Presented at the 24th annual HELA Conference

1. Management in
Hypertension in
Pregnancy
CHUKWUMA I. ONYEIJE, MD, FACOG
ATLANTA PERINATAL ASSOCIATES

2. Take Home Point:
Hypertension is a common complication of
pregnancy.
When severe, it can lead to stroke and death.
However, prompt recognition and treatment
can reduce the risk of these complications

3. Understand why
some
antihypertensive
protocols used for
non-pregnant
individuals must be
modified for the
pregnant woman.

4. Pathologic
and pharmacologic
considerations of
hypertension during
pregnancy.

5. OBJECTIVES
Provide an
evidence based
approach to
acute severe
hypertension in
pregnancy

6. Hypertensive disorders of pregnancy
constitute one of the leading causes
of maternal and perinatal mortality
worldwide.

7. MORTALITY RATE FOR HYPERTENSIVE
DISORDERS.
9
1…
26
0
5
10
15
20
25
30
Africa & Asia United States Latin America & the
Caribbean,

8.  In the United States, the rate of
preeclampsia increased by 25% between
1987 and 2004 (Wallis AB, et al 2008)
 Women giving birth in 1980, those giving
birth in 2003 were at 6.7-fold increased
risk of severe preeclampsia (4).

11. A single death is a tragedy;
a million deaths is a statistic.

12. CLASSIFICATION
OF
HYPERTENSION
IN PREGNANCY
Preeclampsia-
eclampsia
Chronic
(preexisting)
hypertension
Preeclampsia-
eclampsia
superimposed
upon chronic
hypertension –
Gestational
hypertension

13. Preeclampsia-
eclampsia
Preeclampsia-eclampsia
 NEW onset of hypertension and proteinuria
or
 NEW onset of hypertension and end-organ
dysfunction with or without proteinuria
…. most often after 20 weeks of gestation in a
previously normotensive woman
 Eclampsia is diagnosed when seizures have occurred.

14. Preeclampsia
Hypertension after 20 weeks
Proteinuria > 300 mg
Edema
• Systolic > 160
• Diastolic >110 diastolic
• 5 gm protein in 24 hours
• Oliguria
• Cerebral of visual
distrubances
• Pulmonary edema or
cyanosis
• Epigastric or RUQ pain
• Impaired liver function
• Thrombocytopenia
• IUGR
Preeclampsia-
eclampsia
Preeclampsia-
eclampsia

15. Chronic Hypertension
• Present BEFORE pregnancy
• Present BEFORE 20 weeks
• Present AFTER 6 weeks postpartum
Chronic
(preexisting)
hypertension

16. Gestational Hypertension
 Blood Pressure≥140/90
 No proteinuria
 NL BP Postpartum
 May have other signs or symptoms (epigastric pain, low platelets)
 Diagnosis is made in Retrospect
 Associated with some adverse outcomes
 NOTE:
 10% of eclamptics seize without proteinuria
Gestational
hypertension

17. Preeclampsia-eclampsia superimposed
upon chronic hypertension –
 A woman with chronic hypertension develops
Worsening hypertension with
New onset proteinuria or
Other features of preeclampsia
(eg, elevated liver chemistries, low
platelet count).
Preeclampsia-
eclampsia
superimposed
upon chronic
hypertension –

19. What is Hypertension?
CHRONIC HYPERTENSION:
before 20 wks
 Systolic > 140 mm Hg
 Diastolic >90 mm Hg
90% of cases are essential

20. When to Treat Hypertension?
SEVERE HYPERTENSION
(Systolic BP ≥160 mmHg and/or Diastolic BP ≥110 mmHg)
persisting for ≥15 minutes
ALWAYS recommended because
reduces the risk of maternal stroke and other serious
maternal complications.

21. When to Treat Hypertension?
MILD HYPERTENSION
(Systolic BP <150 mmHg and/or Diastolic BP <100 mmHg)
NOT SO CLEAR.
 The benefit treatment for mild hypertension is a reduction in risk of developing
severe hypertension (Ref: AU Abalos, et al.)
 However, this may not be sufficient to warrant exposing the fetus to the
potential adverse effects from these drugs (Ref: von Dadelszen P et al)
 Lowering blood pressure does not affect the course of preeclampsia

22. Why doesn’t
controlling mild
hypertension
NOT eliminate
adverse effects?
The primary pathogenetic process is an abnormality
of the placental vasculature that results in 
placental under perfusion, which leads to 
release of factors that cause widespread maternal
endothelial dysfunction with multiorgan
dysfunction.

