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PubMed2000

[Incidence and prevention of space decompression sickness].

To expound the necessity that space decompression sickness (SDCS) should be separated from altitude DCS, comparison was made between the features of space DCS and altitude DCS. The etiology and pathogenesis of the space DCS and altitude DCS were the same, but the features of the rules leading to their incidences (included influencing factors etc.) were different. For the convenience of getting better systemic and definite knowledge about SDCS, and making effective preventive plans and theoretical expositous, SDCS should be taken as an independent professional term.

Aerospace Medicine↗
PubMed2005

[Early detection of asymptomatic dysbaric osteonecrosis of the shoulder after type 1 decompression sickness: a case report].

INTRODUCTION: Dysbaric osteonecrosis is a rare illness in professional divers and compressed-air workers. The correlation between dysbaric osteonecrosis and previous decompression sickness with osteoarthromuscular pain (type 1 decompression sickness) remains a controversial subject. The probability for ischemic lesions detected with MRI to turn into osteonecrosis after decompression sickness is still not established. EXEGESIS: The authors report the case of a military diver declared definitely medically unfit to dive after the occurrence of advanced dysbaric osteonecrosis of the shoulder, eight months after decompression sickness treated with hyperbaric oxygen, in the same area. A close link between those two events and the requirement for monitoring the follow-up of acute type 1 decompression sickness are discussed. CONCLUSION: Every decompression sickness with osteoarthromuscular pain should be early examined with MRI in order to screen osteomedullar damages liable to worse with diving and change subsequently in bone necrosis.

Adult↗
PubMed1992

[Inner ear decompression sickness following a scuba dive].

Inner ear decompression sickness (IEDCS) is one form of Type II decompression sickness. Most cases of IEDCS have been associated with saturation dives, so there are very few reports of occurrence following shallow scuba dives. We present here the case of a diver who suffered from IEDCS following a shallow scuba dive (30m), and was successfully treated by the protocol outlined in U.S. Navy treatment table 6. This case suggests that there is the possibility of occurrence of IEDCS, even following a shallow scuba dive, if proper decompression procedures are not adhered to. In addition, detailed analysis of diving profiles should be used to distinguish the inner ear dysfunction seen in some divers from inner ear barotrauma which may be attributable to IEDCS.

Adult↗
PubMed1987

Consumption of platelets in decompression sickness of rabbits.

Platelet behavior was studied in rabbit decompression sickness which was brought about by the exposure to 6 ATA for 40 min (bottom time) followed by rapid decompression. Platelet counts significantly decreased after the decompression. Kinetic studies with 111In-oxine-labeled platelets revealed shortened survivals of circulating platelets, and audioradiograms indicated the accumulation of radioactivity in the lungs after the decompression. Although there was no change in the mode volume of platelets after the decompression, the transient appearance of circulating smaller or fragmented platelets suggested a random overdestruction of platelets. Whole and releasable adenine nucleotide contents of platelets were decreased significantly after the decompression. There were no significant changes in cytoplasmic adenine nucleotide contents. Therefore, in decompression sickness, the circulating platelets behaved similarly to those in acquired storage pool disease. Platelet thrombi were found in the pulmonary arteries, compatible with the accumulation of 111In-oxine-labeled platelets. These findings suggest that circulating air bubbles interact with platelets, causing the platelet release reaction, and these activated platelets participate in the formation of thrombi in experimental decompression sickness.

Adenine Nucleotides↗
PubMed2004

[Idiopathic medullary decompression sickness: myth or reality?].

Severe decompression sickness occurs unfrequently, with, generally an identifying cause (error in decompression protocols, promoting factors.). We report a case of severe spinal cord damage; onset after a common dive, neither deep nor long, without any promoting factor, absence of responsiveness to recompression, three hours post-dive, importance of MRI signal abnormalities, make us to point out the confounding variability of onset and evolution of such illness.

Adult↗
PubMed1986

Progressive ulnar palsy as a late complication of decompression sickness.

We report an unusual case of decompression sickness in which a progressive ulnar palsy developed 22 days after the onset of neurological decompression sickness. The initial symptoms of numbness and paresthesias of the hand were treated with recompression therapy, resulting in only partial relief. The patient subsequently developed weakness of the left hand, which increased in severity until the institution of repeated daily hyperbaric oxygen treatments. A total of seven treatments resulted in partial resolution of the patient's signs and symptoms. Recovery was complete within four months.

Adult↗
PubMed1984

Health risk factors for the development of decompression sickness among U.S. Navy divers.

The relationship between the health status and physical characteristics of 185 U.S. Navy divers and their risk for experiencing decompression sickness was examined utilizing historical cohort design. Data on multiphasic medical examinations performed on these men between 1972-1978 were obtained. Cases of decompression sickness before and after examination were identified. Divers who did experience decompression sickness either before or after examination had significantly higher measures of skinfold thickness and weight when compared to those who remained free of decompression sickness. Those divers in the highest quartile of each of three significant skinfold thicknesses measured had risks for decompression sickness that were generally 9 to 10 times as great as those calculated for the combined lower 3 quartiles and 5 to 6 times as great as the average crude risk calculated for all Navy divers over the past 5 yr. These findings suggest that obesity may be a contributory factor to the occurrence of decompression sickness.

