retinal imaging conference

Retinal Imaging Conference

Doug Sigford, M.D.University of Louisville

Department of Ophthalmology and Visual Sciences

1/9/2014

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.

Medical HistoryPOHx: Radial Keratotomy OS

PMH: DM, HIV, hyperlipidemiaCD4 944 cells/μl, viral load undetectable

Meds: Insulin, ezetimibe, atorvastatin, efavirenz,

fosamprenavir, raltegravir , ritonavir

Allergies: NKDA

ROS: Unremarkable, no recent illness

Exam

BCVA P TTP

EOM: Full OU CVF: Full OU

Anterior Segment: unremarkable OU

20/20-3 (-1.00+0.50x65)

4mm

4mm

15

13(-) RAPD

20/20-1 (+0.75 sphere)

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

Mosaic Color Photo OS

Large temporal chorioretinal scar

Autofluorescence OD

OD: Hyperautofluorescence is seen in the periphery of the neurosensory detachment and patchy hypoautofluorescence is seen centrally.

Autofluorescence OS

OS: Mild perifoveal hyperautofluorescence

OCT OD

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

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.

OCT OS

Small PED

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

FA/ICG OD (late)

FA (right) shows increased hyperfluorescence consistent with leakage and pooling. ICG (left) shows stable hyper- and hypofluorescence.

03:45

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

FA/ICG OS (late)

Late FA and ICG show stable macular features as well as the large temporal chorioretinal scar

03:16

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

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

Follow-Up 2 week follow-up showed decreased

subretinal fluid

Initial OCT

Follow-up

Syphilis

Infection caused by the spirochete Treponema pallidum

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

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 placoid chorioretinitis Serous or exudative retinal detachment

Keratouveitis

Syphilis - Stages

Infection caused by the spirochete Treponema pallidum

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

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

Syphilis - Diagnosis

Treponemal tests High specificity FTA-Abs TPPA (treponema pallidum particle

agglutination assay) Remain positive for life

Syphilis - Treatment

Uncomplicated Single dose IM penicillin G or oral

azithromycin

Neurosyphilis IV penicillin for 10 – 14 days Lumbar puncture is recommended

References1. 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. Curr Opin Ophthalmol. 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. Curr Opin Ophthalmol. 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.

Thank You