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Central Retinal Artery Obstruction: Diagnosis & Management | Grand Rounds Conference

Explore a case study of sudden vision loss, differential diagnoses, treatment options, and potential complications of CRAO. Learn about the epidemiology, pathogenesis, and management strategies for this eye condition.

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Central Retinal Artery Obstruction: Diagnosis & Management | Grand Rounds Conference

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  1. Grand Rounds Conference Tala Kassm DO December 10th, 2015 University of Louisville Department of Ophthalmology and Visual Sciences

  2. Subjective • CC: “I can’t see since last night.” • HPI: 81 year old male presents to clinic with complaint of sudden painless vision loss in his left eye for one day. Denies headaches, fevers, weight loss, jaw claudication or temporal tenderness. No associated pain, flashes or floaters. • Review of Systems: per HPI.

  3. History POH: - HRVO with CME OD s/pavastin - POHS OU with macular scar OS - PCIOL OU - BRVO OS (2008) - Mild NPDR OU

  4. History PMH: DMII, HTN, hypothyroidism, CVA, HLD Family Hx: noncontributory Meds: insulin, lisinopril, levothyroxine, xarelto, simvastatin Allergies: NKDA

  5. Clinical Exam OD OS VA(cc,D): 20/40 HM (-1.25+0.75x160) (-1.00+1.00x180) Pupils: 3->2 3->2 2+rAPD OS IOP: 15 14 EOM: FULL FULL CVF: FULL unable to assess Anterior Segment: PCIOL OU

  6. Clinical Exam • Dilated Fundus Exam: • OD OS ON c/d- 0.4 c/d- 0.5 Macula cotton wool spots juxtafoveal POHS scar mild edema retinal whiteningperifoveally VesselsSuperior HRVO small emboli in primary superotemporal artery, box carring Periphery POHS scars OU

  7. OCT Retina - OS

  8. FA OS

  9. FA OS

  10. FA - OS

  11. Assessment • 81 year old male with sudden painless vision loss of left eye. • Diagnosis: Central retinal artery occlusion OS • Differential also includes: • Giant Cell Arteritis

  12. Plan Treatment options discussed at length with patient – 25 gauge pars planavitrectomy Patient declined surgery. Ocular massage attempted. AC paracentesis performed. Carotid doppler ultrasound ordered and 2-D echocardiogram

  13. Follow Up: Three Days Vision: HM OS Pressure OS: 14 mmHg Vessels appeared narrow with box carring, diffuse retinal edema Patient reports he ran out of xarelto three weeks ago Started on a baby aspirin

  14. Follow up: 5 weeks • Vision still HM OS but IOP now 38 mmHg OS • Gonioscopy showed NVA • Diagnosis: • NVG OS secondary to CRAO • Plan: • Avastin OS, PRP in the future • Start Cosopt BID OS

  15. Central Retina Artery Obstruction • Defined as an abrupt decrease of blood flow through the central retinal artery severe enough to cause ischemia of the inner retina • Hallmark symptom: abrupt painless loss of vision in one eye • Initial presenting vision of 20/800 or worse • Light perception to counting fingers in 90% of patients

  16. Presentation Fundus may appear relatively normal in the first few minutes to hours after obstruction Axonal swelling in the nerve fiber layer results in whitening of the retina and arteries appear attenuated In severe obstruction, veins and arteries manifest box-carring or segmentation of blood flow Cherry-red spot: orange reflex from intact choroidal vasculature beneath the fovea

  17. Epidemiology • Accounts for an estimate of 1 in 10,000 outpatient visits to the ophthalmologist • Incidence of 1.9 per 100,000 • Men to women 2:1 ratio • Mean age 60 years • Has been reported to occur from first to ninth decade • Bilateral involvement in 1-2% of cases

