Post-vitrectomy glaucoma is a form of secondary glaucoma that encompasses elevated intraocular pressure occurring after various vitreoretinal surgeries, including pars plana vitrectomy (PPV), scleral buckling, panretinal photocoagulation (PRP), silicone oil (SO) tamponade, and intraocular gas injection.
The pathophysiology of elevated intraocular pressure is classified into open-angle mechanisms, angle-closure mechanisms, or both 1). In open-angle mechanisms, ghost cells (degenerated red blood cells), inflammatory debris, silicone oil emulsification, steroid response, and retinal outer segment fragments (Schwartz syndrome) obstruct the trabecular meshwork1). In angle-closure mechanisms, pupillary block due to gas bubbles, silicone oil, or fibrin, and anterior rotation of the angle due to ciliary body edema are the main mechanisms.
Risk factors vary by surgical procedure, but a history of glaucoma or ocular hypertension is a common risk factor across procedures 1)2). Management primarily involves early postoperative intraocular pressure control and inflammation control, and most cases can be managed with medication. Gas tamponade can cause significant intraocular pressure spikes 1). Long-standing retinal detachment may lead to ischemic neovascularization, and neovascular glaucoma after vitrectomy tends to be refractory.
The incidence of elevated intraocular pressure for each surgical procedure is shown below.
In population-based studies, the cumulative probability of developing glaucoma over 10 years after combined scleral buckling and vitrectomy or vitrectomy alone is 8.9% (95% CI 3.8–14%), which is significantly higher than 1.0% (95% CI 0–2.4%) in the control group (P=0.02).
QHow often does intraocular pressure elevation occur after retinal surgery?
A
It varies greatly depending on the surgical procedure. After vitrectomy, intraocular pressure elevation occurs in 20–60% of cases, but it is often transient. After panretinal photocoagulation, the rate is high at 32–94%, but spontaneous resolution is common. Silicone oil-related cases range from 2.2–56% depending on the report, and the presence of pre-existing glaucoma or aphakia influences the risk. Long-term, the cumulative probability of developing glaucoma over 10 years is reported to be 8.9%.
Eye pain: Occurs with elevated intraocular pressure. Often accompanied by conjunctival injection1)
Blurred vision: Caused by corneal edema or anterior chamber inflammation
Visual loss: Severe and sustained intraocular pressure elevation can lead to optic nerve damage3)
In ghost cell glaucoma, intraocular pressure rises some time after vitreous hemorrhage. The degree of pressure elevation varies depending on the amount of ghost cells migrating into the anterior chamber, but it persists for weeks to months. When pressure elevation is marked, symptoms associated with high intraocular pressure such as corneal edema, eye pain, and nausea occur.
After retinal photocoagulation, shallow anterior chamber, corneal edema, and ciliary injection similar to primary angle-closure glaucoma attack occur, with symptoms including eye pain, headache, and nausea. It is characteristic that these appear several hours after PRP.
Clinical Findings (Findings Confirmed by Physician Examination)
Khaki-colored vesicles are observed in the anterior chamber and vitreous. When ghost cells are abundant, they may form pseudohypopyon. Gonioscopy reveals ghost cells deposited on the lower trabecular meshwork.
It presents as unilateral open-angle glaucoma with relatively large cells in the anterior chamber. Small tears are often located in the far periphery, such as the ora serrata or ciliary body. Over time, strand-like structures may appear under the detached retina. Lens abnormalities (cataract, dislocation, etc.) are also common. It is more frequent in young males, often with a history of blunt trauma or atopic dermatitis.
The rate of required intervention on postoperative day 1 after macular hole surgery is 4.7% (95% CI 3.0–13.9), with the most common reason being elevated intraocular pressure2). In the iFTMH group, 6% had intraocular pressure exceeding 30 mmHg 2). Among cases with elevated intraocular pressure, 50% had a history of glaucoma or ocular hypertension, and 80% had gas tamponade2).
QWhat patterns of intraocular pressure elevation are seen after retinal surgery?
A
It varies by surgical procedure. After vitrectomy, acute intraocular pressure spikes are common within 48 hours. After panretinal photocoagulation, it is detected within 2 hours after treatment. Silicone oil-related elevation can occur from early to several months later. Ghost cell glaucoma develops 1–3 months after vitreous hemorrhage and is characterized by khaki-colored vesicles in the anterior chamber. Schwartz syndrome appears as unilateral open-angle intraocular pressure elevation in eyes with rhegmatogenous retinal detachment.
