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 181 records · Page 10Linked to original sources
PubMed1977

Paraplegia due to decompression sickness.

Eight patients with spinal cord lesions due to decompression sickness are described. The cord lesions were in the cervical cord in four cases and in the upper dorsal cord in the other four, seven patients had incomplete lesions, one had a complete lesion, all patients were spastic. The diving details and description of the onset of paralysis are given and possible pathological processes are discussed. Prophylaxis is by adequate use of decompression stops. The most satisfactory treatment is immediate recompression.

Adult↗
PubMed1986

Urinary problems in decompression sickness.

The records of 25 patients with type II decompression sickness and urinary problems have been reviewed. Seventeen patients were professionals and 8 were above the age of 40. The disease appeared within the 1st hour of emergence from the water in 70% of the cases and within the first 4 hours in the remaining 30%. Nine patients were diagnosed as paraplegic and two as tetraplegic. All patients had urinary disturbances and 14 were on Foley-catheter drainage during the decompression while 11 were on intermittent catheterisation. Fifteen patients had improved urinary function after recompression, 8 had some difficulty, 2 underwent a sphincterotomy and one a transurethral prostatectomy. The low percentage of complete recovery was due to the delayed arrival at the decompression chamber.

Adult↗
PubMed1983

Myelopathy associated with decompression sickness: a report of six cases.

Four scuba divers and 2 professional deep sea divers developed spinal cord symptoms due to decompression sickness. Symptoms developed during or immediately after ascent in 4 cases and were delayed in 2. In 2 cases new symptoms appeared during a jet flight. In 4 cases paraparesis was associated with a sensory level in the mid or low dorsal region indicating the thoracic cord as the major site of involvement. In the other 2 cases the clinical findings were suggestive of combined lesions in the lower cervical and lumbar cord. Therapeutic recompression led to improvement in each case. Three cases who were re-examined after intervals of 3 to 7 years each showed residual corticospinal and minor sensory signs. One of these cases met with a violent death 3.5 years after the acute episode; examination of the cord showed multifocal white matter degeneration in the posterior and lateral columns between C7 and T4 with secondary ascending and descending tract degeneration. The mechanism of spinal cord damage in decompression sickness is discussed.

Adult↗
PubMed1991

Decompression sickness induced hearing loss. A review.

Otologic manifestations of decompression sickness (DCS) occur only rarely. However, with more frequent exposures to deeper depths in recent years, several reports of hearing loss due to DCS have appeared. Nevertheless, the scant literature directly discussing the subject establishes otologic DCS as an important cause of diving-induced hearing loss. When hearing impairment with or without vestibular symptoms is a solitary manifestation of DCS type II, it may be difficult to distinguish from middle and inner ear barotrauma resulting in labyrinthine window fistula. Once a diagnosis is established, immediate recompression treatment with hyperbaric oxygen may result in complete recovery. The pathologic mechanism is discussed and the pertinent literature reviewed.

Atmospheric Pressure↗
PubMed1978

Intracardial gas bubbles and decompression sickness while flying at 9,000 m within 12-24 h of diving.

Intracardial gas bubbles, detected with Doppler ultrasound, and symptoms of decompression sickness were registered at 9,000 m simulated altitude within 12, 18, and 24 h of exposures to 15 or 39 m simulated water depth allowing no stage decompression. With a time interval of 12 h between diving and flying, the earliest intracardial bubbles were found in some subjects already during the first minutes at altitude, and the earliest symptoms of decompression sickness some minutes afterwards. With an 18-h interval, the earliest bubbles and symptoms as well as their average time onsets appeared somewhat later. With a 24-h interval, the earliest bubbles and symptoms were detected slightly later, i.e. after 17 min and 23 min, respectively. Thus, a safe time interval between no-stage decompression dives and flying at 9,000 m cabin altitude for a maximum of 15 min appears to be 24 h. For prolonged such flights, a longer time interval seems to be necessary.

Adult↗
PubMed1990

Bubble-induced dysfunction in acute spinal cord decompression sickness.

