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Acute Ischemic Optic Neuropathy in Severe Preeclampsia
ACUTE ISCHEMIC OPTIC NEUROPATHY IN SEVERE PREECLAMPSIA Roy W. BECK, M.D., JOHN W. GAMEL, M.D., ROBIN J. WILLCOURT, M.D., AND GERALD BERMAN, M.D.
Louisville, Kentucky General examination disclosed obesity, hypertenRetinal changes have been observed in 40% to 100% of cases of preeclampsia. 1-9 sion (170/110 mm Hg), a uterus of 34-week gestational size, trace pedal edema, and 4+ proteinuria. Despite this prevalence, true amaurosis With the onset of seizures, a caesarean section was as a complication of preeclampsia of performed and a live male infant was delivered. The pregnancy is an unusual occurrence, and mother received diazoxide because of sustained increase of the blood pressure. Subsequently, the only isolated case reports have been pressure decreased and a transient Hushing of the published. In most of these cases, loss of optic disks with lessening of the vasoconstriction in vision was secondary to compromise of the disk vessels was observed. Results of an electroencephalogram and computed tomography of the the retinal arterial circulation. To our head were normal. knowledge, no one has reported blindOn the first day after delivery, her visual acuity ness as the result of impairment of the was finger counting at 4 feet in the right eye and 2 feet in the left eye. Results of an ophthalmoscopic blood supply to the prelaminar portion of examination were essentially unchanged from those the optic nerve head. at admission. CASE REPORT A 32-year-old, gravida 4, para 1, abortus 2, woman, 32 weeks pregnant, experienced loss of vision in both eyes. She reported that on the previous evening she had developed a severe, throbbing, right-sided headache, which had persisted throughout the night. Upon arising in the morning, she noted that her vision was blurred. Within 30 minutes visual loss progressed until she could barely perceive light. She had had no previous visual symptoms of any kind but had experienced mild preeclampsia during her pregnancy. Her medical history indicated preexisting untreated hypertension. At the time of initial examination, visual acuity was no light perception in each eye. Ophthalmoscopic examination disclosed chalky-white optic disks with no vessels evident within the substance of the nerve heads. Overlying the optic disks were subtle changes in the vitreous suggestive of a feathery opacification of the posterior aspect of Cloquet's canal (Fig. 1). The retinal arterioles were mildly attenuated but there were no focal spasms. Other findings were unremarkable.
From the Department of Ophthalmology (Drs. Beck, Gamel, and Berman) and the Department of Obstetrics and Gynecology (Dr. Willcourt), University of Louisville School of Medicine, Louisville, Kentucky. This study was supported in part by a grant from the Society to Prevent Blindness, Inc. Reprint requests to John W. Gamel, M. D., 301 E. Walnut St., Louisville, KY 40202. 342
By the third day after delivery, visual acuity had improved to 617.5 (20/25) in each eye. There was only a slight return of color to the optic disks, and the retinal vessels remained mildly and diffusely constricted. Three weeks after delivery, her visual acuity was 616 (20/20) in each eye and there was a partial return of color to the optic disks with persistent slight arteriolar narrowing. We also noted retinal striae in the papillomacular area for the first time (Fig. 2). Two months after delivery, her visual field and color perception were normal in both eyes. DISCUSSION
Retinal changes occurring in preeclampsia were first described by von Graefe in 1855. 10 Most of these changes involve the retinal arterial vasculature, with spasms being the most common finding. Duke-Elder" divided the retinal changes into three stages: Stage 1, Arteriolar spasms; Stage 2, Organic changes in vessels; Stage 3, Edema, hemorrhage, and damage to extravascular tissues. Other ocular findings include retinal detachment'? and spasms of the conjunctival arteries. 11 Transient blindness has been reported in 1% to 3% of patients with eclampsia. 4,12 With early detection and current methods of treatment of preeclampsia, the present incidence is probably much
AMERICAN JOURNAL OF OPHTHALMOLOGY 90:342--346, 1980
VOL. 90, NO.3
OPTIC NEUROPATHY AND PREECLAMPSIA
343
Fig. I (Beck and associates). Fundi of right eye (left) and left eye (right) at first examination.
lower. Only a few case reports of blindness lasting longer than a few minutes have been published. All of these cases were associated with marked spasm of the retinal vessels. Gandhi, Ghosh, and Pillari" described a 20-year-old woman with preeclampsia whose blindness resulted from severe spasms of the retinal arterioles with
marked retinal edema. Within five days visual acuity returned to normal. Matthew, Rajani, and Culati" reported three cases of visual loss secondary to preeclampsia. In two of these patients the most prominent ocular finding was retinal vasospasm; the results of the ophthalmoscopic examination were not noted in the third patient. Radford and Dow 15 report-
Fig. 2 (Beck and associates). Fundi of right eye (left) and left eye (right) three weeks after delivery.
