CORTICAL blindness occurs in approximately 1–3% of preeclampsia and eclampsia patients. 1–3It was reported to occur either before or during the first few days after delivery. 4We report a case of a preeclamptic parturient who suffered transient cortical blindness 26 days after cesarean delivery, related to undiagnosed retained placental fragments.

A 33-yr-old, gravida 2, para 1 parturient was admitted at 38 weeks’ gestation with a chief complaint of abdominal pain. Preeclampsia was diagnosed by the presence of elevated systemic arterial blood pressure (170/100 mmHg) and proteinuria. Physical examination revealed hyperreflexic limbs. Blood tests showed a moderate elevation in liver enzymes (aspartate aminotransferase, 121 U/l) and hyperuricemia (343 μm). Hypertension was controlled with intravenous nicardipine, and an emergent cesarean delivery was performed on the day of admission, using general anesthesia. The patient recovered rapidly from anesthesia, and the results of a neurologic examination performed 2 h later were normal, except for hyperreflexic limbs.

The patient's clinical condition worsened during the first three postoperative days (POD), with the onset of severe hemolysis, elevated liver enzymes, and low platelet count syndrome (aspartate aminotransferase, 4,238 U/l; platelet count, 50,000/ml; and hemolysis, confirmed by elevated nonconjugated bilirubin concentration [59 μm] and decreased haptoglobin concentration). Respiratory distress with severe hypoxemia related to pulmonary edema occurred on POD1, requiring tracheal intubation, mechanical ventilation, and sedation. Acute renal failure (oliguria and creatinine clearance < 5 ml/min) was observed on POD2. A transesophageal echocardiogram ruled out left ventricular dysfunction, and pulmonary artery monitoring was used to optimize hemodynamic status. A head computed tomography (CT) scan without contrast, performed on POD 1 to eliminate intracerebral hemorrhage as a possible diagnosis, was within the normal limits. Three days after admission, a sudden decrease in arterial blood pressure led to the diagnosis of intraabdominal hemorrhage, as well as a subcapsular hematoma of the liver. At this time, CT scan morphology of the uterus was considered normal, with a hyperdensity in the uterine cavity, only suggesting a small amount of intrauterine blood. Intraabdominal blood was surgically evacuated, but the liver was left intact since the Glisson capsule was not ruptured.

The patient's condition improved gradually thereafter. Arterial blood pressure, renal and respiratory function, liver enzyme concentration, and platelet count were all normal by 15 days after delivery. Intravenous sedation was stopped after 1 week, but recovery was slow, and the level of consciousness was sufficient to allow tracheal extubation on POD 14 only. The patient was sleepy, able to be aroused only after verbal stimulation, and confused. The results of a cerebral CT scan performed at this time were normal, and an electroencephalogram revealed diffuse slow waves. The patient's state of consciousness improved gradually, and she was able to perform everyday tasks such as washing, eating without any help, and pouring water into a glass. The results of formal neurologic examinations, repeated several times during this period, were normal.

Three weeks after delivery, hypertension recurred, and treatment with nicardipine was reinitiated. On POD 26, the patient was suddenly unable to perform routine tasks because of complete blindness. Results of a funduscopic examination were normal, pupils were symmetrical and reacted normally to light, and the patient did not react to threat. The results of the remainder of her neurologic examination were normal. Electroencephalography revealed focal posterior paroxysmal spike activity that was unresponsive to intravenous clonazepam and sodium valproate and could only be suppressed with intravenous phenytoin. Head CT scan revealed bilateral occipital hypodensity. Axial T2-weighted magnetic resonance (MR) images with fluid-attenuated inversion recovery sequences showed bilateral hypersignal in the occipital, temporal, and parietal regions, suggesting focal cerebral edema (fig. 1). A recurrence of preeclampsia was suspected. Ultrasound evaluation of the uterus detected echogenic fragments in the uterine cavity. These were removed during a hysteroscopic procedure with general anesthesia. Histologic analysis revealed the presence of placental tissues, including necrotized villi.

Fig. 1. Axial T2-weighted magnetic resonance (MR) image of the brain with fluid-attenuated inversion recovery sequences performed at the onset of cortical blindness on postoperative day 26. The MR image shows bilateral hypersignal in the occipital, temporal, and parietal regions, suggesting focal cerebral edema.

Fig. 1. Axial T2-weighted magnetic resonance (MR) image of the brain with fluid-attenuated inversion recovery sequences performed at the onset of cortical blindness on postoperative day 26. The MR image shows bilateral hypersignal in the occipital, temporal, and parietal regions, suggesting focal cerebral edema.

