Introduction
Ventilator-associated pneumonia (VAP) is a lung disease that develops in a critically ill patient who is on a ventilator. Notably, a ventilator is a machine used to help the patient breathe by providing oxygen using a tube put on the patient’s mouth. More significantly, VAP is among the most commonly encountered hospital-acquired diseases that occur in critical care settings and can be connected to different adverse clinical results. According to the United States Center for Disease Control and Prevention, this kind of infection occurs approximately 48 hours after the commencement of mechanical ventilation (Hanifi et al., 2017). Understandably, VAP can be linked to the increased intake of antibiotics, increase in the rate of multidrug-resistant infections, increase in the time stayed in ICU, and increased mechanical ventilation period, as well as the prolonged stay in the hospital (Hanifi et al., 2017). Such factors also contribute to the increased cost of care for the patient.
Besides, the diagnosis of ventilator-associated pneumonia needs a high clinical suspicion integrated with a bedside inspection, microbiologic examination of the respiratory secretion, and radiographic analysis. Strong surveillance is critical for investigating factors causing VAP as well as the microbiologic situation in a specific unit (Lin et al., 2015). More imperatively, sensible antibiotic utilization is vital, as the resistance organisms perpetually plague the ICU and the critically ill patients. Therefore, respiratory therapy and simple nursing interventions should be explored. The paper seeks to critically analyze the prevention of ventilator-associated pneumonia for patients in a critically ill condition.
Pathophysiology of Ventilator-Associated Pneumonia
For healthy people, multiple techniques work collaboratively to fight the development of pneumonia in the body. Sadly, the presence of a clinical condition of the ICU patients, thus, the supine positioning and sedation, as well as the presence of the endotracheal tube (ETT) usually interfere with the fighting techniques and predisposes the intubated patient to the development of ventilator-associated pneumonia (Hanifi et al., 2017). More significantly, the proper understanding of the pathophysiology is fundamental in the understanding of the strategies targeting the prevention of ventilator-associated pneumonia. Like any pneumonia, ventilator-associated pneumonia often occurs when the bacteria are presented into the sterilized lower respiratory tract and overwhelm the host’s typical defense approach against infection (Lin et al., 2015). The most critical mechanism for the entry of bacteria into the tract is the micro-aspiration of the pathogenic bacteria from the gastrointestinal tract around the endotracheal tube or the upper respiratory.
The other mechanism is through biofilm production in the endotracheal tube
More importantly, the upper respiratory tract for most patients who are under a ventilator is occupied with possibly pathogenic bacteria. Such an outcome was revealed in the study conducted in 1969which recorded the presence of enteric gram-negative microorganisms into the oropharynx of about 75% of the patients under critical care (Lin et al., 2015). The study also suggested that it was due to the overgrowth of the upper gastrointestinal tract as well as because of the retrograde movement. Notably, the aspiration of the secretions consisting of such pathogens allows the infection of the sterilized bronchial tree.
Another research conducted in 2007 also reveals the presence of the same bacteria in the lower respiratory tract of an intubated patient through a comparison between samples of DNA from the microorganisms on the patient’s tongue and those from the Broncho-alveolar lavage (Jackson & Owens, 2019). The other possible source for introducing the bacteria into the lower respiratory tract may be linked to the endotracheal tube. Similarly, the biofilms refer to the network of secretions and the bacteria that develops along the tube or within the lumen. Moving to the lower respiratory tract may lead to infection for the patients who are under ventilation. Also, most studies have always correlated VAP with the presence of a fundamental growth of bacteria from the lung parenchyma and distal airways. The autopsies conducted on patients who are dying due to long stay on ventilation also indicates some patterns, including bronchopneumonia, bronchiolitis, and tracheobronchitis (Jackson & Owens, 2019). The studies based on the patients who are receiving antibiotic treatments indicate a highly variable capacity to predict pneumonia for the quantitative culture more than the threshold. Therefore, it is worth noting that the assumption of the idea that quantitative bacteriologic research accurately demonstrates the histological patterns can be inaccurate in some clinical settings.
Also, patients who are mechanically ventilated are at the risk of being infected by the disease. According to the recent studies, the rate of getting the disease has been demonstrated as three percent every day in the first week of ventilation, two percent in the second week, and one percent in the third week. In general, the overall rate of contracting the disease is spread from 5 % to 67% based on the approach of diagnosis (Lin et al., 2015). Several risk factors have also been identified to accelerate the rate at which ventilator-associated pneumonia occurs. Such risks can be categorized into non-modifiable risk factors such as high age, male gender, presence of cranial trauma, neurological surgery, multiorgan system failure, acute respiratory syndrome, among other factors. The other category is the modifiable risk factors, including the gastric over-distension, supine positioning, low pressure in the endotracheal tube, and series of patient transfer and colonization of the ventilator tract.
