Maternal Characteristics and the Effects of Early and Late-onset Types of Preeclampsia on Maternal and Perinatal Complications

Authors

  • Sintia Damayanti Department of Obstetrics and Gynecology, Dr. Moewardi Hospital/ Faculty of Medicine, Universitas Sebelas Maret
  • Sri Sulistyowati Department of Obstetrics and Gynecology, Dr. Moewardi Hospital/ Faculty of Medicine, Universitas Sebelas Maret
  • Ari Natalia Probandari Department of Public Health, Faculty of Medicine, Universitas Sebelas Maret

Abstract

Background: Preeclampsia is still the main cause of morbidity and mortality not only for mothers but also for fetal. The concept of early and late-onset preeclampsia is a more modern concept, and it is stated that these two entities have different etiologies and must be considered as different forms of the disease. This study aims to analyzing differences in maternal characteristics (age, number of parity, history of hypertension and diabetes mellitus) and laboratory results (platelet, ewitz, Lactic Acid Dehydrogenase/LDH) and to analyzing differences in maternal complications (maternal death, eclampsia, impending eclampsia, pulmonary edema, (hemolysis, elevated liver enzyme levels, and low platelet levels/HELLP syndrome) and perinatal complications (peri­natal death, Intrauterine Growth Restriction/IUGR, fetal hypoxia and fetal distress) between early and late-onset preeclampsia. This study aimed to investigate the maternal characteristics and the effects of early and late-onset types of preeclampsia on maternal and perinatal complications.

Subjects and Method: This was a retrospective cohort study. The study was carried out at Dr. Moewardi Hospital, Surakarta, from January 1, 2016, to December 31, 2017. A total of 548 pregnant mothers with preeclampsia was selected for this study. The dependent variable was the incidence of preeclampsia. The independent variables were age, parity, hypertension, diabetes Mellitus, platelets, LDH, and proteinuria. The data were obtained from the medical record and analyzed by a multiple linear regression.

Results: The number of patients with early-onset (162) was less than late-onset (386). More patients have multiparity in early and late-onset. In early-onset preeclampsia, thrombocytopenia and LDH increase tend to be present, and ewitz >+1. Early-onset preeclampsia tends to result in more maternal and perinatal complications.

Conclusion: The incidence of early-onset is less than late-onset, but early-onset provides worse complications for both maternal and perinatal.

Keywords: Early-onset preeclampsia, late-onset preeclampsia, characteristics, maternal and perinatal complications

Correspondence: Sintia Damayanti. Department of Obstetrics and Gynecology, Dr. Moewardi Hospital/ Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Central Java, Indonesia. Email: sintiadamayan­84@yahoo.co.id. Mobile: 082220020829.

Indonesian Journal of Medicine (2019), 4(4): 329-338
https://doi.org/10.26911/theijmed.2019.04.04.05

References

ACOG (2013). Management of hypertensive crisis in pregnancy, American College of Obstetricians and Gynecologists. Optimizing Protocols in Obstetrics. 4: 1-6.

Ananth CV, Wapner RJ (2013). Pre–eclampsia rates in the United States, 19802010: An age–period–cohort analysis. British Medical Journal. 347: 65-4. https://doi.org/10.1136/bmj.f6564.

Aziz A, Johannes C (2016). The differences of characteristic, management, maternal, and perinatal outcomes among early and late onset preeclampsia. Open Access Library Journal. 3: 27-50. http://dx.doi.org/10.4236/oalib.1102750.

Creasy R (2014). Maternal Fetal Medicine. Principle and practice, America: Saunders. 7: 756S.

Cunningham FG, Donald MPC, Gant NF, Leveno KJ, Gilstrap LC, Hankins GDF (2013). Williams Obstetrics. 22th ed. London: Prentice–Hall International. 567-618.http://dx.doi.org/10.4236/ojpm.2014.411097.

