A 84-year-old man was brought to the emergency department of this hospital intubated after prolonged hypothermia (core temperature 26.0°C at admission). The patient was found unresponsive at his bedside. On examination he was noted to be neglected and malnourished. This condition was probably due to his poor living accommodation. He was unmarried, an obstinate smoker, and he also had abused alcohol for long time.

The patient had a score on the Glasgow Coma Scale of 5-T: eyes, 1 (no opening); verbal, T (could not be evaluated because of tracheal intubation); and motor, 4 (withdrawal from pain). His pulse was 48 beats/min and his blood pressure was 105/70 mm Hg. The initial ECG revealed atrial fibrillation and a giant Osborn wave (with its characteristic arrowhead shape) similar in amplitude to the R wave (fig 1). Laboratory tests showed a white cell count of 12000 per cubic millimetre and a platelet count of 115000 per cubic millimetre. The serum sodium concentration was 132 mmol/l, the serum potassium concentration was 3.1 mmol/l and serum creatinine was 2.1 mg/dl. Other serum electrolyte values, prothrombin time and the partial thromboplastin time were normal. There was no evidence of myocardial ischaemia on enzyme testing and his thyroid function was normal.

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Figure 1

ECG showing giant Osborn wave and atrial fibrillation.

Arterial blood gas measurements while the patient was breathing 100% oxygen revealed a partial pressure of oxygen of 205 mm Hg and a partial pressure of carbon dioxide of 28 mm Hg, bicarbonate 16 mEqL, with a pH of 7.15.

Chest x ray and cranial computed tomography (CT) scan at presentation showed no abnormalities. After active re-warming with warm blanket, warm humidified oxygen and warm intravenous fluids, the Osborn waves decreased in amplitude, and they disappeared after 20 h (fig 2).

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Figure 2

ECG after rewarming.

A subsequent cranial CT scan after 48 h revealed hypodensity in the left temporal lobe consistent with acute arterial ischaemic stroke in the distribution of the left middle cerebral artery. Unfortunately, the cerebral disease progressed and the patient died on the third day of admission.

Electrocardiographic changes in severe hypothermia, including the presence of the J wave, were first described by Osborn in 1953 and the amplitude of the J wave was inversely correlated with body temperature.1

However, Osborn waves are not pathognomonic of hypothermia as they are also seen in “normothermic” patients and differential diagnosis includes common electrocardiographic variant such as early repolarisation.2 The latter ECG pattern was classically considered benign, but recent findings suggest a relationship with sudden cardiac arrest.3

Osborn waves have been reported in cocaine use and haloperidol overdose,4 in severe hypercalcaemia,5 and in central nervous system injury.6 The accentuation of the Osborn waves, immediately before the episodes of ventricular fibrillation, was documented in a patient with a non-Q wave myocardial infarction due to severe coronary vasospasm,7 and the presence of Osborn waves was mentioned in left ventricular hypertrophy and after resuscitation of cardiac arrest.8

The J waves in the Brugada syndrome may be continuously present or intermittently in leads V1 and V2 and sometimes associated with complete or incomplete right bundle branch.9

The patient reported here developed Osborn waves due to hypothermia. The latter usually occurs after exposition to cold environments, but not in this case, because the outside temperature on the date of admission was 15°C. Old age,10 malnutrition, self neglect,11 alcohol consumption, poor quality accommodation, and social isolation12 could have been predisposing factors to hypothermia in our patient. Other risk factors include chronic debilitating conditions, dementia,13 sepsis,14 hypothyroidism, hypopituitarism, hypoadrenalism,15 acute intoxication16 drowning or immersion.17