Jean-Eric Blatteau

Haemodynamic changes induced by submaximal exercise before a dive and its consequences on bubble formation

Objectives: To evaluate the effects of a submaximal exercise performed 2 h before a simulated dive on bubble formation and to observe the haemodynamic changes and their influence on bubble formation. Participants and methods: 16 trained divers were compressed in a hyperbaric chamber to 400 kPa for 30 min and decompressed at a rate of 100 kPa/min with a 9 min stop at 130 kPa (French Navy MN90 procedure). Each diver performed two dives 3 days apart, one without exercise and one with exercise before the dive. All participants performed a 40 min constant-load submaximal and calibrated exercise, which consisted of outdoor running 2 h before the dive. Circulating bubbles were detected with a precordial Doppler at 30, 60 and 90 min after surfacing. Haemodynamic changes were evaluated with Doppler echocardiography. Results: A single bout of strenuous exercise 2 h before a simulated dive significantly reduced circulating bubbles. Post-exercise hypotension (PEH) was observed after exercise with reductions in diastolic and mean blood pressure (DBP and MBP), but total peripheral resistance was unchanged. Stroke volume was reduced, whereas cardiac output was unchanged. Simulated diving caused a similar reduction in cardiac output independent of pre-dive exercise, suggesting that pre-dive exercise only changed DBP and MBP caused by reduced stroke volume. Conclusion: A single bout of strenuous exercise 2 h before a dive significantly reduced the number of bubbles in the right heart of divers and protected them from decompression sickness. Declining stroke volume and moderate dehydration induced by a pre-dive exercise might influence inert gas load and bubble formation.

Blood platelet count and severity of decompression sickness in rats after a provocative dive.

INTRODUCTION Previous animal studies reported that platelet count (PC) is decreased following decompression. Adherence and aggregation of platelets to the bubble surface has been demonstrated in severe decompression sickness (DCS). The present study was designed to clarify the relationship between post-dive platelet levels and the severity of DCS in a rat model. METHODS A total of 57 male Sprague-Dawley rats were assigned to either one experimental group with a hyperbaric exposure (N = 22) or one control group (N = 27). Rats were compressed to 1000 kPa (90 msw) for 45 min while breathing air and decompressed to surface in 38 min with stops at 200, 160, and 130 kPa. Onset of neurological DCS and death time were recorded during a 120-min observation period after surfacing. In the control group, rats were maintained at atmospheric pressure in the same chamber for an equivalent period of time. Blood samples for PC were taken 30 min before and immediately after exposure in two groups. RESULTS Blood PC after hyperbaric exposure had significantly decreased, whereas PC had increased in the control group. We found a correlation between % fall in PC and latency to death time. The platelet loss tended to decrease when fatal DCS was delayed. Rats suffering from severe DCS with a short latency to death presented a pronounced decline in platelets. DISCUSSION The present study highlighted a relationship between the post-dive decrease in PC and DCS severity in rats. Platelet consumption could offer a new index for evaluating decompression stress.

MRI FINDINGS AND CLINICAL OUTCOME IN 45 DIVERS WITH SPINAL CORD DECOMPRESSION SICKNESS

BACKGROUND Decompression sickness (DCS) affecting the spinal cord is the most dangerous form of diving-related injury with potential sequelae. This study was conducted to evaluate the relationship between spinal cord lesions on MRI and clinical findings in divers with spinal DCS. METHODS We studied 45 cases of DCS that were referred to our hyperbaric facility with clinical evidence of spinal involvement during the period 2002-2007. The study included only patients who underwent MRI within 10 d of injury. The severity of spinal DCS for each patient was rated numerically for both the acute event and 1 mo later. The presence or absence of back pain was also noted. RESULTS Spinal cord lesions were significantly more frequent in divers with severe DCS, and did not occur in any diver who experienced a favorable outcome (sensitivity = 67%, specificity = 100%, negative predictive value = 77%, positive predictive value = 100%). The presence of vertebral degenerative changes that impinged on the spinal cord was strongly associated with MRI abnormalities, but not with a negative outcome. Acute back pain was associated with hyperintense lesions and persistence of neurological sequelae [OR = 14 (95% CI, 3.1 to 63.5)]. CONCLUSION The results show that MRI could be helpful in predicting clinical outcome in divers with spinal cord DCS. The presence of medullary compressive factors and vertebral back pain after surfacing indicate increased likelihood of severe myelopathy with incomplete recovery.

Risk factors and treatment outcome in scuba divers with spinal cord decompression sickness

PURPOSE This study was designed to determine the recompression strategy and the potential risk factors associated with the development of severe diving-related spinal cord decompression sickness (DCS). MATERIAL AND METHODS Sixty-three injured recreational divers (52 men and 11 women; 46 +/- 12 years) presenting with symptoms of spinal involvement were retrospectively included. Diving information, symptom latency after dive completion, and time interval between symptom onset and hyperbaric treatment were studied. The severity of spinal cord DCS was rated numerically for both the acute event and 1-month later. Initial recompression treatment at 2.8 atmosphere absolute (ATA) with 100% oxygen breathing or deeper recompression at 4 atmosphere absolute with nitrogen-oxygen or helium-oxygen breathing mixture was also noted. RESULTS Twenty-one divers (33%) had incomplete resolution after 1 month. The clinical severity at presentation was the only independent predictor of poor outcome (odd ratio, 2.68; P < .033). Time to treatment did not influence the recovery with a similar median delay (3 hours) between the divers with or without long-term sequelae. Choice of recompression procedure was not also a determinant factor for treatment outcome. CONCLUSION The initial clinical course before treatment is a major prognostic factor of spinal cord DCS. Delay to recompression less than 3 hours and use of deep treatment tables did not improve outcome in DCS divers.

