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Year : 2017  |  Volume : 60  |  Issue : 2  |  Page : 232-235
Placental histopathological findings in preterm/term and early/late onset small for gestation age: Are they significant?


1 Department of Obstetrics and Gynaecology, University College of Medical Sciences and Guru Teg Bahadur Hospital, New Delhi, India
2 Department of Pathology, University College of Medical Sciences and Guru Teg Bahadur Hospital, New Delhi, India

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Date of Web Publication19-Jun-2017
 

   Abstract 

We undertook a prospective comparison of placental histopathological findings in preterm versus term and early onset versus late onset small for gestation age (SGA) to find more information on the etiological aspects of this disorder. A total of 130 women with nonanomalous SGA were allocated into preterm (n = 60); term (n = 70); early onset (n = 9) and late onset (n = 121) groups. The blinded intergroup placental histopathology comparison was performed both qualitatively (type of lesion) and quantitatively (number of the lesion). All SGA placentae showed varying number of maternal underperfusion (MUP), fetal under perfusion, inflammatory, and others lesions. There was a slight higher percentage of placenta having MUP in preterm and early onset SGA. Perivillous fibrin deposition was peculiar for placenta of preterm SGA (P = 0.043). Both preterm and early onset SGA had a higher number of placental lesions, but there was no statistical difference either in type or number of the placental lesion in any of the examined groups.

Keywords: Fetal growth restriction, placental histopathological lesions, small for gestational age

How to cite this article:
Agarwal R, Tiwari A, Wadhwa N, Radhakrishnan G. Placental histopathological findings in preterm/term and early/late onset small for gestation age: Are they significant?. Indian J Pathol Microbiol 2017;60:232-5

How to cite this URL:
Agarwal R, Tiwari A, Wadhwa N, Radhakrishnan G. Placental histopathological findings in preterm/term and early/late onset small for gestation age: Are they significant?. Indian J Pathol Microbiol [serial online] 2017 [cited 2020 May 29];60:232-5. Available from: http://www.ijpmonline.org/text.asp?2017/60/2/232/208389



   Introduction Top


The placenta has been described as a “diary of intrauterine life” with the potential to reflect many aspects of fetal development.[1] A pertinent question which has been always raised is whether the placental lesions hold any key to adverse fetal outcome observed in small for gestational age (SGA) fetuses. The presence of uteroplacental insufficiency and abnormal blood supply, especially in preterm fetal growth restriction (FGR) placentas have been indicated by many authors.[2],[3],[4],[5],[6] Despite many studies on the aspect, the information still remains sketchy and demands more focused research. We undertook a prospective comparison of placental histopathological findings in preterm versus term and early onset versus late onset SGA to find more information on the etiological aspects of this disorder.


   Materials and Methods Top


The study was conducted in the Obstetrics and Gynaecology Department of a tertiary care center of a low-income country (2014–2016). Prior Ethical Committee clearance and patient consent were obtained for the study. The inclusion criteria for the study was a singleton pregnancy having SGA (actual birth weight <10th percentile for that gestational age).[7] Pregnancy with the anomalous fetus, patients with unsure of dates or irregular menses, known maternal diseases such as diabetes or gestational diabetes, Rh Isoimmunization disorders, thyroid dysfunction, chronic hypertension, smoking history, known collagen vascular disease, liver, and renal disease were excluded from the study.

A total of 130 women with SGA were enrolled prospectively and allocated into four groups:

  • Group 1: Preterm (delivery <37 weeks period of gestation) (n = 60)
  • Group 2: Term (delivery ≥37 weeks period of gestation) (n = 70)
  • Group 3: Early onset (delivery <34 weeks) (n = 9)
  • Group 4: Late onset (delivery ≥34 weeks) (n = 121).


