Nerve Injuries in Orthopaedic Trauma

Peripheral nerve injury accompanies a large share of fractures and dislocations, and the examiner loves the fracture → nerve → clinical deficit triad. This note ties the Seddon/Sunderland classification to the classic limb palsies (wrist drop, claw hand, foot drop), their electrodiagnosis, prognosis, and management.

Classification — Seddon and Sunderland

Two parallel systems are tested. Seddon (1943) is clinical/3-tier; Sunderland (1951) is histological/5-tier and maps onto Seddon. Memorise the correspondence and recovery.

Seddon	Sunderland	Lesion	Wallerian degeneration	Recovery	Surgery
Neurapraxia	Grade I	Myelin damage; axon intact	Absent	Full, days–weeks (≤12 wk)	No
Axonotmesis	Grade II	Axon cut, endoneurium intact	Present	Good, ~1 mm/day	Usually no
—	Grade III	Axon + endoneurium; perineurium intact	Present	Incomplete, scarring	Sometimes
—	Grade IV	Axon + endo + perineurium; epineurium intact (neuroma-in-continuity)	Present	Poor	Yes
Neurotmesis	Grade V	Complete transection, all layers cut	Present	None without repair	Yes (repair/graft)

High-yield: A sixth grade (MacKinnon) = mixed pattern with varying fascicular involvement. But for NEET PG, Sunderland I–V with I=neurapraxia, II=axonotmesis, V=neurotmesis is the answer.

High-yield: Neurapraxia has the best prognosis (no Wallerian degeneration, no axonal loss) and recovers fully. Neurotmesis needs surgical repair. Axonotmesis recovers at the classic rate of ~1 mm/day (≈1 inch/month).

Mnemonic for severity order (mild → severe): "Never Axe Neat" → Neurapraxia → Axonotmesis → Neurotmesis.

Wallerian degeneration

After the axon is severed, the distal segment degenerates (axon + myelin) over ~7 days, cleared by Schwann cells and macrophages. The proximal stump regenerates from the node nearest the injury. Because the distal segment still conducts for the first 3–4 days, nerve conduction studies done too early give false reassurance — wait before prognosticating.

The four trauma-associated palsies (most tested)

1. Radial nerve — humeral shaft fracture

The radial nerve runs in the spiral (radial) groove of the humerus. Mid-shaft fractures, especially the junction of middle and distal third (Holstein–Lewis fracture), threaten it.

• Deficit: Wrist drop — loss of wrist and finger (MCP) extension, loss of thumb extension/abduction, loss of brachioradialis and supinator.
• Sensory: small patch over the dorsal first web space (anatomical snuffbox region).
• Grip: weak because wrist flexion (the extensors normally stabilise the wrist for a strong grip — tenodesis).

High-yield: Saturday night palsy = radial nerve compression in the spiral groove (arm over chair back). Crutch palsy = compression in the axilla → also affects triceps (high lesion). Wrist drop with intact triceps localises the lesion to the spiral groove or below.

Posterior interosseous nerve (PIN) palsy (e.g., Monteggia fracture, proximal radius): finger drop with preserved wrist extension (because extensor carpi radialis longus is spared, wrist deviates radially on extension). No sensory loss — PIN is purely motor.

2. Axillary (circumflex) nerve — shoulder dislocation / surgical neck of humerus

The axillary nerve winds around the surgical neck and passes through the quadrangular space.

• Most common cause: anterior shoulder dislocation (also surgical-neck-of-humerus fracture).
• Deficit: weak deltoid (abduction 15°–90°) and teres minor.
• Sensory: loss over the "regimental badge" area — lateral upper arm over deltoid.
• Test: sensory test is more reliable acutely than deltoid power (pain limits abduction). Always document deltoid sensation before and after reduction.

High-yield: Axillary nerve = most commonly injured nerve in anterior shoulder dislocation. The axillary artery can also be injured (especially in elderly with atherosclerotic vessels).

3. Common peroneal (fibular) nerve — knee / fibular neck

The common peroneal nerve is the most commonly injured nerve in the lower limb, vulnerable as it winds around the neck of the fibula (subcutaneous, fixed).

• Causes: knee dislocation (also injures popliteal artery — limb-threatening), proximal fibula fracture, tight plaster, prolonged squatting/leg-crossing, lateral position on operating table.
• Deficit: Foot drop — loss of dorsiflexion (deep peroneal: tibialis anterior, EHL, EDL) and eversion (superficial peroneal).
• Gait: high-stepping (steppage) gait, foot slap.
• Sensory: dorsum of foot and first web space (deep) / lateral leg (superficial).

High-yield: Knee dislocation = mandatory ankle-brachial index/angiography to exclude popliteal artery injury, plus common peroneal nerve documentation. Foot drop here can be neurapraxia (recovers) or neurotmesis (poor).

