CEREBRAL AIR EMBOLISM, both arterial and venous, acquires considerable significance because of the increase in either diagnostic or reparative cardiovascular procedures that require atmospheric exposure of the intravascular surfaces. Forty of 340 patients after open-heart surgery had signs of arterial embolism, and 34 of these had either psychologic or neurologic deficits attributable to brain air embolism. 1 In a separate study, the incidence of air embolism to the brain following open-heart surgery was estimated at 6 percent.2 Recent, comprehensive reviews of the English medical literature report the rate of complications of percutaneous subclavian catheterization ranging from 0.4 to 9.9 percent.
8Several reports of air embolism as an important complication of venous catheterizations have been published. 4 Venous air embolism to the brain, during posterior fossa craniotomy, occurs at a rate that ranges from 2.6 to 40 percent. 8 Air embolism is also a significant contributor to the number of deaths or illnesses resulting from rapid decompression. Seizures, focal neurologic deficits, unconsciousness and other symptoms in healthy divers have been attributed to air embolism into either the carotid-vertebral or coronary arteries. 8 -7 These deaths and symptoms could be the consequence of either cardiac or cerebral ischemia which, presumably, is induced by the transient mechanical occlusion of blood vessels by the air bubbles.
7The present study was undertaken to a) define some of the ultrastructural brain changes induced by carotid air embolism, and b) compare in the same species, the changes secondary to air embolism with those resulting from ischemia induced by carotid-artery ligation.