Dovepress Accordingly, assays of sFlt-1, placental growth factor, endoglin, and vascular endothelial growth factor, all of which increase 4–8 weeks before onset of the disease, may be useful predictors of pre-eclampsia. Recent data show the protective role of heme oxygenase 1 and its metabolite, car- bon monoxide, in pregnancy, and identify this as a potential target in the treatment of pre-eclampsia.20 Clinical presentation and workup findings Clinical and laboratory tests are intended to define and determine the severity of pre-eclampsia. Headaches, tinnitus, phosphene signals, visual disorders, brisk tendon reflexes, and vigilance disorders are related to cerebral edema; oliguria to acute renal failure; uterine contraction, vaginal bleeding to placental abruption; vomiting to HELLP syndrome; band- like epigastric pain to subcapsular hepatic hematoma; and dyspnea to cardiac failure. Eclampsia, the major neurological complication of pre-eclampsia, is defined as a convulsive episode or any other sign of altered consciousness arising in a setting of pre-eclampsia, and which cannot be attributed to a pre-existing neurological condition. Clinical examination should include resting blood pressure measurement using an appropriate cuff, and screening for weight gain, edema (including signs of acute pulmonary edema and cerebral edema), cardiomyopathy, and acute renal failure. The fetus should be assessed by electrocardiotocography. Laboratory tests include: a complete blood count with platelets, hapto- globin, and lactate dehydrogenase; a blood smear to test for schistocytes; bilirubin, aspartate transaminase, and alanine transaminase in order to identify potential HELPP syndrome; electrolyte, urea, and creatinine assessment to check for acute renal failure or uremia; 24-hour proteinuria; prothrombin, activated thrombin time, and fibrinogen (microangiopathic hemolytic anemia); blood group; and irregular antibody screening. Other examinations include fetal ultrasound with Doppler velocimetry of the umbilical, cerebral, and uterine arteries, estimation of fetal weight, assessment of fetal well-being by Manning score, and examination of the placenta.21 Although the def inition of severe pre-eclampsia varies,1,21,22 several components of this definition are usually accepted: maternal systolic blood pressure $160 mmHg or diastolic blood pressure $110 mmHg; maternal neurological disorders such as persistent headaches, phosphene signals, tinnitus, and brisk, diffuse, polykinetic tendon reflexes, eclampsia, acute pulmonary edema, proteinuria $5 g/day, oliguria ,500 cc/day, creatinine .120 µmol/L, HELLP Vascular Health and Risk Management 2011:7 Pre-eclampsia syndrome, thrombocytopenia ,100,000/mm3, and fetal criteria, especially intrauterine growth retardation, oligohydramnios, or fetal death in utero. Mild pre-eclampsia is defined as diastolic blood pressure $90 mmHg mea- sured on two occasions at least 6 hours apart, combined with proteinuria (two or more occurrences of protein on dipstick, .300 mg total protein in a 24-hour urine collection, or a protein creatinine ratio .30 mg/mmol).1 Immediate emergency management Delivery is the only curative treatment for pre-eclampsia.1 Management is multidisciplinary, involving an obstetrician, an anesthetist, and a pediatrician. In some cases consultation of maternal fetal medicine and hypertension or nephrology subspecialists may be required. Management decisions must balance the maternal risks of continued pregnancy against the fetal risks associated with induced preterm delivery.2 The criteria for delivery are based on two often interrelated factors, ie, gestational age at diagnosis (estimated fetal weight) and severity of pre-eclampsia. Severe pre-eclampsia requires treatment with a dual aim, ie, preventing the harmful effects of elevated maternal blood pressure and preventing eclampsia. Management of severe pre-eclampsia begins with transfer of the mother in a fully equipped ambulance or helicopter to a maternity ward providing an appropriate level of care for both mother and child.2 At admission and daily thereafter, clinical, cardiotoco- graphic, laboratory, and ultrasound testing are required to detect the severity of pre-eclampsia and tailor management accordingly.22 Regardless of the severity of pre-eclampsia, there is no advantage in continuing the pregnancy when pre-eclampsia is discovered after 36–37 weeks.23–25 Nor is expectant management justif ied for severe pre-eclampsia before 24 weeks, in view of the high risk of maternal complications and the poor neonatal prognosis.26–28 The obstetric team must then discuss with the parents the possibility of a medical interruption of pregnancy. Prolongation of pregnancy in the event of mild pre-eclampsia can be discussed and re- evaluated on a regular basis. At 34 –37 weeks, management depends on the severity of the pre-eclampsia. Expectant man- agement is possible for mild pre-eclampsia to limit the risk of induced preterm delivery, but for severe pre-eclampsia, delivery remains the rule due to the increased risk of maternal and fetal complications.2,22 Similarly, at 24–34 weeks, management depends on the severity of pre-eclampsia. The presence of one or submit your manuscript | www.dovepress.com Dovepress 469