SCORE

SRi RamaChandRa
COntinuing ORthOpaEdiC
REviSiOn EduCatiOn

Post Graduate’s Guide

From
Department of Orthopaedics,
Sri Ramachandra Institute of Higher Education
and Research,
Chennai, Tamilnadu

1
 EDITORS

Dr. J.K. Giriraj Harshavardhan Dr. Srijay Sashaank

Dr. K.R. Tarun Prashanth Dr. Abhishek Menon

2
 EDITOR’S NOTE:
Taking a good history and performing an adequate clinical examination is a skill learnt by a doctor
during his study period. These skills improve the communication between the doctor and patient. The
‘touch and feel’ of a doctor can work miracles on the patient. The friendly non-formal atmosphere
would remove the distrust and the medico-legal hassles. It is important that doctors correlate the
patient’s symptoms and findings to the investigations performed. This would avoid unnecessary
interventions. Nowadays even before the patients start talking, they hand over their x-rays and MRIs
for the doctors to have a look. The doctors must resist the temptation to look at the investigations
before performing a clinical examination. This would mislead the doctor – bias. Hence doctors must
follow rigid protocols – history first, clinical examination second, investigations third and
interventions last. Any deviations could lead to misdiagnosis and mis-management.

The idea of this SCORE book is to serve as a tool for quick reference for your examination
and reminder for history and clinical examination. This will be useful for orthopaedic residents in a
busy out patient department as well as for their preparation for the examinations. Once this book is
read, the orthopaedician must be able to elicit the necessary history and perform a complete clinical
examination without missing a single point. All the important theory topics for DNB and MS Ortho
exams are also covered.

Even though not emphasized in this book, doctors must remember that medicine is an art
and not a perfect science. 2+2 in medicine is never 4 and there will always be uncertainties and
differences between patients. That is what makes the practice of medicine very interesting and unique
and not just a robotic job. Doctors are gifted with the kind of knowledge that patients find very
difficult to understand. Doctors must not misuse this knowledge and must practice medicine ethically
and empathetically. This will give true happiness and after all the aim of life is to have a good and
peaceful night’s sleep.

DR. J.K. GIRIRAJ HARSHAVARDHAN, D.Ortho, DNB Ortho,

Associate Professor of Orthopaedics,
Consultant Orthopaedic Surgeon,
Sri Ramachandra Medical Centre,
Sri Ramachandra Medical College and Research Institute, Chennai – 116.
Indian Orthopaedic Association JMRF PaediatricOrthopaedic Fellow.

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S.No Topic Page No

1. General Proforma for examination 7

2. Hip examination 10

Nonunion neck of femur -questions frequently 34

3.
asked

4. Examination of Knee 38

5. Examination of Shoulder Joint 72

6. Examination of the Spine 85

7. Intervertebral disc prolapse 97

8. Scoliosis 100

9. Tuberculosis spine 104

10. Spondylolisthesis 107

6. Examination of Foot and Ankle 109

7. Examination Of Elbow 125

8. Examination of Wrist Joint 139

9. Examination of Swelling 144

10. Examination of a case of Osteomyelitis 157

11. Examination of long bones- Nonunion/Malunion 164

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12. Clinical examination of lower limb deformity 175

13. Examination of knee deformity 184

13. Cerebral Palsy 192

14. Examination of Peripheral Nerves 203

15. Examination of Brachial Palsy 217

16. Avascular necrosis of femoral head 223

17. Cauda equina syndrome 227

18. Blount’s disease 230

19. Biomechanics of hip joint 232

20. Biomechanics of knee 235

21. Cervical myelopathy 237

22. Chondrosarcoma 244

23. Congenital talipes equinovarus deformity 246

24. Congenital vertical talus 251

25. Ewings sarcoma 253

26. Hallux valgus 257

27. Intervertebral disc prolapse - 2 268

28. Developmental dysplasia of the hip 276

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29. Nerve conduction study 286

30. Electromyography 288

31. Orthotics and prosthesis part 1 289

32. Osteomyelitis 295

33. Slipped capital femoral epiphysis 297

34. Tuberculosis of the hip 301

35. Legg-Calve-Perthes disease 306

36. Spondylolisthesis -Part 2 313

Treatment options in fracture neck of femur in 318

37.
young adults

38. Tuberculosis of the spine 325

39. Osteotomies around the hip 329

40. Volkmann ischaemic contracture 339

41. Tendon transfers 344

42. Osteosarcoma 349

43. Ward rounds 354

44. Prosthesis and orthosis part 2 363

45. Last minute revisor 374

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 GENERAL PROFOMA FOR EXAMINATION

Timing Site

Onset- insidious/ acute

Progression, previous episode

Duration , intermittent or constant

Frequency

(if pain) L (location)

Radiation

Trauma and treatment history

Characteristic of pain ( add rest pain and night pain)

Associated symptoms

Triggers – (aggravated/relieved)

Severity(activities of daily living)

Allergies Smoking

Medications Sexual history

Past medical history Diet

Obstetric history Drinking

Past surgical history Alcohol

Family history

Occupation

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 Examination
Conscious, Orientation, Vitals,

Pallor, Icterus, Cyanosis, Clubbing, Lymphadenopathy, Pedal Edema Syndromic Facies

Criteria for ligamentous laxity – Wyne Davis , Bighton criteria Neurocutaneous markers
Features suggestive of spinal dysraphism

1. Inspection
a. Attitude
b. Limb length discrepancy
c. Muscle wasting
d. Skin over limb
e. Scars, sinuses , dilated veins
f. Swelling
g. fullness

2. Palpation
a. Warmth
b. Tenderness
c. Palpation of bony landmarks - Thickening, discontinuity or irregularity
d. Palpation of surrounding soft tissue
e. Palpation of joint

3. ROM deformity and movements

a. Passive
b. Active
c. Painful/ Painless
d. Ass with pain, muscle spasm, crepitus

4. Measurements-
a. Limb length Apparent True
b. Muscle circumference

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5. Special Tests

6. Neuro-
a. Muscle – tone, bulk and power
b. Reflexes- superficial and deep
c. Sensation
d. Fine touch Crude touch Pressure
e. Two point descripination
f. Temperature
7. Pulses
8. Lymph Nodes palpable
9. Other joints
10. Gait

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 HIP EXAMINATION

Patients with hip joint disease may present with an array of complaints the main being
pain, alteration of gait, instability, limitation of functional activity 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.

A proper assessment of the spine, pelvis, and sacroiliac joint or vascular cause needs
to be performed as a routine in order to find where the pathology lies. Rarely hip disease may
present as pain referred to the knee.

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Proforma:
Age Name Sex
Occupation
Chief Complaints :

PAIN

Site- To point the site of pain with a single finger. Note down whether the pain is
localised in the groin, trochanteric area, buttocks etc. and not to use vague terms like pain in
the hip.
Remember that a patient with hip disease may present with knee pain.

Onset – How it started?

Duration – How long the pain is present?

Character – What is the nature of pain? Throbbing pain is due to inflammatory causes,
burning pain is due to neuropathic causes.
Severity- How disabling is the pain is ? Its effect on routine activities, self care, locomotion,
occupation and recreational activities?
Progression – What has happened to the pain after it started? Has it been static ,increased or
decreased in intensity. Is it constant or intermittent?

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.

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Rest pain – pain persistent even at rest seen in malignant tumors and septic arthritis/acute
osteomyelitis
Night Starts/Cries – If there was pain after a period of sound sleep for 2-3 hours in the night
and awakens due to pain, seen in TB arthritis due to loss of protective muscle spasm.

Deformity
From when the deformity was observed? How did it start?
How did it progress and how is it progressing? Any treatment taken?
Any associated symptoms?
Is there any history of trauma or infection?

Limb length discrepancy

How long it is present?
Is it static or progressive? Any aid or support used Associated symptoms?
Any history of infection or trauma?

History to assess function

Walking ability
 Normal or altered
 Restricted or unrestricted
 Aided or unaided
 If aided; which aid is used
 Ability to squat
 Ability to sit cross legged
 Ability to drive car
 Ability to tie shoes
 History of early morning stiffness
 History of small joint pain and swelling
 History of cough with expectoration
 History of burning micturition
 History of altered bowel habits History of watering of eyes

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Past history Hypertension Diabetes mellitus

 Tuberculosis
 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
 How long treatment has been undergone?
 Under any medication or underwent any surgery?

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, cornea, pigmentation of sclera.
 Pinna- Low set, blackish discoloration.
 Cheeks- Malar rash.
 Mouth – Normal dental hygiene, high arch palate.
 air Line- Normal or low.
 Neck – Webbing , thyroid swelling.
 Nipples- Normal level or not.
 Shape of chest wall- Pectus carinatum/ excavatum.

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  Abdomen- Protuberant , undescended testis , hernias.
 Nails- Pitting.
 Palms and soles- Hyperkeratosis.
 Thickening of lower end radius, malleoli and costochondral junctions.

Ligamentous laxity

 Wynne-Davies 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 –
 Tuft of hair in the back
 Midline swelling in the spinal region Café au lait spots
 Shawgreen patches Neurofibroma nodules/swelling

Local Examination
 The steps of local examination are Inspection
 Attitude in general and Inspection of joint in proper Palpation
 Deformities
 Range of Movements Measurements
 Gait analysis Special tests and
 Examination of spine and other joints and other systems.
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
 Skin over the joint Bony contours
 Soft tissue contours Swelling
 Wasting

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  Limb length discrepancy

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.

Deformity is said when there is a fixed contracture of the joint which will prevent the
joint from being brought back to 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 fixed 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.
Attitude must be spoken after telling the patient to keep both limbs as parallel to each other as
it spoken based on comparison to the neighbouring limb.

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.

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 Attitude starts from Position of the lumbar spine ,comment on lumbar lordosis,
position of ASIS ,position of hip, knee, where the patella is facing, position of ankle, position
of lateral border of the foot in order to tell how much the limb is externally rotated.
Muscle wasting of thigh, gluteal and calf segment Limb length discrepancy

Inspection of joint proper Anteriorly from proximal to distal; Level of ASIS

Normal hollowing of iliac fossa Inguinal orifices
Widened perineum
Any visible 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, sinuses
Abnormal masses

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

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Anteriorly:
Local rise of temperature
Anterior joint line tenderness- Anterior joint line is 2-3 cm below and lateral to midinguinal
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
1. Warmth
2. Level in both supero-inferior as well as antero-posterior directions. 3.Surface –
Smooth or irregular or is it thickened.
4. Tenderness both local – using the thumb anteriorly and the other fingers posteriorly
attempt in pressing the trochanter causes pain due to pathology around the trochanter and
thrust tenderness – giving a firm pressure along the lateral aspect of the hip causes pain
due to intrarticular pathology.
5. Broadening or thickening
6. Digital palpation of GT in respect to the trochanter and compare with the normal side.

Posteriorly:
Warmth
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.
PSIS tenderness by palpating the dimple of venous

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Deformity and Movements

Look for active and passive movements in all three axes. Look for sagittal plane -
flexion & extension, coronal plane - abduction & adduction and Axial plane 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.
Normally when a person lies supine on a firm surface the lumbar
spine lies flat on the couch 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.
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.

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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 placed 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 0- 120
Extension 0-10
Abduction 0-40
Internal rotation in flexion 0-35 Internal rotation in Extension 0-30 External rotation in
flexion 0-45 External rotation in Extension 0-40
Movements should be tested both actively and passively.
During the range of movement,its important to look for associated

1. Pain
2. Muscle spasm
3. 3.Crepitus
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 due to excessively sitting cross legged.
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.

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 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? 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 extraarticular cause of pain.
5. Is the limitation of movement due to mechanical causes or due to pain and spasm?
6. 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.
7. 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
8. What is differential rotation?
The change in the amount of internal rotation with the hip in neutral and when hip in
flexion if when increased needs to be inferred as there is a change in the contour of
the femoral head mainly observed in AVN and in other conditions where the contour
of the femoral head is altered i.e Femoro acetabular impingements.
9. Which is the best position to assess rotational movements? Prone position with the
knee flexed.

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.

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Apparent length:
Keep both lower limbs as 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,

Chienes 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 knee joint line medial malleolus tip to.

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 an imaginary 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 3cm 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 90.Palpate from the pubic symphysis laterally and along the inguinal
ligament ,the first bony prominence felt is the Anterosuperior iliac spine (ASIS) and mark it
then posteriorly on running the fingers along the gluteal crease with the hip flexed the most
prominent bony land mark is the Ischial Tuberosity and mark it. Draw a line connecting the
inferior edge of ASIS to the most prominent portion of ischial tuberosity. In the normal hip

21
the tip of greater trochanter will be just touching the line. In patients with supratrochanteric
shortening it will be above the line as the tip of the greater trochanter is migrated proximally..

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 and inferior to
the umbilicus.
Girth measurement is done at the bulkiest part of thigh usually 10-15cm above medial joint
line and calf 7-10cm below the medial joint line ,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 test

Patient position- Supine
Procedure – Stand on the right side of the patient, try to insinuate the dorsal aspect of left
hand under the lumbar spine of the patient and see if the knuckle border is able to cross the
midline, if so it means patient has excessive lumbar lordosis, now with with the other hand
hold the unaffected side. Flex the unaffected knee fully, then flex the unaffected hip till the
dorsal aspect of the lumbar region touches against the hand which infers that 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 which can be seen by trying to
look parallely with the level of the couch ehen the opposite side would be visibl. The angle
between the long axis of thigh and the examination table gives the angle of flexion deformity.

22
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.

Kothari’s parallelogram:
unsquared pelvis – Join
both ASIS and drop perpendicular from each ASIS to midline, measure the angle formed
between lines – this gives idea
of Adduction/abduction in affected hip (can be used as adjunct to classical method and is
easy)

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 50 %
drop is considered normal. If more than 2cm or 50then it is abnormal and suggests abductor
insufficiency.Trendelenberg positive is when Sound side sinks. Insufficiency may be due
to abnormal fulcrum, lever or power of the abductor mechanism.

23
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 90deg and 10deg adduction. Stabilise the pelvis
with one hand with the thumb over the ASIS and other fingers covering the GT posteriorly.
Hold the knee and thigh with the other hand. Push in a to and fro motion in order to feel the
trust/pressure of the proximal femur touching the fingers.
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 90degree 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 30-40degree of
abduction, then a clink will be felt as the femoral head reduces into the acetabulum slipping
over the acetabular rim.

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 90deg 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 30-40deg of
abduction, then a clink will be felt as the femoral head reduces into the acetabulum slipping

24
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

Piriformis test (FADIR):

Flexion, adduction and internal rotation in lateral position stretches piriformis – produces
pain in piriformis tendinitis/syndrome. Same test if produces pain at groin is useful for
femoroacetabular impingement (called impingement sign)

McFarland’s test:
During flexion, hip points to opposite shoulder but in SCFE and Osteonecrosis with
superolateral collapse the hip points to ipsilateral shoulder.

Examination of SI joint
Patrick’s Test: (FABER) Test:
Jansen’s sign: Flexion, abductionand external rotation at hip putting lateral malleolus at
patella – pain produced at SI joint. Same test if produces pain
at groin is useful for femoroacetabular impingement.

Erichson’s pelvis compression test:

Press iliac crests together – pain over SI joint.

25
Gaenslen’s test:
Patient at edge of bed with ipsilateral hip hanging out. Flex both hips together then ask to
release ipsilateral limb to extend hip – pain indicates SI joint affection.

Yeoman’s test for Sacroilitis:

Passive hyperextension of thigh in a prone patient.

Examination of Lumbar Spine Examination of Lymphnodes

External iliac, internal iliac, paraaortic group of lymph
node

Distal neurological and vascular examination:

Check for distal motor deficit especially in sciatic nerve distribution, reflexes and sensations.
Palpate all peripheral pulses (popliteal, anterior and posterior tibial, dorsalis pedis)

Frequently Asked :

Various compensatory mechanisms and what is their importance

Compensation for hip deformity occurs at:
• Spine (often lumbar)
• Pelvis (coronal tilt or flexion/extension)
• Hip joint itself (coronal deformity)
• Knee
• Ankle
• Foot
They are physiological response of body to a pathological condition and must not be thought
of as a disorder! They:
• Conceal deformity
• Maintain equilibrium while standing/ walking by shifting center of gravity
• Stabilize the joint (remember they ‘fix’ the joint)
• Make up for the loss

26
Can all deformities around hip be compensated?
No, there is a limit to compensation for rotational deformities which often remain revealed
unless very mild. Only coronal and saggital plane deformities are corrected, that to only a
certain extent.

How much shortening can be effectively compensated without producing ankle

equinus?
Approximately 2-2.5cm

Prerequisites of performing Thomas test?

The following should be observed:
1. General prerequisites of examination
2. Unilateral deformity (bilateral measured by modification)
3. No bony ankylosis in other hip/knee.
4. Other hip should be painless, ipsilateral hip should not be very painful

How to assess FFD for bilateral limb deformity?

To perform the test in prone position (modification) – both lower limbs dangling off the
couch. Support both thighs and obliterate lumbar lordosis in direct vision then measure the
flexion deformity from imaginary horizontal
Parallel to floor. Other more practical way is to test in lateral position and obliterate lumbar
lordosis.
Modification of Thomas Test.

Which movement is first lost in hip pathology?

Extension followed by rotations, adduction, abduction,
and lastly flexion (this sequence is followed in synovial disorders – increased volume
whereas those in which there is direct injury to cartilage abduction is lost earlier due to
adductor spasm – adductors are stronger!)

27
What is the position of rest for hip joint?
This is the position in which the volume of hip joint is maximal: 10º each of flexion,
abduction and external rotation.

How do you do Trendelenburg test?

There are at least four different methods vaguely described in various textbooks. The
following is the most standard method studied and described.
1. Stand behind patient. Observe the angle between pelvis (line joining iliac crests) and
ground. Ask patient to stand on unaffected side first, lifting affected side foot and flexing hip
between neutral and 30° and knee to clear foot off the ground (this is done to nullify the
effect of rectus femoris). Note the position of pelvis. {In some patients to maintain balance
either a supporting stick can be used on the hand of weight- bearing hip or examiner can
support both shoulders}.
2. Then ask patient to raise the affected side of pelvis as high as possible. (One may
provide support to the patient by holding arm of the weight-bearing side). Correct any
tendency to lean over the weight bearing side by bringing
shoulders at same level.
3. Repeat the same on affected side (the side to be tested).
Interpretation: Normally (“negative test”) one is able to lift the other side (watch iliac crest)
without losing balance for at least 30 sec and the lift is equal to the abduction possible at that
hip.

Gluteal folds have been long propagated as ‘standard’ reference for judging pelvic lift but a
lot of limitations arise primarily due to muscle wasting so common in hip disorders. PSIS is a
good reference if there is significant gluteal wasting or folds are asymmetrical, however it is
too near to midline to judge pelvic lift and be taken as a primary reference.

Alternately one can less reliably stand in front of patient and support patient’s palm. Perform
the test the same way but notice the pressure transmitted by patient’s palm when they attempt
to balance. Increased pressure in opposite side in an attempt to gain support from you
suggests positive test.

28
What constitutes a positive test?
Any of the following constitute a “positive test”: (Abnormal response)
1. Maximal elevation not achieved.
2. Sustained elevation not achieved (for 30 sec) – Delayed abnormal response.
3. Iliac crest not elevated (pelvis parallel to ground).
4. Pelvis drops down (opposite iliac crest).

What does this test assess?

It is a screening test to check integrity of abductor mechanism comprising of head and
acetabular socket as fulcrum, neck and trochanteric region as lever (site of effort), abductor
(primarily Gluteus medius aided by TFL) as power, load is the lower limb distal to
trochanteric region. Hip is a class – 3 lever! Insufficiency at any level is reflected as a
positive test

What can produce a false positive test?

Painful hip, poor balance, uncooperative patient, costopelvic impingement (as in
scoliosis).

What can produce a false negative test?

Use of suprapelvic muscles by patient, use of psoas and rectus femoris, wide lateral
translocation of trunk to allow balance over the hip as a fulcrum.

What are the prerequisites for doing this test?

There are a lot of limitations that itself are frequently seen in hip pathologies, so it is not a
very good test:
• It should not be a very painful hip (spuriously positive).
• There should be no abduction or adduction deformity in any hip.
• Quadratus lumborum must be normal (affected in polio) – this effects a normal
Trendelenburg test.
• In obese and patients with medial shift of lower limb mechanical axis the test may be
pseudo-positive.
• Sacroilitis may produce a positive test.

29
 What are the causes of a positive Trendelenburg test? Gluteus medius paralysis:
• Polio, L5 radiculopathy, girdle muscular dystrophy, cerebral palsy (and other
disjunctive disorders) etc. Power of 5/5 MRC grade is required for normal response
(“negative test”) any power less than or equal to 4 will produce positive test.

Failure of lever:
• Trochanteric avulsion, fracture neck of femur, coxa vara

Disruption of fulcrum:
• Dislocated hip, DDH or subluxating hips, Perthes disease, SUFE, osteonecrosis.

Gluteal inhibition:
• Painful hip due to arthritis/infection, Sacroilitis.

How do you test for telescopy?

Patient supine on bed. Fix pelvis by left hand (trochanter should be embraced by
fingers). Flex hip to more than 60° (preferably to 90°) and adduct the limb slightly (to put hip
in vulnerable position) then apply a Push-Pull force along the axis of shaft and note first the
translation of trochanter and secondly crepitus from joint. (Remember this is a provocative
test and offensive one to the patient – be gentle!) (Now, whether to push or pull first – don’t
be concerned, result will not change!)

What are the prerequisites for telescopy?

Hip and knee should have flexion range of movement; adduction should be possible at
hip, firm mattress, ideally a painless hip.

What are the causes of a telescoping hip? Causes in hip joint:

• Girdlestone arthroplasty,
• Old unreduced dislocation with lax structures
• DDH
• Pathological dislocation e.g. TB
• Charcot’s joint
• Perthes disease

30
• SCFE
• Squeal of septic arthritis
• Osteonecrosis with collapse
• TB hip: Mortar and pestle type, destroyed head, wandering acetabulum
Causes out of hip joint:
• Non-Union fracture neck femur
• Non-Union fracture intertrochanter.

Interpretation of Bryant’s triangle?

Shortening of base: suggests upriding of greater trochanter

seen in – coxa vara, coxa breva, destruction of head, nonunion fracture neck femur, old
dislocations, girdlestone arthroplasty, Perthes disease.

Shortening of perpendicular only: Suggests internal rotation of femur or central migration

of head – old unreduced posterior dislocation, central fracture dislocation etc.

Shortening of hypotenuse: It is always associated with,shortening of either or both of other

lines (Remember Pythagoras theorem).
Isolated shortenings are rare and a combination is often seen:

Base + perpendicular shortening (definite hypotenuse shortening): Central fracture

dislocation, neck resorption, head resorption, protrusio acetabuli.
Base shortened but perpendicular lengthening: Non-union fracture neck femur, anterior
dislocation of hip, SCFE, girdlestone arthroplasty.

Base shortened + lengthened perpendicular: Malunited fracture neck femur All lines
lengthened: Coxa magna, coxa valga.

What are the fallacies of Bryant’s triangle measurement?

Useless in bilateral affections, if ASIS cannot be palpated, lines are quite arbitrary and
errors are easy to occur.

31
 What are the various sites of referred pain of hip joint?
Various patterns observed are:
a. Obturator pattern: Pain deep in groin radiating to medial thigh.
b. Posterior pattern: Deep in the buttock (most common).
c. Femoral pattern: Pain from front of joint radiating along anterior thigh.
d. Lateral pattern: Over greater trochanter radiates along lateral thigh to knee.
e. Uncommonly pain can also radiate to leg and foot.

What are the criteria for making diagnosis of ankylosing spondylitis Rome criteria
(1963): Ankylosing spondylitis (AS) present if
Bilateral Sacroilitis + any of the below:
• Low back pain with stiffness for > 3 months
• Pain and stiffness in thoracic region
• Limited motion in lumbar region
• Limited chest expansion
• History of iritis or its sequel.New York criteria (1968): The following clinical criteria:
1. Limitation of motion of the lumbar spine in anterior flexion, lateral flexion and
extension
2. History of pain in thoracolumbar junction or in the lumbar spine
3. Limitation of chest expansion to < 2.5 cm (1 inch)
• Definite AS = Grade 3-4 bilateral Sacroilitis + at least one clinical criteria “or” grade
3-4 unilateral or grade 2 bilateral Sacroilitis + clinical criteria ‘1’ or both ‘2’ & ‘3’
• Probable AS = Bilateral Sacroilitis without any clinical criteria.
BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) detects the inflammatory
burden of disease. It can help establish the diagnosis of AS in the presence of other factors
like HLA-B27 positivity, persistent buttock or back pain that resolves with exercise, and X-
ray and MRI involvement of sacroiliac joints. (Apart from HLA-B27, two new genes have
been recently associated with AS – ARTS1 and IL23R)

What are the common conditions affecting hip bilaterally?

• Osteonecrosis of hip (bilateral in 50%)
• Perthes disease (10%)
• Coxa Vara (50%)

32
• SUFE/SCFE (25-30%)
• DDH (30-40%).

What triangles you know in relation to hip joint?

Learn the following:
1. Babcock’s triangle
2. Ward’s triangle: Between primary tensile, primary compressive trabeculae and calcar
portion of neck – relevant in osteoporosis and fixation of hip fractures
3. Fairbank’s triangle: Coxa vara
4. Bryant’s triangle
5. Scarpa’s triangle (femoral triangle)
6. Abductor triangle: formed between gluteus medius, ilium, neck of femur (displays
abductor mechanism).

What is the role of manipulation under anesthesia?

Manipulation under anesthesia is indicated in healing disease with less severe deformities
to:
1. Attempt gaining mobility of hip while on treatment when articular cartilage is
supposedly ‘preserved’
2. Provide a functional position (correcting the deformity) to hip lest it goes in fibrous
ankylosis when cartilage is irreparably damaged and functions cannot be regained.

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NONUNION NECK OF FEMUR- QUESTIONS FREQUENTLY ASKED
What will be your differential diagnosis for non union neck of femur?
I will put forward the following differentials:

1. Old ununited Fracture intertrochanteric right femur

2. Old Fracture head of right femur: Telescopy often absent or minimal
3. Malunited fracture acetabulum posterior wall/superior wall/both: very difficult to
differentiate but often internal rotation deformity is observed as the hip is unstable
and dislocates/subluxates posteriorly – not always true, so it is the closest but rarest
differential to be given in exams
4. Old treated TB hip with bony changes (wandering acetabulum/mortar-pestle type):

All said and done traumatic event with typical follow-up should be absent.

What are the causes of non-union in fracture neck femur?

Non-union here is predominantly due to combination of mechanical (points 1-4 below) and
biological (points 5-10) disruptions:
1. Morphologic features: High fracture angle 60º-90º ( shear angle)
2. Displaced fracture: Garden’s III/IV
3. Fracture comminution – Posterior comminution (affects adequacy of reduction,
angulation and stability of fixation)
4. Inadequate reduction and stability of fixation
5. Poor bone quality (osteoporosis)
6. Injury to vascularity: Direct and tamponade effect (Deyerle): Remember head of
femur is already a ‘hypovolemic bone’ (PET studies) even small disturbances put vascularity
at risk.
7. Absence of cambium layer in periosteum
8. Chondrogenic factors in synovial fluid that inhibit callus formation and consolidation
9. Lack of hematoma formation: Synovial fluid prevent hematoma formation
10. Washing away and dilution of osteogenic factors.
Patient’s age (It only decides treatment!), gender, Osteonecrosis has no influence with
non- union # neckfemur.

How does duration of non-union affect planning?

34
Increased duration of fracture is counterproductive in the following ways:
1. Resorption at fracture ends (Resorption begins as early as 3 weeks)
2. Contractures prevent adequate lengthening and reduction
3. Acetabular cartilage damage

How do you radiographically assess the fracture?

Poor prognostic factors:
1. # angulation
2. Osteopenia
3. Bone loss
4. Osteonecrosis
5. Calcar comminution
6. Varus angulation Lateral projection:
1. Flexion/extension
2. Posterior comminution MRI/Bone scan to look for viability of head

How do you radiographically assess osteoporosis?

Singh index on AP radiographic evaluation of trabeculae:
Grade 6 (normal): All trabeculae present
Grade 5: Loss of trochanteric and secondary tensile, attenuated secondary compressive
Grade 4: Loss of secondary compressive, attenuation of primary tensile
Grade 3 (definite osteopenia): Break in primary tensile
Grade 2: Marked loss of primary tensile
Grade 1: Only primary compressive seen but they are also reduced.

When do you call a fracture neck of femur to be a NonUnion?

3 months following fracture.

What are the various treatment options available?

The followings have been successfully practiced (And should be individualistically
given to the patient!):
1. ORIF with cancellous bone grafting
2. ORIF with fibular grafting
3. ORIF with vascularized bone grafting
a. Free vascularized fibula

35
 b. Muscle pedicle bone grafting
4. Neck reconstruction
5. Osteotomy
6. Arthrodesis
7. Arthroplasty
8. Girdlestone type of resection arthroplasty.

How do you plan surgery?

Clinical assessment:
1. Age of patient
2. Presence of Osteonecrosis
3. Prior hip symptoms: Osteoarthritis etc.
4. Co morbidities: Smoking etc.
5. Duration from injury
6. Fracture variables:
a. Site of fracture
b. Fracture configuration.
How would you classify non-union fracture neck femur?
Sandhu et al (Predictive classification):
• Fracture surfaces
– Irregular
– Smooth
• Size of proximal fragment
– 2.5 cm or more
• Gap b/n fragments
– Upto 1 cm
– More than 1 cm
– More than 2.5 cm
Three groups (decided on a combination of above)
• Group three – worst results.

What are the guidelines?

First look for Osteonecrosis:

36
1. Osteonecrosis + Nonunion:
a. <50 years: Pedicle grafting vs. arthrodesis vs. osteotomy (McMurray’s type)
b. >50 years: Arthroplasty
2. Nonunion + anatomy preserved (NO Osteonecrosis):
a. <65 years: Osteosynthesis
i. ORIF with vascularized grafting
ii.ORIF with fibular grafting
b. >65 years: arthroplasty
3. Non-union with destroyed anatomy (e.g. neck resorption)(NO Osteonecrosis)
a. <65 years: Osteotomy (Pauwel’s type) (in a subset of younger people <40 years –
Neck reconstruction also is a suitable option)
b. >65 years: Arthroplasty (This option has become so favourable that for this situation
nearly all patients >40 years are offered arthroplasty!)

37
 EXAMINATION OF A KNEE CASE

Pain: Onset(inciting event- low energy or high energy or twisting),

duration(insidious or long standing), severity(pain threshold, walking distance),
character (aching degenerative, tumor; throbbing - infection), progression (insidious-
degenerative and mechanical; acute- traumatic andinfection), diurnal variation
(morning- inflammatory; evening – mechanical and degenerative; night- inflammatory
and tuberculosis), activity related (degenerative viz. osteoarthritis), radiation (usually to
calf- degenerative and mechanical), pain after prolonged flexion (patellar disorders) ,
pain at other sites (inflammatory, referred pain from lower back), previous
history/episodes.

Deformity: From when the deformity was observed?

How did it start?
How did it progress and how is it progressing? Any treatment taken?
Any associated symptoms?
Is there any history of trauma or infection?
Varus (rickets, osteoarthritis, post-traumatic, etc), Valgus (rickets, rheumatoid arthritis),
Recurvatum (poliomyelitis, generalized joint laxity), flexion (effusion, infection, sequelae,
scurvy, hemophilia), triple deformity (tuberculosis),

Swelling: When? (Onset and duration),

How? (traumatic or atraumatic - infection, inflammatory, tumor), How long?
Associated symptoms? (Fever, pain, etc).
Previous aspiration “Recurrent” - Straw colored (hydrarthosis-inflammatory, osteoarthritis,
loose body; all due to synovial irritation), pus (pyarthrosis- septic arthritis), blood-colored
(haemarthrosishaemophilia, traumatic), Amber colored (Pigmented villonodular synovitis
(PVNS)). Long-standing painless swelling may be meniscal cysts and benign tumors,
osteochondroma (painless), painful swellings – tumors (malignant) and hematoma in soft
tissues.

38
Laxity: sense of the knee giving way
Since when?, How many episodes?, How much disability it causes?
Specifically enquire about “Going out” of knee – Anterior cruciate ligament (ACL) tear,
Patellar dislocation or subluxation (subluxation usually presents with anterior knee pain).
Symptom of “Giving Way” (knee failing to provide support fully – sort of apprehension ±
pain) especially on walking on uneven surfaces usually indicates “Interposition”(meniscus,
cartilage-free bodies, synovial membrane, etc); “Cartilage damage”; “muscle weakness”
(Polio, neuropathy), “generalized joint laxity”

Locking: [Inability to extend fully : free flexion]

“True Locking” also called meniscal locking is usually due to meniscal tear but may
also be caused by loose bodies– “funny” feeling in joint (joint mice) or ACL stump.
“False locking” (difficulty in flexing knee )also called patellar locking rather “catching” may
also be caused by hypertrophied fat pad.

Limitation of movement or stiffness: Painful (inflammatory, degenerative, traumatic,

tumors), painless “mechanical” (soft tissue- contractures of muscles, tendon, fascia,
postoperative, inadvertent- total knee replacement, arthrodesis; bony – malunited
fractures, tumors, osteophytes). Intraarticular (usually painful, bony, sudden stop- firm end
point, postsurgical); extraarticular (developmental, painless, soft-end point).
Noise from joint: Crepitus, snapping syndromes, “Thud” of discoid meniscus. “clunks” and
“clicks” of menisci.

History of early morning stiffness History of small joint pain and swelling History of cough
with expectoration History of burning micturition
History of altered bowel habits History of watering of eyes Treatment history
Past medical and surgery history

EXAMINATION
General and Systemic Examination: ‘Rickets, hypermobility
syndrome (Down’s syndrome, Larsen, Marfan’s, Ehler-Danlos, haemophilia, rheumatoid,
dysplasia, myopathy)

39
LOCAL EXAMINATION
Prerequisites
1. Examine both knees (limbs) together. Expose from flanks to ankle for examination of
knee joints.
2. Firm couch for supine examination.
3. Examine the patient first in standing position then the gait and lastly in “lying down”
position (may require prone position also for some tests). However, if the patient has
significant pain in standing or walking then postpone it till the end.
4. Keep other (“normal”) joint in same position for comparison, e.g. valgus in a knee with
flexion contracture should be commented only by observing the normal joint in same
degree of flexion (Ideally speaking varus is definitely pathological and can be
commented upon even in a flexion deformity, however, it is less well accepted for valgus
deformity).
5. Be gentle and always explain to the patient what you are going to do and what you
expect. Warn if it is going to be painful and be sorry if it hurts!

Inspection
1. Attitude: “Front and Side”- extension at knee joint and hip joint with foot plantigrade
planted fully and patellae looking forwards.
2. Alignment: Patient looking to horizon and you looking head on (i.e. “front only”) -
knee and medial malleoli barely are touching each other with great toe pointing
forwards. (Always speak of “normal alignment” and not as normal joint as there is
inbuilt varus in recurvatum deformity).
a. Genu valgum
b. Genu Varum
c. Windswept deformity
Now inspect joint from “all around”
1. Swelling: Generalized, localized (tumor, bursitis, meniscal cyst, Baker’s cyst,
Osgood- Schlatter disease, Sinding-LarsenJohanson syndrome, Jumper’s knee- patellar
tendinitis, Hoffa’s disease), thickened synovial band seen as swelling at side (meniscal
tear).
2. Effusion (fullness of peri-patellar fossae)
3. Skin: Neurofibromatosis
4. Scars

40
 5. Sinus
6. Patella and extensor apparatus
a. Bipartite patella (swelling at superolateral aspect)
b. Squinting patella (increased femoral ante-version)
c. Frog-eye patella (patella facing out – femoral condyle hypoplasia, subluxed
patella, increased Q angle, etc)
d. Patella magna (osteophytes) and breva (hypoplasia)
7. Wasting especially of vastus medialis.

Gait:
Examine from anterior and posterior perspectives:
1. Valgus thrust gait (single joint- osteoarthritis, malunited tibial plateau #)
2. Valgus thrust with circumduction (both joints affected)
3. Varus thrust gait (osteoarthritis, malunited tibial plateau #, lateral lig. complex
injury.
4. Varus recurvatum thrust (postero-lateral laxity)
5. Duck-footed (Slew-footed) gait (increased femoral anteversion) Lateral
perspective:
1. Antalgic gait
2. Stiff knee gait
3. Flexed knee gait

Examination in sitting position:

1. Patella Alta and Baja
2. J-sign (bony or soft tissue pathology at trochlea – trochlear dysplasia, internal
femoral torsion, tense lateral retinaculum)
3. Dynamic patellar tracking (N- straight line) and patellar tilt. Examination in
supine position: Confirm above findings report any change in findings as
correction of version and deformity (correction denotes intra-articular deformity).
Special attention to effusion and flexion deformity should be given as small
amount may be hidden in standing.

41
Palpation
Basic points while palpating
- look for warmth
- Palpation to rule out synovial thickening
- Palpation of joint lines
- Palpation of bony structures making the knee joint
- Palpation of soft tissue surrounding the knee, attachment sites of tendons and
ligaments

Anterior aspect:
Temperature and Effusion
Fullness or obliteration of parapatellar and suprapatellar recess
- Fluid shift (visible fluid wave  15 ml) – mild effusion.
- Palpable fluid wave (cross fluctuation  30 ml) moderate effusion.
- Ballotable patella sign (patellar tap test) - gross effusion.
- Trans-illumination
- Palpate synovium (from above below feel for thickened bands/doughy thickenings
which “rolls” under the finger) #Patella and extensor apparatus:
- Patellar facet tenderness (push patella medially–feel undersurface)
- Patellar/Quadriceps tendinitis (Jumper’s knee)
- Apical patellar tenderness and bipartite patella (Base)
- Patellar glide/ Slide (<1 cm each side, Sage sign) and tracking
- Patellar lift (“push and lift”, N= none on lateral side, minimal over medial aspect
<10°)
- Patellar grind test (push patella over femur with palm and flex the joint)
- Fairbank’s apprehension test (Glide patella laterally – flex the joint – +ve at around
30°)
- Tibial tubercle

Medial aspect:
# Joint line tenderness (90o flexion: typically elicited medially; laterally obscured by
iliotibial band (ITB))
# Pes Anserinus and bursa, meniscal cysts

42
 # Medial collateral ligament (MCL) - both femoral and tibial ends

Lateral aspect:
# Lateral collateral ligament (LCL), meniscal cysts # Iliotibial band and Gerdy’s
tubercle
# Ober’s test (lateral decubitus position; knee flexion to 90 degrees, hip abduction to
40 degrees, maximum hip extension as permitted -gentle hip adduction is allowed; tests
ITB contracture – inability to adduct hip)
# Allis test (Galleazi sign) – differentiate femoral and tibial shortening

Posterior aspect (prone):

# Confirm and measure flexion deformity
# Baker’s cyst (most prominent in extension) and other swellings (aneurysm,
lymphadenopathy, etc.)
# Craig’s test (Ryder method)

Manipulation and Special Test

Tests for menisci:
1. McMurray’s test (MM – fully flexed knee; external rotation at hind foot + varus stress
extend knee; LM – internal rotation + valgus; patient feels pain and examiner feels
click (uncommon): pain in initial, middle and late extension “suggests” involvement of
posterior, middle portion and anterior horn)
2. Apley’s distraction-compression test – prone patient; stabilize thigh with your knee 
pull leg up in 90o flexion  rotate foot internally and externally: painful  abandon
test: no pain  perform in compression; medial joint line pain- MM tear and vice
versa)
3. Cabot’s maneuver – figure of “4” produces lateral joint line pain
4. Childress’ test – in deep squat walk patient feels respective joint line pain in fully
flexed knee in meniscal tear; retropatellar pain suggests patellofemoral arthritis
5. Passive extension test (Bounce home test) – respective joint line tenderness during
forced extension of knee after maximal active knee extension.

43
 Tests for stability:
• Valgus and Varus laxity
1. Valgus and Varus stress test
a. In extension – damage to MCL and postero-medial capsule (valgus stress); LCL and
posterolateral ligament complex (varus stress)
b. In 20o flexion – more specific for MCL/LCL
2. Cabot’s position
3. Henri Dejour “frog position” – simultaneous evaluation of both knees’ lateral structures.

• Anterior laxity(Tests for ACL)

1. Lachman’s test and Trillat modification
Lachman’s 20-30deg knee flexion , hold femur with left hand,Right hand holds tibia (thumb
on tibial tuberosity- Trillat) Watch end point and anterior translation(Gerdy’s tubercle/medial
condyle

Interpretation- Soft end point

2. Anterior drawer test in neutral, internal and external rotation
3. Pivot shift test of McIntosh and Galway
a. Trace pivot shift “pivot glide” of Henri Dejour
b. Dejour’s test (pivot shift in extension)
c. Hughston’s jerk test
d. Losse test
e. Flexion-Rotation Drawer test

• Posterior laxity(Test fo PCL)

1. Godfrey’s sign – posterior tibial sag in 90/90 position
2. Muller’s test
3. Posterior drawer test and drop-back phenomenon
4. Quadriceps activation test of Daniel

44
• Posterolateral instability:
1. External rotation recurvatum test (varus recurvatum test)
2. External rotation test
3. Reverse pivot shift test
• Anterolateral rotatory instability (ALRI)
1. Slocum’s test

Measurements
• Linear measurements
1. Apparent length
2. True length
3. Femoral and tibial length
4. Inter-malleolar (Genu valgum) and distance between two knees (Genu varum)

• Circumferential measurements
1. Quadriceps wasting (15 cms from knee joint line; > 2 cms is significant)
• Angular measurements
1. Varus and valgus at knee
2. Q angle
3. Tuber sulcus angle
• Torsional measurements
1. Tibial torsion
2. Femoral anteversion
Neurological and vascular status (At least offer to examine)
1. Palpate lower limb pulses (compare)
2. Sensory and motor distribution of tibial, common peroneal and femoral nerves
3. Reflexes (knee, ankle, tibialis posterior)

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TESTS in Detail
STABILITY TESTS: VALGUS AND VARUS LAXITY
The first two stability tests are the valgus and varus stress tests.
In the valgus stress test, a force directed at the midline is applied at the knee while an
opposing force directed away from the midline is applied at the foot or ankle.

The varus stress test is exactly the opposite: a force directed away from the midline is
applied at the knee while an opposing force directed toward the midline is
applied at the foot or ankle.
Valgus Stress Test. The valgus stress test assesses the integrity of the MCL complex. The
superficial MCL is the primary restraint to valgus stress at the knee. The deep fibers of the
MCI. (meniscofemoral ligament and meniscotibial ligament) act as secondary restraints to
valgus stress. The posteromedial capsule is an important restraint to valgus stress when the
knee is in full extension; when the knee is in flexion, the posteromedial capsule is relaxed and
therefore ineffective in resisting valgus stress.

Finally, the cruciate ligaments come into play as tertiary restraints against extreme
valgus stress once the medial structures have failed.

To perform the valgus stress test, have the patient lie supine and relaxed on a flat
examining table. The examiner raises the patient's lower limb off the examining table by
grasping it gently at the ankle with the patient's muscles fully relaxed, If the patient finds
relaxation difficult, the test may be performed without raising the limb by abducting it until
the knee is at the edge of the table so that the patient's thigh is still supported by the table, the
examiner applies a gentle inward force at the knee and a reciprocating outward force at the
ankle. The force is then relaxed. The examiner both looks and feels for a separation of the
femur and the tibia on the medial side of the knee in response to the valgus stress.
In the normal knee, virtually no separation of the medial tibia and femur is felt when the knee
is in full extension.

In the abnormal case, the femur and the tibia are felt to separate when the valgus
stress is applied and to clunk back together when the stress is relaxed. The same test should
be conducted on the opposite, presumably normal, knee for comparison.

46
 Increased laxity on valgus stress with the knee in full extension signifies damage not
only to the superficial and the deep MCL fibers but also to the posteromedial capsule.
In such a knee, the incidence of concomitant injury to one or both cruciate ligaments is
extremely high. If valgus stability in full extension is normal, the examiner then flexes the
patient's knee about 10° or 15° and repeats the test. Flexing the knee relaxes the
posteromedial capsule and concentrates the force on the MCL. (If the examiner flexes the
knee too much, the limb tends to internally rotate at the hip when a valgus force is applied.)
Again, the examiner looks and feels for abnormal separation of the medial tibia and the femur
in response to the valgus stress and the feeling of the two bones clunking back together when
the stress is relaxed. The combination of normal valgus stability when the knee is fully
extended and abnormally increased valgus laxity when the knee is flexed suggests more
isolated damage to the MCL with an intact posteromedial capsule.

Grading Abnormal Laxity. MCL injuries are often divided into three grades according to
the physical findings. The most widely accepted grading system is based on the general
anatomic classification of ligament injuries, in which grade I signifies injury without any
elongation of the ligament, grade II signifies a ligament that is elongated but not
completely disrupted, and grade III signifies a ligament that has lost all structural
integrity. In this system, a grade I injury is one in which the MCL is tender and swollen but
exhibits no increased laxity. In grade II injuries, there is the additional finding of increased
laxity to the valgus stress test but with a firm endpoint. This means that the medial joint
separates more than in the other knee when a valgus stress is applied, but a firm resistance is
eventually felt when the injured ligament pulls taut. In grade III injuries, there is increased
valgus laxity with an indefinite endpoint. In other words, the examiner feels no resistance no
matter how far the medial joint surfaces are separated. Although this is the most widely accepted
system of classification, it does have some problems. The distinction between grade
II and grade III injuries is somewhat arbitrary. Identical injuries may be classified as either
grade II or grade III depending on whether or not the patient is able to relax enough to allow
the examiner to feel an endpoint.

The alternative system of classification, proposed years ago by Fetto and Marshall,
distinguishes between grade II and grade III injuries depending on whether or not there is
increased valgus laxity in full extension, instead of on the endpoint. In this classification,
grade II injuries include all those in which there is increased valgus laxity in flexion but

47
normal valgus laxity in full extension. In grade III injuries, there is increased valgus laxity in
both flexion and extension. Not only is the distinction between grade II and grade III injuries
easier to make with this classification but also it carries greater prognostic significance. As
noted earlier, increased valgus laxity in full extension implies not only damage to the MCL
but also concomitant injury to the posteromedial capsule and usually one or both of the
cruciate ligaments.

Varus Stress Test. The varus stress test is the counterpart of the valgus stress test for
detecting injury to the LCL complex. Again, the patient lies supine and fully relaxed. The
examiner raises the patient's lower limb off the examining table by grasping it at the ankle.
As in the valgus stress test, the knee is first tested in full extension and then in about 10° or
15° of flexion. This time, the examiner applies an outward force at the knee and a
reciprocating inward force at the ankle. Again, the examiner both looks and feels for
abnormal separation of the femur and the tibia, this time on the lateral side of the knee, in
response to the varus stress. In the normal knee, virtually no separation of the lateral tibia and
the femur are felt when the knee is in full extension.

When the lateral ligamentous structures are torn, the femur and the tibia are felt to
separate abnormally when the stress is applied and to clunk back together when the stress is
relaxed.
The major difference between the varus and the valgus stress tests is that most patients have
more natural laxity of the lateral ligaments than the medial ligaments.

This natural laxity is evident when the varus stress test is repeated with the knee in
flexion when,,the varus stress is applied, a definite separation is felt, and when the stress is
relaxed, the femur and the tibia clunk back together. This separation is probably about 3 mm
to 5 mm in the average normal knee. Thus, it is extremely important to compare the two
limbs to verify that the varus laxity felt is increased compared with the other side and not just
a consequence of the patient's physiologic varus laxity. As in the valgus stress test, increased
varus laxity in full extension implies more extensive injury, usually involving the
posterolateral ligament complex and one or both cruciate ligaments.

48
ANTERIOR LAXITY
This is conventionally defined as the ability to translate the tibia anteriorly an
abnormal amount in relation to the femur. It has been shown that increased anterior laxity is a
sign of injury to the anterior cruciate ligament (ACL), although concomitant injury to other
ligaments can increase the magnitude of the abnormal anterior translation. The two most
basic tests for abnormal anterior knee laxity are the anterior drawer and the Lachman tests.

Anterior Drawer Test.

In the anterior drawer test, the patient lies supine with the involved knee bent to a
90° angle. The examiner sits at the end of the examination table with his or her thigh against
the patient's toes to restrain the foot. The examiner then grasps the tibia just below the joint
line and asks the patient to relax. If the patient is properly relaxed, the lower limb should feel
as if it would fall over to the side if the examiner released it. The examiner then pulls forward
with both hands and assesses both the amount of anterior translation of the tibia with respect
to the femur and the quality of the endpoint.

In most patients, the tibia can be felt to move forward at least a few millimeters and
then stop suddenly with a hard endpoint. As in the other stability tests, comparison to the
other side is important. In the case of ACL injury, the tibia is felt to translate forward more
than on the uninvolved side, and the endpoint feels soft Although the anterior drawer test is
the most well known test for abnormal anterior knee laxity, it has some problems and
limitations. First, many patients have considerable normal laxity in the 90° flexed position,
making it more difficult to distinguish between abnormal and normal. Second, it may be
difficult for the patient to flex the knee to 90° if the knee is acutely injured and painful.
Finally, when the knee is flexed 90°, the hamstrings are in an excellent position to mask
abnormal anterior translation in the patient who is unable to relax fully.

Lachman's Test.
For these reasons, the Lachman test has surpassed the anterior drawer test as a basic
screening examination for abnormal anterior knee laxity. This test was first described by Torg
and attributed to his mentor, Lachman. The Lachman test is similar in concept to the anterior
drawer test but is performed with the knee in 20deg to 30° of flexion.

49
 The patient lies supine on the examination table. The examiner stands at the side of
the table near the knee and grasps the lower leg with one hand. Usually, the examiner's
thumb is placed just over the tibial tubercle and the other fingers are wrapped around the rest
of the calf. The other hand is used to grasp the thigh just above the patella. The thumb of this
upper hand presses against the femur through the quadriceps tendon while the other fingers
wrap around the posterior thigh. If the patient is properly relaxed, the limb should feel like a
dead weight. The fingers of the examiner's upper hand, which are supporting the thigh, are
also able to sense any tightening in the hamstrings. If any of the hamstrings are felt to be
tight, identifying the tight muscle to the patient and massaging it a bit often allows the patient
to relax. As with the valgus stress test, better relaxation may sometimes be obtained by
abducting the lower limb and allowing the thigh to rest on the examination table .
In this case, the knee is flexed over the side of the table and the foot rests on the lap of the
seated examiner. Once the patient is adequately relaxed, the examiner pulls forward on the
tibia with one hand while simultaneously pushing backward on the femur with the other hand
in a reciprocating manner. As in the anterior drawer test, the amount of anterior excursion
and the quality of the endpoint are assessed.

One of the differences that makes the Lachman test easier to assess than the anterior
drawer test is that in most normal patients, there is little or no excursion of the tibia when the
Lachman test is performed. Either no translation at all or 1 mm to 2 mm of translation with a
very firm endpoint is appreciated. In the presence of ACL tear, the translation is increased
and the endpoint indefinite. Often, this increased translation can be visibly appreciated by
focusing on the forward movement of the tibia at the tubercle of Gerdy or over the medial
tibial plateau. In subtly abnormal cases, the examiner may not be sure that increased
excursion is present, but he or she may sense a soft end point that differs from the uninjured
knee.
A special case is the incomplete ACL injury, in which the ACL is elongated but not
totally disrupted. In these cases, increased anterior laxity is present but a firm endpoint is still
noted. This endpoint is usually easier to appreciate after the swelling and stiffness of the
acute injury have subsided.
Theoretically, the Lachman test is more specific for injury to the posterior portion of the
ACL, and the anterior drawer test is more specific for injury to the anterior fibers.
This distinction would only be important, however, in the relatively unusual case in which
some of the ACL fibers are torn but the others are relatively intact.

50
PIVOT SHIFT PHENOMENON

The pivot shift test and its variations are dynamic tests that demonstrate the
subluxation that can occur when the ACL is nonfunctional. Thus, they are indirect tests of
ACL injury. An abnormal result usually indicates complete rupture of the ACL but may also
be present when the ligament is excessively elongated but still in continuity. In addition,
some patients with greater than average anterior knee laxity may demonstrate a mild
physiologic pivot shift in the absence of any knee injury. Many patients whose knees
hyperextend can be expected to demonstrate this physiologic pivot shift. In laboratory
studies, sectioning the ACL has been shown to be sufficient to produce a positive pivot shift,
although sectioning the lateral ligament complex usually increases the magnitude of the pivot
shift.

Classic Pivot Shift Test. The classic pivot shift test was described by Galway and Mcintosh.
With the patient supine and relaxed, the examiner lifts the lower limb off the table by the foot
and internally rotates it (Although the classic description of the pivot shift
test is performed with internal rotation of the lower limb, some researchers recommend a
neutral or even externally rotated position.)
If the patient is properly relaxed, the limb feels like a dead weight and the knee naturally falls
into full extension. This may be a straight position or hyperextension, depending on what is
normal for that particular patient.

