Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial

Maureen O. Meade, MD, MSc; Deborah J. Cook, MD, MSc; Gordon H. Guyatt, MD, MSc; Arthur S. Slutsky, MD; Yaseen M. Arabi, MD; D. James Cooper, MD; Andrew R. Davies, MD; Lori E. Hand, RRT, CCRA; Qi Zhou, PhD; Lehana Thabane, PhD; Peggy Austin, CCRA; Stephen Lapinsky, MD; Alan Baxter, MD; James Russell, MD; Yoanna Skrobik, MD; Juan J. Ronco, MD; Thomas E. Stewart, MD; for the Lung Open Ventilation Study Investigators

JAMA. 2008;299(6):637-645.

Context  Low-tidal-volume ventilation reduces mortality in critically ill patients with acute lung injury and acute respiratory distress syndrome. Instituting additional strategies to open collapsed lung tissue may further reduce mortality.

Objective  To compare an established low-tidal-volume ventilation strategy with an experimental strategy based on the original "open-lung approach," combining low tidal volume, lung recruitment maneuvers, and high positive-end–expiratory pressure.

Design and Setting  Randomized controlled trial with concealed allocation and blinded data analysis conducted between August 2000 and March 2006 in 30 intensive care units in Canada, Australia, and Saudi Arabia.

Patients  Nine hundred eighty-three consecutive patients with acute lung injury and a ratio of arterial oxygen tension to inspired oxygen fraction not exceeding 250.

Interventions  The control strategy included target tidal volumes of 6 mL/kg of predicted body weight, plateau airway pressures not exceeding 30 cm H₂O, and conventional levels of positive end-expiratory pressure (n = 508). The experimental strategy included target tidal volumes of 6 mL/kg of predicted body weight, plateau pressures not exceeding 40 cm H₂O, recruitment maneuvers, and higher positive end-expiratory pressures (n = 475).

Main Outcome Measure  All-cause hospital mortality.

Results  Eighty-five percent of the 983 study patients met criteria for acute respiratory distress syndrome at enrollment. Tidal volumes remained similar in the 2 groups, and mean positive end-expiratory pressures were 14.6 (SD, 3.4) cm H₂O in the experimental group vs 9.8 (SD, 2.7) cm H₂O among controls during the first 72 hours (P < .001). All-cause hospital mortality rates were 36.4% and 40.4%, respectively (relative risk [RR], 0.90; 95% confidence interval [CI], 0.77-1.05; P = .19). Barotrauma rates were 11.2% and 9.1% (RR, 1.21; 95% CI, 0.83-1.75; P = .33). The experimental group had lower rates of refractory hypoxemia (4.6% vs 10.2%; RR, 0.54; 95% CI, 0.34-0.86; P = .01), death with refractory hypoxemia (4.2% vs 8.9%; RR, 0.56; 95% CI, 0.34-0.93; P = .03), and previously defined eligible use of rescue therapies (5.1% vs 9.3%; RR, 0.61; 95% CI, 0.38-0.99; P = .045).

Conclusions  For patients with acute lung injury and acute respiratory distress syndrome, a multifaceted protocolized ventilation strategy designed to recruit and open the lung resulted in no significant difference in all-cause hospital mortality or barotrauma compared with an established low-tidal-volume protocolized ventilation strategy. This "open-lung" strategy did appear to improve secondary end points related to hypoxemia and use of rescue therapies.

Trial Registration  clinicaltrials.gov Identifier: NCT00182195

     

Ketoconazole for early treatment of acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. The ARDS Network

