1. ProfessorAbdulsalam Y TahaSchool of MedicineUniversity of SulaimaniIraqhttps://sulaimaniu.academia.edu/AbdulsalamTaha

2. LEARNING OBJECTIVESTo understand:The anatomy and physiology of theoesophagus and their relationship todisease.The clinical features, investigations, andtreatment of benign and malignant diseasewith particular reference to the commonadult disorders. 3. TOPICS Surgical anatomy Physiology Symptoms Investigations Congenital lesions:TOF and AtresiaBenign tumours.Cancer of oesophagusOthers. Foreign bodies. Oesophagealperforation. Gastro-oesophagealreflux diease. Hiatal hernia. Oesophageal motilitydisorders: achalasia anddiffuse spasm. Oesophgeal diverticula. 4. SURGICAL ANATOMY The oesophagus is a fibromuscular tube 25 cm long. Occupying the posterior mediastinum. Extending from the cricopharyngeal sphincter to thecardia of the stomach. 4 cm of this tube lies below the diaphragm. The musculature of the upper one third is mainlystriated, giving way to smooth muscle below. It is lined by squamous epithelium except the lower 3cms which are lined by specialized mucosa. 5. ANATOMY 6. Wall of Oesophagus 7. PHYSIOLOGY To transfer food from the mouth to the stomach. Sequential contraction of oropharyngeal musculature+ simultaneous closure of nasal and respiratorypassages+ opening of the cricopharyngeal sphincter. Involuntary peristaltic wave in the body of oesophagusthen sweeps food bolus downwards. Through a relaxed gastro-oesophageal sphincter zoneinto the stomach. The upper sphincter is normally closed at rest toprevent regurgitation. Failure of it to relax onswallowing may cause propulsion diverticulum. 8. PHYSIOLOGY At the lower end of the oesophagus there is aphysiological sphincter which together with otheranatomical mechanisms prevent reflux of gastric acidand bile. The tone of this sphincter is influenced bygastrointestinal hormones, anti-cholinergic drugs andsmoking. The displaced sphincter loses its tone and permitsreflux to occur. The normal GOJ is 3-4 cm long and has a pressure of30 cm H2O. 9. SYMPTOMS Difficulty in swallowing described as food or fluidsticking ( oesophageal dysphagia). Must rule outmalignancy. Pain on swallowing ( odynophagia). Suggestinflamation and ulceration. Regurgitation or reflux ( heartburn). Common ingastro-oesophageal reflux disease ( GORD). Chest pain; difficult to distinguish from cardiac pain. Loss of weight, anaemia, cachexia and change of voiceare other important symptoms. 10. INVESTIGATIONS Radiography.plain CXR, contrast oesophagography ( barium orgastrographin swallow) and CT scan of chest. Endoscopy: rigid and flexible oesophagoscopy. Endosonography: endoscopic ultrasonography. Oesophageal manametry: to diagnose oesophagealmotility disorders. 24-hour pH monitoring: the most accurate method forthe diagnosis of gastro-oesophageal reflux. 11. BARIUM SWALLOW 12. BARIUM SWALLOW 13. ENDOSONOGRAPHY 14. RIGID OESOPHAGOSCOPY 15. CONGENITAL ABNORMALITIESAtresia with or without tracheo-oesophagealfistula.Stenosis-rare.Short oesophagus with hiatus hernia.Dysphagia lusoria ( compression by anabnormal artery). 16. TYPES OF TOFIT SHOULD BE SUSPECTED IN ALL CASES OF HYDRAMNIOS,A CONDITION WHICH IS PRESENT IN 50% OF CASES OF ATRESIA.RECOGNITION WITHIN FORTY-EIGHT HOURS OF BIRTH,AND SUBSEQUENT SURGICAL CORRECTION, IS THEONLY HOPE OF SURVIVAL. 17. CONGENITAL TRACHEO-OESOPHAGEALFISTULA 18. FOREIGN BODIES IN OESOPHAGUS Adults as well as children are prone to ingest FBs. Varieties of FBs have been encountered. The mostcommon impacted material is food. Dysphagia, odynophagia and drooling of saliva. Plain X- ray +_ contrast study to confirm diagnosis. Removal should be done as early as possible. Complications: perforation of oesophagus, aspiration,fistula formation with aorta. Removal is by rigid or flexible oesophagoscopy.Surgery may be needed for sharp or impacted FBswhich fail to be extracted by endoscopy. 19. SWALLOWED FOREIGN BODIES 20. PERFORATION OF OESOPHAGUS Potentially lethal complication due to mediastinitisand septic shock. Numerous causes, but may be iatrogenic. Surgical emphysema is virtually pathognomonic. Treatment is urgent; it may be conservative or surgical,but requires specialized care. May be spontaneous ( due to barotrauma): Borehaavesyndrome; is the most serious form of perforationbecause of large volume of material that is releasedunder pressure into the mediastinum and pleura. It iscaused by vomiting against a closed glottis, sometimesfollowing labour or weight lifting. The tear is in theweakest point in the lower third. 21. PERFORATION OF OESOPHAGUS Instrumentation is by far the most common cause ofperforation. Diagnostic upper GI endoscopy has a rate of 1: 4000perforation rate. Therapeutic endoscopy has a rate of 1: 400 perforationrate. Diagnosis is based on clinical features, plain x-ray,contrast study and CT scan. Prompt and thorough investigations is the key tomanagement. 