Korean Journal of Cerebrovascular Surgery 2011;13(3):137-142.
Published online September 1, 2011.
Sudden Unilateral Blindness and Ophthalmoplegia after Ruptured Anterior Communicating Artery Aneurysm Surgery: Report of 2 Cases.
Ahn, Sung Yong , Lim, Dong Jun , Kim, Se Hoon , Kim, Sang Dae , Hong, Ki Sun , Park, Jung Yul
Department of Neurosurgery, Ansan Hospital, Korea University Medical Center, Ansan-si, Kyounggi-do, Korea. djlim@korea.ac.kr
The incidence of unilateral blindness and ophthalmoplegia after aneurysm surgery is very rare, especially in an anterior communicating artery (ACoA) aneurysm, but if it occurs, it is mainly caused by intra-operative nerve injury or retinal ischemia. We experienced 2 cases of unilateral blindness immediately after surgery. Both patients were classified into Hunt-Hess grade 1 and Fisher grade 3. Angiographic findings of these patients revealed that the aneurysms were located at the left ACoA. The aneurysms were clipped easily with minimal brain retraction via standard pterional craniotomy. In both cases, injury of the optic nerve during surgery was unlikely. Both patients complained of visual loss with ophthalmoplegia ipsilateral to the site of surgery on the 1st postoperative day and showed evidence of retinal ischemia with central retinal artery occlusion on fundoscopic examination. In our patients, we hypothesize that the complications were most likely related to the intra-orbital ischemia initiated by the collapse of the arterial and venous channels in the orbit and/or to the direct or indirect contusion on the intra-orbital structures. These situations could be produced by inadvertent pressure placed on the eyeball with a bulky retracted frontal skin flap. Visual acuity in both patients ranged from no light perception to finger-counting. Their external ophthalmoplegia had completely disappeared 2 weeks after surgery and visual acuity in one patient began to improve. But in the other patient, the condition was irreversible. The degree of visual recovery seems to be dependent on the duration and severity of retinal ischemia by orbital compression. Unfortunately, there is no satisfactory treatment. We recommend careful surgical manipulation, including the use of an eye shield just before aneurysm surgery to protect the ipsilateral eyeball.
Key Words: Unilateral blindness, Anterior communicating artery aneurysm, Intra-orbital ischemia

Impairment of vision after aneurysmal subarachnoid hemorrhage (SAH) can occur. This condition is mainly caused by retinal, subhyaloid and occasionally vitreous hemorrhage due to acutely elevated intracranial pressure which produces a sudden increase in retinal venous pressure.12) Due to the recent development of microsurgical techniques, neurosurgeons rarely experience blindness in patients caused by direct optic nerve injury or postoperative hematoma surrounding the optic nerve following intracranial aneurysm surgery.
Zimmerman et al. reported that orbital infarction syndrome after intracranial aneurysm surgery has multiple factors; patients with SAH, increased intracranial pressure, anomalous arterial or venous circulation, or impaired orbital venous outflow appear particularly vulnerable.13) The patient’s pathogenesis is not clear, but these authors believe multiple aggravating factors might cause an increase in the risk of orbital infarction in their patients. It will be helpful to prevent these complications in aneurysm surgery if we can elucidate the etiology. To better clarify this problem, we report 2 similar cases to help pinpoint the pathogenesis as well as review the pertinent literature.
Case Reports
Case 1
A 44-year-old woman with normal visual acuity suffered from sudden severe headache with neck stiffness. She had no history of hypertension. Her neurological grade was Hunt-Hess grade 1. A brain computerized tomogram (CT) revealed diffuse subarachnoid hemorrhage (SAH) in the Sylvian cisterns, basal cistern and interhemispheric fissure (Fig. 1). Cerebral digital subtraction angiogram (DSA) showed a left anterior communicating artery (ACoA) aneurysm (Fig. 2). We excluded possible etiological factors such as abnormal systemic ocular conditions and trauma causing the ischemia in intra-orbital structures. The brain was slack after a unilateral frontotemporal craniotomy and an aneurysm clipping was performed without premature rupture and pial injury under normotensive anesthesia without perioperative hypotension. On awakening, she did not complain of blindness, headache and eyelid swelling but we found conjunctival chemosis and blindness of the left eye with left external ophthalmoplegia the next day. A CT scan showed no evidence of hematoma surrounding the aneurysm and intra-orbitally. A subsequent DSA showed no evidence of vasospasm at the anterior circulation flows (Fig. 3). Ophthalmologic consultation was obtained immediately. Visual acuity of the right eye was normal but that of the left eye showed no light perception. Fundoscopy showed diffuse retinal edema with bloodless arterioles. She was treated with 400ml of 25% mannitol, 4 times a day and 500mg of solumedrol. Two weeks later, external ophthalmoplegia began to improve and it had completely disappeared one month after surgery. About 3 months later, her visual acuity had recovered to where she could detect hand motions.
