A 15-year-old girl presented with blurred vision after being hit by an elbow on her left eye. Her best-corrected visual acuity (BCVA) was 16/20. On fundus examination, both a choroidal rupture that formed a crescent shape concentric to the optic disc and a subretinal hemorrhage were detected (fig. ). Optical coherence tomography (OCT) showed that the juxtafoveal retinal pigment epithelial layer with Bruch's membrane was disrupted, and the inner segment/outer segment (IS/OS) of the photoreceptor junction and the external limiting membrane (ELM) layer were distorted with suspected pinpoint disruption (fig. ).\nAfter 3 weeks, her visual acuity reduced to counting fingers. Fundus examination revealed that the subretinal hemorrhage had absorbed and the choroidal rupture had expanded. The crescent-shaped window defect including the fovea was observed on fluorescein angiography (FAG) (fig. ). Wider disrupted layers of the RPE, the IS/OS junction, and the ELM at the corresponding area were detected in OCT. When compared with the first medical examination after the injury, the IS/OS junction and the RPE adjacent to the ruptured site were hardly distinguishable, although they were originally clearly observed (fig. ).\nSteroid pulse therapy (methylprednisolone 500 mg intravenous for 3 days and prednisolone 30 mg oral, tapering for 11 days) was started in another hospital, and 3 months after the injury, visual acuity increased to 20/125. Five months later, OCT revealed that the size of the expanded choroidal rupture had reduced, and the adjacent retina had improved sufficiently to distinguish the IS/OS junction and the RPE. However, FAG disclosed a choroidal neovascular membrane originating from the nasal edge of the choroidal rupture (fig. , fig. ). An intravitreal bevacizumab (Avastin, 1.25 mg/0.05 ml; Genentech, Inc., San Francisco, Calif., USA) injection was administered, and 1 month later, the patient's BCVA of the left eye had improved to 20/32, and the CNV had shrunk (fig. , fig. ). Also the IS/OS junction and the RPE had improved sufficiently and were able to be distinguished (fig. ).
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.