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.

Factors influencing the severity of long-term sequelae in fishermen-divers with neurological decompression sickness.

INTRODUCTION: Numerous studies have been conducted to identify the factors influencing the short-term prognosis for neurological decompression sickness (DCS). However, the long-term sequelae are rarely assessed. The purpose of this study to investigate the factors likely to influence the long-term prognosis. METHODS: Twenty-seven Vietnamese fishermen-divers who on average 9 (SD 6) years beforehand had presented with neurological DCS and ongoing sequelae, were questioned and examined. The severity of the initial clinical profile was quantified using a severity score. The long-term sequelae were clinically evaluated by looking for a motor or sensory deficit or muscular spasticity, and by applying a severity score for the sequelae which focussed on gait and sphincter disorders. RESULTS: An initial severity score of ≥ 15 is significantly associated with a risk of serious long-term sequelae [OR = 13.7 (95% CI 2.4 to 79.5)]. Furthermore, certain treatment practices such as in-water recompression to depths > 17 metres' seawater breathing air are significantly associated with more serious sequelae. The practice of intensive non-standardised hyperbaric oxygen sessions over prolonged durations (median 30 days [IQR 19.5]) delayed after the initial accident (median 4 days [IQR 6]) also seems unfavourable. CONCLUSION: This study establishes a link between the initial DCS severity and the long-term sequelae causing severe gait disorders and sphincter incontinence. Furthermore, this work suggests that certain detrimental treatment practices should be modified. During this field study, we also found that it was possible to reduce sequelae of these divers by offering them an individual programme of self-rehabilitation.

[Hyperbaric oxygen therapy, a little-known discipline]. / L'oxygénothérapie hyperbare, une discipline peu connue.

There are two types of indications of hyperbaric oxygen therapy: it may be used as an emergency treatment in certain acute pathologies or as a therapy for chronic long-term pathologies. The indications are regularly updated and assessed through consensus conferences.

[Hyperbaric medicine and emergency medicine, an example of decompression sickness in diving]. / Hyperbarie et médecine d'urgence, exemple de l'accident de désaturation en plongée.

One of the reasons for the emergency use of a hyperbaric chamber concerns a diving-related accident. Decompression sickness is potentially serious; it requires urgent treatment and hyperbaric recompression. It is caused by the formation of nitrogen bubbles in the organism which appear during the diver's ascent and throughout his or her decompression.

[Nursing care of a patient admitted to a hyperbaric chamber for a chronic wound]. / Prise en charge infirmière d'un patient admis au caisson hyperbare pour une plaie chronique.

The hyperbaric chamber is a particularly relevant therapy for the healing of chronic wounds such as radiation-induced wounds, ulcers, diabetic foot or osteomyelitis. This article describes the pathway of a patient with a chronic wound from the perspective of a hyperbaric medicine nurse.

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.

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.

Risk factors and clinical outcome in military divers with neurological decompression sickness: influence of time to recompression.

BACKGROUND: This study was designed to examine the influence of short delay to recompression and other risk factors associated with the development of severe neurological decompression sickness (DCS) in military divers. METHODS: Fifty-nine divers with DCS treated in less than 6 hours from onset of symptoms to hyperbaric recompression were included retrospectively. Diving parameters, symptom latency and recompression delay were analysed. Clinical symptoms were evaluated for both the acute event and one month later. RESULTS: Median delay to hyperbaric treatment was 35 min (2-350 min). Resolution was incomplete after one month in 25.4 % of divers with DCS. Multivariate analysis demonstrated that severe symptoms, classified as sensory and motor deficits or the presence of bladder dysfunction, were predictors of poor recovery with adjusted odds ratios (OR) of 4.1 (1.12 to 14.92) and 9.99 (1.5 to 66.34) respectively. There was a relationship between a longer delay to treatment and incomplete recovery, but the increased risk appeared negligible with an adjusted OR of 1.01 (1-1.02). CONCLUSION: Our results suggest that neurological severity upon occurrence is the main independent risk factor associated with a poor outcome in military divers with DCS. Clinical recovery was not dramatically improved in this series when recompression treatment was performed promptly.

Prognostic factors of spinal cord decompression sickness in recreational diving: retrospective and multicentric analysis of 279 cases.

