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Summary Table

Category	Details
Risk Factors	Hypertension (strongest association), diabetes mellitus, hyperlipidemia, open-angle glaucoma, hypercoagulable states, increasing age (>50 years), smoking, obesity
Etiology	Compression of a retinal branch vein by a thickened, atherosclerotic arteriole at an arteriovenous (AV) crossing point, leading to turbulent flow, endothelial damage, and thrombus formation
Patient Presentation	Sudden, painless, unilateral decrease in visual acuity or a visual field defect; may range from asymptomatic to severe vision loss depending on macular involvement
Classic Physical Exam	Sectoral (wedge-shaped) flame hemorrhages confined to one quadrant of the retina, following the distribution of the occluded vein; dilated and tortuous veins distal to the occlusion; cotton-wool spots; retinal edema in the affected sector
Key Diagnostic Results	Dilated fundoscopy shows sectoral intraretinal hemorrhages; fluorescein angiography (FA) demonstrates delayed venous filling and capillary non-perfusion; optical coherence tomography (OCT) quantifies macular edema
Management	Observation if vision is preserved; intravitreal anti-VEGF injection (first-line for macular edema); intravitreal corticosteroid implant as alternative; sector/scatter laser photocoagulation for neovascularization
Keywords	"Sudden painless vision loss," "sectoral flame hemorrhages," "AV crossing," "one quadrant," "cotton-wool spots," "macular edema," "neovascularization"

1. Pathophysiology

Branch retinal vein occlusion occurs at arteriovenous crossing points, where a retinal arteriole and venule share a common adventitial sheath. In patients with chronic hypertension or atherosclerosis, the arteriole wall becomes thickened and rigid. This thickened arteriole mechanically compresses the underlying venule against the shared connective tissue sheath. The compression creates turbulent blood flow within the vein, damages the venous endothelium, and activates the coagulation cascade, ultimately forming a thrombus at the AV crossing.

Once the vein is occluded, venous outflow from the upstream retinal territory is blocked. Hydrostatic pressure rises in the capillary bed drained by that vein, causing plasma and red blood cells to leak into the surrounding retinal tissue. This is why the hallmark finding is flame-shaped hemorrhages confined to one sector of the retina rather than all four quadrants (which would indicate central retinal vein occlusion instead).

The increased intravascular pressure also disrupts the inner blood-retinal barrier, leading to macular edema, which is the most common cause of vision loss in BRVO. In more severe (ischemic) cases, widespread capillary closure triggers retinal hypoxia. The ischemic retina responds by upregulating vascular endothelial growth factor (VEGF), which promotes pathological neovascularization. These new, fragile vessels can bleed into the vitreous cavity (vitreous hemorrhage) or grow over the iris (rubeosis iridis), potentially causing neovascular glaucoma.

The superotemporal quadrant is the most frequently affected location because it has the highest density of AV crossings.

2. Classification and Clinical Manifestation

Classification	Capillary Perfusion	Visual Acuity	Retinal Findings	Risk of Neovasc.	Prognosis
Non-ischemic (Perfused) BRVO	Good capillary perfusion; less than 5 disc areas of capillary non-perfusion	Often 20/40 or better	Mild to moderate flame hemorrhages, mild venous dilation, possible macular edema	Low (~2%)	Favorable; ~50-60% recover to 20/40 or better spontaneously
Ischemic (Non-perfused) BRVO	Extensive capillary dropout; 5 or more disc areas of non-perfusion	Often 20/200 or worse	Dense hemorrhages, numerous cotton-wool spots, marked venous dilation and tortuosity	High (~40% develop neovascularization within 3 years)	Guarded; vision recovery is limited

Key clinical features by phase

Phase	Features
Acute (0-3 months)	Sudden visual field defect or decreased acuity; sectoral flame hemorrhages; retinal edema; cotton-wool spots
Subacute (3-6 months)	Hemorrhages begin to absorb; macular edema may persist or worsen; collateral vessels may form at the optic disc
Chronic (>6 months)	Hemorrhages largely resolved; persistent macular edema or cystoid changes; sheathed vessels; possible neovascularization in ischemic cases

