Short Notes of Orthopaedics

Edited by:
Prithwiraj Maiti, MBBS
House physician
Department of Internal Medicine, R.G.Kar Medical College
Author: An Ultimate Guide to Community Medicine
Author: A Practical Hand ook of Pathology Specimens and Slides
[Both published by Jaypee Brothers Medical Publishers, India]
9/9/2016

Table of contents
Chapters Contents Page no.
General principles of Compound fracture [14, supple], Non-union of fracture [13, 1-15
orthopaedics supple], Non-union of closed fracture [09, supple],
Compartment syndrome [12, supple], Crush syndrome [06],
Fat embolism [09], Myositis ossificans [09], Pathological
facture [09] [15], Stress fracture [08, supple], Classification
of nerve injuries [06]
Infections of bones Pyogenic Osteomyelitis [12], Aetiopathogenesis of acute 16-24
and joints osteomyelitis [09], Sequestrum [08] [11, supple] [12,
supple], Ring sequestrum [16], Brodie’s A scess [11] [14,
supple], TB hip joint [10, supple]
Upper limb Fractures occurring due to fall on outstretched hand [14], 25-56
Volkma ’s ischae ic Co tracture [06] [08] [13] [10,
supple] [15], Colles fracture [13] [08, supple], Monteggia
fracture-dislocation [13, supple], Shoulder dislocation [06]
[11], Recurrent dislocation of shoulder [13, supple], Supra
condylar fracture of Humerus [12] [16], Complication of
supracondylar fracture of humerus [08] [09, supple],
 Fracture clavicle [12], Tennis Elbow [12],], Dupuytre ’s
contracture [12] [10, supple], Mallet finger [12], Trigger
finger [11], Fracture olecranon [12, supple], Carpal tunnel
syndrome [11] [09] [13, supple] [14, supple] [16], Frozen
shoulder [08] [11, supple] [14, supple], De Querva ’s
disease [08] [11, supple]
Lower limb Fracture of patella [14] [08, supple], Mechanism of patellar 57-65
fracture [11], Ruptured Tendoachilles [12], Avascular
necrosis of femoral head [10, supple], Fracture neck femur-
types and complication [09]
Spine and vertebra Slipped disc [12, supple], Spondylolisthesis [10], TB spine 66-78
[10], Clinical feature of TB spine [08, supple], Gibbus [08,
supple], Spina bifida [14][09]
Paediatric age group Greenstick fracture [14], CTEV/ Clubfoot [08] [13, supple] 79-82
[11, supple] [10, supple]
Bone cysts and Osteochondroma/ Exostosis [14] [15] [10], Ewi g’s tu our 83-90
tumours [13] [11] [10] [14, supple], Radiological features of
osteosarcoma [12, supple], Management of osteosarcoma
[09, supple], Giant cell tumor [10, supple] [16], Bone cyst
[08, supple]
Miscellaneous Bone graft [13], External fixation [13, supple], Indications of 91-104
limb amputation [12, supple] [09, supple], Ideal amputation
stump [15] [06], Cod a ’s tria gle [11, supple], Bone scan
[10], Paget’s disease of o e [09, supple], Tension band
wiring [09, supple], SP Nail [11, supple]

References: Essential Orthopaedics by J.Maheshwari (5ed), Apley’s System of

Orthopaedics and Fractures (9ed), Handbook of Orthopedic Examination by K.
Banerjee (5ed), Radiopaedia.org and others.
Disclaimers: This document is created for helping the undergraduate MBBS
students for examination purpose. The pictures used in this document are
property of the authors/ publishers and used here solely for educational, non-
commercial use.
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Chapter 1: General Principles of Orthopedics

Compound fracture/ Open fracture:
Introduction:
A fracture with break in the overlying skin and soft tissues, leading to the fracture
communicating with the external environment.
Mechanism:
This type of fracture occurs when enough force hits the bone to cause it break
and stick out through the skin.
Types:
1. Internally open: The sharp fracture end pierces the skin from within
2. Externally open: The object causing the fracture lacerates the skin and soft
tissues over the bone and finally break the bone to cause a fracture.
Symptoms and warning signs:
 History of a major trauma
 Symptoms are mainly due to broken bone and open wound: pain, swelling,
bleeding, infection etc.
 Warning signs to be kept in mind:
i. Stretch pain: Indicates compartment syndrome
ii. Pallor pulselessness: Indicates arterial injury
iii. Foul odour: Indicates infection due to open wound.
Grading of compound fracture [Gustilo classification]:
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Treatment:
Principles and steps of treatment:
1. Primary survey and early resuscitation
2. Bleeding control (by direct pressure)
3. Temporary immobilization of the fracture
4. Decontamination (Wound irrigation with NS [at least 3 litres] ± Antiseptic/
Antibiotic solution)
5. Tetanus prophylaxis (Inj. Tetanus toxoid 0.5 ml IM)
6. Early administration of prophylactic antibiotic (Commonly used: 1st
Generation cephalosporin [type 1 and 2] ± Aminoglycoside [type 3])
7. Thorough wound debridement (Wound exploration + detection and
removal of foreign material + nonviable tissue + bacterial contamination)
8. Repair damaged structures (Consult CTVS surgeon in case of major vascular
injury/ plastic surgeon in case of nerve/ tendon injury)
9. Reduce and stabilize the fracture (External splinting [slab/ cast/ traction];
Early internal fixation [pin/ nail/ plate and screw] ± External fixators:
Method of choice)
10.Wound coverage (Direct suture/ skin graft/ flap).
Complications:
 Infection
 Damaged structures
 Compartment syndrome
 Bone defect: delayed union/ non-union.

Non-union of [closed] fracture:

Introduction:
Non-union is a permanent failure of healing following a fracture.
Definition:
A fracture that in a minimum of 9 months post occurrence and is not healed and
has not shown radiographic progression by 3 months.
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Classification:
There are 2 main types:
1. Atrophic non-union: Osteogenesis seems to have ceased. The bone ends
are tapered or rounded with no suggestion of new bone formation.
2. Hypertrophic non-union: Bone ends are enlarged, suggesting that
osteogenesis is still active but not quite capable of bridging the gap.
Etiological/ Risk factors:

Common sites:
 Femur
 Scaphoid
 Lower third of the tibia
 Lower third of the ulna
 Lateral condyle of the humerus.
Clinical features:
 Persistent pain
 Pain on stressing the fracture
 Mobility
 Increasing deformity at the fracture site.
Radiological features:
 Absence of bridging trabeculae
 Sclerotic fracture edges
 Persistent fracture lines
 Lack of evidence of progressive change toward union in serial X-Ray
 4

 Progressive deformity.
Treatment options:
1. Open reduction + Internal fixation ± Bone grafting: This is the commonest
operation performed for non-union. The grafts are taken from iliac crest.
2. Excision of fragments:
This can only be done where excision of the fragment does not cause any
loss of functions. An excision may or may not need to be combined with
replacement with an artificial prosthesis.
Ex.: In non-union of fracture of the neck of femur in an elderly, the head of
the femur can be replaced by a prosthesis (replacement arthroplasty).
3. No treatment:
Some non-unions do not give rise to any symptoms, and hence require no
treatment.
Ex.: Some non-unions of the fracture scaphoid.
4. Ilizarov’s method:
Ilizarov method is a system in which bone is fixed with thin wires and rings.
Extremity lengthening and reconstruction techniques are used for filling
bone defects and correcting and lengthening bones with deformity.

Compartment syndrome:
Introduction:
Limbs contains muscles, blood vessels and nerves covered by tough fascia. All
these together for s a co part e t .
Introduction:
Compartment syndrome is a clinical condition characterized by an elevation of
intra-compartmental pressure, resulting in a decreased blood supply of the
muscles and nerves within it; causing ischemic damage which may progress into
necrosis of both muscles and nerves.
Risk factors:
1. Direct trauma leading to edema of muscles
 5

2. Soft tissue bleeding from fractures/ operations

3. Prolonged compression by tight plaster/ bandage
4. Direct pressure in a comatose patient lying on a hard surface.
The common sites of fractures notorious for developing compartment syndrome
are elbow, forearm bones, proximal 1/3rd of tibia, multiple fractures of hand and
foot.
Pathophysiology:
 The increased pressure within the compartment compromises the
circulation leading to further muscle ischemia.
 A vicious-cycle is thus initiated and continues until the total vascularity of
the muscles and nerves within the compartment is jeopardized. This results
in ischemic muscle necrosis and nerve damage.
 The necrotic muscles undergo healing with fibrosis, leading to contractures.
 Nerve damage may result in motor and sensory loss.

Types:
According to the progression, compartment syndrome may be of 2 types:
1. Acute:
E : Volk a ’s co tracture
It is a complication of supracondylar fracture of humerus where there is
injury/ compression of the brachial artery, leading to ischemia of flexor
digitorum profundus and flexor pollicis longus, resulting in a permanent
flexion contracture of wrist joint and fingers.
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2. Chronic:
Ex: Chronic exertional compartment syndrome
In some of the long distance runners, there is swelling of the anterior
calf muscle, causing a chronically elevated compartment pressure,
leading to ischemia of deep peroneal nerve, resulting in pain along the
anterolateral aspect of calf; precipitated by muscular exertion.
Clinical features:
I. Often a H/O a risk factor (fracture/ operation/ compression/ infection) is
present
II. Classical features of ischemia (5P):
1. Pain
2. Pallor
3. Paresthesia
4. Paralysis
5. Pulselessness.
- All of these clinical features may not be present, but presence of any of
them should raise suspicion of an impending compartment syndrome in
the mind of the clinician in a background of risk factor(s).
III. Stretch test:
 This is the earliest sign of impending compartment syndrome.
 The ischemic muscles, when stretched, give rise to pain.
 It is possible to stretch the affected muscles by passively moving the
joints in a direction opposite to that of the damaged muscle's action.
Ex: When the toes/ fingers are passively hyperextended, there is
increased pain in the flexors of calf/ forearm.
Diagnosis:
 Confirmation of the diagnosis can be made by measuring the intra-
compartmental pressure.
 A differe tial pressure (ΔP) – the difference between diastolic pressure and
compartment pressure – of <30 mmHg is an indication for immediate
compartment decompression.
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Management:
Compartmental syndrome is a medical emergency:
I. Remove any cast/ bandage/ dressing immediately
II. Elevate the limb to increase blood supply
III. The ΔP should e carefully o itored; if it falls elow 30 Hg, i ediate
open fasciotomy (opening compartments through incisions) is performed.
The wounds should be left open and inspected 2 days later:
 If there is muscle necrosis, debridement can be carried out;
 If the tissues are healthy, the wounds can be sutured (without
tension) or skin-grafted.

Crush syndrome:
Introduction:
This is seen when a limb is compressed for extended periods, e.g. following
entrapment in a vehicle or rubble, but also after prolonged use of tourniquet.
Consequences of Crush syndrome:

Crushed limb Underperfusion Necrosis of muscles

Release of toxic
metabolites (Reactive
Tissue damage Swelling
oxygen metabolites)
when limb is freed

Compartment
Aggravating ischemia
syndrome
 8

 Tissue necrosis also causes systemic problems such as renal failure from
free myoglobin, which is precipitated in the renal glomeruli.
 Myonecrosis may also cause a metabolic acidosis with hyperkalaemia and
hypocalcaemia.
Clinical features:
 The compromised limb is pulseless and becomes red, swollen and blistered;
sensation and muscle power may be lost.
 If not treated adequately within 2-3 days, acute tubular necrosis sets in,
producing signs of deficient renal functions such as scanty urine, apathy,
restlessness and delirium.
Treatment:
 The most important measure is prevention.
 A high urine flow is encouraged with alkalization of the urine with sodium
bicarbonate, which prevents myoglobin precipitating in the renal tubules.
 If oliguria or renal failure occurs then renal haemofiltration will be needed.
 If a compartment syndrome develops, and is confirmed by pressure
measurements, then a fasciotomy is indicated. Excision of dead muscle
must be radical to avoid sepsis.
 Similarly, if there is an open wound then this should be managed
aggressively. If there is no open wound and the compartment pressures are
not high, then the risk of infection is probably lower if early surgery is
avoided.

Fat embolism:
Introduction:
A fat embolism is a type of embolism that is often caused by physical trauma such
as fracture of long bones, soft tissue trauma and burns. Fat embolism occurs in
about 90% of individuals with severe skeletal injuries.
Common skeletal injuries causing fat embolism:
• Fracture femur
 9

• Fracture tibia
• Multiple fractures.

Fat embolism syndrome (FES):

It is distinct from the presence of fat emboli. Symptoms usually occur 1–3 days
after a traumatic injury and consists of the following symptoms:
• Pulmonary: Shortness of breath, hypoxemia
• Neurological: Agitation, delirium, coma
• Dermatological: Petechial rash
• Hematological: Anemia, thrombocytopenia.
Pathogenesis:
• The pathogenesis of fat emboli syndrome probably involves both
mechanical obstruction and biochemical injury.
• Fat microemboli and associated RBC and platelet aggregates can occlude
the pulmonary and cerebral microvasculature.
• Release of free fatty acids from the fat globules exacerbates the situation
by causing local toxic injury to endothelium; and resultant platelet
activation and granulocyte recruitment.
Treatment:
• Oxygen
• Heparinisation
• Low molecular weight dextran
• Ventilator support and ICU management.

Myositis ossificans:
Definition:
Myositis ossificans is defined as heterotopic ossification in the muscles after an
injury.
Age:
The patient is usually a fit young man.
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Most common clinical conditions that may lead to myositis ossificans:

1. Dislocation of elbow.
2. Blow to brachialis/ deltoid/ quadriceps.
3. Unconscious/ paraplegic patients.
Clinical and radiological features:
 Soon after the injury, the patient complains of pain; there is local swelling
and soft-tissue tenderness. X-ray is normal.
 Over the next 2–3 weeks the pain gradually subsides, but joint movement is
limited; X-ray may show fluffy calcification in the soft tissues.
 By 8 weeks the bony mass is easily palpable and is clearly defined in the X-
ray.
Treatment:
 The joint should be rested in the position of function until pain subsides;
gentle active movements are then begun.
 Months later, when the condition has stabilized, it may be helpful to excise
the bony mass.
 Indomethacin or radiotherapy should be given to help prevent a
recurrence.

