Ventilator-Associated Pneumonia

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Table of Contents

Introduction
Etiology
Pathology
References

Introduction

Ventilator Associated Pneumonia (VAP) is the infection of the lungs seen in patients within 2 days after intubation with an endotracheal tube or any other ventilator aid, for instance, the tracheostomy tube that was not there before. It has been regarded as the most common infection in the Intensive Care Unit (ICU) and also the most fatal (Wagh & Acharya, 2009).

Etiology

VAP is a nosocomial infection that is very common. Patients especially those in ICU are at high risk of acquiring VAP. The mechanical ventilators are inserted into the respiratory tree and therefore if contaminated, they can inoculate causative agents into the lower respiratory tract. The causative agents are those common in causing hospital acquired infections like pseudomonas aeruginosa, staphylococcus aureus, Haemophilus influenza, Klebsiella pneumonia and Escherichia coli. The strains of these bacteria are usually drug resistant this being a hospital setting. Infection may also be due to contaminated ventilator equipment and lack of hand washing or using the gloves on multiple patients thus transmitting the disease.

Risk factors include those which increase exposure to these agents or those which reduce host defense mechanisms like longer duration in hospital, mechanical ventilation for long hours, old age, low score in the Glasgow Coma Scale (GCS), other forms of pre-existing pulmonary infection or disease, immunosuppression and poor nutrition (Torpy, 2008).

The aetiology of ventilator associated pneumonia is affected by many factors including time of hospitalization, flora change due to hospital stress, flora change due to various medications including immunosuppressant drugs or antibiotics, presence and amount of nosocomial pathogens and other interventions of the patient (Wagh & Acharya, 2009).

Pathology

Pathogenesis

The pathogenesis of VAP involves destruction of the respiratory parenchyma by the colonies of bacteria that gain access to it through intubation of the ventilators. Infection by bacteria triggers an inflammatory response with infiltration by neutrophils at first and other inflammatory cells later. The inflammatory process is responsible for the purulent sputum seen in these patients. Early onset VAP is that which occurs within 48 hours of intubation and that which occurs after 48 hours, that is, late onset.

They arise from aspiration during the intubation process. Intubation reduces the cough reflex which is a primary defense mechanism; it impairs mucociliary escalator and damages the mucosal lining facilitating colonization by bacteria. Mucous secretion is increased in an attempt to trap the bacteria, further deteriorating the condition. Colonies of bacteria form in the upper respiratory or upper digestive tract, from where they are inoculated into the lower respiratory tract during intubation. Contaminated secretions may also be aspirated. The causative agents can also be the patient’s normal flora especially in gastric aspirations (Augustin, 2007).

Epidemiology

VAP occurs more commonly in patients who stay longer in hospitals and on those with invasive ventilation. Haemophilus influenza and streptococci are very common agents of VAP. Gram negative bacteria are seen when patients stay for prolonged periods on ventilator equipment. Mortality and morbidity are highest in patients with VAP caused by Pseudomonas aeruginosa. Anaerobic bacteria cause VAP following orotracheal intubation more commonly than following nasotracheal intubation.

Diagnosis

Any patient receiving ventilator support is at risk of VAP. Diagnosis may be based on observation of clinical features like fever, elevated white blood cell count, new or progressive infiltrations in the chest radiograph, and purulent sputum production. Chest radiographs may show other related features like atelectasis, pulmonary emboli, pulmonary infarction, pulmonary edema, gastric aspirations, alveolar hemorrhage and even Acute Respiratory Distress syndrome. These are non-specific features hence the need for more specific diagnostic criteria; bacteria culture being the most valuable.

Bronchoscopic methods and nonbrochoscopic techniques have been used in diagnosis. Nonbrochoscopic techniques include Bronchoalveolar Lavage (BAL), Mini-bronchoalveolar Lavage (mini-BAL), Blind Bronchial Sampling (BBS) and Protected Specimen Brush (PSB). The sensitivity of BBS is higher than PSP (Anon, 2007).

Attempts have been made to increase the speed and accuracy of diagnosis. Presence of microbes triggers the alveolar macrophages to release mediators such as tumor necrosis factor alpha (TNF alpha), interleukin-1β and other mediators, making them have diagnostic and prognostic values. Reference ranges for this have not been set and they may be non-specific, making them less valuable in diagnosis.

Several biomarkers have been studied in diagnosis. Elastin Fiber (EF) is released in cases of parenchymal destruction of the lung mucosa, thus it may be useful in differentiating infection, when EF levels are elevated from colonization when its levels are low. Low sensitivity of EF testing makes it less popular in diagnosis. Procalcitonin (PCT) has high sensitivity (87%) in VAP and high specificity (88%). C-reactive protein may also be useful.

