COCLIA 74 Laryngopharyngeal Reflux

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Slide 1 : Laryngopharyngeal Reflux(Extraesophageal Reflux) Samir Undavia Coclia Review 1/7/08
Slide 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
Slide 3 : Factors affecting LES tone Increased Tone Protein Bethanecol Metaclopramide Antacids ??adrenergic drugs Acidification of distal esophagus Decreased Tone Fat Carbs ETOh Cigarettes Carmanitives peppermint, spearmint Theophylline CCB ? -adrenergic drugs Dopamine Sedatives
Slide 4 : Mechanisms resulting in symptoms Acid exposure results in direct mucosal damage Ulceration, hemorrhage, necrosis Damage to mucociliary activity leads to increased viscosity Activated Pepsin (max @ pH 4.5) results in tissue damage Laryngeal Chemoreflex sensory receptors in larynx --> laryngospasm Associated with bradycardia, central apnea and hypotension Vagal Reflex Acid within distal esophagus --> laryngospasm, cough Associated with bronchospasm, increased secretions, tachycardia, hypertension Sudden infant Death Syndrome?
Slide 5 : Common symptoms of LPR ** Globus sensation ** Chronic throat clearing ** Dysphagia ** Sore throat ** Excessive throat mucus Hoarseness / Dysphonia Voice breaks Neck pain Chronic or nighttime cough Vocal fatigue Odynophagia Postnasal Drip Halitosis Ear Pain Laryngospasm Asthma exacerbation Loss of upper singing range Prolonged warm up time for singers Heartburn / regurgitation
Slide 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
Slide 7 : Physical Exam / Laryngoscopy Observations: Voice quality, throat clearing, cough, body habitus Psuedosulcus ventricular obliteration Erythema / hyperemia Vocal fold edema Diffuse laryngeal edema Posterior commisure hypertrophy Thick endolaryngeal mucus / inspisated secretions Granuloma / granulation Leukoplakia Nodules / prenodules Polyps Pachydermia Laryngeus Webs
Slide 8 : Laryngopharyngeal Reflux
Slide 9 : Laryngopharyngeal Reflux
Slide 10 : Laryngopharyngeal Reflux
Slide 11 : Laryngopharyngeal Reflux
Slide 12 : 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: ?
Slide 13 : The association between laryngeal pseudosulcus and laryngopharyngeal re?ux Peter Belafsky, MD, PhD, Gregory Postma, MD, and James Koufman, MD, 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)
Slide 14 : 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
Slide 15 : 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
Slide 16 : Objective Testing pH Probe Testing Gold standard Placed 5 cm above LES (for GERD), and above UES (for LPR) Confirmed by manometry, flouroscopy or endoscopy Positive test: pH 4 (controversial) Negative studies do not rule out LPR, because vagally mediated reflexes may be causing symptoms. Most authors recommend empiric therapy without pH probes. In LPR, can have normal pH @ LES Limitations invasive test, limited senstivity high false negative rate limited reproducibility Indications GERD symptoms partial responses to treatment continued laryngitis despite treatment patients who want proof, evaluation of patients after fundoplication intubated patients with altered mental status Role of Laryngoscopy, dual pH probe monitoring, and laryngeal mucosal biopsy in the diagnosis of pharyngoesophageal reflux (Ann Otol Rhinol Laryngol 2001:299-304.) This prospective blind comparison study compared dual pH probe studies, direct laryngoscopy, and mucosal biopsy in children without symptoms of gastroesophageal reflux who underwent airway evaluation. pH probe not clinically predictive of LPR. Only definitive indicator of LPR and mucosal injury was biopsy. Recommendations: empiric therapy without pH probe testing.
Slide 17 : 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
Slide 18 : Medical Management Behavioral Modification Antacids H2 blockers PPI Promotility agents Other
Slide 19 : 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)
Slide 20 : 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)
Slide 21 : 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)
Slide 22 : 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.
Slide 23 : 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
Slide 24 : 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
Slide 25 : 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
Slide 26 : 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
Slide 27 : 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)
Slide 28 : Disorders in infants and children that are likely reflux related Recurrent Croup Laryngospasm Laryngomalacia Hoarseness Subglottic Stenosis Aspiration Chronic Cough
Slide 29 : Pediatric manifestations of refluxOtolaryngol Head Neck Surg 1999;120:860. 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
Slide 30 : Coclia 1. List the common symptoms of laryngopharyngeal reflux (LPR). 2. Describe laryngoscopy findings in LPR. What is sandifer syndrome? 3. What is laryngeal pseudosulcus? What is the significance of this finding? How does it differ from sulcus vergeture? Oto Head Neck Surg 2002;126:649-652. 4. Discuss the role of objective tests in the diagnosis of LP3R. Ann Otol Rhinol Laryngol 2001;110:299. 5. What behavior and lifestyle modifications are recommended in the medical treatment of LPR. 6. What is the difference between H2 blockers vs. PPI? Which would you prescribe for LPR? 7. Describe your approach to the medical therapy of LPR. How much and how long? Explain persistent symptoms in patients on maximal medical therapy. 8. Discuss sequelae of chronic LPR. Ann Otol Laryngol 2001;110:606. 9. Any data on laryngeal cancer and LPR? 10. When should patients be referred for surgery? What procedures are available to treat LPR/GERD? 11. . Pediatric manifestations of reflux. Otolaryngol Head Neck Surg 1999;120:860.

 


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