retinal imaging conference
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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 - PowerPoint PPT PresentationTRANSCRIPT
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.
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