Background
Posterior reversible encephalopathy syndrome is observed frequently in patients with eclampsia; however, it has also been reported in some patients with preeclampsia.
Objectives
The aim of this study was to determine the incidence of posterior reversible encephalopathy syndrome in patients with preeclampsia and eclampsia and to assess whether these 2 patient groups share similar pathophysiologic backgrounds by comparing clinical and radiologic characteristics.
Study Design
This was a retrospective cohort study of 4849 pregnant patients. A total of 49 patients with eclampsia and preeclampsia and with neurologic symptoms underwent magnetic resonance imaging and magnetic resonance angiography; 10 patients were excluded from further analysis because of a history of epilepsy or dissociative disorder. The age, parity, blood pressure, and routine laboratory data at the onset of symptoms were also recorded.
Results
Among 39 patients with neurologic symptoms, 12 of 13 patients with eclampsia (92.3%) and 5 of 26 patients with preeclampsia (19.2%) experienced the development of posterior reversible encephalopathy syndrome. Whereas age and blood pressure at onset were not significantly different between patients with and without encephalopathy, hematocrit, serum creatinine, aspartate transaminase, alanine transaminase, and lactate dehydrogenase values were significantly higher in patients with posterior reversible encephalopathy syndrome than in those without magnetic resonance imaging abnormalities. In contrast, patients with eclampsia with posterior reversible encephalopathy syndrome did not show any significant differences in clinical and laboratory data compared with patients with preeclampsia with posterior reversible encephalopathy syndrome. In addition to the parietooccipital regions, atypical regions (such as the frontal and temporal lobes), and basal ganglia were also involved in patients with eclampsia and patients with preeclampsia with posterior reversible encephalopathy syndrome. Finally, intraparenchymal hemorrhage was detected in 1 patient with eclampsia, and subarachnoid hemorrhage was observed in 1 patient with preeclampsia.
Conclusions
Although the incidence of posterior reversible encephalopathy syndrome was high in patients with eclampsia, nearly 20% of the patients with preeclampsia with neurologic symptoms also experienced posterior reversible encephalopathy syndrome. The similarities in clinical and radiologic findings of posterior reversible encephalopathy syndrome between the 2 groups support the hypothesis that these 2 patient groups have a shared pathophysiologic background. Thus, magnetic resonance imaging studies should be considered for patients with the recent onset of neurologic symptoms, regardless of the development of eclampsia.
Posterior reversible encephalopathy syndrome (PRES) refers to reversible vasogenic brain edema accompanied with acute neurologic symptoms such as seizure, impaired consciousness, and visual disturbance; brain imaging studies commonly reveal vasogenic edema predominantly involving the bilateral parietooccipital regions. The pathophysiologic condition of PRES is suggested to involve the failure of cerebral blood flow autoregulation; endothelial dysfunction is implicated to play an important role in its development. Eclampsia and preeclampsia are also associated with endothelial dysfunction. Importantly, recent studies reported that PRES was observed frequently in patients with eclampsia; PRES has been suggested as an essential component of eclampsia-mediated primary central nervous system injury. However, PRES was also reported in patients with severe preeclampsia. Thus, we hypothesized that patients with preeclampsia and patients with eclampsia with neurologic symptoms such as severe headaches, visual disturbances, impaired consciousness, or seizures might be experiencing a similar pathophysiologic condition and that this clinical presentation could be radiologically identified as PRES. We conducted magnetic resonance imaging (MRI) studies in patients with neurologic symptoms during the peripartum period to determine the incidence of PRES. We also assessed cerebrovascular condition in these patients using magnetic resonance angiography (MRA). Finally, we analyzed the available clinical and radiologic findings to confirm our hypotheses.
Materials and Methods
This study was a retrospective cohort study conducted in a single medical center at the TOYOTA Memorial Hospital and was approved by the Ethics Committee of the TOYOTA Memorial Hospital. We enrolled patients with preeclampsia and patients with eclampsia with severe headaches, visual disturbances, impaired consciousness, or seizures during the peripartum period; all the patients underwent MRI within 24 hours of the onset of symptoms. The severity of headache was determined clinically; questionnaires and pain scales were not used because of the emergency situation. Of a total of 4849 women who gave birth between February 2007 and July 2015, 49 patients were evaluated with the use of MRI for the onset of new neurologic symptoms; of these, 3 patients were excluded because of a history of epilepsy, and 7 patients were excluded because of the diagnosis of dissociative disorder. Therefore, 39 patients were included in the final analysis of this study. Maternal characteristics, such as age, parity, blood pressure, laboratory data, and radiological findings, were evaluated.
All patients underwent MRI and MRA without contrast with the use of a 1.5 Tesla system within 24 hours after the onset of symptoms; follow-up MRI and MRA studies were conducted within 3 months. The diagnosis of PRES was made based on MRI findings that showed cortical or subcortical fluid-attenuated inversion recovery and T2-weighted hyperintensities within the posterior predominance that resolved or significantly improved on follow-up MRI. Preeclampsia was diagnosed based on the diagnostic criteria established by the American College of Obstetrics and Gynecology. Eclampsia was defined as the occurrence of seizures that could not be attributed to other causes in pregnant patients with preeclampsia.
For data that were considered to be distributed normally, unpaired t test or Welch’s test was used based on the homogeneity of variances. Otherwise, the Mann–Whitney U test was used for continuous data, and Fisher’s exact test was used for categoric data. A probability value of <.05 was considered to be statistically significant.
