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HYPERTENSIVE DISORDERS IN PREGNANCY

HYPERTENSIVE DISORDERS IN PREGNANCY. Hypertension in Pregnancy Classification. Chronic hypertension Gestational hypertension (only during pregnancy) Preeclampsia Superimposed upon chronic hypertension or Renal Disease Preeclampsia - eclampsia

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HYPERTENSIVE DISORDERS IN PREGNANCY

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  1. HYPERTENSIVE DISORDERS IN PREGNANCY

  2. Hypertension in PregnancyClassification • Chronic hypertension • Gestational hypertension (only during pregnancy) • Preeclampsia Superimposed upon chronic hypertension or Renal Disease • Preeclampsia - eclampsia • Transient hypertension (only after pregnancy)

  3. Chronic Hypertension Defined as hypertension diagnosed • Before pregnancy • Before the 20th week of gestation • During pregnancy and not resolved postpartum

  4. Gestational Hypertension • Gestational Hypertension: • Systolic >140 • Diastolic>90 • No Proteinurea • 25% Develop Pre-eclampsia

  5. Gestational Hypertension Diagnosis of gestational hypertension: • Detected for first time after midpregnancy • No proteinuria • Only until a more specific diagnosis can be assigned postpartum If preeclampsia does not develop and • BP returns to normal by 12 weeks postpartum, diagnosis is transient hypertension. • BP remains high postpartum, diagnosis is chronic hypertension. • Proteinurea develops Preeclampsia is diagnosed (25% incidence)

  6. Hypertension in Pregnancy • Complicates 7-10% of pregnancies • 70% Preeclampsia-eclampsia • 30% Chronic hypertension • Eclampsia 0.05% incidence • 20% of Maternal Deaths • Cause of 10% of Preterm birth • Etiology unknown

  7. Hypertension in Pregnancy • Young female 3 fold increased risk • Africans 2 fold increased risk • Multifetal pregnancies • Twins • Triplets • Hypertension • Renal Disease • Collagen Vascular Disease

  8. Blood pressure • Measure blood pressure in the sitting position, with the cuff at the level of the heart. Inferior vena caval compression by the gravid uterus while the patient is supine can alter readings substantially, leading to an underestimation of the blood pressure. Blood pressures measured in the left lateral position similarly may yield falsely low values if the blood pressure is measured in the higher arm and the cuff is not maintained at heart level. • Allow women to sit quietly for 5-10 minutes before measuring the blood pressure.

  9. Record Korotkoff sounds I (the first sound) and IV (the muffling of sound) to denote the systolic blood pressure (SPB) and DPB, 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, record both the fourth and fifth sounds (eg, 120/80/40 with sound I = 120, sound IV = 80, sound V = 40).

  10. Pre-eclampsia Case Study 19 years old lady G1 P0 was seen at the antenatal clinic at 32 weeks gestation for routine check up. On examination she looked generally well, blood pressure was 150/90 pulse 80/m with lower limb oedema +. Uterus was appropriate for date with a viable fetus. Urine analysis showed + protein. Q- what is the diagnosis Q- what investigations to perform Q- what treatment to commence 19 years old lady G1 P0 was seen at the antenatal clinic at 32 weeks gestation for routine check up. On examination she looked generally well, blood pressure was 150/95 pulse 80/m with lower limb oedema +. Uterus was appropriate for date with a viable fetus. Urine analysis showed + protein. Q- what is the diagnosis Q- what investigations to perform Q- what treatment to commence

  11. Pre-eclampsia Case Study 19 years old lady G1 P0 was admitted to the labour word at 32 weeks gestation complaining of headache. On examination she looked generally unwell, irritable, epigastric pain, nausea & blood pressure was 160/110 pulse 90/m with lower limb and abdominal wall oedema ++, reflexes exaggerated. Uterus was small for date with a viable fetus. Urine analysis showed +++ protein. Q- what is the diagnosis Q- what investigations to perform Q- what treatment to commence

  12. Pre-eclampsia ** INCIDENCE: 5-10% 0f all pregnancies . 20% recurrence This is the third most important cause of maternal mortality worldwide • ** DEFINITION OF HYPEWRTENSION: • D.B.P. > 90 mmHg or • S.B.P. > 140 mmHg or • Rise in D.B.P. of at least 15 mmHg (physiological changes) or • Rise in S.B.P. of at least 30 mmHg abandoned • ** PROTIENUREA: • Proteinurea is defined as urinary excretion • 0.3 g protein or greater in a 24-hour • 30 mg/dl (+1 or greater on urine dip specimen) +/- ** OEDEMA: 90% pregnancy. progressive