Context  Three clinical studies have suggested that ketoconazole, a synthetic imidazole with anti-inflammatory activity, may prevent the development of acute respiratory distress syndrome (ARDS) in critically ill patients. However, the use of ketoconazole as treatment for acute lung injury (ALI) and ARDS has not been previously studied. Objective  To test the efficacy of ketoconazole in reducing mortality and morbidity in patients with ALI or ARDS. Design  Randomized, double-blind, placebo-controlled trial conducted from March 1996 to January 1997. Setting  Twenty-four hospitals associated with 10 network centers in the United States, constituting the ARDS Network. Patients  A total of 234 patients with ALI or ARDS. Intervention  Patients were randomly assigned to receive ketoconazole, 400 mg/d (n=117), or placebo (n=117), initiated within 36 hours of fulfilling study entry criteria and given enterally for up to 21 days. Main Outcome Measures  Primary outcome measures were the proportion of patients alive with unassisted breathing at hospital discharge and the number of days of unassisted breathing (ventilator-free days) during 28 days of follow-up. Secondary outcome measures included the proportion of patients achieving unassisted breathing for 48 hours or more, the number of organ failure–free days, and changes in plasma interleukin 6 (IL-6) and urinary thromboxane A₂ metabolites (thromboxane B₂ [TXB₂] and 11-dehydro-TXB₂). Results  In-hospital mortality (SE) was 34.1% (4.3%) for the placebo group and 35.2% (4.3%) for the ketoconazole group (P=.85). The median number of ventilator-free days within 28 days of randomization was 9 in the placebo group and 10 in the ketoconazole group (P=.89). There were no statistically significant differences in the number of organ failure–free days, pulmonary physiology, or adverse events between treatment groups. The median serum ketoconazole level was 1.25 µg/mL and serum levels greater than 0.5 µg/mL were detected in 96% of patients assayed. Plasma IL-6, urinary TXB₂, and 11-dehydro-TXB₂ levels were unaffected by ketoconazole. Conclusions  In these patients with ALI or ARDS, ketoconazole was safe and bioavailable but did not reduce mortality or duration of mechanical ventilation or improve lung function. These data do not support the use of ketoconazole for the early treatment of ALI or ARDS.      

呼气末正压对急性呼吸窘迫综合征绵羊血管外肺水的影响

目的 :探讨呼气末正压 (PEEP)对急性呼吸窘迫综合征 (ARDS)血管外肺水 (EVLW )的影响。方法 :以内毒素持续静脉注射复制绵羊ARDS模型。根据PEEP水平分成 5cmH2 O( 7只 ,1cmH2 O =0 .0 98kPa)、10cmH2 O( 8只 )和 15cmH2 O( 6只 ) 3个组。采用单指示剂热稀释法测定EVLW。应用PEEP前 ( 0h)、应用后 1h和 2h测定EVLW ,同时监测血流动力学、呼吸力学和肺气体交换。结果 :应用PEEP前 ,10cmH2 O和 15cmH2 O组EVLW分别为 ( 16.5± 4.7)ml·kg- 1 和 ( 18.4± 6.0 )ml·kg- 1 ;应用PEEP 2h后 ,EVLW分别为 ( 14 .7± 4.5 )ml·kg- 1 和 ( 15 .3± 3 .7)ml·kg- 1 ,较应用PEEP前显著减少 (P <0 .0 5 )。应用PEEP前 ,15cmH2 O组氧合指数 (PaO2 FiO2 )为 ( 87.3± 2 7.9)mmHg( 1mmHg =0 .13 3kPa) ;应用PEEP 2h后 ,显著升高至 ( 13 8.6± 41.8)mmHg(P <0 .0 5 )。应用PEEP前 ,15cmH2 O组肺静态顺应性为 ( 11.4± 1.9)ml·cmH2 O- 1 ;应用PEEP 2h后 ,显著升高至 ( 14 .8± 2 .3 )ml·cmH2 O- 1 (P <0 .0 5 )。结论 :适当水平的PEEP能显著减少ARDS绵羊EVLW。     

Acute respiratory distress syndrome and acute lung injury

Acute respiratory distress syndrome (ARDS) is a life threatening respiratory failure due to lung injury from a variety of precipitants. Pathologically ARDS is characterised by diffuse alveolar damage, alveolar capillary leakage, and protein rich pulmonary oedema leading to the clinical manifestation of poor lung compliance, severe hypoxaemia, and bilateral infiltrates on chest radiograph. Several aetiological factors associated with the development of ARDS are identified with sepsis, pneumonia, and trauma with multiple transfusions accounting for most cases. Despite the absence of a robust diagnostic definition, extensive epidemiological investigations suggest ARDS remains a significant health burden with substantial morbidity and mortality. Improvements in outcome following ARDS over the past decade are in part due to improved strategies of mechanical ventilation and advanced support of other failing organs. Optimal treatment involves judicious fluid management, protective lung ventilation with low tidal volumes and moderate positive end expiratory pressure, multi-organ support, and treatment where possible of the underlying cause. Moreover, advances in general supportive measures such as appropriate antimicrobial therapy, early enteral nutrition, prophylaxis against venous thromboembolism and gastrointestinal ulceration are likely contributory reasons for the improved outcomes. Although therapies such as corticosteroids, nitric oxide, prostacyclins, exogenous surfactants, ketoconazole and antioxidants have shown promising clinical effects in animal models, these have failed to translate positively in human studies. Most recently, clinical trials with β2 agonists aiding alveolar fluid clearance and immunonutrition with omega-3 fatty acids have also provided disappointing results. Despite these negative studies, mortality seems to be in decline due to advances in overall patient care. Future directions of research are likely to concentrate on identifying potential biomarkers or genetic markers to facilitate diagnosis, with phenotyping of patients to predict outcome and treatment response. Pharmacotherapies remain experimental and recent advances in the modulation of inflammation and novel cellular based therapies, such as mesenchymal stem cells, may reduce lung injury and facilitate repair.     

