hypertensive disorder in pregancy

1. MANAGEMENT OF HYPERTENSIVE
DISEASES IN PREGNANCY
Presenter: Dr Bazambanza Philippe, OB/GYN PGY II
Mentor: Dr Nshimiyumuremyi Emmanuel, OB/GYN
Specialist, MFM Fellow
Nov 10/2023

2. Objectives
• Define, diagnose and manage hypertensive
diseases in pregnancy

3. INTRODUCTION
• Hypertension is defined as SBP≥140 mmHg or
DBP≥90 mmHg).
• It is a common complication of pregnancy and
the incidence is increasing.
• When severe HTN, (SBP ≥160 mmHg or DBP
≥110 mmHg), it can lead to stroke and death,
but prompt recognition and treatment can
reduce the risk of these complications .

4. Classification of Hypertensive
Disorders in pregnancy
By ACOG and Task Force on Hypertension,
classified it into four major classes:
• Chronic hypertension
• Gestational hypertension
• Preeclampsia-eclampsia
• Preeclampsia superimposed on chronic
hypertension

5. 1. CHRONIC HYPERTENSION
• Defined as persistent blood pressures greater
than 140/90 mm Hg diagnosed before
pregnancy or before 20 weeks’ gestation.
• The diagnosis can also be based on
hypertension that is observed for the first
time during pregnancy and persists beyond
the 84th day after birth.

6. EPIDEMIOLOGY
• The prevalence of CHTN increases with
advancing maternal age and obesity.
• For white women, the risk rises from 0.6%
among those 18 to 29 years of age to 4.6%
among those 30 to 39 years of age.
• African-American women have an even higher
risk for chronic hypertension (2% and 22.3%,
respectively).

7. Etiology/Basic pathophysiology
• Most women have essential or primary
hypertension, but around 10% may have
underlying renal, vascular or endocrine
disease, due to genetic or environmental
factors.

8. Classification
• Severe CHTN in pregnancy has been defined as
SBP ≥160 mmHg, or DBP ≥110 mmHg, at least
two measurements 4 hours apart .
• High-risk CHTN has been defined in pregnancy as
that associated with secondary hypertension,
target organ damage (left ventricular
dysfunction, retinopathy, microvascular disease,
prior stroke), dyslipidemia, maternal age >40
years, previous loss, SBP ≥180 mmHg or DBP
≥110 mmHg or other maternal diseases like
obesity and/or diabetes mellitus.

9. Risk factors
• Renal disease (most common cause of
secondary CHTN);
• Collagen vascular disease;
• APS;
• Diabetes; and other disorders such as
thyrotoxicosis, Cushing’s disease,
hyperaldosteronism, pheochromocytoma, or
coarctation of the aorta.

10. Complications
Maternal:
• Worsening CHTN , superimposed pre-
eclampsia (20–50%) with or without severe
features, eclampsia, HELLP syndrome,
gestational diabetes and cesarean delivery.
• Pulmonary edema, hypertensive
encephalopathy, retinopathy, cerebral
hemorrhage, and acute renal failure .

11. Fetal:
- Growth restriction (8–15%); oligohydramnios,
placental abruption (0.7–1.5%, about a two-
fold increase), PTB (12–34%), and perinatal
death (two- to four-fold increase).

12. Management
Principles
- Pregnancy is characterized by increased blood
volume, decreased colloid oncotic pressure.
- Physiologic BP decrease in first and second
trimester may mask CHTN.

13. Initial evaluation
• History. Antihypertensive drugs, prior workup, end-organ
damage, prior obstetrical history, family history of renal or
cardiac disease.
• Physical examination. Blood pressure, cardiac murmurs,
edema.
• Laboratory tests. Baseline values may be useful to be able
to diagnose secondary causes of CHTN and to compare
them in cases of possible superimposed pre-eclampsia:
Liver function test (LFT), platelets, creatinine, urine
analysis, 24-hour urine for total protein (and creatinine
clearance), antinuclear antibodies (ANA) for lupus,
anticardiolipin antibody (ACA) for APS, and lupus
anticoagulant (LA). And early glucose challenge test may be
indicated.

