Yoshimasa Kanawaku

A case of lethal soft tissue injuries due to assault.

A 42-year-old male had been assaulted by his family over the two previous days and went into a deep coma. When the emergency technician arrived, the patient was in a state of cardiopulmonary arrest. On arrival, his electrocardiogram showed asystole. His body showed swelling with subcutaneous hemorrhage, suggesting multiple contusional wounds. Serum biochemistry evaluation revealed blood urea nitrogen of 80 mg/dL, creatinine of 5.99 mg/dL, creatine phosphokinase of 10,094 IU/L, and potassium of 11.0 mEq/L. Advanced cardiopulmonary resuscitation failed to obtain a return of spontaneous circulation. Laboratory findings revealed rhabdomyolysis, renal failure, and hyperkalemia. Autopsy did not indicate the direct cause of death to be traumatic organ injuries. Because trauma was not the direct reason of death, we speculated that the patient died of hyperkalemia induced by multiple contusional soft tissue injuries, following rhabdomyolysis, hemolysis, and acute renal failure. The physician should maintain a high index of suspicion for hyperkalemia induced by rhabdomyolysis and acute renal failure, especially in patients presenting with symptoms of multiple soft tissue injuries with massive subcutaneous hemorrhaging.

Sudden collapse after minor head injury in an elderly man; association with cardiocerebral decompensation and fat embolism syndrome

An 86-year-old man suffering from right hemiparesis and dementia fell from a stretcher and sustained laceration and bruising to his right eyebrow. He was brought to an emergency room, and his wounds were treated. Shortly after discharge, his respiratory and mental status dramatically declined. Despite supportive care, he died about three hours after re-admission. Autopsy revealed a minor laceration to the eyebrow with minor intracranial injuries, mild cardiomegaly (370 g) with right atrial dilatation, pericardial effusion (170 ml) and marked pulmonary edema. Microscopically, fatty droplets were observed in the lung capillaries, the glomeruli and the intracerebral vessels. Although the extent of the original injuries seemed insufficient to cause systemic fat embolism syndrome (FES), the patients decreased cardiac reserves and stress associated with this event likely contributed to his death consistent with the physiochemical model of FES pathogenesis.