Case 2
A 52-year-old man was admitted with a sudden headache, nausea and vomiting (Hunt-Hess grade 1). A brain CT revealed diffuse SAH in the Sylvian cisterns, basal cistern and interhemispheric fissure and a left carotid angiogram demonstrated a left ACoA aneurysm (Fig. 4, 5). An aneurysm surgery was performed via a left frontotemporal craniotomy. The aneurysm was easily clipped without premature rupture. The blood pressure was maintained normotensive during surgery. Immediately after awakening he complained of blindness and pain in the ipsilateral eyeball. Upon ophthalmic examination, the left pupil was 5 mm in diameter and nonreactive to direct or consensual light reflex with afferent papillary defect. The patient’s visual acuity was only light perception in the left eye. The left fundus showed retinal edema throughout the posterior pole and mid-periphery, with cherry-red spots. An emergency follow-up CT scan showed no evidence of hematoma surrounding optic or oculomotor nerve and DSA showed no evidence of vasospasm (Fig. 6). Ophthalmoplegia disappeared but his visual acuity was still limited to the level of light perception at a 3 month follow-up.
Anterior communicating artery (ACoA) aneurysm is the most common form of intracranial aneurysm, accounting for 25~38% of total cerebral aneurysm cases.14) ACoA aneurysms that produce neuro-ophthalmic symptoms usually affect the anterior visual pathway and lead to monocular vision loss, junctional scotoma, or bitemporal hemianopsias often accompanied by retro-orbital pain and headache.2)15) The development of visual loss as a complication of aneurysm surgery is rare, but if it occurs, we are apt to think that direct nerve injury has occurred intraoperatively. We also first considered the possible influence of optic nerve manipulation.
Ischemic events within the orbit are common. Possible etiologies of visual loss and ophthalmoplegia due to intra-orbital ischemia include thromboembolism, coagulopathy, vasculitis, trauma and particular types of surgery. Only a few reports are found in the literature on this type of ischemic ocular complication after surgery. Slocum, et al. suggested visual loss after sectioning of the fifth cranial nerve in the prone position in 1948.11) He speculated that the visual loss was caused by accidental pressure placed on the eye in the presence of lowered blood pressure, due to gravity and blood loss. Givner and Jaffe had four patients in whom unilateral blindness developed following abdominal surgery.5) Two of the four patients were in shock. They attempted to reproduce the same conditions by exerting pressure on the eye of rabbits and monkeys. In their experiments, hemorrhage appeared in the retina of rabbits, but no retinal infarction could be produced. Hollenhorst et al. also reported on 8 patients who experienced sudden unilateral blindness after suboccipital or posterior cervical approaches and they suggested that the cause of that condition was retinal ischemia induced by inadvertent pressure on the ocular structure under prolonged anesthesia induced hypotension.8) The final visual status of the affected eye in their cases ranged from complete recovery of vision to permanent blindness. In relation to aneurysmal SAH, Thygesen and Rosenorn demonstrated a case of bilateral transient blindness due to retinal ischemia caused by cerebral vasospasm after SAH from a ruptured saccular aneurysm.9) Ophthalmoscopy showed bilateral retinal edema with cherry-red spots and spasms of the retinal arteries but without retinal or vitreous hemorrhage. Recently, Borruat et al. defined the orbital infarction syndrome as acute blindness and total ophthalmoplegia resulting from ischemia of all the intraorbital and intra-ocular structures occurring with occlusion of the common carotid artery, giant cellarteritis and mucormycosis.1) Zimmerman et al. described similar features immediately after standard frontotemporal craniotomy for intracranial aneurysm as the orbital infarction syndrome. Their blindness remained permanent.13)
Ocular ischemia is the other major cause of blindness following SAH and aneurysm clipping. It may be due to a variety of intraoperative and postoperative factors. The blood supply to the eye is derived entirely from the ophthalmic artery, which arises from the supraclinoid segment of the internal carotid artery, prior to its entry into the Circle of Willis. Its main branches are the central retinal artery and the ciliary arteries (anterior, long and short posterior). The retina is supplied by the central retinal artery (inner retina) as well as by posterior ciliary arteries (outer retina). Retinal function is dependent on the integrity of both arterial systems.3) The macula is also supplied by cilioretinal arteries which arise from the choroidal circulation. These may protect the macula from ischemia during episodes of diminished central retinal artery flow. The intraocular portion of the optic nerve (anterior to the lamina cribrosa) is supplied by the short posterior ciliary arteries via the choriocapillaris (the inner capillary layer of the choroid). Posterior to the lamina cribrosa, the intraorbital optic nerve is supplied by the central retinal artery, as well as by pial vessels originating from the ophthalmic artery. Finally, the intracanalicular and intracranial portions of the optic nerve are supplied by a pial network originating from the internal carotid and anterior cerebral arteries.
