Hyperbaric oxygen for decompression sickness: 2021 update

2021 ◽  
pp. 195-203
Author(s):  
Richard E. Moon ◽  
◽  
Simon J. Mitchell ◽  

Hyperbaric oxygen for decompression sickness: 2021 update Decompression sickness (DCS, “bends”) is caused by the formation of bubbles in tissues and/or blood when the sum of dissolved gas pressures exceeds ambient pressure (supersaturation). This may occur when ambient pressure is reduced during: ascent from a dive; rapid ascent to altitude in an unpressurized aircraft or hypobaric chamber; loss of cabin pressure in an aircraft [2]; and during space walks. In diving, compressed-gas breathing is usually necessary, although occasionally DCS has occurred after either repetitive or very deep breath-hold dives

2019 ◽  
pp. 685-693
Author(s):  
Richard E. Moon ◽  
◽  
Simon Mitchell ◽  
◽  

Rationale Decompression sickness (DCS, “bends”) is caused by formation of bubbles in tissues and/or blood when the sum of dissolved gas pressures exceeds ambient pressure (supersaturation) [1]. This may occur when ambient pressure is reduced during any of the following: • ascent from a dive; • depressurization of a hyperbaric chamber; • rapid ascent to altitude in an unpressurised aircraft or hypobaric chamber; • loss of cabin pressure in an aircraft [2] and • during space walks.


2019 ◽  
pp. 673-683
Author(s):  
Richard E. Moon ◽  

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac “vapor lock” and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence-based review of adjunctive therapies is presented.


2019 ◽  
pp. 81-85
Author(s):  
Se Hyun Oh ◽  
◽  
Hui Dong Kang ◽  
Sang Ku Jung ◽  
Sangchun Choi ◽  
...  

Decompression sickness is a disease caused by abrupt pressure change and presents various symptoms. To date, acute kidney injury associated with decompression sickness has been reported frequently, but there is no report of hepatic infarction associated with decompression sickness. We report a case of acute kidney injury and acute hepatic infarction treated with hyperbaric oxygen (HBO2) therapy and dialysis in a patient with severe decompression sickness after work diving.


1998 ◽  
Vol 275 (3) ◽  
pp. R677-R682 ◽  
Author(s):  
Susan R. Kayar ◽  
Terry L. Miller ◽  
Meyer J. Wolin ◽  
Eugenia O. Aukhert ◽  
Milton J. Axley ◽  
...  

We present a method for reducing the risk of decompression sickness (DCS) in rats exposed to high pressures of H2. Suspensions of the human colonic microbe Methanobrevibacter smithii were introduced via a colonic cannula into the large intestines of the rats. While the rats breathed H2in a hyperbaric chamber, the microbe metabolized some of the H2diffusing into the intestine, converting H2and CO2to methane and water. Rate of release of methane from the rats, which was monitored by gas chromatography, varied with chamber H2pressure. This rate was higher during decompression than during compression, suggesting that during decompression the microbe was metabolizing H2stored in the rats’ tissues. Rats treated with M. smithii had a 25% (5 of 20) incidence of DCS, which was significantly lower ( P < 0.01) than the 56% (28 of 50) incidence of untreated controls, brought on by a standardized compression and decompression sequence. Thus using a microbe in the intestine to remove an estimated 5% of the body burden of H2reduced DCS risk by more than one-half. This method of biochemical decompression may potentially facilitate human diving.


2015 ◽  
Vol 101 (2) ◽  
pp. 186-187
Author(s):  
A Wrigley

AbstractHypoxia training at the Royal Air Force Centre of Aviation Medicine (RAF CAM) has traditionally involved the use of a hypobaric chamber to induce hypoxia. While giving the student experience of both hypoxia and decompression, hypobaric chamber training is not without risks such as decompression sickness and barotrauma. This article describes the new system for hypoxia training known as Scenario-Based Hypoxia Training (SBHT), which involves the subject sitting in an aircraft simulator and wearing a mask linked by hose to a Reduced Oxygen Breathing Device (ROBD). The occupational requirements to be declared fit for this new training method are also discussed.


2021 ◽  
Vol 51 (1) ◽  
pp. 103-106
Author(s):  
Jacek Kot ◽  
◽  
Ewa Lenkiewicz ◽  
Edward Lizak ◽  
Piotr Góralczyk ◽  
...  

