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PubMed1990

Relationship of menstrual history to altitude chamber decompression sickness.

Records at the USAF School of Aerospace Medicine, Division of Hyperbaric Medicine, were reviewed to determine the relationship between the incidence of altitude chamber decompression sickness (DCS) in females and menstrual history. The study period spans 11 years, from January 1978 to December 1988. There were 81 records suitable for study. A significant inverse linear correlation was noted between the number of days since the start of last menstrual period and the incidence of DCS. This relationship was noted with both Type I and Type II DCS. Lack of information on the population at risk precluded an analysis of the effects of birth control pills on this phenomenon. The underlying mechanism for the correlation between menstrual cycle and susceptibility to development of DCS is unknown. We conclude that women are at higher risk of developing altitude related decompression sickness during menses, with the risk decreasing linearly as the time since last menstrual period increases.

Adolescent↗
PubMed2003

Degassed liquids to prevent/treat decompression sickness.

Recompression and oxygen breathing constitute the primary treatments for decompression sickness (DCS). Increasing the volume of distribution of dissolved gas with high-volume liquid therapy represents an alternative strategy to prevent or treat DCS. Furthermore, degassing of ingested and infused liquids would increase their potential to keep supersaturated tissue gases in solution after decompression. We hypothesize that administration of degassed liquids will prevent or reverse mild-moderate DCS by increasing the volume of distribution of dissolved gas in DCS victims. Degassed perfluorocarbon ingestion offers particularly attractive potential: one liter theoretically dissolves approximately 300ml of N(2) in vivo at 1atm. One could speculate that degassed liquids may adequately treat mild DCS in lieu of recompression, particularly DCS expressed in 'fast compartment' (well-perfused) tissues. Furthermore, degassed liquid administration should prove to be even more effective adjunct therapy for severe DCS than present gas-saturated liquids.

Decompression Sickness↗
PubMed1978

Decompression sickness in the goat: nature of brain and spinal cord lesions at 48 hours.

An investigation was undertaken to determine whether permanent damage to the central nervous system (CNS) is associated with transient decompression sickness in the goat. Twelve goats were compressed in air at 100 fsw for one hour. After decompression over a period of 2.5 min, seven animals showed signs of decompression sickness and four of these were treated by recompression in oxygen. Residual clinical signs after 12 h were present in one animal only. The seven affected goats were killed 48 h after decompression. Lesions in the CNS (other than hemorrhage) were confined to the spinal cord of three animals that had shown paralysis, and consisted of infarction of white matter with occasional microthrombi and perivascular proteinaceous edema of the gray matter. In all seven animals, there was hemorrhage in the spinal cord and in four, hemorrhage in the brain. Infarction of the spinal cord was not present in the four animals that had shown only slight clinical signs (limping); one of these goats had been treated by recompression in oxygen.

Animals↗
PubMed2004

Probabilistic model of decompression sickness based on stochastic models of bubbling in tissues.

BACKGROUND: Decompression sickness (DCS) is caused by gas bubbles formed from pre-existing and new microscopic gas nuclei in blood and tissues. Assuming a random pattern of bubbling processes in living tissues, we developed a probabilistic model of DCS. We hypothesized that symptoms of DCS in an individual exposed to decompression appear when the total volume of bubbles in a unit volume of any tissue, w(t), exceeds the critical specific volume of a free gas phase, wcr. Therefore, one may consider the expectation of w(t)/wcr as a measure of the dynamic risk of gas bubble lesion of a given tissue segment. METHODS: Using the standard approach to estimation of various risks and the sum rule of probabilities of joint events, we defined the cumulative probability of DCS onset by the equation Pcum(t) = 1 - exp[Fcum(t)], where Fcum(t) = sigmaVnQnMnc(t), Qn = 1/wncr, where Vn is the volume of a tissue n. The function Mnc(t) coincides with the function Mn(t), defining a time history of the expectation of wn(t) until it achieves its maximum and then becomes a constant. Evaluating Pcum(t) for particular altitude decompressions, we identified the additive cumulative risk function of development of any DCS symptoms, Fcum-tot(t), with the function defining the cumulative risk of any bubble lesion of the "worst" virtual tissue (WVT) of Type A. On the other hand, we identified the additive cumulative risk function of development of intolerable DCS symptoms, Fcum-int(t), with the function defining the cumulative risk of acute bubble lesion of the WVT of Type phi. RESULTS: We found parameters of the curves Pcum-tot(t) and Pcum-int(t) that fit the known empirical curves for the cumulative probability of DCS onset. For men performing mild exercise at 30 kPa after preoxygenation, our estimated parameters for curves Pcum-tot(t) indicate that the WVTs of Type A have nitrogen washout half-times of 260 and 290 min for preoxygenation times of 75 and 135 min, respectively. On the other hand, the parameters of curves Pcum-int(t) show that the WVTs of Type phi in men performing mild exercise at 20-40 kPa after preoxygenation during 0-6 h are virtual tissues with nitrogen washout half-times of 400 to 615 min. CONCLUSION: Our model provides a new approach to predicting DCS risk for various decompression profiles. By demonstrating the dependence of DCS risk on body tissue parameters, the model explains why resistance to DCS in mammals increases with a lower body mass and greater specific blood flow in tissues.