不同呼气末正压对ARDS患者血管外肺水的影响

目的探讨在ARDS患者中给予不同呼气末正压水平对于患者血管外肺水的影响差异。方法收集35例呼吸窘迫综合征患者,随机分为A、B两组,A组共17例患者,给予呼气末正压8cmH2O治疗,B组共18例患者,给予呼气末正压12cmH2O治疗,监测并比较两组患者在即刻、6、12、24h四个时间点的EVLWI、CI、CVP、MAP、HR数值。结果插管即刻两组的各项观察指标进行比较差异无统计学意义（P〉0．05）。与治疗前比较,治疗后A、B两组的EVLWI的数值均较低．两组的△EVLWI在12h比较差异有统计学意义（P〈0．05）：在24h时比较差异具有高度统计学意义（P〈0．01）,其他的观察指标间差异无统计学意义（P〉0．05）。结论在急性呼吸窘迫综合征患者中给予不同呼气末正压水平（8cm,H2O、12cmH2O）,对EVLWI的影响有显著性,尤其是对于其12h和24h的影响较为显著,对于其他的指标影响不明显。     

急性肺损伤/呼吸窘迫综合征进展

急性肺损伤(acute lung injury,ALI)/呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)是一种常见的、破坏性极大的急性肺损伤综合征。近年来对其定义达成共识,并且在流行病学、自然史和发病机制的研究方面取得大幅度进步,     

Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial.

CONTEXT: Studies have shown that an inflammatory response may be elicited by mechanical ventilation used for recruitment or derecruitment of collapsed lung units or to overdistend alveolar regions, and that a lung-protective strategy may reduce this response. OBJECTIVE: To test the hypothesis that mechanical ventilation induces a pulmonary and systemic cytokine response that can be minimized by limiting recruitment or derecruitment and overdistention. DESIGN AND SETTING: Randomized controlled trial in the intensive care units of 2 European hospitals from November 1995 to February 1998, with a 28-day follow-up. PATIENTS: Forty-four patients (mean [SD] age, 50 [18] years) with acute respiratory distress syndrome were enrolled, 7 of whom were withdrawn due to adverse events. INTERVENTIONS: After admission, volume-pressure curves were measured and bronchoalveolar lavage and blood samples were obtained. Patients were randomized to either the control group (n = 19): tidal volume to obtain normal values of arterial carbon dioxide tension (35-40 mm Hg) and positive end-expiratory pressure (PEEP) producing the greatest improvement in arterial oxygen saturation without worsening hemodynamics; or the lung-protective strategy group (n = 18): tidal volume and PEEP based on the volume-pressure curve. Measurements were repeated 24 to 30 and 36 to 40 hours after randomization. MAIN OUTCOME MEASURES: Pulmonary and systemic concentrations of inflammatory mediators approximately 36 hours after randomization. RESULTS: Physiological characteristics and cytokine concentrations were similar in both groups at randomization. There were significant differences (mean [SD]) between the control and lung-protective strategy groups in tidal volume (11.1 [1.3] vs 7.6 [1.1] mL/kg), end-inspiratory plateau pressures (31.0 [4.5] vs 24.6 [2.4] cm H2O), and PEEP (6.5 [1.7] vs 14.8 [2.7] cm H2O) (P<.001). Patients in the control group had an increase in bronchoalveolar lavage concentrations of interleukin (IL) 1beta, IL-6, and IL-1 receptor agonist and in both bronchoalveolar lavage and plasma concentrations of tumor necrosis factor (TNF) alpha, IL-6, and TNF-alpha, receptors over 36 hours (P<.05 for all). Patients in the lung-protective strategy group had a reduction in bronchoalveolar lavage concentrations of polymorphonuclear cells, TNF-alpha, IL-1beta, soluble TNF-alpha receptor 55, and IL-8, and in plasma and bronchoalveolar lavage concentrations of IL-6, soluble TNF-alpha receptor 75, and IL-1 receptor antagonist (P<.05). The concentration of the inflammatory mediators 36 hours after randomization was significantly lower in the lung-protective strategy group than in the control group (P<.05). CONCLUSIONS: Mechanical ventilation can induce a cytokine response that may be attenuated by a strategy to minimize overdistention and recruitment/derecruitment of the lung. Whether these physiological improvements are associated with improvements in clinical end points should be determined in future studies.     

