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  • 1. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-MilwaukeeEsophageal Swallowing Physiology and Disorders Caryn Easterling, Ph.D. CCC BRS-S Assistant Professor Department of Communication Sciences and Disorders University of Wisconsin-Milwaukee Department of Neurology Department of Pediatric Gastroenterology Medical College of Wisconsin Research Scientist Department of Physical Medicine and Rehabilitation Milwaukee, WisconsinEsophageal Swallowing Physiology and Disorders What Is the Role of the Speech-Language Pathologist in the Evaluation of Swallowing Disorders?Esophageal Swallowing Physiology and Disorders•ASHA Preferred Practice Patterns –Swallowing Assessment refers to the review of the esophageal phase of swallowing –“ …screening of the esophageal phase”•Collaboration between SLPs’ and Radiologists’ observations,impressions, and recommendations from the radiographicexaminationEsophageal Swallowing Physiology and Disorders•Obligated to Document Observations of the SwallowingContinuum in the upright position•Play a key role in the early detection of potential clinicaland radiographic indicators of esophageal swallowingdisorders•Facilitate appropriate medical referrals –(GI/ENT/Neuro/Pulmonary) for further evaluation 1
  • 2. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-MilwaukeeEsophageal Swallowing Physiology & DisordersEsophageal Swallowing Physiology and DisordersDysphagia –Symptom or patient report of swallowing difficulty Often evaluated first using a –Videofluoroscopic Swallow Study (VFSS) –Fiberoptic endoscopic Evaluation of Swallowing (FEES)Key Elements for the SLP•Careful history –will yield the likely anatomical location and pathophysiological process in 80% of the cases•The site of “bolus hold-up” –is not reliable if perceived in the neck•Endoscopy –is virtually always indicated•Precise diagnosis may require manometry and radiographicprocedures•A normal endoscopy and Ba swallow does not adequately rule out astructural eso abnormalityDysphagia•The subjective location of dysphagia does not alwayscorrespond to the anatomical location of the pathology•Patient’s clinical complaints and reporting regarding the siteof dysphagia may be unreliable and does not correlate withthe actual problem –Eg., Distal stricture often referred proximally (Jones et al., 1989)History•Where does the food stick?•Is one or more of the pharyngeal dysfunctions present? –Delay or absent swallow 2
  • 3. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee –Deglutitive nasopharyngeal regurgitation –Deglutitive cough –Repetitive swallows to clear the pharynx•Dysphagia for liquids or solids? –Motor – both –Structural - solidHistory•How long has dysphagia been present; intermittent,progressive? –Long – benign –Long, intermittent, non progressive, solids - structural –Short, rapid progression, weight loss – CA•What does the patient do when it “sticks”? –Do they regurgitate? –Chest Pain?Clinical Indicators of Possible Esophageal SwallowingAbnormality•Fullness or tightening in throat or chest•Localized or radiating Neck, jaw, or chest pain•Liquid or Solid Food Dysphagia•Chronic Cough•Chronic Throat Clearing•Excessive secretions•Paradoxical Vocal Cord Dysfunction•Breathlessness•Hoarseness•Sore throat•Acidic tasteMBS Indicators of Possible Esophageal SwallowingAbnormality: Indicators for medical referrals/further esophagealexaminationModified Barium Swallowing Study: 3
