Retinal Imaging Conference

1. Retinal Imaging Conference Doug Sigford, M.D. University of Louisville Department of Ophthalmology and Visual Sciences 1/9/2014

2. Patient Presentation CC: Routine diabetic eye exam HPI: 51 y/o white male without complaint presented for a routine diabetic eye exam. He had a 38 year history of type 1 diabetes mellitus, but no history of diabetic eye disease.

3. Medical History POHx: Radial Keratotomy OS PMH: DM, HIV, hyperlipidemia CD4 944 cells/μl, viral load undetectable Meds: Insulin, ezetimibe, atorvastatin, efavirenz, fosamprenavir, raltegravir , ritonavir Allergies: NKDA ROS: Unremarkable, no recent illness

4. 4mm 15 4mm 13 Exam BCVA P TTP EOM: Full OU CVF: Full OU Anterior Segment: unremarkable OU 20/20-3 (-1.00+0.50x65) (-) RAPD 20/20-1 (+0.75 sphere)

5. Color Fundus Photos OD: Neurosensory detachment of the inferior macula including the fovea with underlying deep yellow lesions and RPE atrophy. Inferior cotton wool spots are also seen. OS: Deep yellow lesions with areas of RPE atrophy

6. Mosaic Color Photo OS Large temporal chorioretinal scar

7. Autofluorescence OD OD: Hyperautofluorescenceis seen in the periphery of the neurosensory detachment and patchy hypoautofluorescence is seen centrally.

8. Autofluorescence OS OS: Mild perifovealhyperautofluorescence

9. OCT OD OCT through the fovea shows subretinal fluid, RPE disruption, and hyperreflective spots in the outer retina

10. OCT OD OCT inferior to the fovea shows more subretinal fluid, CME, increased disruption of the RPE, and increased hyperreflective spots in the outer retina.

11. OCT OS Small PED

12. FA/ICG OD FA (right) shows early hyperfluorescence primarily in the central portion of the neurosensory detachment. ICG (left) shows both hyper- and hypofluorescence in the same area. 00:41

13. FA/ICG OD (late) FA (right) shows increased hyperfluorescence consistent with leakage and pooling. ICG (left) shows stable hyper- and hypofluorescence. 03:45

14. FA/ICG OS FA (right) shows punctate areas of hyperfluorescence corresponding to the subretinal yellow lesions seen clinically. ICG (left) shows small hypofluorescent and hyperfluorescent areas. 01:01

15. FA/ICG OS (late) Late FA and ICG show stable macular features as well as the large temporal chorioretinal scar 03:16

16. Assessment and Plan • A: 52yo WM with chorioretinitis OD > OS • Differential • Syphilis • TB • Lyme disease • Toxoplasmosis • Chronic central serous chorioretinopathy • P: Check RPR, FTA-ABS, Toxoplasma titers, PPD

17. Follow-Up • RPR 1:1 (previously nonreactive) • FTA-ABS positive • Plan • The patient’s primary doctor was notified and a PICC line was placed for a 2 week course of IV penicillin

18. Follow-Up 2 week follow-up showed decreased subretinal fluid Initial OCT Follow-up

19. Syphilis • Infection caused by the spirochete Treponemapallidum • Occurs in four stages (plus congenital): • Primary – characterized by a skin lesion (chancre) at the point of contact with regional lymphadenopathy • Secondary – four to ten weeks after primary infection, most commonly involves skin, mucous membranes, and lymph nodes • Latent • Tertiary – gummatous, neurosyphilis, or cardiovascular

20. Ocular Syphilis • May affect all structures of the eye • The most common ocular finding in both secondary and tertiary syphilis is uveitis • Iridocyclitis • Posterior Uveitis • Focal or diffuse necrotizing retinitis • Punctate inner retinitis • Vasculitis • Posterior placoidchorioretinitis • Serous or exudative retinal detachment • Keratouveitis

21. Syphilis - Stages • Infection caused by the spirochete Treponemapallidum • Occurs in four stages (plus congenital): • Primary – characterized by a skin lesion (chancre) at the point of contact with regional lymphadenopathy • Secondary – four to ten weeks after primary infection, most commonly involves skin, mucous membranes, and lymph nodes • Latent • Tertiary – gummatous, neurosyphilis, or cardiovascular

22. Syphilis - Diagnosis • Nontreponemal tests • Moderate sensitivity, low specificity • Rapid plasma reagin (RPR) • Venereal disease research laboratory (VDRL) • Detect anti-cardiolipin antibodies through their interaction with diphosphatidyl glycerol • Can be used to monitor therapy and reactivation

23. Syphilis - Diagnosis • Treponemal tests • High specificity • FTA-Abs • TPPA (treponemapallidum particle agglutination assay) • Remain positive for life

24. Syphilis - Treatment • Uncomplicated • Single dose IM penicillin G or oral azithromycin • Neurosyphilis • IV penicillin for 10 – 14 days • Lumbar puncture is recommended

25. References 1. Mattei PL, Beachkofsky TM, Gilson RT, Wisco OJ. Syphilis: a reemerging infection. Am Fam Physician. 2012 Sep 1;86(5):433-40. 2. Aldave AJ, King JA, Cunningham ET Jr. Ocular syphilis. CurrOpinOphthalmol. 2001 Dec;12(6):433-41. 3. Wilhelmus K, Lukehart S: Syphilis. In Ocular Infection and Immunity. Edited by Pepose J, Holland G, Wilhelmus K: Mosby; 1996:1437–1466.  4. Gaudio PA. Update on ocular syphilis. CurrOpinOphthalmol. 2006 Dec;17(6):562-6. 5. Tamesis RR, Foster CS. Ocular syphilis. Ophthalmology 1990; 97:1281–1287. 6. Hughes EH, Guzowski M, Simunovic MP, Hunyor AP, McCluskey P. Syphilitic retinitis and uveitis in HIV-positive adults. Clin Experiment Ophthalmol. 2010 Dec;38(9):851-6. doi: 10.1111/j.1442-9071.2010.02383.x. 7. Kunkel J, Schürmann D, Pleyer U, et al. Ocular syphilis—indicator of previously unknown HIV-infection. J Infect 2009; 58:32–36. 8. Lynn WA, Lightman S. Syphilis and HIV: a dangerous combination. Lancet Infect Dis. 2004 Jul;4(7):456-66.

26. Thank You