急性呼吸窘迫综合征临床转归的相关因素分析

目的分析急性呼吸窘迫综合征（ARDS）临床转归的相关因素。方法对47例ARDS患者临床资料进行回顾性分析。结果本组资料中ARDS患者病死率为72．3％，其中肺内组的病死率（94．1％）明显高于肺外组的病死率（60．0％），P〈0．05；当肺外组合并感染时病死率达95．8％；当胶体渗透压（COP）〈20mmHg（1mmHg=0．133kPa），患者的病死率为83．0％（P〈0．05）。结论肺外组合并感染、COP〈20mmHg可能是预报ARDS病死率高的指标。     

细胞因子与急性呼吸窘迫综合征

细胞因子及其相互作用在急性呼吸窘迫综合征的炎症过程中发挥重要作用。本文综述各种细胞因子在急性呼 吸窘迫综合征发生发展中的作用机制,以期从分子水平揭示其发病机制。     

细胞因子与急性呼吸窘迫综合征

细胞因子及其相互作用在急性呼吸窘迫综合征的炎症过程中发挥重要作用。本文综述各种细胞因子在急性呼吸窘迫综合征发生发展中的作用机制，以期从分子水平揭示其发病机制。     

白细胞整合素与急性呼吸窘迫综合征

白细胞整合素（ＣＤ１１／ＣＤ１８）是粘附分子中整合素的β２亚家族,它仅表达在白细胞上,参与介导白细胞与内皮细胞及其它细胞的相互作用。在急性呼吸窘迫综合征（ＡＲＤＳ）的发病中,多形核白细胞（ＰＭＮ）的渗出与聚集与白细胞整合素的异常表达密切相关,选择性地阻断事素的粘附途径可在阻止炎症的发生发展,减轻肺损伤方面取得一定效果     

急性呼吸窘迫综合征56例临床分析

目的探讨急性呼吸窘迫综合征的诊断和治疗。方法对56例急性呼吸窘迫综合征患者诊断和治疗情况进行州顾性分析。结果56例患者中,27例（占48．21％）患者死亡。结论多种危重病都有可能发生急性呼吸窘迫综合征;多器官功能障碍综合征和呼吸衰竭是导致急性呼吸窘迫综合征患者死亡的主要原因。     

急性肺损伤和急性呼吸窘迫综合征的临床研究

自196 7年Ashbaugh等[1] 报道成人呼吸窘迫综合征(adultrespiratorydistresssyndrome,ARDS)以来,国内外学者作了大量基础与临床研究工作,对ARDS的认识有了明显提高,表现在对ARDS的命名、定义逐渐规范,对其发病机制有了较为深刻的认识,提出了便于临床使用的急性肺损伤(acutelunginjury,ALI)/急性ARDS诊断标准,积累了一些较为成熟的治疗经验和措施,使ALI/ARDS的发病率和病死率均有下降趋势。本文主要就ALI/ARDS的临床研究作简要阐述。一、命名与定义在第一次世界大战期间,Pasteur描述士兵因胸部受伤而发生大面积肺不张时,命名为…     

高海拔区急性呼吸窘迫综合征的监护

为减少高海拔地区呼吸窘迫综合征（Ｈ－ＡＲＤＳ）的病死率,对收入ＩＣＵ的２５２例创伤、感染、大手术患者进行了心电、呼吸、血气、生化连续动态监护。结果：２５２例中有２８例分别于伤后３￣７２ｈ（平均１９．６ｈ）发生了急性呼吸窘迫综合征（ＡＲＤＳ）。除１例死亡外,２７例抢救成活。提示连续动态监护为Ｈ－ＡＲＤＳ的早期诊断、治疗提供了可靠依据,从而减少了病死率。     

严重肺挫伤合并急性呼吸窘迫综合征的诊治

目的提高对严重肺挫伤合并急性呼吸窘迫综合征(ARDS)的认识.方法对24例严重肺挫伤合并ARDS患者的临床资料进行回顾性分析.结果本组患者ARDS占同期外科ICU严重肺挫伤患者(47例)的51.1%,全组死亡6例,死亡率25%,24例均给予机械通气;并发肺炎占12例,感染率50%.结论救治严重肺挫伤合并ARDS患者的关键在于对导致ARDS的原发病肺挫伤有充分认识.早期诊断和治疗,正确使用呼吸机,正确治疗多发性损伤是减少ARDS死亡率的有效方法.     

