Aims

To describe a new objective classification for open fractures of the lower limb and to correlate the classification with patient-centred outcomes.

Aims

To evaluate interobserver reliability of the Orthopaedic Trauma Association’s open fracture classification system (OTA-OFC).

Compartment syndrome, a devastating consequence of limb trauma, is characterised by severe tissue injury and microvascular perfusion deficits. We hypothesised that leucopenia might provide significant protection against microvascular dysfunction and preserve tissue viability. Using our clinically relevant rat model of compartment syndrome, microvascular perfusion and tissue injury were directly visualised by intravital video microscopy in leucopenic animals. We found that while the tissue perfusion was similar in both groups (38.8% (standard error of the mean (sem) 7.1), 36.4% (sem 5.7), 32.0% (sem 1.7), and 30.5% (sem 5.35) continuously-perfused capillaries at 45, 90, 120 and 180 minutes compartment syndrome, respectively versus 39.2% (sem 8.6), 43.5% (sem 8.5), 36.6% (sem 1.4) and 50.8% (sem 4.8) at 45, 90, 120 and 180 minutes compartment syndrome, respectively in leucopenia), compartment syndrome-associated muscle injury was significantly decreased in leucopenic animals (7.0% (sem 2.0), 7.0%, (sem 1.0), 9.0% (sem 1.0) and 5.0% (sem 2.0) at 45, 90, 120 and 180 minutes of compartment syndrome, respectively in leucopenia group versus 18.0% (sem 4.0), 23.0% (sem 4.0), 32.0% (sem 7.0), and 20.0% (sem 5.0) at 45, 90, 120 and 180 minutes of compartment syndrome in control, p = 0.0005). This study demonstrates that the inflammatory process should be considered central to the understanding of the pathogenesis of cellular injury in compartment syndrome.

Cite this article: Bone Joint J 2015;97-B:539–43

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.