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Hypertensive disorders in pregnancy are classified into 5 categories: chronic hypertension, pregnancy-induced hypertension, pre-eclampsia, severe pre-eclampsia, and eclampsia. The etiology is unclear but may involve placental, immunological, biochemical, genetic, and oxidative stress factors. Pre-eclampsia is characterized by new hypertension and proteinuria after 20 weeks of gestation and can lead to multiple maternal and fetal complications if not monitored and managed properly. Treatment involves controlling blood pressure, administering magnesium sulfate to prevent eclampsia, delivering the baby if condition worsens, and monitoring both mother and fetus closely.
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Cme hypertensive disease in pregnancy (1) copy.pdfx-converted
- 2. Classified into 5categories: • Hypertension encountered before 20 weeks of gestation or persists after 6 weeks postpartum. It can be primary or secondary in aetiology. Chronic hypertension • Hypertensive condition in which systolic BP ≥ 140mmHgand / or adiastolic BP ≥ 90mmHgin at least 2 occasions, 4 hours apart, arising de novo after 20 weeks and resolved within 6 weeks postpartum in a previously normotensive woman Pregnancy induced hypertension (gestational hypertension)
- 3. 3 • New hypertension diagnosed after 20 weeks with significant proteinuria. • *Significant proteinuria =24-hour urine protein of >300mg/day (0.3g/day) Pre-eclampsia • Pre-eclampsia with severe hypertension and / or with symptoms, and / or biochemical and / or haematological derangement. Severe pre-eclampsia Eclampsia Pre-eclampsia with convulsion
- 4. 4 •Degree of hypertension: – Mild: SBP:140-149 / DBP:90-99 – Moderate: SBP:150-159 / DBP100-109 – Severe: SBP:≥ 160 / ≥110 Etiology Indefinite etiology, remainunknown Proposed theory: • Placental origin • Immunological origin • Biochemical origin • Genetics • Oxidative stress
- 5. Placental Origin Normal Placental development : Thisis why the maternal blood flow to the placenta canbe increases throughout pregnancy from 50 ml/min in first trimester to 500-750 ml/min at terms.
- 6. Abnormal Placental development: Trophoblast cell fail to invade maternal arteries Spiral arteries retain their pre- pregnancy state Impair perfusion of fetoplacental unit Ischaemic necrosis of acotyledon of placenta Placenta release inflammatory cytokines like TNF-α and IL-6. Dysfunction of vascular endothelial cells Decrease release of nitric oxide & other vasodilator substances Vasoconstricton HPT
- 7. Immunological Origin • Results from some type of immunereactivity in the mother caused by the fetus, which contain the paternalgene. • This theory is supported by the fact that: – Thesymptoms of preeclampsia disappears within a few days after birth of the fetus and its products. – Thickening of the kidney glomerularmembranes (seen in PE,undeterminedcauses)
- 8. Proposed mechanism Maternal immune reaction toward paternal gene in fetus. Deposit &cause thickening of the kidney glomerular membranes Reduces rate of glomerular fluid filtration Thus, to maintain normal formation of urine, arterial pressure elevated HPT
