Caustic keratoconjunctivitis


  • Chemical burn to eye
  • Alkali injuries are more severe than acidic injuries, and are considered an ophthalmologic emergency
  • Prognosis is determined by the extent of injury at the limbus and area/depth of injury to cornea


  • 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


  • 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]


  • 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

Keratoconjunctivitis Types

Clinical Features

  • Severe ocular pain, blepharospasm, reduced visual acuity
  • Altered ocular pH (normal = 7.0-7.2)
  • Appearance
  • Perilimbal ischemia (white ring around iris)
    • Concerning due to co-location of corneal stem cell layer (re-epitheliazation relies on migration of limbal stem cells)

Alkali Burns

  • Rapid penetration through cornea and anterior chamber
  • Causes liquefaction necrosis from hydroxyl ions combining with fatty acids
  • Elevated IOP may be seen in alkali injury[3]
  • Acute injury liquefaction necrosis and ischemia which can be graded on degree of limbal and corneal involvement
  • Early sequelae corneal edema and elevated IOP
  • Later injury after one week - corneal breakdown, ulceration, perforation because of collagenase activity exceeds synthesis

Acid Exposure

  • Injury related to length of exposure and concentration of chemical
  • Causes coagulation necrosis and protein precipitation thus limits depth of penetration
  • Delayed complications corneal and conjunctival scarring, vascularization, glaucoma, uveitis

Other Chemicals

  • Most exposures produce only simple irritation

Roper-Hall classification[4]

Grade Cornea Appearance Limbal Ischemia Prognosis
I Clear None Good
II Hazy/iris details visible <1/3 Good
III Opaque/iris details obscured 1/3-1/2 Guarded
IV Opaque/iris details obscured >1/2 Poor

Differential Diagnosis

Caustic Burns

Conjunctivitis Types

Unilateral red eye

^Emergent diagnoses ^^Critical diagnoses


  • Generally a clinical diagnosis


Caustic Ocular Exposure Management

  • Eye irrigation
    • Immediate irrigation is the most important treatment for caustic ocular injury, and should be started before comprehensive evaluation
    • Irrigate affected eye(s) with copious amounts of fluid (no consensus on volume or length of time)[5]
    • NS, LR, or BSS (Buffered Saline Solution) preferred in the hospital setting[6], but tap water is acceptable, especially in pre-hospital setting.
    • Goal is to remove caustic agent and restore normal ocular pH (7.0-7.2)
    • Do NOT attempt to neutralize pH by adding base to an acidic burn or acid to an alkali burn
    • Use of morgan lens or eyelid speculum will assist with getting more fluid in contact with cornea
  • Remove particulate matter
    • Evert both lids, remove any visible particulate matter with cotton-tipped applicator
  • Anesthesia
  • Antibiotics
  • Control inflammation
  • Ophthalmology consultation for all but minor burns (Severe exposures may require debridement or other surgical intervention)



  • Pediatric patient
  • Corneal haziness, opacity, or limbal ischemia (paleness at limbus)


With 24hr ophthalmology follow-up

  • If only has corneal epithelial injury
    • Encourage use of artificial tears and other lubricating eyedrops

See Also


  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. Lin, M.P., et al., Glaucoma in patients with ocular chemical burns. American journal of ophthalmology, 2012. 154(3): p. 481-485 e1.
  4. Gupta N et al. Comparison of Prognostic Value of Roper Hall and Dua Classification Systems in Acute Ocular Burns. Br J Ophthalmol. 2011;95(2):194-198.
  5. Chau JP, Lee DT, Lo SH. A systematic review of methods of eye irrigation for adults and children with ocular chemical burns. Worldviews Evid Based Nurs. 2012 Aug;9(3):129-38.
  6. Herr RD, White GL Jr, Bernhisel K, Mamalis N, Swanson E. Clinical comparison of ocular irrigation fluids following chemical injury. Am J Emerg Med. 1991 May;9(3):228-31.
  7. Dohlman, C.H., F. Cade, and R. Pfister, Chemical burns to the eye: paradigm shifts in treatment. Cornea, 2011. 30(6): p. 613-4.
  8. Donshik, P.C., et al., Effect of topical corticosteroids on ulceration in alkali-burned corneas. Archives of ophthalmology, 1978. 96(11): p. 2117-20.