Radial nerve palsies associated with paediatric supracondylar humeral fractures: a caution in the interpretation of neurophysiological studies.

Abstract

Traumatic and iatrogenic neurological complications associated with paediatric supracondylar humeral fractures are well recognised. The severity of the nerve injury associated with supracondylar humeral fractures can be difficult to assess clinically and relies upon clinical progression or absence of recovery and neurophysiology. It is accepted that complete nerve palsy with neurophysiological complete block and absence of clinical recovery after three months requires surgical exploration and reconstruction. However, we argue that even a partial nerve palsy that is failing to recover as expected by 3 months should be explored even when the neurophysiology suggests the nerve is in continuity. We report two cases of closed Gartland type III paediatric extension-type supracondylar humeral fractures treated with closed reduction and percutaneous pinning and open reduction and internal fixation, respectively. Both children developed persistent postoperative radial nerve motor palsy. Neurophysiological studies sought prior to exploration indicated a degree of sensory nerve function in both cases, indicating a nerve in continuity. Subsequent surgical exploration revealed interfragmentary radial nerve compression at the fracture site at two levels in one case and at one level in the second case. The site of compression was excised and the nerve grafted. Excellent near-normal radial nerve recovery was achieved except for the persistent loss of extensor carpi radialis function in the first child. We publish these findings to highlight the possibility of misinterpreting the incomplete nerve lesion and the neurophysiology of a nerve in continuity, as a nerve that would spontaneously recover. At exploration, in these two cases, it was clear by the level of interfragmentary compression that the nerve would not have recovered without surgical intervention. We recommend exploration and repair of the radial nerve, when function to the nerve is compromised, even in the face of neurophysiological evidence of an intact nerve.