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Biomedical subjects

M S Niederman

Publications and source records attributed to M S Niederman.

At least 55 records · Page 3Linked to original sources
PubMed1997

Impact of BAL data on the therapy and outcome of ventilator-associated pneumonia.

STUDY OBJECTIVE: To define the impact of BAL data on the selection of antibiotics and the outcomes of patients with ventilator-associated pneumonia (VAP). DESIGN: Prospective observation and bronchoscopy with BAL, performed within 24 h of establishing a clinical diagnosis of a new episode of hospital-acquired VAP or progression of a prior episode of nosocomial pneumonia (NP). SETTING: A 15-bed medical and surgical ICU. PATIENTS: One hundred thirty-two patients hospitalized for more than 72 h, who were mechanically ventilated and had a new or progressive lung infiltrate plus at least two of the following three clinical criteria for VAP: abnormal temperature (> 38 degrees C or < 35 degrees C), abnormal leukocyte count (> 10,000/mm3 or < 3,000/mm3), purulent bronchial secretions. INTERVENTIONS: Bronchoscopy with BAL within 24 h of establishing a clinical diagnosis of VAP or progression of an infiltrate due to prior VAP or NP. All patients received antibiotics, 107 prior to bronchoscopy and 25 immediately after bronchoscopy. RESULTS: Sixty-five of the 132 patients were BAL positive (BAL[+]), satisfying a microbiologic definition of VAP (> 10(4) cfu/mL), while 67 were BAL negative (BAL[-]). The BAL(+) patients had no differences in mortality, prior antibiotic use, and demographic features when compared with the BAL(-) patients. More of the BAL(+) patients (38/65) satisfied all three clinical criteria of VAP than did BAL(-) patients (24/67) (p < 0.05). A total of 50 BAL(+) patients received antibiotic therapy prior to bronchoscopy, and when this prior therapy was adequate (n = 16), as defined by the results of BAL, then mortality was 38%, while if prior therapy was inadequate (n = 34), mortality was 91% (p < 0.001), and if no therapy was given (n = 15), mortality was 60%. When therapy changes were made after bronchoscopy, more patients (n = 42) received adequate therapy, but mortality in this group was comparable to mortality among those who continued to receive inadequate therapy (n = 23). A total of 46 of the 65 BAL(+) patients died, with 23 of these deaths occurring during the 48 h after the bronchoscopy, before BAL results were known. When BAL data became available, 37 of the 42 surviving patients received adequate therapy, but their mortality was comparable to the patients who continued to receive inadequate therapy. CONCLUSIONS: Patients with a strong clinical suspicion of VAP have a high mortality rate, regardless of whether BAL cultures confirm the clinical diagnosis of VAP. When adequate antibiotic therapy is initiated very early (ie, before performing bronchoscopy), mortality rate is reduced if this empiric therapy is adequate, compared to when this therapy is inadequate or no therapy is given. If adequate therapy is delayed until bronchoscopy is performed or until BAL results are known, mortality is higher than if it had been given at the time of first establishing a clinical diagnosis of VAP. When patients were changed from inadequate antibiotic therapy to adequate therapy, based on the results of BAL, mortality was comparable to those who continued to receive inadequate therapy. Thus, even if bronchoscopy can accurately define the microbial etiology of VAP, this information becomes available too late to influence survival.

Aged↗
PubMed1997

[Community-acquired pneumonia in adults. Clinical practice guideline for Argentina. Study Group on Community Acquired Pneumonia].

Community-acquired pneumonia (CAP) affects approximately 1% of the population annually. Initial antimicrobial therapy is most often empirical. Guidelines designed in other countries for the empirical management of CAP are not recommended for use in Argentina. Studies from other countries were considered together with unpublished local data to define the potential etiologic microorganisms and their antimicrobial susceptibility. Recommended diagnostic tests, groups of patients for different therapies and hospitalization criteria were defined. Severe CAP requiring intensive care was distinguished from the rest because of its distinct spectrum of etiologic agents and its high mortality, requiring a more focused therapy. Age, coexisting conditions and severity of illness were taken into account in the election of therapy.

Argentina↗
PubMed1996

Clostridium difficile infection as a cause of severe sepsis.