14. • Other tests: EKG, echocardiogram, and
ophthalmological examination are suggested,
especially in women with long-standing, high-risk, or
severe hypertension.
• Renal ultrasound to rule out polycystic kidney disease
or obstructive disease causing renal failure may be
considered in cases of suspected obstructive uropathy,
or strong family history of kidney disease.
• Also consider toxicology studies, as alcohol,
amphetamines, Ecstasy (MDMA and derivatives), and
cocaine are associated with hypertension.

15. Prevention
• In women with mild hypertension, gestational hyperten-
sive disorders, or a family history of hypertensive disorders,
30 minutes of exercise three times a week may decrease
DBP .
• Maintaining ideal body weight and preconception weight
reduction is recommended if over-weight or obese women.
• A proper diet should be rich in fruits, vegetables, and low-
fat dairy foods, with reduced saturated and total fats.
• Restriction of sodium intake to <2.4 g sodium daily intake,
recommended for essential hypertension, is beneficial in
non-pregnant adults.
• Use of alcohol and tobacco is strongly discouraged.

16. Antihypertensive drugs
Common types:
• Labetalol (alpha- and beta-blocker): is the current
drug of choice of many experts . Labetalol has an
additional arteriolar vasodilating action that
lowers peripheral resistance. It has a rapid onset
of action (within 2 hours). Contraindicated in
Asthma, heart Dse and congestive heart failure.
• Dosing can start at 100 mg twice a day, with
maximum dose of 2400 mg a day in 2–3 divided
doses.

17. • Calcium channel blockers: Calcium channel blockers are
frequently used as first or second option for CHTN in
pregnancy. Nifedipine can be started at 10 mg twice a day,
with maximum dose 120 mg/day. Long-acting nifedipine XL
can be started at 30 mg, with 120 mg as maximum dose.
• Common side effects of nifedipine and amlodipine include
dizziness, headache, peripheral edema, flushing,
tachycardia, and rash.
• Other calcium antagonists such as verapamil and diltiazem
have been used.

18. • Beta-blockers: The safety of beta-adrenergic
blockers is somewhat controversial due to
reports of premature labor, FGR, neonatal
apnea, bradycardia, and hypoglycemia, and
with higher mortality in non-pregnant adults
compared to other agents, should probably
be avoided

19. • Diuretics:
• Not contraindicated in pregnancy, except in
the settings of uteroplacental perfusion
reduction (i.e. pre-eclampsia and FGR).

20. • ACE inhibitor (or AII receptor antagonists):
These drugs are contraindicated in the first
trimester because they might be associated
with a twofold increase in malformations, and
are contraindicated also later in pregnancy
because they are associated with FGR,
oligohydramnios, neonatal renal failure, and
neonatal death.

21. • Methyldopa (Aldomet): A centrally acting α2 sympathetic
agonist was first-line agent historically, and the most studied.
• It is associated with stable uteroplacental blood flow and
fetal hemodynamics.
• It is a mild antihypertensive agent and has a slow onset of
action (3–6 hours). Liver disease is a contraindication.
Initial dose is usually 250 mg two to three times a day, with
highest dose 500 mg four times a day (2 g/day). Can be
associated with significant dry mouth, drowsiness, and
sedation, when high doses are required to control blood
pressure.

22. Recommendations
• The task force of hypertension in pregnancy recommends that
women with mild to moderate hypertension (SBP ≥140 mmHg but
<160 mmHg or DBP ≥90 mmHg but <110 mmHg) without end
organ damage should not be treated with pharmacologic agents .
• In women with known CHTN well controlled on antihypertensive
medications, discontinuation of the medication during the first
trimester is a reasonable alternative as blood pressure is usually
<140/90 at the first visit. Often BP will increase again in the third
trimester, leading to workup for pre-eclampsia, and, if pre-
eclampsia is absent, antihypertensive drugs can be restarted.
• For women with CHTN and end-organ damage (renal disease,
diabetes with vascular disease, or left ventricular dysfunction),
these thresholds should probably be lowered to <140/90 mmHg
to avoid progression of the disease to complications.

