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  • Ophthalmic Pearls

    Glaucoma and High IOP After Vitreoretinal Procedures

    By Sefy Paulose, MD, and Kateki Vinod, MD
    Edited by Jeremiah P. Tao, MD, FACS

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    Glaucoma and elevated IOP can be challenging to manage, particularly when these condi­tions occur secondary to vitreoretinal procedures. Key considerations for successfully managing glaucoma or high IOP in this setting include the preexistence of either condition, the type of vitreoretinal procedure, the timing of IOP elevation, and close collaboration between the vitreoretinal surgeon and other care providers. The choice of treatment should be based on awareness of the pathophysiology, the degree of IOP elevation, and the risk or severity of glaucomatous damage.

    Scleral Buckle

    The incidence of angle-closure glaucoma (ACG) following scleral buckle surgery ranges from 1.4% to 4.4%, and IOP elevation has occurred in up to 28.8% of cases.1,2 The pathophysiology of ACG in these cases involves compression of the vortex veins by the scleral buckle. This compression impedes venous drainage and results in congestion and anterior rotation of the ciliary body, with sub­sequent anterior shift of the lens-iris diaphragm.

    Risk factors for ACG after scleral buckling include preexisting narrow angles, high myopia, and placement of the encircling band anterior to the eye’s equator.

    Management. Most cases of angle closure after scleral buckle resolve with­out intervention, as con-gestion of the ciliary body decreases. Cycloplegia can be helpful to open the angle because it relaxes the ciliary muscle and promotes posterior movement of the lens-iris diaphragm. Note that miotics can worsen angle closure.

    Aqueous suppressants are effective for lowering IOP. Although laser iridotomy is not indicated in these cases because the angle closure is not caused by pupillary block, laser iridoplasty might help to open the angle. In re-fractory cases, trabeculectomy or tube shunt surgery may be required; however, the conjunctival recession and scarring that typically accompany scleral buck­ling may preclude trabeculectomy. Tube shunts have high rates of success, and their endplates can be sutured directly to an existing scleral buckle.

    Another approach to consider is the modified Schocket procedure, in which silicone tubing is used to shunt aqueous from the anterior chamber to the fibrous capsule of an existing scleral buckle.

    Pre-op advice. For eyes at high risk of IOP elevation after scleral buckle, such as those with advanced glaucomatous damage and/or synechial angle closure, it may be prudent to consider placing a tube shunt during the primary buckle surgery.

    Silicone Oil

    Silicone oil is often used when repairing complex retinal detachments. The inci­dence of elevated IOP after injection of silicone oil is approximately 2% at six months and 56% at eight months.3

    There are various mechanisms by which silicone oil can elevate IOP. Therefore, gonioscopy is required to be able to distinguish between a closed angle (in which the glaucoma or ele­vated IOP results from pupillary block, synechial angle closure, intraoperative overfill of silicone oil, or anterior seg­ment neovascularization) and an open angle (in which glaucoma or elevated IOP is due to migrated emulsified oil or an idiopathic cause). The management approach depends on the mechanism.

    Management. IOP elevation on post-op day 1 may signify overfill of silicone oil, necessitating partial aspira­tion of oil by the vitreoretinal surgeon, via the pars plana. Most cases of high IOP related to silicone oil can be man­aged with aqueous suppressants.

    For cases that do not respond to aqueous suppressants, oil removal can be considered if the risk of retinal re-detachment is low. If re-detachment is a concern, placement of a tube shunt can be considered. Given that oil is buoyant in aqueous, the tube should be positioned inferiorly within the anteri­or chamber (especially in aphakic eyes) to avoid escape of oil through the tube, which could lead to tube obstruction and/or subconjunctival inflammation. Another surgical option is cyclophotocoagulation, but repeated treatments may be needed in an oil-filled eye.

    Pupillary block caused by silicone oil requires inferior laser iridotomy or surgical iridectomy. An important and easy-to-miss clinical phenomenon is the aphakic eye without a patent iridot­omy/iridectomy, in which silicone oil prolapses forward and fills the anterior chamber (Fig. 1). High IOP is a result of pupillary block and direct obstruction of the trabecular meshwork. In such cases, the anterior chamber is deep, and the angle appears open on gonioscopy, with angle structures being visible. High-level vigilance is needed to recog­nize the often subtle sheen of silicone oil on the iris surface of these eyes.

    Prophylactic inferior surgical iridec­tomies are often performed at the time of oil injection to prevent pupillary block in aphakic eyes; however, iridectomies are reported to close in 11% to 32% of eyes due to scarring and/or obstruction by capsular remnants.3 An in-office laser iridotomy or a surgical iridectomy allows aqueous to regain access to the anterior chamber and enables return of the oil to the posterior segment.

    A note of caution. Silicone oil is inflammatory; hence, long-term treat­ment with low-dose steroids is crucial to prevent scarring of an iridotomy or iridectomy.

    External photo of eye with oil-filled anterior chamber.
    SILICONE OIL. Aphakic eye with oil-filled anterior chamber, caused by scarring and closure of the surgical iridectomy. Note the subtle sheen of silicone oil on the iris surface.

