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Hypertensive disorders of pregnancy.ppt

  1. 1. 1 Hypertensive disorders of pregnancy Prof. Adel Abul-Heija
  2. 2. 2 Introduction 1. Hypertensive disorders of pregnancy are one of the leading causes of maternal mortality. 2. Worldwide: 50,000 women die each year. 3. Jordan: 4th. Cause of maternal death after (hemorrhage, thrombo-embolism, and sepsis. (Jordan MMR 19.1 per 100000 live birth, 2007-2008)
  3. 3. 3 Diagnosis of hypertension in pregnancy  A systolic BP of > 140 mmHg, a diastolic BP of > 90 mmHg, or both.  Hypertension is considered severe when BP > 160 for systolic or > 110 for diastolic.  It required at lest two determinations with at least 6 hours apart of bed rest.
  4. 4. 4 How to measure BP in pregnant woman  Women should be allowed to sit quietly for 10-20 minutes before each blood pressure measurement.  Blood pressure should be measured in the sitting position, with the cuff at the level of the heart.  Korotkoff sounds I (the first sound) and V (the disappearance of sound) should be used to denote the systolic blood pressure (SBP) and DBP, respectively.  In about 5% of women, an exaggerated gap exists between the fourth (muffling) and fifth (disappearance) Korotkoff sounds, with the fifth sound approaching zero. In this setting, both the fourth and fifth sounds should be recorded (eg, 120/80/40, with sound I = 120, sound IV = 80, and sound V = 40), because the fourth sound will more closely approximate the true DBP.
  5. 5. 5 Diagnosis of Protienurea in pregnancy  Proteinuria:  ≥ 300mg/24 hours urine.  ≥ +1 dipstick. (only applicable if the others are not avialables)  Urinary Protein:creatinine ratio:  At least 0.3 (each measured as mg/dl)
  6. 6. 6 Classifications  Gestational hypertension.  Preeclampsia-Eclampsia.  Chronic hypertension with pregnancy.  Chronic hypertension with Superimposed preeclampsia.
  7. 7. 7 Definitions  Gestational hypertension: – Hypertension for first time after 20 w, without Proteinuria. BP returns to normal before 12 weeks postpartum.  Chronic hypertension with pregnancy: – Hypertension antedates pregnancy and detected before 20 w, & lasts more than 12 weeks postpartum.
  8. 8. 8 Definitions – Preeclampsia:  The development of hypertension and Proteinuria after 20 weeks.  May occur earlier in vesicular mole or multiple pregnancy.  Preeclampsia is diagnosed also in the presence of sever features even in the absence of protienurea (see next slide). – Eclampsia:  The occurrence of tonic-clonic convulsions (without any neurological disease) in a woman with pre- eclampsia.
  9. 9. 9 Definitions  Superimposed pre-eclampsia: ¤ It is the new development of Proteinuria after 20 weeks gestation in a patient with chronic hypertension
  10. 10. 10
  11. 11. 11 Incidence of hypertensive disorders in pregnancy  Gestational hypertension occurs in around 5-6% of all pregnancies. More common in primigravida. Most cases are diagnosed after 34 weeks.  PE complicates 1-2% of all pregnancies. 4-7% of first pregnancies (1 in 4 of PIH) and 1% of subsequent pregnancies, rising to 16% with history of preeclampsia in first pregnancy.  Around 5-10% of PE cases are severe.  Approximately 1% of pregnancies are complicated by chronic hypertension and 20-25% of women with chronic hypertension develop preeclampsia during pregnancy.
  12. 12. 12 Pre-eclampsia (PE): Definition: A diastolic BP > 90 mmHg, on at least two occasions after 20 weeks of gestation accompanied by significant proteinuria (> 300 mg/24h) and/or other systemic severe manifestations mentioned before.
  13. 13. 13 Aetiology of PE: PE is the disease of theories: 1. Damage to the vascular endothelial cells. 2. Abnormal lipid metabolism. 3. Reduced anti-oxidant status. 4. Altered catecholamine homeostasis. 5. Abnormal dietary calcium, magnesium, or selenium. 6. Reduced production of nitric oxide. 7. Abnormal immune response to pregnancy.
