INTRODUCTION TO PERIPHERAL NERVE INJURIES IN ORTHOPAEDIC TRAUMA

Peripheral nerves are highly specialized, viscoelastic structures susceptible to injury from a myriad of insults, including metabolic derangements, collagen vascular diseases, malignancies, endogenous or exogenous toxins, and thermal, chemical, or mechanical trauma. Within the purview of operative orthopaedics, injuries caused by mechanical trauma are of paramount concern. Every patient presenting with an injured limb or limb girdle must undergo an exhaustive evaluation to exclude concomitant musculoskeletal, vascular, and peripheral nerve damage.

The epidemiology of peripheral nerve injuries highlights their significant impact on functional outcomes. During times of armed conflict, 14% to 18% of all extremity injuries involve damage to peripheral nerves. Omer’s seminal report on Vietnam War casualties demonstrated that 22% of patients with upper extremity trauma sustained injuries to major peripheral nerves. While comparable, large-scale epidemiological figures for civilian injuries are less uniformly documented, lacerating or penetrating wounds caused by sharp objects or weapons account for approximately 40% of noncombat peripheral nerve injuries, as reported by Lyons and Woodhall.

Clinical Pearl: Peripheral nerve injuries must be carefully excluded in every patient with an acute extremity injury. Equal diligence must be applied during the postoperative period, following closed reduction, casting, or manipulation, to detect secondary iatrogenic neural injuries.

BIOMECHANICS AND PATHOANATOMY OF NERVE TRAUMA

Understanding the etiology of mechanical nerve injury requires a foundational grasp of nerve biomechanics. Peripheral nerves possess a degree of elasticity, primarily conferred by the undulating arrangement of axons (the bands of Fontana) and the robust perineurium.

• Traction and Stretch: Nerves can safely stretch approximately 8% of their resting length. Stretch exceeding 15% results in complete occlusion of the vasa nervorum, leading to profound ischemia. Stretch beyond 20% to 30% typically results in structural failure of the epineurium and perineurium, culminating in neurotmesis.
• Compression: Sustained mechanical compression induces localized ischemia, microvascular permeability, and intraneural edema. This initiates a fibrotic cascade that can tether the nerve, preventing normal excursion during joint movement and leading to secondary traction injuries.
• Laceration: Sharp trauma transects the neural architecture, necessitating surgical coaptation to guide regenerating axonal cones across the zone of injury.

ETIOLOGY AND MECHANISMS OF INJURY

Gunshot and Ballistic Wounds

Gunshot wounds (GSWs) are frequently complicated by peripheral nerve injury, primarily through cavitational shockwaves rather than direct transection. Consequently, spontaneous recovery is the expected clinical course in the majority of instances.

Historical data robustly supports conservative initial management for ballistic nerve injuries:
* World War I: Foerster reported on 2,915 patients with motor paralysis caused by GSWs, noting that 67% recovered spontaneously.
* World War II: Sunderland reported a 68% incidence of spontaneous peripheral nerve recovery following GSWs.
* Vietnam War: Omer determined that spontaneous recovery occurred in 69% of both high-velocity (> 2,500 ft/s) and low-velocity gunshot wounds.

The expected time to recovery after a GSW ranges from 3 to 9 months, with high-velocity injuries necessitating a longer regenerative period due to a wider zone of blast-induced neurapraxia and axonotmesis (which occur with equal frequency in these wounds).

Surgical Warning: Shotgun wounds exhibit a drastically different clinical profile compared to standard GSWs. Luce and Griffin reported spontaneous recovery of peripheral nerve injuries after shotgun wounds in only 45% of patients. The diffuse pellet spread and severe soft-tissue destruction often result in direct nerve transection, lowering the threshold for early surgical exploration.

Primary vs. Secondary Nerve Injuries

Bone or joint injury is associated with approximately 40% of peripheral nerve lesions, as followed by the Veterans Administration and National Research Council. Lyons and Woodhall noted that 21% of nerve lesions were associated with sufficient skeletal trauma to necessitate combined orthopaedic and neurosurgical care.

• Primary Injury: Occurs at the exact moment of trauma. The nerve is injured by the initial kinetic force, displaced osseous fragments, acute stretching (e.g., during a dislocation), or the initial manipulation.
• Secondary Injury: Develops subacutely or chronically. The nerve becomes compromised by surrounding infection, dense scar tissue formation, exuberant fracture callus, or vascular complications (including expanding hematoma, arteriovenous fistula, localized ischemia, or pseudoaneurysm).

