Preeclampsia: Pathophysiology

Jorge Muniz ·
Educational medical illustration of preeclampsia pathophysiology showing defective trophoblast invasion of spiral arteries leading to placental hypoperfusion, resulting in hypertension, proteinuria, and end-organ damage after 20 weeks gestation, including HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets)
Illustrated guide to preeclampsia pathophysiology — covering defective spiral artery remodeling, placental hypoperfusion, clinical features, risk factors, HELLP syndrome, and eclampsia. Proprietary medical illustration by Jorge Muniz, PA-C.

General Features

  • Preeclampsia is classically defined as the new onset of hypertension and proteinuria after 20 weeks of gestation
    • New onset hypertension with significant end-organ dysfunction (with or without proteinuria) after 20 weeks of gestation also satisfies the diagnosis of preeclampsia
      • Severe headache, epigastric or right upper quadrant pain, visual disturbances, thrombocytopenia, impaired liver function, renal insufficiency, pulmonary edema
      • HELLP syndrome: Hemolysis, Elevated Liver enzymes, Low Platelets
    • Edema may or may not be present
  • Eclampsia = preeclampsia + seizures
  • Risk factors include nulliparity, past history of preeclampsia, preexisting hypertension or renal disease, autoimmune disease, very young or advanced maternal age, diabetes, and obesity
  • Curative treatment is delivery

Pathophysiology

  • Genetic and immunological factors
  • Defective spiral artery remodeling during pregnancy
    • During a normal pregnancy trophoblast cells invade the myometrial segment of the spiral arteries to cause transformation and dilation of the arteries
    • In preeclampsia there is insufficient trophoblast cell invasion, which causes the spiral arteries to remain narrow and leads to placental hypoperfusion
  • Diseased placenta releases proinflammatory proteins
    • Hypertension
    • Vasoconstriction
    • Endothelial cell dysfunction
      • Formation of thrombi
    • End-organ damage

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