无创正压通气在多发伤并发ALI/ARDS中的临床应用

目的:探讨使用无创正压通气(Noninvasive positive pressure ventilation,NIPPV)治疗多发伤并发急性肺损伤/急性呼吸窘迫综合征(Acute lung injury/acute respiratory distress syndrome,ALI/ARDS),总结双水平气道正压通气呼吸模式的临床应用.方法:回顾性分析75例多发伤并发ALI/ARDS患者使用NIPPV或有创机械通气(Invasive mechanical ventilation,IMV)的情况,比较两种通气方式治疗前及治疗后2h动脉血气分析变化及机械通气时间.结果:NIPPV 40例,有创通气35例.无创通气组及有创通气组通气2h后病人动脉血氧分压(Arterial partial pressure of oxygen,PaO2)及血氧饱和度(Oxygen saturation,SaO2)较通气前明显提高(P＜0.0001).无创通气组中5例无创通气3～5d(平均4.2 d)后改IMV,4例因手术需全麻,先予以IMV 20～36 h后改为无创机械通气.35例无创通气3～18d[平均(8±5.5)d]成功脱机,无1例死亡.IMV组通气5～20 d脱机[平均(9±5.5)d],无1例死亡.两组机械通气时间比较无统计学意义(P＞0.05).两组间动脉血气分析治疗前、治疗后变化比较无统计学意义(P＞0.05).结论:多发伤后合并ALI/ARDS早期应用NIPPV治疗,采用双水平气道正压通气的呼吸模式,不仅可取得与IMV治疗相同的效果,而且能减少并发症,提高病人的舒适性.     

Effects of different levels of end-expiratory positive pressure on lung recruitment and protection in patients with acute respiratory distress syndrome

Background It is still controversial as to the implementation of higher positive end-expiratory pressure （PEEP） in patients with acute respiratory distress syndrome （ARDS）. This study was conducted to compare the lower and higher PEEP in patients with ARDS ventilated with low tidal volume, to investigate the relationship between the recruited lung volume by higher PEEP and relevant independent variables and to provide a bedside estimate of the percentage of potentially recruitable lung by higher PEEP. Methods Twenty-four patients with ARDS were studied. A lung recruiting maneuver was performed, then each patient was ventilated with PEEP of 8 cmH20 for 4 hours and subsequently with PEEP of 16 cmH20 for 4 hours. At the end of each PEEP level period, gas exchange, hemodynamic data, lung mechanics, stress index ＂b＂ of the dynamic pressure-time curve, intrinsic PEEP and recruited volume by PEEP were measured. Results Fourteen patients were recruiters whose alveolar recruited volumes induced by PEEP 16 cmH20 were （425_＋65） ml and 10 patients were non-recruiters. Compared with the PEEP 8 cmH20 period, after the application of the PEEP 16 cmH20, the PaO2/FiO2 ratio and static lung compliance both remained unchanged in non-recruiters, whereas they increased significantly in recruiters. Changes in PaO2/FiO2 and static lung compliance after PEEP increase were independently associated with the alveolar recruitment. Analyzing the relationship between recruiting maneuver （RM）-induced change in end-expiratory lung volume and the alveolar recruitment induced by PEEP, we found a notable correlation. Conclusions The results of this study indicated that the potential for alveolar recruitment might vary among the ARDS population and the higher PEEP levels should be limited to recruiters. Improving in PaO2/FiO2, static lung compliance after PEEP increase and the shape of the pressure-time curve could be helpful for PEEP application.     

