Secondary glaucoma occurs after various vitreoretinal surgeries. The procedures involved include pars plana vitrectomy (PPV), scleral buckling, panretinal photocoagulation (PRP), intravitreal anti-VEGF drug administration, intravitreal triamcinolone acetonide injection (IVTA), silicone oil tamponade, and intraocular gas injection.
The pathophysiology of intraocular pressure elevation is classified into open-angle mechanisms, angle-closure mechanisms, or both1). Gas tamponade can induce significant intraocular pressure spikes1). The trabecular meshwork can be obstructed by neovascularization due to proliferative retinopathy, scarring, pigment dispersion, inflammation, or cellular debris from retinal outer segments (Schwartz syndrome)1).
Risk factors vary by surgical procedure, but a history of glaucoma or ocular hypertension is a common risk factor across procedures1)2). In the early postoperative period, management focuses on inflammation and intraocular pressure, and most cases can be controlled with eye drops or oral medications.
Within 48 hours after vitrectomy, about 60% of patients show a rapid increase in intraocular pressure (IOP) of 5–22 mmHg, and about 36% exceed 30 mmHg. There is no significant difference between preoperative IOP and late postoperative IOP, and the increase is often transient.
Clinical findings after vitreoretinal surgery include fibrin exudation in the anterior chamber, silicone oil bubbles in the anterior chamber, angle closure, pupillary block, and ciliochoroidal detachment.
The rate of required intervention on day 1 after macular hole surgery is 4.7% (95% CI 3.0–13.9), with the most common reason being elevated IOP2). In the iFTMH group, 6% had IOP elevation exceeding 30 mmHg 2). Among cases with IOP elevation, 50% had a history of glaucoma or ocular hypertension, and 80% had used gas tamponade2).
QWhat patterns of intraocular pressure elevation are seen after retinal surgery?
A
Although it varies by surgical procedure, acute IOP spikes are common within 48 hours after vitrectomy. After panretinal photocoagulation, they are detected within 2 hours after treatment. Silicone oil-related elevation can occur from early to several months later. Anti-VEGF agents are reported to cause acute transient elevation as well as sustained elevation with repeated injections. With IVTA, about 40% exceed 24 mmHg at 6 months after injection. Most cases are transient and controllable with medication, but persistent cases may require surgical intervention.
Combined with scleral buckling, scatter photocoagulation, PVR
Scleral buckling
Narrow angle, encircling band, high myopia, older age
Silicone oil
Pre-existing glaucoma, DM, aphakia
Intraocular gas
High concentration use, C3F8, combined photocoagulation
Vitrectomy: Combined with scleral buckling, intraoperative scatter endophotocoagulation, and combined pars plana lensectomy increase risk. Vitrectomy for proliferative vitreoretinopathy has a higher likelihood of postoperative intraocular pressure elevation compared to macular hole repair. Fibrin formation is also a risk factor for secondary glaucoma.
Scleral buckling: Pre-existing narrow angle, use of encircling band and placement anterior to the equator, high myopia, older age, and postoperative ciliochoroidal detachment are predisposing factors.
Panretinal photocoagulation: Laser energy may affect incidence and severity. Age and type of diabetes do not influence.
Anti-VEGF: Bevacizumab (9.9%) has a higher prevalence of intraocular pressure elevation than ranibizumab (3.1%). Presence of pre-existing glaucoma and increased injection frequency are also risks.
IVTA: Pre-existing POAG or OHT, family history of glaucoma in first-degree relatives, age (bimodal at 6 years and older age), connective tissue disease, type 1 diabetes, and high myopia are predisposing factors.
Silicone oil: Pre-existing glaucoma, diabetes, and aphakia are major risk factors 1). Amount of emulsified silicone oil in the anterior chamber and use of heavy tamponade agents are associated with postoperative intraocular pressure elevation.
Intraocular gas: High concentration use of expansile gas, use of C3F8, older age, intraoperative photocoagulation, combined lensectomy, combined circumferential scleral buckling, and anterior chamber fibrinous exudate are associated.
IOP measurement: Use a Goldmann applanation tonometer or Perkins tonometer. In gas-tamponade eyes, measure in the sitting position.
Gonioscopy: Differentiation between open-angle and angle-closure determines treatment strategy. Check for peripheral anterior synechiae (PAS), neovascularization, and silicone oil bubbles.
Anterior chamber examination: Evaluate fibrin exudation, silicone oil in the anterior chamber, and inflammatory cells using a slit lamp.