  18. Pathogenesis • Believed that majority are caused by thrombus formation at or proximal to the lamina cribrosa. • An embolus is visible in the central retinal artery in 20-25% of cases. • Other causes: • Inflammation in the form of vasculitis (Ie. varicella) • Local trauma to the optic nerve or blood vessels • Dissecting aneurysm or arterial spasm within central retinal artery • Giant cell arteritis

  19. Management of CRAO • Reduce IOP • IOP- lowering medications • Anterior chamber paracentesis • Ocular massage • Thought to possibly dislodge emboli • 25 gauge vitrectomy • No longer recommended • Carbinogenvasodilatory inhalation therapy • Hyperbaric oxygen therapy • Catheterization of ophthalmic artery with tPA infusion • TransvitrealNd:YAGembolysis

  20. Course and Outcome • Vision loss is permanent due to infarct of inner retina • Irreversible damage to sensory retina after 90-100 minutes of complete CRAO • Vision of 20/400 or worse in 66% of cases • Complications • Iris neovascularization occurs in 18% of eyes • Less than five percent develop neovascular glaucoma

  21. Neovascularization of the Iris • Also known as rubeosisiridis • Occurs after retinal ischemia – most commonly caused by proliferative diabetic retinopathy (PDR), central retinal vein occlusion (CRVO) or carotid artery occlusive disease (CAOD) • Less commonly: • CRAO, sickle cell retinopathy, anterior segment ischemia • Can also occur with tumors, uveitis, chronic RD

  22. Neovascular Glaucoma Neovascularization of the iris and the angle leads to fibrovascular membranes Obstruct trabecular meshwork -> secondary open-angle glaucoma With disease progression the fibrovascular membranes mature and contract, tenting the iris toward the trabecular meshwork -> Peripheral anterior synechiae and angle closure-> secondary angle-closure glaucoma

  23. Neovascular Glaucoma - Treatment Indentify and address underlying etiology Systemic workup for CRVO, PDR, CRAO and carotid artery occlusive disease Mainstay of treatment and prevention is panretinal photocoagulation (PRP) or cryotherapy Medical therapy with atropine 1%, topical steroids and antiglaucoma medications

  24. Mason, John O; Patel, Shyam A; Feist, Richard M; Albert Jr., Michael A; Huishingh, Carrie; McGwinJr, Gerald, Thomley, Martin L. • Investigate the ocular neovascularization rate in eyes with a branch retinal artery occlusion or a central retinal artery occlusion • Study factors that influence ONV rate secondary to CRAO. • Retrospective case series – 83 CRAO’s and 203 BRAO’s.

  25. In the CRAO group, 14.5% developed ONV • Average time for development of ONV was 30.7 days • Diabetes mellitus type 2 was a risk factor for ONV development after CRAO – odds ratio of 5.2 • Patients with DMII should be monitored closely for first 6 months after CRAO for ONV

  26. References Falkenberry SM, Ip MS, Blodi BA, Gunther JB. Optical coherence tomography findings in central retinal artery occlusion. Ophthalmic Surg Lasers Imaging. 2006; 37(6):502-505. BCSC: Retina and Vitreous pages 131-135 Mason, Jason O. Patel, Shyam A. Feist, Richard M. Albert Jr, Michael A. Huisingh, Carrie. McGwinJr, Gerald. Thomley, Martin L. Ocular neovascularization in eyes with a central retinal artery occlusion or a branch retinal artery occlusion. Clinical Ophthalmology 2015 (9): 995-1000. Ryan SJ. Retina. 4th ed. Philadelphia: Elsevier/Mosby; 2013. Park SJ, Choi NK, Seo KH, Park KH, Woo SJ.Nationwide Incidence of Clinically Diagnosed Central Retinal Artery Occlusion in Korea, 2008 to 2011.Ophthalmology. 2014 Jun 7. pii: S0161-6420(14)00383-2. doi: 10.1016/j.ophtha.2014.04.029. [Epub ahead of print]

  27. Thank you for listening

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