Deep vs superficial peroneal: Deep peroneal (anterior compartment) → dorsiflexion + first web-space sensation; this is the nerve threatened in anterior compartment syndrome of the leg.

4. Other examiner favourites

Injury	Nerve at risk	Deficit
Supracondylar fracture humerus (extension type)	Anterior interosseous (AIN, median branch) — most common	Cannot make "OK" sign (loss of FPL + FDP to index) — pinch grip lost, no sensory loss
Supracondylar (flexion type)	Ulnar nerve	Claw hand
Medial epicondyle fracture / cubital tunnel	Ulnar nerve	Claw hand, Froment's sign +
Hip posterior dislocation / acetabular fracture	Sciatic nerve (peroneal division more often)	Foot drop, loss of hamstrings/below-knee
Surgical neck humerus	Axillary	Deltoid
Distal radius (Colles) / lunate dislocation	Median nerve	Acute carpal tunnel
Fracture neck of fibula	Common peroneal	Foot drop

Hand deformity patterns (cross-link with anatomy)

High-yield: "Ulnar paradox" — a higher (proximal) ulnar nerve lesion produces a LESS deformed claw than a low wrist lesion, because the high lesion also paralyses the ulnar half of FDP, so the IP joints flex less. As the nerve recovers, clawing paradoxically worsens.

• Claw hand (ulnar): ring + little finger — hyperextension at MCP, flexion at IP (loss of lumbricals 3,4 + interossei).
• Total claw / "Preacher's hand": combined median + ulnar.
• Ape thumb (median): thenar wasting, thumb adducted, loss of opposition.
• Pope's blessing / hand of benediction: seen on attempted fist in high median nerve lesion (index + middle cannot flex).
• Froment's sign: ulnar palsy — thumb IP flexes (FPL/median substitution) when holding paper because adductor pollicis is weak.

Mnemonic — sensory autonomous zones: Median = tip of index; Ulnar = tip of little finger; Radial = dorsal first web space.

Diagnosis & investigation of choice

Clinical examination (motor, sensory, autonomic, Tinel's sign over the lesion) is first. Electrodiagnosis confirms type, level, and prognosis.

Stepwise diagnostic flow: Clinical localisation → Tinel's sign (advancing = regeneration) → NCS + EMG at 3–4 weeks → MRI/USG/intra-op nerve action potential (NAP) if no recovery → decision: observe vs explore.

Nerve conduction studies (NCS)

• Distinguishes neurapraxia (conduction block across the lesion but normal distal conduction because no Wallerian degeneration) from axonotmesis/neurotmesis (loss of distal conduction after ~7–10 days as Wallerian degeneration completes).
• Timing: do NCS after ~7–10 days for accurate localisation; earlier studies can mislead (distal segment still excitable).

Electromyography (EMG) — investigation of choice for prognosis

• Fibrillation potentials and positive sharp waves = denervation; appear at 2–3 weeks (so EMG is most informative at ~3 weeks).
• Nascent / polyphasic motor unit potentials and reduced recruitment = early reinnervation → favourable.

Feature	Neurapraxia	Axonotmesis	Neurotmesis
Conduction across lesion	Blocked	Lost	Lost
Conduction distal to lesion	Normal	Lost (after Wallerian)	Lost
Fibrillations on EMG	Absent	Present	Present
Wallerian degeneration	No	Yes	Yes
Recovery	Spontaneous, full	Spontaneous, ~1 mm/day	Needs surgery

High-yield: EMG at 3 weeks is the classic "investigation of choice" to assess denervation and prognosticate; NCS done too early is unreliable. MRI neurography / high-resolution USG images structural continuity; intra-operative NAP decides between neurolysis and grafting.

Management / treatment of choice

Principle: closed (low-energy) injuries are observed; open/sharp/high-energy injuries are explored early.

1. Closed fracture with palsy (e.g., radial nerve in closed humeral shaft fracture): most are neurapraxia/axonotmesis → observe with splinting, serial exam and EMG. ~90% recover spontaneously over 3–4 months.
2. Open or penetrating wound with deficit: early surgical exploration (sharp laceration → primary repair within 72 h; ragged/contaminated → delayed repair at 3 weeks).
3. Deficit appearing AFTER manipulation/reduction (iatrogenic, e.g., radial palsy that develops after closed reduction of humerus) → relative indication to explore (nerve may be trapped in fracture site).
4. No clinical or EMG recovery by 3–4 months → explore: neurolysis (Sunderland III), or resection + tension-free nerve graft (sural nerve donor) for neuromas-in-continuity with no NAP / neurotmesis.
5. Repair principles: tension-free epineurial coaptation with 8–0/9–0 nylon; if gap too large → interposition nerve graft or nerve transfer; end-to-end > grafting for outcome.
6. Supportive: splints to prevent contracture (cock-up splint for wrist drop, foot-drop splint/AFO), physiotherapy to maintain ROM, protect anaesthetic skin.

