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 361 records · Page 20Linked to original sources
PubMed2002

The effect of repeated altitude exposures on the incidence of decompression sickness.

INTRODUCTION: Repeated altitude exposures in a single day occur during special operations parachute training, hypobaric chamber training, unpressurized flight, and extravehicular space activity. Inconsistent and contradictory information exists regarding the risk of decompression sickness (DCS) during such hypobaric exposures. HYPOTHESIS: We hypothesized that four short exposures to altitude with and without ground intervals would result in a lower incidence of DCS than a single exposure of equal duration. METHODS: The 32 subjects were exposed to 3 different hypobaric exposures--condition A: 2 h continuous exposure (control); condition B: four 30-min exposures with descent/ascent but no ground interval between the exposures; condition C: four 30-min exposures with descent/ascent and 60 min of ground interval breathing air between exposures. All exposures were to 25,000 ft with 100% oxygen breathing. Subjects were observed for symptoms of DCS, and precordial monitoring of venous gas emboli (VGE) was accomplished with a SONOS 1000 echo-imaging system. RESULTS: DCS occurred in 19 subjects during A (mean onset 70+/-29 min), 7 subjects in B (60+/-34 min), and 2 subjects in C (40+/-18 min). There was a significant difference in DCS incidence between B and A (p = 0.0015) and C and A (p = 0.0002), but no significant difference between B and C. There were 28 cases of VGE in A (mean onset 30+/-23 min), 21 in B (41+/-35 min), and 21 in C (41+/-32 min) with a significant onset curve difference between B and A and between C and A, but not between B and C. Exposure A resulted in four cases of serious respiratory/neurological symptoms, while B had one and C had none. All symptoms resolved during recompression to ground level. CONCLUSION: Data indicate that repeated simulated altitude exposures to 25,000 ft significantly reduce DCS and VGE incidence compared with a single continuous altitude exposure.

Adolescent↗
PubMed1979

Decompression sickness in South African sport divers.

During the period 1 January 1969 to 31 December 1977 56 underwater diving accidents were reported among amateur sport divers in South Africa. Of these, 4 were diagnosed and treated as decompression sickness (DS), an incidence of 7%. Analysis of the 4 cases of DS indicates that they were all in the serious type II neurological category. This is in keeping with results found in Hawaii and Australia, and the reasons for this finding are discussed. An emergency medical system (EMS) for on-site, pre-chamber and decompression chamber treatment is discussed.

Adolescent↗
PubMed1988

Manifestations and treatment of 793 cases of decompression sickness in a compressed air tunneling project in Hong Kong.

In the largest compressed air tunneling contract for the construction of the Island Line of the Mass Transit Railway system in Hong Kong, 154,390 man-decompressions occurred, of which 142,140 were after exposures to 1 bar (1.97 ATA, 14.7 psig) or above. The maximum working pressure (MWP) was 3.30 bar (4.26 ATA, 47.9 psig). There were 792 cases of type I and 1 case of type II decompression sickness. The manifestations of the cases were generally similar to those reported elsewhere. Oxygen treatment was given to 9 cases and all were successfully treated with no recurrence of symptoms. Minimum effective pressure treatment on 783 type I cases was successful, with 9.6% requiring two or more recompressions. The pressure required to relieve symptoms was more closely related to the interval between completion of decompression after work and commencement of treatment than to the delay between onset of symptoms and treatment. For every 1-h interval or every 1-h delay, an additional pressure of 0.04 bar (0.04 ATA, 0.58 psi) above MWP was required for pain relief. Step-wise multiple regression analysis showed that the four predictors for pressure of relief and the highest pressure used in recompression, respectively, were, in order of descending importance, maximum working pressure, interval before treatment, bends sequence (the nth attack of bends experienced in the present contract, i.e., the sum of previous attacks and the present attack), and duration of exposure.

Adult↗
PubMed1992

[Decompression sickness as differential diagnosis in internal medicine emergency admissions].

