Immature villi are usually large sizes and have small, non-dilated vessels, relatively a large number of stroma and absence of SU. They can be present in mature placentas in the form of small isolated islands, which are observed in 97% of mature placentas and are not a pathology. The presence of such villi indicates that villous growth continues in the mature placenta. The second type of immaturity is a delay in villi maturation, i.e. The degree of maturity of the villi lags significantly behind the given gestational age. Delayed villi maturation is observed in diabetes, Rhesus conflict, syphilis, toxoplasmosis, chromosomal abnormalities, especially Down syndrome.

Accelerated maturation. It is characterized by a predominance of mature villi in premature placentas. Seen in preeclampsia, hypertension, habitual miscarriage, etc. Combined with high risk development of fetal asphyxia and IUGR.

All described changes in the villi can be divided into three groups depending on the pathogenesis:

• due to reduction of uteroplacental blood flow (preeclampsia or hypertension) - hyperplasia of the CTP and thickening of the TPB M;
• due to a reduction in fetal blood flow - an increase in the number of SU and stromal fibrosis;
• of unknown origin - fibrinoid villous necrosis, lack of SCM and abnormalities of villous maturity.

Placental mesenchymal dysplasia (PMD), or pseudopartial hydatidiform mole. It is a rare pathology of pregnancy, which macroscopically resembles changes in the placenta during partial hydatidiform mole, but with a normal fetal karyotype. Such cases are often mistaken for partial hydatidiform mole. About 51 cases of PMD have been described in the world literature.

Macroscopically: the placenta is enlarged, the arteries of the chorionic plate are aneurysmatically dilated, and the veins are varicosely dilated, on the maternal surface there are large fields of cystically changed villi (resemble bunches of grapes, as with hydatidiform mole). Microscopically: among the normal placental tissue, fields consisting of enlarged stem villi with cistern-like formations are detected; there may be chorangiomatous changes in the villi. Trophoblast proliferation and trophoblastic inclusions, pathognomonic for partial hydatidiform mole, do not occur in PMD. In addition, with partial hydatidiform mole, a triploid karyotype and a decrease in the level of P-choriogonadotropin in the mother’s blood are observed. With PMD, various fetal pathologies are observed - IUGR, anemia, thrombocytopenia, prematurity and intrauterine death. Maternal complications in combination with PMD are relatively rare. PMD has been described in Wiedemann-Beckwith syndrome.

Tumors of the placenta. Primary nontrophoblastic tumors of the placenta are rare. Chorioangioma, choriocarcinoma, teratoma, hepatocellular adenoma, leiomyoma, heterotopias of adrenal and liver tissue have been described. Metastases of malignant tumors from the mother (melanoma, breast cancer, stomach, rectum, lung, ovary, pancreas, skin, rhabdomyosarcoma, Ewing's sarcoma and medulloblastoma) and from the fetus (neuroblastoma, hepatoblastoma, malignant lymphoma, sarcoma, tumors) occur in the placenta brain and sacral teratomas). In most cases, metastatic tumor cells are localized in the intervillous space; in leukemia, there may be infiltration of the villous stroma. In congenital pigmented nevus of the fetus, nevus cells are observed in the stroma of the villi and grains of melanin pigment in CG cells. Some authors believe that they are the result of aberrant migration of neural crest elements rather than bone marrow metastases.

Transplacental metastases to the fetus are much less common than metastases to the placenta. Of these, metastases of melanoma and lung adenocarcinoma are most often described. In many cases, the fetus dies in utero, but there are observations of spontaneous regression of the tumor.

