Ocular ischemic syndrome Angio Conference Ocular ischemic syndrome R2 한재형/AP.박영훈

Case M/63 신O균 2010년 8월 30일 초진 Chief complaint : Decreased visual acuity(OS) Ocular pain(OS) Past Hx. 2008년 NVG(OD) 진단 후 우안 실명 : LP(-) 약 1년 전부터 점진적인 시력저하 소견 있어 타병원 경유 R/O OIS(OS)로 Evaluation 위해 외래 방문함. DM/HTN(+/+) for 5yrs 2004, 2006 Cat.Op(OU) at local O-COST x2, Iopidine eyedrop x2(OU)

Case M/63 신O균 2010년 8월 30일 초진 VA OD LP(-) OS 0.16(0.63 x-0.75Ds : -1.00Dc Ax 180) IOP OD 25 OS 19 mmHg Pupil : NVI(OU) Gonioscopy PAS(OU) but No NVA(OU)

Case M/63 신O균 2010년 8월 30일 초진 Fundus OS vessel narrowing c CWS Imp : Ocular ischemic syndrome(OS) Plan Carotid Doppler Sonography CT angio 3D carotid bifurcation FAG 신경과 협진 의뢰

Case M/63 신O균 2010년 9월 6일 신경과 진료 Carotid Doppler Sonography & CT angio 3D Carotid bifurcation Marked stenosis of both proximal ICA 신경과 Plan : Admission & evaluation

Case M/63 신O균 2010년 9월 8일 – Fundus photography Corrected VA OS : 0.63

Case M/63 신O균 2010년 9월 8일 - FAG

Case M/63 신O균 2010년 9월 8일 Diagnosis : OIS(OU) 신경과 입원 예정으로 협진하기로 함.

Case M/63 신O균 2010년 9월 17일 VA OS 0.04(n-c) IOP OD 13mmHg OS 13mmHg 신경과 입원 지연으로 9월 16일 입원 4 vessel angiography Rt ICA 78% oclussion Lt ICA 88% oclussion

Case M/63 신O균 2010년 9월 17일

Case M/63 신O균 2010년 9월 17일 - FAG

Case M/63 신O균 2010년 9월 19일 VA OS 0.02(n-c) IOP OD 26 mmHg OS 21 mmHg O-COST x2, O-BMDP x2 /OU, O-LTP xhs/OD Fd stationary, no cherry red spot

Case M/63 신O균 2010년 9월 20일 Lt. Proximal ICA의 Ballooning 시행 후 퇴원

Case M/63 신O균 2010년 9월 30일 VA OS 0.08 IOP OS 32mmHg O-COST x2, O-BMDP x2, O-LTP xhs /OS Pupil : NVI(OS)

Case M/63 신O균 2010년 9월 30일 Imp : NVG(OS) Plan : PRP(OS)

Case M/63 신O균 2010년 10월 4일 VA OS 0.06(0.1 x -2.00Ds : -0.75Dc Ax 10) IOP OD 25 OS 36 2nd PRP(OS) 녹내장 part consult - Reperfusion으로 안압 상승한 것으로 보이 며 수술 필요함.

Case M/63 신O균 2010년 10월 11일 VA OS 0.1(0.125 x -1.75Ds : -1.00Dc Ax 20) IOP OD 20 OS 19 NVI(OS) 감소 Ahmed valve insertion(OS) 시행하기로 함. 10월 18일 시행함.

Case M/63 신O균 2010년 11월 3일 VA OS 0.125(0.16 x -0.75Ds : -0.75Dc Ax 70) IOP OD 23 OS 30 NVI(-) OS

Ocular ischemic syndrome Angio Conference -Review Ocular ischemic syndrome R2 한재형/AP.박영훈

Ocular ischemic syndrome Definition : Caused by a reduction in blood inflow to the eye by obstruction of the carotid artery, and less often ophthalmic artery Ocular effects include manifestation of both posterior and anterior segment ischemia Rubeosis iridis & NVG, Uveitis, retinal Hm., posterior seg. neovacularization, vessel changes Leads to progressive visual loss; Poorer outcome with rubeosis iridis(90% legally blind within one year)

