Hypertensive

Disorders

of Pregnancy

Dr. Fawaz khaza’leh

Presented by : Heba Al-

Omoush

Introduction

• The hypertensive disorders of pregnancy are

major contributors to maternal and perinatal

morbidity and mortality.

• The Centers for Disease Control and

Prevention (CDC) have reported that

preeclampsia/eclampsia is the third leading

causeof maternal mortality in the United

States, primarily due to CNS hemorrhage.

Incidence

• The combined incidence of

hypertensive disorders in pregnancy

varies depending on the population

being studied and on the criteria used

but is reported to range from 12% to

22%, whereas the

preeclampsia/eclampsia syndrome

occurs in about 5% to 8% of

pregnancies.

Classification and Definitions

• Preeclampsia or eclampsia

(hypertension and proteinuria unique to

pregnancy)

• Chronic hypertension

• Chronic hypertension with

superimposed preeclampsia

• Gestational or transient hypertension

CHRONIC HYPERTENSION

• known hypertension before pregnancy,

development of hypertension before20

weeks’ gestation, or, in cases in which

hypertension is first noted during

pregnancy, persistence of elevated

blood pressures greater than 12 weeks’

postpartum.

• It is important to review the

antihypertensive medications being taken

and to discontinue any that are potentially

teratogenic.

• Methyldopa is considered to be the safest

antihypertensive medication in pregnancy,

and calcium channel blockers and

labetalol are also considered to be safe.

• β-Blockers should be used with caution

because they may cause fetal growth

restriction and may affect the

interpretation of the NST.

CHRONIC HYPERTENSION WITH

SUPERIMPOSED PREECLAMPSIA

• The diagnosis of superimposed

preeclampsia should be reserved for

those women with chronic

hypertension who develop new-onset

proteinuria (≥0.3 g in a 24-hour

collection) after the 20th week of

gestation.

GESTATIONAL

HYPERTENSION• The diagnosis of gestational hypertension is

made if hypertension without proteinuria first

appears after 20 weeks’ gestation or within

48 to 72 hours after delivery and resolves by

12 weeks postpartum.

• A significant percentage of women with

apparent gestational hypertension go on to

develop proteinuria and the full preeclampsia

syndrome at a later stage in pregnancy.

• The diagnosis of gestational hypertension

can only be made in retrospect.

Preeclampsia

• a syndrome unique to pregnancy,characterized

by the new onset of hypertension and proteinuria

in the latter half of gestation.

• The following two criteria are essential for the

diagnosis of preeclampsia:

(1) the development of hypertension(systolic

blood pressure ≥ 140 mm Hg or diastolic blood

pressure ≥ 90 mm Hg), in a woman whose blood

pressures were previously normal, after the 20th

week of pregnancy

(2) the development of new-onset proteinuria

after the 20th week of gestation. Proteinuria is

defined as more than or equal to 0.3 g protein in a

preeclampsia is often preceded by, or

associated with, the development of

generalized edema. Dependent edema

(edema of the lower extremities) is very

common in normal pregnancies.

Hand and facial edema are more likely to be

associated with preeclampsia, but if

unaccompanied by hypertension and

proteinuria, they are not diagnostic of the

preeclampsia syndrome.

**predisposing risk factors:

• Primigravida but it also occurs in

multiparas.

• Extremes of age.

• diabetes mellitus, chronic

hypertension.

• Multiple gestation , polyhydrominous .

• Previous hx. Of PET .

• Hydrops fetalis .

• *** When it arises in the early second

trimester (14 to 20 weeks), a

hydatidiform mole or choriocarcinoma

***ETIOLOGY :

Preeclampsia is called a “disease of

theories,” because genetic,

immunologic, vascular, hormonal,

nutritional,and behavioral factors have

all been proposed as causes.

No single, definitive “cause” has been

identified, and the origins of the disease

are considered to be multifactorial.

• The net effect of these processes would

be widespread vasoconstriction leading

to hypoxic and ischemic damage in

different vascular beds.

• the primary underlying pathophysiologic

***Preeclampsia is divided into mild and

severe forms, depending on:

• the severity of the hypertension.

• the amount of proteinuria.

• and the degree to which other organ

systems are affected.

