Ocular Chemical Burns

BASICS

Chemical injury to the eye is a true ophthalmologic emergency with potential for rapid, permanent, and devastating damage.
Alkali burns: More severe—alkalis (e.g., ammonia, lye) penetrate eye rapidly, causing deep necrosis.
Acid burns: Less severe—cause protein coagulation, which limits further penetration, but still can cause significant injury. Hydrofluoric acid acts more like an alkali, with deep penetration and systemic toxicity.
Systems affected: eye, skin/exocrine, nervous system

Alkali (pH >7): Ammonia, lime, lye, ammonium hydroxide; rapid tissue penetration and necrosis, long-term risk of elevated intraocular pressure (IOP)
Acid (pH <7): Sulfuric, hydrochloric, acetic acids; form protein barrier, but may cause significant scarring; hydrofluoric acid can penetrate deeply, bind Ca/Mg, and cause systemic hypocalcemia
Risks: Industrial/chemical work, cleaning agents, cement/plaster, battery explosions, assault

Corneal opacification (alkali > acid), ground-glass cornea (acid), decreased vision
Check for eyelid involvement, conjunctival blanching, limbal ischemia

Thermal burns, traumatic corneal abrasion, infectious keratoconjunctivitis, ruptured globe, foreign body

Immediate pH measurement (litmus paper) of both eyes
Irrigation must not be delayed for further testing
Imaging: CT if intraocular or orbital foreign body suspected (MRI contraindicated)
Full eye exam: Visual acuity, IOP, slit-lamp, fluorescein staining, fundus if possible

Use Roper-Hall or Dua classification to guide prognosis and treatment (extent of limbal/conjunctival involvement)

Start copious irrigation with any available nontoxic fluid immediately (do not wait for ED arrival)
Irrigate until pH neutral (7.2 ± 0.1), check every 30 min; may require 15–30 min (mild) up to 2–4 hours (severe)
Remove all chemical reservoirs by eyelid eversion; sweep fornices to prevent adhesions
Use topical anesthetic for comfort

Broad-spectrum topical antibiotic (e.g., bacitracin-polymyxin B ointment, ciprofloxacin drops)
Artificial tears (preservative-free) q1h initially
Cycloplegics (cyclopentolate 1% TID) for photophobia/uveitis
Topical corticosteroids (prednisolone 1% q1–2h, up to 7–10 days if epithelium intact; rapid taper)
Oral prednisone (20–60 mg daily for 5–7 days if severe)
Vitamin C (ascorbic acid): 500 mg PO QID and/or topical 10% solution q2h to reduce corneal thinning
Acetylcysteine (10–20% topical q4h) may aid healing
IOP-lowering agents if IOP >30 mmHg (e.g., timolol, acetazolamide)
Bandage contact lens (high oxygen permeability) may help healing

Topical steroids: prolonged use (>6 days) can impair healing—use under ophthalmologist’s supervision
Avoid systemic tetracycline in children <8 yrs/pregnancy
Monitor for systemic side effects with IOP-lowering drugs

Biologic fluids (umbilical cord serum, autologous serum, platelet-rich plasma, amniotic membrane drops)
Amniotic membrane transplantation, limbal stem cell transplant (for severe/recurring cases)
Tissue adhesive or tectonic keratoplasty for corneal perforation

Débridement of necrotic tissue
Tenoplasty, conjunctival/mucosal grafting, keratoplasty (for severe or persistent defects)
Enucleation for blind, painful eye (rare)

Depends on injury severity: mild burns often recover, severe burns risk permanent vision loss
Increased limbal and conjunctival involvement → worse prognosis

Immediate irrigation (any available clean water) is critical—do NOT delay.
Alkali burns penetrate deeper and are more severe than acid.
All cases need urgent ophthalmology evaluation.
Prognosis is guarded; time to irrigation and severity of initial injury are major determinants of outcome.