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ION occurs after surgery or nonsurgical bleeding, but it primarily develops spontaneously without warning signs. It is the leading cause of sudden visual loss in patients 50 years or older. Two types of ION are recognized: anterior (AION) and posterior (PION). Of the two, AION is far more common and has been more extensively studied than PION. Both AION and PION are further divided into two types: arteritic and nonarteritic. Arteritic AION is the most serious type and is due to temporal arteritis. This systemic disease, which usually occurs in patients 60 years and older, has a female preponderance. About three fourths of these patients feel ill and have flulike symptoms. Arteritic AION is an emergency and will lead to permanent blindness if untreated.
Nonarteritic ION is much more common and is overwhelmingly the type seen in the perioperative period. Generally found in older patients, it may also occur in young persons with diabetes, malignant hypertension, eclampsia, migraine, systemic lupus, and a number of other systemic vascular diseases. About a quarter of patients with AION will have both eyes involved within 3 years, and about half will be so affected within 10 years. The incidence of nonarteritic ION is estimated to be 2.3 per 100,000 inhabitants per year in the United States,[159] an incidence close to that in a surgical population.[1] ION has been found after a wide variety of surgical procedures, with most having followed cardiothoracic surgery,[84] [86] [90] instrumented spinal fusion operations,[1] [105] [160] head and neck surgery,[78] [92] [95] [100] [106] and surgery on the nose or sinuses.[161] [162] However, cases have also been described after vascular surgery, general surgical and urologic procedures, cesarean section and gynecologic surgery, and liposuction. [2] [68] [71] [74] [80] [91]
It is very important to differentiate arteritic ION from nonarteritic ION because the arteritic form responds to rapid institution of steroid treatment. In arteritic ION, symptoms include a vague feeling of sickness, fever of unknown origin, influenza-like symptoms, scalp tenderness, and usually palpable, hard nodular changes in the temporal arteries. The erythrocyte sedimentation rate and C-reactive protein may be markedly elevated and thus suggest an inflammatory process.[163] In 50% of patients the optic disk swelling typically appears chalky-white because of underlying PCA occlusion. Temporal artery biopsy must be performed to confirm this diagnosis.[163]
PION is characterized by ischemia of the retrolaminar region of the ON. Because the lesion is located further posteriorly than in AION, initial funduscopic examination typically shows no optic disk abnormality. Because of its relative rarity, few studies of PION have been reported in the literature.[164] Like AION, it also has arteritic and nonarteritic forms. PION occurs with giant cell arteritis, systemic lupus erythematosus, sickle cell disease, and fungal infections and after surgical procedures.[165]
Case reports in the literature consist of 51 patients in whom perioperative AION was diagnosed between 1968 and 2002 (see Table 82-2 ). Among this group, 59% of subjects underwent open heart surgery; 12%, nasal, head, or neck surgery; and 12%, spine surgery. The average age was 53 years, and 72% were male. In many cases there are missing data, and hence we cannot be certain that the data are truly a representative sampling, as with any of the collections of case reports that are evaluated. These patients tended to undergo lengthy operations, with an average operative time of 508 minutes. In patients in whom blood pressure was reported, mean arterial pressure averaged 92 mm Hg preoperatively, with an average lowest mean arterial pressure of 65 mm Hg intraoperatively. Preoperative hemoglobin averaged 13.7, the lowest intraoperative value was 8.7, and the postoperative hemoglobin concentration was 8.1 g/dL. The patients received considerable amounts of fluid intraoperatively: an average of 1.4 L of blood replacement, 8.2 L of crystalloids, and 1.0 L of colloids was administered. In 20% of cases, blood loss exceeding 2 L was reported. Coronary artery disease was present in 61%, hypertension in 27%, and diabetes mellitus in 24% of patients. These data may be biased toward a high incidence of these disorders because of the predominance of patients who underwent CABG surgery. In 67% of patients, symptoms of visual loss were not evident until more than 24 hours after surgery because of either delayed onset of the disease or delayed recognition of the symptoms and signs of AION in the perioperative period. Virtually all patients had disk edema, pallor, or both. Over 60% of patients had an afferent pupil defect or nonreactive pupils. The visual field deficit was altitudinal in 14%, 20% had a central scotoma, and in 20%, blindness was the initial symptom. Visual loss was bilateral in 55% and unilateral in 45% of patients. It was indicated in reports that some treatment was attempted in 15 patients, including steroids, aggressive volume replacement, vasopressors, or a combination of these therapies. Treatment did not necessarily result in improvement. Overall in the 51 patients, 47% had no improvement or a worsening of symptoms, 29% improved, and in 25% the outcome was not described.