Chorioangioma is the most common benign tumor of the placenta. Occurs in 1% of cases in unselected placentas. Macroscopically: single, occasionally multiple nodes, round, oval or kidney-shaped. Sometimes the tumor is dark red, soft, reminiscent of fresh blood clots, sometimes it is white, dense, like a heart attack. It is localized in the thickness of the placenta and often bulges above the fruiting surface. Microscopically: it has the structure of a mixed hemangioma (capillary, with cavernous areas). Foci of necrosis, thrombosis and calcification are common, and sometimes there is a predominance of the myxomatous (angiomyxoma) or fibrous (angiofibroma) stromal component. May be combined with hemangioma in the fetus. In most cases clinical significance does not have. Large tumors greater than 5 cm in diameter can have serious consequences. For the mother - polyhydramnios with or without premature birth, antepartum hemorrhage due to separation or rupture of the vascular pedicle of the tumor. For the fetus and newborn - hemangiomas in the liver and skin of the fetus, cardiomegaly, heart failure, IUGR, hydrops, anemia and thrombocytopenia, massive fetoplacental bleeding due to tumor rupture and fetal death. A special variant of chorioangioma is chorangiocarcinoma, which has the structure of chorioangioma, but with the presence of proliferating trophoblastic cells. The tumor is benign; its metastases in the mother or fetus have not been described.

Choriocarcinoma of the placenta (choriocarcinoma in situ) is often not detected macroscopically and is usually mistaken for a heart attack. Microscopically: foci of proliferating syncytioblasts and cytotrophoblasts are observed in the intervillous space, spreading to nearby villi. There may be invasion into the villous stroma and vessels. The consequences of intraplacental choriocarcinoma are variable. In some cases, there is no tumor in the mother and fetus, while in others, lung metastases are observed in both the mother and the fetus. Massive fetoplacental bleeding has also been described. Occasionally, a tumor in the placenta is not detected, despite the presence of metastases in the fetus (in some cases this is due to insufficient examination of the placenta).

Placental insufficiency. The term “placental insufficiency” is used to refer to processes of disruption (mainly reduction) of placental function (perfusion and/or diffusion). It should not be used as a specific nosology in either clinical or pathological diagnoses. The pathologist, based on a thorough morphological examination of the placenta, in his conclusion is obliged to indicate which processes are predominantly disturbed and to speak, at least presumably, about the prognosis for the fetus, and possibly subsequent pregnancies.

Morphological manifestations of a decrease in the diffusion capacity of the placenta include:

• the predominance of delay or arrest of villi development (immaturity) with normal or overweight placenta;
• moderate immaturity of villi with placental hypoplasia;
• chorangiosis or villous hypovascularity;
• SCM deficiency;
• chronic vulitis.

Moderately severe disturbances of placental diffusion occur in 80% of mature placentas, which is accompanied by fetal hypoxia in the last weeks of pregnancy, and with additional hemodynamic disturbances before or during labor, acute asphyxia and fetal death may occur.

A decrease in the perfusion capacity of the placenta is due to a decrease in blood flow in it due to a decrease in the intervillous space and/or fetal vessels in combination with placental hypoplasia, chronic circulatory disorders and/or impaired villous maturation.

Main morphological changes:

• hypoplasia of the placenta and generalized premature ripening villous with intermediate villous deficiency;
• hypoplasia of the placenta with widespread peri- and intravillous fibrinoid deposits or with infarctions occupying more than 30% of the placenta area;
• obliterating angiopathy with fibrosis or immaturity of villous tissue and pronounced fibrinoid deposits with normal given period gestational placental mass;
• increase in the number of SU;
• thickening of the GFBM;
• deficiency of terminal villi in the mature placenta.

Perfusion disorders have adverse consequences for the fetus and newborn - intrauterine asphyxia, IUGR, stillbirth, increased perinatal morbidity (especially hypoxic brain damage) and mortality.

Pathological immaturity of the placenta includes the following options.

Embryonic villi variant- occurs due to stoppage of placental development early stages embryogenesis and is characterized by the persistence of embryonic villi in the placentas of the II–III trimester of pregnancy. Occurs in toxicosis of pregnant women, diabetes mellitus, and some infectious diseases of the mother and fetus. Macroscopically: the placenta is enlarged, edematous, lobular. Microscopically: multi-lobed villi with loose stroma, many Kashchenko-Hoffbauer cells and stromal canals predominate. SCM and syncytial buds are absent, small avascular villi are found, and the intervillous space is expanded. In the case of diffuse spread of embryonic villi, pregnancy most often ends in early spontaneous abortion. Persistence of embryonic villi in the amount of 40–50% of all villi occurs in early gestosis in pregnant women, diabetes mellitus, isoserological incompatibility of maternal and fetal blood, and some specific infections (rubella, syphilis, toxoplasmosis). A typical combination is with abnormalities in the shape of the placenta and umbilical cord attachment, as well as miscarriage or fetal malnutrition.

