Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DECOMPRESSION SICKNESS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2000

[Viral infection, the mask of decompression sickness and decompression sickness diagnosed as viral infection].

Two cases of diving persons: a soldier from the military centre of divers training and a student amateur diver, have been presented in the study. On the basis of similar symptoms--among others: muscular pain, discomfort, subfebrile body temperature, extremely different, incorrect diagnoses were given and improper treatment was introduced. In the case of the soldier suffering from a viral infection decompression sickness was diagnosed only because he served in a divers unit. Whereas, in the second case a physician did not take into consideration all available history data and diagnosed influenza despite evident symptoms of decompression sickness. In the discussion the factors which should have guided the physician in both cases to proper diagnosis and proper therapeutic management have been indicated.

Adult↗
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↗
PubMed2000

Cases from the aerospace medicine residents' teaching file. Decompression sickness.

Decompression sickness is an uncommon but serious risk associated with flying and SCUBA diving with potential for significant morbidity and mortality. It can occur in both novice and experienced individuals. This case illustrates an atypical presentation of decompression sickness in an experienced amateur SCUBA diver. Clinical suspicion must be high, since the presenting symptoms can be nonspecific as in this case. Early recognition and treatment are important for maximum recovery.

Adult↗
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↗
PubMed2001

The physiological kinetics of nitrogen and the prevention of decompression sickness.

Decompression sickness (DCS) is a potentially crippling disease caused by intracorporeal bubble formation during or after decompression from a compressed gas underwater dive. Bubbles most commonly evolve from dissolved inert gas accumulated during the exposure to increased ambient pressure. Most diving is performed breathing air, and the inert gas of interest is nitrogen. Divers use algorithms based on nitrogen kinetic models to plan the duration and degree of exposure to increased ambient pressure and to control their ascent rate. However, even correct execution of dives planned using such algorithms often results in bubble formation and may result in DCS. This reflects the importance of idiosyncratic host factors that are difficult to model, and deficiencies in current nitrogen kinetic models. Models describing the exchange of nitrogen between tissues and blood may be based on distributed capillary units or lumped compartments, either of which may be perfusion- or diffusion-limited. However, such simplistic models are usually poor predictors of experimental nitrogen kinetics at the organ or tissue level, probably because they fail to account for factors such as heterogeneity in both tissue composition and blood perfusion and non-capillary exchange mechanisms. The modelling of safe decompression procedures is further complicated by incomplete understanding of the processes that determine bubble formation. Moreover, any formation of bubbles during decompression alters subsequent nitrogen kinetics. Although these factors mandate complex resolutions to account for the interaction between dissolved nitrogen kinetics and bubble formation and growth, most decompression schedules are based on relatively simple perfusion-limited lumped compartment models of blood: tissue nitrogen exchange. Not surprisingly, all models inevitably require empirical adjustment based on outcomes in the field. Improvements in the predictive power of decompression calculations are being achieved using probabilistic bubble models, but divers will always be subject to the possibility of developing DCS despite adherence to prescribed limits.

Algorithms↗
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↗
PubMed2002

Arterial gas embolism and decompression sickness.

Decompression sickness occurs when a sufficiently large gas phase forms within the tissues of the body after a reduction in ambient pressure. Arterial gas embolism occurs secondary to pulmonary barotrauma when gas is forced into the pulmonary vasculature. Although they may clinically present in a similar fashion, the underlying pathophysiology of the two conditions is quite different.

Decompression Sickness↗
PubMed1995

Paraplegia and decompression sickness.

Decompression sickness may include spinal cord damage, which sometimes persists. Casual divers are exposed, as well as professionals. In this study we have reviewed the clinical records of divers admitted with symptoms of spinal cord injuries in our area in the last 6 years. This study is divided into two groups: those who fully recovered (19 divers) and those with neurological sequelae (12 divers).

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↗
PubMed2001

Effect of ambient temperature on the risk of decompression sickness in surface decompression divers.

