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Assessment of birth weight and morphometry of placenta in pregnancy induced hypertension in sikkimese population.

INTRODUCTION: As per the National family health survey 2005, the prevalence of LBW babies is 22.2% in India. Low birth weight is a primary cause of infant mortality, diseases in early infancy, poor progress and development and accounts for huge amount of stress to the family. PIH is one of the foremost aetiologies of intra uterine growth retardation, foetal distress and infant mortality. The survival, development and growth of the foetus are solely dependent on the proper functioning and development of the placenta which is the foetal organ for exchange of blood gases, nutrition and excretion and is responsible for bringing about all the physiological changes of and maintaining the pregnancy to term. A thorough evaluation of placenta provides an accurate record of any complications which occurred during the prenatal life of the foetus and its consequences in future. The anatomical and pathological placental assessment becomes more precise through morphometric analysis which is non-invasive, indirect method of study of the physiology or pathology of human gestation. Rosana R.M (2008) (1)

If pregnancy is terminated and placenta removed the hypertension and proteinuria resolve within a few hours though some changes take several days or weeks to resolve. The placenta is intimately involved in the aetiology of hypertensive disorders of pregnancy (2). Barker D.J.P. recorded an inverse relationship between weight at birth and blood pressure. Reduced perfusion to the placenta and the foetus is one insult which can permanently alter and program both the structure and physiology of the foetus. In case of maternal hypertension atherosclerosis affects the uterine blood vessels, narrowing their lumen which leads to reduced blood flow at the inter-villous spaces (3).

METHODS: Analytical Study with Prospective cohort design which was carried out from May 2007 to April 2008, at Central Referral Hospital, Sikkim Manipal Institute of Medical Sciences, Tadong. Due to feasibility constraints convenient sample sizes was taken for the study. A total of 90 pregnant women in the age group of 18 years and above who consented to participate were included. Pregnant women with blood pressure ranging from 140/90 to 160/110mmHg with proteinuria were included as "cohort" and 60 pregnant women with normal blood pressure were included as "control". All these women were followed up throughout their pregnancy till delivery to study the final outcome of their pregnancies. Age matching was done to identify each Cohort with two corresponding Controls. The study of gross morphology of placenta was conducted in the Department of Anatomy. Pregnancy induced hypertension was diagnosed as per the WHO criteria in the department of obstetrics and gynaecology. The mothers and neonates were given tags with code numbers for identification. After delivery the placenta were collected from the labour room and operation theatre, washed, dried and examined and fixed in 10% formalin. The newborn babies were examined for any congenital anomalies, weight, and the apgar scoring were noted. The sizes, shape, weight, volume, thickness, number of cotyledons, cord length of the placenta were noted. The placenta was inspected for calcifications, infarctions, infections, site of cord insertion and membranes.

The collected data were tabulated and analyzed using the SPSS (Statistical Package of social sciences), version 10.0 for windows. Findings were expressed in terms of proportion and depicted in the form of Tables. Z-test and Chi-Square Test were applied for univariate analysis to study the effect of each variable over the outcome. A p-value < 0.05 was considered to be statistically significant All these 90 participants had singleton pregnancies and their outcome was live births. Pregnant women who did not give informed verbal consent and twin pregnancies were excluded.


Affects on new born: Though the number of babies with foetal distress, and low Apgar was higher in PIH however this did not show statistical significance.

The Mean birth weight in (MBW) of new born babies in controls was 2.8([+ or -] 0.32), with a maximum of 3.9 kg and minimum of 2.1 kg. The mean birth weight in cases (PIH) was 2.6([+ or -] 0.3) with a maximum of 3.1 kg and 2.0 kg. Out of the 30 cases 18 babies were of low birth weight (< 2.5kg) i.e. 60%, while 12cases were of normal birth weight (40%). The birth weight ranged from 2.0 to 3.0kg in cohorts. The birth weight was significantly less in PIH cases (p-0.0001).

The proportion of Low Birth Weight babies was significantly higher (60%) in PIH. The proportion of LBW babies was found to be significantly higher among the pregnant women in the age group of 30 years and above (45.5) as compared to those in the age group of 25-29 years (17.6%) and less than 25 years (8.9%). Chi-square for linear trend with increase in maternal age was also found to be statistically highly significant.

The number of infarcts, calcifications, and marginal insertion of placenta was more in mothers with PIH compared to normotensive mothers however this was not statistically significant.


