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  2. 2. CLINICAL FEATURES OF OESOPHAGEAL DISEASES • What is odynophagia? • Pain on swallowing • primary peristalsis? • Coordinated oesophageal wave that follows a conscious swallow • Secondary peristalsis? • Is the normal reflex response to a stubborn food bolus or refluxed material designed to clear the oesophagus by a contraction that is not preceded by a conscious swallow. Tertiary contractions? Are nonperistaltic waves that are infrequent (< 10%) during laboratory based manometry, although readily detected if manometry is undertaken while the patient eats a meal
  3. 3. INVESTIGATION • Plain radiographs will show? • foreign bodies. • Contrast radiography?(Barium swallow) • Narrowing, space-occupying lesions, anatomical distortion or abnormal motility. • CT-Scan? • The assessment of Neoplasms of the oesophagus and perforation
  4. 4. 3. - Diagnosis - Clinical presentation - Diagnosis - Treatment
  5. 5. • Endoscopy? 1. View the inside of the oesophagus and the oesophagogastric junction 2. Obtain a biopsy or cytology specimen 3. Removal of foreign bodies 4. Dilate strictures
  6. 6. • Endosonography? • Radial; circular image with the endoscope in the centre, and this type of scanner is widely used to create diagnostic transverse sectional images at right angles to the long axis of the oesophagus
  7. 7. • 24-hour pH recording? • The most accurate method for the diagnosis of gastro-oesophageal reflux An oesophageal pH < 4 at the level of the pH electrode is conventionally considered the cut-off value and, in most oesophageal laboratories, the total time when pH is < 4 in a 24-hour period does not exceed 4% in a healthy adult.
  8. 8. • perforation is more serious • 1-Iatrogenic . • 2-due to barotrauma’ (spontaneous perforation • Boerhaave syndrome) • Boerhaave syndrome is the most serious type of perforation because of the large volume of material that is released under pressure Perforation during diagnostic upper endoscopy. • Who are at increased risk? 1. Those with anterior cervical osteophytes 2. Presence of a pharyngeal pouch 3. Mechanical causes of obstruction 4. Biopsy of a malignant tumor. PERFORATION OF ESOPHAGUS Perforation during therapeutic upper endoscopy is by? 1. Guidewires, graduated dilators or balloons 2. During the placement of self-expanding stents 3. The risk is higher in patients with malignancy.
  9. 9. 1-Defective lower esophageal sphincter (LES) function 2- transient LES relaxations TLESRs) 3- hypotonic LES ** ( e.g. sleroderma) 4- disruption of LES ** ( e.g. resection, balloon rupture)  Hiatal hernia ** ( mal alignment of LES and crural diaphragm) Poor esophageal clearance **  Decreased salivary protection decreased volume ( e.g. sicca syndrome)  Poor gastric emptying with Increased intra-abdominal pressure ( e.g. straining, obesity, pregnancy)  Duodenogastric reflux GERD(GASTROESOPHAGEALREFLEX DISORDER)
  10. 10. Retrosternal burning pain, (heartburn)  epigastric pain regurgitation Pulmonary Asthma Aspiration pneumonia Chronic bronchitis Pulmonary fibrosis Other Chest pain Dental erosion ENT Hoarseness,Laryngitis,Pharyngitis ChronicSinusitis,Subglottic stenosis Laryngeal cancer CLINICAL PRESENTATION
  11. 11.  Barium swallow  Endoscopy  Ambulatory pH monitoring  Esophageal manometry INVESTIGATIONS
  12. 12. GOAL OF TREATMENT  Eliminate symptoms  Heal esophagitis  Manage or prevent complications  Maintain remission
  13. 13. LIFESTYLE MODIFICATIONS Elevate head of bed 4-6 inches Avoid eating within 2-3 hours of bedtime Lose weight if overweight Stop smoking Modify diet Eat more frequent but smaller meals Avoid fatty/fried food, peppermint, chocolate, alcohol, carbonated beverages, coffee and tea OTC medications .
