High blood pressure during pregnancy poses various risks, including: Decreased blood flow to the placenta. If the placenta doesn't get enough blood, your baby might receive less oxygen and fewer nutrients. This can lead to slow growth (intrauterine growth restriction), low birth weight or premature birth.

1. HYPERTENSION
in
PREGNANCY
By: MUKESH SAH
PGI

2.  Diagnosis
 Epidemiology
 Etiopathogenesis
 Pathophysiology
 Prediction and prevention
 Management

3. Epidemiology of Hypertension in Pregnancy
 Maternal Personal Risk Factors
1. Primiparity
2. Primipaternity
3. History of PreEclampsia
4. Obesity
5. Family History of PreEclampsia
6. Ethinicity
7. Maternal Age
8. Smoking

4. Epidemiology of Hypertension in Pregnancy
 Maternal Medical Risk Factors
1.Underlying Medical Conditions
a) Diabetes Mellitus
b) Antiphospholipid Antibody Syndrome
c) Systemic Lupus Erythematosus (SLE)
d) Renal disease
2.Maternal Infection
 Placental/Fetal Risk Factors
1. Multiple Pregnancies
2. Molar Pregnancy

5. Diagnosis of Hypertensive Disorder
 BP > 140 mm Hg systolic or 90 mm Hg diastolic
 Korotkoff phase V is used to define diastolic pressure
 Incremental increases of 30 mm Hg systolic or 15mm Hg diastolic from
midpregnancy blood pressure values
 A sudden rise in mean arterial pressure later in pregnancy—also known
as “delta hypertension”—may also signify preeclampsia even if blood
pressure is < 140/90 mmHg

6. Diagnosis of Hypertensive Disorder
Condition Criteria Required
Gestational hypertension BP > 140/90 mmHg after 20 weeks
in previously normotensive women
Preeclampsia—Hypertension
Proteinuria • ≥ 300 mg/24h, or
• Protein: creatinine ratio ≥
0.3 or
• Dipstick 1+ persistent
or
Thrombocytopenia • Platelets < 100,000/μL
Renal insufficiency • Creatinine > 1.1 mg/dL or doubling
Liver involvement • Serum transaminase levelsc twice
normal
Cerebral symptoms • Headache, visual disturbances,
convulsions
Pulmonary edema

7. Etiopathogenesis
 Are exposed to chorionic villi for the first time
 Are exposed to a superabundance of chorionic villi,
 Have preexisting conditions of endothelial cell activation or
inflammation such as diabetes or renal or cardiovascular disease
 Are genetically predisposed to hypertension developing during pregnancy

8. Etiology
1. Placental implantation with abnormal trophoblastic invasion of uterine
vessels
2. Immunological maladaptive tolerance between maternal,
paternal (placental), and fetal tissues
3. Maternal maladaptation to cardiovascular or inflammatory
changes of normal pregnancy
4. Genetic factors including inherited predisposing genes and
epigenetic influences.

9. Extravillous
trophoblast
InsterstitialET
EndovascularET
Anchoring villi
Syncytiotrophoblast
Cytotrophoblast
Spiral arteries
NORMAL PREECLAMPSIA

10. Pre-eclampsia &
Placental Oxidative Stress
 Placental oxidative stress
plays a pivotal role in
pathogenesis
 Previous assumption:
Deficient trophoblastic
invasion of spiral arteries
→ failure to convert to
large vessels
→ placental hypoxia

11. Pre-eclampsia: Placental Generation
of Free Radicals
Exacerbation of intermittent perfusion-
→ more hypoxia-reoxygenation type placental
injury
→ activation of xanthine oxidase & cleaving of
NAD(P)H
→ free radical-induced placental tissue damage
→ deportation of syncytioblast microvesicles into
maternal circulation

12. Pre-eclampsia: Generation of Free Radicals

13. Cardiovascular system
a. Cardiac output remains normal, and increased total peripheral vascular
resistance
b. Preeclamptic endothelial cells generate less prostacyclin, a vasodilator,
than normal endothelial
cells. Less prostacyclin allows greater vascular sensitivity to angiotensin II,
thus promoting vasospasm and increasing peripheral vascular resistance.

14. Coagulation system
a. Disseminated intravascular coagulation occurs in 10% of patients with
preeclampsia.
b. Because of endothelial damage, most of these patients have mild
procoagulant consumption
and elevated fibrin degradation products.
c. Diffuse intravascular coagulation may arise from vascular damage
sustained during vasospasm.

15. Renal function
a. Glomerularchanges
(1) Glomerular filtration rate (GFR) is usually decreased in preeclampsia.
Deceased renal plasma flow and glomeruloendotheliosis, which
occludes the capillary lumen, account for the lower GFR.
(2) Protein leaks into urine.

