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Show ]. Clin. Neuro-ophthalmol. 3: 239-244, 1983. Ischemic Optic Neuropathy Following General Surgical Procedures SCOTT L. JABEN, M.D. JOEL S. GLASER, M.D. MARK DAILY, M.D. Abstract We report three patients who developed symptomatic visual loss following uncomplicated general surgical procedures. All three patients had ocular examinations and visual field deficits consistent with acute ischemic optic neuropathy. All three had hemoglobin levels below normal limits at the onset of visual symptoms. However, none of the patients suffered intraoperative or postoperative hemorrhaging. Ischemic optic neuropathy may occur following general surgical procedures, not complicated by significant hemorrhaging. Introduction Acute visual loss following profound hemorrhage is a well-recognized entity.I-4 Both nonsurgical and surgical etiologies for hemorrhage have resulted in this condition.s This paper documents three cases of acute ischemic optic neuropathy following general surgical procedures where there was no intraoperative or postoperative hemorrhage. Case Reports Case 1 A 56-year-old man with unstable angina underwent coronary artery bypass surgery on November 11, 1975. Past medical history included hypertension, cigarette smoking, and an acute myocardial infarction in August 1975. Surgery was uncomplicated as verified by review of the operative report and anesthesia record. The preoperative hemoglobin level was 14.0 g%. Immediately postoperatively, the hemoglobin level had fallen to 10.0 g%. Over the ensuing 48 hours, the hemoglobin level fell to 7.8 g%. On the third postoperative day a hypotensive event was documented, and the lowest From the From the Bascom Palmer Eye Institute, Department of Ophthalmology, University of Miami School of Medicine, Miami, Florida, December 1983 blood pressure recorded being 70/50. At no time were there any other signs of hemorrhage symptoms. On the fourth postopertive day the patient complained of blurred vision in both eyes, and he was referred to the opthalmology service. Initial eye examination revealed visual acuities of 20/400, right eye and 2/200, left eye. Visual field examination with a Goldmann perimeter showed bilateral altitudinal defects. The pupils were briskly and equally reactive to light, and demonstrated no afferent pupillary defect. Ocular motility and slit lamp examination of the anterior segments were normal. Tension by applanation was 19 mm right, 17 mm left. Dilated fundus examination revealed diffuse, pale swelling of both optic nerve heads. The maculae, peripheral retina, and retinal vasculature were not abnormal. The patient underwent whole blood transfusion over the following 48 hours to a hemoglobin level of 11.0 g%. Follow-up eye examination 2 months later revealed visual acuities of 20/20, right eye and 20/30, left eye. Repeat visual field testing showed a dense inferior arcuate defect in the right field, and superior and inferior nerve fiber bundle defects in the left, resulting in a temporal and central island of vision (Fig. 1). Dilated fundus examination demonstrated diffuse pallor of the optic nerve heads and retinal arteriolar attenuation (Figs. 2a and 2b). Case 2 A 44-year-old man underwent coronary artery bypass surgery on June 6, 1977. The patient had a history of hypertension, cigarette smoking, and a subendocardial myocardial infarction in January 1977. He experienced unstable angina and recurrent premature ventricular contractions. Surgery was entirely uneventful. Preoperative hemoglobin level was 12.8 g% 1 day prior to surgery. The immediate postoperative hemoglobin level was 239 Ischemic Optic Neuropathy Figure 1. Case 1. Goldmann fields show dense inferior"altitudinal" defect on right, and dense arcuate defects on left. 10.3 g%. Over the ensuing 96 hours, the hemoglobin level gradually decreased to 6.8 g%. There was no evidence of hemorrhage or hypotension. On the fourth postoperative day the patient complained of a visual field defect in the left eye, and he was referred to the ophthalmology service. Examination on June 8 revealed visual acuities of 20/40, right eye and 20/30, left eye. The patient had previously been told of "amblyopia" of the right eye. Visual field testing with a Goldmann perimeter revealed an inferior altitudinal defect in the left field (Fig. 3). Pupil examination showed a left afferent pupillary defect. Motility examination and slit lamp examination of the anterior segments were normal. Tension by applanation was 14 mm right and 12 mm left. The optic nerve head on the right was unremarkable, and the left was diffusely swollen (Fig. 4). A diagnosis of acute ischemic optic neuropathy was made