Alkali ingestion

(Redirected from 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[1]
  • Unlike acids (which cause coagulative necrosis with a protective eschar), alkalis penetrate through tissue layers and can cause transmural injury and perforation[1]
  • Alkali ingestions are more common than acid ingestions in the US and are the most frequent cause of serious caustic GI injury[2]
  • 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[2]
  • 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[3]
  • 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[1]

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[1]

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

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[4]
  • 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)[3]
    • 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[3]
      • 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[5]
    • 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:[5]
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[3]
  • 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)[4]
  • 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[4]

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[1]
  • Do NOT attempt neutralization (i.e. do not give a weak acid) — exothermic reaction causes thermal injury on top of chemical injury[2]
  • Do NOT place a nasogastric tube blindly — risk of esophageal perforation
  • Do NOT give activated charcoal — does not adsorb alkalis; obscures endoscopy; aspiration risk[1]
  • Do NOT perform gastric lavage — contraindicated due to perforation risk[2]

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[2]
  • 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[6]
    • 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:[3]
    • 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[3]
  • Poison Control: 1-800-222-1222

See Also

External Links

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Hoffman RS, Burns MM, Gosselin S. Ingestion of caustic substances. N Engl J Med. 2020;382(18):1739-1748. PMID 32348644.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Alkali Toxicity. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2023. PMID 31082166.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Chirica M, Bonavina L, Kelly MD, Sarfati E, Cattan P. Caustic ingestion. Lancet. 2017;389(10083):2041-2052. PMID 28045663.
  4. ↑ 4.0 4.1 4.2 Rumpf JJ, Settmacher U, Rauchfuss F. Acute emergency care and airway management of caustic ingestion in adults. Scand J Trauma Resusc Emerg Med. 2016;24:45. PMID 27068117.
  5. ↑ 5.0 5.1 Zargar SA, Kochhar R, Mehta S, et al. The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc. 1991;37(2):165-169. PMID 2032601.
  6. ↑ Usta M, Erkan T, Cokugras FC, et al. High doses of methylprednisolone in the management of caustic esophageal burns. Pediatrics. 2014;133(6):e1518-e1524. PMID 24864180.
Retrieved from "https://www.wikem.org/w/index.php?title=Alkali_ingestion&oldid=389192"