Post graduate course Esophageal diseases

1. Post graduate courseEsophageal diseases Prof Dr Yasser M Fouad Prof DrHanaa K Fathelbab DrReem Y MousaDrHamdySayed DrRofida K Moftah

2. DrRofida

3. Anatomy ofOesophagus

4. It is fibro-muscular tube 12 cm in child & 25 cm in adults extends from: the lower border of the cricoid cartilage (C6) to: the cardiac orifice of the stomach T11

5. PARTS OF OESOPHAGUS The esophagus has been subdivided into 3 portions, as follows: • -The cervical portion extends from the cricopharyngeus to the suprasternal notch • -The thoracic portion extends from the suprasternal notch to the diaphragm • -The abdominal portion extends from the diaphragm to the cardiac portion of the stomach.

6. Applied anatomy • -venous drainage : • * cervical part: inferior thyroid vein • * thoracic part :azygos & hemiazygos veins • *Abdominal part :drain into left gastric vein • Varices

7. Applied anatomy • Lymphatic Drainage: • -cervical part: cervical LNs • -Thoracic part: Mediastinal LNs • -Abdominal part: Coeliac LNS • CARCINOMA

8. Arterial supply • The cervical portion : • the inferior thyroid artery • The thoracic portion : • bronchial and esophageal branches of the thoracic aorta • The abdominal portion : • ascending branches of the left phrenic and left gastric arteries

9. Oesphagealconstrications • -from incisor teeth • -15 cm : UOS • -25 cm : Aortic arch • -27 cm : Lt main bronchus • -40 cm : opening in diaphragm • F.B impaction

10. Esophageal Sphincters • -UPPER -LOWER • -Which Anatomical ?? • Upper Esophageal Sphincters

11. Lower Esophageal Sphincter • It is physiological by many factors: • -intra abdominal pressure • -pincock action of diaphragm • -Angle of Hiss • -plug mucosal rosette of stomach

12. DrHamdy

13. HISTOLOGY OF THE ESOPHAGUS

14. Mucosa : Epithelium: non-keratinized stratified squamous epithelium; basal zone has basophilic proliferative cells with minimal cytoplasm, usually 3-4 cells thick, cells then flatten and mature as they approach lumen / surface. Lamina propria: fibrovascular connective tissue between epithelium and muscularis mucosa; folds into slender papillae that projects into epithelium, usually less than 2/3 of epithelial thickness; may contain gastric cardia-like mucus particularly in distal esophagus. Muscularis mucosa: smooth muscle bundles oriented longitudinally; begins at cricoid cartilage and becomes thickened distally. (Z-line is the squamocolumnar junction which is histologically irregular. The lower esophageal sphincter is located in this area.)

15. Submucosa: • Loose connective tissue with vessels, lymphatics, occasional white blood cells, lymphoid follicles (rare), Meissner’s plexus (sparse ganglia) and nerves, submucosal glands lined by mucinous cells that produce acid mucin and bicarbonate. Muscularispropria: • Inner circular and outer longitudinal layers; proximally includes skeletal muscle from cricopharyngeus and inferior pharyngeal constrictor muscles. It contains Auerbach (myenteric) plexus. • Note: longitudinal muscle originates as two bands from cricoid cartilage that incompletely digitate and leaves a bare V-shaped region (area of Laimer) that exposes the underlying circular muscle and creates area of weakness where Zenker’s diverticulum may occur. Adventitia: • loose connective tissue (not consistent serosa), so tumors and infections spread readily.

19. DrReem

20. Physiology of esophegus • The only function of the esophegus is to transport food bolus from the pharynx to the stomach where the process of digestion begins • Efficient transport by the esophagus requires a coordinated, sequential motility pattern that propels food from above and clears acid and bile reflux from below , this movement is known as peristalsis.

21. Peristalsis is a sequential, coordinated contraction wave that travels the entire length of the esophagus, propelling intraluminal contents distally to the stomach. The LES relaxes during swallows and stays opened until the peristaltic wave travels through the LES, then contracts and redevelops resting basal tone.

