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PubMed1998

A loglogistic model for altitude decompression sickness.

BACKGROUND: Altitude decompression sickness (DCS) is a potential hazard encountered during high altitude flights or during extravehicular activity in space. In this study, the loglogistic distribution was used to model DCS risk and symptom onset time. METHODS: The Air Force Research Laboratory, Brooks AFB, TX, has conducted studies on human subjects exposed to simulated altitudes in hypobaric chambers. The dataset from those studies was used to develop the DCS models and consisted of 975 subject-exposures to various altitudes, preoxygenation times, and exercise regimens. Since the risk of DCS is known to increase over time at altitude, and then decrease because of denitrogenation, the loglogistic model was fit to the data. The model assumes that the probability of DCS depends on several risk factors. Maximum likelihood estimates of the parameters were obtained using the statistical software package SAS. Cross validation techniques were provided to examine the goodness of fit of the model. RESULTS: The fitted model indicated that altitude, ratio of preoxygenation to exposure time, and exercise were the most significant risk factors. The model was used to predict the risk of DCS for a variety of exposure profiles. The predicted probability of DCS agreed very closely with the actual percentages in the database. CONCLUSION: The loglogistic distribution was found to be appropriate for modeling the risk of DCS. Based on the cross validation and validation results, we conclude that this model provides good estimates of the probability of DCS over time.

Adolescent↗
PubMed2006

Decompression schedule optimization with an isoprobabilistic risk of decompression sickness.

INTRODUCTION: Divers use decompression schedules to reduce the probability of occurrence of decompression sickness when returning to the surface at the end of a dive. The probability of decompression sickness resulting from these schedules varies across different dives and the models used to generate them. Usually the diver is unaware of this variance in risk. This paper describes an investigation into the feasibility of producing optimized iso-probabilistic decompression schedules that minimize the time it takes for a diver to reach the surface. METHODS: The decompression schedules were optimized using the sequential quadratic programming method (SQP), which minimizes the ascent time for a given probability of decompression sickness. The U.S. linear-exponential multi-gas model was used to calculate an estimate of the probability of decompression sickness for a given dive. In particular 1.3-bar oxygen in helium rebreather bounce dives to between 18 m and 81 m were considered and compared against the UK Navy QinetiQ 90 tables for a similar estimate of probability of decompression sickness. RESULTS: The SQP method reliably produced schedules with fast and stable convergence to an optimized solution. Comparison of the optimized decompression schedules with the QinetiQ 90 schedules showed similar stop times for shallow dives to 18 m. For dives with a maximum depth of 39 m to 81 m, optimizing the decompression resulted in savings in decompression time of up to 30 min. CONCLUSIONS: This paper has shown that it is feasible to produce optimized iso-probabilistic decompression tables given a reliable risk model for decompression sickness and appropriate dive trials.

Decompression↗
PubMed1984

Factitious decompression sickness.

The diagnosis of decompression sickness is made largely by history; there are few physical findings and no radiographic or laboratory tests to support the diagnosis. We present three cases of factitious decompression sickness in which patients fabricated an appropriate history and underwent compression therapy. Due to the potential severity of decompression sickness and the relative safety of compression therapy, the initiation of therapy must not be delayed in a case of decompression sickness. Once therapy is begun, investigation into the particulars of a suspicious case can be made.

Adult↗
PubMed2000

Delayed onset pulmonary barotrauma or decompression sickness? A case report of decompression-related disorder.

A-24-yr-old male professional diver began to complain of substernal pain 3 h after a controlled ascent from a dive of less than 40 ft of sea water (fsw). The diving master who supervised his dive and the physicians who examined him on presentation suspected pulmonary barotrauma rather than decompression sickness (DCS) because he had only descended to a depth of 32 fsw. Hyperbaric oxygen therapy (HBO) by U.S. Navy treatment Table VI was implemented because of his progressively worsening pain. HBO was apparently effective and a relapse was not seen. The author cannot label his condition based on the conventional classification categories, such as decompression sickness (DCS), barotrauma or even decompression illness. This case report is offered as a topic for consideration in the controversy over decompression-related disorders.

Adult↗
PubMed2001

On the likelihood of decompression sickness during H(2) biochemical decompression in pigs.

A probabilistic model was used to predict decompression sickness (DCS) outcome in pigs during exposures to hyperbaric H(2) to quantify the effects of H(2) biochemical decompression, a process in which metabolism of H(2) by intestinal microbes facilitates decompression. The data set included 109 exposures to 22-26 atm, ca. 88% H(2), 9% He, 2% O(2), 1% N(2), for 0.5-24 h. Single exponential kinetics described the tissue partial pressures (Ptis) of H(2) and He at time t: Ptis = integral (Pamb - Ptis). tau(-1) dt, where Pamb is ambient pressure and tau is a time constant. The probability of DCS [P(DCS)] was predicted from the risk function: P(DCS) = 1 - e(-r), where r = integral (Ptis(H(2)) + Ptis(He) - Thr - Pamb). Pamb(-1) dt, and Thr is a threshold parameter. Inclusion of a parameter (A) to estimate the effect of H(2) metabolism on P(DCS): Ptis(H(2)) = integral (Pamb - A - Ptis(H(2))). tau(-1) dt, significantly improved the prediction of P(DCS). Thus lower P(DCS) was predicted by microbial H(2) metabolism during H(2) biochemical decompression.

