Peripheral Nerve Injuries

Introduction

Peripheral nerve injuries form a substantial component of the morbidity of orthopedic trauma, with as many as 15 to 30 percent of major upper extremity injuries and 10 to 15 percent of lower extremity injuries having an identifiable nerve component. The principal concerns in nerve injury are correct classification (which determines prognosis and treatment), recognition of acute injuries requiring urgent intervention (compressive lesions, laceration injuries with sharp transection, vascular compromise), the timing of operative intervention, and the substantial role of rehabilitation and adaptive strategies. The peripheral nerve injuries in orthopedic trauma are closely linked to the specific fracture and dislocation patterns covered in previous chapters — the radial nerve in humeral shaft fractures, the axillary nerve in shoulder dislocations and proximal humerus fractures, the common peroneal nerve in knee dislocations and fibular neck fractures, the sciatic nerve in posterior hip dislocations and acetabular surgery. This chapter addresses the broader principles of nerve injury classification and management, with reference to the specific patterns considered earlier. The chapter draws on Rockwood and Green’s Fractures in Adults, Apley & Solomon’s, Miller’s Review of Orthopaedics, and Dutton’s Orthopaedic Examination.

Peripheral Nerve Anatomy and Pathophysiology

Nerve Structure Peripheral nerves are complex anatomical structures with multiple connective tissue layers and a precisely organized internal architecture: The axon is the conducting element, transmitting impulses from the cell body (in the dorsal root ganglion for sensory neurons, in the anterior horn of the spinal cord for motor neurons) along its length. The axon may be either myelinated (with Schwann cells forming the myelin sheath, conducting impulses by saltatory conduction at high speed) or unmyelinated (with Schwann cells enclosing multiple axons in a non-myelin fashion). The endoneurium surrounds individual axons within a fascicle, providing structural and biochemical support. The perineurium is the strong connective tissue layer surrounding each fascicle, providing the principal mechanical and chemical barrier of the nerve (the blood-nerve barrier). The epineurium is the outermost layer, containing connective tissue, blood vessels, and lymphatics, and binding the fascicles together as a peripheral nerve. The fascicular pattern within a nerve trunk is variable along the length — fascicles may divide, recombine, or transmit between sensory and motor function in complex ways. The implication for surgical repair is that simple end-to-end alignment of the cut nerve ends does not necessarily produce alignment of the corresponding fascicles, with consequent suboptimal functional recovery even in well-performed repairs.

Mechanisms of Nerve Injury The principal mechanisms of nerve injury include: Stretch (traction) injury: Elongation of the nerve beyond its elastic limit, producing varying degrees of intraneural damage. The classical orthopedic settings are the brachial plexus injury from sudden traction in motor vehicle accidents or birth injury (covered in Topic Orth-26), and the peroneal nerve injury in knee dislocation (Topic Trauma-26). Compression: Mechanical pressure on the nerve, either acute (acute compartment syndrome, tourniquet injury, casting that is too tight) or chronic (entrapment neuropathies — discussed separately as a category in Topic Orth-27). Laceration: Sharp transection of the nerve by penetrating injury (knife, glass, sharp bone fragment) or surgical injury. The injury produces immediate functional loss and requires anatomical repair. Contusion: Direct blunt trauma to the nerve, producing localized damage with variable recovery potential. Ischemia: Disruption of the nerve’s blood supply, either from direct vascular injury or from prolonged compression. The nerve has limited tolerance for ischemia (minutes to hours), with progressive injury through this duration. Thermal or chemical injury: Burns, freezing, exposure to caustic chemicals.

Classification of Nerve Injuries

Seddon Classification (1943) The classical Seddon classification organizes nerve injuries into three grades by the pathophysiological severity of injury: Neurapraxia (Grade I): The mildest injury, with localized conduction block but no axonal damage. The nerve fiber is structurally intact; conduction is impaired by transient demyelination at the site of injury. Recovery is typically complete within days to weeks (3 to 12 weeks for full recovery in most cases) as the myelin sheath repairs. Axonotmesis (Grade II): Disruption of the axon with preservation of the surrounding connective tissue layers (endoneurium, perineurium, epineurium). The distal axon undergoes Wallerian degeneration (the orderly distal-to-proximal degeneration of the axon and its myelin), with subsequent axonal regeneration from the proximal stump at approximately 1 mm per day (1 inch per month — useful for clinical prognostication). Recovery is generally complete because the endoneurial tubes provide guidance for regenerating axons back to their original targets. Neurotmesis (Grade III): Complete disruption of the nerve including the connective tissue layers. The endoneurial tubes are no longer continuous, and regenerating axons may fail to find their original targets or may form a neuroma at the site of injury. Spontaneous