BACKGROUND: This study aims to determine the potential risk factors associated with the development of severe diving-related spinal cord decompression sickness (DCS). METHODS: Two hundred and seventy nine injured recreational divers (42 ± 12 years; 53 women) presenting symptoms of spinal cord DCS were retrospectively included from seven hyperbaric centers in France and Belgium. Diving information, symptom latency after surfacing, time interval between symptom onset and hyperbaric treatment were studied. The initial severity of spinal cord DCS was rated with the Boussuges severity score, and the presence of sequelae was evaluated at 1 month. Initial recompression treatment at 2.8 ATA with 100% oxygen breathing or deeper recompression up to 4 or 6 ATA with nitrogen or helium-oxygen breathing mixture were also recorded. RESULTS: Twenty six percent of DCS had incomplete resolution after 1 month. Multivariate analysis revealed several independent factors associated with a bad recovery: age ≥ 42 [OR 1.04 (1-1.07)], depth ≥ 39 m [OR 1.04 (1-1.07)], bladder dysfunction [OR 3.8 (1.3-11.15)], persistence or worsening of clinical symptoms before recompression [OR 2.07 (1.23-3.48)], and a Boussuges severity score >7 [OR 1.16 (1.03-1.31)]. However, the time to recompression and the choice of initial hyperbaric procedure did not significantly influence recovery after statistical adjustment. CONCLUSIONS: Clinical symptoms of spinal cord DCS and their initial course before admission to the hyperbaric center should be considered as major prognostic factors in recovery. A new severity score is proposed to optimize the initial clinical evaluation for spinal cord DCS.

Preconditioning methods and mechanisms for preventing the risk of decompression sickness in scuba divers: a review.

Scuba divers are at risk of decompression sickness due to the excessive formation of gas bubbles in blood and tissues following ascent, with potentially subsequent neurological injuries. Since nonprovocative dive profiles are no guarantor of protection against this disease, novel means are required for its prevention including predive procedures that could induce more resistance to decompression stress. In this article, we review the recent studies describing the promising preconditioning methods that might operate on the attenuation of bubble formation believed to reduce the occurrence of decompression sickness. The main practical applications are simple and feasible predive measures such as endurance exercise in a warm environment, oral hydration, and normobaric oxygen breathing. Rheological changes affecting tissue perfusion, endothelial adaptation with nitric oxide pathway, up-regulation of cytoprotective proteins, and reduction of preexisting gas nuclei from which bubbles grow could be involved in this protective effect.

Risk factors and treatment outcome in scuba divers with spinal cord decompression sickness.

PURPOSE: This study was designed to determine the recompression strategy and the potential risk factors associated with the development of severe diving-related spinal cord decompression sickness (DCS). MATERIAL AND METHODS: Sixty-three injured recreational divers (52 men and 11 women; 46 +/- 12 years) presenting with symptoms of spinal involvement were retrospectively included. Diving information, symptom latency after dive completion, and time interval between symptom onset and hyperbaric treatment were studied. The severity of spinal cord DCS was rated numerically for both the acute event and 1-month later. Initial recompression treatment at 2.8 atmosphere absolute (ATA) with 100% oxygen breathing or deeper recompression at 4 atmosphere absolute with nitrogen-oxygen or helium-oxygen breathing mixture was also noted. RESULTS: Twenty-one divers (33%) had incomplete resolution after 1 month. The clinical severity at presentation was the only independent predictor of poor outcome (odd ratio, 2.68; P < .033). Time to treatment did not influence the recovery with a similar median delay (3 hours) between the divers with or without long-term sequelae. Choice of recompression procedure was not also a determinant factor for treatment outcome. CONCLUSION: The initial clinical course before treatment is a major prognostic factor of spinal cord DCS. Delay to recompression less than 3 hours and use of deep treatment tables did not improve outcome in DCS divers.

Effect of in-water recompression with oxygen to 6 msw versus normobaric oxygen breathing on bubble formation in divers.

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

Pre-dive normobaric oxygen reduces bubble formation in scuba divers.

