DOI: http://dx.doi.org/10.18203/2320-6012.ijrms20190943

Histopathology of placenta in intrauterine growth restriction (IUGR)

Ruchi Khajuria, Megha Sharma

Abstract


Background: Birth of healthy term baby depends on normal placenta. IUGR is a condition associated with placental insufficiency. There is a close relationship between IUGR and placental qualitative changes. The aim of the present study was to evaluate the morphological and histological changes in placentas of IUGR fetuses and in placentas of normal uncomplicated pregnancies and to determine the relationship that exists between morphological change and frequency of IUGR.

Methods: In a cross sectional study conducted in the department of Pathology, GMC Jammu, a total of 60 placenta were received, 30 placenta of IUGR fetus (group 1-case) and 30 placenta of uncomplicated pregnancy with normal single fetus (group 2-control). Exclusion criteria: Twin pregnancy, gestational hypertension, diabetes, congenital anomaly, antepartum hemorrhage and systemic disorder.

Results: Placental weights in IUGR group were significantly lower than control group. Average placental weight in IUGR group was 425 gms while in the control group (normal placenta) it was 550 gms. Infarction, intervillous thrombosis, chorionic villitis, hemorrhagic endovasculitis, placental intravascular thrombi, perivillous fibrin deposition, fibrinoid necrosis and villous edema were found to be more common in IUGR group (Group 1-case group) than Normal (Group 2- control group).

Conclusions: This study highlightened that significant pathological differences were found between the placentas of IUGR fetus and normal fetus. The gross and microscopic measurement of a placenta is a good way to get proper information about IUGR and helps in management of the pregnancy.


Keywords


Intrauterine growth retardation, Foetus infarction, Fibrinoid necrosis, Placenta, Thrombosis

Full Text:

PDF

References


Pardi G, Marconi AM, Cetin I. Placental-fetal interrelationship in IUGR fetuses: a review. Placenta. 2002;23:136-41.

Mardi K, Sharma J. Histopathological evaluation of placentas in IUGR pregnancies. Indian J Pathol Microbiol. 2003;46(4):551-4.

Curtin WM, Krauss S, Metlay LA, Katzman PJ. Pathologic examination of the placenta and observed practice. Obstet Gynecol. 2007J;109(1):35-41.

Tantbirojn P, Saleemuddin A, Sirois K, Crum CP, Boyd TK, Tworoger S, et al. Gross ab-normalities of the umbilical cord: related placental histology and clinical significance. Placenta. 2009;30:1083-8.

Maulik D, Frances Evans J, Ragolia L. Fetal growth restriction: pathogenic mechanisms. Clin Obstet Gynecol. 2006;49(2):219-27.

Fox H, Sebire Nj. Pathology of the Placenta. 3rd ed. Philadelphia: Saundres; 2007.

BenirschkeK, Kaufmann P, Baergen R. Pathology of the Human Placenta. 5th ed. New York Springer; 2006.

Faye-Petersen OM, Heller DS, Joshi VV. Handbook of Placental Pathology. 2nd ed. London: Taylor and Francis; 2006.

Salafia CM, Charles AK, Maas EM. Placenta and fetal growth restriction. Clin Obstet Gynecol. 2006;49(2):236-56.

Smith NM. Broadsheet number 56: Mechanisms of fetal loss. Pathology. 2000;32:107-15.

Laurini R, Laurin J, Marsal K. Placental histology and fetal blood flow in intrauterine growth retardation. Acta Obstet Gynecol Scand. 1994;73:529-34.

Arias F, Romero R, Joist H, Kraus FT. Thrombophilia: a mechanism of disease in women with adverse pregnancy outcome and thrombotic lesions in placenta. J Matern Fetal Med. 1998;7:277-86.

Redline RW, Pappin A. Fetal thrombotic vasculopathy: The clinical Significance of extensive avascular villi. Hum Pathol. 1995;26(1):80-5.

Salafia CM, Minior VK, Pezzullo JC, Popek EJ, Rosenkrantz TS, Vintzileos AM. Intra-uterine growth restriction in infants of less than thirty-two weeks’ gestation: associated placental pathologic features. Am J Obstet Gynecol. 1995;173:1049-57.

Salafia CM. Placental pathology of fetal growth restriction. Clin Obstet Gynecol. 1997;40:740-9.

Chaiworapongsa T, Romero R, Kusanovic JP, Savasan ZA, Kim SK, Mazaki-Tovi S, et al. Unexplained fetal death is associated with increased concentrations of anti-angiogenic factors in amniotic fluid. J Matern Fetal Neonatal Med. 2010;23:794-805.