It is clinically very difficult to ascertain the exact pathophysiologic mechanism responsible for unilateral blindness after intracranial aneurysm surgery. Hollenhorst suggested that these events were initiated by a partial or complete collapse of the arterial and venous channels in the orbit produced by a tamponade action of the ocular contents in the prone position with the face cushioned on a well-padded headrest.8) Zimmerman surmised the pathogenesis of orbital infarction syndrome after intracranial aneurysm surgery as the impairment of ophthalmic artery and collateral arterial perfusion by the combined effects of orbital venous outflow obstruction with increased intra-orbital pressure, resulting in ischemia of the intra-ocular and intra-orbital structures.13) They believed risk factors that aggravate these conditions were increased intracranial pressure, external pressure on the globe or decreased ophthalmic artery perfusion by any mechanism and above all conditions were cumulative. However, in our cases, there was no rise in intracranial pressure or any abnormality in the arteries or veins at the time of the aneurysmal operation. Frontotemporal of “pterional” craniotomy exposure requires a myocutaneous flap to be retracted anteriorly and inferiorly near the orbit, and in some circumstances, this bulky flap could indirectly exert pressure on the globe, especially in individuals with “shallow” orbits or significant orbital congestion. Our patients were in the supine position during the operation, and therefore, the venous outflow obstruction that can occur in the dependent position can be excluded. Further, their mental states were alert and the brain condition was good with minor bleeding intra-operatively and no anesthesia-induced hypotension. There for, intracranial pressure and hypotension were not influencing the ophthalmicartery perfusion. Also, if intracranial pressure and hypotension were to be implicated, the unilaterality of the phenomena would  unlikely explain the cause. One of our patients had hypertension but without any systemic abnormalities; they suffered from unilateral blindness with ophthalmoplegia. This indicates that additional critical factors may be involved to cause these complications.
No examples of global orbital infarction have been reported secondary to ophthalmic artery occlusion because of the rich collateral circulation between the ophthalmic artery and external carotid artery.6)10) Taken together with variability in the degree of ophthalmoplegia and recovery of visual acuity, we think the possible cause of these complications derived from hypoperfusion of one or all of the intra-orbital branches during ophthalmic artery (central retinal artery, ciliary artery, and branches to the extra-ocular muscle or ocular motornerve) caused by intra-operative focal and intra-orbital trauma, rather than hypoperfusion of the ophthalmic artery in addition to its collaterals by systemic abnormalities. Duke-Elder and others described that the mechanism of ocular motor dysfunction resulting from traumatic or iatrogenic causes might be induced by intramuscular edema and hemorrhage.4)7) The skin flap of our patients was also relatively bulky. All things considered, sudden unilateral blindness can occur after surgery with a bulky pad just underneath the reflected frontal flap toward the orbit such as is typically used in frontotemporal craniotomy for intracranial aneurysm surgery. Accordingly, we believe that retinal ischemia and/or the extra-ocular muscle contusion by the retracted skin flap directly contacting the globe is probably the most important pathophysiology of extra-ocular symptoms and permanent blindness.
We propose that the degree of symptoms and signs sudden unilateral blindness and ophthalmoplegia mainly depends on the severity of the pressure exerted on the globe and the duration of resulting orbital ischemia. Once blindness develops, it is difficult to treat, and thus prevention is more important. We recommend routine use of an eye shield to protect the globe, especially in patients who have aggravating factors we already described, or we recommend as gentle a retraction of the skin flap as possible.
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