Laryngopharyngeal reflux

Laryngopharyngeal reflux (LPR),^[1][2] also extraesophageal reflux disease (EERD)^[3] refers to retrograde flow of gastric contents to the upper aero-digestive tract, which causes a variety of symptoms, such as cough, hoarseness, and wheezing, among others. It can be a relevant comorbidity of asthma.^[4]

Although heartburn is a primary symptom among people with gastroesophageal reflux disease (GERD), heartburn is present in fewer than 50% of the patients with LPR. Other terms used to describe this condition include atypical reflux,^[5] silent reflux,^[6] and supra-esophageal reflux.^[7]

Background

Gastroesophageal reflux disease (GERD) was recognized as a clinical entity in the mid-1930s and now is the most prevalent upper gastrointestinal (GI) disorder in clinical practice. Around the same time, in 1934, Bray suggested a link between gut symptoms and airway disease. Acid-related laryngeal ulcerations and granulomas were first reported by Chery in 1968.^[8] Subsequent studies suggested that acid reflux might be a contributory factor in other laryngeal and respiratory conditions. In 1979, Pellegrini and DeMeester were the first to document the link between these airway symptoms and reflux of gastric contents. They also proved that treatment of reflux disease results in elimination of these airway symptoms.^[9]

People who suffer from GERD usually have symptoms such as esophageal damage that result from the stomach acid shooting up into the esophagus. The acid can irritate the tissues of the esophagus resulting in a sore throat and persistent coughing. Patients who suffer from laryngopharyngeal reflux, or LPR, are more likely to experience symptoms as a result of stomach acid refluxing into the larynx.

In recent years, it became apparent that stomach acid is only a part of the equation. Research suggests that the stomach enzyme pepsin plays a crucial role in the complex mechanism behind LPR.^[10][11] The body produces pepsin in the stomach to digest proteins. During reflux episodes, pepsin is delivered into the airways where they are destroying proteins inside of mucosa cells and therefore creating damage. The activity of pepsin correlates with the acidity of the environment. Each time something acid is consumed or acid is refluxed, pepsins are activated and the symptoms worsen.^[12]

Signs and symptoms

Extraesophageal symptoms are the result of exposure of the upper aerodigestive tract to the gastric juice. This causes a variety of symptoms, including hoarseness, postnasal drip, sore throat, difficulty swallowing, indigestion, wheezing, chronic cough, globus pharyngis and chronic throat-clearing. Some people with LPR have heartburn, while others have little or none of these symptoms. This is because the material that refluxes does not stay in the esophagus for very long. In other words, the acid does not have enough time to irritate the esophagus.^[13]

Adults who are afflicted with LPR often experience the acrid taste of bile emanating from the back of their throat. This is also likely to be accompanied by a lump-like sensation in the throat, making it difficult to swallow. The throat may also seem to burn and breathing can be difficult. These symptoms are most often prevalent just after waking.^[14]

LPR may also result in sinusitis and difficulty breathing.^[15]

Diagnosis

As there are multiple potential etiologies for the respiratory and laryngeal symptoms, establishing LPR as the cause based on symptoms alone is unreliable. Laryngoscopic findings such as erythema, edema, laryngeal granulomas, and interarytenoid hypertrophy have been used to establish the diagnosis; but these findings are very nonspecific, and have been described in the majority of asymptomatic subjects undergoing laryngoscopy.^[16] Response to acid-suppression therapy has been suggested as a diagnostic tool for confirming diagnosis of LPR, but studies have shown that the response to empirical trials of such therapy (as with proton-pump inhibitors) in these patients is often disappointing.^[17] Several studies have emphasized the importance of measuring proximal esophageal, or, ideally, pharyngeal acid exposure in patients with clinical symptoms of LPR, to document reflux as the cause of the symptoms.^[18][19]

Before a diagnosis can be made, the doctor will need to record the patient’s medical history and may ask for details about the symptoms that the patient is experiencing. The doctor will then need to perform a physical examination with particular concentration around the head and neck. The doctor may need to use a specialized camera lens made of fiber optic strands. This is gently fed down the patient’s throat which then feeds back images to a monitor. This enables the doctor to get a clearer look at the throat, particularly the larynx. Tell-tale signs include redness, swelling, and obvious irritation. Once a diagnosis is made, the doctor will propose a treatment method.

Treatment

Management of symptoms for patients within this subgroup of the GERD spectrum is difficult. Once these patients are identified, behavioral changes including weight loss and dietary changes are advised. Proton-pump inhibitors have been shown to be ineffective in very young children, and are of uncertain efficacy in older children, for whom their use has been discouraged.^[20] When medical management fails, Nissen fundoplication can be offered.^[21] While proton pump inhibitors may provide limited clinical benefits in some adults, there is insufficient evidence to support routine use.^[20][22] Many studies show that proton pump inhibitors are not more effective than Placebo in treating LPR.^[23] Some studies have pointed to a larger role of pepsin in causing damage to tissue, and of patients having had success with combination of higher dose PPI's and Sodium Alginate preparations (Gaviscon Advanced).

References

External links

• Refluxgate
• Living with Reflux