趋化因子与急性呼吸窘迫综合征

趋化因子是属于细胞因子的一个大家庭,具有相似的特征性结构,可以特异性影响某些类型白细胞游走的方向。本文概括介绍趋化因子的主要特点并着重讨论趋化因子在急性呼吸窘迫综合征发病机制中的作用。     

Retrospective analysis on acute respiratory distress yndrome in ICU

OBJECTIVE: To assess the incidence, etiology, physiological and clinical features, mortality, and predictors of acute respiratory distress syndrome (ARDS) in intensive care unit (ICU). METHODS: A retrospective analysis of 5 314 patients admitted to the ICU of our hospital from April 1994 to December 2003 was performed in this study. The ARDS patients were identified with the criteria of the American-European Consensus Conference (AECC). Acute physiology and chronic health evaluation III (APACHE III), multiple organ dysfunction syndrome score (MODS score), and lung injury score (LIS) were determined on the onset day of ARDS for all the patients. Other recorded variables included age, sex, biochemical indicators, blood gas analysis, length of stay in ICU, length of ventilation, presence or absence of tracheostomy, ventilation variables, elective operation or emergency operation. RESULTS: Totally, 131 patients (2.5%) developed ARDS, among whom, 12 patients were excluded from this study because they died within 24 hours and other 4 patients were also excluded for their incomplete information. Therefore, there were only 115 cases (62 males and 53 females, aged 22-75 years, 58 years on average) left, accounting for 2.2% of the total admitted patients. Their average ICU stay was (11.27+/-7.24) days and APACHE III score was 17.23+/-7.21. Pneumonia and sepsis were the main cause of ARDS. The non-survivors were obviously older and showed significant difference in the ICU length of stay and length of ventilation as compared with the survivors. On admission, the non-survivors had significantly higher MODS and lower BE (base excess). The hospital mortality was 55.7%. The main cause of death was multiple organ failure. Predictors of death at the onset of ARDS were advanced age, MODS > or = to 8, and LIS > or = 2.76. CONCLUSIONS: ARDS is a frequent syndrome in this cohort. Sepsis and pneumonia are the most common risk factors. The main cause of death is multiple organ failure. The mortality is high but similar to most recent series including severe comorbidities. Based on this patient population, advanced age, MODS score, and LIS may be the important prognostic indicators for ARDS.     

Pharmacologic strategies in acute respiratory distress syndrome

Treatment of the acute respiratory distress syndrome includes both supportive measures and correction of the underlying cause. Various pharmacological interventions have been proposed to limit the severity of lung injury and enhance the healing process, including exogenous surfactant, inhaled vasodilators (mainly nitric oxide), corticosteroids, prostaglandin E1, antioxidants (N-acetylcysteine), ketoconazole and other substances. Some of these interventions are administered via the airways, for example inhaled nitric oxide or liquid ventilation with perfluorocarbons. Some have beneficial effects on surrogate end-points such as pulmonary gas exchange. However, in large prospective trials none of these pharmacological approaches have resulted in significantly improved survival in acute respiratory distress syndrome patients.     

Mechanical ventilation in acute respiratory distress syndrome

The acute respiratory distress syndrome occurs commonly in critical care. There is an increasing volume of clinical and experimental evidence that poor ventilatory technique that is injurious to the lungs can propagate the systemic inflammatory response and adversely affect mortality. Many ventilatory techniques have been hypothesized to 'protect' the lungs during mechanical ventilation, including tidal volume limitation, high positive end-expiratory pressure, pressure-controlled inverse ratio ventilation, and prone positioning. Experimental techniques include liquid ventilation, surfactant administration and extracorporeal gas exchange. Despite excellent rationale for their use, few techniques, apart from tidal volume limitation, have been shown to improve survival in randomized controlled trials.     

Supportive care in acute respiratory distress syndrome

Although the central focus of acute respiratory distress syndrome (ARDS) is the pathology within the lung, ARDS is very much a systemic disease. As such, the whole body needs care and support while the disease process within the lung runs its course. The issues of pain management, sedation, fluid balance, nutrition, metabolic and hormonal processes, infection control, and patient positioning are important for any patient in a critical care setting. For patients with ARDS, the required ventilatory support and ARDS-associated systemic inflammation mandate the above supportive measures.     

