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Manifestation and Diagnosis of Pediatric Laryngopharyngeal Reflux Kevin Ho, MD Seckin Ulualp, MD University of Texas Medical Branch Dept. of Otolaryngology Grand Rounds Presentation June 13, 2007
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Manifestation and Diagnosis of Pediatric Laryngopharyngeal Reflux

Apr 06, 2018

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Page 1: Manifestation and Diagnosis of Pediatric Laryngopharyngeal Reflux

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Manifestation and Diagnosis of Pediatric Laryngopharyngeal Reflux

Kevin Ho, MDSeckin Ulualp, MD

University of Texas Medical Branch

Dept. of OtolaryngologyGrand Rounds Presentation

June 13, 2007

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Up to two-thirds of infants exhibit signs of reflux (Nelson 1997)

A majority of those children will outgrow

their reflux by their second year of ageLaryngopharyngeal reflux (LPR) hasgained increasing recognition as a

common pediatric disorder over the pastfew years .

Pediatrics Reflux: IntroductionPediatrics Reflux: Introduction

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± PhysiologicInfrequent reflux symptoms in the absence of abnormalitiesAsymptomaticRarely during sleepOften postprandial

± S econdaryneurologic disease or esophageal dysmotility

± PathologicSymptomaticGERD or LPRD

C lassification

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WHAT IS THE DIFFERENCE BETWEEN GERD & LPR?

Gastroesophageal reflux (GER) ± Retrograde flow of gastric contents

into the esophagus

Laryngopharyngeal reflux (LPR) ± Extraesophageal reflux (EER) ± denotes the gastric contents that

reaches beyond the upper esophageal sphincter (UE S ) intooropharynx and/or nasopharynx

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LPR vs. GER

Stavroulaki. Intern J of Ped Otol 2006

LPR GERDaytime, upright Nighttime, supine

< 10 % < 22 %

Normal esophagealmotility

Esophagealdysmotility

Laryngeal/

Pharyngealsymptoms

Gastrointestinal

symptoms, heartburn

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U pper Esophageal Sphincter

Sivarao Am J Med 2000

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Pathophysiology

Exact etiology unknownDirect acid and/or pepsin injury

Neural-mediated laryngospasm, throatclearing, coughing

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Mucosal injury in LPR

Laryngeal epithelium more susceptibleto damage from refluxate thanesophageal epithelium

Pepsin causes depletion of laryngealprotective proteins and carbonicanhydrasePepsin adhered to laryngeal epitheliumcan be activated during an acidic refluxepisode

Johnston N 2003, 2007

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H istory and Physical

Stavroulaki. Intern J of Ped Otol 2006

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C arr et al. 2000

Retrospective chart review2 groups: ± 214 children diagnosed with GERD

± 8 1 without GERDS ignificant difference in symptoms betweengroups: ± S tertor

± C yanotic spells ± F requent emesis ± C hoking/ gagging ± F ailure to thrive

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Symptoms: Infants

D eal L et al. J Pedi Gastro and Nutrition 2005. EBM B

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Symptoms: Young children

D eal L et al. J Pedi Gastro and Nutrition 2005. EBM B

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C hronic coughRhinosinusitisLaryngitisGlobus pharyngeusDysphagiaAirway obstructionApneaAsthma

Recurrent coupLaryngomalaciaStridor Subglottic stenosisVocal cord nodule/granuloma

Reflux-related Otolaryngologicdisorders

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Esophageal Biopsy Study

Problem Positive Biopsy (%) Negative Biopsy

Asthma 75 25

Recurrent croup 75 25C ough 81 19

Apnea 75 25

Sinusitis 100 0

Stridor 63 27

Laryngomalacia 75 25

Subglotticstenosis

68 32

Post. Glotticedema

81 19

Y ellon R. Am J Med 108: 131S, 2000. EBM B

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C hronic RhinosinusitisReflux-induced chronic inflammation of nasal cavityLack of prospective double-blind R C TC oncurrent role of allergyPhipps C D 2000 (EBM B) : ± Higher incidence of GER in sinusitis patients ± Symptoms improved after GER treatmentBothwell MR 1999 (EBM C ) : ± 89% (25/28) of sinusitis patients who met criteriafor FESS show improvement w/o surgery with

GERD treatment

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Otitis Media

Nasopharyngeal inflammation causingEustachian tube dysfunction

C rapko 2007 ± Prospective non-randomized ± M iddle ear effusion collected after

myringotomy for O M E children

± Pepsin detected in ~ 60% samples ± pH: 6-7.6 (pepsin inactive)

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C hronic cough

Holinger and Sanders 1991 ± Retrospective

± 72 children with chronic cough > 1 monthand normal chest x-ray ± Associated with:

Asthma (32%), sinusitis (23%), GERD (15%)

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A sthma

Esophageal instillation of acid hasbeen shown to induce bronchospasmand reduce peak flow

Debley 2006: ± Prospective cross-sectional study ± 2397 adolescents ±

GERD 8x more common in asthma patients ± Higher morbidity (ER/ clinic visits, missedschool) from asthma if + GERD

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A pnea

Possible mechanisms: Laryngospasm,aspiration, glottic closure reflex

Herbst 1979 ± Retrospective ± 14 infants with apneic events and pH probe

proven GERD ± Apnea resolved after GERD treatment

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Reflux-induced stridor

³ Pseudo-laryngomalacia´Intermittent, not affected by changes in positionMechanisms: ± Acid induced laryngospasm ± Rapid breathing with esophageal irritation

Bouchard S 1999: ±

Retrospective ± 58% of 105 children with stridor and GERD by pH probe ± 83% of those improve with anti-reflux meds