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ed a case of transitory blindness occurring in an eclamptic patient as the result of marked spasm of the retinal vessels. Carpenter, Kava, and Plotkin" described a 22-year-old woman with preeclampsia who developed permanent blindness in association with severe compromise of the central retinal artery circulation. Treatment with intravenously administered papaverine, anticoagulants, and a stellate ganglion block did not alter the course. Sommerville-Large! reported the case of a 26-year-old woman with preeclampsia who developed total blindness in both eyes with spasm of the retinal arterioles, marked edema of the retina and disks, scattered hemorrhages and exudates, and small retinal detachments in both eyes. Bocev" reported two cases of complete visual loss lasting several days in patients with preeclampsia whose fundi showed spasm of the retinal arterioles. Ingiulla" described four other cases of preeclampsia in which amaurosis resulted primarily from spasm of the retinal vessels. In one of these cases retrobulbar injection of procaine HCI (Novocain) was effective in restoring visual acuity, whereas in two of the others intravenously administered procaine HCI had a beneficial effect. In each case, visual acuity completely returned to normal. In all of the preceding reports visual loss could be explained on the basis of severe impairment of the vascular circulation of the retina. Skenderovic and Pestelek" and Kelly20 each described a case of transitory blindness occurring in the presence of optic disk pallor and retinal vascular changes. Both of these cases were presented from the obstetrical standpoint, however, with only cursory reference to ophthalmologic findings; thus, no conclusions about the origin of the amaurosis can be drawn. Cases of blindness occurring with normal fundi have also been reported in association with preeclampsia. 19,21 In some of these
SEPTEMBER, 1980
cases loss of vision has been attributed to occipital lobe ischemia or hysteria. 4,12,16,22 Dieckman" suggested that an occipital lobe disturbance is the usual origin of amaurosis occurring in preeclampsia. In our patient, results of computed tomography of the brain were normal, making this an unlikely possibility. To our knowledge, no documented reports exist in which retinal vascular changes were minimal and profound pallor of the optic disk strongly supported acute ischemic optic neuropathy as the primary cause of blindness in a patient with preeclampsia. The only similar reported case, to our knowledge, was a patient with acute intermittent porphyria. es In patients with porphyria, spasms have been observed in the retinal vessels and, on occasion, generalized angiospastic activity throughout the body has been noted. 24,25 As in preeclampsia, the vasospasms may be secondary to a toxic or biochemical defect, although no specific mechanism has been identified. za In this reported case of porphyria, blindness apparently resulted from ischemic optic neuropathy in a fashion similar to our case. The pathophysiology of selective ischemia of the optic nerve head in preeclampsia is speculative. The blood supplies of the retina and optic disk have been shown experimentally to be distinct. Hayreh.P' Ernest and Potts;" and others have demonstrated in monkeys and humans that the prelaminar optic nerve head receives its blood supply from the posterior ciliary circulation and not from the central retinal artery or its branches. Thus, there is an anatomic basis for selective ischemia of the optic disk. However, the branches of the posterior ciliary artery from the peripapillary choroid and the circle of Zinn, which supply the nerve head, are currently thought to be devoid of musculature within their walls. Thus, vasospasm is an unlikely mecha-
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OPTIC NEUROPATHY AND PREECLAMPSIA
