高原脑水肿64例护理体会

高原脑水肿是急性高原病中的危重型，是人进入高原或急进至更高海拔地区后，由于高原缺氧引起的脑功能障碍，多发生在海拔3000m以上的地区，如不及时积极有效救治，病死率极高。我院驻地海拔约3900m，高原脑水肿是我科常见的危重症之一，护理难度大，笔者对近8年来我科救治的64例高原脑水肿患者的护理进行了系统回顾，现报告如下。     

高原肺水肿合并高原脑水肿124例治疗体会

急性高原病是个体由平原进入高原（海拔3000m以上）或高原进入更高海拔由于缺氧致使机体适应不全而发生的高原地区特有的常见病和多发病，主要包括急性轻型高原病、高原肺水肿、高原脑水肿，并且以上疾病常常同时并存，其中以高原肺水肿合并高原脑水肿较为常见，其发病急，病情变化快，是高原地区危重症之一，加之其救治仍在高原现场进行，缺氧、寒冷、空气干燥、紫外线强等恶劣的自然条件依然存在，故临床救治难度相对较大，若治疗不当或不及时，常危及生命。     

缺氧性胃肠功能障碍与重症急性高原病多器官功能障碍的关系

重症急性高原病病情复杂、凶险、发展变化快,易并发多器官功能障碍(MODS)[1],治疗不及时常危及生命.本文通过回顾性分析我院重症急性高原病病例资料,了解重症急性高原病患者缺氧性胃肠功能障碍及MODS的情况,探讨其相互关系及可能的原因和机制.     

急性高原病脑脊液,血液酸碱及气体成分的改变

作者采用自身对比实验,观察了拉萨市的12例急性高原病治疗前及恢复后的脑脊液、血液的酸碱及其气体成分变化,结果显示急性高原反应及高原肺水肿患者均存在着不同程度的脑水肿,缺氧引起的脑水肿可能是急性高原病发病过程中的重要环节。     

高原肺水肿研究进展

高原肺水肿属急性高原病重症,发病迅速,病死率高.现综述高原肺水肿的发病机制、诊断以及防治措施等方面的研究进展.     

急性高原肺水肿患者血流动力学监测与治疗

由于高原特殊低氧环境,在高原(尤其海拔>4000m)易发生急性高原肺水肿和高原脑水肿,如不及时治疗,预后极差。我们在格尔木市人民医院(海拔2820m)对8例急性高原肺水肿进行了血流动力学监测。对象与方法　(1)一般资料:8例急性高原肺水肿符合中华医学会第三次高原医学学术研讨会推荐的诊断标准[1]。其中5例合并高原脑水肿。年龄27～45岁,平均年龄(35±7)岁。均为汉族。发病时海拔高度在4200～4800m,其中7例是由平原地区5d内直接进入海拔4200m以上地区,1例是当地居民。8例均于进入高海拔地区72h内发病。(2)方法:患者经常规处理后均经右侧颈内静脉…     

高原环境下慢性高原病并发急性高原病的临床回顾

目的：了解在高原环境下慢性高原病患者并发急性高原病的情况。方法：对地处海拔3658米本院40年间（1956年1月至1995年12月）收治的符合筛选标准的18090例住院病历为样本,随访1－15年不等,分为两组,病例组为慢性高原病住院者,对照组为非高原病首次住院者。观察急性高原病的发病情况并进行临床流行病学的分析。结果：（1）对照组急性高原病发病率随观察年限延长而增加,病例组无此现象。急性高原病的逐年发病率与累计发病率,病例组显著高于对照组（P＜0．005）,相对比数比（OR）＝5．03,相对危险度（RR）＝4．33;（2）三型急性高原病发病率除高原高血压组的高原肺水肿与高原心脏病组的高原脑水肿发病率外,余在病例组显著高于对照组（P＜0．05－0．005）。高原心脏病与蒙现组急性高原病发病率分别为23．5％,21．98％。OR＝7．33－6．71,RR＝5．86－5．47;（3）高原心脏病组和蒙赫病组的急性高原病发病率构成以急性轻型高原病为主。结论：慢性高原病患者发生急性高原病风险比高原习服人群增加5倍,尤以高原心脏病与蒙赫病为显著。     

