Printer Friendly

Pediatric laryngopharyngeal reflux.


Laryngopharyngeal reflux (LPR) is common in children. It often affects the airway, and it has been associated with life-threatening disease. The diagnosis and treatment of LPR in children is somewhat different from that in adults.


Pediatric laryngopharyngeal reflux (LPR) has gained increasing recognition over the past few years, and it has been identified as a common pediatric disorder. Its symptoms include benign postprandial vomiting during the first year of life, failure to thrive, esophagitis, and airway disturbances. Vandenpias and Sacre-Smits estimated that the incidence of reflux in all infants is 18%. (1) In some conditions--such as tracheoesophageal fistula, neurologic impairment, or oral motor dysphagia--the incidence might be as high as 70%. (2,3)

As early as 1884, Osler postulated an association between reflux and asthma. (4) In 1993, Kaufman wrote that reflux-related life-threatening airway complications of LPR were more common in children than in adults, but that children rarely complained of heartburn and regurgitation. (5)

Classification of pediatric LPR

Gastroesophageal reflux (GER) in the child is classified as physiologic, functional, pathologic, and secondary. (6) Physiologic reflux entails infrequent entails in children who have no abnormalities on diagnostic studies. It is typically asymptomatic, rarely occurs during sleep, and often occurs in the upright position postprandially. Functional GER is defined as silent or asymptomatic reflux and is identified by esophageal pH monitoring (pH-metry). Pathologic GER (gastroesophageal reflux disease [GERD]) is symptomatic and can cause complications in the gastrointestinal and respiratory tract. It can be quantified clinically and pathologically. Finally, secondary GER is a product of another disorder, such as neurologic disease or esophageal dysmotility. (7)

LPR is usually a self-limited disease, and children generally improve by the end of the first year of life upon their transition to a solid diet. Most symptomatic children require positional treatment. Almost all newborns can be shown to have brief postprandial episodes of reflux on esophageal-probe pH monitoring. (8-10) However, children with persistent LPR who are older than 3 years have a higher rate of complications, and they frequently require medical and/or surgical intervention. (11) Identification and treatment of these children can prevent later morbidity.

Infants are physiologically predisposed to GERD because they have a short intra-abdominal esophagus and an immature lower esophageal sphincter (LES). Children are also prone to excessive exposure to esophageal acid at night because their rate of nocturnal swallowing--and thus their esophageal acid clearance--is less than that of adults.

Pediatric manifestations of LPR

During the past two decades, reports of pediatric LPR have appeared more frequently. (12-16) In the 1970s, Fearon and Brama recognized reflux as a cause of various upper respiratory symptoms in children. (17) Other authors subsequently reported respiratory complications of LPR, including recurrent bronchitis, croup, pneumonia, and chronic asthma. (18-24) LPR has also been reported to be associated with contact ulcers and granuloma. (25,26) Although many of these reports suggest an association between reflux and the development of these conditions, it remains difficult to demonstrate a direct causal role. The effect of LPR in the pediatric airway might be mediated by one or all of three mechanisms: (1) microaspiration with stimulation of the laryngeal adductor reflux, (2) micro-aspiration with chemical pneumonitis, and (3) stimulation of an esophageal-vagal and/or autonomic reflex that results in or potentiates bronchial constriction.

Chronic cough and asthma. A subset of children with asthma or chronic cough refractory to standard medical treatment have been found to have LPR. (18-20,27,28) Coughing can also lead to an increase in intra-abdominal pressure, which can promote reflux. Unfortunately, many patients with chronic cough or asthma have other coexisting medical problems that can complicate the diagnosis and management of reflux. In 1991, Andze et al reported that 76% of 131 children with severe asthma had reflux according to single-probe esophageal pH monitoring. (27) Of those with reflux, 69% experienced clinical improvement in their asthma with medical therapy alone, and 88% had good to excellent results following antireflux surgery.

