Hypertensive Disorders of Pregnancy

BP should be measured in the sitting position with a cuff that is large enough for the subject arm. Hypertension is defined as one of the following :
1. One measurement of diastolic BP of 110 mmHg or more; or
2. Two consecutive measurements of diastolic BP of ? 90 mmHg 4 hours or more apart.
Definition of proteinuria:
1. One 24-h urine collection with a total protein excretion of 300 mg or more; or
2. Two random clean-catch urine specimen with a 2+ or more on reagent strip.

Pre-eclampsia: is defined as hypertension associated with proteinuria arising de novo after the 20th week of gestation in a previously normotensive woman & resolving completely by the 6th postpartum week.

Eclampsia: is a serious life-threatening complication of pre-eclampsia when tonic-clonic convulsion occur in a woman with established pre-eclampsia, in the absence of any other neurological or metabolic cause.

Gestational hypertension: hypertension arising for the first time in the second half of pregnancy without the development of proteinuria, this usually have no important maternal or fetal consequences.

Chronic hypertension: hypertension which is apparent prior to, in the first half of, or persisting more than 6 weeks after pregnancy. The definition of superimposed pre-eclampsia in the presence of chronic hypertension can be difficult to make, but is usually associated with a worsening of the hypertension & the development, or worsening of, proteinuria.




Incidence & Epidemiology:
Pre-eclampsia complicate about 3% of pregnancies. It is more common in primigravid women. Also there is a maternal genetic predisposition as there is a 3-4 fold increase in the incidence of pre-eclampsia in the first degree relatives of affected women. Risk factors for the development of pre-eclampsia include:
1. conditions in which the placenta is enlarged ( multiple gestation, diabetes, hydrops)
2. pre-existing hypertension or renal disease.
3. pre-existing vascular disease (as in diabetes or autoimmune vasculitis.

Aetiology: During normal pregnancy, the cytotrophoblast invade the uterine spiral arteries & the inner part of the myometrium. Invasion of the spiral arteries is associated with degeneration of the tunica media & replacement by fibrinoid material resulting in marked dilatation of the spiral artery & increased intervillous blood flow. In pre-eclampsia, trophoblast invasion is patchy & the spiral arteries retain their muscular walls which will prevent the development of high-flow, low-impedence uteroplacental circulation. Under-perfusion of the placenta causes it to release certain factors (adhesion molecules, von-willebrand factor) into the maternal circulation which target the vascular endothelium & cause dysfunction.

Pathophysiology: The clinical picture of pre-eclampsia is due to activation or dysfunction of vascular endothelial cells. Normal pregnancy is characterized by marked peripheral vasodilatation resulting in a fall in total peripheral resistance despite an increase in cardiac output & circulating volume. This peripheral vasodilatation is accomplished through a reduced vascular sensitivity to vasoconstrictors such as angiotensin. In pre-eclampsia the insensitivity to vasoconstrictors is lost. Vasospasm & endothelial cell dysfunction, with subsequent platelet activation & micro-aggregate formation, account for many pathological features of pre-eclampsia seen in every major organ system. These include: