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.     

Treatment of decompression sickness in swine with intravenous perfluorocarbon emulsion

BACKGROUND: We examined an adjunctive treatment for severe decompression sickness (DCS) to be used when hyperbaric treatment is delayed or unavailable. HYPOTHESIS: It has been hypothesized that intravenous perfluorocarbon (PFC) emulsion combined with 100% inspired O2 would improve the outcome in severe DCS. METHODS: Swine (n = 45) were compressed to 4.9 ATA on air for 22 h and brought directly to 1 ATA at 0.9 ATA min(-1). The animals were then randomized to three groups. The first group breathed ambient air, the second group breathed 100% O2, and a third group received 6 ml x kg(-1) of perflubron emulsion (Oxygent) intravenously and breathed 100% O2. Outcomes of neurological and cardiopulmonary DCS and death were recorded. RESULTS: Animals that received PFC emulsion sustained less DCS (p < 0.01) than the other groups (53% vs. 93%). No animals in the PFC group sustained neurological DCS, which was present in 69% of the subjects in the other two groups. CONCLUSION: O2 breathing postdive did not significantly reduce morbidity or mortality in this model. Postdive treatment with PFC emulsion and 100% O2 decreased the incidence of DCS after nonstop decompression from saturation.     

高压氧对实验性减压病兔脊髓bFGF表达的影响

目的探讨实验性减压病兔脊髓bFGF的改变及高压氧对其影响。方法实验家兔随机分为7组：正常组、减压病3h组、减压病3d组、高压氧3h组、高压氧3d组、常氧高压氮3h组、常氧高压氮3d组。采用快速减压方法制备减压病模型，用免疫组织化学方法检测胸髓及腰髓中bFGF表达。结果（1）快速减压后各组bFGF表达均较正常组增加（P〈0．01），3h组之间无差异（P〉0．05）；（2）减压病3d组较3h组bFGF表达显著增高（P〈0．01），高压氧3d组较3h组显著降低（P〈0．01），常氧高压氮3d组较3h组有所降低（P〈0．05）；（3）高压氧3d组与常氧高压氮3d组均较减压病3d组显著降低（P〈0．01），高压氧3d组较常氧高压氮3d组降低（P〈0．05）。结论减压病脊髓损伤后bFGF表达增加；高压氧和常氧高压氮对减压病脊髓损伤起保护作用，高压氧效果优于常氧高压氮。     

Intravenous perfluorocarbon emulsion increases nitrogen washout after venous gas emboli in rabbits.

Intravenous perfluorocarbon emulsion (IV-PFC) has been shown to provide hemodynamic protection from gas embolism (Venous-VGE or arterial-AGE). The objective of this study was to investigate the mechanism of PFC protection from controlled VGE by quantifying the effects of IV-PFC emulsion on pulmonary elimination of nitrogen (N2). All rabbits received an intravenous pretreatment of PFC emulsion (Oxygent, 2.7 g/kg) or saline, then either a continuous room air infusion (0.25 ml/kg for 10 minutes) or a bolus of air (0.8 ml/kg within 10 seconds) through the femoral vein. Expiratory N2 peaked higher with PFC infusion immediately after air injection. The recovery to baseline of end tidal N2 was faster for PFC-treated animals (40 +/- 4.7 vs. 58 +/- 6.5 minutes). In PFC-treated animals, expired CO2, O2, arterial pressure and central venous pressure returned to baseline faster than the saline group. This study demonstrated that PFC increased pulmonary N2 washout. Correspondingly, PFC treatment better preserved the animals' hemodynamics after VGE injury. The use of IV-PFC promises to be a breakthrough non-recompression therapy for gas embolism in the treatment of Decompression Sickness (DCS) and in surgery.     

Partial pressure of nitrogen in breathing mixtures and risk of altitude decompression sickness

