PURPOSE: To describe variations in the presentation of monocular visual loss associated with intracranial aneurysm rupture. The clinical course, possible etiologies and management of visual loss in three patients are described. CLINICAL FEATURES: The first patient developed Terson's syndrome (vitreal hemorrhage associated with raised intracranial pressure secondary to subarachnoid hemorrhage). Following aneursymal clipping, her postoperative management was conservative and there was no improvement in visual acuity. The second patient underwent surgical clipping of internal carotid aneursysms and sustained visual loss subsequent to surgical dissection and temporary clipping around the optic nerve and anterior choroidal artery. The vessel subsequently thrombosed. Potential contributing factors to visual loss in this case included intraoperative hypotension and anemia. This patient received anti-platelet medications, and experienced subsequent improvement in visual acuity to 6/9. A third patient underwent a right orbito-frontal keyhole craniotomy with the cranial flap retracted across the orbit. Elevated intraocular pressure secondary to external orbital compression may have compromised retinal and choroidal perfusion. This patient also developed vasospasm of both anterior cerebral arteries which resolved partially with papaverine therapy. Hypertension-hypervolemia therapy was instituted, with subsequent partial recovery of visual acuity in her right eye. CONCLUSION: Perioperative monocular visual loss associated with intracranial aneurysm repair is an infrequent occurrence, and clinical presentations may be quite variable. The primary pathophysiological mechanisms are intraocular hemorrhage and ischemia of ocular structures, including the optic nerve. Early detection, via regular fundoscopic examination and treatment aimed at decreasing intraocular pressure and augmenting ocular perfusion may improve outcomes.
PURPOSE: To describe variations in the presentation of monocular visual loss associated with intracranial aneurysm rupture. The clinical course, possible etiologies and management of visual loss in three patients are described. CLINICAL FEATURES: The first patient developed Terson's syndrome (vitreal hemorrhage associated with raised intracranial pressure secondary to subarachnoid hemorrhage). Following aneursymal clipping, her postoperative management was conservative and there was no improvement in visual acuity. The second patient underwent surgical clipping of internal carotid aneursysms and sustained visual loss subsequent to surgical dissection and temporary clipping around the optic nerve and anterior choroidal artery. The vessel subsequently thrombosed. Potential contributing factors to visual loss in this case included intraoperative hypotension and anemia. This patient received anti-platelet medications, and experienced subsequent improvement in visual acuity to 6/9. A third patient underwent a right orbito-frontal keyhole craniotomy with the cranial flap retracted across the orbit. Elevated intraocular pressure secondary to external orbital compression may have compromised retinal and choroidal perfusion. This patient also developed vasospasm of both anterior cerebral arteries which resolved partially with papaverine therapy. Hypertension-hypervolemia therapy was instituted, with subsequent partial recovery of visual acuity in her right eye. CONCLUSION: Perioperative monocular visual loss associated with intracranial aneurysm repair is an infrequent occurrence, and clinical presentations may be quite variable. The primary pathophysiological mechanisms are intraocular hemorrhage and ischemia of ocular structures, including the optic nerve. Early detection, via regular fundoscopic examination and treatment aimed at decreasing intraocular pressure and augmenting ocular perfusion may improve outcomes.
Authors: Albedy Moreira Bastos; Anderson Raiol Rodrigues; Maria Izabel Tentes Côrtes; Eliza Maria da Costa Brito Lacerda; Mônica Gomes Lima; Cláudio Eduardo Corrêa Teixeira; Luiz Carlos de Lima Silveira Journal: Front Neurol Date: 2017-09-21 Impact factor: 4.003