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© 2001 International Anesthesia Research Society
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Abstract |
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Visual loss (acuity or field) secondary to ischemic optic neuropathy (ION) is a rare but devastating complication of cardiac surgery involving cardiopulmonary bypass (CPB). We determined clinical features and risk factors for ION by a retrospective time-matched, case-control study. ION was identified in 17 (0.06%) patients out of 27,915 patients who underwent CPB between January 1, 1976, and December 31, 1994. For each ION patient, two patients who underwent CPB exactly 2 wk before the ION patient were selected as controls. Data were analyzed by using conditional logistic regression with the 1:2 matched-set feature of 17 cases and 34 controls. Two-tailed P values
0.05 were considered significant. From bivariate analysis, smaller minimum postoperative hemoglobin concentration (odds ratio [OR] = 1.9, P = 0.047) and the presence of atherosclerotic vascular disease (OR = 7.0, P = 0.026) were found to be independently associated with ION after CPB, as were smaller minimum postoperative hemoglobin concentration (OR = 2.2, P = 0.027) and preoperative angiogram within 48 h of surgery (OR = 7.2, P = 0.042). In ION patients, 13 (76.5%) of 17 experienced a minimum postoperative hemoglobin value of <8.5 g/dL, whereas only 14 (41.2%) of 34 control patients experienced values <8.5 g/dL. IMPLICATIONS: Patients with clinically significant vascular disease history or preoperative angiogram may be at increased risk for ischemic optic neuropathy after cardiac surgery, especially if the hemoglobin remains low in the postoperative period.
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Introduction |
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Neurologic injury is a well known sequela after cardiac surgery with cardiopulmonary bypass (CPB) and is an important cause of morbidity and mortality (1). Blindness after cardiac surgery with CPB is a rare and poorly understood event. It may be caused by ischemic optic neuropathy (ION), with loss of visual acuity or field, although cortical mechanisms for visual loss are also possible (2,3). The frequency of postoperative visual loss for all types of surgery varies from 0.1% to 0.002% (3–5). Reports of ION in association with cardiac surgery are limited to single or few patient case studies (2–8). In an effort to better understand the pathophysiology and risk factors for ION, we performed a retrospective, time-matched, case-control study of ION associated with cardiac surgery and CPB.
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Methods |
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After IRB approval, the Mayo Clinic Surgical Index and Medical Index were used to identify all patients diagnosed with any type of visual loss after cardiac surgery requiring CPB at Mayo Clinic Rochester between January 1, 1976, and December 31, 1994. The Mayo Clinic Medical Index is a set of databases that serve as an index to the patient’s medical record. The index is created by the coding and classification of diagnoses from a patient’s medical record by using the Master Sheet as the primary source of information (9). Since November 1975, diagnoses have been coded in the Medical Index by using the Hospital Adaptation of the International Classification of Diseases, 2nd ed (HICDA) (10). When performing the initial retrieval from the Medical Index, potential cases of visual loss after cardiac surgery were identified by using the following HICDA codes: 03774–03777, 03779, 03786, 04350, 07713–07715, 07718, 34580–34583, and 34589. Two physicians (JAD and MDA) reviewed the medical records of all patients selected in this initial screen to identify those who experienced new-onset visual loss within 30 days after cardiac surgery. The medical records of these potential cases were subsequently reviewed by an ophthalmologist (JAG) to confirm the diagnosis of visual loss secondary to ION. For each case, two controls who did not experience postoperative visual loss were randomly selected from the pool of all patients undergoing cardiac surgery requiring CPB at Mayo Clinic Rochester exactly 2 wk before the case. By choosing controls from exactly 2 wk before the case, we ensure that the controls underwent surgery on the same day of the week and by the same surgical team as the case. We selected the controls from a time period before the case because we believe that ION is a serious enough complication that after even a single episode, a surgical team may have changed their practice on the basis of what they believed might have contributed to the event.
The medical records of the cases and controls were reviewed, and potential risk factors for blindness were abstracted. The variables included in the data abstraction are presented in Table 1. Valve defect was defined as aortic stenosis, aortic insufficiency, mitral stenosis, or mitral regurgitation. A history of clinically severe vascular disease was defined as claudication, thoracic aneurysm, abdominal aortic aneurysm, history of previous peripheral vascular surgery, transient ischemic attack, cerebral vascular accident, carotid stenosis, or previous carotid endarterectomy. For patients diagnosed with ION, postoperative eye examination included bedside visual acuity in each eye, pupillary reactions, confrontation visual fields, external ocular examination, ocular rotations, applanation tonometry, and a dilated fundus examination. If the medical condition of the patient allowed it, an office examination was performed that also included slit lamp biomicroscopy and visual field testing by tangent screen, Goldmann perimetry, or automated perimetry. Visual field defects included four quadrants, three quadrants, two quadrants, altitudinal, central, and paracentral. The dates of last follow-up and ocular status and examination were also recorded. No eye examination was performed in the control patients.
