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Executive Summary(4)

Executive Summary(4). A shorter duration of ABx therapy ( 7 to 8 days ): recommended for - uncomplicated HAP, VAP, or HCAP - with initially appropriate therapy - a good clinical response - with no evidence of infection with non- fermenting gram-negative bacilli.

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Executive Summary(4)

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  1. Executive Summary(4) • A shorter duration of ABx therapy (7 to 8 days): recommended for - uncomplicated HAP, VAP, or HCAP - with initially appropriate therapy - a good clinical response - with no evidence of infection with non- fermenting gram-negative bacilli

  2. Introduction(1) • HAP: pneumonia occurs  48 hrs after admission ( not intubated at admission) • VAP: pneumonia occurs48-72 hrs after intubation • HCAP: pneumonia occurs including those - hospitalized in an acute care hospital for  2 days within 90 days - received recent IV antibiotic therapy, chemotherapy, or wound care within the past 30 days - resided in a nursing home or long-term care facility - attended a hospital or hemodialysis clinic

  3. Introduction(2) 4 major principles to manage HAP, VAP, HCAP: • Avoid untreated or inadequately treatment; because failure to initiate prompt appropriate and adequate therapy   increased mortality • Avoid the overuse of antibiotics by focusing on accurate diagnosis, tailoring therapy to the results of LRTCs, and shortening duration of therapy to the minimal effective period

  4. Introduction(2) 4 major principles to manage HAP, VAP, HCAP: • 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 • Apply prevention strategies aimed at modifiable risk factors

  5. Epidemiology (1) • Time of onset of pneumonia: an important epidemiologic variable and risk factor for specific pathogens and outcomes • Early-onset HAP and VAP(  4 days): usually better prognosis, more likely to be caused by antibioticsensitive bacteria (Level II)

  6. Epidemiology (2) • Late-onset HAP and VAP ( 5 days ): usually with increased mortality and morbidity, more likely to be caused by multidrug-resistant (MDR) pathogens (Level II) • Early-onset HAP with prior ABx or prior hospitalizationwithin the past 90 days: are at greater risk for colonization and infection with MDR pathogens treat as late-onset HAP or VAP (Level II)

  7. Epidemiology (3)

  8. Epidemiology (4) • HAP/VAP Pts:  risk for colonization and infection with MDR pathogens (Level II) • Incidence of HAP/VAP: difficult to define exactly (overlap with tracheobronchitis) (Level III) • The exact incidence of HAP: usually between 5~15/1,000 admissions (Level II) • The exact incidence of VAP: 6~20-fold greater than in non-ventilated patients (Level II)

  9. Epidemiology (5) • Causes of most cases of HAP, VAP, and HCAP: Bacteria, usually polymicrobial; especially high rate in patients with ARDS (Level I) • Common bacteria: (Level II) - Aerobic GNB: P. aeruginosa, K. pneumoniae, and Acinetobacter species - Aerobic GPC, such as S. aureus ( much MRSA) - Anaerobes: uncommon .

  10. Epidemiology (6) • Rates of L. pneumophila: vary between hospitals, occurs commonly in serogroup1; with colonized water supply and ongoing construction (Level II) • Nosocomial virus and fungal infections: uncommon in immunocompetent patients (Level I) • Outbreaks of influenza: occurred sporadically and risk of infection reduced with widespread effective infection control, vaccination, and use of antiinfluenza agents (Level I)

  11. Epidemiology (7) • Prevalence of MDR pathogens: varies by patient population, hospital, and type of ICU; need for local surveillance data (Level II) • MDR pathogens: (Level II) more commonly isolated from patients - with severe, chronic underlying disease - with risk factors for HCAP - with late-onset HAP or VAP

  12. Pathogenesis (1) • Sources of pathogens: (Level II) - healthcare devices - the environment (air, water, equipment, and fomites) - transfer of microorganisms between patients and staffs • Host- and treatment-related colonization factors: important pathogenesis: (Level II) - the severity of underlying disease - prior surgery - exposure to antibiotics - other medications - exposure to invasive respiratory devices and equipment

  13. Pathogenesis (2) • Primary routes of bacterial entry: (Level II) - aspiration of oropharyngeal pathogens - leakage of secretions which containing bacteria around tube cuff • Uncommon pathogenic mechanisms (Level II) - inhalation or direct inoculation of pathogens - hematogenous spread from infected intravenous catheters - bacterial translocation from GI tract