Pathological fracture:
Definition:
It is defined as a fracture in a bone which has already become week by some
underlying diseases.
Most common cause:
 The most common cause of pathological fracture is osteoporosis.
 The most commonly involved bones are thoracic and lumber vertebral
bodies.
 Other common fractures associated with osteoporosis are fracture neck of
fe ur a d Colles’ fracture.
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Causes of pathological fractures at different ages:

Age Most common cause(s)


At birth Osteogenesis imperfecta


0-5 years Osteogenesis imperfecta


Osteomyelitis


5-20 years Osteomyelitis


Primary bone cyst


Primary bone malignancy


20-50 years Cystic lesions of bone


Malignancy


Osteomalacia


Giant cell tumor


After 50 years Osteoporosis


Multiple myeloma
Metastasis to the bones

Diagnostic clues:
 A fracture without a significant trauma.
 A history of mild discomfort in the region of fracture for some days before
the fracture occurred.
 When patient is already diagnosed with a disease that may cause
pathological fractures (Ex.: malignancy).

Treatment:
The treatment of a pathological fracture consists of:
a. Detection of the underlying disease that is making bone weak.
b. Assessment of the capacity of fractured bone to unite.
c. Achievement of maximum stable fixation.

Detection of the underlying disease that is making bone weak

To detect the underlying disease, the following tests should be done:
 12

1. CBC, ESR.
2. Kidney and liver function tests.
3. Calcium, phosphorus and alkaline phosphatase (Osteoporosis,
Osteomalacia, Bone tumors).
4. Plasma protein electrophoresis (Multiple myeloma).
5. Tumor markers:
a. CA 19-9 (Colorectal cancer).
b. CA 125 (Ovarian cancer).
c. CA 15-3 (Breast cancer).
d. β2-Microglobulin (Lymphoma).
e. Alpha-fetoprotein (Hepatocellular cancer).
f. PSA (Prostatic cancer).
Assessment of the capacity of fractured bone to unite
It is well known that depending upon the etiology of pathological fracture, there
are differences in the capacity of the bone to reunite.
Ex.: In diseases like Osteogenesis imperfecta and Osteoporosis, the fracture is
amenable to reunite with conventional methods whereas, in diseases like
Osteomyelitis and Malignancy, fractures may fail to reunite despite best efforts.
Achievement of maximum stable fixation
Non-operative treatment options:
1. Bisphosphonates.
2. Radiotherapy.
3. Pain control.
4. DVT control.
5. Splints/ traction/ braces etc.

Operative treatment options:

1. Internal fixation: Preferable intra-medullary fixation with/ without bone
grafting/ cementing (in case of big cavities),
2. Resection and replacement.
Note: Surgery should be followed by postoperative radiotherapy to prevent
recurrences.
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Stress fracture:
Introduction:
Stress fracture, also known as hairline fracture; is a special type of fracture
sustained due to chronic repetitive injury (stress) causing a break in bony
trabeculae.
Mechanism:
It results from accumulated trauma from repeated submaximal loading.
Types:
1. Fatigue fracture: Occurs secondary to an abnormal amount of stress
applied to a normal bone.
Ex.: Runners, dancers, military recruits etc.
2. Insufficiency fracture: Occurs with normal stress placed on an abnormal
bone.
E .: Osteoporosis, osteo alacia, Paget’s disease, drug i duced
(corticosteroids and methotrexate).
Clinical features:
 There may be a history of unaccustomed and repetitive activity or a
strenuous physical exercise programme.
 A common sequence of events is: pain after exercise –> pain during
exercise –> pain without exercise.
 The affected site may be swollen or red. It is sometimes warm and usually
tender; the callus may be palpable.
 Occasionally the patient presents only after the fracture has healed and
may then complain of a lump (the callus).
Investigation:
 X-Ray: Early on, the fracture is difficult to detect. When taken a few weeks
later, it may show a small transverse defect in the cortex and/or localized
periosteal new-bone formation.
 Best diagnostic test for unilateral stress fracture is MRI
 14

 Best diagnostic test for bilateral stress fracture is bone scan: will show
increased activity at the painful spot.
Note: The great danger is a mistaken diagnosis of osteosarcoma; scanning shows
increased uptake in both conditions and even biopsy may be misleading.
Treatment:
 Most stress fractures need no treatment other than an elastic bandage and
avoidance of the painful activity until the lesion heals.
 An important exception is stress fracture of the femoral neck. This should
be suspected in all elderly people who complain of pain in the hip for which
no obvious cause can be found. If the diagnosis is confirmed by bone scan,
the femoral neck should be internally fixed with screws as a prophylactic
measure.

Classification of nerve injuries:

Seddo ’s classificatio (1942):
Term Description Example
Neurapraxia A reversible physiological nerve conduction block with loss of Saturday
some types of sensation and muscle power followed by night palsy
spontaneous recovery within a few days or weeks.
Axonotmesis Axonal interruption with loss of conduction but the nerve is in Closed
continuity and the neural tubes are intact. fracture
Distal to the lesion, axons disintegrate and are resorbed by and
phagocytes. This phenomenon is called Wallerian degeneration. dislocations
Recovery takes months to occur.
Neurotmesis When the injury is more severe, whether the nerve is in Open
continuity or not, recovery will not occur. wound
As in axonotmesis, there is rapid Wallerian degeneration, but
here the endoneurial tubes are destroyed over a variable
segment and scarring takes place, which interferes with
regenerating axons regaining entry into the distal segment.
Instead, regenerating fibers mingle with proliferating Schwann
cells a d fi ro lasts i a ju led k ot or neuroma’ at the site
of injury.
 15

Even after surgical repair, many new axons fail to reach the
distal segment.
 16

Chapter 2: Infection of bones and joints

Pyogenic osteomyelitis, Etiopathogenesis:
Introduction:
Infection of bone by any pyogenic organism is called pyogenic osteomyelitis. It is
of 2 types: acute and chronic.
Acute pyogenic osteomyelitis
Responsible organisms:
Staphylococcus aureus (commonest), followed by streptococcus and
pneumococcus.
Route of entry to bone:
1. Primary/ hematogenous (commonest, often seen in children)
2. Secondary (following an open fracture/ bone operation, less common).
Etiopathogenesis:
1. Hairpin arrangement’ of the vessels i the metaphysis of long bone makes
the blood flow sluggish in this area and makes this area being the
commonest area to lodge the organisms (lower femoral metaphysis is the
commonest among them).
2. The host bone initiates an inflammatory reaction in response to the
bacteria. This leads to bone destruction and production of an inflammatory
exudate which may spread to the following directions:

[Spread of pus from metaphysis: A) Along medullary cavity, B) Out of the cortex,
C) To the joint, D) Abscess formation]
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1. Along the medullary cavity:

The pus may spread along the medullary cavity, causing thrombosis of
medullary arteries and veins; cutting blood supply to a portion of bone.
2. Out of the cortex:
The pus travels along Volk a ’s ca als a d co es to lie su -periosteally.
The periosteum is thus lifted off the underlying bone, resulting in damage
to the periosteal blood supply to a part of the bone.
A segment of bone is thus rendered avascular and is called sequestrum.
3. Abscess and sinus formation:
Eventually the periosteum is perforated, letting the pus out into the muscle
or subcutaneous plane, where it can be felt as an abscess. The abscess, if
unattended, bursts out of the skin, forming a discharging sinus.
4. To the joint:
The capsular attachment at the epiphysis - metaphysis junction prevents
the pus from entering the nearby joint. In joints with an intra-articular
metaphysis, the pus can spread to the joint and cause acute pyogenic
arthritis e.g., hip, shoulder etc.
Diagnosis:
Parts of diagnosis Description
Age Childhood

 Acute onset of pain and swelling at the end of a bone

History A recent history of infection (Ex: sore throat, ear discharge etc.)

 Systemic symptoms like fever, malaise etc.

Chief complaints

 Pulse rate is very high and temperature is raised

 Acute tenderness near one of the largest joints
Examination

 Joint movement is restricted (pseudoparalysis)

 Local signs of inflammation (redness, edema, swelling,
warmth) are usually late features and signifies that pus has

 Blood: C‘P↑, ES‘↑, WBC cou t↑ (PMN leucocytes)

escaped from the interior of the bone.

 X-Ray: Earliest classic sign is periosteal new bone formation at

Investigation

the metaphysis (by the 2nd weeks)

 Confirmatory: The most certain way to confirm the clinical
diagnosis is to aspirate pus or fluid from the metaphyseal
 18

subperiosteal abscess/ extra-osseous soft tissues/ an adjacent

joint, followed by gram stain.
Treatment:
Supportive Analgesics at repeated intervals and IV fluid to correct dehydration
Splintage Simple skin traction/ plaster slab for comfort and prevent contracture
Antibiotics Blood and aspiration material is sent immediately, but the
administration of antibiotic should be prompt without waiting for
result. The empirical antibiotic recommendations are:
Age/ group Antibiotic of choice
Upto 6 months IV (Floxacillin + 3rd gen. cephalosporin*
6 months- 6 years -Do-
Older children + IV (Floxacillin + Fusidic acid)
previously fit adults
Elderly + previously IV (Floxacillin + 2nd/3rd gen. cephalosporin)
unfit adults
Sickle cell disease IV (3rd gen. cephalosporin/ fluoroquinolone~)
Drug addicts/ HIV -Do-
MRSA IV (Vancomycin + 3rd gen. cephalosporin)
Drainage If the clinical features do not improve within 36 hours of starting
treatment/ if there are signs of deep pus (swelling, edema,
fluctuation) / if pus is aspirated, the abscess should be drained by
open operation under general anesthesia.
Complications:
1. Chronic osteomyelitis
2. Acute pyogenic arthritis
3. Pathological fracture
4. Growth plate disturbances causing deformity of the limb.

Chronic osteomyelitis
Causes:
1. Delayed and inadequate treatment
2. Reduced host resistance (malnutrition/ HIV etc.)
 19

Diagnosis:


Parts of diagnosis Description


Chief complaints A chronic discharging sinus


The type discharge is sero-purulent


Pain & fever become evident in times of acute exacerbations.


Examination A chronic discharging sinus


Thickened, irregular bone when compared to the normal side


Mild tenderness on deep palpation


Stiffness of the adjacent joint may be present.
Investigation X-Ray:
 Thickening and irregularity of the cortices
 Patchy sclerosis giving the bone a honeycomb appearance
 Sequestrum and involucrum may be visible.
Treatment:
Aims of surgery:
1. Removal of dead bone
2. Elimination of dead space
3. Removal of infected granulation tissue and sinus.
Surgical options:
Option Description Presentation
Sequestrectomy A window is made in the overlying
involucrum and the sequestrum removed.
One must wait for adequate involucrum
formation before performing
sequestrectomy.
 20

Saucerization The bone-cavity is converted into a

'saucer' by removing its wall. This allows
free drainage of the infected material.

Curettage The wall of the cavity, lined by infected granulation tissue, is curetted
until the underlying normal-looking bone is seen.
Excision of the It is done when the affected bone can be excised en-bloc without
infected bone compromising the functions of the limb.
Amputation It is preferred in a long standing discharging sinus when sinus undergoes
malignant change.

Sequestrum, Ring sequestrum:

Introduction:
It is a dead piece of bone which is formed in some infective conditions of bone.
Common conditions associated with sequestrum:
1. Acute osteomyelitis
2. Chronic osteomyelitis
3. TB spine.
Pathogenesis:

 The bacteria gets lodged into the bone (commonly metaphysis) usually
1. In case of acute osteomyelitis:

 In response, the bone initiates an inflammatory reaction against the

through a hematogenous route.

 Whe the pus spread i to edullary cavity, travels alo g the Volk a ’s
invading bacteria, resulting in formation of inflammatory exudate (pus).

 The periosteum is thus lifted off the underlying bone, resulting in damage/
canal and ultimately come to the subperiosteal space.

 A segment of bone becomes avascular and dead.

cut off to the periosteal blood supply to a part of the bone.
 21

2. In case of chronic osteomyelitis:

Delayed and inadequate treatment of acute osteomyelitis results in the pus
giving the time to spread within medullary cavity and sub-periosteally;
resulting in a diminished blood supply and formation of a dead piece of
bone.

 In the commoner paradiscal type of spinal TB, the bacteria lodge in the
3. In case of TB spine:

 The granulomatous inflammation results in erosion of the margins of these

contiguous areas of two adjacent vertebrae.

 The nutrition of the intervening disc, which comes from the endplates of
vertebrae.

 This results in disc degeneration and sequestra formation and as the

the adjacent vertebrae is compromised.

process continues, complete destruction of the vertebra.

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Relevant operative procedures:

Sequestrectomy: This means the removal of sequestrum. If it lies within the
medullary cavity, a window is made in the overlying involucrum (it is the dense
sclerotic bone overlying a sequestrum) and the sequestrum removed. One must
wait for adequate involucrum formation before performing sequestrectomy.

Brodie’s a scess:
Introduction:
It is a special type of subacute osteomyelitis in which the ody’s defe ce
mechanisms have been able to contain the infection so as to create a chronic
bone abscess.
Common age of presentation: 11-20 years
Common sites:
Upper end of the tibia and lower-end of the femur.
Clinical features:
 The patient is usually a child or adolescent who has had chronic persistent
deep boring pain near one of the larger joints for several weeks or even
months.
 The pain may become worse at night and in some instances, it becomes
worse on walking and is relieved by rest.
 He or she may have a limp and often there is slight swelling, muscle wasting
and local tenderness.
 The temperature is usually normal and there is little to suggest an infection.
Laboratory investigations:
The WBC count and blood cultures usually show no abnormality but the ESR is
sometimes elevated.
Radiological features:
 The radiological appeara ce of Brodie’s a scess is diag ostic.
 The typical radiographic lesion is a circumscribed, round or oval radiolucent
cavity’ 1–2 cm in diameter surrounded by a halo of sclerosis.
 23

 Most often it is seen in the tibial or femoral metaphysis.

Management:
 Surgical evacuation and curettage is performed under antibiotic cover.
 If the cavity is large, it is packed with cancellous bone chips.

