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At least 811 records · Page 45Linked to original sources
PubMed2003

Optic neuropathy following an altitude exposure.

This case report describes a 20-yr-old man who presented with retro-orbital pain and blurred vision in his left eye 3 wk after an altitude exposure in a hypobaric chamber. He was found to have significant deficits in color vision and visual fields consistent with an optic neuropathy in his left eye. The patient was diagnosed with decompression sickness and treated with hyperbaric oxygen with a U.S. Navy Treatment Table VI. All signs and symptoms resolved with a single hyperbaric oxygen treatment but recurred. A head MRI revealed a left frontoethmoid sinus opacity. A concomitant sinusitis was diagnosed. The patient had full resolution of symptoms after a total of four hyperbaric oxygen treatments and antibiotic therapy at 6-wk follow-up. Although a para-infectious etiology for this patient's optic neuropathy cannot be excluded, his history of altitude exposure and significant, rapid response to hyperbaric oxygen treatment strongly implies decompression sickness in this case.

Adult↗
PubMed1982

Hyperbaric medicine: state of the art, 1979.

An attempt has been made to determine the clinical usage of hyperbaric oxygen therapy at 83 North American hyperbaric treatment centers from 1971 to 1978. Questions were asked about the conditions or diseases treated, yearly case load for each condition, location of functional hyperbaric chambers, types of chambers used, operating costs, and personnel requirements. Commercial diving chambers that treat decompression sickness and air embolism from diving accidents were included in the last two years of the survey. Fifty-seven responses were received; 30 treatment centers had multiple chambers, 24 had monoplace chambers, and three had both types of chambers. A total of 10,942 patients were treated during the eight-year survey period; 8,408 patients (76%) had category I or II conditions, as defined by the Undersea Medical Society. Of the 20 most commonly treated conditions, 17 were in category I or II. During the survey period, the use of hyperbaric oxygen increased, particularly in the treatment of decompression sickness, carbon monoxide poisoning, and osteomyelitis and osteoradionecrosis.

Brain Ischemia↗
PubMed1994

Influence of carbon dioxide on venous gas emboli production during altitude decompression in goats.

Goats (N = 7) were decompressed from 1,500 m to 9,150, 9,750, or 10,400 m simulated altitude while breathing CO2 tensions of 0, 15, 30, or 46 mm Hg in O2 during 15-min prebreathing and 30-min peak altitude exposures. Risk of decompression sickness was determined by detecting venous gas emboli (VGE) in the pulmonary artery with an implanted Doppler cuff. VGE scores were calculated using the ratio of cardiac cycles containing VGE to total cardiac cycles. The VGE scoring methodology proved sensitive to standard treatment effects (air versus O2 prebreathing). No significant change in VGE scores as a result of varying the inspired CO2 level was detected. Further, no significant change in cardiac index occurred during the various CO2 exposures, and VGE scores were not correlated with cardiac index. Ground-level studies revealed the tension of end-tidal CO2 was significantly elevated at all three levels of inspired CO2, but no change in cardiac index was observed. Short-duration breathing of CO2 in oxygen failed to significantly reduce the risk of decompression sickness as assessed by VGE production.

Altitude↗
PubMed2005

Postural stability before and after hyperbaric oxygen treatment.

OBJECTIVE: The purpose of this study was to determine the effect of hyperbaric oxygenation (HBO) on postural stability in healthy volunteers. The study was performed in accordance with treatment protocols for divers' decompression sickness and carbon monoxide poisoning. METHODS: Twenty-one healthy male divers, aged 31 +/- 6.88 years (mean +/- SD), were tested with quantitative Romberg's test before and after HBO (90 min in a pressure chamber at an ambient pressure of 253 kPa, approximately 15 m of sea water, breathing pure oxygen). The quantitative Romberg's test is a calculation of the average sway for 50 s. RESULTS: No difference was found between sway before and after the HBO (P < 0.05), i.e. we were unable to show that the results of quantitative Romberg's test are affected by HBO. Thus, the quantitative Romberg's test may be a valuable tool in evaluating patients with decompressions sickness, carbon monoxide intoxication and other neurological diseases normally treated with HBO.

