Ventilator associated pneumonia (VAP) is defined as a pneumonia that develops 48-72 hours or greater after endotracheal intubation. It is a subgroup of nosocomial/hospital acquired pneumonia. It is characterised by:
Signs of systemic infection
Changes in sputum characteristics
Detection of a causative organism
There is no gold standard diagnostic tool, and the varying standards of definition affect its incidence.
It is a common complication of mechanical ventilation, affecting around 20-25% of patients ventilated for over 48h. The highest risk appears to be within the first 5 days of ventilation, with risk actually decreasing slightly later on. The mortality rate for VAP varies significantly due to the impact of the underlying disease, but is quoted at between 33-50%.
The development of a VAP is a complex pathophysiological process. There is an interplay between a number of factors:
It is the presence of the ETT that is the major factor. This impairs many of the important normal defences against respiratory tract pathogen, particularly the cough reflex, and impairment of the normal ciliary action. Despite the presence of the cuff, there are still microaspirations occuring around the cuff, allowing organisms to enter the respiratory tract. Some pathogens may develop a biofilm on the ETT itself. Pathogens may also be transmitted to the lower respiratory tract by the suction catheter.
Many pathogens can develop and propagate in the upper airway areas (oropharynx, nasopharynx) or in the upper digestive tract. In critically ill patients, normal flora can be replaced by more problematic pathogens. This pathogenic material can enter the respiratory tract through secretions, and via the mechanical actions of ventilation itself.
The host also plays an important role in the development of VAP. The presence of risk factors will increase the likelihood of development and includes: acute medical pathology, surgery, antibiotic exposure. Critically ill patients often exhibit a degree of relative immunosuppression which appears to contribute to the development of a VAP. Independent risk factors for VAP include:
Male (OR 1.58)
Trauma admission (OR 1.75)
Intermediate underlying disease severity
The most likely pathogens are associated with the timing of the infection:
Early (<4 days) - community pathogens
Late (>4 days) - hospital pathogens, with increased drug resistance.
Before 48 hours, the pathogens are likely to be the same as those causing CAP. Between 2 and 5 days, there could be a mix of community and hospital pathogens. Infections beyond 5 days are more likely to be hospital pathogens. A history of recent ‘healthcare exposure’, also increases the likelihood of the pathogen being more nosocomial in nature.
Gram negative bacilli
Staph. Aureus (20%) - majority MSSA
Enterobacteriaceae (15%) - E. coli, klebsiella, proteus, enterobacter sp.
Streptococcus sp. (10%)
Haemophilus sp. (10%)
Acinetobacter sp. (8%)
Viral and fungal causes are rare. Infections are commonly due to multiple pathogens.
MRSA is increasingly rare as a pathogen, probably due to the impact of infection control measures and the subsequent reduction in colonisation and contamination rates. Pseudomonas is a problem in terms of antibiotic resistance. A lot of these will have specific local resistance patterns.
As patients will be ventilated (or recently extubated) on the critical care unit, a high index of suspicion is needed to detect the changes associated with a VAP. The majority of the assessment will be part of the detailed daily review of an ICU patient e.g. full systematic examination.
A VAP should be considered when there is:
New radiographic changes
Increase in sputum purulence
Increasing WBC count
The clinical findings on examination will be essentially the same as for CAP:
Reduced air entry
A full set of blood tests will commonly be performed due to the critical care setting:
FBC - assessing trends in WBC
Inflammatory markers - CRP, procalcitonin
Peripheral blood cultures
CXR - may show radiological changes of consolidation. Lung ultrasound may have a role in identifying consolidation.
Microbiological sampling of the lower respiratory tract is recommended. Options include:
Endotracheal suctioning with Luken trap
Protected specimen brush
Bronchoalveolar lavage (BAL)
Mini-BAL (blind BAL)
There is no clearly demonstrated difference between these approaches so sterile endotracheal suctioning is commonly employed due to its relative ease. Samples are sent for gram stain and culture. These can be provided as semi-quantitative results which can provide some useful information on the significance of any growth (usually mainly for bronchial washings). Qualitative reporting may be used in more simple collection e.g. tracheal aspirates.
Some organisations performed non-directed BALs routinely on intubated patients. This can provide useful advanced information on potential organisms ahead of any potential deterioration.
This remains challenging, due to the difficulty in differentiating a VAP from the other (often adverse) changes of critical illness and being ventilated. As such, clinical assessment has been shown to have poor specificity and sensitivity, as have a number of assessment tools.
Some institutions use an initial score based on commonly available results (temp, WBC, secretions) to determine when chest radiography should be performed.
CXR signs show a fairly low correlation with VAP, as there are a number of overlapping causes for these found in this patient cohort. However, the absence of radiographic changes has a degree of negative predictive value.
Antibiotic therapy is the appropriate treatment. This will clearly be guided by the most likely pathogens (if no culture results) or targeting the specific pathogen if results are available. In terms of empirical treatment, this will therefore be affected by whether the VAP is early or late, and so the likelihood of responsible pathogens. Local antibiotic policy will provide the best guidance on this, as it will take into account the common local bacteria strains and resistance patterns (but also factors such as cost, familiarity and availability of agents, sensitivity testing that is carried out).
Strong consideration is frequently given to the presence of multi-drug resistant strains, particular in late VAP. Combination therapy may be needed in these cases. Risk factors for this include:
Recent IV antibiotics (within past 90 days) - OR about 12
ARDS preceding VAP
RRT prior to onset
An example regime may be tazocin plus gentamicin. Vancomycin will be considered in cases where MRSA is considered.
Narrowing antimicrobial therapy early is important for patients in critical illness, because of the adverse effects of broad spectrum therapy. This is in terms of both patient benefits (protecting normal flora) and organisational (avoiding resistance).
A 7 day course in usually as effective as a longer course unless there are cases of complications e.g. empyema. Oral step down should be considered when able.
Given the significant impact of VAP, even when promptly treated, prevention is an important goal. A number of interventions have been described, aiming to tackle some of the factors linked to the pathophysiology. Not all of these have a strong evidence base, but they are often incorporated into VAP bundles to try and accumulate any benefits.
The strategies can be broken down into a number of goals:
Prevent colonisation of upper airway/GI tract
Good oral hygiene - chlorhexidine washing
Stress ulcer prophylaxis
Silver/antibiotic coated tubes
Oropharyngeal tube vs nasopharyngeal
Selective gut decontamination
Semirecumbent position - head up 30-45 degrees
Maintain ETT cuff pressure 20-30 mmHg (check 4 hourly)
Use of subglottic suction tubes (NNT 11)
Consideration of small bowel vs gastric feeding
Polyurethane cuffed ETT
Humidification of circuit - preference for HME over warmed
Avoid routine circuit changes
Minimise ventilation duration
Daily sedation holds/holidays
Daily assessment of suitability for extubation
Increased role of NIV
Early tracheostomy (data conflicting)
There are also a number of institutional interventions to help: