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Spectrum of Pathology of The Placenta
Grace F D’costa*, Renu Khode**, Yoganand V Patil*** |
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Abstract
This is a one year and four month prospective study of 75 consecutive placentae. A high percentage (90.6%) showed evidence of pathology, the majority of which (92%) were associated with maternal, foetal or placental risk factors, either singly or in combination. The majority were maternal risk factors, the highest being pregnancy induced hypertension (PIH) – 33.3%. Grossly infarcts and retroplacental haematomas and histological features of accelerated maturation were lesions commonly seen in these cases. In case where the foetal outcome was poor i.e. abortions, intra uterine foetal death (IUFD) and still births, 100% of the placenta, showed evidence of pathology. In preterm deliveries (90%) were abnormal and in term deliveries (68.4%) were abnormal. The commonest gross lesions seen with poor fetal outcome were infarcts and retroplacental haematomas and microscopically, chorioamnionitis (CAM). Chorioamnionitis was given special attention as it is a common risk factor in India. 80% of our cases of acute chorioamnionitis were associated with either stillbirths (57.14%) or abortions (22.85%) and most of our cases (97.14%) were in stage II, III and IV. The prognosis worsens if acute CAM is associated with villous oedema. Particularly in preterm gestation (45%) of our cases with villous oedema were associated with acute CAM and all of them were seen in preterm gestation, all of whom had poor foetal outcome, either still birth (77.77%) or abortion (22.22%), indicating that the deadly combination of villous oedema with acute CAM wrecks havoc on the unborn child. |
Introduction
Over the past fifteen years, interest in the
pathology of placenta has been steadily increasing. Several factors have contributed to this increasing interest. Delayed child bearing and infertility are common in this day and age. When pregnancies fail or there is unexpected outcome, those involved want explanation and assessment of future risks. There is now recognition that placental examination will often yield valuable information for the parents.1 Unfortunately, there is also no question that the current problems in obstetric litigation have stimulated interest in this area. As the placenta may have clues to events occurring throughout gestation, it can potentially help answer questions concerning pregnancy management and foetal outcome.2 The examination of the placenta in cases of poor pregnancy outcome and certain maternal disorders provides proper documentation and information useful to the obstetrician and neonatalogist.3 However there are limitations in clinico- pathologic correlations and there are very few placental processes with invariable consequences and it is frequently not possible to say absolutely that a lesion led to a specific problem however long standing events can frequently be differentiated from recent ones, we are still ignorant of the exact time course of most pathologic processes.4 Still examination of the placenta, in association with pregnancy related and general maternal diseases, is not exercise in futility; hence we attempted such a study and correlated the pathology with the foetal outcome. We also analyzed in detail the areas of chorioamnionitis and villous oedema staged them and correlated them with the pregnancy outcome.
Material and Methods
This is a prospective one year three month study of seventy five consecutive placentae. A special proforma was prepared recording the relevant clinical details of the mother, along with foetal gestation age and foetal outcome. Maternal, foetal and placental risk factors were analyzed and the various gross and microscopic lesions encountered with these risk factors were studied. An attempt was made to correlate placental pathology with foetal outcome and the pathology encountered, when the foetal outcome was poor was analyzed and compared with the control group. Particularly attention paid to chorioamnionitis (CAM) which was staged and correlated with pregnancy outcome. The relationship of villous oedema and various disorders, particularly acute CAM was also studied and was correlated with the foetal outcome.
The placentae were weighed and dimensions noted. The foetal, maternal and cut surface, cord and membranes examined and appropriate sections taken. Hematoxylin and eosin (H and E) stain was used in routine cases. Periodic Acid Schiff (PAS) stain was necessary to access thickening of the basement membrane and Masson’s trichome to access stromal fibrosis.
