Hypertesion in pregnancy Obstetrics

1. ‫الرحيم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬

3. Definition
• Hypertension (HT): sustained elevation of blood
pressure (recorded on at least two occasions).
• Diastolic blood pressure 90 mmHg, or
• Systolic blood pressure 140mmHg,
• Hypertensive disease complicates 5-7 may reach 6-12%
of all pregnancies.
• 16% of pregnancy-related deaths, (63 000 women die
worldwide each year,98% in developing countries )
• Eclampsia 1 in 2000 deliveries.
• More than 10% of women will develop PE in 1st
pregnancy.

4. .
Classification of hypertension in pregnancy‫مهم‬
1. Pre-existing hypertension and/or renal disease.
A. Chronic hypertension(no proteinuria).
B. Chronic renal disease(hypertension and/or
proteinuria).
C. Chronic hypertension with superimposed pre-
eclampsia.
2. Pregnancy induced hypertension(gestational).
A. Gestational hypertension(no proteinuria).
B. Gestational proteinuria(no hypertension).
C. Pre-eclampsia(proteinuria & hypertension).
3. Unclassified hypertension & proteinuria.
4. eclmapsia

5. Pre-eclampsia
PE : iodiopathic disoederof pregnancy .
Hypertension of at least 140/90 mmHg or more
recorded on 2 separate occasions & at least 4 hr.
apart & in the presence of at least 300mg protein
in a 24 hour collection of urine, arising after the
20th weeks of pregnancy in a previously
normotensive woman & resolving completely by
the sixth postpartum weeks.(recently up to
12weeks)
Is a multisystem disease, affecting multiple organ
systems.
PE complicates approximately 2-3% of pregnancies.

6. Etiology
• 1. Abnormal trophoblastic invasion of uterine
vessels.
• 2. Immunological intolerance between maternal
and fetoplacental tissues
• 3. Maternal maladaptation to cardiovascular or
inflammatory changes of normal pregnancy.
• 4. Dietary deficiencies
• 5. Genetic influences. Four fold increase in the first
degree relative of affected women.
• Unexposed to the product of the fetus (paternal
genome),so the disease common in 1st pregnancy

8. Normal placentation:
The maternal blood flow to the placenta
incrsases throughout the pregnancy from
50ml in T1 to 500-750 ml at term.
Trophoblast cells invade the spiral arterioles
within the first 12 weeks of pregnancy &
replace the smooth muscle of the wall of the
vessels, thus converting them to wide bore,
low resistance, large capacitance vessels.
This process is normally complete by 20
weeks gestation.

9. Abnormal trophoblastic invasion

11. Abnormal placentation
In pregnancies complicated by pre-eclampsia, FGR &
or abruptio placentae, there is complete or partial
failure of trophoblast invasion of the myometrial
segments of the spiral arteries.
Spiral arteries retain some of their pre-pregnancy
characteristics being relatively narrow bore and of
low capacitance and high resistance and resulting
in impaired perfusion of the fetoplacental unit.
Affected placentae have gross morphological changes,
which include infarcts & basal haematomas.

12. • An infarct represents an area of ischemic
necrosis of a cotyledon resulting from a spiral
artery occlusion, usually by thrombosis. A
placenta with multiple infarcts is significantly
associated with FGR &IUD.
• Basal hematoma consist of a mass of blood in
the centre of fetal cotyledon due to the
rupture of a damaged spiral artery. This lesion
is associated with maternal hypertension and
increased perinatal mortality.

13. Risk factors for PE
A. First pregnancy.
B. Multiparous with:- PE in any previous pregnancy.
C. Age 40 years or more.
D. BMI of 35 or more.
E. Family history of PE (in mother or sister).
F. Booking diastolic blood pressure of 80 mmHg or
more.
G. Booking proteinuria(of˃or =1+ on more than one
occasion or quantified at ˃or=0.3g/24hr.)
H. Multiple pregnancy.molar pregnancy
I. Certain underlying medical conditions(H.T, renal
disease, diabetes ,SLE , APS).