recovery is poor and surgical repair is required for any chance of meaningful functional recovery. Sunderland Classification (1951) The Sunderland classification refines Seddon’s neurotmesis category and provides a five- grade system: Grade I: Neurapraxia (corresponds to Seddon I). Grade II: Axonal disruption with intact endoneurium. Recovery by axonal regeneration through preserved endoneurial tubes; functional recovery is generally complete. Grade III: Disruption of axon and endoneurium with intact perineurium. Recovery is by axonal regeneration but is less complete because the endoneurial tubes are disrupted and regenerating axons may not reach the correct targets. Grade IV: Disruption of axon, endoneurium, and perineurium with intact epineurium. Recovery without surgical intervention is very poor because the regenerating axons form a neuroma rather than continuing distally. Grade V: Complete transection (corresponds to Seddon’s neurotmesis). The Mackinnon classification adds a Grade VI for mixed injuries with different grades in different fascicles within the same nerve.

Clinical Implications of the Classification The classification is critical because it predicts recovery and guides treatment: Grades I-II (neurapraxia and axonotmesis with intact endoneurium) recover spontaneously without surgical intervention. Grade III recovery is intermediate, with some spontaneous recovery but typically incomplete; surgical exploration and selective repair may improve outcomes. Grades IV and V require surgical repair (anatomical end-to-end coaptation, or nerve graft for gaps that cannot be closed without tension) for any meaningful recovery. The clinical challenge is that at the time of acute injury, the grade is often unknown, and the distinction between recoverable axonotmesis (Grade II) and non-recoverable injury (Grade IV-V) cannot be made on examination alone. Time-based observation with periodic clinical and electrophysiological assessment over 3 to 6 months is often required to determine if recovery is occurring; failure of recovery prompts surgical exploration.

Clinical Assessment of Nerve Injury

The assessment of suspected nerve injury follows a systematic approach:

History: The mechanism of injury (sharp laceration suggesting neurotmesis; stretch or compression suggesting variable injury grade), the timing and progression of symptoms, and any prior nerve dysfunction. Motor examination: Specific testing of muscle groups innervated by the suspected nerve, with grading on the British Medical Research Council (MRC) scale (0 no contraction, 1 flicker, 2 movement without gravity, 3 movement against gravity, 4 movement against some resistance, 5 normal strength). Sensory examination: Light touch, two-point discrimination (normal less than 6 mm at fingertips), pin-prick, vibration. The territory of involvement is mapped systematically. Tinel’s sign: Percussion over the course of the nerve produces paresthesia in the distribution distal to the percussion site. A positive Tinel’s sign at the injury site indicates the location of nerve injury; a progressive distal advancement of Tinel’s sign over time indicates axonal regeneration (and is an encouraging prognostic sign). Autonomic findings: Loss of sweating in the affected distribution (anhidrosis), changes in skin temperature and color, and trophic changes (thinning of the skin, loss of hair, brittle nails) — all reflect denervation and provide additional information about the completeness of the injury. Electrophysiological Studies Electrophysiological studies (electromyography and nerve conduction studies) provide objective evidence of nerve injury and recovery: Nerve conduction studies (NCS) measure conduction velocity and amplitude across segments of the nerve, distinguishing conduction block (suggesting neurapraxia) from absent response (suggesting more severe injury). Electromyography (EMG) assesses muscle electrical activity at rest and with voluntary contraction, with fibrillation potentials appearing approximately 2 to 3 weeks after denervation (axonal injury) and disappearing as reinnervation occurs. Compound motor action potentials (CMAPs) measure the response to nerve stimulation distal to the site of injury; absent CMAP with preserved proximal response indicates conduction block, while absent CMAP with absent proximal response indicates more severe injury. Initial studies are typically performed at 3 to 4 weeks after injury, with serial studies at 3- month intervals to monitor recovery. The studies provide objective evidence of recovery in advance of clinical signs and may help determine the need for surgical exploration.