Five anesthetized dogs undertook a chamber dive, on air, to 300 feet of seawater for 15 min. After the dive, spinal cord decompression sickness was detected by recording a reduced amplitude of the somatosensory evoked potential compared with predive base-line values. After the diagnosis of decompression sickness and rapid perfusion fixation of the animal, the spinal cord was removed and examined histologically. Numerous space-occupying lesions (SOL) that disrupted the tissue architecture were found in each cord, mainly in the white matter. The size and distribution of the SOL were determined using computerized morphometry. Although SOL occupied less than 0.5% of the white matter volume, we tested a number of algorithms to assess whether the SOL may have been directly involved in the loss of spinal cord function that followed the dive. We determined that the loss of somatosensory evoked potential amplitude may be attributed to the SOL if 30-100% of the spinal cord fibers that they displaced were rendered nonconducting. A number of possible mechanisms by which SOL may interfere with spinal nerve conduction are discussed.

Animals↗
PubMed1975

Relationship between saturation exposure pressure and subsequent decompression sickness in mice.

Despite the fact that the pressure reduction is acknowledged to be the single most cogent factor in producing decompression sickness, little has been done to define accurately the allowable limits beyond 2 ATA. This study provides some theoretical guidelines for future manned dives related to this problem. There were 324 albino mice used to define the relationship between saturation exposure pressure and the safe abrupt pressure reduction. The results from both the helium-oxygen and nitrogen-oxygen exposures support the idea of a linear, depth-dependent relationship between the saturation depth and the allowable pressure reduction. Support is presented for the use of a modified decompression ratio P1/P2 (P1 equals saturation pressure and P2 equals pressure following decompression) to account for the observed incidence of decompression sickness. An attempt is made, using the existing human data to relate this empirical relationship to the operational dive setting.

Animals↗
PubMed2006

[Thrombophilic factors in divers with undeserved decompression sickness].

UNLABELLED: In divers with a vascular disease in decompression sickness, who have not committed any technical error, thrombophilic risk factors were sought. Six cases of confirmed divers, without diving technical error, were investigated. Thrombophilic screening included proteins C, S, antithrombin III, and factor VIII assays, and circulating antibodies, Factor V Leiden, and mutation G20210A mutation in Factor II gene research. Total plasma homocysteine (Hcy), an atherosclerosis factor, even when slightly increased, nutitional factors: folate and vitamins B12 and B6, the cofactors of its metabolism, and inversely correlated with Hcy values, were assayed, and subjects were genotyped for mutation C677T in the MTHFR gene. RESULTS: In five divers, Hcy values were moderately increased, and in all the six, folate and/or B12 values were decreased. Three of them showed a genotype TT (mutation C677T), two, the genotype CT, and the sixth, an heterozygous Factor V Leiden. In these divers, a predisposition for vascular diseases, was detected, which was partially curable.

Adult↗
PubMed2002

The relative risk of decompression sickness during and after air travel following diving.

BACKGROUND: Decompression sickness (DCS) can be provoked by post-dive flying but few data exist to quantify the risk of different post-dive, preflight surface intervals (PFSI). METHODS: We conducted a case-control study using field data from the Divers Alert Network to evaluate the relative risk of DCS from flying after diving. The PFSI and the maximum depths on the last day of diving (MDLD) were analyzed from 627 recreational dive profiles. The data were divided into quartiles based on surface interval and depth. Injured divers (cases) and uninjured divers (controls) were compared using logistic regression to determine the association of DCS with time and depth while controlling for diver and dive profiles characteristics. These included PFSI, MDLD, gender, height, weight, age, and days of diving. RESULTS: The means (+/-SD) for cases and controls were as follows: PFSI, 20.7 +/- 9.6 h vs. 27.1 +/- 6.7 h; MDLD, 22.5 +/- 14 meters sea water (msw) vs. 19 +/- 11.3 msw; male gender, 60% vs. 70%; weight, 75.8 +/- 18 kg vs. 77.6 +/- 16 kg; height, 173 +/- 16 cm vs. 177 +/- 9 cm; age, 36.8 +/- 10 yr vs. 42.9 +/- 11 yr; diving > or = 3 d, 58% vs. 97%. Relative to flying > 28 h after diving, the odds of DCS (95% CI) were: 1.02 (0.61, 1.7) 24-28 h; 1.84 (1.0, 3.3) 20-24 h; and 8.5 (3.85, 18.9) < 20 h. Relative to a depth of < 14.7 msw, the odds of DCS (95% CI) were: 1.2 (0.6, 1.7) 14.7-18.5 msw; 2.9 (1.65, 5.3) 18.5-26 msw; and 5.5 (2.96, 1 0.0) > 26 msw. CONCLUSIONS: Odds ratios approximate relative risk in rare diseases such as DCS. This study demonstrated an increase in relative risk from flying after diving following shorter PFSIs and/or greater dive depths on the last day. The relative risk increases geometrically as the PFSI becomes smaller.

