Symptoms Of Decompression Sickness Research Articles

The Level of Knowledge of Decompression Sickness among Divers in Saudi Arabia – A Cross-sectional Study

Abstract Introduction: Decompression sickness (DCS) is a clinical syndrome, i.e. commonly seen in divers. The global prevalence of DCS among professional dive instructors is approximately 3.4%. This study aimed to assess the level of knowledge concerning DCS among divers in Saudi Arabia. Materials and Methods: This is a cross-sectional study conducted among divers in Saudi Arabia. The research team visited several diving resorts to distribute the questionnaires. Furthermore, diving instructors from different cities across the nation were requested to distribute the questionnaire to their colleagues and diving communities. Results: A total of 262 divers participated in the study, of which 252 (96.18%) had a scuba-certified license. The majority of divers (94.27%) reported that they were aware of DCS. Furthermore, 27.48% of the participants reported that they had experienced clinical symptoms of DCS. Only 14 (19.44%) received first aid care, and 17 (6.489%) needed a deco dive/decompression dive. Females demonstrated a higher risk of developing DCS-related symptoms than males (odds ratio = 2.57; 95% confidence interval = 5.44–1.21; P = 0.0135). Conclusion: Majority of the participants were familiar with the nature of the disease and were found to have practiced safe diving. Practically, one-quarter of the participants experienced DCS-related symptoms, and only very few of them received first aid and/or a deco dive. Despite the nature of the study and its small sample size, this study adds to the growing nature of published literature in giving a better understanding of the disease by divers.

Risk assessment of SWEN21 a suggested new dive table for the Swedish armed forces: bubble grades by ultrasonography.

To develop the diving capacity in the Swedish armed forces the current air decompression tables are under revision. A new decompression table named SWEN21 has been created to have a projected risk level of 1% for decompression sickness (DCS) at the no stop limits. The aim of this study was to evaluate the safety of SWEN21 through the measurement of venous gas emboli (VGE) in a dive series. A total 154 dives were conducted by 47 divers in a hyperbaric wet chamber. As a proxy for DCS risk serial VGE measurements by echocardiography were conducted and graded according to the Eftedal-Brubakk scale. Measurements were done every 15 minutes for approximately 2 hours after each dive. Peak VGE grades for the different dive profiles were used in a Bayesian approach correlating VGE grade and risk of DCS. Symptoms of DCS were continually monitored. The median (interquartile range) peak VGE grade after limb flexion for a majority of the time-depth combinations, and of SWEN21 as a whole, was 3 (3-4) with the exception of two decompression profiles which resulted in a grade of 3.5 (3-4) and 4 (4-4) respectively. The estimated risk of DCS in the Bayesian model varied between 4.7-11.1%. Three dives (2%) resulted in DCS. All symptoms resolved with hyperbaric oxygen treatment. This evaluation of the SWEN21 decompression table, using bubble formation measured with echocardiography, suggests that the risk of DCS may be higher than the projected 1%.

About possibility of using liquid respiration to prevent the development of decompression disorders

Introduction. The problem of crew emergency evacuation after prolonged hyperbaric conditions is complicated by the extended decompression necessity. It is impossible to reach normal pressure conditions without risk of decompression sickness in the most cases due to large amount of dissolved indifferent gases in the tissues.
 
 Method for indifferent gases eliminating out of tissues to breathing liquid while liquid breathing is proposed. The absence of dissolved gases in the breathing liquid creates the pressure gradient that allows indifferent gases to diffuse through the alveolar-capillary barrier from the blood into the breathing liquid.
 
 The purpose of the study is to assess the possibility of liquid breathing application to prevent the development of decompression disorders after a long previous stay in conditions of excessive pressure of the gas environment.
 
