Journal of Neuro-Ophthalmology:
Chiasmal Stroke Following Open-Heart Surgery
Fabian, Ido Didi MD; Greenberg, Gahl MD; Huna-Baron, Ruth MD
Goldschleger Eye Institute (IDF, RH-B); Department of Diagnostic Imaging (GG), Sheba Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Hashomer, Israel.
Address correspondence to Ido Didi Fabian, MD, Goldschleger Eye Institute, Sheba Medical Center, Tel Hashomer 52621, Israel; E-mail: firstname.lastname@example.org
A 62-year-old man awoke from aortic valve replacement surgery with a total loss of vision in his right eye and a temporal visual field defect in his left eye. Automated visual field examination confirmed a right-sided anterior junction syndrome, and a right-sided chiasmal infarct was demonstrated by MRI. Although rare, chiasmal stroke is a potential complication of open-heart surgery.
Infarction of the optic chiasm is a rare event since the chiasm is supplied by an extensive collateral network from neighboring major cerebral blood vessels (1,2). We report a patient who developed an infarct affecting the optic chiasm following aortic valve replacement (AVR) surgery.
A 62-year-old man with diabetes mellitus, hypertension, and aortic stenosis but no ocular history was admitted to the thoracic surgical department at our institution for an AVR procedure. The surgery was uneventful, with no hypotension (lowest perfusion pressure: 55 mm Hg), arrhythmia, or severe blood loss (lowest hemoglobin: 8.1 gm/dL). The patient was kept in the supine position for 2.5 hours throughout the procedure and was on a cardiopulmonary bypass membrane oxygenator machine (D905 Avant oxygenator; Sorin Biomedica, Mirandola, Italy) for a total of 1.5 hours.
The patient awoke from surgery complaining of total loss of vision in his right eye and a visual field defect in his left eye. Bedside ophthalmologic examination revealed no light perception in the right eye and J16 near visual acuity in the left eye. The right pupil was amaurotic. Confrontation visual field testing detected a temporal defect in the left eye. Anterior segments were unremarkable, and neither retinopathy nor emboli were noted on dilated funduscopic examination. The rest of the neurological evaluation was normal.
Brain CT showed chronic ischemic changes in the left occipital pole. A chiasmatic lesion was suspected, and 48 hour after AVR, the patient underwent MRI of the brain and orbits. Diffusion-weighted imaging (DWI) showed an abnormality involving the distal aspect of the right optic nerve and the right side of the optic chiasm (Fig. 1), which was also present on T2 images (Fig. 2). MRI also showed an acute cortical infarct in the left occipital pole and 2 other small ischemic foci in the left parietal lobe and the left cerebellar hemisphere. The patient was diagnosed as having multiple brain infarctions.
On the fifth day postoperatively, visual acuity was light perception in the right eye and 20/100 in the left eye. Automated visual field testing revealed a temporal defect in the left eye (Fig. 3A). The patient underwent transthoracic echocardiography and carotid Doppler examination, both of which failed to demonstrate a possible source of emboli.
At 7-week follow-up, MRI showed evolution of the chiasmal infarct (Fig. 4), which was unchanged 2 months later. Five months following surgery, vision had improved to hand motions in the right eye and 20/20 in the left eye. There was minimal improvement in visual field testing (Fig. 3B).
Perioperative visual loss among patients undergoing nonocular surgery occurs in less than 0.001% of cases (3,4), whereas the prevalence of visual loss after cardiac surgery is estimated to be 100 times greater (5-7). The most commonly affected site is the optic nerve with the mechanism being ischemic in origin. If the optic chiasm is involved, it may be the result of an expanding sellar or parasellar mass, such as pituitary apoplexy or a rapidly expanding adenoma (8). An ischemic insult to the chiasm is a rare event due to the fact that the chiasm is supplied by an extensive network of collateral cerebral blood vessels originating from the circle of Willis.
