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Decompression sickness (DCS) is caused by gaseous nitrogen dissolved in tissues forming bubbles during decompression. To date, no method exists to identify nitrogen within tissues, but with advances in positron-emission tomography (PET) technology, it may be possible to track gaseous radionuclides into tissues. We aimed to develop a method to track nitrogen movement in vivo and under hyperbaric pressure that could then be used to further our understanding of DCS using nitrogen-13 ( 13 N 2 ). A single anesthetized female Sprague-Dawley rat was exposed to 625 kPa, composed of air, isoflurane, and 13 N 2 for 10 min. The PET scanner recorded 13 N 2 during the hyperbaric exposure with energy windows of 250-750 keV. The PET showed an increase in 13 N 2 concentration in the lung, heart, and abdominal regions, which all reached a plateau after ∼4 min. This showed that it is possible to gain noninvasive in vivo measurements of nitrogen kinetics through the body while at hyperbaric pressures. Tissue samples showed radioactivity above background levels in the blood, brain, liver, femur, and thigh muscle when assessed using a γ counter. The method can be used to evaluate an array of challenges to our understanding of decompression physiology by quantifying nitrogen load through γ counts of 13 N 2 , and signal intensity of the PET. Further development of the method will improve the specificity of the measured outcomes, and enable it to be used with larger mammals, including humans. NEW & NOTEWORTHY This article describes a method for the in vivo quantification and tracking of nitrogen through the mammalian body whilst exposed to hyperbaric pressure. The method has the potential to further our understanding of decompression sickness, and quantitatively evaluate the effectiveness of both the treatment and prevention of decompression sickness.

Introduction: This is a review of commercial heliox saturation decompression procedures. The scope does not include compression, storage depth or bell excursion dive procedures. The objectives are to: identify the sources of the procedures; trace their evolution; describe the current practice; and detect relevant trends., Methods: Eleven international commercial diving companies provided their diving manuals for review under a confidentiality agreement., Results: Modern commercial diving saturation procedures are derived from a small number of original procedures (United States Navy, Comex, and NORSOK). In the absence of relevant scientific studies since the late 80's, the companies have empirically adapted these procedures according to their needs and experience. Such adaptation has caused differences in decompression rates shallower than 60 msw, decompression rest stops and the decision to decompress linearly or stepwise. Nevertheless, the decompression procedures present a remarkable homogeneity in chamber PO 2 and daily decompression rates when deeper than 60 msw. The companies have also developed common rules of good practice; no final decompression should start with an initial ascending excursion; a minimum hold is required before starting a final decompression after an excursion dive. Recommendation is made for the divers to exercise during decompression., Conclusions: We observed a trend towards harmonisation within the companies that enforce international procedures, and, between companies through cooperation inside the committees of the industry associations., (Copyright: This article is the copyright of the authors who grant Diving and Hyperbaric Medicine a non-exclusive licence to publish the article in electronic and other forms.)

Introduction: Breath-hold (BH) diving has known risks, for example drowning, pulmonary oedema of immersion and barotrauma. There is also the risk of decompression illness (DCI) from decompression sickness (DCS) and/or arterial gas embolism (AGE). The first report on DCS in repetitive freediving was published in 1958 and from then there have been multiple case reports and a few studies but no prior systematic review or meta-analysis., Methods: We undertook a systematic literature review to identify articles available from PubMed and Google Scholar concerning breath-hold diving and DCI up to August 2021., Results: The present study identified 17 articles (14 case reports, three experimental studies) covering 44 incidences of DCI following BH diving., Conclusions: This review found that the literature supports both DCS and AGE as potential mechanisms for DCI in BH divers; both should be considered a risk for this cohort of divers, just as for those breathing compressed gas while underwater., (Copyright: This article is the copyright of the authors who grant Diving and Hyperbaric Medicine a non-exclusive licence to publish the article in electronic and other forms.)

Purpose: Divers can experience cognitive impairment due to inert gas narcosis (IGN) at depth. Brain-derived neurotrophic factor (BDNF) rules neuronal connectivity/metabolism to maintain cognitive function and protect tissues against oxidative stress (OxS). Dopamine and glutamate enhance BDNF bioavailability. Thus, we hypothesized that lower circulating BDNF levels (via lessened dopamine and/or glutamate release) underpin IGN in divers, while testing if BDNF loss is associated with increased OxS., Methods: To mimic IGN, we administered a deep narcosis test via a dry dive test (DDT) at 48 msw in a multiplace hyperbaric chamber to six well-trained divers. We collected: (1) saliva samples before DDT (T0), 25 msw (descending, T1), 48 msw (depth, T2), 25 msw (ascending, T3), 10 min after decompression (T4) to dopamine and/or reactive oxygen species (ROS) levels; (2) blood and urine samples at T0 and T4 for OxS too. We administered cognitive tests at T0, T2, and re-evaluated the divers at T4., Results: At 48 msw, all subjects experienced IGN, as revealed by the cognitive test failure. Dopamine and total antioxidant capacity (TAC) reached a nadir at T2 when ROS emission was maximal. At decompression (T4), a marked drop of BDNF/glutamate content was evidenced, coinciding with a persisting decline in dopamine and cognitive capacity., Conclusions: Divers encounter IGN at - 48 msw, exhibiting a marked loss in circulating dopamine levels, likely accounting for BDNF-dependent impairment of mental capacity and heightened OxS. The decline in dopamine and BDNF appears to persist at decompression; thus, boosting dopamine/BDNF signaling via pharmacological or other intervention types might attenuate IGN in deep dives., (© 2022. The Author(s).)

