Alkali ingestion

Background

• Alkali (caustic/corrosive) ingestion refers to oral exposure to substances with a pH ≥ 12, which cause liquefactive necrosis — saponification of fats, protein denaturation, and cell membrane destruction that penetrates deeply into tissue
• Unlike acids (which cause coagulative necrosis with a protective eschar), alkalis penetrate through tissue layers and can cause transmural injury and perforation
• Alkali ingestions are more common than acid ingestions in the US and are the most frequent cause of serious caustic GI injury
• Common alkali substances:
  • Drain cleaners / oven cleaners: Sodium hydroxide (NaOH) or potassium hydroxide (KOH) — "lye"; most common cause of severe injury
  • Hair relaxers/straighteners: Sodium hydroxide or calcium hydroxide
  • Laundry/dishwasher detergent pods (LDPs): Concentrated alkaline surfactants; increasingly common pediatric exposure
  • Household bleach (NaOCl): Low concentration (3–8%) rarely causes serious injury; industrial-strength bleach or international formulations may have higher concentration
  • Ammonia: Household cleaners
  • Disc/button batteries: Generate alkali via electrolysis at the anode; cause focal liquefactive necrosis on contact with mucosa
• Epidemiology:
  • Children < 5 years: Accidental ingestion; usually small volumes → less severe injury
  • Adolescents / Adults: Intentional ingestion (suicidal); typically larger volumes → more severe injury and higher mortality
• Severity of injury depends on: pH, titratable alkali reserve (TAR), volume ingested, concentration, physical form (liquid vs. solid vs. gel), and duration of tissue contact
• Liquid alkalis tend to cause more extensive injury (spread distally to esophagus and stomach); solid/granular alkalis tend to adhere to oropharynx and proximal esophagus
• Long-term complications: Esophageal stricture (most common long-term sequela), gastric outlet obstruction, and a 1,000-fold increased risk of esophageal carcinoma decades after injury

Clinical Features

• Presentation ranges from asymptomatic to cardiac arrest depending on severity
• Absence of oropharyngeal burns does NOT exclude significant esophageal or gastric injury — up to 10–30% of patients without visible oral burns have esophageal injury on endoscopy

Oropharyngeal

• Oral pain, drooling, dysphagia, odynophagia
• Erythema, edema, ulceration, or white/gray pseudomembranes of the lips, tongue, palate, and posterior pharynx
• Refusal to swallow (children)

Airway

• Stridor, hoarseness, dysphonia — signs of laryngeal/epiglottic edema; may progress rapidly to complete obstruction
• Cough, tachypnea, respiratory distress
• Aspiration → chemical pneumonitis

Esophageal / Gastric

• Chest pain, epigastric pain, back pain
• Hematemesis
• Signs of perforation: severe chest/abdominal pain, rigidity, subcutaneous emphysema

Systemic (Severe Ingestions)

• Hypotension, tachycardia (hemorrhage, third-spacing, sepsis)
• Metabolic acidosis (lactic acidosis from tissue necrosis and hypoperfusion)
• Fever, leukocytosis
• Disseminated intravascular coagulation
• Multiorgan failure

Delayed Complications

• Esophageal/gastric stricture (weeks to months)
• Esophageal perforation (greatest risk in first 5–14 days post-ingestion when tissue is weakest during granulation)
• Esophageal carcinoma (years to decades)

Differential Diagnosis

• Caustic ingestion
• Boric acid ingestion
• Foreign body ingestion (especially button battery)
• Esophageal Perforation (Boerhaave syndrome)
• Infectious esophagitis (candidal, herpetic, CMV — in immunocompromised)
• Pill esophagitis
• Epiglottitis / supraglottitis (if airway symptoms predominate)
• Anaphylaxis (airway edema without history of ingestion)
• Other toxic ingestions (paraquat, formaldehyde)
• Thermal burn to the oropharynx

Evaluation

Workup

• Airway assessment is the first priority — examine for stridor, drooling, voice changes, respiratory distress
• Do NOT delay airway management — early intubation if any concern for progressive airway edema; airway can deteriorate rapidly
• Labs:
  • CBC (leukocytosis may indicate severe injury/necrosis)
  • BMP/CMP (electrolytes, renal function, bicarbonate)
  • VBG/ABG with lactate (metabolic acidosis and elevated lactate are predictive of transmural necrosis)
  • LFTs (hepatic injury in severe cases)
  • Coagulation studies (PT/INR) — coagulopathy may develop
  • Type and screen/crossmatch (anticipate hemorrhage)
  • Lipase (if concern for pancreatic injury)
  • Serum β-hCG in women of reproductive age
• Imaging:
  • CXR and upright abdominal XR: Evaluate for pneumomediastinum, pneumoperitoneum, pleural effusion, aspiration
  • Contrast-enhanced CT (neck/chest/abdomen): Increasingly used as first-line imaging in adults; can identify transmural necrosis (absence of post-contrast wall enhancement), perforation, and extent of injury
    • CT should be performed 3–6 hours post-ingestion per WSES guidelines
    • High specificity for severe injury; may reduce need for emergent endoscopy in some centers
• Endoscopy (EGD):
  • Standard for grading injury severity using the Zargar classification
  • Should be performed within 12–24 hours (do not delay beyond 48 hours — perforation risk increases after this point)
  • Typically performed by GI or surgery; not an ED procedure

