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PubMed1992

A computerized databank of decompression sickness incidence in altitude chambers.

This report describes a hypobaric decompression sickness databank (HDSD) for use with personal computers. The databank consolidates some of the decompression sickness (DCS) information that has accumulated from altitude chamber tests from 1942 to the present. The information was transcribed to a data collection form, screened for accuracy and duplication, and then added to the databank through a computer keyboard. The databank consists of two files; 63 fields contain details of the test conditions in the altitude chamber, the outcome of the test in terms of DCS and venous gas emboli, the physical characteristics of the group of subjects who underwent the test, and the denitrogenation procedures prior to decompression. The HDSD currently contains 378 records that represent 130,012 altitude exposures from 80 sources: scientific journal articles, government and contractor reports, and chapters from books.

Atmosphere Exposure Chambers↗
PubMed1989

Type II altitude decompression sickness (DCS): U.S. Air Force experience with 133 cases.

Type II altitude-related decompression sickness (DCS), due to its wide spectrum of symptoms, is often difficult to diagnose. This difficulty sometimes leads unnecessarily to the permanent grounding of an experienced aviator. So that this condition could be better understood, a total of 133 cases of Type II altitude DCS (on file at the United States Air Force Hyperbaric Medicine Division, School of Aerospace Medicine, Brooks AFB, TX) were reviewed. Most cases (94.7%) followed altitude chamber training. The most common manifestation was joint pain (43.6%), associated with headache (42.1%), visual disturbances (30.1%), and limb paresthesia (27.8%). The next most common symptoms were, in order of decreasing frequency: mental confusion (24.8%), limb numbness (16.5%), and extreme fatigue (10.5%). Spinal cord involvement, chokes, and unconsciousness were rare (6.9%, 6%, and 1.5%, respectively). Hyperbaric oxygen treatment produced fully successful results in 97.7% of the cases. Only 2.3% of the cases resulted in residual deficit; no deaths occurred. A thorough knowledge of the differential diagnosis and predisposing factors is essential to narrow the margins of error in the diagnosis and prevention of decompression sickness in the operational or training environment. A recommendation for favorable consideration of waiver action for those aviators who suffered Type II DCS is presented. These recommendations are based on a unique classification of the severity of symptoms.

Adult↗
PubMed1983

Decompression sickness: USAF experience 1970-80.

During the period 1970-80, there were 58 cases of decompression sickness in one of its forms reported in USAF aircrewmen. These cases occurred in a number of different types of aircraft in which cabin/cockpit depressurization occurred either intentionally (because of operational requirements) or because of mechanical malfunction. The most common manifestation of decompression sickness was bends, although some airmen experienced various degrees of neurological dysfunction. Even though none of the aircraft was lost or damaged due to crew incapacitation, the threat was clearly there. The authors briefly review decompression sickness including prevention, treatment, and aeromedical disposition.

Adult↗
PubMed1991

Decompression sickness: USN operational experience 1969-1989.

This report presents data on the U.S. Navy's experience in decompression sickness occurring in operational flight from 1 January 1969 to 30 December 1989. During these 21 years, decompression sickness was reported in 12 USN aircraft and involved 15 aircrew. The primary cause of decompression, as might be expected, was a loss of cabin or cockpit pressurization. The most common manifestation of decompression sickness was limb or joint pain although some crewmembers experienced various manifestations of neurological dysfunction. One crewmember experienced chokes. Of the 15 afflicted aircrew, 13 (87%) had complete remission of symptoms by the time they landed. Two crewmembers required compression therapy for resolution of symptoms. None of the reported symptoms were incapacitating and none of the aircraft involved crashed or received even minor damage.

Aerospace Medicine↗
PubMed1995

Does the time course of bubble evolution explain decompression sickness risk?

A probabilistic model of decompression sickness (DCS) risk based on linear-exponential (LE) kinetics has given the best fit of the human air and nitrox DCS database. To test the hypothesis that its success may be due to the formation of a gas phase during decompression, we developed a physiologically based bubble evolution model using a numerical solution of a partial differential equation system. Because of the computational intensity of this method, it could not be used to fully explore our hypothesis. Consequently, we compared the solution with that of a computationally simpler approximation that was previously published by Van Liew and found the two approaches gave similar results. Using the simpler model, assuming bubble densities of 1 and 1,000 bubbles/cm3, we found a tissue time constant of at least 80 min (equivalent to perfusion of 1/80 ml.g-1.min-1) was required to achieve a delay in bubble dissolution comparable to the prolonged risk of DCS predicted by the LE model. We suggest that the persistence of single bubbles in a uniformly perfused homogeneous tissue alone is unlikely to explain persistent DCS risk.

Blood Flow Velocity↗
PubMed1976

Decompression sickness during saturation dives.

