DISEASES OF THE OESOPHAGUS BY Dr. ARWA M FUZI Lecture 1

Gastro- esophageal reflux disease GERD

 Affects 30% of the general population.  GERD develops when the esophageal mucosa is exposed to gastro- duodenal contents for prolonged time.  This occur when one of the protective mechanism fail to protect the mucosa.

The natural protective mechanisms of the esophagus  Esophageal peristaltic wave  Neutralization by the alkaline saliva.  The lower esophageal sphincter tone.  The pressure gradient between abdominal and thoracic cavities.  The normal gastric emptying.

Etiological factors  Abnormalities of the lower esophageal sphincter. -Reduced tone or - Frequent inappropriate sphincter relaxation.  Hiatus hernia - Affects 30% of above 50 y population -Loss of he normal pressure gradient between the thoracic and abdominal cavities. -Loss of the oblique angle between the cardia & esophagus. ( HH is very common in asymptomatic patients, some symptomatic pt have no hernia, almost all pt who develop complication of GERD have HH)

 Delayed esophageal clearance - Defective esophageal peristalsis  Gastric contents. - Gastric acid and increased exposure time.  Defective gastric emptying (cause is unknown).  Increased intra-abdominal pressure (pregnancy and obesity)

 Dietary and environmental factors -(Fat, chocolate, alcohol& coffee) relax the lower esophageal sphincter  Patient factors -Visceral sensitivity and pt vigilance

Clinical features  Heart burn &regurgitation (bending, straining, lying).  Water brush  Chocking  Odynophagia, dysphagia  Extra esophageal features -Atypical chest pain -Acid laryngitis -Recurrent chest infection -Chronic cough, asthma

complications  Esophagitis (mild redness to sever, bleeding ulceration, stricture)  Barrett ’ s esophagus (CLO) - Replacement of normal squamous lining of lower esophagus by columnar mucosa, containing areas of intestinal metaplagia - It is a premalignant condition, 10% will develop adenocarcinom -Found in 10% 0f pt with symptoms of GERD -More common in men, > 50y, smocking, severity and duration of GERD -More associated with duedenogastro-esophageal reflux (bile, pancreatic enzyme & pepsin).

-Diagnosed by multiple biopsies to detect intestinal metaplasia & dysplasia -Management of Barrrett ’ s esophagus *Acid suppression & anti reflux surgery will not stop progression or induce regression, treatment only indicated for reflux symptoms or stricture). *Endoscopic therapies ( argon plasma coagulation, radiofrequency ablation & photodynamic therapy) may induce regression. *Regular endoscopic surveillance to detect early dysplasia & malignancy ( every 2-3 years, if dysplasia every 6-12 months) *Esophagectomy for high grade dysplasia

 Anemia - Iron deficiency anemia (chronic blood loss from long standing esophagits or from erosions of the neck of the sac in large HH ) -Other causes of bleeding should be excluded.  Benign esophageal stricture -Fibrous strictures in long standing esophagitis, commenly elderly -Present with dysphagia for solids. -Diagnosis by endoscopy & biopsy to exclude malignancy -Treatment by endoscopic balloon dilatation. Followed by long term therapy by PPI at full dose to prevent recurrence

 Gastric volvulus -Twisting of massive intrathoracic HH -Complete esophageal or gastric obstruction results - Present with sever chest pain, vomiting & dysphagia -Diagnosis by chest x-ray ( air bubble in the chest ), barium swallow - Treated by nasogastric decompression followed by surgery

investigations Indications for investigations -If present in middle or late age -Warning symptoms ( dysphagia, wt loss, anemia) -Presence of atypical symptoms -Suspicion of complications Include:  Endoscopy (to exclude other causes & to identify complications).  24 hr PH monitoring (for unclear cases & befor surgery)

Management  Lifestyle advice (wt loss, diet, elevation of head of bed, stop smocking, avoid late meals).  Drugs - PPIs (can heal esophagitis), -anta-acid -H2-blockers  laparoscopic anti-reflux surgery

Treatment of gastro-oesophageal reflux disease: a 'step-down' approach

Other causes of oesophagitis  Infection - Oesophageal candidiasis ( depletated pt, broad spectrum antibiotics, cytotoxic drugs &AIDS pt)  Corrosives - extensive erosive oesophagitis (Suicide attempt by strong household bleach or battery acid) copmlicated byoesophageal perforation with mediastinitis and by stricture formation.in acute state treatment is conservative, analgesia and nutritional support. barium swallow should be performed to demonstrate the extent of stricture formation. Endoscopic dilatation is usually necessary.

 Drugs (Potassium supplements, NSAIDs &Bisphosphonates ) -Cause oesophageal ulcers.  Eosinophilic oesophagitis -More common in children &young adults - Atopic individuals -Eosinophilic infiltration of the oesophageal mucosa. -Patients present with dysphagia, heartburn, chest pain and vomiting. - Treatment by corticosteroids (fluticasone or betamethasone) inhelar sprayed into the mouth and swallowed, monteleukast, a leukotriene inhibitor used for refractory cases