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Table of Contents
Year : 2019  |  Volume : 16  |  Issue : 4  |  Page : 220-224

Impact of laryngopharyngeal reflux on professional singers

1 Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University (Deemed to be), Bhubaneswar, Odisha, India
2 Department of Otorhinolaryngology, Apollo Hospital, Bhubaneswar, Odisha, India

Date of Submission20-Sep-2019
Date of Acceptance09-Oct-2019
Date of Web Publication12-Dec-2019

Correspondence Address:
Santosh Kumar Swain
Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University (Deemed to be), Bhubaneswar - 751 003, Odisha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/am.am_24_19

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Laryngopharyngeal reflux (LPR) is retrograde flow of gastric content to the larynx and pharynx where these materials come in contact with the upper aerodigestive tract. It is an inflammatory disease associated with voice disorders and lesions in vocal fold. Presence of LPR among professional voice users such as singers can have a dramatic impact on voice quality. Singers are high-risk candidates for LPR because of necessary air support involving higher intra-abdominal pressure, more stress due to professional career, uncomfortable schedules, late meals before going to sleep, and bad food habits such as increased intake of citrus products, fatty, and spicy foods. The objective of this article is to review the current etiopathogenesis, clinical presentations, diagnosis, treatment, and lifestyle modification in cases of singers suffering from LPR and to propose a new patient-related outcome.

Keywords: Dysphonia, laryngopharyngeal reflux, proton-pump inhibitors, singers

How to cite this article:
Swain SK, Pradhan S. Impact of laryngopharyngeal reflux on professional singers. Apollo Med 2019;16:220-4

How to cite this URL:
Swain SK, Pradhan S. Impact of laryngopharyngeal reflux on professional singers. Apollo Med [serial online] 2019 [cited 2022 Dec 7];16:220-4. Available from: https://apollomedicine.org/text.asp?2019/16/4/220/272819

  Introduction Top

Laryngopharyngeal reflux (LPR) occurs due to retrograde movement of gastric acid to the larynx and pharynx. This clinical entity affects the upper aerodigestive tract which is different from gastroesophageal reflux disease (GERD). Patients of LPR often present with dysphonia, foreign body sensation in the throat, presence of phlegm, and chronic cough. In case of professional singers, it will affect extension of the voice, particularly loss of high notes, change in tone of voice that can be expressed as loss of crystal or opaqueness of voice, voice fatigue, trills, and breaks with inability to sing without interruption.[1] The sound produced from the larynx is nothing, but a buzz which is different from that of wonderful voice of singers. This sound coming from the larynx is made up of tones and the tones called harmonics in musical language or overtones in English language.[2] Although LPR is a well-established cause for laryngeal manifestations in adults, it is a less known among singers. At present, LPR in professional singers is still associated with recurrent clinical symptoms and poor quality of voice which has a significant cost for the professional excellence. In this review article, we will discuss the impact of LPR singers including etiopathology, clinical presentations, diagnosis, treatment, and lifestyle modifications.

  Methodology Top

For searching the published article, we conducted an electronic search of the Scopus, Medline and PubMed databases. The search term in the database includes Laryngopharyngeal reflux, singers, and dysphonia. The abstracts of the published article are identified by this search method, and other articles were identified manually from the citations. This review article reviews the current etiopathogenesis, clinical presentations, diagnosis, and treatment of LPR on voice quality of singers and to proposes a new patient-related outcome. This review article makes a baseline from where further prospective trials can be designed and help as a spur for further research in this commonly encountered clinical entity where not many studies are done.

