A 39-year-old woman (gravida 1, para 1) was admitted to Bundang CHA Medical Center. She experienced proteinuria 1 month before delivery, but her blood pressure was within the normal range. Proteinuria persisted throughout the pregnancy and was consistently detected in subsequent urine tests. At 37⁺² weeks of gestation, elective cesarean section was successfully performed in a woman carrying dichorionic diamniotic (DCDA) twins. A few hours after delivery, she experienced a sudden headache with a blood pressure of 140/90 mmHg. She then experienced a seizure that lasted for 2 minutes. She had no significant medical history or neurological symptoms. Upon arrival at Bundang CHA Medical Center, her vital signs were stable: blood pressure 123/ 68 mmHg, SpO₂ 100%, heart rate 58 beats per minute, temperature 36.9℃, and respiratory rate 18 breaths per minute.

A 25-year-old woman (gravida 1, para 1) was transferred to Bundang CHA Medical Center. She was diagnosed with preeclampsia at 31 weeks of pregnancy, but managed to maintain blood pressure within the normal range, which later progressed to mild hypertension without medication. She was carrying DCDA twins, and at 37⁺⁰ weeks of gestation, a cesarean section was performed without any complications. The patient was discharged without complications. Five days after delivery, the patient experienced blurred vision, and her blood pressure was measured with a systolic reading of 150 mmHg. Upon arrival at Bundang CHA Medical Center, her blood pressure was 153/92 mmHg, and she experienced one seizure. She had no significant medical history including neurological disorders. Her vital signs were as follows: SpO₂ 94%, heart rate 85 beats per minute, respiratory rate 18 breaths per minute, and temperature 36.6℃. After the seizure, she became drowsy but recovered the next day and was discharged without complications.

This study was exempted from review by the Institutional Review Board due to its nature as a case report. Informed consent for publication was obtained from the patient

Her urinalysis showed persistent proteinuria (+1), and the complete blood count (CBC) revealed a platelet count of 168×10³/μL, which is on the lower end of the normal range. Serum aspartate transaminase levels were slightly elevated at 49 IU/L, and C-reactive protein (CRP) levels were elevated at 4.87 mg/L (Table 1). Arterial blood gas analysis revealed no significant findings, and the coronavirus disease 2019 (COVID-19) polymerase chain reaction test result was negative. Brain computed tomography (CT) showed no evidence of hemorrhage, and there were no abnormal densities or spaces in the brain parenchyma. Electroencephalography (EEG) was conducted to identify epileptic seizures. No focal or generalized slow activity was observed, and normal responses were elicited with hyperventilation and photic stimulation. As a result, the EEG findings were normal. Chest radiography revealed no signs of pneumonia or pleural effusion (Fig. 1). The echocardiogram results were normal (Fig. 2). Brain MRI was performed to exclude the possibility of cerebrovascular or ischemic diseases. T2 fluid-attenuated inversion recovery (FLAIR) imaging revealed hyperintensities in the bilateral basal ganglia and pons as well as in the bilateral occipital lobes. Susceptibility-weighted angiography showed a punctate hemorrhage in the left parietal lobe (Fig. 3). No findings suggestive of cerebral infarction were observed and no significant abnormalities such as ischemia, tumors, atrophy, or hydrocephalus were noted in the cerebrum, cerebellum, brainstem, ventricles, or cerebrospinal fluid space. Based on the clinical symptoms and blood and imaging test results, PRES appeared to be the most likely cause.

Her urinalysis revealed proteinuria (+2), and the CBC demonstrated a platelet count of 139×10³/μL, which was below the normal range. The CRP levels were elevated at 3.28 mg/dL (Table 2). Arterial blood gas analysis revealed no significant abnormalities, and the COVID-19 test results were negative. Chest radiography revealed mild pleural effusion with radiographic findings suggestive of pulmonary edema (Fig. 4). The electrocardiogram was normal. Brain CT showed no evidence of intracranial hemorrhage. EEG did not demonstrate any epileptiform discharges, indicating no electrophysiological evidence of seizures. Brain MRI was performed to evaluate potential cerebrovascular or ischemic pathologies. T2 FLAIR imaging revealed hyperintensities in the bilateral parieto-occipital lobes and left thalamus. No findings suggestive of cerebral infarction were observed, and no structural abnormalities were noted in the cerebrum, cerebellum, brainstem, ventricular system, or cerebrospinal fluid space (Fig. 5). Based on clinical presentation, laboratory findings, and neuroimaging results, PRES was considered the most likely diagnosis.

