Hospital-Acquired Pneumonia

Kim M. Kerr

Hospital-acquired pneumonia (HAP) is defined as pneumonia occurring 48 hours or more after hospital admission. The definition excludes pulmonary infection that may be incubating at the time of admission. Pneumonia is the second most common hospital-acquired infection, and is associated with the highest mortality rate of all nosocomial diseases. Between 5 and 10 cases of HAP occur per 1,000 hospital admissions, but the incidence is 6 to 20 times higher in mechanically ventilated patients. In this group, the development of pneumonia (ventilator-associated pneumonia [VAP]) is associated with significant morbidity and higher mortality and substantially increases the cost of patient care.

In the immunocompetent host, HAP can be divided into early onset and late-onset infections. Early pneumonia occurs during the first 4 days of hospitalization and is often caused by community-acquired pathogens such as Streptococcus pneumoniae, methicillin-sensitive Staphylococcus aureus, and Haemophilus influenzae. Specific risk factors can alter the likely pathogens. For instance, if a patient has a witnessed aspiration, anaerobes, enteric Gram-negative bacilli, S. aureus should be considered. Recent thoraco-abdominal surgery and the presence of an obstructing foreign body are both additional risk factors for anaerobic pneumonias. Patients with coma, head injury, recent influenza, recent intravenous drug use, diabetes mellitus, or chronic renal failure are at increased risk for S. aureus pneumonias. Corticosteroids predispose patients to pneumonias from fungi, Pseudomonas aeruginosa, and, in some regions of the country, Legionella species.

Late-onset HAP, occurring 4 days or more after admission, is more commonly caused by, S. aureus, P. aeruginosa, or Acinetobacter or Enterobacter species. Resistant organisms such as methicillin-resistant S. aureus (MRSA), P. aeruginosa, and Acinetobacter baumannii tend to emerge after prolonged mechanical ventilation (>7 days), prior antibiotic use, and the use of broad-spectrum antibiotics (third-generation cephalosporins, fluoroquinolones, or carbapenems).

Understanding the pathogenesis of HAP may help in developing mechanisms of prevention. In the normal nonsmoking host, the upper respiratory tract is colonized with aerobic and anaerobic bacteria, whereas the respiratory tract below the vocal cords is sterile. Changes in host defenses can lead to inoculation of the lower respiratory tract with potentially pathogenic bacteria. Colonization and potentially fatal infection can follow inoculation.

Although pathogens can gain access to the lung by inhalation, hematogenous seeding, and contiguous spread, aspiration is the major route of bacterial access in patients with and without endotracheal tubes. Organisms such as P. aeruginosa can be inoculated directly into the endotracheal tube of intubated patients, whereas Enterobacteriaceae usually colonize the oropharynx before the trachea. Studies of oral care in the intensive care unit (ICU) show that chlorhexidine significantly decreases the risk of VAP. Subgroup analysis suggests that favorable effects were most pronounced in patients who were treated with 2% chlorhexidine and in cardiosurgical patients.

Mechanical ventilation almost always requires the presence of an artificial airway (endotracheal tube or tracheostomy tube). However, the presence of such an airway reduces the effectiveness of the cough reflex, compromises mucociliary clearance, can cause direct injury to the tracheal epithelial surface, and provides a direct pathway for pathogens from the ICU environment to the lower respiratory tract. A biofilm of bacteria-laden accretions on the luminal surface of the endotracheal tube also can contribute to the development of VAP if accretions dislodge into distal airways. Novel solutions to the biofilm problem include the development of less-adhesive polymers to prevent accumulation of infected material in the lumen of the tube or coating the tube with antimicrobial agents. Aspiration around the cuff of the endotracheal tube is another mechanism by which bacteria can access the lower respiratory tract. To reduce the amount of secretions pooling on top of the endotracheal tube cuff, a specific endotracheal tube was designed with a separate lumen that allows drainage of secretions from the subglottic space above the tube. Randomized trials have shown a reduction in the incidence of VAP with the use of this technique. Problems with the use of this device are the additional cost and the need to have these endotracheal tubes available when patients undergo endotracheal intubation in a variety of settings (e.g., emergency rooms, operating rooms, ICUs, and hospital wards).

Noninvasive ventilation has been shown to reduce the need for endotracheal intubation and decrease the likelihood of pnenumonia. It should be considered in appropriate patients. The risk of developing VAP is approximately 3% per day for the first 5 days of intubation, 2% per day from days 6 to 10, and 1% per day after that. Some studies suggest that a daily routine of interruption of continuous sedation and assessment of readiness to wean may shorten the duration of mechanical ventilation. Theoretically, shortening the duration of intubation should reduce the incidence of VAP, but these protocols have yet to demonstrate a reduction in VAP.

Nasogastric feeding tubes have been implicated as a risk factor for pneumonia, presumably because of an associated increased incidence of gastroesophageal reflux and aspiration. The supine head position also is a risk factor for the development of VAP, since it has been linked to an increased incidence of aspiration and bacterial colonization of the lower airways in ventilated patients. Clinical data suggest that the simple maneuver of elevating the head of the bed, especially for patients with feeding tubes, may be a safe and inexpensive means of lowering the incidence of VAP.

The role of gastric colonization in facilitating VAP is controversial and has generated multiple clinical trials yielding conflicting data. Central to the controversy is the relationship between VAP, gastric colonization, and stress ulcer prophylaxis. The acidic environment of the gastric lumen prevents bacterial growth under normal physiologic circumstances. However, gastric acidity can be reduced by critical illness, advanced age, and administration of antacids or H₂ antagonists. The cytoprotective agent, sucralfate, may prevent stress ulcers without altering gastric acidity. There have been multiple analyses of more than 20 randomized, controlled clinical trials trying to settle the issue of the effect of stress ulcer prophylaxis on the development of VAP with mixed results: sucralfate decreased gastric colonization and VAP versus H₂ antagonists in some but not all studies. Given its relatively low cost and safe pharmacologic profile, sucralfate is an appealing way of providing stress-related upper gastrointestinal (GI) bleeding prophylaxis. However, sucralfate is not as effective as H₂ antagonists in preventing upper GI bleeding and one must weigh the benefit of the potential decreased risk of VAP against the potential decreased protection against GI bleeding. Whether proton pump inhibitors are more effective than H₂ antagonists in preventing significant upper GI bleeding associated with stress ulcers remains unclear. Limited data suggests the incidence of VAP is similar in those patients who receive H₂ antagonists or proton pump inhibitors for stress ulcer prophylaxis. In summary, the optimal agent that minimizes the risk of both stress ulcers and VAP has yet to be determined.

Although the role of gastric colonization in VAP is uncertain, the evidence is convincing that colonization of the oropharynx often precedes colonization of the trachea and subsequent development of VAP. Selective decontamination of the digestive tract is a strategy designed to prevent oropharyngeal and gastric colonization with aerobic Gram-negative bacilli and Candida species without altering the anaerobic flora of the gut. Some proposed regimens use a combination of nonabsorbable antibiotics applied as a paste to the oropharynx or given through the nasogastric tube, whereas others also include a short course of a systemic antibiotic. Some clinical trials have demonstrated a decrease in the rates of lower respiratory tract infections with selective decontamination of the digestive tract; others, however, have found no difference in the incidence of VAP. Because of concerns about the emergence of antibiotic-resistant organisms with these regimens, the routine use of selective decontamination of the digestive tract to prevent VAP is not recommended at present.

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