Hypertensive

Disorders In Pregnancy

Dr Kailash Kharkwal
Hypertensive Disorders
• Most common medical complication in pregnancy
• 5-10% incidence
• Major cause of maternal and perinatal morbidity worldwide
Hypertension
• BP > 140 mm Hg systolic and /or > 90 mm Hg diastolic (Korotkoff 5
[K5])
• Present on at least 2 occasions, at least 6 hours apart, but within a
maximum of a 1 week period

National High Blood Pressure Education Program Classification

(NHEP) 2000
• Chronic hypertension
• Gestational hypertension
• Preeclampsia and eclampsia syndrome
• Preeclampsia syndrome superimposed upon chronic hypertension
Definitions
Chronic / preexisting hypertension
• SBP ≥140 mmhg and/or DBP ≥90 mmhg that antedates pregnancy or
is present before the 20th week of pregnancy (on at least two
occasions) or persists longer than 12 weeks postpartum
• It can be primary (essential hypertension) or secondary to a variety
of medical disorders
Definitions
Gestational hypertension:
• Hypertension (SBP ≥140 mmHg and/or DBP ≥90
mmHg) for first time after 20 week, without
proteinuria
• BP returns to normal before 12 weeks postpartum
Definitions
Preeclampsia
• Is a multi - system disorder characterized by new onset of
hypertension and proteinuria after 20 weeks of gestation in a
previously normotensive woman
• Increased risk for maternal and/or fetal mortality or serious morbidity
Definitions
Preeclampsia superimposed upon chronic / preexisting hypertension
• New-onset proteinuria 300 mg/24 hours in hypertensive women but
no proteinuria before 20 weeks gestation
• A sudden increase in proteinuria or blood pressure or platelet count <
100,000/mm3 in women with hypertension and proteinuria before 20
weeks gestation
Epidemiology Of Preeclampsia
Incidence:
• Is a disease of humans only
• Is the most common medical disorder complicating pregnancy 5-15%
• Is the most common hypertensive disorder in pregnancy
• More common in primigravidas and elderly multipara
• More common in winter
• More in black races
Preeclampsia: Risk Factors
• Associated with the pregnant woman
• Nulliparity
• Preeclampsia in a previous pregnancy
• Age >40 years or <18 years
• Family history of preeclampsia (mother or sister)
• Chronic hypertension
• Chronic renal disease; APAS or inherited thrombophilia; Vascular or connective tissue
disease; DM (pregestational and gestational)
• High body mass index
• Black race / Filipino
• Woman herself was small for gestational age
• Prolonged interpregnancy interval
Preeclampsia: Risk Factors
• Associated with the pregnant woman’s husband or partner
– First time father (primipaternity)
– Partner related factors (new partner, limited sperm
exposure, after donor insemination; oocyte
donation; embryo donation)
• Associated with the fetus
– Multifetal gestation
– Hydrops fetalis / Triploidy
• Unexplained fetal growth restriction
• Fetal growth restriction, abruptio placentae, or fetal demise in
a previous pregnancy
• Hydatidiform mole
Preeclampsia
• A 2 stage disease?
a) Asymptomatic Placental Stage
b)Symptomatic Maternal Stage

• Stage 1 Poor placentation (early)

• Stage 2 Placental oxidative stress (late)
− Systemic release of placental factors
− Systemic inflammatory response and endothelial activation
• (A)The basic structural units of the placenta are the chorionic villi,
composed of a stromal villous core (VC) with fetal blood vessels,
surrounded by a basement membrane and overlain by vCTBs
• They either fuse to form the multinuclear syncytiotrophoblasts (STBs)
that cover floating villi or join a column of cytotrophoblasts (cCTBs) at the
tips of anchoring villi (AV)
• The anchoring villi, through the attachment of cCTBs, establish physical
connections between the fetus and the mother
• iCTBs penetrate the uterine wall through the first third of the
myometrium

• (B) In PE, the interstitial and the endovascular components of CTB

invasion are restricted.
• As a result, interstitial invasion is shallow and many uterine arterioles
retain their original structures
Placental Oxidative Stress
• Vascular endothelial Dysfunction due to oxidative stress and
inflammatory mediators

