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Retinal artery occlusions
- 1. RETINAL ARTERY OCCLUSION BY DRANJALI MAHESHWARI
- 2. SOURCES Kanski’s –8th edition Ryan’s textbook of retina Yanoff and Duker- 5th edition
- 3. LAYOUT Introduction CRAO BRAO Cilioretinal artery occlusion Ophthalmic artery occlusion Combined artery and vein occlusion Systemic evaluation Treatment
- 4. INTRODUCTION Retinal arterialobstructions are divided anatomically depending on the precise site of obstruction: Central - occurs when the blockage is within the optic nerve substance itself and site of obstruction is not visible on ophthalmoscopy. Branch - occurs when the site of blockage is distal to the lamina cribrosa of the optic nerve More proximal obstructions usually cause a more chronic form of visual problem − the ocular ischemic syndrome
- 5. Majority ofretinal arterial obstructions are either thrombotic or embolic in nature. Branch retinal artery obstruction is far more likely to be embolic than is a central retinal artery obstruction Retinal artery obstructions selectively affect the inner retina only
- 6. BLOOD SUPPLY Theouter retina is supplied by the ciliary arteries via the choriocapillaris and the inner retina by the central retinal artery (CRA). The ophthalmic artery gives rise to both the CRA – its first branch – and the ciliary arteries. Atherosclerosis-related embolism and thrombosis are thought to be responsible for the majority of cases of retinal artery occlusion.
- 8. The originof emboli is most commonly an atheromatous carotid plaque; the ophthalmic artery is the first branch of the internal carotid artery, so embolic material has an easy route to the eye.
- 9. Inflammation inor around the vessel wall : Giant cell arteritis – GCA Systemic lupus erythematosus Wegener granulomatosis Polyarteritis nodosa Vasospasm (e.g. migraine) Systemic hypotension contribute in a minority.
- 10. CENTRAL RETINAL ARTERYOBSTRUCTION. Rare event − it has been estimated to account for about 1 in 10000 outpatient visits to the ophthalmologist. Men are affected more commonly than women in the ratio 2:1. The mean age at onset is about 60years Bilateral involvement occurs in 1–2% of cases
- 11. When botheyes are simultaneously affected by retinal artery obstruction, the differential diagnosis should include : Cardiac valvular disease Giant cell arteritis Other vascular inflammations.
- 12. ETIOLOGY Thrombosis- atlevel of lamina cribrosa Atherosclerosis Congenital abnormality of central retinal artery Coagulopathies Embolism (20-25%) – Origin from atheromatous carotid plaque. Cholesterol (Hollenhorst plaques) Platelet-fibrin Calcific
- 13. Inflammatory Vasculitis(Varicella, SLE, Wegner’s, PAN) Optic neuritis Orbital disorder (Mucormycosis) Local trauma Arterial spasms (dissecting aneurysm)
- 14. Thrombophilic disorders(In one-third of young patients) Hyperhomocystinemia Anti-phospholipid antibody syndrome Sickling hemoglobinopathies Susac syndrome ( Retino-cochleo-cerebral syndrome) Protein C& S deficiency Anti-thrombin III deficiency
- 15. Rare causes Radiation retinopathy Emboli secondary to depot medications around eyes Optic nerve drusens Peripapillary arterial loops Medical examination and manipulation Eg: Carotid angiography, angioplasty , chiropractic neck manipulation
- 16. AMAUROSIS FUGAX Transientmonocular loss of vision Amaurosis fugax study group divides cause into five categories: Embolic Ocular Neurologic Hemodynamic Idiopathic Recovery is in the same pattern as lost.
- 17. CLINICAL FEATURES Thehallmark symptom of acute central retinal artery obstruction is abrupt, painless loss of vision. Pain is unusual and suggests associated ocular ischemic syndrome (OIS). Amaurosis fugax precedes visual loss in about 10% of patients. In cases associated with arterial spasm, a relapsing and remitting course of visual loss precedes central retinal artery obstruction.
- 18. Visual acuityof 20/800 (6/240) or worse. No light perception vision is uncommon except in case of ophthalmic artery obstruction or temporal arteritis. Patent cilioretinal artery - perfuses the fovea, normal central acuity may be present. Afferent pupillary defect on the affected side.
