- Email: [email protected]
Cortical blindness in severe preeclampsia: computed tomography, magnetic resonance imaging, and single-photon-emission computed tomography findings
with ultrasound, ultrafast MRI allowed more precise antenatal brain characterization and spinal cord anomalies in our subject, which shows how ultrafast MRI can help antenatal diagnosis and counseling.
References
8. Hubbard AM, Crombleholme TM, Adzick NS. Prenatal MRI evaluation of giant neck masses in preparation for the fetal exit procedure. Am J Perinatol 1998;15:253–7. 9. Levine D, Barnes PD, Madsen JR, Abbott J, Wong GP, Hulka C, et al. Fetal CNS anomalies revealed on ultrafast MR imaging. AJR Am J Roentgenol 1999;172:813– 8.
Address reprint requests to:
1. Hoyle RM. Surgical separation of conjoined twins. Surg Gynecol Obstet 1990;170:549 – 62. 2. Spitz L. Conjoined twins. Br J Surg 1996;83:1028 –30. 3. Spencer RA. Anatomic description of conjoined twins: A plea for standardized terminology. J Pediatr Surg 1996;31:941– 4. 4. Mansfield P, Stehling M, Ordidge R, Coxon R, Chapman B, Blamire A, et al. Echo planar imaging of the human fetus in utero at 0.5 T. Br J Radiol 1990;63:833– 41. 5. Huppert BJ, Brandt KR, Ramin KD, King BF. Single-shot fast spin echo MR imaging of the fetus: A pictorial essay. Radiographics 1999;S215–27. 6. Amin RS, Nikolaidis P, Kawashima A, Kramer LA, Ernst RD. Normal anatomy of the fetus at MR imaging. Radiographics 1999; S201–14. 7. Quinn T, Hubbard A, Adzick N. Prenatal magnetic resonance imaging enhances fetal diagnosis. J Pediatr Surg 1998;33:553– 8.
Holly L. Casele, MD Evanston Hospital Maternal Fetal Medicine 2650 Ridge Suite 1600 Evanston, IL 60201 E-mail: [email protected]
Cortical blindness in severe preeclampsia: Computed tomography, magnetic resonance imaging, and singlephoton-emission computed tomography findings
head computed tomography and magnetic resonance imaging scans. Follow-up neuroimaging studies 2 weeks later, by which time the patient’s visual acuity had returned to normal, showed complete resolution of radiologic abnormalities. Conclusion: Neuroimaging studies in a woman with severe postpartum preeclampsia complicated by reversible cortical blindness showed that blindness resulted from vasogenic (hydrostatic) cerebral edema and not cerebral vasospasm. (Obstet Gynecol 2000;95:1017–9. © 2000 by The American College of Obstetricians and Gynecologists.)
Katia M. Apollon, MD, Julian N. Robinson, MD, Richard B. Schwartz, MD, PhD, AND Errol R. Norwitz, MD, PhD Background: Cortical blindness is a complication of severe preeclampsia, but it is unclear whether it results from cerebral vasospasm and ischemic injury or vasogenic (hydrostatic) edema due to increased capillary permeability. Case: Reversible cortical blindness in a 33-year-old gravida 2, para 1, with severe postpartum preeclampsia after evacuation of a partial molar pregnancy at 19 weeks’ gestation is presented. Initial neuroimaging studies showed hyperperfusion on head single-photon-emission computed tomography scan, which corresponded with lesions found on
Received November 5, 1999. Received in revised form January 19, 2000. Accepted February 1, 2000.
Copyright © 2000 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
The ophthalmologic manifestations of preeclampsia include retinal detachment, retinal arteriolar vasospasm, thrombosis of the central retinal arteries, and reversible cortical blindness.1,2 However, the pathophysiology of cortical blindness is debated to be from cerebral vasospasm and ischemic injury3,4 or vasogenic edema caused by increased capillary permeability.5,6 We present a case of severe postpartum preeclampsia complicated by reversible cortical blindness after evacuation of a partial molar pregnancy at 19 weeks’ gestation. Neuroimaging studies showed that the cortical blindness resulted from vasogenic edema with selective hyperperfusion of the posterior cerebral circulation. Case
From the Departments of Obstetrics and Gynecology and Radiology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts. Supported by the Reproductive Scientist Development Program through National Institutes of Health (grant 5K12-HD00849) and the Association of Professors of Gynecology and Obstetrics (to ERN).