23. • ACOG recommended giving antihertensive
medication if BP is severe as SBP ≥160 mmHg
or DBP ≥110 mmHg .

24. • The Task Force of hypertension in pregnancy
recommends to start antihypertensive therapy
at SBP >160 mmHg or DBP >105 mmHg on at
least two occasions, with a goal for SBP between
120 and 160 mmHg and DBP between 80 and
105 mmHg, avoiding overly aggressive BP
lowering due to concerns of decreased
uteroplacental blood flow . This is to decrease the
risk of cerebrovascular accidents, and
cardiovascular (e.g., congestive heart failure) and
renal complications.

27. Antepartum testing
• The risk of FGR with uncomplicated CHTN is 8% to 15%,
while with severe and high risk CHTN the risk increases
up to 40%.
• Early detection of FGR can decrease the risk of stillbirth
by 20% , and the addition of umbilical artery Doppler
on those with suspected FGR decreases perinatal
mortality by 29% .
• Initial dating ultrasound, preferably in the first
trimester (FTS at 11–14 weeks), anatomy ultrasound at
around 18 to 20 weeks, and ultrasound for growth at
28–32 weeks are suggested for women with
uncomplicated CHTN

28. • Antenatal testing (usually weekly NST) is
suggested starting around 32 weeks, especially if
poorly controlled HTN, severe HTN, high risk
CHTN, FGR, or superimposed pre-eclampsia is
indicated.
• Umbilical artery Doppler ultrasound is
recommended at least weekly if FGR is present.
• Ultrasound for fetal growth and amniotic fluid
assessment should be performed at diagnosis
and every 3 weeks if still pregnant.

29. Delivery
• The ACOG Committee of opinion
recommends that women with isolated,
uncomplicated CHTN off medications can be
delivered between 38 0/7 to 39 6/7 weeks of
gestation, while of those on medications they
can be delivered earlier from 37 0/7

30. • In women with CHTN on medications requiring
frequent adjustment of antihypertensive medications
consider late preterm delivery starting at 36 0/7 weeks
of gestation.
• Consider late steroid administration for women
diagnosed with superimposed pre-eclampsia with
severe features between 34 0/7 and 36 0/7 weeks.
• The risk of stillbirth is significantly higher at 41 weeks .
• Delivery is typically vaginal, or with C/S if obstetrical
indications.

31. Postpartum/Breastfeeding
• Methyldopa, labetalol, beta-blockers, calcium
channel blockers, are safe with breastfeeding,
with the possible exception of ACE inhibitors,
because even low concentrations in breast
milk could affect neonatal renal function.

32. 2. Gestational hypertension
Definition
• New onset of hypertension (systolic pressure ≥140
mmHg and/or diastolic pressure ≥90 mmHg) at ≥20
weeks of gestation.
• The BP taken on two occasions at least 4 hours apart.
without proteinuria, other signs or symptoms of pre-
eclampsia, or a prior history of HTN.
• Severe GHTN is defined similarly, except that the
cutoffs are ≥160/110 mmHg .
Incidence
• About 6–17% healthy nulliparous women develop
GHTN.

33. Complications
• Progression to pre-eclampsia usually is seen in
1–3 weeks.
• Severe GHTN is associated with higher
morbidities than mild pre-eclampsia, with
incidences of abruption, PTB, and SGA, similar
to severe pre-eclampsia.
• If GHTN develops before 30 weeks or is
severe, there is a high (50%) rate of
progression to pre-eclampsia.

34. Antenatal management
• Before 37 weeks, in the absence of severe GHTN, pre-
eclampsia with severe features or preterm labor, and
in the presence of reassuring fetal testing, expectant
management is suggested.
• Outpatient management with close surveillance of
maternal symptoms, BP (suggest daily as outpatient
with personal BP cuff), proteinuria, and laboratory
tests is suggested.
• Antepartum surveillance also should include daily fetal
kick counts, ultrasonography fetal growth assessment
every 3-4 weeks, BPP or modified BPP every week
starting at the onset of diagnosis.

