Peripheral Nerve Injuries

Peripheral nerve injuries arise from laceration, traction, compression, ischaemia, thermal and chemical injury, and injection. They cause lasting motor, sensory and autonomic disability, and early recognition improves outcome.

Seddon classification

• Neurapraxia: focal conduction block from myelin injury with preserved axons. Recovery occurs within days to 12 weeks and is complete.
• Axonotmesis: axonal disruption with preserved endoneurium and connective tissue. Wallerian degeneration follows, and regeneration proceeds at about 1 mm/day (1 inch/month), with generally good recovery.
• Neurotmesis: complete transection of nerve and connective tissue. No spontaneous recovery, and surgery is needed.

Sunderland grades I to V subdivide this further (I neurapraxia, II axonotmesis, III endoneurial disruption with fascicle preserved, IV only epineurium preserved with scar block, V transection). Grade VI represents a mixed injury.

Mechanisms

• Sharp laceration: glass, knife, or surgical injury, usually neurotmesis.
• Traction: brachial plexus injury in motorcycle crashes and birth injury, common peroneal injury in knee dislocation.
• Fracture association: radial nerve with humeral shaft fractures, axillary nerve with shoulder dislocation and proximal humerus fracture, ulnar and median nerves with elbow fractures, sciatic nerve with posterior hip dislocation, and common peroneal nerve with fibular neck fracture.
• Compression: prolonged tourniquet use, casts, positioning, and compartment syndrome.
• Gunshot: most are in continuity (neurapraxia or axonotmesis).
• Injection: sciatic injury from buttock injection and radial nerve injury from deltoid injection.

Pathophysiology of regeneration

• Distal axons degenerate within 24 to 72 hours. Schwann cells proliferate and form bands of Büngner, guiding regenerating growth cones.
• Motor end plates and muscle degenerate with time. Reinnervation beyond 12 to 18 months is poor, and beyond 24 months is rarely functional.
• Sensory recovery tolerates longer delays.

Outcomes are best for young patients, distal injuries, pure motor or pure sensory nerves, sharp injuries, early repair, and short gaps.

General findings

• Weakness in the muscles supplied, with atrophy appearing from 2 to 4 weeks, and reduced tone.
• Sensory loss in the autonomous zone of the nerve, absent sweating, dry or shiny skin in the denervated area.
• Absent tendon reflexes.
• Tinel sign (percussion along the nerve produces distal tingling), which advances with regeneration.
• Neuropathic pain, which in complete lesions may arise from a neuroma. Early severe burning pain suggests complex regional pain syndrome.

Nerve specific patterns

• Axillary: deltoid weakness, loss of sensation over the lateral shoulder (regimental badge area).
• Musculocutaneous: weak elbow flexion and supination, lateral forearm sensory loss.
• Radial: wrist drop and finger drop, with sensory loss in the first dorsal web space.
• Median: ape hand, loss of thumb opposition and index finger flexion, and loss of sensation on the palmar radial three and a half digits. Anterior interosseous injury causes loss of the OK sign.
• Ulnar: claw hand, Froment sign, weak finger abduction, and loss of sensation on the little finger and ulnar half of the ring finger.
• Femoral: quadriceps weakness, loss of knee jerk, and anteromedial thigh numbness.
• Sciatic: foot drop with weak hamstrings and loss of sensation below the knee except medial leg.
• Common peroneal: foot drop with sensory loss on the dorsum of foot and anterolateral leg.
• Tibial: loss of plantarflexion and sole sensation.

Brachial plexus injury

• Upper trunk (C5 to C6): shoulder abduction and elbow flexion loss, as in the waiter's tip posture.
• Lower trunk (C8 to T1): hand weakness and Horner syndrome.
• Root avulsion signs: Horner syndrome, winged scapula (long thoracic nerve from C5 to C7), rhomboid weakness (dorsal scapular), diaphragm paralysis, severe neuropathic pain, and a negative Tinel sign.

Vascular injury, compartment syndrome and open fracture should be assessed at the same time.

Clinical assessment

• Document motor strength by the 0 to 5 Medical Research Council scale, sensory testing (light touch, pinprick, two point discrimination), reflexes, and sudomotor signs.
• Record the mechanism, time of injury, open or closed nature, and associated injuries.

