有关高原脑水肿诊断问题的探讨

高原脑水肿( HACE)是人体由低海拔地区到高海拔地区,或由高海拔高原地区到更高海拔高原地区由于机体急性缺氧导致的以颅内压升高和(或)意识障碍为主要表现的一组临床综合征,是急性高原病(AHAD)的一个严重类型.目前HACE的诊断标准是1995年中华医学会第三次全国高原医学学术讨论会推荐稿制定的标准[1],笔者根据自己的临床工作经验及国内外有关HACE研究成果,谈谈对“高原脑水肿诊断标准”的看法.     

高原脑水肿早期诊断标准的探讨

目的探讨高原脑水肿（high altitude cerebral edema,HACE）的早期诊断标准。方法应用急性轻型高原病症状分度及评分表对24200例急进高原人员进行筛选,筛选出高度疑似HACE者作为重点观察及随访对象,通过对重点观察及随访对象中非HACE组及HACE组患者的早期症状、体征及辅助检查[包括血常规、血生化、血气分析、脑电图、经颅多普勒超声（TCD）及头颅CT、磁共振（MRI）等]进行对照分析,制定出高原脑水肿的早期诊断标准。结果高原脑水肿的早期诊断标准：①近期由平原进入高原（海拔3000m以上）,或由高原进入更高海拔地区,出现严重头痛、呕吐症状（各症状急性高原反应评分均〉4）;在高原现场经卧床、小流量吸氧及对症治疗后无缓解。②紫绀,眼底异常改变：包括视乳头水肿、视乳头充血、视网膜动脉痉挛。③MRI检查可发现脑实质内T1WI低信号和T2WI高信号的斑点状或小片状改变。④血常规检查可见白细胞总数升高。⑤持续性及进行性发展的低氧血症和呼吸性碱中毒。⑥脑电图检查可见慢波性异常为主的表现。结论早期HAPE在临床症状、体征及相关辅助检查方面均存在一定的特征性改变。①、②、③为必备条件,结合④、⑤、⑥即可对早期HACE做出准确诊断。     

高原肺水肿的发病机制——炎症并非致病因素

一般认为高原肺水肿（high-altitude pulmonary edema,HAPE)的发生为肺泡-毛细血管屏障通透性改变所致。后者继发于强烈的肺血管收缩和高毛细血管压，但是既往在明确诊断的HAPE，支气管肺泡灌洗（bronchoalveolar lavage,BAL)所见亦与炎性致病特征相一致。目的：确定炎症是否为HAPE的主要病变。并明确HEPA病变的时间顺序。     

高原脑水肿

本综述由Hacken,Peter H．和Robert C．Roach．撰写,以《高原脑水肿》为题,发表于《高原医学与生物学》。本文聚焦于高原脑水肿(HACE)的流性病学、临床表现、生理病理、预防和治疗等方面。HACE并不常见,但对突然到高海拔地区,或到过高海拔地区的人来说,这将是致命的并发症。HACE最初会出现意识障碍,进而发展为深度昏迷,以及不同程度的精神变化,意识模糊,运动失调。HACE常常是急性高原病(AMS)或高原肺水肿的并发症。最新的病理生理先导理论认为：HACE是一种血管性水肿。本文将复习各种机理对此进行解释。HACE的预防和治疗与其他高原病类似,但我们把重点放在将患者移至低海拔地区和服用类固醇药物这两方面。最后将用一些病例来解释这一疾病的主要临床特点。     

急性高原脑水肿的救治

高原脑水肿,(high altitude cerebral oedema,HACE),又称脑型急性高原病,是一种恶性高原急病,是人体急速进入3500米以上高原,或从高原迅速进入更高海拔地区时,或久居高原者在某些因素(如过劳、上感、剧烈运动)的诱发下,机体对高原低压性缺氧不适应,由于脑缺氧而引起的严重脑功能障碍,出现严重的神经精神症状,如剧烈头痛、头晕、频繁恶心、呕吐、共济失调、步态不稳、精神萎靡或烦躁,甚至昏迷的一种高原特发病,属急性高原病中最严重类型之一,重者须及时救治.现将HACE的诊断及治疗介绍如下:     

