[Peripheral neurological deficit after fracture of the distal radius.]

The objective of this retrospective study is to compare the results of early and delayed surgery of the carpal tunnel syndrome following fracture of the distal radius. The authors evaluate the quality of their treatment in neurological deficit associated with this injury and recommend the correct procedure. In the submitted study 32 patients with carpal tunnel syndrome after fracture of the distal radius operated in 1976-1978 are evaluated. Damage of the median nerve in the area of the carpal tunnel may develop after injury acutely, subacutely or also chronically. The causes of an acute posttraumatic lesion include haemorrhage into the carpal tunnel area as well as volar dislocated bone fragments. Chronic lesions develop as a result of oedema, excessive callus formation in the carpal tunnel area, persisting dislocation and prolonged immobilization. From the pathophysiological aspect the post-traumatic lesion develops as a result of a chronically elevated pressure in the carpal tunnel which leads to a restricted blood supply in the area of the flexor tendons as well as in the area of the median nerve. The thus developing hypoxia damages the endothelium of the vasa nervorum. Proteins penetrate and oedema develops as a vicious circle. This cascade can be the late consequence of the wrist injury or the consequence of reposition and many weeks' immobilization without adequate physical therapy and in some patients it may act as a "trigger" of Sudeck's syndrome.