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Data are presented as mean ± SD or percentage, as appropriate. The overall frequency of ION was calculated by dividing the number of observed cases by the total number of CPB surgeries performed during the study period. A logistic regression analysis, with visual loss as the dependent variable and year of surgery as the independent variable, was performed with data from all surgeries performed during the study period to determine whether the frequency of visual loss after CPB increased or decreased as a function of calendar time. Visual acuity and visual field loss are summarized by using the most affected eye for each case. For the case-control analysis, potential risk factors for visual loss were assessed with conditional logistic regression, making use of the 1:2 matched-set feature of 17 cases and 34 controls (11,12). Age, body mass index, ejection fraction, hemoglobin, glucose cholesterol, creatinine kinase, blood pressure, duration of CPB, duration of cross-clamp, oxygen saturation, red blood cell (RBC) units transfused, and cardiac output were analyzed as continuous variables. All other risk factors were analyzed as categorical variables. Two-tailed P values
0.05 were considered statistically significant, with no adjustments made for multiple comparisons. All statistical analyses were performed with SAS Version 6.12 (SAS Institute, Inc., Cary, NC). |
Results |
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There were 17 cases of visual loss secondary to ION identified from 27,915 patients who underwent cardiac procedures requiring CPB at Mayo Clinic Rochester during the study period. For these 17 (12 men and 5 women), the mean ± SD age at the time of surgery was 65.4 ± 7.8 yr (range, 43–75 yr). Visual loss was noted a median of 2 days (range, 0–10 days) after surgery and was unilateral in eight patients and bilateral in nine patients. Table 2 shows the results of the postoperative eye examination. The overall frequency of ION during the study period was 0.06%. There was evidence (P < 0.01) that the frequency of this event increased over the study period, with observed event frequencies of 0.01%, 0.03%, and 0.12% for the calendar periods 1976–1981, 1982–1987, and 1988–1994, respectively.
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The univariate associations between the risk factors with visual loss secondary to ION after cardiac surgery requiring CPB are presented in Table 1. Significant univariate risk factors for vision loss include lower minimum postoperative hemoglobin (odds ratio [OR] = 1.9 for each 1 g/dL decrease, P = 0.022), history of clinically severe vascular disease (OR = 7.3, P = 0.012), preoperative angiogram within 48 h of CPB (OR = 5.6, P = 0.034), longer duration of CPB (OR = 1.5 for each 30-min increase, P = 0.026), RBC transfusions (OR = 1.3 for each 1-U increase, P = 0.014), and any use of non-RBC blood components (OR = 4.4, P = 0.028). Because only 17 cases of vision loss were found, no multivariate analysis was included in the initial analysis plan. However, because some of the univariate predictors are probably associated with hemoglobin level, post hoc multivariate analyses were performed to assess the significance of the other risk factors after adjusting for minimum postoperative hemoglobin level (Table 3). From these analyses, a history of clinically severe vascular disease (P = 0.026) and minimum postoperative hemoglobin (P = 0.047) were found to be independent risk factors for vision loss, as were preoperative angiogram within 48 h of CPB (P = 0.042) and minimum postoperative hemoglobin (P = 0.027). Table 4 shows the minimum postoperative hemoglobin values of <8.5 g/dL for the Control group of patients and ION patients with and without a history of clinically severe vascular disease and with and without preoperative angiogram within 48 h of CPB.
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Discussion |
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Loss of vision secondary to ION associated with CPB is a devastating complication of cardiac surgery. We found that ION is an extremely rare event after cardiac surgery, with an overall frequency of 0.06% and evidence of an increase in frequency over the study period (observed event frequencies of 0.01%, 0.03%, and 0.12% for the calendar periods 1976–1981, 1982–1987, and 1988–1994, respectively). This frequency of ION is similar to those previously reported for all types of surgery, with rates from 0.1% to 0.002% (2–5). The finding of an increase in the frequency of ION during the study period is interesting. Whether this represents a true increase in the frequency of ION over time or simply an increase in the number of cases that are diagnosed is difficult to ascertain. The case-control study was designed such that the cases and controls were matched for calendar time. From the case-control study we found that, in case-control sets that were matched on calendar time, lower minimum hemoglobin was associated with ION. As with most institutions, our transfusion practice has changed dramatically since 1976, with lower hemoglobin levels now considered acceptable. Therefore, the observed increase in the frequency of ION over calendar time would be consistent with an association between small hemoglobin concentration and the occurrence of ION.
