HYPERTENSIVE DISORDERS OF

PREGNANCY

JEHAD AL-HARMI
DEPARTMENT OF OBS & GYN
FACULTY OF MEDICINE /KUWAIT UNIVERSITY
 LAKSHMI
– 32 years old. Indian housewife. MF 8/12
– G1. GA = 30/52
– Presented with blurring of vision X 3 h
– O/E BP = 210/120 mmHg
– Admitted to ICU for control of BP
– Suddenly she started shouting at the nurses
to “turn the lights back on”
 LAKSHMI
– 32 years old. Indian housewife. MF 8/12
– G1. GA = 30/52
– Presented with blurring of vision X 3 h
– O/E BP = 210/120 mmHg
– Admitted to ICU for control of BP
– Suddenly she started shouting at the nurses
to “turn the lights back on”
– CORTICAL BLINDNESS
 FAT’HIYA
– 42 year old. Egyptian teacher. MF 3 years
– G5 P0+0+4+0. GA = 34/52
– Delivered by CS for HELLP syndrome 2 d ago
– She went to the toilet unassisted
– Found ½ h later unconscious
– Laparotomy carried out for hemoperitoneum
– Patient died on the table
 FAT’HIYA
– 42 year old. Egyptian teacher. MF 3 years
– G5 P0+0+4+0. GA = 34/52
– Delivered by CS for HELLP syndrome 2 d ago
– She went to the toilet unassisted
– Found ½ h later unconscious
– Laparotomy carried out for hemoperitoneum
– Patient died on the table
– RUPTURED HEPATIC HEMATOMA
 MALEEHA
– 38 year old. Kuwaiti secretary. MF 10 years
– G5 P2+2+0+4. GA = 38/52. No ANC
– Morbidly obese, diabetic & hypertensive
– Presented with loss of FM X 2 d & heavy vaginal
bleeding X 2 h. BP = 200/100 mmHg
– Delivered in RR; macerated SB. BW= 1000g
– She had a fit immediately after delivery; she was
rushed to ICU. Cardiac arrest 10 minutes later
 MALEEHA
– 38 year old. Kuwaiti secretary. MF 10 years
– G5 P2+2+0+4. GA = 38/52. No ANC
– Morbidly obese, diabetic & hypertensive
– Presented with loss of FM X 2 d & heavy vaginal
bleeding X 2 h. BP = 200/100 mmHg
– Delivered in RR; macerated SB. BW= 1000g
– She had a fit immediately after delivery; she was
rushed to ICU. Cardiac arrest 10 minutes later
– ECLAMPSIC FIT
 INTRODUCTION

• Pre-eclampsia (PE) complicates 7% of all

pregnancies
• Second to pulmonary embolism as a cause of
maternal mortality; responsible for 15% of all
maternal deaths
• Important cause of perinatal morbidity & mortality
due to direct fetal effects & iatrogenic preterm
delivery for maternal sake
 TERMINOLOGY - 1

• Many classifications
• National High Blood Pressure Education
Program Working Group revised the
classification system in 2000
• Adopted by ACOG
• 4 categories are recognized
 TERMINOLOGY - 2

1. CHRONIC HYPERTENSION
2. PE
3. GESTATIONAL HYPERTENSION
4. CHRONIC HYPERTENSION WITH
SUPERIMPOSED PE
 TERMINOLOGY - 3
• Chronic hypertension:
– Predates the pregnancy
– Identified before 20/52 gestation
– Exceptions:
• GTD
• Fetal triploidy
• Hydrops fetalis
• Drugs (eg, cocaine)
– Persists > 12/52 postpartum
 TERMINOLOGY - 4
• PE:
– PE is a multi-organ disease process affecting
• Kidneys
• CNS
• Liver
• Hematological system
– Hypertension and proteinuria
– Absolute rather than relative definition for BP
– 24-hour urine collection or dipstick
 TERMINOLOGY - 5

• Gestational hypertension:
– High BP after 20/52 pregnancy without
proteinuria
– Previously termed pregnancy-induced
hypertension (PIH)
• Chronic hypertension with superimposed
PE:
– Increased BP and proteinuria in a woman
known to have chronic hypertension
 EPIDEMIOLOGY - 1

WHAT ARE THE RISK FACTORS FOR

PE?
 EPIDEMIOLOGY - 2

WHAT ARE THE RISK FACTORS FOR PE?