Adult↗
PubMed1986

A blitz of bends: decompression sickness in four students after hypobaric chamber training.

This paper reports three cases of type II and one case of type I decompression sickness occurring in a group of nine vigorously active US Army parachutists who took a hypobaric chamber HALO (high altitude-low opening) training flight to a maximum altitude of 9,908.5 m (32,500 ft). After the cases of decompression sickness were diagnosed and treated, the aviator mask regulators were checked and found to be functioning properly; the oxygen supply was analyzed and found to be pure. All cases fully recovered after treatment on US Navy Diving Table 6 and have returned to full military duty. This HALO training profile is not in use with either the US Navy or the US Air Force and should probably be considered unsafe for future use in training.

Adult↗
PubMed1988

Is there a role for the autochthonous bubble in the pathogenesis of spinal cord decompression sickness?

Histological examination by light and electron microscopy of the spinal cords of four dogs rapidly perfusion-fixed after the onset of decompression sickness revealed the presence of numerous non-staining, space-occupying lesions that were absent in similarly prepared sections of control or ischemic spinal cords. We propose the hypothesis that these lesions are caused by the liberation of a gas phase. The possible significance of these lesions in the evolution of spinal cord dysfunction is discussed with reference to the principal theories of the pathogenesis of spinal cord decompression sickness.

Animals↗
PubMed2001

Inner ear decompression sickness in sport compressed-air diving.

OBJECTIVE: We report our experience over the past 12 years with recreational diving-related inner ear decompression sickness (IEDCS). STUDY DESIGN: Retrospective, consecutive case series. METHODS: Twenty-four divers, representing 29 cases of IEDCS, are presented with regard to evaluation, treatment, and follow-up. RESULTS: These 29 cases represent 26% of the severe decompression sickness (DCS) cases treated in that period. The patient group includes 22 divers who had a single event of IEDCS, one diver who had two events, and one with five repeated episodes. The cause of injury in 23 cases (79%) was violation of the decompression schedule. The mean time from surfacing to appearance of symptoms was 47 +/- 65 minutes. In 83%, symptoms appeared within 1 hour of ascent, in 97% within 2 hours, and in only one diver after 5.5 hours. Ten divers (34%) had pure vestibular involvement, 4 (14%) had cochlear insult alone, and 15 (52%) had combined vestibulo-cochlear injury. Except for one patient who had central as well as peripheral vestibulo-cochlear DCS, all the remaining patients had end organ involvement only, as demonstrated by physical examination and laboratory test results. Fifteen (52%) had isolated IEDCS, whereas 14 had additional symptoms of DCS. Twenty-six cases were treated by hyperbaric oxygenation with supplementary daily hyperbaric sessions. Of the 25 cases with vestibular injury and the 19 with cochlear damage, only 7 (28%) and 6 (32%), respectively, made a full recovery, whereas the others remained with residual damage. Of the 17 treated within 6 hours of symptom appearance, 9 (53%) were cured, compared with one of the 9 treated later (P <.05). CONCLUSIONS: IEDCS related to compressed-air recreational diving is more common than previously thought, and might occur even when no decompression schedule violation took place. Prompt diagnosis leading to the early commencement of hyperbaric oxygen recompression therapy is the key to complete recovery of cochlear and vestibular function.

Adult↗
PubMed1993

[Scuba diving: barotrauma, decompression sickness, pulmonary contra-indications].

