Diving and hyperbaric medicine最新文献

Introduction: Hyperbaric oxygen treatment (HBOT) remains a recognised treatment for acute carbon monoxide (CO) poisoning, but the utility of HBOT in treating CO-induced delayed neurological sequelae (DNS) is not yet established.

Case description: A 26-year old woman presented with reduced consciousness secondary to CO exposure from burning charcoal. She underwent a single session of HBOT with US Navy Treatment Table 5 within six hours of presentation, with full neurological recovery. Eight weeks later, she represented with progressive, debilitating neurological symptoms mimicking Parkinsonism. Magnetic resonance imaging of her brain demonstrated changes consistent with hypoxic ischaemic encephalopathy. The patient underwent 20 sessions of HBOT at 203 kPa (2 atmospheres absolute) for 115 minutes, and received intravenous methylprednisolone 1 g per day for three days. The patient's neurological symptoms completely resolved, and she returned to full-time professional work with no further recurrence.

Discussion: Delayed neurological sequelae is a well-described complication of CO poisoning. In this case, the patient's debilitating neurocognitive symptoms resolved following HBOT. Existing literature on treatment of CO-induced DNS with HBOT consists mainly of small-scale studies and case reports, many of which similarly suggest that HBOT is effective in treating this complication. However, a large, randomised trial is required to adequately determine the effectiveness of HBOT in the treatment of CO-induced DNS, and an optimal treatment protocol.

Bounce diving with rapid descents to very deep depths may provoke the high-pressure neurological syndrome (HPNS). The strategy of including small fractions of nitrogen in the respired gas to produce an anti-HPNS narcotic effect increases the gas density which may exceed recommended guidelines. In 2020 the 'Wetmules' dive team explored the Pearse Resurgence cave (New Zealand) to 245 m breathing trimix (approximately 4% oxygen, 91% helium and 5% nitrogen). Despite the presence of nitrogen, one diver experienced HPNS tremors beyond 200 m. The use of hydrogen (a light yet slightly narcotic gas) has been suggested as a solution to this problem but there are concerns, including the potential for ignition and explosion of hydrogen-containing gases, and accelerated heat loss. In February 2023 a single dive to 230 m was conducted in the Pearse Resurgence to experience hydrogen as a breathing gas in a deep bounce dive. Using an electronic closed-circuit rebreather, helihydrox (approximately 3% oxygen, 59% helium and 38% hydrogen) was breathed between 200 and 230 m. This was associated with amelioration of HPNS symptoms in the vulnerable diver and no obvious adverse effects. The use of hydrogen is a potential means of progressing deeper with effective HPNS amelioration while maintaining respired gas density within advised guidelines.

Introduction: There are inconsistencies in outcome reporting for patients with necrotising soft tissue infections (NSTI). The aim of this study was to evaluate reported outcome measures in NSTI literature that could inform a core outcome set (COS) such as could be used in a study of hyperbaric oxygen in this indication.

Methods: A systematic review of all NSTI literature identified from Cochrane, Ovid MEDLINE and Scopus databases as well as grey literature sources OpenGrey and the New York Academy of Medicine databases which met inclusion criteria and were published between 2010 and 2020 was performed. Studies were included if they reported on > 5 cases and presented clinical endpoints, patient related outcomes, or resource utilisation in NSTI patients. Studies did not have to include intervention. Two independent researchers then extracted reported outcome measures. Similar outcomes were grouped and classified into domains to produce a structured inventory. An attempt was made to identify trends in outcome measures over time and by study design.

Results: Three hundred and seventy-five studies were identified and included a total of 311 outcome measures. Forty eight percent (150/311) of outcome measures were reported by two or more studies. The four most frequently reported outcome measures were mortality without time specified, length of hospital stay, amputation performed, and number of debridements, reported in 298 (79.5%), 260 (69.3%), 156 (41.6%) and 151 (40.3%) studies respectively. Mortality outcomes were reported in 23 different ways. Randomised controlled trials (RCTs) were more likely to report 28-day mortality or 90-day mortality. The second most frequent amputation related outcome was level of amputation, reported in 7.5% (28/375) of studies. The most commonly reported patient-centred outcome was the SF-36 which was reported in 1.6% (6/375) of all studies and in 2/10 RCTs.

Conclusions: There was wide variance in outcome measures in NSTI studies, further highlighting the need for a COS.