    Intraocular Gas

    Sulfur hexafluoride (SF6) and perflu­oropropane (C3F8) are expansile gases commonly used in the surgical man­agement of retinal tears and detachments at the time of pneumatic reti­nopexy or vitrectomy. As the injected gas expands in the vitreous cavity, the lens-iris diaphragm can shift forward and cause secondary angle closure, with or without a pupillary block compo­nent. The incidence of IOP elevation ranges from 6.1% to 67% with SF6 and from 18% to 59% with C3F8.4 The risk of post-op IOP rise can be mitigated by correct titration of gas concentration and volume, along with the patient maintaining a face-down position.

    Management. In most instances, IOP can be controlled with topical glaucoma medications until the gas dissipates. In cases of pupillary block, laser iridotomy is indicated. If surgical intervention is required, tube shunts generally are more successful than trabeculectomy, given the likelihood of conjunctival scarring from the earlier retinal procedure. Re­fractory cases may require gas aspira­tion via the pars plana, at the discretion of the vitreoretinal surgeon.

    Advice for patients. Patients should be advised to avoid traveling to high altitudes, which can cause gas expan­sion and IOP spikes.

    Pars Plana Vitrectomy

    The incidence of elevated IOP after uncomplicated pars plana vitrectomy (PPV) ranges from 15% to 20%, and the rates have been higher for PPV in combination with other intraocular procedures.5 It has been hypothesized that increased oxygen diffusion from the vitreous cavity to the anterior chamber causes oxidative stress within the trabecular meshwork, resulting in elevated IOP.6 The risk appears to be higher for pseudophakic eyes.

    Management. Aqueous suppressants are the first-line treatment to reduce IOP. When surgical intervention is warranted, tube shunts may be the best option because the success rate is better than for trabeculectomy when there is vitrectomy-related conjunctival scarring. Tube insertion into the pars plana can be considered for eyes with corneal endothelial dysfunction or corneal grafts, after confirmation by the vitreoretinal surgeon that the vitreous base has been shaved adequately to prevent vitreous-tube occlusion.

    Intravitreal Injections

    The incidence of elevated IOP after intravitreal steroid injections ranges from 29% to 40%.7,8 These injections increase resistance to aqueous outflow by altering the anatomic structure of the trabecular meshwork through the extracellular matrix; in turn, phago­cytosis is inhibited in the meshwork, causing increased debris buildup and physical obstruction of the outflow system.9 Although some degree of acute IOP elevation is expected because the injection adds volume to the eye, the incidence of sustained IOP elevation after injection of anti-VEGF agents can be as high as 15%.10

    The proposed mechanisms for sus­tained IOP elevation include chronic inflammation, trabecular meshwork obstruction, and damage to the trabec­ular meshwork by the anti-VEGF agent or by particles from the compounding or packaging process. The risk of chron­ic or long-term IOP elevation appears to be higher for patients with preex­isting glaucoma, those with a history of steroid-induced IOP elevation, and those who receive frequent injections.

    Management. Topical aqueous suppressants are the first-line treatment and will adequately control IOP in most cases. If the response to aqueous suppressants is inadequate, incisional glaucoma surgery may be required.

    Panretinal Photocoagulation

    The reported rates of transient IOP elevation after panretinal photocoag­ulation vary widely, from 34% to 97% of cases, and the pressure usually rises immediately after the procedure.11 A high amount of laser energy may cause elevated IOP and ciliary body conges­tion, raising the risk of angle closure.

    When the angle is open, there can be various reasons for IOP elevation, including blood-retinal barrier break­down causing fluid movement from the choroid into the vitreous; ciliary body congestion causing decreased uveo­scleral outflow; and episcleral venous compression by a contact lens, leading to blockage of aqueous outflow.

    Management. IOP elevation after panretinal photocoagulation usually is self-limited and resolves spontaneously. However, cycloplegia and aqueous sup­pression may be needed in refractory cases.

    Takeaway Messages

    After any vitreoretinal procedure, early recognition and prompt treatment of IOP elevation, with or without glau­coma, are essential to reduce the risk of glaucomatous damage and visual decline. Gonioscopy is a crucial tool to identify the underlying mechanism re­sponsible for the IOP rise. The choice of treatment depends on the pathophysi­ology, degree of IOP elevation, and risk or severity of glaucomatous damage. Management options include medical therapy, laser treatment, and surgical intervention. A multidisciplinary approach that involves vitreoretinal specialists is vital to optimize outcomes for patients.

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    1 Kawana K et al. Ophthalmology. 2006;113(1):36-41.

    2 Mansoori T et al. J Curr Ophthalmol. 2022;33(4):444-448.

    3 Honavar SG et al. Ophthalmology. 1999;106(1):169-176;discussion 177.

    4 Kanclerz P et al. J Ophthalmol. 2018;2018:8606494.

    5 Kornmann HL et al. Curr Opin Ophthalmol. 2016;27(2):125-131.

    6 Siegfried CJ, Shui Y. Am J Ophthalmol. 2019;203:12-25.

    7 Roth DB et al. Ophthalmology. 2009;116(3):455-460.

    8 Chin EK et al. Retina. 2017;37(7):1345-1351.

    9 Jones R et al. Current Opin Ophthalmol. 2006;17(2):163-167.

    10 Hoguet A et al. Ophthalmology. 2019;126(4):611-622.

    11 Tsai JC et al. J Glaucoma. 1995;4(1):45-48.

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    Dr. Paulose is an ophthalmology resident and Dr. Vinod is a glaucoma specialist and associate pro­fessor of ophthalmology. Both are at New York Eye and Ear Infirmary of Mount Sinai in New York, New York. Financial disclosures: None.