Although colitis is often seen in critically all patients who have received multiple broad-spectrum antibiotics, there are no reports describing severe sepsis as a result of Clostridium difficile infection. We describe three cases of severe sepsis with local intestinal Clostridium difficile infection as the only identifiable etiology. The mechanism of severe sepsis may be a derangement of the gastrointestinal barrier function. This could result in absorption of microbes or endotoxin or activation of inflammatory cascades in the submucosa of the intestine or liver.

Adult↗
PubMed1996

Evaluation of outcome for intubated patients with pneumonia due to Pseudomonas aeruginosa.

Thirty consecutively intubated patients with pneumonia due to Pseudomonas aeruginosa (cases) were prospectively observed to establish the attributable mortality rate and the prognostic value of APACHE (Acute Physiological and Chronic Health Evaluation) II scores. Four cases did not receive accurate empirical therapy and were excluded from the study. APACHE II scores were calculated within 24 hours of admission (T0), at the time of the diagnosis of pneumonia (T1), and after 72 hours of therapy (T2). The outcomes for these cases (n = 26) were compared with those for matched controls (n = 52) without pneumonia. Six cases died of causes directly related to pneumonia (group D). Two cases whose conditions clinically improved died of cardiac complications, and 18 cases had clinical resolution (group R); however, only 15 of these cases were alive at discharge. The mean APACHE II score at admission was similar (P > .20) for group R, group D, and controls. In contrast, the mean score at T1 (15.40 +/- 6.07 vs. 20.83 +/- 4.66; P < .05) and the mean score at T2 (10.40 +/- 3.57 vs. 25.50 +/- 3.93; P < .01) differed significantly for groups R and D, respectively. The overall observed and predicted mortality rates among cases and controls were 42.3% and 28.1% and 28.8% and 28.7%, respectively, while the attributable mortality rate among cases was estimated to be 13.5% (95% confidence interval, 1.95%-25.04%). We conclude that the attributable mortality rate among intubated patients with pneumonia due to P. aeruginosa is high. The APACHE II score at admission is not useful as a prognostic factor, while progression of organ dysfunction after the onset of pneumonia is an ominous sign.

Adult↗
PubMed1996

New etiopathogenic concepts of ventilator-associated pneumonia.

Ventilator-associated pneumonia develops as a consequence of impaired host defenses and exposure to large numbers of potential pathogens. Both of these processes interact and allow colonization of the airways with enteric gram-negative bacteria to occur through the molecular mechanism of bacterial adherence. Bacterial adherence is a cell-cell interaction mediated by the following variables: (1) host receptors, (2) bacterial adhesins, and (3) the proper microenvironment on the respiratory mucosa. For gram-negative bacteria, an important adhesin may be the pili that project from the cell surface, and important epithelial receptors for adhesins may be glycoproteins contained in respiratory mucus. The proper microenvironment for adherence to take place is a mixture of exposed cell receptors, prolonged bacterial-epithelial cell contact, impaired airway defenses, presence of proteases, and an optimal pH. In some way, all of the risk factors discussed impact either directly or indirectly with this basic molecular process. Once adherence is accomplished, potential pathogens may begin to colonize the respiratory tract. Once colonization occurs, bacteria may proliferate on the respiratory mucosa. At this point, the general status of host defenses determines whether colonization progresses to overt parenchymal lung infection.

Cross Infection↗
PubMed1996

Guidelines for the management of respiratory infection: why do we need them, how should they be developed, and can they be useful?

The management of respiratory infections is a complex and dynamic process, with many areas of controversy and numerous unresolved questions. In an apparent effort to deal with these issues, guidelines for care are being developed for a variety of infections including bronchitis, community-acquired pneumonia, hospital-acquired pneumonia, tuberculosis, HIV infection, and viral illness in immune-compromised patients. As the era of managed care approaches, guidelines will continue to emerge, and several questions about their utility must be answered. In this discussion, the rationale for the popularity of guidelines is examined, along with a review of the processes by which they are developed. Although evidence-based medicine has been suggested as a basis for this process, there are several problems with this approach. Most importantly, evidence-based medicine does not adequately allow for the incorporation of local experience, which is so vital in the management of respiratory infection because of the variability in bacteriology and antimicrobial susceptibilities in different practice settings. If a guideline is developed by a consensus of experts, and viewed as an hypothesis that can be modified based on local data collection, then it can be very useful and can lead to a number of potential benefits for patients with respiratory tract infection.

