Suspected Arterial Gas Embolism After Glossopharyngeal Insufflation in a Breath-Hold Diver

Context:It has been widely believed that tissue nitrogen uptake from the lungs during breath-hold diving would be insufficient to cause decompression stress in humans. With competitive free diving, however, diving depths have been ever increasing over the past decades.Methods:A case is presented of a competitive free-diving athlete who suffered stroke-like symptoms after surfacing from his last dive of a series of 3 deep breath-hold dives. A literature and Web search was performed to screen for similar cases of subjects with serious neurological symptoms after deep breath-hold dives.Case Details:A previously healthy 31-y-old athlete experienced right-sided motor weakness and difficulty speaking immediately after surfacing from a breathhold dive to a depth of 100 m. He had performed 2 preceding breath-hold dives to that depth with surface intervals of only 15 min. The presentation of symptoms and neuroimaging findings supported a clinical diagnosis of stroke. Three more cases of neurological insults were retrieved by literature and Web search; in all cases the athletes presented with stroke-like symptoms after single breath-hold dives of depths exceeding 100 m. Two of these cases only had a short delay to recompression treatment and completely recovered from the insult.Conclusions:This report highlights the possibility of neurological insult, eg, stroke, due to cerebral arterial gas embolism as a consequence of decompression stress after deep breath-hold dives. Thus, stroke as a clinical presentation of cerebral arterial gas embolism should be considered another risk of extreme breath-hold diving.

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Presumed Arterial Gas Embolism After Breath-Hold Diving in Shallow Water

PEDIATRICS ◽

10.1542/peds.2014-4095 ◽

2015 ◽

Vol 136 (3) ◽

pp. e687-e690 ◽

Cited By ~ 2

Author(s):

S. Harmsen ◽

D. Schramm ◽

M. Karenfort ◽

A. Christaras ◽

M. Euler ◽

...

Keyword(s):

Shallow Water ◽

Breath Hold ◽

Gas Embolism ◽

Arterial Gas Embolism

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Hyperbaric treatment of air or gas embolism: current recommendations

Undersea and Hyperbaric Medicine ◽

10.22462/10.12.2019.13 ◽

2019 ◽

pp. 673-683

Author(s):

Richard E. Moon ◽

Keyword(s):

Animal Studies ◽

Decompression Sickness ◽

Bubble Formation ◽

Endothelial Damage ◽

Neurological Deficits ◽

Breath Hold ◽

Gas Embolism ◽

Hyperbaric Treatment ◽

Pulmonary Capillaries ◽

Venous Gas Embolism

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac “vapor lock” and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence-based review of adjunctive therapies is presented.

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