Between 1968 and 2002, 38 patients have been reported with PION (see Table 82-2 ). The nature of the surgical procedures that these patients underwent tended to differ from those in the patients reported with AION. Among this group, 8% of subjects underwent open heart surgery; 24%, nasal, head, or neck surgery; and 39%, spine surgery. The average age was 50 years, with 63% of them male. Although AION is rarely reported in children [166]
In summary, case reports showed similar intraoperative characteristics of AION and PION patients. The main differences were a lower incidence of coronary artery disease in the PION group, the occurrence of PION in younger patients, somewhat more intraoperative blood replacement, more rapid onset or recognition of visual loss, and a greater likelihood that the patient would initially have complete blindness in PION as opposed to visual field loss in AION.
Sadda and associates[164] have recently retrospectively reviewed a relatively large series of patients in whom nonarteritic PION developed spontaneously (38) and patients in whom PION developed in the perioperative period (28). In addition, they segregated patients into spinal surgery (14) versus other types of surgery (14). The spinal surgery patients tended to be younger and to have a lower incidence of coronary artery disease and diabetes, but not hypertension, relative to the other two groups. Unfortunately, intraoperative data were not included, but the postsurgical patients were more likely to have bilateral involvement and a worse visual outcome at initial examination and later follow-up, compared to nonsurgical cases.
Preliminary data from spine surgery patients in the ASA Postoperative Visual Loss Registry[49] showed striking differences between ION patients (n = 43) and those with RAO (n = 8) and similar overall characteristics of the patients to those described in the case report data.[167] The average blood loss in ION patients was 2.3 L versus 0.7 L in the RAO group. The lowest hematocrit was 26% in ION patients and 33% in RAO patients. One of the most interesting findings is that ION developed in eight patients despite being positioned in Mayfield tongs, thus demonstrating that ION can occur even in a setting in which compression of the globe is impossible. The occurrence of ION in patients positioned prone in Mayfield tongs casts doubt on the theory that ION is simply due to external pressure on the eye. Earlier preliminary analysis[168] of all ION patients in the registry had shown a median operating room time of 600 minutes, estimated blood loss of 2.2 L, lowest hematocrit of 24%, and hypotension in only 52% of patients.
The arteritic form of ION is due to giant cell arteritis, whereas postoperative ION is nonarteritic. Nonarteritic AION appears to be caused by embolic or thrombotic occlusion of the PCAs in a watershed zone and results in regional loss of perfusion and infarction of the ONH.[15] [163] [169] The disease is of multifactorial origin and involves patient factors (individual variations in ON anatomy and vasculature and systemic factors), as well as the presence of precipitating events.[170] [171] Neuroretinal rim loss occurs along with the development of optic disk cupping (i.e., acquired excavation of the ONH), similar to the findings seen with glaucomatous optic neuropathy.[21] On the other hand, segmental or diffuse pallor without cupping is the typical disk appearance of nonarteritic AION.[172] Much less is understood about the pathology of nonarteritic AION, but it is thought to be caused by temporary hypoperfusion or nonperfusion of vessels supplying the anterior portion of the ON.[62] [163] In the paragraphs that follow, reference to ION is to the nonarteritic form, which is the variety most often seen in the perioperative period.