Fundus examination: Check for recurrence of retinal detachment, residual gas bubble volume, and optic disc status.
Postoperative review should at minimum include visual acuity assessment, IOP measurement, slit-lamp examination of the anterior and posterior segments, and measurement of residual gas bubble volume 2)3). During postoperative follow-up, also watch for steroid-induced ocular hypertension (usually appearing 7–14 days after surgery) 2). If postoperative day 1 review is omitted, careful consideration should be given to management of expansile gas concentration and prophylactic IOP-lowering medication 2).
Aqueous suppressants: Beta-blockers (timolol) and carbonic anhydrase inhibitors (dorzolamide, oral acetazolamide) are first-line.
Cycloplegics: For angle closure due to ciliary body edema, wait for spontaneous resolution with mydriatics. Be cautious with pilocarpine as it may exacerbate ciliary body tension and worsen the condition.
Anti-inflammatory drugs: For IOP elevation associated with postoperative inflammation, use steroid eye drops 1). However, in steroid responders, IOP may paradoxically increase.
Prophylactic administration: If postoperative day 1 review is omitted, apraclonidine 1% eye drops (2 hours before surgery and at the end of surgery) or timolol 0.5%/dorzolamide 2% combination eye drops (at the end of surgery) significantly reduce IOP spikes 2).
In silicone oil-related glaucoma, topical medications including cycloplegics, steroids, beta-blockers, and prostaglandin analogs achieve IOP control in 30–78% of cases.
Laser iridotomy: Indicated for angle-closure glaucoma due to pupillary block. Prophylactic treatment before surgery may be considered for eyes with narrow angles
Laser iridoplasty: Effective for angle closure after scleral buckling that is resistant to drug therapy. It opens the angle and promotes aqueous outflow
Laser gonioplasty/goniosynechialysis: May be highly effective after the acute phase of angle closure due to ciliary body edema
Transscleral cyclophotocoagulation (CPC): Indicated when the risk of retinal detachment from silicone oil removal is unacceptable or in eyes with poor visual prognosis1)
Anterior chamber paracentesis: Performed to urgently relieve extremely high intraocular pressure
Gas removal: In cases of gas overfill, intraocular pressure is lowered by removing gas from the posterior segment
Silicone oil removal: Expected to relieve mechanical obstruction of the trabecular meshwork, but there are reports of persistent intraocular pressure elevation in all eyes even after removal. It must be weighed against the risk of retinal detachment1)
Aqueous tube shunt: Standard filtration surgery has a poor prognosis due to conjunctival scarring from previous retinal surgery, making drainage devices a more effective option 1). The success rate of inferotemporal Ahmed glaucoma shunt is reported as 86% at 6 months and 76% at 1 year after implantation
Endoscopic cyclophotocoagulation: An option for eyes that require simultaneous silicone oil removal and glaucoma treatment 1)
QHow is intraocular pressure elevation due to silicone oil managed?
A
First, topical medications (beta-blockers, prostaglandin analogs, etc.) are initiated, which can control pressure in 30-78% of cases. Prophylactic peripheral iridectomy at the 6 o’clock position is performed to prevent pupillary block. If medication fails to control pressure, silicone oil removal is considered, but pressure elevation may persist after removal, requiring balance with the risk of retinal detachment. In refractory cases, transscleral cyclophotocoagulation or aqueous drainage devices (e.g., Ahmed shunt) are effective options. Conventional filtration surgery has a poor prognosis due to conjunctival scarring.
