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Neuropathic Joint / Charcot Arthropathy

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1. DEFINITION

• Harrison's Principles of Internal Medicine 22E, p. 3012
• Miller's Review of Orthopaedics 9th Ed, p. 602

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2. HISTORY

• First described by Jean-Martin Charcot in 1868 in patients with tabes dorsalis (neurosyphilis)
• Today, diabetes mellitus is the most common cause
• The term "Charcot joint" honors him; "neuropathic arthropathy" is the more accurate modern term

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3. CAUSES (Etiology) - HIGH-YIELD

• Rheumatology 2-Volume Set 2022, p. 2088
• Campbell's Operative Orthopaedics 15th Ed, Box 7.7

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4. PATHOPHYSIOLOGY - TWO THEORIES

Theory 1: Neurovascular Theory (French theory - Charcot's own)

• Neurologic damage → autonomic dysfunction → arteriovenous shunting → increased local blood flow
• Increased blood flow → bone resorption (osteoclastic > osteoblastic activity)
• TNF-alpha and IL-1B → increased NF-kB → increased osteoclast production → bone loss
• This is the "vascular" mechanism - bone melts away

Theory 2: Neurotraumatic Theory (German theory - Virchow & Volkmann)

• Loss of deep pain and proprioception → protective neuromuscular reflexes gone
• Joint subjected to repeated unperceived microtrauma
• Ligament tears, microfractures accumulate without healing response
• This is the "mechanical" mechanism - joint is beaten to destruction

• Campbell's Operative Orthopaedics 15th Ed (foot & ankle chapter)

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5. JOINT DISTRIBUTION BY DISEASE

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6. INCIDENCE

• Occurs in approximately 1-1.5% of diabetic patients
• Up to 7.5% of diabetics with neuropathy
• Usually occurs at age ≥50 years in someone with diabetes for several years
• Up to 35% present with bilateral disease
• Pain is present in up to 50% of cases (not always painless!)

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7. CLINICAL FEATURES

Symptoms:

• Swelling, warmth, redness, and deformity of the joint
• Disproportionately little pain for the degree of radiographic destruction (classic)
• Pain may occur in up to 50% from intraarticular fractures of osteophytes
• History of trivial or minor trauma triggering acute presentation
• Swelling and redness often improve in the morning (worse with activity)

Signs:

• Progressive joint enlargement (bony overgrowth + effusion)
• Joint instability, hypermobility
• Deformity - "rocker-bottom foot" in diabetic Charcot foot (downward collapse of tarsal bones → convexity of sole)
• Large bony prominences palpable (osteophytes protruding from top of foot)
• Calluses over metatarsal heads → pressure ulcers → osteomyelitis
• Crepitus, loose bodies

Classic Diabetic Charcot Foot:

• Warm, swollen, erythematous foot
• Arch collapse - rocker-bottom deformity
• Often confused with cellulitis or osteomyelitis
• No remembered significant trauma (or only trivial trauma)
• Harrison's 22E, p. 3012

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8. RADIOLOGICAL FEATURES

1. Distension of joint (effusion)
2. Density increased (sclerosis/eburnation)
3. Detritis (loose bodies, intraarticular fragments)
4. Dislocation / subluxation
5. Degenerative changes (joint space loss, osteophytes)
6. Destruction / Disorganization (fragmentation of bone)

• Periarticular bone fragmentation
• Subchondral bone sclerosis (eburnation)
• Large osteophytes at joint margins
• Marked joint destruction out of proportion to clinical pain
• Resorption and tapering of distal metatarsal bones (in diabetic foot)
• "Lisfranc fracture-dislocation" pattern at tarsometatarsal joints

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9. HISTOLOGY

• Osteochondral fragments embedded within the synovium - this is diagnostic of neuropathic arthropathy
• Similar to severe OA: cartilage fragmentation, subchondral eburnation, osteophytes, loose bodies
• More advanced: erosions, devitalized bone, microscopic bone/cartilage fragments
• Synovial fluid: noninflammatory, may be xanthochromic or bloody, contains fragments of synovium, cartilage, and bone

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10. STAGING - EICHENHOLTZ CLASSIFICATION (Most Important)

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11. BRODSKY CLASSIFICATION (Anatomic - Exam Favourite)

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12. INVESTIGATIONS

Imaging:

• Plain X-ray - first line; shows the "6 Ds" as above
• MRI - early detection; differentiates from osteomyelitis; shows bone marrow edema, joint effusion
• Bone scan (Technetium-99m) - increased uptake in BOTH neuropathic joint AND osteomyelitis - cannot differentiate
• Indium-111 labeled WBC scan - increased uptake in osteomyelitis but NOT in neuropathic joint - useful for differentiation
• CT scan - better characterizes bony fragmentation and deformity

Lab:

• ESR, CRP - may be elevated in acute phase
• Blood glucose, HbA1c - to diagnose/control diabetes
• Serologic tests for syphilis (VDRL, TPHA) if suspected
• Synovial fluid analysis: noninflammatory; fragmented cartilage/bone; absence of crystals and low neutrophils (high neutrophils suggest osteomyelitis)

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13. DIFFERENTIAL DIAGNOSIS

• Neuropathic joint: distinct joint margins, Indium-111 WBC scan NEGATIVE
• Osteomyelitis: blurred joint margins, Indium-111 WBC scan POSITIVE
• Technetium bone scan: positive in BOTH - not helpful for differentiation

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14. TREATMENT

Goals:

1. Achieve Eichenholtz Stage 3 (resolution)
2. Maintain alignment and plantigrade foot
3. Preserve ambulatory status
4. Minimize soft tissue breakdown and ulceration

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A. NON-OPERATIVE (Conservative) - First line

• Total Contact Cast (TCC) - gold standard for acute Charcot foot
  • Non-weight-bearing for at least 8 weeks (Harrison's) to 4-6 weeks (acute phase)
  • Distributes pressure evenly, reduces edema
  • Continued until warmth, swelling subside
• Once swelling/warmth resolve → transition to custom brace
  • AFO (Ankle-Foot Orthosis)
  • CROW boot (Charcot Restraint Orthotic Walker)

• Bisphosphonates (e.g., pamidronate, alendronate) - reduce osteoclast activity; useful in acute phase
• Neuroleptic medications (for neuropathic pain)
• Antidepressants (amitriptyline, duloxetine) - neuropathic pain
• Topical anesthetics
• Treatment of underlying cause (glucose control in diabetes)
• Protective inserts and orthotics + regular foot examination - extremely important for prevention

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B. OPERATIVE TREATMENT

1. Stable deformity with recurrent ulcers secondary to bony prominence
2. Unstable/unbraceable deformity
3. Ankle and hindfoot Charcot (high failure rate of conservative management)
4. Failed conservative treatment

• Intramedullary (IM) rod - provides internal stability; can be left indefinitely
• Multiplanar external fixator - alternative option
• Even with radiographic nonunion, many patients can be pain-free and functional

• Generally a relative contraindication
• TKA: fair results reported; requires attention to alignment, ligamentous balancing, bone grafting
• THA: high rates of recurrent dislocation and loosening; surgery only for severe disability

