAGE COMPLEX
8.TORTICOLLIS {CAMPBELL (CONGENITAL
7.VITAMIN D RESISTANT RICKETS TACHDJIAN
ANOMALIES OF TRUNK AND UPPER
CH 32 (METABOLIC&ENDOCRINE DISEASES)
EXTREMITY)}
8.GIANT CELLS (DAV- TUMOURS; GCT)
9.STRENGTH DURATION CURVE(TUREK CH 14
ORTHOPEDIC NEUROLOGY) 9.BONE MINERAL DENSITY
 MAY 2005 3.ISOTOPE BONE SCAN (KUL 1 - 155)

PAPER 1 4.STRUCTURE OF GROWTH PLATE ( DAV PART 1

GENERAL L/3RD )

5.AUTOTRANSFUSION
ESSAY (20 MARKS)
6.GLOMUS TUMOUR
1.DISCUSS THE FACTORS STABILISING THE
GLENOHUMERAL JOINT AND ITS IMPORTANCE 7.ANTALGIC GAIT

IN THE MANAGEMENT OF GLENOHUMERAL

8.NEOADJUVANT CHEMOTHERAPY (DAV -
INSTABILITY.
TUMOURS; M/3RD); CAMPBELL- GENERAL
PRINCIPLES TUMOURS

SHORT ESSAYS (8X10=80 MARKS) 9.STRUCTURE OF INTERVERTEBRAL DISC

(CAMPBELL CH- LOWER BACK PAIN)
2.CHARACTERISTICS OF NORMAL SYNOVIAL
FLUID(TUREK CH13 DISEASES OF JOINT)
 SECTION 8

DORTHO

PAPER 2

-- CALICUT UNIVERSITY (2012-2003)

-- KERALA UNIVERSITY (2012-2005)

 JUNE 2012 NOV 2011

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE CLASSIFICATION, 1. CLASSIFY TIBIAL PLATEAU FRACTURES.

BIOMECHANICS AND MANAGEMENT OF POTTS DESCRIBE THE CLINICAL FEATURES, DIAGNOSIS,
FRACTURE MANAGEMENT AND COMPLICATIONS OF TIBIAL
PLATEAU FRACTURES

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.BLOOD SUPPLY OF SCAPHOID. CLASSICATION
AND MANAGEMENT OF SCAPHOID FRACTURE 2.PES PLANUS

3.BAUMANNS ANGLE 3.SCFE

4.JEFFERSON FRACTURE 4.CHANCE FRACTURE

5.FUNCTIONAL CAST BRACING - STEWART- 5.MULTIDIRECTIONAL INSTABILITY OF

PG215 SHOULDER

6.FRENCH OSTEOTOMY 6.FRACTURE SCAPHOID

7.RUPTURE OF EPL 7.TENNIS ELBOW (CAMPBELL SPORTS

MEDICINE-ELBOW INJURIES)
8.STRESS FRACTURE KULKARNI 1218
8.COMPLEX REGIONAL PAIN
9. COMPLICATIONS OF PELVIC FRACTURES
SYNDROME(CAMPBELL PERIPHERAL NERVE
INJURIES; EFFECTS OF PERIPHERAL NERVE
INJURIES)

9. FLOOR REACTION ORTHOSIS

 MAY 2011 NOV 2010

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE CLINICAL FEATURES, 1. CLASSIFY OPEN FRACTURES. DISCUSS THE

DIAGNOSIS, MANAGEMENT AND PRINCIPLES IN THE MANAGEMENT OF TYPE IIIB
COMPLICATIONS OF TUBERCULOSIS OF THE COMPUND FRACTURES BOTH BONE LEG IN AN
DORSO LUMBAR SPINE YOUNG ADULT

SHORT ESSAY (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.TARSAL TUNNEL SYNDROME 2.ANEURYSMAL BONE CYST (TACHDJIAN ;

BENIGN MUSCULOSKELETAL TUMOUR)
3.HABITUAL DISLOCATION OF PATELLA
3.BONE BANK KULKARNI 1137
4.FRACTURE HEAD OF FEMUR
4.DAMAGE CONTROL ORTHOPAEDICS
5.THORACIC OUTLET SYNDORME
5.RIGID FLAT FOOT
6.LATERAL CONDYLE FRACTURE OF HUMERUS
IN CHILDREN 6.LCP

7.SLAP LESION KULKARNI 1868 7.FAT EMBOLISM GOPALAN PG 68

8.KEINBOCKS DISEASE 8.NEURITIS IN LEPROSY (KUL 1 - 658)

9. KAPLAN LESION 9. PROTRUSIO ACETABULI

 MAY 2010 MAY 2009

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. CLASSIFY CALCANEAL FRACTURES. DISCUSS 1. DISCUSS THE CLINICAL FEATURES,

THE CLINICAL FEATURES, DIAGNOSIS AND MANAGEMENT AND COMPLICATIONS OF
MANAGEMENT OF INTRA ARTICULAR SUPRACONDYLAR HUMERUS FRACTURES IN
FRACTURES OF CALCANEUM CHILDREN

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAY (8X10=80 MARKS)

