Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

CRVO: uncomplicated

1st line – observation plus management of underlying risk factors

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ACUTE
|
CRVO: uncomplicated
1st line – 

observation plus management of underlying risk factors

The main goal of treatment of an uncomplicated central retinal vein occlusion (CRVO), whether it is ischemic or nonischemic, is observation and management of underlying risk factors.

Concomitant medical conditions such as hypertension, atherosclerosis, hyperlipidemia, diabetes mellitus, glaucoma, vasculitis, or hypercoagulable states should be treated if present.

The patient should be closely monitored to detect complications such as macular edema and neovascularization. Patients with ischemic CRVO should be followed more frequently than those with nonischemic CRVO.

CRVO with macular edema

1st line – intravitreal therapy plus management of underlying risk factors

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ACUTE
|
CRVO with macular edema
1st line – 

intravitreal therapy plus management of underlying risk factors

Concomitant medical conditions such as hypertension, atherosclerosis, hyperlipidemia, diabetes mellitus, glaucoma, vasculitis, or hypercoagulable states should be treated if present.

Therapy includes intravitreal injection of a vascular endothelial growth factor (VEGF) inhibitor such as ranibizumab, aflibercept, or bevacizumab.[30][31][32][34][35][36][37][38]

Intravitreal triamcinolone acetonide or dexamethasone (implant) may be considered for persisting macular edema.[39][40][41][42][43][44][45][46][47] [ Cochrane Clinical Answers logo ]

A common approach is to initiate treatment with a VEGF inhibitor. Optical coherence tomography (OCT) can be used to evaluate response to treatment. If there is a good response to treatment after several monthly injections, then the injection interval may be increased.[48] If macular edema persists after several monthly injections, an intravitreal corticosteroid may then be considered, usually to complement anti-VEGF therapy initially (rather than corticosteroid monotherapy). [ Cochrane Clinical Answers logo ]

Only ranibizumab, aflibercept, and dexamethasone implant are approved for the treatment of RVO-associated macular edema. One systematic review reported clinically meaningful improvement in visual acuity and central retinal thickness for up to 5 years in patients treated with VEGF inhibitors or dexamethasone.[49]​ A subsequent systematic review found that VEGF inhibitors are recommended over intravitreal corticosteroids due to fewer adverse effects and better visual outcomes when corticosteroids are given 6-monthly.[50]

Factors to consider when deciding between VEGF inhibitors and intravitreal corticosteroids include duration of action (e.g., depot or implanted corticosteroids may have longer-lasting effects than VEGF inhibitors) and adverse effects (e.g., corticosteroids are associated with cataract progression and IOP elevation, whereas most of the adverse effects of VEGF inhibitors are associated with the intravitreal injection procedure). The long-term adverse effects of VEGF inhibition are not known. A systematic review comparing these two drug classes demonstrated that while dexamethasone required fewer injections, it was less efficacious in treating macular edema than VEGF inhibitors.[51] Intravitreal triamcinolone is preferable to a dexamethasone implant when a patient is aphakic or has an anterior chamber intraocular lens. Migration of the implant into the anterior chamber can lead to corneal edema which requires prompt surgical intervention.

Intravitreal injection with any agent can be complicated by endophthalmitis, retinal detachment, cataract, intraocular pressure elevation, and vitreous hemorrhage.

Primary options

ranibizumab intravitreal: 0.5 mg intravitreally into the affected eye(s) every 4 weeks

OR

aflibercept intravitreal: 2 mg intravitreally into the affected eye(s) every 4 weeks

More

OR

bevacizumab: 1.25 mg intravitreally into the affected eye(s) every 4-6 weeks

Secondary options

ranibizumab intravitreal: 0.5 mg intravitreally into the affected eye(s) every 4 weeks

or

aflibercept intravitreal: 2 mg intravitreally into the affected eye(s) every 4 weeks

More

or

bevacizumab: 1.25 mg intravitreally into the affected eye(s) every 4-6 weeks

-- AND --

triamcinolone intravitreal: 4 mg intravitreally into the affected eye(s) every 3 months

or

dexamethasone intravitreal: 0.7 mg implant injected intravitreally into the affected eye(s) every 3-6 months

OR

triamcinolone intravitreal: 4 mg intravitreally into the affected eye(s) every 3 months

OR

dexamethasone intravitreal: 0.7 mg implant injected intravitreally into the affected eye(s) every 3-6 months

CRVO with neovascularization

1st line – panretinal photocoagulation plus management of underlying risk factors

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ACUTE
|
CRVO with neovascularization
|
with neovascular glaucoma
1st line – 

panretinal photocoagulation plus management of underlying risk factors

Concomitant medical conditions such as hypertension, atherosclerosis, hyperlipidemia, diabetes mellitus, glaucoma, vasculitis, or hypercoagulable states should be treated if present.

