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We describe a healthy 37-year-old man with Bartonella henselae (B. henselae) neuroretinitis with concurrent central retinal vein occlusion and ischemic optic neuropathy resulting in optic atrophy and choroidal ischemia.Case report.A 37-year-old man presented with unilateral decreased vision and a fundus examination consistent with neuroretinitis. Further imaging review supported a concurrent diagnosis of central retinal vein occlusion. Although initially negative, repeat serological testing for B. henselae infection was positive. Multimodal imaging displayed severe outer retinal disruption, ischemic optic neuropathy, and choroidal ischemia. The patient demonstrated near complete resolution of fundus findings and restoration of outer retinal architecture. Residual findings included optic disk pallor and ischemic choroidopathy.B. henselae neuroretinitis may be associated with concurrent retinal vascular occlusive disease and ischemic optic neuropathy. Central retinal vein occlusion and choroidal ischemia leading to optic nerve atrophy are additional sequelae further expanding the clinical spectrum of this entity.

A 44-year-old woman noticed bilateral irregular scotomata associated with photopsias of 6-month duration. Ophthalmoscopic examination demonstrated multiple bilateral, pericentral, hypopigmented, petaloid, macular lesions evident on Amsler grid associated with paracentral hyperreflective lesions on optical coherence tomography in the outer plexiform and nuclear layers. Indocyanine green angiography revealed patches of choroidal ischemia consistent with acute macular neuroretinopathy.

The area of choriocapillaris nonperfusion on optical coherence tomography angiography correlated with the area of macular atrophy on fundus autofluorescence in eyes with exudative age-related macular degeneration. Choroidal ischemia might be involved in macular atrophy in treated age-related macular degeneration., Purpose: To compare the areas of choriocapillaris (CC) nonperfusion and macular atrophy (MA) in treated exudative age-related macular degeneration. Methods: This was a prospective, observational, cross-sectional study. Forty-four eyes exhibiting MA (42 patients with age-related macular degeneration), with a dry macula, underwent fundus autofluorescence and optical coherence tomography angiography. The area of MA detected by fundus autofluorescence and CC nonperfusion detected by optical coherence tomography angiography was measured using image analysis software. The rates of concordance between the MA and CC nonperfusion areas were calculated. We qualitatively and quantitatively compared the areas of MA and CC nonperfusion in age-related macular degeneration eyes. Results: The mean areas of MA and CC nonperfusion were 5.95 ± 4.50 mm2 and 10.66 ± 7.05 mm2, respectively (paired t-test, P < 0.001). In 39 eyes (88.6%), the CC nonperfusion area was larger than the MA area, and the mean CC nonperfusion area was significantly larger than the mean MA area. Fundus autofluorescence matching optical coherence tomography angiography showed that the CC nonperfusion area was almost included in the MA area. The mean concordance rate for the MA area inside the CC nonperfusion area was 87.7 ± 13.9%. Conclusion: The MA and CC nonperfusion areas markedly overlapped. The area of CC nonperfusion correlated with the MA area. Choroidal ischemia might be involved in the pathogenesis of MA in treated age-related macular degeneration.

This review aims to summarize existing information concerning visual disturbances in (pre) eclampsia that have been described in the literature. Preeclampsia is one of the leading causes of maternal and fetal morbidity and mortality worldwide. Visual disturbances in (pre) eclampsia seem to be frequent phenomena. Therefore, the obstetrician/gynecologist may encounter women with serious, and sometimes debilitating, pathology of the visual pathways. Established ophthalmic entities associated with (pre) eclampsia are cortical blindness, serous retinal detachment, Purtscher-like retinopathy, central retinal vein occlusions, and retinal or vitreous hemorrhages. Ensuing visual symptoms include blurry vision, diplopia, amaurosis fugax, photopsia, and scotomata, including homonymous hemianopsia. In general, aside from lowering the blood pressure and preventing (further) seizures with magnesium sulfate, no specific therapy seems indicated for (pre) eclamptic women who experience visual changes. Although in most cases visual acuity returns to normal within weeks to months after the onset of symptoms, rarely permanent visual impairment can occur. Health care providers such as emergency room physicians, obstetricians, family physicians, neurologists, and ophthalmologists should be aware that acute onset of visual symptoms in pregnant women can be the first sign of (pre) eclampsia. Given that visual changes are a diagnostic criterion for severe preeclampsia, obstetricians should appreciate the significance of these changes and discuss appropriate diagnostic options with the ophthalmologist. Affected women can be reassured that most cases are transient.Target Audience: Obstetricians and gynecologists, ophthalmologists, neurologists, family physicians, emergency room physiciansLearning Objectives: After completing this CME activity, obstetricians and gynecologists should be better able to classify visual disturbances at an early stage during pregnancy, interpret acute onset of visual disturbances as the first sign of preeclampsia, and evaluate possible residual visual symptoms during follow-up.

PURPOSE:: To report a case of choroidal ischemia in a professional diver after a decompression sickness accident. METHODS:: A 31-year-old man presented a decompression sickness accident without any systemic manifestation. The symptoms were exclusively ophthalmic with sudden decrease of vision and presence of scotoma predominantly on the left eye immediately after a dive. The patient had a complete clinical ophthalmologic examination as well as fluorescein angiography, optical coherence tomography, central visual field, visual-evoked potentials, and electroretinogram examinations that were repeated during the follow-up over a period of 18 months. RESULTS:: The examinations performed 1 week after the decompression sickness accident and the hyperbaric oxygen therapy showed diminution of foveal reflectivity associated with retinal pigment epithelium modifications, deficit of choroidal perfusion in the macular region, and important central scotoma in both eyes. During the follow-up, the central scotoma disappeared after 6 months. The retinal pigment epithelium presented pigmentary migrations without subretinal fluid accumulation. CONCLUSION:: This case report describes choroidal ischemia resulting from decompression-induced intravascular gaseous microemboli caused by a decompression sickness diving accident. Language: en

Purpose To describe a case of choroidal infarction as illustrated by the "triangular sign of Amalric" after cocaine inhalation. Methods Observational case report. Results A 52-year-old male presented with an acute loss of vision in his left eye immediately after cocaine inhalation. Color photography and fluorescein angiography revealed triangular areas of choroidal ischemia following the distribution of the posterior ciliary arteries. Conclusion Cocaine-induced vasospasm, specifically of the distal short posterior ciliary arteries, may explain the triangular wedge-shaped choroidal infarcts in our patient. A thorough drug history may circumvent unnecessary and costly investigations in such cases.

The authors describe in seven eyes of four patients a form of serpiginous choroiditis beginning in the macula without initial peripapillary activity. Eyes with macular serpiginous choroiditis often had a poor visual prognosis and sometimes developed subretinal neovascularization. Fluorescein angiography of the acute lesions showed hypofluorescence; some cases were thus initially diagnosed as having choroidal ischemia. Fluorescein angiography in one eye, however, suggested that at least some of the hypofluorescence seen acutely in eyes with serpiginous choroiditis is secondary to blocked fluorescence from "opaque" retinal pigment epithelium.