nism for hypoxia in this region. If the short posterior ciliary arteries themselves were in vasospasm, changes in the choroid and outer retinal layers would be expected; yet these were not observed clinically. Conversely, Ernest and Potts 27 have shown in rhesus monkeys that the intravascular pressure in the posterior ciliary circulation to the optic disk is lower than the intravascular pressure in the central retinal artery or its branches. Thus, generalized vasoconstriction in the posterior ciliary and retinal circulations might cause decreased circulation to the prelaminar portion of the optic nerve because of the effective lowering of perfusion pressure in this region by intraocular pressure, while the retinal circulation remained relatively intact. Additionally, a decrease in posterior ciliary circulation to the choroid may have been clinically unapparent. This appears to be the most logical physiologic basis for the events observed in this patient. Although the rapid onset of optic disk pallor in association with severe visual loss may result from acute inflammation, our patient had no inflammatory signs of the optic nerve head. Furthermore, vasospasm is the hallmark of preeclampsia, and the acute infiltration of nerve tissue with inflammatory cells in this clinical setting is extremely unlikely. Thus, we believe selective ischemia of the optic nerve head was the most likely cause of this patient's visual loss and may, indeed, be a more common cause of blindness in preeclamptic patients than has been previously recognized. In some patients, the presence of such changes in the optic nerve may be obscured by the more spectacular and widely reported spasms of the central retinal artery. We were unable to determine precisely the length of time during which our patient was totally blind, but this episode apparently lasted several hours. Com-
345
plete recovery following such an episode is difficult to explain, given our knowledge of the reaction of the central nervous tissue to hypoxia, yet a review of published reports discloses several cases of similar recovery after several hours or even days of complete blindness in association with preeclampsia. The transient flushing of the optic nerve heads observed after delivery is interesting. The role of diazoxide in this vasodilation and in restoration of vision cannot be evaluated on the basis of this single case. SUMMARY
A 32-year-old woman developed bilateral blindness along with severe preeclampsia of pregnancy. Ophthalmoscopic examination disclosed chalky-white optic disks with only minimal changes in the retinal vasculature. After caesarean section, the preeclampsia improved, and complete return of visual acuity occurred during a three-day period. Blindness has rarely been reported as a complication of preeclampsia. In almost all cases it has been associated with severe compromise of the retinal vasculature. Conversely, the ophthalmoscopic findings in our case strongly support acute ischemic optic neuropathy as the cause of blindness. REFERENCES 1. Doderlein, G.: EPH-Gestose und Augenhinterground. Klin. Montasbi. Augenheilkd. 171:896, 1977. 2. Sadowsky, A., Serr, D. M., and Landau, J.: Retinal changes and fetal prognosis in the toxemias of pregnancy. Obstet. Gynecoi. 8:426, 1956. 3. Kranenberg, E. W.: Retinopathia toxaemica gravidarum (in het bijzonder dialysis retinae als complicatie van zwangerschapstoxicose). Ned. Tijdschr. Geneeskd. 100:331, 1956. 4. Dieckmann, W. J.: Toxemia of Pregnancy, 2nd ed. St. Louis, C. V. Mosby, 1952, pp. 240-249. 5. Somerville-Large, L. B.: A case of permanent blindness due to toxemia of pregnancy. Br. J. Ophthalmol. 34:431, 1950. 6. Hallum, A. V.: Changes in retinal arterioles associated with the hypertensions of pregnancy. Arch. Ophthalmol. 37:472, 1947.
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7. Gibson, G. G.: The clinical significance of the retinal changes in the hypertensive toxemias of pregnancy. Am. J. Ophthalmo!. 21:22, 1938. 8. Schultz, J. F., and O'Brien, C. S.: Retinal changes in hypertensive toxemia of pregnancy. A report of 47 cases. Am. J. Ophthalmo!. 21:767, 1938. 9. Wagener, H. P.: Arterioles of the retina in toxemia of pregnancy. J. A. M. A. 101:1380, 1933. 10. Duke-Elder, S., and Dobree, J. H.: Diseases of the Retina. In Duke-Elder, S. (ed.): System of Ophthalmology, vol, 10. St. Louis, C. V. Mosby, 1967, pp. 350-356. 11. Landesman, R, Douglas, R G., and Holze, E.: The bulbar conjunctival vascular bed in the toxemias of pregnancy. Am. J. Obstet. Gyneco!. 68:170, 1954. 12. Hellman, L. M., and Pritchard, J. A.: Williams' Obstetrics, 14th ed. New York, AppletonCentury-Crofts, 1971, pp. 685-747. 13. Gandhi, J., Ghosh, S., and Pillari, V. T.: Blindness and retinal changes with preeclamptic toxemia. N. Y. State J. Med. 78:1930, 1978. 14. Matthew, M., Rajani, C. K., and Gulati, N.: Amaurosis in toxemia of pregnancy. Indian J. Ophthalmo!. 23:25, 1975. 15. Radford, A. J., and Dow, R: Amaurosis in pregnancy. Aust. N. Z. J. Obstet. Gynaeco!. 4:35, 1964. 16. Carpenter, F., Kava, H. L., and Plotkin, D.: The development of total blindness as a complication of pregnancy. Am. J. Obstet. Gyneco!. 66:641, 1953.
