Indocyanine Green Angiography Features in Acute Syphilitic Posterior Placoid Chorioretinitis


Acute syphilitic posterior placoid chorioretinitis (ASPPC) is a rare clinical manifestation of ocular syphilis. The cause of the placoid lesion is still up for debate but could be caused by an impaired choriocapillaris perfusion. However, less attention has been paid to the hypofluorescence of the plaque on late-phase indocyanine green angiography (ICGA). The aim of this study was to comprehensively analyze multimodal imaging findings in patients with ASPPC and to highlight the value of ICGA for the diagnosis of ASPPC.


Retrospective observational case study.


The medical records of patients with uveitis who consulted our tertiary center between 2012 and December 2015 were reviewed. Patients who were diagnosed with uveitis related to syphilis infection with posterior placoid lesions seen on multimodal imaging were included. We compared the aspect of ASPPC on fundus color photography, blue autofluorescence, fluorescein angiography, optical coherence tomography, and early-, mid- and late-phase ICGA.


Fifteen eyes of 12 patients were included in the study. Hypofluorescent plaques were seen on late-phase ICGA in all eyes, corresponding to the placoid lesions visible on blue autofluorescence, while the choriocapillaris filling was normal on fluorescein angiography and ICGA. Within the plaques, optical coherence tomography showed ellipsoid zone disruptions, outer retinal disruptions, and retinal pigment epithelium granulations.


ASPPC could be caused by retinal pigment epithelium dysfunction secondary to an infectious or inflammatory disorder, characterized by a hypofluorescence visible only on late-phase ICGA, and resulting in photoreceptor disruptions. The RPE impairment was reversible after prompt antibiotic treatment.

A cute syphilitic posterior placoid chorioretinitis (ASPPC) is a rare manifestation of ocular syphilis. It was first described by Gass and associates as “large placoid yellowish lesions at the level of the retinal pigment epithelium (RPE) in the macula and juxtapapillary area.” In recent studies focused on ocular complications of syphilis, the placoid type of chorioretinitis has been found in 3% to 58% of patients with ocular findings secondary to syphilis. , Treponema pallidum present in the bloodstream has initially been assumed to enter the choroidal circulation and access the outer retina where the choroidal vascular supply is greatest. It has been hypothesized that the presence of T pallidum in the choriocapillaris could lead to an inflammatory reaction or to antibody release and secondary focal ischemia in the choriocapillaris. Under this hypothesis, outer retinal lesions would be caused by the choriocapillaris nonperfusion. While several publications have described in detail the aspects of syphilitic placoid lesions in relatively large series of eyes, , the respective involvement of the choriocapillaris and RPE remains debated. Less attention has been paid to the meaning of the hypofluorescence of the placoid lesions seen on late-phase indocyanine green angiography (ICGA). The aim of this study was to comprehensively analyze multimodal imaging findings in a series of syphilitic placoid lesions examined in the early stage of the disease. The comparison between fundus color photography, blue fundus autofluorescence (B-FAF), fluorescein angiography (FA), ICGA, and spectral-domain optical coherence tomography (SD-OCT) suggests specific involvement of the RPE and photoreceptors in syphilitic placoid lesions.


The charts of 1493 patients diagnosed with uveitis who consulted our tertiary ophthalmological center (Centre Hospitalier National d’Ophtalmologie des Quinze-Vingts, Paris, France) between January 2012 and December 2015 were reviewed. Among them, 22 patients tested positive for syphilis (confirmed by positive results for the Venereal Disease Research Laboratory test and T pallidum hemagglutination assay) and 14 of these patients had ASPPC. ASPPC was defined by the presence of ≥1 yellowish placoid lesion(s) located at the RPE in the posterior pole. Imaging examinations consisted of fundus color photography acquired with a digital nonmydriatic retinal camera (Canon CR-2 Plus AF), B-FAF (using an excitation wavelength at 488 nm and a barrier filter at 500 nm), FA and ICGA acquired using the Heidelberg Retinal Angiograph confocal scanning laser ophthalmoscope, and the Spectralis SD-OCT (Heidelberg Engineering). All SD-OCT B-scans were acquired using the same protocol: 19 horizontal scan lines over the macular area spaced by 200 μm.

Eyes for which no early-, intermediate-, or late-phase ICGA images were available for interpretation were excluded from the analysis. The findings from the various imaging modalities were compared and correlated based on a multimodal imaging interpretation. In 7 eyes of 6 patients, longitudinal follow-up allowed comparisons of the lesions before and after treatment.

Our study met the tenets of the Declaration of Helsinki.



