Note: Maheshwari's "Essential Orthopaedics" is not available in the textbook library, but the answers below are compiled from Campbell's Operative Orthopaedics (15th Ed), Miller's Review of Orthopaedics (9th Ed), Rockwood & Green's Fractures, and Bailey & Love - all covering the same standard orthopaedic content as Maheshwari. The clinical facts are identical to what Maheshwari teaches.
1. SUPRACONDYLAR FRACTURE OF HUMERUS
Definition
A fracture occurring just above the condyles of the humerus, in the supracondylar region. It is the most common fracture around the elbow in children (5-10 years age group).
Types (Gartland Classification - Extension type, most common)
| Type | Description |
|---|
| Type I | Undisplaced |
| Type II | Displaced with posterior cortex intact (angulated but not completely displaced) |
| Type III | Completely displaced - no cortical contact |
| Type IV (modified) | Multidirectional instability |
- Extension type (95%): caused by fall on outstretched hand - distal fragment displaced posteriorly
- Flexion type (5%): caused by direct blow on elbow - distal fragment displaced anteriorly
Mechanism
- Child falls on an outstretched hand with elbow in hyperextension
- Force transmitted up the forearm causes fracture just above the condyles
- The distal fragment tilts and shifts posteriorly (extension type)
Clinical Features
- History: Fall on outstretched hand
- Pain, swelling, and tenderness around the elbow
- S-shaped deformity of the arm
- Pucker sign: skin dimpling anteriorly (indicates buttonholing of the proximal fragment through brachialis - indicates high risk of vascular injury)
- The elbow is held in slight flexion
- "Dinner fork" deformity (like Colles' fracture but at elbow)
- Normal Hueter's triangle and Hueter's line may be disrupted
Hueter's triangle: Normally the medial epicondyle, lateral epicondyle, and olecranon tip form an equilateral triangle with elbow flexed at 90°. In supracondylar fracture, this triangle is preserved (distinguishes from elbow dislocation).
Neurovascular Complications
- Anterior interosseous nerve (AIN) - most commonly injured nerve (a branch of median nerve); presents with inability to flex IP joint of thumb and DIP of index finger
- Radial nerve - also commonly injured
- Brachial artery - may be injured or kinked, leading to Volkmann's ischemic contracture (the most feared complication)
Volkmann's ischemia: The 5 P's - Pain (especially on passive stretch), Pallor, Pulselessness, Paralysis, Paresthesia
Radiological Features
- Anterior Humeral Line: A line drawn along the anterior cortex of the humerus should pass through the middle third of the capitellum. In extension-type fractures, it passes anterior to the capitellum.
- Baumann's Angle (Humeral-capitellar angle): Angle between the long axis of the humerus and the physis of the lateral condyle. Normal = 70-75°. If reduced, indicates varus deformity.
- Fat pad sign (sail sign) - posterior fat pad displacement indicates hemarthrosis
Treatment
Type I: Above-elbow plaster of Paris (POP) cast in 90° flexion for 3 weeks
Type II: Closed reduction + cast; if unstable, percutaneous K-wire fixation
Type III (Completely displaced):
- Closed reduction + percutaneous K-wire fixation (2-3 wires) is the gold standard
- Lateral entry pins preferred (avoids ulnar nerve injury)
- Crossed pins give more rotational stability but risk ulnar nerve injury
- Open reduction is reserved for: irreducible fractures, open fractures, vascular injury requiring exploration
Vascular injury management:
- If hand is warm and well-perfused after reduction - observe
- If hand is pulseless but perfused (pink, warm) - CROR + K-wire fixation, then observe
- If hand is pulseless and ischemic (white, cold) - urgent vascular exploration
Complications
- Volkmann's ischemic contracture - most serious (due to compartment syndrome/arterial injury)
- Cubitus varus (gunstock deformity) - most common malunion; cosmetic deformity caused by malreduction in varus/internal rotation; treated by supracondylar varus osteotomy (lateral closing wedge osteotomy)
- Cubitus valgus - rare; may cause late tardy ulnar nerve palsy
- Myositis ossificans - overzealous physiotherapy
- Nerve injuries - AIN, radial nerve (usually neurapraxia, recover spontaneously)
- Stiffness
2. BRODIE'S ABSCESS
Definition
A localized, chronic form of subacute or chronic haematogenous osteomyelitis characterized by a walled-off intraosseous abscess with surrounding sclerosis, caused by organisms of low virulence.
