Introduction

   Global orbital infarction results from ischemia of the intraocular and intraorbital structures caused by hypoperfusion of the ophthalmic artery and its branches. It is a rare disorder due to the rich anastomotic vascularization of the orbit.²⁾
   The acute visual loss and/or visual field defect associated with an afferent pupillary defect unilaterally or bilaterally has been reported after various general surgical procedures.^3)6)8)9)10) Initial and follow-up fundoscopic examinations of our both patients were consistent with retinal and choroidal infarction. We report two patients with acute unilateral visual loss and proptosis after clipping of anterior communicating aneurysms.

Case Reports

Case 1 
   A 54-year-old man was admitted with sudden bursting headache and syncope. Computerized tomography (CT) showed subarachnoid blood in the sylvian fissure, interhemispheric fissure and basal cisterns. Cerebral angiography demonstrated a ruptured right anterior communication artery (A-com)aneurysm and hypogenesis of the proximal left anterior cerebral artery. He underwent a standard right frontotemporal craniotomy. We took down the sphenoid ridge and drilled the anterior skull base. During this procedure the periorbita was exposed, but other unexpected events were absent. The aneurysm was clipped successfully. 
   Four hours after surgery, the patient was alert and oriented, but complained of visual loss in the right eye. On examination, marked proptosis, chemosis, and complete ptosis were presented in the same eye. Also an unreactive pupil and ptosis were recorded. Emergency CT showed no evidence of retrobulbar hemorrhage, optic nerve sheath hematoma, orbital mass, or enlarged extraocular muscles. 
   One day after surgery neuro-ophthalmologic consultation disclosed that vision was hand motions in the right eye and 20/50 in the left. The right pupil was minimally reactive to direct light with a marked relative afferent pupillary defect. There was a minimal right consensual pupillary response. Adduction, depression, and elevation were moderately diminished, and no abduction was presented in the right eye. Intraocular pressures (IOP)were 19mmHg in the right eye and 18mmHg in the left. The right retina was edematous, and there were scattered posterior pole blot hemorrhages. No cherry-red spot was evident, and the retinal vessels were normal. Topical agent and systemic acetazolamide were started, and the patient later received intravenous pulse methylprednisolone. 
   One month later, visual acuity was no light perception in the right eye and 20/20 in the left. The right afferent pupillary defect persisted, but the consensual response had normalized. Ptosis, chemosis and proptosis had resolved and motility in the right had improved. There was marked right retinal vascular attenuation, a pale optic disc and diffuse pigmentary retinopathy (Fig. 1). Visual evoked potential(VEP) showed low amplitude waveform and no evidence of normal conduction on the right side (Fig. 2). Two months later, ductions had normalized, but otherwise results of the examination were unchanged. 

Case 2 
   A 64-year-old man had sudden headache, lethargy and seizure. CT showed subarachnoid hemorrhage in the basilar cisterns and intracerebral hemorrhage in the left frontal lobe. Cerebral angiography showed a ruptured left anterior communicating artery aneurysm. The aneurysm was clipped via a left frontotemporal craniotomy without intraoperative complications. On arrival to the intensive care unit after surgery, the patient had ptosis, proptosis and ophthalmoplegia in the left eye. The left globe and orbit were hard by palpation. 
   Two hours later, he was still drowsy and visual acuity of the left eye was no light perception. The left pupil did not react to light with no consensual response. There were complete ptosis, ophthalmoplegia and marked chemosis in the left eye. His emergency CT scan showed a small infarction of the left caudate head and left orbital soft tissue swelling with proptosis. The cornea was clear and depth of the anterior chamber was moderate. Intraocular pressures were 16 mmHg in the left eye and 13 mmHg in the right. A 4+right relative afferent pupillary defect was present. Results of fundoscopy showed retinal edema, arteriolar attenuation, pale optic disc and no cherry-red spot in the left eye.

   Three weeks later, the left retinal edema was recovered, but visual acuity of the left eye was no light perception. The left optic disc was pale, and the retinal vessels were attenuated (Fig. 3). VEP revealed that poor waveform and delayed latency of P100 on the left side (Fig. 4). The proptosis and chemosis were gradually resolved but the ophthalmoplegia and fundus abnormalities still persisted. Two months later, visual acuity was unchanged, and the right afferent papillary defect persisted. The external appearance and eye movements had returned to preoperative condition. 

