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PubMed1999

Inner ear decompression sickness following altitude chamber operation.

Decompression sickness (DCS) is a known hazard of altitude chamber operation. The musculoskeletal, dermal, neurological and pulmonary manifestations of DCS are well recognized, but inner ear injury has not been reported. We present the unusual case of a medical corpsman suffering from vestibular DCS after an altitude chamber exposure to 25,000 ft. The patient had a good clinical response to hyperbaric treatment, but there was laboratory evidence of mild residual vestibular damage with full compensation. This case suggests that aviation medical personnel should be more aware of the possible occurrence of inner ear DCS among subjects exposed to altitude.

Adult↗
PubMed1999

[Severe decompression sickness in divers].

The term "decompression illness (DCI)" is a disorder which arises from the presence of ectopic gas bubbles following decompression. Scuba diving poses the risk of two typically clinical syndromes: decompression sickness (DCS) and arterial gas embolism (AGE). DCS results from the formation of gas bubbles in the tissues of the body and in the blood due to rapid reduction of the environmental pressure. AGE is caused by pulmonary overinflation if the breathing gas cannot be exhaled adequately during the ascent. Although the pathophysiological mechanisms of these two disorders are quite different, both of them lead to the same result: inert gas bubbles that may cause impairment of vital functions due to hypoxia. Recognizing the signs and symptoms of DCI is the first step of the therapy. The emergency treatment contains: basic life support, advanced life support--if necessary, horizontal positioning of the victim, administration of 100% normobaric oxygen via face mask or endotracheal tube, rehydration, rapid transportation to the nearest emergency department/hyperbaric facility for definitive treatment in order to prevent serious neurological sequelae.

Barotrauma↗
PubMed1993

Flying after diving and decompression sickness.

Reports of 1,159 decompression sickness (DCS) incidents during recreational diving were analyzed by logistic regression for the effects of flying on the occurrence of Type II DCS, complete relief of symptoms after one recompression, and residual symptoms 3 months after treatment. The relevant diver populations were those who: 1) did not fly; 2) had symptoms before flying but flew anyhow; 3) and did not have symptoms before flying but developed symptoms during or after flight. Of the total DCS population, 13.9% had preflight symptoms while 5.6% developed symptoms during or after flight. Symptoms which occurred during or after flight were no more serious and their responses to recompression no less successful than symptoms in nonflying divers. There was a statistically significant association between divers who flew with pre-existing symptoms and Type II DCS, incomplete relief with one recompression, and residual symptoms after 3 months.

Adult↗
PubMed1997

Relationship between age and susceptibility to altitude decompression sickness.

BACKGROUND: Susceptibility to altitude decompression sickness (DCS) is influenced by a multitude of factors including, potentially, an individual's age. Previous attempts by authors to determine the effect of age on DCS susceptibility have produced conflicting results. The purpose of this study was to try to clarify that conflict and to quantify the impact of age on DCS risk. METHODS: We examined the Armstrong Laboratory DCS Hypobaric Research Database containing data on 1299 subject flight exposures conducted from 1983-94. Subjects were from 18-45 yr of age. Exposure altitudes ranged from 11,500 ft (3505 m) to 30,000 ft (9144 m). The duration of exposure varied from 3-8 h and preoxygenation time ranged from 0-2 h and 15 min. Data were compiled according to seven age groups. RESULTS: The results show a significant three-fold increase in susceptibility between the age group 18-21 and the group > 42 yr of age. The results also show a trend toward increased susceptibility between the 18-21 group and the groups between 26 and 41 yr of age. However, there was no significant change within the range of 26-41 yr. CONCLUSION: There is a trend toward increased DCS susceptibility with increasing age, with a particularly strong trend for individuals over 42 yr of age.

Adolescent↗
PubMed1999

[Study on testing method of susceptibility to decompression sickness in aerospace].