Animals↗
PubMed1989

The treatment of decompression sickness.

The initial event in decompression sickness is the separation of gas from solution because of supersaturation. If this event gives rise to immediate symptoms, recompression is remarkably effective. This end-point is characteristic of joint pain, that is, Type 1 decompression sickness. Unfortunately the onset of serious Type 2 decompression sickness may be insidious and the delay may be associated with blood-brain barrier dysfunction. Pressure is less effective in the resolution of this problem than a raised partial pressure of oxygen. Standard therapy using oxygen may be associated with worsening of symptoms and air tables with recurrence. Recompression to 4 ata and the use of a mixture of 50% oxygen and 50% helium offers a good working compromise in the treatment of both serious decompression sickness and gas embolism arising in air diving, avoiding the need for a differential diagnosis. Only oxygen or helium and oxygen mixtures should be used in the therapy of decompression sickness in helium and oxygen diving. When therapy has been delayed, intravenous fluids and steroids are important adjuncts.

Atmospheric Pressure↗
PubMed1992

Pathophysiology and treatment of decompression sickness and gas embolism.

Decompression sickness and cerebral gas embolism can present as dramatic and profound sudden onset injuries in patients engaged in tunnel work and compressed gas diving, including scuba. The history and management of these illnesses span centuries. The pathophysiology relates to occurrence of gas bubbles in extrapulmonic sites. Decompression sickness is due to supersaturation of the tissue with dissolved gas and subsequent evolution of gas bubbles. Gas embolism results from the direct transit of molecular gas from a pulmonary or intravascular origin into the arterial circulation causing occlusion of a distal locus. Treatment relates to increasing hydrostatic pressure, thus maximizing the gradient for gas reabsorption and dissolution and subsequently gas excretion via the lungs.

Decompression Sickness↗
PubMed1978

Movement by helicopter of patients with decompression sickness.

Rapid movement of a patient with decompression sickness sometimes poses problems when the site of the hyperbaric treatment facility is located a considerable distance away. Six cases of aviator decompression sickness were diagnosed in altitude chamber participants during an 18-month period. Five cases were uncomplicated decompression sickness and the sixth case was of central nervous system decompression sickness. All cases were transferred by low-level helicopter flight. No complications were noted when the helicopter stayed within 200 ft (61 m) AGL of the take-off point. Symptoms of decompression sickness did worsen however, when this altitude was exceeded. This study shows that movement of patients with decompression sickness by low-level helicopter flight is both safe and effective, especially when pressurized aircraft is neither available nor practical.

Adult↗
PubMed1979

Cross-adaptive effects of cold, hypoxia, or physical training on decompression sickness in mice.

The effects of adaptation to cold, hypoxia, or exercise on hyperbaric decompression tolerance were investigated in two factorial experiments. For either 14 or 28 days, groups of mice were handled (control); exposed discontinuously for 4 h to cold (4 degrees C) or hypoxia (P approximately 379 or 320 Torr); or exercised by swimming (15 min at 31 degrees C) or treadmill excursion (8.1 m/min for 1 or 1.5 h). The animals were divided into subgroups, exposed to one of three hydrostatic pressures (7.6--11.1 ATA) for 30 min, decompressed, and observed to determine survival rate or bends incidence (type II decompression sickness). Decompression sickness was significantly reduced (P less than 0.05) in the treadmill-trained animals, was unchanged in cold-exposed and swim-exercised mice, and tended to increase in animals adapted to hypoxia. Enhanced tolerance by treadmill training is presumably due to lean body conformation, which could reduce nitrogen saturation of tissues, and greater muscle capillarization and cardiovascular fitness, which may improve nitrogen elimination. Reduced tolerance with adaptation to hypoxia may be attributed to rheological changes associated with polycythemia, which facilitate bubble production.

Adaptation, Physiological↗
PubMed1990

Decompression sickness affecting the temporomandibular joint.

Two cases of pain-only decompression sickness of the temporomandibular joint following altitude chamber exposure are presented. A detailed interview of both individuals revealed no other joint involvement or other complaints. A careful neurologic examination failed to disclose abnormalities. In both cases, the pain resolved completely with compression therapy, supporting the diagnosis of decompression sickness. Decompression sickness limited to this small joint is extremely rare, and may be easily confused with other causes of joint pain.

Adult↗
PubMedDate not supplied

[NMR in the diagnosis and treatment of neurologic lesions in decompression sickness].

The case of a decompression sickness in woman, diving to 26 meter depth is reported. The patient was helped by instructor's computer (error!) and she presented risk factors for embolic disease (obesity, smoke, estroprogestinic therapy). She presented with many symptoms of decompression sickness during immersion and during re-ascent (headache, vertigoes and paresthesias). She was not treated on the place of incident, but only 36 hours later at our center of hyperbaric medicine. Her Magnetic Resonance imaging showed hyperintensity lesions of white matter.

Adult↗