  Etiopathogenesis Top

LPR is often a diagnostic challenge due to lack of understanding the etiology and pathophysiology of this clinical condition. There are two theories have been proposed to explain the laryngeal manifestations of LPR. The microaspiration theory postulates that acid-peptic injury occurs to the larynx directly by esophagopharyngeal reflux, whereas the esophagobronchial reflex theory explains that acidification of the distal part of the esophagus may induce laryngeal symptoms by a vagally mediated reflex.[3] Larynx is enormously innervated and reflux in a normal person elicits a protective cough. However, this protective mechanism by the larynx may be altered in LPR. One study reveals reduced laryngeal adductor reflexes in response to endoscopic administration of air pulses in a group of patients.[2] This may cause raised stasis of injurious agents at the larynx. Irritation of laryngeal mucosa is important etiological mechanism in LPR. The chemicals of gastric or gastroduodenal content reflux are acid, pepsin, bile salts, trypsin, and some gastroduodenal proteins which are concerned in chemical injury and inflammation in LPR.[4] Pepsin has been found in intracellular and extracellular laryngeal environments of LPR patients in both clinical and experimental studies.[5],[6] The endocytosis of pepsin damages mitochondria and enhances expression of several genes related to recruitment of inflammatory cells, migration, differentiation, angiogenesis, and growth of laryngeal cells.[7] Acid pepsin also negatively affect expression of growth factors for wound repair and angiogenesis; decrease the mucosal healing and prolongs irritation process. Hence, pepsin is associated with decreased mucosal hydration, inhabitation of mucin and anhydrase carbonic gene expression, and reduction of squamous epithelial heat-shock protein related to cellular protection from chemical and mechanical stress. Microtrauma of vocal fold epithelium by pepsin leading to increased risk of developing benign lesions such as vocal fold sulcus or nodules.[8]

One study demonstrated that the intermittent application of gastric acid to canine vocal folds cause granuloma, which appears as early lesion of human subglottic stenosis (SGS).[8] In the esophagus, carbonic anhydrase helps to neutralize acid reflux to almost neutrality. Carbonic anhydrase is a defense component of the esophageal mucosa which catalyzes the hydration of carbon dioxide, forms bicarbonate, and neutralizes the acid reflux at extracellular space. Increased expression of carbonic anhydrase III may be a cause of epithelial hyperplasia, which is a histological feature of esophagitis. In the presence of pepsin in LPR, the expression of carbonic anhydrase III reduced in the vocal folds, worsening the acid-induced injury and more at the posterior commissure. LPR is also now considered as one of the important causes for development of chronic inflammatory conditions of the middle ear cleft such as otitis media with effusion the damaging effects of gastric acid and pepsin on the subglottic mucosa have been confirmed in the animal models.

  Clinical Presentations Top

Signers suffering from LPR may present with dysphonia which affects the professional duty. The common symptoms in LPR are hoarseness of voice, excessive clearing of throat, coughing, and globus pharyngeus. Hoarseness of voice is usually fluctuating and more in morning time and improves during the daytime as advances.[9] Laryngopharyngeal endoscopic picture shows arytenoid edema, vocal fold edema, interarytenoid pachydermia, and presence of mucous and pseudosulcus.[7] The other laryngeal symptoms in LPR are sensation of fullness in throat, postnasal drip with repeated throat cleaning, chronic cough, and laryngeal spasm. There are no specific clinical presentations of LPR. They often present with a wide range of atypical symptoms and signs. Singers may present with occasional vomiting where they will not realize vomiting, as a problem when it occurs no more than one episode daily. Adult patients of LPR may complain dysphagia and regurgitation or heartburn, whereas some child singers cannot describe their symptoms. The common clinical symptoms are throat clearing or cough. Without these commonly seen symptoms, LPR may not be considered as differential diagnosis, where hoarseness of voice an even more important clue, and sometimes, the only clue for diagnosing LPR. In LPR, some other clinical presentations are dysphonia, chronic cough, reactive airway diseases, excessive throat mucus, postnasal drip, middle ear effusion, and laryngeal carcinoma. Singers are high-risk candidates for LPR because of required air support by intense use of abdominal muscles, raised intra-abdominal pressure, increased mental stress due to career management and busy work schedule, late meals just before sleep, and bad food habits such as more intake of citrus products and fatty and spicy foods.[10] The LPR symptoms in singers may affect and interfere with high-quality voice production. A study revealed the higher prevalence of hoarsed voice and cough among professional Opera Choristers than population sample.[11] Postoperative tonsillectomies patients often present compensatory hypertrophy lingual tonsils which lead to clearing of throat and foreign body sensation. LPR may give rise to various respiratory and otolaryngological conditions, including recurrent bronchitis, refractory bronchial asthma, laryngomalacia, and SGS. Although similarities between LPR and GERDs, there are few clinical distinctions are present between them [Table 1].
Table 1: Difference between laryngopharyngeal reflux and gastroesophageal reflux disease

