Placental infarction occurs when an area of placental tissue dies due to a lack of blood supply. This can happen at any point during pregnancy. The placenta is an organ that develops in the uterus, and its proper function is important for a healthy pregnancy, as it delivers necessary resources to the developing fetus.
Understanding Placental Infarction
The placenta is a temporary organ that forms in the uterus during pregnancy, connecting the mother and the developing fetus. This specialized organ facilitates the exchange of oxygen and nutrients from the mother to the baby, while also removing waste products like carbon dioxide from the baby’s blood. It functions as a barrier, protecting the fetus from some harmful substances and infections, while also producing hormones that support the pregnancy and fetal growth.
An infarction occurs when a blockage in the blood vessels interrupts blood supply to a part of the placenta, causing tissue to die. Small placental infarcts, particularly those at the edge of the placental disc, are sometimes considered a normal finding at term in about a quarter of all pregnancies. However, larger or more extensive infarcts can indicate underlying issues and may compromise the placenta’s ability to function properly.
Factors Contributing to Placental Infarction
Several factors can increase the likelihood of placental infarction, primarily conditions that impair blood flow to the placenta. Preeclampsia, a pregnancy complication characterized by high blood pressure and potential organ damage, is a risk factor. Chronic hypertension, or high blood pressure existing before or developing early in pregnancy, also contributes to the risk by potentially damaging the arteries that supply the placenta.
Maternal thrombophilias, which are conditions that increase the risk of blood clot formation, can lead to placental infarcts by obstructing blood vessels within the placenta. Autoimmune diseases, such as systemic lupus erythematosus, have been linked to an increased risk of preeclampsia and, consequently, placental infarction. Certain genetic factors may also play a role by affecting the normal formation and function of placental blood vessels.
Additional factors include smoking and drug use, which can negatively impact placental blood flow and development. Gestational diabetes and fetal infections are also recognized as potential causes for placental infarction. Advanced maternal age and having given birth multiple times (multiparity) are also considered risk factors that can impair blood flow to the placenta or promote clot formation within its vessels.
Implications for Pregnancy and Fetal Health
The consequences of placental infarction for both the mother and the fetus vary considerably, depending on the size, location, and timing of the infarction. Small infarcts, especially those located at the periphery of the placenta, often have no significant clinical impact and are found in approximately 25% of uncomplicated pregnancies. However, larger infarcts, particularly those involving more than 10-15% of the placental tissue, can lead to more serious complications.
For the developing fetus, extensive placental infarction can compromise the supply of oxygen and nutrients, potentially leading to fetal growth restriction, also known as intrauterine growth restriction (IUGR). This condition means the fetus is not growing at a normal rate. Severe or early-onset infarctions, especially those involving a substantial portion of the placenta (e.g., over 50%), may result in reduced amniotic fluid (oligohydramnios), fetal distress, or, in severe cases, stillbirth.
The mother may also experience implications, including an increased risk of developing pregnancy-induced hypertension or preeclampsia. Placental infarction has also been associated with an increased risk of preterm labor, which is labor that begins before 37 weeks of gestation. While many cases of placental infarction are mild with no significant impact, close monitoring helps identify potential risks and guide management decisions.
Detecting and Addressing Placental Infarction
Placental infarction is often diagnosed incidentally after birth through a pathological examination of the placenta. During pregnancy, it may be suspected if complications like fetal growth restriction or reduced fetal movement arise, prompting further investigation. Ultrasound imaging can sometimes detect placental infarcts, though this method may not always be effective, especially for older or non-hemorrhagic infarcts.
There are no specific symptoms directly indicative of a placental infarction. Instead, symptoms that prompt investigation are usually those of underlying conditions, such as high blood pressure associated with preeclampsia, or signs of fetal distress. Bleeding or spotting might also be an early sign, although these are not always present.
Management of placental infarction primarily focuses on monitoring the well-being of the fetus and addressing any underlying maternal conditions or complications. There is no direct “treatment” to reverse the infarcted tissue. Instead, interventions may include close fetal monitoring through frequent ultrasounds and non-stress testing to ensure adequate blood and nutrient supply to the baby. In some instances, bed rest or hospitalization might be recommended, and corticosteroids may be administered to promote fetal lung maturity if early delivery is anticipated. Depending on the severity of the infarction and the gestational age, early delivery, either by inducing labor or via Cesarean section, might be considered to optimize outcomes for both mother and baby.