Management of the acute respiratory distress syndrome

Significant advances have occurred in the knowledge of the pathogenesis of ARDS. It is now recognized that ARDS is a manifestation of a diffuse process that results from a complicated cascade of events following an initial insult or injury. Mechanical ventilation and PEEP are still important components of supportive therapy. To avoid ventilator-associated lung injury there is emphasis on targeting ventilator management based on measurement of pulmonary mechanics. For those with resistant hypoxia and severe pulmonary hypertension adjunctive modalities, such as prone positioning and low-dose iNO, may provide important benefit. Alternative modes of supporting gas exchange, such as with partial liquid ventilation and extracorporeal gas-exchange, may serve as rescue therapies. Advances in cell and molecular biology have contributed to a better understanding of the role of inflammatory cells and mediators that contribute to the acute lung injury and the pathophysiology of the syndrome that manifests as ARDS. Based on this new understanding, the potential targets for intervention to ameliorate the systemic inflammatory response have proliferated. Examples include the cytokine network and its receptors, antioxidants, and endothelins. Apart from the challenge of testing these agents in experimental models, it seems likely that determination of the optimum combination of agents will become an equally important endeavor. A particular challenge is to develop better methods of predicting which of the many at-risk patients will go on to full-blown ARDS and MODS, thereby targeting subgroups of patients most likely to benefit from anti-inflammatory therapies. Similarly, the adverse effects of immunosuppressive therapy may be diminished by improved, perhaps molecular, techniques to detect microbial pathogens and permit differentiation between Systemic inflammatory response syndrome and sepsis.     

Inflammation and the acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is a clinical syndrome of non-cardiogenic pulmonary oedema associated with bilateral pulmonary infiltrates, stiff lungs and refractory hypoxaemia. ARDS is characterized by an explosive acute inflammatory response in the lung parenchyma, leading to alveolar oedema, decreased lung compliance and, ultimately, hypoxaemia. Although our understanding of the causes and pathophysiology of ARDS has increased, the mortality rate remains in the range of 30-50%. No major advances in pharmacological therapy have been achieved. Mechanical ventilation is the main therapeutic intervention in the management of ARDS. The only approach that has been shown to reduce the inflammatory response and mortality is the use of lung-protective ventilatory strategy with a low tidal volume and high positive-end expiratory pressure. This chapter will review the current state of the literature on the pathogenesis of ARDS and ventilatory and pharmacotherapy approaches to its management.     

Metalloproteinase inhibition prevents acute respiratory distress syndrome

BACKGROUND: The acute respiratory distress syndrome (ARDS) occurs in patients with clearly identifiable risk factors, and its treatment remains merely supportive. We postulated that patients at risk for ARDS can be protected against lung injury by a prophylactic treatment strategy that targets neutrophil-derived proteases. We hypothesized that a chemically modified tetracycline 3 (COL-3), a potent inhibitor of neutrophil matrix metalloproteinases (MMPs) and neutrophil elastase (NE) with minimal toxicity, would prevent ARDS in our porcine endotoxin-induced ARDS model. METHODS: Yorkshire pigs were anesthetized, intubated, surgically instrumented for hemodynamic monitoring, and randomized into three groups: (1) control (n = 4), surgical instrumentation only; (2) lipopolysaccharide (LPS) (n = 4), infusion of Escherichia coli lipopolysaccharide at 100 microg/kg; and (3) COL-3 + LPS (n = 5), ingestion of COL-3 (100 mg/kg) 12 h before LPS infusion. All animals were monitored for 6 h following LPS or sham LPS infusion. Serial bronchoalveolar lavage (BAL) samples were analyzed for MMP concentration by gelatin zymography. Lung tissue was fixed for morphometric assessment at necropsy. RESULTS: LPS infusion was marked by significant (P < 0.05) physiological deterioration as compared with the control group, including increased plateau airway pressure (P(plat)) (control = 15.7 +/- 0.4 mm Hg, LPS = 23.0 +/- 1.5 mm Hg) and a decrement in arterial oxygen partial pressure (P(a)O(2)) (LPS = 66 +/- 15 mm Hg, Control = 263 +/- 25 mm Hg) 6 h following LPS or sham LPS infusion, respectively. Pretreatment with COL-3 reduced the above pathophysiological changes 6 h following LPS infusion (P(plat) = 18.5 +/- 1.7 mm Hg, P(a)O(2) = 199 +/- 35 mm Hg; P = NS vs control). MMP-9 and MMP-2 concentration in BAL fluid was significantly increased between 2 and 4 h post-LPS infusion; COL-3 reduced the increase in MMP-9 and MMP-2 concentration at all time periods. Morphometrically LPS caused a significant sequestration of neutrophils and monocytes into pulmonary tissue. Pretreatment with COL-3 ameliorated this response. The wet/dry lung weight ratio was significantly greater (P < 0.05) in the LPS group (10.1 +/- 1.0 ratio) than in either the control (6.4 +/- 0.5 ratio) or LPS+COL-3 (7.4 +/- 0.6 ratio) group. CONCLUSIONS: A single prophylactic treatment with COL-3 prevented lung injury in our model of endotoxin-induced ARDS. The proposed mechanism of COL-3 is a synergistic inhibition of the terminal neutrophil effectors MMPs and NE. Similar to the universal practice of prophylaxis against gastric stress ulceration and deep venous thromboses in trauma patients, chemically modified tetracyclines may likewise be administered to prevent acute lung injury in critically injured patients at risk of developing ARDS.