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Patterns of placental pathology in preterm premature rupture of membranes

Published online by Cambridge University Press:  18 March 2013

J. Armstrong-Wells ,
M. D. Post ,
M. Donnelly ,
M. J. Manco-Johnson ,
B. M. Fisher  and
V. D. Winn
J. Armstrong-Wells*
Affiliation:
Department of Pediatrics (Neurology), University of Colorado Denver, Aurora, Colorado, USA Department of Obstetrics & Gynecology, University of Colorado Denver, Aurora, Colorado, USA
M. D. Post
Affiliation:
Department of Pathology, University of Colorado Denver, Aurora, Colorado, USA
M. Donnelly
Affiliation:
Department of Obstetrics & Gynecology, University of Colorado Denver, Aurora, Colorado, USA
M. J. Manco-Johnson
Affiliation:
Department of Hematology/Oncology/BMT, University of Colorado Denver, Aurora, Colorado, USA
B. M. Fisher
Affiliation:
Department of Obstetrics & Gynecology, University of Colorado Denver, Aurora, Colorado, USA
V. D. Winn
Affiliation:
Department of Obstetrics & Gynecology, University of Colorado Denver, Aurora, Colorado, USA
*
*Address for correspondence: Dr J. Armstrong-Wells, MD., MPH., Assistant Professor, Director, Perinatal and Hemorrhagic Stroke Programs, UCD Hemophilia and Thrombosis Center, 13199 E. Montview Blvd., Suite 100, Aurora, CO 80045, USA. Email jennifer.armstrong-wells@ucdenver.edu
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Abstract

Inflammation is associated with preterm premature rupture of membranes (PPROM) and adverse neonatal outcomes. Subchorionic thrombi, with or without inflammation, may also be a significant pathological finding in PPROM. Patterns of inflammation and thrombosis may give insight into mechanisms of adverse neonatal outcomes associated with PPROM. To characterize histologic findings of placentas from pregnancies complicated by PPROM at altitude, 44 placentas were evaluated for gross and histological indicators of inflammation and thrombosis. Student's t-test (or Mann–Whitney U-test), χ2 analysis (or Fisher's exact test), mean square contingency and logistic regression were used when appropriate. The prevalence of histologic acute chorioamnionitis (HCA) was 59%. Fetal-derived inflammation (funisitis and chorionic plate vasculitis) was seen at lower frequency (30% and 45%, respectively) and not always in association with HCA. There was a trend for Hispanic women to have higher odds of funisitis (OR = 5.9; P = 0.05). Subchorionic thrombi were seen in 34% of all placentas. The odds of subchorionic thrombi without HCA was 6.3 times greater that the odds of subchorionic thrombi with HCA (P = 0.02). There was no difference in gestational age or rupture-to-delivery interval, with the presence or absence of inflammatory or thrombotic lesions. These findings suggest that PPROM is caused by or can result in fetal inflammation, placental malperfusion, or both, independent of gestational age or rupture-to-delivery interval; maternal ethnicity and altitude may contribute to these findings. Future studies focused on this constellation of PPROM placental findings, genetic polymorphisms and neonatal outcomes are needed.

Keywords

altitude, chorioamnionitis, fetal inflammatory response, funisitis, subchorionic thrombi
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 4 , Issue 3 , June 2013 , pp. 249 - 255
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2013 