2.TERRIBLE TRIAD OF ELBOW 2.DEVELOPMENTAL COXA VARA

3.CONGENITAL VERTICAL TALUS CAMPBELL 3.HEMI VERTEBRA

(CONGENITAL ANOMALIES OF LOWER
4.FLEXIBLE INTRAMEDULLARY NAIL
EXTREMITY)
5.IDIOPATHIC CHONDROLYIS OF HIP
4.LC DCP
6.FAT EMBOLISM SYNDROME GOPALAN PG 68
5.BOTULINUM TOXIN
7.MID PALMAR SPACE INFECTION
6.BONE CEMENT GOPALAN 672
8.WAKE UP TEST(CAMPBELL CH-
7.OSTEOBLASTOMA(TACHDJIAN ; BENIGN
SCOLIOSIS&KYPHOSIS)
MUSCULOSKELETAL TUMOUR) 8.FUNCTIONAL
CAST BRACE STEWART- PG215 9. OBSTETRICAL PALSY

9. BONE TRANSPORT

NOV 2009 (RPT OF MAY 2009)

 DEC 2008 (RPT OF MAY2008) OCTOBER 2007

MAY 2008 PAPER 2

PAPER 2

ESSAY (20 MARKS)

ESSAY (20 MARKS) 1.CLASSIFY NECK OF FEMUR FRACTURES.

DISCUSS THE CLINICAL FEATURES AND
1.DISCUSS ACETABULAR FRACTURES WITH
MANAGEMENT. WHAT ARE THE
EMPHASIS ON MANAGEMENT
COMPLICATIONS.

SHORT ESSAY (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.OSTEOPOROSIS
2.SEQUESTRUM
3.FIBULAR HEMIMELIA
3.BARTONS FRACTURE
4.SHOULDER INSTABILITY
4.TARDY ULNAR NERVE PALSY
5.ACUTE OSTEOMYELITIS
5.GIANT CELL VARIANTS (DAV- TUMOURS;
6.COMPARTMENT SYNDROME( DAV PART 1 GCT)
GENERAL L/3RD )
6.SHOULDER HAND SYNDROME
7.KEINBOCKS DISEASE
7.HETEROTROPHIC OSSIFICATION GOPALAN
8.PERONEAL SPASTIC FLATFOOT PG211

9.SCIWORA 8.MUSCULAR DYSTROPHY

9.OSTEOCHONDRITIS DESSICANS (DAV-LOCAL

COMPLICATIONS OF#; F/3RD) CAMPBELL
SPORTS MEDICINE-KNEE INJURIES)
 MAY 2007 MAY 2006

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1.CLASSIFY SPINAL INJURIES. DISCUSS THE 1.CLASSIFY INJURIES OF ANKLE. DISCUSS THE
MANAGEMENT OF UNSTABLE SPINAL INJURIES CLINICAL FEATURES AND TREATMENT OF
AND REHABILITATION OF PARAPLEGIA FRACTURES OF TALUS.

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.RECURRENT DISLOCATION OF PATELLA 2.NUTRITIONAL RICKETS TACHDJIAN CH

32 (METABOLIC&ENDOCRINE DISEASES)
3.HYPERPARATHYROIDISM
3.HALLUX VALGUS(DAV-LOCAL
4.SENILE KYPHOSIS
COMPLICATIONS OF#; M/3RD) CAMPBELL FOOT
5.CLAW HAND AND ANKLE, DISORDERS OF HALLUX

6.CLASSIFICATION OF DISTAL RADIAL 4.INJURIES OF EXTENSOR MECHANISM OF

FRACTURES KNEE

7.GENU RECURVATUM 5.EQUINUS DEFORMITY

8.JOINT MOUSE 6.FRACTURE HEAD OF RADIUS

9.BONE GRAFT 7.SPRENGELS SHOULDER CAMPBELL

(CONGENITAL ANOMALIES OF TRUNK AND
UPPER EXTREMITY)

8.GIANT CELL TUMOUR OF TENDON SHEATH

9.COLD ABSCESS - (DAV--INFECTION; F/3RD)

 OCTOBER 2006 MAY 2005

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (2X30=60 MARKS)

1.CLASSIFY INJURIES OF PELVIS. DISCUSS THE 1.DISCUSS THE CLASSIFICATION OF OPEN

CLINICAL FEATURES, MANAGEMENT AND FRACTURE. (10)
COMPLICATIONS OF SUCH INJURIES. --HOW WOULD YOU MANAGE A TYPE III OPEN
FRACTURE OF LEG IN AN YOUNG ADULT DUE TO
A HIGH VELOCITY ROAD TRAFFIC ACCIDENT.
SHORT ESSAYS (8X10=80 MARKS) (20)

2.CALCANEAL FRACTURES 2. HOW IS EPIPHYSEAL INJURIES CLASSIFIED

(15)
3.GOUT(TUREK CH 9 METABOLIC BONE
DISEASE) --DISCUSS MANAGEMENT OF TYPE 3 LOWER
TIBIAL INJURY IN ADOLESCENT.(10)
4.COMPLICATIONS OF FRACTURE NECK OF
--HOW WOULD YOU DIAGNOSE A TYPE 5
FEMUR
INJURY.WHAT IS ITS SIGNIFICANCE (5)
5.FIBULAR HEMIMELIA
CAMPBELL VOL2; FRACTURES AND
6.QUADRICEPS CONTRACTURE DISLOCATION IN CHILDREN

7.TENDON TRANSFER FOR FOOT DROP SHORT ESSAYS (4X10=40 MARKS)

8.SEQUESTRA 3.TENSION PNEUMOTHORAX

9.CHONDROSARCOMA 4.FAT EMBOLISM SYNDROME GOPALAN PG 68

5.COMPARTMENT SYNDROME( DAV PART 1

GENERAL L/3RD )