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| Fig. 1: Photograph showing infarction involving 80% of the maternal surface. |
Fig. 2 : Photograph of cut section of the placenta showing old infarction. |
Fig. 3 : Photomicrograph of an old infarct showing ghost villi. |
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| ig. 4 : Photomicrograph showing features of cytotrophoblastic hyperplasia seen in a case of PIH as an indicator of placental ischaemia (H and E, x100). |
Fig. 5 : Photomicrograph showing features of acute chorioamnionitis (Grade 4) (H and E,x40). |
Fig. 6 : Photomicrograph showing features of villous oedema, characterized by villous swelling and microcytic change seen in a case of diabetes mellitus (H and E,x40). |
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Results
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Maternal, foetal and placental risk factors were studied. The majority of cases (92%) were associated with some risk factor, either singly or in combination and a very low number (8%) of cases had no associated risk factor. The majority of cases (66.5%) had a combination of risk factors, the majority (39%), being a combination of all three risk factors. This was followed by the category of only maternal risk factors 16%, the majority of which (58.3%) were pregnancy related, consisting of mainly pregnancy induced hypertension (PIH), abruptio placentae and abortion; this was followed by a combination of pregnancy related and general risk factors (25%) and there were only 16.6% cases of general risk factors. Next came the group of only placental risk factors (5.3%) where acute chorioamnionitis headed the list (100%). Lastly came the category of only foetal risk factors (4%).
Of the pregnancy related risk factors encountered, either singly or in combination, the commonest encountered was PIH (33 3%), followed by abortion (21.6%) and prematurity (18.3%). The commonest gross and microscopic lesions encountered (Table 1) with PIH were infarcts (50%) (Figs. 1, 2 and 3) and features of accelerated maturation like increased syncytial knots (90%), cytotrophoblastic hyperplasia (85%) (Fig.4), microscopic infarcts and stromal fibrosis 60% each. In placentae, where the foetal outcome was abortion, most of the cases did not show significant gross pathology-77%. Subchorial thrombosis (Brues’ mole) was seen in only 15.3% cases. However microscopically secondary changes were noted in 53.8%cases. In the cases where the foetal outcome was prematurity, grossly retroplacental haematomas in 36.36% and infarcts-27.27% cases were seen as the commonest macroscopic lesions and delayed maturation in 36.36% as the commonest microscopic lesion.
General maternal risk factors were not often encountered either singly or in combination with other risk factors. Heart disease headed the list 27.27% followed by disseminated intravascular coagulation (DIC) (18.18%). Most of the lesions however, did not show any significant gross pathology except for the placenta of diabetes and sepsis. The former was a large placenta and showed villous oedema and chorangiosis. Microscopically the latter showed evidence of acute intervillositis.
An analysis between the presence of placental pathology and foetal outcome, recorded that when the foetal outcome was poor i.e. abortion, intrauterine foetal death (IUFD) with maceration and fresh still births (FSB), 100% of the placentae were abnormal. In preterm deliveries 90% were abnormal even in term deliveries 68.4% placentae showed some sort of abnormality and 31 6% were normal. An analysis of the gross and microscopic lesions encountered when the foetal outcome was poor (Table 2) revealed that in most of the categories, grossly the commonest lesions seen were infarcts 35.18% (Figs.1, 2 and 3) and retro-placental haematomas 16.66%, microscopically however chorioamnionitis (Fig.5) headed the list 38.88%, after the secondary changes associated with IUFD were excluded. In the control group of term infarcts, more than 50% of the cases, showed no changes either on gross or microscopy. A small percentage showed evidence of infarcts in 16.6% and retroplacental haematomas in 13.3% grossly and chorioamnionitis (23.3%) microscopically.
Particular attention was paid to chorioamnionitis as infection is a common risk factor in India and it featured prominently when the foetal outcome was poor, but also was present in the control group An attempt was made to stage chorioamnionitis, into 4 stages – I, II, III and IV more than 50% of the cases 54.78% were stage II and half of this number 25.71% into the stage IV. Stage I was rarely encountered 2.8% indicating that our patients probably neglect to seek medical intervention at an earlier stage.