BACKGROUND: Several studies have noted an apparent increase in decompression sickness (DCS) risk with surface decompression diving in warm water or with hot water suits (Van Der Aue 1951, Shields 1986, Leffler 1997), but did not perform statistical tests to control for the pressure-time profile. METHODS: The 1986 data, including 73 DCS cases out of 14,891 dives, were analyzed by Mantel-Haenszel analysis to control for depth and bottom time. Dive profiles from the 1951 U.S. Navy report, including 147 DCS cases from 1507 dives, were analyzed with logistic regression analysis to control for depth, bottom time, and aspects of the decompression profile. RESULTS: In the 1986 data, hot water suits, as compared with passive thermal protection, were associated with an odds ratio (OR) of 1.81 (95% confidence interval, CI = 0.96 to 3.42) for DCS. In the 1951 data, each 10 degree C increase in water temperature yielded an OR for DCS of 1.96 (95% CI = 1.33 to 2.90). The interaction of temperature and bottom time suggested that the effect was more pronounced in shorter dives. Among DCS cases, the OR for type 2 symptoms with hot water suits was not significant in the 1986 data (p = 0.18). In the 1951 data, the probability of type 2 symptoms among DCS cases was better explained by the dive profile than by the temperature. Thermal effects on gas physics, metabolism, hemostasis, and nociception were reviewed. CONCLUSION: Surface decompression divers who are warm at depth face an increased risk of DCS. Vasodilatation in warm divers may result in more rapid on-gassing of tissues with short time constants. A full evaluation of DCS risk should consider physiological and physical effects of ambient temperature.

Decompression Sickness↗
PubMed2002

Kinetic and dynamic models of diving gases in decompression sickness prevention.

Decompression sickness is a complex phenomenon involving gas exchange, bubble dynamics and tissue response. Relatively simple deterministic compartmental models using empirically derived parameters have been the mainstay of the practice for preventing decompression sickness since the early 1900s. Decades of research have improved our understanding of decompression physiology, and the insights incorporated in decompression models have allowed people to dive deeper into the ocean. However, these efforts have not yet, and are unlikely in the near future, to result in a 'universal' deterministic model that can predict when decompression sickness will occur. Divers using current recreational dive computers need to be aware of their limitations. Probabilistic models based on the estimation of parameters using modern statistical methods from large databases of dives offer a new approach and can provide a means of standardisation of deterministic models. Future improvements in decompression practice will depend on continued improvement in understanding the kinetics and dynamics of gas exchange, bubble evolution and tissue response, and the incorporation of this knowledge in risk models whose parameters can be estimated from large databases of human and animal data.

Decompression Sickness↗
PubMed2002

USAF treatment table 8: treatment for altitude decompression sickness.

INTRODUCTION: Altitude decompression sickness (DCS) has been treated with hyperbaric therapy since 1941. Treatment has essentially followed the diving DCS paradigm. Expanding space operations and higher flying, more remotely placed military aircraft have stimulated a re-examination of this paradigm. Can the oxygen and pressure-producing resources in these austere environs be reduced without sacrificing treatment efficacy? METHOD: A prospective series of 12 patients was treated with a new treatment table. USAF Treatment Table 8 (TT8) consists of 100% oxygen delivered at 2 ATA for four 30-min periods with intervening 10-min air breaks (a total oxygen dose of 2 h). Inclusion spanned 1985-1989. RESULTS: There were 10 patients who were treated 11 times for Type I altitude decompression sickness. Treatment was successful in 91%. There was one failure (a recurrence of elbow pain) requiring further therapy. Two patients were treated for Type II altitude decompression sickness. Treatment was successful in 50%. There was one failure (incomplete clearance of sensory deficits and weakness in the shoulder) requiring further therapy. CONCLUSION: Although TT8 had two failures, its successes suggest that a new protocol for the treatment of altitude decompression sickness is viable. In addition, its successes further suggest that a more extensive clinical trial is in order.

Adult↗