Risk factors for immersion pulmonary edema in recreational scuba divers: a case-control study.

BACKGROUND: Immersion can cause immersion pulmonary edema (IPE) in previously healthy subjects. We performed a case-control study to better identify IPE risk factors. METHODS: We prospectively included recreational scuba divers who had presented signs of IPE and control divers who were randomly chosen among diving members of the French Underwater Federation. We sent an anonymous questionnaire to each diver, with questions on individual characteristics, as well as the conditions of the most recent dive (controls) or the dive during which IPE occurred. Univariate logistic regressions were performed for each relevant factor. Then, multivariate logistic regression was performed. RESULTS: Of the 882 questionnaires sent, 480 (54%) were returned from 88 cases (90%) and 392 control divers (50%). Multivariate analysis identified the following independent risk factors associated with IPE: being aged over 50 years ((OR) 3.30, (95%CI) 1.76-6.19); female sex (OR 2.20, 95%CI 1.19-4.08); non-steroidal anti-inflammatory drug (NSAID) intake before diving (OR 24.32, 95%CI 2.86-206.91); depth of dive over 20 m (OR 2.00, 95%CI 1.07-3.74); physical exertion prior to or during the dive (OR 5.51, 95%CI 2.69-11.28); training dive type (OR 5.34, 95%CI 2.62-10.86); and daily medication intake (OR 2.79, 95%CI 1.50-5.21); this latter factor appeared to be associated with hypertension in the univariate analysis. CONCLUSION: To reduce the risk of experiencing IPE, divers over 50 years of age or with hypertension, especially women, should avoid extensive physical effort, psychological stress, deep dives and NSAID intake before diving.

Xenon Blocks Neuronal Injury Associated with Decompression.

Despite state-of-the-art hyperbaric oxygen (HBO) treatment, about 30% of patients suffering neurologic decompression sickness (DCS) exhibit incomplete recovery. Since the mechanisms of neurologic DCS involve ischemic processes which result in excitotoxicity, it is likely that HBO in combination with an anti-excitotoxic treatment would improve the outcome in patients being treated for DCS. Therefore, in the present study, we investigated the effect of the noble gas xenon in an ex vivo model of neurologic DCS. Xenon has been shown to provide neuroprotection in multiple models of acute ischemic insults. Fast decompression compared to slow decompression induced an increase in lactate dehydrogenase (LDH), a well-known marker of sub-lethal cell injury. Post-decompression administration of xenon blocked the increase in LDH release induced by fast decompression. These data suggest that xenon could be an efficient additional treatment to HBO for the treatment of neurologic DCS.

Cost-efficient method and device for the study of stationary tissular gas bubble formation in the mechanisms of decompression sickness.

BACKGROUND: Current in vivo methods cannot distinguish between the roles of vascular and stationary tissular gas bubbles in the mechanisms of decompression sickness (DCS). NEW METHOD: To answer this question, we designed a normobaric-hyperbaric chamber for studying specifically the contribution of stationary tissular gas bubbles in the mechanisms of DCS in individually-superfused tissue samples. For validating our method, we investigated in rat brain slices exposed to 0.4MPa air absolute pressure whether fast decompression rate - the most important cause of cerebral DCS - may induce an increase of lactate dehydrogenase (LDH), a marker of cell injury, compared to slow decompression rate. RESULTS: We provide a technical description of our pressure chamber and show that fast decompression rate of 0.3MPamin(-1) induced a rapid and sustained increase of LDH release compared to slow compression rate of 0.01MPamin(-1) (P<0.0001). COMPARISON WITH EXISTING METHODS: There is no current method for studying stationary tissular gas bubbles. CONCLUSIONS: This report describes the first method for studying specifically in tissue samples the role of stationary tissular gas bubbles in the mechanisms of DCS. Advantageously, according to this method (i) biological markers other than LDH could be easily studied; (ii) tissue samples could be taken not only from the brain but also from any part of the animal's body known of interest in DCS research, allowing performing tissue compartment research, a major question in the physics and theory of decompression research; and (iii) histological studies could be performed from the tissue samples.

Reversible myocardial dysfunction and clinical outcome in scuba divers with immersion pulmonary edema.

Immersion pulmonary edema in scuba divers is a rare disorder that tends to recur and can be potentially fatal, even in the absence of underlying cardiac disease. Anecdotal cases of reversible myocardial dysfunction have been described in this setting, but little is known of its pathogenesis. The purpose of the present study was to determine the clinical outcomes and the determinants associated with this condition. The data from 54 consecutive divers admitted for acute immersion pulmonary edema during a 5.5-year period were retrospectively studied. A diagnosis of myocardial dysfunction was established by the presence of elevated cardiac troponin T levels, coupled with electrocardiographic changes and/or wall motion abnormalities on the echocardiogram. The demographic, clinical, biologic, and diving characteristics were tested as potential predictors of this disorder. All the patients had complete resolution of symptoms within 72 hours, but 3 required intensive ventilation or hemodynamic support at admission. Reversible myocardial dysfunction was observed in 28% and was associated more with age >50 years (odds ratio [OR] 5.5, 95% confidence interval [CI] 1.5 to 21, p = 0.013), hypertension (OR 8.2, 95% CI 2.1 to 32, p = 0.002), diabetes (OR 22.1, 95% CI 1.1 to 458; p = 0.002), and release of natriuretic peptides (OR 9.1, 95% CI 2.4 to 35, p = 0.001). Follow-up investigations at 1 month were obtained for 49 patients and revealed a significant number of patients with occult hypertension. In conclusion, reversible myocardial dysfunction is not uncommon in divers with immersion pulmonary edema. The short-term overall prognosis is not adversely altered, but severe heart failure with a fatal outcome is unpredictable. Close monitoring of older divers with latent cardiovascular risk factors is warranted.