The placentae were collected and were evaluated by a skilled pathologist blinded of maternal pregnancy outcome. The intergroup placental histopathology comparison was performed both qualitatively (type of lesion) and quantitatively (number of lesion). Histological lesions were defined according to the recent Redline's placental classification.[1] The discrete histopathological findings observed in the study were grouped into 15 main lesions and four major pathologic categories for the purpose of statistical analysis:[8] (a) maternal vascular underperfusion (MUP) including villous infarction, villous agglutination, placental syncytial knots (ST), intervillous fibrin, perivillous fibrin deposition, villous hypoplasia, intervillous hematoma, or retroplacental hematoma; (b) fetal vascular underperfusion (FUP) including fetal vasculopathy and avascular villi; (c) inflammatory with villitis, chorioamnionitis or vasculitis lesions; (d) others (stromal fibrosis and calcification). The placental lesions were then compared within the formed groups. We devised a receiver operating characteristic curve taking into consideration 6 significant histopathological lesions (villous infarction, agglutination, ST, intervillous fibrin deposition, stromal fibrosis, calcification) to give optimal lesion threshold for the placental abnormality definition (>3 placental lesions) [Figure 1]. This was used further for intergroup quantitative comparison.
Figure 1: Distribution of main placental histopathological lesions in the examined placentae

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Statistical analysis

Statistical software IBM SPSS Statistics for Windows, Version 20.0. (Armonk, NY; IBM Corp) was used for statistical analysis. Chi-square test (95% confidence interval [CI]), Fischer's exact test were used to determine statistical significance.


   Results Top


Both Group 1 and 2 showed placental lesions of MUP, FUP, inflammatory and others category, although in varying numbers [Table 1] and [Figure 1],[Figure 2],[Figure 3]. There was slightly higher percentage of placenta having MUP lesions (64% vs. 60%) out of total lesion studied in the placenta of preterm versus term SGA. Perivillous fibrin deposition was noted only in the placenta of preterm SGA (P = 0.043). On comparing individual histopathological lesions between SGA Group 1 and 2, no statistically significant difference was found. In Group 1, slightly higher number (50%) placentas were having ≥3 histopathological lesions as compared to 38.5% in Group 2, but this difference again was not statistically significant [Table 2].
Table 1: Comparison of placental findings between preterm and term small for gestation age; early onset and late onset small for gestation age

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Table 2: Comparison of significant histopathological lesions in preterm and term small for gestation age; early onset and late onset small for gestation age

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Figure 2: Main placental histopathological findings indicated maternal underperfusion (H and E, ×200) (a) Syncytial knot (b) Intervillous fibrin deposition (c) Villous infarction (d) Villous agglutination

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Figure 3: Main placental histopathological findings in the others category (H and E, ×200) (a) stromal fibrosis (b) calcification

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On comparison of individual histopathological lesions between Group 3 and 4, again no significant difference was noted [Table 1]. In early onset SGA, placental MUP lesions were noted in 95% versus 74% in late onset SGA. Inflammatory lesions along with stromal fibrosis and calcification were majorly noted in the placenta of late onset SGA. A higher number but not statistically significant, of early onset SGA subjects (Group 3) (66.6%) were having ≥3 significant placental lesions as compared to late onset SGA Group 4 (42.1%) [Table 2].


   Discussion Top


There has been growing interest in placental histopathology associated with intrauterine FGR to find possible implications of these findings and better define, understand, and manage these conditions.[9]

Apel-Sarid et al. conducted a microscopic examination of in 395 placentas in two categories of preterm (<34 and <37 weeks gestation) and compared them with term placenta.[2] They defined uteroplacental insufficiency as placental infarct, fibrosis of chorionic villi, thickening of blood vessels, and poor vascularity of the chorionic villi. They found a significant proportion of preterm FGR cases having pathology findings associated with uteroplacental insufficiency. Another observation was the presence of significant number of ST in preterm FGR cases indicating neonatal exposure to hypoxia and reactive oxygen agents.

Kovo et al. while studying 358 pregnancies, made patient groups and placental classification similar to ours: ≤34 weeks (early-onset FGR) or >34 weeks (late-onset FGR) and compared them with appropriate for age (AGA) neonates controls; placental lesions were too classified as MUP, fetal thrombo-occlusive disease, and inflammatory lesions.[3] The early-onset FGR group had significant higher MUP placental lesions than the late-FGR group. The late-onset FGR group had both placental villous lesions related to MUP and fetal thrombo-occlusive disease than the term AGA group. The authors vowed for severe maternal vascular compromise in early-onset FGR.

In a larger study involving 4617 third-trimester births, Stanek detected 43 placental phenotypes.[4] Based on placental pathologies, he concluded that chronic uteroplacental malperfusion is the dominating etiopathogenetic factor in late preterm and near-term births and acute fetal distress in full-term births. In another research, Salim et al. studied 307 placentae and found maternal obstructive lesions as the most frequent placental lesion among all groups.[5] These placental lesions were highest in early SGA delivered before 34 weeks (76.7%) (P = 0.0004) followed by isolated-SGA delivered at term (45.8%) and least in AGA (20.2%) (P = 0.0006).