VOL. 95, NO. 6, PART 2, JUNE 2000
A 33-year-old woman, gravida 2, para 1, had abdominal ultrasound at 18 weeks’ gestation that found a probable partial molar pregnancy with a single structurally anomalous female fetus. Antenatal course was complicated by intractable nausea and vomiting. Results of pertinent laboratory tests were
0029-7844/00/$20.00 PII S0029-7844(00)00878-4
1017
Figure 1. (A) Axial T2-weighted MRI (3000 ms/80 ms, TR/TE) shows increased T2 signal (arrows) in the peripheral subcortical white matter in the right occipital lobe. (B) Simultaneous axial technetium-99m HMPAO single-photon-emission computed tomographic image shows increased cerebral perfusion (arrows) in the hyperemia in the right posterior temporal cortex, right lateral occipital cortex, and inferior parietal cortex. (C) Follow-up neuroimaging of the woman 8 days after discharge shows resolution of T2-bright signal on MRI and (D) regional hyperperfusion on single-photon-emission computed tomographic image.
-hCG 1,263,520 mIU/mL and TSH 0.44 mU/L (normal range, 0.2– 0.40 mU/L). An uncomplicated dilation and evacuation was done with an autopsy that confirmed the multiple fetal anomalies detected by ultrasound and a fetal karyotype of 69,XXX, consistent with a partial molar pregnancy. Twelve hours after discharge, severe right-sided headache, photophobia, and blurred vision developed, with worsening nausea and vomiting. On readmission, her sitting blood pressure (BP) was 140/90 mmHg. Pelvic examination found a closed cervix and a 14-week-size, mobile, nontender uterus. Trace pedal edema was present. Central nervous system evaluation showed a marked decrease in visual acuity with vision limited to the ability to distinguish between light and dark. Fundoscopy was negative with negative Babinski signs and moderate reflexes bilaterally with no clonus. Results of laboratory tests on admission were normal, including a coagulation screen. Protein was 1⫹ on urine dipstix. Computed tomographic (CT) scan of the head showed decreased attenuation in the occipital poles bilaterally and in the right posterior
1018 Apollon et al
Blindness in Preeclampsia
frontal lobe, and subcortical white matter consistent with focal cerebral edema with no evidence of intracerebral hemorrhage. Results of a lumbar puncture were normal. A diagnosis of hypertensive encephalopathy caused by severe preeclampsia, complicated by cortical blindness was made, and nifedipine therapy (10 mg orally three times a day) was initiated for BP control and magnesium sulfate (6 g intravenous bolus followed by an infusion of 2 g/hour, continued for 48 hours) was prescribed for seizure prophylaxis. On hospital day 2, she had a head magnetic resonance imaging scan (MRI) and singlephoton-emission CT scan. The head MRI showed increased T2-weighted signal within the white matter of the right occipital lobe and right posterior frontal lobe (Figure 1A) indicating vasogenic edema. Simultaneous single-photon-emission CT showed hyperemia in the right posterior temporal cortex, right lateral occipital cortex, and inferior parietal cortex (Figure 1B), more extensive than the lesions on MRI. The subject was discharged 5 days later with adequate BP control and only mildly blurred vision. Follow-up head single-
Obstetrics & Gynecology
photon-emission CT and MRI 8 days after discharge showed complete resolution of abnormalities (Figure 1, C and D) with no residual visual symptoms.