Predive Sauna and Venous Gas Bubbles Upon Decompression from 400 kPa

INTRODUCTION This study investigated the influence of a far infrared-ray dry sauna-induced heat exposure before a simulated dive on bubble formation, and examined the concomitant adjustments in hemodynamic parameters. METHODS There were 16 divers who were compressed in a hyperbaric chamber to 400 kPa (30 msw) for 25 min and decompressed at 100 kPa x min(-1) with a 4-min stop at 130 kPa. Each diver performed two dives 5 d apart, one with and one without a predive sauna session for 30 min at 65 degrees C ending 1 h prior to the dive. Circulating venous bubbles were detected with a precordial Doppler 20, 40, and 60 min after surfacing, at rest, and after flexions. Brachial artery flow mediated dilation (FMD), blood pressure, and bodyweight measurements were taken before and after the sauna session along with blood samples for analysis of plasma volume (PV), protein concentrations, plasma osmolality, and plasma HSP70. RESULTS A single session of sauna ending 1 h prior to a simulated dive significantly reduced bubble formation [-27.2% (at rest) to 35.4% (after flexions)]. The sauna session led to an extracellular dehydration, resulting in hypovolemia (-2.7% PV) and -0.6% bodyweight loss. A significant rise of FMD and a reduction in systolic blood pressure and pulse pressure were observed. Plasma HSP70 significantly increased 2 h after sauna completion. CONCLUSION A single predive sauna session significantly decreases circulating bubbles after a chamber dive. This may reduce the risk of decompression sickness. Sweat dehydration, HSP, and the NO pathway could be involved in this protective effect.

Blood Platelet Count and Bubble Formation After a Dive to 30 msw for 30 min

INTRODUCTION Previous human studies reported that platelet count (PC) is decreased following decompression. Platelet aggregation and adherence to the bubble surface has been demonstrated in severe decompression sickness (DCS). The present study was designed to clarify the relationship between post-dive changes in blood PC and the level of bubble formation in divers. METHODS There were 40 healthy experienced divers who were assigned to 1 experimental group (N = 30) with an open-sea air dive to 30 msw for 30 min in field conditions and 1 control group (N = 10) without hyperbaric exposure. Bubble grades were monitored with a pulsed Doppler according to the Spencer scale and Kissman integrated severity score (KISS). Blood samples for red blood cell counts (RBC), hematocrit (Hct), and PC were taken 1 h before and after exposure in two groups. RESULTS None of the divers developed any signs of DCS. In two groups, the results showed significant increase in RBC count and Hct related with hemoconcentration and no change in PC. Divers with a high KISS score (39 +/- 5.8; mean +/- SD) presented a significantly more pronounced percent fall in PC than divers with a lower KISS score. We found a significant correlation between the percent fall in PC after a dive and the bubble KISS score. DISCUSSION The present study highlighted a relationship between the post-dive decrease in PC and the magnitude of bubble level after decompression. Our primary result is that the post-dive decrease in PC could be a predictor of decompression severity after diving.

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.

Sidenafil Pre-Treatment Promotes Decompression Sickness in Rats

Vascular bubble formation after decompression contributes to endothelial injuries which form the basis for the development of decompression sickness (DCS). Nitric oxide (NO) is a powerful vasodilator that contributes to vessel homeostasis. It has been shown that NO-releasing agent may reduce bubble formation and prevent serious decompression sickness. The use of sildenafil, a well-known, phosphodiesterase-5 blocker, which act by potentiating the vasodilatory effect on smooth muscle relaxation, has never been studied in DCS. The purpose of the present study was to evaluate the clinical effects of sildenafil pre-treatment on DCS in a rat model. 67 rats were subjected to a simulated dive at 90 msw for 45 min before staged decompression. The experimental group received 10 mg/kg of sildenafil one hour before exposure (n = 35) while controls were not treated (n = 32). Clinical assessment took place over a period of 30 min after surfacing. At the end, blood samples were collected for blood cells counts and the level of circulating bubbles in the right cavities was quantified. There were significantly more manifestations of DCS in the sildenafil group than in the controls (34.3% vs 6.25%, respectively, p = 0.012). Platelet count was more reduced in treated rats than in controls (−21.7% vs −7%, respectively, p = 0.029), whereas bubble grades did not differ between groups. We concluded that pre-treatment with sildenafil promotes the onset and severity of neurological DCS. When considering the use of phosphodiesterase-5 blockers in the context of diving, careful discussion with physician should be recommended.

Preconditioning methods and mechanisms for preventing the risk of decompression sickness in scuba divers: a review.

Scuba divers are at risk of decompression sickness due to the excessive formation of gas bubbles in blood and tissues following ascent, with potentially subsequent neurological injuries. Since nonprovocative dive profiles are no guarantor of protection against this disease, novel means are required for its prevention including predive procedures that could induce more resistance to decompression stress. In this article, we review the recent studies describing the promising preconditioning methods that might operate on the attenuation of bubble formation believed to reduce the occurrence of decompression sickness. The main practical applications are simple and feasible predive measures such as endurance exercise in a warm environment, oral hydration, and normobaric oxygen breathing. Rheological changes affecting tissue perfusion, endothelial adaptation with nitric oxide pathway, up-regulation of cytoprotective proteins, and reduction of preexisting gas nuclei from which bubbles grow could be involved in this protective effect.

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.