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Unformatted text preview: Esophargeal Dysphagia Esophargeal Jean Paul Font, MD Michael Underbrink, MD, MBA University of Texas Medical Branch Department of Otolaryngology Grand Rounds Presentation February 6, 2008 Esophageal Anatomy Esophageal Muscular tube connecting the pharynx Muscular to the stomach to Esophagus begins where the inferior Esophagus pharyngeal constrictor merges with the cricopharyngeus – Upper esophageal sphincter (UES) 18 to 26 cm in length Lower esophageal sphincter (LES) Lower – – Thickened circular smooth muscle 40cm from incisors Extrinsic indentations – – – Anterior body of C7 (worsen by Anterior osteophytes) osteophytes) Arch of the aorta, the left mainstem Arch bronchus bronchus Diaphragmatic hiatus Diaphragmatic Four layers: – Mucosa – Submucosa – Muscularis propria – Adventitia; no serosa. Adventitia; Esophageal Mucosa Esophageal – Nonkeratinized, stratified Nonkeratinized, squamous epithelium squamous Gastric lining Gastric – Columnar epithelium Columnar (rugae) (rugae) Z-line – Junction of the squamous Junction epithelium and columnar epithelium epithelium Cephalad movement Cephalad – Barrett’s esophagus. Barrett’s Muscularis propria Muscularis Skeletal and smooth muscle – Skeletal muscle (Proximal 1/3) (Proximal Skeletal – Mixed (Middle 1/3) Mixed (Middle – Smooth muscle (Distal 1/3) (Distal Smooth Inner circular Inner Outer longitudinal layers. Outer Innervation mainly by Vagus n. Innervation Auerbach’s (myenteric) plexus – Between the two muscle layers – Controls esophageal peristalsis – Acetylcholine mediates Acetylcholine contraction contraction – Nitric oxide relaxation Meissner's plexus – – – Submucosal layer Sensory input Sensory Pain sensation overlap with the Pain heart and respiratory system heart Esophageal Peristalsis Esophageal At rest – UES & LES UES tonically contracted tonically Immediately after a Immediately swallow – UES pressure falls UES transiently transiently Shortly thereafter – LES pressure falls LES and remains low until the peristaltic contraction closes the LES Dysphagia Dysphagia Greek dys (difficulty, disordered) and phagia (to eat) Greek dys phagia Sensation that food is hindered in its passage from the Sensation mouth to the stomach mouth Most patients complain that food – “sticks,” “hangs up,” “stops,” or “just won't go down right” sticks,” Anatomically classified into two separate clinical categories: – Oropharyngeal and esophageal. Oropharyngeal Psychiatric disorders can amplify this symptom. Dysphagia is a common symptom Dysphagia – Present in 12% of patients admitted to an acute care hospital Present and in more than 50% of those in a chronic care facility. History History Three questions are crucial: Three (1) What type of food or liquid causes symptoms? – Mechanical vs neuromuscular defect Mechanical – Primarily solids Primarily Structural lesion- peptic stricture, ring, or malignancy Structural – Both solid and liquid Both a motility disorder like achalasia or scleroderma motility (2) Is the dysphagia intermittent or progressive? – Esophageal rings tend to cause intermittent solid food dysphagia Esophageal – Strictures and cancer cause progressive dysphagia (3) Does the patient have heartburn? – Complication of GERD- Esophagitis, stricture & Barrett’s History History Location of dysphagia – Limited value (Referred from any site) Weight loss Weight – Significance and duration of the disease Dietary changes Dietary – Nature and severity of disease. Nature Dysphagia must be distinguished from odynophagia odynophagia – Associated with an inflammatory condition Associated (esophagitis) (esophagitis) Diagnostic Tools Diagnostic Esophagogram Endoscopy Esophageal Manometry pH probe Esophageal Ultrasound CT, MRI Esophagogram Esophagogram Double-contrast barium esophagogram Usually the first specific diagnostic test in Usually the evaluation of esophageal dysphagia the Detect subtle narrowing or esophageal Detect webs that may not be appreciated on endoscopy Endoscopy Endoscopy Procedure of choice to evaluate the mucosa of Procedure the esophagus Detection of structural abnormalities Flexible esophagoscopy – – – – Used by GI service Transorally Diameters approaching 1cm Allows the insufflation of air to distend the esophagus Allows and more easily see all of the mucosa and – Magnified view, suction, irrigation, and biopsy ports. Magnified – Requires intravenous sedation setting Rigid esophagoscopy Rigid – Used by otolaryngologists – Requires general anesthesia – Examine