Flexible laryngoscopy to evaluate for

laryngomalacia

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Laryngomalacia

Most common cause of stridor in infantsProlapse of supraglottic tissues into glottisNegative pressure created by prolapse causes

upward H+

flow50-80% laryngomalacia patients with GERDFlexible laryngoscopyDirect laryngoscopy and bronchoscopy inprolonged symptomatic patients because of risk of synchronous lesion is 15-30 %May peform esophagoscopy and biopsy if airway is robust. Otherwise, perform pH probe

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Subglottic stenosis

Acid causes ulceration, basilar hyperplasia, edemaof the subglottic mucosa

Yellon R 1997:

± Retrospective ± 80% of 26 children who underwent

laryngotracheal reconstruction had at least 1positive test for GER

± Barium swallow/ pH monitoring / esophagealbiopsy / scintiscan

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LaryngoscopyBronchoscopyEsophagoscopy with biopsyBarium EsophagramScintiscan24-hr pH monitoring

Esophageal intraluminal impedance

Diagnostic test for GER/ LPR

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Barium Esophagram

Used mainly if suspect anatomicalabnormalities: Achalacia, web, strictureS ensitivity: 20-60%S pecificity: 64-90%Positive predictive value: 8 0- 8 2%Limitation: High false negative rate due toshort sampling period

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N uclear Scintigraphy

Oral ingestion of technetium-labeled foodAlso detects aspiration, non-acidic reflux, andgastric emptyingSensitivity: 15- 59%Specificity: 83- 100%Limitations: ± Only measure initial postprandial period ± Lack of standardized techniques ± Lack of normative data

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Direct Laryngoscopy andBronchoscopy

Limited data in Pediatric populationC arr MM 2001Prospective non-R CT

Indications for DLB: T rach surveillance,persistent stridor, dysphonia, etc.77 children, 50 (65%) GERD +ve based on:

± pH monitoring ± Barium esophagram ± S cintiscan ± Esophageal biopsy

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C arr et al. ( C ont·d) Example of Laryngeal findings: ± Post-glottic edema ± Arytenoid edema ± TVF edema ± Lingual tonsil enlargement

C ricotracheal findings: ± Edema ± C obblestoning ± Subglottic stenosis ± Blunting of carina ± Increased secretions

M ild symptom (score = 1), severe (score = 2)GERD + group has significantly higher laryngeal and/or cricotracheal scoresS core > 7 ± Sensitivity: 76% ± Specificity: 86%

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Laryngeal Pseudosulcus

C arr MM 2005

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Branski et al. 2002

Prospective randomized blinded trialAdult study120 stroboscopic exam of larynx

Primary complaint of dysphonia x 6 monthsAnalyzed by 5 otolaryngologists5-point scale rating ± Erythema and edema of anterior commissure,

vocal folds, arytenoids ± GER symptoms

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Results of Branski et al.

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Esophagoscopy with biopsy

Mucosal changes: ± Erythema, edema, ulceration, erosion

Structural abnormalities: ± strictures, webs

Histologic esophagitis: ± Basal cell hyperplasia, increased papillary

height, epithelial inflammationHigh positive predictive valueLow negative predictive value

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24-hour p H monitoring

M easure frequency and duration of acid refluxDouble pharyngoesophageal probe ± Proximal: 2 cm above UE S

± Distal: 3 cm above LE S

Reflux episode: ± pH < 4 for 15-30 s ± Pharyngeal event must be preceded by esophageal

event ± Acid exposure time

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Pharynx

Proximal Esophagus

24-hour p H monitoring

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Little JP 1997

Prospective study of 222 childrenAge: 1 day ± 15 years

76 % with abnormal reflux finding at either probe46 % with reflux event at pharyngeal probe butNO T esophageal probePatients with laryngeal abnormalities, and emesis

had significantly more pharyngeal acid reflux thanpatients with non-respiratory symptoms.

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U lualp 2007

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W enzl 2002

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Limitations of p H monitoring

± Patient¶s factor Inconvenience / discomfort

T ime consuming

Insurance coverage / cost ± M ay miss intermittent episodes of LPR ± Does not detect non-acidic episodes ± V ariability in defining a significant reflux

event

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Joniau et al. 2007

Adult studyM eta-analysis of 11 prospective studies192 normal controls

512 reflux laryngitis diagnosed by refluxsymptoms index/ scoreDouble probe 24-hour pH monitoringNo statistical significance in pharyngealreflux events between normal and refluxlaryngitis groupsOnly 38 % reflux laryngitis patients showpharyngeal reflux event in pH monitoring

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Multi-channel IntraluminalImpedance (MII)

± M easure impedance produced by flow of foodbolus (high ionic content and conductivity) inesophagus

± Able to detect passage of solid, liquid, or gaseous bolus

± Intraluminal impedance rapidly decreases asbolus passes through measuring segment

± C an combine with pH probe to detect acidic andnon-acidic episodes

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Proximal

Distal

T utuian 2003

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p H probe vs. Impedance

Rosen R 2006Prospective non-randomized

25 untreated children, 25 treated with PPIS ensitivity in untreated group: Nodifference (~ 8 0 % vs. 76%)

In treated group: sensitivity of impedancegroup significantly higher ( 8 0% vs. 47%)

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Empiric treatment of LPR

W idely used but not validated in PediatricpopulationLifestyle modification: ± T hickening of feeds ± Prone positioning ± W eight loss for older children/ adolescent

Prokinetic agent:Acid suppressive therapy: ± H2 blocker vs. Proton pump inhibitor (limited

data)

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C onclusions

LPR is common among pediatricpopulation and is implicated in manyotolaryngologic disorders

At present, there is no ideal diagnostictool for pediatric LPRW ell-designed controlled studies areneeded to provide more information for diagnosis and management of pediatricLPR

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T hank you!