35. • Severe GHTN usually requires admission to
the hospital for maternal fetal surveillance,
diagnosis and Antihypertensive medications

36. Delivery
• Delivery for women at or beyond 37 weeks
with GHTN, is recommended, rather than
continued observation.

37. • Magnesium sulfate for seizure prophylaxis is
not indicated in GHTN.
• Women with severe GHTN requiring
antihypertensive medications should be
managed as pre-eclampsia with severe
features.
• And delivery is indicated at 34 weeks or after.
• Delivery is typically vaginal, or by C/S if any
obstetrical indications.

38. • Postpartum management of women with
GHTN requires observation of BPs for 72 hours
postpartum and outpatient follow up in 7–10
days, as there is an increased risk of
postpartum pre-eclampsia/eclampsia and
CHTN in these women.

39. 3.Pre-eclampsia
Pre-eclampsia
• Refers to the new onset of hypertension and
proteinuria ≥300 mg in 24 hours or (UPC)
≥0.3, or the new onset of hypertension plus
significant end-organ dysfunction with or
without proteinuria in a previously
normotensive patient, typically after 20 weeks
of gestation or postpartum.

40. Superimposed pre-eclampsia
One or more of the following criteria:
• New onset of proteinuria (≥300 mg in 24 hours,
without prior proteinuria) after 20 weeks in a
woman with chronic HTN
• Sudden increase in proteinuria in a woman with
known proteinuria before or early in pregnancy.
• A sudden increase in hypertension previously
well controlled or escalation of antihypertensive
medication to control BP.

41. Superimposed pre-eclampsia with
severe features
One or more of the following criteria are present:
• Severe high BP (≥160/110 mmHg) despite escalation of
antihypertensive medication
• Platelet count <100,000/mm3
• Increased hepatic transaminases (AST and/or ALT) two
times of the upper limit of normal concentration at a
particular laboratory
• New onset or worsening renal insufficiency (creatinine ≥1.1
mg/dL or a doubling of the serum creatinine.
• Pulmonary edema
• Persistent neurological symptoms (e.g. headache, visual
changes)

42. pre-eclampsia with severe features
Any of the following criteria:
• BP ≥160/110 mmHg (two occasions, ≥4 hours apart)
• Thrombocytopenia, Platelets <100,000/mm3 (and/or evidence of
microangiopathic hemolytic anemia)
• Increased hepatic transaminases (AST and/or ALT) two times of the upper limit of
normal concentration at a particular laboratory
• Progressive renal insufficiency (creatinine ≥1.1 mg/dL or a doubling of the serum
creatinine or oliguria (<500 mL urine in 24 hours) in absence of other renal
disease.
• Persistent headache or other cerebral or visual disturbances (including grand mal
seizures)
• Persistent epigastric (or right upper quadrant) pain
• Pulmonary edema or cyanosis
Proteinuria ≥5 g/24 hours was removed as criteria of severe pre-eclampsia as
expectant management was not associated with worsening maternal or neonatal
outcome, and resolution of renal dysfunction occurred in all women after delivery .

43. Etiology/Basic pathophysiology
• Pre-eclampsia is a systemic disease of unknown etiology. It
is associated with endothelial disease, with vasospasm and
sympathetic over activity.
• Trophoblastic invasion by the placenta into the spiral
arteries of the uterus is incomplete, resulting in reduced
perfusion.
• Hypoxia, free radicals, oxidative stress, and activation of
endothelium are characteristic. Thromboxane (which is
associated with vasoconstriction, platelet aggregation, and
decreased uteroplacental blood flow) is increased, while
prostacyclin (which has opposite effects) is decreased. FGR
is also theorized to develop as a result of defective
placentation and the imbalance between prostacyclin and
thromboxane.

44. • Alterations of the immune response.
• Vascular: Vasospasm and subsequent hemoconcentration
are associated with contraction of intravascular space;
capillary leak and decreased colloid oncotic pressure may
predispose to pulmonary edema.
• Cardiac: Usually reduced cardiac output, decreased plasma
volume, increased systemic vascular resistance.
• Hematological: Thrombocytopenia and hemolysis with
HELLP syndrome (also elevated LDH), disseminated
intravascular coagulation (DIC).
• Hepatic: Elevated AST, ALT; subcapsular hematoma and
liver rupture.