Gas expansion: Occurs when expansion of an intraocular gas bubble exceeds the outflow rate of intraocular fluid without angle closure
Inflammation: Trabecular meshwork obstruction by inflammatory and cellular debris 2). Inflammation is more severe in proliferative diseases with breakdown of the blood-ocular barrier accompanied by fibrin deposition
Silicone oil-related (early): TM obstruction due to migration of silicone oil into the anterior chamber. Often caused by overfill 1)
Silicone oil-related (intermediate): Emulsified SO migrates into the anterior chamber. SO particles partially phagocytosed by macrophages accumulate in the trabecular meshwork (TM) of the superior quadrant, inducing trabeculitis 1)
Silicone oil-related (late): Long-term contact between SO and TM leads to permanent structural changes 1)
Steroid response: Appears usually 7–14 days after postoperative steroid eye drops 2). Involves trabecular meshwork microstructural changes, increased substance deposition, and protease inhibition
Blood-mediated mechanism: TM obstruction by red blood cell breakdown products (ghost cells)
Anti-VEGF-related: Immediate elevation due to injection volume, direct inhibition of TM and uveoscleral outflow pathways, chronic trabeculitis
Pupillary block: Pupillary block by intraocular gas, silicone oil, fibrin, or IOL causes anterior displacement of the lens-iris diaphragm
Ciliary body edema (angle rotation): Scleral buckling impairs vortex vein drainage → ciliary congestion and swelling → anterior rotation of the ciliary body around the scleral spur → angle closure. Includes pupillary block due to mydriasis in narrow-angle eyes and secondary pupillary block from inflammatory posterior synechiae
After panretinal photocoagulation: Ciliary body swelling or fluid shift from choroid to vitreous due to temporary breakdown of the blood-retinal barrier displaces the lens-iris diaphragm anteriorly
Open-angle mechanisms
Gas expansion: When expansion exceeds outflow, intraocular pressure rises
Inflammatory TM obstruction: Caused by debris, fibrin, and ghost cells 2)
Pupillary block: caused by gas, silicone oil, fibrin, or IOL
Angle rotation: ciliary body edema → anterior rotation of the scleral spur axis → angle closure
After panretinal photocoagulation: fluid shift from choroid to vitreous → anterior displacement of the lens-iris diaphragm
Regarding intraocular gas injection, SF6 expands to 2–2.5 times the injected volume, and C3F8 expands to 4 times. Adjusting the concentration to 20% or less for SF6 and 12% or less for C3F8 can avoid unexpected expansion. Maximum gas expansion occurs approximately 24 hours after injection for SF6 and 72 hours for C3F8, but the expansion rate is highest in the first 6 hours, and intraocular pressure elevation begins immediately after gas injection.
After several weeks, attention should also be paid to neovascularization of the iris and angle, as well as side effects of steroid eye drops. In diseases with severe retinal ischemia such as diabetic retinopathy, note that neovascularization may occur postoperatively even if not present preoperatively. In silicone oil-filled eyes after several months or more, intraocular pressure elevation due to emulsified silicone oil can occur.
QWhat are the mechanisms of intraocular pressure elevation after retinal surgery?
A
They are broadly divided into open-angle and angle-closure types. In the open-angle type, causes include gas expansion, trabecular meshwork obstruction by inflammation or debris, silicone oil migration into the anterior chamber, steroid response, and ghost cells (red blood cell breakdown products). In the angle-closure type, the main mechanisms are pupillary block due to gas or silicone oil, and angle rotation due to ciliary body edema. Silicone oil-related mechanisms vary by time: early (anterior chamber migration), intermediate (emulsified SO accumulation, trabeculitis), and late (TM structural changes). Treatment is selected according to the mechanism, so accurate diagnosis by gonioscopy is important.
In the 2023 BEAVRS survey (response rate 35%), 63% of facilities omit the day 1 review 2). Among facilities that omit the day 1 review, 34% perform follow-up within 1 week postoperatively, and 50% within 2 weeks 2). When omitting day 1 review, careful consideration of expansive gas concentration management and prophylactic IOP-lowering medication is recommended 2).
Two RCTs have reported the preventive effect on postoperative IOP spikes 2).
Benz et al.: In an RCT of 50 eyes, timolol 0.5%/dorzolamide 2% fixed combination (administered at the end of surgery) significantly reduced postoperative IOP compared to placebo.
Sciscio & Caswell: In an RCT of 26 eyes with iFTMH, apraclonidine 1% (2 hours before surgery plus at the end of surgery) significantly reduced day 1 postoperative IOP compared to placebo.
Population-based studies show that after combined scleral buckling and vitrectomy or vitrectomy alone, the 10-year cumulative probability of developing glaucoma is 8.9% (95% CI 3.8–14%), significantly higher than 1.0% (95% CI 0–2.4%) in the control group (P=0.02). However, another retrospective study of 111 eyes with a mean follow-up of 49 months found no long-term intraocular pressure elevation, indicating discrepancies between reports.
In anti-VEGF therapy, a prospective study of 312 patients with retinal vein occlusion found that by 60 months, 8% experienced an intraocular pressure increase of ≥10 mmHg from baseline, and 1.6% exceeded 35 mmHg. Switching to OCT-guided PRN dosing may help reduce the risk of sustained intraocular pressure elevation.
Late intraocular pressure elevation has been reported in approximately 4% of cases at 4 years2).
