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Journal of the Anatomical Society of India

Relation between Placental Surface Area, Infarction and Foetal Distress in Pregnancy Induced Hypertension with its Clinical Relevance

Author(s): Udainia A, Bhagwat SS, Mehta CD

Vol. 53, No. 1 (2004-01 - 2004-06)

Department of Anatomy, Government Medical College, Surat - Gujarat

Abstract

Relation between placental surface area, infarction and foetal distress in pregnancy induced hypertension (PIH) with its clinical relevance was studied. The study was carried out on seventy five cases of PIH and twenty four cases of normotensive pregnancy.

It was noted that the mean surface area was significantly less in severe hypertension ( 179.14 cm2) and in mild hypertension (195.98 cm2 ) as compared to the control group ( 242.56 cm2 ). Within the same group, surface area was less for foetal distress cases. Variation in the surface area of placenta was more (coefficient of variation-mild hypertension group: 18.26, Severe hypertension group: 35.43 ) in the cases not having foetal distress as compared to cases having foetal distress (coefficient of variation-mild hypertension group: 15.58, Severe hypertension group: 24.45). Coefficient of variation increases with increase in severity of hypertension.

Placental infarction was present in all the placentae in severe PIH and in 92.5 % placentae in mild PIH as compared to only 29 % placentae in control group. Foetal distress is seen in 37 % cases in severe PIH, 10 % cases in mild PIH and in no case in control group.

Thus severity of hypertension adversely affects both foetal and placental outcome. If PIH is diagnosed at an early stage by frequent monitoring of blood pressure, clinical examination and urine examination, added precautions can be instituted during antenatal period and labour to reduce further risk to the mother and foetus.

Key Words: Placenta, Foetus, PIH, Infarction, Foetal Distress

Introduction

The term " Placenta" was used for the first time in 1559. Placenta is a mirror which reflects the intrauterine status of the foetus. All the anabolites needed for foetal metabolism come from the mother's blood and foetal catabolites are passed back into the mother's circulation through the placenta. Flexner, Cowie, Hellman, Wilde and Voxburgh ( 1948 ) showed enormous margin of placental adequacy in the transfer of some substances across the normal human placenta. So placental inadequacy is not suspected even if the placenta is small, it may be otherwise with oxygen.

The hypertensive disorders complicating pregnancy are quite common. Foetal distress, intrauterine foetal deaths and placental abnormalities are common in pregnancy induced hypertension (PIH). According to Thomson, Billewicz and Hytten ( 1969 ) foetal hypoxia is not uncommon near term and occasionally may lead to foetal distress or death. The risk is increased if placental function has been impaired by preeclampsia, post maturity and threatened abortion. The margin may be narrow and hazard may be greater if the placenta is unusually small. Weight of placenta is "functionally significant" because it is related to villous surface area and to total foetal metabolism.

Browne and Veall ( 1953 ) and Garg, Rath and Sharma ( 1996 ) found that placental surface area is significantly less in PIH, but none have mentioned the exact surface area.

Fox ( 1967 ), noted infarction in placentae from pregnancies complicated by pre eclampsia. He stated that extent and incidence of infarction increases with the increasing severity of toxaemia. But exact relationship between placental surface area, infarction and foetal distress was not very clear.

Present study is aimed at measurement of surface area of placenta, placental infarction and their relationship with foetal distress in PIH.

Materials and Methods

The study of relation between placental surface area, infarction and foetal distress in PIH was conducted in the Department of Anatomy, Government Medical College, Surat. The placentae were collected from Labour Room and Gynaecology Operation Theatre, New Civil Hospital, Surat. A total of 99 full term cases were studied.

Out of 99 cases, 75 cases belonged to parturients having PIH and 24 cases belonged to normal pregnancy ( Control Group ). In PIH, only those cases having blood pressure ranging 140 / 90 mm Hg and above, with and without oedema, and / or proteinuria were included. Some cases also had eclamptic fits. None of these cases had hypertension prior to pregnancy. In normal pregnancy group, only those cases having normal blood pressure without oedema and absent proteinuria were included.

Placenta with cord and membranes were collected immediately after delivery. Any abnormality of cord and membrane was noted. In all the cases, the amnion and chorion were trimmed from the placenta. The umbilical cord was cut at a distance of 5 centimetres from the site of insertion. Placentae were washed in running tap water, dried with the help of blotting paper and weighed. Then surface area of maternal surface of placenta was calculated by taking its imprint on a graph paper.

