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[Decompression sickness in divers treated at the Israel Naval Medical Institute between the years 1992 to 1997].

Clinical characteristics of 125 divers treated for decompression sickness (DCS) in the hyperbaric multiplace chambers of this Institute during 1992-1997 were analyzed retrospectively. In 62 (51%) the diagnosis was DCS Type I (joint pain or skin involvement) and in 60 (49%) DCS Type II (neurological, inner ear or pulmonary disease). Risk factors for the evolution of DCS were depth and duration of the dives involving accidents, violation of recommendations of the decompression tables, and repeated dives. Results were available for 112 of the 125 patients. 54 of them (48%) recovered completely, and another 54 recovered partially; 4 did not respond to treatment. Inner ear DCS was less responsive to hyperbaric oxygen treatment (p = 0.0001). There was significant improvement of neurological function in those with severe neurological injury (p = 0.0001). Rapid diagnosis and transportation of divers with DCS to a hyperbaric chamber is of crucial importance.

Adolescent↗

Escape from a disabled submarine: decompression sickness risk estimation.

Individual crewmember escape from a disabled U.S. Navy nuclear submarine has never been necessary, but remains an important contingency. Decompression sickness (DCS) is one of the foreseeable risks and a robust mathematical model of DCS incidence has been used to estimate the magnitude of this risk under a variety of escape scenarios. The model was calibrated with over 3000 well-controlled human pressure exposures, less than 2% of which simulated pressure profiles of submarine escape. For disabled submarine depths < 300 ft of sea water (fsw) and internal submarine pressures of <11 fsw (arguably the most likely conditions), the DCS risks are comparable to those routinely undertaken by U.S. Navy divers--less than 5%. For progressively deeper depths and especially for higher submarine internal pressures, the risk of DCS becomes much greater, including unknown chances of permanent injury and death. Variations from the baseline escape procedure are explored, including equipment differences, delays in exiting the submarine and changes in the oxygen content of the breathing mix.

Accidents↗

Enhancement of preoxygenation for decompression sickness protection: effect of exercise duration.

INTRODUCTION: Since strenuous exercise for 10 min during preoxygenation was shown to provide better protection from decompression sickness (DCS) incidence than resting preoxygenation, a logical question was: would a longer period of strenuous exercise improve protection even further? HYPOTHESIS: Increased strenuous exercise duration during preoxygenation increases DCS protection. METHODS: There were 60 subjects, 30 men and 30 women, who were exposed to 9,144 m (4.3 psia) for 4 h while performing mild, upper body exercise. Before the exposures, each subject performed three preoxygenation profiles on different days in balanced order: a 90-min resting preoxygenation control; a 240-min resting preoxygenation control; and a 90-min preoxygenation including exercise during the first 15 min. The subjects were monitored at altitude for venous gas emboli (VGE) with an echo-imaging system and observed for signs and symptoms of DCS. RESULTS: There were no significant differences in occurrence of DCS following any of the three preoxygenation procedures. Results were also comparable to an earlier report of 42% DCS with a 60-min preoxygenation including a 10-min exercise. There was no difference between VGE incidence in the comparison of protection offered by a 90-min preoxygenation with or without 13 min of strenuous exercise. The DCS incidence following a 240-min resting preoxygenation, 40%, was higher than observed during NASA studies and nearly identical with the earlier 42% DCS after a 60-min preoxygenation including exercise during the first 10 min. CONCLUSION: The protection offered by a 10 min exercise in a 60-min preoxygenation was not increased with extension of the preoxygenation exercise period to 15 min in a 90-min preoxygenation, indicating an upper time limit to the beneficial effects of strenuous exercise.

Adult↗

Natural history of severe decompression sickness after rapid ascent from air saturation in a porcine model.

We developed a swine model to describe the untreated natural history of severe decompression sickness (DCS) after direct ascent from saturation conditions. In a recompression chamber, neutered male Yorkshire swine were pressurized to a predetermined depth from 50-150 feet of seawater [fsw; 2.52-5.55 atmospheres absolute (ATA)]. After 22 h, they returned to the surface (1 ATA) at 30 fsw/min (0.91 ATA/min) without decompression stops and were observed. Depth was the primary predictor of DCS incidence (R = 0.52, P < 0.0001) and death (R = 0.54, P < 0.0001). Severe DCS, defined as neurological or cardiopulmonary impairment, occurred in 78 of 128 animals, and 42 of 51 animals with cardiopulmonary DCS died within 1 h after surfacing. Within 24 h, 29 of 30 survivors with neurological DCS completely resolved their deficits without intervention. Pretrial Monte Carlo analysis decreased subject requirement without sacrificing power. This model provides a useful platform for investigating the pathophysiology of severe DCS and testing therapeutic interventions. The results raise important questions about present models of human responses to similar decompressive insults.

