HYPERTENSIVE DISORDERS IN

PREGNANCY
Group members
Noela Norah - H12/03897/18
Bovine Omumi – H12/01766/18
Dennis Kiprotich – H12/01758/18
Amos Kipngeno – H12/01750/18
Brian Kiprop – H12/01751/18
Cynthia Cheruto - HP12/07578/18
Collince Obala –H12/01788/18
Bill Clinton - H12/01749/18
Benard Akungu -H12/01754/18
Ashline Awuor - H12/01740/18
Fredrick Ouma - H12/01775/18
Kelvin kipkeu -H12/01767/18
 Introduction

Most common medical complication in pregnancy.

Complicate upto 10% of pregnancies.
Pre- eclampsia 2-8% of pregnancies
One of the leading causes of maternal and perinatal morbidity and
mortality, worldwide.
Globally, 76 000 women and 500 000 babies die each year from
this disorder.
Women in low resource settings are at a higher risk
Classification:

• Chronic hypertension (HTN)

• Gestational HTN
• Preeclampsia with and without severe feature –
Eclampsia
• Preeclampsia superimposed on chronic HTN
CHRONIC HYPERTENSION IN
PREGNANCY

Chronic hypertensive disease (CHD) is the presence of hypertension of any cause

before the 20th week of pregnancy and its presence beyond the 12 weeks after
delivery.
Risk factors for CHD
(i) Age (> 40 years)
(ii) Duration of hypertension (>15 years)
(iii) Level of BP (>160/110 mm of Hg)
(iv) Presence of any medical disorder (Reno vascular)
(v) Presence of thrombophilia's
Classification
Primary (essential) hypertension
Secondary hypertension
Secondary hypertension
Causes
• Primary renal disease
• Oral contraceptives
• Pheochromocytoma
• Reno vascular disease
• Primary hyperaldosteronism
• Cushing syndrome
• Coarctation of aorta
• Sleep apnea syndrome
• hyperthyroidism
ESSENTIAL HYPERTENSION IN PREGNANCY

DIAGNOSIS
Diagnostic criteria:
(1) Rise of blood pressure to the extent of 140/90 mm Hg or more during
pregnancy prior to the 20th week (molar pregnancy excluded)
(2) Cardiac enlargement on chest radiograph and ECG
(3) Presence of medical disorders
(4) Prospective follow up shows persistent rise of blood pressure even after 42
days following delivery.
EFFECTS OF PREGNANCY ON THE DISEASE

(1) There may be a mid-pregnancy fall of blood pressure in about 50%.

However, the blood pressure tends to rise in the last trimester which
may or may not reach its previous level.
(2) In 50%, the blood pressure tends to rise progressively as pregnancy
advances
(3) In about 20%, it is superimposed by pre-eclampsia evidenced by
rise of blood pressure to the extent of 30 mm Hg systolic and 15 mm
Hg diastolic associated with oedema and/or proteinuria
(4) Rarely, malignant hypertension supervenes
(5) In 30%, there is permanent deterioration of the hypertension
following delivery
EFFECT OF THE DISEASE ON PREGNANCY

Maternal risk
In the milder form, the maternal risk remains unaltered but in the severe form or
when superimposed by pre-eclampsia, the maternal risk is much increased.
Fetal risk:
Due to chronic placental insufficiency, there is intrauterine growth retardation.
Preterm birth is high. In the milder form, with the blood pressure less than
160/100 mm Hg, the perinatal loss is about 10%. When the blood pressure
exceeds 160/100 mm Hg, the perinatal loss doubles and when complicated by pre-
eclampsia, it trebles. Risk of placental abruption is high (0.5–10%).
investigation

