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46 Cards in this Set

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  • Back
What are the pre-disposing factors for pre-eclampsia?
Primigravida
Past history of PE
Family history in mother or sister
Existing PE
Multiple pregnancy
BMI > 30
Microvascular disease due to: Diabetes, AI disorder, renal disease, blood-clotting disorders.
What is the aetiology of pre-eclampsia?
Unknown, but thought to arise in the placenta.
This is because: arises only in pregnancy and is cured after delivery of the placenta.
Can also arise in a hydatidiform mole.
What are the clnical features of pre-eclampsia that arise due to direct vascular damage?
Hypertension
Oedema
Platelet aggregation and DIC
Cerebral haemorrhage
Increased incidence of DVTs
What are the secondary effects of pre-eclampsia that arise due to hypoperfusion of tissues?
Kidney - proteinuria.
Brain - eclampsia, CVA.
Liver - dysfunction, haemorrhage.
What are the uteroplacental effects of pre-eclampsia?
Abnormal flow patterns and abnormal invasion of uteroplacental arteries.
IUGR
Oligohydramnios.
How does preeclampsia cause abnormal invasion of the uteroplacental arteries?
In pre-eclampsia, the invasion of the maternal uterine spiral arteries into the trophoblast does not occur consistently. Therefore, the spiral arteries retain their smooth muscle medium and vascular tone, which impairs the blood supply to the uteroplacental vascular bed.
What are the symptoms of pre-eclampsia?
Headache
Visual disturbances
Abdominal pain (hepatic, uterine)
What are the signs of pre-eclampsia?
Hypertension or proteinuria
Clonus, hyperreflexia
Abdominal tenderness (hepatic, uterine)
IUGR on US
What is the cure for pre-eclampsia?
Delivery of the placenta and foetus.
What influences the decision to deliver for pre-eclampsia at 37 weeks plus?
Deliver if any proteinuria
OR unstable blood pressure
OR laboratory evidence of severe disease
OR foetal compromise
What influences the decision to deliver for pre-eclampsia at 32 - 37 weeks?
Must have unequivocal evidence of severe disease to support decision to deliver.
What influences the decision to deliver for pre-eclampsia at 28 - 32 weeks?
Deliver if severe disease after steroid administrion.
What influences the decision to deliver for pre-eclampsia at 23 - 27 weeks?
Deliver if maternal well-being threatened in the presence of very severe disease.
What is the criteria for pre-eclampsia?
1. Development of gestational hypertension (systolic greater than 140 mm Hg or diastolic greater than 90 mm Hg) after 20 weeks of pregnancy in a previously normotensive patient.
2. Objective evidence of systemic maternal disease (hyperuricaemia, proteinuria equal to or greater than 300 mg/day or greater than 30 mg of protein per mmol of creatinine in a random urine sample, or elevated circulating transaminase levels)
3. Absence of a history of primary hypertension or renal disease
4. Return of blood pressure to normal within three months postpartum.
What investigations are appropriate in pre-eclampsia?
1. FBE —a rising haematocrit indicates plasma volume contraction; thrombocytopenia indicates early disseminated intravascular coagulation.
2. Clotting studies: Perform if there is thrombocytopenia or abnormal liver function
3. Serum uric acid—uric acid clearance falls in pre-eclampsia, and there is a reciprocal rise in serum levels. A value exceeding 0.35 mmol/L is clearly abnormal
4. Serum electrolytes—hypokalaemia may suggest a secondary cause for the hypertension
5. Serum creatinine—a level higher than 0.09 mmol/L is abnormal for pregnancy and indicates impaired glomerular filtration rate
6. Liver function tests—a rise in liver enzymes, particularly aspartate aminotransferase (AST), indicates hepatic cellular damage
7. Urinalysis and microscopy. Proteinuria 1+ or more should be quantified using either the spot protein–creatinine ratio (normal is less than 30 mg protein / mmol creatinine) or the 24-hour urinary protein excretion (normal is less than 300 mg/24 hours). Haematuria and/or casts suggest underlying renal parenchymal disease.
How can blood pressure be lowered during pre-eclampsia?
For the acute lowering of blood pressure if systolic blood pressure is 170 mm Hg or above and/or diastolic blood pressure is 110 mm Hg or above, use:
hydralazine 5 mg slowly IV, every 20 minutes, up to 15 mg
and/or hydralazine 5 to 10 mg per hour by IV infusion
OR
nifedipine immediate-release tablets 10 to 20 mg orally,
What drug is given to prevent risk of seziures?
Magnesium sulphate.
What drug is given to promote foetal lung maturity if deliver is imminent?
Betamethasone.
What is superimposed pre-eclampsia?
Developing pre-eclampsia (high blood pressure and proteinuria) in a women with chronic hypertension existing prior to pregnancy.
What is non-proteinuric gestational hyperension?
