Hypertensive Disorders in Pregnancy

JAMOAA HOSPITAL FOR OBS/GYNA – RABAK

Prepared by :
Escander Gabriel Owor, MBBS Alneelian university
 Classification

Hypertension
Risk Factors

Pathophysiology and theories

Complications
Objectives

Diagnosis and
investigation

Management
Case scenario
 case

A 38-year-old woman, G1 P0+0, comes to the office for her first ANC. Her
LMP was12 weeks ago. The patient has had N/V occasionally over the past
few weeks but no other symptoms. She has not seen a health care provider
in years but has no known medical conditions and takes no medications.
Supine blood pressure is 142/96 mm Hg and 138/92 mm Hg on repeat
measurement15 minutes later. Physical examination shows an anxious
woman with mild bilateral ankle edema and an enlarged uterus. Ultrasound
confirms an intrauterine pregnancy consistent with dates. A urinalysis
dipstick is negative for protein and glucose. The patient returns to the office
for a blood pressure measurement a week later and her blood pressure is
152/106 mmHg
Which of the following is the most likely diagnosis in this patient?
A. Chronic hypertension
B. Gestational hypertension
C. Normal pregnancy
D. Preeclampsia
E. White coat hypertension
This patient is at greatest risk of which of the following complications?
A. Fetal heart defect
B. Fetal macrosomia
C. Fetal neural tube defect
D. Placenta accreta
E. Polyhydramnios
F Preterm labor
G. Preterm premature rupture of membranes
 INTRODUCTION

Hypertensive disorders of pregnancy are the second leading

cause of global maternal mortality after maternal hemorrhage,
are significant cause of short and long-term maternal and fetal
morbidity.
incidence is 6-10%.
Complicates 10 - 20 % of pregnancies
The most frequent cause of iatrogenic prematurity.
 Physiological changes

Blood pressure = SVR × COP

Before the increase in COP can adequately compensate for the
fall in SVR, blood pressure begins to decrease in early
pregnancy. It continues to decrease in the second trimester of
normal pregnancy until the nadir in systolic and diastolic blood
pressure is reached by about 22–24 weeks’ gestation.
 From then on, there is a steady rise to pre-pregnancy levels
until term ( due to rise in HR and BV)
 Its usually falls immediately after delivery, although tends to
rise subsequently reaching a peak 3–6 days postpartum

Blood pressure ↓ in midpregnancy and rises during the last

trimester.
Diastolic pressure ↓ more than systolic.
 Hypertension

HTN is Defined as a sustained systolic BP ≥ 140 mm Hg and/or diastolic BP ≥

90 mm Hg in woman seated and at rest, measured twice on two separate
occasions at least 4 hours apart .

Severe hypertension: SBP ≥ 160 mmHg and/or DBP ≥ 110 mmHg

20% pre-existing (chronic)

80% de novo (gestational/pre-eclampsia)
“A scientific discovery is also a religious discovery.
There is no conflict between science and religion.
Our knowledge of God is made larger with every
discovery we make about the world.”

Joseph Hooton Taylor

Classification
Chronic hypertension

Gestational hypertension

Preeclampsia superimposed on chronic hypertension

Pre-Eclampsia -Eclampsia
 Pre-existing (chronic) hypertension

Preexisting HTN is Defined as hypertension prior to the 20th week of gestation, HTN
that existed before pregnancy, or HTN that persists > 12 weeks after delivery.
 Usually not associated with significant proteinuria or end-organ damage
if well controlled.
 Associated with adverse maternal and fetal outcomes (stroke, low birth weight,
NNU admission)
Examples:
 essential hypertension ,
 secondary to chronic renal disorders, coarctation of the aorta, SLE, Cushing,
hyperparathyroidism and pheochromocytoma

 Severe HTN = 160 mmhg or DBP = 110 mmhg

 Gestational hypertension

Also called transient HTN and pregnancy-induced HTN.

A sustained or transient systolic blood pressure (BP) ≥ 140 mm Hg
and/or diastolic BP ≥ 90 mm Hg occurs after the 20th week of gestation in a
previously normotensive patient.
 No proteinuria or end-organ damage
 returning to normal 12 weeks after delivery
 Almost 25% of these develop preeclampsia
 Not usually accompanied by fetal growth restriction.
 Preeclampsia

Definition : It is a multisystem disorder of unknown etiology,

characterized by :
 presence of new hypertension after 20 weeks’ gestation accompanied
by proteinuria and/or evidence of maternal end organ damage .
- Proteinuria: 1+ on dipstick or ≥ 300 mg/24 hr collection of urine or
protein: creatinine ratio of 30mg/mmol
- previously normotensive woman and resolving completely by the 6th
postpartum week.
- Incidence: 5-15%.
 Superimposed preeclampsia:

Preeclampsia in patients with chronic HTN in pregnancy.

