Preeclampsia pdf 2009

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Previous Article Next Article. Article Navigation. Articles September 01 Louis, Mo. This Site. Google Scholar. Joyce M. The risk of pre-eclampsia is 2-fold to 5-fold higher in pregnant women with a maternal history of this disorder. Moreover, nulliparity and a new partner have been shown to be important risk factors Table 1.

Major risk factors for pre-eclampsia Pre-eclampsia may be life-threatening for both mother and child, increasing both fetal and maternal morbidity and mortality. The sole curative treatment being delivery, management must continuously balance the risk—benefit ratio of induced preterm delivery and maternal—fetal complications. Screening women at high risk and preventing recurrences are also key issues in the management of pre-eclampsia. During normal pregnancy, the villous cytotrophoblast invades into the inner third of the myometrium, and spiral arteries lose their endothelium and most of their muscle fibers.

These structural modifications are associated with functional alterations, such that spiral arteries become low-resistance vessels, and thus less sensitive, or even insensitive, to vasoconstrictive substances. Pre-eclampsia has a complex pathophysiology, the primary cause being abnormal placentation.

Defective invasion of the spiral arteries by cytotrophoblast cells is observed during pre-eclampsia. Recent studies have shown that cytotrophoblast invasion of the uterus is actually a unique differentiation pathway in which the fetal cells adopt certain attributes of the maternal endothelium they normally replace.

In pre-eclampsia, this differentiation process goes awry. Moreover, inhibition of maternal synthesis of nitric oxide prevents embryo implantation. This chronic placental ischemia causes fetal complications, including intrauterine growth retardation and intrauterine death. In parallel, oxidative stress induces release into the maternal circulation of substances such as free radicals, oxidized lipids, cytokines, and serum soluble vascular endothelial growth factor 1.

These abnormalities are responsible for endothelial dysfunction 15 with vascular hyperpermeability, thrombophilia, and hypertension, so as to compensate for the decreased flow in the uterine arteries due to peripheral vasoconstriction. Endothelial dysfunction is responsible for the clinical signs observed in the mother, ie, impairment of the hepatic endothelium contributing to onset of the HELLP Hemolysis, Elevated Liver enzymes and Low Platelet count syndrome, impairment of the cerebral endothelium inducing refractory neurological disorders, or even eclampsia.

Depletion of vascular endothelial growth factor in the podocytes makes the endotheliosis more able to block the slit diaphragms in the basement membrane, adding to decreased glomerular filtration and causing proteinuria.

Finally, endothelial dysfunction promotes microangiopathic hemolytic anemia, and vascular hyperpermeability associated with low serum albumin causes edema, particularly in the lower limbs or lungs. The crucial issue to understand is that the prime mover of pre-eclampsia is abnormal placentation. Two common theories appear to be interlinked, ie, a genetic theory 1 , 16 and an immunological theory. Some have been identified, and in candidate gene studies they have provided evidence of linkage to several genes, including angiotensinogen on 1-q42—43 and eNOS on 7q36; other main important loci are 2p12, 2p25, 9p13, and 10q Pre-eclampsia can be perceived as an impairment of the maternal immune system that prevents it from recognizing the fetoplacental unit.

Excessive production of immune cells causes secretion of tumor necrosis factor alpha which induces apoptosis of the extravillous cytotrophoblast. High levels of soluble fms-like tyrosine kinase 1 sFlt-1 , an antagonist of vascular endothelial growth factor and placental growth factor, have been found in women with pre-eclampsia.

Recent data show the protective role of heme oxygenase 1 and its metabolite, carbon monoxide, in pregnancy, and identify this as a potential target in the treatment of pre-eclampsia. 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, haptoglobin, 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; 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.

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. 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. Regardless of the severity of pre-eclampsia, there is no advantage in continuing the pregnancy when pre-eclampsia is discovered after 36—37 weeks.

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 management 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.

Similarly, at 24—34 weeks, management depends on the severity of pre-eclampsia. When emergency delivery is not required, labor can be induced by cervical ripening. Antihypertensive treatment is useful only in severe pre-eclampsia because the sole proven benefit of such management is to diminish the risk of maternal complications cerebral hemorrhage, eclampsia, or acute pulmonary edema.

The four drugs authorized for the treatment of hypertension in severe pre- eclampsia in France are nicardipine, labetalol, clonidine, and dihydralazine.

The algorithm for antihypertensive treatment proposed by French experts 22 is shown in Figure 1. Algorithm for antihypertensive treatment of pre-eclampsia. Pulmonary maturation using corticosteroids must be considered, taking gestational age into account. Betamethasone remains the gold standard at a dosage of two injections of 12 mg 24 hours apart; this treatment reduces the risk of hyaline membrane disease, intraventricular hemorrhage, and neonatal mortality. Magnesium sulfate MgSO4 may be part of the therapeutic armamentarium for severe pre-eclampsia.

It is indicated in the treatment of eclamptic convulsions as well as for secondary prevention of eclampsia, thus replacing treatment by diazepam, phenytoin, or the combination of chlorpromazine, promethazine, and pethidine.

Any manifestation of overdose requires stopping the infusion, considering injection of calcium gluconate, and measuring blood magnesium levels. Eclampsia is generally considered an indication for emergency cesarean section.

Although delivery is the only effective treatment for pre- eclampsia, and despite the fact that clinical symptoms and laboratory abnormalities usually regress in the hours afterwards, the risk of complications persists for some time following delivery. Hemodynamic, neurological, and laboratory monitoring is necessary following delivery for patients with severe preeclampsia. Neurological monitoring consists of checking for signs of imminent eclampsia, including headaches, phosphene signals, tinnitus, and brisk tendon reflexes.

Clinical monitoring must be done several times daily during the week after delivery, a period considered at high risk for complications. If necessary, monitoring can be performed in an intensive care unit. Laboratory monitoring should be done several times daily in the first 72 hours after delivery and thereafter adapted according to progress of the indices.

It must include a complete blood count, liver function tests, and measurement of lactate dehydrogenase. The risk of recurrence of pre-eclampsia during a subsequent pregnancy has to be considered. The relative risk is 15 if pre-eclampsia occurs at 20—33 weeks, 10 at 33—36 weeks, and 8 after 37 weeks. Such screening is intended to check for normalization of blood pressure values and disappearance of proteinuria, and if abnormalities persist, a referral should be made to a nephrologist or a hypertension expert to determine the cause.

This examination is important because pre-eclampsia may unmask previously undiagnosed systemic or kidney disease or thrombophilia. This review focuses on diagnosis, management, and counseling of women who develop these syndromes based on results of recent studies and my own clinical experience.

Abstract There are many obstetric, medial, and surgical disorders that share many of the clinical and laboratory findings of patients with severe pre-eclampsia-eclampsia.

Publication types Review.