EARLY POSTOPERATIVE GLAUCOMA

IOP tends to increase approximately 1 hour after cataract extraction and usually returns to normal within 1 week. Etiologies include retained viscoelastic material or lens particle(s), pupillary block, hyphema, pigment dispersion, and generalized inflammation. Patients at greatest risk include those with ocular hypertension, glaucoma, preoperative IOP >22 mm Hg, and intraoperative complications. Most healthy eyes can tolerate an IOP up to 30 mm Hg for many  months. However, eyes with preexisting optic nerve damage require IOP-lowering medications for any significant pressure increase. Prostaglandin analogs are generally avoided postoperatively because of their proinflammatory characteristics and delayed onset of action. Most eyes with an IOP >30 mm Hg should be treated. If inflammation is excessive, increase the topical steroid dose to every 2 hours while awake and consider a topical NSAID (e.g., ketorolac, flurbiprofen or diclofenac q.i.d., bromfenac b.i.d., or nepafenac daily). See 9.7, Uveitic Glaucoma.

POSTOPERATIVE PUPILLARY BLOCK

Differential Diagnosis

Early Postoperative Period (Within 2 Weeks)

• Aqueous misdirection syndrome (malignant glaucoma). See 9.16, Aqueous Misdirection Syndrome/Malignant Glaucoma.

• Suprachoroidal hemorrhage.

• Anterior chamber lens with vitreous loss: Vitreous plugs the pupil if iridectomy is not performed. Can also occur if patient is aphakic.

• Silicone oil or expansile intraocular gas (e.g., sulfur hexafluoride [SF₆] and perfluoropropane [C₃F₈]) after retinal detachment repair. Gas expansion typically occurs within 4 days of intraocular insertion. Can occur via open-angle or closed-angle mechanisms.

• After endothelial keratoplasty, air or gas can migrate behind iris and cause pupillary block.

• Angle closure after scleral buckling procedure.

Late Postoperative Period (After 2 Weeks)

• Pupillary block glaucoma. See 9.4, Acute Angle Closure Attack.

• Suprachoroidal hemorrhage.

• UGH syndrome. See 9.15.3, Uveitis, Glaucoma, Hyphema Syndrome.

• Aqueous misdirection syndrome (malignant glaucoma): When cycloplegics are stopped. See 9.16, Aqueous Misdirection Syndrome/Malignant Glaucoma.

• Steroid-induced glaucoma. See 9.8, Steroid-Response Glaucoma.

Signs

Increased IOP, shallow or partially flat anterior chamber with anterior iris bowing (iris bombé), absence of a patent PI. Posterior iris adhesions to lens, anterior capsule, or intraocular lens usually present.

Treatment

1. If the cornea is clear and the eye is not significantly inflamed, a PI is performed, usually by YAG laser. Because the PI tends to close, it is often necessary to perform two or more iridotomies. See Appendix 15, YAG Laser Peripheral Iridotomy.

2. If the cornea is hazy, the eye is inflamed, or a PI cannot be performed immediately, then:

   • Mydriatic agent (e.g., cyclopentolate 2% and phenylephrine 2.5%, every 15 minutes for four doses).

   • Topical therapy with β-blocker (e.g., timolol 0.5%), α2 agonist (e.g., brimonidine 0.1% to 0.2%), and CAI (dorzolamide 2%) should be initiated immediately if no contraindication. In urgent cases, three rounds of these medications may be given, with each round being separated by 15 minutes.

   • Systemic CAI (e.g., acetazolamide 250 to 500 mg i.v. or two 250-mg tablets p.o. in one dose if unable to give i.v.) if IOP decrease is urgent or if IOP is refractory to topical therapy.

   • Topical steroid (e.g., prednisolone acetate 1%) every 15 to 30 minutes for four doses.

   • PI, preferably YAG laser, when the eye is less inflamed. If the cornea is not clear, topical glycerin may help clear it temporarily.

   • A surgical PI may be needed.

   • A guarded filtration procedure or tube shunt may be needed if the angle has become closed.

UVEITIS, GLAUCOMA, HYPHEMA SYNDROME

Signs

Anterior chamber cell and flare, increased IOP, hyphema, and possible iris TIDs. Usually  secondary to irritation from a malpositioned anterior or posterior chamber intraocular lens with adjacent iris and ciliary body chafe. UBM may help to confirm diagnosis by demonstrating IOL haptic contact to ciliary body in the sulcus.

Treatment

1. Atropine 1% b.i.d.

2. Topical steroid (e.g., prednisolone acetate 1% four to eight times per day or difluprednate 0.05% four to six times per day) and consider topical NSAID (e.g., ketorolac, flurbiprofen, or diclofenac q.i.d.; bromfenac b.i.d.; or nepafenac daily).

3. Systemic CAI (e.g., acetazolamide 500 mg sequel p.o. b.i.d.) or may consider topical CAI (e.g., dorzolamide 2% t.i.d.).

4. Topical β-blocker (e.g., timolol 0.5% daily or b.i.d.) and α2 agonist (e.g., brimonidine 0.1% to 0.2% b.i.d. to t.i.d.).

5. Consider laser ablation if bleeding site can be identified.

6. Consider surgical repositioning, replacement, or removal of the intraocular lens, especially if patient experiences recurrent episodes, formation of PAS, or persistent CME.

7. Consider YAG vitreolysis if vitreous strands can be seen.