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Emergency and Acute Medicine – Caustic Ingestion
Core Concept
Caustic ingestion causes chemical injury to tissues through acid or alkali exposure. Alkalis dissociate in water to form hydroxyl (OH⁻) ions, producing liquefaction necrosis that primarily damages the esophagus, though gastric injury can occur. Injury progresses from superficial hyperemia and mucosal edema to blistering, ulceration, full-thickness necrosis, perforation, and late fibrosis with esophageal strictures. Alkalis typically do not cause systemic toxicity.
Acids dissociate to form hydrogen (H⁺) ions, leading to coagulation necrosis with eschar formation. Due to rapid esophageal transit, acids mainly injure the stomach, producing edema, inflammation, hemorrhage, necrosis, perforation, and late gastric outlet obstruction. Acids are well absorbed and may cause hemolysis and systemic metabolic acidosis.
Etiologic Sources
Injuries result from direct chemical exposure to acids or alkalis, commonly found in household and industrial products. These include ammonia hydroxide, sodium hydroxide (drain and oven cleaners), sodium hypochlorite (bleach), sulfuric acid (car batteries), hydrochloric acid (toilet cleaners), hydrofluoric acid (glass etching and microchip industries), phenol, formaldehyde, iodine, detergents containing borates or phosphates, rust removers, and button batteries.
Clinical Manifestations
Oropharyngeal findings may include pain, erythema, burns, erosions, ulcers, drooling, hoarseness, stridor, or aphonia; absence of visible lesions does not exclude severe visceral injury. Pulmonary involvement presents with cough, tachypnea, or aspiration pneumonitis. Gastrointestinal symptoms include chest or abdominal pain, dysphagia, odynophagia, emesis or hematemesis, melena, and signs of perforation or peritonitis. Cardiovascular findings include tachycardia and hypotension. Acid ingestion may cause hemolysis. Dermal exposure causes chemical burns, and ocular exposure ranges from conjunctival injection to full-thickness corneal injury. Metabolic acidosis may be present, particularly with acid ingestion.
Essential Initial Assessment
A clear history or signs of exposure are critical. Normal oropharyngeal examination does not rule out esophageal or gastric injury.
Diagnostic Evaluation
Laboratory testing includes CBC, electrolytes, BUN, creatinine, glucose, and arterial blood gas analysis. Blood cultures are indicated if mediastinitis or peritonitis is suspected. Type and cross-match should be obtained when bleeding is a concern. Chest and abdominal radiographs assess for perforation. Esophagogastroduodenoscopy is indicated in symptomatic patients to assess injury severity and should be performed within 12–24 hours, provided the airway is secure and there is no severe pharyngeal injury or respiratory distress. Acute contrast studies are not recommended but may be used later to evaluate strictures.
Key Alternative Diagnoses
Other chemical burns, foreign body ingestion, and upper airway infection or angioedema should be considered.
Prehospital Care
For oral exposure with mild symptoms, rinse the mouth with water or milk if the patient can swallow, has no vomiting, airway compromise, or significant abdominal pain. Copious irrigation is required for ocular or dermal exposure.
Emergency Stabilization
Airway protection is paramount; perform early intubation if respiratory compromise is present, avoiding blind nasotracheal intubation. Treat hypotension with isotonic IV fluids.
Emergency Department Management
Immediate irrigation of skin or eyes with water or normal saline should continue until physiologic pH is achieved, recognizing that alkali exposures require more prolonged irrigation. Induced emesis, activated charcoal, gastric lavage, and neutralizing agents are contraindicated. Limited dilution with water or milk may be considered within 30 minutes of ingestion if there is no airway compromise or suspected perforation; excessive volumes should be avoided. Keep patients NPO after oral exposure. Administer antiemetics and IV acid suppression for symptom control. Initiate broad-spectrum antibiotics if mediastinitis, peritonitis, or corticosteroid therapy is planned. Corticosteroid use to prevent esophageal strictures remains controversial and should be decided collaboratively; antibiotics are required if steroids are used. Surgical consultation is mandatory for suspected perforation or full-thickness necrosis. Hydrofluoric acid exposures require calcium therapy, including topical, intradermal, or intra-arterial calcium gluconate depending on severity and location.
Medications
Supportive medications may include ondansetron for nausea, IV proton pump inhibitors or H2 blockers for symptom relief, and corticosteroids only with multidisciplinary agreement. Calcium gluconate is essential for hydrofluoric acid injuries.
Disposition
All symptomatic patients and all nonaccidental ingestions require hospital admission. Asymptomatic patients with accidental ingestion who can swallow without difficulty and have no concerning findings may be discharged with instructions.
Follow-Up
Psychiatric evaluation is required for intentional ingestions.
Clinical Pearls
Early dilution with water or milk within 30 minutes may limit injury in select patients. Copious irrigation is essential for dermal and ocular exposures, particularly with alkalis. The absence of oral burns does not exclude severe internal injury.