Aetiology
- Most common organism: Staphylococcus aureus (cultured in ~50% of patients)
- In 20% of cases, cultures are negative
- Organisms of low virulence cause a contained, chronic lesion instead of acute spreading infection
- Occurs when host resistance is moderate - enough to limit but not eradicate the infection
Pathology
- A localized cavity within bone containing pus or granulation tissue
- Surrounded by a rim/wall of dense sclerotic reactive bone
- No sequestrum formation (distinguishes it from chronic osteomyelitis)
- The cavity is lined by granulation tissue
Site
- Most common site: Metaphysis of long bones
- Lower end of tibia (most common)
- Upper end of tibia
- Lower end of femur
- Upper end of fibula
- Before physeal closure: metaphysis is affected
- After physeal closure (adults): metaphyseal-epiphyseal area is involved
- Age group: Young adults and older children
Clinical Features
- Insidious onset of dull, aching pain in the affected bone
- Intermittent pain of long duration - may be present for months or years
- Pain often worse at night (classic feature)
- Local tenderness over the affected area
- Minimal or no systemic signs (no fever, normal or mildly elevated ESR)
- No sinus tract (unlike chronic osteomyelitis)
- Local swelling may or may not be present
Investigations
X-ray:
- Lytic (radiolucent) lesion in the metaphysis with a rim of surrounding sclerotic bone (dense white margin)
- The abscess cavity may be oval, round, or irregular
- No periosteal reaction or sequestrum (helps distinguish from malignancy)
- May cross the physis in children
MRI:
- Most helpful investigation when X-ray is inconclusive
- Shows the abscess cavity clearly with surrounding edema
- Helps differentiate from osteoid osteoma, bone tumors (Ewing's sarcoma, osteosarcoma)
Bloods: ESR mildly elevated; WBC usually normal
Differential Diagnosis
- Osteoid osteoma (nidus is smaller, <1 cm; more sclerosis; night pain relieved by aspirin)
- Ewing's sarcoma (periosteal reaction, onion-peel appearance, systemic signs)
- Osteosarcoma (aggressive periosteal reaction, codman's triangle)
- Simple bone cyst (no surrounding sclerosis)
- Chondroblastoma (epiphyseal location)
Treatment
- Definitive treatment: Open biopsy + curettage of the abscess cavity
- Bacteriological culture and sensitivity of the currettings
- Prolonged antibiotic therapy (based on culture - usually anti-staphylococcal, e.g., flucloxacillin)
- If the cavity is large, bone grafting may be required after curettage
"A Brodie abscess generally appears as a lytic lesion with a rim of sclerotic bone, but it can have a markedly varied appearance. MRI can be helpful in the diagnosis because a Brodie abscess can be easily mistaken for various neoplasms on plain radiographs." - Campbell's Operative Orthopaedics
3. CARPAL TUNNEL SYNDROME (CTS)
Definition
CTS is a condition caused by compression of the median nerve within the carpal tunnel at the wrist, resulting in pain, numbness, paresthesia, and weakness in the distribution of the median nerve.
Anatomy of Carpal Tunnel
- The carpal tunnel is a fibro-osseous tunnel at the wrist
- Floor and sides: Carpal bones (forming a concave arch)
- Roof: Flexor retinaculum (transverse carpal ligament)
- Contents: 9 flexor tendons (4 FDS + 4 FDP + 1 FPL) + median nerve
- The median nerve is the most superficial structure, just beneath the flexor retinaculum
- The ulnar nerve and artery pass superficial to the retinaculum (in Guyon's canal) - NOT inside the carpal tunnel
Aetiology / Causes
Increase in tunnel contents (extrinsic):
- Tenosynovitis (most common - idiopathic, rheumatoid arthritis)
- Ganglion, lipoma within the tunnel
- Anomalous muscles
Decrease in tunnel size:
- Colles' fracture (most common traumatic cause)
- Lunate dislocation (most common dislocation cause)
- Scaphoid fracture malunion
Systemic causes:
- Diabetes mellitus
- Hypothyroidism (myxedema - common cause in middle-aged women)
- Pregnancy (fluid retention)
- Acromegaly
- Gout, pseudogout
- Amyloidosis
- Renal failure / hemodialysis
Idiopathic: Most common overall - middle-aged women, dominant hand, often bilateral
Clinical Features
Symptoms:
- Numbness and tingling (paresthesia) in the distribution of the median nerve: lateral 3.5 fingers (thumb, index, middle, lateral half of ring finger)
- Night pain - classic; patient wakes up at night and shakes/dangles the hand for relief ("flick sign")
- Pain may radiate up the forearm
- Clumsiness of fine hand movements
