A study of decompression sickness using recorded depth-time profiles.

Introduction: 122,129 dives by 10,358 recreational divers were recorded by dive computers from 11 manufacturers in an exploratory study of how dive profile, breathing gas (air or nitrox [N2/O2] mixes), repetitive diving, gender, age, and dive site conditions influenced observed decompression sickness (DCSobs). Thirty-eight reports were judged as DCS. Overall DCSobs was 3.1 cases/104 dives. Methods: Three dive groups were studied: Basic (live-aboard and shore/dayboat), Cozumel Dive Guides, and Scapa Flow wreck divers. A probabilistic decompression model, BVM(3), controlled dive profile variability. Chi-squared test, t-test, logistic regression, and log-rank tests evaluated statistical associations. Results: (a) DCSobs was 0.7/104 (Basic), 7.6/104 (Guides), and 17.3/104 (Scapa) and differed after control for dive variability (p ≺ 0.001). (b) DCSobs was greater for 22%-29% nitrox (12.6/104) than for 30%-50% nitrox (2.04/104) (p ≤ 0.0064) which did not differ from air (2.97/10104). (c) For daily repetitive dives (≺12-hour surface intervals (SI)), DCS occurred only following one or two dives (4.3/10104 DCSobs; p ≺ 0.001) where SIs were shorter than after three or more dives. (d) For multiday repetitive dives (SIs ≺ 48 hours), DCS was associated with high multiday repetitive dive counts only for Guides (p = 0.0018). (e) DCSobs decreased with age at 3%/year (p ≤ 0.0144). (f) Males dived deeper (p ≺ 0.001) but for less time than females (p ≺ 0.001). Conclusion: Collecting dive profiles with dive computers and controlling for profile variability by probabilistic modeling was feasible, but analytical results require independent confirmation due to limited observed DCS. Future studies appear promising if more DCS cases are gathered, stakeholders cooperate, and identified data collection problems are corrected.

A proposed in vitro model for investigating the mechanisms of 'joint cracking': a short report of preliminary techniques and observations.

Joint "cracking" is common but not a clearly understood audible phenomenon. In this brief report we propose an in-vitro model to potentially assist in revealing a mechanism for, and therefore source of, this phenomenon. Using a suction cup under tension and de-nucleated fluid to simulate synovial fluid, an audible release with intra-articular cavity formation was elicited. This was followed by a refractory period during which no audible crack could be elicited until the observed cavity had slowly reabsorbed back into the joint fluid. Conversely, if regular fluid containing pre-existing nuclei was used, a cavity formation occurred but with neither an audible release nor subsequent refractory period. With this simple in-vitro model, we were able to reproduce the characteristic audible release, cavity formation and related refractory period typically observed in related experiments in human joints. This simple in-vitro model may be of use in helping to discern both the timing and precise nature of other yet to be discerned mechanisms related to joint cracking.

Le « craquement ¼ des articulations est un phénomène sonore commun, mais mal compris. Dans ce court rapport, nous proposons un modèle in vitro pouvant aider à révéler un mécanisme, et par conséquent une source, pour ce phénomène. À l'aide d'une ventouse sous tension et d'un fluide énucléé ayant pour but de simuler la synovie, on a entendu un son provenant de la cavité intraarticulaire, suivi d'une période réfractaire au cours de laquelle on n'a pas obtenu de craquement sonore jusqu'à ce que la cavité observée se soit réabsorbée lentement dans le liquide articulaire. À l'inverse, lorsqu'on utilisait le liquide régulier contenant les noyaux préexistants, il se produisait une perforation de la cavité, mais sans son ni période réfractaire. Ce modèle in vitro simple a permis de reproduire le son, la cavité et la période réfractaire connexe caractéristiques qu'on observe en général lors d'expériences connexes sur des articulations humaines. Ce modèle in vitro simple peut aussi servir à discerner à la fois le moment et la nature précise d'autres mécanismes qu'on n'a pas encore perçus concernant le craquement des articulations.

The probability and severity of decompression sickness.

