Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DECOMPRESSION SICKNESS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources
PubMed1998

Diving and the risk of barotrauma.

STUDY OBJECTIVES: Pulmonary barotrauma (PBT) of ascent is a feared complication in compressed air diving. Although certain respiratory conditions are thought to increase the risk of suffering PBT and thus should preclude diving, in most cases of PBT, risk factors are described as not being present. The purpose of our study was to evaluate factors that possibly cause PBT. DESIGN: We analyzed 15 consecutive cases of PBT with respect to dive factors, clinical and radiologic features, and lung function. They were compared with 15 cases of decompression sickness without PBT, which appeared in the same period. RESULTS: Clinical features of PBT were arterial gas embolism (n = 13), mediastinal emphysema (n = 1), and pneumothorax (n = 1). CT of the chest (performed in 12 cases) revealed subpleural emphysematous blebs in 5 cases that were not detected in preinjury and postinjury chest radiographs. A comparison of predive lung function between groups showed significantly lower midexpiratory flow rates at 50% and 25% of vital capacity in PBT patients (p < 0.05 and p < 0.02, respectively). CONCLUSIONS: These results indicate that divers with preexisting small lung cysts and/or end-expiratory flow limitation may be at risk of PBT.

Barotrauma↗
PubMed1989

Effect of inert gas switching at depth on decompression outcome in rats.

The present investigation was performed to determine whether inert gas sequencing at depth would affect decompression outcome in rats via the phenomenon of counterdiffusion. Unanesthetized rats (Rattus norvegicus) were subjected to simulated dives in either air, 79% He-21% O2, or 79% Ar-21% O2; depths ranged from 125 to 175 feet of seawater (4.8-6.3 atmospheres absolute). After 1 h at depth, the dive chamber was vented (with depth held constant) over a 5-min period with the same gas as in the chamber (controls) or one of the other two inert gas-O2 mixtures. After the gas switch, a 5- to 35-min period was allowed for gas exchange between the animals and chamber atmosphere before rapid decompression to the surface. Substantial changes in the risk of decompression sickness (DCS) were observed after the gas switch because of differences in potencies (He less than N2 less than Ar) for causing DCS and gas exchange rates (He greater than Ar greater than N2) among the three gases. Based on the predicted gas exchange rates, transient increases or decreases in total inert gas pressure would be expected to occur during these experimental conditions. Because of differences in gas potencies, DCS risk may not directly follow the changes in total inert gas pressure. In fact, a decline in predicted DCS risk may occur even as total inert gas pressure in increasing.

Animals↗
PubMed2005

[Acute decompression illness following hyperbaric exposure: clinical features of central nervous system involvement].

Decompression illness (DCI) is a general term encompassing all pathological changes secondary to reduction of environmental pressure. This condition has two forms: decompression sickness (DCS) and arterial gas embolism (AGE) secondary to pulmonary barotrauma. Moreover, DCS is categorized as minor, such as limb and/or joint pains or skin rash (Type I), and serious, as in cardiopulmonary and/or central nervous system involvements (Type II). Cerebral and spinal injuries have been symptomatically classified into AGE and DCS. Brain scans of patients with AGE or DCS showed multiple cerebral infarctions in the terminal and/or border zones of the cerebral arteries. Brain involvements of patients in both AGE and DCS show no differences in neurological or neuro-radiological findings. From the neurological and radiological standpoint, it is therefore impossible to distinguish these two conditions. Despite established treatments for neurological DCI (both AGE and DCS), it is unclear whether US Navy treatment Table 6 is preferable to standard hyperbaric oxygen therapy such as 2.4 atmospheres pressure for 90 minutes. Japanese laws and regulations have peculiarities that permit air diving to 90 meters depth, but with explicit prohibition of the use of oxygen for decompression, albeit a limited use of mixed gas is permissible. Moreover, currently the health screening for hyperbaric workers does not include detailed examination of the cardiopulmonary or the central nervous system.

Adult↗
PubMedDate not supplied

Monoplace hyperbaric chamber use of U.S. Navy Table 6: a 20-year experience.

