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Pre-eclampsia is a condition that only occurs in women who are at least 20 weeks pregnant, though it may occur a short while after childbirth. It is thought that some form of pre-eclampsia will occur in as many as 10% of all pregnancies, though severe pre-eclampsia affects only 0.5%. The condition is characterised by high blood pressure and protein in the urine, and is due to a reduction of maternal blood supply to the placenta1. Other symptoms, ranging from excessive blood clotting to kidney or liver damage, may occur in the mother if the placenta is damaged by the lack of blood supply. Eclampsia is the name given to a state of convulsions, altered consciousness and eventually coma that may occur following pre-eclampsia, or in some cases entirely out of the blue2. Severe pre-eclampsia and eclampsia are potentially life-threatening, and the only cure is to deliver the foetus and placenta.
The exact cause of pre-eclampsia is not known, but there is thought to be a genetic element, with sisters and daughters of an affected woman being more at risk. Being overweight, aged over 40, developing gestational diabetes or having pre-existing blood pressure or kidney problems also increase the risk of developing pre-eclampsia. The condition may be due to impaired development of the arteries that supply the placenta with the mother's blood – instead of relaxing and allowing blood to flow easily, they remain contracted and impede blood supply to the placenta. This causes tissue damage in the placenta, with the result that it secretes chemicals that cause further contraction of the maternal blood vessels. This leads to a 50% reduction in blood flow to the placenta and an increase in maternal blood pressure. If this situation persists, placental tissue can die and float off into the mother's blood. These pieces of tissue are broken up in the lungs, but this leads to the release of thromboplastins that cause excess clotting and causes deposits of fibrin, a protein that forms part of the body's clotting system, in the kidneys, liver and brain.
The first sign of pre-eclampsia is usually a significant increase in blood pressure compared to that recorded early during the pregnancy. This is often followed shortly by the presence of protein in the urine, which can be detected using urine dipstick testing. Mild pre-eclampsia therefore does not have any symptoms that the woman might notice, and is usually detected during antenatal check-ups. Various problems may occur in severe pre-eclampsia following damage to the placenta:
Neurological symptoms. Deposition of fibrin in the brain may result in severe headaches, confusion, visual disturbance, increased tendon reflexes and the convulsions of eclampsia.
Clotting derangement. Blood clotting can be deranged due to disseminated intravascular coagulation, in which clotting takes place in multiple sites throughout the body, using up platelets and other clotting reserves. This excess clotting thus leads to a lack of clotting, and thus a tendency to bleed.
Renal failure. Deposition of fibrin in the kidneys can lead to acute failure and thus an abnormally low rate of urine production (oliguria).
Liver or lung failure. Deposition of fibrin in the liver or lungs may result in failure of those organs. Damage to the liver may result in abdominal pain, nausea and vomiting.
HELLP syndrome. Deposition of fibrin in small blood vessels, mostly in the liver, leads to a combined syndrome of Haemolysis, Elevated Liver enzymes and Low Platelets. Haemolysis is the destruction of red blood cells and leads to anaemia; liver enzymes are indicators of the state of the liver and are raised due to blockage of the liver's blood supply; platelets are required for blood clotting and are used up as the fibrin causes clotting inside the blood vessels. Each of these may also occur in isolation.
Foetal growth restriction. This occurs over time due to the reduced maternal blood supply to the placenta, which leads to a reduction in nutrients delivered to the foetus. There may also be a lack of fluid around the baby (oligohydramnios), and in severe cases the foetus may end up distressed or even die.
In eclampsia, the above symptoms are all worsened, and are accompanied by swelling of the ankles3, the face and other body parts due to retention of water in the tissues. The convulsions that mark eclampsia begin with a 'tonic' contraction of the muscles and holding of breath, and are followed by a 'clonic' stage in which the body jerks uncontrollably. The convulsions are preceded by restlessness and twitching, and are followed by either more convulsions or a coma lasting upwards of an hour.
Trials have so far failed to find an effective means of preventing pre-eclampsia, though aspirin may improve the risk for women who develop raised blood pressure before 28 weeks of pregnancy. There have been suggestions that changes to lifestyle or diet might help reduce the risk, but there is insufficient evidence regarding such changes.
Treatment of pre-eclampsia aims only to control blood pressure and prevent convulsions – the only cure is to deliver the foetus and placenta. Bed rest and relaxation are of great use in all women with pre-eclampsia, and regular monitoring of blood pressure, urine protein, blood clotting and liver and kidney function are all important. Hospitalisation is required in moderate and severe cases, and antihypertensive drugs such a methyldopa and nifedipine are used to reduce blood pressure.
In women who are less than 35 weeks pregnant, the aim is to manage the pre-eclampsia until the foetus is 35 weeks, so that it has a better chance of survival. Daily foetal movement counts4 or cardiotocography (CTG)5 three times a week can be used to monitor the foetus, and regular ultrasound scans may be used to track its growth. If severe pre-eclampsia or eclampsia develop, the foetus is delivered; otherwise, labour is awaited, and will be induced or a caesarean section performed if the pregnancy exceeds 40 weeks. Once labour begins, CTG is used to detect any foetal distress. Blood pressure is monitored for a week after delivery and should return to normal within six weeks.
Severe pre-eclampsia and imminent eclampsia are treated with intravenous magnesium sulphate, which reduces contraction of the blood vessels, dilates the blood vessels in the brain, reduces platelet usage and protects the placenta from further damage. An excess of magnesium sulphate can cause reduced urine output, depression of breathing and reduced tendon reflexes – this is tested for and is reversed using calcium gluconate if necessary. Once the blood pressure and convulsions have been brought under control, the labour is induced and the foetus delivered. Due to the risk of bleeding, drugs are given to contract the uterus following delivery.
With appropriate treatment, only a handful of women will actually die from severe pre-eclampsia and eclampsia, mostly from heart failure or a bleed into the brain due to the high blood pressure. The outcome for the baby following an urgent delivery depends upon how early it is born, though the existence of specialist neonatal units means that much can be done to support premature infants. Following an episode of pre-eclampsia, around one in three women will have high blood pressure without protein in the urine during a subsequent pregnancy, while less than one in twenty will have another episode of pre-eclampsia. However, pre-eclampsia occurring earlier than 34 weeks into the pregnancy may indicate an underlying problem leading to high blood pressure and this may require further investigation.