HYPERTENSIVE DISORDERS

IN PREGNANCY
DR. SALWA NEYAZI
ASSISSTANT PROF KSU/ CONSULTANT OBGYN
PEDIATRIC & ADOLESCENT GYNECOLOGIST

TYPES OF HYPERTENSIVE DISEASE IN

PREGNANCY
1-Gestational hypertension
2-PET
3-Eclampsia
4-Chronic hypertension
5-PET superimposed on chronic hypertension

Gestational hypertension-1
BP 140/90 mm Hg for the first time during pregnancy
No proteinuria
BP returns to N < 12 Wk postpartum
Final Dx made only postpartum
May have other signs of PET eg. Headache, epigastric
discomfort or thrombocytopenia

PET
Minimum criteria
BP 140/90 mm Hg after 20 Wk gestation
Proteinuria 300 mg/24 hrs or 1+ dipstick
Increased certainty of PET
BP 160/110 mm Hg
Proteinuria 2 gm/24 hrs or 2+ dipstick
Serum creatinine > 1.2 mg/dl unless known to be
previously elevated
Platelets < 100 000/mm

Increased certainty of PET

Microangiopathic hemolysis (increased LDH)
Elevated ALT or AST
Persistant headache or other cerebral/ visual disturbance
Persistant epigastric pain
ECLAMPSIA
Seizures that can not be attributed to other causes in
a woman with PET. 1% of Pt with PET develop EC

CHRONIC HYPERTENSION
BP 140/90 mm Hg before pregnancy or Dx before 20
Wk gestation
HPT first Dx after 20 Wk gestation & persistant after 12
Wk postpartum
PET SUPERIMPOSED ON CHRONIC HYPERTENSION
New onset proteinuria 300 mg/24 hrs in hypertensive
women but no proteinuria before 20 Wk gestation
A sudden increase in proteinuria or BP or
Plt count < 100 000/ mmin women with HPT &
proteinuria before 20 Wk gestation

INCIDENCE & RISK FACTORS

PET occurs in 6-8% of all live birth
RISK FACTORS
Extremes of reproductive age
15 < & >35 Y
Nulliparity
Black race
Hx of PET in a 1st degree female
relative
Hx of PET in prior pregnancy
DM
Chronic renal disease
Ch HPT

Multiple pregnancy twins 13

vs 6%
Hydatidiform mole
Nonimmune hydrops fetalis
Obesity 4.3% BMI < 19.8
kg/m
13.3% BMI 35
kg/m
Smoking risk of HPT

PATHOGENESIS
Endothelial cell injury prostacyclin & thromboxaneA2
Rejection phenomenon (inadequate matenal Ab response)
Compromised placental perfusion
Altered vascular reactivity sensitivity to vaspressin EPN,
NEPN & angiotensin
GFR with retention of salt & water
intravascular volume
CNS irritability
DIC
Uterine muscle stretch & ischemia
Dietary factors
Genetic factors

PATHOGENESIS
Summary of current hypothesis:
Immunological disturbance abnormal placental
implantation placental perfusion production of
substances that activate or injure endothelial cells of the
blood vessels multiple organ system involvement

PATHOPHYSIOLOGY
MULTIPLE ORGAN SYSTEM
INVOLVMENT

CNS- 1
Similar to hypertensive encephalopathy
Petechial Hg
Gross hemorrhages due to ruptured arteries
Thrombosis of the arterioles
Microinfarcts
Fibrinoid necrosis in the walls of blood vessels
Cerebral edema confusion, blurred vision / coma
Brain stem herniation is a serious complication of cerebral
edema death
MECHANISM cerebral hyperperfusion ,vasospasm
&forced dilation

CNS- 1
CT Scan of the pt focal hypodensities in the white
matter / post half of the cerebral hemisphere &
occasionally in the grey matter may represent petechial
Hg
Severe cases IV Hg or subarachnoid Hg
MRI Abnormalities in the cortical & subcortical white
matter of the occipital & parietal areas
EEG nonspecific changes

PULMONARY SYSTEM-2
Pulmonary edema
May occur with sever PET OR EC
Usually postpartum
May be due to excessive fluid administration with
crystalloids + plasma colloid pressure due to
proteinuria
in Pt with ch HPT & hypertensive cardiac disease
Aspiration of gastric content with EC

3-CVS
Plasma volume is reduced, the cause is unknown
theories:
1-Generalized vasoconstriction with vascular
permeability Advocate the use of vasodilators
2-1ry hypovolemia hypoperfusion of the uterus
release of pressor substances HPT
Advocate the use of volume expanders & avoidance
of diuretics

