Preeclampsia was formerly defined as a multisystemic disorder characterized by new onset of hypertension (i.e. systolic blood pressure (SBP) ≥ 140 mmHg and/or diastolic blood pressure (DBP) ≥ 90 mmHg) and proteinuria (> 300 mg/24 h) arising after 20 weeks of gestation in a previously normotensive woman. Recently, the American College of Obstetricians and Gynecologists has stated that proteinuria is no longer required for the diagnosis of preeclampsia. This complication of pregnancy remains a leading cause of maternal morbidity and mortality. Clinical signs appear in the second half of pregnancy, but initial pathogenic mechanisms arise much earlier. The cytotrophoblast fails to remodel spiral arteries, leading to hypoperfusion and ischemia of the placenta. The fetal consequence is growth restriction. On the maternal side, the ischemic placenta releases factors that provoke a generalized maternal endothelial dysfunction. The endothelial dysfunction is in turn responsible for the symptoms and complications of preeclampsia. These include hypertension, proteinuria, renal impairment, thrombocytopenia, epigastric pain, liver dysfunction, hemolysis-elevated liver enzymes-low platelet count (HELLP) syndrome, visual disturbances, headache, and seizures. Despite a better understanding of preeclampsia pathophysiology and maternal hemodynamic alterations during preeclampsia, the only curative treatment remains placenta and fetus delivery. At the time of diagnosis, the initial objective is the assessment of disease severity. Severe hypertension (SBP ≥ 160 mm Hg and/or DBP ≥ 110 mmHg), thrombocytopenia < 100.000/μL, liver transaminases above twice the normal values, HELLP syndrome, renal failure, persistent epigastric or right upper quadrant pain, visual or neurologic symptoms, and acute pulmonary edema are all severity criteria. Medical treatment depends on the severity of preeclampsia, and relies on antihypertensive medications and magnesium sulfate. Medical treatment does not alter the course of the disease, but aims at preventing the occurrence of intracranial hemorrhages and seizures. The decision of terminating pregnancy and perform delivery is based on gestational age, maternal and fetal conditions, and severity of preeclampsia. Delivery is proposed for patients with preeclampsia without severe features after 37 weeks of gestation and in case of severe preeclampsia after 34 weeks of gestation. Between 24 and 34 weeks of gestation, conservative management of severe preeclampsia may be considered in selected patients. Antenatal corticosteroids should be administered to less than 34 gestation week preeclamptic women to promote fetal lung maturity. Termination of pregnancy should be discussed if severe preeclampsia occurs before 24 weeks of gestation. Maternal end organ dysfunction and non-reassuring tests of fetal well-being are indications for delivery at any gestational age. Neuraxial analgesia and anesthesia are, in the absence of thrombocytopenia, strongly considered as first line anesthetic techniques in preeclamptic patients. Airway edema and tracheal intubation-induced elevation in blood pressure are important issues of general anesthesia in those patients. The major adverse outcomes associated with preeclampsia are related to maternal central nervous system hemorrhage, hepatic rupture, and renal failure. Preeclampsia is also a risk factor for developing cardiovascular disease later in life, and therefore mandates long-term follow-up.