If the knee does not fall into full extension, whether due to pain, swelling, or a
displaced meniscus tear, the pivotshift test may not be accurate.
In a patient with a nonfunctional ACL, gravity causes the femur to fall posteriorly when the
limb is held in this manner, resulting in an anterior subluxation of the tibia with respect to the
femur. The examiner then places the palm of the other hand on the lateral aspect of the
proximal leg, just below the knee, and gently applies a force that results in valgus stress as
well as flexes the knee . Somewhere between 20° and 30°, the anteriorly subluxed tibia
spontaneously reduces into its normal position with respect to the femur, due to the pull of the
iliotibial band (pivot) which shifts posterior to the knee joint resulting in a sudden visible
jump or shift. The best place to watch for this jump is at the tubercle of Gerdy. In most
normal individuals, the knee bends smoothly with no such shift. As mentioned, some loose-
jointed individuals exhibit a mild pivot shift in their uninjured knees. Because the pivot shift

51
is a dynamic phenomenon, it is difficult to grade. Some clinicians distinguish a trace pivot
shift or pivot glide in which the tibia can be seen to move smoothly into a reduced position as
the knee flexes, without the sudden jump of the frank pivot shift. In most patients with a
physiologic pivot shift, such a pivot glide is present. At the severe end of the spectrum, the
tibia subluxes so far anteriorly when the knee is extended that a spontaneous reduction does
not occur as the knee flexes. In these cases, the knee appears to be stuck between 20° and 30°
of flexion and docs not flex past the sticking point until the examiner manually pushes the
tibia posteriorly into a reduced position.

Jerk Test. Several variants of the pivot shift test have been described. In the jerk test,
described by Hughston, the procedure is the reverse of the pivot shift test: the examiner
begins with the patient's knee flexed and the tibia reduced and watches the tibia sublux as the
knee is passively extended.

Flexion-Rotation Drawer Test. The flexion-rotation drawer test is a gentler version of the
pivot shift test that has become quite popular. In the flexion-rotation drawer test, the
examiner grasps the patient's leg at the ankle with both hands. The internal rotation, valgus,

and flexion forces are applied indirectly at the ankle . This usually produces a less violent
reduction than the classic pivot shift and is less threatening to the patient with significant
abnormal anterior laxity. A good method is to begin with the flexion-rotation drawer test and
to proceed to the classic pivot shift technique if the results of the flexion-rotation drawer are
equivocal.

POSTERIOR LAXITY
Rupture of the posterior cruciate ligament (PCL) is necessary for a detectable increase
in straight posterior laxity, although damage to the posterolateral structures further increases
the magnitude of the abnormal posterior laxity.

Laboratory research has shown that sectioning the PCL produces the greatest increase
in posterior laxity when the knee is flexed between 70° and 90°. Therefore, the most sensitive
way to test for PCL injury is with the knee flexed between 70° and 90°.

52
Posterior Drawer Test.
The most basic test for PCL injury is the posterior drawer test. The starting position is
essentially the same as that for the anterior drawer test; the patient's knee is flexed 90° and
the foot stabilized. In a patient with a torn PCL, a dropback phenomenon usually occurs in
this position: gravity causes the tibia to sublux posteriorly with respect to the femur, resulting
in an abnormal appearance that is best appreciated when both knees are viewed in profile.
When such a dropback phenomenon occurs, the tibial tubercle appears less prominent and
sagged(Godfrey’s sign) than usual, and the patella appears more prominent than usual. Subtle
changes may often be detected by comparing the injured with the normal knee. In the acute
injury situation, the dropback is less likely to occur or may be masked by acute swelling. The
posterior drawer test is completed by pushing posteriorly on the proximal tibia with both
hands . In the abnormal case, the tibia is felt or seen to sublux further posteriorly with respect
to the femur. If considerable dropback has already occurred, the application of a posterior
force may not sublux the tibia much further. Unlike the anterior drawer test, a fairly firm
endpoint is usually felt once the abnormal posterior laxity has been taken up, even in the case
of complete PCL rupture.

Godfrey's Test.
The Godfrey test is another way of looking for the dropback phenomenon. In
Godfrey's test, the examiner or an assistant holds the patient's legs in the 90/90 position with
both the knees and the hips flexed to 90°. Again, in this position gravity causes the tibia to
sublux posteriorly in a knee with an injured PCL.

Grading Posterior Laxity. The results of the posterior drawer and dropback tests are usually
graded by the relationship of the proximal tibia to the distal end of the femoral condyles.
Normally, the anterior cortex of the proximal tibia sits about 10 mm anterior to the distal end
of the femoral condyles when the knee is flexed about 90°.

Every 5 mm of posterior dropback or posterior drawer is considered a grade of

abnormal laxity. Thus, in a grade 1 posterior drawer, the normal 10 mm of prominence of
the anterior tibia with respect to the femoral condyles is reduced to 5 mm. In a grade 2
posterior drawer or dropback, the proximal tibial cortex is flush with the femoral condyles. In
the grade 3 or grade 4 posterior drawer or dropback, the anterior tibial cortex is respectively
displaced 5 mm or 10 mm posterior to the femoral condyles.

53
Quadriceps Active Drawer Test.
The quadriceps active drawer test, described by Daniel and colleagues, is very
helpful for confirming the presence of posterior subluxation when the dropback is equivocal.
With the patient's knee flexed 90°, the examiner elicits an isometric contraction of the
patient's quadriceps by asking the patient to attempt to slide the ipsilateral foot distally while
the examiner secures it in place and resists such movement .(It is important to confirm, either
visually or by palpation, that such a quadriceps contraction actually occurs.) The examiner
focuses his or her attention on the proximal tibia. In the normal case, the relationship between
the proximal tibia and the distal femur remains constant as the quadriceps contracts. In the
abnormal case, the posteriorly subluxed tibia is seen to shift anteriorly into a reduced position
as the quadriceps contracts. Comparison with the other knee helps to detect subtly abnormal
cases. Occasionally, a small physiologic movement may be observed, but this should be
symmetric with the uninjured knee.

Dynamic Posterior Shift Test. The dynamic posterior shift test is an adjunctive test that
may be abnormal in the presence of abnormal posterior or combined posterior and
posterolateral laxity. In this test, the examiner passively raises the patient's thigh until the hip
is flexed 90°.

The patient's foot is supported with the examiner's other hand so that the knee is
flexed 90° as well. In this position, the hip flexion tightens the patient's hamstrings and thus
may sublux the tibia posteriorly . The examiner then passively extends the patient's knee
while keeping the hip flexed 90°. Although such extension further tightens the hamstrings,
the passive extension causes the subluxed tibia to reduce, sometimes with a sudden noticeable
shift.

POSTEROLATERAL LAXITY
In recent years, further attention has been directed at tests for abnormal
posterolateral laxity. Such laxity reflects injury to the LCL, popliteus tendon, and associated
structures of the posterolateral ligament complex such as the popliteoflbular and
fabellofibular ligaments. Abnormal posterolateral laxity is occasionally present as an isolated
finding, but it is much more commonly found in association with abnormal posterior or
anterior laxity.

54
 When abnormal posterolateral laxity is present, the tibia rotates externally an
abnormal amount with respect to the femur, and the lateral tibial plateau subluxes posteriorly
with respect to the lateral femoral condyle. This can be observed most directly by flexing
the patient's knee to 90° and observing the relationship of the tubercle of Gerdy and fibular
head to the lateral femoral epicondyle as the tibia is rotated externally. Patients with
physiologically lax knees demonstrate considerable external rotation with this aneuver;
therefore, comparison with the contralateral side is important. In such a patient,
distinguishing the increased posterolateral rotation compared with the lax normal side may be
difficult.

Dial Test (External Rotation Test). Another technique for demonstrating increased
posterolateral laxity is to use the position of the foot as an indirect indicator of the amount of
external rotation of the tibia present. In this technique, which may be called the external rotation
test, the supine patient is asked to flex the knees while keeping the knees and ankles together. The
examiner then passively externally rotates the feet and compares the amount of external rotation of the
involved limb with the normal one. Classically, this test is performed with the knees flexed 30° and
again with the knees flexed 90°. In the rare case of isolated posterolateral laxity, increased external
rotation is noted at 30° but not at 90°. Whencombined posterior and posterolateral laxity are present,
increased external rotation is noted in both positions.
30° - PLC alone
30° and 90° - PLC + PCL

Varus Recurvatum Test. Other tests for abnormal posterolateral laxity include the varus
recurvatum test, the posterolateral drawer sign, and the reverse pivot shift test.

In the varus recurvatum test, first described by Hughston and Norwood, the patient lies
supine and relaxed with the legs extended. The examiner grasps one of the patient's great toes
in each hand and lifts them straight up about a foot off the examination table. In the abnormal
case, the knee falls into recurvatum (hyperextension) and varus compared with the uninjured
contralateral knee. This requires a complex injury involving the PCL, the posterolateral
ligament complex, and the LCL. The patient with a positive varus recurvatum test usually
exhibits a varus recurvatum gait and is significantly disabled.

55
Posterolateral Drawer Sign. Hughston and Norwood also described the posterolateral
drawer sign. This is elicited by performing the posterior drawer test with the patient's foot in
external rotation, neutral position, and internal rotation. An increase of the magnitude of the
posterior drawer in external rotation suggests abnormal posterolateral laxity.

Reverse Pivot Shift Test. The reverse pivot shift test, described by Jakob, begins with the
patient in the same supine, relaxed position. To test the right knee, the examiner faces the
patient and rests the patient's right foot on the right side of the examiner's pelvis with the foot
in external rotation. The palm of the examiner's left hand supports the lateral side of the calf
at the level of the proximal fibula. The examiner then bends the knee to 70° or 80°. In
patients with posterolateral rotatory instability, external rotation in this position causes the
lateral tibial plateau to sublux posteriorly in relation to the lateral femoral condyle. This is
perceived as a posterior sag of the proximal tibia. The examiner now allows the knee to
extend, leaning slightly against the foot to transmit an axial and valgus load to the knee. As
the knee approaches 20° of flexion, the lateral tibial plateau reduces from its posterior
subluxed position and a jerk-like shift is appreciated.

The test can also be done in the opposite direction. If the test is begun with the tibia in
the reduced position of full extension and neutral rotation, rapid flexion produces the jerk-like
phenomenon as the tibia subluxes with external rotation posteriorly in relation to the lateral
femoral condyle.

PATELLOFEMORAL JOINT
Besides the observations of patellar malalignment and facet tenderness already
described, the specific patellofemoral joint examination includes tests for patellofemoral
crepitus and instability.

56
Passive Patellar Grind Test.
The passive patellar grind test is probably the most well known test for
patellofemoral crepitus. With the patient supine and relaxed, the examiner presses the patella
against the femur with the palm of one hand while passively flexing the knee with the other.
When degeneration or traumatic irregularity of the articular surface of the patella or the
femoral trochlea is present, the examiner feels a distinctive crunching sensation transmitted
through the patella. Pressure should be light. This test can be uncomfortable even in the
normal knee, and it is very painful in the abnormal one. Because of this, the active patellar
grind test is recommended for routine use. In this variation, the patient sits with the knee
flexed over the end or side of the examination table.

The examiner gently places a hand on the patients patella, asks the patient to actively
extend the knee, and again feels for crepitus. In this case, the patient's own quadriceps
contraction provides the compressive force and the patient can voluntarily stop the process if
it is too painful. The degree of flexion in which the crepitus is felt may also be a clue to the
area of articular cartilage damage. Because the contact pattern of the patellofemoral joint
varies with the position of the knee, crepitus that occurs near extension tends to be associated
with lesions of the inferior portion of the patella or the superior femoral trochlea, whereas
crepitus that occurs deeper into flexion usually represents injury to the superior patella or
inferior trochlea.

Step-Up-Step-Down Test.
The most sensitive test for patellofemoral crepitus is the step-up-step-down test. In
this test, the examiner asks the patient to step up onto a low stool as if climbing a stair, then
to step back down again . Again, the examiner lightly feels for crepitus during the process.
This procedure loads the patellofemoral joint with a multiple of the patient's body weight and
brings out crepitus not detected by the active patellar compression test. In more severe cases
of articular cartilage damage, this crepitus is audible. While performing any of these tests for
patellofemoral crepitus, the examiner should keep in mind that normal or hypertrophied
synovial folds or fronds may produce a much softer popping sensation, which needs to be
distinguished from true cartilaginous crepitus.
Dynamic Patellar Tracking. The next group of patellofemoral tests is for patellar
mobility and functional instability. To assess dynamic patellar tracking, the examiner asks

57
the seated patient to actively extend the knee from 90° to full extension while observing the
movement pattern of the patella from the front. Lightly placing the thumb and the index
finger of one hand on either side of the patella may help the examiner follow the tracking
pattern. In most individuals, the patella appears to move straight proximally, then it often
shifts and tilts a bit laterally near terminal extension. When this lateral shift and tilt are more
marked, the patient is at risk for symptomatic patellar instability. In the unusually extreme
case, termed habitual patellar dislocation, the patella dislocates off the lateral edge of the
femoral trochlea with every active extension.

Patellar Glide Test. The patellar glide test measures passive patellar mobility. In this
test, the patient lies supine with the knees extended and the quadriceps relaxed. (Some
authors recommend that the knees be slightly flexed.) The examiner pushes the patella first
medially, then laterally, each time estimating the excursion of the patella with respect to the
distal femur.This excursion may be estimated in absolute terms (centimeters) or relative
terms (quadrants of the patient's patella). Although the absolute amount of excursion varies
widely, the average is about 1 cm in each direction. In excessive lateral pressure syndrome,
lateral glide is extremely limited. However, not all individuals with diminished lateral glide
have excessive lateral pressure syndrome. Conversely, increased excursion to the lateral glide
test identifies a patient who is at risk for patellar instability but is not sufficient to establish a
diagnosis of patellar instability.

Patellar Apprehension Test.

A test that is more suggestive of clinically symptomatic patellar instability (recurrent
subluxation or dislocation) is the patellar apprehension test, sometimes called the Fairbanks
apprehension test. This test is designed to simulate an episode of patellar instability under
controlled circumstances. With the patient supine and relaxed, the examiner grasps the
symptomatic limb at the ankle and abducts it sufficiently to allow the knee to be flexed over
the side of the table. With the thumb or fingers of the other hand, the examiner performs a
lateral patellar glide, pushing the patient's patella as far laterally as possible. The examiner
then slowly flexes the patient's knee with the other hand. In the patient with a history of
patellar subluxation or dislocation, this maneuver usually creates an apprehension that
another episode of instability is imminent. This apprehension manifests itself with behavior
ranging from verbal expressions of anxiety to an involuntary quadriceps contraction that
prevents further knee flexion. The test is conducted slowly enough so that it can be

58
terminated once the anticipated response is elicited but before causing the patient undue
discomfort.

MENISCAL TESTS
A number of manipulative tests have been developed over the years to diagnose tears
of the menisci. They are variable in their sensitivity and should be thought of as adjuncts to
the finding of joint line tenderness. They are all based on two facts: (1) most meniscal tears
occur in the posterior third of the menisci and (2) as the knee flexes, the femur rolls
posteriorly on the tibial plateau, increasing the contact between the femoral condyles and the
posterior portions of the menisci. All these tests place the knee in a flexed or hyperflexed
position and then compress it, resulting in pain and sometimes clicking localized to the
symptomatic meniscus.

Childress' Test.
In the Childress test, the patient is asked to duck walk, that is, to walk in a deep squat.
As the patient lifts the uninvolved limb to step forward, all the body weight momentarily
compresses the symptomatic knee. If a meniscus tear is present, this maneuver usually causes
pain localized to the joint line of the involved meniscus. This localization is important
because other conditions can produce pain with the Childress test. For example,
patellofemoral pain usually is induced or aggravated by the duck walk, but the patient
localizes the pain to the retropatellar region. When an effusion is present in the knee,
whatever the cause, the patient usually feels pain or discomfort in the popliteal fossa during
the duck walk.

McMurray's Test.
For the McMurray test, the supine patient is asked to flex the involved knee as far as
possible. To test the medial meniscus, the examiner grasps the patient's hindfoot and
externally rotates the foot while placing a varus stress at the knee to compress the medial
meniscus. The knee is then passively extended while the examiner palpates the medial joint
line with the index finger of the other hand.

In McMurray's original description, the test is positive if the patient complains of pain
localized to the medial joint line and the examiner feels a click in this location. In our
experience, the true McMurray click is only occasionally felt, although joint line pain is

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commonly elicited in the absence of such a click and often indicates a meniscus tear. The
pain of osteoarthritis can sometimes also be elicited by the McMurray test.
To test for a lateral meniscus tear, the examiner applies an internal rotation-valgus force to
the hyperflexed knee. In the presence of a lateral meniscus tear, the patient reports pain
localized to the lateral joint line as the knee is passively extended. A click is only rarely felt
with the lateral McMurray test.

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%).

Apley's Test. The Apley test for posterior meniscus tears has two parts. In both
portions, the patient is asked to be prone and to flex the knee to 90°. The examiner then
grasps the foot and asks the patient to relax. For the control or distraction portion of the test,
the examiner stabilizes the patient's thigh using downward pressure from the examiners own
knee while pulling the patient's foot upward to distract the patients knee. The examiner then
alternately externally and internally rotates the patient's foot. The patient should not have pain
with the distraction portion of the test, if pain is experienced during distraction, the test is not
considered reliable (although the patient may still have a meniscus tear) and is abandoned.
If the distraction test causes no pain, the examiner proceeds to the compression test, pushing
downward on the patient's foot to compress the knee while alternately externally and
internally rotating the foot. During the compression test, pain localized to the medial joint
line (usually produced by external rotation) suggests a medial meniscus tear, whereas pain
localized to the lateral joint line (usually produced by internal rotation) suggests a lateral
meniscus tear.

Passive Extension Test.

The final manipulative meniscus test is designed specifically to detect displaced bucket
handle tears, which occur primarily on the medial side. As already mentioned, this condition
should be suspected when the patient is unable to extend the involved knee and tenderness is

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localized to the junction of the medial femoral condyle and medial tibial plateau. In the
passive extension test, sometimes known as the bounce home test, the examiner asks the
patient to actively extend the knee as far as possible. The examiner then gently and slowly
extends the knee a bit further.
In the presence of a displaced bucket handle tear of the medial meniscus, the patient
usually indicates a sharp pain at the junction of the medial femoral condyle and the medial
tibial plateau.

A displaced bucket handle tear of the lateral meniscus will also cause pain when this
test is performed, but the pain is not usually as well localized as with medial meniscus tears.
If a torn ACL stump is preventing extension, the patient usually describes the pain as central
and deep. In the presence of less specific causes of flexion contracture such as effusion and
hamstring spasm, pain may also be produced by this maneuver, but it will not be localized.

Thessaly Test
Patient standson 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%)

OSTEOCHONDRITIS DISSECANS
Wilson test was described as a physical sign of osteochondritis dissecans. It is not
frequently used and has been shown to have a low rate of sensitivity. For the test, the supine
patient is asked to flex the knee. The examiner then passively internally rotates the foot (Fig.
6-73A) and then extends the knee completely. This maneuver is meant to impinge the ACL
against the classic osteochondritis dissecans lesion located adjacent to the intercondylar notch
on the lateral aspect of the medial femoral condyle. In an abnormal test, the patient
experiences pain when the internally rotated knee reaches full extension, and the pain should
subside when the internal rotation force is relaxed

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PHYSICAL FINDINGS IN COMMON CONDITIONS OF THE KNEE
Osteoarthritis
Tibiofemoral joint line tenderness (medial more common than lateral) Patello femoral joint
tenderness (if involved ) Patellofemoral crepitus (if involved) Angular deformity (varus more
common than valgus) Effusion (variable)n Visible osteophytes (variable) Thrust during gait (more
severe cases) (varus thrust more common than valgus thrust)

Anterior Cruciate Ligament Injury Effusion (acutely or after recurrent injury) Lachman's test
abnormal Anterior drawer test abnormal Pivot shift test (flexion rotation drawer test, jerk test,
Losses test) abnormal
Loss of full extension (if the stump of the ligament is impinged)
Signs of associated injuries (other ligament tears, meniscal tears)

Meniscus Tear Joint line tenderness Effusion (variable)

 McMurray's test abnormal (variable) Apley's test abnormal (variable) Childress' test abnormal
(variable)
 Pain reproduced by passive knee flexion (variable)
 Flexion contracture (if a displaced bucket handle fragment is present)
 Bounce home test painful (if a displaced bucket handle fragment is present)

Medial Collateral Ligament Injury Tenderness over the injured portion of the ligament
 Swelling over the injured portion of the ligament
 Effusion (usually mild)
 Valgus stress test abnormal (grade II and grade III injuries)
 Signs of associated injuries (if present)

Patellofemoral Chondrosis or Pain Syndrome

 Patellar facet tenderness
 Patellar crepitus (grind test, step-up—step- down test) (variable)
 Decreased patellar glide (variable) Effusion (more severe cases)
 Stigmata of malalignment (variable) (in-facing patella, increased Q
 angle, increased tubercle-sulcus angle) Patella baja (some postsurgical cases) Lateral
patellofemoral ligament tenderness (excessive lateral pressure syndrome)

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Patellofemoral Instability
 Increased patellar glide (especially lateral) Dysplastic quadriceps mechanism (variable)
Apprehension test abnormal
 Patellar facet tenderness and crepitus (variable)
 Tenderness of medial epicondyle or medial patella (acute injury) Patella aha (variable)
 Lateral patellar tracking (variable)

Posterior Cruciate Ligament Injury

 Dropback Posterior sag sign
 Quadriceps active drawer test abnormal Posterior drawer test abnormal
 Effusion (acute)
 Dynamic posterior shift test abnormal (variable) Signs of other ligament injuries (if present)

Posterolateral Ligament Injury Increased external tibial rotation Dial test

 Varus stress test abnormal
 Varus recurvatum test abnormal (frequently) Posterolateral drawer test abnormal Reverse
pivot shift test abnormal (variable)
 Signs of posterior cruciate ligament injury (frequently) Varus-hyperextension thrust during
gait (more severe cases) Signs of other associated ligament injuries (when present)

Osgood-Schlatter Disease
 Increased prominence of tibial tubercle Tender tibial tubercle
 Pain with resisted knee extension

Patellar Tendon Rupture

 Inability to extend knee against gravity
 Swelling Ecchymosis
 Palpable gap in the patellar tendon (frequent), usually at the inferior pole of the
patella
 Patella alta

Quadriceps Tendon Rupture

 Inability to extend the knee against gravity Swelling Ecchymosis
 Palpable gap in the quadriceps tendon (variable), usually at the

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  superior pole of the patella Effusion (more advanced cases)
 Crepitus) popping or clunking (more advanced cases)
 Abnormal Wilson's test (occasionally) Palpable loose body (occasionally; more
advanced case
Articular Cartilage Injury
 Tenderness of involved portion of knee Effusion (variable)
 Patello-femoral crepitus (If patella or femoral trochlea involved)
Jumper's Knee
 Localized swelling of involved portion of quadriceps mechanism
 (Proximal patellar tendon most common; distal quadriceps tendon or
 distal patellar tendon less common) Localized tenderness of involved area of tendon
 Pain to resisted knee extension

Osteochondritis Dissecans
 Tenderness of involved portion of knee (medial femoral condyle most common)

Common causes of hemarthrosis Cruciate ligament injury Peripheral meniscal injury

Osteochondral injury/ fractures Capsular tear

Causes of giving way Cruciate injury

Recurrent patellar dislocation Collateral ligament injury Extensor mechanism injury

Causes of locking
Bucket handle tears of menisci (true locking) Loose bodies
Recurrent subluxating patella
Cystic lesions arising from the cruciates

Common DDs when you find recurvatum in a posttraumatic knee Injury to

PCL/PLC/Posterior capsule injury
Malunited fractures of L/3rd femur or U/3rd tibia.

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 Difference between locking and extensor lag
 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

What are the structures in the lateral three layers of the knee joint 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

What are the structures in the medial three layers of the knee joint? 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

Radiologic features suggestive of ligamentous injury

 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

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Tests for knee joint effusion
Mild effusion (5-15ml) : bulge test Moderate effusion (15-30ml) : patellar tap Severe
effusion (> 30 ml) : cross fluctuation

How do you examine for synovial thickening

Palpate the superolateral aspect of the knee joint and try to roll the thickened edge of
synovium underneath…doughy feel.

Why superolateral aspect

VMO is wasted first among quads (as it developed later in the evolution of quadriceps)

What is the significance of positive valgus test in 30 deg and 0 deg?

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

Tests for ACL injury Lachman test Anterior drawer test

Pivot shift test of Hughston

Unhappy triad of O’Donoghue

Injury to ACL ,

MCL and
medial meniscus
Whats the most sensitive test for ACL injury
Lachman test.
Can be performed in emergency set up. Look for
Excessive anterior translation Soft end point
Drawbacks of anterior drawer test
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)

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What are the requisites for a positive pivot shift test
A non functioning ACL An intact medial complex An intact iliotibial tract

What is the treatment of ACL injury in skeletally immature patients Conservative

treatment - muscle strenghtening exercises esp. hamstrings Avoid any procedure involving
bony tunnelling until skeletal maturity
If indicated extra-articular reconstruction (eg: McIntosh repair)

Tests of PCL injury 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

Describe the various rotary instabilities and tests used to diagnose it? 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
Which meniscus is commonly injured, why

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Medial meniscus because;
Excursion of medial meniscus (5mm) is less than lateral meniscus (11mm) Attachment of
lateral meniscus to popliteus makes it more mobile

Which meniscus commonly injured in acute ACL injury and chronic ACL injury
Acute ACL – lateral meniscus Chronic ACL – medial meniscus

What are the signs and tests for meniscal injury? 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

Functions of meniscus?
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
Exercises preferred in post ACL reconstructed knee rehabillitation
Closed chain exercises as open chain exercises stresses the reconstructed ACL by quadriceps
pull esp. in terminal extension

List the autograft options for ACL reconstructon

Bone patellar tendon bone
Quadrupled hamstring (semitendinosus & gracilis) Central quadriceps tendon
Iliotibial band

How to treat a case of PCL injury

Acute PCL avulsion – arthroscopic /open fixation
Acute PCL injury in young – reconstruction after attaining full ROM

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Chronic PCL injury – quadriceps strenghtening, correct varus deformity, reconstruct PCL if
still symptomatic

What are the components of posterolateral complex of knee

Iliotibial band Biceps femoris
Lateral collateral ligament Popliteofibular ligament Arcuate complex Posterolateral capsule

Whats the significance of identifying PLC injury

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)

How to palpate for the knee joint line

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.

Give some examples of overuse knee pain syndromes

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

Treatment options for meniscal injury

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.

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Anatomical components of posterolateral corner of the knee joint
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

Tests to diagnose posterolateral corner injury knee

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)

What is the importance of recognizing posterolateral corner injury

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

Treatment of PLC injury

In Acute stage,
Grade I & II – brace in extension X 3weeks
Grade 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

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Anatomy of posterior oblique ligament and oblique posterior ligament 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

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 EXAMINATION OF THE SHOULDER JOINT

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

History
Age, Handedness,
Occupational and recreational activities Shoulder symptoms
Pain - exact site,
duration, onset, progression, 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.
Instability - Duration,
onset, frequency,
precipitating posture or activity,
position of shoulder after the dislocation, and how it gets corrected after an episode.

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 Voluntary/involuntary, associated with which movement, direction, how
frequent,associated neurological injury/ weakness.
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.

Swelling: Spontaneous onset (infective, PVNS, reactive effusion, inflammatory, haemophilia,

degenerative, etc.) or related to trauma (haemarthrosis).
Limitation of movements: Onset (spontaneous over a period – adhesive capsulitis, sub-
acute infections), treatment related (post-traumatic, post-surgical).
Limitations of Activities of daily living
Lack of power: Recurrent subluxation/ dislocations, dead arm syndrome. Causes of radiating
pain (gastric/ duodenal affections, diaphragmatic affections, cardiopulmonary and
mediastinal disorders), polyarthralgia.

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 Past history: Diabetes, hypertension, neurological disorders Past surgical history
Treatment history
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.

Attitude (Carriage/Posture):
– Anterior dislocation of shoulder: Elbow kept away (abduction) and slightly in front and
external rotation with support of the opposite hand.
– Posterior dislocation: Adduction and internal rotation
– Deltoid contracture: Abducted and drooping of shoulder
– Klippel-Feil syndrome: High webbed neck
– Sprengel shoulder: Scapula higher than uninvolved side
– Lateral scapular slide (in throwing athletes) scapula of dominant side drawn away from
midline.
– Prescapular abscess: Shoulder kept in flexion, abduction (away from irritating pus).
– Pyogenic arthritis: Flexion mild abduction and slight external rotation.
• From front : Sternal notch, sternoclavicular joint, clavicle and its contour, supra/infra
clavicular fossae, acromio-clavicular (AC) joint, preglenoid fossa,
anterior axillary fold, coracoids prominence, deltoid mass and shoulder contour, pectoral
muscle, sternocleidomastoid muscle and alignment of chin to suprasternal notch
• From behind: Midline and alignment of nape of neck to both shoulders, trapezius, medial
border of scapula (winging due to serratous anterior weakness or sometimes due to
rhomboids and trapezius also), spinous process of scapula, angle of scapula,
supra/infraspinatous fossae, posterior axillary fold, ‘soft spot’ (1 cm medial and 2 cm inferior
to angle of acromion) to look for swelling.
• From top: AC joint, contour of shoulder

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• From medial aspect: Swelling of lymph nodes, sebaceous gland infection.
At all the sites examine the skin for (SEADS) – swelling, erythema, atrophy (of appendages)
discoloration, suppuration (scars and sinuses).
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,
theinferior 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
shoulderand 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 axiliary fold and pectoralis major is seen patients with pectoralis major tendon
rupture and Poland syndrome. Wasting of supraspinatus and infraspinatus may be seen below
and above the spine of the scapula with prominence of the scapula in toto.

Palpation
Feel for local rise of temperature.

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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.
• Anteriorly: Sterno-clavicular joint, clavicle, AC joint, acromion (for os acromiale),
subacromial bursa (tenderness just anterior to acromion), long head of biceps (for
tendinitis
– palpate along 1-4 cms in front of acromion anteriorly with 10º internal rotation of
shoulder), myositis mass, pectoralis major tendon (by pressing both palms together),
supraclavicular fossa (for brachial plexus injury and ‘burners/stingers’ due to mild
involvement of plexus).
• Lateral aspect: For deltoid mass, step-deformity due to inferior subluxation of
shoulder
• Posterior aspect: Soft spot for swelling
• Medial aspect for pulsations of axillary artery
Look for tenderness, irregularity, thickening, defect, abnormal mobility etc.
Biceps tendon should be palpated in its groove anteriorly with shoulder in neutral and elbow
flexed.

The tenderness over the gleno humeral 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
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.

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 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.
Other movements to be assessed are forward flexion,extension and adduction.

Strength testing
Strength of rotator cuff muscles are measured.
Supraspinatus is assessed in the empty can position; 90 º 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.
Strength of subscapularis is measured with the arm in 90º abduction, elbow at 90º flexion and
the patient is asked to internally 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

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.

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  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.

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.
 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.

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 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.

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 Interpretation


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
fordiagnosis; 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

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

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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. Integrity of subscapularis is assessed separately
for the upper fibres and lower fibres.

Lift off test of Gerber

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 and look at the symmetry of the elbows. 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.

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.

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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.

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.

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 Interpretation – Anterior shoulder pain indicate long head of biceps pathology. Sensitivity-
90%
Specificity – 14%
Yergason test arm by side and elbow flexed to 90º. Patient is asked to flex elbow and pronate
while examiner resists. Pain is felt on anterior aspect of shoulder.

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%.

Tests for dislocated shoulder:

- Hamilton ruler test: Keep a straight ruler along lateral aspect of arm – in a normal
person it does not touch the acromion angle but in dislocated shoulder it does.
This will also be positive in any affection of head of humerus.
- Callaway’s test: Girth of shoulder is normally symmetrical increases in effusion,
suppuration, dislocation of shoulder.
- Duga’s test: on asking the patient to touch his opposite shoulder ,the elbow of the
affected limb cannot be brought to the midline of body
- Bryant’s test: In anterior dislocation of shoulder the anterior axillary fold is
elongated.

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

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Tests for thoracic outlet syndrome:
– Adson’s test: Abduct the arm by 30° and ask patient to take a deep breath while
palpating the pulse (feel the character and compare with other side), then ask the
patient to tilt his head towards the same side – reduction or diminution of pulse
suggests thoracic outlet syndrome.
– Wright’s maneuver: In the above test abduct the shoulder to 90º and externally
rotate the arm.
– Roos test: Abduct the arm and flex elbow to 90° then externally rotate the shoulder so
that the hand faces up. Ask patient to clench and release fist 15 times.
Paresthesia/pain/cramps/ weakness suggest thoracic outlet syndrome.
– Halsted’s test: While patient standing with arm by the side ask patient to turn the
head to other side and extend the neck. Give a downward traction and feel for
diminution / obliteration of pulse.

– Hyperabduction test: Abduct and hyperextend both the arms (behind the body)
simultaneously. Feel for diminution of pulse on affected side.

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 EXAMINATION OF THE SPINE

History
Pain

– Onset
Acute in post-traumatic, jerk, pyogenic infection (discitis), tubercular infection Insidious
onset in mechanical low back pain, spondylitis, facet joints, metastasis (unless precipitated by
trauma), primary bone tumors,hemangioma.

– Site:
Axial (localized pain) at all spinal levels along the midline often result from
‘mechanical’ (non-neurogenic) structures like musculotendinous structures, zygapophyseal
joints, vertebrae and annulus fibrosus whilst
Radiating pain is along the back from the buttock running downward until the great toe due to
the involvement of neurological structures(sciatic nerve) that may be related to disc
herniation, degenerative process, neuroforaminal stenosis or other space-occupying lesions,
intrinsic diseases of cord/nerve root (Herpes zoster).

– Nature:
Throbbing acute unbearable pain result from acute pyogenic infections, traumatic/
pathological fracture (barring osteoporotic #), and
Severe constant pain may result from cauda equina syndrome, advanced tubercular infection,
acute cervical/dorsal/lumbar strain.
Dull constant aching pain is often the result of mechanical problems originating as above.

– Radiation: The radiated (from other site) and radiating (to other site) pain are both
noticed. Pain from lumbar or cervical regions often radiates as ‘lightening sensation’ in the
limbs while dorsal segments radiate in ‘Band-like’fashion. The general rule for
radiating pain (from neurological structures) is simple and constant in that it is the spinal
level of pathology and not the exact structure involved that determines the ‘radiation
pattern’. Axially radiated pain from various sites that require mention include aorta, carotid
arteries, costovertebral and costotransverse articulations, pancreas, lung, pleura, gallbladder,
stomach and proximal duodenum, diaphragm, kidneys, ureter, pelvic organs in female.

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 – Diffuse/localized: Localized pain often result from focal injury to mechanical structures
whereas diffuse pain is often radiated.

– Aggravating and relieving factors:

Rotation and extension was classically attributed to zygapophyseal joints.
Bending forward is painful in discogenic pain. Excursion as such is painful in
inflammatory conditions of spine.
Neuroforaminal stenosis causes neurogenic claudication that comes up after exertion and is
relieved by forward flexion/sitting.

Whereas sitting and getting up from seated position is often painful in discogenic pain,
sleeping with knees and hips flexed often relieves pain.

• Trauma: direct/indirect (like lifting heavy weight, seat belt injuries)

 Deformity: Onset, duration, sudden increase (collapse in pathological fractures),
association with pain and fever (tuberculosis), stiffness (ankylosing spondylitis).
 Loss of balance.
 H/O neurogenic claudication
 H/o weakness: Onset Progression Severity
Diurnal variation
 Associated with involvement of other joints
 H/o Numbness: Onset Progression
Site and region of involvement
 Difficulty in walking
Difficulty in washing face in darkness (s/o ataxia) Perianal sensory loss
 H/o Bowel and bladder involvement: Retention
Urgency Frequency Bladder sensation present or no

 Associated h/o renal, cardiac or GIT complaints H/o pelvic Inflammatory disease
H/o adolescent backpain (spondylolisthesis) and occupation H/o dyspnoea, cyanosis or
palpitation (s/o thoracic component)
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 Polio

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 H/O treatment for the same problem previously
 Drug history
 Past medical and surgical history
 Full Developmental history (Antenatal, natal and postnatal) - R/o any neuromuscular cause of
the deformity.
 Family History R/o Any h/o infection Tuberculosis(contact TB)
Red flag signs in LBA Loss of weight and appetite Fever
Nocturnal pain Rest pain Bilateral sciatica
Sphincter disturbance Age less than 15 or More than 50
H/o trauma, malignancy Gross motor weakness

Examination:
Height Weight US/LS ratio Arm span
Gait and Posture Abnormal movements
Neurocutaneous markers like ash leaf macule/ neurofibromas / café au lait spots / tuft of hair

Inspectiom:
From back:
Head tilt and neck tilt Hairline and
Level of shoulders
Level of scapulae and any rib hump
Arm flank distance
Iliocostal distance
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

Any List: “A list is an abrupt planar shift (no definite curvature) of the spine above a
certain point to one side in coronal plane” – usually seen in lumbar region
Any sideward bending of spine
From Side:
Exaggerated lumbar lordosis Shape of the chest wall
Rib hump Anterior:

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Level of nipples and breast folds Level of the ASIS
Crowding of ribs
Sternum: Pectus excavatum, pectus carinatum
Pot belly

Palpation:
Warmth
Tenderness over the spinous process Point tenderness
Twist tenderness - push the spinous process to either side in an attempt to rotate the vertebra
Thrust tenderness - by gently ‘thrusting’ the spine with
a closed fist.
Feel for any cold abscesses per abdomen as well as superficial Paraspinal muscle spasm
Paraspinal fullness or swelling
Any step deformity as in spondylolisthesis Any knuckle ,gibbus or kyphous deformity

All movements of the cervical spine, dorsal and lumbar spine Schober‘s test
Chest expansion
Limb length discrepancy
From occipital protuberance to tip of coccyx 12th rib to iliac crest
Modified schoebers test
• Flexion: cervical spine – chin to chest, lumbar spine –forward bending (measured by
the final position of trunk in relation to vertical plane or distance of fingers from floor
{normal = 90° or < 10 cm finger floordistance)}
• Extension: cervical spine – looking roof, lumbar spine – backward bending (normally
20- 30°), often limited in patients with facet arthropathy and in foraminal narrowing
as extension further narrows the foramina.
• Lateral rotation to right and left side for cervical spine (normal = 80°)
• Lateral bending (thoracic spine) – floor-fingertip distance
• For flexion and extension of thoracic spine (which is minimal) make the patient sit on
a wooden straight back chair and ask to bend forward and backwards. More accurate
measurement can be made by direct measurement (see below).
• Rotation in sitting position (for lumbar spine) – measure angle between plane of
shoulder to pelvis.

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Measurements:
• Mark two points from T1 to S1 and a point at L1.
Measure and ask patient to bend forward, increase of T1-L1 by >8 cm and L1 to S1
by more than 8-10 cm is normal.

• Modified Schober’s test: mark two points – one point 10 cm above and the other 5
cm below lumbosacral junction.
Measure the distance before and after forward flexion. At least there must be an
increase of
> 5 cm otherwise it is pathological.
• Chest expansion – abnormal is <2.5 cm than the average normal value for age and sex
(measure at the level of the 4th intercostal space).
For males upto 65 years normal is 5.5-7 cm and females 4-5.5 cm.
>65 years of age for males 3-4 cm and females 2.5 to 4 cm. You can safely refer to 5.0
cms as the normal for most healthy adults.

• Iliocostal distance (from front)

• Iliooccipital distance (from back)

Spurling test for cervical spine

Adson test or Roos test for thoracic outlet syndrome Adams Forward bending test for rib
hump
Stretch sign tests –
SLRT – Straight leg raising test (passive test)
Lasegue test for lumbar spine - stop at the hip flexion where pain is induced and dorsiflex
ankle and foot radicular pain exacerbated, strengthens the diagnosis of sciatica.
Bowstring sign of McNab: perform SLRT stop at the hip flexion where pain is produced
flex knee to 90°  press the sciatic nerve in popliteal fossa  strengthens the impression of
sciatica.

Higher mental functions Cranial nerves

Neurological examination:

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 • Cervical spine: lateral rotators (right by left sternocleidomastoid and vice versa),
forward flexors (both SCM together), extensors (posterior intrinsic muscles and
trapezius) and lateral benders (scalene).
• Beevor’s sign (for lower thoracic nerve roots): patient in supine position performs a
quarter squat with hands behind head. Watch the movement of naval up/down or to
any side which indicates involvement of lower abdominal musculature
(below T9)

• Examination of limb muscles (in distribution, myotomes) All four limbs

– Bulk
– Tone
– Power
– Coordination
– Balance
– Involuntary movements (chorea, athetosis, dystonia, tics, myokymia,
hemiballismus, asterixis, myoclonus)

• Sensory examination:
– Fine touch and sharp-dull discrimination.
– Crude touch and sterognosis
– Two point discrimination
– Pressure
– Temperature (cold and hot)
– Vibration sense
– Positional sense (proprioception)

• Reflexes:
– Superficial Reflexes (UMN dependent reflexes)
◆ Trapezius reflex (C3-C4)
◆ Deltoid reflex (C5-C6)
◆ Scapular reflex (C5-T1)
◆ Abdominal muscle reflexes (T7-L1)
◆ Cremastric (T12, L1)

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 ◆ Anal wink reflex(S2-S4): used to determine end of spinal shock
◆ Bulbo-cavernosus (S2-S4)
◆ Plantar reflex (Babinski sign) – this is a pathological reflex and appears only
in UMN lesions
◆ Throckmorton’s reflex (percuss the dorsum of foot in MTP joint region – great
toe extension with flexion of other’s is normal)

– Deep Reflexes (LMN local reflexes with inhibition from UMN) lost in LMN
lesions and becomes hyperactive in UMN lesions (a cervical level is UMN for
lumbar levels!)
◆ Biceps (C5-C6)
◆ Triceps (C6-C7)
◆ Brachioradialis (C6-C7)
◆ Inversion of radial jerk (C5-C6)
◆ Knee (L2-L3-L4)
◆ Ankle (S1-S2)
◆ Medial hamstring (L5)
◆ Tibialis posterior (L5)
– Ankle clonus and patellar clonus (Due to loss from UMN inhibition ).

Autonomic system Cerebellar signs Coordination

Gait:
Shuffling gait (posterior cord syndrome), slapping foot gait (high stepping gait),
broad- based gait (halting gait),
Alderman’s gait- Infective spondylodiscitis festinating gait, antalgic gait, etc.
a. Heel walking: to test ankle dorsiflexors (L5 root).
b. Toe walking: to test ankle plantarflexors (S1 root).

Level Sensory findings Motor deficit Refexes involved

C3 Lateral neck region Trapezius Trapezius reflex

Middle deltoid region in arm Deltoid, Biceps Biceps reflex, deltoid

C4
("Regiment badge area") - Axillary (partial) reflex

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 nerve

Brachioradialis
Dorsum of first web space (Thumb);
Biceps brachii, wrist (supinator) reflex,
C5 lateral forearm - musculocutaneous
extensors inversion of radial reflex,
nerve
biceps (weakness)
Wrist flexors, long
Triceps jerk, scapular
C7 Long finger finger extensors,
reflex
triceps

Little finger, ulnar aspect of palm - Long finger flexors,

C8 Scapular reflex
Ulnar nerve Hand intrinsic

T1 Medial aspect of elbow and lower Intrinsic muscles of

arm - Medial brachial cutaneous hand typically
nerve interossei

T2 Medial upper arm and adjacent chest

T4 Nipple
T10 Umbilicus Flexion of trunk Abdominal reflex
(Beevor's sign)

L1 Anterior proximal thigh at groin fold Iliopsoas Cremastric reflex

(inguinal ligament) –
ilioinguinal nerve
L2 Mid-thigh (pocket region) - Lateral, Iliopsoas
anterior and medial femoral
cutaneous nerves of thigh

L3 Lower thigh and medial aspect of Quadriceps Patellar tendon reflex

patella – obturator nerve (partial)
L4 Medial aspect of leg and Tibialis anterior Patellar tendon
ankle - Saphenous nerve reflex
L5 Lateral and anterolateral aspect of EHL, EDL, Tibialis posterior reflex,
leg, dorsum first web space (medial Gluteus medius medial hamstring reflex
plantar nerve and lateral cutaneous
nerve of calf)

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 S1 Lateral aspect of foot over plantar Gastro-soleus, peronei,
aspect, posterior calf - lateral plantar gluteus maximus Tendo Achilles reflex,
nerve plantar reflex
S2 Posterior thigh region, proximal calf Lax external sphincter
in rectal
examination
S3-5 Perianal area Lax external sphincter Anal reflex,
in rectal bulbocavernosus
examination reflex

How to test for plantar reflex and what is its interpretation?

After Explaining the procedure to the patient , Stroke the lateral aspect of foot from heel
upwards making a ‘J’ at the region of metatarsal heads. Normally there is a progressive
sequence of:
1. Great Toe flexion
2. Ankle dorsiflexion
3. Inversion of foot
This denotes intact innervation up to L5-S1 level.
Mute plantar response can occur in a normal individual and in spinal shock.
The pathological appearance of a different sequence is a Babinski reflex (extensor plantar
response) which is characterized by:
1. Extension of great toe
2. Fanning out of other toes
3. Ankle dorsiflexion
4. Knee flexion followed by ipsilateral hip flexion
5. Contralateral hip and knee extension (withdrawal reflex)
This dramatic sequence can be overridden in a conscious patient and only first few stages are
seen in a typical UMN lesion.
Other ways of eliciting this reflex?
– Squeezing the heel cord (Gordon’s sign)
– Sqeezing the calf
– Pressing firmly the medial border of leg/tibial crest (Oppenheim’s sign)
– Stroking lateral malleolus.

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Pathological reflexes appear in a UMN lesion?
• Hoffman’s reflex {palmar flexion of thumb (and observing a pincer movement
between thumb and index finger) on rapidly tapping the distal phalanx of middle
finger from palmar aspect}
• Inverted radial reflex
• Tromner sign – similar to Hoffman’s reflex but here the middle finger is elevated and
distal phalanx is flicked towards palm
• Crossed adductor’s sign – ipsilateral patellar reflex causes contralateral thigh
adductors to contract
• Chaddock’s sign – abduct little toe and release it to slap against other toes or flick
third and fourth toe down rapidly to look for great toe dorsiflexion.
• Clonus
Bladder dysfunction associated with spinal cord injury?

The following should help explain the mechanism of two different cord bladder
functioning. First there are two differently innervated muscles in bladder control. One is the
bladder motor (detrusor) which is under local spinal control S2-4, whereby any stimulus that
arises due to bladder filling leads to contraction of bladder and emptying. The other one is the
innervations of sphincters which is inhibited (relaxed) by local reflex (S2-4) and stimulated
by sympathetic system (L1-2). Now secondly there is a higher control which has an
inhibitory influence on local reflex (S2-

4). Now if local reflex is released from all upper inhibitions (as happens in UMN lesion) the
bladder becomes an ‘Automatic bladder’ which will contract as soon as it fills up and there
will be detrusor hypertrophy due to hyperactive local reflex (S2-4). If this local reflex is lost
(as will happen in S2-4 lesions like cauda equina syndrome – LMN lesion) the bladder will
not be able to contract due to its lost motor supply and also the sympathetic (L1-L2) reflex is
still activating the sphincters that additionally prevent emptying. This type of bladder keeps
filling till the capacity is exceeded when the urine dribbles due to exceeded competency of
sphincters – ‘atonic bladder’. With time, however intramural reflexes develop whence
witherfilling the bladder may contract due to direct detrusor stimulation – the so called

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‘Autonomous bladder’.
How to predict the level of cord involvement with the vertebral (spinal) level?
The following is the rule of thumb for an adult:
Vertebral level Cord level
C1-C7 Add one to know corresponding cord level T1-6 Add two
T7-9 Add three T10 L1 and L2 T11 L3 and L4 T12 L5 and S1
L1 (cord ends at Rest sacrals and coccygeal segment lower border of L1)
Below L1 Cauda equina

Clonus
It is a pathological hyperreflexia of normal deep tendon reflexes produced due to release of
the normal reflex from higher control. Sustained clonus (> 5 beats of clonus) is
significant and represent UMN lesion.
Ill-sustained clonus can occur in an otherwise normal individual.

How to make Reflexes more prominent if they are not elicited by normal maneuver?
Jendrassik’s maneuver by asking patient to either clench his teeth tight or pulling the
interdigitated fingers of both hands apart to enhance the reflexes.

Rigidity vs Spasticity
Both represent types of hypertonia. Rigidity is pathologically due to extrapyramidal affection.
It can be of cogwheel type (jerky or intermittent regular resistance
to motion) or lead pipe type (present throughout the range of motion).
Spasticity is more of practical concern in the context of spine examination and is due to
affection of pyramidal system (corticospinal pathway). It is classically a UMN lesion and is
of clasp-knife type whereby resistance is offered only to the initial part of movement
and disappears on persisting with the same. A hysterical hypertonia classically increases with
the effort applied.

Central cord syndrome

Central cord syndrome occurs in the cervical level often due to hyperextension injuries or in
an elderly due to stenotic cervical canal.

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 The upper limb is more severely affected with initial affection of pain and temperature and
later involvement of upper limb motor function and lower limb with progression. The
syndrome may also be produced by central canal syrinx or sometimes intraspinal tumors.

Anterior cord syndrome

Due to involvement of ventral portion of cord (interruption of ascending spinothalamic tracts

and descending motor tracts. It is characterized by:
• Loss of pain and temperature sensation
• Loss of motor control below the affected level
• Preservation of proprioception and crude touch

Brown-Sequard syndrome
Hemisection injury of spinal cord:
• Ipsilateral motor loss below the level
• Loss of reflexes at the level
• Contralateral loss of pain and temperature one to three levels below the level of lesion
• Ipsilateral loss of proprioception and position sensationand crude touch

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 INTERVERTEBRAL DISC PROLAPSE

What is the pathognomonic sign of the lumbar IVDP?

A positive cross Straight leg raising test (SLR).

How do you diagnose or what are the signs of upper lumbar disc herniation ? 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.

What are the indications for surgical intervention?

-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

Which disc can produce a false positive finding in MRI? Which is the largest disc?
What percentage of the disc contains water?
L4 L5disc is the largest disc (so it can produce a false positive test) 60-65% of the disc
contains water

What is the difference btw prolapse/extrusions/sequestra

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
What are root tension and root irritating signs?
SLR and bowstring sign - root tension signs Calf tenderness is root irritating sign

How to differentiate between axillary and shoulder disc?

In case of axillary disc, lateral bending to the same side increases the pain. Reverse will
happen if it is a shoulder disc.

What portion of the root lies in the canal?

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Normal extension of root in the canal-3mm What are the signs of L5 root compression?
Sensory -loss anterior, lateral leg and dorsum of foot.
Motor- EHL, Gluteus medius weakness.

Which disc is prolapsed for L5 root involvement?

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.
Differentiate btw neurologic and vascular claudication pain.
Neurogenic: pain relieves with rest, sitting, squatting and bending forwards (to produce
slight flexion relieves vertebrae
Vascular: improves once the patientstops walking
What are the contra indications of epidural steroids?
Local infection, systemic infection, uncontrolled diabetes, congestive cardiac failure

How do you differentiate between referred pain and radicular pain? 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.

What is the most consistent triad in cauda equina syndrome?

Saddle anaesthesia B/L ankle areflexia Bladder symptoms

What is the role of xray in a case of suspected IVDP

rule out infection, tumor and other unsuspected anomalies

What is a positive bowsting sign

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.

How to differentiate between piriformis syndrome and IVDP?

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

What is failed back syndrome?

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 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

What are the complications of dural tear?

Psuedomeningocele, CSF leak through persistent fistula, meningitis

What is fenestration?
surgrgical procedure which removes the ligamentum flavum of one side with
undercutting lamina to increase the space for removing the disc.

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 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

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

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.

What is Adams forward bending test?

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.

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

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)

What are the factors related to progression of AIS ?

Girls > boys Premenarchal age Risser sign of 0
Double curves > single curves Thoracic curves > Lumbar curves More severe curves

What are the problems of untreated scoliosis?

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

Which types of scoliosis are most frequently pathological? Left thoracic curve and right
lumbar curve

What are the types of congenital scoliosis? Failure of formation- (a) Partial –Wedge
vertebrae
(b) Complete- Hemivertibrae

Failure of segmentation- (a) unilateral unsegmented bar

(b) Bilateral- Block vertebrae Mixed type

Which congenital curve is having worst prognosis?

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

What are the types of scoliosis in neurofibromatosis?

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

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

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.

What are the important physical examination points in scoliosis?

Sitting and standing height

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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

How are apical vertebrae and end vertebrae determined?

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.

What are neutral and stable vertebrae?

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

What is mehta”s rib vertebral angle difference?

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.