6.BLUNT INJURY ABDOMEN

 MAY 2004 NOV 2003

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1.DESCRIBE THE CAUSES OF AVASCULAR 1.DISCUSS THE CLASSIFICATION, CLINICAL

NECROSIS OF THE FEMORAL HEAD IN ADULT FEATURES AND MANAGEMENT OF
AND BRIEFLY MENTION THE OPTIONS IN THE INTRACAPSULAR FRACTURE NECK OF FEMUR.
MANAGEMENT OF THE SAME

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.BAMBOO SPINE
2.FRACTURE OF THE LATERAL CONDYLE OF
3.NEUROPATHIC JOINT
HUMERUS IN CHILDREN
4.GENU VARUM
3.HALLUX VALGUS(DAV-LOCAL
COMPLICATIONS OF#; M/3RD) CAMPBELL FOOT 5.GIANT CELL TUMOUR (DAV- TUMOURS;
AND ANKLE, DISORDERS OF HALLUX GCT), CAMPBELL - BENIGN BONE TUMOURS

4.CLASSIFICATION OF FRACTURES OF THE 6.BARTONS FRACTURE

PROXIMAL END OF HUMERUS
7.KEINBOCKS DISEASE
5.CLAW HAND
8.TINELS SIGN
6.SYMES AMPUTATION
9.MALLET FINGER CAMPBELL,
7.COMPLICATIONS OF FRACTURES OF THE (FRACTURE,DISLOC OF HAND CH 64)
ACETABULUM

8.OLLIERS DISEASE

9.CLASSIFICATION OF FRACTURE CALCANEUM

 JUNE 2012 NOV 2010

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DEFINE TIBIAL CONDYLE FRACTURE, 1. CLASSIFY ACETABULAR FRACTURES. DISCUSS

MECHANISM, CLASSIFICATION AND THE MANAGEMENT OF ACETABULAR
TREATMENT. FRACTURES. MENTION THE COMLICATIONS

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.BARTON FRACTURES 2.TRAUMA SCORING SYSTEMS

3.PELVIC FRACTURE COMPLICATIONS 3.MONTEGGIA FRACTURE (CAMPBELL VOL2;

FRACTURES AND DISLOCATION IN CHILDREN)
4.FRO
4.LISFRANC FRACTURE
5.SYMES AMPUTATION
5.OSTEOCHONDRAL LESION OF TALUS
6.LISFRANC INJURIES
6.FLOOR REACTION ORTHOSIS
7.CRUTCH INJURY
7.DUPUYTRENS FRACTURE
8.EPIPHYSEAL INJURIES CAMPBELL VOL2;
FRACTURES AND DISLOCATION IN CHILDREN 8.FAT EMBOLISM SYNDROME GOPALAN PG 68

9.PATHOLOGICAL FRACTURES 9.CHANCE FRACTURE

 JUNE 2010 NOV 2009

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. CLASSIFY ANKLE INJURIES. DISCUSS 1. DESCRIBE NORMAL FRACTURE HEALING.

MANAGEMENT OF PRONATION EXTERNL
DISCUSS THE CLASSIFICATION, CLINICAL
ROTATION INJURY.
FEATURES AND MANAGEMENT OF NON UNION
OF TIBIA.

SHORT ESSAYS (8X10=80 MARKS)

2.FRACTURE DISEASE SHORT ESSAYS (8X10=80 MARKS)

3.CLAW HAND 2.PATHOLOGICAL FRACTURE.

4.SACH FOOT KULKARNI 3941 3.DAMAGE CONTROL ORTHOPAEDICS

5.EMG (KUL 1- 900) (TUREK CH 14 ORTHOPEDIC 4.FRACTURE NECK OF TALUS (DAV-KNEE ANKLE
NEUROLOGY) TRAUMA; F/3RD, M/3RD)

6.BROWN SEQUARD SYNDROME 5.KAPLAN LESION

7.CAST BRACING 6.SHORT WAVE DIATHERMY

8.FRACTURE LATERAL CONDYLE HUMERUS 7.ACROMIOCLAVICULAR SUBLUXATION

9.MYOSITIS OSSIFICANS 8.JONES FRACTURE

9.BIODEGRADABLE IMPLANTS (CAMPBELL

,GENERAL PRINCIPLES OF FRACTURE
TREATMENT; BIOMECHANICS)
 DEC 2008 MAY 2008

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. CLASSIFY INTRACAPSULAR FRACTURE NECK 1. CLASSIFY FRACTURES OF THE ANKLE

OF FEMUR, DISCUSS THE CLINICAL FEATURES ACCORDING TO LAUGE HANSEN. DESCRIBE THE
AND MANAGEMENT OF THIS FRACTURE IN A 55 CLINICAL FEATURES AND MANAGEMENT OF
YR OLD MAN. PRONATION EXTERNAL ROTATION FRACTURES
OF ANKLE.

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.CENTRAL CORD SYNDROME
2.GALLEAZI FRACTURE
3.HOFFAS FRACTURES
3.FRACTURE SCAPHOID
4.PTB PROSTHESIS
4.ANKLE FOOT ORTHOSIS
5.BENNETS FRACTURE
5.FRACTURE PATELLA
6.OLECRANON FRACTURE
6.SMITH FRACTURE
7.LISFRANC FRACTURE DISLOCATION
7.GARDENS CLASSIFICATION OF FRACTURE
8.NERVE CONDUCTION STUDY(TUREK CH 14
NECK OF FEMUR
ORTHOPEDIC NEUROLOGY)
8.SKELETAL TRACTION-STEWART,PG 4
9.PROXIMAL HUMERUS FRACTURE
9.WAX BATH
 MAY 2007 MAY 2007

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. WHAT IS FLOATING KNEE? DESCRIBE THE 1.DISCUSS THE BIOMECHANICS,

MANAGEMENT OF A PATIENT WITH AN OPEN CLASSIFICATION AND MANAGEMENT OF SUB
FLOATING KNEE. TROCHANTERIC FRAACTURES.

