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Laryngopharyngeal Reflux

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Last Update: March 28, 2021.

Continuing Education Activity

Laryngopharyngeal reflux typically results from the effects of reflux on the glottis and vocal cords. Patients may present with a multitude of symptoms ranging from the more common symptoms like hoarseness, globus sensation, and chronic throat clearing to the less common symptoms like heartburn and regurgitation. In contrast to patients with esophageal motor dysfunction, patients with laryngopharyngeal reflux typically have upright, or daytime, reflux. In contrast to patients with gastroesophageal reflux, which is associated with the lower esophageal sphincter, patients with laryngopharyngeal reflux typically have pathologic changes of the upper esophageal sphincter. This activity describes the pathophysiology, evaluation, and management of laryngopharyngeal reflux and highlights the role of the interprofessional team in the care of affected patients.

Objectives:

  • Identify anatomic etiology of laryngopharyngeal reflux.
  • Outline the difference between clinical presentation of a patient with laryngopharyngeal reflux in comparison to gastroesophageal reflux.
  • Review the treatment and management options available for laryngopharyngeal reflux.
  • Explain the role of the interprofessional team to improve care coordination and clinical outcomes in patients with laryngopharyngeal reflux.
Earn continuing education credits (CME/CE) on this topic.

Introduction

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.” [1]  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 vocal cords or glossitis. Reflux is normally sequestered within the stomach and sometimes escapes into the distal 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. Dysfunction in any of the above 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 sphincter 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 muscles, 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 a protective alkaline buffer.

Etiology

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 as well. 

Epidemiology

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.[2]

Pathophysiology

The retrograde flow of gastric acid and pepsin induces laryngeal mucosal damage and impaired mucociliary clearance. Three different theories explain this damage. 1) Direct contact of acid and pepsin with the epithelium induces damage. 2) Gastric refluxate with additional vocal abuse causes symptoms. 3) Mucosal lesions.[3] The esophageal-bronchial reflex theory suggests that acid in the distal esophagus vagally stimulates a chronic cough, which induces laryngeal symptoms.

Histopathology

In one study, post-cricoidectomy epithelial cells from patients suffering from laryngopharyngeal reflux were examined and shown to contain pepsin while the control group cells did not.[3] 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 the uptake of pepsin into cells.

History and Physical

Laryngopharyngeal reflux encompasses many symptoms that could bring a patient into the clinic. Hoarseness is the most prevalent symptom of laryngopharyngeal reflux (100%) with none of the patients with the more common condition of gastroesophageal disease (GERD) reporting hoarseness.[1]

Patients can have a multitude of other symptoms including globus sensation, chronic throat clearing, heartburn, other voice changes, and regurgitation.[4] Patients with laryngopharyngeal reflux typically have upright, or daytime, reflux with good esophageal motor function.[5] This is compared to supine or nocturnal symptoms in patients with reflux who had esophageal motor dysfunction.[6] Patients with gastroesophageal reflux (GERD) have dysfunction of their lower esophageal sphincter in contrast to the upper esophageal sphincter pathology seen in laryngopharyngeal reflux.[7]

Reflux Symptom Index

The reflux symptom index (RSI) is a validated questionnaire to determine the likelihood of positive results of dual diagnoses.[8] RSI greater than 10 is correlated with a high likelihood of reflux pathology. It is an eight-item questionnaire given to patients to score the severity of their symptoms on a scale of 0 to 5 (5 being the most severe). It asks the patient to score:

  • The degree of hoarseness
  • Frequency of throat clearing
  • Degree of throat mucus or postnasal drip
  • Dysphagia
  • Coughing after eating or lying down
  • Breathing difficulties
  • Chronic cough
  • Globus sensation
  • Heartburn

On a physical exam, an otolaryngologist can perform laryngoscopy as well as videostroboscopy. Posterior thickening and pachydermia of laryngeal posterior commissure and post-cricoid mucosa have been associated with laryngopharyngeal reflux.[9] Granulomas of the vocal process have also been highly associated with the disease.[10] Edema along the undersurface of the vocal fold from the anterior to the posterior commissure has a fair sensitivity and specificity for the presence of LPR.[6]

Evaluation

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.[11] 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%.[12] Esophagrams showed a sensitivity of 20% with a specificity of 64% to 90%.[12]

Treatment / Management

Lifestyle modifications are the first step in 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 carbonated 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.

Differential Diagnosis

Laryngeal complaints similar to laryngopharyngeal reflux manifestations have a broad differential.  Most commonly, laryngopharyngeal reflux may be misdiagnosed as gastroesophageal reflux (GERD). Distinctions between these two common conditions have been stated elsewhere in this chapter. As a diagnosis of exclusion, globus hystericus may present with many of these same symptoms. Once LPR has been ruled out via a trial of medical and lifestyle therapy, anxiolytics may be useful.

Prognosis

Long-term untreated laryngopharyngeal reflux can lead to chronic vocal injury with resultant scarring of the true vocal folds. Laryngopharyngeal reflux may also be related to untreated GERD, which can lead to Barrett's esophagitis if left untreated. Also, one study showed in a retrospective chart review that untreated laryngopharyngeal reflux can lead to subglottic stenosis over time.[13]

Complications

As stated above, significant long-term complications of LPR can occur if the disease is left untreated on unrecognized. Commonly listed complications include:

  • Chronic cough
  • Recurrent laryngitis
  • Oral cavity disorders/ulcers
  • Recurrent bronchopulmonary injury/infections

In rare instances, LPR has been identified as a risk factor for laryngeal carcinoma, though this association is under investigation and remains unclear.[14]

Consultations

If a patient continues to have symptoms of hoarseness, dyspnea, and chronic sore throat despite lifestyle changes, an otolaryngologic referral is a good option. Also, a gastroenterologist may need to get involved for possible esophagoscopy to ensure no malignant process is occurring.

