Pre Eclampsia - Lecture notes 2 PDF

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Pre-eclampsia diagnosis, investigations, risks and management...

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MBChB Pre-Eclampsia 1. 1.

 Describe the classifications of hypertensive disorders of pregnancy. Pre-eclampsia o Can have normal BP changes during pregnancy  BP dependent on CO and SVR  Normally falls to minimum in 2nd trimester due to reduced SVR o In HTN - increase in SVR causes increase BP o Classification of hypertensive disorders in pregnancy  Pregnancy induced HTN  When BP >140/90 after 20w gestation de novo  Can be due to  Pre-eclampsia - disorder of HTN + proteinuria appearing in 2nd half of pregnancy  Occurs earlier than 20w in molar pregnancies  Gestational (non-proteinuric HTN) - new HTN presenting in 2nd half without proteinuria  Pre-existing / chronic HTN  When BP >140/90 before pregnancy or before 20w gestation  May already be on anti-HTN meds  Classification  Primary  Secondary - may be due to renal disease etc.  May be accompanied by proteinuria  Higher risk of developing pre-eclampsia

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 Demonstrate an understanding of severe pre-eclampsia and eclampsia including the use of anti-hypertensives and magnesium sulphate. Formulate a management plan for women suffering from pre-eclampsia including the use of anti-hypertensives. Pre-eclampsia o Multi-system disease - usually manifests as HTN and proteinuria o Peculiar to pregnancy - of placental origin  Cured by delivery o Blood vessel endothelial cell damage  With maternal inflammatory response  --> vasospasm / increased capillary permeability / clotting dysfunction o Characterised by  HTN >140/90  Proteinuria >0.3g / 24hr  Occurs after 20w gestation  Normalises after delivery of foetus o Classification  Mild - proteinuria + mild-moderate HTN  Moderate - proteinuria + severe HTN without maternal complication  Severe - proteinuria + severe HTN + maternal complications o Aetiology  Placental disease  Causes unknown  Risk factors

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High risk Previous severe early-onset pre-eclampsia Chronic HTN DM AI disease e.g. antiphospholipid syndrome / SLE / thrombophilia  Moderate risk  1st pregnancy - most at risk  ? Association with abnormal immunological response to foetal genome  Don’t know how they will react as not been pregnant before  >40y/o  Pregnancy interval >10y  BMI >30  FHx of pre-eclampsia  Multiple pregnancy - if 2 placentas!  Uterine artery notching on Doppler IF 1 HIGH RISK + 2 MODERATE RISK - TAKE ASPIRIN 75MG FROM 12W UNTIL DELIVERY Pathophys Stage 1 - development of disease - occurs between 12-13wks of pregnancy  Normal pregnancy - trophoblastic invasion of spiral arterioles --> vasodilation of vessel walls  In pre-eclampsia - invasion is incomplete  Impaired maternofoetal interaction - may be caused by altered immune responses  Incomplete invasion --> spiral arteriole channels not widened  Doesn’t create that low resistance circuit  Spiral arterioles may contain atheromatous lesions resulting in decreased uteroplacental blood flow  "Factor X" - mediatory factor released by placenta  Creates physical manifestations of pre-eclampsia  Causes widespread effects on endothelium throughout the body  Pre-eclampsia is a multi-system disorder Stage 2 - manifestation of disease  Ischaemic placenta - exaggerated by maternal inflammatory response  "Factor X" - mediatory factor released by placenta  Creates physical manifestations of pre-eclampsia  Causes widespread effects on endothelium throughout the body  Pre-eclampsia is a multi-system disorder  Induces widespread endothelial cell damage causing:  Vasoconstriction/vasospasm - increased vascular resistance--> HTN  Increased vascular permeability - proteinuria + oedema    

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Endothelial cell damage --> platelets used --> overall reduction in platelets in blood  Reduced placental blood flow - IUGR  Reduced cerebral perfusion - eclampsia  Cerebral oedema - headaches / visual disturbances In pre-eclampsia - don’t get the physiological 40% increase in blood

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volume   o 

Already under-perfused Means they can't tolerate blood loss

Clinical features Sx        

Can be Asx Headaches Drowsiness Visual disturbances N+V PV bleeding - ?abruption Epigastric pain / RUQ pain - Glisson capsule pain Tonic clonic seizures - severe (eclampsia)

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Signs 

HTN 

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Severe pre-eclampsia >160/110 Proteinuria May have foetal growth restriction - SGA Foetal compromise on USS Reduced liquor volume - OLIGOHYDRAMNIOS Uterus feels full of foetus - feels like less fluid Oedema ?abruption - woody ward uterus

Investigations First line  BP  Urine dip - rule out infection ALSO ?PROTEIN - TRACE/+/++  If +/++  Further investigation --> PCR  Protein-creatinine ratio (PCR)  >30mol/mL protein  Limit is 50 in non-pregnant patients  May be high when do it for the 1st time  + If repeat could get completely different value Monitor maternal complications  Bloods  FBC  U+Es  Increased uric acid + creatinine  Increased Hb  Fall in platelets  Rise in liver enzymes - ALT/ALP  Rise in LDH with liver disease  Long aPPT + PT

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Neuro exam - hyperreflexia, clonus, loss of patellar reflexes Fundoscopy - papilloedema Monitor foetal complications  USS  Umbilical A Doppler  CTG Management 1+ foetal/ maternal complications likely to occur within 2w of onset of proteinuria Assessment  Women w new HTN have BP + urine rechecked  Pts without proteinuria + mild/moderate HTN managed as outpts  BP + urinalysis repeated twice weekly  USS in 2-4w Admission  Necessary when  Symptomatic  Proteinuria 2+ on dipstick OR >0.3g/24hr  BP >160/110  Suspected foetal compromise Principles of management - when BP >160/110  Control HTN  Using known drugs  Don’t want the BP so low that it reduces foetal perfusion  Drugs  Methyldopa  Takes a long time to act  Normally used for chronic HTN in early pregnancy  Labetalol  Alpha and beta blocker - CI in asthma  Can be given in early pregnancy some increased risk of SGA babies  Nifedipine  CCB  ACEi contraindicated!  teratogenic as affect foetal urine production  Prevention of convulsions  Magnesium sulphate  Used for treatment + prevention of pre-eclampsia  IV loading dose followed by IV infusion  Not an anticonvulsant but treats eclampsia by increasing cerebral perfusion  Delivery baby  If baby is delivery whatever the gestation Mode of delivery o Before 34w - CS o After 34w

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IOL w PGs and epidural analgesia - helps reduce BP Anti-HTN drugs used in labour Maternal pushing should be avoided in 2nd stage if BP reaches 160/110  

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Raises intracranial pressure Risks cerebral haemorrhage Oxytocin instead of ergometrine in 3rd stage Ergometrine increases BP

Post-natal care o Post-delivery 24h important o Disease can still manifest then o Monitor  Bloods  Fluid balance - if CVP high - give furosemide  If low give albumin  BP...