Central retinal vein occlusion refer ak khurana
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AK Khurana ophthalmology central retinal vein occlusion CRVO
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I now have all the material needed. Let me compile a comprehensive AK Khurana-style answer on Central Retinal Vein Occlusion.
Central Retinal Vein Occlusion (CRVO)
Note: AK Khurana's Comprehensive Ophthalmology is not in the library catalogue. The following is structured according to Khurana's well-known syllabus format, drawing from Kanski's Clinical Ophthalmology (10th ed.) — the authoritative ophthalmology reference available — supplemented with standard teaching points from Khurana's curriculum.
Anatomy Recap
The central retinal vein (CRV) and central retinal artery share a common adventitial sheath as they pass through the optic nerve, posterior to the lamina cribrosa. Atherosclerotic changes in the artery at this confined crossing can compress and occlude the CRV — this is the anatomical basis of CRVO.
Pathogenesis
Thrombosis occurs at or posterior to the lamina cribrosa, where the CRV is most vulnerable. Three mechanisms contribute (Virchow's triad):
- Endothelial damage — from adjacent atherosclerotic artery or inflammation
- Turbulent flow — at the narrow shared sheath crossing
- Hypercoagulability — thrombophilic states amplify risk
Once occlusion occurs → ↑ venous and capillary pressure → stagnation → retinal hypoxia → capillary endothelial damage → extravasation of blood + fluid → liberation of VEGF → macular oedema and neovascularization.
Risk Factors
| Category | Factors |
|---|---|
| Most important | Age >65 years (>50% of cases) |
| Systemic | Hypertension (2/3 of patients >50 yrs), hyperlipidaemia (1/3), diabetes mellitus (~15%) |
| Ocular | Open-angle glaucoma/ocular hypertension (major ocular risk factor), hypermetropia, shorter axial length |
| Young patients | Oral contraceptive pill (most common in young females), thrombophilia (hyperhomocysteinaemia, antiphospholipid Ab, Factor V Leiden), vasculitis (Behçet, sarcoidosis, Wegener's), myeloproliferative disorders |
| Others | Smoking, dehydration, chronic renal failure |
Classification
CRVO is classified into three types:
1. Impending (Partial) CRVO
- Occurs in younger patients; may be artificial distinction from mild non-ischaemic CRVO
- Symptoms: absent or minor transient blurring, worse on waking
- Fundus: mild venous dilatation and tortuosity, few scattered dot-blot haemorrhages, mild macular oedema
- Prognosis: usually good; some progress to ischaemic CRVO
2. Non-ischaemic CRVO (Venous Stasis Retinopathy)
- More common than ischaemic; ~1/3 progress to ischaemic CRVO within months
Clinical features:
- Symptoms: Sudden painless monocular fall in VA (variable degree)
- RAPD: Absent or mild
- Fundus:
- Tortuosity and dilatation of all 4 quadrant retinal veins
- Dot, blot, and flame haemorrhages — mild to moderate extent
- Cotton-wool spots, disc oedema, macular oedema — common but mild
- Patchy (perivenular) areas of capillary non-perfusion on FA
- Prognosis: Vision returns to normal/near-normal in ~50% if non-ischaemic; VA >6/60 usually portends better outcome
3. Ischaemic CRVO (Haemorrhagic Retinopathy)
- Substantially decreased retinal perfusion with extensive capillary closure and retinal hypoxia
Clinical features:
- Symptoms: Sudden, severe monocular painless visual loss; occasionally painful (NVG)
- VA: Usually counting fingers or worse
- RAPD: Present (important differentiating sign from non-ischaemic)
- Fundus:
- Severe tortuosity and engorgement of all CRV branches
- Extensive deep blot + flame haemorrhages in all 4 quadrants (periphery + posterior pole) — classic "Blood and Thunder" fundus
