Vasopressin has gained wide support as an adjunct vasopressor in patients with
septic shock. This agent exerts its vasoconstriction effects through smooth muscle
V1 receptors and also has antidiuretic activity via renal
V2 receptors. This interaction with the renal
V2 receptors results in the integration of
aquaporin 2 channels in the apical membrane of the renal collecting duct leading to free water reabsorption. Thus,
water intoxication with subsequent
hyponatremia, although rare, is a potentially serious side effect of exogenous
vasopressin administration. We present 2 patients who developed
hyponatremia within hours of initiation of
vasopressin infusion. Extensive diuresis followed its discontinuation with subsequent normalization of serum
sodium. One of the patients required the use of hypertonic saline for more rapid normalization of serum
sodium due to concerns for potential seizure activity. A review of the literature relevant to the incidence of
vasopressin-induced
hyponatremia is provided as well as discussion on additional factors relevant to
septic shock that should be considered when determining the relative risk of
hyponatremia in patients receiving
vasopressin.