BACKGROUND: Many aircraft oxygen systems do not deliver 100% O2. Inert gases can be present at various levels. The purpose of this study was to determine the effect of these inert gas levels on decompression sickness (DCS). METHODS: Subjects were exposed for 4 h to 5486 m (18,000 ft) with zero prebreathe, using either mild (Test A) or strenuous exercise (Test B), and breathing 60%N2/40%O2. Test C used a breathing mixture of 40%N2/60%O2 at 6858 m (22,500 ft) with zero prebreathe and mild exercise. Test D investigated a breathing mixture of 2.8%N2/4.2%argon/93%O2 with 4 h exposures to 7620 m (25,000 ft), mild exercise, and 90 min of preoxygenation. The controls were from previous studies using similar conditions and 100% O2. RESULTS: The DCS risk for Tests A and B and the Control for B was 7%; the Control for Test A was 0% (n.s.). Breathing the 40%N2/60%O2 mixture (Test C) resulted in 43% DCS compared with 53% DCS with 100% O2 (n.s.). When the 2.8%N2/4.2%argon/93%O2 mixture was used, the results showed 25% DCS compared with 31% DCS with 100% O2 (n.s.). CONCLUSIONS: The increased nitrogen and argon levels in the breathing gas while at altitudes of 5486 m to 7620 m did not increase DCS risk. These results support the concept of using the partial pressure gradient of inert gases instead of the percentage of N2 or argon in a breathing gas mixture to determine the risk of DCS during altitude exposure.     

Blood platelet count and severity of decompression sickness in rats after a provocative dive

INTRODUCTION: Previous animal studies reported that platelet count (PC) is decreased following decompression. Adherence and aggregation of platelets to the bubble surface has been demonstrated in severe decompression sickness (DCS). The present study was designed to clarify the relationship between post-dive platelet levels and the severity of DCS in a rat model. METHODS: A total of 57 male Sprague-Dawley rats were assigned to either one experimental group with a hyperbaric exposure (N = 22) or one control group (N = 27). Rats were compressed to 1000 kPa (90 msw) for 45 min while breathing air and decompressed to surface in 38 min with stops at 200, 160, and 130 kPa. Onset of neurological DCS and death time were recorded during a 120-min observation period after surfacing. In the control group, rats were maintained at atmospheric pressure in the same chamber for an equivalent period of time. Blood samples for PC were taken 30 min before and immediately after exposure in two groups. RESULTS: Blood PC after hyperbaric exposure had significantly decreased, whereas PC had increased in the control group. We found a correlation between % fall in PC and latency to death time. The platelet loss tended to decrease when fatal DCS was delayed. Rats suffering from severe DCS with a short latency to death presented a pronounced decline in platelets. DISCUSSION: The present study highlighted a relationship between the post-dive decrease in PC and DCS severity in rats. Platelet consumption could offer a new index for evaluating decompression stress.     

Relation between right-to-left shunts and spinal cord decompression sickness in divers

The role of right-to-left shunting (RLS) in spinal cord decompression sickness (DCS) remains uncertain and could differ according to the distribution of lesion in spinal cord with a higher risk of upper spinal cord involvement in divers presenting a large patent foramen ovale. The aims of this study were to assess the prevalence of RLS with transcranial doppler ultrasonography in 49 divers referred for spinal cord DCS and compare it with the prevalence of RLS in 49 diving controls, and to determine a potential relation between RLS and lesion site of spinal cord. The proportion of large RLS was greater in DCS divers than in healthy control divers (odds ratio, 3.6 [95 % CI, 1.3 to 9.5]; p = 0.017). Shunting was not associated with the increased incidence of cervical spinal cord DCS (OR, 1.1 [95 % CI, 0.3 to 3.9]; p = 0.9) while a significant relationship between large RLS and spinal cord DCS with thoracolumbar involvement was demonstrated (OR, 6.9 [95 % CI, 2.3 to 20.4]; p < 0.001). From the above results, we conclude that the risk of spinal cord DCS in divers with hemodynamically relevant RLS is higher than in divers without RLS, particularly in their lower localization.     

Spinal cord decompression sickness: a comparison of recompression therapies in an animal model

Somatosensory evoked potentials (SEP) were used in an animal model to measure spinal cord electrophysiological function. Animals were submitted to a dive profile resulting in spinal cord decompression sickness (DCS). The animals were treated after a delay allowing the lesion to consolidate. Serial measurements of SEP documented the onset, duration, and outcome of treatment. Physiological data were recorded throughout each experiment. Group A (n = 10) was recompressed to 60 fsw (feet of sea water) breathing 100% oxygen (2.8 ATA) and Group B (n = 8) was treated at 66 fsw breathing 66% oxygen (2.0 ATA). No differences were found between groups in the severity, surface interval before treatment, or the maximum effect of treatment. The maximum effect of treatment was seen by 25 min of treatment. Animals were regrouped into responders and nonresponders. The latter displayed a more rapid onset, a more severe insult, and more adverse physiological effects than the responders. The possibility of a different etiology was considered together with the failure to differentiate between the treatment groups. It was concluded that treatment B was safer but the problems of introducing a new therapeutic table outweighed the safety advantage.     