Adult↗
PubMed2002

Ascent rate, age, maximal oxygen uptake, adiposity, and circulating venous bubbles after diving.

Decompression sickness in diving is recognized as a multifactorial phenomenon, depending on several factors, such as decompression rate and individual susceptibility. The Doppler ultrasonic detection of circulating venous bubbles after diving is considered a useful index for the safety of decompression because of the relationship between bubbles and decompression sickness risk. The aim of this study was to assess the effects of ascent rate, age, maximal oxygen uptake (VO(2 max)), and percent body fat on the production of bubbles after diving. Fifty male recreational divers performed two dives at 35 m during 25 min and then ascended in one case at 9 m/min and in the other case at 17 m/min. They performed the same decompression stops in the two cases. Twenty-eight divers were Doppler monitored at 10-min intervals, until 60 min after surfacing, and the data were analyzed by Wilcoxon signed-rank test to compare the effect of ascent rate on the kinetics of bubbles. Twenty-two divers were monitored 60 min after surfacing. The effect on bubble production 60 min after surfacing of the four variables was studied in 47 divers. The data were analyzed by multinomial log-linear model. The analysis showed that the 17 m/min ascent produced more elevated grades of bubbles than the 9 m/min ascent (P < 0.05), except at the 40-min interval, and showed relationships between grades of bubbles and ascent rate and age and interaction terms between VO(2 max) and age, as well as VO(2 max) and percent body fat. Younger, slimmer, or aerobically fitter divers produced fewer bubbles compared with older, fatter, or poorly physically fit divers. These findings and the conclusions of previous studies performed on animals and humans led us to support that ascent rate, age, aerobic fitness, and adiposity are factors of susceptibility for bubble formation after diving.

Adipose Tissue↗
PubMedDate not supplied

[The ultrasonic location of gas bubbles in the human bloodstream during work in a spacesuit].

The results of testing a procedure of ultrasonic location of the gas bubbles (GB) in man during space suit operations to simulate an extravehicular activity (EVA) are presented. Doppler echotachocardiograph "Rhythm" operating at ultrasonic frequency of 1.76 mHz was used as a GB detector. The device "Rhythm" integrated with a special flat transducer of 23 mm in diameter and 4 mm in width was positioned on the subject chest above the pulmonary artery projection. During 4-6 hour human operations while wearing pressurized (276-290 mm Hg) space suit, in 7 of 12 tests performed a stable and qualitative signal of the arterial blood flow in the lungs was recorded. In case of an unstable signal, in order that its quality be improved the posture of test subject was changed and the signal was recorded during a short-term expired breath-holding. Cardiac GB formation was noted during 6 tests in 2 subjects. The first GBs appeared at the 30th, 33rd, 70th, 111th, 114th and 180th minute after producing an operating reduced pressure in space suit. The time of GB detection on the average was 89.7 min. The maximum intensity of GB signal was 3-4 scores on Spencer's scale, but altitude decompression sickness symptoms did not develop in the test subjects. The risk of developing the altitude decompression sickness as opposed to the results of control experiments without use of space suit is discussed.

Adult↗
PubMed2004

Aerobic exercise before diving reduces venous gas bubble formation in humans.

We have previously shown in a rat model that a single bout of high-intensity aerobic exercise 20 h before a simulated dive reduces bubble formation and after the dive protects from lethal decompression sickness. The present study investigated the importance of these findings in man. Twelve healthy male divers were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min(-1) breathing air and remaining at pressure for 80 min. The ascent rate was 9 m min(-1) with a 7 min stop at 130 kPa. Each diver underwent two randomly assigned simulated dives, with or without preceding exercise. A single interval exercise performed 24h before the dive consisted of treadmill running at 90% of maximum heart rate for 3 min, followed by exercise at 50% of maximum heart rate for 2 min; this was repeated eight times for a total exercise period of 40 min. Venous gas bubbles were monitored with an ultrasonic scanner every 20 min for 80 min after reaching surface pressure. The study demonstrated that a single bout of strenuous exercise 24h before a dive to 18 m of seawater significantly reduced the average number of bubbles in the pulmonary artery from 0.98 to 0.22 bubbles cm(-2)(P= 0.006) compared to dives without preceding exercise. The maximum bubble grade was decreased from 3 to 1.5 (P= 0.002) by pre-dive exercise, thereby increasing safety. This is the first report to indicate that pre-dive exercise may form the basis for a new way of preventing serious decompression sickness.

