Morphological Changes of Placenta Associated with Maternal Anaemia

Abstract

Placenta is the mirror of fetomaternal status. The effect of anemia in pregnancy can be diverse and detrimental to the mother and the fetus. This prompted us to carry out the present study, which aimed to observe and compare the morphological features of placenta at term in anemic and non-anemic mothers of North Bengal and to find out the clinical relevance of such structural changes. Total 30 placentas were collected from each group of selected patients after delivery at labor room. Examination of placenta was conducted according to proforma. A general survey of umbilical cord, membranes, fetal surface, and maternal surface was carried out. The diameters were measured, area was estimated, and shape was noted. Placenta and fetus was weighed in the same scale. The volume was estimated by water displacement method. In anemic mothers, mean baby birth weight was found to be significantly less than that of control group. The mean placental weight in test group was significantly increased in comparison to controls. The mean placental volume and mean placental area in case of test group were significantly increased. Occurrence of morphological features, like subchorionic fibrosis; retroplacental clot, gross calcification, or placental infarction etc were found to be significantly higher in anemic mothers in comparison to non-anemic group. In the present study, it was proved that placenta has considerable functional reserve capacity. It tends to limit the ill-effects of tissue injury and of unfavorable maternal milieu like anemia. Our findings were in accordance with the previous studies in this field. Key-wordsPlacenta, Maternal anaemia, Morphological changes, Placental weight INTRODUCTION Placenta is the most accurate record of the infants’ prenatal experience [1] . It is the vital organ for maintaining pregnancy and promoting normal fetal development. The human placenta is a flattened discoid organ, which connects the fetus with the uterine wall. It has a maternal component, decidua basalis and a fetal component, chorion frondosum. The fetus and the placenta share the same genetic makeup and so therefore both should be expected to possess parallel growth potentials. Maturation of placenta causes an increase in the placental nutrient transfer capacity and thus improves placental efficiency, permitting an increase in the number of grams of fetal weight supported by every gram of placental mass. Not surprisingly “Placental insufficiency” is invoked commonly in case of impaired fetal growth [2] . Access this article online Quick Response Code Website: www.ijlssr.com DOI: 10.21276/ijlssr.2017.3.5.23 At full term the human placenta consists of: 1. Fetal surface, which is smooth, glistening, covered by the amnion and presents the insertion of the umbilical cord close to its centre. 2. Maternal surface rough, irregular consists of 15-30 cotyledons separated by fissures that arise from the folding of the basal plate. 3. Umbilical cord insertion is usually central but may vary in some specimens like battledore/marginal, velamentous, eccentric etc. At full term, the dimensions are as follows: Placental weight is approx. 500gm, diameter: 15-20 cm; thickness: 3cm; volume: 500ml. Length of umbilical cord: 50 cm; breadth: 2cm. These measurements vary widely; there are several types of human placentas with variant cord insertions, and also shape: rounded in 81.6%, oval in 16%, irregular in 2.4% [3-5] . Flattened discoid shape of placenta with an approximately circular outline was described as normal [4] as well as in maternal iron-deficiency anaemial [6] . Size of placenta can be calculated by measuring its diameter, thickness, area, weight and volume [7-8] . Usually, the placenta is 150-200 mm (average 185 mm) in diameter and 10-40mm (average 23mm) in thickness RESEARCH ARTICLE Int. J. Life. Sci. Scienti. Res., 3(5): 1400-1407 SEPTEMBER 2017 Copyright © 2015-2017| IJLSSR by Society for Scientific Research is under a CC BY-NC 4.0 International License Page 1401 [4] . Previously it was observed that presence of low maternal hematocrit was associated with higher placental weight [9] . Recent studies suggested an increase in placental weight in anemic mothers [10] . There is probably a compensatory physiological hypertrophy of the placenta resulting from inadequate oxygen supply to the fetus [11] . Volume of the placenta is proportional to its weight [12] . Placental volume is markedly reduced in abnormally small babies [13] . Volume of placenta is increased in male babies than females [14] . Because of the fact that placenta has a normally unrealized potential for incremental growth [9,15-18] , certain patho-physiological conditions such as high altitude, severe anemia and maternal heart failure are associated