Retinal artery occlusion

Central retinal artery occlusion, ophthalmic artery occlusion, branch retinal artery occlusion, cilioretinal artery occlusion

1. RETINAL ARTERIAL OCCLUSION

2. Ophthalmic artery Ophthalmic artery constitutes the main source of blood supply to orbital structures Ophthalmic artery arises from medial side of the convexity of the fifth bend of the internal carotid artery, just after it has left the roof of cavernous sinus after piercing the dura At its origin ophthalmic artery is medial to ant clinoid process & inf to the optic nerve

3. Central retinal artery Central retinal artery branch of ophthalmic artery Originates from ophthalmic artery close to optic foramen, & runs a wavy course forward below the optic nerve. Here it lies outside the dura but it is adherent to it At about 10-15mm behind the eyeball it bends upwards & pieerces the dura & arachnoid to enter subarachnoid space.

4. Central retinal artery In the subarachnoid space it bends forwards & after a short course it again bends upwards at right angle & invaginate pia to reach the centre of nerve So here it is surrounded by pia matter along with pial vessels & also by sympathetic nerve plexus (nerve of tiedemann ) In the centre of optic nerve it bends forwards & then accompanying with vein (on temp side) it passes anteriorly & pierces lamina cribrosa to appear inside the eye

5. Central retinal artery In the optic nerve head it lies superficially in the nasal part of physiological cup Here it divides into two branches superior & inferior Each of which subdivides into a temporal & nasal branch at or near the margin of the optic disc In the retina the 4 terminal branches of central retinal artery divide dichotomously as they proceed towards the ora serrata where they end without anastomosis

6. The retinal arteries and arterioles remain in the inner retina Only capillaries are found as deep as the inner nuclear layer When two vessels cross, the artery usually lies anterior to the vein And the two vessels share a common adventitial coat Many more arteriovenous crossings occur temporally than nasally because the nasal vessels assume a much straighter course The crossings are important because they represent the most common site of branch retinal vein obstructions.

7. Blood supply of the retina Outer 4 layers of the retina RPE, photoreceptors, ELM, ONL get their nutrition from choriocapillaries Inner 6 layers OPL, INL, IPL, GCL, NFL, ILM get their blood supply from central retinal artery OPL gets its blood supply from both central retinal artery & choriocapillaries Fovea is relatively avascular , get its blood supply from choriocapillaries

8. Blood supply of the retina Macular region get its blood supply from temporal branches of central retinal artery Sometimes cillioretinal artery is seen originating in a hook shaped manner within the temp margin of the disc It runs towards the macula & supplies it Applied :- when present it helps to retain central vision in CRAO

9. Venous drainage The venous drainage of the retina generally follows the arterial supply Veins corresponding to arteries join to form central retinal vein which drains into superior ophthalmic vein Near the superior orbital fissure it is joined by inferior ophthalmic vein Leave the fissure & ultimately drains into cavernous sinus

10. Arterial occlusions

11. Demography Retinal arterial occlusions may occur at any age, but the average age of patients with CRAO found in two large series is 62 & 67 yrs Most series demonstrate a slight male predominance No racial predilection The right and left eyes appear to be involved equally Common systemic risks factors for retinal arterial occlusive disease include Hypertension, Diabetes, Lipid disorders, Cardiac and systemic atherosclerotic disease

12. Mechanism of occlusion The principal mechanisms operative in occlusion of the retinal arterial system are Embolic, Thrombotic, Vaso spastic, Extravascular compression, Vasculitic Other mechanisms such as radiation and elevated intraocular pressure occur much less commonly

13. More than one mechanism may occur An embolism to the retinal arterial circulation can originate as a venous thrombosis reaching the arterial circulation via a right to left cardiac shunt CRAO secondary to giant cell arteritis is primarily a vasculitic phenomenon, with thrombosis being the ultimate occlusive event.

