This document discusses hypertension in pregnancy. It defines gestational hypertension and preeclampsia and describes their characteristics and risk factors. The pathophysiology involves abnormal trophoblast invasion and endothelial cell dysfunction. Screening tests include mean arterial pressure and roll over testing. Management involves controlling blood pressure, preventing complications like eclampsia, and timely delivery. Maternal and fetal wellbeing must both be considered.

1. Hypertension
in
Pregnancy
Anady V. Eleccion
Clinical Clerk
WVSU-Medical Center

2. CHARACTERISTICS OF
WOMEN MOST LIKELY
TO DEVELOP
GESTATIONAL HPN

3. Hypertension
• Appropriately take blood pressure
• >140 mm Hg systolic or 90 mm Hg diastolic

4. Basic Classification of Hypertension
1. Gestational Hypertension
2. Preeclampsia/Eclampsia Syndrome
3. Chronic Hypertension (of any etiology)
4. Preeclampsia superimposed on chronic
hypertension

5. •New-onset of BP elevation after 20 weeks AOG
without proteinuria.
•BP returns to normal by 12 weeks postpartum
•May have other signs or symptoms of preeclampsia
Transient hypertension
Gestational Hypertension

6. •New onset hypertension + new onset Proteinuria
• 24-hour Urinary excretion >300mg
• Urine Protein:Creatinine Ratio ≥ 0.3
• Persistent 30mg/dL protein: dipstick 1+
•BP elevation occurs after 20 weeks AOG and most
often near term
PREECLAMPSIA

7. •In the absence of proteinuria, preeclampsia is diagnosed as
hypertension with the following:
PREECLAMPSIA
Thrombocytopenia Platelet count: <100,000/uL
Renal Insufficiency S. Creatinine >1.1 mg/dL, or doubling of baseline
Liver Involvement Serum Transaminase levels (AST/ALT) twice normal
Cerebral Symptoms Headache, Visual Disturbances, convulsions
Pulmonary Edema

8. !Proteinuria is no longer and important criterion or is
not absolutely required for diagnosis of preeclampsia
PREECLAMPSIA

9. –BP ≥160/110 mmHg on 2 occasions at least 4 hours apart
while the patient is on bedrest
–Thrombocytopenia- platelet count <100,000/uL
–Impaired liver function- abnormally elevated liver enzymes
to 2x normal), severe right upper quadrant pain
–Progressive renal insufficiency- s. crea>1.1mg/dl or doubling
–Pulmonary edema
–New onset of cerebral/visual disturbances
Severe Features of Preeclampsia

10. –Headaches or visual disturbances (such as scotomas)-
premonitory symptoms of preeclampsia
–Epigastric or right upper quadrant abdominal pain-
frequently accompanies hepatocellular necrosis, ischemia,
and edema that stretches the Glisson capsule
Symptoms of Preeclampsia with
Severe Features

11. Mild preeclampsia is no longer used.
Diagnosis is either preeclampsia with severe
features or preeclampsia without severe features
(usually the latter falls under Gestational HPN)

14. –Convulsive phase of the disorder
–New-onset grand mal seizures in a woman with preeclampsia
–It can occur before, during and after labor
–Often preceded by premonitory events, but it can occur in the
absence of warning S/Sx
–Ominous signs: severe headache, epigastric distress,
hyperreflexia
–If seen in a patient, give MgSO4
ECLAMPSIA

15. –High BP before pregnancy or detected before 20
weeks or both
–Failure of BP to normalize postpartum
–If patient has taken anti-hypertensives before pregnancy,
you can surmise that the patient has chronic HPN
–Usual causes: chronic kidney disease (most common),
primary aldosteronism or phaeochromocytoma
CHRONIC HYPERTENSION

16. Categories of Chronic Hypertension
Based on Blood Pressure Levels
Mild to
Moderate
Severe
Systolic 140-159 ≥160
Diastolic 90-109 ≥110

17. –Patients with chronic Hypertension who develop
preeclampsia
–Usually earlier and more severe than pure
preeclampsia
–Associated with fetal growth restriction
CHRONIC HPN WITH SUPERIMPOSED PRE

18. –Includes patents with Hypertension in early gestation
with the following findings:
–Proteinuria develops after 20 weeks
–Proteinuria present before 20 weeks with:
–Sudden exacerbation of Hypertension
–RUQ pain and severe headache, increase in
liver enzymes
–Pulmonary congestion/edema
–Renal insufficiency
–Sudden, substantial and sustained increase in protein excretion
CHRONIC HPN WITH SUPERIMPOSED PRE

