morphological findings and value of placental examination at fetal and perinatal autopsy

APMIS 107: 3 3 7 4 5 , 1999 Printed in Denmark . All rights reserved

Copyright 8 A P M I S 1999

ISSN 0903-4641

Morphological findings and value of placental examination at fetal and perinatal autow

LISE GRUPE LARSEN'y2 and NIELS GRA2M2*3

'Department of Pathology, Central Hospital, Naestved, 'Department of Pathology, Rigshospitalet, Copenhagen and 2Pathological-Anatomical Institute, Herlev Hospital, Denmark

Larsen, L. G. & Grrem, N. Morphological findings and value of placental examination at fetal and perinatal autopsy. APMIS 1999; 107:3374.

The purpose of this study was to report on the morphological findings in placentae from abortions, stillbirths and perinatal deaths, and to assess the value of the results of the placental examinations. The material included 341 placentae and their matched autopsies. Fifty placentae came from abortions induced for medical reasons, 194 from spontaneous abortions, 84 from stillbirths, and 13 from livebirths. Histological slides from all placentae were reviewed and the placental diagnoses were related to the autopsy diagnoses. Frequently observed placental lesions were inflammation of the membranes and/or umbilical cord, placental edema, vascular lesions, single umbilical artery, and degenerative lesions. The placental examination in pregnancies terminating with fetal or perinatal death was of value in half the cases. Some placental lesions provide us with clues when assessing the cause of fetal death, but such lesions are rare. Two important groups of lesions, acute inflammation of the membranes and/or umbilical cord and lesions consistent with uteroplacental vascular insufficiency, seen mainly as infarction and decidual arteriopathy, were observed. Gross examination is informative, though microscopic examination is often necessary.

Key words: Placenta; morphology; abortion; stillbirth; perinatal death.

Lise Grupe Larsen, Department of Pathology, Central Hospital, DK-4700 Nrestved, Denmark.

The events of a pathological pregnancy leading to fetal death, stillbirth or perinatal death are not always obvious from the clinical history and an autopsy of the fetus or the infant, including an examination of the placenta, might be an important diagnostic tool ( 1 , 15, 16). The placenta does not die with the fetus. The placenta un- dergoes morphological changes, and these changes have to be taken into account at the examination (5 ) . However, the placenta will not be macerated at intrauterine death to the same degree as the fetus, and microscopically the placenta might look viable even some time after the death of the fetus. Examination of the placental

Received June 22, 1998. Accepted September 22, 1998.

tissue might provide important information about the pathological pregnancy (22).

The present study reports on placental morphology at abortion, stillbirth and perinatal death, and compares the findings of the placental examination with the results of the autopsies, in order to evaluate the extent to which placental examination provides valuable information about the cause of death and other autopsy results.

MATERIALS AND METHODS

Patients The material consisted of 341 placentae belonging

to a consecutive series of 425 fetal and perinatal autopsies performed at the Pathological-Anatomical In-

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stitute, Copenhagen County Hospital in Herlev, during the 5-year period 1989-1993. During this period the institute performed fetal and perinatal autopsies for the hospitals in Copenhagen County, covering a population of roughly 600,000.

Of the 341 placentae included in the study, 50 came from abortions induced for medical reasons (gestational age 13-27 weeks), 194 from spontaneous abortions (gestational age 9-27 weeks), 84 from stillbirths (gestational age 28-43 weeks), and 13 from live births (gestational age 19-39 weeks; 12 died 0-7 days and 1 died 8-28 days after delivery).

In 84 of the 425 consecutive autopsy cases, no placenta or only fragments had been sent for examination. These 84 cases included 12 abortions induced for medical reasons, 36 spontaneous abortions, 11 stillbirths, and 25 live births. From these figures it is clear that the 13 livebirths examined in the material represent only a fraction of autopsied neonates in the population; it is difficult and often impossible to obtain placenta from children who die some time after delivery.

The study was approved by the Local Ethics Com- mittee and the Danish Data Protection Agency.

Autopsies The fetuses, infants and placentae were submitted

for routine examination, which was performed by one of the two authors, or under their close supervision. The purposes of the autopsies were: 1) to confirm and improve the previous clinical diagnosis, 2) to demon- strate possible complications of diagnostic and thera- peutic procedures, 3) to form a basis for counselling the parents, and 4) to form a basis for perinatal audit. The autopsies were performed according to a protocol which remained unchanged during the 5-year period. In brief, an autopsy included reading the clinical report, external examination, radiography, internal examination and full organ microscopy. Tissue or cells were taken for chromosomal or biochemical studies before or at the autopsy in selected cases. An autopsy report was issued.

