Hypoxic loss of consciousness in air diving: two cases of mixtures made hypoxic by oxidation of the scuba diving cylinder.

Without an adequate supply of oxygen from the scuba apparatus, humans would not be able to dive. The air normally contained in a scuba tank is dry and free of toxic gases. The presence of liquid in the tank can cause corrosion and change the composition of the gas mixture. Various chemical reactions consume oxygen, making the mixture hypoxic. We report two cases of internal corrosion of a scuba cylinder rendering the respired gas profoundly hypoxic and causing immediate hypoxic loss of consciousness in divers.

Therapeutic management of severe spinal cord decompression sickness in a hyperbaric center.

Introduction: Spinal cord decompression sickness (scDCS) unfortunately has a high rate of long-term sequelae. The purpose of this study was to determine the best therapeutic management in a hyperbaric center and, in particular, the influence of hyperbaric treatment performed according to tables at 4 atm (Comex 30) or 2.8 atm abs (USNT5 or T6 equivalent). Methods: This was a retrospective study that included scDCS with objective sensory or motor deficit affecting the limbs and/or sphincter impairment seen at a single hyperbaric center from 2010 to 2020. Information on dive, time to recompression, and in-hospital management (hyperbaric and medical treatments such as lidocaine) were analyzed as predictor variables, as well as initial clinical severity and clinical deterioration in the first 24 h after initial recompression. The primary endpoint was the presence or absence of sequelae at discharge as assessed by the modified Japanese Orthopaedic Association score. Results: 102 divers (52 ± 16 years, 20 female) were included. In multivariate analysis, high initial clinical severity, deterioration in the first 24 h, and recompression tables at 4 atm versus 2.8 atm abs for both initial and additional recompression were associated with incomplete neurological recovery. Analysis of covariance comparing the effect of initial tables at 2.8 versus 4 atm abs as a function of initial clinical severity showed a significantly lower level of sequelae with tables at 2.8 atm. In studying correlations between exposure times to maximum or cumulative O2 dose and the degree of sequelae, the optimal initial treatment appears to be a balance between administration of a high partial pressure of O2 (2.8 atm) and a limited exposure duration that does not result in pulmonary oxygen toxicity. Further analysis suggests that additional tables in the first 24-48 h at 2.8 atm abs with a Heliox mixture may be beneficial, while the use of lidocaine does not appear to be relevant. Conclusion: Our study shows that the risk of sequelae is related not only to initial severity but also to clinical deterioration in the first 24 h, suggesting the activation of biological cascades that can be mitigated by well-adapted initial and complementary hyperbaric treatment.

Validation of sham treatment in hyperbaric medicine: a randomised trial.

INTRODUCTION: This study aimed to determine the lowest possible atmospheric pressure in the 111-152 kPa (1.1-1.5 atmospheres absolute [atm abs]) range that would require the patients to equalise their ears, allowing an effective sham for a 203 kPa (2.0 atm abs) hyperbaric exposure. METHODS: We performed a randomised controlled study on 60 volunteers divided into 3 groups (compression to 111, 132 and 152 kPa (1.1, 1.3, 1.5 atm abs) to determine the minimum pressure to obtain blinding. Secondly, we applied additional blinding strategies (faster compression with ventilation during the fictitious compression time, heating at compression, cooling at decompression) on 25 new volunteers in order to enhance blinding. RESULTS: The number of participants who did not believe they had been compressed to 203 kPa was significantly higher in the 111 kPa compressed arm than in the other two arms (11/18 vs 5/19 and 4/18 respectively; P = 0.049 and P = 0.041, Fisher's exact test). There was no difference between compressions to 132 and 152 kPa. By applying additional blinding strategies, the number of participants who believed they had been compressed to 203 kPa increased to 86.5 %. CONCLUSIONS: A compression to 132 kPa, (1.3 atm abs, 3 metres of seawater equivalent) combined with the additional blinding strategies of forced ventilation, enclosure heating and compression in five minutes, simulates a therapeutic compression table and can be used as a hyperbaric placebo.

[Hyperbaric oxygen therapy for the treatment of radiation-induced cystitis]. / Oxygénothérapie hyperbare dans le traitement de la cystite radio-induite.

