Fibers of the cricopharyngeus muscle represent the upper esophageal sphincter (UES) in thoracic cavity it lies in posterior mediastinum, posterior to the trachea. LES: tonically closed at rest, pressure 20 mmHg, cholinergic mediated, relaxes with swallowing is the major cause of reflux.
Fibers of the cricopharyngeus muscle represent the upper esophageal sphincter (UES) in thoracic cavity it lies in posterior mediastinum, posterior to the trachea. LES: tonically closed at rest, pressure 20 mmHg, cholinergic mediated, relaxes with swallowing is the major cause of reflux.
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Fibers of the cricopharyngeus muscle represent the upper esophageal sphincter (UES) in thoracic cavity it lies in posterior mediastinum, posterior to the trachea. LES: tonically closed at rest, pressure 20 mmHg, cholinergic mediated, relaxes with swallowing is the major cause of reflux.
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Medical Unit III Services Hospital Anatomy of Esophagus Hollow tube formed of striated muscle (upper part) and smooth muscle (lower part). Length about 20-30 cm in adults. Fibers of the cricopharyngeus muscle represent the upper esophageal sphincter (UES). In thoracic cavity it lies in posterior mediastinum, posterior to the trachea. Leaves thorax through diaphragmatic hiatus Lower esophageal sphincter (LES) about 3-5 cm long, ?physiological sphincter. Microscopic Anatomy of esophagus Mucosa: Lined with stratified squamous epithelium, rich in glycogen. Lamina propria muscularis mucosa : thin layer of smooth muscle Submucosa The outer muscular layers: striated in the upper part and smooth in lower 2/3 No serosal covering. Physiology UES: tonically closed, opens 0.2-0.3 sec after a swallow. Peristaltic contractions, duration less than 7 sec and amplitude less than 150 mmHg, velocity less than 8 cm/sec LES: tonically closed at rest, pressure 20 mmHg, cholinergic mediated, relaxes with swallowing. Transient LES relaxation, independent of swallowing is the major cause of reflux. Motor disorders of the esophagus Achalasia Localized esophageal spasm Diffuse esophageal spasm Nutcracker esophagus Non-specific motor abnormalities Achalasia Failure of relaxation of the LES with swallowing and aperistalsis in lower esophagus. Due to decreased or absent intramural esophageal ganglion cells. Symptoms of Achalasia Dysphagia to fluids and solids, intermittent, long -standing. Regurgitation of undigested food Chest pain Aspiration Weight loss Diagnosis of achalasia Esophageal manometry: Absent peristalsis High LES pressure Failure of relaxation of LES. Radiographic studies Endoscopy to exclude organic disease. Normal Achalasia TREATMENT OF ACHALASIA Management Goals Relieve symptoms Improve esophageal emptying Prevent development of megaesophagus TREATMENT OF ACHALASIA Drug therapy Smooth muscle relaxants Botulinum toxin injection 1 to 2 years relief Symptomatic relief Semisoft bland diet Eating slowly Drinking with meals Sleeping with Head end elevated Endoscopic pneumatic dilation Outpatient procedure LES disrupted using balloons of progressively larger diameters Repeat dilations are often required Surgical myotomy DEFINITIONS Gasrtoesophageal reflux: Reflux of gastric contents to the esophagus Gastroesophageal reflux disease (GERD): Any significant symptomatic clinical condition or histopathological changes resulting from reflux. Reflux esophagitis: GERD patients with histopathologically demonstrable changes in the esophageal mucosa. Epidemiology of GERD Heartburn is a very common condition: 3% of population experience heartburn daily 7% frequently 15% weekly 25% monthly Most common in pregnant women: 80% Common in obese and smokers Mechanisms of GERD Transient LES relaxation Hypotensive LES Decreased esophageal acid clearance Hiatus hernia Impaired salivation. CLINICAL PICTURE OF GERD ESOPHAGEAL SYMPTOMS EXTRAESOPHAGEAL SYMPTOMS ESOPHAGEAL SYMPTOMS OF GERD HEARTBURN REGURGITATION Bad Breath Dysphagia Chest pain Water brash Nausea and vomiting Belching Hiccup EXTRAESOPHAGEAL SYMPTOMS OF GERD Chronic cough Asthma recurrent pneumonitis nocturnal choking hoarseness of voice posterior laryngitis with ulceration and granuloma formation. sore throat dental disease Earache Globus sensation Diagnosis of GERD Clinical picture. UGI endoscopy. 24 hour pH monitoring Radioisotope scanning Barium swallow. Complications of GERD Stricture formation Chronic blood loss Barrett’s epithelium Narrow band imaging & chromoendoscopy with methylene blue are used as diagnostic tool. Adenocarcinoma Savary Gillard dilator used for dilatation of esophageal strictures Barrett’s epithelium Barrett’s epithelium Narrow Band Imaging used for diagnosis of barrett’s epthelium Barrett’s epithelium Chromoendoscopy using methylene blue used for diagnosis of Barrett’s Natural history of GERD May be acute condition in a small percentage Mostly chronic condition with recurrent symptoms Majority can be controlled on drugs Majority may require a sort of acid suppressive therapy at 5 years No clear relation exists between symptoms of reflux, amount of reflux or degree of esophagitis. Management of GERD Life- style modification: avoid cigarette smoking dietary manipulation: decrease fatty, spicy and acidic foods decrease weight elevation of the head of the bed avoid tight abdominal binders avoid constipation avoid large meals avoid drugs which decrease LES pressure avoid sleeping after meals for at least 3 hours. Pharmacologic therapy of GERD Antacids: Mg trisilicate Aluminium hydroxide Ca carbonate sodium bicarbonate. H2-blockers: Cimetidine ranitidine famotidine nizatidine Pharmacologic therapy of GERD Proton pump inhibitors: Omeprazole lansoprazole pantoprazole rabeprazole Esomeprazole Tenatoprazole Prokinetic drugs: metoclopramide domperidone. Endoscopic therapy for GERD Sterrata procedure Entyrex Gate keeper anti-reflux repair Gastric plication Antireflux surgery Indications: complicated reflux non compliance for medication refractory GERD patient’s preference severe disease in young person Most popular operation now is laparoscopic fundoplication Treatment of Barrett’s epithelium BE usually occurs in longstanding severe reflux disease BE does not regress after fundoplication or PPI therapy Screening for dysplasia? If high grade dysplasia found: esophagectomy Ablation of BE: Photodynamic therapy Argon plasma coagulation Endoscopic mucosal resection