Oxygen pre-breathing is routinely employed as a protective measure to reduce the incidence of altitude decompression sickness in aviators and astronauts, but the effectiveness of normobaric oxygen before hyperbaric exposure has not been well explored. The objective of this study was to evaluate the effect of 30-min normobaric oxygen (O(2)) breathing before diving upon bubble formation in recreational divers. Twenty-one subjects (13 men and 8 women, mean age (SD) 33 +/- 8 years) performed random repetitive open-sea dives (surface interval of 100 min) to 30 msw for 30 min with a 6-min stop at 3 msw under four experimental protocols: "air-air" (control), "O(2)-O(2)", "O(2)-air" and "air-O(2)" where "O(2)" corresponds to a dive with oxygen pre-breathing and "air" a dive without oxygen administration. Post-dive venous gas emboli were examined by means of a precordial Doppler ultrasound. The results showed decreased bubble scores in all dives where preoxygenation had taken place (p < 0.01). Oxygen pre-breathing before each dive ("O(2)-O(2)" condition) resulted in the highest reduction in bubble scores measured after the second dive compared to the control condition (-66%, p < 0.05). The "O(2)-air" and "air-O(2) "conditions produced fewer circulating bubbles after the second dive than "air-air" condition (-47.3% and -52.2%, respectively, p < 0.05) but less bubbles were detected in "air-O(2) "condition compared to "O(2)-air" (p < 0.05). Our findings provide evidence that normobaric oxygen pre-breathing decreases venous gas emboli formation with a prolonged protective effect over time. This procedure could therefore be beneficial for multi-day repetitive diving.

Predive sauna and venous gas bubbles upon decompression from 400 kPa.

INTRODUCTION: This study investigated the influence of a far infrared-ray dry sauna-induced heat exposure before a simulated dive on bubble formation, and examined the concomitant adjustments in hemodynamic parameters. METHODS: There were 16 divers who were compressed in a hyperbaric chamber to 400 kPa (30 msw) for 25 min and decompressed at 100 kPa x min(-1) with a 4-min stop at 130 kPa. Each diver performed two dives 5 d apart, one with and one without a predive sauna session for 30 min at 65 degrees C ending 1 h prior to the dive. Circulating venous bubbles were detected with a precordial Doppler 20, 40, and 60 min after surfacing, at rest, and after flexions. Brachial artery flow mediated dilation (FMD), blood pressure, and bodyweight measurements were taken before and after the sauna session along with blood samples for analysis of plasma volume (PV), protein concentrations, plasma osmolality, and plasma HSP70. RESULTS: A single session of sauna ending 1 h prior to a simulated dive significantly reduced bubble formation [-27.2% (at rest) to 35.4% (after flexions)]. The sauna session led to an extracellular dehydration, resulting in hypovolemia (-2.7% PV) and -0.6% bodyweight loss. A significant rise of FMD and a reduction in systolic blood pressure and pulse pressure were observed. Plasma HSP70 significantly increased 2 h after sauna completion. CONCLUSION: A single predive sauna session significantly decreases circulating bubbles after a chamber dive. This may reduce the risk of decompression sickness. Sweat dehydration, HSP, and the NO pathway could be involved in this protective effect.

MRI findings and clinical outcome in 45 divers with spinal cord decompression sickness.

BACKGROUND: Decompression sickness (DCS) affecting the spinal cord is the most dangerous form of diving-related injury with potential sequelae. This study was conducted to evaluate the relationship between spinal cord lesions on MRI and clinical findings in divers with spinal DCS. METHODS: We studied 45 cases of DCS that were referred to our hyperbaric facility with clinical evidence of spinal involvement during the period 2002-2007. The study included only patients who underwent MRI within 10 d of injury. The severity of spinal DCS for each patient was rated numerically for both the acute event and 1 mo later. The presence or absence of back pain was also noted. RESULTS: Spinal cord lesions were significantly more frequent in divers with severe DCS, and did not occur in any diver who experienced a favorable outcome (sensitivity = 67%, specificity = 100%, negative predictive value = 77%, positive predictive value = 100%). The presence of vertebral degenerative changes that impinged on the spinal cord was strongly associated with MRI abnormalities, but not with a negative outcome. Acute back pain was associated with hyperintense lesions and persistence of neurological sequelae [OR = 14 (95% CI, 3.1 to 63.5)]. CONCLUSION: The results show that MRI could be helpful in predicting clinical outcome in divers with spinal cord DCS. The presence of medullary compressive factors and vertebral back pain after surfacing indicate increased likelihood of severe myelopathy with incomplete recovery.

Blood platelet count and severity of decompression sickness in rats after a provocative dive.