22. Primary peristalsis is the peristaltic wave triggered by the swallowing center and travels at a speed of 2 cm/s : responsible for pushing the food bolus • The secondary peristaltic wave is induced by esophageal distension from the retained bolus, refluxed material, or swallowed air. The primary role is to clear the esophagus of retained food or any gastroesophagealrefluxate. • Tertiary contractions are simultaneous, isolated, dysfunctional contractions. These contractions are nonperistaltic, have no known physiologic role, and are observed with increased frequency in elderly people. Radiographic description of this phenomenon has been called presbyesophagus.

24. Neuromuscular coordination • Striated muscle regions • The motor innervation to the striated muscle regions of the esophagus is somatic arising from the nucleus ambigus of the brain stem : vagus nerve to give excitatory fibers only to striated muscle fibers through release of acetyl choline

25. Smooth muscle portion has a more complicated innervation: • - extrinsic ( located outside the wall of esophegus) • 1-parasympatheticpreganglionic fibers arise from dorsal motor nucleus : vagusnerve:relay in myenteric plexus through release of acetyl choline to activate nicotinic receptors of myenteric plexus ( exicitatory fibers mediate contraction) • 2-sympathetic postganglionic fibers arise from cervical ,thoracic and celiac ganglia :vagus and peri vascular nerves: myenteric and submucosal plexus : inhibition of nitric oxide release through activation of muscarinic receptors( inhibitory fibers mediating relaxation)

26. -intrinsic ( located inside the wall of esophegus) • 1)myenteric plexus located between the circular and longitudinal layers of muscles • 2)sub mucosal plexus (in sub mucosa) • Each plexus form a network that terminates at the muscle fibers controlling its action • Another type of bipolar cells (interstitial cells of Kajal) is present between the nerve fibers and muscles seems to play a role in neurotransmission

28. Dr Yasser

29. Oesophagus: classification by aetiology • Congenital: atresia, stenosis, fistulas, webs • Infection: fungal infection, viral infection, Chagas’ disease • Physical/Trauma: lacerations • Chemical/Toxic: gastro-oesophageal reflux disease (GORD) • Circulatory disturbances: oeophagealvarices • Immunological disturbance: eosinophilicoesophagitis • Degenerative disorders • Iatrogenic: pill oesophagitis • Idiopathic: achalasia • Various: radiation, psychosomatic • Pre-neoplastic/ Neoplastic: Barrett’s oesophagus -> adenocarcinoma squamous cell carcinoma

30. DR Rofida

31. CASE 1 • A 2-year-old boy presented to a local hospital after ingesting an unknown amount of hair and grease remover. • The patient's past medical and surgical history were unremarkable. • The patient underwent intubation at the outside emergency department because of respiratory distress and was transferred to our facility. • He had obvious burns to the lips and mouth, though not severe. • Doctor took decision of Endoscopy

32. -The Timing of endoscopy ?? - Which type of endoscopy ??

33. The Timing of endoscopy ?? • -are recommending earlier endoscopy and suggesting a wait of only 12 hours and a total wait of no more than 24 hours after ingestion for early assessment and treatment. • -Endoscopy past 48 hours is discouraged because of progressive wall weakening and increased risk of perforation • -Most agree that strong alkali ingestion mandates endoscopy, while asymptomatic or questionable ingestions may be observed, according to some sources

34. The Timing of endoscopy ?? • FIRST 48 hours from ingestion corrosive pass 48 hours!!!  After 14 up to 21 days from ingestion corrosive

35. Which type of endoscopy ?? • -flexible esophagoscopy, • is the most effective method for visualizing the extent of esophageal injury • provides important information about the stomach and duodenum • - Rigid esophagoscopy: • may be used but should not be extended beyond the site of caustic burn because of an increased risk of perforation. • is recommended for nasogastric tube placement and airway management.

36. The patient received flexible endoscopy within the 24 hours following injury. • He was found to have erythemaand small ulcerations in both the esophagus and stomach. His injuries were deemed grade 2a.

