PATHOPHYSIOLOGY

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

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

Thromboplastin Release of bleeding in the decidua basalis

renin
hematoma formation

Glomerular angiotensin I further separation of the placenta

capillary from the uterine wall
endothelial
damaged
angiotensin II pituitary gland abruptio placenta
release of ADH
Protein leak
across the partial separation total separation
capillary sodium water retention
membrane and retention
into urine Marginal Central –
– vaginal conceale massive vaginal
bleeding d bleeding or
edema oliguria conceaaled
bleeding
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
chronic uteroplacental
- monitor vital sign
insufficiency
diet modification
maternal and
Medical
Medical Brain ischemia causes the later
management fetal death
management emergence of convulsions
- IV fluid and
- medication electolyte
administration replacement
Eclampsia
-meds
good
prognosis Occurrence of good prognosis
seizures and can
cause coma

poor prognosis

DEATH