![]() Rarer vascular causes of a VH are prepapillary loops and congenital retinal macrovessels. 6,7 Clinical evidence of a lesion of this nature includes an extensive or multi-layered hemorrhage with or without a possible breakthrough VH. Retinal arterial macroaneurysm lesions may lead to a VH. Third, consider the potential for an abnormal retinal vascular formation to rupture. More rarely, patients with Valsalva retinopathy or Terson’s syndrome may experience a hemorrhage that breaks into the vitreous cavity.ģ. 5 Vessels on the optic nerve head are also susceptible to leakage when there is a shearing force or severe disc edema. 4 It is important to remember that eyes with a VH in the setting of an acute PVD have a 54% to 91% chance of a retinal break. This can occur spontaneously or after ophthalmic trauma and is often seen in retinal tears, detachments and PVDs in part due to the strong vitreoretinal adhesions over retinal vessels. The second cause of VHs is the rupture of a normal blood vessel. 2,3 Ophthalmic conditions such as retinal vein or artery occlusions, ocular ischemic syndrome, chronic uveitis and chronic retinal detachment can also lead to neovascularization and VH.Ģ. 1 Intraocular neovascularization from ischemia can arise from numerous systemic conditions including diabetes, sickle cell anemia and leukemia. The most common etiology of a VH is neovascularization, and PDR remains the number one cause of all VHs. Though exceptions exist, there are four main factors to consider when faced with a VH:ġ. Determining the best treatment underscores the importance of first reaching the correct diagnosis. ![]() VH can present for a multitude of reasons. These two patients have the same diagnosis, but their conditions are very different. Fundus photo of the first patient shows vitreous and subhyaloid hemorrhages with active neovascular fronds extending from the arcades. He was diagnosed with a hemorrhagic PVD and did not require further intervention.įig. At last follow-up, the patient’s vision had improved to 20/25, and no retinal neovascularization or break was visible. Frequent observation with repeat ultrasonography was suggested. The patient was advised to sleep with his head elevated and discontinue any non-prescribed blood thinners. ![]() Due to the limited view of the right fundus, an ultrasound was conducted, revealing a posterior vitreous detachment (PVD) without a retinal break or detachment ( Figure 3). The left eye fundus exam was unremarkable. There was no neovascularization anteriorly, but a diffuse VH was seen in the right eye. She was diagnosed with a VH secondary to proliferative diabetic retinopathy (PDR) in the right eye.Īnother patient, a 67-year-old Hispanic male, presented with blurred vision OD for five days accompanied by dark spots and “spider webs.” Visual acuities were 20/100 OD and 20/20 OS. She reported uncontrolled blood glucose levels consistently measuring above 300mg/dL. The patient’s medical history was significant for type 1 diabetes. The left had hemorrhages and intraretinal microvascular abnormalities without neovascularization. The right fundus had preretinal and vitreous hemorrhages (VHs) centrally, intraretinal hemorrhages and neovascularization along the major arcades ( Figure 1 ). Intraocular pressures, pupils and anterior segment findings were normal. Visual acuities were 20/70 OD and 20/50 OS. A 35-year-old Hispanic female presented to the ophthalmic emergency department with vision loss OD for one week.
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