EFFECTS OF VARIATION IN UMBILICAL ARTERY RESISTIVE INDEX ON PLACENTAL MORPHOLOGY AND BIRTH WEIGHT IN PREGNANCY INDUCED HYPERTENSION
Abstract
Background: Pregnancy induced hypertension results from defective trophoblast invasion and increased umbilical artery resistance which in turn results in decreased blood supply to the placenta and hence to the foetus. This arterial resistance varies in different cases of PIH thus causing variable effects on placenta and foetus. The objective of this study was to study the morpho-metric changes in placenta and alterations in birth weight with differences in umbilical artery resistive index in hypertensive pregnancies. Methods: Ninety pregnant women with pregnancy induced hypertension were selected with gestational age greater than 35weeks. Doppler ultrasound examinations were carried out to record umbilical artery resistive index (UARI). 2 groups were made on the basis of median values of UARI. Plain ultrasound examination was then carried out to record presentation, site of placentation, grade of maturity, insertion of the cord, cord thickness, placental thickness, vacuolation and amniotic fluid index (AFI). After delivery, foetal birth weight was noted and placentae examined for placental weight, infarcts, number of cotyledons, umbilical cord insertion, cord thickness and placental thickness were noted. Foeto-placental weight ratio was also calculated. Results: Significantly higher UARI was seen in the high-resistance group. Significantly lower values of placental thickness, AFI, birth weight, placental weight and placental thickness, whereas greater number of grade-III maturity, infarcts and marginal cord insertion were noted in the high-resistance group. Conclusion: Increased UARI leads to a spectrum of changes in the placenta and also decreased birth weight. Marginal cord insertion causes greater risk of increased UARI.Keywords: PIH, Umbilical Artery, Resistive Index, PlacentaReferences
Ananth CV, Basso O. Impact of Pregnancy-Induced Hypertension on Stillbirth and Neonatal Mortality in First and Higher Order Births: A Population-Based Study. Epidemiology. 2010;21(1):118–23.
Villar J, Carroli G, Wojdvla D, Ablos E, Giordano D, Ba’aqeel H et al. Gestational hypertension and intrauterine growth restriction, related or independent conditions? Am J Obstet Gynecol 2006;194:921–31.
Kaaja R, Kinnunen T, Luoto R. Regional differences in the prevalence of preeclampsia in relation to the risk factors for coronary artery disease in women in Finland. Eur Heart J 2005;26:44–50.
Muhammed Obaid-ur-Rehman M, Salah-ud-din, Siddiqui MA, Rehman S. Incidence of women having pregnancy induced hypertension in Karachi. J Pak Pharmacol 2003;20(1):5–8.
Kumar V, Abbas AK, Fausto N, eds. Robbins and Cotran. Pathologic Basis of Disease. 7th ed. Philadelphia: Saunders Elesware; 2005.
Naicker T, Khedun SM, Moodley J, Pijnenborg R. Quantitative analysis of trophoblast invasion in preeclampsia. Acta Obstet Gynecol Scand 2003;82:722–9.
Goldman-Wohl D, Yagel S. Regulation of trophoblast invasion: from normal implantation to pre-eclampsia. Mol Cell Endocrinol 2002;187(1-2):233–8.
Maynard S, Min J, Merchan J, Lim K, Li J, Mondal S, et al. Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. J Clin Invest 2003;111:649–58.
Levine RJ, Lam C, Qian C, Yu KF, Maynard SE, Sachs BP, et al. Soluble Endoglin and other circulating antiangiogenic factors in preeclampsia. N Engl J Med 2006;355:992–1005.
Roberts JM, Bodnar LM, Lain KY, Hubel CA, Markovic N, Ness RB, et al. Uric Acid Is as Important as Proteinuria in Identifying Foetal Risk in Women With Gestational Hypertension. Hypertension 2005;46;1263–9.
Majumdar S, Dasgupta H, Bhattacharya K, Bhattacharya A. A study of placenta in normal and hypertensive pregnancies. J Anat Soc India 2005;54(2):1–9.
