THE AIRWAY AND BEYOND
| LARYNGOPHARYNGEAL REFLUX IN A RHINOLOGY PRACTICE: THE ROLE OF TNE —Michael Setzen, MD,
Clinical Assistant Professor of Otolaryngology, New York University School of Medicine, New York City
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| Laryngopharyngeal reflux (LPR): different from gastroesophageal reflux disease (GERD); symptoms—mild dysphagia;
dysphonia; globus; sore throat; throat clearing; chronic cough; reasons patients get LPR—sensitive pharynx; unlike
esophagus, pharynx has no protection
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| Patients with LPR: thin; have reflux day and night; heartburn uncommon; intermittent extraesophageal symptoms; esophageal
motility usually normal; physical examination—posterior edema and erythema of larynx
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| Patients with GERD: somewhat obese; reflux usually at night; heartburn; GERD more chronic than LPR
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| Treatment: spelled out in 2002 position paper from American Academy of Otolaryngology—Head and Neck Surgery
(AAOHNS); diet; lifestyle; proton pump inhibitors (PPIs)—bid (vs once daily for GERD); taken for 3 to 6 mo; half
hour before meal; nocturnal breakthrough—medication such as ranitidine (Zantac); taper after improvement (eg, after
3-6 mo)
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| Transnasal esophagoscopy (TNE): brings esophagus back to otolaryngology and allows otolaryngologists to work with
gastroenterologists; patients with LPR prone to getting esophagitis, especially Barrett’s, which can lead to adenocarcinoma;
patients with reflux need TNE
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| Procedure: easy to perform in office; patient npo for 3 hr; anesthetize nose and oral cavity; vasoconstrict nose; pass scope
transnasally, along floor of nose; speaker does not use lubricant or defogging agent; pass down either pyriform fossa; as
going through cricopharyngeus, ask patient to burp or swallow; may need to use air insufflator on scope or ask patient to
sip water as scope passed down; once gastroesophageal junction (Z-line) reached, can brush area gently (risk for perforation
minor); different types of scopes (eg, video-chip scope, regular fiberoptic esophagoscope)
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| Benefits of TNE: safe; patient does not need conscious sedation, eliminating risks (especially safer for elderly and cardiac
patients); done in office, eliminating scheduling problems and lost work time; accurate after brief learning curve (takes 10
procedures to feel comfortable, 25 before being good, 50 to be expert); helps improve survival in adenocarcinoma; cost effective
(eliminates facility fee and anesthesia fee); insurance reimbursement in office setting better than in facility
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| Indications for TNE: dysphagia; reflux for 3 to 6 mo; abnormal esophagography; head or neck neoplasm; concerns about
esophageal neoplasm; note—adenocarcinoma of esophagus fastest-growing carcinoma in United States and Western Europe;
if patients diagnosed early, outcome and survival improved; survival now <10%; TNE indicated for endoscopic surveillance
in patients with GERD and Barrett’s esophagus
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| Complications of esophagoscopy: related to intravenous (IV) sedation; eliminated with TNE
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| Brush biopsy: simple procedure; brush passed along port through scope; gently brush Z-line; more accurate for diagnosing
Barrett’s than visualization only; submit for histopathologic (not cytologic) diagnosis (results in ≈24 hr)
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| Documentation: “proper coding leads to good reimbursement”; good documentation medical necessity; match current procedural
terminology (CPT) codes with International Classification of Diseases, 9th edition (ICD-9) codes; include report
sheet on method, reason, and findings of procedure, and whether brush biopsy done
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| CHRONIC COUGH —Peter C. Belafsky, MD, PhD, Director, Center for Voice and Swallowing, University of California,
Davis, Medical Center
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| Cough: types—acute, duration <3 wk; subacute, 3 to 8 wk; chronic >8 wk; majority of speaker’s patients have cough >1 yr
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| Acute cough: causes—viral upper respiratory tract infection (URI; >80% of patients with common cold report cough
within first 2 days; 25% have persistent cough for 2 wk); bacterial sinusitis; exacerbation of chronic obstructive pulmonary
disease (COPD); pertussis; allergic rhinitis; environmental rhinitis; unusual causes—can be presenting symptom of
pneumonia or congestive heart failure (CHF), especially in elderly (listen to patient’s lungs)
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| Subacute cough: typically postinfectious or secondary to bacterial sinusitis or occasionally, to asthma; listen to lungs, examine
sinuses; consider computed tomography (CT) or x-ray of sinuses or chest
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| Chronic cough: chronic bronchitis secondary to tobacco use number-one cause; although most smokers have chronic cough,
few complain about it; frequently multifactorial; 95% from postnasal drip syndrome, asthma, reflux, chronic bronchitis, eosinophilic
bronchitis, or angiotensin-converting enzyme (ACE) inhibitor; <5% caused by more serious condition (eg, sarcoidosis,