19. ETIOLOGY OF
PREECLAMPSIA

20. ETIOLOGY OF PREECLAMPSIA
1. Abnormal trophoblastic invasion
–Placental implantation with abnormal trophoblastic invasion of uterine
vessels
2. Immunologic Factors
–Maladaptive tolerance between maternal, paternal (placental) and fetal
tissues
3. Endothelial Cell Activation
–Maternal maladaptation to cardiovascular or inflammatory changes of
normal pregnancy
4. Genetic Factors
–Inherited predisposing genes as well as epigenetic influences

21. ABNORMAL TROPHOBLASTIC INVASION
• Defective remodeling of spiral arteries
Normal Placental implantation In Preeclampsia
Proliferation of extravillous
trophoblasts from the anchoring
villous
Defective implantation
characterized by incomplete
invasion of spiral arteriolar wall by
extravillous trophoblasts
Trophoblasts invade the deciduas
and the walls of the spiral arteriole
to replace the endothelium and
muscular wall to create a dilated
low resistance vessel
This results in a small caliber
vessel with high resistance to flow

23. IMMUNOLOGICAL FACTORS
• Loss of tolerance or dysregulation of paternally derived placental and
fetal antigens
• Immune maladaptation – extravillous trophoblasts early in pregnancy
expressed reduced amounts of immunosuppressive nonclassic HLA G
→ defective placental vascularization
• Women with 1597ΔC allele are predisposed to develop preeclampsia
• Possibly shared susceptibility genes with diabetes and
chronic hypertension
histological changes at the maternal-placental interface are
suggestive of acute graft rejection

24. ENDOTHELIAL CELL ACTIVATION
• continuation of defective placentation that leads to inflammatory
and ischemic changes that provokes endothelial cell injury
• Results from extreme activated state of leukocytes in the
maternal circulation
• Oxidative stress generates toxic radicals that injure endothelial
cells
• The toxic radicals from oxidative stress can spread to the
maternal circulation

25. GENETIC FACTORS
• Multifactorial, polygenetic
• Predisposition is likely the result of interactions of
literally hundreds of inherited genes – both paternal
and maternal that controls metabolic and enzymatic
functions on every organ systems

26. PATHOGENESIS AND
PATHOPHYSIOLOGY

28. SCREENING TESTS

29. SCREENING TESTS

30. SCREENING TESTS
• Mean Arterial Pressure (MAP)
-defined as 1/3 systolic BP plus 2/3 the diastolic BP
-MAP value in the second trimester of >90mmHg and a MAP value in
the 3rd trimester of >105mmHg has resulted in an increase incidence
of preeclampsia
• Supine pressor test/ Roll over Test
-done between 28-32 weeks (increased plasma volume)
-an increase of at least 20mmHg in diastolic pressure constitutes a
Positive Roll over Test
-positive predictive value is only 33%

31. Combination of MAP and roll over test
-prediction rate increased to 78%

33. MANAGEMENT

34. Basic management objectives:
•Termination of pregnancy with the least trauma to
mother and fetus
• Consider the safety of the mother first then
delivery of the baby
•Birth of an infant who subsequently thrives
•Complete restoration of health to the mother

35. MATERNAL EVALUATION
A. Laboratory Exam
a. CBC with Platelet
b. S. Creatinine
c. Lactic dehydrogenase
d. Liver enzymes
e. 24-hour urine protein or protein/creatinine ratio
B. Assess for symptoms of severe preeclampsia

37. FETAL EVALUATION
•Sonographic Estimated Fetal Weight
•Non stress test
•Biophysical profile
•Doppler velocimetry
•Fetal weight – to check for presence of IUGR
•Amniotic Fluid – to check for oligohydramnios

38. MANAGEMENT OF SEVERE PREECLAMPSIA
•Aggressive
- High neonatal mortality
and morbidity due to
prematurity
- Prolonged NICU stay
- Long term disability
•Expectant
- Fetal death
- Asphyxial damage in
utero
- Increased maternal
morbidity

41. PHARMACOLOGY
The following drugs are given to immediately lower BP:
•Labetalol – first line because it has decreased S/E of
tachycardia; not available locally; Contraindicated in asthma,
heart disease
•Hydralazine – aka apresoline; available in the Philippines;
maximum dose: 20-25 mg
•Nifedipine – if both drugs are not available
Rule of thumb: There should only be GRADUAL reduction of BP, never
abrupt to preserve adequate fetal circulation.

