Figure 1. Disc photographs of the right (A) and left (B) eyes at the initial visit with corresponding 30-2 Humphrey visual field.
Figure 2. Disc photographs of the right (A) and left (B) eyes at follow-up with corresponding 30-2 Humphrey visual field.
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Giridhar P, Freedman K. Nonarteritic Anterior Ischemic Optic Neuropathy in a 35-Year-Old Postpartum Woman With Recent Preeclampsia. JAMA Ophthalmol. 2013;131(4):542–544. doi:10.1001/jamaophthalmol.2013.2884
Author Affiliations: Department of Ophthalmology, Texas Tech University Health Sciences Center, Lubbock.
Vision loss due to optic neuropathy in the immediate postpartum period can have a variety of causes, including blood loss1 and anesthetic complications.2 We describe a 35-year-old woman with resolving preeclampsia who had sudden unilateral vision loss after giving birth and had a clinical presentation consistent with nonarteritic anterior ischemic optic neuropathy (NAION).
A 35-year-old postpartum woman had sudden loss of vision in her right eye, noted approximately 8 days after vaginal delivery of her full-term baby. The patient had a history of preeclampsia (hypertension, protein in urine 452 mg/24 hours, and leg swelling) diagnosed 2 weeks before delivery. She had continued problems with blood pressure control since delivery, and she also reported severe headache prior to vision loss. There was no history of hypertension, smoking, or medication use. There was no significant ocular history. There was a history of gestational diabetes mellitus for the last 2 months of pregnancy. On initial examination, her blood pressure was 130/82 mm Hg and her weight was 95 kg. Her visual acuity was 20/200 OD and 20/15 OS. There was a relative afferent pupillary defect in the right eye. Ophthalmoscopy revealed superior segmental disc edema with some early pallor in the right eye and a normal disc (with a small cup-disc ratio) in the left eye (Figure 1). Results of the remainder of her ocular examination were normal. Findings on computed tomography and magnetic resonance imaging of the brain and orbits were normal. Results of the laboratory workup including complete blood cell count, erythrocyte sedimentation rate, and C-reactive protein level were normal and she was negative for antinuclear antibodies. Humphrey automated visual field testing (30-2 Sita Fast) demonstrated an inferior altitudinal defect in the right eye and a normal field in the left eye (Figure 1). The working diagnosis was NAION. On follow-up approximately 6 weeks after her initial visit, visual acuity was 20/30 OD and 20/20 OS. Findings of the remainder of the examination were stable except for the development of some segmental superior disc pallor in the right eye (Figure 2). Results of repeated automated visual field testing were also unchanged (Figure 2).
Preeclampsia usually has onset after the 20th week of pregnancy and is characterized by blood pressure higher than 140/90 mm Hg and a urine protein level of 300 mg/24 hours. It has been associated with varied visual disturbances and transient and permanent vision loss. Pathological findings related to vision loss include retinal vessel spasm and occlusion, choroidal infarction or choroidal effusions leading to serous retinal detachment, and focal edema and hemorrhages in the occipital cortex.3 In addition, optic disc edema may arise due to intracranial hypertension, systemic hypertension, or anterior ischemic optic neuropathy.
Two instances of ischemic optic neuropathy associated with preeclampsia have been reported.4,5 However, in contrast to our case, both of these events began before delivery and involved bilateral disc edema and vision loss. Our case appears to be unique in that the symptoms appeared after delivery and the vision loss and disc edema were unilateral. The disc swelling in this case was sectoral and the visual field loss was altitudinal, characteristic of a typical presentation of NAION.
The pathophysiology of preeclampsia is believed to originate from the placenta. Cytotrophoblast cells in the embryo enter the uterine wall and invade the maternal uterine spinal arteries. These cells change from an epithelial phenotype to an endothelial phenotype. This vascular remodeling seems to be disrupted in preeclampsia, resulting in the production of high levels of antiangiogenic factors that enter the maternal circulation; these antiangiogenic factors disrupt the maternal endothelium, resulting in hypertension.6 The exact pathophysiology for NAION in preeclampsia remains elusive, but it is suggested that the uncontrolled hypertension leads to vasoconstriction or ischemia in the posterior ciliary artery circulation.
Correspondence: Dr Giridhar, Department of Ophthalmology, Texas Tech University Health Sciences Center, 3601 Fourth St, MS 7217, Room 2A100, Lubbock, TX 79430 (email@example.com).
Published Online: February 28, 2013. doi:10.1001/jamaophthalmol.2013.2884
Conflict of Interest Disclosures: None reported.
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