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Hypertensive disorders in

pregnancy
Abdallah Al-Mawazreh
Content
• Gestational hypertension.
• Preeclampsia .
• Eclampsia.
• Chronic hypertension with pregnancy.
• Systolic and diastolic blood
pressure (BP) typically fall early in
gestation and are about 5 to 10
mmHg below baseline in the
second trimester, declining to a
mean of about 105/60 mmHg 
•  In the third trimester, blood
pressure gradually increases and
may normalize to nonpregnant
values by term.

Atrial blood pressure is


never normally elevated
in pregnancy
Gestational hypertension
Definition
• Sustained elevation of BP ≥ 140 / 90 Hg after 20 weeks of pregnancy
without proteinuria .

• Gestational hypertension is a temporary diagnosis for hypertensive


pregnant . The diagnosis is changed to:
 Preeclampsia, if proteinuria or severe sympotoms develops
 Chronic hypertension, if blood pressure elevation persists ≥12
weeks postpartum
 Transient hypertension of pregnancy, if blood pressure returns to
normal by 12 weeks postpartum

• Thus, reassessment up to 12 weeks postpartum is necessary to


establish a final definitive diagnosis.
Relation to preeclampsia
• Preeclampsia develops in 15 to 25 percent of women initially
diagnosed with gestational hypertension .
• Women with early onset of gestational hypertension are more
likely to progress to preeclampsia than women with late
onset.
• Women who go on to develop preeclampsia have higher total
vascular resistance at presentation than women with
uncomplicated gestational hypertension
• Serial measurement of sFlt-1 levels reveals a substantial
increase over time in women who go on to develop
preeclampsia, but remain normal or only mildly elevated in
women who maintain a diagnosis of gestational hypertension
Diagnosis
•  The diagnosis of gestational hypertension is clinical .
• The main goals in the initial evaluation of pregnant
women with newly developed hypertension are :
• to distinguish gestational hypertension from
preeclampsia, which has a different course and
prognosis .
• to determine whether hypertension is mild or severe,
which affects management and outcome .
Evaluation
• Determine the severity of hypertension .
• Evaluate for signs/symptoms of severe
preeclampsia .
• Measure protein excretion .
• Perform laboratory evaluation .
• Assess fetal well-being .

Mild VS severe
management 
• Mild gestational hypertension :
• Most patients can be managed safely as outpatients
with weekly antepartum visits.
• Bedrest appears to reduce the risk of worsening
hypertension .
• but neither bedrest nor use of low  dose
aspirin prevent progression to severe preeclampsia,
nor do these interventions improve outcome .
• Patient education and counseling :
- instruct patients to report any symptoms suggestive of severe
disease .
- review signs suggestive of possible fetal/placental impairment ,
such as decreased fetal movement and vaginal bleeding .
• Fetal assessment :
• No antihypertensive therapy :
• data from randomized trials show that medical therapy of mild
hypertension does not improve maternal or neonatal outcome.
• No antenatal glucocorticoids .
• Timing of delivery : 
• induction of labor of hypertensive patients by 40 weeks is
associated with a lower rate of adverse outcome than expectant
management,
• Severe gestational hypertension :

• Medical therapy : 
• Systolic blood pressure ≥160 mmHg or diastolic blood pressure
≥105 mmHg is treated with antihypertensive agents to reduce
the risk of a maternal cerebrovascular event .
• magnesium sulfate ??
• Time of delivery :
• delivery of pregnancies at 34 to 36 weeks and administration
of a course of antenatal glucocorticoids to patients less than 34
weeks is a reasonable approach.
• Recurrence risk :
• Gestational hypertension tends to recur with subsequent
pregnancies.
•  In two large studies, the prevalence of gestational
hypertension in a second pregnancy ranged from 22 to 47
percent among women with gestational hypertension in their
first pregnancy
Preeclampsia
The disease of theories
• Preeclampsia refers to the new onset of hypertension and
proteinuria after 20 weeks of gestation .
• Clinically, preeclampsia can be classified as ‘severe’ when
severe hypertension, severe proteinuria, or other signs
/symptoms of end-organ injury are present .
BURDEN OF DISEASE