Air Pressure↗

[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↗

Treatment of type I decompression sickness using the U.S. Navy treatment algorithm.

The effectiveness of the U.S. Navy (USN) Diving Manual treatment algorithm in treating pain-only decompression sickness (DCS) was analyzed. Treatment logs from the Naval Diving and Salvage Training Center and the Navy Experimental Diving Unit during the decade 1976-1986 were examined. Two hundred and ninety-two cases diagnosed initially as pain-only DCS were identified. Using the treatment algorithm, 208 cases were completed on USN Treatment Table 5 (TT-5), and 84 cases completed on USN Treatment Table 6 (TT-6). Recurrence of symptoms was 4.3% after TT-5, and 3.6% following TT-6. Difference in rate of recurrence was not statistically significant between treatment tables. Overall, the success rate for following the USN treatment algorithm was 95.9%. These data support the use of the shorter TT-5 in accordance with the Navy treatment algorithm.

Algorithms↗

Bubble formation and decompression sickness on direct ascent from shallow air saturation diving.

To find the minimum supersaturation pressure for detectable bubble formation and for contraction of decompression sickness (DCS), three shallow air saturation dives at the depth of 6 m, 7 m, and 8 m were performed. The ultrasonic M-mode method was used for detecting bubbles. The exposure period was 3 d for all dives. Ten subjects were compressed to both 6 m and 7 m, and nine subjects were compressed to 8 m. One bubble streak was shown in the 6-m dive group. A small number of bubbles were seen in four subjects in the 7-m dive. All subjects in the 8-m dive presented various amounts of bubbles. DCS was not observed in the 6-m and 7-m dives. On the other hand, in the 8-m dive, four subjects suffered from DCS and required recompression treatment. The minimum depth for detectable bubble formation was assessed at around 6 m and the direct ascent from saturation at 8 m seems to have a high risk of DCS.

Adult↗

Incidence and risk factors for symptoms of decompression sickness among male and female dive masters and instructors--a retrospective cohort study.

UNLABELLED: The aim was to determine the incidence of symptoms of decompression sickness (DCS) in dive masters and instructors in relation to number of dives and possible risk factors. STUDY DESIGN: Retrospective cohort study of dive masters and instructors in Sweden. STUDY BASE: All dive masters and instructors listed with PADI, NAUI and CMAS in Sweden as of January 1st 1999 (2380 divers). METHODS: The dive masters and instructors received a validated questionnaire on diving activities and symptoms of DCS in 1999. 1516 men and 226 women answered, i.e. 73% of the initial study base. RESULTS: DCS symptoms were reported by 190 divers. The incidence of DCS symptoms was 1.52 for males and 1.27 for females per 1000 dives. Dive masters, divers not performing decompression-stop dives, divers not practicing advanced diving and divers with a low number of total lifetime dives had a higher proportion (p < 0.05) of DCS symptoms per 1000 dives. There were no major differences in DCS symptom incidence related to sex, age, asthma, overweight or alcohol abuse in this study.

Adult↗

The effect of extended O2 prebreathing on altitude decompression sickness and venous gas bubbles.

The purpose of this study was to determine the effect of extended O2 prebreathing on symptom and bubble incidence during decompressions simulating extravehicular activity. The 38 subjects breathed O2 for a 6-h period prior to decompression to 4.3 psi. The subjects performed upper body exercise for 6 h. Subjects were monitored with a Doppler bubble detector and were encouraged to report all symptoms. Eight subjects were exposed to the same protocol after an 8-h prebreathe. Venous bubbles were detected in 18 of 38 subjects decompressed after the 6-h prebreathe. Four of these subjects reported symptoms of altitude decompression sickness. No symptoms or bubbles were detected in the eight subjects who had prebreathed 8 h. The incidence of symptoms and bubbles when combined with prior data on 3.5- and 4.0-hour prebreathes showed an inverse correlation to pre-breathing time. The incidence of symptoms was higher than has been reported for subjects exposed to decompression of shorter duration with less activity.

Adult↗

Spinal cord lipid levels in a porcine model of spinal cord decompression sickness.