24. Things to consider
 Treating the mother
… NOT the fetus
 Intravenous access
 Intravenous hydration
 Intensive care
 Fetal monitoring

25. Is it possible to
predict who will get
preeclampsia?
NICE VS SPREE…

26. PREDICTION
OF
PREECLAMPSIA
ASPRE
NICE
SPREE

27.  Preterm preeclampsia can be substantially decreased by prophylactic use
of aspirn.
 ASPRE - A Multicenter trial of ASpirn vs. Placebo in pregnancy at high risk
for preterm PREeclampsia
 Singleton pregnancies at high risk for preeclampsia at 11-14 weeks until 36
weeks were given 150 mg per day of aspirin VS placebo.
ASPRE
Aspirin versus placebo in pregnancies at high risk for preterm
preeclampsia. NEnglJMed 2017; 377: 613–622.

28.  RESULTS OF ASPRE
 62% Reduction in incidence of PRETERM PREECLAMPSIA.
(95% CI, 26-80)
 No change in risk for TERM PREECLAMPSIA
PROVIDED THAT:
DOSE WAS > 100 mg AND
STARTED BEFORE 16 weeks.
ASPRE
Aspirin versus placebo in pregnancies at high risk for preterm
preeclampsia. NEnglJMed 2017; 377: 613–622.

29. PERINATAL RESPONSE TO THE ASPRE TRIAL
YOU GET BABY ASPIRIN; YOU GET BABY ASPIRIN…

30. But who is
at risk?
 NICE - National Institute for Health and Care Excellence (NICE) guideline.
 High risk = ONE major factor or 2 minor factors:
 MAJOR FACTOR:
 history of hypertensive disease in previous pregnancy,
 chronic kidney disease,
 autoimmune disease,
 diabetes mellitus
 chronic hypertension)
 MINOR FACTOR:
 First pregnancy at age ≥ 40 years,
 interpregnancy interval > 10 years,
 body mass index at first visit ≥ 35 kg/m2
 family history of PE
NICE

31. Is there a
better way?
 FOUR POTENTIALLY USEFUL BIOMARKERS AT 11-13 WEEKS
 Mean arterial pressure (MAP),
 Uterine artery pulsatility index (UtA-PI),
 Serum pregnancy-associated plasma protein-A (PAPP-A)
 Serum placental growth factor (PlGF)9–14.
 BASED ON PREVIOUS STUDIES:
 Wright D, Fetal Diagn Ther 2012; 32: 171–178.
 Akolekar R, Fetal Diagn Ther 2013; 33: 8–15.
 Wright D, Am J Obstet Gynecol 2015; 213: 62.e1–10.
 O’Gorman N, Am J Obstet Gynecol 2016; 214: 103. e1–12.
 Conde-Agudelo A, Obstet Gynecol 2004; 104: 1367–1391.
 Akolekar R, Prenat Diagn 2011; 31: 66–74.
SPREE

32. NICE SPREE
PAST HISTORY
(RETROSPECTIVE)
BIOMARKERS
(A PRIORI)

33. Nonpregnant

36. SPREE

37. THE WINNER
(?)
 Conclusions:
 The performance of screening for preeclampsia as currently recommended by
NICE guidelines is poor and compliance with these guidelines is low.
 The performance of screening is substantially improved by a method
combining maternal factors with biomarkers.
SPREE

38. WHEN & HOW TO TREAT…
 Diastolic BP > 105-110
 Systolic BP > 170
 Avoid rapid BP reduction
 Do NOT normalize BP
 Therapeutic Goal:
 DIASTOLIC BP BETWEEN 90 and 105
 Low BP may precipitate fetal distress

39. Characteristics of Severe Hypertension
Hypovolemia
Clinical assessment of hydration is inaccurate
Unprotected vascular beds are at risk

40. Safe
Antihypertensive
Medications
Methyldopa
Beta blockers
Calcium channel blockers
Hydralazine
Thiazide diuretics / Clonidine

41.  Has been widely used in pregnant women
 Long-term safety for the fetus has been demonstrated
 BUT
 It is a but mild antihypertensive agent
 Slow onset of action (three to six hours).
 Many women will not achieve blood pressure goals on this oral agent or are
bothered by its sedative effect at high doses.
 Some studies (eg, CHIP) utilized this agent and demonstrated that women
treated with methyldopa may have had better outcomes compared with
those treated with labetalol, although these data may be biased by
residual confounding (Ref: Magee LA et al).
Methyldopa

42.  Do Beta blockers increase congenital malformations?
 Not likely.
 InPreSS consortium pooled data from large cohorts drawn from six countries
and reported that beta-blocker use was not associated with large increases in
the relative and absolute risks for major malformations overall
 Labetalol has both alpha- and beta-adrenergic blocking activity,
 Early studies in experimental models suggested that it may preserve
uteroplacental blood flow to a greater extent than traditional beta blockers.
 It has a more rapid onset of action than methyldopa (within two hours versus
three to six hours).
Beta blockers

