A hypertensive syndrome that occurs in pregnant women after 20 weeks' gestation
New-onset, persistent hypertension (defined as a BP of ≥140 mmHg systolic and/or ≥90 mmHg diastolic, based on at least 2 measurements taken at least 4 hours apart)
Pre-eclampsia in previous pregnancy
Family history of pre-eclampsia
Body mass index >30
Maternal age >35 years
Multiple (twin) pregnancy
BP ≥80 mmHg diastolic at booking
Interval of 10 years or more since previous pregnancy
Pre-eclampsia has been reported to occur in about 5% to 8% of all pregnancies in the US. 
The incidence of severe disease and complications varies.
Severe disease, which is associated with an increased risk of morbidity and mortality, has an incidence of only 0.5% in the developed world, 
Rises to 1% in low-income countries. 
Similarly, the incidence of complications such as eclampsia is also variable.
This decrease is observed mostly in the intrapartum and postpartum groups, suggesting a possible beneficial effect of prophylactic magnesium sulphate. 
However, in low-income countries the incidence of eclampsia is 10-fold greater, at about 50 per 10,000 per year. 
Pre-eclampsia is associated with a failure of normal invasion of trophoblast cells leading to maladaptation of maternal spiral arterioles
Associated with hyperplacentation disorders such as diabetes, hydatidiform mole, and multiple pregnancy. 
There are numerous risk factors that increase the probability and severity
However, these risk factors do not account for all cases
Complications such as eclampsia, HELLP syndrome, and fetal growth restriction are not present in all patients.
HELLP is a subtype of severe pre-eclampsia characterised by haemolysis (H), elevated liver enzymes (EL), and low platelets (LP)
>20 weeks' gestation
BP ≥140 mmHg systolic and/or ≥90 mmHg diastolic and previously normotensive
upper abdominal pain
reduced fetal movement
fetal growth restriction
hyper-reflexia and/or clonus
Pre-eclampsia is associated with a failure of the normal invasion of trophoblast cells leading to maladaptation of maternal spiral arterioles. 
The maternal arterioles are the source of blood supply to the fetus.
Maladaptation of these vessels can interfere with normal villous development leading to placental insufficiency and fetal growth restriction.
Not all women with this potential placental trigger develop the syndrome
Therefore, the maternal response must be the decisive factor in development of systemic disease.
This systemic maternal response is what manifests itself as pre-eclampsia. 
Clinically, pre-eclampsia does not manifest until after 20 weeks' gestation.
However, more recent studies suggest that preclinical changes may occur, suggested by the presence of various biomarkers, although none are currently used in routine clinical practice. 
Hypertension and proteinuria are due to the vascular inflammatory response that produces vasoconstriction and capillary leak. 
Other presentations are complications of the vascular inflammation and capillary leak
eclampsia (due to cerebral vascular dysregulation and oedema)
HELLP syndrome (due to liver vascular dysregulation and oedema causing abdominal pain)
pulmonary oedema (due to capillary leak).
1+ protein; urinary excretion of ≥0.3 g protein in 24 hours; or urine protein:creatinine ratio ≥30 mg/mmol
variable depending on severity
no abnormalities in tracing indicate assured fetal wellbeing
may reveal fetal growth restriction
umbilical artery Doppler velocimetry
absence of end diastolic flow is a sign that delivery will probably be necessary in the near future
amniotic fluid assessment
deepest vertical pocket ≥2 cm implies normality; <2 cm is associated with increased fetal morbidity and delivery should be considered
low platelet count is partly diagnostic for HELLP syndrome
Increased transaminase levels are partly diagnostic for HELLP syndrome.
Elevated serum creatinine implies underlying renal disease.
Renal failure is a rare complication, and when it occurs, it is usually acute tubular necrosis associated with co-existing sepsis or placental abruption
May be abnormal with advanced disease affecting the liver, or in association with abruption
hospital admission and monitoring
decision regarding delivery
At <32 weeks' gestation: prolonging the pregnancy is beneficial for the fetus, as long as maternal and fetal assessments are satisfactory
At >36 weeks' gestation: delivery is the most sensible approach
Antenatal corticosteroids are recommended before 34 weeks' gestation to mature fetal lungs
consider for outpatient follow-up when stable
with BP ≥150 mmHg systolic and/or ≥100 mmHg diastolic
close monitoring of fluid balance
continue antihypertensives and magnesium sulphate
Pre-eclampsia is a self-limiting condition of pregnancy that usually resolves once the placenta has been delivered, although it may persist for a few days post delivery.
There are few long-term sequelae; however, there are some long-term disease associations.
The course of pre-eclampsia is altered by treatment, and the condition can be controlled easily in the majority of cases, usually within a few hours of starting treatment.
Once controlled, the length of the disease depends on when delivery is decided.
After delivery, the condition normally settles within 2 to 4 days; however, some women have hypertensive problems and proteinuria for some weeks after.
The overall risk of recurrence in subsequent pregnancies ranges from about 10% to 50%
Depending on the severity of pre-eclampsia, the gestation it occurred at, and subsequent interventions in the next pregnancy.  
Generally, in previous severe or early onset (i.e., <30 weeks) pre-eclampsia, the risk of recurrence is 50%.
In mild to moderate or late-onset pre-eclampsia, the risk of recurrence is reduced to around 10%.