Pre-Eclampsia or Pregnancy - Induced Hypertension

Question: Discuss the causes, risk factors, detection, treatment and complications? Answer: Introduction: Preeclampsia also referred as toxemia or pregnancy-induced hypertension (PIH), is a multisystem disorder which is characterized by de novo hypertension and proteinuria or superimposed maternal hypertension or nephropathy in pregnant woman (Kanasaki Kalluri 2009), (Bell, 2010). This disease affects both the mother and the fetus usually beyond 20 weeks of gestational age. Although the reason behind this disease is not clear till date, but the disease is known to be recognized nearly 200 years ago (Kanasaki Kalluri 2009), (Bell, 2010) Preeclampsia is known to affect 2-5% of pregnancies. The rate exceeds to an approximate of 10-18% in some developing countries. According to a study, UK is one of the leading countries affected with this disease. One out of twenty (5%) women suffers from severe pre-eclampsia or eclampsia causing significant number of maternal deaths in UK. (NICE Clinical guideline). Statistical data reveal that every minute, somewhere in the world death occurs during pre gnancy or childbirth. This amount to an approximate of 1400 number of women death per day; more that 500,000 death every year. Additionally, maternal and fetus mortality is estimated to 13% worldwide in case of undetected preeclampsia (Scazzocchio Figueras 2011), (Marik and Plante, 2008). This multisystem disorder may be categorized into early-onset and late-onset preeclampsia. Early-onset preeclampsia shows fetal-growth restriction (FGR), abnormal uterine and umbilical artery. Doppler waveforms and adverse maternal and neonatal outcomes (Verlohren et al., 2014).Whereas, the late-onset preeclampsia is characterized with lower rate of maternal involvement and favorable perinatal outcomes. Abnormal placental implantation along with endothelial dysfunction is the main features of preeclampsia. Both the renal and vascular systems are affected altogether (Kanasaki Kalluri 2009),(Karumanchi et al., 2005). Causes: The exact cause of preeclampsia is unknown. Experts believe it begins in the placenta the organ that nourishes the foetus throughout pregnancy. In women with preeclampsia, these blood vessels don't seem to develop properly and limits the flow of blood (Redman, 2005), (Segers et al., 2007), (Karumanchi et al., 2005). Recent research show that the causative agent behind the pathogenesis of this disease is maternal endothelial dysfunction, which is mediated be the excess placenta derived soluble VEGF receptor 1 (sVEGFRI or Sflt1) (Venkatesha et al., 2006), (Luft, 2006), (Foidart et al.; 2010). Causes of this abnormal development may include: Insufficient blood flow to the uterus (Redman, 2005), (Karpov, 2010). Damage to the blood vessels (Karumanchi et al., 2005). A problem with the immune system (Segers et al., 2007) Mutation of certain genes likethe prothrombin (Factor II) and the Factor V Leiden (FVL) clotting factor (Karpov, 2010). Risk Factors: Pre-eclampsia develops only as a complication of pregnancy. Risk factors include: History of preeclampsia.A personal or family history of preeclampsia significantly raises your risk of preeclampsia (Jacquemyn, Y. Zemtsova, O., 2010), (Portelinha et al., 2010). First pregnancy.The risk of developing preeclampsia is highest during your first pregnancy (Jacquemyn, Y. Zemtsova, O., 2010), (Nirmalan, 2013). New paternity.Each pregnancy with a new partner increases the risk of preeclampsia over a second or third pregnancy with the same partner (Jacquemyn, Y. Zemtsova, O., 2010), (James, 2013). The risk of preeclampsia is higher for pregnant women older than 40 (Jacquemyn, Y. Zemtsova, O., 2010). (Sibai et al., 2005) The risk of preeclampsia is higher if you're obese (Jacquemyn, Y. Zemtsova, O., 2010). (Sibai, Dekker and Kupferminc, 2005), (Karumanchi et al., 2005). Multiple pregnancies.Preeclampsia is more common in women who are carrying twins, triplets or other multiples (Jacquemyn, Y. Zemtsova, O., 2010), (Nirmalan, 2013). Interval between pregnancies.Having babies less than two years or more than 10 years apart leads to a higher risk of preeclampsia (Jacquemyn, Y. Zemtsova, O., 2010), (Nirmalan, 2013). History of certain conditions.Having certain conditions before you become pregnant such as chronic high blood pressure, migraine headaches, type 1 or type 2 diabetes, kidney disease, a tendency to develop blood clots, or lupus increases your risk of preeclampsia (Jacquemyn, Y. Zemtsova, O., 2010), (KIVEL, 2010). Detection: In the majority of cases, symptoms of preeclampsia aren't noticeable. Women may experience headache, blurred vision, upper abdominal pain and unexplained anxiety. Serious cases of preeclampsia may result in seizures (Tuovinen et al.; 2010). Abnormalities of the liver, kidneys and blood clotting mechanisms may also be present. Dramatic weight gain, a decrease in urine output, blurry vision, nausea, and abdominal pain maybe reasons to watch more closely for the development of preeclampsia. (Sibai et al., 2005). Typically, preeclampsia occurs in the late 2nd or 3rd trimesters of pregnancy (Young, B.C. et al., 2010), (Tuovinen et al.; 2010), (Wood, 2013). Treatment: The only effective treatment for preeclampsia is delivery. Doctors will take into consideration gestation of the fetus in terms of development before inducing labor. If a woman has a good support system in her home, she can manage mild preeclampsia with bed rest and frequent visits to her obstetrical care provider. She may also need to monitor her blood pressure at home on a regular basis. Serious cases of preeclampsia may require admission to the hospital for more intensive monitoring of both the mother and unborn baby. If tests indicate that the health of either of the mother or fetus is at risk, an obstetrician may recommend inducing labor early or performing a caesarean section (Downing, 2010). A study by the Magpie Trial Collaborative Group in June of 2002 found that magnesium sulfate (MgSO4) can ease the symptoms of preeclampsia and has reduced seizures stemming from eclampsiaby56% when given intravenously in a controlled environment by trained staff (Tukur, 2009). Magnesium su lfate has been a standard treatment option in the U.S. since the1950s; however, it is not widely used internationally (Kenny, L.C. et al., 2010), (Tukur, 2009). For women at high risk of pre eclampsia may be detected by the application of ultrasound markers (Mace et al., 2012). Complications: Lack of blood flow to the placenta.Preeclampsia affects the arteries carrying blood to the placenta. If the placenta doesn't get enough blood, your baby may receive less oxygen and fewer nutrients. This can lead to slow growth, low birth weight, or preterm birth. Prematurity can lead to breathing problems for the baby (Jacquemyn, Y. Zemtsova, O., 2010). Placental abruption.Preeclampsia increases your risk of placental abruption, in which the placenta separates from the inner wall of your uterus before delivery. Severe abruption can cause heavy bleeding and damage to the placenta, which can be life-threatening for both you and your baby (Jacquemyn, Y. Zemtsova, O., 2010), (Keiski-Nisula et al., 2009), (Wood, 2013). HELLP syndrome.HELLP which stands for haemolysis (the destruction of red blood cells), elevated liver enzymes, and low platelet count syndrome can rapidly become life-threatening for both you and your baby. Symptoms of HELLP syndrome include nausea and vomiting, headache, and upper right abdominal pain. HELLP syndrome is particularly dangerous because it represents damage to several organ systems. On occasion, it may develop suddenly, even before high blood pressure is detected (Jacquemyn, Y. Zemtsova, O., 2010) (Pourrat et al., 2012), (Clarke and Nelson-Peirsey, 2008). When preeclampsia isn't controlled, eclampsia which is essentially preeclampsia plus seizures can develop. Symptoms that suggest imminent eclampsia include upper right abdominal pain, severe headache, vision problems and change in mental status, such as decreased alertness. Because eclampsia can have serious consequences for both mom and baby, delivery becomes necessary, regardless of how far along the pregnancy is (Jacquemyn, Y. Zemtsova, O., 2010). Cardiovascular disease.Having preeclampsia may increase your risk of future heart and blood vessel (cardiovascular) disease. The risk is even greater if you've had preeclampsia more than once or you've had a preterm delivery. To minimize this risk, after delivery try to maintain your ideal weight, eat a variety of fruits and vegetables, exercise regularly, and don't smoke (Jacquemyn, Y. Zemtsova, O., 2010), (Kajantie et al., 2009). References 1. Bell, M. (2010). A Historical Overview of Preeclampsia-Eclampsia. Journal of Obstetric, Gynecologic, Neonatal Nursing, 39(5), pp.510-518. 2. Clarke, S. and Nelson-Piercy, C. (2008). Pre-eclampsia and HELLP syndrome. Anaesthesia Intensive Care Medicine, 9(3), pp.110-114. 3. Downing, J. (2010). Sildenafil for the Treatment of Preeclampsia. Hypertension in Pregnancy, 29(2), pp.248-250. 4. Felfernig-Boehm, D. et al., 2000. Early detection of preeclampsia by determination of platelet aggregability. Thrombosis Research, 98(2), pp.139146. 5. Foidart, J., Munaut, C., Chantraine, F., Akolekar, R. and Nicolaides, K. (2010). Maternal plasma soluble endoglin at 11-13 weeks' gestation in pre-eclampsia. Ultrasound in Obstetrics and Gynecology, p.n/a-n/a. 6. Jacquemyn, Y. Zemtsova, O., 2010. Risk factors and prediction of preeclampsia. Acta Clinica Belgica, 65(1), pp.112. 7. James, W. (2013). Change in paternity, pre-eclampsia, fetal growth retardation and maternal testosterone concentration. J Obstet Gynaecol, 33(2), p.217. 8. Kajantie, E., Eriksson, J., Osmond, C., Thornburg, K. and Barker, D. (2009). Pre-Eclampsia Is Associated With Increased Risk of Stroke in the Adult Offspring: The Helsinki Birth Cohort Study. Stroke, 40(4), pp.1176-1180. 9. Kanasaki, K. Kalluri, R., 2009. The biology of preeclampsia. Kidney international, 76(8), pp.831837. 10. Karpov, Y. (2010). Book Review: Haywood, H. C., Lidz, C. S. (2007). Dynamic Assessment in Practice: Clinical and Educational Applications. New York: Cambridge University Press. Journal of Psychoeducational Assessment, 28(2), pp.163-166. 11. Karumanchi, S., Maynard, S., Stillman, I., Epstein, F. and Sukhatme, V. (2005). Preeclampsia: A renal perspective. Kidney International, 67(6), pp.2101-2113. 12. Kenny, L.C. et al., 2010. Robust early pregnancy prediction of later preeclampsia using metabolomic biomarkers. Hypertension, 56(4), pp.741749. 