– Chronic renal disease (20X)
– Antiphospholipid syndrome (10X)
– Chronic hypertension (10X)
– Nulliparity (3X) : incidence in primigravidas is 14-22%
compared with 6-7% in multiparous women
– Extremes of age: < 15 or > 35 years (3X for latter)
 EPIDEMIOLOGY - 3

WHAT ARE THE RISK FACTORS FOR PE?

– Family history of PET in a 1st degree relative (5X)
– Multiple pregnancy (4X)
– DM (2X)
– Black race
– Sickle cell disease
– Hydrops fetalis, mirror syndrome
– Altered paternity
 EPIDEMIOLOGY - 4

• Recurrence rate of PE:

– For primigravidas 25%
– For multiparas 50%
– Affected by:
• GA at onset of PE in the index pregnancy
• Severity
• Presence of underlying maternal disease
• No increased risk for chronic hypertension in the
future except in the cases of recurrent PE
 CLINICAL FEATURES - 1

• HYPERTENSION:
– Increase in BP to 140 mm Hg systolic or 90 mm Hg
diastolic
– Sustained (at least 2 readings 6 hours apart within
the same week)
– Ideal measurement in sitting or lateral decubitus
position (upper arm)
– Which is better for diastolic BP IV or V Korotcoff
sound? Why?
 CLINICAL FEATURES - 2

• Classically PE used to be defined as a

triad of hypertension, dependent edema,
and proteinuria

• But nowadays edema is no longer

required to make the diagnosis

• Why?
 CLASSIFICATION - 1

• MILD OR SEVERE
• NO MODERATE CATEGORY IN PE
• Criteria for severity:
– BP>160 mm Hg systolic or 110 mm Hg diastolic
– Proteinuria > 5 g/24 hour (normal < 300 mg). How
does this correlate with the dipstick values?
– Elevated serum creatinine
– Grand-mal seizures (eclampsia)
 CLASSIFICATION - 2

• Criteria for severity:

– Pulmonary edema
– Oliguria (urine output < 500 cc/24 hour)
– Microangiopathic hemolysis
– Thrombocytopenia (platelets < 100)
– Hepatocellular damage (elevated ALT & AST)
– IUGR or IUFD
– Oligohydramnios (AFI < 5 cm)
– Headache, visual disturbances, epigastric or RUQ pain
 ETIOLOGY - 1

UNKNOWN
1. IMMUNE RESPONSE:
– Inadequate maternal antibody production to fetal
allograft resulting in vascular damage from circulating
immune complexes
– This is supported by evidence from cases with:
• Limited prior antigen exposure (young nulliparous women,
altered paternity)
• Increased fetal antigens (large placenta in twins, molar
pregnancy, hydrops fetalis, & DM)
 ETIOLOGY - 2

2. CIRCULATING TOXINS:
3. VASOACTIVE SUBSTANCES:
– Vasoactive substances found in maternal blood,
amniotic fluid, & placenta (eg, nitric oxide
deficiency)
– Increased sensitivity to vasopressin, epinephrine
& norepinephrine
– Loss of third trimester resistance to angiotensin II
 ETIOLOGY - 3

4. ENDOTHELIAL DAMAGE:
– Primary endothelial damage (cause unknown) leads
to decreased prostacyclin (vasodilator) & increased
thromboxane A2 (vasoconstrictor)
– Low-dose aspirin or heparin may play a role in
prevention
5. DIETARY DEFICIENCY:
– Ca supplementation reduces the incidence of PE in
some populations
 ETIOLOGY - 4

6. PRIMARY DIC:
– Thrombi formation & deposition leads to vessel
damage especially in the kidneys & placenta
7. ABNORMAL TROPHOBLAST INVASION:
– 2nd wave of trophoblast invasion at 16/52
– Trophoblasts normally invade muscular layer in
walls of spiral arterioles
 PATHOPHYSIOLOGY - 1

CARDIOVASCULAR ASPECTS:
– Increased BP due to increased systemic
vascular resistance & cardiac output
– Arteriolar vasospasm causes most of the
serious end organ effects
– Loss of blunted pressor response to
angiotensin II
 PATHOPHYSIOLOGY - 2

CARDIOVASCULAR ASCEPTS:
– Increased afterload & decreased ventricular
preload
– Reduction in the synthesis of prostacyclin
relative to thromboxane A2 leads to arteriolar
vasospasm
– Alteration in the synthesis of endothelium
derived relaxing agent (endothelin-I) & nitric
oxide
 PATHOPHYSIOLOGY - 3