14. pathophysiology
Cardiovascular system
Marked peripheral vasoconstriction→hypertension.
High intravascular pressure and loss of endothelial cell
integrity →↑vascular permiability →generalized
oedema.
Renal system
Glomeruloendotheliosis: characteristic lesion specific for
pre-eclampsia, is associated with impaired glomerular
filtration & selective loss of intermediate weight
proteins, such as albumin →proteinuria →↓plasma
oncotic pressure & exacerbates the development of
edema.
• Decrease GFR and renal failure.
• Decrease urate excretion hyperuricaemia

15. Haematological system
• platelets activation and depletion .due to
endothelial damage
• Coagulopathy.
• Reduce plasma volume
• Increase blood viscosity.
Liver
• Subendothelial fibrin deposition is associated with
↑liver enzymes (The presence of haemolysis,
elevated liver enzymes and low platelet count is
called HELLP syndrome).
• Peripheral necrosis.
• Subcapsular hematoma.

16. Neurological system
• Cerebral oedema.
• Cerebral haemorrhage.
• Seizure (eclampsia).
• Retinal haemorrhage ,exudates and papilloedema.
Altered vascular permeability:
• Peripheral oedema.
• Pulmonary oedema.
placenta:
• Fetal growth restriction.
• Fetal hypoxia.
• Abruptio placenta.

17. Clinical presentation
- asymptomatic.
- General vague ,flu-like symptoms
- frontal headache, visual disturbance, epigastric
pain.
Examination.
- High BP.
- Rapid progressive oedema of the face & hands.
- Epigastric tenderness.
- Neurological exa .hyperreflexia, clonus.
- Obstetric exa ,Small for gestational age uterus.
- Urine test for protein.

19. Investigations
• A-haematological
• Haemoglobin &haematocrit. may increased
• Platelets count .
• Uric acid .increased
• Urea & creatinine. Inc =late renal involvment
• Liver function test. AST ,LD
•

20. B-Testing for proteinuria
1. Dipstick urinalysis
Instant result but quantitatively inaccurate.
Results:
- trace: seldom significant.
- 1+ : possible significant.
- ≥ 2+: probable significant.
2. protein:creatinine ratio
Fast(within an hour)
˃ 30mg/mol- probable significant.
3. 24 hour collection
Slow
˃ 0.3 g(300mg)/24 hours- confirmed significant
proteinuria.

21. Principle of management
1. Early recognition of the symptomless syndrome.
2. Awareness of the serious nature of the condition
in its severest form.
3. Adherence to agreed guidlines for admission to
hospital, investigations, & the use of
antihypertensive & anticonvulsant therapy.
4. Well-timed delivery to prevent serious maternal or
fetal complications.
5. Post-natal follow up & counselling for future
pregnancies.

22. prevention
• Salt restriction : ineffective (normal diet)
• Inappropriate diuretic therapy.
• Folic acid supplement.
• calcium, The effect greatest in women at high risk of
developing HT and those with low baseline dietary
calcium.
• Fish oil capsules : modify abnormal PG balance :
ineffective
• Low dose aspirin (75mg) : for all high risk women from
12 weeks.
• Antioxidants : vitamin C & E : reduced endothelial cell
activation , reduction in preeclampsia.
• Antiplatelet prevent preeclampsia.

23. Management & treatment
No cure for PE other than to end the pregnancy by
delivering the baby (and placenta).
- Patients with mild hypertension.
- If diastolic BP is 140-149 /90-99 mmHg with trace
proteinuria or +ve, we can manage the patient as outpatient.
- but require frequent visits to assess maternal & fetal
wellbeing.
- Patients with moderate (150-159/100-109)or severe
(160/110)hypertension, significant proteinuria or
abnormal hematological or biochemical
parameters→admission & inpatient Mx.
- Most of maternal death occur due to multiple organ
failure, DIC, ARDS and renal failure

24. Severe preeclampsia
• BP >= 160/110 mmHg
• Proteinuria 5 g/24hr or >= 2+ dipstick (persistent)
• Cr > 1.2 mg/dl
• Platelets < 100,000 /mm3
• Microangiopathic haemolysis
• Elevated ALT or AST
• Persistent headache , visual disturbance , sever Rt
hypochondria or epigastric pain, vomiting .
• Sudden swelling of the face ,hands ,or feet.

