Branch Retinal Vein Occlusion (BRVO)

Branch Retinal Vein Occlusion (BRVO)
SYMPTOMS Central vision varies as it can be anywhere from 20/20 to 20/200
Peripheral vision is typically abnormal in the area correlating to the BRVO
Patient may also report Mild to severe vision loss in the presence of neovascular glaucoma, an intravitreal hemorrhage, a subhyaloid hemorrhage, and a preretinal hemorrhage, Central vision loss and Metamorphopsia in the presence of cystoid macular edema, Central vision loss and scotoma in the presence of paracentral acute middle maculopathy (PAMM), Central vision loss and Peripheral vision loss in the presence of optic nerve pallor
SIGNS Typically unilateral
Acute occlusion: Dilated and tortuous veins and venules along the distribution of the BRVO, Vessel sheathing along the distribution of the BRVO, Extensive intraretinal hemorrhages (Dot/Blot/Flame) along the distribution of the BRVO, Microaneurysms, Macroaneurysms, Cotton wool spots along the distribution of the BRVO, Exudates along the distribution of the BRVO, Retinal capillary nonperfusion, Cystoid macular edema, Paracentral acute middle maculopathy (PAMM), NVD, NVE, NVA, NVI, Preretinal hemorrhages, Subhyaloid hemorrhages, Intravitreal hemorrhages, Neovascular glaucoma, Sectorial optic nerve edema
There is increased risk of development and severity of these signs with ischemic BRVOs when compared to non-ischemic BRVOs
The signs seen with an acute branch retinal vein occlusion typically resolve in 4-6 months
Chronic/Resolved occlusion: Most intraretinal hemorrhages disappear (some dot/blot/flame hemorrhages will remain for months to years), Cotton wool spots usually disappear, Improvement in the amount of exudates (may remain for months to years), Veins and venules become less tortuous and dilated (due to decrease in pressure against the walls of the vein and venules), Sclerotic retinal vessels, Macular ischemia (enlargement of foveal avascular zone), Collateral vessels, Sectoral optic nerve pallor
WORK-UP Pupils, EOMs, Full eye exam with dilated retinal exam (look closely at the pupillary ruff for NVI especially before dilating), Gonioscopy, OCT analysis of the macula (signs of cystoid macular edema are best seen with an OCT ), OCT analysis of the optic nerve, OCT-Angiography (disruption of the perifoveal capillary plexus correlates with the presence of peripheral retinal ischemia and deep vascular complex nonperfusion), Fluorescein Angiography (greater than or equal to 5DD of capillary nonperfusion is indicative of an ischemic BRVO), Fundus photos, B-scan ultrasound (if unable to view the retina), Watzke-Allen test, Macular photostress test, Amsler grid
TREATMENT Refer to PCP ASAP in order to get any systemic conditions under control and for a full work-up
Give take home Amsler grid in order to monitor for change
Patient needs to use caution with any strenuous exercise or activities in the presence of retinal neovascularization
Patient should sleep with their head elevated in presence of a preretinal, subhyaloid, and/or intravitreal hemorrhage
Non-ischemic or Ischemic BRVO without any evidence of cystoid macular edema and retinal neovascularization: Needs to be monitored closely
Non-ischemic or Ischemic BRVO with evidence of cystoid macular edema and/or retinal neovascularization: Refer to retinal specialist ASAP for treatment
NVI and/or NVA with normal IOP and no evidence of glaucomatous optic nerve damage: Refer to retinal specialist within 48 hours
NVI and/or NVA with elevated IOPs but no evidence of glaucomatous optic nerve damage or with associated secondary open angle glaucoma: Begin treatment with topical and oral glaucoma medications. Refer to retinal specialist within 48 hours
NVI and/or NVA with secondary angle closure with or without glaucoma: The goal is to lower the IOP as quickly as possible in office and then refer to a retinal specialist ASAP. A glaucoma specialist will most likely be involved as well as patient will need a trabeculectomy and/or shunt
FOLLOW-UP Non-ischemic BRVO without any evidence of cystoid macular edema and retinal neovascularization: Should see back in 2-3 months in order to monitor for development of cystoid macular edema, worsening of ischemia, retinal neovascularization, and neovascular glaucoma. If stable, patient should be seen in 4-6 months
Ischemic BRVO without any evidence of cystoid macular edema and retinal neovascularization: Should see back every 1-2 months for the first 6 months in order to monitor for development of cystoid macular edema, worsening of ischemia, retinal neovascularization, and neovascular glaucoma
Once retinal neovascularization becomes involutional or quiescent and the retina and macula is stable, patient should be seen back every 3-6 months
Neovascular glaucoma: Patient will most likely continue care with a retinal specialist and/or glaucoma specialist. If condition is stable and patient is no longer seeing a retinal specialist and/or glaucoma specialist, the patient should be seen every 2-4 months
ADDITIONAL LAB | TESTS If patient is older (50 years old or more), they need to follow-up with their PCP for additional testing if not already done which includes the following: Blood pressure, Fasting blood sugar, HbA1c, Lipid panel, Thyroid panel, CBC with differential, ESR, Plasma protein electrophoresis, Renal function testing, Carotid duplex, Cardiac evaluation
If patient is younger (less than 50 years old), they need to follow-up with their PCP for additional testing if not already done which includes the following: Blood pressure, Fasting blood sugar, HbA1c, Lipid panel, Thyroid panel, CBC with differential, ESR, Plasma protein electrophoresis, Renal function testing, Carotid duplex, Cardiac evaluation, ANA, ACE, Thrombophilia screening (PT, TT, BT, PTT, INR, Protein C, Protein S, Anticardiolipin antibodies)
ETIOLOGY Blockage of blood flow within a branch retinal vein. Venous blockage leads to an increase in back pressure to the capillaries and branch retinal vein which causes damage and subsequent nonperfusion and leakage
DIFFERENTIAL DX Diabetic retinopathy, Hypertensive retinopathy, Anemia retinopathy, Sickle cell retinopathy, Leukemia retinopathy, Branch retinal artery occlusion, Ocular ischemic syndrome
NOTES There are 3 main etiologies of a BRVO
Compression: Sclerosis and hardening of a branch retinal artery (due to various etiologies including diabetes, hypertension, and high cholesterol) leads compression of a branch retinal vein and thrombus formation
Inflammation of the primary vessel walls: Systemic vasculitis (due to various etiologies including tuberculosis, syphilis, and lupus), Localized vasculitis (due to various etiologies such as sarcoids)
Increase in blood stream viscosity: Clotting disorders (due to various etiologies such as antiphospholipid syndrome, protein C deficiency, protein S deficiency, and anticardiolipin antibodies), Drugs such as oral contraceptives, Blood dyscrasias (due to various etiologies such as sickle cell anemia, lymphoma, leukemia, and polycythemia vera)
The highest risk factor for development of a BRVO in older patients is hypertension
BRVOs tend to happen along the superior temporal aspect of the retina
Patients with a BRVO are much less likely to present with retinal ischemia, NVD, NVE, NVI, NVA, neovascular glaucoma, PAMM, and optic nerve edema than patients with a CRVO
Branch Retinal Vein Occlusion (BRVO): Fundus photo demonstrating a superior temporal branch retinal vein occlusion https://imagebank.asrs.org/file/19747/double-macular-branch-retinal-vein-occlusion
Posted in Ocular Conditions, Retina-Vascular