16. Renal function
 Renin–angiotensin–aldosterone system
(a) Potent vasoconstrictor effect of angiotensin II
(b) Stimulation of aldosterone by angiotensin II and consequent sodium
retention
(c) The finding that large doses of angiotensin II can cause proteinuria

17. Other signs of end-organ disease
a. Visual disturbances result
from papilledema and suggest
cerebral involvement.
b. Epigastric pain suggests
hepatocellular dysfunction
and edema and liver capsule
distention.
c. IUGR and
oligohydramnios suggest
placental vasculopathy and
uteroplacental insuffi ciency.

18. Overlapping Roles of Pathology in the Spectrum of Preeclampsia
Blood
Pressure Capillary
Leak
Fibrinolysis
Hemolysis
Symptoms
Normal
Mild
Severe
Epigastric pain
CNS
Bleeding
Nausea/vomiting
Proteinuria
Facial edema
Pulmonary edema
Ascites
Pleural effusions
HELLP
Renal failure
DIC
Low platelets
↑ Liver enzymes

19. Prediction and Prevention
Placental perfusion/vascular resistance
Examples
 Roll-over test
 Isometric handgrip or cold pressor test
 Pressor response to aerobic exercise,
 Angiotensin-II infusion,
 Midtrimester mean arterial pressure,
 Platelet angiotensin-II binding,
 Renin, 24-hour ambulatory blood pressure monitoring, uterine artery or
fetal transcranial
 Doppler velocimetry

20. Prediction
Fetal-placental unit and endocrine dysfunction
Examples
 Human chorionic gonadotropin (hCG), alpha-fetoprotein (AFP), estriol,
pregnancy-associated
 protein A (PAPP A), inhibin A, activin A, placental protein 13,
corticotropin-releasing
 hormone, A disintegrin, ADAM-12, kisspeptin

21. Prediction
Renal dysfunction
Examples
 Serum uric acid, microalbuminuria, urinary calcium or kallikrein,
microtransferrinuria,
 N-acetyl-β-glucosaminidase, cystatin C, podocyturia

22. Prediction
Endothelial dysfunction/oxidant stress
Examples
 Platelet count and activation, fibronectin, endothelial adhesion
molecules, prostaglandins,
 prostacyclin, MMP-9, thromboxane, C-reactive protein, cytokines,
endothelin, neurokinin B,
 homocysteine, lipids, insulin resistance, antiphospholipid antibodies,
plasminogen activator inhibitor
 (PAI), leptin, p-selectin, angiogenic factors such as placental growth
factor (PlGF),
 vascular endothelial growth factor (VEGF), fms-like tyrosine kinase
receptor-1 (sFlt-1), endoglin

23. Prevention
Dietary and Lifestyle modifications
Low Salt diet
Calcium supplementation- 1500-2000mg/day]
Fish oil supplementation
Cardiovascular drugs—diuretics, antihypertensive drugs
Antioxidants—ascorbic acid (vitamin C), α-tocopherol
(vitamin E), vitamin D
Antithrombotic drugs—low-dose aspirin, aspirin/
dipyridamole, aspirin + heparin, aspirin + ketanserin

24. Categories
A. Preeclampsia- Eclampsia
B. Chronic Hypertension
C. Chronic Hypertension with SuperImposed PreEclampsia
D. Gestational Hypertension

25. Preeclampsia
Minimum criteria:
 BP>140/90 mmHg after 20 weeks’ gestation
 Proteinuria > 300mg/24 hours or > 1+ dipstick
Increased certainty:
 BP > 160/110
 Proteinuria
 Increased Serum creatinine
 Thrombocytopeia
 Microangiopathic hemolysis- increased LDH
 Elevated transaminase level-AST/ALT
 Persistent headache, visual disturbance, epigastric pain

26. Hypertension
Edema
Proteinuria
Classic Triad of Preeclampsia

27. Severe PreEclampsia
 Must have one of the following:
 Symptoms of central nervous system dysfunction = Blurred vision,
scotomata, altered mental status, severe headache
 Symptoms of liver capsule distention = Right upper quadrant or
epigastric pain
 Nausea, vomiting
 Hepatocellular injury = Serum transaminase concentration at least
twice normal
 Systolic blood pressure ≥160 mm Hg or diastolic ≥110 mm Hg on
two occasions at least six hours apart
 Thrombocytopenia = <100,000 platelets per cubic milimeter
 Proteinuria = 5 or more grams in 24 hours
 Oliguria = <500 mL in 24 hours
 Severe fetal growth restriction
 Pulmonary edema or cyanosis
 Cerebrovascular accident

