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Hospital-acquired pneumonia (HAP) develops at least 48 h after hospital admission. The most common pathogens are gram-negative bacilli and Staphylococcus aureus; antibiotic-resistant organisms are an important concern. Symptoms and signs include malaise, fever, chills, rigor, cough, dyspnea, and chest paina, but in ventilated patients, pneumonia usually manifests as worsening oxygenation and increased tracheal secretions. Diagnosis is suspected on the basis of clinical presentation and chest x-ray and is confirmed by blood culture or bronchoscopic sampling of the lower respiratory tract. Treatment is with antibiotics. Overall prognosis is poor, due in part to comorbidities.
HAP includes ventilator-associated pneumonia (VAP), postoperative pneumonia, and pneumonia that develops in unventilated hospitalized inpatients.
The most common cause is microaspiration of bacteria that colonize the oropharynx and upper airways in seriously ill patients. Seeding of the lung due to bacteremia or inhalation of contaminated aerosols (ie, airborne particles containing Legionella sp, Aspergillus sp, or influenza virus) are less common causes (see Overview of Pneumonia).
Endotracheal intubation with mechanical ventilation poses the greatest overall risk; VAP constitutes > 85% of all cases, with pneumonia occurring in 9 to 27% of ventilated patients. The highest risk of VAP occurs during the first 10 days of intubation. Endotracheal intubation breaches airway defenses, impairs cough and mucociliary clearance, and facilitates microaspiration of bacteria-laden secretions that pool above the inflated endotracheal tube cuff. In addition, bacteria form a biofilm on and within the endotracheal tube that protects them from antibiotics and host defenses.
In nonintubated patients, risk factors include previous antibiotic treatment, high gastric pH (due to stress ulcer prophylaxis or therapy with H2 blockers or proton pump inhibitors), and coexisting cardiac, pulmonary, hepatic, or renal insufficiency. Major risk factors for postoperative pneumonia are age > 70, abdominal or thoracic surgery, and functional debilitation.
Pathogens and antibiotic resistance patterns vary significantly among institutions and can vary within institutions over short periods (eg, month to month). In general, the most important pathogens are Pseudomonas aeruginosa, methicillin-sensitive Staphylococcus aureus, and methicillin-resistant S. aureus (MRSA).
Other important pathogens include enteric gram-negative bacteria (mainly Enterobactersp, Klebsiella pneumoniae, Escherichia coli, Serratia marcescens, Proteus sp, and Acinetobacter sp).
Methicillin-sensitive S. aureus, Streptococcus pneumoniae, and Haemophilus influenzae are most commonly implicated when pneumonia develops within 4 to 7 days of hospitalization, whereas P. aeruginosa, MRSA, and enteric gram-negative organisms become more common with increasing duration of intubation or hospitalization.
Prior antibiotic treatment (within the previous 90 days) greatly increases the likelihood of polymicrobial infection and antibiotic-resistant organisms, particularly MRSA and Pseudomonas infection. Infection with a resistant organism markedly worsens mortality and morbidity. Other risk factors for polymicrobial infection and antibiotic-resistant organisms include
Current hospitalization of ≥ 5 days
High incidence of antibiotic resistance in the community, hospital, or specific hospital unit
Hospitalization for ≥ 2 days within the previous 90 days
Residence in a nursing home or extended care facility
Home infusion therapy (including antibiotics)
Home wound care
Family member with infection due to an antibiotic-resistant pathogen
Immunosuppressive disease or therapy
However, using these factors may overestimate the risk of polymicrobial and antibiotic-resistant organisms and thus drive overuse of broad-spectrum antibiotics.
High-dose corticosteroids increase the risk of Legionellaand Pseudomonasinfections.
Symptoms and signs in nonintubated patients are generally the same as those for community-acquired pneumonia (see Community-Acquired Pneumonia : Symptoms and Signs) and include malaise, fever, chills, rigor, cough, dyspnea, and chest pain. Pneumonia in critically ill, mechanically ventilated patients more typically causes fever and increased respiratory rate or heart rate or changes in respiratory parameters, such as an increase in purulent secretions or worsening hypoxemia.
Diagnosis is imperfect. In practice, HAP is often suspected on the basis of the appearance of a new infiltrate on a chest x-ray that is taken for evaluation of new symptoms or signs (eg, fever, increased secretions, worsening hypoxemia) or of leukocytosis. However, no symptom, sign, or x-ray finding is sensitive or specific for the diagnosis, because all can be caused by atelectasis, pulmonary embolism, or pulmonary edema and may be part of the clinical findings in acute respiratory distress syndrome. Alternative diagnoses should be sought, particularly in patients who have a pneumonia risk score < 6 (see Table: Hospital-Acquired Pneumonia Risk Index).