Which are the 2 common classification used for scoliosis?

King‖s classification and Lenke‖s classification.
What is the use of Nash-Moe classification and Risser sign?
Nash-Moe classification is used to assess vertebral rotation and Risser sign for skeletal
maturity.
What are the treatment options for idiopathic scoliosis?

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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.

What are the surgical methods of treating AIS?. 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.

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 TUBERCULOSIS SPINE
What are the common levels of involvement of spinal tuberculosis
Thoracic spine -35- 40 % Thoracolumbar spine – 25 – 30 % Lumbosacral spine- 25- 30 %
Cervical spine – 4- 5 %

What are the sites of lesion in the vertebrae

Paradiscal Anterior Posterior Central

Spinal tumour syndrome

What are the problems associated spinal tuberculosis?

Abscess formation Deformity Neurological deficits

Why paradiscal lesions are the commonest type of lesion?

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

Why kyphus deformity is common in children?

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

Which are the common sites of tracking of tuberculous pus?

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.
What are the causes of early onset paraplegia?
Abscess, inflammatory oedema, granulation tissue, sequestrum, thrombosis of anterior spinal
artery.

What are the causes of late onset paraplegia? Stretching of cord over the internal gibbus
deformity. What is spinal tumour syndrome?
Tuberculous extradural granuloma producing neurological deficit without radiological
evidence of vertebral involvement.

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What are the deformities seen in tuberculosis of spine?
A. Knuckle - single vertebra
Gibbus - 2 vertebral involvement
Kyphosis - >3 vertebral involvement
What are the radiological signs of spinal
Q
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

What are the indications for CT scan?

Posterior spinal disease, craniovertebral involvement, sacroiliac joint involvement

What are the indications for MRI scan?

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

What are the investigations in a case of spinal tuberculosis

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

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

What are the regimens used for treating spinal tuberculosis?

A. Hong Kong regimen - Radical surgery
Kenyan regimen - Only ATT
BMRC regimen - Middle path regimen
Q What is Middle path regimen?

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 Initial treatment with ATT and surgery in certain indications
A

What are the indications for surgery in Middle path regimen?

 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.

What are the surgical options for treating D/L tuberculosis?

Anterior decompression and fusion
Anterolateral decompression -Costotransvesectomy
Transpedicular decompression and posterior fusion
Rarely laminectomy - in posterior type

Why is pseudoflexion deformity of hip in spinal tuberculosis?

A. Due to irritation of psoas muscle by abscess.

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

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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.
Low back pain can be due to instability. Radicular pain and neurogenic claudication occurs
due to lateral stenosis – mainly of the foraminal type due to ‘horizontalization’ of the
foramen.

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

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 EXAMINATION OF ANKLE AND FOOT

Age: CTEV present since birth, TEV secondary to polio, neural tube defects, etc.
appear later. CVT noticed at walking age-around 1 year.
Sex: Boys common in CTEV.
Pain: Duration, Site, radiation, type, character, aggravating factors, relieving factors,
diurnal variation and postural variation.
Swelling: Duration, onset (preceding trauma, fever, other joints involvement, morning
stiffness), progress (always increasing as in tumors, regressive as in trauma or
increase with on and off reduction as in infection), aggravating factors
(walking in subtalar arthritis), relieving factors (antibiotics in infection or
chemotherapy in tumours), effect of any treatment received, diurnal and
postural variation.

Associated with deformity in other foot.

Limp: Onset, duration, painful or painless, progressive or not.
Instability: Duration, onset (post-traumatic), unilateral or bilateral (ligament laxity), on
even or uneven surfaces (in stiff subtalar joint)
Deformity: Onset (at birth [CTEV] or appeared later [acquired clubfoot]) (appears at
around 1 year in CVT) (after an episode of fever and myalgia with weakness
of limb muscles in polio), progress (congenital is less progressive than
acquired), any treatment received (casts, surgeries), response to any such
treatment.
Associated diseases: Fever with myalgia and weakness of limbs in polio

From Front
Attitude
Describe from proximal to distal

Sole
 metatarsal heads
o I - sesamoids
o II-V - metatarsalgia
 interdigital neuroma

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  interdigital tenderness
 lateral compression - pain & click
 heel
o origin of plantar fascia

Medial
 1st Metatarsal head
 1st metatarsal-Cuneiform joint (flare of base of 1st MT)
 Navicular Tubercle
Inspection Gait

 Head of Talus (evert forefoot)

 Medial Malleolus
 Sustentaculum Tali (1.5 cm below medial malleolus)
Lateral
 5th Metatarsal head
 Cuboid
 Calcaneum
 Peroneal Tubercle (separates peroneus longus & brevis)
 Lateral malleolus Antalgic, short limbed, foot drop, equinus, stiff 1st MTP joint.

Gait ask patient to walk

 walk away
 walk towards
 Features
o Stiff ankle
o Foot drop
o Fixed equines
o Antalgic
o Rocker Walk to wall & face it

Anterior aspect:
1. Alignment: Great toe (Hallux valgus/ varus), other toes (claw, hammer, mallet),
relations of forefoot, midfoot, hindfoot with each other and lower leg (include tibia
vara, rotation).

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2. Condition of skin: Any discolouration, ulcers, dilated veins, edema (pitting or non-
pitting and up to what level).
3. Toes: Notice transverse skin creases at I-P joints (sometimes lost in polio). Also note
thickened cornified skin over dorsum (heloma durum) seen in toe deformities. Toe
nail deformities in fungal infections. Paronychia (seen as swelling around
base and sides of nail). Ingrown toenail.
4. Osteophytes medially over 1st MTP joint is called bunion and over lateral aspect of
5th MTP joint is called bunionette.
5. Prominence of tendons of EHL and EDL over foot and anterior aspect of ankle by
active contraction of muscles. (structures medial to lateral tibialis anterior, extensor
Hallucis longus, anterior tibial artery, anterior tibial nerve, extensor digitorum longus
and Peroneus tertius).
6. Relation of medial and lateral malleoli: Normally lateral malleoli is below and
posterior to medial malleolus.
7. Any swelling over malleoli: Seen in trauma, tendinitis.
8. Anterior crest of tibia and subcutaneous border may show swelling, deformities.

Deformity
 knee alignment
o physiological valgus
o patella alignment
o valgus with pes planus
 foot rotation
o symmetrical ER
 forefoot
o splaying
 hallux
o valgus / varus Skin
o If abnormal, general comment
 Overriding
 Hammer
 Claw
 Callosities over ipj

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o Pronation
o Lnterphalangeal joint
 Lesser toesscars
 Trophic changes
 Circulatory disturbance
o Hair loss
o Hyperpigmentation
o Varicosities
o Ulcers
 Disuse / denervation

Contour

o Onychomycosis
 Fungal infection of the naildry skin
o dekeratinisation
 Nails
o Paronychia
 Infection of the lateral nail folds
o Eponychia
 Infection of the proximal nail fold
 Swelling
 anterolateral ankle
 navicular
 bunion
 bunionette
 Muscle Wasting
o Calf
o EDB

Lateral aspect
Visualize lateral malleolus, 5th metatarsal base, tendoachilles and peroneus brevis
tendon,lateral border of the foot.
Note for any swelling.

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Deformity
 knee - flexion attitude
 ankle - equinus
Skin
 scars
Contour
 Swelling
 peroneal tendons
Posterior aspect
1. Alignment: Varus/valgus of hindfoot.
“Too many toes sign” – more than 2 toes visible from behind means abduction of
forefoot, usually associated with pes planus.
2. Heel: Size (any broadening), pattern and position.
3. Tell patient to stand on tips of toes (windlass effect-inversion and increased height of
medial longitudinal arch)
4. Plantar fat pad, calcaneal tuberosity (abnormally increased prominence of superior
aspectis Hagelund’s deformity or pump-bump)
5. Retro-calcaneal bursa: Bursitis.
6. Achilles tendon: tendinitis, rupture (2-6 cms above insertion), swelling at level of
malleoli is seen in tendonitis and over whole length is seen in rupture.
7. Calf atrophy (compared to normal): residuum of CTEV, TA rupture or prolonged
immobilization.
From Behind

Deformity
 Back
o Sagital spinal deformity
o Cutaneous manifestastions of spinal dysraphism
 hindfoot
o physiological valgus
o varus
 then ask for Coleman Block
o Valgus
 Single heel raise

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  forefoot
o too many toes
 Skin
o scars
Contour
 Swelling
 calf
 Duchenne
 Tendo Achilles
 heel
o Haglund’s
 Wasting
o calf

Medial aspect
1. Medial longitudinal arch: Cavus or planus or rocker bottom deformity (in diabetics
or improperly treated CTEV)
2. Bony prominences: Medial malleolus, head of 1st MT, calcaneal tuberosity and
navicular tuberosity (prominent in accessory navicular).
3. Tibialis posterior tendon made visible by active contraction.
Structures underneath flexor retinaculum of ankle: tibialis posterior, flexor digitorum
longus, posterior tibial artery, posterior tibial nerve and flexor Hallucis longus.

From Medial Side

 turn affected side away
Deformity
 medial arch is preserved
 pes planus
 pes cavus
Skin
 scars
Contour
 Swelling
 tibialis posterior

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Plantar aspect
1. Callosity suggests point of weight bearing. Normally seen over metatarsal heads and

lateral margin of foot. Painful calluses over MT heads are seen in toe deformities like
claw toes and hammer toes with hyperextension of MTP joints.
2. Corns are localized thickening of skin over pressure areas. Two types: Hard or soft.
3. Ulcerations: Diabetes, abnormal bony prominences

Palpation Anterior
1. Local rise of temperature
2. Tenderness: Over anterior tibial crest (in stress fractures).
Over talar dome: Palpated anterolaterally with maximal passive plantar flexion at
ankle (in OCD). Over navicular in Kohler’s. Over talo-navicular joint in osteoarthritis.
Also palpate cuneiforms, metatarsals (stress fracture esp. in 2nd and 3rd MT. Over 1st
MTP joint in bunions, gout and septic arthritis). 2nd MTP joint (Freiberg’s
infarction).
3. Tenderness in interdigital spaces suggests Morton’s neuromas (commonest b/w 3rd
and 4th metatarsal heads).
4. Swelling: Over stress fractures. Osteophytes over joints. Effusion of joint: Cross
fluctuation can be demonstrated between anterolateral and antero-medial swellings in
full plantar flexion. Also seen between posterolateral and posteromedial swellings in
full dorsiflexion. In between anterior and posterior swellings, it’s seen in neutral
position.
5. Tendons (whether they are taut, tenderness, lump or any gap seen in ruptures, diffuse
swelling, crepitus): Tibialis anterior, EHL, EDL and peroneus tertius.
6. Toes palpated for corns, ingrown toe nails.
7. Tinel’s sign over deep peroneal nerve (at site of dorsalis pedis artery) present in
anterior tarsal tunnel syndrome.
Lateral
1. Lateral malleolus, anterior talo-fibular ligament and calcaneo-fibular ligament for
swelling, tenderness.
2. Peroneal tendons (can’t distinguish 2 separately)
3. Calcaneum, its tuberosity (in Sever’s disease), Calcaneocuboid joint.
4. Over sinus tarsi in subtalar arthritis.

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 5. Over fibular shaft: Stress fractures.

Posterior
1. Over gastro-soleus. In Tendo-Achilles rupture, tenderness, gap and swelling are felt 2-
6 cms above TA insertion.
2. Over posterior tuberosity of calcaneum: Tender swelling in retro-calcaneal bursitis

Medial
1. Medial malleolus and subcutaneous border of tibia
2. Head of talus(by eversion of foot)
3. Navicular tuberosity: Tender swelling seen in accessory navicular.
4. Tendons of FHL, FDL and T.P.
5. Tinel’s signs over posterior tibial nerve and medial and lateral plantar nerves.
Plantar
1. Callosities-tender
2. Sesamoids for tenderness.
3. Plantar fascia-tenderness at calcaneal attachment in fasciitis, tenderness on

hyperextending toes, painful nodules.

4. Plantar fat pad-tenderness.

Tendons
 Tendo Achilles
o insertion
 tenderness
o along tendon
 tenderness (diffuse or focal)
o lump
o retrocalcaneal bursa (pinch tissue anterior to AT)
o calcaneal bursa (posterior to AT)
 Tibialis Posterior
o prominent with plantarflexion & inversion
o thickening
o tenderness

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 o crepitus
o check power if abnormal
o navicular insertion
 Peroneals - Brevis & Longus
o thickening
o tenderness
o dislocation (resisted eversion)
o base of 5th MT insertion
 Tibialis Anterior
o Prominent with dorsiflexion & inversion
o Insertion
 EHL & EDL
 Dorsiflex toes
Ankle Joint
 lateral ligaments
o 1. Anterior Talo-Fibular Ligament (ATFL)
o 2. Calcaneo-Fibular Ligament (CFL)
o 3. Posterior Talo-Fibular Ligament (PTFL)
o 4. Anterior Inferior Tibiofibular Ligament (AITFL)
o 5. Posterior Inferior Tibiofibular Ligament (PITFL)
 joint line
 Deltoid Ligament
 Fluctuance
o effusion or synovial thickening

Forefoot
 bunion
 bunionette
 pulses
o dorsalis pedis
o posterior tibial
 capillary refill
o <2 seconds

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Movements
 Active, Passive, Power
 compare both feet at same time
 Dorsiflexion
o active
 please pull your feet towards your head
o passive
 push patients foot up further
o breaking at midfoot
o power
 “hold foot up” & resist
 Plantarfiexion
 Inversion
 Eversion

Ankle / Tibiotalar (Dorsiflexion/Plantarflexion)

o method
 thumb on talar neck
 grasp heel with other hand
 plantarflex & dorsiflex ankle
 movement occurring at ankle joint
 relate to foot at neutral (90°)
o normal
 dorsiflexion 20°
 plantarflexion 50°

Subtalar (Inversion/Eversion)
o method
 forefoot held in neutral at 90° to tibia (locks wider, anterior part of talar dome into
ankle mortise)
 foot relaxed with thumb on talar neck
 grasp heel with other hand
 invert & evert heel
o normal

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  inversion 10-15°
 eversion 0-5°
o abnormal
 Tarsal Coalition

Midtarsal
o Method
 Foot held at 90° (to lock talus into ankle mortise)
 Calcaneus grasped
o Normal
 Adduct foot (20°)
 Abduct foot (10°)
 Dorsiflexion
 Plantarflexion
1st MTPJ (Flexion/Extension)
o Method
 Stabilise forefoot & IPJ
o Normal
 extension 70-90°
 flexion 45°
1st IPJ (Flexion/Extension)
o Method
 stabilise proximal phalanx
o Normal
 flexion 90°
 extension 0°
Toes (Flexion/Extension)
o extension only occurs at MTPJ
Special Tests Instability
 Anterior Drawer
o Due to complete tear of ATFL
o grasp lower tibia & cup calcaneum
o "clunk" or draw
o compare with other side

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  Lateral instability
o Inversion stress
 gaping of soft tissues
 talar tilt (may occur in normal & must cf. with other side)
 needs to be confirmed on stress views
 Medial Instability
o Eversion stress
o gaping/ widening
o needs to be confirmed on stress views

Gastrocnemius / Soleus Contracture

 test if limited dorsiflexion
o extend knee - dorsiflexion limited by both soleus & gastrocnemius contracture
o flex knee - gastrocnemius relaxed (crosses knee joint)
 if dorsiflexion still limited it is due to soleus contracture
 if limited in extension & not in flexion then due to gastrocnemius contraction
Findings in case of Of CTEV Foot
• Small foot; stretched thin skin on dorsolateral aspect and thrown into creases along the
medial aspect
• Scars and callosities (if patient is ambulatory)
• Head of talus palpable over foot
• Lateral convex border and medial concavity with furrows
• Heel (‘small’) rotated medially and drawn up (empty heel) with deep crease over
posterior aspect

• Ancillary findings:
– Extrinsic/intrinsic type
– Genu valgum Gait: “stumbling” gait ROM: ankle, knee, inversion and eversion at
subtalar joint
Other examination - What else would you like to examine :
• Hip for DDH
• Spine for dysraphism (Meningomyelocele)
• Cerebral palsy
• AMC

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 • Polio – tight ITB (always check!)
• Cleft lip, palate, exomphalos and congenital hernia
• Sensation of foot
• Examine the power of gluteus maximus and quadriceps femoris in particular as
weakness of above can lead to compensatory equinus at ankle. D/D: congenital dislocation of
ankle, tibial hemimelia

Congenital vertical talus

History:
• Deformity in foot present since birth (often noticed when patient starts to walk)
• Toeing out when walking
• Difficulty to fit shoes
Examination:
• Severe uncorrectable equino-valgus deformity of hindfoot.
• Rocker bottom foot (loss of medial longitudinal arch with prominent rounded talar
head as lowermost part of arch).
• Forefoot is abducted, pronated and dorsiflexed with fixed dorsal subluxation of
navicular over talar head.
• Lateral toes are outward looking and everted.
• Soft tissues (tendons of tibialis anterior, long toe extensors and 3 peronei) on
dorsolateral side of foot are contracted.
• Deep creases inferior and lateral to lateral malleolus.
• Tendo-Achilles contracture
• Callosities beneath anterior end of calcaneus and along medial border of foot
superficial to talar head.
• Tendons of peroneus longus, brevis and tibialis posterior are tight and may come to
lie anterior to malleoli (acting as dorsiflexors rather than plantar flexors).
Essential components of deformity:
– Fixed equinus at ankle
– Fixed dorsal dislocation of navicular over talar head)
Always additionally examine spine (for meningo-myelocele, neurofibromatosis), hips and
knees (equino-valgus may be compensatory to knee deformity!).

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Supination and pronation of foot
Supination is a combination of:
• Adduction at fore foot
• Internal rotation and plantar flexion at ankle
• Inversion at subtalar joint
• Medial arch elevation Pronation is a combination of:
• Forefoot abduction
• Hindfoot eversion
• Dorsi flexion at ankle
• Depression at medial arch

When do you say it’s post-polio residual paralysis

1.Asymmetric, patchy, lower motor neuron type paralysis (AFP)
2.Non progressive
3.No sensory loss
4.Prior paralytic poliomyelitis with evidence of motor neuron loss, as confirmed by
history of the acute paralytic illness, signs of residual weakness and atrophy of
muscles on neuromuscular examination, and signs of nerve damage on
electromyography (EMG).
5.A period of partial or complete functional recovery after acute paralytic poliomyelitis,
followed by an interval (usually 15 years or more) of stable neuromuscular function.
6.Symptoms that persist for at least a year.

Commonest deformity in polio foot

Most common is equinovalgus (tibialis anterior paralyzed) followed by
calcaneocavovarus and then equinovarus.
(Valgus is more common than varus).

What is ideal age for tendon transfers and bony procedures in polio
Wait for at least one and a half years after the paralytic attack, i.e., after convalescent
stage has passed off and residual stage has started. The following principles apply:
– Tendon transfers in skeletally immature patients
– Extra-articular arthrodesis between 3-8 years

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 – Triple arthrodesis after 10-11 years
– Ankle arthrodesis after 18 years

Ideally tendon transfers should be done after 5 years when the child can be trained
adequately for rehabilitation.

Results are, however, better after age of 10-11 years. This should be supplemented
with bony procedures (esp.arthrodesis) which should be done before or along with
tendon transfers. Bony blocks to prevent opposite motion may be necessary with tendon
transfers, esp. in children.

This is because in pediatric patients, growth along with slight muscle imbalance even
after tendon transfers causes recurrence of deformities. For example, if tendon is transferred
to cause dorsiflexion of ankle, then posterior bony block to prevent plantar flexion may be
done simultaneously.

First the plantar and dorsiflexion movements are to be balanced before inversion and
eversion. Among the two, plantar flexion strength is to be regained first. If sufficient muscles
are not available for transfer, then joints are to be arthrodesed. For example, if invertors and
evertors are not available, do triple arthrodesis so that only plantar and dorsiflexors are
needed to be balanced.

It is better to be too tight than to be too loose when attaching tendons to new
locations. It is better to wait for 3 weeks in upper limbs and 4-6 weeks in lower limbs for
physiotherapy to start after tendon transplants.

Surgical stabilization of joints (arthrodesis) is ideally done after skeletal maturity.

You should know the actions of groups of muscles namely tibialis anterior, tibialis posterior,
long toe dorsiflexors, long toe plantar flexors and peronei. Transfer to midline if only plantar
and dorsiflexion are to be balanced. If you need eversion, transfer it laterally and transfer
medially if inversion is needed. For example, if you need to transfer a muscle to gain
dorsiflexion and eversion, transfer it to dorsal tarsus (to gain dorsiflexion) and among the
tarsal bones, laterally (to gain eversion).

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Deformity progresses till bone and soft tissue growth ceases. Any splint/passive stretching
cannot prevent development of a deformity. It can only slow down the process.

What is the aim of treatment in foot surgery in polio

Aim is to get a foot which is
• Stable–no abnormal varus/valgus in hindfoot and ankle on weight bearing
• Plantigrade – even distribution of weight on hindfoot, midfoot and forefoot on weight
bearing.
• No significant fixed deformity–without any inversion eversion deformity, with foot to
be able to be brought to right angle passively.
• Adequate muscle power– >3 power in active dorsi and plantar flexors of ankle, i e.,
sufficient power to clear the toes off the ground

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 EXAMINATION OF THE ELBOW JOINT

History:

Handedness Pain Deformity Swelling

Activities of daily living – inability to perform stuff
 H/O trauma (especially note mode of trauma, duration, treatment, h/o massage,
complications, management ever since)
 H/o fever
 H/o septic arthritis,
 H/o increased tendency to bleed/ haemophilia, H/o tuberculosis,
 H/o Hansen‘s disease,
 H/o morning stiffness
 Symptoms of numbness/paraesthesia(ulnar neuritis) H/o weakness
 H/o previous surgery, H/o steroid injections

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,
Wasting of the muscles – arm and forearm
Assessment of normal anatomy ,three point bony relationship, cubital fossa, anconeus
triangle
Para olecranon fossae

Attitude:
Alignment of forearm in relation to arm (carrying angle) compare from normal, flexion
deformity.

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 • From front: Flexion crease (1-2 cms above joint line it is at the level of
interepicondylar axis), swelling (epitrochlear lymph nodes, etc.), medial and lateral
epicondyle, biceps tendon and lacertus fibrosus, common extensor and flexor origin
mass. Widening of the circumference of the distal end of the humerus as a whole.
• From lateral aspect: Anconeus triangle and fullness over soft spot, common extensor
origin, prominence of triceps tendon (elbow dislocation), olecranon process, radial
head (dislocation), olecranon bursa, biceps mass.
• From medial aspect: Medial epicondylar prominence, supracondylar depressions,
common flexor origins
• Posterior aspect (in 90º flexion): Olecranon process, triceps bulge, paraolecranon
fossae, three point relationship.
Palpation
• Superficial palpation: Temperature, superficial tenderness
• Deep palpation:
– Epicondyles, olecranon process, olecranon fossa radial head, capitellum
(Panner’s disease)
– Swelling with all characteristics (site, size, shape, surface, margins,
consistency, tenderness, compressibility/ reducibility, pulsatility)
– Supracondylar ridges:
Palpate both medial and lateral ridges simultaneously for tenderness,
irregularity, thickening,broadening, discontinuity, spur, loss of contour
– Three-point bony relationship( medial epicondyle,olecranon and lateral
epicondyle) compare with the opposite side
– Mass in the cubital fossa - to r/o myositis ossificans
– Medial and lateral condyle
– Radial head
– Ulnar nerve (thickening, subluxation, tenderness) in the cubital tunnel
– Joint line (for tenderness)
– Supratrochlear/epitrochlear lymph nodes
– Anconeus triangle (b/w the olecranon , radial head and the lateral
epicondyle)
– Collateral ligaments
– Brachial artery pulsations Movements

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 Flexion(0-140degree) & Extension(0-5degree)
Supination(80 – 90degree) & Pronation (80-90deg) (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: Measurements

• Linear measurements:
– Arm length (medial and lateral): Lateral length measured from angle of acromion to
lateral epicondyle, medial length is measured from medial epicondyle to an imaginary
soft tissue point on the inner aspect of arm just against the deltoid insertion.
– Forearm length: Lateral length measured from lateral epicondyle to radial styloid
process and medial length from medial epicondyle to ulnar styloid process.
– Three point relationship measurements (in 90º flexion):
Measurement of olecranon tip to lateral and medial epicondyles and interepicondyler
distance.
• Angular measurements: Angle formed between arm and forearm axis. (Axes are
marked by joining the mid-point of lines joining the above bony points, viz. epicondylar line
at elbow, interstyloid line at wrist, line joining deltoid insertion and a point against it).

• Circumferential measurements: For wasting – measure midarm circumference and

forearm circumference at a convenient point (usually 7 cms below medial epicondyle).
Neurological examination:
Motor power of elbow flexors, extensors, supinators, pronators, biceps jerk, triceps jerk and
supinator jerk and sensory testing.
Lyphadenopathy

Special Tests
• Varus stress test: Test in 30° flexion to disengage olecranon.
• Valgus stress test: Test in 30° flexion
• Pivot shift test (for posterolateral rotator instability): For anterior ulnar collateral
ligament by applying valgus and axial compressing forces to elbow and supination torque to

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forearm. This maneuver produces rotator subluxation of ulno humeral joint which is
maximum at 40° of elbow flexion.
• Tests for lateral epicondylitis:
– Resisted wrist extension test
– Long finger extension test: Pain produced just distal to lateral epicondyle suggests
lateral epicondylitis (cf-radial tunnel syndrome)
– Cozen’s test: To an extended elbow and wrist ask the patient to make fist and
passively flex the wrist
– produces pain at the common extensor origin
– Mill’s maneuver: With wrist and elbow extended pronate forearm.
• Resisted pronation: For pronator syndrome
• Resisted flexion and pronation: For medial epicondylitis
• Elbow flexion test for cubital tunnel syndrome.
• Long finger extension test: Pain produced 4 finger breadths below lateral epicondyle
suggests radial tunnel syndrome
• Resisted elbow flexion and resisted forearm supination: For median nerve
compression at lacertus fibrosus

Also examine the shoulder and forearm as the compensations of elbow movements are often
taken up at shoulder and the ill effects are often sustained by forearm

Prerequisites of elbow examination

 Examine both elbows together.
 Examine both elbows in identical position.
 Expose whole upper limb from shoulder girdle to fingers.
 Arms lying by the side of chest is the most comfortable position for the patient.

Interpretations of three point relationship measurements

The olecranon, lateral and medial epicondyle form a nearequilateral triangle in 90°
flexion at elbow. In disruptions of elbow joint, the measurements are altered and can be
interpreted as below:
- Decreased length of medial limb: Posteromedial dislocation, medial rotation of
fractured fragment
- Decreased length of lateral limb: Posterolateral dislocation, lateral rotation

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 - Increased length of medial limb: Fractured medial epicondyle/condyle
- Increased length of lateral limb: Fracture lateral condyle
- Increased base (interepicondylar distance): Malunited fracture intercondylar
humerus.

Fallacies of three-point relationship

• Displaced fracture of medial/lateral epicondyle
• Surgical intervention done leading to altered morphology and inability to palpate
epicondyles
• Excision arthroplasty of elbow
• Lateral spur formation
• Ankylosed elbow in extension
• Charcot’s arthropathy

Importance of Anconeus triangle

The triangle is bounded by radial head, lateral epicondyle and olecranon tip. The
triangle directly overlies joint capsule and anconeus muscle so this ‘soft spot’ becomes
distended early in effusions of elbow joint. Synovial biopsy from elbow joint, injections into
elbow joint can be directly given by approaching this triangle. Anconeus is an important
muscle in EDS studies and can be easily approached here.

How do you look for rotational deformities at elbow joint

Internal/external rotational malalignment at elbow can be measured by measuring the
external and internal rotation at shoulder in 90° abduction and while the arm is by the side
(the movements are to be always compared from other side). Internal rotation deformity at
elbow will restrict external rotation at shoulder and complementary increased internal
rotation. This deficit or excess can be measured and is a quite accurate measure of deformity.
For this measure to be effective there should be no rotational limitation at shoulder or
torsional deformity of humerus and that the deformity should be unilateral. (Remember that
this measure is often only an approximation as the dominant shoulder has an increased
physiological rotation giving fallacious comparison for deformities of left elbow and
masking the ipsilateral deformities)

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 Alternative method (Yamamoto et al): Make the patient bend forward and fully
internally rotate and hyper-extend the shoulder (in an attempt to touch the back). Lift the
hand off the back (in a normal the hand can either be not lifted up or it is minimal). The angle
made by forearm to the horizontal when compared to the opposite side gives an idea of
internal rotation deformity.

How do you palpate for radial head

Locate lateral epicondyle with elbow flexed to 90° then go just in front of it where a
depression is first felt immediately stopped by bony silhouette of radial head.
Confirm by gently rotating forearm for transmitted supination and pronation.

How do you look for flexion deformity of elbow

Make sure that the interepicondylar line is horizontal to the ground before assessing
the flexion deformity.
(Note – in the presence of flexion deformity, never comment on valgus deformity as even the
physiological valgus varies with flexion of elbow. Similarly, however, one can say that there
is varus deformity but do not attempt to quantify (measure) it when flexion deformity
coexists as classically these measurements have been described in elbow extension).

What are the various restraints to elbow joint?

Dynamic:
Anconeus, triceps, brachialis

Static:
• Primary
– Ulnohumeral articulation (only stabilizes in <20deg and >120deg flexion)
– MCL
– LCL
• Secondary:
– Radial head
– Capsule
– Common flexor pronator and extensor origin
Stabilizers of elbow for various stresses:

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 Valgus stress:
• Primary:
MCL
• Anterior bundle: Principle-stabilizer in 30º-120º flexion
• Posterior bundle: Co-restraint
• Secondary: Radial head
• Tertiary: Flexor-Pronator muscle groups (FCR,FDS)

Varus stressPrimary:
– LCL and annular ligament complex
• Secondary:
– Extensor muscles with fascial bands
– Intermuscular septa

How much functional range of movements is required at elbow joint?

For activities of daily living 100o flexion with the functional range of arc from 30deg-
130deg and 100deg rotation (50deg each of pronation and supination) is required.

Various causes of stiff elbow?

• Post-traumatic
- Joint incongruity
- Dislocation/Subluxation
• Heterotopic ossification
• Burns
• Coronoid/olecranon/Radial osteophytes
• Loose bodies
• Triceps/Biceps adhesions
• Chronic infection
• Inflammatory arthritis
• Patient non-compliance
• Post surgery.
How will you differentiate extrinsic from intrinsic stiff elbow?
Intrinsic stiff elbow gives a bony stop to movements while extrinsic stiffness presents
with comparatively soft stop. There is associated deformity in coronal plane in intrinsic

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stiffness. Movements are grossly painful in intrinsic causes due to early development of
arthritis. In extrinsic causes the contracture stands out on pursuing movements. Wasting of all
groups of muscles is more evident in intrinsic stiff elbow.

How to manage patient with stiff elbow ?

Evaluate with radiological investigations (X-ray and/or CT) and then categorization
and management as below:
• Acute: ORIF, continuous passive motion, splints (dynamic and static)
• Sub-acute (<6 months): Splints, anti-inflammatory drugs, close follow-up
• Chronic (> 6 months): X-ray ± CT scan
- Ectopic ossification present
- No ectopic ossification:
 Extrinsic causes: Release
 Intrinsic causes:
– Articular: Soft tissue release or distraction arthroplasty for acceptable
surfaces otherwise elbow arthroplasty (>50 per cent cartilage destroyed)
– Impingement: Coronoid/Olecranon: Excision of bony stop.

What is Column procedure

Posterolateral incision  Dissection between ECU and Anconeus. Separate extensor
tendon from joint capsule and LCL. Expose anterior capsule and release it as wide as
possible. For posterior release dissection proceeds between ECRL and triceps and posterior
capsule is released. Look for and excise the olecranon and coronoid osteophytes. Immediate
CPM is begun followed by dynamic splintage after 3 weeks and gradual weaning over 3
months

What is distraction arthroplasty

Keeps the injured articular surfaces distracted while simultaneously providing joint
motion and protection to collateral ligaments.
Indications:
• Adjuvant to capsule release if ligaments are damaged, or
• Significant dissection making intraoperative motion difficult, or
• > 50 per cent joint surface void of cartilage, or
• Modified joint contour.

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What is fascial interposition arthroplasty
It is an alternative for a poorly articulated or ankylosed joint where painless
movements are desired and elbow replacement cannot be done. Indications:
1. Young patients with post-traumatic ankylosis of elbow with intact broad
contour of distal humerus.
2. Young adult stage I and II rheumatoid arthritis with intact bone.

What materials can be used for interposition arthroplasty

Natural: Fascia, fat patch Synthetic: Synthetic membranes

Ectopic ossification
Formation of bone at abnormal places. Types:
• Heterotropic ossification: Formation of mature lamellar bone in non-osseous tissue
(dystrophic process involving ligaments and capsule; can be metastatic).
• Myositis ossificans (a misnomer): Benign localized reactive proliferative lesion
occurring within soft tissues (muscles) that normally do not ossify.
• Periarticular ossification: Collection of calcium pyrophosphate crystals in soft tissue
(lacks trabecular pattern).

Various causes of myositis ossificans

Classified into three types (etiological classification):
1. Traumatic (myositis ossificans circumscripta, myoosteosis, ossifying hematoma):
Contusions, tearing, post-operative.
2. Neurogenic: Injury to neural axis
3. Myositis ossificans progressiva – inherited disorder More than 1/3rd cases are
idiopathic.

Which muscle is commonly involved in myositis ossificans at elbow

Brachialis muscle, others can be pronator teres and brachioradialis.

What are the clinical features of myositis ossificans

Clinical features depend upon the phase in which patient is seen:

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 • Acute/pseudoinflammatory phase (3rd day – 3rd week): pain, swelling and  ROM
• Subacute/Pseudotumor phase (3-6 weeks): painless hard mass with raised temperature
locally.
• Maturation (3-6 months)
• Resolution (few cases only).

Differential diagnosis of myositis ossificans

The following are often confused with myositis ossificans:
1. DVT in acute phase
2. Osteogenic sarcoma
3. Mesenchymal chondrosarcomas
4. Synovial sarcoma
5. Calcified lipoma
6. Hemangiomas (phleboliths).

What is ‘zonal’ phenomenon

This applies to the functional orientation of fibroblasts to osteoblasts in all ossifying
masses. Myositis ossificans matures from inside to outside. Center is less mature (higher
mitotic figures and cellular atypia), mature cells in periphery. ‘Reverse zoning’ is seen in
tumours. This helps differentiate myositis from otherwise very difficult to differentiate
osteoid forming tumours typically osteosarcoma histologically.

What are the available treatment modalities for ectopic ossification Prophylaxis:

• Chemotherapeutic agents:
- Acute phase: Ice, compression, maintainance of ROM (CPM), support the limb, avoid
massage/forceful passive mobilisation.
- Bisphosphonates: Merely delay the appearance of mass recommended now
- NSAIDS: Started on the first post-operative day and continued for 2 weeks
- Calcitonin ? efficacy – also not recommended
- Thalidomide (for myositis ossificans progressiva)

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• Radiation therapy: Low dose external beam radiation within 96 hrs (20Gy/10
fractions. Coventry (1981) is recommended, other regimes are 10Gy/5 fractions, 6-8
Gy/5 fractions) Excision: Surgery

When to diagnose as a Post-traumatic malunited supracondylar fracture?

History of trauma with relevant treatment. On examination:
• Irregularity over medial and lateral supracondylar ridges
• Maintained three-point relationship
• Medial epicondyle tip is higher
• Hyperextension at elbow
• No widening at intercondylar region
• Internal rotation deformity with restricted external rotation and increased
internal rotation
• No deficiency in the region of trochlea.

Why is supracondylar fracture so common and why does it occur at this site
The following reasons account for the same:
1. Thin wafer of bone
2. Olecranon impinges at the fossa with leverage and delivers point stress
3. Soft tissues often are lax in children which account for possible hyperextension
4. The bone is actively undergoing remodeling at the site during 6-10 years of age
5. Large number of actively growing physes in vicinity account for increased vascularity
at the region and resultant relative hyperemia.
6. Periosteal attachment to olecranon fossa (results in constant transcondylar failure), the
capsule is tight anteriorly and hinges the olecranon tip against fossa.

What is the cause for a higher frequency of posteromedial type fracture

The following bring the distal fragment medially:
1. Pronation of forearm at fall
2. Eccentric pull of biceps
3. Medial column collapse
4. Oblique fracture line.

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What are the displacements of a supracondylar fracture
1. Medial displacement
2. Medial tilt
3. Internal rotation
4. Posterior displacement
5. Posterior tilt
6. Proximal migration

Associated deformities with cubitus varus

Cubitus varus (medial tilt and lateral angulation) is accompanied with:
1. Internal rotation
2. Extension of distal fragment
3. Shortening
4. Medial shift

Cause of fishtail deformity

This is seen in old supracondylar fractures and is due to osteonecrosis of trochlea
producing a smooth gentle curve. Trochlea is supplied by two sources. A distal fracture line
disrupts the supply to lateral part of medial trochlear crista that comes through medial
condyle. The other type of sharp angular wedge is seen after fracture of lateral condyle and is
due to persistence of gap between lateral condular physis ossification center and medial
ossification of trochlea.

Causes of cubitus valgus deformity

1. Non-union fracture lateral condyle
2. Malunited supracondylar fracture humerus
3. Osteonecrosis of lateral trochlea
4. Malunited intercondylar fracture
5. Radial head fracture dislocation
6. Medial epiphyseal injury and growth stimulation.

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Why do you call it fracture of lateral condyle
1. Disturbed three-point relationship
2. Lateral supracondylar ridge thickening
3. Widening of intercondylar region
4. Flexion deformity
5. Tenderness
6. Abnormal mobility of lateral condyle
7. Varus stress test positive
8. Ulnar nerve (may be involved as ulnar neuritis).

When do you call lateral condylar fracture to be not united

After 12 weeks (3 months)

Reason why is non-union common in lateral condyle fractures

The following factors have been put forward:
1. Poor circulation to metaphyseal fragment: Only a very small portion of lateral condyle
is extra-articular and nearly all of blood supply enters from here. Damage to the same
is quite common (trauma/iatrogenic) causing non-union and osteonecrosis.
2. Fragment bathed by synovial fluid
3. Forces exerted by muscles arising from condylar fragment keeping it displaced
4. Displaced fragment with opposition of articular cartilage to the proximal fracture
surface
– in this scenario union is impossible

Why is the cubitus valgus of concern

Not all cubitus valgus deformities will concern us, but particularly the one from
lateral condyle non-union or sometimes with united # is “progressive”. This may lead to
changed elbow mechanics or neurological complications or both and thus concerns us.

What are the causes of progression

1. Non-union with progressive lateral and proximal migration (type II)
2. Damage to ossification center (type I)
3. Bony bar formation (type I and II)

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4. Overgrowth of medial condyle (theoretical).
How does tardy ulnar nerve palsy develop
Tardy ulnar nerve palsy develops due to:
1. Stretching of nerve due to medial angulation and hence resulting lengthier course
2. Friction induced perineuritis, and
3. Adhesions causing entrapment of the nerve in cubital tunnel

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 EXAMINATION OF THE WRIST JOINT
History taking
Try to first ascertain what you are dealing with – deformity/neurological condition/painful or
inflammatory condition,
• Pain: Onset (injury/spontaneous; acute/insidious), type, location, duration, remote
injury (RSD), aggravating and relieving factors, activity restrictions, guarding of wrist
and hand.
• Swelling: Onset (as above), location, duration (also whether temporary or
permanent), relieving and aggravating factors, flare-ups (severity, frequency, duration),
previous treatment if any, association with fever/stiffness, discolouration.
• Deformity: As above + abnormal contours, palm and finger alignment.
• Loss of function: (A key factor as hand in itself is an organ, 45 per cent of hand
function is utilized for grasp, 45 per cent for pinch (key, tip, chuck pinch), 5 per cent for hook
function and in rest 5 per cent hand functions as a paper weight (most primitive function))
• Loss of power: Any decreased strength or dexterity. Apart from above it is very
important to ask for history of hospitalizations and treatment (type, dose, frequency, response
and side effects), details of trauma if present, dominant hand, effect on occupational
functioning and ADL.
Examination Inspection Alignment
• Whether viewed from dorsal or volar aspect with fingers and thumb in adduction – the
forearm, wrist and hand (middle finger) should be in a straight line (axial alignment). Ulnar
deviation of MCP joint and radial deviation of wrist are observed in rheumatoid arthritis
(RA).
• Dislocation of PIP joint is visible as a step off (sagittal malalignment). Rupture of
extensor slip in RA produces flexion deformity of fingers at MCP joint (Vaughan-Jackson
lesion). Dinner fork deformity is seen in Colle’s fracture.
• Rotational malalignment is judged in two ways:
– Ask patient to partially flex the fingers together at MCP joint – nails of index finger
and those of ring and little finger face away from that of long finger in supinated hand.
– Ask patient to flex fully each finger in turn – the fingers should unfailingly point
towards the scaphoid tuberosity.
Dorsal aspect:

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 • Nails: vasculitic changes (local infarction – RA), splinter haemorrhage, periungal
telengiactases (SLE, scleroderma), pin-size pitting (psoriasis), hyperkeratosis, onycolysis,
discolouration, ridges, anaemia, dilated capillary loops over nail fold, paronychia, subungal
haematoma.
• Fingers (examine from DIP to MCP): Mallet finger (avulsion of EDC, EPL for
thumb), redness, sausage shaped digits, nicotine stains, arthritis mutilans, tophi, swan neck/
boutonniere deformity, Z-deformity of thumb, Bouchard’s nodes, Heberden nodes, Garrod
pads, ulnar deviation, benediction attitude, clawing of fingers, contractures, telengiectasia,
mucous cyst, inclusion cyst, sebaceous cyst, skin and appendages (normally there are no hair
from MP and distal).
• Hand: Dropped knuckle (# metacarpal), wasting in first web space, wasting of interossei,
skin and appendages, carpal bossing.

• Wrist: Head of ulna (prominent in pronation disappears in supination), silver fork

deformity, ulnar deviation, volar subluxation, volar-ulnar subluxation, cystic swelling
(ganglion).
Radial aspect:
• Thumb and 1st MCP joint : (gamekeeper’s thumb), swelling (1st MCP arthritis).
• Wrist: Anatomical snuffbox (bound dorsally by EPL and volarly by APL and EPB)
for swelling.
Volar aspect:
• Fingers and palms: As above + pulp spaces for pits (Raynaud’s phenomenon) and
swelling (Felon), swelling over volar aspect of finger (GCT tendon sheath or cystic swelling),
jersey finger (avulsion of FDP), flexion arcade of fingers, palmar skin for pits and cords/
nodules (Dupuytren’s contracture), signs of flexor tendon sheath infection (Kanavel’s signs –
fusiform swelling extending along MP and PP into distal palm + tenderness along volar
aspect + finger held in flexed position + passive extension causes pain), thenar and mid
palmar spaces for infection, thenar and hypothenar wasting.
• Wrist: As above + tendon of Palmaris longus (ask patient to touch the tips of thumb
and little finger and flex the wrist – tightens the palmar fascia and makes tendon prominent),
FCR, FCU, compound palmar ganglion.
Ulnar aspect:

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 • Hypothenar wasting, head of ulna (capita ulna syndrome – in RA the volar
subluxation of carpals and dorsal subluxation of ulnar head accentuates the deformity with
prominent head of ulna).

Palpation
Make a note of temperature.
Dorsal aspect
• Fingers: for mallet finger, collateral ligaments especially for thumb, joint swelling and
effusion, MCP joint for collateral ligament tenderness.
• Metacarpals for deformity, tenderness, first metacarpal base for Bennett’s fracture.
• Wrist for radial styloid, De Quervain’s disease (tenovaginitis of 1st dorsal
compartment – APL, EPB), lister tubercle (2 cm ulnar to radial styloid), anatomic snuff box
(for dorsal branch of radial artery, # scaphoid, 3-4 mm distal to it is basilar joint), 2nd dorsal
compartment (ECRL, ECRB, intersection syndrome, ganglion is most likely to occur
here), 4th dorsal compartment (EDC tendons in RA), TFCC just distal to ulnar styloid.
Palmar aspect
• As in inspection confirm the findings of felon, flexor sheath infection, mid-palmar
space, thenar space
• Swelling of ganglion, GCT tendon sheath, trigger finger (catching of tendon in pulley)
• Tubercle of scaphoid, hook of hamate, pisiform, pisiohamate ligament and Guyon’s
canal, FCR, median nerve (between Pl and FCR), volar carpal ligament (proximal limit
corresponds with the distal radial crease).
Movements
Wrist motion (with elbow flexed in 90º) – dorsiflexion (60-70º), palmar flexion (60-80º),
radial (20º) and ulnar deviation (30-40º)

Finger movements:

Flexion at DIP (70-90º), PIP (110º), MCP joint (80-90º).

Hyperextension at MCP joint is quite normal and is maximum at Index finger (up to 70º).
Other method is to measure the finger tip to transverse palmar crease distance for serial
assessment and follow-up.

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Restricted flexion at IP joints can be due to capsular contracture/ intrinsic contracture
or extrinsic tightness - Perform Bunnell-Littler test to differentiate the two. Passively flex
the IP joint with MCP in extension followed by MCP in flexion. Restriction due to intrinsic
muscle tightness will increase the passive flexion at IP joint with MCP flexion due to
relaxation of intrinsic muscles. In extrinsic tightness the flexion decreases due to tightening
of structures with MCP flexion hence restricting flexion further.

Abduction and adduction: Abduction and adduction is possible at MCP joint due to
“cam effect” – the metacarpal heads are shaped like cam (larger volar articular component as
compared to linear distal) so that in extension the collateral ligaments are lax allowing
movement in coronal plane (this is also the reason for ‘James position’ of immobilization).
This is not possible at IP joints – bicondylar joints without a ‘cam’. The presence of
abduction and power of adduction is more important than the range of abduction! (just
compare with other side).
Thumb movements: Flexion, extension, adduction, abduction, opposition

Motor power and muscle/tendon function:

• Wrist flexors (FCR/ FCU), extensors (ECRL, ECRB, ECU), radial deviators (FCR,
ECRL, ECRB, APL), ulnar deviators (ECU, FCU)
• Finger flexors (FDP – hold PIP individually and ask patient to flex DP; FDS – ask
patient to flex the PIP while holding other three fingers in extension, this
defunctionalises the
FDP as it is a single unit muscle). This test is less reliable for index finger as the FDP
to IF may be separate.
 Abduction (dorsal interossei) and adduction (palmar interossei) of fingers, card test.
• Thumb flexion (FPL, FPB), radial abduction or extension (APL), palmar abduction
(APB), adduction (Adductor pollicis), opposition (APB, OP), froment’s test
(Adductor pollicis) Sensation Testing

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 Percussion:
 Tinel’s test
 Vascularity
Neurological examination for various nerves :
Special tests:
• Carpal tunnel compression tests
1. Tinel’s sign
2. Phalen’s test: Wrist flexed by gravity for 60 sec
3. Durkan’s median nerve compression test: Manual pressure over median nerve at
carpal tunnel for 30 sec
4. Reverse Phalen’s test: Wrist and fingers extended for 2 minutes
5. Tourniquet test: Arm tourniquet inflated above systolic pressure for 60 secs
6. Hand elevation test: Hand elevated above for 60 sec
7. Wrist flexion and carpal compression test: In a supinated forearm with flexed wrist
compress the median nerve with direct pressure
8. Closed fist test: Tight fist for 60 sec

• Stability testing:
1. MCP joint
2. IP joint
• Carpal instability:
1. Scaphoid shift test of Watson: Tests scapholunate instability
2. Luno-triquetral ballottement test for lunotriquetral joint
3. Mid-carpal instability

• DRUK instability:
1. Piano key test
2. DRUJ compression test

• TFCC test: TFCC compression test

• Grind test for basilar (trapezio-metacarpal joint) joint arthritis
• Finkelstein test for de Quervain’s disease.
• Allen’s test for radial and ulnar arterial circulation

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 EXAMINATION OF A SWELLING
History
Age Sex
Swelling -
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
Swelling - Site
Size Shape Number
Surface – irregular/ smooth Borders – well defined/ ill defined Surrounding area
Consistency
Plane of the swelling
Mobility Translucency Pulsation 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.

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 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

When do you call it a benign swelling

history suggests that swelling appeared insidiously followed by pain with chronic duration}.
On inspection:
• The skin is not stretched or shiny smooth.
• There are no dilated veins.
• There is no discolouration.
• There are no secondary skin changes (inflammation, ulcer formation or fungation,
loss of skin appendages)

On palpation:
• Local temperature not raised.
• Non-tender swelling
• Well-defined edge (margins are for ulcer!)
• Smooth surface
• Not-tethered to skin or surrounding soft tissue
• No pain on bearing weight or movements
• No evidence of pathological fracture

How do you determine that the swelling is fixed to or emanating from bone
The swelling is continuous with bone while palpating the edges of the swelling. There is no
intervening tissue between bone and swelling. The swelling congruently moves with the
movements of bone. The swelling arises from beneath the muscles which overlie it.

What other areas/systems should you examine?

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

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How will you differentiate that the swelling is below the muscle or above it
Ask the patient to tense the muscles overlying the swelling by appropriate resistive
maneuver, e.g. pressing the knee down for an anteriorly located lower thigh swelling.
Observe the following:
• Movement of the swelling in the direction of muscle fibers and perpendicular to it
• Prominence of swelling
If the swelling becomes more prominent on tensing the muscle it indicates that the swelling
overlies the muscle otherwise disappearance of swelling suggests that it is deep to the
muscles. A swelling arising from the muscle itself shows variable change depending upon
where it lies within muscle fibers and the support for swelling increases if it lies in the
superficial fibers making it more prominent and vice versa. Now here the assessment of
mobility takes an important role.
The mobility of a swelling that overlies the muscle is not changed while that of a swelling
arising from muscle is lost when movement is attempted in the direction of fibers or
perpendicular to a taught muscle. (Swelling that underlies the muscle often disappears
unless it is large and bony or stony hard!)

How do you determine if a swelling is soft/ firm/hard on clinical examination

A stony hard swelling is not indentable offering some friction or a ‘gritty feeling’ to the
examining hand. Bony or woody hard swelling is also not indentable but is smooth or
lobulated. Rubbery swelling is hard to firm or firm like touching the nose tip. A swelling that
is soft and squashable offering some resilience is ‘spongy’. Swelling feeling like your ear
lobe (spongy and squashable) is a ‘soft’ swelling.
Bony swelling may have some typical surface characteristics like ‘crackling egg-shell
consistency’ of a giant cell tumour (GCT), variable consistency (firm on surface to bony hard
at pedicle) for an osteochondroma.
Swelling may be indentable like a ‘ping pong’ ball in aneurysmal bone cyst (ABC).

Differential diagnosis
• Epiphyseal lesions: Chondroblastoma, chondrosarcoma, giant cell tumour
• Metaphyseal lesions: Any lesion!
• Diaphyseal lesions: Ewing’s sarcoma, osteoblastoma, lymphoma, adamantinoma, fibrous
dysplasia, eosinophilic granuloma
• Flat bones: Ewing’s sarcoma, metastasis, myeloma, chondrosarcoma

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 • Vertebral body: Giant cell tumour, metastasis, Ewing’s sarcoma, eosinophilic granuloma
• Posterior elements of vertebra: Aneurysmal bone cyst, osteoid osteoma, osteoblastoma.

What is sulcus sign

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

How do you stage benign bony swellings

In Enneking classification the benign bone tumors are classified according to activity of the
tumour:
• Latent: Remains static or heals spontaneously like nonossifying fibroma
• Active: Progressive growth limited by natural barriers like ABC
• Aggressive: Progressive growth, invasive, not limited by natural barriers like GCT.

What is Enneking classification of bone tumours

Enneking classified the malignant and benign bone tumours.
Enneking classification of malignant bone tumors is based on a combination of parameters
(grade of tumor
(G1 – low grade, G2 – high grade), compartment involved
(T) and metastasis (M)).

Compartment is defined as a natural barrier to tumour extension like bone, fascia, synovial
tissue, periosteum or cartilage. The tumour may be intracompartmental (T1) or
extracompartmental (T2).

Stage Grade Site Metastasis

IA G1 T1 M0 IB G1 T2 M0 IIA G2 T1 M0 IIB G2 T2 M0
III G1/G2 T1/T2 M1
Stage I is a low grade tumour while II is high grade one.
Sub-stage ‘B’ means an extracompartmental tumor and stage’A’ means inracompartmental
III is a metastatic tumour.

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 How will you stage a primary bone malignancy? 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.

What is a compartment? Give examples

Compartment is an anatomical region surrounded by natural anatomic barriers that
resist spread of neoplasm. Examples are intraosseous lesions, subperiosteal space, muscle
compartments etc.

What neoplasms are extracompartmental from the beginning itself?

Lesions that arise from popliteal fossa, sole of foot, palm of hand, cubital fossa, axilla,
inguinal region etc. are considered extracompartmental from the beginning.

