Essentials of Orthopaedics

PART – 1

(GENERAL ORTHOPAEDICS)

Dr. S A Mahmud & Dr. Santosh Batajoo

 TOPICS PAGE NO
DIAGNOSIS IN ORTHOPAEDICS 5-10
INFECTIONS: OSTEOMYELITIS 9-18
SUBACUTE OM 19-22
CHRONIC OM 26-40
OSTEOARTHRITIS: OA 80
OA of Hip 90
OA of Knee 94
RA 99
JIA 107
Gout 108
Psedogout 114
Anky. Spondylitis 116
AVN 129
AVN of HOF 129
SONK 145
AVN of Talus 148
Kienbock disease 150
Metabolic & Endocrine disease 152
Metabolic Bone Disease. 153
Genetic disorder 167
Genetics. 168
Skeletal dysplasia 171
BONE TUMORS 181
Bone tumor 182
Benign bone tumor 197
BENIGN BONE LESIONS
BENIGN BONE LESIONS 197
CYST & CYST LIKE LESION 206
IN BONE.
SIMPLE BONE CYST 210
FIBROUS DYSPLASIA 212
ABC. ANEURYSMAL BONE 215
CYST.
OSTEOID OSTEOMA & 218
OSTEOBLASTOMA
GCT Giant Cell Tumour. 223
Chondroblastoma. 236
Diaphyseal aclasis. 239
Multiple Exostosis.
Osteochondroma.
ENCHONDROMA 247
Primary malig. bone tumors 249
Osteosarcoma 250
Chondrosarcoma 266
Ewings sarcoma 270
NHL 279
Mul. myeloma 280
Chordoma 283
Adamantinoma 284
Metastatic bone tumor 285
METASTATIC BONE DISEASE 286
Glomus tumor 291
GCT Tendon sheath 293
Neuromuscular disorders 295
Poliomyelitis 297
Leprosy 302
Peri. neuropathy 308
HMSN 311
CP 313
Post cp equinus deformity 335
Peripheral nerve disorders 338
Nerve injury 339
BP Injury 369
OBPI 374
Median N injury 380
CTS 388
Unlar N Injury 400
Radial N injury 417
TOS 227
Cervical rib 434
Foot drop 442
Tarsal tunnel syndrome 447
Tendon injury 456
tendon injury 457
Extensor tendon injury 469
Flexor tendon injury 478
Flexor Zones in Thumb. 489
Tendoachilis Rupture. 491
Mallet Finger. Baseball Finger. 504
Orthopaedic operations 507
Torniquet 508
THROMBOPROPHYLAXIS 512
Fat embolism 512
Tenodesis 517
Arthrodesis 518
Amputation 532
Arthroplasty 547
THR 548
TKR 570
Essentials of Orthopaedics
PART – 1
(GENERAL ORTHOPAEDICS)

1
 Diagnosis in Orthopaedics.
Imagings
Q) ‘Rule of Two’ in X ray examination? APL-693
 Two views:
 Anteroposterior view,
 Lateral view.
 Two joints:
 Joints above & below the fracture must be included.
 Two limbs:
 In children, the appearance of immature epiphysis may confuse the diagnosis of fracture, so x-ray of
uninjured limb is needed for comparison.
 Two occasions:
 Some fractures are notoriously difficult to detect soon after injury, but another x-ray a week or two
week later may show the lesion, eg-stress ≠.
 Two injuries:
 Severe force often causes injuries at more than one level, eg- in case ≠ of calcaneum or femur it is
important to x-ray pelvis and spine.

Two joints: The first x-ray did not include the

elbow.
This was, in fact, a Monteggia fracture – the head
of the radius is dislocated;

Two films of the same tibia: the

fracture may be ‘invisible’ in one view
and perfectly plain in a view at right
angles to that.

Two occasions: A
fractured scaphoid may
not be obvious on the
day of injury, but
clearly seen 2 weeks
later. Two limbs: Sometimes the abnormality can be
appreciated only by comparision with the normal
side; in this case there is a fracture of the lateral
condyle on the left side

2
Q) What are the imagings in orthopaedics?
Imaging in Orthopaedics:

 Plain Radiograph:
 to detect ≠ or dislocation,
 to detect malignancy.

 Contrast Radiograph:
 Sinugraphy,
 Venography / Angiography,
 Myelography.

 Tomography / Computed tomography:

 CT scan,
 CT with 3D Recons.

 Magnetic Resonance Imaging:

 to detect PLID / PID,
 to detect meniscus or ligament tear,
 to diagnose O M,
 to determine presence and extension of malignancy.

 Ultrasonography:
 to detect cystic lesions,
 to diagnose Hip pathologies eg, DDH.
 UST.

 Fluroscopy / C arm:
 to assist in the reduction of ≠ / dislocation,

 DEXA / BMD test:

 T score and Z score to detect osteoporosis / osteopenia.

3
Q) What is MRI? What is the importance in T1 & T2 weighted image in MRI? Role of MRI in orthopaedic
surgery?
MRI:
- Magnetic Resonance Imaging is a modern diagnostic tool that uses magnetic field to create cross sectional
images based on movement of hydrogen atoms.

MRI is ideal for displaying soft-tissue injuries,

particularly tears of the menisci of the knee;
Importance of T1 & T2 weighted image:
 T1 weighted image:
 Images show solid structure and anatomy,
 Fat, Cancellous bone & Bone marrow show highest signal intensity {White}
 Cartilage, Muscle and Spinal canal show varing signal intensity {Grey},
 Fluid, Cortical bone, Ligament, Tendon, Air show lowest signal intensity {Black}
 T2 weighted image:
 Better imaging to detect the pathology,
 Fluid shows Highest signal intensity [ White ],
 Fat shows lowest signal intensity [Dark].
Role of MRI in orthopaedics:
 To detect AVN:
 Early diagnosis of bone ischaemia and necrosis,
 Progression of disease.
 Evaluation of joint:
 To detect any cartilage / ligament injury / meniscal injury,
 To detect any loose bodies,
 To diagnose rotator cuff tear / labrum injury in shoulder,
 To detect any osteochondral lesions.
 To detect spinal disorders:
 like PLID, Cervical PID, Spinal tumour etc.
 To detect Osteomyelitis:
 it can differentiate soft tissue infection and osteomyelitis,
 To detect presence & extension of malignancy:

4
Q) What are the roles of CT scan in orthopaedic surgery? APL-20
Roles of CT scan in orthopaedic surgery:
 To diagnose complex fracture:
 Vertebral body ≠,
 Tibial plateau ≠,
 Calcaneum ≠,
 Pelvis ≠.
 To detect intra articular fracture:
 To detect fracture dislocation,
 To assess tumour size and spread:
 CT guided FNAC: can be employed for guiding soft issue and bone biopsies,
 3D Recons CT: helps to design custom made prosthesis.

Plain x-ray shows a fracture of the vertebral body but one cannot tell precisely how the bone
fragments are displaced.
CT shows clearly that they are dangerously close to the cauda equine.

Plain x-ray shows a fracture of the calcaneum but the details are obscure.
CT sagittal views give a much clearer idea of the seriousness of this fracture.
Limitations:
 Poor soft-tissue contrast when compared with MRI.
 Relatively high radiation exposure to which the patient is subjected.

5
Q) What are the roles of USG in orthopaedic surgery?
Roles of USG in orthopaedic surgery:
 Diagnostic uses:
 For diagnosis of cystic lesions:
 Haematoma,
 Abscess,
 Popliteal cyst,
 Bursitis.
 To detect Synovial fluid effusion,
 To detect Rotator cuff tear,
 To detect DDH in new born babies,
 USG guided FNAC for biopsy.
 Therapeutic uses:
US therapy is used for-
 Scar softening:
 Depuytren’s contracture,
 Fascial scar.
 For palliation:
 Planter fascitis,
 CTS,
 Frozen shoulder.

Q) What are the roles of Radio isotopes in orthopaedic surgery?

Roles of radioisotopes in orthopaedic surgery:
-- Radio isotopes are used in ortho surgery for diagnostic purpose only, following isotopes are used-
 Technetium labelled 99m HDP (99mTc HDP):
 To diagnose Stress ≠ / undisplaced ≠,
 To detect small bone abscess,
 To detect osteoid osteoma,
 To detect aseptic loosening or infection around a prosthesis,
 To diagnose AVN of head of femur,
 To diagnose bony metastasis.
 Technetium labelled Sulphur Colloid (99mTc Sc):

6
  Better indicator of Marrow vascularity,
 Early diagnosis of Femoral head ischemia.
 Gallium 67 (67Ga):
 To detect the sites of hidden infection,
 Investigation of choice of prosthetic loosening after joint replacement,
 Indium 111 labelled Leucocytes (111In):
 Used as a marker of infection.

7
INFECTIONS.

8
 Osteomyelitis.
Camp-725, Apl- 33

Q) Define osteomyelitis? Classify osteomyelitis?

Osteomyelitis:
--- It is defined as inflammation of bone caused by an infecting organism.
camp-725

Classification of osteomyelitis:
a) According to Duration:
 Acute (< 2 wks),
 Sub acute (2 – 3 wks),
 Chronic (>3 wks).
b) According to Route of infection:
 Exogenous: Traumatic,
 Endogenous: Haematogenous / Bacteraemia.
c) According to Host response:
 Pyogenic,
 Non pyogenic.

Q) What are the risk factors of osteomyelitis?

Risk factors / Predisposing factors of osteomyelitis:
 Open fracture,
 Deep punctured wound,
 Iatrogenic injury / Surgery,
 Immuno suppressive conditions:
 Chemotherapy,
 Haemodyalysis,
 Steroid therapy,
 Poorly control DM.
 Malnutrition.
 Diseases impair blood circulation can predispose to OM:
 DM,
 PVD,
 Sickle cell disease.
 Intravenous drug abuser,
 Catheter or I/V line induced infection.

9
Q) What are the complications of acute osteomyelitis?
Complications:
a) Local complications:
 Chronic osteomyelitis,
 Sinus formation,
 Epiphyseal damage,
 Altered bone growth,
 Suppurative arthritis of nearby joint,
 Pathological fracture.
b) Systemic complications:
 Septicaemia,
 Metastatic infections to other site eg. lungs, liver, brain, bone etc.
Q) What are the organisms responsible for acute osteomyelitis?
- Organisms responsible for acute osteomyelitis:
 Neonate:
 E coli,
 Strep ß haemolyticus.

 Child < 4 years:

 E coli,
 Haemophylus influenzae,
 Psedomonus,
 Proteus.
 Older children:
 E coli,
 Pseudomonus,
 Proteus,
 Strep ß haemolyticus.

 Staphylococcus aureus.
 Heroin addict or HIV positive patient:
 Psedomonus,
 Proteus.
 Sickle cell disease:
 Salmonella.
 Chronic ill health taking I/V fluid for nutrition:

10
  Fungal infection.

Osteomyelitis of tibia in sickle cell patient.

Q) Evaluation of Acute Hematogenous Osteomyelitis:

■ History and physical examination
■ Laboratory tests: white blood cell count, erythrocyte sedimentation rate, C-reactive protein
■ Plain radiographs
■ Technetium-99m bone scan ± MRI
■ Aspiration for suspected abscess

Q) What are the pathological stages of acute osteomyelitis?

Pathological stages of acute OM: IS NeR
1. Inflammation {0 – 48 hours},
2. Suppuration {48 – 72 hours} – causes ed intraosseous pressure.
st
3. Necrosis {End of 1 week} – due to vascular stasis, infective thrombi, periosteal stripping.
4. New bone formation {End of 2nd week},
5. Resolution and healing {Reactive bone formation}.

11
Q) Describe the pathogenesis of acute and chronic osteomyelitis?

Septic focus
(Minor skin abrasion or boil or septic tooth or from urethral catheter or dirty needle prick)

Spread through blood / Bacteremia

Settle of bacteria in Metaphysis

Suppuration due to multiplication of bacteria in Metaphysis

(Metaphysial abscess)

Spread of Metaphysial abscess:

 Externally: through Volkmann canal {horizontal canal} to subperiosteal space,
 Along : in to the Medullary cavity,
 In to the joint: if metaphysic is intra-articular.

Sub periosteal abscess

(Acute Osteomyelitis)

Strangulation of blood vessels in Medullary cavity and periosteum due to:

 Stretching of vessels due to oedema,
 Thrombosis of arteries due to inflammatory process,
 Toxic destruction of blood capillaries.
↓
Sequestrum formation due to underlying bone becomes necrosed,
↓
Sinus formation
↓
Subperiosteal new bone formation enclosing Sequestrum (Involucrum)

12
Q) What are the clinical features of acute osteomyelitis?
Clinical features of acute OM:
A) In case of infant:
 Fails to thrive,
 Drowsy and irritable,
 Metaphyseal tenderness,
 Fever,
 Restricted movement of limb / joint.

B) In case of children:
 Pain over the affected part,
 Malaise and fever,
 Recent H/O infection: septic toe, boil, sore throat, discharge from ear etc.
 Age distribution – in children affecting younger than age 2 years and children aged 8 to 12 years.
 Hip joint is the most commonly affected in young patients;

CARDINAL FEATURES OF ACUTE

C) In case of adult:
OSTEOMYELITIS IN CHILDREN
 H/O open ≠ ,
 Pain
 H/O operation of bone,  Fever
 Refusal to bear weight
 Haematogenous infection form distant site.  Elevated white cell count
 Elevated ESR
 Elevated CRP

 Osteomyelitis is in unusual site / caused by unusual organism; found in:

 Heroin addict,
 Sickle cell disease,
 Deficient host defense mechanism / HIV infection.

13
Q) Why osteomyelitis is more commonly involve joint in infant and adult than older children?

--- In children of < 2 years and in adult, acute O M can spread to nearby joint, but in cases of older children –
infection can not be spread to joint because:
 In children < 2 yrs of age, there is common blood supply for metaphysis and epiphysis
which cross the growth plate. So infection may cross from metaphysic to epiphysis and eventually into the nearby
joint.
 In adult, there is no growth plate. So infection may spread directly from metaphysis to
epiphysis and involve the joint.
 In Older children, there is no common circulation like < 2 yrs old children and there is
also presence of growth plate. So infection can not spread to epiphysis and joint usually not involve.

When under pressure, exudate or abscess can extend through Volkmann canals into subperiosteal region and from there into medullary cavity or epiphysis.

Abscess enlarges, intramedullary pressure increases causing cortical ischemia, which may allow purulent material to escape
through the cortex into the subperiosteal space. A subperiosteal abscess then develops.
Q) Why infection is more common in Metaphyseal region in children?
Causes are-
 Metaphyseal region is highly vascular,
 Non anastomoting blood vessels are arranged in hair pin manner,
 Relative vascular stasis favors bacterial colonization,
 Infected emboli are trapped here in small caliber end arteries.
 Relative lack of phagocytic activity in metaphyseal area.

14
Q) Investigations for Osteomyelitis? APL-33

a) Imaging:
 Plain X ray:

Acute osteomyelitis
The first x-ray, 2 days after symptoms began, is normal – it always is;
 Metaphyseal mottling and periosteal changes were not obvious until the second film, taken 14 days later;
 Eventually much of the shaft was involved.
 1st week: X ray shows no abnormality,
nd
 2 week: X ray shows faint extra cortical outline due to periosteal new bone formation
{classic sign of early pyogenic OM},
 Later: periosteal thickening becomes more obvious and there is patchy rarefaction of the
metaphysis.

Causes of visible periosteum:

 ≠ callus
 Myositiis ossificans,
 Scarvey,
 Chr. OM,
 Syphilitic periostitis,
 Deposition of tumour materials eg Codman triangle.

camp-728

15
  USG:
 May detect sub periosteal collection of fluid in early stage of O M but can not distinguish
‘is it pus and haematoma?’
 Radio nuclide scanning:
 Scanning with 99mTc-HDP reveals highly sensitive investigation even in very early stage, but
it has relatively low specificity because of other inflammatory lesions can show similar
changes,
 In doubtful cases: scanning with 67Ga-citrate or 111In labeled leucocytes.
 MRI:
 Extremely sensitive in early phase of O M and differentiate between soft tissue infection
and osteomyelitis.
 It is helpful in case of doubtful diagnosis (bone marrow inflammation) and particularly in
cases of suspected infection in axial skeleton.

b) Blood tests:
 CRP: usually elevated within 12 – 24 hours after onset, check every 2 – 3 days after antibiotic
therapy.
 ESR: usually elevated after 24 – 48 hours of onset.
 WBC Count: often is normal or raised,

 In very young and very old people: these tests are less reliable.
 Hb conc: diminished,

 Anti Staphylococcal antibody: may be raised in atypical cases where diagnosis is in doubt.

c) Blood culture:
 Causative organism can be identified in approximately 50% of patients through blood cultures.
 Bone aspiration usually gives an accurate bacteriological diagnosis and should be performed with 16 or 18
gauge needle in the area of maximal swelling.

16
Q) What are the principles of treatment of acute O M? APL-30,34

Principles of treatment of acute O M:

1. Provide analgesia and general supportive measures,
2. Rest of the affected part,
3. Identify the infective organism and administer effective antibiotic chemotherapy,
4. Drain pus as soon as it is detected,
5. Stabilize the bone if it is fractured,
6. Eradicate avascular and necrotic tissue,
7. Restore the continuity - if there is a gap in the bone,
8. Maintain soft tissue and skin coverage.
 Provide analgesia and General supportive measures:
 Analgesia should be given,
 Consider I/V fluid – as septicaemia and fever can cause severe dehydration.
 Rest of the affected part / splintage:
 To prevent pathological fracture,
 To prevent joint contracture,
 To prevent joint subluxation / dislocation,
 Partly for comfort and rest.
 Identify infecting organism and administer effective antibiotic therapy / Chemotherapy:
 If OM is suspected on clinical ground, aspirate pus / fluid from metaphyseal sub periosteal abscess
and then send it for microbiological examination and sensitivity to antibiotic. Treatment should be started without
waiting for the result of investigation.
 Give antibiotic intravenously until patient’s condition begins to improve and CRP value returns to
normal level, which usually takes 2 to 4 weeks.
 By these times, most appropriate antibiotic should be prescribed on the basis of sensitivity test and
that antibiotic should be administered orally for another 3 to 6 weeks.
 While patient is on oral antibiotic, it is important to check MIC level of antibiotic, CRP, ESR and
WBC count at regular interval and treatment can be discontinued when these tests result seen to be normal.
--- I/V antibiotics : 2 – 4 weeks, then
--- Oral antibiotics : another 3 – 6 weeks.
 Choice of antibiotic:
--- It is based on Highest bactericidal activity, Least toxicity and Lowest cost.
 Duration of antibiotic:
--- Duration of antibiotic therapy is controversial, current trend is toward a shorter course of IV antibiotics
followed by oral antibiotics and monitoring of serum antibiotic levels.

 Drainage of pus as soon as, if it is detected:

17
  If antibiotics are given in early stage within first 48 hours after onset of symptoms – drainage is
often unnecessary,
 If clinical features do not improve within 36 hours of starting treatment or if there is signs of deep
pus {Swelling, Oedema & Fluctuation} or if pus is aspirated - abscess should be drained under GA,
 If pus is found and released – there is little to be gained by drilling into the medullary cavity.
 If there is no obvious abscess – it is reasonable to drill a few holes into the bone in various directions.

 Two main indications for surgery in acute hematogenous osteomyelitis:

 Presence of an abscess requiring drainage,
 Failure of the patient to improve despite appropriate IV antibiotic
treatment.

 Stabilize the bone if it is fractured:

 Eradicate avascular and necrotic tissue:

 Restore the continuity – it there is gap in the bone:

 Maintain soft tissue and skin coverage:

Q) Differential diagnosis of acute OM?

DD of Acute OM:
 Cellulitis,
 Acute suppurative arthritis,
 Streptococcal necrotizing myositis by Group A ß haemolytic streptococci,

 Ewing sarcoma,
 Osteosarcoma,
 Acute rheumatism,
 Sickle cell crisis,
 Gaucher’s disease / Pseudo osteitis.

18
 Subacute Osteomyelitis
Subacute Hematogenous Osteomyelitis.
Camp-730, Apl-32
Q) Radiographic classification of subacute hematogenous osteomyelitis?
GLEDHILL CLASSIFICATION
type 1: Central metaphyseal lesion;

type 2: Eccentric metaphyseal lesion with

cortical erosion;

type 3: Diaphyseal cortical lesion

19
type 4: Diaphyseal lesion with periosteal new
bone formation, but without definite bony lesion;

type 5: Primary subacute epiphyseal

osteomyelitis;

type 6: Subacute osteomyelitis crossing physis

to involve metaphysis and epiphysis.

20
Q) Short note: Brodie’s abscess APL-32

Subacute osteomyelitis
The classic Brodie’s abscess looks like –
 A lytic lesion in metaphysis / metaphyseal epiphyseal area with a rim of sclerotic bone,
 A small walled-off cavity in the bone with little or no periosteal reaction;
 Sometimes rarefaction is more diffuse and
 There may be cortical erosion and periosteal reaction.
Brodie’s abscess:
-- It is a localized form of sub acute osteomyelitis caused by less virulent pyogenic organisms.
Site:
 Usually in the metaphyseal area usually before physeal closure and
 In adult in metaphyseal – epiphyseal area is involved, eg-
 Upper end of tibia,
 Calcaneum,
 Lower end of femur,
 Lower end of humerus.
Causative organisms:
-- Less virulent pyogenic organisms, eg -
 Staphylococcus aureus (50%), Culture report
 Staphylococcus albus,
 20% cases culture report: negative.
Clinical features:
 Patient is usually young adult,
 Intermittent pain at the end of affected long bone for several weeks or months,
 Slight swelling may present,
 May have effusion of adjacent joint,

21
  Temp is usually normal,
 Local tenderness of affected part,
 May have muscle wasting.
Differential diagnosis:
 Osteoid osteoma,
 Non ossifying fibroma,
 Malignant bone tumour.
Investigations:
 CBC: TC – usually normal, ESR - ed.

Brodie abscess in right distal tibial epiphysis of 3-year-old child.

 X ray of the affected part:

 a small walled-off cavity in the bone with little or no periosteal reaction,
 Circumscribed Round or Oval radiolucent area usually in metaphysis,
 Surrounded by halo of sclerotic bone,
 Usually no sequestrum is present.
 Radio isotope scan: ed activity,
 Biopsy: curettage material,
 Pus for C/S:
Treatment:
 Conservative:
 Antibiotic therapy for about 6 weeks,
 Immobilization,
 Follow up.
 Surgery:
 If no sign of healing or improvement after conservative treatment,
 Curettage and if needed fill the gap with bone graft followed by antibiotic.

22
 Chronic osteomyelitis.
Camp-731

Sequestrum of chronic osteomyelitis in tibia

Q) What is chronic osteomyelitis?

Chronic osteomyelitis:
--- It is the infection of bone and marrow which becomes chronic and usually presents with discharging
sinus.
Q) Hallmark of chronic osteomyelitis?
--- ‘Infected dead bone within a compromised soft tissue envelope.’
Q) What are the causes of chronic OM?
Causes of chronic OM:
 Usually Sequel of acute OM: when organism is virulent and host resistance is lower,

 Chronic OM of insidious onset: when organism is less virulent and host resistance is good. Example:
 Chronic non suppurative OM / GARRÉ’S SCLEROSING OSTEOMYELITIS

 Chronic O M caused by Specific organisms:

 TB osteomyelitis,
 Syphilictic OM,
 Stphylococcus epidermidis – in presence of implant,
 Mixed infection by Staph, aureus, E coli, Strep pyogens, Proteus and Pseudomonus.

23
Q) Why recurrence occurs in chronic osteomyelitis?
--- Due to presence of -
 One or more foci of infection within the bone may contain purulent material,
 Infected granulation tissue,
 Presence of sequestrum.
Q) What are the predisposing factors of chronic osteomyelitis?
Predisposing factors of chronic OM:
 Local trauma:
 Open ≠ ,
 Operation to bone,
 Orthopaedic operation where implant used.
 Patient factors:
 Age: extreme of age,
 Diabetic patient,
 Patient with PVD,
 Malnutrition,
 Patient with immune deficiency.
 Virulent organisms:
 Virulent organisms are covered by Protein Poly saccharide Slime (Glycocalyx) that protect from
both host defence and antibiotics, which have the ability to adhere to inert surfaces such as bone sequestrum and
metal implants where they multiply and colonize the area.

Q) What are the surest signs of chronic OM?

 Sprouting granulation tissue at the sinus opening,
 Bone specules comes through sinus tract,
 X ray shows presence of Sequestrum.

24
Q) What is Sequestrum? How it is formed?
Q) Pathogenesis of Chronic osteomyelitis?

Sequestrum:
--- It is a dead piece of bone formed within a living bone by pathological process.

Time required for formation of sequestrum: average 3 months.

Process of formation of sequestrum:

Following Acute O M
↓
Suppuration / Abscess formation
↓
Spread of abscess:
 Externally: via ‘Volkman canal’ giving rise to subperiosteal abscess,
 Along: through medullary cavity.
↓
 Impairment of blood supply of underlying bone,
 Necrosis of bone and dead bone formation due to:
 Stretching of subperiosteal blood vessels
 Toxic thrombosis and destruction of vessels in medullary canal.
↓
Sequestrum formation.

25
Q) What are the features of Sequestrum?

Features of Sequestrum: Normal: pinkish white.

1) Colour: dead white / devoid of periosteum,

2) Surface:
 Inner – Rough: pitted, irregular and moth eaten appearance by granulation tissue,
 Outer – Smooth: smooth and polished due to pressure of pus under periosteum.
3) No bleeding: if it is cut through,
4) On probing: it emits metallic sensation,
5) Sprouting granulation tissue: at the sinus opening,
6) Types of Sequestrum:
 Coraliform: in chronic osteomyelitis,
 Ivory: in syphilis, cortical  feathery,
 Feathery / Sandy: tubercular osteomyelitis
 Black: actinomycosis cancellous  sandy.
 Ring: pin tract infection, amputation stump.
 Tubular: in long bone / diaphyseal sequestrum.
 Lamellar: in flat bone.

26
Q) Why sequestrum is separated?
o Due to loss of blood circulation,
o Detached from living bone.

Q) Why sequestrum is more common in children of > 2 yrs than < 2 yrs of age?
Causes are-
 In children < 2 yrs of age - metaphyseal cortex is thin through which abscess breaks and forms
subperiosteal abscess. So diaphysis is rarely involved and endosteal blood supply of bone is not endangered. Thus
extensive sequestrum does not occur.
 In children > 2 yrs – metaphyseal cortex is thicker. So metaphyseal abscess extends into diaphysis which
jeopardize endosteal blood supply of bone. Periosteum is also thick which leads to large subperiosteal abscess
formation. As a result extensive sequestrum is formed in > 2 yrs old children with chronic OM.

Q) What are the clinical features of chronic osteomyelitis?

Clinical features:
 H/O Acute osteomyelitis,
 Recurrence of pain, pyrexia, tenderness and discharging sinus on the affected area,
 Redness, seropurulent discharge and excoriation of surrounding skin.
 Tissue around the sinus becomes thickened and often puckered.

27
 Anatomical classification of Adult Chronic Osteomyelitis. camp-732

Type I: Intramedullary osteomyelitis; nidus is endosteal

Type II: Superficial osteomyelitis; limited to bone surface

Type III:
Localized osteomyelitis, full thickness of cortex is involved

Type IV: Diffuse osteomyelitis; entire circumference of the

bone is involved.

 Staging for Adult Chronic Osteomyelitis: camp-732

Cierny and Mader Staging System

LESION TYPE / Anatomical STAGE: HOST CATEGORY / Physiological TYPE:
Stage 1: Medullary Type A: Normal
Stage 2: Superficial Type B: Compromised by local or systemic conditions
Stage 3: Localized Type C: Severely compromised by local and systemic conditions
Stage 4: Diffuse

28
Q) Investigations for chronic osteomyelitis?
a) Imaging:
 X ray:

 Mixed osteolytic and osteosclerotic lesion in ----- part of bone,

 Thickening and sclerosis of cortex,
 Frank excavation around an implant,
 Presence of bright chalky piece of bone in the lesion – sequestrum,
 Soft tissue swelling around the lesion.
 Sinugraphy:

Radiographs made in two planes after injection of radiopaque liquid into sinus often are helpful in locating focus of infection in chronic osteomyelitis.

 Sinugraphy can be performed if a sinus track is present and can be a valuable adjunct to surgical
planning,

29
  Radio isotope scintigraphy:
 99m
Tc-HDP: shows increased activity,
 Ga or 111In leveled leucocytes: more specific for osteomyelitis / hidden foci of infection.
67

 CT / MRI:
 Shows extend of bone destruction, reactive oedema, hidden abscess and sequestra.
 CT – it provides excellent definition of cortical bone, especially useful in identifying sequestra.
 MRI – in chronic osteomyelitis well defined rim of high signal intensity surrounding the focus of
active disease {Rim sign},
b) Blood tests:
 WBC count: ed in only 35%,
 ESR: ed,
 CRP: ed.
c) Pus for C/S: 20% cases negative result,
d) PCR & Gel electrophoresis:

‘Gold standard’ CAMP-733

 The “ gold standard ” is to obtain a biopsy specimen for histological and

microbiological evaluation of the infected bone.

 The “ gold standard ” in the diagnosis of osteomyelitis is a biopsy with

culture and sensitivity. A biopsy is not only useful in establishing a
diagnosis, but also is helpful in determining the proper antibiotic regimen.

30
Q) Treatment of chronic osteomyelitis? APL-40, camp- 734

 Treatment of chronic osteomyelitis requires multifaceted approach.

 Antibiotic:
 Antibiotics are administered for 4–6 weeks (starting from the beginning of treatment or the last
debridement) before considering operative treatment.
 The duration of postoperative antibiotics is controversial. Traditionally, a 6-week course of intravenous
antibiotics is prescribed after surgical debridement of chronic osteomyelitis.
 Fluoroquinolone antibiotics are known to have equivalent serum concentrations whether given orally or
intravenously. When deemed appropriate, based on culture sensitivities, oral administration is preferred. Our
practice is to place the patient on 6 weeks of antibiotics, typically given intravenously,
 Fusidic acid, clindamycin and the cephalosporins are good examples. Vancomycin and teicoplanin are
effective in most cases of meticillin-resistant Staphylococcus aureus infection (MRSA).

Q) Why antibiotics are given in chronic osteomyelitis?

 To suppress the infection,
 To prevents the spread of infection to healthy bone,
 To control acute flare / recurrence.

 Local treatment:
 Dressing the wound,
 Colostomy paste to prevent skin excoriation,
 Acute abscess may need urgent incision and drainage.

Affected bone is exposed and sequestrum is removed infected matter is removed.

31
  Debridement of wound:
 Sinus tracks can be injected with methylene blue 24 hours before surgery to make them easier to locate and
excise, camp-734

 All infected soft tissues, dead or devitalized bone & infected implant must be removed,
 Débride necrotic or ischemic bone until the “Paprika Sign” (active punctuate bleeding bone) is achieved,
indicating healthy tissue. Tissue obtained at surgical débridement should be sent for culture and pathology studies.
camp-735

 Sequestrectomy: removal of dead piece of bone.

 Curettage: scraping / scooping means pick up & move,
 Saucerization: excavation / saucer to fascilate drainage.
 Antibiotic covering is continued for at least 4 weeks after last debridement,
 Duration of postoperative antibiotics is controversial. Traditionally, a 6-week course of intravenous antibiotics is
prescribed after surgical debridement of chronic osteomyelitis. camp-734

 Elimination of dead space:

 Porous antibiotic- impregnated beads can be laid in the cavity and left for 2 or 3 weeks and then
replaced with cancellous bone grafts.
 Papineau technique the entire cavity is packed with small cancellous chips (preferably autogenous)
mixed with an antibiotic and a fibrin sealant.
 Where possible, the area is covered by adjacent muscle and the skin wound is sutured without tension.
An alternative approach is to employ a muscle flap transfer: in suitable sites a large wad of muscle, with its blood
supply intact, can be mobilized and laid into the cavity; the surface is later covered with a split-skin graft.
 In areas with too little adjacent muscle (e.g. the distal part of the leg), the same objective can be
achieved by transferring a myocutaneous island flap on a long vascular pedicle.
 A free vascularized bone graft is considered to be a better option, provided the site is suitable and the
appropriate facilities for microvascular surgery are available.

32
  Lautenbach drainage system / Closed suction drain: This involves radical excision of all avascular and
infected tissue followed by closed irrigation and suction drainage of the bed using double-lumen tubes and an
appropriate antibiotic solution in high concentration (based on microbiological tests for bacterial sensitivity). The
‘dead space’ is gradually filled by vascular granulation tissue. The tubes are removed when cultures remain
negative in three consecutive fluid samples and the cavity is obliterated.
 In refractory cases it may be possible to excise the infected and/or devitalized segment of bone
completely and then close the gap by the Ilizarov method of ‘transporting’ a viable segment from the remaining
diaphysis. This is especially useful if infection is associated with an ununited fracture.

Methods to eliminate dead space are: camp-735

(1) Bone grafting with primary or secondary closure;
(2) Use of antibiotic PMMA beads as a temporary filler of the dead space before
reconstruction;
(3) Local muscle flaps and skin grafting with or without bone grafting;
(4) Microvascular transfer of muscle, myocutaneous, osseous, and osteocutaneous
flaps;
(5) Use of bone transport (Ilizarov technique).

 Soft tissue cover:

 Small defect: by split thickness skin graft,
 Large defect: by local musculocutaneous flap or free vascularized flap.

 After care:
 Follow up,
 Local trauma must be avoided,
 Recurrence of symptoms should be taken seriously.

Aims of treatment:
 Surgery for chronic osteomyelitis consists of sequestrectomy and resection of
scarred and infected bone and soft tissue.
 Inadequate debridement may be one reason for a high recurrence rate in chronic
osteomyelitis.

33
Q) Short note: Papineau technique. camp-735

--- Papineau et al. described an open bone grafting technique for the treatment of chronic osteomyelitis.

Aims of technique:
This procedure relies on the formation of healthy granulation tissue in a bed of bone graft that will become rapidly
vascularized. The granulation tissue resists infection and is allowed to adequately drain.

Indication:
 This technique is useful when free flaps or soft tissue transfer options are limited because of
anatomic location or in patients who smoke or are medically compromised.
 Modification of Papineau technique using a vaccum assisted closure and quite useful for
decreasing edema and for closure of soft tissue dead space.

Stages of Papineau technique:

Operation is divided into three stages and usually requires several surgeries:
(1) Débridement and stabilization,
(2) Cancellous autografting, and
(3) Skin closure.

STAGE I: DÉBRIDEMENT AND STABILIZATION

■ Thoroughly débride all sequestra and necrotic bone to healthy and viable soft tissue and bone; thoroughly
irrigate the débrided area.
■ Stabilize the bone with an external fixator or intramedullary nail if needed.

STAGE II: GRAFTING

■ Harvest cancellous bone graft from the iliac crest or proximal tibia.
■ Pack the graft in the bony defect, filling to the subcutaneous level.
■ If indicated, use local muscle pedicle grafts to enhance the blood supply to the grafts, and leave the overlying
skin and subcutaneous tissue open.

STAGE III: WOUND COVERAGE

■ Apply skin grafts or allow the wound to heal by spontaneous epithelialization.

34
 Camp-734

35
Q) Short note: GARRÉ’S SCLEROSING OSTEOMYELITIS APL-41,camp735

Garre’s sclerosing osteomyelitis:

--- It is a form of ‘Chronic Non Suppurative Osteomyelitis’ which is characterized by marked sclerosis
and cortical thickening.
--- Sclerosing osteomyelitis is a chronic form of disease in which the bone is thickened and distended

but abscesses and sequestra are absent.

Site:
 Diffuse enlargement of bone usually at diaphysis of tubular bone or mandible,
 There is usually no abscess.
Cause:
 Cause is unknown,
 Thought to be an infection caused by a low grade, possibly anaerobic bacterium.
Clinical features:
 Patient is typically children / adolescent or young adult,
 Intermittent pain of moderate intensity and usually long duration,
 Long H/O aching and slight swelling & tenderness over the affected bone,
 Recurrent attack of acute pain accompanied by malaise and slight fever.

Sclerosing osteomyelitis of tibia documented by biopsy.

Investigations:
a) X ray of affected part:
 ed bone density and cortical thickening,
 Marrow cavity may be completely obliterated,

36
  There is no abscess cavity / sequestrum.
b) Blood test:
 ESR: usually elevated,
c) Biopsy:
 Low grade inflammatory lesion with reactive bone formation.
 Non specific osteomyelitis and culture usually negative.

Differential diagnosis:
 Osteoid osteoma,
 Ewing’s sarcoma.
 Paget disease.

Treatment:
 Treatment is by operation,
 Abnormal area is excised and exposed surface is thoroughly curetted,
 Bone graft, bone transport or free bone transport may be needed.

Q) Complications of chronic osteomyelitis?

 Bone shortening / lengthening,
 Muscle wasting,
 Pathological fracture,
 Joint stiffness,
 Amyloidosis,
 Epithelioma.

Q) What are the indications of amputation in chronic osteomyelitis?

Indications of amputation in Chronic OM:
 Epithelioma from sinus tract {Squamous cell carcinoma, Fibrosarcoma} 0.2 – 1.6%
 Arterial insufficiency,
 Major nerve palsy,
 Stiffness / joint contracture.

37
 Post Traumatic Osteomyelitis
apl / 8 – 34

-------- Open # is always contaminated and thereby prone to infection.

Causative organisms:
 Staph aureus,
 E coli,
 Proteus,
 Pseudomonus
 Ocasionally anerobic organisms.
Clinical features:
 H/O Open fracture,
 Pain and swelling of affected site,
 Patient become feverish,
 Wound inflamed and seropurulent discharge.
Investigations:
 CBC with ESR,
 CRP,
 RBS,
 Wound swab for C/S.
 X ray of the affected part.
Treatment:
 Cleansing and debridement of wound,
 Leaving the wound open > provision of free drainage,
 Antibiotics:
 Broad spectrum antibiotics,
 Metronidazole for 4 – 5 days,
 Immobilization:
 If stable # then plster slab,
 If unstable then Ex-fix can be given.

38
 Post Operative Osteomyelitis.
apl / 8 – 35

Incidence of infection: 0.2 – 10%

Predisposing factors favor bacterial invasion:
 Extensive soft tissue injury,
 Haematoma formation,
 Bone death,
 Operation of open #,
 Use of foreign implant.
Types (accor. to occurance):
a) Early post operative infection {within 1 month},
b) Intermediate post operative infection {1 month to 1 year},
c) Late post opearative infection {several yrs after opn}
Treatment:
Infection following internal fixation Infection following joint replacement
Broad spec. antibiotic I/V large dose,  Broad spec. antibiotic I/V large dose,
If abscess is formed → it should be drained.  If abscess is formed → it should be drained.
Wound should be left open  If prosthesis is secure and patient have no pain →
long term antibiotics + activity modification
If not heal → meticulous wound debridement,  If prosthesis becomes loose and patient’s general
fixation implant should be retained untit # has united. condition is good → remove prosthesis & cement and
revision arthroplasty.
Loose or ineffectual implant should be removed.  If prosthesis becomes loose and patient’s general
condition is not good → remove prosthesis &
arthrodesis.
After removal of implant if # is unstable then Exfix
shoud be applied.
Regular dressing and long term antibiotic therapy.

39
 Tuberculosis.

Q) Define Tuberculosis?
------ It is a chronic granulomatous infection caused by Mycobacterium Tuberculosis.
Q) Mycobacterium tuberculosis?
 Human type,
 AFB,
 Grows slowly,
 Doubling time – 20 hrs in favorable condition,
 Organisms in droplet during coughing, sneezing, talking then inhaled and reach into alveoli.
Q) Atypical Mycobacterium?
 Affects very rarely,
 Usually in patient of diabetes,
 Immunosuppression for organ transplantation,
 HIV infected patient.
Q) Why atypical mycobacterium is called atypical?
 Rapid growth,
 Pigment production,
 Resistant to anti-TB drugs.
Q) What are the predisposing factors of TB?
 Constitutional: inadequate diet, fatigue, poor sanitation.
 Race: dark skinned people,
 Age:
 Infant < 2 yrs: poor tolerance to infection,
 2 – 15 yrs: infection is usually less severe,
 > 15 yrs: infection is severe and fatal.

Q) Types of tuberculosis?
1) Primary tuberculosis,
2) Progressive primary tuberculosis,
3) Secondary tuberculosis.

40
Q) Primary tuberculosis?
 It occurs in a previously unexposed and thus unsensitized individual with tubercle bacilli.
 Primary tuberculosis occurs after initial infection (first exposure) with MTB or M, bovis.
 Lungs are the usual site of Primary tuberculosis.
 Rare primary sites – intestine, Oropharyngeal locations with M. bovis. Skin is an uncommon
primary site.
Q) What are the primary sites of TB?
 Lungs,
 Intestine,
 Tonsil,
 Skin.
Q) What is Ghon focus / Primary focus?
-------------- Primary tissue lesion usually subpleural, often in the mid to lower zones / lobes caused by M. tubercle
bacilli.
Q) What is Ghon complex / Primary complex?
--------------- Ghon focus + Regional lymph adenopathy.
Regional lymphadenopathy:
-------------- Usually hilar lymph nodes.
Q) Sites of TB lymph nodes?
 Cervical LN,
 Mediastinal LN,
 Mesenteric LN.
Q) What is Ghon body?
-------------- Calcified tubercular lesion (primary complex) is called Ghon body.
Q) What happened when TB bacilli enter into body?
-------- Ghon focus / Primary focus {lungs, tonsil, LN, intestine, skin}  Ghon complex {Ghon focus + Regional
lymph adenopathy}  Ghon body.

Q) Secondary or Post primary tuberculosis?

 It refers to all forms of active infection that occur in a sensitized individual to Mycobacterium.
 It may occur by:
 Reactivation of dormant bacilli from primary lesion (endogenous source) – most cases,
 Reinfection (exogenous source) of tubercle bacilli or

41
  Directly from primary lesion.
Q) What are the fates of tubercular lesion?
 Resolution,
 Fibrosis / Dystrophic calcification,
 Persistent as a low grade infection or Dormant,
 Multiple tubercles,
 Abscess formation.

Q) Organs usually free from TB?

Necrosis:
 Thyroid,  Spectrum of morphological changes that follow cell
 Pancreas, death in living tissues,largely resulting from progressive
degradative action of enzymes on lethally injured cell.
 Skeletal muscle,  Microscopic death of cell in living tissue.
 Cardiac muscle.

Q) What is caseation? How it is formed?

Caseation / Caseous necrosis:

 The term caseous is derived from grass appearance of the area of necrosis i.e. white and cheesy
appearance.
 It is a distinctive form of coagulative necrosis.
 Caseous necrosis is encountered most often in tuberculous infection.
 It is formed by hypersensitivity to the products of the bacilli, tubercular protein and also due to
ischemia.
 It takes about 10 – 14 days to appear.
 Under microscope it looks like homogenous, structure less eosionphilic area.

Q) What is tubercle?
------------ It is the unique lesions of tuberculosis composed of central caseation necrosis surrounded by epitheloid
cells, macrophages with Langhans type of Giant cells with peripheral rim of lymphocytes.

Q) For diagnosis which one is important?

----------- Epithelioid cells surrounded by lymphocytes in a tubercle for TB diagnosis.

42
Q) What are the types of pathological lesions found in TB?
----------- Following 2 types of pathological lesions found in bone and joint TB,
 Wet TB: Caseous exudative type, characterized by –
 Onset is less insidious,
 Constitutional symptoms {local sign of inflammation, swelling} present,
 More destructive, more exudative,
 Abscess formation,
 Sinus formation commonly.

 Dry TB: Granular type, characterized by -

 Insidious onset,
 Usually occurs in adult,
 Less destructive,
 Abscess formation is rare,
 e.g. Caries sicca of shoulder.

Q) Investigation for diagnosis of TB?

 Staining for AFB:
Routine blood test:  Synovial fluid: 10% positive,
 ↓ Hb%,  Synovial tissue: 20% positive,
 Lymph node: 30% positive,
 ↑ ESR,  Osseous cavity: 10% positive.
 ↑ Lymphocyte count.

Detection of AFB:
 Sputum for AFB: positive needs 10,000 bacilli/ml in smear.
 AFB for synovial fluid: 10 – 20%.

Montoux test / Tuberculin test:

 Delayed type of hypersensitivity reaction,
 Mantoux test is significant only in the first 3-4 years of life, adults are usually positive.
 Test becomes positive 4 to 6 wks after tuberculous infection or after BCG vaccination,
Negative test does not rule out tuberculosis.
 Negative test virtually excludes the diagnosis but a positive test merely indicates tuberculous infection.
 Reading:

43
 Positive False Positive
 area of induration ≥ 6mm in diameter.  area of induration < 6mm in diameter.
 in Bangladesh ≥ 10mm in diameter.  in Bangladesh < 10mm in diameter.

Negative False Negative

No area of induration after 72 hours.

 Interpretation:
Positive False Positive
(+)ve result indicates that the patient has False (+)ve result indicates that the patient
been infected with tubercle bacilli, but may be infected with other / atypical type
does not say that whether the infection is of mycobacterium.
already-
 Healed,
 Latent,
 Even Active.

Negative False Negative

(-)ve result indicates that- False (-)ve result may occur in the
 individual is free from tuberculous following conditions,
infection or  Over whelming tuberculosis,
 individual is more susceptible to  Hodgkin’s disease,
tuberculous infection.  Sarcoidosis,
 Measles.

Imaging:
 CXR: can not determine <1.5cm {15mm} lesion,
 Isotope bone scan: can detect 5 mm lesion size as a hot spot,
 CT scan: can detect 1 mm lesion size.

44
 Rapid methods:
 PCR:
 Specificity 100% & Sensitivity 40%,
 Only 10 organisms needed to detect.

 ELISA:
 Antibody to mycobacterial antigen-6,
 Specificity 100% & Sensitivity 94%

 ALS:
 Antibodies produced by peripheral blood lymphocytes in culture supernatant,

 Nucleic Acid Amplification Test {NAAT} / Gene Xpert:

---- DNA or RNA amplification test for rapid diagnosis. May be used sputum or any sterile body fluid. Result
available in < 8 hour. 95% Sensitivity & 99% Specificity.

 Interferon Gamma Release Assays {IGRAs}:

--- New development of TB infection testing. Antigens use to detect people with tuberculosis.

Culture:
 Synovial tissue culture: >50%,
 Bactec 460 media: 4 – 25 days,
 Lowenstein Jensen media: 4 – 6 weeks.

Biopsy:
 Synovial tissue biopsy: 80%,

45
Q) Anti-TB drugs?
First line of drugs:
 These have the greatest level of efficiency and have an acceptable degree of toxicity.
 The following are the first line of drugs used in tuberculosis (mnemonic PRISE).
P—Pyrazinamide
R—Rifampicin IRSEP – 5,10,15,25,35 mg/kg/day
I—INH
S—Streptomycin
E—Ethambutol.
Second line of drugs:
These are useful if the patient develops resistance to the first line of drugs (mnemonic CAKECAT).
They have either low antitubercular efficacy or high toxicity or both, used in special circumstances as
mentioned earlier.
C—Capriomycin
A—Amikacin
K—Kanamycin
E—Ethionamide
C—Cycloserine
A—Amino salicylic acid (PAS).
T—Thiacetazone,
Ciprofloxacin,
Ofoxacin,
Levofloxacin,
Clarithromycin,
Azithromycin.
The second line of drugs is used only for treatment of the diseases caused by resistant microorganisms or
by non-TB mycobacterium.
All drugs are given parenterally and are potentially ototoxic and nephrotoxic.
 Hence, no two drugs from this group should be used simultaneously. These are not used with
streptomycin for the same reasons.

46
Q) Why use Fixed Dose Combination?
----------------- Because bacteriostatic and bactericidal activity to anti-TB drugs against Mycobacterium species in
different growth phases {lag, log and stationary phase}.

Q) Adverse effect of Primary anti-TB drugs?

 INH: Bactericidal

 Hepatitis,
 Peripheral neuropathy.

 Rifampicin: Bactericidal

 Hepatitis,
 Orange discolouration of body secretion.

 Streptomycin: Bactericidal

 Hypersensitivity,
 Ototoxicity,
 Nephrotoxicity,
 Teratogenicity.

 Ethambutol: Bacteriostatic

 Visual disturbance {colour vision, ↓ visual acquity}

 Pyrazinamide: Bactericidal
 Hepatitis,
 Arthralgia.

Q) What is MDR-TB?
----------------- Multi drug resistant TB, mainly resistant to Rifampicin and INH.

Q) What is XDR-TB?
----------------- Extensively Drug Resistant TB,
----------------- XDR-TB is the strains of TB that are resistant to Rifampicin and INH & also resistant to
Fluroquinolone and at least one of the three injectable anti-TB drugs like Capreomycin, Kanamycin or Amikacin.

47
Q) How can you manage drug reaction due to anti-TB drug in your ward?
Management of drug reaction due to anti-TB drugs:
 At first with draw all anti-TB drugs,
 Counseling and reassurance of the patient,
 Maintaining proper hydration, & improve nutritional status,
 Investigations to evaluate liver function:
 S bilirubin,
 SGPT, < 5 times normal, not indication to stop of anti-TB therapy
 SGOT,
 S Alkaline phosphatase,
 Prothombin time.
 Patient should be evaluate for other cause of hepatitis eg, viral hepatitis {viral markers},
 After confirmation, reporting to TB center,
 When liver function becomes normal, then start primary anti-TB drugs one by one with full dose in
an interval of 48 to 72 hours and start with less hepatotoxic drug such as INH at first then
Rifampicin but not Pyrazinamide.
 Instead of Pyrazinamide, suggested regimen is 2 SHE or 1 OHE
 S – Streptomycin,
 H – INH,
 E – Ethambutol,
 O – Ofloxacin.
Q) What are the properties of ideal anti-TB drugs?
 Should be bactericidal in action,
 Should have greatest level of therapeutic efficacy,
 Acceptable degree of toxicity,
 No rapid development of drug resistance.
 Should be available.

 Antibiotic:
---------------- It is the substance (eg. penicillin) that is produced from certain micro-organism
{fungi / bacteria} to destroy or inhibit the growth of other micro-organisms especially bacteria.

 Chemotherapeutic agents:
---------------- These are the synthetic chemicals which are used to destroy infective agents like
bacteria, virus, protozoa, helminthes.

48
Q) What are the rationales of use antibiotics?

Rationale of use antibiotics:

 Use appropriate antibiotic with adequate bacteriological information,
 Antibiotic should be used in proper dose and for appropriate duration,
 Combination antibiotics should be used, where single drug is ineffective or to overcome the chance of
microbial resistance to antibiotic.
 A bactericidal antibiotic should not be used with a bacteriostatic antibiotic at the same time {Antibiotic
antagonism},
 Broad spectrum antibiotic should not be used indiscriminately,
 Consider patient condition during selection of antibiotic,
 Therapy for undiagnosed micro-organisms should be started with broad spectrum antibiotics with
combination {Gram+ve + Gram-ve},
 Should not use newer antibiotic so long as the currently used antibiotic is effective.

Q) What are the common sites of osteoarticular TB?

 Spine (50%),
 Hip (15 – 20%)
 Knee (8 – 10%)
 Elbow,
 Ankle,
 Shoulder (1 – 3%)
 Others.

49
 Pott’s disease.
Tuberculous Spondylitis.
Ebn-551, Moheswari-178

Q) What is Pott’s disease?

-------------- Tuberculosis of spine with destruction of bone resulting in curvature of the spine.

Q) Characteristics of Pott’s disease / tuberculosis of spine?

 Most common form of skeletal tuberculosis constituting about 50% of all cases,
 TB spine is the commonest form of skeletal TB and second common site is Hip {15%},
 10 – 12% TB spine is associated with pulmonary TB,
 5% of TB spine is associated with lymph node TB,
 Named after Sir Percival Pott (1714-88) – described the Gibbus deformity and its sequel, Ebn-551

 Age: no age is immune but most common in 1st to 3rd decade {50% in 1st decade},
 Sex: both sex are equally affected.
Q) Pathology of Pott’s disease?
------------------ Essential pathology of paraplegia is associated with TB spine is the pressure on the spinal cord, as
follows:
 Inflammatory oedema:
 Oedema of spinal cord within the confined space of vertebral canal – due to vascular
stasis and due to toxins from the tuberculous inflammation in the neighboring vertebrae. To subside the oedema,
advice the patient for bed rest or draining paravertebral abscess.

 Extra dural mass:

 Commonest cause of interference of cord function. Abscess in the epidural space
composed of fluid, pus, granulation tissue and caseous material  compression of cord.

 Bony disorders:
 Sequestrum from vertebral body or intervertebral disc  narrowing of spinal canal 
pressure on the cord.
 Angulation of diseased spine  formation of bony ridge or spur called internal
gibbus on the anterior wall of the spinal canal  pressure on the cord.
 Rarely pathological dislocation  pressure on the cord.

50
  Meningeal changes:
 Extradural granulation tissue may contract  cicatrisation (peridural fibrosis)  cord
compression.

 Infarction of spinal cord:

 It is unusual but important cause of paraplegia,
 Infarction is caused by endarteritis, periarteritis or thrombosis of branches of anterior
spinal artery or other spinal arteries  irreparable damage of cord  poor prognosis.

 Changes in spinal cord:

 Unrelieved compression of cord  loss of neuron and fibres  replaced by gliosis.
 Fibres become loss of myelin,
 Thinning and atrophy of spinal cord can be very well visualized by contrast CT or by axial
section of MRI.
Q) Regional distribution?
 Cervical – 12%,
 Cervicodorsal – 5%,
 Dorsal – 42%,
 Dorsolumber – 12%,
 Lumber – 26%,
 Lumbosacral – 3%,
 Skip lesion: 7%
 One or more healthy vertebrae between two lesions,
 Multiple sites,
 eg. Cervical + Lumber or Cervical + Thoracic.

Q) Why tuberculosis is common in dorsal region?

----------------- The reasons cited for this area of predilection are:
 Batson’s plexus – valve less communication between the veins of lungs and thoracic vertebrae,
 Large amount of spongy tissue within the vertebral body,
 Degree of wt bearing, which is comparatively more.
 More vertebral mobility is seen here.

Q) Spread of TB spine?
 Haematogenous route,
 Para-vertebral lymph nodes.

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Q) Types of spinal TB / Location of TB in vertebral column?
1) Typical: affect vertebral body,
2) Atypical: affect lamina or other parts.

Typical Spinal TB:

 Para discal: 70%
 Central: 23%,
 Anterior: 7%.
Atypical Spinal TB:
 Posterior: 1 – 2%.

Para discal type:

 Why common?
 Lower half of upper vertebrae and upper half of lower vertebrae with intervening disk
develop from one sclerotome, which has common source of blood supply.
 Hence, bacteremia involves this embryological section more often.
 It is due to peculiarity of blood supply.
 Intervertebral disc is not involved primarily as it is relatively avascular. Involvement of paradiscal
region jeopardizes the nutrition of the disc and then necrosis of disc occurs.

52
Central type:
 Infection reaches the central part of the body through Batson’s venous plexus or through the
branches of post vertebral artery.
 It is due to peculiarity of Batson’s plexus of vein,
 The diseased vertebral body may show normal bony trabeculae, or may show areas of bone
destruction - body may be expanded / ballooned / collapsed.
 Narrowing of disc space is minimum.

Anterior type:
 Beneath anterior longitudinal ligament and periosteum,
 Common in thoracic spine of children,
 Usually spread from paradiscal or body type lesion,
 Extension of abscess beneath ant. longitudinal ligament.

Posterior / Appendicular type (1% - 2%):

 Pedicle,
 Lamina,
 Transverse process,
 Spinous process,
 Facet joint.

Q) What is Pott’s paraplegia?

--------------- it is the spastic paralysis of the lower part of body and extremities due to pressure on the spinal cord as
the result of tuberculous spondylitis.

Q) Causes of Pott’s paraplegia?

 Extrinsic causes:
 Tubercular abscess,
 Tubercular caseous material,
 Tubercular granulation tissue,
 Sequestered bone and disc,
 Pathological subluxation or dislocation of vertebrae.

53
  Intrinsic causes:
 Tubercular inflammatory oedema involving dura and spinal cord,
 Infective thrombosis of spinal cord,
 Spinal tumour syndrome.

Q) Clinical features of spinal TB / Pott’s paraparesis / paraplegia?

 Symptoms:
 Age: most common 1st to 3rd decades,

 Sex: equally distributed,

 Patient’s complaints:
 Chronic back pain,
 Slowly spontaneous development of twitching of muscles of lower limbs and clumsiness while walking,
 Some patients may present with spinal shock,
 Some patients may present as flaccid type of paralysis & areflexia. But later this flaccid paralysis gradually
changes to spastic paralysis,
 Loss of bowel and bladder function.
 Loss of sensation of lower limbs.
 Cold abscess: Collar stud abscess / Retropharyngeal abscess/Cold abscess in axilla / Para-vertebral abscess /Psoas
abscess.

 Local symptoms:
 Pressure effect associated with cold abscess:
 Cervical region:
 Dysphagia,
 Dyspnoea,
 Hoarseness of voice,
 Restricted movement.

