Blood clots in the placenta form when something disrupts normal blood flow through the network of vessels that connect a pregnant person to their developing baby. The most common trigger is a problem with the spiral arteries, the small blood vessels in the uterine wall that feed the placenta. When these arteries become blocked by a clot, narrowed by disease, or fail to develop properly in early pregnancy, the downstream tissue loses its blood supply. This can cause localized areas of dead tissue (infarcts), pools of trapped blood (hematomas), or widespread clotting that compromises the entire placenta.
How Placental Clots Form
During a healthy pregnancy, cells from the developing placenta invade the spiral arteries of the uterus and remodel them into wide, low-resistance channels. This remodeling is what allows large volumes of oxygen-rich blood to flow freely into the placenta’s exchange spaces. When this remodeling fails or is incomplete, the arteries stay narrow and high-resistance, creating turbulent blood flow in the spaces between the placental villi, the finger-like projections where nutrients and oxygen pass to the fetus.
That turbulence damages the delicate lining of blood vessels and activates the clotting cascade. Small clots begin forming in the spaces between villi, and fibrin, the protein mesh that holds clots together, starts depositing along vessel walls. Over time these micro-clots can grow large enough to block vessels entirely, cutting off sections of the placenta from their blood supply. The result is a placental infarct. If a blocked spiral artery later reopens, blood can surge back into the damaged tissue and create a hematoma, a contained pocket of blood trapped within or behind the placenta.
Clotting Disorders That Raise the Risk
Some people carry inherited or acquired conditions that make their blood more prone to clotting, and these conditions substantially increase the chance of placental complications.
Factor V Leiden mutation is one of the most common inherited clotting disorders. It makes the blood resistant to one of the body’s natural anticoagulant signals, so clots form more easily and break down more slowly. People who carry two copies of the mutation (homozygous) face a significantly higher risk of blood clots during pregnancy than those with one copy.
Antiphospholipid syndrome (APS) is an autoimmune condition in which the immune system produces antibodies that promote clotting in both arteries and veins. APS is one of the most well-established causes of pregnancy-related blood clots, placental insufficiency, preeclampsia, and pregnancy loss. Unlike inherited mutations, APS can develop at any point in life.
MTHFR gene variants, particularly the C677T polymorphism, can impair the body’s ability to process folate. This leads to elevated homocysteine levels in the blood, which damages the inner lining of blood vessels and creates conditions that favor clot formation. When MTHFR variants exist alongside other clotting disorders, the combined effect on thrombotic risk can be much greater than either condition alone.
The Role of Preeclampsia and High Blood Pressure
Preeclampsia, a condition marked by sudden-onset high blood pressure after 20 weeks of pregnancy, is both a cause and a consequence of placental clotting. A poorly functioning placenta releases inflammatory signals into the mother’s bloodstream, triggering widespread damage to the lining of blood vessels throughout the body. That endothelial damage, in turn, promotes further clotting within the placenta, creating a destructive feedback loop.
Chronic high blood pressure that predates pregnancy carries its own risks. Sustained high pressure damages the small arteries supplying the uterus, a process called decidual vasculopathy. These damaged vessels are more likely to develop clots that reduce blood flow to the placenta, leading to infarcts and areas of underperfusion where the tissue doesn’t receive enough oxygen.
Smoking, Cocaine, and Other Lifestyle Factors
Cigarette smoking during pregnancy is a well-documented risk factor for placental clotting, and the risk increases with the number of cigarettes smoked per day in a dose-response pattern. Nicotine and carbon monoxide constrict blood vessels and damage vessel linings, both of which promote clot formation.
Cocaine use carries an even sharper risk. Women who use cocaine during pregnancy are nearly three times more likely to experience placental abruption, a condition where the placenta separates from the uterine wall due to bleeding behind it. They also face elevated odds of placental infarction and preeclampsia. Cocaine causes sudden, intense spikes in blood pressure and powerful vasoconstriction, both of which can rupture or block the fragile spiral arteries that supply the placenta.
Advanced maternal age, generally defined as 35 or older, also increases the likelihood of placental vascular complications including abruption and preeclampsia, likely because blood vessels become less elastic and more prone to damage with age.
Where Clots Form Matters
Not all placental clots carry the same risk. Their location within or around the placenta determines how they affect the pregnancy.
- Retroplacental hematomas form between the back of the placenta and the uterine wall. They are more common in early pregnancy (before 21 weeks) and can lift the placenta away from its blood supply. These carry the highest risk of fetal death among hematoma types.
- Intraplacental hematomas form within the body of the placenta itself, in the spaces between villi. They tend to appear later in pregnancy and result from the breakdown of diseased spiral arteries. This type is associated with the highest rates of growth restriction, preterm delivery, and second-trimester pregnancy loss.
- Subchorionic hematomas form between the placenta’s outer membrane and the uterine wall. These are the type most commonly spotted on early ultrasound. Moderate-sized hematomas that wrap around the gestational sac pose the greatest concern: one study found that 61% of pregnancies that ended in miscarriage had this wrapping pattern.
These different hematoma types have distinct causes and distinct risk profiles, so they are not interchangeable in terms of what they mean for a pregnancy.
How Placental Clots Affect the Baby
The placenta is the baby’s sole source of oxygen and nutrients. When clots block enough of the placental blood supply, the baby doesn’t get what it needs to grow. This is the core mechanism behind fetal growth restriction, where the baby measures significantly smaller than expected for its gestational age.
Small, isolated infarcts are actually common in otherwise healthy placentas and typically cause no problems. The placenta has built-in reserve capacity. But when clotting is widespread, driven by an underlying condition like APS or severe preeclampsia, the cumulative loss of functional tissue can overwhelm that reserve. The consequences range from mild growth restriction to preterm delivery to stillbirth, depending on how much of the placenta is compromised and how early in pregnancy the damage begins.
Placental abruption, the most acute form of retroplacental clotting, affects roughly 0.4% to 1% of pregnancies and is a leading cause of bleeding in the second half of pregnancy. It can develop suddenly and requires urgent medical attention.
Prevention and Management
For people with known clotting disorders or a history of placental complications in a previous pregnancy, preventive treatment typically involves low-dose aspirin, sometimes combined with a daily injection of a blood-thinning medication. Aspirin is usually started early in pregnancy, and injectable blood thinners begin once a viable pregnancy is confirmed on ultrasound, around six weeks. These medications are continued through most of pregnancy and stopped when labor begins.
The evidence for these treatments is strongest in people with antiphospholipid syndrome, where the combination of aspirin and blood thinners has been shown to improve live birth rates. For people with inherited clotting mutations but no history of clots or pregnancy loss, the benefit is less clear, and treatment decisions are made on a case-by-case basis.
Beyond medication, managing modifiable risk factors makes a meaningful difference. Quitting smoking before or early in pregnancy removes one of the most preventable causes of placental clotting. Controlling blood pressure, whether through lifestyle changes or medication, reduces the vascular damage that sets the stage for clots. And for people with elevated homocysteine levels related to MTHFR variants, adequate folate intake helps normalize levels and may reduce thrombotic risk.