Hayreh has suggested that AION is due to individual variations in blood supply to the ON. This theory is supported not only by anatomic studies but also by the variability of visual loss in patients with AION. Reduced perfusion pressure in the region of the paraoptic branches of the sPCAs results in optic disk hypoperfusion.[13] Delayed onset and filling of the prelaminar optic disk, demonstrated by fluorescein angiography, suggest impaired perfusion within the microcirculation of the ONH. Anatomic or physiologic variations in the circulatory supply of the ON may predispose some patients to the development of AION,[33] especially under conditions such as increased IOP or decreased systemic arterial blood pressure. These variations in blood supply could result in underperfused areas.[15] [22]
It has been suggested that a small optic disk (commonly referred to as a small "cup-to-disk ratio") plays a role in a subject's susceptibility to AION.[173] If an optic disk is small, axons of the ON pass through a more narrow opening as they exit the eye and are therefore prone to injury in the presence of edema or decreased blood flow. However, the importance of the cup-to-disk ratio remains controversial.[174] Some have suggested that variability in blood pressure and IOP may predispose patients to the development of AION. Nocturnal hypotension in patients treated with antihypertensive agents could be the mechanism whereby patients are exposed to low-level, albeit repeated decreases in perfusion to the ON, although the importance of this mechanism requires further study.[175] [176]
Disruption of the blood-brain barrier is an early event in AION, and as a result, fluorescein angiography shows dye leakage in the ONH.[62] Clinically, leakage of dye correlates with the early onset of optic disk edema, and it can even be seen before the onset of symptoms.[179] Exactly how disruption of the blood-brain barrier leads to ischemic injury is not known. Immunohistochemical studies of microvessels in the monkey prelaminar ON suggest a lack of classic blood-brain characteristics[180] that could explain the early edema in the ONH after ischemia. Unfortunately, few animal models of AION are available, and hence little is known about the in vivo cellular mechanisms leading to ischemic injury in the ON. Guy showed that 30-minute occlusion of the carotid artery in rats produced ischemia and a swollen ON within 24 hours.[181] The positive nitrotyrosine immunostaining found in the ischemic ON[181] suggests a possible role for nitric oxide and perhaps oxygen free radicals, which would be expected to increase with disruption of the blood-brain barrier.
Because the ON is a white matter tissue, it has no synapses and cell bodies, and the mechanisms of ischemic damage may not be the same as in a gray matter structure. Studies simulating ischemia in ON axons maintained in vitro[152] showed that O2 deprivation sets in motion a series of cytoplasmic and membrane events culminating in axonal destruction. Depletion of adenosine triphosphate when O2 delivery decreased led to membrane depolarization, influx of Na+ and Ca2+ through specific voltage-gated channels, and reversed operation of the Na+ -Ca2+ exchange pump.[153] Ca2+ overload results in direct cellular damage from activation of proteolytic and other enzymes.[154] ION may lead to neuronal injury by apoptotic, or programmed, cell death, which may be stimulated with reduced O2 delivery.[155]
The onset of AION is sudden and painless. Visual field defects are typically an inferior altitudinal hemianopic defect with or without constriction of the visual field or, alternatively, a superior altitudinal defect, nasal hemianoptic defect, or central scotoma. Systemic disease, particularly cardiovascular, is frequently found in AION patients. The prevalence of systemic disease in 406 patients aged 11 to 91 years with AION was compared with that in a race-, gender-, and age-matched group in the general population.[186] Criteria for AION included a history of sudden visual loss with documented optic disk edema that resolved spontaneously within 2 to 3 months and residual optic disk-related visual defects. For all ages, the prevalence of arterial hypertension, diabetes mellitus, and gastrointestinal ulcer was significantly higher in patients with AION. In patients older than 45 years, a significantly higher prevalence of ischemic heart disease and thyroid disease was found. Middle-aged patients had a significantly higher prevalence of chronic obstructive pulmonary disease and cerebrovascular disease. However, a smaller case-control study using better matching criteria suggested that only diabetes was a potential risk factor for the development of AION.[187] Among patients in the Ischemic Optic Neuropathy Decompression Trial (IONDT), 47% were hypertensive, 24% were diabetic, 11% had a previous myocardial infarction, and 3% previously had a stroke.[176] These proportions of patients with "vascular risk factors" might, however, be similar to those in the general population. For ethical reasons, the IONDT could not include a non-ION control group. Smoking might also be a risk factor for the development of ION, but large numbers of patients have not been reported.[188]
When ION follows nonsurgical bleeding, the most frequent site of the bleeding is the gastrointestinal tract, followed by the uterus. The visual loss is usually bilateral and varies from blurred vision to blindness in one or both eyes. Many case reports describe hypotension and profound anemia after the hemorrhage. Hayreh and coworkers hypothesized,[170] [175] based on a review of the literature, that the development of AION after hemorrhage could be due to a combination of three factors: (1) increased peripheral vascular resistance because of release of systemic endogenous vasoconstrictors such as angiotensin, epinephrine, and vasopressin, all of which freely enter the choroidal interstitial fluid and result in vasoconstriction in the ONH vessels and the peripapillary choroidal arteries; (2) a decrease in systemic blood pressure from bleeding and superimposed sleep leading to decreased perfusion of the ONH; and (3) autoregulatory failure of the ON blood supply, also resulting in diminished perfusion.
