Ventilator associated pneumonias including HAP.pptx

Overall summary of ventilator acquired pneumonia

1. VENTILATOR ASSOCIATED PNEUMONIA

2. DEFINITION EPIDEMIOLOGY MICROBIOLOGY PATHOPHYSIOLOGY RISK FACTORS DIAGNOSIS PREVENTION MANAGEMENT

3. DEFINITION HAP is defined as infection of the pulmonary parenchyma that occurs 48 hours or more after admission, was not incubating at the time of admission VAP refers to pneumonia that arises more than 48–72hours after endotracheal intubation HCAP includes any patient who was hospitalized in an acute care hospital for two or more days within 90 days of the infection; resided in a nursing home or longterm care facility; received recent intravenous antibiotic therapy, chemotherapy, or wound care within the past 30 days of the current infection; or attended a hospital or hemodialysis clinic .

4. EPIDEMIOLOGY Infections involving the lungs are the most common nosocomial infections in ICU patients, accounting for 65 % of all nosocomial infections. Over 90% of ICU-acquired pneumonias occur during mechanical ventilation, and 50% of these VAPs begin in the first 4 days after intubation. VAP develops in 10% to 20% of patients who undergo mechanical ventilation for longer than 24 hours and is associated with longer ICU stays, increased costs, and increased mortality.

5. MICROBIOLOGY The isolates in VAP are Gram negative aerobic bacilli such as Pseudomonas aeruginosa , Klebsiella,E.coli . MRSA have become an important cause of VAP

6. Patients with early-onset VAP who have received prior antibiotics or who have had prior hospitalization within the past 90 days are at greater risk for colonization and infection with MDR pathogens and should be treated similar to patients with late-onset VAP.

7. PATHOPHYSIOLOGY Aspiration of pathogens from aerodigestive tract or leakage of bacteria around the endotracheal tube cuff is the primary route of bacterial entry into the trachea. Genomic DNA analysis proved that strains of bacteria from LRT in cases of VAP were identical to strains colonising oropharynx or stomach. Colonization of the endotracheal tube with bacteria encased in biofilm may result in embolization into the alveoli during suctioning or bronchoscopy .

8. ASPIRATION – PRIMARY ROUTE OF BACTERIAL ENTRY INTO LRT

9. BIOFILM FORMATION • It is an aggregate of micro-organisms kept together within a complex matrix of polysaccharides , proteins and DNA. • Develops within hours of intubation. • Provides mechanical scaffold around bacteria. • Protects against host defences and antibiotics.

10. Patient has a baseline period of stability or improvement on the ventilator, defi–ned by 2 calendar days (CDs) of stable or decreasing daily minimum FiO2 or PEEP or values. After a period of stability or improvement on the ventilator, the patient has at least one of the following indicators of worsening oxygenation: 1) Minimum daily FiO2 values increase 0.20 over the daily minimum FiO2 in the preceding 2 CDs (the baseline period) and remain at or above that increased level for 2 CDs. 2) Minimum daily PEEP values increase 3 cmH2O over the daily minimum PEEP in the preceding 2 CDs (the baseline period) and remain at or above that increased level for 2 CDs . Ventilator-Associated Condition (VAC)

11. On or after CD 3 of mechanical ventilation and within 2 CDs before or after the onset of worsening oxygenation (the window period), the patient meets both of the following criteria: 1) Temperature >38°C or <36°C, OR white blood cell count 12,000 cells/mm3 or ”4000 cells/mm3 AND 2) A new antimicrobial agent(s) is started and is continued for 4 CDs. Infection-related Ventilator-Associated Complication (IVAC)

12. POSSIBLE VAP Criteria met for IVAC and during the window period one of the following criteria is met: 1) Purulent respiratory secretions OR 2) Positive qualitative, semi-quantitative, or quantitative cultures from an LRT source. PROBABLE VAP Criteria met for IVAC and during the window period one of the following criteria is met: 1) Purulent respiratory secretions AND 2) Positive quantitative or equivalent semi-quantitative culture of the LRT sources

