Of 48 consecutive children with Gartland III
supracondylar fractures, 11 (23%) had evidence of vascular injury,
with an absent radial pulse. The hand was pink and warm in eight
and white and cold in the other three patients. They underwent colour-coded
duplex scanning (CCDS) and ultrasound velocimetry (UV) to investigate
the patency of the brachial artery and arterial blood flow. In seven
patients with a
This annotation discusses the findings of two papers in the current issue describing the management of the neurovascular complications of supracondylar fractures of the humerus in childhood, with particular reference to the indications for and the timing of exploration of the brachial artery and the affected nerves.
We compared two management strategies for the perfused but pulseless hand after stabilisation of a Gartland type III supracondylar fracture. We identified 19 patients, of whom 11 were treated conservatively after closed reduction (group 1). Four required secondary exploration, of whom three had median and/or anterior interosseus nerve palsy at presentation. All four were found to have tethering or entrapment of both nerve and vessel at the fracture site. Only two regained patency of the brachial artery, and one patient has a persistent neurological deficit. In six of the eight patients who were explored early (group 2) the vessel was tethered at the fracture site. In group 2 four patients also had a nerve palsy at presentation and were similarly found to have tethering or entrapment of both the nerve and the vessel. The patency of the brachial artery was restored in all six cases and their neurological deficits recovered completely. We would recommend early exploration of a Gartland type III supracondylar fracture in patients who present with a coexisting anterior interosseous or median nerve palsy, as these appear to be strongly predictive of nerve and vessel entrapment.
A series of 26 children was referred to our specialist unit with a ‘pink pulseless hand’ following a supracondylar fracture of the distal humerus after a mean period of three months (4 days to 12 months) except for one referred after almost three years. They were followed up for a mean of 15.5 years (4 to 26). The neurovascular injuries and resulting impairment in function and salvage procedures were recorded. The mean age at presentation was 8.6 years (2 to 12). There were eight girls and 18 boys. Only four of the 26 patients had undergone immediate surgical exploration before referral and three of these four had a satisfactory outcome. In one child the brachial artery had been explored unsuccessfully at 48 hours. As a result 23 of the 26 children presented with established ischaemic contracture of the forearm and hand. Two responded to conservative stretching. In the remaining 21 the antecubital fossa was explored. The aim of surgery was to try to improve the function of the hand and forearm, to assess nerve, vessel and muscle damage, to relieve entrapment and to minimise future disturbance of growth. Based on our results we recommend urgent exploration of the vessels and nerves in a child with a ‘pink pulseless hand’, not relieved by reduction of a supracondylar fracture of the distal humerus and presenting with persistent and increasing pain suggestive of a deepening nerve lesion and critical ischaemia.
