Peripheral nerve2
Management – General Considerations

Which require surgery
For those that require surgery, when should you do it?
What surgery should you do?

Which injuries require surgery?

There are two scenarios – the closed injury with nerve dysfunction, and the open injury with nerve dysfunction. The mechanism of injury – compression, ischemia, traction, laceration – can be inferred from the trauma. The majority of acute traumatic nerve injuries are caused by blunt closed trauma, which often stretches and compresses a nerve but leaves it in continuity. Open injuries may be produced sharply or bluntly and may be associated with complete or partial nerve injury. Missile injuries often leave nerves in continuity but produce intraneural damage secondary to cavitation effects. First, a review of the types of nerve injuries:

Sunderland I – Neuropraxic Injuries
– conduction along the axon is physiologically interrupted at the site of the injury, but the axon is not actually disrupted and no wallerian degeneration occurs. The loss of function is variable, usually more profoundly affecting the motor function than sensory.

– Obviously, these injuries do not require surgery. They are detected clinically by fairly well preserved function, and by fairly early recovery.

Sunderland II – Axonotmetic Injuries
– disruption of the axon with wallerian degeneration distal to the point of injury and degeneration proximal for one or more nodal segments occurs. The integrity of the endoneurial tube is maintained, however, so that the anatomic course for regeneration is in place. Any permanent deficit is related to the number of neural cell bodies that die, with cell death occurring more commonly when the injury takes place proximally. Clinically, the neurological deficit is complete, with loss of motor, sensory, and sympathetic function. Motor reinnervation takes place in a progressive manner, and an advancing Tinel sign can usually be followed at the rate of 1 inch per month.

– Because the framework for axonal regeneration is already in place, these would not be improved upon by surgery either. Usually good function is achieved.

Sunderland III
– the axons and endoneurial tubes are disrupted, but the perineurium is preserved. The regenerative effort is impeded by the disruption of the endoneurial tubes and scar formation which obstructs tubes and diverts the sprouting axons. Clinically, the neurological loss is complete, and the duration prolonged. Complete return of neural function does not occur, distinguishing this from the Sunderland II injuries.

– Because it is unlikely that surgical repair could improve upon the intra-neural architecture, these injuries are better left managed non-surgically.

Sunderland IV
– the axons, endoneurium, and perineurium are disrupted, but not completely, so that complete severance of the entire trunk does not occur. Retrograde degeneration with axonal death is more common. Axonal sprouts exit through defects in the perineurium into the surrounding tissues. There will be no advancing Tinel sign.

– The recovery from these is uniformly poor without surgery.

Sunderland V (Neurotonmesis)
– complete transection of the nerve, resulting in a variable distance between the neural stumps. The likelihood of significant bridging by axonal sprouts is remote, as is the possibility of significant functional return.

– Obviously, these are better treated surgically

Type VI injuries (MacKinnon)
– mixed injures in which a nerve trunk is partially severed, and the remaining part sustains fourth, third, second, or even first degree injury.

– These require partial neurorrhaphy, possibly with internal neurolysis.

Unfortunately, patients arrive with neurologic deficits, and not with a Sunderland classification assigned to their injury. The trick is in clinically assessing the patient to determine which type of injury they have. For open wounds, exploration will usually demonstrate whether the nerve is in continuity or not.

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