急性肺损伤的治疗进展

急性肺损伤（acute lung in jury，Au）是指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，临床上以呼吸窘迫、顽固性低氧血症和非心源性肺水肿为特征。其严重阶段称为急性呼吸窘迫综合征（acute respiratory distress syndrome，ARDS）。可进一步发展成多器官功能障碍综合征（multiple organ dysfunction syndrome MODS）或多器官功能衰竭（MOF）。Au的概念包括了ARDS从轻到重的全部连续性的病理生理过程，重症ALI被定义为ARDS，即轻度ALI为ARDS的前奏。ALI作为危重病研究的热点，尽管目前从诊断到治疗方式有了很大进展，但死亡率仍居高不下。许多研究仍有待于临床进一步拓展与追踪。     

急性肺损伤的诊治研究现状及进展

急性肺损伤（acutelunginjury,ALI）及其进展为更严重阶段的急性呼吸窘迫综合征（acute respiratory distress sydrorne,ARDS）是由肺内外的各种病因引起的,以进行性呼吸困难和顽固性低氧血症为特征的机体过度炎症反应急性综合征,甚至并发严重呼吸衰竭。     

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（acute lung injury,ALI）／急性呼吸窘迫综合征（acute respiratory distress syndrome,ARDS）是非心源性的各种内外致病因素如严重感染、创伤、休克、吸人有害气体、中毒等导致的急性、进行性、缺氧性呼吸功能不全或衰竭。     

细胞因子和炎症介质在急性呼吸窘迫综合征发病机制中的作用

急性呼吸窘迫综合征（acute respiratory distress syndrome,ARDS）是由多种原发性疾病过程中发生的急性进行性缺氧性呼吸衰竭（respiratory failure） ,是急性肺损伤（acute lung injury,ALI）的严重阶段,其特征性的病理生理表现为肺实质炎症反应而导致的弥漫性肺泡上皮和肺微血管内皮的严重损伤.在美国每年估计约有190 000 ～200 000例ALI/ARDS成年患者,以及还有大量的ALI/ARDS儿童患者.     

治疗重症哮喘致急性四肢瘫痪性肌病综合征1例

急性四肢瘫痪性肌病综合征（acute quadriplegic myopathy syndrome，AQMS）常见于哮喘急性发作或急性呼吸窘迫综合征（acute respiratory distress syndrome，ARDS）患者，这些患者通常有肌松药和／或皮质类固醇激素使用史，出现急性四肢无力、肌酸激酶升高和肌电图异常^[1]。我科诊治1例，现报道如下。     

无创正压通气治疗急性肺损伤/急性呼吸窘迫综合征研究进展

1994年美国和欧洲呼吸与重症医学学者首次统一急性呼吸窘迫综合征（acute respiratory distress syndrome,ARDS）的定义及诊断标准。在2000年中华医学会呼吸病学分会也讨论通过了中国内地的急性肺损伤（acute lung injury,ALI）/ARDS的诊断标准（草案）：有发病的高危因素;②急性起病：呼吸频数和/或呼吸窘迫;③低氧血症;ALI时动脉血氧分压（PaO2）/吸入氧气浓度（Fi O2）≤300（1mmHg=0.133kPa）;ARDS时PaO2/Fi O2≤200;④胸部X线检查两肺浸润阴影;⑤肺毛细血管前楔压（PCWP）≤18mmHg或临床上能除外心源性     

S100蛋白与急性肺损伤/急性呼吸窘迫综合征

急性肺损伤/急性呼吸窘迫综合征(acute lung injury/acute respiratory distress syndrome,ALI/ARDS)是指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,严重的ALI或ALI的最终严重阶段被定义为ARDS.目前就ALI/ARDS达成的共识是:ALI/ARDS不仅仅是单纯意义上的肺部疾病,也是全身系统炎性疾病的肺部表现,炎性反应和免疫调节失控导致促炎细胞因子释放,并通过细胞间的信息传导,炎性反应进一步放大,促炎与抗炎机制失衡,导致肺损伤加重,最终诱发或加重多器官功能障碍综合征(multiple organ dysfunction syndrome,MODS).     

