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| 1. Anatomy of the esophagogastric junction a) Phrenoesophageal membrane i) Fascial attachments of the esophagus to the diaphragm ii) Attached to esophagus several centimeters above G-E jxn iii) Maintains intraabdominal esophagus |
| 2. Hiatal herniae a) Type I (sliding) i) Phrenoesophageal ligament is stretched ii) G-E jxn can migrate to an intrathoracic position iii) G-E jxn remains cephalad to stomach iv) Reducible, unless esophagus is foreshortened from stricture b) Type II (paraesophageal hiatal hernia) i) Rare ii) Phrenoesophageal ligament remains firm, binding esophagus to preaortic fascia and median arcuate ligament iii) G-E jxn at or near normal location iv) Fundus and body of stomach roll into chest alongside esophagus c) Type III (sliding and rolling hernia) i) E-G jxn and most of greater curve and body of stomach herniate d) Etiology i) Most are acquired ii) Obesity and pregnancy increase intraabdominal pressure, stretching phrenoesophageal ligament |
| 3. Pathophysiology of G-E reflux a) LES - resting pressure, length, site b) Esophageal clearance - gravity and esophageal peristalsis c) Mucosal resistance d) Salivary neutralization e) Gastric secretion i) Sensitivity to gastric acid, pepsin, alkaline bilious material ii) Additive effect iii) Gastric emptying (40% of pts w/reflux esophagitis f) Complications i) Anemia (chronic blood loss) ii) Stricture iii) Barretts esophagus g) Pts w/G-E jxn incompetence should be treated the same as those w/ concomitant hiatal hernia |
| 4. Symptoms a) Most patients are free of symptoms b) Very small risk of incarceration, strangulation, or obstruction of bowel (seldom involved) c) Retrosternal pain, heartburn, postural regurgitation, gaseous eructation d) Symptoms worse after a meal or when supine e) Pain may radiate to jaw, neck, ears or arms f) Respiratory involvement in 20% i) Acid alone may exacerbate asthma g) Shatzki ring i) Membrane or diaphragm on swallow ii) Most are asymptomatic, but may produce intermittent or persistent dysphagia (solid > liquid) iii) Always associated with hiatal hernia iv) Squamous mucosa on top and gastric mucosa on bottom v) Smooth muscle, fibrous tissue and scar between vi) Tx a) Dilatation w/balloon or bougie b) If symptomatic from hiatal hernia-repair hernia and dilate h) Barretts esophagus i) Invariably associated w/sliding hiatal hernia and severe GE reflux 5. Diagnosis a) Radiographic - Ba swallow w/maneuvers to assess reflux b) EGD for all respiratory or GER symptoms c) Formal testing of esophageal function i) Not necessary for typical symptoms of GER ii) 24hr pH monitoring and manometry prior to surgical intervention |
| 5. Medical treatment a) Lifestyle modification i) Elevation of head of bed a) Head 6-10 inches above the feet b) Reduces number of reflux episodes and increases rate of clearance ii) Weight reduction - can improve symptoms iii) Smoking a) Can decrease LES pressure and frequency of GER episodes b) Cessation reduces frequency of episodes iv) EtOH - Lowers LES pressure and impairs peristalsis v) Diet modification a) Coffee, chocolate, peppermint and fatty foods - ¯ LES pressure b) Citrus and tomato juice - direct mucosal irritation c) Cola and milk products stimulate acid secretion d) Timing of meals - avoid recumbency vi) Medications a) Theophylline, dopamine, nitrates, opiates, diazepam, calcium channel blockers - all lower LES pressure b) Pharmacologic therapy i) Cytoprotective agents - sucralfate a) Controversial data on efficacy b) Primary use is adjunctive (add to acid suppression) ii) Antacids - increase LES pressure and alkalinize gastric acid iii) Acid suppression - H2 blockers a) Decrease volume and concentration of gastric acid b) Less effective for GER than for PUD c) 50-60% healing in grade II-III esophagitis (cimetidine) d) Healing is slow-treat for 3-6 months iv) Acid suppression - proton pump inhibitors - omeprazole a) Suppresses basal and stimulated gastric acid secretion b) Superior to placebo, ranitidine and cimetidine for GER c) Recommendation is cessation after 2 months v) Prokinetic agents a) Metachlopramide-dopamine antagonist - disappointing b) Cisapride- enhances acetylcholine release from myenteric plexus (1) Better than placebo for GER symptoms (2) w/ cimetidine is better than cimetidine alone c) Strategy of medical therapy i) First phase = lifestyle changes - behavior, food and drugs ii) Second phase = Pharmacologic management a) H2-blocker, then add cisapride or sucralfate b) Proton pump inhibitor for failure of combo tx c) Continue tx for 3-6 months d) Up to 90% will relapse by one year iii) Surgical treatment for failure of medical tx or complications (stricture, bleeding, severe ulceration) |