  13. Pre-eclampsia Risk Fac tors • Enlarged placenta e.g…………. • Pre-existing hypertension, renal • Pre-existing vascular disease • P0 >>>> multip • Family history • New husband

  14. Pre-eclampsia Aetiology • Abnormal trophoblast invasion… • first 12 weeks, the decidual segments of the spiral arteries are invaded… increased flow to interrvellous space… by 20 weeks trophoblast invades intramyometrial segment of spiral arteries>>> reduce resistance to blood flow to placenta.(high volume) • In P-E trophoblast invasion is patchy & spiral arteries retain their muscular walls…. Reason ????

  15. Pre-eclampsia Pathophysiology • Normal pregnancy: marked peripheral vasodilatation…. 4 fold increase in prostacyclin (PGI2) normal thromboxane and increased nitric oxide by vascular endothelium • Pre-eclampsia: no change/reduction in prostacyclin and N.O. synthesis……. Vasospasm and endothelial cell dysfunction>>> platelet activation and micro aggregate formation • It is a multi organ affecting disease/ syndrome • *hemorrhage and necrosis in many organs,, arteriolar constriction • *kidneys: glomerioloendotheliosis • *acute atherosis of spiral arteries, platelets micro-aggregates&thrombosis • *liver damage>>>> *cerebral vasospasm

  16. Pathophysiology Pathophysiologic Abnormalities in Preeclampsia Generalized vasospasmActivation of coagulation systemAbnormal hemostasisAltered thromboxane-prostacyclin ratioEndothelial cell injuryAbnormal hemodynamicsReduced uteroplacental blood flow

  17. Pathophysiology Heart:Generally unaffected; cardiac decompensation in the presence of preexisting heart disease. Kidney: Renal lesions (glomerular endotheliosis); GFR and renal blood flow decrease; hyperuricemia; proteinuria may appear late in clinical course; hypocalciuria; alterations in calcium regulatory hormones; impaired sodium excretion; suppression of renin angiotensin system.

  18. Pathophysiology Coagulation System:Thrombocytopenia; low antithrombin III; higher fibronectin. Liver: HELLP syndrome (hemolysis, elevated ALT and AST, and low platelet count). CNS: Eclampsia is the convulsive phase of preeclampsia. Symptoms may include headache and visual disturbances, including blurred vision, scotomata, and, rarely, cortical blindness.

  19. Symptoms of Preeclampsia • Visual disturbances typical of preeclampsia are scintillations and scotomata. These disturbances are presumed to be due to cerebral vasospasm. • Headache is of new onset and may be described as frontal, throbbing, or similar to a migraine headache. However, no classic headache of preeclampsia exists. • Epigastric pain is due to hepatic swelling and inflammation, with stretch of the liver capsule. Pain may be of sudden onset, it may be constant, and it may be moderate-to-severe in intensity.

  20. Symptoms of preeclampsia • While mild lower extremity edema is common in normal pregnancy, rapidly increasing or nondependent edema may be a signal of developing preeclampsia. However, this signal theory remains controversial and recently has been removed from most criteria for the diagnosis of preeclampsia. • Rapid weight gain is a result of edema due to capillary leak as well as renal sodium and fluid retention.

  21. Physical Findings in Preeclampsia • Blood Pressure • Proteinurea • Retinal vasospasm or Retinal edema • Right upper quadrant (RUQ) abdominal tenderness stems from liver swelling and capsular stretch

  22. Physical findings in Preeclampsia • Brisk, or hyperactive, reflexes are common during pregnancy, but clonus is a sign of neuromuscular irritability that raises concern. • Among pregnant women, 30% have some lower extremity edema as part of their normal pregnancy. However, a sudden change in dependent edema, edema in nondependent areas such as the face and hands, or rapid weight gain suggests a pathologic process and warrants further evaluation

  23. Pre-eclampsia Screening tests • Why screening • Accuracy. Uterine artery doppler at 24 weeks, notching on both uterine arteries identifies 80% who will develop PET,,, 5% false positive

  24. Pre-eclampsia Investigations **Maternal ** Fetal

  25. Pre-eclampsia Prevention Methods Used to Prevent Hypertensive Disorders of Pregnancy Proper prenatal careLow-salt dietDiureticsAntihypertensive drugsNutritional supplementation Magnesium (365 mg/d)Zinc (20 mg/d)Calcium (1500–200 mg/d)Fish oil Antithrombotic agents Low-dose aspirin (50–150 mg/d)Dipyridamole (225–300 mg/d)Subcutaneous heparin (15,000 IU/d)