+
• Vasospasm due to imbalance between vasodilators (PGI2, NO) &
vasoconstrictors (TxA2, angiotensin 2, endothelin)
Pathology
• PET is the clinical ice-berg tip manifestation of the disturbances in the
maternal homeostasis, involving many systems and organs
Multisystem Features Of Preeclampsia

Hypertension Proteinuria

Systemic blood vessels Kidneys

Multi-organ disease

Cerebral vessels
Liver

Eclampsia
Fetus HELLP syndrome

Intra-uterine growth restriction

Clinical Features and Pathophysiology
Cardiopulmonary
• Hypertension
• Intravascular volume and edema
• Cardiac function - high afterload associated with increase
cardiac filling pressures
• Pulmonary edema
− Pulmobary vascular hydrostatic Pressure > plasma oncotic
Pressure
− Capillary leak, left heart failure, iatrogenic volume overload
Clinical Features and Pathophysiology
Renal
• Proteinuria
– ≥0.3 grams protein in a 24-hour urine specimen or
persistent 1+ (30 mg/dL) on dipstick
– random protein:creatinine ratio >30 mg/mmol
– ≥5 grams of protein in a 24-hour urine collection
(SEVERE)
• Renal Function
– ↓ GFR (30-40%), renal plasma flow
– Rising creatinine and oliguria (UO<500mL/24h) à
PES (secondary to renal vasoconstriction and Na
retention)
Clinical Features and Pathophysiology
Renal
• Hyperuricemia / Hypocalciuria
–increase proximal Na resorption; urate
reabsorption secondary to renal ischemia
• Urine sediment – benign
• Histology – Glomerular Endotheliosis
Clinical Features and Pathophysiology
Hematologic
• Thrombocytopenia
− accelerated platelet consumption
− <100,000/uL à PES
• PT, aPTT, Fibrinogen
− not affected
• Microangiopathic hemolysis
− + schistocytes / helmet cells (PBS)
− Increase LDH; hemoconcentration
Clinical Features and Pathophysiology
Hepatic
• Periportal and sinusoidal fibrin deposition and microvesicular fat
deposition
• Right upper quadrant pain, increase transaminase levels,
coagulopathy, subcapsular hemorrhage or hepatic rupture
• Epigastric pain secondary to stretching of Glisson’s capsule due to
hepatic swelling or bleeding
HELLP Syndrome
Hemolysis
• Abnormal peripheral blood smear (burr cells, schistocytes)
• Elevated bilirubin ≥ 1.2 mg/dL
• Increased LDH of > twice the upper limit of normal for the laboratory
Elevated liver enzymes
• Elevated ALT or AST ≥ twice the upper limit of normal for the
laboratory
• Increased LDH > twice the upper limit of normal for the laboratory
Low platelet count (<100,000/mm 3 )
Clinical Features and Pathophysiology
CNS and eye
• Headache
• Visual symptoms – constriction of retinal arteries
− Photopsia (flashing lights); scotomata (dark
areas/gaps); diplopia or amaurosis fugax (unilat
blindness)
• Generalized hyperreflexia
• Sustained ankle clonus
• Stroke
Clinical Features and Pathophysiology
Fetus and placenta
• Fetal growth retardation
• Oligohydramnios
• Fetal hydrops (mirror or Ballantyne syndrome)
Diagnosis Of Preeclampsia
• Hypertension + Proteinuria = Two facets of a complex
pathophysiological process
Signs
• It is a disease of signs: 2 cardinal signs + or - edema:
• Hypertension:
– Usually precedes proteinuria
• Proteinuria: detected by
– Boiling test.
– Quantitative assay.
– Dipstick test.
+ or - Edema
• Occult or manifest:
− The lower extremities
− Abdominal wall, vulva or may be generalized anasarca
− Face, hands or non-dependent parts
• Usually after hypertension
Peripheral Edema Is Not A Useful Diagnostic Criterion
1) It is common in normal pregnancy
2) PET can occur without edema (dry type)
• So its presence does not ensure a poor prognosis and its absence not
ensure a favorable outcome
Symptoms
These are usually manifestations of severe pre-eclampsia
1. Headache: usually frontal but may be occipital. It is due to cerebral
oedema and hypertension
2. Visual disturbances: blurring of vision, flashes of light or blindness
3. Epigastric or right upper quadrant pain due to enlargement and
subcapsular haemorrhage of the liver
4. Nausea and vomiting due to congestion of gastric mucosa and/ or
cerebral oedema
5. Oliguria or anuria due to kidney pathology
Investigations
A. Laboratory:
• Urine: 24 hour urine, Proteinuria
• Kidney functions: serum creatinine, urea, creatinine clearance and
uric acid.
• Liver functions: bilirubin, Enzymes (SGPT and SGOT)
• Blood: CBC, HCt , Hemolysis and Platelet count (Thrombocytopenia)
• Coagulation Profile: Bleeding and clotting time
TTT of preeclampsia
• Expectant Treatment
• Control of Hypertension
• Prevention of convulsions
• Termination of pregnancy
1) Expectant Treatment
• Rest: Complete Physical and mental rest.
• Diet: Increase protein and carbohydrate with low Na diet !!!!!
• Sedation and Tranquilizer: Phenobarbitone &
Diazepam
• Observation (MATERNAL & FETAL)
Expectant Antepartum Management Of Mild Preeclampsia
Inpatient vs outpatient care
• Close maternal monitoring upon diagnosis of preeclampsia is
important to establish disease severity and the rate of
progression
• Hospitalization is useful for making these assessments and
facilitates rapid intervention in the event of rapid progression
• Outpatient care is a cost-effective option for women with
stable mild preeclampsia after initial dx evaluation
Expectant Antepartum Management Of Mild Preeclampsia
Laboratory follow – up
• Platelet count, serum creatinine, serum AST/ALT à 1-2x/wk,
assess disease progression