Only a limited number of investigators and clinicians have measured the extent of pharyngeal reflux in children with respiratory disease. (29,30) With the exception of infection, LPR is the most common cause of chronic cough in the 0- to 18-month age group, and it is the third most common cause in pediatric patients overall. (31)

Dysphonia. The child with reflux laryngitis can exhibit dysphonia, chronic cough, globus pharyngeus, or a "wet-sounding" voice or cough. (32-34) There is some evidence that reflux treatment might be beneficial in treating persistent nodules in older children in whom speech therapy or surgical excision has failed. Both Burton et al (20) and Walner and Holinger (35) reported an association between GERD and supraglottic stenosis and granulomas.

Laryngomalacia. Attendant to most respiratory diseases is an increased respiratory effort, which creates greater negative intrathoracic pressures and greater intraabdominal pressures. These pressures have been shown to exert a significant potentiating effect on reflux. (33) These pressure increases might be significant in patients with laryngomalacia, and the association between laryngomalacia and reflux has been well documented (figure). (21,22) There is also strong anecdotal evidence that the treatment of severe laryngomalacia can be improved with aggressive reflux management. Children who are being considered for supraglottoplasty should always have their reflux addressed and corrected prior to surgical intervention.

In 1983, the first direct cause-and-effect relationship between stridor and LPR was documented by Orenstein et al. (36) Contencin and Narcy were able to predict the presence of pH-documented LPR in children with stridor with a specificity of 83% and sensitivity of 100%. (29) These results have been supported by the work of Little et al. (30)

Subglottic stenosis. The damaging effects of gastric acid and pepsin on the subglottis have been demonstrated in animal models. (25,37) Reflux increases the risk of stenosis in animal models and is assumed to account for a significant number of patients in whom laryngotracheal reconstruction fails. Antireflux therapy has been recommended for all patients who undergo open laryngotracheal reconstruction. (38,39) Halstead also suggested that antireflux therapy might increase the success of endoscopic repair of subglottic stenosis. (40) However, in 1996, Zalzal et al found no direct correlation between reflux treatment and outcomes following laryngotracheal reconstruction. (41) To date, studies have been limited by a lack of controls. A prospective study examining the effect of reflux treatment on laryngotracheal reconstruction is currently under way at the University of Cincinnati.

Apparent life-threatening events. The evaluation of a child suspected of having apnea or an apparent life-threatening event (ALTE) begins by excluding anatomic laryngeal or tracheal anomalies. Apnea can also arise as a result of both esophageal and laryngotracheal reflux events, which can be caused by direct aspiration, altered gas exchange, or stimulation of the laryngeal chemoreceptor reflex. (42) Apnea can be a significant problem in preterm infants, and there appears to be a 14-fold increase in its frequency in the presence of significant GER. (43) Evidence supports the idea that the normal stimulation of respiration following an apneic episode might not occur in the presence of hypoxia. (44) This hypothesis was supported by a finding in eight infants that direct distal esophageal acid profusion resulted in bradycardia and apnea. (45) The reported incidence of pH-probe-documented reflux in children evaluated for ALTE varies greatly--from 42 to 95%. (46,47) The incidence of both daytime and nocturnal reflu x exceeded that of controls in each of these two reports.

Jolley et al followed 499 children with reflux for 1 year and reported a 9% incidence of sudden infant death syndrome among infants who had a high frequency of GER on pH-metry. (48) Although a direct causal relationship has not been established, it is strongly recommended that any child who has had an ALTE be evaluated for reflux. Animal models have supported these clinical impressions. Wetmore demonstrated that laryngeal instillation of acid causes obstructive apnea secondary to laryngospasm. (49) Duke et al confirmed these data in an immature canine model, and they found evidence that a vagal response from a chemoreceptor probably induced laryngospasm and diaphragmatic arrest in immature canine larynges. (50)

Other considerations. The relationships of LPR to both otitis media and sinusitis are under investigation, but anecdotal reports suggest that reflux might be pathogenic in some cases. (51-54)


A complete history and physical examination should be undertaken, including an evaluation of the child's growth curve. Attention should be paid to the child's birth and perinatal history, feeding, and airway symptoms. The history should elicit the frequency of emesis or regurgitation, the temporal relationship of symptoms to meals, and information on associated respiratory symptoms, associated neurologic or mental disorders, and weight gain. Orenstein et al developed a questionnaire to aid in this task. (55) The presence of signs of neurologic impairment -- such as generalized pharyngeal hypotonia, uncoordinated swallowing, pooling of secretions in the hypopharynx, and signs suggestive of laryngeal irritation (e.g., laryngeal edema and erythema) -- should be investigated by fiberoptic laryngoscopy. Rigid laryngoscopy and bronchoscopy might be indicated to rule out abnormalities, such as the presence of a foreign body, an infection, a subglottic stenosis, a laryngotracheal esophageal cleft, and other anomalies .