- 9. Biochemical origin •Imbalance of vasodilators (eg:prostaglandin) andvasoconstrictors (eg:thromboxane A2) Genetics •Genetic factors are thought to play a role in disease susceptibility •Primigravida women with family history of pre-eclampsia have 2 to 5 folds increased risk of developing the disease compared with primigravida women with no history of pre-eclampsia Oxidative stress •Increase in the levels of placental oxidative stressmay mediate endothelial cell dysfunction and contribute to the pathophysiology of pre-eclampsia
- 10. Biochemical Origin •Imbalance of vasodilators (prostaglandin) and vasoconstrictors (thromboxaneA2) Risk factors Moderate risks • First pregnancy • Age40 years or older • Pregnancyinterval of more than 10years • BMI of ≥ 35kg/m2 at firstvisit • Family hx of pre-eclampsia • Multiple pregnancy Efficacyof aspirin: -17%reduction in risk of pre-eclampsia -8%reduction in relative risk of preterm birth -14%reduction in fetal/neonataldeath -10%reduction in SGAbabies Advice women with >1 moderate risk factor for pre-eclampsia to take75mg of aspirin daily from 12 weeks until the birth of the baby (practice: 36 weeks) • +calcium carbonate 1gBD(promote fetal bone mineralisation & prevention ofgrowth restriction) Aspirin inhibit enzyme cyclo-oxygenase in the platelet and prevent release of thromboxane A2(vasoconstrictor)
- 11. 11 High risks • Hypertensive disease during previous pregnancy • Chronic kidney disease • Autoimmune disease such asSLEor APS • Type 1 or Type 2DM • Chronic hypertension Advice women at high risk of pre-eclampsia to take 75mg of aspirin daily from 12 weeks until 36 weeks of pregnancy • +calcium carbonate 1gBD
- 12. 12 Signs & symptoms ofpre-eclampsia • Severe headache • Problems with vision,such asblurring or flashing before the eyes • Epigastric pain • Vomiting • Sudden swelling of theface, hands or feet (oedema) • Hyperreflexia • Papilloedema • clonus
- 13. Multi-systemic effect of pre-eclampsia Maternal complications • CVA • Eclampsia • Thrombosis • Pulmonary oedema • Pulmonary embolism • PPH • Heart failure • Liver failure • Renal failure • DIVC • HELLPsyndrome • Retinal damage • Maternal death • Increased risk of LSCS Fetal complications • SGA/IUGR • Preterm labour • Placenta abruptio • Oligohydramnios • IUD • Respiratory distress syndrome • Intraventricular haemorrhage
- 14. Cardiovascular system Normal pregnancy: • Marked peripheral vasodilatation →fall in total peripheral resistance despite increase plasma volume& cardiac rate. Pre-eclampsia : • Marked peripheral vasoconstriction due to imbalanceof vasoactive substances →HPT • HPT+loss of endothelial cell integrity due to local disturbances in control of vessel toneproduced by endothelium of vessel wall→ greater vascular permeability & generalizedoedema.
- 15. Renalsystem • Thickened glomerular tufts that containprotein deposit in the basement membrane → Glomeruloendotheliosis • Associated with impaired glomerular filtration & selective loss of intermediate weight proteins(eg : albumin & transferrin) Proteinuria: >300mg per volume in 24 hourcollection Raisedplasma urate levels: >0.35mmol/litres Reduction in plasma oncotic pressure Exacerbate development of oedema
- 16. Haematological system Damageof endothelium Adherence of platelet to damaged area Reduce platelet count-risk of bleeding Increase fibrin deposition-risk of thrombosis Increase production of fibrin Afalling platelet count and changesin clotting factors may proceed to disseminate intravascular coagulation with micro-angiopathic hemolysis secondary to small vessel blockage, revealed by anaemia and the presence of fragmented red cells in peripheral blood.
