A Case of Recurrent and Fatal Hypothermia in a Man with Diabetic Neuropathy

Severe hypothermia most commonly results from accidental exposure to environmental cold temperatures. However, numerous medical conditions can contribute to or even cause hypothermia, including those that increase bodily heat loss (e.g., exfoliative dermatitis), those associated with deficient heat production (e.g., hypothyroidism, liver failure, and malnutrition), and those causing abnormal thermoregulation (e.g., spinal chord injury and sepsis syndrome). Hypothermia in diabetic patients is well described, particularly in association with hypoglycemic episodes (1) and diabetic ketoacidosis (2). Hospital admissions for hypothermia are more frequent among patients with diabetes than among the general patient population (3). Diabetic patients with neuropathy may be at risk for clinical hypothermia because of impairment of physiologic thermoregulatory mechanisms. We report a case of recurrent and fatal hypothermia in a man with diabetes and neuropathy.

P.V., a 40-year-old man with insulin-treated diabetes, was admitted to the intensive care unit of our hospital in January 2001 with hypothermia (rectal temperature 31.5°C) and coma. The patient was found by his wife early on the morning of admission to be cold and unresponsive. The patient had been discharged from our hospital only 1 week prior, and he was known to have diabetes, renal insufficiency, and lower-extremity neuropathy with reduced sensation and deep tendon reflexes. The medical record notes that the patient was also hypothermic (temperature 33.9°C) upon presentation for his prior admission. In the emergency department, his blood pressure was 78/48 mmHg, and his heart rate was 43 bpm and regular. The patient had no focal neurological deficit and a computed tomography scan of his head revealed old lacunar infarct. There was no leukocytosis or gap-acidosis, and his blood area nitrogen, creatinine, and glucose were 16 mmol/l, 504 μmol/l, and 6.9 mmol/l, respectively. The patient was given warmed intravenous fluids and blankets, but had an episode of ventricular tachycardia requiring defibrillation. The patient was moved to intensive care where he quickly recovered and returned to his baseline level of health. The patient’s thyroid function and cortisol response to stimulation were both normal. The chest radiograph showed no infiltrate, and blood cultures and HIV antibody were negative. He had no further episodes of hypothermia or arrhythmia, and he was discharged from the hospital. In February 2001, we received notification that the patient had expired at a local hospital after again being found by his wife to be unresponsive and cold. The medical record notes that the patient’s temperature was 33.9°C upon his arrival to the other facility, where he was resuscitated but subsequently expired of cardiac arrest.

Diabetic patients with autonomic neuropathy may be predisposed to hypothermia by alteration of normal thermoregulatory mechanisms. Peripheral arterial vasomotion as measured with laser Doppler is impaired in diabetic patients with autonomic neuropathy (4), and these patients are at increased risk for intraoperative hypothermia (5). When exposed to external cooling, diabetic patients with autonomic neuropathy demonstrate impaired peripheral vasoconstriction and do not transiently increase their core temperature like nondiabetic patients (6). This case of recurrent and fatal hypothermia was due to the impairment of thermoregulatory mechanisms associated with diabetes and autonomic neuropathy. It is important to counsel diabetic patients, especially those who are elderly and have neuropathy, to guard against accidental cold exposure. Tests of autonomic function (e.g., heart rate variability testing) may identify diabetic patients at increased risk for hypothermia.