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15. COMPLICATIONS

1. Pressure ulcers - over bony prominences/metatarsal heads
2. Osteomyelitis - from infected ulcers; major cause of morbidity
3. Recurrent deformity - especially with high BMI
4. Amputation - in severe, uncontrolled cases with osteomyelitis
5. Deep vein thrombosis - with prolonged immobilization
6. Nonunion after surgical fusion
7. Dislocation/loosening after arthroplasty
8. Bilateral disease in up to 35%

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16. PROGNOSIS / NATURAL HISTORY

• Natural history: acute inflammation → bone resorption → consolidation → stable deformity
• Takes 6-18 months to progress through stages
• Development of Charcot in diabetics is not related to body weight
• Recurrence linked to higher BMI
• Medial column of foot fails before lateral (pull of posterior tibial tendon)
• Sagittal plane deformities more likely to cause ulceration than transverse plane abnormalities
• Early immobilization prevents progression to advanced stages
• Diabetic patients with Charcot have lower quality of life than diabetics without it

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17. KEY EXAM POINTS SUMMARY

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• Campbell's Operative Orthopaedics 15th Edition 2026
• Miller's Review of Orthopaedics 9th Edition
• Harrison's Principles of Internal Medicine 22E (2025)
• Rheumatology 2-Volume Set (2022, Elsevier)

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Foot Drop - Complete Guide for Orthopaedic Postgraduate Exam

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1. DEFINITION

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2. ANATOMY - THE FOUNDATION (Know This Inside Out)

The Common Peroneal (Fibular) Nerve

• Origin: Terminal branch of sciatic nerve (L4, L5, S1, S2)
• Course: Descends in popliteal fossa → winds around the neck/head of fibula (most vulnerable point) → enters peroneus longus muscle → divides into two terminal branches

Two Terminal Branches:

A. Deep Peroneal Nerve (Anterior Tibial Nerve)

B. Superficial Peroneal Nerve

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3. GAIT IN FOOT DROP - STEPPAGE GAIT

1. Exaggerated hip and knee flexion during swing phase
2. Raises the leg higher than normal to prevent the foot dragging
3. Foot "slaps" down on heel strike
4. Characteristic "slap" sound with each step
5. May also circumduct the leg to clear the foot

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4. CAUSES - LEVEL-BY-LEVEL APPROACH (HIGH YIELD)

Level 1: Cortical / Upper Motor Neuron

• Cerebral stroke (parasagittal cortical lesion - leg area)
• Brain tumor
• Cerebral palsy (spastic type)
• Multiple sclerosis

Level 2: Spinal Cord

• Spinal cord injury / trauma
• Spinal cord compression (disc, tumor, abscess)
• Motor neuron disease (ALS)
• Transverse myelitis

Level 3: Nerve Root (L4-L5 Radiculopathy) ← VERY COMMON

• L4-L5 disc prolapse (most common spinal cause)
• L5 root compression by disc or osteophyte
• Cauda equina syndrome
• Key: L5 radiculopathy - also has back pain + dermatomal sensory loss over dorsum of foot

Level 4: Lumbosacral Plexus

• Lumbar plexopathy (diabetes, malignancy)
• Retroperitoneal hemorrhage
• Post-delivery (obstetric palsy - baby's head pressing on lumbosacral trunk)

Level 5: Sciatic Nerve

• Sciatic nerve palsy (deep injection in buttock - commonest iatrogenic cause in India)
• Hip dislocation / acetabular fractures
• Posterior surgical approach to hip

Level 6: Common Peroneal (Fibular) Nerve ← MOST COMMON PERIPHERAL CAUSE

• Compression (most frequent cause):
  • Prolonged squatting - "strawberry picker's palsy", yoga foot drop
  • Leg crossing - habitual leg crossers, especially after weight loss
  • Cast or tight bandage at fibula head
  • Bedridden patients - pressure on outer knee
  • Intraoperative positioning (lateral decubitus, lithotomy position)
  • Post-arthroplasty (TKA/THA) - "post-arthroplasty foot drop"
• Trauma:
  • Proximal fibular fracture
  • Knee dislocation (peroneal nerve injured in 25-45% of knee dislocations!)
  • Tibial plateau fracture
  • Laceration/penetrating injury
• Masses:
  • Intraneural ganglion (from superior tibiofibular joint capsule) - underdiagnosed but treatable
  • Baker cyst
  • Ganglion cyst
  • Osteochondroma
  • Schwannoma
• Leprosy (common in India)
• Stretch injury - forced foot inversion + plantarflexion ("punter's palsy" in footballers)
• Weight loss - nerve becomes vulnerable without subcutaneous fat padding

• TKA - retractor tip compressing nerve against proximal fibula (most common TKA nerve injury)
• THA - especially with valgus-flexion deformity correction
• Tibial osteotomy - EHL nerve supply at risk

Level 7: Anterior Compartment

• Anterior compartment syndrome - pressure necrosis of tibialis anterior and deep peroneal nerve

Level 8: Ankle (Anterior Tarsal Tunnel Syndrome)

• Compression of deep peroneal nerve under the inferior extensor retinaculum
• Causes: fractures, tight shoes, ankle sprain
• Only EDB affected; sensory loss only in first web space

Level 9: Muscle / Tendon

• Tibialis anterior tendon rupture
• Myopathies (rare)
• Scapuloperoneal syndromes

Level 10: Peripheral Neuropathies (Bilateral foot drop)

• Diabetes mellitus
• Charcot-Marie-Tooth disease (hereditary motor-sensory neuropathy)
• Alcohol neuropathy
• Lead poisoning
• Guillain-Barré syndrome
• Leprosy

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5. CLINICAL FEATURES OF COMMON PERONEAL NERVE PALSY (Most Common Cause)

History:

• Inability to lift the foot/toes
• Foot drag while walking
• Frequent tripping/falling
• Numbness/tingling over dorsum of foot and lateral leg
• History of recent weight loss, leg crossing, prolonged squatting, trauma, surgery

Examination:

• Loss of dorsiflexion (ankle) - tibialis anterior
• Loss of toe extension (EHL, EDL)
• Loss of foot eversion (if whole common peroneal involved)
• Plantar flexion and inversion PRESERVED (tibial nerve intact)
• Wasting of anterior and lateral compartment muscles in chronic cases

• Loss over lateral leg (lower 2/3) and dorsum of foot
• First web space involved if deep peroneal involved
• Sole of foot NORMAL (tibial nerve territory) - this distinguishes it from sciatic nerve palsy

• Ankle jerk (S1) PRESERVED (gastrocnemius-soleus is tibial nerve)
• Knee jerk normal
• Plantar response: normal (flexor)

• Foot rests in plantarflexion and inversion at rest (equinovarus posture)
• No inversion of foot on walking (tibialis posterior - tibial nerve - still works)
• Tinel's sign may be positive at fibular head

