Journal of Clinical Sciences

ORIGINAL RESEARCH REPORT
Year
: 2020  |  Volume : 17  |  Issue : 3  |  Page : 61--65

Experience with the management of pediatric laryngopharyngeal reflux in an Indian teaching hospital


Santosh Kumar Swain1, Jasashree Choudhury2,  
1 Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University, Bhubaneswar, Odisha, India
2 Department of Pediatrics, IMS and SUM Hospital, Siksha “O” Anusandhan University, Bhubaneswar, Odisha, India

Correspondence Address:
Dr. Santosh Kumar Swain
Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University, K8, Kalinganagar, Bhubaneswar - 751 003, Odisha
India

Abstract

Aim: Laryngopharyngeal reflux (LPR) is the retrograde flow of gastric content to the larynx and pharynx where these materials come in contact to the upper aerodigestive tract. This clinical entity is less studied among the pediatric population. The objective of this study is to evaluate the impact of LPR in the pediatric population. Materials and Methods: This retrospective study was done in between December 2016 and January 2019. Clinical data such as associated symptoms, endoscopic findings, laboratory testing, therapeutic interventions, and outcome were analyzed. Endoscopic findings were considered to be consistent with LPR in the pediatric age included: Lingual tonsil hypertrophy, postglottic edema, true vocal fold edema and congested and swollen arytenoids, congested inter-arytenoids area. Results: There were 212 children evaluated for dysphonia. There were 38 girls (52.77) and 34 boys (47.22%), and mean age at presentation was 9.32 years with a male-to-female ratio of 0.89:1. Out of 212 children who underwent endoscopy, 72 had shown LPR disease. Five children (6.94%) showed vocal nodules, 3 (4.16%) showed vocal fold cyst, and 2 (2.77%) children showed subglottic edema along with LPR. All the children were treated with anti-reflux measures. By second follow-up visit on 1 month, 68 children (94.44%) had improved symptomatically. Conclusion: LPR appears to cause laryngeal manifestations more commonly in children. In this study, all the children were presenting dysphonia, intermittent cough, foreign-body sensation in throat, and throat-clearing habit. All of them showing congested arytenoids and inter-arytenoid membrane. Early diagnosis and treatment often result in the improvement of hoarseness of voice and prevent complications. LPR in the pediatric population is almost a new diagnosis.



How to cite this article:
Swain SK, Choudhury J. Experience with the management of pediatric laryngopharyngeal reflux in an Indian teaching hospital.J Clin Sci 2020;17:61-65


How to cite this URL:
Swain SK, Choudhury J. Experience with the management of pediatric laryngopharyngeal reflux in an Indian teaching hospital. J Clin Sci [serial online] 2020 [cited 2020 Sep 30 ];17:61-65
Available from: http://www.jcsjournal.org/text.asp?2020/17/3/61/288905


Full Text



 Introduction



Laryngopharyngeal reflux (LPR) is also called as supra-esophageal reflux or extra-esophageal reflux or silent reflux, which refers to a clinical condition where gastroduodenal content goes up to the esophagus and affects throat, particularly the laryngopharynx.[1] In few cases, the gastric contents may reach the nostrils and/or ears through the Eustachian tubes, which aggravates the rhinitis, sinusitis, or otitis media.[2] The findings in laryngeal structures are vocal fold edema, laryngeal edema, and posterior commissure mucosal hypertrophy are important features in pediatric LPR. If LPR is suspected in a pediatric patient, 24 h pharyngeal pH monitoring appears to a useful and well-tolerated diagnostic tool for confirmation. 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.[3] It may give rise to dysphagia, throat pain, and odynophagia. Change in voice is estimated to occur in 6%–23% of children.[4] Although LPR is a well-established cause for laryngeal manifestations in adults,[5] it is a less known among children. In the present study, we evaluate the details of LPR in the pediatric population.

 Materials and Methods



There were 212 children evaluated for dysphonia at the outpatient department of otorhinolaryngology of a tertiary care teaching hospital of Eastern India from December 2016 to January 2019. Out of the 212 children, 72 confirmed the findings for LPR on the basis of clinical presentations and endoscopic findings. There were 72 children, with a mean age of 9.32 years participated in this study where 34 were boys and 38 were girls. The youngest child was 3 years old, and the oldest was 16 years. This is a retrospective study, and it was approved by the Institutional Ethics Committee. Consents from the parents of the participants were obtained for this study. The children those with hoarseness of voice were included in this study and underwent endoscopy. Data collection included age, sex, clinical presentations, endoscopic findings, treatment, and follow-up visits. Children with velopharyngeal insufficiency and children with gastrointestinal diseases under the treatment were excluded from this study. Complaints of the children other than hoarseness of voice such as habit of throat clearing, foreign-body sensation in throat, and blockage feeling in throat were also documented. Detail examinations of the throat, nose, and ear were done in all the children. Flexible nasopharyngolaryngoscopy was performed in the children for the examinations of the larynx and pharynx. Endoscopic assessment was done with the help of flexible nasopharyngolaryngoscopy. Endoscopic findings were documented and reviewed by senior authors. Endoscopic findings considered to be consistent with LPR in pediatric age included: Lingual tonsil hypertrophy, postglottic edema, true vocal fold edema and congested and swollen arytenoids, congested inter-arytenoids area. Children at the time of presentations did not have any gastrointestinal diseases. Adjunct testing for reflux like 24 h dual-channel pH monitoring was done at the department of gastroenterologists. Treatment interventions and their outcome were recorded from two subsequent visits. Treatment included diet modifications, medications (H2 blockers, proton-pump inhibitors, and prokinetics) as per weight of the child, speech language therapy, and anti-reflux surgery.