13. Keski-Nisula, L., Heinonen, S., Remes, S. and Pekkanen, J. (2009). ORIGINAL ARTICLE: Pre-Eclampsia, Placental Abruption and Increased Risk of Atopic Sensitization in Male Adolescent Offspring. American Journal of Reproductive Immunology, 62(5), pp.293-300. 14. KIVEL, T. (2010). Diagnosis of adult ophthalmic tumours: role of clinical history, symptoms and signs. Acta Ophthalmologica, 88, pp.0-0. 15. Luft, F. (2006). Soluble endoglin (sEng) joins the soluble fms-like tyrosine kinase (sFlt) receptor as a pre-eclampsia molecule. Nephrology Dialysis Transplantation, 21(11), pp.3052-3054. 16. Mac, G., Cynober, E. and Carbonne, B. (2012). Ultrasound markers for the detection of women at risk of developing pre-eclampsia. Clinical Chemistry and Laboratory Medicine, 50(6). 17. Marik, P. and Plante, L. (2008). Venous Thromboembolic Disease and Pregnancy. New England Journal of Medicine, 359(19), pp.2025-2033. 18. Nirmalan, P. (2013). Risk for Recurrence of Pre-eclampsia in the Subsequent Pregnancy. JCDR. 19. Portelinha, A., Belo, L., Cerdeira, A., Braga, J., Tejera, E., Pinto, F., Pinto, A., Areias, M., Patrcio, B. and Rebelo, I. (2010). Lipid Levels Including Oxidized LDL in Women with History of Preeclampsia. Hypertension in Pregnancy, 29(1), pp.93-100. 20. Pourrat, O., Neau, J. and Pierre, F. (2012). Bell's palsy in pregnancy: underlying HELLP syndrome or pre-eclampsia?. Obstetric Medicine. 21. Redman, C. (2005). Latest Advances in Understanding Preeclampsia. Science, 308(5728), pp.1592-1594. 22. Scazzocchio, E. Figueras, F., 2011. Contemporary prediction of preeclampsia. Current opinion in obstetrics gynecology, 23(2), pp.6571. 23. Segers, K., Dahlbck, B. and Nicolaes, G. (2007). Coagulation factor V and thrombophilia: Background and mechanisms. Thromb Haemost. 24. Segers, K., Dahlback, B., Bock, P., Tans, G., Rosing, J. and Nicolaes, G. (2007). The Role of Thrombin Exosites I and II in the Activation of Human Coagulation Factor V. Journal of Biological Chemistry, 282(47), pp.33915-33924. 25. Sibai, B., Dekker, G. and Kupferminc, M. (2005). Pre-eclampsia. The Lancet, 365(9461), pp.785-799. 26. Tukur, J. (2009). The use of magnesium sulphate for the treatment of severe pre-eclampsia and eclampsia. Annals of African Medicine, 8(2), p.76. 27. Tuovinen, S., Rikknen, K., Kajantie, E., Pesonen, A., Heinonen, K., Osmond, C., Barker, D. and Eriksson, J. (2010). Depressive symptoms in adulthood and intrauterine exposure to pre-eclampsia: the Helsinki Birth Cohort Study. BJOG: An International Journal of Obstetrics Gynaecology, 117(10), pp.1236-1242. 28. Tuuli, M.G. et al., 2011. Perinatal outcomes in women with preeclampsia and superimposed preeclampsia: Do they differ? American Journal of Obstetrics and Gynecology, 204(6). 29. Venkatesha, S., Toporsian, M., Lam, C., Hanai, J., Mammoto, T., Kim, Y., Bdolah, Y., Lim, K., Yuan, H., Libermann, T., Stillman, I., Roberts, D., D'Amore, P., Epstein, F., Sellke, F., Romero, R., Sukhatme, V., Letarte, M. and Karumanchi, S. (2006). Soluble endoglin contributes to the pathogenesis of preeclampsia. Nat Med, 12(6), pp.642-649. 30. Verlohren, S., Melchiorre, K., Khalil, A. and Thilaganathan, B. (2014). Uterine artery Doppler, birth weight and timing of onset of pre-eclampsia: providing insights into the dual etiology of late-onset pre-eclampsia. Ultrasound Obstet Gynecol, 44(3), pp.293-298. 31. Wood, A. (2013). Second trimester hyperemesis gravidarum is associated with increased risk of preterm pre-eclampsia, placental abruption and small for gestational age birth. Evidence-Based Nursing, 17(3), pp.74-74. 32. Young, B.C., Levine, R.J. Karumanchi, S.A., 2010. Pathogenesis of preeclampsia. Annual review of pathology, 5, pp.173192.