Downloaded 151 times
Uploaded byChamika Huruggamuwa
Ventilator associated pneumonia in the icu
Ventilator-associated pneumonia (VAP) is pneumonia that develops 48-72 hours or more after endotracheal intubation. It is characterized by new infiltrates on chest imaging and signs of infection. Early onset VAP within 4 days is usually caused by antibiotic-sensitive bacteria, while late onset VAP after 4 days often involves multidrug-resistant organisms. Preventing VAP involves care bundles focusing on endotracheal tube maintenance and secretion removal, along with prudent antibiotic usage and limiting intubation time.
More Related Content
Similar to Ventilator associated pneumonia in the icu
![Ventilation Associated Pneumonia [VAP]](https://cdn.slidesharecdn.com/ss_thumbnails/sp2-vap-160224020717-thumbnail.jpg?width=640&height=640&fit=bounds)
Ventilator associated pneumonia in the icu
- 1. Ventilator-Associated pneumonia in theICU BY Dr. Chamika Huruggamuwa Registrar In Anaesthesia TH Kandy
- 3. Introduction • pneumonia thatoccurs 48–72 hours or thereafter following endotracheal intubation, • characterized by the presence of a • new or progressive infiltrate, • signs of systemic infection (fever, altered white blood cell count), • Changes in sputum characteristics, and • detection of a causative agent
- 4. • Early onsetVAP is defined as pneumonia that occurs within 4 days and this is usually attributed to antibiotic sensitive pathogens • Late onset VAP is more likely caused by multidrug resistant (MDR) bacteria and emerges after 4 days of intubation
- 5. Epidemiology • VAP contributesto approximately half of all cases of hospital-acquired pneumonia. • VAP is estimated to occur in 9–27 % of all mechanically ventilated patients • VAP is associated with increased intensive care unit stay, patient ventilator days, and mortality. • The incidence of VAP can be reduced by many means including the use of care bundles and modified TTs.
- 6. • Approximately 50% of all antibiotics administered in ICUs are for treatment of VAP.
- 7. • Independent riskfactors for development of VAP are • male sex, • admission for trauma • intermediate underlying disease severity
- 8. Pathogenesis complex interplay betweenthe Endotracheal tube, Presence of risk factors, virulence of the invading bacteria host immunity
- 9. • The mainpathogenic factor in the development of VAP is biofilm formation within the tracheal tube (TT) microaspiration of secretions
- 10. endotracheal tube violation ofnatural defense mechanisms (the cough reflex of glottis and larynx) against microaspiration around the cuff of the tube
- 11. • Infectious bacteriaobtain direct access to the lower respiratory tract via: • (1) microaspiration, which can occur during intubation itself; • (2) development of a biofilm laden with bacteria (typically Gram- negative bacteria and fungal species) within the endotracheal tube; • (3) pooling and trickling of secretions around the cuff ; • (4) impairment of mucociliary clearance of secretions with gravity dependence of mucus flow within the airways •
- 12. • Pathogenic materialcan also collect in surrounding anatomic structures, such as the stomach, sinuses, nasopharynx and oropharynx, with replacement of normal flora by more virulent strains • constantly thrust forward by the positive pressure • reintubation following extubation increases VAP rates, • the use of non-invasive positive pressure ventilation has been associated with significantly lower VAP rates
- 13. • critically illpatients may have impaired phagocytosis
- 14. Microbiology • Type oforganism depends on the duration of mechanical ventilation • Early VAP is caused by • pathogens that are sensitive to antibiotics, • whereas late onset VAP is caused by multi-drug resistant and more difficult to treat bacteria.
- 15. • Early-onset VAPinclude Streptococcus pneumoniae (as well as other streptococcus species), Hemophilus influenzae, methicillin-sensitive Staphylococcus aureus (MSSA), antibiotic-sensitive enteric Gram- negative bacilli, Escherichia coli, Klebsiella pneumonia, Enterobacter species, Proteus species and Serratia marcescens. • Late VAP are typically MDR bacteria, such as methicillin-resistant S. aureu (MRSA), Acinetobacter, Pseudomonas aeruginosa, and extended-spectrum beta-lactamase producing bacteria
- 16. Diagnosis • Currently, thediagnosis of VAP is based on a combination of clinical, Radiological, and Microbiological criteria • DD ARDS pulmonary oedema pulmonary contusion Tracheobronchitis Thromboembolic disease.
- 17. • no universallyaccepted, gold standard diagnostic criterion for VAP • no radiological criteria pathognomonic of VAP and the interpretation of chest radiographs in ventilated patients is very difficult. • Single air bronchograms and fissure abutment are highly specific, but they lack sensitivity
- 18. • Invasive andnon-invasive sampling techniques are used to Obtain microbiological specimens to diagnose VAP. • Broncho Alveolar Lavage (BAL) mini BALs • Protected specimen brushings (PSB) • Tracheal aspirates • Th e American Th oracic Society (ATS) and the • Infectious Diseases Society of America (IDSA
- 19. BAL gold standardover others,,,,, however • It cannot guarantee sampling from the area of the lung most affected, the sensitivity of this test is low, although the specificity is quite high (significant false-negative rate). • CPIS -clinical, physiological, microbiological and radiographic evidence
- 21. • Scores canrange between zero and 12 with a score of ≥ 6 showing good correlation with the presence of VAP • Despite the clinical popularity of the CPIS, debate continues regarding its diagnostic validity.
