311Page 2retinal ischemia, ischemic optic neuropathy, cortical blindness, and acute angle closure glaucoma. Retinal ischemiacan be central or branch retinal artery occlusion (CRAO or BRAO), and ischemic optic neuropathy is anterior or posterior (AION or PION). Even more uncommon would be acute angle closure glaucoma. Of these, it now appearsthat the most common lesion that results in visual loss after spine surgery is PION.
[2,3]
The discussion below willconcern CRAO and ION. The reader is referred elsewhere for review of other causes of visual loss.
[3]
Specific Mechanisms of Visual Loss
1. Retinal vascular occlusion results in retinal ischemia due to decreased O2 delivery to the retina.
[19]
In most cases,the lesion is unilateral. Cases have been reported after spine surgery, and animal models have directly evaluated themechanisms of injury.
[20-22]
A
.
Mechanisms of injury
: The most common cause of retinal ischemia with spine surgery is compression of the eyethat produces high enough intraocular pressures to stop blood flow in the central retinal artery. In older case reports,compression of the eye was attributed to pressure on the eye exerted by a horseshoe headrest with the patient prone.
[23]
However, there are cases in patients positioned prone on other headrests, where external pressure wasinadvertently exerted on the eye.
[24]
The mechanism of injury is due either to slipping of the head off the headrest, or contact of the eye with some other object, such as goggles placed over the patient’s eyes. Among the spine patientsin the POVL Registry with CRAO, none of them were positioned in a pin-head holder, in contrast to patients whodeveloped ION (see below). All of the retinal artery occlusions in the POVL Registry were unilateral injuries.
[2]
Emboli can occur during lumbar spine surgery,
[25]
but a right-to-left cardiac shunt must be present to produce a paradoxical embolus to the central retinal artery or to a branch retinal artery (BRAO); the latter produces a lesser degree of visual loss
vs
CRAO. There is one published report of paradoxical emboli causing retinal ischemia withBRAO in a 12-year old child who underwent scoliosis repair. The child complained of visual difficulty 4 d postoperatively, at which time she had inferiorly located peripapillary cotton wool spots and loss of visual fields inthe superonasal quadrant in the right eye. There were no signs of external compression. A right-to-left shunt throughan ASD was found by contrast echocardiography.
[26]
B. Clinical presentation
: Patients typically present with a unilateral injury, with no light perception or severe visualfield defects, abnormal pupillary light response, extraocular muscle dysfunction, chemosis, proptosis, and cornealdamage may also be present. Symptoms are usually present within 24 h of the procedure, and often uponawakening.
[3]
The fundus examination shows retinal whitening or edema, and a cherry-red spot. Retinal vessels maydemonstrate sluggish flow, or “boxcar” formation. Weeks or months later there is optic atrophy. MRI of the orbitmay early on show muscle enlargement or edema from compression of the eye.
[27]
The electroretinogram isabnormal. Angiography findings can include filling defects, absent flow, marked stasis, delayed retinal transit timeor retinal hyperpigmentation.
[28]
If the mechanism of visual loss is embolic, it may be possible to see emboli in theretinal vessels upon fundus examination.
C. Pathophysiology
: Numerous studies in several species of animals, including monkeys, cats, and rats havedemonstrated the effects of increased intraocular pressure (IOP) to produce retinal ischemia.
[20]
Similarly, weshowed in cats that increased IOP sufficient to extinguish the b wave activity of the electroretinogram (inner retinaelectrical activity in response to a bright white flash) decreased retinal blood flow to 6% of baseline, and choroidal blood flow to 0.6%.
[29]
Hayreh showed in monkeys a retinal survival time of about 90 min after ligation of thecentral retinal artery, and later reported that surprisingly, survival time was actually longer in atheroscleroticmonkeys.
[21,30]
However, increased IOP is a more severe insult than ligation of the central retinal artery because of the profound simultaneous decreases in both retinal and choroidal blood flow with increased IOP
[29]
and thedifferential susceptibility of some retinal cells to damage from increased pressure.
[31,32]
After retinal ischemia, theretinal circulation is hypoperfused; reperfusion injury may occur and further complicate the injury.
[33]
Several studies have measured IOP with human subjects in the prone position, either in normal volunteers,or in those undergoing spine surgery. These studies generally show increased IOP in the prone position, further increases with the head-down position, and attenuation of the increases by head-up positioning, although there aredifferences in the extent of the changes.
[34-36]
The clinical significance of the changes remains unknown.While hypotension can decrease retinal perfusion, there is efficient autoregulation in the retinal andchoroidal circulations to compensate for decreased blood pressure. Retinal ischemia can also occur due toatherosclerotic disease.
[37]
However, this mechanism would not appear to occur acutely in the perioperative period.Hypotension alone seems to be rarely the cause of retinal vascular occlusion, probably because of efficientautoregulation in the retina, and because of the dual circulation of the retina, where the choroidal circulation is ableto provide O2 delivery via diffusion from the outer retina.
[38]
2. Ischemic Optic Neuropathy (ION) Our understanding of ION after spine surgery is impeded by the lack of controlled studies, the absence of an animal model, and because the pathology of ION has not been well
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