A Report On Air Embolism Essay

A Report On Air Embolism Essay

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Air embolism requires a portal of entry for gas to enter into a vessel and a favorable pressure gradient driving air into the vessel. Even a miniscule amount of air instillation (air bubbles as small as 30 to 60 µm diameter) can cause devastating consequences in the cerebral or coronary vasculature by disrupting distal blood flow and gas exchange. It is known to occur in the setting of SCUBA diving, peripartum and medical procedures that require cannulation of blood vessels or insufflation of air. It has been reported during non-surgical pulmonary procedures, such as transthoracic needle biopsies or tube thoracostomy. It is well acknowledged as a possible complication of argon plasma coagulation (APC) use, during both flexible and rigid bronchoscopy given the direct tissue injury that occurs with the beam but has rarely been described during bronchoscopic procedures. The entry of circulating air can be limited to the thorax and may manifest with cardiovascular collapse.

The pathogenesis of CAGE following a pulmonary procedure requires a portal of entry or a bronchial pulmonary venous connection of some form, whether pre-existing due to tumor or created as a consequence of the procedure. This could occur with needle traversing a bronchus into the pulmonary veins, or a connection created during APC use. Other circumstances such as coughing, or air entry during inspiration during the procedure may further facilitate air entry. Air that enters the pulmonary vasculature can be eliminated by diffusion into the alveoli, but it is conceivable that the amount of air may exceed the capacity for elimination through the pulmonary arteries and enter into the pulmonary veins without any creation of a bronchial venous connection. Of cou...


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Hyperbaric oxygen provides several mechanisms of therapeutic benefit. Increased atmospheric pressure during hyperbaric oxygen treatment compresses air bubbles and hastens the resorption of nitrogen. It also promotes restoration of distal blood flow, decreases endothelial damage, and mitigates reperfusion injury and cerebral edema. Although data is limited, retrospective studies showed decrease in mortality from 90% to 33% and has been demonstrated to be effective in decreasing or resolving neurologic sequelae even 40 hours after the inciting event as the air bubbles may persist. Therefore hyperbaric oxygen treatment should be pursued without delay in all cases where it is available. While no mortality benefit was noted in the cases reviewed in Table I, there does seem to be more favorable neurologic outcomes when hyperbaric oxygen is employed.

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