Parra-Saavedra et al. in a more recent study extended the placental pathology correlation to neonatal outcome.[6] Among 97 histological findings consistent with placental underperfusion (PUP) in 84 SGA pregnancies, maternal vascular supply placental injuries (maldevelopment, obstruction, loss of integrity) were far more in number (79.4%) compared to fetal vascular supply placental lesions. The authors concluded that the presence of histological signs of PUP implies a significantly higher incidence of the emergency cesarean section, neonatal metabolic acidosis at birth and neonatal morbidity.

The varied description of placental pathological types, the FGR groups and their definitions and the nonstandardized method of result reporting make inter study comparison difficult.[2],[3],[4],[5],[6] The major limitation of our study was a lack of AGA control group, and the small cohort studied. Yet we tried to associate placental histopathological findings in different SGA settings both qualitatively (according to lesion) and quantitatively (≥3 placental lesions). There was slightly higher percentage of MUP lesions out of total lesions studied in preterm and early onset SGA. However, there were no other significant differences in individual placental pathological types. Both preterm and early onset SGA group had a higher number (≥3 placental lesions) of abnormal placental lesions compared to other groups, but they were not statistically significant. We could not substantiate any distinct placental etiological category as responsible for SGA fetuses contrary to other studies.[2],[3],[4] Our study further showed that although placenta histopathology grossly reflects placental insult, there are many other factors operational beyond it responsible for FGR.


   Conclusions Top


Preterm and early onset SGA group had a higher number (≥3 placental lesions) of abnormal placental lesion compared to other groups. Maternal placental lesions were more commonly observed in the preterm and early onset SGA group. Perivillous fibrin deposition was noted only in the placenta of preterm SGA. Inflammatory lesions along with stromal fibrosis and calcification were common in the placenta of late onset SGA.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Redline RW. Classification of placental lesions. Am J Obstet Gynecol 2015;213 4 Suppl: S21-8.  Back to cited text no. 1
    
2.
Apel-Sarid L, Levy A, Holcberg G, Sheiner E. Term and preterm (<34 and <37 weeks gestation) placental pathologies associated with fetal growth restriction. Arch Gynecol Obstet 2010;282:487-92.  Back to cited text no. 2
[PUBMED]    
3.
Kovo M, Schreiber L, Ben-Haroush A, Cohen G, Weiner E, Golan A, et al. The placental factor in early- and late-onset normotensive fetal growth restriction. Placenta 2013;34:320-4.  Back to cited text no. 3
    
4.
Stanek J. Comparison of placental pathology in preterm, late-preterm, near-term, and term births. Am J Obstet Gynecol 2014;210:234.e1-6.  Back to cited text no. 4
    
5.
Salim R, Jubran J, Okopnik M, Garmi G. Do placental lesions among term small for gestational age newborns differ according to the clinical presentation? Eur J Obstet Gynecol Reprod Biol 2014;173:38-42.  Back to cited text no. 5
    
6.
Parra-Saavedra M, Crovetto F, Triunfo S, Savchev S, Peguero A, Nadal A, et al. Placental findings in late-onset SGA births without Doppler signs of placental insufficiency. Placenta 2013;34:1136-41.  Back to cited text no. 6
    
7.
Alexander GR, Himes JH, Kaufman RB, Mor J, Kogan M. A United States national reference for fetal growth. Obstet Gynecol 1996;87:163-8.  Back to cited text no. 7
    
8.
Spinillo A, Gardella B, Bariselli S, Alfei A, Silini E, Dal Bello B. Placental histopathological correlates of umbilical artery Doppler velocimetry in pregnancies complicated by fetal growth restriction. Prenat Diagn 2012;32:1263-72.  Back to cited text no. 8
    
9.
Mifsud W, Sebire NJ. Placental pathology in early-onset and late-onset fetal growth restriction. Fetal Diagn Ther 2014;36:117-28.  Back to cited text no. 9
    

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Correspondence Address:
Rachna Agarwal
4/103, East End Apartments, Mayur Vihar, New Delhi - 110 096
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJPM.IJPM_390_16

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    Figures

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    Tables

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