Clazosentan, a potent selective endothelin receptor subtype A antagonist, has been demonstrated to be effective in preventing cerebral vasospasms after subarachnoid hemorrhage. We report the successful management of respiratory failure due to pulmonary edema associated with clazosentan, with a hemodynamic monitoring system. A 49-year-old Japanese man underwent emergency clipping for a right internal carotid-posterior communicating artery aneurysm. The surgery and general anesthesia for the rupture proceeded with no complications. Clazosentan was administered from postoperative day 1 to prevent cerebral vasospasm. He presented with respiratory failure six days post surgery and chest X-ray imaging showed pulmonary edema. In our intensive care unit, the patient's N-terminal pro-brain natriuretic peptide was 476 pg/mL although trans-thoracic echography indicated a normal left ventricular ejection fraction (>60%) and normal diastolic function. The hemodynamic monitoring system showed 11 L/minute cardiac output and a cardiac index of 5.6 L/minute/m2. We thus diagnosed the cause of the patient's respiratory failure as due to excessive volume, as an adverse event of clazosentan. We changed the cerebral vasospasm-preventive drug to fasudil hydrochloride hydrate and forced urination. His body weight dropped approximately 9 kg as of day 9 in the ICU and he was weaned off the ventilator 23 days post surgery. This case indicates the importance of optimal infusion in patients with clazosentan. Optimal fluid management using a hemodynamic monitoring system could be useful for clazosentan-induced respiratory failure.
Keywords: clazosentan; hemodynamic system; hypernatremia; pulmonary edema; respiratory failure.
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