Ventilatory management of acute lung injury and acute respiratory distress syndrome

Context  The acute lung injury and acute respiratory distress syndrome are critical illnesses associated with significant morbidity and mortality. Mechanical ventilation is the cornerstone of supportive therapy. However, despite several important advances, the optimal strategy for ventilation and adjunctive therapies for patients with acute lung injury and acute respiratory distress syndrome is still evolving. Evidence Acquisition  To identify reports of invasive ventilatory and adjunctive therapies in adult patients with acute lung injury and acute respiratory distress syndrome, we performed a systematic English-language literature search of MEDLINE (1966-2005) using the Medical Subject Heading respiratory distress syndrome, adult, and related text words, with emphasis on randomized controlled trials and meta-analyses. EMBASE and the Cochrane Central Register of Controlled Trials were similarly searched. The search yielded 1357 potential articles of which 53 were relevant to the study objectives and considered in this review. Evidence Synthesis  There is strong evidence to support the use of volume- and pressure-limited lung-protective ventilation in adult patients with acute lung injury and acute respiratory distress syndrome. The benefit of increased levels of positive end-expiratory pressure and recruitment maneuvers is uncertain and is being further evaluated in ongoing trials. Existing randomized controlled trials of alternative ventilation modes, such as high-frequency oscillation and adjunctive therapies, including inhaled nitric oxide and prone positioning demonstrate no significant survival advantage. However, they may have a role as rescue therapy for patients with acute respiratory distress syndrome with refractory life-threatening hypoxemia. Conclusions  Volume- and pressure-limited ventilation strategies should be used in managing adult acute lung injury and acute respiratory distress syndrome patients. Further research is needed to identify barriers to widespread adoption of this strategy, as well as the role of alternative ventilation modes and adjunctive therapies.      

Low-dose inhaled nitric oxide in patients with acute lung injury: a randomized controlled trial

Context  Inhaled nitric oxide has been shown to improve oxygenation in acute lung injury. Objective  To evaluate the clinical efficacy of low-dose (5-ppm) inhaled nitric oxide in patients with acute lung injury. Design and Setting  Multicenter, randomized, placebo-controlled study, with blinding of patients, caregivers, data collectors, assessors of outcomes, and data analysts (triple blind), conducted in the intensive care units of 46 hospitals in the United States. Patients were enrolled between March 1996 and September 1999. Patients  Patients (n = 385) with moderately severe acute lung injury, a modification of the American-European Consensus Conference definition of acute respiratory distress syndrome (ARDS) using a ratio of PaO₂ to FiO₂ of 250, were enrolled if the onset was within 72 hours of randomization, sepsis was not the cause of the lung injury, and the patient had no significant nonpulmonary organ system dysfunction at randomization. Interventions  Patients were randomly assigned to placebo (nitrogen gas) or inhaled nitric oxide at 5 ppm until 28 days, discontinuation of assisted breathing, or death. Main Outcome Measures  The primary end point was days alive and off assisted breathing. Secondary outcomes included mortality, days alive and meeting oxygenation criteria for extubation, and days patients were alive following a successful unassisted ventilation test. Results  An intent-to-treat analysis revealed that inhaled nitric oxide at 5 ppm did not increase the number of days patients were alive and off assisted breathing (mean [SD], 10.6 [9.8] days in the placebo group and 10.7 [9.7] days in the inhaled nitric oxide group; P = .97; difference, –0.1 day [95% confidence interval, –2.0 to 1.9 days]). This lack of effect on clinical outcomes was seen despite a statistically significant increase in PaO₂ that resolved by 48 hours. Mortality was similar between groups (20% placebo vs 23% nitric oxide; P = .54). Days patients were alive following a successful 2-hour unassisted ventilation trial were a mean (SD) of 11.9 (9.9) for placebo and 11.4 (9.8) for nitric oxide patients (P = .54). Days alive and meeting criteria for extubation were also similar: 17.0 placebo vs 16.7 nitric oxide (P = .89). Conclusion  Inhaled nitric oxide at a dose of 5 ppm in patients with acute lung injury not due to sepsis and without evidence of nonpulmonary organ system dysfunction results in short-term oxygenation improvements but has no substantial impact on the duration of ventilatory support or mortality.      