Baloch AH, Memon SF, Ansari AK. Comparison of placentae from hypertension associated pregnancies and normal pregnancies. J Liquat Uni Med Health Sci 2012;11(1):3–6.
Kaufmann P, Black S, Huppertz B. Endovascular trophoblast invasion: Implications for the pathogenesis of intrauterine growth retardation and preeclampsia. Bio Reprod 2003;69:1–7.
Helwig JJ, Bouteiller PL. Physiological Smooth Muscle Cell apoptosis contributes to the uterine vascular remodeling in human early pregnancy. Circ Res 2007;100:754–6.
Pijnenborg R, Bland JM, Robertson WB, Brosens I. Uteroplacental arterial changes related to interstitial trophoblast migration in early human pregnancy. Placenta 1983;4:397–413.
Bhatt CJ, Arora J, Shah MS. Role of color Doppler in pregnancy induced hypertension (A study of 100 cases). Indian J Radiol Imaging 2003;3:417–20.
Yalti S, Oral O, Gürbüz B, Ozden S, Atar F. Ratio of middle cerebral to umbilical artery blood velocity in preeclamptic& hypertensive women in the prediction of poor perinatal outcome. Indian J Med Res 2004;120:44–50.
Dicke JM, Huettner P, Yan S, Odibo A, Kraus FT. Umbilical Artery Doppler Indices in Small for Gestational Age Foetuses: Correlation with adverse outcomes and placental abnormalities. J Ultrasound Med 2009;28:1603–10.
Khalid M, Wahab S, Kumar V, Khalid S, Haroon S, Noor AS. Doppler Indices in Prediction of Foetal Outcome in Hypertensive Pregnant Women. Nipal J Obstet Gynaecol 2011;6(1):28–34.
Rasmussen S, Irgens LM. Fetal Growth and Body Proportion in Preeclampsia. Obstet Gynecol 2003;101:575–83.
Stewart VL, Herling P, Dalinka MK. Calcification in soft tissues. JAMA 1983;250:78–81.
Nordenvall M, Ullberg U, Laurin J, Lingman G, Sandstedt B, Ulmsten U. Placental morphology in relation to umbilical artery blood velocity waveforms. Eur J Obstet Gynecol Reprod Biol 1991;40(3):179–90.
Bolz N, Kalache KD, Fotopoulou C, Proquitte H, Slowinski T, Hartung JP, et al. Value of Doppler sonography near term: can umbilical and uterine artery indices in low-risk pregnancies predict perinatal outcome? J Perinat Med 2013;41(2):165–70.
Torres PJ, Gratacós E, Alonso PL. Umbilical artery Doppler ultrasound predicts low birth weight and fetal death in hypertensive pregnancies. Acta Obstet Gynecol Scand 1995;74:352–5.
Published
Issue
Section
License
Journal of Ayub Medical College, Abbottabad is an OPEN ACCESS JOURNAL which means that all content is FREELY available without charge to all users whether registered with the journal or not. The work published by J Ayub Med Coll Abbottabad is licensed and distributed under the creative commons License CC BY ND Attribution-NoDerivs. Material printed in this journal is OPEN to access, and are FREE for use in academic and research work with proper citation. J Ayub Med Coll Abbottabad accepts only original material for publication with the understanding that except for abstracts, no part of the data has been published or will be submitted for publication elsewhere before appearing in J Ayub Med Coll Abbottabad. The Editorial Board of J Ayub Med Coll Abbottabad makes every effort to ensure the accuracy and authenticity of material printed in J Ayub Med Coll Abbottabad. However, conclusions and statements expressed are views of the authors and do not reflect the opinion/policy of J Ayub Med Coll Abbottabad or the Editorial Board.
USERS are allowed to read, download, copy, distribute, print, search, or link to the full texts of the articles, or use them for any other lawful purpose, without asking prior permission from the publisher or the author. This is in accordance with the BOAI definition of open access.
AUTHORS retain the rights of free downloading/unlimited e-print of full text and sharing/disseminating the article without any restriction, by any means including twitter, scholarly collaboration networks such as ResearchGate, Academia.eu, and social media sites such as Twitter, LinkedIn, Google Scholar and any other professional or academic networking site.