Intermediate bristles option is characterized by a predominance of villi with a diameter of 80–110 µm with a small number of lateral, small branches, which indicates a stop in the formation of the villous tree at the stage of development of mid-level villi. In this case, intermediate mature or intermediate immature villi may predominate. The variant with a predominance of intermediate immature villi is more common in spontaneous miscarriages and antenatal fetal death. Dominance of intermediate mature villi occurs more often in spontaneous miscarriages, late gestosis, multiple pregnancy. Sufficient vascularization of the villi allows fetuses to reach a term of 37 weeks or more.

Variant of sclerotic chaotic villi– is formed during the second trimester of pregnancy as a result of the predominant development of the villous stroma and the absence of their capillary bed. Macroscopically: the placenta is reduced (hypoplasia). Microscopically: small villi predominate with single narrow capillaries, their stroma is rich in cells, the syncytium is poorly expressed, syncytial buds are absent, there are few or no embryonic villi. The predominance of this variant of immaturity is observed in spontaneous miscarriages, antenatal fetal death, severe gestosis and multiple pregnancies. In most of them, severe hypoplasia of the placenta, malnutrition of fetuses and newborns was noted. Mortality rate is 40%. Often the fetus dies at 24–25 weeks, less often at the end of pregnancy, but the child can be born alive with low body weight.

Variant of dissociated development– the most common variant of pathological immaturity, occurs at the end of the second – beginning of the third trimester of pregnancy due to the uneven development of individual cotyledons. The placenta, along with mature areas, contains groups or entire fields of embryonic, hypovascularized villi and areas of compensatory capillary hyperplasia. The reasons are not fully understood. It can be observed in late gestosis of pregnant women, latent forms of diabetes mellitus. If the preparations show a sufficient number of mature, small, well-vascularized villi, then full-term newborns are usually born with normal weight or slight malnutrition.

Very rare variants of immaturity include chorangiosis And obliterating angiopathy. The time of their occurrence is the first trimester of pregnancy. For chorangiosis characterized by a diffuse increase in the number of capillaries of the villi, which can be considered primary or secondary ( diabetes) a developmental anomaly, often leading to perinatal mortality. The outcome of pregnancy is often unfavorable, it ends early miscarriage or antenatal fetal death. At obliterating angiopathy the vessels of the stem and intermediate villi are stenotic or obliterated due to filling of the lumen connective tissue varying degrees of maturity. There is an opinion that such obliteration is due to intense smoking of the mother or exposure to occupational factors (red production, etc.). In 30% of cases, the fetus dies in utero or the child is born premature.

Hello Svetlana! I want to immediately express words of support to you regarding what happened to you. And I want to reassure you that if you approach planning your next pregnancy competently and sensitively, then these sad consequences can be avoided by 99%.

Placental insufficiency is one of the main causes of premature birth and spontaneous abortions late dates. Placental insufficiency is usually formed in two ways:

A violation of nutritional function, in which the absorption and assimilation of nutritious foods, as well as the synthesis of the fetus’s own metabolic products, are impaired.

Respiratory failure, which consists of impaired oxygen transport, which happened in your case, judging by the diagnosis of antenatal fetal asphyxia (intrauterine oxygen deficiency). This led to the degradation of the skin and internal organs.

Taking into account the state of protective and adaptive reactions, the following forms of placental insufficiency are distinguished:

. Compensated form feto-placental insufficiency, in which there are initial manifestations of the pathological process in the feto-placental complex. Protective and adaptive mechanisms are activated and experience a certain tension, which creates conditions for the further development of the fetus and the progression of pregnancy. With adequate therapy and management of labor, the birth of a healthy child is possible.

. Subcompensated form feto-placental insufficiency is characterized by an increase in the severity of the complication. Protective-adaptive mechanisms are under extreme stress (the capabilities of the feto-placental complex are practically exhausted), which does not allow them to be implemented sufficiently for an adequate course of pregnancy and fetal development. The risk of complications for the fetus and newborn increases.