Comment The incidence of cortical blindness manifestated by hypertensive encephalopathy in preeclampsia is 1–15%.5,7 It is not known whether cortical blindness results from cerebral vasospasm with ischemic injury, arteriolar necrosis, and cytotoxic edema3,4 or from increased capillary permeability with leakage of fluid and proteins into the surrounding tissues resulting in vasogenic (hydrostatic) edema.5,6 In either case, the end result is focal cerebral edema. The cerebral edema on head CT or MRI is not helpful for defining the mechanism that underlies hypertensive encephalopathy. The availability of improved neuroimaging, including single-photon-emission CT, which can distinguish between areas of hyperperfusion and hypoperfusion, has enabled researchers to conduct more detailed investigations of the response of the cerebral vasculature to hypertension. In 1992, Schwartz et al6 used CT, MRI, and singlephoton-emission CT in 14 women with hypertensive encephalopathy, including eight with preeclampsia. The women had hypodense lesions in their occipital lobes on CT, which correlated with lesions of increased signal intensity on T2-weighted MRI images. Singlephoton-emission CT on two women during hypertensive episodes showed areas of increased cerebral perfusion that corresponded with lesions on CT and MRI. The authors believed the neuroimaging findings supported the concept that hypertensive encephalopathy results primarily from increased capillary permeability, leading to vasogenic edema. Had vasospasm been the etiology, they would have expected decreased cerebral perfusion on single-photon-emission CT with possible infarction. In contrast, Naidu et al4 used CT, singlephoton-emission CT, and transcranial Doppler ultrasound in 65 women with eclampsia, and concluded that vasospasm and resulting ischemia were the primary eclamptic mechanisms. Of 63 women who had singlephoton-emission CTs, including one with bilateral cortical blindness, all had decreased perfusion in the parietal or occipital areas of their brains. However, there was no mention of when single-photon-emission CT scans were done relative to hypertensive events, and because they show dynamic perfusion changes, those scans should be done during the acute disease process. If the scan is done after systemic BP has normalized, the
VOL. 95, NO. 6, PART 2, JUNE 2000
brain perfusion could be normal or focally reduced in areas of edema formation. In our case, the findings of hyperperfusion on singlephoton-emission CT in areas corresponding to lesions found on CT and MRI supported the concept of increased capillary permeability and vasogenic edema as the mechanism of cortical blindness. Further studies in humans using single-photon-emission CT are needed to differentiate between theories of vasospasm and vasogenic edema. As many drugs used in preeclampsia and eclampsia treatment affect the cardiovascular system, a better understanding of blood flow alterations associated with those conditions might improve specificity of medical treatment.
References 1. Jaffe G, Schatz H. Ocular manifestations of preeclampsia. Am J Ophthalmol 1987;103:309 –15. 2. Kesler A, Kaneti H, Kidron D. Transient cortical blindness in preeclampsia with indication of generalized vascular endothelial damage. J Neuroophthalmol 1998;18:163–5. 3. Torres PJ, Antolin E, Gratacos E, Chamorro A, Cararach V. Cortical blindness in preeclampsia: Diagnostic evaluation by transcranial Doppler and magnetic resonance imaging techniques. Acta Obstet Gynecol Scand 1995;74:642– 4. 4. Naidu K, Moodley J, Corr P, Hoffmann M. Single photon emission and cerebral computerised tomographic scan and transcranial Doppler sonographic findings in eclampsia. Br J Obstet Gynaecol 1997;104:1165–72. 5. Crosby ET, Preston R. Obstetrical anaesthesia for a parturient with preeclampsia, HELLP syndrome and acute cortical blindness. Can J Anaesth 1998;45:452–9. 6. Schwartz RB, Jones KM, Kalina P, Bajakian RL, Mantello MT, Garada B, et al. Hypertensive encephalopathy: Findings on CT, MR imaging, and SPECT imaging in 14 cases. AJR Am J Roentgenol 1992;159:379 – 83. 7. Cunningham FG, Fernandez CO, Hernandez C. Blindness associated with preeclampsia and eclampsia. Am J Obstet Gynecol 1995;172:1291– 8.