- 19. Anterior segmentexamination is normal (Except in concurrent OIS with neovascularization of the iris)
- 20. FUNDUS Within thefirst few minutes to hours after the obstruction, the fundus may appear relatively normal. Decreased blood flow results in ischemic whitening of the retina in the territory of the obstructed artery. Most pronounced in the posterior pole (where the nerve fiber layer of the retina is thickest). Acutely arteries appear thin and attenuated.
- 21. Retinal whiteningis very subtle and the retinal vessels appear normal. Fluorescein angiography reveals abnormal arterial filling with a leading edge of dye that confirms central retinal artery obstruction. The same eye 24 hours later- intense retinal whitening with a cherry-red spot is present.
- 22. In severeblockages, both veins and arteries may manifest “box-carring” or segmentation of the blood flow.
- 23. Cherry-red spotof the macula is typical ( arises in because of thin nerve fiber layer). Transmission of the normal choroidal appearance is not diminished, which contrasts distinctly with the surrounding area of intense retinal whitening that blocks transmission of the normal choroidal coloration.
- 24. It alsodepends on the size of fovea.
- 25. OTHER CAUSES OFCHERRY RED SPOT Tay–Sachs disease Farber’s disease Sandhoff’s disease Niemann–Pick disease Goldberg’s syndrome Gaucher’s disease Ganglioside GMI, type 2 Hurler’s syndrome (mucopolysaccharidosis 1 H) β-Galactosidase deficiency (mucopolysaccharidosis VII) Hallevorden–Spatz disease
- 26. Splinter retinalhemorrhages on the disc are common. If pallid swelling is present, temporal arteritis must be ruled out. A patent cilioretinal artery results in a small area of retina that appears normal .
- 27. Prominent cherry-redspot with cilioretinal artery sparing in the papillomacular bundle.
- 28. By 6weeks after the acute event: Retinal whitening resolves Optic disc develops pallor Arterial collaterals forms on the optic disc No foveolar light reflex apparent Fine changes in the retinal pigment epithelium may be visible.
- 29. Secondary ocularneovascularization occuar 8 weeks after the obstruction Iris neovascularization occurs in about 18% of patients with many developing to neovascular glaucoma. Neovascularization of the optic disc occurs after about 2% of central retinal artery obstruction Vitreous hemorrhage may also occur.
- 30. Central retinalartery obstruction caused by a platelet-fibrin embolus. After 3 months, extensive neovascularization of the disc is present.
- 31. DIAGNOSIS AND ANCILLARYTESTING Diffuse ischemic retinal whitening is present in the setting of abrupt, painless visual loss. Fluorescein angiography Optical coherence tomography Electroretinogram Visual field
- 32. FLUORESCEIN ANGIOGRAPHY Delayedarm-to-retina time with a leading edge of dye visible in the retinal arteries is typical Arteriovenous transit is delayed :time elapsed from the appearance of dye within the arteries of the temporal vascular arcade until the corresponding veins are completely filled; normal is less than or equal to 11 seconds Late staining of the disc is common.
- 33. Severe leftcentral retinal artery obstruction with segmentation of the blood column in the retinal vessels (arrows). Fluorescein angiogram at 52 seconds after injection reveals poor filling. The leading edge of dye (arrow) within the inferior retinal arterial system is distinctly abnormal and indicates hypoperfusion. At nearly 6 minutes after injection, the retinal vessels are still poorly filled. The hypofluorescent focus (arrow) on the optic disc corresponds to staining of an embolus within the central retinal artery
- 34. Complete lackof filling of the retinal arteries is unusual and occurs in less than 2% of cases. The choroidal vascular bed in eyes usually fills normally, delays of five seconds or greater seen in about 10% of cases A marked prolongation of choroidal filling in the presence of a cherry-red spot should arouse suspicion of an ophthalmic artery obstruction or a concomitant carotid artery obstruction
- 35. The retinalcirculation has propensity to re-establish the circulation following an acute central retinal artery obstruction. Arterial narrowing and visual loss may persist, but the fluorescein angiogram can revert to normal at varying times after the insult.