Spinal cord lipid content was analyzed in 50 pigs that had experienced a simulated dive known to produce 20-80% incidence of neurologic decompression sickness (DCS). Using air and heliox as breathing mixtures, these animals underwent chamber dives ranging from 200-250 feet of seawater (fsw). These dives were designed to generate spinal cord DCS, which was detected by observing the animals for gross neurologic deficits. Using a standardized method, cylindrical samples of cord were cut from different spinal levels and analyzed for total lipid (TL) content, which produced two cervical, three thoracic, and two lumbar samples. All areas with gross hemorrhage were also sampled. The range of TL (mean) in milligrams per gram from the cervical, thoracic, and lumbar regions were 118-679 (319), 140-635 (366), and 109-658 (307), respectively. Although this implies that TL varies markedly between cords, values within each cord were fairly consistent (+/- 20% from cord mean). The difference in TL values between cord regions with and without hemorrhage was not significant (P > 0.1). This reveals that increased spinal cord TL levels, together with their presumed dissolved inert gas, do not play a major role in the location or incidence of spinal cord hemorrhages in pigs with clinical signs of spinal cord DCS.

Animals↗

Cerebro-spinal decompression sickness: report of two cases.

STUDY DESIGN: Two case reports. OBJECTIVE: To describe two unusual cases of deep diving followed by cerebro-spinal decompression sickness (DCS). SETTING: Midlands Centre for Spinal Injuries, England. METHODS: Observation of the outcome of two different cases of cerebro-spinal DCS, who have received two different modalities of treatment. RESULTS: The first patient's symptoms developed after he surfaced, he was treated according to the US Navy treatment table 6. He also received steroids for almost 3 weeks. His MRI of the brain and spinal cord, which was performed within 24 h of injury did not show any abnormality, while a repeat MRI 3 weeks later revealed abnormal signals in the brain and spinal cord. The second patient's symptoms started before he surfaced, he was treated with Comex 30 treatment table for 14 days and received no steroids, his MRI was performed 3 days after the injury showed high signals in the brain and spinal cord. CONCLUSION: Both divers developed cerebro-spinal dysfunction. They had encephalopathy (manifested by loss of consciousness), which indicates bilateral cerebral dysfunction. DCS can occur even when dives are conducted according to the procedures described by the US Navy. The use of high-dose steroids has not been formally tested in DCS; their use is controversial.

Adult↗

Moderate exercise after altitude exposure fails to induce decompression sickness.

INTRODUCTION: The objective of this study was to determine the effect of exercise after altitude exposure (post-exposure exercise) on subsequent altitude decompression sickness (DCS) incidence. Existing USAF prohibition of exercise following altitude chamber training exposures and interest from operational personnel prompted our evaluation of post-exposure exercise as a DCS-inducing stressor. METHODS: After a 1-h resting preoxygenation, 67 subjects were exposed to 30,000 ft for 2-h while performing mild, upper body exercise. The subjects were monitored for venous gas emboli (VGE) with an echo-imaging system and observed for signs and symptoms of DCS. Subjects without DCS (n = 31) or with DCS which resolved during recompression (n = 29) were randomly assigned to post-exposure rest (control, n = 29) or moderate exercise (50% of peak oxygen uptake, dual-cycle ergometry; n = 31) and both groups were monitored for delayed or recurring DCS. RESULTS: The altitude exposure resulted in 48.3% DCS in the 60 volunteers serving as test or control subjects. Of 31 subjects assigned to the post-exposure exercise group, 15 had developed DCS which resolved during descent. No cases of DCS were observed or reported during or following post-exposure exercise. CONCLUSION: The results show that moderate exercise after exposure did not result in either delayed-onset or recurring DCS.

Adult↗

Decompression sickness in a swine model: isobaric denitrogenation and perfluorocarbon at depth.

INTRODUCTION: Disabled submarine survivors could achieve inert gas tissue saturation likely to cause severe decompression sickness (DCS) on surfacing. This risk increases with time and depth of exposure. Methods to reduce DCS risk and severity are needed specifically for such an operational scenario. METHODS: Yorkshire swine (16.2-26.6 kg) fitted with an external jugular catheter were compressed to 5 ATA for 22 h. They then received an enriched breathing mix of 44% N2 and 56% O2, and an infusion of either saline or a perfluorocarbon (PFC) emulsion, and were observed for 2 h before surfacing without decompression stops. Controls were surfaced after 22 h saturation at 5 ATA. Surface observations continued for another 2 h on all animals and signs of DCS were recorded to the nearest minute. RESULTS: Seizure activity at depth was noted in 0/26 controls, 1/16 in the saline group, and 7/16 in the PFC group. DCS in < 2 h occurred in 25/26 air controls, 2/15 in the enriched mix/saline group, and 4/9 not suffering seizure in the enriched mix/PFC group. Death in < 2 h occurred in 23/26 controls, 1/15 in the saline group, and 1/9 in the PFC group. DISCUSSION/CONCLUSION: This study demonstrates the benefits of breathing increased O2 at depth prior to rapid decompression and the deleterious effects of PFC administration at depth in a swine saturation model with rapid decompression. Future studies should examine a minimal O2 pre-breathe period to offer protection against DCS as well as the role of PFC use after surfacing.