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6. DISTINGUISHING FOOT DROP CAUSES - KEY DIFFERENTIAL POINTS

• Tibialis posterior (inversion) is spared in peroneal palsy but weak in L5 radiculopathy - this is the key distinguishing muscle
• Short head of biceps femoris is supplied by the common peroneal division of sciatic nerve in the thigh - if abnormal on EMG, lesion is ABOVE the fibular head (sciatic nerve), not at fibular head

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7. EVALUATION / INVESTIGATIONS

Step 1: Clinical Localization

• Walk on heels (tests dorsiflexion - will fail)
• Observe gait - steppage gait
• Test all muscles systematically (grade 0-5 MRC scale)
• Test sensation precisely
• Check reflexes
• Tinel sign at fibular head
• Spine examination (SLR, dermatomes)

Step 2: Electrodiagnostic Studies (Most Important Investigation)

• Tests deep and superficial peroneal motor and sensory responses
• Can demonstrate focal conduction block across fibular head
• Compare both sides
• Fibular motor amplitude recording tibialis anterior = best prognostic indicator
• Low/absent amplitude = axonal loss = poor prognosis
• Conduction block across fibula head = demyelination = good prognosis

• Denervation (fibrillations, positive sharp waves) in peroneal-innervated muscles
• Key muscles to test:
  • Tibialis anterior
  • EHL, EDL, EDB
  • Peroneus longus/brevis
  • Short head of biceps femoris - if abnormal, lesion is in thigh/sciatic nerve
  • Tibialis posterior - if abnormal, suggests L5 radiculopathy, NOT peroneal palsy
  • Paraspinal muscles (L4-L5 level) - if abnormal, suggests radiculopathy

• Fibrillations appear 2-3 weeks after nerve injury
• Early EMG (within days) only shows reduced/absent motor unit action potentials
• Repeat at 4-6 weeks for full picture

Step 3: Imaging

• Proximal fibula (fracture, tumor)
• Knee joint (dislocation, degenerative changes, osteochondroma at fibular head)
• Lumbar spine (disc space narrowing, osteophytes, spondylolisthesis)

• MRI lumbar spine - for radiculopathy (disc herniation, spinal stenosis, tumor)
• MRI knee - for intraneural ganglion, Baker cyst, tumors, soft tissue masses at fibular head
• Cross-sectional area of nerve on MRI
• Better than ultrasound for spinal pathology

• Preferred imaging for fibular head lesions - slightly more accurate than MRI for compressive fibular neuropathies
• Shows thickened nerve (cross-sectional area >8 mm² is abnormal)
• Identifies intraneural ganglia, tumors, ganglia, Baker cysts
• Can identify involvement of anterior fascicles (deep peroneal fibers)
• Dynamic assessment possible

• For bony lesions (tumors, osteochondroma, fractures)
• CT myelogram if MRI contraindicated

Step 4: Blood Tests

• Blood glucose / HbA1c - diabetes
• ESR, CRP - inflammatory/infective causes
• Serum B12, folate - nutritional neuropathy
• Heavy metals (lead) - if occupational exposure
• Nerve biopsy - if hereditary neuropathy suspected (CMT)

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8. COMPLETE vs INCOMPLETE FOOT DROP

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9. TREATMENT

A. Non-Surgical (Conservative)

1. Remove cause - remove tight cast, unpad the knee, change position of bed-bound patient
2. For post-TKA peroneal palsy: Remove compressive dressings and flex the knee (reduces tension on nerve) - first treatment
3. Protect foot from pressure sores

• AFO (Ankle-Foot Orthosis) - custom-made plastic AFO
  • Holds foot in 90° or slight dorsiflexion
  • Prevents equinus contracture
  • Allows functional gait
  • Used while awaiting nerve recovery
• Functional electrical stimulation (FES) - emerging option

• Passive range-of-motion exercises (prevent contractures)
• Stretching of Achilles tendon
• Strengthening of partially active muscles
• Gait training with AFO

• Treat underlying cause (control diabetes, treat leprosy, supplement B12)
• Nerve regeneration: no proven pharmacological agents
• Pain management for neuropathic pain

• If nerve not cut: most palsies show return within 3 months (for neuropraxia)
• Axonotmesis: slower recovery, 1 mm/day nerve regeneration
• Watch for: Tinel sign advancing distally = progressing regeneration

B. Surgical

1. No recovery at 3 months + EMG showing no evidence of reinnervation
2. Complete palsy with known structural cause (ganglion, tumor, entrapment)
3. Persistent foot drop >1 year with no recovery
4. Known transection (neurotmesis) - early repair

• For intraneural ganglia, fibular tunnel syndrome, entrapment
• Results: good for demyelinating lesions

• Direct end-to-end repair if gap small
• Sural nerve graft if large gap
• Best results within first 6 months

• Release of scar tissue around nerve
• For traction injuries

• Tibialis posterior (tibial nerve, L4-L5) rerouted to dorsum of foot
• Transferred through interosseous membrane ("transmembranous route") to dorsum of foot
• Attached to mid-dorsum (third cuneiform / base of second metatarsal)
• Prerequisites:
  • Tibialis posterior must be grade 4-5 strength
  • Foot must be passively correctable
  • Joint must be mobile
  • TAL (Tendo-Achilles Lengthening) if equinus present
• Indication: Persistent foot drop >1 year with no neurological recovery

• Peroneus longus to dorsum
• EHL to dorsum (if hindfoot stable)

• For rigid deformity with irreversible foot drop
• Provides stable plantigrade foot
• Triple arthrodesis (subtalar + talonavicular + calcaneocuboid) - for fixed equinovarus
• Lambrinudi's arthrodesis - special triple arthrodesis with dorsal wedge at talonavicular to correct foot drop passively

• Implantable devices for irreversible cases

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10. PROGNOSIS - KEY NUMBERS

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11. POST-TKA / POST-THA FOOT DROP - SPECIAL SCENARIO

• Most common nerve injury after TKA
• Usually due to retractor tip compressing nerve against proximal fibula
• Also with valgus + flexion contracture correction
• Immediate management: Remove compressive dressings + FLEX THE KNEE
• Most recover within 3 months if nerve not cut
• If no recovery at 3 months: EMG/NCS → explore and decompress

• Peroneal division of sciatic nerve most at risk (because it has less movement capacity)
• Risk factors: cementless prosthesis, revision surgery, leg lengthening >2.7 cm
• Immediate management: flex hip, flex knee (reduce tension on sciatic nerve)

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12. KEY EXAM SUMMARY TABLE

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• Localization in Clinical Neurology 8th Edition - comprehensive nerve anatomy and lesion localization
• Bradley and Daroff's Neurology in Clinical Practice - differential diagnosis and electrodiagnostics
• Campbell's Operative Orthopaedics 15th Ed 2026 - surgical management and TKA peroneal palsy
• Miller's Review of Orthopaedics 9th Ed - gait analysis and classification
• Gray's Anatomy for Students - anatomy of common fibular nerve

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Management of Claw Hand - Complete Orthopaedic PG Exam Guide

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1. DEFINITION

• Hyperextension at the metacarpophalangeal (MCP) joints
• Flexion at the proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints

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2. ANATOMY - WHY THE CLAW FORMS (The Key Concept)

