Keywords
prone position - ischemia - vision loss - atlantoaxial dislocation
Introduction
Vision loss after spine surgery is a rare but devastating complication, with incidence
for spinal and cardiac surgery as high as 0.2 and 4.5%.[1] Ischemic optic neuropathy, central retinal artery thrombosis, and cortical blindness
are the three recognized causes of blindness.[2]
[3] Multiple risk factors have been identified in the literature.[2]
[3]
[4]
[5] We report a rare case of unilateral vision loss following surgery for craniovertebral
junction anomaly in the prone position.
Case History
A 16-year-old boy presented with chief complaints of neck pain, progressive spastic
quadriparesis, and tingling paraesthesia in the left upper limb for the past 3 years.
Vision and extraocular movements were regular. Tone was modified ashworth scale (MAS)
grade 2 and power was 4/5 in all four limbs. Deep tendon reflexes were exaggerated.
Abdominal reflex was absent in all quadrants. Plantars were bilateral extensors. Sensory
system was normal. Radiological investigations were suggestive of atlantoaxial dislocation
with occipitalization of atlas ([Fig. 1]). The patient underwent occipito-C2-C3 fixation with foramen magnum decompression
in a prone position with the head resting on a horseshoe headrest ([Fig. 2]). Surgery lasted 6 hours. Postoperatively, the patient had improvement in power
and tingling paraesthesia. On postoperative day 1, the patient complained of loss
of vision from the right eye with orbital swelling. Patient was given injectable methylprednisolone
(30 mg/kg) followed by continuous infusion (5.4 mg/kg/h) for the next 23 hours. Ophthalmology
evaluation revealed a loss of perception of light in the right eye. Fundus examination
showed a cherry red spot with macular ischemia with arteriole attenuation, which was
suggestive of central retinal artery occlusion. Orbital swelling subsided over the
next 1 to 2 days. Extraocular movements were regular. However, there was no improvement
in vision in the right eye.
Fig. 1 Preoperative computed tomography scan of craniovertebral junction with upper cervical
spine, (A) sagittal and (B) axial section, showing atlantoaxial dislocation with rotation of the occipitoatlantal
joint having a bifid anterior and posterior arch of atlas (C1).
Fig. 2 Postoperative images of computed tomography scan of craniovertebral junction demonstrating
(A) three-dimensional reconstruction: (B) axial, (C) sagittal, and (D) coronal section showing occipito-C2-C3 fixation with reduction in the atlantoaxial
dislocation.
Discussion
Multiple case reports in the literature have reported ischemic optic neuropathy after
spinal surgery in the prone position ([Table 1]). Multiple causative factors include:
Table 1
The published cases with possible reasons of visual impairment following surgery in
prone position
|
Sl. no.
|
Study
|
Number of patients
|
Possible diagnosis of vision loss
|
Preoperative risk factors
|
Intraoperative and postoperative risk factors
|
|
1.
|
Stevens et al[1] 1997
|
3,450
|
Posterior optic nerve ischemia, occipital lobe infarcts, central retinal vein thrombosis
|
Paroxysmal atrial fibrillation, hypertension
|
Air embolism, deep venous thrombosis
|
|
2.
|
Myers et al[2]
1997
|
37
|
Ischemic optic neuropathy, retinal artery occlusion, cerebral ischemia
|
Hypertension, diabetes mellitus, smoking, vascular disorders leading to increased
viscosity
|
Hypotension, anemia
|
|
3.
|
Kamming and Clarke[3] 2005
|
1
|
Ischemic optic neuropathy
|
Medullary carcinoma of thyroid
|
Pressure over the eyeball due to headrest, hypotension, anemia
|
|
4.
|
Warner[4] 2006
|
–
|
Ischemic optic neuropathy, central retinal artery occlusion
|
Hypertension, diabetes mellitus, smoking, polycythemia, renal failure, narrow-angle
glaucoma and atherosclerosis
|
Hypotension, anemia
|
|
5.
|
Hunt et al[5] 2004
|
20
|
–
|
–
|
Prone position leads to increase in intraocular pressure
|
|
6.
|
Abraham et al[6] 2003
|
1
|
Ischemic optic neuropathy
|
–
|
Malposition horseshoe headrest, prone position
|
|
7.
|
Ozcan et al[7] 2004
|
10
|
–
|
–
|
Ten degrees of reverse Trendelenburg position also helped decrease the pressure to
normal in the prone position
|
|
8.
|
Hoski et al[8] 1993
|
1
|
Central retinal artery occlusion
|
–
|
Prone position
|
|
9.
|
Merle et al[9] 1994
|
1
|
Central retinal artery occlusion
|
–
|
Prone position
|
|
10.
|
Hayreh[10] 1974
|
25
|
Anterior ischemic optic neuropathy
|
–
|
–
|
-
Preoperative—Hypertension, diabetes mellitus, smoking, polycythemia, renal failure,
narrow-angle glaucoma, and atherosclerosis.
-
Intraoperative—Hypotension and anemia.[6]
-
Postoperative factor—Raised intraocular pressure.
The reasons of ‘raised intra ocular pressure’ include:
-
Due to increased pressure over globe: Inappropriate pressure from padding while lying
on the horseshoe headrest leads to extrinsic pressure over the eyeball, causing raised
intraocular pressure.
-
Raised central venous pressure: Decreased venous return due to low position of the
head, obstruction to venous outflow if head is turned to one side, pressure over the
abdomen along with absence of valves result in central venous pressure changes causing
associated changes in ocular venous pressure.
-
Prone position: Intraocular pressure increases in prone position.[5] Ten degrees of reverse Trendelenburg position also helped decrease the pressure
to normal in prone position.[7]
-
Intraoperative change in the patient's position: Operating team, including an anesthetist,
preoperatively confirmed the position of the head and eye. Change in this position
during surgery could have led to external pressure over the eyeball.
The blindness mechanism is retinal ischemia due to increased intraocular pressure
caused by venous congestion or arterial occlusion. Venous collapse leads to decreased
blood flow when venous pressure is exceeded by intraocular pressure.[8] Dual arterial supply is present in retina—inner layer supplied by central retinal
artery. Retina's outer layer gets its supply due to diffusion from the choroidal plexus.
Hence, in the event of any obstruction to central retina, blindness may result. Arterial
or venous occlusion changes the blood circulation in retina and produces hypoxia in
the affected area. In case of arterial occlusion, severe hypoxia rapidly (in less
than 45 minutes) produces irreversible cell damage in inner layers of the retina.[9] Time duration that the human retina can resist is not precise. Retina of rhesus
monkeys can remain unaffected by ischemia for 95 minutes. Anaerobic glycolysis starts
in vitreous humor after 20 minutes of ischemia. The glucose stored in vitreous humor
is the only source of nutrition to the retina between 40 and 70 minutes of ischemia.
This reserve is the sole determining factor of the time duration of retinal ischemia,
which can be safely tolerated.[10]
We believe that the head position of our patient might have changed during surgery,
leading to the patient's face being trapped inside the horseshoe headrest, resulting
in extrinsic compression over the right eyeball, which developed orbital swelling
and blindness.
Conclusion
Postoperative vision loss after spinal surgery in prone positioning is a rare and
irreversible complication. Proper positioning of the head should be done so that ocular
compression does not happen. Any change in the patient's position intraoperatively
and intraoperative hypotension resulting from excessive blood loss should be avoided.