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.MALLET FINGER CAMPBELL, 2.SPINA VENTOSA

(FRACTURE,DISLOC OF HAND CH 64)
3.PIGMENTED VILLONUDULAR SYNOVITIS-
3.LISFRANC FRACTURE DISLOCATION (DAV, TUMOURS; L/3 RD)

4.NERVE REPAIR 4.NERVE GRAFTING

5.AUTOMATIC BLADDER 5.GIANT CELL VARIANTS (DAV- TUMOURS;

GCT)
6.CEREBRAL PALSY (CAMPBELL VOL 2 ;
NERVOUS SYSTEM DISORDERS IN CHILDREN) 6.PES CAVUS
7.DEQUERVAINS TENOSYNOVITIS
7.SYMES AMPUTATION
8.BANKARTS LESION
8.HIGH TIBIAL OSTEOTOMY
9.FLEXIBLE INTRAMEDULLARY NAIL
9.BOUTONNIERE DEFORMITY
 NOVEMBER 2006 JUNE 2006

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1.CLASSIFY ACETABULAR FRACTURES. GIVE IN 1.DISCUSS THE AETIOPATHOGENESIS,

BRIEF THE TREATMENT PROTOCOL FOR EACH DIAGNOSIS AND MANAGEMENT OF GOUT.
TYPE (TUREK CH 9 METABOLIC BONE DISEASE)

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.SANDERS CLASSIFICTAION OF CALCANEUM 2.SPONDYLOEPIPHYSEAL DYSPLASIA

FRACTURES
3.CLASSIFICATION OF ACETABULAR FRACTURES
3.BIOCHEMICAL CHANGES AND RADIOLOGICAL
4.GAIT CYCLE
FEATURES OF HYPERPARATHYROIDISM
5.CHANCE FRACTURE
4.ENTRAPMENT NEUROPATHIES OF ULNAR
NERVE 6.FIBROMATOSIS

5.FAILED BACK SYNDROME (CAMPBELL CH- 7.MENISCAL INJURY - MANAGEMENT.

LOWER BACK PAIN), KULKARNI (CAMPBELL ; SPORTS MEDICINE CH-KNEE
INJURIES)(CAMPBELL ; CH-ARTHROSCOPY OF
6.AUTOMATIC VS AUTONOMOUS BLADDER
LOWER EXTREMITIES)
7.DIAGBETIC FOOT
8.SPINA VENTOSA
8.FISH TAIL DEFORMITY
9.MANAGEMENT OF FRACTURE HEAD OF
9.PLANTAR FASCITIS (DAV-LOCAL RADIUS
COMPLICATIONS OF#; M/3RD)
 NOVEMBER 2005 MAY 2005

PAPER 2 PAPER 2

ESSAY (20 MARKS) ESSAY (20 MARKS)

1.DISCUSS THE DIAGNOSIS AND MANAGEMENT 1.DESCRIBE THE DIAGNOSIS AND

OF OSTEOSARCOMA OF LOWER END OF FEMUR MANAGEMENT OF PERTHES DISEASE OF HIP IN
IN 15 YR OLD BOY. A 5 YR OLD BOY

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.OSTEOCHONDRITIS DISSECANS. (DAV-LOCAL 2.TARDY ULNAR PALSY

COMPLICATIONS OF#; F/3RD) CAMPBELL
3.CLASSIFICATION OF EPIPHYSEAL INJURY
SPORTS MEDICINE-KNEE INJURIES)
CAMPBELL VOL2; FRACTURES AND
3.BROWN TUMOUR. DISLOCATION IN CHILDREN

4.FUNGAL OSTEOMYELITIS. 4.TRIPLE DEFORMITY OF KNEE

5.CONGENITAL RADIOULNAR SYNOSTOSIS. 5.COMPLICATIONS OF FRACTURE PELVIS

{CAMPBELL (CONGENITAL ANOMALIES OF
6.CODMANS TUMOUR
TRUNK AND UPPER EXTREMITY)}
7.MANAGEMENT OF FRACTURES OF TALUS
6.BONE BANK. KULKARNI 1137
(DAV-KNEE ANKLE TRAUMA; F/3RD, M/3RD)
7.REAMED IM NAILING.
8.SPRENGELS SHOULDER CAMPBELL
8.ACROMIOCLAVICULAR DISLOCATION. (CONGENITAL ANOMALIES OF TRUNK AND
UPPER EXTREMITY)
9.MANAGEMENT AND COMPLICATIONS OF
ACETABULAR FRACTURES. 9.FISH TAIL DEFORMITY
 SECTION 9

DORTHO

PAPER 3

-- CALICUT UNIVERSITY (2012-2003)

-- KERALA UNIVERSITY (2012-2005)

 JUNE 2012 NOV 2011

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DESCRIBE THE BLOOD SUPPLY OF TIBIA. 1. DISCUSS THE RECENT ADVANCES IN TOTAL
CLASSIFY NON UNION AND DISCUSS THE HIP REPLACEMENT WITH SPECIAL EMPHASIS IN
MANAGEMENT OF INFECTED GAP NON UNION CEMENTING TECHNIQUES AND BEARING
OF TIBIA SURFACES KULKARNI 3702, GOPALAN 673