 Thoracic region:
 Knuckle kyphosis: wedging of one or two vertebral body,
 Angular kyphosis / Gibbus: wedging of 3 or more vertebral body.

 Lumber region:
 Cauda eqina syndrome – TB in L4/5 {Disc Protrusion}.

54
  Neurological manifestation: Paresis / Paralysis.
 Most dreadful and crippling complications,
 Incidence: 10% - 30%,
 Highest incidence: associated with TB lower thoracic spine.
 Muscle weakness, clumsiness in walking,
 UMN type lesion – spastic paraplegia,
 At first paraplegia in extension then in flexion.

 Constitutional symptoms: present in only about 20% of cases.

 Low grade fever,
 Evening rise of temperature,
 Night sweets,  Motor functions are almost affected first
than sensory, because:
 Lassitude in the afternoon,
Diseased area of the spine lies
 Loss of appetite, anterior to the cord near motor tracts,
 Loss of weight, Motor tracts are more sensitive to
compression.
 Spinal Tumour Syndrome:
------- In TB spine, there is extradural granulomatous lesion which may be diffuse {diffuse
granulomatous lesion within the spinal canal}. This mimics like a spinal cord tumour, may be anteriorly or posteriorly to the
spinal cord causing mechanical pressure on the cord, which is responsible for neurological complications without any
Radiological evidence of TB involvement of vertebrae.

Q) Cold abscess?

This is a collection of pus and tubercular debris from a diseased vertebra. It is called a cold abscess because it is not
associated with the usual signs of inflammation.

55
Spread of cold abscess:
 If it travels backwards, it may press upon the important neural structures in the spinal canal.
 The pus may come out anteriorly (pre-vertebral abscess) or on the sides of the vertebral body (para-vertebral
abscess).
 Once outside the vertebra the pus may travel along the musculo-fascial planes or neuro-vascular bundles to
appear superficially at places far away from the site of lesion.

Sites of cold abscess in TB spine

Q) Types of Paraplegia / Seddon’s classification of Pott’s paraplegia?

-------------- According to duration / Seddon’s classification:
 Group A / Early onset paraplegia:
 Occurs within first 2 years of active phase,
 Pathology: inflammatory oedema / abscess, granulation tissue, pus, caseous material, tubercular abscess
etc.
 Prognosis: good.
 Group B / Late onset paraplegia:
 After many years (> 2 yrs of onset),
 Paraplegia usually associated with healed disease,
 Pathology:
 Tubercular debris,
 Caseous material,
 Sequestra from vertebral body / disc,
 Internal gibbus: formation of bony ridge or spur called internal gibbus on the anterior wall of the
spinal canal  angulation of diseased spine.

56
  Stenosis of vertebral canal.
 Severe kyphotic deformity,
 Other causes of neurological compression:
 Vascular insufficiency of cord / thrombosis of spinal vessels: prognosis is poor,
 Pathological subluxation or dislocation of spine: prognosis is poor,
 TB meningomyelitis: recovery is incomplete.
 Prognosis: bad.

Q) Stages of TB spine?
 Stage I : Incipient / Pre-destruction,
 Stage II : Early destruction,
 Stage III : Advance destruction,
 Stage IV: Neurological involvement (10% - 20%),
 Stage V : Residual deformity.

Q) Kumar’s classification of Tuberculous paraplegia?

------------------- Classification based on motor weakness,
Stage Clinical features
I Negligible  Unaware of neural deficit,
 Physician detect –
 Planter extensor & Ankle Clonus.
 ↑ Muscle tone,
II Mild  Walk with support.
(Pt aware of motor weakness but manages to walk)
 All signs of spastic paresis are present,
 Spastic gait / Jumpiness during walking.
 No sensory deficit.
III Moderate Non ambulatory / Bed ridden.
 Spastic paraplegia in extension,
 Sensory loss < 50%.
 Bowel & bladder is not involved.
IV Severe  3+ paralysis in flexion / Grade III paraplegia,
 Paraplegia in flexion,
 Sensory loss > 50%,
 Sphincters involve / Bowel & bladder is involved.

57
Q) Kumar’s Clinico-Radiological classification of TB spine? Tuli 4 th
ed: P-223

Stage Features Usual duration

I Pre-destructive  Straightening of curvatures, < 3 months
 Spasm para-vertebral muscles,
 Scinti scan show hyperemia,
 MRI shows marrow oedema.
II Early destructive  Diminished disc space, 2 – 4 months
 Paradiscal erosion,
 Knuckle kyphosis < 100
 MRI – show marrow oedema and break of osseous
margins,
 CT scan – shows marginal erosions or cavitations.
III Mild angular kyphosis 2 – 3 vertebrae involved, 3 – 9 months
(Angle of kyphosis : 100 - 300 )
IV Moderate angular kyphosis > 3 vertebrae involved, 6 – 24 months
(Angle of kyphosis: 300 – 600)
V Severe kyphosis > 3 vertebrae involved, > 2 years.
(Humpback) (Angle of kyphosis: > 600)

Q) Investigation for TB spine?

 Conventional radiography:
Paradiscal type Body / Central type Anterior type

 Narrowing of disc space,  Loss of normal trabeculae,  Erosion at front and side
 Wedge compression of vertebrae,  Body may be expanded or of vertebrae as shallow
 Kyphotic deformity, ballooned, excavation,
 Para-vertebral shadow / abscess.  Areas of lucency,  Vertebral collapse
↓  Collapse of vertebrae / Vertebrae anteriorly,
 In thoracic region: Bird’s nest planna,  Disc space is minimally
appearance, decreased.

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 In lower thoracic region:
A: Concertina collapse,
Bulbous & heart shaped, B: Anterior wedge compression
 In dorsal & dorso-lumber region: Malignancy
fusiform shaped,  Disc space is maintained,
 Body is collapsed.
 In lumber area: lateral bulging of
Psoas outline / Psoas shadow.

X ray Dorsal spine / DL spine showing that:

AP view:
 Disc space reduction {earliest manifestation},
 Fusiform shaped radio-opaque shadow alongside of vertebrae
extending from ……….,

Lat view:
 Trabecular destruction and ant. wedging of vertebrae at the
level ………. {usually takes 3 – 5 months following infection}

 Computed tomography:
 Much better bony detail,
 Irregular lytic lesions,
 Sclerosis,
 Disc collapse & disruption of bone circumference.
 CT guided FNAC: findings may be positive in only about 50% of cases.

59
  MRI:
MRI of LS spine – sagital section. Tuberculous lesion involving L4 & L5 vertebrae.

 Myelography: to exclude-
 Spinal tumour syndrome,
 Spinal tumour,
 Multiple vertebral lesions.
 USG: to detect the size of cold abscess in lumber vertebral disease.
 Haematological investigation / CBC:
 ↓ Hb%,
 ↑ ESR,
 ↑ TC,
 ↑ DC / Lymphocytosis.
 Nucleic Acid Amplification Test {NAAT}:
---- DNA or RNA amplification test for rapid diagnosis. May be used sputum or any sterile body fluid. Result
available in < 8 hour. 95% Sensitivity & 99% Specificity.
 Interferon Gamma Release Assays {IGRAs}:
--- New development of TB infection testing. Antigens uses to detect people with tuberculosis.

Q) D/D of TB spine?
 Pyogenic osteomyelitis: pt is toxic, s/s - acute
 Tumour:
 Benign: Body is usually involved but disc space is maintained. e.g. Haemangioma, GCT, ABC
 Malignant:

60
  Primary: MM, Lymphoma, Ewing’s sarcoma, Osteosarcoma.
 Secondary: from other sites.
 Traumatic fracture / Compression #: Disc space is normal, vertebral body is osteoporotic or sclerotic.

 In TB spine: motor deficit first, then sensory deficit.

 In Traumatic paraplegia: both motor & sensory involvement.

 Spondylolisthesis.

Q) Complications of tuberculosis spine?

• Paraplegia
• Cold abscess
• Sinuses
• Secondary infection
• Amyloid disease
• Fatality

Q) Treatment of TB spine / Pott’s disease?

a} Conservative treatment:
 Complete bed rest 3 – 6 weeks,
 Traction for cervical or cervico-dorsal lesion,
 Anti TB chemotherapy:
 4 FDC: for 3 months,
 2 FDC: for 18 to 24 months.

Q) Before surgery how long you use Anti-TB drug {Tuli 62}?
-------- In general 1 – 4 weeks drug therapy and general treatment is advisable before any major surgical intervention,

Q) How long you use Anti-TB drug in bone TB {Tuli 60}?

-------- Minimum duration 1 year, preferable 18 months, sometimes need 24 months.

 X ray, ESR and Pt is called for follow up 3 to 6 months interval,

 Spinal Brace: gradual mobilization of patient is encouraged in absence of neural deficit with the
help of supportive spinal brace. Spinal brace should be continuing for about 18 to 24 months.
 Cervical region: Cervical collar,
 Thoracic region: Taylor brace,

61
  Lumbosacral region: Corset.

b} Surgical treatment:
Absolute indication: {Tully-271}
 Onset of paraplegia during the course of conservative treatment for 3 – 6 weeks,
 Static or worsening paraplegia in the course of conservative treatment for 3 – 6 weeks,
 Neurological complications fail to respond to conservative treatment,
 Doubtful diagnosis,
 Recurrence of neuro complications / disease,
 Spinal instability,
 Prevention of severe kyphosis or progressive kyphosis.

Other indication:
 Incidence of Surgery:
 Painful paraplegia,
 Uncomplicated cases: 5%,
 Paraplegia of old age,  Complicated cases: 60%
 Recurrent paraplegia,
 Spinal tumour syndrome.
Principles surgery:
 Debridement:
 To minimize the diseased tissue.
 Decompression of spine:
 To relieve pressure.
 Instrumentation with bone graft:
 To maintain stability.

camp-1983
Surgical procedures:
 Posterior Decompression ± Fusion ± Stabilization:

 Post Decompression followed by interbody Fusion with case and bone graft, then
 Stabilization by pedicle screws and rods.
 Costo-transversectomy:

62
 Costotransversectomy:
 This is indicated for a tense paravertebral
abscess.

 Structures remove: excision of the

transverse process of the affected vertebra and
about an inch of the adjacent rib to facilitate
the drainage of abscess.

 Antero-Lateral Decompression (ALD):

Anterolateral Decompression (ALD):
 The structures removed in this
procedure is posterior part of the rib,
transverse process, pedicle and part of the
vertebral body anterior to the cord .

 This is the surgery of choice for Pott’s

paraplegia.

 It helps to effectively remove the solid

and liquid debris.

63
Q) Middle Path Regime? Tully-268
 Rest in hard bed or plaster of paris bed:
 Rest in hard bed,
 POP bed for few uncooperative patients,
 Cervical and cervico-dorsal lesions, traction is used in early stages to put the diseased part at
rest.

 Drugs:
 Intensive phase:
 ING + Rifampicin + Ofloxacin for 5 – 6 months,
 All replicating sensitive mycobacteria are likely to be killed by this bactericidal
regime,

 Continuation phase:
 ING + Pyrazinamide for 3 – 4 months, to be followed by INH + Rifampicin for
another 4 – 5 months,
 Treatment should be last for 7 – 8 months where the aim is to attack the persisters,
slow growing or intermittently growing or dormant or intracellular mycobacteria.

 Prophylactic phase:
 INH + Ethambutol for 4 – 5 months,
 Aim is to offer prophylaxis to the patient during the time his body is developing
adequate protective immunity.
 This is the time when the treated patient is back to his normal working
environments.

The overall incidence of healing by conservative anti-TB therapy in different series {Tuli 1973 / P:294}
varies b/w 83% to 96.8%

 Radiograph & ESR:

 X ray {to see kyphosis} and ESR are taken to patients a 3 – 6 months interval,
 MRI or CT scan may be advisable at 6 months interval for about 2 yrs.

 Gradual mobilization of patient:

 Encouraged in absence of neural deficit with the help of suitable spinal braces as soon as the
comfort at the diseased site permits,

64
  After 3 – 9 weeks of starting of of treatment, back extension exercises 5 – 10 minutes 3 – 4 times
in a day,
 Spinal brace is continued for about 18 months to 2 years.

 Abscesses are aspirated / drained:

 Abscesses are aspirated when near to the surface,
 Open drainage of the abscess is performed if aspiration fails to clear them.
 Prevertebral abscess in cervical region is drained under anaesthesia when complicated by
difficulty in deglutition and respiration.

 Sinuses:
 In majority of cases heal within 6- 12 weeks of onset of treatment.

 Neural complications:
 If progressive recovery of neural complications on triple drug therapy for 3 – 4 weeks, surgical
decompression is unnecessary.
 Decompression of cord for neurological complications should be performed for those cases who
do not show progressive recovery after a fair trial of conservative therapy for few weeks.

 Excisional surgery:
 Is recommended for posterior spinal disease associated with abscess or sinus formation (with or
without neural involvement) because of danger of secondary infection of the meninges – if the
disease does not come under control by drug therapy within 3 – 4 weeks.

 Operative debridement:
 Is recommended for the cases who do not show arrest of activity of spinal lesion after 3 – 6
months of chemotherapeutic regime or cases with recurrence of the disease.

 Posterior spinal arthrodesis:

 Is recommended for symptomatic unstable spinal lesion.

 Postoperative care:
 After decompression or debridement or arthrodesis, patient is nursed on a hard bed for about 2 – 3
weeks,
 In the cases of neural complications, 3 – 5 months after the operation when the patient has made
good recovery then gradually mobilized out of the bed with the help of spinal brace.
 Spinal brace is gradually discarded about 12 to 24 months after the operation.

65
Q) Prognostic factors of TB spine?
 Age of patient: young patient  good prognosis,
 General condition of patient: malnourished pt  bad prognosis,
 Early onset of cord involvement : Early onset  good prognosis,
 Duration of disease: short duration  good prognosis,
 Severity / Degree of cord involvement: partial spinal cord injury  good prognosis.
 Kyphotic deformity: <600 / >600
Q) Paravertebral abscesses?

Para - vertebral abscess: A para - vertebral soft tissue shadow corresponding to the site of the affected vertebra in
the A . P. View indicates a para - vertebral abscess.
It may be of the following types:
(i) Fusiform para - vertebral abscess (Bi rd nest abscess — an abscess whose length is greater than its width),
(ii) Globular or tense abscess: an abscess whose width is greater than the length
(III)Widened mediastinum: An abscess from the dorsal spine may present as a widened mediastinum on the AP X-
ray.
(IV) Retropharyngeal abscess: In cervical spine T.B., a retro-pharyngeal abscess maybe seen on a lateral X-ray.
Normally, soft-tissue shadow in front of t h e C3 vertebral body is 4 mm thick; an increase in its thickness indicates
a retro-pharyngeal abscess.
(V) Psoas abscess: In dorso-lumbar and lumbar tuberculosis, the psoas shadow on an X-ray of t he abdomen may
show a bulge.

66
 TUBERCULAR ARTHRITIS

Tuberculous arthritis – pathology The disease may begin as synovitis (a) or osteomyelitis (b). From either, it can
extend to become a true arthritis (c); not all the cartilage is destroyed, and healing is usually by fibrous ankylosis (d).

An early feature is peri-articular osteoporosis due to synovitis – the left knee in (b). This often resolves with
treatment, but if cartilage and bone are destroyed (c), healing occurs by fibrosis and the joint retains a ‘jog’ of painful
movement

Q) What are the features of joint TB? APL/8 - 45

 Long history,
 Involvement of only one joint,
 Marked Synovial thickening,
 Periarticular muscle wasting,
 Periarticular osteoporosis.

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 TUBERCULOSIS OF HIP
APL – 520, maheswari-180

After the spine, the hip is affected, most commonly.

Usually it occurs in children and adolescents, but patients at any age can be affected.
Pathology:
The disease may start as a synovitis, or as an osteomyelitis in one of the adjacent bones.
↓
Once arthritis develops, destruction is rapid and may result in pathological dislocation.
↓
Healing usually leaves a fibrous ankylosis with considerable limb shortening and deformity.
Clinical features
 The condition starts insidiously with aching in the groin and thigh, and a slight limp;
 Later, pain is more severe and may wake the patient from sleep.
 With early disease (synovitis or osteomyelitis) the joint is held slightly flexed and abducted, and
extremes of movement are restricted and painful,
 If arthritis supervenes the hip becomes flexed, adducted and medially rotated, muscle wasting
becomes obvious, and all movements are grossly limited by pain and spasm.
Sites of Hip TB:
A) Acetabular
roof,
B) Epiphysis,
C) Metaphysis /
Neck,
D) Greater
trochanter.

X-ray
 Radiological classification:
Shanmugasundharam classification:
1. Normal 2. Traveling / Wondering type 3. Dislocating type
4. Perthes type 5. Protrusion acetabuli type 6. Atrophic type
7. Mortar & Pestle type

68
 Clinocoradiological staging:

Stage of Synovitis Stage of Early arthritis Stage of Advanced arthritis Stage of Erosion {subluxation /
dislocation}
 Effusion into the  Articular cartilage is  Cartilage is destroyed,  Further destruction of
joint, involved.  Head and/or the acetabulum and head,
 Attitude - flexion,  This leads to the spasm of acetabulum is eroded.  Wandering acetabulum,
abduction and external the powerful muscles around  There may be a
 Mortle & pestle appearance,
rotation. the hip; flexors and pathological dislocation or
 Reduced joint space,
 As the pelvis tilts adductors are stronger subluxation of t he hip.
 Gross restriction of ROM,
downwards - Affected muscle-groups than the  Attitude - flexion,
limb appears longer extensors and abductors, adduciton and internal
(apparent lengthening),  Attitude - flexion, rotation.
though on measuring adduction and internal  True shortening of the
true limb lengths the two rotation. limb because of the actual
limbs are found to be  As the pelvis tilts upwards destruction of t h e bone.
equal. to compensate for the
adduction, the affected limb
appears shorter (apparent
shortening).

69
Treatment
a) Conservative treatment:
 Antituberculous drugs are essential, and these alone may result in healing.
 Skin traction is applied and, for a child, an abduction frame may be used.
 An abscess in the femoral neck is best evacuated; if the arthritis does not settle, joint ‘debridement’ is performed.
 As the disease subsides, traction is discontinued and movement is encouraged.

b) Operative treatment:

 Synovectomy,
 Debridement of joint,
 Arthrodesis,
 Arthroplasty.

 If the joint has been destroyed, arthrodesis may be necessary once all signs of activity have disappeared, but
usually not before the age of 14.
 In older patients with residual pain and deformity, if the disease has clearly been inactive for a considerable time,
total joint replacement is feasible and often successful; with antituberculous drugs, which are essential, the
chances of recurrence are not great.
 Girdlestone’s excisional arthroplasty is occasionally the only option.

Why traction given?

 To give rest to the joint,
 To give relieve muscle spasm,
 To maintain joint space,
 To prevent deformity.
 To minimize the chance of developing migrating acetabulum.

70
 TUBERCULOSIS OF THE KNEE
mahes- 185, APL-570

Tuberculosis of the knee may appear at any age, but it is more common in children than in adults.
Pathology:
 Bone and joint tuberculosis is always secondary to some primary focus in the lungs, lymph nodes etc. The
mode of spread from the primary focus may be either haematogenous or by direct extension from a neighbouring
focus.
 Commonly, the disease begins in the Synovial membrane (synovial tuberculosis), leading to hypertrophy of the
synovium. In early stages, the disease may be confined to the synovium without significant damage to the joint.
CLINICAL FEATURES
Symptoms:
 Age group of 10-25 years, presents with complaints of pain and swelling in the knee.
 Subsequently, the pain increases and the knee takes an attitude of flexion.
 Child starts limping.
Signs:
• Swelling: The joint is swollen which may be due to synovial hypertrophy or effusion.
• Muscle atrophy: The atrophy of t he thigh muscle is more than can be accounted for by disuse alone. This is an
unexplained feature of joint tuberculosis.
• Cold abscess: There may be swelling due to a cold abscess, either around the knee or in the calf.
• Sinus: There may be discharging or healed sinuses.
• Deformity: In early stages, there is a mild flexion deformity of t h e knee because of effusion in the knee, and
muscle spasm. Later, triple displacement (flexion, posterior subluxation and external rotation) occurs due to
ligament laxity.
• Movements: The movements of the joint are limited. There is pain and muscle spasm on attempting movement.

(a) Lateral views of the two knees. On one side the bones are porotic and the epiphyses enlarged, features suggestive of a severe
inflammatory synovitis. (b) Later the articular surfaces are eroded.

71
X-ray:
 In Synovial TB-
 X-ray is essentially normal in a case of Synovial tuberculosis, except for a soft-tissue shadow corresponding to
the distended knee.
 The joint space may be widened. There is diffuse osteoporosis of the bones around the joint.
 In osseous tuberculosis, one may see juxta-articular lytic lesions. The joint surfaces may be eroded. In later
stages, joint space may be diminished or completely lost.

TREATMENT
• Synovectomy: It may be required in cases of purely synovial tuberculosis. Very often one finds 'melon seed'
bodies within the joint.

• Joint debridement: This may be required in cases where the articular cartilage is essentially preserved. The pus is
drained, the synovium excised, and all the cavities curetted.

• Arthrodesis: In advanced stages of the disease with triple subluxation and complete cartilage destruction the knee
is arthrodesed in functional position, i.e., about 5-10 degrees of flexion and neutral rotation. One popular method of
knee arthrodesis is Charnley ' s compression arthrodesis. Ideal position for fusion is 10–15 degrees of flexion, 7
degrees of valgus and 5 degrees of external rotation.

72
 TB Ankle.
apl- 609
Tuberculous infection of the ankle joint begins as a synovitis or as an osteomyelitis and, because walking is painful,
may present before true arthritis supervenes.

Tuberculous arthritis of the ankle The swelling of the left ankle is best seen from behind.

Clinical features:
 Pain in the affected ankle and walking is painful,
 The ankle is swollen and the calf markedly wasted;
 Skin feels warm and movements are restricted.
 Sinus formation occurs early.
X ray findings:

 X-rays show regional osteoporosis,

 Sometimes a bone abscess and,
 With late disease, narrowing and irregularity of the joint space.
Q) Treatment of TB ankle?
 General treatment (Chapter 2) a removable splint is used to rest the foot in neutral position.
 If the disease is arrested early, the patient is allowed up non-weight bearing in a calliper; gradually taking more
weight and then discarding the calliper altogether.
 Following arthritis, weightbearing is harmless, but stiffness is inevitable and usually arthrodesis is the best
treatment.

73
 TB Shoulder
APL- 358

Tuberculosis of the shoulder is uncommon. This may proceed to abscess and sinus formation, but in some cases the
tendency is to fibrosis and ankylosis. If there is no exudate the term ‘caries sicca’ is used.

Tuberculosis X-ray of the shoulder showing tuberculous abscesses in the head of the humerus.
Clinical features
 Adults are mainly affected. They complain of a constant ache and stiffness lasting many months or years.
 The striking feature is wasting of the muscles around the shoulder, especially the deltoid. In neglected
cases a sinus may be present over the shoulder or in the axilla.
 There is diffuse warmth and tenderness and all movements are limited and painful.
 Axillary lymph nodes may be enlarged.
X-rays
 Show generalized rarefaction, usually with some erosion of the joint surfaces.
 There may be abscess cavities in the humerus or glenoid, with little or no periosteal reaction.
Treatment
Systemic treatment with antituberculous drugs + Shoulder should be rested until acute symptoms have settled.
↓
Thereafter movement is encouraged and, provided the articular cartilage is not destroyed, the prognosis for painless
function is good.
↓
If there are repeated flares, or if the articular surfaces are extensively destroyed, the joint should be arthrodesed.

74
 Tuberculosis of Elbow.
apl – 373,

Tuberculosis of the elbow Muscle wasting is marked

 The elbow is affected in about 10 per cent of patients with skeletal tuberculosis.
 Although the disease begins as synovitis or osteomyelitis,
 The most striking physical sign is the marked wasting.
Clinical features:
 While the disease is active the joint is held flexed, looks swollen, and feels warm and diffusely tender;
 Movement is considerably limited and accompanied by pain and spasm.
 Always feel for the supratrochlear and axillary lymph nodes; they may be enlarged.
X-rays
The typical features are peri-articular osteoporosis and joint erosion.
There may also be subchondral cystic lesions.
Other investigations
Aspiration, synovial biopsy and microbiological investigation will usually confirm the diagnosis.
Treatment
Conservative:
 General antituberculous treatment is essential.
 The elbow is rested until the acute symptoms subside – at first in a splint and positioned at 90 degrees of
flexion and mid-rotation,
 Later simply by applying a collar and cuff. As soon as possible, movement is encouraged.

Operative:
Late residual effects – chronic pain, stiffness or deformity - excisional or replacement arthroplasty or (rarely)
arthrodesis.

75
 TUBERCULOSIS OF WRIST
APL-399

Tuberculosis of the wrist Pointing abscess;

 At the wrist, tuberculosis is rarely seen until it has progressed to a true arthritis.
 Bilateral arthritis of the wrist is nearly always rheumatoid in origin, but when only one wrist is affected
the signs resemble those of tuberculosis.
Clinical features;
 Pain and stiffness come on gradually and the hand feels weak.
 The forearm looks wasted; the wrist is swollen and feels warm.
 Involvement of the flexor tendon compartment may give rise to a large fluctuant swelling that crosses
the wrist into the palm (compound palmar ganglion).
 In a neglected case there may be a sinus. Movements are restricted and painful.

X-ray showing diffuse osteoporosis.

X-rays show localized osteoporosis and irregularity of the radio-carpal and intercarpal joints; there may also be
bone erosion.
Treatment
 Antituberculous drugs are given and the wrist is splinted.
 If an abscess forms, it must be drained.
 If the wrist is destroyed, systemic treatment should be continued until the disease is quiescent and the
wrist is then arthrodesed.

76
 Psoas Abscess.
-------- Paraspinal abscess in psoas muscle, usually caused by lumber tuberculosis.

Cold abscess in the back.

77
78
This cold abscess tracks down along the areas of least resistance and may point in any one of following sites: (i)
Femoral triangle, (ii) inguinal region, (iii) medial side of the thigh, (iv) Greater trochanter, (v) gluteal region, (vi)
ischiorectal fossa, (vii) lateral and posterior aspect of the thigh, and (vii) pelvis.

79
 OSTEOARTHRITIS

INFLAMMATORY RHEUMATIC DISORDERS

CRYSTAL DEPOSITION DISORDERS

80
 Osteoarthritis.
apl-85, ebn-674

OSTEOARTHRITIS APL-85, Ebn-682

Q) What is osteoarthritis?
 Osteoarthritis (OA) is a chronic disorder of Synovial joints in which there is progressive softening and
disintegration of articular cartilage accompanied by new growth of cartilage and bone at the joint margins
(osteophytes), cyst formation and sclerosis in the subchondral bone, mild synovitis and capsular fibrosis.
 Osteoarthritis is a dynamic phenomenon; it shows features of both destruction and repair.
 It is not primarily an inflammatory disorder.

It is also not a purely degenerative disorder, and the term ‘degenerative arthritis’ – which is often used as a
synonym for OA – is a misnomer.
Aetiology / Types of osteoarthritis:
1. ‘Primary’ OA (when there is no obvious antecedent factor),
2. ‘Secondary’ OA (when it follows a demonstrable abnormality).
 Causes for primary osteoarthritis:
 Exact cause is not known,
 Mainly due to wear and tear,
 Following factors are suspected to —
 Obesity,
 Genetics and heredity,
 Occupation involving prolonged standing / sports,
 Multiple endocrinal disorders / Multiple metabolic disorders.

81
 Causes of Secondary osteoarthritis:
 It is generally observed that secondary osteoarthritis occurs in the younger age groups and is more severe than
the primary. • Incongruity of the articular surface, e.g. trauma, Perthe’s,
CDH, slipped epiphysis, etc.
 The causes for secondary osteoarthritis -
• Instability of the hip, e.g. subluxation.
• Obesity.
• Concentration of pressure load, e.g. coxa vara,
• Valgus and varus deformities of the knee. anteversion.
• Intra-articular fractures of the knee, etc. • Direct injury, e.g. infection, trauma, etc.
• Rheumatoid arthritis, infection, trauma, TB, etc. • Constitutional causes, e.g. obesity, hyperthyroidism, etc.
• Hyperparathyroidism.
• Bone diseases like AVN, rheumatoid arthritis, etc.
• Hemophilia.
• Syringomyelia.
• Neurological disease like diabetes.
• Overuse of intra-articular steroid therapy.

 eg. Patients with ‘secondary’ OA of the knee following meniscectomy have been found also to have a higher
than usual incidence of ‘primary’ OA in other joints (Doherty et al., 1983).

 Previous disorders (e.g. Congenital defects, Old fractures, Perthes’ disease or Rheumatoid arthritis) - Such cases
are usually designated as ‘secondary osteoarthritis’,

Non-progressive OA Progressive OA
Non-progressive OA changes are common in Progressive OA changes are seen
older people; here we see them along the characteristically in the maximal load-bearing
inferomedial edge of the femoral head, while area; in the hip this is the superior part of the
the articular cartilage over the rest of the head joint. Articular cartilage has been destroyed,
looks perfect. leaving a bald patch on the dome of the femoral
head.

82
Clinical variants of osteoarthritis:
 MONARTICULAR OSTEOARTHRITIS:
 Septic arthritis,
 Gout,
 Pseudogout,
 Monoarticular RA,
 Reactive arthritis.
 PAUCIARTICULAR OSTEOARTHRITIS:
 JIA.
 POLYARTICULAR (GENERALIZED) OSTEOARTHRITIS:
 Poly articular RA,
 OA,
 Psoriatic arthritis,
 AS,
 Enteropathic arthritis.

Pathogenesis

Pathology
The cardinal features are:

83
(1) Progressive cartilage destruction;
(2) Subarticular cyst formation, with
(3) Sclerosis of the surrounding bone;
(4) Osteophyte formation;
(5) Capsular fibrosis.

Symptoms
Patients usually present after middle age.
A family history is common in patients with polyarticular OA.
Pain - is the usual presenting symptom. For example, pain in the knee from OA of the hip.
Stiffness - is common; characteristically it occurs after periods of inactivity,
Swelling - may be intermittent (suggesting an effusion) or continuous (with capsular thickening or large
osteophytes).
Deformity - may result from capsular contracture or joint instability,
Loss of function - often the most distressing symptom.

Varus deformity of the right knee due to osteoarthritis.

Signs
 Joint swelling - may be due to an effusion,
 Muscle wasting suggests longstanding dysfunction.
 Joint line tenderness is common, and in superficial joints fluid, synovial thickening or osteophytes may be felt.
 Limited movement in some directions,
 Crepitus may be felt over the joint (most obvious in the knee) during passive movements.
 Instability is common in the late stages of articular destruction,
 Other joints should always be examined; they may show signs of a more generalized disorder.

84
 (a,b) The common picture is one of ‘knobbly finger-tips’ due to involvement (c) In some cases the PIP joints are
of the DIP joints (Heberden’s nodes). affected as well (Bouchard’s nodes).

(a) Proximal joints = Rheumatoid arthritis; (b) Distal joints = osteoarthritis; (c) Asymmetrical joints = Gout.

Imaging
a) X-rays

X-ray shows the classic features:

 Disappearance of the joint ‘space’ / loss of articular cartilage seen as narrowing of the ‘joint space’,
 Subarticular cyst formation,

85
 Subarticular sclerosis and
 Osteophyte formation at the margins of the joint.
 Bone remodeling / Remodelling of the bone ends on either side of the joint.

b) Radionuclide scanning
 Scanning with 99mTc-HDP shows increased activity during the bone phase in the subchondral regions of
affected joints.
 This is due to increased vascularity and new bone formation.

c) CT and MRI
To elucidate a specific problem, e.g. early detection of an osteocartilaginous fracture, bone oedema or Avascular
necrosis.

d) Arthroscopy
Arthroscopy may show cartilage damage before x-ray changes appear.

Differential diagnosis of osteoarthritis

 Avascular necrosis
osteoarthritis osteonecrosis

 Osteoarthritis with marked subarticular In primary osteonecrosis articular cartilage is

bone collapse is sometimes mistaken for preserved even while the underlying bone
osteonecrosis. crumbles.
 The clue to the diagnosis is that in OA the
articular ‘space’ (cartilage) is progressively
reduced before bone collapse occurs,

‘Idiopathic’ osteonecrosis causes joint pain and local effusion.

 Inflammatory arthropathies

86
Rheumatoid arthritis, ankylosing spondylitis and Reiter’s disease may start in one or two large joints.

 Polyarthritis of the fingers

Rheumatoid arthritis, Psoriatic arthritis, Tophaceous gout may cause knobbly fingers,

 Diffuse idiopathic skeletal hyperostosis (DISH)

Management of OA

EARLY TREATMENT
Principles are:
(1) Maintain movement and muscle strength;
(2) Relieve pain; and
(3) Protect the joint from ‘overload’;
(4) Modify daily activities.
 Maintain movement and muscle strength / Physical therapy
Maintaining joint mobility and improving muscle strength. Care should be taken to avoid activities which increase
impact loading.

 Analgesic medication / Relieve pain

Pain relief is important, Patients may respond to a simple analgesic such as paracetamol. If this fails to control pain,
a non-steroidal anti-inflammatory preparation may be better.

 Protect the joint from ‘overload’ / Load reduction

Protecting the joint from excessive load may slow down the rate of cartilage loss.

INTERMEDIATE TREATMENT
 Joint debridement (removal of loose bodies, cartilage tags, interfering osteophytes or a torn or impinging
acetabular or glenoid labrum) may give some improvement. This may be done either by arthroscopy or by open
operation.
 Corrective osteotomy may prevent or delay progression of the cartilage damage.

LATE TREATMENT
Progressive joint destruction, with increasing pain, instability and deformity (particularly of one of the
weightbearing joints)  usually requires reconstructive surgery.
Three types of operation have –
 Realignment osteotomy,

87
  Arthroplasty and
 Arthrodesis.

(a) Osteotomy, (b) Arthroplasty, (c) Athrodesis

Realignment osteotomy
 Until the development of joint replacement surgery in the 1970s, realignment osteotomy was widely employed.
 Pain relief is often dramatic and is ascribed to -
(1) Vascular decompression of the subchondral bone, and
(2) Redistribution of loading forces towards less damaged parts of the joint.
(3) After load redistribution, fibrocartilage may grow to cover exposed bone.
 High tibial osteotomy is still considered to be a viable alternative to partial joint replacement for
unicompartmental OA of the knee, and
 Intertrochanteric femoral osteotomy is sometimes preferred for young patients with localized destructive OA of
the hip.
Joint replacement
 Indications-
 Patients with intolerable symptoms,
 Marked loss of function and
 Severe restriction of daily activities.

88
 For OA of the hip and knee in middle-aged and older patients, total joint replacement by modern techniques
promises improvement lasting for 15 years or longer.
 Similar operations for the shoulder, elbow and ankle are less successful but techniques are improving year by
year.
Arthrodesis
Arthrodesis is still a reasonable choice if the stiffness is acceptable.
Complications of OA APL-93

 Capsular herniation
Osteoarthritis of the knee is sometimes associated with a marked effusion and herniation of the posterior capsule
(Baker’s cyst).
 Loose bodies
Cartilage and bone fragments may give rise to loose bodies, resulting in episodes of locking.
 Locking of joint.
 Joint destruction / Deformed joint /FFD,
 Rotator cuff dysfunction
Osteoarthritis of the acromioclavicular joint may cause rotator cuff impingement, tendinitis or cuff tears.
 Spinal stenosis
Longstanding hypertrophic OA of the lumbar apophyseal joints may give rise to acquired spinal stenosis. The
abnormality is best demonstrated by CT and MRI.
 Spondylolisthesis
In patients over 60 years of age, destructive OA of the apophyseal joints may result in severe segmental instability
and spondylolisthesis (so called ‘degenerative’ spondylolisthesis, which almost always occurs at L4/5).

89
 OA of Hip
apl-522

 When no underlying cause is apparent, the term ‘Primary osteoarthritis’ is used. {50%}
Some preceding disorder that leads to articular cartilage damage:
 Obesity,
 Genetics and heredity,
 Occupation involving prolonged standing / sports,
 Multiple endocrinal disorders / Multiple metabolic disorders.
 Obvious underlying cause of ‘Secondary osteoarthritis’:

X-ray findings:

1) Earliest sign is a decreased joint space, usually maximal in the superior weight bearing region but
sometimes affecting the entire joint.
2) Later signs are subarticular sclerosis, cyst formation and osteophytes.

90
 Cartilage softening and thinning are There is a vascular reaction and new-bone formation in the
greatest in the zone of maximal subchondral bone as well as osteophytic growth at the margins of the
stress. joint. These changes, as well as subchondral cyst formation,

Secondary osteoarthritis

(a) After Perthes’ (b) After slipped upper (c) After congenital (d) After rheumatoid (e) Bilateral in a patient with
disease. femoral epiphysis. subluxation. disease. multiple epiphyseal
dysplasia.

Q) Treatment of OA of Hip?
a) Conservative:
 Analgesics and anti-inflammatory drugs may be helpful, and warmth is soothing.
 Patient is encouraged to use a walking stick and to try to preserve movement and stability by non-
weightbearing exercises.
 Activities are adjusted so as to reduce stress on the hip.

b) Operative:
 Indications for operation are:
(1) Progressive increase in pain,
(2) Severe restriction of activities,
(3) Marked deformity and

91
 (4) Progressive loss of movement (especially abduction), together with
(5) X-ray signs of joint destruction.

 Operative procedures:
 Intertrochenteric realignment osteotomy,
 Joint replacement,
 Resurfacement arthroplasty,
 Arthrodesis,
 Osteochondroplasty

 Indications of Total joint replacement: APL-524

Usual case –
 Patient aged over 60 years,
 Long history of pain and
 Increasing disability.

 Operative treatment for OA hip in young patient:

 For preservation of articular cartilage, an intertrochanteric realignment osteotomy may be considered.
 If performed early, it can arrest or delay further cartilage destruction, and if the operation is well
planned it does not preclude later replacement arthroplasty.

 Arthrodesis of Hip:
 Arthrodesis of the hip is a practical solution for young adults with marked destruction of a single joint,
 Advantage - Operation guarantees freedom from pain and permanent stability,
 Disadvantages of restricted mobility and a significant incidence of later backache, as well as deformity and
discomfort in other nearby joints.

 Resurfacement arthroplasty:
 Birmingham hip resurfacing arthroplasty is emerging as an effective alternative to the conventional THR.
 Here only the diseased head is resurfaced and not resected. It is indicated in slightly younger patient.

92
 Intertrochanteric realignment osteotomy
Displacement osteotomy (Mc Murray’s):
moheswari-116

 This is indicated in severe osteoarthritis of hip with large

osteophytes.
 Direction of osteotomy is medially upwards, beginning at the
base of t h e greater trochanter and ending j u s t above the lesser
trochanter.

Osteotomy converts the shearing stress at the

fracture site into compressive forces, thus

enhancing fracture union.

Pauwell’s varus osteotomy:

It is done if osteoarthritis is due to coxa valga.
Valgus osteotomy:
This is more common and is done in adduction deformity of the
hip.

 Aims of the exercises in osteoarthritis hip and knee:

• To increase the range of movements.
• To increase stability and shock absorption.
• To prevent deformity.
• To improve posture.
• To reduce pain and stiffness.

 What are the indications of reconstructive surgery?

 Progressive intolerable pain in affected joint,
 Progressive loss of movement in affected joint.
 Severe restriction of daily activities,
 Marked instability,
 Marked deformity,
 FFD.

93
 Osteoarthritis of Knee
Ebn-678, APL-572

Outer bridge classification:

----- According to arthoscopy,
 Grade I: Softening and swelling of cartilage,
 Grade II: Fragmentation and fissuring of cartilage < ½ inch in diameter.
 Grade III: Fragmentation and fissuring of cartilage > ½ inch in diameter.
 Grade IV: Cartilage loss and exposure of underlying bone.

94
PRIMARY OSTEOARTHRITIS OF THE KNEE
(ALSO CALLED IDIOPATHIC)
Causation of primary osteoarthritis—obesity, genetics and heredity, occupation involving prolonged standing,
sports, multiple endocrinal disorders and multiple metabolic disorders.

SECONDARY OSTEOARTHRITIS OF THE KNEE

Causes for secondary osteoarthritis of the knee are as follows:
• Obesity.
• Valgus and varus deformities of the knee.
• Intra-articular fractures of the knee, etc.
• Rheumatoid arthritis, infection, trauma, TB, etc.
• Hyperparathyroidism.
• Hemophilia.
• Syringomyelia.
• Neurological disease like diabetes.
• Overuse of intra-articular steroid therapy.
Clinical Features
 Predominant symptom is pain which decreases on walking.
 The pain is poorly localized and is dull aching in nature.
 The patient has mild swelling of the knee joint and complains of early morning stiffness.
 The patient complains of early morning stiffness, which subsides over the day after some activity. Genu
varum deformity may be seen in very advanced cases.

95
  Minimal tenderness and coarse crepitus can be elicited.
 If there are loose bodies in a joint, the patient gives history of locking or giving way.
 Terminal movements of the knee are restricted.
 Minimal effusion may be present.
 Radiological examination of the knee joint:

Radiological features seen in osteoarthritis of the knee-

• Loss of joint space (due to destruction of articular cartilage).
• Sclerosis (due to increase cellularity and bone deposition).
• Subchondral cysts (due to synovial fluid intrusion into the bone).
• Osteophytes (due to revascularization of remaining cartilage and capsular traction).
• Bony collapse (due to compression of weakened bone).
• Loose bodies (due to fragmentation of osteochondral surface).
• Deformity and Malalignment (due to destruction of capsules and ligaments).

96
Treatment
Conservative Methods

 Range of motion and flexibility:

Joint stiffness and soft tissue shortening can be reduced with appropriate range of motion (ROM) and stretching
exercises.

 Quadriceps exercises:
Strengthening of quadriceps musculature with either isometric or isotonic, improvement in quadriceps strength,
knee pain, and function.

 Weight Loss:
Obesity is a risk factor for the development of OA,
When people walk, 3-6 times their body weight is transferred across the knee joint;

 Nonopioid analgesics – E.g. Acetaminophen: the drug of first choice. Up to 4 gm/day can be given.

 NSAIDs: If patients fail to respond to paracetamol or other oral or topical analgesics, then the use of an NSAID is
indicated.

 Food supplementation:
Glucosamine and Chondroitin sulfate: Can reduce 20-25 percent pain in mild to moderate OA. Over the counter food
supplements, 1500 mg/day for at least 3 months.

 Intra-articular steroids:
This is indicated if there is effusion and there are signs of inflammation.
Intra-articular corticosteroid injections will often relieve pain, but this is a stopgap, and not a very good one,
because repeated injections may permit (or even predispose to) progressive cartilage and bone destruction.

 Viscosupplementation:
Injection of hyaluronic acid into the joint. Once a week for 3 weeks. Adverse reactions in 2-3 percent.
New forms of medication have been introduced in recent years, particularly the oral administration of glucosamine
and intra-articular injection of hyalourans.

97
 Indications for surgery for OA of Knee:
• Pain refractory to conservative measures.
• History of frequent locking episodes.
• Hemarthrosis due to loose bodies or osteochondral fractures.
• Progressive Deformity, usually genu varum.
• Joint instability.
• Progressive limitation of knee motion.
Arthroscopic washouts:
With trimming of degenerate meniscal tissue and osteophytes, may give temporary relief; this is a useful measure
when there are contraindications to reconstructive surgery.
Realignment osteotomy:

Valgus high tibial osteotomy

 Is often successful in relieving symptoms and staving off the need for ‘end-stage’ surgery.
 The ideal indication is a ‘young’ patient (under 50 years) with a varus knee and osteoarthritis confined to the
medial compartment: a high tibial valgus osteotomy will redistribute weight to the lateral side of the joint.
Replacement arthroplasty
Is indicated in older patients with progressive joint destruction. This is usually a ‘resurfacing’ procedure, with a
metal femoral condylar component and a metal-backed polyethylene table on the tibial side.
Arthrodesis
Is indicated only if there is a strong contraindication to arthroplasty (e.g. previous infection) or to salvage a failed
arthroplasty.

98
 RHEUMATOID ARTHRITIS
APL – 59

 Rheumatoid arthritis (RA) is the most common cause of chronic inflammatory joint disease.
 The most typical features are -
 Symmetrical polyarthritis and
 Tenosynovitis,
 Morning stiffness,
 Elevation of the erythrocyte sedimentation rate (ESR) and
 Appearance of autoantibodies that target immunoglobulins (rheumatoid factors) in the
serum.
Pathology
Rheumatoid arthritis is a systemic disease but the most characteristic lesions are seen in the synovium or within
rheumatoid nodules.
a) JOINTS AND TENDONS:
Synovium is engorged with new blood vessels and packed full of inflammatory cells. Pathological changes, if
unchecked, proceed in four stages.

Stage 1 – Pre- Stage 2 – Synovitis Stage 3 – Destruction Stage 4 – Deformity

clinical
Before RA becomes  Early changes are vascular Persistent inflammation causes Combination of
clinically apparent the congestion with new blood vessel joint and tendon destruction. articular destruction,
immune pathology is formation, proliferation of Articular cartilage is eroded, capsular stretching and
already beginning. synoviocytes and infiltration of the  Partly by proteolytic enzymes, tendon rupture leads to
subsynovial layers by polymorphs,  Partly by vascular tissue in the progressive instability
lymphocytes and plasma cells. folds of the synovial reflections, and deformity of the
 Thickening of the capsular and joints.
structures, villous formation of the  Partly due to direct invasion of
synovium and a cell-rich effusion into the cartilage by a pannus of
the joints and tendon sheaths. granulation tissue creeping over
the articular surface.

99
 b) EXTRA ARTICULAR TISSUES:
 Rheumatoid nodules – small granulomatous lesion consisting of a central necrotic zone surrounded by a radially
disposed palisade of local histiocytes,
 Lymphadenopathy - Not only the nodes draining inflamed joints, but also those at a distance such as the
mediastinal nodes, can be affected.
 Vasculitis - Involvement of the skin, including nailfold infarcts,
 Muscle weakness - Muscle weakness is common. It may be due to a generalized myopathy or neuropathy,
localized sensory and motor symptoms can also result from nerve compression by thickened synovium (e.g. carpal
tunnel syndrome).
 Visceral disease - The lungs, heart, kidneys, gastrointestinal tract and brain are sometimes affected. Ischaemic
heart disease and osteoporosis are common complications.
Clinical features
Onset of RA is usually insidious, with symptoms emerging over a period of months.
In the early stages –
 Polysynovitis, with soft-tissue swelling and stiffness.
 Typically, a woman of 30–40 years complains of pain, swelling and loss of mobility in the proximal
joints of the fingers.
 There may be a previous history of ‘muscle pain’, tiredness, loss of weight and a general lack of well-
being.
 As time passes, the symptoms ‘spread’ to other joints – the wrists, feet, knees and shoulders in order of
frequency.
 Classic feature is generalized stiffness after periods of inactivity, and especially after rising from bed in
the early morning.
 This early morning stiffness typically lasts longer than 30 minutes.

100
Early features of swelling and stiffness of Late hand deformities Occasionally rheumatoid disease
the proximal finger joints and the wrists. starts with synovitis of a single large
joint (in this case the right knee).

Extra-articular features include subcutaneous nodules Features of tendon ruptures

In the later stages-
 Joint deformity becomes increasingly apparent and the acute pain of synovitis is replaced by the more
constant ache of progressive joint destruction.
 The combination of joint instability and tendon rupture produces the typical ‘rheumatoid’ deformities:
 Ulnar deviation of the fingers,
 Radial and Volar displacement of the wrists,
 Valgus knees,
 Valgus feet and
 Clawed toes.
 Joint movements are restricted and often very painful.
 About a third of all patients develop pain and stiffness in the cervical spine.

Investigations
A) Blood investigations:
 Hb: Normocytic, hypochromic anaemia;
 Abnormal erythropoiesis due to disease activity.
 Chronic gastrointestinal blood loss caused by non-steroidal anti-inflammatory drugs.
 ESR & CRP: In active phases the ESR and CRP concentration are usually raised.
 Serological tests:

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  Rheumatoid factor are positive in about 80 percent of patients and
 Antinuclear factors are present in 30 percent.
 Anti-CCP antibodies have added much greater specificity.

A positive test for ‘Rheumatoid factor’ in the absence of the above features is not sufficient evidence of
rheumatoid arthritis, nor does a negative test exclude the diagnosis if the other features are all present.

B) Imaging:
X-rays

Most individuals have evidence of erosions within 2 years.

Early on, x-rays show only the Later stages are marked by the appearance In advanced disease, articular
features of synovitis: soft-tissue of marginal bony erosions and narrowing destruction and joint deformity are
swelling and peri-articular of the articular space, especially in the obvious.
osteoporosis. proximal joints of the hands and feet.
 Flexion and extension views of the cervical spine often show subluxation at the atlanto-axial or mid-cervical
levels; surprisingly, this causes few symptoms in the majority of cases.

Ultrasound scanning and MRI

 Use of other imaging techniques to look at soft-tissue changes and early erosions within joints has become more
common.
 Ultrasound can be particularly useful in defining the presence of synovitis and early erosions.

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C) Synovial biopsy:
 Synovial tissue may be obtained by needle biopsy, via the arthroscope, or by open operation.
 Unfortunately, most of the histological features of rheumatoid arthritis are non-specific.

Presence of tenderness on squeezing across all metacarpophalangeal or metatarsophalangeal joints,

early morning stiffness of at least 30 minutes and a raised ESR are highly suggestive of a diagnosis of
rheumatoid arthritis.

Q) Differential diagnosis of Rheumatoid arthritis?

Differential diagnosis of polyarthritis;
 Seronegative inflammatory polyarthritis: including psoriatic arthritis, adult Still’s disease, systemic
lupus erythematosus and other connective-tissue diseases.

 Ankylosing spondylitis: This is primarily an inflammatory disease of the sacroiliac and intervertebral
joints, causing back pain and progressive stiffness;

 Reiter’s disease: The larger joints and the lumbosacral spine are the main targets. There is usually a
history of urethritis or colitis and often also conjunctivitis.

 Polyarticular gout: Tophaceous gout affecting multiple joints can, at first sight, be mistaken for
rheumatoid arthritis.

 Calcium pyrophosphate deposition: disease This condition is usually seen in older people. Typically it
affects large joints, but it may occur in the wrist and metacarpophalangeal joints as well.

 Sarcoidosis: Sarcoid disease sometimes presents with a symmetrical small-joint polyarthritis and no
bone involvement;

 Osteoarthritis: Polyarticular osteoarthritis (OA), which typically involves the finger joints, is often
mistaken for RA. OA always involves the distal interphalangeal joints and causes a nodular arthritis with
radiologically obvious osteophytes, whereas RA affects the proximal joints of the hand and causes
predominantly erosive features.

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 (a) mainly the proximal joints were (b) the distal joints were the worst (c) There were asymmetrical nodular
affected (rheumatoid arthritis); (Heberden’s osteoarthritis); swellings around the joints (gouty
tophi).

Treatment
 Multidisciplinary approach is needed from the beginning: ideally the therapeutic team should include a
rheumatologist, orthopaedic surgeon, physiotherapist, occupational therapist, orthotist and social worker.
 Poor prognosis is associated with female sex, multiple joint involvement, high ESR and CRP, positive RF and
anti-CCP, younger age and the presence of erosions at diagnosis.
 Prolonged rest and immobility is likely to weaken muscles and lead to a worse prognosis.

PRINCIPLES OF MEDICAL MANAGEMENT

Medical treatment is guided by the principle that inflammation should be reduced rapidly and aggressively.
Treatment should be aimed at controlling inflammation as rapidly as possible.
 Steroids:
 Use of corticosteroids for their rapid onset (initially oral doses of 30 mg of prednisolone or 120 mg
i.m. methylprednisolone may be used). Steroids should be rapidly tapered to prevent significant side effects.
 Injection of long acting corticosteroid preparations into inflamed joints and tendon sheaths. It is
sometimes feared that such injections may themselves cause damage to articular cartilage or tendons. However,
there is little evidence that they are harmful, provided they are used sparingly and with full precautions against
infection.
 DMARD:
 Disease-modifying antirheumatic drugs (DMARDs) should be started at this time. The first choice is
now Methotrexate at doses of 10–25 mg/week. This may be used initially alone or in combination with
Sulfasalazine and Hydroxychloroquine. Leflunomide can also be considered if methotrexate is not tolerated.

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 TNF inhibitors:
 If there is no satisfactory response to DMARDs, it is wise to progress rapidly to biological therapies
such as the TNF inhibitors infliximab, etanercept and adalimumab.
 NSAIDs:
 Control of pain and stiffness with non-steroidal anti-inflammatory drugs (NSAIDs) may be needed,
maintaining muscle tone and joint mobility.

SURGICAL MANAGEMENT
If medical treatment and physiotherapy / occupational therapy fail to restore and maintain function, operative
treatment is indicated.
 Early RA: Soft-tissue procedures (synovectomy, tendon repair or replacement and joint stabilization); in some
cases osteotomy may be more appropriate.
 Late RA: severe joint destruction, fixed deformity and loss of function are clear indications for reconstructive
surgery.

Complications of RA
 Fixed deformities:
The perils of rheumatoid arthritis are often the commonplace ones resulting from ignorance and neglect.
 Muscle weakness:
Even mild degrees of myopathy or neuropathy, when combined with prolonged inactivity, may lead to profound
muscle wasting and weakness.
 Joint rupture:
Occasionally the joint lining ruptures and synovial contents spill into the soft tissues.
 Infection:
Patients with rheumatoid arthritis – and even more so those on corticosteroid therapy – are susceptible to infection.
 Systemic vasculitis:
Vasculitis is a rare but potentially serious complication.
 Spinal cord compression:
This is a rare complication of cervical spine (atlanto-axial) instability.
 Amyloidosis:
This is another rare but potentially lethal complication of longstanding rheumatoid arthritis. The patient presents
with proteinuria and progressive renal failure.

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 Rheumatoid Factor {RF}:
 It is a auto antibody,
 Test to detect RF: Rose Waaler test.
 Following conditions where RF is found raised:
 Rheumatoid arthritis 80%,
 SLE,
 Sjogren’s syndrome 70%,
 Interstitial pulmonary fibrosis,
 Chronic liver disease,
 Tuberculosis,
 Leprosy,
 Sarcoidosis,
 Leukaemia.

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 Juvenile Idiopathic Arthritis (JIA)
APL/9 - 74
--- It can be defined as –
 Inflammatory arthritis,
 Duration > 3 months,
 Occurs in children < 16 yrs of age.
Types:
1. Systemic JIA / Still’s disease.
2. Pauciarticular JIA {Common 60- 70%}
3. Polyarticular JIA,
4. Seronegative spondyloarthropathy / Juvenile AS.

Treatment
General treatment:
 Systemic treatment is similar to that of rheumatoid arthritis, including the use of second-line drugs
such as hydroxychloroquine, sulfasalazine or low-dose methotrexate for those with seropositive juvenile RA.
 Corticosteroids should be used only for severe systemic disease and for chronic iridocyclitis
unresponsive to topical therapy.
Local treatment:
 The priorities are to prevent stiffness and deformity.
 Night splints may be useful for the wrists, hands, knees and ankles; prone lying for some period of
each day may prevent flexion contracture of the hips.
 Between periods of splinting, active exercises are encouraged;
 Fixed deformities may need correction by serial plasters or by a spell in hospital on a continuous
passive motion (CPM) machine;

Complications:
 Ankylosis
 Growth defects
 Fractures
 Iridocyclitis
 Amyloidosis

107
 Gout
CRYSTAL DEPOSITION DISORDERS
APL-77, EBN - 597

Crystal deposition disorders are a group of conditions characterized by the presence of crystals in and around joints,
bursae and tendons.
Three clinical conditions in particular are associated with this phenomenon:
 • Gout
 • Calcium pyrophosphate dihydrate (CPPD) deposition disease
 • Calcium hydroxyapatite (HA) deposition disorders.

GOUT
Gout is a disorder of purine metabolism characterized by hyperuricaemia, deposition of monosodium urate
monohydrate crystals in joints and peri-articular tissues and recurrent attacks of acute synovitis.
Late changes include cartilage degeneration, renal dysfunction and uric acid urolithiasis.

Characteristics:
More widespread in men than in women (the ratio may be as high as 20:1);
Rarely seen before the menopause in females.

Pathology
Hyperuricaemia:
 Nucleic acid and Purine metabolism normally proceeds to the production of hypoxanthine and xanthine; the final
breakdown to uric acid is catalysed by the enzyme xanthine oxidase.
 Monosodium urate appears in ionic form in all the body fluids; about 70 percent is derived from endogenous
purine metabolism and 30 percent from purine-rich foods in the diet.
 It is excreted (as uric acid) mainly by the kidneys and partly in the gut.

Gout:
Urate crystals are deposited in minute clumps in connective tissue, including articular cartilage; the commonest
sites are the small joints of the hands and feet.

