[Decompression sickness and intravenous gas bubbles].
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Inner ear barotrauma with rupture of the round or oval window secondary to diving and decompression sickness (DCS) of the inner ear can be a difficult diagnosis to differentiate. The dive profile or associated elements of DCS will often confirm the diagnosis. Occasionally, diagnosis is made during recompression or during operation. The differential diagnosis is important, since immediate recompression is indicated for inner ear DCS, while it is contraindicated in cases of inner ear barotrauma. We have found no cases reported in the world literature in which both diseases have been diagnosed and proven simultaneously. We present a case of a diver who developed DCS with inner ear manifestations complicated by a round window fistula. Treatment and clinical outcome are discussed along with a brief review of the suspected cause.
The prevalence of right-to-left interatrial shunts was determined by contrast echocardiography in a blind comparison of 61 divers who had had decompression sickness, divided into four predetermined clinical subgroups, and a control group of 63 who had not. The prevalence of shunt was 15/63 in the controls and did not differ significantly in 24 divers with onset of neurological symptoms more than 30 minutes after surfacing (4/24) or 6 with joint pain only (1/6). In divers who had neurological symptoms within 30 minutes of surfacing the prevalence of shunt was 19/29, significantly higher. Rashes soon after surfacing were related to shunts but late rashes were not.
Purpose of the investigation was to assess contribution of repeated (with a 12-hr interval) decompression to the risk of altitude decompression sickness (ADS) by simulation of 6-hr extravehicular activities (EVA) of space crewmembers in altitude chamber. The protocol included "ascents" of 6 essentially healthy male subjects at the age of 24 to 51 to the altitude of 7,600 m (37 kPa) following 30-min prebreathing (elimination of nitrogen from the body by breathing pure oxygen through a mask at the ambient pressure of 73 kPa = 2,600 m). Each subject participated in 2 experimental exposures: first initial and then repeated decompression. None of 24 "ascents" produced clinical signs of ADS. Comparison of the data concerning frequency and time points of detection by ultrasonic Doppler equipment of gas bubbles (GB) in the venous bed during decompression with initial, maximal and mean values of US signal intensity failed to state a significant difference between them. Data of the investigation were confronted with anticipated length of GB dispersion in body tissues.
A 26-yr-old AC-130 gunner developed unilateral temporomandibular joint (TMJ) pain while flying a combat support mission. A diagnosis of decompression sickness (DCS) was made based on his symptoms and risk factors that included prolonged exposure to high altitude (60 to 90 min at 18,000 ft), cold temperature (-11 degrees C), and increased inflight activity. His symptoms resolved with 100% oxygen and he was returned to flying status after 72 h. Altitude related DCS is an unusual occurrence and this is the first reported case of inflight DCS affecting the temporomandibular joint.
The medical history, clinical and neuropathological findings at necropsy are described in a 50-year-old male amateur diver who suffered from Type II decompression sickness, a spinal 'bend'. He survived as a paraplegic for 4 years. In the spinal cord upward Wallerian degeneration in the posterior columns and downward degeneration in the corticospinal tracts was explained by multiple small and medium sized infarcts affecting the centripetal blood supply to the cord. There was preservation of a rim of subpial fibres on the surface of the posterior and lateral columns. The grey matter and nearby white matter (supplied by the centrifugal arterial supply) was unaffected.
BACKGROUND: The Miskito Indian lobster divers of Central America employ very provocative diving profiles and experience severe neurological decompression sickness (DCS) and/or arterial gas embolism (AGE). Scientific data are scarce regarding the clinical patterns of injury, response to treatment, and functional outcomes for such cases. METHODS: A retrospective review of 229 cases of DCS and/or AGE was conducted at 2 hyperbaric units in Central America. RESULTS: The following deficits were recorded on presentation: any neurological deficit: 94%; motor: 79%; sensory: 60%; urinary: 48%; reflex: 45%; and loss of consciousness: 20%. The patterns of weakness (n = 182) were as follows: paraparesis: 27%; paraplegia: 26%; lower extremity monoparesis: 14%; lower extremity monoplegia: 6%; quadriparesis: 4%; hemiparesis: 4%; hemiplegia: 3%; and quadriplegia: 2%. Treatment was delayed by a mean and median of 5 and 2 d, respectively. The majority received hyperbaric oxygen and systemic steroids. Motor function on discharge (n = 182) was as follows: normal: 30%; paraparesis: 15%; lower extremity monoparesis: 15%; paraplegia: 3%; quadriparesis: 2%; hemiparesis: 2%; and missing data/other: 33%. Gait on discharge (n = 182) was as follows: normal: 19%; abnormal: 19%; required one crutch: 10%; required two crutches: 16%; not ambulatory: 5%; and missing data: 31%. DISCUSSION: The majority of severe injuries could be localized to the thoracolumbar spinal cord. One-fifth had bilateral cerebral dysfunction manifested by loss of consciousness. Despite long delays to treatment, divers responded to hyperbaric oxygen. At the time of discharge, almost a third had complete recovery of strength and the majority were ambulatory.
