C T Leffler1. 1. Occupational Health Program, Harvard School of Public Health, Boston, MA, USA. cleffler@pol.net
Abstract
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.
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.