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PubMed1988

Experimental determination of latency, severity, and outcome in CNS decompression sickness.

Twenty-eight dogs underwent a 300 fsw chamber dive designed to generate spinal cord decompression sickness (DCS), which was detected by observing a reduction in the amplitude of the spinal somatosensory evoked potential (SEP). After an interval of 15 min on the surface following diagnosis, the animals received a therapeutic recompression. The latency was defined as the time between surfacing from the dive and the diagnosis of DCS, the severity as the minimum SEP amplitude, and the outcome as the amplitude of the SEP after 2 h of treatment. Significant correlations between latency and severity (P less than 0.05), latency and outcome (P less than 0.01), and severity and outcome (P less than 0.05) were found. Canine spinal cord latency is shown to be very similar to that found in man up to a surface interval of 30 min. The association between latency, severity, and outcome of spinal cord DCS is discussed with reference to the possible mechanisms involved in this disease.

Adrenal Cortex Hormones↗
PubMed1998

Patent foramen ovale and decompression sickness in sports divers.

Patency of the foramen ovale (PFO) may be a cause of unexplained decompression sickness (DCS) in sports divers. To assess the relationship between PFO and DCS, a case-control study was undertaken in a population of Belgian sports divers. Thirty-seven divers who suffered from neurological DCS were compared with matched control divers who never had DCS. All divers were investigated with transesophageal contrast echocardiography for the presence of PFO. PFO size was semiquantified on the basis of the amount of contrast passage. Divers with DCS with lesions localized in the high cervical spinal cord, cerebellum, inner ear organs, or cerebrum had a significantly higher prevalence of PFO than divers with DCS localizations in the lower spinal cord. For unexplained DCS (DCS without commission of any diving procedural errors), this difference was significant for large PFOs only. We conclude that PFO plays a significant role in the occurrence of unexplained cerebral DCS, but not of spinal DCS. We further stress the importance of standardization and semiquantification of future PFO studies that use transesophageal contrast echocardiography.

Adult↗
PubMed2006

Delayed treatment of decompression sickness with short, no-air-break tables: review of 140 cases.

INTRODUCTION: Most cases of decompression sickness (DCS) in the U.S. are treated with hyperbaric oxygen using U.S. Navy Treatment Tables 5 and 6, although detailed analysis shows that those tables were based on limited data. We reviewed the development of these protocols and offer an alternative treatment table more suitable for monoplace chambers that has proven effective in the treatment of DCS in patients presenting to our facility. METHODS: We reviewed the outcomes for 140 cases of DCS in civilian divers treated with the shorter tables at our facility from January 1983 through December 2002. RESULTS: Onset of symptoms averaged 9.3 h after surfacing. At presentation, 44% of the patients demonstrated mental aberration. The average delay from onset of symptoms to treatment was 93.5 h; median delay was 48 h. Complete recovery in the total group of 140 patients was 87%. When 30 patients with low probability of DCS were excluded, the recovery rate was 98%. All patients with cerebral symptoms recovered. Patients with the highest severity scores showed a high rate of complete recovery (97.5%). DISCUSSION: Short oxygen treatment tables as originally described by Hart are effective in the treatment of DCS, even with long delays to definitive recompression that often occur among civilian divers presenting to a major Divers Alert Network referral center.

Decompression Sickness↗
PubMed1988

Effects of exercise on the incidence of decompression sickness: a review of pertinent literature and current concepts.

The effects of exercise on the incidence of decompression sickness (DCS) are not completely understood. This paper reviews studies that have addressed this question. Studies have involved exposures of animals and human subjects to high pressures, which would occur in SCUBA diving operations, and to low pressures, which exist during high-altitude aircraft flights and extravehicular activities during space flight. The temporal course of the exercise in relation to the decompression procedure and the nature of the exercise may influence effects on DCS incidence. Effects of exercise on the uptake and elimination of nitrogen, the production of bubbles due to limb movements, the potential role of carbon dioxide, and current plans for further research are discussed.

Aerospace Medicine↗
PubMed1976

Changes in blood enzyme activity and hematology of rats with decompression sickness.

