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At least 235 records · Page 13Linked to original sources
PubMed1997

Utility of Doppler-detectable microbubbles in the diagnosis and treatment of decompression sickness.

BACKGROUND: Doppler-detectable microbubbles (DMB) are frequently used to evaluate altitude decompression stress. However, the role of DMB in the therapy of decompression sickness (DCS) has not been examined. HYPOTHESIS: The ability of Doppler to detect microbubbles during decompression (Doppler test) may be used in the diagnosis of DCS, and to aid clinical decisions about treatment options for DCS. METHODS: We examined the data on DMB and symptoms from NASA Database on DCS (n = 516). The accuracy of Doppler test was obtained from the Receiver Operating Characteristic (ROC) for DMB (grades I through IV), and efficacy was obtained by calculating predictive or post-test probabilities. Threshold analysis was used to obtain the probabilities for testing and/or treatment decisions. RESULTS: The Doppler test was useful for both screening and confirming DCS, when different criteria (grade I for screening; grade IV for confirming) were used for a positive test. Calculation of predictive values and threshold analysis showed that: 1) early recompression was the therapy of choice when post-test probability of disease was > 0.25 in individuals with non-specific pain at altitude, and early recompression with 100% oxygen for 2 h at site level was optimal therapy when this probability was > 0.33; 2) hyperbaric therapy was optimal when post-test probability was > 0.04 in individuals with uncertain symptoms post-flight. CONCLUSIONS: The Doppler test was of greater utility in excluding DCS than confirming its presence, and was useful in making therapeutic decisions on DCS when confronted with non-specific symptoms at altitude.

Aerospace Medicine↗
PubMed1999

[Decompression sickness after diving and following flying].

A case of delayed symptoms of decompression sickness (DCS) after diving and flying is reported. The diver presented with classical signs of type 2 DCS, probably caused by air travel 16 hours after SCUBA diving. Treatment with hyperbaric oxygen (HBO) in a decompression chamber was successful. Guidelines to prevent DCS for recreational divers who plan to fly after diving are presented.

Adult↗
PubMed1996

Case report on a diver with type II decompression sickness and viral meningitis.

A 33-yr-old man came to the emergency department with the chief complaint of a severe headache and decreased sensation in his right hand following a deep dive on scuba. Physical examination before recompression treatment was remarkable only for hypesthesia on the right hand. We diagnosed type II decompression sickness and the patient underwent standard recompression therapy. The patient experienced near-complete resolution of his symptoms, his only residual complaint being that of neck pain with head movement. To investigate other causes of headache, a computed tomography of the head was performed which was normal, and a lumbar puncture was performed which was consistent with viral meningitis. This is the first reported case of recompression treatment on a patient with viral meningitis and decompression sickness.

Adult↗
PubMed2001

Decompression sickness risk reduced by native intestinal flora in pigs after H2 dives.

Decompression sickness (DCS) risk following a simulated dive in H2 was lower in pigs with a native intestinal flora that metabolized H2. Pigs (n = 27; 19.4 +/- 0.2 kg body mass) were placed in a chamber that was pressurized to 22.2-25.5 atm (absolute; 2.2-2.6 MPa) with 84-93% H2 for 3 h. Chamber concentrations of O2, H2, He, N2, and CH4 were monitored by gas chromatography. Release of CH4 from the pigs indicated that intestinal microbes had metabolized H2 After decompressing to 11 atm, the pigs were observed for DCS. Animals with DCS released significantly less (P < 0.05) methane (0.53 +/- 0.37 ppm CH4; n = 5) than those without DCS (1.40 +/- 0.17 ppm CH4; n = 22). The DCS risk reduction was attributed to the loss of roughly 12% of the total volume of H2 that could be stored in the tissues of the pigs. Thus, H2 metabolism by the native intestinal flora of pigs may protect against DCS following a simulated H2 dive.

Animals↗
PubMed1978

Susceptibility of fetal sheep to acute decompression sickness.

Studies were conducted to determine the susceptibility of the fetus to decompression sickness. Sheep were used because fetal and maternal circulation of sheep and human placentas are dynamically similar. Seven sheep that were within three weeks of parturition were used. A Doppler ultrasonic transducer was placed around an umbilical artery of the fetus in utero and the electrical leads were exteriorized. Umbilical artery blood flow could thus be monitored together with any bubbles appearing in that part of the fetal circulation. Results of 17 dives showed that exposing the mother to a 100-fsw, 25-min standard no-decompression dive produced massive air emboli in the fetus, though no bubbles were detected in the maternal circulation either by Doppler or visual inspection. An 80-fsw dive for 40 min caused an occasional bubble to appear in the fetus. Sixty-fsw dives for 60 and 70 min, respectively, did not produce bubbles in the fetal circulation.

