Carmel Christy MM20505 MD student

L22: Hypertensive disorder of pregnancy

• Introduction
o Most common
o 4 categories
▪ Chronic hypertension → high bp even b4 20weeks of gestation
▪ Preeclampsia/eclampsia
▪ Preeclampsia superimposed on chronic hypertension → Preeclampsia that occurred b4
20 weeks of gestation
▪ Gestational hypertension (pregnancy-induced hypertension) → Hypertension when
pregnant. Hypertension start after 20 weeks of gestation. Usually by 12 weeks
postpartum, hypertension would resolve.
• Chronic Hypertension in Pregnancy
o High bp that either precedes pregnancy, diagnosed within the first 20 weeks or do not resolve
by 12 weeks postpartum
o Prevalence rate are increasing due to delayed childbearing
• Preeclampsia and eclampsia
Preeclampsia Eclampsia
• Systemic syndrome characterized by • Preeclampsia + convulsion
widespread maternal endothelial dysfunction • The development of convulsion in preexisting
presenting clinically with hypertension, preeclampsia or it may appear unexpectedly
oedema, & proteinuria during pregnancy in a patient with minimally elevated blood
• Define → Elevated blood pressure after 20 pressure and no proteinuria
weeks of gestation (of more than 140mmHg • Reverse rapidly on termination of pregnancy
systolic or more than 90mmHg diastolic) plus but can be fatal
proteinuria (of more than 0.3g/24hrs)
• Usually in the last trimester
• Commonly in primigravida (women first preg)
• Btw addition: if new husband also counts as
first preg also hence, risk increase to have

o Other complications of endothelial dysfunction:

▪ Hypercoagulability
▪ Acute renal failure
▪ Pulmonary oedema
o Approximately 10% women with severe preeclampsia develops HELLP syndrome
▪ Hemolysis
Carmel Christy MM20505 MD student

▪ Elevated liver enzymes & low platelets

o Preeclampsia should be distinguished from gestational hypertension that can develop in
pregnancy without proteinuria
• Pathogenesis
o Placenta play central role in patho of preeclampsia
o Symptoms disappear after delivery of placenta
o Critical abnormalities in preeclampsia
▪ Diffuse endothelial dysfunction
▪ Vasoconstriction → Lead to hypertension
▪ Increased vascular permeability → Proteinuria & Oedema
Pathogenesis of preeclampsia
(1) Abnormal • Abnormal trophoblastic implantation & lack of development of physiologic
placental alterations in the maternal vessels required for adequate perfusion of the
vasculature placental bed
• Failure of remodeling (conversion of the decidual spiral arteries from small-
caliber resistance vessels to large capacity uteroplacental vessels lacking a
smooth muscle coat)
• Placental not equipped to meet the increased circulatory demands of the late
gestation and setting the stage for the development of placental ischemia
(2) Endothelial • In response to hypoxia, The ischemic placenta releases factors into the
dysfunction & maternal circulation → Imbalance in circulating angiogenic & antiangiogenic
imbalance of factors → Systemic maternal endothelial dysfunction and the clinical
angiogenic & symptoms of the disease
antiangiogenic • Anti-angiogenic factors → Soluble fms-like tyrosine kinase (sFltl) & endoglin
factors is high in preeclampsia women
• High sFltl & soluble endoglin → Decrease in angiogenesis → Defective
vascular development in the placenta
(3) Coagulation • Preeclampsia is associated with hypercoagulable state
abnormalities • Related to the reduced endothelial production of PGI2 (potent antithrombotic
factor), & increased release of procoagulant factors
• Thrombosis of arterioles and capillaries may occur throughout the body,
particularly in the liver, kidneys, brain, and pituitary.
Carmel Christy MM20505 MD student

• Morphology
Placenta • Placental infarcts
• Retroplacental hematomas → due to bleeding & instability of uteroplacental vessels
• Decidual vessels → Thrombosis, fibrinoid necrosis, or intraintimal lipid deposition
(acute atherosis)
• Reflecting abnormal implantation
• Acute atherosis of uterine vessels in eclampsia:

Liver Gross: Microscopic:

• Irregular • Fibrin thrombi in the portal capillaries
• Focal and foci of hemorrhagic necrosis
• Subcapsular
• Intraparenchymal hemorrhages
Kidney • Bilateral renal cortical necrosis
• Histologically → Fibrin thrombi are present in the glomeruli & capillaries of the cortex
Brain • Gross or microscopic foci of hemorrhage along small-vessel thromboses
• Similar changes are often found in the heart and the anterior pituitary

• Clinical features
Preeclampsia • Most common starts after 34 weeks of gestation
• Begin earlier in women with hydatidiform mole or preexisting kidney disease,
hypertension, or coagulopathies
• Onset → Insidious Characterized by Hypertension & Oedema, with proteinuria
following within several days
• Headache & visual disturbance (Serious indicator, often require delivery)
Eclampsia Central nervous involvement → Convulsions and eventual coma

• Risk factors for preeclampsia

o First pregnancy
o First pregnancy with new partner or long inter-pregnancy interval
o Preeclampsia in previous pregnancy
Carmel Christy MM20505 MD student

o Age <20y or >35y

o Multiple pregnancy (singleton < twin < triplets etc)
o Preexisting hypertension
o Preexisting renal disease
• Investigation
Urinalysis • Look presence of protein in urine
Fetal assessment – • Fetal biometry
Fetal ultrasound - To diagnose or exclude fetal growth restriction (ultrasound 2 weeks
assessment apart)
• Amniotic fluid assessment
Maternal investigation Full blood count
- Reduce platelet in HELLP syndrome
Renal function test
- Serum creatinine → Underlying renal ds
- Serum uric acid → Elevated in severe preeclampsia
Liver function tests
- Increase transaminase level in HELLP syndrome

• Management
o Depend upon gestational age & severity
▪ For long term pregnancies → Delivery
▪ In preterm pregnancies → Close monitoring in mild case
o Indication for delivery (regardless of gestational age)
▪ Eclampsia
▪ Severe preeclampsia with
• Maternal end-organ dysfunction
• Fetal compromise
• HELLP syndrome (hemolysis, elevated liver enzymes & low platelets)
• HELLP syndrome
o Hemolysis, elevated liver enzymes & low platelets
o Usually presents at 27-36 wks of pregnancy with Hypertension, proteinuria and fluid retention
o Jaundice → 5%
o Blood test → Low hemoglobin, with Fragmented red cells, markedly elevated serum
transaminases and rises D-dimers
o Maternal complication → Disseminated intravascular coagulation and placental abruption
o Maternal mortality → 1%
Carmel Christy MM20505 MD student

o Perinatal mortality → up to 30%