The mothers and their neonates identified for this study were given code numbers and studied at the hospital. The placentae along with the umbilical cord identified by corresponding code numbers were preserved in 10 % formalin solution.

All the cases of PIH were divided in to Mild and Severe categories depending upon the frequency and intensity of the abnormalities listed in Table I.

Table I: Indicators of Severity of Pregnancy Induced Hypertension ( PIH )

Indicator Mild PIH Severe PIH
1 Diastolic blood pressure < 100 mm Hg 110 mm Hg or >
2 Proteinuria Trace to 1+ Persistent 2+ or >
3 Convulsions Absent resent(eclampsia)
4 Visual disturbances Absent Present
5 Foetal growth restriction Absent Obvious
6 Headache Absent Present
7 Upper abdominal pain Absent Present
8 Oliguria Absent Present
9 Serum Creatinine Normal Elevated
10 Hyper bilirubinemia Absent Present
11 Thrombocytopenia Absent Present
12 Liver enzyme elevation Minimal Marked
13 Pulmonary oedema Absent Present

Infarction is divided into four categories depending upon gross naked eye examination of placentae. The categories are as under:

  1. Absent: When no foci of infarction is present on the placenta.
  2. Mild: When a few scattered foci of infarction are present on the placenta.
  3. Moderate: When many scattered foci or big areas of infarction are present on the placenta, involving about 10-25 % of total surface area.
  4. Severe: When more than 25 % of total surface area of placenta is infarcted with calcified patches.

Observations and Results

Histogram in Figure 1 shows the observations of surface area of maternal surface of placentae. Statistical analysis has been carried out to find out if the differences between control, mild and severe PIH groups are statistically significant i.e. not by chance.

Surface area of placenta in mild PIH group is shown in Table II. Mean surface area of placenta is significantly less i.e. 153.25 cm2 in cases having foetal distress in comparison to 200.72 cm2 in cases not having foetal distress. Variation in the surface area of placenta is more (Coefficient of variation 18.26) in the cases not having foetal distress as compared to cases having foetal distress (Coefficient of variation 15.58).

Last three columns of Table II show the surface area of placenta in severe PIH group. Mean surface area of placenta is significantly less i.e. 157.31 cm2 in cases having foetal distress in comparison to 192.05 cm2 in cases not having foetal distress. The cases not having foetal distress show much more variation in the surface area of placenta. In the control group, foetal distress is not found. In mild PIH, 4 out of total 40 cases are associated with foetal distress. Mean surface area of foetal distress cases is 153.25 cm2 as compared to 200.72 cm2 in cases not associated with foetal distress. In severe PIH, 13 out of a total 35 cases are associated with foetal distress and their mean surface is 157.31 cm2, which is less than the mean surface area of placentae not associated with foetal distress (192.05 cm2).

Table II: Correlation between Surface Area of Placenta and Foetal Distress in Pregnancy Induced Hypertension (PIH)

  Control Group Mild PIH Group Severe PIH Group
  Total No
Distress
Foetal
Distress
Total No
Distress
Foetal
Distress
Total No
Distress
Foetal
Distress
Mean surface area 242.56 242.71 - 195.98 200.72 153.25 179.14 192.05 157.31
Maximum surface area 299.00 299.00 - 301.00 301.00 183.00 298.00 298.00 222.00
Minimum surface area 204.00 204.00 - 125.00 125.00 132.00 79.00 79.00 90.00
Coefficient of variation 10.91 11.13 - 19.48 18.26 15.58 25.72 35.43 24.45
Standard Deviation 26.46 27.01 - 38.18 36.66 23.88 46.07 46.06 38.46

Thus, it can be concluded that surface area of placenta decreases with increase in severity of PIH. In each group, cases showing foetal distress have lesser surface area in comparison to cases not having foetal distress.

The observations of the infarction of the placentae are shown in Table III. Infarction is present only in 29 % cases in control group as compared to 92.5 % cases in mild PIH and 100 % cases in severe PIH. No case of moderate to severe infarction is found in the control group.

Table III : Incidence of Infarction

  Control Mild PIH Severe PIH
Gr. No. Infarction No. of Cases % No.
of Cases
% No.
of Cases
%
1 Absent 17 71.00 3 7.50 - -
2 Mild 7 29.00 33 82.50 30 85.71
3 Moderate - - - - 2 5.72
4 Severe - - 4 10.00 3 8.57

The observations showing correlation between infarction of placenta and foetal distress are shown in Table IV. Foetal distress is not present in the control group. There are 10 % cases of foetal distress in mild PIH and 37 % cases in severe PIH groups. All the cases of foetal distress in PIH group show infarction in placenta.

