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.

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.

Epidemiological, clinical, and echocardiographic features of twenty 'Takotsubo-like' reversible myocardial dysfunction cases with normal coronarography following immersion pulmonary oedema.

BACKGROUND: Pulmonary immersion oedema is a frequent diving accident. Although its outcome is generally favourable within 72 h, it can nonetheless lead to heart failure or sudden death. Cases of transient myocardial dysfunction have been reported in the literature. This phenomenon is similar to Takotsubo syndrome in many ways. It is characterised by transient myocardial hypokinesia, without associated coronary lesions. METHODS: We report on 20 cases of patients who showed transient alteration of left ventricular kinetics with normal coronary angiography over the course of an immersion pulmonary oedema. RESULTS: The echocardiographic localisation of the myocardial damage was generally focal and not centred on the apex with an average left ventricular ejection fraction of 45%. The main anomalies in the electrocardiographic repolarisation were T wave inversion with corrected QT interval prolongation. We also observed a moderate increase in troponin levels, with discordance between the enzymatic peak and the severity of the left ventricle segmental dysfunction. CONCLUSION: These cases suggest the incidence of a clinical entity strongly reminiscent of Takotsubo phenomenon of atypical topography as a consequence of diving accidents.

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.

Reduction in the Level of Plasma Mitochondrial DNA in Human Diving, Followed by an Increase in the Event of an Accident.

Circulating mitochondrial DNA (mtDNA) is receiving increasing attention as a danger-associated molecular pattern in conditions such as autoimmunity or trauma. In the context of decompression sickness (DCS), the course of which is sometimes erratic, we hypothesize that mtDNA plays a not insignificant role particularly in neurological type accidents. This study is based on the comparison of circulating mtDNA levels in humans presenting with various types of diving accidents, and punctured upon their admission at the hyperbaric facility. One hundred and fourteen volunteers took part in the study. According to the clinical criteria there were 12 Cerebro DCS, 57 Medullary DCS, 15 Vestibular DCS, 8 Ctrl+ (accident-free divers), and 22 Ctrl- (non-divers). This work demonstrates that accident-free divers have less mtDNA than non-divers, which leads to the assumption that hyperbaric exposure degrades the mtDNA. mtDNA levels are on average greater in divers with DCS compared with accident-free divers. On another hand, the amount of double strand DNA (dsDNA) is neither significantly different between controls, nor between the different DCS types. Initially the increase in circulating oligonucleotides was attributed to the destruction of cells by bubble abrasion following necrotic phenomena. If there really is a significant difference between the Medullary DCS and the Ctrl-, this difference is not significant between these same DCS and the Ctrl+. This refutes the idea of massive degassing and suggests the need for new research in order to verify that oxidative stress could be a key element without necessarily being sufficient for the occurrence of a neurological type of accident.

Reliability of venous gas embolism detection in the subclavian area for decompression stress assessment following scuba diving.

INTRODUCTION: Ultrasonic detection of venous gas emboli (VGE) in the precordial (PRE) region is commonly used in evaluation of decompression stress. While subclavian (SC) VGE detection can also be used to augment and improve the evaluation, no study has rigorously compared VGE grades from both sites as decompression stress indicators. METHODS: This retrospective study examined 1,016 man-dives breathing air extracted from the Defence Research and Development Canada dataset. Data for each man-dive included dive parameters (depth, bottom time, total ascent time), PRE and SC VGE grades (Kisman-Masurel) and post-dive decompression sickness (DCS) status. Correlation between SC and PRE grades was analyzed and the association of the probability of DCS (pDCS) with dive parameters and high bubble grades (HBG III- to IV) was modelled by logistic regression for SC and PRE separately for DCS risk ratio comparisons. RESULTS: PRE and SC VGE grades were substantially correlated (R = 0.66) and were not statistically different (p = 0.61). For both sites, pDCS increased with increasing VGE grade. When adjusted for dive parameters, the DCS risk was significantly associated with HBG for both PRE (p = 0.03) and SC (p < 0.001) but the DCS risk ratio for SC HBG (RR = 6.0, 95% CI [2.7-12.3]) was significantly higher than for PRE HBG (RR = 2.6, 95% CI [1.1-6.0]). CONCLUSIONS: The association of bubble grades with DCS occurrence is stronger for SC than PRE when exposure severity is taken into account. The usefulness of SC VGE in decompression stress evaluation has been underestimated in the past.

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.

Cardiovascular Mechanisms of Extravascular Lung Water Accumulation in Divers.

This study assessed the relation between altered cardiac function and the development of interstitial pulmonary edema in scuba divers. Fifteen healthy men performed a 30-minute scuba dive in open sea. They were instructed to fin for 30 minutes and were wearing wet suits. Before and immediately after immersion, cardiac indexes and extravascular lung water were measured using echocardiography and lung ultrasound, respectively. The mean ultrasound lung comet score increased from 0 to 4.6 ± 3.4. The diameter of the inferior caval vein increased by 47 ± 5.2%, systolic pulmonary artery pressure by 105 ± 8.6%, left atrial volume by 18.0 ± 3.3%, and left ventricle end-diastolic volume by 10 ± 2.4% suggesting that both right and left ventricular (LV) filling pressures were elevated. Doppler studies showed an increased mitral E peak (+2.5 ± 0.3%) and E/A ratio (+22.5 ± 3.4%) with a decreased mitral A peak (-16.4 ± 2.7%), E peak deceleration time (-14.5 ± 2.4%) consistent with rapid early LV filling but without a change in LV stroke volume. There was an increase in right/left ventricle diameter ratio (+33.6 ± 4.8%) suggesting a relative increase in right-sided heart output compared with the left. Furthermore, the lung comet score correlated significantly with inferior caval vein diameter, systolic pulmonary artery pressure, right/left ventricle diameter ratio, and E-wave deceleration time. In conclusion, the altered right/left heart stroke volume balance could play an essential role in the development of immersion pulmonary edema. Our findings have important implications for the pathogenesis of cardiogenic pulmonary edema.

