A miscarriage is defined as the spontaneous loss of a pregnancy before 20 weeks of gestation; the second trimester spans from week 13 through week 27. While most miscarriages occur in the first trimester, typically due to chromosomal issues, loss in the second trimester is far less common, occurring in about 1 to 2 percent of pregnancies. The causes of second-trimester loss differ significantly from those in the earlier stage, often relating to structural problems, infections, or underlying maternal health conditions. Understanding these distinct causes is important for future preventative care and provides clarity.
Anatomical and Structural Issues
Physical defects or weaknesses in the mother’s reproductive anatomy can compromise the ability to sustain a growing pregnancy, especially as the fetus gains weight. The most frequently cited cause is cervical insufficiency, sometimes called cervical weakness. This condition involves the painless dilation and effacement (thinning) of the cervix before the pregnancy has reached full term, typically occurring without the contractions that signal labor.
The cervix, the muscular neck of the uterus, normally remains firm and closed until labor begins. With cervical insufficiency, increasing pressure from the growing fetus and amniotic fluid sac causes the weakened cervix to open prematurely. This opening can lead to the membranes rupturing, infection, and the expulsion of the fetus, often happening between 16 and 24 weeks of gestation.
Other structural issues within the uterus can also interfere with the pregnancy. Congenital uterine anomalies, such as a bicornuate or septate uterus, involve an unusually shaped womb that may restrict space for the fetus or compromise blood flow to the placenta. Large uterine fibroids, which are non-cancerous growths, can contribute to second-trimester loss if they obstruct the implantation site or reduce the uterine cavity volume.
Infections and Inflammation
Infections, whether localized to the reproductive tract or systemic, are a major driver of second-trimester miscarriage. These infections trigger a damaging inflammatory response that destabilizes the pregnancy environment. The most common route is an ascending infection where bacteria from the vagina or cervix travel upward into the uterus, leading to inflammation of the fetal membranes and placenta, known as chorioamnionitis.
Bacterial vaginosis (BV) is one localized infection associated with an increased risk of mid-trimester loss and premature rupture of membranes. The presence of these microbes initiates a cascade that releases inflammatory molecules called cytokines. This inflammatory surge can weaken the membranes and stimulate uterine contractions, ultimately leading to preterm labor and miscarriage.
Systemic infections, including certain viruses and bacteria like those in the TORCH panel (Toxoplasmosis, Group B Strep, Rubella, Cytomegalovirus, and Herpes), can directly infect the fetus or placental tissue. A strong association exists between histological chorioamnionitis and spontaneous second-trimester loss, indicating that this inflammatory process often precedes labor. The body’s response to these pathogens creates a hostile internal environment that the pregnancy cannot sustain.
Placental Complications
The placenta is the temporary organ responsible for nutrient, gas, and waste exchange between the mother and the fetus; its malfunction is a frequent cause of later pregnancy loss. Placental insufficiency occurs when the organ does not develop correctly or cannot supply adequate blood flow, oxygen, and nutrients. This poor function can lead to severe growth restriction, placing the fetus at high risk of demise.
A severe complication is placental abruption, the premature separation of the placenta from the inner wall of the uterus before delivery. This separation can be partial or complete, resulting in a loss of the exchange surface, acute fetal distress, and often significant maternal bleeding. Abruption can occur any time after 20 weeks and is a recognized cause of late miscarriage.
Problems can arise from how the placenta attaches to the uterine wall, such as placenta previa, where the placenta covers the cervix. While placenta previa is primarily a bleeding risk, associated complications like severe hemorrhage or localized placental separation can precipitate a second-trimester loss. Failures in the vascular structure, including small clots within the placenta, further compromise its function.
Maternal Systemic Health Factors
Underlying chronic health conditions in the mother can create a systemic environment hostile to the pregnancy, often by affecting blood flow or immune regulation. Autoimmune disorders are particularly relevant, with Antiphospholipid Syndrome (APS) being a recognized cause of recurrent second-trimester loss. In APS, the body produces antibodies that promote blood clot formation, leading to blockages in the small blood vessels of the placenta.
These clots disrupt the blood supply, starving the fetus of oxygen and nutrients. Conditions like uncontrolled diabetes or chronic hypertension also pose a substantial risk. High blood pressure can damage the delicate blood vessels in the placenta, contributing to placental abruption and growth restriction.
Severe thyroid dysfunction, either overactive or underactive, can impact the pregnancy due to its role in regulating maternal metabolism and hormone levels. Lupus (Systemic Lupus Erythematosus) is another autoimmune condition where the body’s overactive immune system can attack placental tissue. Identifying and managing these chronic maternal conditions is a crucial part of preventative care.