Radiation-induced cystitis (RIHC) is a late complication of pelvic radiation therapy defined by irritative lower urinary tract symptoms with recurrent and sometimes refractory hematuria. Conservative or endoscopic treatments are the first lines, but cystectomy in required in refractory cases. Hyperbaric oxygen therapy (HOT) has recently emerged in the management charts for recurrent and refractory hematuria. Thanks to its neoangiogenic and stem-cell stimulation properties, HOT achieves a complete resolution of hematuria in almost two third of patients and appears to be a good therapeutic alternative for this fragile population. However, its geographical availability is currently limited in Switzerland and its implementation can sometimes require long hospital stays.

La cystite radio-induite (CR) est une complication tardive de la radiothérapie pelvienne se présentant notamment sous forme de troubles mictionnels irritatifs ou de macrohématurie récidivante. Le traitement est initialement conservateur ou endoscopique mais peut, dans des cas réfractaires, aboutir à une cystectomie à visée hémostatique ou fonctionnelle. L'oxygénothérapie hyperbare (OHB) a récemment fait son apparition dans les diagrammes de prise en charge de la CR réfractaire. Grâce à ses propriétés néoangiogéniques et à la stimulation des cellules souches, elle permet une résolution complète de l'hématurie chez près de deux tiers des patients et semble être une alternative thérapeutique pour cette population fragile. Actuellement, sa disponibilité géographique reste toutefois limitée en Suisse et sa réalisation implique parfois de longues hospitalisations.

[Hypertension and SCUBA diving]. / Hypertension artérielle et plongée sous-marine.

Hypertension is a major cardiovascular risk factor in our population. This condition is widely recognized as an exacerbating factor for several physiopathological mechanisms, especially under an intense physical effort. In this article we focus on the link between high blood pressure and risk factors in scuba diving. In particular, we illustrate how a hypertensive diver is exposed to an increased risk of acute immersion pulmonary edema, as well as cardiac death.

L'hypertension artérielle est un facteur de risque cardiovasculaire prépondérant dans notre population. Elle est reconnue comme pouvant exacerber de nombreux mécanismes physiopathologiques lors de conditions d'efforts. Dans cet article, nous nous focalisons sur le lien entre l'hypertension artérielle et le risque qu'elle pourrait représenter lors de la pratique de la plongée sous-marine. En particulier, nous illustrerons comment un plongeur hypertendu peut être exposé à un risque augmenté d'œdème pulmonaire aigu d'immersion, ainsi qu'à la mort subite d'origine cardiaque.

Successful Delayed Hyperbaric Oxygen Therapy and Iloprost Treatment on Severe Frostbite at High Altitude.

Magnan, Dre Marie-Anne, Marco Gelsomino, Pierre Louge, and Rodrigue Pignel. Successful delayed hyperbaric oxygen therapy and iloprost treatment on severe frostbite at high altitude. High Alt Med Biol. 23:294-297, 2022.-Frostbite is an injury caused when tissues freeze. Severe frostbite can result in amputation. Hyperbaric oxygen therapy (HBO) may improve frostbite outcome. The patient, a 36-year-old man, was climbing above 6,000 m in Kyrgystan when he fell into a crevasse and lost his gloves. The outside temperature was -30°C. He sustained grade 3 frostbite of both hands, which carries a high amputation risk. He was rescued by local responders and transported to the local hospital: neither rapid rewarming in warm water nor other specific frostbite treatment was given. The patient was repatriated to Geneva (day 2). On day 3, he received medical care including iloprost infusion for 7 days and daily HBO for 3 weeks. His hands healed in <1 month. He suffered no amputation. At 6-month follow-up, no early arthritis was found. Three years later he was able to climb again and play volleyball. He still does not have any clinical arthritis at 4-year follow-up. Iloprost is less effective when initiated longer than 48 hours after frostbite injury. Despite the delay, the patient did not require amputation, as might have been predicted by the injury. The combination of HBO and iloprost may have contributed to this favorable outcome.

Fatal diving: could it be an immersion pulmonary edema? Case report.

Immersion pulmonary edema is a rare, underrecognized, and potentially lethal pathology developing during scuba diving and other immersion-related activities (swimming or apnoea). Physiopathology is complex and not fully understood, but its mechanisms involve an alteration of the alveolo-capillary barrier caused by transcapillary pressure elevation during immersion, leading to an accumulation of fluid and blood in the alveolar space. Diagnosis remains a challenge for clinicians and forensic practionner. The symptoms begin during ascent, with cough, frothy sputum, and hemoptysis. Auscultation reveals signs of pulmonary edema. Pulmonary CT scan, which is the radiological exam of choice, shows ground glass opacities and interlobular thickening, eventually demonstrating a patterned distribution, likely in the anterior segments of both lungs. Apart from the support of vital functions, there is no specific treatment and hyperbaric oxygen therapy is not systematically recommended. We present a case of fatal IPE occurring in a recreational diver who unfortunately died shortly after his last dive. Diagnosis was made after complete forensic investigations including post-mortem-computed tomography, complete forensic autopsy, histological examination, and toxicological analysis.