Plasma activities of lactic dehydrogenase (LDH), creatine phosphokinase (CPK), glutamic pyruvic transaminase (GPT), and alkaline phosphatase (ALP) were studied, along with hematological changes, in rats suffering from various degrees of experimental decompression sickness (DS). By 1 h after decompression, LDH and CPK activities were elevated in moderate and severe DS whereas GOT and GPT were elevated only in severe DS. ALP was reduced in all decompressed rats. Hematological changes indicated hemoconcentration, the degree of which paralleled the severity of DS. By 24 h after decompression, all enzyme activities were approaching control levels with the exception of GOT, which was further elevated from the 1-h value. The observed lung damage in rats with severe DS in conjunction with the hematologic and enzyme data suggested that hypoxemic-hypoxia, incident to bubble embolization of pulmonary vasculature, was a major factor in altering the blood enzyme pattern in DS. Serum enzyme data from two inadequately decompressed divers are also reported.

Alanine Transaminase↗
PubMed1988

Neuropsychologic assessment of cerebral decompression sickness and gas embolism.

A battery of neuropsychologic tests was administered to individuals who had sustained CNS decompression sickness or arterial gas embolism. Testing was intended to assess the presence of residual cognitive impairment. Five clinical cases are presented in which information obtained through this testing played a determining role in the detection and treatment of residual cerebral dysfunction. Recovery of cerebral integrity was documented using the test battery. Even in the absence of clear signs from a standard neurologic examination, sufficient information was gathered by neuropsychologic testing to prompt recompression therapy. Temporary suppression of CNS symptoms by initial recompression was often observed, as documented by follow-up neurologic and neuropsychologic evaluations. Recovery of full cognitive functioning followed repeated hyperbaric treatments, suggesting that CNS insults may be more refractory to therapy than previously thought.

Adult↗
PubMed2006

Dehydration effects on the risk of severe decompression sickness in a swine model.

BACKGROUND: Several physiological factors have been suspected of affecting the risk of decompression sickness (DCS), but few have been thoroughly studied during controlled conditions. Dehydration is a potential factor that could increase the risk of DCS. It has been suggested that hydration may enhance inert gas removal or increase surface tension of the blood. HYPOTHESIS: Dehydration increases DCS risk. METHODS: Littermate pairs of male Yorkshire swine (n=57, mean +/- 1 SD 20.6 +/- 1.7 kg) were randomized into two groups. The hydrated group received no medication and was allowed ad lib access to water during a simulated saturation dive. The dehydrated group received intravenous 2 mg x kg(-1) Lasix (a diuretic medication) without access to water throughout the dive. Animals were then compressed on air to 110 ft of seawater (fsw, 4.33 ATA) for 22 h and brought directly to the surface at a rate of 30 fsw x min(-1) (0.91 ATA x min(-1)). Outcomes of death and non-fatal central nervous system (CNS) or cardiopulmonary DCS were recorded. RESULTS: In the hydrated group (n=31): DCS=10, cardiopulmonary DCS=9, CNS DCS=2, Death=4. In the dehydrated group (n=26): DCS=19, cardiopulmonary DCS=19, CNS DCS=6, Death=9. Dehydration significantly increased the overall risk of severe DCS and death. Specifically, it increased the risk of cardiopulmonary DCS, and showed a trend toward increased CNS DCS. In addition, dehydrated subjects manifested cardiopulmonary DCS sooner and showed a trend toward more rapid death (p < 0.1). CONCLUSION: Hydration status at the time of decompression significantly influences the incidence and time to onset of DCS in this model.

Analysis of Variance↗
PubMed2003

Risk of decompression sickness during exposure to high cabin altitude after diving.

