Hypertensive disorders in pregnancy refer to a group of conditions characterized by high blood pressure during pregnancy, which can include gestational hypertension (high blood pressure that develops after 20 weeks of pregnancy) and preeclampsia (a more severe form of hypertension that can also cause protein in the urine and changes in liver function). These conditions can be serious for both the mother and the baby and may require close monitoring and management. Treatment options may include medications to lower blood pressure, as well as close monitoring of the mother and baby to ensure their health and well-being.

1. HYPERTENSIVE
DISORDERS IN
PREGNANCY

2. INCIDENCE AND SIGNIFICANCE
 10 % of pregnancies suffer hypertensive disorders (most commonly gestational
hypertension )
 3% of pregnancies suffer from PET
 PET is one of the leading causes of maternal death (cerebral hemorrhage as a
main cause of death due to PET )
 Increased perinatal morbidity and mortality ( IUGR, prematurity )

3. CLASSIFICATION OF HYPERTENSIVE
DISORDERS
A. Chronic hypertension
B. Gestational hypertension (non proteinuric pregnancy induced
hypertension )
A. Preeclampsia

4. GESTATIONAL HYPERTENSION
 hypertension that arises for the first time in the second
half of pregnancy(after 20 weeks ) and in the absence of proteinuria
Also called non protinuric pregnancy induced hypertension
 Mild and moderate doesn’t need treatment and has no adverse effect on the
pregnancy while sever should be admitted and treated (more than 160/110)
 1/3 of patients will progress into preeclampsia

5. PREECLAMPSIA
Occur in 3 % of pregnancies
DEFINITION ?
HIGH BLOOD PRESSURE + SIGNIFICANT PROTINURIA AFTER 20 WEEKS
HIGH BLOOD PRESSURE = hypertension of at least 140/90 mmHg recorded on at least two
separate occasions and at least 4 hours apart
SIGNIFICANT PROTINURIA = the presence of at least 300 mg protein in a 24-hour collection of
urine
ARISING AFTER 20 WEEKS OF GESTATION (DE NOVO )

6. RISK FACTORS TO DEVELOP PET
 First pregnancy(PRIMIGRAVIDA)
 Pre-eclampsia in any previous pregnancy
 10 years or more since last baby
 Age 40 years or more
 Body mass index (BMI) of 35 or more
 Family history of pre-eclampsia (in mother or sister)
 Booking diastolic blood pressure of 80 mmHg or more
 Booking proteinuria ( of ≥1+ on more than one occasion or quantified at
≥0.3 g/24 h).
 Multiple pregnancy

7. RISK FACTORS …
 Certain underlying medical conditions:
pre-existing hypertension;
pre-existing renal disease;
pre-existing diabetes;
antiphospholipid antibodies
These risk factors are the same risk factors divided into major and moderate risk factors
where we use low dose aspirin for them if one major or 2 moderate risks to prevent PET *
see later

8. PATHOPHYSIOLOGY
 Normally; trophoblasts invades uterine spiral arterioles muscle layer leading to a vessels
with high capacitance ,high flow and low resistance (by maternal immune system NK
cells )
 In pregnancies that will develop preeclampsia this is defective and process goes into 2
stages :
 First stage : trophoblastic invasion to these vessels is patchy , vessels will still have
their muscular layer ,so the resistance will increase , decreased flow –leading to
uteroplacental ischemia (uteroplacental insufficiency )
 In the second stage, uteroplacental ischaemia results in oxidative and inflammatory
stress, with the involvement of secondary mediators leading to endothelial dysfunction,
vasospasm and activation of the coagulation system leading to systemic disorder

10.  The pregnant lady’s immune system is different than
non pregnant
 NK cells helps trophoblastic cells to invade blood
vessels called spiral arterioles
 The invasion will disrupt the blood vessels muscular
layer but this is good !
 The blood vessels will became dilated containing
more blood and flows more blood into the placenta
 This will not happen in pregnancies that will suffer
preeclampsia

11.  So the blood vessels will have muscular layer which prevent high flow of blood to the placenta
 The placenta will suffer ischemia and release vasoactive substances
 These substances will affect the whole body system trying to increase blood pressure
 The high blood pressure is a trial to help more flow into the placenta
 Blood pressure will be elevated by vasoconstriction that will lead to ischemia and systemic effect
of organs

