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  • Pneumonia in the critically ill hospitalized patient: part 3


In many studies, the measurement of plasma factors to predict ARDS has been disappointing. While various components of activated complement are elevated in septic patients, none has been shown to consistently predict progressive lung injury. Re-cently, a prospective study by Langlois and Gawryl demonstrated the terminal complement complex was increased by an average of 100 percent in septic patients who developed ARDS prior to the onset of clinical lung injury. While interesting, these findings await confirmation at other clinical centers. The neutrophil is also an important participant in the initial phases of lung injury. Despite this, our own data suggest that neither neutrophil turnover nor neutrophil chemoattractant activity can identify which septic patients will develop ARDS.

Dr. Niederman: How does sepsis affect the outcome of ARDS?

Dr. Fein: Advances in the management of respiratory failure have reduced the number of patients who succumb to hypoxemia. Rather, deaths occurring 72 hours or more after the initial insult usually result from uncontrolled pulmonary sepsis. Nosocomial pneumonia is evident in more than 70 percent of patients with ARDS. Infection in a damaged lung potentially influences the outcome by several mechanisms. The additional septic burden further enhances the release of inflammatory mediators including tumor necrosis factor (TNF) and interleukin-1, directly po¬tentiating organ damage and recruiting more neutrophils and macrophages to the lung. These effector cells release proteases and oxidants which promote colonization by micro-organisms and lead to disordered repair of connective tissue matrix and fibrosis. Among ARDS patients with infection, 67 percent died compared to only 7 percent of non-infected patients and those with nosocomial pneumonia may have an even higher mortality. Most infected patients have failure of other organ systems in addition to the lung. It is interesting that following the recovery from ARDS, our patient developed a second episode of respiratory failure, with recovery of both Pseudomonas aeruginosa and Pneumocystis carinii. Both of these organisms are indicators of a markedly compromised host. Host defense impairments are common in the multiorgan failure syndrome and clearly influence outcome. In our patient these compounded the already significant effects of systemic lupus erythematosus, diabetes, and corticosteroid therapy. revatio 20 mg

Proteolytic enzymes, especially neutrophil elastase, are released into the alveolar lining fluid in ARDS. In addition to its effects on connective tissue matrix, elastase may inhibit ciliary function, and degrade 172 immunoglobulin IgG and secretory IgA, thereby inhibiting bacterial clearance and phagocytosis. Likewise, the formation of pulmonary edema fluid may directly inhibit bacterial clearance by macro-phages and washout surfactant, which has antimicrobial activity. While there is no mention in our patient of liver dysfunction, this is a frequent accompaniment of ARDS and multiorgan failure. Liver dysfunction limits clearance of gut bacteria, endotoxin and circulating inflammatory mediators such as TNF, thus enhancing injury. Iatrogenic factors may also impair host defenses. High inspired oxygen tensions used in the patients treatment as well as corticosteroids, impair the phagocytic function of macrophages and neutrophils. It is clear that failure of multiple host defenses contributed to the second episode of acute respiratory failure which he sustained. Dr. Niederman: The patient being discussed today had Gram-negative colonization of the tracheobronchial tree and Gram-negative pneumonia, two findings that are closely interrelated. In addition, the pathogenesis of airway colonization is related to many of the host impairments that our patient demonstrated. He had two eposides of pneumonia, both acquired in the hospital, and at the conclusion of the first episode, he continued to grow Pseudomonas aeruginosa in his lower airway, in the absence of clinical signs of infection. This represented airway colonization which had persisted after an initial pneumonic episode. While still colonized with Pseudomonas aervginosa, he developed a second episode of pneumonia which was due to both Pseudomonas aeruginosa and Pneumocystis carinii. The features of interest in this case are the relationship of airway colonization to the subsequent occurrence of pneumonia, the mechanisms that allow risk factors to lead to colonization of the airway by Gram-negative bacteria, and reasons for persistent lower airway colonization by Pseudomonas aeruginosa.

Colonization of both the upper and lower respiratory tract are frequently associated with the occurrence of nosocomial pneumonia. Rates of Gram-negative colonization of the oropharynx are directly related to the severity of illness for a given patient. In a study by Johanson and colleagues, utilizing multiple cultures of the oropharnyx, it was found that no more than 6 percent of normal individuals had oropharyngeal colonization by Gram-negative bacteria. However, as patients became progressively ill, the incidence of Gram-negative colonization of the upper airway in-creased, such that with multiple cultures, nearly three- quarters of the sickest patients in the hospital were colonized with enteric Gram-negative bacteria. The relevance of this finding to the occurrence of pneumonia was shown in a follow-up study of 213 intensive care unit patients, 26 of whom developed nosocomial pneumonia. Among the patients with pneumonia, 22 of 26 had prior oropharyngeal colonization by Gram- negative bacteria, indicating a high co-association between upper airway colonization and the subse­quent occurrence of parenchymal lung infection. The reason for the close relationship between airway colonization and pneumonia may be the result of two factors. First, once the airway is colonized by Gram- negative bacteria, these organisms are available for aspiration into the tracheobronchial tree. In addition, it is possible that patients who have become colonized in the oropharynx have host impairments which pre­dispose not only to upper airway colonization, but also to lower airway colonization and subsequent pneu­monia. Thus, colonization of both the upper and lower respiratory tract can be viewed as a “marker” of a seriously ill patient who has multiple impairments in respiratory host defenses.
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