25. Investigations
To monitor maternal complications
• FBC: attention for falling platelet count &
rising hematocrit.
• if platelets values are normal, additional
clotting studies are not indicated.
• Serum renal profile(including uric acid).
• Serum liver profile.

26. To monitor fetal complications
Ultrasound assessment of:
- Fetal size.
- Amniotic fluid volume.
- Maternal & fetal Dopplers.
- Antenatal cardiotocography in conjunction
with ultrasound surveillance, to assess fetal
wellbeing.
- A loss of baseline variability or deceleration
may indicate fetal hypoxia.

27. Antihypertensive therapy:
The aim of antihypertensiv therapy is to
lower the blood pressure and reduce the risk
of maternal cerebrovascular accident
without reducing uterine blood flow and
compromising the fetus.
If Bp140-149/90-99 mmhg then review
weekly with test or proteinurea.
If Bp 150 -159/100 -109 mmhg Rx with
labetolol and target Bp 140 -150/80 -
100mmhg . check urea and electrolytes LFT
FBC,review twice weekly for PU.
If Bp >160/>110 ,admit until below
159/109mmhg and Rx as above .

28. DRUGS USED IN ACUTE TREATMENT OF SEVER HTN
1) Hydralazine
5mg bolus iv, repeated at 20-30 min. interval. Iv
infusion in normal saline may be considered if no
response repeated bolus 5mg are required. Up
to15mg
It directly relax the vascular smooth muscles 
reflex tachycardia increase in cardiac
output side effects(restlessness, headache &
palpitation).
Gradual reduction of BP to avoid precipitating fetal
distress(in the form of bradycardia) secondary to
sudden drop in maternal BP that reduce uterine
blood flow.

29. 2) Labetalol(1st line ) :Combined a and B
blockers given as 20 mg iv bolus repeated in
an interval of 10-20 minut(40-80mg).up to
220mg then 40/hr increase up to160mg hr/
3) Nifedipine : 10 mg orally repeated at interval
of 10-20 min. It decrease vascular resistance
by inhibiting trans membrane calcium influx
into vascular smooth muscle cells, it reduce
BP within 10-20 min.
4) 3rd line Na Nitroprusside: 0.25 mg/kg per
min. i.v infusion.
5) Nitroglycerine: 10 mg per minute infusion.

30. Drugs used in long term treatment of HT
A) Methyldopa(Aldomet)
It is regarded as 1st choice in long term treatment of
patient with HT during pregnancy due to it`s
safety.
1 gm loaded dose then 1-2gm /day in divided doses,
increased to maximum of 3 gm.
Action: it decreased central sympathetic outflow by
stimulating brainstem alpha 2 receptors, decrease
vascular resistance without an effect on heart rate
or cardiac output .

31. B) Labetalol: 300 mg in divided doses, increased
to a maximum of 1200 mg/day.
C) Nifedipine: 40 mg/day in divided doses,
increased to a maximum of
120mg/day.
D) Hydralazine :100 mg/day in 4 divided doses,
increased to a maximum of 300 mg/day.

32. Anticonvulsant therapy
The drug of choice for eclampsia is magnesium
sulphate which is given intravenously.
• it reduce the incidence of further convulsion
in women with eclampsia.
• Prevent the onset of convulsion in women
with severe pre-eclampsia.
Steroid
Prior to 34 weeks steroid should be given
intramusculary to reduce chance of neonatal
RDS.

33. Indication of delivery

34. Iatrogenic premature delivery of the fetus is often
indicated in the following condition ‫الوالدات‬ ‫اسباب‬
‫المبكره‬
i. Sever uncontrolled HT > 160/110 mmHg despite
maximum recommended dose of two antiHT
drugs.
ii. HELLP syndrome.
iii. Progressive symptoms( headache, visual
disturbance, epigastric pain).
iv. Pulmonary oedema.
v. Eclampsia.
vi. Fetal distress.
vii. Renal compromise with oliguria.

