RISK FACTORS EXPLAINED

Risk Factors for Pregnancy-Induced Hypertension (PIH) & Their Explanations

Pregnancy-induced hypertension (PIH), including gestational hypertension and

preeclampsia, is influenced by various maternal, genetic, and environmental factors. Below
is a detailed explanation of the listed risk factors:

1. Higher Incidence in Primiparas Below 17 & Above 35 Years

Primiparas Below 17 Years (Teen Pregnancies)

• Immature cardiovascular system: The body may struggle to adapt to increased blood
volume and vascular changes.
• Immune system immaturity: Less tolerance to the fetus can lead to endothelial
dysfunction and inflammation, increasing PIH risk.
• Poor prenatal care & nutrition: Teens may have low calcium, protein, and
micronutrient intake, leading to vascular instability and poor placental
development.
• Higher rates of preterm labor & fetal complications: Poor placental perfusion can
result in intrauterine growth restriction (IUGR) or placental abruption.

Mothers Above 35 Years

• Aging blood vessels: Reduced elasticity leads to increased vascular resistance,

making hypertension more likely.
• Higher prevalence of pre-existing conditions (e.g., chronic hypertension, diabetes,
obesity), which are risk factors for PIH.
• Reduced placental adaptability: The placenta may not function as efficiently, leading
to placental insufficiency and ischemia.

2. Poor Nutritional Status

• Low calcium intake: Leads to vascular contraction and increased blood pressure
due to impaired relaxation of blood vessels.
• Low protein intake: Can cause low oncotic pressure, leading to edema and
worsening preeclampsia.
• Micronutrient deficiencies (e.g., magnesium, zinc, vitamin D): Essential for blood
vessel health and immune regulation.

3. Low Socioeconomic Status (Low Protein Intake)

• Limited access to healthcare → Delayed diagnosis and management of hypertension.

 • Malnutrition → Poor fetal growth, increased risk of placental ischemia, and
endothelial dysfunction.
• Higher stress levels → Increased cortisol levels, which contribute to vascular
dysfunction and inflammation.

4. History of Chronic Hypertension in the Mother

• Women with pre-existing hypertension are at higher risk of developing

superimposed preeclampsia due to already compromised blood vessel function.
• Increased vascular resistance & poor endothelial function make it harder for blood
vessels to adapt to pregnancy changes.

5. Hydatidiform Mole (H-Mole)

• Molar pregnancies involve abnormal trophoblastic proliferation, leading to

excessive production of hCG (human chorionic gonadotropin).
• Excessive hCG stimulates angiogenesis and can lead to vascular abnormalities,
causing hypertension.

6. Diabetes Mellitus

• Hyperglycemia damages blood vessels → Increased risk of endothelial

dysfunction.
• Increased oxidative stress & inflammation → Contribute to vascular constriction
and placental ischemia.
• Higher rates of macrosomia (large babies) → Increased risk of placental
insufficiency and PIH.

7. Multiple Pregnancies (Twins, Triplets, etc.)

• Increased placental mass leads to higher metabolic and oxygen demands.

• More placental ischemia → Higher likelihood of releasing anti-angiogenic factors,
which impair blood vessel function.
• Increased strain on the maternal cardiovascular system, leading to higher blood
pressure.

8. Polyhydramnios (Excess Amniotic Fluid)

 • Increased uterine stretch → Stimulates maternal stress hormones, which can raise
blood pressure.
• Higher fetal metabolic demands → May contribute to placental dysfunction and
vascular stress.

9. Renal Disease

• Impaired kidney function leads to fluid retention and sodium imbalance, increasing
blood pressure.
• Reduced renal clearance of toxins contributes to systemic inflammation and
endothelial dysfunction, worsening preeclampsia.

10. Heart Disease

• Weakened heart function can lead to poor circulation, which exacerbates

hypertension and organ dysfunction.
• Higher risk of cardiovascular complications in pregnancy, including pulmonary
edema and heart failure.