- 36. OPTICAL COHERENCE TOMOGRAPHY Macular optical coherence tomography (OCT) in the acute phase shows inner retinal thickening with shadowing of the outer retina that can be mistaken for subretinal fluid. When the retinal whitening resolves, OCT reveals severe inner retinal thinning. OCT angiography of prior central retinal artery obstruction demonstrates decreased retinal vascularity and attenuation of vessels in the macula
- 37. Optical Coherence Tomography Angiographyand Corresponding Optical Coherence Tomography Structural B-Scan From an Eye With a Prior Central Retinal Artery Obstruction. Paucity of small retinal vessels in the macula and the attenuation of the large retinal vessels. Structural B- scan shows loss of inner retinal tissue.
- 38. ELECTRORETINOGRAPHY Diminution inthe amplitude of the b-wave (corresponding to the function of the Muller and/or bipolar cells) secondary to inner layer retinal ischemia. The a-wave, which corresponds to photoreceptor function, is generally unaffected. In some eyes the study is normal in the presence of decreased vision, possibly because of the re- establishment of retinal blood flow
- 39. Electroretinograms ofa normal right eye (upper tracing) and a left eye (lower tracing) affected by a CRAO. The “b” wave is diminished in the lower tracing of the CRAO eye, but the “a” wave is normal.
- 40. VISUAL FIELD Demonstratea remaining temporal island of vision, presumably because the choroid nourished the corresponding nasal retina. In the presence of a patent cilioretinal artery, small areas of central vision are preserved. Depending upon the degree and the extent of the obstruction, varied portions of the peripheral field may remain.
- 41. SYSTEMIC ASSOCIATIONS About50%–60% of patients have concurrent systemic arterial hypertension, and diabetes is present in 25%. Systemic evaluation reveals no definite cause for the obstruction in over 50% of affected patients. The Retinal Emboli of Cardiac Origin Study Group, a multicenter study, reported on the cardiac findings associated with acute retinal arterial occlusion
- 42.
- 45. DIFFRENTIAL DIAGNOSIS Singleor multiple branch retinal artery obstruction Cilioretinal artery obstruction Severe commotio retinas Necrotizing herpetic retinitis
- 46. COURSE AND OUTCOME Most central retinal artery obstructions result in severe, permanent loss of vision. About one-third of patients experience some improvement in final vision in terms of presentation acuity either with or without conventional treatment. Three or more Snellen lines of improved visual acuity occur in only about 10% of untreated patients. Spontaneous recovery may be more common in young children.
- 47. BRANCHED RETINAL ARTERYOCCLUSION Rare event, less common than central retinal artery obstruction overall. Exception - comparative incidence with young patients, in whom branch retinal artery obstruction is the more common type of retinal artery obstruction. Men are more affected than women by a 2 : 1 ratio, reflects the higher incidence of vasculopathic disease in men. Young patients (less than 50 years of age), women and men are affected equally.
- 48. Mean ageof affected patients is 60 years (Range - second decade to tenth). The right eye (60%) is affected more commonly than the left (40%), which reflects the greater possibility of cardiac or aortic emboli traveling to the right carotid artery. Branch retinal artery obstruction strikes the temporal retinal circulation far more frequently than the nasal.
- 49. Over two-thirdsof branch retinal artery obstructions are secondary to emboli to the retinal circulation. In most cases, the emboli are clearly visible in the arterial tree. Emboli to the retinal circulation may originate at any point in the proximal circulation from the heart to the ophthalmic artery.
- 50. Risk factorsreflect the vasculopathic mechanisms that produce disease within the cardiovascular system: Predisposing family history Hypertension Elevated lipid levels Cigarette smoking Diabetes mellitus
- 51. Three maintypes of retinal emboli have been identified: • Cholesterol (Hollenhorst plaque) • Platelet-fibrin • Calcific
- 52. Cholesterol embolitypically emanate from atheromatous plaques of the ipsilateral carotid artery system, aorta or heart valves may also be a source. Yellow–orange in color, refractile, and globular or rectangular in shape. They are small and can be seen intravascularly without blockage of blood flow.