Introduction: This study aimed to determine the characteristics of decompression illness patients and their treatment outcomes, at the Center of Hyperbaric Medicine, Somdech Phra Pinklao Hospital, one of the largest centres in Thailand., Methods: Past medical records of patients with decompression illness from 2015 to 2021 were retrieved and analysed., Results: Ninety-eight records of diving-related illness from 97 divers were reviewed. Most of the divers were male (n = 50), Thai (n = 86), and were certified at least open water or equivalent (n = 88). On-site first aid oxygen inhalation was provided to 17 divers. Decompression sickness (DCS) cases were characterised according to organ systems involved. The most prominent organ system involved was neurological (57%), followed by mixed organs (28%), musculoskeletal (13%), and pulmonary (2%). There were three cases of arterial gas embolism (AGE). Median presentation delay was three days. Ninety patients were treated with US Navy Treatment Table 6. At the end of their hyperbaric oxygen treatment, most divers (65%) recovered completely., Conclusions: Despite oxygen first aid being given infrequently and long delays before definitive treatment, treatment outcome was satisfactory. Basic knowledge and awareness of diving-related illnesses should be promoted among divers and related personnel in Thailand along with further studies., (Copyright: This article is the copyright of the authors who grant Diving and Hyperbaric Medicine a non-exclusive licence to publish the article in electronic and other forms.)

Inner ear decompression sickness (IEDCS) may occur after upward or downward excursions in saturation diving. Previous studies in nonsaturation diving strongly suggest that IEDCS is caused by arterialization of small venous bubbles across intracardiac or intrapulmonary right-to-left shunts and bubble growth through inward diffusion of supersaturated gas when they arrive in the inner ear. The present study used published saturation diving data and models of inner ear inert gas kinetics and bubble dynamics in arterial conditions to assess whether IEDCS after saturation excursions could also be explained by arterialization of venous bubbles and whether such bubbles might survive longer and be more likely to reach the inner ear under deep saturation diving conditions. Previous data show that saturation excursions produce venous bubbles. Modeling shows that gas supersaturation in the inner ear persists longer than in the brain after such excursions, explaining why the inner ear would be more vulnerable to injury by arriving bubbles. Estimated survival of arterialized bubbles is significantly prolonged at high ambient pressure such that bubbles large enough to be filtered by pulmonary capillaries but able to cross right-to-left shunts are more likely to survive transit to the inner ear than at the surface. IEDCS after saturation excursions is plausibly caused by arterialization of venous bubbles whose prolonged arterial survival at deep depths suggests that larger bubbles in greater numbers reach the inner ear. NEW & NOTEWORTHY Inner ear decompression sickness that occurs during deep saturation diving is explained by arterialization of venous bubbles across intracardiac or intrapulmonary right-to-left shunts and growth of these bubbles if they arrive in the inner ear. Bubbles in arterial blood have prolonged lifetimes at hyperbaric pressures compared with at sea level. This can explain why inner ear decompression sickness is more characteristic of rapid decompressions at great depths than of decompression at sea level.

Introduction: Technical diving is increasing in popularity in Finland, and therefore the number of decompression illness (DCI) cases is also increasing among technical divers. Although hyperbaric oxygen treatment (HBOT) remains the standard of care, there are anecdotal reports of technical divers treating mild DCI symptoms themselves and not seeking a medical evaluation and possible recompression therapy. This study aimed to make an epidemiologic inventory of technical diving-related DCI symptoms, to establish the incidence of self-treatment and to determine the apparent effectiveness of different treatment methods., Methods: A one-year prospective survey with online questionnaires was conducted. Fifty-five experienced and highly trained Finnish technical divers answered the survey and reported their diving activity, DCI symptoms, symptom treatment, and treatment outcome., Results: Of the reported 2,983 dives, 27 resulted in symptoms of DCI, which yielded an incidence of 91 per 10,000 dives in this study. All of the reported DCI symptoms were mild, and only one diver received HBOT. The most common self-treatments were oral hydration and rest. First aid oxygen (FAO 2 ) was used in 21% of cases. Eventually, none of the divers had residual symptoms., Conclusions: The incidence of self-treated DCI cases was 27 times higher than that of HBO-treated DCI cases. There is a need to improve divers' awareness of the importance of FAO 2 and other recommended first aid procedures and to encourage divers to seek medical attention in case of suspected DCI., (Copyright: This article is the copyright of the authors who grant Diving and Hyperbaric Medicine a non-exclusive licence to publish the article in electronic and other forms.)