11. Hereditary Factors

• Women with a family history of PIH or preeclampsia have a higher risk due to:
o Genetic predisposition to endothelial dysfunction.
o Inherited vascular disorders that impair placental blood flow.
o Dysregulated immune response that contributes to inflammation and poor
implantation.
o What Percentage of PIH is Hereditary?
o Research suggests:
✔ 20-40% increased risk if the mother had PIH.
✔ 50-60% increased risk if a sister had PIH.
✔ 2-3 times higher risk if a close female relative (e.g., aunt, grandmother)
had preeclampsia.
✔ Some gene mutations (e.g., related to immune function, blood vessel
development, or clotting) may contribute.
o

12. Previous History of Preeclampsia

• Recurrence risk is high (20-50%) if a woman had preeclampsia in a previous

pregnancy.
 • Indicates underlying vascular dysfunction or autoimmune factors that persist beyond
pregnancy.
• Increased risk of cardiovascular disease later in life, even after pregnancy.

Summary Table: How These Factors Contribute to PIH

Risk Factor How It Leads to PIH

Teen or Advanced Maternal Age Poor vascular adaptation, immune response issues
Poor Nutrition & Low SES Malnutrition → Poor placental health
Chronic Hypertension Pre-existing high BP worsens pregnancy adaptation
H-Mole Excess hCG → Abnormal blood vessel function
Diabetes High blood sugar damages blood vessels
Multiple Pregnancies Higher placental load → More strain on circulation
Polyhydramnios Increased uterine stress hormones raise BP
Renal Disease Poor kidney function → Fluid overload, hypertension
Heart Disease Impaired heart function → Poor circulation
Hereditary Genetic predisposition to endothelial dysfunction
Previous Preeclampsia Persistent vascular damage → Higher recurrence risk
Causes of Pregnancy-Induced Hypertension (PIH) with Unknown Exact
Mechanisms

Although the exact cause of pregnancy-induced hypertension (PIH) and

preeclampsia remains unknown, several theories attempt to explain its
pathophysiology. Here’s a breakdown of the Protein Deficiency Theory, Uterine
Ischemia, and Arterial Vasospasm:

1. Protein Deficiency Theory

Concept:

• This theory suggests that low protein intake leads to poor vascular integrity,
contributing to fluid retention (edema), endothelial dysfunction, and
increased blood pressure.
• Albumin, a key protein in the blood, helps maintain oncotic pressure (the
pressure that keeps fluids in blood vessels).
• Low albumin levels cause fluid to leak into tissues (edema), reducing blood
volume and triggering the renin-angiotensin-aldosterone system (RAAS) to
retain sodium and fluids, leading to hypertension.

How It Contributes to PIH:

• Reduced plasma oncotic pressure → Fluid shifts into tissues → Edema

• Hypovolemia (low blood volume) → Compensatory vasoconstriction →
Hypertension
• Poor placental perfusion → Placental ischemia → Increased release of
inflammatory factors

Current Evidence:

• Some studies show malnutrition (low protein intake) increases the risk of
preeclampsia.
• However, not all preeclamptic patients have protein deficiency, meaning
other factors (genetics, inflammation, and vascular dysfunction) also play a
role.

2. Uterine Ischemia Theory

Concept:
 • Reduced blood flow to the uterus and placenta due to improper remodeling of
the spiral arteries leads to placental ischemia (oxygen deprivation).
• Normally, spiral arteries widen to increase blood supply to the placenta, but in
PIH, they fail to fully dilate, leading to high resistance and poor blood flow.

How It Contributes to PIH:

• Hypoxia (low oxygen levels) → Placental stress → Inflammatory response

• Damaged placenta releases anti-angiogenic factors (sFlt-1, sEng) →
Endothelial dysfunction
• Increased oxidative stress → Further vascular damage and hypertension

Current Evidence:

• Strongest pathophysiological link to preeclampsia.

• Doppler studies confirm abnormal uterine artery blood flow in women with
preeclampsia.
• Uterine ischemia alone does not cause preeclampsia, but combined with
inflammation and genetic predisposition, it significantly increases the risk.

3. Arterial Vasospasm Theory

Concept:

• Widespread vasospasm (narrowing of blood vessels due to excessive

contraction of smooth muscle) is believed to be a major cause of PIH.
• Triggered by abnormal placental factors, leading to high vascular resistance
and hypertension.
• In normal pregnancy, vasodilators (Nitric Oxide & Prostacyclin) balance
vasoconstrictors (Thromboxane & Endothelin).
• In PIH, vasoconstrictors dominate, causing increased blood pressure and
reduced organ perfusion.

