JR - BE - FA - Corrosive Esophagitis.pptx

corrosive esophagitis

1. Corrosive Esophagitis: Mechanisms and Wound Healing Journal Reading Presentan : dr. Faiz Mochammad Silmy Supervisor : dr. Raden Ayu Hardianti Saputri, Sp.THTBKL Department of Otorhinolaryngology, Head and Neck Surgery Faculty of Medicine Padjadjaran University Hasan Sadikin General Hospital Bandung 2025

2. ANATOMY Chaudhry SR, Bordoni B. Anatomy, Thorax, Esophagus . [Updated 2023 Jul 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Cervical:  From cricopharyngeus to suprasternal notch, behind trachea, attached to C6-C8 vertebrae. Thoracic:  From suprasternal notch to diaphragm, passes behind aortic arch (T4-T5) into posterior mediastinum. Abdominal:  From diaphragm (T10) to stomach (T11), passing through right crus of the diaphragm. Esophagus Segments

3. ANATOMY Chaudhry SR, Bordoni B. Anatomy, Thorax, Esophagus . [Updated 2023 Jul 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Length: 23–25 cm in adults. Lined with mucosa, has smooth muscle, and contains two sphincters. Upper Esophageal Sphincter (UES):  Controls food entry into the esophagus . Lower Esophageal Sphincter (LES):  Controls food entry into the stomach. Structure

4. Mahadevan V. Anatomy of the oesophagus . Surgery (Oxford). 2020 Sep 19. Esophageal Constriction lateral diameter (mm) AP diameter (mm) 1. Cricopharyngeal 23 17 2. Arcus Aorta 24 19 3. Left Bronchus 23 17 4. Diaphragma 23 23 At rest diameter esophageal lumen is 20 mm and can increase to 30 mm ANATOMY

5. VASCULARIZATION Chaudhry SR, Bordoni B. Anatomy, Thorax, Esophagus . [Updated 2023 Jul 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Cervical esophagus & UES  → Inferior thyroid artery. Thoracic esophagus  → Aortic esophageal arteries (from bronchial arteries). Abdominal esophagus & LES  → Left gastric artery & left phrenic artery. Venous drainage Submucosal plexus → Superior vena cava. Proximal & distal esophagus  → Azygos system. Mid esophagus  → Left gastric vein (portal vein branch).

6. LYMPHATIC DRAINAGE Chaudhry SR, Bordoni B. Anatomy, Thorax, Esophagus . [Updated 2023 Jul 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Proximal third  → Deep cervical lymph nodes → Thoracic duct. Middle third  → Superior & posterior mediastinal nodes. Distal third  → Gastric & celiac lymph nodes.

7. INNERVATION Chaudhry SR, Bordoni B. Anatomy, Thorax, Esophagus . [Updated 2023 Jul 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.

8. Circular muscle fibers form one component of the physiological sphincter 1/3 superior  striated muscle 1/3 medial  striated + smooth muscle 1/3 inferior  smooth muscle Chaudhry SR, Bordoni B. Anatomy, Thorax, Esophagus. StatPearls. 2021 Modul Utama Bronkoesofagologi: Modul V.12 Divertikulum Zenker. Kolegium Ilmu Kesehatan Telinga Hidung tenggorok Bedah Kepala dan Leher. 2020 ANATOMY

9. Mucosa  non-keratinized squamous epithelium Submucosa  dense connective tissue and coarse elastic fibers, containing blood vessels and submucosal flexuses Esophagus Muscle  longitudinal muscle layer in superficial, circular muscle layer in profundal Fibrosa layer Chaudhry SR, Bordoni B. Anatomy, Thorax, Esophagus . StatPearls . 2021 Modul Utama B ronkoesofagologi : Modul V.12 Divertikulum Zenker. Kolegium Ilmu Kesehatan Telinga Hidung tenggorok Bedah Kepala dan Leher. 2020 HISTOLOGY