Depending on the autopsy findings the 341 autopsies were divided into 9 groups each with common features: 149 autopsies with no specific pathology, 74 with chromosomal abnormalities and/or malformations, 2 with metabolic disease, 4 with hydrops- fetalis, 6 with oligohydramnios, 32 with intrauterine pneumonia, 18 with growth retardation, 16 with se- quelae of asphyxia, and 40 with multiple gestation (twins or triplets).

The degree of maceration was assessed as none, mild, moderate or severe according to Wigglesworth & Singer (27).

Placentae The placentae were fixed in 10% buffered formalin

shortly after delivery. They were weighed after the umbilical cord and the free membranes had been re-

moved. Abnormalities were recorded as well as num- bers and estimated volume of macroscopically visible focal lesions. Sampling for microscopic examination routinely included two to three full-thickness blocks of placental parenchyma, one block of extraplacental membranes, one block with a section of the umbilical cord and blocks from macroscopically visible focal lesions. The tissue was embedded in paraffin and 5 pm sections were cut and stained with haematoxylin- eosin. A separate report not including autopsy data was issued.

Review After the 5-year period, reports on the placental

examinations and matching histological slides were reviewed by one of the authors (LGL). Placental lesions were recorded according to a predetermined list, applying the definitions of Macpherson (1 6) and Kaplan et al. (1 1). The observed lesions were divided into groups and listed in a system modified from Ku- plan et al. (1 1) and Langston et al. (1 5) .

Inflammation of the membranes and the placental parenchyma as well as edema of the villi was graded as mild, moderate or severe. The degree of inflammation of the membranes was assessed according to reference slides as mild (few and small foci), moderate (more diffuse and intense), or severe (widespread intense infiltrate with or without necrosis). The amount of infarction and fibrin deposition was noted as the percentage of the lesions in the total placenta. Decidual arteriopathy was defined as arteries in decidual regions without physiological changes or with atherosis. The other lesions were listed as present or absent. Abruption is not mentioned in this study as the clinical information on the deliveries was insuf- ficient. Information on some macroscopic observations is missing in this retrospective study, e.g. the length of the umbilical cord, and some microscopic observations were too difficult to report objectively, e.g. trophoblast hyperplasia. Other lesions with a rare occurrence, such as maternal floor infarction, were not represented in this material.

Table 1 shows the total observed lesions and in Table 2 the lesions are related to the mode of abortion or delivery. The most frequently observed placental lesions are related to the autopsy groups in Table 3 and to the degree of maceration in Table 4.

Assessment of value of placental examination The value of the placental examination (Table 5 )

for fulfillment of the purposes of the autopsy was assessed by matching the autopsy report and the placental findings using the following terms: 1) Conclus- ive: the placental examination contributed conclus- ively to the combined autopsy and placental examination, e.g. findings of multiple chorioangiomas and a growth retarded fetus. 2) Important: with the results of the placental examination the assessment of the course of the pathological pregnancy was more

338

VALUE OF PLACENTAL EXAMINATION

reliable, e.g. demonstration of moderate or severe acute chorioamnionitis. 3) Supplementary: the results of the placental examination supported the results of the autopsy, but no new information for the assessment of the course of the pathological pregnancy was found, e.g a single umbilical artery and a fetus with malformations. 4) Doubtful: lesions described in the literature as occurring in pathological pregnancies and in normal pregnancies as well, e.g. true knot of the umbilical cord, but with no tissue reaction. 5) Noncontributary: postmortem degenerative changes or minor lesions, and noncontributary for the results of the combined autopsy and placental examination, e.g. postmortem changes such as fibrous sclerosis of

the stem villi and villous fibrosis matching a macerated fetus.

In the evaluation of inflammation of the membranes and of villous edema only moderate or severe lesions were considered significant.