Decompression Sickness↗
PubMed1988

Decompression sickness and bubble formation in females exposed to a simulated 7.8 psia suit environment.

The purpose of this study was to measure female susceptibility to decompression sickness (DCS) during simulated extravehicular activity (EVA) at a candidate (7.8 psia) suit pressure. Thirty female volunteer subjects, in groups of three, were exposed to three consecutive daily EVA simulations at 7.8 psia (5,031 m altitude equivalent) continuously for 6 h. During each altitude exposure, the subjects breathed a gas mixture of 50% oxygen/50% nitrogen, and participated in exercise workloads similar to those expected to be experienced by astronauts during a typical EVA scenario. Precordial Doppler bubble monitoring was accomplished after each cycle of exercise workload simulations. During at least 1 of the 3 days (d) of exposure, 43% of the subjects experienced intravenous bubbling. Of the 30 subjects, 17 (57%) did not experience detectable bubbling on any of the 3 d of exposure and 5 (17%) developed decompression sickness (DCS) during the study. Two cases were delayed, occurring after recompression to ground level; and three subjects required hyperbaric oxygen treatment. The results of this study suggest that female subjects may suffer more delayed DCS symptoms, necessitating hyperbaric oxygen treatment, than their male counterparts under the same experimental conditions. Female subjects did not experience intravenous bubbling as frequently as male subjects when exposed to these study conditions.

Adult↗
PubMed1999

Exercise-induced altitude decompression sickness.

BACKGROUND: It has been known since World War II that exercise at altitude increases incidence of decompression sickness (DCS). However, data on the effects of specific exercise types at altitude are lacking. This research focused on the relative hazards of exercise without motion (isometric, straining) vs. dynamic exercise involving motion. The study also compared arm vs. leg exercise. METHODS: There were 32 healthy male subjects exposed, while resting, to 29,500 ft (8992 m) for 4 h or until DCS occurred, at which time they were brought to ground level. If the subject developed DCS on this exposure, he was exposed in successive months to lower altitudes, using the same procedure, until the subject was free of symptoms for the 4-h exposure. At this symptom-free altitude, as low as 20,000 ft (6096 m), the subject performed isometric arm, isometric leg, dynamic arm and dynamic leg exercises at less than 10% of maximal oxygen consumption, each during separate exposure months. Precordial venous gas emboli (VGE) were monitored every 20 min during each exposure with a Hewlett-Packard SONOS 1000 Echo Imaging System. RESULTS: Dynamic arm, dynamic leg, isometric arm, and isometric leg exercise induced DCS in 50%, 38%, 41% and 31% of the subjects, respectively. VGE incidence varied from 47-66%. No significant differences in DCS or VGE were found. CONCLUSIONS: Under our test conditions, there was no difference between dynamic and isometric exercise in eliciting DCS. Exercise during exposure to the symptom-free altitude for 4 h produced a 40% incidence DCS.

Adult↗
PubMed1995

Decompression sickness: recovery after delayed recompression.

Two patients with Type II decompression sickness with good recovery following delayed recompression therapy are described. These are the first two cases of successful recompression therapy for this diving hazard to be reported in Sri Lanka. The risks taken by Sri Lankan divers and prevention of diving related medical disorders are discussed.

Adult↗
PubMed1986

Intramuscular diclofenac sodium as adjuvant therapy for type I decompression sickness: a case report.

