Caustic burn

(Redirected from Chemical burns)

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

Hand with minor chemical burns exposure to commercial-grade dishwasher with concentrated chlorine.
Chemical burn caused by sodium hydroxide solution (lye) 44 hours after exposure.
Lower leg chemical burn caused by calcium cyanamide.
Water-thinned silver nitrate chemical burn on hand. Left: 7 hours after injury. Right: 26 hours after injury.
Caustic burn caused by exposure to mustard gas (World War I).
Hydrofluoric acid (HF) burns, which were not evident until a day after exposure.
  • Signs and symptoms are inadequate to predict presence or severity of injury after caustic ingestion [3]
  • Exam eyes and skin (splash and dribble injuries may easily be missed)
  • GI tract injury
  • Laryngotracheal injury

Differential Diagnosis

Caustic Burns

Burns

Evaluation

  • 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
  • Brush any dry chemicals off the patient
  • Irrigate all wounds and areas of exposure with copious amounts of water
    • Exception: dry lime, phenol, metals such as potassium and sodium, causes harmful exothermic reaction

Acidic injuries (except Hydrofluoric acid)

Alkali injuries

  • May appear superficial but often are deeper with ongoing burn
  • Treat with 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
  3. Gaudreault, P. et al. Predictability of esophageal injury from signs and symptoms: a study of caustic ingestion in 378 children. Pediatrics. 1983;71(5):767-770.