Whereas AION is the result of interruption of the blood supply to the anterior portion of the ON, PION is produced by decreased oxygen delivery to the more posterior, retrolaminar portion of the nerve. The pathophysiology of PION is even less well understood than that of AION. Blood supply to the retrolaminar portion of the ON is derived from the surrounding pial capillary plexus, with only a small number of capillaries reaching the nerve. Hence, this area is not as well vascularized as the anterior portion of the ON.[22] It appears that decreased blood flow in these vessels or embolic phenomena result in ischemia.[189] However, a low-flow state from systemic hypoperfusion, emboli, or venous stasis could also contribute.
Autopsy studies in postoperative PION have shown edema and enlargement of the ON with central retrolaminar hemorrhagic infarction.[55] [100] [104] [190] A symptom-free period is usually present initially, with minimal or no abnormalities found on ophthalmoscopic examination. An initially normal optic disk and no perfusion abnormalities on fluorescein angiography distinguish PION from AION. Mild disk edema occurs over a period of days. Later (within 5 to 6 weeks), the optic disk shows pale atrophy. The sudden onset of visual disturbance may not affect visual acuity, but a visual field deficit is almost always present.
Only one retrospective study has characterized patients with spontaneously occurring PION.[164] These 38 patients
Perioperative ION appears to be a multifactorial disease, and unlike spontaneously occurring ION, it can occur in younger patients. Because of the paucity of case-control studies and the absence of prospective studies, risk factors have not yet been well defined.[49] Another puzzling feature of this dreaded complication is that it is unclear why AION develops in some patients and PION in others. Possible factors involved in the etiology of perioperative ION are decreased systemic blood pressure, blood loss, increased intraocular or orbital venous pressure, abnormal autoregulation of the ON circulation or anatomic variation in the blood supply to the ON (or both), emboli, the use of vasopressors, the presence of systemic disease (e.g., hypertension, diabetes, and atherosclerosis), and retrobulbar hemorrhage. It seems that one or more of these factors are often involved in an individual patient and in an unpredictable fashion. Because of the poorly defined nature of ION in the perioperative period, it is controversial whether anesthesiologists should alter their practice with respect to the purported risk factors during certain "higher-risk" procedures. These apparently higher-risk operations include open heart, head and neck, and spinal surgery. The incidence of visual loss after spine surgery has been estimated in small studies to approximate 0.07% to 0.20%. [49] [88] After cardiac surgery, the incidence was estimated to be as high as 1.3%[86] in a study of about 800 patients but 0.06% in a large 18-year retrospective study of nearly 28,000 patients at the Mayo Clinic.[191]
Intraoperative hypotension has been cited as an important risk factor by a number of authors of case reports,[68] [77] [97] but because it is not always present,[49] [72] [86] [93] [98] hypotension itself might not be responsible. In a survey of spine surgeons that yielded 24 cases of visual loss after spine surgery, deliberate hypotension was reported to have been used in only 2 cases.[192] In a retrospective survey study of patients undergoing spinal fusion, Myers and colleagues showed that levels of hypotension and anemia were equivalent in patients in whom ION developed versus those in whom it did not.[160] Despite its design flaws, this study is the largest attempt to date to analyze the causes of ION after spinal surgery. Similarly, in a retrospective study of 602 patients who underwent open heart surgery at one institution during a 2-year period, eight cases of ION were found. The lowest perfusion pressure intraoperatively was no different between affected and normal patients.[86] In open heart surgery, hypothermia during cardiopulmonary bypass might play a role in the development of ION through alterations in viscosity, but the contribution of this mechanism has not been studied.
Hypotension can potentially lead to decreases in perfusion pressure in the ON. The anterior ON would be susceptible to damage from hypotension leading to AION either because of anatomic variation in the circulation or because of abnormal autoregulation and an inability to adequately compensate for a decrease in perfusion pressure. The posterior ON would be at potential risk for PION because of the relatively limited blood supply reaching this area, which might be potentiated by hypotension. It is difficult to precisely define the degree of hypotension that is potentially harmful because actual preoperative and intraoperative blood pressure readings were not available in many of the reported cases of ION in the literature, and hence the safe "lower limits" of blood pressure are not known.