高原作业电网施工人员急性高原病发病率及其危险因素分析

目的分析高原作业电网施工人员急性高原病(AMS)发病率及危险因素。方法回顾性将10 956名2019年1月1日—2020年12月31日阿里联网工程高原施工人员纳入研究。由阿里联网工程职工医疗站医疗记录数据库获取对象的基线资料(包括年龄、性别、体质指数、发育及营养状态、相关临床指标等)和AMS发病情况的随访资料, 生命早期居住地所在地和工作环境海拔高度由网站(https://zh-cn.topographic-map.com/legal/)获取。计算不同特征对象AMS发病率, 采用Cox比例风险回归模型探索AMS发病危险因素。结果研究对象年龄为(36.1±10.5)岁, 其中男性占95.27%(10 438名), 随访时间为(17.46±4.23)个月, 生命周期居住地和工作环境海拔分别为(1 959±937)和(4 533±233)m。随访期AMS发病率为15.58%(1 707例), 其中急性高原反应和高原肺水肿(HAPE)发病率分别为15.53%(1 702例)和0.05%(5例), 未发现高原脑水肿(HACE)患者。Cox比例风险回归模型分析显示:工作环境海拔高度每上升100 m...     

高原肺水肿和脑水肿的发病机制及其药物治疗

一氧化氮(NO)合酶mRNA表达减少,使NO合酶活性降低、NO生成减少,是高原肺水肿(HAPE)最重要的因素;其次是肺动脉高压-毛细血管壁高压,造成毛细血管内皮和肺泡表皮层断裂,液体及内含物渗漏;胃肠黏膜损伤,细菌及内毒素入血,引发炎性介质释放,形成肺部炎症及水肿。脑毛细血管压升高和血管内皮生长因子的作用,使毛细血管通透性增加是高原脑水肿(HAPE)主要因素;其次是缺氧使Na+-K+ATP酶活性降低,脑细胞内Na+、Cl-和水分增加;肺通气量增加,H+下降,以及炎性介质释放亦是引起脑水肿的因素。治疗:吸入低浓度的NO,用于治疗HAPE;口服硝苯地平;静脉给氨茶碱或口服β2-受体激动剂;口服乙酰唑胺或呋噻米利尿脱水,严重的HACE用高渗葡萄糖或甘露醇静脉滴注脱水;地塞米松口服或静脉滴注,HAPE和HACE都适用;预防或轻症可选用中药单方或复方。     

血脂质运载蛋白、CysC检测在急性肾损伤患者早期诊断的应用

目的观察血中性粒细胞明胶酶相关脂质运载蛋白(NGAL)、血清半胱氨酸蛋白酶抑制剂C (CysC)水平检测在急性肾损伤(AKI)患者早期诊断的应用。方法选择该院重症加强护理病房(ICU)符合急性肾损伤诊断的患者92例作为研究组,根据诊断将其中79例作为存活组,另外13例作为死亡组,并将同期非急性肾损伤患者30例作为对照组,于入院时行血NGAL、CysC检测,并与血尿素氮(BUN)及血清肌酐(Scr)水平进行分析。结果存活组与死亡组入ICU时NGAL、CysC水平明显高于对照组(P 0.05)。死亡组入ICU时BUN和Scr水平明显高于对照组和存活组(P 0.05)。存活组与对照组BUN和Scr水平比较差异无统计学意义(P0.05)。入院第3天AKI患者NGAL、CysC、BUN和Scr水平持续升高,与对照组比较差异有统计学意义(P 0.05)。入院7、14 d,NGAL、CysC水平呈下降趋势,而7 d时BUN和Scr水平持续升高,14 d呈下降趋势。NGAL截断值为46.29μg/L,敏感性和特异性分别为85.2%和95.4%;CysC截断值为1.31μmol/L,敏感性和特异性分别为90.5%和95.4%;NGAL、CysC敏感性明显高于BUN和Scr,差异有统计学意义(P 0.05)。结论血NGAL、CysC是早期诊断急性肾损伤较有价值的新型标记物,对损伤严重程度和预后的判断均有显著的预测价值。     

