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PubMed1992

The influence of prior exercise at anaerobic threshold on decompression sickness.

This study was conducted to examine the effects of exercise prior to decompression on the incidence of altitude decompression sickness (DCS). In a balanced, two-period, crossover trial, 39 healthy individuals (29 males, 10 females) of mean (S.D.) age 32.5 (7.7) years and body mass index 23.7 (3.4) were each exposed twice, without denitrogenation, to an altitude of 6,400 m (21,000 ft) in a hypobaric chamber. Under the experimental condition, subjects exercised at their predetermined anaerobic threshold levels for 30 min each day for 3 d prior to altitude exposure; the other condition was a non-exercise control. Under both conditions, subjects performed exercise simulating space extravehicular activities at altitude for a period of 3 h, while breathing 100% oxygen. There were nine preferences (untied responses) for DCS, four under control and five under experimental conditions; all were Type I, pain-only bends. No carryover effect between exposures was detected, and the test for treatment differences showed p = 0.56 (95% confidence interval = 0.34-0.58) for symptoms. No significant difference in DCS preferences was found after subjects exercised up to their anaerobic threshold levels during the days prior to decompression.

Adult↗
PubMed1989

Methyl prednisolone in the treatment of acute spinal cord decompression sickness.

Sixteen anesthetized dogs undertook a chamber dive that was designed to induce decompression sickness. Somatosensory evoked potentials (SEP) were used to diagnose and quantify the outcome of spinal cord involvement in the disease. Following diagnosis, 8 animals were treated with methyl prednisolone (MP), 20 mg.kg-1 ("megadose"), as an adjuvant to recompression on an abbreviated U.S. Navy Treatment Table 6. Eight control animals were recompressed in a similar manner, but received the MP diluent only as an adjuvant. Analysis of the SEP at the conclusion of treatment showed that there was no significant difference in outcome for the 2 groups of animals. However, if all the SEP recorded during the treatment period are compared, the MP-treated animals experienced a significantly worse outcome than the diluent-treated controls. The risks and benefit of using corticosteroids in the treatment of human spinal cord DCS are discussed.

Animals↗
PubMed1987

Effects of He-O2 breathing during experimental decompression sickness following air dives.

The effects of ventilation with He-O2 during decompression sickness (DCS) and venous air embolism were studied. Fifteen anesthetized dogs were mechanically ventilated and subjected to repeated air dives until pulmonary artery pressure at least doubled within 10 min postdive. At 30 min postdive, ventilation was either continued with air (controls, n = 7) or changed to He-O2 (n = 8) for an additional 90 min. All animals developed pulmonary hypertension, systemic hypotension, hemoconcentration, hypoxemia, hypercarbia, and pulmonary edema. Breathing air or He-O2 postdive did not alter these responses, but He-O2 breathing produced an 11% increase in pulmonary vascular resistance (PVR). In 3 other anesthetized dogs that were not subjected to dives, ventilation was changed to He-O2 at various times during an intravenous infusion of air; He-O2 breathing caused a 22% increase in PVR. We conclude that breathing He-O2 during DCS resulting from air dive can intensify pulmonary vascular obstruction.

Animals↗
PubMed1988

Central nervous system decompression sickness: latency of 1070 human cases.

Many aspects of central nervous system (CNS) decompression sickness (DCS) are poorly understood, including the temporal pattern of its presentation and the pathogenic mechanisms involved in the development of the disease. Using case histories and clinical series published in the literature and retrieved from treatment center records, this study is an attempt to define the interval between surfacing from a hyperbaric exposure and the onset of symptoms of CNS DCS. The results of 1070 cases of human CNS DCS were included in the study. The results show that the disease generally occurs rapidly: over 50% became symptomatic within 10 min of returning to 1 ATA, and in only 15% of cases was the onset of symptoms delayed for more than 1 h. Cerebral DCS had a more rapid onset than spinal cord disease: 50% of cerebral cases became apparent within about 3 min and a similar proportion of spinal cord cases within about 9 min from surfacing. The influence of these results on the diagnosis and treatment of dysbaric illness, on the safety of certain diving practices, and on possible pathogenic mechanisms is discussed.

Central Nervous System Diseases↗
PubMed1998

Risk of decompression sickness with patent foramen ovale.

Several reports have described populations of divers with decompression sickness (DCS) who have a patent foramen ovale (PFO). The presence of a PFO is known to occur in about 30% of the normal population, hence 30% of divers are likely to have a PFO. Although observations have been made on the presence of a PFO in divers with and without DCS, the risk of developing DCS when a diver has a PFO has not been determined. In this study, Logistic Regression and Bayes' theorem were used to calculate the risk of DCS from data of three studies that reported on echocardiographic analysis of PFO in a diving population, some of whom developed DCS. Overall incidence of DCS was obtained from the sport diving population, from the U.S. Navy diving population, and from a commercial population. The analysis indicates that the presence of a PFO produces a 2.5 time increase in the odds ratio for developing serious (type II) DCS in all three types of divers. Since the incidence of type II DCS in these three populations averages 2.28/10,000 dives, the risk of developing DCS in the presence of a PFO remains small, and does not warrant routine screening by echocardiography of sport, military, or commercial divers.

