1. “Young Female with Painless Blurry Vision”
Mohammad Ali Sadiq, MD – PGY2
March 01, 2019

2. Patient Presentation CC “Blurry vision in right eye” HPI
25 year old white female presented with
Sudden, painless, blurry vision OD for the past one week.

3. History Past Ocular Hx: None Past Medical Hx: Sinus tachycardia
Fam Hx: Mom had a history of a retinal illness when she was 55 years old.
Meds: None

4. History
Allergies: Penicillin Social Hx: No smoking/alcohol ROS: Negative except as in the HPI

5. External Exam OD OS VA 20/25+2 20/20-1 Pupils
Pharmacologically dilated
IOP
21 mmHg
EOM
Full
CVF

6. Anterior Segment Exam SLE OD OS External/Lids WNL Conj/Sclera
White and quiet
Cornea
Clear
Ant Chamber
Deep and quiet
Iris
Flat
Lens

7. Posterior Segment ExamOD OS
Nerve
Few disc hemorrhages, no edema, no NVD
Optic disc pink and sharp
Macula
Scattered dot blot hemorrhages, flame shaped hemorrhages
Normal macula, good foveal reflex
Vessels
Dilated tortuous veins all quadrants
Normal Caliber
Vitreous
Clear
Periphery
Scattered hemorrhages in all quadrants.
No Holes or Tears. Attached 360 Degrees.

8. Fundus Photographs Optic Nerve c/d 0.2, pink and sharp,
Mild elevation inferotemporal
Macula
Foveal/Parafoveal multiple fine yellow/orange granular focal dots
Vessels normal caliber
Subretinal hypopigmented dots ( µm

9. OCT Optic Nerve c/d 0.2, pink and sharp, Mild elevation inferotemporal
Macula
Foveal/Parafoveal multiple fine yellow/orange granular focal dots
Vessels normal caliber
Subretinal hypopigmented dots ( µm

10. Assessment and Plan
A 25 year old white female with who presented with sudden onset, painless decreased vision OD.
Differential Diagnosis:
Impending CRVO
Papillophlebitis
Hyperviscosity retinopathy (waldenstrom, multiple myeloma or blood dyscrasias)
Ocular Ischemic syndrome
Plan:
Ordered extensive coagulopathy/infectious work up.
Re-assess in 2 weeks.

11. Labs CBC ANA Protein-C Factor V Leiden Homocysteine
Antithrombin Activity
Anticardiolipin
RPR, Lyme
Quantiferon
Lipid panel
Punctate hyperfluorescence

12. Update No further visual changes VA 20/25 and 20/20
Work up was negative
Mild macular edema in OD on OCT
Plan:
Continue to observe
Follow up in 3 weeks

13. OCT Optic Nerve c/d 0.2, pink and sharp, Mild elevation inferotemporal
Macula
Foveal/Parafoveal multiple fine yellow/orange granular focal dots
Vessels normal caliber
Subretinal hypopigmented dots ( µm

14. Central Retinal Vein Occlusion
Second most common vascular cause of visual loss after DR
Most commonly associated with advancing age and hypertension.
Vision loss is sudden and painless
Ranging along a spectrum from non-ischemic (mild) to ischemic (severe).
Choroidal changes
Hypoautofluorescence corresponding to sub retinal fluid
Punctate hyperautofluorescence corresponding to elongated photoreceptor outer segments

15. Non-Ischemic CRVO
Also known as partial, perfused or venous stasis retinopathy.
Vision >20/200
Mild or no RAPD
Minimal areas of non-perfusion on FA
Anterior segment neovascularization is rare
Choroidal changes
Hypoautofluorescence corresponding to sub retinal fluid
Punctate hyperautofluorescence corresponding to elongated photoreceptor outer segments

16. Ischemic CRVO
Also known as complete, non-perfused or hemorrhagic retinopathy
Defined as having ≥10 DD of retinal capillary non-perfusion.
Usually associated with poor vision.
Associated with anterior segment neovascularization
Presence of RAPD
More extensive venous dilation/tortuosity and hemorrhages
Only 10 percent having >20/400 vision

17. Anterior Segment Neovascularization
High rate in ischemic CRVO (up to 60%)
Occurs on average 3-5 months after onset of symptoms.
Poor VA is the risk factor most predictive of iris NV in these patients.
Other risk factors include area of non-perfusion and presence of intraretinal blood (CVOS study).
Choroidal changes
Hypoautofluorescence corresponding to sub retinal fluid
Punctate hyperautofluorescence corresponding to elongated photoreceptor outer segments

18. Risk Factors
Most important risk factor is age (>90% are older than 50).
Hypertension
Open-angle glaucoma
Diabetes mellitus
Hyperlipidemia
Hypercoagulability
Choroidal changes
Hypoautofluorescence corresponding to sub retinal fluid
Punctate hyperautofluorescence corresponding to elongated photoreceptor outer segments

19. Hypercoagulability Hyperhomocystinemia Protein S deficiency
Protein C deficiency
Factor V leiden mutation
SLE
Sarcoidosis

20. Management

21. Management Multimodal imaging
Initial evaluation with monthly visits x 6 months
In the CVOS study 16% of initially non ischemic CRVOs converted to ischemic by 4 months. By 36 months, the percentage increased to 34%

22. IMAGING

24. Collateralization

25. CRVO and Cilioretinal Artery Occlusion

26. CRVO and Carotid Cavernous Fistula

27. Fluorescein Angiography

28. OCT-Angiography

29. Management
Laser:
Grid laser not recommended for CRVO with macular edema.
Prophylactic PRP did not result in significant reduction in incidence of iris NV.
PRP when iris neovascularization is observed.

30. Pharmacological Management
Anti VEGF agents have been well-studied for CRVO.
CRUISE – Ranibizumab
COPERNICUS – Aflibercept
SCORE – Intravitreal Triamcinolone
SCORE 2 – Bevacizumab and Aflibercept
Systemic anticoagulation not recommended

31. Other Surgical Approaches
Peripheral laser anastomosis between retinal vein and choroidal circulation
Radial relaxing incision of optic nerve scleral ring
Retinal vein cannulation with infusion of TPA.

32. Conclusions CRVO is a common vascular cause of visual loss.
Mostly seen in patients above the age of 50.
Important to rule out precipitating causes of CRVO in the younger population.
Need to differentiate between ischemic and non-ischemic CRVO.
Anti VEGF therapy plays a critical role
PRP if there is anterior segment neovascularization.
RESTORE trial

33. “If you can’t find a cause for something…. blame it on a VIRUS
“If you can’t find a cause for something…. blame it on a VIRUS !” – Charles Barr, MD

34. Acknowledgements
Charles Barr, MD
Efrat Fleissig, MD