HYPERTENSION IN PREGNANCY

Associate Professor Dr Hanifullah Khan

Objectives

• Understand definitions• Pathophysiology • Presentations of the disease• Important signs and symptoms

INTRODUCTION

Introduction

• H/T in pregnancy – leading cause of maternal & fetal morbidity

• The most frequent cause of iatrogenic prematurity

• PE & eclampsia – delivery is the only effective tx

Definitions – H/T

• H/T – – a DBP of 90mmHg or more, taken on 2

occasions > 4 hrs apart OR– A single DBP of > 110mmHg

• Can occur either in –– Women who already have H/T (10 or 20)– Manifest in 2nd half of pregnancy

Pregnancy HT & Chronic HT

• May be difficult to differentiate• Both have high risk of complications• Chr HT –

– Diagnosed prepregnancy– high BP early in pregnancy

Definitions - PE

• A multisystem disorder characterized by HT + proteinuria– Proteinuria - > 300mg urine pr / 24 hrs

• Occurs > 20 wks gestation• Resolves postnatally• Complications of PE – eclampsia,

HELLP synd

Definition - Eclampsia

• The occurrence of tonic-clonic convulsions in a woman with PE– Pregnancy – Any gestation– No neurological disease

• Gestational hypertension.• Preeclampsia (mild, severe).• Eclampsia.• Superimposed preeclampsia upon

chronic hypertension.• Chronic hypertension with pregnancy.

Classification

Incidence

• PE – 2-8% of all pregnancies– Risk in 1st pregnancy – 4.1%– Risk in later pregnancies – 1.7%– Risk in woman with PE in 1st pregnancies –

14.7%– Risk in woman with PE in previous 2

pregnancies – 31.9%

Summary

• Gestational hypertension: – Hypertension for first time after 20 w, without

proteinuria. BP returns to normal before 12 weeks postpartum.

• Chronic hypertension with pregnancy: – Hypertension antedates pregnancy and detected

before 20 w, & lasts more than 12 weeks postpartum.

PATHOPHYSIOLOGY

Basic understanding

• Complex disease• Appears to be triggered by the placenta

– Can occur in molar pregnancies where fetus absent

Trophoblast

• In normal conditions – – Trophoblast invades myometrium– Spiral arteries converted to low pressure system

• This process is inhibited in PE• Immunological process also involved• Thus HT & PE is caused by abnormal

placentation

Other factors

• Abn placentation → placental insufficiency & IUGR– Development of PE requires further changes

• ↑ Inflammatory activity– Widespread vascular endothelial damage– Capillary leak, vasoconstriction, intravascular

haemolysis, platelet activation– ↑ Immune status - ↑ leucocytes

Pathology • Primarily a disorder of placental dysfunction

– leading to a syndrome of endothelial dysfunction with associated vasospasm

• Evidence of placental insufficiency with associated abnormalities– diffuse placental thrombosis, an inflammatory placental

decidual vasculopathy, and/or abnormal trophoblastic invasion of the endometrium

• This supports abnormal placental development or placental damage from diffuse microthrombosis as being central to the development of this disorder

Pathopyhsiology

1. Placental factorsImmune complex deposition in kidney & placenta

Impair/ inadequate trophoblast invasion to the spiral arteries

Spiral arteries retain their charecteristic (narrow, tortuous, high resistance)

Reduce blood supply to placenta

Result in placental hypoperfusion

As a compensationHigh BP in maternal

2. Altered vascular reactivity

PG12 angiotensin II

vasoconstrict

HPT and reduce placenta blood flow

3. Coagulation disturbance

Activated endothelial cells promote coagulation and increase vasopressor sensitivity

Widespread coagulation occur (DIC)

Fibrin deposition in kidney & placenta

HPT & placental insufficiency

Summary

The development of PE is mediated through the degree of

placental pathology & the maternal inflammatory response

PREECLAMPSIA & ECLAMPSIA

• Is the most common medical disorder complicating pregnancy

• Is the most common hypertensive disorder in pregnancy

• More common in primigravidas and elderly multipara

Occurrence

• Chronic hypertension.• Chronic nephritis.• Past history .• Family history.• Obesity.• Multiple pregnancy.