SEPTEMBER, 1980
17. Bocev, J.: Povodom dva slucaja amauroze kod preeklampsije u trudnoci. Jugos!. Gineko!. Opstet. 16:391, 1976. 18. IngiulIa, W.: Su alcuni casi di amaurosi in gravidanza. Riv. Ostet. Gineco!. 4:287, 1949. 19. Skenderovic, S., and Pestelek, B.: Kasne gestoze komplicirane amaurozom. [ugosl. Ginekol. Opstet. 16:387, 1976. 20. Kelly, K. M.: An unusual case of amblyopia occurring at parturition. Med. J. Aust. 1:745, 1949. 21. Muxi-Olives, M.: Amaurosis en toxicosis gravidica, Acta Obstet. Gineco!. Hisp. Lusit. 3:235, 1968. 22. Wagener, H. P.: Lesions of the optic nerve and retina in pregnancy. J. A. M. A. 103:1910, 1932. 23. DeFrancisco, B. S., Savino, P. J., and Schatz, N. J.: Optic atrophy in acute intermittent porphyria. Am. J. Ophthalmo!. 87:221, 1979. 24. Wolter, J. R, and Clark, R L.: Ocular involvement in acute intermittent porphyria. Am. J. Ophthalmo!. 74:666, 1972. 25. Denny-Brown, D., and Sciarra, D.: Changes in the nervous system in acute porphyria. Brain 68:1, 1945. 26. Hayreh, S. S.: Blood supply of the optic nerve head and its role in optic atrophy, glaucoma, and edema of the optic nerve. Br. J. Ophthalmo!. 53:721, 1969. 27. Ernest, J. T., and Potts, A. M.: Pathophysiology of the distal portion of the optic nerve head. II. Vascular relationships. Am. J. Ophthalmo!. 66:380, 1968.
Louisville, Kentucky General examination disclosed obesity, hypertenRetinal changes have been observed in 40% to 100% of cases of preeclampsia. 1-9 sion (170/110 mm Hg), a uterus of 34-week gestational size, trace pedal edema, and 4+ proteinuria. Despite this prevalence, true amaurosis With the onset of seizures, a caesarean section was as a complication of preeclampsia of performed and a live male infant was delivered. The pregnancy is an unusual occurrence, and mother received diazoxide because of sustained increase of the blood pressure. Subsequently, the only isolated case reports have been pressure decreased and a transient Hushing of the published. In most of these cases, loss of optic disks with lessening of the vasoconstriction in vision was secondary to compromise of the disk vessels was observed. Results of an electroencephalogram and computed tomography of the the retinal arterial circulation. To our head were normal. knowledge, no one has reported blindOn the first day after delivery, her visual acuity ness as the result of impairment of the was finger counting at 4 feet in the right eye and 2 feet in the left eye. Results of an ophthalmoscopic blood supply to the prelaminar portion of examination were essentially unchanged from those the optic nerve head. at admission. CASE REPORT A 32-year-old, gravida 4, para 1, abortus 2, woman, 32 weeks pregnant, experienced loss of vision in both eyes. She reported that on the previous evening she had developed a severe, throbbing, right-sided headache, which had persisted throughout the night. Upon arising in the morning, she noted that her vision was blurred. Within 30 minutes visual loss progressed until she could barely perceive light. She had had no previous visual symptoms of any kind but had experienced mild preeclampsia during her pregnancy. Her medical history indicated preexisting untreated hypertension. At the time of initial examination, visual acuity was no light perception in each eye. Ophthalmoscopic examination disclosed chalky-white optic disks with no vessels evident within the substance of the nerve heads. Overlying the optic disks were subtle changes in the vitreous suggestive of a feathery opacification of the posterior aspect of Cloquet's canal (Fig. 1). The retinal arterioles were mildly attenuated but there were no focal spasms. Other findings were unremarkable.
