An obstetrician may need to divide the anterior lying placenta. In such cases, blood loss is expected to be high and thus blood and blood products are always kept ready. In rare cases, hysterectomy may be required. Complications
Maternal
Antepartum hemorrhage
Malpresentation
Abnormal placentation
Postpartum hemorrhage
Placenta previa increases the risk of puerperal sepsis and postpartum hemorrhage because the lower segment to which the placenta was attached contracts less well post-delivery. Fetal
IUGR (15% incidence)
Hypoxia
Premature delivery
Death

Epidemiology
Placenta previa occurs approximately one of every 200 births globally. It has been suggested that rates of placenta previa are increasing due to increased rate of Caesarian section. Reasons for regional variation may include ethnicity and diet. Africa
Rates of placenta praevia in sub-Saharan Africa are the lowest in the world, averaging 2.7 per 1000 pregnancies. Despite a low prevalence, this disease has had a profound impact in Africa as it is linked with negative outcomes for both the mother and infant. The most common maternal outcome of placenta praevia is extreme blood loss before or after birth (antepartum hemorrhage and postpartum hemorrhage), which is a major cause of maternal and infant mortality in countries like Tanzania. Risk factors for placenta praevia among African women include prior pregnancies, prenatal alcohol consumption, and insufficient gynecologic care. In North Africa placenta praevia rates occur in 6.4 per 1000 pregnancies. Asia
Mainland China has the highest prevalence of placenta praevia in the world, measuring at an average of 12.2 per 1000 pregnancies. Specifically, placenta praevia is most common in Southeast Asia, though the reason for this has not yet been investigated.
Causes
The genetic cause of ULD is known, but research has led to new areas of study that may lead to an increase in knowledge of what causes ULD. Genetic factors
The cause of ULD is known to be a mutation of the gene that produces cystatin B. The disease is autosomal recessive, so both parents of an individual must be carriers of the recessive CSTB gene for the individual to inherit it, and for an individual to show symptoms of ULD, they must have both recessive CSTB genes. Siblings of affected individuals who only have one recessive gene have been monitored and generally do not show the signs of ULD, though in some cases mild symptoms may be present. New developments
New research shows that cystatin B may not be the only factor involved in Unverricht–Lundborg disease. In a study, it was determined that patients with ULD had more dopamine receptors in certain areas of their brain than unaffected individuals. The researchers chose to investigate dopamine receptors because they are known to be a factor in myoclonus, which are a significant part of the symptoms of ULD. The results of this study indicate that the cause of ULD may be more complex than currently thought. Mechanism
While the genetic cause of Unverricht–Lundborg disease is known, the mechanism by which it works is not fully known. Current research has provided promising results that may lead to a confirmation of the mechanism.