the full extent of the esophagus – View is not magnified – Esophagus is not distended – Allows use of instrumentation – The risks of general anesthesia and the rigid The esophagoscopy esophagoscopy Transnasal Esophagoscopy Transnasal Flexible esophagoscopy – Smaller size (5mm) allows their passage through the Smaller nasal cavity Topical anesthesia Topical “Easily” performed clinic procedure Easily” Patient can returned to work after the appointment appointment Allows the insufflation of air to distend the Allows esophagus and more easily see all of the mucosa. Transnasal Esophagoscopy Transnasal Patient is asked to Patient swallow as scope is gently advanced through the UES the Air is insufflated into Air esophagus esophagus If mucosal lesions or If irregularities are found multiple biopsies are taken with biopsy forceps passed through the biopsy port biopsy Postma et al in 2005 – Review of 711 consecutive patients examined Review with transnasal esophagoscopy with – They used a spray combination of 0.05% They oxymetazoline and 4% lidocaine in the nasal cavity – If biopsy or a longer procedure is required, If one Tessalon Perle is used one – Seventeen of 711 procedures (3%) were Seventeen terminated due to a tight nasal vault and 2 due to a self-limited vasovagal response due – 50% incidence of significant findings Esophageal Manometry Esophageal Measures intraluminal pressures – LES, esophageal body & UES With each swallow – – – Strength Timing Sequencing of pressure events Indicated for patients who need recurrent intraluminal Indicated pressure assessment pressure – Achalasia – Diffuse esophageal spasm Diffuse Achalasia Achalasia Primary esophageal motility disorder – Insufficient LES relaxation – Loss of esophageal peristalsis Pathologic – – – Loss of ganglion cell in the myenteric plexus Infiltrate of T lymphocytes, eosinophils, and mast cells Selective loss of postganglionic inhibitory neurons, which contain Selective both nitric oxide and vasoactive intestinal polypeptide both Symptoms – – – Dysphagia to solids and liquid Regurgitation Chest pain Achalasia Diagnosis Achalasia Best initial diagnostic Best study study – Barium esophagram Barium with fluoroscopy with Esophageal dilation Closed LES Loss peristalsis Bird's beak Esophageal manometry Esophageal – Establish the diagnosis Establish Absent or incomplete LES relaxation relaxation Loss peristalsis Endoscopy Endoscopy – Exclusion of Exclusion pseudoachalasia by carcinoma at the GE junction the Treatment Treatment Pneumatic dilation Pneumatic – Should be a surgical candidates Should 2% to 5% risk of perforation 2% – After dilation need a gastrograffin study followed by After barium swallow to exclude esophageal perforation barium – Good to excellent relief of symptoms in 50% to 93% Good of patients Surgical myotomy – – – Myotomy across the LES Laparoscopy with a response rate of 80% to 94% Complication- GERD in 10% to 20% Complication- High risk for pneumatic dilation or surgery High – Botox Effective in about 85% of patients Symptoms recur in more than 50% of patients after Symptoms 6 months months – Pharmacologic treatment with nitrates or Pharmacologic calcium-channel blockers Non-achalasia Motility Disorders Non-achalasia Diffuse esophageal spasm (DES) – Simultaneous and repetitive contractions in Simultaneous the esophageal body the – Normal LES relaxation – Dysphagia if the contraction amplitudes are Dysphagia low low – Chest pain if the contraction amplitudes are Chest high high Diffuse esophageal spasm Diffuse Diagnosis – Esophagogram "corkscrew" esophagus – Manometry Simultaneous and Simultaneous repetitive contractions in the esophageal body Treatment Treatment – Medications that relax Medications the esophagus the Nitrates and calciumchannel blockers Scleroderma Scleroderma Connective tissue disease Peristalsis is absent in the Peristalsis distal two-thirds distal Mild dilation of the distal Mild esophagus esophagus LES becomes incompetent Associated Associated – Aspiration pneumonia – Reflux esophagitis with Barrett's Reflux esophagus esophagus Esophageal Strictures Esophageal Loss of lumen area Loss – Normal 20 mm in diameter Dysphagia main symptom – Less than 15 mm Worse with large food Worse pieces such as meat and bread bread Acid/peptic stricture Acid/peptic accounting for the majority of cases (60%– majority 70%). 