Assessment of fetal well-being

• Daily fetal movement count
• Twice weekly fetal NST with AFI or twice weekly BPS
• UA Doppler indices evaluation
Expectant Antepartum Management Of Mild Preeclampsia
Assessment of fetal growth
• Sonographic estimation of fetal weight done to look for growth
restriction and oligohydramnios at the time of diagnosis, repeated
every 2-3 weeks if the initial examination is normal

Antenatal corticosteroids
• < 34 weeks POG
2) Control of Hypertension:

Parentral drugs:
1. Labetalol :
• First-line therapy (rapid onset of action, good safety profile)
• α and non selective β- adrenergic blocker
• 20 mg IV over 2 minutes followed at 10-minute intervals by
doses of 20 to 80 mg
− Up to a maximum total cumulative dose of 300 mg
− E.g. Give 20 mg, then 40 mg, then 80 mg, then 80 mg, then 80 mg
2) Control of Hypertension:

2. Hydralazine:
• 5 mg IV over 1 to 2 minutes
• If BP goal is not achieved within 20 minutes, give a 5 to 10 mg
bolus depending upon the initial response
− The maximum bolus dose is 20 mg
− If a total dose of 30 mg does not achieve optimal blood pressure
control, another agent should be used.
− The fall in blood pressure begins within 10 to 30 minutes and lasts
from 2 to 4 hours.

3. Diazoxide:
• Used in severe dangerous resistant hypertension as a last resort
• Dose: 50-150mg IV bolus dose
• Repeated every 1-2 minutes until BP decreases
2) Control of Hypertension:
Oral drugs:
1. α-methyl DOPA:
• It is the most commonly used
• It is α-adrenergic agonist causing depletion of catecholamine
stores
• Dose: 250-500mg 4 times/day orally