We report a 20-year experience at LDS Hospital, Salt Lake City, UT using the U.S. Navy Treatment Table 6 (TT6) in an oxygen-filled monoplace hyperbaric chamber (1985-2004). Air breathing was provided via a demand regulator fitted with a SCUBA mouthpiece while the patient wore a nose clip. Intubated patients were mechanically ventilated with a Sechrist 500A ventilator, with a modified circuit providing air, when specified. We treated 90 patients: 72 divers (decompression sickness [DCS] = 67, arterial gas embolism [AGE] = 5), 10 hospital-associated AGE, and 8 miscellaneous conditions. They received a total of 118 TT6 (9 TT6 in intubated patients). Ninety-four percent of the TT6 schedules were tolerated and completed. The intolerance rate from two surveyed multiplace chambers was zero and 3% of 100 TT6 schedules each. Failure to complete the TT6 was due to oxygen toxicity (4) and claustrophobia (3). The U.S. Navy TT6 was well tolerated by patients with DCS or AGE treated in monoplace hyperbaric chambers, but tolerance may not be as high as when treated in the multiplace chamber.

Adult↗
PubMed1997

MR imaging of the central nervous system in diving-related decompression illness.

PURPOSE: This investigation was conducted to determine whether MR imaging showed cerebral or spinal damage in acute diving-related decompression illness, a term that includes decompression sickness (DCS) and arterial gas embolism (AGE). MATERIAL AND METHODS: A total of 16 divers with dysbaric injuries were examined after the initiation of therapeutic recompression. Their injuries comprised: neurological DCS II n = 8; AGE n = 7; combined cerebral-AGE/spinal-DCS n = 1. T1- and T2-weighted images of the brain were obtained in 2 planes. In addition, the spinal cord was imaged in 7 subjects. The imaging findings were correlated with the neurological symptoms. RESULTS: MR images of the head showed ischemic cerebrovascular lesions in 6/8 patients with AGE but showed focal hyperintensities in only 2/8 divers with DCS. Spinal cord involvement was detected in 1/7 examinations, which was the combined cerebral-AGE/spinal-DCS case. There was agreement between the locations of the documented lesions and the clinical manifestations. CONCLUSION: MR readily detects cerebral damage in AGE but yields low sensitivity in DCS. A negative MR investigation cannot rule out AGE or DCS. However, MR is useful in the examination of patients with decompression illness.

Adult↗
PubMed2001

Dysbaric osteonecrosis in Turkish sponge divers.

Skeletal radiographs were performed to determine the prevalence of dysbaric osteonecrosis (DON) in 51 Turkish sponge divers. DON was correlated with the diver's age and experience, maximum diving depth, and decompression sickness (DCS). Thirty-six of the 51 divers had radiographic evidence of one or more lesions, for a prevalence of 70.6% DON. Proximal humerus was the most effected site. Type B (head, neck, and shaft) lesions were most common, comprising 63.6% of all DON lesions. Type A (juxta-articular) lesions were observed in all 10 divers who complained of painful motion of their shoulder or hip joints. DON most commonly affected the proximal humerus. Reportedly, 38 of these 51 (74.5%) divers had experienced DCS. We did not fnd any significant relationship between DON and DCS, maximum diving depth, diving experience, and divers' age.

Data Collection↗
PubMed1986

Direct ascent from shallow air saturation exposures.

Thirty-four healthy human subjects were exposed to shallow air saturation for 48 h [1.77 ATA (25.5 fsw) n = 19, 1.89 ATA (29.5 fsw) n = 15] and then decompressed to 1 ATA (0 fsw) in about 2 min. Symptoms included fatigue, limb and joint pain, headache, myalgias, and pruritus. No subject of 19 was diagnosed as having decompression sickness (DCS) after the shallower exposure, but 4 of 15 were diagnosed and treated for DCS subsequent to the deeper exposure. Almost all subjects in both groups had Doppler-detectable venous gas emboli (VGE) lasting up to 12 h postdecompression. Treated subjects had a recurrence of VGE several hours after the hyperbaric oxygen treatment. Only the duration of VGE, and not the VGE score, correlated with symptoms; and only the subjects body weight and age correlated with the VGE variables. This study indicates that hyperbaric air exposures of this magnitude are not as benign as previously thought.

Adult↗
PubMed2004

Oral and maxillofacial aspects of diving medicine.

