The Ventilator Associated Pneumonia - Research Paper Example

Ventilator Associated Pneumonia affiliation Background: Ventilator-associated pneumonia is the cause of morbidity and mortality in mechanically ventilated patients who have been in the Intensive Care Unit. Aims and objectives: To identify ways in which VAP can be diagnosed, treated, prevented and also its predisposing risk factors. Diagnosis has proven to be a hard task and prevention is the most suitable way of eliminating VAP. Prevention helps in reducing mortality rate, hospital cost and duration of stay in the hospital. Ways of prevention include maintaining good oral care and head elevation by 30 degrees. Treatment of VAP is by use of antibiotics. Keywords: Ventilator-associated pneumonia, mechanical ventilation, endotracheal intubation Introduction Ventilator associated pneumonia (VAP) is one of the main cause of nosocomial and acquired healthcare infections acquired by adults and children in coronary care and intensive care units. VAP has a mortality rate of 25 to 50%. According to National Nosocomial Infection Surveillance System, ventilator associated pneumonia is defined as pneumonia in a patient endotracheal or tracheostomy intubation and mechanical ventilation within 48 hours before the onset of the event (Saramma, Krishnakumar, Dash, & Sarma, 2011). Endotracheal intubation and mechanical ventilation increases the risk of bacterial pulmonary infection because the invasive endotracheal tube allows entry of bacteria into the lower respiratory tract since the tube is located in the trachea. Bacterial colonization in the respiratory tract is facilitated by absence of the cough reflex and excessive mucus secretions in the mechanically ventilated patients. The important pathogenic mechanisms in ventilator associated pneumonia are pharyngeal colonization, micro aspiration and exogenously acquired pathogens (Sherpa, Chakrabarty, DSouza, & Muralidhar, 2014). Ventilated-associated pneumonia can be acquired by aspiration. Aspiration is promoted by supine position and upper airway and nasogastric tube placement. Aspiration occurs outside the endotracheal tube. Aspiration is common among patients with abnormal swallowing, impaired gag reflexes, compromised consciousness due to medication or anaesthesia, delayed gastric emptying or decreased gastric motility (Choudhuri, 2013). Incidence of VAP varies in patients depending on type of hospital, study population and levels of antibiotic exposure. Age and severity of underlying diseases are associated with developing VAP. History of antibiotic exposure and duration of mechanical ventilation are also involved. VAP is a major cause of morbidity, prolonged ICU hospitalization, extended mechanical ventilation and increased costs of hospitalization (Lahoorpour, Delpisheh, & Afkhamzadeh, 2013). Etiology of VAP Studies form as early as 1972 have shown that the airway of mechanically ventilated patients quickly becomes colonised with gram-negative organisms. The primary route of VAP pathogenesis is ac combination of bacterial colonization of the aero digestive tract and the subsequent aspiration into the lower airway (Van Hooser, 2012). If VAP infection occurs within 48-72 hours, it is referred to as early onset and is caused by Staphylococcus aureus (gram positive), Haemophilus infuenzae (gram negative) and Streptococcus pneumoniae (gram negative). These are antibiotic strains present in the ICU. Early onset of VAP is usually less severe associated with a better prognosis and caused by antibiotic sensitive bacteria. Methicillin Resistant Staphylococcus aureus, Pseudomonas aeruginosa and Acinetobacter which are multidrug resistant pathogens cause late onset VAP which occurs after two hours. Late onset VAP is associated with increased mortality and morbidity. Other common pathogens causing VAP include aerobic gram negative rods such as Klebsiella pneumoniae and Escherichia coli (Rit, Chakraborty, Saha, & Majumder, 2014). These gram negative bacilli in the nosocomial pneumonia reach the lower airway through aspiration of gastric contents or of upper airway secretions. Oropharyngeal colonization with gram negative bacilli is unusual in healthy, non-hospitalized individuals. The propensity for colonization of upper airway directly correlates with the severity of the illness. There are several factors that contribute to high rates of VAP in ICU patients. The ICUs have high vulnerable patients who have predisposing lung conditions that compromise with their defence mechanisms in their airways. Aetiological agents differ according to population of the patients in the Intensive Care Unit, duration of hospital stay and prior antimicrobial therapy. Defence mechanisms of the respiratory tract may be overwhelmed despite their function to prevent and eradicate pathogens into the lungs (Choudhuri, 2013). In order for VAP to develop, micro-organisms must gain access to the normally sterile lower part of the respiratory tract. Patients who are critically ill have depressed level of consciousness and impaired gag reflex which may lead to pooling of approximately 100 to 150 ml of contaminated-secretions within a 24 hour period therefore are at a higher risk of infections. The body’s natural defence against infection is impeded by placement of an endotracheal tube by negating effective cough reflexes and mucocilliary clearance of secretions. Impairment of the cough reflex, accumulation of contaminated secretions within the oropharynx and placement of an endotracheal tube