A previously healthy, 12-year-old male presented for a routine visit with complaints of a 2-month history of decreased visual acuity in his left eye (LE). Six months before the visit, he suffered blunt trauma to the LE during a struggle, with no medical observation. At the initial visit, BCVA in the LE was counting fingers and in the right eye, it was 20/20. He had neither restricted eye movements nor afferent pupillary defects. Biomicroscopic examination of the anterior segment was normal. Fundus examination of the LE showed a central macular lesion of 1 disc diameter with fibrosis, increased retinal thickness and intraretinal hemorrhage (fig. , left). Peripheral retinal examination was normal. Spectralis OCT (Heidelberg Engineering Inc., Heidelberg, Germany) showed disruption of the IS/OS junction with corresponding increased reflectivity, loss of the outer nuclear layer, cell infiltration of the retinal wall and subretinal fibrosis. Retinal thickness was 289 µm at the site of the lesion (fig. , right). A fluorescein angiography (FA) revealed early impregnation with no diffusion, increasing with time (fig. ). With support from Pediatrics, off-label, high-steroid pulse therapy (intravenous methylprednisolone 500 mg for 3 days and oral prednisolone 30 mg, tapering for 10 days) was done, resulting in an increase of LE BCVA to 20/200 and a decrease of retinal thickness by 71 µm to 218 µm 1 week after treatment. In an attempt to achieve additional improvement without undesired systemic effects, off-label intravitreal triamcinolone acetonide (IVTA; 0.05 ml/2 mg) was administered 2 weeks after oral treatment. LE BCVA improved to 20/150, and retinal thickness decreased by 10 µm 3 weeks after IVTA. Three months after initial presentation, LE BCVA was 20/125 and retinal thickness was 208 µm. However, the alterations in fundoscopy and OCT remained (fig. ).
A 12-year-old girl presented with decreased vision in the right eye since 6 months following penetrating injury, for which primary repair was done elsewhere. Physical examination by Internist revealed OI. Best corrected visual acuity (BCVA) was 20/1000 in the right eye and 20/80 in the left eye. Refractive error was previously documented as –11 DS and –18 DS in the right and left eye, respectively. Examination revealed blue sclera in both eyes. Adherent leucoma with irregular anterior chamber and peripheral anterior synechiae were noted in right eye; fundus evaluation was not possible. Ultrasound was done and keratoplasty advised. Left eye fundus was unremarkable, except myopic appearance. However, she was lost to follow-up and presented again 3.5 years later with sudden diminution of vision in the left eye since 3 days.\nBCVA was 20/1000 in the right eye and 20/630 in the left. There were no additional findings on biomicroscopic examination in the right eye as compared to the initial visit. Fundus evaluation of the left eye showed the presence of a subfoveal choroidal neovascular membrane (CNVM) []. The clinical findings were confirmed on fundus fluorescein angiography (FFA) and optical coherence tomography (OCT). FFA of the left eye revealed an active subfoveal classic CNVM with profuse leakage. Blocked choroidal fluorescence due to the overlying hemorrhage was also noted [Fig. and ]. OCT revealed subfoveal CNVM and sub-retinal fluid []. The treatment options were explained and informed consent was obtained. The patient was treated with intravitreal injections of Bevacizumab (1.25 mg/0.05 ml). At 1-month follow-up, the patient had a BCVA of 20/200 in the treated eye. Fundus evaluation showed a yellow-white linear streak deep to the retinal layers, suggestive of lacquer crack []. The patient received two re-treatments with intravitreal Bevacizumab at 1-month intervals, following which the CNV regressed. At the last follow-up, 6 months following the last injection, the fundus remained stable [] and visual acuity stabilized at 20/200.