INTRODUCTION: Previous animal studies reported that platelet count (PC) is decreased following decompression. Adherence and aggregation of platelets to the bubble surface has been demonstrated in severe decompression sickness (DCS). The present study was designed to clarify the relationship between post-dive platelet levels and the severity of DCS in a rat model. METHODS: A total of 57 male Sprague-Dawley rats were assigned to either one experimental group with a hyperbaric exposure (N = 22) or one control group (N = 27). Rats were compressed to 1000 kPa (90 msw) for 45 min while breathing air and decompressed to surface in 38 min with stops at 200, 160, and 130 kPa. Onset of neurological DCS and death time were recorded during a 120-min observation period after surfacing. In the control group, rats were maintained at atmospheric pressure in the same chamber for an equivalent period of time. Blood samples for PC were taken 30 min before and immediately after exposure in two groups. RESULTS: Blood PC after hyperbaric exposure had significantly decreased, whereas PC had increased in the control group. We found a correlation between % fall in PC and latency to death time. The platelet loss tended to decrease when fatal DCS was delayed. Rats suffering from severe DCS with a short latency to death presented a pronounced decline in platelets. DISCUSSION: The present study highlighted a relationship between the post-dive decrease in PC and DCS severity in rats. Platelet consumption could offer a new index for evaluating decompression stress.

Echocardiography in military oxygen divers.

BACKGROUND: Oxygen divers undergo environmental stressors such as immersion, ventilation with scuba, cold exposure, and increased ambient pressure. All of these stressors may be responsible for acute hemodynamic modifications. We hypothesized that repeated hyperbaric hyperoxia exposure induces long-term cardiovascular modifications. METHODS: A Doppler echocardiography was conducted on 20 military oxygen divers (average 12 yr diving experience) and compared with 22 controls. Parameters known to be modified by acute hyperoxic exposure, such as left ventricular (LV) function (systolic and diastolic) and arterial compliance, were analyzed. RESULTS: Controls and divers were matched appropriately for age and height, although the divers had a higher body mass index and aerobic capacity. Left atrial and left ventricular diameters did not differ between the two groups. On the other hand, left ventricular mass was significantly higher in the elite military divers (209 +/- 43 g) in comparison with the control group (172 +/- 48 g), even when LV mass was indexed to body surface area. Left ventricular systolic and diastolic function indices, stroke volume, cardiac index, peripheral vascular resistance, and systemic compliance were comparable between the two groups. CONCLUSION: A greater LV mass was observed in oxygen military divers. The echocardiographic differences between divers and controls could be attributed to the high level physical training undertaken by the military divers. Some stressors, such as cold water immersion, repeated hyperoxic exposures, scuba breathing, and long distance swimming, could have participated to the echocardiographic findings in oxygen divers.

Haemodynamic changes induced by submaximal exercise before a dive and its consequences on bubble formation.

OBJECTIVES: To evaluate the effects of a submaximal exercise performed 2 h before a simulated dive on bubble formation and to observe the haemodynamic changes and their influence on bubble formation. PARTICIPANTS AND METHODS: 16 trained divers were compressed in a hyperbaric chamber to 400 kPa for 30 min and decompressed at a rate of 100 kPa/min with a 9 min stop at 130 kPa (French Navy MN90 procedure). Each diver performed two dives 3 days apart, one without exercise and one with exercise before the dive. All participants performed a 40 min constant-load submaximal and calibrated exercise, which consisted of outdoor running 2 h before the dive. Circulating bubbles were detected with a precordial Doppler at 30, 60 and 90 min after surfacing. Haemodynamic changes were evaluated with Doppler echocardiography. RESULTS: A single bout of strenuous exercise 2 h before a simulated dive significantly reduced circulating bubbles. Post-exercise hypotension (PEH) was observed after exercise with reductions in diastolic and mean blood pressure (DBP and MBP), but total peripheral resistance was unchanged. Stroke volume was reduced, whereas cardiac output was unchanged. Simulated diving caused a similar reduction in cardiac output independent of pre-dive exercise, suggesting that pre-dive exercise only changed DBP and MBP caused by reduced stroke volume. CONCLUSION: A single bout of strenuous exercise 2 h before a dive significantly reduced the number of bubbles in the right heart of divers and protected them from decompression sickness. Declining stroke volume and moderate dehydration induced by a pre-dive exercise might influence inert gas load and bubble formation.

Neurological disorders after repetitive breath-hold diving.

We report a case of transient neurological disorder compatible with cerebral decompression illness in a breath-hold diver. A large right-to-left shunt was later detected with contrast transcranial Doppler ultrasound. While the mechanism of brain damage is unclear, this observation highlights the need for breath-hold divers to avoid excessive nitrogen loading and to refrain from forceful Valsalva maneuvers that may contribute to the opening of a patent foramen ovale and lead to paradoxical cerebral embolism. Because decompression illness is a possibility, anyone who experiences unusual symptoms after breath-hold diving should seek immediate medical attention.