Gross anatomy: The placental weight in controls ranged between 425-700 g m. The mean placental weight in hypertensive mothers (PIH) was 511.2([+ or -] 51.5) with a maximum of 600 gm and minimum of 380 gm. Mean placental weight in normotensive mothers was 548.6([+ or -] 72.8) gm with a range of maximum 700 gm and minimum 425gm. It was recorded that 14 placentas of PIH cases weighed between 300-500 gm i.e. 46.6% while 13 placentas weighed >500 gm i.e. 43.3% and 3 placentas weighed less than 300 gm i.e. 10%. In their study Udainia and Jain (2001) recorded that 65.33% of placenta weighed in the range of 300-500 gm while 21.33% weighed less than 300 gm and 13.34% weighed more than 500 gm. Jain et al (2007) revealed that 67% placental weight less than 500 gm in PIH cases. In the present study 56.6% of the placenta in PIH weighed less than 500gm.


Birth Weight: Birth weight is the simplest parameter which serves as the most reliable indicator for the growth, development and sustenance of the neonate. Low birth weight is a major health problem in developing countries like India and hypertension in pregnancy is one of the aetiologies of intra uterine growth reduction. 20 to 25% of babies born to mothers with hypertensive disorders are small for gestational age (SGA). Pre term deliveries occur in 50% of pregnancies with hypertension. Major anomalies occur in 3% off springs and there is increased risk of congenital viral infections especially with cytomegalovirus and hepatitis B. The perinatal mortality rate is around 5-10% in hypertensive disorder of pregnancy.

In our study the mean birth weight of newborn babies of hypertensive mothers was 2.69 kg and that of normotensive babies was 2.84 kg. Jain et al reported 59.10% low birth weight in PIH i.e. (< 2.5 kg). Udainia and Jain (2001) observed the MBW of 2.280 in cases 2.640 in control (4). Majumdar et al (2005) recorded MBW to be 2.04 in Pregnancy PIH and 2.8 kg in normotensives (6) with a range of maximum 3.9 kg and minimum of 2.1 kg.

The proportion of low birth weight was higher in cases (60%) compared to controls (20%) and in conformity to the study of Jain et al (59.10%) (7). Chakravorty (1967) observed the MBW of 2.80 kg in controls and 2.72 kg in hypertensive patients (8).

According to Roberts and Gammil (2005) manifestation of maternal disorder of preeclampsia requires initiation by reduced placental perfusion, followed by maternal response that occurs only in the presence confounding maternal factors (genetic, behavioural or environmental)is associated with reduced perfusion not only to the foeto-placental unit but to all maternal vascular beds (12). Reduced placental perfusion resulting in foetal under nutrition can lead to intra uterine growth restriction and permanent adaptive changes such as endothelial dysfunction. Thus it was noted that in placental insufficiency due to PIH the mean birth weight and the placental weight are both significantly reduced.

In the present study it was observed that the MBW in cases was higher than that of Udainia and Jain (5) & Majumdar (7) but in conformity with that of Chakraborty (9). The MBW in controls was observed to be higher in the present study which could be attributed to better socio-economic status and improved ante-natal care.

Placental Weight: If pregnancy is terminated and placenta removed the hypertension and proteinuria resolve within a few hours though some changes take several days or weeks to resolve. The placenta is intimately involved in the aetiology of hypertensive disorders of pregnancy (2)

The number of meconium stained placenta, infracted areas, thrombosis, and calcifications was higher in PIH but these did not show statistical significance

Incidence of reduced placental weight is significantly higher in PIH which could be due to reduced placental perfusion. The decreased placental weight is attributed to atheromatous lesions in the tunica media of spiral arteries, associated with thrombosis & vascular occlusion and placental infarction (11).

Udainia & Jain (2001) observed that there was significant lowering of placental weight in PIH. An increase in the incidence of intrauterine growth retardation and still birth is found to be associated with lower placental weight. They recorded 12% of placentas in PIH weighed between 251-300 gm and 65.33% between 301-500 gm. They observed that the placental weight ranged from 250 gm-700 gm with a mean of 495([+ or -] 114.11) gm in controls and 405.67 in cases (6).