FRACTURE-NERVE ASSOCIATIONS: EPIDEMIOLOGY AND PATTERNS

The frequency of specific nerve involvement associated with long bone fractures is highly predictable based on regional anatomy. Based on Spurling's review of 300 cases, upper extremity injuries account for 74% of fracture-associated nerve palsies, while lower extremity injuries account for 20%.

Upper Extremity Nerve Injuries

The Radial Nerve:
The radial nerve is the most commonly injured peripheral nerve in orthopaedic trauma. Approximately 14% of all humeral shaft fractures are complicated by radial nerve palsy. The anatomical tethering of the nerve at the lateral intermuscular septum makes it particularly vulnerable.
* 50% of radial nerve injuries are associated with fractures of the distal third of the humerus (Holstein-Lewis fracture).
* 33% are associated with fractures of the middle third of the humerus.
* 7% occur with supracondylar fractures.
* 7% are associated with anterior dislocations of the radial head.

The Ulnar Nerve:
The ulnar nerve is implicated in about 30% of patients with combined skeletal and neural injuries of the upper extremity. It is most frequently compromised in fractures around the medial humeral epicondyle. Furthermore, it is highly susceptible to secondary injury from the formation of hypertrophic callus around the elbow or progressive cubitus valgus (tardy ulnar nerve palsy).

The Median Nerve:
The median nerve is injured in approximately 15% of combined upper extremity neuro-skeletal traumas. Primary injuries are most common during posterior dislocations of the elbow. Secondary injuries frequently manifest as acute carpal tunnel syndrome following distal radius fractures or perilunate dislocations.

The Axillary Nerve:
Axillary nerve stretch injuries occur in approximately 5% of anterior shoulder dislocations, often presenting as deltoid atony and anesthesia over the lateral shoulder (regimental badge area).

Lower Extremity Nerve Injuries

The Sciatic Nerve and Lumbosacral Plexus:
Branches of the lumbosacral plexus are injured in less than 3% of pelvic ring disruptions. However, the sciatic nerve (particularly its peroneal division) is highly vulnerable during hip trauma, being injured in 10% to 13% of posterior hip dislocations.

The Peroneal Nerve:
The common peroneal nerve is most commonly injured at the fibular neck. This occurs frequently during fractures of the proximal tibia and fibula, or as a catastrophic stretch injury during multi-ligamentous knee dislocations (KD-III or KD-IV).

The Tibial Nerve:
Protected deep within the posterior compartment, the tibial nerve is less frequently injured but may be compromised in severe bicondylar tibial plateau fractures or complex fracture-dislocations of the ankle.

CLINICAL EVALUATION AND DIAGNOSTIC WORKUP

A meticulous, documented neurological examination is mandatory before any intervention.

1. Motor Examination: Grade muscle strength (0-5 scale) for specific nerve distributions.
2. Sensory Examination: Assess two-point discrimination and light touch in autonomous sensory zones.
3. Electromyography and Nerve Conduction Studies (EMG/NCS): Baseline studies are of limited value acutely. EMG/NCS should be delayed until 3 to 4 weeks post-injury to allow for Wallerian degeneration to manifest electrically. Fibrillation potentials and positive sharp waves indicate axonal loss.
4. Advanced Imaging: High-resolution Ultrasound (HRUS) and Magnetic Resonance Neurography (MRN) are increasingly utilized to visualize nerve continuity, neuroma formation, or extrinsic compression by hematoma or callus.

SURGICAL INDICATIONS AND TIMING

The decision to explore a peripheral nerve depends heavily on the mechanism of injury and the presence of concomitant trauma.

Indications for Immediate Exploration

• Open Fractures with Nerve Deficit: If the nerve deficit corresponds to the anatomical zone of the open wound, the nerve should be explored during the initial surgical debridement.
• Concomitant Vascular Injury: An ischemic limb requiring emergent vascular bypass or repair mandates concurrent exploration of the adjacent neurovascular bundle.
• Sharp Lacerations: Clean transections (e.g., glass, knife) should be repaired primarily within 72 hours before retraction and epineurial scarring occur.
• Iatrogenic Loss of Function: A new-onset nerve palsy immediately following closed reduction or surgical fixation demands prompt exploration to rule out nerve entrapment within the fracture site or hardware.

Indications for Delayed Exploration (3 to 6 Months)

• Closed Fractures: Most nerve palsies associated with closed fractures (e.g., radial nerve palsy with a closed humeral shaft fracture) are neurapraxic or axonotmetic. Observation for 3 to 4 months is the standard of care. If no clinical or EMG evidence of recovery is present by 12 weeks, exploration is indicated.
• Gunshot Wounds: Given the 69% spontaneous recovery rate, GSW-induced nerve palsies are observed for 3 to 9 months.