- 17. Hepatic System • Vasoconstriction in the hepatic bed leads to periportal fibrin deposition, haemorrhageand hepatocellular necrosis. o Leadsto elevated liver enzymes may occur as part of the HELLPsyndrome (haemolyticanaemia, elevated liver enzymes, and low plateletcount
- 18. Neurological system • In Pre-eclampsia: – Cerebral oedema & haemorrhagic lesions especiallyin posterior hemisphere – Thus, headache & visual disturbances occurs (eg: scotomata, blurred vision. • In Eclampsia: – 1 or more convulsions, not contributable to other cerebral conditions in apatient withpre-eclampsia – Cerebral vasoconstriction leads to focal ischemia& abnormal electrical activity, thus, triggersseizures. • 38%occur antenatally • 18%occur intrapartum • 44%post partum (esp 1st 24-48H)
- 19. Fetal & Placenta • Poor perfusionplacental insufficiency,thus resulting in : – Oligohydramnios – IUGR – PlacentaAbruptio – IUD – Preterm labour
- 20. Investigations • Todetect any evidence of PE,complications of PE& obtain baseline results for future comparison (monitoring) • FBC • Coagulation profile • LFT • RP • UFEME/24H urine protein • PBF • GSH/GXM • Uric acid • Ultrasound assessmentfor fetal growth, AFI,umbilicalartery doppler
- 21. 21 Management • Assessmentand evaluation of patient • Control of blood pressure (aimBP<150/100) • Fetal assessment • Prevention of eclampsia - useof MgSO4 • Plan for delivery – timing andmode • Useof IM dexamethasone (24-34 weeks) –for lung maturity
- 22. 22 Pre-pregnancy care • Women considered tobe at high risk of pre- eclampsia should be referred for pre- pregnancy counselling (to be seenat PPC)to identify modifiable riskfactors. – Lifestyle modification (eg: cessation of smoking and diet adjustment) – Revisemedications to optimize medical conditions and cessation of potentially teratogenic agents(eg: warfarin-> warfarin embryopathy & ACE-I->renal dysgenesis, lung hypoplasia) – Drugs of choice: methyldopa, labetalol,nifedipine
- 23. 23 Antihypertensive drugs • Methyldopa (oral) – MOA: - altered to α-methylnorepinephrine, stimulates inhibitory α-2 adrenergic receptors inhypothalamus - Reducessympathetic tone, total peripheralresistance & bloodpressure. - No direct effect on cardiacfunction. – SE: depression, drowsiness, headache, liver disorder, postural hypotension – CI: acute hepatic disease,history ofdepression – Starting dose: 250mgTDS – Maximum dose: 1gTDS
- 24. 24 Antihypertensive drugs • Nifedipine (oral) – MOA: - Calcium channel blocker. - Inhibits the passageof calcium through the gated channels of smooth and cardiac muscle (vasodilation and musclerelaxation) - Causesdilation of coronary & systemic arteries,decrease peripheral resistance, systemic BP&afterload. – SE: severe headache (mimic worsening disease), flushing, dizziness, palpitations, ankle oedema – CI: Acute MI – Starting dose: 10mgTDS – Maximum dose: 20mgTDS
- 25. 25 Antihypertensive drugs • Labetalol (oral orIV) – MOA: - Exhibits selective α-1 antagonist and nonselectiveβ-2 antagonist effects. - Causesadecrease in systemic arterial blood pressure& systemic vascular resistance without asubstantial reduction in resting heart rate, cardiac output, or stroke volume – SE: tremor, headache, scalptingling – CI: AVheart block, heart failure, bronchialasthma – Starting dose: 100mgTDS – Maximum dose: 400mgTDS
- 26. 26 Antihypertensive drugs • Hydralazine (IV) – MOA: - decreases BPby exerting direct relaxant effect on vascular smooth muscle – SE: reflex tachycardia, Naand H2Oretention, vertigo, myocardial stimulation, SLElikesyndrome – CI: tachycardia
- 27. 27 Monitoring of mother andfoetus Maternal monitoring Fetal monitoring •Vital signs •Full blood count •Serumrenal profile •Serumliver profile •Urinalysis •Sign and symptom of worsening disease process – nausea and vomiting, persistent severe headache, blurred vision •Fundal height •Fetal kick chart •Fetal heart (cardiotocography) •Doppler of umbilical artery •Ultrasound (fetal size,amniotic fluid)-4 weekly or more frequent asindicated
- 28. Timing of delivery • PIHnot on treatment – 40weeks • PIHon treatment – 38 weeks • SeverePIH– 37 weeks • Pre-eclampsia – 34-37 weeks • Eclampsia – immediate delivery oncestable
- 29. 29 Indications for MgSO4 asprophylaxis Severe pre-eclampsia Severe PIH(SBP>160mmHg, DBP>110mmHg) Hypertensive crisis Imminent premature delivery (<32 weeks) forfetal neuroprotection Indications for MgSO4 astreatment Eclampsia If the patient is symptomatic of impending eclampsia • 58%reduced risk of eclampsia • Maternal mortality lower among women allocated with MgSO4 *MOA remains unclear. Possiblemechanisms: -acts asvasodilator, protecting blood brain barrier to decrease cerebral oedema and relieve vasoconstriction.