13. Risk Factors For VAP • Major risk factor = Endotracheal intubation • Factors that enhance colonization of the oropharynx &/or stomach: – Administration of antibiotics – Admission to ICU – Underlying chronic lung disease • Conditions favoring aspiration into the respiratory tract or reflux from GI tract: – Supine position *GERD – NGT placement *Coma/delirium – Intubation and self- extubation – Immobilization • Surgery of head and neck, thorax & upper abdomen • Host Factors: – Extremes of age – Malnutrition – Immunocompromised – Underlying condition/disease process

14. DIAGNOSIS The traditional clinical criteria for the diagnosis of VAP includes :- (a) fever or hypothermia, (b) leukocytosis or leukopenia , ( c) an increase in volume of respiratory secretions or a change in character of the secretions, (d) a new or progressive infiltrate on the chest x-ray

15. -Arterial oxygenation saturation should be measured in all patients to determine the need for supplemental oxygen OR to manage patients who require mechanical ventilation. -Other laboratory studies (complete blood count, serum electrolytes, renal and liver function), can point to the presence of multiple organ dysfunction and thus help define the severity of illness. -A sterile culture of respiratory secretions in the absence of a new antibiotic in the past 72 hours virtually rules out the presence of bacterial pneumonia, but viral or Legionella infection is still possible

16. Microbiological Evaluation Respiratory Sampling :- • Non- bronchoscopic methods:- - tracheal aspirates - mini-BAL • Bronchoscopic methods:- - BAL - Protected specimen brush (PSB)

17. -The bacteriologic strategy uses quantitative cultures of the LRT to confirm or eliminate the diagnosis of VAP based on thresholds of bacterial growth. These thresholds differ depending on the method of respiratory sampling and are as follows: -≥10 5 colony-forming units (CFU)/ mL for an endotracheal aspirate, -≥10 4 CFU/ mL for a BAL, and -≥10 3 CFU/ mL for a PSB. .

18. A diagnostic thoracentesis to rule out a complicating empyema or parapneumonic effusion should be performed if the patient has a large pleural effusion or if the patient with a pleural effusion appears toxic

19. PREVENTION Prevention of VAP centers on minimizing mechanical ventilation and reducing aspiration and bacterial colonisation avoiding intubation and reintubation , shortening the duration of mechanical ventilation, and employing noninvasive methods to improve oxygenation and ventilation when indicated can prevent pneumonia Selective decontamination of the digestive tract(SDD ) administers nonabsorbable antimicrobial agents directly to the oropharynx and stomach to prevent colonization with GNB and S. aureus .

20. Specific prophylaxis against VAP Noninvasive ventilation (NIV) is an alternative approach to the use of artificial airways to avoid infectious complications and injury of the trachea • Semi recumbent positioning • Oscillating and rotating beds • Ventilator circuits management • Enteral feeding methods • Stress ulcer prophylaxis

21. HAND HYGIENE • Infection control measures: staff education, Compliance with alcohol-based hand disinfection, and isolation to reduce crossinfection with MDR pathogens

22. Subglottic Suctioning Specially designed ETT • Continuous suction - 20cm H 2 O • Decreases VAP

23. Selective Oropharyngeal Decontamination Povidone -iodine, chlorhexidine • Oral Chlorhexidine : most studied. • Decreases oropharyngeal colonization. • Used as a standard measure.

24. SILVER COATED ETT Silver : anti-microbial, anti-adhesive properties • Prevents BIOFILM formation. • Limitation: it can only delay ETT colonization, biofilm will eventually form over time as secretions accumulate.

25. VENTILATOR BUNDLE THERAPY • Set of procedures to be implemented together. Head end elevation Oral care with Chlorhexidine Daily sedation hold & SBT Stress ulcer prophylaxis DVT prophylaxis • Shown to reduce VAP rates

26. Extensive pneumonia in both lungs

27. MANAGEMENT Initial therapy should be administered to all patients intravenously, with a switch to oral/ enteral therapy in selected patients with a good clinical response and a functioning intestinal tract.