Panretinal photocoagulation (PRP) is application of laser energy to the retinal periphery for 360°.

It should not be used until the appearance of retinal or anterior segment neovascularization.[53]

The goal of PRP is to prevent further vision loss and to prevent the onset of neovascular glaucoma.

Plus – intraocular pressure control

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ACUTE
|
CRVO with neovascularization
|
with neovascular glaucoma
Plus – 

intraocular pressure control

Treatment recommended for ALL patients in selected patient group

Intraocular pressure can be controlled with ophthalmic beta-blockers, alpha-2 agonists, carbonic anhydrase inhibitors, prostaglandin analogs, or glaucoma surgery.

1st line – panretinal photocoagulation plus management of underlying risk factors

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ACUTE
|
CRVO with neovascularization
|
with vitreous hemorrhage or tractional retinal detachment
1st line – 

panretinal photocoagulation plus management of underlying risk factors

Concomitant medical conditions such as hypertension, atherosclerosis, hyperlipidemia, diabetes mellitus, glaucoma, vasculitis, or hypercoagulable states should be treated if present.

Panretinal photocoagulation (PRP) is application of laser energy to the retinal periphery for 360°.

It should not be used until the appearance of retinal or anterior segment neovascularization.[53]

The goal of PRP is to prevent further vision loss and to prevent the onset of neovascular glaucoma.

Plus – pars plana vitrectomy

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ACUTE
|
CRVO with neovascularization
|
with vitreous hemorrhage or tractional retinal detachment
Plus – 

pars plana vitrectomy

Treatment recommended for ALL patients in selected patient group

A pars plana vitrectomy involves the surgical placement of a vitreous cutter, an infusion cannula, and a third instrument into the vitreous cavity through 3 sclera incisions located in the pars plana.

The primary objective is removal of the vitreous humor.

BRVO or HRVO: uncomplicated

1st line – observation plus management of underlying risk factors

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ACUTE
|
BRVO or HRVO: uncomplicated
1st line – 

observation plus management of underlying risk factors

The main goal of treatment of an uncomplicated branch retinal vein occlusion (CRVO) or hemiretinal vein occlusion (HRVO), whether it is ischemic or nonischemic, is observation and management of underlying risk factors.

Concomitant medical conditions such as hypertension, atherosclerosis, hyperlipidemia, diabetes mellitus, glaucoma, vasculitis, or hypercoagulable states should be treated if present.

The patient should be closely monitored to detect complications such as macular edema and neovascularization. Patients with ischemic BRVO or HRVO should be followed more frequently than those with nonischemic BRVO or HRVO.

BRVO or HRVO with macular edema

1st line – intravitreal therapy plus management of underlying risk factors

Back
ACUTE
|
BRVO or HRVO with macular edema
|
duration ≤3 months
1st line – 

intravitreal therapy plus management of underlying risk factors

Concomitant medical conditions such as hypertension, atherosclerosis, hyperlipidemia, diabetes mellitus, glaucoma, vasculitis, or hypercoagulable states should be treated if present.

Therapy includes intravitreal injection of a VEGF inhibitor such as ranibizumab, aflibercept, or bevacizumab.[37][59]​​[60][61]​​[62][63][64][65][66][82]​​ Intravitreal triamcinolone acetonide or dexamethasone (implant) may be considered for persisting macular edema.[47]​​[67]​​[71]

A common approach is to initiate treatment with a VEGF inhibitor. Optical coherence tomography (OCT) can be used to evaluate response to treatment. If there is a good response to treatment after several monthly injections, then the injection interval may be increased.[48] If macular edema persists after several monthly injections, an intravitreal corticosteroid may then be considered, usually to complement anti-VEGF therapy initially (rather than corticosteroid monotherapy).

Only ranibizumab, aflibercept, and dexamethasone are approved for the treatment of RVO-associated macular edema. All three agents have been studied in patients with BRVO-associated macular edema of <3 months' duration.