37. Endoscopic grading system • Grade 0: Normal • Grade 1: Mucosal edema and hyperemia 2 ULCER • Grade 2A: Superficial ulcers, bleeding, exudates => Excellent prognosis • Grade 2B:Deep focal or circumferential ulcers • 3 NECROSIS • Grade 3A: Focal necrosis => Develop strictures: 70-100% • Grade 3B: Extensive necrosis => Early mortality rate: 65%

38. Endoscopic grading system

39. The patient was given multiple broad spectrum antibiotics without steroids • Analgesia to control pain • . He had repeated endoscopy on day 14

40. DR Yasser

41. Corrosive ingestions

42. Common alkaline-containing sources • Ammonia-containing products • Oven-cleaning products • Swimming pool – cleaning products • Automatic dishwasher detergent • Hair relaxers • Clinitest tablets • Cement • Common acid-containing sources : • Toilet bowl – cleaning products • Automotive battery liquid • Rust-removal products • Metal-cleaning products • Cement-cleaning products • Drain-cleaning products

43. Symptoms • Dyspnea , Dysphagia, Oral pain and odynophagia • Chest pain , Abdominal pain, Nausea and vomiting • life-threatening hypocalcemia following ingestion of hydrogen fluoride (in some rust removers). • Material Safety Data Sheets (MSDS), online databases, and consultations with the local poison center are all ways for a clinician to rapidly familiarize themselves with unfamiliar caustics agents.

44. Physical Examination • Stridor • Hoarseness • Dysphonia or aphonia • Respiratory distress, tachypnea, hyperpnea • Cough Tachycardia • Oropharyngeal burns • Subcutaneous air • Acute peritonitis - Abdominal guarding, rebound tenderness, and diminished bowel sounds • Hematemesis

45. Indications of severe injury include the following: • Altered mental status • Peritoneal signs • Evidence of viscous perforation • Stridor • Hypotension • Shock

46. Laboratory studies may include the following: • pH testing of product and saliva : A pH less than 2 or greater than 12.5 indicates greater potential for severe tissue damage • Complete blood count (CBC) and electrolyte, blood urea nitrogen (BUN), creatinine, and ABG levels may all be helpful as baseline values and as indications of systemic toxicity • Liver function tests and a disseminated intravascular coagulation (DIC) • Urinalysis and urine output may help guide fluid replacement • Serum calcium level and cardiac monitoring and serial ECGs may be needed

47. Upright chest radiograph in all cases of caustic ingestion. Findings may include pneumomediastinum or other findings suggestive of mediastinitis, pleural effusions, pneumoperitoneum, aspiration pneumonitis, or a button battery (metallic foreign body). If contrast studies are obtained, water-soluble contrast agents are recommended because they are less irritating to the tissues in cases of perforation. Computed tomography (CT) scans will often be able to delineate small amounts of extraluminal air, not seen on plain radiographs.

48. Endoscopy Because of the risk of increased injury, esophagoscopy should not be performed in patients with evidence of esophageal or gastrointestinal perforation, significant airway edema, or necrosis and in those who are hemodynamically unstable. Obtaining meaningful information from endoscopy after treatment with activated charcoal is very difficult. Routine use of activated charcoal is not recommended in caustic ingestions.

49. Obtain MSDS sheets when possible for workplace exposures. The product container or labels may be available. Avoid exposure to health care workers. Do not induce emesis or attempt to neutralize the substance by using a weak acid or base. Small amounts of a diluent may be beneficial if administered as soon as possible after a solid or granular alkaline ingestion, to remove any particles that are adhering to the oral or esophageal mucosa.

50. Water or milk may be administered in small amounts. It is very unlikely to be of any benefit after more than 30 minutes. This practice is controversial: Some of the literature available on this topic discourages the use of diluents because of the concern of inducing emesis resulting in re-exposure of tissue to caustic agent. Diluents should not be used with any acid ingestion or liquid alkaline ingestion. The risk of vomiting with re-exposure of the oral or esophageal mucosa to the offending substance can result in worsening injury or perforation.