22. PERFORATION OF CERVICAL OESOPHAGUS 23. Management Options in Perforation of the OesophagusFactors that favour non-operativemanagementFactors that favour operativeRepair Small septic load. Minimal cardiovascularupset. Perforation confined tomediastinum. Perforation by flexibleendoscope. Perforation of cervicaloesophagus. Large septic load. Septic shock. Pleura breached. Boerhave,s synrome. Perforation of abdominaloesophagus. 24. INGESTION OF CORROSIVE AGENTS Corrosives such assodium hydroxide (caustic soda) orsulphuric acid may beingested accidentally orintentionally causingchemical burn ofoesophagus. Severe strictures maydevelop. 25. MANAGEMENT The management in the acute stage iscontroversial. Nothing by mouth, steroids to reduce fibrosis andparenteral nutrition. Followed by carefuloesophagoscopy. Dilatation may be helpful for short strictures. Long strictures are better managed surgically. Surgical options include: replacement ofoesophagus by stomach, colon or jujenum. 26. ACHALASIA CARDIA 27. MANAGEMENTHELLER,S OP DILATATION 28. TOPICSOesophageal Diverticulae.Gastro-oesophageal refluxdiease.Hiatal hernia.Benign tumours.Cancer of oesophagus 29. BENIGN TUMOURS Leiomyomas. Benign intraluminal tumours:Mucosal polypsLipomasFibrolipomasMyxofibromas 30. Leiomyomas Account for two thirds of all benign tumours of theoesophagus. Symptoms: dysphagia occurs when leiyomyomasexceed a diameter of 5 cm as they grow within themuscular wall, leaving the overlying mucosa intact. Diagnosis: Dysphagia, barium swallow andoesophagoscopy. Biopsy is contraindicated. 31. LeiyomyomaThe characteristic radiographic finding of an esophageal leiyomyomaon barium esophagogram, a smooth concave filling defect, createdby a well- defined lesion, with sharp, intact mucosal shadow withabrupt angle where the tumour meets the normal esophageal wall. 32. Surgical treatment Enucleation: in symptomatic patients, thetumour is enucleated from the oesophageal wallwithout violating the mucosa. A limited oesophageal resection is indicated if thetumour lies in the lower oesophagus and can notbe enucleated. 33. Benign intraluminal tumours Oesophagoscopy is performed to confirm thediagnosis and to rule out malignancy. Surgical treatment:Oesophagotomy, removal of the tumour, and repair ofthe oesophagomyotomy.Endoscopy should not be used to remove these tumoursbecause of the possibility of oesophageal perforation. 34. Malignant Tumours Incidence: in the US, the incidence of oesophagealcarcinoma ranges from 3.5 in 1 million for whitesto 13.5 in 100,000 for blacks. The highest incidence of oesophageal carcinomais noted in the Hunan Chinese population with asmany as 130 in 100,000 inviduals affected. 35. Aetiology The exact cause is unknown. Associated factors are:tobacco use, excessive alcohol ingestion,nitrosamines, poor dental hygiene, and hotbeverages. Premalignant conditions:AchalasiaBarrett,s oesophagus. 36. Pathology Squamous cell carcinoma is the most common form. Adenocarcinoma, the next commonest, is the typethat occurs in patients with Barrett,s oesophagus. Rare tumours include mucoepidermoid carcinomaand adenoid cystic carcinoma. Tumour spread: direct invasion, lymphatic andhaematogenic spread. 37. DIAGNOSIS History: dysphagia and weight loss. Contrast study. CT: depth of invasion, lymphatic spread and distantmetastases. Oesophagoscopy: for tissue diagnosis. Endoscopic ultrasonography: depth of invasion andstaging. Bronchoscopy: for proximal lesions to exclude invasionof the bronchial tree. 38. TREATMENT Surgery provides the only cure. Operative mortality is less than 5%. Types: Ivor-Lewis op.Transhiatal oesophagectomy.Left thoraco-abdominal approach.Radiotherapy and chemotherapy: either as adjuvantto surgery or as a primary treatment option.Paliative Treatment for inoperable cases: stenting. 39. GASTRO-OESOPHAGEALREFLUX This is a common condition affecting 80% ofpopulation. LES is a physiological sphincter normally hasan intra-abdominal position. Loss of LESpressure results in gastric reflux. Oesophageal motility causes refluxedsecretions to be cleared by oesophagealperistalsis. Gastric secretions, gastric acid, pepsin and bilereflux produce severe oesophagitis. 40. DIAGNOSIS Symptoms: substernal pain, heartburn andregurgitation. Manometry: decreased LES pressure. Oesophagoscopy: oesophagitis. 24-hr pH monitoring: increased acidity. Cineradiography: correlates the amount of reflux viamotion pictures. 41. TREATMENT MEDICAL:PPI, H2- receptor antagonists, cisapride andmetoclapramide increasing rate of gastricemptying, antacids, weight reduction, abstinencefrom smoking and alcohol and elevation of thehead of bed at night.SURGERY:Antireflux operations: Nissen fundoplication, BelseyMark IV op and Hill repair.