  26. Prevention “Low doses of aspirin do help prevent pre-eclampsia, but there is little information about whether they are of benefit for treatment of established pre-eclampsia “ cochrane 22 April 2003 Pre-eclampsia is a condition in pregnancy involving high blood pressure and protein in the urine. It can lead to serious complications and death. As pre-eclampsia affects blood clotting, antiplatelets (drugs like aspirin which can prevent blood clots) are used for pre-eclampsia. The review of trials found that low doses of aspirin lowered the risk of pre-eclampsia a little (15% lowering in the risk), with a similar lowering in the risk of the baby dying (14%) and a very small lowering in the risk of the baby being born too early (8%). Doses less than 75mg appear to be safe. Higher doses may be better, but as the risks of adverse effects may also increase, more research is needed.

  27. Prevention “Calcium supplements may prevent high blood pressure and help prevent preterm labour” cochrane 22 April 2003 Main results: Eleven studies were included, all of good quality. There was a modest reduction in high blood pressure with calcium supplementation . The effect was greatest for women at high risk of hypertension (relative risk 0.45, 95% confidence interval 0.31 to 0.66) and those with low baseline dietary calcium (relative risk 0.49, 95% confidence interval 0.38 to 0.62). Reviewers' conclusions: Calcium supplementation appears to be beneficial for women at high risk of gestational hypertension and in communities with low dietary calcium intake. Optimum dosage requires further investigation.

  28. SERIOUS COMPLICATIONS: - • HELLP SYNDROME • ABRUPTIO PLACENTAE • PULMONARY OEDEMA • ACUTE RENAL FAILURE • CEREBRAL HAEMORRHAGE • VISUAL DISTURBANCES & BLINDNESS • HEPATIC RUPTURE • ELECTROLYTIC IMBALANCE • POSTPARTUM COLLAPSE

  29. HYPERTENSION DURING PREGNANCY OBJECTIVES OF MANAGEMENT CURE / PREVENT PROGRESSION - CLOSE MONITORING REDUCE BLOOD PRESSURE -TATRGET- 140/90 PROMOTE FOETAL MATURITY PROLONG PREGNANCY (34 - 36 WEEKS) TO ACHIEVE FOETAL MATURITY  TERMINATION DELIVERY- BEST DAY, BEST WAY & BEST PLACE PREVENT / MANAGE COMPLICATIONS

  30. HYPERTENSION DURING PREGNANCY MATERNAL MONITORING LOOK FOR APPEARANCE OF OMINOUS FEATURES DAILY- RECORD B.P 4 TIMES, MONITOR URINE OUTPUT & TEST FOR PROTEINURIA QUALI. / QUANT ALT.DAY- BODY WEIGHT EVERY 4TH DAY- URIC ACID, PLATELET COUNT, L.F.T. (LDH) WEEKLY- CREATININE

  31. HYPERTENSION DURING PREGNANCY FOETAL MONITORING DAILY - CLINICAL FOETAL MONITORING - FHS, FUNDAL Ht. ABDOMINAL GIRTH, LIQUOR, FOETAL MOVEMENT COUNT, C.T.G USG - ON ADMISSION & THEN 3 WEEKLY FOR FOETAL BIOPHYSICAL PARAMETERS, PLACENTA AND LIQUOR VOLUME DOPLLER USG FOR PLACENTAL BLOOD FLOW VELOCITY EVERY 4TH DAY L/S RATIO FOR MATURITY

  32. MANAGEMENT OF PRE-ECLAMPSIA the principles are: • *early recognition of the symptomless syndrome • *awareness of serious nature of the condition in its severe form without over-reacting to mild disease • *agreed guidelines for admission to hospital, investigation, and use of anti hypertensive and anticonvulsant therapy • *well-timed delivery to pre-empt serious maternal or fetal complications • postnatal follow-up and counselling for future pregnancies. Clinical observation and investigation Examination (over and above routine): • palpation of the femoral pulses (to exclude coarctation of aorta) • look for hyperreflexia and ankle clonus • check optic fundi for silver wiring, arterio-venous nipping, exudates and haemorrhage.