12.  High blood pressure in the vessels will lead to, fluid will come out
from vessels leading to edema endothelial dysfunction
 In kidneys it leads to glomeruloendotheliosis associated with
impaired glomerular filtration and selective loss of intermediate
weight proteins, such as albumin and transferrin, leading to
proteinuria
 Loss pf proteins will lead to decrease oncotic pressure and more
edema

13. HELLP SYNDROME
The effect on hematological system + liver
H=hemolysis EL= elevated liver enzyme LP= low platelets
endothelial damage, platelets adhere to the damaged area….. Low
platelets
In the liver, subendothelial fibrin deposition is associated with elevation of
liver enzymes
HELLLLPPP
!

14. HELLP SYNDROME
 Women with HELLP syndrome typically present with epigastric pain,
nausea and vomiting.
 Hypertension may be mild or even absent.
 HELLP syndrome is associated with a range of serious complications
including acute renal failure, placental abruption and stillbirth.
 The management of HELLP syndrome involves stabilizing the mother,
correcting any coagulation deficits and assessing the fetus for delivery

16. CLINICAL PRESENTATION OF PET
 The majority are asymptomatic
 Symptoms : frontal headache, visual disturbance and epigastric pain
 Signs : hypertension is the first early sign
dependent edema usually lower limb
Epigastric tenderness (liver involvement )
hyperreflexia and clonus
Significant proteinuria on urine test (more than 300 mg in 24 hr collection or protein creatinine ratio on
urine spot more than 30 mg/mol )
Urine protein by dipstick more than +1 should be confirmed by 24 hours urine collection

17. MANAGEMENT OF PET
 According to the severity
 According to the gestational age
 The main treatment is termination of pregnancy (delivery )after stabilization (control
blood pressure with convulsion prophylaxis )
 Admit all with penitents with PET , treat moderate and sever with labetalol as first line
treatment if suitable
 PET can be cautiously treated conservatively until 34 weeks but with close monitoring
with low threshold to terminate pregnancy with any maternal or fetal status deterioration
 There is no cure other than delivery; the aim of
management is to stabilize the maternal blood pressure
and prevent seizures and cerebral bleeding

19. SEVER PREECLAMPSIA ?
Preeclampsia is classified as sever if any of these criteria present :
 Systolic bp more than 160
 Diastolic blood pressure more than 110
 Neurological symptoms : headache , visual disturbance (scotomas )
 RUQ pain
 Proteinuria more than 5 g/24 hours urine collection
 Pulmonary edema
 Renal impairment (oliguria less than 500 ml per 24 hours) 0.5 ml /kg or
increase serum creatinine
 Any feature of HELLP syndrome

20. DON’T FORGET THAT THE FETUS IS ALSO AT
RISK (IUGR, OLIGOHYDRAMNIOS )
 To monitor fetal complications:
 Ultrasound assessment of:
 fetal size;
 amniotic fluid volume;
 maternal and fetal Dopplers
 CTG is only needed if there is an abnormal monitoring or decreased
fetal movement (not routine )

21. TREAT HYPERTENSION AND
PREVENT ECLAMPSIA (CONVULSION)
Labetalol is the first line treatment , alpha and beta blocker that is
contraindicated in asthma
Other antihypertensives :
Methyle dopa (centrally acting antihypertensive)
Nefidipine (calcium channel blocker )
In sever cases first line is IV labetalol , next IV hydralazine
The drug of choice for the treatment of eclampsia is magnesium sulphate
Magnesium sulphate should also be used in women with severe pre-
eclampsia to prevent the onset of convulsions

22.  Calcium channel blockers
lead to lower limb edema
 Methyldopa shouldn’t be given
for more than 2 days
postnatally as it may lead to
postpartum depression
 Labetalol is contraindicated in
asthmatic patients

23. DELIVERY
 In sever preeclamsia preterm delivery is often needed
 Delivery before 34 weeks will need corticosteroid for lung maturity
 Preterm delivery is often done by cesarean section
 Cesarean section is not an Indication for preeclampsia unless maternal
or fetal status id deteriorating
 LMWH is needed after delivery if suitable (not DIC or hematological
abnormalities ) and elastic stocking to decrease the risk of VTE
 Don’t use ergometrine
 Epidural is preferred if normal hematological parameters (no DIC and
normal platelets count )
 Follow-up of Bp and proteinuria should be done postnatally