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The laryngoscopic findings in LPR are nonspecific signs of laryngeal inflammation and irritation. The laryngeal pictures show edema, erythema, particularly in the posterior part of the larynx [Figure 1].[12] Granuloma, contact ulcers, and pseudosulcus are also common findings seen in laryngeal examinations. LPR has been implicated in the cause of several laryngeal diseases such as reflux laryngitis, SGS, granuloma, laryngeal carcinomas, vocal nodules, and contact ulcers.[13] Those patients showing vocal fold cyst also showing reflux in endoscopic picture suggesting role of LPR in the development of vocal fold cysts in patients. Vocal nodules are also seen in LPR patients who suggest some nodules are part of the pathophysiologic dynamic with LPR. SGS is the most dreaded complication of LPR, although trauma and infections are two more important causative factors for SGS.
Figure 1: Endoscopic picture of the larynx in a singer suffering with laryngopharyngeal reflux

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  Diagnosis Top

Proper history taking has an important role for clinician to approach hoarseness of voice in professionals like singers. Patients often present with nonspecific mild posterior laryngitis. Progressive or persistent hoarseness lasting more than 2–3 weeks needs detailed examination of the laryngopharynx to rule out other serious entities. It is always good practice to examine the larynx in case of suspected cases of LPR as of apparent known association between LPR and upper aerodigestive area malignancy. LPR should be suspected from clinical history and endoscopic findings of the larynx and hypopharynx. If hoarseness is a prominent clinical symptom, acoustic voice analysis such as frequency, intensity, perturbation, and signal-to-noise ratio gives an objective documentation of symptom severity and progression of the LPR.[14] Laryngeal endoscopic picture often shows signs of nonspecific inflammation of larynx, particularly at posterior part. There are thickening of the vocal folds, congestion, and edema at posterior larynx, although not pathognomonic. On the basis of color analysis, one study quantified the degree of erythema as measure of posterior laryngitis.[13] Sometimes, contact granuloma is associated with LPR. Often, the medial edge of the vocal fold shows a lineal indentation due to infraglottic edema which gives the illusion of the sulcus vocalis. As there are no pathognomonic findings in LPR, Belafsky et al. developed an eight-point clinical scale for assessing and follow-up of the LPR. These laryngeal findings are subglottic edema, ventricular obliteration, hyperemia or erythema, vocal fold edema, diffuse laryngeal edema, posterior commissure hypertrophy, thick endolaryngeal edema, and granuloma.

Diagnosis of LPR may be established by asking questions of the symptoms, videolaryngoscopic examination of the larynx, or double-probe pH monitoring. Ambulatory 24-h double-probe (esophageal and pharyngeal) pH monitoring is highly sensitive and specific for the diagnosis of LPR.[14] There is no ideal diagnostic method for LPR in pediatric age. There are different methods available for diagnosis of LPR and these are pH monitoring, intraluminal impedance, barium studies, scintigraphy, ultrasound, fluoroscopy, and esophageal biopsy. The current gold standard test for LPR is the dual-probe 24-h pH monitoring. However, it is an invasive test with false-negative results reaching as high as 50%.[15] Some additional studies such as radiography, esophageal manometry, and spectrophotometric measurement of bile reflux and biopsy from mucosa.