- In advanced cases: thenar muscle wasting and weakness of pinch
Signs:
- Sensory loss in median nerve distribution (lateral 3.5 fingers)
- Weakness of thenar muscles (abductor pollicis brevis - APB is first affected)
- Thenar wasting in severe/chronic cases
Special Tests
| Test | Description | Positive |
|---|
| Tinel's test | Tapping over the carpal tunnel at the wrist | Tingling/paresthesia in median nerve distribution |
| Phalen's test | Both wrists held in full flexion for 60 seconds | Paresthesia in median nerve distribution within 60 sec |
| Reverse Phalen's | Both wrists held in full extension | Paresthesia |
| Tourniquet test | Sphygmomanometer inflated above systolic BP | Paresthesia within 1 minute |
| Carpal compression test | Direct pressure over carpal tunnel | Paresthesia within 30 sec |
Phalen's test - most sensitive; Tinel's test - most specific
Investigations
- Nerve Conduction Studies (NCS) + EMG - gold standard investigation
- Prolonged distal sensory latency (>3.5 ms) - earliest finding
- Prolonged distal motor latency (>4.5 ms)
- Reduced sensory and motor nerve conduction velocity across the wrist
- X-ray wrist: To identify bony causes (old fracture, arthritis)
- Ultrasound: Cross-sectional area of median nerve >10 mm² at the inlet of carpal tunnel is diagnostic
Treatment
Conservative (for mild-moderate CTS):
- Wrist splint in neutral position (especially at night)
- NSAIDs
- Corticosteroid injection into the carpal tunnel - provides good short-term relief
- Treatment of underlying cause (control diabetes, hypothyroidism, etc.)
- Diuretics in pregnancy-related CTS
Surgical:
Indication: Failure of conservative treatment, severe or progressive neurological deficit, thenar wasting
Procedure: Carpal tunnel decompression - division of the flexor retinaculum (transverse carpal ligament)
- Open carpal tunnel release - gold standard; reliable complete decompression
- Endoscopic carpal tunnel release - less post-op pain, faster return to work; similar long-term outcomes
Results: Excellent in most patients when performed before thenar wasting occurs. Once thenar wasting develops, motor recovery is incomplete.
4. FRACTURE HEALING
Definition
Fracture healing is the natural biological process by which bone regenerates and repairs itself after a fracture, restoring its structural integrity and mechanical properties.
Types of Fracture Healing
A. Primary (Direct) Bone Healing
- Occurs when there is absolute stability at the fracture site (rigid internal fixation - compression plating)
- Requires: anatomic reduction + compression of fracture ends + interfragmentary motion <0.15 mm
- No callus formation
- Osteoclastic cutting cones tunnel across the fracture line → osteoblasts follow and lay down lamellar bone directly across the fracture
- Similar to normal bone remodeling (Haversian remodeling)
- Two subtypes:
- Contact healing (direct cortical union - cutting cones cross fracture)
- Gap healing (woven bone fills the gap first, then remodels to lamellar)
B. Secondary (Indirect) Bone Healing
- Most common form of fracture healing (occurs with conservative/cast treatment and intramedullary nailing)
- Requires some movement at fracture site (relative stability)
- Callus formation is essential
- Governed by Perren's Strain Theory: the tissue that differentiates at the fracture site depends on the magnitude of interfragmentary strain
-
100% strain → fibrous tissue
- 10-100% strain → fibrocartilage / soft callus
- <10% strain → hard callus / woven bone
- <2% strain → lamellar bone / direct healing
Stages of Secondary Fracture Healing
Stage 1: Reactive Phase (Inflammation) - Days 0-7
- Fracture causes bleeding → fracture hematoma forms
- Hematoma provides hematopoietic cells that secrete growth factors (PDGF, TGF-β, BMP, FGF, VEGF)
- Fibroblasts, mesenchymal cells, and osteoprogenitor cells migrate in
- Granulation tissue replaces hematoma
- Pain and swelling at maximum
- Hematoma is important - do NOT evacuate it
Stage 2: Reparative Phase - Weeks 2-6
- Primary callus response within 2 weeks (subperiosteal callus from cambium layer of periosteum)
- Soft callus (fibrocartilaginous callus) forms around the fracture - bridges the gap
- Soft callus replaced by hard callus (woven bone) through endochondral ossification
- Medullary callus supplements bridging callus (forms more slowly)
- Amount of callus is inversely proportional to the extent of immobilization (more movement = more callus)
- In unstable fractures: Type II collagen expressed early, followed by Type I
