Preeclampsia

2–8% of all pregnancies

Nulliparous, or multiparous with previous preeclampsia/eclampsia Hx, advanced maternal age

Increased with Hx of obesity, chronic htn, diabetes, renal disease, SLE, thrombophilia

Increased risk of fetoplacental or maternal deterioration necessitating (often operative) delivery.

Increased risk of fetal death.

Preeclampsia and eclampsia account for about 15% of maternal and perinatal deaths.

Hypertensive crisis leading to intracerebral bleed or LV failure.

Increased interstitial volume leading to edema.

Maternal hypotension producing placental hypoperfusion.

Renal dysfunction progressing to acute renal failure.

Thrombocytopenia may contraindicate regional anesthetic.

Eclampsia (seizure in a severely preeclamptic pt) necessitating difficult tracheal intubation.

Placental abruption.

Risks associated with preterm delivery.

Early onset (<34 wk gestation): High rate of recurrence, strong genetic component, high risk of adverse outcome.

Late onset (<34 wk gestation): Higher incidence, maternal metabolic predisposition.

Marked by Htn, proteinuria (spot urine protein/Cr ratio >0.3).

Maternal hyperdynamic state with diastolic dysfunction, leading to acute cardiorespiratory deterioration.

Proteinuria: Sign of deteriorating renal function and widespread endothelial damage.

Edema: Increasing total body water, proteinuria, Htn; lead to increasing interstitial edema and decreasing intravascular volume.

Hematologic: Widespread endothelial damage often leads to thrombocytopenia.

Epigastric/RUQ pain: Ominous sign of liver subcapsular edema and possible rupture. Delivery should be urgently effected.

HELLP: Poor fetoplacental prognostic sign.

Headache: Seizure may be impending.

Heterogenous disease of unknown etiology.

Immune maladaptation causing placental angiogenesis dysfunction.

Imbalance in circulating mediators of vascular tone and response (e.g., thromboxane vs. prostacyclin) from endothelial damage.

Systemic inflammatory response from placental oxidative stress.

Microangiopathy leading to endothelial change, platelet consumption, hemolysis.