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Complete cortical blindness is defined as bilateral visual loss, absence of optokinetic nystagmus and the lid reflex response to threat, a normal pupillary response and eye motility, and a normal retina and ON. Patients often fail to recognize the blindness themselves, a condition known as Anton's syndrome. [216] Each visual cortex receives input from the contralateral visual field and connects to nearby areas in the occipital and parietotemporal cortex for more advanced visual functions such as analysis of movement, color vision, and three-dimensional form. The primary visual cortex processes retinal information to give a sense of orientation and binocular vision for depth perception. The presence of complete blindness implies damage to both the left and right occipital cortex, whereas a more localized injury produces homonymous hemianopia.
Total blindness from bilateral occipital infarction is rare. Because the visual pathway travels through the parietotemporal lobes, a perioperative cerebrovascular accident affecting the internal carotid, middle cerebral, or basilar or posterior cerebral arteries is the more common scenario that produces cortical blindness. Yet because of collateral circulation, the degree of visual damage is difficult to predict.[7] About 80% of cases of cortical blindness reported postoperatively have followed cardiac or other thoracic surgery. Depending on the sensitivity of the neuropsychological testing profile used, these patients may frequently show evidence of postoperative neurologic sequelae. [217]
Initially, total cortical blindness is usually accompanied by signs of stroke in the parieto-occipital region. The patient may suffer agnosia, an inability to interpret sensory stimuli. Often, vision improves over time, with incomplete lesions left in the visual field combined with visual disorientation. Typical findings are preserved pupillary reflexes and restoration of most of the visual field within days, but impairment in spatial perception and the sense of relationship between sizes and distances may remain. Visual attention may be restricted, and it may not be possible to visualize images formed on all parts of retina at one time.
The incidence of cortical blindness after cardiac surgery was 10 in 808 CABG surgeries in one hospital, with brain scans in five patients showing occipital infarcts (also see Chapter 50 ).[18] In a retrospective series of 700 CABG surgeries and valve replacements by a single surgeon, two patients had unilateral occipital cortical infarcts.[84] Shaw and colleagues [218] prospectively studied 312 patients undergoing CABG surgery and found a 5% incidence of cortical blindness. At least 50% of the patients had associated neurologic deficits. In another study, the onset of visual deficits was shown to follow a time course similar to that of neurologic damage. [219] Among the largest and most recent studies of neurologic dysfunction after cardiac surgery is that of Roach and coworkers.[220] A total of 2108 CABG patients from 24 different hospitals were studied prospectively, with a 6% incidence of neurologic complications. Risk factors included aortic atherosclerosis, old age, previous neurologic dysfunction, hypertension, pulmonary disease, and alcohol consumption. Unfortunately, the incidence of visual disorders was not reported.
Angiography is frequently performed in the preoperative period in patients scheduled to undergo cardiac and vascular surgical operations. Transient (and in one case permanent[54] ) cortical blindness has been reported after intra-arterial injection of iodinated contrast material. An incidence of cortical blindness of 1 in 12,367 coronary angiographies[221] and 10 in 619 patients after vertebral angiography has been reported.[222] Cortical blindness has been seen after angiography of the coronary[223] [224] [225] [226] and cerebral arteries.[227] [228] Vasospasm, emboli, or damage to the blood-brain barrier as a result of lipid solubility or the high osmolality of the contrast material is thought to be responsible.[228] [229]
In case reports of cortical blindness, 55% of cases were reported after CABG surgery and 23% after other thoracovascular operations.[50] Cases have been reported in children. Hypotension was found in 45% of patients, and in 23%, anemia/hemodilution was present. Over half the patients had coronary artery disease, but cortical blindness was found in patients with a wide range of systemic disorders, including congenital heart disease, liver failure, postpartum pulmonary embolism, and hypercholesterolemia. Unfortunately, the time of onset of symptoms was not reported in about half the cases, but for the remaining 50%, onset was within the first postoperative day. As would be expected, funduscopy was normal in virtually all patients when reported, except one, in whom AION was combined with cortical blindness. Visual defects were bilateral in all but one patient, who presented with a lesion near the LGN. The incidence of other objective neurologic findings was relatively high (38%). Confusion was present in 25%. Visual outcome improved in 65% of cases.
Many different etiologies decrease O2 delivery to the visual pathway between the ON and the occipital cortex. Among such etiologies are global ischemia, cardiac arrest, hypoxemia, intracranial hypertension and exsanguinating
CABG surgery is the most common operation associated with cortical blindness, but the pathophysiology of cortical blindness after CABG surgery remains incompletely understood. The major source of brain and visual damage is believed to be embolism from the surgical field, such as fat and atheroma or microemboli of lipid and fibrin-platelet aggregates.[54] [116] [231] A high incidence of emboli in the retinal circulation in patients undergoing CABG surgery has been documented.[204] Patients with aortic atherosclerosis appear to be at particular risk.[220] Cerebral edema could also be responsible for cortical blindness,[232] [233] but a study of early MRI of the brain after CABG surgery showed cortical swelling within 20 to 40 minutes that was not found on follow-up 1 to 3 weeks later, thus leading to a question about its pathogenic role.[234] This edema may somehow contribute to the vague visual disturbances found in up to 25% of CABG patients.[235] In addition to emboli, transient decreases in blood flow to border zones of perfusion between the middle and posterior cerebral arteries, especially in patients with preexistent cerebrovascular disease, are another suspected factor.[20]
Visual recovery from cortical blindness may be prolonged, but previously healthy patients are likely to show a considerable degree of recovery. Therefore, when accompanied by focal neurologic signs, treatment should be directed toward preventing progression of stroke.
The optimal strategy to prevent neurologic injury during cardiac surgery remains controversial. Because of heightened awareness of the risk of embolism from an atherosclerotic aorta,[236] [237] several different techniques have been advocated to decrease intraoperative manipulation of the aorta.[87] [158] [238] Adequate removal of air and particulate matter from the heart during valvular operations may decrease the risk of embolism. In patients younger than 70 years without evidence of cerebrovascular disease, the use of an arterial line filter during cardiopulmonary bypass significantly reduces the number of microemboli detectable by transcranial Doppler ultrasonography. The frequency of subtle neuropsychological and neurologic changes (including nystagmus) was also reduced. No visual defects were found in the study patients.[239] Maintenance of adequate systemic perfusion pressure may prevent episodes of hypoperfusion in patients with cerebrovascular disease, but no controlled studies have associated visual loss and perfusion pressure in open heart surgery. Better development of transcranial Doppler techniques may enable enhanced detection of embolic events. As yet, no proven neuroprotective agents whose use is feasible in these patients are available.[240] Non-bypass heart surgery would be expected to avoid, but not eliminate many embolic complications.[241] [242] To date, no case reports have described visual loss in these patients.
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