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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
VASOCONSTRICTI
ON
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
Pregnancy induced hypertension

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Pregnancy induced hypertension

  • 1. Pregnancy induced hypertension Dr v. l. deshmukh Asso prof GMCH A’bad
  • 2.
  • 3.
  • 4. 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
  • 5. 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
  • 6. 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
  • 7. 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
  • 8. 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
  • 9. 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)
  • 10. classification • PIH • Gestational HT(not asso with proteinuria) • Chronic HT(before 20 wk ) • Eclampsia • PIH-mild/ severe
  • 11. 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
  • 12. 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
  • 13. Risk factors • Genetic predisposition • Primigravida • Positive family history • Vascular ds • Renal ds • Poor SES • Unbooked • Teenage pregnancy
  • 14. pathophysiology •Vasoconstriction •Why? •Vessels more sensitive to vasoconstrictors •Refractory to vasodilators •Vosoconstrictors increase •Vasodilators decrease
  • 15. • Normal preg • BALANCE BETWEEN VCAND VD • Net result is VASODILATATION • PIH • IMBALANCE IN VC AND VD • Net result is VASOCONSTRICTI ON
  • 16. 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
  • 17. 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
  • 18. 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
  • 19. 2.ENDOTHELIAL INJURY • Endothelium-innermost layer of BV • Vasocons-slowing of blood • Decreased nitricoxide • Endothelial injury
  • 20. 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
  • 21. 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
  • 22. DIC • DEPOSITION OF FIBRIN • Kidney=proteinuria, edema, oliguria • CNS=headache,visual disturbances,convulsions • Liver=epigastric pain,hepatic dysfunction • Blood=DIC, haemolysis.
  • 23. Clinical features • H/o amenn • Edema over ankles, abdomen, vulva, face • Headache • Epigastric pain • Oliguria • Blurring of vsion • H/o jaundice
  • 24. C/F • Nausea,vomittings • Loss of FM • BLDG GUMS • Haematuria • F/o abruptio pl • Bldg P/V
  • 25. O/E • Wt gain is more • Bp raised • Edema feet,abd wall edema,vulval edema • Bloated • DTR-brisk
  • 26. investigations • HB%, platelet count,BT/CT • Urine-albumin • PCV • KFT • LFT • Coagulation profile • funduscopy
  • 27. COMPLI--- • Aim-prevent • Detect at the earliest • Treat it timely • Before it endangers life • ALL COMPLICATIONS CAN BE AVOIDED/MINIMISED BY TIMELY INTERFERENCE
  • 28. Inv--- • USG-fetal wt,,AFI, FHS, abruptio pl • BPP • Doppler • NST • Se electrolytes • se uric acid • CT scan
  • 29. 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
  • 30. complications • Maternal • Fetal • IUGR • IUFD • PRETERM • FD
  • 31. COMP--- • MATERNAL • Eclampsia • Abruptio pl • DIC • Oliguria • HELLP • blindness
  • 32. • Preterm labor • PPH • Deep venous thrombosis • Pulmonary embolism • ICH • Saggital sinus thrombosis
  • 33. 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
  • 34. 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
  • 36. COMPLICATIONS • INV WILL POINT TOWARDS COMPLICATION • Pl count- low • LFT-deranged • KFT-deranged • BT/CT- prolonged
  • 37. Timely interference • Maternal factors • Headache, nausea,vomitting,epi pain • DTR brisk • Oliguria • Bldg gums/haematuria • HELLP • ALBUMINURIA 4+
  • 38. TIMELY INTERFERENCE • Fetal • Loss of FM • Oligohydramnions • NST –nonreactive • Doppler-absent/reversed BF • SEVERE IUGR
  • 39. MATERNAL MORTALITY • Better understanding,blood tranfusions, componant therapy,steroids • Causes of death • Eclampsia • PPH • Abruptio pl • embolism