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Caustic Ingestion: Assessment, Investigations and Management

Caustic Ingestion: Assessment, Investigations and Management

Caustic ingestion is exposure of the mouth, pharynx, oesophagus or stomach to a corrosive chemical. Strong alkalis and acids can cause rapidly progressive tissue injury, perforation and later strictures. The absence of visible oral burns does not exclude serious oesophageal or gastric injury.

Emergency priority

Assess and protect the airway first. Stridor, drooling, voice change, respiratory distress, shock, severe chest or abdominal pain, guarding, haematemesis or subcutaneous emphysema require immediate senior, anaesthetic, ENT, surgical and gastroenterology involvement.

Learning objectives

  • Differentiate common alkali and acid exposures and explain their injury patterns.
  • Perform a safe ABCDE assessment and recognise impending airway compromise or perforation.
  • Select appropriate laboratory tests, imaging and endoscopy.
  • Outline acute treatment, complications, follow-up and prevention.

Common corrosive agents

Agent groupExamplesTypical injury
AlkalisDrain/oven cleaners, industrial cleaners, concentrated bleach, some detergentsLiquefactive necrosis with deep tissue penetration; oesophageal injury may predominate.
AcidsToilet cleaners, battery acid, hydrochloric or sulphuric acid preparationsCoagulative necrosis and eschar; gastric injury may be prominent, although any upper-GI level can be affected.
Oxidants and other irritantsConcentrated hypochlorite, peroxide, phenols and industrial chemicalsVariable mucosal, systemic or inhalational toxicity depending on concentration and dose.

Severity depends on pH, concentration, physical form, volume, contact time and whether ingestion was accidental or intentional. Solids may adhere to the oropharynx, while liquids can injure several levels. Intentional ingestion often involves larger volumes and more severe injury.

Pathophysiology

Necrosis begins within minutes. Oedema, vascular thrombosis and inflammation evolve over hours. During the following days the injured wall becomes friable, so perforation may occur early or during the healing phase. Collagen deposition and scar contraction can later produce oesophageal or gastric strictures.

Early phase

Mucosal burns, oedema, bleeding, aspiration, airway compromise, shock and perforation.

Late phase

Dysphagia, odynophagia, malnutrition, oesophageal stricture, gastric outlet obstruction and long-term malignancy risk after severe injury.

Clinical features

  • Burning pain in the mouth, throat, chest or epigastrium.
  • Drooling, refusal to swallow, dysphagia or odynophagia.
  • Hoarseness, stridor, cough, wheeze, hypoxia or respiratory distress.
  • Vomiting, haematemesis or abdominal tenderness.
  • Shock, rigidity, severe chest/back pain or crepitus suggesting perforation.

Symptoms and oral examination correlate poorly with the depth of internal injury. A patient may have significant oesophageal damage despite a normal-looking mouth.

Immediate assessment

  1. Airway: look for drooling, voice change, burns, soot, stridor and progressive oedema. Arrange controlled early intubation by an experienced clinician when compromise is developing; a surgical airway may be required if intubation is unsafe or impossible.
  2. Breathing: give oxygen when indicated, assess aspiration and monitor saturation.
  3. Circulation: obtain IV access, monitor vital signs and treat shock with appropriate fluids and blood products.
  4. Disability and exposure: assess consciousness, associated self-harm, skin/eye contamination and other trauma.
Do not
  • Do not induce vomiting.
  • Do not attempt chemical neutralisation with an acid or alkali; the reaction can generate heat.
  • Do not perform gastric lavage or blind nasogastric-tube insertion.
  • Do not give activated charcoal routinely; it is ineffective for caustics and can obscure endoscopy.
  • Do not delay emergency referral while trying home remedies.

Focused history and examination

  • Identify the product, concentration, amount, time, physical form and container; bring the labelled container safely if available.
  • Clarify accidental versus intentional ingestion, co-ingestants, vomiting and first aid already given.
  • Examine the oral cavity gently without provoking vomiting; assess neck tenderness, chest, lungs and abdomen.
  • Contact the local poison-information service or emergency department for product-specific advice.

Investigations

InvestigationPurpose and interpretation
Full blood count, electrolytes, urea/creatinine, glucoseAssess bleeding, dehydration, renal function and metabolic disturbance.
Blood gas and lactateEvaluate acidosis, ventilation and tissue hypoperfusion in significant exposure.
Liver profile, coagulation and group/crossmatchUseful in severe injury, bleeding or anticipated surgery.
Chest and abdominal radiographsLook for free air, mediastinal gas, pleural effusion or aspiration; a normal film does not exclude deep injury.
Contrast-enhanced CTHelps assess transmural necrosis, perforation and adjacent-organ injury in severe or equivocal cases.
Upper-GI endoscopyGrades mucosal injury and guides feeding/follow-up. In a stable patient it is commonly performed within 12–24 hours by an experienced team; timing is specialist-directed. Avoid when perforation is evident or the patient is too unstable.

Bronchoscopy may be required when inhalational or tracheobronchial injury is suspected. Endoscopy should never delay resuscitation or surgery for perforation.

Management

Initial treatment

  • Remove contaminated clothing and irrigate exposed skin or eyes copiously.
  • Keep the patient nil by mouth until specialist assessment; after immediate mouth decontamination, further oral fluids or diluents should only be given on poison-centre or clinician advice.
  • Provide IV fluids, antiemetics and adequate analgesia while avoiding unnecessary sedation.
  • Use acid suppression, antibiotics and corticosteroids only for defined indications under local protocol and specialist guidance. Antibiotics and steroids are not routine for every ingestion.
  • Arrange early multidisciplinary care involving emergency medicine, anaesthesia, gastroenterology, ENT, surgery, critical care, nutrition and mental-health services when appropriate.

Definitive and supportive care

  • Urgent surgery is required for perforation, peritonitis, mediastinitis, uncontrolled bleeding or established full-thickness necrosis.
  • Nutrition is guided by injury grade: selected mild injuries may resume oral intake after assessment; severe injuries may require enteral access placed under direct vision or parenteral support.
  • Monitor closely for delayed airway oedema, sepsis, bleeding and perforation.
  • After intentional ingestion, provide compassionate psychosocial and suicide-risk assessment once medically stable.

Complications and follow-up

Acute

Airway obstruction, aspiration pneumonitis, haemorrhage, perforation, mediastinitis, peritonitis, fistula, sepsis and death.

Chronic

Oesophageal stricture, recurrent aspiration, malnutrition, gastric outlet obstruction and increased oesophageal cancer risk after major injury.

Progressive dysphagia weeks after ingestion suggests stricture and requires contrast assessment and specialist endoscopic management. Long-term surveillance is individualised according to injury severity.

Prevention

  • Keep chemicals in original labelled containers, locked away from children and separate from food or drink.
  • Never transfer corrosives into beverage bottles.
  • Use protective equipment and safe storage in workplaces.
  • Teach caregivers that vomiting and neutralisation are dangerous first-aid measures.

Key examination points

  • A normal mouth does not exclude severe oesophageal injury.
  • Airway stabilisation and perforation recognition come before endoscopy.
  • Do not induce vomiting, neutralise the chemical or perform blind gastric procedures.
  • Endoscopy and CT answer different questions and are selected by clinical severity.
  • Strictures are important late complications requiring nutritional and specialist follow-up.

References and further reading

For education only. Apply current Uganda Clinical Guidelines, local poison-centre advice, hospital protocols and specialist recommendations.

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