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|LETTER TO EDITOR
|Year : 2015 | Volume
| Issue : 3 | Page : 431-434
Ophthalmic artery occlusion with total ophthalmoplegia following spinal surgery
Jyoti Matalia, Vimal Krishna Rajput, Geetanjali J Chillal, Bhujang K Shetty
Department of Pediatric Ophthalmology and Neuro-Ophthalmology, Narayana Nethralaya-2, Bengaluru, Karnataka, India
|Date of Web Publication||5-Jun-2015|
Department of Pediatric Ophthalmology and Neuro-Ophthalmology, Narayana Nethralaya-2, Bengaluru, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Matalia J, Rajput VK, Chillal GJ, Shetty BK. Ophthalmic artery occlusion with total ophthalmoplegia following spinal surgery. Neurol India 2015;63:431-4
Ocular complications following a non-ocular surgery are uncommon but may be devastating. The incidence of perioperative vision loss (POVL) after non ocular surgery ranges from 0.013% for all surgeries to upto 0.2% for spinal surgeries.  The causes of the sudden visual loss may be the development of ischemic optic neuropathy, central retinal artery occlusion or cortical ischemia. , The simultaneous occurrence of ophthalmic artery occlusion and ophthalmoplegia following non-ocular surgery is very rare. We report a case of an ophthalmic artery occlusion with total ophthalmoplegia that developed following spinal surgery in prone position.
A 68-year-old gentleman presented to the neurosurgery clinic with complaints of progressive tightness and numbness in both upper limbs and the right lower limb. The patient was a known case of type II diabetes mellitus since 15 years and was on oral hypoglycaemic agents and insulin with a good glycaemic control. Following clinical examination and imaging, he was diagnosed with a C4 to C6 spinal canal stenosis with compressive myelopathy. He underwent a C4-6 laminectomy under general anaesthesia. During surgery, he was placed in a prone position with his head supported on a horse-shoe head rest. The total duration of surgery was 3.5 hrs. His haemoglobin was 12.6 g% and the blood counts were normal. There was no significant blood loss or intraoperative hypotension.
On the first postoperative day, he complained of diminution of vision in the left eye with drooping of the left upper eyelid. On examination, the visual acuity was 6/9 in the right eye and the extraocular movements were normal. There was no light perception in the left eye and there was severe ptosis with complete limitation of the extraocular movements in all directions of gaze. The anterior segment showed chemosis in the left eye. The pupil was 3 mm in the right eye with normal reaction to light; while in the left eye, there was a fixed pupil of 6 mm size with a relative afferent pupillary defect. The fundus examination of the left eye revealed retinal edema with a cherry red spot at the macula. Based on these findings, he was diagnosed to be having central retinal artery occlusion with total ophthalmoplegia. Paracentesis was performed in the left eye and the patient was started on oral acetazolamide 1 gram three times per day. The patient was reviewed daily at bedside (as he could not be shifted to the outpatient department) and his visual status remained unchanged until his discharge from the hospital.
One month later, when he was followed up in the neuro-ophthalmic outpatient clinic, there was no improvement in the vision or in the extraocular movements of the left eye. The fundus evaluation of the left eye revealed an optic disc pallor with total vessel attenuation, atrophic changes at the macula and a relatively featureless retina with retinal pigment alterations [Figure 1]a and b. Fluorescein angiography of the fundus showed a delayed choroidal perfusion (32 seconds) and a non-perfusion of the retinal arteries in the left eye that was suggestive of ophthalmic artery occlusion [Figure 2]. At a 3-month follow-up, there was partial improvement of extraocular movements; however, the absence of vision in the left eye persisted.
|Figure 1: (a) Fundus photograph of the right eye showing a normal fundus (b) Fundus photograph of the left eye showing an optic disc pallor with total vessel attenuation, atrophic changes at the macula and a relatively featureless retina with retinal pigment epithelial alterations|
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|Figure 2: Fundus fluorescein angiography of the left eye showing delayed perfusion of choroid (32 seconds) and non-perfusion of retinal arteries suggestive of ophthalmic artery occlusion|
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The main ocular causes of perioperative visual loss following spinal surgery are the ophthalmic artery or retinal artery obstruction. An ophthalmic artery obstruction is acute with the simultaneous presence of occlusion of both the retinal and choroidal circulations and has the following features:  (a) Severe visual loss with barely minimum or no light perception; (b) An intense ischemic retinal whitening that extends beyond the macular area; (c) Small-to-complete disappearance of the cherry-red spot; (d) Marked choroidal perfusion defects on fluorescein angiography; (d) No recordable electroretinogram; and, (e) Late retinal pigment epithelial alterations. In the patients having a CRAO, the fluorescein angiography shows a delay in the retinal arterial filling and the retinal arteriovenous transit time with a normal filling of the choroidal vascular bed. A markedly prolonged choroidal filling with the absence of a cherry red spot should arouse the suspicion of an ophthalmic artery obstruction. 