  14. Pathogenesis (3) • Infected biofilm in the endotracheal tube, with subsequent embolization to distal airways, may be important in the pathogenesis of VAP (Level III) • Stomach and sinuses: potential reservoirs of pathogens, contribute to bacterial colonization of the oropharynx, but their contribution is controversial (Level II)

  15. Modifiable Risk Factors (1) General prophylaxis. • Effective infection control measures: (Level I) -staff education -alcohol-based hand disinfection -isolation: cross-infection with MDR pathogens • Surveillance of ICU infections: (Level II) to identify and quantify endemic and new MDR pathogens, and preparation of timely data for infection control

  16. Modifiable Risk Factors (2) Intubation and mechanical ventilation • Avoid intubation and reintubation (risk of VAP) (Level I) • Noninvasive ventilation should be used whenever possible in selected patients (Level I) • Orotracheal intubation and orogastric tubes are preferred over nasotracheal intubation and nasogastric tubes to prevent nosocomial sinusitis and to reduce the risk of VAP ( direct causality has not been proved) (Level II)

  17. Modifiable Risk Factors (3) Intubation and mechanical ventilation • Continuous aspiration of subglottic secretions: risk of early-onset VAP (Level I) • Cuff pressure  20 cm H2O to prevent leakage of bacterial pathogens (Level II) • Clear contaminated condensate from ventilator circuits and prevent to enter either the endotracheal tube or inline medication nebulizers (Level II)

  18. Modifiable Risk Factors (4) Intubation and mechanical ventilation • Passive humidifiers or heat–moisture exchangers: circuit colonization, but not consistently incidence of VAP not a pneumonia prevention tool (Level I) • duration of intubation and MV: may prevent VAP, achieved by the use of sedation and to accelerate weaning (Level II)

  19. Modifiable Risk Factors (5) Aspiration, body position, and enteral feeding. • Kept in the semirecumbent position (30–45) rather than supine to prevent aspiration, especially when receiving enteral feeding (Level I) • Enteral nutrition: preferred over parenteral nutrition (Level I) -  risk of complications related to CVP - prevent reflux villous atrophyof intestinal mucosa ( whichrisk of bacterial translocation)

  20. Modifiable Risk Factors (6) Modulation of colonization:oral antiseptics and ABx • Routine prophylaxis of HAP with oral antibiotics with or without systemic antibiotics: -incidence of VAP -has helped contain outbreaks of MDR bacteria (Level I) Not recommended especially in patients who may be colonized with MDR pathogens (Level II) • Onset of infection with prior systemic ABx suspicious infection with MDR pathogens (Level II)

  21. Modifiable Risk Factors (7) Modulation of colonization:oral antiseptics and ABx • Prophylactic systemic ABx for 24 hrs at the time of intubation: demonstrated to prevent HAP in patients with closed head injury, but not recommended a routine until more data become available (Level I) • Modulation of oropharyngeal colonization by the use of oral chlorhexidine: has prevented HAP in CABG, but not recommended a routine until more data become available (Level I)

  22. Modifiable Risk Factors (8) Modulation of colonization:oral antiseptics and ABx • Use daily interruption or lightening of sedation to avoid constant heavy sedation and try to avoid paralytic agents, both of which can depress cough and thereby  risk of HAP (Level II)

  23. Modifiable Risk Factors (9) Stress bleeding prophylaxis, transfusion • Sucralfate: VAP, but slightly rate of significant gastric bleeding compared with H2 antagonists. Stress bleeding prophylaxis: H2 antagonists or sucralfate is acceptable (Level I) • Transfusion of RBC with a restricted policy; leukocyte-depleted RBC transfusions can  HAP in selected patient populations (Level I)

  24. Modifiable Risk Factors (9) Hyperglycemia • Intensive insulin therapy: recommended to maintain BS between 80 and 110 mg/dl in ICU patients - nosocomial blood stream infections - duration of mechanical ventilation -  ICU stay -  morbidity -  mortality (Level I)

  25. Diagnose (1)

  26. Diagnosis (2) • Ccomprehensive medical history, PE, CXR, severity of HAP, exclude other potential infection, specific conditions that can influence the likely etiologic pathogens (Level II) • Tracheal colonization: does not require therapy or diagnostic evaluation in the absence of clinical findings or sign of infection (Level II)