How It Contributes to PIH:

• Vasospasm → Reduced placental blood flow → Fetal hypoxia & growth

restriction
• Increased vascular resistance → Hypertension
• End-organ damage (kidneys, liver, brain) → Proteinuria, HELLP syndrome,
eclampsia

Current Evidence:
 • Autopsy studies show vasospasms in the brain, kidney, liver, and placenta of
preeclamptic women.
• Angiotensin II hypersensitivity and increased endothelin levels are
consistent with vasospasm-related hypertension.

Summary Table: Comparing Theories

Theory Main Concept How It Causes PIH Supporting Evidence

Low protein intake Fluid retention, edema, Malnutrition increases
Protein
affects oncotic hypovolemia, PIH risk, but not always
Deficiency
pressure vasoconstriction present in all cases
Strong evidence;
Placental stress, release
Uterine Poor placental blood abnormal uterine artery
of anti-angiogenic
Ischemia flow leads to hypoxia flow found in
factors, oxidative stress
preeclamptic women
Widespread blood
Increased BP, reduced Histological studies
Arterial vessel narrowing
organ perfusion, end- show vasospasms in
Vasospasm increases vascular
organ damage major organs
resistance
Physiological Effects of Pregnancy-Induced Hypertension (PIH) &
Preeclampsia

Pregnancy-Induced Hypertension (PIH) and preeclampsia cause widespread vascular

dysfunction, leading to multiple systemic effects on the heart, blood volume,
clotting system, and red blood cells. Here’s how each factor is affected:

1. Decreased Cardiac Output 🫀

What Happens?

• Vasospasm and increased afterload (vascular resistance) force the heart to

pump against higher pressure, straining the heart.
• Initially, there may be hyperdynamic circulation (increased cardiac output) to
compensate, but as the disease progresses, cardiac output declines due to
increased vascular resistance and endothelial dysfunction.
• In severe cases, left ventricular dysfunction can lead to pulmonary edema
and heart failure.

Key Consequences:

• Poor oxygen delivery to organs

• Risk of pulmonary edema
• Heart strain and potential failure in severe cases

Evidence:

• Echocardiographic studies show reduced cardiac output in severe

preeclampsia.

2. Hemoconcentration (Increased Blood Viscosity)

What Happens?

• Normally, blood volume expands in pregnancy, but in PIH/preeclampsia,

vasospasm and endothelial leakage cause fluid to shift into tissues, leading
to intravascular dehydration.
• This results in higher hematocrit levels (thicker blood), making circulation more
sluggish and increasing clotting risks.

Key Consequences:
 • Increased risk of thrombosis (blood clots)
• Reduced organ perfusion (brain, kidneys, liver)
• Higher risk of stroke

Evidence:

• Studies show higher hematocrit levels in preeclamptic patients, indicating

hemoconcentration.

3. Failure of Blood Volume to Expand (Compared to Normotensive

Pregnant Women)

What Happens?

• In normal pregnancy, blood volume increases by ~40-50% to support fetal

needs.
• In PIH, this expansion fails to occur due to vasoconstriction, endothelial
dysfunction, and increased capillary permeability.
• This worsens hemoconcentration and reduces oxygen delivery to tissues.

Key Consequences:

• Poor placental perfusion → Fetal growth restriction

• Increased risk of hypoxia-related complications

Evidence:

• Studies confirm reduced plasma volume in preeclampsia, worsening maternal

and fetal outcomes.

4. Thrombocytopenia (Low Platelet Count)

What Happens?

• Endothelial dysfunction leads to platelet activation and consumption in tiny

blood clots.
• This causes a drop in platelet levels and is a key sign of HELLP syndrome.
• Thrombocytopenia is usually defined as platelet count <100,000/mm³ in
preeclampsia.

Key Consequences:
 • Increased risk of bleeding (especially postpartum hemorrhage)
• HELLP syndrome progression
• Poor clotting function

Evidence:

• Low platelet count is one of the diagnostic criteria for severe preeclampsia
and HELLP syndrome.

5. Increased Clotting Factors (Prolonged Prothrombin Time - PT)

What Happens?

• In preeclampsia, the liver releases more clotting factors in response to

vascular injury, making blood more prone to clotting.
• However, in severe cases (HELLP, DIC - Disseminated Intravascular
Coagulation), clotting factors are excessively used up, leading to prolonged PT
and increased bleeding risk.