45. • CNS: Eclampsia, intracranial hemorrhage, headache,
blurred vision, scotomata, hyperreflexia, temporary
blindness.
• Renal: Vasospasm, hemoconcentration, and decreased
renal blood flow resulting in oliguria (rarely leading to
acute tubular necrosis, possibly leading to acute renal
failure), proteinuria and hematuria.
• Fetal: Impaired uteroplacental blood flow [FGR,
oligohydramnios, abruption, and nonreassuring fetal
heart rate testing (NRFHT)].

46. Classification
• Pre eclampsia without severe features and
• Pre eclampsia with severe features

47. Prediction
• Abnormal uterine artery Doppler findings in
the second trimester have a sensitivity of 20-
60%
• But the only reliable and currently strategy
for clinical prediction is a Complete medical
history and physical exam to evaluate for risk
factors, strict surveillance and education.

48. Copyrights apply

49. Complications
Most cases of mild pre-eclampsia, at term, do not convey significant
risks. Rates of complications for severe pre-eclampsia are given in the
following subsections in parenthesis .
Maternal
• HELLP syndrome (20%),
• DIC (10%),
• Pulmonary edema (2–5%),
• Abruptio placentae (1–4%),
• Renal failure (1–2%),
• Seizures (eclampsia) (<1%),
• Cerebral hemorrhage (<1%),
• Liver hemorrhage (<1%), death (rare).

50. Fetal/Neonatal
• PTB (15–60%),
• FGR (10–25%),
• Perinatal death (1–2%),
• Hypoxemia-neurologic injury (<1%).

51. Antepartum Management of
Preeclampsia
Three principles:
• First, delivery is always an appropriate therapy for the
mother but not always for the fetus.
• Second, Poor perfusion caused at least in part by
vasospasm is the major factor of preeclampsia leading
to derangement of maternal physiologic function and
ultimately to perinatal mortality and morbidity.
• Third, the pathogenetic changes of preeclampsia occur
long before manifestation of clinical criteria leading to
the diagnosis. Delivery is always an appropriate
therapy

52. Admission
• Admission for 24 hours observation is
acceptable to establish diagnosis and rule out
severe features. Hospitalization may be
indicated in cases in which the woman is
unreliable.
• Admission is indicated in cases of pre-
eclampsia with severe features.

53. 1. Preeclampsia Without Severe
Features:
 Term gestation (≥37 Weeks) prompt delivery
is recommended.

54.  Late Preterm Gestation (34 to 36 6/7 Weeks).
• The decision to deliver depends on the assessment of fetal
well-being.
• ACOG recommends delivery in this period when the
estimated fetal weight is less than 5th percentile,
oligohydramnios is present (<5 cm amniotic fluid index), or
there is nonreassuring fetal testing (BPP 6/10 or less).
• Give antenatal corticosteroids before effecting delivery, if
fetal testing does not warrant immediate delivery.
• In the absence of these findings, expectant management
until 37 weeks can be attempted.

55.  Early Preterm Gestation (<34 Weeks). In the
setting of reassuring fetal testing and the
absence of severe features, expectant
management with administration of antenatal
corticosteroids and frequent monitoring is
recommended.

56. ACOG suggests:
• Weekly BP monitoring and assessment for symptoms of
preeclampsia with severe features.
• Weekly FBC, liver enzyme, and serum creatinine.
• Fetal well-being should be assessed at least twice weekly
with a NST or BPP;
• AFI should be assessed at least weekly and fetal growth
assessed every 3 weeks.
• Additionally, women should be counseled on daily kick
counts
• ACOG does not recommend routine use of magnesium
sulfate in preeclampsia without severe features

57. 2. Preeclampsia With Severe Features
 Magnesium sulfate and antihypertensive
medication
 Term Gestation (≥37 Weeks): prompt delivery
is recommended.