HEMATOLOGICAL ASPECTS:
– Plasma volume contraction leading to
reduced regional perfusion & increased risk of
hypovolemic shock in case of hemorrhage
– Clinically  increased hematocrit (hemo-
concentration)
– This is in spite of increased total body water &
sodium
 PATHOPHYSIOLOGY - 4

HEMATOLOGICAL ASPECTS:
– Arteriolar spasm leads to microangopathic
hemolysis which manifests itself initially as
thrombocytopenia
– HELLP syndrome (Hemolysis, Elevated
Liver enzymes, &/or Low Platelets)
 PATHOPHYSIOLOGY - 5

RENAL ASPECTS:
– Reduced glomelular filtration rate (GFR), proteinuria, &
Na retention
– Reduced GFR due to reduced renal plasma flow &
reduced filtration fraction (GFR/RPF)
– Reduced clearance of uric acid often seen; reflected as
hyperuricemia. This precedes fall of GFR
– Glomelular damage leads to leakage of protein
 PATHOPHYSIOLOGY - 6

NEUOROLOGICAL ASPECTS:
– Hyperreflexia does not correlate with disease
severity
– Generalized tonic-clonic seizures:
• Occur in 1 in 1,000 deliveries or 1% of PE patients
• Seen in many cases that end in maternal death
• May occur up to 24 hours after delivery
• Cause unknown
 PATHPHYSIOLOGY - 7

NEUOROLOGICAL ASPECTS:
– Headache & visual disturbances (blurred
vision & scotomata) occur due to retinal artery
spasm
– Retinal hemorrhage may be seen in severe
cases
– Retinal detachment occurs rarely
– Blindness may be peripheral or central
 PATHOPHYSIOLOGY - 8

PULMONARY EDEMA:
– Due to decreased colloid oncotic pressure,
pulmonary capillary leakage, LVF, iatrogenic
fluid overload, or a combination of the above

HEPATOCELLULAR DAMAGE:
– Due to vasospasm & ischemia. Result in focal
peripheral hemorrhage, infarction, or rupture
 PATHOPHYSIOLOGY - 9

FLUID & ELECTROLYTE BALANCE:

– Increased extravascular volume seen as
increased weight &/or dependant edema
– Decreased bicarbonate level due to lactic
acidosis with compensatory metabolic
alkalosis; especially after eclamptic fits
– Increased ADH & atrial natriuretic factor
 FETAL COMPLICATIONS
1. IUGR
2. Oligohydramnios
3. Placental abruption &/or infarction
4. Consequences of prematurity
5. FD due to utero-placental insufficiency
6. Increased perinatal morbidity & mortality
MATERNAL COMPLICATIONS

1. CNS manifestations: seizures & stroke

2. DIC
3. Increased likelihood of CS
4. Pulmonary edema
5. ARF
6. Hepatic failure or rupture
7. Maternal mortality
 TREATMENT - 1

DELIVERY IS THE ONLY DEFINITIVE

TREATMENT:
– Generally indicated for women near term with
PE of any degree & for women with severe
disease at any gestational age
– Use of corticosteroids is appropriate before
34/52 in some cases
 TREATMENT - 2

• Some manifestations of severe PE

(oliguria, renal failure, HELLP syndrome)
mandate expedient delivery regardless of
gestational age
• For preterm women with mild PE,
conservative management is generally
indicated with close monitoring (BP,
proteinuria, LFT/RFT, CBC, U/S, NST,
BPP)
 TREATMENT - 3

MgSO4 is used for seizure prophylaxis in

severe PE:
– Mechanism of action
– IV loading dose of 4 g over 20 minutes
followed by continuos infusion at 2-3 g/h
– Stop MgSO4 if any of the following occur:
• Loss of deep tendon reflexes
• RR <12/min
• Urine output < 25 cc/h
 TREATMENT - 4

– Therapeutic range = 2-3 mmol/l

– Antidote = 1 g Ca gluconate (10 cc of 10%)
given iv over 2 minutes
– Contraindications
 TREATMENT - 5
Control of maternal BP during labor
using antihypertensive drugs:
– Indicated if systolic BP>170 mm Hg or
diastolic BP>110 mm Hg
– Loss of autoregulation may predispose to the
development of strokes
 TREATMENT - 6

• Hydralazine:
– 5-10 mg boluses repeated every 20 min SOS
– May be given continuously
– Causes tachycardia

• Labetalol:
– 20 mg iv every 10 min; maximum of 300 mg
– Or continuous infusion with BP monitoring
 TREATMENT - 7

