Anesth Analg 2000;91:609-611
© 2000 International Anesthesia Research Society
OBSTETRIC ANESTHESIA
Cortical Blindness in a Preeclamptic Patient After a Cesarean Delivery Complicated by Hypotension
Carl J. Borromeo, MD*,
George T. Blike, MD
,
Christopher W. Wiley, MD, and
Joshua A. Hirsch, MD
Departments of
*Anesthesiology and
Radiology, Lahey Clinic, Burlington, Massachusetts; and
Department of Anesthesiology, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire
Address correspondence and reprint requests to Carl J. Borromeo, MD, Department of Anesthesiology, Lahey Clinic, 41 Mall Rd., Burlington, MA 01805. Address e-mail to carl.j.borromeo{at}lahey.org
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Abstract
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Implications: Visual strokes can occur after prolonged hypotension or as a complication of preeclampsia-eclampsia. This case describes the diagnostic dilemma posed by a patient who developed transient blindness after a hypotensive episode during cesarean delivery for severe preeclampsia-eclampsia.
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Introduction
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Visual disturbances and cortical blindness are hallmarks of posterior cerebral arterial "border-zone infarcts." Studies dating back to the turn of the century have linked these watershed infarcts to prolonged or severe hypotension. Preeclampsia-eclampsia can also have neurological sequelae, including cortical blindness. We report a case of a parturient with severe preeclampsia who suffered severe, but transient, hypotension during cesarean delivery and subsequently developed transient blindness.
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Case Report
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A 36-yr-old parturient at 33 wk gestation was admitted with hypertension and complaints of recurring headaches. Her systemic arterial blood pressures ranged from 150–200 over 70–105 mm Hg. Laboratory examination revealed 3+ urinary protein, hemoglobin 13.5g/dL, aspartate aminotransferase (AST) 78 IU/L (normal 14–36), and alanine aminotransferase (ALT) 66 IU/L (9–52). Her coagulation profile was normal. The patient was started on magnesium sulfate (IV 4-g load, then 1g/h). An elective cesarean delivery was planned for severe pregnancy-induced hypertension.
In the operating room, routine monitors were placed on the patient. One liter of Ringer’s lactate solution was administered IV, and then epidural anesthesia was established to a T4 level by using plain 0.5% bupivacaine. Arterial blood pressures remained approximately 170/80–90 mm Hg, with heart rates 90–99 bpm, until immediately after delivery, when the blood pressure decreased suddenly to 50/30 mm Hg with a decrease in heart rate to 60 bpm. A total of 50 mg of ephedrine, 40 µg of phenylephrine, and IV fluids were administered to increase the blood pressure to 140/80 mm Hg within 3–4 min. She remained conscious and conversant throughout this interval. The remainder of the procedure was uneventful. The patient received 4.5 L of crystalloid for an estimated blood loss of 1.2 L.
Several hours postoperatively, a nurse observed that the patient was unable to perform routine tasks and subsequently discovered that the patient was unable to see. A neurologic examination showed a left homonymous hemianopsia with normal pupillary responses. A head computed tomography scan (CT) without contrast revealed multiple hypodense areas involving the frontoparietal, parietal, and occipital lobes bilaterally. The preliminary conclusion was that these changes were consistent with a watershed infarct. Magnetic resonance imaging (MRI) was not obtained.
The patient’s neurologic examination returned to normal on the second postoperative day. Her liver function tests worsened for 3 days, and her platelet count decreased to 76,000/µL. Thereafter, the laboratory abnormalities returned to premorbid values. Subsequent reading of the CT scan by a neuroradiologist revealed a pattern more consistent with the vasogenic edema seen in preeclampsia-eclampsia, with the characteristic nonarterial cortical and subcortical distribution and the focal petechial hemorrhage (Figs. 1 and 2). She was discharged home on the seventh postoperative day.
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Figure 1. Unenhanced axial CT demonstrates multifocal hypodense areas. These are present in the left occipital and bilateral frontal areas.
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Figure 2. Computed tomography scan through the upper frontal convexities shows a focus of hyperdensity (arrow) characteristic of petechial hemorrhage, which occurs in the setting of pregnancy-induced hypertension or other acute hypertensive disorders.
