HBOT AND AIR OR GAS EMBOLISM

Arterial gas embolism is a major hazard of scuba diving (“diving air embolism”). Its
exact incidence is hard to determine and many victims are probably recorded as
drowning. As a diver begins to ascend, the volume of gas within the lung expands
(in accordance with Boyle’s Law). If the glottis is closed and a diver surfaces too
quickly, as in a panic situation, the only escape for the expanding air mass is through
the thin alveolar walls. Because alveolar rupture requires only a pressure gradient of
approximately 11 kPa air embolism can follow breath holding ascents after taking a
full breath at depth from as shallow as 111 kPa (a depth of approximately 1 metre) to
the surface. Patients with localized areas of obstruction (asthma or secretions)
are at risk to develop pulmonary over-distension even without breath holding. Air
embolism is not restricted to divers. It has been reported in a number of other
traumatic and surgical conditions including blast injuries or penetrating trauma such
as gun shot or stab wounds. Gas may also enter the arterial circulation by
shunting from the venous to the arterial systems. Because 30% of the population
have a probe patent foramen ovale, air sometimes can pass directly from the right to
left heart; therefore, arterial gas embolism can follow either decompression sickness
or medical procedures which permit gas entry into the venous circulation (iatrogenic
air embolism is nearly 200 times as common as diving air embolism, with at least
20,000 cases per year in the USA).
HBOT is approved and recommended for the treatment of air- or gas embolism
based on the same principles as for DCS.