 Results



There were 212 children underwent laryngeal endoscopy for the evaluation of the hoarseness of the voice. Out of the 212 children, 72 revealed LPR features in the larynx. Out of 72 children diagnosed with LPR in this study where 34 were male (47.22%) and 38 were female (52.77%) with a mean age was 9.32 years. Out of 72 children, 9 were exposed to passive smoking from the family members. Eight children had a history of previous tonsillectomy surgery. Five children were professional singers and 9 children were passive smokers [Table 1]. Out of the 72 children, all presented with dysphonia, intermittent cough, and pharyngeal globus, and 72 had throat clearing [Table 2]. Dysphagia heart burning was presented among 65 (90.27%) and 64 (88.88%) children, respectively. All 72 children showed congested arytenoids and interarytenoid membrane [Figure 1]. Lingual tonsillar hypertrophy was seen in 7 children (9.72%). Vocal fold cyst [Figure 2] was observed in three children (4.16%). In five children (6.94%), vocal nodules were observed. Subglottic edema [Figure 3] was seen in two (2.77%) cases [Table 3]. One case associated with Reinke's edema [Figure 4]. The clinical symptoms observed in the pediatric patients are persistent cough, throat clearing, globus pharyngeus, and hoarseness of voice. All the children were sent for gastroenterologist consultation for the proper evaluation and confirmed of gastritis in 13 (18.05%) children and hernia in 2 (2.77%) cases. All the 72 cases confirmed as LPR after the tests of double-probe pH monitor. There were H pylori-positive antrum (gastric) seen in six (8.33%) cases. Children with LPR were treated with proton-pump inhibitor and anti-reflux therapy. A remarkable good therapeutic outcome occurred because of symptomatic relief of the cough and other throat symptoms. There were 72 children with LPR were under follow-up visits after the treatment. Twenty-eight (38.88%) were treated with speech therapy, and 44 (61.11%) children were treated with pharmacotherapy alone. Out of 72 children, 68 (94.44%) improved symptomatically.{Table 1}{Table 2}{Figure 1}{Figure 2}{Figure 3}{Table 3}{Figure 4}

 Discussion



LPR is an inflammatory disease due to backflow of the gastric contents into the laryngopharynx, where it contacts to the tissues of the upper aerodigestive tract.[6] The physiological barriers for preventing LPR include lower esophageal sphincter, esophageal peristalsis, gravity, saliva, and upper esophageal sphincter. When these physiological barriers fail, stomach content come in touch with the laryngopharyngeal tissues, leading to damage of epithelium, ciliary dysfunction, altered sensitivity, and inflammation. The laryngeal symptoms in pediatric LPR include hoarseness of voice, sensation of fullness in throat, postnasal drip with repeated throat cleaning, chronic cough, and laryngeal spasm. There are no specific clinical presentations of LPR in the pediatric populations. They often present with a wide range of atypical symptoms and signs. Children may present with vomiting where parents will not realize vomiting as a problem when it occurs no more than one episode daily. Sometimes children may present with excessive crying, failure to thrive, irritability, and feeding problems. Adult patients of LPR may complain dysphagia, regurgitation, or heartburn whereas pediatric patients 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 gives an even important clue and sometimes the only clue for diagnosing LPR. In LPR, some other clinical presentations are like dysphonia, chronic cough, reactive airway diseases, excessive throat mucus, postnasal drip, middle ear effusion, and laryngeal carcinoma.[7] 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, bad food habits such as more intake of citrus products, fatty, and spicy foods.[8] The LPR symptoms in children may affect and interfere with high-quality voice production. A study revealed a higher prevalence of hoarsed voice and cough among professional opera choristers than population sample.[9] In this study, 5 (6.94%) children were professional singers. Postoperative tonsillectomies children often present compensatory hypertrophy lingual tonsils which lead to clearing of throat and foreign-body sensation. This may aggravate LPR. In this study, 8 (11.11%) children have a history of tonsillectomy surgery in the past.