Normal Intrinsic Function:

1. Flex the MCP joint (via their insertion into the volar plate/flexor aspect)
2. Extend the PIP and DIP joints (via their insertion into the lateral bands of the extensor hood)

What happens when intrinsics are paralyzed:

The "Paradox of Ulnar Clawing" - High vs Low Lesion:

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3. CAUSES OF CLAW HAND

A. Ulnar nerve palsy (Most common cause)

• Ring + little fingers only (ulnar 2 fingers)
• Why? Lumbricals to ring and little fingers = ulnar nerve. Lumbricals to index and middle = median nerve
• Degree of clawing: Ring > little (lumbrical to index/middle fingers partially corrects by median nerve)

B. Combined median + ulnar nerve palsy

• All four fingers involved
• Called "complete intrinsic minus hand" or "ape hand" + claw combined

C. Leprosy (Hansen's disease)

• Most common cause in India
• Ulnar nerve affected at elbow → ulnar claw
• Combined median + ulnar involvement = all finger clawing
• May have fixed contractures

D. Volkmann's ischemic contracture (severe form)

• Post-compartment syndrome
• Intrinsic-minus or claw hand deformity
• Fibrotic muscles, contractures

E. Rheumatoid arthritis

• Intrinsic muscle tightening → intrinsic-plus deformity (opposite) OR
• Intrinsic atrophy from nerve involvement → claw pattern

F. Cerebral palsy / Spastic conditions

• UMN type - different from true claw (has spasticity)

G. Charcot-Marie-Tooth disease

• Hereditary motor-sensory neuropathy
• Progressive clawing of all fingers

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4. CLINICAL ASSESSMENT - THE EXAMINATION SEQUENCE

Inspection:

• Which fingers are clawed? (Ulnar 2 only? All 4?)
• Degree of clawing (mild to severe)
• Wasting of interosseous spaces (hollowing of dorsal web spaces)
• Hypothenar wasting (ulnar palsy)
• Thenar wasting (median palsy)
• Skin changes - anaesthetic skin, ulcers, scars (leprosy)

Assessment of deformity:

• Flexible: can passively correct MCP hyperextension → surgical candidate
• Fixed: contractures present → needs preliminary treatment before tendon transfer

Key Clinical Tests:

1. Bouvier's Test (Most Important for Surgical Planning)

2. Froment's Sign (for adductor pollicis weakness in ulnar palsy)

• Ask patient to hold a flat object between thumb and index finger
• In ulnar palsy: adductor pollicis paralyzed → compensates by flexing thumb IP joint using FPL (median nerve)
• Positive: IP joint flexes during pinch → FPL compensating

3. Assessment of passive correctability:

• Can you passively flex the MCP and extend the PIP? → Prerequisite for tendon transfer
• If NOT passively correctable → splinting first, or PIP arthrodesis

4. Muscle testing (MRC grading 0-5):

• Test all intrinsic muscles: interossei (abduction/adduction), lumbricals
• Test extrinsic muscles: FDP, FDS, FPL, EPL, EDC

5. Sensory assessment:

• Two-point discrimination, monofilament testing
• Maps distribution (ulnar half of ring + entire little finger = ulnar nerve)

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5. PRINCIPLES OF MANAGEMENT

Step 1: Treat the cause (if possible)

• Nerve repair/decompression if nerve injury is recent and accessible
• Leprosy treatment (MDT - multidrug therapy)
• Release of entrapment (cubital tunnel release for ulnar nerve)
• If nerve can recover → wait for recovery (up to 18-24 months)

Step 2: Prevent/correct contractures (Splinting)

• Lively/dynamic splints - hold MCP in slight flexion to prevent fixed hyperextension contracture
• Preserve passive range of motion
• Prerequisites before any tendon transfer:
  • Passive MCP flexion must be possible
  • Passive PIP extension must be possible
  • Skin must be healthy, no ulcers

Step 3: Surgical correction (Tendon transfers or static procedures)

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6. SURGICAL MANAGEMENT - DETAILED

The Goal of Surgery:

1. Bouvier's test result → static vs dynamic
2. Available muscles (not paralyzed, grade 4+, expendable)
3. Pattern of nerve palsy (ulnar only vs combined)
4. Passive correctability of joints

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A. STATIC PROCEDURES

1. Zancolli Capsulodesis (Most Important Static Procedure)

1. Transverse incision in palm at distal palmar crease
2. Expose flexor tendon sheaths at each MCP joint
3. Retract flexor tendons → expose MCP volar plate
4. Resect an elliptical segment of the volar fibrocartilaginous plate (or advance it proximally)
5. Close volar plate with non-absorbable sutures → creates MCP flexion contracture of 10-30°
6. K-wires to maintain position if needed
7. Dorsal splint with MCP in flexion + wrist in extension

2. Fowler Tenodesis

• Activated by wrist flexion (passive, not active)
• Not useful in patients with wrist flexion weakness

3. Riordan Tenodesis

• NOT activated by wrist motion (unlike Fowler)

4. Bone Block (Mikhail)

• Dorsal bone block at MCP joint prevents hyperextension
• Rarely used

5. MCP Joint Arthrodesis

• For severe, irreversible cases
• Sacrifices motion

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B. DYNAMIC PROCEDURES

The Route of Transfer

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1. Modified Stiles-Bunnell Procedure

1. Into bone at base of proximal phalanx (safest)
2. Into flexor sheath
3. Into lateral band (highest risk of intrinsic-plus)

2. Zancolli Lasso Procedure

• FDS tendon is divided distally
• Passed through a slit in the flexor pulley sheath just distal to the MCP joint
• Looped back and sutured to itself
• Creates a dynamic block - when FDS contracts, it flexes the MCP
• Technically a dynamic transfer because FDS is still a functioning muscle-tendon unit

3. Brand Transfer (Paul Brand - Leprosy surgeon)

• Palmar route (through carpal tunnel): Passes under palmar ligaments
• Dorsal route (through interosseous spaces): More common, safer for median nerve

4. Riordan Transfer (FCR-based)

5. Fowler Transfer (Riordan modification - most commonly tested)

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C. COMBINED NERVE PALSIES

Low Median + Low Ulnar Palsy (at wrist)

• All four fingers clawed + thumb opposition + adduction lost
• Clawing: Brand transfer (ECRB with graft) - best option
• Opposition: Riordan transfer (FCR-based)
• Thumb adduction: EIP through third intermetacarpal space to adductor insertion

High Median + High Ulnar Palsy (above elbow)

• FDS, FDP (all fingers), all intrinsics, thenar, hypothenar all paralyzed
• Only radial nerve muscles available for transfer
• Treatment:
  • Arthrodesis of thumb MCP joint
  • Zancolli capsulodesis of all MCP joints (for clawing)
  • ECRL transfer for finger flexion
  • ECRB for thumb and finger extension

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7. SPECIAL CONSIDERATIONS

Leprosy Claw Hand Management

• Most important message: Prevent the claw from becoming FIXED
• Use dynamic splints early during active nerve inflammation
• Prednisolone for acute leprous neuritis (reduces nerve damage)
• Once deformity is fixed → surgical correction