Decompression sickness (DCS), which is caused by inert gas bubbles in tissues, is an injury of concern for scuba divers, compressed air workers, astronauts, and aviators. Case reports for 3322 air and N2-O2 dives, resulting in 190 DCS events, were retrospectively analyzed and the outcomes were scored as (1) serious neurological, (2) cardiopulmonary, (3) mild neurological, (4) pain, (5) lymphatic or skin, and (6) constitutional or nonspecific manifestations. Following standard U.S. Navy medical definitions, the data were grouped into mild-Type I (manifestations 4-6)-and serious-Type II (manifestations 1-3). Additionally, we considered an alternative grouping of mild-Type A (manifestations 3-6)-and serious-Type B (manifestations 1 and 2). The current U.S. Navy guidance allows for a 2% probability of mild DCS and a 0.1% probability of serious DCS. We developed a hierarchical trinomial (3-state) probabilistic DCS model that simultaneously predicts the probability of mild and serious DCS given a dive exposure. Both the Type I/II and Type A/B discriminations of mild and serious DCS resulted in a highly significant (p << 0.01) improvement in trinomial model fit over the binomial (2-state) model. With the Type I/II definition, we found that the predicted probability of 'mild' DCS resulted in a longer allowable bottom time for the same 2% limit. However, for the 0.1% serious DCS limit, we found a vastly decreased allowable bottom dive time for all dive depths. If the Type A/B scoring was assigned to outcome severity, the no decompression limits (NDL) for air dives were still controlled by the acceptable serious DCS risk limit rather than the acceptable mild DCS risk limit. However, in this case, longer NDL limits were allowed than with the Type I/II scoring. The trinomial model mild and serious probabilities agree reasonably well with the current air NDL only with the Type A/B scoring and when 0.2% risk of serious DCS is allowed.

Effects of elevated oxygen and carbon dioxide partial pressures on respiratory function and cognitive performance.

Hyperoxia during diving has been suggested to exacerbate hypercapnic narcosis and promote unconsciousness. We tested this hypothesis in male volunteers (12 at rest, 10 at 75 W cycle ergometer exercise) breathing each of four gases in a hyperbaric chamber. Inspired Po2 (PiO2 ) was 0.21 and 1.3 atmospheres (atm) without or with an individual subject's maximum tolerable inspired CO2 (PiO2 = 0.055-0.085 atm). Measurements included end-tidal CO2 partial pressure (PetCO2 ), rating of perceived discomfort (RPD), expired minute ventilation (V̇e), and cognitive function assessed by auditory n-back test. The most prominent finding was, irrespective of PetCO2 , that minute ventilation was 8-9 l/min greater for rest or exercise with a PiO2 of 1.3 atm compared with 0.21 atm (P < 0.0001). For hyperoxic gases, PetCO2 was consistently less than for normoxic gases (P < 0.01). For hyperoxic hypercapnic gases, n-back scores were higher than for normoxic gases (P < 0.01), and RPD was lower for exercise but not rest (P < 0.02). Subjects completed 66 hyperoxic hypercapnic trials without incident, but five stopped prematurely because of serious symptoms (tunnel vision, vision loss, dizziness, panic, exhaustion, or near syncope) during 69 normoxic hypercapnic trials (P = 0.0582). Serious symptoms during hypercapnic trials occurred only during normoxia. We conclude serious symptoms with hyperoxic hypercapnia were absent because of decreased PetCO2 consequent to increased ventilation.

Protective mechanisms in hypobaric decompression.