Tophi (L. Tophus = porous stone):

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With the passage of time, urate deposits may build up in joints, peri-articular tissues, tendons and bursae; common
sites are around the metatarsophalangeal joints of the big toes, the Achilles tendons, the olecranon bursae and the
pinnae of the ears. These clumps of chalky material are called Tophi.

Classification
Gout is often classified into ‘primary’ and ‘secondary’ forms.
 Primary gout (95 per cent):
Occurs in the absence of any obvious cause and may be due to constitutional under-excretion (the vast majority) or
overproduction of urate.

 Secondary gout (5 per cent):

Results from prolonged hyperuricaemia due to acquired disorders such as Myeloproliferative diseases,
administration of Diuretics or Renal failure.

‘Primary’ hyperuricaemia may develop gout only when secondary factors are
introduced – for example obesity, alcohol abuse, or treatment with diuretics or
salicylates which increase tubular reabsorption of uric acid.

Predisposing factors:

109
Clinical features
Symptoms:
 Patients are usually men over the age of 30 years;
 Women are seldom affected until after the menopause.
 H/O uncontrolled administration of diuretics or aspirin.

Typical ‘gouty type’, with his rubicund face, large olecranon bursae and small subcutaneous tophi over the
elbows. Tophaceous gout affecting the hands and feet; the swollen big toe joint is particularly characteristic.

 Acute gout:
 Sudden onset of severe joint pain which lasts for a week or two before resolving completely is typical of
acute gout.

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  Commonest sites are the metatarsophalangeal joint of the big toe, the ankle and finger joints, and the
olecranon bursa.
 Joint feels hot and extremely tender, suggesting a cellulitis or septic arthritis.
 Sometimes the only feature is acute pain and tenderness in the heel or the sole.
 Chronic gout:
 Recurrent acute attacks may eventually merge into polyarticular gout.
 Joint erosion causes chronic pain, stiffness and deformity; if the finger joints are affected, this may be
mistaken for rheumatoid arthritis.
 Tophi may appear around joints over the olecranon, in the pinna of the ear and – less frequently – in
almost any other tissue. A large tophus can ulcerate through the skin and discharge its chalky material.
 Renal lesions include calculi, due to uric acid precipitation in the urine, and parenchymal disease due to
deposition of monosodium urate from the blood.

X-rays

Typical picture is of large periarticular excavations – tophi consisting of uric acid deposits.
 During the acute attack x-rays show only soft-tissue swelling.
 Chronic gout may result in joint space narrowing and secondary osteoarthritis.
 Tophi appear as characteristic punched-out ‘cysts’ or deep erosions in the para-articular bone ends;
Investigation
Laboratory investigations show
 Leucocytosis and ESR is increased.

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 Synovial fluid study is done under polarized microscopy for the presence of monosodium urate crystals. This is
the most important diagnostic method

Hyperuricaemia is not ‘diagnostic’ and is often seen in normal middle-aged men.

Differential diagnosis
Infection: Cellulitis, septic bursitis, an infected bunion or septic arthritis must all be excluded, if necessary by
immediate joint aspiration.
Reiter’s disease This may present with acute pain and swelling of a knee or ankle,
Pseudogout Pyrophosphate crystal deposition may cause an acute arthritis indistinguishable from gout – except
that it tends to affect large rather than small joints.
Rheumatoid arthritis (RA) Polyarticular gout affecting the fingers may be mistaken for rheumatoid arthritis, and
elbow tophi for rheumatoid nodules. In difficult cases biopsy will establish the diagnosis. RA and gout seldom
occur together.

Treatment
Acute attack
 Acute attack should be treated by resting the joint, applying ice packs if pain is severe, and giving full doses of a
non-steroidal anti-inflammatory drug (NSAID).
 A tense joint effusion may require aspiration and intra-articular injection of corticosteroids.
 Oral corticosteroids are sometimes used for patients who cannot tolerate NSAIDs or in whom NSAIDs are
contraindicated.

Interval therapy
 Between attacks, attention should be given to simple measures such as losing weight, cutting out alcohol and
eliminating diuretics.
 Uricosuric drugs (probenecid or sulfinpyrazone) can be used if renal function is normal.
 Allopurinol, a xanthine oxidase inhibitor, is usually preferred, and for patients with renal complications or
chronic tophaceous gout allopurinol is definitely the drug of choice.

Urate-lowering drugs should never be started before the acute attack has
completely subsided, and they should always be covered by an anti-inflammatory
preparation or colchicine, otherwise they may actually prolong or precipitate an
acute attack.

112
Surgery
Ulcerating tophi that fail to heal with conservative treatment can be evacuated by curettage; the wound is left open
and dressings are applied until it heals.

113
 CALCIUM PYRO-PHOSPHATE DIHYDRATE {CPPD} ARTHROPATHY
(PSEUDOGOUT)
APL- 80

‘CPPD deposition’ encompasses three overlapping conditions:

(1) Chondrocalcinosis – the appearance of calcific material in articular cartilage and menisci;
(2) Pseudogout – a crystal-induced synovitis; and
(3) Chronic pyrophosphate arthropathy – a type of degenerative joint disease.

Acute synovitis (pseudogout)

 The patient, typically a middle-aged woman, complains of acute pain and swelling in one of the larger
joints – usually the knee.
 Untreated the condition lasts for a few weeks and then subsides spontaneously.
 X-rays may show signs of chondrocalcinosis, and the diagnosis can be confirmed by finding positively
birefringent crystals in the synovial fluid.

Chronic pyrophosphate arthropathy

The patient, usually an elderly woman, presents with polyarticular ‘osteoarthritis’ affecting the larger joints (hips,
knees) and unusual joints, such as the ankles, shoulders, elbows and wrists where osteoarthritis is seldom seen.

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X-rays

 Calcium pyrophosphate crystals may be deposited in cartilage,

causing calcification of menisci.
 X-ray of the right knee showed the characteristic features
of articular calcification, loose bodies in the joint and large
trailing osteophytes around the patellofemoral joint.
 Characteristic x-ray features arise from a combination of-
(1) Intra-articular and peri-articular calcification,
(2) Degenerative arthritis in distinctive sites.

Treatment
The treatment of pseudogout is the same as that of acute gout: rest and high-dosage anti-inflammatory therapy.
In elderly patients, joint aspiration and intra-articular corticosteroid injection is the treatment of choice as these
patients are more vulnerable to the side effects of non-steroidal anti-inflammatory drugs.

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 Ankylosing Spondylitis.
APL- 66,

 Like rheumatoid arthritis, this is a generalized chronic inflammatory disease, but its effects are seen mainly in
the spine and sacroiliac joints.
 Ankylosing spondylitis is the most common seronegative spondyloarthropathy to affect the cervical spine.
Characteristics:
 It is characterized by pain and stiffness of the back, with variable involvement of the hips and
shoulders and (more rarely) the peripheral joints.
 Males are affected more frequently than females (estimates vary from 2:1 to 10:1) and the usual age
at onset is between 15 and 25 years.
 There is a strong tendency to familial aggregation and association with the genetic marker HLA-B27.
Cause
 Considerable evidence for regarding ankylosing spondylitis (AS) as a ‘Genetically Determined
Immunopathological Disorder’.
 The disease is much more common in family members of patients than in the general population – HLA-
B27 is present in over 95 per cent of Caucasian patients and in half of their first-degree relatives.
Pathology
 There are two basic lesions:
1) Synovitis of diarthrodial joints and
2) Inflammation at the fibro-osseous junctions of syndesmotic joints and tendons.
 The preferential involvement of the insertion of tendons and ligaments (the entheses) has resulted in the
unwieldy term Enthesopathy.
 Pathological changes proceed in three stages:
(1) An inflammatory reaction with cell infiltration, granulation tissue formation and erosion of
adjacent bone;
(2) Replacement of the granulation tissue by fibrous tissue; and
(3) Ossification of the fibrous tissue, leading to ankylosis of the joint.
 Inflammation of the fibro-osseous junctions affects the intervertebral discs, sacroiliac ligaments, symphysis
pubis, manubrium sterni and the bony insertions of large tendons.
 Ossification across the surface of the disc gives rise to small bony bridges or syndesmophytes linking adjacent
vertebral bodies.

Basic pathology:
 Joints:
Synovial joints: synovitis,
Syndesmotic joints: inflammation -> fibrosis.
 Enthesopathy: inflam. at the insertion of tendons.
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Clinical features
Symptoms:
 The disease starts insidiously: a teenager or young adult complains of backache and stiffness recurring at
intervals over a number of years.
 ‘Simple mechanical back pain’, but the symptoms are worse in the early morning and after inactivity.
Referred pain in the buttocks and thighs may appear as ‘sciatica’.
 Gradually pain and stiffness become continuous and other symptoms begin to appear: general fatigue, pain
and swelling of joints, tenderness at the insertion of the Achilles tendon, ‘foot strain’, or intercostal pain and
tenderness.
Cardinal clinical feature is marked stiffness of the spine.

(a) This patient manages to stand upright by keeping (b) It looks as if he can bend down to touch his toes, but his back is
his knees slightly flexed. rigid and all the movement takes place at his hips.
 Over 10 percent of cases the disease starts with an asymmetrical inflammatory arthritis – usually of the hip,
knee or ankle – and it may be several years before back pain appears. Atypical onset is more common in women,
who may show less obvious changes in the sacroiliac joints.
Signs:
 Early on there is little to see apart from slight flattening of the lower back and limitation of extension in
the lumbar spine.
 There may be diffuse tenderness over the spine and sacroiliac joints, or (occasionally) swelling and
tenderness of a single large joint.
 In established cases the posture is typical: loss of the normal lumbar lordosis, increased thoracic
kyphosis and a forward thrust of the neck; upright posture and balance are maintained by standing with the hips and
knees slightly flexed, and in late cases these may become fixed deformities.

117
  Spinal movements are diminished in all directions, but loss of extension is always the earliest and the
most severe disability. ‘Wall test’: the patient is asked to stand with his back to the wall; heels, buttocks, scapulae
and occiput should all be able to touch the wall simultaneously.

Ankylosing spondylitis – operative treatment

Spinal osteotomy is occasionally performed to correct a severe, rigid deformity.
(a) Before operation this man could see only a (b) After osteotomy his back is still rigid but his posture,
few paces ahead; function and outlook are improved.

 Marked loss of cervical extension may Restrict the line of vision to a few paces.
 Chest expansion, which should be at least 7 cm in young men, is often markedly decreased.
 Peripheral joints (usually shoulders, hips and knees) are involved in over a third of the patients; features
of inflammatory arthritis – swelling, tenderness, effusion and loss of mobility.
Extraskeletal manifestations of AS:
 General fatigue and loss of weight are common.
 Acute anterior uveitis occurs in about 25 percent of patients; it usually responds well to treatment but, if
neglected, may lead to permanent damage including glaucoma.
 Other extraskeletal disorders, such as-
 Aortic valve disease,
 Carditis and
 Pulmonary fibrosis (apical).

118
Q) On Examination?

Look:
 From the front:
 Shoulder height / slight drooping of shoulder,
 Apparent shortening of lower limbs,

 From the side:

 Thoracic Kyphosis / Forward bending of upper trunk,
 Obliteration of lumber lordosis,
 Flexion attitude of hip & knee,

 From the back:

 Mild scoliosis of thoracolumber spine,
 Squating difficultly possible / not possible.

119
Feel:
 Temperature:
 Tenderness:
 Measure chest expansion:

 Trendelenburg test:

120
  Wall test:

 Schober’s test:
Schober’s test Modified Schober’s test

 Positioning the tape measure with 10 cm mark level at dimples

 With the patient upright, select two bony of Venus / post sup iliac spines,
points 10 cm apart and mark the skin ;  Mark the skin at 0 and 15 cm,
 Anchor the top of the tape with a finger and ask the patient to
 as the patient bends forward, the two flex forward as he can,
points should separate by at least a further 5  Note where the 15 cm mark strikes the tape & find out the
cm. increment.
 Normal increment is about 6 – 7 cm.

 Neurovascular status:

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Move:
 ROM of Lumber, Thoracic and Cervical spine:
 Thomas test:
 ROM of Hip:
 Exam of SI joints:

• Gaenslen's test:
The hip and the knee of the joints of the opposite side are
flexed to fix the pelvis, and the hip joint of t he side under
test is hyperextended over the edge of the table. This will
exert a rotational strain over the sacro-iliac joint and give
rise to pain.

• Pump-handle test:
With the patient lying supine, the examiner flexes his hip
and knee completely, and forces the affected knee across the
chest so as to bring it close to the opposite shoulder. This
will cause pain on the affected side.

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Imaging
 X-rays
Cardinal sign:
X ray SI Joint Ferguson view:
Often the earliest – is Haziness and ‘Fuzziness’ of the sacroiliac joints
→ which progress to bony ankylosis.
• Haziness of t he saero-iliac joints
• Irregular subchondral erosions in SI joints.
• Sclerosis of t he articulating surfaces of SI j oints
• Widening of t he sacro-iliac joint space
• Bony ankylosis of t he sacro-iliac joints.
Earliest vertebral change:
X ray LS Spine AP and Lat view.
 Flattening of the normal anterior concavity of the vertebral body
(‘squaring’).
 ‘Squaring’ – Flattening of the normal anterior concavity of

vertebral body - due to combination of osteitis & repair.

 Reactive sclerosis caused by osteitis of the anterior corners of

vertebral bodies with subsequent erosion {Romanous lesion / Shiny

corner sign}, leading to ‘Squaring’ of the vertebral bodies.

Later:
 Ossification of the ligaments around the intervertebral discs
produces delicate bridges (syndesmophytes) between adjacent vertebrae.
 Bridging at several levels gives the appearance of a ‘Bamboo spine’.
 Dagger sign – ossification of supraspinatous and infraspinatous
ligament.

Peripheral joints:
May show erosive arthritis or progressive bony ankylosis.
Hyperkyphosis of the thoracic spine:
Due to wedging of the vertebral bodies.
Osteoporosis is common in longstanding cases.

123
 MRI
MRI allows detailed investigation of sacroiliac joints and may
show typical erosions and features of inflammation such as bone
oedema.

Gadolinium contrast can be used to demonstrate inflammatory

lesions in other areas of the spine.

 Blood Tests:
 ESR and CRP: are usually elevated during active phases of the disease.
 HLA-B27: is present in 95 percent of cases.
 RA Test / Serological tests for rheumatoid factor: are usually negative.

 HLA B 27 / Human Leucocyte Antigen B 27:

 It is a class I surface antigen, encoded by B locus in MHC on chromosome 6 and presents antigenic
peptides to T cells.
 Conditions where HLA B27 positive found:
 Ankylosing spondylitis (90%),
 Reactive arthritis / Reiter’s syndrome,
 Psoriatic arthritis,
 Ulcerative colitis associated with spondyloarthritis.
 Acute anterior uveitis and iritis.

124
Differential Diagnosis OF AS
 Diffuse Idiopathic Skeletal Hyperostosis (DISH) / Forestier disease.
 Common disorder mainly in older men, characterized by widespread ossification of ligaments and
tendon insertions,
 No inflammatory disease,
 Spinal pain and stiffness seldom present,
 SI joints not eroded,
 ESR is normal.

 Other seronegative spondyloarthropathies:

 Reiter disease {Genitourinary and ocular inflammation},
 Psoriatic arthritis,
 Ulcerative colitis / Crohn’s disease.

125
 AS is not usually as damaging as Rheumatoid arthritis and
Treatment OF AS: many patients continue to lead an active life.

 Principles of Treatment consists of:

(1) General measures to maintain satisfactory posture and preserve movement;
(2) Anti-inflammatory drugs to counteract pain and stiffness;
(3) Use of TNF inhibitors for severe disease; and
(4) Operations to correct deformity or restore mobility.
 General measures:
 Patients are encouraged to remain active and follow their normal pursuits as far as possible.
 They should be taught how to maintain satisfactory posture and urged to perform spinal extension
exercises every day.

 Swimming, dancing and gymnastics are ideal forms of recreation.

 Rest and immobilization are contraindicated because they tend to increase the general feeling of stiffness.

126
 Non-steroidal anti-inflammatory drugs:
They do control pain and counteract soft-tissue stiffness, thus making it possible to benefit from exercise and
activity.
 Steroids:
Used when NSAIDs are non effective.
 Local Steroid injection:
-- For persistent synovitis and enthesopathy.
 DMARDs:
-- Extremely effective in case of peripheral form of AS.
 TNF inhibitors:
 These therapies {TNF inhibitors - Infliximab, Etanercept and Adalimumab} are generally reserved for
individuals who have failed to be controlled with non-steroidal anti-inflammatory drugs.
 With the introduction of the TNF inhibitors it has become possible to treat the underlying inflammatory
processes active in AS.
 Operation:
 Incidence of infection is higher than usual and patients may need prolonged rehabilitation.
 Significantly damaged hips can be treated by joint replacement, though this seldom provides more than
moderate mobility.
 If spinal deformity is combined with hip stiffness, hip replacements (permitting full extension) often
suffice.
 Deformity of the spine may be severe enough to warrant lumbar or cervical osteotomy.

Complications
 Spinal fractures:
 The spine is often both rigid and osteoporotic; fractures may be caused by comparatively mild injuries.
 The commonest site is C5–7.
 Hyperkyphosis:
In longstanding cases the spine may become severely kyphotic, so much so that the patient has difficulty lifting his
head to see in front of his feet.
 Spinal cord compression:
 This is uncommon, but it should be thought of in patients who develop longtract symptoms and signs.
 It may be caused by atlanto-axial subluxation or by ossification of the posterior longitudinal ligament.
 Lumbosacral nerve root compression:
Patients may occasionally develop root symptoms, including lower limb weakness and paraesthesia, in addition to
their ‘usual’ pelvic girdle symptoms.

127
AVN

128
 AVN.

Q) What is AVN / Osteonecrosis? Tell about the pathogenesis?

AVN / Osteonecrosis:
Death of bone and bone marrow as a result of deprivation of it’s blood supply.

Pathogenesis:
Four different ways ---
 Severence / cut off the local blood supply,
 Venous stasis → Retrograde arteriolar stoppage,
 Intra-vascular thrombosis,
 Compression of capillaries and sinusoids by
marrow oedema / swelling.

Q) Some examples:
 AVN of Scaphoid ---> Preiser’s disease,
 AVN of Lunate ---> Kienbock disease,
 AVN of Capitulum ---> Panner’s disease,
 AVN of head of Femur --->
 AVN of Talus --->
 AVN of Calcaneum --->
 AVN of Navicular ---> Kohler disease.

AVN of HOF AVN of Head of AVN of Medial Condyle of AVN of Talus AVN of Capitulum.
the Femur,
Humerus

129
Q) What are the common sites of AVN of bone?
Sites particularly vulnurable to ischaemic necrosis / Sites of AVN:
 Femoral head,
 Femoral condyle,
 Head of Humerus,
 Capitulum of Humerus,
 Proximal part of Scaphoid,
 Lunate,
 Proximal part of Talus.

Q) Write in short about the causes of AVN?

Causes of AVN:
 Primary:
Bone cells die after 12–48 hours of anoxia.
- Idiopathic.

 Secondary:
o Traumatic AVN:
-- eg: Displaced # NOF, Dislocation of Hip, Scaphoid ≠, Talus ≠.

o Non-traumatic AVN:
 Haemoglobinopathy: Sickle cell disease
 Infection: Osteomyelitis, Septic arthritis
 Storage disease: Gaucher’s disease,
 Caisson disease: Dysbaric osteonecrosis
 Others:
o Perthe’s disease,
o Pregnancy,
o Ionizing radiation,
o SLE,
o Steroid therapy / Cortisone adminstration,
o Alcohol abuse,
o Anaphylactic shock,
 Coagulation disorders:
o Thrombocytopanic purpura.
o Familial thrombophilia,
o ↑ fibrinolysis.

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Q) Short note: Staging of AVN of Head of Femur. apl (n):531, R-47

Ficat and Arlet’s ARCO Shimuzu Classification

Radiographic Staging Association Research Circulation based of MRI
Osseous
 Stage : 0 o Stage : 0  Grade : I
 No symptom, → Patient is asymptomatic, < 1/3 of femoral
 Radiography normal → All clinical inv. normal, head is involved.
→ Biopsy: osteonecrosis.
Location: medial
 Stage : 1 1/3 of wt. bearing
o Stage : 1
 Little or no pain, area of HOF.
→ X ray: normal,
 Radiography shows no Prognosis: good.
→ MRI or Radionuclide scan:
abnormality. osteonecrosis.
 Grade : II
 Stage : 2 o Stage : 2 ½ of the
 Mild pain, → X ray & / or MRI – Early sign of femoral head is
 Normal head contour. osteonecrosis, involved.
 2A : Sclerosis or → No distortion of bone shape, Location:
Subchondral cyst. 1/3 to 2/3 of
o Stage : 3
 2B : Thin Subchondral ≠ / wt. bearing area,
→ X ray : Crescent sign
Crescent sign – Necrotic Prognosis:
→ Femoral head: still spherical.
Segment. chance of collapse
30%.
o Stage : 4
 Stage : 3 → Sign of flattening or collapse of
 Collapse of Head, femoral head.  Grade : III

 Femoral head distortion, Large part of

 Loss of spherificity. o Stage : 5 femoral head,

→ Changes as above + loss of joint Location:
space (secondary OA). > 2/3 of wt.
 Stage : 4
 Acetabular change, bearing area,
o Stage : 6
 Joint space narrowing, Prognosis:
→ Changes as above + marked
 Signs of secondary OA. chance of collapse
destruction of articular surface.
70% within 3 years.

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 Avascular Necrosis of Head of Femur.
APL-528,103

Q) Clinical features of AVN of head of femur?

 Symptoms:
 H/O trauma over groin – symptoms may take months to appear.
 H/O taking steroid /alcohol / cytotoxic drug / immunosuppressive drugs,
 Children are affected in the conditions such as-
 Perthes’ disease,
 Sickle cell disease,
 Gaucher’s disease.
 Usual complain: Pain over the hip{>50% of cases affect both hips}
 Pain progresses over a period of 2 – 3 years to become quite severe,
 > 10% of cases condition is asymptomatic and discovered incidentally after x ray or MRI
during investigation for a systemic disorder.
 Signs:
 Patients walks with a limp,
 Postive trendelenburg sign,
 Thigh muscle wasting present,
 Limb may be 1 or 2 cm short,
 Movements of hip are restricted, particularly abduction & internal rotation.
 Sectoral sign: internal rotation is full with hip extended, but restricted in flexion --->
suggests pathology in the anterosuperior portion of femoral head, probably due to AVN of HOF.
 Torn acetabular labrum: in young person, pain on internal rotation with hip flexed may
indicate torn acetabular labrum.

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Q) Investigations for AVN of HOF? apl-106

o X ray:
 During early stages plain x ray is normal,
 1st signs appear only 6 – 9 months after the occurrence of bone death,

Articular cartilage (A) remains intact for a long time. The necrotic segment (B) has a texture similar to that of normal bone, but
it may develop fine cracks. New bone surrounds the dead trabeculae and causes marked sclerosis (C). Beyond this the bone
remains unchanged (D).
 Classic feature is increased sclerosis – increased radiographic density appear in the subchondral
bone,
 Trabecular failure in the necrotic segment,

 Thin tangential subchondral fracture line lies just below the articular surface the ‘crescent sign’.

 Earliest x-ray sign is a thin radiolucent crescent just below the convex articular surface where load bearing is

at its greatest.

 Crescent sign: thin radiolucent crescent just below the convex articular surface - thin
subchondral fracture line,
 Distortion / Collapse of articular surface of head of femur,
 Loss of joint space,

 Destruction of articular surface.

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 o MRI:
 1st sign is the band like low intensity signal on T1 weighted film,

(a) Before any change is discernible on the plain x-ray, MRI will (b) In this case the size of the ischaemic segment is
show a typical hypointense band in the T1 weighted image, much larger and the likelihood of bone crumbling
outlining the ischaemic segment beneath the articular surface. much greater.

 Band represents the reactive zone between living and dead bone & thus demarcates the
ischaemic segment,
 Diminished intensity in T1 weighted image,
 Location & extent of demarcated necrotic zone important for Grading of lesion,
 Site & size used to predict the progress of lesion,
 MRI shows characteristic changes in the marrow – a mean of 3.6 months after initiation of
steroid treatment {Sakamoto et al 1997}.
o Radioscintigraphy:
 Radionuclide scanning with 99mTc sulphur colloid is taken up in myeloid tissue may reveal an
avascular segment,

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  Most likely in traumatic avascular necrosis where a large segment of bone is involved or in
sickle cell disease where a ‘cold’ area contrasts significantly with high nuclide uptake – due to increased
erythroblastic activity.
o CT:
 Not very useful for diagnosing osteonecrosis,

 It may be useful in planning surgery.

Q) Treatment of osteonecrosis of Hip? APL-531

 Treatment of Post traumatic osteonecrosis:

 Young patient (< 40 years) or pt reluctant to perform hip replacement can be treated by Realignment
osteotomy with or without bone grafting of the necrotic segment,
 Older patient can be treated by partial or total joint replacement.

 Treatment of Non traumatic osteonecrosis: rahim-48

 Early:
o Shimuzu Grade 1 lesion / Ficat stage I
 Restricted to the medial part of the femoral head,
 Progress very slowly or not at all,
 Symptomatic treatment, reassurance and observe the patient over several years.

o Shimuzu Grade II lesion / Ficat stage IIa:

 Liable to progress,
 Core decompression or Decompression and bone grafting of the femoral head:
 Means of reducing intra-osseous pressure,
 7 mm core of bone is removed by drilling up the femoral neck,
 Symptomatic improvement is seen in 30 – 50% of patients.

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  Ficat stage IIb / III:
 Core decompression
 Realignment osteotomy – for younger patients,
 Partial or total hip replacement – over 45 yrs old pt with increasing symptoms.

o Shimuzu Grade III lesion / Ficat stage IV:

 Have a poor prognosis,
 Decompression is unlikely to have a lasting effect,
 Realignment osteotomy – treatment of choice for younger patient.
 Partial or Total joint replacement – for older patient.
 Late:
 Patient with advanced osteonecrosis and bone collapse (Ficat stage III or IV),
 Reconstructive surgery – osteotomy with or without bone grafting,
 Joint replacement.

 The bone grafts can be introduced with a standard core track technique,
 Grafting through lateral core track.
 “Trapdoor” technique, or
 “Lightbulb” technique.

136
Structural bone grafting techniques after core decompression:
 Structural bone grafting techniques after core decompression have been described using cortical bone, cancellous
bone, vascularized bone graft, and débridement of necrotic bone from the femoral head,
 A prospective case-controlled study comparing vascularized and nonvascularized fibular grafts for large lesions
(involvement of more than 30% of the femoral head) found better clinical results and more effective prevention of
femoral head collapse with vascularized grafting.

137
 Most authors recommend nonvascularized bone grafts for hips with less than 2 mm of femoral head depression
or those in which core decompression has failed and there is no acetabular involvement (Ficat stage I or II).
 Accurate placement of the graft within the lesion and under subchondral bone is essential.

 Trapdoor technique:
 The hip is surgically dislocated, a portion of the chondral surface of the femoral head is lifted

to expose the lesion, the necrotic bone is removed, the cavity is filled with bone graft, and the

cartilage flap is replaced and secured.

 Advantages of this approach include direct evaluation of the cartilage surface and necrotic

femoral head segment and precise placement of the bone graft;

 Disadvantages include technical difficulty, iatrogenic cartilage damage, and risk of iatrogenic

osteonecrosis from the surgical dislocation.

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 Lightbulb technique:
 A bone window measuring approximately 2 × 2 cm is removed at the femoral head-neck

junction with a micro-oscillating saw and osteotomes.

 Through the entry, a mushroom-tipped burr is used to curet a cavity in the femoral head;

removing all the necrotic bone (the shape of the cavity resembles a lightbulb).

 Allograft is packed into the cavity, and the bone plug is replaced and fixed with three 2-mm

absorbable pins.

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  Advantages of this technique are similar to those for the trapdoor technique,

 Disadvantage - the creation of a cortical defect in the femoral neck raises the risk of fracture.
 VASCULARIZED FIBULAR GRAFTING: camp-363

 Rationale for vascularized bone grafting is based on four aspects of the operation and postoperative care:
(1) Decompression of the femoral head, which may interrupt the cycle of ischemia and intraosseous
hypertension that is believed to contribute to the disease;
(2) Excision of the sequestrum, which might inhibit revascularization of the femoral head;
(3) Filling of the defect that is created with osteoinductive cancellous graft and a viable cortical strut to
support the subchondral surface and to enhance the revascularization process; and
(4) Protection of the healing construct by a period of limited weight bearing.

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 Advantages of free vascularized fibular grafting compared with total hip arthroplasty are as follows:
 The presence of a healed femoral head may allow more activity;
 There is no increased risk associated with the presence of a foreign body;
 If performed before the development of a subchondral fracture, the procedure offers the possibility
of survival of a viable femoral head for the life of the patient;
 If total hip arthroplasty is ultimately needed, it is much simpler to perform than is a revision
arthroplasty after a failed total hip arthroplasty.
 Most reports have shown good results in 80% to 91% of patients after vascularized fibular grafting,
and it may be a reasonable option for patients younger than 50 years without collapse of the femoral
head; for patients older than 50, total hip arthroplasty is indicated if symptoms warrant surgical
intervention.
 Concurrent steroid use is not a contraindication for this procedure.
 Disadvantages:
 Longer recovery period and
 Less uniform and
 Less complete relief of pain than after total hip arthroplasty.

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 OSTEOTOMY:

 Transtrochanteric Rotational osteotomy of the femoral head: CAMP-365

 Transtrochanteric rotational osteotomy of the femoral head for idiopathic osteonecrosis was
developed to reposition the necrotic anterosuperior part of the femoral head to a non–weight-bearing locale.

 The femoral head and neck segment is rotated anteriorly around its longitudinal axis so that the
weight-bearing force is transmitted to what was previously the posterior articular surface of the femoral head,
which is not involved in the ischemic process.

142
 VARUS / VALGUS OSTEOTOMY:

143
 RESURFACING HEMIARTHROPLASTY:
 If osteonecrosis involves more than 30% of the head,

 Resurfacing arthroplasty is an attractive alternative for young patients with advanced osteonecrosis
because very little bone is sacrificed.
 TOTAL HIP ARTHROPLASTY AND BIPOLAR HEMIARTHROPLASTY:
 Most series that have examined unipolar and bipolar hemiarthroplasty for the treatment of
osteonecrosis have reported uniformly poor results.
 The results from early reports of total hip arthroplasty for osteonecrosis, although better than
hemiarthroplasty, also were disappointing. Improved results have been reported with modern cementing techniques
and pressfit cementless total hip arthroplasty in patients with osteonecrosis.
 With new bearing surfaces becoming available, such as ceramic-on-ceramic, metal-on-metal,
and highly crosslinked polyethylene, results may improve even more.

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 SONK.
APL-114, 573

SONK / Spontaneous Osteo Necrosis of the Knee:

----> It is due to small insufficiency fracture of the prominent part of the osteoarticular surface
in osteoporotic femoral condyle, vascular supply to the free fragment is compromised.
3 important features:
 Elderly people (usually woman),
 Osteoporotic,
 On the highest part of medial femoral condyle.

2 {3} main categories of osteonecrosis of knee are identified:

 Osteonecrosis associated with definite background disorder [ e.g.
corticosteroid therapy, alcohol abuse, sickle cell disease, SLE etc],
 SONK,
 Post-meniscectomy osteonecrosis.

Clinical features:
 Patients are usually over 60 years,
 Women are affected 3 times more than men,
 Typical H/O sudden, acute pain on the medial side of the joint,
 Pain at rest is common also,
 Small effusion over affected knee,
 Classic feature is the tenderness on pressure on medial femoral condyle or tibial condyle rather than along
the joint line proper,
 May offer H/O similar symptoms in hip or shoulder.

145
 X-ray showing the typical features of subarticular bone
fragmentation and surrounding sclerosis situated in the
highest part (the dome) of the medial femoral condyle. (In
osteochondritis dissecans, the necrotic segment is almost
always on the lateral surface of the medial femoral condyle.

Osteochondritis
dissecans The
osteochondral fragment
usually remains in place
at the articular surface,
site in the medial femoral
condyle,

Investigation:
 X ray of affected knee:
 At the beginning – normal,
 Later – gross osteoporosis.
 MRI of affected knee:
 To visualize bone marrow and to separate necrotic part from viable area.
 To determine the prognosis.
 Radionuclide scan: increased activity on the medial side of knee joint.
 Special investigations: to exclude the cause of osteonecrois.

146
Differential diagnosis:
 Osteochondritis dissecans {age group, site of lesion, aetiology & prognosis}
 Oseoarthritic osteophyte,
 Disruption of degenerative meniscus,
 Stress fracture.

Treatment:
o Conservative:
 In case of 1st instance,
 Analgesics,
 Measures taken to reduce loading over joint.
o Operative:
 Arthoscopic debridement,
 Resurfacing with osteochondral allograft,
 Drilling with or without bone grafting,
 Core decompression of the femoral condyle at a distance from the lesion {for patients with
persistent symptoms & well marked articular surface damage}.

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 Avascular Necrosis of Talus.
Incidence of necrosis:
Overall rate of necrosis of talus about 20 to 60%,
Causes of necrosis;
 It has limited area for vascular portals,
 about 60% of it’s surface is covered by articular cartilage,
 It has no muscular attachment,
 Body of talus is supplied by vessels which enter through talar neck and run anterior to posterior direction,
 In case of # neck of talus, vessels become ruptured. Body of talus becomes ischaemic and then AVN
develops,
 After AVN of talus, process of revascularization begins which takes about 2 to 3 years for it’s completion.

Investigation:
 X ray ankle Mortize view (300 planter flexion):
Hawkin’s sign – Subchondral lucency of talar dome / subchondral atrophy.

 MRI of talus: most sensitive to detect and monitor progress of AVN.

Management:
 Early anatomic reduction and internal fixation,

148
  Non weight bearing crutch walk – until it has been healed,
 Follow up by MRI.
Prognosis:
When AVN with segmental collapse develops – it carries poor prognosis.

Blood supply of Talus:

Blood supply of talus:
 Extra osseous blood supply,
 Intra osseous blood supply.

Extra osseous blood supply:

 Posterior tibial artery:
 Anterior tibial artery:
 Peroneal artery.

Intra osseous blood supply: anastomosis around the Talus.

 Medially by Deltoid artery,
 Laterally by artery of Tarsal sinus,
 Middle part by ananstomosis between the arteries of Tarsal sinus and Tarsal canal.

149
 Kienbock disease.
APL-397

Kienbock disease:
Softening of lunate bone which is a sequel of ischaemic necrosis that usually follows a trauma or
chronic stress.
Clinical feature:
 Painful wrist movement,
 Grip strength is decreased,
 Tenderness over lunate bone,
 Gradual stiffness of wrist movements,
 Relative shortening of ulna (Negative ulnar variance).
Staging:

In stage I Ischaemia without In stage II the bone shows In stage III density is more In stage IV the bone has
mottled increase of density, marked and the lunate collapsed and there is radio-
radiographic abnormality,
but is still normal in shape. looks slightly squashed. carpal osteoarthritis.

Investigation:
 X-ray wrist joint B/V,
 MRI of wrist – detects early changes.

150
Treatment:
a) Non-operative:
 In early stage, splintage of wrist for 6 to 12 weeks which reduce mechanical stress.

(a) Radial shortening; (b) Scapho-capitate fusion.

b) Operative:
-- When conservative treatment fails or in advance cases,
 Up to stage III : shortening of radius (reduction of carpal stress), or
 Radio-carpal arthrodesis (stable pain free wrist).

151
METABOLIC & ENDOCRINE DISORDERS.

152
 Metabolic Bone Disease.
Q) Name some common metabolic bone diseases?

Common metabolic bone diseases:  Osteopetrosis:

Clinical condition characterized by sclerosis & thickening of bone
 Rickets, with ↑ed radiographic density.
 Osteomalacia,
 Osteopenia:
 Osteoporosis, Significant ↓ed in the amount of BMD,
- 1 to – 2.5 value indicates osteopenia.
 Hyperparathyroidism,
 Renal osteodystrophy,
 Scurvey,
 Paget’s disease of bone,
Q) What are the indications of BMD measurement?
Indications of BMD measurement:
 All post menopausal women under 65 years of age,
 Young women following oophorectomy,
 Perimenopausal women with # wrist, ribs, vertebral body or hip.
 Women / Men with x-ray features of osteopenia,
 Men with testosterone deficiency,
 Patients with Hyperparathyroidism, Hyperthyroidism, Renal insufficiency or RA,
 Patients with long term gluco-corticoid / thyroid hormone / thiazide diuretic therapy,
 Patients with dietary deficiency.
Q) Measurement of BMD?
 By Radiological method:
--- Specific for Lumber, Spine, Femoral neck & Distal radius,
 Radiographic absorptiometry,
 Quantitative computed tomography (QCT),
 Single energy x-ray absorptiometry,
 Dual energy x-ray absorptiomety (DEXA):
T score Z score
 0 to – 1 value: Normal bone density, Comparison to:
 - 1 to – 2.5 value: osteopenia,  Age,
 < - 2.5 value: osteoporosis.  Sex,
 Ethnicity.

153
  By Biochemical tests:
 Serum calcium & phosphate level,
 Serum bone alk. phosphatase level,
 Serum PTH,
 Excretion of Pyridinium compound and Telopeptides:
 More sensitive index of bone resorption,
 Useful in monitoring the progress of hyperparathyroidism and other types of osteoporosis.
Q) Short note: Vitamin – D synthesis / Metabolism.
Sunlight

Skin u

7 Dehydro-cholesterol

Diet Cholecalciferol (D3)

PTH

25 Hydroxy – cholecalciferol Liver

(25 HCC)

1,25 Di-hydroxy cholecalciferol Kidney

ACT ON

Intestine

it forms Ca++ binding it stimulates Alkaline it forms Ca++ stimulated
protein in Enteocytes. phosphatase ATPase.

154
 ↑ Ca++ absorption.

Q) Functions of PTH?

1) on GIT:  it is required for conversion of 25(OH)vitD3 to

1,25(OH)2D3 – to ↑ intestinal absorption of Ca++ & PO4--
2) on Bone:  ↑ Bone resorption,  Net effect:
 ↑ Osteoclastic activity, * Bone loss &
 ↓ Osteoblastic activity. * ↑ Blood Ca++ conc.
PTH

3) on Kidney:  ↑ Renal tubular reabsorption of Ca++, Mg++ & H+,

 ↑ Excretion of Na+ & PO4--
4) on Body  Maintain Ca++ conc. in ECF by bone resorption.
fluid:

Q) Define Rickets? What are the biochemical features of rickets? Types of Rickets?
Rickets:
It is a clinical condition characterized by defective mineralization or calcification of bones before
epiphyseal closure; due to deficiency or impaired metabolism of vitamin-D, Calcium or Phosphate.

Biochemical features:
 Normal or ↓ level of serum calcium,
 ↓ level of serum phosphate,
 ↑ level of serum alkaline phosphatase,
 ↓ 25 HCC level in blood (in Vit-D deficiency).

155
Types of Rickets / Causes of Rickets:
a) Nutritional rickets:
due to –
 Malnutrition,
 Malabsorption,
 Biliary disease.

b) Vitamin D Dependent rickets:

 Type I: inability to hydroxylate,
 Type II: receptor insensivity.

c) Vitamin D Resistant rickets / Hypophosphatemic rickets:

It is a form of Rickets that is characterized by low serum phosphate level & resistance to treatment with Vit-D (either ingestion
or ultraviolet radiation).
 X linked Dominant / X linked Hypo-phosphatemic rickets: 80%,
 Autosomal Dominant Hypophostamemic rickets: 20%,
 Fanconi’s syndrome: inadequate reabsorption of phosphate.

156
 d) Rickets secondary to other diseases:
 Tumor induced:
 GCT,
 Non ossifying fibroma.

 Drug induced:
 Phenytoin,
 Phenobarbitone.

 Renal osteodystrophy / Renal Rickets.

Q) What are the clinical and radiological features of Rickets? Maheswari-263

 Nutritional rickets occur in children about 1 yr of old,

 Rickets occur in older children with malabsorption syndrome.

Clinical features of Rickets:

Craniotabes:
Pressure over the soft
membranous bone of skull gives the feeling
of ping pong ball – being compressed &
released,

Bossing of skull:
Bossing of frontal and
parietal bones become evident after the age
of 6 months,

157
 Broadening of the ends of long bones:
Prominently around wrist
and knee are seen around 6 to 9 months of
age.

Harrison’s sulcus:
- Horizontal depression
corresponding to the insertion of
diaphragm,
- Indentation of lower ribs at the
site of attachment to diaphragm.

Rachitic rossary:
Costo-chondral junctions
on the anterior chest wall become
prominent.

Pigeon chest:
Sternum is prominant,

158
 Muscular hypotonia:
Pot belly / Protuberant
abdomen – due to ↑ lumber lordosis.

Knock knee or Bow legs:

Once the child starts
walking.

Child with nutritional rickets:

a) The typical features such as widening of the physis and flaring of the metaphysis are well marked.
b) After treatment the bones have begun to heal but the bone deformities are still noticeable.

Radiological features of Rickets:

 X ray both wrist and knee B/V:
 Radiological signs are:
o Epiphysis:
 Delayed appearance of epiphyses,
 Widening of epiphyseal plate,
o Metaphysis:
 Cupping of metaphysis, Child with classical nutritional rickets
showing:
 Splaying / widening of metaphysis, the well-marked physes,
the flared metaphyses and
o Diaphysis: the bowing deformities of the lower limb bones.

159
  Rarefaction / reduction of density of
diaphysial cortex
o Bony deformity:
 Knock knee,
 Bow leg,
 Coxa vera: in older children.

Q) Outline the treatment of Rickets?

a) Medical treatment:
 inj. vitamin D3 / Cholecalciferol (6 lac units) – mix with milk, Single oral dose.
 if feature of healing (sclerosis on the metaphyseal end of growth plate) not seen on x-ray after 3 – 4
weeks of oral therapy → Same dose may be repeated,
 if there is no response even after Second dose → a diagnosis of Refractory Rickets is made,
 In those cases, where children respond to vit-D therapy, maintenance dose of 400 IU vit-D given
orally per day (Syp. Vit-D3: 1 ml = 200 IU).

b) Orthopaedic treatment:
 Conservative:
 Mild deformity may correct spontaneously as rickets heals,
 Use of specially designed splints (Mermaid splint) or orthopaedic shoe for correction of knee
deformity.

 Operative:
 Surgery can be done after 6 months of starting medical treatment.
 Corrective osteotomy depends upon the nature of deformity.

160
Q) What is osteomalacia? What are the causes of osteomalcia?

Osteomalacia:
-- It is a clinical condition due to inadequate mineralization of bones in adult, characterized by bones
through out the skeleton are incompletely calcified & therefore softened.
Four characteristic features of osteomalacia:

(a) indentation of the acetabula producing the trefoil or

champagne glass pelvis;

(b) Looser’s zones in the pubic rami and left femoral neck;

 Looser’s line (Syn: Pseudofracture, Milkman’s line):

It is transverse, bilaterally symmetrical and incomplete. (c) Biconcave vertebrae; (d) Fracture in the mid-diaphysis
of a long bone following low-
 Presence of Looser’s zones is quite characteristic of energy trauma (the femoral
osteomalacia. cortices in this case are egg-shell
thin).
 Sites:
• Axillary borders of scapula
• Ramus of pubis or ischium
• Neck of femur
• Ribs

161
Causes:
 Vitamin D deficiency: less sunlight exposure,
 GIT surgery: gastrectomy, by pass surgery,
 Coeliac disease: auto immunity against mucosa of small intestine,
 Kidney disease,
 Liver disease,
 Drugs therapy:
 Phenytoin,
 Phenobarbitone.

Q) What is osteoporosis? Mention the sites & causes of osteoporosis?

Osteoporosis:
it is a clinical condition characterized by significant decrease the mass of bone per unit volume of bone
tissue which is accompanied by increased fragility of bone.

Φ Osteoporosis: ↓ Quantity of Bone.

Bone mineralization is normal but ↓ bone mass.

Φ Osteomalacia: ↓ Quality of Bone.

Bone mineralization is defective but bone mass is
normal.

Sites of osteoporosis:
 Vertebral column / Spine,
 Hip,
 Wrist,
 Ribs,
 Pelvis.

Causes of osteoporosis / Classification of osteoporosis:

a) Regional osteoporosis:
 particular bone or group of bones involved eg disuse osteoporosis,

b) Generalized osteoporosis:
i) Primary osteoporosis:

162
  No specific cause,
 Senile osteoporosis,
 ↓ Gonadal activity eg: post menopausal state.

ii) Secondary osteoporosis:

 Nutritional :
 Scurvey,
 Malnutrition,
 Malabsorption.

 Endocrine disorders:
 Hyperparathyroidism,
 Thyrotoxicosis,
 Cushing disease,
 Gonadal insufficiency.

 Malignant disease:
 Multiple myeloma,
 Leukaemia.

 Drug induced:
 Steroids,
 Heparin,
 Anticonvulsant,
 Alcohol,

 Others:
 RA,
 AS,
 TB,
 COPD,
 Chronic renal disease,
 Chronic liver disease.

163
Q) Short note: Marrow oedema syndrome / Transient osteoporosis of the hip. APL532

Marrow oedema syndrome:

 Syndrome characterized by pain and rapidly emerging osteoporosis / Transient osteoporosis of the femoral
head and adjacent pelvis & the cause is unknown.

Clinical features:
 Condition was originally described in woman in the last trimester of pregnancy, but it is now seen in
patients of both sexes and all ages from early adult hood onwards.
 Typically the changes last for 6 – 12 months, after which the symptoms subside and x ray gradually
returns to normal.

Investigation:
 X ray affected hip – shows features of osteopenia,

Bone marrow oedema MRI showing the typical diffuse area of low signal intensity in the right femoral
head in the T1 weighted image.

 MRI of pelvis – features are characteristic of marrow oedema with diffuse changes.

Treatment:
 Condition almost always resolves spontaneously and most patients require no more than
symptomatic treatment,
 If there is any doubt about whether the MRI changes are due to osteonecrosis or marrow oedema,
operative decompression (drilling up the femoral neck) is recommended.

164
Q) Short note: Hyper parathyroidism.

Hyper parathyroidism:
-- It is the syndrome due to over activity of parathyroid glands resulting in excess production of
parathyroid hormone.

Classification:
a) Primary {due to adenoma or hyperplasia}
b) Secondary {due to persistent hypocalcaemia},
c) Tertiary {when secondary hyperplasia lead to autonomous over activity}

Primary hyperparathyroidism:
 Patient is usually middle aged (40 – 60 yrs),
 Woman are affected more than men,
 Stones, Bones, Abdominal groans & Psychic moans.
 Polyuria, Nephrocalcinosis & Chondrocalcinosis.
 Generalised osteoporosis.

Secondary hyperparathyroidism:
 Usually seen in Rickets or Osteomalacia.
 Patient with CRF,

Tertiary hyperparathyroidism:

Investigations:
 S. PTH: ↑
 S. Ca++: ↑
 S. Phosphate: ↓
 S. Alkaline phosphatase: ↑
 X ray features:
 Osteoporosis / Brown tumor,
 Sub periosteal cortical resorption of middle phalanges of fingers {classical &
pathognomic}

165
Q) Short note: Brown tumour? camp-881-2,

Brown tumor / Osteitis fibrosa cystica / Von Rechlinghausen disease of Bone:

-- It is one of the bony manifestations of hyper parathyroidism, usually secondary hyper
parathyroidism.
Clinical features:
 Features of hyper parathyroidism,
 Bone pain with tenderness,
 Pathological fracture.
Investigation:
 S. PTH: ↑,
 S. Ca++: ↑,
 S. Phosphate: ↓,
 S. Alkaline phosphatase: ↑,

Pathological fracture of right

proximal tibia through “brown
tumor” of hyperparathyroidism
in a 55-year-old woman.

 X ray features:
 Atypical cyst like lesion in metaphysis,
 Intense osteoclastic & osteoblastic acivity associated with peritrabecular fibrosis.
Differential diagnosis:
 GCT:
Histopathology:
 Giant cells are little smaller, often occurring in nodular arrangement Microscopic features suggest
especially around the area of haemorrhage, Hyperparathyroidism differ from GCT.
 Characteristic brown colouration result from haemosiderin
deposition,
 Stromal cells are more spindle shaped & delicate,
 Evidence of osseous metaplasia within the stroma is prominent.

Treatment:
 Patients with hyperparathyroidism usually are treated by endocrinologist,
 Orthopaedic management consists of treating actual or impending pathological ≠.

166
GENETIC DISORDERS
SKELETAL DYSPLASIAS

167
 Genetics.
kha path-79

Q) Genetic disorder – due to inherited defect in chromosome or gene.

Q) Chromosome?
 Normal somatic cell contain 46 chromosomes,
 22 pairs autosomes and 1 pair sex chromosome {XX or XY}.
Q) Gene –
 Shortest segment of chromosome within which genetic information is stored.
 Each gene of a pair is called Allele and they may not be identical,
 If the two alleles are identical – the individual is Homozygous,
 If the two alleles are different – the individual is Heterozygous,
 Hemizygous,
 Gene may be dominant – lead s to manifestation,
 Gene may be recessive – trait is not manifested but is capable of being transmitted to offsprings.
Q) Types of Genetic diseases?
 Single gene disorders / Mendelian disorders,
 Chromosomal abnormalities.
Q) Single Gene Disorders?
 Due to defect in a single gene,
 Three patterns of inheritance:
1) Autosomal dominant,
2) Autosomal recessive,
3) X linked: mutant gene is located on sex chromosome.

i) X linked dominant,

ii) X linked recessive.

168
 Autosomal Dominant Disorders Autosomal Recessive disorders
 Dominant trait is one which is manifested in  Recessive traits manifest only in homozygous state,
heterozygous state,  These traits affect both males and females,
 Either parent or male / female may be affected and  The risk of each parent carrying the mutant gene is
can transmit the trait, more common in consanguineous marriage,
 Trait manifests in every generation ,  Siblings have one chance in four of being affected /
 When an affected individual marries a normal Risk is 25% for each birth.
person, then an average half of their children will be
affected.
Examples: Examples:
 Neurobiromatosis,  Thalassaemia,
 Marfan syndrome,  Sickle cell anaemia,
 Achondroplasia,  Neurogenic / Spinal muscular atrophy,
 Osteogenic imperfecta,
 Diaphyseal aclasis / Hereditary
Multiple Exostosis.

X linked Dominant disorder. X linked Recessive disorder.

 An affected male parent transmits to all his  Almost all are X linked recessive,
daughters, but none of his sons – if female parent  Affected male carrying mutant gene received from
is unaffected. mother on X chromosomes are affected as Y chromosomes
 An affected female transmits half her sons and has no allele gene,
half her daughters – if male parent is unaffected.
 Affected males transmit mutant gene in X chromosome to
all daughters but does not transmit the disorder to his sons,

 Highly distinctive pattern of inheritance: an affected male

will pass the gene only to his daughters, who will become
unaffected heterozygous carriers; they, in turn, will transmit
it to half of their daughters (who will likewise be carriers)
and half of their sons (who will be bleeders).
APL-153

169
  A female may be affected if the mutant gene comes from
affected father and carrier mother.
Examples: Examples:
Vitamin D resistant ricket.  Haemophilia A,
 Haemophilia B,
 Duchenne muscular dystrophy,
 Becker muscular dystrophy.

Cytogenetic / Chromosomal disorders:

 Cytogenetic disorders involving Autosomes:
 Trisomy {Extra chromosome 2n+1}: trisomy 21 / Down syndrome.

 Cytogenetic disorders involving Sex chromosome:

 Turner syndrome / monosomy 45 X,
 Klinefelter syndrome / 47 XXY.
 47 XYY.

170
DYSPLASIAS WITH PREDOMINANTLY EPIPHYSEAL CHANGES
 MULTIPLE EPIPHYSEAL DYSPLASIA: apl-157
 Multiple epiphyseal dysplasia (MED) varies in severity from a trouble-free disorder with mild
anatomical abnormalities to a severe crippling condition.
 There is widespread involvement of the epiphyses but the vertebrae are not at all, or only mildly,
affected.
Clinical features:
 Children are below average height and the parents may have noticed that the lower limbs are
disproportionately short compared to the trunk.
 They sometimes walk with a waddling gait and they may complain of hip or knee pain.
 Some develop progressive deformities of the knees and/or ankles. The hands and feet may be short and
broad. The face, skull and spine are normal.
 In adult life, residual epiphyseal defects may lead to joint incongruity and secondary osteoarthritis.
Genetics:
Most cases have an autosomal dominant pattern of inheritance.

X-rays show epiphyseal distortion and flattening at multiple sites, in this case the hips,
X-ray:
 Epiphyseal ossification is delayed, and when it appears it is irregular or abnormal in outline.
 In the growing child the epiphyses are misshapen; in the hips this may be mistaken for bilateral Perthes’
disease {Typical cycle of changes from epiphyseal irregularity to fragmentation, flattening and healing}.

Management
 Children may complain of slight pain and limp, but little can (or need) be done about this.
 At maturity, deformities around the hips, knees or ankles sometimes require corrective osteotomy.
 In later life, secondary osteoarthritis may call for reconstructive surgery.

171
 SPONDYLO EPIPHYSEAL DYSPLASIA / SED

The term ‘spondylo-epiphyseal dysplasia’ (SED) encompasses a heterogeneous group of disorders in which
multiple epiphyseal dysplasia is associated with wellmarked vertebral changes – delayed ossification, flattening of
the vertebral bodies (platyspondyly), irregular ossification of the ring epiphyses and indentations of the end-plates
(Schmorl’s nodes).

 DYSPLASIA EPIPHYSEALIS HEMIMELICA (TREVOR’S DISEASE):

 ‘Hemidysplasia’ affecting just one half (medial or lateral) of one or more epiphyses on one side of the
body.
 It is a sporadic disorder which usually appears at the ankle or knee.
 The child (most often a boy) presents with a bony swelling on one side of the joint; several sites may be
affected – all on the same side in the same limb, but rarely in the upper limb.

 X-rays show an asymmetrical enlargement of the bony epiphysis and distortion of the adjacent joint. At
the ankle, this may give the appearance of an abnormally large medial malleolus.
 Treatment:
 If the deformity interferes with joint function.
 The excess bone is removed, taking care not to damage the articular cartilage or ligaments.

172
 DYSPLASIAS WITH PREDOMINANTLY PHYSEAL AND METAPHYSEAL
CHANGES: APL-160

HEREDITARY MULTIPLE EXOSTOSIS (DIAPHYSEAL ACLASIS):

 Multiple exostosis is the most common, and least disfiguring of the skeletal dysplasias.
 Clinical Features:
The condition is usually discovered in childhood; hard lumps appear at the ends of the long bones and along the
apophyseal borders of the scapula and pelvis.

Sessile exostoses of the femoral neck. Pedunculated exostosis of the distal femur.

 Typically the long-bone metaphyses are broad and poorly modelled, with sessile or pedunculated exostoses arising from
the cortices.
 A mottled appearance around a bony excrescence indicates calcification in the cartilage cap.
 Occasionally one of the cartilagecapped exostoses goes on growing into
 Adult life and transforms to a chondrosarcoma; this is said to occur in 1–2 per cent of patients.

Evolution of the wide metaphysis during growth.

Pathology:
 The underlying fault in multiple exostosis is unrestrained transverse growth of the cartilaginous physis
(growth plate).
 The condition affects only the endochondral bones.
 Cartilaginous excrescences appear at the periphery of the physes and proceed, in the usual way to
endochondral ossification.

173
Genetics:
 The condition is acquired by autosomal dominant transmission; half the children are affected, boys
and girls equally.
 Abnormalities have been identified on chromosomes 8, 11 and 19, referred to as EXT 1, 2 and 3.

Management:
 Exostoses may need removal because of pressure on a nerve or vessel, because of their unsightly
appearance, or because they tend to get bumped during everyday activities.
 Care must be taken not to damage the physes.

174
 ACHONDROPLASIA: apl-163
This is the commonest form of abnormally short stature; adult height is usually around 122 cm (48 inches).

Lumbar lordosis, a prominent thoracolumbar gibbus and bossing of the forehead. X-rays show the short, thick bones (including the
metacarpals).

Clinical Features
 The abnormality is obvious in childhood:
 Growth is severely stunted; the limbs – particularly the proximal segments – are disproportionately
short (rhizomelic shortening) and the
 Skull is quite large with prominent forehead and saddle-shaped nose.
 Frontal bossing and mid-face hypoplasia contribute to the characteristic appearance of people with
achondroplasia.
 The fingers appear stubby and somewhat splayed (trident hands).
 By early childhood the trunk is obviously disproportionately long in comparison with the limbs.
 Joint laxity is common and contributes to the characteristic standing posture: flat feet, bowed legs,
flexed hips, prominent buttocks, lordotic spine and elbows slightly flexed.
 Cervical spine stenosis may cause typical features of cord compression.
 Mental development is normal.
Genetics
 Achondroplasia occurs in about 1 in 30,000 births. Inheritance is by autosomal dominant
transmission;
 The fault is in the gene encoding for the growth suppressing fibroblast growth factor receptor 3
(FGFR-3) on chromosome 4.