58.  Late Preterm Gestation (34 to 36 6/7 Weeks).
Should undergo delivery if the risks associated
with continued expectant management
outweigh the benefits to the fetus of
continuing the pregnancy.
• Give late corticosteroids. However, delivery
should not be delayed , particularly in the
setting of non reassuring fetal status or
worsening maternal disease.

59.  Early Preterm Gestation (<34 Weeks).
• Expectant management may result in fetal benefit.
• Several studies have shown that with close
monitoring, pregnancies complicated by severe
preeclampsia can be managed expectantly, extending
the pregnancy by 5 to 19 days on average and
producing good maternal and neonatal outcomes.
• If expectant management does not result in any
maternal benefit, reevaluate both maternal and fetal
status for prompt delivery.

60. • Expectant management of severe pre-
eclampsia warrants hospitalization at a
tertiary facility for further investigations and
management
• Expectant management was associated with
increased risk of abruptio placentae and SGA.

61. Contraindications to expectant
management
• Eclampsia
• Pulmonary edema
• DIC
• Uncontrollable severe hypertension
• Nonreassuring fetal testing
• Placental abruption
• Stillbirth
• Nonviable fetus

62. Delivery indications less than 34 weeks after
completion of the antenatal
steroids include :
• HELLP
• Persistent neurologic symptoms or epigastric/right
upper quadrant pain
• Maternal serum laboratory abnormalities (platelets
<100,000/µL, transaminase twice the upper limit of
normal, serum creatinine >1.1 mg/dL)
• Fetal growth restriction less than 5th percentile
• Oligohydramnios (amniotic fluid index <5 cm)
• Reversed end-diastolic flow in the umbilical artery
• Labor or PPROM

63. Route of Delivery.
• Delivery is typically vaginal, with C/S if
obstetrical indications.
• Cervical ripening agents may be used if the
cervix is not favorable before induction.
• Although some physicians do not attempt
vaginal delivery when cervical ripening is
required at early gestational ages (<28 to 32
weeks), the incidence of successful induction
is higher than initially thought.
In one cohort, for all inductions less than 34 weeks the
success rate is over 60%.
For those at 24 to 28
weeks being induced for preeclampsia, the success rate
is 39%

64. Use of MgSO4
1. Used prophylactically in severe pre eclampsia
2. Used prophylactically In severe HELLP Sd
3. Therapeutically in eclampsia
4. Short term tocolytic
5. Neuro protection
Compared with placebo or no anticonvulsant, magnesium sulfate is associated
with a 59% reduction in the risk of eclampsia , a 36% reduction in abruption, and a
non-statistically significant but clinically important 46% reduction in maternal
death

65. Antihypertensive therapy
• Labetalol: 20 mg IV bolus, then 40, 80, 80 mg as needed,
every 10 minutes (maximum 220 mg total dose).
• Hydralazine: 5 to 10 mg IV (or IM) every 20 minutes.
Change to another drug if no success by 30 mg (maximum
dose). Hydralazine may be associated with more maternal
side effects and NRFHT than IV labetalol or oral nifedipine .
• Nifedipine: 10 to 20 mg orally, may repeat in 30 minutes.
This drug is associated with diuresis when used postpar-
tum. Nifedipine and magnesium sulfate can probably be
used simultaneously.
• Sodium nitroprusside (rarely needed): Start at 0.25 μ/kg/
min to a maximum of 5 μ/kg/min.

66. 3.Management of CHTN with
superimposed pre-eclampsia without
severe features
• Antihypertensive medications for SBP >160 mmHg or
DBP>105 mmHg
• Maintain BPs between >120/80 mmHg and <160/105
mmHg
• Consider outpatient management in selected population
with easy access to the health system
• Home BPs measurements
• Close follow-up in clinic every week with NST
• Fetal growth evaluation every 3 weeks
• Delivery no less than 37 weeks
• Close postpartum BPs surveillance for first 72 hours
• Close follow up 7–10 days after delivery

67. 4. Management of CHTN with
superimposed pre-eclampsia with
severe features:
• Admission to the hospital for evaluation
• Antihypertensive medications for SBP >160
mmHg or >105 mmHg
• Magnesium sulfate for maternal seizure
prevention
• Expectant management no more than 34 weeks
• Delivery by 34 weeks
• Close postpartum BPs surveillance for first 72
hours
• Close follow up 7–10 days after delivery

68. • Women with renal disease, systemic lupus
erythematosus, insulin-dependent diabetes,
or multiple gestations require a very careful
management if expectantly managed.
• The presence of FGR requires even closer
monitoring, is associated with worse
outcomes, but is usually not in itself a
criterion for delivery, the same as massive
proteinuria.

