Laryngopharyngeal Reflux

Anatomy & Pathophysiology:

Gastroesophageal reflux disease (GERD) is a very common condition characterized by symptomatic reflux of gastric contents into the esophagus. In addition to the esophageal sequelae of reflux, extraesophageal complications may also occur. Laryngopharyngeal reflux (LPR) refers to the effects of GERD on the pharynx and larynx, and exacerbates a number of conditions, including laryngitis, dysphonia, chronic cough, vocal fold lesions, and laryngospasm.

Several physiologic mechanisms exist to prevent reflux. These include the upper esophageal sphincter (UES), the lower esophageal sphincter (LES), and esophageal peristalsis. The UES comprises the cricopharyngeus (CP) and thyropharyngeus muscles, along with the proximal cervical esophagus. Because the UES is the last barrier encountered by refluxed material before reaching the laryngopharynx, its dysfunction is implicated in LPR. Tonic contraction of the CP muscle maintains a closed UES until relaxation is triggered by swallowing. Normally, acid stimulus and physical distention in the distal esophagus increase UES pressure.

LES dysfunction is the primary mechanism implicated in most cases of GERD. Anatomically, the LES is located at the gastroesophageal junction. Like the UES, it is usually closed until the act of swallowing triggers relaxation. Pressure from the surrounding diaphragmatic crura enhances LES competence under normal conditions. Gastric reflux occurs when resting pressure of the LES is lower than gastric pressure, which may be due to transient LES relaxation, chronic LES hypotonia, presence of large hiatal hernia, or increased gastric pressure.

While the esophageal tissue possesses protective mechanisms to counteract the deleterious effects of gastric acid, the mucosa of the larynx and pharynx lacks the equivalent resistance. Therefore, even relatively low levels of exposure of the laryngopharyngeal tissues to acid and digestive enzymes may result in tissue injury. In addition to direct mucosal damage, reflux may also impair mucociliary clearance by respiratory epithelium in the head and neck. GERD can also produce laryngopharyngeal symptoms via indirect pathways. For example, reflux in the distal esophagus can trigger vagally-mediated laryngospasm.


GERD is a common disorder in the United States, with up to 30% of the national population affected. The estimated incidence of GERD among patients seeking treatment from an otolaryngologist is as high as 10%. GERD affects individuals of all ages, including children. The prevalence of LPR among GERD patients has not been documented.


Patients with laryngopharyngeal reflux may present with a variety of symptoms, including hoarseness, change in voice quality, globus sensation, chronic cough, sore throat, excessive secretions, dysphagia, postnasal drip, halitosis, and laryngospasm. Patients may or may not report concurrent symptoms of esophageal reflux, such as heartburn or regurgitation. Absence of classic GERD symptoms does not preclude diagnosis of LPR.

Differential Diagnosis of Laryngopharyngeal Reflux:

  • Acute laryngitis (infectious, overuse)
  • Chronic laryngitis (infectious, allergic)
  • Other infectious or allergic etiology (e.g., allergic rhinitis)
  • Irritant exposure
  • Laryngeal/pharyngeal neoplasm
  • Pharyngoesophageal diverticulum
  • Functional voice disorder



History should include the timing of onset and progression of symptoms (e.g., episodic versus chronic persistent), association with activities or ingestion of particular foods, and exposure to cigarette smoke. The Reflux Symptom Index (RSI) is a survey instrument that can be used to screen for LPR.

Physical Examination

Examination should include flexible fiberoptic laryngoscopy (FFL). The hallmark of LPR on FFL is laryngeal mucosal edema. On the vocal fold, edema may result in the development of a pseudosulcus vocalis. Other findings may include thickened mucosa with a cobblestone appearance and increased mucus secretion or pooling. In severe cases of LPR, ulceration and vocal process granulomas may be present. Erythema is frequently a feature of LPR, but is not as characteristic of the disorder as mucosal edema.

pH Probe Monitoring

The gold standard for diagnosis of GERD is continuous pH probe monitoring. In single probe studies, manometry is typically used to position a pH probe in the distal esophagus, 5 cm proximal to the LES. When evaluating for LPR, a dual probe study is recommended, in which a second probe is placed above the UES. Even with the use of dual probes, pH testing has a false negative rate of up to 50%.