Hypertension arising for the first time in the second half or preganancy and in the absence of proteinuria. It is not associated with adverse pregnancy outcome.
What is the proposed stepwise aetiology of pre-eclampsia?
Genetic predisposition -->
Abnormal immunological response -->
Deficient trophoblast invasion -->
Hypoperfused placenta -->
Circulating factors -->
Vascular endothelial cell activation -->
Clinical manifestations of disease
What is the effect of pre-eclampsia on the cardiovascular system?
Peripheral vasoconstriction, resulting in hypertension.
Therefore loss of endothelial cell integrity.
Leads to greater vascular permeability and generalised oedema.
What is the effect of pre-eclampsia on the renal system?
Development of glomeruloendotheliosis lesion.
Associated with impaired glomerular filtration and selective loss of intermediate weight proteins such as albumin and transferrin, leading to proteinuria.
Reduction in plasma oncotic pressure --> oedema.
What is the effect of pre-eclampsia on the heamatological system?
Platelets adhere to damaged endothelium; also, laying down of fibrin.
What is the effect of pre-eclampsia on the liver?
Subendothelial fibrin deposition leads to elevated LFTs. Can be associated with haemolysis and a low platelet count due to platelet consumption.
i.e. HELLP syndrome.
What is HELLP syndrome and how common and bad is it?
Severe form of pre-eclampsia.
Haemolysis, elevation of liver enzymes, low platelets.
Occus in just 2 - 4% of women with disease.
Associated with high rate of foetal loss (60%).
What is the effect of pre-eclampsia on the neurological system?
Convulsions (eclampsia).
How do the vast majority of pre-eclamptic women present?
Flu like symptoms or asymptomatic.
What is appropriate anti-hypertensive therapy in pre-eclampsia?
Methyldopa: centrally-acting antihypertensive agent. Safe. Unfortunately takes 24 hours to work. SE: sedation, depression.
Labetalol/oxprenolol: alpha- and beta-blocker.
Clonidine: alpha-blocker.
Prazosin: alpha-blocker

If still failing to reach satisfactory BP (135/85) add hydralazine, nifedipine.
What is hydralazine?
Predominantly an arteriolar vasodilator with little effect on venous smooth muscle. Arteriolar vasodilation results in reflex sympathetic stimulation, leading to tachycardia and fluid retention.
What is nifedipine and can you name a side-effect?
Calcium-channel blocker.
Rapid onset of action.
Can cause severe headache (may mimic worsening disease).
What is placental abruption?
The premature separation of a normally sized placenta from the uterine wall.
In placental abruption, where does the blood normally go?
2/3: Separation is at the end of the placenta therefore blood tracks down the cervix and is revealed as vaginal bleeding.
1/3: Bleeding is concealed. Present as maternal shock, foetal distress, foetal death.
What are some of the associations of pre-eclampsia, even though the direct cause is often unknown?
Defective trophoblast invasion.
Abdominal trauma.
High parity.
Uterine over-distension (e.g. polyhydramnios, multiple)
Sudden decompression of the uterus (e.g. after delivery of first twin)
What are some risk factors for placental abruption?
Hypertension
Smoking
Trauma to abdomen
Cocaine use
Anticoagulant therapy
Polyhydramnios
FGR
What is the clinical presentation of placental abruption?
Abdominal pain
Vaginal bleeding
Uterine contractions
If large: maternal shock
Abdominal palp: tender, tense uterus ("woody hard")
Woody hard uterus?
Placental abruption.
What are the complications of placental abruption?
Hypovolaemic shock
DIC
ARF
Fetomaternal haemorrhage
Perinatal mortality
FGR
Why can DIC be triggered by placental abruption?
Triggers: tissue thromboplastin release, endothelial damage to small vessels, pro-coagulant phospholipid production.
Why can placental abruption cause ARF?
Poor renal perfusion secondary to hypovolaemia, hypotension, DIC.
Patient becomes oliguric and may develop acute tubular necrosis.
Usually recover well if adequately resuscitated.
Why is the fetus at risk in placental abruption?
Hypoxia following placental separation.
Premature delivery.
Why does placental abruption sometimes present as contractions?
Due to the irritable effect of blood within the uterus.
Couvelaire uterus
Constant pain associated with a uterus that is very hard on palpation.
Due to a large volume of blood within the myometrium.
Management of severe placental abruption?
DR ABC
Oxygen
IV access
FBC and clotting
LFTs, UEC
Cross-match
Fluid resus
Catheter
Blood transfusion/FFP/platelets/cryoprecipitate
Central venous pressure and arterial lines
Eliminate the cause - deliver baby and placenta
Management of non-severe placental abruption? (i.e. no foetal distress)
Monitor foetal well-being and growth, AFI, doppler US of umbilical artery, CTG
What are the main consequences of abnormal trophoblast invasion?
Pre-eclampsia, FGR, placental abruption, intrauterine death.