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7 - Pre-eclampsia and hypertensive disorders of pregnancy

Published online by Cambridge University Press:  21 August 2009

Alexander Heazell
University of Manchester
John Clift
City Hospital, Birmingham
Egidio da Silva
Specialist Registrar in Anaesthesia and Intensive care University Hospitals, Birmingham, Queen Elizabeth Hospital, Birmingham, UK
Wilson Chimbira
Lecturer in Anaesthesiology, University of Michigan, Ann Arbor, Michigan, USA
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Pre-eclampsia is a multi-system disorder, which primarily affects the cardiovascular system, leading to dysfunction of liver, lungs, kidney and brain. Pre-eclampsia is unpredictable in presentation and progression. At present, there is no curative treatment for pre-eclampsia and the ultimate management is the delivery of the fetus and placenta. Pre-eclampsia can present at any time after the 20th week of gestation, and is an important cause of iatrogenic prematurity, with the associated perinatal morbidity and mortality. In cases of extreme prematurity, pregnancy is prolonged until maternal health is at risk. Success in the management of pre-eclampsia is dependent at least in part on a multidisciplinary approach by the midwifery, obstetric, anaesthetic, intensive care and neonatal teams.

In the UK, pre-eclampsia has an incidence of between 3% and 5%, with severe pre-eclampsia complicating 0.5% of pregnancies. Eclampsia affects only 0.05% of pregnancies in the UK. It is estimated that 1 in 6 stillbirths and 14% of maternal mortality are due to pre-eclampsia and hypertensive disorders of pregnancy.

Aetiology and pathogenesis

Pre-eclampsia is related to placental pathology, probably arising from decreased trophoblast invasion in the first trimester. This reduction in invasion fails to convert the convoluted spiral arteries to high-flow, low-resistance vessels that feed the placenta, thus decreasing placental blood flow, which may result in placental hypoxia and oxidative stress. It is hypothesised that the damaged placenta releases active factor(s) into the maternal circulation that results in endothelial damage and vasoconstriction within the maternal vasculature (Figure 7.1).

Publisher: Cambridge University Press
Print publication year: 2008

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