Electrodiagnostic studies

• Nerve conduction studies and EMG performed too early can mislead. Distal nerve stimulation remains normal for 3 to 7 days after transection.
• Baseline testing is useful at about 3 to 4 weeks, when denervation (fibrillations and positive sharp waves) appears. Serial studies at 3 months and 6 months document reinnervation, shown by nascent motor unit potentials.
• Preserved compound muscle action potential and sensory action potential with a proximal conduction block indicate neurapraxia.
• Absent sensory potentials with preserved dorsal root ganglion function indicates preganglionic root avulsion.

Imaging

• Radiographs for fractures and dislocations.
• High resolution ultrasound defines nerve continuity, neuroma, swelling, and transection, and is useful early in open or closed injuries.
• MR neurography shows nerve signal change, discontinuity and denervation oedema in muscle.
• CT myelography or MRI of the cervical spine for suspected root avulsion, showing pseudomeningocele.
• CT angiography or Doppler studies for arterial injury.

Intraoperative nerve action potential recording on exploration determines whether a lesion in continuity needs resection and grafting.

Immediate care

• Treat life threats, reduce fractures and dislocations, and release compartments.
• Open injuries: irrigation, debridement, tetanus prophylaxis, and cefazolin 2 g IV (add gentamicin for heavy contamination).
• Splint the limb in a functional position, keep joints supple with passive range of motion, and prevent contractures.

Timing of surgery

• Open, sharp transection with deficit: primary repair as soon as feasible, ideally within 72 hours to 7 days of injury. Use tension free epineurial or group fascicular repair with 8-0 to 10-0 nylon sutures under the microscope, with fibrin glue as an adjunct.
• Contaminated, crush or blast injury: debride and tag the nerve ends, with delayed repair at 2 to 3 weeks once the zone of injury is demarcated.
• Closed injury (traction, fracture related): observe with serial examination and electrodiagnostic and ultrasound studies. If there is no clinical or EMG evidence of recovery by 3 to 4 months, explore. Surgery beyond 6 months gives progressively worse results.
• Gunshot wounds: observe for about 3 months, because most are neurapraxic.
• Nerve deficit after fracture reduction or surgery: explore early if the nerve may be entrapped or transected.

Surgical options

• Direct repair: when ends can be approximated without tension.
• Nerve grafting: for gaps over 2 to 3 cm, using sural nerve, or medial and lateral antebrachial cutaneous nerves. Cable grafts are used for large nerves. Processed allografts and conduits suit short sensory gaps.
• Nerve transfers: for proximal injuries, brachial plexus root avulsions and delayed presentation. Examples include spinal accessory to suprascapular nerve, ulnar fascicle to biceps branch (Oberlin), radial triceps branch to axillary nerve, and intercostal nerves to musculocutaneous nerve. The transfer places a donor close to the target muscle and shortens reinnervation time.
• Neurolysis: for lesions in continuity with a conducting nerve action potential.
• Neuroma excision: with burying in muscle or bone, or targeted muscle reinnervation for painful neuromas.

Late reconstruction (beyond 12 to 18 months, or failed repair)

• Tendon transfers: for radial palsy, pronator teres to extensor carpi radialis brevis, flexor carpi radialis to extensor digitorum communis, and palmaris longus to extensor pollicis longus. For foot drop, tibialis posterior transfer through the interosseous membrane. For high ulnar and median palsies, opponensplasty and claw correction.
• Free functioning muscle transfer for brachial plexus injuries with no available donor.
• Joint arthrodesis and bracing (ankle foot orthosis) when transfers are not appropriate.

Adjuncts and rehabilitation

• A single perioperative low frequency electrical stimulation session (20 Hz for 1 hour) enhances axonal regeneration.
• Hand therapy and motor re-education, sensory re-education, desensitisation, and protection of anaesthetic skin.
• Pain management: gabapentin 300 mg at night titrated to 1800 to 3600 mg/day, pregabalin 150 to 600 mg/day, amitriptyline 10 to 75 mg at night, duloxetine 60 mg daily, and lidocaine 5% patches. Early referral for sympathetic block or pain services in suspected CRPS.
• Splints and night positioning, and vitamin B12 repletion when deficient.

Prevention: correct patient positioning, limit tourniquet time (under 2 hours in the upper limb and 2 hours in the lower limb), intramuscular injections only into the safe upper outer quadrant of the buttock or the anterolateral thigh, and avoid tight casts.

Recovery expectations: neurapraxia recovers within weeks, repaired nerves regenerate at about 1 mm/day from the repair site, and recovery is measured by muscle contraction, sensory return, and progression of the Tinel sign.