15. CAUSTICS: INORGANIC ACIDS AND ALKALI

Caustic poisoning occurs when corrosive substances such as inorganic acids or alkalis come into contact with body tissues. These agents cause severe chemical burns, leading to tissue necrosis, perforation, and long-term complications such as strictures. Caustic ingestion is common in accidental exposures among children and intentional self-harm in adults. Early recognition and prompt supportive care are essential for preventing severe morbidity.

Types of Caustic Agents

Inorganic Acids

  • Sulphuric acid
  • Hydrochloric acid
  • Nitric acid
  • Phosphoric acid

Alkalis

  • Sodium hydroxide (lye)
  • Potassium hydroxide
  • Ammonia
  • Bleaching agents containing strong alkali

Mechanism of Injury

Acids

Acids cause coagulation necrosis, forming an eschar that may limit deeper penetration. However, concentrated acids cause severe gastric and esophageal damage.

Alkalis

Alkalis cause liquefaction necrosis, which allows deeper penetration into tissues. This results in extensive damage to the esophagus, leading to perforation and strictures.

Clinical Features

Symptoms develop rapidly after ingestion and depend on concentration, volume, and contact duration.

Local Symptoms

  • Severe mouth and throat pain
  • Drooling and difficulty swallowing
  • Oral burns and ulcerations
  • Vomiting (may contain blood)

Respiratory Symptoms

  • Hoarseness
  • Cough and stridor
  • Airway edema
  • Respiratory distress

Gastrointestinal Effects

  • Retrosternal or epigastric pain
  • Hematemesis
  • Peritonitis due to perforation

Systemic Toxicity

  • Hypotension
  • Shock
  • Metabolic acidosis (in severe exposures)

Complications

  • Esophageal perforation
  • Tracheoesophageal fistula
  • Strictures (weeks to months later)
  • Pulmonary aspiration
  • Sepsis
  • Hemorrhage

Investigations

  • Complete blood count
  • Electrolytes and arterial blood gases
  • Chest X-ray for perforation
  • Endoscopy within 12–24 hours (most important diagnostic tool)
  • CT scan if perforation is suspected

Do NOT perform endoscopy after 48 hours due to risk of esophageal rupture.

Management

1. Initial Stabilization

  • Ensure airway patency
  • Provide humidified oxygen
  • Prepare for early intubation if airway edema is developing

2. Decontamination – What NOT to do

  • No gastric lavage
  • No activated charcoal (obscures endoscopy, limited benefit)
  • No neutralizing agents – exothermic reaction increases injury
  • No inducing vomiting – causes re-exposure to the caustic

3. Supportive Care

  • IV fluids for hydration
  • Analgesics for severe pain
  • Proton pump inhibitors to reduce gastric injury
  • Antiemetics to control vomiting

4. Antibiotics

Use only if there is suspected perforation, fever, or evidence of infection. Prophylactic antibiotics are not routinely recommended.

5. Corticosteroids

Their role is controversial. They may be considered in severe esophageal burns to reduce stricture formation but require concurrent antibiotic coverage.

6. Surgical Intervention

  • Indicated in perforation, mediastinitis, peritonitis, or uncontrolled bleeding

7. Long-Term Management

  • Monitor for esophageal strictures
  • Dilatation procedures for symptomatic strictures
  • Psychiatric evaluation in intentional ingestion cases

When to Admit

  • Any symptomatic patient
  • Difficulty swallowing or drooling
  • Airway involvement
  • GI bleeding or suspected perforation

Detailed Notes:

For PDF style full-color notes, open the complete study material below:

PATH: PHARMD/ PHARMD NOTES/ PHARMD FOURTH YEAR NOTES/ CLINICAL TOXICOLOGY/ CAUSTICS : INORGANIC ACIDS AND ALKALI.

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