Acute respiratory distress syndrome and acute lung injury

被引:229
作者
Dushianthan, A. [1 ]
Grocott, M. P. W. [1 ,2 ]
Postle, A. D. [3 ]
Cusack, R. [1 ]
机构
[1] Southampton Univ Hosp, NHS Trust, Crit Care Res Unit, Southampton SO16 6YD, Hants, England
[2] Univ Southampton, Southampton Univ Hosp, Div Dev Origins Hlth & Dis, Sch Med, Southampton SO16 6YD, Hants, England
[3] Univ Southampton, Southampton Univ Hosp, Div Infect Inflammat & Immun, Sch Med, Southampton SO16 6YD, Hants, England
关键词
END-EXPIRATORY PRESSURE; INHALED NITRIC-OXIDE; NEUROMUSCULAR BLOCKING-AGENTS; ALVEOLAR FLUID CLEARANCE; GAMMA-LINOLENIC ACID; TIDAL VOLUME; ADULT PATIENTS; GAS-EXCHANGE; INTEROBSERVER VARIABILITY; AEROSOLIZED PROSTACYCLIN;
D O I
10.1136/pgmj.2011.118398
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 beta 2 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.
引用
收藏
页码:612 / 622
页数:11
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