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At least 307 records · Page 17Linked to original sources
PubMed1996

A probabilistic model of hypobaric decompression sickness based on 66 chamber tests.

One consequence of the NASA tissue ratio (TR) model is that calculated probability of decompression sickness [P(DCS)] is constant in tests at different ambient pressures so long as the ratio of P1N2 to P2 is the same in each test; P1N2 is N2 pressure in the 360 minute half-time compartment, and P2 is ambient pressure after decompression. We test the hypothesis that constant P(DCS) is better described by TRs that decrease as P2 decreases. Data were from 66 NASA and USAF hypobaric chamber tests resulting in 211 cases of DCS in 1075 exposures. The response variable was presence or absence of DCS while at P2. Explanatory variables were P1N2, P2, exercise at P2, (yes or no), time to DCS (failure time), and time to end of test in those without DCS (censored time). Probability models were fitted using techniques from survival analysis. The log likelihood for the two parameter log logistic survival model was -846 with only failure and censored times, -801 when TR [P1N2/P2] plus exercise were added, and -663 when modified TR [(((P1N2+cl)/P2)-1)c2] plus exercise were added, where c1 and c2 are fitted parameters in the five parameter model. Constant P(DCS) was better described by TRs that decrease as P2 decreases; a conclusion supported by additional empirical observations, and bubble growth models that are independent of DCS data. Exercise increased the P(DCS) at P2. As a description of decompression "dose", the modified TR was superior to TR over a wider range of experimental conditions.

Adult↗
PubMed1991

Decompression sickness: U.S. Navy altitude chamber experience 1 October 1981 to 30 September 1988.

This study reports the incidence of decompression sickness (DCS) occurring in U.S. Navy altitude chambers in association with physiological training of aircrews for the 7-year period from 1 October 1981 to 30 September 1988. There were 140 total cases of DCS in 136,696 chamber exposure, an incidence of 0.10%. Among trainees, there were 78 cases in 111,674 exposures, and incidence of 0.07%. Among inside observers, there were 62 cases in 25,022 exposures and incidence of 0.25%. The incidence of DCS among inside observers was reduced almost two-fold over the last Navy report and is the lowest reported since 1973. Reasons for the reduction are discussed. In addition, analysis of the data includes types of DCS, symptoms, frequency of joint involvement, predisposing factors, altitude and time of onset of DCS, and treatment tables employed.

Aerospace Medicine↗
PubMed1985

[Decompression sickness of the spinal cord. Results of early and of late treatment].

The treatment of 20 scuba divers with decompression sickness of the spinal cord between 1969 and 1984 is reported. Seven patients presented with mild sensomotor impairments, 13 patients were paraplegic and some suffered from additional impairments to the arms. In 12 of the divers the accident that occurred in a Swiss lake and recompression was initiated with a latency of a few hours. These early treatments were successful in 11 patients. The neurologic symptoms already improved during recompression even in the 7 patients who were paraplegic. In a paraplegic woman early treatment failed, but her condition improved under subsequent hyperbaric oxygen treatment. In 9 patients late treatment after an interval of 48 to 192 hours, consisting of repeated hyperbaric oxygen exposures, was performed. 3 patients with mild neurologic disturbances improved completely. 6 patients were paraplegic. In 5 of these early treatment was without success. On 3 occasions, however, early treatment was not started before 15 to 24 hours after the dive. All 6 paraplegic patients improved considerably during late treatment. 8 of the 9 patients undergoing hyperbaric oxygen treatment had been transported by air with slightly reduced cabin pressure from the foreign country to Zurich. No deterioration of neurologic symptoms was observed during air transport.

Adult↗
PubMed2005

Isoproterenol accelerates decompression sickness and death after saturation dives in swine.

