A 39-year-old man presenting with acute delirium is reported who suffered an unexpected cardiac arrest shortly after being sedated. Death followed 2 days later from hypoxic-ischemic encephalopathy. At autopsy, marked pallor and edema of his left sternomastoid muscle was observed which was shown on microscopy to be due to confluent coagulative necrosis. Myoglobin casts in his renal tubules corresponded to an antemortem creatine phosphokinase level of 31,940 U/l. Death was due to rhabdomyolyisis and excited delirium complicating cocaine toxicity with hypoxic-ischemic encephalopathy, against a background of atherosclerotic coronary artery disease. Extensive confluent pallor in a single muscle may be a useful marker of chronic cocaine exposure associated with hyperthermia and muscle necrosis. Confirmatory toxicology is required.

To determine whether vitreous humor sodium levels might be of use in evaluating deaths associated with immersion, samples of vitreous humor were prospectively evaluated at autopsy over a 4-year period from 2006 to 2009. There were 19 cases of saltwater immersion (age range 9-76 years; mean age 44 years; M:F, 2.8:1) and 16 freshwater immersions (age range 2-81 years; mean age 27 years; M:F, 2.2:1). In the group of saltwater drownings, vitreous humor sodium levels were elevated, ranging from 145 to 184 mM (mean = 160.2 ± 9.9 mM), and in the cases of freshwater drowning, the levels were reduced, ranging from 73 to 148 mM (mean = 129.8 ± 17 mM; p < 0.0001). Alterations in electrolyte levels may have been because of hemoconcentration or dilution from electrolyte fluxes in the lungs, or from passive diffusion during immersion. This study has demonstrated that vitreous sodium level is an easily performed test that may be a useful adjunct to the investigation of possible immersion deaths.

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