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Postoperative Ischemic Optic Neuropathy

Williams, E. Lynne MB, BS, FRCA; Hart, William M. Jr., MD, PhD; Tempelhoff, Rene MD

Review Article

Department of Anesthesiology, St. Louis University School of Medicine, St. Louis, Missouri (Williams), and Departments of Ophthalmology and Visual Science (Hart), and Anesthesiology, Washington University School of Medicine, St. Louis, Missouri (Tempelhoff).

Accepted for publication November 23, 1994.

Address correspondence and reprint requests to Rene Tempelhoff, MD, Washington University School of Medicine, Department of Anesthesiology, Box 8054, 660 S. Euclid Ave., St. Louis, MO 63110.

Although uncommon, alteration in vision or blindness after anesthesia, particularly after open heart surgery, is well documented in the nonanesthesiology literature [1-17]Table 1. In some series, the incidence of postoperative visual loss varies between 0.1% and 1% [1,10,14]. Recent retrospective reviews demonstrate one case in 56,000 surgical procedures at one university hospital [18] and six cases over a 10-yr period at another [3]. The recent rate of reporting may be low due to anesthesiologists' concerns regarding litigation, and ophthalmologists' opinion that the occurrence of visual defect after general anesthesia is well established and unremarkable.

Table 1

Table 1

Anesthesia texts limit their discussion of postoperative visual loss to pressure-related eye injuries associated with positioning [19,20]. However, in recent years, the most commonly reported cause of postoperative visual loss is, in fact, ischemic optic neuropathy. Apart from two case reports [3,17], this devastating complication has not been addressed in the anesthesiology literature. Since the anesthesiologist must maintain the patients' safety during surgery, a better understanding of ischemic optic neuropathy is warranted.

This paper focuses on the neurovascular-ophthalmologic mechanisms responsible for postoperative loss of vision. We will review neurovascular-ophthalmic anatomy and the etiology of postoperative ischemic optic neuropathy. Although the visual prognosis of ischemic optic neuropathy is usually grim, we will discuss possible treatment modalities and preventative measures, which in some cases are straightforward, such as ensuring physical protection of the orbit. Others involve more controversial issues, specifically the safe level of hematocrit and arterial blood pressure for the maintenance of perfusion to the visual apparatus [3].

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Anatomy

Blood Supply to the Optic Nerve

The optic nerve Figure 1 may be divided into four parts: anterior (or intraocular), posterior (or intraorbital), intracanalicular, and intracranial. Each part has a unique blood supply which may account for differences in the means by which ischemic damage occurs.

Figure 1

Figure 1

The anterior portion of the optic nerve, which includes the optic disk and the portion of the optic nerve within the scleral canal Figure 1 and Figure 2, is supplied mainly by the short posterior ciliary arteries via the choriocapillaris around the optic disk or via branches to form an anastomotic microvascular ring around the optic nerve [21]. There may also be a double arterial supply from pial branches of the ophthalmic artery [21-23], but the central retinal artery does not furnish branches to the optic nerve in this region.

Figure 2

Figure 2

The posterior portion Figure 3 of the optic nerve has a peripheral vascular supply from pial vessels derived from neighboring branches of the ophthalmic artery. The central retinal artery often supplies branches to the central fibers but the blood flow in the posterior optic nerve is significantly less than that in the anterior portion [24].

Figure 3

Figure 3

The intracanalicular and intracranial portions of the optic nerve Figure 1 and Figure 3 are supplied by the pial network from branches of the internal carotid and anterior cerebral arteries whereas the optic chiasm is supplied by the internal carotid or anterior cerebral artery [25]. The retrogeniculate optic radiation and occipital cortex Figure 1 are supplied by the posterior and middle cerebral arteries [8].

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Blood Supply to the Retina

There are two sources of blood supply to the retina: terminal branches of the central retinal artery to the inner layers and the choriocapillaris to the outer layers Figure 2. However, both circulations must be intact to maintain retinal activity [26,27].