A correlation between the presence of acute chorioamnionitis and pregnancy outcome was drawn (Table 3). In the pregnancies where chorioamnionitis was present, the foetal outcome was poor (80%) i e the end result was death of the foetus, either still birth (57.14%) or abortion (22.85%) and only 20%, survived of which the majority were term babies 14.2%. By contrast in the 34 cases where acute chorioamnionitis was absent (52.9%) survived of which 41.17% were term babies; and 47.05 % succumbed, of which 35.29% were stillbirths and 11.76% were abortions. The relatively high percentage of this group is due to the fact that there were other causes of mortality besides acute chorioamnionitis which contributed.
An association between the occurrence of placental villous oedema (Fig.6) and various disorders encountered (Table 4) reveal a high association with acute chorioamnionitis 45%, again it was more commonly seen in preterm gestations, particularly < 27 weeks (55.5%). The other disorders encountered with villous oedema were abruptio placentae (12.5%), macerated still birth (MSB) (15%) and diabetes, hydrops foetalis, most cases occurred in preterm gestation. In the acute chorioamnionitis cases all succumbed, where in the acute CAM negative cases four survived and seven succumbed.
Discussion
A thorough examination of the placenta contributes significantly towards determining the cause of poor foetal outcome as it is a mirror of not only pure placental pathology, but also of various maternal and foetal risk factors.
Our study was a one year, four months prospective study which included seventy-five consecutive placentae. Of these 90.6% showed evidence of some pathological lesion, emphasizing the need for placental examination The majority 93.3% were associated with some risk factors, either singly or in combination. Our figure of 93.3% is higher than the percentage of Avasthi et al5 from Ludhiana, Punjab whose study included 80% cases with some associated risk factor. We further categorized this group into those having only maternal, only foetal and only placental risk factors. However it was seen that the largest group comprised of more than one risk factor (66.6%), majority being cases with a combination of maternal, foetal and placental risk factors (32%).
This group was followed by the category of only maternal risk factors (16%), the majority of these were pregnancy related (58 3%), mainly PIH, abortion, prematurity and abruptio placentae, this was followed by the group of a combination of pregnancy related and general risk factors (25%) and there were just (16.6%) with general maternal risk factors. Next came the group of only placental risk factors (5.3%), where acute chorioamnionitis headed the list and lastly came the category of only fetal risk factors (4%). In the study of Avasthi et al5 56% showed maternal risk factors. This figure is much higher than ours of 16% and this is explained by the fact that many of our cases with maternal risk factors are grouped in the category of more than one risk factor when this category is further sub-divided. These authors found that the percentage of pregnancy related risk factors was higher than the general risk factors (71.4% and 28.6%) respectively. These findings are similar to ours except that our corresponding figures are lower (58.3% and 16.6%). Our percentage of only fetal risk factors is much lower than that of these authors 4% v/s 24% again for the same reason cited above.
