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A 41-year-old female nurse had cutaneous decompression sickness on two occasions after acting as an inside chamber attendant for patients receiving hyperbaric oxygen. She breathed air during the treatments at pressures equivalent to 14 and 18 metres of seawater, but each time she decompressed whilst breathing oxygen. Latency was 2.5 hours and one hour. She was found to have an 11 mm diameter persistent foramen ovale. It was closed and she returned to work without recurrence of decompression sickness. Review of the literature suggests that shunt mediated decompression sickness is an important occupational risk for individuals with a large right-to-left shunt when working in hyperbaric air, but the manifestations of decompression sickness differ in those who decompress whilst breathing oxygen compared with those who decompress whilst breathing air. [ABSTRACT FROM AUTHOR]

Previous cases of dental barotrauma have been reported in pilots and divers. We report a case of dental barotrauma and barodontalgia in a diving physician accompanying patients during hyperbaric oxygen treatment, and due to pressure changes in the hyperbaric chamber. The physician developed sharp pain localised to the right maxillary molars but radiating to the face, ear and head during decompression from 243 kPa (2.4 atmospheres absolute). The pain intensifi ed following completion of decompression and was consistent with irreversible pulpitis. Clinical examination and panoramic radiography suggested fracture of a heavily restored tooth due to barotrauma. This was managed by tooth extraction. The physician subsequently discontinued accompanying the patients during their hyperbaric oxygen treatment sessions. Dentists and maxillofacial surgery specialists suggest waiting for a minimum of four weeks or until the tooth socket and/or oral tissue has healed suffi ciently to minimise the risk of infection or further trauma before exposure to further pressure change. Although seemingly rare, and despite the comparatively slow pressure changes, dental barotrauma can occur in hyperbaric chamber occupants. [ABSTRACT FROM AUTHOR]

Abstract A key factor affecting survival of fish which are captured at depth and subsequently released is barotrauma. Barotrauma are a suite of injuries which occur as a result of the decreasing ambient pressure experienced by a fish during capture and are caused by expanding swim bladder gas and formation of gas embolisms. Snapper (Chrysophrys auratus) are of key importance to both commercial and recreational fisheries in southern Australia and are often released after capture suffering from barotrauma. Previous research has yielded inconsistent results for survival of C. auratus after suffering barotrauma, in part due to influences related to capture, 'cage' effects and the use of only very short term post-catch and release monitoring. This study therefore used laboratory hyperbaric chambers to simulate the pressure changes associated with capture to investigate whether barotrauma was a direct cause of mortality in C. auratus. The influences of depth and repressurization on mortality, behaviour and symptoms due to barotrauma could therefore be examined in a controlled environment independent of capture and 'cage' effects combined with long-term monitoring (220 d) post-simulation. In a pilot experiment C. auratus (n = 12) were depressurized from 8 bar (≈70 m depth), before being repressurized after 2 min at 1 bar (atmospheric pressure) resulting in agitated in-chamber behaviours and abdominal distension as a result of swim bladder perforation, but 100% survival. A second experiment depressurized C. auratus from 4 bar (≈30 m depth); one treatment group (n = 32) were repressurized after 10 min again resulting in behaviour and symptoms indicative of swim bladder perforation and 100% survival, the other group (n = 32) was left at 1 bar and exhibited many additional external and internal barotrauma symptoms and suffered 16% mortality. Despite the death of a single control individual, statistical analyses found a significant effect of treatment on mortality. Mortality occurred within 15 min of depressurization and the cause of death was consistent with the formation of gas embolisms. Staged post-mortems performed on C. auratus that had been depressurized from 4 bar to induce swim bladder perforation indicated that swim bladders were healed sufficiently to hold gas after just 2 d. C. auratus were shown to be a remarkably robust species to the effects of barotrauma, particularly if repressurized quickly (<10 min) after capture and this resilience is likely reflective of their characteristic semi-pelagic physiology. This study also demonstrated the usefulness of laboratory hyperbaric chambers to examine the long term (>200 d) effects of depressurization on deep water fish species independent of capture and 'cage' effects. [ABSTRACT FROM AUTHOR]