Introduction: This study aimed to investigate whether hyperbaric oxygen treatment (HBOT) could ameliorate ischaemia-reperfusion injury in a rat model of ovarian torsion-detorsion.

Methods: Twenty-seven rats were divided among four groups: surgical sham rats (S) (n = 6) underwent identical anaesthesia and surgical incisions to other groups (n = 7 per group) but with no ovary intervention; torsion rats (T) underwent laparotomy, ovarian torsion, relaparotomy and sacrifice after three hours; torsion and detorsion rats (T/DT) underwent laparotomy, ovarian torsion (three hours), relaparotomy and detorsion, and sacrifice after one week; torsion, detorsion, hyperbaric oxygen rats (T/DT/HBOT) underwent laparotomy, ovarian torsion, relaparotomy and detorsion, and sacrifice after one week during which HBOT was provided 21 times (100% oxygen at 600 kPa for 50 min). In all groups blood collection for markers of oxidative stress or related responses, and ovary collection for histology were performed after sacrifice.

Results: When the T/DT, and T/DT/HBOT groups were compared, 8-hydroxy-2'-deoxyguanosine (a marker of oxidative damage to DNA) and malondialdehyde (a product of lipid peroxidation) levels were lower in the T/DT/HBOT group. Anti-Mullerian hormone levels were higher in the T/DT/HBOT group compared to the T/DT group. In addition, oedema, vascular occlusion, neutrophilic infiltration and follicular cell damage were less in the T/DT/HBOT group than in the T/DT group.

Conclusions: When biochemical and histopathological findings were evaluated together, HBOT appeared reduce ovarian ischaemia / reperfusion injury in this rat model of ovarian torsion-detorsion.

Introduction: To develop the diving capacity in the Swedish armed forces the current air decompression tables are under revision. A new decompression table named SWEN21 has been created to have a projected risk level of 1% for decompression sickness (DCS) at the no stop limits. The aim of this study was to evaluate the safety of SWEN21 through the measurement of venous gas emboli (VGE) in a dive series.

Methods: A total 154 dives were conducted by 47 divers in a hyperbaric wet chamber. As a proxy for DCS risk serial VGE measurements by echocardiography were conducted and graded according to the Eftedal-Brubakk scale. Measurements were done every 15 minutes for approximately 2 hours after each dive. Peak VGE grades for the different dive profiles were used in a Bayesian approach correlating VGE grade and risk of DCS. Symptoms of DCS were continually monitored.

Results: The median (interquartile range) peak VGE grade after limb flexion for a majority of the time-depth combinations, and of SWEN21 as a whole, was 3 (3-4) with the exception of two decompression profiles which resulted in a grade of 3.5 (3-4) and 4 (4-4) respectively. The estimated risk of DCS in the Bayesian model varied between 4.7-11.1%. Three dives (2%) resulted in DCS. All symptoms resolved with hyperbaric oxygen treatment.

Conclusions: This evaluation of the SWEN21 decompression table, using bubble formation measured with echocardiography, suggests that the risk of DCS may be higher than the projected 1%.

Introduction: Quantifying inert gas wash-out is crucial to understanding the pathophysiology of decompression sickness. In this study, we developed a portable closed-circuit device for measuring inert gas wash-out and validated its precision and accuracy both with and without human subjects.

Methods: We developed an exhalate monitor with sensors for volume, temperature, water vapor and oxygen. Inert gas volume was extrapolated from these inputs using the ideal gas law. The device's ability to detect volume differences while connected to a breathing machine was analysed by injecting a given gas volume eight times. One hundred and seventy-two coupled before-and-after measurements were then compared with a paired t-test. Drift in measured inert gas volume during unlabored breathing was evaluated in three subjects at rest using multilevel linear regression. A quasi-experimental cross-over study with the same subjects was conducted to evaluate the device's ability to detect inert gas changes in relation to diving interventions and simulate power.

Results: The difference between the injected volume (1,996 ml) and the device's measured volume (1,986 ml) was -10 ml. The 95% confidence interval (CI) for the measured volume was 1,969 to 2,003 ml. Mean drift during a 43 min period of unlaboured breathing was -19 ml, (95% CI, -37 to -1). Our power simulation, based on a cross-over study design, determined a sample size of two subjects to detect a true mean difference of total inert gas wash-out volume of 100 ml.

