Undersea and Hyperbaric Medicine最新文献

Introduction: The Undersea and Hyperbaric Medical Society (UHMS) is at the forefront of advancing medical knowledge and promoting patient safety in the field of hyperbaric medicine. In the dynamic landscape of healthcare, physicians' critical role in overseeing hyperbaric oxygen treatment (HBO₂) cannot be overstated. This position statement aims to underscore the significance of physician involvement in delivering HBO₂ and articulate UHMS's commitment to maintaining the highest standards of care and safety for patients undergoing hyperbaric treatments.

Abstract: Hyperbaric oxygen treatment demands a meticulous approach to patient management. As the complexity of hyperbaric patients continues to evolve, the direct oversight of qualified physicians becomes paramount to ensuring optimal patient outcomes and safeguarding against potential risks. In this statement, we outline the key reasons physician involvement is essential in every facet of HBO₂, addressing the technical intricacies of the treatment and the broader spectrum of patient care.

Rationale: Physician oversight for hyperbaric oxygen treatment is rooted in the technical complexities of the treatment and the broader responsibilities associated with clinical patient care. The responsibilities outlined below delineate services intrinsic to the physician's duties for treating patients undergoing hyperbaric oxygen treatments.

Objective: This study aimed to systematically analyze the existing literature and conduct a meta-analysis on the acute effects of apnea on the hematological response by assessing changes in hemoglobin (Hb) concentration and hematocrit (Hct) values.

Methods: Searches in Pubmed, The Cochrane Library, and Web of Science were carried out for studies in which the main intervention was voluntary hypoventilation, and Hb and Hct values were measured. Risk of bias and quality assessments were performed.

Results: Nine studies with data from 160 participants were included, involving both subjects experienced in breath-hold sports and physically active subjects unrelated to breath-holding activities. The GRADE scale showed a "high" confidence for Hb concentration, with a mean absolute effect of 0.57 g/dL over control interventions. "Moderate" confidence appeared for Hct, where the mean absolute effect was 2.45% higher over control interventions. Hb concentration increased to a greater extent in the apnea group compared to the control group (MD = 0.57 g/dL [95% CI 0.28, 0.86], Z = 3.81, p = 0.0001) as occurred with Hct (MD = 2.45% [95% CI 0.98, 3.93], Z = 3.26, p = 0.001).

Conclusions: Apnea bouts lead to a significant increase in the concentration of Hb and Hct with a high and moderate quality of evidence, respectively. Further trials on apnea and its application to different settings are needed.

A 60-year-old man with hypertension and dyslipidemia complained of chest pain upon ascending from a maximum depth of 27 meters while diving. After reaching the shore, his chest pain persisted, and he called an ambulance. When a physician checked him on the doctor's helicopter, his electrocardiogram (ECG) was normal, and there were no bubbles in his inferior vena cava or heart on a portable ultrasound examination. The physician still suspected that he had acute coronary syndrome instead of decompression illness; therefore, he was transported to our hospital. After arrival at the hospital, standard cardiac echography showed a flap in the ascending aorta. Immediate enhanced computed tomography revealed Stanford type A aortic dissection. The patient obtained a survival outcome after emergency surgery. To our knowledge, this is the first reported case of aortic dissection potentially associated with scuba diving. It highlights the importance of considering aortic dissection in patients with sudden-onset chest pain during physical activity. In addition, this serves as a reminder that symptoms during scuba diving are not always related to decompression. This report also suggests the usefulness of on-site ultrasound for the differential diagnosis of decompression sickness from endogenous diseases that induce chest pain. Further clinical studies of this management approach are warranted.

Inner ear decompression sickness (IEDCS) is an uncommon diving-related injury affecting the vestibulocochlear system, with symptoms typically including vertigo, tinnitus, and hearing loss, either in isolation or combination. Classically associated with deep, mixed-gas diving, more recent case series have shown that IEDCS is indeed possible after seemingly innocuous recreational dives, and there has been one previous report of IEDCS following routine hyperbaric chamber operations. The presence of right-to-left shunt (RLS), dehydration, and increases in intrathoracic pressure have been identified as risk factors for IEDCS, and previous studies have shown a predominance of vestibular rather than cochlear symptoms, with a preference for lateralization to the right side. Most importantly, rapid identification and initiation of recompression treatment are critical to preventing long-term or permanent inner ear deficits. This case of a U.S. Navy (USN) diver with previously unidentified RLS reemphasizes the potential for IEDCS following uncomplicated diving and recompression chamber operations - only the second reported instance of the latter.