急性高原病

急性高原病(AcuteMountainSicknees,A M S)是暴露于高原时,因高原低氧而在数小时至数天内出现的临床症候群。是发生于高原低氧环境的一种特发性疾病。根据病情程度和预后分为轻型和重型,轻型称为急性轻症高原病(AcuteMildAltitudeDisease,AMAD),重型包括高原肺水肿HighAltitude     

头孢曲松相关急性肾功能不全的临床特征及治疗

目的:探讨应用头孢曲松后可能引起的相关急性肾功能不全临床特征及治疗情况。方法:选择30例应用头孢曲松后出现急性肾功能不全患者为观察组;另选择30例应用头孢曲松后未出现急性肾功能不全患者为对照组。通过对比观察组与对照组的临床表现、体征、实验室检查结果,确定应用头孢曲松后出现急性肾功能不全患者的临床特征及治疗效果。结果:观察组的无尿、少尿表现与Scr、BUN检查结果与另外两组患者差异有统计学意义(P<0.05)。经过治疗后,观察组所有患者的临床症状消失,Scr和BUN回到正常水平。结论:应用头孢曲松后出现急性肾功能不全患者以无尿、少尿表现与Scr、BUN异常升高为主要临床特征,可借助导尿管缓解症状,治疗多可自愈,也可碱化尿液治疗。     

Paraganglioma with acute hyperamylasaemia masquerading as acute pancreatitis

Phaeochromocytomas are rare catecholamine-producing tumours. Although classically described to present with headache, diaphoresis and palpitations, they also present in unusual ways; hyperamylasaemia is one such rare presentation. We describe a man with an extra-adrenal phaeochromocytoma (paraganglioma) presenting with diaphoresis, abdominal pain and multi-organ failure. He had hyperamylasaemia of 1,087 (normal range [NR] 44-161) U/L, which mimicked acute severe pancreatitis. Serum lipase and radiographic imaging of the pancreas appeared normal, and the serial amylase levels normalised over six days upon stabilisation of his condition. 24-hour urinary metanephrines of 10,406 (NR 400-1,500) nmol/day suggested a catecholamine-secreting tumour, and metaiodobenzylguanine scintigraphy confirmed this. We postulate that amylase (of the salivary isotype) is released by hypoxic tissues when high catecholamine levels cause vasoconstriction and that fluctuating hypotension decreases organ perfusion. This case highlights the need for awareness of rare presentations of phaeochromocytomas and encourages physicians to rethink the diagnosis when investigations are inconsistent.     

急性重症胆管炎致急性肺损伤动物模型的制作

目的：复制急性重症胆管炎(ACST)引发的急性肺损伤(ALI)的动物模型。方法：通过胆总管远端结扎,近端注入菌液并封闭的方法,造成大鼠ACST后观察肺功能及病理形态改变。结果：实验组PaO2／FiO2下降;肺系数升高,肺含水量增加;光镜可见充血、水肿、粒细胞浸润和透明膜。结论：此模型符合ALI诊断标准及动物模型的考察指标,说明本模型是成功可靠的。     

