Caustic strictures of the esophagus

Caustic strictures of the esophagus

1. Caustic Strictures of the Esophagus By: Dr. Mahwish Khan

2. Corrosive Ingestion is a disease of industrial age. A major health hazard in children. In rural areas, and in developing countries, caustic soda is used in home industry for soap making, fruit drying and container cleaning on farms. Introduction

3. Most Ingestions occur in children younger than 3-years ---- entirely preventable. Boys are frequently involved. In children more than 5-years is suspect. Ingestion in adolescents (where girls predominate) is usually intentional Epidemiology

4. Mortality is rare, morbidity is devastating, and can be associated with life long consequences. 20% ingestions of caustic substances result in some degree of esophageal injury.

5. Physical form of substance ingested and its pH, play a substantial role in the site and type of post ingestion esophageal injury. pH > 12 or < 1.5 being associated with severe corrosive injuries. Cause

6. Crystalline drain cleaners e:g. sodium hydroxide adhere to oropharynx or become lodged in the upper esophagus, where injury is more severe. Mechanism of Alkali Burns

7. With alkali ingestion Tissue penetration + liquefactive necrosis. Destruction of Epithelium and sub mucosa which may extend to the muscle layer. Ischemia and thrombosis are dominant early processes. Friable eschar develops. Tissue destruction continues until alkali is neutralized.

8. With Acid Ingestion Coagulation Necrosis of mucosa Hard eschar formation Limitation of acid penetration through mucosa occurs. Mechanism of Acid Injestion

9. Cricopharyngeal area Mid esophagus, where it is crossed by aortic arch and left bronchus. Above the GE Junction Sites

10. Immediate spasm and disorganized motility occur Resulting in delayed emptying and even gastic regurgitation. Hemorrhage, thrombosis and marked inflammation with edema seen in first 24-hours Event occurring after corrosive ingestion

11. After 48-hours thrombosis of submucosal vessels occurs, leading to local necrosis and gangrene. Bacterial contamination leading to development of small intramural abscesses occur. After several days , necrotic tissue is sloughed, edema decreases and neovascularization begins.

12. Scar formation begins in 3 rd week. During 3 rd to 6 th week adhesions forms, narrowing or obliterating the esophageal lumen. In transmural injury, necrosis extends to surrounding mediastinum, leading to mediastinitis or tracheo -esophageal or even aorta-esophageal fistulas.

13. Mitomycin C has been reported to be efficient at a dose of 1mg/ml, applied locally with a soaked swab for 4-minutes immediately after dilatation. Recent Advances

14. Few symptoms and signs – One quarter Pain oropharyngeal burns Esophageal injuries unlikely if only the tongue or soft palate involved. Acid Ingestion is associated with rapid transit through the esophagus. Leading to pylorospasm . Clinical Presentation

15. Inflammatory edema of oropharynx. Agitation and tachycardia Drooling and inability to swallow indicate severe posterior pharyngeal or upper esophageal injury. Acute obstruction of upper airway resulting from pharyngeal and laryngeal edema.

16. Maintain Adequate Airway and oxygenation. CVS stability. Few patients require immediate intervention for airway maintenance. History regarding noxious agent, its composition and concentration and circumstances of ingestion. Management and Diagnosis

17. Inducing vomiting Incurring ingestion of any liquid, Passing NG tube. All are contraindicated, Why? Don’ts

18. Fiberoptic endoscopy is both accurate and safe, especially done within 24-48 Hrs , after ingestion. TC labeled sucralfate radio-isotope scanning of esophagus is a screening device Lack of sucralfate adherence indicating the absence of significant injury.

19. In the presence of pharyngeal burns with stridor, early esophagoscopy is contraindicated because of risk of aggravating airway obstruction. IDL is useful to access upper airway. Fever systemic sepsis and upper abdominal signs are indicative of perforation.

20. Water soluble contrast esophagogram may be useful to detect perforation.

21. For patients with First degree burns (grade 1 injury) – No Specific treatment is necessary. Liquid Oral is started and extended to solids. If solids are tolerated, child can be discharged. Follow up at 2-3 weeks. Contrast Examination is done if symptoms of Dysphagia are noted. Treatment – Grade 1 Injury

22. Patient with moderate or severe injuries require further treatment, aimed at prevention of stricture formation, Up to 50% developed strictures. Most patients with grade 2A Injuries recover completely, close follow up, endoscopy and dilatation are required. Moderate Injuries Management

23. Grade 3B Injuries are rare in peads These require immediate and aggressive surgery, if extensive necrosis and perforation are present, especially if stomach is involved. Severe Injuries Management

24. In clinical trials using a variety of dosing regimens, no statistical difference in prevention of stricture formation was e vident. Steroids are not useful for stricture formation More recently, the use of high-dose steroids (dexamethasone1mg/kg/day) has been advocated. Role of Steroids

25. For patients with severe injuries, NG tube may be passed for early feeding purposes. Oral feeding commences as soon as patient can swallow saliva. If dysphagia occurs, esophagogram can identify extent of involvement. Use of anti-fungal agents, antacids and H2 blockers or proton pump inhibitors is widespread, but no proved efficacy.

26. Complications of Injury and Treatment Stricture formation If structure demonstrated on contrast radiography, done 10-14 days, after injury, a program of dilatation is commensed. Dilators used are 1. Mercury filled bougies. 2. Flexible graded bougie dilatation 3.guide wire directed metal olives 4. Various balloon dilators Dilatation should be attempted with great care

27. Initial dilatation is done under G.A with flexible guide wire introduced . Dilatation should be done once a week . Started with catheters that are one or two french sizes smaller than estimated dm of stricture.

28. If dilatation fails and a dense stricture develops it requires Rx Localized strictures may be resected with end to end anastomosis Local injection of steroids(1% triamcenolone acetate) and mitomycin into short strictures is also effective Esophageal stenting by means of indwelling NG tube is also advocated

29. Stents used are silicone and PTFE . Should remain in place for 6 wks until healing occurs . Stents also used in management of esophageal fistulas resulting from caustic injury or dilatation therapy

30. There is still a great need For adult education For legislation To ensure correct labeling and safe packaging and to restrict the strength and availability of caustic agents. Take home Message