Pierre Louge

Preventive effect of pre-dive hydration on bubble formation in divers

Objective: To investigate whether prehydration 90 min before a dive could decrease bubble formation, and to evaluate the consequent adjustments in plasma volume (PV), water balance and plasma surface tension (ST). Methods: Eight military divers participated in a crossover trial of pre-dive hydration using saline–glucose beverage (protocol 1) and a control dive with no prehydration (protocol 2). Drink volume was 1300 ml (osmolality 324 mOsm/l) and drinking time was 50–60 min. The diving protocol consisted of an open sea field air dive at 30 msw depth for 30 min followed by a 9 min stop at 3 msw. Haemodynamic parameters, body weight measurements, urine volume and blood samples were taken before/after fluid intake and after the dive. Decompression bubbles were examined by a precordial pulsed Doppler. Results: Bubble activity was significantly lower for protocol 1 than for protocol 2. PV increased after fluid ingestion by 3.5% and returned toward baseline after diving for protocol 1, whereas it decreased by 2.2% after diving for protocol 2. Differences in post-dive PV between the two conditions were highly significant. Body weight loss before/after diving and post-dive urine volume after diving were significant in both protocols, but the relative decline in weight remained lower for protocol 1 than for protocol 2, with reduction of negative water balance due to higher fluid retention. There were no differences in ST after fluid intake and after diving for the two protocols. Conclusion: Pre-dive oral hydration decreases circulatory bubbles, thus offering a relatively easy means of reducing decompression sickness risk. The prehydration condition allowed attenuation of dehydration and prevention of hypovolaemia induced by the diving session. Hydration and diving did not change plasma surface tension in this study.

Relation between right-to-left shunts and spinal cord decompression sickness in divers.

The role of right-to-left shunting (RLS) in spinal cord decompression sickness (DCS) remains uncertain and could differ according to the distribution of lesion in spinal cord with a higher risk of upper spinal cord involvement in divers presenting a large patent foramen ovale. The aims of this study were to assess the prevalence of RLS with transcranial doppler ultrasonography in 49 divers referred for spinal cord DCS and compare it with the prevalence of RLS in 49 diving controls, and to determine a potential relation between RLS and lesion site of spinal cord. The proportion of large RLS was greater in DCS divers than in healthy control divers (odds ratio, 3.6 [95 % CI, 1.3 to 9.5]; p = 0.017). Shunting was not associated with the increased incidence of cervical spinal cord DCS (OR, 1.1 [95 % CI, 0.3 to 3.9]; p = 0.9) while a significant relationship between large RLS and spinal cord DCS with thoracolumbar involvement was demonstrated (OR, 6.9 [95 % CI, 2.3 to 20.4]; p < 0.001). From the above results, we conclude that the risk of spinal cord DCS in divers with hemodynamically relevant RLS is higher than in divers without RLS, particularly in their lower localization.

Brain MRI signal abnormalities and right-to-left shunting in asymptomatic military divers.

INTRODUCTION We conducted a controlled study to assess the prevalence of brain MRI hyperintense signals and their correlation with right-to-left shunting (RLS) in military divers. METHODS We prospectively enrolled 32 asymptomatic military divers under 41 yr of age and 32 non-diving healthy subjects matched with respect to age and vascular disease risk factors. We examined both groups with a 3-Tesla brain MRI; RLS was detected using transcranial pulsed Doppler in divers only. RESULTS Hyperintense spots were observed in 43.7% of the divers and 21.8% of the control subjects. In particular, divers with significant shunting exhibited a higher prevalence of hyperintensities compared to those with slight or no RLS (75% vs. 25%, respectively). Linear trend analysis also revealed a positive correlation between focal white matter changes, determined using a validated visual rating scale and the RLS grade. CONCLUSION Healthy military divers with a hemodynamically relevant RLS have an increased likelihood of cerebral hyperintense spots compared to age-matched normal subjects. The clinical relevance of these MRI signal abnormalities and their causal relationship with diving remain unclear.

