Acid Eye Injury

Exposure to an acid: sulphuric (car batteries, drain cleaners), hydrochloric (swimming pool and cleaning products), nitric, acetic (vinegar, concentrated forms), hydrofluoric (glass etching, rust removal, semiconductor industry), chromic, phosphoric, and formic acid.

Mechanism: hydrogen ions denature and coagulate proteins, forming a barrier that limits penetration, so acid burns are generally less severe than alkali. Exceptions are strong acids at high concentration (sulphuric, nitric) and hydrofluoric acid, in which the fluoride ion penetrates deeply, binds calcium and magnesium, and causes severe and delayed necrosis and systemic toxicity.

Injuries range from epithelial keratopathy to total corneal opacification, limbal ischaemia, and chemical conjunctival burns. Battery explosions combine acid with thermal and projectile injury.

Pepper spray, vinegar and household acids generally cause mild injury that resolves.

• Immediate pain, blepharospasm, tearing and blurred vision.
• Corneal epithelial defect, whitish ground glass corneal opacity (coagulated epithelium), conjunctival hyperaemia and chemosis, limbal blanching in severe cases, anterior chamber reaction, raised intraocular pressure.
• Lid and facial skin burns; hydrofluoric acid: severe pain disproportionate to findings, delayed progression over hours, skin blanching.
• Systemic signs of hydrofluoric acid toxicity: hypocalcaemia (tetany, prolonged QT, arrhythmia), hypomagnesaemia, hyperkalaemia, cardiac arrest.
• Late: symblepharon, limbal stem cell deficiency, scarring, vascularisation, dry eye, cataract, glaucoma.

• Immediate irrigation first; identify the agent and concentration; check fornix pH before and after irrigation.
• Slit lamp with fluorescein: epithelial defect, stromal haze, limbal ischaemia (clock hours), anterior chamber and lens, intraocular pressure; examine fornices for retained material (cement, battery fragments).
• Hydrofluoric acid: ECG, serum calcium (ionised), magnesium, potassium, and creatinine; repeat during the first 24 hours.
• Slit lamp photographs and serial measurement of the defect.

• Irrigate immediately at the scene with water for at least 15 to 20 minutes, then with 1 to 2 L of normal saline or balanced salt solution (more for severe burns or until pH is 7.0 to 7.4 and stable 5 to 10 minutes after stopping), after topical anaesthesia (proparacaine 0.5 percent) and lid speculum; remove foreign particles from the fornices.
• Medical therapy: cycloplegic (cyclopentolate 1 percent three times daily or atropine 1 percent twice daily), topical antibiotic (chloramphenicol 0.5 percent or ofloxacin 0.3 percent four times daily), preservative free lubricants hourly, topical steroid (prednisolone acetate 1 percent four times daily for 5 to 7 days in moderate injury; every 2 hours while awake for 7 to 10 days in severe injury), ascorbic acid 10 percent drops and oral ascorbic acid 500 mg four times daily, sodium citrate 10 percent drops, oral doxycycline 100 mg twice daily for severe injury, analgesia (paracetamol, oral opioids), and acetazolamide 250 mg four times daily for raised pressure.
• Hydrofluoric acid: irrigate for at least 30 minutes; topical calcium gluconate 1 percent (10 mL of 10 percent calcium gluconate in 90 mL saline) irrigation or drops (avoid calcium chloride, which is corrosive to tissue); skin: calcium gluconate 2.5 percent gel; admit with cardiac monitoring for any significant exposure; IV calcium gluconate 10 percent 10 to 20 mL over 10 to 20 minutes for hypocalcaemia and replace magnesium; sub-conjunctival calcium gluconate is not recommended.
• Surgical for severe burns: amniotic membrane transplantation, limbal stem cell transplantation after 3 to 6 months, and keratoplasty for scarring.
• Follow up: daily until healing, then weekly; monitor pressure and symblepharon formation.