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 10-year-old boy presented to a local doctor with a sudden decrease of vision and a central scotoma in the right eye two days after being hit in that eye with a wooden stick. A hemorrhage was found in the fundus at that time, so the patient was referred to our hospital, where a hemorrhage was observed in the fovea (). Corrected visual acuity was 20/70 and intraocular pressure was 12 mmHg OD. Optical coherence tomography scanning of the right eye showed submacular hemorrhage (). We performed paracentesis (0.3 mL) under general anesthesia to reduce the intraocular pressure. Next, we injected tPA (12.5 μg in 0.05 mL) into the vitreous cavity and waited 15 minutes for the hemorrhage to dissolve. We then performed a further paracentesis (0.1 mL), followed by injection of pure sulfur hexafluoride (SF6, 0.3 mL) into the vitreous cavity. After surgery, we instructed the patient to maintain a prone position as much as possible for a week. One day later, the hemorrhage had started to move out of the fovea, revealing a choroidal rupture beneath (). We considered this choroidal rupture to be the cause of the hemorrhage.\nThe macula was not damaged () and visual acuity improved to 20/16 by four months and 20/13 by seven months after the above treatment. The submacular hemorrhage had been successfully displaced out of the fovea. In spite of the remaining choroidal rupture, the patient has not complained of any symptoms, including metamorphopsia, after 3 years of follow-up.