The central retinal artery enters the optic nerve Figure 3 and divides at the optic disk to form arteriolar branches which form capillary networks in two inner retinal layers except over the fovea which is supplied solely by the choriocapillaris Figure 4. The choriocapillaris is the inner capillary layer of the choroid. Its lobular structure has a feeding arteriole in the center and draining venules at the periphery with each short posterior ciliary artery supplying a distinct area [28] as an end-artery [29], and little cross-circulation between adjacent areas, so that watershed zones may form at their boundaries where blood supply can be tenuous. The watershed zones between short posterior ciliary arteries, which may be situated anywhere between the fovea and the nasal border of the optic disk, play an important role in determining the site and extent of optic nerve head ischemia. The short posterior ciliary arteries and central retinal artery are end-arteries but proximal to these branches; the ophthalmic artery has anastomotic connections with branches of the external carotid arteries [30] although these may be insufficient to protect the optic nerve from ischemia [31]. Although there is both alpha-adrenergic and cholinergic innervation of the choroid, the role of autonomic nerves in control of blood flow is uncertain [27].

Figure 4

Figure 4

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Posterior Scleral Foramen

The optic disk overlies the posterior scleral foramen which is bridged by the lamina cribrosa, a perforated, sieve-like structure composed of collagen and elastic fibers, through which the optic nerve and central retinal vein and artery pass [26]Figure 2. Small posterior foramina, which may constrict the structures passing through them, can be identified ophthalmoscopically as flattening of the normal cup shape of optic disks [32,33].

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Postoperative Loss of Vision

Lesions resulting from an ischemic event in the visual pathway and causing postoperative visual loss are associated with various causes of decreased oxygen delivery Table 2 and can be classified by the main locus of injury Figure 3. Visual losses due to ischemic insult of the optic nerve are separated into anterior ischemic optic neuropathy and posterior ischemic optic neuropathy because these parts of the optic nerve have different blood supplies, different predisposing factors for infarction, and variably different clinical pictures [6,34]. Visual loss associated with the optic radiation and occipital cortex is considered cortical blindness. Rarer etiologies of postoperative visual loss, such as central retinal artery occlusion and obstruction of venous drainage from the eye, will also be discussed.

Table 2

Table 2

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Anterior Ischemic Optic Neuropathy

In the elderly nonsurgical population, anterior ischemic optic neuropathy and optic neuritis are equally prevalent disorders of the optic nerve second only to glaucoma [35]. The visual loss of anterior ischemic optic neuropathy is caused by infarction at watershed zones between the areas of distribution of the small branches of the short posterior ciliary arteries in the choriocapillaris [24,36]Figure 2. Individual variation in blood supply to the optic nerve can affect the pattern and severity of visual loss of anterior ischemic optic neuropathy.

When considering the effects of ischemia on the optic nerve, it should be stressed that damage does not follow an "all or none" law: differing degrees of ischemia produce differing effects [37,38]. Mild ischemia in the anterior optic nerve produces stasis of axoplasmic flow without alteration in visual impulse transmission. Local accumulation of axoplasm, at the site of damage where active axoplasmic transport is interrupted, causes the axons to swell [39]. Asymptomatic optic disk swelling may be the earliest sign of anterior ischemic optic neuropathy [11,37] and may resolve spontaneously without developing into overt ischemic infarction in some juvenile diabetics [40]. Moderate ischemia interferes with both axoplasmic flow and visual impulse transmission resulting in visual loss which is initially reversible, while severe ischemia results in immediate irreversible damage.

Although there is considerable variability, the most common visual field defect in anterior ischemic optic neuropathy is loss of function in the lower hemifield (altitudinal hemianopia) with sparing of the central vision [36,41,42]. This pattern is reflected in the ischemic damage found in postmortem studies of optic nerves. Histologic cross-sections demonstrate complete loss of fibers in the superior half of the nerve, partial peripheral loss in the lower half, while the densely packed, small diameter axons, arising from the center of the visual field are often spared [36].

Anterior ischemic optic neuropathy is classified, depending on its etiology, into two groups: "nonarteritic," the main culprit in the postoperative period, and "arteritic," which is rarer and inflammatory in origin.