Diagnosis

• Diagnosis is clinical — based on history of alkali exposure and consistent symptoms
• Zargar Endoscopic Classification:

Grade	Findings	Prognosis
0	Normal	No injury
1	Mucosal edema, hyperemia	Excellent; heals without sequelae
2a	Superficial ulceration, exudates, friability	Good; low stricture risk
2b	Deep or circumferential ulceration	Moderate; significant stricture risk (~70%)
3a	Focal/scattered necrosis	Poor; high perforation and stricture risk
3b	Extensive necrosis	Surgical emergency; high mortality

• Abnormal labs (severe acidosis, elevated lactate, leukocytosis, thrombocytopenia, elevated CRP, renal injury) are predictive of transmural necrosis and poor outcomes
• Initial normal labs do NOT exclude transmural necrosis — serial monitoring is essential

Management

Airway (First Priority)

• Early intubation if any evidence of airway compromise (stridor, voice changes, drooling, respiratory distress, significant oropharyngeal edema)
• Have a difficult airway plan ready — consider early involvement of anesthesia; awake fiberoptic intubation or surgical airway may be needed if severe laryngeal edema
• 50% of patients with intentional alkali ingestion in one series required intubation

Resuscitation

• IV access (two large-bore) and crystalloid resuscitation
• NPO — nothing by mouth until injury is graded
• Correct coagulopathy and acidosis as needed
• Blood products if hemorrhaging

What NOT To Do

• Do NOT induce emesis — re-exposes esophagus to caustic agent; risk of aspiration and perforation
• Do NOT attempt neutralization (i.e. do not give a weak acid) — exothermic reaction causes thermal injury on top of chemical injury
• Do NOT place a nasogastric tube blindly — risk of esophageal perforation
• Do NOT give activated charcoal — does not adsorb alkalis; obscures endoscopy; aspiration risk
• Do NOT perform gastric lavage — contraindicated due to perforation risk

Dilution (Controversial / Limited Role)

• Small volumes of water or milk (120–240 mL) may be offered within 30 minutes of ingestion of solid/granular alkali only — goal is to dislodge particles adhering to mucosa
• Do NOT use for liquid alkali ingestions (risk of inducing emesis outweighs benefit)
• Do NOT delay other management for dilution

Supportive Care

• Pain management: IV opioid analgesia as needed
• PPI therapy: IV proton pump inhibitor (reduces acid exposure to injured tissue); routinely initiated though evidence is limited
• Antibiotics: Not routinely indicated; give if perforation suspected or documented, or if the patient develops signs of sepsis
• Corticosteroids:
  • Role is controversial
  • Some evidence supports high-dose methylprednisolone (starting within 48 hours) for grade 2b injuries to reduce stricture formation
  • Steroids are NOT indicated for grade 1, 2a (unnecessary) or grade 3 (may mask perforation signs and impair healing)
  • Decision should be made in consultation with GI/surgery after endoscopic grading

Surgical Consultation

• Emergent surgery is indicated for:
  • Evidence of perforation (pneumomediastinum, pneumoperitoneum)
  • Zargar grade 3b on endoscopy (extensive necrosis)
  • Absence of post-contrast wall enhancement on CT (transmural necrosis)
  • Clinical deterioration despite supportive care (peritonitis, hemodynamic instability, worsening acidosis)
• Surgical options include esophagogastrectomy with delayed reconstruction

Disposition

• Discharge after 4–6 hour observation:
  • Asymptomatic patients with accidental ingestion of small volume of low-concentration alkali (e.g. small taste of dilute household bleach, household ammonia cleaner)
  • Must tolerate PO challenge without difficulty prior to discharge
  • Ensure close follow-up; consider outpatient GI referral for delayed EGD
• Admit:
  • All symptomatic patients
  • All intentional ingestions regardless of symptoms
  • All pediatric patients with suspected significant ingestion
  • Any patient requiring endoscopy or CT for injury grading
  • Patients with abnormal labs (acidosis, elevated lactate, leukocytosis)
• ICU admission:
  • Airway compromise or intubation
  • Hemodynamic instability
  • Zargar grade 2b or higher on endoscopy
  • Evidence of perforation
  • Multiorgan dysfunction, DIC, or severe metabolic acidosis
• Surgical consultation: Early for all significant ingestions; emergent for perforation or grade 3b injury
• Psychiatric evaluation: Mandatory for all intentional ingestions prior to hospital discharge
• Poison Control: 1-800-222-1222

See Also

• Acid ingestion
• Caustic ingestion
• Button battery ingestion
• Esophageal perforation
• Boron toxicity
• Toxicology (Main)

External Links

• Ingestion of caustic substances - N Engl J Med 2020
• Caustic ingestion - Lancet 2017
• Alkali Toxicity - StatPearls
• Modified endoscopic classification of caustic burns (Zargar) - Gastrointest Endosc 1991
• Acute emergency care of caustic ingestion in adults - Scand J Trauma Resusc Emerg Med 2016
• ToxCard: Caustic Ingestions Do's and Don'ts - emDOCs