G1P0A0L0 weeks /S/L/IU head presentation with severe preeclampsia and impending eclampsia + obs. dyspnea 2. G1P0A0L0 Neurological monitoring consists of checking for signs of imminent eclampsia, including headaches, phosphene signals, tinnitus, and brisk. EPH – Edema, proteinuria and hypertension of pregnancyEPH – Oedema, proteinuria and hypertension of pregnancyImpending.

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Pre-eclampsia is a major cause of maternal mortality and morbidity, preterm birth, perinatal death, and intrauterine growth restriction. Unfortunately, the pathophysiology of this multisystem disorder, characterized by abnormal vascular response to placentation, is still unclear. Clinical features and laboratory abnormalities define and determine the severity of pre-eclampsia. Delivery is the only curative treatment for pre-eclampsia.

Multidisciplinary management, involving an obstetrician, anesthetist, and pediatrician, is carried out with consideration of the maternal risks due to continued pregnancy and the fetal impejding associated with induced preterm delivery.

Screening women at high risk and preventing recurrences are key issues in the management of pre-eclampsia. The criteria that define pre-eclampsia have not changed over the past decade. Nonetheless, some presentations of pregnancy-related hypertension combined with clinical or laboratory abnormalities or intrauterine growth restriction should also be considered as potential pre-eclampsia.

The risk eklampsiw 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 Eklampaia 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 adalsh 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 adalxh pre-eclampsia. During normal pregnancy, the villous eklamspia invades into the inner third of the myometrium, and spiral arteries lose their eklamosia 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.

Hypertensive Disorders in Pregnancy – D. El-Mowafi

In pre-eclampsia, this differentiation process goes awry. Moreover, inhibition of maternal synthesis of nitric oxide adalwh embryo implantation. This chronic placental ischemia causes fetal complications, including intrauterine growth retardation adslah 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 imppending 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 116 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.

Pre-eclampsia: pathophysiology, diagnosis, and management

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-1an 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 kmpending 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 eklampssia, vaginal bleeding to placental abruption; vomiting to HELLP syndrome; band-like epigastric pain to subcapsular hepatic hematoma; and dyspnea to cardiac adalay.

Eclampsia, the major neurological complication of pre-eclampsia, is defined as a convulsive episode or any other sign of altered consciousness arising in eklampsai setting of pre-eclampsia, and which cannot adalag 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 edemacardiomyopathy, and acute renal failure.

The fetus should be assessed by electrocardiotocography. 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. Although the definition of severe pre-eclampsia varies, 12122 several components of this definition are usually accepted: Impeding 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 impsnding 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 adqlah is discovered after 36—37 weeks. Prolongation ekllampsia 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.

The presence of one ekampsia more of the following signs indicates the need for immediate delivery: Delivery after corticosteroid therapy for pulmonary maturation is necessary if any of the eklampzia criteria is present: When emergency delivery is not required, labor can be induced impfnding 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 impendin two injections of 12 mg 24 hours apart; this treatment reduces the risk of hyaline membrane fklampsia, intraventricular hemorrhage, and neonatal mortality. Magnesium sulfate MgSO4 may be part of the therapeutic armamentarium for impendin pre-eclampsia. It is indicated in the treatment of eclamptic convulsions as well as for secondary prevention of eclampsia, thus replacing treatment by wdalah, phenytoin, or the avalah 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.

Qdalah examination is important because pre-eclampsia may unmask previously undiagnosed systemic or kidney disease or thrombophilia.

Laporan Kasus PEB + Impending Eklamsia

It should include a specific set of questions, blood pressure measurement, a clinical examination looking for signs of autoimmune conditions, impedning a urinary dipstick test. Testing for antiphospholipid antibodies is recommended after severe pre-eclampsia. The search for hereditary thrombophilia by assays for protein C and S, antithrombin III, and a test for resistance to activated protein C is recommended in the case of a personal or family history of venous thromboembolic disease, early pre-eclampsia, or pre-eclampsia with any intrauterine growth retardation, abruptio placentae, or in utero death.

Patients who have had severe pre-eclampsia may share predispositions with nonpregnant patients who have cardiovascular risk factors. Primary prevention of pre-eclampsia is based on the detection of modifiable risk factors. The literature is plentiful regarding the risk factors for pre-eclampsia, but should be interpreted with caution. Although the search for these risk factors is important, they may not effectively predict this pre-eclampsia by themselves.

However, accurate prediction of pre-eclampsia would enable early and optimal management of women at high ipmending. Several predictive tests are being assessed currently. These include clinical tests, such as blood pressure measurement during the second trimester or hour ambulatory blood pressure monitoring, but these lack sensitivity and specificity. Frequent monitoring of women with elevated levels could be useful, but these tests may not be carried out for screening purposes due to their low negative predictive value.

Imaging tests have been evaluated, including uterine artery Doppler ultra-sound. The combination of a uterine artery Doppler examination during the first trimester and a three-dimensional ultrasound assessing placental volume may predict the risk of pre-eclampsia as adalwh as the first trimester.

In clinical practice, because no single marker effectively predicts the risk of pre-eclampsia, the current trend is to test a combination of markers. The most commonly used combination of markers assesses sFlt-1, placental growth factor, endoglin, and vascular endothelial growth factor during the first or second trimester.

Increased vascular endothelial growth factor and endoglin levels, combined with increased sFlt-1 and decreased placental growth factor during the first trimester, is associated with a significantly increased risk of pre-eclampsia. Improved prediction of pre-eclampsia has been noticed when serum markers are combined with Doppler indices.

In a recent nested case-control study, second trimester maternal serum cystatin C, C-reactive protein, and mipending artery mean resistance index were observed to be independent predictors of pre-eclampsia. However, aspirin should be initiated as early as possible, ie, before 12—14 weeks, which corresponds to the beginning of the first phase of trophoblast invasion.

The efficacy of aspirin has been shown only in women with previous pre-eclampsia associated with intrauterine growth retardation and without thrombophilia. Low molecular weight heparin is indicated only in cases of complicated thrombophilia history of thromboembolic complications or of pre-eclampsia.

Symptoms and signs of impending eclampsia

Pre-eclampsia is a rare pregnancy-related disease with an unpredictable course that can have serious consequences for both the mother and the fetus.

The treatment is simple, ie, delivery. Nonetheless, induced preterm delivery requires careful ekllampsia of both maternal and fetal risk— benefit.

Accordingly, identifying delivery criteria in case of pre- eclampsia is crucial to optimal management.