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At least 19 recordsLinked to original sources
PubMed1975

Mechanisms underlying spinal cord damage in decompression sickness.

Decompression sickness, which damaged the spinal cord, was produced in anesthetized dogs using a compression chamber. Cerebrospinal fluid pressure and several intravascular and intracardiac pressures were monitored during the course of the simulated dives. Manometric responses to forcible lung inflation and abdominal compression were measured both predive and postdive after signs of spinal cord damage were evident. Cinevenography of the epidural vertebral venous system was performed both predive and postdive. Histopathologic studies of the brains and cords of both predive and postdive. Histopathologic studies of the brains and cords of paretic animals were carried out. The results indicate that the epidural vertebral venous system becomes obstructed during spinal cord damaging decompression sickness and strongly suggests that spinal cord infarction in decompression sickness is caused by obstruction of cord venous drainage at the level of the epidural vertebral venous system.

Animals↗
PubMed2026

Differential gene transcription following intravenous injection of air bubbles in rats with varying resistance to decompression sickness.

Decompression sickness (DCS) is a pathology caused by the appearance of gas emboli in the bloodstream and tissues. However, the weak correlation between the amount of venous gas emboli (VGE) and the development of DCS, as well as the considerable interindividual variability in DCS susceptibility, suggests that a higher DCS resistance could be associated with a better management of VGE-induced stress. To study the effects of VGE independently of the hyperbaric stress induced by diving, Wistar and DCS-resistant male and female rats received 5 mL/kg of a 0.9% NaCl solution containing air microbubbles through the tail vein. After 120 min, the liver and lungs were harvested. Wet-to-dry weight ratio was determined in the lungs. Gene expression was quantified by reverse transcription-polymerase chain reaction in the liver. Compared with standard Wistar, DCS-resistant rats exhibited a lower lung wet-to-dry weight ratio after air microbubble injection, suggesting lower pulmonary fluid accumulation. In the liver, DCS-resistant rats showed higher tissue factor transcription at the basal state and post-air microbubble injection. Tissue factor pathway inhibitor was lower in DCS-resistant rats at the basal state but higher following air microbubble injection. Levels of heat shock protein 70 (HSP70), heat shock protein 27 (HSP27), and early growth response 1 (Egr-1) were higher in DCS-resistant rats after air microbubble injection. At the basal state, only HSP27 was higher in DCS-resistant rats, with HSP70 lower and Egr-1 not different. These results help clarify the pathways involved in the response to VGE and highlight potential mechanisms underlying resistance to DCS, including enhanced anticoagulant pathways and improved cellular stress responses.NEW & NOTEWORTHY This study suggests for the first time that DCS resistance may be associated with a better tolerance to VGE. This greater DCS resistance could be achieved through improved control of the procoagulant effects of bubbles via TFPI-dependent inhibitory mechanisms and an enhanced cellular stress response to VGE by HSP70, HSP27, and EGR-1. It also suggests that it may be possible to stratify the individual DCS risk based on the thromboinflammatory response to bubbles.

Animals↗
PubMed1991

Microbubble damage to the blood-brain barrier: relevance to decompression sickness.

Decompression sickness affecting the nervous system is still a serious problem in diving, but the mechanisms involved are in dispute. Although microbubbles can be detected in the pulmonary artery on decompression using ultrasound, mammalian lungs are competent filters for microbubbles larger than 20 microns in diameter. It has been assumed that smaller bubbles released by the lungs are harmless, because there is evidence that they do not arrest in the cerebral circulation. We injected 15 +/- 5 microns diameter microbubbles in 5 ml of plasma slowly into the right carotid artery of anesthetized guinea pigs. At intervals of 1, 2, or 3 h postinjection, 2% trypan blue in 2 ml of plasma was injected into the same artery or the contralateral carotid artery. A control animal for each experiment was injected with 5 ml of plasma only, followed by the injection of dye at the same interval. After the animals were killed, the brains were examined for evidence of blood-brain barrier dysfunction. All animals at 1 h, and 9 out of 10 animals at 2 h after the injection of microbubbles, showed extravasation of the albumin-binding dye in the ipsilateral hemisphere, indicating gross blood-brain barrier dysfunction. In each of the matched controls, the barrier in the neocortex remained intact. At Hour 3 the barrier was impermeable to the trypan blue in both experimental and control animals. These experiments demonstrate that microbubbles impair the blood-brain barrier integrity to protein, causing focal edema.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Somatosensory evoked potentials, electroencephalography and CT scans in the assessment of the neurological sequelae of decompression sickness.

Decompression sickness can lead to neurological complications. Recovery may be studied by somatosensory evoked potentials (SEPs), which are more sensitive than normal methods of neurological examination, and by electroencephalography (EEG). The combination of EEG and SEP may be useful in differentiating among spinal, brainstem and cortical pathology.

Adult↗
PubMed1978

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.

Adult↗
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↗
PubMed1985

Doppler bubble detection and decompression sickness: a prospective clinical trial.

Decompression sickness in human beings exposed to high ambient pressure is thought to follow from gas bubble formation and growth in the body during return to low pressure. Detection of Doppler-shifted ultrasonic reflections in major blood vessels has been promoted as a noninvasive and sensitive indicator of the imminence of decompression sickness. We have conducted a double-blind, prospective clinical trial of Doppler ultrasonic bubble detection in simulated diving using 83 men, of whom 8 were stricken and treated for the clinical disease. Diagnosis based only on the Doppler signals had no correlation with clinical diagnosis. Bubble scores were only slightly higher in the stricken group. The Doppler technique does not appear to be of diagnostic value in the absence of other clinical information.

Clinical Trials as Topic↗
PubMed1988

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.

Adult↗
PubMed1987

[Research on the incidence of decompression sickness in compressed air works. The development of its recent five years' study].

Compressed air works have been used as the safest construction work for the basic underground or underwater compressed shield or caisson works in Japan; however, the workers who were exposed to the compressed fields must have put themselves at risk of decompression sickness. Decompression sickness is generally considered to be due to the bubble effects and the bubbles originate from the supersaturated gas dissolved in the blood and other tissues. The standard decompression schedule by the Ministry of Labor has been practically applied at the end of compressed air works, and the laborers decompress slowly from the bottom pressure to the surface according to the schedule. It is difficult to completely prevent the sickness and the average percentage of contracting "bends," using the Japanese standard decompression schedule, is considered to be 0.54%. But previous papers reported higher incidences from 1.42 to 3.3% or more. We have continued an actual investigation on the incidence, and the number of the exposed trials amounted to nearly a hundred thousand. These data were compared between recent five years' group and before. Eventually, it was ascertained that the incidence has been significantly decreased in the recent five years; however, greater care in occupational safety control is still needed.

Adult↗