RESULTS

Observation of placental lesions Of the cases, 30i were from single pregnan-

cies and 40 were from twin or triplet pregnan-

TABLE 1. Placental lesions listed at the review Part of placenta Placental lesions

Observed at the review Placentae Placentae Placentae Grading examined with with

lesions lesions Number Number % (%I

Placenta as a whole

Umbilical cord

Membranes

Maternal uteroplacental vasculature

Fetoplacental vasculature

Villous abnormalities

Abnormal shape Multiple gestation Partial mole Acute funisitis Velamentous insertion True knot Compression Thrombosis Single umbilical artery Acute chorioamnionitis

Amniotic band sequence Amnion nodosum Infarction, >4% Decidual arteriopathy, Retroplacental hemorrhage Intervillous fibrin

deposition, > 19% Intervillous thrombus Villous edema

Diffuse avascular villi Fibromuscular sclerosis in

Chorioangioma Twin transfusion syndrome Villous immaturity Acute villitis Chronic villitis

stem villi

305 34 1 34 1 317 297 318 318 318 31 1 332

334 334 339 296 296

339 340 339

34 1 340

34 1 34 1 340 340 340

7 40 2

53 8 2 1 1

21 154

2 5

23 27

8

13 18

191

70 55

4 2

12 5

62

2.3 11.7 0.6

16.7 2.7 0.6 0.3 0.3 6.8

46.4

0.6 1.5 6.8 9.1 2.7

3.8 5.3

56.3

20.5 16.2

1.2 0.6 3.5 1.5

18.2

Mild (43.5) Moderate (32.5) Severe (24.0)

Mild (63.9) Moderate (33.5) Severe (2.6)

Mild (83.9) Moderate (16.1)

Diffuse villous fibrosis 34 1 125 36.7

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LARSEN er al.

cies. At the review, some placental lesions were observed more frequently, i.e. in more than 5% of the reviewed placentae (Table I). These included inflammation or related lesions (acute chorioamnionitis, acute funisitis and villous edema), vascular lesions (placental infarction, decidual arteropathy, chronic villitis and intervillous thrombus), single umbilical artery and degenerative lesions (diffuse avascular villi, stem

villous fibromuscular sclerosis and villous fibrosis). The rest of the lesions were observed only occasionally.

In Table 2 the placental lesions are related to groups of abortions or deliveries. A single umbilical artery was related to abortions induced for medical reasons. Acute inflammation of the membranes and/or umbilical cord as well as villous edema was related to spontaneous abor-

TABLE 2. Placental lesions observed in the material (number) & related to abortion/delivery (%) Placental lesion Placentae Abortion or delivery

with lesions Abortions Spontaneous Stillbirths Live- at the review induced for abortions births

medical reasons (n=50) (n= 194) (n=84) (n=13) YO % YO % Number

Placenta as a whole Abnormal shape Multiple gestation Partial mole

Umbilical cord Acute funisitis Velamentous insertion True knot Compression Trombosis Single umbilical artery

Acute choriooamnionitis Membranes

mild moderatehevere

Amniotic band sequence Amnion nodosum

Infarction >4% Decidual arteriopathy Retroplacental haemorrhage Intervillous fibrin position > 19% Intervillous thrombus

Fetoplacental vasculature Villous edema

Maternal uteroplacental vasculature

mild moderatekevere

Diffuse avascular villi Fibromusculare Sclerosis in stem villi Chorioangioma Twin transfusion

Villous abnormalities Villous immaturity Acute villitis Chronic villitis Diffuse villous fibrosis

7 40 2

0 0 0

71.4 62.5

100

28.6 32.5 0

0 5.0 0

53 8 2 1 1

21

11.3 0 0 0 0

52.4

71.7 25.0 50.0 0 0

23.8

13.2 75.0 50.0

100 100 23.8

3.8 0 0 0 0 0

67 87 2 5

19.4 3.4 0

40.0

49.3 79.3

100 0

28.3 13.9 0

20.0

3.0 3.4 0

40.0

23 27 8

13 18

8.7 11.1 0 7.7 5.6

34.8 70.4 37.5 38.5 50.0

56.5 18.5 62.5 53.8 44.4

122 69 70

18.9 18.8 7.1

68.0 69.6 65.7

11.5 8.7

1.6 2.9 0 27.2

55 4 2

1.8 0 0

45.5 25.0 0

50.9 75.0 50.0

1.8 0

50.0

25.0 20.0 19.4 10.4 -

12 5

62 125

41.7 40.0 71.0 62.4

25.0 40.0

9.6 25.6

8.3 0 0 1.6

340


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tions. Lesions indicating vascular insufficiency, such as placental infarction, decidual arteriopathy, intervillous fibrin deposition and chronic villitis, were observed in spontaneous abortions and stillbirths. Degenerative lesions, such as diffuse avascular villi, stem villous fibromuscular sclerosis and villous fibrosis, were often observed in spontaneous abortions.

