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. 1999 Nov;106(11):2054-62.
doi: 10.1016/S0161-6420(99)90483-9.

Pathophysiology and hemodynamics of branch retinal vein occlusion

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Pathophysiology and hemodynamics of branch retinal vein occlusion

N L Christoffersen et al. Ophthalmology. 1999 Nov.

Abstract

Purpose: To describe the pathophysiologic and the hemodynamic changes associated with branch retinal vein occlusion (BRVO) on the basis of selected angiographic observations from a cohort of patients with BRVO and related anomalies of retinal blood flow.

Design: Retrospective, observational case series.

Participants: A total of 250 patients with incipient or manifest BRVO and 5 patients with related anomalies.

Methods: Color and red-free gray-scale fundus photography and intravenous fluorescein angiography.

Main outcome measures: Morphologic signs of disturbed retinal blood flow.

Results: All occlusions occurred at arteriovenous crossing sites where the artery is positioned anterior to the vein. Presumptive precursor abnormalities of blood flow at arteriovenous crossings include turbulence and upstream venous dilation. After the onset of BRVO, the clinical course is determined by the location of the BRVO in relation to the fovea, the extent of the involved venous drainage area, and the collateral drainage capacity from the area with compromised venous drainage to the adjacent areas of intact venous drainage. Collateral maturation occurs over a period of 6 to 24 months after the onset of BRVO, when a transient retinal edema may be seen that has a preponderance for foveal involvement because the perifoveal area has the highest density of preformed collaterals between adjacent venous drainage areas.

Conclusions: The treatment of BRVO may possibly benefit from a refined angiographic analysis of the process of collateral formation and new treatment methods aimed at accelerating the process of collateral maturation.

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