Laboratory test and imaging

• Complete blood count
• Urinalysis
• Urea ,electrolyte creatinine
• Lipid profile
• Random blood sugar
• electrocardiography
MANAGEMENT:
The principles of management
(1) To stabilize the blood pressure to below 160/100 mm Hg
(2) To prevent superimposition of pre-eclampsia
(3) To monitor the maternal and fetal well-being
(4) To terminate the pregnancy at the optimal time.
• GENERAL MANAGEMENT:
• adequate rest (physical and mental)
• low salt diet
• The check up should be more frequent 1–2 weeks interval upto 28 weeks and
thereafter weekly.
• In severe cases or in cases of superimposed pre-eclampsia, the patients should
be hospitalized and are placed in the treatment
Antihypertensive drugs:
• Routine use of antihypertensive drug is not favoured. It may lower the blood
pressure and thereby benefit the mother but the diminished pressure may
reduce the placental perfusion which may be detrimental to the fetus.
• antihypertensive drugs should be used only when the pressure is raised beyond
160/100 mm Hg. To prevent target organ damage. In cases, where these drugs
have been used before pregnancy, care should be taken to adjust the dose during
pregnancy, specially, during mid-pregnancy when the blood pressure tends to
fall.
• OBSTETRIC MANAGEMENT
• In mild cases, spontaneous labour is awaited.
• In severe or complicated cases, the aim is to try to continue the pregnancy to at
least 34 weeks otherwise upto the 37th week to attain fetal maturity and then to
terminate the pregnancy.
GESTATIONAL
HYPERTENSION
This is defined as new onset hypertension without
proteinuria or severe features.
Hypertension develops after 20 weeks gestation (typically
after 37 weeks) and remits by 6 weeks postpartum; it
occurs in about 5 to 10% of pregnancies, more commonly in
multifetal pregnancy.
Category includes:
Women who go on to develop preeclampsia
Women with previously undiagnosed chronic HTN
Transient gestational HTN
Specific diagnosis is made postpartum, in retrospect.
It increases the risk of preeclampsia and eclampsia
and of other causes of maternal mortality or
morbidity, including:
• Hypertensive encephalopathy
• Stroke
• Renal failure
• Left ventricular failure
• HELLP syndrome (hemolysis, elevated liver
enzymes, and low platelet count)
Management of Gestational
Hypertension
•Expectant management before 37 weeks’ gestation
•Closely watch for development of severe features
•Establish baseline complete blood count (CBC),
transaminases, creatinine,
LDH, and uric acid
• Antepartum surveillance
• Twice weekly non-stress tests (NSTs) with weekly
amniotic fluid measurement, or biophysical profiles
once or twice per week
• •Growth ultrasonography every 3 to 4 weeks
• Weekly laboratory tests including;CBC,
transaminases (AST, ALT), Creatinine.
• Delivery at 37 weeks’ gestation.
• •Monitor urine protein to determine if condition
has progressed to preeclampsia
 Preeclampsia

New onset gestational hypertension with proteinuria or

end-organ dysfunction occurring after 20 weeks gestation.
SBP ≥ 140 mmHg
DBP ≥90 mmHg
 ◦ Multi- system disorder.
Dependence on proteinuria for diagnosis is eliminated.
In the absence of proteinuria it is diagnosed as new-onset hypertension with
the new onset of any of the following:
◦ Thrombocytopenia (platelet count <100,000/microL)
◦ Renal insufficiency (serum creatinine of >1.1 mg/dL [97 micromol/L] or a
doubling of the serum creatinine concentration in the absence of other
renal disease)
◦ Impaired liver function as indicated by liver transaminase levels at least
twice the normal concentration
◦ Pulmonary edema
◦ Persistent cerebral or visual symptoms
Clinical features

• Symptoms;
• Visual disturbances
• Headache
• Epigastric pain
• Diminished urine output
• Seizures

Signs;

Rise of BP

Oedema/abnormal weight gain (nonspecific)

FH small for gestation

Epigastric tenderness
• Prior preeclampsia x7
• Primigravida x3
• Family history: preeclampsia
1st degree relative, HTN
• Multifetal gestations x3
• Obesity (BMI >30) x2
• New paternity

Medical conditions: DM, chronic
HTN, SLE, thrombophilias, renal
disease

Strong family history of CV
disease( heart dx/stroke in >2
first degree relatives

Advanced maternal age >40yrs
(x1.6)

Foetal congenital anomaly.
Pathophysiology

• There are multiple theories with converging causal pathways.

