Diagnostic Criteria for Corrosive Ingestion Stages
Stage | Endoscopic Findings | Clinical Features | Management |
Grade 1 | Superficial mucosal damage, erythema, edema, and hyperemia. | Minor pain, dysphagia, and oral discomfort. | Observation, analgesia, and gradual reintroduction of oral intake. |
Grade 2A | Deep mucosal and submucosal damage with friability and superficial ulcerations, without circumferential involvement. | Moderate pain, significant dysphagia, possible drooling, and vomiting. | IV fluids, analgesia, proton pump inhibitors (PPIs), and gradual oral intake after 48-72 hours. |
Grade 2B | Deep mucosal and submucosal damage with friability and ulcerations, involving the entire circumference of the esophagus or stomach. | Severe pain, significant dysphagia, vomiting, potential signs of systemic toxicity. | Intensive care monitoring, IV fluids, broad-spectrum antibiotics, and nutritional support. |
Grade 3 | Transmural damage with necrosis, extensive ulcerations, and perforation. | Severe pain, signs of perforation (e.g., subcutaneous emphysema, peritonitis), systemic toxicity, and sepsis. | ICU care, surgical consultation, broad-spectrum antibiotics, parenteral nutrition, and surgery if necessary. |
Introduction
Corrosive ingestion is a critical condition encountered in both gastroenterology and surgery. The ingestion of strong acids or alkalis can cause severe damage to the gastrointestinal tract, necessitating prompt and effective management to mitigate complications.
Etiology
Corrosive ingestion involves substances that cause direct chemical injury to tissues:
Acids: Hydrochloric acid, sulfuric acid, nitric acid.
Alkalis: Sodium hydroxide, potassium hydroxide.
Household products: Drain cleaners, toilet bowl cleaners, batteries.
Pathophysiology
Upon ingestion, corrosives cause chemical burns:
Acids: Cause coagulative necrosis, resulting in eschar formation that limits the depth of injury.
Alkalis: Cause liquefaction necrosis, leading to deeper penetration and more extensive damage.
The injury severity depends on:
Substance concentration.
Volume ingested.
Contact duration.
Physical state (liquid causes more immediate damage compared to solid).
Clinical Presentation
Symptoms:
Immediate oral, pharyngeal, and chest pain.
Dysphagia.
Odynophagia.
Drooling.
Vomiting (may be hematemesis).
Signs:
Oral and pharyngeal burns.
Stridor or hoarseness (indicating airway involvement).
Abdominal tenderness.
Signs of perforation (subcutaneous emphysema, peritonitis).
Diagnosis
History and Physical Examination:
Detailed history of the substance ingested (type, concentration, amount, time of ingestion).
Thorough physical examination focusing on the oropharynx, chest, and abdomen.
Imaging:
Chest and abdominal X-rays: To check for free air indicating perforation.
CT scan: For detailed evaluation of extent and complications.
Endoscopy:
Timing: 24-72 hours post-ingestion (ideal window). Early endoscopy (<24 hours) is avoided due to potential underestimation of injury; late endoscopy (>72 hours) is avoided due to risk of perforation during healing.
Purpose: Assess the extent and severity of esophageal and gastric injuries.
Grading Severity:
Grade 1: Superficial mucosal damage.
Grade 2A: Deep mucosal and submucosal damage without circumferential involvement.
Grade 2B: Deep mucosal and submucosal damage with circumferential involvement.
Grade 3: Transmural damage with risk of perforation.
Management
Initial Management:
Stabilization:
Airway management: Intubation if necessary.
IV fluid resuscitation.
Pain management with opioids.
Avoid:
Nasogastric tube placement.
Gastric lavage.
Activated charcoal administration.
NPO status: To prevent further mucosal damage.
Definitive Management Based on Severity:
Grade 1:
Observation, analgesia.
Gradual reintroduction of oral intake.
Grade 2A:
IV fluids, analgesia, and PPIs.
Gradual oral intake after 48-72 hours.
Grade 2B:
Intensive care monitoring.
Broad-spectrum antibiotics.
Nutritional support (often parenteral).
Grade 3:
ICU care.
Surgery for perforation or significant necrosis.
Broad-spectrum antibiotics, parenteral nutrition.
Follow-Up:
Endoscopy: Repeat at 3 weeks to assess healing and stricture formation.
Nutritional Support: Gradual dietary progression; potential for esophageal dilatation in cases of stricture.
Long-Term Complications
Strictures: Requiring dilatation or stenting.
Malignancy: Increased risk in severe cases; long-term surveillance recommended.
Psychological support: Important in intentional ingestion cases.
Prevention and Education
Patient and Family Education:
Safe storage of corrosive substances.
Importance of childproof containers.
Public Health Measures:
Regulations on labeling and concentration limits of household corrosive.
Conclusion
Corrosive ingestion requires an interdisciplinary approach involving gastroenterology, surgery, critical care, and psychiatry. Prompt diagnosis, appropriate grading of injury, and tailored management based on severity are crucial for optimal patient outcomes. Long-term follow-up is essential to monitor for complications and provide comprehensive care.
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