急性肺损伤和急性呼吸窘迫综合征的诊治思维程序

急性肺损伤和急性呼吸窘迫综合征(ALL/ARDS)是临床较为常见的危急重症,因其病情发展迅速、病死率高而日益为临床所重视.对于ALI/ARDS的早期诊断和正确处理有赖于有效的临床思维程序.     

老年急性呼吸窘迫综合征的诊治

急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)是由于不同原因引起的广泛性肺毛细血管膜损伤和呼吸困难.在上个世纪,Ashbough于1967年报道呼吸窘迫综合征时,他所指的ARDS的A字意指Adult,即成人之意,其时ARDS应是成人呼吸窘迫综合征(adult respiratory distress syndrome);     

早期不同干预方式对犬急性肺损伤呼吸生理的影响

针对严重急性呼吸综合征（SARS）引发的急性肺损伤／急性呼吸窘迫综合征（ALI／ARDS）防治经验，早期应用持续气道内正压（CPAP）和双水平气道内正压（BiPAP）通气可以改善呼吸困难和氧合功能，有可能减少气管插管及病死率，因缺乏严格的对比依据。我们以ALI／ARDS动物模型为研究对象，比较早期应用控制性高浓度氧疗、CPAP、BiPAP不同的干预方式对ALI／ARDS呼吸生理的影响，为临床上早期合理应用无创正压通气治疗ALI／ARDS提供实验依据。     

磷酸二酯酶及其抑制剂在急性肺损伤/急性呼吸窘迫综合征中的研究进展

磷酸二酯酶（PDE）在急性肺损伤／急性呼吸窘迫综合征（ALI／ARDS）的发病机制中起重要作用，PDE抑制剂能调节ALI／ARDS诸个环节，这方面的资料主要来自动物实验及体外细胞培养。本文就PDE及其抑制剂在ALI／ARDS中的研究进展做一综述。     

两种急性肺损伤模型大鼠炎症反应、激素受体水平及其对激素反应的差异研究

糖皮质激素（GC）治疗急性肺损伤（ALI）／急性呼吸窘迫综合征（ARDS）争论已久。GC对严重急性呼吸综合征（SARS）显示出治疗效果。但更多的研究对GC治疗ALI/ARDS提出异议。     

肺表面活性物质在急性肺损伤/急性呼吸窘迫综合征中的研究进展

急性肺损伤／急性呼吸窘迫综合征（ALI／ARES）时肺表面活性物质的成分、功能等均发生变化，研究这些变化对防治ALI／ARDS的发生、发展及预后，都有十分重要的意义。本文综述了肺表面活性物质在ALI／ARDS中的组成成分、代谢、功能改变以及治疗方面的研究进展，为该领域的深入研究提供参考。     

急性肺损伤／急性呼吸窘迫综合征发病机制的研究进展

急性肺损伤（acutelunginjury，ALI）和急性呼吸窘迫综合征（acuterespiratorydistresssyndrome，ARDS）是指由心源性以外的各种肺内外致病因素所导致的急性、进行性缺氧性呼吸衰竭。虽然目前ALI／ARDS发病机制以及相应的治疗手段已经取得了一些进展．但是发病率和病死率仍较高．其病死率高达30％～40％。ALI／ARDS的发病机制十分复杂．涉及的环节多．受损的靶细胞多。     

机械通气在重症急性胰腺炎并发ARDS中的护理

急性重症胰腺炎可引起多种并发症,其中以急性呼吸窘迫综合征(ARDS)最常见,发生率约占60%.     

Toll样受体4/NF-κB信号转导通路在重症急性胰腺炎肺损伤中的表达及血必净的干预作用

急性肺损伤(acute lung injury,ALI)和急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)是重症急性胰腺炎(SAP)最常见的早期并发症,发生率高达33%,发病1周内病死的SAP患者中60%～80%与ALL/ARDS有关[1-2].     

严重胸部外伤合并急性呼吸窘迫综合征28例诊疗体会

2000年1月～2008年12月,我科收治严重胸部外伤合并急性呼吸窘迫综合征（ARDS）患者28例取得良好疗效。现总结如下。 临床资料：本文28例,男22例、女6例,年龄9．0～72．5岁,均为严重胸部外伤合并ARDS。ARDS符合中华医学会重症医学分会“急性肺损伤／急性呼吸窘迫综合征诊断和治疗指南（2006）”中的诊断标准。     

Severe acute pancreatitis in acute hepatitis E.