Although there are many diagnostic options in the evaluation of LPR, few are critical. An initial assessment should be followed by carefully selected diagnostic studies in those patients with presumed or documented sequelae of reflux. The sensitivity and specificity of a symptom-based diagnosis alone is low, (56) and the sensitivity and specificity of testing is improved with the use of multiple tests. (57)

Barium esophagography and radionucleotide reflux scanning. Barium esophagography has the advantage of demonstrating anatomic abnormalities. However, its sensitivity (20 to 60%) and specificity (64 to 90%) for GER/LPR are limited. (33)

Esophageal radionucleotide reflux scanning can be beneficial in identifying reflux in the postprandial child because he or she typically has a neutral or alkaline pH reading, neither of which is identified by standard pH-metry. In certain cases, this reflux might be responsible for the patient's respiratory symptoms. A scintiscan can also determine the rate of gastric emptying. Delayed scintigraphy can be used to identify patients who have pulmonary microaspiration. (58)

Endoscopy with biopsy. Esophagoscopy allows for direct visualization of the mucosal lining. Combined with biopsy, it can show evidence of mucosal inflammation or esophagitis. Direct examination of the larynx also allows for the detection of increased supraglottic vascularity, laryngeal or subglottic edema, interarytenoid pachydermia, and small lymphoid aggregates in the wall of the trachea; all of these findings are suggestive of GERD. A bronchoalveolar lavage can also be performed. The presence of lipid-laden macrophages is approximately 85% sensitive for GERD, according to Nussbaum et al. (59) There is a poor correlation between pH monitoring and esophageal and laryngeal biopsy findings. (60,61)

pH monitoring. Double-probe 24-hour pH studies combined with symptom-based observation andlor respiratory monitoring are believed to be the current diagnostic gold standard. This combination allows the clinician to correlate reflux with cardiac, respiratory, and observational events. During pH-metry, reflux events are measured for 18 to 24 hours and a diary is maintained to record symptoms, activity, and food consumption. In several studies, the reproducibility of pH monitoring was poor. (62,63) The probe test should be repeated if results do not correlate with the clinical picture. The distal probe should be placed approximately 3 cm above the LES in infants and children, and 5 cm above the LES in adolescents. (30) The proximal probe must be placed just above the upper esophageal sphincter in the hypopharynx.

When screening children for ALTE, values are abnormal when the reflux index is greater than 5% in noninfants and greater than 10% in infants. (1) Normative data for pharyngeal reflux events in controls are unavailable, which makes the establishment of pathologic parameters somewhat controversial. Little et al observed reflux in 76% of 222 children on double pH monitoring. (30) It is notable that 46% of these patients had documented acid exposure with normal esophageal probes; these patients tended to experience more respiratory abnormalities. Little et al suggested that the pharyngeal probe allowed for the identification of an additional 46% of patients with LPR in whom esophageal reflux would have been considered physiologic and in whom test results would have been normal if only an esophageal probe had been employed. The exact definition of pathologic LPR continues to be debated. Contencin and Narcy reported a significant incidence of recurrent laryngotracheitis in patients who experienced more than six pha ryngeal episodes, (29) and Halstead suggested that more than 10 pharyngeal episodes within 24 hours are associated with respiratory difficulties. (64)

In light of the pharyngeal probe's poor reproducibility of results and the lack of established normal values, we believe that empiric antireflux therapy might be indicated in those children in whom LPR is strongly suspected. We use pH probe testing to assess the efficacy of therapy and to evaluate those patients in whom the clinical picture is unclear. It is also possible that a child would have alkaline reflux, which is not identified by pH testing. Alkaline refluxate can potentiate acidic damage, and it can cause its own damage to the esophagus and airway. This type of nonacidic reflux could be measured by impedance testing, but such testing is not yet readily available. (65,66)


