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PubMed1988

Manifestations and treatment of 793 cases of decompression sickness in a compressed air tunneling project in Hong Kong.

In the largest compressed air tunneling contract for the construction of the Island Line of the Mass Transit Railway system in Hong Kong, 154,390 man-decompressions occurred, of which 142,140 were after exposures to 1 bar (1.97 ATA, 14.7 psig) or above. The maximum working pressure (MWP) was 3.30 bar (4.26 ATA, 47.9 psig). There were 792 cases of type I and 1 case of type II decompression sickness. The manifestations of the cases were generally similar to those reported elsewhere. Oxygen treatment was given to 9 cases and all were successfully treated with no recurrence of symptoms. Minimum effective pressure treatment on 783 type I cases was successful, with 9.6% requiring two or more recompressions. The pressure required to relieve symptoms was more closely related to the interval between completion of decompression after work and commencement of treatment than to the delay between onset of symptoms and treatment. For every 1-h interval or every 1-h delay, an additional pressure of 0.04 bar (0.04 ATA, 0.58 psi) above MWP was required for pain relief. Step-wise multiple regression analysis showed that the four predictors for pressure of relief and the highest pressure used in recompression, respectively, were, in order of descending importance, maximum working pressure, interval before treatment, bends sequence (the nth attack of bends experienced in the present contract, i.e., the sum of previous attacks and the present attack), and duration of exposure.

Adult↗
PubMedDate not supplied

[Analysis of clinical symptoms of cases of human decompression disease in altitude chamber studies].

Over 2400 altitude chamber ascents in which 130 volunteers participated were performed using different decompression tables. The cases of decompression disease were classified in terms of its types and severity. It is stressed that the experiments involved in decompression studies have to be extremely careful because the disease may have various and sudden manifestations.

Decompression Sickness↗
PubMed1978

Explosive decompression of subjects up to a 20,000-m altitude using a two-pressure flying suit.

The RSAF two-pressure flying suit system to protect the pilot at high altitude has been tested from different medical safety aspects. To secure adequate alveolar oxygen pressure, the suit admits up to 70 mm Hg (9.3 kPa) positive pressure breathing by counter-pressure against the thorax and by a 3.2 times higher pressure in the anti-G suit. After 1 h of oxygen breathing, subjects were exposed to explosive decompression from an altitude of 9,000 m to 17,500 or 20,000 m in 0.5 s in a hypobaric chamber. No symptoms of decompression sickness or of alveolar rupture with gas embolism to the central nervous system were seen. Pulmonary X-rays after the test did not reveal any signs of lung rupture with extrapulmonary gas leakage. With the precordial Doppler ultrasound technique, intracardial gas bubbles (silent bubbles) could be detected only in one subject after explosive decompression to a 20,000-m altitude in the 10 experiments.

Adult↗
PubMed1987

Increase in blood-brain barrier permeability by altitude decompression.

Previous studies indicated that exposure to compression-decompression increases blood-brain barrier (BBB) permeability to vital dyes and antibiotics. This report concerns functional and ultrastructural BBB changes induced by altitude decompression. A 2% trypan blue solution was intravenously injected (4 ml.kg-1) into 29 experimental and 19 control rabbits. Some animals also received horseradish peroxidase. The experimental animals were subjected to 30,000 ft (4.3 psi) for 45 min. Controls were kept at ground level. The animals were sacrificed 90 min postinjection. Gross and microscopic examination and spectrophotometric dye determination revealed significantly greater tracer penetration in experimental brains (mean dye concentration 27.06 +/- 4.42 micrograms.g-1) than in controls (4.52 +/- 1.52 micrograms.g-1). No sex differences were noted. Electron microscopy suggested that the increased BBB permeability was due to transendothelial vesicular transport and, occasionally, to penetration through interendothelial junctions. These observations may have relevance to pharmacotherapy in space and at high altitudes and to the pathogenesis of altitude decompression sickness.

Altitude Sickness↗
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↗
PubMed1979

Mechanical vs. ischemic mechanisms for decompression sickness.

We used 20 kangaroo rats to investigate the effect of exposure to low oxygen levels (0.11 Atm 02 inspired partial pressure) prior to decompression from a steady-state condition. This hypoxia was found to afford significant protection against limb bends as simulated in those animals by tail biting. Yet, it potentiated neurologic symptoms compared with a control exposure on air with the same level of nitrogen supersaturation. However the incidence of simulated limb bends in the same animals was the same with hypoxia as with another control exposure at a pressure estimated to give extravascular bubbles of the same size upon decompression. The results are, therefore, consistent with a simple mechanical basis for limb bends, but are difficult to explain by any ischemic mechanism since a general hypoxia exacerbates any pain produced by oxygen deficiency in the tissues. However, the reverse may be true for some forms of neurologic decompression sickness and the two such cases reported here are consistent with that view, although not statistically significant.