Influence of prehospital management on the outcome of spinal cord decompression sickness in scuba divers.

BACKGROUND: Decompression sickness (DCS) with spinal cord involvement has an unfortunately high rate of long-term sequelae. The objective of this study was to determine the association of prehospital variables on the outcome of spinal cord DCS, especially the influence of the initial clinical presentation and the time to recompression. METHODS: This was a retrospective study using prospectively collected data which included divers with spinal cord DCS seen at a single hyperbaric centre study from 2010 to 2018. Information regarding dive, latency of onset of symptoms, time to recompression and prehospital management, that is, use of oxygen, treatment and means of evacuation, were analysed as predictor variables. The initial clinical severity was estimated by the score of the French society of diving and hyperbaric medicine (MEDSUBHYP). The primary end point was the presence or absence of sequelae at discharge assessed by the modified score of the Japanese Orthopedic Association. RESULTS: 195 divers (48±12 years, 42 women) were included. 34% had neurological sequelae at discharge. In multivariate analysis, a MEDSUBHYP score ≥6 and a time to recompression >194 min were significantly associated with incomplete neurological recovery (OR 9.5 (95% CI 4.6 to 19.8), p<0.0001 and OR 2.1 (95% CI 1.03 to 4.5), p=0.04, respectively). Time to recompression only appeared to be significant for patients with high initial clinical severity. As time to recompression increased, the level of sequelae also increased (p=0.014). CONCLUSION: Determining the initial clinical severity is critical in identifying patients who need to be evacuated for recompression as quickly as possible.

Hyperbaric Oxygen Therapy with Iloprost Improves Digit Salvage in Severe Frostbite Compared to Iloprost Alone.

Background and Objectives: Frostbite is a freezing injury that can lead to amputation. Current treatments include tissue rewarming followed by thrombolytic or vasodilators. Hyperbaric oxygen (HBO) therapy might decrease the rate of amputation by increasing cellular oxygen availability to the damaged tissues. The SOS-Frostbite study was implemented in a cross-border program among the hyperbaric centers of Geneva, Lyon, and the Mont-Blanc hospitals. The objective was to assess the efficacy of HBO + iloprost among patients with severe frostbite. Materials and Methods: We conducted a multicenter prospective single-arm study from 2013 to 2019. All patients received early HBO in addition to standard care with iloprost. Outcomes were compared to a historical cohort in which all patients received iloprost alone between 2000 and 2012. Inclusion criteria were stage 3 or 4 frostbite and initiation of medical care <72 h from frostbite injury. Outcomes were the number of preserved segments and the rate of amputated segments. Results: Thirty patients from the historical cohort were eligible and satisfied the inclusion criteria, and 28 patients were prospectively included. The number of preserved segments per patient was significantly higher in the prospective cohort (mean 13 ± SD, 10) compared to the historical group (6 ± 5, p = 0.006); the odds ratio was significantly higher by 45-fold (95%CI: 6-335, p < 0.001) in the prospective cohort compared to the historical cohort after adjustment for age and delay between signs of freezing and treatment start. Conclusions: This study demonstrates that the combination of HBO and iloprost was associated with higher benefit in patients with severe frostbite. The number of preserved segments was two-fold higher in the prospective cohort compared to the historical group (mean of 13 preserved segments vs. 6), and the reduction of amputation was greater in patients treated by HBO + iloprost compared with the iloprost only.

Decompression illness treated at the Geneva hyperbaric facility 2010-2016: A retrospective analysis of local cases.

