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Doppler bubble detection and decompression sickness: a prospective clinical trial.

Decompression sickness in human beings exposed to high ambient pressure is thought to follow from gas bubble formation and growth in the body during return to low pressure. Detection of Doppler-shifted ultrasonic reflections in major blood vessels has been promoted as a noninvasive and sensitive indicator of the imminence of decompression sickness. We have conducted a double-blind, prospective clinical trial of Doppler ultrasonic bubble detection in simulated diving using 83 men, of whom 8 were stricken and treated for the clinical disease. Diagnosis based only on the Doppler signals had no correlation with clinical diagnosis. Bubble scores were only slightly higher in the stricken group. The Doppler technique does not appear to be of diagnostic value in the absence of other clinical information.

Clinical Trials as Topic↗

On the likelihood of decompression sickness.

The occurrence of decompression sickness in animals and humans is characterized by the extreme variability of individual response. Nevertheless, models and analyses of decompression results have generally used a critical value approach to separate safe and unsafe decompression procedures. Application of the principle of maximum likelihood provides a formal and consistent way to quantify decompression risk and to apply models to data on decompression outcome. By use of the maximum likelihood principle, a number of models were fit to data from dose-response and maximum pressure-reduction experiments with both rats and men. Several different formulations of two- and three-parameter models described the data well. In addition to summarizing data sets, the analyses provide a way to maximize the value of experimental observations, test theoretical predictions, estimate uncertainty in conclusions, and recommend safe practices.

Air↗

Biophysical basis for inner ear decompression sickness.

Isolated inner ear decompression sickness (DCS) is recognized in deep diving involving breathing of helium-oxygen mixtures, particularly when breathing gas is switched to a nitrogen-rich mixture during decompression. The biophysical basis for this selective vulnerability of the inner ear to DCS has not been established. A compartmental model of inert gas kinetics in the human inner ear was constructed from anatomical and physiological parameters described in the literature and used to simulate inert gas tensions in the inner ear during deep dives and breathing-gas substitutions that have been reported to cause inner ear DCS. The model predicts considerable supersaturation, and therefore possible bubble formation, during the initial phase of a conventional decompression. Counterdiffusion of helium and nitrogen from the perilymph may produce supersaturation in the membranous labyrinth and endolymph after switching to a nitrogen-rich breathing mixture even without decompression. Conventional decompression algorithms may result in inadequate decompression for the inner ear for deep dives. Breathing-gas switches should be scheduled deep or shallow to avoid the period of maximum supersaturation resulting from decompression.

Adult↗

Decompression sickness and the role of exercise during decompression.

The risk of decompression sickness (DCS) is greatly increased with exercise at altitude. Bends is the commonest symptom in altitude DCS. Though the adverse effect of exercise at altitude is well known, the role of exercise during decompression is not clear. In this paper, a case of bends occurring with exercise during accidental decompression is presented. The event occurred while exercising on a treadmill at an altitude of approximately 4,572 m (15,000 ft) in the hypobaric chamber. No oxygen pre-breathe was done and ambient air was breathed throughout. The role of hypoxia and exercise during decompression, as well as individual susceptibility, are discussed. Even moderately severe exercise at low altitude may predispose healthy individuals breathing ambient air to DCS, especially when exercise is undertaken during decompression.

Adult↗

Exercise-enhanced preoxygenation increases protection from decompression sickness.

INTRODUCTION: Prevention of decompression sickness (DCS) during exposure to altitude equivalents of 30,000 ft (9144 m) requires extensive denitrogenation. In preparation for extravehicular activity (EVA), present NASA policy is to denitrogenate using a 10.2 psia staged decompression of the entire shuttle for at least 12 h, including 100 min of preoxygenation (breathing 100% oxygen at 14.7 psia prior to decompression), before decompression to the 4.3 psia (30,000 ft; 9144 m) suit pressure. This staged decompression provides the same or better protection from DCS as a 3.5- or 4-h preoxygenation used on earlier Shuttle EVA's. For high altitude reconnaissance flights at similar cockpit altitudes, a 1-h preoxygenation is currently required. METHODS: We have investigated the use of a 1-h and a 15-min preoxygenation period, each beginning with 10 min of dual-cycle ergometry performed at 75% of each subject's peak oxygen consumption (VO2peak) to enhance preoxygenation efficiency by increasing perfusion and ventilation. Male subjects accomplished a 1-h preoxygenation with exercise, a 15-min preoxygenation with exercise, or a 1-h resting preoxygenation before exposure to 4.3 psia for 4 h while performing light to moderate exercise. RESULTS: Incidence of DCS following the 1-h preoxygenation with exercise (42%; n = 26) was significantly less than that following the 1-h resting preoxygenation (77%; n = 26). Incidence and onset of DCS following the 15-min preoxygenation with exercise (64%; n = 22) was not significantly different from the incidence following the 1-h resting control. CONCLUSION: Preoxygenation with exercise has been shown to provide significantly improved DCS protection when compared with resting preoxygenation.