Address reprint requests to:
Errol R. Norwitz, MD, PhD Harvard Medical School Department of Obstetrics and Gynecology Brigham and Women’s Hospital 75 Francis Street Boston, MA 02115 E-mail: [email protected] Received November 17, 2000. Received in revised form January 13, 2000. Accepted January 20, 2000. Copyright © 2000 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
Apollon et al
Blindness in Preeclampsia
1019
References
8. Hubbard AM, Crombleholme TM, Adzick NS. Prenatal MRI evaluation of giant neck masses in preparation for the fetal exit procedure. Am J Perinatol 1998;15:253–7. 9. Levine D, Barnes PD, Madsen JR, Abbott J, Wong GP, Hulka C, et al. Fetal CNS anomalies revealed on ultrafast MR imaging. AJR Am J Roentgenol 1999;172:813– 8.
Address reprint requests to:
1. Hoyle RM. Surgical separation of conjoined twins. Surg Gynecol Obstet 1990;170:549 – 62. 2. Spitz L. Conjoined twins. Br J Surg 1996;83:1028 –30. 3. Spencer RA. Anatomic description of conjoined twins: A plea for standardized terminology. J Pediatr Surg 1996;31:941– 4. 4. Mansfield P, Stehling M, Ordidge R, Coxon R, Chapman B, Blamire A, et al. Echo planar imaging of the human fetus in utero at 0.5 T. Br J Radiol 1990;63:833– 41. 5. Huppert BJ, Brandt KR, Ramin KD, King BF. Single-shot fast spin echo MR imaging of the fetus: A pictorial essay. Radiographics 1999;S215–27. 6. Amin RS, Nikolaidis P, Kawashima A, Kramer LA, Ernst RD. Normal anatomy of the fetus at MR imaging. Radiographics 1999; S201–14. 7. Quinn T, Hubbard A, Adzick N. Prenatal magnetic resonance imaging enhances fetal diagnosis. J Pediatr Surg 1998;33:553– 8.
Holly L. Casele, MD Evanston Hospital Maternal Fetal Medicine 2650 Ridge Suite 1600 Evanston, IL 60201 E-mail: [email protected]
Cortical blindness in severe preeclampsia: Computed tomography, magnetic resonance imaging, and singlephoton-emission computed tomography findings
head computed tomography and magnetic resonance imaging scans. Follow-up neuroimaging studies 2 weeks later, by which time the patient’s visual acuity had returned to normal, showed complete resolution of radiologic abnormalities. Conclusion: Neuroimaging studies in a woman with severe postpartum preeclampsia complicated by reversible cortical blindness showed that blindness resulted from vasogenic (hydrostatic) cerebral edema and not cerebral vasospasm. (Obstet Gynecol 2000;95:1017–9. © 2000 by The American College of Obstetricians and Gynecologists.)
Katia M. Apollon, MD, Julian N. Robinson, MD, Richard B. Schwartz, MD, PhD, AND Errol R. Norwitz, MD, PhD Background: Cortical blindness is a complication of severe preeclampsia, but it is unclear whether it results from cerebral vasospasm and ischemic injury or vasogenic (hydrostatic) edema due to increased capillary permeability. Case: Reversible cortical blindness in a 33-year-old gravida 2, para 1, with severe postpartum preeclampsia after evacuation of a partial molar pregnancy at 19 weeks’ gestation is presented. Initial neuroimaging studies showed hyperperfusion on head single-photon-emission computed tomography scan, which corresponded with lesions found on
Received November 5, 1999. Received in revised form January 19, 2000. Accepted February 1, 2000.
Copyright © 2000 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
The ophthalmologic manifestations of preeclampsia include retinal detachment, retinal arteriolar vasospasm, thrombosis of the central retinal arteries, and reversible cortical blindness.1,2 However, the pathophysiology of cortical blindness is debated to be from cerebral vasospasm and ischemic injury3,4 or vasogenic edema caused by increased capillary permeability.5,6 We present a case of severe postpartum preeclampsia complicated by reversible cortical blindness after evacuation of a partial molar pregnancy at 19 weeks’ gestation. Neuroimaging studies showed that the cortical blindness resulted from vasogenic edema with selective hyperperfusion of the posterior cerebral circulation. Case
From the Departments of Obstetrics and Gynecology and Radiology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts. Supported by the Reproductive Scientist Development Program through National Institutes of Health (grant 5K12-HD00849) and the Association of Professors of Gynecology and Obstetrics (to ERN).