高原康胶囊对快速进入高原者脂质过氧化反应的影响及其意义

人体脑组织富含胆固醇和不饱和脂肪酸，易受到氧自由基的攻击而发生脂质过氧化反应，所以许多急性高原病（AHAD）患者首先表现为神经生理功能的变化，如头痛、头昏等。已有研究证明急性轻型高原病（AMAD）、高原肺水肿（HAPE）、高原脑水肿（HACE）都不同程度地存在脑水肿，因此脂质过氧化反应与AHAD的发病有着密切的关系。     

机械通气在抢救特重型急性高原病中的作用

特重型急性高原病是指同时伴有急性高原性肺水肿和脑水肿的严重疾病。2000年3月至2003年3月，我院收治14例特重型急性高原重症，经常规、氧疗、吸痰、脱水、降颅压、激素、强心、利尿治疗无效后，6例进行机械通气治疗，取得良好疗效。现报告如下。     

急性高原病发病机制的研究进展

高原环境具有低压性低氧、寒冷、辐射强等一系列特点,其中低氧对机体的影响最大。急性高原病是指人在到达海拔超过2500米的高原时,可能发生的急性高原反应、高原脑水肿以及高原肺水肿的总称。随着人们对进入高原地区的需求日益增加,急性高原病的发病机制、预防和治疗也得到了更多的关注。目前,该病的发病机制尚未完全阐明,防治也并未出现更多的进展。本文总结了急性高原病发病的可能机制,旨在为急性高原病的预防和治疗提供新的作用靶点。     

急性高山病的预防与治疗

青藏铁路通行使高原旅行的人数大增,也使得对于处理高原病的知识需要随之增加。急性高原病是人体对急性缺氧习服的失败,包括：高山反应,高原肺水肿和高原脑水肿。急性高原病的特征是发病率极高却又可以有效预防;严重时可以致命但及早发现却可有效治疗。本文总结人体在急性缺氧情况下病生理反应的研究进展和预防处理急性高原病的最新知识。     

Prevention and Treatment of High-Altitude Pulmonary Edema

We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high-altitude pulmonary edema (HAPE). Individual susceptibility is the most important determinant for the occurrence of HAPE. The hallmark of HAPE is an excessively elevated pulmonary artery pressure (mean pressure 36-51 mm Hg), caused by an inhomogeneous hypoxic pulmonary vasoconstriction which leads to an elevated pulmonary capillary pressure and protein content as well as red blood cell-rich edema fluid. Furthermore, decreased fluid clearance from the alveoli may contribute to this noncardiogenic pulmonary edema. Immediate descent or supplemental oxygen and nifedipine or sildenafil are recommended until descent is possible. Susceptible individuals can prevent HAPE by slow ascent, average gain of altitude not exceeding 300 m/d above an altitude of 2500 m. If progressive high altitude acclimatization would not be possible, prophylaxis with nifedipine or tadalafil for long sojourns at high altitude or dexamethasone for a short stay of less then 5 days should be recommended.     

Urinary leukotriene E(4) levels are not increased prior to high-altitude pulmonary edema

STUDY OBJECTIVE: To examine whether increased urinary cysteinyl-leukotriene E(4) (LTE(4)) excretion, which has been found to be elevated in patients presenting with high-altitude pulmonary edema (HAPE), precedes edema formation. DESIGN: Prospective studies in a total of 12 subjects with susceptibility to HAPE. SETTING: In a chamber study, seven subjects susceptible to HAPE and five nonsusceptible control subjects were exposed for 24 h to an altitude of 450 m (control day), and exposed for 20 h to 4,000 m after slow decompression over 4 h. In a field study, prospective measurements at low and high altitude were performed in five subjects developing HAPE at 4,559 m. PARTICIPANTS: Mountaineers with a radiographically documented history of HAPE and control subjects who did not develop HAPE with identical high-altitude exposure. INTERVENTIONS: 24-h urine collections. MEASUREMENTS AND RESULTS: In the hypobaric chamber, none of the subjects developed HAPE. The 24-h urinary LTE(4) did not differ between HAPE susceptible and control subjects, nor between hypoxia and normoxic control day. In the field study, urinary LTE(4) was not increased in subjects with HAPE compared to values obtained prior to HAPE at high altitude and during 2 control days at low altitude. CONCLUSIONS: These data do not provide evidence that cysteinyl-leukotriene-mediated inflammatory response is associated with HAPE susceptibility or the development of HAPE within the context of our studies.     