Sport diving has witnessed explosive growth in the past decade, as 8.5 million people are certified in the United States alone. Even though scuba diving is a relatively safe sport, there are serious risks that all divers must consider. Beyond the better-known sequelae such as decompression sickness, middle ear dysfunction, and potential central nervous system effects, scuba diving also carries inherent risk to the maxillofacial region. Atypical facial pain, temporomandibular joint dysfunction, sinus barotraumas, and barodontalgia have all been reported by dentists and physicians treating military, commercial, and sport divers. Additionally, clinicians must address anatomic concerns for would-be divers, including cleft lip and palate, edentulism, or patients with pre-existing temporomandibular dysfunction, midfacial trauma, or craniomaxillofacial surgery. Health care professionals should have a thorough understanding of the implications of scuba diving for consultation and recommendation regarding diving fitness and the treatment of adverse effects of scuba diving to the maxillofacial region.

Barotrauma↗
PubMed1990

Relative decompression risk of dry and wet chamber air dives.

The difference in risk of decompression sickness (DCS) between dry chamber subjects and wet, working divers is unknown and a direct test of the difference would be large and expensive. We used probabilistic models and maximum likelihood estimation to examine 797 dry (and generally resting and comfortable) and 244 wet (and generally working and cold) chamber dives from the Defence and Civil Institute of Environmental Medicine, supplemented with 483 wet (working, cold) dives from the Navy Experimental Diving Unit. Several analyses considered whether dry and wet data were distinguishable using several models, whether models obtained from one set of exposure conditions would correctly predict the occurrence of DCS in the other condition, and whether a single wet-dry risk difference parameter was different from zero. Although the two conditions may not produce identical risks, immersion appears to change relative risk of DCS by less than 30% and certainly involves less than a doubling of DCS risk. Uncontrolled differences in exercise and temperature stresses unavoidably complicate interpretation. Several methods are presented to extrapolate results from dry-test subjects in decompression trials to expected at-sea performance.

Data Interpretation, Statistical↗
PubMed1987

A case of delayed-onset pulmonary barotrauma in a scuba diver.

A 23-yr-old male scuba diver was admitted to the hyperbaric chamber of the Polish Army Training Centre of Divers and SCUBA Divers for treatment of pneumomediastinum and possible decompression sickness. Medical history suggested a case of pulmonary barotrauma with delayed and exacerbated symptoms. About 36 h after the onset of symptoms the patient was treated successfully according to U.S. Navy Treatment Table 6-A. A recurrence of symptoms was observed more than 3 d after the initial hyperbaric therapy. Signs and symptoms suggested the presence of air in the vessels of the nervous system, and possibly in the heart muscle and bones of the upper limbs. A second recompression therapy began according to method III of the Polish Navy Treatment Tables. Adjunctive therapy included intravenous aspirin, steroids, isosorbide dinitrate, and fluids. Symptoms resolved and did not recur after this second hyperbaric therapy.

Adult↗
PubMed2000

[Severe diving accidents: physiopathology, symptoms, therapy].

Decompression injuries are potentially life-threatening incidents, generated by a rapid decline in ambient pressure. Although typically seen in divers, they may be observed in compressed air workers and others exposed to hyperbaric environments. Decompression illness (DCI) results from liberation of gas bubbles in the blood and tissues. DCI may be classified as decompression sickness (DCS) or arterial gas embolism (AGE), depending on where the gas bubbles lodge. DCS occurs after longer exposures to a hyperbaric environment with correspondingly larger up-take of inert gas. DCS may be classified into type 1 with cutaneous symptoms and musculoskeletal pain only or type 2 with neurologic and/or pulmonary symptoms as well. AGE usually results from a pulmonary barotrauma, and with cerebral arterial involvement, the symptoms are similar to a stroke. The most important therapy, in the field, is oxygen resuscitation with the highest possible concentration and volume delivered. The definitive treatment is rapid recompression with hyperbaric oxygen therapy. Additional therapeutic measures are discussed.

Animals↗
PubMed2003

Mathematical model of diffusion-limited evolution of multiple gas bubbles in tissue.

