The term laryngopharyngeal reflux (LPR) describes the anatomical location of the disease as well as its cause. According to Sataloff, “laryngopharyngeal reflux incorporates a complex spectrum of abnormalities.”. The airway is subdivided anatomically beginning with the oropharynx, then the hypopharynx, supraglottis, glottis, subglottis, and finally, the trachea. The area of concern, and what brings most patients into the clinic, is the effect of reflux on the glottis, or vocal cords. Reflux is normally sequestered within the stomach and sometimes escapes into the esophagus which has been described in other literature.
In healthy individuals, there are four barriers to reflux encroaching on the larynx. The lower esophageal sphincter, upper esophageal sphincter, esophageal peristalsis, and epithelial resistance factors with any dysfunction will lead to symptoms of laryngopharyngeal reflux.
The upper esophageal sphincter is the final gatekeeper in antireflux. The area of the distal pharynx and proximal esophageal only opens for specific physiologic demands, such as swallowing under tonic contraction. This is made up of the cricopharyngeus, thyropharyngeus, and the proximal cervical esophagus, forming a c-shaped sling that attaches to the cricoid cartilage. The tonic pressure induced by these muscles can be decreased with general anesthesia, sleep state, and cigarette consumption.
The lower esophageal sphincter is located at the gastroesophageal junction whose contracture leads to circular closure and prevention of egress of stomach acid. The diaphragmatic crura make up this critical antireflux mechanism.
The esophagus, with the help of gravity and peristalsis, can clear the acid that makes its way more proximal than expected. A mucus layer is present along the esophagus that is a barrier to large molecules, such as pepsin but does not help prevent acid penetration. Also present is the aqueous layer, which helps form an alkaline buffer.
Direct mucosal damage from acidic exposure, typically found in the esophagus, damages the laryngeal epithelium. Ciliary flow is impeded at pH 5.0 and completely halted at pH 2.0. With decreased ciliary flow, there is a decrease in resistance to infection.
It is believed that 10% of patients visiting otolaryngology clinics have symptoms attributed to laryngopharyngeal reflux, and 55% of patients with hoarseness have laryngopharyngeal reflux impacting the quality of their voice.
The retrograde flow of gastric acid and pepsin induces laryngeal mucosal damage and impaired mucociliary clearance. Three different theories explain this damage. Direct contact of acid and pepsin with the epithelium induces damage versus gastric refluxate with additional vocal abuse causes symptoms and mucosal lesions. The esophageal-bronchial reflex theory suggests that acid in the distal esophagus vagally stimulates a chronic cough induces laryngeal symptoms.
In one study, post-cricoid epithelial cells from patients suffering from laryngopharyngeal reflux were examined and shown to contain pepsin while control subject's cells did not. Inactivated pepsin at pH 7 is taken into cells and subsequently reactivated within cells, causing mitochondrial damage and overall cell damage. Cell damage was prevented by blocking uptake of Pepsin into cells.
As stated previously, laryngopharyngeal reflux encompasses many symptoms that could bring a patient into the clinic. That being said, hoarseness was the most prevalent symptom in laryngopharyngeal reflux (100%) with none of the patients with the more common condition of gastroesophageal disease (GERD) reporting hoarseness.
Patients can have a multitude of symptoms with from the common hoarseness, globus sensation, and chronic throat clearing to the less common heartburn and regurgitation. Patients with laryngopharyngeal reflux typically have upright, or daytime, reflux with good esophageal motor function. This is compared to supine, or nocturnal, patients with reflux who had esophageal motor dysfunction. Patients with GERD also often have dysfunction of their lower esophageal sphincter compared to upper esophageal sphincter pathology seen in laryngopharyngeal reflux.
The reflux symptom index (RSI) is a validated questionnaire to determine the likelihood of positive results of dual diagnoses. RSI greater than 10 is correlated with the high likelihood of reflux pathology.
On physical exam, an otolaryngologist can perform laryngoscopy as well as videostroboscopy. Posterior thickening and pachyderma of laryngeal posterior commissure and post-cricoid mucosa have been associated with laryngopharyngeal reflux. Granulomas of the vocal process have also been highly associated. If able to perform videostroboscopy in the office, edema along the undersurface of the vocal fold from the anterior to the posterior commissure fair sensitivity and specificity.
Detection of retrograde flow of stomach acid into the upper aerodigestive tract has been considered the gold standard. This is tested via a single probe or dual probe pH testing. Pathologic reflux is considered present when 0.1% of the study time has a pH of less than 4.0. Radiologic imaging has not been shown to increase the sensitivity of diagnosis. In a study comparing pH probe monitoring versus imaging, Videofluoroscopy showed a sensitivity of reflux diagnosis via imaging ranged from 25% to 33%. Esophagrams showed a sensitivity of 20% with a specificity of 64% to 90%.
Lifestyle modifications are the first step of management. This includes weight loss, small meal size, refraining from lying down within 3 hours of a meal, eating a low fat and low acid diet, avoiding carbonates or caffeinated beverages, stopping tobacco use, and reducing alcohol intake.
If these measures fail to achieve results, medications such as histamine-2 receptor antagonists and proton pump inhibitors can be used to suppress acid production. Surgical therapy such as Nissen fundoplication can also be advocated to decrease symptoms.
Laryngeal complaints similar to laryngopharyngeal reflux manifestations have a wide differential. Most commonly, laryngopharyngeal reflux may be misdiagnosed as GERD. Distinctions between these two common conditions have been stated elsewhere in this chapter.
Long-term untreated laryngopharyngeal reflux will lead to chronic vocal abuse with resultant scarring of the true vocal folds. Laryngopharyngeal reflux may also be related to untreated GERD, which can lead to Barrett esophagitis if left untreated. Also, one study showed in a retrospective chart review that untreated laryngopharyngeal reflux can lead to subglottic stenosis over time.
If a patient continues to have symptoms of hoarseness, dyspnea, and chronic sore throat, an otolaryngologic referral is a good option. Also, gastroenterologists may need to get involved for possible esophagoscopy to ensure no malignant process is occurring.
Laryngopharyngeal reflux can usually be treated with lifestyle modifications that will pay dividends in other aspects of their health. With time, these symptoms can resolve, and the need for anti-reflux medication will abate.
Laryngopharyngeal reflux appears to be common but under diagnosed. The condition is best managed by a multidisciplinary team that includes nurses, pharmacists, and dietitians. Despite the available drugs and surgical procedures to manage this condition, clinicians should know that changes in lifestyle are very important. No treatment will work reliably if the appropriate lifestyle changes are not adopted. Lifestyle modifications are the first step of management. This includes weight loss, small meal size, refraining from lying down within 3 hours of a meal, eating low fat and low acid diet, avoiding carbonates or caffeinated beverages, stopping tobacco use, and reducing alcohol intake.
Patients who adopt a healthy lifestyle see a gradual decrease in symptoms with a low risk of recurrence. Patients who have recurrences need an upper endoscopy and possible PPI treatment.
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