Results
Among a total of 39 patients who fulfilled the criteria, 13 patients were diagnosed with eclampsia. Of these, 12 patients (92.3%) were diagnosed with PRES; 4 of the patients PRES (30.8%) also experienced cerebral vasoconstriction. Thus, only 1 patient with eclampsia did not exhibit any abnormal MRI findings. On the other hand, among 26 patients with preeclampsia who experienced neurologic symptoms such as severe headaches, visual disturbances, or impaired consciousness, 5 patients (19.2%) were diagnosed with PRES; of those, 2 patients (7.7%) experienced cerebral vasoconstriction.
Comparison of clinical and laboratory data at the onset between patients with PRES and patients without MRI abnormalities is shown in Table 1 . Maternal age, frequency of primiparity, blood pressure, platelet counts, blood urea nitrogen, and total bilirubin were not significantly different between the 2 groups. However, hematocrit, serum creatinine, aspartate transaminase, alanine transaminase, and lactate dehydrogenase values were significantly higher in patients with PRES than in those without MRI abnormalities. Table 2 shows the comparison of clinical and laboratory data between patients with PRES and eclampsia or preeclampsia. No significant differences were noted in the clinical and laboratory data between the 2 groups. At the onset, severe hypertension of ≥160/110 mm Hg was observed in 8 of 12 patients (66.7%) with eclampsia with PRES, in all 5 (100%) patients with preeclampsia with PRES, and in 14 of 20 patients (70.0%) without MRI abnormalities.
| Variable | Posterior reversible encephalopathy syndrome (n = 17) | No magnetic resonance imaging abnormalities (n = 20) | P value |
|---|---|---|---|
| Age, y a | 35.4 ± 5.5 | 33.9 ± 4.8 | .36 |
| Primiparity, n (%) b | 12 (70.6) | 8 (40.0) | .10 |
| Systolic blood pressure, mm Hg a | 176 ± 24 | 168 ± 19 | .25 |
| Diastolic blood pressure, mm Hg a | 104 ± 17 | 100 ± 14 | .48 |
| Mean blood pressure, mm Hg a | 128 ± 18 | 123 ± 15 | .34 |
| Hematocrit (%) a | 38.8 ± 5.9 | 33.7 ± 5.5 | .01 |
| Platelet count, 10 4 /μL c | 12.7 (6.1–36.7) | 20.2 (12.0–29.1) | .09 |
| Blood urea nitrogen, mg/dL c | 11.0 (4.0–35.0) | 9.0 (5.0–17.0) | .37 |
| Serum creatinine, mg/dL a | 0.76 ± 0.26 | 0.56 ± 0.14 | < .01 |
| Aspartate transaminase, IU/L c | 43.0 (18.0–1042.0) | 18.0 (11.0–124.0) | < .01 |
| Alanine transaminase, IU/L c | 29.0 (8.0–1008.0) | 10.0 (5.0–139.0) | .01 |
| Total bilirubin, mg/dL c | 0.6 (0.4–2.6) | 0.6 (0.2–1.0) | .59 |
| Lactate dehydrogenase, IU/L c | 553.5 (244.0–2324.0) | 229.5 (129.0–410.0) | < .01 |
a Data are presented as the means ± standard deviation; statistical differences were analyzed with the independent t test or Welch’s test
b Statistical differences were analyzed with Fisher’s exact test
c Data are presented as the median (range); statistical differences were analyzed with the Mann–Whitney U test.
| Variable | Eclampsia (n = 12) | Preeclampsia (n = 5) | P value |
|---|---|---|---|
| Age, y a | 35.6 ± 4.9 | 35.0 ± 7.4 | .85 |
| Primiparity, n (%) b | 8 (66.7) | 4 (80.0) | 1.00 |
| Systolic blood pressure, mm Hg a | 172 ± 25 | 188 ± 17 | .21 |
| Diastolic blood pressure, mm Hg a | 102 ± 17 | 110 ± 18 | .36 |
| Mean blood pressure, mm Hg a | 125 ± 18 | 136 ± 16 | .25 |
| Hematocrit, % a | 39.7 ± 5.0 | 35.9 ± 8.3 | .27 |
| Platelet count, 10 4 /μL a | 17.2 ± 10.7 | 15.9 ± 8.7 | .82 |
| Blood urea nitrogen, mg/dL a | 12.6 ± 5.6 | 16.2 ± 12.4 | .56 |
| Serum creatinine, mg/dL a | 0.69 (0.60–1.30) | 0.70 (0.40–0.60) | 1.00 |
| Aspartate transaminase, IU/L c | 70.0 (18.0–1042.0) | 33.0 (18.0–140.0) | .20 |
| Alanine transaminase, IU/L c | 45.5 (8.0–1008.0) | 18.0 (11.0–103.0) | .44 |
| Total bilirubin, mg/dL c | 0.6 (0.4–2.6) | 0.6 (0.4–1.2) | .65 |
| Lactate dehydrogenase, IU/L c | 562.0 (268.0–2324.0) | 434.0 (244.0–813.0) | .44 |
a Data are presented as the means ± standard deviation; statistical differences were analyzed with the independent t test or Welch’s test
b Statistical differences were analyzed with Fisher’s exact test
c Data are presented as the median (range); statistical differences were analyzed with the Mann–Whitney U test.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