In the category of pregnancy related risk factors PIH headed the list (33.3%) it formed 26.6% of the total risk factors this figure is lower than that of Avasthi et al5 32% who also encountered PIH most frequently. The other risk factor they found in this group was post maturity (8%) whereas we found post maturity in a very small percentage (1.6%) forming 13% of the total risk factors. Abortions, prematurity, abruptio placentae and oligo/polyhydramnios accounted for the remaining risk factors in this group
In the cases of PIH (Table 1) the commonest gross lesions encountered was infarction 50% (Figs.1, 2 and 3).Our findings are consistent with those of other authors Salafia et al6 also found a high percentage of infarction 68.4% in their cases of preterm eclampsia and Das et al7 encountered infarction in 51.4% of their cases with preeclampsia and eclampsia. Retroplacental haematoma was the next common gross lesion encountered by us 20%. This percentage is higher than that Salafia et al6 (12%) and Das et al7 - (8.75%). The commonest microscopic features encountered in PIH were features of accelerated maturation. Increased syncytial knots were seen in 90% cases, this figure is considerably higher than 32% reported by Avasthi et al5 and 40% reported by Salafia et al.6 Cytotrophoblastic hyperplasia (Fig.4) was observed in 85% cases; again this figure is considerably higher than 42% of Salafia et al6 and 10-8% of Avasthi et al.5 However it is lower than the figure of Fox,8 who found it in 96.3% of toxaemic patients. The next common histopathological feature noted was stromal fibrosis (60%) cases, this figure is intermediate between the high percentage of Salafia et al6 (-82%) and a much lower (16%) of Avasthi et al.5 Thickening of the trophoblastic basement membrane was seen in 30% higher than the 19.2% figure of Avasthi et al.5 Villous hypovascularity was also seen in 30% cases, much lower than the 72% figure of Salafia et al.6 Obliterative endarteritis of the foetal stem vessels was seen in 25% cases, which is comparable to the 25% of VV Joshi3 Histologic confirmation of the 10 cases of infarction as seen in all the 70 cases noted grossly and there were two more cases of microscopic infarction detected on histology. So the total number of cases was 60%. This is almost comparable to the findings of Salafia et al6 (-68.4%). Retroplacental haematoma was confirmed microscopically in all the four cases detected grossly, the percentage being 20%, which is less than half of the number of cases detected by Salafia et al6 (-49%) in association with abruptio placentae. A feature that was conspicuous by its absence was acute atherosis, this was probably due the fact that the vessels of the decidua basalis attached to the maternal surface were not included in the tissue sent to us; this is also the reason why it is a feature inconsistently reported in the literature
As far as the other maternal pregnancy related risk factors are concerned we found 21.6% of abortion, the majority of these cases showed no lesions on gross examination and only 15.3% recorded subchorial thrombosis (Brues’ mole) a feature which has been described in association with abortion and may play a role in the cause- Shanklin and Scott.9 Microscopically changes secondary to foetal death like foetal vascular obliteration and stromal fibrosis were seen 53.1% in cases through 30.76% showed normal villi as described by Fox.10 In the cases of prematurity, RPH and infarction were commonly seen- (36.36% and 27.27%) respectively. Microscopically delayed maturation of the villi, was most frequently observed 36.36%. The next risk factor was abruptio placentae (15%) the majority of these cases (77.7%) showed evidence of RPH as expected, which was confirmed on microscopy in all cases. The least commonly encountered risk factor was post maturity (1-6%). This figure is lower than the 8% of Avasthi et al.5 We did not find any lesion on gross examination but found increased syncytial knots and chorangiosis on microscopy- 100% as described by V.V.Joshi.3
General maternal risk factors were often not encountered, either singly or in combination with other risk factors. Heart disease headed the list (27.27%), followed by DIC (18.18%), other risk factors like diabetes, syphilis, TB, sepsis, toxoplasmosis and malaria were encountered rarely -9% each. The study of Avasthi et al3 found anaemia in 16% of the cases; we did not have any case of severe anaemia as most of the cases were under antenatal supervision. Most of the cases did not show any gross or microscopic features as detected by other authors VV Joshi,3 except for the placenta of the diabetic patient which was large and showed villous oedema and chorangiosis on histology, as described by VV Joshi.3 The single case of sepsis showed evidence of intervillositis on histology, though grossly it was unremarkable.
We divided the 75 cases into various groups depending upon foetal outcome abortions (17.3%), IUFD with maceration (30.6%), FSB (12%), preterm delivery (13.3%), term delivery (25.3%) post maturity (1.3%) and analyzed the relationship between the presence of placental pathology and foetal outcome. There were 90.6% abnormal placentae and only 9.3% were normal. The abnormal placentae correlated well with poor foetal outcome. In cases where the foetal outcome was poor, 100% of the placentae were abnormal. In preterm deliveries 90% were abnormal, and even in term deliveries 68.4% showed some sort of abnormality.