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.FIBROFASCITIS 2.ULTRASONOGRAPHY IN DDH

3.KRUKENBURG OPERATION 3.NEOADJUVANT CHEMOTHERAPY (DAV -

TUMOURS; M/3RD) CAMPBELL- GENERAL
4.IMAGE INTENSIFIER IN ORTHOPAEDICS
PRINCIPLES TUMOURS
5.LASSO PROCEDURE
4.MIPPO
6.CHONDROBLASTOMA(TACHDJIAN ; BENIGN
5.DMARD
MUSCULOSKELETAL TUMOUR)
6.BIOABSORBABLE IMPLANTS (CAMPBELL
7.IMMUNO ASSAY IN SKELETAL INFECTIONS
,GENERAL PRINCIPLES OF FRACTURE
8.ASEPTIC LOOSENING OF PROSTHESIS TREATMENT; BIOMECHANICS)

9. VARUS DEROTATION OSTEOTOMY IN 7.LOCKING COMPRESSION PLATE KULKARNI

PERTHES DISEASE PG1433

8.COMPARTMENT SYNDROME OF FOOT( DAV

PART 1 GENERAL L/3RD )

9. PIVOT SHIFT TEST

 MAY 2011 NOV 2010

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE PRINCIPLES, MERITS AND 1. DISCUSS THE RECENT ADVANCES IN THR
DEMERITS OF LCP. DISCUSS THE RECENT WITH SPECIAL EMPHASIS ON BEARING
ADVANCES IN THE MANAGEMENT OF SURFACES, TISSUE INGROWTH, CEMENTING
OSTEOPOROTIC FRACTURES TECHNIQUES AND COMPUTER ASSISSTED
SURGERY

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.ISOTOPE BONE SCAN (KUL 1 - 155)
2.VISCOSUPPLEMENTATION
3.OSTEOID OSTEOMA
3.BIOABSORBABLE IMPLANTS(CAMPBELL
4.BIOLOGICAL FIXATION
,GENERAL PRINCIPLES OF FRACTURE
5.VISCOSUPPLEMENTATION TREATMENT; BIOMECHANICS)

6.GUIDED GROWTH 4.ULTRASOUNG IN DDH

7.DAMAGE CONTROL ORTHOPAEDICS 5.PONSETI TECHNIQUE

8.PELVIC SUPPORT OSTEOTOMY 6.INFECTED IMPLANT

9. CEMENT DISEASE 7.OSTEOGENESIS IMPERFECTA(DAV-LOCAL

COMPLICATIONS OF#; M/3RD) TACHDJIAN CH
32 (METABOLIC&ENDOCRINE DISEASES)

8.MIPPO

9. BONE SUBSTITUTES
 MAY 2010 NOV 2009 (RPT OF DEC 2008)

PAPER 3

MAY 2009

ESSAY (20 MARKS) PAPER 3

1. DISCUSS THE RECENT ADVANCES IN THE

MANAGEMENT OF MALIGNANT BONE
ESSAY (20 MARKS)
TUMOURS WITH EMPHASIS ON LIMB
SALVAGE(DAV) 1. CLASSIFY OPEN FRACTURES. DISCUSS
MANAGEMENT OF GRADE 3 OPEN FRACTURE
BOTH BONE LEG IN A 30YR OLD MALE
SHORT ESSAYS (8X10=80 MARKS)

2.BIOFILM -INTERNET
SHORT ESSAYS (8X10=80 MARKS)
3.SURGICAL DISLOCATION OF HIP
2.ARTHRODIASTASIS
4.TOTAL ELBOW REPLACEMENT
3.FLOATING KNEE
5.SURFACE REPLACEMENT OF HIP KULKARNI
4.PILON FRACTURE
3706

5.MIPPO
6.SINGLE EVENT MULTILEVEL SURGERY IN
CEREBRAL PALSY (CAMPBELL VOL 2 ; NERVOUS 6.BIODEGRADABLE IMPLANT (CAMPBELL
SYSTEM DISORDERS IN CHILDREN) ,GENERAL PRINCIPLES OF FRACTURE
TREATMENT; BIOMECHANICS)
7.VERTEBROPLASTY (KUL 1 - 190)
7.SOMATOS ENSORY EVOKED POTENTIALS
8.CONTINOUS PASSIVE MOTION
(CAMPBELL CH- SCOLIOSIS&KYPHOSIS)
9. FLOOR REACTION ORTHOSIS
8.LCP

9. BOTULINUM TOXIN
 DEC 2008 OCTOBER 2007

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS COMPUTER NAVIGATED 1.DISCUSS THE ETIOLOGY, PATHOLOGY AND

ARTHROPLASTY OF HIP AND ALSO ON MANAGEMENT OF AVN HEAD OF FEMUR (DAV-
CEMENTING TECHNIQUES GENERAL; M/3RD)

SHORT ESSAY (8X10=80 MARKS)

2.PEIZO ELECTRICITY IN ORTHOPAEDICS SHORT ESSAY (8X10=80 MARKS)

