A 9-year-old girl from Equatorial Guinea presented to the emergency department complaining of foreign body sensation in her right eye. A thin and large, translucent, slowly moving, coiled worm was observed underneath the conjunctiva. Anterior segment optical coherence tomography revealed hyperreflective small areas surrounded by larger hyporeflective areas into the subconjunctival space. Loa loa microfilaria was evidenced on blood test. Surgical extraction of the subconjunctival worm was intended on slit lamp and under sedation in the operating room, but it was unsuccessful due to poor cooperation and rapid migration of the larva into the sub-Tenon’s space. The patient received two cycles of oral albendazole and one cycle of diethylcarbamazine before achieving complete microfilaria seroconversion. Abbreviations: AS-OCT = Anterior Segment Optical Coherence Tomography, PCR = Polymerase Chain Reaction, DEC = diethylcarbamazine.

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Introduction: To analyze functional and anatomical outcomes in subtypes of diabetic macular edema treated with a single dexamethasone implant and to assess the usefulness of a pro-re-nata treatment among subtypes. Methods: Retrospective study in morphologic patterns of diabetic macular edema (diffuse retinal thickening n = 15; cystoid macular edema n = 38, and serous retinal detachment n = 17) recalcitrant to anti-vascular endothelial growth factor, treated with dexamethasone implant. Examinations included timing to recidive of diabetic macular edema, best-corrected visual acuity, and central subfield macular thickness at 2, 4, and 6 months. Results: In previously treated patients with a mean of 6.64 ± 3.69 anti-vascular endothelial growth factor injections, the best-corrected visual acuity improved from 61.64 ± 13.71 to 65.71 ± 14.65 as per the Early Treatment Diabetic Retinopathy Study protocol (p = 0.009) and central subfield macular thickness change from 447.46 ± 110.82 to 354.39 ± 80.46 µm (p < 0.005). The best-corrected visual acuity improvement was better in the diffuse retinal thickening group (68.67 ± 13.81 vs 65.26 ± 14.04 in cystoid macular edema and vs 64.12 ± 17.06 in serous retinal detachment), whereas higher central subfield macular thickness thinning was observed in serous retinal detachment group (368.47 ± 29.96 to 310.27 ± 67.47 in diffuse retinal thickening, vs 445.92 ± 105.06 to 364.39 ± 80.28 and 520.59 ± 122.96 to 370.94 ± 81.73 in cystoid macular edema and serous retinal detachment, respectively). Cystoid macular edema group was the group with more recurrences after 6 months (86.8% vs 66.7% in diffuse retinal thickening and 70.6% in serous retinal detachment). Conclusion: Dexamethasone implant is effective for all persistent diabetic macular edema subtypes with sustained functional and morphologic gains in the first 6 months.

Autoimmunity against collapsin response-mediator protein-5 (anti-CRMP-5) has been associated with ocular inflammation in paraneoplastic syndrome. We present a 59-year-old Caucasian man with optic neuritis and vitreous cells in both eyes (OU), at different stages. Despite the fact that the patient did not have any systemic disease, we suspected a paraneoplastic syndrome and requested CRMP-5-IgG and a mediastinoscopy. After performing the tests, a small cell lung carcinoma was diagnosed. Autoantibody CRMP-5-IgG positivity and optic neuritis combined with vitreous inflammation was defined as a paraneoplastic entity, avoiding vitreous biopsy and allowing us to suspect malignancy before systemic symptoms appeared.

SIGNIFICANCE Nutritional and toxic optic neuropathies are rare disorders characterized by visual impairment due to optic nerve damage by a toxin, usually with coexisting nutritional deficiencies. Its pathophysiology is still unclear, and multiple mechanisms implicated act synergistically to bring about this condition. The decline in its incidence and its confusing clinical appearance make diagnosing nutritional and toxic optic neuropathies challenging. PURPOSE This is an observational clinical case report of an atypical clinical case of a nutritional and toxic optic neuropathy with a subacute presentation and papilledema at the time of diagnosis. The patient provided written informed consent for medical information and images to be published. CASE REPORT A 47-year-old man presented with progressive, painless bilateral decrease in central vision over 15 days. The patient had a long-standing history of alcohol abuse and was a heavy smoker. The examination revealed dyschromatopsia, 20/400 visual acuity on both eyes, and no relative afferent pupillary defect. Funduscopy revealed bilateral papilledema. A visual field test showed generalized depression with centrocecal involvement in the left eye. Laboratory studies evidenced decreased vitamin B12/B1 and red blood cell folate levels, increased acute phase reactants, hypertransaminasemia, and macrocytic anemia. Serologies and methanol in urine were negative. After the discontinuation of tobacco use and alcohol accompanied by vitamin supplementation, our patient's visual field, visual acuity, and papilledema improved remarkably. After 5 months, visual acuity and funduscopy were normal. CONCLUSIONS Although some hallmark signs were visible in this case, its subacute presentation and the presence of papilledema at diagnosis caused some diagnostic uncertainty. Nutritional and toxic optic neuropathy is a rare and challenging diagnosis because of a lack of biomarkers. Eye care clinicians should consider nutritional and toxic optic neuropathies to prevent severe and irreversible visual damage resulting from underdiagnosis and mismanagement.