Frequently observed placental lesions were related to the autopsy groups, but specific lesions were only found in a few groups (Table 3). In the group of autopsies with no specific pathology, inflammatory and degenerative lesions of the placenta were observed. When intrauterine pneumonia was observed at autopsy, inflammation was often seen in the membranes or in the umbilical cord. In the group of fetuses with intrauterine growth retardation, half of the placentae showed lesions of vascular insufficiency. For the rest of the autopsy groups, no specific placental lesions were found or there were too few cases for further conclusions to be drawn.

The frequently observed placental lesions were related to the degree of maceration at autopsy (Table 4). If inflammation was observed in the placenta, the fetus was most often pre- served with no maceration. When degenerative placental lesions were observed, more fetuses were macerated.

Value of placental examination The value of the placental examination for

the overall assessment of the case is shown in Table 5. The placental examination was assessed as conclusive in 1.7% of the placentae. This group revealed two partial moles, one matching a triploid fetus and the other matching a fetus with normal karyotype and pneumonia; in one placenta 20% of the parenchyma was replaced by multiple chorioangiomas and the stillborn infant was growth retarded; in a case of amniotic band sequence, a foot of the macerated fetus was observed in the placental membranes; and in a twin pregnancy, the appearance of the two placental parts matched with transfusion syndrome showing one placental part congested and the other part pale with empty villous capil- laries.

The placental diagnosis was important for the purposes of the autopsy in 120 cases (35.2%). Of these, moderate or severe inflam-

341

LARSEN et al.

TABLE 4. The most frequent placental diagnoses related to the degree of maceration of the fetus or infant Placental lesions All Degree of maceration

None Mild Moderate Severe ?

N N (%) N (%) N (%) N (%) N Acute chorioamnionitis moderatehevere 87 68 (78.2) 6 (6.9) 7 (8.0) 6 (6.9) 0 Acute funisitis 53 36 (67.9) 2 (3.8) 9 (17.0) 6 (11.3) 0 Villous edema moderatehevere 69 49 (71.0) 2 (2.9) 14 (20.3) 4 (5.8) 0 Diffuse avascular villi 70 7 (10.0) 2 (2.9) 29 (41.4) 31 (44.3) 1 Fibromuscular sclerosis 55 13 (23.6) 6 (10.9) 19 (34.5) 17 (30.9) 0 Diffuse villous fibrosis 125 35 (28.0) 10 (8.0) 40 (32.0) 39 (31.2) 1 Maceration was graded according to Wigglesworth & Singer (27). N: Number. ?: Grade of maceration unknown.

mation of membranes, funisitis or acute villitis cord was observed in 88 placentae. Vascular lesions observed in 31 placentae included considerable infarctions, decidual arteriopathy, retroplacental hematoma and intervillous fibrin deposition. In the third group in order of importance, compression of the umbilical cord with tissue reaction was observed in one case.

In 24 placentae (7.1%), the examinations were assessed as supplementary. In 12 cases, a single umbilical artery was observed, and chromosomal abnormalities or malformations were reported in the matching fetuses. Four placentae were edematous and the infants were hydropic, three were of unknown etiology, and one autopsy showed adenoid cystic malformation of the lung. The rest of the supplementary placental diagnoses were thrombus in an umbilical artery, moderate inflammation and amnion nodosum in four autopsies with oligohydramnios; and placental granulomas and peripheral retro-

TABLE 5. Value of placental examination for fulfillment of the purposes of the total examination

Value of placental examination Number % Conclusive 6 1.7 Important

(inflammation*) (vascular lesions) (other)

Supplementary Doubtful Noncontributarv

88 25.8 31 9.1

1 0.3 24 7.1 27 7.9

164 48.1 Total 341 100 * Acute moderate and severe inflammation of the

membranes; funisitis or acute villitis was included.

342

placental hematoma in cases with signs of asphyxia at autopsy.

In 27 placental examinations (7.9%), the diagnoses were doubtful as to the result of the combined examination of fetus and placenta. These lesions were umbilical cord lesions such as true knots without tissue reaction, velamentous insertion, and single umbilical artery in singletons, twins or triplets without malformations. Other lesions were villous edema and decidual arteriopathy in fetuses without specific pathology at autopsy.