Available Navy saturation diving data were analyzed for an evaluation of the therapeutic adequacy of decompression sickness treatment procedures and for delineation of precipitant factors in the etiology and treatment of decompression sickness during saturation dives. None of the cases of decompression sickness recorded during saturation dives involved more than musculoskeletal or joint pain, and in 96% of the cases the joint pain was confined to the diver's knees. In 89% of the cases symptoms appeared while the divers were still under pressure. The subsequent recompression treatment of these cases resulted in full relief in only 35% of the cases; the remaining 65% completed the therapy and subsequent decompression with residual pain which diminished over a period of weeks. The adequacy of the recompression appears to be inversely proportional to the depth of reported onset of symptoms and the time required to obtain even partial relief is directly related to the magnitude of the recompression ratio used. Four explanations are suggested for the limited recompression therapy common in saturation diving: increase in musculoskeletal pain with recompression, peer pressure to avoid extension of the chamber confinement, lack of severe neurological symptoms, and the tremendous depths required to obtain a reasonable recompression ratio. The author further suggests that future treatment procedures will require a departure from the accepted concept of radically decreasing the volume of inert gas bubbles by increasing pressure.

Analysis of Variance↗
PubMed1988

Heliox treatment for spinal decompression sickness following air dives.

Enforced delay in treatment of spinal decompression sickness following scuba diving can result in paraplegia. Poor response from initial recompression to 18 m presents the clinician with a difficult management problem. Theoretical objections have been raised to the use of He-O2 as treatment regimen. We report 3 cases that show He-O2 to be an excellent method of treatment in spinal decompression sickness after air diving.

Adult↗
PubMed1993

[Experimental studies of the effects of enriched air nitrox dive on shortening of decompression time and reduction of risks of decompression sickness].

Enriched air nitrox diving has been conducted to shorten decompression time as well as to reduce risks of decompression sickness. Nine volunteer divers served as subjects for nitrox (-a: 60% N2 and 40% O2, and -b: 67.5% N2 and 32.5% O2) and air chamber dives of 20 m/60 min, 30 m/60 min and 40 m/60 min. Venous gas emboli (VGE) were examined after surfacing in a series of nitrox dives and of air dives to compare the risks of decompression sickness (DCS). Three divers as a group were compressed in a chamber for each dive. Decompression was carried out according to the Norwegian Navy nitrox decompression tables for the nitrox dives, and for the air dives the Japanese Ministry of Labor tables were used. Decompression time was much shorter in nitrox diving than in air dives for the same dive profiles. All of nitrox-a and air divers showed no VGE nor DCS symptoms after surfacing of 20 m dives. In case of 30 m dives, VGE appeared in one diver (33%) without DCS symptoms in nitrox-a dive but no VGE nor DCS in nitrox-b dive, whereas for the same air dives two subjects (66%) had VGE and DCS symptoms. When the depth was increased to 40 m in the nitrox dive, nitrox-b did not show both VGE and DCS, while the air dive showed one VGE and one DCS. These results suggest that the nitrox dive with suitable decompression schedule reduces the risks of DCS as well as shortening decompression obligation.

Adult↗
PubMed1991

Decompression sickness presenting as a viral syndrome.

Decompression sickness (DCS) is a well-known hazard of exposure to significant variations in ambient pressure. The diagnosis and management of DCS is frequently a source of confusion. Although the majority of cases are manifested by joint or limb pains (Type I DCS), patients may present with a wide array of symptoms, such as neurologic deficits, headache, fatigue, nausea, and respiratory difficulty. A thorough knowledge of the differential diagnosis and a strong index of suspicion are crucial to the proper management of DCS. Presented herein are two cases of altitude-related DCS which were confused initially with a viral syndrome. A discussion of the symptoms of DCS is included.

Adult↗
PubMed1979

Application of a bubble formation model to decompression sickness in rats and humans.

Although decompression sickness results from bubble formation in blood or tissue, pressure schedules currently in use are essentially empirical and contain little input from cavitation theory. The recent convergence of three lines of investigation suggests that a synthesis of practice and theory may now be possible. The data consist of pressure reduction limits for gelatin, rats, and humans following steady-state exposures. From the gelatin studies, a model has been developed in which bubble formation is initiated by spherical gas nuclei stabilized by surface-active skins of varying gas permeability. We demonstrate that the model is also in good agreement with data on rats and humans over a wide range of pressures and that the model parameters assume sensible values in each case. This suggests that cavitation theory can provide a rationale for current diving practice and can serve to secure, consolidate, and extend this practice.

Animals↗
PubMed1991

Significance of delayed symptom onset and bubble growth in altitude decompression sickness.

Three characteristics of altitude induced decompression sickness (DCS) are: 1) symptoms occur some time after arrival at altitude; 2) symptoms seldom occur below 18,000 ft, even though bubbles are frequently detected at that low altitude; 3) symptoms seldom occur after 4 h at altitude. These observations could be explained if it were postulated that bubbles must reach a threshold size before symptoms of DCS occur. In vitro techniques were used in this study to measure bubble growth at various altitudes. The results indicate that although the growth rate of bubbles depends strongly on the altitude where they form, bubble growth requires time. This helps explain the first observation above. We found that bubbles stop growing early at a small size below 18,000 ft. This helps explain the second observation above. Finally, we found that bubbles stop growing when the fluid immediately surrounding the bubble is cleared of supersaturated gas regardless of the fluid composition a few centimeters from the bubble. This helps explain the last observation above.