 Materials and methods. Syrian hamsters, 4 months old, 120–140 g weight were used in the study. A mixture of perfluorodecalin and perfluorohexane 40:60 ratio was used as a breathing liquid. The animals were divided into four groups: control (№ 1) and three experimental by liquid breathing duration (№ 2, № 3 and № 4 was 15, 30 and 60 minutes, respectively). 
 For isobaric transition from gas to liquid breathing the special test bed was designed. The decompression sickness simulation in laboratory animals was carried out by ultrafast decompression (within 15 seconds) after a 60-minute exposure of 0.6 MPa air gauge pressure. The research method is based on the assessment of decompression disorders clinical picture and pathomorphological studies. The duration of the decompression sickness latent period, severity, animals’ lethality, the average animals’ lethal time, rectal temperature, results of pathomorphological examinations were evaluated. Results. Decompression sickness symptoms such as twitches, convulsions and paresis were observed in the № 1 group animals. Rather less explicit symptoms of decompression sickness were found in the group № 2 in comparison of group № 1. It was assessed by clinical pictures and pathomorphological examinations. Decompression sickness symptoms were not found in none of animals of the groups № 3 and № 4. Conclusions. The technology of liquid breathing with oxygenated and denitrogenated normobaric breathing liquid while hyperbaric conditions is possible to be applied for decompression sickness prevention. The dissolved in tissues nitrogen removal degree depends on the liquid breathing duration.

Flying after diving: a questionnaire-based evaluation of pre-flight diving behaviour in a recreational diving cohort.

Divers are recommended to observe a pre-flight surface interval (PFSI) ≥ 24 hours before boarding a plane following a diving vacation. Decompression sickness (DCS) symptoms may occur during or post-flight. This study aimed to examine the adherence of PFSI ≥ 24 in vacationing divers, and if any perceived signs and symptoms of DCS during or after flight were experienced. An anonymous online survey was publicised through diving exhibitions and social media. Data included diver/diving demographics, PFSI before flight, flight details, and perceived signs and symptoms of DCS during or after flight. Data from 316 divers were examined (31% female) with the age range 17-75 years (median 49). Divers recorded 4,356 dives in the week preceding the flight, range 1-36 (median 14). Overall, 251/316 (79%) respondents reported a PFSI of ≥ 24 hours. PFSIs of < 12 hours were reported by 6 respondents. Diagnosed and treated DCS developing during, and post flight was reported by 4 divers with PFSIs ≥ 24 hours and by 2 divers with PFSIs < 24 hours. Fifteen divers boarded a plane with perceived symptoms of DCS. These data suggest that most divers in this study observed the recommendations of a ≥ 24 hour PFSI with safe outcomes.

Variability in venous gas emboli following the same dive at 3,658 meters

Update: originally posted in Vol 48 #2 Exposure to a reduction in ambient pressure such as in high-altitude climbing, flying in aircrafts, and decompression from underwater diving results in circulating vascular gas bubbles (i.e., venous gas emboli [VGE]). Incidence and severity of VGE, in part, can objectively quantify decompression stress and risk of decompression sickness (DCS) which is typically mitigated by adherence to decompression schedules. However, dives conducted at altitude challenge recommendations for decompression schedules which are limited to exposures of 10,000 feet in the U.S. Navy Diving Manual (Rev. 7). Therefore, in an ancillary analysis within a larger study, we assessed the evolution of VGE for two hours post-dive using echocardiography following simulated altitude dives at 12,000 feet. Ten divers completed two dives to 66 fsw (equivalent to 110 fsw at sea level by the cross correction method) for 30 minutes in a hyperbaric chamber. All dives were completed following a 60-minute exposure at 12,000 feet. Following the dive, the chamber was decompressed back to altitude for two hours. Echocardiograph measurements were performed every 20 minutes post-dive. Bubbles were counted and graded using the Germonpré and Eftedal and Brubakk method, respectively. No diver presented with symptoms of DCS following the dive or two hours post-dive at altitude. Despite inter- and intra-diver variability of VGE grade following the dives, the majority (11/20 dives) presented a peak VGE Grade 0, three VGE Grade 1, one VGE Grade 2, four VGE Grade 3, and one VGE Grade 4. Using the cross correction method for a 66-fsw dive at 12,000 feet of altitude resulted in a relatively low decompression stress and no cases of DCS.

Hyperoxic Effects on Decompression Strain During Alternating High and Moderate Altitude Exposures.

