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PubMed2004

Treatment of decompression sickness in swine with intravenous perfluorocarbon emulsion.

BACKGROUND: We examined an adjunctive treatment for severe decompression sickness (DCS) to be used when hyperbaric treatment is delayed or unavailable. HYPOTHESIS: It has been hypothesized that intravenous perfluorocarbon (PFC) emulsion combined with 100% inspired O2 would improve the outcome in severe DCS. METHODS: Swine (n = 45) were compressed to 4.9 ATA on air for 22 h and brought directly to 1 ATA at 0.9 ATA min(-1). The animals were then randomized to three groups. The first group breathed ambient air, the second group breathed 100% O2, and a third group received 6 ml x kg(-1) of perflubron emulsion (Oxygent) intravenously and breathed 100% O2. Outcomes of neurological and cardiopulmonary DCS and death were recorded. RESULTS: Animals that received PFC emulsion sustained less DCS (p < 0.01) than the other groups (53% vs. 93%). No animals in the PFC group sustained neurological DCS, which was present in 69% of the subjects in the other two groups. CONCLUSION: O2 breathing postdive did not significantly reduce morbidity or mortality in this model. Postdive treatment with PFC emulsion and 100% O2 decreased the incidence of DCS after nonstop decompression from saturation.

Animals↗
PubMed2002

Operation Everest III (Comex'97): altitude-induced decompression sickness during a hypobaric chamber experiment: necessity for circulating venous gas emboli monitoring for the investigators.

INTRODUCTION: Acute exposure to altitude changes increases the risk of decompression sickness (DCS). Altitude-induced DCS incidence is from 15 to 20% and > 30% above 8,000 m. A particular risk occurs for scientific investigators during hypobaric chamber experiments. OBJECTIVE: In the present study, we assess whether the detection of nitrogen venous gas emboli (VGE) could help to screen the investigators at risk for altitude-induced DCS. MATERIAL AND METHODS: During a 32-day hypobaric chamber experiment, we collected clinical episodes of DCS symptoms in the investigators, and performed detection of VGE using two-dimensional (2D) echocardiography and pulsed Doppler ultrasonography guided by 2D images, graded from 0 to 5. RESULTS: Eight investigators made a total of 32 flights, including 8 flights above 8,000 m, with a 15.6% overall incidence of DCS symptoms and a 50% incidence above 8,000 m. VGE detections were systematically performed at or above 8,000 m (eight detections), and some detections were performed at 5,000 m, 6,000 m, and 7,000 m. VGE grades 3 and 4 were present in all but one subject with DCS symptoms and preceded the "bends" in all cases. VGE detection thus confirmed, in a more sensitive way compared to clinical examination, that our precautionary measures for DCS were not optimized. CONCLUSION: VGE monitoring for investigators during hypobaric chamber experiments increased the sensitivity for the detection of subjects at risk for DCS.

Adult↗
PubMed1981

[Blood coagulation processes in decompression sickness and hyperbaric therapy].

The hyperaggregability of platelets is remarkably important in the pathogenesis of decompression sickness. The basis of this phenomenon might consist of an excessive production of metabolites of arachidonic acid (C 20:4) whose action favours aggregation (prostaglandin endoperoxides PGG2 and PGH2 and Tromboxane A2) in respect of the synthesis of its derivatives exerting an antithrombotic action (prostacyclin I2). The antiaggregating therapy usually associated to the hyperbaric treatment involves administration of acetylsalicylic acid in low doses (3.5-5 mg/kg every three days), associated if necessary to dypyridamol. As a prophylaxis against thrombotic phenomena in "risky" subjects, a congruous dietetic assumption of polyunsaturated fatty acids is recommended, such as linoleic acid (C 18:2) and eicosapentaenoic acid (C 20:5) which are forerunners of anti-aggregating prostaglandin derivates. Hyperbaric oxygenation might finally lead to the production of lypid peroxides apt to inhibit the synthesis of PGI2. In such cases it is a rational procedure to administer vitamin E in high doses, as physiological antioxidant of lypids.

Antioxidants↗
PubMed2003

The risk of altitude decompression sickness at 12,000 m and the effect of ascent rate.

