|Year : 2020 | Volume
| Issue : 4 | Page : 141-145
Morpho-Histological Study of Placentae from Pregnancies Complicated by Anemia
Abeer Zubair Khan1, Stuti Srivastava2, Fardan Qadeer3, Mahboobul Haque4
1 Associate Professor, Department of Anatomy, Integral Institute of Medical Sciences and Research, Integral University, Lucknow, Uttar Pradesh, India
2 Assistant Professor, Department of Anatomy, Ananta Institute of Medical Sciences and Research Centre, Siyol, Rajasthan, India
3 Assistant Professor, Department of Pharmacology, Era's Lucknow Medical College and Hospital, Era University, Lucknow, Uttar Pradesh, India
4 Professory and Head, Department of Anatomy, Integral Institute of Medical Sciences and Research, Integral University, Lucknow, Uttar Pradesh, India
|Date of Submission||08-Jul-2020|
|Date of Decision||17-Aug-2020|
|Date of Acceptance||23-Sep-2020|
|Date of Web Publication||7-Dec-2020|
Qadeer Villa, 1 Nabiullah Road, Near City Station, Lucknow - 226 018, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Background: The placenta is an important organ that acts as a conduit for transporting substances from the mother to the fetus and vice versa. It performs many functions and is intimately related to both the mother and the fetus. Anemia is a leading disorder of pregnancy and is seen to effect >65% of pregnant women in India. It is also a known cause of intra-uterine growth retardation, preterm deliveries, low-birth-weight deliveries, etc. Objective: The aim is to study and compare the morphometric and histological changes seen in placentae from normal and anemic mothers. Methods: This study was done in the Department of Anatomy of Shri Ram Murti Smarak Institute of Medical Sciences and Research, Bareilly, Uttar Pradesh, India. One hundred and fifty placentae were collected, 75 each from normal and anemic mothers. A thorough morphometric and histological study of the placentae was done, and the results were recorded. Results: It was observed that the mean weight, diameter, circumference, and chorionic plate area of the placentae from anemic mothers was significantly reduced in comparison to the controls. Histological study showed that there was a significant increase in pathological changes such as syncytial knots, fibrinoid necrosis, calcification, and medial coat proliferation of blood vessels in samples obtained from placentae of anemic mothers in comparison to the controls. Conclusion: It was concluded from this study that maternal anemia has significant consequences on the developing placenta. These morphometric and microscopic changes in placental structure can in turn reduce its function, thus having an adverse effect on fetal outcome.
Keywords: Anemia, morphometry, placenta
|How to cite this article:|
Khan AZ, Srivastava S, Qadeer F, Haque M. Morpho-Histological Study of Placentae from Pregnancies Complicated by Anemia. Natl J Clin Anat 2020;9:141-5
|How to cite this URL:|
Khan AZ, Srivastava S, Qadeer F, Haque M. Morpho-Histological Study of Placentae from Pregnancies Complicated by Anemia. Natl J Clin Anat [serial online] 2020 [cited 2021 Jan 16];9:141-5. Available from: http://www.njca.info/text.asp?2020/9/4/141/302573
| Introduction|| |
The placenta is an organ that connects the developing fetus to the uterine wall. As this complex structure is very closely associated with the fetus throughout gestation, its study provides us an accurate record of an infant’s prenatal period.
Anemia is the most common nutritional deficiency disorder in the world. According to the WHO guidelines, a level of hemoglobin below 11 g/dl is an indication of maternal anemia. It is a hazardous, hematological disorder and, according to the WHO statistics, is seen in 65%–75% of pregnant women in our country. It contributes significantly to maternal morbidity and mortality.
The placenta is a unique organ as it is both a conduit of oxygen to the fetus as well as an expender of oxygen to support its own metabolism and these two functions are perfectly balanced. In patients with anemia there is an underlying deficiency of oxygen-rich blood, and hence, the amount of available oxygen becomes a very critical factor for the development of the placenta, placental blood vessels, and the fetus.
When pregnancy is complicated by maternal anemia, many pathological changes are bound to occur, which can influence morphometry and histology of the placenta. A reduction in weight, circumference, diameter, area, and histological changes such as infarction, calcification, intervillous thrombosis, and fetal vessel hemolysis occurs and reduce the functional villous mass. Hypoxia that occurs as a result of prolonged anemia during pregnancy is associated with an increased risk of preterm delivery, intra-uterine growth retardation (IUGR), low-birth-weight baby, unfavorable APGAR scores and various other undesirable effects on the fetus. Thus, placenta is a focus of increasing interest in modern obstetrics because significant pathological changes afflict the placenta often before affecting the fetus. Placental abnormalities can therefore be an “early warning system” for fetal problems. As most perinatal fetal deaths are related to insufficient oxygen supply in utero, the study of the placenta plays a pivotal role in predicting the outcome of future pregnancies and their management.
