Hydrochloric acid

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Background

  • 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

Differential Diagnosis

Caustic Burns

Evaluation

  • Clinical diagnosis

Work-up

  • 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

Management

  • 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

Ingestion

  • 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
  • Control inflammation
  • Ophthomology consultation for all but minor burns (Severe exposures may require debridement or other surgical intervention)

Disposition

  • Dependant on severity of exposure and complications

See Also

External Links

References

  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.