Pregnancy induced hypertension

Dr v. l. deshmukh

Asso prof

GMCH A’bad

INTRODUCTION

• Global problem

• Complicates 5-10% of pregnancy

• Responsible for 15-20% maternal mortality

• 20-25% PNM

• Haemodynamic changes are complex

• Risk factors still not well understood

defination

• Multysystem disorder

• BP IS RAISED

• Systolic >140 mm of hg

• Diastolic >90 mm of hg

• Asso with proteinuria

• May or may not be asso with edema feet

• Asso with abnormal wt gain

physiology

• Progesteron in pregnancy leads to smooth muscle relaxation

• Results in vasodilatation

• Peripheral resistance falls

• Leads to fall in BP

• THUS BP FALLS IN PREGNANCY

• Instead if it rises it is abnormal-PIH

BP

• Systolic >140

• Diastolic>90

• 15 mm rise in diastolic

• 30 mm rise in systolic

• Over the previous readings

• AFTER 20 WK OF GESTATION

• Important to have BP readings in early pregnancy

proteinuria

• Significant proteinuria is defined as 300 mg/l or more in 24hr urine sample

• Traces=

• 1+=

• 2=+

• 3+=>3gm/l

• 4+=>5 gm/l

Wt gain

• Normal wt gain during pregnancy is 11kg

• If wt gain is more –could be a sign of PIH

• .>1LB/WK

• >500GM/WK

• Wt gain is due to water retention

• Water retention is due to NA+ RETENTION

• Results in edema all over the body ,specially feet(dependant part)

classification

• PIH

• Gestational HT(not asso with proteinuria)

• Chronic HT(before 20 wk )

• Eclampsia

• PIH-mild/ severe

Mild PIH

• BP-140/90 to 160/110 mm of hg

• Proteinuria<2+

• Asso with abnormal wt gain

• May or may not be asso with edema feet

• NOT ASSO WITH WARNING SYMPTOMS

Severe PIH

• BP>160/110 mm of hg

• Proteinuria>2+

• Abnormal wt gain

• Edema +/-

• Asso with warning symptoms

• Asso with abnormal haematological inv

• oliguria.,DIC,IUFD,jaundice

Risk factors

• Genetic predisposition

• Primigravida

• Positive family history

• Vascular ds

• Renal ds

• Poor SES

• Unbooked

• Teenage pregnancy

pathophysiology

•Vasoconstriction•Why?• Vessels more sensitive to vasoconstrictors• Refractory to vasodilators• Vosoconstrictors increase• Vasodilators decrease

• Normal preg

• BALANCE BETWEEN VCAND VD

• Net result is VASODILATATION

• PIH

• IMBALANCE IN VC AND VD

• Net result is VASOCONSTRICTION

Results of vasoconstriction

• Reduced blood supply to uterus=IUGR

• Reduced blood supply to kidney=oliguria

• Reduced blood supply to liver=jaundice

• Reduced blood supply to brain=headache

• Reduced blood supply to eyes=blindness

• Reduced blood supply to heart=chest pain

• Reduced blood supply to liver=epigastric pain

Results of vasoconstriction

• Decreased intravascular compartment

• Less amount of blood• Less amount of plasma volume• Extravasation of excess fluid=edema all over body• Haemoconcentration• Rise in disatolic BP

Vasocon---

• Genetic/immunologic cause

• Altered prostaglandin ratio

• Elevated thromboxane/prostacyclin ratio-(TXB2/PGI2)

• ARTERIAL VASOCONSTRICTION

• Rise in vascular tone and vasospasm

• Increase angiotensin2 synthesis-rise in BP

2.ENDOTHELIAL INJURY

• Endothelium-innermost layer of BV

• Vasocons-slowing of blood

• Decreased nitricoxide

• Endothelial injury

Endo injury---

• Endoth injury leads to platlet aggregation• Platelets get exhausted

•Thrombocytopenia• New platelets thrown in the circulation• New pl are more adhesive in nature• Lead to more pl aggregation

• More thrombocytopenia

Endo injury---

• Pl aggregation further reduce the lumen of BV

• Further depletion in blood supply• Pl agg results in formation of microthrombi

in minute BV

•INTRAVASCULAR COAGULATION= = = DIC

DIC

• DEPOSITION OF FIBRIN

• Kidney=proteinuria, edema, oliguria

• CNS=headache,visual disturbances,convulsions

• Liver=epigastric pain,hepatic dysfunction

• Blood=DIC, haemolysis.

Clinical features

• H/o amenn

• Edema over ankles, abdomen, vulva, face

• Headache

• Epigastric pain

• Oliguria

• Blurring of vsion

• H/o jaundice

C/F

• Nausea,vomittings

• Loss of FM

• BLDG GUMS

• Haematuria

• F/o abruptio pl

• Bldg P/V

O/E

• Wt gain is more

• Bp raised

• Edema feet,abd wall edema,vulval edema

• Bloated

• DTR-brisk

investigations

• HB%, platelet count,BT/CT

• Urine-albumin

• PCV

• KFT

• LFT

• Coagulation profile

• funduscopy

COMPLI---

• Aim-prevent

• Detect at the earliest

• Treat it timely

• Before it endangers life

• ALL COMPLICATIONS CAN BE AVOIDED/MINIMISED BY TIMELY INTERFERENCE

Inv---

• USG-fetal wt,,AFI, FHS, abruptio pl

• BPP

• Doppler

• NST

• Se electrolytes

• se uric acid

• CT scan

HELLP

• Elevated liver enzymes

• Low pl count

• Normal count=>1.5 lac

• 1=1-1.5 lac

• 2=50,000-1 lac

• 3=<50,000

complications

• Maternal

• Fetal

• IUGR

• IUFD

• PRETERM

• FD

COMP---

• MATERNAL

• Eclampsia

• Abruptio pl

• DIC

• Oliguria

• HELLP

• blindness

• Preterm labor

• PPH

• Deep venous thrombosis

• Pulmonary embolism

• ICH

• Saggital sinus thrombosis

T/t

• Principles of mgt

• Control of BP-90-100 DIASTOLIC

• Prevention of complications

• If BP controlled- till term

• If BP not controlled-ignore the fetal maturity & terminate the pregnancy

Control of BP

• Bedrest

• Antihypertensives

• Cap depin-10 mg TDS/QID

• Tab methyldopa-250-500mg TDS/QID

• Tab labetelol-50 mg BD

• HYPERTENSIVE CRISIS- inj labetelol 5-10 mg slowly

Fetal monitoring

USG

DFMC

• BPP

• NST

• Doppler

COMPLICATIONS

• INV WILL POINT TOWARDS COMPLICATION

• Pl count- low

• LFT-deranged

• KFT-deranged

• BT/CT- prolonged

Timely interference

• Maternal factors

• Headache, nausea,vomitting,epi pain

• DTR brisk

• Oliguria

• Bldg gums/haematuria

• HELLP

• ALBUMINURIA 4+

TIMELY INTERFERENCE

• Fetal

• Loss of FM

• Oligohydramnions

• NST –nonreactive

• Doppler-absent/reversed BF

• SEVERE IUGR

MATERNAL MORTALITY

• Better understanding,blood tranfusions, componant therapy,steroids

• Causes of death

• Eclampsia

• PPH

• Abruptio pl

• embolism