Caustic keratoconjunctivitis

(Redirected from Chemical Burns (Eye))


  • 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

Complication of an alkali corneal burn causing ocular surface failure with neovascularisation, opacificatio,n and blindness.
  • 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.