Placental infarction is necrosis of placental tissue caused by a violation of its blood supply. With large areas of damage, it is manifested by a change in the frequency and intensity of fetal movements, bloody discharge from the vagina. When making a diagnosis, data from ultrasound of the uterus, dopplerography of placental blood flow, CTG and phonocardiography of the fetus, laboratory tests are used. The treatment regimen for placental infarction includes etiotropic agents for the correction of the underlying pathology, vasodilators, tocolytic, antihypoxic, antioxidant drugs. Pregnancy is terminated in exceptional cases when there is a threat to the fetus or the woman.
According to experts, intervelous thrombosis and placental infarctions are observed in 25-30% of pregnant women, but only some of them develop fetoplacental insufficiency. The physiological functioning of the placenta is a necessary condition for the full provision of oxygen and nutrients to the fetus, the excretion of its metabolic products. Theoretically, a placental infarction (necrosis), like any other damage to the baby’s place, can pose a threat to the development of the child. However, the compensatory capabilities of the placental tissue ensure adequate operation of the mother-fetus system even with the death of up to 10% of the organ. The probability of pathological disorders with damage to the placenta increases with increasing age of a woman, especially if we are talking about the first pregnancy.
Necrotic changes in placental tissue usually result from local hemodynamic disorders. Thus, diseases and disorders that affect the state of the endothelium, the tone and fragility of the vascular wall, the blood clotting system lead to a heart attack. According to the observations of specialists in the field of obstetrics and gynecology, the most common causes of placental infarction are:
- Prolonged spasm of the spiral arteries. An increase in vascular tone in the placental blood flow system is observed in pregnant women with hypertension, gestosis, symptomatic arterial hypertension in kidney diseases (diffuse glomerulonephritis, chronic pyelonephritis, amyloidosis, hypoplasia, polycystic), congenital and acquired heart and aortic defects, brain tumors, pheochromocytoma, aldosteroma, and other endocrinopathies. Over time, tonic vasoconstriction is aggravated by a decrease in their elasticity and the deposition of insoluble compounds on the walls.
- Damage to the endothelial membrane. Violation of the integrity of the inner layer of the vascular wall increases its adhesive properties, provokes the onset of microthrombosis and sclerosis. Such disorders are characteristic of patients with insulin–dependent, insulin-independent and gestational diabetes, generalized vasculitis, autoimmune processes, including those caused by chronic endometritis. Pronounced capillarotoxicosis develops in a number of infectious diseases: acute sore throat, measles, scarlet fever, chickenpox, herpes, chlamydia, toxoplasmosis, cytomegalovirus infection.
- Hypercoagulation of blood. Chronometric hypercoagulation that occurs in the second trimester of pregnancy is a variant of the norm that prevents significant blood loss during childbirth. Pathological high blood clotting is noted with an increase in the content and activity of procoagulants in patients with thrombocytosis, hyperprothrombinemia. The effect of anticoagulant factors is disrupted in the case of shock, sepsis, large burns, DIC syndrome. Thrombophilia is one of the clinical manifestations of antiphospholipid syndrome (AFS), hyperhomocysteinemia and a number of hereditary fermentopathies.
- Embolism of placental vessels. Infarcts develop with sudden blockage of the vessel by various foreign substances, which are normally absent in the bloodstream. The causes of embolism are detached blood clots with varicose veins and thrombophlebitis of the lower extremities, adipose tissue with extensive fractures of the femur and other large tubular bones, tissue of damaged organs with massive injuries or tumor decay. The ingress of air bubbles into the bloodstream is possible if some invasive medical manipulations (intravenous injections, infusion infusions) are performed incorrectly.
Additional provoking factors for the onset of necrotic processes in the placenta are smoking, physical and psycho-emotional stress, overweight. Nicotine has a damaging effect on the vascular endothelium and increases spasm of peripheral vessels. The negative effect of stress and obesity is associated with a possible increase in blood pressure and blood glucose levels.
The starting point of a placental infarction is the cessation of normal blood supply to placental tissue. Violation of blood flow can be acute (blockage in thromboembolism, thrombosis of the vascular bed in DIC syndrome, rupture of the vessel) or gradually increasing (gradual obstruction of the lumen with sclerosis of the vascular wall in diabetes, hypertension, gestosis, etc.). Violation of local blood supply activates anaerobic mechanisms of glycolysis. Depletion of internal reserves of cells leads to their oversaturation with toxic metabolites and death (necrosis). After some time, the dead areas undergo lysis and gradual replacement with connective tissue. Absorption into the blood of the products of destruction of placental tissue in massive heart attacks can provoke general intoxication of the body and aggravate the course of the underlying disease.
When systematizing various forms of placental infarction, factors such as pathophysiological changes occurring in the necrosis zone, the size and localization of the affected area, the number of foci of tissue death are taken into account. Small marginal infarcts are one of the signs of physiological aging of the placenta, large single foci located in the thickness of the organ usually occur in the presence of predisposing disorders. According to the mechanism of formation , infarcts are distinguished:
- Red. Placental tissues are soaked with blood coming from one or more maternal vessels of the decidual membrane. They are usually an early stage of acute heart attacks, in the absence of premature termination of pregnancy, they turn into a white form.
- White. The affected area has a light grayish or yellowish color, characteristic of ischemic tissues. Such necrosis develops against the background of gradual blockage of blood vessels and deposition of fibrin filaments or becomes the final stage of red heart attacks.