Animals↗
PubMed1979

Doppler detection of thresholds for decompression-induced venous gas emboli in the awake rat.

Awake, unrestrained rats with chronic implants of a Doppler probe on the vena cava, were saturated in a small plexiglass chamber at a maximum pressure (P1), rapidly decompressed to a predetermined pressure (P2) and then monitored for the presence of intravascular bubbles. If there were no indication of bubbles within 1 h, the decompression was considered bubble free. For each saturation pressure, an increasing pressure difference (deltaP = P1 - P2) was tried on each exposure until the threshold for bubble detection was found. The relationship deltaP = a P1 + b, where a and b are constants defining the threshold for bubble detection, was experimentally determined at pressures from 3-10 ATA. The depth-dependent linear relationship deltaP = 0.38P, + 1.29 (r = 0.97, P is less than 0.001) was found for first exposures and deltaP = 0.62 P1 + 0.16 (r = 0.99, p is less than 0.001) for repeat exposures. The chronic Doppler preparation allows a more sensitive threshold determination than past methods for small animals and also allows repeat pressure exposures without the effects of a severe decompression stress.

Animals↗
PubMed1981

Ruthenium red staining of blood-bubble interface in acute decompression sickness in rat.

The ultrastructure of the blood-bubble interface has been studied in rats decompressed experimentally. Subsequent to staining with ruthenium red there was detected by electron microscopy a continuous envelope like layer about 20 nm thick at the bubble-facing surface of the interface. The envelope like structure was visualized also by concanavalin A-ferritin, a glycosyl- and mannosyl residue-recognizing lectin coupled with an electron-dense probe, but the structure was not at all seen by the use of the conventional stains used in electron microscopy, uranyl acetate and lead citrate. No electron-dense layer was discernible on the application of only osmium tetroxide without further staining. The results indicate that material stainable by ruthenium red, and binding concanavalin A (probably a glycoprotein), is concentrated at the blood-bubble interface upon decompression. It is suggested that it plays a role in stabilization of the bubble and in the hematological alterations that are frequently observable in decompression sickness.

Animals↗
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↗
PubMed1983

[Empirical treatment of decompression sickness in Greek sponge divers].

Reports and evidence of the empirical methods of treating decompression sickness long used by Greek sponge divers have been collected. Divers were questioned by a team from Chieti University's School of Underwater and Hyperbaric Medicine during a visit to the island of Kalymnos. There are interesting analogies between modern therapy and ancient empirical methods. The modern methods were devised in response to the enormous incidence of decompression sickness during the fishing season in the Southern Mediterranean. It may well be that the experience of old sponge divers may offer some helpful suggestions for modern therapy of decompression sickness.

Adult↗
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↗
PubMed1982

Clinical and experimental evidence for the use of hypothermia in decompression sickness.

During construction of the Coxwell sewer tunnel and subway in Toronto, a number of patients with decompression sickness failed to respond completely to repressurization alone. After the addition of hypothermia, significant improvement occurred. These observations stimulated an experimental study in which 36 rabbits were exposed to 60 or 70 p.s.i. for 1 h. After sudden decompression over 70 s, they were either observed, cooled in air at 0 degrees C, or cooled in water at 3 degrees C. Immersion in water significantly reduced the mortality rate, while cooling in air did not. These experimental results supported the clinical observations that hypothermia was an effective therapeutic adjunct in the treatment of decompression sickness.

Animals↗
PubMed1981

Acute decompression sickness--report of an autopsy case with widespread fat embolism.

A case of acute decompression sickness presenting severe clinical features was reported. At the time of autopsy, intra- and extravascular air bubbles were found in various organs. Pulmonary fat embolism was also prominent in association with severe circulatory disturbances of the lungs. The spinal cord showed edematous and congestive swelling which was intimately related to the coagulation of blood within the epidural veins that contained innumerable fat droplets. Intravascular fat seemed to be created in and released from the injured adipose tissue, especially that of the bone marrow during decompression and to have acted as an accelerator of intravascular coagulation. The pathophysiological significance of the fat embolism for the development and the progression of decompression sickness is discussed.

