Corrosive Esophagitis: Causes, Pathophysiology, Diagnosis, and Management | A Comprehensive Review

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Introduction

Corrosive esophagitis—also known as caustic esophagitis—is a life-threatening condition caused by ingestion of acidic or alkaline substances that produce varying degrees of esophageal injury. These injuries may range from superficial mucosal ulceration to full-thickness necrosis and perforation. Despite advancements in critical care and endoscopy, corrosive esophagitis remains a major medical and surgical challenge worldwide.

This article provides a comprehensive expert-level review of corrosive/caustic esophagitis, including etiology, pathophysiology, epidemiology, clinical presentation, imaging features, treatment strategies, prognosis, and prevention. The discussion integrates clinical evidence, case-based radiological insights, and modern management guidelines.

Causes and Etiology

The most common causes of corrosive esophagitis are ingestion of alkaline agents (lye, sodium hydroxide, ammonia, dishwasher detergents) and strong acids (sulfuric acid, hydrochloric acid, nitric acid).

  • Alkali ingestion leads to liquefactive necrosis, characterized by deep penetration into the esophageal wall, producing extensive injury.

  • Acid ingestion typically results in coagulative necrosis, which forms an eschar barrier that may limit deeper penetration but still causes severe mucosal damage.

Accidental ingestion is more common in children, whereas intentional ingestion (suicidal attempts) is a major concern among adults.

Pathophysiology

The pathophysiology of corrosive esophagitis is well described in three stages of injury:

  1. Acute Necrosis Stage (0–4 days): Direct chemical burn leads to necrosis, vascular thrombosis, and mucosal sloughing.

  2. Ulceration and Granulation Stage (3–12 days): Inflammatory cell infiltration, tissue edema, and risk of perforation are maximal.

  3. Cicatrization and Stricture Formation (3 weeks to months): Progressive fibrosis leads to esophageal strictures, which can cause chronic dysphagia.

Systemic complications such as mediastinitis, peritonitis (from gastric perforation), aspiration pneumonia, and sepsis may occur.

Epidemiology

  • Global prevalence: Most common in developing countries due to poor labeling and storage of cleaning chemicals.

  • Children: Accidental ingestion accounts for nearly 80% of cases in pediatric populations.

  • Adults: Suicide attempts or psychiatric illness contribute significantly to cases in developed countries.

  • Gender: Higher incidence among women in adult suicidal ingestion, while pediatric cases show equal distribution.

Clinical Presentation

Patients present acutely after ingestion with the following symptoms:

  • Severe odynophagia (painful swallowing)

  • Dysphagia (difficulty swallowing)

  • Chest pain and retrosternal burning

  • Hematemesis or vomiting (sometimes with blood)

  • Abdominal pain if gastric injury occurs

  • Hoarseness and stridor (laryngeal involvement)

Late sequelae include esophageal strictures, malnutrition, and risk of esophageal carcinoma decades later.

Imaging Features

Imaging plays a crucial role in diagnosis, complication detection, and treatment planning.

1. Plain Radiography (Chest/Abdomen)

  • Detects pneumomediastinum (esophageal perforation) or free intraperitoneal air (gastric perforation).

  • May show esophageal dilatation or abnormal contour.

2. Contrast Esophagography

  • In the acute phase, shows diffuse spasm, abnormal motility, or barium pooling.

  • In chronic stage: Demonstrates smooth, tapered strictures in the cervical or upper thoracic esophagus.

3. Endoscopy

  • Gold standard for early evaluation within 24–48 hours.

  • Enables grading of mucosal injury, guides therapy, and helps predict stricture risk.

Case-Based Radiological Illustration

[Figure 1] Images "A" and "B" show distal esophageal mucosal ulcerations after lye ingestion. Image "C" demonstrates an irregular esophageal stricture with significant narrowing.


