Hospital-Acquired Pneumonia

The most common cause of hospital-acquired pneumonia 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 species, Aspergillus species, or influenza virus) are less common causes.

Symptoms and signs of hospital-acquired pneumonia in nonintubated patients are generally the same as those for community-acquired pneumonia Symptoms and Signs Community-acquired pneumonia is defined as pneumonia that is acquired outside the hospital. The most commonly identified pathogens are Streptococcus pneumoniae, Haemophilus influenzae... read more and include malaise, fever, chills, rigor, cough, dyspnea, and chest pain.

Usually, a diagnosis is made based upon a new lung infiltrate combined with clinical features of infection, which include the new onset of fever, purulent sputum, leukocytosis, and decline in oxygenation. However, clinical diagnosis is imperfect. No symptom, sign, or x-ray finding is sensitive or specific for the diagnosis of hospital-acquired pneumonia, because all can be caused by atelectasis Atelectasis Atelectasis is collapse of lung tissue with loss of volume. Patients may have dyspnea or respiratory failure if atelectasis is extensive. They may also develop pneumonia. Atelectasis is usually... read more , pulmonary embolism Pulmonary Embolism (PE) Pulmonary embolism (PE) is the occlusion of pulmonary arteries by thrombi that originate elsewhere, typically in the large veins of the legs or pelvis. Risk factors for pulmonary embolism are... read more , or pulmonary edema Pulmonary Edema Pulmonary edema is acute, severe left ventricular failure with pulmonary venous hypertension and alveolar flooding. Findings are severe dyspnea, diaphoresis, wheezing, and sometimes blood-tinged... read more .

Gram stain and semiquantitative cultures of sputum samples, though not definitive for identifying infection, should be done because they can direct empiric therapy. 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 or serum has not been shown to be reliable in deciding on initiation of antibiotics. 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. Molecular tests that identify the pathogen and resistance patterns in respiratory secretions are emerging and could be useful in guiding treatment.

The mortality associated with hospital-acquired pneumonia is high 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 hospital-acquired pneumonia is suspected, treatment is with antibiotics that are chosen empirically based on

In the 2007 guidelines, the Infectious Diseases Society of America and the American Thoracic Society used very broad criteria for defining the population at risk of infection with antibiotic-resistant pathogens, which resulted in the majority of patients with HAP requiring broad-spectrum antibiotic therapy for MRSA and resistant Pseudomonas. The current, 2016 recommendations (1 Treatment reference Hospital-acquired pneumonia (HAP) develops at least 48 hours after hospital admission. The most common pathogens are gram-negative bacilli and Staphylococcus aureus; antibiotic-resistant... read more ) emphasize use of a narrower spectrum of empiric antibiotics when possible. Empiric therapy for hospital-acquired pneumonia without increased risk for antibiotic-resistant bacteria due to prior IV antibiotic use within 90 days in an institution where MRSA incidence is < 20% (of S. aureus isolates) and P. aeruginosa resistance is < 10% for commonly used empiric antipseudomonal antibiotics, could include any one of the following:

Doses depend on renal function (see table Usual Doses of Commonly Prescribed Antibiotics Usual Dosages of Commonly Prescribed Antibiotics[a] ).

In treatment settings where MRSA rates are > 20%, vancomycin or linezolid should be added. In patients who have risk factors for antibiotic-resistant organisms, or in the absence of reliable local antibiograms, recommendations include triple therapy using 2 drugs with activity against Pseudomonas and 1 drug with activity against MRSA:

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.

Incentive spirometry is recommended to help prevent postoperative pneumonia.