Adult↗
PubMed1981

Cardiac decompression sickness: report and discussion of a case.

A case of first degree atrio-ventricular block, probably representing cardiac involvement by decompression sickness, is presented. The conduction defect resolved spontaneously 36 h after the initiating decompression insult, and was not accompanied by any other cardiovascular changes. The contribution of a recompression treatment, which alleviated accompanying Type I decompression sickness (DCS) symptoms, to the resolution of cardiac DCS is not certain. Cardiac symptoms of DCS do not receive enough consideration. It is suggested that an electrocardiogram should, whenever possible, form part of the basic evaluation of suspected DCS and of the initial workup of candidates for diving. A flow diagram for management of cardiac DCS is proposed.

Adult↗
PubMed1981

[Considerations on 209 cases of decompression sickness treated in Italian hyperbaric centers in 1978 and 1979].

Results of an epidemiological study on the incidence and aethiology of the cases of Decompression Sickness treated in eleven Italian Hyperbaric facilities during 1978 and 1979 are reported 209 cases were treated; 186 recovered completely, 92 improved, 5 had no advantage from treatment, 2 died. The majority of cases were in the age-range 25-29 years (15-55) and in the depth-range 40-50 msw (12-100). Decompression was mandatory in 207 cases and was not respected, mainly because the divers ascended at a wrong rate (20 msw/min in the majority, 10 cass "ballooned" to the surface, 2 cases surfaced at 1-2 msw/min). In a significant number of times decompression was aborted due to exhaustion of compressed air in the bottles. 55% of the 1979 cases referred to repetitive diving (2nd or 3rd dive of the day). The Authors conclude that human error in by far the most recurring aethiological agent in this study and point out the coincidence of the high incidence of D.S. cases south of Rome with the relative lack of diving schools in that area.

Adult↗
PubMed1980

Permeability changes in cerebral, iridic, and retinal vessels during experimental decompression sickness in the rat.

An investigation has been made of the effect of acute decompression sickness upon the permeability of the cerebral, iridic, and retinal vessels of the rat, with sodium-fluorescein as intravenous tracer. No permeability changes were observable during the first 15 min subsequent to decompression, following exposure to 5.1 bar for 50 min. Focal leaky areas were found in the brain parenchyma after exposures to 5.1 bar for 120 min. Although sodium-fluorescein partially permeated the pial vessels in controls, the treatment in a hyperbaric chamber seems to increase the diffusion of the tracer from the pia into the cerebral cortex. Nevertheless, both the iridic and retinal vessels remained "tight." The factors which increase the permeability of microvasculature in brain and possible reasons for the negative results obtained with the iris and retina in decompression sickness are discussed.

Air Pressure↗
PubMed1980

Separation of basic parameters of decompression using fingerling salmon.

The experimental limitations inherent in use of air-breathing vertebrates for studies of decompression are chiefly due to the difficulty in estimating supersaturation levels associated with both symptoms of decompression sickness and bubble formation. The difficulty is because gas elimination begins upon reduction of pressure and therefore complicates any estimates of the supersaturations that promoted the bubbles or symptoms, or both, in the first place. Use of physostomatous fish such as salmonid fingerlings easily available from hatcheries allows decompression of both fish and surrounding water, thereby minimizing gas tension gradients from the fish to the water and the water to the fish. Depending upon the experimental conditions imposed, the important physical properties such as diffusivity and solubility of different diving gases, H2, Ne, He, and N2, can be separated or combined parametrically. Results of these studies indicate that initial bubble formation in vivo is relatively independent of solubility, whereas the bubble growth phase is more dependent on gas concentration.

Animals↗
PubMed1978

Postmortem intravascular bubbling: a decompression artifact?

The relationships between drowning occurring in divers using compressed air, with subsequent recovery of the body to the surface, and the finding of intravascular gas bubbles at autopsy were studied. Guinea pigs were exposed to compressed air in a hyperbaric chamber at various depths [98, 294, and 392 kPa (1,3, and 4 atm)] for various intervals and then drowned at depth. Various decompression schedules were used in returning the drowned animals to the surface. Autopsy examination indicated that large and small intravascular gas bubbles may be found, in the absence of traumatic air embolism or decompression sickness, as a result of the process of decompression alone. Postmortem findings of intravascular bubbles bin drowned divers must be interpreted with caution and the importance of a full history of the incident, including depth and time of diving and evidence of ascent before drowning, are critical to the proper interpretation of intravascular gas bubbles.

Animals↗