Gestational hypertension is the most frequent cause of hypertension during pregnancy and the rate varies between 6 and 17%.14,15 Some women with gestational hypertension will subsequently progress to preeclampsia and the rate of progression depends on gestational age at the time of diagnosis. The rate reaches 50% when gestational hypertension develops before 30 weeks gestation. Preeclampsia is primarily defined as gestational hypertension plus proteinuria. Preeclampsia is considered severe if there is severe gestational hypertension in association with proteinuria (in the normal kidney, during the filtration process that takes place in the glomerulus, proteins do not enter the urinary space and the presence of proteins in urine is always a sign of glomerular disease) or in the presence of multiorgan involvement such as pulmonary edema (i.e. the passage of fluids from the pulmonar interstitial compartment to the alveolar lumen causing a severe obstacle to the diffusion of oxygen from the alveolar space to the blood), seizures, oliguria (i.e. a reduction in the daily urine volume that is associated with a reduction in glomerular filtration rate), thrombocytopenia (i.e. a decrease in platelet count in the blood), abnormal liver enzymes or persistent severe central nervous system symptoms. During preeclampsia both cardiac output and plasma volume are reduced, whereas systemic vascular resistances are increased. These variations cause a reduced placenta, kidney and brain perfusion, resulting in increased foetal and maternal morbidity (i.e. an increase in the incidence of any non-mortal disease) and mortality. The etiology of preeclampsia is still unknown but an endothelial dysfunction (i.e. a decrease in the endothelial function that leads to a decrease in the production of endothelium-derived substances, mainly vasodilators and inhibitors of platelet aggregation) may play a crucial role. Magnesium has been shown to ameliorate endothelial dysfunction in preeclampsia and this may be due either to its direct vasodila-tatory properties or to the ability to stimulate endothelial release of the endothelial vasodilator prostacyclin.
Eclampsia, the occurrence of a seizure in association with preeclampsia, remains a rare but serious complication of pregnancy and is estimated to complicate around 1 in 2000 deliveries in Europe and in other developed countries.16
There are few randomized trials evaluating magnesium to prevent pree-clampsia. All these trials have limited sample size but reveal minimal to no benefit;17 thus magnesium should not be routinely used for this purpose. The results of these studies were the subject of a review.18
As far as the use of magnesium for eclampsia is concerned, a recent review involving 897 women has summarized the evidence about the differential effects of magnesium sulphate when compared with phenytoin for the care of women with eclampsia.19 The comparison was in terms of maternal mortality, recurrence of convulsions and other serious morbidity that could lead to death. Magnesium sulphate reduces the risk of further fits compared with phenytoin and the trend in maternal mortality is also in favour of magnesium sulphate. The review should be viewed in conjunction with those comparing magnesium sulphate with diazepam20 and with lytic cocktail.21 Magnesium sulphate had a 52% lower risk of recurrent convulsions versus diazepam and 67% lower risk of recurrent convulsions versus phenytoin. Overall, there is now compelling evidence in favour of magnesium sulphate rather than phenytoin, diazepam or lytic cocktail for the treatment of eclampsia.
Several protocols for treatment have been used. The most common is a loading dose of 4-6 g of Mg2SO47H2O infused intravenously over 15 to 20min, then a continuous intravenous infusion at 1 g/h for around 24 hours. Because magnesium is excreted in the urine, woman with oliguria or elevated creatinine should be monitored carefully and dosed accordingly. Magnesium sulphate is believed to exert its effects through a non-specific mechanism of action by competing with calcium for entry into myometrial (i.e. muscular cells in the uterus) cells through voltage-operated Ca2+ channels. Because its effect occurs at other sites, magnesium sulphate is associated with a wide range of side effects. Common side effects include flushing, nausea, chest tightness and lethargy, which are directly related to high serum magnesium concentrations. Fetal adverse events have been reported with magnesium sulphate, with a decrease in fetal heart rate and heart rate variability.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...