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References

1.Thornburg, KL, O'Tierney, PF, Louey, S. Review: the placenta is a programming agent for cardiovascular disease. Placenta. 2010; 31(Suppl), S54–S59.Google Scholar
2.Barker, DJ, Thornburg, KL, Osmond, C, Kajantie, E, Eriksson, JG. The prenatal origins of lung cancer II. The placenta. Am J Hum Biol. 2010; 22, 512–516.Google Scholar
3.Barker, DJ, Thornburg, KL, Osmond, C, Kajantie, E, Eriksson, JG. The surface area of the placenta and hypertension in the offspring in later life. Int J Dev Biol. 2010; 54, 525–530.Google Scholar
4.Kajantie, E, Thornburg, KL, Eriksson, JG, Osmond, C, Barker, DJ. In preeclampsia, the placenta grows slowly along its minor axis. Int J Dev Biol. 2010; 54, 469–473.Google Scholar
5.Grether, JK, Nelson, KB, Walsh, E, Willoughby, RE, Redline, RW. Intrauterine exposure to infection and risk of cerebral palsy in very preterm infants. Arch Pediatr Adolesc Med. 2003; 157, 26–32.Google Scholar
6.Redline, R. Cerebral palsy in term infants: a clinicopathologic analysis of 158 medicolegal case reviews. Pediatr Dev Pathol. 2008; 456–464.Google Scholar
7.Nelson, KB. Causative factors in cerebral palsy. Clin Obstet Gynecol. 2008; 51, 749–762.Google Scholar
8.Nelson, KB, Dambrosia, JM, Grether, JK, Phillips, TM. Neonatal cytokines and coagulation factors in children with cerebral palsy. Ann Neurol. 1998; 44, 665–675.Google Scholar
9.Nelson, KB, Willoughby, RE. Infection, inflammation and the risk of cerebral palsy. Curr Opin Neurol. 2000; 13, 133–139.Google Scholar
10.Wu, YW, Colford, JM Jr. Chorioamnionitis as a risk factor for cerebral palsy: a meta-analysis. JAMA. 2000; 284, 1417–1424.Google Scholar
11.Wu, YW, Escobar, GJ, Grether, JK, et al. Chorioamnionitis and cerebral palsy in term and near-term infants. JAMA. 2003; 290, 2677–2684.Google Scholar
12.Yoon, BH, Park, CW, Chaiworapongsa, T. Intrauterine infection and the development of cerebral palsy. BJOG. 2003; 110(Suppl 20), 124–127.Google Scholar
13.Ananth, CV, Vintzileos, AM. Epidemiology of preterm birth and its clinical subtypes. J Matern Fetal Neonatal Med. 2006; 19, 773–782.Google Scholar
14.Dammann, O, Allred, EN, Leviton, A, et al. Fetal vasculitis in preterm newborns: interrelationships, modifiers, and antecedents. Placenta. 2004; 25, 788–796.Google Scholar
15.Hansen, AR, Collins, MH, Genest, D, et al. Very low birthweight placenta: clustering of morphologic characteristics. Pediatr Dev Pathol. 2000; 3, 431–438.Google Scholar
16.Hecht, JL, Allred, EN, Kliman, HJ, et al. Histological characteristics of singleton placentas delivered before the 28th week of gestation. Pathology. 2008; 40, 372–376.Google Scholar
17.Hillier, SL, Martius, J, Krohn, M, et al. A case-control study of chorioamnionic infection and histologic chorioamnionitis in prematurity. N Engl J Med. 1988; 319, 972–978.Google Scholar
18.Mueller-Heubach, E, Rubinstein, DN, Schwarz, SS. Histologic chorioamnionitis and preterm delivery in different patient populations. Obstet Gynecol. 1990; 75, 622–626.Google Scholar
19.Rana, A, Sawhney, H, Gopalan, S, Panigrahi, D, Nijhawan, R. Abruptio placentae and chorioamnionitis-microbiological and histologic correlation. Acta Obstet Gynecol Scand. 1999; 78, 363–366.Google Scholar
20.Guzick, DS, Winn, K. The association of chorioamnionitis with preterm delivery. Obstet Gynecol. 1985; 65, 11–16.Google Scholar
21.Garite, TJ, Freeman, RK. Chorioamnionitis in the preterm gestation. Obstet Gynecol. 1982; 59, 539–545.Google Scholar
22.Ghidini, A, Salafia, CM, Minior, VK. Lack of relationship between histologic chorioamnionitis and duration of the latency period in preterm rupture of membranes. J Matern Fetal Med. 1998; 7, 238–242.Google Scholar
23.Goldenberg, RL, Hauth, JC, Andrews, WW. Intrauterine infection and preterm delivery. N Engl J Med. 2000; 342, 1500–1507.CrossRefGoogle ScholarPubMed
24.Redline, RW. Inflammatory response in acute chorioamnionitis. Semin Fetal Neonatal Med. 2012; 17, 20–25.Google Scholar