Objective. To provide related parameters for astronauts. Method. A study of susceptibility to decompression sickness was carried out in 43 subjects in a hypobaric chamber. Result. Incidence of altitude decompression sickness under rest condition was closely related to age, time of oxygen prebreathing, gas bubble formation rates in the venous blood flow returned to heart and some other physiological indexes. Incidence of decompression sickness was significantly higher in subjects aged 30-36 years than in those aged 19-20 years under the same experimental conditions. In the older subjects body-fat, blood cholesterole and noradrenaline in urine during experiment were significantly higher than those in the younger subjects. It also showed that among persons of the same ages, when prebreathing time was longer, the incidence of decompression sickness was significantly lower under the same experimental conditions. Conclusion. It is desirable that the susceptibility to decompression in astronaut be tested with 1 h oxygen prebreathing before exposure to the altitude of 10000 m for 30 min.

Adult↗
PubMed2003

Multiple sclerosis presenting as neurological decompression sickness in a U.S. navy diver.

A case of clinically definite multiple sclerosis presenting as neurological decompression sickness is presented. A 23-yr-old U.S. Navy diver experienced onset of hypesthesia of the left upper trunk approximately 19 h after making two SCUBA dives. She did not seek medical attention until 3 wk later, at which time she was diagnosed with possible neurological decompression sickness. She was treated with hyperbaric oxygen, but demonstrated no improvement. Further evaluation led to the diagnosis of multiple sclerosis. This case underscores the potential similarity in neurological presentation between multiple sclerosis and decompression sickness. The differential diagnosis of neurological decompression sickness, particularly in atypical cases, should include multiple sclerosis. The appropriateness of medically clearing multiple sclerosis patients for diving is discussed.

Adult↗
PubMed1990

Inner ear decompression sickness following a shallow scuba dive.

Inner Ear Decompression Sickness (IEDCS)--manifested by tinnitus, vertigo, nausea, vomiting, and hearing loss--is usually associated with deep air or mixed gas dives, and accompanied by other CNS symptoms of decompression sickness (DCS). Early recompression treatment is required in order to avoid permanent inner ear damage. We present an unusual case of a scuba diver suffering from IEDCS as the only manifestation of DCS following a short shallow scuba dive, successfully treated by U.S. Navy treatment table 6 and tranquilizers. This case suggests that diving medical personnel should be more aware of the possible occurrence of IEDCS among the wide population of sport scuba divers.

Adult↗
PubMed1992

Decompression sickness: an increasing risk for the private pilot.

Decompression sickness is not an appreciated hazard among the private pilot community. This is of growing concern with the increasing number of nonpressurized aircraft capable of flying to altitudes in excess of 5,468 m (18,000 ft). A case report is presented of a 42-year-old pilot who apparently experienced decompression sickness at flight level 250 which went unrecognized until several months after the incident.

Adult↗
PubMed1976

Intracardial bubbles during decompression to altitude in relation to decompression sickness in man.

Doppler ultrasound was used in five subjects to detect intracardial gas bubbles during decompressions to altitude. At a simulated altitude of 8,000 m, neither intracardial bubbles nor symptoms of decompression sickness occurred. At 9,000 m, bubbles were registered in two subjects, one of which had questionable bends. At 11,500 m, bubbles were registered in all but one subject and two had bends. The three subjects who had not gotten bends were exposed to an air-breathing period of 30 min or, in one case, even 45 min at 2 ATA, for extra nitrogen loading, followed by decompression to 11,500 m. These subjects had heavy showers of bubbles followed by bends. In all cases with decompression sickness during the decompressions to altitude, intracardial bubbles were registered prior to the appearance of symptoms. The technique may be used in studies of decompression sickness without provoking actual symptoms, thus making the studies safer.

Brain Diseases↗
PubMed1976

Incidence of decompression sickness in Navy low-pressure chambers.

This study reports the incidence of decompression sickness occurring in U. S. Navy altitude chambers in association with physiological training of aircrews for the period 1 Jan. 1972 to 31 Dec. 1975. There were 79 cases of decompression sickness in 88,520 altitude chamber exposures, an incidence of 0.089%. Among trainees, there were 22 cases in 73,561 exposures, an incidence of 0.029%. Among chamber inside observers, there were 57 cases in 14,959 exposures, an incidence of 0.38%. This 12-fold greater incidence among inside observers over trainees was statistically significant (p less than 0.01). Reasons for the increased incidence of decompression sickness among inside observers are discussed.