Two men (aged 37 years--patient 1, and 26 years--patient 2), both in good health, had dived as a sport to a depth of 40 and 45 m, respectively, reportedly keeping to the prescribed decompression times on their ascent. Patient 1 immediately developed shortness of breath and pain in the chest, later neurological deficits in both legs, as well as faecal and urinary incontinence. Examination 60 h later revealed paraparesis, increased leg proprioceptor reflexes and paraesthesia below the 10th thoracic vertebra, with abnormal posterior column function. After recompression (hyperbaric oxygenation, 6 treatment sessions of 4 h each over 8 days, as prescribed in US Navy Table No. 6) the signs improved and two months later there were no deficits. Patient 2 developed 30 min after a similar dive painful, doughy swellings and redness over the upper ventral half of the thorax and both upper arms. All signs and symptoms disappeared after recompression treatment (hyperbaric oxygenation for 3 h), begun 28 h after the dive. Previously elevated levels for haemoglobin (18.5 g/dl), haematocrit (0.56) and red blood corpuscles (5.98 x 10(6)/microliters) returned to normal. The described neurological abnormalities are typical for type II, redness and joint pains for type I decompression sickness.

Adult↗
PubMed1991

The use of the pressure cuff test in the diagnosis of decompression sickness.

Records at the Hyperbaric Medicine Division, United States Air Force School of Aerospace Medicine, were reviewed to determine the utility of the pressure cuff test as an aid in the diagnosis of Type I decompression sickness (DCS). Applying local pressure with a blood pressure cuff has been described as a useful test to differentiate the pain of DCS from that of other musculoskeletal conditions. Records were reviewed from January 1985 to December 1989. During this period 179 patients were treated with recompression for extremity pain. Application of a blood pressure cuff to the painful area was used as a diagnostic aid in 87 patients. Only 53 patients (61%) with DCS had a positive test (relief of pain with local pressure). Results did not correlate with the rapidity of relief of symptoms during recompression. We conclude that the failure to respond to the application of local pressure should not be used to rule out the presence of DCS-this must be done with a test of pressure in a hyperbaric chamber.

Adult↗
PubMed1981

Application of bubble formation model to decompression sickness in fingerling salmon.

Recently a new cavitation model has been proposed in which bubble formation in aqueous media in initiated by spherical gas nuclei stabilized by surface-active membranes of varying gas permeability. In previous application of the varying permeability model, good agreement has been obtained with experimental limits in pressure reduction for gelatin, rats, and humans following steady-state exposures. We new extend this investigation to fingerling salmon and demonstrate that a satisfactory description of the decompression data of D' Aoust et al. (Undersea Biomed Res 1980; 7:199-209) is provided by the model with parameter values that are similar to those found for other physical and biological systems. This adds further evidence for the generally of the model as well as for the importance of bubble nucleation as the primary and controlling event in decompression sickness.

Animals↗
PubMed2005

Partial pressure of nitrogen in breathing mixtures and risk of altitude decompression sickness.

BACKGROUND: Many aircraft oxygen systems do not deliver 100% O2. Inert gases can be present at various levels. The purpose of this study was to determine the effect of these inert gas levels on decompression sickness (DCS). METHODS: Subjects were exposed for 4 h to 5486 m (18,000 ft) with zero prebreathe, using either mild (Test A) or strenuous exercise (Test B), and breathing 60%N2/40%O2. Test C used a breathing mixture of 40%N2/60%O2 at 6858 m (22,500 ft) with zero prebreathe and mild exercise. Test D investigated a breathing mixture of 2.8%N2/4.2%argon/93%O2 with 4 h exposures to 7620 m (25,000 ft), mild exercise, and 90 min of preoxygenation. The controls were from previous studies using similar conditions and 100% O2. RESULTS: The DCS risk for Tests A and B and the Control for B was 7%; the Control for Test A was 0% (n.s.). Breathing the 40%N2/60%O2 mixture (Test C) resulted in 43% DCS compared with 53% DCS with 100% O2 (n.s.). When the 2.8%N2/4.2%argon/93%O2 mixture was used, the results showed 25% DCS compared with 31% DCS with 100% O2 (n.s.). CONCLUSIONS: The increased nitrogen and argon levels in the breathing gas while at altitudes of 5486 m to 7620 m did not increase DCS risk. These results support the concept of using the partial pressure gradient of inert gases instead of the percentage of N2 or argon in a breathing gas mixture to determine the risk of DCS during altitude exposure.

Aerospace Medicine↗
PubMed2006

[Decompression sickness accident management in remote areas. Use of immediate in-water recompression therapy. Review and elaboration of a new protocol targeted for a mission at Clipperton atoll].