Combined with scleral buckle, scatter photocoagulation, PVR
Scleral buckling
Narrow angle, encircling band, high myopia, older age
Silicone oil
Pre-existing glaucoma, diabetes, aphakia
Intraocular gas
High concentration use, C3F8, combined photocoagulation
Vitrectomy: Combined use with scleral buckling, intraoperative scatter endophotocoagulation, and concurrent pars plana lensectomy increase the 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 an encircling band placed anterior to the equator, high myopia, older age, and postoperative ciliochoroidal detachment are predisposing factors.
Panretinal photocoagulation: Laser energy level can affect the incidence and severity. It is more likely to occur when a large number of coagulations are performed extensively at once or when the intervals between coagulations are short.
Anti-VEGF: Bevacizumab (9.9%) has a higher prevalence of intraocular pressure elevation than ranibizumab (3.1%). Presence of pre-existing glaucoma and increased frequency of administration are also risk factors.
IVTA: Pre-existing POAG or OHT, family history of glaucoma in first-degree relatives, age (bimodal distribution 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 the main risk factors 1). The amount of emulsified silicone oil in the anterior chamber and the use of heavy tamponade agents are associated with postoperative intraocular pressure elevation.
Intraocular gas: High concentration of expansile gas, use of C3F8, older age, intraoperative photocoagulation, combined lensectomy, combined encircling scleral buckle, and fibrin exudation in the anterior chamber are associated.
Poor prognostic factors in neovascular glaucoma: When neovascular glaucoma develops after vitrectomy, age under 50 years and history of vitrectomy are poor prognostic factors.
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, anterior chambersilicone oil, and inflammatory cells using slit-lamp microscopy.
Fundus examination: Check for recurrence of retinal detachment, residual gas bubble, and optic disc status.
Ultrasound biomicroscopy (UBM): Useful for elucidating pathology, excellent for detecting anterior displacement of the ciliary body and choroidal detachment.
Anterior segment OCT: Allows non-contact evaluation of the degree of angle closure and presence of pupillary block.
B-scan ultrasonography: Used to search for retinal detachment and intraocular lesions when media opacities are present.
Ghost cell glaucoma: Diagnosed definitively by anterior chamber paracentesis and identification of ghost cells with degenerated hemoglobin residues (Heinz bodies) inside the cell membrane.
Schwartz syndrome: Difficult to diagnose based on anterior segment findings alone, but easy if rhegmatogenous retinal detachment is confirmed. Retinal breaks are often difficult to detect due to poor dilation or lens disease; use scleral depression, B-mode ultrasound, UBM, or OCT to search for breaks.
After retinal photocoagulation: History of PRP is key. Anterior segment findings are identical to primary angle-closure glaucoma; differentiate by presence of choroidal detachment or ciliary body anterior rotation on UBM or OCT.
Acute primary angle-closure glaucoma: Angle closure occurs primarily without history of vitreoretinal surgery.
Neovascular glaucoma: Develops due to worsening retinal ischemia after surgery. Neovascularization of the iris and angle is present.
Steroid-induced glaucoma: Open-angle IOP elevation due to postoperative steroid eye drops. Usually appears 7–14 days after surgery 2).
Malignant glaucoma (ciliary block glaucoma): Aqueous misdirection due to anterior rotation of the ciliary body. The anterior chamber is extremely shallow.
Postoperative follow-up should include at minimum: visual acuity assessment, IOP measurement, slit-lamp examination of the anterior and posterior segments, and measurement of residual gas bubble volume 2)3).
Aqueous suppressants: Beta-blockers (timolol) and carbonic anhydrase inhibitors (dorzolamide eye drops, oral acetazolamide) are first-line.
Mydriatics: For secondary angle-closure glaucoma due to pupillary block, try mydriatic eye drops (Mydrin P) to relieve the block. If unsuccessful, iridectomy or lens extraction is needed.
Anti-inflammatory agents: For IOP elevation due to postoperative inflammation, use steroid eye drops 1). However, in steroid responders, IOP may paradoxically increase.
Prophylactic administration: When skipping the postoperative day 1 review, apraclonidine 1% eye drops (2 hours before surgery + at the end of surgery) or timolol 0.5%/dorzolamide 2% combination eye drops (at the end of surgery) significantly reduce intraocular pressure spikes 2)
Specific prescription examples after retinal photocoagulation
The following prescriptions may be used in combination as appropriate.
