An otherwise healthy 13-year-old Japanese boy presented with reduced central vision in his left eye, 3 days after suffering a blunt trauma from being hit by a fishing sinker. Assessment of BCVA showed only the ability to perceive hand motions in the left eye compared to 20/13.3 in the right eye. The intraocular pressure was 8 mmHg in both eyes. The anterior segment of the left eye showed hyphema and laceration of the bulbar conjunctiva. No traumatic cataract or rupture of the globe was seen. Fundus examination of the left eye showed a subretinal hemorrhage extending from the posterior pole to the inferior midperiphery and a slight vitreous hemorrhage (Fig. ). No retinal tear or retinal detachment was seen. In contrast, the right eye appeared normal. Swept-source optical coherence tomography (OCT; DRI OCT-1 Atlantis, Topcon Medical Systems, Tokyo, Japan) showed the presence of a thick submacular hemorrhage in the left eye (Fig. ). Attempts to measure the retinal sensitivity using a microperimeter (MAIA; CenterVue, Padova, Italy) failed, as it was below the detection limits of the instrument (Fig. ). We therefore diagnosed submacular hemorrhage in the left eye, due to choroidal rupture following blunt trauma.\nTwo days after the initial visit, we carried out anterior chamber lavage, vitrectomy, subretinal injection of rt-PA (GRTPA®, Mitsubishi Tanabe Pharma Corporation, Japan) and air tamponade on the left eye under general anesthesia. This operation was performed using the methods reported by Kimura et al. []. Briefly, after performing a 25-gauge micro-incision vitrectomy, 4,000 IU rt-PA in 0.1 ml was injected subretinally using a 38-gauge subretinal infusion needle (MedOne, Sarasota, FL) to liquefy the submacular hemorrhage. Before completing the operation, fluid-air exchange was performed. The patients remained facedown for 3 days after surgery to displace the submacular hemorrhage. The day after the operation, most of the submacular hemorrhage had moved to the inferior periphery.\nOne month after the operation, the BCVA of left eye was 20/1000 and we observed cataract formation, thin remnants of the submacular hemorrhage and juxtafoveal choroidal rupture (Fig. ). We then carried out phacoemulsification and aspiration, intraocular lens implantation and intravitreal injection of 0.05 ml bevacizumab (Avastin®, Hoffmann-la Roche, Basel, Switzerland) in the left eye under general anesthesia. Two months after the second operation, the submacular hemorrhage had totally disappeared (Fig. ) and the BCVA in the left eye had improved to 20/40. As shown in Fig. , the retinal sensitivity had markedly improved.
A 43-year-old married Syrian woman presented at the age of 40 with distortion of central vision in the right eye. Choroidal dystrophy was suspected in Damascus (Syria) ( and ). Rheumatology and infectious workup was negative (syphilis, tuberculosis, anti-double-stranded DNA, anti-single-stranded DNA, rheumatoid factor). CNV was also detected in the macular area in Dubai (United Arab Emirates) and intravitreal injections were advised. She subsequently received three monthly intravitreal ranibizumab injections in Barcelona (Spain) (). Past ocular history revealed myopia of 2.5 D as per patient recollection. She had undergone bilateral refractive surgery (excimer laser 5 years ago followed by laser in situ keratomileusis [LASIK] 3 years ago). Medical history was negative. There was a strong family history of myopia and no parental consanguinity. Fifteen months after initial right eye involvement, the patient expressed the same symptoms in the left eye, such as seeing broken lines and asymmetric faces. She was advised to undergo treatment for CNV in the macular region. She received one injection in Beirut (Lebanon), and subsequently, three monthly injections in Dubai to the left eye. She reported further worsening of vision after each injection. Consultation in London (UK) revealed a best-corrected visual acuity of 20/80 in the right eye and 20/30 in the left eye. Dilated fundoscopy revealed bilateral areas of vertically linear atrophy, more extensive in the right eye, without subretinal fluid or hemorrhage by optical coherence tomography. Fundus autofluorescence imaging revealed areas of reduced autofluorescence corresponding to these areas of atrophy. The reported clinical impression then was myopic chorioretinal degeneration versus lacquer crack-associated myopic degeneration. She was advised to have regular checkup without intravitreal injections as long as the macula stays dry. The patient was frustrated because of both inability to pinpoint a definite diagnosis and gradual decline in vision bilaterally. Nine months later, she initially presented to our clinic with 20/200 visual acuity. Fundoscopy revealed definite widening of the vertical macular choroidal rupture bilaterally (). Stippled changes in the retinal pigment epithelium were observed. Peau d’orange appearance was not present. The patient was emmetropic without keratoconus on corneal topography. Axial length measurement with the IOL Master (Carl Zeiss Meditec AG, Jena, Germany) was 27.35 mm in the right eye and 27.31 mm in the left eye. Keratometry readings were 38.6 D in the right eye and 38.2 D in the left eye. The skin of the neck had tiny pinkish papules suspicious for early goose flesh (). Two separate dermatology consultations and skin biopsies did not favor the diagnosis of pseudoxanthoma elasticum. Even further widening of the choroidal rupture occurred 9 months after presentation. Our working diagnosis was lacquer crack from high myopia (without pseudoxanthoma elasticum) () possibly initiated by LASIK and exacerbated by ocular rubbing and intravitreal injections (). The patient was instructed to avoid ocular rubbing, head-down position, and intravitreal injection (unless an exudative component was present) and to have prior paracentesis before any future intravitreal injections.