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The Histopathology of Placental Insufficiency

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The Histopathology of Placental Insufficiency J Clin Pathol: first published as 10.1136/jcp.29.Suppl_10.1 on 1 January 1976. Downloaded from J. clin. Path., 29, Suppl. (Roy. Coll. Path.), 10, 1-8 Feto-placental function: its nature and assessment The histopathology of placental insufficiency H. FOX From the Department ofPathology, University ofManchester Voltaire, regarded by some as a realist and by others It is only the second of these possibilities which as a cynic, remarked that 'if God did not exist it will be examined here in detail, for if the term would be necessary to invent him'. One suspects that 'placental insufficiency' has any meaning it must be this comment is equally applicable to placental that a placenta receiving an adequate supply insufficiency, a concept that has similarly attracted of nutrients and oxygen is unable to transfer these to not only faithful adherence but also bewildered a normal fetus in quantities sufficient to ensure agnosticism or defiant disbelief. normal growth and development. Placental insufficiency has been largely defined in clinical terms, principally by those who believe that Placental Pathology in Fetal Deprivation the placenta is, during a normal pregnancy, extended to the full limit of its functional capacity. Adherence The functional unit of the placenta is the terminal to this belief implies that any factor which adversely villus and a placenta that is physiologically inade- influences trophoblastic function, by no matter how quate must have either (a) a decreased number of limited an extent, will restrict the fetal supply of functioning villi or (b) a normal number ofvilli which oxygen and nutrients, this resulting in fetal growth are, however, functionally inefficient copyright. retardation, wasting, hypoxia or, in extreme cases, A lesion which clearly reduces the total population death. This clinical concept has been supported, to of functioning villi is placental infarction (fig 1) in some extent, by placental function tests which, which a number of villi undergo ischaemic necrosis however, measure principally the biosynthetic and and become aggregated together to form an easily endocrinological activities of the trophoblast rather visible white plaque. Small infarcts are both common than its capacity for transferring oxygen and and unimportant but necrosis of more than 10 to 15 nutrients to the fetus. The final court of appeal for per cent of the placental parenchyma is associated confirmation of a diagnosis of placental insufficiency with a very high incidence of fetal deprivation and http://jcp.bmj.com/ is the pathologist who finds that the apparently death (Fox, 1967a); indeed, it has been this finding inadequate placentae presented to him for appraisal which has prompted the suggestion that the may be large or small and can vary from being placenta has little or no functional reserve capacity. extensively infarcted and heavily calcified at one That this is too simplistic a view is, however, extreme to complete normality at the other. Many indicated by a consideration of two other lesions pathologists faced with this situation are forced into which cause a reduction not, it is true, in the total an attitude of nihilism and are content not number of villi, but in the population of function- diagnostic on September 28, 2021 by guest. Protected to pursue with any great degree of tenacity the ing villi, these being perivillous fibrin deposition question, to which this paper is directed, ofwhether a and fetal artery thrombosis. In the former (fig 2) a satisfactory pathological basis for placental in- portion of the intervillous space is obliterated sufficiency can be defined. by fibrin which is laid down around the villi as a Clearly the syndrome of chronic fetal deprivation consequence of eddy currents and stasis of maternal may have any one of three fundamental bases: (1) blood and forms an irregular white plaque that is a deficient supply of oxygen or nutrients to the often called an infarct. This is a regrettable mis- placenta either because of an abnormal constitution nomer but it has to be accepted that the villi em- of the maternal blood or because of an inadequate bedded within the fibrinous mass might just as well maternal uteroplacental circulation; (2) a failure of be infarcted for they are no longer available to the placenta to transfer adequately oxygen and fulfil their transfer function. Similarly, following nutrients from maternal to fetal blood; (3) a failure fetal artery thrombosis (fig 3), an event which of the fetus either to take up, or to utilize adequately, usually occurs for no discernible reason, the nutrients and oxygen. avascular villi normally supplied by the occluded J Clin Pathol: first published as 10.1136/jcp.29.Suppl_10.1 on 1 January 1976. Downloaded from 2 H. Fox Fig 1 A placental infarct: this is seen in the left halfof thefield and is characterized by aggregation of villi, obliteration