Of the 22 patients with ocular syphilis, 14 had ASPPC and 2 were excluded because of incomplete multimodal imaging. The lesions were bilateral in 3 cases so that 15 eyes of 12 patients were included. There were 11 men and 1 woman. Seven male patients (58%) were men who have sex with other men. One patient (8%) was HIV-positive. Patients’ mean age was 50 years (34-58 years; median 51.5 years).

Regarding the stage of syphilis, 9 patients (75%) had secondary syphilis, and among them 3 (25%) had neurosyphilis (high leukocyte counts or protein concentration >0.5 g/L in the cerebrospinal fluid or a cerebrospinal fluid polymerase chain reaction study that was positive for T pallidum ), and the remaining patients had unknown stages of syphilis. No fluorescent treponemal antibody absorption test to detect the presence of anti– T pallidum antibodies was performed in 4 patients, but the results of the T pallidum hemagglutination assay and Venereal Disease Research Laboratory test were positive in all patients at the time of diagnosis.


The mean time to ocular diagnosis was 25 ± 25 days (median 14.5 [range 1-90] days). The mean best-corrected visual acuity was 0.91 ± 0.76 logarithm of the minimum angle of resolution (logMAR; Snellen equivalent 20/160 [median 1.15 {range 0-2.3} logMAR]; Snellen equivalent 20/320) before treatment and 0.03 ± 0.10 logMAR (Snellen equivalent 20/20 [median 0 {range −0.2 to 0.2} logMAR]; Snellen equivalent 20/20) after treatment.

On ophthalmoscopic and color fundus examination, deep yellowish placoid lesions extending to the posterior pole were observed. In 8 cases, the plaque was located within the temporal arcades. In 5 cases, it also extended beyond the arcades and/or around the optic disc. In 1 case, it was only located around the optic disc.

The placoid lesion was hyperautofluorescent on B-FAF in all eyes ( Figure 1 ). In 6 eyes, multiple smaller hyperautofluorescent spots were also present around the main plaque ( Figure 1 ). In 10 eyes, there were additional “brighter dots” within the main plaque corresponding to hyperreflective nodular elevations of the RPE on SD-OCT ( Figure 2 ).

Figure 1

Fundus autofluorescence of syphilitic placoid lesions showing their hyperautofluorescence. A through F. Note the presence of satellite hyperautofluorescent dots located outside the main plaque in all cases. In part C, note the presence of brighter spots within the main placoid lesion.

Figure 2

Syphilitic placoid lesion with retinal pigment epithelium clumps. A. Hyperautofluorescence of the placoid lesion and hyperautofluorescent dots (some of them marked with arrows). B. The hyperautofluorescent dots are hypofluorescent on fluorescein angiography and on indocyanine green angiography (ICGA), especially during the late phase (arrows and arrowheads in C and D). E. The optical coherence tomography vertical B-scan shows retinal pigment epithelium clumps (arrowheads corresponding to the hypofluorescent dots seen on late-phase ICGA). The ellipsoid zone is absent within the placoid lesion (large arrow also corresponding to the border of the lesion seen in D).

On early-phase FA, the placoid lesions were isofluorescent in 11 cases ( Figure 3 ) or slightly hyperfluorescent in 4 cases. No early hypofluorescence suggesting delayed choriocapillaris filling was present. The placoid lesion became progressively and variably hyperfluorescent during the middle and late phases of FA in the 15 eyes ( Figure 3 ). The small hyperautofluorescent lesions located outside the main plaque also became hyperfluorescent during the late phase of FA. Eight of 15 eyes presented with papillitis, and 6 with venous vasculitis on FA ( Figure 3 ). None of the patients had inflammation in the anterior segment.

Figure 3

Syphilitic placoid lesion with serous macular detachment. A. Hyperautofluorescent plaque occupying the posterior pole and surrounding the optic disc. B. Early-phase fluorescein angiography showing a slight hyperfluorescence in the area of the plaque. C. The plaque is partially stained and is associated with papillitis and vasculitis (arrows). D. Early-phase indocyanine green angiography (ICGA) showing a normal fluorescence background within the placoid lesion. E. Mid-phase ICGA (7 min) showing that the placoid lesion becomes darker than the surrounding fundus. F. Late-phase ICGA (30 min) showing a deep hypofluorescence of the placoid lesion. G. Horizontal OCT B-scan passing through the fovea showing the serous retinal detachment, retinal pigment epithelium clumps and the loss or attenuation of the ellipsoid zone.

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Sep 11, 2022 | Posted by in OPHTHALMOLOGY | Comments Off on Indocyanine Green Angiography Features in Acute Syphilitic Posterior Placoid Chorioretinitis

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