We performed a trial to assess the safety and tolerability of sequential bronchopulmonary segmental lavage with a dilute synthetic surfactant (Surfaxin) in 12 adults with ARDS. Patients received one of three dosing regimens in which aliquots of Surfaxin were administered via a wedged bronchoscope to each of the 19 bronchopulmonary segments. Suctioning was performed 10-30 s after instillation of individual aliquots. Group 1 patients (n ϭ 3) received one 30-ml aliquot of a 2.5-mg/ml concentration of Surfaxin in each segment, followed by a second 30-ml aliquot with a 10-mg/ml concentration. Group 2 patients (n ϭ 4) received two 30-ml aliquots of the 2.5-mg/ml concentration followed by a third lavage with the 10-mg/ml concentration. Group 3 patients (n ϭ 5) received therapy identical to that received by patients in Group 2 and were eligible for repeat dosing 6 to 24 h later. All patients tolerated the procedure. There were no serious adverse experiences ascribed to either the procedure or the surfactant. The acute respiratory distress syndrome (ARDS) is a lifethreatening disorder characterized by noncardiogenic pulmonary edema and refractory hypoxemia, with a case fatality rate as high as 40-60% (1-7). The pathophysiology of ARDS involves injury to the alveolar-capillary barrier, lung inflammation, atelectasis, surfactant dysfunction, and intrapulmonary shunting. The disorder typically appears within 12 to 24 h of an identifiable clinical event and may be due to direct lung injury, such as with gastric content aspiration, pneumonia, neardrowning, toxic gas inhalation, or chest/lung trauma. In addition, ARDS may be associated with systemic processes such as sepsis, nonthoracic trauma, acute pancreatitis, major surgery, multiple blood transfusions, fat embolism, or shock. No specific therapy for ARDS currently exists. To date, the numerous treatment strategies for the disorder that have been studied have not reduced associated morbidity or mortality.Pulmonary surfactant lines the alveolar epithelium of mature animal lungs. It is a lipoprotein complex that reduces surface tension to assist alveoli expansion, allowing gas exchange. The endogenous surfactant system of patients with ARDS may be compromised in several ways (7,8): the inciting disorder may directly damage type II pneumocytes and decrease the synthesis, secretion, and composition of surfactant or produce abnormal surfactant aggregate forms; plasma proteins in the pulmonary edema fluid may inhibit surfactant properties; and the products of inflammation, such as proteases and reactive oxygen species, may interfere with surfactant function, as well as processing of the substance in the alveolus (7,8).The major pulmonary consequences of ARDS are decreased compliance, decreased oxygenation, loss of lung vol-