.Decompensated form feto-placental insufficiency - there is overstrain and disruption of compensatory-adaptive mechanisms, which no longer provide the necessary conditions for further normal progression of pregnancy. Irreversible morphofunctional disorders occur in the feto-placental system. The risk of developing severe complications for the fetus and newborn (including their death) increases significantly. The clinical picture of feto-placental insufficiency is manifested in violations of the basic functions of the placenta. This form is indicated in the conclusion issued to you.

Infection of the membranes (placenta) was also detected, which is a reflection of violations of the protective function of the placenta when the placental barrier is weakened under the influence of pathogenic microorganisms penetrating the placenta. It is also possible for various toxic substances to penetrate the placental barrier, which also have a damaging effect on the fetus.

In connection with the above, I would like to advise you to now approach planning a subsequent pregnancy with the utmost sensitivity, since your medical history will already include a diagnosis such as placental insufficiency.

First What you should do is check your hormonal levels for the presence of an increased amount of androgens. In all forms of hyperandrogenism, a decrease in the hormones estradiol and progesterone in the blood serum was established in both phases menstrual cycle, as well as from early stages of pregnancy. Primary placental insufficiency develops already at the end of the first, beginning of the second trimester of pregnancy, it leads to a high incidence of fetal malnutrition. In addition, the enzymatic function of the placenta is disrupted, and hemodynamics in the fetoplacental system suffers. Pathological immaturity of the chorion was detected due to intermediate immature villi, microcirculation disorders, hemorrhages, excessive fibrinoid deposition and a high percentage of pathological immune complexes. Hormonal deficiency before pregnancy and in its early stages disrupts the formation of the placenta. Primary placental insufficiency develops, which lies at the origins of the development of late gestosis and chronic fetal hypoxia.

Second Placental insufficiency can develop under the influence of various reasons. Therefore, when planning subsequent pregnancies, you need to check your body for the following diseases:

Diseases of the heart and vascular system (heart defects, circulatory failure, arterial hypertension and hypotension),

Pathology of the kidneys, liver, lungs, blood,

Chronic infections

Diseases of the neuroendocrine system (diabetes mellitus, hypo- and hyperfunction of the thyroid gland, pathology of the hypothalamus and adrenal glands)

Uterine pathologies: endometriosis, myometrial hypoplasia, uterine malformations (saddle-shaped, bicornuate), large uterine fibroids with a predominantly intermuscular location of myomatous nodes.

During pregnancy, to prevent placental insufficiency, early identification and registration of pregnant women at risk for the development of feto-placental insufficiency is recommended.

With the onset of pregnancy, you should properly organize a daily routine with proper rest, including sleep for at least 8-10 hours, including daytime sleep for 2 hours, as well as spending 3-4 hours in the fresh air.

Important for maternal health and proper development the fetus has a rational, balanced diet, with an adequate content of proteins, fats, carbohydrates, vitamins and microelements. Fluid intake (in the absence of edema) to prevent hypovolemia should be 1-1.5 liters. It is important to monitor weight gain during pregnancy. By the end of it, the weight gain should average 10.4 kg.

It is important to be under constant supervision of a doctor, who will individual plan therapeutic measures and timing of their implementation, aimed at preventing the development of placental insufficiency in pregnant women at risk.

Drug prevention enhances the compensatory and adaptive reactions of the mother and fetus, prevents dyscirculatory disorders of the uteroplacental and fetoplacental blood flow and morphological disorders in the placenta.

An integral part preventive measures is to determine their effectiveness, assess the development of pregnancy, the formation of the placenta, the growth and development of the fetus based on the results of ultrasound and laboratory screening. A pregnant woman should be promptly hospitalized in an obstetric hospital to prepare the body for childbirth and decide on the timing and method of delivery.
Additionally

Involutional changes – fibrinoid deposits, calcification, fibrosis (degree of severity – moderate, severe: prevalence – limited marginal, diffuse).