Introduction: This is the first published study on decompression illness (DCI) and its treatment in Finland. Diving conditions are demanding, as even in the summer the water temperature below 20 meters' sea/fresh water (msw/mfw) is 4-10°C. Technical diving has become more popular over the years, so the emphasis of this study was to describe DCI in technical divers and compare it with non-technical recreational divers., Methods: This study includes by estimation over 95% of all hyperbaric oxygen-treated DCI patients during the years 1999-2018 (n = 571). The cases were divided into technical divers (n = 200) and non-technical divers (n = 371). We focused on the differences between these two groups. Technical diving was defined as the usage of mixed breathing gases, closed circuit rebreather diving or planned decompression diving., Results: The mean annual number of treated DCI cases in Finland was 29 (range 16-38). The number of divers treated possibly indicate a shift towards technical diving. Technical dives were deeper and longer and were mainly performed in cold water or an overhead environment. Technical divers were more likely to utilize first aid 100% oxygen (FAO 2 ) and sought medical attention earlier than non-technical divers. Symptom profiles were similar in both groups. Recompression was performed using USN Treatment Table Six in the majority of the cases and resulted in good final outcome. Eighty two percent were asymptomatic on completion of all recompression treatment(s)., Conclusion: This 20-year observational study indicates a shift towards technical diving, and hence a more demanding and challenging style of diving among Finnish divers, with a surprisingly constant number of DCI cases over the years. There is still need for improvement in divers' education in use of FAO 2 for DCI symptoms. Fortunately, the outcome after recompression therapy is generally successful., (Copyright: This article is the copyright of the authors who grant Diving and Hyperbaric Medicine a non-exclusive licence to publish the article in electronic and other forms.)

Objective: An analysis of factors that may indicate both the type and degree of dehydration of a diver's body following a dry chamber hyperbaric exposure., Methods: The study was participated by 63 men - professional divers, with extensive diving experience, aged 24-51 years (average age 32.6). The subjects underwent two hyperbaric exposures, one to a pressure of 0.3 MPa and one to a pressure of 0.6 MPa, with oxygen decompression. The exposures were carried out in a hyperbaric chamber pursuant to the decompression tables of the Polish Navy, with the observance of a 24-hour interval between exposures. Blood samples were collected from the participants in order to perform a blood morphology test. Body weight was measured with the bioelectrical impedance method using the Maltron BioScan 920 device.The results were subjected to statistical analysis. The following blood morphology parameters were analyzed: hematocrit (Ht), erythrocyte size (MCV), color index (MCHC) and body weight composition: total water (TBW), extracellular water (ECW), intracellular water (ICW)., Results: The studies have shown that during a hyperbaric exposure in the chamber the diver's body becomes dehydrated, with observable loss of both intracellular water as evidenced by the reduction of hematocrit content and erythrocyte size, as well as extracellular water, with the accompanying increase in the color index., Conclusions: Hyperbaric conditions are conducive to the dehydration of the diver's body, however to a degree which does not lead to an occurrence of health hazards. Good care for one's health through proper nutrition and hydration are sufficient preventive and protective measures., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Many aspects of the physiological stress related to the exposure to the hyperbaric environment have been studied, but no research has been made to evaluate the impacts of scuba diving on heart rate variability (HRV). We investigated the effects of a simulated dive to 557 KPa (45 meters of salt water) for a 30-minute bottom time on the frequency and time domains estimators of HRV. Electrocardiogram records were obtained with superficial electrodes for 30 minutes before the simulated dive and, subsequently, for one hour after the dive. Each of these time-series was then subdivided into non-overlapping windows of 256 consecutive R-R intervals. A control group was submitted to the same protocol, breathing the same gases used in the simulated dive, while not being exposed to the hyperbaric environment. In the control group we observed a significant increase in SDNN (the square root of the variance of the R-R intervals), RMSSD (the square root of the mean squared differences of successive R-R intervals), and in two bands (high and low) of the power spectrum of frequencies. The subjects in the simulated dive presented only an increase in the low-frequency estimator without any further relevant changes in other estimators of HRV. This study suggests that the low-frequency increase without concomitant high-frequency increase might be an indicator of the physiological stress caused by decompression and that such a dissimilarity in responses might be correlated to the dive-related impairment of the endothelial function., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Introduction: Important developments in the diagnosis of scuba diving fatalities have been made thanks to forensic imaging tool improvements. Multi-detector computed tomography (MDCT) permits reliable interpretation of the overall gaseous distribution in the cadaver. However, due to post-mortem delay, the radiological interpretation is often doubtful because the distinction between gas related to the dive and post-mortem decomposition artifactual gases becomes less obvious., Methods: We present six cases of fatal scuba diving showing gas in the heart and other vasculature. Carbon dioxide (CO₂) in cardiac gas measured by gas chromatography coupled to thermal conductivity detection were employed to distinguish decomposition from embolism based on the detection of decomposition gases (hydrogen, hydrogen sulfide and methane) and to confirm arterial gas embolism (AGE) or post-mortem offgasing diagnoses. A Radiological Alteration Index (RAI) was calculated from the scan., Results: Based on the dive history, the intra-cadaveric gas was diagnosed as deriving from decomposition (one case, minimal RAI of 61), post-mortem decompression artifacts (two cases, intermediate RAI between 60 and 85) and barotrauma/AGE (three cases, maximal RAI between 85 and 100), illustrating a large distribution inside the bodies., Conclusion: MDCT scans should be interpreted simultaneously with compositional analysis of intra-cadaveric gases. Intra-cadaveric gas sampling and analysis may become useful tools for understanding and diagnosing scuba diving fatalities. In cases with short post-mortem delays, the CO₂ concentration of the cardiac gas provides relevant information about the circumstances and cause of death when this parameter is interpreted in combination with the diving profile.