INTRODUCTION: In fighter aircraft, long-duration high-altitude sorties are typically interrupted by refueling excursions to lower altitude. In normoxia, excursions to moderate cabin altitude may increase the occurrence of venous gas emboli (VGE) at high cabin altitude. The aim was to investigate the effect of hyperoxia on VGE and decompression sickness (DCS) during alternating high and moderate altitude exposure.METHODS: In an altitude chamber, 13 healthy men were exposed to three different conditions: A) 90 min at 24,000 ft (7315 m) breathing normoxic gas (54% O₂; H-NOR); B) 90 min at 24,000 ft breathing hyperoxic gas (90% O₂; H-HYP); and C) three 30-min exposures to 24,000 ft interspersed by two 30-min exposures to 18,000 ft (5486 m) breathing 90% O₂ (ALT-HYP). VGE occurrence was evaluated from cardiac ultrasound imaging. DCS symptoms were rated using a scale.RESULTS: DCS occurred in all conditions and altogether in 6 of the 39 exposures. The prevalence of VGE was similar in H-NOR and H-HYP throughout the exposures. During the initial 30 min at 24,000 ft, the prevalence of VGE was similar in ALT-HYP as in the other two conditions, whereas, after the first excursion to 18,000 ft, the VGE score was lower in ALT-HYP than in H-NOR and H-HYP.DISCUSSION: Hyperoxic excursions from 24,000 to 18,000 ft reduces VGE occurrence, presumably by facilitating diffusive gas exchange across the bubble surfaces, increasing the share of bubble content contributed by oxygen. Still, the excursions did not abolish the DCS risk.Ånell R, Grönkvist M, Gennser M, Eiken O. Hyperoxic effects on decompression strain during alternating high and moderate altitude exposures. Aerosp Med Hum Perform. 2021; 92(4):223230.

Does persistent (patent) foramen ovale closure reduce the risk of recurrent decompression sickness in scuba divers?

Interatrial communication is associated with an increased risk of decompression sickness (DCS) in scuba diving. It has been proposed that there would be a decreased risk of DCS after closure of the interatrial communication, i.e., persistent (patent) foramen ovale (PFO). However, the clinical evidence supporting this is limited. Medical records were reviewed to identify Swedish scuba divers with a history of DCS and catheter closure of an interatrial communication. Thereafter, phone interviews were conducted with questions regarding diving and DCS. All Swedish divers who had had catheter-based PFO-closure because of DCS were followed up, assessing post-closure diving habits and recurrent DCS. Nine divers, all with a PFO, were included. Eight were diving post-closure. These divers had performed 6,835 dives (median 410, range 140-2,200) before closure, and 4,708 dives (median 413, range 11-2,000) after closure. Seven cases with mild and 10 with serious DCS symptoms were reported before the PFO closure. One diver with a small residual shunt suffered serious DCS post-closure; however, that dive was performed with a provocative diving profile. Divers with PFO and DCS continue to dive after PFO closure and this seems to be fairly safe. Our study suggests a conservative diving profile when there is a residual shunt after PFO closure, to prevent recurrent DCS events.

Variability in venous gas emboli following the same dive at 3,658 meters

Exposure to a reduction in ambient pressure such as in high-altitude climbing, flying in aircrafts, and decompression from underwater diving results in circulating vascular gas bubbles (i.e., venous gas emboli [VGE]). Incidence and severity of VGE, in part, can objectively quantify decompression stress and risk of decompression sickness (DCS) which is typically mitigated by adherence to decompression schedules. However, dives conducted at altitude challenge recommendations for decompression schedules which are limited to exposures of 10,000 feet in the U.S. Navy Diving Manual (Rev. 7). Therefore, in an ancillary analysis within a larger study, we assessed the evolution of VGE for two hours post-dive using echocardiography following simulated altitude dives at 12,000 feet. Ten divers completed two dives to 66 fsw (equivalent to 110 fsw at sea level by the cross correction method) for 30 minutes in a hyperbaric chamber. All dives were completed following a 60-minute exposure at 12,000 feet. Following the dive, the chamber was decompressed back to altitude for two hours. Echocardiograph measurements were performed every 20 minutes post-dive. Bubbles were counted and graded using the Germonpré and Eftedal and Brubakk method, respectively. No diver presented with symptoms of DCS following the dive or two hours post-dive at altitude. Despite inter- and intra-diver variability of VGE grade following the dives, the majority (11/20 dives) presented a peak VGE Grade 0, three VGE Grade 1, one VGE Grade 2, four VGE Grade 3, and one VGE Grade 4. Using the cross correction method for a 66-fsw dive at 12,000 feet of altitude resulted in a relatively low decompression stress and no cases of DCS.

