Hospital-Acquired Pneumonia


Abstract

Hospital-acquired pneumonia (HAP) is a new infection of the lung parenchyma that develops more than 48 hours after hospital admission. Epidemiologic data suggest that HAP occurs in up to 1.6% of patients, prolongs hospital stay by 2 to 3 days, and represents the most common hospital-acquired infection leading to death in critically ill patients. The morbidity and mortality attributed to HAP are significantly increased if the infection is caused by multidrug-resistant pathogens. The subset of HAP occurring more than 48 hours after initiation of mechanical ventilation is termed ventilator-associated pneumonia (VAP). The concept of a healthcare-associated pneumonia (HCAP), referring to a pneumonia diagnosed outside of the acute care setting, was purposefully removed from the 2016 Infectious Disease Society of American (IDSA)/American Thoracic Society (ATS) guidelines as more recent evidence suggested HCAP pathogens more closely resemble those seen in community-acquired pneumonia than those seen in HAP. Risk factors for HAP/VAP are diverse and include both patient-specific and treatment-associated elements. The diagnostic criteria for HAP/VAP require a new infiltrate on chest radiography in conjunction with typical clinical and laboratory findings of pneumonia. Although microbiologic confirmation is ideal, the optimal diagnostic strategy is debated. Recent trends in the microbial resistance rates for pathogens causing HAP/VAP have led to significant changes in the recommendations for empirical therapy, with an increased reliance on patient-specific factors and local antimicrobial resistance patterns. Limited new antibiotic development and high attributable mortality rates highlight the importance of evidence-based HAP/VAP prevention strategies.

Clinical Vignette

A 72-year-old-man with a history of chronic obstructive pulmonary disease (COPD) sought attention for progressive shortness of breath and wheezing. Two days before presentation, the patient developed subjective fevers, chills, and myalgias. The following morning, his chronic cough had significantly worsened and he was producing more phlegm than usual. By the afternoon, he developed progressive shortness of breath with wheezing that would not respond to his rescue inhalers. His wife called the paramedics, and he was brought into the emergency department.

On exam, the patient had a temperature of 38.4°C, respiratory rate of 32, blood pressure of 147/86 and an oxygen saturation of 86% on 6 L/min of supplemental oxygen. He was dyspneic and unable to speak in full sentences with notable diaphoresis. His pulmonary examination revealed use of accessory muscles with minimal air movement and diffuse expiratory wheezing. The patient was urgently intubated and transferred to the medical intensive care unit (ICU). His complete blood count (CBC) showed a white blood cell count (WBC) of 11,000/mm 3 , and his chest radiograph showed hyperexpanded lungs with no focal consolidations, pleural effusions, or pneumothorax. A respiratory viral panel revealed infection with influenza A and the patient was treated for both his viral infection and a COPD exacerbation with azithromycin, methylprednisone, bronchodilators, and oseltamivir. The patient subsequently defervesced, and his oxygen requirements became minimal.

Five days later the patient developed a new fever and had an increase in his respiratory rate and oxygen requirements. A CBC revealed an increase in his WBC, and a repeat chest radiograph showed a new right lower lobe consolidation. The patient was diagnosed with a VAP and had a tracheal aspirate sent for Gram stain and culture. He was started on empiric broad-spectrum antibiotics, and 2 days later his cultures returned positive for methicillin-resistant Staphylococcus aureus (MRSA). His antibiotics were narrowed to vancomycin monotherapy, and he was successfully extubated 2 days later.

Patients with COPD are prone to developing respiratory failure when exposed to respiratory viruses, such as influenza. This patient’s age and underlying lung disease increased his predilection to develop a VAP, which is a known complication of endotracheal intubation with mechanical ventilation. His severity of illness merited initiation of antimicrobial therapy that covered MRSA, which is a common postinfluenza superinfection.

Epidemiology and Impact

In the United States, pneumonia accounts for 22% of all hospital-acquired infections and is the leading cause of death from nosocomial infection. Although most cases of HAP arise outside the ICU, HAP rates are highest in ICU patients—particularly those who are mechanically ventilated. In this setting, approximately 10% of patients will be diagnosed with a VAP. These patients often experience a prolonged duration of endotracheal intubation, have up to 13% higher rates of mortality, and incur an estimated $40,000 in additional healthcare costs.

Pathophysiology

HAP/VAP—like any other pneumonia—results when microbes penetrate the normally sterile lower respiratory tract, overwhelm local host defenses, and establish infection. Although pathogens are most often introduced in aspirated oropharyngeal secretions, rarely they may enter the lung hematogenously in patients with bacteremia. Intubated patients develop a VAP as a direct consequence of the endotracheal tube acting as a foreign body that bypasses key barriers to infection. VAP ultimately results from varying degrees of aspiration of secretions pooled above the endotracheal tube cuff and/or direct inoculation from the biofilm that forms on the endotracheal tube surface.

Some of the risk factors that predispose patients to develop HAP/VAP are patient specific and include male sex, advanced age, chronic underlying disease (especially pulmonary disease), immunosuppression, obesity or malnutrition, altered level of consciousness, smoking, and alcohol or drug abuse. Other risk factors are treatment related, including intubation, enteral feedings, recent surgery, entry to the ICU, and recent antibiotic exposure ( Fig. 27.1 ).

Fig. 27.1, Risk factors for the development of hospital-acquired pneumonia. ICU, Intensive care unit.

Microbiology

Although causative agents include a wide variety of bacterial pathogens and may be polymicrobial, anaerobes are uncommon in HAP/VAP ( Table 27.1 ). The bacteria that most frequently cause HAP/VAP are stratified into those causing early- and late-onset disease. Early-onset HAP/VAP occurs before hospital day 5 and is often caused by community-acquired organisms such as Streptococcus pneumoniae and Haemophilus influenzae . In contrast, late-onset HAP occurs beyond hospital day 5 and is more frequently caused by hospital-acquired gram-negative bacilli and S. aureus (including methicillin-resistant strains). HAP/VAP caused by S. aureus is more common in patients with head trauma, diabetes, or admission to an ICU. Multidrug resistant pathogens are a growing concern for both community and nosocomial pneumonia, and patients at highest risk are those with higher rates of healthcare contact ( Table 27.2 ). Even though fungi are infrequently implicated as causal pathogens in immunocompetent patients, the use of antifungal therapies has also started to induce a concerning shift in echinocandin resistance among candida species. This dynamic pattern of pathogen resistance evolves over time and varies by geographic location, hospital system, and patient population, highlighting the need for regularly updated local surveillance data.

TABLE 27.1
Common Nosocomial Pneumonia Pathogens
Gram-Positive Pathogens Gram-Negative Pathogens
Staphylococcus aureus
Streptococcus pneumoniae
Enterobacter species
Escherichia coli
Klebsiella pneumoniae
Pseudomonas aeruginosa
Acinetobacter species

TABLE 27.2
Patient-Specific Risk Factors for Antimicrobial-Resistant Pneumonia
Treatment-related risk factors Gastric acid suppression
Hemodialysis
Immunosuppression
Home wound care
Hospitalization for ≥2 days within the past 90 days
Residence in a long-term care facility
Patient-specific risk factors MRSA colonization
Pseudomonas aeruginosa colonization
Prior multidrug resistant infection
Recurrent skin infections
Poor functional status
Structural lung disease (severe COPD, bronchiectasis)
Tracheostomy
Antibiotic-induced resistance Systemic antibiotics within the past 6 months
COPD, Chronic obstructive pulmonary disease; MRSA, methicillin-resistant Staphylococcus aureus .

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