Nonarteritic. This is the most common form of anterior ischemic optic neuropathy and is usually the result of transient decrease in oxygen delivery in the choroid surrounding the optic disk [43]. The proposed etiology is multifactorial: decreased perfusion pressure, increased resistance to blood flow, and decreased oxygen-carrying capacity can each result in decreased oxygen delivery.

Perfusion pressure to the optic nerve head is the difference between arterial pressure and venous pressure or intraocular pressure if that exceeds venous pressure. To maintain the perfusion pressure above a critical level to prevent ischemia, both systemic and local factors are involved.

Anterior ischemic optic neuropathy has been reported after various causes of systemic hypotension including cardiac arrest [44], hemodialysis [45], and even sleep in susceptible patients [37]. It has been reported bilaterally after intraoperative hypotension [3] and after acute severe hemorrhage, usually involving the gastrointestinal tract [11,40,46,47].

It would seem that intraoperative hypotension is only rarely associated with anterior ischemic optic neuropathy as indicated by the American Society of Anesthesiologists' Closed Claims Project which, out of a database of 3000 claims, has only one alleged anterior ischemic optic neuropathy (personal communication, F. W. Cheney, MD, 1994). A combined epidural/general anesthetic technique was used for radical prostatectomy, during which the lowest blood pressure during surgery was 70/40 associated with an episode of acute hemorrhage. However, in other reports of higher incidence of anterior ischemic optic neuropathy after cardiac surgery, hypotension was considered contributory [1,10,14].

Small areas of anterior optic nerve infarction after episodes of hypotension may be unnoticed because the associated visual defects were insignificant. These patients may present at a later date with low-pressure glaucoma and multiple areas of optic atrophy [48,49].

Severe occlusive carotid artery disease, with resulting decreased distal perfusion pressure in the ophthalmic artery and posterior ciliary arteries, occasionally has been associated with anterior ischemic optic neuropathy despite flow from collateral circulation [28].

Increased venous pressure is cited as a contributory factor in postoperative anterior ischemic optic neuropathy after head and neck surgery [15] due to local obstruction of venous outflow. Changes in central venous pressure with changes in body position result in decreased perfusion pressure as well as increased choroidal blood volume resulting in increased intraocular pressure (see below).

Vascular resistance to flow in the short posterior ciliary arteries may be increased due to arterial disease. Anterior ischemic optic neuropathy is more common in smokers [50] and has been reported in patients with atherosclerosis [29,51] and hypertensive vascular disease [42,52,53], diabetic vascular disease [2,47,54-56], migraine [57], Buerger's disease [58], and vasculitides from periarteritis nodosa, and rheumatoid arthritis [59].

The role of vasoconstricting drugs is controversial. In several case reports, endogenous vasoconstrictors, such as sympathetic amines and angiotensin, have been implicated in the development of anterior ischemic optic neuropathy after hemorrhagic shock [1,4,40]. Permanent visual loss has been reported after intranasal epinephrine injection which, presumably, was intraarterial and resulted in vasospasm of the ophthalmic and short posterior ciliary arteries [16]. However, visual loss from anterior ischemic optic neuropathy has been reversed by infusion of norepinephrine to increase perfusion pressure with moderate hypertension [60].

Although some investigators have conflicting observations [61], others [11,27,62] note that anterior ischemic optic neuropathy occurs with increased intraocular pressure, which causes a corresponding decrease in choroidal blood flow [63] rendering the anterior optic nerve vulnerable to ischemia. Intraocular pressure is very high immediately on awakening from sleep [64], a factor which may contribute to the high incidence of anterior ischemic optic neuropathy observed at that time [59]. Also, intraocular pressure changes are directly related to changes in choroidal blood volume, which is directly related to variations in both central venous pressure [65] and carbon dioxide tension [66-68]. Eyes with anterior ischemic optic neuropathy show greater increases in intraocular pressure with changes in position which may represent a critical decrease of perfusion pressure at the optic nerve head [69]. Hyperventilation with 15 degrees head-up tilt has been recommended to minimize intraocular pressure for procedures in the optic globe [66] and may be beneficial for the maintenance of optimal blood flow to the optic nerve head during other surgical procedures, providing there is adequate mean arterial pressure [65].

