Pre Eclampsia

1. Pre Eclampsia S Rajendran

2. Pre eclampsia (PET) • Disorder of the epithelium • Peculiar to pregnancy - arising from the failure of maternal adaptation to pregnancy • Multisystemic • Manifested by • Hypertension • Renal impairment - accompanied by proteinuria • Fluid retention • Intravascular coagulation

3. Pre eclampsia • Impact: • 2 % pregnancies • Significant maternal morbidity & mortality (40 000 deaths worldwide, 14 in UK (2004 CEMD) • Significant neonatal morbidity & mortality • 20% of SCBU/NNU occupancy • 15% of iatrogenic preterm deliveries • Long term : development of hypertension, Diabetes , IHD

4. Risk Factors • 1. Socio demographic • Age>40 • SE status • Ethnic groups • 2. Genetic • Mother/ sister with PET • 3. Pregnancy factors • Multiple pregnancy • Primipara • Previous early onset severe PET • 4. PMH • Obesity • Chronic renal disease • Chronic hypertension • Diabetes • Thrombophilia • SLE

5. Pathogenesis • Theories: • Various • Reduction in placental blood flow • Either due to abnormal placentation • Maternal microvascular disease • Release of circulating factors target maternal vascular endothelial cells

6. Pathogenesis - cont • Early pregnancy • Failure of communication between mother - fetal systems • Failure of physiological adaptation • Therefore - failed trophoblastic invasion of maternal spiral arterioles • Thomboxane (vasosonstrictors) increase rel to PGI2 and NO (Vasodilators) • Failure of plasma volume expansion • Development of high pressure system

7. Pathogenesis - cont • Placenta perfused under high pressure • Endothelial damage • Microthrombi formation • Placetal size reduced • IUGR

8. Pathogenesis - clinical syndrome • 1. CVS/ Pulm • High CO state • High PVR • LVF • Pulmonary odema - ‘leaky endothelium’ • ARDS

9. Pathogenesis - clinical syndrome • 2. Kidneys • Glomerular endothelial cells swell • Block capillaries • ‘leaking’ - proteinuria (>300mg/24hrs) • Impaired renal function tests

10. Pathogenesis - clinical syndrome • 3. Liver • Fibrin deposits - hepatocellular damage • Distension, odema - epigastric pain • Subcapsular haemorrhage • DIC - abnormal LFTs • HEELP

11. Pathogenesis - clinical syndrome • 4. CNS • Vasoconstriction as a protective response - headaches. Visual disturbance • Hyperreflexia • Small vessel damage - infarcts, haemorrhages - Eclampsia , CVA

12. Diagnosis • Hypertension > 160/90 on two occasions • Proteinuria > 300 mg/24 • Altered renal function tests • Raised UA • Raised serum Cr • Altered LFTs • Raised AST/ALT • Derranged clotting factors • Coagulation • Platelet consumption - DIC

13. Management • 1. Treat blood pressure • To prevent CVA • To allow fetal maturity • 2. monitor maternal well being • BP, 24 urine protein • Biochemistry • Symptoms • 3. monitor fetal wellbeing • USS for growth • Doppler • CTG • Steroids (if preterm delivery envisaged)

14. Management • Delivery is the only cure!! • So management relies on delivery as soon as practically possible in the most suitable way possible • Balance between maternal and fetal risks

15. Treatment • 1. Antihypertensives • Long term - methyl dopa safest • But - slow acting . Poor antihypertensive • Other SE • Labetalol - good effective in acute management of severe hypertension (IV and Oral ) But placental hypoperfusion Nifedipine - good in acute management But - placental hypoperfusion Hydralazine - IV only useful in acute management

16. Eclampsia • Fitting !! • Grand mal • Self limiting • BP can be normal • Any woman in pregnancy who fits should have eclampsia management until proven otherwise • Management: • Treat fit - Mg SO4 • Prevent further fitting - Mg SO4 • Stabilise mother & BP • Deliver