Treatment Principles

Immediate Management For the patient with acute peripheral nerve injury:

Documentation of the nerve injury at presentation is essential, both for medical reasons (to monitor recovery) and for medicolegal reasons. Protection of the limb in a functional position with appropriate splinting to prevent contracture during the recovery period. Surgical exploration for acute laceration injuries with suspected complete transection (Sunderland V). The exploration should occur within 72 hours for the cleanest results, although delayed primary repair within 3 weeks is acceptable in selected cases. Surgical exploration for displaced fractures or dislocations with new nerve deficit that did not respond to reduction. The principle is that an irreducible fracture-dislocation with neurological deficit suggests interposed neural tissue or compression requiring direct intervention. Delayed Management For nerve injuries that do not recover spontaneously: Serial clinical and electrophysiological assessment over 3 to 6 months establishes the trajectory. Failure of recovery by 4 to 6 months (depending on the nerve and the distance to the most distal target muscle) prompts surgical exploration. The principle is that time- dependent muscle changes — first reversible muscle atrophy, then progressive irreversible loss of motor end plates and muscle fibrosis — limit the window of opportunity for successful reinnervation. The classical figure is that 18 to 24 months is the limit beyond which motor reinnervation produces poor results, and surgery should be performed well in advance of this limit.

Surgical Techniques Direct neurorrhaphy (end-to-end repair) is the gold standard for complete transection, with epineurial repair (sutures placed in the epineurium without disturbing the internal fascicular pattern), fascicular repair (alignment of corresponding fascicles with grouped fascicular repair), or epineurial repair with fascicular alignment depending on the nerve, the injury pattern, and surgical preference. The principle is tension-free repair; tension at the repair site produces fibrosis, ischemia, and failure of regeneration. Nerve grafting is required when a gap exists between the cut ends that cannot be closed without tension. The classical donor is the sural nerve (the sensory nerve to the lateral foot, with minimal donor-site morbidity), providing a cable graft of approximately 30 to 40 cm length. Cable grafting uses multiple parallel segments to match the cross-sectional area of the recipient nerve. Conduits (synthetic or processed allograft tubes) are used for short nerve gaps (typically less than 3 cm) with reasonable outcomes for sensory nerves and selected motor nerves. Nerve transfers are an alternative to grafting in certain circumstances. The principle is to transfer a functioning nerve from a less critical function to the recipient nerve that has lost

function. The Oberlin transfer (transfer of fascicles of the ulnar nerve to the biceps motor branch) is the prototype, restoring elbow flexion in upper trunk brachial plexus injuries. Wrist extensor transfer (radial-to-axillary transfer for axillary nerve injury), ulnar-to- median sensory transfer, and others have similarly transformed the management of complex nerve injuries. Nerve transfers offer the advantage of providing a closer source for axonal regeneration (with shorter distance to the target muscle), preserving the time- dependent window for successful reinnervation. Tendon transfers are an alternative or supplement to nerve repair when reinnervation is not feasible. The principles include using a donor tendon with one synergistic action, adequate excursion (the distance the tendon can move), expendable function, and appropriate tension at the recipient. Specific transfers include the PT to ECRB transfer for radial nerve palsy (loss of wrist extension), the opponensplasty (using FDS to the index or palmaris longus) for median nerve loss of thumb opposition, and many others. Tendon transfers do not require viable motor end plates in the recipient muscle and are therefore useful in late presentations beyond the window for nerve reinnervation.

Specific Nerve Injuries

Brachial Plexus Injuries Brachial plexus injuries range from minor traction injuries (“stingers” or “burners” in contact sport athletes, with transient symptoms) through complete avulsion of all roots from the spinal cord (severe injury with complete arm paralysis). The classification by location of injury includes: Upper trunk (Erb’s palsy): C5-C6 roots; “waiter’s tip” position (loss of shoulder abduction, external rotation, elbow flexion, forearm supination). Birth injury or motor vehicle accident with shoulder depression. Lower trunk (Klumpke’s palsy): C8-T1; intrinsic hand weakness, finger clawing, sometimes Horner’s syndrome (T1 root involvement). Less common; typically traumatic in adults. Complete plexus injury: All roots; complete flail arm. Catastrophic injury with limited reconstructive potential. The distinction between pre-ganglionic (root avulsion) and post-ganglionic (rupture) injuries is critical to management. Root avulsions involve avulsion of the rootlets from the spinal cord and have no surgical option for direct repair; treatment options are nerve transfers (intercostal nerves, spinal accessory nerve, contralateral C7) to provide some function. Post-ganglionic injuries have viable proximal stumps available for direct repair or grafting. Differentiating features of pre-ganglionic injury include Horner’s syndrome (for T1 root), elevated hemidiaphragm (for C5 phrenic nerve component), severe pain, pseudomeningoceles on imaging, and abnormalities on intraspinal imaging.