The aim of the present study was to determine the effect of postprandial hypertriglyceridemia on the risk of decompression stress following hyperbaric air exposures. The study involved 55 male individuals aged 20-48 years (31.47 ± 5.49 years), body mass index 20.3-33.2 kg/m2 (25.5 ± 2.58 kg/m2). Blood was sampled two hours after a meal each participant had in accordance with individual dietary preferences to determine the following parameters: blood cell counts, activity of aspartate aminotransferase (AST) and alanine ammotransterase (ALT), concentrations of total cholesterol and triglycerides. After each hyperbaric exposure, the presence and intensity of decompression stress were assessed using the Doppler method. Decompression stress was found in 30 individuals. Postprandial hypertriglyceridemia and hypercholesterolemia increased the risk of decompression stress after hyperbaric air exposures.

Introduction: The vast majority of freshwater cave diving in Australia occurs within the limestone caves of the Gambier karst in the south-east of South Australia. The incidence of decompression illness (DCI) in cave divers is presumed to be higher than open-water recreational divers because of the greater depths involved, but has not previously been reported. Our aim was to determine the incidence of DCI in cave divers, the patterns of diving and the outcome of hyperbaric treatment., Methods: This was a retrospective cohort study of cave divers with DCI presenting to the Royal Adelaide Hospital or The Alfred Hospital over a 10-year period between 2002 and 2012. We reviewed case notes of cave divers who were treated for DCI after diving in the Mt Gambier karst. As there are no records of the number of dives performed during the study period we generated a denominator for the incidence of DCI by extrapolating available data and making a number of assumptions about the number of dives per dive permit issued., Results: Sixteen patients were treated for DCI during the study period. The precipitating dive was a single deep decompression dive in seven cases, multiday repetitive dive sequences in eight and a non-decompression dive in one. Three of the 16 cases of DCI involved dives in excess of 90 metres' fresh water (mfw) using trimix. As the total estimated number of dives in the study period was approximately 57,000 the incidence of DCI in Australian cave divers was estimated to be 2.8:10,000 (0.028%). It is possible that the overall incidence of DCI is as high as 0.05%, and even higher when dives to depths greater than 90 mfw are involved., Conclusions: The estimated incidence of DCS in this series is lower than expected but consistent with other series describing DCI in cold-water recreational diving.

Introduction: In studies of decompression procedures, ultrasonically detected venous gas emboli (VGE) are commonly used as a surrogate outcome if decompression sickness (DCS) is unlikely to be observed. There is substantial variability in observed VGE grades, and studies should be designed with sufficient power to detect an important effect., Methods: Data for estimating sample size requirements for studies using VGE as an outcome is provided by a comparison of two decompression schedules that found corresponding differences in DCS incidence (3/192 [DCS/dives] vs. 10/198) and median maximum VGE grade (2 vs. 3, P < 0.0001, Wilcoxon test). Sixty-two subjects dived each schedule at least once, accounting for 183 and 180 man-dives on each schedule. From these data, the frequency with which 10,000 randomly resampled, paired samples of maximum VGE grade were significantly different (paired Wilcoxon test, one-sided P ⋜ 0.05 or 0.025) in the same direction as the VGE grades of the full data set were counted (estimated power). Resampling was also used to estimate power of a Bayesian method that ranks two samples based on DCS risks estimated from the VGE grades., Results: Paired sample sizes of 50 subjects yielded about 80% power, but the power dropped to less than 50% with fewer than 30 subjects., Conclusions: Comparisons of VGE grades that fail to find a difference between paired sample sizes of 30 or fewer must be interpreted cautiously. Studies can be considered well powered if the sample size is 50 even if only a one-grade difference in median VGE grade is of interest.

Technical divers perform deep, mixed-gas 'bounce' dives, which are inherently inefficient because even a short duration at the target depth results in lengthy decompression. Technical divers use decompression schedules generated from modified versions of decompression algorithms originally developed for other types of diving. Many modifications ostensibly produce shorter and/or safer decompression, but have generally been driven by anecdote. Scientific evidence relevant to many of these modifications exists, but is often difficult to locate. This review assembles and examines scientific evidence relevant to technical diving decompression practice. There is a widespread belief that bubble algorithms, which redistribute decompression in favour of deeper decompression stops, are more efficient than traditional, shallow-stop, gas-content algorithms, but recent laboratory data support the opposite view. It seems unlikely that switches from helium- to nitrogen-based breathing gases during ascent will accelerate decompression from typical technical bounce dives. However, there is evidence for a higher prevalence of neurological decompression sickness (DCS) after dives conducted breathing only helium-oxygen than those with nitrogen-oxygen. There is also weak evidence suggesting less neurological DCS occurs if helium-oxygen breathing gas is switched to air during decompression than if no switch is made. On the other hand, helium-to-nitrogen breathing gas switches are implicated in the development of inner-ear DCS arising during decompression. Inner-ear DCS is difficult to predict, but strategies to minimize the risk include adequate initial decompression, delaying helium-to-nitrogen switches until relatively shallow, and the use of the maximum safe fraction of inspired oxygen during decompression.