Pathogenesis of acute lung injury in severe acute pancreatitis

Objective：To study the pathogenesis of acute lung injury in severe acute pancreatitis （SAP）. Methods：Rats were sacrificed at 1, 3, 5, 6, 9 and 12 h after establishment of inducing model. Pancreas and lung tissues were obtained for pathological study, microvascular permeability and MPO examination. Gene expressions of TNF-α and ICAM-1 in pancreas and lung tissues were detected by RT-PCR. Results： After inducing SAP model, the injury degree of the pancreas and the lung increased gradually, accompanied with gradually increased MPO activity and microvascular permeability. Gene expressions of TNF-α and ICAM-1 in pancreas rose at 1 h and reached peak at 7 h. Relatively, their gene expressions in the lungs only rose slightly at 1 h and reached peak at 9-12 h gradually. Conclusion：There is an obvious time window between SAP and lung injury, when earlier protection is beneficial to prevent development of acute lung injury.     

Fluid therapy for severe acute pancreatitis in acute response stage

Background Fluid therapy for severe acute pancreatitis （SAP） should not only resolve deficiency of blood volume, but also prevent fluid sequestration in acute response stage. Up to date, there has not a strategy for fluid therapy dedicated to SAP. So, this study was aimed to investigate the effects of fluid therapy treatment on prognosis of SAP. Methods Seventy-six patients were admitted prospectively according to the criteria within 72 hours of SAP onset. They were randomly assigned to a rapid fluid expansion group （Group I, n=36） and a controlled fluid expansion group （Group II n=-40）. Hemodynamic disorders were either quickly （fluid infusion rate was 10-15 ml.kg-1-h-1, Group I） or gradually improved （fluid infusion rate was 5-10 ml-kg1.h-1, Group II） through controlling the rate of fluid infusion. Parameters of fluid expansion, blood lactate concentration were obtained when meeting the criteria for fluid expansion. And APACHE II scores were obtained serially for 72 hours. Rate of mechanical ventilation, incidence of abdominal compartment syndrome （ACS）, sepsis, and survival rate were obtained. Results The two groups had statistically different （P 〈0.05） time intervals to meet fluid expansion criteria （Group I, 13.5±6.6 hours; Group II, （24.0±5.4） hours）. Blood lactate concentrations were both remarkably lower as compared to the level upon admission （P 〈0.05） and reached the normal level in both groups upon treatment. It was only at day 1 that hematocrit was significantly lower in Group I （35.6%±6.8%） than in Group II （38.5%±5.4%） （P〈0.01）. Amount of crystalloid and colloid in group I （（4028±1980）ml and （1336±816）ml） on admission day was more than those of group II （（2472±1871）ml and （970±633）ml）. No significant difference was found in the total amount of fluids within four days of admission between the two groups （P〉0.05）. Total amount of fluid sequestration within 4 days was higher in Group I （（5378±2751）ml） than in Group II （（4215±1998）ml, P 〈0.05）. APACHE II scores were higher in Group I on days 1, 2, and 3 （P〈0.05）. Rate of mechanical ventilation was higher in group I （94.4%） than in group II （65%, P〈0.05）. The incidences of abdominal compartment syndrome （ACS） and sepsis were significantly lower in Group II （P 〈0.05）. Survival rate was remarkably lower in Group I （69.4%） than in Group II （90%, P〈0.05）. Conclusions Controlled fluid resuscitation offers better prognosis in patients with severe volume deficit within 72 hours of SAP onset. Chin Med J 2009; 122（2）： 169-173     

急性坏死性淋巴结炎1例的护理体会

1病例报告 患者,女34岁。因颈部包块20d余,持续性发热半个月,伴头痛,恶心呕吐1d,于2007年3月22日入院。查体：体温39．7℃,脉搏82次／min,呼吸20次／min,血压110／70mmHg。双侧颈部可扪及数枚大小不等的淋巴结,较大约束力2．5cm×1cm,活动尚可,质硬,触压痛明显,心,肺,腹未见异常。血常规：白细胞1．98×10^9L,中性粒细胞0．14,淋巴细胞0．39,单核细胞0．18,嗜酸性料脑脊检查正常。结核抗体和PPD试验均阴性。