3.CONSERVATIVE MANAGEMENT IN 2.BONE SCAN

OSTEOARTHRITIS
3.DISTRACTION HISTIOGENESIS KULKARNI PG
4.HALLUX VALGUS(DAV-LOCAL 1519
COMPLICATIONS OF#; M/3RD) CAMPBELL FOOT
4.POLLICIZATION
AND ANKLE, DISORDERS OF HALLUX
5.SLAP LESIONS KULKARNI 1868
5.LIMB SALVAGE SURGERY(DAV)
6.FLOATING KNEE
6.LIGAMENTOTAXIS
7.PFN
7.CONTINOUS PASSIVE MOTION
8.EVIDENCE BASED MEDICINE
8.ARTHRODIASTASIS
9.BONE SUBSTITUTES
9. PONSETI TECHNIQUE
 MAY 2007 OCTOBER 2006

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1.DISCUSS THE ROLE OF ARTHROSCOPY IN 1.DISCUSS THE ROLE OF ILLIZAROV RING

DIAGNOSIS AND MANAGEMENT OF TRAUMATIC FIXATION IN THE MANAGEMENT OF NON
AFFECTIONS OF SHOULDER JOINT UNION

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.BIODEGRADABLE IMPLANTS (CAMPBELL 2.CONTINOUS PASSIVE MOBILISATION

,GENERAL PRINCIPLES OF FRACTURE
3.ULNAR DRIFT
TREATMENT; BIOMECHANICS)
4.LAMINOTOMY
3.MANAGEMENT OF RSD
5.EXTERNAL FIXATOR IN HAND INJURIES
4.CHEMONUCLEOLYSIS
6.ENDOSCOPIC CTS RELEASE
5.BONE SCAN IN METASTASIS
7.INTERLOCKING NAIL FOR HUMERUS
6.POLLICIZATION
8.INSTRUMENTATION IN SPONDYLOLISTHESIS
7.DVT
(CAMPBELL CH- SCOLIOSIS&KYPHOSIS)
8.CERAMICS IN ORTHOPAEDICS
9.ULTRASOUND SCAN IN ORTHOPAEDICS
9.OSTEOCHONDRITIS DESSICANS CAMPBELL
SPORTS MEDICINE-KNEE INJURIES) (DAV-LOCAL
COMPLICATIONS OF#; F/3RD)
 MAY 2006 MAY 2005

PAPER 3 PAPER 3

ESSAY (2 X 30 = 60MARKS)

ESSAY (20 MARKS) 1.DESCRIBE THE CLINICAL AND RADIOLOGICAL

FEATURES OF RICKETS.(10)
1.DISCUSS INSTABILITIES OF SHOULDER AND ITS
--WHAT BIOCHEMICAL ABNORMALITIES ARE
RECENT TRENDS IN MANAGEMENT
SEEN (5) --
DISCUSS THE DIFFERENTIAL DIAGNOSIS OF
RICKETS (5)
SHORT ESSAYS (8X10=80 MARKS)
--WHAT ARE THE INDICATIONS AND SPECIFIC
2.BONE BANK KULKARNI 1137 METHODS USED FOR THE ORTHOPAEDIC
MANAGEMENT OF RICKETS (10) TACHDJIAN
3.COMPRESSION SCREW
CH 32 (METABOLIC&ENDOCRINE DISEASES)
4.FAR OUT SYNDROME
2. DESCRIBE THE CLINICAL AND RADIOLOGICAL
5.FNAC FEATURES OF SCFE (10) .DESCRIBE ITS
MANAGEMENT AT DIFFERENT DEGREES OF SLIP
6.BIOLOGICAL FIXATION
(10)
7.LASER DISCECTOMY
WHAT ARE ITS COMPLICATIONS AND ITS
8.CHEMICAL SYNOVECTOMY MANAGEMENT (10)

9.BOTULINUM IN CEREBRAL PALSY(CAMPBELL SHORT ESSAYS (4X10=40 MARKS)

VOL 2 ; NERVOUS SYSTEM DISORDERS IN
3.ARTICULAR SURFACE REPLACEMENT OF THE
CHILDREN)
HIP KULKARNI 3706

4.BONE TRANSPLANT

5.SPINAL CORD MONITORING

6.NEONATAL SEPTIC ARTHRITIS OF THE HIP

 MARCH 2004 NOVEMBER 2003

PAPER 3 PAPER 3

ESSAY (2X30=60 MARKS) ESSAY (20 MARKS)

1.DISCUSS THE SKELETAL MANIFESTATIONS OF 1.DISCUSS THE RECENT ADVANCES IN THE

RHEUMATOID ARTHRITIS. MANAGEMENT OF MALIGNANT BONE
TUMOURS
DESCRIBE THE DRUGS USED IN RHEUMATOID
ARTHRITIS WITH THEIR MECHANISM OF ACTION

2.DESCRIBE THE PRINCIPLES OF MANAGEMENT SHORT ESSAYS (8X10=80 MARKS)

OF IDIOPATHIC SCOLIOSIS. WHAT ARE THE
2.POSTERIOR SPINAL STABILISATION
COMPLICATIOS OF SURGERY PERFORMED FOR
SCOLIOSIS 3.BIOLOGICAL FIXATION

(CAMPBELL CH- SCOLIOSIS&KYPHOSIS) 4.LIGAMENTOTAXIS

SHORT ESSAYS (4X10=40 MARKS) 5.POTTS PARAPLEGIA

3.ROLE OF MRI IN ACL INJURIES KULKARNI CH 6.PILON FRACTURE

12 MRI
7.FUNCTIONAL CAST BRACING STEWART-
4.SURFACE REPLACEMENT OF HIP KULKARNI PG215
3706
8.CHEMONUCLEOLYSIS
5.ANTEVERSION OF FEMORAL NECK IN DDH
9.DENIS BROWNE SPLINT
6.JESS
 JUNE 2012 MAY 2011

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DEFINE SCFE,CLINICAL FEATURES, 1. DESCRIBE THE CLASSIFICATION, DIAGNOSIS

PATHOLOGY, INVESTIGATIONS AND AND MANAGEMENT IN BRIEF OF PERTHES
MANAGEMENT. DISEASE OF HIP.