Recompression during decompression has been suggested to possibly reduce the risk of decompression sickness (DCS). The main objective of the current study was to investigate the effects of FLIRT (First Line Intermittent Recompression Technique) on bubble detection in man. 29 divers underwent 2 simulated dives in a dry recompression chamber to a depth of 40 msw (500 kPa ambient pressure) in random order. A Buehlmann-based decompression profile served as control and was compared to an experimental profile with intermittent recompression during decompression (FLIRT). Circulating bubbles in the right ventricular outflow tract (RVOT) were monitored by Doppler ultrasound and quantified using the Spencer scoring algorithm. Heat shock protein 70 (HSP70), thrombocytes, D-Dimers and serum osmolarity were analyzed before and 120 min after the dive. Both dive profiles elicited bubbles in most subjects (range Spencer 0-4). However, no statistically significant difference was found in bubble scores between the control and the experimental dive procedure. There was no significant change in either HSP70, thrombocytes, and D-Dimers. None of the divers had clinical signs or symptoms suggestive of DCS. We conclude that FLIRT did not significantly alter the number of microbubbles and thus may not be considered superior to classical decompression in regards of preventing DCS., (© Georg Thieme Verlag KG Stuttgart · New York.)

Deep diving is defined as diving to depths more than 50 m of seawater (msw), and is mainly used for occupational and military purposes. A deep dive is characterized by the compression phase, the bottom time and the decompression phase. Neurological and neurophysiologic effects are demonstrated in divers during the compression phase and the bottom time. Immediate and transient neurological effects after deep dives have been shown in some divers. However, the results from the epidemiological studies regarding long term neurological effects from deep diving are conflicting and still not conclusive. Prospective clinical studies with sufficient power and sensitivity are needed to solve this very important issue., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Diving and decompression performed under immersed conditions have been shown to reduce cardiac function. The mechanisms for these changes are not known. The effect of immersion before a simulated hyperbaric dive on cardiomyocyte function was studied. Twenty-three rats were assigned to four groups: control, 1 h thermoneutral immersion, dry dive, and 1 h thermoneutral immersion before a dive (preimmersion dive). Rats exposed to a dive were compressed to 700 kPa, maintained for 45 min breathing air, and decompressed linearly to the surface at a rate of 50 kPa/min. Postdive, the animals were anesthetized and the right ventricle insonated for bubble detection using ultrasound. Isolation of cardiomyocytes from the left ventricle was performed and studied using an inverted fluorescence microscope with video-based sarcomere spacing. Compared with a dry dive, preimmersion dive significantly increased bubble production and decreased the survival time (bubble grade 1 vs. 5, and survival time 60 vs. 17 min, respectively). Preimmersion dive lead to 18% decreased cardiomyocyte shortening, 20% slower diastolic relengthening, and 22% higher calcium amplitudes compared with controls. The protein levels of the sarco-endoplasmic reticulum calcium ATPase (SERCA2a), Na+/Ca2+ exchanger (NCX), and phospholamban phosphorylation in the left ventricular tissue were significantly reduced after both dry and preimmersion dive compared with control and immersed animals. The data suggest that immersion before a dive results in impaired cardiomyocyte and Ca2+ handling and may be a cellular explanation to reduced cardiac function observed in humans after a dive.

This study compared neuroendocrine and psychomotor responses in divers (D, n = 11) and non-divers (ND, n = 9) following 30-minute hyperbaric and decompression stress to 180, 300 and 450 kPa. Venous blood was drawn pre-dive and at 20 and 60 minutes post-dive and analyzed for norepinephrine (NE), epinephrine (E), tryptophan (TRP), cortisol (COR), growth hormone (GH), adrenocorticotrophic hormone (ACTH) and prolactin (PRL). Reaction time was assessed using a psychomotor vigilance task. There was no difference between groups, across time or among levels of hyperbaric stress, for NE, E, TRP or GH. Small decreases over time in COR were noted. ACTH was significantly higher for ND at 20 minutes following 180 kPa and after 60 minutes for 450 kPa exposure. PRL increased significantly more for ND, and changes from baseline following 450 kPa exposure were moderately related (r = 0.52) to the significant slowing of reaction time at 20 minutes (296 +/- 55 msec) and 60 minutes (277 +/- 35 msec) compared with baseline (247 +/- 22 msec), although PRL returned to baseline levels faster than reaction time. It was concluded that for the stress hormones measured, PRL may provide some indication of the adaptation involved with repeated hyperbaric stress, but its relationship to changes in reaction time was weak.

Effect of in-water oxygen prebreathing at different depths on decompression-induced bubble formation and platelet activation in scuba divers was evaluated. Six volunteers participated in four diving protocols, with 2 wk of recovery between dives. On dive 1, before diving, all divers breathed normally for 20 min at the surface of the sea (Air). On dive 2, before diving, all divers breathed 100% oxygen for 20 min at the surface of the sea [normobaric oxygenation (NBO)]. On dive 3, before diving, all divers breathed 100% O2 for 20 min at 6 m of seawater [msw; hyperbaric oxygenation (HBO) 1.6 atmospheres absolute (ATA)]. On dive 4, before diving, all divers breathed 100% O2 for 20 min at 12 msw (HBO 2.2 ATA). Then they dove to 30 msw (4 ATA) for 20 min breathing air from scuba. After each dive, blood samples were collected as soon as the divers surfaced. Bubbles were measured at 20 and 50 min after decompression and converted to bubble count estimate (BCE) and numeric bubble grade (NBG). BCE and NBG were significantly lower in NBO than in Air [0.142+/-0.034 vs. 0.191+/-0.066 (P<0.05) and 1.61+/-0.25 vs. 1.89+/-0.31 (P<0.05), respectively] at 20 min, but not at 50 min. HBO at 1.6 ATA and 2.2 ATA has a similar significant effect of reducing BCE and NBG. BCE was 0.067+/-0.026 and 0.040+/-0.018 at 20 min and 0.030+/-0.022 and 0.020+/-0.020 at 50 min. NBG was 1.11+/-0.17 and 0.92+/-0.16 at 20 min and 0.83+/-0.18 and 0.75+/-0.16 at 50 min. Prebreathing NBO and HBO significantly alleviated decompression-induced platelet activation. Activation of CD62p was 3.0+/-0.4, 13.5+/-1.3, 10.7+/-0.9, 4.5+/-0.7, and 7.6+/-0.8% for baseline, Air, NBO, HBO at 1.6 ATA, and HBO at 2.2 ATA, respectively. The data show that prebreathing oxygen, more effective with HBO than NBO, decreases air bubbles and platelet activation and, therefore, may be beneficial in reducing the development of decompression sickness.