3. Diagnostic Workup

Test	Role	Key Findings
Dilated fundoscopy	Best initial test	Sectoral flame hemorrhages, dilated/tortuous veins, cotton-wool spots in one quadrant
Optical coherence tomography (OCT)	Quantify macular edema; guide treatment	Increased central macular thickness, intraretinal/subretinal fluid, cystoid spaces
Fluorescein angiography (FA)	Most accurate/confirmatory test; classify ischemic vs. non-ischemic	Delayed venous filling, blocked fluorescence from hemorrhage, capillary non-perfusion areas, leakage at macula, collateral vessels
OCT angiography (OCTA)	Non-invasive vascular mapping	Capillary dropout zones, foveal avascular zone enlargement, reduced vascular density
Systemic workup	Identify underlying cause	Blood pressure measurement, fasting glucose, $\text{HbA1c}$, lipid panel; in patients <50 years: hypercoagulability panel (antiphospholipid antibodies, Factor V Leiden, protein C/S, antithrombin III, homocysteine)

The best initial test is a thorough dilated fundoscopic examination. In a clinical vignette, the classic description of flame-shaped hemorrhages limited to one retinal quadrant with dilated veins should immediately point you toward BRVO. No additional testing is needed to make the clinical diagnosis at the bedside.

OCT is then obtained to evaluate the macula. This is the test that drives treatment decisions because persistent macular edema (central subfield thickness typically >300 micrometers) is the primary indication for intravitreal therapy. Without OCT documentation of edema, you do not treat.

Fluorescein angiography serves as the gold standard for classifying the severity of occlusion. The critical determination is whether the BRVO is ischemic or non-ischemic, because ischemic BRVO carries a substantially higher risk of neovascularization. FA identifies areas of capillary non-perfusion: when 5 or more disc areas of capillary dropout are present, the BRVO is classified as ischemic. FA also detects early neovascularization that may not be visible on fundoscopy alone.

A systemic workup is essential because BRVO is frequently the first clinical manifestation of undiagnosed hypertension, diabetes, or hyperlipidemia. In young patients (<50 years) without traditional cardiovascular risk factors, a hypercoagulability panel should be ordered to evaluate for thrombophilic conditions.

4. Management and Treatment

Clinical Scenario	Treatment	Details
BRVO with good vision (20/40 or better), no macular edema	Observation	Monitor every 1-3 months with OCT; address systemic risk factors
BRVO with macular edema causing decreased vision	Intravitreal anti-VEGF injection (first-line)	Ranibizumab 0.5 mg, aflibercept 2 mg, or bevacizumab 1.25 mg (off-label); monthly injections initially, then treat-and-extend
Macular edema refractory to anti-VEGF or pseudophakic patients	Intravitreal dexamethasone implant	Ozurdex 0.7 mg implant; duration of action approximately 4-6 months; monitor for IOP elevation and cataract progression
Neovascularization (disc, retina, or iris)	Sector scatter laser photocoagulation	Applied to the ischemic retinal sector; anti-VEGF may be used as adjunct
Vitreous hemorrhage (non-clearing)	Pars plana vitrectomy	Considered if hemorrhage does not clear within 1-3 months
Neovascular glaucoma	Anti-VEGF + panretinal photocoagulation + IOP-lowering agents	Urgent management to prevent irreversible optic nerve damage

Acute stabilization begins with confirming the diagnosis through fundoscopy and obtaining OCT. If the patient presents with good visual acuity (20/40 or better) and no clinically significant macular edema, observation with serial monitoring every 4 to 6 weeks is appropriate. Systemic risk factor control is paramount: blood pressure optimization, glycemic control, and lipid management.

For patients with vision-reducing macular edema, the first-line treatment is intravitreal anti-VEGF injection. The landmark BRAVO trial established ranibizumab 0.5 mg as effective therapy, and the VIBRANT trial demonstrated aflibercept 2 mg superiority over grid laser. Treatment is initiated with monthly injections for 6 months, followed by a treat-and-extend protocol where the interval between injections is gradually lengthened as long as the macula remains dry on OCT. Most patients require treatment for 2 to 3 years, though some achieve sustained resolution.

Intravitreal dexamethasone implant (Ozurdex, 0.7 mg) is an alternative for patients who are pseudophakic (prior cataract surgery), who respond poorly to anti-VEGF, or who cannot comply with monthly injections. The GENEVA trial supported its use. However, corticosteroid-related complications must be monitored: intraocular pressure (IOP) elevation occurs in approximately 15-20% of patients, and cataract progression is expected in phakic eyes. Because of these side effects, anti-VEGF remains the preferred first-line agent in phakic patients.

