History
- Pain in and around the eye and frontally, blurred vision, seeing round colored halos and lights, nausea, vomiting
- Angle closure induced by medications
- Topical
- Acetylcholinesterase inhibitors
- Sympathomimetics (alpha-1 agonists)
- Periorbital botulinum toxin
- Systemic
- Sulfonamide-containing medications (e.g. antibiotics)
- Antidepressants
- Topiramate (migraine medication)
Etiology
Primary angle-closure glaucoma
The lens and posterior iris shift anteriorly, blocking the pupil and causing what is known as pupillary block. Aqueous humor, produced in the ciliary body, accumulates in the posterior chamber. This pushes the peripheral iris anteriorly and closes the trabecular meshwork, so that aqueous humor can no longer drain from the eye.
Secondary angle-closure glaucoma
- Neovascular glaucoma
- Obstruction by a membrane
- Iridocorneal endothelial syndrome (ICE)
- Posterior polymorphous corneal dystrophy (PPCD)
- Epithelial downgrowth (e.g. after penetrating trauma)
- Phacomorphic angle closure
- Aphakic or pseudophakic pupillary block (vitreous, synechiae, fibrous adhesions, anterior chamber lens)
- Medication side effect
- Topiramate (migraine medication and sulfonamide -> supraciliary effusion -> swelling of the ciliary body -> anterior rotation of the lens-iris diaphragm. Typically bilateral, 2 weeks after starting therapy
- Choroidal swelling (after extensive argon laser coagulation of the retina, scleral buckle, retinal vein occlusion)
- Malignant glaucoma (= aqueous misdirection syndrome)
- Developmental disorder: Axenfeld-Rieger syndrome, Peters anomaly, etc.
Risk Factors
- Age, East Asian ethnicity, female sex, hyperopia, positive family history
- Status after topical mydriatic administration -> triggers angle closure
- Abnormal iris configuration, anterior iris insertion, short axial length (hyperopia)
Diagnostics
- Conjunctiva: injection
- Cornea: microcystic epithelial/stromal/endothelial edema
- Anterior chamber: shallow, especially peripherally; fellow eye also with shallow anterior chamber; existing iridotomy
- Iris/pupil: mid-dilated and fixed, dilated vessels, transillumination, PEX, pigment dispersion
- Lens: pigment deposits, thick, cloudy
- Fundoscopy: increased optic disc cupping, disc margin hemorrhage
- Gonioscopy: closed angle > 180°
- Tonometry: elevated intraocular pressure
Diagnosis
Angle-closure glaucoma, angle-closure glaucoma attack, pupillary block
Treatment
Immediate, parallel initiation of therapy
- Diamox 250mg tablets, 2x
- Contraindicated in topiramate- or sulfonamide-induced secondary angle closure
- Discontinue the causative medication, atropine 0.5% 4x/day
- Potassium
- Cosopt S eye drops 1x, repeat after 30 min
- Iopidine 1% eye drops 1x, repeat after 30 min
- Spersacarpine 2% eye drops 1x every 5 min x4, then every 10 min x3
- Contraindicated in aphakic or pseudophakic pupillary block
- Mydriatic and cycloplegic agent (and Cyclogyl 0.5% every 5 minutes, x8)
- Pred Forte eye drops 1x every 15 min x4
After 30 min, palpatory pressure measurement; if > 35 mmHg
After 30 min, applanation pressure measurement; if > 35 mmHg
If IOP remains persistently elevated -> perform LPI (laser peripheral iridotomy) as an emergency
If pressure does not decrease after LPI -> evaluate for prompt cataract surgery/surgical iridectomy/trabeculectomy
Follow-up
- Daily follow-up examinations (IOP, anterior chamber cells)
- LPI 1-5 days after the attack
- LPI on the fellow eye (caution: 40-80% risk of angle closure within 5-10 years)
- Patient counseling important, document if declined
- Follow-up examinations weekly to monthly, later with visual field and OCT of the optic disc and photography
- In phacomorphic glaucoma -> cataract surgery once IOP and intraocular inflammation are controlled
Prognosis
- LPI can be a definitive solution for the fellow eye
- The acute glaucoma attack typically causes damage to the anterior chamber angle and trabecular meshwork, leading to a chronic stage that subsequently requires long-term treatment