BACKGROUND: Postdive altitude exposure increases the risk of decompression sickness (DCS). Certain training and operational situations may require U.S. Special Operations Forces (SOF) personnel to conduct high altitude parachute operations after diving. Problematically, the minimum safe preflight surface intervals (PFSI) between diving and high altitude flying are not known. METHODS: There were 102 healthy, male volunteers (34 +/- 10 [mean +/- SD] yr of age, 84.5 +/- 13.8 kg weight, 26.2 +/- 4.2 kg x m(-2) BMI) who completed simulated 60 fsw (feet of seawater)/60 min air dives preceding simulated 3-h flights at 25,000 ft to study DCS risk as a function of PFSI. Subjects were dry and at rest throughout. Oxygen was breathed for 30 min before and during flight in accordance with SOF protocols. Subjects were monitored for clinical signs of DCS and for venous gas emboli (VGE) using precordial Doppler ultrasound. DCS incidence was compared with Chi-squared; VGE onset time and time to maximum grade with one-way ANOVA (significance at p < 0.05). RESULTS: Three cases of DCS occurred in 155 subject-exposures: 1/35 and 0/24 in 2 and 3 h flight-only controls, respectively; 0/23, 1/37, and 1/36 for 24, 18, and 12 h dive-PFSI-flight profiles, respectively. DCS risk did not differ between profiles (chi2 [4] = 1.33; crit = 9.49). VGE were observed in 19% of flights. Neither VGE onset time nor time to max grade differed between profiles (82 +/- 38 min [p = 0.88] and 100 +/- 40 min [p = 0.68], respectively). CONCLUSION: Increased DCS risk was not detected as a result of dry, resting 60 fsw/60 min air dives conducted 24-12 h before a resting, 3-h oxygen-breathing 25,000 ft flight (following 30 min oxygen prebreathe). The current SOF-prescribed minimum PFSI of 24 h may be unnecessarily conservative.

Adult↗
PubMed1987

Noncardiogenic pulmonary edema caused by decompression sickness: rapid resolution following hyperbaric therapy.

Noncardiogenic pulmonary edema is a recognized but uncommon manifestation of type 2 decompression sickness. It typically occurs within 6 hours of a dive. Because the adult respiratory distress syndrome in this setting is believed to be due to microbubbles in the pulmonary vasculature, recompression in a hyperbaric chamber has been recommended as a form of therapy. A patient developed noncardiogenic pulmonary edema following a seawater dive to 75 feet. There was complete radiologic and clinical resolution within 5 hours of hyperbaric therapy.

Adult↗
PubMed1995

Ascent rate, post-dive exercise, and decompression sickness in the rat.

The effects of ascent rate and post-dive exercise on the incidence of decompression sickness (DCS) were investigated in six groups of 20 rats exposed for 2 h at a pressure equivalent to 240 feet of sea water (fsw; 735 kPa). Ascent rates were 30, 45, and 60 fsw/min (92, 138, 184 kPa/min), and the rats either rested after the exposure or exercised by walking for 30 min on a treadmill at 1.6 m/min. Post-dive signs included respiratory distress, difficulty walking, paralysis, and death. DCS was scored as non-fatal at 30-min post-dive or fatal at any time. Analysis by ordinal logistic regression indicated more DCS with post-dive exercise (P = 0.0112) and at 45 (P = 0.0011) and 60 fsw/min (P = 0.0001) compared to 30 fsw/min. Survival analysis suggested earlier death at 60 fsw/min compared to 30 fsw/min (P = 0.0006). Similar effects have been reported for the less severe DCS that occurs in humans.

Animals↗
PubMed1992

Time to detection of circulating microbubbles as a risk factor for symptoms of altitude decompression sickness.

This study investigated the association between time at onset of circulating microbubbles (CMB) and symptoms of altitude decompression sickness (DCS), using Cox proportional hazard regression models. The study population consisted of 125 individuals who participated in direct ascent, simulated extravehicular activities profiles. Using individual CMB status as a time-dependent variable, we found that the hazard for symptoms increased significantly (at the end of 180 min at altitude) in the presence of CMB (Hazard Ratio = 29.59; 95% confidence interval [95% CI] = 7.66-114.27), compared to no CMB. Further examination was conducted on the subgroup of individuals who developed microbubbles during the test (n = 49), by using Cox regression. Individuals with late onset of CMB (> 60 min at altitude) showed a significantly reduced risk of symptoms (hazard ratio = 0.92; 95% CI = 0.89-0.95), compared to those with early onset (< or = 60 min), while controlling for other risk factors. We conclude that time to detection of circulating microbubbles is an independent determinant of symptoms of DCS.