From case reports of perioperative ION, it is apparent that on average, patients sustained considerable blood loss and had a decreased hemoglobin concentration intraoperatively. Routine clinical practice based on the National Institutes of Health Consensus Panel on Blood Transfusion[193] and ASA practice guidelines[194] suggests that transfusion is not generally required for hemoglobin values higher than 8.0 g/dL. A number of authors have suggested that allowing hemoglobin to decrease to such low values may be putting patients at increased risk for ION[68] [195] ; however, whether practice should be changed in surgical procedures such as spine or heart surgery—or in any operative procedure—remains controversial. Two retrospective studies examined whether decreased hemoglobin/hematocrit relates to the occurrence of ION. In spine surgery patients, Myers and associates [160] determined that the lowest levels of hematocrit did not differ between patients sustaining ION and those who were not affected. In a case-control study of cardiac surgery patients, Nuttall and coworkers[191] found a somewhat different result. The presence of a lower minimum postoperative hemoglobin was associated weakly with ION (odds ratio, 1.9; P = .047). Looked at another way, 13 of 17 ION patients in their study had a minimum postoperative hemoglobin value less than 8.5 g/dL versus 14 of 34 control patients with this level. This study did not specify the type of ION sustained by the patients, had numerous statistical comparisons, and had a small sample size. Because spine and open heart surgery patients are quite different, it is doubtful that the results can be extrapolated to types of surgery other than cardiac.
In the setting of uncontrolled hemorrhage where blood volume is not maintained, decreased oxygen delivery to the ON could result in either AION or PION.[170] Just how low or for how long the hemoglobin concentration must decrease to lead to this complication is not known. However, the presence of recurrent and profound hemorrhage has been described in many reports. The argument that blood loss in the face of maintained intravascular volume (hemodilution) is harmful seems less scientifically grounded. It has been shown experimentally in minipigs that blood flow in the ONH, as measured by laser Doppler, was maintained during isovolumic hemodilution with a 30% decrease in hematocrit. Moreover, oxygen tension measured at the vitreal surface increased 15%.[196] Hemodilution in cats resulted in a nonsignificant decrease in choroidal oxygen delivery [46] and an increase
AION and PION have been reported in the setting of massive fluid replacement, and many reports include patients that were operated on in the prone position, which raises the possibility that either external pressure on the globe or a buildup of pressure internally within the eye could be related to ION. Regarding external pressure, many cases of ION have been reported in which it was impossible for pressure to have been placed on the eye. Such cases include patients in pin head holders[167] [192] and those in whom the head was turned with the affected eye placed in the upward position.[105] It is unlikely that PION is related to external pressure because the retrolaminar ON is not exposed to the IOP. In addition, an increase in IOP would not be likely to produce an isolated ION without also causing retinal damage because sustained increases in IOP significantly decrease both retinal and choroidal blood flow.[45]
The theory that massive fluid resuscitation could be a pathogenic factor in perioperative ION remains speculative, but it does have some merit. Conceivably, fluid therapy, with or without prone positioning, could result in increased IOP or accumulation of fluid in the ON, or both. The vessels in the ON are small and relatively easily compressible, especially in the posterior ON, so large-volume replacement might lead to decreased arterial supply or increased orbital venous pressure and the risk of venous stasis. Because the CRV and draining veins exit out of the ON, a "compartment syndrome" may occur in the ON. Alternatively, fluid accumulation in the vicinity of the lamina cribrosa might compress axons as they transit this region. In a remarkable report, Cullinane and coworkers[199] found that ION developed in 2.6% of massive trauma patients (>20 L of crystalloid administered in a 24-hour period) who were resuscitated successfully. (Patients were said in this publication to have sustained AION, but from the ocular findings reported, it appears the diagnosis was in fact PION.) These patients received massive blood replacement and were acidotic, most had abdominal compartment syndrome, and the lowest hematocrit ranged from 7.5% to 28%. In addition, very high levels of positive end-expiratory pressure (average, 29 cm H2 O) were used to ventilate these patients. Although these patients had many complicating factors, massive fluid and blood replacement seems to be a possible etiologic factor for ION.