In-Water Recompression (IWR) is defined as a treatment of decompression sickness by immediate underwater recompression after the onset of symptoms in remote areas where hyperbaric chambers are not available. At least three methods of IWR have been published. They used pure oxygen breathing for prolonged periods of time at a depth of 9 m. IWR effectiveness in comparison with standard recompression techniques has not been assessed. IWR should be used in remote localities as an immediate measure to stop the evolution of decompression illness before evacuating the victim for subsequent treatment to the nearest hyperbaric facility. Resulting from environmental conditions, the risks of drowning and hypothermia are the most often quoted, pure oxygen breathing at 9 m can also expose to acute oxygen toxicity. The objectives of this work are: first, to examine existing published methods of IWR; second, to propose a new method of IWR. All published methods of IWR involve victim returning underwater for a long period of time. But dehydration due to a long period of immersion can worsen symptoms of decompression illness and acute oxygen toxicity is also related to the duration of the exposition. In response to these considerations we developed a shorter method of conducting IWR specifically targeted for a diving mission at Clipperton atoll in the Northern Pacific Ocean.

Animals↗
PubMed1986

Spinal cord decompression sickness: a comparison of recompression therapies in an animal model.

Somatosensory evoked potentials (SEP) were used in an animal model to measure spinal cord electrophysiological function. Animals were submitted to a dive profile resulting in spinal cord decompression sickness (DCS). The animals were treated after a delay allowing the lesion to consolidate. Serial measurements of SEP documented the onset, duration, and outcome of treatment. Physiological data were recorded throughout each experiment. Group A (n = 10) was recompressed to 60 fsw (feet of sea water) breathing 100% oxygen (2.8 ATA) and Group B (n = 8) was treated at 66 fsw breathing 66% oxygen (2.0 ATA). No differences were found between groups in the severity, surface interval before treatment, or the maximum effect of treatment. The maximum effect of treatment was seen by 25 min of treatment. Animals were regrouped into responders and nonresponders. The latter displayed a more rapid onset, a more severe insult, and more adverse physiological effects than the responders. The possibility of a different etiology was considered together with the failure to differentiate between the treatment groups. It was concluded that treatment B was safer but the problems of introducing a new therapeutic table outweighed the safety advantage.

Animals↗
PubMed1992

Hyperbaric chamber nurse dies of decompression sickness; unit gets OK.

Experts in the field of hyperbaric medicine say the chambers used to treat dive accident victims and enhance the healing of problem wounds are safe despite the death last August of a nurse. Joyce Vause, 52, died of decompression sickness July 22, 1991 about an hour after she left work at Bay Medical Center, Panama City, FL. Shortly before her death, Vause has been in a hyperbaric chamber attending a patient who had been in a diving accident.

Decompression Sickness↗
PubMed1976

Inner ear decompression sickness.

With recent increases in commercial, military, and sport diving to deeper depths, inner ear injuries during such exposures have been encountered more frequently and noted during several phases of diving: during compression, at stable deep depths, with excessive noise exposure in diving, and during decompression. The pathophysiology of these injuries differs, depending upon the phase of diving in which the injuries occur. In this report, 23 cases of hearing loss, tinnitus, and/or vertigo occurring during or shortly after decompression are presented. Thirteen of these cases occurred in helium-oxygen dives involving a change to air during the latter stages of decompression. A significant correlation is present between prompt recompression treatment, relief of symptoms, and lack of residual deficits. Current knowledge indicates that the management of otologic decompression sickness should include: 1. prompt recompression to at least 99 feet deeper than the symptom onset depth; 2. recompression using the previous helium-oxygen mixture when the injuries occur during or shortly after a switch from helium-oxygen to air during the latter stages of decompression; 3. the use of parenteral diazepam for symptom relief and cyclic inhalations of oxygen enriched treatment gases; and 4. the avoidance of further diving by divers who exhibit permanent inner ear injuries after the acute symptoms have subsided.

Adult↗
PubMed1984

Mesenteric venous thrombosis as sole complication of decompression sickness.

A 27-year-old male commercial diver developed massive mesenteric venous thrombosis following a dive. Symptoms at presentation included abdominal pain and diarrhea. A severe upper gastrointestinal bleed developed. Exploratory laparotomy demonstrated 130 cm of infarcted small bowel. The pathophysiologic events in decompression sickness predispose to vascular obstruction and venous infarction. This patient had a past history of possible thrombophlebitis and pulmonary embolism associated with diving but no identifiable coagulopathy.

Adult↗
PubMed1990

Acute decompression sickness in compressed air workers exposed to pressures below 1 bar in the Singapore Mass Rapid Transit project.