Core Concept
Caustic ingestion causes chemical injury to tissues through acid or alkali exposure. Alkalis dissociate in water to form hydroxyl (OH⁻) ions, producing liquefaction necrosis that primarily damages the esophagus, though gastric injury can occur. Injury progresses from superficial hyperemia and mucosal edema to blistering, ulceration, full-thickness necrosis, perforation, and late fibrosis with esophageal strictures. Alkalis typically do not cause systemic toxicity.
Acids dissociate to form hydrogen (H⁺) ions, leading to coagulation necrosis with eschar formation. Due to rapid esophageal transit, acids mainly injure the stomach, producing edema, inflammation, hemorrhage, necrosis, perforation, and late gastric outlet obstruction. Acids are well absorbed and may cause hemolysis and systemic metabolic acidosis.
Etiologic Sources
Injuries result from direct chemical exposure to acids or alkalis, commonly found in household and industrial products. These include ammonia hydroxide, sodium hydroxide (drain and oven cleaners), sodium hypochlorite (bleach), sulfuric acid (car batteries), hydrochloric acid (toilet cleaners), hydrofluoric acid (glass etching and microchip industries), phenol, formaldehyde, iodine, detergents containing borates or phosphates, rust removers, and button batteries.
Clinical Manifestations
Oropharyngeal findings may include pain, erythema, burns, erosions, ulcers, drooling, hoarseness, stridor, or aphonia; absence of visible lesions does not exclude severe visceral injury. Pulmonary involvement presents with cough, tachypnea, or aspiration pneumonitis. Gastrointestinal symptoms include chest or abdominal pain, dysphagia, odynophagia, emesis or hematemesis, melena, and signs of perforation or peritonitis. Cardiovascular findings include tachycardia and hypotension. Acid ingestion may cause hemolysis. Dermal exposure causes chemical burns, and ocular exposure ranges from conjunctival injection to full-thickness corneal injury. Metabolic acidosis may be present, particularly with acid ingestion.
Essential Initial Assessment
A clear history or signs of exposure are critical. Normal oropharyngeal examination does not rule out esophageal or gastric injury.
Diagnostic Evaluation
Laboratory testing includes CBC, electrolytes, BUN, creatinine, glucose, and arterial blood gas analysis. Blood cultures are indicated if mediastinitis or peritonitis is suspected. Type and cross-match should be obtained when bleeding is a concern. Chest and abdominal radiographs assess for perforation. Esophagogastroduodenoscopy is indicated in symptomatic patients to assess injury severity and should be performed within 12–24 hours, provided the airway is secure and there is no severe pharyngeal injury or respiratory distress. Acute contrast studies are not recommended but may be used later to evaluate strictures.
Key Alternative Diagnoses
Other chemical burns, foreign body ingestion, and upper airway infection or angioedema should be considered.
Prehospital Care
For oral exposure with mild symptoms, rinse the mouth with water or milk if the patient can swallow, has no vomiting, airway compromise, or significant abdominal pain. Copious irrigation is required for ocular or dermal exposure.
Emergency Stabilization
Airway protection is paramount; perform early intubation if respiratory compromise is present, avoiding blind nasotracheal intubation. Treat hypotension with isotonic IV fluids.
Emergency Department Management
Immediate irrigation of skin or eyes with water or normal saline should continue until physiologic pH is achieved, recognizing that alkali exposures require more prolonged irrigation. Induced emesis, activated charcoal, gastric lavage, and neutralizing agents are contraindicated. Limited dilution with water or milk may be considered within 30 minutes of ingestion if there is no airway compromise or suspected perforation; excessive volumes should be avoided. Keep patients NPO after oral exposure. Administer antiemetics and IV acid suppression for symptom control. Initiate broad-spectrum antibiotics if mediastinitis, peritonitis, or corticosteroid therapy is planned. Corticosteroid use to prevent esophageal strictures remains controversial and should be decided collaboratively; antibiotics are required if steroids are used. Surgical consultation is mandatory for suspected perforation or full-thickness necrosis. Hydrofluoric acid exposures require calcium therapy, including topical, intradermal, or intra-arterial calcium gluconate depending on severity and location.
Medications
Supportive medications may include ondansetron for nausea, IV proton pump inhibitors or H2 blockers for symptom relief, and corticosteroids only with multidisciplinary agreement. Calcium gluconate is essential for hydrofluoric acid injuries.
Disposition
All symptomatic patients and all nonaccidental ingestions require hospital admission. Asymptomatic patients with accidental ingestion who can swallow without difficulty and have no concerning findings may be discharged with instructions.
Follow-Up
Psychiatric evaluation is required for intentional ingestions.
Clinical Pearls
Early dilution with water or milk within 30 minutes may limit injury in select patients. Copious irrigation is essential for dermal and ocular exposures, particularly with alkalis. The absence of oral burns does not exclude severe internal injury.
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