Diamox tablets (250 mg) 3 tablets, 3 times daily
Aspara potassium tablets (300 mg) 3 tablets, 3 times daily
Timoptol XE ophthalmic solution (0.5%) once daily
Most cases are transient and spontaneous resolution can be expected. Surgical procedures such as iridotomy or suprachoroidal fluid drainage are rarely required.
Specific prescription examples for ghost cell glaucoma
Depending on the degree of intraocular pressure elevation, the following eye drops are used in combination. If intraocular pressure is sufficiently lowered, discontinue in the order 4) to 1).
In silicone oil-related glaucoma, topical medications including mydriatics, steroids, beta-blockers, and prostaglandin analogs achieve intraocular pressure control in 30–78% of cases.
Laser iridotomy: Indicated for angle-closure glaucoma due to pupillary block. Prophylactic treatment may be considered in eyes with narrow angles before surgery.
Laser iridoplasty: Effective for angle closure after scleral buckling that is resistant to medical therapy. It opens the angle and facilitates aqueous outflow.
Laser gonioplasty/goniosynechialysis: May be highly effective after the acute phase of angle closure due to ciliary body edema.
Anterior chamber paracentesis: Performed to emergently relieve extremely high intraocular pressure.
Gas removal: In cases of gas overfill, intraocular pressure is reduced by removing gas from the posterior segment.
Anterior chamber washout + vitrectomy: Removes ghost cells as a causative treatment for ghost cell glaucoma. If pressure reduction is insufficient, consider outflow reconstruction, filtering surgery, or tube shunt surgery.
Silicone oil removal: Expected to relieve mechanical obstruction of the trabecular meshwork, but some reports indicate persistent intraocular pressure elevation after removal 1). The risk of retinal detachment must be weighed.
Management of refractory cases
Aqueous tube shunt surgery: Standard filtering surgery (trabeculectomy) has poor prognosis due to conjunctival scarring from retinal surgery, making drainage devices a more effective option 1). After vitrectomy, a long tube inserted into the pars plana is indicated. The success rate of inferotemporal Ahmed shunt is reported as 86% at 6 months and 76% at 1 year.
Transscleral cyclophotocoagulation (CPC): Indicated when the risk of retinal detachment from silicone oil removal is unacceptable or in eyes with poor visual prognosis 1).
Endoscopic cyclophotocoagulation: An option in eyes requiring simultaneous silicone oil removal and glaucoma treatment 1).
Cyclodestructive surgery: Includes transscleral cyclophotocoagulation and cyclocryotherapy. These procedures aim to suppress aqueous humor production, but it is difficult to quantify the effect, and if aqueous production decreases excessively, it can lead to phthisis bulbi (shrinkage of the eyeball). Therefore, they are considered a last resort when other surgeries such as filtration surgery are ineffective.
Retinal reattachment is the principle of treatment. Since peripheral retinal breaks are common in young patients, scleral buckling is the first choice of surgical procedure. Vitrectomy or combined cataract surgery may also be selected. If retinal reattachment is successful, intraocular pressure normalizes, and postoperative pressure-lowering medications are rarely needed.
Surgical management of neovascular glaucoma (postoperative)
When neovascular glaucoma develops after vitrectomy, tube shunt surgery is effective. It is indicated when intraocular pressure cannot be lowered by conventional trabeculectomy. After vitrectomy, a long tube inserted through the pars plana is a good option. Preoperative intravitreal injection of anti-VEGF drugs (bevacizumab) reduces perioperative hyphema. The rate of intraocular pressure control to 21 mmHg or below is reported to be approximately 60%.
QHow is intraocular pressure elevation due to silicone oil managed?
A
First, topical medications (beta-blockers, prostaglandin analogs, carbonic anhydrase inhibitors, etc.) are initiated, and pressure can be controlled in 30–78% of cases. Prophylactic peripheral iridectomy at the 6 o’clock position may be performed to prevent pupillary block. If medication fails to control pressure, silicone oil removal is considered, but pressure elevation may persist after removal, and the risk of retinal detachment must be weighed. In refractory cases, transscleral cyclophotocoagulation or aqueous drainage devices (e.g., Ahmed shunt) are effective options, while 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.
Inflammatory trabecular obstruction: Obstruction of the trabecular meshwork by inflammatory and cellular debris 2). Inflammation is more severe in cases with blood-ocular barrier breakdown 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): Migration of emulsified silicone oil into the anterior chamber. Silicone oil particles partially phagocytosed by macrophages accumulate in the trabecular meshwork of the superior quadrant, inducing trabeculitis 1).
