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CORROSIVE ESOPHAGEAL STRICTURE-1233.pptx
- 1. PATHOLOGY AND MANAGEMENT OF CORROSIVEOESOPHAGEAL STRICTURE DR LAWAL ABDULWAHAB SUPERVISING SR; DR EKPENYONG
- 2. Outline • Introduction • Historicalperspective • Epidemiology • Statement of surgical importance • Relevant anatomy • Aetiology • Pathophysiology • Classification • Clinical features • Investigation • Treatment • Trends • Prognosis • Prevention • Conclusion
- 3. Introduction • The consumptionof corrosive substance remains a significant public health concern. • Corrosive oesophageal stricture is a sequel of chemical trauma to the oesophagus • Ranging from varying degrees of difficulty with swallowing solids and liquids to total dysphagia • Effects include not only malnutrition but varying degrees of social and psychological/psychiatric disorders.
- 4. Historical perspective • Therate and severity increased in the early 19th century due to introduction of house hold cleaners with high alkali content • lye products became available for domestic use • Gained prominence in early 20th century • Notable endoscopist chevalier Jackson fought for enactment of the federal caustic act • No such acts in Nigeria
- 5. Epidemiology • Most commoncause of benign dysphagia • Over 80% occur in children < 5years • Alkali constitute majority of cases (main ingredient in house hold cleaners) • Accidental in children • Suicidal /parasuicidal in adults • In Nigeria commoner amongst low socioeconomic groups
- 6. Surgical relevance • Itis a disabling condition, leading to chronic pain and severe malnutrition • Corrosive esophageal stricture pose a risk factor for squamous cell carcinoma of the esophagus • 6.2% incidence rate and 4% prevalence rate • Hence prevention of this occurrence as well as early diagnosis and management of its complication is cornerstone to improving quality of life
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- 9. Aetiology • Acid: • PureHCL, H2SO • From batteries • Alkali: • Pure alkali • Hair relaxers • Cleansing agents • Drugs; • Tetracycline hydrochloride, aspirin/Nsaids, alendronate, ferrous sulfate, potassium chloride, ascorbic acid
- 10. Pathophysiology • Severity ofinjury depends on • Concentration /PH of the substance • Nature: solid or liquid, alkali/acid • Duration of exposure • Quantity ingested
- 11. Pathophysiology • Other factorswhich worsen severity include • Pylorospasm; gastric retention and regurgitation back into the oesophagus • Areas of anatomical narrowing, viz; • The cricopharygeus • Mid-oesophagus at the level of the aortic/left main stem bronchus • Distal oesophagus above the LES
- 12. Pathophysiology Initial injury • Intenseinflammatory reaction • Erythema & oedema of superficial layers • Vascular thrombosis, bacterial infiltration • Cell death and fatty saponification
- 13. Pathophysiology • Within thefirst hour: injured area is not well demarcated • 24-48 hours: cellular degeneration with lymphocyte infiltration • 48-72 hours : angiogenesis + fibroblast migration • 7 days; sloughing of necrotic tissue + granulation tissue formation begins • Wound edge clearly demarcated • Risk of perforation highest due to low tensile strength of deposited collagen
- 14. Pathophysiology • 2nd-3rd week •Wound filled with granulation tissue • Contractile phase of healing begins • Target phase for medications aimed at preventing oesophageal stricture • Continues for months
- 15. Pathophysiology • Classification ofmucosal injury (adapted from zargar et al. • Classification of mucosal injury (adapted from kikendall
- 16. Pathophysiology • The DROOLscore (adapted from uygun et al. • Score ≤ 4 indicates high risk of esophageal strictures, while score < 4 indicates low risk of esophageal strictures.
- 17. Classification of oesophagealburns by depth of injury GRADE DEPTH ENDOSCOSPY 1ST Degree Mucosal Mucosal hyperaemia and oedema 2nd Degree Transmucosal , with or without Involvement of muscularis No extension to peri-oesophageal tissues Hemorrhagic, exudative, exudative, Ulcerative pseudo membranes 3rd Degree Full thickness injury with extension into Per-oesophageal tissues May involve mediastinal or intraperitoneal organs Complete obliteration of of Oesophageal lumen by massive oedema, charring and eschar Full thickness necrosis with perforation
- 18. Classification • Short andlong segment strictures • Simple and complex strictures • Complete and incomplete strictures
- 19. Clinical features/ presentation •Presentation may be; • Acute; Corrosive oesophagitis • Chronic; Corrosive stricture
- 20. Corrosive oesophagitis • Presentationwithin hours or days • History of corrosive ingestion • May complain of; dysphagia, odynophagia, chest pain, dyspnoea, abdominal pain, hematemesis.