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.     

The effect of staged decompression while breathing 100% oxygen on altitude decompression sickness

INTRODUCTION: Space Shuttle extravehicular activity (EVA) requires decompression from sea level pressure (14.7 psia) to a 4.3 psia (30,300 ft) pressure suit. The transition currently involves altering the shuttle atmosphere to allow shirt-sleeve denitrogenation to occur during a 12 to 36-h staged decompression (SD) at 10.2 psia (9,800 ft) with an oxygen-enriched breathing gas (26.5% oxygen, 73.5% nitrogen). The denitrogenation provides protection from decompression sickness (DCS) during EVA in a 4.3 psia pressure suit. Our goal was to determine the highest altitude at which SD while breathing 100% oxygen (SD100) could provide effective protection from development of DCS symptoms after further decompression to 29,500 ft (4.5 psia). METHODS: There were 30 male subjects exposed to at least 6 of 11 conditions in random order on successive months to 29,500 ft for 4 h while performing mild exercise and being monitored for venous gas emboli (VGE) with an echo-imaging system. The subjects received 15 min of ground-level (GL) preoxygenation and an additional 60 or 120 min of SD100 at one of four altitudes between 8,000 ft (10.9 psia) and 18,000 ft (7.3 psia). Control exposures followed a 75- or 135-min ground-level preoxygenation. RESULTS: During SD100, one case of DCS occurred at 18,000 ft, but not at lower staging altitudes. Higher levels of VGE were observed during SD100 at 18,000 ft than during SD100 at any lower altitude. CONCLUSION: Staged decompression at 16,000 ft and below results in decompression risk during subsequent decompression to 29,500 ft similar to that following equivalent periods of ground-level preoxygenation.     

静脉注射全氟碳剂联合酒精湿化吸氧对兔减压病的影响

目的 观察静脉注射全氟碳剂(perfluorocarbon,PFC)联合酒精湿化吸氧对兔减压病发病率、病死率、红细胞和血小板计数的影响.方法 90只4月龄健康雄性新西兰大耳实验兔随机分为5组,包括正常对照组(NC组)、减压病(decompression sickness,DCS)建模组(DCS组)、减压病建模组+静脉注...     

Neurobehavioral and magnetic resonance imaging findings in two cases of decompression sickness

Two divers underwent neurobehavioral examinations and magnetic resonance imaging (MRI) while hospitalized during the first 2 weeks after sustaining decompression sickness (DCS). Their neurologic findings included a Brown-Séquard Syndrome consistent with spinal cord lesion, and focal deficits consistent with cerebral lesion(s). MRI revealed subcortical white matter lesions in the brains of both divers, whereas no lesion of the spinal cord was demonstrated. The patients exhibited neurobehavioral sequelae including disturbances of memory, divergent thinking, and visuospatial and motor functioning. Focal neurologic deficits resolved in both patients, and their cognitive and memory problems improved slowly. Findings in these two divers raise the possibility that cerebral insult more frequently accompanies spinal cord injury in DCS than previously thought.     

The risk of altitude decompression sickness at 12,000 m and the effect of ascent rate

INTRODUCTION: Loss of aircraft cabin pressurization can result in very rapid decompression rates. The literature contains reports of increased or unchanged levels of altitude decompression sickness (DCS) resulting from increasing the rate of decompression. We conducted two prospective exposure profiles to quantify the DCS risk at 12,192 m (40,000 ft), and to determine if there was a greater DCS hazard associated with a much higher rate of decompression than typically used during past DCS studies. METHODS: The 63 human subjects participated in 80 altitude chamber decompression exposures to a simulated altitude of 12,192 m (2.72 psia; 18.75 kPa) for 90 min, following preoxygenation with 100% oxygen for 90 min. Half of the subject-exposures involved an 8-min decompression (1,524 mpm; 5,000 fpm) and the other half experienced a 30-s decompression (mean of 24,384 mpm; 80,000 fpm). Throughout each ascent and exposure, subjects were seated at rest and breathed 100% oxygen. At altitude, they were monitored for precordial venous gas emboli (VGE) and DCS symptoms. RESULTS: The higher decompression rate yielded 55.0% DCS and 72.5% VGE and the lower rate produced 47.5% DCS and 65.0% VGE. Chi square and log rank tests based on the Kaplan-Meier analyses indicated no difference in the incidence or onset rate of DCS or VGE observed during the two profiles. CONCLUSION: Decompression rate to altitude up to 24,384 mpm was found not to have an effect on DCS risk at altitude. However, research is needed to define the DCS risk with decompression rates greater than 24,384 mpm. It was also found that the onset time to DCS symptoms decreases as altitude increases.     

