Good Hope, Heartlands, and Solihull Eye Clinics

Retinal vein occlusion: notes for professionals

David Kinshuck

Blood tests

For older patients

  • 20% RVO recur if cause not addressed
  • blood pressure  <140/80 in clinic
  • FBC, ESR or CRP, lipids, U & Es, Creatinine, eGFR, HbA1c, TSH
  • an ECG will identify a large heart....this would need treatment to lower blood pressure
  • homocysteine, atherosclerotic and thrombophilic
  • ? obstructive sleep apnea  Arch 2010
  • Polycythaemia...need HCT < 45% NEJM 2013
  • ( HTMHFR homozygous O14)

For younger patients review specialist articles see and see and see.

Laser to prevent rubeosis

  • older patients have more ischaemic eyes and are more likely to need laser
  • eyes at risk
    • afferent pupil defect
    • vision 6/36-6/60 or worse
    • lots of retinal ischaemia
    • those with deteriorating vision..this indicates increasing ischaemia see
    • BRVO very unlikely to develop rubeosis, CRVO much more
      (hemispherical RVO in between)
    • older patients
    • > 30 disc areas of ischaemia
  • treat risk factors as above to protect the other eye etc
  • laser 3000 burns 0.02 seconds x 3+ sessions or so if significant ischaemia
    (argon laser...heavier burns than diabetes settings)
  • where time allows (seldom in the UK) review each month to laser when rubeosis evident (iris or angle). This is controversial...about 50% of ophthalmologists like to laser before rubeosis, including DK, that is lasering all severely ischaemic eyes.
  • consider indirect laser
  • CRVO: some patients will need laser for NVD and NVE, not just NVG. Patients with BRVO and hemispherical RVO may need grid laser for CSME especially if oedema substantial, but there is little prospect of improving sight. This is on the basis that increasing/severe CSME may cause even more visual loss.
  • to detect eyes whish may become rubeotic examine the minor arterial circle of the iris with the slit lamp, see
  • look for peripheral ischaemia Retina 2011; risk of rubeosis Retina 2012

Laser for CSME from a branch retinal vein occlusion

If available and there is considerable CSME, anti-VEGF will be more effective.

My current technique (modified from PubMed)

grid laser for CSME

Always laser more than 1 disc diameter from the fovea, further away if the surgeon is inexperienced or the patient is moving.
Laser in green, slow repeat, move away from fovea with small subthreshold burns. If the burn is visible, turn the power a little lower. Laser between vessels as shown. If there is no vessel, 'imagine' one, as a line between 2 two landmarks. The strategy is aimed at avoiding the fovea at all costs. Always know where you are. Anti-VEGF more effective.

 

Laser for/to prevent retinal new vessels

  • If there is lots of retinal ischaemia, retinal new vessels can develop
  • this can follow a severe branch retinal occlusion
  • more likely to follow a central retinal vein occlusion..the more severer forms
  • if the new vessels grow they are likely to bleed and then cause a retinal detachment
  • I would prefer to laser to prevent these....any eye with lots of retinal ischaemia
  • use the PRP settings as for diabetes as here
  • small burns cause less field defect
  • Subthreshold laser may help BJO 2011

Laser to treat rubeosis (NVG) in CRVO, after V Chong

Rubeosis really needs combination treatment

  • Anti-VEGF injection to stop the rubeosis (and this may need to be repeated [regular treatment is not needed]) Anti-VEGF is probably first choice treatment for rubeotic glaucoma, if available
  • cyclodiode laser to lower the pressure (and this may need to be repeated)
  • Once the pressure is down and the retinal view clear, PRP argon laser.

Cyclodiode

  • 1500-2000mw, 1500-2000ms, higher settings for NVG than in a seeing eye
  • good peribulbar anaesthesia....this is very painful without
  • 40 spots, 10 each quadrant, clean plate first, try to avoid pops
  • test laser first on black paper as laser 'wire' fibres become damaged and power can drop off
  • transilluminate for ciliary processes (especially young patients and myopes)
  • after laser, maxidex qid, atropine 1% bd, also ibuprofen 600mg bd
    (note contraindications to ibuprofen), stop anti-glaucoma therapy
  • see 2-3 weeks
  • retreat if necessary. (In practice only very few patients need 3 treatments, and none more.)
  • aim of treatment is to keep a comfortable eye, not really to treat the pressure
  • laser of the ischaemic none-perfused retina (when the eye is treated with anti-VEGF injections) is not needed Retina 2013

If your clinic is getting a lot of patients with NVG, increase prevention such as treating risk factors and more laser as above. There is a lot of controversy in the timing of laser in severe CRVO. Some people laser more (and think they prevent more NVG) others laser less (and think they get no more NVG).

