DEPARTMENT OF OBSTETRICS AND GYNECOLOGY

FEU-NRMF INSTITUTE OF MEDICINE

 GestationalHypertension
 Preeclampsia
 Eclampsia
 Chronic Hypertension
 Superimposed Preeclampsia on

Chronic hypertension
 BP ≥ 140/90mmHg for the first time during
pregnancy after 20 weeks AOG
 No proteinuria
 BP returns to normal before12 weeks’

postpartum transient hypertension

 Final diagnosis made only postpartum
 May have other signs or symptoms of

preeclampsia, for example, epigastric

discomfort or thrombocytopenia
Minimum criteria Increased certainty of
preeclampsia
 BP ≥ 140/90 mmHg  BP ≥ 160/110mmHg after 20
weeks gestation
after 20 weeks  Proteinuria 2.0 g/24 hours or
gestation ≥ 2 + dipstick
 Serum creatinine > 1.2mg/dl
 Proteinuria unless known to be previously
elevated
≥300mg/24 hours  Platelets < 100,000/mm3
or ≥ 1+ dipstick  Microangiopathic hemolysis
(increased LDH)
 Elevated ALT or AST
 Persistent headache or other
cerebral or visual disturbances
 Persistent epigastric pain
 Seizuresthat cannot be attributed to
other causes in a woman with
preeclampsia
 BP ≥140/90 mm Hg before pregnancy or
diagnosed before 20 weeks' gestation not
attributable to gestational trophoblastic
disease;
or hypertension first diagnosed after 20
weeks' gestation and persistent after 12
weeks' postpartum
 New-onset proteinuria 300 mg/24 hours in
hypertensive women but no proteinuria
before 20 weeks' gestation

 A sudden increase in proteinuria or blood

pressure or platelet count < 100,000/mm3
in women with hypertension and proteinuria
before 20 weeks' gestation
 nulliparous women
 race and ethnicity (African-American

ethnicity)
 genetic predisposition
 environmental factors
 chronic hypertension
 multifetal gestation
 maternal age over 35 years
 obesity
 Exposed to chorionic villi for the first time.
 Exposed to a superabundance of chorionic

villi, as with twins or hydatidiform mole.

 Have preexisting vascular disease.
 Genetically predisposed to hypertension

developing during pregnancy.

 Abnormal trophoblastic invasion of uterine
vessels
 Maternal maladaptation to cardiovascular or

inflammatory changes of normal pregnancy

 Immunological intolerance between

maternal and fetoplacental tissues

 Dietary deficiencies
 Genetic influences
 Abnormal trophoblastic invasion of uterine
vessels
 Maternal maladaptation to cardiovascular or

inflammatory changes of normal pregnancy

 Immunological intolerance between

maternal and fetoplacental tissues

 Dietary deficiencies
 Genetic influences
 Abnormal trophoblastic invasion of uterine
vessels
 Maternal maladaptation to cardiovascular or

inflammatory changes of normal pregnancy

 Immunological intolerance between

maternal, paternal and fetoplacental tissues

(APAS), Molar Pregnancy
 Dietary deficiencies and excesses
 Genetic influences
Vasospasm
Endothelial damage
 increased cardiac afterload
 endothelial activation with extravasation

into the extracellular space

 left ventricular hypertrophy
 Blood Volume
- hemoconcentration is a hallmark of
eclampsia

 Blood and Coagulation

- Thrombocytopenia results from platelet
activation, aggregation, and consumption
- The lower the platelet count, the higher the
maternal and fetal morbidity and mortality.
H – Hemolysis ( LDH )
EL – Elevated liver enzymes ( AST
or ALT)
LP – Low Platelet count

“An indication for delivery”

 Endocrine Changes
- normal renin, angiotensin II, aldosterone
- deoxycorticosterone (DOC)
- normal ADH

 Fluid and Electrolyte Changes

- volume of extracellular fluid (edema)
 Renal perfusion and glomerular filtration
(oliguria)
 Plasma uric acid concentration
 Plasma creatinine
 Urine sodium concentration

Anatomical Changes: glomerular capillary

endothelial swelling

PROTEINURIA
 Thecharacteristic lesions commonly
found were regions of periportal
hemorrhage in the liver periphery

