POSTTRAUMATIC PULMONARY INSUFFICIENCY

Abstract

Pulmonary insufficiency is occasionally a life-threatening sequel to severe nonthoracic trauma. A similar disturbance of pulmonary function may be a feature of hepatic cirrhosis, fulminant hepatic failure, liver homotransplantation and major hepatic resection for blunt injury. If failure of some aspect of liver function is responsible for the development of pulmonary insufficiency, it is likely that it is the hepatic RES cells rather than the parenchymal cells which are concerned, because hepatic parenchymal cell failure is not a feature of post-traumatic pulmonary insufficiency. Experimental evidence indicates that hypovolemia increases the load of circulating phagocytosable material and depresses activity of the hepatic RES, while trapping of the pulmonary RES is considerably enhanced. This noxious material, normally dealt with by the hepatic RES, may accumulate during and after hypovolemia in active form in the lungs as a result of the action of 3 mechanisms: direct pulmonary RES phagocytosis from the blood, transfer in hepatic RES cells from liver to lungs and uptake from the blood by polymorphonuclear leukocytes which become sequestered in the lungs. The ensuing pulmonary injury casued by this material may then be manifested by progressive pulmonary insufficiency and the impairment of activity of the hepatic RES by the presence of gram-negative infection.