  14. 14. 14 Patho-physiology of PE:  Abnormal placentation is central to the pathogenesis of PE.  In PE there is reduction in the synthesis of nitric oxide and prostacyclin and increased production of endothelin and sensitivity to angiotensin. This result in to vasospasm and endothelial dysfunction, with subsequent platelet activation and micro thrombus formation. These are responsible for features of PE.
  15. 15. 15 Multi-system Features Of Preeclampsia Multi-organ disease Kidney Systemic blood vessels Liver Fetus Cerebral blood vessels HELLP syndrome IUGR Eclampsia Proteinuria Hypertension
  16. 16. 16 Clinical features of PE: Maternal syndrome: 1. PIH. 2. Proteinuria. 3. Generalized oedema. 4. Hyperuricaemia. 5. Increased haematocrit. 6. Thrombocytopenia & DIC. 7. Reduced antithrombin III. 8. Abnormal liver function tests. 9. Hypocalciuria. 10. Seizures, cortical blindness, retinal detachment (eclampsia). Fetal syndrome: 1. IUGR. 2. Fetal hypoxaemia.
  17. 17. 17 Prevention of PE:  Aspirin: Low dose (81mg/day) increases the prostacycline to thromboxan ratio and prevent platelets aggregation. It should be used from 12 weeks of pregnancy in women at risk.  Calcium supplementation ( may reduce severity in women with low intake of calcium.  Antioxidant: vit.C or vit.E (not effective)  Restriction of dietary salt (not effective)
  18. 18. 18 High risk women that need aspirin  Maternal disorders: – Chronic hypertension – Renal diseases – Diabetes – Autoimmune conditions  First pregnancy  Multiple pregnancy  Maternal BMI > 25  H/O preeclampsia  Age > 40 years
  19. 19. 19 Investigations for PE:  Urinalysis.  24 h urine collection for total protein.  Renal function (urea,uric acid,s. creatinine).  Full blood count (platelets and haematocrit).  Liver function tests.  Coagulation profile if delivery is indicated.  Fetal biophysical profile and Doppler study.
  20. 20. 20 Management of PE:  Diagnosis of PE requires admission for bed rest and close monitoring for mother and fetus.  If the diastolic BP is 90-95mmHg with only 1+ protein in the urine, out-patient management could be followed.  The definitive treatment for PE is delivery. But this depend on gestational age and feto- maternal well-being.
  21. 21. 21 Management of PE (cont.): Antihypertensive therapy:  Treating the hypertension is mainly to reduce the maternal complications. It will not improve fetal condition. Acute treatment of severe hypertension:  Hydralazine: 5mg IV repeated every 20-30 min.  Nifedipine: 10mg orally repeated at 30 min. IV infusion can be used in severe cases.  Labetalol:10-20mg IV .  The dose can be doubled every 10 minutes if proper response is not achieved.  Magnesium Sulphate should be given in the management of all cases of severe preeclampsia to prevent eclampsia.
  22. 22. 22 Indications for delivery in PE:  Term pregnancy.  Severe uncontrolled hypertension (>160/110).  Haemolysis with thrombocytopenia.  Progressive symptoms (headache, visual disturbances, epigastric pain).  Pulmonary oedema.  Renal failure with oliguria.  Eclampsia.  Fetal compromise ( abnormal biophysical profile).
  23. 23. 23 Management of labour and delivery:  The mode of delivery is determined by Bishop’s score and feto-maternal well-being.  Induction of labour is commonly used, but CS is needed in large number of cases.  Fluids input and output should be monitored.  Prolonged pushing by the mother should be avoided.  Ergometrine should be avoided.  Pain relief is optimal (epidural analgesia if no signs of DIC).