Silicone oil-related (late): Long-term contact between SO and TM causes permanent structural changes1)
Steroid response: Appears usually 7–14 days after postoperative steroid eye drops2). Involves trabecular meshwork microstructural changes, increased substance deposition, and protease inhibition
Anti-VEGF-related: Immediate elevation due to injection volume, direct inhibition of TM and uveoscleral outflow, chronic trabeculitis
When vitreous hemorrhage occurs due to surgery, trauma, or retinal disease, red blood cells remain in the vitreous for several weeks or more. The cellular contents are mostly absorbed, leaving only degenerated hemoglobin, forming hollow ghost cells. These ghost cells are less deformable than fresh red blood cells, making it difficult for them to pass through the trabecular meshwork when they migrate into the anterior chamber. Consequently, they obstruct the trabecular meshwork and elevate intraocular pressure.
Red blood cells must be trapped in the vitreous for several weeks (time needed for degeneration into ghost cells)
The anterior vitreous face must be disrupted, creating communication between the vitreous and anterior chamber (pathway for ghost cells to migrate into the anterior chamber)
In rhegmatogenous retinal detachment, photoreceptor outer segments shed into the subretinal space reach the anterior chamber along with viscous subretinal fluid, obstructing the trabecular meshwork. The relatively large cells observed in the anterior chamber correspond to these photoreceptor outer segments.
Pupillary block: Pupillary block caused by intraocular gas, silicone oil, fibrin, or IOL displaces the lens-iris diaphragm anteriorly. In aphakic eyes, silicone oil or a protruding vitreous face can cause pupillary block1)
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 eyes with narrow angles and secondary pupillary block from inflammatory posterior synechiae
After panretinal photocoagulation: Proposed mechanisms include anterior displacement of the vitreous, lens, and ciliary body due to serous choroidal detachment; ciliary body edema from impaired venous drainage; and choroidal perfusion impairment due to breakdown of the blood-retinal barrier. This is more likely when extensive coagulation is performed over a large area at once or when coagulation intervals are short.
Open-Angle Mechanism
Gas expansion: When expansion exceeds outflow, intraocular pressure rises.
Inflammatory TM obstruction: Caused by debris, fibrin, or ghost cells 2).
SO-related 3 stages: Migration into anterior chamber → emulsified SO accumulation → TM structural changes 1).
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 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, 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
It is broadly divided into open-angle and angle-closure types. Open-angle type is caused by gas expansion, trabecular meshwork obstruction due to inflammation or debris, migration and emulsification of silicone oil into the anterior chamber, steroid response, ghost cells, and photoreceptor outer segments (Schwartz syndrome). Angle-closure type is mainly due to pupillary block by gas or silicone oil, and forward rotation of the angle (angle rotation) due to ciliary body edema. Silicone oil-related mechanisms differ by time: early (migration into anterior chamber), 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 omitted the day 1 review 2). Among facilities omitting the day 1 review, 34% performed follow-up within 1 week postoperatively, and 50% within 2 weeks 2). When omitting day 1 review, careful consideration of expansile gas concentration management and prophylactic IOP-lowering medication is recommended 2).
Two RCTs have reported the preventive effect on postoperative intraocular pressure spikes 2). One study reported that administration of timolol 0.5%/dorzolamide 2% fixed combination at the end of surgery significantly reduced postoperative IOP compared to placebo. Another study reported that apraclonidine 1% (2 hours preoperatively plus at the end of surgery) significantly reduced day 1 postoperative IOP compared to placebo 2).
In a population-based study, after combined scleral buckling and vitrectomy or vitrectomy alone, the cumulative probability of developing glaucoma over 10 years was 8.9% (95% CI 3.8–14%), which was significantly higher than 1.0% (95% CI 0–2.4%) in the control group (P=0.02). However, another retrospective study of 111 eyes found no long-term IOP elevation over a mean follow-up of 49 months, indicating variability among reports.
Late IOP elevation has been reported in approximately 4% at 4 years 2).
In anti-VEGF therapy, a prospective study of 312 patients with retinal vein occlusion found that by 60 months, 8% experienced an IOP elevation of 10 mmHg or more from baseline, and 1.6% exceeded 35 mmHg. Sustained IOP elevation with repeated injections is suggested to be due to chronic trabeculitis. Switching to OCT-guided PRN dosing may be useful in reducing the risk of sustained IOP elevation.
