 |
Hospital-acquired
pneumonia develops at least 48 h after hospitalization. The most
common pathogens are gram-negative bacilli and Staphylococcus aureus; drug-resistant
organisms are an important concern. Symptoms and signs are the same
as those for community-acquired pneumonia, but in ventilated patients, pneumonia
may also manifest 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.
Hospital-acquired pneumonia includes ventilator-associated pneumonia, postoperative pneumonia, and pneumonia that develops in unventilated but otherwise moderately or critically ill hospitalized inpatients.
Etiology
The most common cause is microaspiration of bacteria that colonize the oropharynx and upper airways in seriously ill patients.
Risk
factors:
Endotracheal intubation with mechanical ventilation poses the greatest overall risk; ventilator-associated pneumonia constitutes > 85% of all cases, with pneumonia occurring in 17 to 23% of ventilated patients. 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 (from stress ulcer prophylaxis therapy), and coexisting cardiac, pulmonary, hepatic, and renal insufficiency. Major risk factors for postoperative pneumonia are age > 70, abdominal or thoracic surgery, and dependent functional status.
Pathogens:
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 pathogen is Pseudomonas aeruginosa, which is especially common in pneumonias acquired in intensive care settings and in patients with cystic fibrosis, neutropenia, advanced AIDS, and bronchiectasis. Other important pathogens include enteric gram-negative bacteria (Enterobacter sp, Klebsiella pneumoniae
, Escherichia coli
, Serratia marcescens
, Proteus sp, Acinetobacter sp) and both methicillin-sensitive and methicillin-resistant Staphylococcus
aureus.
S.
aureus
, pneumococcus, and Haemophilus influenzae are most commonly implicated when pneumonia develops within 4 to 7 days of hospitalization, whereas enteric gram-negative organisms become more common with increasing duration of intubation.
Prior antibiotic treatment greatly increases the likelihood of polymicrobial infection; resistant organisms, particularly methicillin-resistant S. aureus; and Pseudomonas infection. Infection with a resistant organism markedly worsens mortality and morbidity.
High-dose corticosteroids increase the risk of Legionella and Pseudomonas infections.
Symptoms, Signs,
and Diagnosis:
Symptoms and signs in nonintubated patients are generally the same as those for community-acquired pneumonia (see Pneumonia: Symptoms and Signs). Pneumonia in critically ill, mechanically ventilated patients more typically causes fever and increased respiratory and/or heart rate or changes in respiratory parameters, such as an increase in purulent secretions or worsening hypoxemia. Noninfectious causes of pulmonary deterioration, such as acute respiratory distress syndrome (ARDS), pneumothorax, and pulmonary edema, must be excluded.
Diagnosis is imperfect. In practice, hospital-acquired pneumonia 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 or of leucocytosis. 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 ARDS.
Gram stain and culture of endotracheal aspirates are controversial, 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 seems to yield more reliable specimens, but the effect of this approach on outcomes is controversial. Measurement of inflammatory mediators in bronchoalveolar lavage fluid may play a future role in diagnosis; eg, a concentration of soluble triggering receptor expressed on myeloid cells (a protein expressed and shed by immune cells during infection) > 5 pg/mL may help distinguish bacterial and fungal pneumonia from noninfectious causes of clinical and radiographic changes in ventilated patients. However, this approach requires further investigation, and the only finding that reliably identifies both pneumonia and the responsible organism is a blood or pleural fluid culture that is positive for a respiratory pathogen.
Prognosis
The mortality associated with hospital-acquired pneumonia due to gram-negative infection is about 25 to 50% despite the availability of effective antibiotics. Whether death is due to underlying illness or to the pneumonia itself is uncertain. Women may be at greater risk of death. The mortality rate associated with S. aureus pneumonia is 10 to 40%, in part due to the serious conditions with which it is associated (eg, need for a ventilator, advanced age, cancer chemotherapy, chronic pulmonary disease).