In another report, ION developed in a 27-year-old burn patient who underwent numerous operative procedures and also received massive quantities of fluid on initial resuscitation.[200] Large fluid replacement is generally seen in many case reports (see Table 82-2 ), and increased postoperative weight gain was identified as a risk factor after heart surgery, thus suggesting, though not proving, that fluid replacement might play a role.[86] Other case reports involving spine surgery have also suggested that large-volume transfusions might play a pathogenic role.[72] [93]
Further support of an idea that increases in orbital venous pressure are potentially deleterious can be seen in reports of ION after head and neck surgery in which the internal jugular veins were ligated,[78] [95] [100] [102] [106] as well as reports of ION after superior vena cava syndrome in a liver transplant patient.[76] Finally, additional support for the concept of the importance of orbital venous pressure changes was another case, that of a 24-year-old man suspended upside down for 12 hours after an automobile accident. The patient was blind, with CT of the orbit showing anterior displacement of the globe and stretching of the ON.[201]
Although the relationship to fluid therapy is not clear, Myers and colleagues found that longer surgery was associated with ION.[160] However, cases of ION have been found after widely varying operative times.[168] Some have speculated that facial edema indicates a risk for ION after spine surgery. [96] However, in clinical practice, facial edema is often seen after spinal fusion in many patients in whom ION does not develop, and therefore its relevance remains unclear, and the notion that facial edema is a risk factor is unproven.
Cheng and associates[202] recently provided the first data examining changes in IOP during spine surgery performed with the patient in the prone position. These authors found that in anesthetized patients, IOP increased significantly on initial prone positioning relative to supine (27 ± 2 versus 13 ± 1, P < .05). After 5 hours in the prone position, IOP remained elevated at 40 ± 2 mm Hg. In none of the 20 patients in the study did visual loss develop. Although these data suggest that ocular perfusion pressure might decline even during maintenance of normotension, some experimental design issues must be considered when interpreting these results. The main issues are that the largest increases in IOP were evident near the time that patients were awakening. As such, IOP could have risen because of light anesthesia. Moreover, the study did not have any supine group to control for the effects of fluid administration on IOP. Such control is important because prone positioning itself might not explain the large increases in IOP. These results are valuable as well as worrisome, but further studies are needed to fully evaluate their significance. In summary, fluid administration could be a pathogenic factor in ION, especially in patients positioned prone or undergoing cardiac surgery, but the mechanisms involved, as well as the amounts and nature of fluid required, remain undefined.
Anatomic variation in the ON circulation might predispose patients to the development of ION. The location of potential watershed zones in the ON circulation plus the presence of disturbed autoregulation, even in normal patients,[203] is of great concern but cannot be predicted clinically at this time. Human studies generally show preserved blood flow at clinically used or even lower ranges of perfusion pressure, but these studies have focused their attention primarily on the anterior portion of the ON.[31] [32] [203] However, animal studies show preserved blood flow in various layers of the ON, including the retrolaminar area, even at a mean arterial blood pressure of 40 mm Hg.[26] Although it seems logical to look for guidance from results in the brain, because of anatomic
Emboli may directly obstruct arterial flow to the ON and are most likely to occur during cardiac surgery[158] [204] or with a paradoxical air embolism through a patent foramen ovale.[205] [206] Emboli have been seen postmortem in the PCAs, [207] but the impact of emboli would depend on the anatomic arrangement of the PCAs in the individual patient and the amount of embolized material.
Hayreh and colleagues theorized that AION is related to excessive secretion of vasoconstrictors, which in turn could lower ON perfusion to dangerously low levels.[170] [175] Clinicians use vasopressors to maintain blood pressure in circumstances such as after cardiac surgery. Shapira and coworkers showed an association between prolonged use of epinephrine or long bypass time and ION in patients undergoing open heart surgery.[86] Lee and Lam[98] reported a case of ION in a patient after lumbar spine fusion during which a phenylephrine (Neo-Synephrine) infusion was used to maintain blood pressure. However, no other data suggest that phenylephrine infusion might be harmful for ON perfusion.