AIDS-Related Opportunistic Infections↗
PubMed1995

Cytokines affect pseudomonas binding to tracheal cells via a neutrophil-mediated process.

Critical illness is often associated with gram-negative bacterial colonization of the airways, increasing the risk of nosocomial pneumonia. Cytokines, released in response to endotoxin, might contribute to this phenomenon by causing changes in epithelial cell binding of bacteria. To investigate this possibility, human monocytes and hamster pulmonary macrophages were cultured without or with Escherichia coli endotoxin (10 micrograms/ml) for 4 and 24 h. Hamster and human tracheal epithelial cells were treated with supernates from monocyte cultures for 24 h, and subsequent binding of 14C-labeled Pseudomonas aeruginosa to the epithelial cells was measured (percent adherence). In separate experiments, recombinant human (rh) tumor necrosis factor-alpha (TNF-alpha) (25 to 100 ng/ml) and interleukin-1 beta (IL-1 beta) (2,000 to 8,000 pg/ml) were added to hamster monolayers. Neither monocyte supernates nor purified cytokines were toxic to the epithelial cells for up to 48 h. There was no significant change in P. aeruginosa adherence to either hamster or human tracheal epithelial cells after 24 h of exposure to culture supernates from either endotoxin-stimulated human monocytes or hamster macrophages. Similarly, purified rhTNF and rhIL-1 exposure did not increase bacterial adherence. However, when polymorphonuclear leukocytes were coincubated with the monocyte supernates and epithelial cells, P. aeruginosa adherence was significantly increased. Moreover, this effect was enhanced by an epithelial cell-derived substance. Thus, while inflammatory cytokines may participate in enhancing bacterial colonization of the lung in vivo, they do not do so by a direct action on tracheal epithelial cells but can act via a neutrophil-dependent mechanism.

Animals↗
PubMed1995

New approaches to prevention and treatment of nosocomial pneumonia.

The critical care environment contributes to the development of respiratory infections. The mortality rate of nosocomial pneumonia is as high as 50% to 70%, and approximately half of the deaths are directly attributable to the presence of lung infection. Altered host defenses, emergence of bacterial resistance, and technological advances that result in various therapeutic interventions contribute to pneumonia and its associated mortality in the critically ill population. Nasogastric intubation, elevated gastric pH, large gastric volumes, and endotracheal intubation may all promote exposure of the lungs to large numbers of bacteria. An understanding of the pathogenesis of this serious illness could allow us to devise methods for curbing the incidence and severity of the disease. The clinical setting in which pneumonia develops can be a guide to the organisms responsible, and an understanding of this relationship is helpful in developing a treatment plan. The diagnosis of nosocomial pneumonia is not always accurate, and empiric therapy with appropriately selected antibiotics can be potentially life-saving.

Anti-Bacterial Agents↗
PubMed1995

Prevention of ventilator-associated pneumonia. An attainable goal?

Nosocomial pneumonia is a common and serious problem among hospitalized patients, particularly those treated with mechanical ventilation. This article discusses infection control, the role of respiratory therapy equipment and endotracheal tubes, mobilization of tracheobronchial secretions, the role of the gastrointestinal tract, nutritional support and the role of the stomach, prophylactic antibiotics, and immunomodulation. Although there are no proven modalities for immunoprophylaxis of nosocomial pneumonia, it is possible that early administration of a single agent or combination of immune modulators may prove effective in reducing the mortality associated with nosocomial pneumonia.

Adjuvants, Immunologic↗
PubMed1995

Respiratory infections in the 1990s.

Respiratory infections occur in a variety of settings, affecting patients who live in the community, those who are hospitalized, as well as residents of chronic care facilities. Management of pneumonia and bronchitis is continually changing as the nature of the infecting pathogens, the susceptibility of microbes to antibiotics, and the nature of the host at risk for infection are evolving. Advances in the understanding of disease pathogenesis have led to new approaches for therapy and prevention, using a variety of techniques ranging from immunization to the manipulation of cytokines. One inevitable consequence of this ever-changing field is that our incomplete foundation of knowledge leads to disagreements among experts about the most efficient approach to disease management. In this review, a number of these controversies are examined, with a particular emphasis on the diagnostic approach to pneumonia arising in both the community and the hospital. In addition, a number of pathogenetic and epidemiologic principles are examined, which may have bearing on the prevention of pneumonia in the elderly and the mechanically ventilated patient.

Adult↗