- 21. Corrosive oesophagitis • Examinationof the patient may reveal • General: fever, pallor, cyanosis, dehydration, drooling of saliva, swollen/ulcerated lips and oral mucosa • Tachycardia , ↓BP/shock • Chest: tachypnoea, stridor widespread rhonci/coarse crepitations; hammon’s crunch • Abdominal: tenderness/ features of peritonitis
- 22. Corrosive stricture • Historyof corrosive ingestion weeks to months • Dysphagia, drooling of saliva, regurgitation • Cough, dyspnoea • Weight loss • Signs: marked weight loss, drooling of saliva, pallor, wheezing, scarred lips • CHEST- features of oesophageal lungs
- 23. Investigations • Barium swallowand follow through- done for stricture (not before 3weeks!) • CXR-PA & lateral- may reveal pneumomediastinum, pneumoperitoneum, pleural effusion • Esophagoscopy- rigid or flexible (preferably the latter) • Within first 4- 6 hours of injury but could go up to 24hours for grading, stop on siting first lesion stricture, dilate if short segment(≤2cm) and incomplete also take biopsy • CT-scan- best for perforation and extent of mucosal oedema. • Baseline investigations; FBC, EUCr, LFT
- 24. Long segment midthoracic oesophagealstricture
- 25. Treatment • Depends onthe stage of presentation; corrosive oesophagitis or corrosive stricture.
- 26. Management of corrosive oesophagitis •Admit all patients ;suspected or confirmed • Avoid emetic and gastric lavage • Maintain NPO • Give IV antibiotics, analgesics, sedatives/ tranquilisers
- 27. Management of corrosiveoesophagitis • esophagoscopy within 24hours, pass ng-tube in the process for grades 1-2 (for feeding) • Feeding gastrostomy or jejunostomy • An esophagectomy in case of massive haemoptysis or oesophageal/gastric perforation • Patient stabilised, commence early dilatation(from the 3rd week)
- 28. Management of corrosive stricture Dependson degree of metabolic derangements • Correct dehydration, anaemia • Treat chest infection • May require cervical oesophagostomy • May require feeding gastrostomy/TPN
- 29. Management of corrosive stricture •Role of endoscopic dilatation • Timely evaluation and dilatation plays a central role in achieving better outcome • Avoided within day 5-21 • More number of sessions needed than non corrosive strictures, targeted at regular intervals initial a lumen size 15 mm with complete amelioration of dysphagia (adequate dilatation) • Afterwards, repeated PRN • “Rule of 3”
- 30. Management of corrosive stricture Predictorsof refractory corrosive strictures • Long strictures • Complex strictures • Delayed initiation of treatment • Thickened oesophageal wall
- 31. Management of corrosive stricture Roleof endoscopic dilatation Augmentation – • Nd YAG LASER • Intra lesional injection, e.g. steroids, triamcinolone, mitomycin C ?- controversial • Prosthesis placement • Endoscopic stricture incision
- 32. Management of corrosiveoesophagiti • The role of STENTING • Using removable self- expandable plastic stents • Advantages • Avoids repeated dilatation, • Removable • Disadvantage • Migration, • Expensive, • Mainly used in adults, • Erosion through oesophageal wall
- 33. Management of corrosive stricture Indicationsfor surgery • Complete stricture • Tracheo-oesophageal fistula • Patient intolerant to repeated dilatation • Inability to dilate • Perforation following dilatation • Carcinoma of the oesophagus • Resuscitation; feeding gastro-/jejunostomy, cervical oesophagostomy
- 34. Management of corrosive stricture •Surgical options Incomplete stricture • Short segment - dilate • Long segment- replace/bypass Complete stricture • Short segment- resection and anastomosis • Long segment- replace/bypass
- 35. Management of corrosive stricture CONDUITSADVANTAGES DISADVANTAGES Gastric pull op Single stage, reliable blood supply Acid reflux, bulky Reverse gastric tube Useful when right gastroepiploic supply is poor or disrupted Technically difficult Colon interposition Maintains bowel proportion 3 anastomosis, requires bowel preparation, development of redundancy Jejunal interposition Maintains peristalsis, less gastro-oesophageal reflux, diameter match with oesophagus Require free vascular anastomosis, redundancy develops later, variable vascular anastomosis OPTIONS FOR OESOPHAGEAL REPLACEMENT
- 36. Choice of conduits CONDUITSADVANTAGES DISADVANTAGES STOMACH Proximity to mouth, Richest blood supply, Can go to any distance Single anastomosis, No bowel prep Loss of storage function, Reflux/regurgitation implies head position all the time Mass effect in mediastinum JEJUNUM Rich blood supply, calibre similar to oesophagus, Extends only to distal 3rd of oesophagus, not adapted to solid bolus, prone to small bowel disease, 3 anastomosis RIGHT COLON Extends to any length 3 anastomosis, calibre>oesoph. Requires bowel prep, barium enema/colonoscopy and angiography before use .