Adult↗

[Research on the incidence of decompression sickness in compressed air works. The development of its recent five years' study].

Compressed air works have been used as the safest construction work for the basic underground or underwater compressed shield or caisson works in Japan; however, the workers who were exposed to the compressed fields must have put themselves at risk of decompression sickness. Decompression sickness is generally considered to be due to the bubble effects and the bubbles originate from the supersaturated gas dissolved in the blood and other tissues. The standard decompression schedule by the Ministry of Labor has been practically applied at the end of compressed air works, and the laborers decompress slowly from the bottom pressure to the surface according to the schedule. It is difficult to completely prevent the sickness and the average percentage of contracting "bends," using the Japanese standard decompression schedule, is considered to be 0.54%. But previous papers reported higher incidences from 1.42 to 3.3% or more. We have continued an actual investigation on the incidence, and the number of the exposed trials amounted to nearly a hundred thousand. These data were compared between recent five years' group and before. Eventually, it was ascertained that the incidence has been significantly decreased in the recent five years; however, greater care in occupational safety control is still needed.

Adult↗

Probabilistic modelling for estimating gas kinetics and decompression sickness risk in pigs during H2 biochemical decompression.

We modelled the kinetics of H2 flux during gas uptake and elimination in conscious pigs exposed to hyperbaric H2. The model used a physiological description of gas flux fitted to the observed decompression sickness (DCS) incidence in two groups of pigs: untreated controls, and animals that had received intestinal injections of H2-metabolizing microbes that biochemically eliminated some of the H2 stored in the pigs' tissues. To analyse H2 flux during gas uptake, animals were compressed in a dry chamber to 24 atm (ca 88% H2, 9% He, 2% O2, 1% N2) for 30-1440 min and decompressed at 0.9 atm min(-1) (n = 70). To analyse H2 flux during gas elimination, animals were compressed to 24 atm for 3 h and decompressed at 0.45-1.8 atm min(-1) (n = 58). Animals were closely monitored for 1 h post-decompression for signs of DCS. Probabilistic modelling was used to estimate that the exponential time constant during H2 uptake (tau(in)) and H2 elimination (tau(out)) were 79 +/- 25 min and 0.76 +/- 0.14 min, respectively. Thus, the gas kinetics affecting DCS risk appeared to be substantially faster for elimination than uptake, which is contrary to customary assumptions of gas uptake and elimination kinetic symmetry. We discuss the possible reasons for this asymmetry, and why absolute values of H2 kinetics cannot be obtained with this approach.

Animals↗

A case of decompression sickness at 2,437 meters (8,000 feet).

Among aviators, decompression sickness is a condition that occurs almost exclusively at altitudes above 6,098 m (20,000 ft). Several reports have been published describing the development of decompression sickness after altitude exposures of 3,049 to 4,878 m (10,000-16,000 ft). In most of these cases, the affected individual had a previous history of pain in the involved area due to prior trauma or surgery, or had other risk factors for decompression sickness, such as obesity. Few of these reports have confirmed the presence of decompression sickness by a test of pressure. A case is reported here of multiple joint pains developing after a rapid decompression at 2,439 m (8,000 ft), which improved during descent and rapidly resolved with recompression therapy. There was no prior history of joint pain, trauma, or diving. A brief discussion of decompression sickness is included.

Adult↗

Bubble dissolution physics and the treatment of decompression sickness.

The treatment of decompression sickness often involves both recompressing the victim and administering hyperbaric oxygen in the hope of more rapidly dissolving the bubbles which cause this malady. Although many hundreds of such treatments are conducted each year in the United States alone, the underlying physical principles governing the dissolution of such bubbles are not well understood and only empirically tested. In this paper, we present a mathematical theory of bubble dissolution that is verified by comparison with laboratory experiments. This theory suggests that the commonly employed treatment techniques would be only marginally effective, and that in many situations the bubbles that cause the disease cannot be adequately dissolved using existing techniques and facilities.