Ischemia-related loss of vision after surgery results from lesions in the visual pathway associated with various causes of decreased oxygen delivery. Ischemic insult to the optic nerve is classified into anterior ION (AION) and posterior ION (PION) on the basis of differential blood supplies to the optic nerve. AION results in visual field loss, loss of visual acuity, and swelling of the optic disc. There is no disc swelling with PION, but it presents with acute visual acuity and field losses similar to AION. AION involves the optic disc and the scleral canal portion of the optic nerve, which is supplied by multiple posterior ciliary arteries arising out of the ophthalmic artery. The posterior ciliary arteries communicate with each other to form an incompetent anastomotic ring, the circle of Zinn and Hallen. This area may be a watershed zone, because in most people the circle of Zinn and Hallen is incompetent. The blood supply in this watershed zone can become insufficient under certain physiologic conditions, resulting in nerve injury and disc edema. Twelve of our 17 patients developed AION with optic disc edema. The rest of the patients developed PION. PION results from interference with the blood supply from other branches of the ophthalmic artery and the central retinal artery. This section of the optic nerve is most remote from its arterial supply; it is nourished primarily by easily compressible centripetal pial vessels.
In our study, we found that the smallest postoperative hemoglobin concentration, history of clinically severe vascular disease, and coronary angiogram within 48 hours of surgery were associated with blindness after CPB. Visual acuity and field losses were present in 100% of ION patients, and postoperative follow-up showed no improvement in these findings. The majority of ION patients without a history of clinically severe vascular disease, eight (89%) of nine, experienced a minimum postoperative hemoglobin value of <8.5 g/dL.
The incidence of spontaneous nonarteritic AION in Olmsted County, MN, has been estimated to be 10.2 per 100,000 people per year (13). The risk factors for nonarteritic AION in the nonsurgical population are high serum cholesterol, triglycerides, and glucose (14); hyperlipidemia, hyperfibrinogenemia, and smoking history (15); and diabetes (16). If the incidence rate were assumed to be 10.2 per 100,000 people per year, less than one case of spontaneous AION would be anticipated for a population of 27,915 patients observed for 30 days. Although patients requiring cardiac surgery are undoubtedly different from the general population, the observed rate of AION after cardiac surgery and CPB is much more frequent than the expected frequency of spontaneous AION. Therefore, it is unlikely that surgical AION is simply spontaneous AION that happens to occur immediately after cardiac surgery and CPB.
Many etiologic theories have been proposed for AION. A leading theory is that AION develops secondary to an interruption of oxygen supply to the optic nerve head anterior to the lamina cribrosa that may follow a critical reduction in blood supply or oxygen-carrying capacity. Several surgical and patient factors have been implicated as causing a reduction of blood flow in the posterior ciliary arteries; this will induce ischemia in the watershed zones and subsequently AION. Conditions such as intrinsic small vessel disease secondary to diabetes mellitus, hypertension, prolonged periods of hypotension, and vasospasm induced by large concentrations of circulating catecholamines or other vasoconstrictors are all possible contributing factors. Inflammation induced by CPB via inflammatory mediators with complement activation results in tissue edema, which may reduce perfusion. Anemia can conceivably result in a reduction in oxygen-carrying capacity and subsequent ischemia in the watershed zones. There is an association of AION with hemorrhage (17). Finally, patients with AION have a cup-to-disc ratio that is significantly lower than normal (18). The cup-to-disc ratio correlates anatomically with a narrow scleral canal. A narrow scleral canal may be more susceptible to a vicious cycle of ischemia resulting in edema, which results in further ischemia, although this is controversial.
Embolism is another, although less likely, etiologic possibility for ION that should also be considered. A prospective analysis of 421 patients undergoing coronary artery bypass grafting (CABG) detected a stroke in 5.2% (severe in 2%) (19). Prolonged encephalopathy occurred in 11.6% of patients but usually resolved before discharge. There were five patients with retinal infarctions and two other patients with optic nerve infarctions. Other embolic sources, such as atheromatous debris from the ascending aorta liberated during cross-clamping or left ventricular clots, were among other causes mentioned. Another prospective study of 312 patients who underwent CABG recorded retinal infarction in 17.3% and retinal emboli in 2.6% (20). Brain sections from eight patients and six dogs that died within a few days after open-heart surgery were studied for evidence of emboli (21). Because some of the lesions showed birefringence, the possibility of antifoam agents was mentioned. Embolism to the retina was also demonstrated by intraoperative fluorescein angiography in 10 patients (22). All patients had evidence of microvascular occlusions. Although this study could not determine the nature of the occlusions, the possibilities of vascular spasm, gaseous microbubbles, or particulate microemboli with material such as platelet-fibrin microaggregates were mentioned.
The association between ION and emboli is more difficult to prove. Horton (23) carefully examined two patients who had emboli in the cilioretinal artery. Because the short posterior ciliary arteries supply both the optic disc and the cilioretinal artery, it is theoretically possible for emboli to affect the optic disc with a resultant ION. AION with visible retinal emboli was demonstrated in three patients. Two had undergone CABG, and another had just undergone cardiac catheterization (7). Portnoy et al. (8) reported another case of visible retinal emboli and AION with associated choroidal nonperfusion, as shown by fluorescein angiography. In one study, embolism was histopathologically demonstrated in the short posterior ciliary artery supplying an infarcted optic disc (AION) (24).