Deterrence and Patient Education

Laryngopharyngeal reflux can usually be treated with lifestyle modifications, though LPR can be frustrating as it may not respond as readily to such lifestyle changes as classic GERD. With time, these symptoms can resolve, and the need for anti-reflux medication will abate. For this reason, patient education becomes a crucial aspect of management. Patients need ongoing education on lifestyle modifications including weight loss, reduction in portion size of the meal, and refraining from lying down within 3 hours of a meal. Dietary modifications including adherence to low fat and low acid diet, avoiding carbonated or caffeinated beverages, and reducing alcohol intake is imperative.

Enhancing Healthcare Team Outcomes

Laryngopharyngeal reflux appears to be a common yet under-diagnosed. Despite the available drugs and surgical procedures to manage this condition, it is important to recognize that lifestyle modifications are first-line therapy for this condition. To achieve this goal, an interprofessional team approach is needed. In addition to astute clinicians, treatment and management of LPR requires specialty trained nurses to help educate the patient on lifestyle modifications including weight loss, reduction in portion size of the meal, and refraining from lying down within 3 hours of a meal. Education on dietary modifications including adherence to low fat and low acid diet, avoiding carbonated or caffeinated beverages, and reducing alcohol should be provided by primary care nurses as well as dieticians. When medical therapy is required, the management of the patient requires clinical pharmacists to help assist the clinical team in providing the lowest therapeutic dose of therapy and in adjusting other medications to minimize adverse interactions. A collaborative interprofessional team across multiple disciplines can help improve outcomes in patients with LPR. [Level V]

Continuing Education / Review Questions

References

1.
Sataloff RT. Gastroesophageal reflux-related chronic laryngitis. Commentary. Arch Otolaryngol Head Neck Surg. 2010 Sep;136(9):914-5. [PubMed: 20855686]
2.
Koufman JA. The otolaryngologic manifestations of gastroesophageal reflux disease (GERD): a clinical investigation of 225 patients using ambulatory 24-hour pH monitoring and an experimental investigation of the role of acid and pepsin in the development of laryngeal injury. Laryngoscope. 1991 Apr;101(4 Pt 2 Suppl 53):1-78. [PubMed: 1895864]
3.
Johnston N, Wells CW, Samuels TL, Blumin JH. Rationale for targeting pepsin in the treatment of reflux disease. Ann Otol Rhinol Laryngol. 2010 Aug;119(8):547-58. [PubMed: 20860281]
4.
Burton LK, Murray JA, Thompson DM. Ear, nose, and throat manifestations of gastroesophageal reflux disease. Complaints can be telltale signs. Postgrad Med. 2005 Feb;117(2):39-45. [PubMed: 15745124]
5.
Postma GN, Tomek MS, Belafsky PC, Koufman JA. Esophageal motor function in laryngopharyngeal reflux is superior to that in classic gastroesophageal reflux disease. Ann Otol Rhinol Laryngol. 2001 Dec;110(12):1114-6. [PubMed: 11768699]
6.
Belafsky PC, Postma GN, Koufman JA. Laryngopharyngeal reflux symptoms improve before changes in physical findings. Laryngoscope. 2001 Jun;111(6):979-81. [PubMed: 11404607]
7.
Sivarao DV, Goyal RK. Functional anatomy and physiology of the upper esophageal sphincter. Am J Med. 2000 Mar 06;108 Suppl 4a:27S-37S. [PubMed: 10718448]
8.
Lechien JR, Huet K, Finck C, Khalife M, Fourneau AF, Delvaux V, Piccaluga M, Harmegnies B, Saussez S. Validity and Reliability of a French Version of Reflux Symptom Index. J Voice. 2017 Jul;31(4):512.e1-512.e7. [PubMed: 28069467]
9.
Ylitalo R, Lindestad PA, Ramel S. Symptoms, laryngeal findings, and 24-hour pH monitoring in patients with suspected gastroesophago-pharyngeal reflux. Laryngoscope. 2001 Oct;111(10):1735-41. [PubMed: 11801936]
10.
Noordzij JP, Khidr A, Desper E, Meek RB, Reibel JF, Levine PA. Correlation of pH probe-measured laryngopharyngeal reflux with symptoms and signs of reflux laryngitis. Laryngoscope. 2002 Dec;112(12):2192-5. [PubMed: 12461340]
11.
Smit CF, Tan J, Devriese PP, Mathus-Vliegen LM, Brandsen M, Schouwenburg PF. Ambulatory pH measurements at the upper esophageal sphincter. Laryngoscope. 1998 Feb;108(2):299-302. [PubMed: 9473087]
12.
Johnston BT, Troshinsky MB, Castell JA, Castell DO. Comparison of barium radiology with esophageal pH monitoring in the diagnosis of gastroesophageal reflux disease. Am J Gastroenterol. 1996 Jun;91(6):1181-5. [PubMed: 8651167]
13.
Maronian NC, Azadeh H, Waugh P, Hillel A. Association of laryngopharyngeal reflux disease and subglottic stenosis. Ann Otol Rhinol Laryngol. 2001 Jul;110(7 Pt 1):606-12. [PubMed: 11465817]
14.
Close LG. Laryngopharyngeal manifestations of reflux: diagnosis and therapy. Eur J Gastroenterol Hepatol. 2002 Sep;14 Suppl 1:S23-7. [PubMed: 12570026]
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This book is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to the Creative Commons license, and any changes made are indicated.

Bookshelf ID: NBK519548PMID: 30137832

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