SHORT ESSAYS (8X10=80 MARKS) SHORT ESSAYS (8X10=80 MARKS)

2.TREATMENT OF SKELETAL TB- TULI 2.RHEUMATOID FACTOR

3.CHEMOTHERAPY OF OSTEOGENIC 3.PHOCOMELIA

SARCOMA. (DAV - TUMOURS; M/3RD)
4.DIAGNOSIS OF GOUT(TUREK CH 9
4.HIGH TIBIAL OSTEOTOMY METABOLIC BONE DISEASE)

5.RADIAL CLUB HAND 5.BRODIES ABSCESS

6.CHONDROBLASTOMA(TACHDJIAN ; BENIGN 6.OSGOOD SCHLATTERS DISEASE CAMPBELL ;

MUSCULOSKELETAL TUMOUR) VOL2 OSTEOCHONDROSIS

7. CAUSES AND RISKS OF OSTEOPOROSIS 7.OSTEOID OSTEOMA

8.RENAL OSTEODYSTROPHY 8.DIAGNOSIS OF OSTEONECROSIS

9.FRIEBERG DISEASE 9.RADIOLOGICAL FEATURES OF RICKETS

TACHDJIAN CH 32 (METABOLIC&ENDOCRINE
DISEASES)
 NOV 2010 JUNE 2010

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. CLASSIFY OSTEOMYELITIS. DISCUSS THE 1. DISCUSS THE PATHOLOGY OF PERTHES

CLINICAL FEATURES, DIAGNOSIS AND DISEASE. OUTLINE THE MANAGEMENT OF
MANAGEMENT OF ACUTE HEMATOGENOUS PERTHES DISEASE IN A 7 YR OLD BOY.
OSTEOMYELITIS

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.ANTALGIC GAIT
2.SPINA VENTOSA
3.CLAW HAND
3.TRENDELENBURG SIGN
4.OSTEOID OSETOMA
4.TENNIS ELBOW (CAMPBELL SPORTS
5.COLD ABSCESS-DAV-INFECTION; F/3RD.
MEDICINE-ELBOW INJURIES)
6.KEINBOCKS DISEASE
5.SYNOVIAL CHONDROMATOSIS
7.OSTEOGENESIS IMPERFECTA (DAV-LOCAL
6.RADIOLOGICAL SIGNS OF PERTHES DISEASE
COMPLICATIONS OF#; M/3RD) TACHDJIAN CH
7.TUBERCULOSIS OF KNEE 32 (METABOLIC&ENDOCRINE DISEASES)

8.ACCESSORY NAVICULAR 8.PES PLANUS

9.SPINAL CANAL STENOSIS (CAMPBELL CH- 9.KYPHOSIS

OTHER DISORDERS OF SPINE)
 NOV 2009 MAY 2009

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE CLINICAL FEATURES, DIAGNOSIS 1. DESCRIBE THE CLINICAL FEATURES,

AND MANAGEMENT OF OSTEOSARCOMA RADIOLOGY AND MANAGEMENT OF GIANT
LOWER END OF FEMUR IN A 12 YR OLD BOY. CELL TUMOUR OF BONE. (DAV- TUMOURS;
GCT) CAMPBELL - BENIGN BONE TUMOURS

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.OCHRONOSIS KULKARNI 197
2.SPINA VENTOSA
3.MALLET FINGER CAMPBELL,
(FRACTURE,DISLOC OF HAND CH 64) 3.SPRENGEL SHOULDER CAMPBELL
(CONGENITAL ANOMALIES OF TRUNK AND
4.CONGENITAL VERTICAL TALUS CAMPBELL
UPPER EXTREMITY)
(CONGENITAL ANOMALIES OF LOWER
EXTREMITY) 4.DMARD

5.PLANTAR FASCITIS (DAV-LOCAL 5.GOUT(TUREK CH 9 METABOLIC BONE

COMPLICATIONS OF#; M/3RD) DISEASE)

6.WRIST DROP 6.KEINBOCKS DISEASE

7.MRSA INFECTION IN ORTHOPAEDICS 7.CLUTTONS JOINT

8.SERONEGATIVE SPONDYLOARTHROPATHY 8.PAINFUL ARCH SYNDROME

(KUL 1- 886)
9.FIBROUS DYPLASIA (TACHDJIAN ; BENIGN
9.CHORDOMA ( CAMPBELL - MALIGNANT MUSCULOSKELETAL TUMOUR)
BONE TUMOURS)
 DEC 2008 MAY 2008

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. DISCUSS THE PATHOLOGY OF 1. DEFINE OSTEOMYELITIS. CLASSIFY

OSTEOARTICULAR TUBERCULOSIS. OUTLINE THE OSTEOMYELITIS MENTIONING THE ORGANISMS
MANAGEMENT OF TUBERCULOUS ARTHRITIS CAUSING EACH TYPE. DESCRIBE THE CLINICAL
OF HIP JOINT. FEATURES, RADIOLOGY AND MANAGEMENT OF
ACUTE PYOGENIC OSTEOMYELITIS.