cancer, CHF); <1% habitual (psychogenic); patients—miserable; break ribs; eyes bleed; pass out; cough disabling
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| Work-up: history and physical examination; quality of cough (wet or dry) gives little insight into etiology; timing (cough during
meals could be sign of aspiration; cough after meals or that awakens patient during night likely caused by reflux); previous
treatments; when cough started (many have postviral neuropathy); environmental history; chest x-ray; esophagoscopy (chronic
cough independent risk factor for adenocarcinoma of esophagus; speaker performs pH testing; TNE or esophagogastroduodenoscopy
[EGD] recommended); nasal endoscopy; laryngoscopy
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| Nonsmokers not taking ACE inhibitor: with normal chest x-ray, caused only by postnasal drip syndrome or chronic rhinitis,
reflux, reactive airway disease, pertussis, or eosinophilic bronchitis
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| Postnasal drip syndrome: rhinitis; must dry nose to treat cough; cannot eliminate cough if caused by environmental trigger
that does not change
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| Reflux: find with pH testing; seen in 44% of people with chronic cough; pathophysiology—local irritation of cough receptors
in distal esophagus (does not have to be from acid, so antacids, PPIs, and H2 blockers may not treat reflux causing
cough)
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| Asthma: most patients with classic asthma report chest tightness, wheezing, and dyspnea; symptoms absent in patients with
chronic cough (cough-predominant asthma [silent asthma]); can be stimulated by virus or, occasionally, environment
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| Reactive airway disease: World Trade Center cough; postviral cough; environmental exposure; normal methacholine challenge
test has 100% negative predictive value; treat anyway because of eosinophilic bronchitis; found in 13% of patients
with chronic cough; no bronchial hyperresponsiveness); treatment—inhaled corticosteroids
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| Pertussis: rates increasing in United States; >1000 reported cases in California in 2003; children with pertussis “whoop,” but
adults rarely do; diagnosis—difficult; nasopharyngeal swab for polymerase chain reaction (PCR) or immunofluorescence;
no diagnostic blood test; treatment—macrolide, eg, erythromycin, clarithromycin (Biaxin), azithromycin (Zithromax)
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| Treatment: treatments for rhinitis, postnasal drip syndrome, reflux, asthma, eosinophilic bronchitis, and pertussis overlap;
rhinitis—avoidance, antihistamines, inhaled nasal corticosteroids, anticholinergics; systemic steroids rarely; antibiotics
if infection bacterial; asthma— β2 agonist if true asthma with chest tightness and wheezing; if not, inhaled corticosteroids;
avoidance; anticholinergics; systemic steroids occasionally; postviral reactive airway disease—gabapentin (Neurontin;
shown to suppress ectopic discharge from injured nerves; low adverse effects; few drug interactions);
eosinophilic bronchitis—inhaled corticosteroids; reflux—behavior modification important; bid or tid PPI; H2 blocker
in evening; alginates effective at keeping food in stomach; pertussis—Biaxin for 3 wk; nonspecific cough
suppressants—magnesium, tramadol (Ultram), rarely benzonatate (Tessalon Perles)
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| “Shotgun” protocol: behavior modification; avoidance; bid PPIs; H2 blocker in evening; budesonide (Pulmicort) 2 puffs
bid; Neurontin 300 mg tid; fluticasone (Flonase) 2 puffs bid (double normal dose); azelastine (Astelin) nasal spray (antihistamine);
3 wk of Biaxin; Ultram bid; occasionally amitriptyline (Elavil) in evening for sleep; cost—>$1000/mo;
worth it to patients with chronic cough
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| PEPSIN AND OTITIS MEDIA IN THE PEDIATRIC PATIENT —Dwight Bates, MD, Department of Otolaryngology,
Wake Forest University Baptist Medical Center, Winston-Salem, North Carolina
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| Otitis media (OM): second most common disease of childhood; most common cause of childhood deafness in developed
world; 75% of children have 3 episodes by age 7 yr; in United States, incidence increased 39% in past 10 to 20 yr; $5 billion/yr
spent on surgical and medical management of OM in children <6 yr of age
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| Etiology of OM: eustachian tube flatter and shorter in children than in adults; possibly, reflux of gastric contents into nasopharynx
and eustachian tube; regurgitation in infancy—common problem; 50% of children have 1 episode per day;
number increases and peaks by 4 mo of age, decreasing to 5% by age 10 to 12 mo
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| Research: study—children undergoing ear tube placement for chronic OM with effusion (COME); tested for pepsin using
enzyme-linked immunoabsorbent assay (ELISA) and enzyme activity; 0.8 to 214 µg/mL of pepsin found in 91% of children;
enzymatic assay for function of pepsin found in fewer but still significant number of effusions; study—13 patients with nasopharyngeal
reflux found to have chronic rhinopharyngitis and associated COME; study—ELISA for pepsinogen in 26
tube otorrhea samples; only 8 positive, but concentrations below normal serum reference range (no evidence of significant
reflux)
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| Pepsin: primary aspartic protease in stomach; acts at acidic pH; converted to active form at pH <5; proteolytic activity optimal