VOL. 95, NO. 6, PART 2, JUNE 2000
A 33-year-old woman, gravida 2, para 1, had abdominal ultrasound at 18 weeks’ gestation that found a probable partial molar pregnancy with a single structurally anomalous female fetus. Antenatal course was complicated by intractable nausea and vomiting. Results of pertinent laboratory tests were
0029-7844/00/$20.00 PII S0029-7844(00)00878-4
1017
Figure 1. (A) Axial T2-weighted MRI (3000 ms/80 ms, TR/TE) shows increased T2 signal (arrows) in the peripheral subcortical white matter in the right occipital lobe. (B) Simultaneous axial technetium-99m HMPAO single-photon-emission computed tomographic image shows increased cerebral perfusion (arrows) in the hyperemia in the right posterior temporal cortex, right lateral occipital cortex, and inferior parietal cortex. (C) Follow-up neuroimaging of the woman 8 days after discharge shows resolution of T2-bright signal on MRI and (D) regional hyperperfusion on single-photon-emission computed tomographic image.
-hCG 1,263,520 mIU/mL and TSH 0.44 mU/L (normal range, 0.2– 0.40 mU/L). An uncomplicated dilation and evacuation was done with an autopsy that confirmed the multiple fetal anomalies detected by ultrasound and a fetal karyotype of 69,XXX, consistent with a partial molar pregnancy. Twelve hours after discharge, severe right-sided headache, photophobia, and blurred vision developed, with worsening nausea and vomiting. On readmission, her sitting blood pressure (BP) was 140/90 mmHg. Pelvic examination found a closed cervix and a 14-week-size, mobile, nontender uterus. Trace pedal edema was present. Central nervous system evaluation showed a marked decrease in visual acuity with vision limited to the ability to distinguish between light and dark. Fundoscopy was negative with negative Babinski signs and moderate reflexes bilaterally with no clonus. Results of laboratory tests on admission were normal, including a coagulation screen. Protein was 1⫹ on urine dipstix. Computed tomographic (CT) scan of the head showed decreased attenuation in the occipital poles bilaterally and in the right posterior
1018 Apollon et al
Blindness in Preeclampsia
frontal lobe, and subcortical white matter consistent with focal cerebral edema with no evidence of intracerebral hemorrhage. Results of a lumbar puncture were normal. A diagnosis of hypertensive encephalopathy caused by severe preeclampsia, complicated by cortical blindness was made, and nifedipine therapy (10 mg orally three times a day) was initiated for BP control and magnesium sulfate (6 g intravenous bolus followed by an infusion of 2 g/hour, continued for 48 hours) was prescribed for seizure prophylaxis. On hospital day 2, she had a head magnetic resonance imaging scan (MRI) and singlephoton-emission CT scan. The head MRI showed increased T2-weighted signal within the white matter of the right occipital lobe and right posterior frontal lobe (Figure 1A) indicating vasogenic edema. Simultaneous single-photon-emission CT showed hyperemia in the right posterior temporal cortex, right lateral occipital cortex, and inferior parietal cortex (Figure 1B), more extensive than the lesions on MRI. The subject was discharged 5 days later with adequate BP control and only mildly blurred vision. Follow-up head single-
Obstetrics & Gynecology
photon-emission CT and MRI 8 days after discharge showed complete resolution of abnormalities (Figure 1, C and D) with no residual visual symptoms.
