A mild, self-limited rise in IOP is common after cataract surgery. However, a significant and sustained elevation may require timely management.
Ophthalmic viscosurgical devices (OVDs) retained in the eye after cataract surgery are frequently responsible for early postoperative IOP elevation, which peaks 4–6 hours after surgery. The large molecules of the viscoelastic material can impair aqueous outflow through the trabecular meshwork. Even when all apparent OVDs have been removed from the anterior chamber, residual OVDs can lodge in the posterior chamber or behind the lens implant. In general, IOP elevation usually does not last more than a few days and is amenable to medical treatment.
Marked IOP elevation in the early postoperative period may be temporarily managed by applying gentle pressure on the posterior lip of a preexisting paracentesis incision to release a small amount of aqueous humor. Caution is advised when performing this procedure in the setting of capsule rupture or zonular dialysis because vitreous strands may become incarcerated in the paracentesis. In addition, the surgeon may consider instilling povidone-iodine 5% solution or a topical antibiotic. Topical and/or systemic pressure-lowering agents should also be administered, as IOP reduction after aqueous release is short-lived, with the IOP likely to rise again within 1–2 hours of decompression.
After cataract surgery, elevated IOP without angle closure may also be caused by hyphema, TASS, endophthalmitis, retained lens material (phacolytic or phacoanaphylactic reactions), uveitis, iris pigment release, preexisting glaucoma, corticosteroid use, vitreous in the anterior chamber, or ghost cell glaucoma. Angle-closure glaucoma may be due to pupillary block, malignant glaucoma, epithelial ingrowth, neovascular glaucoma, or PAS. Treatment of the underlying cause of IOP elevation is indicated.
Malignant glaucoma (also known as ciliary block glaucoma, aqueous misdirection, or vitreous block) has been described as a ciliolenticular block induced by anterior movement of the lens–iris interface, poor vitreous fluid conductivity (increased resistance to fluid movement through the vitreous), and choroidal expansion. These factors cause the central and peripheral portions of the anterior chamber to become very shallow and lead to a secondary elevation of IOP due to angle obstruction. Malignant glaucoma occurs most commonly after intraocular surgery in eyes with prior angle-closure glaucoma, but it can also occur in small eyes with open angles.
Malignant glaucoma must be differentiated from pupillary block glaucoma, capsular block, suprachoroidal hemorrhage, and choroidal detachment. Unlike pupillary block, malignant glaucoma is not relieved by iridectomy but requires either intense medical therapy or more aggressive surgical therapy.
Medical treatment consists of cycloplegia and aqueous suppression, as well as hyperosmotic agents (eg, oral glycerin or intravenous mannitol). Use of miotics is not recommended because they can worsen malignant glaucoma by exacerbating anterior displacement of the lens–iris interface.
Surgical intervention consists of Nd:YAG laser irido-zonulo-hyaloidotomy and occasionally vitrectomy to disrupt the anterior vitreous face and vitreous–ciliary body interface, in effect establishing a unicameral eye with an open channel for aqueous to circulate into the anterior chamber. (See also BCSC Section 10, Glaucoma.)
Kaplowitz K, Yung E, Flynn R, Tsai JC. Current concepts in the treatment of vitreous block, also known as aqueous misdirection. Surv Ophthalmol. 2015;60(3):229–241.
Varma DK, Belovay GW, Tam DY, Ahmed II. Malignant glaucoma after cataract surgery. J Cataract Refract Surg. 2014;40(11):1843–1849.
Excerpted from BCSC 2020-2021 series: Section 11 - Lens and Cataract. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.