Diagnosis and Treatment of Eclampsia.

Hypertensive disorders of pregnancy affect approximately 5% to 10% of pregnant women. Eclampsia is a serious hypertensive disorder that is primarily characterized by the onset of grand mal seizure activity in the absence of other causative conditions. While eclampsia is diagnosed clinically, laboratory tests are recommended to assess for complications. Treatment strategies for eclampsia focus on controlling seizures and managing hypertension. Acute care during a seizure is critical because of the need for immediate medical interventions, including the management of the airway, breathing, and circulation, as well as ensuring the safety of the patient during convulsions. Magnesium sulfate is the preferred anticonvulsant drug. Care must be taken during administration to prevent magnesium toxicity. Antihypertensive drugs used in eclampsia include labetalol, hydralazine and nifedipine. The definitive treatment of eclampsia is delivery. Close monitoring of both mother and fetus is important to identify any indications for delivery. The timing and mode of delivery depend on obstetric indications, the severity of eclampsia, the gestational age of the fetus, and the overall clinical status of the patient. Neuraxial anesthesia is the anesthesia of choice for conscious, seizure-free, and with stable vital signs women undergoing cesarean section.

The Molecular Basis of the Augmented Cardiovascular Risk in Offspring of Mothers with Hypertensive Disorders of Pregnancy.

The review examines the impact of maternal preeclampsia (PE) on the cardiometabolic and cardiovascular health of offspring. PE, a hypertensive disorder of pregnancy, is responsible for 2 to 8% of pregnancy-related complications. It significantly contributes to adverse outcomes for their infants, affecting the time of birth, the birth weight, and cardiometabolic risk factors such as blood pressure, body mass index (BMI), abdominal obesity, lipid profiles, glucose, and insulin. Exposure to PE in utero predisposes offspring to an increased risk of cardiometabolic diseases (CMD) and cardiovascular diseases (CVD) through mechanisms that are not fully understood. The incidence of CMD and CVD is constantly increasing, whereas CVD is the main cause of morbidity and mortality globally. A complex interplay of genes, environment, and developmental programming is a plausible explanation for the development of endothelial dysfunction, which leads to atherosclerosis and CVD. The underlying molecular mechanisms are angiogenic imbalance, inflammation, alterations in the renin-angiotensin-aldosterone system (RAAS), endothelium-derived components, serotonin dysregulation, oxidative stress, and activation of both the hypothalamic-pituitary-adrenal axis and hypothalamic-pituitary-gonadal axis. Moreover, the potential role of epigenetic factors, such as DNA methylation and microRNAs as mediators of these effects is emphasized, suggesting avenues for future research and therapeutic interventions.