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PubMed2002

Non-invasive measurement of pulmonary artery pressure in humans with simulated altitude-induced venous gas emboli.

BACKGROUND: Decompression to simulated altitude causes super-saturation of nitrogen desolved in body tissues and can result in venous gas emboli (VGE), which are usually "cleared" in the lung. Large intravenous boli of air administered to animals increase pulmonary artery pressure (PAP), and may induce cross-over of gas to the left side of the heart (creating dangerous arterial gas emboli). This study was conducted to determine whether high VGE grades induced at simulated altitude elevate PAP in humans. METHODS: Eight human subjects with subclinical tricuspid regurgitation were exposed to simulated altitude of > or = 24,000 ft (7315 m) for up to 4 h. Systolic PAP was derived from Doppler ultrasound echo imaging measurements of peak flow velocity of the regurgitant jet. VGE was rated using the Spencer scale. A technique of "bubble titration" was employed with changes in exercise and altitude to maintain sufficient bubbles without decompression sickness. RESULTS: All subjects developed grade III-IV VGE, but 3 developed decompression sickness, resulting in earlier termination. Pre-exposure systolic PAP averaged 24.4 +/- 1.3 (SE) mm Hg. After 1, 2, 3 and 4 h, systolic PAP was 23.7 +/- 1.2 (n = 8), 23.4 +/- 1.1 (n = 8), 23.3 +/- 1.0 (n = 6), and 25.9 +/- 0.6 (n = 5) mm Hg, respectively. Systolic PAP remained unchanged, in spite of bubble grades III-IV for up to 4 h. CONCLUSION: As systolic PAP did not increase with hypobaric exposures that created substantial VGE, the bubble loading was not sufficient to overwhelm the lung clearing capacity. The risk of high PAP resulting in VGE cross-over is low during typical operational altitude exposures.

Aerospace Medicine↗
PubMed1989

Dysbaric disorders: aseptic bone necrosis in tunnel workers and divers.

Dysbaric osteonecrosis is a serious complication for those exposed to a hyperbaric environment, with prevalence of 17% amongst compressed air workers and 4.2% amongst divers. Bone lesions are characteristically multiple and bilateral, occurring frequently in the shafts of the femora or tibiae and the heads of the humeri or femora. A proportion of the lesions will lie next to the joint surface, the so called juxta-articular lesion, and these may progress to a structural failure and secondary osteoarthritis. These lesions can be severely disabling, especially in a young adult male. When related to the occupational history the prevalence of bone lesions, both in compressed air workers and divers, increases with age, experience and with greater pressures of air or at greater depths. Moreover, acute attacks of decompression sickness, the bends, are more liable to be associated with subsequent bone lesions. Current decompression schedules certainly reduce the bends rate but, no matter how strictly adhered to, will not prevent the development of dysbaric osteonecrosis. It is possible that bone necrosis could result solely from exposure to a high pressure of air, either from work in compressed air or diving. Those men with positive bone lesions should be advised to seek expert medical opinion and probably advised to discontinue work in compressed air or diving if a juxta-articular lesion is present. Detection of bone necrosis depends on good quality radiographs with reliable interpretation, preferably by double observation, especially in the early stages. Lesions, especially when early or doubtful, can be confirmed by CT or bone scintigraphy. MRI promises to detect osteonecrosis in the very early stages but is not yet readily available. To detect dysbaric osteonecrosis at an early stage it is important to monitor both compressed air workers and divers with regular radiological skeletal surveys or bone scintigraphy. In 1987, the Bone Necrosis Working Group of the Decompression Sickness Panel recommended that all divers should have a radiological survey on completion of their initial diving training and that bone scintigraphy should be used for subsequent surveillance for certain groups, including those diving deeper than 30 metres, where the time at depth exceeds 4 hours, when experimental decompression is used and in other situations.

Atmospheric Pressure↗
PubMed1989

The influence of diving variables on perceptual and cognitive functions in professional shallow-water (abalone) divers.

Shallow-water diving is regarded as a hazardous occupation due to such dangers as decompression sickness and carbon monoxide poisoning. Recent studies have demonstrated impairments in the neurological and neurobehavioral functioning of professional shallow-water divers, yet the reasons for these deficits are not clear. In this study 80 professional abalone divers were studied using a range of neurobehavioral tests and questioned closely on their diving experience. Multiple linear regression analysis was then performed to determine the extent to which characteristics of the diver's occupation influenced neurobehavioral impairment. The results demonstrated that divers who were at greatest risk of decompression sickness due to their diving technique showed the clearest functional impairments. In particular problems of visual function, psychomotor abilities, and short-term memory were most evident. It appears that professional shallow-water diving is not necessarily a hazardous occupation provided that safe diving practices are observed. However, divers who fail to observe these practices and put themselves at risk of decompression sickness are likely to have impairments in neurobehavioral function which affect their everyday life, and more importantly their responses in emergency situations.

