Eclampsia risk factors

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


The various risk factors associated with the development of eclampsia encompass a personal or family history of pre-eclampsia/eclampsia, nulliparity, primigravida, long interpregnancy intervals, conditions with a large placenta such as multiple gestations(twins or triplets) and H Mole, women with preexisting conditions such as chronic hypertension, history of gestational hypertension in the previous pregnancy, renal diseases, diabetes, gestational diabetes, obesity, certain thrombophilic diseases (such as the antiphospholipid antibody syndrome, protein C deficiency, protein S deficiency, anti-thrombin deficiency), connective tissue disorders, SLE and genetics.

Risk factors

  • History of pre-eclampsia/eclampsia: Personal history of a similar event in the past or family history is a significant risk factor for recurrence in the next pregnancy. Having pre-eclampsia in one pregnancy is a strong predictor for recurrence of pre-eclampsia in future gestations. The risk for women to develop pre-eclampsia during the second pregnancy is approximately 15% if the first pregnancy was affected by pre-eclampsia and 1.1% for those without a history of pre-eclampsia. The risk during the third pregnancy is approximately 30% for women who have had two previous affected pregnancies and remains 1.1% for those without any history. For women with the first occurrence of pre-eclampsia in their second pregnancy, the risk was 15.9% during the third pregnancy and 29.0% during the fourth when they had developed pre-eclampsia in the previous two pregnancies.[1]
  • Nulliparity: The risk for multiparous women without a history of pre-eclampsia was around 1%.[1]
  • Primigravida: The risk of pre-eclampsia is 4.1% in the first pregnancy and 1.7% in later pregnancies overall if none of the previous pregnancies have been affected by pre-eclampsia.[1] This association is the core of theory that says that pre-eclampsia is the consequence of a maternal immune reaction against paternal antigens expressed in the placenta which might result in defective trophoblast invasion and subsequent placental dysfunction. The lower risk of pre-eclampsia among multiparous women has been attributed to desensitisation after exposure to paternal antigens in the placenta during previous pregnancies.[2][3] and to smoother trophoblastic invasion after modification of maternal spiral arteries during the first pregnancy.[4] For this reason pre-eclampsia is also known as a disease of primiparity.
  • Interpregnancy interval: A long interpregnancy interval is associated with increased risk of preeclampsia, supporting the hypothesis that some factors delaying clinically recognized conception may also be in a causal pathway for preeclampsia.[5]
  • Conditions with a large placenta:
    • Multiple gestations: The relative risk of preterm preeclampsia in di-chorionic and mono-chorionic twin pregnancies is similar and substantially higher than in singleton pregnancies. In a study, it was found that the incidence of pre-eclampsia in singleton pregnancies was 2.3% compared to 8% in dichorionic(DC) twin pregnancies and 6% in monochorionic(MC) twin pregnancies. Compared to singletons, the relative risk of total pre-eclampsia was 3.5 for DC twins and 2.6 for MC twins.[6]
    • Hydatiform mole: Hydatiform moles pose a high risk of early-onset preeclampsia if the pregnancy continues with the moles left untreated[7]. Preeclampsia can develop as early as the 2nd trimester in 30–40% of pregnancies with untreated hydatiform moles.[8] [9]
  • Women with preexisting vascular diseases:
    • Chronic hypertension: Chronic hypertension is defined as high blood pressure present before pregnancy or before 20 weeks of pregnancy. If left untreated, it can progress to gestational hypertension, pre-eclampsia, or eclampsia. Development of preeclampsia is the most prevalent complication in pregnancy in women with chronic hypertension[10]. 17% to 25% of women with chronic hypertension develop preeclampsia compared to the general population where the risk is 3-5%.[11] [12] [13]
    • Gestational hypertension: Untreated gestational hypertension can eventually progress to preeclampsia/eclampsia. Approximately 15-25% of patients with gestational hypertension will progress to preeclampsia or severe gestational hypertension[14]. The rate of the progression depends on gestational age at the time of diagnosis and the pregnancy outcome is usually good when the diagnosis is made at ≥ 37 weeks of gestation.[15]
    • Renal diseases
    • Diabetes/ Gestational diabetes/ History of Gestational diabetes: Preexisting diabetes is a risk factor for preeclampsia. In comparison to the relatively low incidence of preeclampsia in non-diabetic women (2-7%)[16] [17] , preeclampsia is diagnosed in 15-20% of pregnancies in women with type 1 diabetes [18][19] [20] and 10-14% of pregnancies in women with type 2 diabetes [21] .
    • Obesity: The risk of preeclampsia and hence eclampsia increases by about 3-fold with obesity, and in developed countries is the leading attributable risk for the disorder. [22]
    • Preexisting thrombophilias: A strong association between maternal thrombophilic disorders and severe preeclampsia has been established in various studies. Examples include:
    • Connective tissue disorders
    • Systemic lupus erythematous
  • Genetics: Patients whose mother or sister had the condition are at a higher risk.[23]