1. If disease is inactive and joints are mobile:
   • Brand transfer or Riordan transfer
2. If skin is anaesthetic: Extra care to avoid pressure ulcers post-surgery
3. Thumb: Opponensplasty for opposition loss (median nerve)

Post-Volkmann's Ischemic Contracture

• Claw hand from intrinsic fibrosis
• Treatment:
  • Muscle slide (origin release of intrinsic muscles) for early/mild cases
  • Tendon lengthening
  • Limited goals; contracture releases improve function partially

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8. PREREQUISITES FOR TENDON TRANSFER

1. Passive correctability - MCP must flex passively, PIP must extend passively
2. Donor muscle grade 4-5 MRC strength (will lose 1 grade after transfer)
3. Stable skeletal framework - no untreated fractures
4. Good soft tissue cover - no active infection, healing scars
5. Patient motivation + compliance for rehabilitation
6. Joint contractures corrected first (by splinting or surgery)
7. If nerve can still recover - wait at least 18-24 months before tendon transfer

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9. SUMMARY TABLE - PROCEDURES AT A GLANCE

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10. KEY EXAM POINTS SUMMARY

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• Campbell's Operative Orthopaedics 15th Edition 2026 - Chapter 76 (Tendon transfers, intrinsic reconstruction)
• THIEME Atlas of Anatomy - General Anatomy and Musculoskeletal System - Ulnar nerve lesions
• Miller's Review of Orthopaedics 9th Edition - Hand surgery

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Rickets, Vitamin D-Dependent Rickets, and Vitamin D-Resistant Rickets

Complete Orthopaedic Postgraduate Exam Guide

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SECTION 1: RICKETS - THE FOUNDATION

1.1 Definition

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1.2 Vitamin D Metabolism - Know This First

SKIN (sunlight on 7-dehydrocholesterol)
        ↓
Vitamin D3 (cholecalciferol) - inactive
        ↓  [Liver 25-hydroxylase (CYP2R1)]
25(OH)D - calcidiol - still inactive (measured to assess stores)
        ↓  [Kidney 1α-hydroxylase (CYP27B1)] ← STIMULATED BY PTH
1,25(OH)2D3 - calcitriol - ACTIVE form (acts on gut, bone, kidney)
        ↓
Actions:
• ↑ intestinal absorption of Ca and PO4
• ↑ renal reabsorption of Ca and PO4
• ↑ bone mineralization
• ↑ bone resorption (with PTH)

• Two hydroxylation steps: Liver (25th position) then Kidney (1st position)
• Active form = 1,25(OH)2D3 = calcitriol = acts on Vitamin D Receptor (VDR)
• FGF23 (Fibroblast Growth Factor 23) - secreted by bone - INHIBITS the 1α-hydroxylase → reduces active vitamin D + promotes phosphate excretion

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1.3 Classification of Rickets

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SECTION 2: NUTRITIONAL RICKETS (Classic Vitamin D Deficiency)

2.1 Causes

• Inadequate sunlight exposure (most common cause worldwide)
• Dietary deficiency of vitamin D or calcium
• Exclusive breastfeeding beyond 3-6 months (breast milk low in Vit D)
• Prematurity - insufficient stores
• Malabsorption (celiac sprue, Crohn's, fat malabsorption) - Vit D is fat-soluble
• Dark skin in temperate climates - less UV penetration
• Maternal Vit D deficiency (congenital rickets - rare, as Vit D preferentially given to fetus)
• Phytate/oxalate-rich diet (binds calcium in gut) - common cause in India, Africa, Bangladesh

2.2 Pathophysiology - Step by Step

1. Low Vit D → ↓ intestinal absorption of Ca and PO4
2. ↓ serum Ca → PTH rises (secondary hyperparathyroidism)
3. PTH does two things:
   • Stimulates osteoclasts → bone resorption to maintain serum Ca
   • Stimulates kidney → phosphate excretion increases (phosphaturia)
4. Result: serum Ca maintained near normal, but serum PO4 falls sharply
5. Both Ca × PO4 product insufficient → osteoid cannot mineralize
6. In the growth plate: zone of provisional calcification fails → widened, disorganized physis
7. Osteoblasts keep laying down unmineralized osteoid → soft, expandable bone

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2.3 Clinical Features - Grouped by System

Skull:

• Craniotabes - softening of skull bones; ping-pong ball consistency on pressing occipital/parietal bones (earliest sign - from 3-6 months)
• Frontal bossing - excess osteoid deposition → prominent forehead
• Delayed closure of fontanelles (anterior fontanelle stays open beyond 18 months)
• Squared head (caput quadratum)

Chest:

• Rachitic rosary (Rickety rosary) - beaded nodularity at costochondral junctions (enlarged ends of ribs)
• Harrison's groove (Harrison's sulcus) - horizontal groove along lower chest margin where diaphragm pulls weakened ribs inward during inspiration
• Pigeon chest (pectus carinatum) - sternum pushed forward
• Barrel chest

Spine:

• Kyphosis or Kyphoscoliosis (especially lumbar region)
• Exaggerated lumbar lordosis in ambulatory children

Long Bones / Limbs:

• Widening of wrists and ankles (expanded metaphyses)
• Genu varum (bow legs) - from medial bowing of tibia/femur - most common in toddlers beginning to walk
• Genu valgum (knock knees) - in older children
• Coxa vara - femoral neck deformity
• Bowing of forearm bones - radius and ulna
• Pathologic fractures (greenstick fractures)

Other:

• Short stature - height below 5th percentile
• Dental abnormalities - delayed teething, enamel defects, dental caries
• Hypotonia and muscle weakness - characteristic; causes "frog posture" in infants
• Waddling gait - from coxa vara + proximal muscle weakness
• Delayed motor milestones (walking, sitting)
• Tetany - carpopedal spasm, Chvostek sign, Trousseau sign (in hypocalcemic form)
• Anemia

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2.4 Radiological Features (HIGH YIELD)

• Wrist (distal radius/ulna) - most useful
• Knee (distal femur / proximal tibia)
• Costochondral junctions

Key radiograph findings:

1. Widening of the growth plate (physis) - hallmark sign
2. Cupping of the metaphysis - concavity of the metaphyseal margin
3. Fraying of the metaphysis - irregular, frayed, "paintbrush" appearance
4. Loss of zone of provisional calcification - normally a bright dense line at physis; absent in rickets
5. Metaphyseal haziness - blurred, poorly defined metaphysis
6. General osteopenia - reduced bone density throughout
7. Bowing of long bones - genu varum (medial bowing of tibia/fibula), coxa vara
8. Codfishing of vertebrae - biconcave vertebral bodies
9. Looser zones (Milkman's fractures / pseudofractures) - more in osteomalacia (adults) - transverse radiolucent bands on compression side of bones; common in femoral neck, pubic rami, scapula
10. Delayed bone age - ossification centres appear late

• Decreased cortical thickness
• Relative radiolucency
• Looser zones / pseudofractures - pathognomonic

