Postextubation dysphagia (PED) is a common problem in critically ill patients with recent intubation. Although several risk factors have been identified, most of them are nonmodifiable preexisting or concurrent conditions. Early extubation, small endotracheal tube size, and small bore of nasogastric tube potentially decrease the risk of PED. The majority of patients receive treatment based on only bedside swallow evaluations, which has an uncertain diagnostic accuracy as opposed to gold standard instrumental tests. Therefore, the treatment decision for patients may not be appropriately directed for each individual. Current treatments are mainly focused on dietary modifications and postural changes/compensatory maneuvers rather than interventions, but recent studies have shown limited proven benefits. Direct therapies in oromotor control, such as therapeutic exercises and neuromuscular stimulations, should be considered as potential effective treatments. P ostextubation dysphagia (PED) is defi ned as the difficulty or inability to eff ectively and safely transfer food and liquid from the mouth to the stomach after extubation. It is commonly seen in trauma and critical care patients requiring endotracheal intubation for mechanical ventilation, especially after cardiac surgery (1, 2). PED may result in aspiration and its ensuing complications, such as aspiration pneumonia, chemical pneumonitis, transient hypoxemia, bronchospasm, or mechanical obstruction with atelectasis. As a result, malnutrition, prolonged hospital stays, fi nancial burden, and increased mortality occur (3, 4). Understanding the treatment modalities and screening tests is essential to minimize complications, improve quality of treatment, and develop standard screening guidelines.
INCIDENCEOf 220,000 survivors of acute respiratory failure requiring mechanical ventilation each year in the US (5), 3% to 62% develop PED. Th e wide range of incidence could be explained by the diff erences in the population studied, diff erences in the sensitivity of diagnostic methods and the timing of the assessment, and the duration of intubation. Th e patients who required prolonged intubation from all diagnosis subtypes were found to have a higher incidence of PED compared to postoperative patients with a shorter duration of intubation (6).
MECHANISMSTh e mechanisms of PED are multifactorial and include mechanical causes, cognitive disturbances, and residual eff ects of narcotics and anxiolytic medications (7). Mechanical causes are directly related to the duration of intubation and endotracheal tube size, since these tubes cause mucosal infl ammation leading to loss of architecture, oropharyngeal muscle atrophy from disuse during intubation, diminished proprioception, decreased laryngeal sensation, and laryngeal injury (edema, granuloma, and vocal cord paralysis) (6). Traumatic brain injury or critical illness may also cause PED by damaging peripheral and bulbar nerves, altering cognition, or causing the dysregulation of the swallowing refl ex (8).
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