and the patient underwent whole blood transfusion over the next 48 hours. The hemoglobin level on June 11 was 13.0 g%. Follow-up eye examination 2 weeks later revealed no subsequent changes. Case 3 A 16-year-old girl with congenital renal hypoplasia underwent renal transplantation in 1973. This was unsuccessful; in 1975, she was begun on hemodialysis. The patient was chronically anemic with a hemoglobin level usually in the range of 7- 240 8.0 g%. She developed hypercalcemia and, in August 1977, she underwent a total parathyroidectomy. Surgery was uncomplicated with no intraoperative hypotension. The first recorded recovery room blood pressure was 100/45. There were no signs or symptoms of hemorrhage in the postoperative period. Preoperative and postoperative hemoglobin levels were in the 7-8.0 g% range. On the third postoperative day the patient complained of blurred vision in both eyes. The patient is said to have had bilateral altitudinal visual fields defects on a eye examination soon after her discharge in August 1977, but the records of this finding were incomplete. Examination in our clinic in March 1979, 11h years following surgery and the onset of visual symptoms, disclosed that there had been no subjective change in the patient's visual status. Visual acuities were 20/30, right eye and 20/15, left eye. The pupils were sluggishly, but equally, reactive. Visual field examination with a Goldmann perimeter revealed a dense right inferior altitudinal defect and a dense left superior altitudinal defect (Fig. 5). Motility examination and slit lamp examination of the anterior segments were normal. Tension by applanation was 13 mm right and 13 mm left. Dilated fundus examination revealed altitudinal pallor and atrophy of the optic nerve heads in both eyes corresponding to the visual field deficits described above (Figs. 6a and 6b ). Journal of Clinical Neuro-ophthalmology Jaben, Glaser, Daily Figures 2a and 2b. Case 1 (a, b). The optic nerves in both eyes show diffuse pallor and arterioi.Jr attenuation. Discussion In 1950, Hollenhorst and Wagener) reviewed 198 cases of 1055 of vision after "distant hemorrhage." They described patients over a wide age range who suffered usually bilateral visual loss following systemic hemorrhages. Most often the hemorrhages were small in amount, but recurrent. December 1983 Such events were rarely seen in healthy individuals after one hemorrhage only, or following trauma. Fifty percent of patients were permanently blind while 10-12% recovered visual function. The pathogenesis was unclear. The most common fundus picture was an ischemic optic neuropathy with pale, edematous optic nerve heads and attenuated retinal arterioles. Optic atrophy subsequently de- 241 Ischemic Optic Neuropathy l~,r 195' Figure 3. Case 2. Goldmann fields show dense inferior altitudinal defect on left. Figure 4. Case 2. Left optic nerve is diffusely swollen. The right was normal. veloped in these eyes. The gastrointestinal tract and uterus were the most common sites of origin of the hemorrhages. The onset of visual symptoms occurred during or immediately after the hemorrhage in 20%, in the first 12-48 hours in 20%, and in the 3-10 day period in 40%. In 1969, Chisholm5 reported three cases of acute visual loss following surgical procedures; specifi- 242 cally, thoracotomy, valvular heart surgery, and cholecystectomy. All of these procedures were complicated by hemorrhage and hypotension. The visual acuity was markedly depressed in all six eyes. The fundus findings included optic nerve edema and adjacent retinal edema in four of the eyes and optic atrophy in the remaining two eyes. Function returned to 20/20 in four of the eyes of two patients. The third patient, who was the only one to receive transfusions of whole blood, retained 20/40 vision in one eye, but had no return in his second eye. Recently, Sweeney et al.6 have reported seven cases of ischemic optic neuropathy as a complication of cardiopulmonary bypass surgery. Five patients experienced loss of vision reported immediately upon waking from anesthesia or within 48 hours. One patient was not alert until the fourth postoperative day, at which point vision was defective, and one patient had no visual complaints until the seventh day. Four of these patients experienced significant hemorrhagic hypotension during bypass surgery, and one experienced postoperative thoracic hemorrhage and hypotension. In all, the clinical syndrome of ischemic optic neuropathy was typical; three patients had bilateral field defects and four had unilateral, but visual acuities were not provided. Hypertension and diabetes were considered predisposing factors, but blood loss with hypotension and shock were