American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · May 2001
Comparative StudyComputed tomography assessment of positive end-expiratory pressure-induced alveolar recruitment in patients with acute respiratory distress syndrome.
Computed tomography (CT) assessment of positive end-expiratory pressure (PEEP)-induced alveolar recruitment is classically achieved by quantifying the decrease in nonaerated lung parenchyma on a single juxtadiaphragmatic section (Gattinoni's method). This approach ignores the alveolar recruitment occurring in poorly aerated lung areas and may not reflect the alveolar recruitment of the entire lung. This study describes a new CT method in which PEEP-induced alveolar recruitment is computed as the volume of gas penetrating in poorly and nonaerated lung regions following PEEP. ⋯ PEEP-induced alveolar recruitment was 499 +/- 279 ml whereas distension and overdistension of previously aerated lung areas were 395 +/- 382 ml and 28 +/- 6 ml, respectively. The alveolar recruitment according to Gattinoni's method was 26 +/- 24 g and no correlation was found between both methods. A significant correlation was found between PEEP-induced alveolar recruitment and increase in Pa(O(2)) only when recruitment was assessed by the new method (Rho = 0.76, p = 0.003), suggesting that it may be more accurate than Gattinoni's method.
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Am. J. Respir. Crit. Care Med. · May 2001
Resolution of infectious parameters after antimicrobial therapy in patients with ventilator-associated pneumonia.
Although recommended durations of antimicrobial therapy for ventilator-associated pneumonia (VAP) range from 7 to 21 d, these are not based on prospective studies and little is known about the resolution of symptoms after start of antibiotics. Resolution of these symptoms was investigated in 27 patients. VAP was diagnosed on clinical, radiographic, and microbiological criteria, including quantitative cultures of bronchoalveolar lavage. ⋯ Newly acquired colonization, especially with P. aeruginosa and Enterobacteriaceae, occurred in the second week of therapy. Six patients developed a recurrent episode of VAP, four of them with P. aeruginosa. Clinical responses to therapy for VAP occur within the first 6 d of therapy, endotracheal colonization with Gram-negative bacteria persists despite susceptibility to therapy, and acquired colonization usually occurs in the second week of therapy and frequently precedes a recurrent episode.
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Am. J. Respir. Crit. Care Med. · May 2001
Comparative StudyQuality-adjusted survival in the first year after the acute respiratory distress syndrome.
There is little information on long-term outcome after acute respiratory distress syndrome (ARDS). We measured quality-adjusted survival in the first year after ARDS in a prospective cohort (n = 200). All patients met traditional criteria for ARDS. ⋯ QWB was low at 6 and 12 mo (0.59 +/- 0.015 and 0.60 +/- 0.015), yielding a quality-adjusted survival of 36 QALYs per 100 patients (sensitivity range: 21 to 46 QALYs). We conclude that ARDS developing in previously healthy patients is associated with poor quality-adjusted survival. These data are important for cost-effectiveness analyses and long-term care.
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Am. J. Respir. Crit. Care Med. · May 2001
Comparative StudyPulmonary edema fluid from patients with acute lung injury augments in vitro alveolar epithelial repair by an IL-1beta-dependent mechanism.
Efficient alveolar epithelial repair is crucial for the restoration of the injured alveolar epithelial barrier in patients with acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS). We hypothesized that pulmonary edema fluid from patients with ALI /ARDS would inhibit alveolar epithelial repair as measured in an in vitro epithelial wound-repair model using the human alveolar epithelial-like cell line A549. In contrast to our initial hypothesis, pulmonary edema fluid from patients with ALI/ARDS increased alveolar epithelial repair by 33 +/- 3% compared with pooled plasma from healthy donors (p < 0.01). ⋯ Inhibition of interleukin-1beta (IL-1beta) activity by IL-1 receptor antagonist reduced alveolar epithelial repair induced by ALI/ARDS edema fluid by 46 +/- 4% (p < 0.001), indicating that IL-1beta contributed significantly to the increased epithelial repair. In summary, pulmonary edema fluid collected early in the course of ALI/ARDS increased alveolar epithelial repair in vitro by an IL-1beta-dependent mechanism. These data demonstrate a novel role for IL-1beta in patients with ALI/ARDS, indicating that IL-1beta may promote repair of the injured alveolar epithelium.