8.6 Ventilatory Associated Pneumonia Flashcards
What do you understand by the term ventilator associated pneumonia (VAP)?
The definition of VAP is the most subjective of the common device-related
healthcare-associated infections.
The National Institute of Clinical Excellence (NICE) 2008 defines VAP as the
nosocomial pneumonia that develops 48 hours or more after mechanical
ventilation given by means of endotracheal tube or tracheostomy.
The American Thoracic Society refers to VAP as pneumonia that arises more
than 48–72 hours after endotracheal intubation.
It is the most common nosocomial infection encountered in the intensive
care unit (ICU), ranging from 9%–28% of all mechanically ventilated patients
with the peak incidence occurring around day 5 of ventilation.
Mortality ranges from 24% to 50% and depends on the pathogen and underlying
clinical condition of the patient.
What are some other types of pneumonias?
- Hospital-acquired pneumonia (HAP),
or nosocomial pneumonia, develops
after 48 hours or more after admission to a hospital.
Hospitalised patients may have many risk factors for pneumonia,
including mechanical ventilation,
malnutrition,
underlying comorbidities,
and immune disturbances.
The microorganisms responsible include
Methicillin Resistant Staphylococcus Aureus (MRSA),
Pseudomonas, Enterobacter, and Serratia.
- Healthcare-associated pneumonia is the pneumonia that occurs in
patients who are hospitalised for at least 2 days in the past 90 days, or
are residents of a nursing home or treated with IV antibiotics, received
chemotherapy in the last 30 days or haemofiltration in any setting. - Community-acquired pneumonia is defined by the British Thoracic
Society as comprising symptoms of acute lower respiratory tract illness
with new focal chest signs, at least one systemic feature such as fever,
sweating, or a temperature > 38°C, and no other explanation for the
illness.
Streptococcus pneumoniae is the most common cause of
community-acquired pneumonia worldwide. - Atypical pneumonia is the pneumonia caused by certain pathogens such
as Legionella, Mycoplasma, and Chlamydia.
The clinical and radiological features are usually different from commonly occurring pneumonias.
- Aspiration pneumonia is the inhalation of either oropharyngeal or gastric
contents into the lower airways.
The resulting lung inflammation is not an infection,
but if the aspirated material contains anaerobic bacteria,
it can contribute to infection. - Opportunistic pneumonia includes those that affect immunocompromised
individuals.
Main pathogens are Cytomegalovirus, Pneumocystis jiroveci, Mycobacterium avium-intracellulare, and Candida.
What are the clinical and radiological features of VAP?
Accurate diagnosis is usually difficult, and a high index of suspicion is
needed.
Empirical antibiotic therapy with broad-spectrum antibiotics is
started early after appropriate cultures are taken.
The diagnostic criteria include:
a) Clinical:
Chest infection with signs such as fever,
purulent aspirations,
and leucocytosis.
b) Microbiological:
bacteriological evidence of pulmonary infection.
c) Radiological:
X-ray evidence of lung infection—
new or progressive pulmonary infiltrates.
Diagnostic Scoring system
The Clinical Pulmonary Infection Score (CPIS)
has been devised to increase the accuracy of diagnosis.
The CPIS takes into account
- clinical
(temperature, presence of tracheal secretions), - physiological
leucocytosis and worsening gas exchange), - microbiological (positive culture of tracheal aspirate),
- radiographic evidence to assign a numerical value.
Scores can range from 0 to 12
with a score of ≥ 6 showing
good correlation with the presence of VAP
although both the sensitivity (77%) and specificity (42%)
of the score is low.
The appearance of new infiltrates on CXR
plus two or more signs of pulmonary infection,
such as new purulent secretions,
worsening gas exchange, leucocytosis, or pyrexia,
increases the likelihood of VAP.
What are the common pathogens associated with VAP?
Mainly caused by gram-negative organisms,
but gram-positive bacteria such
as MRSA are not uncommon.
Typically, bacteria causing early onset VAP include
Streptococcus pneumoniae,
Haemophilus influenzae,
methicillin-sensitive Staphylococcus aureus (MSSA),
Gram-negative bacilli,
Escherichia coli,
Klebsiella pneumonia,
Enterobacter and Proteus species,
Serratia marcescens.
Culprits of late VAP are drug-resistant organisms such as
MRSA,
Acinetobacter,
Pseudomonas aeruginosa,
extended-spectrum beta-lactamase producing bacteria (ESBL).
What are the risk factors for VAP?
Patient factors:
advanced age,
low serum albumin,
ARDS, COPD
other lung diseases,
impaired consciousness,
trauma and burns,
multiple organ failure,
large volume gastric aspirates,
upper respiratory tract colonisation.
Interventional factors:
Interventional factors
Interventional factors:
prolonged ventilation,
level of sedation,
use of neuromuscular blocking agents,
antacids,
proton pump inhibitors (PPI) and
H2 blockers, nasogastric tube, supine position, frequent circuit changes, and
transfer outside ICU.
What is the pathological process of VAP?
It is thought to be caused by entry of infected secretions into distal bronchi.
Patients are usually immunosuppressed,
their oropharynx becomes colonised with organisms,
especially gram-negative bacteria. oral and nasal
tubes cause trauma, leading to infections such as sinusitis.
The natural protections like cough reflex, tracheobronchial secretions,
mucociliary linings, saliva, and nasal mucosa are less effective in these
patients.
The pathogens enter the lower lung through mechanical routes such as
around the endotracheal tube cuff, suction catheter, and ventilation tubings.
How do you prevent VAP?
General measures:
Use of sterile equipment,
regular hand washing,
using barrier nursing such as gloves and an apron,
minimal contact with patient usually
reduce the incidence of any infection in ICU.
Specific measures:
This include reducing the load of pathogens and their
entry into lower respiratory tract
- Reducing aero-digestive colonisation
- Reducing aspiration
- Reducing aero-digestive colonisation
° oral decontamination using topical antiseptics such as chlorhexidine
mouthwash
° Selective decontamination of digestive tract (SDD) using
nonabsorbable antimicrobials such as polymyxin E and amphotericin
B has been tried with variable success.
Although studies suggest that SDD is effective in reducing the incidence of VAP, this intervention is not commonly used in the UK because of fears of encouraging
Clostridium difficile, antimicrobial resistance, and the emergence of
multi-drug resistant pathogens.
- Reducing aspiration
° Nursing the patient in semi-recumbent position
is crucial and proven to
reduce VAP significantly.
° Colonisation and leak around the tracheal cuff is a cause for
migration of pathogens to lungs.
Secretions should be cleared from top of the cuff regularly
by subglottic suctioning, and cuff pressures
are maintained at acceptable levels (> 20 cms H2o)
to prevent micro-aspiration.
Minimising duration of ventilation
Minimising duration of ventilation
° This is achieved by early tracheostomy,
which has proven to lower the incidence of VAP.
Periodic ‘sedative interruptions’ and daily
assessment of readiness to extubate
may reduce the duration of
mechanical ventilation.
- Choice of drugs to change pH of gastric contents
° Reducing the acidity of stomach in stress ulcer prophylaxis is claimed
to increase the incidence of VAP by increasing the proliferation of
gram-negative bacteria. Use of H2 blockers or sucralfate, instead of
PPIs, are suggested to reduce the risk.
° Enteral feeding can increase the risk of VAP by altering the gastric
acidity and risk of aspiration, but benefits of enteral feeding usually
outweigh this small risk.