Adult↗
PubMed1989

[Diving profiles and work loads of fishermen's "Oikomi Gyoho" diving].

Diving profiles of fishermen divers in the Izu Islands were investigated and recorded by DDR (Diving Data Recorder). Consumed air volume during diving work was also checked in each dive and the work load was measured by VO2 during diving. It was recognized that divers repeatedly experienced extreme descents and ascents, that were accompanied by increases of oxygen consumption. This suggested that the load of their work was far beyond that of sports divers. The particular diving method used, called the "Oikomi Gyoho method" is to repeatedly dive several times to catch fish. Each bottom (diving) time is rather short and the dept changes from deeper to shallower areas gradually. This profile is considered to be a safe diving method for the prevention of DCS (Decompression Sickness). However, stopping for decompression during ascent is sometimes required to prevent DCS according to analysis of the diving profiles. It is pointed out that the risk of DCS still remains with this diving method.

Decompression Sickness↗
PubMed2006

Gas nuclei, their origin, and their role in bubble formation.

Gas bubbles are the primary agent in producing the pathogenic effects of decompression sickness. Bubble formation during decompression is not simply the consequence of inert gas supersaturation. Numerous experiments indicate that bubbles originate as pre-existing gas nuclei. Radii are on the order of 1 microm or less. Heterogeneous nucleation processes are involved in generating these gas entities. Musculoskeletal activity could be the main promoter of gas nuclei from stress-assisted nucleation. The half-life and faculty for nuclei to initiate bubble formation during decompression depend on many factors. Oxygen window and surface tension are involved in resolving bubbles. Two factors have been proposed to stabilize gas nuclei against dissolution: gas nuclei trapped in hydrophobic crevices and gas nuclei coated with surface-active molecules such as surfactants. Diffusion and surface tension could play an important role in the formation of gas nuclei crevices. However, while the concept of in vivo hydrophobic crevices remains a theoretical possibility, none have yet been identified in tissues and/or in microcapillaries. Moreover, while surfactants seem present in numerous tissues and could play a role in gas nuclei stabilization, they could also be involved in bubble elimination. The understanding of such mechanisms is of primary importance to neutralize nuclei and for modeling bubble growth. Here we present in a single document a summary of the original findings and views from authors in this field.

Animals↗
PubMed1987

Shoulder pain and pneumoperitoneum following a diving accident.

We present the case of a diver who experienced the acute onset of shoulder pain after a rapid ascent. It was determined that the patient had decompression sickness ("the bends") of the right shoulder and pulmonary barotrauma resulting in secondary pneumoperitoneum. He underwent decompression, with prompt resolution of symptoms. Of the 14 cases of isolated pneumoperitoneum due to barotrauma reported in the world literature, three were due to gastric rupture. Shoulder pain in association with pneumoperitoneum may be due to diaphragmatic irritation or may be an isolated symptom of decompression sickness. Correctly determining the etiology of these findings is crucial to the appropriate management of the patient.

Adult↗
PubMed1983

Decrease of ether induction time after exposure to dysbaric conditions in rat.

In 22 adult male albino rats (means = 565 g) it was consistently observed that the time required to anesthetize them with 5 ml of diethyl ether after a hyperbaric exposure of 6 ATA using compressed air decreased depending on the severity of the animals' post-decompression reaction to the compression-decompression exposure. Monitoring the time required to lightly anesthetize adult male rats with diethyl ether to a point of losing the righting reflex after a particular compression-decompression exposure provided an indication of the rats' post-exposure state of health. This technique aided in correctly establishing if a rat developed a degree of decompression sickness that may have otherwise gone unnoticed. The loss of resistance to ether induction as a result of decompression sickness may be related to alterations in the blood-brain barrier, blood perfusion inequities, or changes in cardiopulmonary mechanics due to the presence of gaseous emboli. Rats that survived the compression-decompression exposures showed a marked resistance to ether induction after 24 h of recovery.

Animals↗
PubMed2004

[Severe vertigo after a scuba-dive to 29 meters].