There are three phases in the treatment of LPR: lifestyle modification (phase 1), pharmacologic treatment (phase 2), and antireflux surgery (phase 3). (67) The level of treatment is based on the severity of the reflux. It is important to realize that many infants respond to lifestyle and positional therapy alone. Also, many of the drugs used for LPR are not approved by the U.S. Food and Drug Administration (FDA) for infants, despite their widespread use; therefore, establishing a diagnosis prior to pharmaco-therapy is important in these patients. Generally, reflux treatment begins with conservative measures, including elevation of the head of the bed, milk thickening, avoidance of substances that can decrease LES tone, and fasting before bedtime.

If behavior modification fails, the clinician can turn to pharmacologic treatment with either a cytoprotective agent, an [H.sub.2] receptor antagonist, a prokinetic agent, or a proton-pump inhibitor. Pharmacologic therapy for reflux is successful in 80% of cases. Mild reflux can be treated with a combination of conservative measures, an antacid, and an [H.sub.2] blocker. Because proton-pump inhibitors have not been approved by the FDA for use in infants, their use is controversial. It is our belief that proton-pump inhibitors are warranted for severe or life-threatening symptoms.

Surgical intervention is reserved for patients in whom aggressive medical therapy fails and who continue to have life-threatening complications of reflux. The most common surgical procedure is Nissen fundoplication, which carries a 90% success rate and a 1% mortality rate. (68,69) Pennell et al reported improved surgical outcomes in children who did not have respiratory symptoms. (3,70)

A significant percentage of children with reflux also have respiratory disorders. Treatment of these respiratory disorders might be unsuccessful until the reflux is successfully managed. Close monitoring and follow-up of these patients is essential to optimize outcomes.


(1.) Vandenplas Y, Sacre-Smits L. Continuous 24-hour esophageal pH monitoring in 285 asymptomatic infants 0-15 months old. J Pediatr Gastroenterol Nutr 1987;6:220-4.

(2.) Hrabovsky EE, Mullett MD. Patterns of pediatric gastroesophageal reflux. Am Surg 1985;51:212-6.

(3.) Pennell RC, Lewis JE, Cradock TV, et al. Management of severe gastroesophageal reflux in children. Arch Surg 1984;l 19:553-7.

(4.) Osler W. The Principles and Practice of Medicine: Designed for the Use of Practitioners and Students of Medicine. New York: Appleton, 1892.

(5.) Koufman JA. The otolaryngologic manifestations of gastroesophageal reflux disease (GERD). In: Myers N, Buston CD, Breckman DE, Krause CJ, eds. Advances in Otolaryngology-Head and Neck Surgery. Vol.7. St. Louis: Mosby, 1993:13-15.

(6.) Demeester TR, Johnson LF, Joseph GJ, et al. Patterns of gastroesophageal reflux in health and disease. Ann Surg 1976;184:459-70.

(7.) Boyle JT. Gastroesophageal reflux in the pediatric patient. Gastroenterol Clin North Am 1989;18:315-37.

(8.) Orenstein SR. Controversies in pediatric gastroesophageal reflux. J Pediatr Gastroenterol Nutr 1992;14:338-48.

(9.) Carre IJ. The natural history of partial thoracic stomach (hiatus hernia) in children. Arch Dis Child 1959;34:344-53.

(10.) Kibble, MA. Gastroesophageal reflux and failure to thrive in infancy. In: Gellis SS, ed. Gastroesophageal Reflux: Report of the Seventy-Sixth Ross Conference on Pediatric Research. Columbus, O.: Ross Laboratories, 1979:39-42.

(11.) Treen WR, Davis PM, Hyams JS. Gastroesophageal reflux in the older child: Presentation, response to treatment and long-term follow-up. Clin Pediatr 1991 ;30:435-40.

(12.) Coben RM, Weintraub A, DiMarino AJ, Jr., Cohen S. Gastroesophageal reflux during gastrostomy feeding. Gastroenterology 1994;106:13-8.

(13.) Hebra A, Hoffman MA. Gastroesophageal reflux in children. Pediatr Clin North Am 1993;40:1233-51.