The placental examination was assessed as noncontributory in 164 placentae (48.1Y0). Many of these changes were signs of postmortem degeneration, such as stromal fibrosis, diffuse avascular villi and fibrous sclerosis of the vessels. Other lesions of no known significance for the result of the combined examination of the fetus and placenta were foci of immature villi in the second trimester, small chorioangiomas, intervillous thrombus, minimal edema or minimal chorioamnionitis.

DISCUSSION

Placental lesion were observed with different frequency (Tables 1 & 2). The most frequent lesions were inflammation and edema, vascular lesions, single umbilical artery and degenerative lesions, as reported previously (1).

Acute chorioamnionitis is accepted as an important entity leading to premature onset of labour, fetal infection and several associated complications (2, 15, 16, 28). In many instances,


pathogens are not recovered by conventional aerobic and anaerobic bacteriological methods (28), and many cases with histological evidence of membrane inflammation have been reported as clinically silent (9). Acute inflammation of the membranes or the umbilical cord, in this study deemed an important placental diagnosis, was observed in 88 placentae (25.8%), most often related to spontaneous abortions (Tables 2 & 5 ) . If the autopsy revealed infection of the fetus, the placenta was often inflamed. Further- more, in the autopsy group with no specific pathology, the placental examination often showed inflammation (Table 3). Only moderate or severe inflammation of the membranes was included in the study in order to be sure that the influence of the inflammation was considerable. There is no correlation between mild chorioamnionitis and fetal infection or positive bac- terial cultures (28). Marked inflammation has been identified as an indicator of significant infection of the fetus and of premature labour (9). Labour might be stimulated as a response to the infection due to production of prostaglandins and of cytokines from activated macrophages. The produced substances attract inflammatory cells from fetal vessels in the membranes or in the umbilical cord. In cases of acute chorioamnionitis without fetal infection, fetal com- promise is due to increased metabolic demands of the fetus or vasoconstriction of umbilical cord vessels on account of the accumulation of thromboxanes and prostaglandins (2, 16). Mor- bidity and mortality in association with chorioamnionitis have also been related to placental edema (lo), because the edema of the villi com- promises the fetal blood flow (19). The placental edema in this study was not observed more frequently if the membranes or the umbilical cord were inflamed. The incidence of acute chorioamnionitis varies in different series, but has been reported to be as high as 85% (20). Micro- scopic examination is necessary for the diagnosis. The distribution of the inflammation in the membranes is thought to be diffuse (20). Sampling one block of the free membranes and two blocks of placental tissue including the chorionic plate is believed to be sufficient to re- veal considerable inflammation (20), but no sys- tematic studies on sampling have been pub- lished. Reporting of acute chorioamnionitis and of acute funisitis is important when discussing

the actual pregnancy (9). Acute funisitis indi- cates an infection prior to fetal death, since the inflammatory response is only possible in a live fetus (16). An observation of acute chorioamnionitis with Gram-positive cocci might indicate an infection by P-hemolytic streptococci with a risk of recurrence in the next pregnancy (8), but the importance of most of the inflammatory lesions with respect to future pregnancies is unknown.

Lesions indicating uteroplacental vascular insufficiency, including infarctions, decidual arteriopathy, retroplacental hematoma and increased intervillous fibrin deposition, were observed in 31 placentae (9.1%). The lesions of vascular insufficiency reflect impaired maternal perfusion of the intervillous space (16, 24). In normal pregnancies, dilation of the spiral arteries by invasion of intermediate trophoblast in the 14th to 20th gestational week is an essential part of placentation with the establishment of an adequate maternal blood flow (16). If trophoblast invasion is inhibited, vascular insufficiency results. Infarction of the placental parenchyma occurs, and the artery wall might change, which is seen as atherosis (13, 14). The consequent fetoplacental ischaemia is the pri- mary event in many placentae from pregnancies complicated with growth retardation and/or preeclampsia (12, 16, 23). The uteroplacental and fetoplacental circulation regulate each other, with disturbances on the one side leading to disturbances on the other (18). It is generally assumed that destruction of 20% of the placental parenchyma may result in fetal death (4). However, the outcome for the fetus depends on the functional capacity of the surviving tissue rather than the proportion of the placenta that has been destroyed, and an infarction of 5% of the placental parenchyma might indicate more diffuse and serious lesions of the vasculature in- volving a greater part of the placenta (4). Pla- cental infarction and/or decidual arteriopathy was observed in about half the growth-retarded fetuses or infants in this material, and these lesions were rarely observed in the other groups of autopsies (Table 3). In most cases of chronic villitis, no infection is observed and chronic villitis has been related to conditions of low uteroplacental circulation (23), but in the present material, chronic villitis was not specific in the autopsy group with growth retardation. In the

