Hydrochloric acid


  • Strong acid, causes coagulation necrosis due to denaturation of proteins
  • Most household bleaches are only 3-6% hydrochlorite solutions, but patients may have occupational exposures if working in steel picking, chemical manufacturing, oil/gas-well acidizing, and food processing
  • HCl is combustion product of polyvinyl chloride (PVC), can cause chemical inhalation injury, can persist in air for up to an hour after fire extinguished

Clinical Features

  • Can be systemically absorbed and → metabolic acidosis, hemolysis, AKI
  • Dermal caustic burns
  • Ingestion
    • All patients with serious esophageal injuries have some initial sign/symptom
    • Dysphagia, odynophagia, epigastric pain, vomiting
    • Laryngotracheal injury: dysphonia, stridor, respiratory distress
      • Occurs via aspiration of caustic or vomitus or inhalation of acidic fumes
  • inhalation injury
    • PVCs and other arrhythmias
    • Delayed onset (2-12 hours) pulmonary edema
    • Dyspnea, chest pain
  • Caustic keratoconjunctivitis
    • Severe eye pain, blepharospasm, reduced visual acuity
    • Altered ocular pH (normal = 7.0-7.2)
    • Conjunctival injection OR blanching, chemosis, hemorrhage, epithelial defects, corneal loss OR edema, perilimbal ischemia (white ring around iris)

Differential Diagnosis

Caustic Burns


  • Clinical diagnosis


  • Only necessary in patients with significant injury or volume of ingestion
  • CBC, metabolic panel, lactate, serum calcium (if concern for hydrofluoric acid exposure
  • ECG
  • Tylenol/ASA levels if concerned about coingestion (suicidal patients)
  • Ingestion, consider:
    • 3-View CXR: look for free air under diaphragm or mediastinal free air
    • CT: if suspect perforation but CXR negative


  • Decontaminate first: use appropriate personal protective equipment, remove all patient's clothing, decontaminate patient
  • Irrigate areas of dermal or ocular exposure, early and copiously!
  • Airway management
    • Monitor closely for stridor, airway edema, hoarseness, or other signs of airway injury
    • Intubate early if signs of airway injury exist, before airway becomes more difficult to manage.
    • Consider awake fiberoptic or video laryngoscopy if concern for difficult airway
    • Blind nasotracheal intubation is contraindicated in caustic ingestion due to the potential for perforations and false passages
    • Bronchodilators for bronchospasm if concern for inhalational injury

Systemic Exposure


  • Airway management especially important!
  • Endoscopy
    • Indications:
      • All intentional ingestions (higher likelihood of high volume ingestion)
      • Any ingestion with stridor, drooling, significant oropharyngeal burns, vomiting, food refusal
    • Perform within 12-24 hours of ingestion (too early can underestimate extent of injury, too late increases risk of wound softening and perforation)
  • Esophageal stricture mitigation[1]
  • Surgical intervention: indicated if perforation or peritoneal signs
  • Contraindicated (or controversial) therapies:
    • Antibiotics (unless giving steroids]]
    • Activated charcoal (may consider when coingestants pose a risk for severe systemic toxicity)
    • Gastric lavage: contraindicated due to potential to cause reflux of caustic agent into esophagus, creating more damage
    • Dilution with water or milk: causes vomiting, elevating risk for perforation
    • Neutralization (e.g. with milk or mag citrate): generates excess heat

Caustic Ocular Exposure Management

  • Eye irrigation
    • Immediate irrigation is the most important treatment for caustic ocular injury, and should be started before comprehensive evaluation
    • Irrigate affected eye(s) with copious amounts of fluid (no consensus on volume or length of time)[2]
    • NS, LR, or BSS (Buffered Saline Solution) preferred in the hospital setting[3], but tap water is acceptable, especially in pre-hospital setting.
    • Goal is to remove caustic agent and restore normal ocular pH (7.0-7.2)
    • Do NOT attempt to neutralize pH by adding base to an acidic burn or acid to an alkali burn
    • Use of morgan lens or eyelid speculum will assist with getting more fluid in contact with cornea
  • Remove particulate matter
    • Evert both lids, remove any visible particulate matter with cotton-tipped applicator
  • Anesthesia
  • Antibiotics
    • Erythromycin ophthalmic ointment QID for minor burns
    • Topical fluoroquinolone for more severe burns
  • Control inflammation
  • Ophthalmology consultation for all but minor burns (Severe exposures may require debridement or other surgical intervention)


  • Dependant on severity of exposure and complications

See Also


  1. High Doses of Methylprednisolone in the Management of Caustic Esophageal Burns. Pediatrics 2014;133:e1518–e1524
  2. Chau JP, Lee DT, Lo SH. A systematic review of methods of eye irrigation for adults and children with ocular chemical burns. Worldviews Evid Based Nurs. 2012 Aug;9(3):129-38.
  3. Herr RD, White GL Jr, Bernhisel K, Mamalis N, Swanson E. Clinical comparison of ocular irrigation fluids following chemical injury. Am J Emerg Med. 1991 May;9(3):228-31.
  4. Dohlman, C.H., F. Cade, and R. Pfister, Chemical burns to the eye: paradigm shifts in treatment. Cornea, 2011. 30(6): p. 613-4.
  5. Donshik, P.C., et al., Effect of topical corticosteroids on ulceration in alkali-burned corneas. Archives of ophthalmology, 1978. 96(11): p. 2117-20.
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