What will you see on an X-Ray

Specifically I will look for parent bone and changes (site, extent, cortical breach, etc.),
tumour mass, destruction pattern, periosteal reaction and tumour mineralization patterns
(osteoid, chondroid, reactive bone mineralization).

What are the various types of periosteal reactions

Takes 10 days to three weeks to appear:
• Type I: Solid periosteal reaction
– Shell formation: Simultaneous bone removal of bone from endosteal surface with
surface deposition of bone. Thickness depends on the balance between the two
– Smooth shells: Associated with benign tumours
– Lobulated shells: Due to focal variation in growth rate
– Ridged shell: Trabeculated, septated or soap-bevel reaction. This is due to uneven
destruction. Seen in non-ossifying fibroma, GCT, ABC, enchondroma and some
malignant tumours like chondro/fibrosarcoma, plasmacytoma and metastasis from
thyroid, melanoma, renal.
• Type II: Continuous periosteal reaction with cortical persistence

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 – Solid periosteal reaction: Multiple layers of bone deposition due to chronic
stimulation of bone by a relatively slow growing bony lesion, e.g. osteoid osteoma,
sub-acute osteomyelitis. It is referred to as cortical thickening or hyperostosis.
– Single lamellar reaction: Single layer of new bone in the form of a uniform
radiodense line considered hallmark of benign process, e.g. histiocytosis X, osteoid
osteoma,
• Dense undulating periosteal reactions are a variant seen with low-grade osteomyelitis,
osteoarthropathy associated with paraneoplastic lesions or varicose veins, periosteitis
– Lamellated reactions: Seen with active bone-destroying lesions like acute
osteomyelitis, Ewing’s sarcoma and osteosarcoma
– Parallel speculated reaction: (Hair-on-end appearance) seen with more rapidly
destroying malignant process due to bone formation along the radial
neovascularisation
• Type III: Interrupted periosteal reactions seen with aggressive tumours reaching
sub- periosteal location after cortical breach:
– Buttress: Solid bone formation at cortical margins of a slowly but constantly growing
lesion
– Codman angle: Represents the buttress lesion in an aggressive neoplasm. First
described by Ribbert was elaborated upon by Codman in 1926. It can be seen in any
lesion that aggressively lifts the periosteum like acute osteomyelitis, ABC, osteoma,
osteosarcoma, chondrosarcoma. They result from subperiosteal bleeding and bone
formation and are themselves free from tumour!

• Type IV: Complex periosteal reactions

– Divergent speculated pattern aka sunburst pattern:
Combination of reactive bone formation and malignant bone formation, it contains areas of
reactive and sarcoma bone with intervening areas of cellular tumour and tumour products.
It is highly suggestive of osteosarcoma but can also be seen in osteoblastic active metastasis
and haemangioma.

What are the various types of bone destructions

Bone destruction has to be analyzed on the following grounds before grouping them:
1. Pattern of bone destruction and configuration of marginal interface

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 2. Cortical breach
3. Presence of sclerotic rim
4. Expansion of parent bone

Type I: Geographic bone destruction:

A. Geographic lesion with sclerotic margin: Seen in nonossifying fibroma, unicameral
bone cyst, chondroblastoma, fibrous dysplasia
B. Geographic lesions without sclerotic margins: GCT
C. Geographic lesions with ill-defined margins: Seen in GCT, fibrosarcoma, and
chondrosarcoma. Aggressive benign neoplasms such as enchondroma,
chondroblastoma, desmoplastic fibroma.

Type II: Moth-eaten destruction (regional invasion): Multiple scattered holes that vary in
size interspersed with apparently preserved bone. This pattern is seen in Ewing’s sarcoma,
primary lymphoma, chondrosarcoma, fibrosarcoma and osteosarcoma, sometimes acute
osteomyelitis.

Type III: Permeative destruction: Poorly demarcated with indistinct margins. Can be seen
in numerous destructive processes not limited only to neoplastic (round cell tumours,
angiosarcoma, high grade chondrosarcoma, etc.), mechanical, inflammatory (acute
osteomyelitis) and metabolic lesions of bone.

What else would you like to do and why

I would get detailed radiological investigations to determine and plan management:
• Bone scan:
– Intramedullary extent of tumour – classically the bone was cut 6 cms proximal to the
lesion demarcated by scintigraphy
– Polyostotic disease
– Metastasis
– Biological activity of tumour
• CT scan: Bony extent and margins of tumour and cortical breach.
• MRI:
– Medullary extent

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 – Soft-tissue component and extent
– Involvement of vital structures

• Angiography:
– Tumour blood supply
– Embolisation to reduce intra-operative bleeding
– Relationship of major vessels to tumour
– Feasibility of intra-arterial chemotherapy.

Which bone tumour metastasizes to bones

Osteosarcoma

What are the principles of bone biopsy

1. Should be done at the conclusion of staging (to avoid radiological artifacts)
2. Avoid sampling error, take multiple samples from the lesion (this is necessary for
sarcomas but single specimens may suffice for carcinomas)
3. The biopsy tract should be incorporated into the planned surgical incision
4. Biopsy should be done from the representative tissue
5. Biopsy tract should be the shortest way to tumour
6. Should not violate more than one compartment
7. Should not be done from intermuscular planes
8. Should be remote from the main neurovascular bundle
9. Try not to violate the cortex and take sample from the extracortical bone tissue (to
prevent weakening the bone by creating a stress riser defect)
10. Bone window should not have any sharp corners (avoiding stress risers) –
prefer an oblong window
11. Avoid transverse incisions (prefer longitudinal incisions)
12. Do a sharp dissection, close with a sub-cuticular stitch
13. Obtain meticulous hemostasis (to avoid haematoma formation); a drain if absolutely
needed must be placed in the line of incision, or through the wound
14. For an incisional biopsy take tumour tissue, reactive tissue, pseudo-capsule, capsule
15. Biopsy should be ideally done by the surgeon going to finally operate the patient.

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 What are the various types of biopsy
1. FNAC (not very useful for sarcomas)
2. Core/Trephine biopsy using a 14-gauge needle (usually recommended for most bone
tumours)
3. Incisional biopsy (for failed core biopsy, vascular bone tumours, ABC)
4. Excisional biopsy (usually done for small lesions <2-3 ms in longest diameter).

What surgery will you do for this patient and what are the various advantages and
disadvantages of the resection procedures
Four types of excision based on the relationship of dissection plane to the tumour and
pseudocapsule.
1. Intralesional excision: Performed within the tumour mass and removes only a portion of
tissue, the pseudocapsule and macroscopic tumour are often left behind
2. Marginal excision: Dissection plane passes through the pseudocapsule, may leave
microscopic tissue behind
3. Wide (en-bloc) excision: Removal of tumour tissue, pseudocapsule, and a cuff of normal
tissue (some > 1 cms) peripheral to the tumour tissue in all directions. This is often the
desired procedure for a sarcoma but the normal tissue is a matter of controversy.
4. Radical excision: Removal of tumour and entire containing compartment, taking care of
skip metastasis 1, 2 done for benign lesions or for palliative procedures in metastases. 3, 4
for curative malignant lesion.

What is the difference between a satellite lesion and a skip lesion

“Skip lesions” are present in the same anatomical compartment; they are ‘not’ in
continuity with the main tumour mass that forms outside the pseudocapsule. “Satellite lesions”,
in turn, are formed within the pseudocapsule and are in continuity with the main tumour mass.

What is three-strike rule

The four key components are:
1. Bone
2. Nerves
3. Vessels
4. Soft tissue envelope
If any of the three key components are involved then limb salvage is not worth considering
‘three-strike rule’.

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 What are the types of chemotherapy
• Adjuvant chemotherapy: Given after surgical procedure for control of residual
tumour and metastasis or micrometastasis.
• Neo-adjuvant chemotherapy: Given before the surgical procedure and after it
(‘Sandwich technique’) often for a limb salvage procedure. It is aimed to:
– Chemotherapeutic drugs start acting immediately helping control micrometastasis
– Reduce the stage of tumour (at least 90 per cent kill is desired, if < 90 per cent then
change agents – there is no evidence of increased survival in those that do not
respond to initial/ deemed most effective agents)
– Determine the response of tumour to chemotherapy (sort of ‘sensitivity testing’ for
drugs)
– Reduce mass and vascularity of tumour
– Buy time for surgical intervention and prosthetic design.
–
• Definitive chemotherapy: For tumours that are highly chemosensitive (Ewing’s sarcoma)
• Palliative: For tumours that cannot be resected.

What is the role of radiotherapy

Adjuvant radiotherapy had been largely replaced with chemotherapy. Use of mega-
voltage and orthovoltage radiation to control micrometastasis and tumour volume reduction
has now but immensely helped the limb salvage procedures. It can be given in neoadjuvant or
adjuvant modes. Radiotherapy acts by rupture of chemical bonds of complex molecules,
generation of highly reactive free radicals and hydrolysis, direct DNA damage and
strand breakage and lastly to damage to vascularity which is quite prominent in sarcomas.
The damage is more pronounced in rapidly dividing cells (high turnover) but success is
dependent on the rate of recovery of surrounding normal tissue.

Dosage is measured in terms of Rad (radiation absorbed dose) which is a measure of

the energy imparted to the matter by ionizing radiation per unit mass (1 Rad – 0.01j/kg).
Grays (Gr) = 1 joule of energy absorbed by a mass of 1 kg tissue (= 100 Rad). Radiation is
given in daily fractionated doses resulting in repair of normal tissues but exponential kill of
tumour tissue. Multisite radiation (multiaxial radiation) protects the normal tissue from

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excessive radiation but the total energy delivered to the tumour is high often in the form of
‘limit,
movement’ (large amount of energy delivered in packets over few seconds). Tumours that are
amenable to radiotherapy are few and include Ewing’s sarcoma, osteosarcoma, myeloma.

What is neo-adjuvant chemotherapy? Why is it needed?

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.

When will you do the surgery after neo-adjuvant chemotherapy

Usually after 2 cycles of chemotherapy.

What is the most common soft tissue tumor in children

Hemangioma.

What is the most common soft tissue tumor in adults

Lipoma.

What is the most common malignant soft tissue tumor in children and adults
It is rhabdomyosarcoma for children and malignant fibrous histiocytoma for adults.

What is the most common primary benign and malignant bone tumor
Osteochondroma and osteosarcoma.

What is the most common bone tumor of hand

Enchondroma.

What is the most common secondary benign bone tumor

Aneurysmal bone cyst.

What is the most common secondary malignancy of bone

In the order – malignant fibrous histiocytoma, osteosarcoma and fibrosarcoma.

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What is the most common sarcoma of foot and ankle
Synovial sarcoma.

What is the most common sarcoma of hand

Epithelioid sarcoma.

What are the common anterior spinal tumors

Giant cell tumor, hemangioma, eosinophilic granuloma, metastasis, chordoma, multiple
myeloma.

What tumors do you find in posterior spinal elements

Aneurysmal bone cyst, osteoid osteoma, osteoblastoma.

Can you tell characteristic immunostains for some tumors

Lymphoma (+CD20), Ewings sarcoma (+CD99), Chordoma (Keratin, S100), Adamantinoma
(Keratin).

Is it benign or malignant clinically 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

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 What are the principles of doing a biopsy
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

What all tests will you send the specimen for

All specimens should be sent for both culture and histopathologic study.

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.

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 EXAMINATION OF OSTEOMYELITIS
Clinical features suggestive of chronic osteo myelitis. Symptoms:
H/o pain, swelling, discharge, fever, trauma, surgery,
discharging bone pieces, sinus fixed to bone, inability or loss of function Contact
tuberculosis LOW/LOA
Burning micturition
Upper Respiratory tract infection sore throat
Dental caries
Other joint involvement
Treatment and drug history

Signs:
fullness, swelling, redness,
skin puckered scar exposed necrotic bone, soft tissue contracture, warmth,
bony tenderness, irregular surface, fixed sinus, .
Irregular thickened bone Bony deformity
Surgical hardware Lymphadenopathy

Common Xray findings Sequestrum Involucrum

Ill defined bone destruction Local irregular thickening
Loss of corticomedullary differentiati

What is a Sequestrum
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.

What are the types of sequestrum

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

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What are the gross charecteristics of sequestra
White, brittle bone piece with smooth pus facing and rough granulation facing surface lying
free from parent bone
No punctuate bleeding – no paprika sign
Sinks in water
Dull note on percussion
Histology - Closed haversian canal

What is involucrum
Immature, subperiosteal, reactive, living new bone formation around a dead bone

What is the common sites of OM and why 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.
What are causes of diaphyseal OM
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.

What is sequestrum and what is its importance

Separated microscopic/macroscopic necrotic fragment of usually cortical bone (which
appears radiodense) surrounded by infected granulation tissue and pus (radiolucent) from
viable parent bone
Diagnostic importance: Necessary to make diagnosis of chronic osteomyelitis
Biological importance: It serves as a focus for continuing infection leading to recurrent bouts
of acute and chronic osteomyelitis.
(It takes  2-3 months for sequestrum to isolate and separate.

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Sequestrum may be absent in children <12 months of age – whole bone becomes a
sequestrum as periosteum is loosely attached, also small sequestra may be absorbed over
time)

Why is the sequestrum dense on X-ray

1. Avascular -  resorption of bone (unable to take part in remodeling)
2. Surrounded by radiolucent granulation tissue and pus enhancing the contrast
3. Hyperemia of surrounding bone due to inflammation making it relatively osteopenic.

Types of sequestra According to shape:

• Pencil like – infants
• Cylindrical/tubular – infants
• Ring – external fixator
• Conical – amputation stump
• Annular – amputation stump
• Coralliform – Perthes
Consistency:
• Coke like – Tuberculosis
• Feathery – Syphilis
• Sand like – tubercular osteomyelitis in metaphysis
Coloured:
• Black – amputation stump and long exposure of necrotic bone air while also attached
to parent bone (formation of ferrous sulphide), fungal infection
• Green – pseudomonal osteomyelitis

Miscellaneous:
• Muscle – Volkmann’s ischemic contracture.

What is involucrum and its importance

Immature, subperiosteal, reactive, living new bone formation around a dead bone.
Biological importance: It walls off abscess; it surrounds and can merge with parent bone or
become perforated with holes ‘cloacae’ through which pus and granulation tissue
may pout or pus discharges.

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 Treatment related importance: Only if three walls of sequestrum are seen fully on two
perpendicular views should sequestrectomy be undertaken otherwise a pathological # will
result and it will get converted into infected nonunion.

D/D of involucrum include

a. 50% infants <6 months age  B/L symmetrical thin layer along diaphysis of femur, radius,
humerus
b. Hypervitaminosis A
c. Metastatic leukaemia
d. Neuroblastoma.

What is Ciery and Mader classification for chronic OM

Based on anatomical and physiological criteria To determine stage of infection

Anatomical Type
I Medullary Endosteal disease
Cortical surface infected
II Superficial
because of coverage defect
Cortical sequestrum that
III Localized can be excised without
compromising stability
Features of I, II, and III plus
mechanical instability
IV Diffuse
before or after
debridement
Physiological Class
Immunocompetent with
A host Normal
good local vascularity
Local (L) or systemic (S)
Compromise d
B host factors that compromise
immunity or healing
Minimal disability,
prohibitive morbidity
C host Prohibitive anticipated, or poor
prognosis
for cure

Cierny and Mader Staging System for Chronic Osteomyelitis What is the cause of chronicity of
infection
1. Presence of unabsorbed and retained sequestra serving as a constant source of infection
2. Unobliterated cavities (dead spaces alive with bacteria!)
3. ‘Microbiological shift’ (change of aerobic cocci to gram negative or anaerobes)

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4. Multiple types of bacteria “mixed infection” and antimicrobial resistance.
How would you explain the role of bone scan? Tc bone scan
Triphasic scan
Three phases
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.

What are the specific types of OM

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

How do you differentiate a tubercular sinus from pyogenic sinus

The following points help one differentiate the two:
1. Tubercular sinus has bluish margins and is undermined.
2. There is serous discharge unless there is superadded infection or extravagant
infection.
3. Anaesthesia or paresthesia in the skin surrounding the sinus.

How do you clinically differentiate cellulitis from osteomyelitis

Cellulitis has peau d’orange appearance of skin with features of lymphangitis and bleb
formation.

What is the differential diagnosis for chronic osteomyelitis?

Tumour: Ewing’s sarcoma, eosinophilic granulomas, lymphoma, osteoid osteoma,
intraosseous ganglion and osteosarcoma
Trauma: Stress fracture

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Osteonecrosis: Especially of hip, knee (femoral condyles – with corticosteroid therapy or
HIV infection)
Miscellaneous: Fibrous dysplasia, Paget’s disease, cellulitis, haemophilia, Gaucher’s disease
(pseudo-osteitis), Caffey’s disease (infants), hypervitaminosis A, chronic cutaneous and
subcutaneous infections (deep mycotic infections).

In what forms of osteomyelitis will you not see a periosteal reaction

HIV associated osteomyelitis, tubercular osteomyelitis (some cases), long standing resolving
osteomyelitis that began in childhood.

What are the principles of treatment of chronic osteomyelitis

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

Principles for treatment of chronic osteomyelitis

Treatment for osteomyelitis is initiated along the following path:
1. Thorough debridement of necrotic tissue and bone: Sinus tract, necrotic bone,
infected granulation tissue, sequestra, eburnated bone is removed and saucerisation
done for providing wide window.
2. Stabilization of bone
3. Obtaining intra-op cultures
4. Dead space management
5. Soft tissue coverage
6. Limb reconstruction
7. Systemic antibiotic treatment

What are the surgical treatment options in osteomyelitis

Sequestrectomy and curettage
Open bone grafting [Papineau technique]

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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

What are the complications of osteomyelitis Growth disturbancesIncreased rate of growth

Decreased rate of growth
Pathological # Muscle contracture Septic arthritis
Secondary septicaemia Epithelioma
Joint stiffness Amyloidosis Recurrences & relapses

What is bead pouch technique

Used as an interim method between wound excision and definitive coverage Cavity
filled with antibiotic impregnated beads and covered by sterile transparent adhesive covering.

What is biofilm
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.

What is pulse lavage

Iriigation with 10-14 litres of saline Fluid pressure 50-70 pounds/sq inch 800 pulses /minute

What is Garres OM
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

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 EXAMINATION OF LONG BONES-NON-UNION
/MALUNION
Common Findings Inspection:
• Scar, discolouration (due to plaster treatment), sinus(es) –infection
• Deformity (angular/rotational)
• Shortening
• Bayoneting of fragments
• Swelling (hypertrophic)
• Wasting

Palpation:
• Temperature
• Tenderness (deep palpation and palpate with nail of your thumb)
• Palpable defect (palpate with nail of thumb running from above down)
• Abnormal mobility (check in two planes)
• Crepitus
• Loss of transmitted movements (rotate the distal part)
• Telescopy and distraction of fragments (lax non-unions and pseudoarthrosis)
• Prominence or absence of other bone (fibula) and its status

Movements: Check for ROM of nearby joints as stiffness due to previous treatment is
common.
Neurovascular status distally
Both iliac crests and legs for bone graft.

How do you define non-union, delayed union, slow union, and pseudoarthrosis
Non-union: Simply, when a fracture fails to unite permanently of its own. Comprehensively
“non-union of fracture is said to exist when the fracture shows clinically, radiologically and
biologically no signs for progression of healing after giving adequate time (US FDA
considers this as 9 months with failure of progression for 3 consecutive months) for the type
and site of fracture which will not unite unless some fundamental alteration in the line of

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management is undertaken” (quite vague and demands speculation for future events).
According to Brinker non-union is a fracture that according to treating physician will not heal
unless some intervention is required. This is a permanent end situation.
Delayed union: Fracture is said to have gone into delayed union when healing has not
advanced at the average rate for the location and type of fracture. This is a “temporary” phase
(fracture still shows progress towards healing) and will progress to permanency of union or
sometimes non-union.

Slow union: Here the fracture takes longer than usual to unite but passes through the stages
of healing without departure from normal both clinically and radiologically.
The ultimate outcome is union. Some people differentiate between slow union as being slow
to start with from delayed union where fracture struggles in later stages of healing.

Pseudoarthrosis: This is a distinct nonunion characterized by hypermobility at the fracture

site with cleft formation between ends and lined by pseudo-capsule. The cavity is usually
fluid-filled.

What are the causes of non-union Local factors:

Fracture related:
1. Open
2. Infected
3. Comminuted
4. Segmental
5. Fractures of irradiated bone
6. Intra-articular fractures
Treatment related:
1. Inadequate immobilization (most common)
2. Inadequate reduction
3. Inadequate fixation
4. Inadequate blood supply
5. Inadequate soft tissue cover
6. Interposition of soft tissue
7. Inadequate apposition “Distraction”

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Systemic:
1. Age (elderly)
2. Mal-nutrition (Albumin< 3.4 g/dl; lymphocyte count <1500/mm3)
3. Corticosteroid therapy
4. Immunosuppressive treatment
5. Systemic (hepatic, renal) disease
6. Metabolic bone disease
7. Anticoagulants
8. Burns
9. Smoking
10. Alcohol
11. Radiation

How do you classify non infected non-union:

Umiarov’s classification
Type I: Normotrophic without shortening
Type II: Hypertrophic with shortening
Type III: Atrophic with shortening
Type IV: Atrophic with bone and soft tissue defect usually with shortening
May’s classification for Tibia (actually it is a classification for osteomyelitis of tibia, however
type III, IV, V include non- union)
Type III: Tibial defect 6 cm or less with intact fibula
Type IV: Tibial defect >6 cm, intact fibula
Type V: Defect > 6 cm with no usable fibula.

Non-infected non-union: Weber and Cech Hypervascular non-union:

1. “Elephant foot”: Inadequate fixation/immobilisation, premature weight bearing
2. “Horse hoof”: Moderately unstable fixation
3. “Oligotrophic”: Inadequate apposition, displaced fracture

Avascular non-union:
1. Torsion wedge: Intermediate fragment healed to one main fragment of bone but not to
other
2. Comminuted (necrotic): Has one or more necrotic fragments

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 3. Defect (gap): Loss of intermediate fragment
4. Atrophic: Ends porotic and atrophic usually loss of blood supply

What is the basis of Weber and Cech classification

Viability of bone ends determined by strontium85 uptake.

Paley’s classification for tibial non-union (clinical and radiological):

• Type A (<1cm bone loss)
– A1: Mobile deformity
– A2: Fixed deformity
• A2-1: Stiff non-union without deformity
• A2-2: Stiff non-union with fixed deformity

• Type B (>1cm bone loss)

– B1: Bony defect no shortening
– B2: Shortening but no defect
– B3: Both (shortening with defect)

How do you clinically determine that this is a non-union and not delayed union or
pseudoarthrosis
Presence of painless abnormal mobility at the site in two perpendicular planes is deemed
pathognomonic of nonunion. Other findings are:
• Crepitus
• Telescopy of fragments (lax non-union)
• Loss of transmitted movements
• Palpable gap or defect in avascular nonunions.
Patient is unable to bear weight if it is in lower limb.
In delayed union there is residual pain at fracture site and tenderness on manipulation of the
fracture with abnormal mobility usually in one plane. Abnormal mobility if at all
present is not gross. Pseudoarthrosis is characterized by gross abnormal mobility typically in
all directions and crepitus is often absent as the ends are covered by fibrocartilage.

Is it necessary that a non-union has to be painless

No, following are the causes of painful non-union:

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1. Infected non-union
2. Interposition of soft tissue especially viable muscle and nerves
3. Non-unions of intra-articular fractures
4. Bayonet non-unions impinging surrounding tissues with adventitial bursa formation and
bursitis.

How do you clinically differentiate a stiff from a lax non-union

Stiff non-unions have arc of motion  7º (classically < 1 cm defect) that is not adequately
bridged by fibrocartilage to resist movements grossly. Often only micromotion can be
elicited; even the patient may bear weight partially in such cases. They are also called non-
mobile non-unions(or short fibrous non-unions).
Lax non-unions (Arc of motion >7º) on the contrary are inadequately supported by
connective tissue and demonstrate the classical signs of non-union. These are also called long
non-unions or mobile non-unions.
(Intra-articular short fibrous nonunion (fibrous Ankylosis) are often painful and the concept
of painless nonunion does not apply to them.)

Do all non-unions demonstrate abnormal mobility? (Or can you tell me something
about non-mobile nonunions)
Not necessarily. As above stiff nonunions typically hypertrophic ones may not at all
demonstrate abnormal mobility, also some site specific nonunions like in diaphyseal tibial
non-union where fibula is intact mobility may be masked at least in mediolateral plane.
Some metaphyseal tibial and femoral non-unions also ingeniously mask abnormal mobility
only on the sheer basis of proximity to mobile joint – judgment testifies the surgeon’s clinical
competence. (In these cases give the clinical diagnosis as malunion if deformity is present but
there is no tenderness or if tenderness is present then – uniting fracture when time frame from
injury is short or delayed union if time period is long. If there is no
deformity/tenderness/abnormal mobility then case will not be kept in exam and better search
for something else or you are grossly missing something!)
What are the common sites of occurrence of nonunions
Typical sites include – fracture femoral neck, fracture of carpal scaphoid, fracture
neck of talus,
fracture lateral condyle humerus, fracture capitellum,
fractures of distal third shaft of tibia.

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What are the causes of non-union for fracture shaft of tibia
Distal third of tibia is poorly surrounded by muscles so that segmental periosteal
blood supply (derived from anterior tibial artery) is limited.
Secondly these fractures are often open and caused by high velocity injury further
compromising the blood supply.
Surgical intervention is an added risk factor for jeopardizing the blood supply.
Lastly in middle third fractures of tibial shaft the endosteal blood supply derived from
posterior tibial artery that supplies 90 per cent of cortex is most severely affected.

How do you clinically identify infected non-union

Following are the features of infected non-union: (Infected non-unions fall into Cierney
Madar type IV osteomyelitis)

1. Painful non-union (painless if there is significant gap (>1cm) filled with mature
fibrous tissue)
2. Raised local temperature
3. Discharging sinus
4. Scar healed by secondary intention with “puckering”.
5. Tethered skin
6. Irregularity of bone on either side (representing osteomyelitis)

What will you do next

Radiograph of involved extremity (to confirm diagnosis) with adjacent joints.

Diagnosis
Describe the location, type of non-union along with condition of bones and ancillary
findings of infection and soft tissue. Comment on joints, status of hardware and deformities.
Delayed union:
• Slight resorption of bone ends with “Wooly” appearance [No e/o sclerosis or very slight].
• Medullary canal is open at both ends.
• Fracture line is clearly visible.
• External and internal callus are minimal. Nonunion:
• Marked sclerosis of ends with rounding off appearance.
• Medullary canal closed.

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 • Diffuse osteoporosis of both fragments.
• Fracture gap persists and widened due to unsuccessful bridging.
• Proximal end convex and distal end concave (pseudoarthrosis).

How does infection affect fracture healing

Infection is not an etiological factor for nonunion i.e., it does not cause non-union;
fractures are known to unite in the presence of infection. However, active ongoing
uncontrollable infection is a predisposing factor for non-union of fracture. Various
mechanisms are responsible to this effect:
• Dissection of pus through planes and periosteum – devascularising the ends.
• Fragmentation and dissolution of fracture hematoma.
• Inflammatory mediators that promote fibrous tissue formation.
• If fixation was done then implant failure occurs destabilizing the fragments.
• Increased catabolic response at fracture ends than anabolic activity (this also causes
porotic ends).
How does non-union develop
The inherent tendency of fracture is to heal and to this end there is a fine interplay of
innumerable factors that also have a reserve capacity, i.e., some deviations are tolerated but
not constant and gross distractions from normal process. Quality of bone, vascularity,
protection and stress are some of important mechanical and biological factors that can be
modulated to produce positive effect. Response to stress is as follows:

• Intermittent compressive hydrostatic stress (pressure)

• Chondrogenesis
• Intermittent strain & Fibrogenesis
• Low levels of mechanical stimuli (micro motion)

– Good vascularity  Ossification (Osteogenesis)

– Poor vascularity  Chondrogenesis.

Type of healing also depends on type of stabilization:

What are the various types of callus response with your chosen mode of treatment?
1. Cast (Closed treatment)  Periosteal bridging callus and interfragmentary enchondral
ossification
2. Compression plate  Primary cortical healing (cutting cone type)

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 3. Intramedullary healing  Early – Periosteal bridging callus and late – Medullary
callus
4. External fixator  depends on rigidity
• Less rigid – periosteal bridging callus
• More rigid – primary cortical healing
5. Inadequate immobilisation with
a. Adequate blood supply  Hypertrophic non-union (failed endochondral ossification)
b. Poor blood supply  Atrophic (Avascular) non-union
6. Inadequate reduction with displacement at fracture site  Oligotrophic nonunion.

What are various types of bone grafts

Bone grafts or bone transplants are natural bone tissues obtained to provide either structural
stability (cortical) or stimulate osteogenesis (cancellous) or both (usually).
(Bone graft substitute are synthetic or semi-synthetic derivatives that have various effects
on bone healing.)

Vascularised: Fibula (free vascularise/double barrel fibula transfer, centralization of fibula,

reversed flow vascularised pedicle), iliac crest, greater trochanter,coracoid process (with
muscle), rib.

Non-vascular graft:
Cortical: Fibula, tibia, autoclaved diaphyseal grafts.
Cancellous: Iliac crest mulberry grafts, tibial condyles, femoral condyles, olecranon, excised
head of femur, posterior superior iliac spine, malleoli.
Cortico-cancellous: Tibial upper metaphysis, tricortical iliac graft.
Mesh cage bone graft technique: Metallic cage (slightly smaller than adjacent bone) filled
with cancellous bone chips and demineralised bone matrix.
Grafts may also be classified as autograft, syngraft (isograft – from identical twin), allograft
(homograft), xeno(hetero)graft or according to shape, composition and method of application
(onlay (single or dual of Boyd)), inlay, intercalary, peg (neck femur, epiphysiodesis), Hgraft,
chip, shell, osteoperiosteal, pedicle, sliding and intramedullary (augments stability, improves
screw purchase, added potential for intramedullary healing between host bone and graft, e.g.
humeral non-union).

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What is the mechanism by which grafts enhance healing Biological properties of bone
grafts are
Osteoinduction (process that supports the mitogenesis of undifferentiated
mesenchymal cells, leading to the formation of osteoprogenitor cells that form new bone),
Osteoconduction (property of a matrix that supports the attachment of bone-forming
cells for subsequent bone formation) and
Osteogenesis (combination of above to form bone).
Osteogenic property is defined as propensity to generate bone from bone forming cells.

How do grafts heal

Cancellous (osteoinduction more prominent than osteoconduction): By a process
called “creeping substitution” (Phemister) whereby capillaries invade the tissue followed by
granulation tissue and macrophages that resorb the
bone while simultaneously also the process of osteogenesis is going on over the scaffold of
graft.
Cortical (mainly serves as structural graft, osteoconduction prominent): Process is
somewhat similar but slow resorption occurs along haversian canals and then regeneration
occurs. This may take years to complete depending on size and vascularity.

What grafting options are available for infected non-union

1. Papineau open bone grafting (Three stage technique):
a. Debridement (usually multiple at 5-7 days interval) with intramedullary stabilization
b. Grafting: Once granulation tissue appears use “matchstick” cancellous grafts 3-6 cms
× 3 mm × 4mm in overlapping circular fashion with or without saline irrigation and
wound packing.
c. Skin cover: Either spontaneous or various flaps/graft for coverage
2. Mini-Papineau
3. Postero-lateral bone grafting of tibia (Harmon’s method, especially if anterior skin is
unhealthy)
4. Phemister bone grafting
5. Friedlander technique – thorough debridement + stabilization and closure followed by
open bone grafting
6. Ilizarov method with or without bone grafting

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7. Huntington’s two-stage tibialization of fibula for infected gap nonunion (quiescent
infection).

What is phemister bone grafting and modified phemister grafting

Technique for treating delayed unions and established non-union of tibia (even infected
ones) by placing “sub-periosteal” “cortical” bone grafts (onlay) across fracture site. The
fracture site was not opened. Modification (Charnley and Forbes) included
placing “cortico-cancellous” grafts “subcortically” by raising “osteoperiosteal” flaps.
Charnley additionally used “Shingling” (raising osteoperiosteal flaps of bone longitudinally
across fracture site)
Philosophy of Phemister grafting:
• Fibrous union should not be broken down by refreshing or resection as it disturbs the
ongoing healing process and increases instability.
• Nonunion heals if induced to do so
• Rigid immobilisation is unnecessary
• Can be used in presence of recent sepsis provided graft is inserted through normal tissues
away from fracture site.

What are the various modalities of enhancing fracture healing

1. Autogenous (vascular/non-vascularised) Bone grafting
2. Bone marrow injection (app. 20 ml of marrow harvested from iliac crest or greater
trochanter for nonunions < 5mm)
3. Stem cell injection (100-150 ml bone marrow centrifuged to produce 2-4 ml aspirate
containing multipotent marrow cells and osteogenic stromal cells)
4. Platelet rich plasma and related peripheral blood concentrates
5. Electrical: What can be modulated?
a. Piezoelectric effect of Yasuda
b. Bioelectric/steady state potentials (Friedenberg and Brighton) How?

1. Constant direct current stimulation (invasive percutaneous electrodes)

– stimulates inflammatory like response – stage I of fracture healing
2. “Capacity coupled generators” (alternating current) – affects cAMP; collagen synthesis
and calcification during repair
3. PEMF (pulsed electro magnetic field, time varying inductive coupling) –

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 calcification of fibrocartilage (not fibrous tissue)
6. Ultrasound
7. External shockwave treatment
8. Bone morphogenic proteins
a. BMP-2 (rhBMP-2; 1.5 mg/kg in collagen sponge)
b. BMP-7 (rhBMP-7 aka OP-1{osteogenic protein – 1})
c. BMP-14 (GDF-5/MP-52)

What are bone graft substitutes Osteoinductive

• Allograft bone
• Demineralized bone matrix (contains Type-I collagen, noncollagen protein and
osteoinductive growth factors like TGF- superfamily, BMP, GDF)
• Purified human BMP
• OP-1 device
• INFUSE (rhBMP-2/ACS{absorbable collagen sponge})

Osteoconductive
• CaPO4 – available as powder, ceramics (coralline, synthetic, etc. prepared by sintering
(heating to temp. >100ºC) cements and composite
• CaSO4
• Allograft (stored at (–60ºC); tested for HIV, HBV, HCV, Syphilis- India; additionally for
HTLV-I and II and CMVUS, sterilized by -irradiation/Ethylene oxide) Hydroxyapatite
Bioactive glass (beads of silica, calcium oxide, disodium oxide and pyrophosphate)

Osteogenic and osteopromotive

• Bone marrow aspirate injection/implantation
• Platelet-rich plasma and blood concentrates
• Stem cells

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CLINICAL EXAMINATION OF LOWER LIMB 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

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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.

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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.

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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.

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 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

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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.

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

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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.

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 Deformity is defined as a deviation from normal structure or function which may be
symptomatic or has the potential to produce symptoms.

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 and 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.

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.

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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.

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 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:
Stature,
upper segment lower segment ratio, facies ,
teeth,
metaphyseal thickening,
hand, nails,
features of rickets, proximal muscle weakness
Examination of hip: to r/o coxa vara. Anteversion of hip
Intermalleolar /Intercondylar Distance: on standing and sitting Thigh leg angle
Thigh –foot angle Transmalleolar axis
Knee flexion to find the component of the varum / valgum Q angle:
ITB contracture;
Fibular Hemimelia/ Tibial Hemimelia Examination of foot and ankle: Metatarsus varus:
Calcaneo Valgus, Equinus: Standing:
• Genu varum/valgum

• External (valgum)/internal (in toeing) rotation of foot

• Patella subluxation/dislocation (lateral in valgum)
• Flat feet (valgum)

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 Gait:
• Abnormal foot progression angle
• Varus/Valgus thrust gait
• Stigmata of associated disease
– Rickets
– Dysplasia (acral shortening)
– Cerebral palsy
– Ligamentous laxity
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

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What is j sign
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.

What are the investigations you will do

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.

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.

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.

What is the difference between full length x ray and scanogram?

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.

What is the normal alignment of a limb

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

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the angle formed is 7 degree valgus. Any deviation from this value will produce undue force
on the respective side of the joints.

What is MAD?
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.

What would you do to confirm the location of disease?

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.

What is the normal change of the angle during development of the limb
6-12 months - moderate genu varum 18 – 24 months – leg straight
4 years – pjysiological genu valgus 6 years – leg straight
What are volkman law and wolf law
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.

How do you define genu varum/valgum?

These are angular deformities (coronal malalignment) of lower limb; some centers
include it under orthopaedic cosmetology.

Valgum (knock-knees) or varum (bow-legs) refer specifically to abnormal coronal

alignment” in which the leg is shifted away from midline (Valgum-medial angulation) or
towards it (Varum-lateral angulation). In a normal person standing with heels/knees touching
each other, ASIS-center of patella-center 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. Upto 1 cm separation
can be allowed for soft tissue in obese patients.

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How do you measure these?
Measured in standing position. Two methods:
1. Femoro-tibial alignment: Angle formed between lines joining ASIS to center of
patella and line joining center of inter-malleolar line to center of patella. Subtract
normal valgus from the measured alignment (7º for males, 8º for females >7 yrs) for a
valgus malalignment and add the same for varus. Varum or Valgum is said to exist if
the angle is outside two standard deviations from the normal for males and females
for that age.
2. Measure the intermalleolar distance in cms (normal < 10 cms) using measuring tape
for valgus, and distance between two knees for varus (normal < 8 cms). It can also be
expressed in “finger-breadth” albeit crudely.
For unilateral deformities measure from midline (plumb line from nape of neck).
The first method is more specific and reproducible,however, it is limited by age factor
and charts are not readily available. Second method although crude but can be readily
pursued to judge the progression of deformity. Also distance in cms is not absolute for
all – same distance is much more significant for a short statured person.

How do you differentiate if the deformity is in femur or tibia

Supine position in a relaxed patient, flex the knee fully (heel touching ischial tuberosity is
normal alignment) –
• If the deformity disappears altogether, then it should have been in femur,
• If it persists it should be tibial,
• If it is partially corrected then it could be in both.

This is because the non-weight bearing posterior femoral condyles are usually
relatively spared (HeuterVolkman law) of deformity (unless it is epi/metaphyseal
dysplasia/trauma, tc). In full flexion the tibia is in articulation with posterior femoral
condyles; if the deformity is tibial it persists however if femoral – it corrects. There is usually
only a partial correction in dysplasia. Patient can also be made to squat to demonstrate this.
This method is usually applicable for metabolic and some developmental causes only.
Ideally it should be assessed radiologically.

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What are the signs of rickets
1. Infant rickets symptoms:
a. Deformed skulls
b. Late-closing fontanelles
c. Rib-breastbone joint enlargement
d. Delayed milestones
2. Knobby enlargements on the ends of bones
3. Distorting pelvis under weight
4. Spinal curvature
5. Restlessness
6. Lack of sleep
7. Retarded growth
8. Mental retardation
9. Thin top of skull (craniotabes)
10. Thin back of skull
11. Bossing (frontal bossing)
12. Harrison groove
13. Beading where rib joins cartilage (rachitic rosary)
14. Bowed legs
15. Knock-knees
16. Weak muscles (floppy-baby syndrome, rickety myopathy)
17. Pot belly and widening of perineum
18. Deformed chest (pigeon chest)
19. Weak ribs
20. Abnormal teeth development
21. Tooth decay
22. Fragile bones if untreated
23. Fractures if untreated (especially greenstick fractures)
24. Double malleoli sign
25. Windswept deformity (Tackle deformity)
26. Tetany spasms.

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What would you do next?
I would like to get an AP and lateral view of both lower limbs fully including femur
and tibia in standing position.
If not possible then I will get orthoscannogram/ computed scannogram of both lower limbs.
(Remember for genu varum radiographs are indicated only if child is short [dwarfism],
asymmetric deformity, age >3 yrs, progressive deformity).

What do you see on X-rays?

Look for
1. Confirmation of diagnosis
2. Site of disease
3. Degree of malalignment (magnitude in degrees–tibiofemoral angle, mechanical axis, and
metaphysealdiaphyseal angle for differentiating tibia vara from genu
varum >16º = tibia vara)

4. Associated disorders and assessment of physes

Signs of rickets:
i. Rarefaction of the provisional zones of calcification
ii. Irregularly frayed and cupping metaphysis
iii. Deepened physes, rarefaction of the margins of theepiphyses
iv. Diffuse rarefaction of the shafts with thinning of the cortex and coarsened texture
v. In healing rickets – zones of provisional calcification become denser than the
diaphysis.
What would you do to confirm the location of disease “or” what if the malalignment is
not very clear on X-ray
Measure CORA ( center-of-rotation of angulation)
This reveals:
• Site “apex” of deformity (femoral/tibial/metaphyseal/diaphyseal sometimes at joint
line!)
• Number of deformity in complex deformities/ both femoral and tibial involvement
• Magnitude
• Planning guide
• Reveals additional deformities like bowing of bones and torsional deformities.

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 What is pseudo valgum and varum
Excessive femoral anteversion and compensatory tibial extorsion produces appearance of
genu valgum. Femoral anteversion only or with tight posterior hip capsule without tibial
compensation appears like genu varum in supine position.
What is hemichondrodiastasis
Asymmetrical physeal lengthening (“distraction”) by
fixator to correct angular deformities.
What deformities does iliotibial band contracture produce
• At lumbar spine: Ipsilateral lumbar scoliosis, increased lumbar lordosis.
• At pelvis: Pelvic obliquity due to abduction contracture
• At hip: Flexion, abduction, external rotation (FABER)
• At knee: Genu valgum and knee flexion contracture
• At leg: External tibial torsion with or without knee subluxation
• At Ankle and foot: (secondary deformities) – talipes equino varus, heel varus
• Whole leg: Shortening (true), initially there may be apparent lengthening due to
abduction contracture at hip and pelvic obliquity.
What is triple deformity of knee
Classically described for tuberculosis of knee. However, it is also found in various long
standing chronic diseases like rheumatoid arthritis and in ITB contracture.
Deformity components:
1. Flexion deformity at knee (due to chronic nature of diseases and synovial effusion
knee is commonly kept in position of maximum joint space – 30º which persists to
produce flexion deformity of knee).
2. Posterolateral subluxation of tibia (most of chronic destructive diseases joint
subluxates
3. laterally – reasons are not clear; one explanation could be that in rheumatoid disease which
commonly affects females there is already more physiological valgus which leads to
increased stresses over lateral joint compartment, other more plausible one is that in
destructive diseases there is exaggeration of the physiological alignment – remember there is
a physiological valgus and posterior tibial slope in a normal knee joint).
4. External rotation of tibia over femoral condyles– various reasons; quadriceps pull,
popliteus action, ITB, etc

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 CEREBRAL PALSY
History:

Prenatal history
Mother – drug intake, infections, irradiation, PIH(BP, swelling of feet), post partum
haemorrhage
Which child (other children – are they normal)
Mode of delivery ? Difficult labour (cord around the neck, oligohydramnios) Whether
premature ? IUGR ?
Whether child cried immediately after birth
History of jaundice/ convulsions in the neonatal period ? Any other treatment / PICU
admission
Difficult in sucking/ swallowing Dribbling at the mouth
Baby feeling stiff/ wriggling awkwardly Developmental Milestones – Motor / Social
(Social smile, head control, turning in bed, crawling, sitting, standing, walking without
support, climbing stairs, uttering single words)
Mode of ambulation, mobility Activities of daily living Education, Communication

Examination

Spinal balance – sitting control? Able to sit without support with straight spine (good
prognosis)
Fixed / Correctable deformities Spine – Scoliosis
Hip – Flexion, Adduction, Internal rotation ( look for telescopy) Knee – flexion
Ankle – Equinus, calcaneus Subtalar joint – Varus/Valgus
Forefoot – Abduction/Adduction Pes Cavus/ Planus Hallux Vagus/ Claw toes Tone
Special tests for muscle spasm

Tests for adductor and medial hamstring tightness and to differentiate between both Test for
hamstring spasticity ans contracture (poplitel angle)
Prone rectus test

Tests for gastroctneus contracture and spasticity and to differentiate between both Not
necessary to measure range of movements of joints

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Power of muscles – only in older children who are able to understand instructions Most
important is power of knee extensors
Observe gait Aided/ Unaided

Must carefully observe the position of joints during all phases of gait and look for paucity of
movements of joints during gait

Eg.Knee flexion may be impeded during swing phase due to tight rectus femoris Equinus
gait, jump gait , crouch gait

Example:
9 year old male/female child brought by mother with difficulty walking since 1 year of age.
Progressive?
Painful or not?
Hx tendency to fall? How many times
Underwent physio at 1 for a year then discontinued It til last week. Any orthoses use?
Birth History – Antenatal,Natal,Post natal No maternal infections,
Consanguinousmarriage/non consanguinous Term/Preterm – cause for preterm
3 kg baby
Born with a normal vaginal delivery , cried immediately after birth. stayed in the ICU for 1
day ,
No jaundice, Fever, Convulsions,
Normal Bowel and bladder habits
Develpmental – speech,handedness, neck holding, tripod position, sit up, stand with
support,walk,gait pattern
Immunization Treatment history
O/E
(patient attitude- was unable to sit, so examined in lying)
Syndromic features – low hair line, flattened nose, widened intercanthal distance, low set
ears,high arched palate, syndactyly)
Neurocutaneous markers Inspection (LLD, muscle wasting) Callosities knee?
Spine – tuft of hair,swelling,deformity.balance From posterior aspect-

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 Head is in the centre, Shoulder same level, no scoliosis, or abnormal folds, PSMS, Tuft of
hair or any neurocutaneous marker
From lateral aspect, no gibbus, normal thoracic kyphosis with lumbar lordosis From anterior
nipples normal, as are the folds.
Chest movements + Thoracolumbar /abdomino thoracic movements (to check if diaphragm is
working.)
Level of ASIS
Position of the Greater trochanter, projection of patella.
Scar over the calf – tendoachilles lengthening or gastrosoleus, or gastrocnemius. Depending
on scar position.

Palpation
No PSMS, No Gibbus
Patella alta – normally, the inferior pole of the patella is at the joint line, and normally the
superior pole is just 1 fingerbreadth above the adductor tubercle . If it is above this, then it is
patella alta.
Palpate the posterior gluteal region Hip dislocation posterior

Neurological exam:
Higher Functions Normal ( does she follow your clicks or does she smile when you or mom
looks at her)
1. Cranial Nerves
2. Tone(feel muscle and opposite movement)
3. Bulk
4. Power always check abductors( keep knee flexed and abduct in lateral position)
5. Check extensors knee
6. Check till evertors and invertors.
7. For ankle dorsiflexion, confusion test, flex hip, and ankle will flex.

8. Reflexes –DTR’s superficial , abdominal , and babinskis and Clonus - ill sustained( maybe
false positive, ) ; sustained( indicative of UMN lesion
9. sensation

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 Upper limb
No spasticity ( modified ashworth score)
Fixed deformity UL? – (usually adduction, Internal rotation of shoulder, Elbow flexion,
forearm pronation, thumb in hand)
Check dorsiflexion of wrist ( Adaptive muscle shortening.)

ROM and deformity

1. No FFD of hip. (staheli test is more useful in cp to check extension of the hip. ) Then only do
Thomas test if there is FFD.
2. Rectus Femoris Test (Ely’s) Flex knee in prone position and see if the butt is lifting up. If
when pressing it disappears I tis spasm, if it doesn’t disappear, contracture)

3. Obers Test - Tightness of iliotibial tract

4. Hamstrings - Popliteal angle The max angle till which we can extend the knee with hip in
flexion 90( different from ffd which we should see in extension of hip, person may have a
popliteal angle of even eg. 130 but no ffd.) angle of holt is the corollary of popliteal angle( if
popliteal angle 130, angle of holt Is 50.) >50 degrees popliteal angel is positive
The holt angle is the functional hamstring tightness.
Hamstring shift Test: Hamstring tightness or pelvic tilt hamstrings shift due to anterior
pelvic tilt). Make opposite hip flexed like in Thomas test and then perform popliteal angle.
This is because if the pelvic is flexed , the hamstrings will be falsely shortened. This will
show the true hamstring contracture)

5. Phelps Gracilis Test : Keep patient at side of bed. With hips and knees flexed. See the
degree of abduction, then see in with knees extended and see if it gets decreased.
Hip In flexion- 45 abduction atleast required to prevent probable subluxation. Hip extended-
30 abduction

6. Silverskiolds test : Only do it if ankle is in equinus. And do it with the subtalr joint In
inversion to decrease the possibility of the subtalar joint faking dorsiflexion by inversion.
Check the plantarflexion especially in a crouch gait, as ta lengthening may produce an ankle
calcaneus .

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 ROM: T1 and T2 for all muscles
Hamstrings Test : Supine, Make patient flex hip then attempt to extend the knee, T1 is the
first resistance felt with low velocity. T2 is the second resistance felt at higher velocity.
7. Patellar tracking
8. Q angle measuremt

Torsional deformity :
1. Femur (prone): Craigs Test – Palpate the most prominent part in the GT sometimes
difficult therefore then, completely internally rotate and ER to see maximum angles Increased
femoral anteversion leased to keeping entire limb internally rotated
One femur will be more intorsioned, therefore will have more internal rotation than
external rotation.
2. Tibia :
1. Thigh foot angle.-
Patient prone position with hips and knee flexed, the Angle subtended between long axis of
the thigh and a line drawn from the centre of the heel to the foot( If foot is normal )

2. intermalleolar axis.
20-30 ( If foot is abnormal) keep patient supine, and make sure femoral condyles horizontal
then check intermalleolar axis anddifference in angle)
3. Foot – Heel bisector line should bisect 2nd webspace. Balance.
Coronal and sagittal balance
Gait:
1. Head – Midline
2. Shoulder same level or drooping
3. Spine any scoliosis
4. Pelvis level or dropping
5. Hips- Flexed??
6. Knee
7. Heel strike, If there is no heel strike, then probably equinus.
8. Scissoring
Crouching gait- Hips flexed , knees flexed, heels on ground. ( ankles dorsiflexed)
Vs Jumping gait- hips and knees flexed and ankles plantarflexed ( heel not on floor)

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Diagnosis
NAPE
Neurological – UMN/LMN lesion Anatomical diagnosis – diplegia Pathological – spastic
cerebral palsy Etiology- perinatal hypoxia/ preterm
Compications – with no fixed flexion deformities and no torsional deformities with GMFS
score of (FMS score)
With gait

Treatment:
1. Communication- with mother/scholastic performance
2. Activities of daily living- toileting/ personal care Grades
3. Physiotherapy for muscle spasm.

Related Theory

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.

Define cerebral palsy

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 structurallyand
biochemically normal
The brain lesion must be fix and non progressive
The abnormality of the brain result in motor impairment

What is the aetiology of cerebral palsy 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

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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

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- one side UL
more than LL
Diplegic CP- Both LL more than UL Triplegic CP – 3 limbs involved Quadreplegic CP – all
4 limbs involved
Double Hemiplegic CP - all 4limbs involved both UL more than LL What are the
histopathological findings of the brain in CP children Periventricular leukomalasia
Intraventricular and periventricular hemorrhage
Can severity of spasticity be measured
There is no clear best test. Modified Ashworth Scale is the most widely used method for the
clinical assessment.
Grade Description

0 No increase in muscle tone

Slight increase in muscle tone, manifested by a catch and
release, or by minimal resistance at the end of the range
of motion when the affected part(s) is moved in flexion or
1
extension

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 Slight increase in muscle tone, manifested by a catch,
followed by minimal resistance throughout the remainder
(less than half) of
2
the range of movement (ROM)
More marked increase in muscle tone through most
3 of ROM, but affected part(s) easily moved
Considerable increase in muscle tone, passive movement
4 difficult
Affected part(s) rigid in
5 flexion and extension

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

What is the prognosis for hand function

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

What are the non surgical treatments of cerebral palsy 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)

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Mention the indications for bracing
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

Describe the medical treatments of cerebral palsy.

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.

Mention the common indications for Botulinum toxin injection

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
equinus
If parents refuses surgery and desires injections

What are the general considerations for Surgery

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.

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

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)

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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.

What is the surgery for scissoring gait

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.

What is the surgery for the flexed knee gait

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

What are the current operations for the valgus foot in skeletally immature child

Mosca procedure ( open wedge interfacet calcaneal osteotomy)

Grice green procedure (Sub talar extra articular arthrodesis)

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

equinus foot
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

Mention the techniques of gastrocnemius recession

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

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What is the role of hand surgery in CP
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.

When should the surgery of Lower limb be done?

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.

What are the indications for the triple arthrodesis?

Fixed varus or valgus deformity in a skeletaly mature patient

What is the most common type of hand deformity and how can it be corrected?
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

How and when should scoliosis be treated in CP

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.

What is Single Event Multi-Level Surgery

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.