43.  Beta blockers are generally avoided in patients with asthma as they may
precipitate bronchospasm.
 In a study of a large study, status asthmaticus occurred more often in women
with asthma treated with labetalol than those treated with other
antihypertensive drugs
 (6.5 versus 1.7/1000 delivery hospitalizations of women with asthma).
 Ref: Booker WA et al, Obstet Gynecol. 2018
Beta blockers

44.  Data on the safety of calcium channel blockers during pregnancy are
mixed.
 A 2017 systematic review found evidence of increased risks of
 stillbirth (OR 3.0, 95% CI 1.0-8.7),
 preterm birth (OR 4.6, 95% CI 2.9-7.3),
 congenital cardiovascular malformations (OR 1.4, 95% CI 1.2-1.7)
 HOWEVER:
 the odds ratios were based on single studies, and
 studies did not evaluate the effect of treated versus untreated hypertension and did
not specify the type of hypertensive disorder being treated (Ref Fitton CA et al.
Calcium channel blockers

45.  Intravenous Hydralazine has been widely used for many years in the
setting of acute hypertension in pregnancy and is an acceptable
antihypertensive drug in this setting
 However, the hypotensive response to hydralazine is less predictable than
that seen with other parenteral agents.
 Hydralazine can also be taken orally; however,
 it causes reflex tachycardia &
 fluid retention,
 which limits its usefulness in pregnancy.
Hydralazine

46.  Controversial.
 Some guidelines suggest that these agents can be continued in women
with chronic hypertension who were taking them prior to pregnancy (Ref:
Collins et al)
 Significant volume depletion is not likely in this setting since most of the
fluid loss occurs within the first two weeks of us
 Assuming that drug dose and dietary sodium intake are relatively constant.
 Diuretics are not generally used in women with
preeclampsia unless pulmonary edema has developed.
Thiazide diuretics

47.  Clonidine has a similar mechanism of action as methyldopa
 Can be an effective drug for treatment of mild hypertension in pregnancy
 Bothersome side effects and the possibility of rebound hypertension if it is
stopped suddenly,
 Use for patients who cannot tolerate
 methyldopa, nifedipine, or labetalol
 Clonidine is available as a transdermal patch,
 Useful for patients who cannot take an oral antihypertensive drug.
Clonidine

48. Acute Medical
Therapy
Labetalol
Hydralazine
Nifedipine
Nitroprusside
Diazoxide
Clonidine

49. LABETALOL – FIRST-LINE THERAPY
 Mechanism: Alpha and Beta block
 Dose: Every 10 minutes, 20mg,
then 40, then 80 for a total of 300
mg
 ALTERNATIVELY: A constant
infusion of 1 to 2 mg/min can be
used instead of intermittent
therapy.
 Onset: 1-2 minutes
 Duration: 3 - 6 hours
 Side effects: hypotension

50. HYDRALAZINE
 Mechanism: Peripheral vasodilation
 Dose: 5-10 mg every 20 minutes
 Onset: 10-20 minutes
 Duration: 2-4 hours
 Side effects: headache, flushing,
tachycardia, lupus like symptoms
 If a total cumulative dose of 20 to 30 mg in 24
hours does not achieve optimal blood pressure
control, another agent should be used.

51. Vasodilator Precautions
GIVE 250-500 CC OF
FLUID IV
AVOID MULTIPLE DOSES
IN RAPID SUCCESSION
ALLOW TIME FOR DRUG
TO WORK
MAINTAIN LEFT LATERAL
POSITION
AVOID OVER TREATMENT

52. NIFEDIPINE
 Mechanism: Calcium
channel block
 Dose: 10 mg po
 Not sublingual
 Onset: 5-10 minutes
 Duration: 4-8 hours
 Side effects: chest pain,
headache, tachycardia

53. CLONIDINE
 Mechanism: Alpha agonist, works centrally
 Dose: 1 mg po
 Onset: 10-20 minutes
 Duration: 4-6 hours
 Side effects: unpredictable, avoid rapid
withdrawal

54. NITROPRUSSIDE
 Mechanism: direct vasodilator
 Dose: 0.2 – 0.8 mg/min IV
 Onset: 1-2 minutes
 Duration: 3-5 minutes
 Side effects:
 cyanide accumulation
 hypotension

55. Seizure Prophylaxis
Magnesium sulfate 4-6 g bolus 1-2 g/hour Monitor urine
output and DTR’s
Lower dose with
renal dysfunction,

56. Magnesium
Sulfate
Is not an antihypertensive agent
Centrally acting anticonvulsant
Blocks neuromuscular conduction
Serum levels: 6-8 mg/dL