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2.5 Laboratory Findings

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2.6 Treatment of Nutritional Rickets

Medical (First line):

• Recommended daily intake: 600 IU (age 1-70 years) / 800 IU (>70 years)
• Deficiency treatment: 50,000 IU weekly for 3-12 weeks → then maintenance 800 IU/day
• In children: 1,000-6,000 IU daily based on weight

• Single oral/IM dose of 600,000 IU (or 100,000-300,000 IU)
• Used in non-compliant patients or where daily therapy not feasible
• Results in healing within weeks

• 1.5-2 g/day of elemental calcium
• Essential alongside Vit D (without calcium, Vit D alone gives incomplete response)

• Normocalcemia within 1 week of therapy
• PTH and ALP normalize in 3-6 months
• Radiographic healing: cupping/fraying begins resolving in 3-6 months
• Most deformities (bowing) resolve spontaneously with medical treatment if treated early

Surgical (For residual/progressive deformities):

1. Deformity persists or worsens despite adequate medical treatment
2. Active rickets must first be treated medically - never operate on active/uncontrolled rickets (bones too soft, poor healing)
3. Significant angular deformity causing functional disability
4. Age: generally after 3-4 years old when bone is stronger

• Valgus osteotomy of distal femur and/or proximal tibia - for genu varum
• Stapling / guided growth (hemiepiphysiodesis) - for ongoing deformity correction in growing children
• Dome osteotomy / closed wedge osteotomy - for severe cases
• Fixation: K-wires in plaster, or internal fixation depending on age/severity

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SECTION 3: VITAMIN D-DEPENDENT RICKETS (VDDR)

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3.1 VDDR Type I (Pseudovitamin D-Deficiency Rickets)

Biochemistry:

Clinical Features:

• Presents in children under 2 years (earlier/more severe than nutritional)
• Severe bony changes of rickets
• Hypocalcemic tetany and seizures (characteristic)
• Muscle hypotonia
• Radiological features identical to nutritional rickets

Treatment:

• Calcitriol (1,25(OH)2D = the active hormone) - bypasses the deficient enzyme
• Dose: 0.25-1 μg/day (physiologic doses sufficient - this is what distinguishes it from Type II)
• OR Alfacalcidol (1α-hydroxyvitamin D) - also bypasses the kidney step
• Calcium supplementation (1.5-2 g/day)
• Responds well to physiologic doses of calcitriol - excellent prognosis with treatment

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3.2 VDDR Type II (Hereditary Vitamin D-Resistant Rickets)

Biochemistry:

Clinical Features:

• Presents in infants under 1 year (earlier and more severe than Type I)
• Similar bony changes to nutritional rickets
• Alopecia (partial or total) - pathognomonic feature! Hair follicles have VDR; without functioning VDR → alopecia
• Poor dentition
• Hypocalcemic tetany and seizures
• Does NOT respond to normal or even high doses of vitamin D

Treatment:

• Very difficult to treat due to end-organ resistance
• Long-term nocturnal calcium infusions (IV calcium drip overnight) - normalizes PTH → reduces urinary phosphate → improves rickets and growth
• High-dose calcitriol (supraphysiologic) - may partially help mild cases
• Hair growth does NOT restore with treatment (alopecia is permanent)
• Outcome: improved skeletal disease but not alopecia

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3.3 VDDR Type III (Rare)

• Mutation in CYP3A4 gene → accelerated catabolism of Vit D metabolites
• Both 25(OH)D and 1,25(OH)2D are low
• Similar to phenytoin-induced Vit D deficiency

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SECTION 4: VITAMIN D-RESISTANT RICKETS (VDRR) / HYPOPHOSPHATEMIC RICKETS

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4.1 Pathophysiology - The FGF23 Story

• Produced by osteocytes and osteoblasts in bone
• Functions:
  1. Inhibits renal tubular phosphate reabsorption → phosphaturia → hypophosphatemia
  2. Inhibits renal 1α-hydroxylase → reduces 1,25(OH)2D production

• PHEX gene mutation (phosphate-regulating endopeptidase on X chromosome) → PHEX normally degrades FGF23 → without PHEX, FGF23 accumulates → extreme phosphaturia + suppressed Vit D activation

PHEX mutation → ↑ FGF23 → ↑ renal PO4 excretion → ↓ serum PO4
                          → ↓ 1α-hydroxylase → ↓ 1,25(OH)2D → ↓ gut PO4 absorption
Result: SEVERE hypophosphatemia + INAPPROPRIATELY LOW 1,25(OH)2D (should rise to compensate, but doesn't)

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4.2 Types of Hypophosphatemic Rickets

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4.3 X-linked Hypophosphatemic Rickets (XLH) - The Classic Form

Biochemistry:

• Ca is NORMAL (not low) - no secondary hyperparathyroidism
• PTH is NORMAL (no hypocalcemia to stimulate it)
• 25(OH)D is NORMAL (sunlight exposure/diet fine)
• Phosphaturia - key finding

Clinical Features:

• Usually presents after child begins to walk (1-2 years)
• Severe bowing deformities - more pronounced than nutritional rickets
• Short stature - disproportionate, lower limbs especially shortened
• Dental abnormalities - abscess, enamel defects, pulp anomalies
• Generally no tetany (Ca is normal)
• Muscle weakness less prominent than nutritional rickets
• May have craniosynostosis
• Rachitic bone changes on X-ray
• Does NOT respond to normal doses of vitamin D - hence "resistant"

Treatment:

1. Oral phosphate supplementation (elemental phosphate 1-2 g/day in divided doses, 4-5 times/day)
   • Multiple daily doses required (phosphate poorly retained)
   • Side effects: diarrhea, secondary hyperparathyroidism
2. Calcitriol (0.5-1 μg/day for adults; 0.025-0.05 μg/kg/day in children)
   • To counteract the FGF23-induced suppression of 1,25(OH)2D
   • Monitor for hypercalcemia and nephrocalcinosis

• Burosumab (Crysvita) - anti-FGF23 monoclonal antibody (IgG1)
  • Binds and neutralizes FGF23 → restores phosphate reabsorption + normalizes 1,25(OH)2D
  • FDA approved for children (≥1 year) and adults with XLH
  • Dose in children: 0.8-2 mg/kg every 2 weeks subcutaneously
  • Dramatically superior to phosphate + calcitriol for growth, rickets healing, bowing
  • Monitor: serum phosphate, alkaline phosphatase, 1,25(OH)2D

• Corrective osteotomy for residual bowing after medical control
• Only after disease is biochemically controlled
• Valgus osteotomy of distal femur + proximal tibia
• External fixator or internal fixation
• High recurrence rate if medical treatment not maintained

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SECTION 5: COMPARISON TABLE - THE KEY EXAM DIFFERENTIATOR

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SECTION 6: OTHER RELATED CONDITIONS

Renal Osteodystrophy

• Chronic renal failure → impaired 1α-hydroxylation → ↓ 1,25(OH)2D
• PLUS: phosphate retention → hypocalcemia → secondary hyperparathyroidism
• Combined features of rickets/osteomalacia + osteitis fibrosa cystica (from PTH)
• Radiograph: rickets features + subperiosteal resorption + "salt and pepper skull"
• Treatment: calcitriol + phosphate binders + calcium

