Decompression Illness in Repetitive Breath-Hold Diving: Why Ischemic Lesions Involve the Brain?

Abstract

Nitrogen (N2) accumulation in the blood and tissues can occur due to breath-hold (BH) diving. Post-dive venous gas emboli have been documented in commercial BH divers (Ama) after repetitive dives with short surface intervals. Hence, BH diving can theoretically cause decompression illness (DCI). “Taravana,” the diving syndrome described in Polynesian pearl divers by Cross in the 1960s, is likely DCI. It manifests mainly with cerebral involvements, especially stroke-like brain attacks with the spinal cord spared. Neuroradiological studies on Ama divers showed symptomatic and asymptomatic ischemic lesions in the cerebral cortex, subcortex, basal ganglia, brainstem, and cerebellum. These lesions localized in the external watershed areas and deep perforating arteries are compatible with cerebral arterial gas embolism. The underlying mechanisms remain to be elucidated. We consider that the most plausible mechanisms are arterialized venous gas bubbles passing through the lungs, bubbles mixed with thrombi occlude cerebral arteries and then expand from N2 influx from the occluded arteries and the brain. The first aid normobaric oxygen appears beneficial. DCI prevention strategy includes avoiding long-lasting repetitive dives for more than several hours, prolonging the surface intervals. This article provides an overview of clinical manifestations of DCI following repetitive BH dives and discusses possible mechanisms based on clinical and neuroimaging studies.

Breath-Hold Diving Injuries — A Primer for Medical Providers

“…The symptoms of decompression illness (DCI) present between 0 and 120 min and usually start mild and may be transient and improve or may persist and worsen over time (66,69). Common symptoms include headache, dizziness/ vertigo, nausea, numbness, weakness, visual disturbances, seizure (61), loss of consciousness, hearing loss, euphoria, trouble concentrating, and/or sudden death (70).…”

“…Long deep dives over 100 m (65) also allow for potential gas buildup and diffusion. It is postulated that intrapulmonary arteriovenous anastomoses allow for right-to-left shunting of venous gas emboli that develop at depth (66), and that hypoxia, hypercapnia, and exercise during a dive all contribute to the opening of these shunts (67) which then allow gas bubbles to enter the arterial bloodstream. These circulating bubbles have been implicated in the cause of endothelial damage to the blood-brain-barrier and resultant reversible encephalopathy (68).…”

“…MRI may show areas of hyperintensity in large vessels as well as watershed areas (59). Areas of infarct have been found to involve the cerebral cortex, subcortex, basal ganglia, brainstem, and cerebellum (66). Areas of partial hemorrhage may be seen as well (61).…”

Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia

“…Commercial divers who engage in breath-hold diving (referred to as "Ama" in Japan) are subjected to frequent and prolonged episodes of hypercapnic hypoxia [194]. This circumstance, in turn, may decrease the likelihood of ischemic stroke and enhance the resilience of the brain to ischemic-reperfusion injury.…”

Breath-Hold Diving-Related Decompression Sickness with Brain Involvement: From Neuroimaging to Pathophysiology

“…Currently, DCS with neurological symptoms is estimated to occur in 2.7 out of 10,000 divers [ 3 ]. Although previous studies have been published attempting to correlate neuroradiological findings with the pathophysiology of neurological DCS, especially in breath-hold diving, this remains unclear at present [ 4 , 5 , 6 , 7 ].…”