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PubMed1994

Probabilistic model of altitude decompression sickness based on mechanistic premises.

To develop a predictive equation and to test ideas about the mechanisms involved in hypobaric decompression sickness, we performed statistical analyses on published results of 7,023 exercising O2-breathing men subjected to one-step decompressions in altitude chambers. The dependent variable was signs or symptoms so severe that the person's trial was terminated (forced descent). The three independent variables were 1) duration of 100% O2 breathing at ground level (prebreathing), 2) atmospheric pressure after ascent, and 3) exposure duration. The best model, chosen from trial-and-error combinations of premises about bubble behavior, indicates that decompression sickness outcome depends on 1) prebreathing time, but with an unexpectedly long washout half time for N2; 2) time at altitude, as if bubbles grow; and 3) the estimated difference, raised to the fifth power, between the partial pressure of N2 in tissue before and that in bubbles after decompression, perhaps an index of the number of bubbles generated. We expect the model to provide accurate predictions for decompressions matching those of the bulk of the data; the mechanistic cues should be considered hypotheses for further investigation.

Altitude Sickness↗
PubMed1978

Reduction of the incidence of decompression sickness in rats by smooth-muscle activating factor (SMAF).

Normal rats were injected with a smooth-muscle activating factor (SMAF) to examine the dose-response relationshio of SMAF to the incidence of decompression sickness. After injections of saline or 1.0, 5.0, or 10.0 mg/kg SMAF, the animals were compressed to 6 ATA breathing air for 1 h and were then rapidly decompressed to 1 ATA. Results indicate that predive injections of SMAF or exposure to the SMAF substance protected rats against decompression sickness and that higher doses appear to offer more protection.

Animals↗
PubMed1991

The effect of delay on treatment outcome in altitude-induced decompression sickness.

Records at the USAF School of Aerospace Medicine, Hyperbaric Medicine Division, were reviewed to determine whether a relationship exists between the length of time from development of symptoms of altitude chamber decompression sickness (DCS) to start of compression therapy and the outcome of treatment. During the 5-year period from 1 January 1984 to 31 December 1988, 233 cases of altitude chamber DCS were treated in USAF hyperbaric chambers. Information obtained from each record included age, sex, time from exposure to symptom onset, time from symptom onset to start of compression therapy, time required for resolution of symptoms, and number of treatment failures (failure to resolve during the first treatment dive or recurrence of symptoms after the first dive). Analysis of the data obtained from treatment records reveals a direct relationship between length of delay to treatment with compression therapy and outcome of treatment. Patients successfully treated with a single treatment dive had an average delay to treatment of 10.6 h. Patients that failed treatment after one dive (failed to resolve or recurred) had an average delay to treatment of 18.2 h. The difference between these groups is significant (p less than 0.05). Outcome of treatment was not significantly related to patient age, sex, or type of symptoms. A discussion of factors causing delays in treatment of decompression sickness is included.

Adult↗
PubMed2003

Gender not a factor for altitude decompression sickness risk.

INTRODUCTION: Early, retrospective reports of the incidence of altitude decompression sickness (DCS) during altitude chamber training exposures indicated that women were more susceptible than men. We hypothesized that a controlled, prospective study would show no significant difference. METHODS: We conducted 25 altitude chamber decompression exposure profiles. A total of 291 human subjects, 197 men and 94 women, underwent 961 exposures to simulated altitude for up to 8 h, using zero to 4 h of preoxygenation. Throughout the exposures, subjects breathed 100% oxygen, rested or performed mild or strenuous exercise, and were monitored for precordial venous gas emboli (VGE) and DCS symptoms. RESULTS: No significant differences in DCS incidence were observed between men (49.5%) and women (45.3%). However, VGE occurred at significantly higher rates among men than women under the same exposure conditions, 69.3% and 55.0% respectively. Women using hormonal contraception showed significantly greater susceptibility to DCS than those not using hormonal contraception during the latter two weeks of the menstrual cycle. Significantly higher DCS incidence was observed in the heaviest men, in women with the highest body fat, and in subjects with the highest body mass indices and lowest levels of fitness. CONCLUSION: No differences in altitude DCS incidence were observed between the sexes under our test conditions, although men developed VGE more often than women. Age and height showed no significant influence on DCS incidence, but persons of either sex with higher body mass index and lower physical fitness developed DCS more frequently.

Aerospace Medicine↗
PubMed1986

In vivo microbubble detection in decompression sickness using a second harmonic resonant bubble detector.