It is generally accepted that the incidence of decompression sickness (DCS) from hyperbaric exposures is low when few or no bubbles are present in the circulation. To date, no data are available on the influence of in-water oxygen breathing on bubble formation following a provocative dive in man. The purpose of this study was to compare the effect of post-dive hyperbaric versus normobaric oxygen breathing (NOB) on venous circulating bubbles. Nineteen divers carried out open-sea field air dives at 30 msw depth for 30 min followed by a 9 min stop at 3 msw. Each diver performed three dives: one control dive, and two dives followed by 30 min of hyperbaric oxygen breathing (HOB) or NOB; both HOB and NOB started 10 min after surfacing. For HOB, divers were recompressed in-water to 6 msw at rest, whereas NOB was performed in a dry room in supine position. Decompression bubbles were examined by a precordial pulsed Doppler. Bubble count was significantly lower for post-dive NOB than for control dives. HOB dramatically suppressed circulating bubble formation with a bubble count significantly lower than for NOB or controls. In-water recompression with oxygen to 6 msw is more effective in removing gas bubbles than NOB. This treatment could be used in situations of "interrupted" or "omitted" decompression, where a diver returns to the water in order to complete decompression prior to the onset of symptoms. Further investigations are needed before to recommend this protocol as an emergency treatment for DCS.

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.

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.

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.

We compare outcomes of experimental air dives with prescriptions for ascent given by various air decompression tables. Among experimental dives compiled in the U.S. Navy Decompression Database, many profiles that resulted in decompression sickness (DCS) have longer total decompression times (TDTs, defined as times spent at decompression stops plus time to travel from depth to the surface) than profiles prescribed by the U.S. Navy table; thus, the divers developed DCS despite spending more time at stops than the table requires. The same is true to a lesser extent for the table used by the Canadian forces. A few DCS cases occurred in profiles having longer TDTs than those of the VVal-18 table and a table prepared at the University of Pennsylvania. The TDTs for 2.2% risk according to the probabilistic NMRI'98 Model are often far longer than TDTs of experimental dives that resulted in DCS. This analysis dramatizes the large differences among alternative decompression instructions and illustrates how the U.S. Navy table provides too little time at stops when bottom times are long.

Objectives: The French Navy uses the Marine Nationale 90 (MN90) decompression tables for air dives as deep as 60 msw. The resulting incidence of decompression sickness (DCS) for deep dives (45-60 msw) is one case per 3000 dives., Methods: Three protocols with experimental ascent profiles (EAPs) were tested in the wet compartment of a hyperbaric chamber. For each protocol, eight subjects dove to 50 or 60 msw and ascended according to the standard MN90 table or an EAP. Precordial bubbles were monitored with Doppler sensors at 30-min intervals after surfacing. Protocol I went to 60 msw and used deep stops beginning at 27 msw. Protocol II was a repetitive dive to 50 msw with a 3-h surface interval; the EAP made the first deep stop at 18 msw. Protocol III again went to 60 msw, but the EAP used a single, shorter deep stop at 25 msw., Results: For Protocol I, all divers developed bubbles at Spencer grade 2-3 and still had bubbles 120 min after surfacing; there was no statistical difference between bubbling for the MN90 and EAP, but one diver presented a case of DCS after the EAP. For Protocol II, the EAP produced severe bubbling for the eight divers. Those findings led to stopping the EAPs with the longer deep stops used in Protocols I and II. Protocol III again showed no difference between the standard and modified profiles., Discussion: The addition of deep stops requires careful consideration. Two of our EAPs made no difference and one produced increased bubbling.