The absence of gestational restructuring of the myometrial segments of the uteroplacental arteries leads to a gradual reduction of blood flow from the mouths of these arteries into the intervillous space, or creates a limit of uteroplacental blood flow, thereby limiting the growth of the placenta and the degree of its diffusion capacity. Characteristic was a pronounced dissociation of the deficit in the weight of newborns (on average 25.5%) and only a relative decrease in the weight of their placentas (10.6% less than control values). The structure of the villous tree generally corresponded to HS (72.7%), or pathological immaturity - the predominance of intermediate differentiated villi (20.2%) or dissociated development of cotyledons (9.1%).

Basal plate – without pathological changes.

Placental tissue – consistency (dense, spongy, flabby), color (bluish, dark bluish, pale bluish), without pathological changes;

Classification of placental insufficiency.

Diameters (maximum, minimum)

hemorrhages, blood clots (size, location, adhesions)

Risk factors – systemic vascular pathology of HIV/AIDS.

Thus, the isolated placental form of chronic PN, which is morphologically diagnosed in 22.6% of placental dysfunction, differs from the first more pronounced placental hypoplasia due to early immaturity of the villi and the prevalence of sclerosis and reduction of the lumens of the fetal capillaries, as well as thickening of the placental barrier. The results of Doppler measurements reflect mainly the relative preservation of the uteroplacental blood flow and a significant increase in resistance in the capillary bed of the placenta.

Normal viable newborn (level 1)

edema (+,++,+++), fibrinoid (+,++,+++), fibrin (+,++,+++), pseudoinfarctions (+,++,+++), calcifications ( +,++,+++), thrombosis of the intervillous space (+,++,+++), dystrophic changes in the villous stroma and vascular walls (+,++,+++), fibroblastic reaction (+,++ ,+++), villous sclerosis (+,++,+++).

1) Uteroplacental form.

The umbilical cord arteries had an expanded lumen, which was accompanied by ectasia of the arteries in the chorionic plate and supporting villi. This phenomenon is explained by a decrease in the total volume of the capillary bed of the villous tree, i.e., expansion of the arterial segment in front of the reduced capillary segment of the placental-fetal circulation with a corresponding expansion of its venous part. In biopsy specimens of the placental bed of the uterus, either normal gestational changes (68.5%) or the absence of such changes (28.5%) in the uteroplacental arteries were noted; occasionally hyperplastic arteriosclerosis was detected (3%) with partial preservation of the lumen of the vessels.

5. Ascending bacterial infection of the placenta (stage). Exudative inflammation of the membranes (choriodeciduitis, membranitis), placenta (subchorial intervillusitis, chorioamnionitis), umbilical cord (varieties of funiculitis)

Trophoblastic layer – clear cell, dark cell, uniform, uneven; hyperplasia, hypoplasia;

At the same time, severe rheological shifts also occur outside the infarction zones; they are causally related to the ultrastructural pathology of syncytiotrophoblast microvilli - the main site of hemostasis regulation.

III degree – severe changes

Forms – compensated, subcompensated (chronic edema of the umbilical cord).

A common symptom for the placental form of chronic PN is a pronounced decrease in fetal weight (-33.2%) and a synchronous, significant deficit in placental weight (-43.7%), which is explained by a violation of the ratio of the volume of the capillary bed and stroma in immature villi. In the chaotically branching, sclerotic villi, active fibroblasts and multiple collagen fibers predominated, compressing the few capillaries from the outside. An electron microscopic study of villi revealed that in all cases of pathological immaturity of placental tissue, but especially with chaotic sclerotic villi, a sharp thickening of the placental barrier occurs due to the accumulation of fields of collagen fibers and fibroblast processes in the basal layer.

The pathogenesis of the placental form of chronic PN consists of immaturity and progressive sclerosis of the stroma of small villi, reduction of their capillary network, local hypoxia, thickening of the placental barrier, severe diffusion disorders, development of chronic PN.

6. Hematogenous infection of the placenta with damage to the membranes (focal exudative-necrotic deciduitis), placenta (productive hypertrophic villusitis, basal productive deciduitis), umbilical cord (thrombvasculitis, exudative-necrotic funiculitis).

1) Acute disorders of the uteroplacental circulation.

ruptures, defects (size, quantity, location);

2) Acute disorders of the placental-fetal circulation.

Risk factors are hypoxic cardiopathy, encephalopathy.

Form: hyperplastic, hypoplastic, dysplastic, angiospastic.