42. PHARMACOLOGY
Antihypertensive medications for urgent BP control during
pregnancy
•Labetalol – 10-20mg IV then 20-80mg q20-30min to
a maximum dose of 300mg
•Hydralazine – 5mg IV or IM then 5-10mg IV q15-20
min or constant infusion of .5-10mg/h
•Nifedipine – 10-20mg orally, repeat in 30 mins if
needed then 10-20mg q 2-6H

43. PHARMACOLOGY
Maintenance Medications
Do NOT give methyldopa for the purpose of immediate
reduction of BP. It should only be for maintenance.

44. OBJECTIVES FOR TREATMENT
A. Prevent complications such as:
•Congestive heart failure
•Myocardial ischemia
•Renal injury or failure
•Ischemic or hemorrhagic stroke

45. OBJECTIVES FOR TREATMENT
B. Prevent and control Eclampsia
Premonitory S/Sx of eclampsia
•Presence of headache, visual disturbances and scotomata
•Epigastric or RUQ pain
•Hyperreflexia

46. Magnesium Sulfate (MgSO4) Prophylaxis
Can be given as an continuous IV infusion or intermittent IM
injections
•Should be given up to 24Hours after delivery
•Monitor urine output, reflexes and respiration
•Loading dose: 4g IV diluted in 100 ml IVF given for 15 min
•Continuous infusion: 2g/hr
•10g IM (5g per buttock)
•Maintenance: 5g every 4h or 1-2g IV
Do NOT stop MgSO4 after delivery because eclampsia may still occur!

47. DELIVERY
Termination of the pregnancy is the only cure for
preeclampsia
• AOG – preterm, term
• Presence or absence of severe features
• Presence of eclampsia, HELLP syndrome
• Presence of maternal or fetal compromise –
placental abruption, IUGR
If in the presence of eclampsia, you should DELIVER the baby
after the patient was stabilized.

48. Maternal Indications for Delivery in
Women With Severe Preeclampsia
• Oliguria (<500ml/24hr)
• HELLP syndrome
• Platelet counts <100,000/mm3
• Deterioration of renal function
(serum creatinine >/=1.5 mg/dl)
• Suspected abruptio placenta, progressive labor,
and/or rupture of membranes
Sibai et al AmJOG 2007

49. Fetal Indications For Delivery In Women
With Severe Preeclampsia
• Repetitive late or severe variable deceleration
• Biophysical profile </=4 on 2 occasions at 6 hours
apart
• IUGR (Estimated fetal weight <5th percentile)
• Umbilical artery Doppler with reverse end
diastolic flow
• Severe oligohydramnios
Sibai et al AmJOG 2007

50. Mode of Delivery
• Vaginal delivery
- Inducible cervix
- No fetal distress
• Cesarean section

51. GLUCOCORTICOIDS FOR LUNG
MATURATION
•Steroids to improve fetal lung maturity in preterm infants
•Decrease incidents of respiratory distress
•Improve fetal survival

52. HOSPITALIZATION
Recommendation for immediate hospitalization
(gestational hypertension and preeclampsia without
severe features)
•New S/Sx of severe preeclampsia
• Evidence of fetal growth restriction
• Elevation of liver enzymes
• Thrombocytopenia

53. COMPLICATIONS

54. Maternal complications
- Cerebrovascular accident – hemorrhage/infarction
- Abruption placenta and DIC
- Aspiration pneumonia
- Pulmonary edema
- Renal failure
- C-P arrest
ECLAMPSIA

55. Fetal Complications
- Fetal death
- Prematurity- in cases of preterm pregnancies
- Fetal complications may be due to placental
insufficiency or abruption placenta
ECLAMPSIA

57. PREVENTION OF
HYPERTENSION IN
PREGNANCY

58. PREVENTION OF HPN IN PREGNANCY
•Low dose aspirin – recommended in reducing the risk
of preeclampsia in patients who are moderate to high
risk
• Dose – 60-80mg/day
•Calcium supplementation – may prevent preeclampsia
in patients with low dietary intake of calcium
•Dose – 1.5-2g elemental calcium/day
•Vit C, Vit E, selenium, Vit A, Fish oil – not effective

59. PREVENTION OF HPN IN PREGNANCY
•Early and frequent prenatal check-ups and
good nutrition is still the most effective
means of decreasing the incidence and
severity of HPN in pregnancy