Oncogenic Osteomalacia (Tumor-Induced)

• Rare mesenchymal tumors secrete FGF23 → identical to XLH
• Phosphatonin-mediated
• Treatment: find and remove the tumor → cure; if not found: phosphate + calcitriol or burosumab

Drug-Induced Rickets

• Phenytoin, rifampicin → induce CYP enzymes → accelerate catabolism of Vit D metabolites → functional deficiency
• Treatment: higher doses of Vit D supplementation

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SECTION 7: ORTHOPAEDIC SURGICAL MANAGEMENT OF DEFORMITIES

When to Operate

1. Deformity persists after 1-2 years of adequate medical treatment
2. Deformity is progressive or severe causing disability
3. Active rickets MUST be controlled first - biochemically quiescent disease
4. Child old enough for surgery (typically ≥4 years)

Types of Deformity Correction

Post-operative Care

• Immobilization in plaster/cast
• Continue medical treatment throughout (phosphate + calcitriol for VDRR)
• Monitor healing carefully - may be delayed if disease reactivates
• Recurrence is high in VDRR if medical treatment not maintained

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SECTION 8: EXAM SUMMARY - QUICK REVISION TABLE

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• Harrison's Principles of Internal Medicine 22E (2025, McGraw Hill) - Vit D metabolism, VDDR types
• Grainger & Allison's Diagnostic Radiology - X-ray features
• Guyton & Hall Textbook of Medical Physiology - Pathophysiology
• Miller's Review of Orthopaedics 9th Edition - Classification and orthopaedic management
• Robbins & Kumar Basic Pathology - Morphology and histology
• Rheumatology 2-Volume Set (Elsevier, 2022) - Biochemistry comparison table
• Rockwood & Green's Fractures in Adults 10th Ed (2025) - Causes and mechanisms

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Soft Tissue Flaps - Complete Orthopaedic Postgraduate Exam Guide

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1. DEFINITION

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2. THE RECONSTRUCTIVE LADDER

1. Supportive measures - dressings, negative pressure wound therapy (NPWT/VAC)
2. Direct/Primary closure - simplest; tension-free approximation
3. Secondary intention healing - granulation, small wounds
4. Skin graft - STSG or FTSG; needs vascular recipient bed
5. Local or regional flap - fasciocutaneous, muscle (brings blood supply)
6. Free flap - microsurgical transfer for complex/large defects

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3. INDICATIONS FOR FLAP COVERAGE

1. Exposed bone stripped of periosteum
2. Exposed tendon stripped of paratenon
3. Exposed joint/articular cartilage
4. Exposed orthopaedic implant (nail, plate, external fixator pin tract)
5. Exposed nerve or vessel
6. Irradiated tissue (poor vascularity)
7. Infected wounds where a vascularized flap adds defense
8. Large defects requiring bulk/dead space filling
9. Sensate coverage needed (e.g., weight-bearing areas of sole)

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4. CLASSIFICATION OF FLAPS

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A. By Blood Supply (Most Important Classification)

1. Random Pattern Flap

• No single named artery - relies on dermal and subdermal plexus (microcirculation)
• Blood supply unpredictable
• Length:breadth ratio must be respected:
  • Upper limb/face: up to 3:1
  • Lower limb: 1:1 or 2:1 (less rich blood supply)
• Examples: rotation flap, advancement flap, transposition flap
• Simple, widely available, no need to identify named vessels

2. Axial Pattern Flap

• Contains a single named arteriovenous pedicle running along its axis
• More predictable and reliable blood supply
• Greater resistance to infection
• Can have greater length:breadth ratio than random
• Can be pedicled (vessels kept intact) or used as free flap (vessels divided and reanastomosed)
• Examples: radial forearm flap (radial artery), latissimus dorsi flap (thoracodorsal artery), groin flap (superficial circumflex iliac artery)

3. Perforator Flap (Modern concept)

• Based on perforating vessels that emerge from deep vessels through muscle/fascia to skin
• Allows harvest of skin and fat alone without sacrificing the underlying muscle
• Lower donor site morbidity
• Requires Doppler marking of perforators preoperatively
• Examples: DIEAP (deep inferior epigastric artery perforator), ALT (anterolateral thigh), propeller flap
• Common perforator flaps: DIEAP, ALT, thoracodorsal artery perforator (TDAP), superior/inferior gluteal artery perforator (SGAP/IGAP)

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B. By Tissue Composition (Tissue Type)

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C. By Donor Site / Location of Transfer

1. Local Flap

• Tissue immediately adjacent to defect
• Requires that adjacent tissue is healthy (outside zone of injury)
• Subtypes by movement pattern (see Section 5)
• Examples: rotation flap, advancement flap, Z-plasty

2. Regional Flap

• Tissue from same anatomical region but not immediately adjacent
• Pedicle remains in continuity
• Examples: gastrocnemius for proximal tibia, pectoralis major for chest wall

3. Distant Flap (Pedicled)

• Tissue from a different anatomical region
• Pedicle bridges across - staged procedure usually needed
• Examples: groin flap for hand (degloved hand placed in abdominal pocket), cross-leg flap
• Disadvantages: requires multiple stages, immobilization

4. Free Flap (Free Tissue Transfer)

• Tissue completely divided from donor site including its vessels
• Vessels anastomosed to recipient vessels near defect (microsurgery)
• Single-stage procedure
• Most versatile - can reach any site
• Requires microvascular expertise

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D. By Method of Transfer (Movement)

1. Advancement Flap

• Tissue moved directly forward in a straight line to fill the defect
• No rotation
• Types: V-Y advancement, Moberg flap (for fingertip)
• V-Y: triangular incision → advanced → closed as Y shape

2. Rotation Flap

• Semicircular flap rotated into defect around a pivot point
• Random pattern in blood supply
• Rule: rotated flap should be no longer than width of its base
• Back-cut increases arc of rotation but reduces blood supply to base

3. Transposition Flap

• Flap transposed over an intervening bridge of tissue into adjacent defect
• Can be geometric (rhomboid/Limberg flap) or non-geometric
• May be axial or random
• Examples: Z-plasty, rhomboid flap

4. Propeller Flap (Modern)

• Islanded on a perforator pedicle, rotated up to 180° around the perforator axis
• Like a propeller spinning around its axis
• Used for pretibial/medial leg defects
• Identified with hand-held Doppler preoperatively
• Advantages: minimal donor morbidity, single stage, no need for microsurgery

5. Interpolation Flap

• Flap raised from nearby but non-adjacent area, passed over intact skin to reach defect
• Pedicle divided at second stage (3 weeks later)
• Example: cross-finger flap, forehead flap

6. Tube/Tubed Pedicle Flap

• Flap rolled into a tube to protect the pedicle
• Historical technique; rarely used today
• Example: Italian flap (Tagliacozzi)

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5. Z-PLASTY - THE CLASSIC LOCAL FLAP