  33. Laboratory investigation • Proteinuria-. If present also check urine microscopy andculture to exclude urinary infection. *Serum urate levels increase early in pre-eclampsia. Levels >350 pmol/L are abnormal in pregnancy but gradually increasing levels are more significant. •Serum urea and creatinine. Rising levels are significant but not such sensitive indicators of pre-eclampsia as uric acid. The upper limits of normal in pregnancy are 5 mmol/L for serum urea and 100 pmol/L for creatinine, but trends are even more important than specific levels. • Platelet count gradually falls if disseminated Intravascular coagulation is occurring.

  34. Laboratory investigation • Liver function-this should be checked once persistent proteinuria is present, or if platelet count is significantly reduced. It can be detected by elevation of liver enzymes (not alkaline phosphatase, which is normally raisedbecause it is produced by the placenta). •Coagulation studies should be carried out if plateletcount is reduced, and in severe disease. • Tests of fetal growth and well-being • Each of these tests should be repeated as often as is clinically necessary.

  35. Pre-eclampsia Treatment ** definite treatment is delivery (ending the pregnancy). But, Mother vs. Fetus

  36. Pre-eclampsia Treatment ** Mild pre-eclampsia: diastolic /90-95 & proteinurea trace-1+ ** Moderate pre-eclampsia ** Severe pre-eclampsia ** Does the treatment improve the condition? Then why. Adv/disadv

  37. Management of mild (non-proteinuric) pre-eclampsia The principles are: *uncomplicated hypertension is suitable for careful supervision at home by the primary health care team *anti hypertensive therapy is not indicated * admission to hospital is indicated when: +-SBP is 160 and/or DBP 100 mmHg or greater -proteinuria is detected in a clean (i.e. mid-stream) urine sample in the absence of a urinary infection }-the patient is symptomatic with e.g. visual disturbances, unusual headache, epigastric pain, or vomiting (URGENT!) there is clinical evidence of intrauterine growth retardation +tests of fetal welfare have deteriorated -4-a previous bad obstetric history suggests that closer surveillance would be worthwhile.

  38. MANAGEMENT OF SEVERE HYPERTENSION The maternal risks of cerebrovascular accident and of left ventricular or renal failure begin to increase significantly when hypertension is severe. • The choice has then to be made between delivery and anti­hypertensive therapy. • Among the factors to be considered are: ~gestational age-it is seldom justified to commence long-term oral therapy from 34 weeks the severity of other signs and symptoms availability of intensive neonatal care facilities. >K• Treatment neither influences the progression of underlying pre­eclampsia nor significantly improves fetal outcome. It helps to protect the mother and enables many pregnancies to continue that otherwise would be ended because of maternal risk.

  39. CONTROL OF ACUTE SEVERE HYPERTENSION • There is no consensus on the optimum acute treatment. • The important objective is to reduce the blood pressure to safe levels (but not too low!). • Parenteral hydralazine is used most commonly but oral nifedipine should be considered . LONGER-TERM CONTROL OF SEVERE HYPERTENSION The combined a- and (B- blocking agent labetalol is commonly used. The potent vasodilator and calcium channel blocker nifedipine is a useful second-line treatment. Its major drawback is severe headache. Angiotensin-converting enzyme (ACE) inhibitors have deleterious fetal effects and their use is not recommended. If a woman with chronic hypertension becomes pregnant on an ACE inhibitor, change to another anti-hypertensioe agent is advised.

  40. LONGER-TERM CONTROL OF SEVERE HYPERTENSION • There is still insufficient trial evidence to determine whether the benefits outweigh any disadvantages. • If it is to be used, the suggested indications are: ,-DBP >_100 mmHg -pregnancy <_34 weeks *fetal and maternal state otherwise good. •Methyldoparemains the drug of first choice. The combined a- and (B- blocking agent labetalol is commonly used. The potent vasodilator and calcium channel blockernifedipine is a useful second-line treatment. Its major drawback is severe headache. Angiotensin-converting enzyme (ACE) inhibitors have deleterious fetal effects and their use is not recommended. If a woman with chronic hypertension becomes pregnant on an ACE inhibitor, change to another anti-hypertensioe agent is advised.

  41. TTiming of delivery • The most common grounds for delivery are: progressive fetal compromise (i.e. when the baby is safer delivered) uunacceptable risk to maternal health, e.g. uncontrollable BP, impending renal failure or heart failure, HELLP syndrome, DIC, eclampsia (see below). . •

  42. The mode of delivery (caesarean section versus vaginal) depends on: -the seriousness of the situation -the gestational age -the degree of fetal/maternal compromise. • Epidural analgesia is the method of choice for labour (as longas a coagulation defect has been excluded). • Appropriate facilities for the care of the newborn available

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