Am Fam Physician. 2005 Mar 1;71(5):856-861.
to the editor: Although preeclampsia is typically diagnosed in the prenatal period, we would like to describe an unusual case of late-onset eclampsia presenting postpartum as sudden bilateral cortical blindness.
The patient was a healthy, 21-year-old black woman, gravida three, para one, with a previous normal pregnancy and no history of hypertension or preeclampsia. She had an unremarkable prenatal course and her blood pressure prenatally ranged from 98/62 mm Hg to 130/80 mm Hg one week before delivery. Urine protein was zero or trace at all visits. She delivered a healthy 2,670 g (5 lb, 8 oz) male infant at term. Blood pressures immediately postpartum were mostly 120s to 130s/60s to 70s mm Hg with occasional pressures of 140 to 150/80 to 90 mm Hg.
Eight days after delivery, the patient awoke with a severe bilateral frontal headache and blurry vision. Over several hours, this progressed to acute bilateral cortical blindness. Initial evaluation showed blood pressure of 169/99 but without proteinuria. Subsequent 24-hour urine collection showed 0.28 grams protein. Computed axial tomography of the brain demonstrated bilateral low attenuation lesions in the cerebral hemispheres; magnetic resonance imaging revealed diffuse altered T2 signals in a posterior distribution. Cerebral angiogram was normal. Twenty hours after the onset of symptoms the patient developed altered mental status and had two tonic-clonic seizures, at which point she was treated with phenytoin (Dilantin) and magnesium.
The patient’s headache and vision quickly improved and by 48 hours her vision had returned to 20/20 acuity. Her blood pressure continued to be elevated throughout her hospital stay, at one point reaching 200/110 mm Hg. Three days after admission, she was discharged home on metoprolol.
Preeclampsia in pregnancy is defined as new-onset elevated blood pressure (>140/90 mm Hg) along with proteinuria after 20 weeks of gestation.1,2 Severe cases may progress to eclampsia characterized by seizures. A multicenter review3 of preeclampsia found up to one third of cases developed postpartum with 80 percent of these occurring three to 14 days after delivery. One case report4 describes onset 26 days after delivery.
Although visual changes such as blurry vision or scotoma are common, they may be more typical of late-onset disease.3,5 One study reported visual symptoms in 44 percent of patients with late-onset preeclampsia.3 Acute cortical blindness has been estimated to occur in 1 to 3 percent of patients with eclampsia, although a review of 15 cases noted a prevalence of 15 percent.5 Our patient was similar to patients in that case series including the transient nature of visual loss (four hours to eight days in their review) and mental status changes (three of their 15 patients) but had minimal urine protein and relatively mild hypertension on initial presentation.
Because 90 percent of women presenting with late postpartum preeclampsia have a headache and close to one half have some type of visual disturbance, physicians providing obstetric care should be alert for these symptoms as an unusual presentation of this disease. This case demonstrates that preeclampsia is less common in multiparous patients, but it can be severe when it develops.
1. ACOG Committee on Obstetric Practice. ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. No. 33, January 2002. American College of Obstetricians and Gynecologists. Obstet Gynecol. 2002;99:159–67.
2. Lipstein H, Lee CC, Crupi RS. A current concept of eclampsia. Am J Emerg Med. 2003;21:223–6.
3. Chames MC, Livingston JC, Ivester TS, Barton JR, Sibai BM. Late postpartum eclampsia: a preventable disease? Am J Obstet Gynecol. 2002;186:1174–7.
4. Delefosse D, Samain E, Helias A, Regimbeau JM, Deval B, Farah E, et al. Late onset of cortical blindness in a patient with severe preeclampsia related to retained placental fragments. Anesthesiology. 2003;98:261–3.
5. Cunningham FG, Fernandez CO, Hernandez C. Blindness associated with preeclampsia and eclampsia. Am J Obstet Gynecol. 1995;172:1291–8.
Send letters to Kenneth W. Lin, MD, MPH, Associate Deputy Editor for AFP Online, e-mail: email@example.com, or 11400 Tomahawk Creek Pkwy., Leawood, KS 66211-2680.
Please include your complete address, e-mail address, and telephone number. Letters should be fewer than 400 words and limited to six references, one table or figure, and three authors.
Letters submitted for publication in AFP must not be submitted to any other publication. Possible conflicts of interest must be disclosed at time of submission. Submission of a letter will be construed as granting the American Academy of Family Physicians permission to publish the letter in any of its publications in any form. The editors may edit letters to meet style and space requirements.
Copyright © 2005 by the American Academy of Family Physicians.
This content is owned by the AAFP. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP. Contact firstname.lastname@example.org for copyright questions and/or permission requests.
Want to use this article elsewhere? Get Permissions