Causes of Pain

• Corneal decompensation: Fluorescein-staining defect(s) on slit lamp examination. Pain improves with topical anesthetic.
• Uveitis: Anterior chamber or vitreous white blood cells. Corneal opacification may obscure the view of an inflammatory reaction.
• Glaucoma with elevated IOP.
• Hypotony: Ciliary body shutdown, retinal detachment, choroidal detachment, and ciliary body detachment. See 13.11, HYPOTONY SYNDROME.

1. Sterile corneal decompensation (if it appears infected, see 4.11, BACTERIAL KERATITIS).
   • Antibiotic or lubricating ointment (e.g., erythromycin or bacitracin–polymyxin B) daily to q.i.d. to the eye for weeks to months (or even permanently). Can also add cycloplegic agent (e.g., atropine 1%) for additional comfort. Consider nightly taping of eyelids.
   • Consider a tarsorrhaphy, amniotic membrane graft, or Gunderson conjunctival flap in refractory cases.
2. Uveitis.
   • Cycloplegia (e.g., atropine 1% b.i.d.).
   • Topical steroid (e.g., prednisolone acetate 1% q1–6h). See 12.1, ANTERIOR UVEITIS (IRITIS/IRIDOCYCLITIS).
   • Endophthalmitis should be ruled out if severe uveitis or a hypopyon is present.
3. Markedly increased IOP.
   • Topical beta-blocker (e.g., timolol 0.5% daily or b.i.d.) with or without an adrenergic agonist (e.g., brimonidine 0.1%, 0.15%, or 0.2% b.i.d. to t.i.d.). Topical carbonic anhydrase inhibitors (e.g., dorzolamide 2% t.i.d.) are effective, but potential systemic side effects may not warrant their use for pain relief; miotics and prostaglandin analogs may increase ocular irritation.
   • If the IOP remains markedly increased and is thought to be responsible for the pain, a cyclodestructive procedure (e.g., diode laser cyclophotocoagulation) may be attempted. The potential for sympathetic ophthalmia must be considered.
   • If pain persists despite the previously described treatment, a retrobulbar alcohol block may be given.
4. Hypotony.
   • Resolve causes of hypotony (e.g., repair wound leak, treat uveitis or ciliochoroidal detachment). If retinal detachment is found, repair may resolve hypotony.
5. Cause of pain unknown.
   • Cycloplegia (e.g., atropine 1% t.i.d.).
   • Topical steroid (e.g., prednisolone acetate 1% q1–6h).
   • Retrobulbar injections of neurolytic agents can be considered. See Appendix 10, TECHNIQUE FOR RETROBULBAR/SUBTENON/SUBCONJUNCTIVAL INJECTIONS.
6. Ocular pain refractory to topical medication therapy and/or retrobulbar injections.
   • Consider enucleation or evisceration of the eye. Evisceration should not be performed if intraocular malignancy is suspected. Enucleation does not relieve facial paresthesias.
   • Consider postinfectious or postsurgical neuralgia, in which case referral to pain management is indicated.

NOTE:

Technique: 2 to 3 mL of lidocaine is administered in the retrobulbar region. The needle is then held in place while the syringe of lidocaine is replaced with a 1-mL syringe containing 95% to 100% alcohol (some physicians use 50% alcohol). The contents of the alcohol syringe are then injected into the retrobulbar space through the needle. The syringes are again switched, so a small amount of lidocaine can rinse out the remaining alcohol. The retrobulbar needle is then withdrawn. Patients are warned that transient eyelid droop or swelling, limitation of eye movement, or anesthesia may result. Retrobulbar chlorpromazine (25 to 50 mg, using 25 mg/mL) or phenol can also be used. See Appendix 10, TECHNIQUE FOR RETROBULBAR/SUBTENON/SUBCONJUNCTIVAL INJECTIONS.

NOTE:

Monocular patients should wear protective eye wear (e.g., polycarbonate lenses) at all times to prevent injury to the contralateral eye.

Depends on the degree of pain and clinical examination. Once the pain resolves, patients are reexamined every 6 to 12 months. B-scan US should be performed periodically (typically every 3 years) to rule out an intraocular tumor when the posterior pole cannot be visualized.

Patients with a nonseeing eye and unsalvageable vision can experience mild-to-severe ocular pain for a variety of reasons.