1. Grand Rounds Eddie Apenbrinck M.D.
University of Louisville School of Medicine
Department of Ophthalmology & Visual Sciences
4/1/2016 1 1

2. Subjective
CC: sudden painless loss of vision OD HPI: 80 year old white male referred to Retina clinic for sudden painless loss of vision in the right eye. Loss of vision occurred over seconds and was not associated with any pain, flashes or floaters.

3. POH: Pseudophakia OU (2006) PMHx: HTN, NIDDM, Hyperlipidemia ROS: denies any temporal artery tenderness, headaches, jaw claudication, fatigue, weight loss, appetite changes Meds: Metformin, Simvastatin, Lisinopril Allergies: NKDA

4. Exam VA(cc,n): 20/25 20/20 -0.50 sphere -1.00+0.50x150
OD OS
VA(cc,n): / /20
-0.50 sphere x150
Pupils: no APD
IOP:
CVF: Very Constricted Full
EOM: Full OU 4

5. Exam Anterior Segment L/L: WNL OU C/S: WNL OU Cornea: WNL OU
OD OS
Anterior Segment
L/L: WNL OU
C/S: WNL OU
Cornea: WNL OU
AC: No cell or flare OU
I/L: PCIOL OU
Vitreous: WNL OU 5

6. HVF 30-2 OS OD

7. Fundus Photos OD OS
Normal

8. BAF OD OS

9. OCT: Fovea OD OS

10. OCT: OD Fovea

11. OCT: OD

12. Fluorescein Angiogram OD

13. FA OD OS

14. Assessment and Plan Assessment Plan
80 year old male with CRAO with patent cilioretinal artery
Plan
Observe
Obtain Carotid, Echocardiogram

15. Work-up Echocardiogram: unremarkable Carotid ultrasound
Right ICA: 50-69% stenosis based on peak systolic velocity
Left ICA: poor study, recommend CTA
CTA: significant atherosclerotic calcifications involving left carotid bulb and proximal internal carotid artery indicating high grade stenosis vs occlusion

16. 1 month follow-up No significant changes in vision per patient
BCVA OD: 20/25 OS: 20/20
IOP: OD 11 OS 12
DFE OD: New NVD and VH (inferiorly)

17. FA OD

18. Assessment/Plan
80yo with CRAO with patent cilioretinal OD and new NVD and VH OD
Plan
PRP OD: #1000 burns, 360 degrees in periphery

19. 2 Month follow-up 4 Month follow-up
BCVA OD: 20/25
DFE OD: NVD with resolving VH
OCT OD: VMT
Plan:
Observe
4 Month follow-up
BCVA OD: 20/25
DFE OD: Optic Disc Collaterals and resolving VH
OCT OD: VMT
Plan:
Observe

20. OCT OD: 2 month F/U
OCT OD: 4 month F/U

21. Central Retinal Artery Occlusion
Characterized by unilateral, sudden, painless
vision loss
Visual acuity at the time of initial presentation ranges from counting fingers to light perception in 74-90% of eyes
A patent cilioretinal artery is seen in approximately one- third of cases.

22. Epidemiology
The estimated incidence of CRAO is 1 in 10,000 cases at tertiary referral centers.
The average age at presentation is in the early sixties
Men are affected more frequently than women
1-2% of cases may manifest bilaterally

23. Central Retinal Artery Occlusion
CRAO is often caused by arthrosclerosis-related thrombosis occurring at the level of the lamina cribrosa
Evaluation of embolic source
Carotid Doppler Imaging (presence or absence of plaque)
Echocardiography
Hypercoagulability work-up in patients <50 yo

24. CRAO Treatment NaturalCourse Current conventional therapy
Less than 10% of cases report improvement in VA
Current conventional therapy
Dislodging emboli: ocular massage, Yag laser embolectomy
Reducing IOP: anterior chamber paracentesis
Vasodilation: Carbogen (95% O2 & 5% CO2), nitrates
Maintaining retinal oxygenation: hyperbaric oxygen
Thrombolytics: streptokinase, urokinase, and tissue plasminogen activator
None of these treatments have proven effective and their use is largely based on anecdotal reports and small case series.

25. Retrospective case series of 168 cases of CRAO
NVD developed in three patients after CRAO, an occurrence rate of 1.8%.
Rubeosis iridis also developed in two of the three patients.
All three eyes received panretinal laser photocoagulation, with eventual resolution of the NVD

26. Lit Search
Retrospective case series of consecutive patients (286 total eyes: 83 CRAOs and 203 BRAOs)
Twelve (14.5%) of the 83 eyes with a CRAO developed ocular neovascularization
(91.7%) had iris neovascularization
(83.3%) had neovascular glaucoma
(16.7%) had neovascularization of the optic disc.
2 of the 203 eyes with a BRAO developed iris neovascularization
Diabetes mellitus type 2 was a risk factor for ONV development following a CRAO with an adjusted odds ratio of 5.2

27. References
BCSC: Retina and Vitreous. Central Retinal Artery Occlusion. Pgs
Ryan SJ. Retina. 4th ed. Philadelphia: Elsevier/Mosby; 2013.
Rumelt S, Dorenboim Y, Rehany U. Aggressive systematic treatment for central retinal artery occlusion. Am J Ophthalmol 1999;128:733–8.
Brown GC, Magargal LE. Central retinal artery obstruction and visual acuity. Ophthalmology 1982;89:14–9.
Hayreh SS, Zimmerman MB. Central retinal artery occlusion: visual outcome. Am J Ophthalmol 2005;140:376–91.
Biousse V, Calvetti O, Bruce BB, et al. Thrombolysis for central retinal artery occlusion. J Neuroophthalmol 2007;27:215–30.
Park SJ, Choi NK, Seo KH, Park KH, Woo SJ. Nationwide Incidence of Clinically Diagnosed Central Retinal Artery Occlusion in Korea, 2008 to Ophthalmology Jun 7. pii: S (14) doi: /j.ophtha [Epub ahead of print]
Tang WM, Topping TM, Vitreous surgery for central retinal artery occlusion. Arch Ophthalmol 2000 Nov;118(11):
Hayreh SS, Jonas JB. Optic disk and retinal nerve fiber layer damage after transient central retinal artery occlusion: an experimental study in rhesus monkeys. Am J Ophthalmol 2000;129:786–95.