(14.) Boyle JT, Altschuler SM, Patterson BL, et al. Reflux inhibition of the lower esophageal sphincter (LES) following stimulation of pulmonary vagal afferent receptors [abstract]. Gastroenterology 1986;90:1353.

(15.) Sondheimer JM. Clearance of spontaneous gastroesophageal reflux in awake and sleeping infants. Gastroenterology 1989;97:821-6.

(16.) Sondheimer JM. Upper esophageal sphincter and pharyngoesophageal motor function in infants with and without gastroesophageal reflux. Gastroenterology 1983;85:301-5.

(17.) Fearon B, Brama I. Esophageal hiatal hernia in infants and children. Ann Otol Rhinol Laryngol 1981;90:387-91.

(18.) Euler AR, Byrne WJ, Ament ME, et al. Recurrent pulmonary disease in children: A complication of gastroesophageal reflux. Pediatrics 1979;63:47-5 1.

(19.) Malfroot A, Vandenplas Y, Vernlinden M, et al. Gastroesophageal reflux and unexplained chronic respiratory disease in infants and children. Pediatr Pulmonol 1987;3:208-13.

(20.) Burton DM, Pransky SM, Katz RM, et al. Pediatric airway manifestations of gastroesophageal reflux. Ann Otol Rhinol Laryngol 1992;101:742-9.

(21.) Belmont JR, Grundfast K. Congenital laryngeal stridor (laryngomalacia): Etiologic factors and associated disorders. Ann Otol Rhinol Laryngol 1984;93:430-7.

(22.) Matthews BL, Little JP, McGuirt WF, Jr., Koufman JA. Reflux in infants with laryngomalacia: Results of 24-hour double-probe pH monitoring. Otolaryngol Head Neck Surg 1999;120:860-4.

(23.) Bauman NM, Sandler AD, Schmidt C, et al. Reflex laryngospasm induced by stimulation of distal esophageal afferents. Laryngoscope 1994;104:209-14.

(24.) Boggs DF, Bartlett D, Jr. Chemical specificity of a laryngeal apneic reflex in puppies. J Appl Physiol 1982;53:455-62.

(25.) Delahunty JE, Cherry J. Experimentally produced vocal cord granulomas. Laryngoscope 1968;78:1941-7.

(26.) Koufman JA. Contact ulcer and granuloma of the larynx. In: Gates GA, ed. Current Therapy in Otolaryngology-Head and Neck Surgery. 5th ed. St. Louis: Mosby, 1994:456-9.

(27.) Andze GO, Brandt ML, St. Vil D, et al. Diagnosis and treatment of gastroesophageal reflux in 500 children with respiratory symptoms: The value of pH monitoring. 3 Pediatr Surg 1991;26:295-300.

(28.) Jolley SG, Herbst JJ, Johnson DG, et al. Esophageal pH monitoring during sleep identifies children with respiratory symptoms from gastroesophageal reflux. Gastroenterology 1981;80:1501-6.

(29.) Contencin P, Narcy P. Gastroesophageal reflux in infants and children. A pharyngeal pH monitoring study. Arch Otolaryngol Head Neck Surg 1992;118:1028-30.

(30.) Little JP, Matthews BL, Glock MS, et al. Extraesophageal pediatric reflux: 24-hour double-probe pH monitoring in 222 children. Ann Otol Rhinol Laryngol Suppl 1997:169:1-16.

(31.) Holinger LD, Sanders AD. Chronic cough in infants and children: An update. Laryngoscope 1991;10l:596-605.

(32.) Contencin P, Maurage C, Ployet MJ, et al. Gastroesophageal reflux and ENT disorders in childhood. Int J Pediatr Otorhinolaryngol 1995;32(Suppl):S135-44.

(33.) Orenstein SR. Gastroesophageal reflux. In: Wyllie R, Hyams JS, eds. Pediatric Gastrointestinal Disease: Pathophysiology, Diagnosis, Management. Philadelphia: W.B. Saunders, 1993:337-69.

(34.) Gumpert L, Kalach N, Dupont C, Contencin P. Hoarseness and gastroesophageal reflux in children. J Laryngol Otol 1998;112: 49-54.