- 53. Cholesterol embolus(arrow) in the fundus of an asymptomatic woman. Embolus is present at the bifurcation, since it is trapped as the lumen of the artery narrows
- 54. Platelet-fibrin emboliare long, smooth, white-colored, intra-arterial plugs that may be mobile or break up over time. Usually they are associated with carotid or cardiac thromboses.
- 55. Calcific emboliare solid, white, nonrefractile plugs associated with calcification of heart valves or the aorta.
- 56. Less commonlyseen embolic types : Tumor cells from atrial myxoma or a systemic metastasis Septic emboli associated with septicemia or endocarditis Fat emboli associated with large bone fractures Emboli dislodged during angioplasty or angiography Depot drug preparations from intra-arterial injections around the eye or face
- 57. Rarely, localocular conditions produce branch retinal artery obstruction including: Inflammatory diseases such as toxoplasmosis Acute retinal necrosis Mechanical compression from anterior ischemic optic neuropathy Structural entities such as optic disc drusen or prepapillary arterial loops
- 58. Systemic hematologicalor clotting problems - isolated branch retinal artery obstruction or multiple recurrent branch retinal artery obstruction Systemic vasculitides, such as polyarteritis nodosa Local vasculitis associated with varicella infection Oral contraceptive use and cigarette smoking - in young, otherwise healthy women
- 59. CLINICAL FEATURES Symptoms. Sudden and profound painless altitudinal or sectoral visual field loss. Can sometimes go unnoticed, particularly if central vision is spared. VA Variable In patients where central vision is severely compromised, the prognosis is commonly poor unless the obstruction is relieved within a few hours .
- 60. RAPD isoften present. Amaurosis fugax occurs in about one-fourth of patients prior to frank obstruction, especially case of carotid disease. Bilateral simultaneous branch retinal artery obstruction, which can mimic homonymous field defects can occur rarely.
- 61. Fundus signsmay be subtle : Attenuation of arteries and veins with sludging and segmentation of the blood column (‘cattle trucking/ boxcarring’). Cloudy white oedematous (ground glass) retina corresponding to the area of ischaemia. One or more occluding emboli may be seen, especially at bifurcation points. The affected artery is likely to remain attenuated. Recanalization may leave absent ophthalmoscopic signs.
- 62. A syndromeof multiple, recurrent, bilateral branch retinal artery obstruction in young, otherwise healthy patients has been reported. A few of the patients also manifest vestibuloauditory Susac’s syndrome, a rare disorder that manifests as a microangiopathy of the central nervous system.
- 63. Inferotemporal occlusion– embolus visible over the disc Superior branch retinal artery occlusion due to an embolus at the disc
- 64. FA showslack of arterial filling of the involved artery and hypofluorescence of the involved segment due to blockage of background fluorescence by retinal swelling
- 65. Small macularbranch artery occlusion and it’s FA
- 66. In thechronic phase, when the retinal whitening has diminished, a loss of the nerve fiber layer in the affected area is apparent. Arteriolar collaterals on the optic disc or at the site of obstruction may develop
- 67. ANCILLARY TESTING Visualfield testing confirms the defect, which rarely recovers. FA shows delay in arterial filling and hypofluorescence of the involved segment due to blockage of background fluorescence by retinal swelling OCTA demonstrates vascular features that correlate with FA and provide improved visualization of the microvasculature compared to FA.
- 68. OCT initiallyreveals thickening and hyperreflectivity consistent with intracellular edema of the inner retina in the territory of the obstructed artery. Over time, corresponding inner retina will be severely thinned.
- 69. Review in3 months is warranted to review the appearance of the fundus and visual fields Provide advice on prognosis and confirm that systemic management has been carried out appropriately.
- 70. DIFFRENTIAL DIAGNOSIS Cotton–woolspot(s) Central retinal artery obstruction Cilioretinal artery obstruction Retinal astrocytoma Inflammatory or infectious retinitis
- 71. CILIORETINAL ARTERY OCLUSION A cilioretinal artery is present in 15–50% of eyes Its main importance is that when present it may facilitate preservation of central vision following central retinal artery occlusion, provided the fovea is supplied.
