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.

Chest CT scan for the screening of air anomalies at risk of pulmonary barotrauma for the initial medical assessment of fitness to dive in a military population.

Introduction: The presence of intra-pulmonary air lesions such as cysts, blebs and emphysema bullae, predisposes to pulmonary barotrauma during pressure variations, especially during underwater diving activities. These rare accidents can have dramatic consequences. Chest radiography has long been the baseline examination for the detection of respiratory pathologies in occupational medicine. It has been replaced since 2018 by the thoracic CT scan for military diving fitness in France. The objective of this work was to evaluate the prevalence of the pulmonary abnormalities of the thoracic CT scan, and to relate them to the characteristics of this population and the results of the spirometry. Methods: 330 records of military diving candidates who underwent an initial assessment between October 2018 and March 2021 were analyzed, in a single-center retrospective analysis. The following data were collected: sex, age, BMI, history of respiratory pathologies and smoking, treatments, allergies, diving practice, results of spirometry, reports of thoracic CT scans, as well as fitness decision. Results: The study included 307 candidates, mostly male, with a median age of 25 years. 19% of the subjects had abnormal spirometry. We identified 25% of divers with CT scan abnormalities. 76% of the abnormal scans were benign nodules, 26% of which measured 6 mm or more. Abnormalities with an aerial component accounted for 13% of the abnormal scans with six emphysema bullae, three bronchial dilatations and one cystic lesion. No association was found between the presence of nodules and the general characteristics of the population, whereas in six subjects emphysema bullae were found statistically associated with active smoking or abnormal spirometry results. Conclusion: The systematic performance of thoracic CT scan in a young population free of pulmonary pathology revealed a majority of benign nodules. Abnormalities with an aerial component are much less frequent, but their presence generally leads to a decision of unfitness. These results argue in favor of a systematic screening of aeric pleuro-pulmonary lesions during the initial assessment for professional divers.

Cecal Metabolomic Fingerprint of Unscathed Rats: Does It Reflect the Good Response to a Provocative Decompression?

On one side, decompression sickness (DCS) with neurological disorders lead to a reshuffle of the cecal metabolome of rats. On the other side, there is also a specific and different metabolomic signature in the cecum of a strain of DCS-resistant rats, that are not exposed to hyperbaric protocol. We decide to study a conventional strain of rats that resist to an accident-provoking hyperbaric exposure, and we hypothesize that the metabolomic signature put forward may correspond to a physiological response adapted to the stress induced by diving. The aim is to verify and characterize whether the cecal compounds of rats resistant to the provocative dive have a cecal metabolomic signature different from those who do not dive. 35 asymptomatic diver rats are selected to be compared to 21 rats non-exposed to the hyperbaric protocol. Because our aim is essentially to study the differences in the cecal metabolome associated with the hyperbaric exposure, about half of the rats are fed soy and the other half of maize in order to better rule out the effect of the diet itself. Lower levels of IL-1ß and glutathione peroxidase (GPX) activity are registered in blood of diving rats. No blood cell mobilization is noted. Conventional and ChemRICH approaches help the metabolomic interpretation of the 185 chemical compounds analyzed in the cecal content. Statistical analysis show a panel of 102 compounds diet related. 19 are in common with the hyperbaric protocol effect. Expression of 25 compounds has changed in the cecal metabolome of rats resistant to the provocative dive suggesting an alteration of biliary acids metabolism, most likely through actions on gut microbiota. There seem to be also weak changes in allocations dedicated to various energy pathways, including hormonal reshuffle. Some of the metabolites may also have a role in regulating inflammation, while some may be consumed for the benefit of oxidative stress management.

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.

Cecal metabolome fingerprint in a rat model of decompression sickness with neurological disorders.

Massive bubble formation after diving can lead to decompression sickness (DCS), which can result in neurological disorders. We demonstrated that hydrogen production from intestinal fermentation could exacerbate DCS in rats fed with a standard diet. The aim of this study is to identify a fecal metabolomic signature that may result from the effects of a provocative hyperbaric exposure. The fecal metabolome was studied in two groups of rats previously fed with maize or soy in order to account for diet effects. 64 animals, weighing 379.0_20.2 g on the day of the dive, were exposed to the hyperbaric protocol. The rats were separated into two groups: 32 fed with maize (Div MAIZE) and 32 fed with soy (Div SOY). Gut fermentation before the dive was estimated by measuring exhaled hydrogen. Following hyperbaric exposure, we assessed for signs of DCS. Blood was analyzed to assay inflammatory cytokines. Conventional and ChemRICH approaches helped the metabolomic interpretation of the cecal content. The effect of the diet is very marked at the metabolomic level, a little less in the blood tests, without this appearing strictly in the clinic status. Nevertheless, 37 of the 184 metabolites analyzed are linked to clinical status. 35 over-expressed compounds let suggest less intestinal absorption, possibly accompanied by an alteration of the gut microbial community, in DCS. The decrease in another metabolite suggests hepatic impairment. This spectral difference of the ceca metabolomes deserves to be studied in order to check if it corresponds to functional microbial particularities.