INTRODUCTION: Loss of aircraft cabin pressurization can result in very rapid decompression rates. The literature contains reports of increased or unchanged levels of altitude decompression sickness (DCS) resulting from increasing the rate of decompression. We conducted two prospective exposure profiles to quantify the DCS risk at 12,192 m (40,000 ft), and to determine if there was a greater DCS hazard associated with a much higher rate of decompression than typically used during past DCS studies. METHODS: The 63 human subjects participated in 80 altitude chamber decompression exposures to a simulated altitude of 12,192 m (2.72 psia; 18.75 kPa) for 90 min, following preoxygenation with 100% oxygen for 90 min. Half of the subject-exposures involved an 8-min decompression (1,524 mpm; 5,000 fpm) and the other half experienced a 30-s decompression (mean of 24,384 mpm; 80,000 fpm). Throughout each ascent and exposure, subjects were seated at rest and breathed 100% oxygen. At altitude, they were monitored for precordial venous gas emboli (VGE) and DCS symptoms. RESULTS: The higher decompression rate yielded 55.0% DCS and 72.5% VGE and the lower rate produced 47.5% DCS and 65.0% VGE. Chi square and log rank tests based on the Kaplan-Meier analyses indicated no difference in the incidence or onset rate of DCS or VGE observed during the two profiles. CONCLUSION: Decompression rate to altitude up to 24,384 mpm was found not to have an effect on DCS risk at altitude. However, research is needed to define the DCS risk with decompression rates greater than 24,384 mpm. It was also found that the onset time to DCS symptoms decreases as altitude increases.

Adult↗
PubMed1997

Probabilistic gas and bubble dynamics models of decompression sickness occurrence in air and nitrogen-oxygen diving.

Probabilistic models of the occurrence of decompression sickness (DCS) with instantaneous risk defined as the weighted sum of bubble volumes in each of three parallel-perfused gas exchange compartments were fit using likelihood maximization to the subset of the USN Primary Air and N2-O2 database [n = 2,383, mean P(DCS) = 5.8%] used in development of the USN LE1 probabilistic models. Bubble dynamics with one diffusible gas in each compartment were modeled using the Van Liew equations with the nucleonic bubble radius, compartmental volume, compartmental bulk N2 diffusivity, compartmental N2 solubility, and the N2 solubility in blood x compartmental blood flow as adjustable parameters. Models were also tested that included the effects of linear elastic resistance to bubble growth in one, two, or all three of the modeled compartments. Model performance about the training data and separate validation data was compared to results obtained about the same data using the LE1 probabilistic model, which was independently implemented from published descriptions. In the most successful bubble volume model, BVM(3), diffusion significantly slows bubble growth in one of the modeled compartments, whereas mechanical resistance to bubble growth substantially accelerates bubble resolution in all compartments. BVM(3) performed generally on a par with LE1, despite inclusion of 12 more adjustable parameters, and tended to provide more accurate incidence-only estimates of DCS probability than LE1, particularly for profiles in which high fractional O2 gas mixes are breathed. Values of many estimated BVM(3) parameters were outside of the physiologic range, indicating that the model emerged from optimization as a mathematical descriptor of processes beyond bubble formation and growth that also contribute to DCS outcomes. Although incomplete as a mechanistic description of DCS etiology, BVM(3) remains applicable to a wider variety of decompressions than LE1 and affords a conceptual framework for further refinements motivated by mechanistic principles.

Decompression Sickness↗
PubMedDate not supplied

Efficacy of Doppler ultrasound [correction of utrasound] for screening symptoms of decompression sickness during simulated extravehicular activities.

Doppler ultrasound is frequently used for monitoring circulating microbubbles during decompression to assess the symptoms of Decompression Sickness (DCS). This analysis was carried out to evaluate its effectiveness for screening symptoms of DCS during simulated extravehicular activities (EVA). The information from various hypobaric chamber studies carried out at the NASA Johnson Space Center, Houston, TX was used in this analysis (n=516). The circulating microbubbles were detected in the precordial area in 42% (218/516), and symptoms were reported in 16% (81/516) of these exposures. The accuracy of Doppler-detectable bubbles (Spencer grades) on all symptoms of DCS was examined by calculating measures of sensitivity and specificity. The efficacy of Doppler as a screening device was examined by calculating their positive predictive value (PPV) and negative predictive value (NPV). The results of these analyses indicated that the sensitivity of Doppler decreased, and the PPV increased with higher Spencer grades. However, the likelihood of detecting true negative cases (NPV) was consistently higher with all bubble grades. Due to the high false-positive rate and low prior probabilities of the risk of DCS, Doppler was found to be more useful to identify those who did not develop DCS, than to detect positive cases of DCS in the simulated EVA exposures.

Decompression Sickness↗
PubMed1990

Complement activation involvement in decompression sickness of rabbits.

