Ventilator Associated Pneumonia

OVERVIEW

Ventilator Associated Pneumonia (VAP) is pneumonia occurring in people who had mechanical ventilation within 48 hours of the onset of infection

  • VAP is a subgroup of hospital-acquired pneumonia
  • VAP applies to patients with an endoctracheal tube or a tracheostomy tube – does not include patients receiving non-invasive ventilation (NIV)
  • common complication in ICU (15-20% incidence if >48h ventilation)
  • a gold standard test for diagnosis does not exist

PATHOGENESIS

Events leading to VAP:

  • Colonization of the oral cavity, upper airway, endotracheal tube and circuit with pathogenic organisms
  • Passage of pathogenic bacteria from the above sites into the lower airways through aspiration or microaspiration of secretions and suction catheters

Endotracheal cuffs

  • effective at preventing macro-aspiration
  • small folds on the surface of the cuff act as conduits for microaspiration of secretions pooled above the cuff
  • In older patients, who may have tracheomalacia, there may be a leak around the cuff despite high intra-cuff pressure

CAUSATIVE ORGANISMS

< 48 hours in hospital

  • often community organism

48 hours – 5 days:

  • community + hospital organisms

> 5 days

  • often hospital grown multi-resistant organisms (MROs) such as methicilin-resistant Staphylococcus aureus (MRSA) and Gram-negative bacilli (GNB):
    • Pseudomonas aeruginosa
    • Klebsiella
    • Enterobacter
    • Acinetobacter baumannii
    • Stenotrophomonas maltophilia

RISK FACTORS

  • See preventative measures below

ASSESSMENT

Clinical suspicion of VAP when:

  • new infiltrates are present on chest x-ray, and
  • at least one of the following is present:
    • Fever
    • leukocytosis
    • or purulent tracheo-bronchial secretion

INVESTIGATIONS

  • see diagnostic criteria below
  • microbiological sampling options:
  1. Lukens trap (deep suctioning via sterile catheter)
  2. bronchscopic protected catheter brush
  3. bronchoscopic alveolar lavage (BAL)
  • no conclusive evidence in favour of any approach, so a Lukens trap is commonly used because is practical

DIAGNOSTIC CRITERIA

Clinical

  • lung findings such as fremitus, dullness, bronchial breathing, crackles
  • purulent sputum
  • fever

Laboratory

  • inflammatory marker elevation
  • positive cultures (sputum or blood)
  • 4 fold increase in antibody titres
  • histopathology consistent with pneumonia

Radiological

  • infiltrate or consolidation consistent with pneumonia

MANAGEMENT

Empiric antibiotics initially (use local guidelines)

  • cover MDR organisms
  • stop antibiotics for VAP at 6-8 days (evidence that longer courses lead to colonisation with MROs)
  • treat Pseudomonas aeruginosa, Acinetobacter species or Stenotrophomonas maltophilia for 15 days

-> tazocin or timentin or cefepime
-> AND gentamicin to cover MDR organisms (use ciprofloxacin if age >65y, GFR <50 or recently on gentamicin)
-> if suspected MRSA add in vancomycin (pre-existing long-term lines, prior MRSA, in hospital > 7day or recent admission <3 months)
-> add teicoplanin if VRE colonized

-> if treatment fails:  cover MRSA with vancomycin or linezolid or teicoplanin + gram negatives with amikacin or tobramycin or colistin

Other

  • supportive care including a protective lung ventilation strategy
  • physiotherapy
  • sputum clearance

PROGNOSIS

  • VAP event adds 6 days to mean ICU LOS
  • overall attributable mortality is 13%, with higher rates for surgical patients (Melsen et al, 2013)

PREVENTION

Not all measures used have been proven to prevent VAP

Implementation

  • MDT approach with staff commitment (doctors, nurses, infectious diseases team, physiotherapy, management)
  • Recognition of the problem (determine VAP base rate in the unit)
  • Identify interventions that improve outcome
  • Educate staff (nursing education shown to decrease VAP incidence)
  • implement preventative strategy as a ‘bundle of care’ with ongoing education and reminders
  • audit and feedback results