The prognosis for PRES is generally favorable, with reports indicating that 75%-90% of patients achieve full recovery (Gewirtz et al., 2021). However, 10%-20% of patients may experience neurological sequelae, and in severe cases, permanent vision loss or even death has been reported (Frick et al., 2017; Liman et al., 2014; So et al., 2015).

The most widely accepted view is that PRES is caused by hypertension and endothelial damage, leading to the disruption of cerebral autoregulation. Normally, cerebral blood flow is maintained through the dilation and constriction of vessels to ensure adequate tissue perfusion and to prevent excessive increases in intracranial pressure. However, when blood pressure rises excessively, autoregulation fails, resulting in breakdown of the blood-brain barrier and extravasation of proteins and fluids into the interstitial space, causing vasogenic edema (Parasher & Jhamb, 2020).

In particular, the increased plasma volume and cardiac output during pregnancy necessitate adaptation of the cerebral circulation to maintain consistent blood flow within the brain. Acute hypertension during pregnancy can contribute to the failure of cerebral autoregulation, reduced cerebral vascular resistance, and elevated blood pressure. In addition, women with preeclampsia have elevated levels of circulating factors, such as vascular endothelial growth factor and placental growth factor, increasing vascular permeability and contributing to vasogenic edema. In women with preeclampsia, oxidative stress in the placental circulation changes low-density lipoprotein (LDL) to oxidized LDL (oxLDL), which then binds to lectin-like oxLDL receptor (LOX-1). This mechanism triggers inflammation and increases superoxide production within endothelial cells, adversely affecting endothelial function (Fishel Bartal & Sibai, 2022). Endothelial damage is another common trigger of PRES and can contribute to the likelihood of PRES in women with preeclampsia.

The primary goals in the management of PRES include reduction of cerebral edema, achieve blood pressure control, and seizure management. In patients with acute hypertension, careful and gradual lowering of blood pressure is essential, avoiding reductions of more than 20%-25% in the initial hours. The target mean arterial pressure should be maintained between 105 and 125 mmHg. Currently, no standardized protocols exist for the administration of antiepileptic medications in PRES; hence, treatment should be tailored to an individual patient's clinical status. In cases of eclampsia, magnesium sulfate is particularly beneficial because of its vasodilatory effects and ability to decrease vascular permeability, thereby reducing cerebral edema (Zhu & Huang, 2023).

Although, PRES is rare and often associated with a good prognosis, it can sometimes be accompanied by serious sequelae. Therefore, we concluded that continuous monitoring of mothers during the antenatal and postpartum periods is essential to prevent eclampsia and PRES. Emphasis should be placed on identifying at-risk groups through blood pressure elevation, blood tests, and biomarkers in women with preeclampsia and suspected preeclampsia, and implement continuous monitoring to prevent PRES. Currently, evidence regarding impact of early diagnosis of PRES on clinical management of eclampsia is limited. Further research is needed to clarify the clinical relevance of differentiating eclampsia from PRES in patients without persistent neurological sequelae.

Postpartum eclampsia is associated with the persistence of gestational hypertension, preeclampsia, and proteinuria and can also arise from other causes. Symptoms of postpartum eclampsia can range from mild to life-threatening, and include seizures and cerebrovascular accidents. Therefore, diagnosis and management should be continuous and conducted in a stepwise manner, requiring a multifaceted approach that considers the diagnosis of preeclampsia before delivery, its risk factors, time of onset, and associated signs. Symptoms of preeclampsia and proteinuria are generally treated within the first week postpartum and blood pressure usually decreases within 48 hours. However, in some patients, worsening postpartum hypertension and neurological symptoms may lead to postpartum eclampsia or the HELLP syndrome (Sibai, 2012).

Consideration of risk factors for the development of postpartum preeclampsia is essential. Among maternal characteristics, advanced maternal age, particularly age >35 years, has been associated with an approximately twofold increase in risk. Prepregnancy obesity is another significant factor, with a body mass index ≥40 linked to up to a 7.7-fold increased risk. Nulliparity also appears to confer a greater risk than multiparity, and women with a history of hypertensive disorders in prior pregnancies are more likely to experience postpartum preeclampsia. Intrapartum factors also contribute to the risk. Cesarean delivery is associated with a 2- to 7-fold increased risk of postpartum preeclampsia when compared with vaginal delivery. Additionally, large volumes of intravenous fluid administered during labor have been associated with an increased risk, potentially due to fluid shifts that result in postpartum volume overload and hypertension (Hauspurg & Jeyabalan, 2022).

The 2 previous cases also involved instances of eclampsia resulting from postpartum hypertension. Therefore, it is important to understand how to manage mothers with nonsevere preeclampsia and persistent proteinuria suspected to be related to preeclampsia, both prenatally and postpartum.