The otolaryngologic manifestations of gastroesophageal reflux disease (GERD) or extraesophageal reflux in patients, including primarily hoarseness, cough, globus sensation, and throat clearing, constitute an increasingly significant portion of an otolaryngologist's practice. Various descriptions and terminology have been employed to delineate laryngopharyngeal reflux (LPR), including supraesophageal GERD, extraesophageal complications of GERD, and atypical GERD. Patients and clinicians often confuse and conflate the signs and symptoms of GERD and LPR. However, current research suggests that, although there may be some overlap, GERD and LPR may represent 2 distinct conditions with different management approaches. The underlying premise remains that reflux of gastric contents is a primary cause of laryngeal pathology, even in the absence of GERD symptoms.
Patients presenting with chronic laryngeal symptoms or a persistent cough pose diagnostic challenges. Although visible reflux-related injuries to the upper airway may be identified, many of these patients report no heartburn, regurgitation, chest pain, nausea, or vomiting, supporting the idea that GERD and LPR may be separate conditions. Acid-pepsin injury from direct contact might only be part of the explanation for LPR. Additionally, LPR could also result from a vagal reflex arc between the esophagus and the upper aerodigestive tract, triggered by acid reflux, leading to symptoms such as globus, throat clearing, and chronic cough.
Four barriers prevent reflux from reaching the larynx: the lower esophageal sphincter, the upper esophageal sphincter, esophageal peristalsis, and epithelial resistance factors. Dysfunction in any of these areas can cause symptoms of LPR. The upper esophageal sphincter acts as the final gatekeeper against refluxed gastric contents. The distal pharynx and upper esophageal sphincter should open only during specific physiological states, such as swallowing, and remain closed otherwise. The muscle group forming this acid barrier includes the cricopharyngeus, thyropharyngeus, and proximal cervical esophageal muscles, which create a C-shaped sling attached to the cricoid cartilage. However, the tonic pressure from these muscles can decrease during general anesthesia, sleep, and cigarette smoking. Research suggests that a deficiency of epithelial cadherin, the intercellular junctional complex protein, and carbonic anhydrase isoenzyme III, in relation to the presence of intracellular pepsin in laryngeal epithelium, may occur in patients with LPR.
The clinical diagnosis of LPR mainly depends on the patient's history of chronic laryngitis symptoms such as globus, throat clearing, cough, and hoarseness. The physical exam may include nasopharyngoscopy, fiberoptic laryngoscopy, and, more recently, videostroboscopy of the larynx. Clinicians look for signs like erythema and edema of the posterior commissure, as well as cobblestoning. Often, patients present with pseudosulcus vocalis or infraglottic edema extending from the anterior commissure to the posterior larynx, especially in patients with pH-confirmed LPR.
Workup may include barium esophagography, but its utility may be limited. More useful procedures include laryngoscopy, esophageal endoscopy, and ambulatory 24-hour pharyngoesophageal pH monitoring. Some advocate flexible endoscopic evaluation of swallowing with sensory testing.
Management can be individualistic and involve multiple factors. Medical treatment usually begins with an empirical trial of proton pump inhibitors, histamine-2 receptor antagonists (H2 blockers), prokinetic agents, and mucosal cryoprotectants. Patients who need ongoing or increasing acid suppression may be good candidates for Nissen fundoplication, especially if long-term medication negatively impacts their quality of life. Lifestyle modifications include dietary changes, regular exercise, elevating the head during sleep, and avoiding tobacco and alcohol. Some patients may also benefit from swallowing therapy administered by a speech-language pathologist. Most patients benefit from long-term follow-up, repeat laryngoscopy or testing, and lifestyle prevention.
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