25% of patients with chronic HTN in pregnancy develop preeclampsia.
Diagnose by:
A. acute-onset proteinuria
B. Worsening of hypertension (increase of 30 mmHg or more in
systolic BP or 15 mmHg or more in diastolic BP)
Often occurs earlier in pregnancy, has more severe fetal growth
restriction than preeclampsia without chronic HTN, and is also
associated with ↑ risk of placental abruption.
 Pathophysiology and Theories

The pathophysiology likely to be multifactorial with genetics,

immunology and endothelial dysfunction each having roles.

Pre-eclampsia can be thought of as a two-phases disorder:

 abnormal perfusion of the placenta.
 maternal systemic response
Failure of normal trophoblast invasion lead to maladaptation of
maternal spiral arterioles which in turn interfere with normal
villous development leading to placental insufficiency and
consequently fetal growth restriction.
Maternal systemic response result in vasoconstriction and capillary
leaking leading to hypertension and complication.
Raised level of pro-inflammatory and anti-angiogenic cytokines
contribute to this.

 Renin- angiotensin system

 Atrial natriuretic peptide (ANP)
 Prostaglandins ( Prostacycline , PGI2 )
 anti-angiogenic{Soluble Flt1 (sFlt1) and soluble endoglin (sEng)}
produce systemic endothelial dysfunction
by antagonizing VEGF and TGF-β1 signalling.
.
 Pathological Changes

a) Vasospasm
b) Coagulopathy
c) Sodium and water retention.
 RISK FACTORS for PREECLAMPSIA

1. Age >40 years

DEMOGRAPHIC

1. Multiple gestation 4. nullparity

2. Molar pregnancy 5. Previous pre-eclampsia
OBSTETRICS 3. Non-immune 6. Long interval between
hydrops pregnancy >10 years
1. Diabetes mellitus
2. Chronic HTN
3. Renal disease
4. SLE,
MEDICAL
5. Antiphospholipid
6. SCD
 Psychological stress & strain Obesity BMI> 35
Genetic kg/m2
Smoking

Genetic
Predisposition

Family History

Race & Ethnicity

More Common in black & Asians

Pregnancy by ovum
donation
 Types of pre-eclampsia

A. Pre-eclampsia without severe feature( mild): HTN + proteinuria with

no signs of end organ damage or severe HTN
B. Pre-eclampsia without severe feature( severe) : HTN with/without
proteinuria + one or more signs of end organ damage or severe HTN +
heavy proteinuria
 SIGN and SYMPTOMS for SEVERE PREECLEMPSIA

Symptoms Signs Lab

Headache Oliguria (<400ml/day or <30 Elevated Liver enzymes
ml/hr).

Epigastric pain Edema Thrombocytopenia (<

100,000
Visual changes Pulmonary edema and Proteinuria (≥ 5.0 g/24 hr)
cyanosis
Nausea and vomiting Hyperreflexia Serum creatinine >
1,1mg/dl
SBP > 160 or DBP > 110
 Diagnosis

Baseline
History Exam Investigations
(symptoms & BP
risk factors)
There is no diagnostic test for pre-eclampsia, therefore much of
the antenatal care is directed towards screening for this condition.

Hypertension
Blood pressure of 140/90 mmHg or more or an increase of 30
mmHg in systolic and/or 15 mmHg in diastolic blood pressure
over the pre-or early pregnancy level
 Investigations
• Urine:300mg/24 hour, +1on dipstick or PCR 30mg/mmol
• Kidney functions (serum creatinine, urea, creatinine clearance and serum uric
acid.
• Liver functions ( Raised hepatic enzyme levels ) bilirubin
• Blood: CBC, HCt , Hemolysis and Platelet count (Thrombocytopenia).
• Coagulation Profile: Bleeding and clotting time ( Abnormal coagulation
profile )
• Serum uric acid level >4.5 mg/dl indicates presences of pre-eclampsia
• Ophthalmoscope

• Antenatal fetal monitoring: Done by clinical examination , Daily fetal kick

count ,USG of fetal growth ,Liqour pockets , Cardiotocography
( CTG )
• Umbilical artery flow velocimetry ( Doppler study )
• Bio-physical profile
Complications
 Maternal
Convulsions (eclampsia)
Cerebral haemorrhage.
Renal failure.
Heart failure (left ventricular systolic or diastolic dysfunction).
Liver failure and HELLP syndrome
Disseminated intravascular coagulation.
Abruptio placentae.
Residual chronic hypertension in about 1/3 of cases.
Recurrent pre-eclampsia in next pregnancies.