INTRODUCTION: The Geneva hyperbaric chamber is the main treatment centre for decompression illness (DCI) in Switzerland. The characteristics, symptomatology, treatment and short-term outcome of divers treated at this chamber have not previously been investigated. METHODS: This was a retrospective study of patients treated with hyperbaric oxygen (HBO) for DCI from 2010 to 2016. Data were analysed to provide a description of the cases and statistical analysis for possible factors associated with an unfavourable outcome. RESULTS: One hundred and thirty-five patients were treated for DCI. Ninety-two were included in the study. Sixty-four presented with neurological and 28 with mild DCI. One hundred and thirty-five patients were treated for DCI. Ninety-two were included in the study. Sixty-four presented with neurological and 28 with mild DCI. Patients with mild DCI mainly had musculoskeletal symptoms (79%). Patients with neurological DCI mainly had spinal (55%), followed by vestibular (36%) symptoms. Arterial gas embolism was diagnosed in 30% of cases. Diving depths ranged between 15 and 142 metres, and dive times between two and 241 min. Median time to treatment was 6 h. Patients with neurological DCI had a high rate (25%) of persisting deficits after treatment. Older age was associated with an unfavourable outcome in univariate but not in multivariate analysis. No adverse effects of HBO were observed. For spinal DCI, a high Boussuges score was associated with persisting deficits after treatment. CONCLUSIONS: Our findings are consistent with other series. Severe DCI was associated with a high rate of persisting deficits. No single factor was associated with a negative outcome. A Boussuges score > 7 had sensitivity of 90% and positive predictive value 53% for predicting an unfavourable outcome in spinal DCI.

Can preventive hyperbaric oxygen therapy optimise surgical outcome?: A systematic review of randomised controlled trials.

BACKGROUND: A primary underlying cause of postoperative complications is related to the surgical stress response, which may be mitigated by hyperbaric oxygen therapy (HBOT), the intermittent administration of oxygen at a pressure higher than the atmospheric pressure at sea level. Promising clinical studies have emerged suggesting HBOT's efficacy for reducing some postoperative complications. Notwithstanding, the effectiveness (if any) of HBOT across a range of procedures and postoperative outcomes has yet to be clearly quantified. OBJECTIVE: This systematic review aimed to summarise the existing literature on peri-operative HBOT to investigate its potential to optimise surgical patient outcome. DESIGN: A systematic review of randomised controlled trials (RCTs) with narrative summary of results. DATA SOURCES: MEDLINE, EMBASE, CINAHL and the Cochrane Central Register of Controlled Trials were searched without language restrictions through to 19 June 2018. ELIGIBILITY CRITERIA: Studies were included if they involved patients of any age undergoing any surgical procedure and provided with at least one HBOT session in the peri-operative period. Two independent reviewers screened the initial identified trials and determined those to be included. Risk of bias was assessed using the Cochrane Risk of Bias tool for RCTs. RESULTS: The search retrieved 775 references, of which 13 RCTs were included (627 patients). Ten RCTs (546 patients) reported treatment was effective for improving at least one of the patient outcomes assessed, while two studies (55 patients) did not find any benefit and one study (26 patients) found a negative effect. A wide range of patient outcomes were reported, and several other methodological limitations were observed among the included studies, such as limited use of sham comparator and lack of blinding. CONCLUSION: Peri-operative preventive HBOT may be a promising intervention to improve surgical patient outcome. However, future work should consider addressing the methodological weaknesses identified in this review. TRIAL REGISTRATION: The protocol (CRD42018102737) was registered with the International ProspectiveRegister of Systematic Reviews (PROSPERO).

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

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

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.

Physiological stress markers during breath-hold diving and SCUBA diving.

This study investigated the sources of physiological stress in diving by comparing SCUBA dives (stressors: hydrostatic pressure, cold, and hyperoxia), apneic dives (hydrostatic pressure, cold, physical activity, hypoxia), and dry static apnea (hypoxia only). We hypothesized that despite the hypoxia induces by a long static apnea, it would be less stressful than SCUBA dive or apneic dives since the latter combined high pressure, physical activity, and cold exposure. Blood samples were collected from 12SCUBA and 12 apnea divers before and after dives. On a different occasion, samples were collected from the apneic group before and after a maximal static dry apnea. We measured changes in levels of the stress hormones cortisol and copeptin in each situation. To identify localized effects of the stress, we measured levels of the cardiac injury markers troponin (cTnI) and brain natriuretic peptide (BNP), the muscular stress markers myoglobin and lactate), and the hypoxemia marker ischemia-modified albumin (IMA). Copeptin, cortisol, and IMA levels increased for the apneic dive and the static dry apnea, whereas they decreased for the SCUBA dive. Troponin, BNP, and myoglobin levels increased for the apneic dive, but were unchanged for the SCUBA dive and the static dry apnea. We conclude that hypoxia induced by apnea is the dominant trigger for the release of stress hormones and cardiac injury markers, whereas cold or and hyperbaric exposures play a minor role. These results indicate that subjects should be screened carefully for pre-existing cardiac diseases before undertaking significant apneic maneuvers.