10. Methods: Retrospective evaluation (2008–2020) Patients undergoing surgery for caustic ingestion complications Conducted by two independent gastro-pathologists Corrosive induced esophageal and gastric injury: Histopathological evaluation of surgically resected specimens over a decade in a tertiary care center Objective: to evaluate various histological changes in esophageal /gastric resected specimens from patients who underwent surgery for various indications after caustic ingestion. Caustic ingestion: common clinical problem in gastroenterology Children: 70–80% of cases (accidental) Resected specimens provide key histopathological insights Few studies available on histopathological changes in caustic-induced esophageal /gastric injury Shah J, Jena A, Shweta S, Vaiphei K, Gupta V, Kumar N, et al . Corrosive induced esophageal and gastric injury: Histopathological evaluation of surgically resected specimens over a decade in a tertiary care center . Indian J Pathol Microbiol 2024;67:379-84.

11. Shah J, Jena A, Shweta S, Vaiphei K, Gupta V, Kumar N, et al . Corrosive induced esophageal and gastric injury: Histopathological evaluation of surgically resected specimens over a decade in a tertiary care center . Indian J Pathol Microbiol 2024;67:379-84. Parameter N (%) Age (years) 28.66 9.31 Gender (Male) 24 (61.6%) Nature Acid Alkali Not known 24 (61.6%) 11 (28.2%) 4 (10.2%) Site of involvement Esophagus Stomach Both 9 (23.1%) 7 (17.9%) 23 (59.0%) Esophageal involvement Upper Middle Lower Middle + Lower Diffuse 5 (12.8%) 4 (10.2%) 6 (15.4%) 9 (23.1%) 7 (17.9%) Parameter N (%) Age (years) Gender (Male) 24 (61.6%) Nature Acid Alkali Not known 24 (61.6%) 11 (28.2%) 4 (10.2%) Site of involvement Esophagus Stomach Both 9 (23.1%) 7 (17.9%) 23 (59.0%) Esophageal involvement Upper Middle Lower Middle + Lower Diffuse 5 (12.8%) 4 (10.2%) 6 (15.4%) 9 (23.1%) 7 (17.9%) Parameter N (%) Time from ingestion of corrosive <7 days 7-30 days 1-3 months >3 months 3 (7.7%) 4 (10.2%) 2 (5.1%) 30 (77.0%) Indication of surgery Immediate perforation Severe gastro-intestinal bleed Long/refractory stricture latrogenic perforation Missing data 7 (17.9%) 1 (2.6%) 20 (51.3%) 7 (17.9%) 4 (10.3%) Table 1: Baseline characteristics of included 39 patients of corrosive ingestion

12. Shah J, Jena A, Shweta S, Vaiphei K, Gupta V, Kumar N, et al . Corrosive induced esophageal and gastric injury: Histopathological evaluation of surgically resected specimens over a decade in a tertiary care center . Indian J Pathol Microbiol 2024;67:379-84. Parameter N (%) Esophageal ulcer Deep mucosal Submucosal Transmural 28.66 9.31 Presence of granulation tissue 24 (61.6%) Esophageal inflammation (extent) Sub-epithelial Transmural 24 (61.6%) 11 (28.2%) 4 (10.2%) Esophageal inflammation (severity) Mild Moderate Severe 9 (23.1%) 7 (17.9%) 23 (59.0%) Parameter N (%) Esophageal ulcer Deep mucosal Submucosal Transmural Presence of granulation tissue 24 (61.6%) Esophageal inflammation (extent) Sub-epithelial Transmural 24 (61.6%) 11 (28.2%) 4 (10.2%) Esophageal inflammation (severity) Mild Moderate Severe 9 (23.1%) 7 (17.9%) 23 (59.0%) Parameter N (%) Esophageal fibrosis Submucosal Transmural Esophageal hypertrophied muscularis mucosa Esophageal reactive LN Esophageal vascular thrombosis Esophageal dysplasia Table 2: Histopathological details of esophageal specimens (n=32) of the study cohort