TB hip:
Introduction:
Hip is the second most common site for bone TB (after TB spine) is the
commonest cause of pain in the hip in children in countries where TB is still
prevalent.
Initial focus of infection:
1. Acetabular roof (most common)
2. Head of femur.
Stages along with clinical features:


Stage Pathology Clinical feature
Stage of Joint effusion Flexion, abduction and external rotation


synovitis (FAbER) deformity


Apparent lengthening of the affected limb.
Stage of early Damage to the Flexion, adduction and internal rotation


arthritis articular damage (FAdIR) deformity


Apparent shortening of the affected limb.
Stage of late Gross destruction of Flexion, adduction and internal rotation


arthritis articular cartilage, (FAdIR) deformity
femoral head ±

True shortening of the affected limb
acetabulum

Considerable restriction of hip movements.


Stage of Pathological Migrating (Wandering) acetabulum
advanced dislocation or Mortar and pestle appearance: Femoral
arthritis subluxation of the hip head and neck grossly destroyed, collapsed
and small in size.
 24

Radiological features:
1. Haziness of the bones around the hip: Earliest sign
2. Reduction of joint space: Due to arthritis of cartilage
3. Irregular outline of articular surface of bone: Because of destruction
process
4. Acetabular changes: Wandering acetabulum/ Mortar & pestle appearance.
Other diagnostic tools:
1. CBC: Lymphocyte count ↑
2. ESR: May be ↑
3. Aspiration of synovial fluid
4. Aspiration of cold abscess (if any)
5. Biopsy and histopathological examination from lesion
6. CXR: Should be routinely done to rule out pulmonary TB.
Treatment:
A. Conservative management:
I. Care of the hip: The affected hip is put to rest by immobilisation
using below-knee skin traction.
II. General care:
 High protein diet
 Control of infection by prompt initiation of anti-tubercular
chemotherapy. Start with HRZE for 3 months.
III. Gradual mobilisation of the hip.
B. Operative intervention:
I. FNAC/ Biopsy: When diagnosis is in doubt
II. Cold abscess: Aspiration/ evacuation
III. To provide a painless, mobile but unstable joint: Excision arthroplasty
(Girdlestone arthroplasty)
IV. To provide a painless, stable but fixed joint: Arthrodesis (surgical
fusion of the joint).
 25

Chapter 3: Upper limb

Fractures occurring due to fall on outstretched hand (FOOSH):
Depending on where the forces from FOOSH are applied, fractures and
dislocations can occur at the wrist, forearm or elbow.
Wrist fractures
Mechanism:
When falling on outstretched hand, palm strikes the ground with the wrist in
hyperextension.
Diagram shows lateral view of bones of
forearm and wrist: humerus (HUM),
which includes capitulum (CAP); radius
and radial head articulating with
capitulum; ulna and olecranon wrapping
around trochlea; and scaphoid (S)
articulating with distal articular surface of
radius.

Arrow indicates hyperextension of wrist

that occurs during fall on outstretched
hand. Inset shows enlargement of area
indicated by outline and rotated to
typical orientation of wrist radiographs.
Lightning bolts represent common sites
of fractures due to falls on outstretched
palm:

Fractures caused: A = Colles, B = Dorsal

Barton, C = Scaphoid.

Examples of wrist fractures resulting from FOOSH:

Example General description
Colles fracture Transverse fracture through the distal metaphysis of radius
Dorsal Burton Fracture through the dorsal rim of distal articular surface of
fracture radius
Scaphoid fracture Usually non-displaced fracture of the scaphoid
 26

Forearm and elbow fractures

Mechanism:
Not only does a FOOSH cause hyperextension of the wrist, but it also transmits an
axial load along the length of the forearm, from wrist to elbow, which may result
in specific patterns of fractures.

Diagram shows frontal view of bones of

forearm: humerus (HUM), which
includes capitulum (CAP) and trochlea
(TRO); radius with head articulating
with capitulum; ulna with olecranon
wrapping around trochlea; and carpus
as one unit. Falling on outstretched
hand (downward arrow) results in
transmission of axial forces up forearm
(upward arrows).

Examples of forearm and elbow fractures resulting from FOOSH:

(See pictures on next page)
Example General description
Both Bone Forearm Transverse fractures of the shafts of both the radius and
Fracture ulna, particularly seen in children
Monteggia Fracture- Ulnar shaft fracture with radial head dislocation
Dislocation
Galeazzi Fracture- Radius fracture with dislocation of the distal ulna at the
Dislocation distal radioulnar joint
Radial head fractures Simple radial head fractures are common and usually are
isolated injuries. Severely comminuted radial head
fractures are uncommon; ex.: Essex-Lopresti fracture.
 27

Monteggia Fracture-Dislocation
Galeazzi Fracture-Dislocation
Essex-Lopresti fracture:

I. Application of axial load to

radius alone, impacting radial
head into capitulum (CAP) and
causing comminuted radial
head fracture.
II. Asymmetric axial load between
radius and ulna causes tearing
along length of interosseous
membrane (IOM) and disrupts
distal radioulnar joint (DRUJ).

Volk ann’s ische ic contracture VIC :

Definition:
VIC is the result of vascular insult to deep tissues of limb producing ischemia,
primarily of the muscles and secondarily of nerves, as a sequel of compartment
syndrome (an elevation of interstitial pressure in a closed osseofascial
compartment).
Causes:
1. External compression (tight bandage/ plastering)
2. Crush injuries
3. Fractures
4. Post burn contracture
5. Repeated intra-arterial injections (in drug addicts)
6. Internal bleeding (hemophilia).
 28

Common sites:
1. Volar aspect of forearm
2. Hand and foot
3. Anterior and deep posterior compartments of leg
Pathology:

Raised intra-
Vascular Ischemia of Infarction of
compartmental
compromise muscles muscles
pressure

Muscles can't Replaced by Contracture

regenerate fibroous tissue (VIC)

Clinical features: (4Ps)

 Pain: It increases with extension of fingers i.e. stretching of flexor muscles.
So it is called stretching pain . Ge tle passive e te sio of fi gers causes
severe pain.
 Pallor: Earliest feature.
 Paresthesia: Late feature.
 Pulselessness: It is not a constant feature of VIC as radial pulse is often
found in ischemic hand.
Volkmann’s sign:
 When wrist is extended, MCP and IP joints become more flexed.
 When wrist is flexed, MCP and IP joints can be extended.
Management:
Impending VIC (It is a medical emergency)
 All bandage/ plasters/ splints are removed immediately.
 Limb is elevated to the level of heart.
 Elbow is straightened to 30° flexion.
 Limb is frequently observed for signs of ischemia.
 29

 If no improvement occurs, fasciotomy operation must be done to

decompress the osseofascial compartment.
Established VIC
Mild variety Splinting and physiotherapy.
Moderate Max page muscle slide operation + Neurolysis + Tendon transfer
Severe Scar excision +- Muscle slide +- Proximal row carpectomy +- Wrist
arthrodesis.

Colles fracture:
Introduction: It is the most common fracture in people >40 years of age.
Site: This is a transverse fracture of distal end of radius, at the cortico-cancellous
junction (2 cm proximal to distal articular surface).
Relevant anatomy: Normally, the radial styloid is about 1 cm distal to the ulnar
styloid. In Colles fracture, both the styloids lie almost at the same level.
Mechanism: Fall on an out-stretched hand/ post-menopausal osteoporosis.
Typical deformities:

 Dorsal displacement.
 Dorsal tilt.
 Lateral displacement.
 Lateral tilt.
 Impaction of fragments.
 Supination.

Clinical features:
The patient presents with pain, swelling and deformity of the wrist. On
examination, tenderness and irregularity of the lower end of the radius is found.
There may be a classical 'dinner-fork deformity'.
 30

The wrist is broadened and radially deviated with prominent ulnar head and there
is dorsal and lateral tilt. Wrist movements are restricted.
Radiological features:
 Most of the displacements are evident on X-Ray, except Supination which
can be appreciated only clinically.
 A-P view: Normally the distal articular surface of radius is faced medially.
When it faces laterally, a lateral tilt is present.
 Lateral view: Normally the distal articular surface of radius is faced
ventrally. When it faces neutral/ dorsal position, a dorsal tilt is present.
This dorsal tilt is the most characteristic displacement of Colles fracture.
Treatment:
 For an undisplaced fracture, immobilisation in a below-elbow plaster cast
for 6 weeks is sufficient.
 For displaced fractures, the standard method of treatment is manipulative
reduction followed by immobilisation in Colles' cast.
Technique of closed manipulation:
 The muscles of forearm must be relaxed, either by general or regional
anesthesia. The surgeon grasps the injured hand as if he were 'shaking
hands'.
 The first step is to disimpact the fragments which have often been driven
together. This is achieved by firm longitudinal traction to the hand against
the counter-traction by an assistant who grasps the arm above the flexed
elbow. Some displacements are corrected by traction alone.
 The surgeon now presses the distal fragment into palmar flexion and ulnar
deviation using the thumb of his other hand.
 31

 As this is done, the patient's hand is drawn into pronation, palmar flexion
and ulnar deviation. A plaster cast is applied extending from below the elbow
to the metacarpal heads, maintaining the wrist in palmar flexion and ulnar
deviation. This is Colles' cast.

Colles cast:

(a) In palmar flexion.

(b) In ulnar deviation.

Monteggia fracture-dislocation:
Introduction:
Fracture of the upper-third of the ulna with dislocation of the head of radius.
Mechanism of injury:
Fall on outstretched hand.
Types:
Type Angulation of ulnar Angulation of radial
fracture fragment dislocation
Extension Anteriorly Anteriorly
Flexion Posteriorly Posteriorly
 32

Clinical features:
 The ulnar deformity is usually obvious but the dislocated head of radius is
masked by swelling.
 A useful clue is pain and tenderness on the lateral side of the elbow.
 Wrist and hand should be examined for signs of injury to radial nerve.
Diagnosis:
With isolated fractures of the ulna, it is essential to obtain a true antero-posterior
[A-P] and true lateral view of the elbow. Always obtain a full length X-Ray of
forearm and hand.
Treatment:

Confirmation of diagnosis

Attempt at reduction under general

anaesthesia

Successful Failed

Open reduction and

Check X-rays weekly for
internal fixation using a
the initial 3-4 weeks
plate

Complications:
1. Nerve injury
2. Mal-union
3. Non-union.
 33

Dislocation of shoulder:
Shoulder joint is the most commonly dislocated joint among the large joints. The
causes behind this vulnerability are:
a. Shallow glenoid socket.
b. Extraordinary range of movement.
c. Sheer vulnerability of this joint during stressful activities of upper limb.
Anterior dislocation
Mechanism:
Dislocation is usually caused by a fall on the hand. The head of the humerus is
driven forward, tearing the capsule and producing avulsion of the glenoid labrum
(the Bankart lesion).
Clinical features:
 Severe pain.
 Patient support the affected arm with the opposite arm.
 The arm must always be examined for nerve and vessel injury before
reduction is attempted.
X-Ray:
 A-P view: It will show the overlapping shadows of the humeral head and
glenoid fossa, with the head usually lying below and medial to the socket.
 Lateral view: It will show the humeral head out of line with the socket.
 34

Treatment:
a. Stimson’s techni ue: The patient is left prone with the arm hanging over
the side of the bed. After 15 or 20 minutes the shoulder may reduce.
b. Hippocratic method: Gently increasing traction is applied to the arm with
the shoulder in slight abduction, while an assistant applies firm counter-
traction to the body.
c. Kocher’s method: TEA-I (Traction, external rotation, adduction and internal
rotation applied serially). This technique has been abandoned due to high
risk of injury to vessels and nerves and bone fracture.
Post-operative care:
 An x-ray is taken to confirm reduction and exclude a fracture.
 When the patient is fully awake, active abduction is gently tested to
exclude an axillary nerve injury and rotator cuff tear.
 The median, radial, ulnar and musculocutaneous nerves are also tested.
 The pulse is felt.
Complications:
Early complications Late complications
Rotator cuff tear Shoulder stiffness
Nerve injury (axillary nerve: most common) Unreduced dislocation (in the elderly)
Vessel injury (axillary artery: most common) Recurrent dislocation (in case of tear
Fracture-dislocation of proximal humerus of capsule of shoulder joint)
 35

Posterior dislocation
It is rare (<2% of all shoulder dislocations).
Mechanism:
Indirect force producing marked internal rotation and adduction needs be very
severe to cause a posterior dislocation. This happens most commonly during a fit
or convulsion or with an electric shock.
Clinical features:
 The arm is held in internal rotation and is locked in that position.
 The front of the shoulder looks flat with a prominent coracoid, but swelling
may obscure this deformity.
 When seen from above, the posterior displacement is usually apparent.
X-ray:
 A-P view: As humeral head is medially rotated, it looks abnormal in shape
(like an electric light bulb). The humeral head stands away from the glenoid
fossa (the empty glenoid sign).
 Lateral view: It is very important to take as it actually shows the posterior
dislocation/ subluxation.
Treatment:
Reduction of dislocation by ADLRI (adduction, lateral rotation and immobilization
done serially).
Complications:
 Unreduced dislocation.
 Recurrent dislocation and subluxation.

Recurrent dislocation of shoulder:

Introduction:
 If an anterior dislocation tears the shoulder capsule, repair occurs
spontaneously following reduction and the dislocation may not recur.
 36

 But if the glenoid labrum is detached (particularly in young patients) or the

capsule is stripped off in front of the neck of glenoid, repair is less likely and
recurrence is more common.
Epidemiology:
1. Common in young patients (~20 years)
2. Common in males
3. Most recurrences occur within first 2 years of first episode
4. May be classified into 2 types: traumatic and atraumatic.
Clinical features:
 History: The history is diagnostic. The patient complains that the shoulder
dislocates with relatively trivial everyday actions. Often he can reduce the
dislocation himself.
 Any doubt as to diagnosis is quickly resolved by
the apprehension test. if the patie t’s ar is
passively placed behind the coronal plane in a
position of abduction and lateral rotation, his
immediate resistance and apprehension are
pathognomonic.
Radiological features:
1. Hill sach’s lesion: Posterolateral humeral head compression fracture
2. Bankart’s lesion: Fracture-dislocation of anteroinferior aspect of glenoid.
Treatment:
Surgery is indicated for patients having >3 episodes. Commonly done operations
are:
1. Bankart's operation: Glenoid labrum and capsule are re-attached to the
front of the glenoid rim
2. Arthroscopic Bankart repair: Faster and easier rehabilitation but expensive
procedure
3. Putti-Platt operation: Double-breasting of the subscapularis tendon to
prevent recurrences.
 37

Supracondylar fracture of humerus:

Introduction:
This is one of the most serious fractures in childhood as it is often associated with
complications.
Mechanism:
 Fall on outstretched hand
 As the hand strikes the ground, the elbow is forced into hyperextension
resulting in fracture of the humerus above the condyles
 The fracture line extends transversely through the distal metaphysis of
humerus just above the condyles.
Types:
Depending upon the displacement of the distal fragment, supracondylar fracture
may be of 2 types:
A. Extension type (80%): The distal fragment is extended (tilted backwards) in
relation to the proximal fragment.
B. Flexion type (20%): The distal fragment is flexed (tilted forwards) in relation
to the proximal fragment.