A 27-year-old flight instructor experienced 5 to 10 minutes after a scuba-dive to 29 m, which lasted totally 50 minutes, dizziness, nausea and severe vertigo. The symptoms lasted about an hour. The patient vomited several times and noted sudden onset headache and vertigo lasting the following three days. Hyperbaric oxygen therapy was started 30 hours after the event because decompression sickness was suspected. Transthoracic echocardiographic evaluation showed a patent foramen ovale. Diving accidents may be caused by decompression sickness, the formation of a free intravascular gas phase (bubbles) may result in transatrial shunting in the presence of a patent foramen ovale and may lead to neurological signs and symptoms. In this context the diver was advised to undergo closure of the atrial septal defect. Five months after the incident the patient underwent successful transcatheter occlusion of the PFO.

Adult↗
PubMed1974

Isobaric bubble growth: a consequence of altering atmospheric gas.

During certain treatments of decompression sickness following dives made with compressed air, the U.S. Navy advocates breathing helium-oxygen mixtures. However, stable nitrogen bubbles created within gelatin by decompression have been found to enlarge when the atmosphere was switched from nitrogen to helium without changing ambient pressure. This suggests that decompression sickness would be worsened by switching from nitrogen to helium in the breathing gas mixture.

Atmosphere Exposure Chambers↗
PubMed1985

Preemployment medical examinations in a compressed air tunneling project in Hong Kong.

One thousand workers intended to be employed in a compressed air tunneling project in Hong Kong had preemployment medical examinations for fitness to work in compressed air. Only 69.3% were declared fit and the overall unfit rate was 22.1%. The major disqualifying medical conditions were lung and heart abnormalities and chronic otitis media. Chest x-ray was found to be the most useful procedure in detecting the disqualifying conditions. The type I bends rate of the contract during the same period of examination was low: 1.39% at maximum working pressure of 2.45 kg/cm2, and there was no case of type II decompression sickness. Although many factors may affect the bends rate, it is suggested that the strict criteria adopted in the selection of workers might have contributed to the satisfactory outcome in the prevention of decompression sickness.

Decompression Sickness↗
PubMed2001

Simulation of dynamic bubble spectra in tissues.

Decompression sickness (DCS) is the result of bubble formation in the body due to excessive/rapid reduction in the ambient pressure. Existing models relate the decompression stress either to the inert gas load or to the size of a single bubble in a tissue compartment. This paper presents a model that uses the gas exchange equations combined with bubble dissolution physics and population balance equations to produce a new mathematical framework for DCS modeling. This framework, the population balance model for decompression sickness (PBMDS), simulates the number of bubbles with their corresponding size distributions in a compartmental tissue array. The model has a modular structure that enables one to explore different modeling results with respect to key aspects of DCS, such as gas exchange, nucleation, and surface tension. The paper's goal is to present the derivation of PBMDS in detail, however, three simple application case studies are provided. The aim of these case studies is to suggest that PBMDS supplies additional information on bubble distribution while supporting the results from current practice.

Computer Simulation↗
PubMed1984

A model of spinal cord dysbarism to study delayed treatment: I. Producing dysbarism.

This paper reports the development of a model of spinal cord decompression sickness (DCS) which lends itself to studies of treatment in anesthetized dogs. Models tried early in this development could be used in the future to study blow-up and cerebral decompression sickness. We found that a dive with a bottom time of 12-15 min at 300 ft breathing air and decompressed in 5.5 min produced a high incidence of cord DCS, as diagnosed by changes in spinal evoked potentials (SEP). Furthermore the animals could generally be sustained on the surface using intravenous fluids, without going into shock, before treatment by compression was begun. The findings are discussed in the light of previous studies.

Anesthesia, Intravenous↗
PubMed1977

Scuba diving accidents.

The principal scuba diving medical problems of barotrauma, air embolism and decompression sickness have as their pathophysiologic basis the Ideal Gas Law and Boyle's Law. Hyperbaric chamber recompression therapy is the only definitive treatment of air embolism and decompression sickness. However, with a basic knowledge of diving medicine, the family physician can provide effective supportive care to the patient prior to initiation of hyperbaric therapy.

Accidents↗
PubMed2000

Cases from the Aerospace Medicine Resident's Teaching File: unsuspected pulmonary barotrauma.

A USAF pararescue specialist developed chest pain during scuba diving duty. Initial evaluations considered decompression sickness and musculoskeletal etiologies. Pulmonary barotrauma was not contemplated because of the relatively mild presentation. Later, a very significant pneumothorax was discovered and successfully treated without sequelae. Decompression sickness is briefly discussed followed by a more in-depth examination of the presentation, diagnosis, treatment, and aeromedical aspects of spontaneous and "deserved" pneumothoraces.