13. Shah J, Jena A, Shweta S, Vaiphei K, Gupta V, Kumar N, et al . Corrosive induced esophageal and gastric injury: Histopathological evaluation of surgically resected specimens over a decade in a tertiary care center . Indian J Pathol Microbiol 2024;67:379-84. Parameter <7 days (n=3) 8-90 days (n=6) >90 days (n=30) P Esophageal ulcer Presence of granulation tissue Inflammation (severity) (moderate/severe) Esophageal fibrosis Esophageal reactive LN Esophageal vascular thrombosis Esophageal hypertrophied muscularis mucosa Gastric ulcer Presence of granulation tissue Inflammation (moderate/severe) Gastric fibrosis Hypertrophied muscularis mucosa Vascular thrombosis 3 (7.6%) 1 (2.5%) 2 (5.1%) 1 (2.5%) 0 (0) 2 (5.1%) 2 (5.1%) 3 (7.7%) 1 (2.5%) 1 (2.5%) 1 (2.5%) 1 (2.5%) 2 (5.1%) 4 (10.2%) 4 (10.2%) 3 (7.7%) 4 (10.2%) 1 (2.5%) 0(0) 4 (10.2%) 4 (10.2%) 4 (10.2%) 3 (7.7%) 4 (10.2%) 2 (5.1%) 1 (2.5%) 22 (56.4%) 18 (46.1%) 15 (38.4%) 22 (56.4%) 2 (5.1%) 0 (0) 19 (48.7%) 11 (28.2%) 9 (23.1%) 10 (25.6%) 20 (51.2%) 13 (13.3%) 0 (0) 0.733 0.686 0.743 0.373 0.907 0.001 0.989 0.070 0.080 0.794 0.140 0.740 0.001 Table 4: Relation of histopathological findings with duration between caustic ingestion and surgery (n=39)*

14. Histopathology Shah J, Jena A, Shweta S, Vaiphei K, Gupta V, Kumar N, et al . Corrosive induced esophageal and gastric injury: Histopathological evaluation of surgically resected specimens over a decade in a tertiary care center . Indian J Pathol Microbiol 2024;67:379-84. Shah J et al (a) Chronic changes in the esophagus where the mucosa is intact however shows extensive replacement fibrosis of submucosa, muscularis mucosae, and propria; (b) the thin and atrophic gastric mucosa with extensive full‑thickness replacement fibrosis of gastric wall. (HE, 150) (a and b) Different pictures showing the absence of deep mucosa and submucosa along with hemorrhages and bland necrosis of muscularis propria (HE, ×150)

15. Discussion Shah J, Jena A, Shweta S, Vaiphei K, Gupta V, Kumar N, et al . Corrosive induced esophageal and gastric injury: Histopathological evaluation of surgically resected specimens over a decade in a tertiary care center . Indian J Pathol Microbiol 2024;67:379-84. Stage 1:   Necrosis with neutrophil invasion Stage 2:   Vascular thrombosis Stage 3:   Sloughing of superficial tissue Stage 4:   Healing Histopathological Changes After Corrosive Ingestion Risk of perforation, lasts 14–21 days) With collagen deposition, granulation tissue, and re-epithelialization Eskander et al Kochhar R et al Endoscopic biopsies: Basal cell hyperplasia Dilated intra-epithelial & vascular spaces Hyperkeratosis and parakeratosis Scar tissue with chronic irritation may progress to malignancy (reported after 3–4 decades)

16. Discussion Shah J, Jena A, Shweta S, Vaiphei K, Gupta V, Kumar N, et al . Corrosive induced esophageal and gastric injury: Histopathological evaluation of surgically resected specimens over a decade in a tertiary care center . Indian J Pathol Microbiol 2024;67:379-84. Advenier et al Surgery performed from  <1 week to >3 months  post-ingestion Common esophageal findings: Mucosal ulceration:  90.6% Transmural inflammation:  68.8% Transmural fibrosis:  62.5% No correlation  between timing of surgery & type/extent of ulceration, inflammation, fibrosis, or granulation tissue Within 1 day: massive wall damage, nonspecific changes At 3 days: erosive & necrotic lesions, no fibrosis, intense inflammation Long-term (27–81 days): fibrosis & mucosal thickening Current study