CVS-3
High systemic vascular resistance & hyperdynamic
ventricular function avoid aggressive fluid
adminstration
Loss of the normal refractoriness to angiotensin II

BLOOD-4
Hemoconcentration
Thrombocytopenia < 150 000 15-20% of PT
Fibrinogen
Thrombin time in 1/3 of the Ptwith EC
FDP 20% of the Pt
DIC 5%
Microangiopathic hemolytic anemia 5%
HEELP hemolytic anemia, liver enzymes, low Plt
-LDH > 600 U/L
-T bilirubin >1.2 mg/dl
-AST > 70U/L
-Plt < 100 000/mm
Found in 10% of the Pt with severe PET

5-KIDNEY
Characteristic lesion glomeruloendotheliosis swelling
of the gromelular capillary endothelium GFR
creatinine clearance/ plasma creatinine
uric acid
Proteinuria
Renal tubular necrosis &renal failure
6-Eyes
Visual disturbances due to retinal artery vasospasm
Retinal detachment
Cortical blindness occipital lobe ischemia infarction or
edema lasting hrs up to 8 days

Liver-7
Minimal involvement with fibrin deposition
Periportal hemorrhagic necrosis serum liver
enzymes
Bleeding from these lesions Subcapsular hematoma
hepatic rupture
Hepatic infarction
HEELP SYNDROME

Endocrine & metabolic changes-8

plasma renin, angiotensin II & aldosterone to the
normal prepregnancy values
Vasopressin levels are N
Atrial natriuretic peptide
Volume expansion in PET ANP COP &
periephal vascular resistance
Expansion of the extracellular fluid volume (edema)
Proteinuria plasma oncotic pressure
displacement of intravascular fluid to interstitium

Uteroplacental perfusion-9
Vasospasm compromised placental perfusion
perinatal morbidity & mortality
Doppler velocimetry (systolic /diastolic velocity ratio of
umbilical& uterine arteries )20% N
15% N Umbilical / Abnormal uterine
40% Both Abnormal
Histological changes in placental bed
Defective trophoblastic invasion of spiral arteries / decidual
vessels but not myometrial vessels are invaded by
trophoblast
Charecteristic lipid rich lesions in the uteroplacental arteries

PREVENTION
Calcium supplementation??
Fish oil ineffective
Low dose aspirin selective supression of throboxane
synthesis by the plt & sparing endothelial prostacyclin
production Not effective in preventing PET
Antioxidants Vit C & E supplementation significant
reduction in PET

SYMPTOMS & SIGNS

BP
Proteinuria
Edema of the face & hands ( but it has been dropped of
the definition due to poor predictive value)
Headache
Visual disturbance
Epigastric pain
Exaggerated reflexes

Fetal & maternal risks

Fetal
IUGR
Oligohydramnios
Placental infarcts
Placental abruption
Prematurity
Uteroplacental
insufficiency
Perinatal death

Maternal
CNS seizures & stroke
DIC
CS
Renal failure
Hepatic failure or rupture
Death

CLASSIFICATION OF PET
SEVERE PET
Systolic BP >160 mmHg or diastolic >110 mmHg on two
occasions at least 6 hrs apart
Proteinuria 5 g/24 hrs
Oliguria < 500 cc /24 hrs
Cerebral or visual symptoms
Epigastric or Rt upper quadrant pain
Pulmonary edema or cyanosis
Low PLt
liver enzymes
IUGR
MILD PET any PET that is not considered severe

MANEGEMENT OF PET &

EC

Manegement
OBJECTIVES
Terminaton of pregnancy with the least possible trauma
to the mother & fetus
Birth of an infant who subsequently thrives
Complete restoration of health to the mother
1- Hospitalization
Women with new onset BP 140/90
Worsening BP
Development of proteinuria in addition to existing BP

INITIAL HOSPITAL MANAGEMENT

Observe for headache , visual disturbance, epigastric
pain & rapid wt gain
Wt daily
Analysis for proteinuria every 2 days / daily
BP in sitting position every 4 hrs except during sleep
Blood investigations Hct, Plt, S creatinine, liver
enzymes
Frequent evaluation of fetal size & AF
Reduced physical activity but not absolute bed rest
N diet & fluid intake

FURTHER MANAGEMENT
Depends on:
Severity of PET
Duration of gestation
Condition of the Cx
Complete resolution of the signs & symptoms does not
occur till after delivery
Lines of management
Termination of pregnancy
Antihypertensive therapy
Anticonvulsant therapy
Home health care if BP improved within few days Pt
can be managed as outpatient Home BP & urine
protein monitoring . Instruction to come to hospital if she
has waning symptoms . Rest at home