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.[1] In this study, all the 72 (100%) patients presented with congestions of the arytenoids and interarytenoid membrane. Granuloma, contact ulcers, and pseudosulcus are also the common findings seen in laryngeal examinations. LPR has been implicated in the cause of several laryngeal diseases such as reflux laryngitis, subglottic stenosis (SGS), granuloma, laryngeal carcinomas, vocal nodules, and contact ulcers.[10] In this study, 5 (6.94%) children were showing vocal nodules and 2 (2.77) children showed subglottic edema. Those patients showing vocal fold cyst also showing reflux in the endoscopic picture, suggesting the role of LPR in the development of vocal fold cysts in pediatric patients. In this study, 3 (4.16%) children showed vocal fold cysts. 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 complications of LPR, although trauma and infections are two more important causative factors for SGS. The damaging effects of gastric acid and pepsin on the subglottic mucosa have been confirmed in the animal models. One study demonstrated that the intermittent application of gastric acid to canine vocal folds cause granuloma, which appears as early lesion of human SGS.[11] In the esophagus, carbonic anhydrase helps to neutralizes acid reflux to almost neutrality. Carbonic anhydrase is a defense component of the esophageal mucosa which catalyzes the hydration of carbon dioxide, form bicarbonate and neutralizes the acid reflux at the extracellular space. Increased expression of carbonic anhydrase III may be a cause of epithelial hyperplasia, which is a histological feature of esophagitis.[12] 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. There are three approaches for confirming the diagnosis of the LPR. First is clinical presentations of the patients and empirical medical treatment; second is endoscopic findings; and third one is demonstrations of the reflux events by pH monitoring and multichannel impedance. The diagnosis of LPR may be established by asking questions of the symptoms, videolaryngoscopic examination of the larynx, or double-probe pH monitoring.[13] 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 the pediatric age. There are different methods available for the diagnosis of LPR, and these are pH monitoring, intra-luminal 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] All of our 72 children confirmed as LPR after tests of double-probe pH monitor. Some additional studies such as radiography, esophageal manometry, spectrophotometric measurement of bile reflux, and biopsy from mucosa. The endoscopic examination can be done by flexible or rigid laryngoscopy in suspected cases.

The aim of the treatment of LPR in the pediatric populations is to heal the mucosal damage, relieve the symptoms, and prevent recurrence. The treatment of pediatric LPR is often challenging as it is difficult to differentiate between the physiological reflux from pathological reflux. Treatment includes dietary changes and changes of habits such as stop smoking (active and passive), reduce weight (in obese child), avoid alcohol, and not take meal immediately bedtime. Dietary restrictions include chocolate, caffeine, fat, tomato sauce, red wine and gasified beverages.[16] LPR is often associated with bad dietary habits. LPR can be reduced by changing dietary habits. Children are advised to eat dinner early (at least 2 h before bedtime). The children with LPR should avoid spicy foods, carbonated drinks, high fat foods, and chocolates.[17] 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 the 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.[18] The anti-reflux treatment for LPR is optimized by taking medications in the morning and again later in the evening before dinner. In case of long-standing LPR, patients need treatment for months with twice daily dose to resolve the symptoms. Patients should be educated for taking proton-pump inhibitors such as omeprazole, esomeprazole, rabeprazole, lansoprazole, and pantaprazole which work best if taken 30–60 min before meals. Children diagnosed with LPR those are under treatment with speech therapy and pharmacotherapy have higher rate of improvement than those who received medical/drug therapy alone. In children with LPR and vocal nodules have higher rate of improvement than either therapy alone.[19] In this study, 28 (38.88%) children were treated with speech therapy, and 44 (61.11%) children were treated with pharmacotherapy alone. Duration of ongoing injury due to acid reflux, exposure to irritants such as smoke and alcohol may account for the treatment period. Surgical treatment is reserved for the children in whom medical therapy failed or associated with life-threatening symptoms. Early treatment of LPR in the pediatric patients results in the improvement of laryngeal symptoms such as hoarseness of voice. The endoscopic examination of the larynx is usually sufficient to guide the treatment without requirement for other diagnosis tests.

LPR in pediatric population is almost a new diagnosis. Unless clinician is carefully assessing the larynx, many of the findings may be missed as one focuses only on the vocal folds and not over the entire larynx. Furthermore, inflammation and edema of the vocal folds in LPR may be confused with vocal fold nodules.

