Rhabdomyolysis: a neglected priority in the early management of severe limb trauma

Abstract

Potentially dangerous muscle damage is often overlooked in the salvage of severely injured limbs. Muscle damage may be due to direct injury with crush, laceration or contusion. This may be complicated by ischaemia through prolonged compression at the time of injury or later as a result of raised compartmental pressure. The result of muscle damage, irrespective of cause, is rhabdomyolysis, in which alteration of the cell membrane occurs with release of intracellular contents. The systemic effect of rhabdomyolysis can vary from transient mild hyperkalaemia, hypocalcaemia, myoglobinaemia and elevated creatinine phosphokinase to the lifethreatening crush syndrome with hypovolaemic shock, cardiac arrhythmias and acute myoglobinuric renal failure. The local effect is increased capillary permeability resulting in accumulation of tissue fluid and raised compartment pressure. Rhabdomyolysis may therefore cause compartment syndrome; however, the converse is true, with prolonged compartment syndrome small vessel thrombosis may cause cellular death with subsequent rhabdomyolysis despite axial vessel patency (Kitka et al., 1987). The crush syndrome was first described in air raid victims trapped under falling masonry (Bywaters and Beall, 1941); however, it may be encountered in peacetime as is illustrated by the following three cases.