Objective: To analyze Hyperbaric Oxygen Therapy Registry (HBOTR) data to estimate the Medicare costs of hyperbaric oxygen therapy (HBO₂) based on standard treatment protocols and the annual mean number of treatments per patient reported by the registry.

Methods: We performed a secondary analysis of deidentified data for all payers from 53 centers registered in the HBOTR from 2013 to 2022. We estimated the mean annual per-patient costs of HBO₂ based on Medicare (outpatient facility + physician) reimbursement fees adjusted to 2022 inflation using the Medicare Economic Index. Costs were calculated for the annual average number of treatments patients received each year and for a standard 40-treatment series. We estimated the 2022 costs of standard treatment protocols for HBO₂ indications treated in the outpatient setting.

Results: Generally, all costs decreased from 2013 to 2022. The facility cost per patient per 40 HBO₂ treatments decreased by 10.7% from $21,568.58 in 2013 to $19,488.00 in 2022. The physician cost per patient per 40 treatments substantially decreased by -37.8%, from $5,993.16 to $4,346.40. The total cost per patient per 40 treatments decreased by 15.6% from $27,561.74 to $23,834.40. In 2022, a single HBO₂ session cost $595.86. For different indications, estimated costs ranged from $2,383.4-$8,342.04 for crush injuries to $17,875.80-$35,751.60 for diabetic foot ulcers and delayed radiation injuries.

Conclusions: This real-world analysis of registry data demonstrates that the actual cost of HBO₂ is not nearly as costly as the literature has insinuated, and the per-patient cost to Medicare is decreasing, largely due to decreased physician costs.

For over five decades, many experimental and clinical studies have shown predominantly positive but controversial results on the efficacy of hyperbaric oxygen (HBO₂) therapy in burns. The study aimed to define a common denominator or constellations, respectively, linked to the effects of HBO₂ in burns with a special focus on dosage parameters. Based on original work since 1965, species, number of individuals, type of study, percentage of total body surface area (TBSA), region, depth of burn, causative agent, interval between burn and first HBO2 session, pressure, duration of individual session, number of HBO₂ sessions per day, cumulative number of HBO₂ sessions and type of chamber were assessed. Out of 47 publications included, 32 were animal trials, four were trials in human volunteers, and 11 were clinical studies. They contained 94 experiments whose features were processed for statistical evaluation. 64 (67.4%) showed a positive outcome, 16 (17.9%) an ambiguous one, and 14 (14.7%) a negative outcome. The only factor independently influencing the results was pressure with ATA (atmospheres absolute) lower than 3 ATA being significantly associated with better outcomes (p=0.0005). There is a dire need for well-designed clinical studies in burn centers equipped with hyperbaric facilities to establish dedicated treatment protocols.

A widely accepted belief is that Nathaniel Henshaw was the first practitioner of hyperbaric medicine. He is said to have constructed the first hyperbaric chamber where he treated several disorders and provided opportunities to prevent disease and optimize well-being. While there is little doubt Henshaw was the first to conceptualize this unique medical technology, careful analysis of his treatise has convinced this writer that his was nothing more than a proposal. Henshaw's air chamber was never built. He would have failed to appreciate how its structural integrity could be maintained in the presence of enormous forces generated by envisioned changes in its internal pressure and, likewise, how its door could effectively seal the chamber during hypo-and hyperbaric use. Henshaw would have also failed to appreciate the limitations of his two proposed measuring devices and the toxic nature of one. Neither of these would have provided any quantitative information. The impracticality of his proposed method of compressing and decompressing the chamber is readily apparent. So, too, the likely toxic accumulation of carbon dioxide within the unventilated chamber during lengthy laborious periods required to operate it. Henshaw recommended pressures up to three times atmospheric pressure and durations for acute conditions until their resolution. Such exposures would likely result in fatal decompression sickness upon eventual chamber ascent, a condition of which nothing was known at the time. It would be another 170 years before a functional air chamber would finally become a reality. Henshaw's legacy, then, is limited to the concept of hyperbaric medicine rather than being its first practitioner.