Atmospheric Pressure↗

Climatic and environmental factors in the aetiology of decompression sickness in divers.

As decompression sickness (DCS) may occur unexpectedly after 'safe' dives it was hypothesised that the weather and tidal factors could contribute to the risk. One hundred and seventy seven cases of DCS were identified from the Institute of Naval Medicine's diving accident records and allocated to a 'safe' group or control 'risky' group, depending on the dive profiles. Comparison of the prevailing environmental conditions between groups revealed significant differences in air temperature and windchill (p = < 0.001 for all dives) and for air minus water temperature (p = < 0.01 for all dives). The results imply that exposure to a cold thermal environment following diving, particularly when the air temperature is colder than the water temperature, may be a previously unrecognised risk factor for DCS.

Air↗

Experimental respiratory decompression sickness in sheep.

Respiratory decompression sickness (RDCS, "the chokes") is a potentially lethal consequence of ambient pressure reduction. Lack of a clearly suitable animal model has impeded understanding of this condition. RDCS, unaccompanied by central nervous system signs, occurred in 17 of 18 unanesthetized sheep exposed to compressed air at 230 kPa (2.27 ATA) for 22 h, returned to normal pressure for approximately 40 min, and taken to simulated altitude (0.75 ATA, 570 Torr). Respiratory signs, including tachypnea, sporadic apnea, and labored breathing, were accompanied by precordial Doppler ultrasound evidence of marked venous bubble loading. Pulmonary arterial pressures exceeded 30 Torr in five catheterized sheep that died or became moribund. Hypoxemia (arterial Po2 less than 40 Torr), neutropenia, and thrombocytopenia were observed. Peribronchovascular edema was the most prominent necropsy finding. Chest radiography indicated interstitial edema in most affected sheep. High body weight and catheterization predisposed the sheep to severe RDCS. It appears that this protocol reliably provides a useful animal model for studies of RDCS and obstructive pulmonary hypertension, that the precipitating event is massive pulmonary embolization by bubbles, and that venous bubbles, detected by Doppler ultrasound, can signal impending RDCS.

Altitude↗

Towards new paradigms for the treatment of hypobaric decompression sickness.

Altitude induced (hypobaric) decompression sickness (DCS) has long been treated with ground level oxygen and U.S. Navy Treatment Tables 5 and 6. These treatment tables originate from surface excursion diving and, when implemented, require significant resource allocation. Although they are effective treatment regimens, these tables were not developed for treating hypobaric DCS which has an etiology similar to saturation diving DCS. In this review, different treatment options for hypobaric DCS are presented. These options include more aggressive use of ground level oxygen and treatment tables using a maximum pressure of 2 atmospheres (ATA). Specific attention is given to USAF Table VIII, an experimental hypobaric DCS treatment-table, and space suit overpressurization treatment. This paradigm shift for DCS treatment is based on a projected increase in hypobaric DCS treatment from exposure to low pressure during several operational conditions: cruise flight in the next generation aircraft (e.g., F-22); high altitude, unpressurized flight by special operations forces; and the extraordinary amount of extravehicular activity (EVA) required to construct the international space station. Anticipating the need to treat DCS encountered during these and other activities, it is proposed that 2 ATA or less hyperbaric oxygen (HBO) treatment conjoined with new collapsible chamber technology can be used to address these issues in a safe and cost effective fashion.

Aerospace Medicine↗

Treatment of decompression sickness with a perfluorocarbon emulsion (FC-43).

Decompression sickness is caused by the production of tissue and blood stream inert gas bubbles. Perfluorocarbon emulsions (PFC) have enhanced O2 and N2 solubilities as well as a small particle size as properties. The effects of treatment with a PFC (FC-43) and 100% oxygen on decompression sickness were investigated in 24 Sprague-Dawley rats compressed to 6.8 ATA and rapidly decompressed. Survival in animals receiving PFC and 100% oxygen was significantly longer (P = 0.01) than in those receiving a 6% hetastarch (H) treatment. The PFC survivors at 24 h did not demonstrate any neurologic deficits, whereas the 1 H animal surviving at 24 h was ataxic and not eating. Those animals who died most often did so within minutes after decompression, suggesting a hemodynamic demise. We conclude that PFC treatment when coupled with 100% oxygen breathing provides both hemodynamic and neurologic protection from decompression sickness.