BACKGROUND: To reduce bubble formation and growth during hypobaric exposures, a denitrogenation or nitrogen "washout" procedure is performed. This procedure consists of prebreathing oxygen fractions as close to one as possible (oxygen prebreathe) prior to depressurization before ascending to the working altitude or low spacesuit pressures. During the NASA prebreathe reduction program (PRP), it was determined that the addition of a light arm exercise to short, individually designed, performance-based heavy exercise (dual cycle ergometry) during an abbreviated 2-h prebreathe (F1O2 - 1.0) reduced the occurrence of decompression sickness (DCS). Heavy-exercise-induced DCS reduction is likely to be related to the enhancement of the tissue nitrogen washout during the oxygen prebreathe. In addition to the heavy-exercise-induced microcirculatory adaptation, we hypothesized that the light exercise would not cause sufficient microcirculatory changes in the limbs to explain alone this further DCS protection. We evaluated microcirculatory changes as minimal by replicating the exercise characteristics of the PRP trials in 13 healthy subjects. METHODS: Noninvasive near infrared spectroscopy (NIRS) allowed observation of instantaneous variations of total, oxygenated, and deoxygenated hemoglobin/myoglobin concentrations in the microcirculatory networks (probes facing the vastus lateralis and deltoid muscles) of active limbs during dynamic exercise. RESULTS: The high-intensity leg exercise alone produced the changes in NIRS parameters; the light arm exercise induced minimal microcirculatory volume changes. However, this coupling appeared to be critical in previous altitude PRP chamber studies by reducing DCS. DISCUSSION: With only minimal microcirculatory blood volume changes, it is unlikely that light exercise alone causes significant nitrogen tissue washout. Therefore, our results suggest that in addition to nitrogen tissue washout, another unknown exercise-induced effect may have further enhanced the DCS protection, possibly mediated via the anti-inflammatory effect of exercise, gas micronuclei reduction, NO pathways, or other molecular mechanisms.

Per-capita claims rates for decompression sickness among insured Divers Alert Network members.

Decompression sickness (DCS) in recreational diving is a rare and usually self-limiting injury, but permanent disability can occur. Incidence rate estimates are difficult to establish because the number of divers at risk is usually unknown in population samples with well-documented DCS. We estimated the annual per-capita DCS incidence rates for 2000-2007 based on insurance claims submitted by members of the Divers Alert Network (DAN), Durham, N.C., with dive accident insurance. The overall per-capita DCS claims rate (DCR) was 20.5 per 10,000 member-years. Based on the age-adjusted DCR, males submitted 28% more claims than females. Male-to-female difference was greatest between 35 and 40 years of age and disappeared by the mid-50s. Highest rates were observed in the 30- to 39-year age category, after which DCR declined with increasing age. Highest yearly DCR was estimated in 2002. Insurance dropout rate was greater among those who had DCS in the first year of their insurance compared to those who did not have DCS in their first year.

Decompression illness.

Decompression illness is caused by intravascular or extravascular bubbles that are formed as a result of reduction in environmental pressure (decompression). The term covers both arterial gas embolism, in which alveolar gas or venous gas emboli (via cardiac shunts or via pulmonary vessels) are introduced into the arterial circulation, and decompression sickness, which is caused by in-situ bubble formation from dissolved inert gas. Both syndromes can occur in divers, compressed air workers, aviators, and astronauts, but arterial gas embolism also arises from iatrogenic causes unrelated to decompression. Risk of decompression illness is affected by immersion, exercise, and heat or cold. Manifestations range from itching and minor pain to neurological symptoms, cardiac collapse, and death. First-aid treatment is 100% oxygen and definitive treatment is recompression to increased pressure, breathing 100% oxygen. Adjunctive treatment, including fluid administration and prophylaxis against venous thromboembolism in paralysed patients, is also recommended. Treatment is, in most cases, effective although residual deficits can remain in serious cases, even after several recompressions.

A computationally advantageous system for fitting probabilistic decompression models to empirical data.

To investigate the nature and mechanisms of decompression sickness (DCS), we developed a system for evaluating the success of decompression models in predicting DCS probability from empirical data. Model parameters were estimated using maximum likelihood techniques. Exact integrals of risk functions and tissue kinetics transition times were derived. Agreement with previously published results was excellent including: (a) maximum likelihood values within one log-likelihood unit of previous results and improvements by re-optimization; (b) mean predicted DCS incidents within 1.4% of observed DCS; and (c) time of DCS occurrence prediction. Alternative optimization and homogeneous parallel processing techniques yielded faster model optimization times.

Marginal DCS events: their relation to decompression and use in DCS models.

