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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