Purtscher’s retinopathy followed by neovascular glaucoma
A 66-year-old Japanese man presented to our hospital with blurred vision and a central scotoma in his left eye 1 month after suffering from a head injury, which was reported to have occurred following a blow received on his left forehead during a fight. The patient initially noticed the ophthalmic symptoms 1 week after the injury. According to his medical records after the injury occurred, there were no contusions or subcutaneous hemorrhages in the facial region. Computed tomography of his head revealed no fracture, brain damage, or intracranial hemorrhage. Furthermore, there was no history of bone fracture, strong compressions to the chest and abdomen, or direct globe contusion. Although he had a history of hypertension and angina pectoris that were satisfactorily controlled by beta-blocker therapy, there was no history of diabetes and hyperlipidemia. He was a chronic smoker (20 cigarettes per day for 40 years).\nAt initial presentation, his best-corrected visual acuity (BCVA) on a decimal chart was 1.5 oculus dexter and 0.6 oculus sinister. The intraocular pressure (IOP) was 12 mmHg in both eyes. The critical flicker frequency was 38 Hz oculus dexter and 24 Hz oculus sinister. A relative afferent pupillary defect was present in his left eye. Fundus examination revealed no distinct abnormalities in the right eye; however, it revealed multiple white lesions surrounding the optic disk of the left eye, without retinal neovascularization (). Goldmann perimetry demonstrated paracentral scotomas in the left eye (). Optical coherence tomography demonstrated retinal edema, particularly in the inner retina of the left eye ( and ). Furthermore, carotid artery ultrasonography was performed to rule out ocular ischemic syndrome. Although there were slight plaques bilaterally, no significant coarctation was observed. On the basis of these findings, a clinical diagnosis of Purtscher’s retinopathy of the left eye was made. The patient was followed up without treatment.\nOne month after the initial examination, visual acuity in the left eye deteriorated, and the BCVA and IOP became 0.01 in decimal chart and 37 mmHg, respectively. Gonioscopy revealed angle neovascularization in all quadrants. The angle was wide open with no peripheral anterior synechiae. In addition, fluorescein angiography demonstrated a delay of 33 seconds in the arm-to-retina circulation time, with a mild leak observed from the peripheral vessels as well as from nonperfused areas in the peripheral retina; however, there was no retinal neovascularization (). A diagnosis of neovascular glaucoma of the left eye was made, and treatment with intravitreal bevacizumab injection (1.25 mg/0.05 mL) and a total of 2,764 shots of panretinal photocoagulation was initiated to rapidly decrease IOP and avoid peripheral anterior synechiae.\nOne month after treatment (3 months after the head injury), BCVA and IOP in the left eye recovered to 0.4 in decimal chart and 8 mmHg, respectively, under latanoprost treatment. Five months after the head injury, BCVA and IOP in the left eye were 0.4 in decimal chart and 7 mmHg, respectively, without hypotensive drugs. The angle neovascularization and white lesions gradually regressed (). The visual field defect partially recovered (). Optical coherence tomography showed retinal thinning in the inner layers ( and ).