Displacements and Radiological investigation:

Commonly, a supracondylar fracture is displaced. The distal fragment may be
displaced in the following directions:
Displacements Evident in which view of X Ray?
1. Proximal shift
2. Lateral/ medial shift A-P view
 38

3. Medial tilt
1. Proximal shift
2. Dorsal shift Lateral view
3. Dorsal tilt
Internal rotation is not visible in X Ray and only diagnosed clinically

Diagnosis:
Chief complaint
The child is brought to the hospital with a history of fall on outstretched hand
followed by pain, swelling, deformity and inability to move the affected elbow.
Examination

 Unusual posterior prominence of 

Early presentation Late presentation


Gross swelling makes the diagnosis difficult
tip of olecranon (because of dorsal Signs of ischemia may be present (5P: Pain,

 Since the fracture is supra- 

tilt) may be present pallor, paresthesia, paralysis, pulselessness)


Radial and ulnar pulses may be absent
condylar, the 3 bony point

Look for median nerve injury (pointing-index)
relationship is maintained, as in a Look for radial nerve injury (wrist-drop).
normal elbow.

Classification of supracondylar fracture:

Classification Description
Type 1 Undisplaced
 39

Type 2 Angulated fracture with posterior cortex still in continuity

Type 2a Distal fragment merely angulated
Type 2b Distal fragment is angulated and malrotated
Type 3 A completely displaced fracture

Treatment of choice according to classification

Classification Treatment of choice
Type 1 Immobilization in plaster slabs for 3 weeks, with elbow in maximal flexion
and forearm in pronation that does not jeopardize the radial pulse.
Extent of plaster is from deltoid muscle insertion to proximal palmar
crease just short of the knuckles, excluding the thumb.
Type 2a Reduction under general anesthesia by the following step wise maneuver:
1. Traction and counter traction above the elbow
2. Reduction by pressure over olecranon, while maintaining traction
3. Gradual elbow flexion and forearm pronation, while checking radial
pulse and capillary return.

Type 2b & 3 The fracture should be reduced under general anesthesia as soon as
possible, by the method described above, and then held with
percutaneous crossed smooth K-wires.
Other options for severe fractures:
1. Open reduction
2. Continuous traction (Ex: Dunlop traction).
 40

Complication of supracondylar fracture of humerus:


Nature Time Name


Immediate At the time of fracture Vascular injury
Nerve injury
Within first 2-3 days of fracture Volk a ’s ische ia

Early


Late Weeks to months after fracture Malunion


Myositis ossificans
Volk a ’s ische ic
contracture (VIC)
Immediate complications


Vascular injury


Commonly injured artery: Brachial artery
Mechanism of injury:
The brachial artery is usually injured by the sharp edge of the proximal


fragment.
Complications:
 Forearm edema and compartment syndrome
 Absent pulse
 Volkmann's ischemia (ischemic damage to flexors of forearm)
 Peripheral gangrene.
 Definite management options:
 Extension of elbow and removal of all dressings
 Repair/ grafting of vessel + fasciotomy
 Operative exploration in extreme cases.

 Commonly injured nerves:

Nerve injury

 Radial nerve
 Median nerve
 Ulnar nerve.
 Management:
 Loss of function is usually temporary and recovery is expected within
3-4 months.
 If there is no recovery then the nerve should be explored.
 41

Early complications
Volkmann’s ischemia
 Introduction:
This is an ischemic injury to the muscles and nerves of the flexor
compartment of the forearm caused by occlusion of brachial artery by a

 Commonly affected muscles:

complicated supracondylar fracture of humerus.

The muscles supplied by the anterior interosseous artery are most

susceptible to ischemic damage because this artery is an end-artery. Most
commonly affected muscles are the flexor pollicis longus and flexor

 Clinical features:
digitorum profundus (medial-half).

Early diag osis of Volk a ’s ische ia is of e tre e i porta ce.

 Severe pain in the forearm
 Stretch pain: Pain in the flexor aspect of forearm when fingers are
extended passively
 Inability to move fingers fully
 Tenderness on pressing forearm muscles.
 Treatment:
Volk a ’s ische ia is a e erge cy of highest order:
 Remove any splints or bandages
 Elevate the forearm
 Encourage to move the fingers
 If no improvement within 2 hours: Perform fasciotomy operation.

Late complications


Malunion


This is the commonest complication of a supracondylar fracture.
Cause:
 Failure to achieve good reduction
 Displacement of the fracture fragment within plaster.


Type of deformity: Cubitus varus.
Other a e: Gunshot deformity’.
 42

 Treatment: Supracondylar corrective osteotomy (French osteotomy).

 introduction:
Myositis ossificans

It is characterized by ectopic new bone formation around the elbow joint,

 Cause: Massage following the injury.

resulting in stiffness.

 Treatment:
 Early stages:
 Elbow is put to rest by an above-elbow slab
 Gentle elbow mobilization is started.
 Late stages:
Treatment options are:
 Excision of the myositic bone
 Excision arthroplasty of elbow.
Volkmann’s ischemic contracture VIC
 Introduction:
This is a sequel to Volkmann's ischemia. The ischemic muscles are gradually
replaced by fibrous tissue, which contracts and draws the wrist and fingers
into flexion.

If the peripheral nerves are also affected, there will be sensory loss and

 Clinical features: (4Ps)

motor paralysis in the forearm and hand.

 Pain: Pain in the flexor aspect of forearm when fingers are extended
passively. It is called stretchi g pai ’.
 Pallor: Earliest feature.
 Paresthesia: Late feature.
 43

 Pulselessness: It is not a constant feature of VIC.

Volkmann’s sign:
 When wrist is flexed, MCP and IP joints can be extended.
 When wrist is extended, MCP and IP joints become more flexed.

 Treatment:
Severity of deformity Treatment options
Mild Passive stretching of muscles using Volkmann’s splint
Moderate Maxpage operation: Here the flexor muscles are
released from their origin at medial epicondyle and ulna
Severe Bone operations such as shortening of the forearm
bones, carpal bone excision etc. may be required

Fracture clavicle:
Introduction:
In children the clavicle fractures easily, but it almost invariably unites rapidly
without complications. In adults this can be a much more troublesome injury.
Classification/ types:
Clavicle fractures are usually classified into 3 types on the basis of their location:
 44

Fracture clavicle

Group 1: Middle Group 2: Lateral Group 3: Medial

third fracture third fracture third fracture
(69-82%) (21-28%) (2-3%)

Group 2b:
Group 2a:
Coracoclavicular Group 2c: Intra-
Coracoclavicular
ligament torn/ articular fracture
ligament intact
detached*

[*Group 2b fractures are unstable and often cause asymptomatic non-union]

Mechanism of injury:
 Cause: Fall on outstretched hand/ shoulder
 In the common middle third fracture:
 The inner half is held upwards by the sternomastoid muscle and
 The outer fragment is pulled downwards by the gravity and pull by
pectoralis major muscle.

 In the less common lateral third fracture:

 2a: There is little displacement
 2b: There may be severe displacement.
 45

Clinical features:
Diagnosis is simple in most cases. There is a history of trauma followed by pain,
swelling, crepitus etc. at the site of fracture. One must look for any evidence of
neuro-vascular deficit in the upper limb on the affected side.
Imaging:
 X Ray of shoulder:
1. Antero-posterior view
2. 30⁰ cephalic tilt view
 The fracture is usually in the middle third of the bone, and the outer
fragment usually lies below the inner.
 With medial third fractures it is also wise to obtain X-Rays of the sterno-
clavicular joint.
Treatment:
Type of fracture Recommendations
Middle third Non-operative management: application of a sling for 1–3 weeks
(Group 1) until the pain subsides, followed by mobilization within the limits
of pain.
Lateral third 2a Non-operative management: application of a sling for 2–3
(Group 2) weeks until the pain subsides, followed by mobilization
within the limits of pain (as group 1).
2b Surgery to stabilize the fracture (reserved for cases of

 Use of a coracoclavicular screw

symptomatic non-union only):

 Plate and hook plate fixation

 Suture and sling techniques.
Medial third Non-operative management unless the fracture displacement
(Group 3) threatens the mediastinal structures.

Complications of fracture clavicle:

Early complication Late complication
Injury to subclavian vessels/ brachial Shoulder stiffness
plexus Symptomatic non-union
 46

Tennis elbow (lateral epicondalgia):

Introduction:
Pain and tenderness over the lateral epicondyle of the humerus is a common
complaint among tennis players, but even more common in non-players who
perform similar activities involving forceful repetitive wrist extension.
Pathology:
The extensor carpi radialis tendon (which automatically extends the wrist when
gripping) is pathological in tennis elbow.
Age of presentation: 30-40 years
Typical history:
 Pain comes on gradually, often after a period of unaccustomed activity
involving forceful gripping and wrist extension.
 It is usually localized to the lateral epicondyle, but in severe cases it may
radiate widely.
 It is aggravated by movements such as pouring out tea, turning a stiff door
handle, shaking hands or lifting with the forearm pronated.
Examination:
 The elbow looks normal; flexion and extension are full and painless.
 Characteristically there is localized tenderness at/ just below the lateral
epicondyle
 The pain can be reproduced actively by having the patient extend the wrist
with the elbow straight/ passively by stretching the wrist extensors (by the
e a i er acutely fle i g the patie t’s wrist with the forearm pronated).
 47

Treatment:
 90% of te is el ows’ will resolve spo ta eously withi 6–12 months.
 The first step is to identify, and then restrict, those activities which cause
pain.
Symptomatic treatment:
 The patient is initially treated with analgesics-anti-inflammatory drugs for a
week or so.
 If there is no response, a local injection of hydrocortisone at the point of
maximum tenderness generally brings relief.
Operative treatment:
Tennis elbow surgery may involve:
 Releasing the tendon
 Removing inflamed tissue from the tendon
 Repairing tendon tears.

Dupuytren’s contracture:
Introduction:
This is a condition characterized by a flexion deformity of one or more fingers due
to a thickening and shortening of the palmar aponeurosis.
Epidemiology:
Dupuytre ’s co tracture is co o i Europea s, epileptics receivi g phe ytoi ,
diabetic and cirrhotic patients.
Relevant anatomy:
 Normally, the palmar aponeurosis is a thin but tough
membrane, lying immediately beneath the skin of the palm.
 Proximally, it is in continuation with the palmaris longus
tendon.
 Distally, it divides into slips, one for each finger. The slip
blends with the fibrous flexor sheaths covering the flexor
tendon of the finger, and extends up to the middle phalanx.
 48

Pathoa ato ical cha ges i Dupuytre ’s co tracture:

 The esse tial pro le i Dupuytre ’s co tracture is proliferation of
myofibroblasts, the cause of which remains unknown.
 After an initial proliferative phase, fibrous tissue within the palmar
aponeurosis slowly contracts, drawing the fingers into flexion at the
metacarpophalangeal (MCP) and proximal interphalangeal joints (PIP).
 The ring finger is the one affected most commonly. The contracture is
generally limited to the medial 3 fingers.

History and chief complaint:

 The patient (usually a middle-aged man) complains of a nodular thickening
in the palm.
 Gradually this extends distally to involve the ring or little finger.
 Pain may occur early on but is seldom a marked feature.
 The palm is puckered, nodular and thick.
 If the subcutaneous cords extend into the fingers they may produce flexion
deformities at the MCP and PIP joints.
 About 60% of patients give a family history.
 49

Differential diagnosis:
1. Skin contracture: Previous skin laceration is obvious
2. Tendon contracture: Finger deformity changes with wrist position
3. PIP contracture: History of joint injury.
Treatment options:
1. Non-surgical:
a. High energy radiation therapy (usually X Ray)
b. Injection of enzyme (Collagenase clostridium histolyticum).
2. Surgical (from mild to severe cases):
a. Needle fasciotomy
b. Open fasciotomy
c. Fasciectomy under general anesthesia.

Mallet finger:
Introduction:
After a sudden flexion injury (e.g. stubbing the tip of the finger), the terminal
phalanx droops and cannot be straightened actively.
Types of injuries:
2 broad types of injuries can occur in a mallet finger:
1. Avulsion of the most distal part of extensor tendon
2. Avulsion of a bone fragment (small/large) from base of terminal phalanx.
 50

Treatment:
The 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.
Duration of splint:
1. For tendon avulsion: 8 weeks constant + 4 weeks only at night
2. For bone avulsion: 6 weeks (as bone heals early than tendon).

Complications:
1. Non-union
2. Persistent droop
3. Swan neck deformity.

