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Dear Sir,A 19-year-old generally healthy male soldier was diagnosed with heat stroke complicated by rhabdomyolysis and acute renal failure following a 90-km march in the Negev desert. On admission, blood pressure was 150/60 mm Hg, temperature 42°C, pulse rate 120, and respiratory rate 40. The patient exhibited delirium without meningeal or focal neurological signs. Laboratory results were as follows: sodium 123 mmol/l, potassium 4.9 mmol/l, creatinine 141 µmol/l, urea 8.5 mmol/l, creatine kinase 6,957 U/l, and serum myoglobin 8,830 ng/ml (normal 0–120). Shortly after admission he developed generalized tonic-clonic seizures. Treatment included cooling, intravenous hypertonic saline, bicarbonate and diazepam. Approximately 12 h after admission his delirium resolved accompanied by improvement in renal function, electrolyte, myoglobin, and creatine kinase abnormalities. Two days later he complained of right anterior tibial pain, swelling, and limitation of movement. Physical examination showed localized tenderness and edema encompassing the right anterior tibial area associated with drop foot and pain exacerbation with passive movement. Abnormal conduction along the right common peroneal nerve was demonstrated on nerve conduction studies. No sensory deficit was elicited. An ultrasound duplex examination of the right lower extremity veins was normal. A diagnosis of anterior tibial compartment syndrome was made. Mannitol treatment was started, as illustrated in figure 1, with subsequent reduction in edema and improvement in the patient’s strength and range of motion. He was discharged 10 days after admission with mild residual weakness confined to the right lower extremity.Acute compartment syndrome (ACS) is a serious complication of rhabdomyolysis, induced by increased intracompartmental pressure and subsequent muscle tamponade [1]. Clinical manifestations include induration and edema of the involved compartment, pain with passive motion of those muscles situated in the compartment, weakness and neurological disturbances [2]. ACS requires emergent surgical decompression when intracompartmental pressure is greater than 40 mm Hg and/or clinical symptoms and signs are present [3]. However, fasciotomy has a high complication rate because it converts a closed necrotic muscle injury into an open wound with potential dissemination of infection [4]. Mannitol was first proposed as a noninvasive alternative therapy for ACS after encouraging results were obtained with mannitol infusion for the treatment of ACS in a canine model [5]. Mannitol extracts water by extracellular fluid hyperosmolarity, hence ameliorating muscle edema. Our report is the first documentation of a salutary effect of mannitol therapy for ACS in humans and warrants further investigative efforts for this conservative treatment of ACS.
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Daniels et al. (1998) studied this question.
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