Infrastructure and general measures

  • infection control: hand hygiene compliance, cross control of infection, surveillance, close communication
  • antibiotic cover: adequate cover to reduce risk of MDR organisms
  • good staffing levels: decreases cross contamination
  • environment: targeted environmental sampling, disinfection during outbreaks

Patient Care

Prevent colonization of the upper respiratory and gastrointestinal tract

  • good oral care (use 0.12-0.2% chlorhexidine twice daily with a sponge swab, brushing teeth)
  • Oropharyngeal decontamination or selective digestive decontamination (reduces VAP rate but generally not used due to concern over MDR organism selection)
  • Stress ulcer prophylaxis only when indicated (i.e. high risk: burns, traumatic brain or spinal cord injury, severe sepsis, coagulopathy and those receiving steroids equivalent of hydrocortisone > 250mg/day; or active peptic ulcer disease)
  • silver coated ETT shown to decrease the rate of VAP
  • probiotics (decreases VAP)

Prevent aspiration

  • Maintain the head of the bed at 30-45° unless contraindicated (decreases VAP)
  • Subglottic secretion drainage (SSD) (decreases VAP with NNT=11 if ventilated for more than 24-48h, but when combined with head up nursing no difference observed)
  • maintain ETT cuff pressures between 20-30 cmH2O, check q4h
  • No benefit from ultrathin or tapered cuff endotracheal tubes (Jaillette et al, 2017)
  • Consider early gastrostomy if indicated (may decrease microaspiration)

Minimize the duration of mechanical ventilation

  • Assess readiness for extubation daily
  • Optimize use of sedation and analgesia (avoid oversedation, decreases time on mechanical ventilation and thus VAP)
  • Early mobilization
  • Early tracheostomy (data controversial, only applicable to selected patients e.g. neurosurgical patients, high spinal patients)
  • Use NIV if appropriate (decreases VAP)

Endotracheal suction, humidification and care of the circuit

  • Endotracheal suction when airway secretions are present (closed and open suction with a single use catheter are equivalent)
  • Humidification and heating of the inspired gases (HME vs heated humifiers: data conflicting, considered equivalent if heated humidification with heating wire in the inspiratory or both limbs of the circuit is used to prevent condensation)
  • Avoid routine ventilator circuit change (frequent changes doesn’t change VAP rate)

Other

  • use blood conservation strategies (transfusion independently increases VAP)

References and Links

Journal articles

  • Coppadoro A, Bittner E, Berra L. Novel preventive strategies for ventilator-associated pneumonia. Crit Care. 2012 Dec 12;16(2):210. doi: 10.1186/cc11225. [pubmed]  [article]
  • Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. American Journal of Respiratory and Critical Care Medicine. 2005; 171(4):388-416. [pubmed] [article]
  • Guillamet CV, Kollef MH. Ventilator associated pneumonia in the ICU: where has it gone? Current opinion in pulmonary medicine. 2015; 21(3):226-31. [pubmed]
  • Jaillette E, Girault C, Brunin G, et al. Impact of tapered-cuff tracheal tube on microaspiration of gastric contents in intubated critically ill patients: a multicenter cluster-randomized cross-over controlled trial. Intensive care medicine. 2017; epublished [pubmed]
  • Melsen WG, Rovers MM, Groenwold RH. Attributable mortality of ventilator-associated pneumonia: a meta-analysis of individual patient data from randomised prevention studies. The Lancet. Infectious Diseases. 2013; 13(8):665-71. [pubmed]
  • Nair GB, Niederman MS. Ventilator-associated pneumonia: present understanding and ongoing debates. Intensive care medicine. 2015; 41(1):34-48. [pubmed]

FOAM and web resources


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health, a Clinical Adjunct Associate Professor at Monash University, and the Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Education Committee. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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