175
Pathology
 This is essentially an abnormality of endochondral longitudinal growth resulting in diminished
length of the tubular bones.
 Membrane bone formation is unaffected, hence the normal growth of the skull vault and the
periosteal contribution to bone width.

X-Rays
 All bones that are formed by endochondral ossification are affected, so the facial bones and skull
base are abnormal but the cranial vault is not.
 The tubular bones are short but thick, the metaphyses flared and the physeal lines somewhat
irregular; sites of muscle attachment, such as the tibial tubercle and the greater trochanter of the femur, are
prominent.
 Proximal limb bones are disproportionately affected (rhizomelia), changes are also seen in the wrists
and hands, where the metaphyses are broad and cup shaped. The epiphyses are surprisingly normal.
Differential diagnosis:
 Pseudoachondroplasia,
 ‘Dwarfism’,
 Morquio’s disease.
Management
 During childhood, operative treatment may be needed for lower limb deformities (usually genu varum).
 During adulthood, spinal stenosis may call for decompression. Intervertebral disc prolapse
superimposed on a narrow spinal canal should be treated as an emergency.
 Advances in methods of external fixation have made leg lengthening a feasible option. This is
achieved by distraction osteogenesis. However, there are drawbacks / complications, including nonunion, infection
and nerve palsy, may be disastrous; and the cosmetic effect of long legs and short arms may be less pleasing than
anticipated.

176
 DYSCHONDROPLASIA (ENCHONDROMATOSIS; OLLIER’S DISEASE)
 The condition is not inherited; indeed, it is probably an embryonal rather than a genetic disorder.
 Disorder in which there is defective transformation of physeal cartilage columns into bone.

Multiple chondromas.
Clinical Features
 Typically the disorder is unilateral; indeed only one limb or even one bone may be involved.
 An affected limb is short,
 The fingers or toes frequently contain multiple enchondromata, which are characteristic of the disease and
may be so numerous that the hand is crippled.
 A rare variety of dyschondroplasia is associated with multiple haemangiomata (Maffucci’s disease);
X-Rays
 The characteristic change in the long bones is radiolucent streaking extending from the physis into
the metaphysis – the appearance of persistent, incompletely ossified cartilage columns trapped in bone.
 In the hands and feet the cartilage islands characteristically produce multiple enchondromata.
 Beware of any change in the appearance of the lesions after the end of normal growth; this may be a
sign of malignant change, which occurs in 5–10 per cent of cases.
Treatment
Bone deformity may need correction, but this should be deferred until growth is complete; otherwise it is likely to
recur.

MAFFUCCI’S DISEASE
This rare disorder is characterized by the development of multiple enchondromas and soft-tissue haemangiomas of the skin and
viscera.

177
 DYSPLASIAS WITH PREDOMINANTLY - DIAPHYSEAL CHANGES
 OSTEOPETROSIS (MARBLE BONES / ALBERS–SCHÖNBERG DISEASE)
 Osteopetrosis is one of several conditions which are characterized by sclerosis and thickening of the
bones which appear with increased radiographic density.
 This is the result of an imbalance between bone formation and bone resorption;
 In the most common form, osteopetrosis, there is failed bone resorption due to a defect in osteoclast
production and/or function.

 Osteopetrosis tarda:
 The common form of osteopetrosis is a fairly benign,
 Autosomal dominant disorder that seldom causes symptoms and may only be discovered in
adolescence or adulthood after a pathological fracture or when an x-ray is taken for other reasons – hence the
designation tarda.
 X-rays show increased density of all the bones: cortices are widened, leaving narrow medullary
canals; sclerotic vertebral end-plates produce a striped appearance (‘football-jersey spine’); the skull is thickened
and the base densely sclerotic.
 Treatment is required only if complications occur.
 Osteopetrosis congenital:
 This rare, Autosomal recessive form of osteopetrosis is present at birth and causes severe disability.
 Bone encroachment on marrow results in pancytopenia, haemolysis, anaemia and
hepatosplenomegaly.
 Foraminal occlusion may cause optic or facial nerve palsy.
 Osteomyelitis following, for example, tooth extraction or internal fixation of a fracture is quite
common.
 Repeated haemorrhage or infection usually leads to death in early childhood.
 Treatment, in recent years, has focused on methods of enhancing bone resorption and
haematopoeisis, e.g. by transplanting marrow from normal donors and by long-term treatment with gamma-
interferon.

178
 DIAPHYSEAL DYSPLASIA (ENGELMANN’S OR CAMURATI’S DISEASE)

 This is another rare childhood disorder in which xrays show fusiform widening and sclerosis of the
shafts of the long bones, and sometimes thickening of the skull.
 The condition is notable because of its association with muscle pain and weakness. Children complain of
‘tired legs’ and have a typical wide-based or waddling gait.

 Candle bones (Melorheostosis / Leri’s

disease)
 This rare, non-familial, condition is sometimes
discovered (almost accidentally) in patients who
complain of pain and stiffness in one limb.
 X-rays show irregular patches of sclerosis,
appearance is reminiscent of wax that congeals on the
side of a burning candle.
 Spotted bones (osteopoikilosis)
 The condition is inherited as an autosomal
dominant trait.
 Routine x-rays sometimes show (quite incidentally)
numerous white spots distributed throughout the
skeleton.
 Striped bones (osteopathia striata)
X-rays show lines of increased density parallel to the
shafts of long bones,

179
 COMBINED AND MIXED DYSPLASIAS
A number of disorders show a mixture of epiphyseal, physeal, metaphyseal and vertebral defects.

 SPONDYLOMETAPHYSEAL DYSPLASIA:
 PSEUDOACHONDROPLASIA:
Characterized by short limbed dwarfism associated with ligamentous laxity, exaggerated lumbar lordosis and bow-
leg deformities.

 CLEIDOCRANIAL DYSPLASIA:

Cleidocranial dysplasia The ‘squashed face’ and sloping shoulders which can be brought together anteriorly are pathognomonic.
NAIL–PATELLA SYNDROME:

The Nail–Patella syndrome The dystrophic nails, minute patellae, pelvic ‘horns’ and subluxed radii combine to give an
unmistakable picture.

180
BONE TUMOURS.

181
 BONE TUMOR.
Q) What is Neoplasia?
Neoplasia:
It is an abnormal mass of tissue; the growth of which exceeds & uncoordinated with that of normal tissue
and persist in the same excessive manner after cessation of stimuli that evoked the change.
Q) Classify bone tumour?
Q) WHO 1994 clssification of Bone tumour?
Q) Enumerate Malignant bone tumour? APL (n)-181

182
Q) Classify Bone tumour according to Site? B & L – 534

Q) Common bone tumour according to age group:

1st decade (<10 yrs):
 Benign: E. granuloma, SBC, Osteochondroma
 Malignant: Ewings sarcoma
2nd – 3rd decade (>10 – 30yrs):
 Benign: SBC, ABC, NOF, Fibrous dysplasia, Chondroblastoma, Osteoid osteoma.
 Malignant: Ewings sarcoma, P osteosarcoma.
3rd – 4th decade (30 – 40 yrs):
 Benign: GCT, Osteoblastoma
 Malignant: Lymphoma, Parosteal osteosarcoma, S Chondrosarcoma.
5th decade:
 Malignant: MM, Metastasis, P Chondrosarcoma., S osteosarcoma.

183
Q) Common Diaphyseal tumours according to age: B & L 534

Age Most common Diaphyseal tumour

< 10 years Eosinophil granuloma
Teenage Ewing’s sarcoma
Adult Lymphoma
> 60 years Metastasis / Myeloma

Q) Pre-malignant conditions of Bone:

 GCT,
 Polyostotic Paget’s disease of bone,
 Fibrous dysplasia,
 Multiple enchondromatosis / Ollier’s disease,
 Enchondromatosis & angiomas of soft tissue / Maffucci syndrome,
 Multiple osteochondroma.

Q) Tumours that producing cartilage: B & L - 533

 Osteochondroma : cartilage capped; grows away from physis,
 Enchondroma : inside bone; most common in hands & feet,
 Chondroblastoma : in the epiphyses of adolescents,
 Chondrosarcoma : of varying malignancy.

Q) Tumour that producing Bone: B & L – 531

o Osteoid osteoma – small painful tumour producing dense cortical reaction,
o Osteoblastoma – larger & more aggressive.
o Osteosarcoma - malignant, most commonest in lower femur & upper tibia.

Q) Warning signs of Bone tumour: B & L : 535

 Non mechanical bone pain,
 Especially around the knee in young adolescent,
 Concerning x-rays.

184
Q) Warning signs of soft tissues tumour: B & L : 536
Each of these factors
 Larger than 5 cm or increasing in size, has a 25% risk of
 Painful, Malignancy.
 Position: deep to fascia,
 Recurrence after previous excision.

Q) Benign Bone Tumours:

 Fibrous cortical defect,
 Fibrous dysplasia,
 Osteoid osteoma,
 Osteoblastoma / Giant osteoid osteoma,
 Chondroma,
 Chondroblastoma,
 Chondromyxoid fibroma,
 Osteochondroma,
 ABC,
 GCT,
 Eosinophilic granuloma.

Q) Name some Benign Aggressive Bone tumours?

o GCT,
o Chondroblastoma,
o Osteoblastoma / GOO,
o Langerhans cell histiocytosis:
 Eosinophilic granuloma (isolated single bone),
 Hand Schuller Christian disease:
 Skull lesion,
 Exophthalmos,
 Diabetes insipidus.

185
Q) Enneking staging of Bone tumour: B & L: 535, APL (N)-191
Grade Site Metastasis Stage
Intracompartmental no IA
a) Low grade
Extracompartmental no IB

Intracompartmental no IIA
b) High grade
Extracompartmental no IIB

Intacompartmental
c) Any grade Present III
(Low / High) Extracompartmental

 Staging of Benign Tumour: TNM Staging for Primary Sarcoma of Bone

Latent: apl/N - 181
Tumour– node–metastasis (TNM) staging has been applied to
Φ Well defined margin,
primary sarcomas of bone.
Φ Grows slowly & then stop, i.e
osteochondroma.
Active:
Φ Progressive growth limited by natural
barriers,
Φ Not self limiting, i.e osteoid osteoma,
ABC
Aggressive:
Φ Growth not limited by natural barriers,
i.e GCT.

 Grading of tumour: kh – 66, b&l -534, apl(n)-191

 Assessment of degree of malignancy or aggressiveness,

 Grading is done on:
 Degree of differentiation / degree of resemblance to normal tissue,
 Nuclear size,
 Pleomorphism / variation in size & shape,
 Mitotic activity.

186
  Grading system:
 G I: > 75% cell differentiation,
 G II: 50 to 75% cell differentiation,
 G III: 25 to 50% cell differentiation,
 G IV: < 25% cell differentiation.

Q) Assessment of bone or soft tissue tumour:

--- 3 phases:
Phase 1 Phase 2 Phase 3
(within 24 hours) (within 1st week)
At district hospital At tumour treatment
centre
Ǿ History & examination Bone scan Φ CT scan of lesion
Ǿ Bloods, USG whole abdomen, Φ MRI of lesion
Ǿ X-ray whole bone, CT scan chest Φ Biopsy
Ǿ CXR.

Q) Clinical features of bony tumour?

 Age:
 Primary bone tumours; osteosarcoma and Ewing’s sarcoma have preponderance for children, adolescents
and young adults,
 Chondrosarcoma typically occurs in older patients.
 Metastatic tumour occurs usually at elderly age.
 Pain:
 Most common symptom experienced by a patient with a bone tumour is pain.
 Pain is initially mild but then gets worse as the tumour increases in size.
 Night pain is a particularly worrying symptom.
 Referred pain is not uncommon, particularly with pelvic tumours which can present with abdominal, back or
leg pain.
 Swelling and tenderness:
 Swelling and tenderness over the affected bone are the most common findings but there will be limitation of
joint movement if there has been irritation of the joint by the tumour, or the tumour has grown into the joint.
 Size:
 All superficial soft-tissue lesions measuring greater than 5 cm and all deep-seated lesions should be
considered a sarcoma until proven otherwise.
 Pathological fracture:
 Has been reported in between 5 and 12% of osteosarcomas and up to 21% of chondrosarcomas,

187
Q) What are the investigations you will do to diagnose bone tumour? apl-189

 Imaging:
 X rays:

If other forms of imaging are planned (bone scans, CT or MRI), they

should be done before undertaking a biopsy, which itself may distort the
appearances.

 CT scan:
 Shows more accurately both intraosseous and extraosseous extension of the tumour and the
relationship to surrounding structures.
 CT is essential to complete systemic staging and re-staging in bone and softtissue sarcomas and
metastatic disease to identify pulmonary metastases.

 MRI:
 Assessment of tumour spread: (a) within the bone, (b) into a nearby joint, and (c) into the soft tissues.
 Blood vessels and the relationship of the tumour to the perivascular space are well-defined, which
aids greatly in preoperative assessment and the prediction of resection margins for limb-salvage surgery.
 It may demonstrate features consistent within certain lesions (e.g. fluid-fluid levels within an
aneurysmal bone cyst (ABC) or telangiectatic osteosarcoma).

 Whole body scan:

 Can be helpful in revealing the site of a small tumour (e.g. an osteoid osteoma),
 Useful for detecting skip lesions,
 Evidence of metastatic disease as part of the initial staging process.

 Laboratory investigations:
 Hb: ↓
 ESR: 

188
  S Alkaline phosphatase: Non-specific findings, but if other causes are excluded they may help in
differentiating between benign and malignant bone lesions.
 S acid phosphatase: suggests prostatic carcinoma.
 S Protein electro phoresis: reveal an abnormal globulin fraction,
 Urine for Bence Jones protein.
INVESTIGATING THE ‘SUSPICIOUS BONE LESION’
 Differential diagnosis of a bone abnormality will depend on
 the Age of the patient,
 the Location of the lesion and
 the Radiographic or MRI characteristics of the lesion.
 Some lesions have absolutely typical presentations: for example,
 In a child an epiphyseal lesion is likely to be either a chondroblastoma or infection,
 While at the same location in an adult it is more likely to be a clear cell chondrosarcoma or a giant-
cell tumour.

 Well-demarcated lesions tend to be benign while ill-defined lesions are more likely to be malignant or metastatic.

 Metastases to bone are increasingly likely after the age of 35, particularly if the patient has a past history of
malignancy.

 CT scans of the chest; abdomen and pelvis will be helpful to identify occult primary carcinomas. Biochemical tests will
help to exclude prostate cancer (PSA) or myeloma (serum electrophoresis and urinary Bence-Jones proteins) as
possible causes.

 Infection can be a great mimic of tumours and it is good practice to assess the CRP and ESR in all these patients.

Q) What is Biopsy? What are the types of biopsy?

Biopsy:
It is a surgical technique of taking sample of tissue from disease part in a living body; in order to discover
the cause or presence and extent of that disease.
Types of Biopsy:
--- According to histopathological processing:
a) With fixative : (10% Formalin / Formal dehyde – preserve morphology)
 Mucosal biopsy,
 Punch biopsy,
 Needle biopsy,
 Curetting,

189
  Excision,
 Resection.

b) Without fixative:
 Frozen section biopsy.

Q) What are the principles of biopsy? B & L – 537, EBN – 617

Principles of Biopsy:
 Only biopsy done - once staging is completed,
 Biopsy should be performed at the centre who will undertaking the main surgery,
 Image guided biopsy is more reliable,
 Jamshidi needles for bone and Trucut needles for soft tissues.
 Tourniquet can be used, but exsanguination should be avoided – as this can release tumour cells in the
circulation,
 No transverse incision,
 Collected sample should contain normal tissue, pseudocapsule and tumour cells.
 If bone sample is to be taken, make a small circular or oval hole in the bone to prevent pathological fracture,
 Do not cross the compartments,
 Biopsy track will have to be excised at the time of definitive surgery,
 Drain should be avoided, if drain is needed it should be pass through incision line.

Techniques of Open biopsy:

 If a needle biopsy could place neurovascular structures at risk, an open biopsy may be considered.
 The site is selected so that it can be included in any subsequent operation.
 As little as possible of the tumour is exposed and a block of tissue is removed, ideally in the boundary
zone, so as to include normal tissue, pseudocapsule and abnormal tissue.
 If bone is removed, the raw area is covered with bone wax or methylmethacrylate cement, to reduce
bleeding and contamination from the cut bone edge.
 If a tourniquet is used, it should be released and haemostasis achieved before closing the wound.
 Drains should be avoided, so as to minimize the risk of tumour contamination, but where used they
should be placed in line with the wound to allow excision at the time of definitive tumour resection.
 Taking a biopsy at the time of fixing a pathological fracture can be condoned only if the patient has
known metastatic cancer.

190
Purposes of Biopsy:
 To confirm diagnosis,
 Grading of tumor,
 For treatment planning,
 Medicolegal purpose.

Q) Techniques of Tumour Excision? APL (N) 192

191
 Intracapsular / Intralesional excision & curettage: ‘Prophylactic fixation’ is indicated-
 Incomplete form of tumour ablation, If a lytic lesion is -
(a) Greater than half the diameter of the
 Adjunctive treatment such as use of acrylic bone;
cement after curettage decreases the risk of (b) Longer than 3 cm on any view, or
(c) Painful, irrespective of its size. APL-865
local recurrence,
 Applicable for:
 Benign tumour with very low risk of
recurrence,
 For incurable tumour which need debulking to
relieve local symptom.

Marginal excision:
 Excision goes beyond the tumour but
dissection is carried out through reactive zone,
 Risk of recurrence: 50%.

Wide excision:
Surgery has been carried out through completely normal
tissue, well away from the tumour.
 Applicable for:
 Grade IA: low grade intra-compartmental lesion,
 Grade IIA in conjunction with chemotherapy.
 Risk of recurrence: below 10%.

Radical resection:
 Entire compartment in which the tumour lies is
removed en bloc without exposing the lesion,
 Applicable for high grade tumour (IIA or
IIB),
 True Radical resection: amputation at a
level above the compartment involved.

Surgical Margins: B & L -538

192
 a) Intralesional excision: Incomplete removal of tumour,
b) Marginal excision: Resection through the reactive zone of tumour
c) Wide excision: Resection outside the reactive zone of tumour,
d) Radical resection: Excising the whole affected compartment.

Q) Surgical options for Malignant Primary Bone Tomour?

 Amputation or van Ness rotationplasty,
 Excision alone,
 Excision and Replacement with graft or prosthesis.

Q) What are the routes of metastasis of malignant bone tumour?

Routes of metastasis of malignant bone tumour:

 Local spread,
 Distant spread:
 Lymphatic spread:
 Lymphatic embolism,
 Permeation – malignant cells grow along lymphatic vessel in retrograde direction,
 Skip lesion – metastasis occur by passing regional L N.
 Haematogenous spread:
 Implantation: implantation into the peritoneal cavity, pleural cavity.

Q) Mention the common sources of metastatic bone diseases?

Common sources of metastatic bone disease: --> About 10% of cases no
 Carcinoma of Breast, primary tumour is found.
 Carcinoma of Prostate, --> 93% from Breast, Bronchus,
 Carcinoma of kidney, Thyroid, Prostate & Kidney.
b&l-529
 Carcinoma of lungs,
 Carcinoma of thyroid,
 Carcinoma of UB,
 GIT carcinoma.

Q) What are the primary sites of bone metastasis?

Primary sites / common sites of bone metastasis:
o Spine / vertebrae,

193
 o Proximal femur,
o Proximal humerus,
o Skull,
o Visceral tumour can spread directly into adjacent bones eg: pelvis, ribs etc.

Q) What are the features of malignant transformation of benign tumour?

Features of malignant transformation of benign tumour:
a) Clinical features:
 Typical position of tumour,
 Pain & tenderness of affected part,
 Rapidly increasing size of bony lump,
 Recurrence after previous excision,
 Patient may present with feature of pathological #,
 Features of metastasis in LN, lungs, liver etc.

b) Radiological features:
 Irregular & indistinct tumour margins (endosteal & periosteal),
 Moth eaten appearance of bone destruction,
 Periosteal reaction:
 Onion peel appearance,
 Codman’s triangle.
 Soft tissue extension / Sun ray or burst appearance,

Q) Bone tumor mimics? APL/ N- 186

 Soft-tissue haematoma
 Myositis ossificans
 Stress fracture,
 Tendon avulsion injuries,
 Infection,
 Gout,
 Osteopetrosis / Marble bone disease / Albers-Schönberg disease,
 Osteopoikilosis:
 Melorheostosis:

194
 Painful mass in the adductor compartment of the
right thigh.
Lamellar periosteal reaction (‘onion-skin periostitis’)
X-rays demonstrate periosteal calcification.
Radiographs demonstrate a with a permeative pattern in the femoral diaphysis.
CT confirms the calcific mass.
classic dripping candle wax These features are remarkably similar to those seen

appearance. in femoral diaphyseal Ewing’s sarcoma but in this

case biopsy confirmed osteomyelitis.

195
BENIGN BONE LESIONS

196
 BENIGN BONE LESIONS
apl-194

NON-OSSIFYING  Commonest benign lesion of bone,

 It is asymptomatic and is almost always encountered
FIBROMA (FIBROUS
in children as an incidental finding on x-ray.
CORTICAL DEFECT)
 Developmental defect in Commonest sites are the metaphyses of long bones;
which a nest of fibrous
 X-ray appearance more or less oval radiolucent area
tissue appears within the
surrounded by a thin margin of dense bone; lesion that appears
bone.
to be ‘central’ is actually adjacent to or within the cortex,
hence the alternative name ‘fibrous cortical defect’.

Treatment is usually unnecessary

FIBROUS DYSPLASIA X-rays show

Fibrous dysplasia is a
 Radiolucent ‘cystic’ areas in the metaphysis or shaft;

developmental disorder in because they contain fibrous tissue with diffuse spots of
which areas of trabecular immature bone, the lucent patches typically have a
bone are replaced by cellular slightly hazy or ‘Ground-glass’ appearance.
fibrous tissue containing
flecks of osteoid and woven  Weight bearing bones may be bent, and one of the
bone. classic features is the ‘shepherd’s crook’ deformity of the
proximal femur.
 Osteoid bone:

 Woven bone:

197
OSTEOID OSTEOMA Patients are usually under 30 years of age and males
predominate.
Tiny bone tumour (less than
Patient complains of persistent pain, sometimes well
1 cm in diameter),
Any bone except the skull localized but sometimes referred over a wide area. Typically

may be affected, but over half the pain is relieved by salicylates.

the cases occur in the femur or
X-ray:
tibia.
 Feature is a small radiolucent area, the so-called
‘Nidus’.
 Lesions in the diaphysis are surrounded by dense
sclerosis and cortical thickening.
 Lesions in the metaphysis show less cortical
thickening.
Lesions in cancellous bone produce
far less periosteal reaction and are
CT scan - nidus can be seen only in fine cut CT scans.
easily mistaken for a Brodie’s
abscess. 99mTc-MDP scintigraphy - reveals intense, localized
activity.
OSTEOBLASTOMA No risk of malignant transformation
Only effective treatment is complete removal or destruction
(GIANT OSTEOID
of the nidus. Excised in a small block of bone or destroyed by
OSTEOMA) CT localized radio-ablation. The specimen should be x rayed
Similar to an osteoid osteoma immediately to confirm that it does contain the little tumour.
but it is larger (more than 1
cm in diameter), more
cellular.

198
CHONDROMA X-ray
 Shows a well-defined, centrally placed radiolucent area at
(ENCHONDROMA) the junction of metaphysis and diaphysis; sometimes the bone
 Islands of cartilage may is slightly expanded.
persist in metaphyses of bones  In mature lesions there are flecks or wisps of calcification
formed by endochondral
within the lucent area; when present, this is a pathognomonic
ossification;
feature.

 Chondromas are usually

Malignant change –
asymptomatic and are
 Probably less than 2 % (and hardly ever in a child) for
discovered incidentally on x-
patients with solitary lesions,
ray or after a pathological
fracture.  High as 30% in those with multiple lesions (Ollier’s
disease) and
 Up to 100% in patients with associated haemangiomas
(Maffucci’s syndrome).

CHONDROBLASTOMA X-ray
 Shows a rounded, well-demarcated radiolucent area in
 Benign tumour of immature
cartilage cells appear
the Epiphysis with no hint of central calcification; this

primarily in the Epiphysis, site is so unusual that the diagnosis springs readily to
mind.
 Usually of the proximal
humerus, femur or tibia.  Sometimes the lesion extends across the physeal line.

 Patients are affected around  Occasionally the articular surface is breached.

the end of the growth period
or in early adult life; there is a
predilection for males.

199
CHONDROMYXOID X-rays
 Are very characteristic: there is a rounded or ovoid
FIBROMA
radiolucent area placed eccentrically in the Metaphysis;
 Benign cartilaginous
lesions, seen mainly in  In children it may extend up to or even slightly across
adolescents and young the physis.
adults.
 Endosteal margin may be scalloped, but is almost
 It may occur in any always bounded by a dense zone of reactive bone
bone but is more common extending tongue-like towards the diaphysis.
in the lower limb.
 Cortex may be asymmetrically expanded. Sometimes
there is calcification in the ‘vacant’ area.

OSTEOCHONDROMA X-ray
 Well-defined exostosis emerging from the metaphysis,
(CARTILAGE-CAPPED
EXOSTOSIS)
 Typical features of a large cartilage-capped exostosis;
cartilage cap does not show on x-ray unless it is calcified.
The bony part may be sessile, pedunculated or
cauliflower-like.

BONE ISLAND X Ray show: CAMP-864

Bone islands, also called  Bone islands usually can be diagnosed by plain
Enostoses, are benign radiographs.
lesions of cancellous  They typically are small, round or oval areas of
bone. homogeneous increased density within the cancellous
They usually are bone.
asymptomatic and are

discovered incidentally. CT scans show:

Thickened trabeculae that merge with the surrounding

200
Almost any bone can be bone. MRI usually shows well-defined lesions that are
involved, but the pelvis isointense to cortical bone and thus dark on T1- and T2-
and the femur are the weighted images.
most common sites.
Treatment:
Most patients with bone islands can be treated with
observation with serial plain radiographs. As long as the
lesions remain asymptomatic and do not grow, no further
intervention is indicated. If a patient experiences pain, or
if the lesion grows, biopsy is indicated to rule out more
aggressive lesions, such as a sclerosing osteosarcoma,
blastic metastasis, or sclerotic myeloma.

201
Solitary cyst or Unicameral bone cyst
Appears during childhood, typically in the metaphysis of one of the long bones and
most commonly in the proximal humerus or femur.

X-rays
 Show a well-demarcated radiolucent area in the metaphysis,
 Often extending up to the physeal plate;
 Cortex may be thinned and the bone is expanded.

ANEURYSMAL BONE CYST

 Aneurysmal bone cyst may be encountered at any age and in almost any bone,
 More often in young adults and in the long-bone metaphyses.

X-rays
 Show a well-defined radiolucent cyst, often trabeculated and eccentrically placed.
 Growing tubular bone it is always situated in the metaphysis.
 It usually does not extend right up to the articular margin.
 Occasionally it causes marked ballooning of the bone end.

FIBROUS CORTICAL DEFECT

Developmental defect in which a nest of fibrous tissue appears within the bone and persists
for some years before ossifying.

x-ray
 More or less oval radiolucent area surrounded by a thin margin of dense bone;
 Views in different planes may show that a lesion that appears to be ‘central’ is actually
adjacent to or within the cortex, hence the alternative name ‘fibrous cortical defect’.

FIBROUS DYSPLASIA
Fibrous dysplasia is a developmental disorder in which areas of trabecular bone are
replaced by cellular fibrous tissue containing flecks of osteoid and woven bone.
X-rays show
 Radiolucent ‘cystic’ areas in the metaphysis or shaft; because they contain fibrous tissue
with diffuse spots of immature bone,
 Lucent patches typically have a slightly hazy or ‘ground-glass’ appearance.
 The weightbearing bones may be bent, and one of the classic features is the ‘shepherd’s
crook’ deformity of the proximal femur.

202
CHONDROMA (ENCHONDROMA)
Islands of cartilage may persist in the metaphyses of bones formed by endochondral
ossification;

X-ray shows
 A well-defined, centrally placed radiolucent area at the junction of metaphysis and
diaphysis;
 Sometimes the bone is slightly expanded.
 In mature lesions there are flecks or wisps of calcification within the lucent area; when
present, this is a pathognomonic feature.

CHONDROMYXOID FIBROMA
Benign cartilaginous lesions, this is seen mainly in adolescents and young adults. It may
occur in any bone but is more common in the lower limb.
X-rays are
 Very characteristic: there is a rounded or ovoid radiolucent area placed eccentrically in
the metaphysis; in children it may extend up to or even slightly across the physis.
 The endosteal margin may be scalloped, but is almost always bounded by a dense zone
of reactive bone extending tongue-like towards the diaphysis.
 The cortex may be asymmetrically expanded. Sometimes there is calcification in the
‘vacant’ area.

CHONDROBLASTOMA
Benign tumour of immature cartilage cells, appear primarily in the epiphysis - usually of
the proximal humerus, femur or tibia.

X-ray shows
A rounded, well-demarcated radiolucent area in the epiphysis with no hint of central
calcification;

203
GIANT-CELL TUMOUR
Lesion of uncertain origin that appears in mature bone,

X-rays show
 A radiolucent area situated eccentrically at the end of a long bone and bounded by the
subchondral bone plate.
 The endosteal margin may be quite obvious, but in aggressive lesions it is ill-defined.
 The centre sometimes has a soap-bubble appearance due to ridging of the surrounding
bone.
 The cortex is thin and sometimes ballooned; aggressive lesions extend into the soft
tissue.
 The appearance of a ‘cystic’ lesion in mature bone, extending right up to the
subchondral plate - is so characteristic.

Brown tumour

Estimations of blood calcium, phosphate and alkaline phosphatise concentrations so as

exclude an unusual ‘brown tumour’ associated with hyperparathyroidism.

Feature of Hyperparathyroidism:
 Primary: due to adenoma / hyperplasia. Stones, bones, abdominal groans, psychic
moans.
Secondary: due to persistent hypocalcaemia (↓Ca). eg- Rickets, Osteomalacia.
 Tertiary: secondary hyperplasia. eg-CKD.

204
Q) Benign bone tumours in Epiphysis?
 Chondroblastoma,
 GCT,
Q) Benign bone tumours in Metaphysis?
 Non ossifying fibroma / Fibrous cortical defect,
 Chondroma / Enchondroma,
 Chondromyxoid fibroma,
 Osteochondroma,
 SBC,
 ABC,
 Osteochondroma.
Q) Benign bone tumours in Diaphysis?
 Osteid osteoma,
 Giant osteoid osteoma / Osteoblastoma,
 Fibrous dysplasia.

205
 CYST & CYST LIKE LESION IN BONE.
APL-200

Cysts and cyst-like lesions of bone

(a) Simple bone cyst: (b) Chondromyxoid (c) Aneurysmal bone cyst: (d) Giant-cell tumour:
Fills the medullary cavity but fibroma: Expansile cystic tumour, always on Hardly ever appears before
does not expand the bone Looks cystic but it is actually a the metaphyseal side of the physis. epiphysis has fused, the
radiolucent benign tumour; pathognomonic feature is that
always in the metaphysis; hard it extends right up to the
boundary tailing off towards subarticular bone plate;
the diaphysis. sometimes malignant.

206
 Simple bone cyst Aneurysmal bone Chodroblastoma Chondromyxoid Fibrous dysplasia
cyst fibroma

Usually appears during Age : 10 – 30yrs Age: at the end of Mainly seen in Usually occurs in childhood
childhood. growth period or in adolescent and & adolescence.
early adult life. young adults.
--> Typically Always involve Appears May occur in any Ǿ Developmental disorder
metaphyseal region of metaphyseal primarily in the bone, found in the metaphysis or
long bone, region of long epiphysis, More common in diaphysis,
--> Most commonly: in bone, Usually in the the bones of lower Ǿ Common sites: Proximal
proximal humerus or proximal humerus, limb. femur, tibia, humerus, Ribs,
femur. femur or tibia. Craniofacial bones.
C/F: C/F: C/F: C/F: C/F:
-->Usually Φ Pain in the Predilection for Pt seldom ~ Monostotic: affect one
asymptomatic, affected part, males, complain, bone,
Φ Swelling on the ~ Monomelic: affect one
-->Usually discovered affected part. Constant ache in Incidental finding limb,
after a pathological # or affected joint, or may present with ~ Polyostotic: affect many
as an incidental finding pathological #. bones.
on x ray. Tenderness in > Single lesion: may
the adjacent bone. asymptomatic,
> Large lesion: pain or
pathological #.
X ray: X ray: X ray: X ray: X ray:
--> well demarcated Φ Well defined Rounded, well Rounded or ovoid > Radiolucent cystic area in
radiolucent area in the radiolucent cyst, demarcated radiolucent area the metaphysis or shaft,
metaphysis, radiolucent area in placed eccentrically > Lucent area typically
Φ Often the epiphysis, in the metaphysis. have slightly hazy or
--> SBC fills the trabeculated & Endosteal margin Ground glass appearance.
medullary cavity but eccentrically placed. Sometimes may be scalloped, > Weight bearing bones
does not expand the lesion extends may be bent eg: Shepherd’s

207
bone. Φ Does not extend across the physeal crook deformity of
right up to articular line, proximal femur.
margin,

Occasionally
Φ Occasionally articualar surface is
causes marked breached,
ballooning of the
end of bone.

H/P/E: H/P/E: H/P/E: H/P/E: H/P/E:

--> Lining membrane

consists of filmsy
fibrous tissue, often
containing giant cells. Φ Tumour lining Benign tumour Benign
> Loose cellular fibrous
consists of fibrous of immature cartilaginous lesion,
tissue with widespread
tissue with cartilage cells, 3 types of tissues
patches of woven bone &
vascular spaces, Large collection can be identified:
scattered giant cells.
deposits of of chondroblasts stellate cells, islands
> Malignant transformation
haemosiderin and surrounded by of hyaline cartilage
to Fibrosarcoma (0.5 – 5%).
multinucleated immature fibrous and fibrous tissues.
giant cells tissue,
Φ Malignant Tumours do not
transformation undergo malignant
does not occur. change but may be
locally aggressive
and may extend
into the joint.
Treatment: Treatment: Treatment: Treatment: Treatment:
--> Active cyst: Curettage + After the end of Excision of lesion + > Small lesion: needs no
(enlarging in sequential chemical growth period – autogenous BG. treatment,
x rays,) cauterization + marginal excision > Large lesion / painful /
Ǿ Aspiration of fluid + bone graft. of the lesion and threatening to #: curettage +
inj. Methylprednisolone replaced by BG with or without bone
/ autologous BG. autogenous bone cement.
Ǿ If cyst goes on graft.

208
enlarging or
pathological # present –
curettage + BG.
Ǿ If risk of # -
prophylactic fixation.
asymptomatic lesion:
can be left alone,

209
 SIMPLE BONE CYST
Apl-200

Simple bone cyst: Fills the medullary cavity but does not expand the bone,
Cyst – on expanding the cortex & Fracture through a cyst

Q) What is Simple Bone Cyst?

-- This lesion (also known as a solitary cyst or unicameral bone cyst) appears during childhood, typically in the
metaphysis of one of the long bones and most commonly in the proximal humerus or femur.

Q) Is it tumour?
-- It is not a tumour, it tends to heal spontaneously and it is seldom seen in adults.

Q) Clinical features of simple bone cyst?

The condition is usually discovered after a pathological fracture or as an incidental finding on x-ray.

Q) Pathology of SBC?
Pathology The lining membrane consists of flimsy fibrous tissue, often containing giant cells.

Q) Differential diagnosis of SBC?

Non-osteogenic fibroma, fibrous dysplasia and the benign cartilage tumours are solid and merely look cystic on x-
ray.

210
Q) Treatment of SBC?
 Treatment depends on whether the cyst is symptomatic, actively growing or involved in a fracture.

 Asymptomatic lesions in older children can be left alone but the patient should be cautioned to avoid
injury which might cause a fracture.

Typical solitary (or unicameral) cyst – on the shaft side of the physis and expanding the cortex, Injection with methylprednisolone, and
healing.

 ‘Active’ cysts (those in young children, usually abutting against the physeal plate and obviously
enlarging in sequential x-rays) should be treated, in the first instance, by aspiration of fluid and injection of 80–160
mg of methylprednisolone or autogenous bone marrow. This often stops further enlargement and leads to healing of
the cyst.

 If the cyst goes on enlarging, or if there is a pathological fracture, the cavity should be thoroughly
cleaned by curettage and then packed with bone chips, but great care should be taken not to damage the nearby
physeal plate. If the risk of fracture is thought to be high, prophylactic internal fixation should be applied.

 If curettage is thought to be necessary, material from the cyst should be submitted for examination.

Q) Complication of treatment of SBC?

-- There is always the risk that the cyst will recur and more than one operation may be needed.

211
 FIBROUS DYSPLASIA
Apl-195

Q) What is Fibrous dysplasia?

-- Fibrous dysplasia is a developmental disorder in which areas of trabecular bone are replaced by cellular fibrous
tissue containing flecks of osteoid and woven bone.
Q) What are the common sites of Fibrous dysplasia?
-- Most common sites of occurrence are the
 Proximal femur,
 Tibia,
 Humerus,
 Ribs and
 Cranio-facial bones.
Q) What are the varieties of Fibrous dysplasia?
-- Fibrous dysplasia may affect one bone (monostotic), one limb (monomelic) or many bones (polyostotic).

Q) What are the clinical features of Fibrous dysplasia?

 Small, single lesions are asymptomatic.
 Large, monostotic lesions may cause pain or may be discovered only when the patient develops a
pathological fracture.
 Patients with polyostotic disease present in childhood or adolescence with pain, limp, bony
enlargement, deformity or pathological fracture.
 Untreated, the characteristic deformities persist through adult life,
eg. in the upper femur (with the so-called ‘shepherd’s crook’ appearance)
 Occasionally the bone disorder is associated with café-au-lait patches on the skin and (in girls)
precocious sexual development (Albright’s syndrome).

212
Q) What the X ray features of Fibrous dysplasia?

Monostotic fibrous dysplasia of the upper femur (with the so-called ‘shepherd’s crook’ appearance) & Polyostotic fibrous dysplasia.

 X-rays show -
 Radiolucent ‘cystic’ areas in the metaphysis or shaft; because they contain fibrous tissue with diffuse spots
of immature bone, the lucent patches typically have a slightly hazy or ‘ground-glass’ appearance.
 The weight bearing bones may be bent, and one of the classic features is the ‘shepherd’s crook’ deformity
of the proximal femur.

 Radioscintigraphy shows - marked activity in the lesion.

Q) Histological features of Fibrous dysplasia?

Histological picture is of loose, cellular fibrous tissue with widespread patches of woven bone and scattered giant
cells.

213
Q) Complications of Fibrous dysplasia?
 If the lesions are large, the bone is considerably weakened and pathological fractures or progressive
deformity may occur.
 Malignant transformation to fibrosarcoma occurs in 0.5 per cent of patients with monostotic lesions
and up to 5 per cent of patients with Albright’s syndrome.

Q) Treatment of Fibrous dysplasia?

 Treatment depends on the extent of the defect and the presence or absence of deformities.
 Small lesions need no treatment.
 Those that are large and painful or threatening to fracture (or have fractured) can be curetted and grafted,
but there is a strong tendency for the abnormality to recur. A mixture of cortical and cancellous bone grafts may
provide added strength even if the lesion is not eradicated.
 For very large lesions, the grafts can be supplemented by methylmethacrylate cement. With large cysts,
the bone often bleeds profusely at operation: forewarned is forearmed.
 Deformities may need correction by suitably designed osteotomies.

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 ABC.
ANEURYSMAL BONE CYST.
APL/N-201

Aneurysmal bone cysts (ABCs) are benign, expansile lesions of bone composed of blood-filled cystic spaces.
ABCs appear as a subperiosteal, poorly defined osteolytic lesion, elevating and progressively eroding the cortex.

Characteristics:
 They predominantly affect children and teenagers with an equal sex distribution.
 ABCs can affect any bone but are most commonly seen in the metaphyses of long bones, particularly the
femur, tibia and humerus.
 They may occur in the spine where they typically affect the posterior elements.
 They are destructive lesions and, while they are histologically benign, they can result in significant
disability.
 The lesion may demonstrate rapid progression, but equally it may resolve spontaneously following trauma,
either fracture or biopsy.
 Malignant transformation does not occur. apl-202

Clinical features:
 Patients typically present with pain and swelling.
 When affecting the spine, presentation can be with nerve root impingement and neurological impairment.

Investigations:
 X ray:

 Show a well-defined radiolucent cyst, often trabeculated and eccentrically placed.

 In a growing tubular bone it is always situated in the metaphysis.
 Expansile, lytic lesion in the metadiaphysis area with a pathological fracture.
 It usually does not extend right up to the articular margin.
 Occasionally it causes marked ballooning of the bone end.

215
  MRI:

 MRI demonstrates the typical cystic features with multiple intralesional septations and fluid levels.
 Fluid-fluid levels are seen within the lesion which is highly suggestive of an aneurysmal cyst.
Histopathology:

 Histologically, ABCs are composed of blood-filled, cystic spaces separated by fibrous septae,
 Cyst contained blood and lined by loose fibrous tissue containing numerous giant cells.
 Histologically the lining consists of fibrous tissue with vascular spaces, deposits of

haemosiderin and multinucleated giant cells.

Differential diagnosis:
 GCTs,
 Chondroblastoma,
 Osteoblastoma and
 Fibrous dysplasia,

Treatment:
 The lesion may demonstrate rapid progression, but equally it may resolve spontaneously following trauma,
either fracture or biopsy.
 Curettage of the lesion at the time of biopsy (‘Curopsy’), debriding the cystic cavity wall, is often effective
though recurrence can occur in up to 20% of cases.
 During curettage there may be considerable bleeding from the fleshy lining membrane.
apl- 202

216
  Cyst should be carefully opened, thoroughly curetted and then packed with bone grafts. Sometimes

the graft is resorbed and the cyst recurs, necessitating a second or third operation.
 Radiation is effective at stimulating cyst calcification but must be offset by the risk of secondary sarcoma or of
growth arrest due to damage to the nearby physis.

217
 OSTEOID OSTEOMA & OSTEOBLASTOMA
Apl-196

OSTEOID OSTEOMA OSTEOBLASTOMA

(GIANT OSTEOID OSTEOMA)

X-ray appearance depends on the site of the lesion.

(a) With cortical tumours there is marked reactive bone
thickening leaving a small lucent nidus, which may itself have a
central speck of ossification.
(b) Lesions in cancellous bone produce far less periosteal
reaction and are easily mistaken for a Brodie’s abscess.

This tiny bone tumour (less than 1 cm in diameter) (more than 1 cm in diameter),

Patients are usually under 30 years of age and males Usually seen in young adults, more often in men
predominate. than in women.

Any bone except the skull may be affected, but over It tends to occur in the spine and the flat bones;
half the cases occur in the femur or tibia.
Patient complains of persistent pain, sometimes well Patients present with pain and local muscle
localized but sometimes referred over a wide area. spasm.
Typically the pain is relieved by salicylates.
If the diagnosis is delayed, other features appear: a
limp or muscle wasting and weakness; spinal lesions
may cause intense pain, muscle spasm and scoliosis.
X-ray feature is a small radiolucent area, the so-called X-ray shows a well-demarcated osteolytic lesion
‘nidus’. Lesions in the diaphysis are surrounded by which may contain small flecks of ossification.
dense sclerosis and cortical thickening; this may be so There is surrounding sclerosis but this is not
marked that the nidus can be seen only in fine cut CT always easy to see, especially with lesions in the
scans.
flat bones or the vertebral pedicle.
99mTc-MDP scintigraphy reveals intense, localized
Radioisotope scan will reveal the ‘hot’ area.
activity.

218
Treatment is complete removal or destruction of the Treatment consists of excision and bone grafting.
nidus. The lesion is carefully localized by x-ray and/or
CT and then excised in a small block of bone or
destroyed by CT localized radio-ablation.
D/D: Brodie’s abscess, Ewing sarcoma.

Characteristics of Osteoid osteoma: camp-859

 Most osteoid osteomas are found in the second or third decades of life, but an occasional lesion has been
reported in older patients.
 No malignant change has ever been documented.
 The lesion consists of a small (<1.5 cm) central radiolucent nidus with surrounding bony sclerosis.
 Microscopic appearance consists of fibrovascular tissue with immature bony trabeculae that are rimmed
by prominent osteoblasts. Osteoclasts and occasional giant cells can be seen. There are no aggressive features.

Treatment:
 If the patient’s symptoms are adequately controlled, and the patient is willing to undergo long-term
medical management, antiinflammatory medication can be used as the definitive treatment. Patients treated in this
manner usually experience spontaneous healing of the lesion within 3 to 4 years.
 Most patients with lesions of the pelvis or long bones of the extremities can be treated with percutaneous
radiofrequency ablation. This technique involves a CT-guided core needle biopy after which a radiofrequency
electrode is inserted through the cannula of the biopsy needle. The temperature at the tip is increased to 90°C for 6
minutes. Recurrence rates are less than 10%.The procedure may not be indicated for vertebral lesions (due to risk
of thermal injury to the spinal cord) or lesions of the small bones of the hands or feet (due to risk of thermal injury
to the skin).

219
 Osteoid osteoma in a 17-year-old girl
who complained of left thigh pain for
several months. Anteroposterior view of
left hip shows small radiolucent lesion
with thick sclerotic rim of reactive bone.

 Surgical management involves removal of the entire nidus. This can be accomplished by curettage or
en bloc resection. The latter is associated with a low recurrence rate but is rarely indicated for lesions in the long
bones because of an increased risk of postoperative pathological fracture.

DIFFERENTIAL DIAGNOSIS:
 GARRÉ’S SCLEROSING OSTEOMYELITIS APL-41,camp735

Garre’s sclerosing osteomyelitis:

--- It is a form of non suppurative osteomyelitis which is characterized by marked sclerosis and cortical
thickening.
--- Sclerosing osteomyelitis is a chronic form of disease in which the bone is thickened and distended

but abscesses and sequestra are absent.

Site:
 Diffuse enlargement of bone usually at diaphysis of tubular bone or mandible,
 There is usually no abscess.
Cause:
 Cause is unknown,
 Thought to be an infection caused by a low grade, possibly anaerobic bacterium.
Clinical features:
 Patient is typically children / adolescent or young adult,
 Intermittent pain of moderate intensity and usually long duration,
 Long H/O aching and slight swelling & tenderness over the affected bone,
 Recurrent attack of acute pain accompanied by malaise and slight fever.

220
 Sclerosing osteomyelitis of tibia documented by biopsy.

Investigations:
d) X ray of affected part:
 ed bone density and cortical thickening,
 Marrow cavity may be completely obliterated,
 There is no abscess cavity.

 Brodie’s abscess:
-- It is a localised form of sub acute osteomyelitis caused by less virulent pyogenic organisms.

Site:
-- Usually in the metaphyseal area usually before physeal closure and in adult in metaphyseal – epiphyseal
area is involved, eg-
 Upper end of tibia,
 Calcaneum,

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  Lower end of femur,
 Lower end of humerus.

Causative organisms:
-- Less virulent pyogenic organisms, eg -
 Staphylococcus aureus (50%), Culture report
 Staphylococcus albus,
 20% cases culture report: negative.

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 GCT
Giant Cell Tumour.
APL (N)-202

GCT:
This is a benign but locally aggressive bone tumour, composed of proliferation of mononuclear cells with scattered
macrophages.
It is an osteolytic lesion of uncertain origin, appears usually in the Epiphysis of Mature bone (after closure of
epiphysis).
Synonym:
Osteoclastoma.

Giant-cell tumours The tumour always abuts against the joint margin.

Q) Why GCT is more accurate term than Osteoclastoma?

 Giant cells represent as Fused Oval or Spindle shaped cells, not osteoclast cells.
 Bone destruction by Giant cells rather than Osteoclast cells.

Q) Characteristics of GCT:
Pulmonary Mets:
 5% of all Primary bone tumours, --> Mortality 15%
 GCT,
 Benign >90% & Malignant 5 – 10 %,  Chondroblastoma.
 Hardly ever seen before closure of physis,
 About 3% of GCT is metastasized to lungs.
 Pathological # occurs in 10 – 15% of cases 15%:
 Pathological ≠,
 Age:
 Recurrence,
o 20 – 40 years of age,  Mortality – in case of pulmonary Mets.
o Peak incidence – 3rd decade.

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  Sex: Female > Male.
 Malignant transformation: 1 – 13%,
 1% to 2% may be synchronously or metachronously multicentric. camp-887

 Site:
 Distal femur, ---> About 60% around knee.
 Proximal tibia,
 Distal radius, --------------> 3rd most common site.
 Proximal humerus.
 Other bone can be affected.

Hardly ever appears before epiphysis has fused, the Pathognomonic feature is that it extends right up to the subarticular bone plate;
sometimes malignant.

Q) Which bone is immune for GCT?

No bone is immune for GCT, but some sites are rare eg- patella, ribs.

Q) A young adult with GCT at distal radius, why called GCT of bone?
 Characteristics: 3E,
 Age: Young adult; so after closer of epiphysis,
 Site: 3rd Common site – distal radius.

Q) Clinical features:
 Pain:
 Pain at the end of long bone,
 Dull aching in nature,
 Chronic & constant,
 Worst at night,
 Increases with activity.

 Swelling:

224
  Towards end of the affected limb / one side of affected bone,
 Gradually increasing size,
 Extends right up to subarticular bone plate,
 Sometimes rapidly growing / aggressive variety,
 Skin over the bone is shiny, but no dilated vessels.
 3E: Epiphyseal, Eccentric & Expansile.

 Joint movement:
 Usually joint is not involved,
 Joint movements may be restricted in late stage when articular surface has been breached.

 Pathological # :
 Pathological # occurs in 10 – 15% of cases.

Q) On examination:
a) Look:
 Swelling at the end of limb,
 Shape of swelling – globular / diffuse / circumscribed,
 Overlying skin shiny,
 Veins are not dilated,
 Muscle wasting present / absent,
 In case of lower limb – gait & squatting.

b) Feel:
 Temp : raised,
 Tenderness : present,
 Size : --- x --- cm,
 Consistency : hard, Egg shell cracking sound may present on applying pressure,
 Swelling fixed to underlying bone,
 Overlying skin : free,
 Regional LN : not palpable,
 Neurovascular status : normal,

c) Move:
 ROM of nearby joint : usually normal,
 Movements may be restricted if articular surface has been breached.

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Q) Differential diagnosis:

Cystic lesion in Epiphysis.

 Chondroblastoma,

 ABC,
 Simple bone cyst,
 Fibrous dysplasia, Cystic lesions in Metaphysis.
 Chondromyxoid fibroma,
 Brown tumour of hyperparathyroidism.
Q) Investigations FOR GCT?
i) X ray of the affected part:

 Epiphyseal & Expansile radiolucent lesion situated Eccentrically at the end of a long bone and bounded
by subchondral bone plate,
 Endosteal margin is quite obvious, but in aggressive lesion is ill defined;
 Cortex is thinned & sometimes ballooned; when cortical breakage present – soft tissue spillage may
seen,
 Center sometimes / early stage - has a soap bubble appearance due to ridging of the surrounding bone
(trabeculation with marginal sclerosis),
 Campanacci’s Radiological Grading:

apl/10- 199

226
 ii) Blood test:
 Serum acid phosphatase: ↑ed, Stromal & Giant cells contain acid phosphatase,
 Serum alkaline phosphatase:
 Serum calcium: ↑ed in Brown tumour.
 Serum phosphate:

To see:
iii) CT scan:  Extension of tumour,
 Staging of tumour
iv) MRI:  Invasion into joint.

v) Arthroscopy:

vi) Chest X ray {Inspiratory & Expiratory phase}: to see pulmonary metastasis.

vii) Biopsy:
 Excisional biopsy:
 Frozen section:

Q) Enneking Staging of GCT?

Stage Findings
Stage I Latent / Inactive Φ Incidental finding,
(10 – 15%) Φ No symptom,
Φ Eccentric subchondral lucency.
Stage II Active Symptomatic,
(70%) Thinning of cortex with Expansile lesion,
Sometimes present with pathological #.
Stage III Aggressive Rapidly growing,
(10 – 15%) Pathological # (10- 15%),
Cortex breached & spillage to surrounding,
Lungs metastasis 3%.

227
Q) Histological findings of GCT?

Giant-cell tumour – Histology A low-power view of the biopsy shows the abundant multinucleated giant cells lying in a stroma composed
of round and polyhedral tumour cells. There are numerous mitotic figures

 Numerous multinucleated giant cells scattered on a background of stromal cells with little or no visible
intercellular tissue (striking feature),

 Nuclei of mononuclear spindle cells are identical with the nuclei of giant cells,

 Number of nuclei varies from 15 – 150 which are centrally placed, TUREK

Multinucleated giant cells (typically 40 to 60 nuclei per cell). camp-887

 Aggressive lesions tend to show more cellular atypia and mitotic figures,

 Histological grading is unreliable as a predictor of tumour behaviour.

 Jaffe’s Histological criteria:

Grade Criteria
Grade I Φ Multinucleated giant cells with background of stromal cell,
Φ Well differentiated spindle shaped mononuclear cell.
Grade II Ǿ Number of giant cells increased within the stromal cells,
Ǿ Poorly differentiated spindle shaped mononuclear cells.
Grade III Nucleus of giant cells becomes identical,
Undifferentiated spindle shaped mononuclear cells.

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Q) Treatment of GCT?

a) Well confined, slow growing lesion with benign histology:

 Curettage: GCTs appear as fleshy / meaty,
 Stripping of the cavity with Burrs and Gauges: reddish-purple tissue

 Chemical cauterization:
 Swabbing with H2O2 / 5% Phenol + 70% Alcohol / Liquid nitrogen,
 Wash with Normal saline.
 Cavity is then packed with bone chips / bone cement.

b) More aggressive or Recurrent lesion:

 Excision of tumour mass followed by Bone grafting or Prosthetic replacement.

Q) Recurrence rate of different treatment modalities:

Treatment modalities Recurrence rate

1. Curettage only 85%
2. Curettage + Chemical cauterization (5% phenol + 70% alcohol) 45%
3. Curettage + Bone graft 41%
4. Curettage + Chemical cauterization + Bone graft 14%
5. Curettage + Chemical cauterization + Bone graft + Bone cement 5 – 10%
6. Curettage + Cryosurgery with liquid nitrogen + Bone graft 1.9%
7. Wide excision + Bone graft / Massive allograft 5 – 7%
8. Marginal excision + Bone graft 36%
9. Amputation / Disarticulation 0%
10. Radiation – inaccessible sites / inoperable sites (spine, pelvis, 50 – 70%
sacrum etc)

Q) Treatment of GCT? APL/N-199

 Stage 1 and 2 lesions, extended intralesional curettage with a detailed debridement of the lesional wall will be
effective.

 Stage 3 disease can often be treated by thorough curettage though in some cases en-bloc resection is required.

 Denosumab has a role in advanced stage 3 lesions or lesions in inoperable locations.

 Anti-RANKL antibodies such as Denosumab can be used to stop the osteolytic process and switch the balance
towards bone formation.

229
  Response of the tumour can be dramatic.

 Side-effect can result in significant morbidity, including hypocalcaemia, osteonecrosis of the jaw and atypical
fracture patterns.

RANK- Receptor Activator of Nuclear Factor Kappa B

RANKL- Receptor Activator of Nuclear Factor Kappa B Ligand.

Q) What is cauterization? What are the types of cauterization?

Cauterization: Burning of a part of structure,
Types: 2 types
1) Thermal cauterization: with
a. Diathermy
b. Liquid nitrogen,
2) Chemical cauterization.

Q) What types of bone grafts are used in the treatment of GCT?

 Autograft:
 Autograft from iliac creast,
 intercalary graft – usually shaft of fibula,
 Vascular / Non vascular fibular graft,
 Ribs can be used, when fibular graft is not possible.

Giant-cell tumour – treatment

(a) Excision and bone grafts.
(b) Block resection and replacement with a large allograft.

230
  Allograft:
 Osteoarticular Allograft / bone graft + articular cartilage.

Q) What are the disadvantages of using only bone graft?

o Wt bearing joint must be protected for prolong time to prevent pathological #,
o Does not give immediate stability,
o Tumour recurrence is often difficult to distinguish, due to graft resorption,

Q) What is Sandwich technique?

Curettage + Chemical cauterization – followed by:
1) Bone graft
2) Gel foam
3) Bone cement SANDWICH.
4) Gel foam
BG-C-GB
5) Bone graft

Q) What are benefits of using bone cement?

o Provides immediate stability,
o Wt bearing joint must not be protected for prolong time to prevent pathological #,
o Allow earlier detection of recurrence,
o May kill residual tumour cells by the heat (800 to 850C) of polymerization.

231
Q) Procedure of chemical cauterization?

After proper curettage fill up the cavity with 5% phenol and keep it for 20 – 30 seconds,
(Phenol is acidic which lysis of cells both normal & tumour cells)

Then apply 70% alcohol / Methyl alcohol and keep it for 30 – 40 seconds for 3 – 4 times,
(Alcohol neutralizes phenol to prevent further destruction of normal cells)

Suck out alcohol after each application,

Then wash the cavity with normal saline,

Finally apply bone graft with or with out cement.