Factors to consider when deciding between VEGF inhibitors and intravitreal corticosteroids include duration of action (e.g., depot or implanted corticosteroids may have longer-lasting effects than VEGF inhibitors) and adverse effects (e.g., corticosteroids are associated with cataract progression and IOP elevation, whereas most of the adverse effects of VEGF inhibitors are associated with the intravitreal injection procedure). The long-term adverse effects of VEGF inhibition are not known. A systematic review comparing these two drug classes demonstrated that while dexamethasone required fewer injections, it was less efficacious in treating macular edema than VEGF inhibitors.[51] Intravitreal triamcinolone is preferable to a dexamethasone implant when a patient is aphakic or has an anterior chamber intraocular lens. Migration of the implant into the anterior chamber can lead to corneal edema which requires prompt surgical intervention. 

Intravitreal injection with any agent can be complicated by endophthalmitis, retinal detachment, cataract, intraocular pressure elevation, and vitreous hemorrhage.

Primary options

ranibizumab intravitreal: 0.5 mg intravitreally into the affected eye(s) every 4 weeks

OR

aflibercept intravitreal: 2 mg intravitreally into the affected eye(s) every 4 weeks

More

OR

bevacizumab: 1.25 mg intravitreally into the affected eye(s) every 4-6 weeks

Secondary options

ranibizumab intravitreal: 0.5 mg intravitreally into the affected eye(s) every 4 weeks

or

aflibercept intravitreal: 2 mg intravitreally into the affected eye(s) every 4 weeks

More

or

bevacizumab: 1.25 mg intravitreally into the affected eye(s) every 4-6 weeks

-- AND --

triamcinolone intravitreal: 4 mg intravitreally into the affected eye(s) every 3 months

or

dexamethasone intravitreal: 0.7 mg implant injected intravitreally into the affected eye(s) every 3-6 months

OR

triamcinolone intravitreal: 4 mg intravitreally into the affected eye(s) every 3 months

OR

dexamethasone intravitreal: 0.7 mg implant injected intravitreally into the affected eye(s) every 3-6 months

1st line – grid laser photocoagulation plus management of underlying risk factors

Back
ACUTE
|
BRVO or HRVO with macular edema
|
duration >3 months and eligible for laser treatment
1st line – 

grid laser photocoagulation plus management of underlying risk factors

Concomitant medical conditions such as hypertension, atherosclerosis, hyperlipidemia, diabetes mellitus, glaucoma, vasculitis, or hypercoagulable states should be treated if present.

Grid laser photocoagulation can be considered for patients with macular edema persisting for >3 months, despite intravitreal therapy, or for those patients who cannot receive corticosteroids (e.g., because of advanced or uncontrolled glaucoma). Grid laser photocoagulation involves the application of laser energy in a grid configuration in areas of leakage (as seen on fluorescein angiography) in the macula.

The Branch Vein Occlusion Study (BVOS) classified eligibility for laser treatment as follows: visual acuity worse than 20/40, <5 disk areas of nonperfusion on fluorescein angiography, no hemorrhage in the foveal center, and duration of disease of at least 3 months.[68] [ Cochrane Clinical Answers logo ]

Patients in the BRAVO study were eligible to receive grid laser photocoagulation if needed.[60] Eligibility for laser treatment was as follows: visual acuity ≤20/40 or central subfield thickening ≥250 micrometers and <5 letters or <50 micrometer improvement compared with the visit 3 months prior. Additionally, macular hemorrhage had to have resolved.

The BVOS found that eyes treated with grid laser photocoagulation had improved vision and less macular edema than untreated eyes at 3 years' follow-up.[69] 

The utilization of grid laser alone or in combination with ranibizumab has been investigated, and grid laser was not shown either to improve eventual visual function or to prolong time between anti-VEGF injections (i.e., reduce treatment burden).[70] [ Cochrane Clinical Answers logo ]

1st line – intravitreal therapy plus management of underlying risk factors

Back
ACUTE
|
BRVO or HRVO with macular edema
|
duration >3 months and ineligible for laser treatment
1st line – 

intravitreal therapy plus management of underlying risk factors

Concomitant medical conditions such as hypertension, atherosclerosis, hyperlipidemia, diabetes mellitus, glaucoma, vasculitis, or hypercoagulable states should be treated if present.