I degree – minimal changes.

Quick involvement in pathological process The placental barrier explains the predominance of severe degrees of malnutrition of the fetus and newborn and the high level (40%) of perinatal losses.

During the first trimester, the most characteristic form of embryochorial insufficiency is the formation of a retrochorial hematoma, which causes the death of the embryo. Its pathogenesis is determined by the imperfection of hemostasis in this period of placental development, in particular the brush border of the syncytiotrophoblast. A clear immunomorphological marker of the brush border is placental alkaline phosphatase (PLAP).

Relief (smoothed, bumpy); without pathological changes;

Blood clots, heart attacks (structure, degree of organization).

Blood filling (anemia, moderate plethora, hyperemia, thrombosis).

MORPHO-FUNCTIONAL STATE OF THE AFTERMISSION:

SCHEME FOR DESCRIPTION OF THE PLACENTA OF A NEWBORN

manifestations of hematogenous infection (villusitis, intervillusitis);

Attachment (central, paracentral, marginal, shell)

These changes were recorded in almost all biopsies of placental tissue, i.e. were widespread in small placentas.

For the fetus – amniotic pneumonia, sepsis (taking into account viability)

Normoplastic type of placenta structure. Reactive changes in the placenta.

Shape (round, oval, irregular)

4.5 Morphofunctional basis of placental insufficiency

2nd degree (average volume of lesion, or subcompensated phase);

The decidua layer is compact, spongy, thin, pronounced,

Decidua (thin, thickened; compact, spongy), cellular infiltration (composition, severity), necrosis (structure, size, cellular reaction), hemorrhage (structure, size, cellular reaction).

The most striking histological signs of this form of chronic PN were large ischemic infarctions of varying duration, which histologically looked like total necrosis of groups of villi with surrounding hemorrhages in the intervillous space.

Traditional temporary approaches to the treatment of chronic PN from the moment when fetal malnutrition is detected (most often in the 3rd trimester) cannot be considered pathogenetic, since after the end of cytotrophoblast migration into the RA it is difficult to count on their gestational restructuring.

variant of embryonic villi, variant of immature intermediate villi, variant of mature intermediate villi, variant of chaotic sclerotic villi.

Hemorrhage (localization, severity - minor, moderate, extensive).

2) isolated placental form of chronic PN;

For the mother - UGI, endocervicitis, endometritis.

2) Placental form.

Option – minimal manifestations of ascending bacterial infection of the placenta (focal choriodeciditis), a reaction to normal microflora.

The first two are typical for the third trimester and will be discussed in the corresponding chapter.

cytolytic changes (focal, diffuse),

absent, insignificant (focal), pronounced (widespread).

Forms: paretic (placental shock), ischemic (cardiogenic shock).

A. Blastopathy and implantation pathology, including complications of multiple pregnancies, disturbances in the shape of the placenta and umbilical cord attachment.

LEVELS OF STUDY

vascular condition (blood filling, vasculitis),

E. Chronic placental insufficiency:

TBX vascularization (normal, decreased, increased);

leukocyte infiltration (focal, diffuse), accumulations of leukocytes in the submesodermal zone.

HISTOLOGICAL STUDY OF THE PLACENTA

3. COMPENSATORY REACTIONS (no, +, ++, +++):

II degree – changes of moderate severity

leukocyte infiltration (degree of severity, diffuse or focal),

B. Pathology of the placenta and initial organogenesis of the embryo.

IV degree – with death.

Number of vessels (3,2,4).

2 Complex A (micro -10 kus. IFLA, partial blood test)

Pathological changes - (edematous, cloudy, dull, colored).

3) Placental-fetal form.

B. Pathology of extraembryonic structures and initial histogenesis of the embryo.

Hemorrhages (location, size)

1 degree (minimal amount of changes, or compensated phase);

Amniotic membrane – edema (severity), adhesion (focal, diffuse), leukocyte infiltration.

Morphological criteria for acute and chronic placental insufficiency (Milovanov).

The structure of blood vessels (normal, pathological - hypoplasia, dysplasia, edema, leukocyte infiltration).