Adult↗
PubMed1997

Modeling the effects of exercise during 100% oxygen prebreathe on the risk of hypobaric decompression sickness.

BACKGROUND: Several previous studies indicated that exercise during prebreathe with 100% O2 decreased the incidence of hypobaric decompression sickness (DCS). We report a meta-analysis of these investigations combined with a new study in our laboratory to develop a statistical model as a predictive tool for DCS. HYPOTHESIS: Exercise during prebreathe increases N2 elimination in a theoretical 360-min half-time compartment decreasing the incidence of DCS. METHODS: A dose-response probability tissue ratio (TR) model with 95% confidence limits was created for two groups, prebreathe with exercise (n = 113) and resting prebreathe (n = 113), using nonlinear regression analysis with maximum likelihood optimization. RESULTS: The model predicted that prebreathe exercise would reduce the residual N2 in a 360-min half-time compartment to a level analogous to that in a 180-min compartment. This finding supported the hypothesis. The incidence of DCS for the exercise prebreathe group was significantly decreased (Chi-Square = 17.1, p < 0.0001) from the resting prebreathe group. CONCLUSIONS: The results suggested that exercise during prebreathe increases tissue perfusion and N2 elimination approximately 2-fold and markedly lowers the risk of DCS. Based on the model, the prebreathe duration may be reduced from 240 min to a predicted 91 min for the protocol in our study, but this remains to be verified. The model provides a useful planning tool to develop and test appropriate prebreathe exercise protocols and to predict DCS risks for astronauts.

Clinical Protocols↗
PubMed2005

Altitude decompression sickness susceptibility: influence of anthropometric and physiologic variables.

INTRODUCTION: There is considerable variability in individual susceptibility to altitude decompression sickness (DCS). The Air Force Research Laboratory Altitude DCS Research Database consists of extensive information on 2980 altitude exposures conducted with consistent procedures and endpoint criteria. We used this database to quantify the variation in susceptibility and determine if anthropometric and/or physiologic variables could be used to predict DCS risk. METHODS: There were 240 subjects who participated in at least 4 of 70 exposure profiles in which between 5 and 95% of all subjects tested developed DCS symptoms. A subject/study ratio (SSR) was calculated by dividing the DCS experienced by a subject during all their exposures by the DCS incidence for all subjects who participated in the identical exposures. The SSR was used to identify the relative susceptibility of subjects for use in analyzing possible relationships between DCS susceptibility and the variables of height, weight, body mass index, age, percent body fat, and aerobic capacity. RESULTS: The DCS incidence was 46.5% during 1879 subject-exposures by subjects exposed at least 4 times. A significant relationship existed between higher DCS susceptibility and the combination of lower aerobic capacity and greater weight (p < 0.05). DISCUSSION: Despite a correlation, less than 13% of the variation in DCS susceptibility was accounted for by the best combination of variables, weight and VO2max. CONCLUSION: Differences in DCS susceptibility cover a wide range and appear to be related to some anthropometric and physiologic variables. However, there was insufficient correlation to allow prediction of an individual's susceptibility.

Adaptation, Physiological↗
PubMedDate not supplied

Decompression sickness following breath-hold diving.