Hospital-Acquired Pneumonia Risk Index
Gram stain and culture of endotracheal aspirates are of uncertain benefit because specimens are likely to be contaminated with bacteria that are colonizers as well as pathogens, and a positive culture may or may not indicate infection. Bronchoscopic sampling of lower airway secretions for quantitative culture yields more reliable specimens that can differentiate colonization from infection. Information gained from bronchoscopic sampling reduces antibiotic use and assists in switching from broader to narrower antibiotic coverage. However, it has not been shown to improve outcomes.
Measurement of inflammatory mediators in bronchoalveolar lavage fluid has not been shown to be reliable. An increase in serial serum procalcitonin levels can identify patients with impending deterioration. The only finding that reliably identifies both pneumonia and the responsible organism is a pleural fluid culture (obtained via thoracentesis in a patient with pleural effusion) that is positive for a respiratory pathogen. Blood cultures are relatively specific if a respiratory pathogen is identified but are insensitive.
The mortality associated with HAP ranges from 25 to 50% despite the availability of effective antibiotics. However, not all mortality is attributable to the pneumonia itself; many of the deaths are related to the patient's other underlying illness. Adequacy of initial antimicrobial therapy clearly improves prognosis. Infection with antibiotic-resistant gram-negative or gram-positive bacteria worsens prognosis.
If HAP is suspected, treatment is with antibiotics that are chosen empirically based on
Early-onset pneumonia occurs within the first 4 days of hospitalization. Late-onset pneumonia occurs after ≥ 5 days of hospitalization.
Recommendations for patients with early-onset HAP without risk factors for antibiotic-resistant organisms include any one of the following:
Doses depend on renal function (see Table: Usual Doses of Commonly Prescribed Antibiotics).
Recommendations for patients with late-onset disease or with risk factors for antibiotic-resistant organisms include triple therapy using 2 drugs with activity against pseudomonas and 1 drug with activity against MRSA:
An antipseudomonal cephalosporin (cefepime or ceftazidime) or an antipseudomonal carbapenem (imipenem, meropenem) or a β-lactam/β-lactamase inhibitor (piperacillin/tazobactam)
An antipseudomonal fluoroquinolone (ciprofloxacin or levofloxacin) or an aminoglycoside (amikacin, gentamicin, or tobramycin)
Linezolid or vancomycin
While indiscriminate use of antibiotics is a major contributor to development of antimicrobial resistance, adequacy of initial empiric antibiotics is a major determinant of a favorable outcome. Therefore, treatment must begin with initial use of broad-spectrum drugs, which are then changed to the narrowest regimen possible based on clinical response and the results of cultures and antibiotic susceptibility testing. Alternative strategies for limiting resistance that have been tried but have not been proven efficacious include stopping antibiotics after 72 h in patients whose pulmonary infection scores (see Table: Hospital-Acquired Pneumonia Risk Index) improve to < 6 and regularly rotating empirically chosen antibiotics (eg, q 3 to 6 mo).
Among cases of HAP, the most effective preventative measures are those that focus on VAP. Semiupright or upright positioning reduces risk of aspiration and pneumonia compared with recumbent positioning and is the simplest and most effective preventive method. Noninvasive ventilation using continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) prevents the breach in airway defense that occurs with endotracheal intubation and eliminates the need for intubation in some patients.
Continuous aspiration of subglottic secretions using a specially designed endotracheal tube attached to a suction device seems to reduce the risk of aspiration.
Selective decontamination of the oropharynx (using topical gentamicin, colistin, chlorhexidine, vancomycin cream, or a combination) or of the entire GI tract (using polymyxin, an aminoglycoside or quinolone, and either nystatin or amphotericin B) is controversial because of concerns about resistant strains and because decontamination, although it decreases incidence of VAP, has not been shown to decrease mortality.
Surveillance cultures and routinely changing ventilator circuits or endotracheal tubes have not been shown to decrease VAP.
Incentive spirometry is recommended to help prevent postoperative pneumonia.
Hospital-acquired pneumonia (HAP) includes ventilator-associated pneumonia, postoperative pneumonia, and pneumonia that develops in unventilated patients who have been hospitalized for at least 48 h.
Mechanical ventilation is the most important risk factor for HAP.
Likely pathogens differ from those causing community-acquired pneumonia and require initial empiric antibiotic therapy that is active against antibiotic-resistant organisms.
Diagnosis is difficult, with culture of a potential pathogen from pleural fluid or blood being the most specific finding.
Reassess patients several days after intiation of treatment, and change antibiotics based on available culture and clinical data.
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