- 72. Isolated cilioretinal arteryocclusion and FA of the eye shows hypofluorescence in the affected area due to reduced filling and masking by retinal oedema Isolated- rare; occur in young patients with an associated systemic vasculitis. Isolated; (B) FA of the eye in (A) shows hypofluorescence in the affected area due to reduced filling and masking by retinal oedema;
- 73. Isolated cilioretinalartery obstruction Fluorescein angiogram demonstrates poor filling of the obstructed cilioretinal artery and retinal capillary nonperfusion within the area of distribution of the vessel.
- 74. Combined withCRVO- occlusion is transient and the prognosis is better than in isolated cilioretinal artery occlusion.
- 75. Combined withanterior ischaemic optic neuropathy typically affects patients with GCA and carries a very poor prognosis.
- 76. OPHTHALMIC ARTERY OCCLUSION Acute simultaneous obstruction of both the retinal and choroidal circulations is referred to as an ophthalmic artery obstruction. Cases of ophthalmic artery obstruction usually have associated local orbital or systemic diseases including: Orbital mucormycosis Orbital trauma Retrobulbar anesthesia Depot corticosteroid injection Atrial myxoma Carotid artery disease.
- 77. Ophthalmic arteryobstructions can be differentiated clinically from central retinal artery obstruction by the following features: • Severe visual loss—bare or no light perception. • Intense ischemic retinal whitening that extends beyond the macular area. • Little to no cherry-red spot. • Marked choroidal perfusion defects on fluorescein angiography. • Nonrecordable electroretinogram. • Late retinal pigment epithelium alterations
- 78. COMBINED ARTERY ANDVEIN OBSTRUCTIONS Central retinal artery obstruction combined with simultaneous central retinal vein obstruction rarely occurs. Patients typically present with acute, severe loss of vision. Examination shows a cherry-red spot combined with features of a central retinal vein obstruction, which include dilated, tortuous veins that have retinal hemorrhages in all four quadrants
- 80. Associated systemicor local disease is the rule— Collagen vascular disorders Leukemia Orbital trauma Retrobulbar injections Mucormycosis The visual prognosis is generally poor and the risk of neovascularization of the iris is about 75%.
- 81. SYSTEMIC EVALUATION Urgentspecialist vascular evaluation, typically within 24 hours, is the standard of care following a retinal arterial event, including amaurosis fugax Risk of a stroke is relatively high in the first few days after a transient ischaemic attack (TIA). The detection of atrial fibrillation is of particular importance as admission for anticoagulation may be indicated.
- 82. ALL PATIENTS Smoking Symptoms of GCA (1–2% of central retinal artery occlusion – CRAO) : Headache, jaw claudication, scalp tenderness, limb girdle pain, weight loss and existing polymyalgia rheumatica Extremely unlikely under 55–60 years. Constitutes an ophthalmic emergency
- 83. Pulse -detect arrhythmia, particularly atrial fibrillation. Blood pressure. Cardiac auscultation for a murmur. Carotid auscultation is of limited value as the absence of a bruit does not exclude significant stenosis. ECG to detect arrhythmia and other cardiac disease. ESR and CRP to identify possible GCA.
- 84. Other bloodtests include : CBC (platelets may be raised in GCA) Glucose Lipids Urea and electrolytes
- 85. Carotid duplexscanning is a non-invasive screening test involving a combination of high-resolution real-time ultrasonography with Doppler flow analysis. If significant stenosis is present, surgical management may be considered
- 86. SELECTED PATIENTS Consideredon a targeted basis in some patients, particularly if younger and with no known cardiovascular risk factors, or there is an atypical clinical picture.
- 87. Further carotidimaging Cranial magnetic resonance imaging (MRI) or computed tomography (CT) may be indicated to rule out intracranial or orbital pathology. Echocardiography- Usually performed in young patients or if there is a specific indication such as a history of rheumatic fever, known cardiac valvular disease, or intravenous drug use. Chest X-ray. Sarcoidosis, tuberculosis, left ventricular hypertrophy in hypertension. 24-hour ECG to exclude intermittent arrhythmia.