  14. 14. H2-Receptor Antagonists (H2RAs) Cimetidine (Tagamet®) Ranitidine (Zantac®) Famotidine (Pepcid®) Nizatidine (Axid®) Proton Pump Inhibitors (PPIs) Omeprazole (Prilosec®) Lansoprazole (Prevacid®) Rabeprazole (Aciphex®) Pantoprazole (Protonix®) Esomeprazole (Nexium ®) ACID SUPPRESSION THERAPY FOR GERD
  15. 15. BARRETT’S ESOPHAGUS; DEFINITION • defined short segment (3 cm or low) orlong segment (more than 3 cm) barrett’s esophagous. • The present definition requires both endoscopic recognition of colummar lining and biopsy-established intesttinal metapolism in the esophagous. • the tube that carries food from the mouth to the stomach -- changes to tissue that resembles the lining of the intestine. About 10% of people with chronic symptoms of GERD develop Barrett's esophagus.
  16. 16. Etiology 1. GERD → esophageal acid exposure and bile exposure → Barrett’s esophagus → esophageal Adenocarcinoma 2. Chronic GERD is the mian risk factors developing Barrett’s esophagus 3. Obesity 4. Cigarette smoking and a high-fat diet 5. Genetic component
  17. 17. BARRETT’S ESOPHAGUS Complications of Barrett’s esophagus : (1)ulcer (2)stricture (3)dysplasia (4)cancer Endoscopy land & biopsy technique; • Four-quadrant biopsies should be obtained at 2 cm intervals through the columnar-lined esophagus from distal to proximal. • Detection Barrett’s length.
  18. 18. Another pathologist ← Repeated biopsy ← Intestinal metaplasia without dysplasia Low grade dysplasia Repeated Biopsy High grade dysplasia Barrett’s esophagus Medical treatment Two biopsy (3 years) One biopsy per year High grade dysplasia +Cancer ? Positive Negative Careful survillance ← Endoscopic ablation therapy ← Esophagectomy ← Esophagectomy ←
  19. 19. TREATMENT • Barrett’s esophagus without high grade dysplasia or cancer (A): First medical treatment: → (proton pump inhibtor better than H2 blocker) → 95% with errosive gastritis and barrett’s ulcer healed. → decrease DGE (bile) reflux (decrease secretion). → medical therapy can’t regress Barrett’s EP but improved symptoms.
  20. 20. SURGICAL TREATMENT • Anti reflux surgery can’t regress Barrett’s EP and complete prevention of Adeno carcinoma. Indication for surgery: 1. Transmural penetrated ulcer 2. Severe stricture 3. Perforated ulcer 4. High grade dysplasia & cancer. 5. Massive & uncontroled bleeding from ulcer 6. Fistula fo rmation 24
  21. 21. CARCINOMA OF THE OESOPHAGUS • Risk factor • - SCC: • smoking and alcohol consumption, • dietary (N-nitroso compounds, hot food, betel nut, poor nutrition), HPV infection, Endemic areas (China) • - adeno: • smoking, obesity, GERD, long term use of theophylline, and beta agonists ) ? ( 25
  22. 22. WHAT ARE THE CLINICAL FEATURES OF CA ESOPHAGOUS? 1. Early disease; non-specific dyspeptic symptoms 2. Dysphagia, regurgitation, vomiting, odynophagia 3. Weight loss 4. Chronic GI blood loss is common & may result in iron deficiency anemia. • Acute bleeding is rare. (erosion to aorta or pulmonary arteries.)
  23. 23. WHAT ARE THE CLINICAL FEATURES OF CA ESOPHAGOUS? 1. Advanced malignancy include recurrent laryngeal nerve palsy, Horner’s syndrome, chronic spinal pain and diaphragmatic paralysis. 2. Cutaneous tumour metastases or enlargedsupraclavicular lymph nodes 3. Respiratory symptoms can be caused by aspiration and direct invasion of the tracheobronchial tree.
  24. 24. DIFFERENTIAL DIAGNOSIS OF DYSPHAGIA 1. Esophageal carcinoma 2. Achalasia 3. Peptic strictures due to reflux 4. Benign esophageal tumors (rare)
  25. 25. 6. Diagnosis
  26. 26. ACHALASIA
  28. 28. EsophagealCancer
  29. 29. Squamous cell carcinoma of Esophagus - “Esophagus: contrasted barium shows squamous cell carcinoma in the middle portion of
  30. 30. Figure 1. Initial CT scan revealed a large mass in the distal third of the esophagus. Post-chemotherapy CT scan showed a significant reduction of the tumor size.
  31. 31. Carcinoma esophagus- a barium swallow showing irregular narrowing with "shouldered edges" suggestive of a malignant stricture!!
  32. 32. 36