The following have been identified as risk factors for placenta previa:

- Previous placenta previa (recurrence rate 4–8%), caesarean delivery, myomectomy or endometrium damage caused by D&C.

- Women who are younger than 20 are at higher risk and women older than 35 are at increasing risk as they get older.

- Alcohol use during pregnancy was previous listed as a risk factor, but is discredited by this article.

- Women who have had previous pregnancies ( multiparity ), especially a large number of closely spaced pregnancies, are at higher risk due to uterine damage.

- Smoking during pregnancy; cocaine use during pregnancy

- Women with a large placentae from twins or erythroblastosis are at higher risk.

- Race is a controversial risk factor, with some studies finding that people from Asia and Africa are at higher risk and others finding no difference.

- Placental pathology (Vellamentous insertion, succinturiate lobes, bipartite i.e. bilobed placenta etc.)

- Baby is in an unusual position: breech (buttocks first) or transverse (lying horizontally across the womb).

Placenta previa is itself a risk factor of placenta accreta.

In rare cases, inherited bleeding disorders, like hemophilia, von Willebrand disease (vWD), or factor IX or XI deficiency, may cause severe postpartum hemorrhage, with an increased risk of death particularly in the postpartum period. The risk of postpartum hemorrhage in patients with vWD and carriers of hemophilia has been found to be 18.5% and 22% respectively. This pathology occurs due to the normal physiological drop in maternal clotting factors after delivery which greatly increases the risk of secondary postpartum hemorrhage.

Another bleeding risk factor is thrombocytopenia, or decreased platelet levels, which is the most common hematological change associated with pregnancy induced hypertension. If platelet counts drop less than 100,000 per microliter the patient will be at a severe risk for inability to clot during and after delivery.

The prognosis of this complication depends on whether treatment is received by the patient, on the quality of treatment, and on the severity of the abruption. Outcomes for the baby also depend on the gestational age.

In the Western world, maternal deaths due to placental abruption are rare. The fetal prognosis is worse than the maternal prognosis; approximately 12% of fetuses affected by placental abruption die. 77% of fetuses that die from placental abruption die before birth; the remainder die due to complications of preterm birth.

Without any form of medical intervention, as often happens in many parts of the world, placental abruption has a high maternal mortality rate.

Placental abruption occurs in approximately 0.2–1% of all pregnancies. Though different causes change when abruption is most likely to occur, the majority of placental abruptions occur before 37 weeks gestation, and 14% occur before 32 weeks gestation.

Antepartum bleeding (APH), also prepartum hemorrhage, is bleeding during pregnancy from the 24th week (sometimes defined as from the 20th week) gestational age to full term (40th week). The primary consideration is the presence of a placenta previa which is a low lying placenta at or very near to the internal cervical os. This condition occurs in roughly 4 out of 1000 pregnancies and usually needs to be resolved by delivering the baby via cesarean section. Also a placental abruption (in which there is premature separation of the placenta) can lead to obstetrical hemorrhage, sometimes concealed. This pathology is of important consideration after maternal trauma such as a motor vehicle accident or fall.

Other considerations to include when assessing antepartum bleeding are: sterile vaginal exams that are performed in order to assess dilation of the patient when the 40th week is approaching. As well as cervical insufficiency defined as a midtrimester (14th-26th week) dilation of the cervix which may need medical intervention to assist in keeping the pregnancy sustainable.

Placenta previa occurs approximately one of every 200 births. It has been suggested that incidence of placenta previa is increasing due to increased rate of Caesarian section.

Perinatal mortality rate of placenta previa is 3-4 times higher than normal pregnancies.

There is also an increased risk for cardiovascular complications, including hypertension and ischemic heart disease, and kidney disease. Other risks include stroke and venous thromboembolism. It seems pre-eclampsia does not increase the risk of cancer.

Lowered blood supply to the fetus in pre-eclampsia causes lowered nutrient supply, which could result in intrauterine growth restriction (IUGR) and low birth weight. The fetal origins hypothesis states that fetal undernutrition is linked with coronary heart disease later in adult life due to disproportionate growth.

Because preeclampsia leads to a mismatch between the maternal energy supply and fetal energy demands, pre-eclampsia can lead to IUGR in the developing fetus. Infants suffering from IUGR are prone to suffer from poor neuronal development and in increased risk for adult disease according to the Barker hypothesis. Associated adult diseases of the fetus due to IUGR include, but are not limited to, coronary artery disease (CAD), type 2 diabetes mellitus (T2DM), cancer, osteoporosis, and various psychiatric illnesses.

The risk of pre-eclampsia and development of placental dysfunction has also been shown to be recurrent cross-generationally on the maternal side and most likely on the paternal side. Fetuses born to mothers that were born small for gestational age (SGA) were 50% more likely to develop preeclampsia while fetuses born to both SGA parents were three-fold more likely to develop preeclampsia in future pregnancies.