The Singapore Mass Rapid Transit (MRT) project started compressed air work in Oct 1984. Eleven km of underground tunnels out of 20 km were built using this method. Cases of decompression sickness (DCS) arising from compressed air work are rare with working pressures less than 1 bar gauge. However, there were 10 cases of DCS in the MRT project who were exposed to less than 1 bar pressure. The authors present their clinical features and attempt to explain the observations in relation to theories of bubble nuclei formation, gas loading and rate of decompression. The formation of bubble micronuclei are correlated with physical factors like heavy exertion, and the use of vibrating tools. The concept of extremely long tissue half-times in the absorption of nitrogen in the body is discussed as a contributory factor to the development of DCS under 1 bar.

Acute Disease↗
PubMed1982

The permeability alteration of brain and spinal cord vasculature to horseradish peroxidase during experimental decompression sickness as compared to the alteration in permeability induced by hyperosmolar solution.

The permeability of microvasculature in the cerebral cortex, neostriatum, and spinal cord to i.v. injected horseradish peroxidase (HRP) has been investigated in rats following experimental compression to 6.1 bars (abs.) air for 90 min, and subsequent decompression to the ambient pressure in 1 min. For comparison, 1 ml of 2.0 M urea was injected into the right common carotid artery of rats during 15 s. After exposure to compression-decompression, under the light microscope focal leaky areas were found in all the regions examined. The leakage was most prominent in the grey matter of the spinal cord, and the cerebral cortex. In decompressed rats, arterioles were most often the site of peroxidase extravasation, whereas extravasation of HRP was less frequently displayed by capillaries and venules. In urea-treated rats, capillaries and venules frequently displayed extravasation of HRP as well. Parenchymal cells accumulated the trace adjacent to the leaky areas. Under the electron microscope, the extravasation of HRP was associated with peroxidase-containing pleomorphic vesicular structures in the endothelium, both in decompressed and urea-injected rats. Moreover, in contrast to decompressed rats, the junctions between endothelial cells were penetrated by the trace in urea-treated rats. Accordingly, the results indicate that during decompression sickness the pathway for the extravasation of proteins is through vesicular transfer, whereas the injection of hyperosmolar urea induces extravasation, both through vesicular transfer and junctions between the endothelial cells.

Animals↗
PubMed1976

Cinephotomicrography of dog spinal vessels during cord-damaging decompression sickness.

Thirty-three dogs were anesthetized, laminectomized in the lower thoracic, upper lumbar region, and exposed to simulated 220 ft air dives of 5 to 60 minutes. Cinephotomicrography of the epidural vertebral venous system and dorsal pial vessels was done predive and postdive. The epidural vertebral venous system became blocked by bubbles in 24 animals. Eighteen animals evaluated for clinical and/or pathologic signs of cord damage all manifested positive signs. In 10 dives made by eight dogs, epidural vertebral venous system obstruction did not occur, and signs of cord damage were absent after nine of these dives. After one dive, a dog manifested cervical cord damage remote to the region of epidural vertebral venous system under observation. Acute pulmonary hypertension and central venous congestion were not essential prerequisites for epidural vertebral venous system occlusion to occur. These experiments permit further analysis of the pathogenesis of spinal cord damage in decompression sickness.

Animals↗
PubMed1983

An evaluation of plasma volume expanders in the treatment of decompression sickness.

Each of 29 goats was instrumented with an ultrasonic flowmeter transducer around the left common carotid artery and a silastic catheter in the anterior vena cava. Following recovery from the surgery the goats were subjected to a dive protocol designed to elicit symptoms of decompression sickness (DCS). The goats were returned to the surface and, following a 20-min observation period, were either left untreated (controls) or treated with one of five different plasma volume expanders. The plasma volume expanders were evaluated based on their ability to decrease the severity of DCS and the number of arterial bubbles that could be counted. Analysis of the results shows that all of the five plasma volume expanders used appeared to reduce the severity of the signs of DCS and to decrease the number of arterial bubbles detected but that these tendencies were not statistically significantly except for Mannitol and Dextran 40. Animals that did not develop arterial bubbles tended to respond better to fluid therapy than did those that did develop bubbles.

Animals↗
PubMed1980

Nature and treatment of decompression sickness occurring after deep excursion dives.

During Predictive Studies IV (PS IV), the fourth in a series of collaborative undersea investigations, plans were made for excursion compressions to 1200 and 1600 feet of sea water (fsw) from saturation depths of 800 and 1200 fsw, respectively. Three cases of decompression sickness (DCS) occurred in the excursion phases of PS IV; all were relieved by prompt treatment, and there were no residual effects. This paper describes the rationale and treatment regimen used for deep excursion DCS, reports the results of the treatment, and makes specific recommendations of the therapy of DCS occurring after such excursions.

Decompression Sickness↗