In our study, diabetes mellitus, smoking, and hyperglycemia were not found to be significantly associated with developing blindness after CPB. These nonsignificant findings should be interpreted with caution, because these risk factors are present in many patients requiring cardiac surgery and, with only 17 cases, our case-control study had limited statistical power to detect such risk factors. Shapira et al. (2) also noted that these were not risk factors for cardiac surgical patients who developed AION. They noted an increased incidence of AION over a one-year period and performed a comparative study of 8 patients who developed AION out of 602 consecutive cardiac surgery patients. The development of AION was associated with a prolonged duration of CPB, lower hematocrit levels, greater perioperative weight gain, and the perioperative use of epinephrine and amrinone. They theorized that prolonged duration of CPB was associated with greater inflammation and higher levels of endogenous catecholamines. The combination of exogenous vasoactive drugs with endogenous catecholamines stimulated by CPB or low cardiac output syndrome and reduced hematocrit may have acted synergistically to produce vasoconstriction and ischemia in the posterior ciliary circulation, resulting in AION. There is a possibility that those patients in our study receiving exogenous vasoactive drugs with low cardiac output may have died before they were able to disclose their visual loss.
Myers et al. (6) reported on 37 patients who experienced visual loss after spine surgery secondary to AION, retinal artery occlusion, or cerebral ischemia. Twenty-eight of these patients were compared with matched controls without visual loss. The visual loss patients had longer durations of surgery and much larger blood loss, but the hematocrit and blood pressure values were nearly identical. Spinal surgery patients are very different from CPB patients.
Brown et al. (4) reported a case series of six patients having different types of surgery who developed ION. They noted that all of the patients had episodes of prolonged (
0.25 hours) hypotension (lowest mean blood pressure 68 mm Hg) and anemia (hemoglobin 8.0 g/dL). Although they had no control group for comparison, they concluded that the practice of allowing smaller acceptable hemoglobin concentrations in more extensive surgeries with an increased risk for excessive blood loss might predispose patients to ION.
The increased risk of ION associated with preoperative angiogram within 48 hours of CPB is difficult to explain, although transient cortical blindness has been reported after coronary angiography (25). We have documented a reduction in preoperative hemoglobin of 1.8 g/dL associated with coronary angiography performed <14 days before cardiac surgery (26). Surgenor et al. (27) noted that cardiac catheterization during the same hospitalization was 1 of the 10 factors significantly associated with RBC transfusions in CABG surgery patients. Another possibility is that preoperative angiogram within 48 hours of CPB may be a surrogate measure of worse patient condition.
There are several limitations of our study. Patients may have died or had severe postoperative cognitive dysfunction such that the diagnosis of visual loss could not be ascertained. Because of the rarity of this complication, we chose to collect data for a large number of potential risk factors (Table 1) and perform the analysis without adjusting for multiple comparisons. By doing so, we have chosen to control the per-comparison error rate rather than the per-experiment error rate. Given the number of comparisons performed, it is possible that one or more comparisons have been declared falsely significant. Furthermore, this study is limited by a small sample size that results in limited statistical power for detecting risk factors and prevents precision in estimating the OR for a given risk factor, as demonstrated by the width of the 95% confidence intervals presented in Table 1. This lack of precision should be considered when interpreting the increased risk associated with a given risk factor. For these reasons, the extent of conclusions we can make about postoperative hemoglobin concentration is limited. Although our study does not definitively demonstrate a causal relationship between small hemoglobin concentration and the occurrence of ION or a determination of an appropriate hemoglobin level for prevention of ION, our results support the conclusion that lower hemoglobin is associated with an increased risk of ION. The hemoglobin concentration of 8.5 g/dL, which we use as a cut-point in Table 4, is consistent with prior group and consensus conference recommendations and results of prior publications (28,29).
There have been several studies that suggest that maintenance of a smaller hemoglobin concentration in the intensive care unit was not harmful to the patient (30–32). We found a significant association between smaller postoperative hemoglobin concentration, history of clinically severe vascular disease, and a preoperative angiogram with visual loss after cardiac surgery. It is important to note that association does not prove causation, and the hemoglobin value of 8.5 g/dL is only a rough guideline that has no physiologic or medico-legal significance in absolute terms. Patients with clinically significant vascular disease history or preoperative angiogram may be at increased risk for ION after cardiac surgery, especially if the hemoglobin level remains low in the postoperative period.
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Acknowledgments |
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Supported by the Mayo Foundation for Medical Education and Research, Rochester, MN.
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References |
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