As anemia in pregnancy is known to have a detrimental effect on the placenta, the present study was undertaken to analyze the spectrum of changes that may occur when pregnancy is associated with this underlying disorder.
The purpose of this study was to evaluate the morphometric and histological changes seen in placentae from anemic mothers and to compare the findings with the control group.
| Materials and Methods|| |
This study was done in the Department of Anatomy of Shri Ram Murti Smarak Institute of Medical Sciences and Research, Bareilly, Uttar Pradesh, in association with the Department of Obstetrics and Gynaecology and the Department of Pathology after taking required ethical clearance from the institutional ethical committee. One hundred and fifty full-term placentae were randomly collected over a period of 1 year, from mothers who delivered either vaginally or by cesarean section. Relevant history was taken, and the results of hematological investigations were recorded.
The placentae were classified into the control and study group (anemic group). Under each group, 75 placentae were studied. Placentae from women with single, uncomplicated pregnancies of gestational age between 37 and 41 weeks were included in this study. Placentae from mothers with hemoglobin ≥11 g/dL were taken as control group, while those from mothers with hemoglobin ≤11 g/dL were taken as the study group. Placentae from women with associated obstetric or medical complications of pregnancy, i.e., gestational hypertension, fibroids, retroversion of uterus, cervical cancer, ovarian cysts, venous thromboembolism, etc., or with systemic disorders and chronic maternal illnesses were excluded from the study. Placentae obtained as a result of twin pregnancies were also excluded.
Morphometric and histological examination
The placenta was first inspected, and its various morphometric measurements were recorded. The following parameters of the placenta were then measured: weight, diameter, circumference, and chorionic plate area.
- Weight was measured in grams by an electronic weighing scale
- Diameter was measured by a digital vernier caliper. Both maximum and minimum diameters were measured in centimeters up to one decimal point
- Circumference was measured in centimeters up to one decimal point by a thread which was wound around the entire circumference of the placenta and cut at the point of crossing after one round. The length of the cut thread was measured by stretching it between the two arms of the digital caliper.
- From the diameter of the placenta, the mean chorionic plate area was also calculated by using the following formula:
Where A is area of an ellipse, dL is the largest diameter and dS is the smallest diameter.
For the histological study we obtained full-thickness tissue from the placenta and prepared it for routine H and E. In the light microscopic examination, the placental villi were quantitatively screened for syncytial knots, fibrinoid necrosis, cytotrophoblastic cellular proliferation, calcification, and endothelial changes in blood vessels. All the slides were first observed in low power (×10) and then the presence of the aforementioned parameters was recorded per low power field (per lpf). Three random and different areas of the slide were screened, and the range and mean of the values obtained per low power field was recorded. Histological photographs were taken with the help of an Olympus CX21i compound microscope, which had an attached camera.
A comparison between the control and study group was made by calculating the mean, median with standard deviation and P-value for each parameter by using t-test.
| Results|| |
[Table 1] shows the various morphometric measurements of the control and study group. It was observed that in the anemic group; the mean weight, minimum diameter, circumference, and chorionic plate area were reduced in comparison to the control group and this reduction was found to be statistically significant (P ≤ 0.05). The maximum diameter of placentae from the anemic group was also reduced in comparison to the controls, but this reduction was statistically not significant.
[Table 2] shows a comparison between various histological features observed in placentae from both the control and anemic group.
|Table 2: Histology by hematoxylin and eosin staining per lpf (low power field-×10)|
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On light microscopic examination of placentae from anemic mothers, it was observed that syncytial knots [Figure 1], fibrinoid necrosis [Figure 2], areas of calcification and medial coat proliferation of blood vessels [Figure 3] were significantly increased in anemic groups in comparison to the controls.
|Figure 3: Showing medial coat proliferation of blood vessels in study group|
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Cytotrophoblastic cellular proliferation [Figure 4] was slightly reduced in the anemic group in comparison to the controls, but this reduction was not statistically significant.
|Figure 4: Showing cytotrophoblastic cellular proliferation in study group|
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| Discussion|| |
Anemic disorders of pregnancy are one of the leading causes of maternal and perinatal mortality and morbidity. The present study deals with changes in morphometry and histological structure of the placenta in mothers with anemia. A total of one hundred and fifty placentae were meticulously studied. It can be inferred from the results of the present study that the mean of all morphometric parameters of the placenta was reduced in the anemic group in comparison to the controls.
The mean chorionic plate area of anemic group was also reduced in comparison to the controls. This corresponds to a decreased diameter and circumference in the study group in comparison to the controls. It was seen that in mothers suffering from gestational anemia the placental size was smaller as compared to the placentae from normal, healthy mothers.