14. Atherosclerosis-related thrombosis Atherosclerosis-related thrombosis at the level of the lamina cribrosa is by far the most common underlying cause of CRAO About 80% The incidence of atherosclerosis increases with age & is accelerated by Hypertension, Hyperlipidaemia , Diabetes, Oral contraceptives and Hyperhomocysteinaemia Other risk factors include obesity, tobacco smoking and a sedentary lifestyle

15. Carotid embolism Origin of emboli is most often from an atheromatous plaque at carotid bifurcation and sometimes from aotic arch.

16. Types of emboli Emboli may be of following types: 1.Cholesterol emboli - hollenhorst plaques Intermittent showers of minute ,bright, refractile , golden to yellow-orange crystals, Often located at arteriolar bifurcation Rarely cause significant obstruction

17. Types of emboli 2.calcific emboli Single,non -scintillating often on or close to the disc They may be overlooked when present on the disc They are more dangerous because they may cause permanent occlusion

18. Types of emboli 3.fibrin –platelet emboli : Dull grey, elongated particles, usually multiple ,occasionally fill the entire lumen They may cause a retinal transient ischaemic attack and resultant amaurosis fugax Occasionally they may cause permanent obstruction

19. Uncommon causes Giant cell arteritis Cardiac emboli Periarteritis : Dermatomyositis , SLE, PAN, Wegener granulomatosis , Bechet syndrome Thrombophilic disorders: defects of natural anticoagulants, antiphospholipid antibody syndrome, hyperhomocystenaemia Sickle cell disease Migrane (reflex vasospasm) Susac syndrome: triad of retinal artery occlusion, sensorineural deafness and encephalopathy

20. Local conditions in the eye and orbit Peripapillary arterial loop Optic nerve head drusen Intraocular foreign body Elevated intraocular pressure secondary to angle-closure glaucoma External compression of the ophthalmic artery or central retinal artery caused by orbital cellulitis , orbital hemorrhage, abscess formation, cavernous sinus thrombosis, and neoplastic disease

21. BRAO in right eye secondary to prepapillary arterial loop

22. Inferior BRAO secondary to intraocular foreign body imbedded in the retina with distal occlusion of the inferior temporal artery . There is hemorrhage overlying the intraocular foreign body.

23. Histopathology RAO Reduced/no perfusion Reduced glucose & O2 delivery Ischaemia Opacification of ganglion cell layer

24. The opacification is most prominent in the macular region where the multiple layers of ganglion cells reside Retinal opacification generally decreases toward the periphery as the ganglion cell population diminishes, and is also absent from the avascular zone of the foveola where ganglion cells are absent. The classic ‘cherry red spot ’ is a result of the visible red reflex of the perfused choroid at this location

25. CRAO Sudden ,profound, painless loss of vision VA : severely reduced except if a portion of papillomacular bundle is supplied by cilioretinal artery ,where central vision is preserved Afferent pupillary defect Visual fields are depressed in the area of the ischemic retina The retina shows ischemic whitening the retinal arterials and veins manifest boxcarring Cherry red spot FFA: delay in arterial filling and masking of background choroidal fluorescence by retinal swelling

26. Characteristics Findings on OCT Increase in inner layer reflectivity and Muted outer layer reflectivity around the foveola With normal reflectivity of the retinal pigment epithelium beneath the foveola

27. OCT of CRAO demonstrating increased thickness in the inner retinal layers and muted outer layer/retinal pigment epithelium reflectivity surrounding the foveola . Note that there is normal reflectivity of the retinal pigment epithelium at the foveola

28. Prognosis Poor due to retinal infarction After few days oedema disappears ,arteries remain attenuated . Inner layers of retina become atrophic. Optic atrophy,permanent loss of vision Rubeosis iridis may require PRP,NVD NVG

29. OPHTHALMIC ARTERY OCCLUSIONS Profound painless unilateral loss of vision Visual acuity ranges from CF to no PL An afferent pupillary defect Fundus picture is that of an acutely infarcted retina with extensive retinal whitening Pallid swelling of the optic disk No cherry red spot Boxcarring or segmentation of the blood column of the retinal vessels FFA :- no or markedly delayed background choroidal flush and minimal or delayed filling of the retinal vasculature

30. Chronic ophthalmic artery occlusion in right eye. Pale disk and ischemic retinal arteries and veins.

31. Visual recovery is rare in cases of ophthalmic artery occlusion. Electroretinographic testing can help differentiate ophthalmic artery occlusions from CRAO In ophthalmic artery occlusions, both the B wave and A wave are absent In CRAO with intact choroidal perfusion, the A wave is present.