Treatment and Management

1. Initial Emergency Care

  • Airway protection (intubation if respiratory compromise)

  • Avoid gastric lavage or emesis induction (may worsen injury)

  • IV fluids, analgesics, proton pump inhibitors, and broad-spectrum antibiotics in severe cases

2. Endoscopic Intervention

  • Performed within 24–48 hours to assess mucosal injury.

  • Avoided after 72 hours due to high risk of perforation.

3. Nutritional Support

  • Nasogastric feeding or parenteral nutrition in severe dysphagia.

  • Long-term: Gastrostomy/jejunostomy if strictures develop.

4. Stricture Management

  • Endoscopic dilation (bougie or balloon dilators)

  • Intralesional steroid injections may reduce recurrence.

  • Surgical esophageal replacement (colon interposition or gastric pull-up) for refractory strictures.

5. Cancer Surveillance

  • Patients with chronic strictures are at increased risk of squamous cell carcinoma.

  • Lifelong endoscopic monitoring is recommended.

Prognosis

Prognosis depends on:

  • Type and concentration of agent

  • Volume ingested

  • Promptness of medical intervention

  • Mild cases: Recovery with supportive therapy.

  • Severe cases: High risk of strictures, perforation, fistula formation, and long-term carcinoma risk.

  • Mortality: Ranges from 5–20% in severe corrosive ingestion.

Prevention

  • Child-proof storage of household cleaning agents

  • Proper labeling and packaging of industrial chemicals

  • Public health education on the hazards of caustic ingestion

  • Psychiatric support for individuals with suicidal tendencies

Quiz

1. Which mechanism best explains alkali-induced esophageal injury?

A) Coagulative necrosis
B) Liquefactive necrosis
C) Caseous necrosis
D) Fibrinoid necrosis

2. What is the most common long-term complication of corrosive esophagitis?

A) Mediastinitis
B) Stricture formation
C) Tracheoesophageal fistula
D) Esophageal perforation

3. Which imaging finding is most suggestive of chronic corrosive esophagitis?

A) Diffuse esophageal spasm
B) Smooth tapered narrowing on contrast study
C) Free intraperitoneal air
D) Patchy mucosal enhancement on CT

Answer & Explanation

1. Answer: B) Liquefactive necrosis. Explanation: Alkali penetrates deeply into tissue, producing liquefactive necrosis with saponification of fats and protein dissolution.

2. Answer: B) Stricture formation. Explanation: Chronic fibrosis and scar contracture lead to esophageal strictures, typically developing within weeks to months.

3. Answer: B) Smooth tapered narrowing. Explanation: Chronic strictures appear as smooth, tapered stenosis on barium esophagography, distinguishing them from acute spasm or perforation signs.

Conclusion

Corrosive esophagitis remains a significant medical emergency with acute and chronic implications. Understanding the etiology, pathophysiology, clinical features, imaging, and treatment is essential for effective management. Prevention through public awareness and safe handling of chemicals is the best strategy.

References

[1] J. Zargar et al., "Management of caustic ingestion in adults," Lancet, vol. 360, no. 9349, pp. 1731–1736, 2002.
[2] S. R. Contini and A. Scarpignato, "Caustic injury of the upper gastrointestinal tract: A comprehensive review," World J Gastroenterol, vol. 19, no. 25, pp. 3918–3930, 2013.
[3] L. Kikendall, "Caustic ingestion injuries," Gastroenterol Clin North Am, vol. 20, no. 4, pp. 847–857, 1991.
[4] M. Mamede and J. M. de Mello Filho, "Treatment of caustic ingestion: An analysis of 239 cases," Dis Esophagus, vol. 15, pp. 210–213, 2002.
[5] G. R. Katzka, "Caustic injury to the esophagus," Curr Treat Options Gastroenterol, vol. 13, no. 1, pp. 59–70, 2015.
[6] C. Poley et al., "Caustic esophageal injury: Prognostic factors and treatment," Endoscopy, vol. 36, pp. 111–118, 2004.
[7] W. S. Kochhar et al., "Long-term management of corrosive strictures," Indian J Gastroenterol, vol. 29, no. 1, pp. 1–5, 2010.

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