We consider the nature and utility of marginal decompression sickness (DCS) events in fitting probabilistic decompression models to experimental dive trial data. Previous works have assigned various fractional weights to marginal DCS events, so that they contributed to probabilistic model parameter optimization, but less so than did full DCS events. Inclusion of fractional weight for marginal DCS events resulted in more conservative model predictions. We explore whether marginal DCS events are correlated with exposure to decompression or are randomly occurring events. Three null models are developed and compared with a known decompression model that is tuned on dive trial data containing only marginal DCS and non-DCS events. We further investigate the technique by which marginal DCS events were previously included in parameter optimization, explore the effects of fractional weighting of marginal DCS events on model optimization, and explore the rigor of combining data containing full and marginal DCS events for probabilistic DCS model optimization. We find that although marginal DCS events are related to exposure to decompression, empirical dive data containing marginal and full DCS events cannot be combined under a single DCS model. Furthermore, we find analytically that the optimal weight for a marginal DCS event is 0. Thus marginal DCS should be counted as no-DCS events when probabilistic DCS models are optimized with binomial likelihood functions. Specifically, our study finds that inclusion of marginal DCS events in model optimization to make the dive profiles more conservative is counterproductive and worsens the model's fit to the full DCS data.

Resolution and severity in decompression illness.

omegaWe review the terminology of decompression illness (DCI), investigations of residual symptoms of decompression sickness (DCS), and application of survival analysis for investigating DCI severity and resolution. The Type 1 and Type 2 DCS classifications were introduced in 1960 for compressed air workers and adapted for diving and altitude exposure with modifications based on clinical judgment concerning severity and therapy. In practice, these proved ambiguous, leading to recommendations that manifestations, not cases, be classified. A subsequent approach assigned individual scores to manifestations and correlated total case scores with the presence of residual symptoms after therapy. The next step used logistic regression to find the statistical association of manifestations to residual symptoms at a single point in time. Survival analysis, a common statistical method in clinical trials and longitudinal epidemiological studies, is a logical extension of logistic regression. The method applies to a continuum of resolution times, allows for time varying information, can manage cases lost to follow-up (censored), and has potential for investigating questions such as optimal therapy and DCI severity. There are operational implications as well. Appropriate definitions of mild and serious manifestations are essential for computing probabilistic decompression procedures where severity determines the DCS probability that is acceptable. Application of survival analysis to DCI data would require more specific case information than is commonly recorded.

Phosphodiesterase-5 inhibitors oppose hyperoxic vasoconstriction and accelerate seizure development in rats exposed to hyperbaric oxygen.

Oxygen is a potent cerebral vasoconstrictor, but excessive exposure to hyperbaric oxygen (HBO(2)) can reverse this vasoconstriction by stimulating brain nitric oxide (NO) production, which increases cerebral blood flow (CBF)-a predictor of O(2) convulsions. We tested the hypothesis that phosphodiesterase (PDE)-5 blockers, specifically sildenafil and tadalafil, increase CBF in HBO(2) and accelerate seizure development. To estimate changes in cerebrovascular responses to hyperoxia, CBF was measured by hydrogen clearance in anesthetized rats, either control animals or those pretreated with one of these blockers, with the NO inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME), with the NO donor S-nitroso-N-acetylpenicillamine (SNAP), or with a blocker combined with l-NAME. Animals were exposed to 30% O(2) at 1 atm absolute (ATA) ("air") or to 100% O(2) at 4 or 6 ATA. EEG spikes indicated central nervous system CNS O(2) toxicity. The effects of PDE-5 blockade varied as a positive function of ambient Po(2). In air, CBF did not increase significantly, except after pretreatment with SNAP. However, at 6 ATA O(2), mean values for CBF increased and values for seizure latency decreased, both significantly; pretreatment with l-NAME abolished these effects. Conscious rats treated with sildenafil before HBO(2) were also more susceptible to CNS O(2) toxicity, as demonstrated by significantly shortened convulsive latency. Decreases in regional CBF reflect net vasoconstriction in the brain regions studied, since mean arterial pressures remained constant or increased throughout. Thus PDE-5 blockers oppose the protective vasoconstriction that is the initial response to hyperbaric hyperoxia, decreasing the safety of HBO(2) by hastening onset of CNS O(2) toxicity.