Anterior ischemic optic neuropathy can occur with both high- and low-pressure glaucoma [11,48,49], after ocular pneumoplethysmography [70], and after cataract extraction in patients with increased intraocular pressure [71]. A case report of intraoperative external ocular compression due to tight occlusive plastic eye protectors which resulted in postoperative anterior ischemic optic neuropathy presumably was associated with raised intraocular pressure [72].

During cardiac surgery, when cardiopulmonary bypass is initiated with crystalloid priming solution [73], there is an increase in intraocular pressure which may contribute to the occasional development of postoperative anterior ischemic optic neuropathy [74,75]. However, these intraocular pressure findings during cardiopulmonary bypass are controversial since some studies do not show an increase in intraocular pressure with cardiopulmonary bypass [76,77].

Anterior ischemic optic neuropathy occurs more often in congenitally small optic disks [78,79]. The small cross-sectional area of the posterior scleral foramen has little space for expansion of nerve fibers in response to hypoxia of the optic nerve [21,22,80]. A vicious cycle may occur with increased pressure from swollen fibers locally compressing the blood supply, worsening ischemia, and increasing the swelling of the nerve fibers.

Increased viscosity can reduce blood flow. Anterior ischemic optic neuropathy has been reported in patients with increased blood viscosity attributable to abnormal red blood cells, such as sickle cell disease [81], or polycythemia [11]. Anterior ischemic optic neuropathy after cardiopulmonary bypass has been attributed, in part, to hypothermia, by increasing the viscosity of plasma [1]. This is controversial since studies of plasma viscosity [82] have shown that increases in plasma viscosity do not alter tissue flow or oxygenation.

Postmortem studies demonstrate that anterior ischemic optic neuropathy is not usually caused by emboli [29]. It does not occur more in patients with carotid disease [83,84] since emboli preferentially lodge in the central retinal artery rather than the short posterior ciliary arteries. However, occasional reports of anterior ischemic optic neuropathy have been associated with emboli from a septic focus [85], metastatic chondrosarcoma [86], multiple cholesterol fragments either from carotid disease [12,29,51,62,87], after crossclamping of the aorta [2,13], or in association with cardiac catheterization [12,62]. Also, anterior ischemic optic neuropathy has been reported simultaneously with retinal artery emboli [13,17,29,83] and with microemboli after coronary artery bypass surgery [2].

Anterior ischemic optic neuropathy has been associated with anemia due to iron-deficiency [88] or hemorrhage with or without hypotension [1,5,46,89]. Experimental isovolemic hemodilution to a hematocrit of 20%-22% in cats resulted in an increase in retinal blood flow but a decrease in choroidal blood flow [90]. This may imply a decrease in oxygen delivery to the outer layers of the retina and the anterior optic nerve, rendering those areas more vulnerable to ischemia [90].

Patients who develop anterior ischemic neuropathy are most commonly over 50 yr old, the age group with a high incidence of conditions affecting the peripheral vasculature, such as diabetes, hypertension, or atherosclerosis [53,91,92]. However, anterior ischemic optic neuropathy also presents rarely in young adults [93].

The usual presentation of anterior ischemic optic neuropathy is sudden, painless monocular visual deficit, varying in severity from a slight decrease in visual acuity to no light perception [43]. However, it can occur in small stages, eventually presenting an appearance that mimics glaucoma [48,49]. When associated with acute hemorrhage, the symptoms may appear immediately or be delayed for up to several weeks [40]. There is also a progressive form of anterior ischemic optic neuropathy, characterized by continuing deterioration of visual function over several weeks [41,56,94].

The deficit is often discovered on waking in the morning [59] and the patient may be only vaguely aware of the visual defect [41]. Most commonly, there is loss of the inferior visual field. Other defects may present, but they rarely include central visual loss [95]. In moderate to severe cases, a relative afferent pupillary defect is present [95].