A hypothesis has been proposed that claims much of the phenomena of decompression sickness (DCS) are mediated by the complement system of blood plasma. This "complement hypothesis" can be used to explain the variation in susceptibility of individuals to DCS, including the phenomena of acclimatization and de-acclimatization. In this study, certain predictions of the complement hypothesis were examined by exposing rabbits to a particular pressure profile; some were observed to have symptoms of DCS and some showed none. Those that were observed to have symptoms were also found to have native complement systems that were activated by air bubbles, and those that did not show symptoms of DCS when exposed to the same pressure profile had native complement systems that were not activated by air bubbles. Rabbits that had shown symptoms of DCS the first 2 times that they were exposed to the pressure profile could be acclimatized to the pressure profile by pharmacologically decomplementing them in vivo. After being decomplemented, they showed no symptoms of DCS when they were exposed to the same pressure profile for a third time. When the decomplemented rabbits were allowed to remain inactive for a period of time that was sufficient to allow their complement systems to return to normal, after having been decomplemented, and were then subjected to the pressure profile for the fourth time, they were each again observed to have symptoms of DCS, i.e., they became de-acclimatized when their complement systems had returned to their native sensitivity. These results provide further experimental support for the complement hypothesis.

Animals↗
PubMed1999

[Human resistance to decompression sickness and nonspecific methods of its elevation].

The object of this study was the dependence of decompression sickness (DCS) tolerance determined by the intensity of venous gas embolism on functioning of the cardiovascular and respiratory systems, and micro-circulation which predetermine wash-out of an indifferent gas. Efficiency of nonspecific methods, e.g. hypercapnic training, hyperbaric oxygenation, exposures to pulse current to enhance human tolerance to DCS was experimentally substantiated.

Adult↗
PubMed1998

Probable decompression sickness in a trainee with atopic dermatitis.

Hypobaric chamber training has a potential risk of inducing decompression sickness (DCS). A case of a patient with an atopic dermatitis who complained of paresthesia and numbness in his left arm and shoulder during the altitude exposure is presented here. His symptoms were severe enough for the attending medical officer to diagnose Type II DCS, but it turned out to be a probable case of simple skin bends requiring no treatment. The author can find no better explanation for this discrepancy than the contribution of dermatitis. The possibility of atopic dermatitis confounding the correct diagnosis of the severity of DCS is proposed.

Adult↗
PubMed1987

Failure of heparin, superoxide dismutase, and catalase to protect against decompression sickness.

The effects of heparin (HEP), superoxide dismutase (SOD), and catalase (CAT) on the course of decompression sickness (DCS) were studied in anesthetized dogs (Canis familiaris). Animals were divided into 4 groups: a drug assay group (n = 4) received HEP + SOD or HEP + SOD + CAT but were not dived; a control group (n = 14) was dived without drug treatment; a HEPSOD group (n = 11) received HEP + SOD predive and postdive; and a HEPSODCAT group (n = 15) received HEP + SOD + CAT before diving. All dived animals were subjected to repetitive air dives to 10 ATA until pulmonary artery pressure at least doubled within 10 min postdive. Physiologic variables were measured for 3 h postdive or until death. Animals were not recompressed. More early deaths occurred in the HEPSOD (7/11) and HEPSODCAT (8/15) groups than in the control group (5/14). All dived animals developed pulmonary hypertension, systemic hypotension, hemoconcentration, acidosis, hypoxemia, and interstitial pulmonary edema postdive. Drug therapy did not alter these responses to decompression. We conclude that without recompression, treatment with either HEP + SOD OR HEP + SOD + CAT does not improve the outcome of severe DCS in this animal model.

Animals↗
PubMed1988

Air vs. He-O2 recompression treatment of decompression sickness in guinea pigs.

Air vs. He-O2 (20.9% O2) recompression treatment was examined in a model of severe decompression sickness (DCS) using male albino guinea pigs (Cavia porcellus, 500-600 g). Following decompression to the surface from simulated air dives at 200 or 250 fsw, both anesthetized and unanesthetized animals often exhibited responses indicative of a fatal bout of DCS (including hypotension, cardiac arrhythmia, and tachypnea). Upon recompression with air back to depth, good recovery of animals with DCS was observed. Comparison of air vs. He-O2 recompression responses of unanesthetized animals with recompression back to initial depth (200 fsw) revealed a slower recovery from tachypnea with He-O2. Recompression partially back to depth following 200-fsw air dives produced significant differences in the breathing recovery vs. recompression depth relationship between air and He-O2. Treatment effectiveness improved with increasing depth with air, but not with He-O2. These data indicate potential differences in recompression response to air vs. He-O2 when using ventilatory recovery as a measure of effectiveness in treatment of DCS in guinea pigs following air dives.

Air↗