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 EXAMINATION OF PERIPHERAL NERVES:
Occupation Hand Dominance
Deformity – onset,duration,progression H/o Trauma
Weakness Paraesthesia/numbness Inability to perform functions H/o native splinting
Treatment history
H/o Rheumatoid H/o Hansens H/o seizure
Common Things to look for in a case of peripheral nerve injury 1.Attitude and position of the
joints
2. Inspectory findings – describing the deformities, skin condition, scarring, muscle wasting,
mention about contours of the normal musculature.
3. Palpate the surrounding bones and look for tenderness, thickening, broadening,
discontinuity, palpate surrounding soft tissue, palpate the joints, palpate the nerve and
look for tenderness, continuity, thickening and tinel’s sign.
4. Deformities, Range of movements – passive and active, differentiate between spasm and
contracture.
5. Motor- bulk, tone, power and reflex
6. Sensation – Pressure, Temperature, light touch, crude touch ,two point discrimination,
pain
7. Distal vasculature 8.Special Tests 9.Lymphnodes Diagnosis:

Example :
Post-traumatic / idiopathic Recovering / nonrecovering, Complete / incomplete Right
/ left High / low radial nerve palsy for past 9 months (with or without non-union/
united fracture of humerus)

Course of radial, ulnar and median nerves :

Radial nerve (C5-T1):
Formed in front of subscapularis from posterior cord  passes anterior to lattissimus
dorsi muscle  to pass through triangular space accompanied with profunda brachii artery to
posterior aspect of humerus into radial groove (not spiral groove; radial groove is few mm
above spiral groove) where it is separated from bone by medial head of triceps coursing
obliquely laterally  pierces the lateral intermuscular septum around 12cm above lateral

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epicondyle  passes into anterior compartment emerging beneath brachioradialis  deep
branch (PIN) pierces supinator muscle to emerge into extensor compartment of forearm
 forms cauda equina of spinner 8 cms distal to elbow joint.

Ulnar nerve (C8-T1, rarely C7 also):

Formed from medial cord of brachial plexus  runs inferomedial to axillary artery to
continue behind brachial artery over triceps muscle  passes straight to posterior aspect of
medial epicondyle in “ulnar groove” between medial epicondyle and olecranon process 
passes between two heads of FCU (the so-called “cubital tunnel” better called humeroulnar
aponeurosis  remains deep to FCU overlying FDP muscle accompanied with ulnar artery 
passes superficially; emerging beneath FCU to reach Guyon’s canal at wrist.

Median nerve (C6-T1):

Formed from medial and lateral roots of median enters arm in close relation to
brachial artery. In the cubital fossa nerve lies lateral to brachialis tendon and passes b/n two
heads of pronator teres  gives AIN  continues in forearm sandwiched b/n FDS and FDP 
emerges just proximal to wrist b/n FDS and FCU  passes through carpal tunnel  lies
anterior and radial to FDS tendons  divides in hand into recurrent
motor and sensory branches

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

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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)
What function is lost in nerve (radial/median/ulnar) palsy Radial:
1. Inability to extend fingers (1,2,3,4,5) {low} and wrist {low+high}
2. Inability to stabilize the wrist (wrist drop) and thumb (radial abduction of thumb)
{low+high}
3. Loss of grip strength (accessory forearm flexion) {High}
4. Accessory forearm supination {Very High}
5. Sensory loss (radial 2/3 dorsal sensation)

Ulnar
1. Loss of grip strength (impairment of power grip > precise grasp) {High}
2. Flexion of distal phalanx 4,5 {High}
3. Digital balance 4,5 {High}
4. Loss of finger function (flexion (partial), adduction, abduction) {High+Low}
5. Loss of thumb adduction and weakness of thumb flexion {High+Low}
6. Sensory loss (medial 1½ digits – Low; Ulnar 1/3 volar – High)

Median nerve:
1. Loss of thumb opposition, finger stabilization 1,2 {Low+High}
2. Weakness of wrist and partial loss of finger flexion 2,3; complete for 1 {High}
3. Forearm pronation {High}
4. Sensory loss (Radial volar 2/3 hand)

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Combined low median and ulnar nerve:
1. Thumb opposition+ adduction + flexion (partial)
2. Finger abduction and adduction
3. Finger stabilization
4. Sensory loss (volar hand + dorsal ulnar 1½)

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 through the ulnar groove
behind the medial epicondyle. Then it enters the forearm between two heads of FCU through
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.

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) Abductor digiti minimi
(Can be palpated, power tested)
First dorsal interossei (last muscle supplied)

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

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.
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.

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Low ulnar palsy – lesion below elbow, usually below wrist with sparing of FCU and FDU.

Tests for ulnar nerve palsy

Test FCU – differentiate high and low nerve palsy Card test – tests palmar interossei
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
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

Boundaries of Guyon’s canal

Wall formed proximally by pisiform and distally by hook of hamate Floor by transverse
carpal ligament, hamate and triquetrum bones Roof by pisio-hamate ligament.

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)

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

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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.

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.

What is intrinsic minus hand

Fingers: Hyperextension at MCP joint + flexion at IP joints ± adduction of fingers Thumb:
adduction and hyperextension at MCP joint + Flexion at IP joint.

Radial Nerve Palsy :

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.

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

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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.

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)

How will you localize level of lesion in 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

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

Holstein Lewis fracture and what is its importance

Spiral fracture of M/3rd and L/3rd junction of humerus with proximal spike over lateral
aspect just at the site where radial nerve touches humerus. Commonly radial nerve palsy was
thought to be associated with fracture.

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 :

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.

How to 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

Clinical features of median nerve palsy:

Wasting of the flexor prominence radial aspect Thenar wasting

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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) Ask patient to form ‘O’
with Index finger and thumb using tips – patient will extend DIP of Index finger and IP of
thumb making peacock’s eye instead

Compression neuropathies of median nerve

Carpal tunnel syndrome Anterior interosseous syndrome Pronator syndrome

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.

What is the structure of a peripheral nerve

Epineurium has two parts-internal and external, former permeates the nerve
ensheathing individual fascicles and the latter is a condensation of collagen encasing the
fascicles as a group. Epineural fibrosis and scar formation after nerve injury is a function of
epineurium. Perineurium is an extension of blood-brain-barrier made up of up to 10
concentric lamellae of flattened cells that are ‘dove-tailed’. Removal of perineurium causes
nerve function to fail. Up to 15 per cent stretch, there is no injury to perineurium but it fails
for stretch >20 per cent. Endoneurium acts as a packing material of collagen tissue. There is
no elastin. Participates in the formation of Schwann cell tube.

What is fascicle
Termed funiculus by Sunderland it is the smallest unit of nerve that can be
manipulated surgically.

Wallarian degeneration :
It is the reactive change of a nerve to injury whereby distal stump is cleared of
axoplasm and myelin along with regenerative changes in proximal stump. It is initiated by
macrophage ingrowth stimulating Schwann cells. Schwann cell proliferation peaks around

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 3rd day and continues up to 2 weeks. The distal stump once cleared by Schwann cells and
macrophages is left in the form of a tube that shrinks in size. Proliferating Schwann cells
form ‘bungers bands’. The proximal stump degenerates till nearest node of ranvier from
where new sprouts grow (2-5 sprouts within 6 hrs). Those sprouts that establish end organ
contact
persist rest all (those entangled at scar site ‘scar delay’ and those missing their ‘receptive
tubes’) are pruned away.

What is topographic sensitivity

Reinnervation of correct muscle within motor system or correct patch of skin in sensory
system.

How do you classify nerve injuries

Seddon’s classification:
Neurapraxia ( ‘Sunderland’s type I); only physiological disruption of nerve function –
recovers of its own.
Axonotomesis ( ‘Sunderland’s type II-IV); physiological disruption with partial anatomical
(increasing) disruption of nerve – recovery possible (70%) but later
may need surgical intervention in higher grades.
Neurotemesis ( ‘Sunderland’s type V); complete anatomical and physiological disruption of
nerve – always needs surgical intervention.

What are synergistic muscles

Synergism is the endless repeated coordination of anatomically different groups of muscles to
perform a given action e.g., wrist extensors + finger flexors + finger adductors “or” wrist
flexors + finger extensors + finger abductors.

What are the prerequisites for tendon transfer

In order of importance:
1. Correction of contractures (all joints must be supple)
2. Adequate strength of the transferred tendon
a. 85 per cent of power is a must (Steindler) – graded as good power

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 b. “Omer” stated that a muscle loses at least one grade of strength after transfer so for
useful post-operative movements 4/5 power is a must.
3. Straight line of pull: No pulley is ideal or minimum number of pulleys should be made.
4. One tendon – One function, i.e., flex or extend
5. Synergism: Synergistic transfer should be preferred as much as possible, however, there are a
lot of violations of this rule.
6. Expendable donor: There should be no functional morbidity following use of a tendon
7. Tissue should be in equilibrium (tissue equilibrium – termed by Steindler)
a. Soft tissue induration should subside
b. No reaction in wounds
c. Joints are supple
d. Scars should be as soft as possible
8. Pass tendon below fascial planes/sheaths and not below incision line/scar (best b/n
subcutaneous fat and fascial sheath).
9. Amplitude of transferred tendon should be as near to the original tendon for which the
transfer is being done.
10. Try preserving the nerve and vascular supply to muscle and vascular supply to tendon.
11. Insertion of the tendon should be as close to the insertion of paralyzed tendon; at same
angle; if split transfer then keep both slips in same tension.
12. Try to restore sensibility of distal organ before treatment.
13. Arthrodesis/joint procedure should be done before tendon transfer.
14. The disorder should be a non-progressive one.
15. Keep dissection to a minimum around the muscle to be transferred and achieve meticulous
hemostasis to prevent adhesion formation.

What if the amplitude of transferred tendon is less than the tendon for which transfer
has been contemplated
Amplitude can be increased by two ways:
1. Converting a monoarticular muscle into bi/multiarticular, e.g., (FCU/FCR  EDC). The
effective amplitude of motion is enhanced due to tenodesis effect by active volar flexion of
wrist.
2. Muscle release from surrounding, e.g., brachioradialis transfer.

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 When will you do a tendon transfer
In general, till the time a functional recovery is expected to occur; one can wait else do a
tendon transfer.
Early transfer can be done if there is gap > 4 cms or there is excessive scarring/skin loss over
the nerve, some may also include injection palsy and gunshot injuries in this category.
Otherwise, transfer is usually done after waiting for around 1 year following injury (whether
an interim repair has been attempted or not).

Why do you wait for a year

To give adequate time for the nerve to regrow and possibly re-innervate the muscle. Neuro-
muscular junctions in the muscle degenerate if not re-innervated in about a year’s time, so it
is prudent to do tendon transfer after year as the likelihood of regaining function is meager.
Moderate to severe atrophy of muscles is seen by 3 months, mod-severe fibrosis seen by 11
months, beyond 3 years there is fragmentation and disintegration of muscle fibers; hence
ideal reinnervation can be expected after 1-3 months, functional reinnervation up to 1 years,
no reinnervation >3 yrs.

What are the various tendon transfers for radial nerve injury
I. JONES transfer Classical (1916):
1. PT ECRL and ECRB;
2. FCU EDC III-IV;
3. FCR EPL; EDC II, EIP Classical (1921):
1. PT ECRL and ECRB
2. FCU EDC III-IV
3. FCR EDC II, EIP, EPL, EPB, APL
Modified JONES: PT ECRB and rest as above
II. FCR transfer (of Starr; Brand; Tsuge)
1. PT ECRB
2. FCR EDC II-V
3. PL rerouted APL
III. Boyes Transfer (Superficialis transfer)
1. PT ECRB
2. FCR APL and EPB

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 3. FDS III EDC II-V via interosseous membrane
4. FDS IV EIP; EPL via interosseous membrane
IV. FCU Transfer (Standard Transfer, this is not modified Jones transfer)
1. PT ECRB
2. FCU EDC
3. PL rerouted EPL

What will you do for a patient who comes with fracture of humerus with radial nerve
palsy
Will wait for return of nerve function as according to Steindler’s formula for nerve
regeneration [(1mm = 1Day) + 30 days for motor recovery to manifest (N-M junction)
and nerve ends to sprout]. Usually for, e.g., nerve injury is 90-120 mm above lateral condyle.
Now for brachioradialis to get reinnervated that arises 20 mm above lateral condyle it will
take 70-100 days + 30 days = 4-5 months. This is the time duration one can wait (calculate as
for other fractures). This is based on the premises that often the nerve injury is apraxia or
axonotomesis with nerve in continuity and fair recovery is seen in over 90 per cent cases.

Will you always follow this regime ‘or’ will you always prefer to wait
No, early exploration of radial nerve must be done for patient with palsy associated with:
1. Radial nerve injury secondary to manipulation of fracture (absolute indication)
2. Open fractures
3. Fractures in which satisfactory alignment is not possible by closed methods
4. Fractures with associated vascular injury
5. Patients with multiple trauma.

How to overcome nerve gap

Following in isolation or combination are often required:
1. Mobilization
2. Transposition
3. Limb positioning
4. Resection osteotomy
5. Nerve stretching and bulb suture (neuroma to glioma suture)
6. Neuromatous neurotisation (e.g., intercostal nerve for brachial plexus)
7. Nerve grafting

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 8. Nerve crossing (ulnar  median)
9. Addition of non-neural tubes (e.g., vein segment).

How much mobilization can be done for a nerve

Depends on the type of nerve but in general mobilization>6-8 cms  perfusion. ( 8 per
cent tension  venular flow, 10-15 per cent - tension: blood flow arrest).
What are various types of nerve grafting
The various options are:
1. Trunk grafting using full-thickness segment of major nerve trunk (disadvantage –
central necrosis/total graft dissolution)
2. Cable graft using multiple strands of cut nerve sewn at both ends (drawback – wastes
axons and ignores anatomic localization of function)
3. Pedicle grafting often preferred for high combined ulnar and median nerve palsy
where ulnar nerve is used as a pedicle graft to repair median nerve.
4. Interfascicular nerve graft (group fascicular nerve grafting)
5. Individual fascicular nerve grafting – often done for paucifascicular nerve, e.g., ulnar
nerve at elbow or for thin/terminal nerves, e.g., motor thenar branch of distal
digital nerve.
6. Free vascularised nerve graft.

From where one can harvest nerve for graft

1. Autogenous:
a. Lateral cutaneous nerve of thigh
b. Medial brachial and antebrachial cutaneous nerve
c. Radial sensory nerve
d. Sural nerve (up to 40 cms of graft)
e. Lateral cutaneous nerve of forearm (up to 20 cms)
f. Terminal branch of PIN (for digital nerves)
2. Autologous vessels and muscle
3. Allograft nerve
4. Artificial conduits (veins/collagen conduits).

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 5.

EXAMINATION OF BRACHIAL PLEXUS

RTA (High velocity)
Hand dominance
If hx of LOC( how long)

Loss of function immediately following trauma

Rate of progression of deformity. Any improvement in symptoms,

Has there been any improvement since then??

Hx of pain in brachial plexus means that that specific nerve root may be avulsed. (therefore
preganglionic)
Sensation?
Activities daily living – eat, use his hand

History similar to plexus injuries – outstretched elevevated arm History of # scapula ribs,
clavicle.
Difficulty in vision in the evenings (s/o Horner‘s)
In Obstetric palsy, antenatal / natal / and post natal history.

Rx history

Examination:
Walk the plexus
1. Inspection
Eyes. Ptosis is there ( horners indicates only T1 root avulsion(preganglionic) and its abcense, the
lesion is
Head not tilted ( paraspinal muscles working, otherwise tilted to side of the lesion)
Supraclavicular fossa ? Fullness clavicle # Muscle wasting
Supraspinatus and infraspinatus wasting Medial scapular wasting
Biceps triceps
Sulcus sign
Scars , sinuses
Trophic changes of hand(dryness, excoriations), change in hand shape, (ulnar border) Thumb in hand
sign

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2. Palpation
I. Tap just posterior to scm (tinels sign) means there is a naked nerve root lying there. (
therefore if tinels sign is positive it is postgangionic ; as in preganglionic it is covered by the vertebra
and wont hurt if tapped)
Tinels from distal to proximal
II. Clavicle bony irregularity.(maybe # clavicle)
III. Humerus, scapula and other bones
IV. Palpation of ulnar nerve

3. ROM – Check if there is any fixed deformities shoulder elbow and pronation supination , wrist,
fingers
4. Neurological exam( brachial plexus)
a) Tone flaccidity
b) Bulk
c) Power

I. Trapezius ( spinal acces nerve)(useful to transfer muscle)

II. Rhomboids( retract shoulder and feel medial border scapula. ( relax the trapezius by bending
the neck that side dorsal scapular nerve from early roots of c5 which indicates preganglionic
lesions
III. Serratus anterior -stable elbow in 90, shoulder abd 90 and internally rotate ( or ask then to
fall on your hands and push.. or push against the table then look at medial border scapula)(
indicstes c5, c 6, c 7 root avulsions. )
IV. Lattismus Dorsi – (thoracodorsal nerve by posterior cord) hold limb abducted and ask the
patient to adduct against resistance, and palpate posterior axillary fold.
V. Deltoid.
VI. Biceps
VII. Triceps
VIII. Pronation supination
IX. Finger flexion
X. Wrist extension
XI. Interossei.
d) Reflexes
e) Sensation C5 to T1 check.

Pulse may not be present but limb may still be viable.

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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
Horners in brachial plexus. C8 T1 ( as the sympathetic ganglion arises from c8-t1)

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

Treatment
6 months cut off
Aim for
1.Shoulder abduction 2.Elbow flexion
3.Sensation along radial aspect of forearm and hand Nerve grafting
Beyond six months Tendon transfers.
Free functioning muscle transfer. X
Ncs and Emg always after 3-4 weeks for wallerian degeneration to occur if intact sensory path then
it means it’s a pre ganglionic injury. Which is worse and untreatable

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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

Middle finger
C7 Finger Extensor Wrist Flexor Triceps

C8 Finger Flexion Medial forearm, ring small finger

Finger Adduction Finger

T1 Medial Arm
Abduction

Describe the supply of components of brachial plexus:

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.

What are the features of preganglionic lesion Involvement of dorsal scapular and long thoracic
nerve Long tract signs
Cervical spine fractures

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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.

Describe the representation of C5 to T1 nerve roots

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.

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

What is mean by Erb’s point

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.

What are the components of Erb’s palsy

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)

Aims of reconstructive surgery

To restore
Shoulder abduction Elbow flexion
Sensation of medial side of hand.
How will you treat shoulder internal rotation contracture Mild to moderate: SEVER‘S anterior
subscapular release. Severe: ROGER‘S derotational osteotomy.

What are the options to regain shoulder abduction

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

How will you restore Elbow flexion

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.

What is meant by neurotisation

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

What are the late radiological features of Erbs palsy

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

What is SOMSAK procedure

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

What is Oberlin transfer

Transfer of ulnar nerve to musculocutaneous nerve

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 AVASCULAR NECROSIS OF THE FEMORAL HEAD
The causes for hip pain in the young include

1. Avascular necrosis
2. Femoro acetabular impingement
3. Inflammatory
–Ank Spond
- Rheumatoid
-Gout/Pseudogout
4.Low grade pyogenic infections
5.Tuberculosis of the hip
6. Pigmented vilonodular synovitis
7. Synovial Chondromatosis
8. Transient synovitis

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 Definition:
Cellular death of bone components due to interruption of blood supply; the bone structures
then collapse, resulting in pain, loss of joint function and long term joint damage.

Causes:
Traumatic
1. Femoral neck fractures
2. Posterior dislocation of femoral head
3. Head of femur fractures
Non Traumatic
1. Alcoholism
2. Corticosteroids
3. Smoking
4. Thrombophilias
5. Renal osteodystrophy
6. Scleroderma
7. Skin disorders
8. Solid organ transport
9. Haemoglobinopathies
10. HIV
11. Gauchers disease
12. Hyperlipedemia
13. Polyarteritis nodosa
14. Chemotherapy
15. Radiotherapy
16. Liver diseases
17. Gout
18. Rheumatoid arthritis
19. Giant cell arteritis
20. Pancreatitis
21. Caisons disease
22. Idiopathic- CHANDLERS DISEASE
23. Pregnancy
24. Genetic

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Theories:
1.Direct cellular toxicity
2. Extraosseous venous blockage
3. Extraosseous arterial disruption
4. Intraosseous extravascular
5. Intraosseous intravascular
6. Hypersensitivity
7.Multifactorial

Pathogenesis:
Death of Haematopoietic elements- 6-12 hours of ischemia.
Bone cells- 12-48 hours of ischemia.
Fat cells > 48 hours of ischemia.

Pathology:
1. Loss of fat cell outlines
2. Inflammatory cell infiltration
3. Marrow edema
4. Appearance of tissue histiocytes
5. Replacement of necrotic marrow by undifferentiated mesenchymal tissue.

Clinical Features:
1. Pain
2. Stiffness
3. Reduced range of movements of the hip

Signs:
1. Tenderness
2. Spasm/Fixed deformities
3. Reduced and Painful ROM
4. Sectoral sign +
5. Shortening
6. Axis deviation

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 Investigations:
1. X rays
2. MRI- Kerboul angle

Classifications:

1.Ficat and Arlet

2.ARCO MUST KNOW
3. University of Pennsylvania
4. Steinbergs classification

MANAGEMENT:
STAGE 0/ STAGE I

-Stanzolol (Anabolic steroid)

- Lovastatin
-Alandronate
-Enoxparin

Stage II
Core decompression +/- Bonegrafting
Vascularised/ non vascuralised fibular bone graft
“Trap door” procedures- through articular cartilage
Stem cells
Bone morphogenic proteins
Tantlam rods RECENT ADVANCES

STAGE III/ STAGE IV

- Realignment osteotomies( Sugioka)

- Resurfacing arthroplasty
- Arthrodesis( usually not done as it is b/l condition)
- Arthroplasty

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 CAUDA EQUINA SYNDROME
Cauda equina syndrome is defined by a constellation of symptoms that result from terminal
spinal nerve root compression in the lumbosacral region
considered one of the few true medical emergencies in orthopaedics
key features
bilateral leg pain
bowel and bladder dysfunction
saddle anesthesia
lower extremity sensorimotor changes
Epidemiology
1-6% of lumbar disc herniations
Pathophysiology
space-occupying lesion within lumbosacral canal, including
disc herniation (most common)
spinal stenosis
tumors
trauma (retropulsion of fracture fragment, dislocation or collapse)
spinal epidural hematoma
epidural abscess
Associated conditions
deep vein thrombosis (DVT)
is a well known complication after spinal trauma or spine surgery
Anatomy
Spinal cord
conus medullaris
tapered, terminal end of the spinal cord
terminates at T12 or L1 vertebral body
filum terminale
non-neural, fibrous extension of the conus medullaris that attaches to the coccyx
cauda equina (horse's tail)
collection of L1-S5 peripheral nerves within the lumbar canal
compression considered to cause lower motor neuron lesions
Bladder

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receives innervation from
parasympathetic nervous system (pelvic splanchnic nerves and the inferior hypogastric
plexus) and
sympathetic plexus (hypogastric plexus)
external sphincter of the bladder is controlled by the pudendal nerve
lower motor neuron lesions of cauda equina will interrupt the nerves forming the bladder
reflex arcs

Presentation
Symptoms
back pain
unilateral or bilateral leg pain is the most common presenting symptom after back pain
saddle anesthesia
impotence
sensorimotor loss in lower extremity
neurogenic bladder dysfunction
disruption of bladder contraction and sensation leads to urinary retention and eventually to
overflow incontinence
bowel dysfunction is rare
Physical exam
Inspection
Lower extremity muscle atrophy with insidious presentations (e.g. spinal stenosis)
fasciculations are rare
Palpation
lower back pain/tenderness is not a distinguishing feature
palpation of the bladder for urinary retention
Neurovascular examination
bilateral lower extremity weakness and sensory disturbances
decreased or absent lower extremity reflexes
Rectal/genital examination
reduced or absent sensation to pinprick in the perianal region (S2-S4 dermatomes), perineum,
and posterior thigh
decreased rectal tone or voluntary contracture

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diminished or absent anal wink test and a bulbocavernosus reflex
Imaging
MRI
study of choice to evaluate neurologic compression
CT myelography
study of choice if patient unable to undergo MRI
Treatment
Operative
urgent surgical decompression within 48 hours
indications
significant suspicion for CES
severity of symptoms will increase the urgency of surgical decompression
techniques
diskectomy
laminectomy
outcomes
studies have shown improved outcomes in bowel and bladder function and resolution of
motor and sensory deficits when decompression performed within 48 hours of the onset of
symptoms
Surgical Techniques
Surgical decompression of neural elements
Approach
posterior midline approach to lumbar spine
Diskectomy vs. wide laminectomy and diskectomy
no comparison studies between microdiskectomy alone and wide decompression combined
with microdiskectomy.
Complications
Delayed presentation or decompression
sexual dysfunction
urinary dysfunction requiring catheterization
chronic pain
persistent leg weakness

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 BLOUNT’S DISEASE
- First described by Dr.Blount in 1937
- Tibia vara caused due to deformity at the medial side of the proximal tibial physis
TWO TYPES DEPENDING ON AGE
INFANTILE ADOLOSCENT
<8YEARS >8YEARS

- Can be unilateral or bilateral

- H/O early walking is present usually
CLASSIFICATION:
- Described by Langenskoild
- Radiological classification varying with advancing age
- Stage 1-4, increased metaphyseal beaking and sloping
- Stage 5-6, epimetaphyseal bone bridge
CLINICAL FEATURES:
- Progressive deformity
- Limb length discrepancy
- Instability
- Early waling and obesity
- Bowing
- Ligamentous laxity
X-RAY: AP and lateral views:
- Medial tibial epiphysis – deficient
- Medial tibial physis – widening
- Medial tibial metaphysis – beaking
- Tibial diaphysis – bowing
- Knee – genu varum
- Tibia – lateral shift
- Fibula – posterior shift
Angles to be measures:
- Tibio-femoral angle
- Metaphyseal-diaphyseal angle

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- Mechanical axis of the limb
TREATMENT:
1. LESS THAN 3 YEARS: stage 2 deformity
- Bracing, >20hours a day, until correction is present for at least one year or surgical correction
is required
2. 3-8 years:
- Usually stage 2 or 3
- Osteotomy is done
- Over correction is performed as deformity can recur
3. For stage 4 and 5 of disease:
- Physiological closure of physis is mostly happened, if so corrective osteotomy
- If closure has not occurred, lateral epiphysiodeis

4. For stage 6:
- There is a bony bridge across physis
- If growth is present less than 2 years, then corrective osteotomy with lateral epiphysiodesis
can be done
- If growth is present more than 2 years, then corrective osteotomy with lateral epiphysiodesis
and lengthening procedure should be done
COMPLICATIONS:
1. Common peroneal nerve injury
2. Recurrence
3. Anterior tibial artery injury

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 BIOMECHANICS OF HIP JOINT
Joint reaction force defined as force generated within a joint in response to forces acting on
the joint in the hip, it is the result of the need to balance the moment arms of the body weight
and abductor tension (see diagram to right) maintains a level pelvis Coupled forces when two
movements and associated forces are coupled Joint congruence relates to fit of two articular
surfaces high congruence increases joint contact area Instant center of rotation point about
which a joint rotates often changes during rotation due to joint translation center of gravity of
human is just anterior to S2 Friction and lubrication not a function of contact area lubrication
decreases friction examples coefficient of friction of human joints is .002 to .04 TJA (metal
on PE) is .05 to .15
Hip Free Body Analysis

Free body analysis diagram

W = gravitational force
weight of the body minus weight of ipsilateral extremity (or5/6 body weight)
My = abductor muscle force
R = joint reaction force
can reach 3 to 6 times body weight
Solving for joint reaction force (R)
step 1: calculate My
principle
sum of all moments equals 0
in this case, the moments are created by My and W
equation
(A x My) + (B x W) = 0
assume A = 5cm and B = 12.5cm (this information will be given to you)
My = 2.5W

232
step 2: calculate Ry
Ry = My + W
Ry = 2.5W + W
Ry = 3.5W
step 3: calculate R
R = Ry / (cos 30°)
R = 3.5W / (cos 30°)
R = ~4W

Clinical Implications
Actions that decrease joint reaction force include
increase in ratio of A/B (shift center of rotation medially)
acetabular side
moving acetabular component medial, inferior, and anterior
femoral side
increasing offset of femoral component
long stem prosthesis
lateralization of greater trochanter
by using increased offset neck/prosthesis
varus neck-shaft angulation
increases shear across joint
patient's gait
shifting body weight over affected hip
this results in Trendelenburg gait
cane in contralateral hand
reduces abductor muscle pull and decreases the moment arm between the center of gravity
and the femoral head
carrying load in ipsilateral hand
produces additional downward moment on same side of rotational point
Actions that increase joint reaction force include
valgus neck-shaft angulation
decreases shear across joint

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Stability
Deep-seated “ball-and-socket” joint is intrinsically stable.
Sourcil
Condensation of subchondral bone under superomedial acetabulum
R is maximal at this point.
Trendelenburg gait - A cane in the contralateral hand produces an additional moment. This
can reduce R up to 60%. Carrying a load in the ipsilateral hand also decreases R

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 BIOMECHANICS OF KNEES

1. Kinematics
ROM
Ten degrees of extension (recurvatum) to 130 degrees of flexion.
Functional ROM is nearly full extension to about 90 degrees of flexion.
117 degrees: required for squatting and lifting
110 degrees: required for rising from a chair after TKA
Rotation varies with flexion.
At full extension, rotation is minimal.
At 90 degrees of flexion, ROM is 45 degrees of external rotation and 30 degrees of internal
rotation.
Amount of abduction or adduction is essentially 0 degrees.
A few degrees of passive motion is possible at 30 degrees of flexion.
Knee motion is complex, about a changing instant center of rotation.
Polycentric rotation
Excursions of 0.5 cm for the medial meniscus and 11 cm for the lateral meniscus are possible
during 120-degree arc of motion.
Joint motion
Instant center traces a J-shaped curve about the femoral condyle.
Moves posteriorly with flexion
Flexion and extension involve both rolling and sliding.
Femur internally rotates (external tibial rotation) during the last 15 degrees of extension.
“Screw home” mechanism
Related to different in radii of curvature for the medial and lateral femoral condyles and the
musculature
Posterior rollback increases maximum knee flexion.
Tibiofemoral contact point moves posteriorly.
Normal rollback is compromised by PCL sacrifce, as in some TKAs.
Axis of rotation of the intact knee is in the medial femoral condyle.
Patellofemoral joint has sliding articulation.
Patella slides 7 cm caudally with full flexion.
Instant center is near the posterior cortex above the condyles.

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2. Kinetics
Knee stabilizers
Ligaments and muscles play the major stabilizing role
ACL:
Typically subjected to peak loads of 170 N during walking
Up to 500 N with running
Ultimate strength in young patients: about 1750 N
Failures by serial tearing at 10% to 15% elongation
PCL: Sectioning increases contact pressures in the medial compartment and the
patellofemoral joint.
Joint forces
Tibiofemoral joint
Knee joint surface loads
Three times body weight during level walking
Up to four times body weight with stair walking
Menisci
Help with load transmission
Bear one third to half body weight
Removal increases contact stresses
Up to four times the load transfer to bone
Quadriceps produces maximum anterior force on the tibia at 0 to 60 degrees of knee flexion.
Patellofemoral joint
Patella aids in knee extension.
Increases the lever arm
Stress distribution
It has the thickest cartilage in the entire body.
Bears the greatest load
Bears half the body weight with normal walking
Knee Stabilizers
Medial Superfcial MCL (primary), joint capsule, medial meniscus, ACL/PCL
Lateral Joint capsule, IT band, LCL (middle), lateral meniscus, ACL/PCL (90 degrees)
Anterior ACL (primary), joint capsule
Posterior PCL (primary), joint capsule; PCL tightens with internal rotation
Rotatory Combinations: MCL checks external rotation;ACL checks internal rotation

236
 CERVICAL MYELOPATHY
Cervical spondylosis result in three clinical entities:
Discogenic neck pain (axial pain)
Radiculopathy (root compromise)
Myelopathy (cord compression) and combinations of these conditions

Epidemiology
Cervical myelopathy is more common in men and tends to present earlier than in women.
Changes are more common in patients with RA where 85% of those with moderate to severe
disease will have x-ray changes.
When patients with cervical myelopathy present in the third or fourth decade of life it is
usually secondary to congenital stenosis.

If it presents later in life, degenerative spondylosis is usually the underlying cause.

Patients who have a congenitally narrow canal are predisposed to the effects of spondylotic
changes earlier, as there is less space in the canal to accommodate the compressing lesions.

Pathological process
The underlying cause of the condition is compression of the long tracts in the spinal cord.
The normal diameter of the cervical spinal canal is between 17 mm and 18 mm.
When this diameter falls below 12 mm to 14 mm for any reason this is likely to cause
stenosis and myelopathic symptoms.
The average diameter of the spinal cord in the cervical spine is 10 mm.
The common pathological processes underlying cervical myelopathy are outlined below:
 Disc Herniation.
Discogenic disease may cause myelopathy in the acute setting as a large central soft disc
herniation causing cord compression. Disc disease is also often seen as part of the
compressive lesion in spondylotic disease.
 Congenital.
Myelopathy due to congenital stenosis does not have a specific underlying lesion. It is caused
by a canal diameter which is narrower from birth. It is often not symptomatic until secondary
degeneration further narrows the canal.

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 Spondylosis.
CSM is the result of degenerative changes which develop with age, including ligamentum
flavum hypertrophy or buckling, facet joint hypertrophy, disc protrusion and posterior
spondylotic ridges. One or all of these changes contribute to an overall reduction in canal
diameter which may result in cord compression. Spondylolisthesis usually occurs in the lower
cervical spine. It is caused by arthrosis of the facet joints combined with disc degeneration
leading to instability.
 Post traumatic myelopathy.
Trauma may induce myelopathy or precipitate symptoms of an underlying stenosis of the
spinal canal. Smaller diameter canals have an increased chance of neurological injury in
trauma.
 Ossification of the posterior longitudinal ligament (OPLL).
This is a common feature in patients with cervical myelopathy with up to 25% being affected.
It is particularly common in patients from the far east. It is seen on imaging as areas of
ossification behind the vertebral bodies. The extent is best defined by CT.
 Myelopathy due to tumour expansion.
Intraspinal tumours are a relatively uncommon cause of cervical myelopathy but must always
be considered given the potentially catastrophic consequences of the diagnosis being missed.
Tumours may originate in the spinal cord (intramedullary tumours) or compress from outside
(extramedullary tumours). Metastatic deposits are usually slow growing with gradual onset of
symptoms.

Symptoms
Patients may present with a range of symptoms and many of these are non-specific. It is
important to remember that although cervical myelopathy is a disease of the cervical spine it
may manifest with lower as well as upper limb symptoms.
The classical presentation is
1. loss of balance with poor coordination,
2. decreased dexterity,
3. weakness,
4. numbness and
5. paralysis in severe cases.
Pain is a symptom in many patients but it is important to remember that it may be absent

238
which often leads to a delay in diagnosis.
In older patients it often manifests with a rapid deterioration of gait and hand function.
Cervical lesions in the region of C3 - C6 cause a loss of manual dexterity with difficulties
in writing and nonspecific alteration in arm weakness and sensation.
Cervical lesions from C6 - C8 tend to lead to a syndrome of spasticity and loss of
proprioception in the legs. These patients often have gait disturbance and suffer multiple
falls. Multilevel disease is common causing a mixture of symptoms.
Common presenting complains are:
• Heavy feeling in the legs
• Poor exercise tolerance
• Radiculopathy
• Poor fine motor skills
• L’Hermitte’s phenomenon - intermittent electric shock sensations in the limbs, exacerbated
by neck flexion
• Numbness and tingling in the limbs
Late in the disease where compression is severe, if surgical decompression is not performed
the symptoms progress to sphincter dysfunction and quadriparesis.
Examination findings
Patients present with a number of clinical findings which are predominantly upper motor
neuron signs.
• Weakness is more severe in the upper limbs.
• Gait is usually affected with an ataxic broad based gait.
• Hypertonia - increased resting muscle tone identified by passive movement.
• Hyperreflexia - exaggerated response to normal physiological reflexes.
• Ankle clonus - forced dorsiflexion at the ankle giving rise to sustained beats of clonus
(more than three beats is considered pathological).
• Babinski sign - extension of the great toe on scratching of the sole of the foot.
• Hoffman’s reflex - flicking of the terminal phalynx of the middle or ring finger causing
concurrent flexion at the terminal phalynx of the thumb and index finger.
• Finger escape sign - the small finger spontaneously abducts due to weak intrinsic muscles.
Classification
The most comprehensive classification system widely in use is The Nurick classification
probably the most useful classification to be used for stratifying the level of functional
restriction in mobility, caused by cervical myelopathy.

239
The Ranawat classification is used to categorise patients who have rheumatoid myelopathy
based on their history and examination findings. It can be used to predict recovery after
surgical intervention.

Nurick’s Functional Scale

Grade Level of Neurological Involvement
Grade I No difficulty in walking
Grade II Mild gait involvement not interfering with employment
Grade III Gait abnormality preventing employment
Grade IV Able to walk only with assistance
Grade V Chairbound or bedridden
Ranawat Classification of Neurological Deficit
Class Level of Neurological Involvement
Class I No neural deficit
Class II Subjective weakness, dysaesthesia and hyperreflexia
Class III A Objective weakness and long tract signs; patient ambulatory
Class III B Objective weakness and long tract signs; patient no longer ambulatory

Imaging
There are a number of ways that imaging can be used to diagnose the condition and help
decide on a management plan. They are often used in combination to give a clear overall
view of the pathology.

X-ray.
Plain x-ray is the initial imaging modality of choice. Anteroposterior (AP) and lateral views
should be requested. These will show spondylolisthesis, fusion and osteophytes clearly.
Absolute measurements of the canal size are not reliable from x-ray. However, Pavlov’s ratio
can be used as a guide to indicate narrowing. It is worked out as the AP diameter of the spinal
canal divided by the AP diameter of the vertebral body. Where instability is suspected to be
the cause of symptoms (especially in RA) flexion and extension views of the cervical spine
will show abnormal motion.
MRI.
MRI gives a detailed three-dimensional image of the cervical spinal cord and any
compression present. It has been key in recent years in diagnosing the condition early. The
advantages of MRI are that it involves no radiation and gives excellent imaging of the disc

240
and nerves including intrinsic changes in the cord and nerve roots . The extent of panus in
patients with RA is also well demonstrated. In recent years new techniques have become
more prevalent which reduce the impact of artifact caused by instrumentation. MRI is not as
good at identifying the extent of osteophytes and disc calcification so when these are
suspected MRI should be supplemented with CT.

CT.
There are two main uses for CT scanning in the diagnosis of cervical myelopathy.
There are some patients who are unable to undergo MRI imaging, often because of an
implanted cardiac device. For these patients a CT myelogram offers an imaging option which
is almost as sensitive as MRI.
In general CT can also give additional information on the presence of osteophytes or other
bony compressive lesions which are underestimated on MRI scans

Conservative management
Cervical myelopathy is predominantly progressive and only a small number of patients
experience regression in their symptoms. Some patients are medically co-morbid making
surgery high risk. In these patients a trial of conservative management should certainly be
considered.
Non-operative management should involve regular analgesia.

Gabapentin should be considered as an adjunct to simple analgesics for patients who have
significant pain from radicular symptoms.

A soft collar may be used, especially when instability is a significant cause of symptoms
which is often the case in patients with RA.

Physiotherapy may be of use in patients who can tolerate it which can involve traction, heat
and ultrasound therapy.

Activity modification can be a useful way of limiting factors which provoke symptoms.
Extension of the cervical spine and restriction of heavy lifting can be particularly helpful.
The use of epidural steroid injection is controversial. They are primarily used in patients who
have significant radicular symptoms. Patients who suffer a failure of at least three months

241
conservative management should be considered for operative intervention. Particularly if
symptoms impair activities of daily living surgical intervention should be considered. Any
patient who exhibits progressive neurological deficit should undergo operative intervention
unless the risk of surgery makes this impossible. It should be made clear to the patient that
the main aim of operative intervention is to prevent progression of the neurological
symptoms and that recovery is unpredictable and cannot be guaranteed.

Surgical management

The primary goal of any surgery is to restore the diameter of the spinal canal such that
compression of the spinal cord is relieved. The choice of operation depends to a degree on the
surgeon’s experience with any particular procedure. However, the location of stenosis and the
vertebral body alignment will guide whether an anterior or posterior approach is suitable.
Although controversial, there have been studies which show that even when a patient is
bedridden because of cervical myelopathy, there is a benefit to operative intervention.
Surgical interventions can be divided into two anatomical areas; the upper (C0-C2) and
lower cervical spine (C3-C7) and two approaches; anterior and posterior. When considering
approach, the decision making process has to consider a number of factors

• Main site of cord compression

• whether compression comes from the front or the back
• the number of levels involved
• Bone quality
• Deformity (mainly kyphosis)
• Instability (stepladder deformity in RA patients - multiple sequential levels of subluxation)
• Presence of fused segments
• Patient wishes and expectations

Procedures
Combined anterior (cervical) Smith-Robinson discectomy and fusion (ACDF)
Involves excision of osteophytes and corpectomy with a strut graft fusion with or without
instrumentation
Anterior plating may increase the fusion rate in multilevel discectomies with fusion and will
protect a strut graft in multilevel corpectomies.

242
Adjunctive posterior plating may be considered in cases involving prior laminectomy,
multilevel corpectomy and strut grafting, or three-level ACDF.
Early postoperative complications:
Dysphagia from esophageal retraction (9.5%)
Surgical site hematoma with airway compromise (1%-11%)
Recurrent laryngeal nerve injury
Higher incidence from right-sided approach (controversial)
Late postoperative complications:
Nonunion
Single level: 5%
Two levels: 6%
Three levels: 10%
Treatment of a nonunion should be posterior fusion.
Adjacent segment disease
Symptomatic disease in 25% at 10 years after ACDF

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 CHONDROSARCOMA

Classification:

WHO classification Bone

1. Conventional chondrosarcoma- Primary or Secondary
2. Juxtacortical chondrosarcoma
3. Mesenchymal chondrosarcoma
4. Dedifferentiated chondrosarcoma
5. Clear cell chondrosarcoma

Soft tissues
1. Extraskeletal myxoid chondrosarcoma
2. Mesenchymal chondrosarcoma

Important points/ Salient points:

 90% are primary conventional type

 Secondary chondrosarcoma occurs at a younger age group
 Adulthood- 3rd decade of life + 5th-7th decades peak incidences
 Male are twice commonly affected
 Solitary osteochondroma < 1 %cof malignant transformation
 Osteochondromatosis- 5%
 Ollier’s disease or Maffuci’s syndrome-25 to 30% risk for malignant transformation
 Cartliage cap > 2 cm
 Sudden onset of pain
 Lysis around calcification (cortical destruction + soft tissue mass)

Conventional types:
- Murphy et al suggested that based on Xrays two types of lesion
Adaptive- Expansile and thickening of > 2/3rd of the cortex
Aggressive- Cortical disruption + soft tissue expansion

244
 Rosenthal et al( Radiographs)
Low grade High grade

Dense calcifications rings or spicules Faint amorphous calcifications

Wide spread uniformly distributed calcifications Large non calcified area
Eccentric lobular soft tissue mass Concentric growth of soft tiss

Classification based on histology:

Evan’s histologic classification
Grade I
- Small densely staining nucleus
- Chondroid or myxoid matrix
- Multiple nuclei in one lacuna
- Calcification and bone formation are usually not present
Grade II
- Moderate size of nuclei
- Mitosis < 2 / high power field
- Increased cellularity
- Polar staining and have visible intranuclear detail
Grade III
- > 2 mitoses/ high power field
- Greatest cellularity in the peripheral of tumor lobules
- Dense cellularity- no matrix seen

Treatment:
Radioresistant and Chemoresistant
Surgery:
Enchondroma or Chondrosarcoma in situ – Intralesional curettage or wide excision
Grade II/ Grade III- Wide excision + reconstruction.

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 CONGENITAL TALIPES EQUINO VARUS

Introduction
Idiopathic deformity of the foot of unclear etiology
Epidemiology
demographics
most common birth defect
1:250 to 1:1000 depending on population
highest prevalence in Hawaiians and Maoris
more common in males
location
half of cases are bilateral
Genetics
genetic etiology is strongly suggested
unaffected parents with affected child have 2.5% - 6.5% chance of having another child with a
clubfoot
familial occurrence in 25%
recent link to PITX1, transcription factor critical for limb development
common genetic pathway may exist with congenital vertical talus
Associated conditions
hand anomalies (Streeter dysplasia)
diastrophic dysplasia
arthrogryposis
tibial hemimelia
myelodysplasia
amniotic band syndrome
Pierre Robin syndrome
Opitz syndrome
Larsen syndrome
prune-belly syndrome
absent anterior tibial artery

246
Anatomy
Muscles contractures lead to the characteristic deformity that includes (CAVE)
midfoot Cavus (tight intrinsics, FHL, FDL)
forefoot Adductus (tight tibialis posterior)
hindfoot Varus (tight tendoachilles, tibialis posterior, tibialis anterior)
hindfoot Equinus (tight tendoachilles)
Bony deformity consists of
talar neck is medially and plantarly deviated
calcaneus is in varus and rotated medially around talus
navicular and cuboid are displaced medially
Table of foot deformity muscle imbalances

Presentation
Physical exam
inspection
small foot and calf
shortened tibia
medial and posterior foot skin creases
foot deformities
hindfoot in equinus and varus
differentiated from more common positional foot deformities by rigid
equinus and resistance to passive correction
midfoot in cavus
forefoot in adduction
Imaging
Radiographs
recommended views
dorsiflexion lateral (Turco view)
shows hindfoot parallelism between the talus and calcaneus
will see talocalcaneal angle < 35° and flat talar head (normal is talocalcaneal angle >35°)
AP
talocalcaneal (Kite) angle is < 20° (normal is 20-40°)

247
talus-first metatarsal angle is negative (normal is 0-20°)
also shows hindfoot parallelism
Ultrasound
helpful in prenatal diagnosis (high false positive rate)
can be diagnosed as early as 12 weeks of gestational age
Treatment
Nonoperative
serial manipulation and casting (Ponseti method) indications there has been a trend away from
surgery and towards the nonoperative
Ponseti method due to improved long term results outcomes Ponseti method has 90% success rate
with appropriate treatment, children can be expected to walk and run Operative

posteromedial soft tissue release and tendon lengthening

indications resistant feet in young children "rocker bottom" feet that develop as a result of serial
casting syndrome-associated clubfoot delayed presentation >1-2 years of age performed at 9-10
months of age so the child can be ambulatory at one year of age outcomes requires postoperative
casting for optimal results extent of soft-tissue release correlates inversely with long-term function
of the foot and patient

medial column lenthening or lateral column-shortening osteotomy, or cuboid decancellation

indications older children from 3 to 10 years triple arthrodesis indications in refractory clubfoot at
8-10 years of age
contraindicated in insensate feet due to rigidity and resultant ulceration talectomy indications
salvage procedure in older children (8-10 yrs) with an insensate foot

multiplanar supramalleolar osteotomy

indicationssalvage procedure in older children with complex, rigid, multiplanar clubfoot
deformities that have failed conventional operative management gradual correction by means of
ring fixator (Taylor Spatial Frame) application complex deformity resistant to standard methods of
treatment

248
Techniques
Serial manipulation and casting (long leg cast)
goal is to rotate foot laterally around a fixed talus
order of correction (CAVE)
midfoot cavus
forefoot adductus
hindfoot varus
hindfoot equinus

Ponseti Method
Month 1- Weekly serial • First correct cavus with forefoot SUPINATED (NOT pronation)
4 casting (with knee in by aligning the plantar-flexed 1st MT with the remaining
90° of flexion ) metatarsals (forcible pronation would increase cavus deformity
with forefoot as the 1st MT is plantar-flexed further)
supination, then • Secondly correct adduction and heel varus by rotating
forefoot abduction calcaneus and forefoot around talus (head of talus acts as a
fulcrum) into forefoot ABDUCTION

Tendoachilles • Equinus correction last with tendinoachilles lengthening (TAL)

lengthening (TAL) at • Perform when foot is 70° abducted and heel is in valgus
week 8 required in • Ponseti method uses a complete transverse cut of achilles
80% • Cast in maximal dorsiflexion after TAL

Month 4- Foot abduction • With Denis-Brown bar in external rotation (70° in

8 orthosis (FAO) clubfoot and 40° in normal foot)
• 23 hours a day for 3 • Fit FAO on day of TAL
months after
correction
• night time/nap time
only until age 4 years

2-4 years Tibialis anterior • 10-20% will need TA transfer with or without repeat
tendon transfer (TA TAL for recurrent supination, varus, and/or equinus
transfer) at 2 yrs of • Indicated if the patient demonstrates supination of the
age (10-20% will foot during dorsiflexion (a dynamic intoeing gait)
require)

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Complications
Complications with nonoperative treatment deformity relapse relapse in child < 2 years early relapse
usually the result of noncompliance with FAO treat with repeat casting relapse in child > 2 years
treat initially with casting consider tibialis anterior tendon transfer to lateral cuneiform (can only
perform if lateral cuneiform is ossified) consider repeat Achilles tendon lengthening dynamic
supination treat with whole anterior tibial tendon transfer (preferred in OITE question over split
anterior tibial tendon transfer) Complications with surgical treatment residual cavus result of
placement of navicular in dorsally subluxed position pes planus results from overcorrection
undercorrection intoeing gait osteonecrosis of talus
results from vascular insult to talus resulting in osteonecrosis and collapse dorsal bunion caused by
dorsiflexed first metatarsal (FHB and abductor hallucis overpull secondary to weak plantar flexion)
and overactivity of anterior tibialis treat with capsulotomy, FHL lengthening, and FHB flexor to
extensor transfer at MTP joint

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 CONGENTIAL VERTICAL TALUS
- The talus is vertically placed in the foot at birth
- A milder form is called as oblique talus
Other names:
- Rocker bottom foot
- Persian slipper foot
- Convex pes valgus
ETIOLOGY:
- Unknown
- Associated with arthrogryposis and myelomeningocele
- 50% bilateral
- Equal in both sexes
PATHOANATOMY:
- Hind foot in equinus
- Forefoot in dorsiflexion
- Navicular dislocated dorsally
- Calcaneocuboid dislocation
- Everted foot
CLASSIFICATION:
COLEMAN:
- Type 1: Associated with calcaneocuboid dislocation
- Type 2: No calcaneocuboid dislocation

CLINICAL FEATURES:
- Present at birth
- Abnormality present at forefoot, midfoot and hindfoot
- Talus aligns as an hourglass with the tibia on walking
- Callosities over foot
- Peg-leg gait(walking with heels on)
- Heel does not touch the ground
X-RAY:
- AP view and plantar flexed lateral view(Eyre brook view)

251
- The long axis of the 1st metatarsal passes dorsal to the long axis of talus, which normally
passes plantigrade
- Look for meary angle

TREATMENT:
AIM:
- Restoration of normal anatomy and maintain it
- Functionally stable and pain free foot
NON OPERATIVE METHODS:
- For younger children
- Serial manipulation and casting
- Usually not very effective
SURGICAL MANAGEMENT:
Children between 1-4 years of age:
- Joystick technique
- Open reduction and realignment
- Long leg cast for 8 weeks
- AFO for 6 months
Children between 4-8 years:
- Open reduction
- Soft tissue release
- Extra articular arthrodesis(Grice green technique)
Children more than 8 years with severe deformity:
- Triple arthrodesis
- Cast for 12 weeks
- Non weight bearing waling

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 EWINGS SARCOMA
Introduction
A distinctive small round cell sarcoma
Epidemiology
demographics
typically found in patients from 5-25 years of age
second most common malignant bone tumor in children
uncommon in African Americans and Chinese
locations
~50% are found in the diaphysis of long bones
most common locations pelvis, distal femur, proximal tibia, femoral diaphysis,
and proximal humerus
5% metaphysis
Genetics
t(11:22) translocation
Staging
almost all tumors are MSTS stage IIB or III
Prognosis
survival
5 yr survival
65-80% for localized disease
25-40% for metastatic disease
10 yr survival
60% for localized disease
30% for metastatic disease
poor prognostic factors
tumor size/location
tumors greater than 100cm3 or >8cm in size
spine and pelvic tumors (worst) > proximal extremities > distal extremities
(best prognosis)
age and sex
older age (>14) worse prognosis
male worse prognosis

253
laboratory parameters
elevated lactic dehydrogenase levels (>200IUml) indicates large tumors/metastatic
disease
anemia and elevated WBC indicates extensive disease
molecular pathology
p53 mutation in addition to t(11:22) translocation
overexpression of cell proliferation antigen Ki-67
overexpression of HER-2/neu
metastases (most important prognostic indicator)
presence of mets has poor prognosis
lung metastases better prognosis than bone/bone marrow mets
skip metastases (same bone) better pronosis than metastases to another site
chemotherapy response
< 90% necrosis with chemotherapy
Symptoms
Presentation
pain often accompanied by fever
often mimics an infection
Physical exam
swelling and local tenderness
Imaging
Radiographs
required images
AP and lateral of affected area
findings
large destructive lesion in the diaphysis or metaphysis with a permeative moth-
eaten appearance
lesion may be purely lytic or have variable amounts of reactive new bone formation
periosteal reaction may give "onion skin" or "sunburst" appearance
Bone scan
indications
required as initial staging workup

