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

2. 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)

3. 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)

4. 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

5. 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

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

7. Case M/63 신O균 2010년 9월 8일 - FAG

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

9. 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

10. Case M/63 신O균 2010년 9월 17일

11. Case M/63 신O균 2010년 9월 17일 - FAG

12. 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

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

14. 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)

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

16. 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.

17. 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.

18. 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

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

20. 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)

21. 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%

22. The carotid system

23. 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.

24. 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

25. 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

26. 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

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

28. 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.

29. 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 seconds of first dye in arteries
But you can also see this is CRAO, CRVO

30. 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

31. 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

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

33. 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?