Cases reported "Decompression Sickness"

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1/9. 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.
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2/9. risk of decompression sickness during exposure to high cabin altitude after diving.

    BACKGROUND: Postdive altitude exposure increases the risk of decompression sickness (DCS). Certain training and operational situations may require U.S. Special Operations Forces (SOF) personnel to conduct high altitude parachute operations after diving. Problematically, the minimum safe preflight surface intervals (PFSI) between diving and high altitude flying are not known. methods: There were 102 healthy, male volunteers (34 /- 10 [mean /- SD] yr of age, 84.5 /- 13.8 kg weight, 26.2 /- 4.2 kg x m(-2) BMI) who completed simulated 60 fsw (feet of seawater)/60 min air dives preceding simulated 3-h flights at 25,000 ft to study DCS risk as a function of PFSI. Subjects were dry and at rest throughout. oxygen was breathed for 30 min before and during flight in accordance with SOF protocols. Subjects were monitored for clinical signs of DCS and for venous gas emboli (VGE) using precordial Doppler ultrasound. DCS incidence was compared with Chi-squared; VGE onset time and time to maximum grade with one-way ANOVA (significance at p < 0.05). RESULTS: Three cases of DCS occurred in 155 subject-exposures: 1/35 and 0/24 in 2 and 3 h flight-only controls, respectively; 0/23, 1/37, and 1/36 for 24, 18, and 12 h dive-PFSI-flight profiles, respectively. DCS risk did not differ between profiles (chi2 [4] = 1.33; crit = 9.49). VGE were observed in 19% of flights. Neither VGE onset time nor time to max grade differed between profiles (82 /- 38 min [p = 0.88] and 100 /- 40 min [p = 0.68], respectively). CONCLUSION: Increased DCS risk was not detected as a result of dry, resting 60 fsw/60 min air dives conducted 24-12 h before a resting, 3-h oxygen-breathing 25,000 ft flight (following 30 min oxygen prebreathe). The current SOF-prescribed minimum PFSI of 24 h may be unnecessarily conservative.
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3/9. An adolescent scuba diver with 2 episodes of diving-related injuries requiring hyperbaric oxygen recompression therapy: a case report with medical considerations for child and adolescent scuba divers.

    Worldwide, more than 1000 scuba (self-contained underwater breathing apparatus) diving injuries per year requiring hyperbaric recompression are documented. Approximately 80 to 90 fatalities per year are reported in north america. On average, there were 16 diving injuries requiring hyperbaric recompression therapy in scuba divers aged 19 years and younger in north america between 1988 and 2002. The youngest injured diver was 11 years old, and the youngest fatality was 14 years old during this time period. In the year 2000, certifying recreational scuba diving organizations lowered the minimum age to 8 from age 12 years for participation in the sport. We report a case of a highly trained adolescent scuba diver who, despite having advanced diving certifications, had 2 separate episodes of diving-related injuries requiring hyperbaric recompression therapy. A discussion of medical considerations in the care of the child and adolescent scuba diver is included.
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4/9. 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.
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5/9. Aseptic necrosis in compressed air tunnel workers using current OSHA decompression schedules.

    Aseptic necrosis (dysbaric osteonecrosis) was discovered in two compressed air tunnel workers who had used the present occupational health and safety Administration (OSHA) decompression tables for compressed air tunneling at pressures greater than 36 pounds per square inch gauge (psig). A roentgenographic study was made of 21 men who had worked at pressures up to 43 psig using the OSHA schedules. Bone scanning was also included. Seven of the men (33%) were found to have aseptic necrosis involving the shoulders, hips or distal femoral shafts and proximal tibia. It became evident that the present OSHA schedules caused not only an unacceptable incidence of decompression sickness but also aseptic necrosis at pressures over 36 psig. New interim tables that are more conservative and that use either air or oxygen as a breathing gas during decompression are undergoing laboratory and worksite evaluation.
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6/9. The transportable recompression rescue chamber as an alternative to delayed treatment in serious diving accidents.

    This report summarizes experience in the use of a Transportable Recompression Rescue Chamber (TRRC) for one man in the rapid initiation of treatment and evacuation in severe scuba diving accidents. An evacuation system is described which incorporates the centralized management of all diving accidents and standardized TRRCs capable of interlocking under pressure with the stationary medical chamber. oxygen breathing capability in the TRRC allows the use of up-to-date U.S. Navy oxygen treatment tables. Included are 19 cases of Type II decompression sickness and pulmonary barotrauma with neurological manifestations, most of which occurred at remote diving sites with no nearby walk-in chambers. Case analysis includes distance and means of evacuation, delay in initiating therapy, time spent in TRRC, and initial and final outcome. Together, TRRCs and airborne evacuation to a stationary medical chamber insures a minimal delay between the onset of symptoms and the start of recompression therapy. The use of the TRRC is a prime factor in minimizing delay. No complications associated with the use of TRRCs have been encountered. Ideally, evacuation should be made in a pressurized two-compartment (for a victim and an attendant) chamber. However, if this is not available we strongly advocate the use of one-man pressurized TRRCs over unpressurized evacuation.
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7/9. nitrogen-oxygen saturation therapy in serious cases of compressed-air decompression sickness.

    decompression sickness and arterial air embolism which follow exposure to raised environmental pressures of compressed air are usually adequately treated by accepted recompression procedures of relatively short durations. With serious cases, however, conventional treatment may not allow sufficient time at depth for the complete resolution of manifestations because of the need to avoid pulmonary oxygen toxicity which is associated with a prolonged period of breathing compressed air. Treatment by nitrogen-oxygen saturation at a pressure equivalent of 30 m (100 ft) sea water is proposed. Based upon the success of three refractory cases treated by this procedure, recommendation are made for the conversion of standard compressed-air chambers into an emergency saturation mode for therapy.
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8/9. 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.
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9/9. biochemistry and hematology at decompression sickness: a case report.

    A 24-year-old hospital corpsman, a volunteer in a series of dry chamber air dives to a simulated pressure equivalent to 188 FSWG (57.3 MSWG), developed left knee pain shortly after standard decompression. A tentative diagnosis of decompression sickness was made and recompression therapy was initiated with alleviation of pain occurring at 60 FSWG (18.3 MSWG). A U.S. Navy Treatment Table "5 (oxygen breathing) regimen was then selected and completed uneventfully. The subject had been undergoing biomedical evaluation for several days prior to diving; thus, a clinically diagnosed case of dysbarism with subsequent treatment was available for study. This individual was then monitored for a 10-d period. The acute phase of decompression sickness was characterized by a marked shortening of clotting time and a thrombocytopenia with accompanying increased platelet aggregates. The recovery phase was categorized by a variety of hematological and bio-chemical changes. hemodilution, an elevated megathrombocyte index, and a tendency toward eosinopenia were evident for most of the 10-d observation period. Other persistent alterations detected during this period included a relative hyperglycemia, depressed urine Na /K , and increased ketosteroid excretion. These observations indicate that abatement of pain after treatment of dysbarism can be followed by the onset of a variety of biochemical and hematological changes. Moreover, complete recovery may require upwards of 10 d.
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