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.

Perilymphatic fistula after underwater diving: a series of 11 cases.

INTRODUCTION: Onset of cochleovestibular symptoms (hearing loss, dizziness or instability, tinnitus) after a dive (scuba or breath-hold diving) warrants emergency transfer to an otology department. One priority is to investigate the possibility of the development of decompression sickness with a view to hyperbaric oxygen treatment of bubble-induced inner-ear damage. If this injury is ruled out, inner-ear barotrauma should be considered together with its underlying specific injury pattern, perilymphatic fistula. METHODS: We report on a series of 11 cases of perilymphatic fistula following ear barotrauma between 2003 and 2015, eight after scuba diving and three after free diving. All patients underwent a series of laboratory investigations and first-line medical treatment. RESULTS: Seven patients had a perilymphatic fistula in the left ear and four in the right. Eight cases underwent endaural surgical exploration. A fistula of the cochlear fenestra was visualised in seven cases with active perilymph leakage seen in six cases. After temporal fascia grafting, prompt resolution of dizziness occurred, with early, stable, subtotal recovery of hearing in seven. Of six patients in whom tinnitus occurred, this disappeared in two and improved in a further two. Two patients were not operated on because medical treatment had been successful, and one patient refused surgery despite the failure of medical treatment. Median follow-up time was 7.4 years (range 0.3 to 12). CONCLUSION: The diagnosis of perilymphatic fistula is based on clinical assessments and various laboratory findings. When there was strong evidence of this condition, surgery yielded excellent functional outcomes in all patients treated early.

Colonic Fermentation Promotes Decompression sickness in Rats.

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

Serum albumin as a biomarker of capillary leak in scuba divers with neurological decompression sickness.

BACKGROUND: Prior reports have shown that decompression sickness (DCS) in scuba divers is accompanied by vascular endothelium damage attributed to gas emboli formation, resulting in capillary leak with hemoconcentration. The significance of serum albumin as a biomarker of vascular permeability in this condition has been insufficiently investigated. We studied whether there was a relationship between low serum albumin values on admission and the occurrence of neurological DCS. METHODS: Demographic, diving, and laboratory data of 52 randomly selected DCS divers were compared with those of 52 asymptomatic divers referred for inadequate decompression. The diagnostic performance of serum albumin in predicting neurological DCS was assessed. RESULTS: Both groups did not differ from the variables examined. Serum albumin was significantly lower in injured divers than in controls (38.7 ± 3 g · L(-1) vs. 41 ± 2.9 g · L(-1)). At a cut-off value of 35.2 g · L(-1), we found a specificity of 98% (95% CI 90-100) and a sensitivity of 16% (95% CI 7-28) for the prediction of neurological DCS development. CONCLUSION: Our findings suggest that hypoalbuminemia at initial presentation, albeit rare, accurately predicts the occurrence of neurological DCS in scuba divers. The prognostic value of this biomarker and the potential beneficial role of albumin infusion in more severe cases remain to be investigated.

Neuron-specific enolase and S100B protein levels in recreational scuba divers with neurological decompression sickness.

INTRODUCTION: Neuron-specific enolase (NSE) and S100B protein are brain-origin proteins commonly described to assess the presence and severity of neurological injury. To date, there are limited data examining the influence of scuba diving on these biomarkers, particularly when symptoms of decompression sickness (DCS) occur. The purpose of this controlled study was to determine whether these serum neurochemical markers could be used as 1) indicators of neurological DCS and 2) predictors of incomplete recovery. METHODS: Fifty-nine divers with neurological DCS and 37 asymptomatic divers admitted for inadequate decompression, serving as controls, were consecutively enrolled between 2010 and 2012. Blood samples were collected at initial presentation up to 6 hours after dive completion (controls) or onset of symptoms (DCS divers). Biomarkers were quantified in nonhaemolysed samples only. Clinical outcome was assessed at 6 months post-injury. RESULTS: The two groups did not differ regarding the variables examined, except for the total dive time which was slightly shorter in the control group. NSE, but not S100B protein, was higher in the DCS group than in controls (P < 0.0001). An NSE level > 15.9 µg L⁻¹ determined by ROC analysis predicted DCS development with a specificity of 100% (95% confidence interval (CI) 90 to 100) and a sensitivity of 24% (95% CI 14 to 36). There was a trend towards a higher likelihood of residual neurological deficits above this cut-off value (P = 0.08). CONCLUSIONS: Early determination of NSE was found to be useful for the diagnosis of neurological DCS with a high specificity. However, its clinical applicability in decision making for determining treatment as well as its prognostic value remains to be established. Reliability of S100B protein was not demonstrated in the present study.