The gross and microscopic pathology of the placenta with poor foetal outcome, was further analyzed and compared with a cohort group (Table 2). In the former IUFD with maceration formed the largest group (30.6%) followed by abortion (17.3%), FSB’s (12%) and IUGR (9.3%) Hydrops foetalis and twin pregnancy was encountered in 1.3% each. In cases of IUFD with maceration, the commonest gross lesion was infarction and retroplacental haematoma 52% and 17.3% cases which was confirmed on histology, microscopically however the commonest lesions were changes secondary to IUFD like villous hypovascularity and showed fibrosis 78.2% each, foetal stem vessel sclerosis (60.9%), Cytotrophoblastic hyperplasia and basement membrane thickening (60.9%) villous oedema (47.8%) and increased syncytial knots (34%). The study of Avasthi et al,5 found a lower percentage of villous fibrosis (40%), cytotrophoblastic hyperplasia 30% and microscopic infarction (15%), however they found a higher percentage of increased syncytial knotting (50%) but the study of fox,10 cytotrophoblastic hyperplasia was seen in almost 100% cases. Following the group of secondary changes was seen chorioamnionitis (56%) (Fig.5) on microscopy. Avasthi et al5 found much lower percentage of 10%, which is comparable with the low figures of Hovatta et al11 and Rayburn et al12 – 4.9% and 7.8% respectively. In cases of fresh still births, the commonest gross and microscopic lesions encountered were infarcts and retroplacental haematoma 55.5% each. When both MSBs and FSBs are combined, the incidence of infarctions and RPH (gross and microscopy) are 50.3% and 28.1%, higher than the percentage of Hovatta et al11 which are 14.8% and 14.4% respectively. The incidence of maternal floor infarction in our study was 13.3%. 60% of cases were associated with IUFD, higher than the 40% of Andres et al13 and 17% of Naeye.14
We had 9.3% of IUGR which is comparable with the 8% of Avasthi et al5 and 7.6% of Salafia et al.6 we did find evidence of maternal floor infarction which is described in cases of IUGR and found in study of Andres et al.14 Microscopically, cytotrophoblastic hyperplasia with basement membrane thickening was found most frequently in 85.7% cases and villous hypovascularity with showed fibrosis in 42.8% cases which is comparable with the percentage of Avasthi et al5 70% and 50% respectively. The study of Salafia et al,8 also found the latter lesions in 50% cases. In the control group of 30 cases, through more than 50% of the cases showed no changes either on gross or microscopy, a small percentage showed evidence of infarcts 16.6% retroplacental haematoma 13.3%, grossly and chorioamnionitis microscopically 23.3% Avasthi et al,5 also found evidence of 8% infarction in their normal control group, however they did not find any evidence of retroplacental haematoma or chorioamnionitis in this group.
Particular attention was paid to chorioamnionitis, as infection is a common risk factor in India and it featured prominently when the foetal outcome was poor, but surprisingly was also present in the control group of normal foetal outcome. An attempt was made to stage CAM in four stages I, II, III, IV as described by salafia et al.15 more than 50% of the cases i.e. 54.28% fell into the stage IV category. Stage I was rarely encountered 2.8% indicating that our patients probably neglect to seek medical intervention at an earlier stage.
A correlation between the presence of acute CAM and pregnancy outcome was drawn (Table 3). In the pregnancies where acute CAM was present, the foetal outcome was poor (80%) i.e. the end result was death of the foetus, either stillbirths 57.14% or abortion 22.85% and only 20% survived, the majority of which were term babies 14.2% by contrast in the 34 cases where acute CA was absent 52.9% survived, of which 41.7% were term babies and 47.05% succumbed, of which 35.29% where stillbirths and 11.76% were abortion. The relatively higher percentage of this group is due to the fact that there were other causes of mortality besides acute CAM which contributed. Thus acute CAM was a major risk factor in adverse foetal outcome. Our figures compare well with those of Quinn et al,16 who also found a higher percentage 90% of poor foetal outcome, either stillbirths or neonatal deaths in acute CAM positive cases and a much lower percentage – 42.4% when acute CAM was negative, the finding of Koh et al17 indicate a much lower percentage (10.8%) of cases with poor foetal outcome in cases of CAM and preterm delivering has been reported in the literature, suggesting that occult antepartum infection of the genital tract may be an important cause of preterm delivery. We found a higher percentage (14.2%) of term babies compared to preterm babies (5.7%) when ACA was present. These findings are at variance with those of Guzick et al,18 who found CAM in higher percentage in preterm babies (32.8%) than in term babies (10%).
