Altitude decompression sickness: hyperbaric therapy results in 528 cases

We reviewed 528 cases of decompression sickness (DCS) resulting from altitude exposure (either aircraft or altitude chamber) during the period 1 January 1977 through 31 December 1986, and treated with hyperbaric therapy. Data collected include age, sex, date and place of origin, duty position, type of exposure, altitude, diagnosis, treatment, and result. Analysis of the data described maximum altitudes of exposure, time to onset of symptoms, diagnosis, and the treatment tables used. Significant results include an increased incidence of altitude DCS requiring hyperbaric therapy among females (relative risk for females is 4.3 times that of males), no significant difference in incidence rates between duty positions in the altitude chamber exposures reviewed, and confirmation of the efficacy of hyperbaric oxygen therapy.     

Vascular leukocyte sequestration in decompression sickness and prophylactic hyperbaric oxygen therapy in rats

BACKGROUND: Evidence for a causal relationship between decompression sickness (DCS) and leukocyte sequestration was assessed in a rat model based on the effects of interventions which impede cell-to-cell adherence, including hyperbaric oxygen therapy (HBO2). HYPOTHESIS: We hypothesized that leukocyte adhesion to vessels may play a role in DCS. METHODS: Rats were subjected to decompression stress and their ability to ambulate on a rotating drum was assessed to quantify functional neurological deficits. Leukocyte adherence in the brain was measured by a myeloperoxidase (MPO) radioimmunoassay. Interventions included infusion of antibodies to render rats neutropenic or to inhibit leukocyte beta2 integrin adhesion molecules. Tissue gas bubbles were imaged and quantified using a transmission ultrasound camera. RESULTS: Decompressed rats manifested a deficit in their ability to ambulate and a five-fold elevation in concentration of MPO in brain. Neutropenic rats, and those infused with antibody fragments to inhibit leukocyte beta2 integrins, did not exhibit brain MPO elevations, nor a deficit in ambulatory function. HBO2 was used in a prophylactic manner to address its ability to inhibit leukocyte beta2 integrin-mediated adherence without reducing the presence of decompression-induced bubbles. Prophylactic HBO2 prevented cerebral leukocyte sequestration and the performance deficit. CONCLUSIONS: The results implicate beta2 integrin-mediated leukocyte adhesion in neurological deterioration after decompression stress, and offer new insight into the therapeutic action of HBO2. Immunomodulatory approaches, including prophylactic HBO2, may improve the safety of decompression procedures in undersea and space exploration.     

快速减压后大鼠模型视网膜电生理的变化

目的 观察快速减压(RD)后大鼠视网膜电图(ERG)的变化,并探讨减压病造成视网膜早期功能损伤的特点。方法 20只大鼠按数字表法随机分为4组,分别为正常对照(NC)组、安全减压(SD)组、快速减压处理后0 h(RD0)组和6 h(RD6)组,SD组、快速减压处理各组大鼠暴露于加压舱内,舱内气压在30 s内升至1.0 MPa,维持5.5 min,快速减压各组打开放气阀用55 s减至常压,SD组采用动物安全减压方案减到常压。按照国际临床视觉电生理学会的标准化方案,采用国特医疗系统和银-氯化银角膜电极以及银针电极对大鼠进行暗视视网膜电图(Scot-ERG)、振荡电位(OPs)、明视视网膜电图(L-ERG)记录。结果 快速减压后大鼠ERGa、b波以及OPs O2波幅值降低,潜伏期明显延长。快速减压后6h,Scot-ERG b波和OPs O2波幅值增加,RD6组[b波(134.5±27.9) μV,O2波(27.1±9.2)μV]较RD0组[b波(56.5±21.1) μV,O2波(8.1±1.9) μV]高(P＜0.05)。SD组比RD0组和RD6组视网膜电活动受抑制程度轻,SD组Scot-ERG b波和OPs O2波幅值[b波(266.5±25.2) μV,02波(44.1±5.6) μV]高于快速减压后RD0组和RD6组(P＜0.05)。结论 快速减压会造成大鼠视网膜电生理异常,安全减压可有助于减轻这种功能损伤。     

