Central Bouquet Hemorrhage in Association with Terson Syndrome Following Ruptured ACOM Aneurysm

Introduction

Terson syndrome, first identified by Albert Terson in 1900, involves intraocular hemorrhage that accompanies acute intracranial bleeding, most commonly subarachnoid hemorrhage (SAH). The proposed mechanism involves a sudden increase in intracranial pressure, leading to rupture of small ocular vessels and hemorrhage into the vitreous or sub-internal limiting membrane (sub-ILM) [1]. The underlying mechanism of Terson syndrome is believed to involve a rapid elevation of intracranial pressure that induces venous congestion and obstruction of normal venous drainage, resulting in rupture of fragile peripapillary capillaries and subsequent intraocular hemorrhage [2], [3], [4]. These mechanisms explain the spectrum of hemorrhages observed, which can involve the vitreous, sub-ILM, preretinal, intraretinal, and subretinal layers. Clinically, Terson syndrome causes sudden vision loss due to vitreous hemorrhage and is frequently associated with neurological findings stemming from intracranial disease [2], [3], [4]. Diagnosis using ocular ultrasound, OCT, and fluorescein angiography is essential for identifying retinal involvement [2], [3], [4]. OCT imaging was essential in confirming these findings and monitoring resolution. If vitreous hemorrhage persists, pars plana vitrectomy may be required to avoid complications like epiretinal membrane formation, macular holes, and retinal detachment. The management of Terson syndrome requires a two-step approach: initial stabilization and treatment of the causative intracranial pathology, followed by ophthalmic evaluation and intervention to restore visual function. In selected cases, a conservative strategy involving observation is justified, since spontaneous clearance of intraocular hemorrhage may occur gradually over time [3].

Central bouquet hemorrhage (CBH) was characterized by a deep retinal hemorrhage with well-defined, round margins located in the central fovea, often accompanied by petaloid hemorrhages radiating into the surrounding Henle fiber and outer nuclear layers. Cross-sectional OCT consistently demonstrated a clearly demarcated, round hyperreflective lesion involving the central fovea of these layers [5]. CBH is more commonly reported in retinal vascular disorders but is rarely described in the context of Terson syndrome. Underlying causes of CBH were predominantly neovascular age-related macular degeneration (40%), followed by lacquer cracks in pathological myopia (30%), macular telangiectasia Type 2 (10%), proliferative diabetic retinopathy (10%), and ocular trauma linked to angioid streaks (10%). Spontaneous resolution occurs in approximately 30% of cases and is associated with partial improvement in visual acuity [5].

This report aims to describe the rare coexistence of Terson syndrome and CBH following a ruptured anterior communicating artery aneurysm, emphasizing the role of multimodal imaging in its recognition and demonstrating the potential for favorable visual outcomes with carefully monitored conservative management.

Publication History

Received: 04 November 2025

Accepted: 17 November 2025

Accepted Manuscript online:
20 November 2025

Article published online:
26 January 2026

• References

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