70%). ETIOLOGY OF ESOPHAGEAL STRICTURES STRICTURES Intrinsic strictures Extrinsic strictures Acid peptic Pulmonary/mediastinal malignancies Pill-induced Anomalous vessels and aneurysms Chemical/lye Metastatic submucosal infiltration (breast cancer, mesothelioma, adenocarcinoma of gastric cardia) Post-nasogastric tube Infectious esophagitis Sclerotherapy Radiation-induced Esophageal/gastric malignancies Surgical anastomotic Congenital Systemic inflammatory disease Epidermolysis bullosa Diagnosis Diagnosis Esophagogram – Initial diagnostic study – Delineate the stricture Distal stricture Caustic ingestion Endoscopy – Evaluate the mucosa Evaluate normal mucosa Barrett's metaplasia Treatment Treatment Esophageal dilation – Depends on the length and diameter – Tight or complex strictures Tight Less than 10 mm in diameter Less Greater than 2 cm in length Best managed with wire-guided bougies under fluoroscopic and Best endoscopic control endoscopic – Simple strictures can be dilated with Maloney dilators – Progressively over weeks to months with a gradual increase in Progressively the diameters of the dilators the – Most patients have relief of dysphagia after dilation to a diameter Most of 40 to 54 French with no requirement for maintenance dilations of – Radiation-induced or malignant strictures are at higher risk of Radiation-induced perforation Treatment Treatment To minimize the risk of perforation, the "rule of To threes" applies threes" – No more than three sequential dilators should be No performed per session performed – Refractory strictures can be treated endoscopically Refractory with injection of triamcinolone into the stricture in all four quadrants prior to dilation four – More recently, endoscopically placed temporary More nonmetallic expandable stents (Polyflex) nonmetallic Effective in refractory benign strictures Esophageal Rings & Webs Esophageal Symptoms – Intermittent solid food dysphagia, Intermittent dysphagia aspiration, and regurgitation aspiration, Rings – Circumferential – Mucosa or muscle – Most commonly occur in the distal Most esophagus esophagus – Schatzki's ring occurs at the GEJ Schatzki's Webs – – – – Only part of the esophageal lumen Always mucosal Located in the proximal esophagus Association with iron deficiency Association (Plummer and Vinson) (Plummer Diagnosis Diagnosis Barium Esophagogram – Most sensitive test Endoscopic visualization – Normal-appearing mucosal – Cervical webs are associated Cervical with carcinoma with Treatment – Endoscopic dilation – Large bougie or balloon (15 to Large 20 mm) so as to fracture the ring ring – Refractory rings Pneumatic dilation (large Pneumatic balloon) balloon) Electrosurgical incision Surgical resection Treat GERD Dysphagia lusoria Dysphagia Aberrant right subclavian artery – Arises from the left side of the aortic arch Arises – Compress the posterior esophagus Compress – 20% of cases anterior 20% Barium esophagogram Barium – Indentation at the level of the third and fourth thoracic vertebrae Confirmation – CT, MRI, arteriography, or EUS Endoscopy – Right radial pulse may diminish with compression of the right subclavian artery Esophageal manometry – High-pressure zone at the location of the aberrant artery Symptoms usually respond to changes in diet to soft consistency and small Symptoms size size When necessary, surgery relieves the obstruction by reanastomosing the When aberrant artery to the ascending aorta aberrant Gastroesophageal Reflux Disease Disease GERD is recognized in about 10-15% of the population Reflux esophagitis – Changes in the esophageal mucosa – Present in 30% to 40% Barrett's esophagus – 10% to 20% Defects in the esophagogastric barrier such as Defects – LES incompetence – Transient relaxation of LES – Hiatal hernia GERD Diagnosis GERD Classic symptom is heartburn – Retrosternal burning discomfort and acid Retrosternal regurgitation regurgitation – Other symptoms are dysphagia, odynophagia, Other and belching and Laryngopharyngeal reflux (LPR) – Hoarseness, throat clearing, dysphagia, Hoarseness, increased phlegm and globus sensation Management Management Treatment Treatment – Initial empiric trial in the absence of alarm Initial signs signs – Diagnostic testing Diagnostic if there is a failure to respond to an empiric course of antisecretory therapy if alarm signs such as dysphagia, odynophagia, weight loss, chest pain, or choking are present. pH probe pH Ambulatory 24-hour Ambulatory esophageal pH monitoring esophageal – Gold standard for the diagnosis Gold of GERD of – Detect and quantify Detect gastroesophageal reflux gastroesophageal – Correlate symptoms temporally Correlate with reflux with Bravo pH probe Bravo Size of a capsule Placed endoscopically Placed – 6 cm above the