Nosocomial pneumonia in adults

1. Nosocomial pneumonia in adults References: 1)Thomas M File, Jr,MD UpToDate Online 13.3 2) Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 2005; 171:388. Presented by Intern 鍾葛鈞

2. Definition of ATS/IDSA guidelines: 1)Hospital-acquired pneumonia (HAP) is pneumonia that occurs 48 hours or more after admission, which was not incubating at the time of admission. 2)Ventilator-associated pneumonia (VAP) refers to pneumonia that develops more than 48 to 72 hours after endotracheal intubation. 3)Healthcare-associated pneumonia (HCAP) includes any patient who was either hospitalized in an acute care hospital for two or more days within 90 days of the infection; or resided in a long term care facility; or received intravenous antimicrobial therapy, chemotherapy, or wound care within the 30 days prior to the current infection; or attends a hospital or hemodialysis clinic

3. Principles underlie the management of HAP, VAP, and HCAP Principle (1) • Avoid untreated or inadequately treated HAP, VAP, or HCAP, because the failure to initiate prompt appropriate and adequate therapy has been a consistent factor associated with increased mortality.

4. Principle (2) • Recognize the variability of bacteriology from one hospital to another, specific sites within the hospital, and from one time period to another, and use this information to alter the selection of an appropriate antibiotic treatment regimen for any specific clinical setting.

5. Principle (3) • Avoid the overuse of antibiotics by focusing on accurate diagnosis, tailoring therapy to the results of lower respiratory tract cultures, and shortening duration of therapy to the minimal effective period.

6. Principle (4) • Apply prevention strategies aimed at modifiable risk factors.

7. ETIOLOGY • HAP, VAP, and HCAP • aerobic gram-negative bacilli (eg, Escherichia coli, Klebsiella pneumoniae, Enterobacter spp, Pseudomonas aeruginosa, Acinetobacter spp) • gram-positive cocci (eg, Streptococcus spp, Staphylococcus aureus, including methicillin-resistant S. aureus [MRSA • viruses or fungi is significantly less common except in the immunocompromised patient.

8. Risk factors for MDR pathogens 1.Receipt of antibiotics within the preceding 90 days 2.Current hospitalization of 5 days 3.Admission from a healthcare-related facility (eg, long-term care facility, dialysis unit) 4.High frequency of antibiotic resistance in the community or in the specific hospital unit 5.Presence of risk factors for HCAP including: hospitalization for two days or more in the preceding 90 days; residence in an extended care facility; home infusion therapy; chronic dialysis; home wound care; and a family member with an MDR pathogen 6.Immunosuppressive disease and/or therapy

9. Risk Factors Of VAP In Patientreceiving Mechanical Ventilation • Age >70 years • Chronic lung disease • Depressed consciousness • Large volume aspiration • Chest surgery • Frequent ventilator circuit changes • The presence of an intracranial pressure monitor or nasogastric tube • H-2 blocker or antacid therapy • Transport from the ICU for diagnostic or therapeutic procedures • Previous antibiotic exposure, particularly to third generation cephalosporins • Reintubation • Hospitalization during the fall or winter season • Mechanical ventilation for acute respiratory distress syndrome (ARDS)

10. Prevention of HAP • Role of gastric pH • Decontamination of the digestive tract • Patient positioning • Subglottic drainage

11. Role of gastric pH • gastric pH by H-2 blockers or antacids HAP • macroscopic gastric bleeding (P > 0.2) Sucralfate >ranitidine>antacid = 10% > 6% > 4% • Early-onset pneumonia was not statistically different (P > 0.2). • Late-onset pneumonia(4 days ) (P = 0.022). Sucralfate >antacid >ranitidine = 5% >16% > 21% • Mortality : no statistically difference

12. Role of gastric pH(2) • Sucralfate : lower median gastric pH (P < 0.001) and less frequent gastric colonization (P = 0.015) • Molecular typing, 84% late-onset GNB pneumonia have gastric colonization with the same bacteria before pneumonia developed • CONCLUSION: Stress ulcer prophylaxis with sucralfate reduces the risk for late-onset pneumonia in ventilated patients compared with antacid or ranitidine

13. Decontamination of the digestive tract • preventing oropharyngeal and gastric colonization with aerobic GNB and Candida spp, without disrupting the anaerobic flora • locally administered nonabsorbable antibiotic (eg, polymyxin) and an aminoglycoside or fluoroquinolone + amphotericin B or nystatin. • ( oral cefotaxime or trimethoprim) • One RCS showed decrease in pneumonia due to GNB w/o decrease in pneumonia from all causes

14. Decontamination of the digestive tract (2) • A large prospective randomized trial of ICU in the Netherlands (p’t 934) : SDD group →lower mortality both in the ICU and during hospitalization (mortality :15 vs 23% ICU, 24 vs 31 % hospital) • The preventative effects of SDD for HAP have been considerably lower in ICUs with high rates of endemic MDR pathogens • selection for resistant organisms

15. Patient positioning • Several studies → supine position vs semirecumbent → predisposed to microaspiration of gastric contents position • lower incidence of both clinically suspected and microbiologically confirmed HAP in semirecumbent versus supine patients • No difference in mortality • Suggest : place intubated patients in the semirecumbent position unless contraindicated.