From the Department of Ophthalmology (Drs. Beck, Gamel, and Berman) and the Department of Obstetrics and Gynecology (Dr. Willcourt), University of Louisville School of Medicine, Louisville, Kentucky. This study was supported in part by a grant from the Society to Prevent Blindness, Inc. Reprint requests to John W. Gamel, M. D., 301 E. Walnut St., Louisville, KY 40202. 342
By the third day after delivery, visual acuity had improved to 617.5 (20/25) in each eye. There was only a slight return of color to the optic disks, and the retinal vessels remained mildly and diffusely constricted. Three weeks after delivery, her visual acuity was 616 (20/20) in each eye and there was a partial return of color to the optic disks with persistent slight arteriolar narrowing. We also noted retinal striae in the papillomacular area for the first time (Fig. 2). Two months after delivery, her visual field and color perception were normal in both eyes. DISCUSSION
Retinal changes occurring in preeclampsia were first described by von Graefe in 1855. 10 Most of these changes involve the retinal arterial vasculature, with spasms being the most common finding. Duke-Elder" divided the retinal changes into three stages: Stage 1, Arteriolar spasms; Stage 2, Organic changes in vessels; Stage 3, Edema, hemorrhage, and damage to extravascular tissues. Other ocular findings include retinal detachment'? and spasms of the conjunctival arteries. 11 Transient blindness has been reported in 1% to 3% of patients with eclampsia. 4,12 With early detection and current methods of treatment of preeclampsia, the present incidence is probably much
AMERICAN JOURNAL OF OPHTHALMOLOGY 90:342--346, 1980
VOL. 90, NO.3
OPTIC NEUROPATHY AND PREECLAMPSIA
343
Fig. I (Beck and associates). Fundi of right eye (left) and left eye (right) at first examination.
lower. Only a few case reports of blindness lasting longer than a few minutes have been published. All of these cases were associated with marked spasm of the retinal vessels. Gandhi, Ghosh, and Pillari" described a 20-year-old woman with preeclampsia whose blindness resulted from severe spasms of the retinal arterioles with
marked retinal edema. Within five days visual acuity returned to normal. Matthew, Rajani, and Culati" reported three cases of visual loss secondary to preeclampsia. In two of these patients the most prominent ocular finding was retinal vasospasm; the results of the ophthalmoscopic examination were not noted in the third patient. Radford and Dow 15 report-
Fig. 2 (Beck and associates). Fundi of right eye (left) and left eye (right) three weeks after delivery.
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AMERICAN JOURNAL OF OPHTHALMOLOGY
ed a case of transitory blindness occurring in an eclamptic patient as the result of marked spasm of the retinal vessels. Carpenter, Kava, and Plotkin" described a 22-year-old woman with preeclampsia who developed permanent blindness in association with severe compromise of the central retinal artery circulation. Treatment with intravenously administered papaverine, anticoagulants, and a stellate ganglion block did not alter the course. Sommerville-Large! reported the case of a 26-year-old woman with preeclampsia who developed total blindness in both eyes with spasm of the retinal arterioles, marked edema of the retina and disks, scattered hemorrhages and exudates, and small retinal detachments in both eyes. Bocev" reported two cases of complete visual loss lasting several days in patients with preeclampsia whose fundi showed spasm of the retinal arterioles. Ingiulla" described four other cases of preeclampsia in which amaurosis resulted primarily from spasm of the retinal vessels. In one of these cases retrobulbar injection of procaine HCI (Novocain) was effective in restoring visual acuity, whereas in two of the others intravenously administered procaine HCI had a beneficial effect. In each case, visual acuity completely returned to normal. In all of the preceding reports visual loss could be explained on the basis of severe impairment of the vascular circulation of the retina. Skenderovic and Pestelek" and Kelly20 each described a case of transitory blindness occurring in the presence of optic disk pallor and retinal vascular changes. Both of these cases were presented from the obstetrical standpoint, however, with only cursory reference to ophthalmologic findings; thus, no conclusions about the origin of the amaurosis can be drawn. Cases of blindness occurring with normal fundi have also been reported in association with preeclampsia. 19,21 In some of these
SEPTEMBER, 1980
