The lesions of fifteen hundred placentas considered from a clinical point of view

THE IIESIONS CONSIDERED

C)F’ .L1’LFTEEN IIUNIIREII E‘R(.)M A C1JXIC:;2I~ POINT

PLACENTAS OF VIEW

UR understanding of the pathologic lesions of the placenta is in an unsatisfactory state, both as regards their et,iology and clasThe work of Eden, sification, as well as their clinical significance. Williams, Dieckmann and XteNalley, Siddall and Hartman in the English and American litemttm~ and that of Grosser and .Hinselmann in the (Jerman have contributed the bulk of what we now know. However, they leave the reader with the imprtssion that, the subject is st’ill vague from the pathologic and clinical points of view, This is particularly true of the latter. The meanin g of the abnormal changes in the placenta to the obstetrician ant1 his patients does not seem lo bavp emerged from the efforts of t,hesc ;~r~lhors to cata.logue and explain the lesion itself. That this fetal organ is the seat of a number of different forms of proliferations and dcge~irratioris. which alter its form and possibly its fun&ions, has been proved. t
0

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553

width, and the depths of the placenta carefully examined for lesions. Any abnormality is noted and those which seem to be of significance from t,lie clinical point of view are given further study by histologic methods. In addition, microscopic preparations are made from the placentas of all syphilitic mothers and of those with premature or stillborn fetuses. In this way, over 1,500 placentas have passed through our laboratories. Lesions of special interest have been worked up by means of differential staining methods as these were indicated. Our study is based upon this material, In selecting and analyzing the lesions to be included, only those have been accepted which were of sufficient size, or if diffuse, of sufficient extent to have clinical significance. In the case of obliterative lesions (infarcts) and cysts, we have accepted as our criterion a diameter of 2 em. in the gross. This attitude is a point of departure from the work of our predecessors in this field. We realize that in taking it we are open to criticism because of our attempt to differentiate lesions that may have clinical importance from those having none. However, this is to be a practical study, in which, if it is to be of value to clinicians, such differentiation is of the utmost importance because the minor lesions occur with such frequency, in cases showing no other abnormality, that, unless discrimination is shown, the net result will be obscured in a mass of data that cannot be analyzed. Our plan is to divide the study into four parts. First, we wish to make clear the incidence of lesions in the whole group of 1,500 placentas and compare our findings with those of other workers. Second, the incidence of the same lesions in normal mothers and infants will be considered. Then, with this as a background, the lesions occurring in a series of abnormal mothers and infants will be presented, and, finally, the findings in the placentas of all women with nonsyphilitic stillborn infants will be shown in an effort to indicate the signific.ance of placental lesions in this group. Table I reveals the incidence of the various lesions in the entire series of 1,500 placentas. The largest group is that called “obstructive and proliferative lesions. ” This is to be considered as embracing all types of “infarcts.” It is divided into two subgroups labelled “red” and “white, ” as these may have different etiologic significance. The red infarcts have an incidence of 5.4 per cent and the white 13 per cent, together making a total of 18 per cent. In view of our method of selecting lesions, it will be important to indicate the findings of Williams who quotes 63 per cent for this group, Ravenstein 42 per cent, and Siddall and Hartman 67.7 per cent. These latter figures are undoubtedly correct from a pathologic point of view, but, since they include a majority of small lesions, we feel that our figure is a much more useful one and still includes all those abnormalities which could

TRAIJT

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PI,.\CEST.Z

In Table III, 232 pregnancies which were diagnosed as abnormal The out,standing feat.ures of this summary clinically, are analyzed. seem to be the relatively high incidence of infarction in eclampsia and preeclampsia, 40 per cent,; syphilis ‘Ji per cent; and premature

SERIES

Obliterative

OF

and

1,268

“NORAIAL

proliferative (‘Linfai-cts”)

cysts Tumors Hydatidiform mole Vesicular degener:ttion Rrtroplacental lwmorrhage

NUMBER OF CASES

CASES”

lesions

Red White :;-

PER CENT OF WHOLE

52 141 ‘) g 0 0

j

4.0 11.0 0.0 0.2 I)

