OCCLUSIVE VASCULAR DISORDERS OF THE RETINA

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Benedict Chapman
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1 OCCLUSIVE VASCULAR DISORDERS OF THE RETINA

2 Learning outcomes By the end of this lecture the students would be able to Classify occlusive vascular disorders (OVD) of the retina. Correlate the clinical features of OVD of the retinal with the underlying pathophysiological changes. List treatment modalities for OVD List the complications of OVDs

3 Let us look at a case a 54-year-old school teahcer presented with acute visual loss in the left eye. He had history of uncontrolled hypertension and open angle glaucoma. Laboratory tests including complete hypercoagulability and thrombotic workup were completed. Ophthalmologic exam showed best corrected visual acuity (BCVA)of 6/9 OD, 6/60 OS. Pupil exam showed sluggish right pupil with relative afferent papillary defect, and a reactive pupil on the left. Intraocular pressures were 19 mmhg in the right, and 11 mmhg in the left. Slit lamp exam showed normal anterior segments with open angles bilaterally.

5 Retinal vein occlusion Central retinal vein occlusion (CRVO) Branch retinal vein occlusion (BRVO) Hemiretinal vein occlusion (HRVO)

6 BRVO CRVO HRVO

7 Epidemiology Retinal vein occlusion is the second most common cause of visual loss due to retinal vascular disease BRVO is the most common type It is a significant cause of severe visual loss in people over the age of 40 yrs

8 Pathophysiology Can you think of some anatomical factors that could predispose retinal veins to occlusion?

9 Pathophysiology Various local and systemic factors play a role in the pathological closure of the retinal veins The central retinal artery and vein share a common adventitial sheath as they exit the optic nerve head and pass through a narrow opening in the lamina cribrosa. Retinal arterioles and their corresponding vein share the adventitia. Thickening & hardening of the arteries can compress the veins. This anatomical position predisposes to thrombus formation in the central retinal vein by various factors, including slowing of the blood stream, changes in the vessel wall, and changes in the viscosity of the blood. Arteriosclerotic changes in the central retinal artery transform the artery into a rigid structure and impinge upon the pliable central retinal vein, causing hemodynamic disturbances, endothelial damage, and thrombus formation.

retina increased production of vascular endothelial growth factor (VEGF) neovascularization of the

10 With occlusion of the central retinal vein (CRVO) increased venous & capillary pressure stagnation of the blood in the retinal venous system and increased resistance to venous blood flow ischemic damage to the retina increased production of vascular endothelial growth factor (VEGF) neovascularization of the posterior and anterior segment Capillary leakage Neovascular Glaucoma, NVD, NVE,RD Complications of RVO Macular oedema

11 CRVO With occlusion of the vein there is increased venous & capillary pressure and stagnation of the blood in the retinal venous system and increased resistance to venous blood flow. ischemic damage to the retina increased production of vascular endothelial growth factor (VEGF) in the vitreous cavity. Increased levels of VEGF stimulate neovascularization of the posterior and anterior segment responsible for secondary complications due to RVO. VEGF causes capillary leakage leading to macular edema. The prognosis depends upon the reestablishment of patency of the venous system by recanalization, dissolution of clot, or formation of optociliary shunt vessels.

12 Risk factors Blood Systemic Vessel wall

13 Risk factors Age: 50% of these cases occur in patient over 65 years of age Systemic diseases like diabetes mellitus, hypertension, hyperlipidemics states, smoking & obesity Inflammatory diseases like sarcoidosis, Bechet disease Hyperviscosity syndromes like polycythemia, paraproteinemias Clotting disorders - Activated protein C resistance, lupus anticoagulant, anticardiolipin antibodies, protein C, protein S, antithrombin III Raised Intraocular pressure (IOP) Oral contraceptive use

14 CRVO Clinical presentation Clinical entities Non ischemic CRVO (about 75% of cases) Ischemic CRVO (worse prognosis) How would you diagnose retinal ischemia?

15 CRVO Clinical presentation Asymptomatic Decreased vision Visual loss sudden or gradual, over a period of days to weeks. ranges from mild to severe. Patients can present with transient obscurations of vision initially, later progressing to constant visual loss. Photophobia Redness of eyes Painful blind eye

16 Clinical examination Patients should undergo a complete eye examination, including visual acuity, pupillary reactions, slit lamp examination of the anterior and posterior segments, undilated examination of the iris, gonioscopy, Dilated fundus examination

17 Signs Visual acuity: (Best-corrected vision acuity) It is one of the important indicators of the final visual prognosis. Pupillary reactions: normal/ relative afferent pupillary reflex. If the iris has abnormal blood vessels, the pupil may not react. Conjunctiva: Advanced stages may show congestion on conjunctival and ciliary vessels. Cornea: Advanced stages may show diffuse corneal edema obscuring the visibility of internal structures. Iris: normal/ neovascularization The anterior chamber angle: it may show neovascularization with open angles and later show total peripheral anterior synechia and closed angles.

18 Signs Fundus examination: Retinal hemorrhages Dilated tortuous veins Optic disc edema Cotton-wool spots Macular oedema Late signs: Neovascularization (NVD, NVE), optic disce cupping, optociliary shunt vessels at the disc (a prognostic sign), pigmentary changes in the macula

25 Rubeosis 100 day glaucoma

26 Investigations Risk factors screening (Lab tests) FFA Electro-retinogram (ERG)- amplitude of the b-wave is decreased relative to the a-wave

28 TREATMENT Depends on the type & stage of CRVO Principles of treatment are Treat the underlying cause Monitor Treatment modalities Intravitreal corticosteroid and anti-vegf injections Dexamethasone intravitreal implant Laser photocoagulation Chorioretinal venous anastomosis

29 Follow -up Regular follow up babysit" 1 for these eyes during that period when they are at maximum risk of developing neovascular glaucoma, i.e. first 7-8 months

30 Prognosis For nonischemic CRVO, complete recovery with good visual recovery occurs only in about 10% of cases. Fifty percent of patients will have 6/60 or worse vision. About one third of patients convert to ischemic CRVO within 3 years; 15% within the first 4 months. For ischemic CRVO, more than 90% of patients will have 6/60 or worse vision. About 60% of patients develop ocular neovascularization About 10% of patients can develop CRVO or other type of vein occlusions within either the same eye or the contralateral eye within 2 years.

31 Conclusion? Lacrimal system Cornea Conjunctiva Cataract Refractive errors

Vascular Disease Ocular Manifestations of Systemic Hypertension

Vascular Disease Ocular Manifestations of Systemic Hypertension Maynard L. Pohl, OD, FAAO Pacific Cataract & Laser Institute 10500 NE 8 th Street, Suite 1650 Bellevue, WA 98004 USA 425-462-7664 Cerebrovascular