Q) Procedure of Cryosurgery?

- 600 - single time,

--> Liquid nitrogen /
Thermal cauterization - 210 - three times.
(freezing)
--> After that, cavity is filled up with bone graft.

Q) Complications of Cryosurgery / liquid nitrogen?

 Skin necrosis,
 Nerve injury.
 Pathological #,
 Prolong healing time,

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Q) What are the complications of GCT? apl/N -199

 Recurrence (15%)
 Pathological # (15%),
 Malignant transformation (Osteosarcoma, Fibrosarcoma ) / Malignant GCT: 1 – 13%.
 Metastasis to lungs 3%
Q) What are the causes of Recurrence of GCT?
o Incomplete curettage / removal,
o Incomplete filling of cavity,
o Aggressiveness of the tumour,
o Soft tissue involvement.
Q) What are the characteristics of Malignant GCT?
 Painful rapidly growing tumour,
 Tumour extend to surrounding tissue,
 Metastasis to lungs,
 Histology shows:
 More cellular atypia and mitotic figure,
 Increased number of stromal cells / spindle cells,
 Pleomorphism,
 Hyperchromatic nuclei.

Q) What are the indications of amputation in GCT?

 Malignant GCT
 Wide spread aggressive tumour,
 Invading surrounding soft tissue,
 Repeated recurrence.
 Tumor with fungating growth.

Q) Follow up after treatment?

 3 monthly for 1 years,
 6 monthly for 2 years,
 Then yearly.

233
Q) Special operations according to the site of GCT?
A) GCT in Lower end of femur / Upper end of tibia:
 For Benign local tumour: Curettage + Bone graft + Bone cement.
 Large tumour encroaches subchondral bone: Curettage + BG + Bone cement.
 Invasion into articular cartilage:
 Enbloc excision + Arthrodesis,
 Arthrodesis + Fibular bridging on both sides,
 Arthroplasty with custom made prosthesis,
 Turn Y plasty.
B) GCT in Lower end of radius:
 Curettage + Bone graft,
 Excision of tumour mass {En bloc} +
 Centralization of ulna,
 Radialization / Translocation of ulna,
 Vascularized / non-vascularized proximal fibular graft,
 Allograft,
Points Centralization of ulna Translocation of ulna / Radialization of
ulna (U→R)
a) Indication: GCT in distal radius GCT in distal radius.
b) Advantages: Ǿ Easy procedure, Φ Wrist movements are preserved,
Ǿ Duration of surgery – short, Φ Supination & pronation movements are
Ǿ Chance of nonunion – rare, preserved
Ǿ Chance of implant failure – less, Φ No deviation of hand,
Ǿ Stable wrist. Φ Grip strength: good,
c) Disadvantages: --> Restriction of wrist movements (90 – 95%), --> Chance of non union,
--> Restriction of supination & pronation, --> Chance of implant failure,
--> Deviation of hand either radial or ulnar side, --> Duration of surgery: long,
--> ↓ Grip strength.

d) Procedure: >In centralization of ulna – Scaphoid or Lunate is

used for ulno-carpal fusion,
> Fusion of ulna with scaphoid – more stable,
> Fusion of ulna with lunate – less stable.

234
 Centralization of ulna
C) GCT in Upper end of humerus: Wide excision + Custom made prosthesis,

D) GCT in Shaft of humerus: Wide excision + Fibular bone graft (Strut graft),

E) GCT in talus:
 Curettage + Bone graft,
 Talectomy,
 Arthrodesis.

F) GCT in spinal column: Radiotherapy,

G) GCT in clavicle / fibula: Excision of affected part,

H) GCT in tendon sheath: Excision of tendon (entirely),

I) Lungs mets treatment: lobectomy.

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 Chondroblastoma.
APL-198, APL/N- 195

Chondroblastoma:
--- Benign tumour of immature cartilage cells which appear primarily in the epiphysis.
---- Less than 1% of all bone neoplasms and are more common in males.

Site: Usually appears in proximal humerus, femur or tibia.

Age: patients are affected around –

 The end of growth period or
 In early adult life.

Characteristics / Clinical features:

 Predilection for males,
 Constant ache in the affected joint,
 Tender spot in the adjacent joint,
 Tumour does not undergo malignant change,
 Tumour may be locally aggressive and extend into the joint.

X ray findings:

 Rounded, well demarcated radiolucent area in the epiphysis with no hint of central calcification,
 This site is so unusual that the diagnosis springs readily to mind,
 Sometimes the lesion extends across the physeal line,
 Occasionally articular surface is breached.

236
Lytic lesion in the proximal tibial physis crossing the MRI demonstrates a typical chondroblastoma with secondary ABC

physeal scar and abutting the subchondral plate. transformation (note fluid-fluid levels).

Histopathology:

More faintly staining islands of

chondroid tissue composed of Round
cells (‘chondroblasts’) and scattered
multinucleated giant cells.

 Histologically, they appear as ‘wet-sawdust’ with areas of chondroid matrix, calcification and haemorrhage.
 Areas resembling an ABC may be seen in 35% of cases.

D/D: Aneurysmal bone cyst.

Treatement:
 Majority of cases can be treated with simple curettage with or without bone grafting to the defect to support the
subchondral plate.
 High risk of recurrence (about 10% of cases) after incomplete removal.
 More aggressive, en-bloc resection may be required for recurrent disease.

237
Chondroblastoma in 16-year-old boy. Patient had left shoulder pain for 1 year.

A, Anteroposterior radiograph of left shoulder reveals lytic lesion in

proximal left humerus extending across open physis.

B, CT scan shows calcification of lesion.

MR images show fluid-fluid level. Incision

biopsy confirmed diagnosis of
chondroblastoma with secondary
aneurysmal bone cyst.

Anteroposterior radiograph after curettage and bone grafting.

238
 Diaphyseal aclasis.
Multiple Exostosis.
Osteochondroma.
(CARTILAGE-CAPPED EXOSTOSIS)
Apl-199

-- It is an Autosomal dominant disorder characterized by multiple cartilage capped bony outgrowth –

arise from metaphysis of long bones or along the apophyseal border of scapula / pelvis.

Apophysis:
Normal bony outgrowth that arise from separate ossification center and fuses with the bone in
the course of time.

Genetics:
o It is an autosomal dominant disorder,
o Abnormalities in chromosome 8, 11 & 19.

Pathology:
 Aberration of growth - Unrestricted transverse growth of the cartilagenous physis,
 Effects only on the enchondral bone,
 Cartilagenous excrescences appear at the periphery of physis and proceed in the usual way to enchondral
ossification.
 Typically, the cap is only a few millimeters thick in adults, although it may be 2 cm thick in a child.
 A bursa frequently overlies the tumor and may contain osteocartilaginous loose bodies.

239
Theory of histogenesis: EBN – 619, TUREK- 599

 Cambium layer of periosteum produces embryonic tissue that is the common forerunner for bone
and cartilage. Tumor may represent a ‘perverted activity of the periosteum’ which reverts to its role
as perichondrium.
 At the point of tendinous insertion, there is focal accumulation of embryonic connective tissue.

Types of Exostosis:
 According to number:
1) Solitary exostosis,
2) Multiple exostosis.
 According to shape:
1) Sessile (wide / broad based) – more chance of malignant change.
2) Pedunculated.

Clinical features:
 Patient is usually teenager or young adult,
 Multiple lump over the ends of bones,
 Osteochondromas may occur on any bone preformed in cartilage but usually are found on the metaphysis of
a long bone near the physis.
 Pain over the lump (due to overlying bursitis or impingement of nerve or soft tissue),
 Paresthesis due to stretching of adjacent nerve,
 Difficulty in the movements of affected limb.
 Osteochondroma usually do not recur after operation but if does it always recur as osteosarcoma.

240
On Examination:
a) Look:
 Number:
 Site / Sites:
 Shape:
 Compare both limbs,
 Hemispherical / oval / diffuse protuberance,
 Overlying skin: any scar mark / hair distribution,
 Gait.

b) Feel:
 Temp,
 Tenderness,
 Size,
 Surface is smooth,
 Bony hard in consistence,
 Overlying skin is free / fixity to overlying skin,
 Often possible to feel the base which may be quite narrow,
 Distal neurovascular status,
 Palpate regional lymph nodes.

c) Move:
 Lump is fixed to underlying bone,
 Measure the range of movement of adjacent & distal joint.

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X-ray examination showed the typical features of a large cartilage-capped exostosis; of course the cartilage cap does not show on x-ray
unless it is calcified. The bony part may be sessile, pedunculated or cauliflower-like.

Q) X ray findings:
 Well defined bony growth from metaphysis,
 Cartilage and capsule are not seen.

Q) Features suggestive of malignant changes?

a) Clinical features: Chance of malignant transformation:
 Solitary: 1% - 2%,
Enlargement of tumour in successive examination,  Multiple: 5% - 6%
Painful further enlargement after the end of growth period
Skin change: Venous engorgement,
Warm and tender swelling.
Tumor in pelvic bone or scapula.
Malignant transformation to chondrosarcoma.

b) Radiological changes:
Bulky cartilage cap (> 1cm in thickness: Apl, > 2 cm in Campbell),
Irregularly scattered flecks of calcification within the cartilage cap,
Spread into the surrounding soft tissue, (seen by MRI).

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 Histological sections show that the exostosis is
always covered by a hyaline cartilage cap from
which the bony excrescence grows.

Complications:
o Dwarfism,
o Pressure effect of exostosis,
o Deformities,
o Tendency to undergo malignant change (chondrosarcoma): 1% for solitary lesion and 6% for multiple
lesions / Incidence of malignant degeneration to be approximately 1% for patients with a
solitary osteochondroma and 5% for patients with multiple hereditary exostoses. camp-868

Features of Malignant transformation:

 Malignant transformation should be suspected when a previously quiescent lesion in an adult grows
rapidly;
 It usually takes the form of a low-grade chondrosarcoma.
 In these cases, the cartilage cap usually is more than 2 cm thick.
 Risk factors for malignant change:
 Multiple exostosis {> 1},
 Sessile variety,
 Flat bone is more affected {scapula, pelvic bone}
 Malignant transformation is best evaluated by CT or MRI.

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Differential diagnosis:
 Multiple enchondromatosis (Olier’s disease),
 Trevor’s disease.
 Ivory exostosis / Compact osteoma.

OLLIERS DISEASE

Trevor disease (dysplasia epiphysealis hemimelica):

It refers to an intraarticular epiphyseal osteochondroma. When multiple joints are involved, it is usually unilateral
(hemimelica). Commonly seen in males < 10yrs of age.

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Indications of operation:
 If tumour causes symptoms – it should be excised:
 Mechanical obstruction – ↓ ROM,
 Cosmetic,
 Nerve compression or stretching,
 Painful.
 In case of adult, tumour becomes bigger recently or painful - then operation is urgent.
 Surgery (en bloc resection) is indicated when the lesion is large enough to be unsightly or produce
symptoms from pressure on surrounding structures or when imaging features suggest malignancy.
Treatment:
 Extra-periosteal marginal excision including cartilagineous cap and overlying perichondrium,
 Cartilaginous cap should not be damaged during removal,
 Bone base should be removed by piece meal.

 Do not resect subperiosteally which may lead to recurrence.

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Q) What are the indications of operation of osteochondroma?
Tumour obstructing joint movement,
Painful bursitis,
Fracture of bony stalk – may occur due to trauma,
Pressure over neighboring vessels and nerves,
Malignant change (1 – 2%)

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 ENCHONDROMA
APL/N-193

Intramedullary neoplasm made of well differentiated hyaline cartilage.

Commonest location is the tubular bones of the hand, followed by the femur and humerus.

intraosseous chondroid lesion within the right proximal humerus.

Radiographically, the lesion is most commonly central with rounded, well-defined, lobulated edges and a thin rind
of reactive sclerosis. It contains glandular, popcorn, ring-like opacities.

247
 Enchondroma:
--- Chondroma growing within medullary cavity of bone close to growth plate.

 Echondroma:
---- Chondroma growing on the surface of bone.

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PRIMARY MALIGNANT BONE TUMOURS

249
 Osteosarcoma.
APL(N)-207, CAMP-909.

Osteosarcoma:
It is a malignant primary bone tumour of mesenchymal origin in which mesenchymal tumour cells have the ability
to produce neoplastic osteoid or immature bone.

It is a primary malignant tumour characterized by production of osteoid by malignant cells.

Cells of origin: Multipotential Mesenchymal cells,
 Osteogenic –> osteoid tissue predominent – Sclerosing type osteosarcoma,
 Collagenic –> collagen tissue predominent – Fibrosarcomatous type,
 Chondrogenic –> cartilage tissue predominent – chondrosarcomatous type.

Incedence:
 2nd most common primary malignant tomour of bone, next to MM,
 20% of primary malignancies of bone.

Age:
 Primary high grade osteosarcoma – 2nd decade of life (10 – 20 years of age),
 Parsoteal osteosarcoma – 3rd to 4th decade,
 Secondary osteosarcoma -- > 5th decade / older age.

Sex:
Male > Female

Sites: Metaphysis region of long bone,

 Distal femur : 50%,
 Proximal tibia: 20%,
 Proximal humerus: 10%.
 Other sites.

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Metaphyseal site; increased density, cortical erosion and Proximal tibia of 11-year-old boy Proximal humerus of 8-year-old
periosteal reaction are characteristic. with chondroblastic boy with osteoblastic
Sunray spicules and Codman’s triangle; osteosarcoma. osteosarcoma.

Classification:
a) On the Basis of Cause & nature of presentation: 2 types,
i. Primary or Denovo osteosarcoma:
 Arises denovo, in absence of bone disease,
 Types: 6 types,
 Conventional / Central / Classic / Medullary high grade:
Histologically it may be-
 Osteoblastic,
 Fibroblastic,
 Chondroblastic.
 Low grade central osteosarcoma,

 Surface osteosarcoma:
 High grade surface,
 Par-osteal osteosarcoma,
 Periosteal osteosarcoma,

 Telangiectic osteosarcoma: – highly vascular & bony changes like ABC,

 Small cell osteosarcoma: high grade lesion resemble of Ewing sarcoma or lymphoma.

ii. Secondary osteosarcoma: {occur at the site of another disease process}

 Usually occurs in elderly / > 5th decade,

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  Extremely rare,
 Factors associated with secondary os include Paget disease and previous Radiation therapy,
 Some pre-malignant conditions often associated:
 Paget’s disease – about 1% (usually in pelvis),
 Fibrous dysplasia,
 Irradiation / radiation induced os 10 – 15%,
 Multiple osteochondroma,
 Chronic osteomyelitis,
 Osteogenic imperfecta.

b) On the basis of Histology:

 Osteoblastic / Sclerosing type – new bone formation, around 50%
 Chondroid / Chondroblastic – being cartilage cell, >50%
 Fibroblastic – basic cells are fibroblasts, rare.

c) According to Radiological finding:

 Osteosclerotic / Osteoblastic – dense irregular bone seen in metaphysis,
 Osteolytic – radiolucent area seen at metaphysis with ↑ed density at the edge,
 Mixed / Classic (Osteosclerotic + osteolytic) – usually at metaphysis but may be at mid shaft,

Variants of osteosarcoma:
a) Par-osteal osteosarcoma:
 Rare,
 Low grade malignancy,
 Arises on the surface of bone and invades the medullary cavity only at late stage,
 Peculiar tendency to occur as a lobulated ossified mass on the posterior aspect of distal femur,

b) Peri-osteal osteosarcoma:
 Intermediate grade malignancy arises on the surface of bone,
 Most common locations are the diaphysis of femur and tibia.
 Usually occurs in slightly older age group.

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 Parosteal osteosarcoma :
X-rays show an ill-defined extraosseous tumour –
note the linear gap between cortex and tumour.

D/D:
Myositis ossificans {ossification in myositis
ossificans is more mature at the periphery of the
lesion, whereas the center of parosteal os is more
heavily ossified},

Osteochondroma {CT scan of osteochondroma

shows a medullary cavity containing marrow in
continuity with the medullary canal of the involved
bone}.

Anteroposterior and lateral radiographs of proximal femur of 67-year-old woman with periosteal osteosarcoma.
MR image shows lesion arising from surface of bone. Marrow does not seem to be involved.
Points Par-osteal o s Peri-osteal o s
1) Situated on Arises on the surface of tubular bone & Arises on the surface of bone.
invades medullay cavity at late stage.
2) X-ray Φ Dense bony mass on the surface of Φ Tumour mass on the surface of cortex,
shows bone or encircling it, Φ Superficial defect on the cortex,
Φ Cortex is not eroded, Φ No gap remains b/w cortex & tumour.
Φ A thin gap remains between cortex
and tumour,

3) Usual -> Peculiar tendency to occur as a -> Common location at diaphysis of femur

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 location lobulated ossified mass on the posterior or tibia.
aspect of distal femur.
4) Characteristics Ǿ Rare, Ǿ intermediate grade malignancy,
Ǿ Low grade malignancy.

Anteroposterior and lateral

radiographs of parosteal
osteosarcoma arising in its most
common location.

CT scan and MR image show lesion arising from posterior surface of distal femur without involvement of marrow
cavity.

E.S : Swelling → Pain.

Clinical features:
O.S : Pain → Swelling.
o Pain – is usually the first symptom,
 Constant,
 Worse at night / Night pain {present only in about 25% of patients},
 Gradually increase in severity / Progressive pain.
o Swelling,
o Limping gait – if wt bearing bone is involved,

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 o Pathological # / Deformity,
o Metastatic features – 10% cases early metastasis in lungs / Haemoptysis,
o Constitutional features.

On examination:
Average delay from onset of symptoms to confirm
 Look:
diagnosis : about 15 weeks,
 Skin:
Patient delay {time b/w onset of symptom to initial
 Tense, physician encounter} : 6 weeks,
 Shiny, Physician delay {time from 1st visit to correct diagnosis}:
 Glossy, 9 weeks.
 Dilated veins Causes of physician delay:
 Swelling:  Failure to obtain radiograph at the initial visit,

 Diffuse swelling,  Failure to repeat radiograph when patient’s

 Shape: symptoms persisted or worsened.

 Gait & Squatting.

 Feel:
 ↑ temp,
 Tenderness,
 Variable consistency (soft to stony hard),
 Indurated, fixed with underlying bone.
 Regional LN: may be palpable,
 Systemic Exam: chest.

 Move:
 Joint movements: may be restricted,
 If fracture present: abnormal mobility present.

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Differential diagnosis:

i) Subacute OM,

ii) Ewing’s sarcoma,

iii) Chondrosarcoma,

iv) Fibrosarcoma,

v) Metastatic tumour.

Osteosarcoma Osteomyelitis
1) Malignant osteiod matrix in the back 1) Reactive new bone formation in the
ground of spindle cells back ground of dead bone,
2) Formation of osteoid which is 2) Formation of mature bone /
immature / unmineralized, involucrum,
3) Osteoid do not having Haversian 3) Involucrum having Haversian
system system.
4) Malignant cells - present 4) Absent,
5) Inflammatory cells - absent 4) Present,
6) Granulation tissue - absent 6) Present.

The metaphyseal site; increased density, cortical erosion and periosteal reaction are characteristic.
Sunray spicules and Codman’s triangle;

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Investigation:

a) X ray of affected part:

 Hazy osteolytic area / Dense osteoblastic area,

 Endosteal margin: poorly defined, Moth eaten appearance,

 Cortex: breached & tumour extends into adjacent tissue,

 Sun burst appearance / Hair on end appearance:

 Streaks of new bone radiating outwards from the cortex.

 Codman’s triangle:
 Reactive new bone formation at the angles of periosteal elevation.

 Pathological # seen in osteolytic lesion.

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b) CBC (↓Hb%, ↑ESR)

c) S. alkaline phosphatase: ↑,

d) CXR : to see pulmonary metastasis (> 5 mm lesion),

e) Pulmonary CT : to see pulmonary metastasis (upto 1 mm lesion),

About 15% of patients have

f) CT / MRI : to see
pulmonary metastasis by the time they
 Size of tumour, are first seen / at the time of
diagnosis.
 Extent of tumour,
 Neurovascular invasion.

g) Bone scan: to see skip lesion / skeletal metastasis.

X-rays of a distal femoral osteosarcoma in a child.

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 MRI examination: coronal, sagittal and axial
scans showing the intra-and extra-osseous
extensions of the tumour and its proximity to
the neurovascular bundle.

Pale tumour tissue is seen occupying the distal third of the femur and extending through the cortex.

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Biopsy:
 It should be taken from non-calcified peripheral zone,
 Representative tissue must contain:
 Normal tissue (normal bone) : Red,
 Reactive tissue (Pseudocapsule) : Orange,
 Tumour tissue : Gray.

Histology / Pathology:

Malignant stromal tissue showing osteoid formation, Same tumour showed areas of chondroblastic
differentiation.

 Pink staining malignant osteiod matrix in the back ground of spindle cells ( Stromal cells),
 Several samples are needed for diagnosis of osteosarcoma, unless there is evidence of osteoid formation.

Treatment:
o Multidisciplinary approach: consultation & co-operation between Orthopaedic surgeon, Radiologist,
Pathologist, Oncologist, Radiotherapist, Orthotic Prosthetic designer & Rehabilitation specialist.

o Aim of treatment:
 Removal of tumour mass,
 Prevention of metastasis,
 Reconstruction of affected limb,
 Rehabilitation of patient.

o Treatment modalities:

260
  Chemotherapy,
 Surgery,
 Radiotherapy.

o Treatment protocol:
 Pre-operative biopsy & staging is mandatory,
 Neoadjuvant chemotherapy :
 Surgery:
 Adjuvant chemotherapy.

Neoadjuvant chemotherapy:
 Given for 8 – 12 weeks before operation,
 3 weeks interval, 3 cycles & 3 weeks gap before operation;
 Doxorubicin, Methotrexate, Cyclophosphamide (DMC)
 Aim:
 To kill tumour cells,
 To prevent micrometastasis,
 To reduce the vascularity of tumour,
 To ↓ the size of tumour,
 To prevent shedding of tumour cells during operation,
 To make non operable tumour operable.

Adjuvant chemotherapy:
 To kill any remaining cancer cells,
 To stop them from spreading.

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 Postoperative x-rays showing an endoprosthetic replacement following wide
resection of the lesion (Stanmore Implants Worldwide).

Surgery:
 Limb Salvage Surgery:
 1st step consists of wide excision of tumour with preservation of neurovascular
stuructures,
 Resulting defect is then dealt with:
 Short diaphyseal segment can be replaced by vascularized or non-vascularized bone
graft,
 Osteo-articular segment can be replaced by large allograft, endoprosthesis or allgraft
prosthetic composite.
 In growing children, extendible implants are used to avoid the need of repeated
operation but may need to be replaced at the end of growth.
 Outcome:
 Wound breakdown and infection,
 10 yrs survival rate of these prostheses with mechanical failure is 75% and for
failure due to any cause is 58%,
 Limb salvage rate at 20 years is 84%.

 Amputation & early rehabilitation:

 If there are difficulties of limb sparing surgery,

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  Particularly for high grade tumour,
 If there is doubt about whether the lesion is intracompartmental.

 Modular: a number of inter-changeable components which can be

assembled easily and quickly into prosthesis.
Endoprosthesis:
 Custom made.

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Treatment plan according to stage:
o Stage I: surgery + adjuvant therapy
o Stage II: neoadjuvant + surgery + adjuvant,
o Stage III: neoadjuvant + palliative surgery + adjuvant

8 – 12 weeks, 6 – 12 months.

o A (intra-compartmental) – wide local excision,

o B (extra –compartmental) – radical resection / amputation.

The Enneking staging system for bone tumours:

Low-grade - Intracompartmental 1A
Extracompartmental 1B  Important prognostic factor is the tumour staging at the
High-grade  Intracompartmental 2A time of diagnosis.
Extracompartmental 2B
 Next important prognostic factor is the grade of lesion.

Any grade  Metastases 3

Outcome of treatment / Survival rate:

 5 years survival rate,
Tumour without metastasis:
 Amputation only ---> 5-10%
 Surgery + Adjuvant ---> 41%,
 Neoadjuvant + Surgery + Adjuvant ---> 60 - 70%,
 Surgery only ---> 25%,

Tumour with metastasis:

 Neoadjuvant + Amputation + Adjuvant --> 24 – 40%.

Patient with pulmonary resection + adjuvant therapy: 60%

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 Patient with no treatment after onset of metastasis: about 2.9 months.
Prognostic factors / Poor prognostic factors:
o High grade of tumour --> poor prognosis,
o Secondary osteosarcoma --> poor prognosis,
o Rapid relapse after initial treatment,
o Location --> more proximal tumour – worse prognosis,
o Pulmonary Metastasis:
 pulmonary metastasis at the time of diagnosis {15%}  < 20% long term survival,
 > 8 pulmonary nodules,
 larger (>3 cm) pulmonary nodule,
 Unresectable pulmonary nodule.
o Patient with nonpulmonary metastasis (eg. bone metastasis) shows worse prognosis, with < 5% long term
survival,
o Patient with ‘Skip Metastasis’ (metastasis within the same bone as the primary tumour or across the joint
from the primary tumour) have poor prognosis as the patient with distant metastasis.

Specimen of osteosarcoma:
 The jar containing specimen of resected part of lower part of femur with about – x--- cm growth,
 The growth with intact capsule,
 No engorged vein is present,
 Cortical erosion presents posteriorly.
 Diagnosis: osteosarcoma involving lower part of femur.

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 CHONDROSARCOMA
apl-205, APL/N-209

 Chondrosarcomas are the second most common primary malignant bone tumours after
osteosarcoma,
 Chondrosarcoma is one of the commonest malignant tumours originating in bone.

 The highest incidence is in the fourth and fifth decades and men are affected more often

than women. {3rd to 8th decade / peak 40 – 70yr}

 Tumours are slow-growing and are usually present for many months before being discovered.

 Site:
 Chondrosarcoma may develop in any of the bones that normally develop in cartilage; almost 50%
appear in the metaphysis of one of the long tubular bones, mostly in the lower limbs.
 Next most common sites are the pelvis and the ribs.

 Clinical features:
 Patients may complain of a dull ache or a gradually enlarging lump.
 Medullary lesions may present as a pathological fracture.

 Primary chondrosarcoma: 4th – 5th decade,

 Secondary chondrosarcoma: 2nd – 3rd decade.

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 Types of Chondrosarcoma:

a) According to source:

 Primary chondrosarcoma:

 Low grade:
 Clear cell chondrosarcoma,
 High grade:
 Dedifferentiated chondrosarcoma,
 Mesenchymal chondrosarcoma.
 Secondary chondrosarcoma:
- arises from ‘Benign cartilage lesion’s including,
 Osteochondroma,
 Multiple hereditary exostosis,
 Enchondromas,
 Ollier’s disease,
 Maffucci’s syndrome.

b) According to location:
 Central chondrosarcoma,
 Peripheral chondrosarcoma,
 Juxtacortical (periosteal) chondrosarcoma

Central chondrosarcoma
The tumour develops in the medullary cavity of either tubular or flat bones, most commonly at the proximal

end of the femur or in the innominate bone of the pelvis.

Peripheral chondrosarcoma
This tumour usually arises in the cartilage cap of an exostosis (osteochondroma) that has been present

since childhood.

Juxtacortical (periosteal) chondrosarcoma

Here the lesion appears as an excrescence on the surface of one of the tubular bones – usually the femur.

It arises from the outermost layers of the cortex, deep to the periosteum. X-ray changes comprise features

of both a chondrosarcoma and a periosteal osteosarcoma: an outgrowth from the bone surface, often

267
containing flecks of calcification, as well as ‘sunray’ streaks and new-bone formation at the margins of the

stripped periosteum.

Clear-cell chondrosarcoma
Despite the fact that it is very slow-growing, it does eventually metastasize.

Mesenchymal chondrosarcoma
This is an equally controversial entity. Histology shows a mixture of mesenchymal cells and chondroid tissue.

X RAY FINDINGS:

 Mixed lytic or blastic lesion with reactive thickening of cortex.

 Intralesional ‘Popcorn’ / Honeycomb calcification may be seen.

Treatment
 Low grade chondrosarcoma:

 Extended curettage,

 Intraoperative adjuvant therapy: liq nitrogen, argon beam radiation.

 Excision of surrounding soft tissue.

 High grade chondrosarcoma;

 Wide excision & Prosthetic replacement – for slow-growing and metastasize late,

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  Chemotherapy:

 No role in the treatment of conventional chondrosarcoma.

 Currently chemotherapy is being evaluated for the treatment of defiffertiated and

mesenchymal chondrosarcoma.

 Radiation therapy:

 limited role,

 Palliative measure for surgically inaccessible lesion.

 Amputation - may be preferable in case of unacceptable loss of function;

 Patient should therefore be followed up for 10 years or longer. Overall 5-year survival is
approximately 50%.

 Prognosis of Chondrosarcoma: camp - 916

 Low grade: > 90% patients with 10 years survival.

 High grade: 20% - 40% patients with 10 years survival

 Dedifferentiated chondrosarcoma: 5 years survival in < 15% patients.

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 Ewing’s Sarcoma.
Reticulum Cell Sarcoma
camp-918, apl-212

Q) Name some bone marrow tumours?

 Marrow itself: -- Myeloma.

 Supporting marrow structure / Reticuloendothelial tissue:

 Undifferentiated Round cell Sarcoma / Endothelial myeloma,
 Round cell sarcoma,
 Haemangio-endothelioma.

Q) Name some malignant Round Cell Tumour?

 Ewing’s sarcoma,
 Reticulum cell sarcoma / Non-Hodgkin’s lymphoma,
 Medullary neuroblastoma,
 Eosionophilic granuloma.

Q) What is Ewing’s sarcoma?

--- It is primary malignant tumour of bone arises from reticuloendothelial cells of medullary cavity /
endothelial cells in bone marrow.

Q) Incidence of Ewing’s sarcoma?

 3rd most common primary malignancy of bone,
 2nd most common (aftet osteosarcoma) in patients younger than 30 yrs of age,
 Most common in patients younger than 10 years of age,
 About 9% of primary malignancies of bone.

Q) Characteristics of Ewing’s sarcoma?

 Age:
 5 – 25 years,
 10 – 20 years,
 < 10 years (most common).

 Sex: Male : Female = 1.5 : 1,

 Race: exceedingly rare in African descent.

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  Predisposing factor: there are no known predisposing factors,
 Site:
 Most common location including the metaphyses of long bones, often with extension into the diaphysis,
 And flat bones of the shoulder and pelvic girdle,
 Rarely, occurs in spine or in small bones of feet or hands.
 Usually occurs in a tubular bone and especially in the tibia, fibula or clavicle.

Q) Clinical features?
o Swelling:
 Warm & tender, E.S : Swelling → Pain.
 Dilated vein over skin, O.S : Pain → Swelling.
 Firm in consistency,
 Fixed with underlying bone.
o Pain:
 Throbbing pain & worse at night.
o Generalized illness:
 Warm & tender swelling,
 Pyrexia,
 Suggestive of a diagnosis of osteomyelitis.
o Metastatic features of lungs – may present.

Q) On examination:
a) Look:
 Swelling over the affected limb,
 Usually diffuse swelling,
 Shape:
 Dilated vein over the skin,
 Any scar mark over the skin,
 Muscle wasting,
 Gait – in case of lower limb.

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b) Feel:
 Temp: ↑,
 Tenderness: present,
 Size:
 Consistency: firm & fixed with underlying bone,
 Overlying skin free from underlying mass,
 Neuro-vascular status:
 Chest exam – if any metastatic features of lungs found.

c) Move:
 ROM of nearest and distal joints.

Q) Differential Diagnosis of Ewing’s sarcoma / Malignant Round Cell Tumour?

 Subacute osteomyelitis -----→ Blood culture,
 Osteosarcoma ------→ Biopsy,
 Retinaculum cell sarcoma / Non Hodgkin’s lymphoma, (APL-213)
 Metastatic neuroblastoma.

Q) Investigations for Ewing’s sarcoma?

 Blood picture:
 CBC: leukocytosis,
 Hb%: ↓↓,
 ESR: ↑↑,
 CRP: ↑↑↑,
 Lactate dehydrogenase: ↑.

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 Ewing’s tumour Examples of
Ewing’s tumour in -
(a) the humerus,
(b) the mid-shaft of the fibula and
(c) the lower end of the fibula.

 X – ray:
 Area of bone destruction, predominantly in the mid-diaphysis;
 Onion peel (Apl 212) / Onion skin (Camp918):
New bone formation may extend along the shaft and sometimes it appears as fusiform layers of bone around
the lesion.
 Often tumour extends into surrounding soft tissues with radiating streaks of ossification (Sunray appearance)
& reactive periosteal bone at the proximal and distal margins (Codman’s triangle).

 MRI:
 MRI of entire bone should be ordered to evaluate the full extent of the lesion,
 Helpful to evaluate the extent of soft tissue mass, which is often very large.

 CT scan + MRI: reveal large extra osseous component.

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  CT scan of chest: lungs is the most common site of metastasis.

 Bone scan:
 It should be performed because bone is the second most common site of metastasis.
 It may show multiple areas of activity in the skeleton.
 Although ‘skip’ metastases (similar to those that occur in osteosarcoma) are not reported in Ewing sarcoma.

 Biopsy: to confirm the diagnosis.

Anteroposterior and lateral radiographs of left fibula of 7-year-old girl with Ewing sarcoma. Involvement of large portion
of bone (or even entire bone) is typical of Ewing sarcoma. C, MR image shows a large soft tissue mass. D, Typical
microscopic appearance of Ewing sarcoma. E and F, Anteroposterior and lateral radiographs after completion of
neoadjuvant chemotherapy. Note increased ossification of lesion. G, Repeat MR image after neoadjuvant chemotherapy
shows marked reduction in size of soft tissue mass. H and I, Anteroposterior and lateral radiographs of left tibia after
wide resection of tumor. Distal fibular physis was preserved.
Wide resection avoids complications associated with radiation therapy in growing child.

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Q) Pathology / Histopathological findings?
a) Macroscopically:
 Tumour is lobulated and often fairly large,
 Looks grey (like brain) or red (like redcurrant jelly) – if hge occurred into it.
b) Microcopically:
 Abnormal fibrohistocytic cells, many of & some of which are binucleate or multinucleate,
 No ground substance is seen.

Q) Treatment of Ewing’s sarcoma?

--- Best result is achieved by combination of Radiotherapy, Chemotherapy and Surgery.
a) For accessible site:
 Neoadjuvant chemotherapy

 Surgery (wide local excision / amputation / disarticulation)

 Adjuvant Chemotherapy for 1 year.

b) For inaccessible site:

 Neoadjuvant Radiotherapy

 Surgery (wide local excision)

 Adjuvant chemotherapy for 1 year.

c) Post operative Radiotherapy:

-- It may be added if the resected specimen is found not to have a sufficiently wide margin of
normal tissue.

Radiotherapy:
 Ewing’s sarcoma is highly sensitive to radiotherapy. As it is known as ‘Melting Tumour’.
 But unfortunately recurrence is common,

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  Radiotherapy has a dramatic effect on tumour mass, but overall survival is not much enhanced.

Chemotherapy:
 Vincristine,
 Cyclophosphamide,
 Adriamycin.

Surgery:
 Surgery alone does little to improve it.

Q) Outcome of treatment?
 Combination therapy: 3 – 5 years survival rate → 50 – 70%,
 Radiation + Amputation: 2 years survival rate → 15%

 Without metastasis → Radio + Chemo + Surgery → 70%

 With metastasis → Radio + Chemo + Surgery → 10 – 20%

Q) Prognosis of Ewing’s sarcoma?

o Age: older age poor prognosis (with a cutoff around 12 to 15 yrs old),
o Sex: male > female,
o Site: proximal part poor prognosis than distal,
o Size: large size shows poor prognosis,
o Metastasis: distant metastasis poor prognosis,
o Patient with local recurrence: 5 yrs survival rate → 20%,
o Patient relapse with distant metastases: 5 yrs survival rate → 10%.

Q) What is the importance of grading of Ewing’s sarcoma?

---------- There is no importance of grading because Ewing’s sarcoma is regarded as a High grade sarcoma.

276
Q) What are the difference between osteosarcoma and Ewing’s sarcoma?

Points Osteosarcoma Ewing’s sarcoma

1. Age: 10 – 20 yrs, more common in 5 – 25 yrs, more common in 1st decade.
2nd decade.
2. Sex: M>F M>F
3. Site: Metaphysis of long bone Metaphysis to Diaphysis of long bone
4. Clinical feature: Swelling→ pain → Pain → swelling → constitutional symptoms.
constitutinal symptoms
5. Pathology: primary bone tumour of Supporting marrow structure / Reticuloendothelial
mesenchymal origin tissue:
Undifferentiated Round cell Sarcoma.
6. Blood picture: S. alkaline phosphatase: ↑ S. lactate dehydrogenase: ↑
7. X ray findings: Φ Codman’s triangle, Ǿ Onion peel appearance,
Φ Sunburst appearance Ǿ Codman’s triangle,
Ǿ Sunburst appearance.
8. Radiotherapy: Less sensitive Highly sensitive.
9. Prognosis: worse prognosis worst prognosis

Q) What are the difference b/w acute pyogenic OM with Ewing’s sarcoma?

Points Acute pyogenic OM Ewing’s sarcoma

1. Defination: Inflammation of bone and bone Primary malignant bone tumour arises from
marrow, usually due to infection. endothelial cells of bone marrow.
2. Age: it may occur at any age, 5 – 25 yrs, commonly 2nd decade.
3. Bone involve: it may occur in any bone, Usually occur in tubular bone & especially in
tibia, fibula or clavicle.
4. Site: Usually involve metaphysis of Usually involve diaphysis of long bone.
long bone.
5. Clinical features: Generalized illness, pyrexia, Generalized illness, pyrexia, together with
warm and tender swelling over warm & tender swelling, H/O night pain.
involved region.
6. Investigations: WBC count, ESR, CRP: ↑ WBC count, ESR, CRP: ↑
X ray of affected part: X ray: Onion peel appearance,

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 CT & MRI:
7. Treatment: 4 Steps; Ǿ Neoadjuvant chemotherapy,
a) Supportive treat. for pain & Ǿ Surgery,
dehydration, Ǿ Adjuvant chemotherapy,
b) Splintage of affected part, Ǿ Postoperative radiotherapy.
c) Antibiotic therapy,
d) Surgical drainage

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 NON-HODGKIN’S LYMPHOMA
(RETICULUM-CELL SARCOMA)
APL-213

Like Ewing’s sarcoma, this is a round-cell tumour of the reticuloendothelial system.

Site: It is usually seen in sites with abundant red marrow: the flat bones, the spine and the long-bone metaphyses.

Age: The patient, usually an adult of 30–40 years, presents with pain or a pathological fracture.

X-ray
Shows a mottled area of bone destruction in areas that normally contain red marrow;

X-ray showing moth-eaten appearance of the ilium.

Pathology
Histologically this is a marrow-cell tumour with collections of abnormal lymphocytes.

Treatment
The preferred treatment is by chemotherapy and radical resection; radiotherapy is reserved for less accessible lesions.

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 MULTIPLE MYELOMA
APL-213

Multiple myeloma is a malignant B-cell lymphoproliferative disorder of the marrow, with plasma cells
predominating.

Clinical features:
 Patient, typically aged 45–65, presents with Weakness, Backache, Bone pain or a Pathological fracture.
 Hypercalcaemia may cause symptoms such as thirst, polyuria and abdominal pain.
Bone resorption leads to hypercalcaemia in about one-third of cases.
 Associated features of the marrow-cell disorder are plasma protein abnormalities, increased blood viscosity
and Anaemia.
 In late cases there may be signs of Cord or Nerve root compression, Chronic nephritis and Recurrent
infection. Late secondary features are due to renal dysfunction and spinal cord or root compression caused by
vertebral collapse.
 Localized tenderness and restricted hip movements could be due to a plasmacytoma in the proximal femur.

Characteristic ‘pepper-pot’ appearance of the

skull

Vertebral compression fractures, Characteristic x-ray features are bone rarefaction,

Punched-out areas in the skull and the long bones.

X-rays
 X-rays often show nothing more than generalized osteoporosis;
 ‘Classical’ lesions are -
 Multiple punched-out defects with ‘soft’ margins (lack of new bone) in the skull, pelvis and
proximal femur,

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  A crushed vertebra, or
 A solitary lytic tumour in a large-bone metaphysis.
 The effects on bone are due to marrow cell proliferation and increased osteoclastic activity resulting in
osteoporosis and the appearance of discrete lytic lesions throughout the skeleton.
Investigations
 Mild anaemia is common, and an almost constant feature is a high ESR.
 Blood chemistry may show a raised Creatinine level and Hypercalcaemia.
 Over half the patients have Bence Jones protein in their urine,
 Serum protein electrophoresis shows a characteristic abnormal band.
 A Sternal marrow puncture may show plasmacytosis, with typical ‘myeloma’ cells.

There are dense sheets of plasma cells with eccentric nuclei.

Differential diagnosis:
 Metastatic bone disease.
 Gammopathies.

Treatment
 Principles of treatment:
 General supportive measures include correction of fluid balance and (in some cases) hypercalcaemia.
 Immediate need is for pain control and, if necessary,
 Treatment of pathological fractures:
 Limb fractures are best managed by internal fixation and packing of cavities with methylmethacrylate cement
(which also helps to staunch the profuse bleeding that sometimes occurs).
 Spinal fractures carry the risk of cord compression and need immediate stabilization – either by effective
bracing or by internal fixation.
 Unrelieved cord pressure may need decompression.
 Perioperative antibiotic prophylaxis is important as there is a higher than usual risk of infection and wound
breakdown.

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 Solitary plasmacytomas can be treated by radiotherapy.
 Specific therapy is with alkylating cytotoxic agents (e.g. melphalan).
 Corticosteroids are also used especially if bone pain is marked – but this probably does not alter the course of the
disease.

Prognosis:
Prognosis in established cases is poor, with a median survival of between 2 and 5 years.

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 CHORDOMA
APL-215
Rare malignant tumour arises from primitive notochordal remnants.

Chordomas are rare tumours arising from remnantsof the notochord. They most commonly present in the sacrum where they can cause a
painful mass or lower bowel and urinary symptoms which may require colostomy and bowel resection to achieve a satisfactory margin.

Clinical features:
 It affects young adults and usually presents as a slow-growing mass in the sacrum;
 Patient complains of longstanding backache.
 The tumour expands anteriorly and, if it involves the sacrum, may eventually (after months or even years)
cause rectal or urethral obstruction; rectal examination may disclose the presacral mass. In late cases there may also
be neurological signs.

Investigations:
 X-ray shows a radiolucent lesion in the sacrum.
 CT and MRI reveal the extent of intrapelvic enlargement.

It arise anywhere within the spine, in this case at the lumber vertebrae which was treated by en-bloc resection

Treatment
 This is a low-grade tumour, though often with extracompartmental spread.
 After wide excision there is little risk of recurrence.
 If there are doubts in this regard, operation should be combined with local radiotherapy.

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 ADAMANTINOMA
APL- 215
 Adamantinoma is a low-grade tumour which metastasizes late – and usually only after repeated and inadequate
attempts at removal.
 This rare tumour has a predilection for the anterior cortex of the tibia but is occasionally found in other long
bones.

Bubble-like appearance in the mid-shaft of the tibia is typical. X-rays demonstrated an expansile, soap bubble lesion.

Clinical features:
 Patient is usually a young adult who complains of aching and mild swelling in the front of the leg.
 On examination there is thickening and tenderness along the subcutaneous border of the tibia.

Investigations:
 X-ray shows a typical bubble-like defect in the anterior tibial cortex; sometimes there is thickening of the
surrounding bone.
 Early on it is confined to bone; later, CT may show that the tumour has extended inwards to the medullary canal
or outwards beyond the periosteum.
Treatment
 Preoperative CT and MRI are essential to determine how deep the tumour penetrates; if it is confined
to the anterior cortex, the posterior cortex can be preserved and this makes reconstruction much easier.
 If the lesion extends to the endosteal surface, a full segment of bone must be excised; the gap is filled
with a vascularized graft or a suitable endoprosthesis, or managed by distraction osteogenesis.
 If there has been more than one recurrence, or if the tumour extends into the surrounding soft tissues,
radical resection or amputation is advisable.

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METASTATIC BONE DISEASE

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 METASTATIC BONE DISEASE
APL- 216, APL / N - 220

 The skeleton is one of the commonest sites of secondary cancer;

 The commonest Source is carcinoma of the breast; next in frequency are carcinomas of the prostate, kidney,
lung, thyroid, bladder and gastrointestinal tract.
 In about 10 percent of cases no primary tumour is found.
 Commonest Sites for bone metastases are the vertebrae, pelvis, the proximal half of the femur and the
humerus.
 Spread is usually via the blood stream; occasionally, visceral tumours spread directly to adjacent bones (e.g.
the pelvis or ribs).
 Metastases are usually Osteolytic, and pathological fractures are common. Bone resorption is due to
 Direct action of tumour cells or
 Tumour-derived factors TNFα, IL1, IL6 and PTHrP) that stimulate osteoclastic activity.
 Osteoblastic lesions are uncommon; they usually occur in prostatic carcinoma.

Metastasis is defined as follows: ‘Transmission of

pathogenic micro-organisms or cancerous cells from an
original site to one or more sites elsewhere in the body
usually via blood vessels or lymphatics.’

Clinical features:
 Patient is usually aged 50–70 years;
 Pain is the commonest and often the only clinical feature.
 Some deposits remain clinically silent and are discovered incidentally on x-ray examination or bone
scanning, or after a pathological fracture.
 Symptoms of Hypercalcaemia may occur (and are often missed) in patients with skeletal metastases.
These include-
 Anorexia,

 Nausea,

 Thirst,

 Polyuria,

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  Abdominal pain,

 General weakness and

 Depression.

 Children under 6 years of age, metastatic lesions are most commonly from adrenal Neuroblastoma.
The child presents with bone pain and fever; examination reveals the abdominal mass.

Imaging

Patients over 60 with vertebral

compression fractures may
simply be very osteoporotic, but
they should always be
investigated for Metastatic bone
disease and Myelomatosis.

A) X-rays:
 Most skeletal deposits are osteolytic and appear as -
 Rarified areas in the medulla or
 Produce a moth-eaten appearance in the cortex;
 Osteoblastic deposits suggest a prostatic carcinoma;

Radioisotope scan revealed many deposits in different parts of the skeleton.

B) Radioscintigraphy:
Bone scans with 99mTc-MDP are the most sensitive method of detecting ‘silent’ metastatic deposits in bone;

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Special investigations / Blood Test:
 Hb: ↓,
 ESR: 
 Serum alkaline phosphatase: 
 Serum acid phosphatase:  {In prostatic carcinoma the acid phosphatase also is elevated}
 Tumour markers:

Treatment
A) Counselling: about-
 Disease,
 Management plan &
 Prognosis.
B) Multidisciplimary approaches.

C) General treatment:
 Despite a poor prognosis, patients deserve -
 To be made comfortable, to enjoy (as far as possible) their remaining months or years, and
 To die in a peaceful and dignified way.
 Control of pain:
Most patients require analgesics, but the more powerful narcotics should be reserved for the terminally ill.

D) Treatmentl of Metastatic activity:

 Radiotherapy is used both to control pain and to reduce metastatic growth.
 Secondary deposits from Breast or Prostate can often be controlled by hormone therapy:
Stilboestrol for prostatic secondaries and Androgenic drugs or oestrogens for breast carcinoma.
 Disseminated secondaries from Breast carcinoma are sometimes treated by oophorectomy
combined with adrenalectomy or by hypophyseal ablation.
 Treatment of Solitary secondary deposit: Occasionally, Radical treatment (combined
chemotherapy, radiotherapy and surgery) targeted at a solitary secondary deposit and the parent primary lesion may
be rewarding and even apparently curative.
 Treatment of Multiple secondaries: Those with multiple secondaries, treatment is entirely
symptomatic.

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E) Treatment of Hypercalcaemia:
 It includes renal acidosis, nephrocalcinosis, unconsciousness and coma.
 It should be treated by ensuring adequate hydration, reducing the calcium intake and, if necessary, administering
bisphosphonates.

F) Treatment of limb fractures:

 Most cases intramedullary nailing is the most effective method; fractures near joints (e.g. the distal femur or
proximal tibia) may need fixation with plates or blade plates, and sometimes replacement by an endoprosthesis.
 Pain is immediately relieved, nursing is made easier and the patient can get up and about or attend for other types
of treatment without unnecessary discomfort.
 Postoperative irradiation is essential to prevent further extension of the metastatic lesion.

Surgical timidity may condemn the patient to a painful lingering death.

 Radiotherapy used as a preoperative adjunct has been shown to increase the postoperative infection rate
(Jeys et al., 2005).

G) Prophylactic fixation:
 As a rule of thumb, where 50 percent of a single cortex of a long bone (in any radiological view) has been
destroyed, pathological fracture should be regarded as inevitable.
 Mirel’s scoring system: to evaluate fracture risk and therefore act as a guide as to whether (and when) a
fracture should be fixed or not.

H) Treatment of Metastatic spinal disease:

 Metastatic spinal disease is 40 times more common than all primary tumours of the spine together.
 If there are overt symptoms and signs of cord compression, treatment is urgent.

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 Operative intervention (vertebrectomy and reconstruction) appears to provide a better functional outcome than
radiotherapy. Patients remain ambulatory and continent for longer and the 5-year survival rate is around 18 percent.
 Radiotherapy alone is reserved for patients with softtissue compression and as palliation for inoperable cases.

‘Prophylactic fixation’ is indicated-

If a lytic lesion is -
(a) Greater than half the diameter of the bone;
(b) Longer than 3 cm on any view, or
(c) Painful, irrespective of its size. APL9 - 865

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 Glomus tumor
Glomangioma.

Q) What is Glomus body?

-- It is composed of tortous arteriole and communicates directly with venule and surrounded by network of nerves.

Q) What is the function of Glomus body?

-- It helps to regulate body temperature.

Q) Where glomus body is found commonly?

-- Commonly found in nail bed of the tip of finger and toes & in the palmar surface of phalanges.

Q) What is Glomus tumor?

-- It is a rare benign neoplasm that arises from neuroarterial structure which is called Glomus body.

Q) Histological features of Glomus tumor?

-- Histologically, Glomus tumor consists of mixture of blood vessels, nerve tissues and muscle fibres derived from
wall of arterioles, so this is known as ‘Angio-myo-neuroma’.

Q) Common sites of Glomus tumor?

-- 50% in finger tip and 50% in sub-ungual area / under the nail bed.
--- Occur more often in the hand (75%) than elsewhere and are located beneath the fingernail in 25%
to 65% of patients
Q) Clinical features of Glomus tumor?
 Pain, cold sensitivity, and point tenderness are the characteristic symptoms of a glomus tumor,
 Small bluish circumscribed swelling at the tip of affected finger,
 Pain over the affected area which is aggravated by touching / pressure effect,
 Pain also aggravates by exposure of the affected part to sudden change of temp.
 Affected site is extremely tender to touch / pressure.

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Q) Investigation for Glomus tumor?
-- MRI of nail bed.

Q) How to treat Glomus tumor?

-- Excision of tumor mass.

Q) Size of Glomus tumor?

Glomus tumors usually are less than 1 cm in diameter, often being only a few millimeters in diameter,

Q) Test for Glomus tumor?

Direct pressure on the tumor by a small, firm object, such as a pinhead, causes excruciating pain (Love test), whereas pressure
applied slightly to one side of it elicits no pain.
camp-3672

 Most of these tumors are benign; however, if the lesion exceeds 2.0 cm and histologic parameters suggest
malignancy, then metastatic rates exceed 25%.

 These tumors can be removed with the patient under local anesthesia and should be accurately localized by
marking the lesion just before surgery.

 Meticulous and complete excision of the usually well-encapsulated lesions is curative, although reoperation rates
of 12% to 24% have been reported most likely from incomplete tumor extirpation.

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 GIANT CELL TUMOR OF THE TENDON SHEATH
(XANTHOMA)
camp- 3667

Giant cell tumor on the flexor surface of the ring finger. Surgical dissection showing well-encapsulated giant cell tumor
with typical yellowish brown color.

 Occur more often as firm lobulated masses on the volar lateral side of the index and middle fingers.

 Multiple xanthomas may be associated with hypercholesterolemia.

 Clinical features:
 Xanthomas usually grow slowly and can remain the same size for many years.
 Pain and tenderness are rare.
 If xanthomas occur at a joint (often the proximal interphalangeal joint), they can become large
enough to interfere with joint motion.
 Histology:
 Grossly, the tumors appear as well-encapsulated yellow or tan lobular masses.
 Histological sections reveal spindle cells, fibrous tissue, cholesterol-laden histiocytes, multinucleated
giant cells similar to osteoclasts, and hemosiderin.
 Surgical technique:
 Extensile surgical approaches are frequently required, and
 Gentle blunt dissection should be performed to minimize fragmentation of the encapsulated tumor
mass.
 Magnified vision is helpful to discover discolored synovial tumor,

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 Recurrence:
 18 - 27% recur even after meticulous excision of the friable fragments.
 Risk factors for recurrence or persistence include adjacent degenerative joint disease, location at the
finger distal interphalangeal and thumb interphalangeal joint, bony invasion, multifocal disease and
poor surgical technique.

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NEUROMUSCULAR DISORDERS.

295
 Neuromuscular disorders
apl-229

• Dystonia  This term refers to abnormal posturing (focal or generalized) that may affect any part
of the body
 Often aggravated when the patient is concentrating on a particular motor task such as
walking.

• Antalgic gait  Markedly shortened stance phase on one side.

• Spastic gait  Crouching posture (flexed hips and knees and feet in equinus)
‘Scissoring’ (legs crossing each other), due to muscle imbalance.
• Drop-foot gait  During swing, the foot ‘drops’ into equinus;
 This is caused by disorder or damage to the peripheral nerves supplying the foot
dorsiflexors.
• High-stepping  Due to a bilateral foot drop.
gait
• Waddling  Trunk is thrown from side to side with each step.
(Trendelenburg)  Seen in patients with functionally weak abductor muscles (or dislocation) of the hip.
gait
• Ataxic gait  Irregular loss of balance, which is compensated for by a broad-based gait, or
sometimes uncontrollable staggering.

Neuromuscular disorders:
 CEREBRAL PALSY
 LESIONS OF THE SPINAL CORD
 POLIOMYELITIS
 Motor neuron disease (amyotrophic lateral sclerosis)
 Spinal muscular atrophy
 PERIPHERAL NEUROPATHIES
 HEREDITARY NEUROPATHIES / Peroneal muscular atrophy,
 METABOLIC NEUROPATHIES
 Diabetic neuropathy
 Alcoholic neuropathy
 INFECTIVE NEUROPATHY:
 Neuralgic amyotrophy (acute brachial neuritis)
 Guillain–Barré syndrome (Acute Inflammatory Demyelinating Polyneuropathy –
AIDP)
 Leprosy.

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 POLIOMYELITIS
APL-251, EBN-603

Poliomyelitis is an acute infectious viral disease, spread by the oropharyngeal route that passes through several
distinct phases.

Anterior horn cells are affected in poliomyelitis

Viral infection of the anterior horn cell of the spinal cord or nerve cells of brainstem, resulting in temporary or
permanent paralysis.
Characteristics:
 Only around 10 per cent of, patients exhibit any symptoms at all and
 Involvement of the CNS occurs in < 1 % of cases with effects on the anterior horn cells of the spinal
cord and brain-stem, leading to LMN (flaccid) paralysis of the affected muscle groups.

Shortening and wasting of the This long curve is typical of a paralytic Paralysis of the right deltoid and supraspinatus
left leg, with equinus of the ankle. scoliosis. makes it impossible for this boy to abduct his right
arm.

297
Clinical features

(A) Polio lower limb (B) Foot deformities in polio (C) Upper limb deformities in polio

Poliomyelitis typically passes through several clinical phases,

 The acute illness:

Early symptoms are fever and headache; in about one-third of cases the patient gives a history of a minor illness
with sore throat, mild headache and slight pyrexia 5–7 days before. Symptoms increase in severity, neck stiffness
appears and meningitis may be suspected.

 Paralysis:
Soon muscle weakness appears; it reaches a peak in the course of 2–3 days and may give rise to difficulty with
breathing and swallowing. Pain and pyrexia subside after 7–10 days and the patient enters the convalescent stage.

 Recovery and convalescence:

A return of muscle power is most noticeable within the first 6 months, but there may be continuing improvement
for up to 2 years.

 Residual paralysis:
If Recovery is incomplete and then left with some degree of asymmetric flaccid (LMN) paralysis or unbalanced
muscle weakness that in time leads to joint deformities and growth defects.

 Post-polio syndrome:
Pattern of muscle weakness became firmly established by 2 years, it is now recognized that in up to 50 per cent of
cases reactivation of the virus results in progressive muscle weakness in both old and new muscle groups,

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 Lower limb deformities in poliomyelitis

 Polio usually affects children less than 12 months.