Other Studies

Other diagnostic modalities that may be considered in evaluation of GERD include barium esophagram and esophagoscopy. Barium esophagography allows for the identification of hiatal hernia, esophageal stricture, and motility disorder. Esophagoscopy is primarily useful in evaluating for presence of esophageal inflammation, metaplasia or neoplasm. Unfortunately, neither of these investigations is effective for identifying LPR. As a result, most patients are treated empirically with anti-reflux medication and only undergo investigations if they do not respond to pharmacotherapy.

Laryngeal sensory testing evaluates the presence of the laryngeal adductor reflex, which causes adduction of the vocal folds in response to tactile stimulus, delivered in the form of an air pulse. In LPR, it is thought that edematous laryngeal mucosa requires a larger pressure stimulus to cause the reflex than normal mucosa. Positive results on laryngeal sensory testing have been reliably correlated with positive pH probe test results. Finally, impedance testing may play a useful role in LPR evaluation as it allows for the assessment of reflux independent of pH. Both acid and nonacid reflux events may occur in GERD, although only the former may be detected using conventional pH probe studies. Studies suggest that LPR symptoms may, in fact, be caused more by nonacid reflux events.


Many of the principles of LPR treatment are identical to those for GERD. Behavioral changes, such as elevating the head of the bed during sleep, avoidance of foods that exacerbate symptoms, and not eating within 3 hours of lying down may be effective in reducing symptoms in up to half of patients with LPR.

Pharmacotherapy for GERD includes antacids (such as bicarbonate or magnesium-based compounds), histamine type 2 blockers (e.g., cimetidine), and proton pump inhibitors (PPIs, e.g., omeprazole). Of these, PPIs are the most effective; however, resistance is not uncommon in patients with LPR.

Nissen fundoplication is a surgical option for treatment of refractory GERD. It involves wrapping the gastric fundus around the abdominal esophagus to enhance LES competence. Small studies of patients with LPR undergoing Nissen procedures have demonstrated significant symptomatic improvement after surgery.

Complications, Prognosis & Follow-Up:

The majority of patients with pH probe-proven GERD and LPR improve with anti-reflux therapy. Studies have reported anti-reflux medication success rates of over 90% within 4 months of treatment initiation in patients with chronic reflux laryngitis. However, symptom recurrence was also reported when treatment was discontinued. Nissen fundoplication has a reported success rate of between 70-85% for relief of LPR symptoms, although this is not generally indicated for LPR alone due to the associated complications, which include hemorrhage, splenic injury, dysphagia, early satiety, pneumothorax, diarrhea, and gastric ulceration.

In patients whose symptoms do not respond to treatment or continue to progress, the possibility of an underlying aerodigestive tract malignancy should be considered. Endoscopic evaluation of the hypopharynx, larynx, and esophagus may be undertaken in these cases to rule out the presence of tumor.

Key Points

  • Laryngopharyngeal reflux (LPR) refers to the effects of gastroesophageal reflux (GER) on the pharynx and larynx, and may contribute to a number of conditions, including laryngitis, dysphonia, chronic cough, vocal fold lesions, and laryngospasm.
  • Presenting symptoms of LPR may include hoarseness, change in voice quality, globus sensation, chronic cough, sore throat, excessive secretions, dysphagia, postnasal drip, halitosis, and laryngospasm.
  • Characteristics of LPR on laryngoscopy include mucosal edema, erythema, mucosal thickening or granulation, increased mucus secretion or pooling, pseudosulcus vocalis, ulceration, and granuloma formation.
  • Although no investigations are required in most patients, evaluation of LPR may include a dual probe pH study, as it is possible to have laryngopharyngeal reflux despite normal distal esophageal pH levels.
  • Treatment options for GERD include behavioral modifications, pharmacotherapy, and surgical intervention.
  • A low index of suspicion for possible malignancy should be maintained in those patients whose symptoms fail to respond or progress despite reflux therapy, with careful endoscopic evaluation of the larynx, hypopharynx and esophagus considered.