Models of gas bubble dynamics employed in probabilistic analyses of decompression sickness incidence in man must be theoretically consistent and simple, if they are to yield useful results without requiring excessive computations. They are generally formulated in terms of ordinary differential equations that describe diffusion-limited gas exchange between a gas bubble and the extravascular tissue surrounding it. In our previous model (Ann. Biomed. Eng. 30: 232-246, 2002), we showed that with appropriate representation of sink pressures to account for gas loss or gain due to heterogeneous blood perfusion in the unstirred diffusion region around the bubble, diffusion-limited bubble growth in a tissue of finite volume can be simulated without postulating a boundary layer across which gas flux is discontinuous. However, interactions between two or more bubbles caused by competition for available gas cannot be considered in this model, because the diffusion region has a fixed volume with zero gas flux at its outer boundary. The present work extends the previous model to accommodate interactions among multiple bubbles by allowing the diffusion region volume of each bubble to vary during bubble evolution. For given decompression and tissue volume, bubble growth is sustained only if the bubble number density is below a certain maximum.

Air Pressure↗
PubMed1995

Complement activation in divers after repeated air/heliox dives and its possible relevance to DCS.

Plasma levels of the anaphylatoxin C5a were measured in 19 divers performing repeated air dives. Blood samples were collected immediately before the first dive and 2 h after the first and the second or third dive. Serum obtained at the same times was subjected to complement activation in vitro by air bubbles. Six divers developed symptoms of decompression sickness (DCS). Most intravascular bubbles were observed in divers with the lowest plasma levels of C5a. Postdive plasma levels of C5a did not increase compared with predive levels, nor were postdive levels significantly different after two or three dives compared with the first dive. Repeated dives did not influence the amounts of C5a generated in vitro. Neither plasma levels of C5a nor C5a generated in vitro were significantly different in divers who experienced symptoms of DCS vs. divers without symptoms of DCS. We conclude that plasma level of C5a and measurement of C5a generation in vitro cannot be used to predict DCS.

Adult↗
PubMed1997

Risk factors for pulmonary barotrauma in divers.

STUDY OBJECTIVES: Pulmonary barotrauma (PBT) of ascent is a feared complication in compressed air diving. Although certain respiratory conditions are thought to increase the risk of suffering PBT and thus should preclude diving, in most cases of PBT, risk factors are described as not being present. The purpose of our study was to evaluate factors that possibly cause PBT. DESIGN: We analyzed 15 consecutive cases of PBT with respect to dive factors, clinical and radiologic features, and lung function. They were compared with 15 cases of decompression sickness without PBT, which appeared in the same period. RESULTS: Clinical features of PBT were arterial gas embolism (n=13), mediastinal emphysema (n=1), and pneumothorax (n=1). CT of the chest (performed in 12 cases) revealed subpleural emphysematous blebs in 5 cases that were not detected in preinjury and postinjury chest radiographs. A comparison of predive lung function between groups showed significantly lower midexpiratory flow rates at 50% and 25% of vital capacity in PBT patients (p<0.05 and p<0.02, respectively). CONCLUSIONS: These results indicate that divers with preexisting small lung cysts and/or end-expiratory flow limitation may be at risk of PBT.

Adult↗
PubMed1989

Effect of peripheral temperature on the formation of venous gas bubbles.

Temperature of the tissue affects the many components involved in the formation of tissue gas phase formation: diffusion, perfusion, and inert gas solubility. Since the effects of perfusion and inert gas solubility may be counteracting in terms of enhancing growth of gas bubbles, the optimal thermal status of divers throughout a dive remains unresolved. To elucidate the role of peripheral body temperature on gas phase formation, four subjects were exposed to a 10 degree and 40 degree C environment for 3 h on two separate occasions, after a no-stop decompression from a 12-h dive to 9.14 m (30 fsw) on air. The 3-hour exposures to either a cold or warm air environment resulted in a significant difference in mean skin temperature (P less than or equal to 0.01) with no alteration in rectal temperature. Total peripheral resistance during the 10 degree C exposure was 13.8 +/- 1.9 mmHg.liter-1.min-1 and significantly higher than that observed during the 40 degree C exposure (10.4 +/- 3.5 mmHg.liter-1.min-1). Gas bubbles in the venous return were monitored with a Doppler ultrasonic transducer placed in the precordial region, both at rest and after a deep knee bend. Venous bubbles were only detected in 1 subject following the warm air exposure, whereas 3 of the 4 subjects developed Doppler-detectable bubbles during the cold air exposure. Although both the cold and warm air exposures (3 h postdecompression) were uneventful, a hot shower taken by the subjects on completion of the cold air exposure (6 h postdecompression) precipitated mild type I symptoms of decompression sickness. These symptoms were not present after a hot shower following the warm air exposure. The present results indicate that despite the assumed greater inert gas solubility of tissues expected during cold air exposure, the decrease in the perfusion may have played a more significant role in the observed levels of detectable venous gas bubbles. Development of type I symptoms following a 12-h saturation, a 3-h cold exposure, and a subsequent hot shower suggests that a rapid rise in peripheral temperature may cause a significant rise in tissue gas tension. This increase in tension does not seem to be sufficiently reduced by increased perfusion to the tissues to prevent bubble formation.