• Both maternal and fetoplacental factors implicated.
• The placenta plays a critical role in the development of
preeclampsia.
• It can occur in absence of a fetus (H.mole) but not in absence of
a placenta and remits after delivery of the placenta.
• Preeclampsia has been described as a disease of theories
because the cause is unknown.
Abnormal Development of the Placenta

• In normal pregnancy, the cytotrophoblast cells invade maternal spiral

arteries of the uteroplacental bed.
• In1st trimester(10-12weks) invasion is up to the decidual segments, in
nd
2 trimester(16-18weeks) a 2 wave of trophoblasts invade up to the
myometrium.
• The endothelial lining is replaced and the musculoelastic arterial wall is
destroyed and replaced by fibrinoid material.
• This facilitates transformation from small muscular spiral arterioles to
large tortuous capacitance vessels(uteroplacental arteries) of low
resistance hence increased placental blood flow.

In preeclampsia, cytotrophoblast cells infiltrate decidual portion
only. There is impaired invasion of the myometrium.

Spiral arteries remain narrow hence failure to establish maternal
circulation leading to placental hypoperfusion.
 Hypoperfusion, Hypoxia, Ischemia

• Both a cause and consequence of abnormal placental development.

• Hypoperfusion is more pronounced with rising gestation as the
abnormal uterine vasculature is unable to accommodate rising blood
flow to fetus/placenta
• Hypoperfusion, hypoxia and ischemia of placenta lead to local
oxidative stress.
• There is subsequent release of factors into maternal blood leading to a
systemic inflammatory response and endothelial cell dysfunction.
Hypoperfusion, hypoxia, Ischemia

Factors supporting this theory;

a)medical conditions with vascular insufficiency have been
associated with increasedrisk of abnormal placentation and
preeclampsia
b)Obstetric conditions with increased placental mass without
increasing blood flow implicated in ischemia and preeclampsia
c) preeclampsia common in women at high altitudes
Vascular Endothelial Dysfunction


An imbalance between proangiogenic factors and anti-angiogenic factors leads to
angiogenic imbalance and vascular endothelial dysfunction

Vascular Endothelial Growth Factor(VEGF) and Placenta Growth Factor 1(PlGF1) are
important pro-angiogenic factors.

Soluble endoglin(sEng) and fms-like tyrosine kinase 1(sFlt1) receptors are anti-
angiogenic factors.

SFlt1 is secreted by the placenta. Its release is thought to be triggered by placental
ischemia.

In preeclampsia patients, it increases earlier at 21-24 weeks instead of 33-36weeks. It
binds VEGF and PIGF1 preventing their interaction with endogenous receptors.

Sflt-1:PIGF1 ratio is thought to be a possible predictor of preeclampsa

There is therefore no activation of eNOS, no vasodilation.

Instead there is increased vascular permeability

Decreased production of endothelial-derived vasodilators, such as nitric oxide
and prostacyclin, and increased production of vasoconstrictors, such as
endothelins and thromboxane leads to vasocontriction and hypertension
Immunologic Factors


Immunologic abnormalities similar to those observed in organ rejection graft
versus host disease, have been observed in preeclamptic women

Extravillous trophoblast cells express unusual combination of HLA class I antigen
cells (C, E & G).

In preeclampsia, conflict between maternal & paternal genes is believed to
induce abnormal placental implantation through increased NK cell activity.

Factors supporting this: Patients with less exposure to fetopaternal antigens have
less risk of developing preeclampsia and vice versa.

Risk factors related to reduced exposure include:
A) Nulliparous women
B) Change partners between pregnancies
C) Long interpregnancy intervals
D) Use barrier contraception
E) Conception via intracytoplasmic
Genetic Factors


Factors supporting this theory:

Primigravid women with a family history of preeclampsia have 2-5-fold higher risk of
the disease.
A) The risk of preeclampsia is increased more than 7-fold in women who have had
preeclampsia in a previous pregnancy
B) The spouses of men who were the pro product of a pregnancy complicated by
preeclampsia are more likely to develop preeclampsia than spouses of men without
this history
C) A woman who becomes pregnant by a man whose previous partner had preeclampsia
is at higher risk of developing the disorder than if the pregnancy with the previous
partner was normotensive

Diagnosis of Preeclampsia

New-onset HTN after 20 weeks’ gestation with proteinuria:

