A Case of Multiple Organ Failure due to Heat Stoke Following a Warm Bath
A 68-year-old man was admitted to emergency room for loss of consciousness. He was discovered in bathtub filled with warm water and he was unconscious. He was presumed to have been in a warm bath for 3 hours at the time of discovery. He had been taking an oral hypoglycemic agent for his diabetes for 9 years.\nHis body temperature was 41℃, the blood pressure was 80/50 mmHg, the pulse rate was 124 beats/min and the respiratory rate was 48 breaths/min. On arrival, he was semicomatous, areflexic and flaccid, but he had no lateralizing signs or neck stiffness. His skin was hot and dry. His blood glucose was 150 mg/dL, and the arterial blood gas analysis showed a mixed high anion gap metabolic acidosis and respiratory alkalosis (pH: 7.42, pO2: 47.2 mmHg, pCO2: 28 mmHg, and HCO3-: 18 mmol/L). On admission, laboratory findings were as follows: WBC: 6,300/L, Hb: 17.5 g/dL, platelets: 70,000/L, prothrobin time (PT): 12.8 sec (89%, INR 1.12), activated partial thromboplastin time (aPTT): 21.7 sec, aspartate aminotrasferase (AST): 98 IU/L, alanine aminotransferase (ALT): 97 IU/L, bilirubin: 0.7 mg/dL, amylase: 39 IU/L, Na/K/Cl: 140/4.1 /100 mmol/L, BUN: 32 mg/dL, creatinine: 2.3 mg/dL and myoglobin: 223 ng/mL. Brain MRI showed no hemorrhage or infarction and there was no abnormal finding on the chest X-ray.\nAfter 30 min, his body temperature was still 39.5℃. Despite further decreasing the body temperature to 38℃ via external cooling and infusion of fluids, the semicomatous mentality was not changed and so endotracheal intubation and mechanical ventilation were started. On day 2, the PT decreased to 13% (INR 7.57), and the aPTT was also prolonged to an uncheckable range. The AST/ALT increased to 2136/1838 IU/L and the total bilirubin increased to 3.2 mg/dL (). The fibrinogen decreased to 185.6 mg/dL (normal range: 230-480), and the fibrin/fibrinogen degradation products (FDPs) were elevated to >20 ug/dL. The laboratory findings were considered to represent acute hepatic failure combined with acute renal failure (ARF) and disseminated intravascular coagulation (DIC) following heat stroke. Other causes of fulminant liver failure like viral hepatitis and fulminant Wilson's disease were ruled out by the patient's history and/or the appropriate laboratory tests. On the third day, continuous venovenous hemofiltration (CVVHF) was started because of the progressive oligouria despite continuous infusion of diuretics and the worsening metabolic acidosis (pH: 6.93, pO2: 117 mmHg, pCO2: 41.8 mmHg and bicarbonate: 8.6 mmol/L). The serum transaminase was decreased, but the PT remained prolonged despite daily infusion of fresh frozen plasma (FFP). The serum bilirubin level increased further to 50 mg/dL.\nOn day 15, abdominal distension developed and the ascitic fluid analysis showed inflammatory exudates. At the same time, Acinetobacter baumannii and Enterococcus faecium were cultured in the blood and the appropriately sensitive antibiotics were started under the impression of septic peritonitis. In spite of treatment with CVVHF and the best supportive care, the hepatic failure (bilirubin to 53 mg/dL) and DIC progressed with superimposed infection. The patient passed away on day 25.