Retinal Vein Occlusion

•   CRV bifurcates at laminar cribrosa and divides into 4 main veins (supertemporal/nasal and interotemporal/nasal)

•   20% of the time CRV bifurcates inside the nerve

Definition

Types of retinal vein occlusion:

•   CRVO

o   Non-ischaemic – 75%

o   Ischaemic – 25%

-   Defined by evidence of neovasculaisation on the surface of the iris or ischaemia (defined by angiography) of area greater than 10x size of optic disc.

•   Hemi-CRVO

o   Ischaemic

o   Nonischaemic

•   BRVO

o   Major branch

o   Macular branch

 

Epidemiology

•   Overall Prevalence            5.2/1000

•   BRVO                              4.42/1000

•   CRVO                              0.8/1000

•   M=F

•   Chance of second eye involvement within 4 years = 7%

•   Increases with age – 50% of cases are >65yrs age

Pathogenesis/risk factors

•   Pathogenesis

o   CRVO

-   Occlusion occurs in the region of the lamina cribrosa

-   Vein and artery share a common adventitial sheath

-   A thickened and rigid artery at this site may compress the thin walled vein

o   BRVO

-   Occlusion occurs at sites of AV crossing

-   There is however often no clear evidence of ongoing venous compression at the site of an occlusion

-   It is suggested the artery intermittently compressing the vein results in damage to the vessel wall with resultant turbulence and eventual thrombosis

 

•   Local risk factors:

o   Elevated IOP

•   Systemic risk factors:

o   HTN

-   CRVO OR (of having HTN) 3.8, BRVO OR 3.0

o   Hyperlipidaemia

-   Both types OR 2.5

o   DM

-   OR 1.5 (CRVO OR 2.0, BRVO OR 1.1)

o   Atherosclerotic vascular disease

•   Other disease associations:

o   Vasculitis – SLE, sarcoid, syphilis

o   Neoplasia – leukaemia, myeloma

o   Medications – OCP, diuretics

•   Haematological disorders

o   No trials large enough to elucidate link with thrombophilia

o   Probably more likely in patients <65 and without cardiovascular risk factors

o   Hyperhomocystinaemia – significant risk elevation in some studies

o   Thrombophilia

-   Factor V leiden/APC resistance – significance in some studies (OR 1.49)

-   Protein C and S deficiency, PT gene mutation, ATIII – Possible link but NS in trials to date

-   Antiphospholipid syndrome – significant

Clinical

•   Sudden painless visual loss

•   Macular oedema is the most important cause of reduced vision

•   Retinal haemorrhages

o   Flame shaped, dot or blot

o   Dilated tortuous veins

o   +/- optic disc oedema

o   Hard exudates – yellow lipid deposits at the junction of the normal and oedematous retina

o   Cotton wool spots – ischaemia of the nerve axons

•   BRVO distribution

o   Superotemporal – 66%

o   Inferotemporal – 43%

Investigations/Diagnosis

•   Diagnosis based on clinical appearance.

•   Determination of ischaemia is of importance in determining prognosis and need for treatment. Predictors of ischaemia are:

o   Defined by fluorescein angiogram (however very arbitrary cutoff – spectrum of risk)

o   Very poor poor visual acuity (i.e. 6/120 ~ hand movements)

o   Presence of RAPD

•   Flourescein angiography

o   Useful to

-   Confirm occlusion

-   Extent of retinal non-perfusion (to allow definition as ischaemic)

-   To distinguish neovascularisation from venous collateral/shunt vessels

-   Acutely 50-60% of patients may have non-diagnostic scan due to swelling

o   Indication for use in BRVO:

•   OCT

o   Used to measure macular oedema

o   Gauge treatment response

Prognosis

•   Causes of visual loss

o   Macular oedema

o   Retinal ischaemia

o   Secondary complications

-   Vitreous haemorrhage

-   Retinal detachment

-   Neovascular glaucoma

•   BRVO

o   >50% of eyes achieve >6/12

•   CRVO

o   Non-ischaemic

o   ­­­­­­­­­­­­Ischaemic

 

Treatment

•   No evidence for aspirin or anticoagulation

•   If ischaemic/significant macula oedema

o   Anti-VEGF

o   Pan retinal laser