Adult↗
PubMed1984

Optimum weights for commercial divers.

Obesity is one of the factors which increase the risk of decompression sickness. It has been suggested that any diver whose weight is more than 20% in excess of that derived from currently accepted tables should therefore be stopped from diving until he has lost enough weight. Published tables of average and standard weights for men, however, are unsuitable for application to men recruited for commercial diving, as the populations on which the tables were based differ in important respects from divers. Furthermore, the tables may assume that men are weighed and measured clothed and in shoes, whereas in most medical examinations the measurements are made on men without shoes and partially clad . Analysis of weight measurements of 1520 divers whose records are in the Decompression Sickness Central Registry in Newcastle upon Tyne suggests that divers as a group are substantially heavier than other populations on whom height-weight tables have been based. A table derived from American data of 1935-53 is often used as a guide. If this table is used the percentage of divers rejected as overweight may be as high as 13.6%. More recent and more appropriate data on heights and weights are required for use as reference standards for divers, or perhaps another measurement indicating obesity should be used.

Adult↗
PubMed2005

Evaluation of a porcine model to study in vivo platelet activation.

INTRODUCTION: In order to investigate if decompression sickness involves platelet activation an animal model was evaluated. MATERIALS AND METHODS: Twenty-four thiopentone-midazolam-fentanyl-anaesthetized pigs in four groups received 5-min infusions of adenosine diphosphate (25 mg/kg) or platelet activating factor (0.4 microg/kg). Groups 1 and 2 (adenosine diphosphate, n=6 and platelet activating factor, n=6) were studied for 30 min and then sacrificed. Groups 3 and 4 (adenosine diphosphate, n=6 and platelet activating factor, n=6) were sacrificed immediately afterwards to study short-term changes. Haemodynamics, platelet counts and post mortem lung platelet aggregates were registered. Groups 1 and 2 also had indium platelet labelling, lung scintigraphy and platelet accumulation index calculations performed. RESULTS: Adenosine diphosphate induced immediate and more profound transient shocks. Platelet and leukocyte count decreases and occurrences of post mortem lung platelet aggregates were significantly more profound in the 5-min adenosine diphosphate group (Group 3) than in the platelet activating factor group (Group 4). With platelet labelling there were positive platelet accumulation index trends in the 30-min adenosine diphosphate group (Group 1). Adenosine diphosphate also produced platelet aggregation in platelet-rich porcine plasma. Only adenosine diphosphate (an intermediate platelet agonist) showed signs of platelet activation when considering all platelet parameters. The model should be further evaluated with different bolus doses of adenosine diphosphate, but may be used to evaluate if gas bubbles introduced into the circulation (as with decompression sickness), or possibly if clinical drugs, might produce platelet activation in vivo.

Animals↗
PubMedDate not supplied

Diving injuries to the inner ear.

Most of the previous literature concerning otologic problems in compressed gas environments has emphasized middle ear barotrauma. With recent increases in commercial, military, and sport diving to deeper depths, inner ear disturbances during these exposures have been noted more frequently. Studies of inner ear physiology and pathology during diving indicate that the causes and treatment of these problems differ depending upon the phase and type of diving. Humans exposed to simulated depths of up to 305 meters without barotrauma or decompression sickness develop transient, conductive hearing losses with no audiometric evidence of cochlear dysfunction. Transient vertigo and nystagmus during diving have been noted with caloric stimulation, resulting from the unequal entry of cold water into the external auditory canals, and with asymmetric middle ear pressure equilibration during ascent and descent (alternobaric vertigo). Equilibrium disturbances noted with nitrogen narcosis, oxygen toxicity, hypercarbia, or hypoxia appear primarily related to the effects of these conditions upon the central nervous system and not to specific vestibular end-organ dysfunction. Compression of humans in helium-oxygen at depths greater than 152.4 meters results in transient symptoms of tremor, dizziness, and nausea plus decrements in postural equilibrium and psychomotor performance, the high pressure nervous syndrome. Vestibular function studies during these conditions indicate that these problems are due to central dysfunction and not to vestibular end-organ dysfunction. Persistent inner ear injuries have been noted during several phases of diving: 1) Such injuries during compression (inner ear barotrauma) have been related to round window ruptures occurring with straining, or a Valsalva's maneuver during inadequate middle ear pressure equilibration. Divers who develop cochlear and/or vestibular symptoms during shallow diving in which decompression sickness is unlikely or during compression in deeper diving, should be placed on bed rest with head elevation and avoidance of maneuvers which result in increased cerebrospinal fluid and intralabyrinthine pressure. With no improvement in symptoms after 48 hours, exploratory tympanotomy and repair of a possible labyrinthine window fistula should be considered. Recompression therapy is contraindicated in these cases...

