Pregnancy induced hypertension Dr v. l. deshmukh Asso prof GMCH A’bad.
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Transcript of Pregnancy induced hypertension Dr v. l. deshmukh Asso prof GMCH A’bad.
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