Pathophysiology

Pre-eclampsia has been known as 'The Disease of Theories', as the exact course of events that lead to the clinical syndrome have not been elucidated. However, there is an increasing understanding of these events. It is known that pre-eclampsia is fundamentally related to poor tro-phoblast invasion in the myometrium and this results in maternal spiral arteries being hampered in their normal physiological vasodilatation [8]. The maternal syndrome of pre-eclampsia must be related to additional factors as inadequate trophoblast invasion is also seen in pregnancies complicated by fetal growth restriction without maternal disease. It is clear that impaired intervillous blood flow results in inadequate perfusion and ischaemia in the second half of pregnancy. This probably results in the production of reactive oxygen species. Once the normal endogenous antioxidants are overwhelmed, a condition of oxidative stress exists. This is probably fundamental to the clinical syndrome of pre-eclampsia. Either through oxida-tive stress or other vasoactive substances being released from the placenta, activation of the vascular endothelium occurs [9]. The vascular endothelium is known to supply all organ systems and this explains the widespread

Table 25.2 Risk factors for pre-eclampsia at antenatal booking

Relative risk

Confidence intervals

Antiphospholipid

9.72

4.34-21.75

syndrome

Previous history of

7.19

5.83-8.83

pre-eclampsia

Pre-existing diabetes

3.56

2.54-4.99

Multiple pregnancy

2.93

2.04-4.21

Nulliparity

2.91

1.28-6.61

Family history

2.90

1.70-4.93

Raised BMI

(a) before pregnancy

2.47

1.66-3.67

(b) at booking

1.55

1.28-1.88

Age over 40

1.96

1.34-2.87

Raised diastolic blood

1.38

1.01-1.87

pressure (>80 mmHg)

aspects of the syndrome. Markers of endothelial damage are frequently raised. In addition there is abnormality in lipid profiles, such that triglycerides and free fatty acids are roughly doubled. There is an increase in lipid peroxidation both systemically and in the placenta suggesting that oxidative stress is fundamentally involved in the endothelial cell damage.

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