A 65-year-old hypertensive man presents with sudden, painless inferior field defect in the right eye. Visual acuity is 6/12. Fundoscopy reveals a wedge-shaped sector of superotemporal flame hemorrhages, dot-blot hemorrhages, dilated tortuous superotemporal vein, and cotton-wool spots that sharply respect the horizontal raphe through the macula. The structure marked **A** in the diagram shows these characteristic sectoral hemorrhages. Which of the following best explains the PATHOGENESIS of the hemorrhages marked **A** in this clinical scenario?
A. Diabetic microangiopathy causing selective weakening of the venous wall in the superotemporal quadrant
B. Venous occlusion from primary thrombophilia leading to stasis and spontaneous rupture of retinal capillaries
C. Sclerotic arterial thickening compresses the vein at the arterio-venous crossing, causing turbulent shear injury, endothelial damage, and thrombosis
D. Hypertensive crisis causing acute elevation in intraluminal venous pressure with diffuse retinal hemorrhages across all quadrants
Explanation
Why option 1 is right
The sectoral flame hemorrhages marked A in superotemporal BRVO result from a specific pathogenic mechanism: at every retinal arterio-venous crossing, the artery and vein share a common adventitial sheath. Sclerotic arterial thickening (from hypertension and atherosclerosis) compresses the vein at this crossing, slowing blood flow and triggering turbulent shear injury to the endothelium, leading to endothelial damage and thrombosis. This explains why the superotemporal quadrant is involved in 60–70% of cases — arterio-venous crossings are most numerous there and the artery typically lies over the vein. The hemorrhages stop abruptly at the horizontal raphe because retinal nerve fibres do not cross it, creating the characteristic wedge-shaped sectoral pattern seen in A. This mechanism is the textbook explanation in AAO BCSC Retina and is central to understanding BRVO pathophysiology.
Why each distractor is wrong
Option 2: While thrombophilia can cause BRVO in younger patients, it is not the primary mechanism in a 65-year-old hypertensive man. The clinical scenario explicitly points to hypertension-driven arterial sclerosis as the dominant pathogenic factor, not primary thrombophilia. Spontaneous capillary rupture from thrombophilia alone does not explain the specific arterio-venous crossing compression mechanism.
Option 3: Diabetic microangiopathy causes diffuse retinal hemorrhages and microaneurysms, not the sharply demarcated sectoral flame hemorrhages that respect the horizontal raphe. There is no mention of diabetes in this patient's presentation, and diabetic retinopathy does not produce the wedge-shaped pattern characteristic of BRVO marked A.
Option 4: Hypertensive crisis causes acute, diffuse retinal hemorrhages across multiple quadrants (including flame, dot-blot, and blot hemorrhages), not the sharply sectoral pattern that respects the horizontal raphe. The hemorrhages in A are confined to the superotemporal sector precisely because they follow the territory of a single branch vein, not a systemic pressure phenomenon.
High-YieldNEET PG
BRVO = artery-over-vein compression at the crossing → turbulent shear injury → thrombosis; hemorrhages stop at horizontal raphe (nerve fibre boundary); superotemporal quadrant most common (60–70%).
AAO BCSC Retina; BRAVO/VIBRANT trials
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