considered the immediate cause of optic nerve infarction. No mention was made of hemoglobin levels. Neither Journal of Clinical Neuro-ophthalmology Jaben, Glaser, Daily Figure 5. Case 3. Goldmann fields reveal an inferior'" altitudinal'" defect on the right, and a superior'"altitudinal'" defect in the left. (a J Figures 6a and 6b. Case 3 (a, b). Optic nerves were segmentally pale, corresponding to the visual field defects seen in fig. 5. the effect of transfusion nor ultimate visual outcome was noted. We believe that the three cases recorded in the present report represent visual loss due to acute ischemic optic neuropathy. These patients had several common features. Onset of symptoms oc- December 1983 curred 3-4 days after a surgical procedure. Two cases had bilateral visual loss and all three had systemic illnesses. Fortunately, the involved eyes recovered to good levels of central visual acuity. The major exception that distinguishes our cases from those described previously is the lack of any 243 Ischemic Optic Neuropathy internal or external hemorrhage. However, all three suffered from conditions characterized by decreased oxygen carrying capacity. In the cases of coronary artery bypass surgery, there was a dramatic diminution postoperatively of the hemoglobin levels. Hemodilution and accelerated hemolysis, both resulting in lowered hemoglobin levels, are well-recognized phenomena following extracorporeal circulation procedures.7 In case 3, the patient had the anemia typical of chronic renal failure. Hayreh has provided evidence that adequate perfusion pressure to the posterior ciliary arteries is necessary for the nourishment of the anterior portion of the optic nerve.s This perfusion pressure is determined by the mean arterial blood pressure, minus the intraocular tension. We believe that decreased perfusion pressure coupled with the limited oxygen-carrying capacity of the blood led to the development of a peculiar variety of anterior ischemic optic neuropathy. There was evidence of decreased mean arterial blood pressure in two of our patients. The reversal of visual defects documented in case 1, and in those patients reported by Chisolm,15 is remarkable and largely atypical for anterior ischemic optic neuropathy.9 It is unclear if a different pathophysiologic mechanism need be invoked to explain the clinical course of these patients. Hayreh has theorized that neuronal axoplasmic flow and impulse conduction may be reduced by ischemia alone, and that these defects may be restored if the process has not progressed to full-blown infarction. lO Indeed, one of our two patients treated with whole blood transfusion had a favorable response with impressive return of visual function, in addition to one of Chisholm's patients.5 Therefore, whole blood replacement may be helpful in preserving the visual pathways. In summary, we have presented three cases of acute ischemic optic neuropathy following surgical 244 procedures that were not complicated by systemic hemorrhage. Treatment in two cases where the hemoglobin levels had dropped acutely consisted of whole blood transfusion. Visual prognosis was unexpectedly good. The phenomenon of atypical ischemic optic neuropathy following surgical procedures should be recalled in the situation of acute visual loss during the immediate postsurgical period, and whole blood transfusion may be beneficial to the visual outcome. References 1. HoJlenhorst, R.W., and Wagener, H.P.: Loss of vision after distant hemorrhage. Am. f. Med. 219: 209218, 1950. 2. Lazaro, E,J., Cinotti, A.A, Eichler, P.N., and Khawager, A.A.: Amaurosis due to massive gastrointestinal hemorrhage. Am. f. Gastroenterol. 55: 50-53, 1971. 3. Harren, AT.: Blindness following gastrointestinal hemorrhage. Ann. Intern. Med. 36: 882-888, 1952. 4. Drance, 5.]., Morgan, R. W., and Sweeney, V.P.: Shock induced optic neuropathy. N. Engl. j. Med. 288: 392-395, 1973. 5. Chisholm, LA: Optic neuropathy of recurrent blood loss. Br. j. Ophthalmol. 53: 289, 1969. 6. Sweeney, P.]., Breuer, AC., Selhorst, ].B., et al.: Ischemic optic neuropathy: A complication of cardiopulmonary bypass surgery. Neurology 32: 560562,1982. 7. Schwartz, S.I.: Textbook of Surgery (3rd ed.). McGraw-Hili Book Co., New York, 1979, p. 823. 8. Hayreh, 5.5.: Anterior ischemic optic neuropathy. I Terminology and pathogenesis. Br. j. Ophthalmol. 58: 955, 1974. 9. Boghen, D.R., and Glaser, J.S.: Ischemic optic neuropathy. Brain 98: 689-708, 1975. 10. Hayreh, S.5.: Anterior ischemic optic neuropathy. Arch. Ophthalmol. 99: 1030, 1981. Write for reprints to: Joel S. Giaser, M.D., Bascom Palmer Eye Institute, P.O. Box 016880, Miami, Florida 33101. Journal of Clinical Neuro-ophthalmology |