硝普钠治疗高原肺水肿的疗效分析

目的:探讨硝普钠对高原肺水肿的治疗效果。方法:对62例高原肺水肿的住院患者,进行常规治疗(34例)或在常规治疗的基础上静脉滴注硝普钠(28例),观察患者肺部音消失时间、胸片阴影消失时间、临床治愈时间。结果:62例患者中,硝普钠组的肺部音消失时间、胸片阴影消失时间及临床治愈时间较常规治疗组明显缩短(P<0.01)。结论:硝普钠对高原肺水肿有明显的辅助治疗作用。     

Prevention and treatment of high-altitude illness in travelers

High-altitude illness is the collective term for acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). These syndromes can affect unacclimatized travelers shortly after ascent to high altitude (especially higher than 2500 m). AMS is relatively common and usually is mild and self-limiting; HACE and HAPE are uncommon but life-threatening. Gradual ascent is the best strategy for preventing or minimizing high-altitude illness, although chemoprophylaxis may be useful in some situations. Acetazolamide remains the chemoprophylactic agent of choice, although other drugs, such as gingko biloba, are being investigated. Immediate descent remains the cornerstone of treatment for HACE and HAPE, although pharmacologic and hyperbaric therapies may facilitate this process.     

Gene polymorphisms and high-altitude pulmonary edema susceptibility: a 2011 update

High-altitude pulmonary edema (HAPE) is a severe disease caused by high-altitude hypoxia. Since some individuals are more susceptible to high altitude than others, the incidence is variable and cannot be predicted. Furthermore, multiple genes can contribute to the occurrence of HAPE, making it even more difficult to predict. The genes associated with HAPE include those in the renin-angiotensin-aldosterone system pathway, the nitric oxide pathway and the hypoxia-inducible factor pathway. Other genes associated with HAPE include tyrosine hydroxylase (TH), vascular endothelial growth factor (VEGF), pulmonary surfactant proteins and β(2)-adrenergic receptor. The association of the polymorphisms of these genes with HAPE susceptibility has previously been investigated. Among the genes evaluated, polymorphisms of NOS3, ACE, CYP11B2, Hsp70 and endothelin-1 and pulmonary surfactant proteins A1 and A2 were shown to be associated with HAPE incidence, while associations between TH, VEGF and HAPE remain to be fully elucidated. Novel technological approaches, including genome-wide association studies and next-generation sequencing, are currently being used to identify new HAPE susceptibility genes. The goal of this review article is to summarize the current literature and to define the outstanding areas of research that need to be explored to advance our ability to predict when HAPE will occur.     

High-altitude-related disorders--Part I: Pathophysiology, differential diagnosis, and treatment

As increasing numbers of people choose to sojourn or retire to the mountains, high-altitude illness is becoming a pathological phenomenon about which healthcare providers should have greater awareness. Hypoxia is the primary cause of high-altitude illness, but other stressors on the sympathetic nervous system, such as cold and exertion, also contribute to disease development and progression. Although variable across persons, symptoms of high-altitude disorders usually occur at altitudes over 7000 feet, and typically in 1 of 3 forms: acute mountain sickness (AMS), high-altitude cerebral edema (HACE), or high-altitude pulmonary edema (HAPE). Major symptoms include nausea, poor sleep, headache, lassitude, cough, dyspnea on exertion and at rest, ataxia, and mental status changes. As a rule, illness occurring at high altitude should be attributed to the altitude until proven otherwise. Treatment is best accomplished by descent and by oxygen or pharmacologic intervention if necessary. Under no circumstances should a person with worsening symptoms of high-altitude illness delay descent. As will be discussed in part II of this article, gradual ascent and subsequent acclimatization to altitude is the most effective prevention, though acetazolamide (Diamox) may be a useful prophylactic measure in some.     

Medical therapy of altitude illness

Acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE) continue to cause significant morbidity and occasional deaths among mountain recreationists and residents. Descent to lower altitude is still considered the treatment of choice, but an increased role for medical therapy is emerging. Acetazolamide is currently the drug of choice for prevention of AMS, and probably HAPE as well. Numerous studies have demonstrated the drug's effectiveness when it is started 12 to 24 hours before ascent. Suggestions for indications, dosage, and regimen vary with different authors. Lower dosage offers adequate protection with fewer side effects. Acetazolamide has still not been adequately studied for treatment of altitude illness. Oxygen effectively treats HAPE and mild AMS, but is not as useful for cerebral edema. Dexamethasone recently was found effective for treatment of AMS, including early cerebral edema, but not for advanced cerebral edema. Side effects limit its use for prophylaxis, but dexamethasone offers an alternative to acetazolamide for those with sulfa intolerance.