BACKGROUND: Disabled submarine (DISSUB) survivors are expected to achieve inert gas tissue saturation that would likely cause severe decompression sickness (DCS). Rescue procedures in a DISSUB scenario cannot accommodate a staged decompression and the availability of recompression treatment chambers is limited. Alternatives to the standard recompression procedures for treating DCS are needed. Experimentally, isoproterenol has successfully addressed many underlying physiological concerns expected to result in cardiopulmonary DCS in this group. HYPOTHESIS: We hypothesized that isoproterenol would reduce the incidence of cardiopulmonary DCS in a saturation dropout model. METHODS: Yorkshire swine (21.8 +/- 1.68 kg) were fitted with an external jugular catheter and compressed to 4.33 ATA in a dry chamber for 22 h. They were infused with isoproterenol (0.002 mg x kg(-1)) while still at depth and returned to the surface without decompression stops. They received additional infusions every 10 min throughout a 2-h observation period. Signs of DCS were recorded to the nearest minute. RESULTS: Isoproterenol administration resulted in a significant increase in the incidence of severe cardiopulmonary DCS (13/34 control vs. 12/18 isoproterenol) and death from DCS (10/34 control vs. 11/18 isoproterenol). There was no difference in the incidence of severe neurological DCS. CONCLUSIONS: Administering isoproterenol as an intervention/treatment for DCS significantly increases the risk of cardiopulmonary DCS and death following saturation dropout in 20-kg swine. As an adjunctive therapy or alternative to staged decompression, isoproterenol in the dose regimen delivered here is not expected to improve outcome in a DISSUB mass casualty scenario.

Adrenergic beta-Agonists↗
PubMed1983

[Evaluations of 169 cases of decompression sickness treated in Italian hyperbaric centers 1980-1981].

An assessment was made of 169 cases of decompression sickness occurring during the period 1980-81. Nearly all (95,6%) were attributable to superficial planning and execution of the immersion and reascent to the surface marker as the result of panic. Breakdown in the diving apparatus was only responsible in 4.4% of cases. Irrispective of the intermediate decompression stages, the rate of reascent was more than 10 metres a minute in 71.6% of cases. Full recovery as a result of hyperbaric management was obtained in 78,2% type I sickness and 61.9% type II, with improvements in 17.3% and 35.1% respectively. The interval between emersion and treatment ranged from 1 to 72 hr, though the results of treatment were not significantly related to the rapidity of intervention (p greater than 0.05). Good results were dependent on the type of treatment employed, with a significantly better outcome (p less than 0.01) from U.S. Navy tables 2-2A, 3-3A, 4, 5 and 6 and the 2 + 6 recompression protocol, than from tables 5A and 6A.

Decompression Sickness↗
PubMed1989

Neurobehavioral and magnetic resonance imaging findings in two cases of decompression sickness.

Two divers underwent neurobehavioral examinations and magnetic resonance imaging (MRI) while hospitalized during the first 2 weeks after sustaining decompression sickness (DCS). Their neurologic findings included a Brown-Séquard Syndrome consistent with spinal cord lesion, and focal deficits consistent with cerebral lesion(s). MRI revealed subcortical white matter lesions in the brains of both divers, whereas no lesion of the spinal cord was demonstrated. The patients exhibited neurobehavioral sequelae including disturbances of memory, divergent thinking, and visuospatial and motor functioning. Focal neurologic deficits resolved in both patients, and their cognitive and memory problems improved slowly. Findings in these two divers raise the possibility that cerebral insult more frequently accompanies spinal cord injury in DCS than previously thought.

Adult↗
PubMed1986

Consequences of U.S. Navy diving mishaps: decompression sickness.

This study identified the short- and long-term health effects among U.S. Navy divers (n = 328) who suffered decompression sickness (DCS) between January 1968 and December 1979 and compared their post-DCS hospitalization rates with a matched sample of divers (n = 1,086) who had no recorded diving accidents. Results identified 251 individuals (76.5%) whose records contained no diving-related medical events after the DCS incident; the other divers (23.5%) had records of a subsequent hospital admission and/or a physical disability separation. Only three physical disabilities were attributed to DCS or diving, and there were no DCS-related deaths. DCS divers had significantly higher rates than controls for total hospitalizations, symptoms and headache, and diseases of the arteries and veins. These two clusters, which included such conditions as pain in the joint, abnormal involuntary movement, pain in the limb, and arterial embolism, were identified as potential risks for divers who suffer a DCS mishap. Previous hospitalizations and age were not associated with DCS; however, divers in the DCS group were significantly heavier than all other divers.

