CURATING A DEFAULT VIEW

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3 5 (5.1%) 1 (1.9%)

Pearson’s Chi-square = 1.942 P value = 0.585 df = 3

CHAPTER 5

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are been reported in blacks than in Caucasian studies.⁴⁷ Another study in Mannitoba, Kenya reported an incidence of 64.5% with a much higher

incidence of large FMH compared with other studies.¹ In a recent study which looked at FMH in women undergoing caesarean section, an incidence of 28.1% was also reported.⁴⁸

The incidence of large FMH of 1.4% recorded in this study was consistent with most studies which had reported an incidence of between 0.3- 2.5%, ⁴⁸ though a sharp contrast to 6.14% incidence of large FMH reported by Adeniji et al.³⁹ Wiley and D’Alton (2010) did a review of publications of FMH from January 1966 – December 2008 and concluded that there were inconsistencies in incidences of FMH reported.⁴⁹ These inconsistencies may be due to poor reproducibility reported and the fact that FMH studies are highly dependent on technical skills and possibility of false positive results when adult cells

containing HbF, which also stain cherry red are erroneously counted. These reasons may not be solely responsible for the high incidence in this study. It is also likely due to the fact that this study was also conducted among blacks as suggested earlier by Kizza A. P. et al (1990)⁴⁷ that incidences are higher in blacks.

Maternal obstetric risk factors and maternal blood group had been implicated as determinants of FMH.^{1, 2} However, individual studies in literature have

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reported inconsistencies in risk based approaches to FMH ^{2, 12} In this study, parity (p = 1.000), EGA (p = 0.193), baby birth weight (p = 0.247), maternal blood group (p = 0.193) and age of parturients (p = 0.735), did not show any significance for FMH (Tables 2 and 3). Maternal Rh factor (p = 0.081) did not also pose a significant risk factor for FMH as there was no significant FMH between the Rh positive and Rh negative groups (Table 4). The Rh negative parturient is important because of the possible iso-immunization that could occur when carrying a Rh positive fetus. The 42 years review of FMH by Wiley and D’Alton also confirmed these inconsistencies and maintains that more than 80% of cases of FMH remained unexplained.⁴⁹

Placental parameters studied in this population showed similarity with other studies.^{17, 40} The mean of placental parameters reported here (Table1) when compared with those reported in standard texts show slight differences. The mean volume and weight of 506.51mls and 516.89g respectively are slightly higher than the reported means of 497mls and 508g. The mean thickness of 21.44mm reported here is however lower than that of 23mm reported earlier.¹⁷ It should be noted that these means are from Caucasian studies and there is paucity of research work in Africans to compare with. A wide variation has been reported in literature for these individual placenta parameters17, 18, 19, 20

and when the means are considered as a range as reported in some literature,¹⁷ these results are also within the range. No study was cited in Nigeria reporting placental parameters.

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The positive correlation between USS thickness and baby birth weight (0.641), placental weight and placental volume (0.999) and placental weight with USS thickness (0.643) (Table 5) is in accordance with all other studies comparing placental parameters. 24, 25, 40, 50 In this study, there were linear relationships between all these placental parameters; placentae with reduced thickness on USS was associated with a low birth weight baby, reduced placental weight and volume at birth. Also, in those with increased placental thickness, there was increase in placental weight and placental volume. It can be inferred that one placental parameter is predictive of the other and eventual birth weight of the baby.

In this study, none of these morphological parameters of the placenta

including grade of placenta proved significant statistically for FMH (Tables 6- 9). This study aimed at assessing whether placental anatomy (weight, volume and thickness) influences the occurrence and severity of FMH in normal

pregnancies. Assuming these placental parameters in this study showed a significant difference between the two groups, the placenta could then have been suggestive of FMH. Considering that we already know that a positive correlation exists between these placental parameters, if obstetric USS was done at 36 weeks and the placental thickness was suggestive of FMH, this would lead to increased surveillance for FMH in Rh D Negative pregnant women. In such women the placental weight and volume would be measured at birth to further predict severity of FMH and identify those Rh D Negative

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pregnant women who would require Kleihauer-Betke test to determine volume of FMH and dose of anti- D immunoglobulin to be administered. The findings in this study did not show that placental parameters could be used as

determinants of FMH. This result appears as an isolated report as no other study was cited in literature comparing placental morphology with FMH.

Sivarao, S. (2002)¹⁰ and Mayhew, T. M. (2005)²³ had suggested that placental morphology and parameters can provide valuable information on pregnancy outcomes. Some studies have implicated the placenta in some case reports of FMH. Diseases of inflammation of the placenta such as preeclampsia and chorioamnionitis were reported to be associated with FMH.⁵¹ Some other studies have also reported an association between the placenta and low birth weight babies, maternal diabetes mellitus, intra uterine growth restriction and fetal hydrops. Some of these changes include placentomegaly while some have small placenta with reduced thickness.15, 24, 41, In a review by Wiley and D’Alton, (2010),⁴⁹ it was suggested that certain placental lesions such as intraplacental haemorrhage, intervillous thrombosis, placental infarcts and retroplacental haematoma were more frequently observed in pregnancies with evidence of FMH.⁴⁹ However, the morphology of these placentae were not mentioned. Another study by Al-Mufti et al, (2003),⁴² which compared FMH and its severity with number of fetuses, reported that there was increased severity with higher order pregnancies. Also, Adeniji et al, (2008),³⁹ suggested similar relationship. Al-Mufti went further to suggest that the increase in

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fetomaternal cell trafficking was possibly related to increased placental

surface area and vasculature. In another study by Wegrzyn, P. et al, (2005),⁵² which looked at placental parameters at 11-14 weeks and prediction of

chromosomal defects, the study did not prove significant except for trisomies 13 and 18 which were associated with early onset fetal growth restriction.

In all these highlighted pathological situations, the placenta is either smaller than the average or there is placentomegaly, but, in none of them was the placenta morphology directly examined as a contributor to FMH.

The placental grade in this study did not also influence occurrence of FMH (Table 9). FMH occurred in the different grades of placenta and there was no consistency. No study was cited relating placental grade with occurrence of FMH. Earlier studies had only implicated the grade of placenta in the

prediction of fetal pulmonary maturity.¹⁵

As stated earlier, in this study there was no statistical significance between placental parameters and FMH. This may probably be due to the fact that pathological conditions were not present in the study group. One may then ponder to ask whether it is the pathological conditions of the placenta without the influence of morphology that contributes to FMH.

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