- 88. Additional bloodtests : Fasting plasma homocysteine level to exclude hyperhomocysteinaemia. ‘Thrombophilia screen’ - refers to heritable thrombophilias, which have predominantly been implicated in venous rather than arterial thromboses. Plasma protein electrophoresis to detect dysproteinaemias such as multiple myeloma. Thyroid function tests, especially if atrial fibrillation is present; may be associated with dyslipidaemia.
- 89. Autoantibodies: Rheumatoidfactor, anticardiolipin antibody, antinuclear antibody, anti-double stranded DNA antibodies, principally looking for vasculitis in younger patients. Syphilis serology. Blood cultures.
- 91. TREATMENT Retinal arteryocclusion is an emergency because it causes irreversible visual loss unless the retinal circulation is re-established prior to the development of retinal infarction. Theoretically, timely dislodgement of thrombus or emboli may ameliorate subsequent visual loss Treatments may be tried in patients with occlusions of less than 24–48 hours’ duration at presentation, though evidence of benefit is limited.
- 92. The numberof measures tried and the intensity of treatment should be tailored to the individual More aggressive if lower duration of occlusion, good general health, monocularity More aggressive systemic treatment may be avoided in the frail elderly Lack of evidence for clear benefit and the risks, should be discussed before use
- 93. Adoption ofa supine posture: Might improve ocular perfusion and should always be implemented
- 94. Ocular massage: Using a three-mirror contact lens (allows direct artery visualization). Aim is to mechanically collapse the arterial lumen and cause prompt changes in arterial flow, improving perfusion and potentially dislodging an embolus or thrombus. One described method consists of positive pressure for 10–15 seconds followed by release, continued for 3–5 minutes. Self-massage through closed eyelids can be continued by the patient.
- 95. Breathing ahigh oxygen (95%) and carbon dioxide (5%) mixture, ‘carbogen’, has been advocated for a possible dual effect of retarding ischaemia and vasodilatation. ‘Rebreathing’ into a paper bag in order to elevate blood carbon dioxide and respiratory acidosis has been advocated, as this may promote vasodilatation
- 96. Anterior chamberparacentesis Using 27-gauge needle to withdraw 0.1–0.2 ml of aqueous is controversial but has been advocated by some authorities. Povidone-iodine 5% and topical antibiotic are instilled a few minutes prior to the procedure, with a short course of antibiotic afterwards. It may be prudent for ocular massage to be avoided following paracentesis.
- 97. Transluminal Nd:YAGlaser embolysis or embolectomy : BRAO or CRAO in which an occluding embolus is visible Shots of 0.5–1.0 mJ or higher are applied directly to the embolus using a fundus contact lens. Embolectomy has been said to occur if the embolus is ejected into the vitreous via a hole in the arteriole. The number of shots described in reports is extremely variable. The main complication is vitreous haemorrhage
- 98. Topical apraclonidine1%, timolol 0.5% and intravenous acetazolamide 500 mg to achieve a more sustained lowering of intraocular pressure. Sublingual isosorbide dinitrate to induce vasodilatation Hyperosmotic agents Mannitol or glycerol have been used for their possibly more rapid IOP-lowering effect as well as increased intravascular volume
- 99. Thrombolysis: Extrapolatingfrom successful treatment of stroke and myocardial infarction, various strategies have been used to deliver thrombolytic agents to the ophthalmic artery, including local arterial (internal carotid and ophthalmic) and intravenous infusion. A recent large trial of local intra-arterial fibrinolysis with recombinant tissue plasminogen activator (rtPA) showed no benefit over conservative treatment that included isovolaemic haemodilution Nearly 40% adverse reaction rate in the rtPA group.
- 100. OPD MANGEMENT Aimshould be to decrease IOP as it cause : Dislodgement of embolus Produce retinal dilatation and increase perfusion
- 101. Ocular massageis of utmost important especially with goldmann contact lens – done till re-establishment of continuous laminar flow and increase in width of blood column and disappearance of fragmented flow. IOP lowering agents Carbogen inhalation AC paracentesis
- 102.