Predicting the effect of decompression sickness on survival following submarine tower escape

Purpose The purpose of the present study was the development of a methodology for translating predicted rates of decompression sickness (DCS), following tower escape from a sunken submarine, into predicted probability of survival, a more useful statistic for making operational decisions. Design/methodology/approach Predictions were made, using existing models, for the probabilities of a range of DCS symptoms following submarine tower escape. Subject matter expert estimates of the effect of these symptoms on a submariner’s ability to survive in benign weather conditions on the sea surface until rescued were combined with the likelihoods of the different symptoms occurring using standard probability theory. Plots were generated showing the dependence of predicted probability of survival following escape on the escape depth and the pressure within the stricken submarine. Findings Current advice on whether to attempt tower escape is based on avoiding rates of DCS above approximately 5%–10%. Consideration of predicted survival rates, based on subject matter expert opinion, suggests that the current advice might be considered as conservative in the distressed submarine scenario, as DCS rates of 10% are not anticipated to markedly affect survival rates. Originality/value According to the authors’ knowledge, this study represents the first attempt to quantify the effect of different DCS symptoms on the probability of survival in submarine tower escape.

An echo from the past: Building a Doppler repository for big data in diving research

Decompression sickness (DCS) remains a major operational concern for diving operations, submarine escape and high-altitude jumps. Aside from DCS symptoms, venous gas emboli (VGE) detected with ultrasound postdive are often used as a marker of decompression stress in humans, with a specificity of 100% even though the sensitivity is poor [1]. Being non-invasive, portable and non-ionizing, ultrasound is particularly suited to regular and repeated monitoring. It could help elucidate interand intra-subject variability in VGE and DCS susceptibility, but analyzing these recordings remains a cumbersome task [2].

A review of diving practices and outcomes following the diagnosis of a persistent (patent) foramen ovale in compressed air divers with a documented episode of decompression sickness.

The presence of a persistent (patent) foramen ovale (PFO) increases the risk of decompression sickness (DCS) whilst diving with pressurised air. After the diagnosis of a PFO, divers will be offered a number of options for risk mitigation. The aim of this study was to review the management choices and modifications to diving practices following PFO diagnosis in the era preceding the 2015 joint position statement (JPS) on PFO and diving. A retrospective study was conducted of divers sourced from both the Alfred Hospital, Melbourne and the Divers Alert Network Asia-Pacific during the period 2005-2015. Divers were contacted via a combination of phone, text, mail and email. Data collected included: diving habits (years, style and depths); DCS symptoms, signs and treatment; return to diving and modifications of dive practices; history of migraine and echocardiography (ECHO) pre- and post-intervention; ECHO technique(s) used, and success or failure of PFO closure (PFOC). Analyses were performed to compare the incidence of DCS pre- and post-PFO diagnosis. Seventy-three divers were interviewed. Sixty-eight of these returned to diving following the diagnosis of PFO. Thirty-eight underwent PFOC and chose to adopt conservative diving practices (CDPs); 15 chose PFOC with no modification to practices; 15 adopted CDPs alone; and five have discontinued diving. The incidence of DCS decreased significantly following PFOC and/or adoption of conservative diving practices. Of interest, migraine with aura resolved in almost all those who underwent PFOC. Many divers had already adopted practices consistent with the 2015 JPS permitting the resumption of scuba diving with a lowering of the incidence of DCS to that of the general diving population. These results support the recommendations of the JPS.

Risk factors of decompression sickness in scuba diving

BackgroundRecreational diving with aqualung can be called an extreme sport because the divers are exposed to physical and psychological risks. A serious danger in diving is the very exposure to a change in pressure underwater, which every diver must deal with. That kind of danger may cause many problems related to any pressure exposure and unfortunately, diving-related illnesses have shown the increasing tendency. Recreational divers are the most numerous group among the people who suffer from decompression sickness (DCS) and alas, similar condition can be expected in future years. Aim of this literature review was to determine the risk factors of decompression sickness after scuba diving.Materials and methodsMaterial for this literature review was found by two independent authors searching PubMed, Cochrane library and ScienceDirect databases by using a combination of keywords: „scuba diving”, „risk factors”, „decompression sickness”, „DCS”. Finally, 4 publications qualified for a review of literature.ResultsMany authors presented factors such as patent foramen ovale, BMI and fat mass, age, diving exposure, heavy exercise, sex, strong current, workload during diving, circulatory right-to-left shunt and the lack of changes in the diving style to have an impact on developing DCS. In the opposite, one study stated that overweight and gender had minor contribution to DSC.ConclusionsRisk factors of decompression sickness in scuba diving could be: high-grade PFO, age, diving exposure, strong current, heavy exercise, workload during diving, dehydration, repetitive diving, violation of dive profiles, experience in diving, presence of circulatory right-to-left shunt and the lack of changes in the diving style after previous DCS episode. Further research is needed to verify the role of gender and fat mass in developing symptoms of decompression sickness.