Despite convincing evidence of a relationship between breath-hold diving and decompression sickness (DCS), the causal connection is only slowly being accepted. Only the more recent textbooks have acknowledged the risks of repetitive breath-hold diving. We compare four groups of breath-hold divers: (1) Japanese and Korean amas and other divers from the Pacific area, (2) instructors at naval training facilities, (3) spear fishers, and (4) free-dive athletes. While the number of amas is likely decreasing, and Scandinavian Navy training facilities recorded only a few accidents, the number of spear fishers suffering accidents is on the rise, in particular during championships or using scooters. Finally, national and international associations (e.g., International Association of Free Drives [IAFD] or Association Internationale pour Le Developpment De L'Apnee [AIDA]) promote free-diving championships including deep diving categories such as constant weight, variable weight, and no limit. A number of free-diving athletes, training for or participating in competitions, are increasingly accident prone as the world record is presently set at a depth of 171 m. This review presents data found after searching Medline and ISI Web of Science and using appropriate Internet search engines (e.g., Google). We report some 90 cases in which DCS occurred after repetitive breath-hold dives. Even today, the risk of suffering from DCS after repetitive breath-hold diving is often not acknowledged. We strongly suggest that breath-hold divers and their advisors and physicians be made aware of the possibility of DCS and of the appropriate therapeutic measures to be taken when DCS is suspected. Because the risk of suffering from DCS increases depending on depth, bottom time, rate of ascent, and duration of surface intervals, some approaches to assess the risks are presented. Regrettably, none of these approaches is widely accepted. We propose therefore the development of easily manageable algorithms for the prevention of those avoidable accidents.

Decompression Sickness↗
PubMedDate not supplied

Probability of decompression sickness in no-stop air diving and subsaturation diving.

Probabilistic models allow estimation of the probability (Pdcs) that decompression sickness (DCS) will occur in any particular dive. Our objective is to provide Pdcs estimates for no-stop diving instructions used by the U.S. Navy and various other navies. To do so, we develop statistics-based (probabilistic) and intuition-based (deterministic) models using dive-outcome data from the U.S. Navy Decompression Database. We give special attention to subsaturation dives (defined as no-stop dives shallower than 40 fswg with bottom times between 4 hr and one day), for which experimental dives are scarce. According to our models, probability of DCS is 2% or less for current U.S. Navy no-stop air dive schedules and near 1% for the navies of Great Britain, Canada, and France; also the current U.S. Navy prescriptions for subsaturation dives seem to be appropriate. Our probabilistic models fail for deep dives; they do not avoid observed DCS cases in the calibration dataset and provide longer no-stop times than allowed by tables used operationally; we advocate prescriptions by our deterministic model for deep no-stop dives.

Algorithms↗
PubMed1985

Oxygen in the treatment of spinal cord decompression sickness.

Twenty-five anesthetized dogs were used to find the optimum Po2 for the delayed treatment of spinal cord decompression sickness (DCS). They were instrumented for the measurement of physiological variables and somatosensory spinal evoked potentials (SEP) given an air dive of 15 min at 10 bar (300 ft) and decompressed in under 6 min. At the surface SEP were observed for signs of DCS. Fifteen minutes after cord DCS was observed in the SEP, the dogs were compressed to 5.0 bar breathing one of 5 gas mixtures giving a Po2 of 1.0, 1.5, 2.0, 2.5, or 3.0 bar. At the start of therapy all groups were in a similar physiological state with a similar loss of SEP. Between 40 and 120 min, recovery was significantly different (P less than 0.05) between the groups, most SEP recovery having occurred within 15 min. The treatments ended with 22, 32, 70, 66, and 42% recovery, respectively. It would appear that the optimum Po2 is around 2.0 bar.

Animals↗
PubMed1998

Decompression sickness risk in rats by microbial removal of dissolved gas.

We present a method for reducing the risk of decompression sickness (DCS) in rats exposed to high pressures of H2. Suspensions of the human colonic microbe Methanobrevibacter smithii were introduced via a colonic cannula into the large intestines of the rats. While the rats breathed H2 in a hyperbaric chamber, the microbe metabolized some of the H2 diffusing into the intestine, converting H2 and CO2 to methane and water. Rate of release of methane from the rats, which was monitored by gas chromatography, varied with chamber H2 pressure. This rate was higher during decompression than during compression, suggesting that during decompression the microbe was metabolizing H2 stored in the rats' tissues. Rats treated with M. smithii had a 25% (5 of 20) incidence of DCS, which was significantly lower (P < 0.01) than the 56% (28 of 50) incidence of untreated controls, brought on by a standardized compression and decompression sequence. Thus using a microbe in the intestine to remove an estimated 5% of the body burden of H2 reduced DCS risk by more than one-half. This method of biochemical decompression may potentially facilitate human diving.

Animals↗