Medico-legal aspects of peripheral nerve injury

Iatrogenic nerve injuries are always a matter for concern. This article will address the common causes, diagnosis and management of iatrogenic peripheral nerve injuries. The most widely used classification of peripheral nerve injury is that described by Seddon in 1943.1 He divided nerve injuries into three types: neurapraxia, axonotmesis and neurotmesis. Neurapraxia (inactivity of the nerve) is a non-degenerative lesion of a nerve characterised by a complete or partial failure to propagate an action, potentially resulting in motor and/or sensory loss. It is usually caused by compression or ischaemia, resulting in ischaemia of the myelin sheath. The nerve remains intact and Wallerian degeneration does not occur. It is reversible if the injurious agent is removed. If the distal segment of the nerve is stimulated, there is a motor response. The lesion recovers by remyelination of the distal segment and takes between two and 12 weeks, depending on the age of the patient and the site of the injury. In practice, it is unwise to assume that a lesion is a neurapraxia rather than a more severe injury because this will lead to delay in diagnosis and a poorer outcome. The presence of persistent pain suggests that the injurious agent is continuing to act. The diagnosis should not be made in the presence of a strong Tinel test which indicates that axons have been ruptured. An axonotmesis (cutting of the axon) is the result of disruption of the axon and its myelin sheath. The supporting structures, Schwann cells, endoneurium, perineurium and epineurium remain intact. It is usually the result of severe compression or a crush injury. Wallerian degeneration occurs distally, and proximally to the closest node of Ranvier. Repair is by a combination of collateral sprouting in lesser injuries and axonal regeneration in more severe injuries. The latter occurs at …