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Caustic burns
From WikEM
Contents
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), ammonia (NH3)
- Found in: bleach, drain openers, oven cleaners, toilet cleaner, hair relaxers
Acids
- Proton donor → free hydrogen ion → cell death 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
- However, due to pylorospasm and pooling of acid, high-grade gastric injuries are common
- Can be systemically absorbed and → metabolic acidosis, hemolysis, AKI
- Examples
- Hydrochloric acid (HCl), hydrofluoric acid (HF), Sulfuric acid (H2SO4)
- Found in: auto batteries, drain openers, metal cleaners, swimming pool products, rust remover, nail primer
Clinical Features
- Signs and symptoms are inadequate to predict presence or severity of injury after caustic ingestion [1]
- 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
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
See Also
References
- ↑ 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.