Caustic burn: Difference between revisions

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Revision as of 13:14, 22 March 2016

Background

Caustics

  • Substances that cause damage on contact with body surfaces
  • Degree of injury determined by pH, concentration, volume, duration of contact
  • Acidic agents cause coagulative necrosis
  • Alkaline agents cause liquefactive necrosis (considered more damaging to most tissues)
  • Corrosive agents have reducing, oxidising, denaturing or defatting potential

Alkalis

  • Accepts protons → free hydroxide ion, which easily penetrates tissue → cellular destruction
    • Liquefactive necrosis and protein disruption may allow for deep penetration into surrounding tissues
  • Examples
    • Sodium hydroxide (NaOH), potassium hydroxide (KOH)
      • Lye present in drain cleaners, hair relaxers, grease remover
    • Bleach (sodium hypochlorite) and Ammonia (NH3)
      • Cleaning products such as oven cleaners, swimming pool chlorinator
      • Household bleach ingestion (4-6% sodium hypochlorite) rarely causes significant esophageal injury[1][2]

Acids

  • Proton donor → free hydrogen ion → cell death via denatured protein → coagulation necrosis and eschar formation, which limits deeper involvement
    • However, due to pylorospasm and pooling of acid, high-grade gastric injuries are common
      • Mortality rate is higher compared to strong alkali ingestions
  • Can be systemically absorbed and → metabolic acidosis, hemolysis, AKI
  • Examples
    • Hydrochloric acid (HCl), hydrofluoric acid (HF), Sulfuric acid (H2SO4), Phosphoric acid, Oxalic Acid, Acetic acid
      • Found in: auto batteries, drain openers, toilet bowl, metal cleaners, swimming pool cleaners, rust remover, nail primer

Clinical Features

  • All pts w/ serious esophageal injuries have some initial sign or symptom
    • E.g. stridor, drooling, vomiting
  • Exam eyes and skin (splash and dribble injuries may easily be missed)
  • GI tract injury
    • Dysphagia, odynophagia, epigastric pain, vomiting
  • Laryngotracheal injury
    • Dysphonia, stridor, respiratory distress
    • Occurs via aspiration of caustic or vomitus or inhalation of acidic fumes

Differential Diagnosis

Caustic Burns

Diagnosis

  • Clinical diagnosis

Work-up

Only necessary in patients with significant injury or volume of ingestion

Consider:

  • CBC
  • Metabolic panel
  • Lactate
  • Calcium level (if Hydrofluoric acid exposure)
  • ECG
    • May show QT-prolongation if hypocalcemic secondary to Hydrofluoric acid
  • APAP/ASA levels if concerned about coingestion (suicidal patients)

Management

First prevent personal exposure to the caustic agent by removing all clothing and decontaminating the patient

Acidic injuries (except Hydrofluoric acid)

May also have non-anion gap acidosis (e.g. HCl)

  • Respond well to copious saline or water irrigation

Alkali injuries

  • May appear superficial but often are deeper w/ ongoing burn
  • Treat w/ copious irrigation and local wound debridement to remove residual compound

Disposition

  • Admit the following:
    • Injuries that cross flexor or extensor surfaces
    • Facial injuries
    • Perineum injuries
    • Partial-thickness injuries >10-15% of BSA
    • All full-thickness burns

See Also

References

  1. Wasserman RL, Ginsburg CM. Caustic substance injuries. J Pediatr. 1985;107(2):169-174. doi:10.1016/s0022-3476(85)80119-0
  2. Harley EH, Collins MD. Liquid household bleach ingestion in children: a retrospective review. Laryngoscope. 1997;107(1):122-125. doi:10.1097/00005537-199701000-00023