35. Delivery
Steriod indicated when delivery plland befor 37 wk .
 In spontaneous or induced labour and if clotting
studies are normal, epidural anasthesia is
recomended and it help to control blood pressure.
B P measument(mercury SM) every 15 min in S1.
Ergometrine is avoided in the Mx. of 3rd stage as it
can significantly increase blood pressure.
Patients are at risk of thromboembolism, and
should be given prophylactic subcutaneous heparin
and antithrombotic stockings.

37. Post-natally
• Blood pressure and proteinuria will resolve.
• One or both may persist beyond 6 weeks in
minority of patients, which suggest the presence of
underlying chronic hypertension or renal disease.
Screening
There is currently no screening test for PE. But
*Doppler assesserment of maternal utrine circulation.
Elevated AFP .GCH and inhibin-A or decreased PAPP

38. Complications of PE
1.Eclampsia.
2.Cerebral haemorrhage.
3.Pulmonary oedema.
4.HELLP syndrome .
5.Acute renal failure.
6.Placental insufficiency IUGRIUD.
7.Abruptio placenta.
CNS
RP
LIVER +BLOOD

40. Eclampsia
Definition: occurrence of convulsions(grand mal) in patient
with pre-eclampsia. Usually short lasting 60-75 sec, and self
limiting. A serious complication of PE with increase the fetal
and maternal mortality.
Eclamptic fit occurs classically in 2nd half of pregnancy and up
to 10 days postpartum, it is tonic clonic convulsion followed
by brief period of coma.
Incidence: Antepartum: 40%
Intrapartum: 20%
Postpartum: 40%
Imminent eclampsia(fulminating PE ): is a transitional
condition characterized by increasing symptoms and signs
of PE. Severe PE is more common than eclampsia.

41. • The seizure may be divided into 2 phases:
– Phase 1 lasts 15-20 seconds and begins with facial twitching. The
body becomes rigid, leading to generalized muscular contractions.
– Phase 2 lasts approximately 60 seconds. It starts in the jaw, moves
to the muscles of the face and eyelids, and then spreads
throughout the body. The muscles begin alternating between
contracting and relaxing in rapid sequence.
• A coma or a period of unconsciousness follows phase 2.
– Unconsciousness lasts for a variable period.
– Following the coma phase, the patient may regain some
consciousness.
– The patient may become combative and very agitated.
– The patient has no recollection of the seizure.
• A period of hyperventilation occurs after the tonic-clonic seizure. This
compensates for the respiratory and lactic acidosis that develops
during the apneic phase.
• Seizure-induced complications may include tongue biting, head
trauma, broken bones, or aspiration.

42. Diagnosis of severe PE
• Severe PE is identified by BP≥ 160/ 110 mmHg &
proteinuria on dipstick testing.
Symptoms of severe PE that may precede eclampsia:
1. Frontal headache.
2. Visual disturbance(blurred vision & flashing lights).
3. Epigastric pain.
4. General malaise & nausea.
5. Restlessness.
6. Amnesia and other mental status changes
To the developement of grand mal convulsions.
- Preceding PE suggest eclampsia but in 1/3 of cases
eclamptic fit precedes other signs.

43. • Differential Diagnosis
• Adrenal Insufficiency and Adrenal Crisis Cerebellar Hemorrhage
• Cerebral Aneurysms Cerebral Venous
Thrombosis
• Encephalopathy, Hypertensive Encephalitis
• Gestational Trophoblastic Neoplasia Head Trauma
• Hyperaldosteronism, Primary Hypertensive
Emergencies
• Hypoglycemia Meningitis Neoplasms, Brain
• Epilepsy Shock, Septic
• Stroke, Hemorrhagic Stroke, Ischemic
• Subarachnoid Hemorrhage
• Systemic Lupus Erythematosus
• Thrombotic Thrombocytopenic Purpura
• Withdrawal Syndromes Angiomas
• Cerebral Vasculitis Drug Overdose Metabolic Disorders
• Undiagnosed Brain Tumors
• cysticercosis(tapeworm infection caused by Taenia solium),