Conclusions: We present a portable device with acceptable precision and accuracy to measure inert gas wash-out differences that may be physiologically relevant in the pathophysiology of decompression sickness.

Pulmonary oxygen toxicity (POT), an adverse reaction to an elevated partial pressure of oxygen in the lungs, can develop as a result of prolonged hyperbaric hyperoxic conditions. Initially starting with tracheal discomfort, it results in pulmonary symptoms and ultimately lung fibrosis. Previous studies identified several volatile organic compounds (VOCs) in exhaled breath indicative of POT after various wet and dry hyperbaric hypoxic exposures, predominantly in laboratory settings. This study examined VOCs after exposures to 81 metres of seawater by three navy divers during operational heliox diving. Univariate testing did not yield significant results. However, targeted multivariate analysis of POT-associated VOCs identified significant (P = 0.004) changes of dodecane, tetradecane, octane, methylcyclohexane, and butyl acetate during the 4 h post-dive sampling period. No airway symptoms or discomfort were reported. This study demonstrates that breath sampling can be performed in the field, and VOCs indicative of oxygen toxicity are exhaled without clinical symptoms of POT, strengthening the belief that POT develops on a subclinical-to-symptomatic spectrum. However, this study was performed during an actual diving operation and therefore various confounders were introduced, which were excluded in previous laboratory studies. Future studies could focus on optimising sampling protocols for field use to ensure uniformity and reproducibility, and on establishing dose-response relationships.

Introduction: Capnography aids assessment of the adequacy of mechanical patient ventilation. Physical and physiological changes in hyperbaric environments create ventilation challenges which make end-tidal carbon dioxide (ETCO₂) measurement particularly important. However, obtaining accurate capnography in hyperbaric environments is widely considered difficult. This study investigated the EMMA capnograph for hyperbaric use.

Methods: We compared the EMMA capnograph to sidestream capnography and the gold standard arterial carbon dioxide blood gas analysis in a hyperbaric chamber. In 12 resting subjects breathing air at 284 kPa, we recorded ETCO₂ readings simultaneously derived from the EMMA and sidestream capnographs during two series of five breaths (total 24 measurements). An arterial blood gas sample was also taken simultaneously in five participants.

Results: Across all measurements there was a difference of about 0.1 kPa between the EMMA and sidestream capnographs indicating a very slight over-estimation of ETCO₂ by the EMMA capnograph, but fundamentally good agreement between the two end-tidal measurement methods. Compared to arterial blood gas pressure the non-significant difference was about 0.3 and 0.4 kPa for the EMMA and sidestream capnographs respectively.

Conclusions: In this study, the EMMA capnograph performed equally to the sidestream capnograph when compared directly, and both capnography measures gave clinically acceptable estimates of arterial PCO₂.

Delayed post-hypoxic encephalopathy can occur after an episode of anoxia or hypoxia. Symptoms include apathy, confusion, and neurological deficits. We describe a 47-year-old male patient who inhaled gas from a kitchen stove liquid petroleum gas cylinder. He was diagnosed with hypoxic ischaemic encephalopathy 12 hours after his emergency department admission. He received six sessions of hyperbaric oxygen treatment (HBOT) and was discharged in a healthy state after six days. Fifteen days later, he experienced weakness, loss of appetite, forgetfulness, depression, balance problems, and inability to perform self-care. One week later, he developed urinary and fecal incontinence and was diagnosed with post-hypoxic encephalopathy. After 45 days from the onset of symptoms, he was referred to the Underwater and Hyperbaric Medicine Department for HBOT. The patient exhibited poor self-care and slow speech rate, as well as ataxic gait and dysdiadochokinesia. Hyperbaric oxygen was administered for twenty-four sessions, which significantly improved the patient's neurological status with only hypoesthesia in the left hand remaining at the end of treatment. Hyperbaric oxygen has been reported as successful in treating some cases of delayed neurological sequelae following CO intoxication. It is possible that HBO therapy may also be effective in delayed post-hypoxic encephalopathy from other causes. This may be achieved through mechanisms such as transfer of functional mitochondria to the injury site, remyelination of damaged neurons, angiogenesis and neurogenesis, production of anti-inflammatory cytokines, and balancing of inflammatory and anti-inflammatory cytokines.