This document discusses hypertension in pregnancy, including definitions of gestational hypertension, preeclampsia, and eclampsia. It covers the pathophysiology of preeclampsia, which involves abnormal placentation leading to placental ischemia and endothelial dysfunction. Clinical presentations are described, including headaches, visual changes, abdominal pain, and seizures in severe cases. Evaluation involves assessing risk factors, measuring blood pressure and testing urine for protein. Treatment focuses on controlling blood pressure, preventing and treating seizures, and often requires delivery of the baby and placenta. Prognosis depends on severity, with risks of maternal and infant complications and mortality increasing in severe preeclampsia and eclampsia.

1. HYPERTENSION IN PREGNANCY
Associate Professor Dr Hanifullah Khan

2. Objectives
• Understand definitions
• Pathophysiology
• Presentations of the disease
• Important signs and symptoms

3. INTRODUCTION

4. Introduction
• H/T in pregnancy – leading cause of
maternal & fetal morbidity
• The most frequent cause of iatrogenic
prematurity
• PE & eclampsia – delivery is the only
effective tx

5. Definitions – H/T
• H/T –
– a DBP of 90mmHg or more, taken on 2
occasions > 4 hrs apart OR
– A single DBP of > 110mmHg
• Can occur either in –
– Women who already have H/T (10
or 20
)
– Manifest in 2nd
half of pregnancy

6. Pregnancy HT & Chronic HT
• May be difficult to differentiate
• Both have high risk of complications
• Chr HT –
– Diagnosed prepregnancy
– high BP early in pregnancy

7. Definitions - PE
• A multisystem disorder characterized
by HT + proteinuria
– Proteinuria - > 300mg urine pr / 24 hrs
• Occurs > 20 wks gestation
• Resolves postnatally
• Complications of PE – eclampsia,
HELLP synd

8. Definition - Eclampsia
• The occurrence of tonic-clonic
convulsions in a woman with PE
– Pregnancy
– Any gestation
– No neurological disease

9. • Gestational hypertension.
• Preeclampsia (mild, severe).
• Eclampsia.
• Superimposed preeclampsia upon
chronic hypertension.
• Chronic hypertension with pregnancy.
Classification

11. Incidence
• PE – 2-8% of all pregnancies
– Risk in 1st
pregnancy – 4.1%
– Risk in later pregnancies – 1.7%
– Risk in woman with PE in 1st
pregnancies –
14.7%
– Risk in woman with PE in previous 2
pregnancies – 31.9%

12. Summary
• Gestational hypertension:
– Hypertension for first time after 20 w, without
proteinuria. BP returns to normal before 12 weeks
postpartum.
• Chronic hypertension with pregnancy:
– Hypertension antedates pregnancy and detected
before 20 w, & lasts more than 12 weeks
postpartum.

13. PATHOPHYSIOLOGY

14. Basic understanding
• Complex disease
• Appears to be triggered by the placenta
– Can occur in molar pregnancies where fetus
absent

15. Trophoblast
• In normal conditions –
– Trophoblast invades myometrium
– Spiral arteries converted to low pressure
system
• This process is inhibited in PE
• Immunological process also involved
• Thus HT & PE is caused by abnormal
placentation

16. Other factors
• Abn placentation → placental
insufficiency & IUGR
– Development of PE requires further changes
• ↑ Inflammatory activity
– Widespread vascular endothelial damage
– Capillary leak, vasoconstriction, intravascular
haemolysis, platelet activation
– ↑ Immune status - ↑ leucocytes

17. Pathology
• Primarily a disorder of placental dysfunction
– leading to a syndrome of endothelial dysfunction with
associated vasospasm
• Evidence of placental insufficiency with associated
abnormalities
– diffuse placental thrombosis, an inflammatory placental
decidual vasculopathy, and/or abnormal trophoblastic invasion
of the endometrium
• This supports abnormal placental development or
placental damage from diffuse microthrombosis as being
central to the development of this disorder

18. Pathopyhsiology
1. Placental factors
Immune complex deposition in kidney & placenta
Impair/ inadequate trophoblast invasion to the spiral arteries
Spiral arteries retain their charecteristic (narrow, tortuous, high
resistance)
Reduce blood supply to placenta
Result in placental hypoperfusion
As a compensation
High BP in maternal

19. 2. Altered vascular reactivity
PG12 angiotensin II
vasoconstrict
HPT and reduce placenta blood flow

20. 3. Coagulation disturbance
Activated endothelial cells promote coagulation and
increase vasopressor sensitivity
Widespread coagulation occur (DIC)
Fibrin deposition in kidney & placenta
HPT & placental insufficiency

21. Summary
The development of PE is
mediated through the degree of
placental pathology & the
maternal inflammatory response

22. PREECLAMPSIA & ECLAMPSIA

23. • Is the most common medical disorder
complicating pregnancy
• Is the most common hypertensive disorder
in pregnancy
• More common in primigravidas and elderly
multipara
Occurrence

24. • Chronic hypertension.
• Chronic nephritis.
• Past history .
• Family history.
• Obesity.
• Multiple pregnancy.
Epidemiology

25. Maternal personal risk factors for preeclampsia
First pregnancy
Multigravida pregnant by a different partner
Age younger than 18 years or older than 35 years
History of preeclampsia
Multiple pregnancy
Family history of preeclampsia in a first-degree relative
Obesity
Preexisting diabetes
Chronic hypertension
Renal disease
Smoking

