INHALED PROSTAGLANDIN E-1 FOR TREATMENT OF ACUTE LUNG INJURY IN SEVERE MULTIPLE ORGAN FAILURE

Acute lung injury is characterized by hypoxemia due to pulmonary venti lation/perfusion-mismatching. IV administered prostaglandin E-1 (PGE(1 )), a vasodilator with a high pulmonary clearance, has been studied in acute lung injury. Inhalation of the vasodilators nitric oxide and pr ostacyclin improved oxygenation by selective dilation of the pulmonary vasculature in ventilated lung areas. Ln the present study, PGE(1) in halation was used for treatment of acute lung injury. Fifteen patients with acute lung injury defined as Pao(2)/fraction of inspired oxygen (FIO2) <160 mm Hg were treated with PGE(1) inhalation in addition to s tandard intensive care. The drug was continuously delivered via a pneu matic nebulizer. Acute physiology and chronic health evaluation system II and multiple organ failure scores were (mean +/- SEM) 33 +/- 2 and 10 +/- 0.3, respectively. Inhaled PGE(1) was administered for 103 +/- 17 h at a dose of 41 +/- 2 mu g/h. The Pao(2)/FIO2 ratio increased fr om 105 +/- 9 to 160 +/- 17 mm Hg (P < 0.05) and to 189 +/- 25 mm Hg (P < 0.05) after 4 h and 24 h, respectively. PGE(1) inhalation decreases in mean pulmonary artery pressure and central venous pressure were no t statistically significant. Mean arterial pressure, pulmonary capilla ry wedge pressure, cardiac output, and heart rate remained unchanged. Intensive care unit mortality was 40%. The present data suggest that i n haled PGE(1) is an effective therapeutic option for improving oxygen ation in patients with acute lung injury. Whether inhaled PGE(1) will increase survival in acute lung injury should be investigated in a con trolled prospective trial. Implications: Ln patients with severe acute lung injury and multiple organ failure, inhaled prostaglandin E-1 imp roved oxygenation and decreased venous admixture without affecting sys temic hemodynamic variables. Controlled clinical trials are warranted.