Body Weight↗
PubMed1987

Role of oxygen in the production of human decompression sickness.

In the calculation of decompression schedules, it is commonly assumed that only the inert gas needs to be considered; all inspired O2 is ignored. Animal experiments have shown that high O2 can increase risk of serious decompression sickness (DCS). A trial was performed to assess the relative risks of O2 and N2 in human no-decompression dives. Controlled dives (477) of 30- to 240-min duration were performed with subjects breathing mixtures with low (0.21-0.38 ATA) or high (1.0-1.5 ATA) Po2. Depths were chosen by a sequential dose-response format. Only 11 cases of DCS and 18 cases of marginal symptoms were recorded despite exceeding the presently accepted no-decompression limits by greater than 20%. Analysis by maximum likelihood showed a shallow dose-response curve for increasing depth. O2 was estimated to have zero influence on DCS risk, although data variability still allows a slight chance that O2 could be 40% as effective as N2 in producing a risk of DCS. Consideration of only inert gases is thus justified in calculating human decompression tables.

Decompression Sickness↗
PubMed2003

[Study of platelet membrane glycoprotein expression in mice with decompression sickness].

OBJECTIVE: To investigate the role of expression of platelet membrane glycoprotein CD31, CD61 and CD62p in the pathogenesis of decompression sickness. METHODS: Mice were randomly divided into decompression sickness group and normal control group. The animals in decompression sickness group were exposed to 600 kPa compressed air for 60 minute, then they were rapidly decompressed to normal pressure in one minute. At 60th minute after reducing to normal pressure, the expression of CD31, CD61 and CD62p on platelet membrane in mice was measured by flow cytometry. RESULTS: The mean fluorescence intensity of CD31, CD61 and positive percentage of CD62p on platelet membrane [(18.64 +/- 1.01), (271.06 +/- 24.25), (4.48% +/- 0.43%) respectively] in decompression sickness group were significantly increased compared with normal control group [(16.89 +/- 1.69), (234.09 +/- 15.96), (3.00% +/- 0.66%) respectively] (P < 0.05, P < 0.01). CONCLUSION: Inadequately rapid decompression may induce up regulation of platelet membrane glycoprotein CD31, CD61 and CD62p expression in mice, which may lead to thrombosis.

Animals↗
PubMed1987

Relation between complement activation and susceptibility to decompression sickness.

The consequences of complement activation and the symptoms of decompression sickness are similar. Consequently, the relation between the sensitivity of individuals to complement activation by air bubbles and their susceptibility to decompression sickness has been examined. Plasma samples from 34 individuals were incubated with air bubbles, and the concentration of the fluid phase metabolites of complement activation C3a, C4a, and C5a were measured with radioimmunoassays. It was found that both the anaphylatoxins C3a and C5a were produced by the presence of air bubbles but that the anaphylatoxin C4a was not. This finding indicates that air bubbles activate the complement system by the alternate pathway. One group of individuals was found to be particularly sensitive to complement activation by this pathway. They produced 3.3 times more C3a and 5.3 times more C5a in their plasma samples incubated with air bubbles as did the other group. Sixteen individuals were subjected to a series of pressure profiles that were severe enough to produce bubbles in their circulatory system that could be detected by Doppler ultrasonic monitoring. The group of individuals that had been identified as being more sensitive to complement activation by the alternate pathway was also found to be more susceptible to decompression sickness.

Adult↗
PubMed1998

Probabilistic models of the role of oxygen in human decompression sickness.

Probabilistic models of human decompression sickness (DCS) have been successful in describing DCS risk observed across a wide variety of N2-O2 dives but have failed to account for the observed DCS incidence in dives with high PO2 during decompression. Our most successful previous model, calibrated with 3,322 N2-O2 dives, predicts only 40% of the observed incidence in dives with 100% O2 breathing during decompression. We added 1,013 O2 decompression dives to the calibration data. Fitting the prior model to this expanded data set resulted in only a modest improvement in DCS prediction of O2 data. Therefore, two O2-specific modifications were proposed: PO2-based alteration of inert gas kinetics (model 1) and PO2 contribution to total inert gas (model 2). Both modifications statistically significantly improved the fit, and each predicts 90% of the observed DCS incidence in O2 dives. The success of models 1 and 2 in improving prediction of DCS occurrence suggests that elevated PO2 levels contribute to DCS risk, although less than the equivalent amount of N2. Both models allow rational optimization of O2 use in accelerating decompression procedures.

Air Pressure↗
PubMed1993

[Clinical aspects, pathophysiology and therapy of decompression sickness].

