Fig. 1.1
Spiral arteries of the decidua capsularis. The arterial wall, without the action of the trophoblast, preserves the myometrial layer. The lumen is very narrow
Fig. 1.2
Decidua in an 8-week pregnancy. The interstitium and the arterial wall are invaded by the trophoblast. Trophoblastic cells are present on arterial endothelium and in one artery occlude entirely the lumen
This apparently paradoxical phenomenon has a series of advantages: (i) it reduces the oxidative stress of the foetus in a particular moment of development, (ii) it induces a rapid maturation of the villi in hypoxia, (iii) it expands the peripheral regions of the placenta in the passage to the II trimester, (iv) it allows a more rapid transformation of the arterial wall attacking it both externally and internally, and (v) it allows a progression of the trophoblast against the flow, so progressively extending the transformation of the arterial wall to the vessels of the myometrium.
Intercommunicating clefts appear in the syncytiotrophoblast and these lacunae fill with maternal blood (Fig. 1.3). The columns between the lacunae, originally formed only of the syncytiotrophoblast, now form a central core of cytotrophoblastic cells (primary villus stems), this is followed by a mesenchyme core growth into the stems (secondary villous stems), and finally they are vascularised (tertiary villus). Finally branching occurs and the villi are formed.
Fig. 1.3
Early stage of a blastocyst in endometrium. The wall of the blastocyst is composed of an internal layer of cytotrophoblast and a thick layer of syncytiotrophoblast in which a complex labyrinth of channel is promptly occupied by maternal blood
The precise description of the placental structure can be found in the specific texts; however, the chorionic plate (on the foetal side) is smooth and shiny due to the presence of amniotic epithelium, and the allantochorionic vessels can be glimpsed which spread from the insertion zone of the funiculus. The maternal side is irregularly separated by deep septa (corresponding to the septa of the decidua) into 16–20 lobules known as maternal cotyledons. The foetal cotyledon is instead the primary stem of a chorionic villus and its branches and sub-branches, that is, the functional unit of the villous tree coming from the chorionic plate. The latter being more numerous than the former, each maternal cotyledon can contain more than one foetal cotyledon.
Near the centre of the maternal cotyledon, the villi are thinned out and form a haematic lacuna (Fig. 1.4) which causes a reduction in the speed of the blood flow and a corresponding reduction in hydrostatic pressure necessary for mother-foetus transfer. It is also the area with the highest levels of oxygen, and therefore the most recent and immature villous branching can be found around it. Various villous typologies are found within the placenta:
- 1.
Stem villi (Fig. 1.5): the primary stem with an artery and a vein with a muscular wall, connective tissue and a trophoblast mantle. They can have up to eight orders of branching, reducing in calibre but not in structure. Some are embedded in fibrin and anchored to the basal plate to give stability to the organ.
- 2.
Immature intermediate villi (Fig. 1.6): large villi with a reticulate stroma occupied by active macrophagic Hofbauer cells and capillaries at various distances from the trophoblast surface. They guarantee transfer in the first phase of pregnancy and continue to branch, maturing into stem villi or mature intermediate villi
- 3.
Mesenchymal villi (Fig. 1.7): they are the first generation of villi becoming immature intermediate villi. Starting as trophoblastic sprouts from the underlying mesenchymal layer they undergo a proliferation of cytotrophoblastic cells within the trophoblast mantle. Capillary formation completes their transformation into new immature intermediate villi.
- 4.
Mature intermediate villi (Fig. 1.8): The reticulate stroma disappears reducing the diameter of the villi, and the capillaries reach the outer mantle of the structure. On the surface and the extremities of the villus, we find the terminal villi.
- 5.
Term villi (Fig. 1.9): they are formed of looping capillaries (4–6, but in section they seem less) which are very close to the basal membrane of trophoblast so creating the vasculo-syncytial membrane, that is, the optimal structure for maternofoetal transfer.
Fig. 1.4
Low magnification of a maternal cotyledon. The haematic lacuna is evident near the centre. Some immature intermediate villi are present around the lacuna
Fig. 1.5
Term placenta. In this picture many principal villi of different sizes are present. All villi are characterised by thick mesenchymal stroma in which two vessels (arteria and vein) are evident. The surface often lacks of the trophoblast, and a layer of fibrin separates the villus by the maternal blood. The size of the villi depends on the degree of ramification of the single villus. In the insertion we observe a principal villus anchoring to the basal fibrinoid layer
Fig. 1.6
The immature intermediate villus is large, and its stroma shows a reticular shape for the presence of a very complex network of channel. In each lacuna the Hofbauer cells show a dark nucleus anchored by thin cytoplasm projections to the channel wall. The capillary vessels are arranged at different distances from the trophoblast. The maternofoetal changes are possible but in low entity
Fig. 1.7
Two mesenchymal villi characterised by a cap of proliferating cytotrophoblast cells, an edematous stroma and absence of vessels
Fig. 1.8
The intermediate mature villi are smaller than the immature ones. Their axes contain expanded capillary vessels. Several term villi are exposed on their surface
Fig. 1.9
Term villi are composed of some loops of capillary vessels, few interstitium and trophoblast. The dilated vessels are very close to the basal membrane in a region of the trophoblast without nuclei. The distance between foetal and maternal blood is minimal, and the maternofoetal changes reach the maximum of possibility
All types of villi are not always present during the pregnancy. The mature intermediate villi and the terminal villi proliferate in the third trimester to satisfy the increased needs of the foetus, even if around the haematic lacuna we still find immature intermediate and mesenchymal villi to allow for placenta growth. On the maternal side, we find the fibrinoid deposits forming the Rohr and Nitabuch striae which create a physical and immunological barrier and the decidual endometrium infiltrated by extravillous trophoblast.