低流速法选择急性呼吸窘迫综合征最佳呼气末正压的临床研究

目的 :用低流速法测定准静态肺顺应性曲线 ,探讨以曲线低位转折点压力 (Pinf)选择急性呼吸窘迫综合征 (ARDS)最佳呼气末正压 (PEEP)的可行性。方法 :以 8例早期ARDS患者为研究对象 ,用低流速法测定准静态肺顺应性曲线 ,确定Pinf。分别以Pinf、Pinf -4、Pinf -2、Pinf+ 2、Pinf+ 4和Pinf + 6作为PEEP值 ,观察不同PEEP对ARDS患者血流动力学和氧代谢、肺气体交换和肺机械力学的影响。结果 :8例患者的准静态肺顺应性曲线均存在Pinf ,为 (11.0± 3 .2 )cmH2 O(1cmH2 O =0 .0 98kPa)。PEEP从Pinf-4增加到Pinf + 6时 ,动脉氧分压 (PaO2 )、动脉氧饱和度 (SaO2 )、平均气道压 (Pm)和气道峰值压 (PIP)均显著增加 (P <0 .0 5 )。与Pinf比较 ,Pinf -4时 ,SaO2 显著降低 ,Pinf+ 2、Pinf+ 4和Pinf+ 6时 ,SaO2 显著增加(P <0 .0 5 ) ;Pinf + 6时 ,心脏指数 (CI)显著降低 (P <0 .0 5 ) ,氧输送 (DO2 )无显著性差异 ,但当PEEP高于Pinf或低于Pinf -2时 ,CI与DO2 均呈降低趋势。与Pinf+ 6相比 ,Pinf-2时动态顺应性显著增高。结论 :ARDS患者机械通气时 ,以低流速法测定的准静态肺顺应性曲线为依据 ,Pinf-2或Pinf为最佳PEEP ,可获得最大DO2 。     

肺牵张指数指导急性呼吸窘迫综合征最佳呼气末正压的选择

目的 研究以不同的肺牵张指数指导急性呼吸窘迫综合征(ARDS)患者呼气末正压(PEEP)的选择.方法 14例ARDS患者实施肺复张后容量控制通气,用回归法求得方程P=a×timeb+c,b为肺牵张指数.调整PEEP使b<1(0.61(1.11时PEEP分别为(8.3±1.5)cm H2O、(15.0±1.9)cm H2O和(18.4±1.9)cm H2O,差异有统计学意义(P<0.001).b=1和b>1时的PaP2/FiO2明显高于复张前.与b=1时相比,b>1时的肺静态顺应性显著降低(P<0.05).h=1和b>1的复张容积较b<1增大.结论 充分复张后b=1时患者氧合、顺应性、肺复张容积明显改善,可指导ARDS患者最佳PEEP的选择.     

Early use of the pulmonary artery catheter and outcomes in patients with shock and acute respiratory distress syndrome: a randomized controlled trial

Context  Many physicians believe that the pulmonary artery catheter (PAC) is useful for the diagnosis and treatment of cardiopulmonary disturbances; however, observational studies suggest that its use may be harmful. Objective  To determine the effects on outcome of the early use of a PAC in patients with shock mainly of septic origin, acute respiratory distress syndrome (ARDS), or both. Design, Setting, and Patients  A multicenter randomized controlled study of 676 patients aged 18 years or older who fulfilled the standard criteria for shock, ARDS, or both conducted in 36 intensive care units in France from January 30, 1999, to June 29, 2001. Intervention  Patients were randomly assigned to either receive a PAC (n = 335) or not (n = 341). The treatment was left to the discretion of each individual physician. Main Outcome Measures  The primary end point was mortality at 28 days. The principal secondary end points were day 14 and 90 mortality; day 14 organ system, renal support, and vasoactive agents–free days; hospital, intensive care unit, and mechanical ventilation–free days at day 28. Results  The 2 groups were similar at baseline. There were no significant differences in mortality with or without the PAC at day 14: 49.9% vs 51.3% (mortality relative risk [RR], 0.97; 95% confidence interval [CI], 0.84-1.13; P = .70); day 28: 59.4% vs 61.0% (RR, 0.97; 95% CI, 0.86-1.10; P = .67); or day 90: 70.7% vs 72.0% (RR, 0.98; 95% CI, 0.89-1.08; P = .71). At day 14, the mean (SD) number of days free of organ system failures with or without the PAC (2.3 [3.6] vs 2.4 [3.5]), renal support (7.4 [6.0] vs 7.5 [5.9]), and vasoactive agents (3.8 [4.8] vs 3.9 [4.9]) did not differ. At day 28, mean (SD) days in hospital with or without the PAC (0.9 [3.6] vs 0.9 [3.3]), in the intensive care unit (3.4 [6.8] vs 3.3 [6.9]), or mechanical ventilation use (5.2 [8.5] vs 5.0 [8.5]) did not differ. Conclusion  Clinical management involving the early use of a PAC in patients with shock, ARDS, or both did not significantly affect mortality and morbidity.      

