This document discusses laryngopharyngeal reflux (LPR), also known as extraesophageal reflux. It begins by describing the barriers to reflux in the upper esophageal sphincter and lower esophageal sphincter. It then discusses the various factors that can increase or decrease lower esophageal sphincter tone. The document goes on to explain the mechanisms by which reflux can cause symptoms, common symptoms of LPR, objective tests used to diagnose LPR, and treatment options including behavioral modifications, medications, and surgery. It concludes by discussing potential sequelae of untreated LPR and its relationship to various pediatric disorders.

1. LARYNGOPHARYNGEAL
REFLUX
(EXTRA-ESOPHAGEAL REFLUX)
BY :- DR SANJIV KUMAR (MS-ENT FINAL YEAR STD)
DARBHANGA MEDICAL COLLEGE, LAHERIASARAI (BIHAR)
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2. BARRIERS TO REFLUX
 Upper Esophageal Sphincter (final barrier)
 C-shapped : cricopharyngeus, thyropharyngeus,
cervical esophagus
 Lower Esophageal Sphincter ( most critical)
 Esophageal Acid Clearance
 Peristalsis & gravity
 Epithelial Resistance Factors
 Mucus + aqueous layer.
 Esophageal epithelium > respiratory epithelium
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3. FACTORS AFFECTING LES TONE
 Increased Tone  Decreased Tone
Fat
Protein Carbs
Bethanecol ETOh
Metaclopramide Cigarettes
Antacids Carmanitives
 peppermint, spearmint
adrenergic drugs
Theophylline
Acidification of distal CCB
esophagus -adrenergic drugs
Dopamine
Sedatives
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4. MECHANISMS RESULTING IN SYMPTOMS
 Acid exposure results in direct  Laryngeal Chemoreflex
mucosal damage sensory receptors in larynx -->
Ulceration, hemorrhage, laryngospasm
necrosis Associated with bradycardia, central
apnea and hypotension
 Damage to mucociliary activity  Vagal Reflex
leads to increased viscosity Acid within distal esophagus -->
laryngospasm, cough
 Activated Pepsin (max @ pH Associated with bronchospasm,
4.5) results in tissue damage increased secretions, tachycardia,
hypertension
Sudden infant Death Syndrome?
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5. COMMON SYMPTOMS OF
LPR
 ** Globus sensation  Vocal fatigue
 ** Chronic throat clearing  Odynophagia
 ** Dysphagia  Postnasal Drip
 ** Sore throat  Halitosis
 ** Excessive throat mucus  Ear Pain
 Hoarseness / Dysphonia  Laryngospasm
 Voice breaks  Asthma exacerbation
 Neck pain  Loss of upper singing range
 Chronic or nighttime cough  Prolonged warm up time for singers
 Heartburn / regurgitation
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6. THE REFLUX SYMPTOM
INDEX
 Within the past month, how did the following problems affect you? Rank
them from 0 (no problem) to 5 (severe problem).
 Hoarseness or a problem with your voice
 Clearing your throat
 Excess throat mucus or post nasal drip
 Difficulty swallowing foods, liquids or pills
 Coughing after you have eaten or after lying down
 Breathing difficulties or choking episodes
 Troublesome or annoying cough
 Sensations of something sticking in your throat or a lump in your throat
 Heartburn, chest pain, indigestion, or stomach acid coming up
 > 10: high likelihood of a positive dual-channel pH probe study showing reflux
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7. PHYSICAL EXAM / LARYNGOSCOPY
Granuloma / granulation
Observations:
• Voice quality, throat clearing,
cough, Leukoplakia
body habitus
Psuedosulcus Nodules / prenodules
ventricular obliteration
Polyps
Erythema / hyperemia
Vocal fold edema
Pachydermia Laryngeus
Diffuse laryngeal edema
Posterior commisure hypertrophy Webs
Thick endolaryngeal mucus /
inspisated secretions
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8. SANDIFERS SYNDROME
 Spasmodic torsional dystonia, arching of the
back and rigid opisthotonic posturing, mainly
involving the neck, back, and upper
extremities, associated with either GERD or a
hiatal hernia
 Posturing, typically occuring shortly after
feeding, that lasts 1-3 minutes
 Age: observed from infancy to early childhood.
Most children outgrow symptoms by early
childhood. Mentally impaired individuals may
have persistence of symptoms into adolescence
 Often confused with a seizure disorder
 Incidence: < 1% of children with reflux
 Pathophysiology: ?
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9. THE ASSOCIATION BETWEEN LARYNGEAL PSEUDOSULCUS
AND LARYNGOPHARYNGEAL REflUX
 Psuedosulcus Vocalis
 Pattern of infraglottic edema on the
ventral surface of the vocal fold
 Sulcus Vergeture
 a depression in the mucous membrane
of the free edge of the true vocal fold
due to adherence of the epithelium to
the vocal ligament owing to absence
of the lamina propria
 70% of patients with documented LPR had
Pseudosulcus (not pathogneumonic, but close)
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10. OBJECTIVE TESTING
Voice Analysis
• Before and after therapy - ? significance
Esophagram
• Useful for GERD, not LPR
• Hiatal hernia, erosive esophagitis, strictures,
barrett’s, esophageal rings, compression,
motility disorders, diverticula, cricopharyngeal
spasm, aspiration
EGD
• In pts with GERD, may be helpful to find Barretts, strictures, esophagitis early
• Should patients with LPR without symptoms of GERD be referred to have EGD?