Venous gas embolism in chamber attendants after hyperbaric exposure.

An initial occupational survey (OS) was initiated to investigate the prevalence of venous gas embolism (VGE) in chamber attendants assisting hyperbaric oxygen (HBO2) treatments. Nine female subjects were exposed for three consecutive days to the routine hospital procedure of compressed air exposure to 240 kPa for approximately 115 min with 12 min of terminal oxygen (O2) breathing. VGE was monitored with ultrasound Doppler in 15 min intervals for 2h after the first and third exposure. A follow-up experimental study was completed to investigate whether changed breathing gases and decompression would affect the high incidence of VGE observed in the OS. Ten female subjects were randomly exposed to the routine or revised profile (12 and 24 min of terminal O2 breathing respectively), and a Nitrox profile (breathing gas 40.5% O2 in Nitrogen during 90 min of the isobaric phase). VGE was monitored with transthoracic ultrasound scanner and Doppler. In the OS precordial VGE grade III (Doppler) was observed in five subjects, but median resting precordial VGE was Grade 0 both days and VGE score at all sites were equal Days 1 and 3. In the experimental study, median resting precordial VGE was Grade 0 (Doppler) and Grade 1 (Scanner). VGE Grade III (Doppler) was observed in all series, but VGE scores were not significantly different between the series. We conclude that chamber attendants assisting HBO2 treatment at 240 kPa for approximately 115 min are exposed to a significant decompression stress using the profiles tested in the present study.     

Pharmacological interventions to decompression sickness in rats: comparison of five agents

INTRODUCTION: This research investigated whether decompression sickness (DCS) risk or severity could be reduced using drug interventions that are easier to implement and equal to or more efficacious than recompression therapy. METHODS: Using a rat model of DCS, anti-inflammatory or anticoagulant drugs, including lidocaine, aspirin (ASA), methylprednisolone (MP), alpha-phenyl-N-butylnitrone (PBN), and transsodium crocetinate (TSC) were tested to determine their effect on incidence of DCS, death, and time of symptom onset. Each treatment group consisted of approximately 40 animals that received the drug and approximately 40 controls. Animals were exposed to one of five compression and decompression profiles with pressure ranging from 6.3 ATA (175 fsw) to 8.0 ATA (231 fsw); bottom time was either 60 or 90 min; and decompression rate was either 1.8 or 15 ATA x min(-1). Following decompression, the rats were observed for 30 min while walking on a wheel. DCS was defined as an ambulatory deficit or abnormal breathing. RESULTS: None of the drugs reached statistical significance for all DCS manifestations. Lidocaine post-dive and MP were the only treatments with marginally (P < 0.15) significant differences in DCS outcomes compared to controls. Lidocaine post-dive significantly decreased the incidence of neurological DCS from 73-51%. MP significantly extended the time of onset of death from DCS from 5.4 min to 7.1 min. DISCUSSION: Of the treatments investigated, lidocaine given post-dive has the best chance of success in adjuvant therapy of DCS. Future studies might investigate adjuvant drugs given in combination or during recompression.     

Electrocardiographic changes in serious decompression sickness

Electrocardiographic changes observed in 21 dogs suffering from spinal cord decompression sickness (DCS) are described. Changes seen included P wave peaking and P-R depression compatible with right heart strain; S-T segment and T wave changes suggestive of myocardial ischemia; and ventricular arrhythmias ranging from unifocal premature ventricular contractions to ventricular tachycardia. Compression therapy did not always restore the ECG changes promptly to normality. The changes are discussed in association with concurrent physiological events. These included pulmonary hypertension, systemic hypertension and hypotension, and cerebral DCS. Possible mechanisms ranging from local cardiac DCS or coronary gas embolism to autonomic nervous system disturbances arising from cerebral and spinal cord DCS are reviewed. It is concluded that ECG recordings should be made more often when treating clinical DCS.     

Effect of heliox, oxygen and air breathing on helium bubbles after heliox diving.