Key Consequences:

• Increased risk of clot formation (DVT, pulmonary embolism)

• Potential for DIC (Disseminated Intravascular Coagulation) → Life-
threatening
• Risk of excessive postpartum bleeding

Evidence:

• Higher fibrinogen levels and prolonged PT are observed in severe

preeclampsia cases.

6. Abnormal RBC Formation (Mishappen & Short Life Span)

What Happens?

• Microangiopathic Hemolysis (RBC damage due to narrowed blood vessels)

occurs in HELLP syndrome.
• Increased vascular resistance forces RBCs to squeeze through narrowed
vessels, damaging their structure (schistocytes seen in blood smear).
• RBCs break down faster, leading to anemia and increased bilirubin levels.
 Key Consequences:

• Hemolysis (RBC destruction) → Anemia → Fatigue & weakness

• Jaundice (due to increased bilirubin from hemolysis)
• Risk of worsening oxygen delivery

Evidence:

• Blood smears show fragmented RBCs in severe preeclampsia and HELLP

syndrome.

Summary Table: Physiological Effects of PIH/Preeclampsia

Effect Cause Consequences Clinical Findings

Reduced organ Heart strain, left
Decreased Cardiac Increased vascular
perfusion, risk of ventricular
Output resistance
pulmonary edema dysfunction
Fluid shifts out of Thickened blood, High hematocrit
Hemoconcentration
blood vessels increased clot risk levels
Poor vascular
Failure of Blood Hypoxia, poor fetal Lower plasma
adaptation in
Volume Expansion growth volume
pregnancy
Increased platelet Bleeding risk, HELLP Platelet count
Thrombocytopenia
consumption syndrome <100,000/mm³
Elevated
Increased Clotting Clot formation, risk of
Endothelial damage fibrinogen,
Factors DIC
prolonged PT
Abnormal RBC Microangiopathic Hemolysis, anemia, Schistocytes in
Formation hemolysis jaundice blood smear

Final Takeaway

• Preeclampsia is a multisystem disorder that affects the heart, blood volume,

clotting system, and red blood cells.
• Severe complications include HELLP syndrome, DIC, and organ failure.
• Early detection and management (e.g., blood pressure control, magnesium
sulfate for seizure prevention) can prevent serious outcomes.
Hormonal Changes in Pregnancy-Induced Hypertension (PIH) &
Preeclampsia

Pregnancy normally causes significant hormonal changes to regulate blood pressure

and fluid balance. However, in PIH and preeclampsia, these hormonal systems
become dysregulated, contributing to hypertension, fluid retention, and vascular
damage.

1. Increased Renin Levels

What Happens?

• Renin, produced by the kidneys, is responsible for activating the renin-

angiotensin-aldosterone system (RAAS) to regulate blood pressure.
• Normally, pregnancy downregulates renin due to increased blood volume, but
in PIH, renin levels remain high due to poor placental perfusion and kidney
ischemia.
• Vasoconstriction & sodium retention increase, leading to high blood
pressure.

Key Consequences:

• Increased vascular resistance (vasoconstriction)

• Worsening hypertension
• Further kidney damage

Evidence:

• Studies show elevated renin activity in preeclampsia despite high blood

pressure, suggesting an abnormal response.

2. Increased Angiotensin II (ANG II) Levels

What Happens?

• Angiotensin II is a powerful vasoconstrictor that increases blood pressure

and stimulates aldosterone release.
• Normally, pregnancy reduces vascular sensitivity to ANG II, but in
PIH/preeclampsia, the body becomes more sensitive to its effects, causing
excessive vasoconstriction.
 • This leads to high blood pressure, kidney damage, and endothelial
dysfunction.

Key Consequences:

• Increased blood pressure (worsened hypertension)

• Decreased uteroplacental blood flow → Fetal growth restriction
• Increased endothelial damage → Proteinuria, HELLP syndrome

Evidence:

• Women with preeclampsia have higher vascular responsiveness to ANG II,

leading to more severe hypertension.

3. Increased Aldosterone Levels

What Happens?

• Aldosterone, secreted by the adrenal glands, promotes sodium & water

retention to maintain blood volume.
• Normally, pregnancy increases aldosterone to compensate for expanded
blood volume, but in PIH/preeclampsia, aldosterone levels paradoxically
rise despite vasoconstriction and fluid retention.
• This leads to excessive fluid retention, contributing to edema and
hypertension.