Common Peroneal Nerve Injury The common peroneal nerve courses superficially around the neck of the fibula and is at substantial risk of injury in knee dislocations (Topic Trauma-26), fibular neck fractures, prolonged compression (against a stretcher or operating table), and crossed-leg habits in patients with weight loss (loss of subcutaneous padding). The injury produces foot drop (loss of dorsiflexion, eversion, and toe extension) and sensory loss over the dorsum of the foot and lateral leg. The treatment of acute peroneal nerve injury depends on the mechanism. Compression injury typically recovers spontaneously over weeks to months. Traction injury in knee dislocation has a poor prognosis, with only 50 to 80 percent of patients recovering useful function. Sharp laceration requires urgent repair. Failed recovery at 4 to 6 months prompts exploration with neurolysis, repair, or grafting; late presentation with permanent palsy is treated with tendon transfers (typically posterior tibial tendon transfer through the interosseous membrane to the dorsum of the foot) or with ankle-foot orthosis (AFO) for non-surgical management. Axillary Nerve Injury The axillary nerve is at risk in anterior shoulder dislocation, proximal humerus fractures, and surgical approaches to the shoulder. The injury produces weakness of deltoid (shoulder abduction beyond 30 degrees) and sensory loss over the lateral aspect of the deltoid. Acute injury is typically neurapraxic and recovers spontaneously over 3 to 6 months. Failure of recovery at 6 months may prompt exploration; nerve grafting or transfer (triceps motor branch of the radial nerve to the axillary nerve) may restore deltoid function.

Radial Nerve Injury The radial nerve is the most commonly injured nerve in long bone fractures, with the Holstein-Lewis distal third humeral shaft fracture being the classical association (Topic Trauma-14). The injury produces wrist drop (loss of wrist and finger extension) and sensory loss over the dorsum of the first webspace. The management of radial nerve palsy associated with humeral shaft fracture follows the principles discussed in Topic Trauma-14: expectant management for closed injuries (with 75 to 90 percent spontaneous recovery), surgical exploration for open injuries, secondary palsy after manipulation, and failed recovery at 4 to 6 months. Tendon transfers for established radial nerve palsy (PT to ECRB for wrist extension, FCR to EDC for finger extension, palmaris longus to EPL for thumb extension — the standard pattern) provide reliable restoration of function. Median Nerve Injury The median nerve is at risk in distal radius fractures (acute carpal tunnel syndrome), supracondylar humerus fractures in children (typically the anterior interosseous branch), and direct trauma. Loss produces thumb opposition weakness (abductor pollicis brevis),

forearm pronation weakness (in proximal injuries with pronator teres involvement), and sensory loss over the thumb, index, middle, and radial half of the ring finger. The acute median nerve palsy with carpal tunnel syndrome from acute fracture is a surgical emergency requiring carpal tunnel release. Ulnar Nerve Injury The ulnar nerve is at risk in distal humerus fractures, elbow injuries, and direct trauma at the wrist. Loss produces intrinsic hand weakness with clawing (the Wartenberg sign of small finger abduction; the Froment sign with thumb adduction weakness producing IP joint flexion to compensate), and sensory loss in the small finger and ulnar half of the ring finger. Cubital tunnel syndrome (chronic compression) is a common entrapment neuropathy. Acute injuries follow the same principles as other nerve injuries; late presentations are addressed by transfer procedures (the AIN to motor branch of ulnar nerve transfer being increasingly performed). Sciatic Nerve Injury The sciatic nerve is at risk in posterior hip dislocations (Topic Trauma-20) and during operative approaches to the acetabulum. The peroneal division is typically more affected than the tibial division because of its more lateral and posterior position. Recovery rates are 50 to 80 percent for the tibial component but only 30 to 50 percent for the peroneal component. Direct injury during surgery may require immediate repair; traction injuries typically warrant observation. Femoral Nerve Injury The femoral nerve is at risk in surgical approaches to the hip and acetabulum (particularly the ilioinguinal approach), in retractor placement during anterior hip approaches, and rarely in injuries to the iliopsoas region. Loss produces quadriceps weakness and sensory loss over the anterior thigh. Recovery is generally good for compression injuries.

Nerve Injuries in Children

Pediatric nerve injuries deserve specific consideration because of several features that distinguish them from adult injuries: Birth-related brachial plexus injuries are the prototype, with the classical Erb’s palsy (upper trunk injury from traction during difficult delivery) being the most common pattern. Spontaneous recovery in newborn brachial plexus palsy is excellent in the majority of cases, with 80 to 95 percent achieving complete or near-complete recovery without surgical intervention. Failure of antigravity biceps function by 3 to 6 months is the principal indication for surgical exploration (microsurgical reconstruction with nerve grafting or transfer). Pediatric peripheral nerve injuries generally recover better than equivalent adult injuries because of the greater regenerative capacity and the shorter distance to target muscles. Surgical management follows similar principles to adult injuries, with attention to the open growth plates and the rehabilitation considerations in growing children.

