Pulmonary reperfusion injury is a clinical syndrome with no single and recognized pathophysiologic mechanism. It is a major cause of morbidity and mortality following lung transplantation, cardiogenic shock, or cardiopulmonary bypass. The underlying mechanisms remain uncertain. Lung inflammatory injury induced by lipopolysaccharide, characterized by rapid sequestration of neutrophils in response to inflammatory chemokines and cytokines released in the lungs is an acceptable theory. Structural or functional impairment of surfactant has been noted in pulmonary reperfusion injury. The pathological changes may include bilateral pulmonary infiltrates, reduced lung compliance and worsening of gas exchange in the immediate posttransplant period. Recruitment maneuver and high positive end-expiratory pressure can relieve postoperative respiratory failure, especially in the patient with reperfusion pulmonary edema after pulmonary thromboendarterectomy. Pharmaceutical agents, including inhaled nitric oxide, soluble complement receptor type 1, prostaglandin E1 and exogenous surfactant, attenuate pulmonary reperfusion injury through distinct mechanisms. Extracorporeal membrane oxygenation and Novalung are temporary assistance in bridging to lung transplantation, stabilization of hemodynamics during transplantation and treatment of severe lung dysfunction and primary graft failure. Modulation of heme oxygenase-1 expression, ischemic conditioning and gene therapy are future directions for pulmonary reperfusion injury management.
Key words: cardiopulmonary bypass, pulmonary hypertension, respiratory insufficiency