17. STRENGTH Shah J, Jena A, Shweta S, Vaiphei K, Gupta V, Kumar N, et al . Corrosive induced esophageal and gastric injury: Histopathological evaluation of surgically resected specimens over a decade in a tertiary care center . Indian J Pathol Microbiol 2024;67:379-84. LIMITATION First study on  histopathological evaluation of resected surgical specimens  in corrosive injuries Avoids limitations of  endoscopic biopsies  (which may show minimal/altered changes, especially post-dilatation trauma) More representative of  true caustic-induced histological changes Retrospective design Cases involved  mainly acidic agents  → limited generalizability Type/brand of caustic agents  not available → effect on histology not assessed

18. CONCLUSION Caustic ingestion leads to mucosal ulceration, transmural inflammation, and transmural fibrosis which might be the reason for refractory stricture in such patients. In the acute stage of caustic ingestion, vascular thrombosis is commonly seen; however, apart from that, all other factors were similar among patients who operated after different periods of caustic ingestion.

19. Esophageal Epithelial Barrier Fang Yang, Yiwei Hu, Zewen Shi, Mujie Liu, et al. The occurrence and   development mechanisms of   esophageal stricture: state of   the   art review. Journal of Translational Medicine.(2024).22:123 EEB effectively block the attack of foreign antigens and allergens, H + ions, etc. Keratin 14 (KRT 14) & filaggrin (FLG) are important proteins in the formation of the cornified envelope of the EEB structure. E-cadherin (E-cad) & Zonula Occludens (ZO-1) are important proteins for the esophageal epithelial cell junctions.

20. >26.000 patients ingest corrosive substances in United States each year Lusong MAAD, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World journal of gastrointestinal pharmacology and therapeutics. 2017 First peak Second peak 1 to 5 year old age group Adolescent and young adult (21 years and older) age group Corrosive Esophagitis

21. Corrosive Agents 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Sulfuric (batteries) Hydrochloric (WC cleaner) Nitric (metal cleaner) Phosphoric (antirust) Oxalic Na-hydroxide (soda) K hydroxide Ammonia Sodium carbonate Calcium oxide Sodium hypochlorite (bleach) Hydrogen peroxide K-permanganate Strong acids (pH <2) Strong alkali (pH >12) Kolegium ilmu kesehatan telinga hidung tenggorok bedah kepala dan leher . Modul utama bronkoesofagologi esophagitis korosif 2022 Flint PW, et al. Cummings otolaryngology head and neck surgery. Elsevier. 2021

22. Patophysiology Ingested corrosives Acids Alkalis (+ tissue proteins) coagulative necrosis production eschar formation limits further penetration and depth of injury deeper penetration into tissues thrombosis in blood vessels liquefactive necrosis limits blood flow to already damaged tissue Andon Chibisev .Post-corrosive Late Complications in Esophagus and Stomach – Role of the Esophageal Rest; 2010 Temiz A. Caustic Ingestion [Internet]. Pediatric and Neonatal Surgery. InTech ; 2017. Available from: http://dx.doi.org/10.5772/67526

23. Severe odynophagia Hoarseness and dyspnea Chest pain (if perforated) Asymptomatic (if mild) Odynophagia begin to disappear Swallowing become normal Progressive dysphagia from solid food to liquid Clinical Presentation Acute phase Sub-acute / latent phase Chronic phase Kolegium ilmu kesehatan telinga hidung tenggorok bedah kepala dan leher . Modul utama bronkoesofagologi esophagitis korosif 2022 Lusong MAAD, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World journal of gastrointestinal pharmacology and therapeutics. 2017

24. Biological Mechanisms of   E sophageal Stricture Inflammatory respons Excessive differentiation of fibroblasts Damage of   the   esophageal epithelial barrier (EEB) Fang Yang, Yiwei Hu, Zewen Shi, Mujie Liu, et al. The occurrence and development mechanisms of esophageal stricture: state of the art review. Journal of Translational Medicine.(2024).22:123