Animals↗
PubMed2002

Decompression sickness during construction of the Great Belt Tunnel, Denmark.

Thirteen cases of decompression sickness (DCS) occurred during the construction of the 8-km long railway tunnel under the Great Belt in Denmark between January 1992 and February 1996. 320 compressed air workers were subjected to 9018 pressure exposures in four tunnel boring machines. Overall DCS incidence was 0.14%. Working pressures ranged between 0.25 bar (1.25 atm abs or 126.3 kPa) and 2.95 bar (3.91 atm abs or 396.3 kPa) and working times ranged between 2 minutes and 339 minutes. During the first 1798 pressure exposures 7 DCS cases occurred using French air decompression tables from 1974. The following 7220 exposures were then decompressed in accordance with the newly issued French air decompression tables of 1992. After changing schedules 6 DCS cases occurred and DCS incidence was reduced to 0.08%. Two of the first seven DCS cases had permanent residual symptoms after recompression treatment. All DCS cases, except one, occurred among the 30% of exposures that imposed the greatest decompression stress. DCS incidence among these exposures was 0.42%.

Adult↗
PubMed1997

Helium and oxygen treatment of severe air-diving-induced neurologic decompression sickness.

BACKGROUND: The use of helium and oxygen recompression treatment of neurologic decompression sickness (DCS) has several theoretical advantages over the traditionally used air and oxygen recompression tables that have been confirmed by findings from recent animal experiments. OBJECTIVES: To evaluate the outcome of patients with neurologic DCS who had been treated with a helium-oxygen protocol and to compare it with that of a retrospective control group that was treated with air-oxygen tables. DESIGN: The study and control groups included 16 and 17 diving casualties, respectively. The severity of neurologic DCS was estimated according to a 9-point scale weighting motor, sensory, and sphincter control functions. The study group was treated with a helium-oxygen decompression protocol, and the control group was treated with the US Navy air-oxygen Table 6 or 6A. Persistent residual dysfunction was treated in both groups with daily hyperbaric oxygen sessions, at 2.5 absolute atmospheres for 90 minutes, until no further clinical improvement was noted. SETTING: The Israel Naval Medical Institute (Israel's national hyperbaric referral center), Haifa. RESULTS: Significant clinical score increments were found for both the helium-oxygen- and air-oxygen-treated groups: 2.8 +/- 2.4 (mean +/- SD) and 7.4 +/- 1.1 at presentation vs 7.6 +/- 2.1 and 8.1 +/- 1.5 at discharge, respectively (P < .001 and P = .005, respectively). Although the score at presentation was significantly lower for the helium-oxygen-treated group (P < .001), no difference was found between the groups' average outcome scores. While most of the improvement in the patients in the study group could be attributed to the helium-oxygen treatment and not to the supplemental hyperbaric oxygen, in the control group, no significant difference could be demonstrated between the scores at presentation and at completion of the air-oxygen recompression table. In 5 patients who were treated with the use of the air-oxygen tables, deterioration was observed after recompression. No deterioration or neurologic DCS relapse occurred in the helium-oxygen-treated group. CONCLUSION: The results suggest an advantage of helium-oxygen recompression therapy over air-oxygen tables in the treatment of neurologic DCS.

Decompression Sickness↗
PubMed1990

Altitude decompression sickness: hyperbaric therapy results in 528 cases.

We reviewed 528 cases of decompression sickness (DCS) resulting from altitude exposure (either aircraft or altitude chamber) during the period 1 January 1977 through 31 December 1986, and treated with hyperbaric therapy. Data collected include age, sex, date and place of origin, duty position, type of exposure, altitude, diagnosis, treatment, and result. Analysis of the data described maximum altitudes of exposure, time to onset of symptoms, diagnosis, and the treatment tables used. Significant results include an increased incidence of altitude DCS requiring hyperbaric therapy among females (relative risk for females is 4.3 times that of males), no significant difference in incidence rates between duty positions in the altitude chamber exposures reviewed, and confirmation of the efficacy of hyperbaric oxygen therapy.

Adult↗
PubMed1987

Hormonal changes during decompression sickness.

Changes in plasma hormone levels were studied in anesthetized dogs during decompression sickness. Hormone levels were measured in 4 groups: control (no dive, n = 9); air group (air dive, ventilated with air postdive, n = 6); helium-oxygen (He-O2) group (air dive, ventilation changed to He-O2 at 30 min postdive, n = 9); nonsurvivor group (air dive, died within 30 min postdive, n = 9). Dived animals were subjected to repetitive dives until pulmonary artery pressure doubled. Plasma epinephrine (Epi) and norepinephrine (NE) concentrations rapidly increased postdive in all animals. Serum angiotensin-converting enzyme (ACE) activity increased postdive in the He-O2 group only, and these increases were small. Diving did not alter serum concentrations of cortisol, thyroxine (T4), or triiodothyronine (T3); however, T4 and T3 fell in all animals, probably as a consequence of anesthesia. He-O2 breathing did not affect concentrations of Epi, NE, cortisol, T4, T3, or serum ACE activity.