Accidents, Occupational↗
PubMed2005

Altitude decompression sickness between 6858 and 9144 m following a 1-h prebreathe.

INTRODUCTION: The zero prebreathe altitude threshold for developing 5% decompression sickness (DCS) symptoms in men has been reported to be 6248 m (20,500 ft). However, such an altitude threshold when 1 h of oxygen prebreathe is used has not been well documented and was the primary purpose of this study. METHODS: The 51 male human subjects were exposed to 9144 m (30,000 ft), 8382 m (27,500 ft), 7620 m (25,000 ft), and/or 6858 m (22,500 ft) for 8 h. They were monitored for symptoms of DCS and venous gas emboli (VGE). RESULTS: DCS symptom incidence after 4 h of exposure decreased with exposure altitude from 87% at 9144 m to 26% at 6858 m. VGE were lower during the 4-h 6858-m exposures (32%) than at the higher altitudes (76-85%). The symptom incidences during the first 4 h of exposure were lower at 6858 m and 7620 m following a 1-h prebreathe as compared with analogous zero-prebreathe exposures. There were no differences between incidences of VGE or DCS at any of the four altitudes after 8 vs. 4 h of exposure. CONCLUSION: The altitude threshold for 5% DCS symptoms is below 6858 m after 1 h of prebreathe. However, during 6858-m and 7620-m exposures, a 1-h prebreathe is highly beneficial in reducing DCS incidence and delaying the onset of DCS, keeping the incidence to less than 6% during the first 90 min of exposure. Use of 4-h vs. 8-h exposures does not appear to underestimate DCS risk at or above 7620 m.

Adult↗
PubMed1998

Information about venous gas emboli improves prediction of hypobaric decompression sickness.

HYPOTHESIS: Information about venous gas emboli (VGE) detected in the pulmonary artery such as the occurrence of VGE, Grade of VGE, the time when VGE first appear, and the time course of the Grade or occurrence of VGE, could be used to better assess the probability of decompression sickness [P(DCS)] in any hypobaric decompression. We hypothesized that these data would improve the estimate of P(DCS) since objective measurements of the decompression stress are available for the individual. METHODS: A binary correlation and survival analysis approach were used on information from 1,322 hypobaric chamber exposures to establish the relationships between VGE and DCS. RESULTS: Based on the correlation analysis, the absence of VGE is highly correlated with the absence of a DCS symptom, as evident from a negative predictive value of 0.98. However, the presence of VGE in the pulmonary artery is not highly correlated with a subsequent DCS symptom, as evident from a positive predictive value of 0.39 for Grades III and IV VGE. The correlation results suggest the presence of VGE in the pulmonary artery is a necessary, but not sufficient, condition for DCS. Based on the survival analysis, the log logistic survival model, a one-variable model with two parameters gave a log likelihood (LL) of -757. This model was expanded to include seven additional variables, including four about VGE, and the nine-parameter model gave a better LL of -481. CONCLUSION: Information about VGE plus other variables known to influence DCS is useful to better assess the P(DCS) for hypobaric decompressions.

Adult↗
PubMed1984

Perfluorochemicals as a treatment of decompression sickness in rats.

