RESUMO
Terson's Syndrome describes intraocular hemorrhage secondary to an acutely raised intracranial pressure (ICP). Although Terson's Syndrome is common amongst patients with subarachnoid hemorrhage (SAH), it is underdiagnosed and often overlooked. This review discusses the current understanding of the etiopathogenesis, clinical features, and management of Terson's Syndrome and highlights the visual and prognostic implications to stress the importance of timely diagnosis and management. The origin of intraocular hemorrhage in Terson's Syndrome has been debated. A recognized theory suggests that an acutely raised ICP induces effusion of cerebrospinal fluid into the optic nerve sheath which dilates the retrobulbar aspect of the sheath in the orbit. Dilatation mechanically compresses the central retinal vein and retinochoroidal veins resulting in venous hypertension and rupture of thin retinal vessels. A commonly reported clinical feature is decreased visual acuity and blurred vision. These may be accompanied by symptoms of increased ICP including loss of consciousness and headache. Diagnosis is established using evidence from the clinical presentation, ophthalmoscopy, and, when required, imaging including B-mode ultrasound, CT, MRI, and fluorescein angiography. Terson's Syndrome is managed conservatively by observation for mild cases and with vitrectomy for bilateral cases and for patients whose hemorrhage has not spontaneously resolved after an observational period. Terson's Syndrome can be used as a prognostic indicator of morbidity and mortality in underlying pathology like SAH. Fundoscopy of patients with SAH, acutely raised ICP or visual disturbance with unknown etiology can help establish a timely Terson's Syndrome diagnosis. This may avoid the risk of permanent visual impairment.
