Classification and causes
By time of onset, two main forms of the syndrome are distinguished:
- Primary: starts before 16 weeks of gestation. Based on endogenous factors (genetics, infections, endocrinopathies) that disrupt normal chorionic villi differentiation and angiogenesis.
- Secondary: occurs after 16 weeks against the background of an already formed organ. Exogenous causes are to blame: maternal extragenital pathologies and obstetric complications affecting blood flow.
Important: the primary form can transition into the secondary form, and secondary PI itself often develops due to subclinical processes established early on.
Pathogenesis: where does the system break?
Placental insufficiency is based on three fundamental failures:
- Blockade of the first wave of endovascular trophoblast migration (in the 1st trimester). Result: delayed formation of the uteroplacental bed and necrotic changes in the placental bed.
- Defect of extravillous chorion invasion. Spiral arteries do not undergo complete gestational remodeling (especially in myometrial segments). They retain their muscular layer and ability to spasm in response to vasoconstrictors, leading to placental hypoplasia.
- Impaired villous differentiation. Villi mature unevenly, and vasculosyncytial membranes fail to form properly. Gas exchange and trophic functions drop critically.
Stages of chronic placental insufficiency
The chronic form has a prolonged course and develops in the second half of pregnancy. Three severity stages are distinguished:
| Grade | Placental morphology | Dopplerometry | Fetal condition (Ultrasound and CTG) |
|---|---|---|---|
| Compensated | Moderate dystrophy, robust compensation (vascular growth) | Isolated blood flow disorders | No FGR or grade I, initial hypoxia |
| Subcompensated | Pronounced dystrophy, membrane thickening | Combined disorders (mother–placenta–fetus) | Grade I–II FGR, oligohydramnios, moderate hypoxia |
| Decompensated | Villous sclerosis, vascular reduction, weak compensation | Critical blood flow, centralization | Grade III FGR, oligohydramnios, pronounced hypoxia |
Fetal growth restriction (FGR)
Fetal growth restriction is the main clinical companion of placental insufficiency. According to fetometry, three forms are distinguished:
- Symmetrical: proportional reduction of all body dimensions. Established in early gestation due to chromosomal abnormalities, intrauterine infections (TORCH complex), or severe toxic effects.
- Asymmetrical: only the fetal abdominal size lags behind. Typical for the 3rd trimester against the background of chronic hypoxia (preeclampsia, maternal hypertension, autoimmune processes).
- Mixed: disproportionate lag of all parameters, but with a predominant reduction in abdominal dimensions.
Risk factors
The development of PI and FGR is triggered by a wide spectrum of factors:
- Socio-demographic: maternal age (under 18 or over 30 years), heavy physical labor, psycho-emotional stress, smoking, alcohol, and malnutrition.
- Extragenital: heart, kidney, and lung diseases, diabetes mellitus, and blood system pathologies.
- Obstetric and gynecological: uterine myoma, genital malformations, history of infertility, as well as complications of the current pregnancy (preeclampsia, multiple pregnancy, threatened abortion, thrombophilias).
Briefly: answers to topical questions
Which specific TORCH infections most frequently cause symmetrical fetal growth restriction?
Symmetrical fetal growth restriction is caused by the following intrauterine infections included in the TORCH complex:
- Toxoplasma (Toxoplasma gondii) — the causative agent of toxoplasmosis.
- Rubella virus (Rubella virus) — the causative agent of rubella.
- Cytomegalovirus (Cytomegalovirus) — the causative agent of cytomegalovirus infection, which is the most frequently detected condition.
- Herpes simplex virus (Herpes simplex virus) — the causative agent of herpesvirus infection.
Syphilis, which belongs to the group of other infections in this complex, is also among the causes of the symmetrical form.
How does the level of synthesized hormones change in placental insufficiency?
In placental insufficiency, the level of placental lactogen in the pregnant woman's blood decreases. This protein hormone is synthesized exclusively in the placenta, enters the maternal bloodstream, and participates in her carbohydrate and lipid metabolism. A low level of placental lactogen is a marker of placental insufficiency.
What drugs are used for the medical treatment of compensated placental insufficiency?
Currently, there is no effective medical treatment for placental insufficiency. However, complex therapy includes drugs with vasoactive action:
- Antiplatelet agents — improve microcirculation in the placenta, increase prostaglandin I₂ synthesis, and reduce platelet activation and aggregation.
- Low-molecular-weight heparin preparations — are of great importance in patients with thrombophilias (timing and duration are selected individually).
What are the indications for emergency premature delivery in placental insufficiency?
Indications for emergency premature delivery in placental insufficiency and concomitant fetal hypoxia are:
- Inefficacy of therapy for pronounced chronic fetal hypoxia.
- Onset of acute fetal hypoxia.
- Grade III fetal growth restriction.
- Lack of growth in fetometric parameters for 2 weeks and worsening oligohydramnios.
- Impaired fetal condition (decompensated form of placental insufficiency with centralization of blood circulation).
To remember IUGR forms: Symmetric — Start of pregnancy (early onset, genetics/infections, whole body is affected). Asymmetric — Abstetrical/placental issues (late onset, only the abdomen suffers due to blood flow redistribution).
Class and exam questions
What is the difference between acute and chronic placental insufficiency?
Acute onset occurs suddenly due to catastrophic events (placental abruption, placental infarction, uterine rupture). Chronic develops slowly in the second half of pregnancy, against the background of maternal diseases or gestational complications.
What is centralization of fetal circulation?
This is a protective reaction in decompensated hypoxia, where blood is redirected to vital organs (brain, heart) to the detriment of peripheral tissues.
Why does the failure of spiral artery remodeling cause hypoxia?
When chorionic invasion is defective, the arteries do not lose their muscular layer. They retain the ability to spasm, which chronically reduces maternal blood flow to the placenta.
What else to study on this topic
- Hydatidiform mole: complete and partial (genetics, morphology, and pathogenesis)
- Invasive mole and risks of developing malignant trophoblastic tumors
- Diagnostics of gestational trophoblastic disease (the role of β-hCG, ultrasound, and theca-lutein cysts)
- Management tactics and monitoring of patients after vacuum aspiration of a hydatidiform mole
- Impact of specific TORCH infections on the development of symmetric IUGR
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