24. PREVENTION OF PREECLAMPSIA
 Screening for preeclampsia may be done by history and blood pressure measurement since
the first visit and every visit , uterine artery doppler showing notch or biochemical tests (low
PlGF)
 Low dose aspirin in high risk patients (75 mg aspirin once daily before 20 weeks )
reduces PET
 Calcium may decrease PET risk in patients with low diet intake of calcium

25. WHEN TO GIVE ASPIRIN ?
 One major risk factor
 2 or more moderate risk factors

26. ECLAMPSIA
The development of convulsions in a woman
with pre-eclampsia
Vasospasm and cerebral edema leads to
convulsion
Its an emergency !

27. ECLAMPSIA
 Preeclampsia +convulsion – neurological disorders
 Most common cause of death is cerebral hemorrhage
 Prevented by magnesium sulphate for preeclamptic patients
 Risk factors:
difficult to predict, uncontrolled hypertension, two or fewer prenatal care
visits, primigravidity, obesity, black ethnicity, history of diabetes and age
<20 years
 Warning signs:
epigastric pain and right upper quadrant tenderness, headache,
uncontrolled hypertension, agitation, hyper-reflexia and clonus, facial
(especially periorbital) oedema, poor urine output, papilloedema.

28. MANAGING ECLAMPTIC FIT
 Call for help
 ABC protocol (airway breathing cardiac )
 Magnesium sulphate 4g IV loading then 1g IV per hour for 24 hours
(first line )
 Delivery of the baby after stabilization
 Monitor respiratory rate , heart rate , urine output , deep tendon reflexes
(magnesium toxicity )
 In case of magnesium toxicity stop magnesium , check serum level of
magnesium , give antidote if sever as in cardiac arrest or respiratory
failure )
 Antidot for magnesium sulphate is calcium gluconate 10 ml 10 % iv
slowly

29. CHRONIC HYPERTENSION
 Presence of high blood pressure before pregnancy or first time before
20 weeks
 May lead to preeclampsia (superimposed preeclampsia )
 Can lead to abruptio placenta , heart failure and intracerebral
hemorrhage

30. CHRONIC HYPERTENSION
Causes :
Idiopathic.
Essential hypertension.
Vascular disorders.
Renal artery stenosis.
Coarctation of the aorta.
Renal disease.
Polycystic disease.
Diabetic nephropathy.
Chronic glomerulonephritis.
 Most common cause is essential
 Secondary causes should be excluded with the majority of
secondary cause is RENAL
Nephrotic and nephritic syndrome
Collagen vascular disease.
Systemic sclerosis.
Systemic lupus erythematosus.
Rheumatoid disease.
Endocrine disease.
Phaeochromocytoma.
Conn’s syndrome.
Cushing’s syndrome.
Diabetes mellitus.

31. SUPERIMPOSED PREECLAMPSIA IN
CHRONIC HYPERTENSION
The risk of developing PET in patients with chronic hypertension increases more in sever chronic
hypertension or renal disease related hypertension, in addition to the following group of patients :
 Renal disease.
 Maternal age >40 years.
 Pre-existing diabetes.
 Multiple pregnancy.
 Connective tissue disease (e.g. antiphospholipid syndrome).
 Coarctation of the aorta.
 Blood pressure ≥160/100 mmHg in early pregnancy.
 Pre-pregnancy BMI >35.
 Previous pre-eclampsia.
 Antiphospholipid syndrome.

32. MANAGEMENT OF CHRONIC
HYPERTENSION IN PREGNANCY
 Screen for end organ failure (kidney function, cardiac ….etc)
 Review drugs safety (ACE, ARBS ?)
 Watch for superimposed preeclampsia
 Watch for fetal complications as IUGR
 Delivery around 39 weeks in controlled cases
 Follow up post partum , discuss contraception and review drugs
regarding safety in breastfeeding
 Mild cases needs no treatment especially in the first trimester
(physiological decrease in Bp )
 Treatment should be given for moderate and sever cases