Author: Cristian Metrangolo (Italy)
Co-authors: Laura Premoli, Marco Mazzola, Marisa Rubino, Liviana Fontanel, Walter Messina, Simone Donati
Purpose
The aim of this case report is to evaluate whether the clinical features developed in this patient clinical case were due to a simple posterior ocular inflammation after surgery or if they were related to a posterior uveitis of uncertain origin. The ultimate aim is to underline the importance of a correct diagnostic pathway in bilateral posterior uveitis and the value of multidisciplinary collaboration.
Setting/Venue
Medical Retina Service, Ophthalmology Unit, ASST Sette Laghi - University of Insubria, Varese, Italy
Methods
We collected the clinical history of a patient undergoing a bilateral IOL scleral fixation in 2019 and 2020. After the surgery on each eye, he referred a visual acuity decrease, with a diagnosis of macular edema persisting for several months he had stopped follow-ups and treatments due to COVID19 restrictions. On January 2021, coming back for a check, we decided to perform a diagnostic pathway to evaluate the aetiology of ocular inflammation. We performed fluorescein (FA), green indocianine angiography (ICGA) and SD-OCT examination. The exams showed a petaloid macular edema associated to hyperfluorescent spots diffused on the whole retina on FA, and hypofluorescent spots on ICGA which could be related to a suspected tuberculosis or sarcoidosis. A local therapy with indomethacin eye drops twice/day and dexamethasone eye drops five/day was started, and in the meantime a complete serological and radiological examination for uveitis was performed. As the Mantoux and QuantiFERON TB Gold tests resulted positive, with a negative chest CT, in agreement with the infectious specialist, we decided to start a therapy based on a prophylactic treatment with isoniazid 5mg/kg/day for six months and oral prednisone starting with 1mg/kg/day to control retinal inflammation.
Results
After the application for 30 days of a topical therapy with indomethacin and dexamethasone, the patient showed an increase in visual acuity in both eyes (RE from 0.5 to 0.7 Snellen, LE from 0.025 to 0.05) and a decrease of central retinal thickness CRT (RE from 566 to 382 micron; LE from 517 to 340 micron). We also appreciated an improvement of inflammatory retinal signs on fluorescein angiography. Considering the persistence of macular edema, we added oral steroids and isoniazid. After 1 month of systemic therapy, we appreciated a complete visual recovery in RE (0.9 Snellen) and a slight improvement in LE (0.1 Snellen). Macular edema was completely resolved in both eyes with a CRT of 317 micron in RE and 267 in LE. Fluorescein angiography performed at the same time showed an almost complete resolution of retinal inflammation in RE, while in LE we appreciated a persistence of inferior-temporal hyperfluorescent retinal spots. The patient is now visited monthly to evaluate the presence of recurrences.
Conlusions
Because of the persistence and the severity of macular edema and retinal inflammation, we performed a wide screening with instrumental and serological examinations. Indeed, the evidence of a severe macular edema associated to hyperfluorescent spots in the retinal periphery in both eyes did not confirm the diagnosis of post-surgical macula edema. For this reason, the positivity of serological tests and the presence of retino-choroidal signs on ICGA addressed for a hidden role of TBC in the pathology. It’s reported that TBC could cause an immuno-mediated reaction without a direct involvement of the bacteria, presenting angiographic features referable to our patient. However, a systemic isoniazid therapy was added to avoid the development of a clinical TBC, when oral steroids had started to resolve inflammation. Finally, the efficacy of the applied therapy supported our clinical hypothesis of multiple aetiology: surgical intervention and a concomitant immuno-based reaction which caused a posterior uveitis with a severe and persistent macular edema in this patient.
Financial Disclosure
None
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