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Central retinal artery occlusion and ophthalmoplegia following spinal surgery
  1. M J Halfon,
  2. P Bonardo,
  3. S Valiensi,
  4. M C Zaffaroni,
  5. M M Fernandez Pardal,
  6. D Ribero Ayerza,
  7. R Ebner,
  8. P Anderson,
  9. R C Reisin
  1. Hospital Britanico, Perdriel 74, Buenos Aires C1280AEB, Argentina
  1. Correspondence to: Dr Mario J Halfon Hospital Britanico, Perdriel 74, Buenos Aires C1280AEB, Argentina;

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Visual loss and ophthalmoplegia are very infrequent complications after spinal surgery.1,2 Visual loss may be caused by ischaemic optic neuropathy, central retinal artery or vein occlusion, or occipital stroke.2,3 Previous reports have attributed this complication to patient positioning, intraoperative blood loss, and controlled hypotension or shock.2–5 Associated risk factors include anaemia, prolonged surgical time, bradyarrhythmia, hypertension, diabetes, smoking, vascular disease, and increased blood viscosity.2,6 Ophthalmoplegia after spinal surgery is even more unusual than visual loss, and only few reports exist in the literature.6–8 Moreover, magnetic resonance image (MRI) studies to differentiate between cavernous sinus thrombosis and direct compression of orbital contents have not been previously described. We therefore report two patients who developed this unusual combination of ophthalmoplegia and central retinal artery occlusion (CRAO) after spinal surgery.

Case 1

A 62 year old male ex-smoker underwent a L2–L3 posterior spinal decompression and segmental instrumentation for lumbar stenosis and scoliosis, in prone position with ocular protection (gauze swab and tape). The surgery lasted 2 hours and 45 minutes. Before the procedure blood pressure was 140/60 mm Hg and during operation it was maintained at 90/60 mm Hg. Just after surgery he complained of visual loss and left ocular and nasal pain. Examination revealed left palpebral oedema, local erythema, blindness, and total ophthalmoplegia of the left eye. Left pupil was dilated and fixed. The funduscopic examination showed retinal oedema, a central cherry-red spot at the macula, and attenuated arteries. The rest of his neurological examination was normal.

The haematocrit dropped from 43% to 34%. The brain MRI was normal and the orbit MRI revealed enlargement and hyperintensity of left ocular muscles in T2 weighted images sparing their tendons (fig 1). Ocular motility recovered in 4 weeks but visual loss persisted until the last follow up at 7 months.

Figure 1

 MRI of the orbit. T2 weighed image shows proptosis and oedema of extraocular muscles in the left eye, sparing their tendons.

Case 2

A 23 year old man with a history of tobacco abuse and asthma underwent a prolonged cervical arthrodesis in prone position caused by C7 vertebral collapse with spinal contusion. Immediately after surgery he complained of left visual loss and he was referred to our hospital. Details of duration of surgery, ocular protection, intraoperative blood pressure, and haematocrit were unavailable. Upon examination he showed blindness of the left eye with palpebral oedema, orbital pain, and total external ophthalmoplegia. The funduscopic examination revealed a pale retina with a macular cherry-red spot. The pupil was dilated and fixed. The MRI studies showed a normal brain, but swelling of the left extraocular muscles; MRI angiography and ophthalmic echo Doppler were normal. After 3 months vision did not recover but ocular motility partially improved.


Our two patients developed complete ophthalmoplegia and CRAO after spinal surgery. Intraoperative ocular protection was used at least in the first patient. Common features included prone position and postoperative signs of orbital swelling. Imaging studies revealed signs of oedema in extraocular muscles sparing their tendons. To our knowledge, extraocular muscles abnormalities in MRI have not been previously reported. Ophthalmoplegia partially improved in one patient and fully recovered in the other within a few weeks, but visual loss persisted in both cases.

Stevens et al,2 in a retrospective review of 3450 spinal surgeries, identified seven patients (incidence 0.2%) with visual loss caused by ischaemic optic neuropathy, occipital infarction, or central retinal vein occlusion, but neither presented with CRAO or extraocular muscle abnormalities.

Only few patients with CRAO following surgery have been previously described in the English literature (table 1). Moreover, Little1 analysed 27 930 cases of controlled hypotension anaesthesia and found only three cases of CRAO. No details of surgical positioning or procedure were given. Since the original report of Slocum et al,9 it has been emphasised that CRAO may be the result of extrinsic ocular pressure caused by head rest or anaesthetic mask malposition in the presence of hypotension, shock, and prolonged anaesthesia.4,5,8–10

Table 1

 Reported patients with postoperative CRAO, ophthalmoplegia, or both

Ophthalmoplegia related to spinal surgery is also an exceptional complication. West et al7 described a patient who developed unilateral total external ophthalmoplegia and unilateral visual loss following scoliosis surgery. An orbit computed tomography scan performed 1 week later showed left proptosis and swelling of the left medial rectus and ruled out cavernous sinus thrombosis. The authors suggested that perioperative ocular compression might be the cause. Wolfe et al6 reported a young woman who suffered a right CRAO after an instrumented spinal surgery. Postoperatively, the patient had blindness, moderate ptosis, restriction of the extraocular movements, and paraesthesias in the supraorbital region of the same eye. A CT scan of the brain and orbits showed only mild oedema of the right optic nerve. Ocular motility improved but the visual loss did not. Although prognosis is usually very poor, a recent patient described in Japan was treated successfully with urokinase and PGE1, stellate ganglion block, and hyperbaric oxygen therapy.11

Hollenhorst et al8 reported eight cases of unilateral visual loss after inadvertent orbital pressure during general anaesthesia for neurosurgical procedures. The most severe cases had proptosis, ptosis, and paralysis of extraocular musculature with no recovery. Moreover, they provoked visual loss and ophthalmoplegia by orbital compression for 60 minutes in seven rhesus monkeys, in the setting of hypovolaemia and hypotension. They proposed that partial or complete collapse of the arterial and venous channels of the orbit, occurred as a result of a tamponade action of the ocular contents. When the external pressure is released, the ischaemic vascular channels dilate and there is a transudation of fluid through the permeable walls into the tissue spaces. This results in orbital oedema, proptosis, paresis of ocular movement, and massive oedema of the retina. Based on findings from this animal model, it is likely that external pressure during the surgical procedure induces occlusion of the arterial and venous orbital vessels. The increased MRI signal in extraocular muscles is probably the expression of post-ischaemic oedema facilitated by the richer vascular supply and the more prominent extravascular space characteristic of these muscles.12 Reversibility of ophthalmoplegia will probably depend on the degree of ischaemia suffered by both the extraocular muscles and the III, IV, and VI cranial nerves.

CRAO and ophthalmoplegia are unusual, but severe, complications after spinal surgery. Postoperative signs of orbital swelling, only in the affected eyes, were clear evidence of intraoperative compression in our patients.

The increase in intraorbital pressure associated with hypotension, shock, anaemia, prolonged operative time, and bradyarrhythmia are considered to be the main risk factors for developing CRAO and ophthalmoplegia. Adequate eye protection during surgery, and meticulous attention to keep the eyes free from pressure, can reduce the risk of these potentially avoidable serious complications.


We thank Dr John Stewait for his critical reading of the manuscript.