有关急性呼吸窘迫综合征（ARDS）诊断标准的评介

1 ARDS的诊断标准 自1967年，Ashbaugh等报道12例因各种原因引起的急性呼吸衰竭病人以来，对此症的定义和诊断标准一直颇有争议。20世纪80年代初，Petty和Ashbaugh等将其命名为“成人呼吸窘迫综合征”（adult respiratory distress syndrome，ARDS）。1994年第一次美欧ARDS专题讨论会（American—European consensus conference，AECC）提出将“成人”呼吸窘迫综合征改称为“急性”（acute而不是adult）呼吸窘迫综合征，并推荐新的ARDS和急性肺损伤的标准（见表1）。     

急性重症呼吸衰竭与体外膜肺氧合

急性重症呼吸衰竭（severe acute respiratory failure）是由于肺外或肺内的严重疾病引起肺损伤导致气体交换障碍,产生严重的低氧血症和／或高碳酸血症,其病情较重,病死率高。尽管在呼吸危重病治疗方面已取得一些进展,但由于急性肺损伤／急性呼吸窘迫综合征（acute lung injury／acute respiratory distress syndrome,ALI／ARDS）病因复杂,     

急性肺损伤的早期修复与重建

急性肺损伤(acute lung injury,ALI)/急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)是由于多种肺部或肺外的因素引起的肺泡-毛细血管膜弥漫性损伤,进而导致气体交换功能障碍.近年来发现,肺组织的修复与重建在ALI/ARDS的早期阶段即可发生,并且影响着ALI的急性炎症反应.因此,研究ALI/ARDS修复与重建过程中的细胞、细胞因子及其作用机制,有利于深入了解ALI/ARDS早期的发生、发展过程,进而寻找出早期、有效的干预措施.     

Myocarditis associated with acute nasopharyngitis and acute tonsillitis

Thirty-five instances of fatal myocarditis atributable to acute nasopharyngeal and tonsillar infections have been reported. The available evidence indicates that these are samples of a not uncommon type of cardiac disease which fortunately has a relatively good prognosis. Further investigation should be carried on to establish fully the etiological agent and the pathogenesis of the lesion. Although the pathologic observations indicated that all patients died of cardiac failure, heart disease was suspected clinically in only three, and in fifteen patients death was unexpected. Significant clinical observations which would seem to be of importance in the recognition of the process were: disproportion of the temperature and pulse rate, hypotension, thready or feeble pulse, and substernal oppression. Cyanosis, dyspnea, and orthopnea occurred frequently.Autopsy findings included significant enlargement of the heart in many cases. The microscopic changes, similar in both nasopharyngeal and tonsillar infections, have been classified in three overlapping groups. In all of these the inflammatory process was observed to be patchy, frequently showing considerable variation in intensity from one area to another and having no predilection for a particular portion of the myocardium. Significant (moderate or marked) degrees of muscle degeneration observed in the diffuse type of myocardial lesion were not present in the interstitial form. The cellular reaction, which was characteristically more intense than that observed in diphtheritic myocarditis, was predominantly mononuclear, but significant numbers of polymorphonuclear leucocytes accumulated at sites of more severe inflammation.Although the figures are too small to justify conclusions, there appears to be significant correlation between the clinical occurrence of hypotension and the estimated severity of the myocarditis, since it was a feature in every severe case in which the blood pressure was recorded. The only available electrocardiograms (four), abnormal in every case, were from patients whose hearts showed muscle degeneration of moderate or marked degree. Anginal pains were related to the presence of hypotension. Fibrosis of the heart muscle was related both to the muscle degeneration and to duration of illness.In therapy, attention is called to the danger involved in the administration of intravenous fluids.     

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.     

Philadelphia chromosome-positive acute lymphoblastic leukemia preceded by acute pleuropericarditis

A 69-year-old woman was admitted with sudden chest pain and high fever. Electrocardiography showed negative T waves in the precordial leads. Subsequently, pleural and pericardial effusion developed, but the symptoms and signs subsided without specific therapy. On day 31, fever, left shoulder pain and pleural effusion reappeared. 67Ga scintigraphy showed abnormal uptake in the chest and left shoulder. Blasts were detected in the peripheral blood on day 44, and in the pleural effusion and bone marrow on day 45. The blasts were positive for Philadelphia chromosome, CD10, CD19, CD33, CD34 and IgH-chain rearrangement and negative for myeloperoxidase. The clinical picture of the preceding pleuropericarditis was that of viral or idiopathic origin, but its relationship with acute lymphoblastic leukemia was unclear. Inflammatory chemokines in the pleural space may have induced invasion of the leukemic cells.     

Fatal idiopathic acute eosinophilic pneumonia with acute lung injury

A fatal case of idiopathic eosinophilic pneumonia with acute lung injury is described. The patient required treatment with mechanical ventilation and intravenous corticosteroids, however, she died on the third hospital day. At autopsy, both exudative and proliferative phases of diffuse alveolar damage were observed bilaterally. Marked eosinophilic infiltrate was noted in the alveolar wall and within the alveolar cavities with occasional abscess-like features. To our knowledge, this is the first report of fatal acute eosinophilic pneumonia, and provides important information for the management of this condition.