1. Release of scar contracture (web space contractures, burns, flexor surface scars)
2. Reorientation of scar into RSTL
3. Correction of skin web deformities
4. Release of trapdoor deformities

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6. MATHES AND NAHAI CLASSIFICATION OF MUSCLES (Vascular Anatomy of Muscles)

• Type I and II = most reliable for free flap transfer
• Type IV = unreliable as free flap; too risky
• Type V (latissimus dorsi) = the workhorse free flap

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7. SPECIFIC FLAPS - TIBIAL FRACTURE COVERAGE (MOST EXAM-RELEVANT)

• Proximal third → Gastrocnemius flap
• Middle third → Soleus flap
• Distal third → Free flap (no reliable local muscle) OR fasciocutaneous flap OR propeller flap

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A. Gastrocnemius Flap (Proximal Third)

• Posterior midline incision
• Separate gastrocnemius from soleus
• Preserve sural nerve and great saphenous vein
• Pes anserinus may restrict rotation - can be released
• Muscle surface covered with split-thickness skin graft (STSG) Donor site: Primary closure of posterior calf Limitation: Cannot reach knee joint above joint line; cannot cover distal leg

B. Soleus Flap (Middle Third)

• Proximal: branches from popliteal artery
• Medial: posterior tibial artery branches
• Lateral: peroneal artery branches Unique feature: Can be used as a hemisoleus flap (split longitudinally) to cover different areas Use: Proximally based for middle third; distally based for distal third Technique: More complex dissection than gastrocnemius Limitation: Limited arc of rotation; within zone of injury for high-energy tibial fractures Donor site: Partial sacrifice acceptable (other head remains); STSG needed on muscle

C. Fasciocutaneous Flaps (All Thirds, Especially Middle and Distal)

• Based on medial perforators from posterior tibial artery
• Covers medial tibial defects
• Risk: great saphenous vein and saphenous nerve must be spared
• Secondary defect requires STSG

• Based on peroneal artery perforators in lateral compartment
• Less frequently used - reduced rotational reach
• Risk to superficial peroneal nerve

• Island of skin rotated 180° on a single perforator (identified by Doppler)
• Used for pretibial/medial leg defects including distal third
• Modern workhorse for many leg defects
• No muscle sacrifice; single stage

• Historical landmark: first described that including deep fascia allows longer, thinner, more reliable fasciocutaneous flaps in the lower extremity
• This observation led to the development of fasciocutaneous flap concept

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8. FREE FLAPS - KEY WORKHORSE FLAPS

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9. MUSCLE FLAP vs FASCIOCUTANEOUS FLAP - COMPARISON

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10. TIMING OF FLAP COVERAGE - CRITICAL FOR ORTHOPAEDICS

• Ideal: within 72 hours (before bacterial colonization becomes established)
• Definitive coverage within 7 days: significantly reduces infection rates
• Delay >7 days → higher risk of infection and flap failure
• "Fix and flap": bone fixation and soft tissue coverage at same operative setting is ideal (single-stage "orthoplastic" approach)
• Emergency fixation (external fixator) first, then formal fixation + coverage when patient stable

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11. FLAP MONITORING

• Color - pink (healthy), pale (arterial problem), blue/purple (venous congestion)
• Temperature - warm = good; cool = arterial compromise
• Capillary refill - <2 seconds = healthy
• Turgor/tension - soft = good; tense/firm = venous congestion
• Pin-prick bleeding - bright red = arterial flow; dark/no bleeding = problem
• Skin paddle "monitor" - LD muscle flap can have a de-epithelialized skin island left externally for monitoring

• Implantable Doppler - monitors vessel patency (Doppler signal continuously)
• Near-infrared spectroscopy - non-invasive tissue oxygenation
• Transcutaneous oxygen tension
• Handheld Doppler - check pedicle signal through skin

• Used for venous congestion of flaps (arterial supply intact, venous outflow blocked)
• Hirudo medicinalis (medicinal leech) - bites and allows blood to drain; secretes hirudin (anticoagulant) and histamine
• Risk: Aeromonas hydrophila infection → must cover with ciprofloxacin/trimethoprim

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12. COMPLICATIONS OF FLAPS

Early:

1. Flap necrosis - partial or total
   • Arterial: pale, cold flap → urgent re-exploration
   • Venous: congested, purple → leeches then re-exploration
2. Haematoma - compresses vessels → venous congestion → necrosis
3. Infection - especially in contaminated open fractures
4. Wound dehiscence
5. Seroma - especially with LD flap (use drains)

Late:

1. Partial necrosis requiring regrafting
2. Hypertrophic/keloid scarring
3. Contracture of donor site or flap
4. Flap bulkiness requiring revision/thinning (liposuction or direct excision)
5. Loss of sensation at donor site
6. Functional deficit at donor site (e.g., shoulder function after LD harvest)
7. Aesthetic issues

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13. SPECIFIC REGIONAL FLAP EXAMPLES FOR ORTHOPAEDICS

For the Hand:

• Thenar flap - for fingertip defect; PIP flexion contracture risk
• Cross-finger flap - for volar fingertip; distant from amputated finger; sensory recovery
• Homodigital flag flap - based on digital artery; homodigital (same finger) or heterodigital (adjacent finger)
• Moberg advancement flap - V-Y advancement on thumb; based on bilateral digital arteries
• Radial forearm free flap - large dorsal/palmar hand defects
• Groin flap (SCIA) - degloved hand placed in groin pocket; distant pedicle flap; 3-week wait

For the Foot/Ankle:

• Sural artery flap - distally based neurocutaneous flap on sural nerve + small saphenous vein; covers heel and ankle
• Dorsalis pedis flap - covers small foot/ankle defects
• Instep flap - sensate; excellent for heel/sole coverage
• Free flap (ALT, gracilis, LD) - for large/complex defects

For Hip/Thigh/Pelvis:

• Tensor fasciae latae (TFL) - Type I muscle; covers groin/trochanteric/perineal/hip defects
  • Pedicle: transverse branch of lateral femoral circumflex artery (from profunda femoris)
  • 10 × 30 cm skin flap available
  • Can be osteocutaneous (include iliac crest bone)
  • Motor: superior gluteal nerve; sensory: T12 + lateral femoral cutaneous nerve
• Rectus femoris - covers groin/lower abdominal wall defects
• Biceps femoris - covers ischial pressure sores
• Gluteus maximus - ischiallpressure sore coverage; Type III muscle

For the Knee:

• Medial gastrocnemius - proximal tibial defects + knee defect coverage
• Patellar/knee - rotation flaps from thigh/calf

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14. KEY EXAM CONCEPTS - QUICK SUMMARY

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• Rockwood & Green's Fractures in Adults 10th Edition (2025) - Reconstructive ladder, tibial coverage, free flaps table
• Miller's Review of Orthopaedics 9th Edition - Classification, Z-plasty, upper extremity
• Campbell's Operative Orthopaedics 15th Edition 2026 - TFL flap, perforator flaps
• Mulholland & Greenfield's Surgery 7th Ed - Mathes-Nahai classification, workhorse flaps