Hypertensive Disorders in Pregnancy

1. Hypertensive Disorders in Pregnancy Azza Alyamani Prof. of Obstetrics & Gynecology

2. Classification Women who are pregnant and hypertensive must be divided into : * chronic hypertension. * pregnancy induced hypertension (PIH) or gestational hypertension. those with PIH further subdivided : * proteinuric PIH (preeclampsia)minority * non-proteinuric PIHmajority

3. Therefore : women with hypertension in pregnancy are classified as having: 1. preeclampsia (proteinuric hypertension). 2. non – proteinuric hypertension. 3. chronic hypertension: •primary (essential) hypertension. 95%. •secondary hypertension.5%. ..renal dis. ..adrenal dis. ..hyperthyroidism. The aetiology and management of the three conditions are different .

4. Incidence: Worldwide , maternal mortality from hypertensive disease accounts for : 100.000 deaths per year. preeclampsia occurs in 5% . non – proteinuric PIH 15%. it accounts to 15 – 20% of maternal mortality in the developed cuonteris.

5. Definition: pregnancy induced hypertension (PIH) is : Hypertension that occurs after 20 weeks gestation and unrelated to other pathology. protienuria is the excretion of 300mg or more of protein in 24 hours urine. hypertension and protienuria define preeclampsia.

6. Preeclampsia : *is a multisystem disorder involving the placenta , liver , kidneys , blood , neurological and cardiovascular systems. * both maternal and fetal morbidity / mortality are more likely to occur with early – onset disease as; placental abruption ,acute renal failure ,cerebral Hge ,DIC and IUGR ,prematurity as delivery is the only cure. therefore , ANC is directed towards identifying women with hypertension and protienuria.

7. * severity ranges from : • a milddisorder (transient hypertension in the later part of the pregnancy) to • a life-threatening disorder with seizure HELLP syndrome, fetal hypoxia, and growth retardation. • * more severe disease: 0.5 per 1000 deliveries

8. Chronic Hypertension : is the presence of persistent hypertension of whatever cause , before 20 weeks gestation or persistent hypertension beyond 6 weeks postpartum. sustained bl. p of 140/90 mmHg or > on two occasions 6 hours apart is considered hypertensive.

9. Aetiology Pregnancy induced hypertension (PIH) Preeclampsia: is unknown , believed to be involved : = immune maladaptation. = placental ischemia. = oxidative stress. = genetic predisposition.

10. Genetic Predisposition Faulty interplay bet. invading trophoblast and decidua Decreased bl. supply to feto-placental unit Release of circulating factors Endothelial cell alteration IUGR Hypertension Proteinuria

11. Management Screening for preeclampsia : Risk Factors 1. +ve family history in the first –degree relative increase the risk of PET 4 – 8 fold. 2. primiparety 3. medical disorders as : * history of PET. * chronic hypertension. * diabetes. * obesity. * antiphospholipid syndrome. * molar pregnancy. * multiple pregnancy. * hydropsfetalis.

12. Screening and assessment for chronic hypertension : Women who is found to be hypertensive before pregnancy can be advised about : 1. weight loss. 2. restrict salt and alcohol intake. 3. change her antihypertensive agents , diuretics , angiotensin-converting enzyme (ACE) inhibitors and β blockers to other alternatives.

13. Diagnosis Screening tests: to predict PET and superimposed preeclampsia on chronic hypertension. (1) US it is quick ,non-invasive and inexpensive . Uterine artery Doppler : analysis of its waveform is an early predictor of poor placental perfusion and development of PET , there is resistance circulation with notch. Its predictive value is greater at 24 weeks or more.

14. Uterine art. Doppler in PET diastolic notch

15. (2) Biochemical tests in preeclampsia : * HB , and Hematocrit concentrations. * CBC with platelets count. * serum uric acid . * endothelial activation markers are increased. * urinary excretion of Ca and microalbuminuria

16. in severe chronic hypertension: * urine analysis. * 24h urine for protein , creatinine clearance, catecholamine metabolites and free cortisol. * bl. Urea and electrolytes as Na & k. * Lupus anticoagulant and anticardiolipin in APS. * serum lipids. in addition (3) fundoscopy. (4) ECG & ECHO. (5) X ray chest.

17. Symptoms & Signs

19. * Criteria of severe preeclampsia = blood pressure : > 160 mmHg systolic or • > 110 mm Hg diastolic • = Proteinuria: > 3 g in 24 hours • = Persistent and severe cerebral or visual disturbances (headache, blurred vision) • = Persistent and severe epigastric pain or right upper quadrant pain. = Pulmonary edema or cyanosis. = Oliguria ( < 500 ml urine / 24 hour). = Eclampsia ( grand mal seizures). = HELLP syndrome.

20. Maternal and fetal assessment: *the GA at which woman present with hypertension is an important factor in establishing risk . Late onset hypertension after 37weeks rarely result in serious maternal or fetal complications. * Superimposed pre eclampsia on chronic hypertension is diagnosed by identifying proteinuria, raised uric acid levels or failing platelets count . chronic hypertension is associated with preeclampsia in 20% and abruptio placenta in 2%.