 Subcapsular hematoma and liver

rupture
headaches and visual symptoms
gross hemorrhage due to ruptured arteries
principal postmortem lesions in eclampsia
- edema
- hyperemia
- ischemia
- thrombosis
- hemorrhage
Blindness (amaurosis)
 Compromised uteroplacental perfusion
from vasospasm is almost certainly a major
culprit in the genesis of increased perinatal
morbidity and mortality
 Roll over test
 Uric acid
 Fibronectin
 Coagulation activation
 Oxidative stress
 Cytokines
 Placental peptides
 Fetal DNA
 Uterine artery doppler velocimetry
 Dietary manipulation
 Calcium supplementation
 Fish oil supplementation
 Antioxidant (Vit. C & E )
 Low dose aspirin
“Delivery is the definitive
cure for preeclampsia”
 Basic management objectives for any
pregnancy complicated by preeclampsia are:

1. Termination of pregnancy with the least

possible trauma to mother and fetus.
2. Birth of an infant who subsequently thrives.
3. Complete restoration of health to the mother
 Pregnancy complicated by hypetension is managed
according to severity of the disease and gestational age
of the fetus.
 Know the accurate gestational age and classify the

severity of the disease

 Pregnancy complicated by hypetension is managed
according to severity of the disease and gestational age
of the fetus.
 Know the accurate gestational age and classify the

severity of the disease.

 Severe disease is delivered at 34 weeks.
 Severed disease at < 34 weeks is managed

conservatively provided maternal and fetal conditions

are good.
 Mild disease or non-severe disease: await

spontaneous labor but with more frequent check-ups

compared to non-hypertensives
1. Detailed examination followed by daily
scrutiny for clinical findings such as
headache, visual disturbances, epigastric
pain, and rapid weight gain
2. Weight on admittance and every day
thereafter
3. Analysis for proteinuria on admittance and
at least every 2 days thereafter
4. Blood pressure readings in the sitting
position with an appropriate-size cuff
every 4 hours, except between midnight
and morning.
5. Measurements of CBC and platelets, serum
creatinine, LDH and liver enzymes
6. Frequent evaluation of fetal size and
amniotic fluid volume either clinically or
with sonography.
7. Steroids to accelerate fetal lung maturity
given between 24-34 weeks.
 Preeclampsia complicated by generalized
tonic–clonic convulsions.

Differential Diagnosis:
◦ Epilepsy
◦ Encephalitis
◦ Meningitis
◦ Cerebral tumor
◦ Cysticercosis
◦ Ruptured cerebral aneurysm
1. Control of convulsions using an intravenously
administered loading dose of magnesium
sulfate, followed either by a continuous
infusion of magnesium sulfate or by an
intramuscular loading dose and periodic
intramuscular injections.
2. Intermittent intravenous or oral administration
of an antihypertensive medication to lower
blood pressure whenever the diastolic pressure
is considered dangerously high.
3. Avoidance of diuretics and limitation of
intravenous fluid administration.
4. Delivery.
 Magnesium intoxication is avoided by ensuring
- urine output is adequate
- the patellar or biceps reflex is present
-no respiratory depression
 Therapeutic level: 4 to 7 mEq/L
 Toxic Levels:
- 10 mEq/L Patellar reflexes disappear
- >10 mEq/L respiratory depression develops,
- >12 mEq/L respiratory paralysis and arrest follow
 Antedote: Calcium gluconate, 1 g intravenously
Magnesium sulfate
is an
ANTICONVULSANT
not an
ANTIHYPERTENSIVE
 Given intravenously whenever the diastolic blood
pressure is 110 mm Hg or higher or the systolic
blood pressure is more than 160 mm Hg.

 Administered in 5- to 10-mg doses at 15- to

20-minute intervals until a satisfactory response
is achieved.

 A satisfactory response antepartum or

intrapartum is defined as a decrease in diastolic
blood pressure to 90 to 100 mm Hg, but not
lower lest placental perfusion be compromised.
 Labetalol
- Intravenous labetalol, an 1‫ס‬- and
nonselective ß-blocker, is also used to treat
acute hypertension of pregnancy

 Nifedipine
- in a 10-mg oral dose to be repeated in 30
minutes if necessary.
 Methyldopa: drug of choice during
oral treatment of hypertensive
disorder during pregnancy
 Diuretics: AVOIDED unless there is

pulmonary edema
Possible Causes:
- underlying chronic hypertension
- mobilization of edema fluid with
redistribution in to the intravenous
compartment

Management:
 drugs uses antepartum can be used

postpartum
 Diuretics can be used
 Epiduralanalgesia for women with
severe preeclampsia was promoted to
ameliorate vasospasm and lower
blood pressure.
 Women with gestational HPN or
preeclampsia during the index pregnancy
are at higher risk of hypertension on
subsequent pregnancies.

 Hypertension during pregnancy is a marker

for increased rates of later cardiovascular-
related diseases, renal and neurological
sequelae.