Six experimental investigations of various mechanical aspects of the spinal cord are described relevant to its injury by gas deposited from solution by decompression. These show appreciable resistances to gas pockets dissipating by tracking along tissue boundaries or distending tissue, the back pressure often exceeding the probable blood perfusion pressure--particularly in the watershed zones. This leads to a simple mechanical model of spinal decompression sickness based on the vascular "waterfall" that is consistent with the pathology, the major quantitative aspects, and the symptomatology--especially the reversibility with recompression that is so difficult to explain by an embolic mechanism. The hypothesis is that autochthonous gas separating from solution in the spinal cord can reach sufficient local pressure to exceed the perfusion pressure and thus occlude blood flow.
A significant change of occurrence (p=0.0343) of type 1 and type 2 decompression sickness (DCS) of divers in Croatia was observed in the period from 1991 to 2002 (type 1: n=26, 37.68% and type 2: n=43, 62.32%) compared with the period from 1967 to 1990 (type 1: n=93, 52.84% and type 2: n=83, 47.16%). The change was attributed to the extensive usage of diving computers and artificial gas mixtures which enable extended bottom times and deeper dives, thus putting divers at an increased decompression risk. The importance of the results of this report is in the fact that permanent neurological deficit occurs only after type 2 DCS. Injured divers with permanent loss after type 2 DCS are not fit for diving and require a long term medical care, thus becoming a significant public health problem.
The purpose of this study was to determine the minimum spacesuit pressure required to prevent decompression sickness (DCS) during operational conditions in a 50% oxygen/50% nitrogen environment. In this study, 30 male volunteer subjects were exposed in groups of three, to three consecutive daily extravehicular activity (EVA) simulations at 7.8 psia (5,031 m altitude equivalent) for a continuous period of 6 h. During each altitude exposure, the subjects participated in similar exercise workloads expected to be experienced by astronauts during a typical EVA scenario. Precordial Doppler monitoring revealed that 73.3% of the subjects had intravenous bubbling during at least 1 d of the 3 d of exposure, with 26.7% remaining bubble-free during the entire study. No correlation was found between either body fat or age and incidence of bubble formation. One case of DCS occurred during the study indicating that 7.8 psia is not sufficient pressure to totally preclude DCS in a 50% oxygen/50% nitrogen environment. The necessary pressure awaits further study.
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We tested the possible occurrence of a neurological insult secondary to high-frequency sound exposure. Immersed, anesthetized rats were subjected to a simulated diving profile designed to induce decompression sickness, while exposed to the transmission of an acoustic beacon. Intermittent sound at a pressure level of 184.5 dB re 1 microPa at 1 m (1.7 kPa), a frequency of 37 kHz, and with a duration of 4 ms, was transmitted in a duty cycle of 0.26%. Four groups, each containing nine animals, were included in the study as follows: group 1, immersion only, no sound exposure; group 2, immersion with sound exposure; group 3, diving simulation when immersed, no sound exposure; group 4, diving simulation when immersed, with sound exposure. Somatosensory evoked potentials (SSEPs) were recorded the day before the study, and a second recording was made 30 min after immersion. Some of the SSEP components disappeared after the dive in 3 rats from group 3 and 2 rats from group 4. SSEP components could not be identified in a significantly larger number of animals from groups 3 and 4, compared with groups 1 and 2. No differences were found in wave latency, amplitude or conduction time. Our data show that the high-frequency sound exposure employed did not contribute to the development of the neurological insult.
We do not yet know why whales occasionally strand after sonar has been deployed nearby, but such information is important for both naval undersea activities and the protection of marine mammals. Jepson et al. suggest that a peculiar gas-forming disease afflicting some stranded cetaceans could be a type of decompression sickness (DCS) resulting from exposure to mid-range sonar. However, neither decompression theory nor observation support the existence of a naturally occurring DCS in whales that is characterized by encapsulated, gas-filled cavities in the liver. Although gas-bubble formation may be aggravated by acoustic energy, more rigorous investigation is needed before sonar can be firmly linked to bubble formation in whales.