细菌感染在急性肺损伤/急性呼吸窘迫综合征中的作用

目的　探讨细菌感染在急性肺损伤 (ALI)和急性呼吸窘迫综合征 (ARDS)发病及进展中的作用。方法　分析10年间发生ALI、ARDS的 60 4例住院患者的临床资料。结果　①导致直接肺损伤的首要原因为肺部感染 ,导致间接肺损伤的首要原因为全身性感染 ;②在所分离的致病菌中 ,革兰阳性球菌 ( 5 0 .76%)和革兰阴性杆菌 ( 4 0 .15 %)基本相等 ,金黄色葡萄球菌和铜绿假单胞菌分别为第一和第二位致病菌 ;③随SIRS分级的提高 ,感染患者ALI和ARDS的发病率均显著增加 (P <0 .0 5 ) ;④随发生功能障碍器官数的增多 ,感染患者ALI的发病率显著增加 (P <0 .0 5 ) ,当发生 2个以上器官 (即 1个肺外器官 )功能障碍时 ,感染患者ARDS病死率显著增加 (P <0 .0 5 ) ;⑤在治疗原发病、氧疗及抗感染基础上的综合治疗可显著提高患者的治愈率 (P <0 .0 5 )。结论　感染是ALI和ARDS发病的主要诱因 ;机会致病菌是导致感染的主要细菌 ;以治疗原发病和抗感染为主的综合治疗可改善二者的预后     

Noninvasive positive-pressure ventilation for postextubation respiratory distress: a randomized controlled trial

Context  Noninvasive positive-pressure ventilation (NPPV) has been demonstrated to be effective in preventing the need for endotracheal intubation in some patients who present with acute respiratory failure. It is also used for patients who develop acute respiratory distress after extubation, but there are no randomized controlled trials that address its effectiveness in this population. Objective  To determine the effectiveness of NPPV compared with standard medical therapy in preventing the need for endotracheal reintubation in high-risk patients who develop respiratory distress during the first 48 hours after extubation. Design  Randomized, controlled, unblinded study with concealed allocation conducted between August 1, 1996 and October 31, 1999. Setting  An intensive care unit (ICU) in an academic, tertiary care hospital in Ontario. Patients  Eighty-one patients with a history of cardiac or respiratory disease or who initially required ventilatory support for more than 2 days and who developed respiratory distress within 48 hours of extubation. Interventions  Patients were randomly assigned to receive standard medical therapy alone (supplemental oxygen to maintain oxygen saturation by pulse oximetry 95%; n = 42) or NPPV by face mask plus standard medical therapy (n = 39). Main Outcome Measures  Rates of reintubation, duration of mechanical ventilation, lengths of ICU and hospital stay, and hospital mortality. Results  Comparing the NPPV group with the standard-therapy group, there was no difference in the rate of reintubation (72% vs 69%; relative risk, 1.04; 95% confidence interval, 0.78-1.38) or hospital mortality (31% for both groups; relative risk, 0.99; 95% confidence interval, 0.52-1.91). Similarly, no difference was found in duration of mechanical ventilation or length of ICU or hospital stay. Conclusions  The addition of NPPV to standard medical therapy does not improve outcome in heterogeneous groups of patients who develop respiratory distress during the first 48 hours after extubation.      

急性肺损伤/急性呼吸窘迫综合征治疗进展

急性肺损伤/急性呼吸窘迫综合征是临床常见的危重病症之一,起病急、发展快、病死率高,尽管在过去几年中,重症医学的发展使得ARDS的院内发生率和死亡率大幅下降,但目前临床上仍缺乏特效的治疗手段.肺保护通气、积极抗感染治疗和限制性液体管理是目前主要西医治疗策略,近年来有部分改进从而进一步降低该病的死亡率.此外,关于ARDS异...