- 30. Management of Pre-Eclampsia – Anti-hypertensive medication: • Aim BP<150/100 • 1st line: labetalol(oral/IV) • 2nd line: nifedipine,methyldopa – PEprofiles: FBC,RP ,LFT ,Coagulation profiles, uric acid – Fetal monitoring: Growth scan,AFI,umbilicalartery doppler – CTG – IM dexamethasone ifconsidering delivery (24-34 weeks) – For IV MgSO4asprophylaxis or symptomatic of impending eclampsia
- 31. Indication for EarlyDelivery - Timing of delivery: • Determine by severalfactors: Severe refractory hypertension= BPremains uncontrolled despite maximal medicaltherapy Deteriorating maternal or fetalconditions Availability of neonatalcare Completion of corticosteroid • After 37weeks: recommend delivery within24- 48hours
- 32. 32 Management of Eclampsia • Anti-convulsant – MgSO4 – Loading dose: • IV =4g(8mls) +12mls NSgiven over 15minutes • Recurrent convulsion =further dose 2g(4mls) +8mls NS given over 15minutes • IM =10g with 5g(10mls) given ateach buttock – Maintenance dose: • 24.7g +500mls NSto run at 21mls/hour =1g/hour • Maintenance dose to continue up till 24hours post- delivery or 24 hours from the last convulsion (whichever occurslater)
- 33. 33 Management of Eclampsia o Sideeffects of MgSO4:neuromuscular blockade, loss of tendon reflex, respiratory & cardiac depression • Sign of toxicity : respiratory rate depression, prolong QRS complex, cardiac arrest • Aim urine output at least (30mls/hour) – to prevent retention of magnesium in thecirculation * Urine output is not a sign of toxicity • Antihypertensive drugs: hydralazine,labetalol • Plan for delivery once patientstable
- 34. 34 MgSO4 level(mmol/L) Effects 0.8 to 1.0 Normal plasma level 1.7 to 3.5 Therapeutic range 2.5 to 5.0 ECGchanges (P-Qinterval prolonged, widen QRScomplex) 4.0 to 5.0 Reduction in deep tendon reflex >5.0 Lossof deep tendon reflexes >7.5 Sino-atrial and atrioventricular blockade, respiratory paralysis and CNSdepression >12 Cardiac arrest Antidote for MgSO4 toxicity: - 1gm Calcium gluconate (10ml of 10% solution) given IV slow bolus over 3minutes
- 35. HELLPSyndrome •Variant of severe pre-eclampsia/eclampsiawith biochemical evidenceof – Haemolysis (H) – Elevated Liver enzymes (EL) – Low platelets (LP) •Occursat various gestational ages-ranging from mid- 2nd trimester of pregnancy until several days postpartum(20%) • A/w increase maternal and perinatalcomplication - Mortality rate: maternal-24%, perinatal-30-40%
- 36. 36 Management of HELLPsyndrome • Early recognition- investigations and evaluation of patient • Control HPT • Assessfetal condition • Plan for delivery – timing andmode • Platelet transfusion if <50,000/uL orsymptomatic • Prevention of seizure- use of MgSO4
- 37. 37 Post-partum care • All patients should have their their blood pressure monitored during home visits orin primary health carecentres. • Ensurecompliance if patient isdischarged with medication. • Patients should be counselled about contraception, spacing and risk of developing similar problems in subsequentpregnancies • Longterm follow-up is advised for development of chronichypertension
- 38. References • NICEclinical guideline107 • Labour ward manual SGH • Clinical Protocols in O&Gfor Malaysians Hospitals • Obstetrics by Tenteachers • Journal of cerebral circulation:Magnesium sulphate treatment for the prevention of elampsia • European journal of obstetric &gynaecology and reproductive biology