25. Inflammatory Respons Immune activation begins with macrophage phagocytosis → faster pathogen clearance. Macrophages regulate inflammation and fibrosis. Myofibroblasts emerge, enabling cell signaling and communication. Macrophages secrete TGF-β, promoting fibrosis if inflammation persists. In the esophagus: unresolved inflammation → ECM accumulation → fibrosis → stricture. Fang Yang, Yiwei Hu, Zewen Shi, Mujie Liu, et al. The occurrence and development mechanisms of esophageal stricture: state of the art review. Journal of Translational Medicine.(2024).22:123

26. Fang Yang, Yiwei Hu, Zewen Shi, Mujie Liu, et al. The occurrence and development mechanisms of esophageal stricture: state of the art review. Journal of Translational Medicine.(2024).22:123

27. Excessive differentiation of fibroblasts Myofibroblasts: vital for repair, but excessive activity → hyperfibrosis. Chronic inflammation → ECM over-deposition → esophageal stricture. Fibrotic diseases → major cause of organ dysfunction (~45% deaths in developed countries). CCL2/MCP-1 drives fibroblast over-differentiation → fibrosis. Therapeutic potential: Cenicriviroc inhibits CCL2/MCP-1 → anti-fibrotic effect. Fang Yang, Yiwei Hu, Zewen Shi, Mujie Liu, et al. The occurrence and development mechanisms of esophageal stricture: state of the art review. Journal of Translational Medicine.(2024).22:123

28. Fang Yang, Yiwei Hu, Zewen Shi, Mujie Liu, et al. The occurrence and development mechanisms of esophageal stricture: state of the art review. Journal of Translational Medicine.(2024).22:123

29. Fang Yang, Yiwei Hu, Zewen Shi, Mujie Liu, et al. The occurrence and development mechanisms of esophageal stricture: state of the art review. Journal of Translational Medicine.(2024).22:123

30. Damage of EEB Mucosal ulcers → damage to esophageal epithelial barrier (EEB). Cytokines such as IGF-1 and PDGF-C → activate myofibroblasts → secrete collagen → scar formation. Scar/ulcer presence is linked to esophageal stricture, but EEB damage-stricture connection is not well-established. EEB structure stability is vital as a barrier in the esophagus. Genes like TGM1, TGM3, CSTA, IVL, LOR → regulate cornified envelope proteins → maintain EEB integrity. Gene abnormalities → impaired protein synthesis → weakened cell–cell junctions, shown in skin diseases; esophageal role not yet reported. Fang Yang, Yiwei Hu, Zewen Shi, Mujie Liu, et al. The occurrence and development mechanisms of esophageal stricture: state of the art review. Journal of Translational Medicine.(2024).22:123

31. Substances Causing Caustic Injury Household bleaches (sodium hypochlorite) Drain openers Toilet bowl cleaners Dishwashing agents and detergents Toilet bowl cleaners Anti-rust compounds Swimming pool cleaners Vinegar Formic acid (rubber tanning industry) COMMON ALKALINE AGENTS COMMON ACIDIC AGENTS Denmark, Israel, UK, Peru, Spain, Australia, Saudi Arabia, Turkey India ( cheaper, more available) De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90. 

32. Pathophysiology De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90.  Colorless , tasteless, viscous, minimal odor → ingested in larger amounts. Cause liquefactive necrosis → deeper tissue penetration, risk of transmural injury. Damage esophagus (longer mucosal contact, neutralization in stomach). ALKALINE AGENTS Pungent odor , unpleasant taste → ingested in smaller amounts, rapidly swallowed. Cause coagulation necrosis → protective eschar limits full-thickness injury. Damage stomach (rapid esophageal transit, more stomach injury). ACIDIC AGENTS

33. Timeline of Mucosal Injury De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90.  Within minutes: necrosis, hemorrhagic congestion, small vessel thrombosis. 4–7 days: mucosal sloughing, bacterial invasion, granulation, collagen deposition. ~3 weeks : healing begins, but tensile strength lowest (risk of perforation). Day 5–15: endoscopy avoided due to high perforation risk. 3rd week onward: scar retraction, stricture formation, impaired LES → worsened acid reflux. Factors Influencing Severity Concentration of agent. Amount ingested. Duration of tissue contact. pH of substance.