High-yield: Radial nerve palsy with closed humeral shaft fracture → conservative/observe (functional bracing). Explore only if palsy is secondary to open fracture, develops after manipulation, or shows no recovery by 8–12 weeks. Tendon transfers are a salvage option for irrecoverable wrist drop.

High-yield: Best functional results after repair occur in young patients, distal lesions, sharp transections repaired early, and short gaps. Outcome worsens with proximal lesions (long way to grow, motor end-plates fibrose after ~18–24 months — repair before then).

Complications

• Permanent motor/sensory loss, muscle wasting, joint contracture, anaesthetic-skin trophic ulcers.
• Neuroma (painful stump neuroma; neuroma-in-continuity).
• Complex Regional Pain Syndrome (CRPS) type II (causalgia) — burning pain, allodynia, vasomotor/sudomotor changes after a partial nerve injury (median/sciatic classically). CRPS-I (RSD) has no definable nerve lesion.
• Disuse osteopenia, fixed deformity, loss of function/employment.
• Failed reinnervation if repair delayed beyond ~18 months (motor end-plate degeneration).

Key differentials

• Root vs plexus vs peripheral nerve lesion: root lesions follow dermatomes/myotomes; plexus lesions (e.g., Erb's C5–C6 "waiter's tip", Klumpke's C8–T1 claw) cross multiple nerves.
• Compartment syndrome — pain out of proportion, pain on passive stretch, paraesthesia; nerve dysfunction here is ischaemic, an emergency (fasciotomy), not primary nerve transection.
• Volkmann's ischaemic contracture — sequela of missed forearm compartment syndrome (supracondylar fracture) mimicking median/ulnar deficit.
• Tendon rupture vs nerve palsy: e.g., post-fracture EPL rupture (after Colles) mimics radial palsy — distinguish by tenodesis test and intact sensation.
• Central causes (stroke) — UMN signs, no muscle wasting, no fibrillations.

Recently asked / exam angle

• Nerve injured in surgical neck of humerus / anterior shoulder dislocation = axillary; sensory loss over regimental badge area. (Repeat favourite.)
• Holstein–Lewis fracture (distal-third humerus) → radial nerve palsy.
• Supracondylar fracture, extension type → AIN (anterior interosseous) most commonly; tested via inability to make the "OK" sign / pinch.
• Sunderland classification — match grade to layer: Grade II = endoneurium intact, Grade IV = neuroma-in-continuity (epineurium intact only), Grade V = complete transection.
• EMG fibrillations appear at 2–3 weeks → why we wait ~3 weeks to prognosticate.
• Common peroneal nerve = most commonly injured nerve in lower limb, at fibular neck; knee dislocation → also rule out popliteal artery.
• Ulnar paradox: proximal lesion → less clawing.
• Closed humeral shaft fracture with wrist drop → observe (most recover); image-based "what next" answers favour conservative + splint.
• Recovery rate of regenerating axon = 1 mm/day; Tinel's sign advances distally with regeneration.
• Causalgia (CRPS II) follows partial injury of median/sciatic nerve.

Rapid revision

1. Neurapraxia → no Wallerian degeneration, full recovery; neurotmesis → needs surgery.
2. Sunderland: I = neurapraxia, II = axonotmesis (endoneurium intact), V = neurotmesis (complete cut).
3. Axon regeneration = 1 mm/day ≈ 1 inch/month.
4. Radial nerve → spiral groove → wrist drop, sensory loss at dorsal first web space; humeral shaft (Holstein–Lewis) fracture.
5. PIN palsy = finger drop with preserved wrist extension, NO sensory loss.
6. Axillary nerve → anterior shoulder dislocation/surgical neck → deltoid weakness + regimental badge sensory loss.
7. Common peroneal nerve → fibular neck → foot drop, steppage gait; check popliteal artery in knee dislocation.
8. AIN (supracondylar extension #) → can't make the "OK" sign, no sensory loss.
9. Ulnar paradox — proximal ulnar lesion gives less clawing than a distal one.
10. EMG at ~3 weeks (fibrillations) and NCS after ~7–10 days for prognosis; EMG is the prognostic investigation of choice.
11. Closed fracture + palsy → observe & splint (~90% recover by 3–4 months); open/iatrogenic/no-recovery → explore.
12. Causalgia = CRPS II after partial nerve injury (median/sciatic); explore before 18–24 months to beat motor end-plate fibrosis.