Animals↗

Hyperbaric oxygen therapy: treatment for spinal cord decompression sickness.

Spinal cord injury (SCI) may result from decompression sickness associated with sport and commercial diving. Decompression sickness is caused by the formation of gas bubbles in the vessels and tissues secondary to a reduction in ambient pressure. A complete or incomplete spinal cord injury may result from decompression sickness. Recompression and hyperbaric oxygen therapy is the primary treatment. The use of hyperbaric oxygen therapy (HBO) as a treatment for these injuries can greatly influence the patient's outcome. Early intervention in a recompression chamber may result in complete recovery. If treatment is delayed however, the prognosis for recovery is poor.

Decompression Sickness↗

[Probability models for altitude decompression sickness].

Objective. To study the probability or risk of decompression sickness in high altitude flight and to establish a probability model. Method. Survival analysis technique was used in the analysis of the information about altitude decompression sickness. Result. It was found that the risk of decompression sickness initially increases up to a certain time point, and then decreases because of denitrogenation. The hazard function may describe the characteristics of this pattern in changes of risk. The parameters of probability models for altitude decompression sickness can be estimated by using the maximum likelihood method. Conclusion. Prediction with the survival models based on the logistic distribution is good.

Aerospace Medicine↗

Preventive effect of a vasodilator on the occurrence of decompression sickness in rabbits.

The effect of terbutaline on the occurrence of decompression sickness was studied in seven rabbits. Terbutaline is a vasodilator, a sympathomimetic beta2-receptor stimulator. The rabbits were given a hyperbaric exposition at 2 ATA followed by oxygen breathing at 1 ATA and a hypobaric exposition at 0.2 ATA. Each rabbit got a hyperbaric exposition long enough for symptoms of decompression sickness to occur at the hypobaric exposition. With a time interval of at least 1 week, each rabbit received an identical pressure exposition, except that terbutaline was injected intravenously at the beginning of the denitrogenation period at 1 ATA. Of the seven experiments with the drug, only one case of decompression sickness occurred and with a delayed appearance. This may be compared to rapid-appearing decompression sickness in all cases in the control series. The results may be of importance in diving routines and, possibly, in the treatment of decompression sickness.

Animals↗

Epidemic decompression sickness: case report, literature review, and clinical commentary.

BACKGROUND: Decompression sickness (DCS) is a syndrome of symptoms caused by bubbles of inert gas. These bubbles are produced by a significant ambient pressure drop. Although cases are usually solitary there have been several episodes of DCS clusters. This paper reports an episode of epidemic decompression sickness and reviews the literature. METHODS: The case reported describes six aircrewmen with DCS following an unpressurized AC-130 flight (maximum altitude 17,000 ft). Two obvious concerns-the low altitude at which DCS was encountered and the potential for epidemic hysteria-are discussed and discounted. In addition, factors contributing to this case are recounted in depth. Moreover, the literature was examined for similar cases of epidemic decompression sickness. Four other instances were discovered. Detailed qualitative analysis of these five reports was performed. RESULTS: With this information epidemic decompression sickness is defined and classified. Two types are described-individual-based (Epi-I) and population-based (Epi-P). Epi-I is a cluster of DCS following a solitary exposure; whereas, Epi-P is a cluster of DCS following multiple exposures over time. Investigation of Epi-P follows the classical rules of outbreak investigation (time, place, person, and environment); whereas, Epi-I does not. In fact, the focus in Epi-I is almost entirely the environment. Following this outline should produce an etiology that control measures can be directed against. However, it is prudent to look beyond the etiology. Enter the Haddon Matrix, a classic public health tool that considers counter-measures before, during, and after the event. CONCLUSION: These many concepts are illustrated with the presented case. Following this template, both the expert and the novice flight surgeon have a systematic and reproducible approach to these difficult puzzles.

Adult↗

The pathophysiology, presentation, and triage of altitude-related decompression sickness associated with hypobaric chamber operation.

Decompression sickness following excursions to low atmospheric pressures has recently been a topic of confusion and concern. This article provides a reference for management of decompression sickness occurring after exposure to a reduction in ambient pressure in a hypobaric chamber. The pathophysiology, recognition, classification, initial management, definitive treatment, and eventual disposition of these cases are presented in a form which is applicable to all flight surgeons and flight physiologists, especially those with responsibility for utilization of hypobaric chambers.

Aerospace Medicine↗