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TRAUMA-ICU NURSING EDUCATIONAL SERIES VAP: what, how, and why ? Bradley J. Phillips, M.D. Critical Care Medicine Boston Medical Center Boston University School of Medicine Nosocomial Pneumonia Leading cause of death from hospitalacquired infections, with an associated mortality rate of 30 %. VAP is a sub-type of nosocomial pneumonia specifically referring to a bacterial source Kollef. NEJM 1999 “VAP” defined as parenchymal lung infection occurring more than 48 hrs after the initiation of mechanical ventilation Morehead & Pinto. Arch Int Med 2000 VAP: a framework (1) Early-onset VAP occurs within 48 – 72 hrs after tracheal intubation often from aspiration during the intubation process usually due to antibiotic-sensitive bacteria Oxacillin-sensitive Staph aureus Haemophilus influenzae Strep pneumoniae Kollef. NEJM 1999 VAP: a framework (2) Late-onset VAP occurs after 72 hrs of mechanical ventilation multiple theories behind it’s actual development usually due to antibiotic-resistant bacteria Oxacillin-resistant Staph aureus (“MRSA”) Pseudomonas aeruginosa Acinetobacter species Enterobacter species Kollef. NEJM 1999 Why are we talking about VAP ? Single most common ICU nosocomial infection Incidence: 20 - 25% (though controversial !) Mortality Differing reports throughout the world… range 20 - 80% depends on type of ICU and organism difficult to ascertain actual incidence Varying definitions Varying populations Varying techniques & diagnostic methods Epidemiology Mechanically ventilated patients Morbidity 9 – 24 % incidence some authors report as high as 44% increased ICU length of stay (5x longer) increased total length of stay (2x longer) increased ventilator days (7x longer) Costs Additional $8,800 for VAP Papazian et al. Am J Res CCM 1996. Craven et al. Am Rev Res Dis. 1996. Kollef. JAMA 1993. Torres et al. Am Rev Res Dis 1990. Pathogenesis of VAP 2 Key Steps a. Bacterial colonization of the aerodigestive tract b. Aspiration of contaminated secretions into the lower airway Kollef, NEJM 1999 Pathophysiology Bacterial entry into the lower airway (1) Inhalation Hematogeneous (“seeding”) Contributing factors impaired gastric and intestinal motility altered LOC diminished gag reflex decreased mucociliary clearance Pathophysiology (2) the endotracheal tube creates an abnormal continuum between the upper airway and the trachea as well as establishing a subglottic reservoir of secretions rich in bacterial pathogens… those secretions, over time, become part of a biofilm that lines the ET tube – allowing distal aerosolization of particulate matter via the ventilatory cycle Morehead et al. Arch Intern Med 2000 The Airway Intubation (1) Greatest risk factor !! increased incidence 7 - 21 fold reintubation 47% compared to 10% in matched controls ICU stay and crude mortality higher Etiology Microaspiration Oral and gastric bacteria colonize subglottic area ET quickly invested with biofilm above and below cuff Intubation (2) Mechanical factors Glottis is eliminated primary barrier to aspiration lost Balloon cuff erodes tracheal epithelium Allows direct bacterial invasion Role of low-pressure cuffs…? Airway desiccation loss of mucus/antibody production in oral cavity Role of humidified circuits…? Role of the Gastric Tube Intubated patients have gastric tubes Decrease gastric distension Access for enteral feedings Provides a conduit for bacterial migration Higher rate of reflux and sinusitis (NGT vs. OGT) H-2 Blockers Gastric alkalinization Promotes bacterial overgrowth Presumably higher rates of significant aspiration Gastric pH > 4 predisposition to GNR/S. aureus Use of sulcrafate associated with lower rates of VAP ( Am J med 1987 and 1991, Ann Int Med, 1995 Infec Control Hosp Epidemiol 1994) VAP: sulcrafate 5%, antacid 10%, ranitidine 21% Benefit: lack of gastric alkalinization and lower bacterial colonization Stress Ulcer Prophylaxis and VAP Controversial Topic ! A Meta-analysis of previous studies found no significant difference Prospective randomized trials Simms et al, J Trauma, 1991 Thomason et al, J Trauma, 1996 99 trauma patients on antacids, cimetidine, or sulcralfate No difference in nosocomial pneumonia or gastric bacteria 242 intubated ICU patients on antacid, ranitidine, or sulcralfate No difference in rates of VAP or GI bleeding Markowicz et al, Am J Respir Crit Care Med, 2000 Multicenter, prospective trial Found sulcrafate significantly associated with pneumonia in ARDS ? mechanism Diagnosis: Nosocomial Pneumonia Difficult in ventilated patient Typical criteria Clinical Radiographic Laboratory Statistically, a specific combination of clinical diagnostic criteria has not been identified to reliably diagnose bacterial pneumonia What is “VAP” ? Reliability of Clinical Signs Signs Fever, pulmonary infiltrate, and purulent tracheal secretions Fagon et al, Am J Med, 1993 23 patients with tracheobronchitis clinical “pneumonia” criteria, but negative protected brushings and BAL Matched with patients unsuspected to have pneumonia Mortality rates were similar (26% vs. 27%) Lower than patients with a “proven” pneumonia ( BAL) Diagnosis: Nosocomial Pneumonia Objective tests can be unreliable After 48 hrs, endogenous flora of aerodigestive tract replaced by hospital microflora Antibiotic usage allows for selection and overgrowth of resistant organisms CXR has been notoriously inaccurate No single radiographic sign has > 68% accuracy