Perfluorodecalin and perfluorotripropylamine which have N2 solubility coefficients of 28.4 and 35.7 ml/dl, respectively, were used for treatment of decompression sickness in this study. Rats with chronically implanted venous catheters were held for 30 min at 800 kPa (7 bar, 8 ATA) by introducing compressed air into a chamber in which they were kept; a relatively short period of decompression followed (200 kPa/min). Immediately thereafter injections of the perfluorochemicals (PFCs) in a dose of 10 g/kg were given, controls received saline in the same volume or remained without treatment. An observation period of 2 h followed; after this time the incidence of death amongst the experimental animals (as compared with controls tested by the chi 2-test) showed that PFC treatment increased the likelihood of survival. Probit-log time relationship for the incidence of death also revealed a significant decrease in lethality in treated rats 30 min after the end of decompression. The mean lethal times Lt50 differed significantly, too. A still greater effect might be expected if the PFC emulsion were deprived of its normal nitrogen content by oxygenation before administration. Under the conditions of the present experiments PFCs produced an improvement in N2 exhalation at least in terms of the survival rate after compression followed by a very short decompression time.

Animals↗
PubMed1985

Pressure in the treatment of spinal cord decompression sickness.

Previous work had shown that a Po2 of about 2.0 bar was the optimal Po2 for the treatment of spinal cord decompression sickness (DCS). With 20 anesthetized dogs the hypothesis was tested that pressures in excess of a threshold, taken as 3 bar, did not enhance recovery of spinal cord DCS. Dogs were subjected to a 15-min air dive at 10 bar (300 ft) and decompressed over 5.5 min. At the surface, spinal cord evoked potentials (SEP) were observed for changes indicating DCS. Fifteen minutes after DCS was first detected the dogs were recompressed to 3, 5, 7, or 2.8 bar breathing 66, 40, 29, or 100% oxygen which gave a Po2 of 2.0 bar except in the 2.8 bar group. The recovery of the SEP over 2 h was observed. Group mean recoveries at 67, 62, 29, and 42% were not significantly different after 120 min. As the hypothesis was supported, a tentative proposal for changing current therapy was made.

Animals↗
PubMed2000

A trial to determine the risk of decompression sickness after a 40 feet of sea water for 200 minute no-stop air dive.

BACKGROUND: The USN93 probabilistic model of decompression sickness (DCS) predicts a DCS risk of 3.9% after a 40 ft of seawater (fsw) for 200 min no-stop air dive, although little data is available to evaluate the accuracy of this prediction. Based on an analysis of Navy Safety Center data from diving on U.S. Navy standard air decompression tables, the observed incidence of DCS for this type of dive is 0.11%. Knowing the true incidence of the dive is important for deciding whether or not to adopt proposed probability based decompression procedures for U.S. Navy diving. HYPOTHESIS: The risk of DCS after a 40 fsw for 200 min no-stop air dive is 3.9%. METHODS: We conducted a closed sequential trial to determine the DCS incidence on this dive. RESULTS: Of 30 military divers who completed 91 dives, there were 2 cases of DCS (2.2%, 95% CI: 0.27 7.7%). The study was terminated early after the second DCS case because of the presence of neurological symptoms and signs. CONCLUSIONS: This study demonstrates that the incidence of DCS in a laboratory setting is higher than observed in fleet diving. Use of the 40 fsw for 200 min schedule in a decompression computer is likely to result in DCS incidence 2.5- to 70-fold greater than that observed in U.S. Navy diving using table-based procedures.

Adult↗
PubMed1997

Lower decompression sickness risk in rats by intravenous injection of foreign protein.

We have identified a novel means of reducing the risk of decompression sickness (DCS) in rats. A substantial reduction in DCS, from 55% in untreated animals to 24% in animals injected intravenously with a hydrogenase of bacterial origin, was documented for animals breathing a mixture of oxygen and hydrogen. However, this reduction was clearly not a function of metabolic elimination of H2; injections of proteins lacking hydrogenase activity also elicited a lower DCS incidence, and animals breathing hyperbaric helium had the same protective advantage as animals breathing H2. The reduction in DCS risk was shown to be caused by intravenous injection of a foreign protein. The magnitude of the effect varied: two foreign proteins tested did not induce a statistically significant response. We speculated that the foreign protein elicited an immune reaction pre-dive, which diminished the subsequent response of the immune system in DCS. Identifying the underlying mechanism may be important to understanding the pathophysiology of this malady, and may ultimately lead to a therapy applied pre-decompression for reducing DCS risk in human diving.