32. BRANCH RETINAL ARTERY OCCLUSIONS Presentation : painless loss of visual field in the distribution of the occluded artery Fundus : narrowing of arteries and veins with sludging and segmentation of blood column. Cloudy white retina may not occur in nasal branch artery occlusions due to the single layer of ganglion cells present there FFA:- delayed transit of the dye through the affected vessel, and often retrograde filling of the vessel can be observed later in the angiogram

33. Inferior BRAO with calcific emboli at inferior margin of the optic disk beneath overlying vein. Fluorescein angiogram of inferior BRAO showing delayed perfusion of inferior retina with retrograde filling of inferior retinal veins

34. RE fundus photo revealing whitening of the superior retina with a calcified plaque at the disc within the supero temporal artery (arrow); (B) SDOCT revealed hyper-reflectivity and increased thickness of the inner retinal layers in the superior compared to inferior retina, decreased reflectivity of the outer retinal layers (including retinal pigment epithelial layer) in the superior retina as compared to inferior retina probably due to optical shadowing

35. CILIORETINAL ARTERY OCCLUSIONS 35% of eyes and 50% of people have cilioretinal arteries Typical symptom pericentral scotomas , often subtle, in the distribution of the artery APD are often not present Although any of the described mechanisms of occlusion may be operational May occur in conjunction with central retinal venous occlusive disease and anterior ischemic optic neuropathy

36. Cilioretinal artery occlusion. (A) Isolated; (B) combined with central retinal vein occlusion; (C) combined with anterior ischaemic optic neuropathy; (D) FA shows hypofluorescence at the macula due to lack of filling and masking by retinal swelling

37. Management Management of the acute occlusive event in an attempt to restore visual function Workup of the patient looking for potential systemic conditions requiring treatment Management of the remote complications and sequelae of the arterial occlusive event

38. Management of the acute occlusive event Digital ocular massage Simple treatment with low morbidity No statistical benefit has been noted Reduction of intraocular pressure through ocular antihypertensives and paracentesis Which theoretically may also dislodge an embolus Have been attempted to improve retinal arterial circulation. Studies have shown no significant difference in final versus initial visual outcomes in use of topical beta blockers, oral acetazolamide , or paracentesis

39. Medical vasodilatation utilizing sublingual nitroglycerin, calcium channel blockers and pentoxifylline Used to improve the retinal arterial circulation. While results of one study found that the pentoxifylline group had less neovascularization compared to standard treatment, there was no definitive improvement in visual outcomes To date there are only anecdotes of effectively treating CRAO with nitroglycerin

40. Carbogen 95% oxygen and 5% carbon dioxide inhalation treatment that may cause dilation of retinal arterioles not shown benefit to final visual outcome and is generally no longer used thrombolytic therapy There are case reports of thrombolytic therapy improving visual recovery even when initiated more than 2 h after occlusion. However, less than 16% of CRAO cases are due to platelet fibrin obstruction

41. lack of clinical evidence of improved visual outcome potential for systemic complications, and inherent difficulty establishing nonembolic etiology The decision to attempt fibrinolytic therapy using drugs like TPA should be made carefully. in patients with CRAO, if giant cell arteritis is suspected by clinical and laboratory parameters, high-dose steroid therapy should be initiated while awaiting temporal artery biopsy

42. Surgical treatments Laser photo disruption of an embolus Vitrectomy with cannulation of the central retinal artery No randomized trial data have confirmed the efficacy of any of these treatments.

43. Systemic workup In up to 30% of patients , no systemic associated condition leading to arterial occlusion is documented

44. Thank-you