(35.) Walner DL, Holinger LD. Supraglottic stenosis in infants and children. A preliminary report. Arch Otolaryngol Head Neck Surg 1997;123:337-41.

(36.) Orenstein SR Orenstein DM, Whitington PF. Gastroesophageal reflux causing stridor. Chest 1983;84:301-2.

(37.) Little FB, Koufman JA, Kohut RI, Marshall RB. Effect of gastric acid on the pathogenesis of subglottic stenosis. Ann Otol Rhinol Laryngol 1985;94:516-9.

(38.) Gray S, Miller R, Myer CM III, Cotton RT. Adjunctive measures for successful laryngotracheal reconstruction. Ann Otol Rhinol Laryngol 1987;96:509-13.

(39.) Bauman NM, Oyos TL, Murray DJ, et al. Postoperative care following single-stage laryngotracheoplasty. Ann Otol Rhinol Laryngol 1996;105:317-22.

(40.) Halstead LA. Gastroesophageal reflux: A critical factor in pediatric subglottic stenosis. Otolaryngol Head Neck Surg 1999;120:683-8.

(41.) Zalzal GH, Choi SS, Patel KM. The effect of gastroesophageal reflux on laryngotracheal reconstruction. Arch Otolaryngol Head Neck Surg 1996;122:297-300.

(42.) Wennergren G, Bjure J, Hertzberg T, et al. Laryngeal reflex. Acta Paediatr Suppl 1993;82(Suppl 389):53-6.

(43.) Menon AP, Schefft GL, Thach BT. Apnea associated with regurgitation in infants. J Pediatr 1985;106:625-9.

(44.) Lanier B, Richardson MA, Cummings C. Effect of hypoxia on laryngeal reflex apnea--implications for sudden infant death. Otolaryngol Head Neck Surg 1983;91:597-604.

(45.) Ramet J, Egreteau L, Curzi-Dascalova L, et al. Cardiac, respiratory, and arousal responses to an esophageal acid infusion test in near-term infants during active sleep. J Pediatr Gastroenterol Nutr 1992;15:135-40.

(46.) Newman LI, Russe J, Glassman MS, et al. Patterns of gastroesophageal reflux (GER) in patients with apparent life-threatening events. J Pediatr Gastroenterol Nutr 1989;8:157-60.

(47.) Sacre L, Vandenplas Y. Gastroesophageal reflux associated with respiratory abnormalities during sleep. J Pediatr Gastroenterol Nutr 1989;9:28-33.

(48.) Jolley SG, Halpern LM, Tunell WP, et al. The risk of sudden infant death from gastroesophageal reflux. J Pediatr Surg 1991;26:691-6.

(49.) Wetmore RF. Effects of acid on the larynx of the maturing rabbit and their possible significance to the sudden infant death syndrome. Laryngoscope 1993; 103:1242-54.

(50.) Duke SG, Postma GN, McGuirt WF, Jr., et al. Laryngospasm and diaphragmatic arrest in immature dogs after laryngeal acid exposure: A possible model for sudden infant death syndrome. Ann Otol Rhinol Laryngol 2001;l10:729-33.

(51.) Parsons DS. Chronic sinusitis: A medical or surgical disease? Otolaryngol Clin North Am 1996;29:l-9.

(52.) Barbero GJ. Gastroesophageal reflux and upper airway disease. Otolaryngol Clin North Am 1996;29:27-38.

(53.) Rozmanic V, Velepic M, Ahel V, et al. Prolonged esophageal pH monitoring in the evaluation of gastroesophageal reflux in children with chronic tubotympanal disorders. J Pediatr Gastroenterol Nutr 2002;34:278-80.

(54.) Tolia V. Gastroesophageal reflux and supraesophageal complications: Really true or ballyhoo? J Pediatr Gastroenterol Nutr 2002;34:269-73.

(55.) Orenstein SR, Cohn JF, Shalaby TM, Kartan R. Reliability and validity of an infant gastroesophageal reflux questionnaire. Clin Pediatr (Phila) 1993;32:472-84.