44. Signs of severe PE prior tp E
1. Agitation.
2. Hyper-reflexia & clonus.
3. Facial oedema(periorbital).
4. Right upper quadrant tenderness.
5. Poor urine output.
6. Papilledema.
7. Marked proteinuria
8. Tachycardia ,
9. Tachypnea
The fetus
Appear small, with oligohydramnios and reduced fetal
movements.
CTG may shows signs of hypoxia with fetal tachycardia,
reduced variability and decelerations

45. Management of Eclampsia
• ABC approach should be used.
• Put the patient in quite darken room .
• Call for help from senior obstetric & anaesthetic colleagues,
consultant haematologist.
• The patient should be moved to left lateral position.
• Oxygen applied.
• Large bore i.v cannulae should be sited and blood taken for FBC,
clotting studies, renal and liver function test & cross matching.
• 1. control of convulsions using IV MgSO4.
• 2. Intermittent IV or oral of antihypertensive drug to lower
Diastolic BP <100.
• 3. Avoidance of diuretics(Diuretics are used only in the setting of
pulmonary edema),
• limit IV fluid administration ,
• avoid hyperosmotic agents
• 4. Delivery

46. • Urgent stabilization of mother condition before
considering delivery by:
Prevention & treatment of fits by intravenous
magnesium sulphate.
- initial loading dose of 4g is given, followed by infusion
of 1g/hour.
- Magnesium sulphate overdose→respiratory & cardiac
depression.(this can be reveresed by calcium
gluconate-10ml of 10% solution).
• Therapeutic level: 4-7 meq/L
• Patellar reflexes lost: 8-10 meq/L
• Respiratory depression: 10-15 meq/L
• Respiratory paralysis: 12-15 meq/L
• Cardiac arrest: 25-30 meq/L
• Cr >1.3 : half dose MgSO4
Blood pressure control. to prevent intracranial
hemorrhage which may lead to death.

47.  Management of fluid balance.
In PE there is peripheral vasoconstriction with reduced
plasma volume, together with redistribution of
extracellular fluid.
UOP fall and fluid overload may lead to cerebral and
pulmonary oedema
Restrict fluid intak to 80ml/ hour until postpartum
diurrsis established .
• Renal failure is uncommon and if it occur usually
reversible.
• Unless unusual fluid loss : N/V , diarrhea , excessive
blood loss. And persistent minimal urine output,
invasive monitoring may help to avoiding fluid over
load.
• Women with eclampsia already has excessive
extracellular fluid

48. Delivery :
 should follow stabilization of patient condition.
• Delivary of the placenta remainsthoonly intevention which
lead to resolution of the clinical biochemical manfestation
of PE .the woman with PE should be delivared in an
enviroment of closely monetered and approperiately
maneged, with contenouse post natal surveillance . The
mode of delivary depend upon gestation ,severity o
maternal diseas degreeof featl compromise.
• Anesthesia in Preeclampsia.
• GA : caused by tracheal intubation, sudden increased in
BP,pulm edema , intracranial hge
• Epidural preferred : no serious maternal or fetal
complication , lower MAP , Cardiac output not fall

49. Post-delivery care should include :
• Maternal observations should be conducted every 5-15
minutes until stabilization of the mother.
• Fluid balance.
• BP measurement.
• Renal, hepatic & CNS function, urine output.
• Keep MgSo4 infusion for 24 hrs. at 1g/hr. drip. It`s toxicity is
assessed by loss of deep tendon reflexes & respiratory
depression, biochemically by measuring plasma Mg level (
therapeutic range 2-5 mg/dl).
• Prophylaxis for thromboembolism (SC heparin & compression
stock).
• Patients with persistent hypertension past 8 weeks'
puerperium or neurologic changes may need medical
referral.

