With the exception of certain nerve injuries, all soft tissues heal by the formation of collagenous scar tissue. Prompt, careful, and anatomic reapproximation of injured tendon, muscle, and skin provides the best basis for a functional and satisfactory result. Failure to achieve repair of an injured tendon often results in significant functional loss.
Effective repair of a lacerated tendon remains a great surgical challenge because tendons often heal with an excess of scar tissue and loss of their natural gliding function. The principles of tendon repair therefore include thorough debridement of the wound, precise anatomic reapproximation, and protected active range of motion during healing to help maintain the mobility essential for normal function. The range of motion allowed after repair is limited by the particular tendon injured, the location of the laceration along the course of the tendon, and the strength of the surgical repair.
Peripheral nerve injury was described by Seddon as either neurapraxia, axonotmesis, or neurotmesis and later further subdivided by Sunderland. Neurapraxia (Sunderland 1) involves local damage to myelin, often from compression or stretch associated with an injury. There is no disruption in axon continuity, and no distal degeneration takes place so no permanent loss of function is expected; recovery typically takes weeks to months. Axonotmesis involves loss of continuity with varying damage to surrounding connective tissue. Sunderland subdivided this with type 2, retaining intact endoneurium, perineurium, and epineurium, which helps guide healing axons and prevents infrafascicular healing so complete functional recovery may take place, but on the order of months. Sunderland type 3 involves disruption of the endoneurium, and recovery is often incomplete. In Sunderland type 4, the perineurium is disrupted as well, leaving only epineurium, and may require excision and surgical repair of the damaged segment. Neurotmesis, equivalent to Sunderland type 5 injuries, involves complete disruption of the nerve. Laceration of a peripheral nerve disrupts the axons that normally carry impulses to and from the central nervous system, and restoration of nerve function depends on the effective repair of these axons. The distal segment undergoes wallerian degeneration, leaving the basal lamina of the Schwann cells to serve as guiding structures for the growth cone at the tip of the regenerating axon to it is hoped grow through. Complete nerve lacerations should be referred for surgical evaluation to an orthopaedic or plastic surgeon trained in microsurgical nerve repair. The principles of peripheral nerve repair include adequate debridement, careful anatomic repair by means of group fascicular repair, and/or simply epineurial repair (controversy still exists between the two). When primary repair cannot be achieved without tension, autografts, allografts, and entubulation chambers are therapeutic options being investigated. Failure to achieve satisfactory repair of a lacerated peripheral nerve results in permanent loss of its function and often produces a painful neuroma at the injury site.
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