343

LARSEN et al.

further examination of placenta on suspicion of vascular insufficiency, other lesions not included in this study such as fetal erythroblastosis (2, 25), iron deposition in villi (17, 18, 24), trophoblast volume (2, 16) and occurrence of endovas- cular trophoblast in decidual arteries (14) might contribute to the diagnosis. The listed lesions of uteroplacental vascular insufficiency are associated with preeclampsia, maternal hypertension and growth retardation, and for some of the lesions a risk of recurrence in future pregnancies (1 5).

The finding of a single umbilical artery was assessed as a supplementary observation. The phenomenon is reported in 1% of pregnancies (11). A single umbilical artery or amniotic bands are markers of dysmorphogenesis (4). If a single artery is observed, the frequency of associated congenital anomalies varies in different studies from 20% to 50% (1 1, 16). We observed such combinations in more than half the cases with chromosomal anomalies and malformations in the fetus in the supplementary group (Table 3). However, cases with a single umbilical artery were also reported in the autopsy groups without signs of dysmorphogenesis. In multiple pregnancies, a single artery is seen more frequently (3), as indicated in our material.

Serious umbilical cord lesions as seen in this material with compression of the cord and tissue reaction are very important, and should be confirmed microscopically with thrombus, bleeding or inflammatory reactions (16).

Rare placental diagnoses will often provide crucial information about the course of a pathological pregnancy. The placental examination can provide the definitive clue, as in the six conclusive cases (1.7%) in the present study. In one placenta, multiple chorioangiomas were observed replacing 20% of the placental parenchyma. Chorangiomas are benign vascular tu- mors associated with perinatal morbidity and mortality, because fetal growth is affected by the shunting of fetal blood from functioning villous tissue (23). In the case with amniotic band sequence, the fetus was too macerated for proper examination, but on examination of the membranes, fetal remnants were observed. Twin transfusion syndrome might be difficult to an- ticipate clinically (26) and the report on the placental examination with marked difference of

the two placental parts grossly and microscopically is important (7). The diagnosis of partial mole, especially in the second trimester, might be difficult to obtain on gross examination of the placenta, but on careful examination of the placental disc, the cystic villi are observed and microscopy will confirm the observation. In all six conclusive cases, the macroscopic examination indicated the pathological condition, but a histological examination was helpful in con- firmation of the diagnosis. Of these placental diagnoses, only moles have a risk of recurrence in future pregnancies (21).

The observed degenerative lesions, such as stem villous fibromuscular sclerosis (1 6.2%), diffuse avascular villi (20.5%) and villous fibrosis (36.7%), are regarded as postmortal phenomena ( 5 , 6), often related to maceration (Table 4) and especially found in the group of spontaneous abortions (Table 2). These degenerative lesions are probably a reaction sec- ondary to cessation of fetal blood flow at fetal death (16). The significance of the lesions is highly questionable and probably of no importance. Morphological changes in the placenta following intrauterine death are marked after 2 weeks (6). Other focal but important lesions might be diagnosed even at that time, but diffuse lesions seem to be hidden in the degenerative changes.

Lesions in the large group of placentae pro- viding no contributary information, besides the degenerative lesions described above, were sub- chorionic fibrin deposition, foci of immature villi, small chorioangiomas and intervillous thrombi. At present, the relation of the lesions to fetal death is unknown. Whether mild acute chorioamnionitis is the early stage of inflammation or is related to lesser pathogenicity than a more severe grade of inflammation is unknown, and mild inflammation has no relation to fetal morbidity (28).

The results of the present study showed that placental examination in pregnancies terminating with fetal or perinatal death was of value in half the cases, in agreement with Agapitos et al. (1). If clinicians, microbiologists and pathologists continue to work in close collaboration, even better results might be obtained (4). How- ever, assessment of the value of placental examinations is subjective and in some cases it is difficult to interpret the placental findings.

344


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