of the intervillous space and necrotic changes in the villi(H&E x 56). copyright. vessel play no part in transferring oxygen or nutrients usually therefore the visible hallmark, and only to the fetus. It is therefore surprising that neither of occurs as a complication, of a severely compromised these lesions appears to affect adversely the fetus, this utero-placental circulation and it is this, rather than applying not only to small lesions but also to those in the simple loss of villi, that is the true cause of the which as many as 30 per cent of the villi are rendered fetal complications. functionally inactive (Fox, 1967b) That the placenta As already mentioned, infarction may also be due can withstand the loss of nearly a third of its to retroplacental bleeding. A sharp distinction functional parenchyma without any fetal embarrass- has been drawn between the chronic condition of http://jcp.bmj.com/ ment bears eloquent witness to the fact that, far from premature separation of the place'ita and the acute being physiologically extended, it has a very con- catastrophe of abruptio placentae (Gruenwald et al, siderable functional reserve capacity. Why then the 1968); tbe former results in the formation of a paradox that a similar, or even much less substantial, retroplacental haematoma which indents the basal loss of villi because of infarction is of such gloomy plate of the placenta and causes infarction of the import for fetal growth and development? Placental overlying villi but does not usually produce any infarction is due either to a retroplacental haema- clinical symptoms whilst the latter produces a on September 28, 2021 by guest. Protected toma or thrombosis of a maternal utero-placental dramatic clinical picture, is usually followed rapidly vessel; if those due to retroplacental bleeding are, for by delivery of the fetus and may not leave any the moment, excluded it is clear that extensive pathological imprint on the placenta. Retro- infarcts are due to widespread thrombosis of placental haematomata are found in about 5 per cent maternal arterioles (Brosens and Renaer, 1972), a of pregnancies but the vast majority are small and of phenomenon that would not be expected to occur in no importance; they are only associated with fetal a healthy vascular tree. Indeed, a significant degree of deprivation if more than a third of the placental infarction is found only in placentae from women parenchyma is separated by the haematoma from the suffering from the hypertensive complications of maternal utero-placental vessels or if the bleeding pregnancy and these are precisely the conditions in occurs in a pregnancy already complicated by a which the utero-placental vessels are markedly hypertensive condition. abnormal (Robertson et al, 1975) and in which, as a It could, of course, be argued that the most consequence, maternal blood flow through the obvious manner in which the villous population is placenta is diminished. Extensive infarction is diminished, namely, by the development of an J Clin Pathol: first published as 10.1136/jcp.29.Suppl_10.1 on 1 January 1976. Downloaded from The histopathology ofplacental insufficiency 3 4: 3k.~. -s~rr'~~. '\*- '4' -I L N' 2 ; Cr ..< ' s copyright. \ 44 SS+W1sSX ~ /b ............................. Fig 3 Avascular villi resulting from thrombosis ofa fetal stem artery (H & E x 350). Fig 2 Perivillousfibrin deposition: the intervillous space is filled in byfibrin which completely envelops the widely are readily visible and thus serve as convenient pegs separated villi (H & E x 350). upon which to hang a diagnosis of placental inadequacy. This perhaps emphasizes that the macroscopicSt.4'o study of the placenta is not often of any http://jcp.bmj.com/ unusually small placenta, is often associated with great value to the pathologist concerned with poor fetal growth and that in such cases the defining placental insufficiency. It is true that this inadequate growth of the fetus is a direct result of the may reveal the crater marking the site of an old small placental size. If, however, fetal growth were retroplacental haematoma or the very uncommon rigidly limited by placental size it would indicate that large haemangioma which may, possibly because it the placenta is functioning at the limit of its capacity, acts as an arteriovenous shunt and thus allows the a view which appears to be incorrect. It is much more return of unoxygenated blood to the placenta, be on September 28, 2021 by guest. Protected probable that the reverse situation is the case and associated with fetal deprivation and that circum- that when the fetus is small the placenta, being a vallate placentation is accompanied unduly often by fetal organ, shares in the generally diminished a minor degree of fetal growth retardation but most growth of the fetus, the small placenta being thus a other visible lesions are quite banal. Thus sub- manifestation, rather than a cause, of poor fetal chorionic fibrin plaques, intervillous thrombi, small growth (Gruenwald, 1975).
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