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PATHOPHYSIOLOGY

unknown etiology
Predisposing factors Precipitating factors
Age preeclampsia in previous
Sex decreased placental perfusion pregnancy
Family History multigravidity
Diet (high in cholesterol, saturated
Placental production of endothelin fat, and sodium intake)

vasospam

Endothelial cell damage

vasoconstriction

hypertension

Platelet cluster at the site of endothelial


damage

rise in peripheral resistance

reduced blood supply


decreased perfusion in kidneys decreased perfusion in placenta

bleeding in the decidua basalis


Thromboplastin Release of renin

hematoma formation

Glomerular angiotensin I further separation of the placenta from the


capillary uterine wall
endothelial
damaged
angiotensin II pituitary gland abruptio placenta
release of ADH
Protein leak across
the capillary partial separation total separation
membrane and into sodium retention water retention
urine
Marginal Central
vaginal concealed massive vaginal
bleeding bleeding bleeding or
edema oliguria conceaaled
proteinuria hemmorhage

preeclampsia
if treated: if not treated: if treated: if not treated:

Nsg. management Nsg. management


- bed rest Fetal risks include acute and - monitor VS poor prognosis
- monitor vital sign chronic uteroplacental
diet modification insufficiency

Medical management
maternal and
Brain ischemia causes the later
Medical management
emergence of convulsions - IV fluid and electolyte fetal death
- medication replacement
administration -meds

Eclampsia

good prognosis
Occurrence of good prognosis
seizures and can
cause coma

poor prognosis

DEATH