Trigger finger/ Digital Tenovaginosis:

Introduction:
It is a condition characterized by
entrapment of a flexor tendon at the
entrance into fibrous digital sheath,
preventing free gliding of that contained
flexor tendon.
Epidemiology:
 Female > Male
 Common age group: 40-60 years
 Predisposing diseases:
1. Diabetes mellitus
2. Rheumatoid arthritis.
Pathophysiology:
 The flexor tendon can become irritated as it slides through the tendon
sheath tunnel. As it becomes more and more irritated, the tendon may
 51

thicken and nodules may form, making its passage through the tunnel more
difficult.
 The tendon sheath may also thicken, causing the opening of the tunnel to
become smaller.
Symptoms:
 Initially, the only symptom is pain at the base of the affected finger,
especially on trying to passively extend
the finger.
 Any digit may be affected, but the thumb,
ring and middle fingers most commonly;
sometimes several fingers are affected.
 The affected finger initially remains bent
at the PIP joint but with further effort it
suddenly straightens with a snap.
 A tender nodule can be felt in front of the
MCP joint and the click may be
reproduced at this site by alternately
flexing and extending the finger.
Treatment:
Injection of
Recurrent cases (especially in
In early stage corticosteroid into the
diabetics)
digital tendon sheath

Operation: The fibrous sheath is incised

A second injection is often needed Refractory cases
until the tendon moves freely

Fracture olecranon:
Introduction:
This is usually seen in adults. It results from a direct injury as in a fall onto the
point of the elbow.
 52

Clinical Presentation:
Patients typically present with the upper extremity supported by the contralateral
hand with the elbow in relative flexion.
Clinical evaluation:
 Look: Abrasions over olecranon or hand can be indicative of the mechanism
of injury
 Feel: Palpable defect at fracture site
 Move: Inability to extend the elbow actively against gravity indicates
discontinuity of triceps mechanism
 Neurosensory evaluation: Associated ulnar nerve injury is possible,
especially with comminuted fractures from high-energy injuries.
Mayo classification of olecranon fracture with treatment options of choice:
Type Subtype Description Treatment of choice
1 1A Non-comminuted Long arm cast or posterior splint
(Nondisplaced) 1B Comminuted with early mobilization
2 (Displaced, 2A Non-comminuted Tension band wiring/
stable): Intramedullary fixation
Most common 2B Comminuted Tension band wiring + Additional
type interfragmentary plate & screw
fixation/ Fragment excision &
triceps advancement (in elderly)
3 (Displaced, 3A Non-comminuted Rigid plate and screw fixation
unstable) 3B Comminuted Rigid plate & screw fixation ±
External fixator ± Bone graft

Complications:
1. Hardware prominence requiring removal (most common)
2. Stiffness
3. Non-union
4. Miscellaneous:
a. Ulnar neuropathy
b. Post-traumatic arthritis
 53

c. Infection
d. Heterotopic ossification.

Carpal tunnel syndrome:

Definition:
It is a syndrome characterized by compression of median nerve as it passes
beneath the flexor retinaculum.
Age group involved: 40-50 years, common in females.

Causes:
MEDIAN TRAP
 Myxoedema
 Edema premenstrually
 Diabetes
 Idiopathic
 Agromegaly
 Neoplasm
 Trauma
 Rheumatoid arthritis
 Amyloidosis
 Pregnancy.
 54

Clinical features:
The patient is usually a middle aged woman, complaining of:
a. Tingling and numbness in thumb and radial 2½ fingers.
b. The tingling is more prominent during sleep.
c. There is a feeling of clumsiness while carrying out fine
movements.
d. Sensory symptoms can often be reproduced by
percussing over the median nerve (Tinel’s sign) or by
holding the wrist fully flexed for less than 60 seconds
(Phalen’s test).
Treatment:
Temporary relief:
1. Steroid injection into carpal tunnel.
2. Light splints that prevent wrist flexion.
Definitive surgery:
Open surgical division of transverse carpal ligament followed by decompression of
median nerve.

Frozen shoulder:
Definition:
It is a well-defined disorder characterized by progressive pain and stiffness of the
shoulder which usually resolves spontaneously after about 18 months.
Associated conditions:
The disease is commoner in diabetics.
Clinical features:
1. The patient, aged 40–60, may give a history of trauma, often trivial,
followed by pain in the arm and shoulder. Pain gradually increases in
severity and often prevents sleeping on the affected side.
2. After several months it begins to subside, but as it does so stiffness
becomes an increasing problem, continuing for another 6–12 months after
pain has disappeared.
3. Gradually movement is regained, but it may not return to normal and some
pain may persist.
 55

Examination:
Apart from slight wasting, the shoulder looks quite normal; tenderness is seldom
marked. The cardinal feature is a stubborn lack of active and passive movement in
all directions.
Diagnosis:
The diagnosis of frozen shoulder is clinical, resting on 2 characteristic features:
1. Painful restriction of movement in the presence of normal X-Rays; and
2. A natural progression through three successive phases (pain, stiffness and
regaining of movements).
Treatment:

 Analgesics and anti-inflammatory drugs to relieve pain

Conservative treatment

 Reassure the patient

 E ercise: ‘egular pe dulu ’ e ercise is encouraged where the patient

 Manipulation under general anesthesia

leans forward at the hips and moves his arm like a pendulum

 Injecting a large volume of sterile saline into the joint under pressure.

 Arthroscopic capsular release: Indicated only in prolonged and disabling

Surgical treatment

restriction of movement which fails to respond to conservative treatment.

De-Quervain’s disease:
Introduction:
De-Quervai ’s disease is a ste osi g te osy ovitis characterized y painful
thickening of the common tendon sheath containing abductor pollicis longus and
extensor pollicis brevis tendons at the radial styloid process.
Risk factors:
The predisposing factors are related to repetitive strain injury while doing
activities that requires the thumb to be held in abduction and extension:
 Grasping/ pulling/ pushing
 Bowling
 Golf and fly-fishing
 Piano-playing
 56

 Sewing
 Typing
 Use of Mouse.
Women are affected more often than men. The syndrome commonly occurs
during and after pregnancy.
Clinical features:
 Pain on the radial side of the wrist
 Tenderness is most acute at the very tip of the radial styloid
 A history of the predisposing activities is commonly present
 The pathognomonic sign is elicited by Finkelstein’s
test: The examining physician grasps the thumb
and ulnar deviates the hand sharply. If there is an
increased pain in the radial styloid process and
along the length of the extensor pollicis brevis and
abductor pollicis longus tendons, then the test is
positive for De Quervai ’s disease.
Treatment:

Rest + Splintage +
In early stage If failed
NSAIDS

Operation (Slitting the

Corticosteroid
thickened tendon
injection into the Resistant cases
sheath) [Danger: Injury
tendon sheath
to the radial nerve]
 57

Chapter 4: Lower limb

Fracture of patella, Mechanism:
Introduction:
Patella fracture is one of the most common knee injuries.
Mechanism of injury:
The mechanism of injury may be direct or indirect.
 In a direct injury, as may occur by a blow on the anterior aspect of the
flexed knee, usually a comminuted fracture (a fracture causing formation of
>2 separated bone components) results. The comminution may be limited
to a part or whole of the patella. The latter is also called a stellate fracture.
 In an indirect injury, a sudden violent contraction of the quadriceps in a
flexed knee gives rise to a fracture with the fracture-line running
transversely across the patella, dividing it into 2; the so-called two-part
fracture.

Types of patella fractures:

a) Two-part fracture

b) Stellate fracture

Clinical features:
Symptoms:
 Pain and swelling over the knee (main symptoms)
 Additional symptoms may include:
 58

a. Inability to straighten the knee

b. Inability to walk.
Signs:
 Bruising (a sign of direct trauma)
 Knee may be swollen (due to hemarthosis resulting from trauma)
 Crepitus may be felt (in case of comminuted fracture)
 Gap between fracture fragments may be felt (in case of displaced fracture)
 Extensor lag: The patient will not be able to lift his leg with the knee in full
extension; it remains in a position short of full extension (due to disruption
of the extensor apparatus).
Diagnosis:
X Ray (A-P and Lateral view of knee joint) will show a fracture with wide
separation of fracture fragments. A sunrise/ skyline view may be required.

Treatment:
1. Initially:
 Ice application,
 Cylinder plaster slab (from above ankle to the groin).
 59

2. Non-operative:
I dicated for closed fractures + i i u displace e t ( 2 c ) + i tact
extensor retinaculum.
 Cylinder plaster cast for 6-8 weeks
 Isometric quadriceps exercises
 Encouragement of early weight bearing
 After cast removal, gradual knee flexion and isotonic quadriceps
exercises are started.
3. Operative:
I dicated for fracture with 2 c displace e t/ extensor retinaculum
tears/ open fractures.
Operative options are:
 Tension band wiring
 Circumferential wiring
 Partial patellectomy.

Ruptured tendoachilles:
Epidemiology:
Rupture of tendoachilles is common in sports requiring an explosive push-off.
Ex: Football, Tennis, Badminton etc.
Predisposing factors:
1. Poor muscle strength and flexibility
2. Failure to warm up and stretch before sport
3. Previous injury/ tendinitis
4. Previous H/O corticosteroid injection.
Typical site of rupture:
The typical site for rupture is at the vascular atershed’ area a out 4 cm a ove
the insertion of the tendon, an area where the blood supply to the tendon is
poorer than elsewhere.
 60

Clinical feature:
A ripping or popping sensation is felt, and often heard, at the back of the heel. The
patient will often report having looked round to see who had hit them over the
back of the heel, the pain and collapse are so sudden.
Examination:
 Plantar flexion of the foot is usually inhibited and weak.
 There is often a palpable gap at the site of rupture; bruising comes out 1-2
days later.
 Calf s ueeze test Thompson’s/ Simmond’s test :
 It is diagnostic of Achilles tendon rupture
 Normally, with the patient prone, if the calf is squeezed the foot will
plantarflex involuntarily
 If the tendon is ruptured the foot will remain still.

Treatment:
Non-operative:
1. Plaster cast/ special boot with the foot in equinus (plantar flexion)
2. Physiotherapy to be started within 4-6 weeks.
Operative:
1. Percutaneous surgery
2. Open surgery (in serious rupture).
 61

Avascular necrosis/ osteonecrosis of femoral head:

Mechanism/ Pathophysiology:
1. Traumatic: After a fracture through the neck, all the
medullary blood supply and most of the capsular
blood supply to the head are cut off. The viability of
the femoral head may therefore depend almost
entirely on the blood supply through the ligamentum
teres. If this blood supply is insufficient, avascular
necrosis of a segment or whole of the head occurs.
2. Non-traumatic: Over 80% of these cases are
associated with high-dosage corticosteroid medication or alcohol abuse.

High dose
Fat cell
corticosteroid ↑Marrow fat Sinusoidal Trabecular
swelling in the Ischemia
and/or volume compression bone death
marrow
alcohol abuse

A small part is attributed to coagulopathies like sickle cell disease

(increased coagulability), SLE (antiphospholipid deficiency); where the
primary mechanism is arterial occlusion.
Among the infective causes, TB hip is an important issue to look for.
Clinical features:
 The earliest stage of bone death is asymptomatic; by the time the patient
presents, the lesion is usually well advanced.
 Pain is a common complaint. It is felt in or near hip joint and only with
certain movements.
 In the later stages the joint becomes stiff and deformed.
Investigations:
1. MRI: It is the most reliable way of diagnosing marrow changes and bone
ischemia at a comparatively early stage.
 62

2. Bone scan: More often the picture is dominated by an increased activity,

reflecting hyperaemia and new bone formation in the area around the
infarct. Sometimes it may also show a cold’ area, particularly if a large
segment of bone is completely avascular (e.g. after fracture of the femoral
neck).
3. X-Ray: The early signs of ischemia cannot be detected by plain x-ray
examination. They appear usually 3 months after the onset of ischemia:
 Early stages: An area of increased radiographic density appears in the
subchondral bone. Soon afterwards, suitable views may show a thin
tangential fracture line just below articular surface (Crescent sign).
 Late stages: Distortion of the articular surface and intense sclerosis,
Note: The joint space retains its normal width because the articular
cartilage is not destroyed until very late.
ARCO staging of AVN of femoral head:
Stage Description
0 Patient asymptomatic and all clinical investigations are normal but
biopsy shows osteonecrosis
1 X-rays normal. MRI or radionuclide scan shows osteonecrosis
2 X-rays and/or MRI show early signs of osteonecrosis but no distortion of
bone shape or cresce t sig ’
3 X-ray shows crescent sign’ ut fe oral head still spherical
4 Signs of flattening or collapse of femoral head
5 Changes above + Loss of joint space (secondary osteoarthritis)
6 Changes above + Marked destruction of articular surfaces

Treatment options:
1. In young individuals: Arthrodesis/ Bipolar arthroplasty/ Meyer’s procedure
2. In elderly individuals: Hemi-replacement arthroplasty
3. Where there is an associated damage to the hip: Total hip replacement.
 63

Fracture neck femur: types and complications.

Classification of fracture neck femur:
A. Anatomical classification:
Subcapital A fracture just below the head.
Transcervical A fracture in the middle of the neck.
Basal A fracture at the base of the neck.

The more proximally the fracture located, the worse the prognosis.
B. Pauwel’s classification:
This classification is based on the angle of inclination the fracture line
makes in relation to the horizontal plane (Pauwel's angle).
Type 1 Pauwel angle is <30°.
Type 2 Pauwel angle is 30°-50°.
Type 3 Pauwel angle >50°.

The more the angle (higher type), the more unstable is the fracture, and
worse the prognosis.
 64

C. Garden’s classification:
This is based on the degree of displacement of the fracture (mainly
rotational displacement) . The degree of displacement is judged from
change in the direction of the medial trabecular stream of the neck in
relation to the bony trabeculae in the weight-bearing part of the head and
acetabulum.

Stage 1 The fracture is incomplete with the head tilted in

posterolateral direction so that there is an obtuse angle
laterally at the trabecular stream.
Stage 2 The fracture is complete but undisplaced so that there is a
break in the trabecular stream with little angulation.
Stage 3 The fracture is complete and partially displaced. As the
distal fragment rotates externally, it causes internal
rotation of the head.
Stage 4 The fracture is complete and fully displaced. As the distal
fragment rotates further outwards, it loses contact with
the head, which springs back to its original position.