GEJ cm Transmits to a recording device device 48 hours of pH data Falls off after 4 to 10 days Falls Patients prefer this device over the catheter-based system due to reduced discomfort to Endoscopy Endoscopy – Reflux esophagitis Reflux Erosions or ulcerations – pH probe results are pH normal in 25% of patients with erosive esophagitis esophagitis Barrett's esophagus Barrett's Potentially serious complication of longstanding GERD Stratified squamous epithelium of the Stratified distal esophagus is replaced by intestinal columnar metaplasia columnar It is the most significant outcome of It chronic GERD and predisposes patients to the development of esophageal adenocarcinoma. MALIGNANT STRICTURES 12,000 new cases each year in the United States 12,000 Squamous cell carcinoma (SCC) Squamous – – – – Black males Alcohol and tobacco abuse History of caustic esophageal injury Other conditions including achalasia, Plummer-Vinson Other syndrome, and a history of head and neck SCC syndrome, – Have also been associated with human papillomavirus. Have Adenocarcinoma – – – white males well-documented association with GERD Barrett's esophagus MALIGNANT STRICTURES MALIGNANT Malignant obstruction – Late presentation and carries a poor prognosis – Dysphagia is rapidly progressive – Diagnosis Endoscopy with mucosal biopsy Evaluation includes staging Evaluation – CT and Endoscopic US – Staging is based on the TNM classification Staging – T1 or T2 without nodal or metastatic disease, can be T1 treated with surgery alone treated – Patients with more advanced disease Patients Neoadjuvant chemotherapy/radiation before surgical resection resection Cricopharyngeal Dysfunction The cricopharyngeus remains contracted between swallows between Cricopharyngeal achalasia achalasia – Muscle fails to Muscle completely relax completely – smooth posterior smooth impression on the hypopharynx hypopharynx Zenker’s Diverticulum Zenker’s Esophageal diverticula are classified based on: Esophageal – Anatomic location – Mechanism of origin (pulsion or traction). Mechanism Zenker's diverticulum (ZD) Zenker's – Pulsion type diverticulum Herniation of esophageal mucosa and submucosa through Herniation an area of weakened esophageal musculature an – Annual incidence of 2 per 100,000 people per year – Males predominance (2 to 3 times) Zenker’s Diverticulum Zenker’s Killian's dehiscence or Killian's triangle triangle – Between the Between cricopharyngeal muscle and inferior constrictor muscle muscle Killian-Jamieson's area – between the oblique and between transverse fibers of the cricopharyngeal muscle cricopharyngeal Laimer's triangle – Between the Between cricopharyngeal muscle and the most superior esophageal wall circular muscles Diagnosis Diagnosis History – Progressive dysphagia Progressive 90% of patients presenting with ZD presenting – – – Regurgitation of food Unprovoked aspiration Noisy deglutition Barium Barium Esophagogram Esophagogram Treatment Treatment Surgery – Cricopharyngeal Cricopharyngeal myotomy External – cricopharyngeal cricopharyngeal myotomy – Diverticulum is excised Diverticulum and the defect closed Endoscopic Endoscopic References References Bechi P: Long-term ambulatory enterogastric reflux monitoring: validation of a new Bechi fiberoptic technique. Dig Dis Sci 1993; 38:1297-1306. Dig Devault KR, Castell DO: Updated guideline for the diagnosis and treatment of Devault gastroesophageal reflux disease. Am J Gastroenterol 1999; 94:1434-1442. Am Elluru RG, Willging JP. Endoscopy of the Pharynx and Esophagus. Cummings Elluru CW, ed. Otolaryngology Head & Neck Surgery. Philadelphia: Elsevier Mosby; 2005, 1825-1834. 1825-1834. Mittal RK: Transient lower esophageal sphincter relaxation. Mittal Gastroenterology 1995; 109:601-610 Gastroenterology Postma GN, Cohen JT, Belafsky PC, et al. Transnasal Esophagoscopy: Revisited Postma (over 700 Consecutive Cases). Laryngoscope 2005;115:321-323. 2005;115:321-323. Postma GN, Bach KK, et al. The Role of Transnasal Esophagoscopy in Head and Postma Neck Oncology. Laryngoscope 2002;112:2242-2243. Laryngoscope Tobin RW: Esophageal rings, webs, and diverticula. J Clin Tobin Gastroenterol 1998; 27:285. Gastroenterol Vaezi MF, Richter JE: Diagnosis and management of achalasia. Am J Vaezi Gastroenterol 1999; 12:3406-3413. Gastroenterol Vollweiller JF, Vaezi MF. The Esophagus: Anatomy, Physiology, and Diseases. Vollweiller Cummings CW, ed. Otolaryngology Head & Neck Surgery. Phaladelphia: Elsevier Mosby, 2005, 1835-1998. Mosby, ...
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