28. Management of Severe PreEclampsia <34wks
Observe in the LR/DR for 24/48hrs
MgSo4 for 24hrs
Antihypertensives
Utrasonography, monitoring of FHT
and symptoms, labs
Any of the FF present?
Eclampsia
Pulmonary edema
DIC
Suspected abruptio
NRFS
PROM
Magnesium sulfate
Delivery

29. Management of Severe PreEclampsia <34wks
Any of the FF present?
Eclampsia
Pulmonary edema
DIC
Suspected abruptio
NRFS
PROM
Steroids
• MgSO4 for 24hrs
• Antihypertensives
• Steroids
• Daily eval of
Maternal-Fetal
condition
• Delivery if with
Indications
• Deliveryat 34wks
<24wks 24- 33 6/7wks
Terminate
Pregnancy

30. Maternal and Fetal Monitoring
 Maternal Assessment
-VS, Fluid intake and UO should be monitored every
hour
-Symptoms of severe preEclampsia, uterine contractions,
rupture of membranes and bleeding should be monitored
atleast every 8hours
-Laboratory Testing daily

31. Maternal and Fetal Monitoring
 Fetal Assessment
-Kick count and NST daily
-BPS twice weekly
-Serial Fetal growth, Umbilical artery doppler studies
should be performed every 2weeks

32. B. Chronic Hypertension “Preexisting Hypertension”
 Definition
 Systolic pressure ≥ 140 mmHg, diastolic pressure ≥90 mmHg, or both.
 Presents before 20th week of pregnancy or persists longer than 12 weeks
postpartum.
 Causes
 Primary = “Essential Hypertension”
 Secondary = Result of other medical condition (ie: renal disease)

33. Management
1) Referral to an internist
2) Anti-hypertensive therapy in severe chronic hypertension
3) Antihypertensive therapy for mild to moderate chronic hypertension
4) Antihypertensive for continuous therapy in chronic hypertension in
pregnancy
5) Second line antihypertensives for continuous therapy in chronic
hypertension in pregnancy

34. 6) Antihypertensive drugs that should not be used
during pregnancy
7) Antihypertensive drugs for use in urgent control of
severe chronic hypertension in pregnancy
8) Fetal surveillance for IUGR in chronic hypertension
9)Surveillance for fetal well-being in chronic
hypertension in pregnancy with IUGR
10) Timing of delivery complicated by mild to moderate
chronic hypertension in pregnancy

35. C. Chronic hypertension with Superimposed
preeclampsia New-onset proteinuria >300mg/24 hors in hypertensive women but no
proteinuria before 20 weeks’ gestation.
 A sudden increase in proteinuria or blood pressure or platelet count
<100,000u/L in women with hypertension and proteinuria before 20
weeks’ gestation.

36. C. Chronic Hypertension with Superimposed
Preeclampsia
 Severe hypertension i.e. systolic BP≥160 mmHg or
diastolic BP ≥110mmHg or both
 Thrombocytopenia (platelets<100,000/uL
 Elevated liver transaminases (2x upper limit of
normal)
 New onset renal insufficiency (sudden increase in
serum creatinine)
 Pulmonary edema
 Cerebral or visual disturbances

37. Gestational Hypertension
 It is new onset of threshold BP elevations after 20
weeks gestation in the absence of proteinuria
 SBP > 140 or DBP > 90 mmHg for first time during
pregnancy
 BP returns to normal before 12 weeks postpartum
 Final diagnosis made only postpartum.
 May have other signs or symptoms of preeclampsia,
for example, epigastric discomfort or
thrombocytopenia.
 Reclassified by some as transient hypertension.

38. Eclampsia:
Diagnosis, Prevention &
Management

39. Eclampsia
 Diagnosis secure – if
with classic triad &
convulsion
 Symptoms: Persistent
headache, photophobia,
blurred vision, epigastric
&/or RUQ pain, altered
mental status

40. Is eclampsia preventable ?
Pathogenesis unknown → limited strategies
 Primary – prevention of preeclampsia
 Secondary – pharmacologic agents to prevent convulsion in
diagnosed preeclampsia
 Tertiary – prevention of subsequent convulsion in diagnosed
eclampsia
Currently - no preventive therapy for preeclampsia

41. Is eclampsia preventable ?
 Onset of convulsions may be abrupt –
not gradual progress
 20% do not have premonitory signs
& symptoms prior
 50% of eclamptics develop 1st
convulsion in hospital
 Percentage of eclampsia
considered unpreventable –
ranged from 31% - 87%

42. Management of Eclampsia
Management Plan
1. Prevent maternal injury & support
respiratory & cardiovascular function
2. Prevent recurrent convulsions
3. Control blood pressure
4. Assess fetal well being
5. Delivery
6. Postpartum care

