Crush syndrome le syndrome de compression

The first detailed cases of crush syndrome were described in 1941 in London after victims trapped beneath bombed buildings presented with swollen limbs, hypovolemic shock, dark urine, renal failure, and ultimately perished. The majority of the data and studies on this topic still draw from large databases of earthquake victims. However, in Africa, a continent with little seismic activity, the majority of crush syndrome cases are instead victims of severe beatings rather than earthquake casualties, and clinical suspicion by emergency personnel must be high in this patient group presenting with oliguria or pigmenturia. Damaged skeletal muscle fibres and cell membranes lead to an inflammatory cascade resulting in fluid sequestration in the injured extremity, hypotension, hyperkalemia and hypocalcemia and their complications, and renal injury from multiple sources. Elevations in the serum creatinine, creatine kinase (CK), and potassium levels are frequent findings in these patients, and can help guide critical steps in management. Fluid resuscitation should begin prior to extrication of trapped victims or as early as possible, as this basic intervention has been shown to in large part prevent progression of renal injury to requiring haemodialysis. Alkalinization of the urine and use of mannitol for forced diuresis are recommended therapies under specific circumstances and are supported by studies done in animal models, but have not been shown to change clinical outcomes in human crush victims. In the past 70 years the crush syndrome and its management have been studied more thoroughly, however clinical practice guidelines continue to evolve.