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. In severe preeclampsia, systolic blood pressure can be 160 mmHg or greater and diastolic blood pressure can be 110 mmHg or greater. These extreme blood pressures can lead to a hemorrhagic stroke or placental abruption, which the placenta detaches prematurely from the uterine wall.

Now, there can also be local areas of vasospasm, which means that less blood might reach certain parts of the body. For example, reduced blood flow to the kidneys, which are particularly susceptible, can cause glomerular damage leading to oliguria—which is abnormally low amounts of urine, as well as proteinuria . Normally, the glomeruli of the kidneys do a good job of preventing protein from spilling into the urine, so proteinuria can be a sign of glomerular damage and is a classic sign of preeclampsia. Reduced blood flow to the retina can cause blurred vision, the sensation of seeing flashing lights, and the development of a scotoma. A scotoma is when a small part of the visual field has slightly worse visual acuity, which is kind of like having a blurry spot on an otherwise normal computer monitor.

Reduced blood flow to the liver can cause severe liver injury and swelling, which can cause an elevation in liver enzymes and stretches out the capsule around the liver. Stretching of the liver capsule typically causes right upper quadrant pain, or epigastric pain, which is one of the cardinal symptoms of severe preeclampsia.

Endothelial injury also leads to the formation of lots of tiny thrombi in the microvasculature, which is a process that uses up massive amounts of platelets. Having all of these tiny blood clots in the blood is a bit like having dozens of boulders in the middle of a fast moving river. It becomes treacherous for red blood cells to navigate through, and before long, they slam up against a clot and get destroyed, which is a process called hemolysis. Together these make up HELLP syndrome, H for hemolysis, EL for elevated liver enzymes, and LP for low platelets. HELLP syndrome develops in about 10 to 20% of women with severe preeclampsia or eclampsia.

Finally, endothelial injury increases vascular permeability, which is when water is allowed to slip out of blood vessels between neighboring endothelial cells and get into the tissues. Because there’s also a loss of protein from the blood due to the proteinuria, even more fluid moves from the blood vessels into the tissues.

And this causes generalized edema which is often seen in the legs, face and hands; pulmonary edema which can cause cough and shortness of breath; and cerebral edema which can cause headache, confusion, and seizures. These seizures define the onset of eclampsia.

Because all of the problems of preeclampsia and eclampsia stem from placental dysfunction, the ultimate treatment is delivery of the fetus and placenta. The decision to induce delivery depends heavily on the gestational age of the fetus as well as the severity of the disease and how it’s affecting both maternal and fetal health. If the onset of symptoms comes after delivery, then the goal is to manage the symptoms which slowly subside on their own. Additional measures are aimed at managing any end-organ damage by offering supplemental oxygen, as well as medication to manage seizures, and other complications like stroke or placental abruption.

All right, as a quick recap, preeclampsia is a disorder that occurs after 20 weeks gestation and up to 6 weeks following delivery. It is defined by a new onset of hypertension and proteinuria but can affect a lot of organs, particularly the kidneys, eyes, liver, and brain. Eclampsia is diagnosed when a patient with preeclampsia develops seizures.

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