Toxemia · What Is It, How It Is Managed, and More

Toxemia in pregnancy is an outdated term for what is now known as preeclampsia. The term toxemia was a common term in the 19th and early 20th centuries before the discovery of specific pathophysiological mechanisms. Now it has been mostly replaced by more precise terms (e.g., sepsis, preeclampsia, toxicity, uremia, etc.). 

Preeclampsia is a complication of pregnancy characterized by new-onset high blood pressure and signs of damage to various organs, like the liver or kidneys. It’s a disorder that only occurs in pregnant individuals, and it happens after 20 weeks’ gestation, although in some cases it can develop up to 6 weeks after delivery.  

The main signs of preeclampsia are new-onset hypertension and proteinuria, or the presence of proteins in the urine, which is a marker of kidney damage. Other symptoms may include persistent headaches, visual disturbances, upper right abdominal pain, nausea or vomiting, and decreased urine output. Signs and symptoms of preeclampsia vary in severity and can develop gradually or abruptly. Some individuals may not experience any symptoms of preeclampsia or only mild ones, while for others it can turn into a life-threatening illness.  

The exact cause of preeclampsia is unclear, but it’s thought to arise from a disruption in the development of the placenta. During a healthy pregnancy, the spiral arteries in the uterus undergo significant changes—they expand up to 5 to 10 times their usual size and transform into wide, low-resistance vessels capable of supplying a large amount of blood to the growing fetus.  

In preeclampsia, however, this remodeling process doesn’t take place. The arteries remain narrow and take on a fibrous structure, restricting blood flow to the placenta. Early on in pregnancy, the placenta can easily meet the fetus’s needs despite the abnormal blood supply. Around 20 weeks of gestation, as the fetus's need for oxygen and nutrients increases, the placenta responds to the insufficient blood and oxygen supply by releasing inflammatory mediators into the mother’s circulation. These molecules (e.g., sFlt-1, sEng) trigger widespread dysfunction in the vascular endothelium—the thin layer of cells lining blood vessels—contributing to the systemic symptoms of preeclampsia. 

Although rarer, it’s possible for preeclampsia to occur up to 6 weeks after delivery. That’s because even though the placenta is gone, the harmful effects of the inflammatory molecules can linger in the maternal bloodstream for hours to days, continuing to damage the endothelium.  

While anyone can develop preeclampsia, it 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 chronic high blood pressure, diabetes, obesity, or a family history of preeclampsia, as well as being Black and/or Hispanic. 

Preeclampsia can lead to serious complications, including maternal death and fetal demise, if left untreated. Severe forms of preeclampsia or those that occur early in pregnancy (i.e., before 34 weeks’ gestation) are associated with greater risks for both the pregnant individual and the fetus.  

Complications for a person with preeclampsia may include excessive bleeding due to low platelet levels in the blood, as well as damage to the liver, lungs, kidneys, eyes, or heart. A stroke or heart attack can also result. In addition, preeclampsia may cause the placenta to separate from the wall of the uterus, which can deprive the fetus of oxygen and nutrients and may lead to premature birth, restricted growth of the fetus, and fetal demise, in severe cases. 

Another severe complication of preeclampsia is eclampsia, which is characterized by coma and seizures in addition to the characteristic preeclampsia symptoms. While most individuals recover fully from eclampsia, there's a small risk of brain damage and permanent disability.   

HELLP syndrome is another life-threatening complication of preeclampsia. The acronym HELLP stands for hemolysis (i.e., the destruction of red blood cells), elevated liver enzymes, and low platelet count. This syndrome is a more severe form of preeclampsia, capable of rapidly becoming life-threatening for both the pregnant individual and fetus. The majority of pregnant individuals with HELLP syndrome will have high blood pressure and the presence of protein in the urine. 

Diagnosis of preeclampsia is established in pregnant individuals who present with blood pressure readings over 140/90 mmHg consistently along with signs of organ damage after 20 weeks’ gestation. Those who develop hypertension during their pregnancy but show no signs of organ damage are diagnosed with gestational hypertension instead.  

Early and consistent prenatal visits may help diagnose and treat preeclampsia in early stages to avoid further complications. Blood pressure will be monitored regularly, and blood tests may be ordered to assess platelets, clotting factors, and kidney and liver function. Urine tests may also be ordered to assess protein levels in the urine. Additionally, regular fetal surveillance may also be recommended to monitor the health and growth of the fetus. A diagnosis of preeclampsia may be made based on lab values alone, regardless of the presence of clinical symptoms.  

Yes, there are predictive tests for preeclampsia, which aim to identify individuals at high risk for the condition before clinical symptoms appear, allowing for early intervention (e.g., low-dose aspirin).  

The best current predictive method for early-onset preeclampsia is a first-trimester combined screening including clinical factors, uterine artery Doppler, and biomarkers like PlGF or PAPP-A. Later in pregnancy, the sFlt-1/PlGF ratio can be used to detect or rule out preeclampsia, especially in uncertain cases. A high ratio indicates placental dysfunction, while a low ratio has a strong negative predictive value, meaning preeclampsia is unlikely to develop in the next week or two. 

Treatment of preeclampsia varies depending on the severity of clinical presentation and stage of pregnancy. Because 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.  

In preeclampsia without severe features, management involves regular monitoring of blood pressure and serial laboratory tests to detect any signs of organ damage, as well as fetal surveillance with non-stress tests and serial ultrasounds. Antihypertensive medications, like hydralazine or nifedipine may be started. If no complications arise, delivery is typically recommended at 37 weeks’ gestation.  

On the other hand, in preeclampsia with severe features, individuals may be admitted to the hospital for the remainder of their pregnancy for close maternal and fetal monitoring. Antihypertensives may be prescribed to control blood pressure, and magnesium sulfate may be given to prevent seizures. If the individual is less than 34 weeks pregnant, they may be given corticosteroids to promote fetal lung maturity. If maternal and fetal status are reassuring, delivery may be induced at 34 weeks, or at the time of diagnosis if further along. Alternatively, if the individual becomes unstable or if eclampsia occurs, delivery may be induced right away to prevent further worsening.  

After delivery of the baby, signs and symptoms of preeclampsia typically resolve. In rare situations, preeclampsia may appear after delivery, so follow-up care with a clinician after delivery is very important. 

Maintaining regular prenatal appointments is the most effective method of detecting preeclampsia early. Eating a nutritious diet, exercising, and managing pre-existing chronic conditions may also reduce an individual’s risk of developing preeclampsia. For pregnant individuals with high-risk characteristics, a clinician may advise they start taking a low dose of aspirin early in pregnancy to help reduce preeclampsia risk.