Ophthalmoscopic examination initially shows optic disk edema, which may include all or part of the disk and frequently is accompanied by splinter hemorrhages at the disk margin [96]. The degree of visual loss may not correspond to the severity of disk edema. Fluorescein angiography during the initial phase shows filling defects in the disk, the surrounding choroid, and choroidal watershed zones [87]. Electroretinography is normal, but the amplitude of visual evoked potentials is decreased in patients with anterior ischemic optic neuropathy, confirming moderate ischemic damage to the retina and to the axons of the optic pathway [97] in both eyes. The disk edema usually resolves in approximately 2 mo and is replaced by optic atrophy [96].

Prognosis varies: the most common outcome is little recovery of visual function [40,59], despite the return of normal choroidal circulation demonstrated by fluorescein angiography after 2-3 wk [96]. However, there have been case reports of partial, spontaneous remission of the visual field defect after a few weeks [11,98] and improvement of visual acuity in up to 30% of patients [41,93,99], despite persistent disk pallor [100]. In the progressive type of anterior ischemic optic neuropathy, there is no further loss of vision, after approximately 6 wk, possibly because constrictive pressure in the lamina cribrosa is relieved, as swollen optic nerve axons atrophy [56,94].

Anterior ischemic optic neuropathy usually starts unilaterally, but after a variable time, the other eye usually becomes affected [41,42,51,54,56,59,95]. Ischemic changes in visual evoked potentials and electroretinography can be found bilaterally in all patients with anterior ischemic optic neuropathy even if the visual defect is unilateral, suggesting a degree of subclinical damage in the asymptomatic, contralateral eye. Also, the contralateral eye often demonstrates an optic disk with less than normal cupping and evidence of crowding of the optic nerve fibers in the scleral foramen [21,80]. Postoperative anterior ischemic optic neuropathy associated with hemorrhagic hypotension usually presents bilaterally with a fixed visual deficit [40].

Many types of therapy have been tried, including retrobulbar steroid injections [101], antiplatelet therapy [102], anticoagulants [51], phenytoin [102], norepinephrine infusion [60] and adequate blood replacement [103], but none have been consistently successful [43]. Carbonic anhydrase inhibitors to decrease intraocular pressure and steroids to decrease axonal swelling have been administered within 48 h of the onset of visual loss to improve anterior optic nerve circulation, and have met with variable success [11,41]. A recent small series demonstrated that mild hemodilution has been associated with improvement of central vision [104].

Surgical optic nerve sheath fenestration is a new therapy for nonarteritic anterior ischemic optic neuropathy, currently undergoing a multicenter, prospective, randomized clinical trial [102,105]. It increases blood flow velocity in the central retinal artery and decreases vascular resistance in the posterior ciliary arteries [106]. Some reports have been favorable in patients with progressive [106-108] and nonprogressive anterior ischemic optic neuropathy [102,109,110], while others have been less favorable [111-114] and point out that the spontaneous remission rate is approximately the same as the success rate of the optic nerve sheath decompression [100]. Occasionally, the contralateral eye's vision may improve if it has been previously affected by anterior ischemic optic neuropathy [109]. However, anterior ischemic optic neuropathy has been reported in the previously unaffected contralateral eye 1 to 2 mo after the procedure [102], and possibly associated with scarring at the sites of incision. The incidence of vascular and neural complications is 2% [115] and there is occasional aggravation of visual loss [116].

Arteritic. Arteritic anterior ischemic optic neuropathy is less common than the nonarteritic type [43]. It typically presents in patients older than 60 yr with severe loss of vision and complaints of aches, myalgias, malaise, headache, scalp tenderness, and other vague systemic symptoms. There is inflammation of the blood vessels and the diagnosis is made by temporal artery biopsy demonstrating giant cell arteritis. Unlike nonarteritic anterior ischemic optic neuropathy, the primary lesion of the short posterior ciliary arteries is occlusion due to thrombosis. Ophthalmoscopic examination reveals extreme disk pallor with greater retinal pathology than in the nonarteritic form and fluorescein angiography demonstrates extensive filling defects [43]. Although rare, coincidental arteritic anterior ischemic optic neuropathy has been reported in the postoperative period [117]. It is important to diagnose arteritic anterior ischemic optic neuropathy since, if untreated, it progresses very rapidly to bilateral blindness. The therapy for arteritic anterior ischemic optic neuropathy is steroids at high dosage to protect the contralateral eye and to arrest progression of the disease. Although the treatment is usually effective, most patients require steroids indefinitely [59,101].