Due to high incidence of SIRS and ARDS in ICU, the validity of a radiographic infiltrate becomes less reliable Differential Diagnosis Pulmonary Edema Cardiogenic Non-cardiogenic Atelectasis Infarction Nosocomial pneumonia Hemorrhage Systemic Inflammatory Response Syndrome Adult Respiratory Distress Syndrome (ARDS) Diagnosis Remember, VAP is a sub-type of nosocomial pneumonia defined specifically in relation to a bacterial etiology ? Role of Candida species… Why an accurate diagnosis ? Inappropriate treatment of pneumonia has been shown to correlate directly with an increased mortality Indiscriminate use of antibiotics leads to the development of multi-resistant strains Empiric antibiotic therapy predisposes to infection with more virulent strains Fagon et al, Am Rev Respir Dis, 1989 Increased proportion of pneumonias due to Pseudomonas and Acinetobacter from 19% to 65% when antibiotics were administrated before the development of an actual pneumonia Increased mortality in previously-treated group (48% vs. 83%) Diagnostic Tests Tracheal aspirations Selective airway sampling Bronchoalveolar lavage (BAL) Protected specimen brush Direct airway visualization Quantitative Cultures Becoming a mainstay in the “academic diagnosis” of VAP However, regardless of technique, laboratory standardization is essential Cumbersome Labor intensive Associated Costs Tracheal Aspirates (TA) Gram stains plagued by low specificity Tracheal colonization Correlate with cultures in only 46% (EAST Study) GNR better predictive, whereas gram positive or no bacteria was unreliable Quantitative cultures and TA Probably comparable to invasive procedures Sensitivity (82% vs. 64%) and specificity (83% vs. 96%) Overall more cost-effective than invasive procedures Diagnostic Tests: TA Presence of elastin fibers in TA Specific indicator of pulmonary necrosis Increased specificity to 73-100% Shlaes et al, Chest, 1984 Sputum samples strongly correlated to radiographic evidence of pulmonary necrosis Histologically proven positive in 9 cases without radiographic findings Can be non-specific for noninfectious causes of necrotizing lung diseases Bronchoaveolar Lavage (BAL) Performed by bronchoscopy BAL samples larger portion of lung than TA Increased with protected catheter Sensitivity 72-100%, specificity 69-100% Sens 92%, Spec 97% Recommend threshold of 104 CFU/ ml Blind mini-BAL Can be done by respiratory technicians Protected catheter-approach Compares favorably to bronchoscopic BAL Protected Specimen Brush Performed via bronch or non-bronchoscopic Sensitivity and specificity varies Sensitivity 70-100% Specificity 60-92% Sensitivity drops with antibiotic use (13%) Threshold 103 CFU/ml Combination of Test Inherent drawback with BAL and PSB Delays in cultures of 24-48 hrs. Lower than acceptable sens. and spec. when either method used alone Combined BAL and PSB BAL recovered cells determine empiric antibiotic if more than 5% of infected cells Therapy is altered based on PSB with 103 CFU cutoff Improves sensitivity 100% and specificity 96% Prevention is Critical… Intubation Intubate only if necessary Early extubation if criteria meet…though need to minimize the risk of re-intubation ! ? Semi-upright positioning ? Subglottic continuous aspiration ? Use of oral gastric tubes instead of NGT ? Limited use of gastric alkalinization ? Selective digestive decontamination Subglottic Continuous Aspiration Valles et al, Ann Int Med, 1995 Randomized blinded study Reduction of VAP Controls 39.6 episodes /1000 vent days Intervention 19.9 episodes / 1000 vent days Increased time to developing VAP (control) 5.9 days to (intervention) 12 days Drawbacks Expensive specialized ET tubes Semi-Upright Positioning Evidence For: (Torres et al, Ann Int Med, 1992) Used radioactive labeling of gastric contents Significantly less aspiration with 45 degree elevation Magnitude of supine aspiration time-dependent Evidence Against: (Ibanez et al, JPEN, 1992) Similar study in 70 patients No statistical difference in supine vs. upright Significant difference of reflux in patients with NGT Use of Oral Gastric Tubes Use significantly reduces Incidence of infectious sinusitis Incidence of VAP Recommendations Convert NGT to OG Consider gastrostomy if long term use necessary Sample Current Practice ? Empirical Antibiotics: VAP Why such a concern: Abx-Resistance MMWR – July 5, 2002 VRSA in Michigan MMWR - October 11, 2002 VRSA in Pennsylvania Wake-up Call…. Antibiotics & VAP what is the “appropriate use” of antibiotics in either suspected or “proven” VAP ? Mortality related to Abx-Coverage VAP: Summary of Approach Critical Care Medicine Boston Medical Center Boston University School of Medicine Nonpharm. Prevention Measures Kollef, NEJM 1999. Pharm. Prevention Measures Kollef, NEJM 1999. VAP: Conclusions Most common nosocomial infection in the ICU Most significant risk is intubation/reintubation ? Preventable Disease Treatment should be rationale Hospital-based patterns of infection (i.e. biograms) Unit-specific protocols validated through time Accurate & accepted diagnosis of VAP Clinical, radiographic, and laboratory findings Such a diagnosis may be most accurate with quantitative cultures via either TA, BAL, PSB VAP: Questions Critical Care Medicine Boston Medical Center Boston University School of Medicine Ventilator-Associated Pneumonia Critical Care Medicine Boston Medical Center Boston University School of Medicine Bradley J. Phillips, M.D.