Incidence Mean age : 65 years old (50’s to 80’s) No preference for race Males > Females (2:1) Incidence estimated ~ 7.5 case/million Unilateral in 80%, bilateral in 20%

The carotid system

OIS Etiology 1. 70% or greater stenosis of the ipsilateral carotid system (CC or ICA) 90% decreases CRA perfusion pressure by 50% For bilateral OIS, usually 100% occlusion of one ICA and 50% stenosis contralaterally Cause is most often atherosclerosis of the carotid artery Less commonly giant cell arteritis, vasospasm, trauma 2. Can be due to ophthalmic artery obstruction or other occlusive diseases in aortic arch, CRA or ciliary arteries(chronic obstruction). Also thromboembolism, vasculitis.

Presentation and Symptoms 1. Vision loss Reported by 90% of patients 2/3: vision loss gradual over a few weeks 12% : vision loss abrupt; see cherry red spot 2. Reduced recovery time after bright light exposure Due to macular ischemia 3. History of amaurosis fugax in 10% Loss of vision for a few seconds or minutes 1/3 of amaurosis fugax have a 75% or greater carotid artery obstruction 4.Pain Described as a dull ache “ocular angina” May be caused by NVG or because of globe/dura ischemia

Anterior segment findings Rubeosis Iridis (iris neovascularization) 2/3 of patients at time of presentation Causes NVG Only a little more than 50% develop IOP increase because of decreased ciliary body perfusion. May see hypotony instead. Cells/Flare in the anterior chamber Usually in eyes with rubeosis iridis Cells are found in 1/5 of eyes, usually not > 2+ Lens opacification

Course of NVG Prerubeosis stage Preglaucoma stage Normal IOP, rubeosis iridis begins: dilated capillaries near pupil margin that first begin intrastromally Open-Angle Glaucoma stage Elevated IOP, more neovascularization, AC reaction, hyphema Angle-Closure Glaucoma Stage Flat iris stroma with fibrovascular membrane that undergoes contraction Peripheral anterior synechiae Severe glaucoma; need surgical intervention

NVG Theories for neovascularization Retinal hypoxia Angiogenesis factors (e.g. VEGF) Local hypoxia of iris -> iris vessel dilation -> new vessel formation

Posterior segment findings 1. Narrowed retinal arteries 2. Dilated retinal veins But, NOT tortuous contrast with CRVO(tortuous veins) May also see beading Occurs because of ischemia 3. Retinal hemorrhage(80%) 4. NV NVD in 35% of eyes 5. Cherry red spot & CWS etc.

FAG 1. Delayed or patchy choroidal filling (60%) Normal choroidal filling is complete 5 seconds after you see the dye; sometimes this can be delayed for a minute or more Most specific FA sign in OIS 2. Prolonged retinal arteriovenous transit time(95%) Normal is complete filling of major veins in temporal arcade within 10-11 seconds of first dye in arteries But you can also see this is CRAO, CRVO

3. Retinal vessel staining (85%) Arteries > veins due to ischemic damage to epithelial cells 4. Macullarr edema (1/6) Due to hypoxia, endothelial damage, microaneurysms But, not as much edema as diabetic retinopathy or ocular surgery 5. Retinal capillary nonperfusion Due to endothelial and pericyte damage

Treatment: Carotid Endarterectomy Can initially help save vision, but still get poor vision 1 year after the surgery Can get IOP increase after endaterectomy with rubeosis iridis and angle blockage

Treatment : PRP Can increase IOP after surgery -> AION or retinal ischemia Only about 36% of patients will get NVI regression after treatment

Treatment : NVG PRP/Panretinal cryotherapy Goniophotocoagulation in anterior chamber Effective in early stages; prevent closure Medical management Open-angle stage Not miotics (inc. inflammation/discomfort) Cyclocryotherapy (to reduce ciliary body blood flow and pain), Transscleral Nd:YAG cyclophotocoagulation Filtering surgeries(trabeculectomy or full thickness filtering procedure) Silicone oil injection?