34. Clinical Presentation Upper respiratory tract: hoarseness, stridor → suggest epiglottis/larynx involvement (life-threatening risk). Esophageal injury: dysphagia, odynophagia. Gastric involvement: hematemesis, epigastric pain. Symptoms depend on location of injury Short-Term Complications Perforation ( esophagus or stomach) → may occur within 2–3 weeks. Sudden worsening of symptoms or acute deterioration → suspect perforated viscus. Chronic Complications Stricture formation Presents with dysphagia, substernal pressure (≥3 weeks after ingestion). Gastric outlet obstruction Early satiety, post-prandial nausea/vomiting, severe weight loss (first 5–6 weeks). Malignant transformation Esophageal carcinoma De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90. 

35. Diagnosis and Staging De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90.  Do not directly correlate with severity/outcome. Independent predictors of death: Age, WBC >20,000 cells/mm³, Gastric deep ulcer or necrosis Laboratory Tests Chest X-ray : mediastinal or subdiaphragmatic gas → suggests perforation. UGI series (water-soluble contrast) : used if perforation suspected. Traditional Radiology

36. Diagnosis and Staging De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90.  Endoscopic ultrasound (EUS): evaluates esophageal wall. Findings: muscularis destruction → predictor of stricture, poor response to balloon dilatation. Ultrasound Slightly higher diagnostic yield than endoscopy. Shows necrosis depth, transmural damage, threatened/established perforations. CT Scan Limited advantage over CT. Pros: no ionizing radiation. Cons: poor differentiation of esophageal wall layers, slower throughput, movement artifacts in acutely ill patients. MRI

37. Esophagogastroduodenoscopy (EGD) Gold standard for diagnosis and management guidance. Best performed within  12–48 hours  post-ingestion (safe up to 96 h). Avoid  between days 5–15 (healing stage → tissue friability, perforation risk). Symptomatic or intentional ingestions  → emergent endoscopy recommended. Asymptomatic accidental ingestions  with low-potency substances → endoscopy may not be required. Indications Hemodynamic instability. Severe respiratory compromise. Suspected perforation. Contraindications De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90. 

38. Esophagogastroduodenoscopy (EGD) Grade 0, I, IIA → recover without sequelae. Grade IIB & III → high risk of stricture formation and complications. Every increase in injury grade → 9-fold rise in morbidity & mortality. Zargar classification Description Grade 0 Normal mucosa Grade I Edema and erythema of the mucosa Grade IIA Hemorrhage , erosions, blisters, superficial ulcers Grade IIB Circumferential lesions Grade IIIA Focal deep gray or brownish-black ulcers Grade IIIB Extensive deep gray or brownish-black ulcers Grade IV Perforation De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90. 

39. Endoscopic pictures of Zargar classification 0 to IIIB De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90. 

40. Management algorithm for caustic substance ingestion De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90. 

41. Management algorithm for caustic substance ingestion De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90. 

42. Management De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90.  Previously recommended, but  no longer advised . Risk: cause  thermal injury  & further tissue destruction. Neutralizing Agents Routine placement not recommended  before endoscopy. Risks: retching, vomiting → reflux exposure; foreign body → infection, delayed healing. Nasogastric Tube H2 blockers and IV PPIs often used. Sucralfate: Small RCTs suggest ↓ stricture formation in corrosive esophagitis. Gastric Acid Suppression & Mucosal Protection

43. Management De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90.  1992 study: antibiotics + steroids → may reduce strictures, but effect not separable. Consensus : if steroids are given, antibiotics should also be administered. Antibiotics Systemic Steroids Triamcinolone  (40–100 mg/session): Used to augment stricture dilatation. Mitomycin-C  (0.4 mg/mL topical application): Antifibroblastic effect. Benefits: ↓ number of dilatations, improved dysphagia relief compared to triamcinolone. Intralesional Therapy Dexamethasone > Prednisolone in stricture prevention (38.9% vs 66.7%). Systematic review : no additional benefit for grade II esophageal burns.

