Placental pathology

Mechanisms of placental insufficiency development

Chronic placental insufficiency (PI) is based on three fundamental microscopic failures:

1. Failure of the first wave of trophoblast migration. Occurs in the first trimester. Uteroplacental blood flow forms with a delay, leading to necrotic lesions of the placental bed.
2. Defective invasion of the extravillous chorion. Spiral arteries do not remodel completely—changes affect the decidual segments, but bypass the myometrial ones. As a result, the vessels continue to respond to vasoconstrictive stimuli. The resulting spasm disrupts blood flow, causing hypoplasia of the placenta (placenta).
3. Abnormal villous differentiation. Villi mature unevenly and slowly. Because of this, syncytiocapillary membranes form incorrectly, which critically undermines the placenta's ability to nourish the fetus and supply it with oxygen.

Fetal growth restriction (FGR) as a consequence of dysfunction

Impaired placental function inevitably affects the child. There are two main clinical and pathogenetic forms of FGR:

• Symmetrical form. Starts in early gestation. Most often triggered by genetic abnormalities (e.g., trisomies 13, 18, 21, or monosomies), intrauterine infections (in utero — rubella, toxoplasmosis, herpes, syphilis), and severe toxic exposures, including maternal smoking, alcohol, and poor nutrition.
• Asymmetrical form. Develops in the third trimester. This is a classical consequence of chronic PI. It is caused by maternal extragenital diseases (bronchial asthma, hypertension, autoimmune processes), preeclampsia, and multiple pregnancy.

Compounding factors: myoma and anemia

Placental formation and attachment are often complicated by underlying maternal conditions.

Uterine myoma occurs in 0.5–2.5% of pregnant women. If the placenta forms over an intermuscular (interstitial) node, the risk of PI increases sharply. In addition, myoma increases the likelihood of premature placental abruption, abnormal placental attachment, and fetal malpresentation. The tumor itself may enlarge, become edematous, or undergo necrosis during gestation.

Iron deficiency anemia (IDA) is another potent trigger of placental complications, detected in a third of patients. Iron deficiency (against a normal requirement of 7 mg per day) provokes not only PI, but also polyhydramnios, uterine inertia, preterm labor, and hemorrhage.

Multiple pregnancy and nutritional status

Multiple pregnancy is a serious challenge for the uteroplacental complex. Carrying twins involves specific types of placentation that require careful ultrasound monitoring. Multiple pregnancy itself is a risk factor for asymmetrical FGR and preeclampsia.

Maternal nutritional status is critically important for maintaining placental function. The demand for micronutrients increases enormously due to the transfer of substances to the fetus and accelerated metabolism. In the second half of gestation, fractional nutrition is required (5–6 times a day) focusing on protein (lean meat, fish, cottage cheese) and mandatory compensation for deficiencies in folic acid, iodine, magnesium, and zinc. Ignoring these rules leads to morphofunctional immaturity of the newborn.

Class and exam questions

What else to study on this topic

• Ultrasound diagnosis of multiple pregnancy and placentation anomalies.
• Specific complications and obstetric management in monozygotic and dizygotic twins.
• Isthmic-cervical insufficiency associated with cervical-isthmic myoma.
• Principles of diet therapy and nutritional support for the prevention of placental disorders.
• Intranatal complications and indications for cesarean section in multiple pregnancies.

Other topics in the "Obstetrics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.