Introduction: The main pathologies that require a recompression therapy are decompression sickness (DCS) and arterial gas embolism (AGE), boths can be caused by pressure-related activites and certain amount of gas (dissolved or not) in the Victim's blood. Besides diving other pressure-related activities put the person in risk of this pathologies. Aim: To investigate the main place of production of these pathologies and their physiological base. Methods: we reviewed all charts of patients with DCS and AGE from 1970-2017 at Centro de Buceo de la Armada (Cartagena). Results: There were 392 cases, 345 (88%) diving related, 36 (9,18%) hyperbaric chamber-related, 6 (1,53%) submarine activities related and 4 (1,02%) hypobaric activities-related. Conclusions: Diving injuries rates are the most important but any pressure-related activity can be risky even hyperbaric chamber activity, considered the safest pressure-related activity. [ABSTRACT FROM AUTHOR]

The probabilities of decompression sickness (DCS) among diving fishermen are higher than in any other group of divers. Diving behavior of artisanal fishermen has been directed mainly to target high-value species. The aim of this study was to learn about the occurrence of DCS derived from sea cucumber harvesting in the Yucatán Peninsula, Mexico. We conducted a retrospective chart review of diving fishermen treated at a multiplace hyperbaric chamber in Tizimín, Mexico. In total, 233 recompression therapies were rendered to 166 diving fishermen from 2014 to 2016. The average age was 36.7 ± 9.2 years (range: 20-59 years); 84.3% had experienced at least one DCS event previously. There was a correlation between age and DCS incidents (F: 8.3; R2: 0.07) and differences in the fishing depth between seasons (H: 9.99; p<0.05). Musculoskeletal pain was the most frequently reported symptom. Three divers, respectively, suffered permanent hearing loss, spinal cord injury and fatal outcome. Diving fishermen experience DCS at an alarmingly high rate, probably due to the type of species targeted, given the requirements in each case. Understanding divers' behaviors and their incentives while in pursuit of high-value species such as sea cucumber could help to find ways to mitigate health risks and help enforce regulation. [ABSTRACT FROM AUTHOR]

Background: Inside attendants (IAs) exposed to high pressure during hyperbaric oxygen (HBO2) therapy. The aim of this study was to evaluate the alterations of pulmonary functions in IAs over time. Methods: IAs in our hyperbaric center constituted the IA group (n=11). A sex- and age-matched control group (n=15) was constituted from hospital staff who had not dived or been exposed to hyperbaric environments before. We measured the respiratory function of all subjects at two time points: 1) at the start of the study; and 2) 12 months after the first measurement. The following parameters were recorded: forced vital capacity (FVC), forced expiratory volume in one second (FEV1), rate of FEV1 to FVC (FEV1/FVC%), forced expiratory flow at 25% to 75% vital capacity (FEF25-75%), forced expiratory flow at 50% vital capacity (FEF50%), forced expiratory flow at 25% vital capacity (FEF25%). Results: Both groups were similar in terms of age, sex, smoking and body mass index. We found that FEV1, FEV1/FVC%, FEF25-75% and FEF50% significantly reduced in both groups after 12 months (p<0.05). However, the rate of change in all parameters was similar in both groups (p>0.05). In the IA group, the total number of exposures within the 12 months was positively correlated with the rate of reduction in FEF25% (r=0.788, p=0.004). Conclusion: Working as an IA does not deteriorate pulmonary function in the short term. However, there is a need for long-term follow-up studies. [ABSTRACT FROM AUTHOR]

Background Current in vivo methods cannot distinguish between the roles of vascular and stationary tissular gas bubbles in the mechanisms of decompression sickness (DCS). New method To answer this question, we designed a normobaric–hyperbaric chamber for studying specifically the contribution of stationary tissular gas bubbles in the mechanisms of DCS in individually-superfused tissue samples. For validating our method, we investigated in rat brain slices exposed to 0.4 MPa air absolute pressure whether fast decompression rate – the most important cause of cerebral DCS – may induce an increase of lactate dehydrogenase (LDH), a marker of cell injury, compared to slow decompression rate. Results We provide a technical description of our pressure chamber and show that fast decompression rate of 0.3 MPa min −1 induced a rapid and sustained increase of LDH release compared to slow compression rate of 0.01 MPa min −1 ( P < 0.0001). Comparison with existing methods There is no current method for studying stationary tissular gas bubbles. Conclusions This report describes the first method for studying specifically in tissue samples the role of stationary tissular gas bubbles in the mechanisms of DCS. Advantageously, according to this method (i) biological markers other than LDH could be easily studied; (ii) tissue samples could be taken not only from the brain but also from any part of the animal's body known of interest in DCS research, allowing performing tissue compartment research, a major question in the physics and theory of decompression research; and (iii) histological studies could be performed from the tissue samples. [ABSTRACT FROM AUTHOR]

The article offers information on a study that examined the influence of delay to recompression on mild/moderate neurological decompression sickness (DCS) in divers. The study explored the medical histories of 28 divers treated at a hyperbaric facility in the Maldive Islands. Its results show encouragement to remotely situated hyperbaric chambers as well as in third-world resort areas.