Confidence Intervals↗
PubMed1978

[Fatal decompression sickness following therapeutic hyperbaric environment (author's transl)].

In Hannover/Germany in 1976 a so called "Society for Regenerative Hyperbaric Therapy" (Gesellschaft für Regenerative Uberdruck-Therapie) subjected 20 patients within two coupled multi-place chambers to a simulated hyperbaric environment, equivalent to a maximum of 4 ata, followed usually by gradual reductions of the pressure. The patients were of an average age of 67.2 years and were afflicted by various disorders. During one of the "dives" a patient developed air embolism of the central nervous system. During ensuing confusion of the chamber was opened suddenly, with resultant explosive reduction of the high pressure. This resulted in five letal accidents of decompression sickness. Post mortem examination revealed diffuse distribution of gas bubbles throughout the entire body. By elecronmicroscopy each bubble was covered by an osmiophilic coat. Post mortem findings are discussed and correlated with well-known and new clinical symptomes. These observations present for the first time fatal accidents of decompression sickness in humans, associated with hyperbaric air-therapy.

Aged↗
PubMed2002

Diving methods and decompression sickness incidence of Miskito Indian underwater harvesters.

Diving conditions, dive profiles, and symptoms of decompression sickness (DCS) in a group of Miskito Indian underwater seafood harvesters are described. Dive profiles for 5 divers were recorded with dive computers, and DCS symptoms were assessed by neurological examination and interview. Divers averaged 10 dives a day over a 7-day period with a mean depth of 67 +/- 7 FSW (306 +/- 123 kPa) and average in-water time of 20.6 +/- 6.3 minutes. Limb pain was reported on 10 occasions during 35 man-days of diving. Symptoms were typically managed with analgesic medication rather than recompression. Indices of the decompression stress were estimated from the recorded profiles using a probabilistic model. We conclude that the dives were outside the limits of standard air decompression tables and that DCS symptoms were common. The high frequency of limb pain suggests the potential for dysbaric bone necrosis for these divers.

Adult↗
PubMed1998

Decompression sickness presenting as forearm swelling and peripheral neuropathy: a case report.

Neurological symptoms after decompression from a dive are usually thought to be manifestations of central nervous system (CNS) decompression sickness (DCS). We present a case of DCS in which neurological symptoms are present but which the clinical findings, magnetic resonance imaging and electroneuromyographic studies suggest were caused by muscle injury and exacerbation of an existing peripheral neuropathy. This finding supports the alternative hypothesis that some neurological symptoms and signs in DCS are due to effects on peripheral nerves rather than the CNS.

Adult↗
PubMedDate not supplied

Diving behaviour and decompression sickness among Galapagos underwater harvesters.

Diving conditions, dive profiles, vascular bubbles, and symptoms of decompression sickness (DCS) in a group of Galapagos commercial divers are described. They harvest sea cucumbers from small boats with surface supplied air (hookah). Dive profiles for 12 divers were recorded using dive loggers, and bubble formation was measured in the pulmonary artery. DCS symptoms were assessed by interview. A total of 380 immersions were recorded over a nine day period. The divers did on average 6.3 immersions per day, in a yo-yo pattern. Mean overall depth was 34.5 FSW. Maximum recorded depth was 107 FSW. Average bottom time per day per diver was 175 minutes. 82 % of all ascents exceeded the recommended maximum ascent rate of 30 FSW/ min. High bubble grades were observed on six occasions, but the test was unreliable. Muscle and joint pain was reported on five occasions, in three different divers. Symptoms were typically managed by analgesics, in-water recompression or not at all. The divers were extremely reluctant to seek professional help for DCS symptoms, mostly due to the high costs of treatment. We conclude that the fishermen dive beyond standard no-decompression limits, and that DCS symptoms are common.

Adolescent↗
PubMed1981

Ruthenium red staining of blood-bubble interface in acute decompression sickness in rat.

The ultrastructure of the blood-bubble interface has been studied in rats decompressed experimentally. Subsequent to staining with ruthenium red there was detected by electron microscopy a continuous envelope like layer about 20 nm thick at the bubble-facing surface of the interface. The envelope like structure was visualized also by concanavalin A-ferritin, a glycosyl- and mannosyl residue-recognizing lectin coupled with an electron-dense probe, but the structure was not at all seen by the use of the conventional stains used in electron microscopy, uranyl acetate and lead citrate. No electron-dense layer was discernible on the application of only osmium tetroxide without further staining. The results indicate that material stainable by ruthenium red, and binding concanavalin A (probably a glycoprotein), is concentrated at the blood-bubble interface upon decompression. It is suggested that it plays a role in stabilization of the bubble and in the hematological alterations that are frequently observable in decompression sickness.