21. * Uterine artery Doppler velocity waveforms is used to assess risk . * bl.pressure and urine analysis are checked every 2 weeks. sudden and profound rise should alert the clinicianto the possibility of PET. * high uric acid and low platelet count may pre –date proteinuria by some weeks.

22. Management Pre eclamptic Toxaemia A) PET remote from term Early onset PET is associated with : a. placental insufficiency resulting in IUGR and fetal death. Therefore ; Fetal Wellbeing must be carefully considered. 1. monitoring of fetal movements. 2. serial symphesis -fundal height . 3. serial US to confirm fetal growth ,AF volume and Umbilical A. Doppler waveform .

23. b. involvement of other organ systems resulting in increased maternal morbidity and mortality. 1.serial platelets count as platelets are consumed due to endothelial activation. Thrompocytopenia <100.000/ml. delivery should be considered. 2.increased HB and haematocrit values indicate hypovolaemia. 3.clotting abnormalities indicate DIC. .

24. 4.raised uric acid a measure of fine renal tubular function is used to assess severity of the disease. raised urea and creatinine indicate late renal involvement . 5.severe proteinuria > 3g /24 hours urine resulting in fall of circulating albumin and increasing the risk of pulmonary edema.

25. 5.HELLP syndrome it is severe variant of PET, Haemolysis , Elevated Liver enzymes and Low Platelets . PET can cause subcapsular hematoma, liver rupture and hepatic infarction which result in raised liver transaminases as AST indicating hepatocellular damage and liver involvement and the need to consider delivery.

26. Delivery : should be considered once fetal lung maturity is likely ( at 32 weeks gestation) ,especially if either multi-organ involvement or fetal compromise is proved. Corticosteroids are given to enhance fetal lung maturity. Steroid therapy may enhance recovery from HEELP syndrome. Delivery before term is usually by CS .such patients are risk of thromboembolism and should be given prophylactic SC heparin and stockings.

27. Indications of termination of pregnancy in PET : 1. uncontrollable hypertension. 2. deteriorating liver or renal function. 3. progressive fall in platelets. 4. neurological complications as cerebral Hge. 5. deteriorating fetal condition as non-reactive CTG.

28. B) PET near term Lat onset preeclampsia rarely results in serious morbidity to mother or fetus . Drug therapy should be considered: a) antihypertensive the aim is to lower the bl. pressure and lower the risk of maternal cerebrovacular accident without uterine bl. flow and compromising the fetus.

29. 1. Labetolol ą &β blockers . can be given IV and orally. safe during pregnancy. 2. Methyldopa centrally acting agent. very safe during pregnancy. only given orally . takes 24 h for its effect. 3. Nifedipine is Ca channel blocker . with rapid onset of action. cause severe headache.

30. NB: Diuretics ,Angiotensin-converting enzyme (ACE) inhibitors and β-blockers are contraindicated . b) Low dose aspirin results in significant reduction in preeclampsia associated fetal death and preterm delivery. c) for prophylaxis Ca , fish oil , antioxidants , vit. C , vit. E

31. Management of severe fulminating preeclampsia and impending eclampsia : 1. IV antihypertensive Hydralazine / labetolol IV infusion titration rapidly against changes in the blood pressure . 2. Anticonvulsant therapy Magnesium Sulfate : * it is the anticonvulsant of choice as ttt. of eclampsia and also as prophylaxis which reduce the risk of fits to half. Diazepam and phenytoin can be used but less effective .

32. * mode of action = anticonvulsant. = muscle relaxant. =vasodilator. reduce the intracerebral ischaemia. * dose 2 g IV as a loading dose then 1-2 g / h as maintenance infusion. * toxicity is detected by : absence of the patellar reflexes. respiratory arrest . may be cardiac arrest. * antidote is: 10 ml of 10% Ca gluconate.

33. 3. Fluid management a Folly′s catheter should be inserted and fluid balance recorded. * oliguria without a rising serum urea or creatinine is a manifestation of severe PET and not renal failure. however , if creatinine or potassium rises , haemodialysis is necessary. * diuretics should only be given if there are signs of pulmonary edema.

34. Postpartum Care * in severe PET and eclampsia, a severe type of of eclamptic fitsoccur postpartum , intensive monitoring is required for 48 h. after delivery. * bl. Pressure is frequently at its highest levels 3 -4 days after delivery . Therefore , antihypertensive therapy is need to be continued after discharge home.

35. * a postnatal care visit 6 -8 w. is mandatory for measuring bl.p , urine analysis , RFT, LFT and predisposing factors as thrompophilia or APS should be excluded. * in women with severe chronic hypertension must be carefully monitored for at least 48h after delivery as they are at increased risk of renal failure , pulmonary edema and hypertensive encephalopathy.

36. Thank you