These factors have been cited in case reports but are not present in all patients in whom ION has developed. Moreover, they are typically found in patients undergoing cardiac surgery, but ION develops in few of these patients. No case-control data show an association of these factors with the development of ION in spine surgery patients. In a prospective study of nonsurgical patients, ION was not associated with the presence of carotid artery disease.[208] A basis for the theoretical notion that perioperative ION is related to atherosclerosis is that the ON vasculature would respond abnormally to changes in perfusion pressure (i.e., demonstrate disturbed autoregulation). This association has not been studied in humans, and animal data are sparse and inconclusive.[30]
Because of the close anatomic relationship of the sphenoid sinus and ethmoidal cells to the orbit and ON, surgery on the nose and paranasal sinuses poses a special risk of damage. The bone is very fragile in this area, and there is anatomic variation inasmuch as pneumatization depends on the individual pattern of growth developmentally.
Retrobulbar hemorrhage may follow surgical damage to the fragile lateral wall of ethmoidal cells, the lamina papyracea. Sinus endoscopy has improved visualization of structures in the surgical field significantly, but blindness has occasionally been reported.[161] [209] [210] Direct surgical damage to the ON may occur, [211] but indirect damage by compression from retrobulbar hematoma leading to ION has been reported more often. Most authors do not describe findings at funduscopy, and therefore the cases cannot be classified into AION or PION. Paresis of eye muscles (mostly the medial rectus muscle), including ptosis, is often seen.[120] [162] [212] The outcome is poor; in only one case was temporary blindness reported,[213] whereas all other reported cases of retrobulbar hematoma resulted in permanent blindness.[50]
The pathogenesis of perioperative AION is not yet completely understood. Multiple factors that could contribute to ION are frequently present in patients undergoing open heart, spine surgery, or head and neck operations. ION can occur after any other type of surgery as well. A patient may have risk factors such as anatomic variation and abnormal autoregulation in the ON, but these anomalies are currently undetectable in the preoperative period. Preexisting as well as intraoperative factors may interact in an unpredictable fashion and lead to ION. Further studies are necessary to gain a better understanding of the mechanisms leading to ION in the perioperative period.
Unfortunately, there is no proven treatment of ION. Williams and coauthors[195] have reviewed the attempted treatments. Acetazolamide lowers IOP and may improve flow to the ONH and retina.[155] [214] Diuretics such as mannitol or furosemide reduce edema. In the acute phase, corticosteroids may reduce axonal swelling, but in the postoperative period, they increase the risk of wound infection. Because steroids are of unproven benefit, their use must be carefully weighed. Increasing ocular perfusion pressure or hemoglobin concentration may be appropriate when ION occurs in conjunction with significant decreases in blood pressure and hemoglobin concentration. Maintaining a head-up position could be valuable if increased ocular venous pressure is suspected. Similarly, IOP should be lowered if an increase is documented. ON decompression is an operative procedure that could restore circulation in the ON. However, in a multicenter trial sponsored by the National Eye Institute, this operation was found to be ineffective and possibly harmful; because of the adverse findings, this study was terminated prematurely.[215]
The major stumbling blocks in recommending prevention strategies are that the status of the patients' ON circulation is not known preoperatively and no effective or practical method is available for monitoring the ON intraoperatively. However, some general recommendations can be made. In patients with preexistent cardiovascular disease, long-standing or poorly controlled hypertension, or end-organ damage or those with known visual disorders such as glaucoma, it would seem prudent to maintain systemic blood pressure as close to baseline values as possible and to avoid prolonged decreases in ocular perfusion pressure. These caveats might be even more relevant during prolonged surgery in the prone position because of the potential accompanying increases in IOP. No rational guidelines have been established at this time to define safe percent decreases in blood pressure or the time limits of such decreases. If vasopressors such as phenylephrine are used to maintain blood pressure, the impact of their prolonged use on the ON microvasculature is not known. Any recommendation to maintain blood pressure has to be weighed against possible surgical needs for deliberate hypotension to decrease blood loss and maintain adequate operative exposure.
Whether patients should be warned about the possibility of ION during the process of informed consent, especially those undergoing apparently higher-risk operations such as CABG and complex instrumented spinal fusion surgery, is controversial. [49] Few clinicians seem to include the complication in informed consent discussions. Despite the devastating nature of this injury, our limited understanding of the pathogenesis of this disorder does not yet enable us to make rational recommendations that are likely to completely prevent its occurrence at this time.
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