Caustic burn

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
- 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

Caustic ingestion
Caustic eye exposure (Caustic keratoconjunctivitis)
Caustic dermal burn
Airbag-related burns
Hydrofluoric acid
Tar burn
Cement burn

Burns

Smoke inhalation injury (airway compromise)
Chemical injury
- Acrolein
- Hydrochloric acid
- Tuolene diisocyanate
- Nitrogen dioxide
Systemic chemical injury
- Carbon monoxide toxicity
- Cyanide toxicity
Specific types of burns
- Caustic burns
- Electrical injuries
  - Lightning Injuries
Associated toxicities

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)

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 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

References

↑ Wasserman RL, Ginsburg CM. Caustic substance injuries. J Pediatr. 1985;107(2):169-174. doi:10.1016/s0022-3476(85)80119-0
↑ 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
↑ 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.

Authors:

[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.

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