Noncardiogenic pulmonary edema as the first manifestation of pheochromocytoma: a case report

We report here a case of pheochromocytoma presenting with noncardiogenic pulmonary edema, which is an unusual first manifestation of pheochromocytoma. Chest radiograph showed diffuse consolitaion and ground-glass opacity on both lungs. Neither pleural effusion nor cardiomegaly was present. High-resolution computed tomography (HRCT) showed widespread ground-glass opacity with fine intralobular reticular opacity (so-called "crazy-paving" appearance) and consolidation in a strikingly dependent distribution. The areas of ground-glass opacity and consolidation were sharply marginated by interlobular septa, showing a geographic appearance. The pulmonary edema and dyspnea resolved over three days without cardioactive or diuretic treatment. Noncardiogenic pulmonary edema is an unusual first manifestation of pheochromocytoma. It is important to recognize this unusual manifestation in the emergency situation.     

Radionuclide lung imaging in respiratory decompression sickness: potential role in the diagnosis and evaluation of hyperbaric therapy

Of the more than 3.5 million trained divers in the United States, many will experience various illnesses specific to divers. Most of these illnesses are related to the changes in absolute pressure that divers experience while diving. During and after ascent, a diver is at risk for decompression sickness and pulmonary barotrauma. A very rare casualty is pulmonary decompression sickness from immersion. This is a literature review and case report of a young woman with acute respiratory decompression sickness who had defects on perfusion lung imaging after a diving accident and after hyperbaric oxygen therapy. However, the perfusion defects reverted to normal in less than 24 hours. Possible explanations for the changes in the appearances of the scans are offered and discussed. This case report shows the potential utility of lung scanning in the diagnostic examination of these patients and the evaluation of the adequacy of treatment with hyperbaric oxygen therapy. A greater use of ventilation-perfusion lung scans in the treatment of such patients may establish its role more definitely.     

Reascent following resolution of high altitude pulmonary edema (HAPE)

There is an absence of information in the literature regarding reascent to high altitude following resolution of HAPE (high altitude pulmonary edema). This report presents three cases of HAPE that are notable for later reascent to a high summit (up to 8,850 m) within the time course of each expedition. These cases illustrate that careful, gradual reascent following recovery and acclimatization after an episode of HAPE precipitated by rapid ascent may be considered. The pathophysiology of HAPE is reviewed with a focus on the evidence for rapid reversibility of pulmonary vascular injury. The evidence for protective pulmonary vascular remodeling is discussed to further support such a recommendation for cases of uncomplicated HAPE.     

Fibroblast response to rapid decompression and hyperbaric oxygenation.

INTRODUCTION: The cellular basis for symptoms associated with rapid decompression and the use of hyperbaric oxygenation treatment (HBO) is not established. METHODS: Image analysis, sulforhodamine B assay and bromodeoxyuridine (BrDU) incorporation were used to identify cellular changes associated with rapid decompression (RD) or hyperbaric oxygenation (HBO). Human fibroblasts were exposed to RD or HBO and compared with untreated cells. Immediately following treatment, the fraction of cells synthesizing DNA was measured by detection of cells incorporating the BrDU. At 1 d and 3 d following the treatments, total cell protein adherent to the bottom of wells was measured using a sulforhodamine B assay. Cell density was observed with light microscopy and quantified with image analysis. RESULTS: RD increased total protein significantly, (p < 0.05) relative to control, while HBO had less effect. The fraction of cells synthesizing DNA was increased by HBO and reduced by RD relative to control (p < 0.05). Image analysis showed that cell density at day 1 was: control>HBO>RD; and at day 3: RD>HBO>control, indicating an increase in proliferation induced by the treatments. CONCLUSION: This data shows that HBO and RD increase the proliferation of fibroblasts for 24 h following treatment. HBO increased DNA replication. While there was a decrease in DNA replication following RD, protein synthesis was enhanced.     

