Central Bouquet Hemorrhages in Retinal Vein Occlusion: A Distinct Pathway to Macular Atrophy

To characterize central bouquet hemorrhages (CBHs) in retinal vein occlusion (RVO) and evaluate their association with long-term visual and anatomical outcomes, in particular macular atrophy. This is a retrospective longitudinal cohort study of 403 treatment-naïve eyes with RVO (mean age, 62.9 ± 15.4 years; 59% male).

CBH was identified on spectral-domain optical coherence tomography as vertically oriented light-absorbing masses centered at the fovea, above the external limiting membrane. Clinical characteristics, imaging findings, and intravitreal treatment frequency were compared between eyes with and without CBH. Baseline and longitudinal visual acuity analyzed with multivariable regression models, the prevalence of CBH-related features, and the cumulative incidence and predictors of macular atrophy assessed with Cox regression models were assessed.

CBH were observed in 28% of eyes (n = 111) at baseline. Affected eyes were older, had more systemic vascular comorbidities, and presented with more severe macular edema, peripapillary hemorrhages, and cotton-wool spots (all P < 0.001). Ischemic markers-including arteriolar paracentral acute middle maculopathy (P = 0.04) and increased ischemic index on fluorescein angiography (P = 0.02)-were more common in CBH eyes. Over time, CBH reabsorbed, often leaving a plaque-like RPE thickening, which progressed to outer retinal atrophy in 69% of cases over 36 months. Severe cystoid macular edema and full-thickness macular holes were also common. CBH was independently associated with worse baseline visual acuity (β = 0.09 logMAR; 95% confidence interval [CI], 0.01-0.18; P = 0.04) and slower visual recovery (β for CBH × Time = -0.002 logMAR/month; P < 0.001). Intravitreal treatments reduced the risk of macular atrophy (hazard ratio, 0.28; 95% CI, 0.08-0.96; P = 0.04), and each additional injection conferred a protective effect (hazard ratio, 0.96; 95% CI, 0.93-0.99; P = 0.02).

CBH represents a characteristic hemorrhagic manifestation in RVO, likely reflecting the localized effects of elevated venous pressure and macular ischemia that contribute to structural disruption and poor visual outcomes. Its presence warrants close monitoring and sustained treatment to mitigate long-term retinal damage.