The impact of inspiratory pressure level on prevention of ventilator-associated pneumonia: A double-blind, randomized clinical trial


Ventilation-associated pneumonia (VAP) occurs at least 48 hours after endotracheal intubation. The most common pathogens are Gram-negative bacilli and Staphylococcus aureus. Antibiotic-resistant bacteria are a major concern. In ventilated patients, pneumonia is usually accompanied by fever, increased white blood cell count, decreased oxygenation, and increased purulent tracheal secretions. Diagnosis may be suspected based on clinical presentation and chest radiograph and confirmed by positive blood cultures for the same pathogen found in respiratory secretions or by bronchoscopy of the lower respiratory tract with quantitative Gram stain and culture. Treatment is with antibiotics. The overall prognosis is poor, partly due to comorbidities. A recent report showed that patients with coronavirus disease 2019 requiring ventilators in the ICU were more likely to be affected by non-COVID-19 patients on ventilators in the same unit and viral infections caused by the virus. A higher risk of ventilator-associated pneumonia has been shown compared to patients with pneumonia. The reason for the existence of this increased susceptibility remains unclear, as the reports mentioned adjusted for ventilation durations and the increased susceptibility is likely related to impaired innate immunity in the lung. However, several observational studies have identified glucocorticoid use as a factor associated with her increased risk of VAP and other nosocomial infections. Ventilator-associated pneumonia is pneumonia that develops at least 48 hours after endotracheal intubation. This is a subset of hospital-acquired pneumonia, including pneumonia in non-ventilated hospitalized patients. VAP has more resistant pathogens and often worse outcomes than other forms of hospital-acquired pneumonia. The most common cause of ventilator-associated pneumonia is microaspiration of bacteria that colonize the oropharynx and upper respiratory tract of critically ill patients. Endotracheal intubation compromises airway defenses, impairs cough and mucociliary clearance, and facilitates microaspiration of bacteria-laden secretions that accumulate over the inflated endotracheal tube cuff. In addition, bacteria form biofilms on and within the endotracheal tube, protecting them from antibiotics and host defenses. The highest risk of VAP is in his first 10 days after intubation. Ventilator-associated pneumonia occurs in 9–27% of her ventilator-using patients. Diagnosis is incomplete. In practice, ventilator-associated pneumonia is a new symptom or sign (e.g., fever, increased secretions, worsening hypoxemia) or a new invasion on a chest radiograph taken to assess leukocytosis. is often suspected based on the appearance of However, no symptoms, signs, or radiographic findings are present, as they may all be due to atelectasis, pulmonary embolism, or pulmonary edema, and may be part of the clinical presentation of acute respiratory distress syndrome. Not diagnostically sensitive or specific. Despite the availability of effective antibiotics, the mortality rate from ventilator-associated pneumonia is high. However, not all mortality is due to pneumonia itself. Many of the deaths are related to the patient's underlying medical conditions. Adequacy of early antibiotic therapy clearly improves prognosis. Infections with antibiotic-resistant bacteria worsen the prognosis. There are several measures that can help prevent ventilator-associated pneumonia. A semi-upright or upright position reduces the risk of aspiration and pneumonia compared to lying down and is the simplest and most effective method of prevention. Noninvasive ventilation using continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BPAP) prevents the compromise of airway defenses that occurs with endotracheal intubation and eliminates the need for intubation in some patients with pneumonia.