| 6. Surgical therapy a) Failure of medical tx or complications (stricture, bleeding, severe ulceration) b) Significant symptoms and esophagitis in a young pt. c) Operative approach i) Restore 4-6cm of intraabdominal esophagus ii) Thoracic approach a) Shortening of the esophagus - to immobilize esophagus b) Prior esophageal procedure c) Esophageal dysmotility requiring myotomy d) Suggested mechanisms for improvements i) LES manipulation ii) Accentuation of angle of His iii) Increased opening of the cardia e) Procedures i) Complete fundoplication - Nissen/Nissen-Rosetti a) 87% free of symptoms long-term b) 3cm loose Nissenà4% free from post-op symptoms ii) Partial fundoplication a) Belsey Mark IV - 240° wrap b) Lind - 300° c) Toupet - 180° iii) Angelchick prosthesis a) 20% persistent dysphagia b) Migration |
| Barretts esophagus 1. Anatomy and physiology a) Definition=esophagus is lined w/columnar mucosa more than 3cm proximal to the distal end of the muscular esophageal tube b) 3 types of mucosa - gastric fundic, junctional, specialized columnar (80%) c) Acid (and pepsin and gastrin) is produced, but amount is insufficient to explain peptic ulceration of Barretts |
| 2. Pathogenesis a) Nearly every patient has pathologic reflux b) Metaplasia of pleuropotential cells in submucosa c) Migration of gastric mucosa not felt to be mechanism |
| 3. Epidemiology a) 1% in pts w/o symptoms who undergo endoscopy b) 10-20% in pts w/symptoms of reflux c) 8-13% of children endoscoped for GER d) Age 50-60 e) Men=3xwomen f) Relative lack in African-Americans |
| 4. Diagnosis a) GER symptoms b) Symptoms may improve with progression of Barretts c) >80% - hiatal hernia d) 75% - stricture e) Nearly 50% - ulcer f) Endoscopy i) Irregular squamocolumnar junction ii) Strictures typically involve squamocolumnar junction iii) Biopsy at multiple levels g) LES pressure is lower in pts w/Barretts than normal people and lower than pts w/reflux but w/o Barretts |
| 5. Benign (non-neoplastic) complications i) Stricture, bleeding, mucosal ulceration ii) Severe bleeding - 25% (rare in GER) iii) Penetrating ulcer in 10% a) May be successfully treated w/acid suppression b) Resection for mediastinal perforation |
| 6. Dysplasia and adenocarcinoma i) Persistent acid reflux responsible for Barretts is involved in dysplasia and malignant change ii) Other premalignant markers a) Increased G2 tetraploidy b) DNA aneuploidy c) ras oncogenes (H- ras, K- ras, N- ras) - not a factor iii) Risk of malignant degeneration related to a) Duration and severity of GER b) Tobacco c) Overall extent of columnar spread iv) Cancers a) Arise almost exclusively in specialized columnar epithelium b) Most have transmural extension with + nodes at time of dx v) 1/140 pt years = 40x usual risk in this country = 10-20% of all esophageal ca |
| 7. Medical management a) Lifestyle changes - behavior, food and drugs b) Medications c) Resolution of symptoms does not correlate with regression of Barretts |
| 8. Surveillance a) Surveillance allows detection at an early stage and improves long-term survival b) Endoscopy at least every year |
| 9. Surgical treatment of benign disease a) Indications = failure of medical tx or complications (same as for GERD) b) Unknown whether regression of Barretts or reversion of dysplasia can be expected c) Fundoplication and resection if necessary i) Remove all Barretts mucosa ii) Cervical esophagogastrostomy (intrathoracic esophagogastrostomy carries a high d) Surgical treatment of dysplasia and adenocarcinoma i) High grade dysplasia (separate from carcinoma in situ) ii) Intensive med tx w/rebiopsy q 3months or resection iii) When resecting, remove all Barretts epithelium |
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