43. Prevent Maternal Injury &
Supportive Respiratory & CV Care
 During/immediately after
acute convulsion – prevent
serious maternal injury
 Prevent aspiration
 Maintain oxygenation

44. Prevent Recurrent Convulsions
 Magnesium Sulfate – drug of choice
Loading: 6 g IV over 15-20 min.
Maintenance: 2 g/h cont.IVdrip
LD: 4g IV, given slowly over 5-10 minutes and
10g deep intramuscular (IM) (5g to each buttock), then
5g IM every 4 hours until 24 hours after delivery
OR
LD: 4g IV followed immediately by IV infusion of 2g/
hour. (4-10mL ampules of 50% MgSO4) to 1000mL
D5W or D5NM and infuse IV at a rate of 100mL/hour.
The rate of the drip may be reduced to 1g/hr after 24
hours.

45. Effects of Magnesium at
Different Serum Levels
Effect Level (mEq/L)
 Seizure prophylaxis 4–6
 Loss of deep tendon refl exes 10
 Respiratory depression 15
 General anesthesia 15
 Cardiac arrest 25

46. Eclampsia: Blood Pressure Control
 Reduce BP but avoid significant hypotension
 Objective: avoid loss of cerebral autoregulation & prevent CHF
without compromising cerebral perfusion or jeopardizing
uteroplacental blood flow
 Maintain BP at 140-160/90-110
 Hydralazine (5-10 mg every 15 min.) or Nifedipine (10-20 mg oral
over 30 min.)
(Maximum dose- 50 mg in a hour)

47. Assess Fetal Well-being
 Maternal hypoxemia & hypercarbia →
FHR & uterine activity changes
(Bradycardia, transient late decelerations, ↓beat-to-
beat variability, compensatory tachycardia, ↑
frequency & tone)
 Spontaneously resolve within 3-10 minutes
after convulsion & hypoxemia correction
 Emergency CS only if bradycardia &/or
recurrent late decelerations persist
beyond 10-15 minutes

48. Eclampsia: Proper Mode of Delivery
 Not an indication to do CS especially with mother
stable
 Factors considered in choosing method:
 Fetal gestational age & condition
 Presence of labor & Bishop score
 In labor – allow vaginal delivery in absence of
obstetric complications
 Not in labor:
a. initiate with oxytocin/prostaglandin if >30 wks;
if < 30 wks with ripe cervix
b. CS if< 30 wks, not in labor & unripe cervix

49. Eclampsia: Labor & Delivery Pain Relief
 Systemic opioids or epidural anesthesia
 For CS – either epidural, spinal or combined
techniques of regional anesthesia
 Coagulopathy or severe thrombocytopenia –
regional anesthesia contraindicated
 General anesthesia - ↑ risk of aspiration, Failed
induction due airway edema, Marked ↑ systemic
& cerebral pressure during intubation &
extubation

50. Eclampsia: Postpartum Management
 Close monitoring of vital signs, symptoms &
input & output
 Magnesium sulfate continued for at least 24
hrs after delivery &/or after last convulsion
 Shift to oral antihypertensive medications

51. HELLP Syndrome
Triad:
(1) Microngiopathic hemolysis
(2) Liver dysfunction
(3) Thrombocytopenia

52. Laboratory Criteria for the Diagnosis of
HELLP Syndrome
I. Hemolysis
1. Abnormal peripheral blood smear (Burr cells, Schistocytes)
2. Elevated bilirubin > 1.2 mg/dl
3. Low serum haptoglobulin
4. Significant drop in hemoglobin level unrelated to blood loss
II. Elevated liver enzymes
1. Elevated AST or ALT > 2x the upper limit of normal for the laboratory
2. Increased LDH > 2x the upper limit of normal f normal for the
laboratory
III. Low platelet count (<100,000/mm3)

53. Classifications for Laboratory Diagnosis
of HELLP Syndrome
Mississippi Classification Tennessee Classification
Class I
Platelets < 50,000
AST or ALT > 70 IU/L
LDH > 600 IU/L
Complete or True
Platelets < 100,000
AST > 70 IU/L
LDH > 600 IU/L
Class II
Platelets =50,000-100,000
AST or ALT > 70 IU/L
LDH > 600 IU/L
Partial or Incomplete
Severe preeclampsia with any one
of the following:
ELLP, HEL, EL, LP
Class III
Platelets =100,000-150,000
AST or ALT > 40 IU/L
LDH > 600 IU/L

54. Management
 Stabilize the mother, Assess fetal condition and decide whether prompt
delivery is indicated.

55. THE END
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