Hematogenous Infection and Villitis
Inflammation of the placental villi—villitis—is the primary morphological indicator of hematogenous infection. Such lesions are most characteristic of viral etiologies. However, inflammation can also be caused by bacteria (Treponema pallidum, Listeria, Mycobacterium, Brucella, Chlamydia), parasitic infestations (Toxoplasma, Trypanosoma), and fungi.
Depending on the extent of the process, villitis is classified as focal or diffuse (which can be total, generalized, or segmental). By the nature of the inflammatory response, it is categorized as exudative (most commonly purulent) and productive, frequently accompanied by marked alterative changes. The outcome of chronic inflammation is fibrosis of the villous stroma accompanied by obliteration of fetal blood vessels.
In clinical practice, villitis is extremely dangerous: it serves as a direct source of fetal infection and often leads to intrauterine fetal death due to bilateral infectious involvement (affecting both maternal and fetal organisms) and impaired placental function.
Anomalies of Shape and Insertion
A normal placenta has a round or oval disc shape. Structural anomalies include placenta membranacea (diffuse placenta), placenta fenestrata (fenestrated placenta), annular placenta, bilobate or multilobate placenta, and circumvallate placenta. An atypical shape alone usually has no clinical significance, but it can occasionally provoke antepartum hemorrhage and abnormal umbilical cord insertion.
Pathologies of placental localization pose a particular threat:
- Placenta previa: The embryo implants in the lower uterine segment, causing the placenta to completely or partially cover the internal cervical os. It occurs in 0.2–0.9% of pregnancies (partial previa is more frequent). In the second half of gestation, this causes uterine bleeding. With complete previa, vaginal delivery poses a severe threat to the woman's life.
- Placenta accreta: Develops due to the absence or significant thinning of the decidua basalis. Villi firmly attach to the myometrium, invading the superficial layers or the entire thickness of the uterine wall. Following delivery, the placenta fails to separate spontaneously, triggering massive hemorrhage. This condition is frequently associated with placenta previa and results in uterine rupture in 14% of cases. It requires manual removal and sometimes hysterectomy.
Placental Circulation Disorders
Blood flow disorders can result from dysfunctions in either the maternal or fetal vascular networks. Sometimes they are detected even in uncomplicated pregnancies, but their frequency and severity increase significantly in preeclampsia, chronic hypertension, and other extragenital pathologies.
Impaired blood circulation leads to inadequate oxygen supply to the fetus. This carries the risk of acute or chronic intrauterine hypoxia, intrauterine growth restriction (IUGR), and fetal demise.
The most important types of circulatory disorders include:
- Placental infarction (identified histologically using hematoxylin and eosin staining).
- Intervillous space thrombosis.
- Retroplacental hematoma.
Note: Impairment of blood flow within the intervillous space is a key factor in disrupting fetal oxygenation. Nevertheless, the placenta possesses a robust reserve capacity: involvement of up to 10–15% of the villi can be entirely 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 (possessing an elastic membrane), whereas the arteries carry deoxygenated blood away from the fetus (lacking an elastic membrane).
The vessels are surrounded by a resilient gelatinous tissue—Wharton's jelly (composed of a mucoid substance and a network of fibroblasts), which protects them against compression and stretching.
Key umbilical cord pathologies:
- Single umbilical artery (aplasia of one vessel): occurs in ~1% of cases, frequently associated with congenital malformations and intrauterine growth restriction.
- Short umbilical cord (less than 32 cm): limits fetal movement, and severe tension during labor can disrupt blood flow or cause placental abruption.
- Long umbilical cord (greater than 70 cm): increases the risk of nuchal cord, true knots, and cord prolapse during labor, leading to vascular compression and hypoxia.
- Vascular thrombosis: arises from blood flow disruption (due to knots or nuchal cord) or inflammation of the cord. Occlusive thrombi most commonly affect the umbilical vein and frequently result in intrauterine death from acute hypoxia.