2. Calcium Channel Blocker:

• Nifedipine (adalat or Epilat)
• Dose: 10-30mg 3-4 times/day orally

3. β-adrenergic blockers:
• Labetalol (Trandate) 100-400mg 2 times daily
• Atenolol (tenormin) 50-100mg once daily
Target BP
• 130 to 150 mm Hg systolic and 80 to 100 mm Hg diastolic OR reduce
MAP by no more than 25% over 2 hours
• Cerebral or myocardial ischemia or infarction can be induced by
aggressive antihypertensive therapy if the blood pressure falls below
the range at which tissue perfusion can be maintained by
autoregulation
TTT of Preeclampsia
3) Prevention of convulsions
4) Termination of pregnancy
Magnesium Sulfate (MgSO4):
• IV regimen:
– Initially 4-6 gm (20%) in 100ml solution, given
over 15-20 minutes.
– Then, 1-2 gm/hour by IV drip

• IM regimen:
– 10 gms of 50% solution are given deeply IM (5
gms in each buttock)
– Maintain with 5 gm/4 hours of 50% solution
Preeclampsia: Termination of Pregnancy
• Definitive treatment: DELIVERY!
• Based on the factors:
a) POG
b) Severity of PE
c) Maternal / Fetal condition
Timing of delivery:
• Mild or Severe pre-eclampsia is usually treated conservatively till the
end of the 36th week to ensure reasonable maturation of the fetus
Mild Preeclampsia :
• Deliver at ≥37 weeks of gestation
• Labor induction encouraged
Indications of termination before 36th week include:
• Fetal
• Maternal
Fetal:
a) Intrauterine growth restriction,
b) Oligohydramnios,
c) Reduced fetal movements,
d) Abnormal fetal heart patterns, or
e) Failing biochemical results.

Maternal:
a) Blood pressure is sustained or exceeds 160/110 mmHg
b) Urine proteinuria > 5 gm/24 hours
c) Oliguria
d) Evidence of DIC
e) Imminent or already developed eclampsia
Severe Preeclampsia:
• Deliver regardless of gestational age

Method of delivery
• Vaginal delivery
• Caesarean section
Method of delivery
Vaginal delivery may be commenced in vertex presentation by:
a) Amniotomy + oxytocin if the cervix is favourable
b) Prostaglandin vaginal tablet (PGE2) if the cervix is not favourable.

Caesarean section is indicated in

a) Fetal distress
b) Late deceleration occurs with OCT
c) Failure of induction of labour
d) Other indications as contracted pelvis and malpresentations
Intrapartum care
a) Close monitoring of the fetus is indicated
b) Proper sedation and analgesia to the mother
c) Hypotensives may be given if needed
d) 2nd stage of labour may be shortened by vacuum extraction or
forceps
Postpartum care
a) Ergometrine is better avoided as it may increase the blood pressure
b) Continue observation of the mother for 48 hours for blood pressure
c) Sedatives and hypotensive drugs are continued in a decreasing dose
for 48 hours
Eclampsia
• Development of grand mal seizures in a woman with preeclampsia, in
the absence of other neurologic conditions that could account for the
seizure
• Occurs in 2 to 3 percent of severely preeclamptic women not
receiving anti-seizure prophylaxis
Diagnosis Of Eclampsia:
Eclamptic fit stages (4 stages):
• Premonitory stage (1/2 minute)
• Tonic stage (1/2 minute)
• Clonic stage (1-2 minutes)
• Coma
Treatment of Eclampsia
1. General and first aid measures:
• Isolation in a single, quite, semi dark room (eclampsia room)
• Ensure patent airway with tracheal and bronchial suction
• Put the patients in Trendlenburg position (to avoid aspiration of
secretions)
• Insert a catheter
• Nasogastric tube may be inserted
• Nothing by mouth and fluid chart
• Full laboratory investigations
Treatment of Eclampsia
2. Observation:
• Pulse, temperature, BP and
RR
• Level of consciousness
• Duration of coma
• Fetal heart sounds
• Urine output and
albuminuria
• Number of convulsions
Treatment of Eclampsia:
3. Control of Convulsions:
a) Magnesium Sulfate (MgSO4): Main stay of
management
b)Phenytoin: The dose is 15mg/kg slow IV
c) Diazepam (Valium): Initially 10-20mg IV slowly
4. Control of hypertension
over 5-10 minutes followed by 40mg in 5%
5. Other drugs:
dextrose slow IV infusion
• Antibiotic for infection.
• IV glucose 25% as a liver support, increases the urine output and
improves hemo-concentration