The article discusses a study that compares the number of venous gas bubbles observed following a short, deep and shallow, long air dive performed in a hyperbaric chamber and actual dives in open water. Using the Eftedal and Brubakk grading method, the study showed that diving in water produces significantly more gas bubble formation than dry diving. Results of the study suggest that decompression procedures should aim at keeping venous bubble formation as low as possible.

Decompression Sickness (DCS) may occur when divers decompress from a hyperbaric environment. To prevent this, decompression procedures are used to get safely back to the surface. The models whose procedures are calculated from, are traditionally validated using clinical symptoms as an endpoint. However, DCS is an uncommon phenomenon and the wide variation in individual response to decompression stress is poorly understood. And generally, using clinical examination alone for validation is disadvantageous from a modeling perspective. Currently, the only objective and quantitative measure of decompression stress is Venous Gas Emboli (VGE), measured by either ultrasonic imaging or Doppler. VGE has been shown to be statistically correlated with DCS, and is now widely used in science to evaluate decompression stress from a dive. Until recently no mathematical model has existed to predict VGE from a dive, which motivated the development of the Copernicus model. The present article compiles a selection experimental dives and field data containing computer recorded depth profiles associated with ultrasound measurements of VGE. It describes a parameter estimation problem to fit the model with these data. A total of 185 square bounce dives from DCIEM, Canada, 188 recreational dives with a mix of single, repetitive and multi-day exposures from DAN USA and 84 experimentally designed decompression dives from Split Croatia were used, giving a total of 457 dives. Five selected parameters in the Copernicus bubble model were assigned for estimation and a non-linear optimization problem was formalized with a weighted least square cost function. A bias factor to the DCIEM chamber dives was also included. A Quasi-Newton algorithm (BFGS) from the TOMLAB numerical package solved the problem which was proved to be convex. With the parameter set presented in this article, Copernicus can be implemented in any programming language to estimate VGE from an air dive. [ABSTRACT FROM AUTHOR]

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The article discusses saturation treatment in shore-based chambers for divers with deteriorating cerebro-spinal decompression sickness (DCS). Two cases are presented that include air saturation treatment and helium saturation treatment. The article also outlined the basic principles and delivery protocols of saturation treatment.

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. [ABSTRACT FROM AUTHOR]

The article analyzes problems with a preclinical treatment algorithm for diving accidents based on hyperbaric situation in Switzerland. It offers a brief historical perspective of the development of deep diving physiology and practice in the country. It discusses the availability of hyperbaric chambers for assessment and recompression treatment (HBOT) and helicopter-based medevacuation in the country. It also offers a look at international recommendations for decompression illness.

The article presents information on a study which investigated the incidence and severity of work-related health issues facing multiplace chamber attendants exposed to increased pressure at a full-time clinical hyperbaric unit. It describes the working environment of the multiplace hyperbaric chamber for health-care personnel. It discusses the incidence of barotrauma and decompression sickness among hyperbaric chamber attendants. The study concludes that a multiplace hyperbaric chamber is a relatively safe working environment.

The article presents information on a study which investigated the extent and significance of decompression stress experienced by chamber attendants using Doppler analysis. A brief overview is given on hyperbaric oxygen therapy. It also assesses the demographic variation within the hyperbaric attendant population and its association to decompression stress. It relates the limitation of Doppler analysis in assessing decompression stress.

Disabled submarine (DISSUB) survivors are expected to achieve saturation with inert gas. However, rescue procedures may not accommodate staged decompression, raising the potential for severe decompression sickness (DCS). Alternatives to standard recompression therapy are needed. It has been demonstrated in humans that isobaric oxygen "prebreathing" (OPB) can accelerate decompression in a DISSUB scenario. In-70 kg swine saturated at 2.82 atm absolute (ATA), I h of OPB eliminated death and reduced severe DCS. We hypothesized that even shorter periods (<1 h) of OPB before no-stop decompression from saturation at 2.82 ATA could reduce the incidence of DCS in a large animal model. Catheterized Yorkshire swine (68.8 ± 1.7 kg) in individual Plexiglas boxes within a large animal hyperbaric chamber were compressed to 2.82 ATA for 22 h. Following saturation and while still at depth, breathing gas was switched to >95% O2 for 45 mm (OPB45), 15 mm (OPB15), or 5 mm (OPB05) of OPB, or no OPB (control). The chamber was then decompressed without stops (0.91 ATA/min). Observers then entered the chamber and recorded signs of DCS for 2 h. All OPB periods significantly reduced the risk of developing type II DCS. OPB45 eliminated severe DCS. Controls had a 2.5 times greater risk of developing type II DCS than OPB05 (P 0.016). OPB45 and OPB15 significantly reduced type I DCS compared with controls. These results support the potential of OPB as an alternative to staged decompression and that OPB could be expected to improve outcome in a DISSUB rescue scenario. [ABSTRACT FROM AUTHOR]