Discussion

   Sudden blindness occurs from retinal infarction caused by hypoperfusion of the central retinal artery, and from anterior ischemic optic neuropathy and choroidal ischemia due to compromise of the short ciliary arteries. Ophthalmoplegia results from hypoperfusion of the long ciliary arteries and from impaired arterial supply to the extraocular muscles or ocular motor nerve.⁷⁾
   The ophthalmic artery originates from the internal carotid artery and has numerous ocular and orbital branches, including the central retinal and ciliary arteries. Among the branches of the ophthalmic artery, only the central retinal artery and the short posterior ciliary arteries are terminal vessels. The ophthalmic artery occlusion alone does not cause the orbital infarction because the blood supply of the orbit is derived from rich anastomoses between the internal carotid artery (ophthalmic artery and its branches) and external carotid artery (maxillary, facial, superficial temporal arteries, and their branches). However, if collateral blood flow is compromised by other factors, orbital infarction may develop seriously. 
   Borruat et al in 1993 reported three patients who suffered from acute blindness, ophthalmoplegia and proptosis, and they defined ischemia of all the intraocular and intraorbital structure as orbital infarction syndrome. They suggested that the possible mechanisms for orbital infarction were either the occlusion of an anomalous ophthalmic artery (lacking anastomoses)or the occlusion of both the ophthalmic artery and its anastomoses. This syndrome can occur with common carotid artery occlusion, orbital mucormycosis, giant cell arteritis and myelofibrosis.²⁾
   Visual loss is a rare complication of aneurysm surgery;procedures requiring general anesthesia and cardiopulmonary bypass, in which hypovolemia, hypotension or hypothermia occur, particularly can be at risk.¹⁾ Hollenhorst et al reported eight patients who were blind suddenly after neurosurgical procedure. They postulated that the cause of blindness was retinal ischemia developed by a tamponade action of the ocular structure under the prolonged anesthesia induced hypotension.⁴⁾
   Reduced blood pressure and direct pressure on the globe due to improper positioning of the patient may be responsible for postoperative visual loss in some patients. Jayam et al describe a patient with irreversible unilateral ischemic retinopathy and peroneal neuropathy after an alcohol-induced loss of consciousness, and referred to "saturday night retinopathy". The mechanism was thought to be increased orbital pressure due to the prolonged dependent position of the patient, causing pressure on the globe and compromising the retinal and ciliary artery.⁵⁾
   Only a few reports concerning retinal ischemia and intraorbital ischemia as an isolated complication of surgery are found in the literature. Zimmerman et al described six cases with orbital infarction syndrome after frontotemporal craniotomy for intracranial aneurysm. They suggested that these conditions such as increased intracranial pressure, external pressure on the globe or decreased ophthalmic artery perfusion pressure by any mechanism might increase the risk for orbital infarction.¹¹⁾ Wolfe et al experienced a similar condition as a complication of positioning in a patient with no cardiologic or hematologic diseases during adult scoliosis surgery.¹⁰⁾
   The cause of orbital infarction syndrome in our cases is probably multifactorial;Firstly, subarachnoid hemorrhage and/or cerebral infarction cause the intracranial hypertension, increasing the orbital pressure and lowering ophthalmic artery perfusion. Secondly, we generally take down the sphenoid ridge more radically and drill the anterior skull base more flatly in surgery for this site aneurysm than other;it can be done under constant irrigation to prevent thermal damage to the optic nerve. But occasionally, a hole of orbital wall is made in the process of inadvertent removal of sphenoid bone. Once, irrigation fluid leaks through the hole, it results in swelling and strangulation of the intraorbital structure, and compromising the retinal and ciliary circulation. Finally, inadvertent pressure placed on the eyeball with a tightly retracted scalp flap might provoke intraocular and/or retinal ischemia. 
   Orbital infarction syndrome should be managed aggressively. Significant proptosis and elevated IOP should be controlled. Retrobulbar or optic nerve sheath hematoma should be identified promptly because some patients may benefit from mergency surgery. Despite of aggressive treatment, prognosis for significant visual recovery after orbital infarction is poor. 

Conclusion

   Visual loss caused by ophthalmic artery occlusion often is profound and irreversible. So, every precaution should be taken to minimize known risk factors. All operative procedures were performed precisely, especially taking down the sphenoid ridge and drilling the anterior skull base. In addition, increased intracranial pressure and systemic blood pressure should be controlled adequately. 

REFERENCES

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4. Hollenhorst RW, Svien HF, Benoit CF. Unilateral blindness occurring during anesthesia for neurosurgical operations. Arch Ophthalmol 52:819-30, 1954

5. Jayam AV, Hass WK, Carr RE, Kumar AJ. Saturday night retinopathy. J Neurol Sci 22:413-8, 1974

6. Johnson MW, Kincaid MC, Trobe JD. Bilateral retrobulbar optic nerve infarctions after blood loss and hypotension:a clinicopathologic case study. Ophthalmology 94:1577-84, 1987

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8. Lee EC, Kim TH, Jung JM, Seo SW. A case of orbital infarction syndrome caused by compression of bulky bicoronal scalp flap. J Korean Ophthalmol soc 43:795-800, 2002

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10. Wolfe SW, Lospinuso MF, Burke SW. Unilateral blindness as a complication of patient positioning for spinal surgery:a case report. Spine 17:600-5, 1992

11. Zimmerman CF, Van Patten PD, Golnik KC, Kopitnik TA, Anand R. Orbital infarction syndrome after surgery for intracranial aneurysms. Ophthalmology 102:594-8, 1995