44. Endoscopy De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90.  Normal / very mild injury  → discharge. Grade I–IIA  → in-hospital observation; gradual diet progression (liquids in 24–48h). ≥ Grade IIB  → close monitoring; possible endoscopically-guided nasoenteric tube (bypass necrotic areas) for feeding + trial of oral intake. Grade III  → monitor response to therapy & feeding for ≥1 week. Management by Endoscopic Grade (Zargar) Role : guides diagnosis, staging, and treatment decisions.

45. Late Complications and Management Esophageal stricture  → most common sequela. ~70% in Grade IIB, >90% in Grade III injuries. Typically develops at  8 weeks , but can occur as early as 3 weeks. Endoscopic Dilatation Weekly  bougie dilatation + intralesional triamcinolone  → safe, effective, ↓ frequency of sessions, maintained lumen ≥14 mm. Intervals : 1–3 weeks in studies;  3–4 weeks recommended . Goal : Relieve dysphagia. Maintain luminal diameter ~15 mm. De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90. 

46. Late Complications and Management Esophageal Stents Types : SEMS (Self-Expanding Metal Stents)  → high necrosis, ulceration, hyperplasia, fistula, embedding (not preferred). Plastic stents  → less hyperplasia, but higher migration, weaker radial force, require removal. Biodegradable (BD) stents  → avoid retrieval, lower migration, but limited long-term data. Surgical Indication : Severe strictures, failed/unsafe endoscopic therapy. Options : Esophagectomy + gastric pull-up Advantages: faster, only 1 anastomosis. Disadvantages: reflux, recurrence of stricture, metaplasia risk. Colonic interposition  (preferred if stomach spared) More complex (3 anastomoses). More stable long-term outcome, less recurrent stricture. De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90. 

47. CONCLUSION The severity and outcomes of injury depend on the substance’s concentration, volume, contact time, and pH, with the esophagus and stomach being the most affected sites. Early endoscopic evaluation is the cornerstone of diagnosis and management, as it guides treatment, predicts complications, and helps prevent long-term sequelae such as strictures and malignancy

48. CRITICAL APPRAISAL JBI CRITICAL APPRAISAL CHECKLIST FOR TEXTUAL EVIDENCE: NARRATIVE

49. 1. Is the generator of the narrative a credible or appropriate source? Yes. The article was written by gastroenterologists from the Philippine General Hospital, published in the  World Journal of Gastrointestinal Pharmacology and Therapeutics , and underwent peer review 2. Is the relationship between the text and its context explained? Yes. The review clearly sets the context: caustic ingestion as a global public health issue, the typical settings (children accidentally, adults often intentional), the anatomical sites involved ( esophagus , stomach, airway), and the consequences. 3. Does the narrative present the events using a logical sequence so the reader or listener can understand how it unfolds? Yes. The article is organized systematically—starting with epidemiology, substances involved, pathophysiology, clinical presentation, complications, diagnosis, and management. The flow is logical, allowing readers to follow the “story” of how caustic ingestion occurs, causes injury, and is managed. De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90. 

50. De Lusong MAA, Timbol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):90-98. doi : 10.4292/wjgpt.v8.i2.90.  4. Do you, as reader or listener of the narrative, arrive at similar conclusions to those drawn by the narrator? Yes. Conclusions are evidence-based, with clear causal links (e.g., alkali injury depth, role of endoscopy, limited steroid benefit, long-term risks). The logic is clear, leading readers to similar conclusions as the authors. 5. Do the conclusions flow from the narrative account? Yes. The review moves from describing the problem (caustic ingestion), its mechanisms, clinical manifestations, and finally to management recommendations. The conclusions about management (e.g., endoscopy as cornerstone, limited benefit of corticosteroids, risk of malignancy after decades) are supported by the prior discussion. 6. Do you consider this account to be a narrative? Yes . he degree of narrativity is moderate: it does not rely on emotional persuasion but on logical, scientific persuasion. The “narrative” here is structured around medical events and evidence rather than personal storytelling.

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