Tetranomial decompression sickness model using serious, mild, marginal, and non-event outcomes

Abstract Decompression sickness (DCS) is a condition resulting from reductions in ambient pressure, causing inert gas bubbles in tissues. This work focuses on hyperbaric exposures, specifically DCS resulting from underwater diving. Signs and symptoms of DCS can range from mild skin rashes and joint pain to serious neurological and cardiological malfunction, and even death. Marginal DCS is defined as symptoms associated with DCS that resolve spontaneously without recompression treatment. There are two categories of decompression modeling used to mitigate risk of DCS: deterministic and probabilistic; neither address DCS symptom severity. Symptom severity is important to U.S. Navy dive planning, as the Navy has different limits for the number allowable cases of mild-symptom DCS and more severe-symptom DCS for a given dive. In this work, a probabilistic model for predicting the tetranomial outcomes of serious, mild, marginal, and no DCS was developed, analyzed, and compared with trinomial and trinomial marginal models from our previous works. Six variants of exponential-exponential (EE1) and linear-exponential (LE1) models were calibrated with 3322 air and N2–O2 dive exposures detailed in the BIG292 empirical human dive trial data set. Two methods of symptom severity splitting were compared. The log likelihood difference test indicated the LE1 model using a previously-disclosed Type A/B splitting provided the best fit to the empirical dive data of all tetranomial models tested in this work. When comparing this tetranomial model to our previous trinomial and trinomial marginal models using the Pearson chi-squared statistic, we find that the tetranomial and trinomial marginal models’ predictions of marginal DCS are not aligned well with the incidence of marginal DCS in the data. Both the trinomial marginal model in our previous work and tetranomial model presented here are unable to accurately replicate the occurrence of marginal DCS events observed in the BIG292 dataset. These marginal DCS events may hinder model fit during calibration. We recommend the use of the trinomial model from our previous work, which simultaneously predicts the probability of mild, serious, and no DCS.

Demonstration by Infra-Red Imaging of a Temperature Control Defect in a Decompression Sickness Model Testing Minocycline.

The prevention, prognosis and resolution of decompression sickness (DCS) are not satisfactory. The etiology of DCS has highlighted thrombotic and inflammatory phenomena that could cause severe neurological disorders or even death. Given the immunomodulatory effects described for minocycline, an antibiotic in widespread use, we have decided to explore its effects in an experimental model for decompression sickness. 40 control mice (Ctrl) and 40 mice treated orally with 90 mg/kg of minocycline (MINO) were subjected to a protocol in a hyperbaric chamber, compressed with air. The purpose was to mimic a scuba dive to a depth of 90 msw and its pathogenic decompression phase. Clinical examinations and blood counts were conducted after the return to the surface. For the first time they were completed by a simple infrared (IR) imaging technique in order to assess feasibility and its clinical advantage in differentiating the sick mice (DCS) from the healthy mice (NoDCS). In this tudy, exposure to the hyperbaric protocol provoked a reduction in the number of circulating leukocytes. DCS in mice, manifesting itself by paralysis or convulsion for example, is also associated with a fall in platelets count. Cold areas ( < 25°C) were detected by IR in the hind paws and tail with significant differences (p < 0.05) between DCS and NoDCS. Severe hypothermia was also shown in the DCS mice. The ROC analysis of the thermograms has made it possible to determine that an average tail temperature below 27.5°C allows us to consider the animals to be suffering from DCS (OR = 8; AUC = 0.754, p = 0.0018). Minocycline modulates blood analysis and it seems to limit the mobilization of monocytes and granulocytes after the provocative dive. While a higher proportion of mice treated with minocycline experienced DCS symptoms, there is no significant difference. The infrared imaging has made it possible to show severe hypothermia. It suggests an modification of thermregulation in DCS animals. Surveillance by infrared camera is fast and it can aid the prognosis in the case of decompression sickness in mice.

