Variability in venous gas emboli following the same dive at 3,658 meters

2021 ◽  
pp. 119-126
Author(s):  
Hayden W Hess ◽  
◽  
Courtney E Wheelock ◽  
Erika St. James ◽  
Jocelyn L Stooks ◽  
...  

Exposure to a reduction in ambient pressure such as in high-altitude climbing, flying in aircrafts, and decompression from underwater diving results in circulating vascular gas bubbles (i.e., venous gas emboli [VGE]). Incidence and severity of VGE, in part, can objectively quantify decompression stress and risk of decompression sickness (DCS) which is typically mitigated by adherence to decompression schedules. However, dives conducted at altitude challenge recommendations for decompression schedules which are limited to exposures of 10,000 feet in the U.S. Navy Diving Manual (Rev. 7). Therefore, in an ancillary analysis within a larger study, we assessed the evolution of VGE for two hours post-dive using echocardiography following simulated altitude dives at 12,000 feet. Ten divers completed two dives to 66 fsw (equivalent to 110 fsw at sea level by the Cross correction method) for 30 minutes in a hyperbaric chamber. All dives were completed following a 60-minute exposure at 12,000 feet. Following the dive, the chamber was decompressed back to altitude for two hours. Echocardiograph measurements were performed every 20 minutes post-dive. Bubbles were counted and graded using the Germonpré and Eftedal and Brubakk method, respectively. No diver presented with symptoms of DCS following the dive or two hours post-dive at altitude. Despite inter- and intra-diver variability of VGE grade following the dives, the majority (11/20 dives) presented a peak VGE Grade 0, three VGE Grade 1, one VGE Grade 2, four VGE Grade 3, and one VGE Grade 4. Using the Cross correction method for a 66-fsw dive at 12,000 feet of altitude resulted in a relatively low decompression stress and no cases of DCS.

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.


2015 ◽  
Vol 114 (3) ◽  
pp. 1521-1529 ◽  
Author(s):  
Dror Tal ◽  
Hofit Shachar-Bener ◽  
Dov Hershkovitz ◽  
Yehuda Arieli ◽  
Avi Shupak

Mass stranding of cetaceans (whales and dolphins), in close association with the activity of naval sonar systems, has been reported on numerous occasions. Necropsy showed bubble-associated lesions similar to those described in human decompression sickness (DCS). We examined the hypothesis that exposure to underwater sound may potentiate DCS. Rats were subjected to immersion and simulated dives with and without simultaneous acoustic transmissions at pressure levels and frequencies of 204 dB/8 kHz and 183.3 dB/15 kHz. DCS severity was assessed using the rotating wheel method. Recording of somatosensory evoked potentials (SSEPs) was employed under general anesthesia as an electrophysiological measure of neurologic insult. A significantly higher rate of decompression sickness was found among animals exposed to the 204-dB/8-kHz sound field. Significantly higher pathological SSEPs scores were noted for both underwater sound protocols. Pathological SSEPs scores in animals immersed during the acoustic transmissions, but without changes in ambient pressure, were comparable to those observed in animals exposed to the dive profile. The results demonstrate induction of neurological damage by intense underwater sound during immersion, with a further deleterious effect when this was combined with decompression stress. The study outcome has potential implications for human diving safety and may provide an explanation for the mass stranding of cetaceans purportedly associated with sonar activity.


2019 ◽  
pp. 217-220
Author(s):  
Eduardo Briceño-Souza ◽  
◽  
Nina Méndez-Domínguez ◽  
Ricardo j Cárdenas-Dajda ◽  
Walter Chin ◽  
...  

Diving as a method of fishing is used worldwide in small-scale fisheries. However, one of the main causes of morbidity and mortality among fishermen is decompression sickness (DCS). We report the case of a 46-year-old male fisherman diver who presented with chronic inguinal pain that radiated to the lower left limb. Living and working in a fishing port in Yucatan, he had a prior history of DCS. A diagnosis of avascular necrosis in the left femoral head secondary to DCS was made via analysis of clinical and radiological findings. The necrosis was surgically resolved by a total hip arthroplasty. Dysbaric osteonecrosis is a more probable diagnosis. In this region fishermen undergo significant decompression stress in their daily fishing efforts. Further studies regarding prevalence of dysbaric osteonecrosis among small-scale fisheries divers are needed. In a community where DCS is endemic and has become an epidemic, as of late, the perception of this health risk remains low. Furthermore, training and decompression technique are lacking among the fishing communities.


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.


2021 ◽  
pp. 57-58
Author(s):  
Virginie Papadopoulou ◽  
◽  
Peter Lindholm ◽  

Decompression sickness (DCS) remains a major operational concern for diving operations, submarine escape and high-altitude jumps. Aside from DCS symptoms, venous gas emboli (VGE) detected with ultrasound post-dive are often used as a marker of decompression stress in humans, with a specificity of 100% even though the sensitivity is poor [1]. Being non-invasive, portable and non-ionizing, ultrasound is particularly suited to regular and repeated monitoring. It could help elucidate inter- and intra-subject variability in VGE and DCS susceptibility, but analyzing these recordings remains a cumbersome task [2].


1962 ◽  
Vol 202 (6) ◽  
pp. 1041-1044 ◽  
Author(s):  
D. C. Smith ◽  
J. Q. Barry ◽  
A. J. Gold

Exposure of restrained, unanesthetized dogs to a simulated altitude of 30,000 ft consistently resulted in respiratory alkalosis and marked hypokalemia. When alkalosis was prevented by increasing the pCO2 of inspired air during decompression, a smaller but statistically significant decrease in plasma potassium concentration still occurred. In comparison with previous studies, the hypokalemia observed in these restrained, unanesthetized dogs was greater than that found in either unrestrained or anesthetized dogs subjected to the same decompression stress. Consequently, the suggestion is made that in the unanesthetized, restrained dog, the hypokalemic response not attributable to respiratory alkalosis is of adrenal mediation and results from the "stress" of restraint plus hyperventilation, rather than to hypoxemia or the decompression stress, per se.


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