Exposure to the underwater environment is associated with several unique disorders that may require recompression in a hyperbaric chamber. Increasing pressure during descent reduces the volume of the paranasal sinuses and middle ear, which, if not properly equalized, will sustain injury due to barotrauma. Barotrauma of the inner ear results in vertigo, tinnitus, and often permanent hearing loss. During ascent, expanding gas can produce lung injury accompanied by pneumothorax, mediastinal and subcutaneous emphysema, injection of air into the pulmonary veins, and arterial air embolism to the brain. Divers with pulmonary barotrauma often present with unconsciousness, seizures, or other evidence of cerebral dysfunction. Rapid treatment with recompression often reverses the cerebral deficits. Air embolism lesions are usually diffuse, in contradistinction to a stroke which usually follows the distribution of a single cerebral artery. Decompression sickness is a disorder caused by evolution of supersaturated dissolved gas in tissues and blood following exposure to increased pressure. Protocols for avoiding excess supersaturation during ascent from depth have been available for more than 100 years, and diving is considered safe when established decompression schedules are followed. Decompression sickness causes pain in the joints of the upper and lower extremities, and can injure the spinal cord. Paralysis, paresthesias, sensory loss, and bowel and bladder paralysis accompany spinal cord injury. Treatment involves recompression and oxygen. Platelet inhibitors and other anti-inflammatory drugs are also useful. A diving disorder must be considered in any patient with a neurologic syndrome, vertigo, hearing loss, or joint pain following diving. [ABSTRACT FROM AUTHOR]

The article looks at the development of recompression chamber facilities in Malaysia that started in the early 1960s. The first recompression facility in a hospital was established in 1996 at the Armed Forces Hospital in Lumut. The Malaysian Science University Hospital was the first university hospital in 2004 to establish recompression chamber facilities, with a monoplace recompression chamber.

Production of blood-borne microparticles (MPs), 0.1–1 µm diameter vesicles, and interleukin (IL)-1β in response to high pressure is reported in lab animals and associated with pathological changes. It is unknown whether the responses occur in humans, and whether they are due to exposure to high pressure or to the process of decompression. Blood from research subjects exposed in hyperbaric chambers to air pressure equal to 18 meters of sea water (msw) for 60 minutes or 30 msw for 35 minutes were obtained prior to and during compression and 2 hours post-decompression. MPs and intra-particle IL-1β elevations occurred while at pressure in both groups. At 18 msw (n = 15) MPs increased by 1.8-fold, and IL-1β by 7.0-fold (p < 0.05, repeated measures ANOVA on ranks). At 30 msw (n = 16) MPs increased by 2.5-fold, and IL-1β by 4.6-fold (p < 0.05), and elevations persisted after decompression with MPs elevated by 2.0-fold, and IL-1β by 6.0-fold (p < 0.05). Whereas neutrophils incubated in ambient air pressure for up to 3 hours ex vivo did not generate MPs, those exposed to air pressure at 180 kPa for 1 hour generated 1.4 ± 0.1 MPs/cell (n = 8, p < 0.05 versus ambient air), and 1.7 ± 0.1 MPs/cell (p < 0.05 versus ambient air) when exposed to 300 kPa for 35 minutes. At both pressures IL-1β concentration tripled (p < 0.05 versus ambient air) during pressure exposure and increased 6-fold (p < 0.05 versus ambient air) over 2 hours post-decompression. Platelets also generated MPs but at a rate about 1/100 that seen with neutrophils. We conclude that production of MPs containing elevated concentrations of IL-1β occur in humans during exposure to high gas pressures, more so than as a response to decompression. While these events may pose adverse health threats, their contribution to decompression sickness development requires further study. [ABSTRACT FROM AUTHOR]

An abstract of the article "Monoplace Hyperbaric Chamber Use of US Navy Table 6: A 20-Year Experience," by L. K. Weaver is presented.