Animals↗
PubMed1996

Testing of hypotheses about altitude decompression sickness by statistical analyses.

This communication extends a statistical analysis of forced-descent decompression sickness at altitude in exercising subjects (J Appl Physiol 1994; 76:2726-2734) with a data subset having an additional explanatory variable, rate of ascent. The original explanatory variables for risk-function analysis were environmental pressure of the altitude, duration of exposure, and duration of pure-O2 breathing before exposure; the best fit was consistent with the idea that instantaneous risk increases linearly as altitude exposure continues. Use of the new explanatory variable improved the fit of the smaller data subset, as indicated by log likelihood. Also, with ascent rate accounted for, replacement of the term for linear accrual of instantaneous risk by a term for rise and then decay made a highly significant improvement upon the original model (log likelihood increased by 37 log units). The authors conclude that a more representative data set and removal of the variability attributable to ascent rate allowed the rise-and-decay mechanism, which is expected from theory and observations, to become manifest.

Altitude↗
PubMed2001

A review of the relationship between patent foramen ovale and type II decompression sickness.

The significance of patent foramen ovale (PFO) in the pathophysiology of Type II decompression sickness (DCS) remains controversial. PFOs are common, occurring in approximately one quarter of the normal population, thus making right-to-left shunting of venous gas emboli (VGE) a theoretical concern in both hyper- and hypobaric situations. Despite this high prevalence of PFO in the general population, and the relatively common occurrence of venous gas bubbles in diving and altitude exposures, the incidence of Type II DCS in diving or with altitude is remarkably low. Although the literature supports a relationship between the presence and size of PFO and cryptogenic stroke, and an increased relative risk of Type II DCS with a PFO in divers, the absolute increase in risk accrued is small. Hence, the value of screening is also controversial. This paper presents a summary of the literature on PFOs and DCS in animals, and in human altitude and diving, focusing on the latter; as well the analogous literature on cryptogenic stroke. The results of an examination of the literature on detection of, screening for, and treatment of PFOs is also presented.

Altitude↗
PubMed2004

Altitude decompression sickness at 7620 m following prebreathe enhanced with exercise periods.

INTRODUCTION: Over 80% altitude decompression sickness (DCS) was reported during a 4-h exposure with mild exercise to 7620 m (25,000 ft) without prebreathe. Prebreathe for more than 1 h would be necessary to reduce the DCS risk below 40%. Use of a single period of exercise to enhance prebreathe effectiveness has been successfully tested and used during some U-2 operations. The current tests used multiple exercise sessions to enhance prebreathe (MEEP) as a means of improving denitrogenation efficiency. METHODS: Two MEEP profiles, 30 or 60 min, preceded 4-h exposures to 7620 m with mild, upper-body exercise while breathing 100% oxygen. Resting prebreathe controls were from published studies at the same laboratory. Both MEEP profiles involved 10 min of strenuous dual-cycle ergometry (75% of maximal oxygen uptake) at the beginning of prebreathe. After a 15-min rest period during the 60-min prebreathe, an additional 5 min of strenuous ergometry was performed. Mild exercise was performed during 15 of the last 20 min of both prebreathe profiles. RESULTS: The 60-min MEEP resulted in 25% DCS and the 30-min MEEP 40% DCS (N.S.). The 25% incidence of DCS following the 60-min MEEP profile was significantly less than the 63% DCS following an equal-time, resting prebreathe control. Following the 30-min MEEP, DCS incidence was not greater than the incidence following a 60-min, resting prebreathe control. There was a lower incidence of venous gas emboli during the MEEP exposures than during resting control exposures. CONCLUSION: Denitrogenation with multiple periods of exercise provides a shorter alternative to resting prebreathe for reducing DCS risk during exposure to 7620 m.

Adolescent↗
PubMed2002

Vascular leukocyte sequestration in decompression sickness and prophylactic hyperbaric oxygen therapy in rats.