(56.) Costantini M, Crookes PF, Bremner RM, et al. Value of physiologic assessment of foregut symptoms in a surgical practice. Surgery 1993;l14:780-7.

(57.) Tolia V, Calhoun JA, Kuhns LR, Kauffman RE. Lack of correlation between extended pH monitoring and scintigraphy in the evaluation of infants with gastroesophageal reflux. J Lab Clin Med 1990;115:559-63.

(58.) Fisher RS, Malmud LS, Roberts GS, Lobis IF. Gastroesophageal (GE) scintiscanning to detect and quantitate GE reflux. Gastroenterology 1976;70:301-8.

(59.) Nussbaum E, Maggi JC, Mathis R, Galant SP. Association of lipid-laden alveolar macrophages and gastroesophageal reflux in children. J Pediatr 1987;l10:190-4.

(60.) Heine RG, Cameron DJ, Chow CW, et al. Esophagitis in distressed infants: Poor diagnostic agreement between esophageal pH monitoring and histopathologic findings. J Pediatr 2002;140:14-19.

(61.) McMurray JS, Gerber M, Stern Y, et al. Role of laryngoscopy, dual pH probe monitoring, and laryngeal mucosal biopsy in the diagnosis of pharyngoesophageal reflux. Ann Otol Rhinol Laryngol 2001;110:299-304.

(62.) Vandenplas Y, Helven R, Goyvaerts H, Sacre L. Reproducibility of continuous 24 hour oesophageal pH monitoring in infants and children. Gut 1990;31:374-7.

(63.) Mahajan L, Wyllie R, Oliva L, et al. Reproducibility of 24-hour intraesophageal pH monitoring in pediatric patients. Pediatrics 1998;l0l:260-3.

(64.) Halstead LA. Role of gastroesophageal reflux in pediatric upper airway disorders. Otolaryngol Head Neck Surg 1999;120:208-14.

(65.) Wenzl TG, Schenke S, Peschgens T, et al. Association of apnea and nonacid gastroesophageal reflux in infants: Investigations with the intraluminal impedance technique. Pediatr Pulmonol 2001;31:144-9.

(66.) Wenzl TG. Investigating esophageal reflux with the intraluminal impedance technique. J Pediatr Gastroenterol Nutr 2002;34:261-8.

(67.) Silva AB, Hotaling AJ. Advances in pediatric gastroesophageal reflux disease. Curr Opin Otolaryngol Head Neck Surg 1994;2:508-14.

(68.) Fung KP, Seagram G, Pasieka J, et al. Investigation and outcome of 121 infants and children requiring Nissen fundoplication for the management of gastroesophageal reflux. Clin Invest Med 1990;13:237-46.

(69.) Little AG, Ferguson MK, Skinner DB. Reoperation for failed antireflux operations. J Thorac Cardiovasc Surg 1986;91:511-17.

(70.) Di Lorenzo C, Orenstein S. Fundoplication: Friend or foe? J Pediatr Gastroenterol Nutr 2002;34:117-24.
COPYRIGHT 2002 Medquest Communications, LLC
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2002, Gale Group. All rights reserved. Gale Group is a Thomson Corporation Company.

Article Details
Printer friendly Cite/link Email Feedback
Author:Postma, Gregory N.
Publication:Ear, Nose and Throat Journal
Geographic Code:1USA
Date:Sep 1, 2002
Previous Article:Treatment of laryngopharyngeal reflux.
Next Article:A personal information resource. (Editorial).

Related Articles
Candida esophagitis. (Esophagoscopy Clinic).
A large left vocal fold mass. (Laryngoscopic Clinic).
Laryngopharyngeal reflux 2002: a new paradigm of airway disease. (Introduction).
Laryngopharyngeal reflux is different from classic gastroesophageal reflux disease.
Symptoms and findings of laryngopharyngeal reflux.
Laryngopharyngeal reflux testing.
Clinical manifestations of laryngopharyngeal reflux.
Treatment of laryngopharyngeal reflux.
Bilateral vocal process papillomas: report of a case.
Pulsed-dye laser in the treatment of recurrent respiratory papillomatosis of the larynx.

Terms of use | Privacy policy | Copyright © 2021 Farlex, Inc. | Feedback | For webmasters