26. Multisystem Features Of
Preeclampsia
Hypertension Proteinuria
Eclampsia HELLP syndrome
Intra-uterine growth restriction
Multi-organ disease
Cerebral vessels
Fetus
Liver
Systemic blood vessels Kidneys

27. Diagnosis Of PE
Hypertension + Proteinuria
=
Two facets of a complex pathophysiological
process

28. Peripheral oedema
• Not a useful diagnostic criterion
– Common in pregnancy
– PE can occur without oedema

29. • Headache.
• Blurring of vision.
• Nausea and vomiting.
• Epigastric pain (distension of the liver
capsule)
• Oliguria or anuria
Symptoms – non-specific

30. –The frequency and intensity of
the signs and symptoms.
–The more the severity of PE, the
more likely the need to terminate
pregnancy
Severity of PE

31. • Eclamptic fit stages ( 4 stages):
– Premonitory stage (1/2 minute):
●
Eye rolled up
●
Twitches of the face and hands.
– Tonic stage (1/2 minute):
●
Generalized tonic spasm with opisthotonus.
●
Cyanosis.
●
Tongue may be bitten between the clenched teeth.
Diagnosis of Eclampsia

32. EVALUATION

33. Evaluation of Hypertension in
Pregnancy
History
 ID and Complaint
 HPI (S/S of Preeclampsia)
 Past Medical Hx, Past
Family Hx
 Past Obstetrical Hx, Past
Gyne Hx
 Social Hx
 Medications, Allergies
 Prenatal serology, blood
work
 Assess for Hypertension in
Pregnancy risk factors
Physical
 BP (essential)
 Oedema
 Hyperreflexia
 Clonus
 Fondoscopy
 Urine dipstick test
 Cardiovascular
 Respiratory
 Abdominal = Epigastric
pain, RUQ pain

34. Cardiovascular
• Generalized vasospasm
• Increased peripheral resistance
• Reduced central venous/
pulmonary pressure
Hematological
• Platelet activation and depletion
• Coagulopathy
• Decreased plasma volume
• Increased blood viscosity
• Proteinuria
• Decreased glomerular filtration
rate
• Decreased urate excretion
Renal
Hepatic
• Periportal necrosis
• Subscapular
hematoma
• Cerebral oedema
• Cerebral haemorrhages
Central Nervous System
Organ Specific Changes associated with
Pre-eclampsia

35. Clinical presentation
Symptoms Signs
•Headache (frontal/ occipital)
• Visual disturbance
•Nausea & vomiting
• Epigastric and right upper
abdominal pain
•Oliguria / anuria
• Maybe asymptomatic
• Rapid rise in BP
• Papilloedema
•Fluid retention (non-
dependent edema)
• Hyperreflexia
•Clonus
• Uterus and fetus may feel
small for gestational age

36. Investigations
• Urine - 24 hour urine, Proteinuria.
• Kidney functions - serum creatinine, urea,
creatinine clearance and uric acid.
• Liver functions - bilirubin, Enzymes (SGPT
and SGOT).
• Blood - CBC, HCt , Hemolysis and Platelet
count (Thrombocytopenia).
• Coagulation Profile - Bleeding and clotting
time

37. Differential Diagnosis:
• A. Hypertension With Pregnancy.
• B. Proteinuria With Pregnancy.
• C. Edema With Pregnancy:

38. Differential Diagnosis Convulsions
Convulsions With Pregnancy:
• Eclampsia.
• Epilepsy.
• Hysteria.
• Meningitis and Encephalitis.
• Tetanus.
• Tetany.
• Brain tumors.
• Uremic convulsions

39. Differential Diagnosis
HELLP Syndrome:
• Acute fatty liver in pregnancy.
• Hepatitis.
• Thrombocytopenia purpura.
• Hemolytic Uremic syndrome.

40. Treatment
• PREVENTION.
• Antepartum
●
Proper antenatal care
●
Expectant treatment.
●
Control hypertension.
●
Treatment of eclampsia .
●
Prevention and control of convulsions.
●
Termination of pregnancy .
• Intrapartum care.
• Postpartum care.

41. Control of Convulsions:
• Magnesium Sulfate (MgSO4):
●
It is the drug of choice.
●
Mechanism:
– CNS depression.
– Mild VD.
– Mild diuresis.
– Inhibits platelet aggregation.
– Increase PGI2 synthesis.

42. Prognosis:
• BP usually normalize after placental delivery .
• Hypertension may persist.
• Postpartum eclampsia carries the worst prognosis.
• Maternal mortality is about 2% in severe preeclampsia and
10% in eclampsia.
• Perinatal mortality rate is about 5% in mild cases, 25% in
severe cases and 30% in eclampsia.

43. CONCLUSIONS

44. Summary
Hypertension diagnosed prior to 20 weeks' gestation, is
generally due to preexisting chronic hypertension rather
than pregnancy induce hypertension
Pre- eclampsia may be diagnose by a combination of fetal
and maternal features, including IUGR, hematological or
biochemical abnormalities as well as clinical symptom and
signs

45. Maternal deaths
• Confidential Enquiry into Maternal and
Child Health UK (2003-2005)
– 18 deaths from PE & eclampsia
– 10 deaths caused by IC haemorrhage
●
Due to uncontrolled BP

46. References
• Obstetrics by Ten Teachers 18th
Edition
• Obstetrics illustrated 6th
Edition
• Lecture Notes Obstetrics and
gynaecology 3rd
Edition
• http://emedicine.medscape.com/article/26
1435-overview