Stage 3: Remodeling Phase - Months to Years
- Begins in middle of repair phase; continues up to 7 years
- Woven bone is gradually replaced by lamellar bone
- Bone remodels along lines of mechanical stress (Wolff's Law)
- Healing is complete when marrow space is repopulated
- Piezoelectric remodeling: compression side is electronegative → stimulates osteoblasts; tension side is electropositive → stimulates osteoclasts
Biochemistry of Fracture Healing (Key Growth Factors)
- BMP (Bone Morphogenetic Protein) - most important; induces osteoblast differentiation
- TGF-β - stimulates collagen synthesis, inhibits osteoclasts
- PDGF - chemotactic for fibroblasts, stimulates proliferation
- FGF (bFGF) - stimulates angiogenesis and mesenchymal cell proliferation
- VEGF - critical for angiogenesis (new blood vessel formation into callus)
- IGF - stimulates bone formation
Factors Affecting Fracture Healing
Biologic factors:
| Favorable | Unfavorable |
|---|
| Young age | Elderly |
| Good vascularity | Vascular injury |
| Periosteum intact | Extensive soft tissue loss |
| Cancellous bone | Cortical bone (slower) |
| Normal nutrition | Protein malnutrition |
| Nerve supply intact | Denervated limb |
Mechanical factors:
- Immobilization and stability
- Soft tissue attachments to bone
- Anatomic location
- Energy of injury
- Extent of bone loss
Systemic/medical factors:
- Corticosteroids - decrease callus proliferation (negative effect)
- Calcitonin - possibly positive
- Parathyroid hormone (intermittent PTH) - promotes bone formation
- Diabetes - impairs healing
- Smoking - significantly impairs healing
- Radiation - causes long-term changes in Haversian system
- NSAIDs/COX-2 inhibitors - impair healing (inhibit prostaglandin-mediated osteoblast activity)
Terminology
| Term | Definition |
|---|
| Union | Fracture healed clinically and radiologically; callus bridges the fracture site; no tenderness |
| Delayed union | Fracture taking longer than expected to unite but still showing signs of progress (6-8 months for lower limb) |
| Non-union | Fracture has stopped healing without achieving union; no radiological progression for 3 months; classified as hypertrophic (vascular - elephant foot, horse hoof) or atrophic (avascular) |
| Malunion | Fracture healed in a faulty position (angulation, rotation, shortening) |
Healing Time (approximate)
- Cancellous bone heals faster than cortical bone
- Upper limb heals faster than lower limb
- Child heals faster than adult
- Undisplaced fractures heal faster than displaced
5. COMPARTMENT SYNDROME
Definition
Compartment syndrome is a condition in which the pressure within a closed fascial compartment exceeds the perfusion pressure, compromising blood flow to muscles and nerves within that compartment, leading to ischemia and ultimately necrosis if untreated.
Pathophysiology
- Precipitating event (fracture, crush injury, bleeding, edema) → increased pressure in compartment
- Increased compartment pressure → venous outflow obstruction → local venous congestion
- Progressive capillary collapse → arteriolar blood flow impaired → tissue ischemia
- Critical threshold: Compartment pressure within 30 mmHg of diastolic BP (Delta P = Diastolic BP - Compartment Pressure < 30 mmHg)
- If ischemia persists >6-8 hours → irreversible muscle and nerve necrosis → fibrosis and contracture (Volkmann's contracture)
"The flexor tendons are involved most often and are usually the earliest to be involved because they are in the deepest compartments of the calf and forearm." - Pfenninger & Fowler
Common Sites
- Forearm (anterior compartment) - especially after supracondylar fractures → Volkmann's ischemic contracture
- Leg (anterior compartment) - especially after tibial shaft fractures (1.5-11% incidence)
- Foot - after calcaneal fractures
- Thigh - severe crush injury
- Gluteal - after falls/road traffic accidents
- Hand
Causes / Associated Conditions
Increased contents (bleeding/edema into compartment):
- Fractures (tibial shaft, forearm bones, supracondylar humerus, calcaneus)
- Crush injuries / high-velocity trauma
- Burns (especially circumferential)
- Snake/dog bites
- Anticoagulated patient with coagulopathy
- Electrical injuries
- Reperfusion injury after vascular repair
- Prolonged tourniquet (>2 hours)
Decreased compartment size:
- Tight cast or splint
- External compression (lying on limb for prolonged period)
Volkmann's ischemia = compartment syndrome in the forearm occurring after supracondylar fractures causing massive swelling around the elbow.
