CRVOMuhammad Hatab

Anatomy

Epidemiology• The prevalence ranges from 0.7% in patients aged 49-60 years to

4.6% in patients older than 80 years.

• Nonischemic CRVO:• 10% resolve completely• 50% vision may be 6/60 or worse.• One third the ischemic type(6-12 months)

• Ischemic CRVO:• > 90% final visual acuity may be 6/60 or worse. • > 60% Anterior segment neovascularization (with NVG). (few

weeks and up to 1-2 years afterward).

Pathophysiology

Clinical Presentation

Symptoms:• Blurred vision

VA of an eye with pure CRVO at first presentation will never be below 0.05

• The usual VA is 0.1– 0.5

Clinical PresentationEarly features

Late features• Venous sheathing • Resorption of

hemorrhages, • Macular pigment

disturbance, • Collateral vessels

at the arcade and optociliary shunt vessels on the optic nerve.

Workup

• Laboratory Studies??• Imaging Studies• Color Doppler imaging• OCT

Workup• FFA

When & Why?

Ischemic vs Non-ischemic

• Four functional tests1. Relative afferent pupillary defect (RAPD)2. Electroretinography (ERG)3. Visual fields 4. Visual acuity

• Two morphologic tests 1. Fluorescein fundus angiography2. Ophthalmoscopy

Ischemic vs Non-ischemic

Differential DiagnosisCharacteristic difference Differential diagnosis

No peripheral bleedings Anterior ischemicneuropathy

EarlyCRVO

No drop in visual acuity Papilledema

Both eyes involved Hypertensive retinopathyDiabetic retinopathyHyperviscosity syndrome

Dot and blot bleedingsNot marked papilledema

Ocular ischemia

No collaterals on papilla Geographic atrophy oflate AMD

LateCRVO

No leakage in fluorescein angiogram

Neovascular disease

Natural Course

• 32% of non-ischemic and 85 % of ischemic CRVO eyes result in a visual acuity of 0.1 or less after 1 year

• The better the initial visual acuity, the better the final outcome.

• The lower the initial visual acuity, the sooner iris neovascularization develops

Natural Course

• Even non-ischemic CRVO may develop iris neovascularization

• The overall rate of neovascular disease is 16 %, ranging from 10 % in perfused eyes to 40 % in non-perfused eyes

• Patients with low vision must be observed closely during the first weeks and months so as not to miss neovascular disease

Natural Course

Reasons for a poor outcome ?• The continuous breakdown of the blood

retinal barrier leads to chronic macularedema or exudative retinal detachment

• The ischemic inner retina with still functioning photo-receptor cells causes neovascular complications.

Natural Course

Unfavorable factors in CRVO that may cause a poor prognosis

Signs

Ischemic CRVO (iris neovascularization within weeks)Bleedings in central cystsDark, widespread dense bleedingsVery low initial visual acuity ≤ 0.05

Ophthalmologicfactors

Badly treated arterial hypertensionDiabetic retinopathyPatients’ age over 80 years

General factors

Complications

• Ocular neovascularizationAnterior segment neovascular glaucoma. Posterior segment vitreous hemorrhage.NVI > NVD > NVE

• Macular edemaCME lamellar or full-thickness macular hole

• Cellophane maculopathy and macular pucker

• Optic atrophy

Treatment

• The goal of CRVO therapy should be to prevent:1. Chronic macular edema and macular scarring2. Neovascular complications

• The main treatments can be divided into two categories: 1. Early intervention to improve the visual outcome2. Late treatment to avert painful blinding

Early Treatment

• Medical Care• No known effective medical treatment is

available for either the prevention of or the treatment of central retinal vein occlusion (CRVO)

• Lowering of risk factors may inhibit CRVO’s progression from a non-ischemic to the ischemic form, or reduce the frequency of recurrences or involvement of the second eye

Early TreatmentTreatment Rationale

Lowering blood pressureHyperlipidemia

Cardiovascular risk factors

Carbogen inhalationDrug-induced

Vasodilatation

Coumarin, heparinLowering platelet aggregation

Anticoagulation

Systemic fibrinolysis high dose Systemic fibrinolysis low dose Selective fibrinolysis Retinal endovascular lysis

Intravitreal lysis

Thrombolysis

Isovolemic hemodilution Hypervolemic hemodilution

Hypovolemic hemodilution

Blood viscosity

Systemic corticosteroids Intravitreal

Steroids

Intravitreal injection

• Triamcinolone ( 1- 4 mg/0.1 ml)• Bevacizumab ( 1.25 mg/ 0.05 ml)• Ranibizumab (0.3 mg or 0.5 mg )• Aflibercept ( 2mg)• Dexamethasone intravitreal implant (0.35 mg

and 0.7 mg)

Surgical Care• Laser photocoagulation• CVOS concluded that prophylactic PRP did not prevent the

development of iris neovascularization and recommended to wait for the development of early iris neovascularization and then apply PRP.

• Argon green laser usually is used (1500–2000 x500 μm x0.05–0.1 sec)• If ocular media is hazy for laser to be applied, cryoablation of the

peripheral fundus is performed.• About 16-32 transscleral cryo spots are applied from ora serrata

posteriorly.• Macular grid photocoagulation was effective in reducing

angiographic evidence of macular edema, but it did not improve visual acuity in eyes with reduced vision due to macular edema from CVO Not recommended

Surgical Care

• Chorioretinal venous anastomosis

• Radial optic neurotomy

• Vitrectomy

Summary of recommendations for management of CRVO