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