Decompression Sickness↗
PubMed1990

Combined arterial gas embolism and decompression sickness following no-stop dives.

Decompression sickness (DCS) has been clinically classified as Type I (predominantly joint pain) or Type II (predominantly spinal cord lesions). We present 3 cases that are all characterized by severe (Type II) DCS with signs and symptoms of spinal cord injury occurring in conjunction with arterial gas embolism (AGE). We consider the AGE "minor" because only 2 of the 3 subjects initially lost consciousness, and in all cases the signs and symptoms of the AGE had essentially resolved within 1 h or by the time recompression therapy began. DCS was resistant to recompression therapy, even though treatment began promptly after the accident in 2 of the 3 cases. None of the cases had a good neurologic outcome and there has been one death. None of the divers exceeded the U.S. Navy "no-stop" limits for the depths at which they were diving. We have observed a previously unreported clinical syndrome characterized by severe Type II DCS subsequent to AGE following pressure-time exposures that would normally not be expected to produce DCS. We postulate that AGE may have precipitated or predisposed to this form of DCS.

Adult↗
PubMed1989

A case of decompression sickness in a commercial pilot.

We report a case of decompression sickness (DCS) followed by pulmonary edema in a 47-year-old commercial pilot who operated a non-pressurized turboprop twin at flight level 290. He became unconscious and recovered after an emergency descent. The pilot collapsed and a pulmonary edema occurred 8 h after landing. The patient improved rapidly with fluid replacement and without hyperbaric therapy, which was not available at that time. This course of DCS is unusual because it is reported that fluid replacement without hyperbaric therapy normally cannot recover severe cases of DCS. The considerable increase in body weight of this pilot within the last 6 months may have been a predisposing factor for development of decompression sickness.

Aerospace Medicine↗
PubMed1981

Corticosteroids in treatment of serious decompression sickness.

Although high-dose corticosteroids have been widely recommended as an adjunctive measure in the treatment of serious decompression sickness, there are few objective data to support their efficacy in this disease. An unusual case of neurological decompression sickness which seemed to demonstrate a therapeutic response to steroids independent of recompression is presented. The various manifestations of decompression sickness and the effectiveness of delayed treatment are discussed.

Adrenal Cortex Hormones↗
PubMed1978

Relationship between CO2 levels and decompression sickness: implications for disease prevention.

Extensive data concerning the incidence of decompression sickness among workers participating in the deepest caisson operation in Japan to date have been collected and analyzed for the period April through August, 1976. When the bottom pressure was between 3.0 and 3.2 ATA, the incidence of decompression sickness was 3.05%; subsequently, the incidence was only 0.96% between 3.2 and 3.4 ATA. The man lock (i.e., decompression chamber) had never been ventilated during the former group of decompressions and the level of CO2 had ranged between 1.8 and 2.3% (v/v); in the latter group of decompressions, the CO2 level ranged between 0.3 and 0.8% with ventilation. All other conditions, including the decompression table used, were the same. Moreover, based upon the nature of the muscular activity required of the caisson workers just prior to decompression, their most common site of affliction was found to lie within the body region where the highest tissue tensions of CO2 would be expected during decompression.

Adult↗
PubMed1993

Spinal cord decompression sickness in sport diving.

OBJECTIVE: To summarize 16 years' experience in the diagnosis and treatment of spinal cord decompression sickness in Israel. DESIGN: The survey data were collected firsthand by physicians trained in underwater diving medicine. SETTING: The Israeli Naval Medical Institute, Israel's national hyperbaric referral center. PATIENTS: Sixty-eight sport divers diagnosed as having spinal cord decompression sickness. INTERVENTIONS: Hydration and 100% oxygen breathing until the patient reached the hyperbaric chamber. All patients received recompression therapy on US Navy treatment tables using oxygen, except for six who were treated by Comex Treatment Table CX-30, which uses helium in addition to oxygen. MAIN OUTCOME MEASURES: Neurological examination after the completion of recompression therapy. RESULTS: Forty-one percent of the dives were performed within the decompression limits of the US Navy standard decompression tables. Risk factors were fatigue, circumstances suggesting dehydration, and extreme physical effort. The most common presenting symptoms were paresthesias, weakness of the legs, lower back pain, or abdominal pain. Full recovery was achieved in 79% of the patients. Spinal symptoms appeared immediately on surfacing in six of the eight patients who continued to have multiple neurological sequelae. CONCLUSIONS: United States Navy air decompression tables appear not to be completely safe for sport divers. Even mild spinal symptoms identified on surfacing should be treated vigorously. High-pressure oxygen-helium therapy seems to be a promising alternative in cases of severe spinal cord decompression sickness.

Adult↗