Grid/sector laser photocoagulation was historically the standard treatment for macular edema based on the Branch Vein Occlusion Study (BVOS). The BVOS recommended grid laser for eyes with macular edema and visual acuity of 20/40 or worse that persisted for at least 3 months. While still a valid treatment, grid laser has been largely supplanted by anti-VEGF in current practice. Laser remains the primary treatment for retinal neovascularization: scatter (sector) photocoagulation is applied to the ischemic retinal territory when neovascularization is detected.

Contraindications and cautions: In pregnant patients, anti-VEGF agents are generally avoided due to potential teratogenic effects from systemic VEGF inhibition; observation or laser is preferred. In patients with recent thromboembolic events (stroke, myocardial infarction within 3 months), the theoretical systemic risk of anti-VEGF should be weighed against benefits, though intravitreal doses result in minimal systemic absorption.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Central Retinal Vein Occlusion (CRVO)	Also presents with sudden painless vision loss, flame hemorrhages, dilated veins, and cotton-wool spots	CRVO produces hemorrhages in all four quadrants ("blood and thunder" fundus), while BRVO hemorrhages are confined to one sector/quadrant
Diabetic Retinopathy	Both show intraretinal hemorrhages, cotton-wool spots, macular edema, and neovascularization	Diabetic retinopathy is bilateral and symmetric, develops gradually over years, and shows microaneurysms as the earliest sign; BRVO is unilateral, acute, and sectoral
Hypertensive Retinopathy	Both share risk factor of hypertension; both show flame hemorrhages and cotton-wool spots	Hypertensive retinopathy is bilateral with arteriolar narrowing, AV nicking, and copper/silver wiring; hemorrhages are diffuse and bilateral, not confined to one vein's territory
Central Retinal Artery Occlusion (CRAO)	Both cause sudden, painless, unilateral vision loss	CRAO shows a pale/whitened retina with a cherry-red spot at the fovea and no hemorrhages; BRVO shows a hemorrhagic, edematous retina
Ocular Ischemic Syndrome	Can present with dilated veins, hemorrhages, and neovascularization	Ocular ischemic syndrome results from carotid artery stenosis, causes dot-and-blot hemorrhages in the mid-periphery (not flame-shaped), and is associated with orbital/periorbital pain and a low IOP; FA shows prolonged arterial filling time
Papilledema	Both may show disc hemorrhages and swelling	Papilledema is bilateral, associated with headache and transient visual obscurations, and caused by elevated intracranial pressure; the hemorrhages are peripapillary rather than sectoral

6. Traps and High-Yield Pearls

The single most common trap with BRVO questions is confusing it with CRVO. Both conditions share the same risk factors and present with sudden painless vision loss, retinal hemorrhages, and dilated veins. The discriminating feature is the distribution of hemorrhages: BRVO is sectoral (one quadrant), while CRVO involves all four quadrants. If a vignette describes hemorrhages "in the superotemporal quadrant" or "along the distribution of a single vein," that is BRVO. If the vignette describes a "diffuse" or "four-quadrant" hemorrhagic picture, that is CRVO.

A second frequent error involves treatment sequencing. Students sometimes select grid laser photocoagulation as the first-line treatment for macular edema because it appears in older references. Current guidelines and landmark trials (BRAVO, VIBRANT) have established intravitreal anti-VEGF as the standard first-line therapy for vision-reducing macular edema. Grid laser is now considered a second-line or adjunctive option. However, for neovascularization, laser photocoagulation remains the primary intervention, not anti-VEGF alone.

A third pitfall is forgetting the systemic workup. BRVO is not merely an eye disease. It is a marker of underlying cardiovascular disease. A vignette may present a patient with new-onset BRVO and ask for the "most important next step" beyond ophthalmic treatment. The answer is blood pressure measurement and cardiovascular risk factor screening (fasting glucose, lipid panel). In a younger patient without conventional risk factors, the tested concept shifts to ordering a hypercoagulability panel.

Finally, be alert to the complication timeline. The most common cause of vision loss in BRVO is macular edema (not neovascularization). Neovascularization is a later complication that occurs primarily in ischemic BRVO, typically developing within the first 6 to 12 months. A question asking about the "most likely cause of persistent decreased vision at 3 months" in a BRVO patient is testing your knowledge that the answer is macular edema, not hemorrhage obscuring the macula (hemorrhages often clear) and not neovascularization (too early and only in ischemic subtype).

The core competency being tested is your ability to recognize the sectoral hemorrhage pattern, correctly classify the vascular event, initiate appropriate imaging (OCT for treatment decisions, FA for ischemic classification), choose anti-VEGF as first-line for macular edema, and connect the ocular finding to underlying systemic disease.

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