Hypoxia, centralization of blood in pulmonary vessels, and increased cardiac output during physical exertion are the pathogenetic pathways of acute pulmonary edema observed during exposure to extraordinary environments. This study aimed to evaluate the effects of breath-hold diving at altitude, which exposes simultaneously to several of the stimuli mentioned above. To this aim, 11 healthy male experienced divers (age 18-52y) were evaluated (by Doppler echocardiography, lung echography to evaluate ultrasound lung B-lines (BL), hemoglobin saturation, arterial blood pressure, fractional NO (Nitrous Oxide) exhalation in basal condition (altitude 300m asl), at altitude (2507m asl) and after breath-hold diving at altitude. A significant increase in E/e' ratio (a Doppler-echocardiographic index of left atrial pressure) was observed at altitude, with no further change after the diving session. The number of BL significantly increased after diving at altitude as compared to basal conditions. Finally, fractional exhaled nitrous oxide was significantly reduced by altitude; no further change was observed after diving. Our results suggest that exposure to hypoxia may increase left ventricular filling pressure and, in turn, pulmonary capillary pressure. Breath-hold diving at altitude may contribute to interstitial edema (as evaluated by BL score), possibly because of physical efforts made during a diving session. The reduction of exhaled nitrous oxide at altitude confirms previous reports of nitrous oxide reduction after repeated exposure to hypoxic stimuli. This finding should be further investigated since reduced nitrous oxide production in hypoxic conditions has been reported in subjects prone to high-altitude pulmonary edema.

Introduction: Indigenous populations renowned for apneic diving have comparatively large spleen volumes. It has been proposed that a larger spleen translates to heightened apnea-induced splenic contraction and elevations in circulating hemoglobin mass (Hb_mass), which, in theory, improves O₂ carrying and/or CO₂/pH buffering capacities. However, the relation between resting spleen volume and apnea- induced increases in Hb_mass is unknown. Therefore, we tested the hypothesis that resting spleen volume is positively related to apnea-induced increases in total Hb_mass.

Methods: Fourteen healthy adults (six women; 29 ± 5 years) completed a two-minute carbon monoxide rebreathe procedure to measure pre-apneas Hb_mass and blood volume. Spleen length, width, and thickness were measured pre-and post-five maximal apneas via ultrasound. Spleen volume was calculated via the Pilström equation (test-retest CV:2 ± 2%). Hemoglobin concentration ([Hb]; g/dl) and hematocrit (%) were measured pre- and post-apneas via capillary blood samples. Post-apneas Hb_mass was estimated as post-apnea [Hb] x pre-apnea blood volume. Data are presented as mean ± SD.

Results: Spleen volume decreased from pre- (247 ± 95 mL) to post- (200 ± 82 mL, p<0.01) apneas. [Hb] (14.6 ± 1.2 vs. 14.9 ± 1.2 g/dL, p<0.01), hematocrit (44 ± 3 vs. 45 ± 3%, p=0.04), and Hb_mass (1025 ± 322 vs. 1046 ± 339 g, p=0.03) increased from pre- to post-apneas. Pre-apneas spleen volume was unrelated to post-apneas increases in Hb_mass (r=-0.02, p=0.47). O₂ (+28 ± 31 mL, p<0.01) and CO₂ (+31 ± 35 mL, p<0.01) carrying capacities increased post-apneas.

Conclusion: Larger spleen volume is not associated with a greater rise in apneas-induced increases in Hb_mass in non-apnea-trained healthy adults.

We present two cases of cricoid chondronecrosis treated with hyperbaric oxygen (HBO₂) therapy. Both patients presented with biphasic stridor and dyspnea several weeks after an intubation event. Tracheostomy was ultimately performed for airway protection, followed by antibiotic treatment and outpatient HBO₂ therapy. Both patients were decannulated within six months of presentation and after at least 20 HBO₂ therapy sessions. Despite a small sample size, our findings are consistent with data supporting HBO₂ therapy's effects on tissue edema, neovascularization, and HBO₂ potentiation of antibiotic treatment and leukocyte function. We suggest HBO₂ therapy may have accelerated airway decannulation by way of infection resolution as well as the revitalization of upper airway tissues, ultimately renewing the structural integrity of the larynx. When presented with this rare but significant clinical challenge, physicians should be aware of the potential benefits of HBO₂ therapy.