(See also Chap. 81: Infections Acquired in Health Care Facilities)
Potential etiologic agents of VAP include MDR and non-MDR pathogens; the prominence of the various pathogens depends on the length of hospital stay at the time of infection and the presence of other risk factors.
Prevalence estimates of VAP are 6–52 cases per 100 pts, with the highest hazard ratio in the first 5 days of mechanical ventilation.
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 results in less antibiotic use and lower mortality. The more distal in the respiratory tree the diagnostic sampling, the more specific the results.
NO RISK FACTORS FOR RESISTANT GRAM-NEGATIVE PATHOGEN | RISK FACTORS FOR RESISTANT GRAM-NEGATIVE PATHOGENa (CHOOSE ONE FROM EACH COLUMN) | |
---|---|---|
Piperacillin-tazobactam (4.5 g IV q6hb) Cefepime (2 g IV q8h) Levofloxacin (750 mg IV q24h) | Piperacillin-tazobactam (4.5 g IV q6hb) Cefepime (2 g IV q8h) Ceftazidime (2 g IV q8h) Imipenem (500 mg IV q6hb) Meropenem (1 g IV q8h) | Amikacin (15–20 mg/kg IV q24h) Gentamicin (5–7 mg/kg IV q24h) Tobramycin (5–7 mg/kg IV q24h) Ciprofloxacin (400 mg IV q8h) Levofloxacin (750 mg IV q24h) Colistin (loading dose of 5 mg/kg IV followed by maintenance doses of 2.5 mg × [1.5 × CrCl + 30] IV q12h) Polymyxin B (2.5–3.0 mg/kg per day IV in 2 divided doses) |
Risk factors for MRSAb (add to above) | ||
Linezolid (600 mg IV q12h) or Adjusted-dose vancomycin (trough level, 15–20 mg/dL) |
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 |
Less well studied than VAP, HAP more commonly involves non-MDR pathogens. Anaerobes may also be more commonly involved in non-VAP pts because of the increased risk of macroaspiration in pts who are not intubated.
Bronchiectasis is an irreversible airway dilation that involves the lung in either a focal (due to obstruction) or a diffuse (due to a systemic or infectious process) manner. Bronchiectasis can arise from infectious or noninfectious causes.
The most widely cited mechanism of infectious bronchiectasis is the “vicious cycle hypothesis,” in which susceptibility to infection and poor mucociliary clearance result in microbial colonization of the bronchial tree. Proposed mechanisms for noninfectious bronchiectasis include immune-mediated reactions that damage the bronchial wall and parenchymal distortion as a result of lung fibrosis (e.g., postradiation fibrosis or idiopathic pulmonary fibrosis).
Presenting pts typically have a persistent productive cough with ongoing production of thick, tenacious sputum.
The diagnosis of bronchiectasis is based on clinical presentation with consistent CXR findings, such as parallel “tram tracks,” a “signet-ring sign” (a cross-sectional area of the airway with a diameter at least 1.5 times that of the adjacent vessel), lack of bronchial tapering, bronchial wall thickening, or cysts emanating from the bronchial wall.
Treatment of infectious bronchiectasis is directed at the control of active infection and at improvements in secretion clearance and bronchial hygiene.
Lung abscess—necrosis and cavitation of the lung following microbial infection—can be categorized as primary (∼80% of cases) or secondary; alternatively, it can be categorized as acute (<4–6 weeks in duration) or chronic (∼40% of cases).
Initial presentation of lung abscess may be similar to that of pneumonia.
Chest CT is the preferred radiographic study for precise delineation of the lesion.
Treatment depends on the presumed or established etiology.