  Treatment Top

The management of LPR in singers includes lifestyle modifications and pharmacological treatment. Counseling for diet and lifestyle modifications are an important part of the treatment. The positive impact of alkaline and low-fat diet is helpful for singers whose symptoms are refractory to proton-pump inhibitors (PPIs).[16] Dietary changes and changes of habits such as stop smoking (active and passive), reduce weight (in obese), avoid alcohol, and not take meal immediately bedtime. Dietary restrictions such as chocolate, caffeine, fat, tomato sauce, red wine, and gasified beverages.[9] LPR can be reduced by changing dietary habits. Patients are advised to eat dinner early (at least 2 h before bedtime). They should avoid spicy foods, carbonated drinks, high-fat foods, and chocolates. Larynx is more susceptible to injury due to refluxate than esophagus, so acid must be suppressed adequately around the clock. The treatment for LPR should be more aggressive than treatment of gastroesophageal disease (GERD). The traditional treatment of GERD such as dietary and lifestyle modifications and use of antacids, H2 antagonist, or proton-pump inhibitor fail to control LPR in as many as 50% of the patients suffering from LPR.[15] The antireflux treatment for LPR is optimized by taking medications in the morning and again later in evening prior to dinner. In case of long-standing LPR, patients need treatment for months with twice daily dose to resolve symptoms. At present, most common drugs used for treating LPR are PPIs, which suppress the production of acid by acting directly on the H +-K + ATPase of the parietal cells. PPIs may not only protect from exposure of the upper aerodigestive tract, but also decrease the injury from the enzymatic activity of pepsin, which need an acid medium for activation.[9] Patients should be educated for taking proton-pump inhibitors such as omeprazole, esomeprazole, rabeprazole, lansoprazole, and pantoprazole which work best if taken 30–60 min before meals. Singers diagnosed with LPR, who are under treatment with speech therapy and pharmacotherapy, have higher rate of improvement than those who received medical/drug therapy alone. In patients with LPR and vocal nodules have higher rate of improvement than either therapy alone.[17] Duration of ongoing injury due to acid reflux, exposure to irritants such as smoke and alcohol may account for the treatment period. Early treatment of LPR in patients results in improvement of laryngeal symptoms like hoarseness of voice. The endoscopic examination of the larynx is usually sufficient to guide treatment without requirement for other diagnostic tests. Duration of injury due to acid reflux and exposure to irritants such as smoke and alcohol may account for the treatment period. Early treatment of LPR in patients results in improvement of laryngeal symptoms like hoarseness of voice. The endoscopic examination of the larynx is usually sufficient to guide treatment without requirement for other diagnostic tests. Surgical treatment is reserved for the children, in whom medical therapy failed or associated with life-threatening symptoms. Surgery for LPR is helpful to avoid long-term medications. However, recent data suggests surgery has high rate of failure along with morbidity and mortality. Singers those have no respiratory symptoms have better surgical outcome. There should be more randomized controlled trials for assessing the antireflux surgery in atypical pediatric LPR. Patients for surgery should have a definite diagnosis of LPR and prolonged and aggressive PPI medications for considering fundoplication. A patient who's LPR fails to resolve after medical or surgical treatment must be followed indefinitely with proper examination of the upper aerodigestive area for signs of complications.

  Lifestyle Modifications Top

Singers of LPR are advised to do regular exercise for at least 30 min each day as a guard against reflux symptoms. Patients, who are less active physically, are prone for developing reflux symptoms.[18] Singers are advised to stop smoking, as it can cause acid production.[19] Cigarette smoking is directly associated with acid retention leading to slow clearance of esophageal acid. Smokers have been shown a higher incidence of reflux symptoms than nonsmokers. Alcohol consumption is associated with higher chance of reflux symptoms than nonalcoholics. White wine has more effect on acid exposure than does red wine consumption. Weight gain of the singers aggravates reflux symptoms, whereas weight loss can lead to reverse effect, allowing them to reduce for taking reflux medications.[20] Excessive tea, coffee, and spicy food aggravate LPR among singers so suggested to avoid it. They are also advised to avoid prolonged empty stomach and sleep 2–3 h after meals.

  Conclusion Top

LPR in singers is suspected from the clinical history and endoscopic findings. The various clinical presentations of LPR in children are usually nonspecific. The clinical presentations are postnasal drip, globus sensation in throat, throat clearing, cough, and chocking sensation in the throat. It may give rise to dysphagia, throat pain, and odynophagia. The endoscopic findings in laryngeal structures such as vocal fold edema, laryngeal edema, and posterior commissure mucosal hypertrophy are important features in LPR among singers. If LPR is suspected in singers, 24-h pharyngeal pH monitoring appears to a useful well-tolerated diagnostic tool for confirmation. There are no specific tests for diagnosing LPR. Empirical treatment with PPIs has been widely accepted as diagnostic tests and treatment options of LPR. Other treatment are lifestyle and dietary modifications such as quitting smoking and drinking alcohol, weight loss, and avoid caffeine.

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  References Top

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Johnston N, Yan JC, Hoekzema CR, Samuels TL, Stoner GD, Blumin JH, et al. Pepsin promotes proliferation of laryngeal and pharyngeal epithelial cells. Laryngoscope 2012;122:1317-25.  Back to cited text no. 4
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  [Table 1]


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