cases loss of vision has been attributed to occipital lobe ischemia or hysteria. 4,12,16,22 Dieckman" suggested that an occipital lobe disturbance is the usual origin of amaurosis occurring in preeclampsia. In our patient, results of computed tomography of the brain were normal, making this an unlikely possibility. To our knowledge, no documented reports exist in which retinal vascular changes were minimal and profound pallor of the optic disk strongly supported acute ischemic optic neuropathy as the primary cause of blindness in a patient with preeclampsia. The only similar reported case, to our knowledge, was a patient with acute intermittent porphyria. es In patients with porphyria, spasms have been observed in the retinal vessels and, on occasion, generalized angiospastic activity throughout the body has been noted. 24,25 As in preeclampsia, the vasospasms may be secondary to a toxic or biochemical defect, although no specific mechanism has been identified. za In this reported case of porphyria, blindness apparently resulted from ischemic optic neuropathy in a fashion similar to our case. The pathophysiology of selective ischemia of the optic nerve head in preeclampsia is speculative. The blood supplies of the retina and optic disk have been shown experimentally to be distinct. Hayreh.P' Ernest and Potts;" and others have demonstrated in monkeys and humans that the prelaminar optic nerve head receives its blood supply from the posterior ciliary circulation and not from the central retinal artery or its branches. Thus, there is an anatomic basis for selective ischemia of the optic disk. However, the branches of the posterior ciliary artery from the peripapillary choroid and the circle of Zinn, which supply the nerve head, are currently thought to be devoid of musculature within their walls. Thus, vasospasm is an unlikely mecha-
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OPTIC NEUROPATHY AND PREECLAMPSIA
nism for hypoxia in this region. If the short posterior ciliary arteries themselves were in vasospasm, changes in the choroid and outer retinal layers would be expected; yet these were not observed clinically. Conversely, Ernest and Potts 27 have shown in rhesus monkeys that the intravascular pressure in the posterior ciliary circulation to the optic disk is lower than the intravascular pressure in the central retinal artery or its branches. Thus, generalized vasoconstriction in the posterior ciliary and retinal circulations might cause decreased circulation to the prelaminar portion of the optic nerve because of the effective lowering of perfusion pressure in this region by intraocular pressure, while the retinal circulation remained relatively intact. Additionally, a decrease in posterior ciliary circulation to the choroid may have been clinically unapparent. This appears to be the most logical physiologic basis for the events observed in this patient. Although the rapid onset of optic disk pallor in association with severe visual loss may result from acute inflammation, our patient had no inflammatory signs of the optic nerve head. Furthermore, vasospasm is the hallmark of preeclampsia, and the acute infiltration of nerve tissue with inflammatory cells in this clinical setting is extremely unlikely. Thus, we believe selective ischemia of the optic nerve head was the most likely cause of this patient's visual loss and may, indeed, be a more common cause of blindness in preeclamptic patients than has been previously recognized. In some patients, the presence of such changes in the optic nerve may be obscured by the more spectacular and widely reported spasms of the central retinal artery. We were unable to determine precisely the length of time during which our patient was totally blind, but this episode apparently lasted several hours. Com-
345
plete recovery following such an episode is difficult to explain, given our knowledge of the reaction of the central nervous tissue to hypoxia, yet a review of published reports discloses several cases of similar recovery after several hours or even days of complete blindness in association with preeclampsia. The transient flushing of the optic nerve heads observed after delivery is interesting. The role of diazoxide in this vasodilation and in restoration of vision cannot be evaluated on the basis of this single case. SUMMARY
A 32-year-old woman developed bilateral blindness along with severe preeclampsia of pregnancy. Ophthalmoscopic examination disclosed chalky-white optic disks with only minimal changes in the retinal vasculature. After caesarean section, the preeclampsia improved, and complete return of visual acuity occurred during a three-day period. Blindness has rarely been reported as a complication of preeclampsia. In almost all cases it has been associated with severe compromise of the retinal vasculature. Conversely, the ophthalmoscopic findings in our case strongly support acute ischemic optic neuropathy as the cause of blindness. REFERENCES 1. Doderlein, G.: EPH-Gestose und Augenhinterground. Klin. Montasbi. Augenheilkd. 171:896, 1977. 2. Sadowsky, A., Serr, D. M., and Landau, J.: Retinal changes and fetal prognosis in the toxemias of pregnancy. Obstet. Gynecoi. 8:426, 1956. 3. Kranenberg, E. W.: Retinopathia toxaemica gravidarum (in het bijzonder dialysis retinae als complicatie van zwangerschapstoxicose). Ned. Tijdschr. Geneeskd. 100:331, 1956. 4. Dieckmann, W. J.: Toxemia of Pregnancy, 2nd ed. St. Louis, C. V. Mosby, 1952, pp. 240-249. 5. Somerville-Large, L. B.: A case of permanent blindness due to toxemia of pregnancy. Br. J. Ophthalmol. 34:431, 1950. 6. Hallum, A. V.: Changes in retinal arterioles associated with the hypertensions of pregnancy. Arch. Ophthalmol. 37:472, 1947.