Adult↗
PubMed2002

Mathematical model of diffusion-limited gas bubble dynamics in unstirred tissue with finite volume.

Models of gas bubble dynamics for studying decompression sickness have been developed by considering the bubble to be immersed in an extravascular tissue with diffusion-limited gas exchange between the bubble and the surrounding unstirred tissue. In previous versions of this two-region model, the tissue volume must be theoretically infinite, which renders the model inapplicable to analysis of bubble growth in a finite-sized tissue. We herein present a new two-region model that is applicable to problems involving finite tissue volumes. By introducing radial deviations to gas tension in the diffusion region surrounding the bubble, the concentration gradient can be zero at a finite distance from the bubble, thus limiting the tissue volume that participates in bubble-tissue gas exchange. It is shown that these deviations account for the effects of heterogeneous perfusion on gas bubble dynamics, and are required for the tissue volume to be finite. The bubble growth results from a difference between the bubble gas pressure and an average gas tension in the surrounding diffusion region that explicitly depends on gas uptake and release by the bubble. For any given decompression, the diffusion region volume must stay above a certain minimum in order to sustain bubble growth.

Air Pressure↗
PubMed2004

Caisson disease during the construction of the Eads and Brooklyn Bridges: A review.

The Eads Bridge (St. Louis) and the Brooklyn Bridge (New York City) were testing grounds for caisson construction. These caissons were enormous compressed air boxes used to build riverine piers and abutments anchoring the bridges. Caisson meant faster and cheaper construction, but there was a hidden cost---caisson disease (decompression sickness). Within caissons, workers labored at pressures as high as 55 psig and caisson disease was common. This discourse is a brief history of the caisson, a brief discussion of the illness as viewed in the mid 1800's, and an abbreviated history of the Eads and Brooklyn Bridges. It also provides a detailed description and evaluation of the observations, countermeasures, and recommendations of Dr. Alphonse Jaminet, the Eads Bridge physician, and Dr. Andrew Smith, the Brooklyn Bridge physician, who published reports of their experience in 1871 and 1873, respectively. These and other primary sources permit a detailed examination of early caisson disease and Jaminet's and Smith's thinking also serve as good examples from which to study and learn.

Decompression Sickness↗
PubMed1992

Loss of cabin pressurization in U.S. Naval aircraft: 1969-90.

During the 22-year period from 1 January 1969 to 31 December 1990, there were 205 reported cases of loss of cabin pressure in US Naval aircraft; 21 were crew-initiated and 184 were deemed accidental. The ambient altitudes varied from 10,000 ft (3048 m) to 40,000 ft. (12192 m). The most common reason for crew-initiated decompression was to clear smoke and fumes from the cockpit/cabin (95%). The most common cause for accidental loss of cabin pressure was mechanical (73.37%), with aircraft structural damage accounting for the remaining 26.63%. Serious physiological problems included 1 pneumothorax, 11 cases of Type I decompression sickness, 23 cases of mild to moderate hypoxia with no loss of consciousness, 18 cases of hypoxia with loss of consciousness, and 3 lost aircraft with 4 fatalities due to incapacitation by hypoxia. In addition, 12 ejections were attributed to loss of cockpit pressure. Nine of the ejections were deliberate and three were accidental, caused by wind blast activation of the face curtain. Three aviators lost their lives following ejection and seven aircraft were lost. While the incidence of loss of cabin pressure in Naval aircraft appears low, it none-the-less presents a definite risk to the aircrew. Lectures on the loss of cabin/cockpit pressurization should continue during indoctrination and refresher physiology training.

Accidents, Aviation↗