69. 4. HELLP syndrome
• HELLP syndrome can have an antepartum or postpartum
onset and it is associated with increased maternal
morbidity and mortality.
• The following criteria are most commonly used (Tennessee
Classification): Hemolysis as evidenced by an abnormal
peripheral smear in addition to either serum LDH >600
IU/L, or total bilirubin ≥1.2 mg/dL (≥20.52 μmol/L);
elevated liver enzymes, (AST and/or ALT) two times of the
upper limit of normal concentration at a particular
laboratory, and platelets <100,000 cells/mm3. If all the
criteria are met, the syndrome can be also called
“Complete”; if only one or two criteria are present, the
term “partial HELLP” is preferred.
• See Mississippi classification also

70. • HELLP syndrome is a severe manifestation of pre-
eclampsia and complicates approximately 0.5–0.9% of
all pregnancies and 10-20% of cases with severe pre-
eclampsia.
• The onset can be 72% antepartum, and 28%
postpartum .
• HELLP syndrome detected before fetal viability may
identify a pregnancy complicated by partial
mole/triploidy, trisomy 13, APS, autoantibodies to
angiotensin AT(1)-receptor, or severe preterm pre-
eclampsia with “mirror” syndrome .
Epidemiology

73. Complications
• Complications of HELLP syndrome are somewhat
similar to those of severe pre-eclampsia.
• If profound hypovolemic shock occurs, suspect liver
hematoma.
• If confirmed, liver hematoma is best managed
conservatively. Contributing factors to deaths of
women with HELLP syndrome are:
- Stroke, cardiac arrest,
- DIC, adult respiratory distress syndrome, renal failure,
sepsis, hepatic rupture, and hypoxic encephalopathy .

74. Management

75. Delivery
Timing
• Prompt delivery is indicated if HELLP is diagnosed at ≥34 weeks, or even
earlier if multiorgan dysfunction, DIC, liver failure or hemorrhage, renal
failure, possible abruption, or NRFHT are present.
• Delivery can only be delayed for a maximum of 48 hours between 24 and
33 6/7 weeks to give steroids for fetal maturity.
• Although some women may have improvement in laboratory values in
these 48 hours, delivery is still indicated in most cases.
Mode
• Mode of delivery should generally follow obstetrical indications, with
HELLP syndrome not being an indication for cesarean .
• Counseling and management should include the information that the
incidence of cesarean delivery in trials of labor with HELLP at <30 weeks is
high. With a platelet count <100,000/mm3, a drain may be indicated
under and/or over the fascia in cases of cesarean delivery.

76. 5. Eclampsia
Definition
• is the occurrence of new onset of ≥1 grand
mal seizure(s) in association with pre-
eclampsia and/or HELLP syndrome.

77. Epidemiology/Incidence
• The incidence is 0.1% in Europe and 2.7 in
Africa
• The onset can be antepartum (40-50%),
intrapartum (20–35%), or postpartum (10-
40%). Late post-partum eclampsia (>48 hours
but <4 weeks after delivery) is rare, but can
occur.

78. Symptoms
• Persistent headache or other cerebral or visual
disturbances, altered mental status (including
grand mal seizures), persistent epigastric (or
right upper quadrant) pain, severe range BPs.
Massive proteinuria and/or edema may be
present.