• Verapamil:
– 10 mg S/L repeated after 30 min

• Na nitroprusside:
– Last resort
 TREATMENT - 8

DELIVERY:
– Vaginal route preferable over CS even in
patients with severe disease
– Cervical ripening with PGE2 or Foley catheter
can be considered
 TREATMENT - 9

ANESTHESIA:
– For labor & delivery:
• Parenteral analgesia. Pethidine!
• Epidural block. But beware of hypotension &
thrombocytopenia

– For CS:
• GA associated with elevation of BP during induction
& reversal
• Epidural block
 PREVENTION

1. LOW-DOSE ASPIRIN:
60-80 mg OD. May be appropriate for women at
high risk for developing PE.
Not recommended for prophylaxis in unselected,
normotensive patients
1. REDUCED NA INTAKE
2. CA SUPPLEMENTATION:
2 g Ca gluconate OD. 3X reduction in PE in
angiotensin-sensitive women
 CHRONIC HYPERTENSION - 1

Mild-moderate chronic hypertension:

– Systolic BP= 140-180 mmHg, diastolic BP= 90-100
mmHg
– Unlikely to have any significant deleterious
maternal effects
– May have serious detrimental effects on the fetus
such as IUGR, placental abruption & IUFD
– No apparent benefits to treatment
 CHRONIC HYPERTENSION - 2

Severe hypertension:
– Systolic BP > 180 mmHg, diastolic BP> 100
mmHg
– May require antihypertensive therapy to
prevent maternal morbidity & mortality
 CHRONIC HYPERTENSION - 3

• Patients already on medication may

continue therapy (even in second trimester)
• If therapy is to be initiated during pregnancy,
the first line agent is alpha-methyl dopa (250
mg X 3 - 500 mg X 4)
• Beta-blockers (labetalol 100 mg X 2- 300 mg
X 4 or atenolol 50-100 mg X 1). Beware of
IUGR
 CHRONIC HYPERTENSION - 4

• ACE inhibitors are contraindicated because

they may lead to fetal anomalies, renal
failure & oligohydramnios, IUFD & NND

• Diuretics should not be started during

pregnancy. The reduced plasma volume
may have adverse fetal effects. Used as last
resort only
 CHRONIC HYPERTENSION - 5

• Increased risk of IUGR. Serial U/S & NST

to monitor fetal well-being

• Significant risk for superimposed PE.

Monitor BP & proteinuria; & deliver at term
 OTHERS
• Management of:
– Gestational hypertension:
• Less likelihood of complications
• Less need for intervention

– Chronic hypertension with superimposed PE:

• Similar to management of PE arising de novo
during pregnancy
• Role of prophylaxis
 CONTRACEPTION

• Patients with PE can use the combined oral

contraceptive pill (OCP) 2/52 after delivery if
BP has returned to normal
• Women with well-controlled & monitored
hypertension < 35 years old may try OCP (<
35 mg ethinyl estradiol) if otherwise healthy
& without end-organ vascular disease
• ALTERNATIVES
 CASE - 1

MARIUM
– 19 year old. MF 9/12
– G1. GA = 35/52
– C/O headache & epigastric pain X 1 day
– BP = 180/120 mm Hg
– Proteinuria 4 +

– OUTLINE MANAGEMENT
 CASE - 2

AMEENA
– 36 year old. MF 9 years
– G7 P2+1+3+2. GA = 30/52
– Previous CS at 28/52 for severe PE.
BW 500 g. NND after 2/7
– Routine ANC visit, BP = 150/90 mm Hg

– OUTLINE MANAGEMENT
 CASE - 3

HESSA
– 40 year old. MF 15 years
– G7 P6+0+0+6. All FTND. GA = 12/52
– C/O vaginal bleeding X 2/7
– O/E BP = 160/100 mm Hg. Proteinuria 2+
– P/V uterus = 16/52. Os closed

– DISCUSS DIFFRENTIAL DIAGNOSIS &

MANAGEMENT
 CASE - 4

FATMA
– 32 year old. MF 1 year
– G1. GA = 30/52
– Routine ANC visit
– BP = 150/95 mm Hg
– Proteinuria 1+

– DISCUSS FURTHER MANAGEMENT

 CASE - 5

AYSHA
– 38 year old. MF 12 years
– G6 P4+0+1+4. All FTND. GA = 12/52
– First ANC. BP = 160/105 mm Hg

– OUTLINEM MANAGEMENT
THE END