The residual pain of type I decompression sickness (limb bends) occurring despite recompression therapy is due to an acute inflammatory reaction in the soft tissue around the joint. This case history reports an excellent response in resolving residual pain by the use of an intramuscular injection of the nonsteroidal anti-inflammatory drug, diclofenac sodium. The theoretical reasons for this are discussed.

Adult↗
PubMed2006

Nitrogen load in rats exposed to 8 ATA from 10-35 degrees C does not influence decompression sickness risk.

INTRODUCTION: Environmental temperature is commonly thought to modulate decompression sickness (DCS) risk, but the literature is mixed regarding which conditions elicit the greatest risk. If temperature is a risk factor, then managing thermal exposure may reduce DCS incidence. We analyzed whether hot or cold conditions during or immediately after a hyperbaric exposure altered DCS incidence in a rat model. METHODS: Rats (eight groups of five animals in each of nine conditions; mean body mass +/- SD = 259.0 +/- 9.2 g) were placed in a dry chamber that was pressurized with air to 70 m (8 ATA) for 25 min, followed by rapid (< 30 s) decompression under a series of temperature conditions (35 degrees, 27 degrees, or 10 degrees C during compression; 35 degrees, 20 degrees, or 10 degrees C post-decompression). Animals were observed for 30 min post-decompression for signs of DCS. DCS incidence in the 27 degrees C compression/20 degrees C post-decompression group was 50% by design. Data from all nine groups of paired temperature conditions were compared with each other using analysis of variance, Chi-square tests, and logistic regression. RESULTS: No significant differences in DCS incidence were found among the groups (30-52.5% DCS incidence per group, 42% DCS incidence overall). DISCUSSION AND CONCLUSIONS: This animal model emphasized potential temperature effects attributable to tissue N2 load acquired during compression; there was no evidence that environmental temperature from 10-35 degrees C during or post-dive modulated DCS incidence. It remains to be determined if temperature modulates DCS risk as a function of variable N2 elimination rates.

Animals↗
PubMed1997

A case of spinal cord decompression sickness presenting as partial Brown-Sequard syndrome.

Type II decompression sickness (DCS) usually manifests as myelopathy; however, there are no reports of Brown-Sequard syndrome in association with diving accidents. We report a 35-year-old man who developed type II DCS presenting as partial Brown-Sequard syndrome. MRI of the thoracic spine revealed two punctate foci of increased signal intensity in the right T6 spinal cord.

Adult↗
PubMed1997

Prevention of decompression sickness during extravehicular activity in space: a review.

Extended and more frequent extravehicular activity (EVA) is planned in NASA's future space programs. The more EVAs are conducted, the higher the incidence of decompression sickness (DCS) that is anticipated. Since Japan is also promoting the Space Station Freedom project with NASA, DCS during EVA will be an inevitable complication. The author reviewed the pathophysiology of DCS and detailed four possible ways of preventing decompression sickness during EVA in space: (1) higher pressure suit technology; (2) preoxygenation/prebreathing; (3) staged decompression; and (4) habitat or vehicle pressurization. Among these measures, development of zero-prebreathe higher pressure suit technology seems most ideal, but because of economic and technical reasons and in cases of emergency, other methods must also be improved. Unsolved problems like repeated decompression or oxygen toxicity were also listed.

Aerospace Medicine↗
PubMed1984

The functional and biochemical changes of platelets in experimental decompression sickness of rabbits.

The functional and biochemical changes of rabbit platelets were studied after an exposure to 6 ATA (atmosphere absolute) for 40 min (bottom time). Platelet counts significantly decreased after the decompression. Platelet aggregation induced by collagen was not changed. Although there was no change in the mode volume of platelets after the decompression, the transient appearance of circulating smaller or fragmented platelets suggested a random over-destruction of platelets. Whole and releasable adenine nucleotide contents of platelets were decreased significantly after the decompression. There were no significant changes in cytoplasmic adenine nucleotide contents. Therefore, in decompression sickness, the circulating platelets behaved similarly to those in acquired storage pool disease. Platelet thrombi were found in the pulmonary arteries. These findings suggest that circulating air-bubbles interact with platelets, causing the platelet release reaction, and these activated platelets participate in the formation of thrombi in experimental decompression sickness.

