Skerrett S J, Niederman M S, Fein A M
Department of Medicine, University of Washington School of Medicine, Seattle.
Clin Chest Med. 1989 Dec;10(4):469-502.
We have discussed the relationship between systemic illness, infection, and lung disease. As we have seen, patients with a wide variety of disease states, including advanced age, diabetes mellitus, alcoholism, collagen vascular disease, cancer, heart failure, and organ transplantation are potentially at increased risk for pneumonia because of disease-related impairments in host defenses. In addition, two virtually ubiquitous conditions in hospitalized patients, malnutrition and therapeutic interventions (especially with common medications), frequently add to the risk of airway invasion by bacterial pathogens. Systemic illness not only makes lung infection more common, but may adversely affect outcome and resolution, as well as determine the clinical presentation of pneumonia. In one particular population, the intubated and mechanically ventilated patient, the risk of infection is particularly high, and nosocomial pneumonia is a major cause of mortality. To the extent that the host response itself leads to the symptoms and signs of infection, systemically ill individuals may have subtle clinical features when serious bacterial invasion is present. Many components of the host defense system can become abnormal with serious illness, but a common mechanism that ties many systemic diseases to pneumonia is an alteration in airway epithelial cell receptivity for bacteria, namely, bacterial adherence, a process that mediates airway colonization, the first pathogenetic step on the road to pneumonia. The impetus for understanding how serious illness promotes lung infection is that once these mechanisms are identified, potential preventative strategies to minimize infection risk in the individual with systemic disease may be developed. The relationship among systemic illness, the lung, and infection also exists in a different direction: infection of a systemic nature (the septic syndrome) can lead to disease in the lung (ARDS). We have described the features of the septic syndrome and identified how it may lead to lung injury, usually by indirect means, through activation of inflammatory mediators that are carried to the lung via the vasculature. Although it is frequently impossible to predict which specific patient with systemic sepsis will develop acute lung injury, the current state of knowledge does permit us to identify high-risk individuals. Surprisingly, clinical assessment rather than biochemical testing is the best predictor of the development of acute lung injury. Patients with severe injury, profound shock and multiple systemic insults are most prone to acute lung injury in the presence of systemic sepsis.(ABSTRACT TRUNCATED AT 400 WORDS)
我们已经讨论了全身性疾病、感染与肺部疾病之间的关系。如我们所见，患有多种疾病状态的患者，包括高龄、糖尿病、酗酒、胶原血管病、癌症、心力衰竭和器官移植患者，由于宿主防御方面与疾病相关的损害，患肺炎的风险可能会增加。此外，住院患者中两种几乎普遍存在的情况，即营养不良和治疗干预（尤其是常用药物），常常会增加细菌病原体侵入气道的风险。全身性疾病不仅使肺部感染更为常见，还可能对预后和病情缓解产生不利影响，并决定肺炎的临床表现。在一个特定人群，即插管并接受机械通气的患者中，感染风险特别高，医院获得性肺炎是主要的死亡原因。就宿主反应本身导致感染的症状和体征而言，当存在严重细菌入侵时，全身性疾病患者可能具有不明显的临床特征。宿主防御系统的许多组成部分在重病时可能会变得异常，但将许多全身性疾病与肺炎联系起来的一个共同机制是气道上皮细胞对细菌的接受性改变，即细菌黏附，这一过程介导气道定植，是通往肺炎的第一个致病步骤。理解重病如何促进肺部感染的动力在于，一旦确定了这些机制，就可以制定潜在的预防策略，以将患有全身性疾病个体的感染风险降至最低。全身性疾病、肺部与感染之间的关系在另一个方向上也存在：全身性感染（脓毒症综合征）可导致肺部疾病（急性呼吸窘迫综合征）。我们已经描述了脓毒症综合征的特征，并确定了它如何通常通过间接方式，即通过激活经血管系统输送到肺部的炎症介质，导致肺损伤。虽然通常无法预测哪些患有全身性脓毒症的特定患者会发生急性肺损伤，但目前的知识状态确实使我们能够识别高危个体。令人惊讶的是，临床评估而非生化检测是急性肺损伤发生的最佳预测指标。在全身性脓毒症存在的情况下，严重受伤、深度休克和遭受多次全身性损伤的患者最容易发生急性肺损伤。（摘要截选至400字）
