Caustic keratoconjunctivitis

Background

• Chemical burn to eye
• Alkali injuries are more severe than acidic injuries

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

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

Diagnosis

• 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

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

Management

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

• Ocular alkali exposures are an ophthalmologic emergencies
• Prior to aggressive lavage with 2L water first check for globe perforation

1. Anesthesia
   1. Apply topical anesthesia (e.g. tetracaine)
2. Irrigation
   1. Apply for at least 30min (1-2L) or at least 40min (4L) for alkali exposure
   2. Perform immediately and before any examination
   3. NS or LR works best
   4. Treat until pH is >7.4 when checked 30min after the last irrigation
      1. Avoid testing pH of the irrigation fluid (wait few min before checking ocular fluid)
3. Remove particulate matter with cotton applicator
4. Measure acuity and IOP (may be increased if trabecular meshwork has been damaged)
5. Cycloplegic for pain control
   1. Avoid phenylephrine
6. Abx
   1. Erythromycin ointment QID
7. Ophtho consultation for all but minor burns
   1. Severe exposures may require anterior chamber irrigation

Disposition

1. Admit all pts w/ corneal haziness or opacity or limbal ischemia (paleness at limbus)
2. Discharge w/ 24hr f/u if pt only has corneal epithelial injury (fluorescein uptake)

Prognosis

After irrigation perform complete eye exam. The prognosis is determined by the extent of injury at the limbus and area/depth of injury to cornea.

Sources

• Brodovsky SC, et al: Management of alkali burns: An 11-year retrospective review. Ophthalmology 2000; 107:1829-1835

See Also

• Eye Algorithm (Main)
• Caustic burns