Action Potentials↗
PubMed2000

Effects of heterogeneous structure and diffusion permeability of body tissues on decompression gas bubble dynamics.

To gain insight into the special nature of gas bubbles that may form in astronauts, aviators and divers, we developed a mathematical model which describes the following: 1) the dynamics of extravascular bubbles formed in intercellular cavities of a hypothetical tissue undergoing decompression; and 2) the dynamics of nitrogen tension in a thin layer of intercellular fluid and in a thick layer of cells surrounding the bubbles. This model is based on the assumption that, due to limited cellular membrane permeability for gas, a value of effective nitrogen diffusivity in the massive layer of cells in the radial direction is essentially lower compared to conventionally accepted values of nitrogen diffusivity in water and body tissues. Due to rather high nitrogen diffusivity in intercellular fluid, a bubble formed just at completion of fast one-stage reduction of ambient pressure almost instantly grows to the size determined by the initial volume of the intercellular cavity, surface tension of the fluid, the initial nitrogen tension in the tissue, and the level of final pressure. The rate of further bubble growth and maximum bubble size depend on comparatively low effective nitrogen diffusivity in the cell layer, the tissue perfusion rate, the initial nitrogen tension in the tissue, and the final ambient pressure. The tissue deformation pressure performs its conservative action on bubble dynamics only in a limited volume of tissue (at a high density of formed bubbles). Our model is completely consistent with the available data concerning the random latency times to the onset of decompression sickness (DCS) symptoms associated with hypobaric decompressions simulating extravehicular activity. We believe that this model could be used as a theoretical basis for development of more adequate methods for the DCS risk prediction.

Atmospheric Pressure↗
PubMed1984

Diving medicine.

This discussion focuses on the several pressure-related syndromes that are peculiar to diving and that are collectively known as dysbarism. These include barotrauma of descent, barotrauma of ascent, and air embolism. Also considered are nitrogen narcosis and decompression sickness.

Decompression Sickness↗
PubMed1981

Blood cell changes in asymptomatic divers.

Many recent reports have suggested that diving and decompression cause changes in blood cells even when no overt symptoms of decompression sickness are present. This study subjected 10 normal persons to a pressure exposure of 100 fsw (30.5 msw) for 60 min followed by the standard U.S. Navy decompression schedule. No subject had symptoms of clinical decompression sickness. Repeated blood samples over a 3-week period spanning the simulated dive were analyzed for numbers of red cells, white cells, reticulocytes, platelets (by three methods), and size distribution of platelets. The study was designed to detect postdive changes of less than 5%. Small but definite decreases were found in levels of red cells, white cells, hematocrit, and platelets (by microscopic methods but not by machine), and the proportion of large platelets rose. The changes were too mild to support a proposed mechanism of decompression damage.

Blood Cell Count↗
PubMed1986

Aseptic necrosis in caisson workers: a new set of decompression tables.

There is a high incidence of aseptic necrosis and decompression sickness among caisson workers due to inadequate decompression using the current OSHA decompression tables (1-7). Because of this, a new set of tables--Autodec III-O2--was developed which more effectively eliminates nitrogen from the body and, therefore, should decrease the incidence of both bends and aseptic necrosis. The Autodec III-O2 schedule's superiority was statistically significant at a level of 0.08 compared to the OSHA table. It is our conclusion that OSHA should adopt the Autodec III-O2 schedule as a replacement for the current decompression tables.

