Pre-eclampsia overview

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2]

Overview

Preeclampsia is one of the leading causes of maternal and perinatal mortality worldwide and is defined as new-onset hypertension after 20 weeks of gestation or near the term accompanied by proteinuria or other [[maternal] organ involvement.Right upper quadrant or epigastric pain may be due to periportal and focal parenchymal necrosis, hepatic cell edema, or Glisson’s capsule distension.




periportal and focal parenchymal necrosis, hepatic cell edema, or Glisson’s capsule distension, or a combination. However reeclampsia is gestational hypertension accompanied by ≥1 of the following new-onset conditions at or after 20 weeks’ gestation:  Proteinuria  Other maternal organ dysfunction, including:   AKI (creatinine ≥90umol/L; 1 mg/dL)   Liver involvement (elevated transaminases, eg, alanine aminotransferase or aspartate aminotransferase >40 IU/L) with or without right upper quadrant or epigastric abdominal pain   Neurological complications (examples include eclampsia, altered mental status, blindness, stroke, clonus, severe headaches, and persistent visual scotomata)   Hematological complications (thrombocytopenia–platelet count <150 000/μL, disseminated intravascular coagulation, hemolysis)  Uteroplacental dysfunction (such as fetal growth restriction, abnormal umbilical artery [UA] Doppler wave form analysis, or stillbirth)


Pre-eclampsia (US: preeclampsia) is a medical condition where hypertension arises in pregnancy (pregnancy-induced hypertension) in association with significant protein in the urine. Its cause remains unclear, although the principal cause appears to be a substance or substances from the placenta causing endothelial dysfunction in the maternal blood vessels.[1] While blood pressure elevation is the most visible sign of the disease, it involves generalized damage to the maternal endothelium and kidneys and liver, with the release of vasopressive factors only secondary to the original damage.

References

  1. Drife JO, Magowan (eds). Clinical Obstetrics and Gynaecology, chapter 39, pp 367-370. ISBN 0-7020-1775-2.

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