Key Consequences:

• Increased fluid retention → Edema (swelling)

• Hypertension due to increased sodium & water reabsorption
• Higher risk of pulmonary edema in severe cases

Evidence:

• Elevated aldosterone levels are detected in preeclamptic women, worsening

fluid overload and hypertension.

4. Increased Antidiuretic Hormone (ADH) Levels

What Happens?
 • ADH (vasopressin) regulates water balance by reducing urine output and
increasing water retention.
• In PIH/preeclampsia, ADH secretion increases abnormally due to
endothelial dysfunction and low circulating blood volume (despite fluid
retention).
• This causes further fluid overload, worsening edema and hypertension.

Key Consequences:

• Oliguria (low urine output) despite high blood pressure

• Fluid retention → Worsened pulmonary & peripheral edema
• Risk of seizures in severe eclampsia (cerebral edema)

Evidence:

• Increased ADH activity is associated with fluid imbalance and oliguria in

severe preeclampsia.

Summary Table: Hormonal Changes in PIH & Preeclampsia

Clinical
Hormone Effect Consequence
Findings
Activates RAAS, Worsens vasoconstriction, High blood
Renin increases ANG II & hypertension, kidney pressure,
aldosterone damage proteinuria
Increases BP, reduces Worsened fetal
Angiotensin II Potent vasoconstrictor
placental blood flow growth restriction
Swelling,
Promotes sodium & Increases edema, worsens
Aldosterone pulmonary
water retention hypertension
edema
Oliguria,
Antidiuretic Reduces urine output, Causes fluid overload,
neurological
Hormone (ADH) retains water cerebral edema
symptoms

Final Takeaway

• In PIH/preeclampsia, these hormones become dysregulated, worsening

hypertension, fluid retention, and organ damage.
• Management focuses on blood pressure control (e.g., antihypertensives)
and fluid balance monitoring to prevent severe complications like eclampsia
and HELLP syndrome.
Renal Changes in Pregnancy-Induced Hypertension (PIH) &
Preeclampsia

In PIH and preeclampsia, renal function is significantly impaired due to

vasospasm, endothelial dysfunction, and decreased blood flow to the kidneys.
This results in reduced filtration, fluid retention, and accumulation of waste
products, which can lead to kidney damage and multi-organ complications.

1. Reduced Renal Perfusion & Glomerular Filtration Rate (GFR)

What Happens?

• Vasospasm and endothelial dysfunction cause narrowing of renal arteries,

reducing blood flow to the kidneys.
• This leads to a decrease in the glomerular filtration rate (GFR), meaning the
kidneys filter less blood per minute.
• The body retains more waste products and fluids, worsening hypertension
and edema.

Key Consequences:

• Fluid retention → Increased blood pressure and swelling

• Accumulation of waste products (urea, creatinine, uric acid)
• Increased risk of acute kidney injury (AKI) in severe cases

Evidence:

• GFR is significantly reduced in preeclampsia, leading to impaired kidney

function and fluid overload.

2. Elevated Creatinine, Uric Acid, and Urea

What Happens?

• With reduced kidney filtration, waste products (creatinine, urea, and uric acid)
accumulate in the blood.
• Creatinine is a marker of kidney function, and its elevation indicates kidney
impairment.
• Uric acid levels increase due to endothelial damage and reduced excretion,
contributing to further vascular dysfunction.
 Key Consequences:

• Increased risk of kidney damage and acute kidney injury (AKI)

• Hyperuricemia (high uric acid) → Worsens endothelial dysfunction &
hypertension
• Neurological symptoms (confusion, drowsiness) in severe cases

Evidence:

• Serum creatinine, urea, and uric acid levels are significantly elevated in
preeclamptic women, often indicating renal impairment.

3. Decreased Urinary Excretion of Calcium

What Happens?

• Normally, pregnancy increases calcium excretion in urine.

• In preeclampsia, calcium retention occurs due to impaired renal function,
leading to low urinary calcium levels.
• Low calcium levels may contribute to increased blood pressure by affecting
vascular smooth muscle contraction.

Key Consequences:

• Increased risk of kidney stones due to retained calcium

• Worsened vasoconstriction and hypertension
• Potential link to fetal growth restriction

Evidence:

• Studies show low urinary calcium excretion in preeclampsia, suggesting a

role in hypertension development.