FEEST
• Can provide direct visualization of LPR
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11. OBJECTIVE TESTING
Manometry
• Useful for GERD and surgical planning of antireflux surgery, not for LPR
• May show ineffective esophageal motility, low LES tone
Reflux Scan
• Radionucleotide study ( oral technetium)
• Low senstivity for LPR
Acidification Testing (Bernstein Test)
• NGT with HCL + H2O titrated until symptoms occur
Brochoalveolar lavage
• Good to track pulmonary complications of reflux + aspiration
• Look for lipid-laden macrophages ( shown to be increased in children with pulm complications of aspiration
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12. OBJECTIVE TESTING
Limitations
pH Probe Testing
• invasive test,
• limited senstivity
Gold standard • high false negative rate
• limited reproducibility
Placed 5 cm above LES (for GERD), and above
UES (for LPR)
• Confirmed by manometry, flouroscopy Indications
or
• GERD symptoms
endoscopy
• partial responses to treatment
• continued laryngitis despite treatment
Positive test: pH 4 (controversial)
• patients who want proof,
• evaluation of patients after
Negative studies do not rule out LPR, because fundoplication
vagally mediated reflexes may be causing
• intubated patients with altered mental
symptoms.
status
Most authors recommend empiric therapy
without pH probes.
In LPR, can have normal pH @ LES
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13. TREATMENT: BEHAVIORAL MODIFICATION
Avoid Eating 3 hours before lying down
No tobacco products
No alcohol, fried foods, fatty foods,
chocolate, caffeine, spicy foods,
peppermints
Avoid tight fitting clothes
Elevate HOB 6-8 inches
Chew gum for 1 hour after food intake
Walk for 1 hour after food intake
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14. MEDICAL MANAGEMENT
Behavioral Modification
Antacids
H2 blockers
PPI
Promotility agents
Other
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15. MEDICAL TREATMENT OF
LPR
 Antacids
 Neutralize pH, increase LES tone
 Sought out by patients prior to seeking medical attention
 Increase pH, thus deactivate pepsin
 Gaviscon
 Alginic acid
 Helps with GERD, but does not increase LES tone
 Common Antacids
 Maalox (aluminum hydroxide/magnesium hydroxide/simethicone)
 Mylanta (aluminum hydroxide/magnesium hydroxide/simethicone)
 Tums (calcium carbonate)
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16. H2 BLOCKERS
Competitive histamine type 2 receptor blocker
• Reduced acid secretion and pepsin production
Can be used for minor LPR, adjunctive treatment,
or in weaning patients from PPI’s
Long term high dose H2 blockers not as effective nor
as cost effective as PPI’s
Commonly used:
• Zantac (ranitidine)
• Pepcid (famotidine)
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17. PROTON PUMP
INHIBITORS
Inhibit Hydrogen-Potassium ATPase
• Last step in Acid production in parietal cell
More effective than H2 blockers
Take 1 hour prior to eating
Common PPI’s:
• Aciphex (Rabeprazole)
• Nexium (esomeprazole)
• Prevacid (lansoprazole)
• Prilosec (omeprazole)
• Protonix (pantoprazole)
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18. PROMOTILITY AGENTS
Reglan (Metaclopramide)
• Dopamine antagonist
Erythromycin
Increases LES tone, gastric emptying and esophageal clearance
May be helpful for those with DM, dystrophia myotonica, anorexia
secondary to delayed gastric emptying times in these conditions.
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19. OTHER MEDICAL
THERAPY
Sulcrafate
• Salt of sucrose
• Increases mucosal resistance to trauma, promotes healing in
duodenal ulcers
Bethanechol
• Cholinergic
• Increases LES tone, decreased GER, improves salivary
flow, improves GI motility, detrusor muscle tone
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20. HOW TO TREAT LPR
Behavioral modifications
Start with PPI
• Mild LPR can be given trial of H2 blocker, or OTC meds
• Can increase to BID, and add H2 blocker
• Refer to GI with increasing needed dose
• Workup structural causes of GERD/LPR
Treat for 6-8 weeks, with reevaluation. Then attempt at weaning.
Weaning:
• Downgrade from PPI to H2 blocker
• BID to Qdaily
• Continuation of behavioral modification
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21. SURGICAL TREATMENT
For those who fail medical therapy
Replacing LES into abdomen, and
augmentation of LES into better barrier
Nissen Fundoplication
• 360o wrap of gastric fundus around
intraabdominal esophagus
• > 73% show dramatic improvement
of LPR symptoms
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22. SEQUELAE OF LPR
Chronic Laryngitis (> 3mo)
Contact Ulcer
Laryngeal Granuloma
• Treat with PPI, behavioral modifications, voice therapy, possibly
with intralaryngeal Botulinum toxin for refractory cases, then
surgery
Suglottic Stenosis
• Strong association btw LPR & SGS.
• Causal or synergistically with other causes of SGS
• 5 of 7 patients with idiopathic SGS had signs of reflux
• Evaluation of SGS should always include evaluation of LPR
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23. LPR AND HEAD AND NECK
CANCER
Reflux not established as a carcinogen
May contribute to complications of surgical management and
radiation treatment of SCCA.
High incidence of LPR and GERD ( documented by pH probes)
exists in patients with SCCA of the head and neck.
Bile acid and acidic conditions can be tumorigenic in the esophagus
(through over expression of COX 2)
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24. DISORDERS IN INFANTS AND
CHILDREN THAT ARE LIKELY
REFLUX RELATED
Recurrent Croup
Laryngospasm
Laryngomalacia
Hoarseness
Subglottic Stenosis
Aspiration
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Chronic Cough
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25. PEDIATRIC MANIFESTATIONS OF REFLUX
100 % of patients with laryngomalacia had at least 1 episode of
reflux in a 24 hour period
Whether this is causal is not known. However, reflux is known to
harm respiratory epithelium in an already compromised airway
Whether treating them will help the laryngomalacia is not known
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