BAL fluid may be tested for levels of Soluble Triggering Receptor Expressed on Myeloid cells (sTREM)-1 as this can be useful in differentiating bacterial from fungal infections. Levels of endotoxin in BAL can be invaluable, since it is elevated in patients with Gram-negative bacteria rather than Gram-positive. It can also differentiate colonization from infection of the pulmonary tissue. STREM, PCT and CRP are potentially useful in diagnosis. EF and endotoxin are less reliable (Rea-Neto et al., 2008).

Treatment

Being a bacterial infection, administration of antibiotics is the mainstay in treatment for VAP. Results from the culture sensitivity lab are important in choosing the type of antibiotic to use. VAP is acquired in hospitals, which means that most of the causative agents are Multi-Drug Resistant, and therefore antibiotics normally chosen are those with activity against Multi-Drug Resistance bacteria. VAP is a debilitating disease and it usually requires palliative care, intensive care with mechanical ventilator aid. The risk for Antibiotic resistant bacteria is increased if the patient was receiving antibiotics previously.

A combination of piperacillin, tazobactam and amikacin are commonly used in treatment. Studies have shown that a combination of cefepime and levofloxacin are more effective, but there are concerns about their use especially in patients with Acute Renal Failure (Ahmed et al., 2007).

Prevention

Prevention of VAP is achieved primarily by reducing the risk factors. Vaccination also is very valuable in prevention. People handling patients especially in ICU, nurses and doctors should play a major role in reducing the risk factors. They should aim at reducing bacterial colonization on the oro-pulmonary tracts by observing hygiene. Hand washing with soap and a lot of water is helpful immediately before attending to the patients. They should always wear gloves and avoid using them on multiple patients. This may be achieved by placing it on notice boards and doors in ICUs that they should observe these basic and cost-effective strategies. Protective attire should be worn especially when drug-resistant strains have been isolated in cultures.

Mechanical interventions can be used to reduce colonization in the mouth and upper part of the respiratory tree. These include effective and regular tooth brushing and thorough rinsing with clean water. The secretions can be suctioned using relevant equipment as this is invaluable in reducing colonization of bacteria.

Colonization in the oropharynx can also be decreased by applying pharmacologic interventions like use of chlorhexidine oral rinse twice daily. Other solutions have also been used e.g. colistin, vancomycin (especially where drug-resistant strains are suspected) and gentamicin. Stress ulcer prophylaxis can also be done to reduce bacterial colonization of the stomach since risk of aspiration is high in ICU patients.

Accumulated mucus can home many colonies of bacteria hence the need for aseptic methods when performing intubations. Saline lavage should be avoided since its risks outweigh the benefits. It transports bacteria from the endotracheal tubes to the lower airways and has been shown to increase the incidence of VAP. Prophylactic administration of antibiotics does not reduce the incidence of VAP and it should be avoided because it leads to development of the drug-resistant strains.

Turning patients every 1 hour or so has been shown to reduce the incidence of VAP. Special beds are available for this purpose but are not cost-effective in most clinical settings. These methods act by increasing drainage of the lungs. Infection from contaminated ventilator circuits or those with bacterial colonies can be minimized by changing them frequently and cleaning them thoroughly. VAP caused by aspiration can be minimized by monitoring and preventing incidences of weaning or extubation.

Aspiration can also be prevented by elevating the head of the patient up to about 35° and also facilitating gastric emptying. Thorough suctioning of the upper respiratory tract is very useful in decreasing the risk of aspiration. Cuff pressure should be high to reduce aspiration of secretions. There are various studies underway to investigate the possibility and cost effectiveness in using endotracheal tubes that are coated with silver nitrate as this has been shown to reduce colonization in other animals (Augustin, 2007).

References

Ahmed et al. (2007). Treatment of ventilator-associated pneumonia with piperacillin-tazobactum and amikacin vs cefepime and levofloxacin: A randomized prospective study. Web.

Anon. (2007). Ventilator Associated Pneumonia. Web.

Augustin, B. (2007). Ventilator-Associated Pneumonia. Web.

Rea-Neto et al. (2008). Diagnosis of ventilator-associated pneumonia: a systematic review of the literature. Web.

Torpy, J. (2008). Ventilator-Associated Pneumonia. Web.

Wagh, H and Acharya, D. (2009). Ventilator Associated Pneumonia – an Overview. Bjmp. Web.

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