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Discussion
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Cortical blindness signifies a (usually incomplete) loss of vision caused by lesions of the geniculocalcarine visual pathways in the posterior hemispheres (1). Because the post-geniculate visual pathways lie in a tenuously supplied "arterial border zone," cortical blindness and other visual disturbances have long been associated with hypoperfusion-related watershed infarcts (2,3). Cortical blindness has also been reported as a complication of preeclampsia-eclampsia (4–7), with an incidence as much as 15% in women with eclampsia (6).
This case report describes a confusing scenario caused by the overlapping clinical and radiologic features of these two conditions. Initially, this patient’s neurologic findings were incorrectly attributed to a hypotension-related watershed infarct. Subsequently, subtle radiologic clues and her clinical course helped establish the diagnosis of preeclampsia-induced cortical blindness. The cortical blindness resulting from either watershed infarcts or preeclampsia-eclampsia differ in their associated radiologic findings, pathophysiologies, and natural histories.
Similar, but not identical, radiologic findings are seen in both conditions. Bilateral, focal to diffuse low-density lesions on CT and hyperintense lesions on T2-weighted MRI images are the most common neuroradiologic abnormalities in patients with severe preeclampsia-eclampsia. These changes represent focal increases in brain water content (4–6,8,9). This edema is most consistently seen in the posterior hemispheres, particularly in areas approximating the "arterial border zones," or may be more diffuse, involving anterior deep white matter regions and the basal ganglia (8,9). In severe cases, radiologic evidence of gross or petechial hemorrhages may also be present (10,11). Hypotension-related watershed infarcts demonstrate the same type of edematous changes (hypodensity on CT and hyperintensity on T2-weighted MRI) but in very specific "distal field" territories of the middle cerebral artery and posterior cerebral artery (2,11). The parietooccipital border zone is most susceptible to hemodynamic ischemic injury, as it is the most peripheral region of the anterior, middle, and posterior cerebral arterial circulations. Hemodynamic watershed infarction is very rarely hemorrhagic.
The cause of these focal increases in brain water is different in hypotension-related watershed infarcts and preeclampsia-eclampsia. Ischemia and infarction secondary to hypoperfusion lead to cytotoxic edema in border zone infarcts. In this case, sodium and water enter damaged neurons, producing intracellular edema. Conversely in preeclampsia-eclampsia, there is hyperperfusion and the loss of normal protective autoregulation (breakthrough), resulting in forced vasodilation, passive overdistension, and vasogenic extracellular edema (11,12). The typical watershed-like distribution of the lesions in pregnancy-induced hypertension can be explained by histopathologic studies that have shown breakthrough vasculopathic changes in areas that correspond to arterial "border zones" (13). This pattern may be the result of differential innervation of the posterior and anterior cerebral circulations, with the internal carotid system more generously supplied by protective sympathetic nerves than the vertebrobasilar system, resulting in the loss of autoregulation and forced arteriolar dilation predominantly in the "watershed" occipital lobes (12). This breakthrough vasculopathy, in its severest form, results in fibrinoid necrosis of the vessel wall, leading to extravasation and the characteristic small perivascular petechial hemorrhages seen in advanced cases of preeclampsia-eclampsia and hypertensive encephalopathy (12,13).
The prognosis for cortical blindness depends on etiology (1). Bilateral occipital abnormalities caused by hypotension are associated with a poor prognosis (1,2). However, cortical blindness associated with preeclampsia-eclampsia almost always resolves (6,11), further supporting the theory that the radiographic lesions represent vasogenic edema and are not caused by vasospasm and ischemia. Table 1 summarizes the differences between preeclampsia-eclampsia- and watershed infarct-induced cortical blindness.
Finally, because of the possible involvement of the visual association cortex, patients with cortical blindness from either cause may be unaware of or unconcerned about their deficits. Some will deny or make excuses for their blindness (Anton Syndrome) (3). In these very rare instances, only a meticulous neurologic examination, including visual field testing, will reveal the condition.
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Accepted for publication June 5, 2000.
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Abstract
Introduction