- 22. • The Johannsoncriteria • The HELICS criteria • The United States Centre for Disease Control (CDC) definition
- 23. Treatment • antibiotic dependson the duration of mechanical ventilation. • Late onset VAP (> 4 days) broad spectrum antibiotics • Early onset (≤ 4 days) limited spectrum antibiotics
- 24. • The usualduration of treatment for early onset VAP is 8 days and longer in the case of late-onset VAP or if MDR organisms are suspected or identified • Despite therapy, if no response is observed, it may be prudent to reconsider the diagnosis, reassess the organism being treated or search for other reasons for signs and symptoms.
- 25. Prevention • The roleof care bundles A care bundle refers to a group of evidence-based interventions related to a particular condition which when applied together significantly improves patient outcome.
- 26. TT modification • TTcuff design to prevent microaspiration. Cuff pressure control • cuff pressure <20 cm H2O favors increased passage of secretions between the cuff and the wall of the trachea, while >30cmH2O may cause tracheal mucosal damage.
- 27. Subglottic secretion drainage Ameta-analysis of 13 randomized controlled trials showed that subglottic secretion drainage was effective at reducing VAP rates, also reducing the time to onset of first VAP, reduced duration of mechanical ventilation, and reduced ICU LOS.
- 28. TT cuff design highvolume–low pressure cuff Vs A tapered cuff shape
- 29. TT coating Silver-coated TTor a standard TT chlorhexidine and titanium dioxide. Significant reduction in VAP rates NO Reduction in ICU LOS or duration of ventilation NASCENT TRIAL
- 30. Nebulized gentamicin • Nebulizedgentamicin attained a higher concentration within the TT and there was a lower incidence of biofilm formation
- 31. Kinetic therapy Mucociliary clearanceis inhibited by immobility. • Mechanical rotation of patients with 40° turns achieves more significant clearance of secretions than current standard therapy of 2 hourly turns Lower the incidence of VAP No effect on duration of ventilation, LOS, or mortality. Requires specialist equipment and has been associated with significant complications such as intolerance to rotation, unplanned extubations, loss of vascular access, and arrhythmias.
- 32. Care of airwayequipment • Studies have shown that TT colonization and biofilm formation begins within 24 h of intubation. Reducing biofilm formation can be achieved by, Strict attention to hand hygiene when handling the TT, closed-circuit suction systems, use of heat and moisture exchangers, limiting ventilator tube changes to whenever they are soiled,
- 33. Feeding • early establishmentof enteral feeding is of benefit to critical care patients. • reflux and aspiration of gastric contents is the main cause of VAP. • post-pyloric feeding may reduce the incidence of VAP.
- 34. Intubation-related events Reducing theduration of intubation with the use of sedation holds and weaning protocols reducing unplanned extubations minimizing re-intubation have also been shown to reduce VAP incidence
- 36. The major goalsof VAP management early, appropriate antibiotics in adequate doses followed by de- escalation based on microbiological culture results and the clinical response of the patient. Antimicrobial stewardship programs involving pharmacists, physicians and other healthcare providers optimize antibiotic selection, dose, and duration to increase efficacy in targeting causative pathogens and allow the best clinical outcome
Editor's Notes
- #6 Earlier studies placed the attributable mortality for VAP at between 33–50 %, but this rate is variable and relies heavily on the underlying medical illness [1]. Over the years, the attributable risk of death has decreased and is more recently estimated at 9–13 % [9], [10], largely because of implementation of preventive strategies
- #11 Functions of upper airway
- #16 Patients with a history of hospital admission for ≥ 2 days in the past 90 days, nursing home residents, patients receiving chemotherapy or antibiotics in the last 30 days and patients undergoing hemodialysis at outpatient centers are susceptible to drug resistant bacteria
- #18 Daily bedside evaluation in conjunction with chest radiography can only be suggestive of the presence or absence of VAP, but not defi ne it
- #19 Th e American Th oracic Society (ATS) and the Infectious Diseases Society of America (IDSA) guidelines recommend obtaining lower respiratory tract samples for culture and microbiology
- #20 Endotracheal aspirate: Easiest to obtain, does not require provider involvement. 2. Bronchoalveolar lavage (BAL): Requires bronchoscopic guidance. 3. Mini-bronchoalveolar lavage (mini-BAL): Performed ‘blind’, i. e., without bronchoscopic guidance. 4. Protected specimen brush (PSB): Utilizes a brush at the tip of the catheter which is rubbed against the bronchial wall.
- #29 Tapperd cuff made of ultra thin polyurethane reduce the secretion channeling.