  • 4. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee•Is Not Diagnostic Exam for Esophageal SwallowingDisorders or Gastroesophageal Reflux Disease (GERD)•Includes only observations of potential indicators ofesophageal swallowing disordersMBS Indicators of Possible Esophageal SwallowingAbnormality: Indicators for medical referrals/further esophagealexamination•Large air column just below UES•Pocket of contrast just posterior and distal to UES (Zenker’sDiverticulum)•Slow or obstructed esophageal clearance of contrast in theupright position (± tertiary contractions) AnatomyAnatomy of the Human EsophagusThe esophagus: –22 to 26 centimeters in length –Length varies with body size –Tubular structure composed of skeletal (proximal 1/3rd) and smooth (distal 2/3rds) muscle. (Christensen, 1987; Roman, 1982)Anatomy of the Human Esophagus•Organ of transport –Peristalsis•Peristalsis is the progression of a pressure wave through the body ofthe esophagus –Body position is important in evaluation of peristalsis 4
  • 5. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee•Striated esophageal muscle demonstrates both: –Primary peristalsis during the esophageal phase of swallowing ….and –Secondary or bolus initiated peristalsis (Kendall, Thompson, Day, & Garvie, 1987)Anatomy of the Human Esophagus 1/3 Striated Muscle 0.9 cm (4% ) --- Mixed 7.6 cm (34%) 2/3 Smooth Muscle 14.3 cm (62%)Anatomy of the Human Esophagus•Striated muscle of the esophagus has both an external andan internal layer of muscle –Outer - longitudinal muscle –Inner - circular muscle –Interact in a stereotypic pattern during peristaltic propulsion of the luminal contents (Hendrix, 1993)Anatomy of the Human Esophagus•Layers of the Esophageal Wall –Squamous Epithelium –Lamina Propria –Muscularis mucosaBoundaries of the Esophagus are Defined by twoSphinctersBoundaries of the Esophagus are Defined by twoSphinctersUpper Esophageal Sphincter (UES)/ PharyngoesophagealSphincter (PES) Biomechanical Sphincter: 5
  • 6. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee –Relaxation –Traction force to open •Superior and anterior pull by posterior cricoid cartilage away from the posterior pharyngeal wall •Contraction of the suprahyoid muscles –Distension (elasticity of the UES) •Intrabolus pressureBoundaries of the Esophagus are Defined by twoSphincters•Lower Esophageal Sphincter (LES) –Passive Relaxation –DistentionNeural Control of Swallowing•Motor neurons involved in oropharyngeal and esophagealswallowing –Trigeminal (V) - striated muscle –Facial (VII) - striated muscle –Vagus (X) – striated muscle –Glossopharyngeal (IX) - striated muscle –Hypoglossal (XII) nuclei - striated muscle –Nucleus ambiguous (nA) - striated muscle –Dorsal motor nucleus of the vagus nerve (dmnX) - smooth muscleNeural Control of the Human Esophagus•Esophageal Body: innervated extrinsically –Autonomic nerves 6
  • 7. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee •Via vagus nerve and branches of the sympathetic nerves •Motor function: brainstem, medulla and pons•Highly dependent on the peripheral sensory input fromoropharyngeal structures –LES relaxation may occur independently of eso body (LESR)Neural Control of the Human Esophagus•Intrinsic innervation of the EB –Myenteric plexus •Ganglionic cells •Nerve fibers –(Dodds et al., 1974; Gilbert & Dodds, 1986)Neural Control of the Human Esophagus•UES – motor innervation –Glossopharyngeal nerve –Pharyngeal branch of the vagus –Recurrent laryngeal branch of the vagus•Cervical esophagus –Recurrent laryngeal nerve•Distal esophagus –Branches of the thoracic vagal trunksMoving the Bolus:Esophageal Peristalsis is InitiatedTwo Ways•Primary Peristalsis – Swallow initiated•Secondary Peristalsis – Distension of esophagealbody•Remember position mattersEsophageal Peristalsis•Above the bolus 7
