Definition of nerve injury:

The mildest grade is called neurapraxia. Neurapraxia is a reduction or complete block of conduction across a segment of a nerve with axonal continuity conserved. More specifically, it is dysfunction and/or paralysis without loss of nerve sheath continuity and peripheral wallerian degeneration. Nerve conduction is preserved both proximal and distal to the lesion but not across the lesion. A person's foot "falling asleep" after his legs have been crossed is an example of a functional loss without abnormal change.

Axonotmesis is a more severe grade of nerve injury compared to neurapraxia. Axonotmesis is a result of damage to the axons with preservation of the neural connective tissue sheath (endoneurium), epineurium, Schwann cell tubes, and other supporting structures. Thus, the internal architecture is relatively preserved. This can guide proximal axonal regeneration to reinnervate distal target organs. Distal wallerian degeneration occurs in axonotmesis.

Neurotmesis is the most severe grade of peripheral nerve injury. It occurs when the axon, myelin, and connective tissue components are damaged and disrupted or transected. Recovery through axonal regeneration cannot occur. This grade of injury includes nerve lesions in which external continuity is preserved but intraneural fibrosis occurs and blocks axonal regeneration.

Frequency:

Nerve injury can be associated with fractures and fracture- dislocations. The probability of nerve injury is doubled with fracture associated with shoulder dislocation. Approximately 95% of peripheral nerve injuries associated with a fracture occur in the upper extremity. The most common form is radial nerve injuries associated with humeral fractures. The most common injury resulting from dislocations or fracture-dislocation of the elbow seems to be ulnar nerve neurapraxia, which spontaneously resolves after a closed reduction. Radial nerve palsy after fracture of the humerus is the most common nerve lesion in long bone fractures.

Neural injury is more common with dislocations, which result in stretch injuries to the nerve, occurring in 18% or more of knee dislocations and more than 13% of posterior hip dislocations. Nerve injury is common in dislocations of the shoulder, with an incidence rate of 48%.

Iatrogenic etiology is another possible cause of injury. The incidence of nerve injuries varies from 1-10% in patients with closed forearm fractures treated by plating. However, determining whether the injury resulted from fracture or operative intervention often is difficult. Associated trauma can increase the probability of nerve injury. For example, a hematoma formation at the site of injury increases the probability of nerve injury 4.4-fold.

Etiology:

The first mechanism of injury is mechanical injury. Two examples of mechanical injury are "Saturday-night paralysis" of the radial nerve and tourniquet paralysis.

The second mechanism of injury is crush and percussion injury. This injury can be described through an animal model. With this model, the usual method is squeezing the nerve with smooth- tipped forceps, which induces focal compression injury. In humans, compression injuries can be induced by fractures, hematomas, and compartment syndrome. Proximal venous ligation, direct trauma to muscle, infection, burns, and localized pressure by casts or by circular dressings also are causes of compartment syndrome.

Compartment syndrome injuries cause high pressure in the surrounding tissue. Pressure compresses the arterial blood supply of the nerve, predisposing the nerve to ischemic cell damage and cell death. Even though the peripheral nervous system is relatively resistant to ischemia, long periods of stretch and compressive force can cause vascular compromise and neuronal ischemia. Delays in assessment and treatment of compartment syndrome can lead to nerve injury in the forearm. Concussion or compression of the nerve causes neurapraxia. Other causes of neurapraxia include ischemia secondary to vascular compromise, metabolic derangement, and diseases or toxins causing demyelination of the nerve.

A third mechanism of injury is laceration injury caused by blunt or penetrating trauma. The nerves in these injuries are not cleanly sectioned but are damaged in an irregular pattern.

The fourth mechanism of injury is penetrating trauma, whereby peripheral nerves are partially or completely severed. Penetrating trauma is caused by stab wound lacerations and by glass and surgical incisions.

The fifth mechanism of injury is stretch injury. The internal anatomy of nerves permits the nerve to stretch approximately 10-20% before structural damage occurs. Stretch injuries or severe blows to a nerve cause axonotmesis. In axonotmesis caused by stretch injuries, axons over long segments of nerve are disrupted. In axonotmesis caused by severe blows, axons are disrupted only at the site of impact .

