Severe Esophageal Necrosis Following Caustic Ingestion

CASE REPORT

Keywords: caustic ingestion; sodium hydroxide; esophageal necrosis; liquefactive necrosis; caustic injury grading; early endoscopy; vocal cord injury; esophageal perforation; alkali ingestion; Zargar classification

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Clinical History

A 58-year-old male presented to the emergency department after intentional ingestion of sodium hydroxide, a common alkaline cleaning material, in a suicide attempt. The patient was hemodynamically unstable with signs of severe upper airway compromise. Endoscopy was performed approximately 6 hours after ingestion to assess the extent of esophageal injury. At the time of the procedure, the patient was already receiving ventilatory support in the intensive care unit.

Endoscopic Findings

Upon entering the esophagus, extensive necrosis and sloughing of the esophageal mucosa was immediately evident at the level of the vocal cords (Figure 1A). Significant damage to the vocal cords themselves was noted, indicating direct caustic contact or aspiration during the ingestion event. Advancing through the proximal esophagus, diffuse necrotic changes and ulceration were observed (Figure 1B), with the mucosa showing a friable, devitalized appearance. Further examination revealed progressive esophageal involvement with necrotic tissue and dark discoloration extending throughout the mid-esophagus (Figure 1C). A more distal view confirmed extensive mucosal damage and friability involving the entire visible esophageal circumference (Figure 1D). The scope was deliberately not advanced beyond the esophagogastric junction due to the severity of necrotic changes and the high risk of iatrogenic perforation.

Discussion

Caustic ingestion is a medical emergency with high morbidity and mortality, particularly when the ingested substance is an alkaline agent such as sodium hydroxide. Unlike acid ingestion, which produces coagulative necrosis and a protective eschar that may limit tissue penetration, alkali substances cause liquefactive necrosis — dissolving tissue proteins and saponifying fats, allowing the caustic agent to penetrate deep into the esophageal wall and beyond. This mechanism explains the extensive transmural destruction seen in severe alkali ingestion and the high risk of subsequent perforation, mediastinitis, and fistula formation.

Early endoscopy, ideally within 12 to 24 hours of ingestion, is the cornerstone of injury assessment. The Zargar classification system grades caustic esophageal injury from grade 0 (normal examination) to grade 3b (extensive circumferential necrosis). The findings in this case — diffuse circumferential necrosis extending from the vocal cords through the visible esophagus — are consistent with Zargar grade 3b, which carries the highest morbidity and mortality. However, endoscopy must be performed with great caution in these patients. Advancing the scope through areas of severe circumferential necrosis risks iatrogenic perforation. The decision to limit the examination to the esophagus and not cross the esophagogastric junction was appropriate given the severity of mucosal damage observed.

The involvement of the vocal cords is a particularly ominous finding, as it suggests direct caustic contact with the supraglottic structures during ingestion or aspiration of the caustic material. Vocal cord injury further complicates the clinical course by contributing to airway compromise and increasing the need for prolonged ventilatory support. In this patient, the combination of extensive esophageal necrosis and respiratory compromise requiring mechanical ventilation indicated a grave prognosis.

Survivors of severe caustic esophageal injury face significant long-term morbidity, most commonly esophageal stricture formation, which may develop weeks to months after the initial injury. Management of strictures often requires serial endoscopic dilation, stent placement, or in refractory cases, surgical reconstruction with esophageal replacement. Nutritional support via jejunostomy or parenteral nutrition is essential during the acute and subacute phases of recovery.