254
findings
will show very "hot" lesion
MRI
indications
required as initial staging workup to identify soft-tissue extension and marrow
involvement
findings
often shows a large soft tissue component
CT chest
indications
required as initial staging workup to look for pulmonary metastasis
Studies
Labs
ESR is elevated
WBC is elevated
anemia is common
lactic dehydrogenase
Bone marrow biopsy
required as part of workup for Ewing's to rule out metastasis to the marrow
Histology
Gross appearance
may have liquid consistency mimicking pus
Characteristic findings
sheets of monotonous small round blue cells
prominent nuclei and minimal cytoplasm
may have pseudo-rosettes (circle of cells with necrosis in center)
Immunostaining
positive
CD99 (in 95%)
MIC2
vimentin
PAS positive (intracellular glycogen)

255
neuron specific enolase (NSE)
S100
Leu7
negative
cytokeratin
reticulin (positive in lymphoma)
neurofilament (positive in neuroblastoma)
Differentials
Small-round-cell tumor differential (by age)
< 5 yrs: neuroblastoma or leukemia
5-10 yrs: eosinophilic granuloma
5-30 yrs: Ewing's sarcoma
>30 yrs: lymphoma
> 50 yrs: myeloma
Osteosarcoma
Osteomyelitis
Treatment
Nonoperative
chemotherapy + radiation therapy
indications non-resectable tumors (eg. large spinal tumors) sites where functional deficit is unacceptable
trend is towards surgical resection / away from RT because of morbidity associated with radiation and
risk of secondary malignancies Operative
chemotherapy + limb salvage resection ± adjuvant radiation
indications standard of care in most patients where primary tumor can be completely removed
(expendable and surgically reconstructible sites) chemotherapy vincristine, doxorubicin,
cyclophosphamide, and dactinomycin preoperative chemotherapy given for 8-12 weeks followed by
surgical resection and maintenance chemotherapy for 6-12 months adjuvant radiation not necessary if
margins are adequate and there is good response to chemotherapy indications positive post-resection
surgical margins patients who present with widely metastatic disease where chemotherapeutic
response has been poor

256
 HALLUX VALGUS
Introduction

 Not a single deformity, but rather a complex deformity of the first ray
o often accompanied by deformities and symptoms in lesser toe
o two forms exist
 adult hallux valgus
 adolescent & juvenile hallux valgus
 Epidemiology of adult hallux valgus
o more common in women
o 70% of pts with hallux valgus have family history
 genetic predisposition with anatomic anomalies
o risk factors
 intrinsic
 genetic predisposition
 increased distal metaphyseal articular angle (DMAA)
 ligamentous laxity (1st tarso-metatarsal joint instability)
 convex metatarsal head
 2nd toe deformity/amputation
 pes planus
 rheumatoid arthritis
 cerebral palsy
 extrinsic
 shoes with high heel and narrow toe box
 Pathoanatamy
o valgus deviation of phalanx promotes varus position of metatarsal
o the metatarsal head displaces medially, leaving the sesamoid complex laterally
translated relative to the metatarsal head
o sesamoids remain within the respective head of the flexor hallucis brevis tendon and
are attached to the base of the proximal phalanx via the sesamoido-phalangeal
ligament
o this lateral displacement can lead to transfer metatarsalgia due to shift in weight bearing
o medial MTP joint capsule becomes stretched and attenuated while the lateral

257
 capsule becomes contracted
o adductor tendon becomes deforming force
 inserts on fibular sesamoid and lateral aspect of proximal phalanx
o lateral deviation of EHL further contributes to deformity
o plantar and lateral migration of the abductor hallucis causes muscle to plantar
flex and pronate phalanx
o windlass mechanism becomes less effective
 leads to transfer metatarsalgia
 Associated conditions
o hammer toe deformity
o callosities
 Juvenile and Adolescent Hallux valgus
o factors that differentiate juvenile / adolescent hallux valgus from adults
 often bilateral and familial
 pain usually not primary complaint
 varus of first MT with widened IMA usually present
 DMAA usually increased
 often associated with flexible flatfoot
o complications
 recurrence is most common complication (>50%), also overcorrection
and hallux varus
Anatomy

Presentation

Symptoms
presents with difficulty with shoe wear due to medial eminence
pain over prominence at MTP joint
compression of digital nerve may cause symptoms

258
Physical exam
Hallux rests in valgus and pronated due to deforming forces illustrated above
examine entire first ray for
1st MTP ROM
1st tarsometatarsal mobility
callous formation
sesamoid pain/arthritis
evaluate associated deformities
pes planus
lesser toe deformities
midfoot and hindfoot conditions
Imaging

 Radiographs
o views
 standard series should include weight bearing AP, Lat, and oblique views
 sesamoid view can be useful
o findings
 lateral displacement of sesamoids
 joint congruency and degenerative changes can be evaluated
 radiographic parameters (see below) guide treatment

259
Radiographic Measurements in Hallux Valgus

Hallux valgus Long axis of 1st MT and prox. Identifies MTP Normal
(HVA) phal. deformity < 15°

Intermetatarsal Between long axis of 1st and < 9°

angle (IMA) 2nd MT

Distal metatarsal Between 1st MT long. axis and Identifies MTP joint < 10°
articular (DMAA) line through base of distal incongruity
articular cap

Hallux valgus Between long. axis of distal < 10 °

interphalangeus phalanx and proximal phalanx
(HVI)

Treatment - Adult Hallux Valgus

 Nonoperative
o shoe modification/ pads/ spacers/orthoses
 indications
 first line treatment
 orthoses more helpful in patients with pes planus or metatarsalgia
 Operative
o surgical correction
 indications
 when symptoms present despite shoe modification
 do not perform for cosmetic reasons alone
 technique
 soft tissue procedure
o indicated in very mild disease in young female (almost never)
 distal osteotomy
o indicated in mild disease (IMA < 13)
 proximal or combined osteotomy
o indicated in more moderate disease (IMA > 13)

260
 1st TMT arthrodesis
o arthritis at TMT joint or instability
 fusion procedures
o indicated in severe deformity/spasticity/arthritis
 MTP resection arthroplasty
o only indicated in elderly patients with low functional demands
Treatment - Juvenile and Adolescent Hallux valgus

 Nonoperative
o shoe modification
 indications
 pursue nonoperative management until physis closes
 Operative
o surgical correction
 indications
 best to wait until skeletal maturity to operate
o can not perform proximal metatarsal osteotomies if physics
is open (cuneiform osteotomy OK)
 surgery indicated in symptomatic patients with an IMA > 10° and
HVA of > 20°
 severe deformity with a DMAA > 20 consider a double MT
osteotomy to correct orientation of MT head articular cartilage
 technique
 soft tissue procedure alone not successful
 similar to adults if physis is closed (except in severe deformity)

Techniques

Soft Tissue Procedures

modified McBride
indications
goal is to correct an incongruent MTP joint (phalanx not lined up with
articular cartilage of MT head). Usually done in patients with
a HVA less than 25 degrees

261
IMA deformity less than 15 degrees
usually in patient 30-50 years of age
rarely appropriate in isolation
usually performed in conjunction with
medial eminence resection
MT osteotomy
1st TMT arthrodesis (Lapidus procedure)
technique
includes
release of adductor from lateral sesamoid/proximal phalanx
lateral capsulotomy
medial capsular imbrication
(original McBride included lateral sesamoidectomy)
Metatarsal Osteotomies
distal metatarsal osteotomy
indications
mild disease (HVA ≤ 40, IMA < 13)
distal metatarsal osteotomies include
Chevron
biplanar Chevron (corrects DMAA)
Mitchell
may be combined with proximal phalanx osteotomy (Akin-medial
closing wedge osteotomy)
proximal metatarsal osteotomy
indications
moderate disease (HVA >40°, IMA >13°)
proximal metatarsal osteotomies include
crescentic osteotomy
Broomstick osteotomy
Ludloff
Scarf
double (proximal and distal) osteotomy
indications

262
severe disease (HVA 41-50°, IMA 16-20°)
first cuneiform osteotomy
indications
severe deformity in young patient with open physis
Proximal phalanx osteotomies
Akin osteotomy
indications
hallux valgus interphalangeus
congruent joint with DMAA <10°
as a secondary procedure if a primary procedure (e.g., chevron or distal soft-tissue procedure) did not
provide sufficient correction due to a large DMAA or HVI
some authors perform Akin together with/at the time of proximal osteotomy+distal soft tissue correction
because this results in progressive increase in HVI
Fusion procedures
Lapidus procedure (1st metatarsocuneiform arthrodesis with modified McBride)
indications
severe deformity (very large IMA)
arthritis at 1st TMT
metatarsus primus varus
hypermobile 1st TMT joint
concomitant pes planus
MTP Arthrodesis
indications are hallux valgus in
cerebral palsy
Down's syndrome
Rheumatoid arthritis
Gout
Severe DJD
Ehler-Danlos

Resection arthroplasty
proximal phalanx (Keller) resection arthroplasty

263
 indications
largely abandoned
rarely indicated in some elderly patient with reduced function demands

Surgical Indications for Various Techniques to treat Hallux Valgus

HVA IMA Modifier Procedure
Mild < 25° <13° Distal osteotomy Chevron osteotomy. Biplanar if
DMAA > 10° usually with mod McBride

Moderate 26-40° 13 - Proximal osteotomy Chevron/mod McBride + Akin osteotomy

15° +/- distal osteotomy
Proximal MT osteotomy and mod McBride
Severe 41-50° 16 - Double - Proximal MT osteotomy plus biplanar
20° osteotomy DMAA chevron, mod McBride
> 15°
Lapidus procedure plus Akin
Elderly/very low Keller
demand patient
Juvenile/Adolescent Double osteotomy of first ray
with DMAA > 20

Surgical Indications for Specific Conditions

Juvenile/Adolescent with First cuneiform osteotomy

open physis

Hypermobile 1st MT Lapidus procedure

DJD MTP Arthrodesis

Skin breakdown simple bunionectomy with medial eminance removal

Gout MTP Arthrodesis

Recurrence with pain in 1st Lapidus procedure

TMT joint

Rheumatoid arthritis MTP Arthrodesis

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Down's syndrome, CP, MTP Arthrodesis
Ehler-Danlos

Procedure Technique Indications Complications

Modified Includes release of 30-50 y/o female -Recurrence
McBride adductor from lateral withHVA 15-25 -Hallux varus
sesamoid/proximal IMA <13
phalanx, lateral IPA < 15
capsulotomy, medial
capsular imbrication
Original included lateral -never indicated -Hallux Varus
McBride sesamoidectomy and has
been abandoned
Chevron Distal 1st MT osteotomy reserved for mild to -AVN of MT head
(intra-articular). Can moderate deformities -recurrence
perform in two planes in adults -dorsal malunion with transfer
(Biplanar distal Chevron) and children, metatarsalgia
biplanar chevron--
>correct increased
DMAA
Mitchell Distal 1st MT osteotomy same as Chevron. -recurrence
(extra-articular). More reserved for mild to -malunion
proximal than Chevron) moderate -transfer metatarsalgia
deformities, rarely
utilized
Akin proximal phalanx medial -combined with
closing wedge osteotomy Chevron in moderate
to severe deformities
-hallux valgus
interphalangeus
Scarf / Ludloff Metatarsal shaft -IMA 14-18° -dorsal malunion with transfer
/ osteotomies. -DMAA is normal or metatarsalgia

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Mau increased -recurrence
Proximal Proximal metatarsal Severe deformity -hallux varus
crescentric or osteotomies. (plus IMA > 20 -dorsal malunion with transfer
Broomstick modified McBride) HVA > 50 metatarsalgia
-recurrence
Keller Include medial eminence largely abandoned -cock-up toe deformity
resection removal and resection of due to -poor potential for correction
arthroplasty base of proximal phalanx complications. of deformity
indicated only in
older patients with
reduced functional
demands
MTP -indicated in
arthrodesis moderate to severe
hallux valgus
- DJD of 1st MTP
- painful callosities
beneath lesser MT
heads
Lapidus first TMT joint -moderate or severe Nonunion (may or may not be
procedure arthrodesis with distal deformity symptomatic)
soft tissue procedures -hypermobility of dorsiflexion of the first
(medial eminence first ray metatarsal with transfer
removal, first web space metatarsalgia
release of AdH, lateral
capsule release)
First Opening wedge -children with Nonunion (may or may not be
Cuneiform osteotomy (often requires ligamentous laxity, symptomatic)
Osteotomy autograft) flatfoot, and
hypermobile first ray
- adolescent with an
open physis

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 Complications

Recurrence
most common cause of failure is insufficient preoperative assessment and failure
to follow indications
e.g., failure to recognize DMAA > 10°
inadequate correction of IMA
e.g., failure to do adequate distal soft tissue realignment
more common in juvenile/adolescent population
noncompliant patient that bears weight
Avascular necrosis
medial capsulotomy is primary insult to blood flow to metatarsal head
distal metatarsal oseotomy and lateral soft tissue release inconjunction do not
increase risk for AVN (Chevron plus lateral release thought to increase risk in the past)
Dorsal malunion with transfer metatarsalgia
due to overload of lesser metatarsal heads
risk associated with shortening of hallux MT
Lapidus
proximal crescentric osteotomies
Hallux Varus
caused by
overcorrection of 1st IMA
excessive lateral capsular release with overtightening of medial capsule
overresection of medial first metatarsal head
lateral sesamoidectomy
Cock up toe deformity
due to injury of FHL
most severe complication with Keller resection
2nd MT transfer metatarsalgia
Neuropraxia

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INTERVERTEBRAL DISC PROLAPSE -2
Function
- allows spinal motion and provides stability
- links adjacent vertebral bodies together
- responsible for 25% of spinal column height
Composition
Annulus fibrosus
- Outer structure that encases the nucleus pulposus
- composed of type I collagen that is obliquely oriented, water, and proteoglycans
- characterized by high tensile strength and its ability to prevent intervertebral distraction
- remains flexible enough to allow for motion
- high collagen / low proteoglycan ratio (low % dry weight of proteoglycans)
- fibroblast-like cells - responsible for producing type I collagen and proteoglycans

Nucleus pulposus
- Central portion of the intervertebral disc that is surrounded by the annulus fibrosis
- composed of type II collagen, water, and proteoglycans approximately 88% water
- hydrophilic matrix is responsible for height of the intervertebral disc
- characterized by compressibility a hydrated gel due to high polysaccharide content and high
water content (88%) proteoglycans interact with water and resist compression
Aggrecan is a proteoglycan primarily responsible for maintaining water content of the disc
viscoelastic matrix distributes the forces smoothly to the annulus and the end plates
- low collagen / high proteoglycan ratio (high % dry weight of proteoglycans)
- chondrocyte-like cells responsible for producing type II collagen and proteoglycans
survive in hypoxic conditions
Blood Supply
The disk is avascular with capillaries terminating at the end plates
Nutrition reaches nucleus pulposus through diffusion through pores in the endplates
- annulus is not porous enough to allow diffusion
Innervation
The dorsal root ganglion gives rise to the sinuvertebral nerve which innervates the superficial fibers
of annulus
- no nerve fibers extend beyond the superficial fibers

268
Neuropeptides thought to participate in sensory transmission include
- substance P, calcitonin, VIP, CPON
Fixation
Attached to vertebral bodies by hyaline cartilage

Disc Biomechanics
Disc
Viscoelastic characteristics
- demonstrates creep which allows for deformity over time
- demonstrates hysteresis which allows for energy absorption with repetitive axial compression
this property decreases with time
Stresses
Annulus fibrosus - highest tensile stresses
Nucleus pulposus - highest compressive stress
Intradiscal pressure is position dependent
pressure is lowest when lying supine
pressure is intermediate when standing
pressure is highest when sitting and flexed forward with weights in the hands
when carrying weight, the closer the object is to the body the lower the pressure
Stability
following subtotal discectomy, extension is most stable loading mode

Pathoanatomy
Disc Herniation
Herniated disks are associated with a spontaneous increase in the production of
- osteoprotegrin (OPG)
- interleukin-1 beta
- receptor activator of nuclear factor-kB ligand (RANKL)
- parathyroid hormone (PTH)
Disc aging leads to an overall loss of water content and conversion to fibrocartilage. Specifically
there is a
decrease in
nutritional transport water contentabsolute number of viable cells proteoglycans pH increase in

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an increase keratin sulfate to chondroitin sulfate ratio lactate degradative enzyme activity
density of fibroblast-like cells fibroblast-like cells reside in the annulus fibrosus only
no change in absolute quantity of collagen Spectrum of Pathological Changes in Facet Joints and Discs and
Interaction of These Changes

PHASES OF SPINAL DEGENERATION

1.Dysfunction Phase
Facet Joints
Synovitis ← Circumferential tears
Hypermobility
Continuing degeneration
Pathological Result
Dysfunction -> Herniation
Intervertebral Disc

Circumferential Tears
Radial tears

2.Instability phase
Facet Joints
Capsular laxity
Subluxation
Pathological Result
Instability
Lateral nerve entrapment
Intervertebral Disc
Internal disruption
Disc resorption

3.Stabilization phase
Facet Joints
Enlargement of articular processes
Pathological Result

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 One-level stenosis
Multilevel spondylosis and stenosis
Intervertebral Disc
Osteophytes

TABLE 42-1
Nerve root anatomy
key difference between cervical and lumbar spine is
pedicle/nerve root mismatch
cervical spine C6 nerve root travels under C5 pedicle (mismatch)
lumbar spine L5 nerve root travels under L5 pedicle (match)
extra C8 nerve root (no C8 pedicle) allows transition
horizontal (cervical) vs. vertical (lumbar) anatomy of nerve root
because of vertical anatomy of lumbar nerve root a paracentral and foraminal disc will affect different
nerve roots because of horizontal anatomy of cervical nerve root a central and foraminal disc
will affect the same nerve root

 Epidemiology
o 95% involve L4/5 or L5/S1 levels
L5/S1 most common level
o peak incidence is 4th and 5th decades
o only ~5% become symptomatic
o 3:1 male:female ratio

 Pathoanatomy
o recurrent torsional strain leads to tears of outer annulus which leads to herniation of nucleus
pulposis
 Prognosis
o 90% of patients will have improvement of symptoms within 3 months with nonoperative
care.
o size of herniation decreases over time (reabsorbed)
 sequestered disc herniations show the greatest degree of spontaneous reabsorption
 macrophage phagocytosis is mechanism of reabsorption

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 Classification
Location Classification
central prolapse
often associated with back pain only
may present with cauda equina syndrome which is a surgical emergency
posterolateral (paracentral)
most common (90-95%)
PLL is weakest here
affects the traversing/descending/lower nerve root
at L4/5 affects L5 nerve root
foraminal (far lateral, extraforaminal)
less common (5-10%)
affects exiting/upper nerve root
at L4/5 affects L4 nerve root
Axillary
can affect both exiting and descending nerve roots
Anatomic classification
Protrusion
eccentric bulging with an intact annulus
Extrusion
disc material herniates through annulus but remains continuous with disc space
Sequestered fragment (free)
disc material herniates through annulus and is no longer continuous with disc space

Presentation
Symptoms
can present with symptoms of
Axial back pain (low back pain)
this may be discogenic or mechanical in nature
Radicular pain (buttock and leg pain)
often worse with sitting, improves with standing
symptoms worsened by coughing, valsalva, sneezing
cauda equina syndrome (present in 1-10%)

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 bilateral leg pain
LE weakness
saddle anesthesia
bowel/bladder symptoms
Physical exam
motor exam
- ankle dorsiflexion (L4 or L5) test by having patient walk on heels
- EHL weakness (L5) manual testing
- hip abduction weakness (L5)
have patient lie on side on exam table and abduct leg against resistance
- ankle plantar flexion (S1)
have patient do 10 single leg toes stands
Provocative tests
straight leg raise
a tension sign for L5 and S1 nerve root
technique
can be done sitting or supine
reproduces pain and paresthesia in leg at 30-70 degrees hip flexion
most important and predictive physical finding for identifying who is a good candidate for surgery
contralateral SLR
crossed straight leg raise is less sensitive but more specific
Lasegue sign
SLR aggravated by forced ankle dorsiflexion
Bowstring sign
SLR aggravated by compression on popliteal fossa
Kernig test
pain reproduced with neck flexion, hip flexion, and leg extension
Naffziger test
pain reproduced by coughing, which is instigated by lying patient supine and applying pressure
on the neck veins gait analysis Trendelenburg gait due to gluteus medius weakness which is
innervated by L5
Imaging
Radiographs

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may show
loss of lordosis (spasm)
loss of disc height
lumbar spondylosis (degenerative changes)
MRI without gadolinium
modality of choice for diagnosis of lumbar and cervical disc herniations
1.highly sensitive and specific
2.helpful for preoperative planning
3.useful to differentiate from synovial facet cysts
however high rate of abnormal findings on MRI in normal people
Indications for obtaining an MRI
pain lasting > one month and not responding to nonoperative management or
red flags are present
infection (IV drug user, h/o of fever and chills)
tumor (h/o or cancer)
trauma (h/o car accident or fall)
cauda equina syndrome (bowel/bladder changes)
MRI with gadolinium
useful for revision surgery
allows to distinguish between post-surgical fibrosus (enhances with gadolinium) vs. recurrent
herniated disc (does not enhance with gadolinium)

Non Operative
rest and physical therapy, and antiinflammatory medications
indications
first line of treatment for most patients with disc herniation
90% improve without surgery
technique
bedrest followed by progressive activity as tolerated
medications
NSAIDS
muscle relaxants (more effective than placebo but have side effects)
oral steroid taper
physical therapy

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extension exercises extremely beneficial
traction
chiropractic manipulation
selective nerve root corticosteroid injections
indications
second line of treatment if therapy and medications fail
technique
epidural
selective nerve block
outcomes
leads to long lasting improvement in ~ 50% (compared to ~90% with surgery)
results best in patients with extruded discs as opposed to contained discs
Operative
laminotomy and discectomy (fenestration discectomy,microdiscectomy)
Micordiscectomy – gold standard, done with an operating microscope for better visualization
indications
persistent disabling pain lasting more than 6 weeks that have failed nonoperative options
(and epidural injections) progressive and significant weakness cauda equina syndrome
technique can be done with small incision or through "tube" access rehabilitation
patients may return to medium to high-intensity activity at 4 to 6 weeks
outcomes outcomes with surgery compared to nonoperative improvement in pain and function
greater with surgery positive predictors for good outcome with surgery
leg pain is chief complaint positive straight leg raise weakness that correlates with nerve root
impingement seen on MRI married status negative predictors for good outcome with surgery
worker's compensation WC patients have less relief from symptoms and less improvement in
quality of life with surgical treatment
far lateral microdiskectomy
indications for far-lateral disc herniations technique
utilizes a paraspinal approach of Wiltse

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 DEVELOPMENTAL DYSPLASIA OF THE HIP
Introduction
A disorder of abnormal development resulting in dysplasia and possible subluxation or dislocation
of the hip secondary to capsular laxity and mechanical factors DDH encompasses a spectrum of
disease that includes dysplasia a shallow or underdeveloped acetabulum subluxation dislocation
teratologic hip dislocated in utero and irreducible on neonatal exam presents with a pseudoacetabulum
associated with neuromuscular conditions and genetic disorders commonly seen with arthrogryposis,
myelomeningocele, Larsen's syndrome late (adolescent) dysplasia mechanically stable and reduced but
dysplastic Epidemiology incidence most common orthopaedic disorder in newborns dysplasia is 1:100
dislocation is 1:1000 location most common in left hips in females bilateral in 20% demographics more
commonly seen in Native Americans and Laplanders rarely seen in African Americansrisk factors
firstborn female (6:1 over males) breech family history oligohydramnios Pathophysiology initial
instability thought to be caused by maternal and fetal laxity, genetic laxity, and intrauterine and
postnatal malpositioning pathoanatomy initial instability leads to dysplasia dysplasia leads to gradual
dislocation typical deficiency is anterior or anterolateral acetabulum in spastic cerebral palsy,
acetabular deficiency is posterior-superior Associated conditions associated with "packaging"
deformities which include congenital muscular torticollis (20%) metatarsus adductus (10%) congenital
knee dislocation conditions characterized by increased amounts of type III collagen
Pathology:
At birth, hip joint slides in and out of the acetabulam posterior surface is flattened and thickened, the
part of the acetabulam (posteriosuperior) develops a rim of thickened articular cartilage called as
NEOLIMBUS .
Sliding of the head in and out produces a clunk produced by the neolimbus
A few dislocated hips stay dislocated, for which secondary barriers of reduction develop, they are:
Pulvinar – fatty tissue within the depth of the acetabulam thickens
Ligamentum teres also thickens and elongates
Transverse acetabular ligament thickens
Inferior capsule- hour glass shape
Classification
Can be classified as a spectrum of disease involvement (phases)
dislocated
Ortolani-positive early when reducible; Ortolani-negative late when irreducible

276
dislocatable
Barlow-positive
subluxatable
Barlow-suggestive
Presentation
Physical exam (< 3 months) mainstay of physical diagnosis is palpable hip subluxation/dislocation on
the exam Barlow dislocates a dislocatable hip by adduction and depression of the flexed femur
Ortolani reduces a dislocated hip by elevation and abduction of the flexed femur Galeazzi (Allis)
apparent limb length discrepancy due to a unilateral dislocated hip with hip flexed at 90 degrees and
feet on the table femur appears shortened on dislocated side hip clicks are nonspecific findings
Barlow and Ortolani a rarely positive after 3 months of age because of soft-tissue contractures about
the hip.
Physical exam (> 3 months to 1 year) limitations in hip abduction most sensitive test once contractures
have begun to occur occurs as laxity resolves and stiffness begins to occur decreased symmetrically in
bilateral dislocations leg length discrepancy predominate Physical exam (> 1 year - walking child)
pelvic obliquity lumbar lordosis in response to hip contractures resulting from bilateral dislocations in a
child of walking age Trendelenburg gait results from abductor insufficiency toe walking compensate
for the relative shortening of the affected side.
Imaging
 Radiograph
o indications
 becomes primary imaging modality at 4-6 mo after the femoral head begins to ossify
 positive physical exam
o leg length discrepancy recommended views
 AP of pelvis measurements hip dislocation Hilgenreiner's line a horizontal line through right
and left triradiate cartilage femoral head ossification should be inferior to this line Perkin's line
o line perpendicular line to Hilgenreiner's through a point at lateral margin of acetabulum
 femoral head ossification should be medial to this line Shenton's line
 arc along inferior border of femoral neck and superior margin of obturator foramen arc line
should be continuous delayed ossification of the femoral head is seen in cases of dislocation hip
dysplasia
o acetabular index (AI) the angle formed by a line drawn from a point on the lateral triradiate
cartilage to point on lateral margin of acetabulum and Hilgenreiners line should be less than 25° in

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patients older than 6 months center-edge angle (CEA) of Wiberg the angle formed by a vertical line
from the center of the femoral head and a line from the center of the femoral head to the lateral edge of
the acetabulum
o less than 20° is considered abnormal reliable only in patients over the age of 5 years acetabular
teardrop not typically present prior to hip reduction for chronic dislocations since birth development of
teardrop after reduction is thought to be a good prognostic sign for hip function

 Ultrasound
 indicationsprimary imaging modality from birth to 4 months may produce spurious results if
performed before 4-6 weeks of age positive physical exam risk factors (family history or breech
presentation)
 the AAP recommends a US study at 6 weeks in patients who are considered high risk (family
history or breech presentation) despite normal exam monitoring of reduction during Pavlik harness
treatment
 most studies show is not cost effective for routine screening findings evaluates for acetabular
dysplasia and/or the presence of a hip dislocation allows view of bony acetabular anatomy, femoral
head, labrum, ligamentum teres, hip capsule normal ultrasound in patients with soft-tissue 'clicks' will
have normal acetabular development measurements alpha angle the angle created by lines along the
bony acetabulum and the ilium normal is greater than 60° beta angle the angle created by lines along
the labrum and the ilium normal is less than 55° femoral head is normally bisected by a line drawn
down from the ilium
 Smaller α angle- shallow bony acetabulam Smaller β angle - better cartilaginous acetabulam
 GRAF’s classficataion:
 Class 1- normal

278
  Class 2- immature
 Class 3- subluxated
 Class 4- dislocated
 Arthrogram
o indications
 used to confirm reduction after closed reduction under anesthesia help identify possible blocks
to reduction inverted labrum labrum enhances the depth of the acetabulum by 20% to 50% and
contributes
to the growth of the acetabular rim in the older infant with DDH the labrum may be inverted and may
mechanically block concentric reduction of the hip inverted limbus
 represents a pathologic response of the acetabulum to bnormal pressures caused by superior
migration of the head consists of fibrous tissue transverse acetabular ligament hip capsule is constricted
by iliopsoas tendon causing hour-glass deformity of the capsule pulvinar ligamentum teres CT.CT is
historically the study of choice to evaluate reduction of the hip after closed reduction and spica casting
MRI
increasingly used to evaluate reduction of hip after closed reduction and spica casting, to minimize
radiation compared to CT.
Kashiwagi classification:
Group 1- sharp acetabular rim
Group 2- Rounded acetabular rim
Group3 – Inverted acetabular rim
o
 Screening
 All infants require screening
o physical exam
 successful screening requires repetitive screening until walking age
o ultrasound
 ultrasound screening of all infants occurs in many countries, however, it has not been proven to
be cost-effective
 USA recommendations is to perform ultrasound at 4 to 6 weeks in patients with
 risk factors
 positive physical findings
 utilized to follow Pavlik treatment or for equivocal exams

279
Treatment in Children
Nonoperative
abduction splinting/bracing (Pavlik harness)
indications
DDH < 6 months of age and reducible hip Pavlik harness treatment is contraindicated in teratologic
hip dislocations is a dynamic splint that requires normal muscle function for successful outcomes
contraindicated in patients with spina bifida or spasticity outcomes overall Pavlik harness has a success
rate of 90% dependent upon age at initiation of treatment and time spent in the harness abandon Pavlik
harness treatment if not successful after 3-4 weeks If Pavlik harness fails, consider converting to semi-
rigid abduction brace with weekly ultrasounds for an addition 3-4 weeks before considering further
intervention
closed reduction and spica casting
indications DDH in 6 - 18 months of age failure of Pavlik treatment arthrography performed at the time
of reduction
medial dye pool >7mm associated with poor outcomes and osteonecrosis
wide abduction associated with osteonecrosis (aim at <55 degrees abduction) Operative
open reduction and spica casting
indications DDH in patient >18 months of age failure of closed reduction open reduction and
femoral osteotomy indications DDH > 2 yr with residual hip dysplasia anatomic changes on femoral
side (e.g., femoral anteversion, coxa valga) femoral head should be congruently reduced with
satisfactory ROM, and reasonable femoral sphericity best in younger children (< 4 yr) after 4 yr, pelvic
osteotomies are utilized
open reduction and pelvic osteotomy indications DDH > 2 yr with residual hip dysplasia severe
dysplasia accompanied by significant radiographic changes on the acetabular side (increased acetabular
index) used more commonly in older children (> 4 yr) decreased potential for acetabular remodeling as
child ages
Techniques
Abduction splinting/bracing (Pavlik harness)
goals treatment is based on an early concentric reduction in order to prevent future degeneration of the
hip
risk, complexity, and complications are increased with delays in diagnosis position in bracing
goal is 90-100° flexion (controlled by anterior straps) and abduction of 50° (controlled by posterior
straps)

280
 o extreme positions can cause
AVN due to impingement of the posterosuperior retinacular branch of the medial femoral circumflex
artery
seen with extreme abduction (> 60°) placement of abduction within 'safe zone' transient femoral nerve
palsy seen with hyperflexion discontinue if hip is not reduced by 3-4 weeks to prevent Pavlik disease
erosion of the pelvis superior to the acetabulum and prevention of the development of the posterior
wall of the acetabulum worn for 23 hours/day for at least 6 weeks or until hip is stable wean out of
harness over 6-8 weeks after hip has stabilized until normal anatomy develops confirm position with
ultrasound or xray and monitor every 4-6 week
Closed reduction and spica casting
performed under general anesthesia excessive force can result in AVN arthrogram used to confirm the
reduction concentric reduction must be obtained with less than 5mm of contrast pooling medial to
femoral head and the limbus must not be interposed the arthrogram will also help identify anatomic
blocks to reduction:
spica casting
following reduction immobilize in a spica cast with hip flexion of 100 deg. and abduction of 45 deg
with neutral rotation for 3 months 'human position' change cast at 6 weeks adductor tenotomy
performed if the patient has an unstable safe zone used if excessive abduction required to maintain the
reduction
confirm reduction with CT scan in spica cast with selective cuts to minimize radiation to the child

Open reduction
anterior approach (Smith-Peterson) most common to decrease risk to the medial femoral circumflex
artery

281
 capsulorrhaphy can be performed after reduction ued if the patient is older than 12 months other
possible approaches include medial adductor approach, a variation of Ludloff pros directly addresses
block to reduction can be used in patients under 12 months of age less blood loss cons unable to
perform a capsulorrhaphy higher association of AVN anteromedial approach posteromedial approach
remove possible anatomic blocks to reduction iliopsoas contracture, capsular constriction, inverted
labrum, pulvinar, hypertrophied ligamentum teres adductor tenotomy performed if the patient has an
unstable safe zone if excessive abduction required to maintain the reduction immobilize in functional
position of 15° of flexion, 15° of abduction and neutral rotation

Femoral Osteotomy (VRDO)

used to correct excessive femoral anteversion and/or valgus femoral osteotomy and shortening may be
needed to prevent AVN decrease tension produced by reduction of a previously dislocated hip
Pelvic Osteotomies
indications increase anterior or anterolateral coverage used after reduction is confirmed on abduction-
internal rotation views and satisfactory ROM has been obtained

TREATMENT:
In neonate:
Pavlik Harness: Hips should be reducible.
- Chest straps at level of nipple and hips flexed 120° and moreover posterior strap should not
force the hips into abduction.
- Hyper flexion can cause femoral nerve palsy and hips to dislocate inferiorly
- Review using ultrasonography at 3-4 weeks interval
- Continue for 6 weeks, if hips in place, only monitoring by xrays required until skeletal
maturity
- If found dislocated after 6 weeks, arthrogram is done and managed using closed / open
reduction

In 1-6 month old child:

- Pavlik harness: First choice, if reduction present, continue harness until 6 weeks.
- No reduction: Discontinue harness and open/closed reduction is required
- Pavlik harness disease: Composes of
Failure to reduce hip

282
 Femoral nerve palsy
AVN of head
- Other splints:
- Von Rosen splint
- Craig splint

In 6 months-2yrs child:
- AIM: To obtain and maintain the reduction of the hip without damaging the femoral head
- Either done by closed or open reduction following traction
- Reduction should be done after the ossific nucleus has developed to have lesser chances of
AVN
- Closed reduction: Under GA
- Hips flexed to 90° and then general slow abduction is done(Ortolani)
- After reduction, ROM is assessed to see where it dislocates
- Adduction and internal rotation is measured to construct the safe zone.
- Considered stable if there is wide safe zone
- Considered unstable if 10-15° of internal rotation is needed or wide abduction is required
- Once considered stable- immobilize using hip spica for 6 weeks
- If there is medial joint space more than 6mm, considered improper reduction
- Open reduction:
- Done when there is failure to obtain stable hip by closed reduction, approaches used:
- Medial approach most preferred:
 Minimal dissection
 Obstructions to reduction are encountered directly
 But limited view of the hip
 Interruption of medial circumflex femoral artery
 Capsulorhaphy cannot be done
- Anterior approach:
 Better view of hip joint and capsulorhaphy can be done
- Once reduction is done, hip spica is applied with hips flexed to 90° with minimal abduction
Open reduction with femoral osteotomy:
- Done if excessive pressure is applied over the head during reduction
- If child more than 2 years of age

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- Subtrochanteric or intertrochanteric osteotomy is done and fixed using blade plate
Open reduction and innominate osteotomy:
- Child more than 18months
- Head placed in extension neutral rotation and abduction
- If more than 1/3rd of the head is visible, osteotomy will provide lateral coverage
- Salter and pemberton osteotomy are types of pelvic osteotomy
In children 2yrs or more:
- Femoral shortening osteotomy
- Primary Salter/Pemberton osteotomy
- More than 3yrs- also do acetabular osteotomy to cover head (Steel,Ganz,shelf,chiari)
- When acetabular and femoral osteotomy are combined, posterior dislocation of hip can
happen
Complications:
 Osteonecrosis
o seen with all forms of treatment
o increased rates associated with
 excessive or forceful abduction
 previous failed closed treatment
 repeat surgery
o diagnosis based on radiographic findings that include
 failure of appearance or growth of the ossific nucleus 1 year after the reduction
 broadening of the femoral neck
 increased density and fragmentation of ossified femoral head
 residual deformity of proximal femur after ossification
 Delayed diagnosis
o bilateral dislocations
 patients typically functions better if hips are not reduced if 6 years of age or older
o unilateral dislocation
 better outcomes without surgical treatment if the patient is 8 years of age or older
 epiphysiodesis can be performed for treatment of limb length discrepancy
 Recurrence
o approximately 10% with appropriate treatment
o requires radiographic follow-up until skeletal maturity

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 Transient femoral nerve palsy
o seen with excessive flexion during Pavlik bracing

285
 Nerve Conduction Study
 Definition
o comprises nerve conduction velocity (NCV) studies and electromyography (EMG)
o used to localize areas of compression and neuropathy
o distinguish
 lower vs upper motor neuron lesions
 spinal root, trunk, division, cord or peripheral nerve lesion
o determine severity and prognosis
 neuropraxia has good prognosis
 axonotmesis/neurotmesis has poor prognosis
o demonstrate denervation, reinnervation, aberrant reinnervation, motor end plate lesion
o valuable in worker's compensation patients with secondary gain issues
 Indications
o carpal tunnel syndrome
o cubital tunnel syndrom
o cervical radiculopathy
o lumbar radiculopathy
o nerve dysfunction of the shoulder (e.g., scapular winging)
Nerve Conduction Velocity
 Definition
o tests performed on peripheral nerves to determine their response to electrical stimuli
 Technique
o constant voltage electric stimulator evokes a response from muscle (motor nerve study) or
along
the nerve (sensory nerve study)
 standard stimulus is 0.1 to 0.2ms square wave
o for motor nerve studies, an additional stimulus is measured along the proximal segment
between
2 points on the nerve
 to overcome inherent delay across neuromuscular junction if the recording electrode were
placed on the muscle

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  Measures
o NCV = distance divided by latency
 distance traveled is from the cathode of the stimulating electrode to the recording
electrode
 latency is the time from the onset of stimulus to the onset of response
 onset latency = time from site of stimulation + time to activate postsynaptic
terminal (neuromuscular transmission time) + time for action potential to
propagate along muscle membrane to recording potential
 NCV is determined by
 myelin thickness
 internode distance
 temperature
 age
o NCV in newborns are 50% of adult values
o NCV in 1 year olds are 75% of adult values
o NCV in 5year olds are 100% of adult values
o Amplitude
 from baseline to negative peak (in mV)
 area under peak is proportional to number of muscle fibers depolarized
 provides estimate of number of functioning axons and muscles
o Duration
 reflects range of conduction velocities and synchrony of contraction of muscle fibers
 if there are axons with different CVs (acute demyelination), duration will be greater
o Late responses evaluate proximal nerve lesions (near spinal cord, e.g. Guillain-Barre
syndrome)
 F-wave amplitude
 H-reflex
 stimulate Iα fibers at knee, with recording at the soleus (S1 root)
 affected by sensory neuropathies, motor neuropathies of the tibial
or sciatic nerves, and S1 root lesions
Demyelination leads to increase latencies (slowing) of NCV distal sensory latency of > 3.2 ms
are abnormal for CTS motor latencies > 4.3 ms are abnormal for CTS decreased conduction
velocities less specific than latencies velocity of < 52 m/sec is abnormal

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 ELECTROMYOGRAPHY
Definition
 to study electrical activity of individual muscle fibers and motor units
 differentiate between diseases of nerve roots, peripheral nerves or skeletal muscles
 determine if disease is acute or chronic, and if there is reinnervation
 determine if there is nerve continuity
Technique
 insert needle electrode through the skin into muscle to determine insertional and spontaneous activity

Types of activity
insertional activity
1. shows state of muscle and innervating nerve as needle is inserted
2. normal muscle has baseline electrical activity
3. abnormal insertional activity (>300-500ms) shows early denervation
 polymyositis
 myotonic disorders
 myopathies
4.reduced insertional activity occurs after prolonged denervation
muscle undergoes fibrosis
contraction activity
 patient is asked to contract muscle and shape/size/frequency of motor unit potentials are recorded
spontaneous activity
 normal spontaneous activity includes end plate potentials and end plate spikes
 abnormal spontaneous activity indicates some nerve/muscle damage
1. sharp waves
2. fibrillations
 spontaneous action potentials from single muscle fibers caused by oscillations in resting membrane
potential of denervated fibers
 seen 3-5wk after nerve lesion begins, and stays until it resolves or muscle becomes fibrotic
 also seen in muscle disorders e.g. muscular dystrophy
3. fasciculations
 spontaneous discharge of group of muscle fibers
 found in amyotrophic lateral sclerosis, progressive spinal muscle atrophy and anterior horn
degenerative diseases e.g. polio, syringomyelia
 seen as "undulating bag of worms" on physical exam
4. complex repetitive discharges
5. myokimic discharges

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 ORTHOTICS AND PROSTHESIS PART 1
An orthosis (orthos (G.) – straight) is a device designed to supplement or augment the
function of an existing limb or body part. It controls the abnormal movement or
allows restricted normal movements. The following can be devised as functions of splints:
Static splints (Immobilize or stabilize joints)
– Protection
– To put joints to rest
– To decrease inflammation
– To decrease pain
– To prevent undesired motion
– To resolve fixed joint contractures (e.g. serial casting)
– To substitute for lost muscle function
– To substitute for loss of a digit
Dynamic splints (Mobilisation or traction to joints)
– To resolve tendon tightness
– To resolve joint contracture
– To increase activity range on motion to given joints
– To increase muscle strength.
Goals of Orthoses
• Maintenance or correction of body segment alignment
• Assistance or resistance to joint motion
• Axial loading of the orthosis & therefore relief of distal weight bearing forces
• Protection against physical insult
Lower Extremity Orthoses:
• FO foot orthosis
• AFO ankle foot orthosis
• KO knee orthosis
• KAFO knee ankle foot orthosis
• HKAFO hip knee ankle foot orthosis
• HO hip orthosis
Most common orthosis
1. Metal bars 2. Total Contact 3. Floor reaction 4. Unweighting
5. Immobilizing – Most AFO’s can be articulating or non-articulating

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 PROSTHESIS

Prosthesis is a device designed to replace as much as possible the function or appearance of a

missing limb or body part.
Prosthesis may be classified in three broad categories:
1. Endoskeletal: Most widely used for lower limbs throughout the world. This type of
prosthesis consists of a central structural tube to which a joint and socket can be attached.
The central tube is mostly made of carbon fiber or aluminum. This basic structure can then be
covered by an outer cosmesis in form of shaped foam.
2. Exoskeletal: In these prostheses, the main structural component is the “outer visible skin”.
Now a days, mostly DURAL (aluminum alloy) or plastic laminates are used.
Majority of the upper limb prosthesis are of plastic exoskeletal structure.
3. Temporary “pylon” prosthesis: This consists of two self locking side struts resembling
above knee calipers. They are rarely used in the current circumstances.
The term pylon is also used to describe the central structural tube in the endoprostheses.
Following details have to be furnished while prescribing prosthesis:
1. Type of prosthesis
2. Level of amputation
3. Type of socket
4. Material of socket
5. Hip, knee, elbow mechanism
6. Foot/ankle or hand/terminal appliance
7. Suspension
8. Cosmesis

What are various types of sockets

From the viewpoint of patient, socket is the single most important factor in prosthesis.
• Sockets may be made of various materials for E.g. Leather, polypropylene, fiberglass, etc.
• Sockets may be standard sockets, which are worn over a stump sock. Now a days, suction
sockets are available which remain in close contact to the skin and are worn without a sock.
• Recently, silicone impregnated sock or sock lined by a layer of polyurethane gel have been
developed to increase comfort and reduce sweating.

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What are various types of suspension mechanisms?
The prosthesis may be:
A. Suspended with the help of belt, cuff or sleeve.
B. Self suspending: These may again be divided into mechanical or suction.

SACH Foot:
SACH stands for (solid ankle cushion heel).
No true ankle joint, contains a ‘simulated ankle joint’ by compressed wedge shaped rubber
heel. Consists of a solid wooden keel, high density rubber for dorsum, low density rubber for
toes and plantar aspect (ensures smooth transition from toe-off to heel strike, variable density
rubber for heel. The advantages are as follows:
• Absorbs the impact of heel strike.
•  vertical excursion of centre of gravity.
• Allows some simulated movement of metatarsal head.
Jaipur Foot
Appearance similar to normal foot
Can be worn without shoe but if someone wishes to wear one he can use a flat heel shoe.
No restriction of movements at ankle as the metallic keel (carriage bolt) is confined to ankle
only and all movements take place at natural site.
Squatting possible (dorsiflexion adequate)
Cross-legged sitting is possible (adequate forefoot adduction and internal rotation possible)
Walking on uneven ground possible(good inversion and eversion)
Cosmetic skin colour
Barefoot walking possible
No heel and toe height difference
Myoelectric (externally powered , switch controlled Upper limb prosthesis)
Myoelectric components are controlled by voluntary muscle action via an electronic signal.
The signal is picked up and amplified by electrodes placed over muscle fibers and the
downloaded over to a computer to provide a specific function. Before prescribing this type of
prosthesis, myoelectric testing has to be done.
Advantages:
– Better cosmesis
– No need for harness

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– Prevents repetitive injury
– Increased anatomic function
– Voluntary wrist rotation
Disadvantages:
– Heaviest
– Slower response time
– Expensive
– Frequent maintenance
– Battery dependent
– Less durable, non water proof
– Longer training period
What is post-prosthetic care
Balancing, stretching and muscle strengthening exercises may be started as soon as possible.
This helps in maintaining flexibility, prevent flexion contractures and preserve muscle mass
and strength.
2. An aerobic conditioning program must be designed and incorporated in the rehabilitation
process.
3. Gait training should begin with first step. Initially walking stick or walker may be allowed
but there use should be terminated as soon as possible.
4. In case of upper limb amputations, early fitting of prosthesis and promotion of two handed
function leads to reduced rejection rate.
Milwaukee brace
A brace designed by Blount, Schmidt and Bedwell (1958) known by the city of origin of
these men. This brace is
used for controlling curve deterioration and to maintain the post-operative correction in
patients with scoliosis. The brace has three parts:
– The pelvic mould
– Vertical bars
– Mandibulo-occipital assembly
The pelvic girdle uniformly fits over the iliac crests and is the most important part of brace. It
helps reduce lordosis, derotates the spine, and corrects frontal deformity.
Uprights have localized pads to apply transverse force which is effective for smaller curves.
The main corrective force is the thoracic pad which attaches to two posterior and one anterior
upright. Discomfort from the same creates a righting response.

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 Neck ring is another corrective force and is designed to give longitudinal traction. The throat
mould allows the use of distraction force without producing jaw deformity.
Complications
• Pain
• Skin breakdown
• Jaw deformity
• Unsightly appearance
• Increased energy expenditure with ambulation, etc.

Floor reaction Orthoses

Revolutionary orthosis:
 Custom fabricated, moulded plastic device that supports the ankle and foot area of the body
and extends from below the knee down to and including the foot
 It was described by Saltiel for the use of patients with weak quadriceps or plantar flexors in
1969.
 It holds the ankle in equinus to prevent the heel from touching the ground.As the body weight
brings the heel downwards, the suprapatellar band will press the knee back preventing knee
from buckling during stance phase.
It allows the knee to flex during swing phase when the foot is of the ground.
 The Floor Reaction Orthoses is designed to lock the ankle and to provide maximum
resistance to ankle dorsiflexion
 It is a stance phase control orthosis.

Use:
 It can be used in lower limb paralysis with weak quadriceps like in patients with post polio
residual paralysis
 Management of crouch gait , which is characterised by excessive ankle dorsiflexion,increased
knee flexion and increased hip flexion in midstance.

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 Contraindication:
 Hip flexion contracture >30 degree
Knee Flexion Contracture >20degree and a
 Thigh foot angle >15degree external.
Advantages over other AKO’s:
 Light Weight
 Swing phase is not laboured
 Prevents knee from buckling
 Stabilises knee without muscle action
 Ground clearance is easier
 Good patient compliance
 Cosmetically acceptable – can be worn under shoe.

Disadvantages
 Must correct fitting or else it wont function
 Has to be custom made

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 OSTEOMYELITIS
Osteomyelitis implies inflammation of the bone and its marrow regardless of whether it is due to
pyogenic organisms ,tuberculosis, syphilis, specific virus.

Acute osteomyelitis is a rapidly destructive pyogenic infection, usually hematogenous in

origin,occuring most frequently in infants and children.

It starts in the metaphysis of an actively growing long bone and runs a fulminating septic course that
may terminate fatally.

Metaphysis of long bones

Lower extremity upper extremity
Femur : 27% humerus:12%
Tibia : 22% radius: 4%
Fibula: 5% ulna: 3%

Bacteria can be introduced into the bone by

 Haematogenous spread,
 Local invasion from a contigous infection,
 Direct inoculation from a penetrating trauma
Transient bacteremia is relatively common in childhood- otitis
media,sinusitis,pharyngitis,uti’s.
Symptoms
 High grade fever-associated with chills
 Decreased activity,not moving the affected limb
 Pain
 Swelling
 Incessant cry
 Refusal to take feeds
Signs
 Febrile
 Tenderness over the affected limb
 “toxic” looking child in case of associated sepsis
 Tachycardia
 Tachypnoea
 Extremity is held in semi flexion with surrounding muscles in spasm
 Passive movements are resisted by the patient due to pain

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 Acute osteomyelitis
Specific non specific
(Tb, Syphilis, Viral) (pyogenic org)

Treatment:
Medical management:

Parenteral antibiotics-emprical initially and later based on c/s

Duration of antibiotics-controversial
4 weeks of parenteral antibiotics followed by 2 weeks of oralantibiotics
Opat-followed now a days

Surgical
 Extensive open irrigation and drainage of pus
 Cortical drilling or fenestration
 Curettage of the medullary canal

Complications:
 Fulminant sepsis
 Septic arthritis
 Pathological fracture
 Deep vein thrombosis
 Pulmonary embolism
 Avascular necrosis
 Chronic osteomyelitis
 Growth disturbances

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 SLIPPED CAPITAL FEMORAL EPIPHYSIS

- Displacement of proximal femoral epiphysis

- Also called as femoral capital epiphysiolysis
- Children in the growth spurt are more affected
- Age – 10years and more
- Boys are more affected than girls
- Left side more than right (25% chance to become bilateral)

Etiology:
- Children are either fat or extremely tall and thin
- Hormonal imbalance:
Pititary hormone responsible for rapid growth and increase physeal hypertrophy.
Gonadal hormone responsible for physeal maturation and epiphyseal fusion
Disparity between both, physis is unable to tolerate the increased stress due to
increase in body weight
- Hypothyroidism
- Oestrogen- increased physeal strength, so less common in girls
- Minor local trauma
- The perichondrial ring is thin in this age group

PATHOLOGY:
- Femoral shaft goes into internal rotation and neck goes forward
- Physis is separated at the hypertrophic zone and placed posterior to the femoral neck
- Anterior retinacular vessels can be torn
- Posterior vessels are the only supply now

Physeal disruption
˅
Premature closure of physis and bony remodelling
˅
Fixed external rotation deformity and coxa vara

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 CLINICAL FEATURES:

Usually minor episodes rather than one sudden event

- In bilateral slips, second slip happens within 18 months
- Child is usually around 10 years, nearing puberty
- Over weight / tall and thin
- Pain- groin and thigh
- Limp
- Child is aware that leg is turning out
- O/E: leg is externally rotated
Shortening present
Limitation of flexion abduction and medial rotation
Increase in external rotation as hip flexes

IMAGING:
1. XRAY: AP and frog lateral/lateral views taken:
- Trethowan’s sign:
- Metaphyseal blanch sign of steel:
- double density sign at the level of metaphysis in AP view
- due to overlap of femoral neck and slipped physis

- Capener’s sign:
-In lateral view, also called as sham’s sign
-In normal hip inferomedial wall of the femoral neck overlaps the posterior wall of acetabulam
forming a triangular density
-This density is lost due to the slip
- In lateral view: Southwick angle
Metaphyseal angle of steel

- Other signs:
1. Decreased epiphyseal height
2. Physeal widening

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3. Lesser trochanter prominent due to external rotation
4. Posterior metaphyseal new bone formation
2. USG: Shows joint effusion
3. MRI: Done to detect avascular of femoral head

GRADING OF SLIP CLINICALLY:

1. PRE SLIP:
Groin/knee pain, increased on exertion
Limp with decreased internal rotation
2. ACUTE SLIP:
Symptoms less than 3 weeks
Painful range of motion with external rotation deformity and shortening
3. CHRONIC SLIP:
Symptoms more than 3 weeks
Loss of internal rotation, abduction and flexion
Shortening present
4. ACUTE ON CHRONIC SLIP:
Long history with acute exaceberation

RADIOLOGICAL GRADING:
According to the percentage of slip in relation to the femoral neck width
Mild: displacement less than 1/3rd of femoral neck width
Moderate: displacement between 1/3rd and half
Severe: displacement more than half of the femoral neck width

TREATMENT:
AIM:
1. To preserve epiphyseal blood supply
2. To stabilize the physis
3. To correct any residual deformity
In minor slips:
- less than 1/3rd of the width of the epiphysis in AP view and less than 20° tilt in lateral
view.