at pH 2 to 3; normal concentration in stomach 1000 µg/mL (Tasker study showed 0.2-214.0 µg/mL in middle ear)
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| Speaker’s study: hypotheses—reflux of gastric contents into nasopharynx can cause eustachian tube dysfunction and thus
COME in children; detection of pepsin in middle ear effusion can be used as marker for past reflux events; study—
samples from 27 ears of 19 children <4 yr of age, undergoing myringotomy tube placement for COME; Western blot—
antibody specific for end terminus of pepsin; no effusion contained pepsin; specific enzymatic assay—done at pH 2 to 3;
14 of 19 effusions showed proteolytic activity; conclusion—first hypothesis unproven; by specific enzymatic assay, pepsin
or pepsinogen appears to be present in middle ear of children with COME, but concentration probably very low; question
of whether concentration of pepsin normally present in middle ear high enough to cause damage; pepsin may still be
good marker for past reflux episodes, but not detectable with Western blot
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| NEUROLOGIC DISEASES OF THE LARYNX —Milan Amin, MD, Assistant Professor, Department of Otolaryngology,
New York University School of Medicine, and Director, New York University Voice Center, New York City
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| Functions of larynx: protects airway—primary function to prevent aspiration; redundant mechanisms; actively participates
in respiration—role in regulating airflow; feedback via airflow receptors; produces voice—least vital function;
latest to develop evolutionarily; complex function that requires multiple muscles
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| Peripheral disorders: paralysis and paresis; vocal cord paralysis and paresis—common; may affect any nerve; unilateral
or bilateral; left side more common than right because of length of recurrent laryngeal nerve; synkinesis—common;
found on electromyography (EMG) in patients with abnormal movement of vocal cords; causes—surgical; tumor; virus;
idiopathic; intubation; trauma; symptoms—“breathy” voice; vocal fatigue (most common complaint); inability to
project; weakness (inability to valsalva secondary to poor glottal closure); shortness of breath (SOB)—inadequate
movement in larynx; treatment—voice therapy useful only in mild unilateral cases; surgical interventions investigational;
partial cordectomy, arytenoidectomy, or tracheotomy for SOB or airway obstruction due to bilateral vocal cord paralysis
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| Myasthenia gravis: affects larynx; autoimmune disorder of neuromuscular junction; patients present with weak, breathy
voice; severe vocal fatigue; decreased maximum phonation time; ineffective cough, leading to aspiration; diagnosis—
edrophonium test using objective voice measures
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| Stroke: may result in vocal cord paralysis or paresis; if in brainstem, may produce dramatic changes in larynx; articulation
disorders—present in majority of patients; otolaryngologist cannot treat effectively; significant dysphagia—in 50% of
patients; problems may include pharyngeal motor weakness, vocal cord paralysis or paresis
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| Amytrophic lateral sclerosis (ALS): uncommon; progressive motor neuron disorder; respiratory failure—biggest problem;
patients lack muscle strength to expand lungs; aspiration pneumonia usual cause of death; voice and speech
disorders— usually occur late, but early involvement detectable; weak, breathy voice due to laryngeal weakness; poor
breath support because of muscle weakness in rib cage; dysarthria because of tongue and pharyngeal muscle weakness; dysphagia
and aspiration—weak protective reflexes (eg, larynx does not elevate properly, so epiglottis does not fold properly;
weak glottal closure); manometry—many patients have hyperactive cricopharygeus muscles, preventing bolus from
entering esophagus; sensory dysfunction—new reports show ALS not purely motor disorder; sensory axons in spinal cord
affected; adds to dysphagia
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| Parkinson’s disease: 70% of patients have significant voice and speech problems related to tremor, bradykinesia, and rigidity
in peripheral muscles and larynx; swallowing difficulties less common; characteristic pitch-locked vocal quality
(monotone); voice weak; appearance of vocal cord bowing; voice fades at end of breath; tremor only in late stages; decreased
articulation; treatment—difficult; occasionally, vocal cord augmentation, but does not produce dramatic improvement
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| Swallowing disorders: common sequelae of neurologic disorders; may be result of many factors (eg, sensory deficits, laryngeal
muscle weakness, changes in pharyngeal tone, tongue weakness, cricopharyngeal muscle incoordination);
evaluation—modified barium swallow; pharyngeal and esophageal manometry; treatment—depends on cause; cricopharyngeal
myotomy or botulinum toxin type A (Botox) if muscle hyperactive; vocal fold augmentation for improper
closure of larynx; for severe muscle disorder with inadequate elevation of larynx, consider laryngeal elevation or suspension;
sensory innervation for certain unilateral sensory deficits
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Educational Objectives
| The purpose of this program is to educate the listener about the role of transnasal esophagoscopy (TNE) in an otolaryngology
practice, chronic cough, pepsin and otitis media (OM) in the pediatric patient, and neurologic diseases of the larynx.