Dive problems and risk factors for diving morbidity.

INTRODUCTION: Running out of air, buoyancy problems and rapid ascents are known risk factors for diving morbidity and mortality. The effects of the diving environment and equipment and the influence of individual diver characteristics on these risks were studied. METHODS: Between 1995 and 2004, Project Dive Exploration prospectively recorded 52,582 recreational dives made by 5,046 adult divers. Data regarding diver characteristics, dive environment, recorded depth-time profiles and reported dive problems were collected. Ascent rates were calculated from depth-time profiles. Human factors (age, sex, certification status) were tested by logistic regression for association with running out of air, buoyancy problems and rapid ascents. To control for human factors, dives where a problem was reported (case dives) were compared to dives made by the same divers in which each risk factor was not reported (control dives), again using a logistic regression model. RESULTS: Running out of air and buoyancy problems were significantly associated with older females, whereas rapid ascents were associated with younger males. Certification status also affected which type of problem was experienced. Maximum depth and dive time had only weak effects upon the type of problem experienced. All three problems were associated with charter boat and live-aboard diving, the most significant environmental association being the perceived workload of the dive. CONCLUSIONS: We recommend dive instructors give greater emphasis during training to monitoring gas reserves, buoyancy control techniques and slow ascents, coupled with practical methods of gauging ascent rate. Dive boat crews should consider likely workloads when selecting dive sites and warn divers against overexertion.

Scuba injury death rate among insured DAN members.

We calculated the annual rates of diving-related deaths among DAN-insured members in the period from 2000 to 2006 and investigated the effects of age and sex on death rate by logistic regression. We determined relative risks for divers < 50 and ≥ 50 years of age for drowning, arterial gas embolism, and cardiac incidents, the three most common disabling injuries associated with diving death. There were 1,141,367 insured member-years and 187 diving-related deaths. Males made up 64% of the members. Individuals ≥ 50 years of age constituted 31% of the fatalities. Insured mean age increased from 40 ± 12 to 43 ± 13 years over the seven-year study period. Annual fatality rates varied between 12.1 and 22.9 (average 16.4, 95% confidence intervals 14.2, 18.9) per 100,000 persons insured. The relative risk for male divers in their thirties was six times greater than the risk for female divers in the same age range. Fatality rates increased with age for both sexes, but the higher relative risk for males progressively decreased until the rates became similar for both sexes after age 60. Death associated with cardiac incidents was 12.9 times more likely in divers ≥ 50 years of age. We recommend that older divers adjust their participation in diving according to health status and physical fitness, maintain fitness with regular exercise, and abstain from diving in conditions likely to require unaccustomed physical activity.

Statistical models of acute mountain sickness.

Acute mountain sickness (AMS) is caused by exposure to altitudes exceeding 2500 m and often resolves by acclimatization without further ascent. Statistical models of AMS score and the probability of an AMS diagnosis were developed to allow the combination of dissimilar exposures for simultaneous analysis. The study population was 302 trekkers from a previous investigation who provided self-reported symptoms upon arrival at 3840 m during hikes through altitudes of 1500 to 6200 m. AMS score (Hackett scale) was estimated by linear regression and the probability of an AMS diagnosis (Lake Louise criteria) by logistic regression. AMS score or probability was significantly associated with exposure day and altitude. Increased altitude over the prior 3 days resulted in higher estimated AMS score or probability and decreased altitude in lower score or probability. The odds ratio (OR) of AMS was 3.6 if not on acetazolamide. Females appeared slightly more susceptible than males (1.5 OR). The approach offers the advantages of (1) improved statistical power by combining exposures, (2) insight into the dose-response relationship of altitude exposure and AMS risk, (3) quantitative tests for the significance of factors that might affect AMS susceptibility, and (4) practical tools to track individual climbers and plan operational ascents.