A 28-year-old male complained of a sudden loss of vision in the left eye for 1 week when presented to our hospital. He had hypertension for more than 3 years without regular treatment but had no history of any other systemic illness, drug use, myopia, and trauma. Three weeks ago, he was admitted to other hospital due to sudden severe pain and blurred vision of the left eye for 1 h. At the time of admission, the blood pressure was 230/120 mmHg, the intraocular pressure was 69 mmHg, there were conjunctival hyperemia and corneal edema, the pupil diameter was 2.5 mm. Skull CT and MRI detected abnormal signal shadows in the left eye and no abnormalities in the brain. B-ultrasonography indicated an occupying lesion in the left eye. The hospital considered the diagnosis of glaucoma and choroidal occupying lesion. The patient was given symptomatic treatment to reduce the intraocular and blood pressure, including mannitol by intravenous drip, Catinolol Hydrochloride and Brinzolamide eye drops, oral antihypertensives. Due to which, the symptoms improved. However, after 2 weeks, the patient came to our hospital for treatment due to the sudden loss of vision in the left eye. Further examination revealed the following: the blood pressure was 200/120 mmHg, best-corrected visual acuity was 20/20 in the right eye and hand motion in the left eye, and the anterior segment was normal, there were no hyperemia, corneal edema and mydriasis, the intraocular pressure was normal. Fundus camera displayed disc hemorrhage near the optic disc and hard and soft exudates at posterior pole in the right eye; fundus details could not be evaluated in the left eye because of hemorrhage in the vitreous cavity. B-ultrasonography of the left eye revealed a dense, diffuse intravitreal hemorrhage. Skull MRI revealed abnormal signal shadow in the left eyeball (beside the lateral wall), considering the possibility of intraocular hemorrhage. Laboratory examination showed that serum creatinine was 178.0 (53–106 mol/L), and total cholesterol was 6.63 (2.83–5.20 mmol/L). The blood routine and coagulation function were normal, serum infection and immune tests were within normal limits, tumor marker were negative, and no abnormality was found on chest CT or abdominal ultrasound. Thus, the following diagnosis was considered: left eye vitreous hemorrhage, right eye hypertensive retinopathy, hypertension combined with hypertensive crisis, and hyperlipidemia. We recommended a medical consultation for blood pressure reduction, kidney protection, lipid regulation, and other treatments. After the blood pressure was stabilized, vitrectomy combined with silicone oil tamponade of the left eye was performed, retinal vascular abnormalities were ruled out in the vitrectomy performed. In order to keep the refractive medium transparent, silicone oil was used as an endotamponade. The intraoperative finding was an inferotemporal subretinal focal elevated lesion with distinct boundary and yellow color. Since the nature of the elevated lesion could not be determined, it was not treated. No abnormal cells were found in the pathology of vitreous fluid during the operation. Any obvious abnormality was not observed in the macular optical coherence tomography (OCT) of the left eye after surgery. Infrared photography showed a dome-shaped bulge in the peripheral part of the inferotemporal region of the left eye. ICGA showed low fluorescence occlusion and no abnormal fluorescence leakage in the elevated lesion. Combined with the results of systemic and ocular examination, SSRH in the left eye was considered. After close follow-up, the SSRH was found to be gradually reabsorbed, albeit at a slower rate, best-corrected visual acuity was 20/20 in the right eye and 20/25 in the left eye at 1 month after the operation, silicone oil was removed 9 months after surgery. The SSRH was mostly absorbed in his last follow-up visit (1 year after the vitrectomy).