  • 8. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee –What is going on? •The circular muscle contracts and the longitudinal muscle relaxes to produce a propulsive segment that travels the length of the esophagus during the swallowEsophageal PeristalsisCan it be modified?•Peristalsis in the striated muscle is modified –bolus volume –temperature change Indicating that sensory inputs from the esophagus modulate the central vagal output that controls peristalsis in the striated muscle of the esophagus (Dodds, Hogan, Reid, Stewart & Arndorfer, 1973)Ingestion of Cold Substances Causes Inhibition ofEsophageal Peristalsis & Can Produce PainSingle Swallow: Observe primary peristalsisFrequent Swallows: Inhibit Propagation of Peristalsis into theDistal EsophagusCompetence of the GE Junction•Two Major Components –Sphincter pressure - LES •Muscle tone •Diaphragm –Transient sphincter relaxations •Specific mechanisms not knownLES Resting & Relaxation Pressure 8
  • 9. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee•LES pressure during rest and deglutition is the sum ofsphincteric muscle tone and the phasic changes of thediaphragm –LES Pressure increases with inspiration•Transient lower esophageal sphincter relaxation (TLESR’S)Esophageal Causesof Dysphagia – Four Categories•Motility Disorders or Abnormalities•Structural Abnormalities –Obstructs passage of the bolus •Web, ring, or stricture –Benign or malignant tumor –Numerous causes of both•Infection•Neural DysfunctionESOPHAGEAL FUNCTION TESTINGObservations during an Esophagram (radiographicevaluation of the esophagus)•Esophageal bolus transit –Gravity assisted •Esophageal clearance in the upright position•Esophageal shortening•UES opening (assume relaxation)•UES closure (assume contraction)•LES opening (assume relaxation)•LES closure (assume contraction)Components of an Esophagram•Recumbent Position•Sufficient Bolus Size 9
  • 10. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee•Observation of Sufficient Swallows•Abdominal Compression? –Gastroesophageal reflux?•Bolus Challenge (marshmallow)?Esophageal Motor Function& Bolus Motility•1° peristaltic wave - initiated by swallow•2° peristaltic wave - initiated by distended esophagus –2° bolus residual –Reflux event•Tertiary contractions - non-propulsive events•Manometry and esophagram are complimentary –Manometry quantitative –Esophagram qualitativeEsophageal Manometry•Measurement of pressure changes in the body of theesophagus•Indirect measure of contraction and function•No direct observation of bolusClinical Indications For Esophageal Manometry•Evaluation of patients with dysphagia –Primary motility disorders •Achalasia: motor disorder of smooth muscle of eso –LOSS OF INTRAMURAL NEURONS –LES DOES NOT RELAX –NON PERISTALTIC CONTRACTIONS •Spastic disorders –Secondary motility disorders •Scleroderma 10
  • 11. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-MilwaukeeClinical Indications For Esophageal Manometry(cont.)•Evaluation of patients with GERD –Evaluate peristalsis and LES integrity •GER severity •Prior (after) fundoplication –Assist in placement of pH probe (location of UES/LES)•Evaluation of patients with non-cardiac chest painINTRALUMINAL IMPEDANCEINTRA-ESOPHAGEAL pH MONITORING•Prolonged pH recording in the study of gastro-esophagealreflux. (Spencer J, 1969)•Laryngopharyngealreflux (LPR)•Globus pharyngeous (Cook, 2007)DEFINITION OF REFLUX•Defined by fall in pH to <4.0 until returnto >4.0•Rationale: –Clearly distinct from usual intra-esophageal - pH of 6-7 –Pepsin inactivated at pH >4.0 –Good association between reflux Sx and pH 4.0REFLUX PARAMETERS•Percent acid exposure (pH <4.0) –Upright –Recumbent –Total•Total number of reflux episodes•Number of episodes >5 minutes 11
