Na. Moussa et al., ACUTE HYPONATREMIC ENCEPHALOPATHY AFTER A CEREBROVASCULAR ACCIDENT, The American journal of the medical sciences, 316(1), 1998, pp. 56-59
A 66-year-old hypertensive male with acute intracerebral hemorrhage de
veloped acute hyponatremic coma 3 days after the addition of enalapril
and a combination of amiloride and a thiazide diuretic td his hypoten
sive regimen. The patient recovered consciousness and serum sodium nor
malized 2 days after fluid restriction and withdrawal of both medicati
ons. Three weeks later, upon inadvertent reinstitution of enalapril an
d indapamide, severe hyponatremic encephalopathy promptly recurred; re
covery was again rapid following fluid restriction and withdrawal of b
oth medications. This temporal relationship establishes the thiazide d
iuretic or the angiotensin converting enzyme inhibitor or both as the
cause of the profound symptomatic hyponatremia in this patient. Result
s of simultaneous serum and urine osmolality assays on several occasio
ns were consistent with a decrease in free water clearance, a result o
f either increased antidiuretic hormone (ADH) secretion or potentiatio
n of its peripheral action, and thiazide-induced natriuresis. The use
of a thiazide diuretic in the presence of either of these aberrations
of ADH homeostasis most likely explains the profound and rapid develop
ment of hyponatremia. Drug-induced disturbances in serum osmolality ar
e a potentially reversible cause of deterioration of the mental state
in a patient with an acute cerebrovascular accident.