A 78-year-old male patient visited our clinic for visual disturbance of the left eye which had developed one day previously. The patient had no ophthalmologic history, and he had been taking hypoglycemic agents for the control of diabetes mellitus for 3 years and was being medicated for chronic renal failure by the Department of Internal Medicine at our hospital. One day prior to presentation to our department, he developed systemic edema, and oral administration of 160 mg furosemide (Lasix; Handok Pharmaceuticals Co., Seoul, Korea) was administered by the Department of Renal Internal Medicine for the treatment of systemic edema. His blood pressure was 161 / 90. The basic data describing his systemic condition including body weight and height was not taken during his visit to the Internal Medicine Department. He did not have any history of furosemide treatment due to systemic edema. Blood tests at that time revealed an increase of blood urea nitrogen (BUN, 47 mg/dL) and creatinine (1.8 mg/dL), and urinary albumin was detected (500 mg/dL). On presentation to our department, the best corrected visual acuity of the right eye was 0.5, and that of the left eye was 0.125. The intraocular pressure of both eyes was within normal range. Upon fundus examination of the left eye, retinal edema was observed in the posterior pole, including the macula.

On fluorescein angiography, macular edema caused by vessel leakage was detected in the left eye (Fig. 1A). Macular edema was confirmed by optical coherence tomography (Fig. 1C). Two days after the oral administration of furosemide, the visual acuity of both eyes had improved to 0.6 and 0.3, respectively. After 7 days, the visual acuity of both eyes had improved to 0.9 and 0.6, respectively. Fundus examination and optical coherence tomography revealed complete disappearance of the sub-retinal fluid in the left eye (Fig. 1D). Before the oral administration of furosemide, the right eye showed a mild abnormality on fluorescein angiography (Fig. 1B). Because visual acuity of the right eye improved after administration of furosemide, we speculated that sub-retinal fluid was also present in the right eye.

A 43-year-old female patient diagnosed with non-proliferative diabetic retinopathy and under regular ophthalmological examination developed visual disturbance in the left eye. Ophthalmological tests were thus performed. This patient had a disease history of intermittent systemic edema and thus a history of taking furosemide (Lasix). At admission, all blood tests were normal except for the elevation of BUN (44 mg/dL) and creatinine (1.8 mg/dL). In the past, her renal function test was within the normal range. The best-corrected visual acuity of the right eye was 0.5, that of the left eye was 0.4, and the intraocular pressure of both eyes was within the normal range. In the fundus of the right eye, scattered flame-shaped retinal hemorrhages were observed in the posterior pole. In the fundus of the left eye, in addition to scattered flame-shaped retinal hemorrhage, new vessels were also observed (Fig. 2A). On optical coherence tomography, edema was present in the posterior pole including the macula (Fig. 2B), but routine blood and urine tests were normal. Panretinal photocoagulation and the oral administration of 120 mg furosemide were initiated for the treatment of macular edema, especially serous retinal detachment. After 3 weeks of oral administration of furosemide, macular edema, especially serous retinal detachment, had improved, but visual acuity had not improved (Fig. 2C). Bevacizumab (1.25 mg; Avastin, Genentech, San Francisco, CA, USA) was injected intravitreally at this stage in order to treat the remaining cystoid macular edema and subretinal fluid. One month after the injection, complete resolution of the subretinal fluid and cystoid macular edema was seen, but the visual acuity had still not improved (Fig. 2D).