  • 12. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee•Time of single longest episodeAMBULATORY PH MONITORING:Clinical Indications•Reflux symptoms –Chest pain –Hoarseness –Bronchospasm –Non-ulcer dyspepsia•Typical heartburn with negative workup•Pre-operative evaluation for fundoplication•Follow-up of anti-reflux therapy –During medical therapy –Post-fundoplicationSYMPTOM INDEX = Number of Times Symptom Occurred when pH <4AMBULATORY GER MONITORING(MII-pH)•GER episodes identified by MII•GER episodes categorized as acid or non-acid by pH –Non-acid reflux = refluxate with pH >4 (<10% bile)POTENTIAL MII-pH APPLICATIONS•Diagnosis of patient with persistent symptoms while on PPI Rx Elucidate the role of non-acid GER•Evaluation of atypical GERD Correlate acid & non-acid GER episodes to sx Quantify proximal extent of GER•Evaluate postprandial GER pH is blind during early postprandial period 12
  • 13. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee Postprandial is prime time for reflux and sxPERSISTENT SYMPTOMS ON PPIPossible causes•Acid not controlled by medications ~20%•Symptoms due to “non-acid” reflux ~40%•Symptoms not due to reflux ~40%NON-ACID REFLUX•Detected by combined impedance-pH monitoring•Does it cause injury? –It does cause symptoms!•Laryngopharyngeal reflux (LPR) –Visual findings & pH monitoring lack specificity –Laryngeal irritation is multi-factorial –Longer time to disappear compared to symptoms (Belafsky et al., Laryngoscope; 2001) –Empiric BID PPI (omeprazole etc.) best (4-6 months) (Park et al., Laryngoscope; 2005)Globus pharyngeus•Globus pharyngeus: –Feeling of a lump or foreign body in the throat –Crumb-like sensation, constriction causing choking –45% of population experiences•Globus “hystericus” –Wilson et al., (1995,96), UKGlobus pharyngeus•Cook et al., (2007) –How valuable is videofluoroscopy and ambulatory pH in monitoring patients with globus 13
  • 14. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee –pH helpful only in those who had GER with GP –All accompanying pharyngeal dysfunction noted on VFSS•Cook et al., (1998) –Hypertensive UES –No association with GER•Consistent presence of mucous in the epipharynx•PPI & anti-depressiveESOPHAGEAL MOTILITY ABNORMALITIESClassification of Esophageal MotilityDisorders•Primary –those disorders not related to underlying disease•Secondary –those related to underlying diseasePrimary Motility/Motor Disorders•Achalasia•Diffuse esophageal spasm•Intestinal pseudo-obstruction•Presbyesophagus•Neonatal achalasia•Affect neural as well as muscular elements of the esophagus andLES•Pain and dysphagia –Calcium channel blockers –Anti-anxiety medication –Botox vs. muscle relaxantsSecondary Motility Disorders•Connective tissue –Scleroderma 14
  • 15. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee•Chemical or physical –Reflux esophagitis (peptic) –Caustic esophagitis –Vagotomy –Radiation•Endocrine•Infection –Fungal: moniliasis –Bacterial: TB –Parasitic: Chagas’ disease –Viral: Herpes simplex•Metabolic –Diabetes –ETOH –Amyloidosis –Serum pH and electrolye disturbancesSecondary Motility Disorders•Neurologic disease –Myositis –Parkinsonism –Huntington’s chorea –Wilson’s disease –Cerebrovascular disease –Multiple sclerosis –ALS –CNS neoplasmABNORMAL ESOPHAGEAL MOTILITYTraditional Classifications•Achalasia•Diffuse esophageal spasm•Nutcracker esophagus•Hypertensive lower esophageal sphincter•Non-specific esophageal motility disorderABNORMAL ESOPHAGEAL MOTILITYNew Classification•Inadequate LES relaxation (RP >8 mmHg) –Classic achalasia – absence of peristalsis –Atypical patterns 15
  • 16. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee•Uncoordinated motility –Diffuse esophageal spasm (>10% simultaneous contractions, >30 mmHg)•Hypercontraction –Body = nutcracker esophagus (mean amplitude >180 mmHg) –LES = hypertensive LES (>45 mmHg)•Hypocontraction (≥ –Body = IEM (≥30% contraction < 30 mmHg) –LES = Hypotensive LES (<10 mmHg)ABNORMAL ESOPHAGEAL MOTILITY•Clinical Importance•Achalasia –Establish diagnosis and direct therapy•DES, nutcracker esophagus, hypertensive LES: –Relation to Sx usually not clear –Only suggests therapy (no pathology