The primary treatment of decompression illnesses (arterial gas embolism and all types of decompression sickness) is recompression therapy, combined with hyperbaric oxygen breathing. It is essential to initiate treatment as soon as the symptoms arise. However, prior to hyperbaric oxygen therapy--particularly with any delay in starting recompression--specific supportive therapy for severe decompression-related injuries is mandatory after first-aid treatment has been given. The preferred supportive treatment would be 100% normobaric oxygen breathing, oral or better i.v. fluids (crystalloids or dextrose saline), flat position on the back, and organization of appropriate means of transportation to the nearest hyperbaric center. Large doses of corticosteroids as well as anticoagulants are under discussion, but there is some evidence that steroids and medium doses of acetylsalicylic acid, given initially, may be of certain benefit for patients suffering from cerebral- and spinal-cord trauma due to decompression accidents. There is evidence that latency of onset of decompression illnesses is a prognostic indicator. Nevertheless, urgent HBO therapy in a hyperbaric chamber suitable for intensive care under pressure is mandatory for all severe decompression disorders.

Decompression Sickness↗
PubMed1977

Altitude decompression sickness: hyperbaric therapy results in 145 cases.

Most cases of decompression sickness that occur at altitude resolve upon descent to lower altitudes. Before the use of hyperbaric therapy, cases that did not resolve accounted for some of the most difficult medical management problems in military aerospace medicine. On 27 March, 1941, the U.S. Navy Diving School successfully used hyperbaric therapy for a case of altitude-induced decompression sickness that did not resolve on return to ground level. Since then, over 145 such cases have been treated by hyperbaric therapy. At first, treatments involved using compressed air, with varying success. Current medical management of altitude-induced decompression sickness requires immediate compression to 2.8 ATA, equivalent to 60 ft of sea water (FSW) pressure, and a series of intermittent oxygen and air breathing periods during the subsequent slow decompression to surface. This report confirms the treatment recommendations set forth by Behnke and Downey, and crystallized by Goodman in 1964. Conclusions are based on treatment experience in the management of 120 cases in U.S. Air Force hyperbaric chambers, and a survey of hyperbaric facilities which have treated 25 other cases.

Adult↗
PubMed1980

Ventricular dysrhythmia associated with serious decompression sickness.

A case of serious decompression sickness complicated by frequent, unifocal, premature ventricular contractions (PVC) is presented. Although no cardiac monitoring was available, a continuous lidocaine infusion was used during recompression treatment to treat the PVCs, and it appeared to produce no untoward side effects. The concerns about using lidocaine in the dysbaric patient subjected to a hyperbaric oxygen environment are discussed.

Adult↗
PubMed1991

Decompression sickness presenting as optic neuropathy.

Decompression sickness (DCS) is a systemic disorder caused by an abrupt decrease in the ambient atmospheric pressure to which an individual is exposed. A previously healthy 23-year-old male parachutist developed optic neuropathy after a series of multiple repeated hypobaric exposures; his symptoms improved promptly with recompression and hyperbaric oxygen therapy. We believe this to be the first reported case of DCS presenting as optic neuropathy.

Adult↗
PubMed2003

Prophylactic high dose methylprednisolone fails to treat severe decompression sickness in swine.

INTRODUCTION: Controlled decompression from saturation conditions is not always an option, particularly in a disabled submarine scenario. Hypothesis Prophylactic high dose methylprednisolone (MP) would improve outcome in severe cases of decompression sickness (DCS). METHODS: Littermate pairs of male Yorkshire swine (n = 86, mean weight +/- SE = 19.3 +/- 0.2 kg) were randomized to one of three groups, then compressed on air to 4.3 ATA (33 msw) for 22 h and brought directly to surface pressure (1 ATA) at 0.9 ATA x min(-1). The MP-50 group received i.v. infusion of 50 mg x kg(-1) of MP dissolved in 60 cc normal saline (NS) immediately prior to the hyperbaric exposure. The NS group received 60 cc NS i.v. immediately prior to the hyperbaric exposure. The MP-10 group received i.v. infusion of 10 mg x kg(-1) MP dissolved in 60 cc NS during the hyperbaric exposure, 7 h before the decompression. RESULTS: Outcomes of severe DCS and death were recorded. NS group: 14 DCS, 4 died; MP-50 group: 19 DCS, 12 died; MP-10 group: 19 DCS, 10 died. Compared with the NS group, logistic regression analysis suggested that animals in the MP-10 group were more likely to get severe DCS and to die (p < 0.01) and animals in the MP-50 group were more likely to die from their disease (p < 0.01). DISCUSSION: Prophylactic high dose MP exerts no protective effect against severe DCS and actually worsens mortality in this model. An earlier group of untreated controls (UC, n = 44, 30 DCS, 11 died, mean weight +/- SE = 19.9 +/- 0.3 kg) exposed to the same profile was also available for analysis. Comparison of the UC and NS animals suggested that pre-dive NS treatment may protect against severe DCS.

Analysis of Variance↗