57. Magnesium Toxicity
RESPIRATORY RATE
< 12
DTR’S NOT
DETECTABLE
ALTERED
SENSORIUM
URINE OUTPUT
< 25-30
CC/HOUR
ANTIDOTE: 10 ML OF
10% SOLUTION OF
CALCIUM GLUCONATE
1 V OVER 3 MINUTES

58. Treatment of Eclampsia
FEW PEOPLE DIE OF
SEIZURES
PROTECT PATIENT AVOID INSERTION OF
AIRWAYS AND PADDED
TONGUE BLADES
IV ACCESS BOLUS MGSO4 AT 4-6
BOLUS, IF NOT EFFECTIVE,
GIVE ANOTHER 2 G

59. Alternate Anticonvulsants
Diazepam 5-10 mg IV
Sodium Amytal 100 mg IV
Pentobarbital 125 mg IV
Dilantin 500-1000 mg IV infusion

60. After the Seizure
ASSESS MATERNAL LABS FETAL WELL-BEING EFFECT DELIVERY TRANSPORT WHEN
INDICATED
NO NEED FOR IMMEDIATE
CESAREAN DELIVERY

61. Other Complications
PULMONARY EDEMA OLIGURIA PERSISTENT
HYPERTENSION
DIC / HELLP / AFLP

62. Pulmonary Edema
FLUID OVERLOAD REDUCED COLLOID OSMOTIC PRESSURE MORE COMMON FOLLOWING DELIVERY AS
COLLOID ONCOTIC PRESSURE DROPS FURTHER
AND FLUID IS MOBILIZED

63. Treatment of
Pulmonary
Edema
 PREVENTION:
 Avoid over-hydration
 Restrict fluids
 Lasix 10-20 mg IV
 Usually no need for
albumin or Hetastarch

64. Oliguria
25-30 CC PER HOUR
IS ACCEPTABLE
IF LESS… SMALL
FLUID BOLUSES OF
250-500 CC AS
NEEDED
LASIX IS
GENERALLY NOT
NECESSARY
ANTICIPATE
POSTPARTUM
DIURESIS
SWAN GANZ
CATHETER RARELY
NECESSARY

65. Persistent Hypertension
BP MAY REMAIN ELEVATED FOR
SEVERAL DAYS
DIASTOLIC BP LESS THAN 100 DO
NOT REQUIRE TREATMENT
BY DEFINITION, PREECLAMPSIA
RESOLVES BY 6 WEEKS

66. Disseminated Intravascular Coagulopathy
RARELY OCCURS WITHOUT
ABRUPTION
LOW PLATELETS IS NOT DIC REQUIRES REPLACEMENT BLOOD
PRODUCTS AND DELIVERY

67. Simplified Management of HELLP
and AFLP at Term
Third trimester patient with elevated
LFTs +/- hypertension
HELLP diagnosedAFLP diagnosed
Maternal Stabilization 
Delivery 
Maternal Recovery
Maternal Stabilization 
Delivery 
Maternal Recovery

68. Detailed Algorithm for AFLP
AFLP diagnosed
Correction of
coagulopathy
Seizure or coma
present?
Correction of
Hypoglycemia
Intensive care /
Intubation
FFP,
Cryoprecipitate
Glucose Replacement
and fluid resuscitation
Expedited Delivery – Virtually No Place for Conservative
Management
Following Delivery, the fetus is at risk for acidosis, nonketotic
hypoglycemia and fatty liver. Evaluation for LCHAD deficiency may give
information regarding risk of recurrence.

69. Detailed (and oversimplified)
Algorithm for HELLP
HELLP diagnosed
Mild BP elevation,Stable
mother, 32-34 weeks, No
IUGR, No Distress
Mild BP elevation,
Stable mother, <32
weeks, No IUGR, No
Distress
Severe HTN,
unstable, > 34
weeks, IUGR, Fetal
distress, maternal
coagulopathy
Administer
dexamethasone,
observe, deliver when
other factors change
Administer steroids and
deliver in 24-48 hours
(sooner if status
changes)
STABALIZE AND DELIVER
Following Delivery, fetal outcome is principally related to EGA at delivery
and presence or absence of intrapartum complications. Risk of
recurrence is 19 to 27%.

70. Conservative Management
CONTROVERSIAL STEROIDS REQUIRES TERTIARY CARE MUST HAVE STABLE LABS
AND REASSURING FETAL
STATUS
MAY USE
ANTIHYPERTENSIVES

71. SUMMARY
Clear criteria for diagnosis
Laboratory and fetal assessment
Magnesium sulfate seizure prophylaxis
Timing and place of delivery

73. REFERENCES:
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