16. Subglottic drainage Hi-Lo EVAC tube (CASS)

17. Subglottic drainage (2) • Lessen risk of aspiration • 5 studies (896 intubated p’t) The use of CASS reduced the incidence of VAP by nearly half - risk ratio 0.51 (95% CI 0.37-0.71). • The effect of CASS in limiting VAP was most pronounced among patients expected to require >72 hours of mechanical ventilation.

18. Diagnosisof Pneumonia Clinical definition – • New or progressive infiltrate • Fever • Leukocytosis • Purulent tracheobronchial secretions • unreliable compared with the gold standard of lung histology • One study compared the clinical diagnosis of HAP with the histopathologic diagnosis obtained at autopsy: pneumonia was diagnosed correctly in only 2/3 of cases

19. Noninfectious causes of fever and pulmonary infiltrates in VAP • Chemical aspiration without infection (Aspiration pneumonitis) • Atelectasis • Pulmonary embolism • Acute respiratory distress syndrome (ARDS) • Pulmonary hemorrhage • Lung contusion • Infiltrative tumor • Radiation pneumonitis • Drug reaction • Bronchiolitis obliterans organizing pneumonia (BOOP)

20. Diagnosis • Imaging • Gram's stain and culture • Bronchoscopy

21. Imaging • limited value in ventilated patients. • In one study, only 1/3 of ventilated patients with a new or worsening alveolar infiltrate had pneumonia at autopsy • No single radiologic sign was clearly correlated with the diagnosis. • The most reliable sign was the finding of air bronchograms, but predicted pneumonia in only 64 percent of cases. • ARDS and alveolar hemorrhage were the most common disorders mistaken for pneumonia.

22. Gram's stain and culture • unreliable due to contamination with bacteria colonizing the oropharynx • The presence of many polymorphonuclear leukocytes (and few epithelial cells) and bacteria, which are morphologically consistent with bacteria found on culture, improve the predictive power • In addition, the lack of isolation of a pathogen (eg, MRSA or Pseudomonas) from a well-collected and adequate expectorated sputum sample can be used to narrow the antimicrobial regimen • Blood cultures are extremely helpful when positive, but the yield is low

23. Bronchoscopy Protected brush specimen (PBS) • Using a threshold of >10(3) colony forming units (CFU)/mL • sensitivity : 64 to 100 % • specificity : 60 to 100 % Bronchoalveolar lavage (BAL) • Samples approximately one million alveoli, recovers 5x -10x the number of organisms obtained by PBS. Quantitative cultures using a threshold of >10(4) CFU/mL • sensitivity : 72 - 100 % • specificity : 69 - 100 %

24. 1) Baseline 2) When VAP is clinically suspected 3) 3 days later

25. Patients with no known risk factors for MDR pathogens • Ceftriaxone (2 g QD) • Ampicillin/sulbactam (3 g Q6H) or piperacillin/tazobactam (4.5 g Q6H) (eg, Enterobacter spp, Serratia spp, Pseudomonas spp) • Levofloxacin (750 mg daily) or ciprofloxacin (400 mg every eight hours) • Ertapenem (1 g daily)

26. Patients with known RF for MDR pathogens • 3 combination Antipseudomonal cephalosporin eg, cefepime (2 g Q8H) or ceftazidime (2 g Q8H) OR Antipseudomonal carbapenem eg imipenem (500 mg Q6H) or meropenem (1 g Q8H) OR Piperacillin-tazobactam (4.5 g Q6H)+ Antipseudomonal FQ, preferred regimen if Legionella is likely, eg, levofloxacin (750 mg QD) or ciprofloxacin (400 mg Q8H) OR Aminoglycoside eg, gentamicin or tobramycin (7 mg/kg QD adjusted to a trough level <1 µg/mL) or amikacin (20 mg/kg QD adjusted to a trough level <4-5 µg/mL)+ (if MRSA is suspected, there are MRSA risk factors, or high incidence of MRSA locally): Linezolid (600 mg Q12H) OR Vancomycin (15 mg/kg Q12H, dosed so that trough levels are 15 to 20 µg/mL)