Alcaligenes↗
PubMed1991

Decompression sickness: risk factors and the monoplace chamber--a case report.

Discussions regarding the use of monoplace chambers for the treatment of decompression sickness (DCS) have continued for some time. Recently the role of these chambers has been reviewed by Kindwall (12) and critiqued by Moon (13). Various principles and concerns presented in their articles are illustrated by this case presentation of type II (serious) DCS with pulmonary and neurologic manifestations. Closely timed recurrent altitude exposure is discussed as a risk factor for DCS. Also, a newly defined risk factor (menstrual phase) is considered relevant to this case. Finally, we recommend that arrangements be made early in the management of DCS cases for transfer to a chamber which can provide definitive therapy.

Adult↗
PubMed1990

Threshold altitude resulting in decompression sickness.

A review of case reports, hypobaric chamber training data, and experimental evidence indicated that the threshold for incidence of Altitude Decompression Sickness (DCS) was influenced by various factors such as prior denitrogenation, exercise or rest and period of exposure, in addition to individual susceptibility. Fitting these data with appropriate statistical models has the potential for estimating the frequency of occurrence of DCS at various altitudes under different experimental conditions and allows us to examine the influence of various factors on the threshold for DCS. This approach was illustrated by logistic regression analysis on the incidence of DCS below 9,144 m (30,000 ft). Estimations using these regressions showed that under a noprebreathe, 6-h exposure, simulated extravehicular activity profile, the threshold for symptoms occurred at approximately 3,353 m (11,000 ft); while under a no-prebreathe, 2-h exposure profile with knee-bends exercise, the threshold occurred at 7,925 m (26,000 ft). These examples showed that definition of threshold altitude should be qualified by the particular combination of experimental variables under which it was observed.

Aerospace Medicine↗
PubMed1996

The distribution of limb pain in decompression sickness.

BACKGROUND: For many years there has been a widely held but largely unsubstantiated belief that pain in the upper limb in decompression sickness (DCS) is associated with bounce diving, whereas compressed air workers, saturation divers and high altitude aviators are more susceptible to involvement of the lower limbs. HYPOTHESIS: The hypothesis of counter current exchange of inert gas, modulated by changes in tissue temperature, has been evaluated as a possible mechanism to explain the reported distribution of limb pain in DCS. METHODS: An extensive review of over 19,000 cases of limb pain decompression illness has been undertaken from case reports stored in the diving accident database at the Institute of Naval Medicine, in the published literature, and from unpublished clinical and experimental reports. RESULTS: There was a predominance of upper limb involvement in bounce divers and, in contrast to traditional teaching, in aviators. By contrast, the lower limbs were more commonly involved in compressed air workers and saturation divers. CONCLUSION: Each of the occupational exposures has been discussed individually with reference to counter-current exchange and other factors as potential influences on the distribution of disease. We conclude that counter-current exchange of inert gas may be implicated in the distribution of limb pain in DCS.

Acid-Base Equilibrium↗
PubMed1979

Mechanical vs. ischemic mechanisms for decompression sickness.

We used 20 kangaroo rats to investigate the effect of exposure to low oxygen levels (0.11 Atm 02 inspired partial pressure) prior to decompression from a steady-state condition. This hypoxia was found to afford significant protection against limb bends as simulated in those animals by tail biting. Yet, it potentiated neurologic symptoms compared with a control exposure on air with the same level of nitrogen supersaturation. However the incidence of simulated limb bends in the same animals was the same with hypoxia as with another control exposure at a pressure estimated to give extravascular bubbles of the same size upon decompression. The results are, therefore, consistent with a simple mechanical basis for limb bends, but are difficult to explain by any ischemic mechanism since a general hypoxia exacerbates any pain produced by oxygen deficiency in the tissues. However, the reverse may be true for some forms of neurologic decompression sickness and the two such cases reported here are consistent with that view, although not statistically significant.

Animals↗