Epidemiology

Maternal personal risk factors for preeclampsia

First pregnancyMultigravida pregnant by a different partnerAge younger than 18 years or older than 35 yearsHistory of preeclampsiaMultiple pregnancyFamily history of preeclampsia in a first-degree

relativeObesity Preexisting diabetesChronic hypertensionRenal diseaseSmoking

Multisystem Features Of Preeclampsia

Hypertension Proteinuria

Eclampsia HELLP syndrome

Intra-uterine growth restriction

Multi-organ disease

Cerebral vessels

Fetus

Liver

Systemic blood vessels Kidneys

Diagnosis Of PE

Hypertension + Proteinuria =

Two facets of a complex pathophysiological process

Peripheral oedema

• Not a useful diagnostic criterion– Common in pregnancy– PE can occur without oedema

• Headache.• Blurring of vision.• Nausea and vomiting.• Epigastric pain (distension of the liver

capsule)• Oliguria or anuria

Symptoms – non-specific

–The frequency and intensity of the signs and symptoms.

–The more the severity of PE, the more likely the need to terminate pregnancy

Severity of PE

• Eclamptic fit stages ( 4 stages):– Premonitory stage (1/2 minute):

● Eye rolled up● Twitches of the face and hands.

– Tonic stage (1/2 minute):● Generalized tonic spasm with opisthotonus.● Cyanosis.● Tongue may be bitten between the clenched teeth.

Diagnosis of Eclampsia

EVALUATION

Evaluation of Hypertension in PregnancyHistory

ID and Complaint HPI (S/S of

Preeclampsia) Past Medical Hx, Past

Family Hx Past Obstetrical Hx, Past

Gyne Hx Social Hx Medications, Allergies Prenatal serology, blood

work Assess for Hypertension

in Pregnancy risk factors

Physical BP (essential) Oedema Hyperreflexia Clonus Fondoscopy Urine dipstick test Cardiovascular Respiratory Abdominal =

Epigastric pain, RUQ pain

Cardiovascular

• Generalized vasospasm• Increased peripheral

resistance• Reduced central venous/

pulmonary pressure

Hematological

• Platelet activation and depletion

• Coagulopathy• Decreased plasma volume• Increased blood viscosity

• Proteinuria• Decreased glomerular

filtration rate• Decreased urate excretion

Renal

Hepatic

• Periportal necrosis• Subscapular

hematoma

• Cerebral oedema• Cerebral haemorrhages

Central Nervous System

Organ Specific Changes associated with Pre-eclampsia

Clinical presentationSymptoms Signs

•Headache (frontal/ occipital)• Visual disturbance•Nausea & vomiting• Epigastric and right upper abdominal pain•Oliguria / anuria• Maybe asymptomatic

• Rapid rise in BP• Papilloedema•Fluid retention (non-dependent edema)• Hyperreflexia•Clonus • Uterus and fetus may feel small for gestational age

Investigations

• 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

Differential Diagnosis:

• A. Hypertension With Pregnancy. • B. Proteinuria With Pregnancy.

• C. Edema With Pregnancy:

Differential Diagnosis ConvulsionsConvulsions With Pregnancy:• Eclampsia.• Epilepsy.• Hysteria.• Meningitis and Encephalitis.• Tetanus.• Tetany.• Brain tumors.• Uremic convulsions

Differential DiagnosisHELLP Syndrome:

• Acute fatty liver in pregnancy.• Hepatitis.• Thrombocytopenia purpura.• Hemolytic Uremic syndrome.

Treatment• PREVENTION.• Antepartum

● Proper antenatal care● Expectant treatment.● Control hypertension.● Treatment of eclampsia .● Prevention and control of convulsions.● Termination of pregnancy .

• Intrapartum care.• Postpartum care.

Control of Convulsions:

• Magnesium Sulfate (MgSO4):● It is the drug of choice.● Mechanism:

–CNS depression.–Mild VD.–Mild diuresis.– Inhibits platelet aggregation.– Increase PGI2 synthesis.

Prognosis:

• BP usually normalize after placental delivery .• Hypertension may persist.• Postpartum eclampsia carries the worst prognosis.• Maternal mortality is about 2% in severe preeclampsia and

10% in eclampsia.• Perinatal mortality rate is about 5% in mild cases, 25% in

severe cases and 30% in eclampsia.

CONCLUSIONS

SummaryHypertension diagnosed prior to 20 weeks'

gestation, is generally due to preexisting chronic hypertension rather than pregnancy induce hypertension

Pre- eclampsia may be diagnose by a combination of fetal and maternal features, including IUGR, hematological or biochemical abnormalities as well as clinical symptom and signs

Maternal deaths

• Confidential Enquiry into Maternal and Child Health UK (2003-2005)– 18 deaths from PE & eclampsia– 10 deaths caused by IC haemorrhage

● Due to uncontrolled BP

References

• Obstetrics by Ten Teachers 18th Edition• Obstetrics illustrated 6th Edition• Lecture Notes Obstetrics and gynaecology

3rd Edition• http://emedicine.medscape.com/article/

261435-overview