Animals↗

Epidemiology of decompression sickness under simulated space extravehicular activities.

Several ground-based trials were conducted by NASA at the Lyndon B. Johnson Space Center, Houston, TX, during 1982-90 to examine the risk of altitude decompression sickness (DCS) during space extravehicular activities. There were 22 different pressure profiles involving single and staged decompression procedures, each lasting from 180 to 360 min at the final altitude. A total of 164 healthy subjects participated in 426 exposures to altitude. Symptoms of DCS occurred in 17% (74/426) and circulating microbubbles by precordial Doppler ultrasound were detected in 42% (179/426) of all exposures. About 27% (20/74) of exposures with symptoms resulted in test abort, and one-third of all test aborts required treatment in the hyperbaric chamber. There was about 3.20 times (95% Confidence Interval [95% CI] = 1.56-6.66) higher risk of symptoms in the presence of Doppler-detectable microbubbles. Examination of individual risk factors showed that there was about 4.3 times (95% CI = 1.62-11.50) higher risk of symptoms with increasing number of exposures. These findings emphasize the importance of evaluating risk factors from ground-based trials for application in operational decision-making and treatment strategies.

Adult↗

Electroencephalography and magnetic resonance imaging in neurological decompression sickness.

The purpose of this study was to evaluate the use of electroencephalography (EEG) and magnetic resonance imaging (MRI) in the clinical evaluation of acute decompression sickness (DCS) in the central nervous system (CNS). Twenty-one patients treated because of acute DCS in the CNS during 1999-2001 were included, 15 patients with clinical cerebral DCS and five with clinical spinal cord DCS. Seven patients had abnormalities in their EEG, five with cerebral DCS and two with spinal cord DCS. MRI showed high intensity lesions in the spinal cord in four patients with clinical spinal cord DCS and in one with clinical cerebral DCS. Cerebral lesions were not identified by MRI in any patient. In conclusion, EEG showed unspecific abnormalities in only one third of the cases. Conventional MRI with a 1.5 T scanner may be of help in the diagnosis of DCS in the spinal cord, but not in the brain. EEG and MRI have low sensitivity in the diagnosis of acute DCS in the CNS. Recompression treatment of DCS should still be guided by clinical neurological examination and assessment of symptoms.

Adolescent↗

Detection of right to left shunts in decompression sickness in divers.

The diagnostic accuracy of bubble contrast transthoracic and transesophageal echocardiography and transcranial Doppler sonography in the detection of patent foramen ovale in divers with decompression sickness was assessed. Transcranial Doppler has a better positive and negative predictive value than the other modalities.

Adult↗

Short oxygen prebreathing and intravenous perfluorocarbon emulsion reduces morbidity and mortality in a swine saturation model of decompression sickness.

Disabled submarine (DISSUB) survivors will achieve inert gas tissue saturation within 24 h. Direct ascent to the surface when saturated carries a high risk of decompression sickness (DCS) and death, yet may be necessary during rescue or escape. O(2) has demonstrated benefits in decreasing morbidity and mortality resulting from DCS by enhancing inert gas elimination. Perfluorocarbons (PFCs) also mitigate the effects of DCS by decreasing bubble formation and increasing O(2) delivery. Our hypothesis is that combining O(2) prebreathing (OPB) and PFC administration will reduce the incidence of DCS and death following saturation in an established 20-kg swine model. Yorkshire swine (20 +/- 6.5 kg) were compressed to 5 atmospheres (ATA) in a dry chamber for 22 h before randomization into one of four groups: 1) air and saline, 2) OPB and saline, 3) OPB with PFC given at depth, 4) OPB with PFC given after surfacing. OPB animals received >90% O(2) for 9 min at depth. All animals were returned to the surface (1 ATA) without decompression stops. The incidence of severe DCS < 2 h after surfacing was 96%, 63%, 82%, and 29% for groups 1, 2, 3, and 4, respectively. The incidence of death was 88%, 41%, 54%, and 5% for groups 1, 2, 3, and 4, respectively. OPB combined with PFC administration after surfacing provided the greatest reduction in DCS morbidity and mortality in a saturation swine model. O(2)-related seizure activity before reaching surface did not negatively affect outcome, but further safety studies are warranted.

Animals↗