Complication of fracture neck of femur:

1. Non-union:
It is due to inadequate immobilisation and poor blood supply to the
proximal fragment. The main complaint is pain and inability to bear weight
on the affected limb. The limb is short and externally rotated.
 65

Treatment:
 In elderly patients: Replacement arthroplasty.
 In younger patients:
 Neck reconstruction.
 Pauwel’s osteoto y.
2. Avascular necrosis:
After a fracture through the neck, all the medullary blood supply and most
of the capsular blood supply to the head are cut off. The viability of the
femoral head may therefore depend almost entirely on the blood supply
through the ligamentum teres. If this blood supply is insufficient, avascular
necrosis of a segment or whole of the head occurs.
Treatment:
 In elderly patients: Hemi-replacement arthroplasty.
 In younger patients:
 Arthrodesing the hip.
 Bipolar arthroplasty.
 Meyer’s procedure.
3. Osteoarthritis:
It develops following fracture of the neck of the femur after a few months
to a few years. It occurs due to:
a. Avascular deformation of the head; or
b. Union in faulty alignment.
The patient presents with pain and stiffness of the joint. Initially the pain is
intermittent, but later it persists.
Treatment:
 In elderly patients: Total hip replacement.
 In younger patients:
 Inter-trochanteric osteotomy.
 Arthrodesing the hip.
 66

Chapter 5: Spine and vertebra

Slipped disc:
Relevant anatomy:
The intervertebral disc consists of three distinct components:
1. Nucleus pulposus: Inner structure containing
gelatinous material
2. Annulus fibrosus: Outer structure containing
fibro-cartilaginous tissue
3. Cartilage end-plates: Thin layer of hyaline
cartilage in between vertebral bodies which help
maintain nutrition in intervertebral discs.
Pathophysiology:

Nucleus degeneration Disc protrusion Disc extrusion (the nucleus

(weakening of fragmentation comes out of the annulus
of nucleus and posterior part (the nucleus tends to bulge though it has yet not lost
of annulus) through the defect) contact with the parent disc)

Degeneration and joint

Disc sequestration (with a
complete rupture, part of the
nucleus lose contact with
parent disc and lie free in the
spinal canal)
displacement: With chronic
Stage of repair: Residual
degeneration, the disc space
nucleus fiibrosed, extruded
narrows and posterior facet
nucleus fibrosed and calcified
joints are displaced, giving
rise to osteoarthritis
 67

Common level: The commonest level of disc prolapse is between L4-L5 in the
lumbar spine and C5-C6 in the cervical spine.
Common site of exit: The site of exit of the nucleus is usually posterolateral.
Clinical features:
 Common age of presentation: 20-40 years
 Commonest symptom: LBP ± Sciatica
 LBP may be acute or chronic in onset:
 An acute backache is severe with the spine held rigid by muscle
spasm, and any movement at the spine painful
 In chronic backache, the pain is dull and diffuse, usually made worse
by exertion, forward bending, sitting or standing in one position for a
long time and relieved by rest.
 Sciatic pain radiates to the gluteal region, the back of the thigh and leg.
 Neurological symptoms:
 They may occur when prolapsed disc compresses over a nerve
 Patie t co plai s of paraesthesia, ost ofte descri ed as pi s a d
needles’ correspo di g to the dermatome of the compressed nerve
root
 There may be numbness in the leg or foot.

 Cauda equina syndrome*:

 It occurs when large disc material compresses the theca and roots:
I. Irregular LMN type paralysis in the lower limbs
II. Bilateral absent ankle jerks
III. Hypoaesthesia in the region of L5 to S4 dermatomes
IV. Urinary and bowel incontinence.
Clinical examination:
1. Posture: The patient stands with a rigid, flattened lumbar spine. Whole
trunk is shifted forwards on the hips. The trunk is tilted to one side.
2. Movements: The patient is unable to bend forwards; any such attempt
initiates severe muscle spasm in the paraspinal muscles.
 68

3. Tenderness: There is diffuse tenderness in the lumbo-sacral region,

localized tenderness is found occasionally.
4. Straight leg raising test (SLRT): A positive SL‘T at 40° is suggestive of root
compression.
5. Neurological examination:
 A careful neurological examination would reveal a motor weakness,
sensory loss or loss of reflex corresponding to the affected nerve
root.
 Of special importance is the examination of the muscles of the foot
supplied by L4, L5 and S1 roots, as these are the roots affected more
commonly.
 The extensor hallucis longus muscle is exclusively supplied by L5 root
and its weakness is easily detected by asking the patient to dorsiflex
the big toe against resistance.
Investigation:
MRI is the investigation of choice.
Treatment:
 Conservative management:
 Complete bed rest for 2-4 days: It is most important
 Drugs: Analgesics and muscle relaxants
 Physiotherapy.
 Operative management:
Indications:
 Failure of conservative treatment
 Cauda equina syndrome
 Severe sciatic tilt.
Operative techniques:
 Fenestration
 Laminotomy
 Hemi-laminectomy
 Laminectomy.
 69

Spondylolisthesis:
Introduction:
Spondylolisthesis is defined as forward displacement of a vertebra over the one
below it.
Common site:
 Between L4 and L5
 Between L5 and S1.
Relevant anatomy:
Normally, forward displacement of a vertebral body is prevented by:
1. Engagement of its articular processes with that of the vertebra below it
(most contribution)
2. Intervertebral disc and ligaments (less contribution).
- Any disturbance in these mechanisms may lead to spondylolisthesis.
Types:
There are 6 types of spondylolisthesis:
1. Lytic/ isthmic type (50%):
 This is the commonest variety.
 There is either a defect in pars interarticularis (part of the vertebra
bridging the superior and inferior articular facets) or elongation of the
pars
 The defect allows the separation of the two halves of the vertebra
(anterior and posterior).
2. Degenerative (25%):
 Common in elderly people
 The posterior facet joints becomes unstable because of osteoarthritis,
permitting forward slip.
3. Dysplastic (20%):
 The superior sacral facets are congenitally defective, leading to slow but
severe displacement
 Associated anomalies (usually spina bifida occulta) are common.
 70

4. Post-traumatic:
Unusual fractures may result in destabilization of the lumbar spine.
5. Pathological:
Bone destruction (due to TB or neoplasm) may lead to vertebral slipping.
6. Iatrogenic:
Excessive operative removal of bone in decompression operations may
result in progressive spondylolisthesis.
Clinical features:
 Age of presentation:
- Isthmic variety: Adolescents and young adults
- Degenerative variety: Elderly people.
 Principle symptom is back pain ± sciatica.
 Symptoms become worse on standing or walking.
 On examination, following signs may be detected:
- Visible or palpable 'step' above the sacral crest
- Hamstring tightness (as evidenced by SLRT)
- Increased lumbar lordosis.
Diagnosis:
 Diagnosis is confirmed by X-Ray.
 Lateral view shows the forward shift of the upper part of the spinal column
on the stable vertebra below.
 Oblique view shows defect in pars
interarticularis.
- Normal: Scottish dog sign
- Spondylolisthesis: Head of the
Scottish dog’ is separated fro
neck.
Management:
Degree Symptom Management
Mild No symptoms No treatment is required
Mild Mild symptoms Conservative: Brace and spinal
exercises
 71

Moderately  Symptoms hampering An operation may be required:

 Slip 50%
severe or more daily activity Decompression of the
compressed nerves if any,
 Neurological followed by fusion of the
compression is severe affected segments of the spine.

TB spine/ Pott’s disease, Clinical features:

Introduction:
Bone is the 2nd most common site of TB (after lung) and the spine is the
commonest site of bone TB; the dorso-lumbar spine being the one affected most
frequently.
Source of infection:
TB of the spine is always secondary. The bacteria reach the spine via the
hematogenous route, from the lungs or lymph nodes. It spreads via the para-
vertebral plexus of veins.
Types:

1. Paradiscal type (98%):

Lower ½ of one vertebra + Upper ½ of adjacent vertebra + Intervening disc
are involved (all have a common blood supply).
2. Central type:
Body of a single vertebra is affected, leading to early collapse of the
weakened vertebra.
 72

3. Anterior type:
Infection is localised to the anterior part of the vertebral body, involving
anterior longitudinal ligaments.
4. Posterior type:
Posterior complex of the vertebra [pedicle, lamina, spinous process and
transverse process] is affected.
Clinical features:
 Back pain: Commonest symptom
 Radicular pain
 Stiffness: Earliest symptom
 Cold abscess: May present as a para-vertebral swelling
 Gibbus: Gradually increasing prominence of the spine
 Tenderness over spinous process
 Paraplegia: Most serious complication in neglected cases ->
I. Ankle/ patellar clonus: Earliest sign
II. Spastic paraplegia (early) -> Flaccid paraplegia (late).
Radiological changes:
 Early changes:
I. Reduction of disc space: Earliest change
II. Localized osteopenia.
 Late changes:
I. Collapse of vertebral body: Seen in central type
II. Aneurysmal sign: Sometimes seen in anterior type
III. Evidence of cold abscess:
 Paravertebral abscess: Seen in Paradiscal type
 Retropharyngeal abscess: Seen in TB cervical spine
 Psoas abscess: Seen in dorso-lumbar/ lumbar TB
Other diagnostic modality:
1. CT scan: May detect a small abscess undetected by standard X-Ray
2. MRI spine
3. Definitive diagnosis is by biopsy and culture.
 73

Treatment:
o Conservative management:
o This consists of providing rest to the spine during the acute phase,
followed by guarded mobilisation.
o High protein diet
o Control of infection by prompt initiation of anti-tubercular
chemotherapy. Start with HRZE for 3 months.
o Operative management:
o Cold abscess: Aspiration and evacuation
o Indications of surgery:
I. Patients not responding to conservative management
II. Patie ts with eurological co plicatio s/ Pott’s paraplegia
III. Recurrence of the disease
IV. Doubtful diagnosis.
o Surgical procedures of choice: Anterolateral decompression or Anterior
decompression.

Gibbus:
Introduction:
Gibbus deformity is a short-segment structural thoracolumbar kyphosis resulting
in sharp angulation of spine.
Common causes:

Gibbus deformity

Congenital Acquired

Achondroplasia Osteomyelitis Compression fracture

Cretinism Pyogenic spinal osteomyelitis Osteoporosis

Hurler syndrome TB spine (Pott's disease) Vertebral metastasis

 74

Associated clinical features and investigations:

Suspected cause Associated clinical features to look for Investigation
Acquired causes
Pyogenic spinal Symptoms are similar in both type. Symptoms of CBC, CRP, ESR, MRI
osteomyelitis toxicity may be present especially in pyogenic spine, aspiration and
TB spine osteomyelitis (fever, swelling at infection site, night biopsy from a cold
sweat), persistent back pain, stiffness, muscle abscess.
spasms, cold abscess, neurological deficit.
Osteoporosis Commonly seen in elderly patients; presents with Serum Ca++, PO4---,
fragility fractures especially at vertebral column Vit-D, PTH, ALP, Dual-
(back pain ± sciatica), ribs, hip and wrist. energy X-ray
absorptiometry (DXA)
Vertebral Look for any symptom(s) of associated underlying MRI
metastasis primary source of cancer in the body.
Congenital
Achondroplasia Short stature in infants, shortening of limbs and Can be detected by
fingers, large head with prominent forehead, small prenatal ultrasound
midface with flattened nasal bridge, kyphosis/ and a complete
lordosis. skeletal survey
Cretinism Mild: Excessive sleeping, poor muscle tone, low or Serum FT4, TSH;
hoarse cry, infrequent bowel movements, often a Tc-99m
exaggerated jaundice and low body temperature. thyroid scan is done
Severe: Large anterior fontanel, persistence of a to rule out any
posterior fontanel, an umbilical hernia and a large structural anomaly
tongue (macroglossia).
Hurler’s syndrome Dwarfism, enlarged liver, spleen, heart; recurrent Urine tests, Enzyme
URTI/ ear infections, distinct facial features (flat assays (detects
face, depressed nasal bridge and bulging forehead), excess
inguinal/ umbilical hernia. mucopolysaccharide)

Treatment:
According to the underlying cause.
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Spina bifida:
Definition:
Spina bifida is a congenital disorder where two halves of the posterior vertebral
arch fail to fuse at one or more levels.
Developmental background:
 The vertebral bodies develop from the mesoderm around the notochord.
 From the centre of each body extend two projections which grow around
the neural canal to form the vertebral arch.
 The two halves of the arch fuse in the thoracic region, from where the
fusion extends up and down.
 Failure of fusion of these arches gives rise to spina bifida. It is often
associated with mal-development of the spinal cord and the membranes.

Types:
According to the severity of lesion, spina bifida is of two types:
a. Spina bifida occulta.
b. Spina bifida cystica.
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Spina bifida occulta:

 It is the mildest and commonest form of spina bifida.
 In most cases, there is only a midline defect between the
laminae. Most cases are discovered incidentally on spine X
Rays (defect lies commonly at L5 level).
 When several vertebrae are involved, some tell-tale defects
in the overlying skin may be seen. Ex.: a dimple, a pit, a tuft
of hair.

Spina bifida cystica:

 It is the severe form of spina bifida.
 Here vertebral laminae are missing and the contents of the vertebral canal
prolapse through the defect.
The abnormality takes one of several forms discussed below:

a. Meningocele:
 It is the least serious abnormality.
 Here the dura matter is open posteriorly but the
meninges are intact and a CSF-filled meningeal sac
protrudes under the skin.
 The spinal cord and nerve roots remain inside the
vertebral canal and there is usually no neurological
abnormality.

b. Myelomeningocele:
 It is the most common and most serious abnormality.
 It usually occurs in the lower thoracic spine or the lumbosacral
region.
 Part of the spinal cord and nerve roots prolapse into the
meningeal sac.
 In some cases the neural tube is fully formed and the sac is
covered by a membrane and/or skin: a closed’
myelomeningocele.
 77

 In others the cord is in a more primitive state, the unfolded neural

plate forming the roof of the sac: an open’ myelomeningocele. It
is always associated with a neurological deficit distal to the level
of the lesion.

Myelomeningocele

Closed Open
variety variety

 If neural tissue is exposed to the air, it may become infected,

leading to more severe abnormality and even death.

Clinical features:
In spina bifida occulta:
 Normal people.
 A posterior midline dimple.
 A tuft of hair.
 A pigmented nevus.
 Children may present with mild neurological symptoms: enuresis, urinary
frequency or intermittent incontinence; neurological examination may
reveal weakness and some loss of sensibility in the lower limbs.

In spina bifida cystica:

 A saccular lesion is present at birth overlying the lumber spine, often
covered by membrane +/- skin.
 There is almost always some sort of neurological deficits like:
 Equinovarus or calcaneovalgus of the feet,
 Recurvatum of the knee,
 78

 Hip dislocation,
 Loss of sensation and sphincter control.
 Signs of hydrocephalus.
Investigations:
1. X-Ray and CT scan: Extent of bony lesion and other vertebral anomalies.
2. MRI: Assessment of neurological deficits.
Treatment:
Age Procedure
1 day Close skin defect
1 week Ventriculo-caval shunt
1 month Stretch and strap
6 months- 3 years Orthopaedic operations
Whenever needed Urogenital operations
 79

Chapter 6: Pediatric age group

Greenstick fracture:
Introduction:
Greenstick fracture is a special type of pediatric incomplete long bone fracture.
Because a child's bones are much more flexible than adult bone, an incomplete,
or 'greenstick' fracture may occur. A "greenstick fracture" means that one side of
the fracture has broken and one side is bent.
Pathophysiology and mechanism of injury:
 Greenstick fractures occur when the force applied to a
bone results in bending of the bone such that the
structural integrity of the convex surface is overcome,
resulting in fracture of the convex surface.
 However, the bending force applied doesn't break the
bone completely and the concave surface of the bent
bone remains intact.
 This can occur following an indirect trauma following a
fall on an outstretched arm/ a direct blow.