Inner ear decompression sickness following altitude chamber operation

Decompression sickness (DCS) is a known hazard of altitude chamber operation. The musculoskeletal, dermal, neurological and pulmonary manifestations of DCS are well recognized, but inner ear injury has not been reported. We present the unusual case of a medical corpsman suffering from vestibular DCS after an altitude chamber exposure to 25,000 ft. The patient had a good clinical response to hyperbaric treatment, but there was laboratory evidence of mild residual vestibular damage with full compensation. This case suggests that aviation medical personnel should be more aware of the possible occurrence of inner ear DCS among subjects exposed to altitude.     

Altitude decompression sickness symptom resolution during descent to ground level

INTRODUCTION: Altitude decompression sickness (DCS) is a health risk associated with the conduct of high altitude airdrop operations, high altitude reconnaissance, future fighter operations, hypobaric chamber training, unpressurized flight, and extravehicular activity (EVA) in space. The treatment for DCS includes the provision of 100% oxygen (O2) at ground level (GLO) and/or hyperbaric oxygen therapy (HBO). In this paper we examine the effect of repressurization to ground level from hypobaric conditions on DCS symptoms. Timely recompression (descent at first recognition of any DCS symptom) may be a safe, effective treatment for the large majority of DCS symptoms. METHODS: Data from altitude chamber exposures recorded in the Air Force Research Laboratory (AFRL) Altitude DCS Database were reviewed to determine the level of recompression required for complete resolution of 1,699 observed symptoms. RESULTS: Of the 1,699 DCS symptoms reviewed, 66 (3.9%) resolved at altitude, 117 (6.9%) resolved at ground level, and 1,433 (84.3%) resolved during descent. Increasing the pressure by 138 mmHg from the altitude of exposure where symptoms occurred resolved roughly 50% of symptoms. Little resolution of symptoms was noted with recompressions of < 50 mmHg. The greatest rate of symptom resolution occurred with recompressions of 50-250 mmHg. CONCLUSION: These findings support the concept that descent and postflight, ground-level oxygen may be sufficient to relieve the majority of altitude DCS symptoms. HBO may be reserved for serious, recurring, delayed, or refractory symptoms. The findings also suggest a need for further study of DCS symptom resolution.     

高空减压病氧气疗法发展动向

目的 综述国外近10年来高空减压病氧气疗法在实际应用及科学研究工作中的进展。资料来源与选择、主要资料选自1990年以来发表的有关高空减压病氧气疗法的文献。资料引用 国内外发表的文献11篇，资料综合 美国在空军加压治疗表（表5及表6）的基础上提出了两个方面的建议：（1）引进美国海军减压病加压治疗表4及表7凤提高对严重病例及复发病例的疗效；（2）采用地面呼吸纯氧及加压值≤2ATA（1ATA=101.3kPa)的高压氧疗法治疗单纯屈肢症病例，以适应航空、航天活动中应用方法更简单、合用、可就地实施的需要。结论 所提建议在实践及理论上皆有合理的根据，值得试行推广。     

Inner ear decompression sickness following a shallow scuba dive

Inner Ear Decompression Sickness (IEDCS)--manifested by tinnitus, vertigo, nausea, vomiting, and hearing loss--is usually associated with deep air or mixed gas dives, and accompanied by other CNS symptoms of decompression sickness (DCS). Early recompression treatment is required in order to avoid permanent inner ear damage. We present an unusual case of a scuba diver suffering from IEDCS as the only manifestation of DCS following a short shallow scuba dive, successfully treated by U.S. Navy treatment table 6 and tranquilizers. This case suggests that diving medical personnel should be more aware of the possible occurrence of IEDCS among the wide population of sport scuba divers.     

Pathogenesis of pulmonary edema caused by blast waves]

In the study of pathogenetic mechanisms of pulmonary edema to blast wave generated by detonation of the aerosol explosive in the open air, the dynamics of changes of the eicosanoid contents, the products of the energy metabolism as well as the glucose metabolism in the lung tissue of sheep have been examined. On the basis of data from the literature as well as own results the authors have given the original scheme of possible mechanisms of pulmonary edema caused by effects of the blast wave.     

