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HBOT For Air/ Gas Embolism


Air or Gas Embolism is caused when gas bubbles enter the arteries, veins and/or capillaries. It can take place as simple as small amounts of air getting into the blood circulation accidentally during surgery or other medical procedures (for example a bubble entering an intravenous fluid) and can be a consequence associated with diving. When a diver's airway is shut on ascent the expanding air in the lungs can provoke a rupture of the alveoli, thereby causing air to move into the arteries. Air bubbles (emboli) block arterial blood flow. Air emboli may lodge distally in the smaller arteries and arterioles of brain and obstruct the flow of blood resulting in ischemia, hypoxia and cerebral edema. Secondary effects of air embolism include platelets clumping all over (as they are considered foreign body) and damage to blood vessel walls. Obstructed vessels leak fluid into surrounding tissues. The resulting swelling further reduces tissue blood flow.

Benefits of HBOT :

HBO is the first line of treatment in these conditions. Under hyperbaric conditions, oxygen diffuses into the bubbles, displacing the nitrogen from the bubble and into solution in the blood. In organs with relatively poor collateral circulation, air embolism may induce ischemia or infarction, while surgery and trauma are the main causes of cerebral arterial air embolism. Air emboli can directly affect brain circulation, and patients are often accompanied by circulatory failure and secondary reduction of cardiac output; thus, such patients will develop focal neurological deficits, hemiplegia, and changes in mental state. Air embolism can also stimulate endothelial cells to release inflammatory factors, thereby causing secondary vasospasm and capillary exudation. When arterial air embolism occurs, it is recommended that the patient is placed in the supine position, because the Trendelenburg position may aggravate cerebral edema. It is recommended that the patient should receive high-flow oxygen until hyperbaric oxygen is available, to promote the reabsorption of nitrogen from the air emboli into the blood and reduce the volume of air emboli. Thereby improving the ischemia of the diseased organs and reducing the fatality rate. It would be best for the patient to receive hyperbaric oxygen therapy within 4–6 h after the occurrence of air embolism. Even if the patient misses the best time of treatment, hyperbaric oxygen therapy within 30 h after the occurrence of embolism would also be of benefit to a certain extent HBO induced vasoconstriction inhibits air embolism redistribution and decreases cerebral edema. It also reduces blood sludging (blood in which the red blood cells become massed along the walls of the blood vessels and reduce the lumen of the vessels and the rate of blood flow) and improves WBC function.

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