◦ BP ≥140/90 mm Hg on two occasions taken 4 hours apart
◦ BP ≥160/110 mm Hg once

Proteinuria is defined by:

◦ 24-hour protein level ≥300 mg or protein/creatinine ratio of ≥0.3
◦ Timed urine protein level extrapolated out to 24-hour value
◦ Urine dip +1 or more (only if other methods are not available)
◦ Proteinuria is NOT required for diagnosis if the patient has new onset HTN with severe criteria.
Diagnosing Preeclampsia without
Proteinuria.
• New-onset HTN with any of these findings:
• Platelets <100,000/uL
• Creatinine >1.1 mg/dL or doubled from baseline
• Transaminases twice the normal levels
• Pulmonary edema
• Cerebral or visual symptoms
Severe Features Of Preeclampsia

• New on onset headache or visual disturbances

• Pulmonary edema
• Hepatic dysfunction
-Transaminase levels x2
-Right upper quadrant or epigastric pain
• Platelets <100,000 /ul
• Elevated creatinine ( >1.1 mg/dl or x2 baseline)
• SBP ≥ 160 mmHg
• DBP ≥ 110 mmHg
Complications.
Management of Preeclampsia
without severe features
• management before 37 weeks’ gestation
• Closely watch Expectant for development of severe features
• Establish baseline complete blood count (CBC), transaminases,
creatinine, LDH, and uric acid
• Antepartum surveillance
• Twice weekly non-stress tests (NSTs) with weekly amniotic fluid
measurement, or biophysical profiles once or twice per week
• Growth ultrasonography every 3 to 4 weeks
• Weekly laboratory tests
• CBC, transaminases (AST, ALT), Creatinine.
• No need to monitor urine protein because even >5 g is not considered a
“severe feature” and does not affect timing of delivery
• Delivery at 37 weeks’ gestation
Management of Preeclampsia
with severe features
• Admit to hospital and monitor closely on
bedrest
• Treatment goals:
• Prevent seizures
• Control BP to prevent cerebral hemorrhage
• Expedite delivery, balancing maternal and fetal
condition and fetal maturity and fetal
surveillance
Antepartum management
measures
• 1. BP control
• 2. Maternal monitoring: SPO2, RR, DTRs, GCS
• 3. Fluid management- input/output monitoring
• 4. Thromboprophylaxis: TED stockings
• 5. Seizure prophylaxis
• 6. Steroids for fetal lung maturation
• 7. Fetal assessment and monitoring: U/S +
Dopplers, CTG
• 8. Prevention and management of complications
Maternal evaluation during expectant
management of severe preeclampsia
• Symptom assessment at least every 8 hours
• Assessing for headache, visual changes, RUQ or epigastric pain,
retrosternal pain or pressure
• Vital signs, neurologic examinations, and deep tendon reflexes
every 15 minutes until stable, then hourly if administering
magnesium sulfate (MgSO4)
• Monitor intake and output; insert Foley catheter, if needed –
Notify delivering clinician for <30 mL/hour of urine
• Laboratory tests daily; may decrease to every other day when
stable
• CBC, transaminases, creatinine
• Consider peripheral blood smear and coagulation profile – Type and
screen in labor
Severe BP Control
• Labetalol
• Initial dose: 20 mg IV bolus over 2 minutes
• If BP remains ≥160/110 mm Hg, then repeat 10 minutes later with
40 mg IV, and 10 minutes later at 80 mg IV. If BP remains
≥160/110 mm Hg, switch to hydralazine
• Maximum daily IV dose of 300 mg Hydralazine
• Initial dose: 5 or 10 mg IV over 2 minutes
• After 20 minutes, if BP remains ≥160/110 mm Hg, may repeat
with 10 mg IV
• Nifedipine
• 10 mg orally; if BP >160/110 mm Hg in 20 minutes, administer 20
mg and may repeat in 20 minutes for a total of 50 mg
• If BP remains elevated, administer 40 mg IV labetalol
Magnesium Sulfate
• Preferred anticonvulsant (prevent seizures)
• It is safer and more effective for prevention of
recurrent seizures than phenytoin, diazepam or lytic
cocktail (ie, chlorpromazine, promethazine, and
pethidine).

