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Introduction The term pregnancy induced hypertension PIH suggests a disorder of blood pressure that arises because of the presence of pregnancy. Such a simple view detracts from the fundamental pathological process that underlies this condition: PIH, pre-eclampsia and its variants are part of a multisystem disorder that can affect every organ system in the body and collectively are the second highest cause of direct maternal deaths in the UK.

Although pre-eclampsia is associated with abnormal trophoblast invasion in the first half of pregnancy, it is not until later in the pregnancy that the clinical syndrome of pre-eclampsia is seen. The mechanisms by which the abnormal placentation and subsequent impaired placental perfusion cause the widespread vascular endothelial dysfunction that characterizes pre-eclampsia are not fully understood. Pre-eclampsia is defined as hypertension with proteinurial. It is, however, a very heterogeneous condition such that the timing of onset and the clinical course are unpredictable.

In some, hypertension and proteinuria are the only manifestation, while others may present with severe renal or liver impairment, and in yet others the most prominent feature might be intrauterine fetal growth restriction secondary to placental disease. Eclampsia is a generalized seizure that occurs during pregnancy in association with the features of pre-eclampsia.

In a proportion of women with with eclampsia, however, the features of pre-eclampsia are notevident at the time of the first seizure. The only cure for these conditions is delivery. Hypertension in pregnancy is calssified into three groups, depending on the timing of onset and the associated clinical features:.

Hypertension In normal pregnancy the maternal blood pressure falls slightly during the first trimester, predominantly as a consequence of reduced system vascular resistance. Maternal blood pressure continues to fall during the second trimester and reaches a nadir at approximately weeks gestation.

Thereafter, maternal blood pressure steadily aincreases during the third trimester to reach pre-pregnancy levels. Maternal blood pressure falls immediately after delivery of the baby, but then rises and peaks on the 4th postnatal day. Maternal blood pressure should be measured in the siting position with an appropriatesized cuff that is palced on the upper arm at the level of the heart fig.

Phase V Korotkoff sounds i. A diastolic blood pressure of mmHg on any one occasion or a systolic blood. A systolic blood pressure of 30 mmHg above the booking systolic blood pressure or a diastolic blood pressure of mmHg above the booking diastolic blood pressure are alternative and widely used criteria for the diagnosis of hypertension in pregnancy.

Hypertension in pregnancy may be pre-existing or related to pregnancy PIH or pre-eclampsia. An increased maternal blood pressure in early pregnancy before 20 weeks gestation is usually.

In a young woman with pre-existing hypertension, consideration should be given to identify the rare secondary causes of hypertension such as renal disease, cardiac disease, phaeochromocytoma and endocrine disorders such as Cushings syndrome.

The diagnosis of essential hypertension may be made retrospectively if the materbal bllodpressure has not returned to normal within 3 months of delivery of the baby. PIH and pre-eclampsia rarely occur before 20 weeks gestation unless associated with trophoblastic disease or fetal triploidy. The hypertension associated with preeclampsia usually resolves within 6 weeks of delivery.

A Measurement of blood pressure reproduced with permission. B Testing for urinary protein. Essential hypertension Essential hypertension is more common in older women and the prognosis for pregnancy is generally good; the main risk is from superimposed pre-eclampsia.

Women with essential hypertension are also at increased risk of placental abruption and intrauterine fetal growth restriction. Some women taking antihypertensive drugs may be able to discontinue their medication during pregnancy, particularly during the first and second trimesters.

Drugs that are commonly used for the treatment of essential hypertension during pregnancy include methyldopa, labetalol and nifedipine.

Diuretics and angiotension-converting enzyme ACE. It is established, however, that women who develop pre-eclampsia have a genetic or phenotypic susceptibility and that there are two distinct phases to the conditions development: first there is inadequate trophoblast invasion during early pregnancy, and secondly, in later pregnancy, there is reduced placental perfusion and uteroplacental ischemia, which in turn gives rise to the clinical syndrome.

Box The precise mechanism by which this abnormal placentation causes the multisystem disorder that characterizes pre-eclampsia is not known. It has been suggested that there is a trigger which promotes widespread vascular endothelial dysfunction in response to the reduced placental perfusion. This endothelial dysfunction subsequently causes metabolic changes, an exaggerated maternal inflammatory response and reduced organ perfusion. Maternal susceptibility The evidence for genotypic susceptibility to developing pre-eclampsia is strong.

Large epidemiological studies demonstrate a three-to fivefold increased risk of pre-eclampsia in the first-degree relatives of affected women. While it is possible that a single maternal gene in some families may be important, no single gene has been identified. It may be that multiple genes maternal, paternal and fetal interact, and that environmental factors may effect their expression. Certain phenotypes are also more susceptible.

Women with insulin resistance and central obesity are at increased risk of developing pre-eclampsia, possibly on account of an exaggerated metabolic response. Those with connective tissue disease, such as systemic lupus erythematosus, are also at increased risk, possibly because of an exaggerated immune response.

In addition, those with an inherited thrombophilia are more likely to develop pre-eclampsia. These associations suggest that the pathophysiology of pre-eclampsia involves a significant interaction between metabolic, immunological and coagulation processes, possibly mediated through vascular endothelial dysfunction and damage. Phase 1 abnormal placentation In normal pregnancy, placentation occurs between 6 and 18 weeks gestation.