- 37. Choice of conduits CONDUITSADVANTAGES DISADVANTAGES LEFT COLON More adaptable than right to solid content, extends to any length, same calibre as the oesophagus As in right colon FREE GRAFT (SMALL LARGE BOWEL) Can be positioned anywhere, Requires 5 anastomosis; 2 vascular, 3-bowel.
- 38. Approaches to theoesophagus APPROACH ADVANTAGES DISADVANTAGES TRANSHIATAL No thoracotomy-less pain, one anastomosis Blind , likely more bleeding, difficult with severe perioesophageal fibrosus MCKEOWN Oesophago- gastric/colonic anastomosis in the neck 3-incision-most stressful LEWIS-TANNER 2-incision 2-incision- more stressful LEFT THORACO- ABDOMINAL Single incision, no position change Long incision, diaphragmatic incision
- 39. Choice of routesfor conduits ROUTES COMMENTS POSTERIOR MEDIASTINUM Shortest route=>replacement after oesophagectomy ANTERIOR MEDIASTINUM Longer route, pleura can be opened=> hemopneumothorax SUBCUTANEOUSLY Cosmesis; descent of swallowed food seen on anterior chestwall Injury to conduit from minor trauma to the anterior chest TRANSPLEURAL Where other route are unavailable TRANSLUMINAL Mainly done for in-situ ca oesophagus; mucosa stripped off leaving a tube of muscularis and adventitia
- 40. Complications Early, Late, oriatrogenic • Malnutrition • Aspiration • Recurrent pneumonia • Chronic chest pain • Esophageal perforation • Fistula formation • Bleeding, hemorrhage • Recurrent stricture • Stricture formation • Esophageal carcinoma
- 41. Current trends • Laparoscopicassisted surgeries • Total minimal invasive bypass procedure
- 42. Prognosis • Patients withcorrosive esophageal stricture have high prevalence of underlying psychological morbidity, impaired quality of life, and higher disability. • Studies have shown that the grade of dysphagia strongly correlates with quality of life and associated disability, with higher dysphagia being associated with poorer prognosis • Nutritional status
- 43. Prevention • Prevention hasa paramount role in reducing the incidence of corrosive ingestion especially in children. • Primary prevention • Secondary prevention • Tertiary prevention
- 44. Conclusion • Corrosive oesophagealstricture is a severe long term complication of corrosive ingestion with significant adverse effect on quality of life • Efforts should channelled its prevention, as well as early intervention and appropriate management • Surgery remains the mainstay of therapy where endoscopic management fails or is contraindicated
- 45. References • Chirica M,Bonavina L, Kelly MD, Sarfati E, Cattan P. Caustic ingestion. Lancet 2017;389(10083):2041– 2052. DOI: 10.1016/S0140-6736(16)30313-0. • Ananthakrishnan N, Kalayarasan R, Kate V. Corrosive injury of esophagus and stomach. In: ed. PK, Mishra ed. Textbook of Surgical Gastroenterology,New Delhi, India: Jaypee; 2016. • Lakshmi CP, Vijayahari R, Kate V, Ananthakrishnan N. A hospital-based epidemiological study of corrosive alimentary injuries with particular reference to the Indian experience. Natl Med J India 2013;26(1):31–3
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