3. Chronic placental insufficiency:

Arteries with a slit-like lumen and hypertrophy of the internal, longitudinal layer of smooth muscles predominated in the umbilical cord. For the umbilical cord vein, lumen ectasia is more typical, often with blood clots. When examining biopsies of the placental bed, normal gestational changes or their partial absence in the uteroplacental arteries were revealed.

4. Acute placental insufficiency:

7. Chronic umbilical cord insufficiency caused by vascular dysplasia (arterial aplasia, varicose vein dysplasia, combined arteriovenous dysplasia).

Without pathological changes (thin, transparent, shiny)

Developmental anomalies (ridge, rim, accessory lobe, etc.)

Features of retrochorial hematoma.

COMPLIANCE OF THE PLACENTA WITH THE GESTATIONAL TERM (yes, no)

II. Placental insufficiency developing in the II and III trimesters:

D. Pathology of the placenta and late organogenesis, including spontaneous miscarriages and “frozen” pregnancies.

Violation of villi maturation (no, +, ++, +++):

3) predominantly fetoplacental form of chronic PN.

Newborns at risk (level 2)

Pathology of the placenta. 1) types of maturation disorders 2) causes and morphology of primary and secondary, acute and chronic failure placenta 3) their effect on the fetus 4) inflammation: types, nomenclature, morphology depending on the route of infection 5) the effect of inflammation on the fetus.
1) Types of maturation disorders:
1. Accelerated maturation of chorionic villi (usually in the last 8-10 weeks of pregnancy) with:
1) late gestosis in pregnant women
2) habitual miscarriage
3) long-term threat of miscarriage
4) chronic pyelonephritis
Morphology:
ü elongation of the villi and a decrease in their thickness with the formation of a typical villous tree with big amount terminal villi
ü there is no fibrosis of the stroma of old, centrally located villi and their transformation into stem ones
ü new peripherally located immature villi are formed
ü terminal and resorption villi are not formed
2. Slow maturation of chorionic villi with:
1) isosensitization by Rh factor
2) in some forms of diabetes mellitus
3) for a number of infectious diseases (syphilis, toxoplasmosis, etc.)
Morphology:
ü villi remain stromal and continue to grow and branch due to the formation of additional branches
ü large placenta with a small number of terminal villi
3. Dissociated maturation of chorionic villi - often associated with fetal congenital malformation or chronic villusitis.
Morphology: presence of villi different sizes, varying degrees maturity and vascularization
2) Placental insufficiency is a syndrome in which the placenta is not able to maintain adequate exchange between the mother’s body and the fetus.
a) Primary PN - occurs during the formation of the placenta during the period of implantation, early embryogenesis and placentation.
The reasons are various factors acting on the parents’ gametes, zygote, blastocyst, and developing placenta:
1. genetic
2. endocrine (for example, with enzymatic deficiency of decidual tissue due to ovarian dysfunction)
3. infectious
Morphology of primary PN:
ü anatomical changes in the structure, location, attachment of the placenta
ü vascularization defects and impaired chorion maturation
b) Secondary PN - caused by the action of exogenous factors on the formed placenta, usually in the second half of pregnancy. It can develop acutely or chronically.
1) Acute secondary PN:
ü premature detachment of a normally located placenta with the formation of a retroplacental hematoma
ü extensive circulatory disorders in the form of hemorrhages in the intervillous space, decidua, villous stroma
ü blood clots, fresh heart attacks, plethora, villous angiomatosis
2) Chronic secondary PN: develops early, at the beginning of the second half of pregnancy, and lasts a long time. It can be relative and absolute.
1. Relative chronic secondary PN:
A number of changes in the placenta:
a) compensatory (increase in the number of resorption and terminal villi, capillaries, functioning syncytial nodules, syncytiocapillary membranes)
b) involutive-dystrophic (increased amount of fibrinoid, narrowing of the intervillous space, villous fibrosis, vascular sclerosis, calcification of nodules)
c) inflammatory (not always)
d) circulatory (infarction, thrombosis, hyperemia, decrease in villous vascularization, hyperplasia of villous capillaries)
e) disruption of the maturation process of the chorion (accelerated, delayed, dissociated maturation)
f) often - hypoplasia of the placenta and its pathological immaturity
