Hematogenous infection and villitis
Inflammation of the placental villi — villitis — is the primary morphological indicator of hematogenous infection. This type of lesion is most characteristic of viruses. However, inflammation can also be caused by bacteria (
Based on the prevalence of the process, villitis is divided into focal and diffuse (which may be total, generalized, or segmental). According to the clinical course, exudative inflammation (most commonly purulent) and productive inflammation are distinguished, frequently accompanied by marked alterative changes. The outcome of chronic inflammation is sclerosis of the villous stroma with obliteration of fetal blood vessels.
In clinical practice, villitis is extremely dangerous: it acts as a direct source of fetal infection and frequently leads to intrauterine fetal death due to bilateral infectious involvement (of both maternal and child organisms) as well as impaired placental function.
Anomalies of shape and insertion
A normal placenta has a round or oval disc shape. Structural anomalies include diffuse placenta (placenta membranacea), fenestrated placenta (placenta fenestrata), annular placenta, bilobate and multilobate placenta, as well as circumvallate and circummarginate placenta. An atypical shape alone is of no clinical significance in most cases, but it can occasionally provoke antepartum hemorrhage and umbilical cord insertion anomalies.
Localization pathologies pose a particular threat:
- Placenta previa (placenta previa): the embryo implants in the lower uterine segment, causing the placenta to completely or partially cover the internal os. It occurs in 0.2–0.9% of pregnancies (partial previa being more common). In the second half of gestation, this causes uterine bleeding. With complete previa, unassisted vaginal delivery poses a severe threat to the woman's life.
- Placenta accreta (placenta accreta): develops against the background of the absence or significant thinning of the basal decidua. The villi firmly attach to the myometrium, growing into the superficial layers or through the entire thickness of the wall. After delivery, the placenta does not separate spontaneously, and severe bleeding begins. The condition is frequently combined with placenta previa and leads to uterine rupture in 14% of cases. It requires manual removal and sometimes hysterectomy.
Placental circulatory disorders
Blood flow disorders can be caused by disruptions in both the maternal and fetal vascular networks. Sometimes they are detected even in normal pregnancies, but their frequency and severity increase significantly in preeclampsia, hypertension, and other extragenital pathologies.
Impaired blood circulation leads to inadequate oxygen supply to the fetus. This is fraught with acute or chronic intrauterine hypoxia, intrauterine growth restriction (IUGR), and even fetal death.
The most important types of disorders include:
- Placental infarction (histologically detected with hematoxylin and eosin staining).
- Intervillous space thrombosis.
- Retroplacental hematoma.
Note: it is the disruption of blood flow in the intervillous space that is the key factor in the failure of fetal oxygen supply. Nevertheless, the placenta possesses a robust reserve: damage to up to 10–15% of the villi may be completely asymptomatic.
Umbilical cord pathology
The average length of a normal umbilical cord is 59 cm. It contains three vessels: one umbilical vein and two arteries. The vein transports nutrient- and oxygen-rich arterial blood from the placenta to the fetus (it has an elastic membrane), while the arteries carry venous blood away from the fetus (they lack an elastic membrane).
The vessels are surrounded by an elastic gelatinous tissue — Wharton's jelly (composed of a mucoid substance and a network of fibroblasts), which protects them from compression and stretching.
Important umbilical cord pathologies:
- Single umbilical artery (aplasia of one of the vessels): occurs in ~1% of cases, often combined with congenital malformations and intrauterine growth restriction.
- Short umbilical cord (less than 32 cm): restricts fetal movements, and during labor, strong tension can disrupt blood flow or cause placental abruption.
- Long umbilical cord (more than 70 cm): increases the risk of nuchal cord, true knots, and prolapse of the cord loops during labor, leading to vascular compression and hypoxia.
- Vascular thrombosis: arises due to blood flow disruption (in cases of knots or nuchal cord) or inflammation of the cord. Occlusive thrombi most commonly affect the umbilical vein and frequently lead to intrauterine death from acute hypoxia.
Briefly: answers to topical questions
What grades of placenta accreta are distinguished depending on the depth of villous invasion?
Depending on the depth of invasion, three degrees of invasive placenta are distinguished:
- Accreta — adhesion to the myometrium.
- Increta — invasion into the myometrium.
- Percreta — perforation through the myometrium.
What are the clinical and morphological stages of placental insufficiency?
According to severity, three forms of chronic placental insufficiency are distinguished: compensated, subcompensated, and decompensated.
- Compensated form — moderate involutional and dystrophic changes in the placenta are combined with significant compensatory-adaptive reactions, including villous vascularization and the development of syncytiocapillary membranes. Initial isolated circulatory disorders are detected; initial signs of fetal hypoxia may be determined; fetal growth restriction is absent or minimal.
- Subcompensated form.
- Decompensated form.
To avoid confusion with vascular physiology, remember that in the umbilical cord they operate "in reverse" relative to the maternal organism: the single vein carries arterial blood to the fetus, and the two arteries carry venous blood away from it.
What else to study on this topic
- Spontaneous abortions: etiology, pathogenesis, and morphological changes
- Ectopic pregnancy: classification and morphological characteristics
- Preeclampsia: theories of development, impact on the fetus, and morphology of the mother-placenta-fetus system
- Trophoblastic disease: forms, clinical significance, and manifestations
Master the entire topic in the "Pathological Anatomy" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Placental Pathology" and 4,414 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 153 video lessons on the subject
Other topics in "Chapter 21. Pathology of Pregnancy"
The entire section «Chapter 21. Pathology of Pregnancy»Free video lessons: pathological anatomyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.