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.WADDLING GAIT
2.CARIES SICCA
3.PAINFUL ARC SYNDROME
3.ABDUCTOR MECHANISM OF HIP
4.BRYANTS TRIANGLE
4.MADELUNG DEFORMITY
5.GENU RECURVATUM
5.MULTIPLE MYELOMA
6.SPINA BIFIDA
6.OSGOOD SCHLATTERS DISEASE (CAMPBELL
7.HOUSEMAIDS KNEE
VOL 2 ; OSTEOCHONDROSIS)
8.FOOT DROP
7.ACHONDROPLASIA (TACHDJIAN,
9.TORTICOLLIS {CAMPBELL (CONGENITAL ORTHOPEDIC DISORDERS)
ANOMALIES OF TRUNK AND UPPER
8.NEUROPATHIC JOINT
EXTREMITY)}
9.GOUT(TUREK CH 9 METABOLIC BONE
DISEASE)
 MAY 2007 MAY 2007

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1. WHAT IS COLD ABSCESS? DESCRIBE THE 1. DISCUSS THE CURRENT TRENDS IN THE
ANATOMICAL BASISOF COLD ABSCESS AT DIAGNOSIS AND MANAGEMENT OF BONE AND
VARIOUS SPINE LEVELS JOINT INFECTIONS.

DAV -- INFECTION; F/3RD.

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS) 2.MANAGEMENT OF PERIPROSTHETIC

FRACTURES AFTER THR
2.OSTEOCLASTOMA
3.FLOOR REACTION ARTHROSIS
3.RENAL RICKETS TACHDJIAN CH 32
(METABOLIC&ENDOCRINE DISEASES) 4.RECENT ADVANCES IN FIXATION OF SPINE
TRAUMA
4.FIBULAR HEMIMELIA
5.FREE VASCULARISED BONE TRANSPLANT
5.SPRENGELS SHOULDER CAMPBELL
(CONGENITAL ANOMALIES OF TRUNK AND 6.MICRO LUMBAR DISCECTOMY
UPPER EXTREMITY)
7.BONE MORPHOGENIC PROTEIN
6.GOUT(TUREK CH 9 METABOLIC BONE
8.EVALUATION AND STAGING OF
DISEASE)
MUSCULOSKELETAL SARCOMAS
7.INTRINSIC PLUS DEFORMITY
9.MANAGEMENT OF LIUMB LENGTH
8.MULTIPLE MYELOMA INEQUALITY OF LOWER LIMBS IN CHILDREN

9.GROWTH PLATE ( DAV PART 1 GENERAL

L/3RD )
 MAY 2006 MAY 2005

PAPER 3 PAPER 3

ESSAY (20 MARKS) ESSAY (20 MARKS)

1.CLASSIFY TIBIAL CONDYLAR FRACTURES. 1.DESCRIBE THE CLASSIFICATION OF DORSO

DISCUSS THE MANAGEMENT OF TIBIAL LUMBAR SPINE FRACTURES AND THE RECENT
CONDYLAR FRACTURES IN ADULT WITH TRENDS IN THEIR MANAGEMENT.
EMPHASIS ON RECENT TRENDS.

SHORT ESSAYS (8X10=80 MARKS)

SHORT ESSAYS (8X10=80 MARKS)
2.CARPAL TUNNEL SYNDROME-DIAGNOSIS
2.CLASSIFY PERIPROSTHETIC FRACTURES. CAMPBELL ; CH - THE HAND

3.DISCOID MENISCUS. (CAMPBELL ; CH- 3.SPINAL CORD MONITORING ON SPINAL

ARTHROSCOPY OF LOWER EXTREMITIES) SURGERY.
4.HETEROTROPIC OSSIFICATION GOPALAN
4.STAGING OF BONE TUMOURS
PG211
5.BISPHOSPHONATES
5.NEOADJUVANT CHEMOTHERAPY (DAV -
TUMOURS; M/3RD) CAMPBELL- GENERAL 6.BONE SUBSTITUTES
PRINCIPLES TUMOURS 6.PROXIMAL FEMORAL
7.CLASSIFICATION OF FRACTURES OF
NAIL
ACETABULUM
7.GAIT ANALYSIS- METHODS
8.LIGAMENTOTAXIS
8.CERAMICS IN ORTHOPAEDICS
9.BONE TRANSPORT
9.CUBITUS VALGUS.
 SECTION 10

BOOKS

CAMPBELL - REFERENCE BOOK ,BUT IF U HAVE FOLLOWED IT THROUGHOUT GO WITH IT

TACHDJIAN -- PEDIATRIC TOPICS LIKE SCFE,DDH,PERTHES ....

ROCKWOOD -- BETTER TO READ IF KOVAL DOESNT GIVE IT IN DETAIL

ZUKERMAN,KOVAL -- MOST TRAUMA QUESTIONS CAN BE GOT FROM THIS TINY CHAMP

TULI -- ALL TB RELATED QUESTIONS

DAV -- DAVENGRE NOTES (F/3 --FIRST THIRD) , (L/3 --LAST THIRD) -- MOST TOPICS BUT GOTTA
SEARCH

GOPALAN-- LAST MINUTE READ, GOOD ONLY IF U HAVE READ /LEARNED THE TOPIC EARLIER FROM
BOOKS THAT GIVE THE TOPIC IN DETAIL

KULKARNI - ONLY LIMITED TOPICS. SOME CHAPTERS ARE TOO GOOD, SOME REALLY BAD

TUREK --BASIC SCIENCES CHAMP

APLEY

FINALLY FOR SOME ELUSIVE TOPICS (LIKE BIOFILMS) DO SEARCH THE NET.

321 | Q & A
322 | Q & A