Preeclampsia: Difference between revisions
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'''Original Editor '''- [[User: | '''Original Editor '''- [[User:Lucinda hampton|Lucinda hampton]] | ||
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Revision as of 02:26, 6 March 2024
Original Editor - Lucinda hampton
Top Contributors - Lucinda hampton, Ayodeji Mark-Adewunmi, Kirenga Bamurange Liliane and Carina Therese Magtibay
Introduction[edit | edit source]
Preeclampsia is a life-threatening cardiovascular disorder associated with pregnancy. Preeclampsia is marked by hypertension and proteinuria at 20 weeks of gestation. The underlying cause is not precisely known but likely heterogenous. Ample research suggests that for some women with preeclampsia, both maternal and placental vascular dysfunction plays a part in its' evolution and can carry on into the postpartum period. Possible changes include impaired placentation, and endothelial damage.[1]
Maternal Consquences[edit | edit source]
Preeclampsia is associated with an increased relative risk for the development of end-stage kidney disease (ESKD) in the mother.
Research shows that women with a history of preeclampsia are 60% more likely to experience ischemic stroke and also have an increased risk of hemorrhagic stroke and venous thromboembolism[2].
Women with a history of preeclampsia have increased white matter hyperintensities on brain magnetic resonance imaging9,106, a marker of cerebral small vessel disease that is highly associated with stroke and dementia [3]
Neonatal Consequences[edit | edit source]
The neonatal outcomes of preeclampsia identified are; preterm birth, stillbirth, low birth weight (LBW), low Apgar score, intrauterine growth reduction (IUGR), neonatal intensive care unit (NICU) admission.[4]
Other differences include delayed physical development and sensorimotor reflex maturation, increased body mass index, changes in neuroanatomy and reductions in cognitive function, and hormonal changes.[2]
Preeclampsia is one of three conditions that constitute the syndrome of ischaemic placental disease, a group of pathologies that also includes placental abruption and intrauterine growth restriction.[5]
Resources[edit | edit source]
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References[edit | edit source]
- ↑ Opichka MA, Rappelt MW, Gutterman DD, Grobe JL, McIntosh JJ. Vascular dysfunction in preeclampsia. Cells. 2021 Nov 6;10(11):3055.Available:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8616535/ (accessed 5.3.2024)
- ↑ 2.0 2.1 Turbeville HR, Sasser JM. Preeclampsia beyond pregnancy: long-term consequences for mother and child. American Journal of Physiology-Renal Physiology. 2020 Jun 1;318(6):F1315-26.Available:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7311709/ (accessed 5.3.2024)
- ↑ Miller EC. Preeclampsia and cerebrovascular disease: the maternal brain at risk. Hypertension. 2019 Jul;74(1):5-13.Available:https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.118.11513 (accessed 5.3.2024)
- ↑ Atamamen TF, Naing NN, Oyetunji JA, Wan-Arfah N. Systematic literature review on the neonatal outcome of preeclampsia. Pan African Medical Journal. 2022 Jan 31;41(1).Available:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8977357/ (accessed 5.3.2024)
- ↑ Parker SE, Werler MM, Gissler M, Tikkanen M, Ananth CV. Placental Abruption and Subsequent Risk of Pre‐eclampsia: A Population‐Based Case–Control Study. Paediatric and perinatal epidemiology. 2015 May;29(3):211-9.Available:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4400232/ (accessed 5.3.2024)