The practice of scuba diving is associated with two specific medical problems: barotrauma directly related to changes in ambient pressure, and decompression sickness related to the uptake and the release of inert gases by the body. Neurological symptoms are frequent in severe diving accidents. They may arise following either barotrauma or decompression sickness, and often require urgent treatment in a hyperbaric chamber. Asthma, chronic obstructive pulmonary disease, and spontaneous pneumothorax increase the risk of lung barotrauma and represent contraindications to diving.

Asthma↗
PubMed2001

[Prevention of altitude decompression sickness during simulation of egress from the cabin of space vehicle with hypobaric artificial atmosphere].

Based on the proposed semiempiric nomograms, the study was aimed at selection and investigation of normoxic N2-O2 hypobaric atmosphere (HA) at 93-73 kPa, and evaluation of effectiveness of the gas mixture against the altitude decompression sickness (ADS) during 6-hr simulation of extravehicular activities at 37 kPa without prebreathing. Subjects were 22 healthy males from 20 to 50 yr. old. In all, 115 experiments were performed. Twenty-four hours in HA at 93 kPa and subsequent transition to 37 kPa led up to development of ADS symptoms by one subject in one of 27 experiments (3.7%), and emergence of venous gas bubbles (USI) with the intensity of 2, 70, and 19 points by the Spenser scale in 9 experiments (33.3%). Lower HA pressures (86 kPa, 80 kPa and 73 kPa) did not give rise to ADS though the occurrence of venous GB distinctly tended downward (30.6%, 14.3% and 11.8%) and so did the intensity of their entry into the pulmonary circulation (2, 40, 18 points; 1, 80, 19 points, and 2, 00, 15 points, respectively). Minimal ADS risk was observed in HA at 80 kPa and 73 kPa and did not reach 4% at the confidence level of 95%.

Adult↗
PubMed2004

Acclimatization to neurological decompression sickness in rabbits.

Diving acclimatization refers to a reduced susceptibility to acute decompression sickness (DCS) in individuals undergoing repeated compression-decompression cycles. We demonstrated in a previous study that the mechanism responsible for this acclimatization is similar to that of stress preconditioning. In this study, we investigated the protective effect of prior DCS preconditioning on the severity of neurological DCS in subsequent exposure to high pressure in rabbits. We exposed the rabbits (n = 10) to a pressure cycle of 6 absolute atmospheres (ATA) for 90 min, which induced signs of neurological DCS in 60% of the animals. Twenty-four hours after the pressure cycle, rabbits with DCS expressed more heat-shock protein 70 (HSP70) in the lungs, liver, and heart than rabbits without signs of disease or those in the control group (n = 6). In another group of rabbits (n = 24), 50% of animals presented signs of neurological DCS after exposure to high pressure, with a neurological score of 46.5 (SD 19.5). A course of hyperbaric oxygen therapy alleviated the signs of neurological DCS and ensured the animals' survival for 24 h. Experiencing another pressure cycle of 6 ATA for 90 min, 50% of 12 rabbits with prior DCS preconditioning developed signs of DCS, with a neurological score of 16.3 (SD 28.3), significantly lower than that before hyperbaric oxygen therapy (P = 0.002). In summary, our results show that the occurrence of DCS in rabbits after rapid decompression is associated with increased expression of a stress protein, indicating that the stress response is induced by DCS. This phenomenon was defined as "DCS preconditioning." DCS preconditioning attenuated the severity of neurological DCS caused by subsequent exposure to high pressure. These results suggest that bubble formation in tissues activates the stress response and stress preconditioning attenuates tissue injury on subsequent DCS stress, which may be the mechanism responsible for diving acclimatization.

Acclimatization↗
PubMed1985

Neurologic presentation of decompression sickness and air embolism in sport divers.

In a retrospective study of scuba divers with neurologic injuries, we found that mild symptoms were common. Seventy divers had decompression sickness, most often with paresthesias or numbness, rarely with paresis. Thirty-nine divers had air embolism that often caused unconsciousness or mild symptoms of cerebral injury. Many divers with neurologic decompression sickness gave histories of dives that were within conventional limits, and many with air embolism gave no history of breath-holding during ascent. Mild symptoms sometimes regressed spontaneously. Recompression delays were responsible for poor responses to therapy.

Adolescent↗