HEALTH CARE–ASSOCIATED PNEUMONIA
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Potential etiologic agents include MDR and non-MDR pathogens; the prominence of the various pathogens depends on the length of hospital stay at the time of infection (See Also Chap. 78).
Epidemiology, Pathogenesis, and Clinical Manifestations
Prevalence estimates of VAP are 6–52 cases per 100 pts, with the highest hazard ratio in the first 5 days of mechanical ventilation.
- Three factors important in the pathogenesis of VAP are colonization of the oropharynx with pathogenic microorganisms, aspiration of these organisms to the lower respiratory tract, and compromise of normal host defense mechanisms.
- Clinical manifestations are similar to those in other forms of pneumonia.
Application of clinical criteria consistently results in overdiagnosis of VAP. Use of quantitative cultures to discriminate between colonization and true infection by determining bacterial burden may be helpful; the more distal in the respiratory tree the diagnostic sampling, the more specific the results.
- See Table 132-2 for recommended options for empirical therapy for HCAP.
- Higher mortality rates are associated with inappropriate initial empirical treatment.
- Broad-spectrum treatment should be modified when a pathogen is identified.
- Clinical improvement, if it occurs, is usually evident within 48–72 h of the initiation of antimicrobial treatment.
- Treatment failure in VAP is not uncommon, especially when MDR pathogens are involved; MRSA and P. aeruginosa are associated with high failure rates.
- VAP complications include prolongation of mechanical ventilation, increased length of ICU stay, and necrotizing pneumonia with pulmonary hemorrhage or bronchiectasis. VAP is associated with significant mortality risk.
- Strategies effective for the prevention of VAP are listed in Table 132-3.
|Patients without Risk Factors for MDR Pathogens|
Ceftriaxone (2 g IV q24h) or cefotaxime (2 g IV q6–8 h) or
Moxifloxacin (400 mg IV q24h), ciprofloxacin (400 mg IV q8h), or levofloxacin (750 mg IV q24h) or
Ampicillin/sulbactam (3 g IV q6h) or
Ertapenem (1 g IV q24h)
|Patients with Risk Factors for MDR Pathogens|
|Pathogenic Mechanism||Prevention Strategy|
|Oropharyngeal colonization with pathogenic bacteria|
|Elimination of normal flora||Avoidance of prolonged antibiotic courses|
|Large-volume oropharyngeal aspiration around time of intubation||Short course of prophylactic antibiotics for comatose ptsa|
|Gastroesophageal reflux||Postpyloric enteral feedingb; avoidance of high gastric residuals, prokinetic agents|
|Bacterial overgrowth of stomach||Avoidance of prophylactic agents that raise gastric pHb; selective decontamination of digestive tract with nonabsorbable antibioticsb|
|Cross-infection from other colonized pts||Hand washing, especially with alcohol-based hand rub; intensive infection control educationa; isolation; proper cleaning of reusable equipment|
|Large-volume aspiration||Endotracheal intubation; rapid-sequence intubation technique; avoidance of sedation; decompression of small-bowel obstruction|
|Microaspiration around endotracheal tube|
|Endotracheal intubation||Noninvasive ventilationa|
|Prolonged duration of ventilation||Daily awakening from sedation,a weaning protocolsa|
|Abnormal swallowing function||Early percutaneous tracheostomya|
|Secretions pooled above endotracheal tube||Head of bed elevateda; continuous aspiration of subglottic secretions with specialized endotracheal tubea; avoidance of reintubation; minimization of sedation and pt transport|
|Altered lower respiratory host defenses||Tight glycemic controlb; lowering of hemoglobin transfusion threshold|