A resonant bubble detection method based on a second harmonic technique has been used to monitor the femoral vascular system of dogs subjected to rapid decompression. For this study, the detector consisted of two acoustic transducers mounted at right angles to each other that were packaged in a perivascular cuff configuration. This detector responds selectively only to bubbles near resonant size (4.2 mum in diameter); solid particles and large bubbles produce no response. The detector was used to monitor a total of 15 dogs. Eleven dogs were subjected to a series of simulated underwater dives until acute symptoms of decompression sickness occurred; 4 dogs served as controls. In the dived group, either the femoral vein or the femoral artery was monitored. Resonant bubbles were observed in the femoral veins of all 6 dogs monitored at this location. During arterial monitoring, most dogs showed no response, but an occasional weak response was observed in 2 of the dogs. No resonant bubbles were detected in the femoral artery or the femoral vein in any of the controls. The data suggest that this bubble detection method is feasible for in vivo use. Furthermore, 4 mum diameter bubbles are much more prevalent in the veins of dogs suffering from decompression sickness than they are in dog arteries, presumably because they are filtered out effectively by the pulmonary circulation. Modifications of this method are discussed to enhance its accuracy and applicability for quantifying bubble size, location, and number.

Animals↗
PubMed2001

Increasing activity of H(2)-metabolizing microbes lowers decompression sickness risk in pigs during H(2) dives.

The risk of decompression sickness (DCS) was modulated by varying the biochemical activity used to eliminate some of the hydrogen (H(2)) stored in the tissues of pigs (19.4 +/- 0.2 kg) during hyperbaric exposures to H(2). Treated pigs (n = 16) received intestinal injections of Methanobrevibacter smithii, a microbe that metabolizes H(2) to water and CH(4). Surgical controls (n = 10) received intestinal injections of saline, and an additional control group (n = 10) was untreated. Pigs were placed in a chamber and compressed to 24 atm abs (20.6-22.9 atm H(2)). After 3 h, the pigs were decompressed and observed for symptoms of DCS for 1 h. Pigs with M. smithii had a significantly lower (P < 0.05) incidence of DCS (44%; 7/16) than all controls (80%; 16/20). The DCS risk decreased with increasing activity of microbes injected (logistic regression, P < 0.05). Thus the supplemental tissue washout of the diluent gas by microbial metabolism was inversely correlated with DCS risk in a dose-dependent manner in this pig model.

Animals↗
PubMed1981

[Disability evaluation in decompression sickness treated with hyperbaric therapy].

The Authors report 41 cases of decompression sickness following air scuba diving observed during the last three years at the Istituto di Medicina del Lavoro of the University of Genoa and discuss about consequent injuries and damages (period of hospitalization, temporary and permanent disability). The Authors say that in 12 cases remain permanent disability with limitation more or less serious of the working capacity. They, at last, emphasize that neurological symptoms are getting better during several months so to be necessary to wait for two years at least before estimating definitively advise.

Adult↗
PubMed1985

Electrocardiographic changes in serious decompression sickness.

Electrocardiographic changes observed in 21 dogs suffering from spinal cord decompression sickness (DCS) are described. Changes seen included P wave peaking and P-R depression compatible with right heart strain; S-T segment and T wave changes suggestive of myocardial ischemia; and ventricular arrhythmias ranging from unifocal premature ventricular contractions to ventricular tachycardia. Compression therapy did not always restore the ECG changes promptly to normality. The changes are discussed in association with concurrent physiological events. These included pulmonary hypertension, systemic hypertension and hypotension, and cerebral DCS. Possible mechanisms ranging from local cardiac DCS or coronary gas embolism to autonomic nervous system disturbances arising from cerebral and spinal cord DCS are reviewed. It is concluded that ECG recordings should be made more often when treating clinical DCS.

Animals↗
PubMed1996

The initial signs and symptoms of altitude decompression sickness.

BACKGROUND: With the potential for higher aircraft and cabin altitudes, the way in which altitude decompression sickness (DCS) presents continues to be of interest. The majority of previous papers on the symptomatology of DCS are retrospective reviews of patients treated hours or days post-exposure. The initial presentation while still at altitude is the form of DCS that aircrew must be able to recognize in order to respond correctly. This paper reports the initial manifestations of DCS that occurred during a series of prospective hypobaric chamber studies. These studies had been specifically designed to investigate DCS. METHODS: This paper presents a prospective analysis of DCS symptoms from 447 subjects, recorded over an 11-yr period at the Armstrong Laboratory (AL), and is an attempt to provide an accurate representation of the initial presentation of altitude DCS. RESULTS: Of the 447 cases, 83.2% had musculoskeletal involvement, 2.7% had chokes, 2.2% skin manifestations, 10.8% paresthesia, and 0.5% frank neurological features. CONCLUSIONS: The most common presenting feature was musculoskeletal, with knee pain predominating (occurring in 70% of these cases). A very low incidence of neurological features was seen in the AL database, which was in contrast to data from many other sources. Reasons for this difference may include the use of preoxygenation and the policy of prompt recompression upon symptom development at AL. There is also the possibility that individuals in the training and operational environments are more likely to report frank neurological involvement than other forms of DCS.