Danielle A, Samita S, Gita D (2014). The association between dietary factors and gestational hypertension and preeclampsia: a systematic review and meta-analysis of observational studies. BMC Medicine. 12:157. https://doi.org/10.1186/s12916–014–0157–7.

Gathiram P, Moodley (2016). Preeclampsia: its pathogenesis and pathophysiology. Cardiovascular Journal of Africa. 27(2): 77. https://dx.doi.org/10.5830%2FCVJA2016009.

Halenur B, Fatma B, Kadir G, Sedef R, Esra A, Ilke T, Ahmet G (2015). The frequency and feto-maternal outcomes of early and late onset preeclampsia: The experience of a single tertiary health center in the bustling metropolis of Turkey; Istanbul. Medeniyet Medical Journal. 30: 163-169. https://dx.doi.org/10.5222/MMJ.2015.163.

Hutcheon JA, Lisonkova S, Joseph KS (2011). Epidemiology of preeclampsia and the other hypertensive disorders of pregnancy. Best Practice Clinical Obstetrics Gynaecol. 25(4):391–403. doi: 10.1016/j.bpobgyn.2011.01.006

Lisonkova S, Joseph KS (2017). Incidence of preeclampsia: Risk factors and outcomes associated with early versus late onset disease. American Journal of Obstetrics Gynecology. 209 (544): 1–12.https://doi.org/10.1016/j.ajog.2013.08.019.

Mateus J, Bytautiene E, Lu F, Tamayo E, Betancourt A, Hankins G (2011). Endothelial growth factor therapy improves preeclampsia like manifestation in Murine model induced by expression of SVEGR–1. American Journal of Physiological Society. 30(5):

-7. https://doi.org/10.1152/ajpheart.00373.2011.

Mifsud W, Sebire N (2014). Fetal Diagnosis and Therapy: Placental pathology in early onset and late–onset fetal growth restriction. London: Karger. 36: 117. https://doi.org/10.1159/000359969.

Peter V, Laura A, James M, Robert M (2003). Sub classification of preeclampsia. Hypertension in pregnancy. 22(2): 143–148. https://doi.org/10.1081/PRG–120021060.

Priscila V, Moises E, Dinara D, Jose A (2011). Distress conditions during pregnancy may lead to pre–eclampsia by increasing cortisol levels and altering lymphocyte sensitivity to glucocorticoids. Elsevier. 77: 188-191. https://doi.org/10.1016/j.mehy.2011.04.007.

Simsek A, Uludag S, Tuten A, Oncul M, Acikgoz AS, Uludag S (2016). Maternal and prenatal outcomes in earlyonset and late–onset preeclampsia. Department of Obstetrics and Gynecology. Istanbul. 15th World Congress in Fetal Medicine. Retrieved from https://fetalmedicine.org/abstracts/2016/var/pdf/abstracts/01542.pdf.

Srinivas S, Edlow A, Neff, Sammel M, Andrela C, Elovitz M (2009). Rethinking IUGR in pre–eclampsia: dependent or independent of maternal hypertension? Journal of Perinatology. 29: 680–684. https://doi.org/10.1038/jp.2009.83.

Sulistyowati S, Soetrisno S, Kartika NH (2016). Ekspresi human leukocyte antigen–C di trophoblastdan natural killer cell di desiduapada preeklampsia berat. Jurnal Kedokteran Brawijaya. 29(1): 59-63. Retrieved from https://jkb.ub.ac.id/index.php/jkb/article/view/1154/499.

Woods A, Hoffmann D, Weydert C, Butler S, Zhou Y, Sharma R (2011). Adenoviral delivery of VEGF 121 early in pregnancy prevents spontaneous development of pre–eclampsia in BPH/5 Mice. Hypertension. American Heart Association. 94-102. https://doi.org/10.1161/HYPERTENSIONAHA.110.160242.

Downloads

Published

2019-10-10

Issue

Section

Articles