Clinical features:
Similar to a classical long bone fracture:
 Pain at the injured area
 There may be swelling and redness at fracture site
 The child may cry inconsolably
 As Greenstick fractures are stable (continuity of bone intact), they only
causes a bend at the injured part, rather than a deformity.
Diagnosis:
X Ray is diagnostic. It shows a fracture which is usually:
 Mid-epiphyseal
 Incomplete
 Angulated.
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Treatment:
 Most fractures of the arms and legs require a cast to keep the bones in
good alignment while the break heals. If the bones are in a poor alignment,
they may need to be repositioned, typically under sedation.
 X-rays are required in a few weeks to make sure the fracture is healing
properly, to check the alignment of the bone, and to determine when a cast
is no longer needed. Most fractures or breaks require 4-8 weeks for
complete healing.
 After the cast is removed, the child should avoid high-impact activities for
another 1-2 weeks to keep from re-injuring the arm or leg.

Congenital talipes equino-varus (CTEV)/ Clubfoot:

Introduction:
It is the commonest congenital foot disorder.
Tali= talus Pes= foot
Talipes = Walking on talus of foot.
E uino = Plantar flexion Varus = Inversion.
Equinovarus = Pla tar fle io + Inversion.
Epidemiology:
 Incidence: 1 in 1000 live births
 Male : Female= 2:1
 Bilateral in 60% of the cases.
Etiology:
1. Primary/ Idiopathic: Commonest
2. Secondary:
a. Neuropathic: Spina bifida/ Poliomyelitis/ Sacral agenesis
b. Muscular: Myelodysplasia/ Arthrogryposis multiplex congenita/
Congenital constriction band
c. Miscellaneous: Post burn contracture/ VIC of leg/ Leprosy.
 81

Foot abnormalities in CTEV: [Mnemonic: CAVE]

1. Cavus of midfoot: Exaggeration of longitudinal arch
2. Adductus of forefoot: At metatarsal joint
3. Varus (inversion) of hindfoot: At subtalar joint
4. Equinus (plantar flexion) of hindfoot: At ankle joint.

Grading of CTEV and their features:

Mild/ mobile variety Severe/ rigid variety
On passive manipulation, the foot can be O passive a ipulatio , the foot ca ’t
corrected appreciable to an anatomically be corrected appreciable to an
neutral position. anatomically neutral position.
Calf muscles are not so atrophied. Calf muscles are severely atrophied.
Heel size comparable to opposite side. Small sized heel.
No crease. Deep crease just above the heel and in
the medial border of the foot.
Size/ shape of foot comparable to Small sized foot.
opposite side.
Borders of foot is comparable to the Concave medial border, convex lateral
opposite side. border.
 82

Radiological features:
 Preferred investigation: A-P and Lateral view of foot
 Findings:
 Kite’s a gle (Talo-calca eal a gle) is or ally >35◦, i CTEV : ↓↓ .
Treatment:
Age Treatment of choice
<1 year Manipulation of foot and above knee casting
1-4 years Turco operation (posteromedial soft tissue release)
4-12 years  Dilwyn-Evans operation: Wedge excision of

 Dwyer’s operatio : Osteoto y of calca eu .

calcaneocuboid joint

>12 years Triple arthrodesis

Severe uncorrected Talectomy
clubfoot
 83

Chapter 7: Bone cyst and tumors

Osteochondroma/ Exostosis:
Introduction:
This is the commonest benign tumor of the bone. This is not a true neoplasm
because its growth stops with cessation of growth of epiphyseal plate.
Special growth pattern of this tumor:
 It starts as a small overgrowth of cartilage at the edge of the physeal plate.
 Then it develops by endochondral ossification into a bony protuberance still
covered by the cap of cartilage. For this reason, this tumor is also called
cartilage capped exostosis .
 Any bone that develops in cartilage may be involved; the commonest sites
are the fast-growing ends of long bones and the crest of the ilium.
 It may go on growing but at the end of the normal growth period for that
bone it stops enlarging.
 Any further enlargement after the end of the growth period is suggestive of
malignant transformation.
Epidemiology:
 Osteochondromas can present at any age but commonly develop during
childhood (period of most rapid skeletal growth), but once formed remain
for the rest of the individual's life
 Male > Female.
Clinical features:
 Usually asymptomatic and most frequently found incidentally
 Pain occasionally may occur due to: bursitis/ vascular compression/ nerve
compression/ malignant transformation (which is very rare)
 On palpation, a firm non-tender swelling fixed to the bone is the
commonest clinical finding.
Diagnosis:
The X Ray appearance is diagnostic. It shows:
 A well-defined exostosis emerging from the metaphysis
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 Its base co-extensive with the parent bone

 It looks smaller than it feels because the cartilage cap is usually invisible on
X Ray
 However, large lesions undergo cartilage degeneration and calcification and
then the X Ray shows the bony exostosis surrounded by clouds of calcified
material.
 Multiple lesions may develop as part of a heritable disorder – hereditary
multiple exostosis.

Treatment:
 When symptomatic, the tumor should be excised.
 The excision includes the periosteum over the exostosis; since leaving it may
result in leaving a few cartilage cells which will grow again and may cause
recurrence of the swelling.

Ewing’s tu or/ sarcoma:

 Introduction:
Ewi g’s tu or is the most common malignant tumor of flat bones. It is also
the most common tumor which has multicentric origin.
 Cell of origin: Endothelial cells of bone marrow.
 Age of occurrence: 10-20 years.
 Commonly affected bones: The affected bone is usually tubular flat bones.
Ex.: tibia, fibula, clavicle.
 Site of bone affected: Mid-diaphysis.
 85

 Clinical features: The patient presents with pain: often throbbing (rhythmic
beating) in character and swelling.
 Differential diagnosis:
1. Osteomyelitis: Generalized illness and pyrexia, together with a warm,
tender swelling and a raised ESR suggest a diagnosis of osteomyelitis.
2. Osteosarcoma: A biopsy is needed to differentiate these 2 tumors.
 Radiological features:
1. X-Ray:
 The tumor is mid-diaphyseal in location.
 New bone formation may extend along the shaft and sometimes it
appears as fusiform layers of bone around the lesion – the so called
classical onion-peel’ effect.
 Often the tumor extends into the surrounding soft tissues, with
radiating streaks of ossification and reactive periosteal bone at the
proximal and distal margins.
Note: These features (the su ray’ appeara ce a d Cod a ’s
triangles) are usually associated with osteosarcoma, but they are just
as co o i Ewi g’s sarco a [so, they are ot differe tiati g
features].
2. CT/MRI:
They will reveal large extraosseus component.
3. Radioisotope scan:
It will show multiple areas of activity.
 Pathology:
 Gross appearance: The tumor is lobulated and often fairly large. It
may look grey or red if hemorrhage has occurred into it.
 Microscopic appearance: Sheets of small dark polyhedral cells with
no regular arrangement and no ground substance.
 Treatment:
Ewi g’s sarco a is a highly radiose sitive tumor. It dramatically melts in
radiotherapy, only to recur shortly. Surgery alone gives little survival
benefit to the patient. Chemotherapy alone has a 5 year survival rate of
50%. So, the best results are achieved by a combination of all 3 methods
available:
 A course of preoperative neoadjuvant chemotherapy +
 86

 Wide excision if the tumor is in a favorable site/ radiotherapy

followed by local excision if it is less accessible +
 Then a further course of chemotherapy for 1 year.
Note:
Postoperative radiotherapy may be added if the resected specimen is found
not to have a sufficiently wide margin of normal tissue.

Radiological features of osteosarcoma:

Common sites:
Distal femur, proximal tibia, proximal humerus.
X-Ray
1. Area of irregular destruction in the metaphysis, sometimes over-shadowed
by new bone formation
2. Cortical erosion over the lesion with new bone formation in the matrix of
the tumor
3. Wide zone of transition, permeative or moth-eaten appearance
4. Aggressive periosteal reaction, which is irregular in nature and due to lifting
of the periosteum by the tumor
A. Cod a ’s tria gle: A triangular area of sub-periosteal new bone seen at
the tumor-cortex junction
B. Sun-ray/ Sun-burst appearance: As the periosteum is unable to contain
the tumor, it grows into the overlying soft tissues. New bone is laid
down along the blood vessels within the tumor centrifugally, giving rise
to this appearance.
C. Onion skin reaction.
5. Tumor matrix ossification/ calcification.
CT/ MRI
Rarely done, before planning limb sparing surgery to note cortical break/ soft
tissue involvement.
Bone scan
To search for skip lesions.
 87

CXR
To look for pulmonary metastasis.

Management of osteosarcoma:
Line of management:
1. Low grade osteosarcoma: Treated by surgery alone
2. High grade osteosarcoma: Neo-adjuvant chemotherapy -> Surgery ->
Adjuvant chemotherapy.
Chemotherapy
 Introduction of systemic chemotherapy has dramatically improved survival
rates.
 Before the routine use of chemotherapy, treatment was immediate wide or
radical amputation and 80% patients died of metastasis eventually, though
metastasis was not evident on presentation.
 Chemotherapy used in osteosarcoma are of 2 types:
a. Neo-adjuvant chemotherapy: Administered before the surgical
resection of primary tumour
b. Adjuvant chemotherapy: Administered postoperatively to treat
presumed micro-metastasis.
 Chemotherapeutic agents commonly used are: Cisplatin (most successful
agent), Cyclophosphamide, Doxorubicin, Decarbazine, Dactinomycin,
Vincristine, Methotrexate.
 After induction of chemotherapy (lasting about 2 months) surgical resection
is to be carried out. Surgery is contemplated 3-4 weeks after last dose of
chemotherapeutic agent. Adjuvant chemotherapy again started 2 weeks
after operation.
Surgery
 Surgery is the mainstay of treatment.
 There are 2 options: Limb salvage surgery and Amputation. Choice between
these 2 entities must be made on the basis of the expectations and desires
of the individual patient and the family.
 88

 Limb salvage surgery has become an accepted standard of care for patients
with skeletal malignancies including osteosarcoma.
 Important Guidelines to be followed during surgery:
 Wide resection of affected bone with a normal muscle cuff all around
 En-block removal of all biopsy sites & contaminated tissue
 Resection of bone 3-4 cm beyond abnormal uptake
 Resection of adjoining joint & capsule.
 Adequate motor reconstruction
 Adequate soft tissue coverage.
 Commonly used surgical techniques:
I. Bone grafting
II. Rotationplasty
III. Resection/ Arthrodesis
IV. Prosthesis.
Special Note: Radiotherapy in osteosarcoma:
 Role of radiotherapy is limited in the treatment of osteosarcoma as it is a
relatively radioresistant tumor.
 Indications of radiotherapy:
I. Postoperative: When surgical margins are involved
II. Inoperable sites: Skull, vertebral, ilium, sacrum
III. Palliation of pain in metastatic disease
IV. Bilateral lung irradiation in case of pulmonary metastasis.

Giant cell tumor (GCT):

Introduction:
 It is an osteolytic bone tumour
 Arises from the epiphysis
 It is a benign but locally aggressive tumour.
Epidemiology:
 Almost always occurs in patients who attained skeletal maturity
 Common age group: 15-35 years
 89

 Female > Male.

Site:
 Epiphysis of long bone
 Eccentric in position
 MC site: Lower end of femur
 Other areas: Epiphyseal areas of tibia, radius and humerus.
Clinical features:
 A young patient complains of pain at the end of a long bone with limitation
of joint movements
 On examination, an eccentric swelling is noted at the end of a long bone
 Overlying skin is stretched and shiny but no redness, raised temperature or
dilated veins are noted
 On palpation, the swelling is warm, tenderness may be noted
 Characteristic egg shell crackling sound may be elicited where there is too
much thinning of cortex
 NO CALCIFICATION & NO NEW BONE FORMATION
 Pathological fractures may occur late in the course.
Pathology:
 Gross: It is grossly seen as an encapsulated tumour consisting of friable
bleeding tissues + blood clots + cysts + cavities.
 Microscopic: Presence of abundant multinucleated giant cells in a
background of mononuclear stromal cells.
 The giant cells contain acid phosphatase which serves as a tumour marker.
X-RAY appearance:
1. An eccentric radiolucent area in the epiphysis of a long bone
2. Cortex is expanded and thin but intact
3. No periosteal reaction
4. Characteristic soap bubble appearance: Due to thin septae of bone
traversing the tumour.
 90

Treatment:
 En-bloc resection with bone grafting/ allograft/ prosthesis/ bone cement:
Treatment of choice
 GCT commonly recurs after excision and may become malignant after
unsuccessful removal
 Other treatment options:
i. Simple curettage
ii. Extended curettage
iii. Sandwich technique.

Bone cyst:
There are numerous cystic lesions of bone described. We will only discuss the two
most common types: simple (unicameral) bone cyst and aneurysmal bone cyst in a
comparative manner.
Points Simple bone cyst Aneurysmal bone cyst
Age group (MC) <20 years Young adults
Sex Common in males Common in females
Location Metaphysis Metaphysis
Site (MC) Proximal humerus Lower leg
Note: Both of them may involve any bone.
Pathology Aspiration: Straw coloured fluid and Contains blood, hemosiderin
characteristic giant cells present deposits and giant cells
Clinical feature Often asymptomatic; may present Often asymptomatic; may present
with pain, redness, warmth, swelling with pain, visible/ palpable

 Well demarcated radiolucent area  Well demarcated expansile

in case of pathological fracture progressively expansile swelling
Radiology

 Fallen fragment sign: Seen in MRI

in the metaphysis radiolucent lytic lesion in the

only: fracture fragment falls within  Double density fluid level: Seen
metaphysis

the cyst cavity. in CT/ MRI only.