Pitfall: Failing to obtain serial clinical examinations and EMG studies at 6 and 12 weeks can lead to missed windows for nerve grafting. Motor endplates undergo irreversible fibrosis by 18 to 24 months post-denervation; therefore, reinnervation must be achieved before this critical threshold.

OPERATIVE PRINCIPLES AND SURGICAL APPROACHES

When surgical intervention is indicated, meticulous microsurgical technique is paramount. The primary goals are to restore neural continuity, decompress the nerve from extrinsic tethering, and provide a well-vascularized soft-tissue bed.

General Operative Setup

• Magnification: Operating loupes (3.5x to 4.5x) or an operating microscope are mandatory.
• Instrumentation: Microsurgical instruments, jeweler's forceps, and micro-scissors.
• Hemostasis: A pneumatic tourniquet is utilized for the approach but must be deflated prior to nerve repair to ensure absolute hemostasis, as postoperative hematoma is a primary cause of secondary nerve failure. Bipolar electrocautery is used strictly away from the nerve tissue.

Step-by-Step: Radial Nerve Exploration in Humeral Shaft Fractures

When exploring a radial nerve that has failed to recover following a humeral shaft fracture, the approach depends on the fracture location.

1. Positioning: The patient is positioned lateral or supine with the arm draped free across the chest.
2. Incision: A longitudinal incision is made on the lateral aspect of the arm, extending from the lateral epicondyle proximally toward the deltoid insertion.
3. Superficial Dissection: The deep fascia is incised. The interval between the brachioradialis (anterior) and the triceps (posterior) is identified distally.
4. Nerve Identification (Distal to Proximal): Always identify the nerve in virgin, unscarred tissue. The radial nerve is located in the intermuscular interval anterior to the lateral epicondyle. It is traced proximally into the zone of injury (the fracture callus).
5. Neurolysis: Using tenotomy scissors, the epineurium is carefully freed from the surrounding fracture callus or scar tissue. If the nerve is entrapped within the bone, a high-speed burr is used to unroof the bony tunnel, protecting the nerve with a malleable retractor.
6. Assessment: If the nerve is in continuity but thickened (neuroma-in-continuity), intraoperative nerve stimulation is performed. If a compound muscle action potential (CMAP) is present, external neurolysis is sufficient. If no conduction is present, the neuroma must be resected back to healthy fascicles, followed by sural nerve cable grafting.

Step-by-Step: Common Peroneal Nerve Decompression at the Fibular Neck

Indicated for secondary compression from callus, hematoma, or severe stretch injuries.

1. Positioning: Supine with a bump under the ipsilateral hip to internally rotate the leg.
2. Incision: A curved incision is made posterior to the biceps femoris tendon, curving anteriorly across the fibular neck.
3. Dissection: The common peroneal nerve is identified medial to the biceps femoris tendon in the popliteal fossa.
4. Decompression: The nerve is traced distally as it wraps around the fibular neck. The superficial fascia of the peroneus longus is incised. The fibrous arch of the peroneus longus must be completely released to decompress the nerve as it divides into its deep and superficial branches.
5. Handling: The nerve is handled exclusively by its epineurium using vessel loops. Traction must be strictly avoided.

POSTOPERATIVE PROTOCOLS AND REHABILITATION

The postoperative management of peripheral nerve injuries is as critical as the surgical execution.

• Immobilization: Following primary nerve repair or grafting, the limb is splinted in a position that minimizes tension on the neurorrhaphy site for 3 weeks. For example, following an ulnar nerve repair at the elbow, the elbow is splinted in 45 to 60 degrees of flexion.
• Early Passive Motion: While the nerve repair is protected, adjacent joints must undergo passive range of motion (ROM) to prevent debilitating contractures.
• Nerve Gliding: At 3 to 4 weeks, the splint is removed, and gentle, progressive nerve gliding exercises are initiated to prevent epineurial adhesions to the surrounding soft tissue bed.
• Orthotic Support: Dynamic splinting is utilized to prevent overstretching of denervated muscles and to assist with function (e.g., a dynamic extension splint for radial nerve palsy, or an Ankle-Foot Orthosis [AFO] for peroneal nerve palsy).
• Monitoring: Clinical recovery is monitored by advancing Tinel's sign (progressing at approximately 1 mm per day or 1 inch per month) and serial EMG/NCS at 3-month intervals.

In conclusion, the etiology of peripheral nerve injuries in orthopaedics is deeply intertwined with the mechanics of the primary skeletal trauma. A profound understanding of fracture-nerve associations, coupled with disciplined clinical evaluation and precise microsurgical technique, is essential for the modern orthopaedic surgeon to optimize functional recovery in these complex injuries.