乙醇治疗急性减压病的实验研究

目的 探讨乙醇治疗急性减压病的病因学及其作用机制.方法 将实验兔32只复制成急性减压病(ADCS)模型,随机分为治疗组和对照组,每组16只.放人动物舱内在5 min内加压至0.6MPa,停留30 min,然后用10 min匀速减至常压(0.1 Mpa)出舱.出舱后每隔5 min定时测定Doppler气泡音.戊巴比妥纳20 mg/kg耳缘静脉麻醉后,手术暴露后腔静脉约10 cm作为观察段.治疗组ADCS模型兔在测定Doppler气泡音后,用25%乙醇溶液3 ml/kg,由耳缘静脉缓慢注射入血管内;对照组则由耳缘静脉缓慢注射10 ml生理盐水.然后经后腔静脉直接观察气泡消长情况,分次解剖,整体观察.结果 对照组16只兔,出舱后30 min相继死亡8只,其余在60～100 min时仍有Ⅰ～Ⅲ级Doppler气泡音,后腔静脉、皮下、肌肉、内脏器官及循环系统可见大量气泡,部分血管完全被气泡阻塞.治疗组无死亡,Doppler气泡音在30～60 min内消失.后腔静脉、皮下、肌肉、内脏器官的血管直径增加一倍以上,血流显著增快.血循环内无气泡或有极少量单个气泡.结论 乙醇疗法是一种快速有效、经济实用的消除急性减压病的新方法.     

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。     

创伤性脑水肿的发生机制及治疗研究进展

颅脑创伤作为一种严重的创伤类型,无论平时还是战时均有较高的发生率,严重威胁人类生命安全。颅脑创伤后,均有不同程度的脑水肿的发生和存在,对脑水肿的治疗效果直接关系到疾病的预后。本文就创伤性脑水肿的分类、发生机制及治疗进展作了全面综述。     

结合运动的氧气预呼吸对减压病的预防作用

目的 综述国外氧气预呼吸过程中进行体育运动以提高对减压病预防作用的科研工作进展。资料来源与选择 主要资料选自公开发表的氧气预呼吸过程中进行体育运动以提高对减压病预防作用的文献。资料引用 参考文献16篇。资料综合 氧气预呼吸过程中进行体育活动可以减少减压病发生率，这已为低压减压实验及数学模型初步证实，这种作用可能是因为体育运动能使肺通气量、心输出量及组织灌流增加引起排氮效率提高的结果。结论 结合运动的氧气预呼吸可以缩短氧气预呼吸时间而保持预防效果，符合高空飞行及航天员出舱活动的需要，故此方法值得深入研究。     

高压氧对实验性减压病兔脊髓诱发电位的影响

目的　探讨实验性减压病兔脊髓诱发电位的改变及高压氧 (HBO)对其影响。方法　将 3 2只实验兔放入加压舱中 ,于 5min内用压缩空气加压至 0 .6MPa,停留 60 min ,然后于 3～ 5m in内减至常压。分别于进舱前、出舱后 3 h和 3 d,进行脊髓诱发电位检查。 HBO组 :出舱后 1 h至 3 d,每天接受HBO治疗 1次 (0 .2 5MPa) ;常氧高压氮组 :出舱后 1 h至 3 d,每天暴露常氧高压氮 1次 (0 .2 5MPa) ;对照组 :出舱 1 h至 3 d,每天暴露舱内常压空气 1次。结果　 (1 )三组家兔减压后 3 h脊髓诱发电位 N2 1潜伏期均较进舱前延长 (P<0 .0 1 )、波幅有降低趋势 (P<0 .0 5) ;(2 ) HBO和常氧高压氮可使 N2 1潜伏期缩短 (P<0 .0 1 ) ,波幅增高 (P<0 .0 5)。结论　 (1 )快速减压可造成家兔减压病脊髓损伤 ,表现脊髓诱发电位 N2 1改变 ;(2 ) HBO和常氧高压氮对减压病脊髓损伤均有治疗作用 ,但 HBO疗效优于常氧高压氮