- Prominent cotton-wool spots (infarcts)
- Optic disc swelling and hyperaemia
- NVI (Rubeosis iridis): Develops in ~50%, usually 2–4 months post-occlusion → "100-day glaucoma" / "90-day glaucoma"
- FA: Markedly delayed arteriovenous transit, extensive capillary non-perfusion (>10 disc areas), vessel wall staining and leakage
- ERG: Depressed (used to assess neovascular risk)
Differentiating Ischaemic vs Non-ischaemic CRVO
| Feature | Non-ischaemic | Ischaemic |
|---|---|---|
| VA | Variable, often better than 6/60 | Usually CF or worse |
| RAPD | Absent/mild | Present |
| Cotton-wool spots | Few | Numerous/prominent |
| Haemorrhages | Moderate | Extensive ("blood and thunder") |
| Capillary non-perfusion on FA | <10 disc areas | >10 disc areas |
| NVI/NVG | Rare | ~50% |
| ERG | Near normal | Depressed |
| Prognosis | Better | Very poor |
Systemic Assessment
All patients:
- Blood pressure, fasting glucose, lipids
- ESR/plasma viscosity, FBC, urea/electrolytes/creatinine
- ECG
Additional in patients <50 years, bilateral CRVO, or recurrent CRVO:
- Thrombophilia screen: antiphospholipid Ab, protein C/S, factor V Leiden, homocysteine
- Autoimmune screen: ANA, ANCA
Complications
- Macular oedema — commonest cause of chronic poor vision
- Rubeosis iridis (NVI) → Neovascular glaucoma — "100-day glaucoma"
- Vitreous haemorrhage (from retinal NV)
- Macular ischaemia → permanent VA loss
- Epiretinal membrane, subretinal fibrosis (rare)
Management
Systemic
Control hypertension, diabetes, hyperlipidaemia. Investigate for underlying cause.
Treatment of Macular Oedema
Indicated when VA <6/9 and/or central macular thickness >250 μm on OCT:
| Treatment | Key Trial | Outcome |
|---|---|---|
| Intravitreal anti-VEGF (ranibizumab, aflibercept, bevacizumab) | CRUISE (ranibizumab), COPERNICUS (aflibercept) | First-line; monthly injections × 6 months improve VA vs placebo |
| Intravitreal dexamethasone implant (Ozurdex) | GENEVA study | Effective; risk of IOP rise and cataract |
| Intravitreal triamcinolone | SCORE study | >3 lines improvement in 25% vs 7% controls; 1 mg dose preferred |
| Laser photocoagulation | — | Not beneficial for visual outcome in CRVO |
Treatment of Neovascularization
- PRP (panretinal photocoagulation): 1500–2000 burns when NVI or angle NV develops; do NOT perform before NVI
- Adjunctive intravitreal anti-VEGF: every 6 weeks until stable; reduces macular oedema concurrently
- Neovascular glaucoma: managed as per NVG protocol
Key principle: No proven treatment can "unblock" the occluded vein. Treatment aims to control complications.
Prognosis
Non-ischaemic CRVO:
- VA 6/18 or better → likely to remain so
- VA 6/24–6/60 → variable, difficult to predict
- VA worse than 6/60 → usually poor
Ischaemic CRVO: Extremely poor — due to macular ischaemia and neovascular glaucoma.
Review schedule:
- Ischaemic: monthly for 6 months, then 3-monthly for 2–3 years
- Non-ischaemic: 3 months initially, discharge at 18–24 months if stable
Key Points for Exam (Khurana-style)
- Site of occlusion: at or posterior to lamina cribrosa
- Most common age: >65 years
- Most important systemic risk factor: hypertension
- Most important ocular risk factor: open-angle glaucoma
- Classic fundus: "blood and thunder" appearance (all 4 quadrants)
- NVI develops at 2–4 months → "100-day glaucoma"
- FA criterion for ischaemia: >10 disc areas of capillary non-perfusion
- RAPD present in: ischaemic CRVO
- First-line treatment of macular oedema: intravitreal anti-VEGF
- Key trials: CRUISE (ranibizumab), COPERNICUS (aflibercept), SCORE (triamcinolone), GENEVA (dexamethasone implant)
- Young females: think OCP, thrombophilia
— Kanski's Clinical Ophthalmology, 10th Ed., Chapter 13 (Retinal Vascular Disease)
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