increase the risk for VAP in critically ill patients (Sedwick, Lance-Smith, Reeder, & Nardi, 2012). Risk factors The endotracheal tube is the largest risk factor for VAP. The tube prevents cough, upper airway filtering and upper airway humidification. The endotracheal tube inhibits cilliary transport by the epithelium and epiglottic and upper airway reflexes (Van Hooser, 2012). Independent risk factors associated with VAP include mechanical ventilation, antibiotic exposure, duration of hospitalization were associated with acquisition of VAP (Lahoorpour, Delpisheh, & Afkhamzadeh, 2013). Patient risk factors include age if they are over 65 years, underlying chronic illness such as Chronic Obstructive Pulmonary Disease, immunosuppression, depressed consciousness, thoracic or abdominal surgery, previous antibiotic therapy and previous pneumonia or remote infection (Van Hooser, 2012). Signs and symptoms Patients with VAP will have chest X-ray showing new progressive and persistent diffuse infiltrate which may not attributed to another disease appearing on chest radiographs. Onset of purulent tracheobronchial sputum will be observed. Patients will also have a fever greater 38.5oC (101oF), leucocytosis of 10,000\mm3 or more and positive sputum and blood cultures (Van Hooser, 2012). Diagnosis Early diagnosis of VAP is difficult because of many conditions common to ICU patients like sepsis, acute respiratory distress syndrome (ARDS) or pulmonary atelectasis. Diagnosis of VAP is based on systemic signs of infection, new or worsening infiltrates seen on chest X-ray and bacteriological evidence of pulmonary parenchymal infection (Choudhuri, 2013). Ventilator associated pneumonia was considered when its onset occurred after 48 hours and patients after 48 hours of mechanical ventilation and diagnosed when patients showed signs and symptoms for the condition. In cases of clinically suspected pneumonia endotracheal aspirate was performed early in the morning and diagnosis of VAP was established with positive quantitative culture. Prevention of VAP Staff education, colonization reduction and aspiration avoidance are three basic principles that can be used to prevent ventricular associated pneumonia. In order to reduce VAP in ICUs, education and reinforcement is required to change the behaviour of health practitioners (Van Hooser, 2012). Study done by (Sherpa, Chakrabarty, DSouza, & Muralidhar, 2014) among critical care providers of ICU’s in Kasturba Hospital Manipal, Udupi District, Karnataka indicated a high proportion had inadequate knowledge and there is a need to impart training to the ICU care providers about VAP for its prevention. VAP can be prevented by avoiding intubation and invasive mechanical ventilation in patients without contraindications. Hemodynamically stable patients with respiratory failure should be offered non-invasive positive pressure ventilation. The patients should be cooperative, have a reserve, are not facing impending respiratory arrest and do not have contraindications like excessive secretions, facial injury or claustrophobia. In absence of non-invasive ventilators, regular ventilators can be used to provide no-invasive ventilation with appropriate facial interface. These patients need to be monitored closely and placed on invasive mechanical ventilation on early signs of worsening (Saydin, 2014). Colonized secretions reside in both the gastrointestinal tract and oropharynx. The 2004 US Centres for Disease Control and Prevention (CDC) guidelines for prevention of VAP by educating workers in health epidemiology and VAP control procedures. The guidelines advice the thorough cleaning of all ventilator and circuit equipment, contaminated hands should be washed frequently and thoroughly with water and soap or an alcoholic antiseptic solution to reduce colonization. Gloves and gowns are effective in preventing nosocomial spread of antibiotic resistant bacteria. When clinical conditions cease, it is advisable to remove to remove endotracheal tubes and tracheostomy tubes. Poor oral hygiene in patients undergoing mechanical ventilation is associated with secondary colonization of the respiratory tract leading to development of pneumonia. Proper hygiene will reduce VAP therefore reduce mortality in the ICU. Microbes colonising the mouth Removal of endotracheal secretions is a primary step in preventing VAP and can be carried out continuously or at scheduled intervals. Pathogens linked to VAP in orally intubated patients become colonised in dental plaque and in the oral mucosa. Within 48 hours of admission to an ICU, patients have changes in the oral flora which gram-negative and other virulent organisms. Dental plaque provide an environment for respiratory pathogens such as methicillin resistant Staphylococcus aureus and Pseudomonas aeruginosa. Periodic aspiration of secretions after installation of isotonic saline seems to reduce VAP incidence in patients with tracheotomies (Di Filippo, Casini, & De Gaudio, 2011). To avoid aspiration, a semi-recumbent body position reduces aspiration in the lower airways compared to a supine position. Deeply sedated and relaxed patients are at a higher risk of aspiration therefore relaxation and paralytic medication should be avoided (Choudhuri, 2013). Elevation of the head of the bed to 30 degrees is highly recommended as a preventive strategy that lowers the risk of aspiration. Semi-recumbent position is low cost and effective (Van Hooser, 2012). The endotracheal tube prevents glottis closure therefore the