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- Position can be accepted
- Percutaneous inning using one or two cannulated cancellous screws
In moderate slips:
- Slip between 1/3rd and half in AP view and tilt between 20-40° in lateral view
- Deformity and disability will persist
- Percutaneous pinning and after deformity is present femoral osteotomy is done
- Careful pinning should be done as physis is posterior, pins can damage the posterior
retinacular vessels
- Bone graft epiphysiodesis is also an option In severe slips:
- AP view more than 2/3 of the physis is slipped
- Lateral view more than 40° tilt
- Unacceptable, as it causes severe deformity
- Closed reduction should not be attempted

OPEN REDUCTION:
DUNN’S OSTEOTOMY:
- Femoral neck is resected after preserving the posterior retinacular vessels
For less experienced surgeons:
- Fix physis as in moderate slip and latter do intertrochanteric osteotomy
- May result in shortening of 2-3cms

COMPLICATIONS:
1. Slipping of opposite side physis, hence prophylactic pinning is recommended
2. AVN of femoral head- avoid forceful manipulation
3. Articular chondrolysis
4. Coxa vara
5. Secondary osteoarthritis

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 TUBERCULOSIS HIP
What is the cause of night cries?
Destruction of cartilage exposes the subchondral nerve endings. In the night
with muscle relaxation, the splinting effect is taken away and the bony surfaces
rub across each other causing severe pain.

How will you confirm diagnosis in a case of TB Hip?

I will get an X-ray of pelvis done (AP) view with
radiographs of right hip in AP and lateral projections.
Blood tests:
• Serial ESR
• ELISA: IgG and IgM response to A60 Antigen complex (interspecific antigen
and is common to typical and atypical mycobacteria) – sensitivity of 60-80%
• PCR is highly sensitive and specific (lots of them are available, still more
reliable and specific is the RNA testing but is much expensive)
Skin tests: False positives and negatives high; strongly positive reaction in
previously negative patient is highly suggestive (but hardly found in an adult
patient).
Synovial fluid examination/ synovial biopsy/bone biopsy:
•  Protein, poor formation of mucin clot etc. in synovial fluid examination
• Staining (Ziehl-Neelson)
• Culture:
– Provides ultimate diagnosis
– But is very slow (Rapid alternatives are BACTEC TB- 460, BACTEC
MGIT960 etc.)
• Rapid methods:
– Centrifuged samples
– Thin-layer and gas-liquid interphase chromatography for detection of lipids
and long-chain fatty acids

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– Radioactive labeled DNA probes: specific to diagnose family, genus, species,
sub-species – result in 2-8 hours
– MDR rapid diagnosis: genotypic analysis of six codon regions rpoB531,
rpoB526, rrs513, rpsL43, embB306, and katG315
– Molecular hybridization techniques.
Staining requires around 10,000 bacilli/mm3, culture requires 1000
bacilli/mm3.

What do you expect to see on an X-ray?

As per the examination I expect to see involvement ofboth femur and
acetabulum with reduction of joint space, cystic sclerotic lesions in head and
acetabulum, acetabular widening and/or destruction of femoral head, upriding
of greater trochanter, flexion adduction and external rotation deformity, with or
without subluxation of joint and displacement of fat plane.

How do you clinico-radiologically classify TB Hip?

Shanmugasundaram classification:
1. Normal hip
2. Travelling acetabulum
3. Dislocating type
4. Perthes type
5. Mortar and pestle type
6. Atrophic type
7. Protrusio acetabuli
(More commonly in Adult the Atrophic form; in children: normal, perthes and
dislocation types, while mortar & pestle, wandering and protrusion types are
seen in both)

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What are the common radiological signs of TB hip?
Osteoporosis is the earliest sign, ‘Cat-Bite’ lesion in articular margin,  joint
space, destructive changes. Bony lamellae undergo osteoporosis in early stages
(osteoclasts and howships lacunae) later with healing there is osteosclerosis
(osteoblastic activity).

What are the radiological signs of healing?

The following are seen in healing TB:
1.  in thickness of trabeculae
2.  density of bone
3. Recommencing of epiphyseal growth

How do you stage TB hip?

Clinical staging (this is the sequence of untreated TB, treatment may arrest it
anywhere!):
Stage Pathology Attitude
1. Stage of apparent lengthening
(due to pelvic tilt to compensate for abduction deformity. >75% pain free
movements, No true shortening)
2. Stage of apparent shortening (pelvic tilt to compensate adduction deformity
(spasm), movements restricted beyond 50%, true shortening either none or <1
cm)
3. Stage of true shortening. (Fixed deformities, movements restricted to <25%,
Real shortening
>1 cm)
4. Stage of aftermath and destruction (wandering acetabulum, pathological
dislocation, destruction of head, fibrous ankylosisetc.)
Ongoing gross destruction
Advanced arthritis

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Early arthritis
Synovitis/Effusion
FABER (flexion,abduction, external rotation)
FADER (Flexion, adduction, external rotation)
FADER with shortening
Shortening s further, deformities can vary depending on the final
outcome.

Why do the deformities differ in different stages

In stage I due to effusion and d requirement for space hip goes into FABER
deformity, later in stage II the deformities are due to spasm of muscles. Flexors
and adductors are stronger than other groups so characteristic FADER
deformity is exhibited. Moreover irritation of inferomedial joint capsule by
debris irritates obturator nerve causing adductor spasm and direct irritation of
iliopsoas occurs by underlying swollen, hyperemic capsule. In stage III there is
eburnation of cartilage and generalized spasm increasing bony contact and
enhancing destruction but above two groups dominate to maintain FADER
deformity.

Can you still see flexion, abduction, internal/external rotation deformity in

a patient in stage II/III?
YES:
• Patient treated by prolonged traction
• Patient maintained in hip spica
• Elderly or debilitated patients who prefer to lie in lateral position and continue
with initial posture for relief of pain,moreover they have weak muscles
• Destruction of iliofemoral ligament (inverted Y-ligament of Bigelow)
• Patient who continues to bear weight in the initial deformed position.

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What is Phemister triad?
Classically described for tuberculosis of hip consists of:
1. Juxtaarticular osteoporosis
2. Peripherally located osseous lesion
3. Gradual narrowing of joint space.

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 LEGG-CALVE-PERTHES DISEASE
A REVIEW by

Dr. J.K. Giriraj Harshavardhan,

Perthes disease is a self-limiting, non-inflammatory condition affecting the capital femoral
epiphysis with stages of degeneration and regeneration, the basic pathogenesis of which is
ischaemia of the femoral head.
In 1910, the condition was described independently by Arthur Legg of Boston, USA.,
Jacques Calve of Berk, France and George Perthes of Tubingen, Germany. However the
credit should actually go to Waldenstrom who in 1909 described the 4 stages of the disease.
Epidemiology
- It usually occurs between the ae group of 3-12 years and most common between 5 – 7 years.
- Boys are affected 4 times more commonly than girls.
- Girls have a poorer prognosis than boys probably because girls reach skeletal maturity earlier
than boys and therefore have less remodeling potential.
- Frequency of left and right hip involvement is almost equal
- Bilateral involvement is seen in 10 – 20 % of patients.
- Familial in 8 – 12 % of cases.
Etiology and pathogenesis
The etiology of this disease remains an enigma but the cardinal step in the pathologenesis
is ischaemia of the femoral head.
Between the age of 4 to 7 years, the femoral head is entirely dependent on the lateral
epiphyseal (retinacular ) vessels for its blood supply and venous drainage (upto 4 years the
metaphyseal vessels which penetrate the growth disc also supplies the femoral head; after 7
years the vessels in the ligamentum teres contribute to the blood supply). The lateral
epiphyseal vessels located in the retinacula makes them susceptible to stretching and to
pressure from an effusion (venous stasis rise in intraosseous pressure  ischaemia). Hence
contributory factors causing ischaemia may include trauma, increased blood viscosity
(antithrombotic factor deficiencies, hypofibrinolysis), etc.,

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Clinical features
Typical patient – a boy of 4 -8 years Hip pain (commonly referred to knee- hence any
child with knee pain, examine the hip!) Limp Child appears to be well (cf. infective hip
pathology), though often somewhat undersized Hip looks normal – may be a little wasting
(cf. infective hip pathology) Movements – terminally restricted and painful suggestive of
synovitis, abduction (specially in flexion) is nearly always limited and usually internal
rotation also, usually no fixed deformities

Pathological stages of the disease (Waldenstrom, Elizabethtown)

NECROTIC STAGE
Part or all of the epiphysis is infarcted, but the articular cartilage which receives its
nourishment from the synovial fluid continues to grow. Radiologically these changes are
demonstrated as a small capital epiphysis and an apparent increased thickening of the
articular cartilage that gives the impression of increased medial joint space (Waldenstrom’s
sign). Subsequently the necrotic portion of the femoral head becomes radiologically dense.
Subchondral fractures (crescent sign) and crushing of the necrotic bone due to continued
stresses leads of loss of height of the bony epiphysis. Lasts approximately for 6 months.

RESORPTION (FRAGMENTATION) STAGE

Reparative process begins and the dead marrow is gradually replaced by fibrovascular tissue
(revascularization). When this happens, the alternating areas of sclerosis and fibrosis appear
on the x-ray as ‘fragmentation’ of the epiphysis. Lasts approximately for 6 months.

REOSSIFICATION STAGE
Reossification of the fibrovascular tissue will occur. Reossification generally begins at the
margins of the epiphysis and progresses until the entire epiphysis is ossified. Radiologically
this will be seen as an increase in epiphyseal density. Lasts approximately 1.5 to 3 years.

REMODELLING (HEALING) STAGE

Continues until skeletal maturity. The femoral head may regain its normal (or near-normal)
shape; however, in less fortunate cases the femoral head becomes mushroom-shaped, larger
than normal and laterally displaced in a dysplastic acetabular socket.

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(Note: Containment procedures (non-surgical or surgical) is attempted only in the
necrotic and fragmentation stage. It will not have any effect in the reossification and
remodelling stages)
Classifications

Herring classification
Greater degree of predictive value for the outcome of the Perthes changes
Utilizes a well taken AP x-ray of the hips
Capital epiphysis is divided into lateral, central and medial pillars
Group A – normal height of the lateral pillar
Group B – partial collapse (but still more than 50 % hight) of the lateral pillar
Group C – severe collapse (less than 50 % of normal height) of the lateral pillar

Salter and Thompson classification

Group A – less than 50 % involvement of femoral head
Group B – more than 50 % involvement

Caterall classification
Requires AP and frog leg lateral x-rays of the hips
Lacks inter-observer reliability
Group 1 – Epiphysis has retained its height (no collapse), less than half the nucleus is
sclerotic (usually only anterior portion is involved)
Group 2 – Upto 50 % of the nucleus is sclerotic and there may be some collapse of the central
portion
Group 3 – Most of the nucleus is involved with sclerosis, fragmentation and collapse of the
head. Metaphyseal resorption may be present.
Group 4 – Whole head is involved, the ossific nucleus is flat and dense and metaphyseal
resorption is marked

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 Head at risk signs
Radiographic signs which presage increasing deformity and displacement of the femoral head
1. Progressive uncovering of the epiphysis (lateral subluxation)
2. Calcification in the cartilage lateral to the ossific nucleus
3. Radiolucent area at the lateral edge of the bony epiphysis (Gage’s sign)
4. Severe metaphyseal resorption (metaphyseal cyst)
5. Horizontal growth plate
Stulberg classification
Used for determining outcome of the disease.
Based on the concept of sphericity and congruity.
Applicalble to patients who have reached skeletal maturity.
Class I – Normal femoral head
Class II – Spherical femoral head with shortened femoral neck (coxa breva) and coxa magna
Class III – Nonspherical or ovoid femoral head that is not flat
Class IV – Flat femoral head with a flat acetabular roof
Class V – Flat femoral head with a normal acetabulum
Based on the above classification, the hips are considered as:
Spherical Congruency – class I and II hips. Arthritis does not usually develop.
Aspherical Congruency – class III and IV hips. Mild to moderate arthritis usually develops in
mid or late age.
Aspherical Incongruency – class V hips. Severe arthritis develops before the age of 50 years.
Mose classification
Used for determining outcomes of treatment
Good result – Outline of the femoral head fits a concentric circle, with a deviation of 1 mm or
less, on both AP and frog-leg lateral views, and the 2 circles have the same radius
Fair result – Outline of the femoral head on the 2 circles (i.e AP and L) varied by 2mm
Poor result – Outline of the femoral head deviated more than 2mms from a concentric circle
on at least one of the x-rays.

Differential diagnosis
Transient synovits
Slipped femoral epiphysis
Infective arthritis

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 Morquio’s disease, cretinism, multiple epiphyseal dysplasia, sickle-cell disease and
Gaucher’s disease may resemble Perthes’ disease radiologically, especially if they are
bilateral; however, in bilateral Perthes’ disease the two sides are likely to be in different
stages.

Goals of treatment
1) Relief of symptoms
2) Containment of the femoral head
3) Restoration of range of motion
Containment
Collapse of the necrotic bone may lead to lateral extrusion of the the epiphysis
(cartilaginous/bony) beyond the confines of the margins of the acetabulum. If reossification
of the epiphysis and healing occurs with the epiphysis extruded laterally, ultimately there will
be a deformation of the femoral head (coxa magna/irregularis). This would lead to early
arthritis of the femoral head.

Containment means taking active steps to seat the femoral head congruently and as fully as
possible in the acetabular socket, so that it may retain its sphericity and not become displaced
during the period of healing. The theory is that the acetabulum will act as a mould for the
deformed femoral head once it is contained well in the acetabulum. Hence containment is
useful only when it is done in the necrotic and fragmentation stage. It will not be useful in
the re-ossification and healing stages as no further change in the shape of the deformed
femoral head will occur.

The pre-requisites for containment are: - 1) near normal range of movement and 2) hips
should be containable. X-rays do not reveal the cartilaginous portion of the epiphysis. Hence
an arthrogram needs to be done to ascertain whether the hip is containable. If on abduction,
the arthrogram reveals that the ‘whole’ (cartilaginous and bony) femoral head is located
within the acetabulum, then containment is possible. If there is severe deformation of the
femoral head, on abduction of the hip, the femoral head may subluxate (by hinging over the
lateral margin of the acetabulum) instead of getting contained in the acetabulum. This is
known as ‘hinged abduction’ and is a contra-indication for containment procedures. MRI
may also be useful to determine the containability of the hip by assessing the shape of the
whole femoral epiphysis.

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 Containment is achieved by:
1) holding the hips widely abducted, in plaster or in a removable brace- ambulation, though
awkward, is just possible, but the position must be maintained for at least a year till the re-
ossification stage
2) operation – varus osteotomy of the femur or an innominate osteotomy of the pelvis, or both –
this offers the advantages of improved containment and early mobilization over non-
operative contain
Symptomatic treatment
Traction for few days to weeks till pain subsides
Movements are then encouraged – preservation of abduction is especially important –
muscles releases of adductors may be useful for restoration of range of motion. If the range
of motion of slow to recover or is lost again, it indicates deforming epiphysis and hence some
form of containment treatment is advocated.
Avoidance of sport and strenuous activities
Anti-inflammatory medication
Wheel chair use and crutch walking should be discouraged in order to avoid unnecessary
joint stiffness and contracture.
Review of literature
Most of the reported studies have simply lacked the controls necessary to allow valid
scientific conclusions to be drawn. The great disparity in results is related to many factors,
including a lack of controls for known variables (age at the onset of the diseases, sex and
duration of the disease) and a lack of precision and poor interobserver reliability of the
classification systems. It is also difficult to compare the results of any treatment with the
natural history of the disease. Hence there is no general agreement on the ‘correct’ course of
treatment for all cases.
Guidelines to treatment
Based on a critical review of the literature, Herring has suggested the following guidelines:
1. Children under 6 years
No specific form of treatment has much influence on the outcome. Symptomatic treatment is
appropriate
2. Children aged 6-8 years
In this group, the bone age (using the atlas of Gruelich and Pyle) is more important than the
the chronological age

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a. Bone age at or below 6 years
Herring Group A and B or Catterall stage I and II – symptomatic treatment
Herring Group C or Catterall stage III and IV – abduction brace
b. Bone age over 6 years
Herring Group A and B or Catterall stage I and II – abduction brace or osteotomy
Herring Group C or Catterall stage III and IV – outcome probably unaffected by treatment,
but some would operate
3. Children 9 years or older
Except in very mild cases which is rare, operative containment is the treatment of
choice The above are just guidelines. Some surgeons may have a more aggressive
philosophy of treatment and some may be more conservative. Benjamin Joseph adopts a
more aggressive approach by performing surgical containment (open wedge subtrochanteric
varus ostotomy with derotation or extension and a trochanteric epiphyseodesis) in all children
over 7 years of age with Catterall II, III and IV involvement. The short term results of this
approach have proved to be satisfactory. Excessive varization must be avoided (the neck
shaft angle should be reduced to below 120 degrees) to avoid excessive shortening and
excessive weakening of gluteus medius due to elevation of the greater trochanter. If
excessive varization is required to contain the femoral head, a combination of femoral
osteotomy and innominate (eg. Salter) osteotomy is indicated.
Salvage procedures
Indications
1) Hinged abduction
2) Deformed femoral head in re-ossification or healing stage
Procedures
Proximal femoral valgus osteotomy
Distal and lateral transfer of greater trochanter
Shelf arthroplasty
Cheilectomy
Chiari medial displacement pelvic osteotomy
These procedure do not appear to delay the onset of degenerative arthrosis.

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 SPONDYLOLISTHESIS - 2
Definition
Herbiniaux a belgian obstetrician noted a bone prominence.
 Killian in 1854 used the term spondylolisthesis ,spondylos meaning ‘vertebra’ and
olisthenein ‘to slip’
 Defined as anterior or posterior slipping or translation of one segment of the

 spine on the next lower segment.

Degenerative Spondylolisthesis
 A condition characterized by lumbar spondylolithesis without a defect in the pars
o absent of pars defect differentiates from adult isthmic spondylolithesis
 Epidemiology

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 o prevalence
 ~5% in men
 ~9% in woman
o demographics
 more common in African Americans, diabetics, and woman over 40 years of age
 8 times more common in woman than men
 increase in prevalence in women postulated to be due to increased ligamentous laxity
related to hormonal changes
o location
 degenerative spondylolithesis is 5-fold more common at L4/5 than other levels
 this is different that isthmic spondylolithesis which is most commonly seen at L5/S1
o risk factors
 sacralization of L5 (transitional L5 vertebrae)
 sagittally oriented facet joints

 Pathoanatomy
o forward subluxation (intersegmental instability) of vertebral body is allowed by
 facet joint degeneration
 facet joint sagittal orientation
 intervertebral disc degeneration
 ligamentous laxity (possibly from hormonal changes)
o degenerative cascade involves
 disc degeneration leads to facet capsule degeneration and instability
 microinstability which leads to further degeneration and eventual macroinstability and
anterolithesis
 instability is worsening with sagittally oriented facets (congenital) that allow forward
subluxation
o neurologic symptoms caused by
 central and lateral recess stenosis
 a degenerative slip at L4/5 will affect the descending L5 nerve root in the lateral recess
o caused by slippage, hypertrophy of ligamentum flavum, and encroachment into the spinal
o canal of osteophytes from facet arthrosis
 foraminal stenosis

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 a degenerative slip at L4/5 will affect the L4 nerve root as it is compressed in the foramen
vertical foraminal stenosis (loss of height of foramen) caused by loss of disk height osteophytes
from posterolateral corner of vertebral body pushing the nerve root up against the inferior surface
of the pedicle anteroposterior foraminal stenosis (loss of anterior to posterior area) caused by
degenerative changes of the superior articular facet and posterior vertebral body

Classification

Myerding Classification
Grade I < 25%
Grade II 25 to 50%
Grade III 50 to 75% (Grade III and greater are rare in degenerative
spondylolithesis)
Grade IIII 75 to 100%
Grade IV Spondyloptosis (all the way off)

Presentation
Symptoms mechanical/ back pain most common presenting symptom usually relieved with
rest and sitting neurogenic claudication & leg pain second most common symptoms
defined as buttock and leg pain/discomfort caused by upright walking relieved by sitting
not relieved by standing in one place (as is vascular claudication) may be unilateral or
bilateral same symptoms found with spinal stenosis cauda equina syndrome (very rare)

Physical examination
L4 nerve root involvement (compressed in foramen with L4/5 DS) weakness to quadriceps
best seen with sit to stand exam maneuver weakness to ankle dorsiflexion (cross over with
L5) best seen with heel-walk exam maneuver decreased patellar reflex L5 nerve root
involvement weakness to ankle dorsiflexion (cross over with L4) best seen with heel-walk
exam maneuver weakness to EHL (great toe extension) weakness to gluteus medius (hip
abduction) provocative walking test have patient walk prolonged distance until onset of
buttock and leg pain have patient stop but remain standing upright if pain resolves this is

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consistent with vascular claudication
have patient sit
if pain resolves this is consistent with neurogenic claudication (DS)
hamstring tightness
commonly found in this patients, and must differentiate this from neurogenic leg pain
Imaging
Radiographs
recommended views
weight bearing lumbar AP, lateral neutral, lateral flexion, lateral extension
findings
slip evident on lateral xray
flexion-extension studies
instability defined as 4 mm of translation or 10° of angulation of motion compared to
adjacent motion segment
MRI
indications
persistent leg pain that has failed nonoperative modalities
best study to evaluate impingement of neural elements
views
T2 weighted sagittal and axial images best to look for compression of neurologic elements
CT
useful to identify bony pathology
CT myelogram
helpful in patients in which a MRI is contraindicated (pacemaker)

Treatment
Nonoperative
physical therapy and NSAIDS
indications
most patients can be treated nonoperatively
modalities include
activity restriction NSAIDS

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Physiotherapy
epidural steroid injections indications second line of treatment if non-invasive methods fail
Operative
lumbar wide decompression with instrumented fusion
indications most common is persistent and incapacitating pain that has failed 6 mos. of
nonoperative management and epidural steroid injections progressive motor deficit
cauda equina syndrome outcomes ~79% have satisfactory outcomes improved fusion rates
shown with pedicle screws improved outcomes with successful arthrodesis worse outcomes
found in smokers risk of adjacent segment degeneration requiring surgery is greater than
30% at 10 years
posterior lumbar decompression alone
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 outcomes ~69% treated with decompression alone are satisfied
~ 31% have progressive instability
anterior lumbar interbody fusion (ALIF)
indications reserved for revision cases with pseudoarthrosis outcomes injury to superior
hypogastric plexus can cause retrograde ejaculation
Posterior lumbar interbody fusion
Trans-foraminal lumbar interbody fusion

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 TREATMENT OPTIONS IN FRACTURE NECK OF FEMUR
IN YOUNG ADULTS
A REVIEW BY
DR.J.K. GIRIRAJ HARSHAVARDHAN,
INTRODUCTION
We generally consider patients who are younger than 60 years as “young”. But physiologically
those who are active and have high functional demands, good bone quality, and minimal medical
problems are considered “young”(It is these “young people” we will be reviewing in this article).
Whereas those who have low functional demands (use an assistive device to walk), chronic illnesses,
or poor bone quality are considered “elderly”

Femoral neck fractures in any age group is an enigma. We can never definitively predict the
positive outcome of fixation of fractures because of the peculiar femoral head blood supply which
increases the risk of femoral head osteonecrosis and nonunion. Hence for an elderly patient, the goals
are to restore mobility with weight-bearing as tolerated and to minimize complications seen with
prolonged bed rest. A hemiarthroplasty or total hip replacement often accomplishes these goals best.
The patient’s age makes preservation of the femoral head of little importance. But for a
physiologically young and active adult, the goals are to preserve the femoral head, avoid
osteonecrosis, and achieve union. Avoiding an arthroplasty is ideal.
ETIOLOGY
Femoral neck fractures occur less commonly in younger individuals due to high velocity
trauma (commonly associated with femoral shaft fractures). Axial loading of the hip in the abducted
position usually leads to these fractures. Stress fractures may occur due to repeated cyclical loading.
In general femoral neck fractures in young adults tend to be more distal, more vertical and more
unstable. Femoral neck fractures in young adults are associated with higher incidences of femoral
head osteonecrosis and nonunion, ranging from 12 to 86%. Salvage procedures, such as osteotomy,
and other reoperations have high failure rates, and arthroplasty procedures are not ideal, given the
patient’s young age and higher level of activity.

RADIOLOGICAL EVALUATION AND CLASSIFICATION

Radiographic evaluation includes x-ray of the pelvis with both hips AP view ( for Garden
classification), x-ray of the pelvis AP view with traction and internal rotation of the the affected hip
(for Pauwels classification) and x-ray of the affected hip translateral view (to assess posterior
comminution). In doubtful cases as in impacted fractures, MRI (rather than CT) is beneficial. There is
a great degree of inter-observer variation with the Garden’s classification and hence it is more
practical to classify these fractures as non-displaced (Garden I or II) or displaced (Garden III or IV).

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The Pauwels classification is more descriptive of femoral neck fractures in young adults. The fracture
pattern can indicate the relative stability of the fracture and predict the difficulty of obtaining stable
fixation. Type III fractures are the least stable and more difficult to treat and are associated with
increased risks of fixation failure, nonunion, malunion and AVN.

MANAGEMENT OF ACUTE FRACTURES

Principles – ANATOMIC REDUCTION AND STABLE INTERNAL FIXATION

Surgical fixation should be done as soon as the patient is medically optimized. Complication rates
MAY be reduced by immediate or early fixation. There is no benefit of pre-operative traction.
Traction may actually be detrimental by internally rotating the hip and increasing intracapsular
pressure.

The role of capsulotomy remains controversial. Decompressing the intra-capsular haematoma

MAY decrease the risk of AVN. This may be done by aspiration or percutaneous capsulotomy.
Once patient is anaesthetized, closed reduction is attempted by Leadbetter or Whitman’s technique.
The reduction is assessed by Garden alignment index and Lowell C curve. ONLY an anatomic
reduction must be accepted. If it is not possible, open reduction must be done through the Watson-
Jones approach.

Following the anatomic closed/open reduction, the fracture needs to be stably fixed. There are
various fixation methods- cannulated large fragment cancellous screws, DHS, blade plates, DCS,
fixed angle proximal femoral locking plate. Fixation with multiple cancellous lag screws is
recommended for most femoral neck fractures. At least 3 parallel screws are used in an inverted
triangle configuration (to reduce the risk of sub-trochanteric fracture). Pauwels Type I and II are most
amenable to this type of fixation. For basicervical fractures with comminution, sliding hip screw
(DHS) provides a more stable fixation than 3 cancellous screws. A derotational screw is used
superior to the sliding hip screw to prevent rotation of the femoral head during insertion of the
compression screw. The use of these large compression hip screws raises several concerns, including
the amount of bone removed if subsequent reconstruction is required for treatment of nonunion and
the risk of disrupting the blood supply to the femoral head if the hip screw is imperfectly placed. Any
of the 5 fixation methods mentioned above may be used in Pauwels type III. Various studies offer
differing opinions and it is difficult to advocate a particular method for these fractures. Some
surgeons peform a primary valgus ostetomy (recommended by DePalma) to change the vertical shear
force to a compression force at the fracture site. But this treatment method has been nearly given up
due to reasons mentioned later in this article.

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POST OPERATIVE FOLLOW UP
Following stable internal fixation, patient can be mobilized toe-touch weight bearing with crutches
or walker for 3 months. Monthly radiographs are made to assess healing and to identify any evidence
of osteonecrosis. A reasonable clinical indicator that the femoral head is still viable is relative
femoral head osteopenia on the injured side as compared with the normal side on an AP pelvis x-ray.
A single-photon-emission computed tomography (SPECT) can be obtained to evaluate the chance of
femoral head osteonecrosis developing. If the uptake is <90%, there is an increased chance of
osteonecrosis developing. MRI is NOT a good predictor of posttraumatic osteonecrosis. Patients in
whom femoral head osteonecrosis develops usually have persistent groin and trochanteric pain that
does not resolve with time. If the patient does not have pain and has normal radiographs at 24
months, osteonecrosis is unlikely to develop. A femoral neck fracture is deemed to be healed when
the patient is asymptomatic and the fracture line is fading. It is completely healed when the patient is
asymptomatic and the fracture is no longer visible. If there is any question (due to perisistent pain)
about healing at 4 to 6 months postoperatively, a CT scan should be obtained to assess the fracture
line.

TOTAL HIP REPLACEMENT IN ACUTE FRACTURES IN YOUNG PATIENTS

Total hip replacement may be considered in adults over 40 years of age with displaced fractures if
there is significant osteoporosis due to chronic diseases, steroid intake. These are the patients who
have a high risk of failure of internal fixation. Even patients who abuse alcohol are at high risk of
failure. But total hip replacement in this condition may be associated with higher incidences of
dislocation.

SALVAGE PROCEDURES
In our county, it is common to see neglected cases of fracture neck of femur (truly neglected or
following indigeneous treatment). In evaluating these patients, we must determine the viability of the
head, the degree of femoral neck resorption that has occurred, and the degree of osteoporosis that is
present. After these factors are analyzed, we have 2 choices – 1) to salvage the patient’s own femoral
head or 2) to discard the femoral head in favour of an arthroplasty. The duration of nonunion per se
has no role in the decision making process. But long standing nonunions are likely to be associated
with resorption of the femoral neck or associated degenerative changes in the hip, and this must be
taken into account.

Osteonecrosis, the actual death of bone secondary to ischaemia is an early phenomenon after
fracture of the femoral neck and can be considered a microscopic event. Late segmental collapse is
the collapse of the subchondral bone and articular cartilage that overlies the infarcted bone. This
collapse, results in joint incongruity, pain and eventually, degenerative joint disease. Not all patients

320
with osteonecrosis will have late segmental collapse because those femoral heads with partial necrosis
may revascularize and repair before routine stresses on the hip result in collapse of the infarcted area.
Even those femoral heads determined to be avascular by scanning may function well and not undergo
late segmental collapse. Union is possible in the presence of osteonecrosis. When union to an
avascular femoral head occurs, complications generally do not develop until resorption of the
avascular bone in the head occurs, resulting in segmental collapse. H.ence it must be clearly
understood that the mere radiographic presence of osteonecrosis is not a contra-indication for femoral
head salvage procedures in young patients. But it must be remembered that osteonecrosis
substantially lowers the likelihood of success with internal fixation and bone grafting.

Following internal fixation, if there is evidence of instability- particularly if there is a halo

about the fixation device-operative intervention is indicated, as further delay is unlikely to lead to
fracture union If union does not occur within 6 months, a nonunion is likely.

If there is no femoral neck resorption and when the femoral head is viable, femoral head
salvage procedures such as valgus osteotomy or fibular grafting may be tried. These procedures may
be done in an avascular head without collapse but with less successful results. A muscle-pedicle bone
graft may be considered in an effort to revascularize the head if there is no segmental collapse of the
head and no bone stock loss that would make stable fixation likely. But if there is AVN with
segmental collapse or extensive resorption of the femoral head, total hip arthroplasty or arthrodesis
will have to be done.

VALGUS INTERTROCHANTERIC OSTEOTOMY

The principle of valgus ostetomy is to shift the weight-bearing line medially and most importantly,
to place the fracture plane more horizontally to reduce the shear stress on the fracture. This
osteotomy can be useful when the fracture line is vertical and resistant to valgus reduction. If there is
varus angulation at the fracture site as in delayed presentation or loss of reduction after fixation, a
change in position will require force, or dissection that is likely to interrupt the blood supply. These
cases can be safely treated with a valgus osteotomy without open reduction. Since the procedure is
performed in the inter-trochanteric region, the risk of AVN is minimal. But valgization can shorten
the trochanteric lever arm (producing a Trendlenburg gait) and increase the axial loads on the hip
(leading to early cartilage degeneration). Hence extreme valgization greater than 150 degrees must be
avoided. The devices useful for the osteotomy are the double angle blade plate, Meine blade plate and
the double angle DHS. Valgus osteotomy also makes a subsequent total hip replacement difficult in
case of failure.

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OPEN REDUCTION, INTERNAL FIXATION AND FIBULAR AUTOGRAFT
Nagi et al treated many cases of nonunion with open reduction, fixation by compression hip screw
and a free fibular graft with reasonable results. There was a considerable number of late failures.
Probably a free microvascularized fibular graft may provide superior results

MEYER’S PEDICLE BONE GRAFT

Here the quadratus femoris muscle with an attached block of bone is mobilized and inserted into
the posterior femoral head. This procedure may be useful in nonunion to revascularize the head.

HIP ARTHRODESIS
This is indicated in young individuals with active lifestyles. Because of the absence of the femoral
head and neck, fusion is difficult. To maintain length, ischiotrochanteric fusion may be necessary.

TOTAL HIP REPLACEMENT IN NONUNION

When there is AVN with segmental collapse or extensive resorption of femoral neck , the femoral
head is not salvageable and THR may be necessary. The average lifespan of a prosthesis is around 15
years by current standards. The patient will have a mobile and stable hip. Bipolar arthroplasty is
better avoided in younger patients as they are associated with poorer hip scores similar to unipolar
arthroplasty.

EXCISIONAL ARTHROPLASTY AND PELVIC SUPPORTIVE OSTEOTOMY

Here the femoral head alone is removed. The patient ends up with a very unstable but mobile hip
which some Indian patients may prefer. But the patients usually continue tol have pain due to
capsular stretching because of the instability and hence usually younger patients are very unsatisfied
with the procedure. The stability and abductor power may be improved to some extent by a pelvic
supportive osteotomy. Pelvic supportive ostetomy is a proximal femoral valgus osteotomy done in
level with the ischium. This seats the ischium on the proximal femur and decreases the Trendlenburg
lurch. The valgization lengthens the abductors improving its power. The limb may also be
lengthened additionally to improve the gait of the patient.

CONCLUSION
There will always be some confusion in the mind of any orthopaedic surgeon regarding the
management of femoral neck fractures in young adults. This confusion is compounded in the case of
delayed presentations and nonunions. Hence these fractures remain an unsolved mystery!

MUST READ FOR STUDENTS (NOT INCLUDED IN THIS ARTICLE)

Blood supply of the femoral head

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Classication of femoral neck fractures – Garden, Pauwel, AO-OTA
Singh’s index
Trabecular pattern of proximal femur
Closed reduction techniques – Leadbetter, Whitman
Watson Jones approach to the hip
Garden alignment index
Lowell curves
Operative techniques – cannulated cancellous screws fixation, DHS fixation
Basics of unipolar, bipolar and total hip arthroplasty

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 TUBERCULOSIS OF SPINE (POTT’S SPINE)
Introduction:
 It is most common in the 2nd decade of life
 Males and females are equally affected
 Spinal tuberculosis constitue about 50% of the entire osteoarticular tuberculosis
 Spinal tuberculosis is usually secondary to pulmonary/visceral /glandular primary foci

Signs &Symptoms:
Active Stage:
1. Fever
2. Night sweats
3. Pain-night cries
4. Loss of weight and appetite
5. Severe muscle spasms
6. Cold abscess
7. Tuberculous sinuses
8. Knuckle, Gibbus,Kyphosis
9. Neurologic deficits
Healed Stage:
1. Regain weight
2. Sinuses are not active
3. Deformity persisting
4. Neurologic deficits

Incidence
 Dorsal-42%
 Lumbar-26%
 Cervical-12%
 Dorsolumbar-12%
 Cervicodorsal-5%
 Lumbosacral-3%

Classification:
 Anterior
 Central
 Paradiscal

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 Appendicial
 Synovial

Central:
 Through the bateson’s plexus of veins
 Not much of disc involvement ,endplate destruction occurs
Anterior:
 Infection along ALL
 Should be distinguished from paradiscal type with extensive abscess- long standing cases
 “Saw toothed “ appearance/ Scalloping effect
Paradiscal:
 Most common
 Development as “somites”- embryology
 Share common blood supply
 Disc space narrowing is the first pathology in Xray
 Requires 50-60% of calcium in the bone to be reduced for showing destructive lesion in X ray.
Appendicial:
 Spinous process + Transverse process+ Facet+Lamina+Post neural arch
 Combined with paradiscal types have also occurred.
Synovial:
 Occurs only in the zygoapophyseal joints in the spine.

X-rays/Radiographic classification: (Kumar-1988)

Pre destructive
I- Early destructive
II- Mild kyphosis < 3 vertebra k- 10 to 30.
III- Moderate kyphosis > 3 vertebra k-30 to 60.
IV- Severe kyphosis > 3 vertebra k- > 60.

Other features in X ray:

Pre/para vertebral soft tissue shadows
1. C- spine: Distinguish between the trachea and pharynx; 1.5 cm above the cricoid and 0.5 cm below it.
2. C7 to D4: Good penetration X rays are required.
3. Dorsal spine: ‘V’ shaped lucency pushing the lung shadows.
4. Lumbar spine:”Fusiform”/ “Spindle” shaped abscess.

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 Cold Abscess (Common sites)
- Paraspinal region
- Axilla C spine + Upper Dorsal
- Anterior/Posterior triangles of neck
- Intercostal spaces

- Chest wall
- Petit’s triangle Lower Dorsal + Lumbar
- Psoas
- Illiacus muscle

Above the insertion of the diaphragm in the vertebra- cold abscess in the thoracic cavity below the
diaphragm is the Psoas/ Iliacus.

Neurologic deficits:
Classification:
Kumar’s (1988)/ Tuli’s (1985)

Stage I: Not aware of weakness

Treating physician finds the lesion
Plantar- extensor
Exaggerated DTR’s
Stage II: “Clumpsiness” or “ Jumpiness”
Walks with or without support
Stage III: Not able to walk
Spasctic extensor
Sensory deficit< 50%
Stage IV: Not able to walk
Spastic flexor, Bowel bladder involved, Flaccidity

Pathology of deficits
1. Inflammatory edema
2. Extradural compression- Abscess/Caseous material/Granulation
3. Bony –Collapse,Kyphosis,Seuestration debris
4. Meningeal changes- ‘Pseudofibrosis’
5. Infarctions: End arteries,periarteritis+ thrombosis

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6. Spinal tumor syndrome
Treatment:
Middle path regimen:
1.Rest/ ATT(11/2 years)
2.ATT-
Intensive phase: 5-6 months
Continous phase- 7-8 months
Prophylactic phase- 4-5 months
Intensive phase:
H+R+O ; H-300-400 mg H-Isoniazid
R-450-600 mg R-Rifampicin
O-400-600 mg O-Ofloxacin
Continuation phase:
H+Z ; H-300-400 mg
Z-1500 mg Z-Pyrizinamide
Prophylactic phase:
H+ E ; E-1200 mg E-Ethambutol
Surgical intervention is done if:
1.No signs of “progressive recovery” to a satisfactory level after ATT of 3-4 weeks.
2. Worsening of neurology
3.Onset of neurologic deficits
4.Recurrence of neurologic deficits
5.Cervicothoracic lesions with problems in deglutition or respiration
6.Advanced cases with marked sensory + flaccidity+ bowel bladder involvement.

Followed up with:
ESR + X rays
Exercise
Sinuses are removed
Abscess – drained or aspirated.
Surgery:
Anterior + Anterolateral decompression.
Spine at risk signs: Rajasekharan et al
1.Toppling
2. Lateral shift
3.Separation of facet joint
4. Posterior retropulsion of diseased vertebral segments

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 OSTEOTOMIES AROUND THE HIP
A review by
DR.J.K. GIRIRAJ HARSHAVARDHAN,
CLASSIFICATION
According to anatomic location
Femoral
1. Cervical – eg. Modified Dunn osteotomy done for slipped capital femoral epiphysis
2. Intertrochanteric – eg. Sugioka transtrochanteric rotational osteotomy for avascular necrosis of
femoral head
3. Subtrochanteric – eg. Schantz pelvic supportive osteotomy done for unstable hip
4. Greater trochanteric – eg. Flip osteotomy done during Ganz safe surgical dislocation of hip
Pelvic
1. Reconstructive – single, double, triple, periacetabular
2. Salvage – Chiari, Shelf
Indications
Dysplastic hips
Dysplastic hips are characterized by a shallow acetabulum and increased acetabular index. There
may be associated subluxation or dislocation. Following reduction of head into the acetabulum,
osteotomies are usually done in children over the age of 1.5 years to provide anterior coverage,
improve acetabular index and prevent instability of the hip.
When an open reduction is done, femoral osteotomy and shortening is done to decrease the
pressure on the femoral head and facilitate easy reduction. Varization and derotation may be added to
the femoral shortening osteotomy.
Single pelvic (ilium) osteotomies such as the Salter and Pemberton osteotomies improve
acetabular index and are usually indicated over the age of 4 years when the acetabulum fails to
develop in a reduced hip. The osteotomy may just redirect the acetabulum as in a Salter osteotomy or
may reduce the volume of the acetabulum (acetabuloplasty) as in a Pemberton osteotomy. As the
child becomes older double (ilium +pubis)or triple osteotomes (ilium +pubis + ischium) may be
necessary to redirect the acetabulum. Periacetabular osteotomies popularized by Ganz are ‘powerful’
osteotomies which are technically difficult but can redirect the acetabulum in any direction. It can be
done at any age even after skeletal maturity.
Salvage procedures such as the Chiari osteotomy or shelf procedure are done in older children
with subluxed hips to improve coverage of the femoral head. No attempt is made to reduce the
subluxed femoral head (that is why they are called salvage procedures) because of the high risk of
avascular necrosis of femoral head.

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Perthes’ disease
Varus osteotomy of the proximal femur is indicated in Elizabeth Town stage of necrosis and
fragmentation when the head is ‘at risk’ (lateral extrusion of the capital femoral epiphysis which
usually occurs in Herring’s type B and C). Varization of the proximal femur brings the laterally
extruded head under the acetabulum so that the head will eventually remodel to a reasonably ‘round’
head. This is called containment. Varus osteotomy should not be done in the late reossification and
residual/ healed stages as the femoral head loses its biological plasticity and its ability to mould in
these late stages. Varus osteotomy is also contra-indicated when there is a hinged abduction. Hinged
abduction means that laterally extruded portion of the femoral head abuts or impinges on the
acetabular edge (when there is a large extrusion) during abduction and causes subluxation of the
femoral head. This can be easily detected by an arthrogram which shows medial pooling of the dye
on abduction of the hip. Varus osteotomy should be performed only after the hip irritability reduces
with rest and traction. If stiffness of hip persists even after prolonged rest and traction it may imply
that the lateral extrusion is severe and there may be a hinged abduction. When there is a hinged
abduction, valgus (not varus) osteotomy should be done to improve congruity.

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Technique of varus containment osteotomy and greater trochanter apophyseodesis advocated by Prof Benjamin Joseph

In late stages (re-ossification and residual), salvage procedures such as the shelf procedure and
Chiari osteotomy may be done to improve femoral head coverage and delay osteoarthritis. But
nowadays in experienced hands this can be tackled by a safe surgical dislocation and reshaping of the
femoral head.
Slipped capital femoral epiphysis
In SCFE, the capital femoral epiphysis slips posteriorly and medially leading to retroversion and
varus. In situ pinning is the treatment of choice. But in moderate and severe slips in situ pinning
leads to a proximal femur deformity which may need to be corrected at a later date with proximal
femur osteotomies. The principle of the osteotomy is to correct the varus and retroversion(ex-toeing).
The distal fragment has to be valgized and internally rotated. The osteotomy can be done at the neck,
basicervical, intertrochanteric or subtrochanteric level. It can be expected that an osteotomy closer to
the head will produce a better correction of the deformity. But as the corrective osteotomy is done
closer to head the risk of avascular necrosis of femoral head and non-union increases.
Nowadays paediatric orthopaedicians are more aggressive in the initial management of moderate
and severe slips. Closed reduction should not be done because of the increased risk of avascular
necrosis. Open reduction may be done through an anterolateral approach before pinning. Safe
surgical dislocation of the hip may be done and the exposed capital femoral epiphysis may be
repositioned on the femoral neck and pinning done.
Avascular necrosis of femoral head and Osteoarthritis of the hip
With the longevity of total hip replacement improving (15 to 20 years), osteotomies are less
frequently performed for AVN and OA hip. Valgus or varus osteotomy of the proximal femur may be
done in Stage II B or III AVN and early OA to reposition the collapsed/arthritic area of femoral head
from the weight bearing region (dome). Sugioka transtrochanteric rotational osteotomy has been
described for AVN but the results of this osteotomy could not be replicated by other surgeons.

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Paralytic subluxation/dislocation of hip
Typically subluxation and dislocation of the hip occurs in paralytic disorders such as cerebral
palsy, spinal dysraphism, etc. due to flexion and adduction contractures of the hip. Migration
percentage/index can be used to identify early subluxation. Early subluxation may be managed by
soft tissue releases alone but subsequently bony procedures may be required if there is a relapse or
progression. A combination of femoral varus derotation osteotomy (to tackle coxa valga and
excessive femur anteversion) and pelvic osteotomy to improve posterior coverage of the acetabulum
(cf. dysplastic hip where the anterior coverage is deficient) is needed. Transiliac Dega osteotomy is
usually preferred as the coverage can be improved wherever needed.
Hip subluxation/dislocation is very common in non-walkers in cerebral palsy. Even though child
may not be walking, the problem has to be tackled so that the hip can be abducted and perineal
hygiene can be maintained.
Delayed union/non-union of fracture neck femur
Valgus osteotomy of the proximal femur is done in delayed union (after internal fixation) and non-
union of fracture neck of femur in younger individuals to improve the union rates. Valgization makes
the fracture line more horizontal and converts the shearing forces acting across the fracture into
compressive forces making it more conducive for fracture healing.

Primary valgization may be done in type III Pauwell acute fracture where the fracture line is very
vertical on a traction internal rotation view. But later conversion to THR may become difficult.
Hence it is preferred to use a fixation device with side plate (eg. DHS, angled blade plate) rather than
primary valgus osteotomy for such fracture patterns.

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Nonunited/malunited intertrochanteric fracture
Coxa vara and retroversion occurs as a result of improperly treated(neglected/indigenously
treated) /failed treatment (after internal fixation) of intertrochanteric fractures. Valgus osteotomy and
internal fixation can improve the leg length discrepancy, lurch and extoeing. When well planned and
executed union can be achieved without a necessity for a prosthetic replacement in younger
individuals.
Improvement of surgical exposure
Greater trochanteric osteotomy is used to facilitate and improve exposure in many hip surgeries
eg. internal fixation of acetabulum fractures through the posterior approach, safe surgical dislocation
of the hip (Ganz)

Ganz safe surgical dislocation utilizes a greater trochanter osteotomy as illustrated above

Extended trochanteric osteotomy is used in revision surgery to facilitate removal of femur prosthetic
component and intramedullary cement.
Improvement of stability in unstable hips
In neglected congenital dislocation of the hip and in excised hips (following Girdlestone
arthroplasty) patients have an unsightly abductor lurch which is also energy consuming. The stability
of the hip can be improved by a pelvic supportive osteotomy(not a pelvic osteotomy) popularized by
Schanz and later Ilizarov.

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 Valgus osteotomy of the femur is done at the the level of the ischium( i.e where the femur is
in line with the ischial tuberosity in the horizontal plane on the xray). The distal fragment is valgized
to the extent that no free adduction is possible (degree of valgization = degree of free adduction + 10
degrees). When the osteotomy is done the proximal fragment is prevented from excessively
translating proximally during weight bearing by the ischium (i.e the ischium sits on the proximal
fragment). The power of the hip abductors is improved as the adducted proximal fragment stretches
and tightens the lax abductors. Hence the abductor lurch is reduced and gait improved. But the
valgization shifts the mechanical axis laterally. This increases the stress on the lateral compartment of
the knee joint predisposing to early osteoarthritis of the lateral tibio femoral compartment of the knee.
This can be prevented by performing a distal femur varization osteotomy to reposition the mechanical
axis through the centre of the knee joint. Also lengthening can be performed with the distal femur
osteotomy by using a Ilizarov fixator.

Osteotomies of historical interest (not commonly performed nowadays)

Lorenz bifurcation osteotomy
McMurray’s osteotomy
Dickson’s high geometric osteotomy
Dimon Houghston osteotomy
Sarmiento’s osteotomy
Pauwel’s varus/valgus/Y osteotomy
Sugioka’s transtrochanteric rotational osteotomy
Varus derotation osteotomy of Axer
Albee acetabuloplasty
Important osteotomies
Salter osteotomy
Indications – anterolateral acetabular deficiency (commonly seen in DDH), < 15 degrees of
acetabular index correction required
Prerequisites –congruous hip reduction, iliopsoas and adductor contractures must be released, range
of motion of the hip must be good
Age – 18 months to 6 years
Transverse iliac osteotomy is made just above the acetabulum (from sciatic notch to just below the
anterior inferior iliac spine) . Using the pubic symphysis as a hinge the distal fragment is rotated
without displacement of the posterior aspect of the osteotomy to cover the anterolateral deficiency.
The gap is filled with bone graft and the displacement is held with K wires.

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Pemberton osteotomy (acetabuloplasty)
Pemberton described a pericapsular osteotomy of the ilium in which the osteotomy is made
through the full thickness of the bone from just superior to the anterior inferior iliac spine anteriorly
to the triradiate cartilage posteriorly (posterior part of ilium remains intact): the triradiate cartilage
acts as a hinge on which the acetabular roof is rotated anterioly and laterally (bends on the triradiate
cartilage). Anterior and lateral coverage of femoral head is improved but posterior coverage
remains unchanged. It is indicated when more than 10 to 15 degrees of acetabular index correction is
required for dysplastic acetabulum. It is technically more difficult than a Salter osteotomy but
internal fixation is not required. It can be done between 18 months to 10 years of age (till there is an
open triradiate cartilage)

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Dega osteotomy (acetabuloplasty)
Dega procedure is an incomplete iliac osteotomy similar to a Pemberton osteotomy. The difference
is that there is a larger posterior hinge (horizontal limb of the tri-radiate cartilage) and less inner table
is osteotomized. Medial part of the ilium is intact. Therefore it relies on the plasticity of the superior
acetabular margin rather than the triradiate cartilage acting as a hinge unlike the Pemberton
osteotomy. Overall femoral head coverage is improved (anterior, posterior and lateral). Hence this is
suitable for both DDH as well as in paralytic hip instability.

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Steel triple innominate osteotomy

Indications: Adolescents and skeletally mature individuals with residual dysplasia in a congruous hip
in whom acetabular remodelling is no longer anticipitated
This is a redirectional osteotomy and is technically difficult. The ilium, ischium and superior pubic
ramus is divided to make the acetabulum rotationally free. The acetabulum can be rotated to cover
any defect as illustrated above. But in contrast to a salvage procedure, the femoral head is still
covered by articular cartilage (cf. Chiari osteotomy and shelf procedure where the femoral head is
additionally covered by fibro-cartilage). But this procedure may distort the pelvis such that natural
childbirth in adulthood may not be possible.

Chiari osteotomy
Chiari osteotomy is a transverse osteotomy which is done just superior to acetabulum. The distal
fragment with femur is medially displaced and fixed with screws/pins. This is also called capsular
interpositional arthroplasty as capsule is interposed between the shelf and femoral head. It is
indicated as a salvage procedure in incongruous joints with early osteoarthritis.

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Staheli Shelf procedure
Shelf procedure is performed to increase the volume of the acetabulum to cover the subluxated hip
(as in DDH) or extruded femoral head (as in Perthes’). This is a salvage procedure which is
performed in subluxated (non-concentric) dysplastic hips in children over the age of 5 years. The
hip may still remain subluxated after multiple attempts at open reduction. In older children when the
acetabulum is grossly deficient redirectional osteotomies may not be sufficient. In such cases this
procedure can be done to decrease the rate and risk of progression to osteoarthritis. Similarly in
Perthes’ disease this procedure is performed in the reossification and residual stage as well as when
there is a hinged abduction when containment procedures are contra-indicated.

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A supraacetabular slot is created. Iliac graft strips are inserted into the slot and checked
radiographically to be as low as possible. The reflected head of rectus femoral is used to secure the
graft and cancellous bone graft is placed over it.

Ganz periacetabular osteotomy

This triplanar osteotomy is for adolescent and adult hips with residual dysplasia and minimal
arthritic changes. A large amount of correction can be obtained in all directions as the osteotomy is
closer to the hip joint. The posterior column remains mechanically intact allowing immediate crutch
walking with minimal internal fixation. Unlike the Steel triple osteotomy, the shape of the true pelvis
is unaltered permitting normal child delivery.