In helium saturated rat abdominal adipose tissue, helium bubbles were studied at 101.3 kPa during breathing of either heliox(80:20), 100% oxygen or air after decompression from an exposure to heliox at 405 kPa for one hour. While breathing heliox bubbles initially grew for 15-115 minutes then shrank slowly; three out of 10 bubbles disappeared in the observation period. During oxygen breathing all bubbles initially grew for 10-80 minutes then shrank until they disappeared from view; in the growing phase, oxygen caused faster growth than heliox breathing, but bubbles disappeared sooner with oxygen breathing than with heliox or air breathing. In the shrinking phase, shrinkage is faster with heliox and oxygen breathing than with air breathing. Air breathing caused consistent growth of all bubbles. With heliox and oxygen breathing, most animals survived during the observation period but with air breathing, most animals died of decompression sickness regardless of whether the surrounding atmosphere was helium or air. If recompression beyond the maximum treatment pressure of oxygen is required, these results indicate that a breathing mixture of heliox may be better than air during the treatment of decompression sickness following heliox diving.     

Decompression Sickness: An Update

In brief: Until 20 years ago, the physical phenomenon of bubbling was the primary consideration in decompression sickness (DCS). Now the physiological aspects of DCS and the physiochemical states that lead to bubbling are better understood. This paper discusses four important developments in the study of DCS: (1) the recognition of the importance of hydration states and flow in the microcirculation, (2) the documentation of intravascular bubble formation during asymptomatic decompressions, (3) the recognition of pharmacological substances that influence DCS, and (4) the development of an animal model to understand spinal cord bends. More attention will probably be given to the use of pharmacological agents in treating DCS in the future.     

静脉注射全氟化碳乳剂对大鼠减压病防治作用的研究

目的 观察静脉注射全氟化碳乳剂(perfluorocarbon emulsion,PFCE)对大鼠减压病(decompression sickness,DCS)的防治作用.方法 以"700 kPa-60 min空气暴露、3 min减压"方案制备SD大鼠减压病模型,在高气压暴露前或暴露后即刻静脉注射PFCE(7 ml/kg),观察大鼠行为学(包括发病和死亡)以及肺、大脑和脊髓组织的病理变化.高气压暴露后以生理盐水处理,或者不经任何处理作为对照.结果 高气压暴露后即刻静脉注射PFCE的动物发病率(21.7%)显著低于生理盐水组(60.0%)(P<0.05)和空白对照组(66.7%)(P<0.01),死亡率(13.0%)显著低于空白对照组(42.9%)(P<0.05);大部分行为学及病理学指标显著改善(P<0.05).高气压暴露前静脉注射PFCE的动物发病率(80.0%)和死亡率(45.0%)与生理盐水组、空白对照组相比差异无统计学意义.结论 高气压暴露后即刻静脉注射PFCE对大鼠急性DCS具有良好的防治作用.     

Staged decompression to 3.5 psi using argon-oxygen and 100% oxygen breathing mixtures

INTRODUCTION: The current extravehicular activity (EVA) space suit at 4.3 psia causes hand and arm fatigue and is too heavy for Martian EVA. A 3.5 psia EVA pressure suit requires increased preoxygenation time but would reduce structural complexity, leak rate, and weight while increasing mobility, comfort, and maintainability. On Mars, nitrogen and argon are available to provide the inert gas necessary for a fire-resistant habitat atmosphere, eliminating need for transport. This study investigated breathing argon/oxygen and 100% oxygen gas mixtures during staged decompression prior to exposure to 3.5 psia. METHOD: During this study, 40 subjects each completed 3 hypobaric exposures to 3.5 psia for 3 h in a reclined position: (A) a 4-h 25-min 14.7-psia (ground level) denitrogenation (100% oxygen breathing) prior to exposure to 3.5 psia; (B) the same as A, utilizing a 7.3-psia stage denitrogenation; and (C) the same as B, with 62% argon-38% oxygen (ARGOX) during the stage. Venous gas emboli (VGE) were monitored with echocardiography. RESULTS: Decompression sickness (DCS) incidence at 3.5 psia with ARGOX at 7.3 psia (C) was significantly higher than with oxygen breathing with or without staged decompression: there was 78% DCS for C compared with 33% and 55% DCS, respectively, for A and B. The corresponding VGE incidences were 73% (C) compared with 33% (A) and 45% (B). CONCLUSION: Preoxygenation at a 7.3-psia stage resulted in a higher DCS risk at 3.5 psia than ground level preoxygenation. It is suggested that an 8.0-psia stage pressure could eliminate this difference. Unfavorable results after preoxygenation with ARGOX indicate argon on-gassing was significant.