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AMERICAN JOURNAL OF OPHTHALMOLOGY
7. Gibson, G. G.: The clinical significance of the retinal changes in the hypertensive toxemias of pregnancy. Am. J. Ophthalmo!. 21:22, 1938. 8. Schultz, J. F., and O'Brien, C. S.: Retinal changes in hypertensive toxemia of pregnancy. A report of 47 cases. Am. J. Ophthalmo!. 21:767, 1938. 9. Wagener, H. P.: Arterioles of the retina in toxemia of pregnancy. J. A. M. A. 101:1380, 1933. 10. Duke-Elder, S., and Dobree, J. H.: Diseases of the Retina. In Duke-Elder, S. (ed.): System of Ophthalmology, vol, 10. St. Louis, C. V. Mosby, 1967, pp. 350-356. 11. Landesman, R, Douglas, R G., and Holze, E.: The bulbar conjunctival vascular bed in the toxemias of pregnancy. Am. J. Obstet. Gyneco!. 68:170, 1954. 12. Hellman, L. M., and Pritchard, J. A.: Williams' Obstetrics, 14th ed. New York, AppletonCentury-Crofts, 1971, pp. 685-747. 13. Gandhi, J., Ghosh, S., and Pillari, V. T.: Blindness and retinal changes with preeclamptic toxemia. N. Y. State J. Med. 78:1930, 1978. 14. Matthew, M., Rajani, C. K., and Gulati, N.: Amaurosis in toxemia of pregnancy. Indian J. Ophthalmo!. 23:25, 1975. 15. Radford, A. J., and Dow, R: Amaurosis in pregnancy. Aust. N. Z. J. Obstet. Gynaeco!. 4:35, 1964. 16. Carpenter, F., Kava, H. L., and Plotkin, D.: The development of total blindness as a complication of pregnancy. Am. J. Obstet. Gyneco!. 66:641, 1953.
SEPTEMBER, 1980
17. Bocev, J.: Povodom dva slucaja amauroze kod preeklampsije u trudnoci. Jugos!. Gineko!. Opstet. 16:391, 1976. 18. IngiulIa, W.: Su alcuni casi di amaurosi in gravidanza. Riv. Ostet. Gineco!. 4:287, 1949. 19. Skenderovic, S., and Pestelek, B.: Kasne gestoze komplicirane amaurozom. [ugosl. Ginekol. Opstet. 16:387, 1976. 20. Kelly, K. M.: An unusual case of amblyopia occurring at parturition. Med. J. Aust. 1:745, 1949. 21. Muxi-Olives, M.: Amaurosis en toxicosis gravidica, Acta Obstet. Gineco!. Hisp. Lusit. 3:235, 1968. 22. Wagener, H. P.: Lesions of the optic nerve and retina in pregnancy. J. A. M. A. 103:1910, 1932. 23. DeFrancisco, B. S., Savino, P. J., and Schatz, N. J.: Optic atrophy in acute intermittent porphyria. Am. J. Ophthalmo!. 87:221, 1979. 24. Wolter, J. R, and Clark, R L.: Ocular involvement in acute intermittent porphyria. Am. J. Ophthalmo!. 74:666, 1972. 25. Denny-Brown, D., and Sciarra, D.: Changes in the nervous system in acute porphyria. Brain 68:1, 1945. 26. Hayreh, S. S.: Blood supply of the optic nerve head and its role in optic atrophy, glaucoma, and edema of the optic nerve. Br. J. Ophthalmo!. 53:721, 1969. 27. Ernest, J. T., and Potts, A. M.: Pathophysiology of the distal portion of the optic nerve head. II. Vascular relationships. Am. J. Ophthalmo!. 66:380, 1968.