Comment The incidence of cortical blindness manifestated by hypertensive encephalopathy in preeclampsia is 1–15%.5,7 It is not known whether cortical blindness results from cerebral vasospasm with ischemic injury, arteriolar necrosis, and cytotoxic edema3,4 or from increased capillary permeability with leakage of fluid and proteins into the surrounding tissues resulting in vasogenic (hydrostatic) edema.5,6 In either case, the end result is focal cerebral edema. The cerebral edema on head CT or MRI is not helpful for defining the mechanism that underlies hypertensive encephalopathy. The availability of improved neuroimaging, including single-photon-emission CT, which can distinguish between areas of hyperperfusion and hypoperfusion, has enabled researchers to conduct more detailed investigations of the response of the cerebral vasculature to hypertension. In 1992, Schwartz et al6 used CT, MRI, and singlephoton-emission CT in 14 women with hypertensive encephalopathy, including eight with preeclampsia. The women had hypodense lesions in their occipital lobes on CT, which correlated with lesions of increased signal intensity on T2-weighted MRI images. Singlephoton-emission CT on two women during hypertensive episodes showed areas of increased cerebral perfusion that corresponded with lesions on CT and MRI. The authors believed the neuroimaging findings supported the concept that hypertensive encephalopathy results primarily from increased capillary permeability, leading to vasogenic edema. Had vasospasm been the etiology, they would have expected decreased cerebral perfusion on single-photon-emission CT with possible infarction. In contrast, Naidu et al4 used CT, singlephoton-emission CT, and transcranial Doppler ultrasound in 65 women with eclampsia, and concluded that vasospasm and resulting ischemia were the primary eclamptic mechanisms. Of 63 women who had singlephoton-emission CTs, including one with bilateral cortical blindness, all had decreased perfusion in the parietal or occipital areas of their brains. However, there was no mention of when single-photon-emission CT scans were done relative to hypertensive events, and because they show dynamic perfusion changes, those scans should be done during the acute disease process. If the scan is done after systemic BP has normalized, the
VOL. 95, NO. 6, PART 2, JUNE 2000
brain perfusion could be normal or focally reduced in areas of edema formation. In our case, the findings of hyperperfusion on singlephoton-emission CT in areas corresponding to lesions found on CT and MRI supported the concept of increased capillary permeability and vasogenic edema as the mechanism of cortical blindness. Further studies in humans using single-photon-emission CT are needed to differentiate between theories of vasospasm and vasogenic edema. As many drugs used in preeclampsia and eclampsia treatment affect the cardiovascular system, a better understanding of blood flow alterations associated with those conditions might improve specificity of medical treatment.
References 1. Jaffe G, Schatz H. Ocular manifestations of preeclampsia. Am J Ophthalmol 1987;103:309 –15. 2. Kesler A, Kaneti H, Kidron D. Transient cortical blindness in preeclampsia with indication of generalized vascular endothelial damage. J Neuroophthalmol 1998;18:163–5. 3. Torres PJ, Antolin E, Gratacos E, Chamorro A, Cararach V. Cortical blindness in preeclampsia: Diagnostic evaluation by transcranial Doppler and magnetic resonance imaging techniques. Acta Obstet Gynecol Scand 1995;74:642– 4. 4. Naidu K, Moodley J, Corr P, Hoffmann M. Single photon emission and cerebral computerised tomographic scan and transcranial Doppler sonographic findings in eclampsia. Br J Obstet Gynaecol 1997;104:1165–72. 5. Crosby ET, Preston R. Obstetrical anaesthesia for a parturient with preeclampsia, HELLP syndrome and acute cortical blindness. Can J Anaesth 1998;45:452–9. 6. Schwartz RB, Jones KM, Kalina P, Bajakian RL, Mantello MT, Garada B, et al. Hypertensive encephalopathy: Findings on CT, MR imaging, and SPECT imaging in 14 cases. AJR Am J Roentgenol 1992;159:379 – 83. 7. Cunningham FG, Fernandez CO, Hernandez C. Blindness associated with preeclampsia and eclampsia. Am J Obstet Gynecol 1995;172:1291– 8.
Address reprint requests to:
Errol R. Norwitz, MD, PhD Harvard Medical School Department of Obstetrics and Gynecology Brigham and Women’s Hospital 75 Francis Street Boston, MA 02115 E-mail: [email protected] Received November 17, 2000. Received in revised form January 13, 2000. Accepted January 20, 2000. Copyright © 2000 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
Apollon et al
Blindness in Preeclampsia
1019