The association of CAM with poor fetal outcome is known, however there are studies Naeye19 and Schwarz,20 which indicate that the prognosis worsens if CAM is associated with villous oedema (Fig.6), particularly in preterm babies who are more prone to villous oedema. Villous oedema produces a reduction of the intervillous space and a decreased number of chorionic villi per unit area hence might affect maternal intervillous blood flow and foetal oxygen supply and therefore would be a cause of higher foetal mortality. We therefore analyzed our 20 cases of placental villous oedema (Table 4) to see if there was any significant association with CAM 45% of these cases were associated with CAM, all of these were seen in preterm gestation , thus we found a significant association with CAM. Shen Schwarz et al20 and Naeye et al19 also found that villous oedema associated with CAM was more frequent in preterm babies and that it strongly correlated with antenatal hypoxia and poor foetal outcome. The most of the cases 55% were associated with abruptio placentae, MSB, diabetes, hydrops foetalis, most occurred in preterm gestation. These findings are in concordance with the findings of Naeye et al,19 who found more lesions like maternal hypertension, PROM, placental growth retardation, placenta praevia, maternal sepsis, in addition to those described above. Shen Schwarts20 however found more preterm gestation in the cases of diabetes. Thus we endorse the association of villous oedema with chorioamnionitis, particularly in preterm gestations. A further analysis of the cases of villous oedema in association with ACA shows that all 9 succumbed , these were 6 MSBs , 1 FSB and 2 preterm and 2 term babies and 7 succumbed i.e. 5 MSBs and 2FSBs. Thus the lethal combination of villous oedema and acute CA can be a potentially powerful enemy to the unborn child, and it is probably chorioamnionitis, which is the evil partner of villous oedema, which wrecks more havoc. Our findings thus endorse those of Naeye et al19 and shen Schwartz et al.20
Conclusions
In the one year, four months prospective study of the 75 consecutive placentae we encountered a high percentage 90.6% of abnormal placentae. The majority of cases 92% were associated with some risk factor; maternal, foetal or placental, either singly or in combination. The latter was more frequent 66.6%. The highest maternal risk factor was PIH- 33.3% and fetal risk factor was IUFD with maceration 30.6%, present either singly or in combination with other risk factors. The cases of pregnancy related maternal risk factors showed more placental pathology than the cases with general maternal risk factors. The commonest gross lesions detected were infarcts and retroplacental haematomas and the commonest microscopic lesions detected were increased villous syncytial knotting, cytotrophoblastic hyperplasia, villous stromal fibrosis and hypovascularity, particularly associated with PIH indicating accelerated maturation. In abortions secondary changes predominated. In cases where the foetal outcome was poor 100% of the placentae were abnormal. In preterm deliveries 90% were abnormal and in term deliveries 68.4% were abnormal. The commonest placental pathology associated with poor foetal outcome were infarcts and retroplacental hematomas on gross examination and secondary changes associated with intrauterine foetal death, followed by CAM on microscopy. CAM was given special attention, as infection is a common risk factor in India, it is known to be associated with either still births 57.14% or abortions 22.85% and most of our cases were in stage II, III,IV. (97.14%) indicating that our patients probably neglect to seek medical intervention at an early stage. The prognosis worsens if acute CAM is associated with villous oedema and all of them were seen in preterm gestations. All these cases had a poor fetal outcome i.e. they were either stillbirths 77.77% or abortions 22.22% compared to the acute CAM negative cases, indicating that the deadly combination of villous edema with acute cam wrecks have on the unborn child.
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