We report an 18-year-old boy with severe acute pancreatitis developing during acute hepatitis E and complicated by sepsis and acute renal failure. The patient recovered on supportive management.     

重症急性胰腺炎患者发生急性期急性肺损伤的危险因素分析

目的探讨重症急性胰腺炎(SAP)患者发生急性期急性肺损伤(ALI)的相关危险因素。方法选取114例SAP患者为研究对象,根据其发生急性期ALI的情况分成损伤组(n=36)和非损伤组(n=78)。回顾性分析两组患者的临床资料,对单因素分析后存在显著性差异的指标行非条件Logistic回归分析。结果(1)两组患者性别、病因、平均住院天数、血糖浓度及慢性疾病史等一般资料比较差异无统计学意义(P0.05);损伤组年龄、病程、Ranson评分均显著高于非损伤组(P0.01);且损伤组器官受累≥2个、腹腔感染率、机械通气治疗率、合并全身炎症反应综合征(SIRS)率均显著高于非损伤组(P0.01);APACHEⅡ评分8分率、吸烟史率则显著低于非损伤组(P0.01)。(2)非条件Logistic回归方程显示年龄、病程、合并SIRS、器官受累情况、机械通气治疗、腹腔感染、Ranson评分等均为SAP患者发生急性期ALI的独立危险因素(P0.05);吸烟及APACHEⅡ8分则为SAP患者发生急性期ALI的保护因素(P0.05)。结论年龄、病程、器官受累情况、机械通气治疗、腹腔感染、Ranson评分、合并SIRS等均为SAP患者发生急性期ALI的独立危险因素,需引起临床重视。     

Intensified therapy in acute lymphoblastic and acute undifferentiated leukemia in adults

One hundred seventy adult patients with acute lymphoblastic leukemia (ALL) or acute undifferentiated leukemia (AUL) were entered into a prospective multicenter therapy trial at 25 hospitals. The aim of the trial was to improve remission duration by using a modified form of an intensified induction regimen that was successful in childhood ALL, to define immunologic subtypes of ALL by use of cell-surface markers, and to extract other possible prognostic factors. The overall complete remission rate was 77.8%. The median overall survival time was 26 months, being 4 months for nonresponders and 32 months for responders. The median remission duration for the 126 patients with complete remission was 20 months. Prognostically favorable factors for remission duration were response to chemotherapy within 4 weeks, age less than 35 years, a low initial leukocyte count, and the immunologic subtypes c- ALL with early response to therapy and T-ALL, where 61% and 58%, respectively, are still in complete remission at 3 years. An adverse influence on remission duration was observed for the subtype null-ALL, with a median survival of 13 months, and for patients with a delayed response to induction therapy, independent of phenotype.     

Hyperlipidemia in acute pancreatitis

Whether hyperlipidemia is a pre-existing metabolic disorder or a consequence of acute pancreatitis is still debated. Mild to moderate elevation of serum triglyceride levels are likely to be an epiphenomenon of the pancreatic disease. A marked hyperchylomicronemia and hypertrygliceridemia would be needed to trigger acute pancreatitis; a relevant defect in the lipid catabolism and clearance should therefore pre-exist. The aim of the present study was to investigate whether patients with acute pancreatitis and marked hyperlipidemia have an impaired clearance capacity of exogenous lipids, which would define the hyperlipidemia as a preexistent abnormality and therefore a potential cause of the pancreatic disease. With this aim, the kinetics of the removal of exogenous triglycerides from the circulation have been analyzed. Twenty patients with acute pancreatitis have been studied. Ten of them suffered from an episode of acute pancreatitis with marked hyperlipidemia (serum triglyceride levels>20mmol/L). Four to six months after recovery from the pancreatitis, a two-stage infusion of Intralipid 20% was carried out and the fractional removal rate (K₂) and the maximal clearance capacity (K₁) of exogenous triglycerides were calculated. At low infusion rates a first order kinetics for removal was observed, whereas at high infusion rates a zero order kinetics was operating. All patients with a previous attack of normolipidemic acute pancreatitis had normal K₂ and K₁ values. Five patients with previous hyperlipidemic acute pancreatitis had an abnormally low clearance capacity of exogenous triglycerides, whereas the remaining five had normal removal values. The present study provides new information in the association between hyperlipidemia and acute pancreatitis by showing that even a marked elevation of serum lipid levels should not be invariably considered as the etiological factor of the pancreatic disease, even if other potential causes are not evident.