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For older patients

• blood pressure
• FBC, ESR or viscosity
• fasting blood sugar and lipids
• lupus anticoagulent and anti-phospholipid antibody
• U & Es, Creatinine, TSH
• an ECG will identify a large heart....this would need treatment to lower blood pressure
• homocysteine

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

• add thrombophilia screen, especially if patient has had other venous-thromboembolic disease
• this includes factor V leiden, antithrombin 111, protein C & S

• older patients have more ischaemic eyes and are more likely to need laser
• young patients may need systemic steroids as above
• 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 1500 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 was 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.
• Chorio-retinal anastomosis laser does not seem to maintain vision (initial studies suggested it may), this is being investigated further as results are unclear
• to detect eyes whish may become rubeotic examine the minor arterial circle of the irs with the slit lamp, see

CSME = clinically significant macular oedema.

My current technique (modified from PubMed)

• area centralis lens
• 50 microns
• 0.05 seconds
• grid pattern...laser...2 spaces ...burn
• ~80 mw, more if there is oedema (~130mw)
• first 2 laser session no FFA
• if oedema reamins after 2 gird lasers, FFA, then laser applied to ischaemic area ONLY as defined by FFA
• if CSME recent, consider IVT or IVA
• these are the same settings used for a macular grid for diabetes

• If there is lots of retinal ischaemia, retinal vew vessels can develop
• this can follow asevere 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 cuase 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

PRP as above, but is this is not possible, either accept (eye may become painful as well as blind) or treat

• IVA is probably first choice treatment for rubeotic glaucoma, of available
  
  
• cyclodiode see
• but follow up is not long yet as this is a new technique
• treat if painful
• 1500-2000mw, 1500-2000ms, higher settings for NVG than in a seeing eye
• leave 11 o'clock-1 o'clock space unlasered
• 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 2-3months
• 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

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).

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

This is experimental, some results are good. Results are not yet consistent and are not recommended for general use as yet.

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

Incidence is 2/1000 over 5 years

Risk factors include

• blood pressure
• abnormalities of FBC, ESR or viscosity , total protein, immunoglobulins, fasting blood sugar
• hyperlipaemia
• smoking (controversial)
• Dodson reports a direct relationship between RVO and platelet glycoprotein genetic differences. This is in the GpIa/IIa complex, which intiates 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 homocyteine levels. There may be a gentic cause of this, but levels can be lowered (and vascular occlusions generally be prevented) by a healthy diet woth 9 (men) 7 (women) portions of vegetables/fruit/day.
• 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

For younger patients

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

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 separated mechanism)
6. thrombin forms
7. thrombin & occlusion extends
8. inflammation in vessel wall
9. angiogensis of occluded vessel
10. (vein bursts and retinal haemorrhages evident)
11. multiple vascular channels develop
12. micoraneurysms 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 ot the risk of rubeosis.

IVT is emerging 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 .

This paper used 8mg and showed definite benefit. The same author discussed complications here,  but the standard dose is 4mg. A recent paper suggests the IVT is best given early for best results.  Moschos...benefit is temporary

Intravitreal bevacizumab (Avastin) treatment of macular edema in central retinal vein occlusion: a short-term study.   Intravitreal Avastin is likely to be extremely helpful, and usually improves sight if given early. Full article.

Kreutzer...34 patients,repeated injections, some vision improvement