25.Salafia, CM, Weigl, C, Silberman, L. The prevalence and distribution of acute placental inflammation in uncomplicated term pregnancies. Obstet Gynecol. 1989; 73(Pt 1), 383–389.Google Scholar
26.Kramer, MS, Chen, MF, Roy, I, et al. Intra- and interobserver agreement and statistical clustering of placental histopathologic features relevant to preterm birth. Am J Obstet Gynecol. 2006; 195, 1674–1679.Google Scholar
27.Aziz, N, Cheng, YW, Caughey, AB. Neonatal outcomes in the setting of preterm premature rupture of membranes complicated by chorioamnionitis. J Matern Fetal Neonatal Med. 2009; 22, 780–784.Google Scholar
28.Pacora, P, Chaiworapongsa, T, Maymon, E, et al. Funisitis and chorionic vasculitis: the histological counterpart of the fetal inflammatory response syndrome. J Matern Fetal Neonatal Med. 2002; 11, 18–25.Google Scholar
29.Yoon, BH, Romero, R, Yang, SH, et al. Interleukin-6 concentrations in umbilical cord plasma are elevated in neonates with white matter lesions associated with periventricular leukomalacia. Am J Obstet Gynecol. 1996; 174, 1433–1440.Google Scholar
30.Kim, CJ, Yoon, BH, Park, SS, Kim, MH, Chi, JG. Acute funisitis of preterm but not term placentas is associated with severe fetal inflammatory response. Hum Pathol. 2001; 32, 623–629.Google Scholar
31.Salafia, CM, Vogel, CA, Vintzileos, AM, et al. Placental pathologic findings in preterm birth. Am J Obstet Gynecol. 1991; 165(Pt 1), 934–938.Google Scholar
32.Arias, F, Rodriquez, L, Rayne, SC, Kraus, FT. Maternal placental vasculopathy and infection: two distinct subgroups among patients with preterm labor and preterm ruptured membranes. Am J Obstet Gynecol. 1993; 168, 585–591.Google Scholar
33.Germain, AM, Carvajal, J, Sanchez, M, et al. Preterm labor: placental pathology and clinical correlation. Obstet Gynecol. 1999; 94, 284–289.Google Scholar
34.Hessol, NA, Fuentes-Afflick, E. The perinatal advantage of Mexican-origin Latina women. Ann Epidemiol. 2000; 10, 516–523.Google Scholar
35.Wu, YW, Xing, G, Fuentes-Afflick, E, et al. Racial, ethnic, and socioeconomic disparities in the prevalence of cerebral palsy. Pediatrics. 2011; 127, e674–e681.Google Scholar
36.Chaiworapongsa, T, Romero, R, Kim, JC, et al. Evidence for fetal involvement in the pathologic process of clinical chorioamnionitis. Am J Obstet Gynecol. 2002; 186, 1178–1182.Google Scholar
37.van Hoeven, KH, Anyaegbunam, A, Hochster, H, et al. Clinical significance of increasing histologic severity of acute inflammation in the fetal membranes and umbilical cord. Pediatr Pathol Lab Med. 1996; 16, 731–744.Google Scholar
38.Katzman, PJ, Metlay, LA. Fetal inflammatory response is often present at early stages of intra-amniotic infection, and its distribution along cord is variable. Pediatr Dev Pathol. 2010; 13, 265–272.Google Scholar
39.Machin, G. Funisitis and chorionic vasculitis: relation to chorioamnionitis, timing and scoring. Fetal Pediatr Pathol. 2011; 30, 414–430.Google Scholar
40.Salafia, CM, Misra, D, Miles, JN. Methodologic issues in the study of the relationship between histologic indicators of intraamniotic infection and clinical outcomes. Placenta. 2009; 30, 988–993.Google Scholar
41.Sebire, NJ, Goldin, RD, Regan, L. Histological chorioamnionitis in relation to clinical presentation at 14–40 weeks of gestation. J Obstet Gynaecol. 2001; 21, 242–245.Google Scholar
42.Harteman, JC, Nikkels, PG, Kwee, A, Groenendaal, F, de Vries, LS. Patterns of placental pathology in preterm infants with a periventricular haemorrhagic infarction: association with time of onset and clinical presentation. Placenta. 2012; 33, 839–844.Google Scholar
43.Koeppen, M, Eckle, T, Eltzschig, HK. The hypoxia-inflammation link and potential drug targets. Curr Opin Anaesthesiol. 2011; 24, 363–369.Google Scholar
44.Kovo, M, Schreiber, L, Ben-Haroush, A, et al. The placental factor in spontaneous preterm labor with and without premature rupture of membranes. J Perinat Med. 2011; 39, 423–429.Google Scholar
45.Khalid, ME, Ali, ME, Ali, KZ. Full-term birth weight and placental morphology at high and low altitude. Int J Gynaecol Obstet. 1997; 57, 259–265.Google Scholar