In patients with sudden transient loss of consciousness, accident and emergency departments begin by looking for a cardiac or a neurological explanation. Occasionally the cause proves to be one of the rare conditions that produce severe hypotension through vasodilatation.
CASE HISTORYAn Asian man aged 50 was found by his work colleagues unconscious with laboured breathing, but recovered spontaneously. In the preceding two weeks he had experienced two episodes of sweating and weakness, each lasting a few minutes, without loss of consciousness. He had type 2 diabetes treated with diet alone and was taking amlodipine 5 mg daily for hypertension. There was a family history of type 2 diabetes. He consumed half a bottle of whisky a day and was an ex-smoker.On examination he was fully conscious and normotensive, with a tachycardia. He had bilateral parotid enlargement, greater on the right than the left, and wasting of proximal limb muscles without demonstrable weakness; these signs were attributed to alcohol. Arcus senilis was present. On the electrocardiogram there was sinus tachycardia with ST depression in the lateral leads. The haemoglobin was 15.9 g/dL, white blood count 20.9610 9 /L with neutrophilia, and platelet count 225610 9 /L. He was mildly hypokalaemic (3.2 mmol/L); random glucose was 20.7 mmol/L. Tests that gave normal results included serial cardiac enzymes, creatinine, liver function tests, bone pro®le, thyroid function tests, lipid pro®le, erythrocyte sedimentation, exercise electrocardiography, 24-hour Holter monitoring, echocardiography and coronary angiography.After coronary angiography, however, he complained of palpitations and of feeling hot and sweaty. He was observed to have bloodshot eyes, sinus tachycardia (rate 140/min) and hypotension (systolic blood pressure 60 mmHg). Symptoms and signs resolved within 30 minutes. On continuous electrocardiographic monitoring for several days no arrhythmias were seen. A further episode of hypotension and sinus tachycardia occurred in the presence of medical staff, during which initially there was no palpable cardiac output and he had a grand mal seizure. Central venous access was achieved, but recovery was spontaneous. During a third episode, central venous pressure, measured via the right internal jugular line, proved to be low during the period of hypotension and sinus tachycardia, pointing to a primary vasodilatory mechanism.A full septic screen was negative. The initial neutrophilia had resolved. Amlodipine was discontinued. Autonomic function tests were normal. Although mild hypokalaemia was recorded during two attacks he was normokalaemic at other times. Screening tests for rare conditions associated with the episodic release of vasodilatory mediators were performed. Urinary 5-hydroxyindoleacetic acid concentrations, urinary catecholamine concentrations, and serum calcitonin concentrations and gut neuropeptide concentrations (vasoactive intestinal peptide, pancreatic polypeptide, gastrin, glucagon, neurotensin, somatostatin) were normal, excluding re...