Our patient had perception of light and a cherry red spot on day 1, but the vision worsened to no perception of light. The fundus evaluation showed optic disc pallor with retinal ghost vessels and retinal pigment epithelium alterations and macular atrophy. The electroretinogram was not performed but fluorescein angiography done at follow up showed markedly delayed choroidal perfusion and absent retinal filling confirming the presence of the ophthalmic artery obstruction.
Various mechanisms have been proposed for the development of ischemic neuropathy and ophthalmoplegia. Hollenhorst et al.  reproduced visual loss and ophthalmoplegia experimentally in seven rhesus monkeys by orbital compression for 60 minutes along with systemic hypovolemia and hypotension. A mechanism of partial or complete collapse of the arterial and venous channels of the orbit that were produced by a tamponade action of the ocular contents was the proposed mechanism. Halfon et al.  suggested that the reversibility of ophthalmoplegia would depend on the degree of ischemia suffered by the extraocular muscles and the III, IV and VI cranial nerves.
The intraoperative position of the patient with his head resting on the horse-shoe head rest could have led to a direct pressure on the globe resulting in raised intraocular pressure causing ophthalmic artery occlusion and total ophthalmoplegia. Although a protective foam rest is usually placed over the patient's face, there are high chances of the same being displaced during surgery resulting in direct pressure on the ocular structures.
Cases with simultaneous ophthalmic artery occlusion causing visual loss and total ophthalmoplegia as a surgical complication following prolonged compression of the eye are very few in the literature.  Kothari et al.  presented a case of ophthalmic artery occlusion that occurred following spinal surgery but their patient did not have an ophthalmoplegia. West et al.  reported a similar case with ophthalmic artery occlusion and ophthalmoplegia in a 50-year old patient following scoliosis surgery and attributed it to pressure on the orbital contents during surgery. Ophthalmic artery occlusion has also been reported following a mammoplasty  and a pars plana vitrectomy. 
No proven therapy exists for this complication and significant visual recovery usually does not occur. Some of the ophthalmic complications are preventable by an early recognition of the entity and by taking adequate precautions to prevent this complication. The American Society of Anesthesiologists have proposed a Practice Advisory for prevention of the perioperative visual loss associated with spine surgery.  The intraoperative management suggested by this advisory includes the following: (1) Blood pressure management: Systemic blood pressure should be monitored continually in high-risk patients and the use of deliberate hypotension for these patients should be determined on a case-by-case basis; (2) Management of intraoperative fluids: Central venous pressure monitoring should be considered in high risk patients and the intravascular volume maintained in patients who have substantial blood loss; (3) Management of anemia: Hemoglobin or hematocrit values should be monitored periodically during surgery in high-risk patients who experience substantial blood loss. The Task force believes that there is no documented lower limit of hemoglobin concentration that has been associated with the development of perioperative visual loss; (4) Use of vasopressors: They can be used on a case-by-case basis because there is insufficient evidence to provide guidance for their use; (5) Patient positioning: There is no evidence that ocular compression causes isolated perioperative anterior or posterior ischemic optic neuropathy (ION). However, direct pressure on the eye should be avoided to prevent arterial occlusion. The high-risk patient should be positioned so that the head is at level with or higher than the heart, whenever possible. The high-risk patient's head should be maintained in a neutral forward position whenever possible (that is without significant neck flexion, extension, lateral flexion, or rotation); and, (6) Staging of surgical procedures may entail additional costs and patient risks (e.g., infection, thromboembolism, or neurologic injury) but may decrease the risk of perioperative visual loss in some patients.
The consensus of the Task Force regarding the postoperative management of patients is that a high-risk patient's vision should be assessed when the patient becomes alert (e.g., in the recovery room or the intensive care unit). If there is a concern regarding potential visual loss, an urgent ophthalmologic consultation should be obtained to determine its cause. Additional management may include optimizing the hemoglobin or hematocrit values, the hemodynamic status, and the arterial oxygenation. The Task Force believes that there is no role for antiplatelet agents, steroids, or intraocular pressure-lowering agents in the treatment of perioperative ION. 
In conclusion, a permanent visual loss and total ophthalmoplegia following a non-ocular surgery, although rare, can be a serious and devastating complication. The anaesthetists and surgeons should be aware of this potential complication and take appropriate preventive measures.
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[Figure 1], [Figure 2]