Ventilator Associated Pneumonia

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  Ventilator Associated Pneumonia
  Dr Swapnil Pawar

Ventilator-associated Pneumonia

Blog Written by Dr Jose Chacko

CDC definitions

Ventilator-associated event (VAE)

Ventilator-associated condition (VAC): increase in daily minimum PEEP ≥ 3 cm H2O or FiO₂ ≥ 0.20 sustained for at least 2 calendar days following a baseline period (2 calendar days) of stability or improvement

Infection-related ventilator-associated complication (IVAC): Altered leukocyte count (≥ 12,000 cells/mm3 or ≤ 4000 cells/mm3) and/or temperature (> 38 °C or < 36 °C), a new antimicrobial prescription has been started and sustained for at least 4 calendar days

Possible or probable VAP: Above plus microbiological confirmation of a lower respiratory tract infection,

After the first 48 hours

Early: Days 1–4

Late: Day 5 and later

Peak: days 5–9

Incidence

The discrepancy between reports from the US and Europe (1–2.5 vs. 18.5 per 1000 ventilator days)

Differences in definition, diagnostic criteria, sampling techniques, type of intensive therapy unit (ITU), and patient population

Incidence varies depending on the underlying disorder – high in cancer, TBI, COPD, ARDS

Age does not correlate

Higher incidence in males

Outcomes

Prolongs duration of ventilation and hospitalization

Unclear whether there is attributable mortality (1% on day 30 and 1.5% on day 60)

Based on data from 58 RCTs, attributable mortality was 9%

Micro-organisms

Duration of mechanical ventilation

Length of hospital and ICU stay

Timing and cumulative exposure to antimicrobials

The local microbial ecology

Other ICU-dependent factors

Gram negative: Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, and Acinetobacter species

Late onset more likely to be MDR; it may occur with prior exposure to antibiotics

Resistance to third- and fourth generation cephalosporins in Enterobacteriaceae strains due to the expression of acquired extended-spectrum β-lactamases (ESBLs) and/ or AmpC β-lactamases is a major concern

Carbapenemase producing strains

Colistin resistance

Diagnosis

Clinical suspicion

Radiographic infiltrates

Microbiological confirmation

CPIS criteria (Pugin et al.): temperature, blood leukocytes, tracheal secretions aspect, oxygenation, radiographic infiltrates, and semi- quantitative cultures of tracheal aspirates with Gram stain

More recent: at least 2 of new onset of fever, purulent endotracheal secretions, leukocytosis or leucopenia, increase in minute ventilation, decline in oxygenation, and/or increased need for vasopressors to maintain blood pressure. However, these findings may exist in non-infective etiology

Poor sensitivity of plain chest radiographs

Biomarker generally non-beneficial

Microbiological diagnosis

Distal tracheal secretions

Gram stain has limited sensitivity and specificity

BAL vs. tracheal aspirate – overdiagnosis with tracheal aspirate alone and unnecessary antibiotic use

Meta-analysis of 5 RCTs did not show the difference in outcomes between quantitative cultures vs. non-invasive techniques

When to commence antibiotics?

General recommendation to withhold if clinically stable; however, has to be based on clinical judgment

If cultures are negative, or antibiotics are administered prior to culture, reassess after 48-72 hours whether antibiotics need to continue

Stop antibiotics based on procalcitonin levels: if the procalcitonin level is <0.5 ng/mL or has decreased more than 80% from baseline levels

Future: molecular methods – PCR. May be oversensitive

VAP prevention

Oral chlorhexidine: may be harmful

Stress ulcer prophylaxis: may be harmful

Oral and digestive decontamination: not useful in ICUs with a high level of antimicrobial resistance

Modified cuff: not useful

Routine cuff pressure monitoring: not useful

Subglottic secretion drainage: lower rates of VAP; does not shorten the time to extubation, reduce ICU length-of-stay, prevent ventilator-associated events, or reduce lower mortality rates

Head-up position: may be useful

Shorten the duration of ventilation

VAP treatment

Empirical treatment: severity of the underlying illness, risk factors for MDR pathogens, and the local resistance patterns

Septic shock at VAP onset, ARDS prior to VAP onset, acute renal replacement therapy prior to VAP

Non-immunocompromised, early-onset: third-generation cephalosporin

In other situations, initial empiric treatment should include a broad-spectrum β-lactam targeting Pseudomonas aeuroginosa and/ or ESBL-producing Enterobacteriaceae. We use betalactam – betalactamase inhibitor (Pip-taz) or carbapenem

We have a high incidence of ESBL-producing Enterobacteriaceae hence carbapenem is often used as the first line

Ceftazidime-avibactam: carbapenem-resistant Enterobacteriaceae or XDR Pseudomonas aeruginosa. Effective against extended-spectrum β-lactamase, AmpC-, Klebsiella pneumoniae carbapenemase- and OXA-48-producing Enterobacteriaceae and drug-resistant Pseudomonas aeruginosa isolates; it is not active against metallo-β-lactamase-producing strains.

MRSA cover if incidence is common

Importance of de-escalation; switch to monotherapy, reduce the duration of treatment

7 days is enough for most patients – robust evidence

Nebulized antibiotics: generally, not effective. Not effective if there is bacteremia. Repeated nebulization may prolong the duration of ventilation.

Restrict patients with VAP to XDR-Gram-negative pathogens susceptible only to colistin or aminoglycosides

XDR: non-susceptibility to at least one agent in all but two or fewer antimicrobial categories

Summary –

Awareness of VAP in ICU is important.

VAP prevention bundles should be implemented in each ICU.

Minimising the duration of mechanical ventilation and early extubation when feasible is the key to preventing VAP.

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