This descriptive, nonrandomized, multicenter-based study compares the treatment outcomes of two major categories of recompression treatment tables for recreational sport SCUBA divers suffering from decompression sickness and/or arterial gas embolism. Stratified and logistic regression analyses were used to compare the enhanced tables, which use pressures of 165 fsw (feet of salt water) or 60 fsw with extended recompression time, to the regular tables, which use pressures of 60 fsw or less without extended recompression time. A total of 113 cases were treated with enhanced tables, 54 being successes. A total of 214 cases were treated with regular tables, 135 being successes. The final logistic statistical model after adjusting for confounding factors found a significant improvement in successful treatment outcomes for divers treated with tables that use pressures of 60 fsw or less without extended recompression time (OR = 0.47, 95% CI = 0.28-0.78).
Pregnant hamsters were exposed to 7.1 ATA (200 fsw) of compressed air breathing for 40 min. Comparisons were made between three groups of pregnant hamsters: (a) those that developed decompression sickness (DCS); (b) those that did not; and (c) a control (non-divided) group. As reported previously, maternal DCS if untreated resulted in frequent and severe teratogenic effects. Furthermore, fetuses from those females who apparently did not develop DCS were significantly smaller at term than fetuses from the control animals. However, fetuses from females that were treated for DCS did not differ from controls. This suggests that 40-min, 200-fsw dives per se are detrimental to fetal development in hamsters.
For the first manned flight of Hermes there will be a capability of performing EVA. The European EVA Space Suit will be an anthropomorphic system with an internal pressure of 500 hPa of pure oxygen. The pressure reduction from the Hermes cabin pressure of 1013 hPa will induce a risk for Decompression Sickness (DCS) for the EVA crewmember if no adequate protective procedures are implemented. Specific decompression procedures have to be developed. From a critical review of the literature and by using knowledge gained from research conducted in the past in the fields of diving and aerospace medicine safe protective procedures are proposed for the European EVA scenario. An R factor of 1.2 and a tissue half-time (t1/2) of 360 minutes in a single-tissue model have been identified as appropriate operational values. On the basis of an acceptable risk level of approximately 1%, oxygen prebreathing times are proposed for (a) direct pressure reduction from 1013 hPa to a suit pressure of 500 hPa, and (b) staged decompression using a 700 hPa intermediate stage in the spacecraft cabin. In addition, factors which influence individual susceptibility to DCS are identified. Recommendations are also given in the areas of crew selection and medical monitoring requirements together with therapeutic measures that can be implemented in the Hermes scenario. A method for demonstration of the validity of proposed risks and procedures is proposed.
Trimix (a mixture of helium, nitrogen, and oxygen) has been used in deep diving to reduce the risk of high-pressure nervous syndrome during compression and the time required for decompression at the end of the dive. There is no specific recompression treatment for decompression sickness (DCS) resulting from trimix diving. Our purpose was to validate a rat model of DCS on decompression from a trimix dive and to compare recompression treatment with oxygen and heliox (helium-oxygen). Rats were exposed to trimix in a hyperbaric chamber and tested for DCS while walking in a rotating wheel. We first established the experimental model, and then studied the effect of hyperbaric treatment on DCS: either hyperbaric oxygen (HBO) (1 h, 280 kPa oxygen) or heliox-HBO (0.5 h, 405 kPa heliox 50%-50% followed by 0.5 h, 280 kPa oxygen). Exposure to trimix was conducted at 1,110 kPa for 30 min, with a decompression rate of 100 kPa/min. Death and most DCS symptoms occurred during the 30-min period of walking. In contrast to humans, no permanent disability was found in the rats. Rats with a body mass of 100-150 g suffered no DCS. The risk of DCS in rats weighing 200-350 g increased linearly with body mass. Twenty-four hours after decompression, death rate was 40% in the control animals and zero in those treated immediately with HBO. When treatment was delayed by 5 min, death rate was 25 and 20% with HBO and heliox, respectively.
In the Singapore Mass Rapid Transit Project (MRT), 11 km of underground tunnels were built using compressed air. 1,737 compressed air workers (CAWs) were employed in the project. They underwent 188,538 man decompressions at the various compressed air worksites. 160 CAWs developed Type I decompression sickness (DCS) and 4 developed Type II DCS. This gave an overall incidence of 0.087%. The adoption of strict medical selection, strict adherence to decompression procedures and the provision for acclimatization of newstarters contributed greatly to this low incidence. Prompt treatment of DCS accounted for the low relapse rate. The clinical presentation of DCS is discussed here. Prevention of DCS by worksite environmental and work-practice monitoring are advocated.