INTRODUCTION

Terson syndrome (TS) is characterized by the presence of intraocular hemorrhages—often multilayered—in conjunction with an intracranial hemorrhage, most commonly subarachnoid hemorrhage. The reported incidence of TS ranges from 10% to 50% following subarachnoid hemorrhage [1]. Although the exact pathophysiological mechanism remains unknown, it is generally hypothesized that the syndrome occurs in the setting of subarachnoid hemorrhage accompanied by raised intracranial pressure (ICP). Elevated ICP may impede ocular venous outflow, resulting in the rupture of peripapillary and retinal capillaries, or alternatively, it may facilitate the reflux of blood from the subarachnoid space via the glial-lymphatic system, thereby producing intraocular hemorrhages [2–4]. Despite raised ICP being the postulated mechanism underlying TS, its association with papilledema is rarely described. Here, we report a case of TS presenting with subarachnoid hemorrhage, multilayered intraocular hemorrhages, and concurrent papilledema, all of which resolved with conservative medical management.

CASE REPORT

A 35-year-old male patient was brought to casualty following a road traffic accident, presenting with loss of consciousness. His initial Glasgow Coma Scale score was seven. A computed tomography (CT) scan of the brain revealed a thin interhemispheric subarachnoid hemorrhage along the falx cerebri, accompanied by bifrontal contusions (Fig. 1A). With no significant midline shift evident, he was managed conservatively with phenytoin sodium in tablet form (100 mg) three times daily, glycerol syrup (30 mL) twice daily, ondansetron in tablet form (4 mg) twice daily, and tramadol hydrochloride in tablet form (100 mg) three times daily. Six days later, as his sensorium improved, he reported diminished vision in both eyes and was referred for ophthalmic evaluation. On examination, visual acuity was 20/80 in the right eye and counting fingers at 1 m in the left eye. The anterior segment appeared unremarkable bilaterally. Fundus examination revealed vitreous and preretinal hemorrhages, along with disc oedema and peripapillary hemorrhages in both eyes (Fig. 1B, C). There was no evidence of direct ocular trauma, and the patient had no systemic conditions (such as diabetes, hypertension, or blood dyscrasias) that might predispose him to intraocular hemorrhages. The presence of multilayered hemorrhages (in the vitreous, preretinal, and retinal layers) against the background of a subarachnoid hemorrhage led to the diagnosis of TS with papilledema. In light of his recent major head injury, observation was chosen as the management strategy for the intraocular hemorrhages. The patient was subsequently referred back to the neurophysician for management of raised ICP, as evidenced by the bilateral papilledema. He was commenced on oral acetazolamide (500 mg) three times daily to decrease cerebrospinal fluid secretion and reduce ICP. The patient later discharged himself against medical advice and was lost to follow-up for 2 months.

He returned to the ophthalmology outpatient department 2 months later. His vision had improved to 20/60 in the right eye and was 20/200 in the left. A repeated CT scan of the brain demonstrated a resolving subarachnoid hemorrhage, with bifrontal encephalomalacia changes (Fig. 2A). Fundus examination revealed a reduction in vitreous hemorrhage and complete resolution of disc oedema in both eyes (Fig. 2B, C). Given the improvement in vision and the resolving vitreous hemorrhage, continued observation was recommended.

Ethics statement

Written informed consent for publication of the research details and clinical images were obtained from the patient.

DISCUSSION

TS has classically been described as the coexistence of intraocular hemorrhage—whether in the vitreous, sub–internal limiting membrane, or subhyaloid spaces—with an intracranial hemorrhage, predominantly subarachnoid hemorrhage. The condition is strongly associated with acute head injury [5–8]. It is frequently underdiagnosed due to the presence of other life-threatening conditions at presentation or because patients with impaired sensorium are unable to communicate effectively. Although several theories have been proposed to explain the occurrence of intraocular hemorrhages in TS, the raised ICP hypothesis is generally regarded as the most plausible explanation. A recent theory, termed the “glymphatic reflux theory,” suggests that a glial-lymphatic (or glymphatic) system exists between the central nervous system, the optic nerve, and the retina. When ICP exceeds intraocular pressure, blood from the subarachnoid space may reflux into the globe, causing hemorrhages at multiple retinal levels [8]. The mechanism of raised ICP following posttraumatic intracranial hemorrhage accounts for the development of both papilledema and TS, although their simultaneous occurrence is rarely documented. In our case, a delay in fundus evaluation made it difficult to determine whether TS preceded the papilledema or if both arose concurrently. While both conditions are related to raised ICP, TS is generally considered an acute event, typically manifesting within 24 to 48 hours after head injury [1], whereas papilledema usually requires a longer period, generally between 1 and 3 weeks, to become evident [9,10].

The management of TS is determined by the evolution of the intraocular hemorrhage. Observation is appropriate in cases with mild hemorrhage or in patients who have significant systemic conditions. In cases where there is persistent vitreous hemorrhage or the development of an epiretinal membrane, a vitrectomy may be required [6,11]. Immediate vitrectomy may be indicated in instances of submacular hemorrhage, bilateral visual impairment, or in pediatric patients to prevent amblyopia. In our patient, conservative management was chosen for the vitreous hemorrhage owing to his systemic condition (raised ICP and recent recovery from altered sensorium) and the reasonably good vision in one eye. By the 2-month follow-up, the vitreous hemorrhage had decreased significantly, and the papilledema had resolved completely. This improvement is likely attributable to the spontaneous resolution of the subarachnoid hemorrhage and the associated brain parenchymal oedema. It should be noted that the occurrence of TS in conjunction with subarachnoid hemorrhage and papilledema generally carries a poor prognosis for survival [8,12,13]. The presence of papilledema alongside TS is indicative of persistently raised ICP, which necessitates prompt treatment with oral acetazolamide, oral glycerol, or intravenous mannitol. In our patient, timely management of raised ICP likely facilitated the natural resolution of both the intracranial and intraocular pathologies. A dilated fundus examination should be routinely performed in any patient presenting with intracranial hemorrhage, especially subarachnoid hemorrhage, to detect associated intraocular hemorrhages. Early recognition and management of papilledema in such cases may be lifesaving.

ARTICLE INFORMATION

Author contributions

Conceptualization: all authors; Investigation: HR, AG; Methodology: all authors; Project administration: all authors ; Writing–original draft: HR; Writing–review & editing: all authors. All authors read and approved the final manuscript.

Conflicts of interest

The authors have no conflicts of interest to declare.

Funding

The authors received no financial support for this study.

Data availability

Data sharing is not applicable as no new data were created or analyzed in this study.

Fig. 1.

Imaging at the time of presentation. (A) Computed tomography scan of the brain showing a thin subarachnoid hemorrhage (asterisks) along the falx cerebri and bifrontal contusion injury (arrows). (B) Fundus image of the right eye displaying a preretinal (sub–internal limiting membrane) hemorrhage and inferior vitreous hemorrhage. (C) Fundus image of the left eye showing both preretinal and vitreous hemorrhages.

Fig. 2.

Follow-up imaging at 2 months. (A) Computed tomography scan of the brain demonstrating a resolving subarachnoid hemorrhage (asterisks) with bifrontal encephalomalacia changes. (B) Fundus image of the right eye showing a resolved sub–internal limiting membrane hemorrhage alongside a diminishing vitreous hemorrhage. (C) Fundus image of the left eye demonstrating resolving vitreous hemorrhage.

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