The placental weight in controls ranged between 425-700 g in the present study. Hosemann (1946) in his study of normal term pregnancy found the placental weight of 400-1000 gm (6). Majumdar et al (2005) observed that the mean placental weight in control group was 485.85 ([+ or -] 47.31) and 399.10 ([+ or -] 90.31) in cases (7). K. Jain et al (2007) in their study revealed that 67% of placentas in PIH weighed less than 500 mg (8). The present study reveals that the mean placental weight is 511.2([+ or -] 51.2) in cases and 548.6([+ or -] 72.8) in controls, and 56.6% placentas weighed less than 500gm in PIH cases while Udainia & Jain (2001) (6) in their study reveal 77.33% of placenta in PIH weighed less than 500 gm which is slightly lower than the observations by the above authors.

Similar reduced weight of placenta in PIH was recorded by Chakravorty (1967) (9) Jain et al (2007) (8), Armitage, Hamilton & Rowe (1967) and Majumdar (2005) (7) and is confirmed by the present study. It is observed that the birth-weight as well as the placental weight was higher in both controls and cases in the present study which could be attributed to improved antenatal care and better socioeconomic status of the mothers in the present times.

The main feature of abnormal placentation is the inadequate trophoblastic invasion of maternal spiral arteries which fail to dilate and leads to high resistance low flow chorio-decidual circulation. The spiral arteries are unable to dilate to accommodate the required increase in blood flow resulting in placental dysfunction which manifests as pre-eclampsia (11). The reduced placental weight in PIH as shown by Chakravorty (1967) (10), Jain et al (9), Udainia & Jain (2001) (6), Majumdar (6), Boyd, Hamilton and Rowe (1967) (14), Garg, Rath and Sharma (1996) (16) is confirmed by the present study.

CONCLUSION: The mean birth weight of newborns is reduced in PIH p-value 0.001. The incidence of LBW babies was found to be more in preterm deliveries (38.1%) than full term deliveries (10.1%). Foetal distress, and the number of meconium stained placenta was higher in PIH cases but did not show significant variations.

The placentas of PIH mothers weighed less than that of normotensive mothers and were statistically significant (p 0.014). The placenta of patients with PIH weighed significantly less and the mean birth weight was also reduced in PIH as compared to controls with a significant (p-0.0001). The placentas of cases were smaller with more infarcts, calcifications, and fibrinoid deposits though the number of cotyledons did not show any significant variation.


(1.) R.R.M. Correa et al; (2008).Arch of Gynaecol and Obstet, 277: 201-206

(2.) Robson S.C: Hypertension and renal disorders; Dew Hurst Text book of Obstetrics and Gynaecology for Postgraduates. Edwards D. K. Blackwell Science Publications, London. 6th edition. 1995, 166-185.

(3.) Barker D.J.P. et al. (1998). Mothers, Babies ND Health in Later Life. Edinburgh, United Kingdom: Churchill Livingstone

(4.) Salvatore, A.C. (1968). The placenta in acute toxemia, Am J of Obstet and Gynecol, 102: 347-53.

(5.) Udainia A, Jain M.L, (2001). Morphological Study of Placenta in Pregnancy Induced Hypertension: J of Anatomical Society of India 50 (1): 24-27

(6.) Hosemann H. (1946). Duration of Pregnancy and weight of the placenta. Arch of Gynaecol. 176: 453.

(7.) Majumdar S, Dasgupta H, Bhattacharya K, Bhattacharya A. (2005). A Study of Placenta in normal and hypertensive pregnancies. J. Anatomical Society of India 54(2) 1-9.

(8.) Jain K, Kavi V, Raghuveer CV, Sinha R. (2007) Placental pathology in pregnancy--induced hypertension (PIH) with or without intrauterine growth retardation. Indian J of Pathology and Microbiology, 5:3

(9.) Chakravorty A.P. (1967), Fetal and placental weight changes in normal pregnancy and pre-eclampsia. J of Obstet and Gynaecol British Commonwealth. 74: 247-253.

(10.) Armitage P, Boyd J.D, Hamilton W, Rowe B.C, (1967). Journal of British Commonwealth. A Statistical analysis of a series of birth weights and placental weight. Human Biology. 39: 430.

(11.) Zeek P.M, Assali N.S. (1950). Vascular changes in the deciduas associated with eclamptogenic toxemia of pregnancy. Am J Clin Pathol. 20:1099-1109.

(12.) Norwitch E, Chaur-Dong H.S.U, Rapke J.T, 2002, Acute complications of Pre-eclampsia. Clinical J Obst & Gynaecol, 45(2):308-29.

(13.) Roberts J.M, Gammill H. S, 2005, Pre-eclampsia: Recent insights. Hypertension, 46: 1243-1249.

(14.) Hamilton W.J. and Girmes D, 1969, A statistical analysis of the growth of the human placenta correlated with the foetus. Journal of Anatomy. 105: 204.

