Clinics in chest medicine
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Clinics in chest medicine · Mar 2001
ReviewRespiratory infection in the chronically critically ill patient. Ventilator-associated pneumonia and tracheobronchitis.
The long-term ventilated patient is at high risk for developing nosocomial pneumonia or tracheobronchitis. In general, the frequency of infection increases with the duration of mechanical ventilation, but the risk appears to be greatest in the first week of intubation. Although these types of infection are common and may have morbidity and mortality impact, the daily risk is less in the long-term ventilated patient than in the acutely ill intubated patient. ⋯ In some patients, colonization can be eliminated. When the long-term ventilated patient does develop infection, it generally involves highly resistant gram-negative or gram-positive organisms and therapy should be prompt and appropriate. Not all such patients respond to systemic antibiotics, and the use of adjunctive aerosol therapy may have benefit for those with either tracheobronchitis or pneumonia, especially if highly resistant pathogens are present.
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Clinics in chest medicine · Sep 2000
ReviewMechanical ventilation in acute lung injury and acute respiratory distress syndrome.
Mechanical ventilation provides life-sustaining support for most patients with acute lung injury and acute respiratory distress syndrome; however, traditional approaches to mechanical ventilation may cause ventilator-associated lung injury, which could exacerbate or perpetuate respiratory failure caused initially by conditions such as pneumonia, sepsis, and trauma. This article reviews the theory, laboratory data, and results of recent clinical trials that suggest that modified ventilator strategies can reduce ventilator-associated lung injury and improve clinical outcomes.
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Dysfunction of the surfactant system of the lung in the setting of acute lung injury (ALI) is likely to contribute to the pathophysiology of that syndrome. Multiple mechanisms, including injury to alveolar type II cells and inhibition by plasma proteins contribute to this loss of function. Similar injury occurs in animal models of acute lung injury and, in that setting, treatment with exogenous surfactant causes marked improvement in gas exchange. Clinical studies of surfactant treatment of ALI suggest benefit, and definitive phase III trials are now in progress.
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Clinics in chest medicine · Sep 2000
ReviewPulmonary pathology of acute respiratory distress syndrome.
Lung morphology in ARDS reflects the rapid evolution from interstitial and alveolar edema to end-stage fibrosis consequent to injury of the alveolocapillary unit. This morphologic progression, termed diffuse alveolar damage, has been subdivided into sequentially occurring exudative, proliferative, and fibrotic phases. Pulmonary lesions correlate with the phase of alveolar damage rather than its specific cause. ⋯ The factors that govern which patients will develop the fulminant syndrome are poorly understood. It must be re-emphasized that the lung is stereotyped in its response to injury and, consequently, descriptive, or even quantitative, studies of lung morphology can only provide clues regarding the initiating factors and pathogenetic mechanisms of ARDS. Progress in understanding the pathogenesis of ARDS and development of rational approaches to therapy will ultimately depend on careful clinical and experimental studies and the application of immunohistochemical and molecular biology techniques to unravel basic mechanisms of cellular injury and response.
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Since last reviewed in this forum, there have been remarkable advances in our understanding of the acute inflammatory process and how it contributes to the development of ALI. As stated in the beginning of this article, it is not possible to even begin to review all the specific advances that have been made. ⋯ These include the recognition that patients at risk for and with ARDS represent a heterogeneous population, that mediators or markers of inflammation cannot be considered in isolation, that a balance between proinflammatory mediators and inflammatory modulators may be important, and that there are several genetic factors that could contribute to the susceptibility for the development of ARDS. Hopefully these concepts can be expanded and clarified so that the next review of this topic can report on successful therapeutic interventions for the prevention and the treatment of ARDS.