4. Decreased Urine Output (Oliguria)

What Happens?

• Severe vasoconstriction reduces kidney perfusion, leading to low urine

production (oliguria).
• The body retains more fluid, worsening hypertension and edema.
 • If urine output drops too low (<500 mL/day), it may indicate acute kidney
injury (AKI), requiring urgent treatment.

Key Consequences:

• Fluid overload → Pulmonary edema (difficulty breathing)

• Severe kidney damage (acute renal failure)
• Risk of metabolic imbalances (electrolyte disturbances, acidosis)

Evidence:

• Oliguria (<500 mL/day) is a sign of severe preeclampsia and kidney

dysfunction.

5. Proteinuria (Protein in Urine)

What Happens?

• Glomerular endothelial damage causes leakage of proteins (especially

albumin) into urine.
• Loss of albumin in urine leads to low oncotic pressure, causing fluid to leak
into tissues → worsening edema.
• Proteinuria (>300 mg/day) is a key diagnostic criterion for preeclampsia.

Key Consequences:

• Severe swelling (face, hands, feet) due to loss of albumin

• Increased risk of kidney failure
• Indicates worsening endothelial damage & progression toward HELLP
syndrome

Evidence:

• Proteinuria is a major marker of kidney dysfunction in preeclampsia and

helps differentiate it from gestational hypertension.

Summary Table: Renal Changes in PIH & Preeclampsia

Renal Change Cause Consequence Clinical Findings

Reduced renal Vasospasm, Impaired filtration, fluid High BP, edema,
perfusion & GFR endothelial retention kidney injury
 Renal Change Cause Consequence Clinical Findings
dysfunction
Waste buildup, High blood urea,
Elevated creatinine,
Decreased filtration worsened creatinine, uric
uric acid, & urea
hypertension acid
Decreased calcium Impaired kidney Hypertension, kidney Low urinary
excretion function stone risk calcium
Decreased urine Severe Fluid overload, kidney Low urine output
output (oliguria) vasoconstriction failure risk (<500 mL/day)
Worsened edema, Protein >300
Proteinuria Endothelial damage
kidney dysfunction mg/day in urine

Final Takeaway

• Renal function is severely affected in PIH and preeclampsia, leading to fluid

retention, high blood pressure, and waste buildup.
• Proteinuria and oliguria indicate worsening disease and may progress to
kidney failure if untreated.
• Monitoring kidney function (creatinine, urine output, proteinuria) is crucial
to prevent severe complications.
Warning Signs of Severe Preeclampsia & Imminent Eclampsia 🚨

Preeclampsia can rapidly progress into a life-threatening condition if not managed

promptly. The following warning signs indicate severe preeclampsia or impending
eclampsia, requiring immediate medical attention.

1. Rapid Weight Gain (4-5 lbs in a Single Week)

What Happens?

• Excess fluid retention (edema) due to leaky blood vessels causes sudden
weight gain.
• Normally, weight gain in pregnancy is gradual, but in preeclampsia, rapid
weight gain suggests severe fluid retention and worsening vascular
dysfunction.

Why It’s Dangerous?

• Sign of worsening endothelial damage & kidney dysfunction

• Can lead to fluid overload & pulmonary edema (difficulty breathing)

2. Sudden Swelling (Edema)

What Happens?

• Swelling occurs due to fluid leaking from blood vessels into surrounding
tissues.
• Normally, mild swelling in pregnancy is common, but in preeclampsia, it
becomes sudden, severe, and persistent.

Why It’s Dangerous?

• Indicates worsening kidney damage (proteinuria) & vascular dysfunction

• Severe swelling can signal pulmonary edema (fluid in the lungs), leading to
breathing difficulty

3. Swelling of the Face & Hands

 What Happens?

• Swelling in non-dependent areas (face, hands) suggests severe vascular

leakage rather than normal pregnancy-related swelling.
• This occurs due to low oncotic pressure from protein loss in urine
(proteinuria).

Why It’s Dangerous?

• Severe preeclampsia marker

• Can progress to pulmonary edema & brain swelling (cerebral edema),
increasing the risk of seizures (eclampsia)

4. Swelling of Ankles & Feet That Does Not Go Away After a 12-Hour
Rest

What Happens?

• Normally, mild swelling in pregnancy reduces with rest.

