Citation

Clarke D, Gerard W, Norris T. Aviat. Space Environ. Med. 2002; 73(2): 139-146.

Affiliation

Department of Hyperbaric Medicine, Palmetto Richland Memorial Hospital, University of South Carolina, Columbia 29203, USA. dick.clarke@palmettohealth.org

Copyright

(Copyright © 2002, Aerospace Medical Association)

DOI

unavailable

PMID

11846183

Abstract

Pulmonary barotrauma-induced cerebral arterial gas embolism (CAGE) continues to complicate compressed gas diving activities. Inadequate lung ventilation secondary to inadvertent breath holding or rapid buoyant ascent can quickly generate a critical state of lung over-pressure. Pulmonary over-pressurization may also occur as a consequence of acute and chronic pulmonary pathologies. Resulting barotrauma frequently causes structural failure within the terminal distal airway. Respiratory gases are then free to embolize the systemic circulation via the pulmonary vasculature and the left heart. The brain is a common target organ. Bubbles that enter the cerebral arteries coalesce to form columns of gas as the vascular network narrows. Small amounts of gas frequently pass directly through the cerebral circulation without occlusion. Larger columns of gas occlude regional brain blood flow, either transiently or permanently, producing a stroke-like clinical picture. In cases of spontaneous redistribution, a period of apparent recovery is frequently followed by relapse. The etiology of relapse appears to be multifactoral, and chiefly the consequence of a failure of reperfusion. Prediction of who will relapse is not possible, and any such relapse is of ominous prognostic significance. It is advisable, therefore, that CAGE patients who undergo spontaneous recovery be promptly recompressed while breathing oxygen. Therapeutic compression will serve to antagonize leukocyte-mediated ischemia-reperfusion injury; limit potential re-embolization of brain blood flow, secondary to further leakage from the original pulmonary lesion or recirculation of gas from the initial occlusive event; protect against embolic injury to other organs; aid in the resolution of component cerebral edema; reduce the likelihood of late brain infarction reported in patients who have undergone spontaneous clinical recovery; and prophylax against decompression sickness in high gas loading dives that precede accelerated ascents and omitted stage decompression.

Language: en