Adult↗
PubMedDate not supplied

Abnormal serum biochemistries in association with arterial gas embolism.

Although diving-associated arterial gas emboli have been thought to embolize the cerebral circulation preferentially, more recent evidence suggests that gas bubbles disseminate widely and may cause dysfunction in multiple organ systems. We performed a retrospective survey of the records of patients presenting with diving-associated gas embolism over a 10-yr period to determine the maximal levels of serum transaminases and lactate dehydrogenase after a diving accident. Twenty-nine subjects with arterial gas embolism were identified whose dive profiles suggested that decompression sickness was unlikely. Maximal transaminase levels (aspartate amino transaminase = 442 +/- 187 IU/L; alanine amino transaminase = 315 +/- 205 IU/L) and lactate dehydrogenase level (800 +/- 227 IU/L) were significantly greater in the gas embolism patients than those levels measured in a group of normal individuals undergoing training dives of similar depth and duration. These preliminary studies suggest that arterial gas embolism frequently produces significant abnormalities in serum enzyme activity in sport divers whose dives would not be expected to produce decompression sickness. Arterialized gas bubbles may circulate widely, causing injury outside of the cerebral circulation.

Adolescent↗
PubMed1981

Lack of teratogenic effects of air at high ambient pressure in rats.

The purpose of the research was to determine if pregnant rats subjected to a maximum tolerated duration of exposure to air at 6 atmospheres absolute pressure (ATA) (50.3 meters seawater) would have an increased frequency fetal death, resorption, low birth-weight, or malformations. Ninety pregnant rats were assigned to one of three exposure schedules during organogenesis: days 9-11, 12-14, or 15-17, and were randomized between one treatment and two control groups. The treatment group was subjected to 6 ATA for 70 minutes with compression and decompression at 1.8 ATA (18.3 meters seawater)/minute. Control groups were exposed to either 1 ATA of air (surface) within the hyperbaric chamber, or 1 ATA of air outside the chamber. For 30 minutes following decompression, chamber-treated animals were placed in a slow, motor-driven rotating cage, and assessed for gait disturbances from decompression sickness. On Day 20 of gestation, laparotomy was performed, and corpora lutea, implantations, and resorptions were counted. Fetuses were weighed, sexed, and examined for gross malformations. Subsequently, they were fixed, sectioned, and examined for visceral anomalies. Minor visceral anomalies and anatomical variations were present in 16.3% of all fetuses; however, no significant differences existed between groups. Similarly there were no significant differences when number of resorptions, number of dead fetuses, mean fetal weights, and malformations were compared by analysis of variance. Finally, there was no relation between symptoms of decompression sickness and any of the above measures. These results indicate that exposing rats to air at increased atmospheric pressure does not affect fetal health or survival.

Air Pressure↗
PubMed1985

Seal lungs collapse during free diving: evidence from arterial nitrogen tensions.

Arterial blood nitrogen tensions of free-diving Weddell seals (Leptonychotes weddelli) were measured by attaching a microprocessor-controlled blood pump and drawing samples at depth to determine how these marine mammals dive to great depths and ascend rapidly without developing decompression sickness. Forty-seven samples of arterial blood were obtained from four Weddell seals during free dives lasting up to 23 minutes to depths of 230 meters beneath the sea ice of McMurdo Sound, Antarctica. Peak arterial blood nitrogen tensions of between 2000 and 2500 millimeters of mercury were recorded at depths of 40 to 80 meters during descent, indicating that the seal's lung collapses by 25 to 50 meters. Then arterial blood nitrogen tensions slowly decreased to about 1500 millimeters of mercury at the surface. In a single dive, alveolar collapse and redistribution of blood nitrogen allow the seal to avoid nitrogen narcosis and decompression sickness.

Animals↗
PubMed1990

[Chronology of scheduling repeated dives and its importance in professional diving].

Repeated dives are frequently performed in diving practice. The value of proper chronology of sequencing repeated dives into different depths was verified by analyzing three professional tabular decompression systems. Sequencing of dives from greater to smaller depths proved to be the only correct algorithm. Such an algorithm plays an important role in preventing the development of critical supersaturation with inert gas and of potential manifestations of decompression sickness in divers.

Decompression Sickness↗