  27. Diagnosis (3) • Blood cultures: All patients should collect; A positive result indicate pneumonia or extra-pulmonary infection (Level II) • Sample collection: Protected specimen brush samples- specificity>sensitivity; Endotracheal aspirate, BAL-sensitivity>specificity (Level II) • Diagnostic threshold of quantitative culture: PSB 103 cfu/ml; BAL 104~105 cfu/ml; tracheal aspirates 106 cfu/ml

  28. Diagnosis (4) • A sterile culture without a new antibiotic in the past 72 hours: virtually rules out the presence of bacterial pneumonia (NPV 94%), but viral or Legionella infection is still possible (Level II) • Semiquantitative cultures of tracheal aspirates cannot bereliably as quantitative cultures to define the presence of pneumonia and the need for antibiotic therapy (Level I)

  29. Diagnosis (5) • Bronchoscopic bacteriologic strategy:  14-day mortality, compared with a clinical strategy in VAP (Level I) should not postpone diagnostic studies in clinically unstable (Level II)

  30. Treatment (1)

  31. Treatment (2)

  32. Treatment (3) Penicillin-resistant S. pneumoniaeand multidrug-resistant S. pneumoniae: frequency; levofloxacin or moxifloxacin are preferred to ciprofloxacin and the role of other new quinolones, such as gatifloxacin, has not been established

  33. Treatment (4) • ESBL strain: such as K. • pneumoniae or • Acinetobacter: • carbepenem is a • reliable choice. • L. pneumophila: • combination antibiotic • regimen should include • macolide (azithromycin) • or a fluoroquinolone • (e.g., ciprofloxacin or • levofloxacin) • MRSA risk factors are • present or there is a • high incidence locally: • Vancomycin or linezolid

  34. Treatment (5) Trough levels: for gentamicin and tobramycin  1 g/ml; and for amikacin  4–5 g/ml; for vancomycin: 15–20 g/ml.

  35. Treatment (6) • Initial IV form; a switch to oral/enteral therapy; Highly bioavailable agents, such as quinolones and linezolid, may be easily switched to oral therapy (Level II) • Aerosolized antibiotics have not been proven to have value in the therapy of VAP (Level I) However, they may be considered as adjunctive therapy in MDR gram-negatives pathogens, not responding to systemic therapy (Level III)

  36. Treatment (7) • Combination therapy: for possible MDR pathogens (Level II); No documented superiority compared with monotherapy, except to enhance likelihood of initially appropriate empiric (Level I) • Combination with aminoglycoside: stopped after 5–7 days in responding patients (Level III) • Monotherapy: Only in the absence of resistant pathogens (Level I)

  37. Treatment (8) • If initially appropriate ABx: efforts to shorten duration from the traditional 14~21 to 7 days, except P. aeruginosa, and with good clinical response & resolution of clinical features (Level I) • In P. aeruginosa pneumonia: combination recommended (  resistance on monotherapy); combination will not necessarily prevent the development of resistance, but avoid inappropriate and ineffective tx (Level II)

  38. Treatment (9) • In Acinetobacter species: the most active agents are the carbapenems, sulbactam, colistin, and polymyxin; no data documenting an improved outcome with combination regimen (Level II) • In ESBL Enterobacteriaceae: monotherapy with a third-generation cephalosporinshould beavoided. The most active agents are carbapenems (Level II)

  39. Treatment (10) • Adjunctive inhaled aminoglycoside or polymyxin: should be considered for MDR gram-negative pneumonia, especially not improving with systemic therapy (Level III) • Linezolid: an alternative to vancomycin for MRSA (Level II),preferred in renal insufficiency or receiving other nephrotoxic agents, but more data are needed (Level III).

  40. Treatment (11) • Antibiotic restriction: limit epidemic infection with specific resistant pathogens • Heterogeneity of antibiotic prescriptions: including formal antibiotic cycling   overall frequency of antibiotic resistance long-term impact of this practice: unknown (Level II)

  41. Response (1) • Serial assessment of clinical parameters to define the response to initial empiric therapy (Level II) • Clinical improvement: takes 48–72 hours don’t change therapy during this time; unlessrapidclinical decline (Level III) • Non-response: evident by Day 3, using an assessmentof clinical parameters (Level II)

  42. Response (2)

  43. Response (3) • In responding patient: de-escalation of antibiotics, narrowing therapy to the most focused regimen on the basis of culture data (Level II) • In nonresponding patient: evaluate for -noninfectious mimics of pneumonia -drug-resistant organisms -extrapulmonary sites of infection -complications of pneumonia and its therapy. (Level III)

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