known)•IEM, hypotensive LES: –Usually indicates GERD –Important information prior to fundoplicationABNORMAL ESOPHAGEAL MOTILITYDiffuse Esophageal Spasm•Chest pain –Associated with high amplitude esophageal peristaltic pressure wave –Repetitive non-propulsive contractions•Similar to early “vigorous” achalasia –Except normal LES relaxation –Manometric analysisAchalasia•Lack of relaxation of the lower esophageal sphincter (LES) –Absent or markedly decreased 10 and 20 esophageal peristalsis –Disruption of motility•Early- “vigorous” numerous tertiary contractions –Without normal 10 wave•Late stage - dilated esophagus –Large air-fluid level –“Bird beak-like” appearance of the LES•Amyl Nitrate - smooth muscle relaxant –Improves LES relaxation –Lowers barium column level –Excludes underlying tumor 16
  • 17. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-MilwaukeeBarrett’s Esophagus•10% prevalence of adenocarcinoma in patient’s withBarrett’s•Risk of adenocarcinoma 30 to 40 times greater in Barrett’spatients•Classic Presentation: –High esophageal stricture –GERD and/or hiatal herniaPREVALENCE OF BARRETT’S BY AGEIneffective Esophageal Motility (IEM)A SPECIFIC MANOMETRIC ABNORMALITY•Contraction abnormality of the distal esophagus where≥30% of wet swallows are –Low-amplitude contractions (<30 mm Hg) or –Nontransmitted contractions•Occurs in about 30% of GERD patientsScleroderma•Weak-to-absent distal peristalsis (smooth muscle)•Normal proximal peristalsis & UES (striated muscle)•Absent 1° and 2° peristaltic pressure waves•Dilated esophagus•Abnormal esophageal motility•Patulous LES with free GER•Long term GERD leads to esophagitis, strictures –Possible Barrett’s esophagus –Adenocarcinoma of the esophagusIEM – “Presbyesophagus”•Increased number of tertiary contractions•Esophageal aperistalsis•Older individuals 17
  • 18. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee•Diabetes- weakened 10 peristalsis –Frequent tertiary contractionsMotor Disturbances•Non-specific dysmotility•Breaking 1° peristaltic pressure wave•2° clearing - common•Tertiary contractions – common and increase with age•Low amplitude of peristaltic pressure wave•Prolonged duration of peristaltic pressure waveObstruction to Passage of Bolus•Webs, Rings, & Strictures –Webs - often incomplete • 1-2 mm in length • Cervical esophagus –Rings- 3-5 mm length •Schatzki’s ring –Gastroesophageal junction –Strictures - longer than 1cm • Can be very longCervical Esophageal Webs•Upper esophagus•Usually incomplete•Anterior location•If complete with narrowing –Dysphagia•Often incidental, non-symptomaticPlummer Vinson Syndrome•Dysphagia due to esophageal webs•Iron deficiency anemia•Pharyngoesophageal carcinomaZenker’s diverticulum•Hypopharnyx•Posteriorly just above upper esophageal sphincter 18
  • 19. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee –Killian-Jamieson’s dehiscence•Can lead to: –Globus –Retrograde aspiration•Hypothesis: –Incoordination of pharyngeal pressure wave contraction & UES relaxationSchatzki’s Ring•At the gastroesophageal junction•Greater than 20 mm –B ring•Less than 12 mm –Symptomatic Schatzki’s•Between 12-20 mm –?•Marshmallow ChallengeSchatzki Ring•Case report (Gawrieh., et.al, 2005) –Three patients •Schatzki Ring (2) •hypertensive peristaltic waves (1) –Cardiac syncope during swallowing –Treatment – cardiac pacemaker •Syncope when swallowing resolvedBenign Strictures•Peptic / GERD –Barrett’s esophagitis –NG intubation –Scleroderma•Caustic ingestion•Pill esophagitis•Radiation•Rare: –Congenital esophageal stenosis –Crohn’s disease –Eosinophilic esophagitis (increased dx) 19