1.5 Anomalies of Shape, of Structure or of Function?
The understanding of placental pathology has made great strides in recent years both because of demands from clinical research and legal medicine and because of the new genetic and molecular techniques. We now know that many “lesions” over which many words have been spilt are much less important than they seemed. Even modifications of shape, thickness and structure which fascinated traditional pathologists have been found to be of little practical interest.
Modern placental diagnosis, like in all the daily practice of the pathologist, must aim to give a convincing interpretation of the pathological event. For this reason the diagnostic process has to include three phases.
- 1.
Correct information on the clinical data and perinatal risk: possible maternal causes of foetal damage, age of the pregnancy, foetal weight and evolution of the pregnancy and of the delivery.
- 2.
Correct examination of the placenta: macroscopic assessment, observation of the membrane and the funiculus, evaluation of the lesions for character, age (recent or old), intensity and extension.
- 3.
Correct interpretation for a correct conclusion: assessment of the extent of the damage and its incidence on the evolution of the disease, presence of multiple causal or concausal factors and discriminatory assessment of causal signs from consequent signs. These last observations can account for inappropriate past assessments such as the fact that fibrous obliteration of the stem villi arteries is a consequence of the death of the foetus, not the cause.
From what is written above it becomes clear that a presentation of placental pathology can start only from the solution to specific clinical queries.
1.6 Placental Anomalies Secondary to the Intrauterine Death of the Foetus
The examination of the placenta after a pregnancy complicated by the intrauterine death of the foetus is a classic example when the observer can be misled into confusing “the signs of death”, that is, the alterations secondary to foetal death, with the signs actually linked to the cause of death.
An accurate discrimination not only allows us to distinguish between the two phenomena but also can give us information on the time of death which is more accurate than that given by thanatological observations of the foetal autopsy. In fact the thanatological alterations of the foetus are subject to several variables such as the temperature, the quantity of amniotic fluid, the presence of meconium, infections prior or consequent to death and the concurrence of anaemia and/or haemolysis, which drastically interfere in the evolution of the phenomena [4]. Differently, the placenta, which depends on maternal blood for its oxygenation and tropism, at the moment of death of the foetus, begins to show a precise series of events which are correlated to the cessation of foetal circulation [5, 6]. This has enormous value in medical-legal disputes as it allows the objective description of a relatively precise time span for interpretation of time of death of the foetus over and above the subjective opinions of the mother and the obstetrician.
Many of the foetuses suffering an intrauterine death are expelled within the first 24 h, but the exact percentage is not known. Conversely, there have been cases of foetal retention lasting more than a week. The alterations observable in the placenta are for the most part linked to the arrest of foetal circulation and proceed over time from the large vessels of the funiculus to the foetal capillaries. These are joined by lesions caused by the suffering of the vessel walls and of the haematic crasis of the foetus.
In conclusion, based on the literature and on our experience, we can use the following time scale to be able to determine the time passed between the death of the foetus and its expulsion:
- (a)
After a few hours: “fibromuscular” thickening of the walls of the umbilical arteries (Fig. 1.10) and swelling of the endothelium of the arteries of the stem villi (Fig. 1.11). These aspects, tightly linked to vascular collapse due to cardiac arrest, are non-specific because they are also found in a prolonged afterbirth expulsion.
- (b)
After 6 h: the start of intracapillary karyorrhexis of the villi (Fig. 1.12). It progresses with time. The start of intimal fibrous sedimentation of the vessels of the stem villi.
- (c)
After 24–48 h: the start of mineralisation of the villi (a non-specific phenomenon because it can be found in living foetuses with anomalies of the metabolism), the anomalies of the vascular lumina increase (Fig. 1.13), regressive areas of Wharton jelly are observed, and haemoglobinic diffusion begins (Fig. 1.14).
- (d)
- (e)
After 7 days: fibrosis of the villi is more and more compacted (Fig. 1.17).
Fig. 1.10
Few hours after the foetal death, the arteries of the umbilical cord are contracted, the lumen is often virtual and the wall is apparently thickened
Fig. 1.11
In the stem villi the contracted arteries have an endothelial swelling. This picture was in the past confused with a glycogenic degeneration in diabetic placenta
Fig. 1.12
Intravascular karyorrhexis. Nuclear fragments of the leukocytes are present in the lumina of the capillary vessels
Fig. 1.13
Regressive aspects of the villar arteries, with intimal fibrosis, some days after the foetal death
Fig. 1.14
Diffusion of the erythrocytes in the Wharton jelly of the umbilical cord. Macroscopically the cord appears red brown some days after the foetal death
Fig. 1.15
Coagulative necrosis of the muscular cells of the cord vessels, with cytoplasm hypereosinophilia and absence of nuclei. The foetus is dead from 1 week
Fig. 1.16
Complete dissociation of the arterial wall after the disappearance of the lumen
Fig. 1.17
(a–c) Disappearance of vessels, progressive fibrosis and reduction of cells in villi after a week of foetal death. The trophoblastic nuclei are amassed in large and dark nodules
The above listed alterations, important for the definition of the time of death of the foetus, must not be used to define the cause of death, which must be studied with accuracy and patience to avoid inconclusive diagnostic opinions which suggest that the post-mortem alterations mask the causes of death. The criterion must be that of defining the lesions which are common and synchronous, so leading to retention of the dead foetus, and focal lesions not in line with the time of death, which more probably pertain to its cause.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