This overall reduction in the size of the placentae from mothers of the study group indicates that anemia has a detrimental effect on placental development, and it can be attributed to the lower oxygen-carrying capacity of the blood and the resulting hypoxia. Most authors like Rohini et al. reported that the mean weight of placentae from anemic mothers was 410 g. This finding was similar to the findings of the present study. Mongia et al., who have studied placental morphometry in Indian women and other ethnicities, have also found similar results. But some authors like Godfrey et al. and Agboola, who also studied placentae from anemic mothers, reported that anemia and iron deficiency during pregnancy were associated with large placental weight and size, and thus, they found a positive correlation between maternal anemia and placental weight. They also observed that placental hypertrophy appeared to be a uniform, proportional, physiological compensatory growth. This was in contrast to the findings of the present study, where placental weight was found to be significantly reduced in anemic group. A review of data published by a few other authors also reveals that hypoxia may initially cause hypertrophy of the placenta, but with the advancement in the pregnancy, i.e., toward term, placental growth retardation is observed., This hypotrophy of the placenta may be dependent on the duration, time, and severity of anemia.
One of the main functions of the placenta is that it acts as a barrier between the fetus and the mother by separating the fetal blood vessels from the maternal blood present in the intervillous spaces. The structure of this placental barrier can be observed under a light microscope. The barrier is selectively permeable and allows certain substances such as water, oxygen, hormones, and other nutritive molecules to pass from the maternal blood to the fetal blood vessels and excretory products to pass from the fetus to the mother. The components of the placental barrier from maternal to fetal side are:
- Trophoblastic basement membrane
- Connective tissue core of the villus derived from the fetus (extraembryonic mesoderm)
- Basement membrane of fetal capillaries
- Endothelium of fetal capillaries.
With increasing gestational age, this barrier reduces in thickness and this appears to be a normal change seen with placental maturity. Closer to term, we also observed that the syncytiotrophoblast layer became thin and syncytial knots were increased. The cytotrophoblast layer also reduced and was seen as clumps and fragments. Increased deposition of fibrin was seen on the villus surface as well as in the tunica of the blood vessels. These changes are a sign of placental maturity and are seen in normal placentae, but their increased incidence in placentae from anemic mothers signifies that these changes in the placenta are not proportional to the gestational age.
On histology of placentae from anemic mothers, we observed that there was a significant increase in the presence of calcification, medial coat proliferation of blood vessels, syncytial knots, and fibrinoid necrosis in comparison to the controls. Areas showing fibrinoid necrosis were significantly increased, and fibrin deposit was seen even in the tunica of blood vessels. Fibrinoid necrosis of blood vessels leads to intervillous hemorrhage, which was also observed in few anemic cases but not in controls. Al-Hakeem et al. studied changes in placentae from anemic mothers and found an increase in histomorphological abnormalities like thickening of the capillary basement membrane, cytotrophoblastic proliferation, syncytial knots, and fibrosis. Mehrotra et al. and Biswas et al. reported a similar increase in villous fibrosis and syncytial knots in placentae from anemic mothers. Increased syncytial knots, fibrinoid necrosis, and a reduction in cytotrophoblastic cellular proliferation are all effects of reduced perfusion and oxygen concentration. Tripathi and Sudele and Soni and Nair conducted a similar histopathological study on placentae from anemic mothers, and they found that the areas showing cytotrophoblastic cellular proliferation were significantly increased in the study group in comparison to the controls. This is contrary to our finding, but it is essential that gestational age and severity of anemia be considered before these values can be accurately compared. It is postulated that when the placenta develops in hypoxic conditions like anemia the villi show many changes, including an increase in angiogenesis and terminal capillaries. These changes appear to be a compensatory mechanism to fulfill the needs of the developing fetus. Placental changes characterized by endothelial or vascular abnormalities like medial coat proliferation may present with increased permeability of the vessels, which can even lead to fetal anemia.
These histological changes are also an indicator of placental maturity as the placentae from mothers who delivered postterm (beyond 42 weeks of gestation) usually present with a higher incidence of these features. An early appearance of signs of placental maturity can be a signal for induction of labor and spontaneous preterm delivery. This can be extremely dangerous for a yet under-developed fetus and can explain why anemia is a known and leading cause of preterm delivery, IUGR, and abnormal APGAR scores at birth.
| Conclusion|| |
From the various morphometric changes observed, it is concluded that placentae obtained from anemic mothers show a significant reduction in placental size. On histopathological analysis, these placentae also show an increase in signs of ischaemic damage to tissues along with maldeveloped terminal villi. These findings may account for impaired gas and nutrient transfer to and from the fetus in these disorders, thereby resulting in perinatal mortality and morbidity. This also helps us establish that IUGR, abnormal APGAR scores of the baby and preterm deliveries seen in anemic mothers can be caused due to microscopic changes in the structure of the placenta and fetal hypoperfusion. It is essential that the spectrum of placental changes and their effects on the fetus be studied further and evaluated qualitatively to establish such a correlation.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2]