The supracondylar humerus fracture in children has specific nerve injury patterns — the anterior interosseous nerve (AIN) palsy is the most common (loss of FPL and FDP to the index finger, producing inability to perform the “OK” sign), typically neurapraxic, and recovers spontaneously over 3 to 6 months. The median nerve, radial nerve, and ulnar nerve can all be affected; the classical association of ulnar nerve injury with flexion-type supracondylar fractures (much less common than extension type) is well-recognized.

Rehabilitation After Nerve Injury

Rehabilitation is a substantial component of nerve injury management and includes: Splinting in functional positions to prevent contractures during the recovery period. For radial nerve palsy, dynamic extension splints (with elastic bands providing passive wrist and finger extension while permitting active flexion) maintain hand position. For peroneal nerve palsy, an AFO maintains foot dorsiflexion during ambulation. Range of motion exercises to prevent joint stiffness and capsular contracture. Passive range of motion is performed if active range is impaired by motor weakness. Sensory re-education for sensory nerve injuries, with structured programs to retrain interpretation of sensory stimuli as reinnervation occurs. Motor re-education for transfer procedures (whether nerve or tendon), with structured programs to retrain the new muscle function. For nerve transfers, the patient must learn to activate the donor function to produce the recipient function (e.g., contracting the ulnar nerve fascicles to produce biceps contraction after Oberlin transfer); this is a substantial cognitive task and requires dedicated therapy. Adjunctive modalities including electrical stimulation (with mixed evidence for stimulation of denervated muscle to maintain motor end plates during reinnervation period), neurodynamic exercises (mobilization of the nerve to prevent or reduce adhesions), and pain management. Psychological support is important given the prolonged and uncertain recovery course of many nerve injuries.

Complex Regional Pain Syndrome (CRPS) After Nerve Injury

Complex regional pain syndrome (CRPS), addressed in detail in Topic Trauma-8, can develop after nerve injury (CRPS type II, formerly causalgia) or without identifiable nerve injury (CRPS type I, formerly RSD). The recognition by Budapest criteria, the role of multidisciplinary management, and the avoidance of common pitfalls (inadequate early treatment, excessive immobilization, missed Stener-like lesions) all apply.

Summary and Take-Home Points

Peripheral nerve injuries are classified by the Seddon system (neurapraxia, axonotmesis, neurotmesis) and the refined Sunderland system (grades I-V) based on the pathophysiological severity of injury. The classification predicts recovery: neurapraxia

and axonotmesis with intact endoneurium (Sunderland I-II) recover spontaneously; partial structural injury (Sunderland III) has intermediate recovery; complete structural injury (Sunderland IV-V) requires surgical repair. The clinical assessment of nerve injury combines motor and sensory examination, Tinel’s sign, and autonomic findings, supplemented by electrophysiological studies (NCS, EMG) for objective characterization and monitoring. The time course of injury includes Wallerian degeneration of the distal axon (1 to 2 weeks), the appearance of fibrillation potentials on EMG (2 to 3 weeks), and axonal regeneration at approximately 1 mm per day (1 inch per month). The principles of management include immediate surgical exploration for sharp laceration injuries and for irreducible fracture-dislocations with new neurological deficit, expectant management for closed injuries with serial assessment, surgical exploration at 4 to 6 months for failure of recovery, and avoidance of the 18 to 24 month limit beyond which motor reinnervation produces poor results. The surgical techniques include direct neurorrhaphy (epineurial or fascicular repair) for tension-free repair, nerve grafting (typically sural nerve cable graft) for gaps that cannot be closed without tension, nerve conduits for short gaps, nerve transfers as an alternative or supplement to direct repair (the Oberlin transfer for elbow flexion in upper plexus injuries is the prototype), and tendon transfers as a late reconstruction option independent of nerve reinnervation. The specific nerve injuries — brachial plexus, axillary, radial, median, ulnar, sciatic, common peroneal, femoral — each have specific clinical patterns, fracture associations, recovery prospects, and reconstructive options as discussed throughout this and previous chapters. Pediatric nerve injuries generally have better recovery than equivalent adult injuries because of greater regenerative capacity and shorter distances to target muscles. Rehabilitation with splinting, range of motion, sensory re-education, motor re-education for transfers, and psychological support is a substantial component of management. The chapter that follows turns to vascular injuries and compartment syndrome — the final topic of the trauma section before moving to the anatomy and surgical approaches that complete the curriculum.