Niederman M S, Fein A M
Medical and Respiratory Intensive Care Unit, Winthrop-University Hospital, Mineola, New York.
Clin Chest Med. 1990 Dec;11(4):633-56.
Systemic sepsis and pneumonia are common predisposing factors for ARDS, which can serve as the initial manifestation of the multisystem organ failure syndrome. Primary pneumonia that necessitates ICU admission leads to ARDS in approximately 10% of patients. Systemic infection can also lead to ARDS, but when bacteremia alone is present, the risk is low (probably less than 5%). If the septic syndrome with a hemodynamic and end-organ response develops, the ARDS may follow in as many as 40% of patients. When multiple risk factors for acute lung injury are present, the risk of developing ARDS rises dramatically. The septic syndrome, acute lung injury, and multiorgan failure are closely tied to one another because bacterial cell walls can activate inflammatory mediators, such as interleukin-1 and tumor necrosis factor, which can in turn lead to the septic syndrome and inflammatory injury to the lung. Clinical features, more than serum markers, have been the best predictors of whether lung injury will follow sepsis, indicating that the mere presence of mediators alone cannot cause ARDS and that there are individual susceptibility factors in the effects of these mediators. With the advent of monoclonal antibodies and new anti-inflammatory drugs, prevention of progression from sepsis to multiorgan failure may become possible. Pneumonia is the most common infection that complicates ARDS once it is established, and the mortality rate may approach 90%. The existence of acute lung injury, its predisposing conditions, coexisting illnesses, and the therapeutic interventions used for patients with lung injury all can interfere with lung host defenses and set the stage for bacterial infection of the already-injured lung. This infection appears to add to the propagation of the multiple system organ failure that has already begun. In the future, it may become possible to prevent this infection, which would be a welcome development, because currently, we are stymied in our efforts to diagnose and treat pneumonia in the setting of acute lung injury. Preventive efforts will follow from an understanding of the pathogenesis of pneumonia and in the future may include topical antibiotics, selective digestive decontamination, and prophylactic passive immunotherapy.
全身性败血症和肺炎是急性呼吸窘迫综合征（ARDS）常见的诱发因素，ARDS可作为多系统器官功能衰竭综合征的初始表现。需要入住重症监护病房（ICU）的原发性肺炎在约10%的患者中会导致ARDS。全身性感染也可导致ARDS，但仅存在菌血症时，风险较低（可能低于5%）。如果出现伴有血流动力学和终末器官反应的脓毒症综合征，则多达40%的患者可能会继而发生ARDS。当存在多种急性肺损伤危险因素时，发生ARDS的风险会急剧上升。脓毒症综合征、急性肺损伤和多器官功能衰竭彼此密切相关，因为细菌细胞壁可激活炎症介质，如白细胞介素-1和肿瘤坏死因子，进而导致脓毒症综合征和肺部的炎症性损伤。临床特征而非血清标志物一直是脓毒症后是否会发生肺损伤的最佳预测指标，这表明仅介质的存在并不能导致ARDS，而且这些介质的作用存在个体易感性因素。随着单克隆抗体和新型抗炎药物的出现，预防脓毒症发展为多器官功能衰竭可能成为现实。一旦ARDS确立，肺炎是最常见的使其复杂化的感染，死亡率可能接近90%。急性肺损伤的存在、其诱发条件、并存疾病以及用于肺损伤患者的治疗干预措施，均会干扰肺部宿主防御功能，并为已受损肺部的细菌感染创造条件。这种感染似乎会加剧已经开始的多系统器官功能衰竭的进展。未来，有可能预防这种感染，这将是一个令人欣喜的进展，因为目前在急性肺损伤情况下诊断和治疗肺炎的努力受阻。预防措施将源于对肺炎发病机制的了解，并可能在未来包括局部使用抗生素、选择性消化道去污和预防性被动免疫治疗。