Adult↗
PubMed1985

Light and electron microscopic alterations in spinal cord myelin sheaths after decompression sickness.

Pathological examination of spinal cords from animals subjected to experimental decompression sickness (DCS) was undertaken in an attempt to explain the disparate response to treatment observed. Eight experimental animals, four undived control animals, and two dived but untreated animals were perfusion fixed, and the spinal cords were removed. Light microscopy of toluidine blue stained, ultrathin sections from dived animals demonstrated a distinctive widened myelin sheath showing a banded pattern of myelin disruption. This pattern was confirmed by electron microscopy and showed the separation to be between abutting double layers of myelin. Artifactual changes were also present in dived and undived animals. These previously unreported changes may be caused by DCS. They are compatible with the major mechanisms proposed in the pathophysiology of spinal cord DCS and may also account for the response to treatment seen in our experimental animals. It is suggested that these findings may also explain the response to treatment seen in patients, together with the formation of late lesions described in the spinal cords of long-term survivors of DCS.

Animals↗
PubMed1994

Survivorship models for estimating the risk of decompression sickness.

Several approaches have been used for modeling the incidence of decompression sickness (DCS) such as Hill's dose-response and logistic regression. Most of these methods do not include the time-to-onset information in the model. Survival analysis (failure time analysis) is appropriate when the time to onset of an event is of interest. The applicability of survival analysis for modeling the risk of DCS is illustrated by using data obtained from hypobaric chamber exposures simulating extravehicular activities (n = 426). Univariate analysis of incidence-free survival proportions were obtained for Doppler-detectable circulating microbubbles (CMB), symptoms of DCS and test aborts. A log-linear failure time regression model with 360-min half-time tissue ratio (TR) as covariate was constructed, and estimated probabilities for various TR values were calculated. Further regression analysis by including CMB status in this model showed significant improvement (p < 0.05) in the estimation of DCS over the previous model. Since DCS is dependent on the exposure pressure as well as the duration of exposure, we recommend the use of survival analysis for modeling the risk of DCS.

Computer Simulation↗
PubMedDate not supplied

[Acute myelopathy in a diver caused by decompression sickness. A case description and a survey of the literature].

INTRODUCTION: Decompression sickness (DS) is caused when bubbles of an inert gas usually nitrogen, since oxygen is metabolised in the tissues are released into the bloodstream and tissues during fast ascents once the atmospheric pressure is lowered near the surface. Neurological complications are its most serious form of expression and include vertigo, headache, stroke and acute myelopathy, among others. DS that affects the spinal cord is infrequent. CASE REPORT: A male, 42 years old, who presented progressive tetraparesis 15 minutes after returning to the surface following several immersions up to 40 metres deep in the same day. Neurological exploration revealed tetraparesis that was predominantly distal and in the lower limbs, a posterior cord syndrome, urinary incontinence and neurogenic pain. Total column magnetic resonance imaging showed areas of diffused hypersignal in the T2 sequence in the thoracic and cervical (C2 to C6) regions, predominating in the posterior cords. The echocardiogram, transcranial Doppler and spirometric studies ruled out an arterial gas embolism following pulmonary barotrauma. CONCLUSIONS: Spinal DS can give rise to a serious myelopathy, which affects the pyramidal pathway, posterior cords and sphincteral control, and which generally appears after sudden ascents from the deep dives.

Adult↗
PubMed1996

Prevalence of decompression sickness among U-2 pilots.

BACKGROUND: Though it is rarely reported, decompression sickness (DCS) is an expected risk for U-2 aviators. The potential for chronic sequelae of untreated DCS in this population has never been addressed. METHODS: After conducting a preliminary survey at an active-duty U-2 squadron, a cohort of 416 U-2 pilots (active-duty and retired) were mailed two sequential anonymous surveys to assess demographic data, career prevalence of DCS symptoms, and overall health status with an emphasis on chronic musculoskeletal problems. RESULTS: The response rate for each mail-in survey was over 60%. During their career, 75.5% of pilots experienced DCS symptoms such as joint pain, skin manifestations, and/or various neurological problems. Symptoms generally started during flight and resolved upon descent. Many pilots voluntarily increased their oxygen prebreathing time, or inflated the pressure suit during flight to prevent or treat symptoms. At some point in their career 12.7% of those experiencing symptoms either altered the flight profile or aborted a mission as a result. The association of past DCS with current arthritic problems was not statistically significant. CONCLUSIONS: The career prevalence of DCS symptoms in U-2 pilots is higher than previously reported, and these symptoms sometimes affect mission completion. We found no evidence that chronic musculoskeletal sequelae (e.g., arthritis or dysbaric osteonecrosis) are causally associated with DCS in this population.