 Mild episode of fever, headache and diarrhea.
 Lower limbs are more commonly affected and the paralysis could be partial or total (paralytic stage)
 The paralysis of the muscles whether spinal (75%) or bulbar (25%) usually lasts until two months.
 Involvement is asymmetric.
 Tibialis anterior is most often completely paralyzed.
 Sensory system is not affected.
 Then there may or may not be recovery for a period of two years.
 Any residual paralysis after two years of affection is permanent with no chance of recovery.
 Bulbar poliomyelitis is rare and affects the respiratory muscles. It may be fatal.
 Common deformities are:
– Hip—Flexion, Abduction and External rotation.
– Knee—Flexion, triple deformity and Genu valgum.
– Foot —Talipes equinovarus.

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Early treatment
During the acute phase the patient is isolated and kept at complete rest, with symptomatic treatment for pain and
muscle spasm. Active movement is avoided but gentle passive stretching helps to prevent contractures.
Late treatment
 Isolated muscle weakness without deformity:
- Which can be treated by tendon transfer.

 Passively correctible deformity:

Any unbalanced paralysis (i.e. muscle weakness on one aspect of a joint and greater power in the antagonists) can
lead to deformity. An appropriate tendon transfer may solve the problem permanently.

 Fixed deformity:
Fixed deformities cannot be corrected by either splintage or tendon transfer alone; it is important also to restore
alignment operatively and to stabilize the joint, if necessary, by arthrodesis. Occasionally a fixed deformity is
beneficial. Thus, an equinus foot may help to compensate mechanically for quadriceps weakness; if so, it should not
be corrected.
 Flail joint:
If the joint is unstable or flail it must be stabilized, either by permanent splintage or by arthrodesis.
 Shortening:
Discrepancies of up to 3–5 cm can, (in theory), be compensated for with a shoe raise although this tends to make
the shorter (and weaker) leg clumsier. apl-253

300
Treatment of Foot deformity:
 Instability and foot-drop can be controlled by an ankle–foot orthosis or a below-knee calliper.
 Often there is imbalance causing varus, valgus or calcaneocavus deformity; fusion in the corrected
position should be combined with tendon re-routing to restore balance, otherwise there is risk of the deformity
recurring.
 For varus or valgus the simplest procedure is to slot bone grafts into vertical grooves on each side of the
sinus tarsi (Grice); alternatively, a triple arthrodesis (Dunn) of subtalar and mid-tarsal joints is performed,
 With associated foot-drop: Lambrinudi’s modification is valuable; triple arthrodesis is performed but the
fully plantarflexed talus is slotted into the navicular with the forefoot in only slight equinus: foot-drop is corrected
because the talus cannot plantarflex further, and slight equinus helps to stabilize the knee.
 With calcaneocavus deformity: Elmslie’s operation is useful - triple arthrodesis is performed in the
calcaneus position, but corrected at a second stage by posterior wedge excision combined with tenodesis using half
of the tendo achillis.
 Claw toes,
 If the deformity is mobile, are corrected by transferring the toe flexors to the extensors;
 If the deformity is fixed, the interphalangeal joints should be arthrodesed in the straight position and
the long extensor tendons reinserted into the metatarsal necks.

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 Leprosy
APL-53, 260

Leprosy – ulnar nerve paralysis

Ulnar nerve paralysis is relatively common in longstanding leprosy.

Characteristics:
 Still a frequent cause of peripheral neuropathy in Africa and Asia.
 Mycobacterium leprae, an acid-fast organism, causes a diffuse inflammatory disorder of
the skin, mucous membranes and peripheral nerves.
 Depending on the host response, several forms of disease may evolve.
 Infection is acquired mainly by respiratory transmission;
Pathology
 Granulomatous lesions in the peripheral nerves, the skin and the mucosa of the upper respiratory tract.
 Indeterminate leprosy: Some develop a few skin lesions, appearing as vague hypopigmented
macules that recover spontaneously.
 Tuberculoid leprosy: occurs where there is Delayed Type Hypersensitivity (DTH) to M. leprae
antigens, combined with some decrease in cell-mediated immunity (CMI). The granuloma in tuberculoid leprosy is
focal and circumscribed and is made up of epithelioid cells,
 Lepromatous leprosy: is seen in patients who are unable to mount effective CMI against M. leprae.
Here the granuloma is diffuse and extensive and it consists of macrophages, many loaded with acid-fast bacilli.
 Borderline types: are intermediate forms that show some features of both of the above conditions.
Without treatment, they tend to progress increasingly towards the lepromatous form.
 The chronic course of leprosy is often punctuated by acute inflammatory episodes – so-called ‘reactions’ –
which are due to the deposition of immune complexes (Erythema Nodosum Leprosum or ENL or Type II reaction)
or due to an increase in CMI and DTH levels (reversal reaction or RR or Type I reaction).

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 Patches on the body

Tuberculoid leprosy:
 Most severe neurological lesions are seen.
 Anaesthetic skin patches develop over the extensor surfaces of the limbs;
 Loss of motor function leads to weakness and deformities of the hands and feet.
 Thickened nerves may be felt as cords under the skin or where they cross the bones (e.g. the ulnar nerve behind
the medial epicondyle of the elbow).
 Trophic ulcers are common and may predispose to osteomyelitis.
Lepromatous leprosy:
 It is associated with a symmetrical polyneuropathy, which occurs late in the disease.
Clinical features:

Leprosy – late features lost all the fingers of both hands.

Symptoms:
 Hypopigmented skin patches with impaired sensibility develop in all types of leprosy.
 Deformities of the hands and feet may also be seen.
 Trophic ulcers, causing progressive destruction of the affected part, appear in the hands and feet.

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  Coarsening of the facial skin and loss of eyebrows may produce typical leonine features. Lepromatous
ulceration of the nasal mucosa leads to destruction of the nasal septum and nasal deformity.
 Clinical defects in nerve function appear early in tuberculoid leprosy but much later in lepromatous
leprosy.
Signs:
 Thickened cutaneous nerves may be seen and thickened nerve trunks may be felt where they are
superficial, especially where they cross a bone (typically behind the medial condyle of the humerus at the elbow).
 Skin lesions in tuberculoid leprosy are sparse, well-demarcated, hypopigmented and anaesthetic.
 In lepromatous leprosy, the skin is affected diffusely and extensively and the lesions present as multiple,
symmetrically distributed macular patches with some sensory impairment.
 Peripheral nerves are affected extensively in lepromatous leprosy whereas in tuberculoid leprosy the
neural lesions are few and focal in distribution.
 Except for the Vth and VIIth nerves, the cranial nerves are not affected.
 Nerve lesions in tuberculoid leprosy may undergo caseation and liquefaction resulting in an ‘intraneural
cold abscess’ mimicking an intraneural tumour, or the pus may break through the epineurium to present as a
chronic collar-stud abscess.
 ‘Drop-foot’ occurs in 1–2 % of leprosy patients, because of paralysis of muscles in the anterior and lateral
compartments of the leg consequent to damage to the common peroneal nerve.
Patterns of nerve involvement
 Nerve trunks of the upper limbs are involved more often than those of the lower limbs.
 In the upper limb ulnar nerve paralysis is the most common and combined ulnar and median nerve paralysis is
seen less frequently.
 Occasionally, triple nerve paralysis (paralysis of ulnar, median and radial nerves) may occur.

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Treatment:
For purposes of treatment, patients are categorized as having-
 Paucibacillary (cases of indeterminate and Tuberculoid leprosy) or
 Multibacillary (cases of Lepromatous and Borderline leprosy) leprosy.
MULTIDRUG THERAPY
Recommendations of the World Health Organization,
 Paucibacillary disease are treated with Rifampicin 600 mg once monthly and Dapsone 100 mg once daily,
for 6 months;
 Patients with Multibacillary disease are given Rifampicin 600 mg and Clofazimine 300 mg once monthly
and dapsone 100 mg and clofazimine 50 mg once daily, for 12 months.
 Reactions, especially acute neuritis, are treated with anti- inflammatory medication, of which prednisolone
is the most important, and other supportive therapy.

NERVE DECOMPRESSION
Surgical decompression is indicated:
(a) In acute neuritis when, even while under treatment with corticosteroids, there is increasing neurological deficit;
and
(b) In cases of severe, unresponsive nerve pain, for relief of pain.

Decompression involves-
A} Tunnel release (often with excision of the medial epicondyle for the ulnar nerve),
B} Combined with incision of the epineurium over the entire sclerosed segment of the nerve.

Aim of Decompression:
 To improve perfusion of the nerve
 Allow the anti-leprosy and anti-inflammatory drugs to reach the affected segment and thus prevent
or abort nerve damage.
 Muscle weakness, particularly intrinsic muscle paralysis due to ulnar nerve involvement, may require
multiple tendon transfers.

Complications of Leprosy:
The notorious deformities and disablement result from:
(a) Local leprous granulomas (as in the face);
(b) Damage to nerves of the hands and feet and consequent muscle paralysis;
(c)‘Trophic lesions’ (ulcers, shortening of digits and mutilations) arising from injuries to insensitive hands and feet.

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 THE FOOT IN LEPROSY apl-298

Problems include
 Drop-foot,
 Claw toes,
 Plantar ulceration and
 Tarsal disorganization.
Drop-foot
‘Drop-foot’ occurs in 1–2 per cent of leprosy patients, because of paralysis of muscles in the anterior and lateral
compartments of the leg consequent to damage to the common peroneal nerve.
Mobile drop-foot - This is corrected by transfer of tibialis posterior tendon, which is almost never paralysed in
leprosy. Circumtibial, two-tailed tibialis posterior tendon transfer to extensor hallucis and extensor digitorum
longus tendons over the dorsum of the foot is most commonly done; When only the anterior compartment muscles
are paralysed, a similar transfer of peroneus longus is done.
Fixed drop-foot deformity - Fixed equinus or equinovarus usually requires triple arthrodesis of the hindfoot
(Lambinudi’s operation), which should provide the patient with a plantigrade foot.

Claw-toes
This condition, due to plantar intrinsic muscle paralysis, is more common than drop-foot.

Plantar ulceration (trophic ulcers)

Painless chronic ulcers that occur ‘spontaneously’ are commonly seen in the soles of neurologically compromised
feet.

Neuropathic foot - Neuropathic

tarsal disorganization

Neuropathic tarsal disorganization

 ASEPTIC DISORGANIZATION
Aseptic tarsal disorganization is uncommon.
 SEPTIC TARSAL DISORGANIZATION
Infection may spread from a plantar ulcer to underlying tarsal bones and joints and destroy these structures.

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 Clinical features of paralytic Hand deformities in leprosy APL-296

Total claw-hand deformity in combined paralysis Partial claw-hand deformity in ulnar nerve paralysis:
of ulnar and median nerves. ring and little fingers are clawed

(a) ‘Claw-thumb’ (hyperextended at the basal and flexed at the middle and distal joints) in combined ulnar
and median nerve paralysis. Note wasting of the thenar eminence.
(b) Illustrating pinch in thenar paralysis. Only the lateral or ‘key-pinch’ is possible for these hands.

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 PERIPHERAL NEUROPATHIES
APL-256

 Disorders of the peripheral nerves may affect motor, sensory or autonomic functions,
 There are over 100 types of neuropathy;
 Abnormalities may be -
 Predominantly sensory (e.g. diabetic polyneuropathy),
 Predominantly motor (e.g. peroneal muscular atrophy) or
 Mixed.
Types of peripheral neuropathy:
1. Radiculopathy – involvement of nerve roots, most commonly by vertebral trauma, intervertebral disc herniation
or bony spurs, space-occupying lesions of the spinal canal and root infections like herpes zoster.
2. Plexopathy – direct trauma (e.g. brachial plexus traction injuries), compression by local tumours (Pancoast’s
tumour), entrapment in thoracic outlet syndrome, and viral infection such as neuralgic amyotrophy.
3. Distal neuronopathy – involvement of neurons in distinct peripheral nerves, which is usually subdivided into:
a. Mononeuropathy – involvement of a single nerve, usually mixed sensorimotor (e.g. nerve injury,
nerve compression, entrapment syndromes and nerve tumours). Mononeuropathies – mainly nerve
injuries and entrapment syndromes.
b. Multiple mononeuropathy – involvement of several isolated nerves (e.g. leprosy and some cases of
diabetes or vasculitis).
c. Polyneuropathy – widespread symmetrical dysfunction (e.g. diabetic neuropathy, alcoholic
neuropathy, vitamin deficiency, Guillain– Barre syndrome.
 Causes of polyneuropathy:

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Clinical features

Peripheral neuropathy Two typical deformities in patients with peripheral neuritis:

(a) ulnar claw hands and (b) pes cavus and claw toes.

 Patients usually complain of sensory symptoms: ‘pins and needles’, numbness, a limb ‘going to sleep’,
‘burning’, shooting pains or restless legs.
 They may also notice weakness or clumsiness, or loss of balance in walking.
 Occasionally (in the predominantly motor neuropathies) the main complaint is of progressive deformity, for
example, claw hand or cavus foot.
 There may be a history of injury, a recent infective illness, a known disease such as diabetes or malignancy,
alcohol abuse or nutritional deficiency.
 Examination may reveal motor weakness in a particular muscle group.
 In the polyneuropathies the limbs are involved symmetrically, usually legs before arms and distal before
proximal parts.
 In polyneuropathy, there is a symmetrical ‘glove’ or ‘stocking’ distribution.
 Trophic skin changes may be present.
 If pain sensibility and proprioception are depressed there may be joint instability or breakdown of the
articular surfaces (‘Charcot’ joints).

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 Hereditary Motor and Sensory Neuropathy (HMSN)
APL-258

Hereditary neuropathies – peroneal muscular atrophy This patient has the typical wasting of the legs, cavus
feet and claw toes associated with peroneal muscular atrophy.

Which includes-
 Peroneal muscular atrophy,
 Charcot– Marie–Tooth disease and
 Some benign forms of spinal muscular atrophy.

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 METABOLIC NEUROPATHIES
APL-258

 Diabetic neuropathy,
 Alcoholic neuropathy,

INFECTIVE NEUROPATHY
APL-259

 Herpes zoster (shingles)

 Neuralgic amyotrophy (acute brachial neuritis)
 Guillain–Barré syndrome (acute inflammatory demyelinating polyneuropathy – AIDP)
 Leprosy.

Neuralgic amyotrophy A common feature of neuralgic amyotrophy is winging of the scapula due to serratus anterior
weakness. Even at rest (a) the right scapula is prominent in this young woman. When she thrusts her arms forwards against
the wall (b) the abnormality is more pronounced.

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 CP
CEREBRAL PALSY
CAMP- 1204, APL- 235
Q) What is Cerebral palsy?
The term ‘cerebral palsy’ includes a group of disorders that result from non-progressive brain damage during early
development and are characterized by abnormalities of movement and posture.
Q) Causes of Cerebral palsy?
a) Prenatal causes: Developmental milestone:
 Neck control: 3 month,
 Maternal infection (TORCH),
 Able to sit: 6 month,
 Multiple pregnancy,
 Crawling: 9 month,
 Premature rupture of membrane (PROM),
 Walking: 12 month.
 Rh incompatibility.
b) Perinatal causes {delivery upto 28 days}:
 Birth asphyxia,
 Birth trauma,
 Breach delivery,
 LBWB (<1.5 kg),
 Kernicterus.
c) Post natal causes:
 Meningitis,
 Encephalitis,
 Head injury.
Q) Classification of CP?
a) According to Motor dysfunction / Clinico-pathological types:
1) Spastic palsy:
 Pyramidal tract is involved,
 Commonest variety (>60%),
  muscle tone,
 Hyper active reflexes.
2) Athetosis:
 Extra pyramidal tract is involved,
 Continuous involuntary writhing movements.
3) Ataxic:
 Muscular incordination during voluntary movements.
 Balance is poor,

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  Wide based gait.
4) Dystonia:
 Generalized increase in muscle tone and abnormal positions induced by activity.
5) Hypotonia:
 It is usually a phase, lasting several years during early childhood before the features of
spasticity become obvious.
6) Mixed palsy:
 Combination of spasticity and athetosis.

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b) According to Topogrpphic / Area of distribution:
1) Monoplegia: involvement of one limb,
2) Hemiplegia: involvement of upper & lower limb on one side of body,
3) Diplegia: involvement of 4 limbs, lower limbs are more severe.
4) Quadriplegia: involvement of all 4 limbs & trunk.
5) Total body involvement:
 Involvement of all 4 limbs,
 Trunk & neck with varying degree of severity,
 Low IQ,
 Unable to walk.

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316
Q) CP Presentation?
a) UPPER LIMB:
Upper limb deformities are seen most typically in the child with spastic hemiplegia or total body involvement and
consist of flexion of the elbow, pronation of the forearm, flexion of the wrist, clenched fingers and adduction of the
thumb.
 Elbow flexion deformity,
 Forearm pronation deformity,
 Wrist flexion deformity,
 Flexion deformity of the fingers,
 Thumb-in-palm deformity.
b) LOWER LIMB:
 SPASTIC HEMIPLEGIA:
 Equinovarus foot deformity: Tibialis anterior is invariably weak and the patient develops an equinovarus foot
deformity.
 Leg length discrepancy Due to discrepancies in growth,
 SPASTIC DIPLEGIA:
 Hip adduction deformity The child walks with the thighs together and sometimes even with the knees crossing
(‘scissors gait’). This may be combined with spastic internal rotation. Adductor release is indicated if passive
abduction is less than 20 degrees on each side.
 Hip flexion deformity This is often associated with fixed knee flexion (the child walks with a ‘sitting’ posture) or
else hyperextension of the lumbar spine. Operative correction is indicated if the hip deformity is more than 30
degrees.
 Hip internal rotation deformity Internal rotation is usually associated with flexion and adduction. If so, adductor
release and psoas lengthening will be helpful.
 Hip subluxation Subluxation of the hip occurs in about 30 percent of children with cerebral palsy. A persistent
flexion-adduction deformity leads to femoral neck anteversion. If the abductors are weak and the child is not fully
weightbearing, there is a risk of acetabular dysplasia and subluxation of the joint; in non-walkers there may be
complete dislocation. Correction of flexion and adduction deformities (see above) before the age of 6 years may
have a role in preventing subluxation.
 Knee flexion deformity This is one of the commonest deformities; it is usually due to functional hamstring
tightness. Spastic flexion deformity may be revealed only when the hip is flexed to 90 degrees so that the
hamstrings are tightened.
 Spastic knee extension This can usually be corrected by simple tenotomy of the proximal end of rectus femoris.
 External tibial torsion This is easily corrected by supramalleolar osteotomy,

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 Equinus of the foot The child with spastic diplegia usually toe-walks.
 Varus deformity,
 Equinovalgus and a ‘Rocker-bottom’ foot.

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323
324
325
326
327
328
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333
 apl-243
The diplegic patient usually has problems at all levels, Soft-tissue and bony surgery to both limbs can be performed
at one sitting or staged over a few weeks.

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 Post CP Equinus Deformity.
APL-243

Spastic equinus (a) Standing posture of a young girl with bilateral spastic equinus deformities. (b) Tendo Achillis lengthening resulted in
complete correction and a balanced posture.

Post CP equinus deformity:

It is a common variety of CP deformity.
On Examination:
Look:
 The child with spastic diplegia usually toe-walks. This triggers an excessive plantarflexion– knee extension
couple that may be manifested as knee hyperextension.
 In children with limited dorsiflexion, the gastrocnemius is often more affected than the soleus.
 Gait – equinus gait,
 Squating – difficultly possible.
Feel:
 Temperature:
 Tenderness;
 Silfver-ski-öld test: APL- 238

 With the child lying supine on the examination couch, the knee is flexed to a right angle and the ankle is dorsiflexed; this
tests soleus tightness.
 The knee is then fully extended on the couch and ankle dorsiflexion is repeated; now it is mainly gastrocnemius tightness
that is being tested.
 Popliteal angle;

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Move:
 ROM of ankle:
 ROM of knee:
 ROM of hip:

 Splints are used -

To prevent muscle contracture,
X Ray imaging:
Maintain joint position and
 X ray pelvis including both hip, Improve movement and hence function.
 X ray knee B/V,
 X ray ankle B/V.

Treatment of post CP equinus deformity:

a) For mild & flexible deformity:
 Manual stretching,
 Serial casting,
 Use of custom made orthosis / AFO,
 Chemo-denervation of Gastro-soleus complex with Botulinum toxin
↓
It causes temporary (approx 3 months) selective muscle paralysis by blocking Acetylcholine
release at N – M junction.

b) For fixed deformity:

 If ankle can be brought passively to neutral when knee is flexed, but fall into equinus as the knee is
extended – Gastrocnemius shortening is addressed. Gastrocnemius can be lengthened by-

Vulpius or Baker procedure Strayer procedure.

Lengthening of Gastrocnemius aponeurosis just Selective lengthening of Gastrocnemius.

before it joins to the aponeurosis of Soleus.

336
 If ankle remains in significant equinus despite knee flexion, then Gastrosoleal complex is lengthened
either open or per cutaneous lengthening technique.

337
PERIPHERAL NERVE DISORDERS.

338
 Nerve.
APL-269

Diagram of the structural elements of a peripheral nerve.

Q) Draw a cut section of a peripheral nerve? What are the common causes of peripheral nerve injury?
Causes of nerve injury:
 Open / closed fracture and / or dislocation,
 Direct injury: cut or laceration,
 Mechanical injury:
 Traction,
 Compression,
 Pressure effect.
 Thermal injury:
 Frost bite,
 Heat.
 Infection: leprosy,
 Electric shock,
 Ischemic injury: VIC,
 Radiation injury.

339
Q) What is upper motor and lower motor neuron lesion? What are the clinical
features of UMNL and LMNL?

Upper motor neuron:

Pyramidal cells of motor cortex and their axons up to anterior horn cells of spinal cord are
called UMN.

Lower motor neuron:

Cell bodies of anterior horn of spinal cord, motor neuclei of cranial nerves and their axons are
called LMN.

Clinical features of UMNL & LMNL:

Points UMNL LMNL
1. Paralysis Spastic paralysis Flaccid paralysis
2. Muscle wasting No muscle wasting Wasting of muscle
3. Muscle tone ↑ed muscle tone ↓ed muscle tone.
4. Reflex Superficial reflexes lost, deep Superficial and deep reflexes are lost.
reflexes are exaggerated.
5. Clonus Present Absent
6. Fasciculation & Absent Present
Fibrillation
7. Babinski sign (Extensor (+) ve (-) ve
Planter Response)
8. Example  CVA,  MND,
 Intracranial tumour,  Polio (ant. horn cell affected),
 Peripheral neuropathy,

Q) What type of lesion you will find if the injury in cervical, dorsal & lumber region?
Injury to Cervical region: UMN type of lesion,
Injury to Dorsal region: UMN type of lesion,
Injury to Lumber region: LMN type of lesion,
Injury to Thoracolumber region: Mixed pattern.

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Q) What are the different types of nerve injury? / Classify nerve injury?
A) Seddon’s classification:

i) Neuropraxia:
 Reversible physiological nerve conduction block,
 It is due to mechanical pressure causing segmental demyelination,
 eg; saturday night palsy, milder type of tourniquet palsy.
 Investigation:
 Tinel’s sign: absent,
 EMG: conduction block at injury site, distally normal conduction.

ii) Axonotmesis:
 Seen typically after closed # or dislocation,
 Axonal interruption,
 Loss of conduction but nerve is in continuity / Neural tubes are intact,
 Axonal processes grow (degeneration) at a speed of about 1 mm / per day,
 Investigation:
 Tinel’s sign: advancing,
 EMG: conduction block at injury site, distally denervation.

iii) Neurotmesis:
 Division of nerve fiber, usually occurs in an open wound / #,
 Neuroma: regenerating axonal fibers mingle / mix with proliferating Schwann cells & fibroblasts
that make a jumbled knot.
 Investigation:
 Tinel’s sign: static,
 EMG: conduction block at injury site, distally denervation.

b) Sunderland classification:

i. 1st degree injury:

→ Transient ischaemia and neuropraxia.

ii. 2nd degree injury:

→ Axonal degeneration takes place / Axonotmesis,
→ Endoneurium is preserved, so regeneration can lead to complete or near complete
repair,

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 → Recovery without need of intervention.

iii. 3rd degree injury:

→ Endoneurium is disrupted but Perineural sheath is intact,
→ Chance of axons reaching their target are good but fibrosis & cross connection
will limit recovery.

iv. 4th degree injury:

→ Only Epineurium is intact,
→ Nerve trunk is still in continuity but internal damage is severe,
→ Recovery unlikely, injured segment should be excised and nerve should be
repaired or grafted,

v. 5th degree injury:

→ Nerve is divided and will have to be repaired.

Q) Clinical features of nerve injury?

 Acute nerve injuries:

 Symptoms:
 Easily missed, especially if associated with fracture or dislocation,
 Always test for nerve injuries following any significant trauma,
 If nerve injury is present, look for accompanying vascular injury.
 Abnormal posture of limb eg wrist drop,

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  Signs:
 Numbness, paresthesia or muscle weakness in the related area,
 Sudomotor changes may be found in the same topographic areas, skin feels dry due to lack of
sweating.

 Chronic nerve injuries:

 Anaesthetic skin may be smooth and shiny with evidence of diminished sensibility such as cigarette
burn of the thumb in median nerve palsy or foot ulcer with sciatic nerve palsy.

Q) Assessment of nerve functional recovery / function? APL-273

 It can be revealed by simple clinical tests:

 Tests of sensitivity to light touch and pin prick.
 Tests of muscle power,
 Tests for sudomotor changes.

 In case of nerve injury – Motor recovery is slower than Sensory recovery.

Tests of Sensitivity:
 Sensory status / Locognosia:
 Locognosia is the ability to localize touch and can be tested with standardized hand map.

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 Sudomotor change / Plastic pen test:
 Sudomotor changes may be found in the same topographic areas,
 Skin feels dry due to lack of sweating,
 Smooth barrel of the pen is brushed across the palmar surface of hand; normally there is a sense of slight
stickiness due to thin layer of surface sweat.
 When skin is denervated - pen slips along smoothly with no sense of stickiness in the affected area.
 Tinel’s sign:
 Peripheral tingling or dysaesthesia provoked by percussion the affected nerve,

 In case of Neuroproxia: Tinel’s sign is negative.

 In case of Axonotmesis:
 Tinel’s sign is positive & advancing at the site of injury, because of sensitivity of the regenerating
axon sprouts,
 After a delay of a few days or weeks – Tinel’s sign will then advance @ of about 1 mm / day, as the
regenerating axons progress along the Schwann cell tube,
 Failure of Tinel’s sign to advance suggests 4th or 5th degree injury and need for early exploration.
 In case of Neurotmesis: Tinel’s sign is static.

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 Nerve Conduction Velocity:

 Electromyography {EMG}:
 If a muscle loses its nerve supply, EMG will show denervation potentials by 3rd week,
 EMG excludes neuropraxia but it does not distinguish between axonotmesis and neurotmesis.

 Two point discrimination:

 It is a measure of innervation density.

TWO POINT DISCRIMINATION

Finger tip: 3 mm,
Palm of Hand: 10 mm,
Sole of foot: 3 cm.

 Two point discrimination gives information about how completely nerve has recovered?
 After nerve regeneration or repair, a proportion of proximal sensory axons will fail to reach their
appropriate sensory end-organ; they will either have regenerated down the wrong Schwann-cell tube or will be
entangled in a neuroma at the site of injury.
 Static two point discrimination measures slowly adapting sensors {Merkel cell} – normal static two
point discrimination is about 6 mm.
 Moving two point discrimination measures rapidly adapting sensors {Meissner corpuscles and
Pacinian corpuscles} – moving two point discrimination is more sensitive and returns earlier. Normal moving two
point discrimination is about 3 mm.

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Test for Motor power:
Motor power is graded on the Medical Research Council scale as:
0 - No contraction.
1 - A flicker of activity.
2 - Muscle contraction but unable to overcome gravity / Contraction when gravity eliminated,
3 - Contraction able to overcome gravity / Contraction against the gravity.
4 - Contraction against resistance.
5 - Normal power.
Q) Evaluation of patient with nerve injury? camp-3367

-- Four areas of consideration are important when evaluation of a patient with nerve injury especially in hand,
 Type of injury,
 Sensibility evaluation,
 Motor function,
 Sudomotor (sweating) function.

Type of injury:
 Caused by several mechanisms including direct trauma – blow, fracture etc, laceration, traction or
stretching and entrapment or compression.

Sensibility evaluation:
 Autonomous sensory distributions of Median, Radial and Ulnar nerves in volar pulp of the index
finger, volar pulp of the little finger and the thumb index web space.

Test each area three times. Start at a width of 10 mm,

and gradually decrease the distance.

Two-point discrimination testing

 Customary methods used to evaluate damaged sensory nerves include the use of a sharp pin to assess
pain, a cotton tipped applicator or a finger eraser to assess light touch and tips of paper clip to assess two point
discrimination.
 If nerve is transected, patient would not feel light touch, would not appreciate pin as a sharp stimulus
and would be unable to discriminate between one and two points.

346
  Patients with closed injuries or partial injuries to nerves may show spotty appreciation of light touch
and pain and have markedly widened two point discrimination.

Motor function: MRC grading

Sudumotor function:
 Usually a denervated area shows no sweating within about 30 minutes after a nerve injury,
 Compare normal and suspected injured areas by palpation with a dry fingertip.

Q) Types of Nerve repair? Rohim-41

 For sharp clean injury:

 Primary repair: within first 6 to 8 hours,
 Delayed primary repair: within first 7 to 18 days,
 Secondary repair: 18 days to 3 weeks.
 For lacerated injury: from 3 to 6 weeks.

Q) What are the types of nerve repair? camp-3370

--- According to timing of repair, 3 types-

 Primary repair:
 Immediately after injury or within 6 to 12 hours,
 Delayed repair:
 Usually within first 2 to 2.5 weeks,
 Secondary repair:
 After 2.5 to 3 weeks.

Q) Critical time for nerve repair?

Nerve High lesion Low lesion
Median nerve: 9 months 12 months
Ulnar nerve: 9 months 15 months
Radial nerve: 15 months 9 months {PIN}

Generally, the longer the delay in repair, the poorer the return of motor function that can be
expected.

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Q) Principles of treatment of nerve injury? APL-274

Options are-
 Nerve exploration,
 Primary repair,
 Delayed repair,
 Nerve guides,
 Nerve grafting,
 Nerve transfer.

Nerve exploration: CAMP-3083

 Indication of exploration:
 If nerve was seen to be divided and needs to be repaired,
 If the type of injury {knife wound / high energy injury} suggests that nerve has been divided
or severely damaged,
 If recovery is inappropriately delayed and diagnosis is in doubt.
 Vascular injuries, unstable / comminuted, soft tissue and tendon divisions should be dealt with before
nerve lesion.

Stumps are correctly orientated and attached by fine sutures through the epineurium.

Primary repair:
 A divided nerve is best repaired as soon as this can be done safely.
 Primary suture at the time of wound toilet has considerable advantages – the nerve ends have not retracted
much, their relative rotation is usually undisturbed and there is no fibrosis.

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  A clean cut nerve is sutured, a ragged cut margin may need paring of the stumps with sharp blade, but this
must kept to a minimum.
 Stumps are anatomically oriented and fine (10/0) sutures are inserted in the epineurium.
 Tension free repair can usually be obtained by:
 By positioning the nearby joints or
 By mobilizing and re-routing the nerve.
 Nerve graft must be considered:
 If tension free repair does not solve the problem or
 If flexion needs to be excessive.
 If tourniquet is used it should be pneumatic one, it must be released and bleeding points should be stopped
before the wound is closed.
 Limb is splinted in a position to ensure minimal tension on the nerve.
 If splint is retained for 3 weeks thereafter physiotherapy is encouraged.

PRIMARY NEURORRHAPHY:

EPINEURIAL NEURORRHAPHY

PERINEURIAL (FASCICULAR)
NEURORRHAPHY

EPI-PERINEURIAL NEURORRHAPHY

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INTER-FASCICULAR GRAFTING

Technique of partial neurorrhaphy.

Delayed repair:
 Indication of late repair {eg. weeks or months}:
 Closed injury which was left alone but shows no sign of recovery at expected time,
 Diagnosis was missed and patient presents late.
 Primary repair has failed.
 How to deal with the Gap?
 Nerve must be sutured without tension,
 Nerve ends are brought together by gently mobilizing the proximal and distal segments,
 By flexing nearby joints to relax the soft tissues or in case of ulnar nerve by transposing the nerve
trunk to the flexor aspect of the elbow,
 Gap of 2 cm in Median nerve, 4 – 5 cm in ulnar nerve and 6 – 8 cm in sciatic nerve can usually be
closed.
 Limb being splinted in the ‘relaxing’ position for 4 – 6 weeks after the operation. Gap of more than 1 – 2
cm usually require grafting.

350
  Options must be carefully weighed: if the patient has adapted to functional loss, if it is a high lesion and
re-innervation is unlikely within the critical 2 year period or if there is a pure motor loss which can be
treated by tendon transfer – it may be best to leave well alone.

Q) What are the methods of closing nerve gap?

 Nerve mobilization,
 Nerve transposition,
 Joint flexion,
 Nerve graft,
 Bone shortening.

Q) Critical gap of nerve that can be apposed by mobilization?

 Radial nerve: 2 - 3 cm,
 Median nerve: 2 to 3 cm,
 Ulnar nerve: 3 to 5 cm,
 PIN: 1 cm.
 Sciatic nerve: 6 – 8 cm.

Nerve guides:
 Nerve gaps can regenerate through a tube which excludes the surrounding tissue from each end.

Weber et al. conduit repair technique. Minimal distance between

nerve stumps is 5 mm, even in instances in which ends can be
coapted without tension. camp-3373

 The tubes can be autogenous vein, freeze dried muscle, silicone or metal, soluble guides (flexible at body
temperature) which dissolve over weeks or months are also used.
 This technology offers a simple way of avoiding a nerve graft.

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Nerve grafting: APL-275, CAMP-3084

 Gap of 2 cm in Median nerve, 4 -5 cm in Ulnar nerve and 6 – 8 cm in Sciatic nerve – usually be closed.
Elsewhere, gaps of more than 1 – 2 cm usually require grafting.
 Sural nerve is most commonly used, up to 40 cm can be obtained from each leg,

Nerve grafts placed between nerve ends

Nerve grafts sutured in place

Interfascicular nerve grafting

 Advantages of Sural nerve:

 Nerve diameter is small,
 Several strips may be used,
 Graft should be long enough to lie without any tension,
 It should be routed through a well vascularized bed,
 Graft is attached at each end either by fine sutures or with fibrin glue.
 What are the types of nerve graft?
3 types of nerve graft,
i) Cable graft: eg- sural nerve graft used as several strips.

ii) Pedicle graft: eg- if ulnar and median nerves are both damaged {e.g. in Volkmann’s ischaemia}; a
pedicle of ulnar nerve is used to bridge the gap in median nerve.

iii) Vascularized graft: eg- used in the treatment of brachial plexus injury.

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Nerve transfer / Neurolization:
 In Root avulsions of the upper brachial plexus too proximal for direct repair, nerve transfer can be used.
 Spinal accessory nerve can be transferred to suprascapular nerve and intercostals nerves can be transferred
to musculocutaneous nerve.
 Entire muscle (Gracilis or Latissimus dorsi) can be transferred as a free flap, attached between elbow and
shoulder and then innervated by joining intercostals nerves or spinal accessory nerve to the stump of the
original nerve supplying that muscle.

Spinal accessory nerve to suprascapular nerve transfer

camp-3084

TRANSFER OF THE ULNAR NERVE FASCICLES TO DOUBLE FASCICULAR TRANSFER

NERVE OF THE BICEPS MUSCLE FROM ULNAR AND MEDIAN
NERVES
(OBERLIN ET AL.) (MACKINNON AND COLBERT)

353
 Transfer of ulnar nerve fascicles to nerve to biceps Double fascicular transfer for musculocutaneous nerve.
muscle A, Redundant flexor carpi ulnaris fascicle from ulnar nerve is
transferred to biceps branch.
B, Redundant flexor carpi radialis fascicle from the median
nerve transferred to the brachialis branch.

Q) Post operative assessment of nerve repair? camp-3369

--- In evaluating the progress of peripheral nerve injury and repair – following tests are important.
Sensibility evaluation:
 Basic minimum test recommended for sensibility evaluation are stationary two point discrimination
and moving two point discrimination,
 Normal two point discrimination usually is 6 mm or less.
Motor function:
 Basic tests are recommended for motor function: Grip strength, Key pinch and Tip pinch strength.
 Squeeze grip dynamometer, pinch dynamometer etc should be used to measure.
Subjective evaluation:
 Evaluation of patient for the presence of pain, cold intolerance, dysthesia and functional disabilities.
Sudumotor function:
 Loss of sweating is an indicator of nerve disruption and loss of sympathetic function,
 Sweating may return without a return of two point discrimination.
 Usually it returns with the return of two point discrimination.

Q) How to care the paralysed parts?

 Skin – must the protected from friction damage and burn,
 Joints – should be moved through their full range twice daily to prevent stiffness
 Dynamic splints – may be helpful / to prevent muscle wasting.

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Q) Name the common deformities occur in High radial nerve palsy, low ulnar nerve palsy and
Erb’s palsy?
Deformities of High Radial Nerve Palsy:
 High lesion usually occurs due to # of SOH or after prolonged torniquet pressure.
 Wrist drop with finger drop – due to weakness of extensors of wrist and metacarpophalangeal joints.
 Sensory loss over small patch on the dorsum around the anatomical snuff box.

Deformities of Low ulnar nerve palsy:

 Caused by cut on shattered glass or sharp object,
 Numbness over ulnar one & half finger and also over skin of hypothenar eminance.
 Hypothenar and interosseous muscle wasting.

Deformities of Erb’s palsy:

 Arm : hangs by the side of body, adducted and internally rotated,
 Forearm: extended and pronated,
 Wrist: flexed,
 Deformity is known as Policeman tip hand or Porter’s tip hand,

Brachial Plexus

Q) What is brachial plexus? How brachial plexus is formed? APL-276

Q) Draw the branches of post. cord of brachial plexus?

Brachial plexus:
It is a network of nerves running from spine which is usually formed by anterior rami of lower four
cervical (C5 – C8) and 1st thoracic nerve (T1).

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 APL-276

Formation of brachial plexus:

It is formed by Roots, Trunks, Divisions and Cords.
 Roots:
-- Formed by ant. primary rami of spinal nerves C5,6,7,8 & T1 with contribution from ant. primary
rami of C4 & T2.

 Trunks:
-- Roots of C5 & C6 join to form upper trunk.
-- Roots C7 forms middle trunk,
-- Roots C8 & T1 join to form lower trunk.

 Divisions:
-- Each trunks divide ant and post divisions,
-- These divisions join to form cords.

 Cords:
-- Lateral cord is formed by union of ant. division of upper & middle trunk,
-- Medial cord is formed by lower trunk,
-- Posterior cord is formed by union of post. divisions of all three trunks.

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 camp-3086

357
358
359
Q) Causes of Brachial plexus injury?
 Open injury:
 Penetrating injury,
 Gunshot injury,
 Tumor removal,
 Excision of cervical rib.
 Close injury:
 Traction injury:
 Birth injury,
 Falling of heavy object
on shoulder,
 RTA / bike injury,
 Shoulder dislocation.
 Irradiation.

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Q) Types of Traction injury?
 Supra-clavicular lesions: 65%
 Neck and shoulder are wrenched apart eg motor cycle accident,
 Injury to root and trunk level,
 Subclavian artery may be injured.

 Infra-clavicular lesions: 25%

 Usually associated with fracture or dislocation of shoulder,
 Fracture of clavicle rarely damage plexus and only if caused by direct blow,
 Axillary artery is torn in about a quarter of cases.

 Combined: 10%

Q) Types of brachial plexus injury?

According to location of injury:
 Middle trunk: C7
 Upper trunk / Erb’s palsy – C5,6
 Lower trunk / Klumpke’s palsy – C8T1
 Total palsy / Mixed.
 T1 root – alone may be involved.

Q) If T1 root is only involved?

Causes:
 Incomplete lower obstetrical palsy,
 Cervical spondylosis,
 Cervical rib syndrome,
 Neurofibromatosis,
 Apical & metastatic carcinoma.
Signs:
 Wasting of small muscles of hand including thenar group,
 Sensory loss on the medial side of hand only.

361
Q) Classify BP injury?
Leffert classification:
------ According to mechanism of injury,

i) Open injury (stab injury)

ii) Closed injury (RTA)

iia – Supraclavicular injury:
 Preganglionic
 Post ganglionic.
iib – Infraclavicular injury.
 Upper trunk injury,
 Middle trunk injury
 Lower trunk injury

iii) Radiation injury

iv) Obstetric injury:

 Erb’s palsy
 Klumpke palsy.

Points Preganglionic injury Postganglionic injury

Mechanism of injury High energy trauma Traction injury
Nerve root Avulsion of nerve roots Roots remain intact
Pain in affected limb Crushing / Burning pain if anesthetic limb Usually no pain
Paralysis of muscle Parralysis of scapular muscles Usually intact
Wasting of muscle Scapular muscles Scapular muscles usually normal
Horner syndrome Present Absent
Pseudomeningocele Present in MRI Absent in MRI
Histamine test Triple response No response

362
Q) Level of injury
a) Preganglionic lesion:
 Avulsion of nerve root from spinal cord / disruption proximal to dorsal root ganglion,
 Can not recover,
 Surgically irreparable,
 Features suggesting Root avulsion:
 Crushing / Burning pain in anesthetic hand,
 Paralysis of scapular muscle or diaphragm,
 Horner’s syndrome,
 Severe vascular injury,
 Associated fracture of cervical spine,
 Spinal cord dysfunction / hyper-reflexia in lower limb.
 Histamine test:
o Intradermal injection of histamine usually causes a triple response in the surrounding skin
{Central capillary dilatation, Wheal and Flare},
o If the flare reaction persists in an anaesthetic area of skin – lesion must be proximal to dorsal root
ganglion – Preganglionic lesion,
o If the flare reaction Not persists - Post ganglionic lesion – test will be negative because nerve
continuity between skin and dorsal root ganglion is interrupted.

b) Post ganglionic lesion:

 Rupture of nerve distal to dorsal root ganglion - can be in trunk, division or cord.
 Potentially capable of recovery,
 Surgically repairable.

363
Q) Investigation for brachial plexus injury?
 X ray of cervical spine:
 X ray chest:

Myelogram shows leakage of the contrast medium, indicating root avulsion.

 CT myelography or MRI:
 Pseudomeningocele is produced by root avulsion,
 During first few days a ‘positive’ result is unreliable because dura can be torn, without there being root
avulsion.

 Nerve conduction study:

 If there is sensory conduction from an anaesthetic dermatome - this suggests a preganglionic lesion
{because nerve distal to ganglion is not interrupted},
 NCV test becomes reliable only after a few weeks because wallerian degeneration in post ganglionic lesion
will block nerve conduction.

Q) Examination of Brachial plexus injury patient?

 Look:
 Exposure:
 Attitude of limb:
 Skin & hair distribution:
 Apparent muscle wasting:
 Horner syndrome:
 Obvious deformity:

364
 Feel:
 Temperature of affected limb:
 Tenderness of affected limb:
 Measurement of muscle wasting arm / forearm / hand,
 Sensory status:
 Tinel sign:
 Tap vigorously at the side of Neck – above downwards – in the line of nerve roots,
 Test is positive - if there is marked painful paresthesia in the corresponding dermatomes eg,
tapping over C6 root produces severe pain and tingling in the thumb.
 Positive test generally indicates a ruptured nerve root and a post ganglionic lesion.

 Move:
 Shoulder / Elbow / Wrist / Finger – active and passive.
 Special test for muscle power:
 Serratus anterior – winging of scapula,
 Rhomboid,
 Trapezius,
 Supra spinatus and infra spinatus, Deltoid.
 Biceps, Brachialis, Brachioradialis.
 Triceps.

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Q) Management of brachial plexus injury? APL/9 -278

 Emergency surgery for brachial plexus injury:

 It is associated with penetrating wound, vascular injury or severe soft tissue damage whether open or
closed,
 Clean cut nerves then repaired or grafted,
 Best perform by specialized team.
 Timing of surgery:
 In early days – operative exposure is easier and response of repair is more reliable,
 Repair is performed after 6 months unlikely to succeed.
 Early reconstruction:
 Nerve grafting:
 For restoration of shoulder and elbow function are quite good,
 Outcome for lesions affecting forearm and hand is disappointing.
 Nerve transfer / Neurotization:
 Alternative way of providing functioning axon,
 If C5 & C6 are avulsed:
 Spinal accessory nerve can be transferred to Suprascapular nerve,
 2nd or 3rd intercostal nerves can be transferred to Musculocutaneous nerve.
 If one nerve root is available (eg C5):
 This should be grafted on to the lateral cord which will supply elbow flexion, finger flexion and
sensation over the radial side of the hand.
 If two roots are available (eg C5,6):
 These can be grafted on to the lateral and posterior cords,
 These procedures bypass the suprascapular nerve which is joined to the spinal accessory nerve.
 If complete preganglionic loss:
 Contra lateral C7 root can be extended across the chest with autologous graft and then used as an
axon source into the plexus.
 Phrenic nerve:
 Result:
 Two or Three years must pass before the final results of plexus reconstruction are apparent.

Objectives are to regain - APL-278

 Shoulder abduction, Elbow flexion, Wrist extension, Finger flexion, and

 Sensibility over the lateral (radial) side of the hand.

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 Late reconstruction:
 Indications:
 If the patient is not seen until very late after injury or
 If the plexus reconstruction has failed.

 Procedures:
 Tendon transfer to achieve abduction of shoulder:
 Trapezeus to Deltoid.
 Tendon transfer to achieve elbow flexion:
 Pectoralis major to Biceps,
 LD to Biceps,
 Triceps to Biceps.
 Free muscle transfer:
 Gracilis, Rectus femoris or contralateral Latissimus dorsi can be transferred as a free flap,
 Innervated with 2nd or 3rd intercostal nerves or contralateral C7,
 Elbow flexion and wrist extension can be regained.

367
  Shoulder arthrodesis:
 Arthrodesis is usually reserved for unstable or painful shoulder,
 Perhaps after failure of re-innervation of the supraspinatus,
 Position of shoulder – must be tailored to the needs of the particular patient.

SURGICAL GOALS CAMP-3089

The surgeon should have clear and reasonable surgical goals, which are, in order of priority,
(1) Restoration of elbow flexion,
(2) Restoration of shoulder abduction, and
(3) Restoration of sensation to the medial border of the forearm and hand.

Q) What are the signs indicating poor prognosis in traumatic plexus lesion?
1. Complete lesion involving all five {C5 to T1} roots,
2. Severe pain in anaesthetic arm,
3. Sensory loss above clavicle,
4. Horner’s syndrome,
5. Paralysis of Rhomboids and Serratus anterior muscle,
6. Fracture of transverse process,
7. Retention of sensory conduction in the presence of sensory loss.

Nerve graft using fibrin polymer glue

368
369
370
371
Neurotization – implantation of a nerve into a paralyzed muscle.

372
373
 OBPI

Q) Obstetrical Brachial Plexus Palsy? apl-279

OBPI:

Paralysis of the abductors and external rotators of the shoulder, as well as the forearm supinators, results in the typical posture
demonstrated in this baby with Erb’s palsy of the left arm.

Cause:
 Caused by excessive traction on the brachial plexus during childbirth
 eg. by pulling the baby’s head away from the shoulder or by exerting traction with the baby’s arm in
abduction.

Types of OBPI: 3 types-

 Upper root injury {Erb’s palsy}: 60%,
 Lower root injury {Klumpkey’s palsy}: 5%,
 Total plexus injury: 35%.

Clinical features:
 Diagnosis is usually obvious at birth: after a difficult delivery baby with a floppy or flail arm,
 One or two days later – type of brachial plexus injury can be detected.

374
 Erb’s palsy:
 Caused by injury of C5,6 & sometimes 7,
 Abductors and external rotators of the shoulder and supinator is paralysed,
 Arm is held to the side, internally rotated and pronated.
 There may be loss of finger extension,
 Sensation can not be tested in a baby.
 Klumpkey’s palsy:

Young boy with Klumpke’s palsy of the right arm.

 Due to injury of C8 & T1,

 Baby lies with arm supinated and elbow is flexed,
 Loss of intrinsic muscle power in hand,
 Reflexes are absent,
 There may be unilateral Horner’s syndrome.
 Total plexus injury:
 Baby’s arm is flail and pale,

 All finger muscles are paralysed and there may also be vasomotor impairment,
 Unilateral Horner’s syndrome.

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 APL / 10 - 290

Investigation:
 X ray chest: to exclude ≠ of shoulder or clavicle.
 MRI of Brachial plexus:

Management:
 Paralysis may recover completely:
 Many (perhaps most) of the upper root lesions recover spontaneously,
 A fairly reliable indicator is return of Biceps activity by 3rd month,
 Absence of Biceps activity does not completely rule out later recovery.

 Paralysis may improve:

 A total lesion may partially resolve, leaving the infant with a partial paralysis.

 Paralysis may remain unaltered:

 More likely with complete lesions, especially in the presence of Horner’s syndrome.

 Operative management:
 If there is no Biceps recovery by 3 months – operative intervention should be considered,
 Unless the roots are avulsed – it may be possible to excise the scar and bridge the gap with free Sural
nerve grafts,
 If the roots are avulsed – nerve transfer may give a worthwhile result.
 Shoulder is prone to fixed internal rotation and adduction deformity. Subscapularis release will be
needed, sometimes supplemented by a tendon transfer. In case of older children – deformity can be
treated by rotation osteotomy of humerus.

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Q) Short note: Erb’s paralysis
Q) What do you mean by Erb’s palsy?
Erb’s palsy:
Trauma induced (usually birth trauma) paralysis of muscles of upper arm; due to lesion in the upper
trunk of brachial plexus.
Site of injury: upper trunk of brachial plexus.
Causes of injury:
 Birth injury,
 Fall on shoulder,
 During anaesthesia.
Nerve roots involved: mainly C5 and partly C6.
Muscles paralysed:
 Mainly Biceps, Brachialis, Brachioradialis & Deltoid,
 Partly Supraspinatus, Infraspinatus & Supinator.

Deformity:
** GOOD
 Arm:
HAND
 Hangs by the side,
BUT
 Adducted,
BAD
 Medially rotated,
SHOULDER**
 Forearm:
 Extended,
 Pronated.
 Wrist:
 Flexed.
Name of deformity:
 Policeman’s tip hand or
 Porter’s tip hand.
Disability:
 Arm : abduction & lateral rotation of arm is lost,
 Forearm : flexion & supination of forearm is lost,
 Jerks : Biceps & Supinator jerks are lost,
 Sensation lost: small area over lower part of deltoid / Regimental badge area.

377
Q) Short note: Klumpke’s paralysis.

Site of injury: lower trunk of brachial plexus,

Nerve root involved: mainly T1 & partly C8.

Causes of injury:
 Undue abduction of arm with clutching something with hand when falling from height,
 Birth injury.

Muscles paralysed:
 Intrinsic muscles of hand (T1)
 Ulnar flexors of wrist & fingers (C8)

Deformity: Claw hand deformity.

Disability:
 Clawing of ring and little finger of hand,
 Cutaneous anaesthesia over ulnar border of forearm and hand,
 Horner’s syndrome:
--> This is due to injury to the
 Ptosis,
sympathetic fibres of head & neck that
 Miosis,
leave the spinal cord through T1.
 Anhydrosis,
 Enophthalmos,
 Loss of ciliospinal reflex.

378
Q) What is Winging of Scapula?

Long thoracic nerve palsy Winging of the scapula is demonstrated by the patient pushing forwards against the wall. If the serratus anterior is paralysed, the
scapula cannot be held firmly against the rib-cage.

Winging of Scapula:
When Serratus anterior muscle is paralysed due to injury to the nerve to serratus anterior / long
thoracic nerve, then medial border of scapula gets raised when pushing movement is attempted – this is called
Winging of Scapula.

379
 Median Nerve Injury.
APL (8) - 229

Level of injury:
a) Low lesion / Near to wrist,
b) High lesion / in the forearm

Low lesion:
 Mechanism of injury: Wasting of the thenar eminence on the right side.
 Cut in front of wrist or
 By carpal dislocation.

 Clinical feature:
 H/O injury,
 Unable to abduct thumb (Pen test),
 Opposition of thumb is difficult (OK sign +ve),
 Thenar muscles are wasted / Paralysis of thenar muscles – Ape thumb deformity.
 Sensory loss over the skin of lateral three & half finger and over thenar eminance.

High lesion:
 Mechanism of injury:
 # in forearm or
 Elbow dislocation.

In high median nerve lesions, the long flexors to the

 Clinical feature: thumb and index fingers are also paralysed and the
patient shows the ‘pointing index sign’.
 Pointing index finger / pointing sign,
 Pinch defect
– Thumb & index flexors are deficient
 Opposition of thumb is difficult.
 Thenar muscles are wasted,
Paralysis of thenar muscles – Ape thumb deformity.
Typical area of sensory loss.

380
  Sensory loss over flexor surface of forearm along radial border, dorsum of hand,
lateral 3 & ½ finger and also over thenar eminance.

Isolated AIN injury:

Examination: Signs are similar to High median nerve injury without any sensory loss.
 OK Sign : + ve,
 Oschner clasping test : + ve,
 Pen test : +ve
 Sesory loss: over tip of index finger.

Investigation:
 NCV
 EMG.

Treatment:
 Surgical exploration, repair of median nerve end to end or repair by nerve graft.

381
Q) Pen test for Median nerve?

Median nerve – testing for abductor power (a) The hand must remain flat, palm upwards. (b) The patient is told to
point the thumb towards the ceiling against the examiner’s resistance.

382
On examination:
a) Look:

383
b) Feel:

384
c) Move:

Testing FCR
Testing FPL

Testing FDP of Index

Median nerve – testing for abductor power

(a) The hand must remain flat, palm upwards.
(b) The patient is told to point the thumb towards the
ceiling against the examiner’s resistance.

385
Q) Short note: Median nerve entrapment. APL (8) – 248
CTS Pronator Syndrome AIN compression
Median nerve is compressed Φ Proximal MN compression, Compressive neuropathy of AIN
within the carpal tunnel. Φ Compressive neuropathy of MN at results in motor deficit only, no
or below the level of elbow. sensory changes.
Causes of CTS: Sites of compression: Sites of compression:
 Endocrine,  Supracondylar process,  Edge of Bicipital
 Inflammation,  Ligament of Struthers, aponeurosis,
 Trauma,  Bicipital aponeurosis,  Tendinous edge of deep
 Pregnancy,  B/W ulnar & humeral heads of head of pronator teres
 Tumour pronator teres, (most common),
 Menopause.  FDS aponeurotic arch.  FDS arcade.
Clinical features: Clinical features: Clinical feature:
1) Burning pain, tingling, 1) Aching pain over proximal volar 1) No complain of pain, unlike
numbness & paresthesia forearm, CTS or Pronator syndrome,
over radial 3 & ½ digits, 2) Paresthesis over thumb, index,
2) Symptoms are more acute middle finger & radial half of ring
2) Weakness to grip & pinch
at night, finger,
(specially thumb, index and
3) Pt have to move fingers to 3) Sensory disturbance along the
middle finger flexion),
get relief, distribution of palmar cutaneous
4) Difficulty in carrying out branch of median nerve which
3) Unable to make OK sign (Test
fine movements such usually arise 4 to 5 cm proximal
sewing, writing. to carpal tunnel. of FDP & FPL)

Examination: Examination: 3 Deep Flexor Muscles are

a) Phalen test: pain &  Paresthesis becomes worse suppliced by AIN:
paresthesia along the with repetitive prono-supination,
distribution of MN,  Resisted elbow flexon with 1. FDP (index & middle),
forearm supination – compression of 2. FPL (thumb),
b) Tinel sign: +ve, MN at Bicipital aponeurosis, 3. Pronator quadratus.
 Resisted forearm pronation
with elbow extension – compression
c) Abduction & Opposition of MN at 2 heads of pronator teres.
of thumb: weak,  Resisted flexion of FDS to
middle finger – compression of MN

386
 at FDS apneurotic arch.
Investigation: Investigation: Investigation:
 NCV:  X ray elbow joint B/V: bony  NCV,
 X ray cervical spine: to spur at the attachment of  EMG:
exclude cervical Struther’s ligament. May reveal
spondylosis, cervical  NCV: can localize the level of abnormalities in FPL, FDP
rib. compression. (index & middle finger),
 EMG. pronator quadratus muscle.
Treatment: Treatment: Treatment:
a) Conservative: a) Conservative: 3 months 1. Conservative: 8 to 12 weeks,
 NSAIDs,  Rest,  Rest,
 Light splint that prevent  NSAIDs,  NSAIDs,
wrist flexion,
 Splinting,  Splinting,
 Corticosteroid inj. into
 Physiotherapy.  Physiotherapy.
carpal tunnel.

b) Operative:
 Open surgical division of b) Operative: after 3 months of 2. Operative: after conser. treat,
transverse carpal conser. treat,  Surgical exploration &
ligament,  Surgical exploration & decompression of AIN.
 Endoscopic division of decompression of MN.
flexor retinaculum,  Decompression of all possible
c) Treatment of cause. 5 sites
Outcome: Outcome:
About 80% patients relieve from symptoms. About 75% patients relieve from
symptoms.

