Why are women still dying in pregnancy, and what can you actually do about it?

Preeclampsia begins with failed remodeling of uterine spiral arteries, starving the placenta of blood flow. The placenta sends distress signals into the mother's circulation, spiking blood pressure and damaging organs. If caught early, careful delivery timing and magnesium sulfate prevent the worst outcomes. If caught late, the cascade kills.

According to Ngene and Moodley (2024), the frequency of preeclampsia is rising due to increasing obesity, diabetes, advanced maternal age, and multifetal pregnancies. Preeclampsia alone accounts for approximately 50,000 maternal deaths worldwide each year. Scott et al.'s systematic review of 17 international guidelines found universal agreement: low-dose aspirin before 16 weeks prevents early-onset preeclampsia, and magnesium sulfate treats severe cases. Richards et al. confirmed aspirin's efficacy specifically for women with chronic hypertension. A medication that costs pennies. Universally recommended across every guideline on earth. And women are still dying from it. I find that inexcusable, and you should too. The problem with maternal morbidity and mortality from preeclampsia is not that we lack solutions. It is that we fail to apply them consistently.

Let me explain the biology because understanding the mechanism helps you advocate for yourself. During normal pregnancy, the spiral arteries in the uterine wall are remodeled by trophoblast cells to become wide, low-resistance vessels that deliver adequate blood to the growing placenta. In preeclampsia, this remodeling fails. The arteries remain narrow and high-resistance. The placenta becomes chronically underperfused, essentially starving for oxygen. In response, the placenta releases anti-angiogenic factors, primarily sFlt-1 and soluble endoglin, into the maternal circulation. These factors damage the endothelial lining of blood vessels throughout the mother's body, causing the hypertension, proteinuria, liver dysfunction, and cerebral oedema that characterise severe preeclampsia.

The ASPRE trial, published by Rolnik et al. in the New England Journal of Medicine, demonstrated that 150mg aspirin taken nightly starting before 16 weeks of gestation reduced the incidence of preterm preeclampsia by 62%. Sixty-two percent. For a medication that costs less than a dollar per month. The mechanism is straightforward: aspirin inhibits thromboxane A2 production in the placental vasculature, improving blood flow and reducing the inflammatory cascade that leads to spiral artery dysfunction. Every major obstetric guideline now recommends aspirin for women at moderate to high risk. Yet implementation remains inconsistent. Some women are never screened for risk factors. Others are prescribed aspirin too late, after 16 weeks, when the window for prevention has already closed. This is what I mean when I say maternal morbidity and mortality is a story of neglect, not complexity.