Medical personnel in hyperbaric treatment centres are at occupational risk for decompression sickness (DCS) while attending patients inside the multiplace hyperbaric chamber (MHC). A 51-year-old male hyperbaric physician, also an experienced diver, was working as an inside attendant during a standard hyperbaric oxygen therapy (HBOT) session (70 minutes at 253.3 kPa [2.5 atmospheres absolute, 15 metres’ seawater equivalent]) in a large walk-in MHC. Within 10 minutes after the end of the session, symptoms of spinal DCS occurred. Recompression started within 90 minutes with an infusion of lignocaine and hydration. All neurological symptoms resolved within 10 minutes breathing 100% oxygen at 283.6 kPa (2.8 atmospheres absolute) and a standard US Navy Treatment Table 6 was completed. He returned to regular hyperbaric work after four weeks of avoiding hyperbaric exposures. Transoesophageal echocardiography with a bubble study was performed 18 months after the event without any sign of a persistent (patent) foramen ovale. Any hyperbaric exposure, even within no-decompression limits, is an essential occupational risk for decompression sickness in internal hyperbaric attendants, especially considering the additional risk factors typical for medical personnel (age, dehydration, tiredness, non-optimal physical capabilities and frequent problems with the lower back).


2021 ◽  
pp. 287-295
Author(s):  
Ya Li ◽  
◽  
Xiaona Xu ◽  
Junxiang Bao Bao ◽  
Wenlan Wang ◽  
...  

Objective: Decompression sickness (DCS) causes serious brain hypoxic-ischemic injury. This experiment was designed to observe whether hyperbaric oxygen (HBO2) pretreatment played a neuroprotective effect in decompression sickness rat models and to explore the mechanism of protective effects. Methods: Sprague-Dawley (SD) male rats were pretreated with HBO2 and then underwent decompression to establish the DCS rat model. Antioxidant capacities were evaluated by detecting peroxides (GPx), superoxide dismutase (SOD), catalase (CAT) activity and malondialdehyde (MDA) content in brains. The levels of metal elements manganese (Mn), zinc (Zn), iron (Fe) and magnesium (Mg) in brain tissues were assessed by flame atomic absorption spectrometry. Necrosis and apoptosis of neurons were assessed by H-E staining and immunohistochemical staining. Results: HBO2 pretreatment reduced the degree of necrosis and apoptosis in brain tissues of decompression sickness rat models. In addition, HBO2 pretreatment increased GPx, SOD and CAT activities and reduced MDA accumulation. It also increased the content of Mn, Zn, Fe and Mg in brain tissue, which are all related to free radical metabolism. Conclusion: These results suggested that HBO2 pretreatment has protective effects on brain injury of rats with decompression sickness. The mechanism of the protective effects may be related to reducing oxidative damage by affecting metal elements in vivo.


2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Alexander Patrician ◽  
Ivan Drvis ◽  
Tony Dawkins ◽  
Barak Otto ◽  
Geoff Coombs ◽  
...  

2012 ◽  
Vol 523-524 ◽  
pp. 1041-1046 ◽  
Author(s):  
Tappei Higashi ◽  
Masato Sando ◽  
Jun Shinozuka

High-speed orthogonal cutting experiments with cutting speeds of up to 200 m/s with a high-speed impact cutting tester of air-gun type are attempted. In this tester, a light projectile with a small built-in cutting tool is loaded into a tube, being accelerated by a compressed gas. The projectile captures the chip that is indispensable to analyze the cutting mechanism. The projectile holding the chip is decelerated by another compressed gas just after finishing the cutting, being stopped without damage in the tube. Successful experiment can be accomplished by setting adequate values of the operation parameters for the experiment, which are the pressure of each gas and the opening and shutting time of the solenoid-controlled valve for each compressed gas. In order to determine the adequate values of these parameters, a ballistic simulator that simulates the velocity and position of the projectile traveling in the tube is developed. By setting the values of these parameters obtained by the simulator, the cutting speed of 200 m/s is achieved when the ambient pressure is set to be a vacuum and helium is used for each compressed gas. This paper describes the ballistic simulator developed and shows the experimental results of the high-speed cutting of aluminum alloy A2017.


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