Adenine Nucleotides↗
PubMed2001

Altitude decompression sickness. Case presentation.

The in-flight altitude-related decompression sickness (DCS) is not as common as DCS occurring after working or recreational diving, or, at least, it is not commonly described in the medical literature. Though modern aircraft are safer and more reliable, occupants are still subject to the stress of high altitude flight, and altitude DCS still represents a risk to the occupants, mostly if they are exposed to altitudes of 25,000 ft or higher. The authors report their experience about two different accidents involving a US Air Force pilot and a navigator, treated at the Service of Hyperbaric Medicine at Landspitallin Fossvogur, the University of Reykjavik City Hospital, Iceland, because of occurrence of type II altitude-related DCS. A US Navy Oxygen Treatment Table 6 was successfully applied in both cases. Also considered are some aspects related to physiopathology, clinical presentation and therapy of DCS, with particular regard to the occurrence of DCS during flight.

Adult↗
PubMed2004

Altitude decompression sickness symptom resolution during descent to ground level.

INTRODUCTION: Altitude decompression sickness (DCS) is a health risk associated with the conduct of high altitude airdrop operations, high altitude reconnaissance, future fighter operations, hypobaric chamber training, unpressurized flight, and extravehicular activity (EVA) in space. The treatment for DCS includes the provision of 100% oxygen (O2) at ground level (GLO) and/or hyperbaric oxygen therapy (HBO). In this paper we examine the effect of repressurization to ground level from hypobaric conditions on DCS symptoms. Timely recompression (descent at first recognition of any DCS symptom) may be a safe, effective treatment for the large majority of DCS symptoms. METHODS: Data from altitude chamber exposures recorded in the Air Force Research Laboratory (AFRL) Altitude DCS Database were reviewed to determine the level of recompression required for complete resolution of 1,699 observed symptoms. RESULTS: Of the 1,699 DCS symptoms reviewed, 66 (3.9%) resolved at altitude, 117 (6.9%) resolved at ground level, and 1,433 (84.3%) resolved during descent. Increasing the pressure by 138 mmHg from the altitude of exposure where symptoms occurred resolved roughly 50% of symptoms. Little resolution of symptoms was noted with recompressions of < 50 mmHg. The greatest rate of symptom resolution occurred with recompressions of 50-250 mmHg. CONCLUSION: These findings support the concept that descent and postflight, ground-level oxygen may be sufficient to relieve the majority of altitude DCS symptoms. HBO may be reserved for serious, recurring, delayed, or refractory symptoms. The findings also suggest a need for further study of DCS symptom resolution.

Aerospace Medicine↗
PubMed2004

Central nervous system decompression sickness and venous gas emboli in hypobaric conditions.

INTRODUCTION: Altitude decompression sickness (DCS) that involves the central nervous system (CNS) is a rare but potentially serious condition. Identification of early symptoms and signs of this condition might improve treatment. METHODS: We studied data from 26 protocols carried out in our laboratory over the period 1983-2003; all were designed to provoke DCS in a substantial proportion of subjects. The data set included 2843 cases. We classified subject-exposures that resulted in DCS as: 1) neurological DCS of peripheral and/or central origin (NEURO); 2) a subset of those that involved only the CNS (CNS); and 3) all other cases, i.e., DCS cases that did not have a neurological component (OTHER). For each case, echo imaging data were used to document whether venous gas emboli (VGE) were present, and their level was classified as: 1) any level, i.e., Grade 1 or higher (VGE-1); and 2) high level, Grade 4 (VGE-4). RESULTS: There were 1108 cases of altitude DCS in the database; 218 were classified as NEURO and 49 of those as CNS. VGE-1 were recorded in 83.8% of OTHER compared with 58.7% of NEURO and 55.1% of CNS (both p < 0.001 compared with OTHER). The corresponding values for VGE-4 were 48.8%, 37.0%, and 34.7% (p < 0.001, compared to OTHER). Hyperbaric oxygen (HBO) was used to treat about half of the CNS cases, while all other cases were treated with 2 h breathing 100% oxygen at ground level. DISCUSSION: Since only about half of the rare cases of hypobaric CNS DCS cases were accompanied by any level of VGE, echo imaging for bubbles may have limited application for use as a predictor of such cases.

Altitude↗