Stretch injuries can be induced by traction. For example, forcible depression of the shoulder or traction of the arm can injure the brachial plexus. This results in a stretch injury. Traction injuries to the peripheral nerve trunk limb girdle plexuses or to spinal nerve roots can occur in a number of ways. Injuries to the lumbosacral plexus or to the lumbosacral roots commonly are associated with fractures of the pelvis. Displacement of fractures and joint dislocations can result in stretch injury to peripheral nerves. Stretch injury to peripheral nerves may occur during operative or other surgical procedures. Stretching of the nerve around the radial neck during a closed reduction is an example of procedural etiology for stretch injury.

A sixth mechanism of injury is high-velocity trauma caused by motor vehicle accidents and gunshot wounds.

A seventh mechanism of injury is cold injury. Frostbite leads to necrosis of all involved tissues, including the peripheral nerves. Several hours of nonfreezing exposure with a temperature above -2.5°C and below 10°C damages peripheral nerves because they are more vulnerable than the surrounding tissue.

An eight mechanism involves injury to nerves from physiologic healing processes. For example, the sciatic nerve can be compressed from scar formation and massive heterotopic ossification after a hip trauma. After elbow trauma, scarring can jeopardize the normal gliding of the ulnar nerve in the elbow due to adherence to scar tissue, fracture callus, or heterotopic bone.

Lastly, iatrogenic injury is another possible cause of acute nerve injury. Iatrogenic injury to the axillary nerve can occur in shoulder instability surgery. Here, the axillary nerve injury can be secondary to tension, suture compression, or iatrogenic laceration. Furthermore, in rotator cuff surgery, overzealous muscle splitting places the axillary nerve at risk for injury. Posterior interosseous and median nerve injury can occur during elbow arthroscopy. Iatrogenic causes of traumatic posterior interosseous nerve injury around the proximal forearm have been documented.

Clinical Presentation:

In some cases, the injury does not match the clinical presentation. Operative findings of nerve injury may or may not match clinical findings. Data exist of gross operative evidence of nerve injury without clinical evidence of neurological dysfunction, such as with sheath hematoma and compression by fracture fragments. Conversely, data exist of intraoperative grossly normal-appearing nerves with clinical paresis. These deficits may develop after initially appearing with a normal neurological examination.

More specifically, following a traumatic hip dislocation, some patients may develop sciatic nerve deficits even after an initial normal neurological examination. Hence, when a nerve is damaged, it may continue to appear normal in a neurological examination. In truth, damage can be revealed only through diagnostic studies.

In many instances, acute nerve injury associated with complex trauma complicates a thorough neurological examination. For example, of the patients with traumatic hip dislocations who are treated in the emergency department, many also present with concomitant head, visceral, or skeletal injuries. With these cases, a thorough neurological examination of the affected extremity becomes difficult to perform. Furthermore, in many patients, nerve injury may remain undetected because joint and/or bony injury may dominate the clinical picture.

Certain presenting traumas should alert the clinician to the possibility of associated nerve injury. For example, for patients with trauma and obvious skeletal deformities to the shoulder, such as glenohumeral dislocation and/or fracture, be aware of the potential for associated nerve injury. Nerve injury may be apparent immediately after injury. For example, immediate paralysis of common peroneal nerve function and foot drop with loss of eversion of the foot usually are reported at the time of a stretch/contusion injury without fracture or dislocation at the knee level. In an aggravated patient who is vigorously moving all of his extremities, a motionless upper extremity strongly suggests brachial plexus involvement.

Indications for Surgery and Intervention:

Deciding the timing of surgery is very important. In clean lacerating injuries in which the nerve ends are visible in the wound or when clinical examination reveals obvious motor and sensory deficits resulting from the injury at the laceration, immediate primary repair may be indicated. In blunt transections resulting from lacerations, delayed repair has a better surgical result. Injuries that do not demonstrate evidence of early spontaneous recovery, such as those caused by bullets, crushing blows, traction, fractures, or injections, are explored 2 months after the injury. For a nerve injury within 2 -3 inches of recoverable muscle, 2 months is required for the growing axons to begin the process of muscle reinnervation. Therefore, an additional delay of 1 month is justified before surgical exploration. Brachial plexus stretches or contusions are observed for 4 months. If no evidence of recovery is present, the plexus is explored.