387
 Carpal Tunnel Syndrome.
APL- 288, camp - 3637

--- In this condition, median nerve is compressed as it passes through carpal tunnel.
--- Elevation of carpal tunnel pressures of more than 20 to 30 mm Hg impedes epineurial blood flow and nerve
function is impaired.
Q) What is carpal tunnel?
--- It is a fibro-osseous tunnel formed by carpal bones dorsally and flexor retinaculumn anteriorly.

Q) What are the structures passes through this tunnel?

 9 tendons:
 4 tendons of FDS,
 4 tendons of FDP,
 1 tendon of FPL.
 1 nerve:
 Median nerve.

Median nerve compression (a) Thenar wasting in the right hand, (b) sensory loss.

388
Q) Clinical features of CTS?
 Burning pain, Tingling, Numbness & Paresthesia in radial 3 & ½ digits,
 Symptoms more during night,
 Difficulty in doing fine movements eg. Sewing, writing etc.
Q) On examination of CTS?
Look:
 Expose both upper limbs upto cervical region {cervical rib, cervical spondylosis},
 Wasting of thinner eminence,

Feel:
 Temp:
 Tenderness:
 Sensory status:
 ↓ sensation in thumb, index and middle finger,
 ↓ sensation in autonomous zone in index finger.

Tinel’s test; B&L-446

Median nerve compression test

 Tinel sign: Sensory symptoms can often be reproduced by percussing over the median nerve (Tinel’s sign).
 Carpal compression test / Durkan test: in which direct compression is applied to the median nerve for 30
seconds with the thumbs or an atomizer bulb attached to a manometer, was found to be more specific (90%)
and more sensitive (87%) than either the Tinel or Phalen test. Patients with carpal tunnel syndrome usually
have symptoms of numbness, pain, or paresthesia in the median nerve distribution.
 Vascular status:

Move:
 Phalen test:
 Sensory symptoms can often be reproduced by holding the wrist fully flexed for less than 60 seconds
(Phalen’s test). APL-288

389
 Phalen’s test. B&L- 446

 Acute flexion of the wrist for 60 seconds (Phalen test) increases the paresthesia. camp- 3638

 Pen test: weak,

 Abduction & opposition of Thumb: weak,
 Movement of Wrist joint: Most hand functions are performed with the wrist in ulnar deviation;

0
 Normal wrist in ulnar deviation is about 50 ,
From the neutral position dorsiflexion is
 Normal radial deviation is only about 15°.
slightly less than palmarflexion.

Q) Investigations of CTS?
 NCS: Electrodiagnostic tests, which show slowing of nerve conduction across the wrist, are reserved

for those with atypical symptoms.

 X ray cervical spine B/V: Radicular symptoms of cervical spondylosis may confuse the diagnosis and
may coincide with carpal tunnel syndrome.

 X ray wrist B/V,

 Blood test:
 CBC:
 ESR:

390
  CRP:
 S creatinine.
 RA test:
 TSH:

Q) What are the causes of carpal tunnel syndrome?

 Endocrine:
o Hypothyroidism,
o Myxoedema,
o Acromegaly.
 Inflammation:
 RA,
 TB,
 Gout.
 Pregnancy:
 Menopause:
 CRF:
 Trauma:
o Lunate dislocation,
o Complication of Colles’ fracture.
 Tumor / Ganglion.

Q) Differential diagnosis?
 Cervical rib / TOS,
 Cervical spondylosis.

391
Causes: camp-3638

Anatomy Physiology

392
Q) Treatment of CTS?
 Conservative:
 Light splint to prevent wrist flexion:

Carpal tunnel splint

 When patient presents with night pain only,

 CTS with pregnancy related symptoms.

Carpal tunnel injection,

 Corticosteroid inj into carpal tunnel – provides temporary relief.

 If mild symptoms have been present, and there is no thenar muscle atrophy, the use of night splints
and injection of cortisone preparations into the carpal tunnel may provide temporary relief, but long-term benefit is
obtained in only about 10% of patients treated with corticosteroid injection and splinting. Care should be taken not
to inject directly into the nerve. camp- 3639

 Operative:

Open carpal tunnel release.

 Surgical division of Transverse Carpal Ligament,

 Endoscopic release of flexor retinaculum.
 Limited approaches, such as the “double incision” of Wilson and the “minimal incision” of
Bromley may offer rapid recovery.

393
“MINI-PALM” OPEN CARPAL TUNNEL RELEASE

“Double incision” of Wilson “Minimal incision” of Bromley.

 Transverse incision proximal to anterior wrist Thenar crease takes a variable course,
crease between flexor carpi ulnaris and flexor carpi and palmar incisions should be well ulnar
radialis tendons. to it to avoid the median nerve palmar
 Distal longitudinal incision made between proximal cutaneous branch.
palmar crease and 1 cm distal to hamate hook in line
with radial border of ring finger.
Avoid cutting the palmar cutaneous

sensory branch, which lies in the interval

between the palmaris longus and the

flexor carpi radialis tendons.

Maintain longitudinal orientation so that the
incision is generally to the ulnar side of the
long finger axis or radial border of the ring
fourth ray.
 When severed, the palmar sensory

branch frequently causes a painful

neuroma that may later require excision

from the scar.

 Should this nerve be severed, do not

attempt to repair it but section it at its

394
 origin.

Avoid injury to the superficial palmar

arterial arch, which is 5 to 8 mm distal to

the distal margin of the transverse carpal

ligament.

395
Post operative care:
 A light compression dressing and a volar splint may be applied.
 The hand is actively used as soon as possible after surgery, but the dependent position is avoided. Usually
the dressing can be removed by the patient at home 2 or 3 days after the surgery, and then gentle washing and
showering of the hand is permitted.
 Gradual resumption of normal hand use is encouraged.
 The sutures are removed after 10 to 14 days.
 A splint may be continued for comfort as needed for 14 to 21 days.

396
ENDOSCOPIC RELEASE. camp- 3644

Advantages:
 Less palmar scarring,
 Less ulnar “pillar” pain,
 Rapid and complete return of strength, and return to work and activities at least 2 weeks sooner than for
open release.

Limitations:
Problems related to Endoscopic carpal tunnel release include
(1) A technically demanding procedure;
(2) A limited visual field that prevents inspection of other structures;
(3) The vulnerability of the median nerve, flexor tendons, and superficial palmar arterial arch;
(4) The inability to control bleeding easily; and
(5) The limitations imposed by mechanical failure.

Methods:
Two methods can be divided into
 Single-portal (Chow) and
 Two-portal (Agee) techniques.

Single-portal (Chow) Two-portal (Agee)

397
Q) Incision for open surgical division of transverse carpal ligament?

 The incision should be kept to the ulnar side

of the thenar crease so as to avoid accidental
injury to the palmar cutaneous (sensory) and
thenar motor branches of the median nerve.

 Internal neurolysis is not recommended.

Q) What are the dangers of surgery & how to avoid it?

-- Two nerves are always kept in mind;
 Palmer cutaneous branch of Median nerve:
 It passes superficial to the retinaculumn,

 On radial side of Palmaris longus,

 Supplies skin of thenar eminence.

398
  Recurrent motor branch of Median nerve:
 It leaves Median nerve on its lateral side,

 It emerges from carpal tunnel to turn back to give motor supply to thenar

muscle.

-- To avoid injury to these nerves:

 Incision should be placed on the ulnar side midline / ulnar side of median nerve,
 A longitudinal incision is made from distal flexor crease & extended distally for about 5cm in line
with the ulnar aspect of 3rd digit.

Q) Complications of CTS release?

Early / Per operative:
 Injury to palmer cutaneous branch of Median nerve,
 Recurrent motor branch of Median nerve,
 Injury to superficial palmer arch.
Late:
 Unrelieved or Recurrent carpal tunnel syndrome.

CAMP- 3649

 Recurrence rate after primary carpal tunnel release is approximately 2%.

 Unrelieved symptoms may lead to repeat operation in 12% of patients.
 Causes of Recurrent CTS:
 Incomplete release of the transverse carpal ligament,
 Re-formation of the flexor retinaculum,
 Scarring in the carpal tunnel, median or palmar cutaneous neuroma,
 Palmar cutaneous nerve entrapment,
 Recurrent granulomatous or inflammatory tenosynovitis, and
 Hypertrophic scar in the skin.

399
 Ulnar Nerve Injury.

Ulnar Nerve Injury:

a) Sites of injury:
 Near the wrist (Low lesion),
 Near the elbow (High lesion),
 Open wound may damage it at any level.
b) Clinical features:
 Low lesion:
o H/O cut by shattered glass or any sharp object,
o Entrapment of ulnar nerve in piso-hammate tunnel / Guyon’s canal.
o Claw hand deformity,
o Numbness over the skin of ulnar one and half finger & also over hypothenar eminance.
o Hypothenar and interosseous muscle wasting.

 High lesion:
o H/O injury (cut / # / dislocation) around the elbow,
o Ulnar nerve entrapment in cubital tunnel,
o High ulnar paradox,
o Numbness over the skin of medial border of forearm, hand, ulnar one and half finger & also over
skin of hypothenar eminance.
o Muscles wasting over medial side of forearm, hypothenar and interosseous group.

c) Examination:
 Froment’s sign: (+)ve,
 Card test: (+)ve,
 Sensory loss: over the tip of little finger.

400
 d) Investigation:
 NCV,
 EMG.
Q) Critical time for nerve repair?
Nerve High lesion Low lesion
Median nerve: 9 months 12 months
Ulnar nerve: 9 months 15 months
Radial nerve: 15 months 9 months {PIN}

Q) What are the types of nerve repair? camp-3370

--- According to timing of repair, 3 types-

 Primary repair:
 Immediately after injury or within 6 to 12 hours,
 Delayed repair:
 Usually within first 2 to 2.5 weeks,
 Secondary repair:
 After 2.5 to 3 weeks.

Q) Treatment:
 Exploration and repair of ulnar nerve, either by-
 Neurolysis,
 End to end repair or,
 Repair by nerve graft.
 Anterior transposition of ulnar nerve at elbow permits closer of gap up to 5 cm.

401
Q) Short note: Ulnar nerve compression / Entrapment neuropathy of ulnar nerve.
Cubital Tunnel Syndrome Ulnar Tunnel Syndrome / Handle Bar Palsy
a) Compressive neuropathy of ulnar nerve at the level of Ulnar nerve can be compressed in Guyon’s canal / Piso-
elbow, Hammate tunnel (length: 2 – 3 cm) at the ulnar border of
nd
b) 2 most common compressive neuropathy of upper wrist.
extremity.
Sites of compression: Causes:
At the level of elbow within cubital tunnel:  Ganglion from Triquetro-hammate joint (most
 by bony abnormality, ganglion or hypertrophied common),
synovium.  # hook of Hammate,
 Pisiform dislocation,
Proximal to cubital tunnel:  Ulnar artery aneurysm,
 by Arcade of Struthers (hiatus of medial  Inflammatory arthritis,
intermuscular septum)

Distal to cubital tunnel:

 by two heads of FCU.

Clinical features: Clinical features:

Numbness & tingling sensation over little and ring  Presentation depends on location of
finger, compression within Guyon’s canal & it may be
Weak pinch (70% pinch will lost)  Pain & paresthesia over ulnar one and half

402
 Weak to grip, finger,
Slight clawing,  Ulnar clawing,
Hypothenar & intrinsic muscles wasting found.  Wasting of hypothenar & interrosi muscles.
 Weak to pinch & grasp.
Test: Test:
 Tinel’s percussion test:  Tinel’s percussion test:
 Tenderness over nerve behind medial epicondyle. Tenderness over nerve behind medial epicondyle.
 Sensory test: ↓ed over tip of little finger.  Sensory test: ↓ed over tip of little finger.
 Froment’s sign:  Froment’s sign:
 Card test:  Card test:
Investigation: NCV.
Treatment: Investigation:
a) Conservative: NCV,
 NSAIDS, X ray / CT wrist: # hook of Hammate.
 Activity modification, MRI wrist: ganglion, ulnar artery aneurysm.
0
 Splintage of elbow in mid extension (45 ) at night,
b) Operative: Treatment:
 U. N decompression without transposition,  It depends on cause,
 U. N. decompression with ant. transposition.  Surgery needs to decompress ulnar nerve
 Medial epicondylectomy. entrapment at wrist.

Q) How you ensure that ulnar nerve entrapment occurs at wrist rather than elbow?

Ulnar nerve entrapment occurs at wrist, because:

 power of FCU & FDP to little finger is maintained,
 Dorsal branch of ulnar nerve which leaves the ulnar nerve proximal to Guyon’s canal is intact.

 About 5 cm proximal to wrist,

 It runs along the ulnar side of back of wrist & hand, then divides into 2 dorsal digital branches
for little and ring finger.

403
Q) What is Claw hand deformity?
Q) Short note: Claw Hand.

Claw hand:
-- It is a deformity of hand due to various causes characterized by hyperextension of MCP joints &
flexion of IP joints of fingers.

Types:
-- 2 types,
a) Ulnar claw hand:
-- Ulnar nerve lesion involving ring and little finger,
b) True claw hand:
-- Combined median & ulnar nerve lesion involving all fingers of hand.

Causes:

i) Isolated ulnar nerve injury / ulnar claw hand,

ii) Combined median & ulnar nerve injury,

iii) Cervical rib,

iv) Leprosy,

v) Amyotrophic lateral sclerosis,

vi) Advanced rheumatoid arthritis, Typical area of sensory loss.

vii) Volkmann’s ischaemic contracture,

viii) Spinal cord lesion: Syringomyelia, Poliomyelitis.

404
On examination:
 Clawing of little & ring finger / all fingers of hand,
 Trophic change over the skin of finger,
 Thenar / hypothenar & interosseous muscles wasting,
 Sensory loss – over the distribution of affected nerve.
Investigation:
 NCV,
 X ray neck – thoracic inlet view,
 RA test,
 CBC.

Treatment:
 Treatment according to cause,
 In case of injury: surgical exploration, neurolysis / repair of nerve end to end / repair by nerve graft.

Q) What are the difference between claw hand & Dupuytren’s contracture?

Points Claw Hand Dupuytren’s contracture

1) Definition Deformity of hand characterized by Deformity of hand characterized by nodular
hyper-extension of MCP joints & hypertrophy & contracture of superficial palmar
flexion at IP joints of ring and little fascia / palmar aponeurosis.
finger / all fingers of hand.
2) Causes:  Isolated injury to UN,  Due to proliferation of myofibroblast
 combined injury to UN + MN, within palmar fascia,
 Leprosy,  Inherited autosomal dominant trait.
 VIC,
 Spinal cord lesion.
3) Clinical  Claw hand deformity,  Nodular thickening in palm extends to
features:  Wasting of thenar / hypothenar & ring & little finger,
interosseous muscles,  Flexion deformity at MCP & PIP joints
 Cutaneous anaesthesia along the of ring and little finger,
distribution of ulnar or ulnar +  Sometimes dorsal knuckle pad is

405
 median nerve. thickened – Garrod’d Pad,
 Loss of pinch action over thumb.  Similar nodules may seen on sole of
foot – Ledderhose’s disease.
 Fibrosis of corpus cavernosum –
Peyronie’s disease.

4) Associated Often associated with H/O trauma or Associated with DM, Epilepsy treated with
Conditions cut injury or disease affecting ulnar phenytoin, Smoking, PTB, Alcoholic
nerve or ulnar and median nerve. cirrhosis / CLD, AIDS.

Q) Short note: Tardy Ulnar Nerve Palsy. EBN - 304

Tardy ulner nerve palsy:

-- It is late onset ulner nerve palsy characterized by difficulty to perform fine movements.

Causes:
i) # Medial epicondyle of humerus,
ii) Malunited or non-united # medial condyle of humerus,
iii) Dislocation of elbow,
iv) Recurrent sublaxation of elbow due to inadequate fibrous arch,
v) Shallow ulnar groove,
vi) Hypoplasia of humeral trochlea,
vii) Cubitus valgus deformity,
viii) Nerve contusion (traction, compression & pressure effect).

Clinical features:
 H/O trauma / fracture around elbow,
 Difficulty to perform fine movements,
 Muscle wasting over ulnar side of forearm and hand,
 Sensory deficit along the distribution of ulnar nerve,

Investigation:

406
  NCV,
 EMG

Treatment:
 Treatment of the cause,
 Surgical treatment includes:
 Exploration and neurolysis.
 Medial epicondylectomy or
 Anterior transposition of ulnar nerve.

407
Q) On examination of Ulnar nerve palsy:
Look:
 Expose both upper limbs up to shoulder,
 Attitude of hand:
 Ulnar paradoxical claw hand,
 Clawing of little and ring finger,
 Visible muscle wasting:
 Wasting of ulnar side of forearm muscles & hypothenar muscle,
 Wasting of hypothenar muscle & interrossi muscles.
 Skin condition: any scar mark present or not
Feel:
 Temp:
 Tenderness:
 Measure muscle wasting: in forearm.
 Sensory status:
 Sensory loss over little & medial ½ of ring finger,
 Loss of sensation in dorsum – indicates lesion proximal to wrist.
 Muscle power:
 FDS of Ring & Little finger: normal due to median nerve is intact.
 FDP of Ring & Little finger:
 In low lesion – flexion of DIP possible, due to escape of FDP muscle.
 In high lesion – fail to flex DIP, due to paralysis of inner half of FDP.
 FCU:
 1st Dorsal Interrossi:
 Abduction & adduction of fingers:
Move:
 Special tests:

408
Q) Critical time for nerve repair?
Nerve High lesion Low lesion
Median nerve: 9 months 12 months
Ulnar nerve: 9 months 15 months
Radial nerve: 15 months 9 months {PIN}

Q) What are the types of nerve repair? camp-3370

--- According to timing of repair, 3 types-

 Primary repair:
 Immediately after injury or within 6 to 12 hours,
 Delayed repair:
 Usually within first 2 to 2.5 weeks,
 Secondary repair:
 After 2.5 to 3 weeks.
Q) Treatment of ulnar claw hand? apl / 10 – 297,

 Exploration and repair of ulnar nerve, either by-

 Neurolysis,
 End to end repair or,
 Repair by nerve graft.

 Anterior transposition of ulnar nerve at elbow permits closer of gap up to 5 cm.

Exploration and suture of a divided nerve are well worthwhile, and anterior transposition at the elbow permits
closure of gaps up to 5 cm.

409
  Distal nerve transfer from the anterior interosseous nerve may be considered in high lesions of the ulnar
nerve.

 While recovery is awaited,

 Skin should be protected from burns.
 Hand physiotherapy keeps the hand supple and useful.

o Tendon transfer for correction of claw hand deformity:

 Brand procedure: Metacarpophalangeal flexion can be improved by extensor carpi radialis
longus to intrinsic tendon transfers (Brand), or
 Zancolli procedure: By looping a slip of flexor digitorum superficialis around the opening of the
flexor sheath (Zancolli procedure).
 Index abduction is improved by transferring extensor pollicis brevis or extensor indicis to the
interosseous insertion on the radial side of the finger.

Q) If no recovery of ulnar nerve in expected time or no treatment – then what will happen?
If there is no recovery after nerve division, hand function is significantly impaired -
 Grip strength is diminished because the primary metacarpophalangeal flexors are lost, and
 Pinch is poor because of the weakened thumb adduction and index finger abduction.
 Fine & coordinated finger movements are also affected.

Q) What will happen if anterior transposition of ulnar nerve is not done at elbow after medial epicondyle ≠
reduction?
--- In all cases of ORIF, Ulnar nerve should be transported a anteriorly to prevent –
 Damage of ulnar nerve by friction,
 Entrapment of ulnar nerve in callous.

Q) Claw hand?
-- It is a deformity of hand due to various causes characterized by hyperextension of MCP joints &
flexion of IP joints of fingers.

410
Types:
-- 2 types,
a) Ulnar claw hand:
-- Ulnar nerve lesion involving ring and little finger,
b) True claw hand:
-- Combined median & ulnar nerve lesion involving all fingers of hand.

Causes:
 Isolated ulnar nerve injury / ulnar claw hand,
 Combined median & ulnar nerve injury,
 Cervical rib,
 Leprosy,
 Amyotrophic lateral sclerosis,
 Advanced rheumatoid arthritis,
 Volkmann’s ischaemic contracture,
 Spinal cord lesion: Syringomyelia, Poliomyelitis.

On examination:
 Clawing of little & ring finger / all fingers of hand,
 Trophic change over the skin of finger,
 Thenar / hypothenar & interosseous muscles wasting,
 Sensory loss – over the distribution of affected nerve.

411
Investigation:
 NCV,
 X ray neck – thoracic inlet view,
 RA test,
 CBC.

CAMP-3510

 Fowler technique:

It split the extensor proprius tendons of the index and little fingers to form four slips and
attached one each to the extensor aponeuroses on the radial side of the index and middle
fingers and on the ulnar side of the ring and little fingers.

412
413
 Brand technique:

It using the extensor carpi radialis longus / brevis tendon lengthened by a free graft from the plantaris tendon; the
distal end of the graft is split into four slips, or tails, and each tail is passed to the volar side of the deep transverse
metacarpal ligament and is attached on the radial side of each proximal phalanx to the extensor aponeurosis except
in the index finger, where it is attached on the ulnar side. In his opinion, index finger pinch can be secured more
firmly.

414
 Zancolli capsuloplasty or a tenodesing procedure:
--- To stabilize the metacarpophalangeal joints:

 Zancolli Lesso tech:

415
416
 Radial Nerve Injury.
APL/10 – 296, camp - 3516

Q) Sites of injury:
a) Low lesion (at the elbow)
b) High lesion (in upper arm),
c) Very High lesion (in axilla)

Low lesion / at Elbow:

1. Mechanism of injury:
 # or dislocation Head / Neck of Radius,
 Inadvertent injury during excision of radial head /
Iatrogenic injury to PIN.

2. Clinical features:
 Patient can not extend M/C joints of fingers (finger drop),
 Unable to extend thumb.

High lesion / Radial grove:

1. Mechanism of injury:
o # SOH,
o Trauma over arm,
o After prolonged tourniquet pressure,

2. Clinical features:
o Wrist drop + finger drop,
o Unable to extend thumb,
o Sensory loss over the skin around anatomical snuff box.

417
Very high lesion / Axilla:
1. Mechanism of injury:
 Chronic compression in axilla by ill fitting crutch.
 Fracture or Dislocation around shoulder.

2. Clinical features:
 above all +
 Unable to extend elbow, Triceps reflex: absent.

Typical area of sensory loss.

418
Sites of injury: Q) Name the muscles supplied by PIN?
d) Low lesion (at the elbow)
e) High lesion (in upper arm), Φ 4 (7) superficial muscles of extensor comp. of
f) Very High lesion (in axilla) forearm:

i) ECRB,
Low lesion:
ii) ED,
3. Mechanism of injury:
iii) Ext. digitiminimi
 # or dislocation Head / Neck of Radius,
 Inadvertent injury during excision of radial iv) ECU

head / Iatrogenic injury to PIN.

Φ 5 deep muscles of extensor comp. of forearm:

i) Supinator,
4. Clinical features:
 Patient can not extend M/C joints of fingers ii) Abd. pollicis longus,

(finger drop), iii) Ext. pollicis brevis,

 Unable to extend thumb. iv) Ext. pollicis longus.

v) Ext. indicis.
High lesion:
3. Mechanism of injury: Q) What are the functional losses of PIN injury?
o # SOH,
o Trauma over arm, Pure motor disorder, no sensory deficit,
o After prolonged tourniquet pressure, Weakness / Fail to extend MCP joints of
fingers (finger drop),
4. Clinical features: Weakness / Fail to abduct & extend IP
o Wrist drop + finger drop, joints of thumb,
o Unable to extend thumb, Weakness in the ulnar deviation of wrist.
o Sensory loss over the skin around anatomical
snuff box.

Very high lesion:

3. Mechanism of injury:
 Chronic compression in axilla by ill fitting
crutch.
 Fracture or Dislocation around shoulder.

419
4. Clinical features:
 above all +
 Unable to extend elbow,
 Triceps reflex: absent.

420
Q) Short note: Radial nerve entrapment. APL (O) – 299

Posterior Interosseous Syndrome. Radial Tunnel Syndrome (RTS)

Resistent Tennis Elbow.
--> Compressive neuropathy of PIN --> Due to entrapment of Radial nerve at the level
of lateral aspect of elbow.
Pathophysiology / Causes / Mech. of injury: Clinical features:
 Microtrauma : repetitive prono-supination movement,  Pain in the lateral aspect of upper forearm,
 Trauma : Monteggia # dislo, Radial head #,  Pain is aggravated often work related or at
 SOL: ganglion, lipoma. night,
 Inflammation: Rheumatoid synovitis of Radio-  Wrist movement precipitates pain.
capitellar joint
 Iatrogenic: Surgery.
Level of Compression: Level of compression:
i. (F) Fibrous tissue anterior to Radio-capitellar joint, FREAS
ii. (R) Leash of Henry : Recurrent branch of Radial
artery at the level of Radial neck,
iii. (E) ECRB’s edge,
iv. (A) Arcade of Frohse : proximal edge of Supinator
muscle,
v. (S) Distal edge of Supinator muscle.

Clinical features:
As low lesion of R. N
Investigation: Investigation:
 X ray forearm including elbow B/V
 MRI of affected part,
 NCV,
 EMG
Treatment: Treatment:
a) Conservative: c) Conservative:
 Rest,  Rest,
 Activity modification,  Activity modification,

421
  NSAIDs,  NSAIDs,
 Splinting,  Splinting,
 Physio-therapy.  Physio-therapy.
b) Operative: d) Operative:
 Surgical exploration & decompression of  Surgical exploration & Radial nerve
PIN, usually after 3 months of conservative should be freed beneath ECRB and
treatment. Supinator mucle.
 Tendon transfer.

Q) On examination of Wrist Drop?

Look:
 Expose both upper limbs up to shoulder and compare,
 Attitude of limb:
 Wrist drop;
 Finger drop.
 Scar mark present or not,
 Visible muscle wasting {triceps, BR,
extensor muscles of forearm}.

Feel:
 Temp:
 Tenderness:
 Sensory status:
 In Very / High lesion – anaesthesia on dorsum of the base of thumb, 1st interosseous space
and dorsum of hand + forearm.
 In low lesion – anaesthesia limited to anatomical snuff box.
 Muscle power:
 Triceps:
 Brachioradialis:
 Wrist extension:
 Finger extension:
 Tinel sign:
 Vascular status:

422
Move:
 In Very High lesion:
 Inability to extend the elbow, wrist and finger at MCP joints {Extension of fingers permitted by
action of lumbricals and interossei, when hand is supported at MCP joints},
 Flexion of elbow at mid prone position / BR,
 Supination of elbow in extended elbow / Supinator,
 Extension of elbow / Triceps.

 In High lesion:
 Wrist and Finger drop,
 Flexion of elbow at mid prone position – not possible,
 Supination of elbow in extended elbow – not possible,
 Extension of elbow – Possible.

 In low lesion:
 Finger drop: present,
 Wrist can be extended, but radially deviated as Extensor carpi radialis is lost,
 Flexion of elbow at mid position – possible,
 Supination of elbow – possible,
 Extension of elbow – possible.

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Q) Investigation for Radial nerve injury?
 NCS,
 EMG.

Q) Treatment of wrist drop? apl- 283, camp- 3515

 Open injuries:
Should be explored and the nerve repaired or grafted as soon as possible.
 Closed injuries:
 If the palsy is present on admission, one can afford to wait for 12 weeks to see if it starts to recover.

 If it does not, then EMG should be performed; if this shows denervation potentials and no active potentials then
a neurapraxia is excluded and the nerve should be explored.

 The results, even with delayed surgery and quite long grafts, can be gratifying as the radial nerve has a
straightforward motor function.

 If it is certain that there was no nerve injury on admission, and the signs appear only after manipulation or
internal fixation, then the chances of an iatropathic injury are high and the nerve should be explored and – if
necessary – repaired or grafted without delay.

 Dynamic Cock up Splint: While recovery is awaited, the small joints of the hand must be put through a full range
of passive movements. The wrist is splinted in extension.

 Tendon transfer: If recovery does not occur, the disability can be largely overcome by tendon transfers:

424
 Brand suggested:

APL / 10 - 296

TRANSFER OF THE - CAMP- 3516

 PRONATOR TERES TO EXTENSOR CARPI RADIALIS BREVIS,

 FLEXOR CARPI RADIALIS TO EXTENSOR DIGITORUM COMMUNIS,
 PALMARIS LONGUS TO EXTENSOR POLLICIS LONGUS.

 Boyes devised transfers:

(1) Pronator teres to Extensor Carpi Radialis Longus and Extensor Carpi Radialis Brevis,
(2) Flexor Carpi Radialis to Extensor Pollicis Brevis and Abductor Pollicis Longus,
(3) Middle Flexor Digitorum Sublimis to Extensor Digitorum Communis, and
(4) Ring Flexor Digitorum Sublimis to Extensor Pollicis Longus and Extensor Indicis Proprius.

425
Q) Post operative care after tendon transfer?
 Although the sutures can be removed 10 to 14 days postoperatively, the wrist is kept in 40
degrees of extension, the metacarpophalangeal joints in full extension, and the thumb radially abducted
and extended for 3 weeks.
 Supervised physical therapy is begun at this time.
 A removable custom-molded splint keeping the wrist, fingers, and thumb in the postoperative
position is worn at night and between therapy sessions for approximately 3 months postoperatively.

426
 Thoracic Outlet Syndrome
TOS
APL-293

Q) What is TOS?
--- Neurological and Vascular symptoms & signs in the upper limb may be produced by compression of lower trunk
of brachial plexus (C8 & T1) and subclavian vessels between clavicle and 1st rib.

Q) What are the causes of TOS?

 Cervical rib,
 Scalenus anticus syndrome,
 Costoclavicular syndrome / Eden’s syndrome,
 Hyper abduction syndrome.
 Wide 1st Rib / Clavicle,
 ≠ 1st Rib / Clavicle,
 Tumor arising from upper lobe of lungs.

427
Q) What are the sites of compression?
--- 3 sites,
1. 1st narrowing area / interscalene triangle:
 Interscalene triangle is bordered by anterior scalene muscle anteriorly, middle scalene muscle
posteriorly and medial surface of 1st Rib inferiorly.
 Presence of scalene minimus muscle and the fact that both anterior and middle scalene muscles have
their insertion in the 1st Rib can cause a narrow space and therefore compression.
 Brachial plexus and subclavian artery pass through this space.

2. 2nd passage way / Costoclavicular triangle:

 Costoclavicular triangle is bordered anteriorly by middle third of clavicle, posteromedially by the
first rib and posterolaterally by upper border of scapula.
 Subclavian vessel and brachial plexus cross costoclavicular triangle.

3. 3rd passage way / Subcoracoid or Sub-pectoralis minor space:

 This passageway is beneath the coracoid process just under pectoralis minor muscle.
 Borders include coracoid process superiorly; pectoralis minor anteriorly and ribs 2 – 4 posteriorly.
 Shortening of pectoralis minor can lead to narrowing of this space and therefore compression of
neurovascular structures during hyperabduction.

428
Q) Complications of TOS?
 Subclavian artery compression → result in post stenotic dilatation → stasis → favours thrombosis →
thrombi break and migrate distally causing embolization → blockade of distal artery causing ischaemia and
gangrene of upper limb.
 Compression of brachial plexus →

Q) Differential diagnosis of TOS?

 Cervical spondylosis,
 Rotator cuff syndrome,
 Ulnar nerve compression,
 Pancoast tumor.

429
Q) On examination of TOS?
Look:
 Expose the patient up to the waist,
 Compare both upper limb,
 Any muscle wasting present or not,
 Any sign of ischaemia – Discolouration, Gangrene, Sweating.
 Any supraclavicular swelling present or not.

Feel:
 In case of Supraclavicular swelling {Examine from back}
 Measure muscle wasting in both arm and forearm,
 Sensory examination – at autonomous zone,
 Compare Radial pulse on both sides.

430
 Unfortunately these tests are neither sensitive nor specific enough to clinch the diagnosis.
APL-293

Move:
 Adson’s test:
Adson’s test
The patient’s neck is extended and turned towards
the affected side while he or she breathes in
deeply; this compresses the interscalene space and
may cause paraesthesia and obliteration of the
radial pulse. APL-293

431
  Wright’s test:
--- Arms are abducted and externally rotated again the symptoms recur and pulse disappear on the affected
side.

 Roos test:
Wright’s test
Arms are abducted and externally rotated; again the symptoms recur and
the pulse disappears on the abnormal side. The examination is continued
by asking the patient to hold his or her arms high above their head and
then open and close the fingers rapidly; this may cause cramping pain on
the affected side (Roos’s test).
APL-293

3 minutes.

 Allen test:

432
Q) What is intermittent Claudication test?
--- Arm is abducted and elevated & fingers are exercised,
 If pain develops after 1 minute → it is normal {Negative},
 If pain develops before 1 minute → test is positive.

Q) Investigations for TOS?

 X ray cervical spine B/V,
 X ray Shoulder AP,
 CXR,
 Angiography and Venography,
 Nerve conduction study,
 ECG – to exclude cardiomegaly.
Q) Treatment of TOS?
 Conservative:
 Analgesics,
 Physiotherapy,
 Exercises like shoulder shrugging.
 Operative:
 Indication:
 Pain is severe,
 Muscle wasting is obvious,
 Vascular disturbance.
 Procedure:
 Removal of 1st thoracic rib:
 Posterior approach,
 Trans-axillary approach,
 Anterior approach.
 Removal of Cervical rib,
 Scalenotomy.

433
 Cervical Rib Syndrome.
Scalenus Syndrome.
Superior Thoracic Aperture Syndrome.
vattacharia-211, APL-293

--- This is a condition characterized by pain, paresthesia and muscular wasting of the upper extremity due to some
pathology at the thoracic outlet, commonly due to cervical rib.
--- Cervical rib syndrome is found in about 0.5% of normal population, of which only about 10% produce
symptoms.

Q) Pathology of cervical rib?

 Subclavian artery and 1st thoracic nerve going to form Brachial plexus pass through a triangle bounded by
scalenus anterior in front, scalenus medius behind and 1st rib at the base.
 In the Scalene triangle – neurovascular bundle may be stretched or angulated. Angulation or compression of the
artery and / or 1st thoracic nerve.

 Artery:
 Subclavian artery is rarely compressed rather than angulated. Owing to elevation → angulation, there is
constriction or narrowing of the lumen over rib.
 Subclavian artery is rarely compressed but the lumen may contract due to irritation of its sympathetic
supply, or else its wall may be damaged leading to the formation of small emboli. Even more unusual are signs of
venous compression – oedema, cyanosis or thrombosis.

434
  Nerves:
 Following stretching or compression of 1st thoracic nerve / lower trunk – friction neuritis causing at the
beginning sensory disturbances and later motor disturbance along the distribution of C8 & T1.
 Irritation of peri-arterial sympathetic fibres or paralysis of sympathetic fibres in the lower trunk may be
responsible for vasomotor disturbance.
Q) Causes of cervical rib?
 Extra rib:
Extra rib arises from 7th cervical vertebrae and extra rib may by-
 Complete rib:

 Incomplete rib:

 Incomplete rib ends by a fibrous band to 1st rib:

 No rib but only a fibrous band:

 Abnormality of muscle:
 There may be an additional scalene muscle,
 There may be a close approximation of the insertion of scalenus anterior and scalenus medius.

435
  Angulation of 1st thoracic nerve:
 When the Brachial plexus is post fixed, 1st thoracic nerve becomes stretched or acutely angulated over
the 1st rib.
Q) Clinical features of Cervical rib?

Amadeo Modigliani’s painting of Madame Zborowska (courtesy of the Tate Gallery, London).

 Common in woman,
 Thin woman with long narrow neck is more susceptible,
 Usually above the age of 30 years.
 Symptoms are usually unilateral and appear towards the end of the day or at night and often
improved by raising the limb.
 Symptoms:
 Sensory disturbances:
 Pain and paraesthesia extending from the shoulder, down the ulnar aspect of the arm
and into the medial two fingers.
 Symptoms tend to be worse at night and are aggravated by bracing the shoulders
(wearing a back-pack) or working with the arms above shoulder height.
 Pain becomes worse after carrying a heavy weight eg. shopping basket or ironing.

 Motor disturbances:
 In addition to sensory disturbances, weakness of the hand with clumsiness in
performing fine action.
 Later wasting of small muscles of hand may develop.

 Vasomotor disturbances:
 Coldness of the fingers, periodic changes in the skin colour, cyanosis, excessive
sweating, trophic changes with ulceration / gangrene of the tips of fingers.

436
  Early symptoms and signs can be mistaken for ulnar nerve compression. In fact, ulnar
neuropathy may accompany thoracic outlet compression as a manifestation of the double-crush syndrome. There is
pain and numbness over the medial side of the forearm and hand. In severe cases there will be wasting of all the
intrinsic muscles (T1) and weakness of the long flexors (C8).

Unfortunately these tests are neither sensitive nor specific enough to clinch the diagnosis.
APL-293

 Signs:
 Signs in the neck:
 Gradual sagging of shoulder girdle, perhaps in association with some atrophy /
wasting of the regional musculature,
 If a female, the patient is often long-necked with sloping shoulders (like a Modigliani
painting).
 Palpable lump in supraclavicular region:
 Lump may be pulsatile / subclavian artery being elevated by abnormal rib,
 Tender / on pressure → symptoms may increase.

 Adson test:
Adson’s test
The patient’s neck is extended and turned towards the
affected side while he or she breathes in deeply; this
compresses the interscalene space and may cause
paraesthesia and obliteration of the radial pulse.
APL-293

 Signs in the affected limb:

 Wasting of small muscles of hand supplied by C8 & T1:

437
  Interroseous muscles,
 Thenar muscles,
 Hypothenar muscles.
 Examination may show mild clawing of the ulnar two fingers with wasting and weakness of the
intrinsic muscles.
 Increased sweating or cynosis.
 Evidence of finger tip necrosis / gangrene.
 Sensory changes along C8 - T1 distribution.

 Wright’s test:
--- Arms are abducted and externally rotated again the symptoms recur and pulse disappear on the affected
side.
 Roos test:

 Allen test:

438
Q) Differential diagnosis of Cervical rib?
 Cervical spondylosis:
Cervical spondylosis is sometimes discovered on x ray. However, this disorder seldom involves the T1 nerve root.
 Pan coast tumour:
Pancoast’s syndrome, due to apical carcinoma of the bronchus with infiltration of the structures at the root of the
neck, includes pain, numbness and weakness of the hand. A hard mass may be palpable in the neck and x-ray of the chest
shows a characteristic opacity.
 Rotator cuff lesion:
Rotator cuff lesions sometimes cause pain radiating down the arm. However, there are no neurological symptoms
and shoulder movement is likely to be abnormal.
 Raynaud’s disease.
 CTS,
 Brachial neuritis.

Q) Investigations for Cervical rib?

X-ray of a long-necked woman: all the vertebrae down to T1 are above the clavicle.

 X ray cervical spine AP & Lateral view: X-rays of the neck occasionally demonstrate a cervical rib or an
abnormally long C7 cervical process.

439
 Cervical rib (a) Unilateral on right side and (b) bilateral.

 X ray Chest – to see apical tumour.

 Angiography and Venography are reserved for the few patients with vascular symptoms.
 MRI of cervical spine and thoracic inlet.
 Electrodiagnostic tests are helpful mainly to exclude peripheral nerve lesions such as ulnar or
median nerve compression which may confuse the diagnosis.
Q) Treatment of Cervical rib?
 Conservative treatment:
 Exercises of muscles of shoulder girdle:
 Strengthen the muscles,
 To lessen the tendency of shoulder to drop.
 UST or SWD,
To relief of pain.
 Analgesics,
 Advice:
 Not to carry any heavy weight.
 Operative treatment:
 Indications:
 When conservative treatment fail.
 Presence of severe pain.
 Muscle wasting is obvious.
 If there are vascular disturbances.
 Approaches:
 Supraclavicular approach or
 Transaxillary approach.
 Essentials of operation:
 Thoracic outlet is decompressed by removing the first rib (or the cervical rib). APL-294

 Division of Scalenus anterior muscle and / or,

440
  Excision of extra rib / fibrous band:
 These procedures may not cause relief of symptoms.
 So some surgeons advocate to cut all the three sides of scalene triangle ie, division of
both scalene anterior and medius muscles, excision of cervical rib / fibrous band and in absence of cervical rib or band – a
portion of 1st rib is excised.
 When cervical rib is excised, it should be removed along with it’s periosteum, other
wise there is a chance of regeneration.
 If vasomotor symptoms are prominent:
 Above operation should better be supplemented with sympathetic denervation of the
nd rd
upper limb, when 2 and 3 thoracic ganglion as well as lower third of the stellate ganglion are removed.
 Patients with arterial obstruction, distal embolism or a local aneurysm will need
vascular reconstruction as well as decompression.
 Care must be taken to prevent injury to the brachial plexus and subclavian vessels, or
perforation of the pleura.

441
 Nerve supply of leg
BD - 93
Sciatic nerve

Sural nerve

Tibial nerve Common peroneal nerve

Post. comp

 Superficial: Sup. Peroneal N. Deep Peroneal N./

 Gastrocnemius, Ant. Tibial Nerve.
 Soleus,
 Plantaris.
Lat comp.
Ant comp
 Deep:
 Popleteus,
 TP,
 FDL,
 FHL
Peroneus brevis TA
Peroneus longus EHL
EDL
PT

442
 Sensory loss following division of –
Complete sciatic nerve

Common peroneal nerve

443
 Posterior tibial nerve

Trophic ulcers because of sensory loss

Anterior tibial nerve.

Q) What are the muscles supplied by common peroneal nerve?

Q) What will happen if CPN become injured? BD-81

Common Peroneal Nerve (CPN):

-- Smaller terminal branch of Sciatic nerve.

Root value: L4, 5 S1, 2

444
Branches:
-- Sciatic nerve is divided into 2 parts: Tibial nerve & CPN at the apex of popleteal fossa. Then
CPN descends laterally & then it winds round posterolateral aspect of neck of fibula piercing peroneus longus
muscle, where it gives following 2 branches:
1) Superficial Peroneal Nerve,
2) Deep Peroneal Nerve / Anterior Tibial Nerve.

Muscles supplied by CPN:

 Superficial peroneal nerve:
 Peroneus longus,
 Peroneus brevis.

 Deep peroneal nerve / ATN:

 Tibialis anterior,
 EHL,
 EDL,
 Peroneus tertius.

Results of injury to CPN:

 Foot drop:
 Loss of power of inversion (TA) & eversion (PL & PB) of foot,
 Loss of power of extension of great {EHL} & other toes {EDL},
 Loss of sensation over the skin of :
 Dorsum of foot --> Superficial peroneal nerve injury,
 Cleft in b/w 1st & 2nd toes --> ATN injury / Deep peroneal nerve.

445
Q) Short note: Foot drop. EBN – 345, SHAH – 41/1

Foot drop:
-- It is the condition of foot when the power of dorsiflexion of foot is lost.

Causes of foot drop:

 General :  Complete Foot Drop: CPN injury.
 Peripheral neuropathy,
 Incomplete Foot Drop: Anterior Tibial Nerve injury.
 Leprosy,
 Poliomyelitis,
 Cerebral palsy.
 CVD,
 DM,
 Multiple sclerosis.
 TB of spine,

 Local:
 At the Spine:
 Spina bifida,
 Spinal tumour,
 Disc prolapse. Most common causes:
 Tight plaster / poor
padding,
 At the Hip:  UTST,
 # Neck of fibula,
 Posterior dislocation of hip,  Fasciotomy.
 # around the hip,
 # acetabulum.

 At the Gluteal region:

 Deep intramuscular injection → Injury to Sciatic nerve.

 At the Thigh:
 # SOF,
 Penetrating / gunshot injury.

446
  At the Knee (common causes):
 Dislocation of knee,
 # lateral condyle of tibia,
 # neck of fibula,
 Tight plaster around the knee,
 Damage of CPN during application of UTST.

 At the Leg / Ankle:

 Extensor tendon injury,
 Ant / Lat compartment syndrome,
 Gun shot injury.
Level of lesion:
a) High lesion:
 Above knee, both tibial & CP nerve is injured,
 Total foot drop.

b) Low lesion:
 Below knee injury,
 Foot drop is usually incomplete,
 2 types:
 Type : 1 (Deep Peroneal nerve / Ant. tibial nerve injury)
o Power loss: TA, EHL, EDL, PT
o Sensation loss: 1ST web space of foot.
o Spared: PL & PB,
o Complain: pt can not dorsiflex and invert the foot but eversion is possible.
o Muscle wasting: front of leg.

 Type: 2 (Sup. Pernoneal Nerve injury)

o Power loss: PL & PB
o Sensation loss: over outer leg and dorsum of foot.
o Spared: TA, EHL, EDL & PT.
o Complain: pt can not evert but can dorsiflex & invert the foot.
o Muscle wasting: outer half of leg.

447
 Injury to Superficial Peroneal Injury to Deep Peroneal Nerve Injury to Tibial Nerve
Nerve
Sensory loss: Sensory loss; Sensory loss:
Lateral aspect of leg upto dorsum of Cleft between 1st and 2nd toe. sole of foot,
foot, except cleft of 1st and 2nd toe.
Motor loss: Motor loss: Motor loss;
Loss of eversion power of foot. loss of dorsiflexion of foot, Loss of planter flexion of foot,
loss of extension of toes, loss of flexion of toes,
Inversion of foot: weak. inversion of foot: weak

Clinical features:

i) H/O nerve or extensor tendon injury over leg,

ii) High stepping gait,

iii) Sensory loss,

iv) Inability to dorsiflex the foot,

v) Inability to inversion & / or eversion of foot.

On examination: rohim-144
 Look:
 From front:
 Attitude of limb,
 Wasting of muscles,
 Scar mark,
 Pelvic tilting.
 From side:
 Scar mark,
 Any equinus deformity.
 From back:
 Spine: any gibbus,
 Pelvis: any tilting,
 Wasting:
 Calf muscle,
 Gluteal muscle.

448
  Any Scar mark.
 Gait / Walking:
 High stepping gait,
 Heel walking: -ve,
 Toe walking: +ve.
 Squating:
 Feel:
 Temp:
 Tenderness:
 Measure muscle wasting:
 Tinel sign:
 Nerve thickening:
o Post auricular nerve,
o Ulnar nerve.
 Sensory status:
 Muscle power:
 EHL:
 TA:
 FHL:
 Inversion:
 Eversion:

 Move:
 ROM of ankle,
 ROM of subtalar joint,
 ROM of mid tarsal joint.

Investigation:
 NCV,
 EMG.
 X ray of ankle B/V

449
Treatment:
a) Treatment at early stage:
 High incidence of recovery,
 Conservative treatment with a view to encourage recovery (for a least 1 year) should be carried out.
 Splintage of knee in 200 flexion and ankle in 900 for Night time & in Day time, walking is allowed
by using ‘Foot drop appliance’.
 Foot drop appliance / Brace:
Two verities:
 Dynamic – Spring shoe,
 Static – Backstop shoe.

b) If conservative treatment fails:

 For complete foot drop:
 TP to Dorsum → 3rd MT or 3rd Cuneiform bone.

TP tendon released from it’s insertion and rerouted through interroseous

membrane to ant compartment & then anchored to the base of 3rd MT or 3rd cuneiform bone by pull out suture.

 TP to EHL & EDL:

Circumtibial two tailed TP tendon transfer to EHL & EDL.

450
 For incomplete foot drop: (loss of dorsiflexion but presence of evertors)
 Anterior transposition of TP tendon & then fixed to EHL, combined with -
 PB transfer to EDL. (to prevent excessive valgus – due to strong evertor)
(OBER) (BARR)

451
 camp-1270
 Ober anterior transfer of posterior tibial tendon. A, Insertion of posterior tibial tendon has been
exposed. Note line of skin incision over muscle.
 Through a medial longitudinal incision 7.5 cm long, free the posterior tibial tendon from its
attachment to the navicular.

 B, Tendon has been freed from its insertion,  Cut a generous window in the interosseous
and muscle has been dissected from tibia. membrane but avoid stripping the periosteum
 Strip the periosteum obliquely on the medial from the tibia or fibula.
surface of the tibia so that when the tendon is  Pass the posterior tibial tendon through the
moved into the anterior tibial compartment only window between the bones, taking care that it is

452
the belly of the muscle will come in contact with not kinked, twisted, or constricted and that the
denuded bone. The tendon must not be in vessels and nerves to the muscle are not
contact with the tibia. damaged.

C, Tendon and muscle have been passed through anterior tibial compartment to dorsum of foot,
and tendon has been anchored in third metatarsal.

 Post operative care:

 The cast is removed at 3 weeks, the wounds are inspected, the sutures are removed, and a
short-leg walking cast is applied with the foot in the neutral position and the ankle in slight dorsiflexion.
 Six weeks after surgery the cast is removed, and a program of rehabilitative exercises is
started that is continued under supervision until a full range of active resisted function is obtained.
 The transfer is protected for 6 months by a double-bar foot-drop brace with an outside T-
strap.

453
Q) Short note: Tarsal Tunnel Syndrome. APL (8)-252 / 514

Tarsal Tunnel Syndrome:

-- Pain & sensory disturbance over the planter surface of foot due to compression of posterior tibial
nerve behind and below the medial malleolus.
Causes:
 SOLs eg: ganglion, haemangioma, varicosity etc,
 Displaced # of distal tibia, talus or calcaneum,
 Tenosynovitis of adjacent tendon sheath,
 Neural tumour,
 Perineural fibrosis.
Clinical features:
 Paresthesia & numbness over sole,
 Pain is thrombing in nature, often worse at night.
 Patient seeks relief from pain by walking around or stamping,
 Tinel percussion test – usually positive behind medial malleolus.
Investigation:
 NCV: may show slowing of motor or sensory conduction,
 X – ray of foot with ankle B/V,
 MRI of foot.

454
Treatment:
a) Conservative treatment:
 NSAIDs,
 Physiotherapy,
 Apply medial arch support in shoe to hold foot into slight varus position.

b) Operative treatment:
-- Neurolysis posterior tibial nerve behind medial malleolus & followed into the sole.

455
TENDON INJURY

456
 Tendon Injury

Q) Anatomy of Tendon?
 Tendon consists of Type-1 collagen,
 Loose connective tissue condenses on the surface – called Epitenon,
 Mesotenon -
 Paratenon –
 Tendon is separated from adjacent structures by Teno-Synovial sheath.
 Enthesis -
Q) Nutrition and blood supply of Tendon?
--- From 2 basic sources:
 Synovial fluid: produced within tenosynovial sheath.
 Blood supply:
 Longitudinal vessels in the paratenon,
 Intraosseous vessels at the tendon insertion,
 Muscular vessels at myotendinous junction,
 Vincular circulation through vinculum or mesotenon.

Q) What are the phases of tendon healing?

--- 3 phases:
1. Inflammatory phase {48 – 72 hours},
2. Fibroblastic phase {5 days – 4 weeks}:
a) Intrinsic: from tendon,
b) Extrinsic: from surroundings.
3. Remodeling phase {4 weeks – 14 weeks}

457
Q) What are the types of tendon repair?
Q) Timing of Tendon repair?
a) Primary repair: within first 12 hours – 24 hours of injury,
b) Delayed primary repair: 24 hours – 2 weeks,
c) Secondary repair: after 2 weeks – 4 weeks,
d) Late secondary repair: after 4 weeks.
e) Reconstruction: after 6 weeks.

Q) Prerequisite of repair / reconstruction? camp-3273

i) Skin coverage – should be adequate,

ii) Wound – should be minimally contaminated, well healed.

iii) Oedema / erythema – has to be subsided,

iv) Fracture fixation / healing – must be optimum,

v) Joints – allow useful range of passive motion,

vi) Gliding area – must be relatively free of scar,

vii)Sensation – to be normal or at least one digital nerve should be intact.

The presence of Palmaris longus tendon should be determined before any grafting procedure; its presence can be
exhibited by having the patient appose the tips of the thumb and little finger while flexing the wrist.

458
Q) What are the principles of ideal tendon repair?
Q) What are the characteristics of Tendon repair?
1) Easy and appropriate placement of suture on tendon ends,
2) Secure the suture knots,
3) Smooth juncture of tendon ends,
4) Minimal gapping at repair site,
5) Minimal interference of tendon vascularity,
6) Sufficient strength to permit early motion stress to tendon.
Q) Principles of tendon transfer?
 Which muscle is missing?
a) Assess the problem:
 Which muscle is available?

 Have adequate power at least MRC grade 4.

b) Donar muscle should be:  Must be agonist or synergist.
 Should be expandable.

 Must be stable.
c) Recipient site should be:
 Must have mobile joint / Joint must be shuffled

 Have a straight line of pull.

d) Transferred tendon should be:
 Capable of firm fixation.
Patient considerations - Age—minimum 5 years*

459
Minimum age when a child can be trained for using the transferred muscle.

Q) Testing the flexor tendons APL-797

Testing for-
(a) Flexor digitorum profundus (FDP) lesser fingers,

(b) Flexor digitorum superficialis (FDS) lesser fingers,

(c) FDP index,

(d) FDS index.

460
Q) Techniques of tendon repair? apl-796, camp-3251

Core suture:

Circumferential suture:

a) End to End suture:

Bunnell stitch:

Criss-cross stitch:

Kessler:

461
Modified Kessler:

Tajima modification of Kessler:

Interlocking:

Bevel technique:

Four Strands Cruciate repair

462
b) End to Side repair / Pulvertaft / Fish mouth technique:
FISH-MOUTH END-TO-END SUTURE (PULVERTAFT)

Pulvertaft technique of suturing tendon of small diameter to one of larger diameter.

Steps in technique of end-to-side anastomosis. End of tendon has been buried

463
c) Roll stitch:
Roll stitch using 4-0 wire or 4-0
monofilament nylon is especially
useful in suturing lacerated
extensor tendon over or near
head of metacarpal.

d) Tendon to Bone:

Pull out suture:

Tied over button

Koch (1944) & Bunnell (1940) Eyre− Brook Wilson et al (1985)

Pulvertaft (1965)

464
Q) Suture materials for Tendon repair?
 Stainless steel wire – highest tensile strength,
 Nylon – maintain strength longer than Prolene,
 Prolene – strength longer,
 PDS – strong as Prolene,
 Catgut, Dexon & Vicryl – absorbable and weak.

Q) Size of suture materials?

Sites Core suture Circumferential suture
Smaller digit  4.0 Prolene 6.0 Prolene
Larger digit, 3.0 Prolene 6.0 Prolene

Palm, 
Forearm
Medium sized  2.0 Prolene 4.0 Prolene
Tendo-achilles  No 1 Prolene 3.0 or 4.0 Prolene.

465
Q) From where the tendon grafts are taken? camp-3277
 Palmaris longus –
 Most common, in about 15% population it is absent.
 Max length – about 15 cm long,

PT

 Plantaris –
 in about 9 - 10% of population - it is absent,

 Long toe extensor tendons.

 Extensor indicis, EDC for index.

 Flexor digitorum sublimus.

466
Q) What are the causes of failure of tendon repair?
 Formation of adhesion {3 – 5 mm of tendon glide is sufficient to prevent adhesion},
 Rupture of repaired tendon: due to-
 ↓ed strength of suture materials,
 < 3 mm gap is required to avoid bridging fibrous tissue.

Q) Complications of tendon repair? Camp-3278

 Re-rupture,
 Adhesion,
 Stiffness of Joint,
 Bowstring,
 Infection,
 Lumbrical plus hand,
 Quardiga effect.

 Lumbrical plus hand:

 The pull of the profundus muscle, applied through the lumbrical muscle, creates extension of the
proximal and distal interphalangeal joints.
 This usually occurs if the tension on a tendon graft is not appropriately set and the graft is relatively too
“long”.
 The condition also may be seen when amputations have occurred through the middle phalanx after
avulsion of the insertion of the flexor digitorum profundus or division of the flexor profundus tendon.

A, Severance of flexor digitorum profundus

(FDP) (produces paradoxical extension).

B, Avulsion of FDP.

C, Overly long flexor tendon graft.

D, Amputation through middle phalanx.

467
  The treatment of this condition consists of transection of the involved lumbrical tendon through a
longitudinal incision in the web space to the radial side of the involved finger, usually after use of a local anesthetic.

 Quardiga effect:
 If the tension on the tendon graft is set too tightly, when the patient attempts to flex the fingers, the
grafted finger flexes and reaches the palm before the remaining fingers.
 Usually occurring in the long, ring, and little fingers.

Q) What are the indications of Tenolysis?

 Passive range must be more than active range,
 Surgical scars must be supple and there should not be indurated around,
 Minimum of 3 months of physiotherapy must be given and must have reached a plateau in
improvement.

