The placenta is a temporary organ that develops during pregnancy, acting as the life support system for the developing fetus. It serves as the interface between the mother’s and baby’s circulations, performing the functions of the baby’s lungs, kidneys, and liver until birth. Understanding how systemic infections, such as COVID-19, alter the placenta’s structure and function is important for obstetric care. The SARS-CoV-2 infection can induce changes in the placenta that differ significantly from its healthy state, primarily related to inflammation and disruptions in blood flow.
Baseline: The Role of a Healthy Placenta
The placenta is formed by specialized cells that create the villous tree, maximizing the surface area for exchange between the mother’s and baby’s bloodstreams. Maternal blood fills the intervillous spaces surrounding the chorionic villi, which contain the fetal capillaries. This arrangement allows for the transfer of oxygen and nutrients without the mixing of maternal and fetal blood.
The organ plays a multi-faceted role beyond simple exchange. It is an active endocrine gland, producing hormones such as human chorionic gonadotropin (hCG) and progesterone, which are necessary to maintain the pregnancy. The placenta also functions as a selective barrier, regulating the transfer of substances and providing an immunological defense. It actively transports necessary compounds like amino acids and glucose to the fetus, which is the baby’s main energy source. Waste products, such as urea and carbon dioxide, are simultaneously transferred back into the maternal circulation for disposal.
Structural Changes Observed in COVID-19 Placentas
In placentas from mothers infected with SARS-CoV-2, pathologists frequently observe distinct structural abnormalities not typically seen in a healthy placenta. These changes are broadly categorized into issues affecting the maternal circulation, the fetal circulation, and increased inflammation. The most common finding relates to problems with maternal blood flow, known as maternal vascular malperfusion (MVM). This can manifest as abnormal development of the maternal blood vessels that supply the placenta, including a condition called decidual arteriopathy.
MVM features often include the presence of intervillous thrombi—small blood clots in the spaces where maternal blood pools—and excessive fibrin deposition, which is a protein involved in clotting. These blockages physically obstruct the flow of maternal blood, reducing the amount of oxygen and nutrients that can reach the villi. The resulting lack of oxygen, or hypoxia, can lead to areas of dead tissue within the placenta called villous infarcts.
The fetal side of the circulation can also be affected, a condition termed fetal vascular malperfusion (FVM). FVM involves damage to the fetal blood vessels within the villi, sometimes leading to thrombosis within the fetal vessels themselves. These micro-clots reduce the capacity for the baby’s blood to exchange gases and nutrients across the placental barrier. While the virus can directly infect the placenta in some cases, most structural damage is thought to be an indirect consequence of the mother’s systemic inflammation and hypercoagulable state.
A third, less frequent but more severe finding is chronic histiocytic intervillositis. This inflammatory condition is characterized by an abnormal accumulation of immune cells in the intervillous space. This severe inflammation is often associated with a high risk of adverse fetal outcomes, including fetal growth restriction and stillbirth. The presence of these combined vascular and inflammatory lesions creates a placenta that is structurally compromised compared to a normal organ.
Impact on Fetal Nutrient and Oxygen Transfer
The structural damage observed in COVID-19 placentas directly impacts the organ’s ability to perform its core functions of nutrient and gas exchange. Maternal and fetal vascular malperfusion create placental insufficiency, meaning the organ is less efficient at transferring substances. When blood flow is restricted by clots and vessel damage, the amount of oxygen and glucose delivered to the fetus is lowered. This reduced supply can result in fetal growth restriction, where the baby does not grow as expected in the womb.
The decreased oxygenation capacity indicates a functional impairment even after the mother’s acute illness has passed. Furthermore, the vascular damage caused by the infection is sometimes linked to an increased risk of preeclampsia in the mother. Preeclampsia is a pregnancy complication characterized by high blood pressure and organ damage, which shares common pathways with the placental vascular issues seen in COVID-19. The presence of these lesions increases the risk for adverse outcomes, including preterm birth and, in severe cases, intrauterine fetal death.
Assessing the Risk of Vertical Transmission
A separate concern is the risk of the SARS-CoV-2 virus passing directly from the mother to the fetus, known as vertical transmission. The placenta is normally an effective barrier against most viruses. Studies show that while placental structural damage is frequent, the actual transmission of SARS-CoV-2 across the placental barrier to cause a confirmed fetal infection is rare.
Confirmed vertical transmission, defined by detecting the virus in samples such as umbilical cord blood or amniotic fluid, occurs in a very low percentage of cases. The risk of transmission is higher if the mother experiences a severe case of COVID-19 requiring oxygen support or intensive care. The virus must overcome several hurdles to cross the placenta, including the effectiveness of the placental barrier itself. Therefore, the primary concern is the indirect harm caused by compromised placental function resulting from the mother’s systemic illness.