50. Complications of Eclampsia
• As many as 56% of patients with eclampsia may have transient
deficits, including cortical blindness.
• there is an increased risk for cerebrovascular accidents (CVAs) and
coronary artery disease (CAD) in eclamptic mothers later in life.
• Other potential complications of eclampsia include the following:
• Permanent neurologic damage from recurrent seizures or
intracranial bleeding
• Renal insufficiency and acute renal failure
• Fetal changes – IUGR, abruptio placentae, oligohydramnios
• Hepatic damage and rarely hepatic rupture
• Hematologic compromise and DIC
• Increased risk of recurrent preeclampsia/eclampsia with
subsequent pregnancy
• Maternal or fetal deat

51. HELLP syndrome
• A combination of hemolysis, elevated liver enzymes
and low platelets, is seen in severe PE(12%). May be
asymtomatic ,malaise ,nausea ,epigastric or right upper
quadrant tenderness .Dx laboratory
• More common in multiparous woman.
• It may be associated with placental abruption,
disseminated intravascular coagulation, acute renal
failure, subcapsular liver hematoma and fetal death.
• The only effective treatment is prompt delivery of the
baby.
• The DIC is treated with fresh frozen plasma to replenish
the coagulation proteins, and the anaemia may require
blood transfusion.
• In mild cases, corticosteroids and antihypertensive
drugs may be sufficient.

52. Chronic hypertension
• Present prior to pregnancy , or in the 1st half or persist
after 6 weeks postpartum .
Causes
1. Idiopathic- essential hypertension. 90% of cases.
2. Renal disease. (Polycystic disease, diabetic
nephropathy, chronic glomerulonephritis, nephrotic
syndrome).
3. Vascular disorder.(Renal artery stenosis, coarctation of
aorta).
4. Collagen vascular disease.(Systemic sclerosis, SLE,
rheumatoid disease).
5. Endocrine disease.(Pheochromocytoma, Conn′s
syndrome, cushing′s syndrome, D.M).

53. Essential hypertension account for 90 % of cases, but we
have to exclude other causes before diagnosis:
• Serum creatinine.
• Electrolytes and urate.
• Liver function test.
• Urine analysis(blood, protein, glucose).
• 24 hours urinary protein/creatinine clearance.
• Renal ultrasound.
• Autoantibody screen.
• ECG & echocardiography.
• Maternal risk of pre-existing hypertension
1. Pre- eclampsia.
2. Abruption.
3. Heart failure.
4. Intracerebral haemorrhage.

54. Risk factors for developing superimposed pre-
eclampsia
1. Maternal age ˃ 40 years.
2. Pre-pregnancy BMI ˃ 35.
3. Blood pressure ≥ 160/100mmHg in early
pregnancy.
4. Multiple pregnancy.
5. Antiphospholipid syndrome.
6. Coarctation of aorta.
7. Pre-existing diabetes.
8. Renal disease.
9. Previous pre-eclampsia.

55. Management of chronic hypertension
In mild cases(˂ 150/100 mmHg).
- no treatment.
- Monitor pregnancy to detect rising blood pressure,
or features of PE, or FGR by serial US scans.
Most authorities stop the treatment of chronic HT,
if diastolic BP <110 mmHg and in the 1st trimester
and low risk pat., because the BP decrease.
ACEI is contraindicated because it cause fetal
death and neonatal renal failure.

56. • If BP ˃ 150/100 mmHg, antihypertensive
medication will need to be taken(to reduce
the risk of intracerebral hemorrhage).
The aim of antihypertensive treatment is to
maintain BP in the region of 140-160/ 80-
100mmHg.
Treatment does not prevent placental
abruption, super imposed PE, nor perinatal
outcome.
Methyldopa is given first, if this fail to control
then Nifedipine is added.

57. Obstetric Mx of pre-existing hypertension:
1. Close monitoring for the develpement of
superimposed PE (elevated BP, new onset or
worsening proteinuria, FGR).
2. Early delivery is indicated if BP difficult to control.
3. In general, await spontaneous labour or attempt
vaginal delivery by induction of labour(at around
38 weeks).
4. Post-natally: careful observation of BP.
5. The standard antihypertensive medications are not
C.I in breast feeding mothers.
6. Follow up for BP, and protein uria in 1-2 weeks.