Diagnosis of Ventilator-Associated Pneumonia Patient
Clinical Diagnosis
Ventilator-associated pneumonia is often predicted if a patient develops an advancing infiltrate on the chest radiograph, infected tracheobronchial secretion, and leukocytosis. Contrary to community-acquired pneumonia, the recommended clinical technique for pneumonia is inadequate diagnostic value for identifying the incidence of ventilator-associated pneumonia. During postmortem research that was conducted on the histologic analysis, where lung samples from the occurrence of death were utilized as references; the sensitivity significantly reduced with about 23%, while the utilization of a single variable led to a tremendous decline in specificity by approximately 33% (Lin et al., 2015). There is usually inaccuracy in the clinical technique in the diagnosis of VAP due to the invariability of the purulent tracheobronchial secretions in patients undergoing prolonged ventilation and are rarely triggered by pneumonia.
Similarly, the symptoms of pneumonia, including leukocytosis, tachycardia, and fever, are not precise; they can be a result of any process producing cytokines, tumor necrosis, and gamma interferon. Such conditions include surgery, vein thrombosis, trauma, pulmonary infarction, and pulmonary embolism, among other examples. The clinical rationale technique for the presence of VAP can be a patient with high temperature and a new patient who has taken 48hours in ventilation or less.
The sensitivity of the clinical mechanism for the diagnosis of VAP is even reduced, especially for patients with ARDS, in which it can be more difficult to identify fresh radiographic infiltrates. For ARDS patients, previous research has revealed a false-negative rate of approximately 46% for the clinical diagnosis of the disease (Pileggi et al., 2011). Therefore, the feeling for the incidence of VAP in the conditions of ARDS patients should be higher. Also, when a fever, purulent sputum, leukocytosis, and positive sputum culture are suspected in the absence of a new lung infiltrate, then the finding of the nosocomial tracheobronchitis should be tolerated.
Based on the previous studies regarding mechanically ventilated patients, the nosocomial tracheobronchitis is usually linked to the long stay in the ICU as well as too much time in the ventilator without an increased rate of fatalities. In a randomized trial of intubated patients who suffer from community-acquired tracheobronchitis, antibiotic therapy reduces cases of continuous occurrence of pneumonia and death (Pileggi et al., 2011). In general, the possible randomized controlled trials should be conducted before prescribing antibiotic therapy for the normal treatment of nosocomial tracheobronchitis. Notably, differentiating the tracheobronchitis from pneumonia can be based on the radiograph that is portable in the ICU. Therefore, the clinicians need to use a clinical pulmonary infection score for the therapy.
Radiologic Diagnosis
Despite chest radiograph being the most fundamental way of diagnosing ventilator-associated pneumonia patients, the criteria are still having challenges with its specificity and sensitivity. More precisely, low-quality films compromise the accuracy of the X-rays performed on the patient’s chest. In a study conducted on a surgical patient, approximately 26% of the opacities were identified through computed tomography scans instead of the portable X-ray on the chest (Villar et al., 2016). The asymmetric pulmonary infiltrate constant with ventilator-associated pneumonia may be triggered by several noninfectious disorders such as chemical pneumonitis, atelectasis, pulmonary embolism, asymmetric cardiac, pulmonary, and drug reaction, among other noninfectious conditions. According to the research, the radiographic specificity of the pulmonary opacity, which is constant with the disease is between 27% and 30% (Villar et al., 2016).
However, due to the high specificity, some chest radiographic outcomes may be significant in identifying the diagnosis of ventilator-associated pneumonia. According to several studies, including the one focusing on the autopsy, the significant results include air bronchogram, air space abutting a gap, and quick cavitation of pulmonary infiltrate (Villar et al., 2016). Understandably, such abnormalities of radiography are not common.
Microbiologic Diagnosis
Even though the spread of VAP into the blood is approximately 10% of the cases and below, if the bacteria causing pneumonia is cultured into the clinically suspected pneumonia, treatment of the disease is necessary (Tanguay et al., 2018). As a result, most studies have suggested a thoracentesis and two sets of blood culture for the non-loculated pleural effusions of about 10 mm wide for the chest radiograph to comprise the process of evaluating the suspected disease. Also, the use of ultrasound may be required in case the effusion is loculated. Nonetheless, it is more imperative to understand that the sensitivity of the blood culture for VAP diagnosis is not more than 25% as well as understanding that the when the sensitivity is positive, the bacteria may have come from the extra-pulmonary locations of the disease as revealed by more than 64% of the cases (Tanguay et al., 2018).
More importantly, the non-quantitative and gram-staining cultures of the tracheal secretion have the benefits of reproducibility, and it requires little skills without specialization in any technique. However, according to previous research, the upper respiratory tract can quickly be colonized by possible pulmonary pathogens even in the absence of pneumonia; thus, when the bacteria is cultured, it is not clear whether it causes pneumonia or colonization.
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