Adult↗
PubMed1999

Predicting risk of decompression sickness in humans from outcomes in sheep.

In animals, the response to decompression scales as a power of species body mass. Consequently, decompression sickness (DCS) risk in humans should be well predicted from an animal model with a body mass comparable to humans. No-stop decompression outcomes in compressed air and nitrogen-oxygen dives with sheep (n = 394 dives, 14.5% DCS) and humans (n = 463 dives, 4.5% DCS) were used with linear-exponential, probabilistic modeling to test this hypothesis. Scaling the response parameters of this model between species (without accounting for body mass), while estimating tissue-compartment kinetic parameters from combined human and sheep data, predicts combined risk better, based on log likelihood, than do separate sheep and human models, a combined model without scaling, and a kinetic-scaled model. These findings provide a practical tool for estimating DCS risk in humans from outcomes in sheep, especially in decompression profiles too risky to test with humans. This model supports the hypothesis that species of similar body mass have similar DCS risk.

Algorithms↗
PubMed2002

Decompression sickness latency as a function of altitude to 25,000 feet.

INTRODUCTION: Current Air Force Instructions (AFIs) allow flight of unrestricted duration in unpressurized aircraft up to 25,000 ft. Supplemental oxygen is required to prevent hypoxia, but decompression sickness (DCS) is not adequately considered in current oxygen use guidelines. Recent information from the Air Force Research Laboratory (AFRL) DCS database, combined with a projected increase in exposure to these altitudes under proposed USAF missions, suggests that DCS may be operationally significant in certain circumstances. METHODS: The AFRL Altitude Decompression Sickness Risk Assessment Computer (ADRAC) model was used to develop a family of curves representing DCS latency (time to symptom onset) as a function of altitude for the case of zero preoxygenation and mild exercise. The DCS database was then searched for serious DCS cases among subjects under the same conditions (n = 175). An upper limit for DCS incidence that avoided serious DCS symptoms was selected and exposure time limits were determined. Preoxygenation requirements necessary to remain below the selected DCS incidence limit were also evaluated using ADRAC and provide an alternative to time limits. RESULTS AND DISCUSSION: The 20% DCS curve met the above criteria. Based on this, continued unlimited exposure time is recommended for 21,000 ft and below. The 20% DCS risk curve for zero-prebreathe exposures to 25,000 ft, 24,000 ft, 23,000 ft, and 22,000 ft are reached at 45 min, 70 min, 120 min, and 200 min, respectively. Consistent with existing AFIs, flying unpressurized above 25,000 ft is not recommended. These times should be reduced for crewmembers engaged in heavy physical activity at altitude. CONCLUSIONS: This article proposes time limits for unpressurized flight above 21,000 ft to reduce DCS risk.

Aerospace Medicine↗
PubMed1976

Biochemistry and hematology at decompression sickness: a case report.

A 24-year-old hospital corpsman, a volunteer in a series of dry chamber air dives to a simulated pressure equivalent to 188 FSWG (57.3 MSWG), developed left knee pain shortly after standard decompression. A tentative diagnosis of decompression sickness was made and recompression therapy was initiated with alleviation of pain occurring at 60 FSWG (18.3 MSWG). A U.S. Navy Treatment Table "5 (oxygen breathing) regimen was then selected and completed uneventfully. The subject had been undergoing biomedical evaluation for several days prior to diving; thus, a clinically diagnosed case of dysbarism with subsequent treatment was available for study. This individual was then monitored for a 10-d period. The acute phase of decompression sickness was characterized by a marked shortening of clotting time and a thrombocytopenia with accompanying increased platelet aggregates. The recovery phase was categorized by a variety of hematological and bio-chemical changes. Hemodilution, an elevated megathrombocyte index, and a tendency toward eosinopenia were evident for most of the 10-d observation period. Other persistent alterations detected during this period included a relative hyperglycemia, depressed urine Na+/K+, and increased ketosteroid excretion. These observations indicate that abatement of pain after treatment of dysbarism can be followed by the onset of a variety of biochemical and hematological changes. Moreover, complete recovery may require upwards of 10 d.

Adult↗