This Article Résumé de cet Article Full Text Full Text (PDF) Submit a scholarly reply Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Chong, C. T. Articles by Singh, K. Search for Related Content PubMed PubMed Citation Articles by Chong, C. T. Articles by Singh, K.

Case series: Monocular visual loss associated with subarachnoid hemorrhage secondary to ruptured intracranial aneurysms

[Perte visuelle monoculaire associée à une hémorragie sous-arachnoïdienne secondaire à la rupture d’anévrysmes intracrâniens]

Chin Ted Chong, MBBS^*, Ki Jinn Chin, MMED(ANAES)^*, Leonard W. Yip, MRCSED MMED(OPHTH) and Kulgit Singh, MMED(ANAES)^*

^* From the Department of Anesthesiology,
The Eye Institute, Tan Tock Seng Hospital, National Healthcare Group, Singapore.

Address correspondence to: Dr. Chin Ted Chong , Department of Anesthesiology, Tan Tock Seng Hospital, 11 Jalan Tan Tock Seng, Singapore 308433. Phone: 65-63577771; Fax: 65-63577772; E-mail: chintedchong{at}yahoo.com.sg

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.