Pneumonia in the critically ill hospitalized patient: part 7
Dr. Craven: When a patient is mechanically ventilated, the lower respiratory tract may become colonized more readily with bacteria. In the 1960s, the Dallas group reported that ventilators with contaminated mainstream nebulizers could generate bacterial aerosols that infiltrated the terminal bronchioles and alveoli, resulting in a necrotizing Gram-negative pneumonia. Most ventilators now heat and humidify the inspiratory phase gas with humidifiers that do not generate significant bacterial aerosols.
While ventilators rarely infect patients, secretions from patients are a common source of bacterial contamination of the mechanical ventilator tubing and condensate present in the tubing. If the condensate is inadvertently flushed back into the patient, pneumonia can result, because the patient receives a large inoculum of bacteria in a volume of fluid which can be inoculated directly into the lungs, thereby overwhelming host defenses. Several devices have been advocated to remove condensate from the circuit. One of these devices, the heat moisture exchanger, eliminates the condensate problem, but may not provide optimal humidity to the patient.
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In-line medication nebulizers are a potential source of bacterial aerosols that may penetrate to the terminal bronchioles and avoid host defenses. These devices may become contaminated by reflux of condensate from the tubing. Humidifying cascades appear to be ain unlikely risk factor for pneumonia and ventilator circuit colonization. Humidifying cascades should be filled with sterile water and because of the high temperature in the cascade, bacterial growth of the most nosocomial pathogens is limited. Dr. Niederman: Please explain how gastric colonization may serve as a risk factor for pneumonia and discuss how we could approach intestinal bleeding prophylaxis so as to minimize pneumonia risk. Dr. Craven: First, let me briefly discuss the subject of stress ulcer prophylaxis. In contrast to the 1970s, when stress bleeding was a serious complication for intensive care patients, the incidence in the 1980s appears to be less frequent, perhaps because of improvements in mechanical ventilation, nutritional support, and early treatment of shock. For this reason, it is critical to carefully assess the needs of each specific patient and the risk-benefit ratio of any prophylactic agent.
Many critically ill patients receive prophylaxis against stress bleeding with antacids which may neutralize gastric acid or H2-blockers that block gastric acid secretion. Antacids and/or H2-blockers such as cimetidine and ranitidine have been used for prophylaxis against stress bleeding in critically ill patients with variable effectiveness. The efficacy depends on the criteria used to assess stress bleeding, the doses administered, and the patient population studied. Antacids have been most effective in studies where they were administered every 2 hours to maintain gastric pH above 3.5. H2-blockers have been most effective in earlier studies of stress bleeding prophylaxis, and for critical care patients who have a moderate risk of bleeding. When macroscopic bleeding is used as the criterion for efficacy and when combining results of all studies, antacids and H2- blockers appear to have similar efficacy and appear more effective than placebo.
Prophylaxis against stress bleeding can also be achieved with sucrose octasulfate which acts by a different mechanism. In contrast to the potential effects of antacids and H2-blockers on gastric pH, sucrose octasulfate (sucralfate) activity is independent of hydrogen diffusion or neutralization. In addition, sucralfate has little buffering capacity and appears to act by adhesion to the mucosa, altering gastric mucus, increasing PGE2 in the gastric lumen, and by absorbing pepsin. In studies reported to date, sucralfate appears to provide protection against stress bleeding that is similar to antacids and H2-blockers. Although suspensions of sucralfate are only available in Europe, a useable preparation for critically ill patients can be made by putting the tablet in solution, making a suspension, and then flushing it down the nasogastric tube. It is very important that the sucralfate tablet not be crushed before adding the saline solution or sterile water, and that the nasogastric tube be flushed after the sucralfate is given, to avoid clogging the tube. viagra plus
Let me now briefly discuss the role of nasogastric tubes and gastric colonization in the pathogenesis of oropharyngeal colonization and pneumonia. Gastric colonization may be an important prerequisite for retrograde colonization of the oropharynx and the development of nosocomial pneumonia. The bactericidal activity of hydrochloric acid (pH-1) and gastric secretions was first demonstrated in 1939 by Garrod. Normally, the stomach maintains near-sterility by its acid pH. Changes in the gastric flora may occur in patients with increased age, malnutrition, achlor- hydria, or other gastrointestinal diseases.