The aim of the study was to evaluate the presence of cerebral lesions in asymptomatic scuba divers and explain the causes of them: potential risk factors associating cardiovascular risk factors, low aerobic capacity, or characteristics of diving (maximum depth, ascent rate). Experienced scuba divers, over 40 years of age, without any decompression sickness (DCS) history were included. We studied 30 scuba divers (instructors) without any clinical symptoms. For all of them, we carried out a clinical examination with fatty body mass determination and we questioned them about their diving habits. A brain Magnetic Resonance imaging (MRI), an assessment of maximal oxygen uptake, glycemia, triglyceridemia, and cholesterolemia were systematically carried out. Cerebral spots of high intensity were found at 33 % in the scuba diving group and 30 % in the control group. In the diving group, abnormalities were related to unsafe scuba-diving or metabolic abnormalities. In our study, we did not find a significant relationship between the lesions of the central nervous system, and the age, depth of the dives, number of dives, and ergometric performances (maximal oxygen uptake, V.O (2max), serum level of blood lactate). Nevertheless, we found a significant relationship between the lesions of the central nervous system and ascent rate faster than 10 meters per minute (r = 0.57; p = 0.003) or presence of high level of cholesterolemia (r = 0.6; p = 0.001). We found concordant results using the Cochran's Test: meaningful link between the number of brain lesions and the speed of decompression (Uexp = 14 < Utable = 43; alpha = 0.05, p < 0.01). We concluded that hyperintensities can be explained by preformed nitrogen gas microbubbles and particularly in presence of cholesterol, when the ascent rate is up to 10 meters per minute. So, it was remarkable to note that asymptomatic patients practicing scuba diving either professionally or recreationally, presented lesions of the central nervous system. This survey permitted us to highlight in a population of professional divers, neurological and also cardiovascular abnormalities (ventricular arrhythmias); although none of them present any symptoms today. It seems therefore important to us to propose in the future, for a better prevention of neurological injuries, a systematic follow-up by maximal oxygen consumption measure, brain MRI, and cholesterolemia. In the same way, our results suggest a modification of the diving tables with a maximal decompression rate at 9 m . mn (-1).

Background: Many occupational diving groups have substantially different diving patterns to those for which decompression schedules are validated., Aims: To evaluate tuna farm occupational diving practice against existing decompression models and describe a method for collecting and modelling self reported field decompression data., Methods: Machine readable objective depth/time profiles were obtained from depth/time recorders worn by tuna farm occupational divers. Divers' health status was measured at the end of each working day using a self administered health survey that produces an interval diver health score (DHS) with possible values ranging from 0 to 30. Depth/time profiles were analysed according to existing decompression models. The contribution of diving exposure and between diver variability to DHS was evaluated using linear regression., Results: The mean risk of decompression sickness was calculated as 0.005 (SD 0.003, n = 383). The mean DHS following diving was 3 (SD 2, n = 383) and following non-diving activities was 1 (SD 1, n = 41). After accounting for between diver variability in intercept, DHS was found to increase one unit for every 1% increase in the risk of decompression sickness., Conclusions: A method has been established for the collection and analysis of self reported objective decompression data from occupational diving groups that can potentially be used as the basis for development of purpose designed occupational diving decompression schedules.

A decline in expiratory flow rates in divers has recently been attributed to chronic exposure to hyberbaric air. Airway hyperresponsiveness (AHR) to stimuli due to a hyperbaric environment may play a certain role in this context. The aim of this study was to determine the prevalence of AHR in compressed air divers and to assess the value of bronchial challenges for prediction of fitness to dive. A cross-sectional sample of 59 healthy male volunteers--28 divers and 31 diving candidates (controls)--who had been found fit to dive in a diving medical examination underwent additional allergy screening (skin prick and serum IgE) and a histamine bronchial challenge. Pre- and postchallenge body plethysmography was completed to assess AHR. AHR to histamine was significantly increased among divers and positively related to diving experience whereas divers and controls did not differ significantly with respect to age, anthropometric data, current smoking habits, skin prick reaction, and elevated serum IgE. Our results indicate an increased prevalence of AHR to nonspecific inhalation stimuli in experienced divers. Bronchial challenge tests may be helpful to detect asthmatics in the medical assessment of fitness to dive and for follow-up examinations during a diver's career.

The aim of this study was to determine the utility of pulsed Doppler and 2D echocardiography for the detection and the quantification of circulating bubbles after decompression. Twenty-three sport divers performed 60 SCUBA dives (mean 32 msw). An evaluation of circulating bubbles was performed using 2D images one hour after diving. Circulating bubbles were also detected with pulsed Doppler. The sample volume was placed in the outflow area of the right ventricle 1-2 cm below the pulmonary valve. 2D echocardiography showed circulating bubbles in right cavities of the heart in 32 cases. Short axis parasternal view and right cavities long axis view were the best incidences. Pulsed Doppler confirmed the results in these 32 cases and detected circulating bubbles in seven other cases. Isometric contraction of muscle limb must be performed to increase the sensitivity of detection. The count of the bubbles may be evaluated when using a combination of Spencer's and Powell's grading. We conclude that 2D echocardiography is less accurate than pulsed Doppler in the detection of circulating bubbles after decompression. Further studies are needed to compare pulsed Doppler guided by 2D echocardiography to continuous Doppler for the detection of circulating bubbles.

The authors offer a way of estimation of safety modes of decompression, based on definition of intensity of venous gas embolism (VGE) at each decompression and account of probability of illness of divers in series of tests. Intensity of VGE was determined with the help of ultrasonic gas bubbles Doppler radar. Comparative safety of standard modes of decompression of divers of the Navy was estimated, and also the modes, designed in accordance with mathematical model of decompression, offered by I. A. Voĭtsekhovich (1990), were done. The results testify, that use of ultrasonic radar for estimation of intensity of VGE at decompression and account of average and maximum probability of decompression illness in series of tests of modes permit to receive the comparative characteristic of safety of modes at small number of decompressions.