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Posterior Ischemic Optic Neuropathy

Posterior ischemic optic neuropathy presents as acute loss of vision and visual field defects similar to anterior ischemic optic neuropathy. It is thought to be caused by decreased oxygen delivery to the posterior portion of the optic nerve Figure 1 between the optic foramen at the orbital apex and the central retinal artery's point of entry where the optic nerve is most vulnerable to ischemia. This section is farthest from an arterial supply, being nourished only by centripetal pial vessels [32,33] which can be compressed readily. In comparison, the anterior, intracanalicular and the intracranial portions of the optic nerve have a more luxuriant blood supply.

Posterior ischemic optic neuropathy occurs spontaneously less frequently than anterior ischemic optic neuropathy [41], whereas the former is reported with a greater frequency in postoperative patients associated with hemorrhagic hypotension [3,6,15,118,119], and in anemic patients after severe hypotension [118-120]. Posterior ischemic optic neuropathy is not associated with occlusive vascular disease as often as anterior ischemic optic neuropathy, possibly because the pia exerts less occlusive pressure to the vessels passing through it than the more rigid lamina cribrosa. On the other hand, when the vasculature is normal, the greater blood supply to the anterior optic nerve [32] may protect it from the combination of anemia and hypotension better than the posterior portion.

The posterior optic nerve has relatively less constriction than the anterior portion, so that a hypoxic insult results in a slower development of ischemic damage, and a symptom-free period often precedes the loss of vision [118]. There are often no abnormal ophthalmoscopic findings initially, reflecting the retrobulbar involvement of the optic nerve, but mild disk edema occurs a few days later. Computed tomography scan of the orbit can show enlargement of the intraorbital optic nerve [118].

Postoperative posterior ischemic optic neuropathy has been reported after diverse procedures such as laparotomy, open heart surgery, radical neck dissection, and hip arthroplasty [15,118,119,121-125]. The etiology is not well understood but appears to be multifactorial: severe hypotension and anemia are combined with at least one other factor (e.g., congenital absence of the central retinal artery, infection, or venous obstruction).

Nonsurgical scenarios in which posterior ischemic optic neuropathy has occurred include cardiac arrest associated with toxic megacolon [126], aggressive therapy for malignant hypertension [127], severe anemia due to massive gastrointestinal hemorrhage [6,128,129], and blunt trauma to the eye [130].

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Differential Diagnosis

There are vascular etiologies of postoperative loss of vision other than ischemic optic neuropathy Table 3. Cortical blindness, retinal artery occlusion, and ophthalmic venous obstruction therefore should be excluded.

Table 3

Table 3

Cortical Blindness. Cortical blindness may follow emboli or sustained, profound hypotension, such as cardiac arrest, resulting in infarction of watershed areas in parietal or occipital lobes. It has been reported after coronary artery bypass surgery [8-10,131], craniotomies, and laryngectomy [132]. Occipital infarctions may also result from air or particulate emboli during cardiopulmonary bypass [13]. Cortical blindness is characterized by loss of visual sensation with retention of pupillary reaction to light [132] and normal funduscopic examination. The patient may not be conscious of the loss of vision, which improves in most cases but may leave residual hallucinations. Computed tomography scan or magnetic resonance imaging abnormalities in the parietal or occipital lobes confirm the diagnosis.

