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

Kiyotaka Kohshi,Petar J Denoble,Hideki Tamaki,Frédéric Lemaître,Yoshitaka Morimatsu,Tatsuya Ishitake

doi:10.3389/fphys.2021.711850

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.

Highlights

Underwater breath-hold (BH) diving is practiced casually by millions of beachgoers and snorkelers
The BH diving neurological deficit, both acute stroke-like manifestations and asymptomatic lesions, in our opinion, are decompression disorders initiated by gas embolism
Underlying injuries occur in the external watershed areas and the territories of perforating arteries of the brain, an area vulnerable to arterialized venous gas bubbles, which in the conditions of repetitive BH diving can grow inducing processes that lead to decompression illness (DCI)

Summary

Introduction

Underwater breath-hold (BH) diving is practiced casually by millions of beachgoers and snorkelers. The causes and DCI in Breath-Hold Divers mechanisms of neurological post-dive conditions are not clear yet, and the term BH diving neurologic deficit (BHDND) was suggested in a symposium (Table 1; Wong, 2006). The strokelike manifestations and time relation to BH diving in acute cases are suggestive of DCS, cerebral arterial gas embolism (CAGE), and hypoxic brain injury as the most likely causes. Imaging of brains in BHDND reveals lesions similar to stroke and micro-stroke caused by embolism of various origins. While this does not exclude hypoxic injury due to hypoxemia or hemodynamic hypoperfusion, it shifts the focus of discussion toward various forms of decompression illness (DCI), including paradoxical venous gas emboli (VGE), CAGE, and intraarterial growth of bubbles from nanobubble buds on hydrophobic vascular surfaces

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