Microaspiration in Intubated Critically Ill Patients: Diagnosis and Prevention

Abstract

Microaspiration of contaminated oropharyngeal secretions and gastric contents frequently occurs in intubated critically ill patients, and plays a major role in the pathogenesis of ventilator-associated pneumonia. Risk factors for microaspiration include impossible closure of vocal cords, longitudinal folds in high-volume low-pressure polyvinyl chloride cuffs, and underinflation of tracheal cuff. Zero positive end expiratory pressure, low peak inspiratory pressure, tracheal suctioning, nasogastric tube and enteral nutrition increase the risk for microaspiration. Other patient related factors include supine position, coma, sedation, and hyperglycemia. Technetium 99 labelled enteral feeding is probably the most accurate marker of microaspiration in critically ill patients. However, use of this radioactive marker is restricted to nuclear medicine departments. Blue methylene is a reliable qualitative marker of microaspiration. However, fiberoptic bronchoscopy is required to diagnose microaspiration of blue dye in ICU patients. Quantitative pepsin measurement in tracheal aspirates is accurate in diagnosing microaspiration of gastric contents in critically ill patients. In addition, this marker is easy to use in routine practice. However, pepsin should be detected rapidly after aspiration. In vitro, and clinical studies suggested that semirecumbent position, polyurethane cuffs, positive end expiratory pressure, low-volume low-pressure cuff, and continuous control of cuff pressure were efficient in reducing microaspiration in ICU patients. Other preventive measures such as subglottic aspiration, tapered shape cuff, guayule latex cuff, lateral horizontal patient position, gastrostomy tube, and postpyloric feeding require further investingation.

Airway Pepsin Levels in Otherwise Healthy Surgical Patients Receiving General Anesthesia With Endotracheal Intubation

“…Toward a more causal mechanism, an increasing number of investigators have independently developed their own pepsin assays and successfully identifi ed pepsin in the airways of a variety of lung pathologies: lung transplant patients, 28,29 interstitial lung disease, 30 pediatric patients, 10 and the critically ill. 6,11 Recognizing that pepsin itself is directly cytotoxic not just to the esophagus but also to the respiratory epithelium, 31 it may help to fi nally link the relationship between refl ux and lung pathology and explain why gastric acid-suppressive therapies have largely been ineffective in the treatment of presumed pulmonary manifestations of refl ux. 27,32 Unfortunately, controls in these airway pepsin studies have not consistently been reported, and, to our knowledge, only one study has tried to specifi cally examine for the presence of airway pepsin in a controlled setting using a qualitative pepsin assay in normal adults.…”

Pepsin and Amylase in Oral and Tracheal Secretions: A Pilot Study

“…A value of 0.6 μmol/min per milliliter (approximately 1305 IU/L) C ritically ill patients treated with mechanical ventilation are at increased risk for microaspiration of secretions, which may include oral contents, gastric contents, or both, around the cuff of the endotracheal tube. 1 Oral secretions are laden with bacteria, increasing the risk for infection in the event of aspiration. Aspiration of gastric contents is associated with inflammation and infection.…”

“…4,5 Pepsin is widely used to detect aspiration of gastric contents; however, specimens must be obtained within a short period after aspiration occurs because pepsin breaks down quickly. 1 Aspiration of oral secretions has been typically assessed by culturing tracheal aspirates, which is costly and time consuming. Researchers 1,5-8 have proposed that amylase, normally present in the mouth, could be used as a biomarker for aspiration of oral contents.…”

Aspiration lung disorders in bovines: A case report and review

“…The gastric acid prevents bacterial growth in the early stages. Aspiration of significant amounts can be readily noticed by non-productive coughing, acute tachypnoea and dyspnoea, wheezing, bloody or frothy sputum, hypoxia and tachycardia developing into severe respiratory distress after 2-5 hours (Nseir et al 2011). Bronchospasm occurs later and the cellular injury enables fluids and cellular elements to leak into the interstitial space and the alveoli, which can dilute and decrease production of surfactant, resulting in atelectasis (De Bendictus, Carnielli & De Benedictis 2009).…”