  1. 1.0 1.1 1.2 Hernández-Díaz S, Toh S, Cnattingius S (2009). "Risk of pre-eclampsia in first and subsequent pregnancies: prospective cohort study". BMJ. 338: b2255. doi:10.1136/bmj.b2255. PMC 3269902. PMID 19541696.
  2. Luo ZC, An N, Xu HR, Larante A, Audibert F, Fraser WD (2007). "The effects and mechanisms of primiparity on the risk of pre-eclampsia: a systematic review". Paediatr Perinat Epidemiol. 21 Suppl 1: 36–45. doi:10.1111/j.1365-3016.2007.00836.x. PMID 17593196.
  3. Saftlas AF, Levine RJ, Klebanoff MA, Martz KL, Ewell MG, Morris CD; et al. (2003). "Abortion, changed paternity, and risk of preeclampsia in nulliparous women". Am J Epidemiol. 157 (12): 1108–14. doi:10.1093/aje/kwg101. PMID 12796047.
  4. Moore MP, Redman CW (1983). "Case-control study of severe pre-eclampsia of early onset". Br Med J (Clin Res Ed). 287 (6392): 580–3. doi:10.1136/bmj.287.6392.580. PMC 1548969. PMID 6411232.
  5. Basso O, Weinberg CR, Baird DD, Wilcox AJ, Olsen J, Danish National Birth Cohort (2003). "Subfecundity as a correlate of preeclampsia: a study within the Danish National Birth Cohort". Am J Epidemiol. 157 (3): 195–202. doi:10.1093/aje/kwf194. PMID 12543618.
  6. Francisco, C., Wright, D., Benkő, Z., Syngelaki, A. and Nicolaides, K.H. (2017), Hidden high rate of pre-eclampsia in twin compared with a singleton pregnancy. Ultrasound Obstet Gynecol, 50: 88-92.
  7. Iriyama, T., Wang, G., Yoshikawa, M. et al. Increased LIGHT leading to sFlt-1 elevation underlies the pathogenic link between hydatidiform mole and preeclampsia. Sci Rep 9, 10107 (2019).
  8. Kohorn, E. I. Molar pregnancy: presentation and diagnosis. Clinical obstetrics and gynecology 27, 181–191 (1984).
  9. Soto-Wright, V., Bernstein, M., Goldstein, D. P. & Berkowitz, R. S. The changing clinical presentation of complete molar pregnancy. Obstetrics and gynecology 86, 775–779, (1995)
  10. Chronic Hypertension in Pregnancy Ellen W. Seely and MD Jeffrey EckerMD Originally published18 Mar 2014 2014;129:1254–1261
  11. Sibai BM. Chronic hypertension in pregnancy.Obstet Gynecol. 2002; 100:369–377.
  12. Rey E, Couturier A. The prognosis of pregnancy in women with chronic hypertension.Am J Obstet Gynecol. 1994; 171:410–416.
  13. McCowan LM, Buist RG, North RA, Gamble G. Perinatal morbidity in chronic hypertension.Br J Obstet Gynaecol. 1996; 103:123–129.
  14. Saudan P, Brown MA, Buddle ML, Jones M. Does gestational hypertension become pre-eclampsia? Br J Obstet Gynaecol. 1998 Nov;105(11):1177-84. doi: 10.1111/j.1471-0528.1998.tb09971.x. PMID: 9853766.
  15. Obstetrics and Gynecology Gestational Hypertension – Preeclampsia Baha M. Sibai Fadi G. Mirza
  16. Knuist M, Bonsel GJ, Zondervan HA, Treffers PE. Intensification of fetal and maternal surveillance in pregnant women with hypertensive disorders. Int J Gynaecol Obstet. 1998;61(2):127–33. doi:S0020729298000241 [pii]
  17. Hauth JC, Ewell MG, Levine RJ, Esterlitz JR, Sibai B, Curet LB, et al. Pregnancy outcomes in healthy nulliparas who developed hypertension. Calcium for Preeclampsia Prevention Study Group. Obstet Gynecol. 2000;95(1):24–8. doi:S0029784499004627
  18. Jensen DM, Damm P, Moelsted-Pedersen L, Ovesen P, Westergaard JG, Moeller M, et al. Outcomes in type 1 diabetic pregnancies: a nationwide, population-based study. Diabetes Care. 2004;27(12):2819–23. doi:27/12/2819
  19. Persson M, Norman M, Hanson U. Obstetric and perinatal outcomes in type 1 diabetic pregnancies: A large, population-based study. Diabetes Care. 2009;32(11):2005–9. doi:dc09-0656 [pii] 10.2337/dc09-0656.
  20. Knight KM, Thornburg LL, Pressman EK. Pregnancy outcomes in type 2 diabetic patients as compared with type 1 diabetic patients and nondiabetic controls. J Reprod Med. 2012;57(9-10):397–404.
  21. Groen B, Links TP, van den Berg PP, Hellinga M, Moerman S, Visser GH, et al. Similar adverse pregnancy outcome in native and nonnative dutch women with pregestational type 2 diabetes: a multicentre retrospective study. ISRN obstetrics and gynecology. 2013;2013:361435. doi: 10.1155/2013/361435.
  22. Roberts JM, Bodnar LM, Patrick TE, Powers RW (2011). "The Role of Obesity in Preeclampsia". Pregnancy Hypertens. 1 (1): 6–16. doi:10.1016/j.preghy.2010.10.013. PMC 3082136. PMID 21532964.
  23. Chesley LC, Annitto JE, Cosgrove RA. "The familial factor in toxemia of pregnancy". Obstet Gynecol 1968;32:303.

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