The placenta is a temporary organ that provides oxygen and nutrients to the developing fetus while removing waste products. When a portion of this organ experiences a lack of blood flow, the resulting tissue damage is known as placental infarction. This condition is a localized area of ischemic necrosis, or tissue death, caused by an interruption of the maternal blood supply. The severity depends heavily on the extent and location of the damaged tissue.
Understanding Placental Infarction
Placental infarction represents a localized area of ischemic necrosis within the villous tree, the functional unit of the placenta where nutrient and gas exchange occurs. The primary mechanism involves the occlusion of maternal spiral arteries that supply blood to the intervillous space. This blockage starves the downstream placental tissue of oxygen and nutrients, leading to cell death.
Small, isolated infarctions, especially those located at the periphery, are common findings in up to 25% of uncomplicated term pregnancies and are typically not clinically significant. However, large or multiple infarctions, particularly those affecting more than 10% to 15% of the placental mass, indicate substantial compromise. These widespread infarctions significantly reduce the functional capacity of the placenta, which can impact fetal well-being.
The distinction between different types of infarctions is based on their location and extent. Infarctions are classified as segmental when they affect a distinct region supplied by one or more spiral arteries. Central infarctions, occurring deep within the placental disc, are generally more concerning than marginal infarctions found at the edge. The infarcted tissue appears as a firm, pale, or white area on gross examination due to the loss of blood flow.
Identifying Contributing Factors
The underlying cause of placental infarction is often a failure in the normal vascular adaptation process of pregnancy, broadly termed maternal vascular malperfusion (MVM). During a healthy pregnancy, the maternal spiral arteries are remodeled into wide, low-resistance vessels to ensure high blood flow to the placenta. When this remodeling is defective, the arteries remain narrow, high-resistance vessels, leading to inadequate blood supply.
Maternal conditions that cause poor blood flow and endothelial damage are strongly associated with placental infarction. Chronic hypertension and preeclampsia are primary factors, as the high pressure damages the blood vessels supplying the placenta. The severity of placental infarction often correlates with the severity of the hypertensive disorder.
Autoimmune disorders and clotting abnormalities also contribute to the risk by promoting thrombus formation within the spiral arteries. Conditions such as antiphospholipid syndrome or inherited thrombophilias can increase the likelihood of blood clots forming, which then block the maternal blood flow. These underlying vascular and clotting issues create the ischemic environment.
Impact on Fetal and Maternal Health
When placental infarction affects a substantial portion of the organ, the reduced surface area for exchange results in placental insufficiency, which directly impacts the fetus. One frequent consequence is intrauterine growth restriction (IUGR), where the fetus fails to reach its growth potential due to insufficient nutrient supply. This restricted growth places the fetus at risk for complications both during and after birth.
A significant infarction can also lead to decreased blood flow to the fetus, triggering a redistribution of fetal circulation to preserve oxygen supply to the brain. This adaptive response can result in decreased renal perfusion, often leading to oligohydramnios, a reduction in amniotic fluid volume. Oligohydramnios further complicates the pregnancy by raising the risk of umbilical cord compression and developmental issues.
In the most severe cases of extensive placental damage, the fetus faces elevated risks of stillbirth or perinatal death. The association between placental infarction and preeclampsia also extends to maternal health, as women with severe placental malperfusion are at an increased risk of developing severe preeclampsia. A history of placental infarction is also a marker for an increased risk of recurrence in future pregnancies, signaling a potential underlying maternal predisposition to vascular dysfunction.
Monitoring and Management Strategies
There is no intervention that can reverse or cure infarcted placental tissue once the damage has occurred. Therefore, the management strategy focuses on vigilant monitoring of fetal well-being and managing any associated maternal conditions. Diagnosis is often made incidentally during routine prenatal ultrasound examinations, where the infarcted areas may be visualized as masses or regions of altered echogenicity.
Doppler velocimetry of the umbilical artery is a primary surveillance tool used to assess blood flow resistance in the fetal-placental circulation. Abnormal Doppler findings, which indicate increased resistance due to placental compromise, alert clinicians to the need for intensified monitoring. This non-invasive assessment helps determine the degree of placental dysfunction and guides subsequent decision-making.
Ongoing fetal surveillance involves frequent non-stress tests (NSTs) and biophysical profiles (BPPs). The NST assesses the fetal heart rate response to movement, while the BPP evaluates parameters including fetal breathing, movement, tone, and amniotic fluid volume. If these tests indicate progressive fetal compromise, such as a BPP score falling below 6, the decision to proceed with delivery becomes a consideration. The timing of delivery is a delicate balance between the risks of prematurity and the risk of continued deterioration in the compromised intrauterine environment.