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.

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.

Stimulating fermentation by the prolonged acceleration of gut transit protects against decompression sickness.

Massive bubble formation after diving can lead to decompression sickness (DCS). Gut fermentation at the time of a dive exacerbates DCS due to endogenous hydrogen production. We sought to investigate whether medium-term stimulation of fermentation as a result of polyethylene glycol (PEG)-induced acceleration of bowel transit before diving exacerbates DCS in rats. Seven days before an experimental dry dive, 60 rats were randomly divided in two groups: an experimental group treated with PEG (n = 30) and an untreated control group (n = 30). Exhaled hydrogen was measured before the dive. Following hyperbaric exposure, we assessed for signs of DCS. After anaesthetisation, arterial blood was drawn to assay inflammatory cytokines and markers of oxidative stress. PEG led to a significant increase in exhaled H2 (35 ppm [10-73] compared with control 7 ppm [2-15]; p = 0.001). The probability of death was reduced in PEG-treated rats (PEG: 17% [95% CI 4-41] vs control: 50% [95% CI 26-74]; p = 0.034). In addition, inflammatory markers were reduced, and the antioxidant activity of glutathione peroxidase was significantly increased (529.2 U.l-1 [485.4-569.0] versus 366.4 U.l-1 [317.6-414.8]; p = 0.004). Thus, gut fermentation might have a positive effect on DCS. The antioxidant and neuroprotective properties of the fermentation by-products H2 and butyrate may explain these results.

Tirofiban, a Glycoprotein IIb/IIIa Antagonist, Has a Protective Effect on Decompression Sickness in Rats: Is the Crosstalk Between Platelet and Leukocytes Essential?

In its severest forms, decompression sickness (DCS) may extend systemically and/or induce severe neurological deficits, including paralysis or even death. It seems that the sterile and ischemic inflammatory phenomena are consecutive to the reaction of the bubbles with the organism and that the blood platelet activation plays a determinant role in the development of DCS. According to the hypotheses commonly put forward, the bubbles could either activate the platelets by direct contact or be the cause of abrasion of the vascular epithelium, which would expose the basal plate glycogen and then prompt the platelets to activate. The purpose of this study is to confirm anti-platelet drugs specific to GPIIb/IIIa integrin could prevent DCS, using a rat model. There is a significant difference concerning the incidence of the drug on the clinical status of the rats (p = 0.016), with a better clinical outcome for rats treated with tirofiban (TIR) compared with the control rats (p = 0.027), even if the three anti-GPIIb/IIIa agents used have limited respiratory distress. TIR limited the decrease in platelet counts following the hyperbaric exposure. TIR help to prevent from DCS. TIR is specific to GPIIb/IIIa whereas eptifibatide and abciximab could inhibit αVß3 and αMß2 involved in communication with the immune system. While inhibiting GPIIb/IIIa could highlight a platelet-dependent inflammatory pathway that improves DCS outcomes, we wonder whether inhibiting the αVß3 and αMß2 communications is not a wrong approach for limiting mortality in DCS.

[Is it possible to dive again after decompression sickness?] / Peut-on replonger après un accident de désaturation ?

Decompression sickness in underwater diving exposes the diver to a risk of clinical sequelae which require specific care. In the absence of sequelae or after clinical recovery, the question of diving again may be raised. As part of a secondary prevention approach, the hyperbaric practitioner measures the physical, psychological and social impact of re-exposure to pressure and the immersion of the patient-diver.

Immersion pulmonary oedema in a healthy diver not exposed to cold or strenuous exercise.

In healthy divers, the occurrence of immersion pulmonary oedema (IPE) is commonly caused by contributory factors including strenuous exercise, cold water and negative-pressure breathing. Contrary to this established paradigm, this case reports on a 26-year-old, well-trained combat swimmer who succumbed to acute IPE during static immersion in temperate (21°C) water, while using a front-mounted counterlung rebreather. The incident occurred during repeated depth-controlled ascent practice at the French military diving school. It was discovered that the diver had attempted to stop any gas leakage into the system by over-tightening the automatic diluent valve (ADV) (25th notch of 27) during the dive, thus causing a high resistance to inspiratory flow. The ventilatory constraints imposed by this ADV setting were assessed as a 3.2 Joules·L⁻¹ inspiratory work of breathing and -5 kPa (-50 mbar) transpulmonary pressure. This report confirms the key role of negative pressure breathing in the development of interstitial pulmonary oedema. Such a breathing pattern can cause a lowering of thoracic, airway and interstitial lung pressure, leading to high capillary pressure during each inspiration. Repetition of the diving drills resulted in an accumulation of interstitial lung water extravasation, causing pathological decompensation and proven symptoms.

Thirty-five Day Fluoxetine Treatment Limits Sensory-Motor Deficit and Biochemical Disorders in a Rat Model of Decompression Sickness.