Troponins in scuba divers with immersion pulmonary edema.

Immersion pulmonary edema (IPE) is a serious complication of water immersion during scuba diving. Myocardial ischemia can occur during IPE that worsens outcome. Because myocardial injury impacts the therapeutic management, we aim to evaluate the profile of cardiac markers (creatine phosphokinase (CPK), brain natriuretic peptide (BNP), highly sensitive troponin T (TnT-hs) and ultrasensitive troponin I (TnI-us) of divers with IPE. Twelve male scuba divers admitted for suspected IPE were included. The collection of blood samples was performed at hospital entrance (T0) and 6 h later (T0 + 6 h). Diagnosis was confirmed by echocardiography or computed-tomography scan. Mean ± S.D. BNP (pg/ml) was 348 ± 324 at T0 and 223 ± 177 at T0 + 6 h (P<0.01), while mean CPK (international units (IUs)), and mean TnT-hs (pg/ml) increased in the same times 238 ± 200 compared with 545 ± 39, (P=0.008) and 128 ± 42 compared with 269 ± 210, (P=0.01), respectively; no significant change was observed concerning TnI-us (pg/ml): 110 ± 34 compared with 330 ± 77, P=0.12. At T0 + 6 h, three patients had high TnI-us, while six patients had high TnT-hs. Mean CPK was correlated with TnT-hs but not with TnI-us. Coronary angiographies were normal. The increase in TnT during IPE may be secondary to the release of troponin from non-cardiac origin. The measurement of TnI in place of TnT permits in some cases to avoid additional examinations, especially unnecessary invasive investigations.

The Key Roles of Negative Pressure Breathing and Exercise in the Development of Interstitial Pulmonary Edema in Professional Male SCUBA Divers.

BACKGROUND: Immersion pulmonary edema is potentially a catastrophic condition; however, the pathophysiological mechanisms are ill-defined. This study assessed the individual and combined effects of exertion and negative pressure breathing on the cardiovascular system during the development of pulmonary edema in SCUBA divers. METHODS: Sixteen male professional SCUBA divers performed four SCUBA dives in a freshwater pool at 1 m depth while breathing air at either a positive or negative pressure both at rest or with exercise. Echocardiography and lung ultrasound were used to assess the cardiovascular changes and lung comet score (a measure of interstitial pulmonary edema). RESULTS: The ultrasound lung comet score was 0 following both the dives at rest regardless of breathing pressure. Following exercise, the mean comet score rose to 4.2 with positive pressure breathing and increased to 15.1 with negative pressure breathing. The development of interstitial pulmonary edema was significantly related to inferior vena cava diameter, right atrial area, tricuspid annular plane systolic excursion, right ventricular fractional area change, and pulmonary artery pressure. Exercise combined with negative pressure breathing induced the greatest changes in these cardiovascular indices and lung comet score. CONCLUSIONS: A diver using negative pressure breathing while exercising is at greatest risk of developing interstitial pulmonary edema. The development of immersion pulmonary edema is closely related to hemodynamic changes in the right but not the left ventricle. Our findings have important implications for divers and understanding the mechanisms of pulmonary edema in other clinical settings.

Reliability of right-to-left shunt screening in the prevention of scuba diving related-decompression sickness.

OBJECTIVES: The aim of this study was to investigate the relationship between right-to-left shunt (RLS) and the clinical features of decompression sickness (DCS) in scuba divers and to determine the potential benefit for screening this anatomical predisposition in primary prevention. METHODS: 634 injured divers treated in a single referral hyperbaric facility for different types of DCS were retrospectively compared to 259 healthy divers. All subjects had a RLS screening by contrast Transcranial Doppler (TCD) ultrasound according to a standardized method. The number of bubbles detected defined the degree of RLS (small if 5-20 bubbles, large if >20 bubbles). RESULTS: TCD detected 63% RLS in DCS group versus 32% in the control group (p<0.0001) The overall prevalence of RLS was higher in divers presenting a cerebral DCS (OR, 5.3 [95% CI, 3.2-8.9]; p<0.0001), a spinal cord DCS (OR, 2.1 [95% CI, 1.4-3.1]; p<0.0001), an inner ear DCS (OR, 11.8 [95% CI, 7.4-19]; p<0.0001) and a cutaneous DCS (OR, 17.3 [95% CI, 3.9-77]; p<0.0001) compared to the control group, but not in divers experiencing ambiguous symptoms or musculoskeletal DCS. There was in increased risk of DCS with the size of RLS. The determination of diagnostic accuracy of TCD testing through the estimation of likelihood ratios revealed that predetermination of RLS did not change significantly the prediction of developing or not a DCS event. CONCLUSION: The assessment of RLS remains indicated after an initial episode of spinal cord, cerebral, inner ear and cutaneous form of DCS but this approach is definitely not recommended in routine practice.