Influence of repetitive open sea dives and physical exercises on right-to-left shunting in healthy divers

Objective: Paradoxical gas embolism through right-to-left (R/L) shunts is considered as a potential cause of certain types of decompression sickness. Aim: To assess whether 4 months of repetitive diving and strenuous exercises would lead to an increased prevalence of R/L shunting in a group of military divers. Methods: Using a standardised contrast-enhanced transcranial Doppler technique, 17 divers were re-examined for the presence of a R/L shunt 4 months after their initial examinations. R/L shunts were classified as type I if observed only after a straining manoeuvre, and type II if present at rest. Results: Initial prevalence of R/L shunt was 41%: six type I shunts and one type II. At the second examination, prevalence was 47%, with the appearance of one type I shunt that was not previously present. We found no significant increase in the prevalence and size of R/L shunts. Conclusion: It is speculated that diving-related phenomena, such as variations in right atrial pressures during the end stages of or events immediately after a dive could generate an R/L shunt. However, extreme conditions of repetitive diving and strenuous exercises do not cause permanent modification in R/L permeability over a period of 4 months.

Severe Capillary Leak Syndrome after Inner Ear Decompression Sickness in a Recreational Scuba Diver

BACKGROUND Post-decompression shock with plasma volume deficit is a very rare event that has been observed under extreme conditions of hypobaric and hyperbaric exposure in aviators and professional divers. CASE REPORT We report a case of severe hypovolemic shock due to extravasation of plasma in a recreational scuba diver presenting with inner ear decompression sickness. Impaired endothelial function can lead to capillary leak with hemoconcentration and hypotension in severe cases. This report suggests that decompression-induced circulating bubbles may have triggered the endothelial damage, activating the classic inflammatory pathway of increased vascular permeability. CONCLUSION This observation highlights the need for an accurate diagnosis of this potentially life-threatening condition at the initial presentation in the Emergency Department after a diving-related injury. An elevated hematocrit in a diver should raise the suspicion for the potential development of capillary leak syndrome requiring specific treatment using albumin infusion as primary fluid replacement.

Colonic Fermentation Promotes Decompression sickness in Rats.

Massive bubble formation after diving can lead to decompression sickness (DCS). During dives with hydrogen as a diluent for oxygen, decreasing the body’s H2 burden by inoculating hydrogen-metabolizing microbes into the gut reduces the risk of DCS. So we set out to investigate if colonic fermentation leading to endogenous hydrogen production promotes DCS in fasting rats. Four hours before an experimental dive, 93 fasting rats were force-fed, half of them with mannitol and the other half with water. Exhaled hydrogen was measured before and after force-feeding. Following the hyperbaric exposure, we looked for signs of DCS. A higher incidence of DCS was found in rats force-fed with mannitol than in those force-fed with water (80%, [95%CI 56, 94] versus 40%, [95%CI 19, 64], p < 0.01). In rats force-fed with mannitol, metronidazole pretreatment reduced the incidence of DCS (33%, [95%CI 15, 57], p = 0.005) at the same time as it inhibited colonic fermentation (14 ± 35 ppm versus 118 ± 90 ppm, p = 0.0001). Pre-diveingestion of mannitol increased the incidence of DCS in fasting rats when colonic fermentation peaked during the decompression phase. More generally, colonic fermentation in rats on a normal diet could promote DCS through endogenous hydrogen production.

Predictive factors of dysbaric osteonecrosis following musculoskeletal decompression sickness in recreational SCUBA divers.

Joint Bone Spine - In Press.Proof corrected by the author Available online since jeudi 8 octobre 2015

Specific diving training-induced arterial circulation changes

Objective: Several stressors such as cold water immersion, hyperoxic exposure and decompression-induced circulating bubbles can alter arterial circulation after a dive. The aim of this study was to investigate the arterial modifications induced by a specific diving training including repeated hyperbaric exposures and physical training. Method: Arterial pressure measurement and pulse wave velocity (PWV) recordings were performed in 12 student military divers before and after 15 weeks’ training. The results were compared with the same investigations performed in 12 non-diver healthy subjects. Results: A decrease in systolic blood pressure and pulse pressure was observed at both upper and lower limbs in student military divers after the training. Non-significant decreases in both carotido-femoral PWV and carotido-pedal PWV were found after the training. When the pulse time transit was divided by the cardiac cycle length between two R peaks ((RR) interval), a significant increase was observed between the carotid and femoral sensors. On the other hand, some differences were noticed between military divers and controls. Controls and divers were matched appropriately according to age and height, although the divers had a higher aerobic capacity as well as lower resting heart rate and lower pulse wave velocity. Conclusion: In trained military subjects, a training which includes repeated diving exposures and endurance exercises leads to vascular modifications suggesting an increase in central arterial compliance. There was no sign of arterial alteration induced by repeated diving exposures.

Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness.

AbstractImmersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal. IPE is thought to involve hemodynamic and cardiovascular disturbances, but its pathophysiology remains largely unclear, which makes IPE prevention difficult. This observational study aimed to document IPE pathogenesis and improve diagnostic reliability, including distinguishing in some conditions IPE from decompression sickness (DCS), another diving-related disorder.Thirty-one patients (19 IPE, 12 DCS) treated at the Hyperbaric Medicine Department (Ste-Anne hospital, Toulon, France; July 2013–June 2014) were recruited into the study. Ten healthy divers were recruited as controls. We tested: (i) copeptin, a surrogate marker for antidiuretic hormone and a stress marker; (ii) ischemia-modified albumin, an ischemia/hypoxia marker; (iii) brain-natriuretic peptide (BNP), a marker of heart failure, and (iv) ultrasensitive-cardiac troponin-I (cTnI), a marker of myocardial ischemia.We found that copeptin and cardiac biomarkers were higher in IPE versus DCS and controls: (i) copeptin: 68% of IPE patients had a high level versus 25% of DCS patients (P < 0.05) (mean ± standard-deviation: IPE: 53 ± 61 pmol/L; DCS: 15 ± 17; controls: 6 ± 3; IPE versus DCS or controls: P < 0.05); (ii) ischemia-modified albumin: 68% of IPE patients had a high level versus 16% of DCS patients (P < 0.05) (IPE: 123 ± 25 arbitrary-units; DCS: 84 ± 25; controls: 94 ± 7; IPE versus DCS or controls: P < 0.05); (iii) BNP: 53% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 383 ± 394 ng/L; DCS: 37 ± 28; controls: 19 ± 15; IPE versus DCS or controls: P < 0.01); (iv) cTnI: 63% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 0.66 ± 1.50 &mgr;g/L; DCS: 0.0061 ± 0.0040; controls: 0.0090 ± 0.01; IPE versus DCS or controls: P < 0.01). The combined “BNP-cTnI” levels provided most discrimination: all IPE patients, but none of the DCS patients, had elevated levels of either/both of these markers.We propose that antidiuretic hormone acts together with a myocardial ischemic process to promote IPE. Thus, monitoring of antidiuretic hormone and cardiac biomarkers can help to make a quick and reliable diagnosis of IPE.

GUT FERMENTATION SEEMS TO PROMOTE DECOMPRESSION SICKNESS IN HUMANS

Massive bubble formation after diving can lead to decompression sickness (DCS) that can result in neurological disorders. In experimental dives using hydrogen as the diluent gas, decreasing the bodys H2 burden by inoculating hydrogen-metabolizing microbes into the gut reduces the risk of DCS. In contrast, we have shown that gut bacterial fermentation in rats on a standard diet promotes DCS through endogenous hydrogen production. Therefore, we set out to test these experimental results in humans. Thirty-nine divers admitted into our hyperbaric center with neurological DCS (Affected Divers) were compared with 39 healthy divers (Unaffected Divers). Their last meal time and composition were recorded. Gut fermentation rate was estimated by measuring breath hydrogen 1-4 h after the dive. Breath hydrogen concentrations were significantly higher in Affected Divers (15 ppm [6-23] vs. 7 ppm [3-12]; P = 0.0078). With the use of a threshold value of 16.5 ppm, specificity was 87% [95% confidence interval (CI) 73-95] for association with neurological DCS onset. We observed a strong association between hydrogen values above this threshold and an accident occurrence (odds ratio = 5.3, 95% CI 1.8-15.7, P = 0.0025). However, high fermentation potential foodstuffs consumption was not different between Affected and Unaffected Divers. Gut fermentation rate at dive time seemed to be higher in Affected Divers. Hydrogen generated by fermentation diffuses throughout the body and could increase DCS risk. Prevention could be helped by excluding divers who are showing a high fermentation rate, by eliminating gas produced in gut, or even by modifying intestinal microbiota to reduce fermentation rate during a dive.