Our patient experienced loss of vision following AVR surgery under general anesthesia. MRI showed multiple ischemic foci in the brain, as well as a right-sided chiasmal infarct involving the prechiasmal portion of the right optic nerve. Visual field examination confirmed a right anterior junction syndrome (9). Although no definite source was found, we assume that the insult is most likely embolic in nature. Cerebral emboli have been reported to occur frequently following cardiopulmonary bypass procedures and confirmed both with fluorescein angiography (10) and autopsy studies (11,12).
Anatomic studies have detailed the complex blood supply of the chiasm and visual pathways (1,2). This rich vascular network includes 2 major components, a superior group and an inferior group. The superior group of vessels emanate from the anterior cerebral arteries and occasionally anterior communicating arteries, whereas the inferior blood supply is derived from branches of the internal carotid artery, basilar, posterior cerebral, and posterior communicating arteries. The complex nature of this network is characterized by numerous anatomical variations, collateral feeders, and crossing-over phenomenon (1). Based on the location of the chiasmatic infarct in our case, we propose involvement of branches arising from the A1 segment of the right anterior cerebral artery or from the distal right internal carotid artery.
In conclusion, MRI, and DWI in particular, may play a valuable role in evaluating patients with perioperative visual loss due to ischemia of the anterior visual pathways.
1. Wollschlaeger PB, Wollschlaeger G, Ide CH, Hart WM. Arterial blood supply of the human optic chiasm and surrounding structures. Ann Ophthalmol. 1971;3:862-869.
2. Bergland R, Ray BS. The arterial supply of the human optic chiasm. J Neurosurg. 1969;31:327-334.
3. Roth S, Thisted RA, Erickson JP, Black S, Schreider B. Eye injuries after nonocular surgery: a study of 60,965 anesthetics from 1988 to 1992. Anesthesiology. 1996;85:1020-1027.
4. Warner ME, Warner MA, Garrity JA, MacKenzie RA, Warner DO. The frequency of perioperative vision loss. Anesth Analg. 2001;93:1417-1421.
5. Kalyani SD, Miller NR, Dong LM, Baumgartner WA, Alejo DE, Gilbert TB. Incidence of and risk factors for perioperative optic neuropathy after cardiac surgery. Ann Thorac Surg. 2004;78:34-37.
6. Nuttall GA, Garrity JA, Dearani JA, Abel MD, Schroeder DR, Mullany CH. Risk factors for ischemic optic neuropathy after cardiopulmonary bypass: a matched case/control study. Anesth Analg. 2001;93:1410-1416.
7. Sweeney PJ, Breuer AC, Selhorst JB, Waybright EA, Furlan AJ, Lederman RJ, Hanson MR, Tomsak R. Ischemic optic neuropathy: a complication of cardiopulmonary bypass surgery. Neurology. 1982;32:560-562.
8. Biousse V, Newman NJ, Oyesiku NM. Precipitating factors in pituitary apoplexy. J Neurol Neurosurg Psychiatry. 2001;71:542-545.
9. Schiefer U, Isbert M, Mikolaschek E, Mildenberger I, Krapp E, Schiller J, Thanos S, Hart W. Distribution of scotoma pattern related to chiasmal lesions with special reference to anterior junction syndrome. Graefes Arch Clin Exp Ophthalmol. 2004;242:468-477.
10. Blauth CI, Arnold JV, Schulenberg WE, McCartney AC, Taylor KM. Cerebral microembolism during cardiopulmonary bypass. Retinal microvascular studies in vivo with fluorescein angiography. J Thorac Cardiovasc Surg. 1988;95:668-676.
11. Moody DM, Bell MA, Challa VR, Johnston WE, Prough DS. Brain microemboli during cardiac surgery or aortography. Ann Neurol. 1990;28:477-486.
12. Challa VR, Moody DM, Troost BT. Brain embolic phenomena associated with cardiopulmonary bypass. J Neurol Sci. 1993;117:224-231.
© 2010 Lippincott Williams & Wilkins, Inc.