Fetal
Intrauterine growth retardation (IUGR).
Intrauterine fetal death.
Prematurity and its complications.
 Assignment

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 Management

 Screening and Prophylaxis

 Treatment
 Fetal surveillance
 Timing and Method of deliver
 Screening and Prophylaxis

Proper antenatal care:

Regular ANC detect the high risk patients who may develop PIH through:
 Good Hx and frequent Examination of BP
 Screening tests e.g regular blood tests( CBC, RFT) and
Urinalysis if proteinuria (≥1+) is detected, PCR or measurement of
24-hour protein excretion.
 A low PlGF or raised SFlt can predict or help to diagnose pre-eclampsia

Prophylaxis
 Low-dose aspirin (75to 150) : It inhibits thromboxane production from the
platelets and the AII binding sites on platelets,from 12 wk to 36wk.
 Calcium and vitamin D: Low maternal serum 25(OH)D conc increase pre-
eclampsia risk, and vitamin D supplementation lowers this risk.
 Management of Gestational and Chronic HTN
 BP 140-159/90-109mmHg can be managed as an outpatient.
 Stop ACE inhibitors or ARBs or thiazide diuretics and offer alternatives
 Lifestyle advice (weight management/exercise/diet/reducing salt intake)\
 Weekly BP measurement
 Offer aspirin 75-150mg OD from 12 weeks
 PlGF test between 20 week up to 35 weeks if suspected of developing pre-
eclampsia
 fetal assessment ( Fundal height for FGR) and 2-4 weekly ultrasound

BP target control 135/85mmHg (previously 150/100mmHg)

 Inform pt about warning symptoms and signs .
 The exact level BP at which to institute antihypertensive treatment is controversial
 MAP more then 150,has risk of cerebral hemorrhage due to loss of cerebral auto
regulation therefore SBP = OR > 160/ DBP = OR > 110 mmhg require
Antihypertensive treatment

 Admit if severe (160/110mmHg), but manage as hypertension if falls below

 Offer treatment and record BP every 15-30minutes until 135/85mmHg.
 Offer continued pharmacological treatment
 Daily urine dipstick while inpatient.
 Measure FBC, U+Es, LFTs at presentation then weekly.
 Carry out PlGF testing
 Fetal assessment
 Antihypertensive medication
Labetalol PO: 100mg BD, increase if necessary to 200mg increment until an
effective dose is reached ( max 2.4g daily) avoided in women with asthma.

Methyldopa PO: 250mg 2 to 3 times daily then increase if necessary.( max 3g

daily) side effects, including depression, sedation and postural hypotension.
Nifedipine
Alpha blocker and vasodilators such as oral hydralazine can be used
 Incase of Tx failure these drug can be combined
 Diuretics , ACE inhibitors and ARB are contra –indicated
 Do not stop Antihypertensive treatment abruptly
 If mother is taking labetalol, monitor neonate for 72h after birth. ( risk of
hypoglycemia bradycardia and Respiratory distress)
 Timing of birth

•Do not offer planned early birth before 37 weeks if blood pressure is lower than
160/110mmHg unless there are other medical indications
•If birth is necessary, offer steroids and Magnesium Sulphate in line with NICE guidance
on preterm labour and birth.
 Management of pre-eclampsia without
severe feature
Delivery of the fetus and placenta is the definitive treatment of pre-eclampsia.
General measures:
 hospitalization ; rest and monitoring of BP
 Assess the risk for FGR
 Normal Sodium and caloric intake
 Oral Antihypertensive
Before 37 weeks LMP: expectant management
After 37 weeks LMP: induce labor as soon as cervix is favorable or CS within
24- 48 H
 Management of pre-eclampsia with severe
features
Care is best organized with multidisciplinary team(OBGYN, Anaesth and
midwife)
General measures:
 hospitalization ; rest and monitoring of BP
 Assess the risk for FGR
 Fluid balance (limit maintenance fluids to 80 ml/hour unless there are other
ongoing fluid losses)
 CBC, platelets, and liver function tests should be checked daily

 Magnesium sulfate and IV antihypertensives may be given initially while

betamethasone is administered for fetal lung maturity
Magnesium sulfate
 Monitoring of mgso4