According to the OECD statistical base for 2014, anti-depressants will, on average, be distributed at a rate of 62 daily doses per 1,000 inhabitants for the 25 countries surveyed (Health at a glance: Europe 2014; OECD Health Statistics; World Health Organization and OECD Health Statistics, 2014). Divers must be concerned. On another hand, divers are potentially exposed to decompression sickness including coagulation inflammation and ischemia, which can result in neurological lesions or even death. The purpose of this study is to assess whether chronic treatment with anti-depressants may represent a contraindication to the practice of an at-risk activity, such as, scuba diving, or even presents a benefit by attenuating the severity of the symptoms. We study for the first time the effect of a 35-day fluoxetine treatment (20 mg/kg) on the occurrence of decompression sickness in laboratory rats (n = 79). Following exposure to the hazardous protocol, there is a significant correlation between the type of treatment and the clinical status of the rats in favor of a better clinical prognosis for the rats treated with fluoxetine with a significantly higher number of No DCS status and a lower number of Severe DCS status in the Flux, compared to Controls. The treatment modifies the rat performances both significantly and favorably during the physical and behavioral tests, just like their biological and biochemical constants. After decompression, rats under treatment display lower sensory-motor deficit and lowers biochemical disorders. From a biological point of view, we conclude fluoxetine should not be seen as a contraindication for diving on the basis of anticipated increased physiological risk.

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.

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.

Fluoxetine Protection in Decompression Sickness in Mice is Enhanced by Blocking TREK-1 Potassium Channel with the "spadin" Antidepressant.

In mice, disseminated coagulation, inflammation, and ischemia induce neurological damage that can lead to death. These symptoms result from circulating bubbles generated by a pathogenic decompression. Acute fluoxetine treatment or the presence of the TREK-1 potassium channel increases the survival rate when mice are subjected to an experimental dive/decompression protocol. This is a paradox because fluoxetine is a blocker of TREK-1 channels. First, we studied the effects of an acute dose of fluoxetine (50 mg/kg) in wild-type (WT) and TREK-1 deficient mice (knockout homozygous KO and heterozygous HET). Then, we combined the same fluoxetine treatment with a 5-day treatment protocol with spadin, in order to specifically block TREK-1 activity (KO-like mice). KO and KO-like mice were regarded as antidepressed models. In total, 167 mice (45 WTcont 46 WTflux 30 HETflux and 46 KOflux) constituting the flux-pool and 113 supplementary mice (27 KO-like 24 WTflux2 24 KO-likeflux 21 WTcont2 17 WTno dive) constituting the spad-pool were included in this study. Only 7% of KO-TREK-1 treated with fluoxetine (KOflux) and 4% of mice treated with both spadin and fluoxetine (KO-likeflux) died from decompression sickness (DCS) symptoms. These values are much lower than those of WT control (62%) or KO-like mice (41%). After the decompression protocol, mice showed significant consumption of their circulating platelets and leukocytes. Spadin antidepressed mice were more likely to exhibit DCS. Nevertheless, mice which had both blocked TREK-1 channels and fluoxetine treatment were better protected against DCS. We conclude that the protective effect of such an acute dose of fluoxetine is enhanced when TREK-1 is inhibited. We confirmed that antidepressed models may have worse DCS outcomes, but concomitant fluoxetine treatment not only decreased DCS severity but increased the survival rate.

Fluoxetine stimulates anti-inflammatory IL-10 cytokine production and attenuates sensory deficits in a rat model of decompression sickness.

Despite "gold standard" hyperbaric oxygen treatment, 30% of patients suffering from neurological decompression sickness still exhibit incomplete recovery, including sensory impairments. Fluoxetine, a well-known antidepressant, is recognized as having anti-inflammatory effects in the setting of cerebral ischemia. In this study, we focused on the assessment of sensory neurological deficits and measurement of circulating cytokines after decompression in rats treated or not with fluoxetine. Seventy-eight rats were divided into a clinical (n = 38) and a cytokine (n = 40) group. In both groups, the rats were treated with fluoxetine (30 mg/kg po, 6 h beforehand) or with a saccharine solution. All of the rats were exposed to 90 m seawater for 45 min before staged decompression. In the clinical group, paw withdrawal force after mechanical stimulation and paw withdrawal latency after thermal stimulation were evaluated before and 1 and 48 h after surfacing. At 48 h, a dynamic weight-bearing device was used to assess postural stability, depending on the time spent on three or four paws. For cytokine analysis, blood samples were collected from the vena cava 1 h after surfacing. Paw withdrawal force and latency were increased after surfacing in the controls, but not in the fluoxetine group. Dynamic weight-bearing assessment highlighted a better stability on three paws for the fluoxetine group. IL-10 levels were significantly decreased after decompression in the controls, but maintained at baseline level with fluoxetine. This study suggests that fluoxetine has a beneficial effect on sensory neurological recovery. We hypothesize that the observed effect is mediated through maintained anti-inflammatory cytokine IL-10 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.