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Erstellt von Anna Walker
vor fast 10 Jahre
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Frage | Antworten |
When does pre-eclampsia manifest in a pregnancy? | After 20 weeks, unless pregnancy is a hydatidiform mole. |
What are the clinical features of PET? | HTN, proteinuria, oedema, multiorgan involvement, fetal compromise, significant maternal morbidity. |
What are the risk factors for PET? | FHx, previous PET, extremes of age, socio-economic status, multiple pregnancy (larger placenta), primigravida, assisted conception, obesity, DM. |
What is PET caused and cured by? | CAUSED by pregnancy, CURED by delivery (of placenta). |
What is the pathophysiology of the endothelial cell disorder that is PET? | An excessive inflammatory response to syncytial trophoblast-related cells released into maternal blood. |
How is the placenta abnormally formed in PET? | Trophoblast cells fail to invade into maternal endometrium and myometrium. Maternal spiral arteries continue to have thick muscular walls. This leads to high resistance and low flow into the placenta. This in turn leads to damage of the villi. |
What are the risks for the fetus in PET? | IUGR, IU hypoxia, prematurity, abruption, still birth, metabolic syndrome (fetal programming). |
What are the risks for the mother in PET? | Endothelial cell dysfunction, leading to increased capillary permeability, tissue oedema, tissue oedema, vasospasm and DIC. 1. Tissue oedema 2. HTN (altered production of vasodilators) 3. Clotting dysfunction (abnormal production of procoagulants). Organ hypoperfusion - kidneys, liver, brain (presents with headaches, blurred vision etc). May get LVF/pulmonary oedema. Seizures, cortical blindness, intracranial bleeds, renal failure, liver capsule haemorrhage. |
What maternal monitoring should be undertaken in PET? | BP 4-6 hourly. FBC, U&Es, serum creatinine especially, urates. Urinalysis +/- quantify proteinuria (PCR, 24h collection), signs and symptoms, fluid balance. |
What fetal monitoring should be undertaken in PET? | USS for size and growth. CTG (>26 weeks). Movements. Umbilical artery Doppler - is there flow throughout cardiac cycle? Fluid volume. |
What are some indications for delivery in PET? | If maternal BP cannot be controlled with antihypertensives. Eclampsia. Pulmonary oedema. Renal, hepatic or coagulation impairment. Fetal distress. Milder pre-eclampsia at term. Need steroids if pre-term birth (ideally for a week). |
What is the definition of hypertension in pregnancy? | >140/>90 in a pregnant woman. OR >30 systolic or >15 diastolic up from booking BP. |
How much protein is needed to count as the proteinuria in pre-eclampsia? | A 24h collection containing 300mg of protein. |
What is Pregnancy-Induced Hypertension (PIH)? | This is when the BP rises above 140/90 after 20 weeks. It can either be due to pre-eclampsia or transient hypertension. Pre-eclampsia is a disorder in which hypertension and proteinuria (>0.3g/24h) appear in the second half of pregnancy, often with oedema. Occasionally proteinuria is absent, e.g. in early disease, when it is not always distinguishable from gestational hypertension, which is new hypertension presenting after 20 weeks without proteinuria. |
What is the epidemiology of pre-eclampsia? | Affects 6% of nulliparous women. Less common in multiparous women unless additional risk factors are present. Approximate 15% recurrence rate. This is up to 50% if there has been severe pre-eclampsia before 28 weeks. |
Describe the pathophysiology of PET. | Incompletely understood but appears to be a two-stage process. Stage 1 accounts for the development of the diseasse, occurs before 20 weeks and causes no symptoms. Incomplete invasion of spiral arterioles, and vessel walls do not vasodilate as they should. This impaired maternofetal trophoblast interaction may be caused by altered immune responses. In addition, spiral arteries may contain atheromatous lesions. The result is descreased uteroplacental bloodflow. Stage 2 is the manifestation of the disease. The ischaemic placenta, probably via an exaggerated maternal inflammatory response, induces widespread endothelial cell damage, causing vasoconstriction, increased vascular permeability and clotting dysfunction. This causes the clinical manifestationd of the disease. |
What is HELLP syndrome? | Consists of Haemolysis (H), elevated liver enzymes (EL) and a low platelet count (LP). Disseminated intravascular coagulation, liver failure and live rupture may also occur. The woman typically experiences severe epigastric pain; occasionally this is the presenting feature of pre-eclampsia, and it may occur postnatally in a hitherto well woman. Haemolysis turns the urine dark. Treatment is supportive and includes magnesium sulphate prophylaxis against eclampsia. Intensive care therapy is required in severe cases. |
What does NICE recommend women at risk of PET do to reduce their risk? | Take low-dose aspirin (75mg) starting before 16 weeks modestly reduces the risk. |
Describe the use of Methyldopa in PET. | Use to bring down BP if intending to keep pregnancy going for weeks. Acts centrally, stop after delivery (can cause post natal depression). |
Which drugs would you use for intermediate-acting control of BP in PET? Short-acting? | B-blockers, Calcium channel blockers (e.g. Nifedipine). Short-acting = hydralazine occasionally used, but avoided due to the side effect of headaches. Diuretics are NOT used - woman is already leaking fluid from vasculature - if you make her lose more she will clot more. Anaesthetists occasionally may opt to use them. |
Describe the use of Magnesium Sulphate in PET. | Used to treat eclamptic fits. Muscle relaxant and treats cerebral oedema. Very narrow therapeutic margin before toxic dose. 2.5g IM is a therapeutic dose. At 4 there is a loss of patellar reflexes (1st sign of toxicity). Need to make sure next dose will not push it up to 4g - need regular blood tests to check Mg levels; if >3, omit next dose. If anuria, don't give it as patient cannot excrete it. |
Describe the postnatal care of a pre-eclamptic woman. | Whilst delivery is the only cure for pre-eclampsia it often takes at least 24h for severe disease to improve and it may worsen during that time. Liver enzymes, platelets and renal function should still be monitored. Low platelets usually return to normal in a few days. Fluid balance monitoring is essential: pulmonary oedema and resp failure may follow uncontrolled administration of IV lfuid, which is restricted to 80ml/h plus losses. If the urine output is persistently low, the central venous pressure (CVP) monitoring will guide management. The BP is maintained at aroun 140/90. The highest level tends to be reached about 5 days after birth. Postnatal treatment is usually with a B-blocker and may be needed for several weeks. Long-term management involves communication with the GP and community midwives for BP monitoring after discharge. At 6 weeks women with persistent proteinuria or HTN should be referred to a renal/HTN clinic. |
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