The Branch Vein Occlusion Study (BVOS) classified eligibility for laser treatment as follows: visual acuity worse than 20/40, <5 disk areas of nonperfusion on fluorescein angiography, no hemorrhage in the foveal center, and duration of disease of at least 3 months.[68] [ Cochrane Clinical Answers logo ]  

Patients in the BRAVO study were eligible to receive grid laser photocoagulation if needed.[60] Eligibility for laser treatment was as follows: visual acuity ≤20/40 or central subfield thickening ≥250 micrometers and <5 letters or <50 micrometer improvement compared with the visit 3 months prior. Additionally, macular hemorrhage had to have resolved.

If ineligible for laser treatment, then therapy includes intravitreal injection of a VEGF inhibitor such as ranibizumab, aflibercept, or bevacizumab.[37][59]​​[60]​​[62][63][64][65][66][82]​​ Intravitreal triamcinolone acetonide or dexamethasone (implant) may be considered for persisting macular edema.[47]​​[67]​​[71]

A common approach is to initiate treatment with a VEGF inhibitor. Optical coherence tomography (OCT) can be used to evaluate response to treatment. If there is a good response to treatment after several monthly injections, then the injection interval may be increased.[48] If macular edema persists after several monthly injections, an intravitreal corticosteroid may then be considered, usually to complement anti-VEGF therapy initially (rather than corticosteroid monotherapy).

Only ranibizumab, aflibercept, and dexamethasone are approved for the treatment of RVO-associated macular edema.

Factors to consider when deciding between VEGF inhibitors and intravitreal corticosteroids include duration of action (e.g., depot or implanted corticosteroids may have longer-lasting effects than VEGF inhibitors) and adverse effects (e.g., corticosteroids are associated with cataract progression and IOP elevation, whereas most of the adverse effects of VEGF inhibitors are associated with the intravitreal injection procedure). The long-term adverse effects of VEGF inhibition are not known. A systematic review comparing these two drug classes demonstrated that while dexamethasone required fewer injections, it was less efficacious in treating macular edema than VEGF inhibitors.[51] Intravitreal triamcinolone is preferable to a dexamethasone implant when a patient is aphakic or has an anterior chamber intraocular lens. Migration of the implant into the anterior chamber can lead to corneal edema which requires prompt surgical intervention. 

Intravitreal injection with any agent can be complicated by endophthalmitis, retinal detachment, cataract, intraocular pressure elevation, and vitreous hemorrhage.

Primary options

ranibizumab intravitreal: 0.5 mg intravitreally into the affected eye(s) every 4 weeks

OR

aflibercept intravitreal: 2 mg intravitreally into the affected eye(s) every 4 weeks

More

OR

bevacizumab: 1.25 mg intravitreally into the affected eye(s) every 4-6 weeks

Secondary options

ranibizumab intravitreal: 0.5 mg intravitreally into the affected eye(s) every 4 weeks

or

aflibercept intravitreal: 2 mg intravitreally into the affected eye(s) every 4 weeks

More

or

bevacizumab: 1.25 mg intravitreally into the affected eye(s) every 4-6 weeks

-- AND --

triamcinolone intravitreal: 4 mg intravitreally into the affected eye(s) every 3 months

or

dexamethasone intravitreal: 0.7 mg implant injected intravitreally into the affected eye(s) every 3-6 months

OR

triamcinolone intravitreal: 4 mg intravitreally into the affected eye(s) every 3 months

OR

dexamethasone intravitreal: 0.7 mg implant injected intravitreally into the affected eye(s) every 3-6 months

BRVO or HRVO with neovascularization

1st line – scatter laser photocoagulation plus management of underlying risk factors

Back
ACUTE
|
BRVO or HRVO with neovascularization
1st line – 

scatter laser photocoagulation plus management of underlying risk factors

Concomitant medical conditions such as hypertension, atherosclerosis, hyperlipidemia, diabetes mellitus, glaucoma, vasculitis, or hypercoagulable states should be treated if present.

Scatter laser photocoagulation, applied directly to areas of nonperfusion, reduces the incidence of retinal neovascularization in patients with nonperfused (5 disk areas of nonperfusion on fluorescein angiography) branch retinal vein occlusion (BRVO) by 50%, from 40% of affected patients to 20% of affected patients.[68]

Scatter laser also reduces the number of patients who develop vitreous hemorrhage.[68]

Scatter laser should only be performed once neovascularization has developed, because a large percentage of patients with nonperfused BRVO never develop neovascularization.[68]

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Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer

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