Adult↗
PubMed1984

Several new aspects of bubble-induced central nervous system injury.

Ischaemia is a major mechanism underlying central nervous system (c.n.s.) damage in decompression sickness. Some recent experimental observations on the effect of bubble-induced ischaemia on c.n.s. tissue sharpen and extend our understanding of the pathophysiology of decompression sickness. After bubble-induced brain ischaemia, a measurable increase in 111In-labelled leucocytes occurs in the injured hemisphere. By 4 h into the recovery period the cells are concentrated in zones of low blood flow, as measured by the [14C]iodoantipyrine technique. The presence of these cells during the critical early hours of c.n.s. ischaemia suggests that they may contribute to the evolution of neuronal damage. Oedema is often cited as the cause of clinical deterioration after c.n.s. ischaemia or trauma. Recent evidence indicates that the presence and degree of circumscribed brain oedema is not a good predictor of the amount of nerve cell recovery (by using cortical sensory evoked response) after bubble-induced brain ischaemia. This brings into question the role of circumscribed oedema of the c.n.s. in dysfunction of post-ischemic nerve cells.

Animals↗
PubMed1997

Decompression comparison of helium and hydrogen in rats.

The hypothesis that there are differences in decompression risk between He and H2 was examined in 1,607 unanesthetized male albino rats subjected to dives on 2% O2-balance He or 2% O2-balance H2 (depths < or = 50 ATA, bottom times < or = 60 min). The animals were decompressed to 10.8 ATA with profiles varying from rapid to slow, with up to four decompression stops of up to 60 min each. Maximum likelihood analysis was used to estimate the relative decompression risk on a per unit pressure basis (termed "potency") and the rate of gas uptake and elimination, both factors affecting the decompression sickness risk, from a specific dive profile. H2 potency for causing decompression sickness was found to be up to 35% greater than that for He. Uptake rates were unresolvable between the two gases with the time constant (TC) estimated at approximately 2-3 min, leading to saturation in both cases in < 15 min. Washout of both gases was significantly slower than uptake, with He washout (TC approximately 1.5-3 h) substantially slower than H2 washout (TC approximately 0.5 h). It is unknown whether the decompression advantage of the faster washout of H2 or the disadvantage of its increased potency, observed in the rat, would be important for human diving.

Animals↗
PubMed1987

Dysbaric cerebral air embolism in Hawaii.

Cerebral air embolism is a major cause of death and disability among sport scuba divers. To better define the epidemiologic and clinical manifestations of this infrequently encountered disorder, the records of all recompression treatments in Hawaii from 1976 through 1979 were reviewed. Forty-two cases of dysbaric air embolism (DAE) were identified on the basis of clinical criteria, accounting for 18% of the patients undergoing recompression treatment for diving-related disorders during this four-year period. In 22 patients (52%), DAE was part of a dysbarism syndrome that involved one or more forms of decompression sickness and/or in which DAE could not be differentiated from neurologic decompression sickness. The presenting signs and symptoms varied, with asymmetric multiplegia being the most common finding. Two patients died, giving a case fatality rate of 5% for those who survived until reaching the recompression chamber. Overall, 78% of the cases manifested either complete (61%) or substantial (17%) recovery with recompression and adjunctive medical measures. Traditional concepts of dysbaric cerebral air embolism are not adequate to explain the spectrum of clinical manifestations encountered in this condition.

Adolescent↗
PubMed1988

Effect of N2-He-O2 on decompression outcome in rats after variable time-at-depth dives.

No study of decompression sickness has examined both variable gas mixtures and variable time at depth to the point of statistical significance. This investigation examined the effect of N2-He-O2 on decompression outcome in rats after variable time-at-depth dives. Unanesthetized male albino rats were subjected to one of two series of simulated dives: 1) N2-He-O2 dives (20.9% O2) at 175 feet of seawater fsw) and 2) N2-O2 dives (variable percentage of O2; depths from 141 to 207 fsw). Time at depth ranged from 10 to 120 min; rats were then decompressed within 10 s to surface pressure. The probability of decompression sickness (severe bends symptoms or death) was analyzed with a Hill equation model, with parameters for gas potency and equilibrium time for the three gases and weight of the animal. Relative potencies for the three gases were of similar magnitude for bends and statistically different for death in ascending order: O2 less than He less than N2. Estimated gas uptake rates were different. N2 took three to four times as long as He to reach full effect; the rate of O2 appeared to be considerably shorter than that of N2 or He. The large influence of O2 on decompression outcome questions the simplistic view that O2 cannot contribute to the decompression requirement.

Animals↗