79. Complications
• The risk of maternal death is around 1-2% in the
developed world and up to 10% in developing
countries.
• Perinatal mortality is 6-12% in the developed
world and up to 25% in developing countries.
• Other complications are similar and possibly
more severe than severe pre-eclampsia cases
(maternal-abruption 7-10%, DIC 7-11%, HELLP 10-
15%, pul-monary edema 3-5%, renal failure 5-9%,
aspiration pneumonia 2-3%, PTB 50%).

80. Management
Principles.
• In about 15% of cases, hypertension or proteinuria may be absent
before eclampsia.
• A high index of suspicion for eclampsia should be maintained in all
cases of hypertensive disorders in pregnancy, in particular those
with CNS symptoms (headache, visual disturbances).
• The first priorities are airway, breathing, and circulation.
• Multidisciplinary care is essential, as several people are needed for
immediate stabilization. Interventions include airway assessment
and placing the patient in the lateral decubitus position (to avoid
aspiration). Maintain oxygenation with supplemental oxygen via 10
L/min mask. Obtain vital signs and assess pulse oximetry.
Supportive care includes inserting a tongue blade between the
teeth (avoiding inducing a gag reflex), and preventing maternal
injury.

81. Workup.
• Cerebral imaging is usually not necessary for
the diagnosis and management of most
women with eclampsia.
• It might be helpful in cases complicated by
neurologic deficits, coma, refractory to
magnesium, or seizures >48 hours after
delivery.

82. Therapy.
• Magnesium sulfate is the drug of choice to
treat eclampsia and prevent recurrent
convulsions.
• Loading dose of 4 g, followed by an infusion of
1 g/hour ( Zuspan regimen).
• Increasing the loading dose to 6 g and the
infusion rate to 2 g/ hour has also been
suggested in imminent eclampsia. (SIBAI
regimen).

83. MgSO4 toxicity

84. Antepartum testing
• NRFHT occurs in many cases of eclampsia, but
usually resolves spontaneously in 3-10
minutes by fetal in utero resuscitation with
maternal support. Therefore, NRFHT is not an
indication for immediate cesarean delivery in
case of eclampsia, unless it continues >10-15
minutes despite normal maternal
oxygenation.

85. Delivery
• Delivery should occur expeditiously, but only
when the mother is stable. This requires a
multidisciplinary, efficient, and timely effort.

86. Long-term counseling
• In a large cohort study, the recurrence risk of
pre-eclampsia is around 15% in the second
pregnancy for women who had had pre-
eclampsia in their first pregnancy and 30% for
women who had pre-eclampsia in the
previous two pregnancies .
• Family planning is required / permanent
family planning method is a better option.

87. Prevention of pre-eclampsia and
eclampsia in subsequent pregnancies
• Low-dose aspirin, 100-150mg OD should be
initiated before 16 weeks (and, if possible, as
early as at 12 weeks) of gestation until 36
weeks of gestation.
As shown in a meta-analysis of 34 RCTs [56]. Low-dose aspirin initiated before 16
weeks is associated with a significant decrease in the incidence of gestational
hypertension (69%), pre-eclampsia (53%), severe pre-eclampsia (90%), IUGR (54%),
and PTB (78%) in women identified to be at risk for pre-eclampsia, therefore it is
recommended to start prior to 16 weeks of gestation.

88. • Calcium supplementation is also associated
with a 24% reduction in the risk of PTB overall,
and by 55% in women at high risk of pre-
eclampsia.
In one study, childhood systolic blood pressure
>95th percentile is reduced by 41%. Overall,
these results support the use of calcium
supplementation during pregnancy, especially
for women at high risk of developing pre-
eclampsia and for those with low dietary
intake

89. References
1. CREASY & RESNIK’S MATERNAL-FETAL
MEDICINE, EIGHTH EDITION
2. MATERNAL-FETAL EVIDENCE BASED GUIDELINES,
FOURTH EDITION
3. RWANDA STANDARD TREATMENT GUIDELINES
Obstetrics and gynecology Volume 4
4. GABBE’S OBSTETRICS Normal and Problem
Pregnancies 8TH EDITION
5. Gestational hypertension and preeclampsia:
ACOG Practice Bulletin, Number 222. Obstet
Gynecol 2020; 135:e237.