After hearing and assimilating this program, the clinician will be better able to:
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 | 1. Evaluate the role of TNE as an office-based procedure.
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| 2. Discuss the benefits of TNE in the early diagnosis of laryngopharyngeal reflux (LPR).
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| 3. Differentiate between acute, subacute, and chronic coughs.
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| 4. Discuss the role pepsin might play in pediatric OM.
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| 5. Describe the effect of neurologic diseases on the larynx, with emphasis on myasthenia gravis, stroke, amyotrophic
lateral sclerosis, and Parkinson’s disease.
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Discussed on This Program
Amitriptyline HCl [Elavil]
Azelastine HCl [Astelin, Optivar]
Azithromycin [Zithromax]
Benzonatate [Benzonatate Softgels, Tessalon, Tessalon Perles]
Botulinum toxin type A [Botox, Botox Cosmetic, Dysport]
Budesonide [Pulmicort Turbuhaler, others]
Erythromycin (many trade names)
Clarithromycin [Biaxin, Biaxin XL]
Edrophonium chloride [Enlon, Reversol, Tensilon]
Fluticasone propionate [Flonase, others]
Gabapentin [Neurontin]
Magnesium (many trade names)
Ranitidine HCl [Zantac, others]
Tramadol HCl [Ultram]
Suggested Reading
Andrus JG et al: Transnasal esophagoscopy: a high-yield diagnostic tool. Laryngoscope 115:993, 2005; Aviv JE et al:
Office-based esophagoscopy: a preliminary report. Otolaryngol Head Neck Surg 125:170, 2001; Bocskei C et al: The influence
of gastroesophageal reflux disease and its treatment on asthmatic cough. Lung 183:53, 2005; Fleischer S et al: Office-based
laryngoscopic observations of recurrent laryngeal nerve paresis and paralysis. Ann Otol Rhinol Laryngol
114:488, 2005; Fukae J et al: Hoarseness due to bilateral vocal cord paralysis as an initial manifestation of familial amyotrophic
lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord 6:122, 2005; Kalpaklioglu AF et al:
Evaluation and impact of chronic cough: comparison of specific vs generic quality-of-life questionnaires. Ann Allergy
Asthma Immunol 94:581, 2005; Kastelik JA et al: Investigation and management of chronic cough using a probability-
based algorithm. Eur Respir J 25:581, 2005; Keles B et al: Pharyngeal reflux in children with chronic otitis media with effusion.
Acta Otolaryngol 124:1178, 2004; Koufman JA: Laryngopharyngeal reflux 2002: a new paradigm of airway disease.
Ear Nose Throat J 81(9 Suppl 2): 2, 2002; Lee B, Woo P: Chronic cough as a sign of laryngeal sensory neuropathy:
diagnosis and treatment. Ann Otol Rhinol Laryngol 114:253, 2005; Mainie I et al: Fundoplication eliminates chronic
cough due to non-acid reflux identified by impedance pH monitoring. Thorax 60:521, 2005; Miyamoto RC et al: Bilateral
congenital vocal cord paralysis: a 16-year institutional review. Otolaryngol Head Neck Surg 133:241, 2005; Oyamada Y
et al: Asymmetry of the vocal folds in patients with vocal fold immobility. Arch Otolaryngol Head Neck Surg 131:399,
2005; Postma GN et al: Transnasal esophagoscopy: revisited (over 700 consecutive cases). Laryngoscope. 115:321, 2005;
Tasker A et al: Is gastric reflux a cause of otitis media with effusion in children? Laryngoscope 112:1930, 2002; Tasker A
et al: Reflux of gastric juice and glue ear in children. Lancet 359:493, 2002
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue Dr. Setzen has
disclosed that he is a consultant for Gyrus ENT and BrainLab, and is on the Speakers’ Bureau of Aventis Pharmaceuticals,
Merck & Co., Inc., and GlaxoSmithKline.
Dr. Setzen addressed the New York Rhinology Update, held April 8-10, 2005, in New York City, and sponsored by New
York University Post-Graduate Medical School and the Albert Einstein College of Medicine. Drs. Belafsky, Bates, and
Amin addressed Laryngology and Office-Based Surgery: State of the Art and Beyond, held May 20-21, 2005, in Winston-Salem,
North Carolina, and sponsored by The Center for Voice and Swallowing Disorders of Wake Forest University.
The Audio-Digest Foundation thanks the speakers and sponsors for their cooperation in the production of this program.
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