Arterial gas embolism Gas in the arterial system can be carried to the blood vessels of the brain and other vital organs. It typically causes transient embolism similar to thromboembolism but of shorter duration. Where damage occurs to the endothelium inflammation develops and symptoms resembling stroke may follow. The bubbles are generally distributed and of various sizes, and usually affect several areas, resulting in an unpredictable variety of neurological deficits. Venous gas can be admitted to the systemic circulation and become arteriolised by passing through pulmonary or intracardial shunts, bypassing the pulmonary filter. Unconsciousness or other major changes to the state of consciousness within about 10 minutes of surfacing or completion of a procedure are generally assumed to be gas embolism until proven otherwise. The belief that the gas bubbles themselves formed static emboli which remain in place until recompression has been superseded by the knowledge that the gas emboli are normally transient, and the damage is due to inflammation following endothelial damage and secondary injury from inflammatory mediator upregulation. Hyperbaric oxygen can cause downregulation of the inflammatory response and resolution of oedema by causing hyperoxic arterial vasoconstriction of the supply to capillary beds. High concentration normobaric oxygen is appropriate as first aid but is not considered definitive treatment even when the symptoms appear to resolve. Relapses are common after discontinuing oxygen without recompression.
Barotrauma
Blast injury
Polytrauma
Rheotrauma
Penetrating trauma
Microtrauma
Trauma
Blunt trauma