Treatment
A few patients may have a pneumonia risk score (see Table 5: Pneumonia: Hospital-Acquired Pneumonia Risk Index ) low enough to suggest that alternative diagnoses should be sought. Otherwise, treatment is with antibiotics that are chosen empirically based on local sensitivity patterns, specific patient risk factors, and the conditions noted in Table 2: Pneumonia: Community-Acquired Pneumonia in Adults .
|
Table 5
|
| | |
|
Hospital-Acquired Pneumonia
Risk Index
|
|
Factor
|
Points
|
|
Temperature (°C)
|
|
|
0
|
|
|
1
|
|
|
2
|
|
Blood leukocytes, μL
|
|
|
0
|
|
|
1
|
|
|
1
|
|
Tracheal secretions
|
|
|
0
|
|
|
1
|
|
|
2
|
|
Oxygenation: Pao
2/Fio
2, mm Hg
|
|
|
0
|
|
|
2
|
|
Pulmonary radiography
|
|
|
0
|
Diffuse (or patchy) infiltrate
|
1
|
|
|
2
|
|
Progression of infiltrate*
|
|
|
0
|
Progression (heart failure and ARDS excluded)
|
2
|
|
Growth of pathogenic bacteria on tracheal aspirate culture*
|
No, rare, or light growth
|
0
|
|
|
1
|
Same bacteria as on Gram stain
|
1
|
|
Pao
2/Fio
2 = ratio of arterial O2 pressure to fraction of inspired O2; ARDS = acute respiratory distress syndrome.
|
|
*Criteria applicable 72 h after initial diagnosis.
|
|
Score > 6 suggests hospital-acquired pneumonia.
|
|
Score < 6 suggests alternative process.
|
|
Adapted from Singh N, Rogers P, Atwood CW, et al: Short-course empiric antibiotic therapy for patients with pulmonary infiltrates in the intensive care unit. American Journal of Respiratory and Critical Care Medicine 162:505–511, 2000.
|
|
Indiscriminate use of antibiotics is a major contributor to development of antimicrobial resistance. Therefore, treatment may begin with initial use of broad-spectrum drugs, which are replaced by the most specific drug available for the pathogens identified by culture. Alternative strategies for limiting resistance that has not proven effective include stopping antibiotics after 72 h in patients whose pulmonary infection scores (see Table 5: Pneumonia: Hospital-Acquired Pneumonia Risk Index) improve to < 6 and regularly rotating empirically chosen antibiotics (eg, q 3 to 6 mo).
Initial antibiotics:
Multiple regimens exist, but all should include antibiotics that cover both resistant gram-negative and gram-positive organisms. Options include a carbapenem ( imipenem-cilastatin 500 mg IV q 6 h or meropenem 1 to 2 g IV q 8 h), monobactam ( aztreonam 1 to 2 g IV q 8 h), or antipseudomonal β-lactam ( ticarcillin 3 g IV with or without clavulanic acid q 4 h, piperacillin 3 g IV with or without tazobactam q 4 to 6 h, ceftazidime 2 g IV q 8 h, or cefepime 1 to 2 g q 12 h), given alone or combined with an aminoglycoside ( gentamicin or tobramycin 1.7 mg/kg IV q 8 h or 5 to 6 mg/kg once/day or amikacin 5 mg/kg q 8 h) and/or vancomycin 1 g q 12 h. Linezolid may be used for some pulmonary infections involving methicillin-resistant S. aureus, especially in patients who cannot take vancomycin . Daptomycin should not be used for pulmonary infections.
Prevention
Noninvasive ventilation using continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP) prevents the breach in airway defense that occurs with endotracheal intubation and eliminates the need for intubation in some patients. Semi-upright or upright positioning reduces risk of aspiration and pneumonia compared with recumbent positioning.
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, and vancomycin cream) or of the entire GI tract (using polymyxin, an aminoglycoside or quinolone, and either nystatin or amphotericin) also seems to be effective, although it may increase the risk of colonization with resistant organisms.
Surveillance cultures and routinely changing ventilator circuits or endotracheal tubes have not been shown to decrease ventilator-associated pneumonia.
Last full review/revision November 2005
Content last modified November 2005
| |