Retinal Artery Occlusion. Most retinal occlusions due to emboli during open heart surgery resolve within 30 min of the discontinuation of cardiopulmonary bypass, but rarely some persist and present as postoperative visual loss [133]. Central retinal artery occlusion presents as painless monocular blindness, and occlusion of a branch of the artery results in a limited field defect or blurred vision. The visual deficit of retinal artery obstruction is often severe initially but it improves, unlike ischemic optic neuropathy which usually has a moderate but permanent deficit. Ophthalmoscopic examination of eyes with retinal artery occlusion reveals a pale edematous retina, cherry-red spot at the fovea, and platelet-fibrin or cholesterol emboli in the narrowed retinal arterioles [13]. Optic atrophy, the usual final outcome in ischemic optic neuropathy, occurs in only 50% of eyes with central retinal artery occlusion [134].

Unlike ischemic optic neuropathy, central retinal artery occlusion often is caused by emboli from an ulcerated atherosclerotic plaque of the ipsilateral carotid artery [134]. It is important therefore to diagnose retinal artery occlusion in case carotid artery surgery is indicated [82]. However, the clinical picture may not always be clear, because visual loss due to retinal emboli may be accompanied by ischemic optic neuropathy [5,12,17] or cerebral emboli [2].

Vasospasm or thrombosis may also cause central retinal artery occlusion after radical neck surgery complicated by hemorrhage and hypotension [135,136], and after intranasal injection of alpha-adrenergic agonists [16,137]. Stellate ganglion blockade has been successful in improving vision in some patients [136].

Ophthalmic Venous Obstruction. Obstruction of venous drainage from the eye may occur intraoperatively when patient positioning results in external pressure on the eyes. Increased awareness has probably contributed to the lack of reports of this cause of postoperative visual loss in the last 40 yr [7,8]. Ophthalmoscopic examination in severe cases revealed normal or dilated retinal arterioles, engorgement of the veins, and edema of the macula and the retina surrounding the optic disk, which gradually absorbed but without recovery of vision. Less severe cases were observed in patients in whom immediate loss of vision was less, and partial or complete recovery ensued [7].

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Management of Postoperative Visual Loss

Diagnosis and Treatment

The diagnosis of ischemic optic neuropathy should be suspected if a patient complains of visual loss during the first postoperative week, especially if it is painless, is first noticed upon awakening from sleep, and affects the lower peripheral fields, sparing the central vision. Funduscopy will reveal disk edema in anterior ischemic optic neuropathy but not usually in posterior ischemic optic neuropathy. However, the clinical presentation varies considerably and can be misleading. Ophthalmologic consultation may be delayed for various reasons: the onset of symptoms may not occur immediately after surgery, patients may consider altered vision to be a normal part of recovery from anesthesia [3,137], the pathology may be misdiagnosed as confusion or delirium [14], or the loss of vision itself may lead to a confusional state.

Early diagnosis of the site of the lesion is of the utmost importance since the prognosis varies. Many retrogeniculate lesions demonstrate visual improvement, whereas most cases of ischemic optic neuropathy do not. If there is an embolic origin, a source should be searched for, such as carotid artery disease, which may need investigation and perhaps surgery. Coincidental arteritic anterior ischemic optic neuropathy needs to be excluded since these patients require long-term steroids to avoid progression of their disease.

If ischemic optic neuropathy is suspected in the postoperative period, urgent ophthalmologic consultation should be sought to establish the diagnosis and to decide on therapy. Ischemic optic neuropathy has a poor visual prognosis, but osmotic diuretics and high-dose steroids in the first 48 h after the ischemic insult may decrease the nerve fiber edema and assist the residual circulation in the anterior optic nerve [15,59]. Also, surgical optic nerve decompression may be considered in patients with nonarteritic anterior ischemic optic neuropathy [108]. Other measures, such as the maintenance of normal to mildly mean arterial pressure [60] and normal hematocrit [88], may have some therapeutic benefit, and it seems logical to maintain these to prevent deterioration of the eye pathology.

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Prevention

Obvious precautions include avoiding intraoperative external pressure on the ocular globe and minimizing micro- and macroemboli during cardiopulmonary bypass. In addition, our review of the literature points to a frequent association between postoperative visual loss and decreased blood pressure and hematocrit, irrespective of the anatomic lesion in the visual pathway.