 Conclusion



LPR suspected from the clinical history and endoscopic findings. Failure to respond to medical treatment and lifestyle modification need confirmatory studies. In this study, girls were more affected than boys. All the children were presenting dysphonia, intermittent cough, foreign-body sensation in throat, and throat-clearing habit. All of them showing congested arytenoids and inter-arytenoid membrane. Multichannel intra-luminal impedence and pH monitoring studies are useful for the confirmation of LPR. There are no specific tests for diagnosing LPR. Empirical treatment with PPIs has been widely accepted as a diagnostic tests and treatment options of LPR. Speech therapy helps in case of LPR with hoarseness of voice. Other treatments include lifestyle and dietary modifications such as quitting smoking and drinking alcohol, weight loss, and avoid caffeine.

Limitations of the study

There are few limitations of this study. There is variability in the interpretation of endoscopic pictures by clinicians. There is also variability among clinicians for children identified with hoarseness of voice on the basis of physical and systemic examinations. There is another limitation of the study is a lack of consistency among clinicians to use other objective tests for confirming LPR.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Campagnolo AM, Priston J, Thoen RH, Medeiros T, Assunção AR. Laryngopharyngeal reflux: Diagnosis, treatment, and latest research. Int Arch Otorhinolaryngol 2014;18:184-91.
2Alharethy S, Baqays A, Mesallam TA, Syouri F, Al Wedami M, Aldrees T,et al. Correlation between allergic rhinitis and laryngopharyngeal reflux. Biomed Res Int 2018;2018:1-6.
3Sataloff RT, Hawkshaw MJ, Gupta R. Laryngopharyngeal reflux and voice disorders: An overview on disease mechanisms, treatments, and research advances. Discov Med 2010;10:213-24.
4Swain SK, Behera IC, Sahoo L. Hoarseness of voice in pediatric age group. Our experiences at an Indian teaching hospital. Indian J Child Health 2019;62:74-8.
5Smit CF, van Leeuwen JA, Mathus-Vliegen LM, Devriese PP, Semin A, Tan J,et al. Gastropharyngeal and gastroesophageal reflux in globus and hoarseness. Arch Otolaryngol Head Neck Surg 2000;126:827-30.
6Koufman JA, Aviv JE, Casiano RR, Shaw GY. Laryngopharyngeal reflux: Position statement of the committee on speech, voice, and swallowing disorders of the American Academy of Otolaryngology-Head and Neck Surgery. Otolaryngol Head Neck Surg 2002;127:32-5.
7Abdel-aziz MM, Abd El-Fattah AM, Abdalla AF. Clinical evaluation of pepsin for laryngopharyngeal reflux in childrenwith otitis media with effusion. Int J Pediatric Otorhinolaryngol 2003;77:1765-70.
8Weber B, Portnoy JE, Castellanos A, Hawkshaw MJ, Lurie D, Katz PO, et al. Efficacy of anti-reflux surgery on refractory laryngopharyngeal reflux disease in professional voice users: A pilot study. J Voice 2014;28:492-500.
9Cammarota G, Masala G, Cianci R, Palli D, Capaccio P, Schindler A, et al. Reflux symptoms in professional opera choristers. Gastroenterology 2007;132:890-8.
10Belafsky PC, Postma GN, Koufman JA. Validity and reliability of the reflux symptom index (RSI). J Voice 2002;16:274-7.
11Karkos PD, Leong SC, Apostolidou MT, Apostolidis T. Laryngeal manifestations and pediatric laryngopharyngeal reflux. Am J Otolaryngol 2006;27:200-3.
12Axford SE, Sharp N, Ross PE, Pearson JP, Dettmar PW, Panetti M,et al. Cell biology of laryngeal epithelial defenses in health and disease: Preliminary studies. Ann Otol Rhinol Laryngol 2001;110:1099-108.
13Beaver ME, Stasney CR, Weitzel E, Stewart MG, Donovan DT, Parke RB Jr., et al. Diagnosis of laryngopharyngeal reflux disease with digital imaging. Otolaryngol Head Neck Surg 2003;128:103-8.
14Postma GN, Belafsky PC, Aviv JE, Koufman JA. Laryngopharyngeal reflux testing. Ear Nose Throat J 2002;81:14-8.
15Stavroulaki P. Diagnostic and management problems of laryngopharyngeal reflux disease in children. Int J Pediatr Otorhinolaryngol 2006;70:579-90.
16Bove MJ, Rosen C. Diagnosis and management of laryngopharyngeal reflux disease. Curr Opin Otolaryngol Head Neck Surg 2006;14:116-23.
17El-Serag HB, Satia JA, Rabeneck L. Dietary intake and the risk of gastro-oesophageal reflux disease: A cross sectional study in volunteers. Gut 2005;54:11-7.
18Koufman JA. Laryngopharyngeal reflux is different from classic gastroesophageal reflux disease. Ear Nose Throat J 2002;81:7-9.
19Block BB, Brodsky L. Hoarseness in children: The role of laryngopharyngeal reflux. Int J Pediatr Otorhinolaryngol 2007;71:1361-9.