Termination of pregnancy
Indications
Term pregnancy with mild or severe PET
Severe PET regardless of the gestational age
Warning signs headache , visual disturbance, epigastric
pain, oliguria
Eclampsia Pt must be stabilized & delivered immediately
Preterm with mild PET Assess fetal wellbeing by NST,
BPP, Doppler
Methods of termination
IOL with prostaglandines to ripen the Cx followed by IV
oxytocin
Elective CS Severe PET with unfavorable Cx

Antihypertensive therapy
Mild PET
There is no benefit of antihypertensive therapy
Reduction in the maternal BP with labetalol or nifedipine
IUGR
ACI contraindicated IUGR, boney malformations, limb
contracture, PDA, pulmonary hypoplasia, RDS, hypotension
&death
Severe PET
Antihypertensive therapy is used to control BP untill the Pt
delivers or in preterm for 48 hrs to allow time for
glucocorticoid administration for fetal lung maturity then
delivery

Antihypertensive therapy for severe PET & EC

Hydralazine
IV infusion or IV 5-10 mg bolus at 15-20 min interval
when diastolic BP 100-110 mm Hg or systolic BP
160 mmHg
Nifedipine 10 mg po repeated in 30 min
Labetalol 10 mg IV / 20 mg after 10 min/ 40mg after
10min/80 mg (not to exceed 220 mg)
Nitroprusside used only in PT not responding to other
drugs
Diuretics not recommended because intravascular
volume depletion already exists in PET

Fluid therapy
Hyperosmotic agents not recommended because
intravascular influx of fluid subsequent escape of
fluid to vital organs pulmonary edema & cerebral
edema
LR 60-120 ml/hr Excessive fluid administration
pulmonary edema & cerebral edema

PREVENTION /CONTROL OF CONVULSIONS

Magnesium sulfate IV infusion 4 gm loading dose in 100
ml of IV fluid over 20 min 2 gm /hr maintenance
Measure serum MG level at 4-6hrs maintain at 4-7 mEq /L
D/C 24 hrs after delivery25% of seiz occur post partum
Avoid toxicity by :
-monitoring patellar reflexes
-respiratory rate
-urine output
Antidote calcium gluconate 1gm IV
MgS myometrial contractility
Compared to phenytoin or diazepam 50% in maternal
mortality ,67% in convulsions
Infants were less likely to be admitted to NICU/ intubation

Prognosis
Maternal death rare due to cerebral Hg, aspiration
pneumonia, hypoxic encephalopathy, thromboembolism,
hepatic rupture, renal failure, ansthesia
Recurrence 25-33% primipara
70% multipara
PG, PET before 30 wk 40%
HEELP 5%

CHRONIC HYPERTENSION
in pregnancy

CHRONIC HYPERTENSION
Incidence of ch HPT 0.5-4%
80% essential HPT
20% due to renal disease
Symptoms & signs
risk in Age > 30, obese, multipara, DM, renal disease,
black race, family Hx
Difficult to deffirentiate HPT with superimposed PET from
HPT with renal disease both have proteinuria

INVESTIGATIONS
Chest x ray cardiomegaly
ECG Lt vent hypertrophy
serum creatinine, creatinine clearance & proteinuria
5-10%
MATERNAL COMPLICATIONS
Superimposed PET in 1/3 of Pt
risk of abruptio placentae 0.4-10% DIC, acute
tubular & cortical necrosis
If renal function is well creatinine < 1.5 mg/dl
pregnancy does not change the coarse of renal
disease
If renal function is affected prior to pregnancy
deterioration of renal function occur more rapid in
pregnancy

FETAL COMPLICATIONS
Prematurity 25-30%
IUGR 10-15%
Stillbirth & fetal distress due to abruptio placentae or ch
intrauterine asphyxia

TREATMENT
No benefit of treating mild CH HPT ( 140-179/90-109)
in pregnancy should be monitered for worsening HPT or
superimposed PET
Pt with severe CH HPT should have their BP controlled
before pregnancy & continue Rx in pregnancy
Methyle Dopa
Calcium channel blockers
B blockers can be used but IUGR
Labetalol

Obstetric management
Serial U/S for fetal growth. BPP, NST 34wk
Follow up every 2 wks till 30 then weekly
Warn the mother about symptoms of superimposed PET
Investigations Renal function test,uric a , calcium ,LFT, 24hrs
urine for creatinine clearance & protein, CBC, Urinalysis,
ECG.GTT
Early U/S for dating of preg
Not allowed to continue past 40wks
IOL at40 wks
Regular diet no salt restriction
IOL for superimposed PET,IUGR, fetal distress, worsening
renal function