• Persistent swelling despite rest suggests severe fluid overload & kidney
dysfunction.

Why It’s Dangerous?

• Indicates progressive kidney damage & worsening hypertension

• High risk of developing pulmonary edema

5. Rise in Blood Pressure (BP)

What Happens?

• Preeclampsia is characterized by sustained high blood pressure (≥140/90

mmHg).
• Severe preeclampsia is defined as BP ≥160/110 mmHg.

Why It’s Dangerous?

• Increased risk of stroke, seizures (eclampsia), and placental abruption

• Decreased placental blood flow → Fetal distress & growth restriction
6. Proteinuria (Protein in Urine)

What Happens?

• Leaky glomerular membranes allow protein (especially albumin) to escape

into urine.
• Loss of protein leads to low oncotic pressure, worsening edema and fluid
overload.

Why It’s Dangerous?

• Key diagnostic feature of preeclampsia (>300 mg protein/day in urine)

• Indicates significant kidney damage and progression to HELLP syndrome

When to Seek Emergency Care?

If a pregnant woman experiences any of these symptoms, urgent medical attention

is required.
Other severe symptoms include:

• Severe headache (sign of cerebral edema)

• Vision changes (blurry vision, seeing spots) (retinal damage)
• Upper right abdominal pain (RUQ pain, epigastric pain) (liver damage)
• Seizures (eclampsia)

7. Severe Headaches

What Happens?

• Vasoconstriction and increased blood pressure cause reduced blood flow

to the brain.
• Cerebral edema (brain swelling) further worsens the headache.
• The pain is usually persistent, throbbing, and unrelieved by medication.

Why It’s Dangerous?

• Warning sign of impending eclampsia (seizures)

• Risk of stroke (intracranial hemorrhage) due to high BP
• Can indicate hypertensive crisis
8. Blurry Vision

What Happens?

• Hypertension and vasospasms reduce blood flow to the retina, leading to

visual disturbances.
• Fluid leakage into the optic nerve (papilledema) can also cause blurred vision.
• Retinal detachment may occur in severe cases.

Why It’s Dangerous?

• Sign of severe cerebral vasospasm & retinal damage

• Increases risk of seizures (eclampsia)
• Possible permanent vision loss if untreated

9. Seeing Spots (Scotoma) or Light Flashes

What Happens?

• Vasospasms in the retinal arteries cause temporary blindness, light

sensitivity, or flashing lights.
• Often occurs with blurry vision and headaches.

Why It’s Dangerous?

• Indicates severe preeclampsia with neurological involvement

• May precede an eclamptic seizure
• Risk of retinal detachment or permanent visual impairment

10. Severe Pain Over the Stomach & Under the Ribs (Epigastric or RUQ
Pain)

What Happens?

• Liver swelling & ischemia (reduced blood flow) cause upper right quadrant
(RUQ) pain.
• May be due to HELLP syndrome (Hemolysis, Elevated Liver Enzymes, Low
Platelets).
• Liver capsule distension & microvascular damage cause intense pain.
 Why It’s Dangerous?

• Indicator of HELLP syndrome → Risk of liver rupture or failure

• Severe pain + nausea/vomiting = Critical emergency
• Associated with increased risk of internal bleeding

11. Decrease in the Amount of Urine (Oliguria)

What Happens?

• Reduced kidney perfusion due to vasoconstriction leads to low urine

output.
• Kidneys cannot effectively filter waste, causing fluid retention, swelling, and
worsening hypertension.
• Oliguria (<500 mL urine/day) suggests renal impairment.

Why It’s Dangerous?

• Sign of kidney failure (acute kidney injury - AKI)

• High risk of metabolic imbalances & fluid overload
• May require dialysis if severe
SCRIPT PATHOPHYSIO
Pathophysiology of Hypertensive Disorders of Pregnancy (Based on the Image)

The image outlines the development of preeclampsia, hypertension, proteinuria, and HELLP
syndrome, beginning with modifiable and non-modifiable risk factors. Here’s a step-by-step
breakdown of the process:

Step 1: Risk Factors

Risk factors are divided into two categories:

A. Modifiable Risk Factors (Can be changed through lifestyle and medical intervention)

1. Obesity – Increases inflammation and vascular dysfunction, leading to endothelial damage.

2. Physical Inactivity (Sedentary Lifestyle) – Reduces cardiovascular health, making the

circulatory system more susceptible to dysfunction.