Criteria for Severe

Preeclampsia• Severe hypertension (systolic blood pressure ≥160

mm Hg, or diastolic blood pressure ≥ 110 mm Hg)at

rest, on two occasions at least 6 hr apart

• Heavy proteinuria (at least 5 g in a 24-hr collection or

a qualitative value of 3+ in urine samples collected 4

hr apart)

• Oliguria (<500 mL in 24 hr)

• Cerebral or visual disturbances

• Pulmonary edema or cyanosis

• Epigastric or right upper quadrant pain

• Impaired liver function (elevated liver enzymes)

• Thrombocytopenia

• Fetal growth restriction

HELLP syndrome

• This syndrome occurs in preeclamptic

women with evidence of hemolysis,

elevated liver enzymes, and low platelets

(thrombocytopenia).

Complications of

preeclampsia***Maternal complications:

• Multiorgan system dysfunction including renal failure, hepatic Failure

• central nervous system (CNS) hemorrhage ,stroke.

• pulmonary edema

• placental abruption

• disseminated intravascular coagulation (DIC).

*** Fetal and neonatal complications:

• growth restriction.

• prematurity, and perinatal death.

Management of preeclampsia

• Hx.

• Physical examination

• Labs .

• Treatment.

***By Hx.:

• should focus on whether there is any

past history of elevated blood

pressures or renal disease, either

before pregnancy or during previous

pregnancies.

• The patient should be carefully

questioned regarding symptoms of

severe preeclampsia or its

complications, including headache,

visual changes, nausea, vomiting,

abdominal or epigastric pain, and

vaginal bleeding.

*** by PE:

• Assessment of blood pressure, weight gain, edema, fundal height, and reflexes.

• a qualitative assessment of urinary protein excretion with a dipstick.

• In addition, findings consistent with severe preeclampsia such as

• epigastric or right upper quadrant tenderness, uterine

tenderness, petechiae due to low platelets, and signs of

pulmonary edema should be sought.

• If there is severe headache or visual symptoms, an ophthalmic examination may be indicated.

*** Initial Laboratory Evaluation :

Complete blood count, platelet count, lactate

dehydrogenase: If abnormal, order d-dimers,

Coagulation panel, and smear

• Renal studies: Serum blood urea nitrogen,

creatinine, and uric acid; urinalysis; 24-hr

urine for protein and creatinine

• Liver function tests: serum aspartate

aminotransferase,alanine aminotransferase,

and bilirubin.

*** A careful fetal evaluation is also

indicated.

• Delivery is the only

definitive cure for

preeclampsia.

• hospitalize patients with a presumed diagnosis of preeclampsia to determine the disease’s severity and maternal and fetal stability.

• if mild and if there is no evidence of fetal compromise,management consists of rest and observation ,watching for possible progression to severe preeclampsia. No antiHTN or MgSO4 are used.

• Delivery if <36 wk with IV oxytocin to induce labour C/S only for obstetrical indication.

• MgSO4 for seizure prophylaxis (4 g load and 2 g/hr maintenance) during labor and delivery and continued for 12-24 hrs postpartum

***If Severe :

• Aggressive prompt delivery is

indicated for any GA with evidence of

maternal or fetal risk:

- Give IV MgSO4 , loading dose 5-gm ,

then maintenance infusion of 2 g/h

- IV hydralazine and/or lebetelol

- vaginal delivery with IV oxytocin if

mother & fetus are stable

• The goal of antihypertensive therapy in

severe preeclampsia is to lower blood

pressure carefully to prevent CNS

hemorrhage.

• In general the blood pressure should not be

lowered to “normal levels” or less than

130/80 mm Hg. Caution must always be

exercised to not lower the arterial pressure

too much or too rapidly because either may

result in decreased uteroplacental blood flow

and fetal distress, which may necessitate

emergent cesarean delivery in an unstable

• Oral nifedipine has been used

successfully, but should be used

cautiously to avoid hypotension,

particularly when used in conjunction

with magnesium sulfate.

Eclampsia• Is the presence of tonic-clonic seizures in a

woman with preeclampsia that cannot be attributed to other causes.

• Eclamptic seizures can also occur before the development of classic signs of preeclampsia.

• use of magnesium sulfate intrapartum and postpartum for seizure prophylaxis in women with preeclampsia.

• In a recent review of this subject, 38% to 53% of eclamptic seizures occurred before labor, 18% to 36% occurred during labor, and 11% to 44% occurred after delivery (usually within the first 24 to 48 hours postpartum).

***Management of eclamsia:

• Protect mother airway & tongue

• Give IV MgSO4 5g to stop seizure, then

maintenance 2 g/h

• Aggressive prompt delivery at any GA after

stabalize the mother & the fetus

Thank You