2. Absolute chronic secondary PN (the most severe form, develops against the background of impaired chorion maturation):
ü predominance of involutive-dystrophic processes
ü a sharp decrease in the rate of vascularization of villi (a large number of avascular villi)
3) Effect on the fetus various types Mon:
Primary PN:
Ø occurrence of non-developing pregnancy
Ø congenital malformations of the fetus
Ø threat of miscarriage or spontaneous abortion in early dates pregnancy
Secondary acute PN: fetal death and termination of pregnancy
Secondary relative chronic PN:
Ø compensatory-adaptive processes are preserved and even intensified, pregnancy can end in timely delivery of a viable healthy child
Ø possible developmental delay of the fetus, and in unfavorable obstetric situations - development of chronic fetal hypoxia and intrauterine death
Secondary absolute chronic PN:
Ø malnutrition and chronic hypoxia of the fetus up to its intrauterine death
Ø pregnancy against the background of threatened abortion or premature birth
4) Types of inflammation of the placenta:
a) the nature of inflammation in the placenta can be
ü exudative (usually serous-purulent, sometimes fibrinous or serous-hemorrhagic)
ü proliferative
b) along the way, inflammation in the placenta may be
ü sharp
ü chronic
Causes:
a) more often bacterial flora, less often viruses, fungi, mycoplasma, chlamydia, toxoplasma
b) change in pH amniotic fluid and other irritants (aseptic or sterile inflammation)
Nomenclature - according to the localization of inflammation:
Intervillesitis - inflammation in the intervillous space
1) subchorial intervillesitis - under the chorionic plate in the form of a strip of abundant accumulation of leukocytes and fibrin
2) central - away from the chorionic and basal plates
3) basal - localized directly above the basal plate.
Villusitis (from villus - villus) - inflammation of the villus
a) terminal
b) stem
Basal deciduitis is inflammation of the basal lamina.
Placental chorioamnionitis is inflammation of the chorionic plate.
Funiculitis - inflammation of the umbilical cord
Membraneitis (parietal amniochoriodeciduitis) - inflammation of the extraplacental membranes, if all three layers are involved in the inflammatory process (amnion, smooth chorion, true acadia)
Parietal chorioamnionitis (choriodeciduitis) - if two layers are affected.
Parietal amnionitis or deciduitis - when only one layer is affected.
Morphology depending on the route of infection.
a) ascending route - the pathogen from the vagina through the cervical canal penetrates into the amnion cavity, most often with early rupture of the membranes and discharge of water (infection is often intranatal or in the last hours of the antenatal period)
Inflammatory changes (so-called amniotic type of inflammation):
a) aqueous membrane (both parietal and placental)
b) chorionic plate of the placenta and its vessels
c) intervillous space adjacent to the chorionic plate
d) smooth chorion outside the placenta
e) sometimes - the adjacent falling membrane, as well as the umbilical cord
In the fetus, with an ascending route of infection, the following may be affected:
a) any areas of the skin surface and mucous membranes that come into direct contact with infected waters
b) respiratory tract, alveolar ducts, alveoli by aspiration
c) digestive tract (if swallowed)
b) hematogenous route of infection - the pathogen is introduced into the placenta from the mother’s blood through the spiral arteries of the placental membrane of the placenta or through the endometrial vessels in the true membrane of the placenta (more often infection is antenatal)
Inflammatory changes (so-called parenchymal type of inflammation):
a) intervillous space, without predominant localization under the chorionic plate
b) villi and their vessels
c) basal lamina of the placenta
d) true falling shell
In the fetus, there is damage to organs, especially those richly supplied with blood and not bordering the external environment - primarily the liver, adrenal glands, kidneys, spleen, etc.
c) descending route of infection - depends on which part of the placenta is adjacent to the opening of the fallopian tube
d) mixed routes of infection - the process often begins as an ascending or hematogenous one.
5) Consequences for the fetus:
ü absence of clinical manifestations (with limited chorioamnionitis)
ü intrauterine growth retardation (with perivillusitis)
ü development of infection in the fetus with damage to individual organs (with villusitis)
ü premature birth
ü infection of the fetus with the development of local and generalized purulent-inflammatory diseases of the fetus and newborn