with unusually large placental volume. Placenta extrachorialis, the commonest developmental variant of the placenta is found in 25% of all placentas. Circumvallate form of placenta extrachorialis, whether partial or complete, is associated with an increased incidence of low birth weight [12,19-21] , congenital malformation [22] , prematurity, prenatal bleeding and abruption [23] . The normal placenta can contain 8 20 cotyledons [24] . Reduced number of cotyledons can be seen in maternal malnutrition, especially in severe anemia [25] . Calcification of placenta is a sign of physiological maturity of placenta [26] . More mature and heavy the placenta more is the extent of calcified patches [27] . Placental calcification occurs earlier in pregnancy in cigarette smokers [28] . Placenta is subjected to cystic degeneration also, related to maturation [29] . Out of a series of 630 placentas collected from cases of toxemia and diabetes, 40 had cystic changes [30] . Placental infarction is described as an area of necrotic changes; extensive infarction is the hallmark of a severe circulatory compromise in placenta [31] . Woodling et al. [32] described “The placental infarct as a consequence of necrosis of maternal cotyledon caused by occlusion of the utero-placental artery those supplies it”. V. Paul Wentworth [26] divided infarct into “red infarcts” and “other true infarcts” and also found two similar macroscopic lesions and termed them “perivillous fibrin deposition” and “mottled infarct”. Thrombosis within the tissue is a feature of both normal and abnormal placentas. The clinical significance of such thrombosis is either not known or proved to be none [33] . Relevance of present study: Placental change in Anemia Placenta is the mirror of the fetomaternal status. The effect of anemia in pregnancy can be so diverse and detrimental to both mother and developing fetus that it prompted us to carry on the present study to know whether placenta, an organ acting as a bridge between mother and fetus, is associated with major changes in anemia. Finally, an attempt has been made to confirm, agree or deny the findings of the previous workers in this field. MATERIALS AND METHODS The study was conducted during the period of June-2006 to May-2007 in the Department of Anatomy in collaboration with the Department of Pathology and Department of Obstetrics & Gynaecology, North Bengal Medical College & Hospital, Darjeeling, India, which caters for patients from all possible social status. The placentas were collected from booked cases delivered in the Department of Obstetrics & Gynecology. Permission from the ethics committee was taken; informed consent was taken from the patients. Gravid females up to third parity (Po to P3), aged between 17-30 years; height ranging of 148-170 cm and weight ranging from 50-60 kg were taken into consideration. Routine investigations such as blood grouping, Rh typing, Hemoglobin percentage, Fasting Blood sugar, VDRL, Urine for routine examination were conducted and recorded separately for future references both for test and control groups. Patients suffering from complications such as hypertension, pre-eclampsia, eclampsia, diabetes, antepartum hemorrhage, heart disease and other gross maternal systemic disorders were excluded. Control Group (Group I): This group included healthy non-anemic mothers free from significant medical, surgical and obstetrical complications and 30 placentas were collected in this series following live birth only. Test Group (Group II): This group includes anemic mothers diagnosed clinically and hematologically otherwise free from significant medical, surgical and obstetrical complications and 30 placentas were collected in this series following live birth. Fresh placentas were collected from the patients selected beforehand. After delivery at labor room, placenta were collected and placed in a bowl for subsequent examination. Examinations of placenta were conducted according to proforma adopted by Benirschke [1] . Immediately on collection of placenta, a general survey of umbilical cord, membranes, fetal surface and maternal surface was carried out. Then membranes of placenta were trimmed off by a sharp scissor near the margin as described by Aherne [13] . The placentas were subsequently cleansed free and washed in water. Following parameters of the placenta were determined: (a) Dimensions: The maximum & the minimum diameters were measured by the measuring tape. Thickness of each placenta was measured at its centre & three other places by piercing the placenta by a long needle calibrated in cm. The average thickness of the placenta was measured to the nearest 0.1 cm. (b) Area: The area of placenta was estimated in sq. cm using the formula for the area of an ellipse. Therefore Placental area (cm. 2 ) = π ax Diameter (cm.)/2