28. NON-INFECTIOUS CAUSES OF CHEST INFILTRATES • Atelectasis • Aspiration • Pulmonary embolism • Cardiogenic pulmonary edema . • Acute respiratory distress syndrome (ARDS ) • Fluid overload. • Cryptogenic organizing pneumonia . • Pulmonary hemorrhage

29. VAP with No risk for MDR pathogens and hospitalized <5 d Streptococcus pneumonia Haemophilus influenzae Methicillin -sensitive Staphylococcus aureus Escherichia coli Klebsiella pneumoniae Enterobacter species Proteus species Serratia marcescens Third-generation cephalosporin ( Ceftriaxone ) Or Ampicillin–sulbactam Or Respiratory fluoroquinolone ( Levofloxacin orMoxifloxacin ) Or Non- antipseudomonal carbapenem ( Ertapenem )

30. VAP At risk for MDR pathogens or hospitalized for ≥5 d Pseudomonas aeruginosa Klebsiella pneumonia (extended-spectrum β - lactamase +) Acinetobacter species Legionella pneumophila Methicillin -resistant S. aureus Antipseudomonal cephalosporin ( Cefepime , Ceftazidime ) Or Antipseudomonal carbapenem ( Imipenem or Meropenem ) Or Antipseudomonal penicillin with β- lactamase inhibitor( Piperacillin–tazobactam ) Plus Antipseudomonal fluoroquinolone (Ciprofloxacin or Levofloxacin ) Or Aminoglycoside ( Gentamycin , Tobramycin , or Amikacin ) Plus Anti-MRSA agent ( Linezolid or Vancomycin

31. If L. pneumophila is suspected, the combination antibiotic regimen should include a macrolide (e.g., azithromycin ) or fluoroquinolone ( e.g.,ciprofloxacin or levofloxacin ) rather than an aminoglycoside . If P. aeruginosa pneumonia is documented, combination therapy is recommended. The principal justification is the high frequency of development of resistance on monotherapy .

32. Carbapenems are often effective against ESBL organisms( E. coli, Klebsiella ) or Acinetobacter species For patients with penicillin allergy consider substituting β- lactam with: • Aztreonam • Meropenem (<1% crossreactivity to penicillin allergy) Inhaled antibiotics have been used in selected populations and should be used only after consultation with a subspecialist

33. Risk Factors for MDR Pathogens : -Antimicrobials in previous 90 d -Current hospitalization for 5 d or greater. -Hospitalization for 2 d or greater in the previous 90 d Nursing home -Home infusion therapy -Chronic dialysis in previous 30 d -Wound care at home - Immunosuppression

34. Combination therapy vs Monotherapy Combination therapy should be used (agents from different antibiotic classes) if patients are likely to be infected with MDR pathogens. Monotherapy with selected agents can be used for patients with VAP in the absence of resistant pathogens. Patients in this risk group should initially receive combination therapy until the results of lower respiratory tract cultures confirm that organism grown is not MDR

35. Response To Therapy Clinical improvement usually takes 48–72 hours, and thus therapy should not be changed during this time unless there is rapid clinical decline. Non response to therapy is usually evident by Day 3, using an assessment of clinical parameters Serial quantitative microbiologic studies of lower respiratory tract secretions can also define resolution end points.

36. The CPIS combines clinical, radiographic, physiological (PaO2/FiO2), and microbiologic data into a single numerical result. Baseline is calculated from the first five variables. For positive culture, two points are added to the CPIS baseline score. A score of more than six at baseline or after incorporating the culture result is considered suggestive of pneumonia

37. Improvement in the CPIS occurring during the first 3 days of empiric treatment was associated with hospital survival whereas a lack of improvement in the CPIS predicted mortality.

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