Table IV : Correlation between Infarction of Placenta and Foetal Distress

  Control Mild PIH Severe PIH
  No. of Cases % No. of Cases % No. of Cases %
Foetal Distress - - 4 10 13 37
Infarction - - Present   Present  

Discussion

Brown and Veall ( 1953 ) found a small placenta in PIH. Garg et al. ( 1996 ) mentioned that the size of placenta and its weight decreases with increase in severity of PIH, But none have mentioned the exact surface area of placenta.

In the present study, the mean surface area is 179.14 cm2 in severe PIH and 195.98 cm2 in mild PIH as compared to 242.56 cm2 in control group. Thus it can be concluded that severity of PIH has an adverse effect on the surface area of placenta and there of on foetal growth and development. Figure 2 shows that in the PIH groups, surface area of placenta is correlated with foetal distress and that the mean surface area is less in cases having foetal distress as compared to cases not having foetal distress. Recently Rath, Garg and Sood ( 2000 ) reported mean placental surface area of 209.36 cm2 in severe PIH, 251.73 cm2 in mild PIH and 254.63 cm2 in the control group. Comparable figures in the present study are towards the lower side. It could be due to regional variations or other socio-economic variations in the two population groups.

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Fig 2: Comparison of Surface area of Placenta of Foetal Distress cases with those of No Foetal Distress Cases

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Zeek and Assali ( 1950 ) defined placental infarction as a zone of ischaemic necrosis of a group of villi due to complete interference with their blood supply in the decidua or in the local state by thrombosis of a spiral arteriole or a retroplacental haemorrhage. Fox ( 1967 ) stated that in pregnancies complicated by pre eclamptic toxaemia, the incidence of placental infarction was very considerably raised, above that found in uncomplicated pregnancies. The incidence of placental infarction was related to the severity of PIH in these cases and not to any other maternal factor. In the present study also, placental infarction is present in 96 % cases in PIH. Fox ( 1978 ) found infarction in 25 % of normal term placentae. In the present study, infarction is found in 29 % cases in the control group. Present study also shows that all the placentae in severe PIH and 92.5 % placentae in mild PIH are infarcted. This indicates that the severity of hypertension adversely affects the placental infarction.

Chakravorty (1967 ) reported that foetal distress is correlated with severe infarction In present study also all cases of foetal distress in PIH are associated with infarction. Therefore, from the present study it can be concluded that in PIH, placental infarction and there of foetal distress are the outcome of a single disease process i.e. PIH.

By visualising the placenta during the antenatal period by ultra sound or Colour Doppler Imaging, one can predict the status of foetus in utero. If appropriate measures are instituted at an early stage to check the severity of PIH, one can reduce the risk of foetal distress.

References

  1. Brown JCM, Veall N. The maternal blood flow in normotensive and hypertensive women. Journal of Obstetrics and Gynaecology of British Empire 1953; 60 : 141-147.
  2. Chakravorty AP . Foetal and placental weight changes in normal pregnancy and pre-eclampsia. Journal of Obstetrics and Gynaecology of British Common wealth 1967; 74 : 247 253.
  3. Flexner LB, Cowie DB, Hellman LM, Wilde WS, Voxburgh GJ. The permeability of the human placenta to sodium in normal and abnormal pregnancies and the supply of sodium to the human foetus as determined with radioactive sodium. American Journal of Obstetrics and Gynaecology 1948;55 : 469-480.
  4. Fox H. Abnormalities of the foetal stem arteries in the human placenta. Journal of Obstetrics and Gynaecology of British Common wealth 1967; 74: 734-738.
  5. Fox H. The Pathology of the Placenta in The placenta in maternal disorders. Vol 7. WB Saunders Co. Philadelphia ; pp. 213-251,1978.
  6. Garg K, Rath G, 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.
  7. Rath G, Garg K, Sood M. Insertion of umbilical cord on the placenta in hypertensive mother. Journal of Anatomical Society of India 2000; 49 (2) : 149-152.
  8. Thomson AM, Billewicz WZ, Hytten FE. The weight of the placenta in relation to birth weight. Journal of Obstetrics and Gynaecology of British Common wealth 1969; 76 : 865-872.
  9. Zeek PM, Assali NS. Vascular changes in the decidua associated with eclamptogenic toxaemia of pregnancy. American Journal of Clinical Pathology1950; 20 : 1099-1109.
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