• Slows neuromuscular conduction and decreases

central nervous system irritability
• No significant effect on BP
• Decreases risk of placental abruption
Regimen
• Pritchard Regimen
• 14 g of MgSO4 loading dose
• 4g (20% solution) IV over 5-15 min
• 10g (50% solution) IM (5 g in each buttock).
• Subsequently, 5 g is given intramuscularly into alternate buttocks every 4
h.

• Zuspan regimen
• Initial intravenous dose of 4 g (10% solution) slowly over 10-15 min
• maintenance dose of 1-2 g every hour given by an infusion pump

• Indication: severe features

• Administer for 24 hrs after delivery or after last seizure-
whichever comes last • Recurrent fit load again with2-4g MgSO4
Toxicity
• MgSO4 toxicity is uncommon with
normal renal function • Check
magnesium level if:
• Urine output <30 mL/hour
• Elevated serum creatinine
• Symptoms of MgSO4 toxicity-
-Loss of patellar reflexes
• Antidote — Calcium gluconate 15 to 30 mL of
a 10% solution (1500 to 3000 mg) IV over 2-5
min. + Furosemide
• Alternative calcium chloride
• SE: N,V flushing, diaphoresis
• CI: Myasthenia Gravis
• limit maintenance fluids to 80 ml/hr to reduce
risk of iatrogenic pulmonary edema
Delivery Decisions for Severe
Preeclampsia SVD VS CS?
• Vaginal delivery is preferred because of:
• Lower risk of bleeding, infection, anesthesia reaction,
and surgical complications – Quicker recovery
• Lower risk for future deliveries • Cesarean delivery is
indicated for:
• Continuous seizures or other emergent signs and symptoms –
Fetal distress
• Unfavorable cervix with severe prematurity (<30 weeks’ gestation)
• Anesthesia methods:
• Epidural/spinal preferred versus general
• General anesthesia is indicated if platelet count <50,000 mcL
• Avoid ergometrine for PPH
Timing of delivery
• Pre eclampsia with severe features
•≥ 34wks – deliver
• Pre-viable gestation - deliver
• Expectant management can be considered
≥24weeks to <34 weeks to reduce risk of
neonatal morbidity due to prematurity
• Monitor for s/s of severity
• Administer steroids
• Neonatology and anesthesia review
Pathogenesis of eclampsia

Theories:

A) hypertension>breakdown of the auto regulatory system of the cerebral
circulation>hyperperfusion, endothelial dysfunction, and vasogenic and/or
cytotoxic oedema.

B)hypertension>activation of the auto regulatory system>vasoconstriction of
cerebral vessels>hypoperfusion, localized ischemia, endothelial dysfunction,
and vasogenic and/or cytotoxic oedema
Eclampsia
• The onset of seizures in a patient with preeclampsia, in
the absence of other explanations
• Etiology uncertain

• – cerebral edema and cerebral ischemia are possible

causes
• BP levels are often significantly elevated; however, in
15% of cases, BP levels are normal (diastolic ≤90 mm
Hg)
• Can occur before, during, or after delivery
• Fetal bradycardia can occur for 3-5min after fit: Recovers
Seizure Management

• Avoid anticonvulsant polypharmacy

• Protect airway to minimize aspiration
• Prevent maternal injury
• Administer MgSO4 to control convulsions
• When stable, plan for delivery
•HELLP • Clinical Presentation of HELLP
Syndrome