Pulmonary ventilation-perfusion mismatch: a novel hypothesis for how diving vertebrates may avoid the bends.

Hydrostatic lung compression in diving marine mammals, with collapsing alveoli blocking gas exchange at depth, has been the main theoretical basis for limiting N2 uptake and avoiding gas emboli (GE) as they ascend. However, studies of beached and bycaught cetaceans and sea turtles imply that air-breathing marine vertebrates may, under unusual circumstances, develop GE that result in decompression sickness (DCS) symptoms. Theoretical modelling of tissue and blood gas dynamics of breath-hold divers suggests that changes in perfusion and blood flow distribution may also play a significant role. The results from the modelling work suggest that our current understanding of diving physiology in many species is poor, as the models predict blood and tissue N2 levels that would result in severe DCS symptoms (chokes, paralysis and death) in a large fraction of natural dive profiles. In this review, we combine published results from marine mammals and turtles to propose alternative mechanisms for how marine vertebrates control gas exchange in the lung, through management of the pulmonary distribution of alveolar ventilation () and cardiac output/lung perfusion (), varying the level of in different regions of the lung. Man-made disturbances, causing stress, could alter the mismatch level in the lung, resulting in an abnormally elevated uptake of N2, increasing the risk for GE. Our hypothesis provides avenues for new areas of research, offers an explanation for how sonar exposure may alter physiology causing GE and provides a new mechanism for how air-breathing marine vertebrates usually avoid the diving-related problems observed in human divers.

Specifics of Gas Bubble Formation and Growth in Tissues during Decompression after Saturation Dives

It is shown that the decompression schedules after saturation diving to the depth of 30 m designed to hold the nitrogen supersaturation for the most “slow” tissues at the acceptable levels is significantly shorter than the decompression schedules with zero supersaturation of these tissues with nitrogen and all dissolved gases. Equality of the risk for decompression sickness (DCS) onset during this decompression schedule to the risk of DCS onset under non-stop ascent to the surface after saturation diving to the depth of 6.1 m indicates that the effect of the high ambient pressure decreases the density of gas bubble seeds in tissues and the growth rate of their total volume. The DCS symptoms in the experienced divers under dangerous decompression profiles not appear due to the lower density of gas bubble seeds in their tissues relatively to the average level inherent to the many of humans.

Evidence of Heritable Determinants of Decompression Sickness in Rats.

Decompression sickness (DCS) is a complex and poorly understood systemic disease caused by inadequate desaturation after a decrease of ambient pressure. Strong variability between individuals is observed for DCS occurrence. This raises questions concerning factors that may be involved in the interindividual variability of DCS occurrence. This study aimed to experimentally assess the existence of heritable factors involved in DCS occurrence by selectively breeding individuals resistant to DCS from a population stock of Wistar rats. Fifty-two male and 52 female Wistar rats were submitted to a simulated air dive known to reliably induce about 63% DCS: compression was performed at 100 kPa·min up to 1000 kPa absolute pressure before a 45-min long stay. Decompression was performed at 100 kPa·min with three decompression stops: 5 min at 200 kPa, 5 min at 160 kPa, and 10 min at 130 kPa. Animals were observed for 1 h to detect DCS symptoms. Individuals without DCS were selected and bred to create a new generation, subsequently subjected to the same hyperbaric protocol. This procedure was repeated up to the third generation of rats. As reported previously, this diving profile induced 67% of DCS, and 33% asymptomatic animals in the founding population. DCS/asymptomatic ratio was not initially different between sexes, although males were heavier than females. In three generations, the outcome of the dive significantly changed from 33% to 67% asymptomatic rats, for both sexes. Interestingly, survival in females increased sooner than in males. This study offers evidence suggesting the inheritance of DCS resistance. Future research will focus on genetic and physiological comparisons between the initial strain and the new resistant population.

Dive Risk Factors, Gas Bubble Formation, and Decompression Illness in Recreational SCUBA Diving: Analysis of DAN Europe DSL Data Base.