Altitude↗
PubMed1989

Ethanol treatment for acute decompression sickness in rabbits.

Rabbits developed acute decompression sickness after staying at 6 ATA for 30 min followed by decompression to 1 ATA in 20 min or less. If the rabbits received an i.v. injection of 25% ethanol upon surfacing, all survived, whereas half the untreated control group died within 15-35 min after decompressing. In ethanol-treated animals, no bubbles were seen in blood vessels of visceral organs, muscles, and subcutaneous tissues at autopsy 60 min after treatment. Decompression reduced platelet counts markedly in all rabbits, but in the control group the count stayed low, whereas with ethanol treatment the counts had reached the precompression level after 1 h and 24 h.

Animals↗
PubMed1994

Protective effect of oxygen and heliox breathing during development of spinal decompression sickness.

A rat model of spinal decompression sickness (DCS) allows study of spinal cord function for at least 3 h after decompression to 1 atm abs (101 kPa) after an exposure to air at 3.8 atm abs (385 kPa) for 1 h. During these 3 h, spinal evoked potentials (SEPs) elicited by peroneal nerve stimulation may be reduced or disappear, and histologic lesions in the spinal cord are observed. Three groups of animals were given either air, oxygen, or heliox (80/20) to breathe at 1 atm abs for 3 h after decompression. Both oxygen and heliox breathing impeded the development of DCS significantly as judged by the mortality of the animals and disappearance of the SEPs. The effect of heliox seemed to be superior to that of oxygen. The latency time from stimulation to the first SEP peak increased significantly during both air and oxygen breathing, whereas no significant increase was seen during heliox breathing. Histologic examination of the spinal cords of animals breathing air, oxygen, or heliox (80/20) showed focal lesions in the white and gray matter. In the white matter, degenerated myelin sheaths as well as expanded extracellular spaces compatible with bubble formation were seen. In the gray matter, perikaryal degeneration was observed. The extracellular space in the white matter was increased in all decompressed animals compared with controls (P < 0.01). Oxygen and heliox breathing caused a smaller increase in extracellular space as compared with air-breathing animals (P < 0.05) and (0.10 > P > 0.05), respectively. It is concluded that breathing of oxygen or heliox (80/20) at 1 atm abs has a preventive effect on the development of DCS when compared with air breathing; the effect of heliox seems to be superior to that of oxygen.

Air↗
PubMed1994

Role of extravascular gas bubbles in spinal cord injury induced by decompression sickness in the rat.

We have evaluated the contribution of extravascular gas bubbles to spinal cord injury in decompression sickness. For this purpose, a model of decompression sickness was developed by subjecting rats to simulated dives using compressed air. Various diving profiles were tested and the presence of spinal cord injury was demonstrated by electrophysiologic measurements. To evaluate the space occupying lesions induced by gas bubbles in the white matter, the spinal cord was fixed by perfusion with 10% buffered formalin. Tissue blocks from cervical, thoracic, and lumbar spinal cords were embedded in paraffin. Tissue sections were double stained with luxol fast blue and hematoxylin and eosin. The space occupying lesions were quantified with a digitizer tablet. The fractional area of the lesions was 0.009% in controls and 0.026% in rats subjected to diving. We conclude that the volume of extravascular free gas present in the cord of rats with spinal decompression sickness is small and that artifacts of tissue preparation contribute to the volume estimate. As far as can be judged from the results in this animal model, the contribution of extravascular gas bubbles to spinal cord decompression injury is minor.

Animals↗
PubMed1983

[Empirical treatment of decompression sickness in Greek sponge divers].

Reports and evidence of the empirical methods of treating decompression sickness long used by Greek sponge divers have been collected. Divers were questioned by a team from Chieti University's School of Underwater and Hyperbaric Medicine during a visit to the island of Kalymnos. There are interesting analogies between modern therapy and ancient empirical methods. The modern methods were devised in response to the enormous incidence of decompression sickness during the fishing season in the Southern Mediterranean. It may well be that the experience of old sponge divers may offer some helpful suggestions for modern therapy of decompression sickness.