patient is unable to cough and remove secretions in a natural way. However, accumulation or pooling of oropharyngeal secretions above the endotracheal tube cuff occurs and then these fluids can be aspirated. Removal of these secretions by suction can reduce risk of aspiration and may be cost effective and safe intervention. Cuffed endotracheal tubes are essential in adults when positive pressure ventilation is used. The correct pressure within the cuff is to prevent aspiration around the cuff yet maintain ventilation and adequate capillary perfusion of the contacted mucosa. Pathogenic laden secretions are able to migrate between the cuff and tracheal wall through minute channels which may be created when the pressure drops and the cuff is manipulated, It is advisable that the cuff pressure should be recorded regularly. When the tube is repositioned, oral care and subglottic suction should be performed to reduce disruption and aspiration of colonized bacteria (Van Hooser, 2012). When gastric feeding tubes are placed, the gastroesophageal sphincter is violated which can cause or contribute to reflux. The tube can provide a route for microbial access and colonisation. Delivering feeding solution through percutaneous enteral gastric tube reduces gastroesophageal regurgitation, increases nutrient delivery, provides a shorter feeding time and most important lowers the VAP rate. Continuous feeding is tolerated by the patient better than bolus feeding since it keeps the stomach from becoming over distended and preserve peptic acidity at levels lethal to bacteria (Van Hooser, 2012). Patients receiving mechanical ventilator support are susceptible to gastrointestinal haemorrhage. Prophylactic agents such as antacids and histamine type 2 antagonists are often used protectively reduce peptic acidity. In this changed pH environment, the stomach may be colonized with pathogenic bacteria. As the gastric volume is increased, micro aspiration may occur at any time (Van Hooser, 2012). Treatment Antibiotics should be initiated as soon as VAP has been diagnosed. Appropriate material for cultures should be obtained prior to initiation of antibiotics. A broad spectrum of antibiotics are started based on the clinical presentations and institutional patterns of bacterial sensitivity and resistance. Delays in administering of antibiotics leads to increased mortality. After culture results are available and patients are stabilised, antibiotic therapy needs to be de-escalated and tailored to the clinical scenario (Saydin, 2014). Detection of causative organisms and their antibiotic susceptibility is crucial for diagnosis of VAP in order to initiate the appropriate antibiotic treatment therefore reducing the adverse effects of inadequate antibiotic treatment on the patient prognosis (Goel, Hogade, & Karadesai, 2012). Routine use of prolonged courses of antibiotics not supported by the results of microbial cultures should be discouraged to minimise the risk of subsequent antibiotic resistant infections. Elimination of unnecessary antibiotic administration for a prolonged period can reverse the trend of increasing antibiotic resistance among hospital-acquired infections. The use of aerosolized antibiotics has also been discouraged because of inefficacy and propensity for the emergence of antibiotic resistant infections. Routine use of selective digestive tract decontamination does not have any demonstrated effect mortality, emergency of antibiotic resistance infections and additional toxicity (Choudhuri, 2013). References Choudhuri, A. H. (2013). Ventilator-Associated Pneumonia: When to hold breath? International Journal of Critical Illness and Injury Science, 169-174. Di Filippo, A., Casini, A., & De Gaudio, A. R. (2011). Infection prevention in the intensive care unit: Review of the recent literature on the management of invasive devices. Scandinavian Journal of Infectious Diseases, 243-250. Goel, V., Hogade, S. A., & Karadesai, S. G. (2012). Ventilstor associated pneumonia in a medical intensive care unit: Microbial aetiology, susceptibility patterns of isolatedmicro-organisms and outcome. Indian Journal of Anaesthesia, 558-562. Lahoorpour, F., Delpisheh, A., & Afkhamzadeh, A. (2013). Risk factors foracquisition of ventilator-associated pneumonia in adult intensive care units. Pakistan Journal of Medical Sciences, 1105-1107. Rit, K., Chakraborty, B., Saha, R., & Majumder, U. (2014). Ventilator associated pneumonia in a tertiary care hospital in India: Incidence, etiology, risk factors, role of multidrug resistant pathogens. International Journal of Medicine and Public Health, 51-60. Saramma, P. P., Krishnakumar, K., Dash, P. K., & Sarma, P. S. (2011). Alcohol-based hand rub and ventilation-associated pneumonia after elective neurosurgery: An interventional study. Indian Journal of Critical Care Medicine , 203-208. Saydin, G. (2014). Ventilator-associated pneumonia in advanced lung disease: A wakeup call. Lung India, 1-4. Sedwick, M. B., Lance-Smith, M., Reeder, S. J., & Nardi, J. (2012). Using Evidence-Practice to Prevent Ventilator-Associated Pneumonia. American Association of Critical-Care Nurses, 41-50. Sherpa, P. C., Chakrabarty, J., DSouza, P. J., & Muralidhar, V. (2014). Knowledge of Critical Care Provider on Prevention of Ventilator Associated Pneumonia. Journal of Krishna Institute of Medical Sciences University, 80-84. Van Hooser, T. D. (2012). Ventilator Asociated Pneumonia (VAP): Best Practice Strategies for Caregivers. Kimberly-Clark Health Care, 1-20. Read More