Preeclampsia is a disorder that only happens in pregnant women, and it happens after 20 weeks’ gestation, and in some cases develops up to 6 weeks after delivery.
Preeclampsia causes new-onset hypertension and proteinuria, which is a marker of kidney damage, and can also cause damage to other organs like the brain and liver.
There can be a wide range of symptoms. For some women there may be no symptoms or only mild ones, whereas for others, it can turn into a life-threatening illness.
If a woman with preeclampsia develops seizures, she is then said to have eclampsia.
Preeclampsia tends to occur more often during a first pregnancy, in pregnancies with multiple gestations, or in mothers 35 years or older.
Other risk factors include having hypertension, diabetes, obesity, or a family history of preeclampsia.
Alright, but why do these changes happen in preeclampsia and eclampsia?
Well, the exact cause is unclear, but a key pathophysiologic feature though is the development of an abnormal placenta.
Normally, during pregnancy, the spiral arteries dilate to 5-10 times their normal size and develop into large uteroplacental arteries that can deliver large quantities of blood to the developing fetus.
In preeclampsia, these uteroplacental arteries become fibrous causing them to narrow, which means less blood gets to the placenta.
A poorly perfused placenta can lead to intrauterine growth restriction and even fetal death in severe cases.
This hypoperfused placenta starts releasing pro-inflammatory proteins.
These then get into the mother’s circulation and cause the endothelial cells that line her blood vessels to become dysfunctional.
Endothelial cell dysfunction causes vasoconstriction—narrowing of the blood vessels—and also affects the kidneys in a way that makes them retain more salt, both of which result in hypertension.
When diagnosing preeclampsia, hypertension is defined as a systolic blood pressure of 140 mmHg or greater or diastolic blood pressure of 90 mmHg or greater.