• Increase risk for life-threatening events, including placental


abruption, acute renal failure, cerebral hemorrhage, hepatic
failure or rupture, pulmonary edema, disseminated
intravascular coagulation, and progression to eclampsia. 
• Worldwide, 10 to 15 percent of direct maternal deaths (ie,
resulting from obstetric complications of pregnancy) are
associated with preeclampsia/eclampsia .
  In the United States, preeclampsia/eclampsia is one of four
leading causes of maternal death, along with hemorrhage,
cardiovascular conditions, and thromboembolism .
• Morbidity and mortality are also increased for the fetus
/neonate because of the greater risk of restricted fetal growth
and preterm birth in affected pregnancies. 
RISK FACTORS

• past history of preeclampsia . (RR 7.19 )


• First pregnancy (nulliparity) .
• A family history of preeclampsia in a first degree relative .
• Twin pregnancies .
• Advanced maternal age .
• Preexisting medical conditions:
• Pregestational diabetes
• Blood pressure ≥130/80 mm Hg at the first prenatal visit .
• Antiphospholipid antibodies
• Body mass index ≥26.1
PATHOPHYSIOLOGY  
Multi-factorial !!
• involves both maternal and fetal / placental factors .
• abnormalities in the development of the placental vasculature early
in pregnancy,
• These abnormalities can result in placental underperfusion, and
possibly hypoxia and ischemia.
• release of circulating antiangiogenic factors (soluble fms–like
tyrosine kinase [sFlt-1], soluble endoglin [sEng]) and other
substances
• cause widespread maternal systemic endothelial dysfunction
(increased vascular permeability, vasoconstriction, activation of
coagulation system, microangiopathic hemolysis), resulting in
hypertension, proteinuria, and the other clinical manifestations of
preeclampsia
In the future ?!!
• Clinical applications for these observations have not been
established.
• Measurement of serum sFlt-1 is still investigational and its
ability to predict development of preeclampsia needs to be
determined in prospective, longitudinal studies.
• Measurement of sFlt-1:VEGF (or sFlt-1:PlGF) ratio in urine
appears to be a better test to identify those women at high
risk of developing preeclampsia, and also for confirming
clinical diagnosis of the disorder. A high sFlt-1:PIGF may also
identify women at risk of requiring delivery within two weeks
because of severe preeclampsia .In the future, apheresis or
drugs that bind to sFlt-1 may be used to reduce sFlt-1 levels
and thereby to prevent or treat preeclampsia .
CLINICAL MANIFESTATIONS

• In most women it first become apparent after 34 weeks of


gestation, including when the woman is in labor “late onset
preeclampsia” .
• In about 10 percent of women, hypertension and proteinuria
develop before 34 weeks of gestation “early onset
preeclampsia” .
• and in about 5 percent, preeclampsia is first recognized
postpartum “postpartum preeclampsia” . usually within 48
hours of delivery .
CLINICAL MANIFESTATIONS

• The degree of maternal hypertension and proteinuria, and


the presence/absence of other clinical manifestations of the
disease are highly variable .
• Most patients have only mild preeclampsia .
• About 25 percent develop severe preeclampsia .
Signs and symptoms

• Severe hypertension (systolic blood pressure ≥160 mm Hg or diastolic


≥110 mm Hg on two occasions at least six hours apart)
• Persistent and/or severe headache,
• Visual abnormalities (scotomata, photophobia, blurred vision, or
temporary blindness [rare])
• Upper abdominal or epigastric pain
• Nausea, vomiting
• Oliguria
• Dyspnea, retrosternal chest pain
• Fetal growth restriction
• Oligohydramnios
• Altered mental status
Laboratory abnormalities

• Hemoconcentration
• Microangiopathic hemolytic anemia (abnormal peripheral
smear, elevated bilirubin, or low serum haptoglobin
levels U/L)
• Thrombocytopenia (<100,000/microL)
• Elevated serum creatinine concentration (>1.3 mg/dL)
• Elevated liver enzymes (twice the upper limit of normal)
• Severe proteinuria (≥5 grams in 24 hours)
DIAGNOSIS

