Sir: Volume overload, left ventricle failure, lung injury after reperfusion, and pulmonary embolus can cause pulmonary hypertension (PHT) and pulmonary edema in patients undergoing orthotopic liver transplantation (OLT). These events are currently managed by mechanical ventilation, high fractional inspired oxygen (FIO 2 ), fraction, inotropic support, diuretics, and systemic vasodilators [1,2]. However, the lack of selectivity for pulmonary vessels often hinders the use of systemic vasodilators. On the contrary, the very short half life makes inhaled nitric oxide (iNO) a useful selective vasodilator to manage PHT and hypoxemia [3,4].We report the successful use of iNO in a 59-year-old postnecrotic cirrhotic male patient with severe PHT and hypoxemia after OLT. At the beginning of the surgical procedures, pulmonary gas exchange and cardiovascular parameters were in the normal range (Table 1), and they remained quite stable in the anhepatic and reperfusion stages in spite of severe surgical bleeding during liver isolation. Two hours after reperfusion (i) mean arterial pressure (MAP) suddenly decreased, (ii) heart rate, mean pulmonary arterial pressure (MPAP), and pulmonary artery occlusion pressure increased, and (iii) cardiac index (CI) decreased slightly (Table 1). We immediately started dobutamine infusion, with an improvement in MAP. Surgical procedures ended within 1 h and the patient was admitted to the intensive care unit (ICU). During surgery, 5 l of packed red cells, 8 l of fresh frozen plasma, and 7 l of crystalloids were infused with a fluid balance of + 6 l.One hour later at ICU admission, MAP was restored to normal values but MPAP remained higher than pre-OLT data (Table 1). Chest X-ray showed pulmonary edema and subtle pleural effusions. Arterial blood gas analysis indicated a serious reduction of gas exchange efficiency and severe mixed acidosis. The serum albumin concentration was 24 g l ±1 . We continued dobutamine infusion and mechanical ventilation with positive end expiratory pressure. We started furosemide infusion and also attempted nitroglycerine, which produced a sudden drop in MAP. Because of severe PHT and hypoxemia, permission was requested and granted to start iNO (15 ppm). One hour after iNO was started, MPAP and pulmonary vascular resistance decreased and the arterial oxygen tension/ FIO 2 ratio (PaO 2 /FIO 2 ) increased. Thereafter, normal values were achieved in 48 h (Table 1). Two days after ICU admission, fluid balance and albuminemia were ±2.0 l and 34 g l ±1 , respectively. Thirty hours after the start of iNO, it was reduced step by step and discontinued 16 h later. On the third postoperative day, we extubated the patient, who was discharged from the ICU 4 days later.In order to manage pulmonary edema and PHT, we used inotropes, mechanical ventilation, diuretics, and systemic vasodilators. Unfortunately, the latter procedure failed and, therefore, we chose iNO. Having an immediate positive effect on pulmonary gas exchange and PHT, iNO allowed us to set diuretic infusion and mecha...