BACKGROUND: Evidence for a causal relationship between decompression sickness (DCS) and leukocyte sequestration was assessed in a rat model based on the effects of interventions which impede cell-to-cell adherence, including hyperbaric oxygen therapy (HBO2). HYPOTHESIS: We hypothesized that leukocyte adhesion to vessels may play a role in DCS. METHODS: Rats were subjected to decompression stress and their ability to ambulate on a rotating drum was assessed to quantify functional neurological deficits. Leukocyte adherence in the brain was measured by a myeloperoxidase (MPO) radioimmunoassay. Interventions included infusion of antibodies to render rats neutropenic or to inhibit leukocyte beta2 integrin adhesion molecules. Tissue gas bubbles were imaged and quantified using a transmission ultrasound camera. RESULTS: Decompressed rats manifested a deficit in their ability to ambulate and a five-fold elevation in concentration of MPO in brain. Neutropenic rats, and those infused with antibody fragments to inhibit leukocyte beta2 integrins, did not exhibit brain MPO elevations, nor a deficit in ambulatory function. HBO2 was used in a prophylactic manner to address its ability to inhibit leukocyte beta2 integrin-mediated adherence without reducing the presence of decompression-induced bubbles. Prophylactic HBO2 prevented cerebral leukocyte sequestration and the performance deficit. CONCLUSIONS: The results implicate beta2 integrin-mediated leukocyte adhesion in neurological deterioration after decompression stress, and offer new insight into the therapeutic action of HBO2. Immunomodulatory approaches, including prophylactic HBO2, may improve the safety of decompression procedures in undersea and space exploration.

Animals↗
PubMed2004

Decompression sickness risk model: development and validation by 150 prospective hypobaric exposures.

INTRODUCTION: High altitude exposure has an inherent risk of altitude decompression sickness (DCS). A predictive DCS model was needed to reduce operational risk. To be operationally acceptable, such a theoretical model would need to be validated in the laboratory using human subjects. METHODS: The Air Force Research Laboratory (AFRL) has conducted numerous studies on human subjects exposed to simulated altitudes in hypobaric chambers. The database from those studies was used to develop a statistical altitude DCS model. In addition, a bubble growth model was developed using a finite difference method to solve for bubble radius as a function of time. The bubble growth model, integrated with the statistical model, constitutes the AFRL DCS Risk Assessment Model. Validation of the model was accomplished by comparing computer predictions of DCS risk with results from subsequent prospective human subject exposures. There were five exposure profiles, not previously found in the database, covering a wide parameter of ranges of altitude (18,000-35,000 ft), exposure time (180-360 min), prebreathe time (0-90 min), and activity level (rest-strenuous) that were used. The subjects were monitored for DCS symptoms and venous gas emboli. RESULTS: There were 30 subjects who were exposed to each of the 5 altitude profiles. The DCS incidence onset curves predicted by the model were not significantly different from the experimental values for all scenarios tested and were generally within +/- 5% of the actual values. CONCLUSION: A predictive altitude DCS model was successfully developed and validated.

Altitude Sickness↗
PubMed2000

Computed chest tomography in an animal model for decompression sickness: radiologic, physiologic, and pathologic findings.

This study was conducted to investigate the early pulmonary effects of acute decompression in an animal model for human decompression sickness by CT and light microscopy. Ten test pigs were exposed to severe decompression stress in a chamber dive. Three pigs were kept at ambient pressure to serve as controls. Decompression stress was monitored by measurement of pulmonary artery pressure and arterial and venous Doppler recording of bubbles of inert gas. Chest CT was performed pre- and postdive and in addition the inflated lungs were examined after resection. Each lung was investigated by light microscopy. Hemodynamic data and bubble recordings reflected severe decompression stress in the ten test pigs. Computed tomography revealed large quantities of ectopic gas, predominantly intravascular, in three of ten pigs. These findings corresponded to maximum bubble counts in the Doppler study. The remaining test pigs showed lower bubble grades and no ectopic gas by CT. Sporadic interstitial edema was demonstrated in all animals--both test and control pigs--by CT of resected lungs and on histologic examination. A severe compression-decompression schedule can liberate large volumes of inert gas which are detectable by CT. Despite this severe decompression stress, which led to venous microembolism, CT and light microscopy did not demonstrate changes in lung structure related to the experimental dive. Increased extravascular lung water found in all animals may be due to infusion therapy.

Acute Disease↗
PubMed1992

Predicting the time of occurrence of decompression sickness.

Probabilistic models and maximum likelihood estimation have been used to predict the occurrence of decompression sickness (DCS). We indicate a means of extending the maximum likelihood parameter estimation procedure to make use of knowledge of the time at which DCS occurs. Two models were compared in fitting a data set of nearly 1,000 exposures, in which greater than 50 cases of DCS have known times of symptom onset. The additional information provided by the time at which DCS occurred gave us better estimates of model parameters. It was also possible to discriminate between good models, which predict both the occurrence of DCS and the time at which symptoms occur, and poorer models, which may predict only the overall occurrence. The refined models may be useful in new applications for customizing decompression strategies during complex dives involving various times at several different depths. Conditional probabilities of DCS for such dives may be reckoned as the dive is taking place and the decompression strategy adjusted to circumstance. Some of the mechanistic implications and the assumptions needed for safe application of decompression strategies on the basis of conditional probabilities are discussed.

Decompression Sickness↗