Terson’s Syndrome (TS) was originally described as intraocular hemorrhage associated with aneurysmal subarachnoid hemorrhage (SAH)[1]. It is a consequence of sudden rise in intracranial pressure (IP) that reduces venous return to the cavernous sinus or obstruct the retinochoroidal anastomoses and central retinal vein, culminating in venous stasis and ocular hemorrhage ([Figure]). TS has also been reported in nonaneurysmal SAH, severe traumatic injuries or venous thrombosis[2].
Figure 37 year-old woman with sudden headache progressed to seizures and decreased level of consciousness. Nonenhanced CT (A) showed basilar cisterns and sulcal effacement due to intracranial hypertension, additionally to subarachnoid hemorrhage that thickens and increases the attenuation of the tentorium cerebelli bilaterally (arrows). Note bilateral intraocular hemorrhage (arrowheads). The 3D-reconstruction of CTA (arterial phase) showed a berry aneurysm (arrow) in the supraclinoid segment of the right internal carotid artery (B). The coronal reformatted CTA image (C) and CT perfusion axial image (D), performed 4 days later, depicted absence of contrast opacification of intracranial vessels and diffusely absent cerebral blood flow, endorsing the concurrent diagnosis of brain death in the follow-up.
Current literature has highlighted TS as an important life-threatening prognostic finding[3],[4]. Recognizing TS on fundoscopy or CT is recommended and effective control of IP is imperative to reduce the risk of mortality in this critical setting[5].