Initial Severity Scoring and Residual Deficit in Scuba Divers with Inner Ear Decompression Sickness.

BACKGROUND: Inner ear decompression sickness (IEDCS) in scuba diving results in residual vestibulocochlear deficits with a potential impact on health-related quality of life. The aim of this study was to determine the predictive factors for poor clinical recovery and to try to establish a prognostic score on initial physical examination. METHODS: The medical records of injured divers with IEDCS treated in our facility between 2009 and 2014 were retrospectively analyzed. The clinical severity of the deficit was evaluated on admission using a numerical scoring system taking into account the intensity of vestibular symptoms and the presence of cochlear signs. The clinical outcome was assessed at 3 mo by telephone interview. After multivariate analysis of potential risk factors for sequelae, the discriminating value of the score and these prognostic reliability indices were calculated. RESULTS: Among the 99 patients included in the study, 24% still had residual symptoms. Statistical analysis revealed that only a high clinical score [OR = 1.39 (95% CI 1.13-1.71)] and a delay in hyperbaric recompression >6 h [OR = 1.001 (95% CI 1-1.003)] were independently associated with incomplete recovery. The advantage of the score lay in its highly specific nature (92%) rather than its sensitivity (48%) for a threshold of 10. CONCLUSION: Results suggest that the severity of IEDCS can be easily determined by a clinical score during the acute phase. Recompression treatment should not be delayed. Gempp E, Louge P, de Maistre S, Morvan J-B, Vallée N, Blatteau J-E. Initial severity scoring and residual deficit in scuba divers with inner ear decompression sickness. Aerosp Med Hum Perform. 2016; 87(8):735-739.

Gut fermentation seems to promote decompression sickness in humans.

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

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

Immersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal. IPE is thought to involve hemodynamic and cardiovascular disturbances, but its pathophysiology remains largely unclear, which makes IPE prevention difficult. This observational study aimed to document IPE pathogenesis and improve diagnostic reliability, including distinguishing in some conditions IPE from decompression sickness (DCS), another diving-related disorder.Thirty-one patients (19 IPE, 12 DCS) treated at the Hyperbaric Medicine Department (Ste-Anne hospital, Toulon, France; July 2013-June 2014) were recruited into the study. Ten healthy divers were recruited as controls. We tested: (i) copeptin, a surrogate marker for antidiuretic hormone and a stress marker; (ii) ischemia-modified albumin, an ischemia/hypoxia marker; (iii) brain-natriuretic peptide (BNP), a marker of heart failure, and (iv) ultrasensitive-cardiac troponin-I (cTnI), a marker of myocardial ischemia.We found that copeptin and cardiac biomarkers were higher in IPE versus DCS and controls: (i) copeptin: 68% of IPE patients had a high level versus 25% of DCS patients (P < 0.05) (mean ±â€Šstandard-deviation: IPE: 53 ±â€Š61 pmol/L; DCS: 15 ±â€Š17; controls: 6 ±â€Š3; IPE versus DCS or controls: P < 0.05); (ii) ischemia-modified albumin: 68% of IPE patients had a high level versus 16% of DCS patients (P < 0.05) (IPE: 123 ±â€Š25 arbitrary-units; DCS: 84 ±â€Š25; controls: 94 ±â€Š7; IPE versus DCS or controls: P < 0.05); (iii) BNP: 53% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 383 ±â€Š394 ng/L; DCS: 37 ±â€Š28; controls: 19 ±â€Š15; IPE versus DCS or controls: P < 0.01); (iv) cTnI: 63% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 0.66 ±â€Š1.50 µg/L; DCS: 0.0061 ±â€Š0.0040; controls: 0.0090 ±â€Š0.01; IPE versus DCS or controls: P < 0.01). The combined "BNP-cTnI" levels provided most discrimination: all IPE patients, but none of the DCS patients, had elevated levels of either/both of these markers.We propose that antidiuretic hormone acts together with a myocardial ischemic process to promote IPE. Thus, monitoring of antidiuretic hormone and cardiac biomarkers can help to make a quick and reliable diagnosis of IPE.