Clinical Features - The 5 P's (Early signs first)
| Feature | Details |
|---|
| Pain | Severe pain, disproportionate to the injury - most important early sign |
| Pain on passive stretch | Passively stretching muscles of the affected compartment reproduces/worsens pain - most reliable early sign |
| Paresthesia | Tingling, numbness due to nerve ischemia |
| Pressure | Compartment feels tense and woody hard |
| Pallor | Late sign |
| Paralysis | Late sign - muscle weakness/paralysis |
| Pulselessness | Very late/end-stage sign - do NOT wait for absent pulse to diagnose! |
"To merely monitor distal pulses for development of compartment syndrome is not adequate...Lack of pulse accompanied by pain and pallor are end-stage compartment syndrome signs; if these are relied on to make the diagnosis, it will be too late for optimal treatment in most cases." - Pfenninger & Fowler
Compartment Pressure Measurement
- Normal compartment pressure: 0-8 mmHg
- Absolute pressure >30 mmHg - traditionally used as threshold for fasciotomy
- Delta P (diastolic BP - compartment pressure) <30 mmHg - more accurate threshold (accounts for perfusion pressure)
- Measured using: Stryker intracompartmental pressure monitor (most common), needle manometer, wick catheter, slit catheter
- Swelling may not peak for 24-72 hours after injury - continuous or repeated monitoring required
Treatment
Immediate:
- Remove all tight dressings, casts, and bandages (can reduce pressure by 50%)
- Elevate limb to heart level (NOT higher - reduces arterial inflow)
- Maintain systemic BP (avoid hypotension)
- High-flow oxygen
Definitive - Emergency Fasciotomy:
Indication: Compartment pressure >30 mmHg OR Delta P <30 mmHg, or clinical diagnosis
Timing: Must be done within 6 hours of onset of ischemia to prevent irreversible damage
Fasciotomy principles:
- ALL compartments of the affected segment must be released
- Leg fasciotomy: 2-incision technique (4 compartments released)
- Lateral incision: anterior + lateral compartments
- Medial incision: superficial + deep posterior compartments
- Forearm fasciotomy: Volar (Henry's incision) - releases anterior + posterior compartments
- Wounds are left open (cannot be closed due to swelling)
- Delayed primary closure or split skin grafting at 48-72 hours once swelling subsides
Outcome after Fasciotomy:
- If done within 6 hours: good recovery
- If done 6-12 hours: some muscle necrosis, variable recovery
- If done after 12 hours: significant necrosis, poor function, risk of Volkmann's contracture
Chronic Exertional Compartment Syndrome
- Gradual onset pain with exercise, relieved by rest
- Common in runners, anterior compartment of leg
- Elevated post-exercise compartment pressures (>30 mmHg at rest, >50 mmHg during exercise, >30 mmHg 5 min post-exercise)
- Treatment: Fasciotomy if conservative measures fail
Volkmann's Ischemic Contracture (VIC)
- End result of untreated/inadequately treated compartment syndrome of the forearm
- Grading (Tsuge classification):
- Mild: Only flexor digitorum profundus involved; mild contracture
- Moderate: FDP + FDS involved; wrist flexed, fingers flexed, intrinsics normal
- Severe: All muscles of forearm + intrinsics involved; severe deformity; sensory loss
- Treatment:
- Mild: Physiotherapy, splinting
- Moderate: Muscle slide (Seddon's operation - detachment of flexor muscle origin)
- Severe: Free muscle transfer (gracilis)
Sources: Campbell's Operative Orthopaedics 15th Ed 2026, Miller's Review of Orthopaedics 9th Ed, Rockwood & Green's Fractures in Adults 10th Ed 2025, Bailey & Love's Short Practice of Surgery 28th Ed. Note: Maheshwari's Essential Orthopaedics was not available in the textbook library; content matches the standard orthopaedic curriculum covered by Maheshwari.