During normal placentation development, major structural alterations of the spiral arteries occur, allowing an increase in blood supply to the placentation. Trophoblast invasion of the maternal spiral arteries cause the diameter of these arteries to increase approximately five-fold, converting a high-resistence, low-flow system to one with a low resistance and high flow.

In women who develop pre-eclampsia, adequate trophoblast invasion does not seem to occur, or the trophoblastinvation is limited to the decidual portions of the vessels. The result is inadequate placental perfution. This type of abnormal placentation is also associated with intrauterine fetal growth restriction that occurs independently of pre-eclampsia.

During early pregnancy, trophoblast invasion is regulated ed at the maternal decidual barrier by the action of the factors expressed wuthin the decidua and on the trophoblast cells. These regulatory factors include cell adhesion molecules CAMs and the extracellular mattix ECM , proteinases and their inhibitors, growth factors and cytokines. Abnormalities in any one of these factors may lead to invasion and subsequent pre-eclamsia.

It has been suggested. Abnormal placentation may be the resulst of material immune rejection of paternal antigens expressed by the fetus. HLA-G is a class 1B major histocompatibility antigen that is expressed by extra-villous trophoblast and may protect cells from natural killer cell lysis. Women who develop pre-eclampsia in first pregnancies and the protective effect of pairty further support an immunological mechanism for the condition. Phase 2 endothelial dysfunction The second phase of pre-eclampsia is characterized by widespread endothelial damage and dysfunction.

Women with pre-eclampsia have increased circulating levels of markers of endothelial dysfunction. Endothelial damage promotes platelet adhesion and thrombosis, and disturbs the normal physiological modulation of vascular tone, further amplifying the respons. The underlying pathophysiology of this second phase of pre-eclampsia is characterized by an exaggerated maternal systemic inflammatory response, with associated activation of leucocytes, platelets and coagulation system.

Pre-eclampsia is also associated with other markers of inflammation. Features of oxidative stress and dyslipidemia are also evident and the overall effect is reduced organ perfusion. Normal pregnancy is a state of systemic inflammation. In normal pregnancy there is leuccocytosis and an increase in leucocyte activation. Women with pre-eclampsia appear to have an excessive inflammatory response to pregnancy.

Animal models have demonstrated that the administration of endotoxin during pregnancy can cause hypertension and proteinuria.

It has been suggested that the exaggerated maternal inflammatory response that is seen in pre-eclampsia may lead to endothelial dysfunction and damage. Other systemic metabolic. This atherogenic lipid profile may also be a contributor to endothelial dysfunction in women with pre-eclampsia.

Many of the features of the second phase pre-eclampsia are the result of reduced organ perfusion caused by vasoconstriction, activation of the coagulation system and reduction of plasma volume.

The resulting organ damage caused by hypoperfusion gives rise to the clinical features of pre-eclampsia, eclampsia and HELP syndrome see later table Normal pregnancy is associated with an increase in angiotensin II levels. Angiotensin II is a potent vasoconstrictor. However, during normal pregnancy, despite increased angiotensin II levels, peripheral vascular resistance falls.

This appears to be because normal pregnant women are resistant to the effects of angiotensin II, a phenomen that seems to be lost in women who develop PIH and pre-eclampsia. This suggests that abnormalities in the renin-angiotensinaldosterone system may play a role in the pathogenesis of the condition.

Women pre-eclampsia are also more responsive to other vasoconstrictors such as vasopressin and noradrenaline and appear to be less responsive to vasodilators such as nitric oxide and prostacyclin PGI2. In pre-eclampsia, organ perfusion is further compromised by activation of the coagulation cascade.

Altered platelet function is seen in most women with pre-eclampsia. In normal pregnancy there is increase biosynthesis of eicosanoids, particularry prostacyclin and thromboxane A2. Prostacyclin is a vasodilator with platelet-inhibitory properties and thromboxane A2 is a vasoconstrictor with a tendency to promote platelet aggregation. Prostacyclin and thromboxane A2 usually increase in proportion to one another and consequently there is a net neutralization, and homeostasis is disrupted due to a relative deficiency of prostacyclin.

This occurs either because of a reduction in prostacyclin synthesis or because of an increased production of thromboxane A2. This imbalance leads to plateletstimulstion and also vasoconstriction and hypertension. In pre-eclampsia, plasma volume is reduced as a consequence of increased capillary permeability. This further reduces organ perfusion. Table Potential secondary effects of the metabolic, inflammatory endothelial alterations in preeclampsia CVS.

Increased peripheral resistance leading to hypertension Increased vascular permeability and reduced maternal plasma volume Laryngeal and pulmonary oedema Glomerular damage leading to proteinuria,. Hepatic rupture Thrombosis and fibrinoid necrosis of the cerebral arterioles Eclampsia. Linking phase 1 and phase 2 It has been suggested that reduced placental perfusion that is a feature of the first phase of pre-eclampsia is associated with oxidative stress.

Women who develop pre-eclampsia have reduced levels of the antioxidant ascorbic acid, as well as increased levels of markers of oxidative stress. Furthermore, women who develop pre-eclampsia have increased cytrophoblast levels of xanthine oxidase, a superoxide-generating enzyme. The oxidative stress that is. Oxidative stress may also cause placental apoptosis and result in the shedding of placental debris into the maternal circulation. This debris, along with the free radicals produced by osidative stress, may then lead to vascular endothelial damage that characterizes the maternal syndrome of the second phase of preeclampsia.


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