Adult↗
PubMed2002

Modulation of decompression sickness risk in pigs with caffeine during H(2) biochemical decompression.

In H(2) biochemical decompression, H(2)-metabolizing intestinal microbes remove gas stored in tissues of animals breathing hyperbaric H(2), thereby reducing decompression sickness (DCS) risk. We hypothesized that increasing intestinal perfusion in pigs would increase the activity of intestinal Methanobrevibacter smithii, lowering DCS incidence further. Pigs (Sus scrofa, 17-23 kg, n = 20) that ingested caffeine (5 mg/kg) increased O(2) consumption rate in 1 atm air by ~20% for at least 3 h. Pigs were given caffeine alone or caffeine plus injections of M. smithii. Animals were compressed to 24 atm (20.5-23.1 atm H(2), 0.3-0.5 atm O(2)) for 3 h, then decompressed and observed for signs of DCS. In previous studies, DCS incidence in animals without caffeine treatment was significantly (P < 0.05) lower with M. smithii injections (7/16) than in controls (9/10). However, contrary to our hypothesis, DCS incidence was marginally higher (P = 0.057) in animals that received caffeine and M. smithii (9/10) than in animals that received caffeine but no M. smithii (4/10). More information on gas kinetics is needed before extending H(2) biochemical decompression to humans.

Animals↗
PubMed1989

Patent foramen ovale and decompression sickness in divers.

30 patients with a history of decompression sickness were examined for the presence of patent foramen ovale by bubble contrast, two-dimensional echocardiography and colour flow doppler imaging. With bubble contrast, 11 (37%) of the patients had right-to-left shunting through a patent foramen ovale during spontaneous breathing. 61% of a subset of 18 patients with serious signs and symptoms had shunting. This number was significantly higher than the 5% prevalence seen with the same diagnostic technique in 176 healthy volunteers. The presence of patent foramen ovale seems to be a risk factor for the development of decompression sickness in divers.

Acute Disease↗
PubMed1989

Decompression sickness and arterial gas embolism in sports scuba divers.

Diving underwater with breathing apparatus is an increasingly popular sport. Consequently, the number of diving-related accidents, including both decompression sickness and arterial gas embolism, have increased. Though both involve bubbles, decompression sickness is a disease which involves gas bubbles forming in tissues and venous blood, while arterial gas embolism results from the introduction of gas bubbles directly into the arterial circulation. Although the pathologies and natural histories of decompression sickness and arterial gas embolism are different, the treatment of these conditions is essentially the same. Compression in a recompression chamber is the definitive treatment of both decompression sickness and arterial gas embolism, and any delay before treatment must be minimised if a good outcome is desired.

Arteries↗
PubMed1997

Magnetic resonance findings in scuba diving-related spinal cord decompression sickness.

Scuba diving is associated with risk of severe decompression sickness (DCS type II), which results from rapid reduction of the environmental pressure sufficient to cause the formation into tissue or blood of inert gas bubbles previously loaded within tissues as a soluble phase. DCS type II constitutes a unique subset of ischemic insults to the central nervous system (CNS) with primarily involvement of the spinal cord. Ten patients with diving-related barotrauma underwent neurologic examination. Two of them presented progressive sensory and motor loss in the extremities at admission and were presumed affected by spinal cord DCS. Magnetic resonance imaging (MRI) demonstrated abnormalities in the white-matter tracts of the spinal cord in these patients, in each case corresponding to an area of the cord believed to be clinically involved. After a course of therapeutic recompressions, one patient was able to stand and walk a short distance, and MRI revealed a decreased extension of areas of spinal cord abnormalities. MRI has proved to be reliable in the detection of pathologic changes of spinal cord decompression sickness that were previously undetectable by other neuroimaging methods and also has proved to be useful in the follow-up during therapeutic hyperbaric recompressions.

Adolescent↗