•  International guidelines generally agree that the diagnosis of


preeclampsia should be made in a previously normotensive
woman with new onset of hypertension and proteinuria after
20 weeks of gestation
• Criteria for diagnosis are:
• Systolic blood pressure ≥140 mmHg or diastolic blood
pressure ≥90 mmHg, and
• Proteinuria ≥0.3 grams in a 24-hour urine specimen or
protein:creatinine ratio ≥0.3 mg/mg or >30 mg/mmol
• For women with chronic / preexisting hypertension who have
proteinuria prior to or in early pregnancy, superimposed
preeclampsia is difficult to diagnose definitively, but should be
suspected when there is a significant worsening of
hypertension (especially acutely) in the last half of pregnancy
[ systolic ≥ 30 or diastolic ≥ 15 ] or development
of signs/symptoms associated with severe preeclampsia .
Post-diagnostic evaluation 

• The purpose of the post-diagnostic evaluation is :


• to determine the severity of disease .
• assess maternal and fetal well-being.

 These factors, as well as gestational age, guide


management
Post-diagnostic evaluation 
• Severity of hypertension (systolic blood pressure ≥160 mm Hg
or diastolic blood pressure ≥110 mm Hg on two occasions at
least six hours apart)
• Severity of proteinuria (≥5 grams/day) .

•  the history and physical examination should evaluate the patient


for:
•Persistent and/or severe headache
•Visual abnormalities (scotomata, photophobia, blurred vision, or
temporary blindness)
•Upper abdominal or epigastric pain
•Nausea, vomiting
Oliguria
Dyspnea
Post-diagnostic evaluation 

• post-diagnostic laboratory/imaging evaluation should include:


• Platelet count
• Serum creatinine
• Serum aspartate aminotransferase (AST) or alanine
aminotransferase (ALT)
• Obstetrical ultrasound (fetal weight, amniotic fluid volume)
• Fetal assessment (biophysical profile or nonstress test)
Management of PE
• The definitive treatment of PE is delivery to prevent
development of maternal or fetal complications from disease
progression.
• Patients with mild or severe PE at or near term should be
delivered.
• Evidence of serious maternal end-organ dysfunction or non-
reassuring tests of fetal well-being are indications for prompt
delivery at any gestational age.
• On the other hand, when mother and fetus are stable, a
conservative approach is reasonable in order to achieve further
fetal growth and maturity
Management of mild PE
•Women with mild PE delivered at ≥37 weeks of gestation.
•Expectant management include :
-Inpatient maternal monitoring initially to establish disease
severity, then follow as outpatient.
-Lab follow-up: plt count, serum creatinine, and serum AST.
(Repeated once or twice weekly).
-Fetal wellbeing can be assessed weekly (ultrasound for fetal
growth, AFI, NST) .
-Antenatal corticosteroids.
-The use of antihypertensive drugs to control mildly elevated BP
does not alter the course of the disease.( not recommended)
Management of sever PE

 Hospitalization until delivery.


 Bed rest.
 Monitor BP every 2 to 4 hours.
 Assess maternal symptoms every 2 to 4 hours.
 Strict fluid intake /output.
 CBC, LFT, KFT (twice weekly if not daily).
 Administer antenatal corticosteroids
 Assess fetal well-being daily with NST and BPP.
 Delivery should occur after 32 to 34 weeks gestation.
Management of sever PE

 Severe hypertension should be treated to prevent maternal


vascular complications ( stroke, heart failure).
• Acute therapy :
- labetalol: 20 mg IV over 2 minutes, repeat after 10-minute by
doses of 20 to 80 mg up to a maximum total cumulative dose
of 300 mg.
- Hydralazine :5 mg IV over 1-2 minutes; if the BP goal is not
achieved within 20 minutes, give 5-10 mg bolus depending upon
the initial response.
Management of sever PE

• Nifedipine :10 mg orally, with repeat doses every 30 minutes


as needed.
For maintenance dosing, 10 to 20 mg can be given every 3 to 6
hours.
• Seizure prophylaxis with magnesium sulfate
Prevention

• Low-dose aspirin is the only drug for which


there is some evidence of benefit in reducing
the risk of preeclampsia. ??
• Ca supplement ?

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