Management 1. Observation (in inactive cyst) 1. Excision
options 2. Aspiration and injection of steroid 2. Embolization
3. Curettage & bone grafting. 3. Curettage & bone grafting.
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Chapter 8: Miscellaneous
Bone graft:
Introduction:
Bone grafting is an operation whereby pieces of bone (bone grafts) taken from
some part of a patient's body are placed at another site.
Indication:
(i) Non-union of fractures- to promote union.
(ii) Arthrodesis of joints- to achieve fusion between joint surfaces.
(iii) Filling of defects/ cavities in a bone.
Purpose:
Bone grafts are both osteoinductive and osteoconductive:
1. Osteoinductive: They are able to stimulate osteogenesis through the
differentiation of mesenchymal cells into osteoprogenitor cells.
2. Osteoconductive: They provide linkage across defects and a scaffold upon
which new bone can form.
Types:
 92

1. Autograft:
Graft is taken from the same person. This is the gold standard bone grafting
technique. The commonest site is iliac crest.
a. Free graft:
These grafts do not survive because blood supply is not intact; but they
provide a scaffold upon which new bones are laid down.
I. Cancellous bone grafting: Choice in non-union.
Ex.: Iliac crest.
II. Cortical bone grafting: Choice in filing bone gaps/ defects.
Ex.: Fibula.
b. Vascularized graft:
These grafts are placed to the receptor area with blood supply
maintained. So, these are ideal bone grafts.
I. Muscle-pedicle grafting:
The bone graft is taken along with a pedicle of muscle. The muscle
(with its intact blood supply) continues to supply blood to the
graft.
Ex.: Non-union of fracture neck of femur.
II. Free-vascularized grafting:
In this, the bone (usually fibula) is taken along with the vessels
supplying it. It is placed at new site, and its vessels anastomosed
to a nearby vascular bundle.
2. Allograft:
Bone grafts are taken from another human. These are usually required
when enough bone is not available from the host, i.e. where a big defect is
created following a tumor resection.
a. From live donor:
Ex.: From mother to child.
b. From dead body:
These are called cadaveric grafts.
3. Xenograft:
Bone grafts are taken from another species.
Ex.: Bovine grafts.
 93

Special note: Artificial bone:

This is a new option in the developed countries. It is hydroxy-apetite with porous
structure and supposed to have osteoconductive potential.

External fixation:
Introduction:
It is a process of rigid stabilization of fractures by percutaneously placed pins or
tension wires, which are then connected to an external frame.
Commonly used external fixators:
 Ilizarov apparatus
 Taylor spatial frame
 Hoffman external fixation system
 Rail external fixator etc.
Types:
1. Pin fixators: In these, 3–4 mm sized pins are passed through the bone. The
same are held outside the bone with the help of a variety of tubular rods
and clamps.
2. Ring fixators: I these thi K’ wires (1–2 mm) are passed through the bone.
The same are held outside the bone with rings.
Indications:
There are no absolute indications and each case must be individualized. Common
indications are:
1. Open fractures (Gustilo grade 3)
2. Fracture with bone loss
3. Infected non-union/ fractures
4. Some cases of pelvic fractures
5. Fractures associated with burns
6. Arthrodesis
7. Temporary stabilization of fractures
 94

8. Limb lengthening
Done with ring fixators
9. Deformity correction
Contraindications:
1. Immunocompromised patients
2. Non-compliant patient
3. Pre-existent internal fixators that prohibit placement of external fixators
4. Bone pathology involving pin fixators.
Advantages and disadvantages of external fixators:
Advantages Disadvantages
1. Decreased chance of infection 1. Psychological burden
2. Preservation of vascularity 2. Most patients need a second
3. Allows monitoring of open wounds to operation for permanent fixation.
assess the viability of soft tissue and
also permits dressing/ skin grafting
without disturbing the fracture
4. Prevents joint stiffness, muscle
atrophy and osteoporosis.

Complications:
 Pin tract infection
 Neurovascular injury
 Impalement of soft tissues
 Re-fractures
 Compartment syndrome.

Indications for limb amputation:

Introduction:
Amputation is a procedure where a part of the limb is removed through one or
more bones.
 95

Indications:
1. Trauma:
 It is the most common indication for limb amputation in developing
countries. The common causes are either road traffic accident or
gunshot wounds/ violence.
 The only absolute indication for primary amputation is an irreparable
vascular injury in an ischemic limb.
 Ideally, the decision to amputate should be made immediately; and a
late amputation dictated by developing sepsis in an inadequately
debrided limb represents a failure of management.
2. Peripheral vascular diseases (PVD):
 It is the most common indication for limb amputation in developed
countries.
 It is the most common indication for lower limb amputation primarily in
elderly persons with diabetes mellitus, who often experience peripheral
neuropathy that progresses to trophic ulcers and subsequent gangrene
and osteomyelitis.
3. Bone tumors:
 The goal in treating malignant bone tumors is to remove the lesion
with the lowest risk of recurrence.
 With the advent of advanced techniques, limb-salvage surgery has
replaced amputation as the primary treatment for bone tumors.
4. Infections:
In cases of difficult to manage infections, eradication of infection from a
body part necessitates removal of the affected digit or limbs. The major
indications are:
 Chronic osteomyelitis
 Severe surgical site infection
 Necrotizing fasciitis.
5. Congenital:
Congenital absence and limb malformations account for a small percentage
of amputations. Such amputations are performed primarily in the pediatric
population because of failure of partial or complete formation of a portion
of the limb.
 96

Ideal amputation stump:

An ideal amputation stump should assure the following characteristics:
 Ideal length and shape
 Bone end well covered with muscles
 Non adherent incision scar
 Muscle with good power
 Absence of neuroma
 Free from infection
 Full and free movements at the joint above
 No fixed deformity.
Ideal length and shape
To predict the level of amputation, some methods are used to assess the
vascularity of primary wound healing. Ex.:
 Trans cutaneous measurement of oxygen tension (Best method)
 Tissue uptake of IV fluorescein
 Thermography
 Laser Doppler flowmetry.
The importance of ideal length and shape of an amputation stump lies in the fact
that when stump length is less than ideal or when the ideal shape is not possible,
it can potentially compromise the function; in that case amputation at the next
higher level is recommended.
Bone end well covered with muscles
An ideal stump should have end bearing, i.e. it should have side pad/ bony surface
of sufficient size that can bear weight for varying period – especially in partial foot
amputations. Disarticulation (separation of two bones at their joints) is
recommended for this purpose in growing children and elderly.
Non adherent incision scar
The scar should not adhere to the bone. To reduce the problem of adhesion, skin
and muscle flap over the stump should be thick.
 97

Muscle with good power

Muscle should be divided at least 5 cm distal to the intended bone resection.
The muscle should be stabilized by myodesis (muscle/ tendon sutured to bone) or
by myoplasty (muscle/ tendon sutured to periosteum/ fascia) of which myodesis
is better option because of stronger insertion and greater strength.
Absence of neuroma
Nerves are transected using any of the preferred methods (end-loop
anastomosis/ perineural closure/ ligation/ cauterization/ bury nerve end in bone
or muscle) to reduce risk of developing neuroma.
Free from infection
It is an absolute requirement of ideal amputation stump.
Full and free movements at the joint above & no fixed deformity
 Excessive periosteal stripping is not advised as it results in ring sequestra
and bone overgrowth.
 Bone prominence not covered by adequate soft tissue should be resected.
 Definitive prosthesis should be fitted – strong and functional stump is a pre-
requisite for maximum prosthetic use.

Cod an’s triangle:

Introduction:
It is a triangular area of new subperiosteal bone formation
usually formed when an aggressive lesion lifts the
periosteum away from the bone.
Pathophysiology:
With aggressive lesions, the periosteum does not have time
to ossify with shells of new bone, so only the edge of the
raised periosteum will ossify.
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Common causes for Cod a ’s tria gle:

 Osteosarcoma
 Ewi g’s sarco a
 Subperiosteal abscess (from osteomyelitis)
 Aneurysmal bone cyst
 Metastasis.
Diagnostic modality:
 Digital X-Ray for detection
 MRI for characterization.
Management:
According to the cause.

Bone scan:
Introduction:
It is a procedure in which a bone seeking radioisotope is injected intravenously
and photon emission by these nucleotides taken up by bone is recorded by either
simple scanner or Gamma camera, to produce an image which reflects the
current activity of the tissue.
Commonly used radioisotope: Technetium labelled hydroxy-methylene
diphosphonate (99� �� − ���).
Phases:
After the isotope is injected intravenously, its activity is recorded in 2 phases:
1. Early perfusion phase: Shortly after injection, when the contrast is still in
the blood stream/ perivascular space
2. Bone phase: After 3 hours when isotope has been taken up by the bone.
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Findings:
Normal findings
In early perfusion phase, the
vascular soft tissue around the
joint produces the darkest image.
After 3 hours of injection, this
Abnormal findings
↑Activity Due to ↑soft tissue lood flow:
Acute/ chronic synovitis/ a highly
vascular tumor/ fracture/ regional
sympathetic dystrophy.
↓Activity Local vascular insufficiency
↑Activity Fracture/ infection/ local tumor/

 Absent blood supply

activity fades away and the bone [Hot spots] healing after necrosis
outlines get more clear. ↓Activity
[Cold spots]  Replacement of bone by
pathological tissue.

Indications:
 Diagnosis of stress fracture that are not evident on plain X-Ray
 Detection of small bone abscess/ an osteoid osteoma
 Investigation of loosening of/ infection around a prosthesis
 Diagnosis of femoral head ischemia i Perthes’ disease or avascular ecrosis
in adults
 Early detection of bone metastasis.

Paget’s disease of bone:

Introduction:
It is a common bone disorder, characterized by a chronic progressive disturbance
in bone metabolism that primarily affects older persons.
Epidemiology:
Commonly affects males. Male: Female= 3:2
Pathology:
The disease passes through 3 stages:
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1. Osteolytic/ hot phase:

Overactive osteoclastic bone resorption
2. Intermediate/ mixed phase:
Osteoclastic bone resorption is followed by compensatory increase in
osteoblastic new bone formation
3. Sclerotic/ cold phase:
Osteoblastic activity is greatly increased, leading to marked thickening of
bony trabeculae and cortex.
It should be noted that pagetic bones are structurally disorganized and more
susceptible to bowing and fracture.
Symptoms:
1. Pain: MC symptom: Due to increased bone vascularity/ expansile lytic
lesions/ fractures/ bony deformities
2. Back pain: Due to enlarged pagetic vertebrae/ vertebral compression
fractures/ kyphosis
3. Gait abnormalities: Due to bowing of the femur/ tibia
4. Secondary osteoarthritis of hip/ knee joint
5. Sensorineural hearing loss: Due to compression of cochlear nerve from
temporal bone involvement
6. Cranial nerve palsies
7. Headache/ frontal ossing/ ↑ head size: Due to involvement of skull bones
8. Facial deformities: Due to involvement of facial bones.
*Osteosarcoma arising in an elderly patient is almost always due to malignant
transformation i Paget’s disease. The fre ue cy of alig a t change is 1%.
Diagnosis:
1. Biochemical:
The biochemical evidence of concomitant bone formation and resorption
co fir s the diag osis of Paget’s disease:
 ↑ Alkali e phosphatase ( arker of ew o e for atio )
 ↑ Uri ary hydro yproli e ( arker of o e resorptio )
 Normal Ca++ and PO4--- levels.
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2. Radiological:
Radiological findings depend upon the stage of the disease:
Early osteolytic  Radiolucent wedge shaped areas within long
phase o es: Ca dle fra e / Blade of grass

Late osteoblastic  Thickening of the cortex/ coarse trabeculation/

appearance

 Picture frame vertebra: Cortical thickening of

phase enlargement of a long bone/ areas within it

 Ivory vertebra: Diffuse radiodense enlargement

superior and inferior end plates of a vertebra

 Cotton ball appearance: Focal patchy densities

of a vertebra

 Disruption/ fusion of sacro-iliac joints.

in skull X-ray (Characteristic)

Treatment:
1. Calcitonin
2. Bisphosphonates: Risedronic acid, Alendronic acid, Pamidronic acid,
Etidronic acid
3. Surgery: The main indication for operation is a pathological fracture, which
(in a long bone) usually requires internal fixation.

Tension band wiring (TBW):

Introduction:
 When wire is used for internal fixation
of fracture and the wire is applied on
the tensile surface of the bone, the
procedure is called TBW.
 The tension band technique converts a
tensile force into a compressive force.
This enables improved fracture healing
as stability is improved when tensile
forces are reduced at the fracture site.
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Mechanism:
 When a fractured bone is centrally loaded, there is uniform compression at
fracture site.

 But if it is eccentrically loaded, then there is distraction on tensile surface.

 If the tensile strength is kept fixed, the eccentric force cannot open up the
fracture and the distracting tensile force is changed to compressive force.
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Some common indications:

Pre-requisites for a successful TBW:

1. Bony cortex on the compressive side must be sufficiently strong enough to
withstand the compressive loads generated; otherwise it may cause
comminution fracture (fixation failure).
2. The wire used must be strong enough to withstand the distracting tensile
forces, otherwise it may cause wire breakage (implant failure).
3. Adjoining joint movement must be encouraged very early after operation.
4. Pre-stressing the wire is a must.
5. K wires are co o ly used as a adjuva t i pla t, which preve ts
fracture translation, shearing, rotation and provides anchorage points for
the wire.
Advantages:
 Minimal implant material is used to achieve maximum fracture fixation
 Provides dynamic compression at fracture site
 Minimal postoperative immobilization is required
 Cost effective.
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Disadvantages:
 Subcutaneously placed wire may cause hardware prominence: skin
irritation, pain and even skin breakdown
 Wire may break early/ may get out of the bone
 Needs a second operation for implant removal.

SP Nail:
Introduction:
 It is type of orthopedic implant
 Full name: Smith Peterson nail
 It is a flanged metal nail used to fix the femoral head in fractures of femur
neck.
Indications:
1. SP nail: For fracture neck femur; it is used in Garden type 3 and type 4 in
patients aged less than 60 years
2. SP nail + McLaughlin plate: For intertrochanteric fracture.
Advantage:
1. Less blood loss
2. Cost effective.
Disadvantage:
1. Non-union
2. Avascular necrosis of femoral head
3. Failure of fixation.