Pateller reflex, BP, HR, Respiratory rate every 15 minute in first Hour then
hourly, With urine out put.
Signs of magnesium sulfate overdose:
1. Disappearance of the patellar reflex at 8 to 10 mEq/L
2. Hypotension
3. Arrhythmia
4. Respiratory depression (RR < 12)
If the patellar reflex Disappears, stop magnesium sulfate immediately and give
Calcium gluconate 1g iv
If UOP Drops ( 30ml/h or 100ml/4h: stop MgSO4 and deliver as quickly as possible
 Antihypertensive medication

is indicated for patients with a systolic BP of 160 mm Hg or greater or diastolic

BP of 110 mm Hg or greate.
It is reasonable to reduce the patient's systolic BP to 140 to 155 mm Hg and
the diastolic BP to 90 to 100 mm Hg. It is more important to decrease the
diastolic pressure.
Excessive fall in maternal BP will result in placental hypo perfusion and fetal
death. DBP SHOULD NOT GO BELOW 90mmgh.
 Timing of delivery

Severe pre-eclampsia is usually treated conservatively till the end of the 36th
week to ensure reasonable maturation of the foetus.

 From 34 to 36wk+6D: Continue surveillance unless there are

indications for early birth
 After 37 weeks: Initiate birth within 24 to 48 hours
 Before 34 weeks: expectant management is acceptable if BP is
adequately controlled with antihypertensive agents, fetal testing is
reassuring, and there is no evidence of IUGR
 Thresholds for considering planned early
birth
Include any of the following known features of severe pre-eclampsia:
 inability to control maternal blood pressure despite using 3 or more classes
of antihypertensives in appropriate doses
 maternal pulse oximetry less than 90%
 progressive deterioration in liver function, renal function, haemolysis, or
platelet count
 ongoing neurological features, such as severe intractable headache,
repeated visual disturbances ,
 eclampsia
 placental abruption,
 reversed end-diastolic flow,
 abnormal CTG or stillbirth.
 Severe pre-eclampsia is usually treated conservatively till the end of the 36th
week to ensure reasonable maturation of the foetus.
Classical
indications
Indications of termination before 36th week include:

Foetal :
 intrauterine growth
retardation,
 oligohydramnios,
 reduced foetal movements,
 Fetal distress/Non
Reassuring , or
failing biochemical results
Maternal :
 blood pressure is sustained or
exceed 180/110 mmHg
 oliguria ,
 evidence of DIC , or HELLP
 Eclampsia
 Maternal symptoms
 Method of deliver
Vaginal delivery may be commenced in vertex presentation by:
amniotomy + oxytocin if the cervix is favourable.

Caesarean section is indicated in :

 Foetal distress.
 Late deceleration occurs with oxytocin challenge test.
 Failure of induction of labour.
 Other indications as contracted pelvis, and malpresentations.

 Delivery indicated within 24 to 48 hour

 If CS is performed, Regional Anaesthesia is perferred beceacuse GA cried Risk of
fluctuation in BP,This helps control of hypertension by reduction of pre- and
afterload
 Ergometrine should be avoided as it may produce an acute rise in blood pressure
Answer

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 Fetal surveillance

At the diagnosis:
 ultrasound for fetal growth and amniotic fluid volume assessment
 umbilical artery doppler velocimetry
 Cardiotocography

 Pt instructed regarding fetal movement

 NST at least weekly
 Postpartum management
Pre-eclampsia resolve after delivery however one third of eclampsia occur in
postpartum, therefore MgSO4 prophylaxis is continued for 24h PP.

Continue monitoring of the mother for 48 hours for blood pressure control, fluid
balance, hematology and biochemistry.
NSAID avoided because of the risk of AKI especially in volume deplete patients and
fluid retention that may cause pulmonary oedema.
Anti- hypertensive drugs are continued in a decreasing dose for 48 hour

Postpartum hypertension

Methyldopa should be avoided PP because of its tendency to cause depression.

β-blockers (e.g., atenolol 50–100 mg o.d.), with the addition of a calcium antagonist (e.g.,
nifedipine 10–20 mg b.d. or amlodipine 5–10 mg o.d.) and/or an ACE inhibitor (e.g., enalapril 5–
20 mg b.d.)
 Prediction Models

Recently designed tool which assesses maternal signs, symptoms, and laboratory
findings to generate a valid and reliable algorithm for predicting adverse maternal
and perinatal outcome in patients with preeclampsia

 FullPIERS Pre-eclampsia Integrated Estimate of Risk

 PREP-S
 PlGF
 Summary

•main types of hypertension in pregnancy.

•Management is similar in all cases, but needs to be
individualised for each women using an MDT approach
•Prediction tools and PlGF may be useful
•Risk of complications continues after birth
•Implications for longterm cardiovascular and renal health
 References
BMJ
Medscape
MSF
NICE
Handbook of Obstetric Medicine - 5E
Johns Hopkins Manual of Gynecolo
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