  24. 24. 24 Complications of severe PE: Eclampsia: Occurrence of convulsions in association with PE.  Incidence: 5 in 10 000 deliveries and 1-2% of severe PE cases.  High maternal and fetal mortality.  It can occur ante-natally, intra-partum and post-partum.  The patho-physiology is cerebral vasospasm leading to ischemia and cerebral edema.
  25. 25. 25 Eclampsia: Diagnosis:  Women manifest excitability or hyperflexia prior to onset of seizure.  Tonic-clonic convulsions with small period of coma.  Prolonged coma mains CVA.
  26. 26. 26 Management of eclampsia:  During seizure: Maintain airway, Administer oxygen and avoid supine hypotension.  Anticonvulsant therapy: 1. Magnesium sulphate 4-6 g IV followed by a maintenance infusion of 1-2 g / h. 2. Diazepam 20mg IV followed by a maintenance infusion as required. 3. Phynenton  Anticonvulsant should be continued for at least 24 h after the last convulsion.  CS is indicated unless the mother is in active labour.
  27. 27. 27 Magnesium Sulfate (MgSO4):  It can be given IV or IM or SC – The therapeutic level is 4-7mEq/L. – The total dose of MgSO4 should not exceed 24 gms in 24 hours .  The dose of MgSO4 is monitored by:  Preserved patellar reflex. (7-10 mEq/L)  Respiratory rate >16/min. (10-13 mEq/L)  Urine output >100ml/4hours. (15-25 mEq/L)  Serum Mg++ level.  Is stopped 24 hours after delivery.  Antidote is ca gluconate
  28. 28. 28 Complications of severe PE: HELLP syndrome: Occurs in the absence of hypertension. H: haemolysis. EL: elevated liver enzymes. LP: low platelet count.  Present with epigastric pain, tender liver, nausea & vomiting.  Headache and arterial hypertension.  Carries high maternal (acute renal failure & pulmonary odema) and fetal mortality.  Treatment similar to eclampia & DIC. Platelet transfusion and cortico-steroids are necessary.  Delivery is the treatment of choice.
  29. 29. 29 Chronic hypertension in pregnancy Causes of CHT: 1. Essential hypertension. 2. Renal diseases (glomerulonephritis, polycystic disease, diabetic nephropathy, renal artery stenosis). 3. Collagen vascular diseases ( systemic lupus erythematosus, scleroderma). 4. Coarctation of the aorta. 5. Phaeochromocytoma.
  30. 30. 30 Chronic hypertension in pregnancy  The main concern that one third of these women will develop superimposed PIH. Risk factors for preeclampsia in CHT: 1. Renal disease. 2. Maternal age > 40 years. 3. Diabetes. 4. SLE. 5. Coarctation of the aorta. 6. BP > 160/100 mmHg in early pregnancy.
  31. 31. 31 Chronic hypertension in pregnancy Feto-Maternal risks: 1. Eclampsia. 2. Abruptio-placenta. 3. Heart failure. 4. Intracerebral haemorrhage. 5. IUGR.
  32. 32. 32 Long-term treatment of hypertension This is used mainly in CHD.  Methyldopa is the most common in use (least side effects). 1-2 g / day in three divided doses.  Nifedipine 40 mg / day in two divided doses.  Labetolol and Hydralazine can also be used.  ACE inhibitors, Angiotensin II blocker, and Chlorothiazide should be avoided because of teratogenic effect.
  33. 33. 33 Chronic hypertension in pregnancy Management:  Investigations should be performed to diagnose the cause of hypertension.  If the woman is on antihypertensive drugs, she should continue on it, except for angiotensin converting enzyme inhibitors (captoprel) because of risk of fetal damage. Care should be taken not to excessively lower the BP as this may affect the fetal healthy.  Maternal and fetal well-being should be monitored through the pregnancy.
  34. 34. 34 Chronic hypertension in pregnancy Management (cont.):  In severe cases admission is needed.  The obstetric management is similar to that of preeclampsia.  Timing the delivery must be individualized according to the feto-maternal well-being.  Induction of labour or CS should be selected according to the case.
  35. 35. 35