 

Incipient RVO

Treat incipient RVO actively to prevent progression, lower eye pressure if borderline

The other eye may be at risk Retina15

 

Identify ocular ischaemic syndrome

See This can be identified by FFA features:

  • delayed and patchy filling
  • venous tortusosity and beading
  • mid-peripheral blot haemorrhages
  • more often bilateral, one eye may have good vision

Epidemiology etc

Incidence is 2/1000 over 5 years. Risk factors include

  • blood pressure
  • abnormalities of FBC, ESR or viscosity , total protein, immunoglobulins, fasting blood sugar
  • hyperlipidaemia
  • smoking (controversial)
  • Dodson reports a direct relationship between RVO and platelet glycoprotein genetic differences. This is in the GpIa/IIa complex, which initiates platelet adhesion at the start of a thrombosis. Strangely, it is not related to DVTs. It seems to synergistically with other factors.
  • high homocysteine  and here  Many patients have high homocysteine levels. There may be a genetic cause of this, but levels can be lowered (and vascular occlusions generally be prevented) by a healthy diet with 9 (men) 7 (women) portions of vegetables/fruit/day.  See how to lower levels.
  • factor 12 deficiency
  • other genes see
  • Ten-year incidence of retinal vein occlusion in an older population: the Blue Mountains Eye Study : age, blood pressure, and obesity are related.
  • 15 year study, Klein . Analysis suggest migraine increases risk of branch rvo, diabetes central, and so on. The burden of RVO  Eye 11
  • Prevalence/associations India Retina 2013

For younger patients

  • the 'pill', which should be stopped
  • HRT, which should be stopped
  • Protein C or S abnormalities (anticoagulants needed), factor V leiden
  • APL syndrome (antiphospholipid antibody) (need anticoagulation)
  • ask about mouth ulcers...if present and recurrent consider Behcets

Pathogenesis

  1. genetic differences as above
  2. shorter eyes are also linked to RVO's short axial length
  3. artery & vein are in close contact, in the optic nerve or in a sheath in the retina
  4. artery presses on vein
  5. endothelium is damaged also (a separate mechanism)
  6. thrombin forms
  7. thrombin & occlusion extends
  8. inflammation in vessel wall
  9. angiogenesis of occluded vessel
  10. (vein bursts and retinal haemorrhages evident)
  11. multiple vascular channels develop
  12. microaneurysms develop
  13. vein re-canalises, but retina damaged around
  14. healthy cells produce HIF (hypoxic inducing factor), but this is rapidly broken down
  15. in hypoxia, it is not broken down, and stimulates cells to make VEGF
  16. Studies confirm the concentration of AC VEGF is directly proportional to the risk of rubeosis.
  17. serous detachments..look for peripharal abnormalities Retina 12
  18. inflammation after the rvo JAMA 13
  19. collaterals are not related to better visual outcome  Retina 14

Intravitreal triamcinolone (IVT)

We have nearly stopped using this treatment and prefer intravitreal steroid implants, Avastin & laser, see. IVT was considered as a new treatment for the macular oedema that occurs with retinal vein occlusion, see. IVT may improve the sight, but the effect may not last long. There are risks, see , 10% patients developed severe glaucoma.

  • Complications are discussed here,  but the standard dose is 2mg
  • A recent paper suggests the IVT is best given early for best results (Oh 07)
  • Cheng 2009: triamcinolone no benefit versus Avastin and more adverse events
  • Moschos...benefit is temporary
  • For branch retinal vein occlusions this SCORE report suggests 1mg intravitreal triamcinolone & grid laser is no more effective than grid laser alone, but the 1 mg dose was safer than the 4 mg dose. Laser is best, Score 6
  • For central retinal vein occlusions in this SCORE report IVT repeated at regular intervals, improves vision by 25%
  • For central rvo, comparing IVT to IVA (triamcinolone to Avastin) IVT reduces oedema more but causes more side effects (glaucoma) Tao 2010
  • does not influence shunt vessels Retina 2013

Osardex (intravitreal seroid implant)

Anti-VEGF in RVO

 

Anti-VEGF Central

  • now standard treatment
  • start early...much more effective
  • wil need retreatment
  • PRP laser also if lots of retinal ischaemia
  • stop treatment if poor response
  • treatment  plan Eye 16 , here modified here considerably

CRVO 3 monthly injections anti-VEGF

oct

 

Complete responder fluid on oct
  • follow up increasing interval
partial response poor response

continue injections

? extend interval between injections

dexamethasone implant
consider PRP laser; look for ischaemic areas clinically or with FFA

 

Anti-VEGF hemispherical

  • also sector PRP laser also if lots of retinal ischaemia
  • stop treatment if poor response

Anti-VEGF branch

Case 1 (cases presented at Congress) bus driver

  • 57 y bus driver
  • hand movements..svere CRVO, very ischaemic
  • anti-VEGF and and PRP laser..but will not get enough sight back to drive bus

Case 2

  • afro-carribean, hyertensive, diabetes, longstanding macular oedema from retinal vein occlusion, no response to anti-VEGF

Case 3

  • brvo, cmo, osardex, vision improved, repeated osardex, cataract, phaco, removed, CMO still, prp sector, do you continue osardex?

Case 4

  • 66y patient,, small brvo, cmo, lucentis reduced oedema, stayded dry, patient discharged or virtual clinic?

Case 7

  • severe cme, dry with lucentis, recurred, patient had MI

Case 8

  • patient pregnant, no injections, new vessels developed, had PRP laser, delived baby, then avastin

Notes about anti-VEGF

A mild then later a much more severe central retinal vein occlusion

This situation is not uncommon: a patient presents with reasonable vision and and central rvo with haemorrhages. But 4 months later, the sight becomes much worse and the haemorrhages (and ischaemia) increases (laser etc is needed).
Recent suggestions indicate such a patient might have had a second vein occlusion. Such a patient illustrated here. We cannot explain the 'second' occlusion; the high viscosity (ESR) may be relevant.

 

possibly a second retinal vein occlusion
November
CF vision; lots of haemorrhages, more macular oedema
July
6/12 vision, scattered retinal haemorrhages
Male, 86y, minor rvo July. in November much worse. BP ok, high CRP & ESR  (ESR 35) enlarge