Atsumi N, Gomi S, Kanemoto S, Mihara W, Shigeta O, Terada Y, Jikuya T, Sakakibara Y, Mitsui T, Ninomiya H
Department of Surgery, University of Tsukuba, Japan.
Nihon Kyobu Geka Gakkai Zasshi. 1996 Dec;44(12):2123-9.
Among 176 pediatric patients who underwent open heart surgery from 1990 to 1996, 7 developed severe pulmonary hypertensive crisis (PHC) postoperatively. All patients were treated with conventional medical therapy consisting of hyperventilation and deep sedation. Prostaglandin E1 and/or amrinone were administered initially as a pulmonary vasodilator, and in 3 of the 7 patients this resulted in immediate improvement in hemodynamics. These patients subsequently weaned off ventilatory support and they were discharged from the hospital. In 4 other patients, pulmonary vasodilator therapy with prostaglandin E1 and amrinone had failed and they were treated with inhaled nitric oxide (NO). In all patients, inhalation of NO resulted in immediate decrease in pulmonary pressure without significant change in systemic arterial pressure. Two patients successfully weaned from the ventilator, whereas in 2 patients decrease in pulmonary pressure was transient. They developed airway bleeding and died as a result of respiratory insufficiency. Although inhaled NO effectively reduced pulmonary pressure in patients with PHC, this effect was not maintained over 12 hours in patients associated with bronchopulmonary dysplasia. In patients at risk for severe PHC, rapid treatment with NO inhalation after initial event as well as the prevention of lung injury caused by mechanical ventilation were found to be important in the postoperative management.