Pregnancy induced hypertension

PIH, for obstetricians, undergraduates, postgraduates

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

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

35. Fetal monitoring
USG
DFMC
•BPP
•NST
•Doppler

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