15=h ~/ / I

I

births 31 per cent,. It is also notable that these lesions do not have as high an incidence in nephritis (14.5 per cent) as they do in the whole series of 1,500 cases. This would seem to be a contradiction to the results of other workers who find infarcts, especially of the ’ ’ red ’ ’ variet,y, more frequently in nephritis than in any other condition. We can offer one possible explanation. In our clinic, the incidence of chronic nephritis is relatively low, being only 3 per cent. This woulcl of course recluce the number of lesions that might be regarded as associated with permanent kidney damage. Another point of interest is the incidence of vesicular degeneration of the villi in 10 per cent of the placentas of premature births. This finding is in accordance wit,11 the work of Dr. Streeter, who has recently called attention to it. As would be expected, retroplacental hemorrhage is frequent in abortions and in premature separation of the normally implanted placenta. In fact, it, is so constant a finding that it might be considered as the normal mechanism for separation of t,lir placenta. from the llt,erine wall in the abortion group. In view of the fact that this study is an attempt to point out the influence that placental lesions may have upon the welfare of the mother or the fetus, it is thought important to study the placentas associated with all nonsyphilitic stillborn infants. There were 38 such place&as (Table IV). Of these infants, 17 can be assumed t,o have died of extraplacental causes, such as prolapsed cord, multiple loops of cord about the neck, severe intrapartum infections, and hydrocephalus, an assumption which is borne out by the fact that no placental lesions were founcl excepting in the cases of intrapartum infection, and in t,hese, although there was a definite infiltration of the tissues with the infective organisms, there was no clefinit,e reason for supposing that this was the cause of neonatal death.

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PI,ACENTA

This leaves a group of 21 eases, diagnosed clinically as atelectasis, anomalies, and asphyxia. Seven of these cases showed no placental lesions of importance. The remaining fourteen, or 38 per cent, of this group of 38 stillborns, showed marked infarction. These are ontlittetl rtntler the diagnosis of the mother. The severe toxemias, eclatrtpsia, preeclanipsia, and nephritis account for 42 per cent of the 14, ant1 normal mothers account for the rema.ining 57 per cent. This would scent t.o indicate that. in this small series, t.he nmternal abnormality TABLE SERIES

OF

38

Iv

NONSYPHILITIC

S’l’ILI,BOKN

A. Cause of death probably extraplacental.

Prolapsed cord Cord about neck Intrapartum inf. Hydrocephalus

B. Cause

Atelectasis Anomalies Asphyxia

of death

*Theso 1. Eclampsia 2. Nephritis, 3. Normal

doubtful

I4 cases fall

into

and preeclampsia, 2 with 4 case% 2 with mothers

the

INFANT’S

Clinical diagnosis

I-

Clinical diagnosis

following

Maternal

17 cases

Ko marked placental lesions

21 cases

“14 of this group had large placental lesions

Groups

38 per

cent.

2 cases, both with large red “infarcts” large red “infarcts” laroe \yllite 4 ‘infarcts’ 7

Premature izfants, “infarcts” ’ Full-term infants, “infarcts”

6 cases

all

2 eases,

both

with with

large large

Toxemias 42% white red

I

57’;‘o

may have had something to do with the occurrence of infarcts in the placenta, particularly as the placental lesions were of sufficient extent to suggest the possibility of their having contributed in part, at least, toward the infant’s death before birth. In summary it may be said that, in this study of 1,500 placentas, the chief abnormality found was some form of obliterative process which has been considered as having the same effect upon t.he placenta whatever its variety or origin. An attempt to associate these lesions with abnormalities in the mother has led to the conclusion that there seems to be no connection, as the incidence of placental lesions in the abnormal group was almost identical with those in the whole series of cases,the incidence in both being 1s per cent. In the stillborn group there may be some connection between placental infarcts and severe toxemias, even though normal mothers who had marked infarction of their placentas had a higher incidence of stillbirths. However, Siddall and Hartman observed t.hat mothers suffering from a toxemia of pregnancy, with large infarcts of the placenta, had infants with decreased birth weight, while the infants were