Q) Post operative protocol of tendon repair?

i) Good dressing,
ii) Drain removal and start passive movement 3 – 5mm at 2nd POD,
iii) Passive flexion within the cast – for 2nd POD to 2 weeks,
iv) Passive flexion and Active hold – for 2 weeks to 4 weeks,
v) From 4 weeks: Gentle-
 Active flexion with Passive assist,
 Active extension with Passive assist.
vi) Plaster will be remove 6 wks later and
vii) Dynamic Splint kept for a minimum period of 8 weeks. {Kleinert protocol / Duran protocol}

Q) Position of immobilization for Flexor Tendon Injury after repair?

 Wrist: 300 flexion,
 MCP joint: 700 flexion,
 PIP & DIP joints: slight flexion.

Q) Position of immobilization for Extensor Tendon Injury after repair?

 Wrist: in full extension,
 Fingers: should remain parallel,
 PIP & DIP: neutral.

468
FIXATION OF TENDON TO BONE. CAMP-9

Fixation of tendon to bone.

469
470
 Extensor Tendon Injury.
camp-3290
1) Zone –I: DIP
 Disruption of insertion of Extensor tendon,
 DIP joint of fingers &

T I – Distal phalanx & IP joint of thumb {EPL}.

 Mallet finger deformity.
2) Zone – II: Middle phalanx.
 Disruption of extensor tendon over-
Middle phalanges &

T II  Proximal phalanx of thumb {EPL}.

3) Zone – III: PIP
 Disruption of extensor tendon over –
PIP joint of fingers {central slip}

T III MCP joint of thumb {EPL & EPB}.

 Boutonniere deformity / (BUTTONHOLE DEFORMITY)
4) Zone – IV:
camp-3290
 Disruption of extensor tendon over –
T - Thumb
Proximal phalanx of fingers &

T IV  1st Metacarpal over thumb.

5) Zone – V:
 Disruption of extensor tendon over –
MCP joint of fingers &

T V  CMC joint of thumb.

6) Zone – VI:
 Disruption of ext tendons over metacarpal bones level.
7) Zone – VII:
 Disruption of ext tendons over wrist.
8) Zone – VIII:
 Disruption of ext tendons proximal to wrist.

471
Function of lumbricals:
 Flexion of MCP and Extension of IP Joints {PIP & DIP} of digit.

Q) Swan neck and Boutoniere deformity? apl- 419

Swan Neck deformity Boutonniere deformity

 DIP flexion & PIP hyperextension.  DIP hyperextension & PIP flexion.

472
 Causes / Injuries include- Causes / Injuries include-
 RA {MCP joint volar subluxation},  Zone III extensor tendon injury,
 FDS laceration,  Rheumatoid arthritis:
 Mallet finger, (Rupture of central slip)
 Intrinsic contracture.
(Extension force > Flexion force)
Treatment: Treatment:
 FDS tenodesis for FDS rupture,  Central slip repair,
 Central slip tenotomy.  PIP arthrodesis.

Q) Treatment of extensor tendon rupture?

 Early repair gives better result,
 Meticulous surgical technique is essential,
 Four strand core suture with epitendinous circum suture is now accepted method,

On examination:

473
Q) Position for immobilization for extensor tendon injury?
 Dorsal splint,
 Fingers should remain parallel to forearm with wrist in full extension,
 PIP & DIP – neutral.

Q) Post operative rehabilitation for extensor tendon injury?

 3 wks immobilization,
 Early motion / 3 motion protocols-
 Exercise begins at 4th – 5th POD,
 Prior to active flexion, passively full flexion for 10 times or more is advised,
 Active flexion 20 – 30 times, 4 – 5 times in a day, from full extension to ½ to 2/3rd range of flexion is
encouraged.
 After 6 weeks splint is discarded and normal motion resume.

Stack splint for Zone – 1 rupture 6 – 8 weeks and at night only for additional 1 week.

474
TRAUMATIC DISLOCATION OF THE EXTENSOR TENDON AT THE METACARPOPHALANGEAL
JOINT camp-3297

Sagittal band injury / Boxer’s knuckle:

----- It leads to dislocation of extensor tendon at MCP.

Mechanism of injury:
 Traumatic:
 Forceful resisted flexion or extension.
 Laceration of extensor hood,
 Direct blow to MCP joint,
 Inflammatory:
 Rheumatoid arthritis.

Site of injury:
 Middle finger is most commonly involved-
 Index 14%,
 Middle finger 48%,
 Ring 7%,
 Little 31%.
 Radial sagittal band injury is more common {radial:ulnar= 9:1}

Sagital band:
 Radial and Ulnar sagital band arise from volar plate attached to extensor tendon,
 Function:
 Primary stabilizer of extensor tendon at MCP joint,
 Resists ulnar deviation of tendon, especially during MCP flexion.
 Prevent tendon bowstring during MCP joint hyperextension.

Characteristics:
 Traumatic dislocation of the extensor tendon toward the ulnar aspect of the metacarpophalangeal
joint occurs most commonly in the long finger.
 The dislocation usually occurs as a result of a tear in the proximal radial portion of the shroud
ligament (sagittal bands) and the more proximal fascia as the finger is suddenly extended against a force, as in a
flicking or thumping motion.

475
  Ulnar side disruption with radial displacement of the tendon is rare. More violent mechanisms may
cause collateral ligament and joint surface injury.

Types Sagittal band injury:

Type I,
Mild injury with no instability;

Type II,
Moderate injury with extensor tendon
subluxation;

Type III,
Severe injury with tendon dislocation.

Treatment:
 If seen within the first few days, this dislocation can be treated effectively with splinting of the
metacarpophalangeal joint and wrist in extension for 3 to 4 weeks, followed by 3 to 4 weeks of removable splinting
or buddy taping to the adjacent finger on the radial side in the case of ulnar displacement.

 Within 1 week of acute injury:

 Extension splint for 4 to 6 weeks.

 More than 1 week of chronic injury:

 Primary repair can be tried.

 Chronic injury:
 Extensor centralization procedures;
 Trap door flap:
 Ulnar based partial thickness capsular flap created,

476
  Flap resutured to capsule.
 Kilgore tendon slip:
 Carroll tendon slip:
 McCoy tendon slip:

A, Cross section of metacarpal head in which ulnar B, Ulnar-based loop formed from extensor
subluxation of extensor tendon is shown. tendon passed in distal-to-proximal direction
around radial collateral ligament and sutured to
extensor tendon.

 Postoperative care:
 Sutures are removed after 10 to 14 days, and the splint is maintained with the
metacarpophalangeal joint extended for 3 to 4 weeks.
 Protected motion and splinting is maintained for about 8 weeks, and a gradual
increase in activities is allowed thereafter.

477
 Flexor Tendon Injury
apl-796. camp-3261

Q) Normal position of fingers of hand?

--- Flexion of –
 Index – 400,
 Middle – 500,
 Ring – 600,
 Little – 700.

Q) ROM of finger?
 ROM of MCP: 00 – 900,
 ROM of PIP: 00 – 1000,
 ROM of DIP: 00 – 800.

478
The zones of injury:
I – Distal to the insertion of flexor digitorum superficialis {Distal to FDS insertion}
II – Between the opening of the flexor sheath (the distal palmar crease) and the insertion of flexor
superficialis {Distal palmar crease to FDS insertion},
IIII – Between the end of the carpal tunnel and the beginning of the flexor sheath.
{End of Carpal tunnel to Distal palmar crease}
IV – Within the carpal tunnel
V – Proximal to the carpal tunnel.

479
 5 Annular pully: A1, A2, A3, A4, A5
 A2 & A4 are critical / important to prevent bowstring effect,
 A1, A3 & A5 – overlie MCP, PIP & DIP.
 A1 – most commonly involved in Trigger finger.

 3 Cruciate pully: C1, C2, C3

 Function: to prevent collapse of sheath.

A1 A2 C1 A3 C2 A4 C3

Camp- 3261

480
 Camper’s Chiasma:

--- FDS divides and passes around FDP tendon, two portions of FDS reunite at ‘Camper’s Chiasma.’

 Excursions of FDP & FDS:

 Up to 9 cm of flexor tendon excursion may be required to produce composite wrist and digital flexion,
 Only 2.5 cm of excursion is required for full digital flexion with the wrist stabilized in neutral position.

481
Q) How to manage Flexor tendon injury at Zone-II? rahim-84, apl-799, ferquherson-39
 History:
 Age of patient:
 Occupation:
 Dominant hand:
 Mechanism of injury:
 Sharp cut injury: glass cut, sharp weapon.
 Machinery injury:
 Penetrating injury:
 H/O injury / Age of injury. (Zone II - more dramatically,‘no man’s land’
because injuries in this zone are the most
 Treatment taken after injury:
dangerous).
 Examination:
 Look:
 Attitude of hand / finger:
 Nature of wound: site, size, healthy or unhealthy.
 Skin condition:
 Apparent muscle wasting:
 Feel:
 Temp:
 Tenderness:
 Vascular status / circulation: hand / digit,
 Sensory status: hand / finger or digit,
 Tinnel sign:

482
  Move:
 Movement of joints:
 Power of muscle:

 Investigation:
--- X ray of affected part.

483
 Treatment:
Q) Treatment of FDS / FDP at Zone-II?
 Isolated injury of FDP at Zone-II:
 Fresh case: repair of tendon,
 Late case: arthrodesis of DIP joint at 300 flexion.
 Isolated injury of FDS at Zone-II:
 No need to repair,
 Division of the superficialis tendon noticeably weakens the hand and a swan neck deformity can
develop in those with lax ligaments. At least one slip should therefore always be repaired.
apl-799
 Late effect: Swan Neck deformity.

 Both FDP & FDS injury at Zone-II:

 Recent injury:
 Without Pulley involvement:
 Both tendons should be repair.
 With Pulley involvement: A2, A4
 Pulley reconstruction and tendon repair.
 Old / Neglected injury:
 Without pulley involvement:
 Tendon reconstruction.
 With pulley involvement:
 Two stage reconstruction.

Two stage reconstruction:

 1st stage repair: pulley reconstruction with silastic tube insertion through the pulley.

 2nd stage repair: after 6 – 8 weeks, tendon reconstruction.

 Primary repair: apl-799

 Primary repair with fastidious postoperative supervision gives the best outcome
by high level of expertise and specialized physiotherapist,

 Secondary repair:
 Tendon graft of palmaris longus or plantaris can be used.

484
 Post operative management: rahim-70
 Posterior cast for 3 weeks:
 Wrist: 200 - 300 flexion,
 MCP joint: 500 - 700 flexion,
 PIP & DIP joints: slight flexion.

 Movement:
viii) Drain removal and start passive movement 3 – 5mm at 2nd POD,
ix) Passive flexion and extension within the dressing – for 2nd POD to 2 weeks,
x) Passive flexion and Active hold – from 2 weeks,
xi) From 4 weeks: Gentle-
 Active flexion with Passive assist,
 Active extension with Passive assist.
xii) Plaster usually removes 6 wks later or
xiii) Dynamic Splint kept for a minimum period of 8 weeks. {Kleinert protocol / Duran protocol}

 Normal use of hand at 10 – 12 wks after repair.

485
Q) Reconstruction of Pulley A2 & A4? CAMP-3280, orthobullet

■ Make a zigzag (see Fig. 64-16B and C), midlateral (see Fig. 64-17), or volar oblique (see Fig. 64-16D) incision.

■ If a two-stage tendon reconstruction is planned, insert a Silastic rod (Hunter) of appropriate size and attach it
distally either to the remaining profundus tendon stump or to the bone by a small screw (Fig. 66-55), as described
for the two-stage Hunter rod technique.

Reconstruction of flexor tendon pulleys. 66-56 ■ In another technique, advocated by Lister, extensor retinaculum from the wrist
can be harvested and used as an encircling pulley reconstruction as well (Fig. 66-
57).

 Fibro-osseous rim of the flexor

sheath.

 Extensor retinaculum from the

wrist.

■ Several techniques are available for pulley reconstruction. If a tendon graft is to be used for a pulley substitute,
use a thin strip measuring at least 6 cm in length and 0.25 cm in width. If the original fibro-osseous rim of the flexor
sheath is satisfactory, weave the tendon through this rim and secure it with mattress sutures. Weave the strip over
the silicone rod beginning at about the A2 pulley level (Fig. 66-56).
■ The A2 and A4 pulleys can be reconstructed individually in this method. If the fibroosseous rim is insufficient,
pass the tendon graft around the phalanx and suture it to itself with several mattress sutures.

 Principles / Goals of Pulley reconstruction:

 Preserve / reconstruct at least 3 or 2 pulleys,
 A2 and A4 is important.

 Graft materials:
 Extensor retinaculum,
 Excised tendon materials:
 Palmaris longus,
 Plantaris,
 FDS,
 Flexor tendon allograft.
 Techniques:

486
  Encircling technique / Around the bone:
 Single loop {Bunell},
 Triple loop {Okutsu}.
 Non encircling technique:
 Belt loop {Karev},
 Extensor retinaculum {Lister}.

 Complications of Pulley reconstruction:

 Chance of phalanx fracture,
 Stiffness,

Flexor tendon avulsion

487
Camp-3272

488
 Flexor Zones in Thumb.

camp-3273

Zone I: area at the interphalangeal joint and the insertion of the flexor pollicis longus.
 IP joint to insertion of FPL.

Zone II: includes the fibroosseous sheath extending just proximal to the metacarpal head and the
metacarpophalangeal joint.
 Proximal phalanx to MCP joint + MC head.

Zone III: includes the area of the metacarpal beneath the thenar muscles.

Zone IV: corresponds to the carpal tunnel,

Zone V: corresponds to the distal forearm just proximal to the wrist.

Further advancement becomes necessary and lengthening of the tendon by Z-plasty just proximal to the wrist
should be done. This tendon is unique in that it can be advanced without disturbing its blood supply because it does
not have a vinculum. Tendon advancement rather than tendon grafting has been recommended because
paratendinous adhesions are not as likely to form after advancement.

489
 Hand incisions ‘Permissable’ incisions in hand surgery. Incisions must not cross a skin crease or an interdigital
web or else scarring may cause contracture and deformity.

The position of safe immobilization The knuckle joints are 90º flexed, the finger joints extended and the thumb
abducted. This is the position in which the ligaments are at their longest and splintage is least likely to result in
stiffness. Apl-431

490
Tendoachilis Rupture.
CAMP-2321, APL (N10)-638

Common sites of tendon rupture:

• Supraspinatus tendon
• Bicep's tendon—long head
 Achilles tendon
• Extensor pollicis longus tendon
• Quadriceps tendon
• Patellar tendon

491
Characteristics of T A rupture:
 The Achilles is the tendonous extension of Gastrocnemius and Soleus.
 It is the thickest and strongest tendon in the body.
 It is about 15 centimetres (6 in) long,
 It is inserted into the middle part of the posterior surface of the calcaneus,
 The tendon can receive a load stress 3.9 times body weight during walking and 7.7 times body weight when
running.
 3rd most common tendon injury.
 Common in middle aged athletes.
 Causes of rupture:
 Iatrogenic: – intra tendinous steroid injection,
 Spontaneous:- avascular degeneration,
o Tendinitis
o Tendinosis – tendon degeneration without associated inflammation.
o Peritendinitis / Tenosinovitis.
 Traumatic: - due to fall on sharp object.

Q) Sites of rupture?

Mid substance / Water shed line

 Myotendinous Jxn
(4 – 14%)

 Midsubstance / Water shed line.

2-6 cm proximal to insertion (72 – 73%)

 Avulsion from insertion (14 – 24%)

--> Pathological tear / rupture usually takes place about 3 – 5 cm above the
insertion of tendoachilis.

492
Q) Mechanisms of TA rupture?
o Pushing off with the weight bearing forefoot while extending the knee,
o Sudden unexpected dorsiflexion of the ankle,
o Violent dorsiflexion of the planter flexed foot as in a fall from a height,
o Direct blow to the contracted tendon or from a laceration.

Q) Clinical features of ruptured tendoachilis?

 Patient is usually middle aged,
 H/O intra lesional steroid injection,
 H/O sudden agonizing pain at the back of heel while running or jumping,
 Patient is able to walk but with a limp.
 Running, Jumping and Activities such as ascending or descending stairs are severely compromised.
 Plantarflexion of the foot is usually inhibited and weak (although it may be possible, as the long flexors of the toes are
also ankle flexors eg. FHL, FDL).

Q) Blood supply to TA?

Post Tibial artery,

Peroneal artery,
Osseous b/s through calcaneum

493
Q) On examination?

a. Look:
 Bruising over lower part of affected leg,
 Visible gap seen about -------- cm above heel,
 Gap is more prominent with dorsiflexion of foot,
 Patient is unable to Stand on tip toe on the affected leg (pt is asked to raise the heel from the ground while
standing upon the affected leg only).
 Gait: limping gait.
 Toe walking – not possible,
 Heel walking – possible,
b. Feel:
 Temp over the affected area: normal,
 Tenderness: present,
 A palpable gap is felt about ----- cm above it’s insertion,
 Palpate the distal stump,
 Thompson squeeze test / Simmond’s test: positive,

 Matles test:
 Pt is placed prone with the lower legs extending off the bed is asked to actively flex the knees to 900.

494
 Foot falls into neutral or
slight dorsiflexion in
position.

 Active flexion of the knee should cause the gastrocnemius to shorten thus causing planter flexion of
the foot,
 If the foot falls into neutral or slight dorsiflexion - the achilles tendon is likely ruptured.
 O’Brien needle test:

c. Move:
 Planter flexion of the affected foot is weak in comparison with opposite foot,
 Dorsiflexion of the affected foot,
 Power of Peroneus brevis:
 Power of FHL:
 Inversion & Eversion of foot: normal

Q) Investigation?
 X ray ankle B/V ----------> to exclude avulsion #,
 USG of the affected part to detect the gap,
 MRI of lower part of leg with ankle ------> for exclude complete tear or tendinosis.

Q) Ultra sound based criteria for choosing non-operative treatment?

 Gap of less than 5 mm with maximal planter flexion,
 Gap of less than 10 mm with the foot in neutral position,
 More than 75% tendon apposition with the foot in 200 planter flexion.

Q) Types of T.A rupture?

1) Acute rupture: diagnosed & treated less than 48 hrs after injury,

495
 2) Chronic rupture: ranged from those, diagnosed & treated more than 48 hrs after injury; to
those diagnosed and treated up to 2 months after injury.

Q) Treatment? camp-2323
 Non operative: functional bracing and aggressive rehabilitation protocol,
 Operative:
 For acute rupture:
 Open repair,
 Minimally invasive percutaneous repair.
 For chronic rupture:
 Reconstruction:
 Primary repair (uncommon),
 Augmentation:
o Free fascia tendon graft,
o Fascia advancement / Local tendon transfer,
o Synthetic or allograft augmentation.
 If the tendon defect is < 3 cm after debridement and the injury is < 3 months of old – direct
repair often possible,
 If the tendon gap is > 3 cm, additional techniques must be used such as local tissue transfer,
tissue augmentation, synthetics and allografts.

Q) What are techniques for repairing acute achilles tendon rupture?

 Open repair / Primary repair - with or without augmentation (tendon transfer, local fascial turndown,
allograft),
 Percutaneous or minimally invasive repair,
 Suture techniques:
 Single and double Bunnell,
 Kessler and
 Krackow (locking loop).

Q) Why open repair is called ‘Gold standard’ of operative treatment?

 Historically low rate of rerupture,
 High rate of return to Activity / Sports,
 ↓ ed complication rate with newer techniques,

496
Q) Name some open repair techniques with augmentation?
 Lindholm technique: CAMP-2325

 Lynn technique:
 Method is useful for injuries less than about 10 days old,
 Later the plantaris tendon becomes incorporated in the scar tissue and can not be identified
easily.

497
  Plantaris tendon is fanned out to make a membrane 2.5 cm or more wide for reinforcing the
repair.

 Teuffer technique:

498
  Turco and Spinella modification:
PB is passed through mid coronal slit in distal stump of Achilles tendon and suture to
stump & to the tendon.

 Minimum invasive percutaneous technique: Ma & Griffith.

Q) What are the advantages of minimum invasive technique?

 Smaller incisions to speed recovery,
 Minimize complications, especially infection and nerve injury.

Q) What are the disadvantages of minimum invasive technique?

o Risk of sural nerve injury,
o Failure to appose tendon ends or malalignment of tendon ends,
o Lower strength of repair,

499
Q) Techniques for reconstruction of chronic / NEGLECTED achilles tendon rupture?
 Augmentation:
 Free fascia tendon graft:
 Fasia lata,
 Donor tendons (Semitendinosus, peroneal, Gracilis, patellar tendon),

 Fascia advancement:
 V – Y plasty / Abraham & Pankovich:
 It is useful when 1 to 3 cm of tendon must be resected.

 V – Y plasty / Abraham & Pankovich:

 Gastrocnemius soleus fascia turn down graft / Bosworth tech:

500
  Wapner technique:

 Synthetic or Allograft augmentation:

 Polyglycol threads,
 Marlex mesh,
 Dacron vascular graft,

Synthetic materials such as Carbon

fiber or Marlex mash have been used as
a bridge between torn tendon ends.

 Carbon fiber,
 Allograft tendon.

501
o Modified Teuffer:

o Maffulli et al.:

502
 After Treatment.
After operation • Apply short leg cast in grav ity equinus.

• cast is remov ed.

• wound is inspected.
At 2 week • sutures are remov ed.
• apply another short leg cast in grav ity equinus f or additional 2 wks.
• partial wt bearing crutch walk during 2nd week period.

At 4 week •cast is changed.

• f oot is gradually brought to plantigrade position ov er next 2 wks.

• short leg walking cast is applied.

At 6 to 8 weeks • f oot is in plantigrade position.
• f ull wt bearing is allowed.

• rev erse 900 ankle stop brace or similar dev ice is fitted
At 12 weeks • and is worn until a nearly full range of motion & strength 80% that of opposite extremity
hav e been obtained – usually within 6 months.

503
 Mallet Finger.
Baseball Finger.
apl-418,791

--- It is the fixed flexion deformity of DIP joint of finger.

--- After a sudden flexion injury (e.g. stubbing the tip of the finger) the terminal phalanx droops and cannot be
straightened actively.

Mechanism:
Three types of injury are recognized:
 Avulsion of the most distal part of the extensor tendon;
 Avulsion of a small flake of bone from the base of the terminal phalanx;
 Avulsion of a large dorsal bone fragment, sometimes with subluxation of the terminal
interphalangeal (TIP) joint.

Clinical features:
 H/O injury over tip of finger,
 Localized pain and swelling,
 Inability to extend the distal finger.

Q) Questions to be asked?

Q) On examination:
Look:
 Expose both hands and compare,
 Hand deformity – DIP joint of the affected finger is flexed.
 Localized swelling – if presents early,

504
Feel:
 Localised tenderness – if presents early.
Move:
 Ask the patient to extend the distal phalanx – but patient can not do it,
 Passive extension – possible, but when finger is released terminal phalanx falls back into 300 flexion.

Q) Differential diagnosis?

With the extensor mechanism unbalanced, the PIP joint may become hyperextended (‘swan-neck’).

Q) Investigation?

--- X ray of local part.

Q) Treatment of Mallet finger? apl- 418, 719

 If no fragment is avulsed or if avulsed fragment is not significantly displaced – hold terminal

phalanx in a splint in full extension for 6 weeks.

TIP joint should be immobilized in slight

hyperextension, using a special mallet-finger
splint which fixes the distal joint but leaves
the proximal joints free.

 A mallet finger without bone injury is treated with a plastic splint with the DIP joint in extension for
8 weeks, followed by 4 weeks of night splintage.
 If avulsed fragment is displaced – it can be fixed with thin K wire,

505
  Operative treatment is considered only if there is a large fragment (>50%) and subluxation of the
DIP joint.
 If there is subluxation then K-wires or small screws are used to fix the fragment in place.
 If injury is > 3 weeks old – operative fixation is rarely helpful. Because the deformity can be ignored
as it is minimal and functional loss is also minimal.
 Surgery is ill advised, as the complication rate is high and it is unlikely to improve the outcome.

COMPLICATIONS OF MALLET FINGER. apl-792

 Non-union This is usually painless and treatment is not needed.

 Persistent droop About 85 per cent of mallet fingers recover full extension. If there is a

persistent droop this can be treated by tendon repair supported by K-wire fixation of the joint, but the

results are often disappointing. The alternative would be joint arthrodesis, best achieved with a buried

intramedullary double-pitch screw.

 Swan neck deformity Imbalance of the extensor mechanism can cause this in lax-jointed

individuals. A central slip tenotomy is straightforward and can give a very good result.

506
ORTHOPAEDIC OPERATIONS.

507
 Orthopaedic Operations
APL-303

RADIATION EXPOSURE
 Intraoperative radiography involves the risk of exposure to radiation; both the patient and surgeon are affected.
 The dose limit for the general public is 1 mSv per year, which is the equivalent of 1000 chest x-rays.
 Using a hip procedure as an example, lead aprons will reduce the effective dose received by a factor of 16 for
anteroposterior projections and by a factor of 4–10 for lateral projections. Using a thyroid shield decreases the dose
by another 2.5 times.

THE ‘BLOODLESS FIELD’

TOURNIQUET
It is a surgical epuipment which is applied over limb to make operative field blood loss.
Purposes:
 To improve the visibility in surgery,
 To reduce blood loss.
Types:
 Pneumatic
 Non pneumatic.
Principles of Tourniquet:
 Exsanguinate the limb prior inflating tourniquet,
 Tourniquet cuff should be as wide as the diameter of limb,
 Apply as proximally as possible,
 Apply padding to the site, without creases.
 When tourniquet is inflated, time must be noted.
 When tourniquet is removed – the site should be inspected for any damage and the return of circulation. These
informations should be recorded in notes.

TOURNIQUET CUFF
 Only a pneumatic cuff should be used and it should be at least as wide as the diameter of the limb.
 A layer of wool bandage beneath the pneumatic tourniquet will distribute the pressure and prevent wrinkling of
the underlying skin.
 During skin preparation, it is essential that the sterilizing fluid does not leak beneath the cuff as this can cause a
chemical burn.

508
EXSANGUINATION
 Elevation of the lower limb at 600 for 30 seconds will reduce the blood volume by 45 per cent; increasing the
elevation time does not alter the percentage significantly.
 These methods reduce blood volume by an additional 20 per cent.

TOURNIQUET PRESSURE
A tourniquet pressure of –
 150 mmHg above systolic is recommended for the lower limb and
 80–100 mmHg above systolic for the upper limb.

Tourniquet time
 An absolute maximum tourniquet time of 3 hours is allowed, although it is safer (and more advisable) to keep
this under 2 hours;
 Transient nerve-related symptoms may occur with 3-hour tourniquet times but full recovery is usual by the fifth
day.

Finger tourniquet
 This is suitable for relatively minor hand operations.
 A sterile rubber glove-finger makes a good cuff; the tip is cut and the margin is then rolled back proximally.

MEASURES TO REDUCE RISK OF INFECTION

a) SKIN PREPARATION AND DRAPING
Hair removal
If hair removal is deemed necessary, they can be used the day before surgery without an increase in wound
problems.

Skin cleaning
 The limb may benefit from washing with soap to remove particulate matter and grease. This is particularly useful
in managing open fractures and in cases where the limb has been wrapped in a cast or splint for some time.
 Skin preparation prior to surgery should be carried out with an alcohol-based preparation where safe; alcohol is
not to be applied over open wounds, exposed joints or nerve tissue.

509
Drapes
 These function to isolate the surgical field from the rest of the patient and reduce contamination from outside.
 Plastic adhesive coverings, some impregnated with iodine, function primarily to secure the drapes, especially if
the limb is moved during surgery. This method of skin isolation was thought to reduce wound contact with some of
the resident bacteria around the skin incision; however there is no evidence that they reduce surgical site infections
and they may even increase them! (Webster and Alghamdi 2007).

b) SURGICAL ATTIRE
Gowns
Function to isolate the surgical field from the rest.

Gloves
Double gloving, with a coloured inner glove (so-called indicator glove) reduces the number of inner glove
perforations and allows outer glove perforations to be picked up more quickly, but a difference in surgical site
infections has yet to be established (Tanner and Parkinson, 2006).

Face mask
This ‘hallmark of the surgeon’ in theatre has been questioned in its ability to reduce surgical site infections.

c) VACCINATION
 There is a risk of transmission of blood-borne infections to orthopaedic surgeons, not least because of the nature
of surgery but also due to frequent handling of instruments and bone fragments with sharp edges.
 Vaccination reduces the likelihood of accidental needle-stick injury but will need augmenting by prophylaxis
through vaccination.

Hepatitis B
 Transmission may occur through inoculation or even from contact with a contaminated surface

(the virus is able to survive for a week in dried blood).

 There is a 30 per cent risk of transmission from a single inoculation of an unvaccinated person

(Alter et al., 1976).

 Vaccination is safe, effective and immunity, for those who respond after a course of injections,

indefinite.

 Those who do not respond to immunization will need post-exposure prophylaxis using a

combination of hepatitis B immunoglobulin and the vaccine.

510
Hepatitis C
 The risk of accidental transmission is lower than for hepatitis-B (less than 7 per cent).

 Unfortunately neither effective vaccines nor post-exposure protection is available.

Human immunodeficiency virus

 The risk of human immunodeficiency virus (HIV) infection after accidental injury is very low (less

than 0.5 per cent) (Ippolito et al., 1999), although this may vary between individuals.

 Vaccination is not available but post-exposure treatment with antivirals is essential.

511
 THROMBOPROPHYLAXIS
APL-307

Acute thrombophlebitis. Chronic venous insufficiency

Venous Thrombo-Embolism (VTE):

Venous thromboembolism (VTE) is the commonest complication of lower limb surgery. It comprises three
associated disorders-
 Deep vein thrombosis (DVT),
 Pulmonary embolism (PE) and
 Later complication of Chronic venous insufficiency.
Deep venous thrombosis
 DVT occurs most frequently in the veins of the calf and less often in the proximal veins of the thigh and pelvis.
 Fragments sometimes get carried to the lungs, where they may give rise to symptomatic pulmonary embolism
(PE) and in a small percentage of cases, fatal pulmonary embolism (FPE).
Risk factors of DVT:
 Old age,
 Obesity,
 Smoking,
 Varicose vein,
 Malignant disease,
 Prolong operation,
 Pelvic / Hip surgery,
 Past H/O DVT / Pulmonary embolism.

512
Pathophysiology of DVT / Virchow’s triad:
Triad of changes in venous system –
 Endothelial injury,
 Venous stasis,
 Hypercoagulability.

Prophylaxis of DVT:
 General preventive measures:
 Assessment of risk factors,
 Stop smoking 4 weeks preoperatively,
 Stop OCP 6 weeks preoperatively,
 Adequate hydration in perioperative period,
 Avoid calf pressure in perioperative period,
 Early post operative mobilization.

 Specific Physical methods :

 Graduated elastic compression stocking,
 Intermittent pneumatic calf compression device,
 Electric calf muscle stimulation.
 Inferior vena cava filters resemble an umbrella and are percutaneously

passed through the femoral vein and lodged in the inferior vena cava. They merely catch an

embolus to prevent it from reaching the lungs.

 Therapeutic measures:
 Unfractionated Heparin:
 S/C 5000 unit unfractionated Heparin pre operatively 2 hours before surgery and then 12
hourly daily post operatively, until patient become mobile.
 Low molecular weight Heparin:
 For moderate thromboembolism risk {abdominal surgery} recommended dose 20mg to
40mg (1mg/kg) S/C 2 hours before surgery, once daily until patient is ambulatory.
 For high risk thromboembolism {orthopaedic surgery} recommended dose usually 40mg S/C
12 hours before surgery, then once daily until patient is ambulatory.

513
Treatment of established DVT:
 Loading dose of 5000 units {1 ml = 5000 units} of heparin I/V stat, followed by daily weight
adjusted dose of LMWH {1mg/kg body wt},
 Warferin is started with loading dose of 10mg tab daily for 3 days, thereafter dose is adjusted
until the INR is stable at 2.0 -3.0 and then heparin is discontinued.

Incidence of DVT:
 Approximately one in 30–40 patients operated on for hip fractures or hip and knee replacements will develop a
symptomatic thromboembolic complication despite the use of prophylaxis during their hospital stay.
 Traditional recommendations suggesting that it should be continued until the patient is fully mobile have been
superseded by evidence that the cumulative risk for VTE lasts for up to 1 month after knee replacement surgery and
3 months with hip surgery (Bjornara et al., 2006).

514
 FAT EMBOLISM SYNDROME (FES)

Fat embolism;
----- it is process by which fat emboli passes into blood stream and lodge within blood vessels.

Fat embolism syndrome:

----- Manifestation of fat embolism occasionally cause multi system dysfunction, mainly lungs and next to brain is
involved.

Incidence:
 Single bone #: 1 – 3%,
 Bilateral or double bone #; 5 – 10%,
 Onset usually 24 – 72 hours after initial insult.
 Mortality rate 10 – 20%.

Triad of FES:
1. Hypoxemia,
2. Neurological abnormalities,
3. Petechial rash.

Causes of FES:
A) Trauma related:
 Long bone #,
 Burn injury.
 Bone marrow harvesting / transplant
B) Non trauma related:
 DM,
 Pancreatitis,
 Osteomyelitis
 Panniculitis,
 Steroid therapy
 Fat infusion

515
Clinical features of FES;
Gurdi criteria-
Major criteria Minor criteria
Respiratory insufficiency: Tachycardia
Hypoxia
Dyspnoea
Pleural friction rub
ARDS
CNS menifestation: Pyrexia
Seizure / focal deficit
Mild delirium to coma
Petechial rash Retinal change
Renal dysfunction / Jaundice

Investigations
CBC:
Hb: decrease
ESR: increase
Platelet count: decrease.
CXR: bilat snowstorm appearance.
Urine for RME

Treatment;
 Counselling
 Prompt stabilization of # bone,
 ET tube intubation and PPV.
 ICU care,
 Supportive treatment,
 Recovery is unpredictable and mortality rate is high.

516
TENODESIS.

517
 Arthrodesis.
APL-323

ARTHRODESIS

--- It refers to surgical fusion of joint,

--- Most reliable operation for a painful or unstable joint.

Principles of Arthrodesis:
The principles of arthrodesis are straightforward and involve four stages:

(1) Exposure – both joint surfaces need to be well visualized, but some smaller joints are now

accessible by arthroscopic means;

(2) Preparation – both articular surfaces are denuded of cartilage and sometimes the subchondral bone

is ‘feathered’ to increase the contact area;

(3) Coaptation – the prepared surfaces are apposed in the optimum position, ensuring good contact;

(4) Fixation – the surfaces are held rigidly by internal or external fixation. Sometimes bone grafts are

added in the larger joints to promote osseous bridging.

Indications of Arthrodesis:
 Painful joint,
 Instability of joint,
 Failure of joint replacement.

Complications of Arthrodesis:
Main complication is non-union with the formation of a pseudoarthrosis.

Rigid fixation lessens this risk; where feasible (e.g. the knee and ankle), the bony parts are squeezed

together by compression-fixation devices.

518
 Shoulder Arthrodesis:

Indication:
 Stabilization of paralytic disorders,
 Brachial plexus palsy,
 Reconstruction after tumor resection,
 Painful ankylosis after chronic infection,
 Recurrent shoulder instability which has failed previous repair attempts
Contraindication:
 Ipsilateral elbow arthrodesis,  200 – 300 →

 Contralateral shoulder arthrodesis, Abduction,

 20 – 300 →
0
 Progressive neurological disorders,
Forward
 Elderly patient.
flexion,
 200 – 300 → Internal
rotation.

0
Fusion position: [30 – 300 – 300]

519
 Arthrodesis of Elbow: APL-381, Stanmore- 79

 It is a technically difficult and very disabling procedure.

 Even with normal wrist and shoulder function it is not possible to fuse the elbow in a position

which would facilitate both feeding (i.e. 100 degrees of flexion) and perineal hygiene (about 45 degrees

of flexion).

Indication:
 Septic arthritis of elbow joint,
 Post traumatic arthritis,
 Failed elbow arthroplasty,
 Severely comminuted intra
articular fracture.

Contraindications:
 Contralateral elbow fusion,
 Ipsilateral shoulder fusion,
 Charcot arthropathy.

520
 Stanmore - 100

521
 Arthrodesis of joints of the hand Stanmore - 121

522
 Arthrodesis of Hip: apl-535, Stanmore - 145

 Surprisingly, although the joint is fused, the patient retains a great deal of ‘mobility’ because lumbosacral
tilting and rotation are preserved and often increased.
 For sitting comfortably the hip needs 600 of flexion; for climbing stairs 450; and for walking 200.

Screw plus bone graft;

Arthrodesis Stiffness of the hip is largely disguised by mobility of the spine and knee.

 Technical considerations:
The recommended position for arthrodesis is
 200 – 300 of flexion,
 00 – 100 of adduction (unless the leg is short) and
 About 50 of external rotation.

523
  Indications: Arthrodesis should be considered when there are serious contraindications to osteotomy or
arthroplasty: for example, a patient who is too young, a hip that is already stiff but painful and previous infection.

 Contraindications: Elderly patients, lack of bone stock and abnormalities in the ‘compensating joints’
(lumbar spine, knees and opposite hip).

 Complications of Hip Arthrodesis:

(1) Failure to fuse and
(2) Malposition, which hampers function and puts unwanted strain on other joints.
Late complications are –
(3) Compensatory deformities in other joints (knees and opposite hip) and
(4) Low backache, which occurs in over 60% of patients 20 years after fusion.
(5) Women may complain of difficulty with sexual intercourse, and
(6) Squatting is impossible.

524
 Knee Arthrodesis: apl-581

Indication:
 Irremediable instability due to the late effects of poliomyelitis and
 Painful loss of mobility due to tuberculosis or chronic pyogenic infection.
 Commonest indication is failed total knee replacement (either septic or aseptic).

Compression Arthrodesis
TECHNIQUE
 A vertical midline incision is used.
 Posterior vessels and nerves are protected and the ends of the tibia and femur removed by means of
straight saw cuts,
 Position of Fusion:
 150 of flexion and
 70 of valgus.
 Charnley’s method, using thick Steinman pins inserted parallel through the distal femur and proximal
tibia, and connecting these with compression clamps, was for many years the standard method.
 Nowadays, multiplanar external fixation is used,

525
526
 Ankle Arthrodesis: apl- 613, Stanmore - 218

The ideal position for fusion:

 Zero in the sagital plane (the foot therefore plantigrade) and
 50 of valgus.

Complications:

527
528
 SUBTALAR ARTHRODESIS

Indications:
 Idiopathic / post traumatic arthritis,
 Inflammatory arthritis of sub talar joint,
 Flat foot / cavo varus foot reconstruction – optional.

Subtalar mid-tarsal fusion.

529
 TRIPLE ARTHRODESIS

LAMBRINUDI ARTHRODESIS
Indications:
 Post traumatic arthritis,
 Degenerative arthritis,
 CTEV,
 Polio,
 CP,
 RA,
 Pes cavus,
 Pes plano valgus deformity,
 Tarsal coalition,
 Tibialis post tendon dysfunction. A, Kocher approach to ankle.
B, Kocher approach to calcaneus.
 Charcot’s arthropathy. C, Ollier approach to midtarsal and subtalar joints.

530
Complications of Triple arthrodesis:
 Early:
 Chance of injury to adjacent blood vessels and nerves.
 Anaesthesia of skin,
 Infection,
 Late:
 Delayed union,
 Pseudoarthrosis,
 Non union,
 AVN of talus.

Contraindications:
 Young child less than 12 years, because the procedure limits growth of foot, Bones are cartilaginous in
nature at this age and attempt to fuse leads to AVN of talus and fibrous union occur instead of bony union.
 Condition can be adequately corrected and maintained by bracing / soft tissue procedure / tendon balancing.
 Smoking,

531
 Amputation.
APL-325

Amputation:
--It means removal of a limb / part of limb or organ by surgical technique.

Mangled extremity: {Mangle – destroy or severely damaged by tearing}

-- It is the injury to extremity so severe that salvage is often questionable and amputation is a possible
outcome.

Indication of amputation:
 Dead:
 PVD,
 Limb death due to severe trauma / burn / frostbite.

 Dangerous:
 Malignant bone / soft tissue tumour,
 Lethal sepsis,
 Crush injury / Crush syndrome.

 Damn nuisance:
 Severe pain,
 Paralysis of limb,
 Gross malformation,
 Recurrent sepsis.

Varieties of amputation:
 Provisional amputation:
 May be necessary because primary healing is unlikely,
 Limb is amputated as distal, skin flaps are cut & sutured loosely over pack,
 Re-amputation is performed when stump condition is favourable.

532
 Definitive End bearing amputation:
 When pressure or weight is to be borne through the end of stump,
 Scar must not be terminal and bone end must be solid not hollowed,
 It must be cut through or near a joint,
 Example:
o Amputation through knee,
o Gritti stokes,
o Syme’s amputation.

 Definitive Non end bearing / Cone bearing amputation:

 Commonest variety,
 When pressure or weight is not to be borne through the end of stump,
 Scar can be terminal.
 Example:
o Above knee amputation,
o Below knee amputation.

533
Amputations at sites of election:
 Most lower limb amputations are for ischaemic disease and are performed through the site of election below the
most distal palpable pulse,
 Selection of amputation level can be aided by Doppler indices,
 Sites of election are determined by the demands of prosthertic design and local function.

534
Principles of technique:
 Tourniquet:
 A tourniquet is used unless there is arterial insufficiency.

 Skin flap:
 Skin flaps are cut so that their combined length equals 1.5 times width of the limb at the site of
amputation.
 As a rule, anterior and posterior flaps of equal length are used for upper limb & for transfemoral
(above knee) amputations and below knee amputation – long posterior flap is usual.

 Muscles:
 Muscles are divided distal to the proposed site of bone section,
 Opposing groups are sutured over the bone end to each other and to the periosteum, thus providing
better muscle control as well as better circulation.
 It is also helpful to pass the sutures that anchor the opposing muscle groups through drill holes in the
bone end – creating an Osteomyodesis.

 Nerve:
 Nerves are divided proximal to the bone cut to ensure a cut nerve end will not bear weight.

 Bone:
 Bone is sawn across at the proposed level.
 In case of transtibial amputation – front of tibia is usually bevelled and filed to create a smoothy
rounded contour & fibula is cut 3 cm shorter.

 Haemostasis:
 Main vessels are tied, tourniquet is removed and every bleeding points meticulously ligated.

 Closure:
 Skin is sutured carefully without tension.
 Suction drainage is advised,
 Stump is covered without constricting passes
of bandage; figure of eight passes are better suited
and prevent the creation of venous tourniquet
proximal to the stump.

535
After care:
 Drain off and dressing at 3rd POD,
 If haematoma forms, it is evacuated as soon as possible,
 Stitches off at 14th POD,
 After satisfactory wound healing, gradual compression stump socks are used to help shrink the
stump and produce a conical limb end,
 Muscles must be exercised, joints kept mobile and patient is taught to use prosthesis.
Q) Examples:

 Forequarter / Inter-scapulo thoracic amputation: mutilating operation

 Eradication of malignant tumour in upper limb,

536
  Palliation for intractable sepsis or pain,
 Traumatic avulsion of upper limb / dead limb.

 Disarticulation at shoulder:
 If 2.5 cm of humerus can be left below anterior axillary fold, it is possible to hold the stump in
a prosthesis.

 Amputation in the forearm:

 Shortest forearm stump that will stay in a prosthesis in 2.5 cm, measured from front of flexed
elbow,
 Even a shorter stump may be useful as a hook to hang things from.

537
 Hindquarter / Hemi-pelvectomy amputation:
 Performed only for malignant disease.

 Disarticulation through the hip:

 Prosthetic fitting is difficult,
 If the femoral head, neck and trochenter can be left, it is possible to fit a tilting table prosthesis.

 Transfemoral amputation:
 A longer stump offers the patient better control of the prosthesis and it is usual to leave at least
12 cm below the stump for knee mechanism.
 Recent gait studies suggest some latitude is present as long as the amputated femur is at least
57% of the length of contralateral femur.

 Amputation around the knee:

 Gritti Stokes operation – {in which the trimmed patella is apposed to the trimmed femoral
condyle}- is rarely performed because the bone may not unite securely,
 End bearing stump is rarely satisfactory.
 Fitting a modern knee mechanism is troublesome and the sitting position reveals the knees to be
grossly unequal in level,
 Main indication for around knee amputation procedure is in children because the lower femoral
physis is preserved, effectively permitting a stump length equivalent to an above knee
amputation to be reached when the child is mature.

538
 Transtibial / Below knee amputation:
 Healthy below knee stumps can be fitted with excellent prosthesis allowing good function and
nearly normal gait,
 Even 5 – 6 cm stump may be fitted with a prosthesis in a thin patient, greater length makes fitting
easier.
 There is no advantage in prolonging the stump beyond the conventional 14 cm.

539
540
  Above the ankle / Syme’s amputation:

 In adults it is well accepted by men, but women find it cosmetically undesirable.

 The stump is designed to be end bearing, scar is brought away from the end by cutting a long posterior flap,
 Flap must contain not only skin of the heel but the fibrofatty heel pad so as to provide a good surface for
weightbearing,
 The bones are divided just above the malleoli to provide a broad area of cancellous bone to which the flap
should stick firmly; otherwise the soft tissues tend to wobble about.

541
Syme’s amputation

542
 Pirogoff’s amputation:
 The back of the os calcis is fixed onto the cut end of the tibia & fibula.

 Partial foot amputation:

 Foot may be amputated at any convenient level, for examples- through the mid tarsal joints {Chopart}, through
the tarsometatarsal joints {Lisfranc}, through the metatarsal bones or through the metatarsophlangeal joints

 Amputation in the foot:

 Where feasible, it is better to amputate through the base of proximal phalanx rather than through
meatarsophalangeal joint,
 With diabetic gangrene, septic arthritis of the joint is not uncommon; the entire ray {toe + metatarsal bone}
should be amputated.

543
Q) Complications of amputation?
 Early complications:
 Reactionary haemorrhage,
 Breakdown of skin flaps: due to -
 Ischaemia,
 Suturing under excess tension,
 In case of below knee amputation – an unduly long tibia pressing against the flap.

544
  Gas gangrene:
 Clostridia and spores from the perineum may infect a high above knee amputation or
re-amputation,
 Especially if performed through ischaemic tissue.

 Late complications:
 Skin:
 Eczema is common,
 Ulceration is usually due to poor circulation.

 Muscle:
 If too much muscle is left at the end of stump, the resulting unstable ‘cushion’ induces feeling of
insecurity for proper use of prosthesis.

 Nerve:
 A cut nerve always forms a neuroma which is painful and tender,
 Excising 3 cm of the nerve above neuroma sometimes succeeds.

 Phantom limb:
 Feeling that the amputated limb is still present.
 Patient should be warned of the possibility.

 Joint:
 Joint above the an amputation may be stiff or deformed,
 Common deformity: fixed flexion or fixed abduction at hip in above knee amputation,
 It should be prevented by exercises.

 Bone:
 A Spur often forms at the end of bone, but usually painless,
 If there is infection then spur may be enlarged and painful and necessary to excise.
 If the bone is transmitting little weight, it becomes osteoporotic and liable to fracture, such
fractures are best treated by internal fixation.

545
Q) Short notes: Microsurgery in Orthopaedics / Replantation Surgery? APL-325

Microsurgery in orthopaedics:
--- Microsurgical techniques are used for repairing-
 Nerves,
 Vessels,
 Transplanting bone with a vascular pedicle,
 Substituting a less essential digit {eg. Toe} for a more essential one {eg. Thumb},
 For re-attaching a severed limb or digit.
Pre-requisites:
 Operating microscope,
 Special instruments,
 Micro suture,
 Special chair with arm support,
 Specialized surgeon & team.

Caution:
 Warm ischaemic period of greater than 6 hours are likely to result in permanent muscle damage and may
even produce severe systemic upset in the patient when reperfusion of the muscle occurs.

Techniques:
 Severed part should be kept cool during transport,
 More muscle in the amputated part – shorter the period it will last,
 A finger tip may survive for 24 hours and forearm only for a few hours,
 Bones are shorter to reduce tension and fixed with internal or external fixator first,
 Next vessels: veins first  after that artery,
 Nerves & Tendons next need to repair.

Limitation:
 Time consuming procedure,
 Often unsuccessful,
 Expensive procedure.

546
Arthroplasty.

547
 THR
APL- 536,

 Charnley’s (1979) three major contributions to the evolution of hip replacement were:
(1) The concept of low-friction torque arthroplasty;
(2) The use of acrylic cement to fix the components; and
(3) The introduction of high-density polyethylene as a bearing material.

548
TOTAL HIP REPLACEMENT
GENERAL PRINCIPLES / Rationale APL-536

(1) The prosthetic implants must be durable;

(2) They must permit extraordinary low friction movement at the articulation;
(3) They must be firmly fixed to the skeleton; and
(4) They must be inert and not provoke any unwanted reaction in the tissues.

 Usual combination is a metal femoral component (stainless steel, titanium or cobalt– chrome alloy) articulating
with a polyethylene socket.
 Ceramic components have better frictional characteristics but are more easily broken.

Stanmore – 145, apl- 536

 Because of the tendency for implants to loosen with time, joint replacement was customarily
reserved for patients over 60 years.
 Improved cementing techniques and rapid advances in the design of uncemented prostheses, the
operation is being offered to younger patients with destructive hip disorders, and occasionally even to children
severely crippled with rheumatoid disease.

549
550


 Technical considerations
 Infection can be prevented by-
 Prophylactic measures,
 Use of special ultraclean-air operating theatres,
 Occlusive theatre clothing and
 Perioperative antibiotic cover.
 Some surgeons routinely use antibiotic-laden cement.

551
  The choice of implant should depend on sound biomechanical and biological testing. The argument of
‘cemented versus cementless’ goes on.
 Postoperatively the implant should be protected from full loading until osseointegration is advanced; 6
weeks on crutches is not unreasonable.

 Results
Implant survival rates of more than 95% at 15 years are being reported.

 Fixation Principles:

Prosthetic fixation Fixation between cement and bone is by -

(a) Interlock (interdigitation of large irregularities in cement and bone) and, more completely, by
(b) Osseointegration (intimate penetration of cement between endosteal trabeculae).

 Fixation is either by embedding the implant in methylmethacrylate cement, which acts as a grouting
material filling the interstices, or by fitting the implant closely to the bone bed without cement. Cement is a grout,
not a glue, and fixation is achieved by a mechanical interlock in the bony interstices.

552
  The ‘bond’ between bone and the implant surface, or cement, is never perfect.
 The best that can be hoped for is ingrowth of trabecular bone on the implant or cement
(osseointegration).
 Various ways of enhancing Fixation process:
(1) If acrylic cement is used, it is applied under pressure and allowed to cure without
movement or extrusion after the implant has been inserted;
(2) Ling and his co-workers have shown that a smooth, tapered and collarless femoral
prosthesis will continue settling within the cement mantle even after polymerization, thereby maintaining expansile
pressure between cement and bone (Fowler et al., 1988);
(3) Uncemented implants may be covered with a mesh or porous coating that
encourages bone ingrowth (Engh et al., 1987);
(4) The implant may be coated with hydroxyapatite, an excellent substrate for
osteoblastic new-bone formation and osseointegration.

 IMPLANT SELECTION
a) Cemented implants:
 Cement is a grout, not a glue, and fixation is achieved by a mechanical interlock in the bony interstices.
 Cemented stems embrace two broad concepts:
 Taper-slip or Force-closed design,
 Composite beam or Shape-closed design.

Taper slip is a highly polished tapered stem designed to settle within the cement mantle and reengage the taper
optimizing the load distribution to the surrounding bone and cement.

553
 Taper slip stems, such as the Exeter prosthesis, have gained increasing popularity among cemented implants.

554
b) Uncemented implants

c) ‘Hybrid hip’:

555
d) Modular system.

e) Ceramic implant,

f) Custom made.

556
 Non cemented prosthesis:
Advantages Limitations
No bone cement related complication Not suitable for osteoporotic bone.
Decrease incidence of aseptic loosening. Acetabular cup have porous coating. So bone ingrowth
over porous coating takes much time.
No chance of aggresive osteolysis. Not gives immediate stability. So implat should be
protected from full weight bearing, until
osteointegration in advance. {about 6 wks]
Acetabular cup and screw gives secure fixation. Periprosthetic # more common {7.4%].
Hydroxyapatite over stem gives quick
osteointegration.
Suitable for young patient.

Cemented prosthesis
Advantages Limitations
Suitable for osteoporotic bone. Bone cement related complications.
Gives immediate stability. Aggressive osteolysis.
Antibiotic mixed bone cement decreases the risk of Aseptic loosening.
post operative infection.
Periprosthetic fracture incidence less. Not suitable for young patient.

557
 Complications:

 Deep vein thrombosis is more common than with other elective operations.

 Infection is the most serious postoperative complication.

 With adequate prophylaxis the risk should be less than 1% {0.1% - 1%},

 It is higher in the very old, in patients with rheumatoid disease or psoriasis, and in those on

immunosuppressive therapy (including corticosteroids).

558
  Intraoperative complications include perforation or even fracture of the femur or acetabulum.

 Sciatic nerve palsy (usually due to traction but occasionally caused by direct injury) may occur with any
type of arthroplasty but is more common with a posterior approach (Most cases recover spontaneously).

 Postoperative dislocation is rare if the prosthetic components are correctly placed.

 Reduction is easy and traction in abduction usually allows the hip to stabilize.

 If malposition of the femoral or acetabular component is severe, revision may be needed, or

possibly augmentation of the socket.

 Heterotopic bone formation around the hip is seen in about 20 percent of patients 5 years after joint
replacement.
 Cause is unknown, but patients with skeletal hyperostosis and ankylosing spondylitis are particularly

at risk.

 Ossification can be prevented in high-risk patients by giving either a course of nonsteroidal anti-

inflammatory drugs for 3–6 weeks postoperatively or a single dose of irradiation to the hip.

 Aseptic loosening of either the acetabular socket or the femoral stem is the commonest cause of longterm
failure.

Ten years after a hip replacement there is a distinct radiolucent line around this femoral implant as well as resorption of the calcar.
 With modern methods of implant fixation, there is likely to be radio graphic evidence of

 loosening in less than 10 percent of patients 15 years after operation;

 At microscopic level many stable implants show cellular reaction and membrane formation at the

bone–cement interface.

559
 Aggressive osteolysis, with or without implant loosening, is sometimes seen.

Aggressive osteolysis.
 It is associated with granuloma formation at the interface between cement (or implant) and bone.

 This may be due to a severe histiocyte reaction stimulated by cement, polyethylene or metal

particles.

560
561
562
 Hip Replacement Components:

563
 Acetabular Reaming:

564
BEARING SURFACES
The issue of osteolysis had not been resolved by the implantation of uncemented implants.

 Highly cross-linked polyethylene (XLPE)

Gamma irradiation of polyethylene causes cross-linking, which greatly improves the wear resistance compared to
conventional polyethylene.

 Ceramic-on-ceramic
Alumina ceramics were introduced as a bearing material in the 1970s.
They are‘wettable’, have very low wear rates, are scratch-resistant and their particulate debris is not biologically
very active.
However, ceramics are brittle and are susceptible to fractures.

 Metal-on-metal
Metal bearing surfaces have very low wear rates and are self-polishing, which allows for self healing of surface
scratches.

565
Screw positioning:

566
 Preparation of Femoral component: CAMP-164

567
 Vertical height (vertical offset) - is determined primarily by the base length of the prosthetic neck plus the length
gained by the modular head used. Vertical height and offset increase as the neck is lengthened, Neck length
typically ranges from 25 to 50 mm,

 Offset / Horizontal offset - is the distance from the center of the femoral head to a line through the axis of the
distal part of the stem and is primarily a function of stem design.

 Version of the femoral neck (Anterior offset) - Version refers to the orientation of the neck in reference to the
coronal plane and is denoted as anteversion or retroversion.
Restoration of femoral neck version is important in achieving stability of the prosthetic joint. The normal femur has
10 to 15 degrees of anteversion of the femoral neck in relation to the coronal plane when the foot faces straight
forward, and the prosthetic femoral neck should approximate this.
Proper neck version usually is accomplished by rotating the component within the femoral canal. This presents little
problem when cement is used for fixation; however, when press-fit fixation is used, the femoral component must be
inserted in the same orientation as the femoral neck to maximize the fill of the proximal femur and achieve
rotational stability of the implant.

568
IMPORTANCE OF OFFSET:
 Inadequate restoration of offset shortens the moment arm of the abductor musculature and results in increased
joint reaction force, limp, and bone impingement, which may result in dislocation.
 Offset can be increased by simply using a longer modular neck, but doing so also increases vertical height,
which may result in overlengthening of the limb. This is accomplished by reducing the neck-stem angle (typically
to about 127 degrees) or by attaching the neck to the stem in a more medial position

 Rehabilitation
 The length of inpatient stay has been reduced to 4–6 days in most hospitals.
 Patients are well mobilized on crutches or sticks before discharge, and will have negotiated stairs
independently.
 Progress to full weightbearing without support will usually take 6–8 weeks at the patient’s own pace.

569
 TKR

Types of TKR:
 Partial / unicompartmental replacement,
 Minimally constrained TKR,
 Constrained TKR
 Minimally invasive TKR.

570
Complications:

571