- Calcareous. The necrosis site is calcified, contains white solid inclusions. Infarcts of this type usually form gradually as the placenta ages or against the background of sclerosis of spasmodic vessels, on the damaged endothelium of which calcium is deposited.
The clinical picture of necrosis of the child’s place depends on the size of the ischemia zone and the number of damaged areas. Single marginal infarcts of small size are asymptomatic, often regarded as a variant of the norm. If a heart attack is caused by a rupture of a large vessel in the central part of the placenta, a limited hematoma is usually formed. In this case, there may be painful sensations in the uterus, during long periods of pregnancy, when the placenta is located on the anterior uterine wall, it is sometimes possible to feel a dense formation. Rupture of peripheral vessels leads to the development of uterine bleeding. However, usually with placental necrosis, there are no pronounced symptoms, it is possible to suspect pathology only by changing the activity of the fetus due to oxygen starvation. A prognostically unfavorable sign is a sudden sharp increase in the child’s movements with its subsequent fading for 6 or more hours.
Placental infarction poses the greatest threat to the fetus. Its most common consequence is fetoplacental insufficiency with hypoxia, fetal development delay and even stillbirth. The first signs of insufficient supply of oxygen and nutrients appear in the presence of multiple microinfarcts up to 3 cm in diameter and extensive damage to more than 15% of placental tissue. If the necrosis area exceeds 30%, the condition is assessed as threatening to the fetus and requires urgent medical care.
The long-term consequences of AF, which arose against the background of placental necrosis, are considered to be an increased risk of asphyxia by amniotic fluid during childbirth, delays in mental and speech development, hyperexcitability of the child, and other neurological disorders. In addition to fetoplacental insufficiency, a heart attack can provoke premature placental abruption and massive bleeding. In rare cases, the death of large areas disrupts the endocrine function of the organ, and a decrease in the secretion of estrogens, placental lactogenic hormone, chorionic gonadotropin leads to weakness of labor, hypotonic bleeding in childbirth, hypogalactia in the postpartum period.
When signs of fetoplacental insufficiency or spotting spotting from the vagina appear in a woman predisposed to vascular and thrombotic disorders, the diagnostic search is aimed at assessing morphological processes in the tissues of the placenta and the functional state of the child. The survey plan includes the following methods:
- Ultrasound of the uterus and fetus. Sonography makes it possible to identify the infarction zone, which usually has the form of multiple small or single extensive hyperechoic inclusions with clear contours. The study also determines the compliance of fetometric indicators with the term of pregnancy
- Cardiotocography and phonocardiography of the fetus. The methods are aimed at obtaining data on the heart activity of the child. A possible placental insufficiency as a consequence of a heart attack is indicated by a change in the rhythm and frequency of heart contractions — tachycardia, bradycardia, arrhythmia.
- Dopplerography of uteroplacental blood flow. Doppler examination provides an objective assessment of the features of blood circulation in the placenta and reveals the absence of pulsation in the vessels during tissue necrosis. The method has diagnostic value in the second half of pregnancy.
- Laboratory blood tests. In the general analysis, taking into account the underlying pathology, there may be a reduced or increased platelet count, erythropenia and a decrease in hemoglobin levels. During the study of the hemostasis system, thrombin time, APTT and a number of other indicators were changed.
Additionally, to clarify the causes that caused necrotic disorders in the placenta, a biochemical blood test, diagnosis of the immune status, studies to determine the causative agents of infectious diseases (ELISA, PCR) are prescribed. Differential diagnosis is carried out with severe forms of gestosis, premature placental abruption, isoserological incompatibility of maternal and fetal blood, chorioamnionitis and other causes of fetoplacental insufficiency. According to the indications, the patient is examined by an endocrinologist, an infectious disease specialist, an immunologist, a cardiologist, a urologist.
In the presence of signs of hypoxia and fetal growth retardation, therapeutic measures are aimed at eliminating the causes that led to necrosis of the child’s place, and compensating for disorders in the fetoplacental system. If there is no threat to the life of the fetus and the pregnant woman, complex conservative therapy is recommended. Emergency delivery in the form of stimulation of premature birth or cesarean section is performed only for vital indications. The standard scheme of management of pregnant women involves solving the following tasks:
- The effect on the etiological factor. Taking into account the nosology complicated by placental necrosis, hypotensive, hypoglycemic, antibacterial, hormonal agents, immunocorrectors are used. In case of violations in the hemostasis system, anticoagulants, antiplatelet agents and other drugs that affect blood clotting are prescribed. A specialist of the appropriate profile is involved in the selection of medicines for the treatment of the underlying disease.
- Stabilization of the uteroplacental system. To improve the perfusion of nutrients and oxygen in the intact part of the placenta, agents with a vasodilating effect, low doses of tocolytics are used. Effective drugs that improve blood rheology and microcirculation. To increase the resistance of the fetus to hypoxia, actovegin is used, antioxidants, the appointment of which reduces the likelihood of brain damage.
Prognosis and prevention
In most cases, the prognosis for placental infarction is favorable. Small areas of necrosis do not affect the development of the child, and timely diagnosis and adequate treatment for large lesions can prevent or minimize the possible consequences of pathology. For preventive purposes, pregnant women from the risk group are recommended to register in a women’s clinic in a timely manner, regular visits to an obstetrician-gynecologist and ultrasound screenings, careful implementation of recommendations for the treatment of concomitant pathology. An important role in the prevention of infarction of a children’s place is played by smoking cessation, diet, normalization of sleep and rest.