PubMed · 10206942
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R W Hamilton. 1999. Evoked potentials and decompression.. https://pubmed.ncbi.nlm.nih.gov/10206942/
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Decompression sickness occurs when a sufficiently large gas phase forms within the tissues of the body after a reduction in ambient pressure. Arterial gas embolism occurs secondary to pulmonary barotrauma when gas is forced into the pulmonary vasculature. Although they may clinically present in a similar fashion, the underlying pathophysiology of the two conditions is quite different.
Decompression sickness (the "bends") is a well-known risk of scuba diving. The pathophysiology and treatment is well documented. In the urologic data, no reference to the development of a neurogenic bladder as a result of an episode of the bends was found. We present the evaluation and management of a previously asymptomatic man who developed detrusor hyperreflexia after an episode of decompression sickness. Urologists in coastal communities should be aware of the potential risk of the development of neurogenic bladder.
BACKGROUND: Several studies have noted an apparent increase in decompression sickness (DCS) risk with surface decompression diving in warm water or with hot water suits (Van Der Aue 1951, Shields 1986, Leffler 1997), but did not perform statistical tests to control for the pressure-time profile. METHODS: The 1986 data, including 73 DCS cases out of 14,891 dives, were analyzed by Mantel-Haenszel analysis to control for depth and bottom time. Dive profiles from the 1951 U.S. Navy report, including 147 DCS cases from 1507 dives, were analyzed with logistic regression analysis to control for depth, bottom time, and aspects of the decompression profile. RESULTS: In the 1986 data, hot water suits, as compared with passive thermal protection, were associated with an odds ratio (OR) of 1.81 (95% confidence interval, CI = 0.96 to 3.42) for DCS. In the 1951 data, each 10 degree C increase in water temperature yielded an OR for DCS of 1.96 (95% CI = 1.33 to 2.90). The interaction of temperature and bottom time suggested that the effect was more pronounced in shorter dives. Among DCS cases, the OR for type 2 symptoms with hot water suits was not significant in the 1986 data (p = 0.18). In the 1951 data, the probability of type 2 symptoms among DCS cases was better explained by the dive profile than by the temperature. Thermal effects on gas physics, metabolism, hemostasis, and nociception were reviewed. CONCLUSION: Surface decompression divers who are warm at depth face an increased risk of DCS. Vasodilatation in warm divers may result in more rapid on-gassing of tissues with short time constants. A full evaluation of DCS risk should consider physiological and physical effects of ambient temperature.