3. Dietary Factors (High-Salt Intake) – Causes fluid retention, increasing blood pressure.

4. Smoking – Causes vasoconstriction and oxidative stress, damaging blood vessels.

5. Stress – Increases cortisol and sympathetic activity, raising blood pressure.

6. Imbalance of Th17/T-reg Cells – Leads to an exaggerated immune response, increasing

inflammation and endothelial damage.

B. Non-Modifiable Risk Factors (Cannot be changed)

 1. Previous Preeclamptic Pregnancies – Women with past preeclampsia have a higher risk due to
vascular and immune system memory.

2. Multiple Gestation (Higher Placental Mass) – More placenta means higher demand on blood
supply, increasing risk.

3. Primigravida (First Pregnancy) – The first pregnancy exposes the maternal immune system to
placental factors, making it more vulnerable to dysfunction.

4. Advanced Maternal Age (>35 Years Old) – Blood vessels are less elastic, increasing the risk of
hypertension.

5. Genetic Factors (Family History of Hypertension) – Inherited vascular sensitivity and

endothelial dysfunction increase susceptibility.

6. Collagen Vascular Disease – Autoimmune diseases affecting blood vessels (e.g., lupus)
increase endothelial dysfunction risk.

Step 2: Abnormal Uterine Vascular Remodeling in Early Pregnancy

• Normally, trophoblast cells invade maternal spiral arteries, transforming them into low-
resistance, high-capacity vessels to ensure adequate blood flow to the placenta.

• In hypertensive disorders, this remodeling is incomplete, leading to narrow, high-resistance

vessels that limit blood flow to the placenta.

Step 3: Reduced Placental Perfusion

• Due to poor remodeling of spiral arteries, the placenta receives insufficient blood supply.

• This results in placental hypoxia (low oxygen levels) and oxidative stress.

Step 4: Placental Dysfunction

• The hypoxic placenta fails to function properly, leading to the release of inflammatory
mediators, anti-angiogenic factors (like sFlt-1), and oxidative stress molecules into the
maternal circulation.

• These factors cause widespread endothelial dysfunction.

Step 5: Systemic Maternal Endothelial Dysfunction

The endothelium (inner lining of blood vessels) becomes damaged and dysfunctional, leading to:
 1. Increased Angiotensin II (ANGII) Sensitivity – Blood vessels overreact to normal levels of
ANGII, causing excessive vasoconstriction and increased blood pressure.

2. Increased Thromboxane (TBX) – Promotes vasoconstriction and clot formation, reducing

placental and systemic blood flow.

3. Increased Endothelin (ET) – A potent vasoconstrictor that further narrows blood vessels,
worsening hypertension.

4. Decreased Prostacyclin (PGI₂) – Reduces vasodilation and increases clotting, further

increasing vascular resistance.

5. Decreased Nitric Oxide (NO) – Prevents blood vessels from relaxing, maintaining high blood
pressure.

These changes lead to renal pressure natriuresis (impaired ability of the kidneys to excrete sodium
and fluid), further increasing blood volume and hypertension.

Step 6: Clinical Consequences

Depending on how severe the endothelial dysfunction is, different complications arise:

1. Hypertension – Due to excessive vasoconstriction from ANGII, TBX, and ET, along with
reduced PGI₂ and NO.

2. Proteinuria (Glomerular Endotheliosis) – Kidney damage causes protein to leak into urine, a
key sign of preeclampsia.

3. HELLP Syndrome (Hemolysis, Elevated Liver Enzymes, Low Platelets) –

o Hemolysis: Small blood clots damage red blood cells.

o Elevated Liver Enzymes: Blood clots reduce liver blood flow, leading to liver damage.

o Low Platelets: Platelets are used up in small clots, leading to a low platelet count.

Final Summary

The pathway starts with modifiable and non-modifiable risk factors, leading to poor placental blood
flow, hypoxia, and placental dysfunction. This triggers endothelial dysfunction, leading to
hypertension, kidney damage (proteinuria), and severe complications like HELLP syndrome.

The timing of preeclampsia onset (early vs. late) depends on various maternal, fetal, and placental
factors. Some women experience it early in pregnancy (before 34 weeks), while others develop it later
(after 34 weeks, often near term).