When certain cases are unresponsive to conservative treatment, surgery is the only alternative. Surgery is indicated for patients with neurotmesis. Therefore, accurate grading of an acute traumatic injury is essential. Accurate grading is necessary for identifying high-grade injuries that may benefit from early surgery and for preventing unnecessary early exploration of grade I and II lesions.

Evolution of nerve injuries is important in indicating the need for open treatment. If nerve function is progressively deteriorating as per electrodiagnostic study findings, surgery may be indicated because the status of the connective tissue cannot be assessed without direct exploration.

Treatment Options:

The use of analgesics can help patients control pain from nerve injuries. Antivirals and steroids help to decrease endoneurial edema, an etiology of nerve injury. Hyperbaric oxygen (HBO) is an approved adjunctive treatment for acute traumatic ischemic reperfusion injury.

In surgical therapy, primary repair is direct reconnection of the nerve immediately after injury. In an epineurial repair, the epineuriums of the separated nerve endings are sutured together using a microsuture (usually 8-0 or 10-0 Ethicon). Best results occur when the nerves are either purely sensory or purely motor and when the intraneural connective tissue component is small and the fascicles have been clearly aligned.

Sharp lacerations without loss of nerve substance or partial lacerations with proper alignment are good examples of injuries that benefit from epineurial repair. In a crushing or delayed repair requiring trimming of the nerve ends, group fascicular repair improves fascicular alignment without an excessive number of sutures. Excessive sutures add to scar tissue production. Individual fascicle repair is not practiced widely because it requires numerous sutures and because it is technically difficult.

Secondary repairs are delayed repairs that may entail different strategies. Bones can be shortened to add length to a nerve. Nerve transposition across a flexed joint (eg, the ulnar nerve in the elbow) is another strategy for gauging nerve length in secondary repairs. These techniques can gain as much as an approximate 10% increase in available nerve length. However, within 3 weeks after injury, a nerve may lose as much as 8% of its length. Many surgeons prefer delayed suture to primary suture because this allows the wound to heal and it decreases the risk of infection. In addition, during a delayed repair, scarred ends of the nerve can be defined more accurately and trimmed back to normal fasciculi. The epineurial suture is more secure because the sheath has toughened. The suture of a severed nerve should not be delayed beyond 1 month.

Neurolysis is performed on intraneural and extraneural scar tissue to release regenerating nerve fibers in the hope of improving functional recovery. Contaminated wounds, such as gunshot wounds and avulsions with severe tissue disruption, benefit from a secondary repair. Severely damaged nerves may require a nerve graft. For example, a graft would be necessary if, after resection of injured nerve ends (including neuroma), the defect could not be closed without tension.

Studies show that sensation can return after nerve grafting. Extensive research has focused on the use of allograft nerves to replace peripheral nerves that require a long nerve graft. Allografts can survive if the patient is immunosuppressed and if the nerve allograft is preserved to maintain cell viability. Immunosuppression can be discontinued when the nerve graft has been incorporated with an ingrowth of Schwann cells from the host nerve ends. Nevertheless, results from autograft use are slightly more favorable than allograft use.

Intraoperative electrodiagnostic monitoring is important for assessing the functional integrity of motor and sensory peripheral nerves. The patient is draped to allow observation of the tested muscle groups. Intraoperative SSEPs and direct electrical stimulation can be used. Regional and local anesthetic blocks or tourniquets are avoided to facilitate intraoperative electrophysiological testing.

Important Complications:

Outcome and Prognosis:

Neuropraxic injuries usually are reversible, and patients recover within days to weeks. In axonotmesis, although axons will regenerate, functional recovery depends on the associated injuries, the amount of healthy proximal axon remaining after injury, and the age of the patient.