Introduction: The popularity of SCUBA diving is steadily increasing together with the number of dives and correlated diseases per year. The rules that govern correct decompression procedures are considered well known even if the majority of Decompression Sickness (DCS) cases are considered unexpected confirming a bias in the “mathematical ability” to predict DCS by the current algorithms. Furthermore, little is still known about diving risk factors and any individual predisposition to DCS. This study provides an in-depth epidemiological analysis of the diving community, to include additional risk factors correlated with the development of circulating bubbles and DCS.Materials and Methods: An originally developed database (DAN DB) including specific questionnaires for data collection allowed the statistical analysis of 39,099 electronically recorded open circuit dives made by 2,629 European divers (2,189 males 83.3%, 440 females 16.7%) over 5 years. The same dive parameters and risk factors were investigated also in 970 out of the 39,099 collected dives investigated for bubble formation, by 1-min precordial Doppler, and in 320 sea-level dives followed by DCS symptoms.Results: Mean depth and GF high of all the recorded dives were 27.1 m, and 0.66, respectively; the average ascent speed was lower than the currently recommended “safe” one (9–10 m/min). We found statistically significant relationships between higher bubble grades and BMI, fat mass, age, and diving exposure. Regarding incidence of DCS, we identified additional non-bubble related risk factors, which appear significantly related to a higher DCS incidence, namely: gender, strong current, heavy exercise, and workload during diving. We found that the majority of the recorded DCS cases were not predicted by the adopted decompression algorithm and would have therefore been defined as “undeserved.”Conclusion: The DAN DB analysis shows that most dives were made in a “safe zone,” even if data show an evident “gray area” in the “mathematical” ability to predict DCS by the current algorithms. Some other risk factors seem to influence the possibility to develop DCS, irrespective of their effect on bubble formation, thus suggesting the existence of some factors influencing or enhancing the effects of bubbles.

Evolution of the plasma proteome of divers before and after a single SCUBA dive.

Decompression sickness (DCS) is a poorly understood and complex systemic disease caused by inadequate desaturation following a reduction of ambient pressure. A previous proteomic study of ours showed that DCS occurrence but not diving was associated with changes in the plasma proteome in rats, including a dramatic decrease of abundance of the tetrameric form of Transthyretin (TTR). The present study aims to assess the impact on the human blood proteome of a dive inducing significant decompression stress but without inducing DCS symptoms. Twelve healthy male divers were subjected to a single dive at a depth of 18 m of sea water (msw) with a 47-min bottom time followed by a direct ascent to the surface at a rate of 9 msw/min. Venous blood was collected before the dive as well as 30 min and 2 h following the dive. The plasma proteomes from four individuals were then analyzed by using a two-dimensional electrophoresis-based proteomic strategy. No protein spot showed a significantly changed abundance (fdr< 0.1) between the tested times. These results strengthen the hypothesis according to which significant changes of the plasma proteome measurable with two-dimensional electrophoresis may only occur along with DCS symptoms.

Effect of simulated air dive and decompression sickness on the plasma proteome of rats.

Decompression sickness (DCS) is a poorly understood systemic disease caused by inadequate desaturation following a reduction in ambient pressure. Although recent studies highlight the importance of circulating factors, the available data are still puzzling. In this study, we aimed to identify proteins and biological pathways involved in the development of DCS in rats. Eighteen male Sprague-Dawley rats were subjected to a same simulated air dive to 1000kPa absolute pressure and divided into two groups: no DCS or DCS. A third control group remained at atmospheric pressure. Venous blood was collected after hyperbaric exposure and the plasma proteomes from four individuals per group were analyzed by using a two-dimensional electrophoresis-based proteomic strategy. Quantitative analysis identified nine protein spots with abundances significantly changed (false discovery rate < 0.1) between the tested conditions. Three protein spots, identified as Apolipoprotein A1, Serine Protease Inhibitor A3K (Serpin A3K), and Alpha-1-antiproteinase, appeared increased in DCS animals but displayed only weak changes. By contrast, one protein spot identified as Transthyretin (TTR) dramatically decreased (i.e. quite disappeared) in animals displaying DCS symptoms. Before diving, TTR level was not different in DCS than nondiving group. These results may lead to the use of TTR as an early biomarker of DCS.