• Extremely variable presentation

Syndrome •
of symptoms
Common findings:
• RUQ pain, epigastric pain,
• A presentation of nausea, and vomiting
preeclampsia with • 85% hypertensive
• Differential diagnosis can
severe features include biliary colic,
• HELLP acronym: pancreatitis, acute fatty liver of
• Hemolysis pregnancy (AFLP),
gastroesophageal reflux
• Elevated Liver disease, hepatitis, idiopathic
enzymes thrombocytopenic purpura, and
• Low Platelets thrombotic thrombocytopenic
purpura
Lab Findings In HELLP
Syndrome
• Hemolysis
• Abnormal peripheral smear
• LDH level elevated
• Liver enzymes
• Transaminase levels ≥2 × normal
• Platelet count
-<100,000/mcL
• N/B; Need all three to diagnose HELLP Syndrome;
however, any one of the three is diagnostic of
preeclampsia with severe features when elevated
BP is also present
Management of HELLP
• Similar to preeclampsia with severe
features
• Stabilize woman
• Evaluate fetus for compromise
• Determine optimal timing/route of delivery
• Use continuous fetal monitoring
• Manage BP and fluid status
• All women should receive MgSO4 while
symptomatic or in labor
 Postpartum Preeclampsia and
HELLP management
• Improvement is typically rapid after delivery
• Risk of seizures is greatest in the first 24 hours after birth
• Diuresis signals resolving of the disease process
• Monitor BP and urine output
• Laboratory testing every 12 hours until resolved
• When already administering MgSO4, continue until clinically
stable
• Typically at least 24 hours postpartum

• Women who have not required MgSO4 prior to delivery may

require postpartum initiation of MgSO4. Examples include:
• New-onset HTN with cerebral symptoms (eg, headache, blurred
vision)
• Preeclampsia with severe HTN (≥160/110 mm Hg) • Eclampsia
• 24 hours
- Continue MgSO4 if severe preeclampsia
-Monitor intake and output
• 72 hours
• BP monitoring in hospital or equivalent at home
• Treat persistent HTN
• If two values ≥150/100 mm Hg at least 4 to 6 hours apart
• Persistent BP levels ≥160/110 mm Hg (goal is to treat
within 1 hour)
• Use oral nifedipine or labetalol (good safety profiles and fast
onset
 Superimposed Pre-
Eclampsia on Chronic
Hypertension
Definition
• New onset proteinuria in women with hypertension
and no proteinuria before 20 weeks of pregnancy
or;
• In women with hypertension and proteinuria,
severe excercebation in hypertension with onset of
new symptoms or thrombocytopenia or abnormal
liver enzymes
• 20 to 20% of patients with chronic hypertension
usually end up with severely elevated levels of BPs
by 24wks(diagnosis of Pre-eclampsia)
Cont’
• ACOG further sub categorises superimposed pre-
eclampsia as
1) Superimposed PE – sudden increase in BPs that were
previously well controlled even after escalation of
antihypertensive medications to control the BPs
2) New onset Proteinuria- proteinuria >= 300mg/24hrs or
Protein creatinine ratio > 0.3 or sudden increase in
proteinuria in women with known proteinuria
Compared with regular PE, superimposed PE tends to
appear early in pregnancy, with more severity and is
accompanied by fetal growth restriction.
Superimposed PE with severe
features
1. severe-range BP (160 mm Hg systolic or ≥110 mm
Hg diastolic) despite escalation of antihypertensive
therapy;
2. persistent cerebral symptoms such as headaches or
visual disturbances;
3. significant increase in liver enzymes (at least two
times the upper limit of normal concentration for a
particular laboratory);
4. thrombocytopenia (platelet count <100,000/µL); or
5. new-onset and/or worsening renal insufficiency
Risk Factors
• Severe baseline BPs (>= 130/80 mmHg)
• Patients need for antihypertesive therapy
• Presence of end-organ damage/failure e.g. baseline
proteinuria
Clinical Features
• Worsening hypertension,
• New-onset proteinuria,
• Neurological symptoms such as severe headaches
and visual disturbances,
• Generalized edema,
• Oliguria, and certainly,
• Convulsions or pulmonary edema
Management
• Women with superimposed preeclampsia before 34 weeks’
gestation may be candidates for expectant management at
facilities with adequate maternal and neonatal ICU resources
(ACOG 2018) – allow for foetal maturity
• Foetal asessment to monitor fetal growth restriction and still
births
• Magnesium sulfate neuproprophylaxis is initiated for
eclampsia prevention
• Anti-hypertensive drug therapy to lower blood pressure
• Treatment of underlying end organ failure
• Delivery if there is risk to mothers life irrespective of
gestation age
Prevention
• Low Dose Aspirin (81 mg/d) starting at 12 to 28
weeks until delivery to reduce the likelihood of
developing subsequent PE, preterm birth, or FGR
• Anti-hypertensive drugs
• Regular clinic follow-up of at risk mothers with
close monitoring
END