It was established that professional divers who never suffered from decompression sickness had fundus changes similar to those changes which could be seen in divers who have had this disease. A many years diving may lead to permanent degenerative changes at the eye fundus.

As the pathogenesis of dysbaric osteonecrosis is not fully understood, we investigated the effects of compressed air, decompression, and elevated oxygen levels on bone blood flow. Bone blood flow was measured in 4 groups of rabbits using the radioactive-labeled microsphere technique. In the Control and Oxygen groups it was measured at normal pressure (1 ATA) at the end of 4-h exposures to air and 100% oxygen, respectively. In the Pressure group it was measured "at pressure" at the end of a 4-h exposure to compressed air (3 ATA) and in the Decompression group it was measured after decompression following a 3.5-h exposure to compressed air (3 ATA). Femoral head blood flow was significantly lower (P = 0.027) in both the Pressure (7.5 ml.100 g-1.min-1) and Decompression (7.1 ml.100 g-1.min-1) groups than in the Control group (13.0 ml.100 g-1.min-1). Moreover, the distribution of blood flow between the cortex and marrow of the humerus differed significantly (P = 0.044) between the Control and Pressure groups. No differences were found between the bone blood flow rates of the Control and Oxygen groups. It is concluded that femoral head blood flow is reduced by prolonged exposure to compressed air (without decompression) and that this is not solely an effect of the high partial pressure of oxygen.

Postmortem human tissue from recently deceased divers was processed histologically to assess any inner and middle ear damage that could have resulted from the effects of pressure during diving. The following new findings are particularly noteworthy. In one diver, ascent while breath holding resulted in the rupture of the ear drum and blood in the middle ear, in addition to pulmonary barotrauma. In a second diver, following inner ear decompression sickness, new bone growth, similar to that described earlier in experimental studies with the squirrel monkey, was observed in the arms of one of the semicircular canals. These observations are further confirmation that otologic disorders can be a serious threat to divers.

An M-mode ultrasound system was used to obtain a reliable method for the evaluation of microbubbles caused by decompression. When the probe is focused in the outflow tract of the right ventricle it is easy to recognize a linear configuration of the echoes caused by the microbubbles. A quantitative study of microbubbles can be done by counting the number of linear echoes per second. Application of this method is reported following saturation diving decompression. We think the reported method is worthy of further use.

The effect of simulated standard no-decompression dives to 60 and 100 ft of seawater was tested in 12 near term sheep carrying 16 fetuses. In the immediate postdive period there were no significant changes in fetal blood pressure or fetal placental or renal blood flow, but the maternal blood pressure was elevated and the maternal placental blood flow was depressed. Six surgically prepared fetuses were dived to 100 ft. Five died within 20 min of ascent and the sixth suffered severe cardiac arrhythmia and hypotension. At autopsy all fetuses were observed to have massive bubbling in the arterial system and heart. Five fetuses were dived to 100 ft without surgery. Two were alive 3 h later and no bubbles were present at autopsy, and three were born alive at term. With the 60-ft dives, three fetuses were subjected to surgery and all suffered massive bubbling. Two fetuses were dived to 60 ft without surgery; one was alive after 3 h and the other was born alive at term. We conclude that surgery and monitoring result in the formation of postdive gas bubbles that would not otherwise appear.

Retinal fluorescein angiography was used to examine the ocular fundi of 84 divers. The retinal capillary density at the fovea was low and microaneurysms and small areas of capillary nonperfusion were seen. The divers had significantly more abnormalities of the retinal pigment epithelium than a comparison group of non-divers. Furthermore, the prevalence of fundus abnormality was related to length of diving history. All observed changes were consistent with the obstruction of the retinal and choroidal circulations. Such obstruction could be due either to intravascular bubble formation during decompression, or to altered behaviour of blood constituents and blood vessels in hyperbaric conditions.

Thirteen paraplegias after decompression have been treated in the 5 centres of Lyons, Geneva, Mulhouse, Basel and Strasbourg. All these cases are somehow comparable: 12 males, 1 female, skilled and well-trained divers are involved from 27 to 50 years. Submersion between 30 and 42 metres, during 15 to 30 minutes. Ascension with or without decompression stops. Beginning with sudden posterior thoracic, 4 feeling sick, 2 becoming briedly unconscious, paralysis after a while (until 1 hour). All have received hyperbaric oxygenation (from 1 to 5 hours later), with an improvement for 10. Neurological findings. 5 tetraplegics, 7 para-(5 with Brown-Sequard), and one LI. Quickly, the tetraplegics improved to a thoracic level. In two cases, paraplegia remained complete at thoracic level. The others had a better evolution; the paralysis improved slowly, with marked spasticity, impaired sensation did not improve to such an extent, often localised at a lower level, with sexual impotence. Micturitions became normal but with often urine leakages. This rather favourable evolution allowed 11 to go back to work.

Four divers in a compression chamber system were suddenly decompressed from 9 atm to 1 atm. One of the divers was about to close the door between the chamber system and the trunk when the accident happened. He was shot out through the door and severely mutilated. The three others died on the spot. The autopsy results are described. The most conspicuous finding was large amounts of fat in the large arteries and veins and in the cardiac chambers, as well as intravascular fat in the organs, especially the liver. This fat can hardly have been embolic, but must have "dropped out" of the blood in situ. It is suggested that the boiling of the blood denatured the lipoprotein complexes, rendering the lipids insoluble.