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Query: UMLS:C0040586 (tracheobronchitis)
 449 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary infections are the most life-threatening infections in mechanically ventilated patients. Methods to avoid these infections by prophylactic systemic or local administration of antibiotics may promote resistance and selection of distinct groups of pathogens. In mechanically ventilated patients we studied the impact of early diagnosis and specific therapy on the prevention of pulmonary infections. Due to the very short interval between colonization and infection, daily microscopic and microbiologic examinations of tracheobronchial secretions proved to be essential for early and successful therapy and even prevention of pulmonary infections. PATIENTS AND METHODS. The present study comprised a total of 190 patients admitted to the surgical intensive care unit who required mechanical ventilation for a period of at least 48 h: 56 were admitted for multiple trauma; 38 had peritonitis; and the remainder had postoperative complications such as renal failure, cardiac problems, septicemia or pneumonia. Multitraumatized patients (16.5 days) and those with peritonitis (13.8 days) needed the most extensive ventilatory support. After admission antibiotic therapy was started with a second-generation cephalosporin or amoxicillin/clavulanic acid. Further antibiotic treatment was directed strictly against the isolated pathogens. Tracheobronchial secretions were monitored daily by microscopy and cultures. Microscopic evaluation was essential to discriminate between colonization and inflammation, and often indicated the infective agent. If infections were suspected provisional antibiograms were performed on the material. This procedure allowed a specific antibiotic treatment to be initiated 8-12 h later. In patients with pulmonary infections, additional bronchoscopic material was taken in order to correlate these findings with those gained from the tracheobronchial secretions. RESULTS. In 85% of cases massive colonization of the trachea with Pseudomonas aeruginosa, enterobacteria, Staphylococcus aureus or Streptococcus pneumoniae resulted in pulmonary infections 24-48 h later. The reduced virulence of Pseudomonas species (non-aeruginosa) and Acinetobacter species is reflected by an infection rate of 50% and an extended period of time to establish an infection (2-4 days). Only 30% of patients highly contaminated with Candida developed pulmonary infections after 3-6 days. A fair correlation (86%) was found between pathogens isolated in tracheobronchial secretions and bronchoscopic material. In the population studied, 68 patients (35.7%) developed pulmonary infections, 32 of them pneumonia (16.8%), and the others purulent tracheobronchitis with fever. Both groups were treated with antibiotics. Patients with multiple trauma, often accompanied by lung contusion, were most frequently affected. In 59 patients (87%) pulmonary infections were treated successfully by specific antibiotic therapy; 9 patients died so rapidly, that the pulmonary complication could not account for the fatal outcome. In 38 patients with massive contamination of the tracheobronchial system by enterobacteria, Pseudomonas aeruginosa or Staph. aureus, progression from colonization to infection was prevented by early administration of specific therapy. CONCLUSIONS. Because pulmonary infections in most cases arise very soon after pathogens have gained access to the tracheobronchial system daily monitoring of tracheobronchial secretions is required for early initiation of specific therapy.
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PMID:[Microbiological care of ventilated intensive care patients. Feasibility of diagnosis and therapy of pulmonary infection]. 195 44

Pulmonary infection in cystic fibrosis (CF) is primarily a purulent tracheobronchitis. Antibiotics are available that are active in vitro against bacteria isolated from sputum from patients with CF. Despite efficacious antibiotic concentrations in serum, however, the results of treatment are frequently suboptimal. A widely accepted explanation for this limited efficacy is poor penetration of orally or intravenously administered antibiotics into respiratory secretions. The bioactivity of antibiotics in respiratory secretions is not identical to that found in vitro. Laboratory conditions are standardized and selected to approximate serum. Deviations from these conditions can markedly influence the results. Differences in composition between sputum and laboratory culture media, as well as variation in growth and metabolism of the pathogen in respiratory secretions, must be considered when predicting in vivo activity in sputum. Thus, when defining criteria for antibiotic susceptibility or resistance in the treatment of pulmonary infection in patients with CF, the concentrations achievable in bronchial secretions as well as the bioactivity in this environment should be considered.
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PMID:Antibiotic activity in sputum. 370 36

Pulmonary infections span a wide spectrum, ranging from self-limited processes (e.g., tracheobronchitis) to life-threatening infections including both community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP). Together, pneumonia and influenza rank as the sixth leading cause of death in the United States and lead all other infectious diseases in this respect. Pneumonia is the second-most-common hospital-acquired infection in the United States, accounting for 17.8% of all hospital-acquired infections and 40,000 to 70,000 deaths per year. HAP is the most common nosocomial infection occurring in patients requiring mechanical ventilation, developing in 6.5% of patients after 10 days and in 28% of patients after 30 days of ventilatory support. Patients acquiring HAP have a greater risk of mortality than comparably ill ventilated patients who do not develop pneumonia. Ventilator-associated pneumonia (VAP) specifically refers to a bacterial pneumonia developing in patients with acute respiratory failure who have been receiving mechanical ventilation for at least 48 hours. The etiologic bacteriologic agents associated with VAP typically differ based on the timing of the occurrence of the infection relative to the start of mechanical ventilation. VAP occurring within 96 hours of the onset of mechanical ventilation is usually due to antibiotic-sensitive bacteria that colonize the patient prior to hospital admission (e.g., Streptococcus pneumoniae, Haemophilus influenza, oxacillin-sensitive Staphylococcus aureus). VAP developing after 96 hours of ventilatory support is more often associated with antibiotic-resistant bacteria including oxacillin-resistant Staphylococcus aureus, Acinetobacter species and Pseudomonas aeruginosa. However, more recent data suggest that hospitalization and exposure to antibiotics prior to the start of mechanical ventilation are important risk factors for the occurrence of VAP attributed to antibiotic-resistant bacteria. Therefore, these risk factors should be considered when deciding on an appropriate empiric antibiotic regimen regardless of the onset of VAP. VAP and catheter-associated bloodstream infections are the leading causes of infection acquired in the intensive care unit (ICU) setting. Patients in the ICU have rates of HAP that are as much as five to ten times higher than the rates in general hospital wards. Additionally, like nosocomial bloodstream infections, VAP is associated with an attributable mortality beyond that accounted for by patients' severity of illness. The attributable mortality associated with VAP appears to be greatest for "high-risk'' antibiotic-resistant bacteria including Pseudomonas aeruginosa and oxacillin-resistant Staphylococcus aureus. The greater hospital mortality associated with these "high-risk'' pathogens has been attributed to the virulence of these bacteria and the increased occurrence of inadequate initial antibiotic treatment of VAP due to the presence of antibiotic resistance. This review provides an overview of the clinical importance of VAP. We then describe how this nosocomial infection influences the management and outcomes of patients with the acute respiratory distress syndrome (ARDS).
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PMID:Ventilator-associated pneumonia complicating the acute respiratory distress syndrome. 1608 83