Hematocrit. Blood flow increases with a lower hematocrit due to decreased viscosity [138]. However, the concept that this results in increased oxygen delivery is open to question. A review of the available human data shows that cerebral oxygen delivery is maximal at a hematocrit of 42% [139]. Also, isovolemic hemodilution failed to improve the outcome of stroke [140,141]. There are two probable explanations: 1) Although hemodilution decreases the viscosity of whole blood in vessels until the precapillary level, it does not affect viscosity at the capillary level where oxygen availability (and therefore hematocrit) is the critical factor for tissue oxygen uptake [142]; 2) lowered hematocrit results in increased cerebral blood flow by vasodilation. Ischemic areas are already vasodilated, and therefore hemodilution would tend to exacerbate the hypoxia by decreasing oxygen delivery [143]. Since they are both neural tissue, a parallel might be drawn between the brain and the optic nerve with respect to their tissue oxygen delivery. Also, as discussed above, choroidal circulation is decreased with experimental hemodilution [90]. For these reasons, it seems more likely that isovolemic hemodilution would contribute to, rather than protect against, ischemic optic neuropathy in the perioperative period [3].

Brown et al. [3] point out that recent changes in transfusion practice may lead to an increase in the incidence of postoperative ischemic optic neuropathy [144]. Although current guidelines have not been specific, there have been inferences that blood transfusion can be safely withheld until the hemoglobin is 7 or 8 g/dL [145]. Also, conclusions from animal experiments have been misleading: Levine et al. [146] concluded, after animal experiments of isovolemic hemodilution showed no morbidity, that this was evidence that patients could tolerate a lowered hematocrit. However, no other perturbations, such as hypotension or cardiovascular disease, were included in the experiments, so it is arguable that extrapolation can be made from these results to many clinical situations.

Perfusion Pressure. Systemic hypotension is mentioned in most reports of ischemic optic neuropathy but there is little discussion concerning a safe level of mean arterial pressure. Although autoregulation occurs in the retinal arteries [147], it does not appear to play an important part in choroidal [148] or optic nerve circulation [27]. Blood flow in these parts is related directly to the arterial pressure [65,148]. Therefore, it would seem that the maintenance of normotension is a key factor in the prevention of ischemia to the optic nerve. However, postoperative optic nerve ischemia has been reported in one instance despite normal blood pressure and hematocrit [3], indicating the contribution of other factors in its etiology.

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Conclusion

Postoperative ischemic optic neuropathy is the result of multiple factors. It is usually associated with hypotension and often with blood loss. However, there are often other contributing variables, such as venous obstruction or vascular abnormalities. Because systemic vascular occlusive diseases (e.g., diabetes and arteriosclerosis) are common predisposing conditions more likely to be encountered in the elderly population, postoperative loss of vision may become more frequent as the age of the surgical population increases. Also, since a low hematocrit in the presence of other factors may predispose more surgical patients to visual loss, it may be that the current low level of hematocrit, at which blood transfusion is deemed to be indicated, may not be as safe as previously supposed, especially in the presence of hypotension.

During the process of "informed consent," it might be advisable to indicate to patients that postoperative loss of vision is a rare complication, but that it has been known to occur, particularly in situations of hypotension and low hematocrit. This discussion may be most appropriate for patients reluctant to receive blood transfusion who are about to undergo procedures associated with induced hypotension or probable massive hemorrhage. During the postoperative visit, an assessment of visual function by means of brief questions and examination by the anesthesiologist may minimize delays in diagnosis of visual defects by ensuring prompt ophthalmologic consultation and treatment, thus optimizing the patient's chance of regaining vision.

Addendum: The Ischemic Optic Neuropathy Decompression Trial Research Group has recently published the data of a cooperative study (Optic Nerve Decompression Surgery for Nonarteritic Anterior Ischemic Optic Neuropathy (AION) Is Not Effective and May Be Harmful. JAMA 1995;273:625-32). This study demonstrates no effectiveness in the surgical treatment of AION and, in some cases, a worsening of the visual symptoms.

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