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The patient's clinical condition rapidly improved after surgery. She was able to distinguish bright light 12 h after curettage, and she could identify the shape of usual items after 48 h. Visual function was considered normal by the ophthalmologist after 4 days. Within 1 week, arterial blood pressure was normalized, level of consciousness was improved, and electroencephalographic abnormalities disappeared. A week later, occipital hypersignal on T2-weighted MR imaging had nearly disappeared. The patient was discharged 38 days after cesarean section delivery.

The present case illustrates an uncommon evolution of severe preeclampsia with secondary onset of neurologic symptoms associated with intrauterine retention of placental products.

An initial improvement in preeclampsia-related symptoms is common after delivery, but relapse often occurs within 24 h. In our case, severe hepatic, hematologic, cardiovascular, and renal complications occurred in a classic timing, within the first 3 days after delivery. 5Our patient's very slow clinical improvement during the first 3 weeks was less expected, since recovery is usually complete within 1 week. However, persistent elevated blood pressure related to preeclampsia has been described 6 weeks postpartum. 6 

In contrast, the recurrence of hypertension and delayed onset of focal occipital seizures and cortical blindness are very uncommon. Because preeclampsia can only occur in the presence of a placenta, the hypothesis of placental tissue retention should be considered when unusual evolution is observed after delivery. In our case, it should have been suggested as soon as hypertension returned on POD 21. Physiopathologic alterations of preeclampsia and eclampsia are the result of an initial placental trigger and a maternal systemic response. 7Maternal symptoms are related to the synthesis of placentally derived vasoactive substances and to abnormal maternal systemic inflammatory response to an overload of placental debris shed from the syncytiotrophoblast into maternal circulation. 8,9Our case shows that even a small quantity of necrotized villous tissue retained in the uterine cavity can result in persistent preeclampsia and lead to further worsening of neurologic symptoms.

We arrived at the diagnosis of retained placenta very late in our observation of the patient. Despite spontaneous separation and controlled cord traction, it is sometimes difficult to ascertain that the entire placenta has been delivered. 10Placental retention has been reported to result in several complications, including bleeding, sepsis, and pain. In our case, postoperative uterine contraction and bleeding were considered to be nonspecific, despite severe blood coagulation disorders. An abdominal CT scan performed on POD 3 only showed hyperdensity in the uterine cavity, suggesting a small amount of intrauterine blood, and the diagnosis of retained placental products was suspected because of the recurrence of preeclampsia-related symptoms.

Although visual disturbances are common in severe preeclampsia, cortical blindness is rare, with an incidence of 1–3% and 3–14% in preeclamptic and eclamptic patients, respectively. 2Blindness may be the primary clinical presentation of preeclampsia and may be isolated or associated with an altered state of consciousness. 4In eclampsia, it may precede seizures for several hours. 2Patients may experience a complete loss of vision or may still perceive bright light shone directly into their eyes. 11The diagnosis should be evoked in the presence of loss of vision when (1) normal ophthalmoscopic examination results rule out retinal disease and (2) normal pupillary response to light and absence of blinking in response to threat suggest postgeniculate insult. Several pathologic features have been proposed to explain the neuropathologic mechanism of cerebral insult in eclampsia-related cortical blindness. Cerebral vasogenic edema in the cortex and subcortical white matter in the occipital lobes is commonly seen on MR imaging. 11–13An alteration in posterior cerebral blood flow autoregulation also has been suggested to favor arterial vasoconstriction and cerebral ischemia. 14Rarely, microinfarctions and focal hemorrhage may contribute to cerebral dysfunction. 2,15Cerebral imaging is of major importance in the diagnosis of cortical blindness. Head CT scan may reveal occipital hypodensities suggesting cerebral edema, described recently as posterior leukoencephalopathy syndrome. 16It is helpful to rule out hemorrhage and to detect thromboembolic phenomena. Occasionally, the head CT scan may be within normal limits, suggesting that the transient and limited extent of increased fluid shift may be beyond the resolution of a CT scan. 11MR imaging is increasingly used for the diagnosis of cortical blindness, since it exhibits superior soft tissue contrast and multiplanar resolution. It is the technique of choice to obtain images of the visual pathways. 11Hyperintense signal lesions on T2-weighted MR images are consistent with focal edema.

Management of preeclamptic or eclamptic women in whom cortical blindness develops is the same as for patients without this complication, and the management guidelines are now straightforward. 6Delivery should not be postponed unnecessarily, and the prognosis of cortical blindness is good, with a mean (± SD) duration of blindness of 34 ± 27 and 92 ± 67 h in eclamptic and preeclamptic patients, respectively. 2Scotomas or long-lasting alterations in visual function are uncommon and are typically related to severe focal ischemia or hemorrhage.

In conclusion, this case illustrates that retention of placental tissue should be suspected in the presence of an unusual evolution of preeclampsia-related symptoms. Uterine vacuity should be assessed even when placental delivery is considered to be complete, since it is the key to treating preeclampsia.

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