Proximal femur varus osteotomy

Indications – 1. Containment procedure for Perthes’ disease 2. Paralytic subluxation/ dislocation
Disadvantages – Shortening of the limb, Trendlenburg gait (due to laxity of abductors) , prominence
of the greater trochanter
Tips – Medial displacement of 10 to 15 mm of distal fragment should be preferably done to maintain
the mechanical axis
Proximal femur valgus osteotomy
Indications – 1. Hinged abduction in Perthes’ disease 2. Coxa vara 3. Delayed union/ Nonunion neck
femur
Disadvantages – lengthening, Trendlenburg gait (due to shortening of power lever arm.

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 VOLKMANN ISCHAEMIC CONTRACTURE

It is a condition that results in shortening, weakening and fibrosis of forearm muscles as

a result of loss of blood supply, usually following a fracture of the upper arm bone or an
elbow injury .
Richard Von Volkmann of Halle described this condition resulting from tight bandage for
injured extremity.

Common cause of VIC

Long bone fractures either as a primary cause or secondarily due to ill-supervised or ignored
treatment.
In the upper limb fracture supracondylar humerus in children is the most common cause
Fracture both bones of leg is the most common cause of compartment syndrome (not of
proximal tibial metaphyseal fracture!).
Usually presents with History of trauma followed by swelling and functional loss. Slowly
developing contracture. Wasting and fibrosis of muscles, involvement of skin with scar
(contracted).Typical posture of hand and attitude of limb. Volkmann’s sign positive and other
findings as above.

Findings
• Wrist flexion
• Volkmann’s sign
• Pronated forearm, Wasting
• Flexed elbow
• Cord- like induration on the flexor side, extensors affected/ spared
• MP joints flexed/extended and IP joints flexed/extended
• Paraesthesia or anaesthesia in the hand and fingers
• Flexed and adducted thumb
• Claw hand
• Deformity and trophic changes due to ulnar and median nerve involvement.

Volkmann sign is the inability to actively extend fingers (at IP and/or MCP joints) without
flexing wrist and passive extension of fingers possible only with wrist flexion (or conversely

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wrist flexion with passive finger extension). It differentiates the deformity due to nerve
palsy and those due to intrinsic muscle contracture of long flexors. Also it can
differentiate between intrinsic minus hand from long flexor contracture.

Pathophysiology - Ischaemic Zone of Injury

Seddon described ischemic zone of injury usually following brachial artery injury that
acquires ellipsoid shape which is in general different from conical ischemic zones observed
in lung and liver ischemia. The long axis of the ellipse runs usually around anterior
interosseous artery with center just above mid-forearm. Nerve at the center is the one most
affected in VIC; which is often median nerve whereas ulnar nerve often is at periphery
and is variably involved. FDP and FPL lying on either side of vessel are the most severely
affected muscles. Necrotic muscle is colloquially termed “muscle sequestrum”.

Median nerve more commonly involved

Median nerve is often entrapped at the center of ischemic ellipsoid and contracting cicatrix in
later stages hence it suffers maximum damage.
Ulnar nerve situated at periphery of the zone is variably involved depending on the severity
of disease and involvement.
Radial nerve is involved only in extensive disease process spilling on to extensor region.
Muscles commonly involved
FDP (partial or complete) and FPL are the first ones to be involved; then depending on the
severity of involvement FDS, PT, flexors of the wrist, pronator quadratus, extensors in that
order may be affected.

Classifications:

Seddon:
Grade I: Ischaemia
Grade II: Ischaemic contracture
Grade III: Ischaemic contracture with nerve involvement
Zancolli:
Type I: Contracture involving forearm muscles with normal intrinsic muscles
Type II: Contracture involving forearm muscles with paralysis of intrinsic muscles

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Type III: Contracture involving forearm muscles with contracture of the intrinsic muscles
Type IV: Combined type

Tsuge (Types):
Mild (aka localized VIC): Further subdivided into proximal (pronator teres chiefly
involved) or distal (pronator quadratus) or middle third (flexor digitorum profundus)
involvement.
No or mild nerve involvement, e.g. ulnar nerve in proximal type. Often presents with
involvement of RF/MF but in advanced cases there may also be involvement of IF/LF.
Moderate: Deep muscles (FDP, FPL) + superficial muscles (FDS, wrist flexors, pronator
teres) + involvement of thumb and nerve involvement.
Severe: Moderate + extensors (often partial) and skin involvement + severe contractures and
joint stiffness.

Assessment before surgery

Muscle groups involved and spared (for tendon transfer),
nerve involvement, skin involvement (there may not be enough initial space available for free
vascularised transfer due to skin contracture).
Thence we stage the disease and decide treatment.

Time for surgery

Ideal is to wait for at least 3 months {Seddon; for necrotic region to segregate and
spontaneous recovery of muscle and nerves stops (some say 6 months)} and should be
done within a year (Tsuge) to produce good results.
Deformity is said to be established if the interval from injury is more than 6 months.

Modalities of management
Treatment is devised according to the stage of presentation
I. Acute Stage (up to 24 hrs):
Treat like compartment syndrome.
II. Sub-Acute or delayed stage (from 24 hrs to 3-6 months):
Presenting as edema and induration of forearm with paresthesia or anaesthesia and motor
weakness or loss.

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The deformities are progressing during this stage. It is an opportunity to improve sensations
and motor function and prevent stiffness and deformity.
Mobilization and supervised physiotherapy (Dynamic splinting, stretching) is undertaken.
Surgery is indicated if there is
neurological impairment,
failure of conservative treatment or
radiological (MRI) evidence of fibrosis.
Neurolysis and displacement of nerve from contracting cicatrix to subcutaneous plane,
excision of scar is done.
If nerve damage is severe then excision followed by grafting may be attempted.
III. Established VIC (Tsuge classification of disease severity):
Mild type:
a. Stretching and physiotherapy: If muscle mass is available.
b. Tendon transfer/lengthening when there is loss of muscle mass by Z-Plasty (of involved
FDS, FDP, FPL tendons) or FDS to FDP transfer {Parkes} (by attaching cut distal end of
FDS to cut proximal end of FDP “motorization of FDP”).
c. The other way of transfer is to transfer extensor tendon to flexor. For involvement of
multiple tendon units prefer muscle sliding operation (Page’s operation) or less favourably
proximal row corpectomy.
Moderate type (Classic type):
Initial stretching followed by:
a. Muscle sliding operation (of Maxpage) with neurolysis (preferred for preserved muscle
mass).
b. When there is no useful finger flexion left or there is proximal skin problem then
BR/ECRL transfer to flexors (FPL and FDP respectively) and complete release of contracture
and neurolysis is the usual option.
Other options are proximal row carpectomy or forearm shortening by 2-3 cms (Garre’s
operation).
Severe type:
Preferred treatment includes early excision of all necrotic tissue with complete neurolysis of
ulnar and median nerves to give them fair chance to recover (at least 3 months ). This can be
followed by tendon transfer as above or if no tendons are available then gracilis (muscle after
expanding skin with tissue expanders) or latissimus dorsi/medial gastrocnemius
(Myocutaneous) free innervated muscle graft. Carpectomy (Griffiths) and wrist arthrodesis

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are other uncommonly performed operations in isolation.

In old cases with no available motor, severe contracture and non-salvageable nerve
injury; a combined procedure of flexor tenodesis with intermetacarpal fusion with thumb in
opposition can be done. Non-salvageable (damn useless) limb can even be amputated.
Thumb function needs to be addressed in moderate and severe types: Release of 1st web
space contracture followed by reconstruction of motor function by use of extensors or by
intermetacarpal fusion with thumb in opposition.

Muscle slide operation

It is the distal slide (by 3 cms) of flexor pronator mass subperiosteally from common flexor
origin and interosseous membrane protecting carefully the ulnar nerve and anterior
interosseous nerve, artery and vein.
FCU may need to be elevated till the level of wrist. This is followed by anterior transposition
of ulnar nerve. The muscles are dissected in the order (ulnar nerve  FCU PT  FDP 
PT (distal origin)  Palmaris longus and FCR  FDS  FCU at interosseous membrane).
Advantages are – simple surgery, can be completed in one operation and secondary tendon
transfers are possible after this procedure.

Disadvantages of muscle slide operation

1. Ineffective for paralyzed muscle.
2. Some scar tissue is left behind.
3. There is a risk of recurrence of contracture with growth of the bone.
4. There is a decrease in strength of grip especially in flexion of the DIP joint.
5. All flexor muscles are treated alike irrespective of the severity of damage.

Differential diagnosis
Cases are usually very evident but some milder versions may be confused with:
• Post traumatic haematoma and resulting contracture
• Osteomyelitis and muscle involvement either by intervention or disease process
• Haemangioma of forearm muscles
• Pseudo-VIC (tethering of muscle often FDP to healing fracture).
• Burns.

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 TENDON TRANSFERS
Introduction
Three main principles:
The transfer should not significantly decrease the remaining function of the hand.
The transfer should not create a deformity if a significant return of function occurs following
a repair.
The transfer should be phasic or capable of phase conversion
Fundamental Principles:
Correction of contracture
Adequate strength
Straight line of pull
One tendon, one function
Synergism
Expendable donor
Timing of tendon transfer
All joints must be fully passively mobile.
All skin and soft tissue must be pliable and mobile.
Principles of tendon transfers match muscle strength
force proportional to cross-sectional area
greatest force of contraction exerted when muscle is at resting length
amplitude proportional to length of muscle
work capacity = (force) x (amplitude)
motor strength will decrease one grade after transfer
should transfer motor grade 5
appropriate tensioning
appropriate excursion
can adjust with pulley or tenodesis effect
Smith 3-5-7 rule
3 cm excursion - wrist flexors, wrist extensors
5 cm excursion - EDC, FPL, EPL
7 cm excursion - FDS, FDP
surgical priorities

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elbow flexion (musculocutaneous n.)
shoulder stabilization (suprascapular n.)
brachiothoracic pinch (pectoral n.)
sensation C6-7 (lateral cord)
wrist extension and finger flexion (lateral and posterior cords)
selection
determine what function is missing
determine what muscle-tendon units are available
evaluate the options for transfer
basic principles
donor must be expendable and of similar excursion and power
one tendon transfer performs one function
synergistic transfers rehabilitate more easily
it is optimal to have a straight line of pull
one grade of motor strength is lost following transfer
Prognosis
age
leading prognostic factor
worse after age 30
location
distal is better than proximal
Presentation
Physical exam
brachial plexus injury
Horner's sign
correlates with C8-T1 avulsion
often appears 2-3 days following injury
severe pain in anesthetic limb
indication of root avulsion
loss of rhomboid function
indication of root avulsion
radial nerve palsy
classified according to location of lesion proximal or distal to the origin of PIN

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low radial nerve palsy
PIN syndrome
high radial nerve palsy
loss of radial nerve proper function (triceps, brachioradialis, ECRL plus muscles innervated
by PIN)
median nerve palsy
classified according to location of lesion proximal or distal to the origin of AIN
low median nerve palsy
loss of thumb opposition (APB function)
high median nerve palsy
loss of thumb opposition
loss of thumb, index finger, and middle finger flexion
ulnar nerve palsy
low ulnar nerve palsy
loss of power pinch
abduction of the small finger (Wartenberg sign)
clawing
results from imbalance between intrinsic and extrinsic muscles
high ulnar nerve palsy
loss of ring and small finger FDP function
primary distinguishing deficit
clawing less pronounced because extrinsic flexors are not functioning
Studies
Sensory and motor evoked potentials
better than standard EMG/NCS

Treatment
Nonoperative
physical therapy, splinting, and antispasticity medications indications decreased passive
range of motion spasticity Operative early surgical intervention (3 weeks to 3 months)
indications total or near-total brachial plexus injury high energy injury
late surgical intervention (3 to 6 months) indications partial upper-level brachial plexus
palsy

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low energy injury postoperative care protect for 3-4 weeks then begin ROM
continue with protective splint for 3-6 weeks synergistic transfers are easier to rehabilitate
(synergistic actions occur together in normal function, e.g., finger flexion and wrist
extension)

Specific Transfers & Indications

Goal to regain FROM: Donor tendon (working) TO: Recipient Tendon (deficient)
Axillary nerve palsy
Shoulder stability glenohumeral arthrodesis glenohumeral arthrodesis
(flail shoulder)
Musculocutaneous nerve palsy
Elbow flexion pectoralis major, latissimus dorsi to biceps
Elbow flexion common flexor mass point more proximal on humerus
(Steindler flexorplasty)
Radial nerve & PIN palsy
Elbow extension deltoid, latissimus dorsi, or biceps to triceps
Wrist extension PT ECRB
Finger extension FDS, FCR, or FCU EDC
Thumb extension PL or FDS EPL
Low median nerve palsy
Thumb opposition FDS (ring) base proximal phalanx or APB
and abduction tendon (use FCU as pulley - classic
Bunnell opponensplasty)
EIP APB (pulley around ulnar side of
wrist)
High median nerve palsy
Thumb IP flexion BR FPL
Index and long FDP of ring and small finger (ulnar FDP of index and middle (side-to-
finger flexion nerve) side transfer)

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Ulnar nerve palsy
Thumb adduction FDS or ECRB adductor pollicis
Finger abduction APL, ECRL, or EIP 1st dorsal interosseous
(index most
important)
Reverse clawing FDS, ECRL (must pass volar to lateral bands of ulnar digits
effect transverse metacarpal ligament to
flex proximal phalanx)

Complications
Adhesions
necessitate aggressive therapy and possible secondary tenolysis

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 OSTEOSARCOMA

Introduction:
-Highly malignant bone tumor that is characterized by the invariable formation of neoplastic osteoid
and tumor tissue.
-It is the most common primary bone tumor (excluding haematologic origin)

Epidemiology:
-Incidence is 2 to 3 per 10,00,000 cases in USA
-It is common in 2nd decade , with a peak again in older age group (bimodal peak)
-Annually 600-800 cases are reported in USA
- Male: Female ratio is 3:2
-Rare in children < 10 years of age
- Bones around the knee, proximal humerus, spine, pelvis and jaws in elderly are affected.

Etiology:
- Hereditary: Loss of heterozygosity (LOH) of chromosome arms 3q,13q,17p &18q are frequently
involved.
- Retinoblastoma gene (Rb gene)
- Li-fraumeni syndrome (p53) gene
- Rothmund Thomson syndrome
- Environmental factors : Chemical agents like 20- methyl cholanthrene are known to produce
osteosarcoma
- Viral aetiology: Polyoma virus, SV -40 virus are some DNA viruses that produce osteosarcoma.
Clinical Features:
1. Pain: -pain precedes swelling
- Night pain
- Rest pain
2. Swelling: -Enlarges in size
-Skin over the swelling appears stretched and shiny
-Engorged veins are seen over the swelling
-Local signs of inflammation
3. Restriction of movements: Mechanical restriction (or) pathological fractures
4. Ulceration and fungation in later stages
5.Features of metastases – Caccexia - Cough +/- Haemoptysis

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 Investigation:
1. Complete blood count/ Routine blood investigations
2. X ray : - Permeative bone lesion
-Indistinct margins
-Cortical erosions
- Sun ray appearance
-Codmans triangle
3. MRI : - Soft tissue extension
-Skip lesion
- Neurovascular structures if involved
-Intramedullary extent of the lesion
4.Angiogram: -To know the vascularity/ feeder vessels/ neo angiogenesis
5.Bone scan (PET scan)
6. CT/HR CT of thorax :Micro metastases in the lungs.
7. Biopsy

Pathology:
- Malignant spindle cells directly producing tumor osteoid
- Tumor cells should be adjacent to the osteoid,no intervening normal osteoblasts.
- Other cells like cartilage , fibrous tissue, vascular spaces, sheets of small round cells can be present
- Stromal cells :
Anisocytosis
Poikilocytosis
Nuclear pyknosis
Pleomorphism
Polyhederal contours

350
 Classifications
Based on pathologic features:
1. High grade intramedullary
2. Low grade intramedullary
3. Parosteal
4. Periosteal
5. High grade surface osteosarcoma
6. Telangiectatic
7. Small cell osteosarcoma
DHALIN ET AL

Osteoblastic Chondroblastic Fibroblastic

COPELAND & GESCHICKTER ET AL

Osteolytic Osteosclerotic

STAGING
MSTS (Musculoskeletal tumor society)
1. ENNEKING
2. AJCC ( American Joint Committee for Cancers)

Prognosis:
Elevated alkaline phosphatase and lactate dehydrogenase have worse prognosis

Treatment:
Neoadjuvant Chemotherapty
Surgical Procedure
Continue chemo and radiotherapy

351
 Chemotherapy:
1. HDMTX (High dose methotrexate)
2. Doxorubicin
3. Cisplatin
4. Bleomycin
5. Dactinomycin
6. Cyclophosphamide
7. Ifosfamide

BDC regime is the most commonly followed.

MULTIDRUG PROTOCOL
1.Vincristine 1.5mg/m2 on day 1
2.HDMTX 200 to 300 mg/kg on day 2 + CFR Citovorum factor release 9 mg every 6 hours for a
period of 12 days
3.After 2 weeks; Adriamycin 15 mg/kg/day x 2 weeks
Total period for a cycle is 56 days.

Surgery:
1. Allografts
2. Autografts
3. Endoprosthesis
4. Composite fixation

Radiotherapy:

Megavoltage radiotherapy 230 rads/day or 1000 rads/week

Pulmonary resection- Treatment of metastases

RECENT ADVANCES IN TREATMENT OF OSTEOSARCOMA

1. Intra arterial chemotherapy

2. Intensification of regional limb perfusion
3. GCSF- Granulocyte colony stimulating factor
4. GMCSF-Granulocyte macrophage colony stimulating factor
5. Role of p-glucoprotein, DHFTR amplification

352
6. Non cytotoxic drugs like- MTP PE Muramyl tripeptide phosphoethonolamine : Lipophillic
analogue of muramyl di peptide,it can activate circulating monocytes and pulmonary macrop
hages, inducing them to be tumoricidal.
7. Interferons/BCG’sSurgical
- Expandable prosthesis
- Allografts (Bone banks)

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 WARD ROUNDS-
DR. SRIJAY SASHAANK, DR. J.K. GIRIRAJ HARSHAVARDHAN
1. Plaster of Paris
Chemical formula?
Setting time?
Factors affecting setting time?
Applications?
Complications?

Chemical formula-Ca so4.1/2 H2o

Setting time: 4-5 minutes
Factors affecting setting: Temperature of water, impurities, Humidity, Room temperature
Applications: Slab, Cast, Functional cast bracing
Complications: NVD, Compartment syndrome,Fracture disease, Wasting
2.

Identify: POSI- position of safe immobilization

Sister James position
Priciples: MCP’s flexed so as to permit the tautness of the collateral ligaments (are stretched to
maximum length to prevent contractures)
Shape of the metacarpals also contribute to the need for flexion at the MCP joint.

3. Patella tendon bearing cast

Principle: “Continuing function while a fracture is uniting”
Pascal’s law: When a limb is loaded there is generation of intracompartmental pressure around
fracture site that exerts pressure on the wall of the fascial compartment.
Pre requisite: No Pain on minimal movement,Reasonable reistance to telescopy,shortening should not
exceed 0.25” for tibia and 0.5” for femur

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Contra indications:Non compliant pateint,Neuro muscular disorder,Altered sensitivity ,Isolated tibia
fracture(fibula intact)

4. Synthetic fibre glass plaster

Composition: Fiber glass impregnated with polyurethane polymer
Setting time:1-2 minutes
Advantages: light weight, water resistant,lesser setting time

5. Chlorhexidine gluconate
Effects:Antiseptic in lower concentration,Bactericidal in higher concentration
Uses: For surgical hand scrub,Post operative wound cleaning
Commonly available in 2% and 4 %

6. Gauze
Properties100% Cotton fabric with loose open weave
Bleached to white
Quick absorbent property
Adsorbent
Prepared in long sheets
Number of holes per square centimeter 4x4=16
Uses: Dressings

7. Compound benzoin tincture

Composition: Bensoin resin in alcohol
Effect: Adhesive and anti septic
Uses: before skin traction application, before application of dressing as wound sealant.

8. Elastocrepe bandage
Composition: Cotton,polyester and elastic yarns
Functions: Stable pressure around area of application leading to reduction of venous blood flow and
thus reduces the swelling around the injured area
Hemostatic effect due to compression
Uses:For strapping of sprain and strain around joints,Splinting of fractures,post op compressive
dressings.

355
9. Dressing trolleys
Materials kept
Surgical drum with sterile gauze pieces,dressing pads,roller bandages
Cidex tray with Scissors,Artery forceps,needle holder and thumb forceps
Kidney tray :Concavity confirms to the curvature of the body part
Transparent glass bottle with cheatle’s forceps
Minimum of two dressing trolleys( one for infected dressings and one for clean cases)

10. Povidone iodine solution

PVI:Polyvinyl pyrrolidone iodine
Effects:Antiseptic- effective against bacteria,fungi,protozoa and yeast
Disadvantages: Insolublity+Instablity. Irritant,stains
Available forms: 5% and 10%solutions
7.5% scrub
10% ointments

11. Hip spica cast

Position: 45 degree of hip flexion,and 30 degree of abduction
Knee joint 45 degree of flexion
Ankle- neutral position
Uses: Paediatric femur fractures, Paediatric hip surgeries
Complications:Superior messentric artery syndrome  Ischemia to the bowel

12. EUSOL
Identify:Edinburgh University solution
Composition: Boric acid 1.25 g,Bleaching powder1.25 g, Sterile water 100 ml
Mechanism: Release of nascent chloride
Uses:Desloughing agent
To separate slough from infected wounds,bed sores,ulcers and burns
Eusol II contains additional sodium acetate and glacial acetic acid to tackle pseudomonas infection
Vinegar can be added if pseudomonas infection is suspected
(acetic acid,ascorbic acid,citric acid and tartaric acid)

356
13. Hydrogen peroxide solution
Chemical formula:20 Volumes of H2O2
Effect: Cleansing
Uses: Frothing brings debris out of wound
Destroys anaerobic organism
Used as chemical cauterisation
Removes blood stain from clothes
Non orthopaedic use: Staining and Dying units

14. Thomas splint

Designed by Robert Jones for immobilisation –proposed its name as Thomas splint in memory of his
maternal uncle Hugh Owen Thomas.
Components:
Well padded circular or oval ring
Outer bar with proximal angulation-angulation clears the greater trochanter.
Inner bar
W shaped Joint of two bars.

357
15. Bohler Braun frame

Designed by Braun,modified by Bohler

USE of the pulleys:
1st pulley in the line of the leg-for calcaneum and distal tibial traction
2nd pulley in line of supracondylar area-for upper tibial pin traction
3rd pulley to change the angle of traction and prevent equinus deformity at ankle
Advantages-Change the angle of traction as required.Multiple traction can be given simultaneously

16. Skin traction

Traction kit contains: Skin strap,crepe bandage,spreader Cotton rolls
Applying a traction: Medial Strap should be anterior (Shin of the tibia),Lateral strap should be along
the long axis of greater trochanter to the lateral malleoli
This prevents external rotation from occuring
Complications: Pressure sores, Common peroneal nerve palsy, Skin itching,allergic reactions

17. Buck’s frame or pulley

358
Components: Three pulleys as upper ,middle, lower+Bed holding frame
Preferred Pulley wheels: Wheel diameter 5-6.25 cm
Axel diameter:6 mm
Uses: Different pulleys are used for alignment of distal fragment in relation to proximal fragment by
adjusting traction cords on at different heights.

18. Cervical skeletal traction by crutchfield tongs

Application: Requirement: Crutchfield tong,guarded drillbit
Three finger breadths above pinna and in line of mastoid, the drilling should be in the parietal bone,
penetration should not exceed 3 mm in children and 4 mm in adults.
Traction weight: 2.5 kg + ½ kg for each cervical vertebra
Contraindications: C2 hangman fracture,Cervical flexion distraction injuries(Facetal dislocation)
leading to disc herniation
Tip - Technique of reduction of unilateral and bilateral facetal dislocations of the cervical spine is
commonly asked during ward rounds. Read it in detailed from standard textbooks

19. AO external fixator

What is the full form of AO?
What are the components of the fixator?
Types of Schantz screws (self tapping) – non tapered, tapered – differences

Factors affecting the stability:

Number of pins and their diameter
Distance between pins
Number of parallel rods and their diameter
Distance between the bone and rod
Pin placement nearer to the fracture site.

359
How to identify pin tract infection:
Discharge
To tap the the pins and see for the resonant sound, if dull note is present then its indicative of
infection.
Tenderness on palpating around the pin tract sites.

How will you dynamize an AO external fixator?

Needs a unilateral uniplanar frame fixed with 2 rods. Proximal to the fracture nuts are loosened on
one of the rods. Distal to the fracture nuts are loosened on the other rod.

20. Balkan frame

The frame was first used in the Balkan War – first World War
Components: Vertical uprights,Horizontal bars,Monkey trapeze, Pulleys.
Uses:Trapeze used for personal hygiene and physiotherapy. Bars and pulleys for applying various
types of tractions.

21. Venous compression stockings

Specialised hosiery to prevent occurrence of progression of venous disorder
Principle: Compression of limbs reduces the diameter of peripheral veins. This increases venous flow
and effectiveness of valve.
Indications: Limb edema,Chronic peripheral venous insufficiency,Varicose veins,Lymphedema.

22. Pneumatic compression devices

Two types: Intermittent PCD and Sequential PCD
Pressure range:19-150 mm hg
Indications: Prolonged recumbent patient, post op THR,TKR, Venous disorder,Patients in whom
chemical prophylaxis is contraindicated

360
23. Incentive spirometry
Principle:Opening of deflated alveloi of lungs under forced inspiration
Indication:For bed ridden patients, after chest surgery, after trans thoracic surgery.

24. Cheatle forceps

Use:Its to be kept in a transpatent glass bottle- wide mouth-sterile cotton at the

base of the bottle with chlorhexidine solution. Used to transfer gauze, pads and
instruments from bin to trays/doctor

25. CIDEX Solution

Composition:It contains 2%glutaraldehyde solution.
Change solution every 14 days
Uses: For sterilising sharp instruments like scissors.
26. Biomedical waste management

361
27. Joshi External Stabilization System (JESS)
Designed by Dr. Brij Bushan Joshi (the first MS Ortho postgraduate in India from Bombay
University) in the 1980s for hand injuries – did not choose to patent the fixator
Extrapolated to the use in CTEV deformity

Components
Untensioned Kirschner wires (cf. Ilizarov)- to fix fixator to bone
Knurled rods (cf. Ilizarov – threaded rods)- straight, L shaped, Z shaped
Distractors – double hole, fish mouth, split block, biaxial hinge
Allen key
Link joints

WHAT IS NOT COVERED IN THIS ARTICLE

Tourniquet – Refer chapter 19 Traction and Orthopaedic appliances – Stewart/Hallett

Walking aids - Refer chapter 17 Traction and Orthopaedic appliances – Stewart/Hallett

Ilizarov fixator and components- Refer chapter 8 and 9 Textbook of Ilizarov surgical techniques –
Golyakhovsky/Frankel

362
 PROSTHESIS AND ORTHOSIS PART 2
‘For revision’ article prepared by
DR. J. K. GIRIRAJ HARSHAVARDHAN
DIFFERENCE BETWEEN PROSTHESIS AND ORTHOSIS
PROSTHESIS – replaces a missing part of the body
ORTHOSIS – appliance fitted – improves function of that part of the body to which it is fitted

PROSTHESIS

• Exoskeletal-
outer laminated shell,
durable,
not adjustable
• Endoskeletal –
pylon made of metal or carbon fibre,
shaped foam covers – not very durable needs to replaced often
adjustable, modular

363
 PARTS OF A PROSTHESIS
TYPES OF SOCKETS
BELOW KNEE PROSTHESIS – patella tendon bearing socket, total surface bearing socket,
supracondylar extension, suprapatellar extension
ABOVE KNEE PROSTHESIS-

Methods of suspension of sockets –

1. belts,
2. shuttle lock system (pin engages into a shuttle lock in the bottom of the socket),
3. lanyard system ( a strap or cord fixed to the liner is routed through the distal socket
and used to pull the residual limb into the socket),
4. suction (as the residual limb is pushed into the sucket is air is expelled out through a
valve and creates a negative pressure environment),
5. vacuum pump attached to socket

364
PROSTHETIC KNEE UNITS
Single axis or polycentric
Manual locking or Hydraulic or Pneumatic or Microprocessor technology

PROSTHETIC FEET
Nonarticulated –
1. Rigid keel – eg. SACH foot
2. Flexible/elastic keel – Dynamic response foot

Articulated –
1. Single axis
2. Multi axis
3. Micro-processor – small computer controlled sensors

SACH (SOLID ANKLE CUSHIONED HEEL) FOOT

Inelastic keel or core made of wood
No ankle joint
Cushioned heel of microcellular or spongy rubber
Moulded polymer of rubber

365
366
JAIPUR FOOT
Designed by P.K. Sethi and Ramachandra Sharma
• Forefoot and heel blocks made of sponge rubber
• Ankle block made of light wood
• 3 components bound together, enclosed in a rubber shell and vulcanized
• Cheap but not standardized
• Labour intensive
• Does not require any shoe
• Waterpoof
• Permits enough movements- easier to walk on uneven surfaces
• Light weight

367
MADRAS FOOT
Modification of the SACH foot
Space between keel and ground filled with spongy rubber (not only the heel portion unlike SACH)
Toes shaped like normal, TendoAchilles like shape made
Additional rubber sole for barefoot walking

368
ORTHOSIS
Nomenclature and parts

369
 BARLOCK JOINT- when pt walks the knee is locked in extension by pushing down the lock which
can be released when the pt needs to bend the knee and sit

FLOOR REACTION ORTHOSIS (Anterior floor reaction ankle foot orthoses)

370
Fabricated to hold the ankle in few degrees of plantarflexion.
Restricts the ability of the tibia to roll forward over the foot in the second/ankle rocker of gait,
creating an extension moment that stabilizes the knee during stance. As the body weight brings the
heel downwards, the suprapatellar band will press the knee backwards preventing the knee from
buckling during stance phase (Refer page 290) Indicated for weakness of the quadriceps
Contraindications – 1. hip and knee flexion contractures exceeding 10 degrees, 2. notable recurvatum
during stance, 3. cruciate ligament insufficiency

FOOT WEAR MODIFICATIONS FOR SYMPTOMATIC FLEXIBLE PES PLANUS

Etiology of pain – Heel valgus stretches the medial structures (especially tibialis posterior) leading
pain
Footwear modifications
• Thomas heel with medial heel raise- most important
• Medial arch support- less important

371
FOOT ABDUCTION ORTHOSIS AFTER COMPLETION OF PONSETI’S TECHNIQUE FOR
CORRECTION OF CONGENITAL TALIPES EQUINOVARUS DEFORMITY

372
WALKING WITH CRUTCHES/WALKER/STICK
How to assess whether the height of support is correct?
Head up
Back straight with the pelvis over the feet as much as possible
Shoulders depressed not hunched
Support tips around 15 cms in front of and lateral to the tip of the toes
Elbows in a position of 30 degrees of flexion when the palm of the hands is on top of the handgrips
(most important point)
---------------------------------------------------------------------------------------------------------------------------
-----------
What is not covered in this article – please refer ‘Traction and Orthopaedic Appliances –
Stewart/Hallett)-
Pavlik harness
Prescription of orthoses
Spinal orthoses
Crutch walking

373
 LAST MINUTE REVISOR
Prepared by: DR. J.K. GIRIRAJ HARSHAVARDHAN, D.Ortho, DNB Ortho,
Consultant Orthopaedic Surgeon and Ass. Professor of Orthopaedics,
Sri Ramachandra Medical Centre,
Sri Ramachandra Medical College and Research Institute, Chennai

LIST OF COMMON EXAMINATION CASES

SPINE
Tuberculosis spine without neurological deficit
Tuberculosis spine with neurological deficit
Post-traumatic paralysis
Scoliosis
Kyphosis - traumatic, infective, tumour
Spinal dysraphism
Cervical myelopathy
Cervical and lumbar disc prolapse
Lumbar canal stenosis
Ankylosing spondylitis

HIP
Perthes’ disease
Slipped capital femoral epiphysis
Tuberculosis
Avascular necrosis
Monoarticular rheumatoid arthritis
Osteoarthrosis
Coxa vara – developmental, malunited intertrochanteric #
Nonunion # neck femur
Post septic sequelae
Ankylosing spondylitis
Congenital dislocation
Neglected traumatic dislocation

TRAUMA
Nonunion of any long bones – aseptic, infected
Malunion of any long bones
Cubitus varus – malunited supracondylar #
Cubitus valgus – nonunion # lateral humeral condyle
Malunited distal radius
Nonunion avulsion # patella
Unreduced shoulder, elbow dislocation
Internal derangement knee

OTHERS
Bone tumours – osteosarcoma, GCT, exostoses,etc
Peripheral nerve injuries – ulnar, radial, median, peroneal, brachial plexus, etc
Chronic osteomyelitis
Post polio residual paralysis
Cerebral palsy
Any congenital deformity – torticollis, club foot, Sprengel’s, tibia pseudarthroses, etc

374
Arthritis of any major joint
Genu valgum/varum/recurvatum
Hansen’s disease
Periarthritis shoulder
Rickets
Neglected TendoAchilles rupture
Volkmann’s ischaemic contracture
Reflex sympathetic dystrophy
Post-traumatic elbow/knee stiffness
Heterotopic ossification

I can assure you that the cases kept in the examination will definitely be present in this list. So make
sure that the you know about the cases in detailed.

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ULNAR NERVE PALSY

Look for
Wasting of hypothenar eminence, 1st dorsal web space
Clawing of fingers
Test for
Adduction and abduction of fingers (interosseoi)
Card test
Froment’s test (for adductor pollicis brevis, 1st palmar and dorsal inteosseoi)
FDP – little and ring finger (flexion of DIP jt)
FCU (flexion and ulnar deviation of wrist)
Sensation – tip of little finger

MEDIAN NERVE PALSY

Look for
Wasting of thenar eminence
Ape thumb deformity (thumb externally rotated and lies in the plane of palm)
Test for
Abductor polices brevis (Pen test)
Flexor polices brevis (flexion of MCP joint of thumb)
Flexor polices longus (flexion of IP joint of thumb)
Flexor digitorum profundus middle and ring finger (flexion of DIP jt)
Flexor digitorum superficialis of medial 4 fingers (flexion of PIP jt- tested after stabilizing other
fingers in extension)
Flexor carpi radialis (flexion and radial deviation of wrist)
Palmaris longus
Pronator teres and quadratus (pronation of forearm)
Sensations – tip of index finger

RADIAL NERVE PALSY

Look for
Wrist drop, fingers drop and thumb drop
Test for
Tricepts (extension of elbow)
Brachioradialis ( flexion of elbow in midprone position of forearm)

375
Extensor carpi radialis longus and brevis (extension of wrist)
Extensor digitorum (extension of medial 4 fingers at MCP joints and not the IP joints- IP joint
extension occurs by action of interosseoi and lumbricals)
Extensor carpi radialis longus and brevis (extension of thumb at MCP and IP jt)
Sensations – 1st dorsal web space

COMMON/DEEP PERONEAL NERVE PALSY

Common peroneal palsy implies that both superficial and deep peroneal nerves are involved
Look for
Foot drop
Test for
Tibialis anterior and peroneus tertius (dorsiflexion of ankle)
Extensor digitorum and hallucis longus (extension of toes)
Sensations - !st dorsal web space
Superficial peroneal nerve
Peroneus longus and brevis (eversion of subtalar joint)
Sensations – dorsum of foot other than 1st dorsal web space, medial and lateral border
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PAIN
Most important symptom in orthopaedics – collect detailed information about the pain
Duration
Site
Radiation
Character – dull aching/throbbing/pricking/burning/etc
Progress
Continous/Intermittent(remissions and exacerbations)
Severity (ideal is to rate the pain using Visual Analogue Scale/Numerical Rating Scale)
Associated symptoms if any (eg.limp)
Aggrevating factors
Relieving factors
Any history of rest pain
Any history suggestive of night cries (patient woken up during sleep due to pain)
How is the pain affecting the patient’s activities of daily living?
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----

ELICITING A HISTORY OF SKELETAL TUBERCULOSIS

Commonest sites – spine, hip, knee, elbow
Pain – usually severe, rest pain and night cries may be present
History of loss of weight and appetite (absent in 50% of cases)
History of evening rise of temperature (absent in 50% of cases)
History of pulmonary tuberculosis – chronic cough and expectoration ,haemoptysis
History of contact with tuberculosis
History of tuberculosis treatment (long duration of drugs, red coloured urine)
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ELICITING A HISTORY OF RHEUMATOID ARTHRITIS

Multiple joints pain and swelling x 6 weeks
Bilateral symmetrical involvement of joints

376
Characteristically PIP and MCP joints of fingers involved
History of early morning stiffness of fingers for more than 1 hour
EXAMINATION OF A JOINT
Inspection
Attitude
Swelling/deformity
Muscle wasting
Limb length discrepancy
Look at all sides of the joint
Palpation
Warmth
Tenderness
Soft tissues around the joint, synovium
Bones around the joint – irregularity, thickening
Bony prominences and their relationship
Movements
Fixed deformities
Active and passive
Measurements
Limb length
Muscle bulk, etc
Others
Special tests to assess stability of the joint
Special tests for soft tissue inflammation – eg. tendinitis
Regional lymphadenopathy
Distal neurovascular status
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EXAMINATION OF KNEE
Inspection
Attitude
Swelling- effusion, cysts
Deformity – genu valgum, varum, recurvatum
Muscle wasting
Limb length discrepancy
Popliteal fossa
Palpation
Warmth
Tenderness – Joint line (medial,lateral, patellofemoral), surrounding bones (distal femur, patella,
proximal tibia and fibula)
Tests for effusion – patellar tap, fluctuation, bulge test
Sorrounding bones – irregularity, thickening
Special tests
For valgus and varus instability (collateral ligaments)
Anterior and posterior Drawer’s test
Lachman’s test
Pivot shift test
For PCL and posterolateral complex – dial test, quadriceps drawer test,etc
McMurray’s test
Appley’s grinding test

377
Apprehension test for recurrent patella dislocation
Others
Movements – active, passive, range of flexion, any fixed flexion deformity, any extensor lag
Measurements – limb length, muscle wasting
Inguinal lymphadenopathy
Distal neurovascular status

DIFFERENTIAL DIAGNOSIS OF CHRONIC SYNOVITIS OF THE KNEE JOINT

Infective- Tuberculosis
Subacute pyogenic
Gonococcal
Inflammatory Rheumatoid arthritis
Reiter’s disease (so called reactive arthritis)
enteropathic arthritis
ankylosing spondylitis
Juvenile chronic arthritis
Others Pseudogout
Haemophilia
Traumatic
Pigmented villonodular synovitis
Synovial chondromatosis

EXAMINATION OF SHOULDER
Commonly kept cases
Periarthritis shoulder
Chronic arthritis – TB, RA
Tumours of proximal humerus
Recurrent dislocation
Nonunion # proximal humerus
Post-traumatic stiffness
Inspection
Attitude
Swelling/ deformity
Contour of deltoid
Bryant’s sign
Muscle wasting
Limb length discrepancy
Palpation
Warmth
Tenderness
Bony irregularity/thickening – proximal humerus, spine of scapula and acromion, clavicle
Movements
Abduction, adduction, flexion, extension, internal and external rotation, circumduction (Refer Das)-
look for painful arc of abduction and drop arm test
Others
Measurements – limb length, muscle, Callaway’s test
Apprehension test
Duga’s test
Hamilton’s ruler test
Abduction paradox or drop arm test
Neer’s and Hawkin’s test

378
Speed’s test
Axillary lymphadenopathy
Distal neurovascular status (examine axillary nerve)
Look for sources of referred pain – cardiac, abdomen (diaphragmatic irritation)
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EXAMINATION OF ELBOW
Commonly kept cases
Cubitus varus due to malunited supracondylar fracture
Cubitus valgus due to nonunion lateral humeral condyle #
Post-traumatic stiffness – malunited intercondylar # humerus, myositis ossificans
Nonunion avulsion # olecranon
Congenital radio-ulnar synostosis
Neglected Monteggia # dislocation and its variants
Neglected elbow dislocation
Chronic arthritis – TB, RA, etc

Inspection
Attitude
Swelling – anterior and posterior
Deformity – cubitus varus/valgus, FFD, hyperextension
Muscle wasting
Limb length discrepancy
Palpation
Warmth
Tenderness- soft tissue/bony
Bony irregularity and thickening – medial and lateral supracondylar ridges, medial and lateral
humeral condyles and epicondyles, olecranon, radial head (identified by forearm rotations), any
abnormal masses suggestive of myositis
Synovial thickening
Relationship between the 3 bony prominences- medial and lateral epicondyles, tip of olecranon

Movements
Flexion
Forearm rotations (whether transmitted to radial head)
Measurements
Upper limb – angle of acromion – lateral epicondyle of humerus – radial styloid
3 bony prominences (normally form a triangle)
Muscle bulk
Others
Valgus varus instability
Cozen’s and reverse Cozen’s test for epicondylitis
Axillary lymphadenopathy
Distal neurovascular status
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EXAMINATION OF WRIST
Commonly kept cases
Malunited distal radius fracture
Reflex sympathetic dystrophy
Madelung’s deformity

379
GCT of distal ulna or radius
Compound palmar ganglion
Chronic arthritis – TB, RA
Inspection
Attitude
Swelling/deformity
Scars, sinuses
Muscle wasting
Limb length discrepancy
Palpation
Warmth
Tenderness- soft tissue/bony
Bony irregularity/thickening – distal radius, distal ulna, carpal bones
Relationship between radial and ulnar styloid process
Movements
Palmar and dorsi flexion
Radial and ulnar deviation
Forearm rotations
Others
Measurements – limb length, muscles
Finkelstein test
Piano key sign for DRUJ instability
Special tests for carpal instability (refer Appley)
Regional lymphadenopathy
Distal neurovascular status
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EXAMINATION OF A TUMOUR
Commonly kept cases
Osteochondroma
Enchondroma
Fibrous dysplasia
Giant cell tumour
Aneurysmal bone cyst
Osteosarcoma
Soft tissue sarcoma
Ewing’s sarcoma, etc
INSPECTION OF THE MASS/SWELLING
Site
Size – in at least 2 dimensions
Shape – eg. Hemispherical, cylindrical, spherical, etc
Skin over swelling – colour, ?shiny, ?dilated veins, scars
Margins – well/ill defined
Sorrounding skin
Deformity
Muscle wasting
PALPATIONS
Warmth
Tenderness?

380
Site – in relation to bone – epiphysis, metaphysic, diaphysis
Consistensy – Soft, cystic, firm, hard, variable
Shape, Size
Plane of swelling – skin, subcutaneous tissue, muscle or bone
Edges – ill defined, well defined
Mobility
Pulsations
Fluctuation
Ulcer if present
Abnormal mobility (pathological #)
OTHERS
Auscultation for bruit
Movements of adjacent joints
Regional lymphadenopathy
Distal neurovascular status
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BRACHIAL PLEXUS INJURIES

Attitude of limb

To identify involved roots or trunks

Examine muscles supplied by a particular myotome
Myotome Muscles
C5 Deltoid
C6 Biceps
Wrist extensors (ECRL, ECRB)
C7 Triceps
Wrist flexors (FCR)
Finger extensors (EPL, ED)
C8 Long digital flexors (FDP, FPL)
T1 Finger abductors and adductors (Interossei)
Test sensations according to dermatomes
Dermatome Sensory area
C4 Lateral neck
C5 Area over middle deltoid
C6 Dorsum of 1st web space and thumb
C7 Middle finger
C8 Little finger and ulnar side of hand
T1 Medial aspect of elbow
T2 Medial upper arm and adjacent chest

To know whether it is pre or post- ganglionic look for

Power of serratus anterior, levator scapulae and rhomboids
Horner’s syndrome
Long tract signs

To plan treatment
Check for passive ROM of all joints to rule out contractures
Test power of muscles usually used for tendon transfers-

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 Trapezius
Latissimus dorsi
Pectoralis major
Sternocleidomastoid
Triceps
Flexor- pronator mass
Supraspinatus, infraspinatus, subscapularis
Wrist extensors, extensor indicis, extensor digiti minimi

SPINE

Expected cases-
Trauma
Tuberculosis
Scoliosis
Spinal dysraphism
Disc prolapse
Ankylsing spondylitis

Inspection
Curvature – scoliosis, kyphosis (gibbus)
Obvious swelling/ deformity (search for cold abscess)
Scars/ sinuses
Cutaneous markers of spinal dysraphism

Palpation
Tenderness (C7 – vertebra prominens, D3- medial end of spine of scapula, D7- inferior
angle of scapula, L4 L5 – highest point of iliac crest)
Paraspinal muscle spasm ( consistency of muscles, whether able to pinch up muscle)
Cold abscess

Movements if not contra-indicated

Coin test
Schober’s test

Neurological examination of upper and lower limbs

Bulk of muscles, tone, power, reflexes including clonus, sensations, bowel/bladder

Special tests
Cervical rib – Adson’s test
Cervical myelpathy- Hoffman’s sign, Lhermitte’s sign, inverted radial reflex, look for
myelpathy hand
Lumbar disc prolapse- SLR, Lassegue, look for involvement of L5 and S1 nerve roots
and cauda equina syndrome (perianal sensations, anal contractions)
Ankylosing spondylitis- chest expansion, Schober’s test, special tests for SI joints
(Gaenslen, Gillie), wall test
Scoliosis – curve correction with lateral flexion, bending forward, plumbline, ribhump

HIP

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Expected cases
DDH Ankylosing spondylitis
Perthes’ Osteoarthrosis
SCFI Coxa vara
TB Nonunion # neck of femur
AVN Malunited intertrochanteric #
Rheumatoid arthritis Neglected traumatic dislocation

HISTORY
Name
Age/Sex
Occupation
Complaints – duration

Pain- duration, site, radiation, character, severity, aggrevating factors, relieving

factors,
remissions and exacerbations, rest pain, night cries, is it affecting ADL
Limp – duration, painless/ful

h/o trauma – mode of injury, was he able to stand or walk after injury, treatment
taken –
? indigenous
h/o fever, chronic cough, hemoptysis, loss of weight/appetite, night sweats, evening
rise of temperature, exertional dyspnoea
h/o other joint pains, early morning stiffness
h/o bleeding diathesis
h/o low back ache, stiffness, dyspnoea

Activities of daily living- how affected

Standing, walking, climbing stairs, squatting, sitting crosslegged, toilet activities,
occupation

Family history eg. RA

Alcoholic, smoker
?Steroid intake
h/o contact with TB patients
Any previous surgeries
? Known DM/HT/asthmatic/APD

If patient is a child – Which child?, Delivery ?premature, mode of delivery, walking

Milestone

GENERAL EXAMINATION

Constitution
? Anemia
Temp.

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Abdomen - ?hepatosplenomegaly
RS- , CVS-
Lymphadenopathy
Child – height, weight (cf. expected height and weight), secondary sexual
characteristics ?
Hand, foot- swelling, deformity
Rheumatoid nodules

LOCAL EXAMINATION

Inspection
? Exagerrated lumbar lordosis
ASIS – levels
Attitude lower limb
Muscle wasting
Shortening (Perform Allis test/Galleazi sign)
Any swelling, masses
Scars, sinuses
Gluteal folds, creases
Greater trochanter

Palpation
Exagerrated lumbar lordosis
ASIS levels
Warmth
Tenderness base of Scarpa’s triangle
Vascular sign of Narath
Greater trochanter- smooth or irregular, ?broadened, ?tender, ?elevated
Any other masses – does it move with rotation of the limb

Movements
Fixed deformities- Thomas’ test, squaring pelvis
Movements- active and passive (cf. opposite hip)
Flexion – knee extended, knee flexed
Extension
Abduction (with hip flexed important in DDH)
Adduction
Internal rotation- hip flexed, hip neutral (look for differential rotation or sectoral
sign)
External rotation- hip flexed, hip neutral

Measurements
Apparent
True ( Bryant’s triangle)
Nelaton’s line
Schoemaker’s test
Morris bitrochanteric test
Muscle wasting

Special tests

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Axis deviation – should be done only if hip can be brought to neutral rotation in
extension
Telescopy test
Trendlenburg test
Gait
Rectal examination if central dislocation is suspected

Inguinal/iliac lymphadenopathy

Distal neurovascular deficit

Lumbosacral spine, opposite hip and ipsilateral knee

If bilateral hip pathology, look for

Rheumatoid arthritis – finger and toes deformity and stiffness
Ankylosing spondylitis- chest expansion, modified Schober’s test, sacro-iliac joints
(Genslen and Gillie tests), movements of cervical spine, wall test

POST POLIO RESIDUAL PARALYSIS LOWER LIMBS

HISTORY
Onset
Previous surgeries
Use of orthoses

EXAMINATION

Gait
Aided/unaided
quadriceps hand to knee gait, gluteus maximus gait, gluteus medius gait

Deformties and fixed contractures

Spine – scliosis
Pelvic obliquity
Hip- look for fixed deformities, telescopy and Trendlenburg test
Ober’s test for IT band contracture
Knee- FFD, recurvatum, valgus
Ankle – equinus, calcaneus
Subtalar joint – varus, valgus
Pes cavus / planus
Toe deformities and dorsal bunion

Surgical scars

Passive range of movements of all joints

Wasting of muscles

Hypotonia

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Power of muscles
Hip abductor, flexors, extensors
Knee flexors, extensors
Tibialis anterior, EHL, EDL
Gastrosoleus, tibialis posterior, FHL, FDL
Peroneus
Reflexes – knee, ankle, plantar

Measurements
Limb length discrepancy
Muscle wasting

Sensations
Bowel / bladder (to rule out other conditions)

CEREBRAL PALSY

HISTORY

Pre-natal history
Mother- drug intake, infections, irradiation, PIH (BP, swelling of feet), haemorrhage
Which child (other children- how are they?)
Mode of delivery- ? difficult labour
Whether premature
Whether cried immediately after birth
? Jaundice, convulsions
Any other treatment history
Difficulty in sucking, swallowing
Dribbling at the mouth
Baby feeling stiff or baby wriggling awkwardly

Developmental milestones – Motor, Social

(Social smile, head control, turning in bed, crawling, sitting, standing, walking with
support¸ walking without support, climbing stairs, uttering single words)

Mode of ambulation, mobility

ADL
Education, communication

EXAMINATION

Spinal balance – sitting control ? able to sit without support with straight spine (good
prognosis)

Fixed/ correctable deformities

Spine – scoliosis
Hip- Flexion, adduction, internal rotation (look for telescopy)
Knee- flexion
Ankle- equinus, calcaneus
Subtalar joint – varus, valgus

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Forefoot – abduction, adduction
Pes cavus, planus
Hallux valgus, claw toes

Tone

Special tests for muscle spasm (refer Campbell)

Tests for adductor and medial hamstring tightness and to differentiate between both
Tests for hamstring spasticity and contracture (popliteal angle)
Prone rectus test
Tests for gastrosoleus contracture and spasticity and to differentiate between both

Not necessary to measure range of movement of joints

Power of muscles – only in older children who are able to understand instructions
Most important is power of knee extensors

Observational gait analysis

Aided/ unaided
Must carefully observe the position of joints during all phases of gait and look for
paucity of movements of joints during gait
Eg. Knee flexion may be impeded during swing phase due to tight rectus femoris
Equinus gait, jump gait, crouch gait

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 SRIHER -DEPARTMENT OF ORTHOPAEDICS
Prof. P.V. Vijayaraghavan
Prof. P. Gopinath Menon
Dr. Kannan Karthik Kailash (Head of Department of Spine Surgery)
Prof. M. Mohan Kumar
Prof. D. Gokul Raj
Prof. R. Dorai Kumar
Prof. N. Jambu
Prof. Srinivasa Rajappa
Dr. J.K. Giriraj
Dr. U. Thiagarajan
Dr. B. Mohan Choudhary
Dr. Ganesan. G. Ram
Dr. S. Vignesh Jayabalan
Dr. L. Senthil
Dr. M. Mohammed Sameer
Dr. Sundar Surya Kumar
Dr. T. R. Ashok
Dr. G. Venkatesh Kumar
Dr. M. R. Thirunthaiyan
Dr. Pravin K Vanchi
Dr. B. Raghavendran
Dr. C. Sitsabesan
Dr. R. Muthu Manickam
Dr. G. Sudhir
Dr. P. Pradeep
Dr. K. R. Tarun Prashanth
Dr. S. Srijay Sashaank
Dr. Sanjay. A.K
Dr. Sundararaja. B
Dr. Dheepan Kumar
Dr. Raghav

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DEPARTMENT OF ARTHROSCOPY AND SPORTS MEDICINE
Prof. S. Arumugam
Dr. P. Suresh
Dr. Prakash Ayyadurai
Dr. K.A. Thiagarajan
Dr. V.J. Parthiban
Dr. Karthik Anand

Prof. P.V. Vijayaraghavan – Vice Chancellor, SRIHER

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