Animals↗
PubMed2006

A latent class model to assess error rates in diagnosis of altitude decompression sickness.

BACKGROUND: Prospective testing of denitrogenation protocols to reduce the risk of decompression sickness (DCS) in astronauts requires pre-defined accept and reject criteria. We assume that the end-point of a test, the presence or absence of signs and symptoms attributable to DCS, is unequivocal. However, diagnosis of DCS is not perfect, nor is there is a gold standard to assess diagnosis error rates. These error rates could cause consistent bias in the decision to accept or reject proposed protocols. We used a Latent Class Model (LCM) incorporating inter-rater agreement to estimate false-positive and negative rates of DCS diagnosis for each of six symptomatic (covariate) strata. METHODS: Case descriptions from 135 reports collected since 1982 were available with 103 diagnosed as DCS (73.1%). There were 3 subsets of 45 descriptions that were randomly selected, information about the original diagnosis omitted, and were sent to 15 physicians (raters), all experts in altitude DCS. Subsets were diagnosed for DCS by either four, five, or six raters. We then used a LCM to estimate false-positive and false-negative error rates for the original NASA test diagnosis, even though a gold standard was not available. RESULTS: Estimates of false-positive rates in the NASA diagnoses ranged from 13% to 83% and from 1% to 32% for false-negative rates over the six strata of symptomatic response variables. CONCLUSIONS: Our findings suggest that use of current DCS diagnostic outcomes as if they were error free would likely produce an inflated rejection rate of acceptable protocols in future testing if adjustments are not made.

Adult↗
PubMed2002

Pulmonary decompression sickness at altitude: early symptoms and circulating gas emboli.

INTRODUCTION: Pulmonary altitude decompression sickness (DCS) is a rare condition. 'Chokes' which are characterized by the triad of substernal pain, cough, and dyspnea, are considered to be associated with severe accumulation of gas bubbles in the pulmonary capillaries and may rapidly develop into a life-threatening medical emergency. This study was aimed at characterizing early symptomatology and the appearance of venous gas emboli (VGE). METHODS: Symptoms of simulated-altitude DCS and VGE (with echo-imaging ultrasound) were analyzed in 468 subjects who participated in 22 high altitude hypobaric chamber research protocols from 1983 to 2001 at Brooks Air Force Base, TX. RESULTS: Of 2525 subject-exposures to simulated altitude, 1030 (41%) had symptoms of DCS. Only 29 of those included DCS-related pulmonary symptoms. Of these, only 3 subjects had all three pulmonary symptoms of chokes; 9 subjects had two of the pulmonary symptoms; and 17 subjects had only one. Of the 29 subject-exposures with pulmonary symptoms, 27 had VGE and 21 had severe VGE. The mean onset times of VGE and symptoms in the 29 subject-exposures were 42 +/- 30 min and 109 +/- 61 min, respectively. In 15 subjects, the symptoms disappeared during recompression to ground level followed by 2 h of oxygen breathing. In the remaining 14 cases, the symptoms disappeared with immediate hyperbaric oxygen treatment. CONCLUSIONS: Pulmonary altitude DCS or chokes is confirmed to be a rare condition. Our data showed that when diagnosed early, recompression to ground level pressure and/or hyperbaric oxygen treatment was 100% successful in resolving the symptoms.

Adult↗
PubMed2002

The effect of simulated weightlessness on hypobaric decompression sickness.

BACKGROUND: A discrepancy exists between the incidence of ground-based decompression sickness (DCS) during simulated extravehicular activity (EVA) at hypobaric space suit pressure (20-40%) and crewmember reports during actual EVA (zero reports). This could be due to the effect of gravity during ground-based DCS studies. HYPOTHESIS: At EVA suit pressures of 29.6 kPa (4.3 psia), there is no difference in the incidence of hypobaric DCS between a control group and group exposed to simulated weightlessness (supine body position). METHODS: Male subjects were exposed to a hypobaric pressure of 29.6 kPa (4.3 psi) for up to 4 h. The control group (n = 26) pre-oxygenated for 60 min (first 10 min exercising) before hypobaric exposure and walking around in the altitude chamber. The test group (n = 39) remained supine for a 3 h prior to and during the 60-min pre-oxygenation (also including exercise) and at hypobaric pressure. DCS symptoms and venous gas emboli (VGE) at hypobaric pressure were registered. RESULTS: DCS occurred in 42% in the control and in 44% in simulated weightlessness group (n.s.). The mean time for DCS to develop was 112 min (SD +/- 61) and 123 min (+/- 67), respectively. VGE occurred in 81% of the control group subjects and in 51% of the simulated weightlessness subjects (p = 0.02), while severe VGE occurred in 58% and 33%, respectively (p = 0.08). VGE started after 113 min (+/- 43) in the control and after 76 min (+/- 64) in the simulated weightlessness group. CONCLUSIONS: No difference in incidence of DCS was shown between control and simulated weightlessness conditions. VGE occurred more frequently during the control condition with bubble-releasing arm and leg movements.

