Hyperthyroidism during pregnancy is a relatively rare event, but poor control of hyperthyroidism during pregnancy is associated with a host of issues. These include intrauterine fetal demise, hypertensive disorders of pregnancy, preterm delivery, low birth weight, intrauterine growth restriction, and maternal congestive heart failure. One of the most feared sequelae of hyperthyroidism is thyroid storm, which has a mortality rate >10%. Patients who develop thyroid storm present several challenges to anesthesiologists including hemodynamic instability and medication management. Here, we present the anesthetic management for a parturient whose delivery was complicated by signs and symptoms consistent with thyroid storm.

Cilostazol is an inhibitor of phosphodiesterase type III that possesses both antiplatelet and vasodilator effects. The present study aimed to determine the vasodilator effect of cilostazol in eNOS deficient (eNOS−/−) mice. Mouse aorta was contracted with sub‐maximal concentration of phenylephrine and concentration‐dependent relaxations to cilostazol (10−8–10−5 mol/L) were obtained in aortic rings, isolated from wild type and eNOS−/− mice. As previously reported, in aortas of wild type mice with intact endothelium, relaxations to cilostazol were significantly augmented as compared to aortas without endothelium. Surprisingly, genetic inactivation of eNOS significantly enhanced relaxations to cilostazol suggesting that chronic loss of nitric oxide may unmask compensatory vasodilator mechanisms significantly enhanced by the treatment with cilostazol. The augmentation of relaxations to cilostazol in aortas of eNOS−/− mice was endothelium independent and not inhibited by indomethacin, a cyclooxygenase inhibitor. Our findings support the view that patients suffering from vascular endothelial dysfunction induced by reduced availability of nitric oxide, may exhibit enhanced vasodilator reactivity to cilostazol.