Cerebral decompression disorders differ from those of the spinal cord in that there is no experimental evidence suggesting autochthonous or venous stasis mechanisms. Accordingly, greater emphasis is placed on embolic and inflammatory mechanisms.
Cerebral DI has a very short latency. In the review by Francis, 75% of the 311 cerebral DI cases became symptomatic within 10 minutes (even with all cases of overt pulmonary barotrauma specifically excluded) 72. This leaves paradoxical gas embolization as an attractive alternative possibility.
Clinical Features Systemic Gas Embolism (SGE):
Gas embolism is by its nature a systemic disease although clinically it primarily affects the myocardium and the brain. While coronary embolism may account for some diving fatalities, it is not associated with long term morbidity. Cerebral events, on the other hand, are associated with both short term mortality and long term morbidity.
SGE gain access to the cerebral circulation via the carotid and vertebral arteries that converge at the base of the brain forming the circle of Willis. Depending on the volume of gas and region of the brain involved the clinical outcome of gas embolism ranges from instant death to spontaneous uneventful recovery. Relapses have been reported in up to 30% of patients with arterial gas embolism following submarine escape, irrespective of preceding or concurrent recompression 89-91. A subset of patients may also suffer subclinical damage only visualized by medical imaging 74.
Irrespective of the cause, the ultimate outcome of cerebral gas embolization appears to depend on the anatomical location, gas volume, delivery rate, pre-embolic gas saturation as well as co-morbid factors such as hypotension or dysfunction of vital centers.
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