Adolescent↗
PubMedDate not supplied

[Probability of altitude decompression sickness following a drop in pressure from 840 to 308 mm Hg].

The decompression from the hyperbaric air atmosphere with the pressure 840+/-5 mm Hg and subsequent 40 min exposure to the hypobaric atmosphere 308+/-1 mm Hg containing 40 to 95% O2 cause a decompression disease in 5-40% cases. The probability of the disease depends on the duration of nitrogen saturation at an increased pressure, physical fitness and individual susceptibility to decompression sickness.

Adult↗
PubMed1975

Prevention of decompression sickness during a simulated space docking mission.

This study has shown that repetitive exchanges between the American Apollo space vehicle atmosphere of 100% oxygen at 5 psia (258 torr) and the Russian Soyuz spacecraft atmosphere of 30% oxygen-70% nitrogen at 10 psia (523 torr), as simulated in altitude chambers, will not likely result in any form of decompression sickness. This conclusion is based upon the absence of any form of bends in seven crewmen who participated in 11 tests distributed over three 24-h periods. During each period, three transfers from the 5 to the 10 psia environments were performed by simulating passage through a docking module which served as an airlock where astronauts and cosmonauts first adapted to each other's cabin gases and pressures before transfer. Biochemical tests, subjective fatigue scores, and the complete absence of any form of pain were also indicative that decompression sickness should not be expected if this spacecraft transfer schedule is followed.

17-Hydroxycorticosteroids↗
PubMed1988

Fatal pulmonary decompression sickness: a case report.

A 51-year-old civilian pilot flying a high performance aircraft for the USAF presented for medical attention approximately 1.5 hours after developing substernal chest pain and dyspnea while flying unpressurized at FL 280 (8,534 meters) for 30 minutes. In spite of recompression about 3 hours later, the pilot expired while ascending from 6 atmospheres, 2.5 hours into the dive. This represents the first reported fatality due to altitude-induced decompression sickness since 1959. Pathologically, this case is similar to cases presented in the past. In addition, this case serves to reemphasize many of the "risk factors" for decompression sickness, especially age and obesity. Furthermore, the evidence presented points to maintaining only the highest standards of physical health in those who fly high performance aircraft.

Decompression Sickness↗
PubMed2004

Exercise and nitric oxide prevent bubble formation: a novel approach to the prevention of decompression sickness?

Nitrogen dissolves in the blood during dives, but comes out of solution if divers return to normal pressure too rapidly. Nitrogen bubbles cause a range of effects from skin rashes to seizures, coma and death. It is believed that these bubbles form from bubble precursors (gas nuclei). Recently we have shown that a single bout of exercise 20 h, but not 48 h, before a simulated dive prevents bubble formation and protects rats from severe decompression sickness (DCS) and death. Furthermore, we demonstrated that administration of N(omega)-nitro-l-arginine methyl ester, a non-selective inhibitor of NO synthase (NOS), turns a dive from safe to unsafe in sedentary but not exercised rats. Therefore based upon previous data an attractive hypothesis is that it may be possible to use either exercise or NO-releasing agents before a dive to inhibit bubble formation and thus protect against DCS. Consequently, the aims of the present study were to determine whether protection against bubble formation in 'diving' rats was provided by (1) chronic and acute administration of a NO-releasing agent and (2) exercise less than 20 h prior to the dive. NO given for 5 days and then 20 h prior to a dive to 700 kPa lasting 45 min breathing air significantly reduced bubble formation and prevented death. The same effect was seen if NO was given only 30 min before the dive. Exercise 20 h before a dive suppressed bubble formation and prevented death, with no effect at any other time (48, 10, 5 and 0.5 h prior to the dive). Pre-dive activities have not been considered to influence the growth of bubbles and thus the risk of serious DCS. The present novel findings of a protective effect against bubble formation and death by appropriately timed exercise and an NO-releasing agent may form the basis of a new approach to preventing serious decompression sickness.

Animals↗
PubMed1976

Air embolism and decompression sickness in scuba divers.

The recognition and prompt treatment of air embolism and decompression sickness by the emergency physician can do much to reverse the unfavorable outcome of these two medical emergencies. Recognition depends on the physician maintaining a high index of suspicion. While the primary treatment for these disorders is recompression, other forms of therapy are outlined which must be instituted promptly.

Decompression Sickness↗