  • 20. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee –Graft vs. host diseaseCaustic Ingestion•Ingestion of strong acids or bases –Lye, Drano•Long severe stricture formation –1-3 months after event•Chronic lye strictures –Increased risk for esophageal carcinomaPill Esophagitis•Tetracycline and doxycycline - most common –Superficial ulcers –Eventually heal•Quinidine, potassium chloride, alendronate, aspirin, NSAIDs –Severe esophagitis with ulcers & strictures•Direct irritant at areas of hang-up in the esophagus – aortic arch –left mainstem bronchus –heartRadiation•High doses (5000 cGy (rads) or more) –Dysphagia from stricture formation –4-8 months after Radiation Therapy•Acute esophagitis (1-4 weeks)•Smooth, long strictures•Within radiation portal•Differential Dx: –Recurrent tumor – irregular, nodular shapeEosinophilic Esophagitis (EE)•1966 – Dysphagia – proximal rings (Kelly: JAMA 197: 143)•1978 – EE in an adult (Landes: Gastroenterology 74:1298)•1993 – EE in group 12 adults (Attwood: Dig Dis Sci 38:109)•2001 – Small Caliber Esophagus (Vasilopoulos: Gastroenterology 55:99) 20
  • 21. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-MilwaukeeEosinophilic Esophagitis (EE)•Structural Abnormalities –Small caliber esophagus –Corrugations/multiple concentric rings –Proximal stenosis –Whitish surface vesiclesEosinophilic Esophagitis (EE)•Diagnostic evaluations –Endo - 93% –Radiologic - 69% –Structural alterations 23 - 25 patients –GERD-like features: 2 patients –No unique features: 2 patients•Solid food dysphagia is the clue!Graft vs. Host Disease•Bone marrow transplant patients•Bullae, ulcers, mucosal desquamation•Long stricturesCongenital Esophageal Stenosis•In adults- mild form•Children –Severe form requiring surgery•Ring-like indentations –? Remnants of cartilage or –Related to GERBenign Tumors•Submucosal –Leiomyoma •50% - benign tumors –Neurofibroma –Hemangioma –Fibroma 21
  • 22. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee –Lipoma –Granular cell myoblastoma –Hemangiopericytoma –CondylomaaccuminataMalignant Obstruction•Squamous Cell Carcinoma•Adenocarcinoma•Carcinoid•Sarcoma•Lymphoma•MetastasesSquamous Cell Carcinoma•50-70% of esophageal tumors•Dysphagia develops late•5 year survival <10%•Risk factors –Smoking –AlcoholConditions With Increased Risk ofEsophageal Cancer•Squamous Cell –ENT Cancer –Achalasia –Lye Stricture –Celiac Disease –Plummer-Vinson –Radiation•Adenocarcinoma –Barrett’s –Scleroderma 22
  • 23. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-MilwaukeeRadiologic Appearance•Superficial esophageal cancer•Varicoid•Apple-core lesions•Infiltrating•Polypoid•Plaque-like•UlcerativeAdenocarcinoma•30-50% of esophageal malignancies•Virtually always on a background of Barrett’sesophagus –10% prevalence of adenocarcinoma in patient’s with Barrett’s –Risk of adenocarcinoma 30-40x greater in Barrett’s than general populationInfection•Viral - often in immunocompromised host•Fungal - often in immunocompromised hostCandida albicans•Immunosuppressed 2° –Malignancy –Diabetes –AIDS –Debilitating illness•Most common - opportunisitic esophagitis –Odynophagia –Dysphagia –Chest pain•May (but not always) also have oral thrush•Longitudinal plaques or nodular lesions•Late Stage - “shaggy” esophagusHerpes 23
  • 24. C. Easterling, Ph.D. CCC BRS-S ASHA 2007Assistant Professor, University of Wisconsin-Milwaukee•Immunocompromised patients –Second most common opportunisitic esophagitis•Herpes Simplex Virus I•Acute, severe odynophagia with chest pain•Vesicles rupture- small superficial ulcers•Clustered or spread apartCytomegalovirus (CMV)•AIDS patients –Less likely in other immunocompromised patients•Severe odynophagia•Ulcers, fold thickening, nodularity- –May mimic herpes•Large flat ulcers or elongated –Indistinguishable from HIVHIV•AIDS patients with odynophagia•Giant ulcers•Dfferential Dx: CMV- negative brushings for CMVCase Presentations:Overlapping Disorders of Oropharyngeal andEsophageal Function •Caryn Easterling caryn@uwm.edu 24