(15.) Garg K, Rath G and Sharma S. Association of birth weight, placental weight and the site of umbilical cord insertion in hypertensive mothers. Journal of Anatomical Society of India (1996), 44:4

(16.) Boyd, P.A. and Scott, A. (1985). Quantitative structural studies on human placentae associated with pre-eclampsia, essential hypertension and intrauterine growth retardation. British J of Obstet and Gynaecol, 92: 714-721.


[1.] Kalpana Chhetri

[2.] Poonam Shilal

[3.] Binod Kumar Tamang


[1.] Assistant Professor, Department of Anatomy, Sikkim Manipal Institute of Medical Sciences, Central Referral Hospital.

[2.] Assistant Professor, Department of Anatomy, Sikkim Manipal Institute of Medical Sciences, Central Referral Hospital.

[3.] Associate Professor, Department of Anatomy, Sikkim Manipal Institute of Medical Sciences, Central Referral Hospital.


Dr. Kalpana Chhetri, Department of Anatomy, Sikkim Manipal Institute of Medical Sciences, 5th mile, Tadong, Sikkim--737102.

Date of Submission: 30/08/2013.

Date of Peer Review: 31/08/2013.

Date of Acceptance: 02/09/2013.

Date of Publishing: 06/09/2013
Table 1: Comparison of Obstetric Parameters between
PIH mothers and Normotnsive mothers

Serial   Obstetric                HTN Mean
No.      Parameters               ([+ or -] 2SD)

01       Birth Weight (kg)        2.6(0.2)
02       Age of pregnant woman    26.9(4.3)
03       Parity                   1.9(1.1)
04       Gestational age          37.0(1.5)

Serial   Normotensive Mean    P-Value from Z
No.      ([+ or -] SD)        test result

01       2.8(0.3)             0.0001 *
02       24.4(2.8)            0.001 *
03       2.3(1.4)             0.194
04       38.2(1.4)            0.0001 *

* p-value < 0.05 was considered to be statistically

Table 2: Comparison of Morphology of Placenta &
Cord between PIH mothers and normotensive mothers

Serial   Morphology of           HTN Mean
No       Placenta & Cord         ([+ or -] 2SD)

01       Placental Weight(gm)    511.2(51.5)
02       No. of Cotyledons       19.4(2.1)
03       Placental diameter      19.2(1.8)
04       Placental thickness     2.7(0.3)
05       Placental volume(cc)    461.5(63.6)
06       Cord length(cm)         55.0(2.8)

Serial   Normotensive Mean    P-value
No       ([+ or -] 2SD)       from Z test

01       5486(72.8)           0.014 *
02       19.9(2.8)            0.406
03       18.8(2.2)            0.361
04       2.7(0.5)             0.609
05       450.7(90.1)          0.561
06       57.5(3.2)            0.782

* p-value of < 0.05 was considered to be statistically

Table III: Correlates of low birth weight identified by the study

                              WEIGHT        WEIGHT

                              n     (%)     n     (%)
1.        ANTENATAL
          Cohort(PIH)         18    60      12    40
          Control             12    20      48    80
2.        AGE GROUP
          < 25yrs             4     8.9     41    91.1
          25-29yrs            64    17.6    28    82.4
          [greater than       5     45.5    6     54.5
            or equal to]
3.        PARITY
          [less than or       11    17.2    53    82.8
            equal to] 2
          > 2                 4     15.4    22    84.6
          Central             6     15.8    32    84.2
          Eccentric           3     10      27    90
          Marginal            6     27.3    16    72.7
          < 37weeks           8     38.1    13    61.9
          [greater than       7     10.1    62    89.9
            or equal to]

Sl. No.   CORRELATES          [X.sup.2],    VALUE

1.        ANTENATAL
          Control             17.64         0.001
2.        AGE GROUP
          < 25yrs
          25-29yrs            8.55          0.014
          [greater than
            or equal to]
3.        PARITY
          [less than or       0.04          0.835
            equal to] 2
          > 2
          Eccentric           2.76          0.251
          < 37weeks           9.06          0.003
          [greater than
            or equal to]

* p-value < 0.05 was considered to be statistically
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Author:Chhetri, Kalpana; Shilal, Poonam; Tamang, Binod Kumar
Publication:Journal of Evolution of Medical and Dental Sciences
Article Type:Clinical report
Geographic Code:9INDI
Date:Sep 9, 2013
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