In low-risk pregnancies, the association between cigarette smoking and a reduced risk of pre-eclampsia has been consistent and reproducible across epidemiologic studies. High-risk pregnancies (those with pregestational diabetes, chronic hypertension, history of pre-eclampsia in a previous pregnancy, or multifetal gestation) showed no significant protective effect. The reason for this discrepancy is not definitively known; research supports speculation that the underlying pathology increases the risk of preeclampsia to such a degree that any measurable reduction of risk due to smoking is masked. However, the damaging effects of smoking on overall health and pregnancy outcomes outweighs the benefits in decreasing the incidence of preeclampsia. It is recommended that smoking be stopped prior to, during and after pregnancy.

Studies suggest that marijuana use in the months prior to or during the early stages of pregnancy may interfere with normal placental development and consequently increase the risk of preeclampsia.

Gestational hypertension is one of the most common disorders seen in human pregnancies. Though relatively benign on its own, in roughly half of the cases of gestational hypertension the disorder progresses into preeclampsia, a dangerous condition that can prove fatal to expectant mothers. However, gestational hypertension is a condition that is fairly rare to see in other animals. For years, it has been the belief of the scientific community that gestational hypertension and preeclampsia were relatively unique to humans, although there has been some recent evidence that other primates can also suffer from similar conditions, albeit due to different underlying mechanisms. The underlying cause of gestational hypertension in humans is commonly believed to be an improperly implanted placenta. Humans have evolved to have a very invasive placenta to facilitate better oxygen transfer from the mother to the fetus, to support the growth of its large brain.

Placental insufficiency can affect the fetus, causing Fetal distress. Placental insufficiency may cause oligohydramnios, preeclampsia, miscarriage or stillbirth. Placental insufficiency is most frequent cause of asymmetric IUGR.

According to the theory of thrifty phenotype, placental insufficiency triggers epigenetic responses in the fetus that are otherwise activated in times of chronic food shortage. If the offspring actually develops in an environment rich in food it may be more prone to metabolic disorders, such as obesity and type II diabetes.

With treatment, maternal mortality is about 1 percent, although complications such as placental abruption, acute renal failure, subcapsular liver hematoma, permanent liver damage, and retinal detachment occur in about 25% of women. Perinatal mortality (stillbirths plus death in infancy) is between 73 and 119 per 1000 babies of woman with HELLP, while up to 40% are small for gestational age. In general, however, factors such as gestational age are more important than the severity of HELLP in determining the outcome in the baby.

"Maternal floor infarcts" are "not" considered to be true placental infarcts, as they result from deposition of fibrin around the chorionic villi, i.e. perivillous fibrin deposition.

A placental infarction results from the interruption of blood supply to a part of the placenta, causing its cells to die.

Small placental infarcts, especially at the edge of the placental disc, are considered to be normal at term. Large placental infarcts are associated with vascular abnormalities, e.g. hypertrophic decidual vasculopathy, as seen in hypertension. Very large infarcts lead to placental insufficiency and may result in fetal death.

It is recommended that women with vasa previa should deliver through elective cesarean prior to rupture of the membranes. Given the timing of membrane rupture is difficult to predict, elective cesarean delivery at 35–36 weeks is recommended. This gestational age gives a reasonable balance between the risk of death and that of prematurity. Several authorities have recommended hospital admission about 32 weeks. This is to give the patient proximity to the operating room for emergency delivery should the membranes rupture. Because these patients are at risk for preterm delivery, it is recommended that steroids should be given to promote fetal lung maturation. When bleeding occurs, the patient goes into labor, or if the membranes rupture, immediate treatment with an emergency caesarean delivery is usually indicated.

The risk of a repeat GTD is approximately 1 in 100, compared with approximately 1 in 1000 risk in the general population. Especially women whose hCG levels remain significantly elevated are at risk of developing a repeat GTD.

It is associated with gestational diabetes, smoking and high altitude.

Maternal causes

- Obesity

- Mothers under 20 or over 40 years old

- Past history of diabetes mellitus, hypertension and renal disease.

- Adolescent pregnancy.

- chronic hypertension

- New paternity.

- Thrombophilias (anti-phospholoipid syndrome, protein C/S deficiency, factor V Leiden)

- Having donated a kidney.

Pregnancy

- Multiple gestation ( twins or triplets, etc.)

- Placental abnormalities:

Family history

- Family history of pre-eclampsia.

- African American race

In sheep, intrauterine growth restriction can be caused by heat stress in early to mid pregnancy. The effect is attributed to reduced placental development causing reduced fetal growth. Hormonal effects appear implicated in the reduced placental development. Although early reduction of placental development is not accompanied by concurrent reduction of fetal growth; it tends to limit fetal growth later in gestation. Normally, ovine placental mass increases until about day 70 of gestation, but high demand on the placenta for fetal growth occurs later. (For example, research results suggest that a normal average singleton Suffolk x Targhee sheep fetus has a mass of about 0.15 kg at day 70, and growth rates of about 31 g/day at day 80, 129 g/day at day 120 and 199 g/day at day 140 of gestation, reaching a mass of about 6.21 kg at day 140, a few days before parturition.)

In adolescent ewes (i.e. ewe hoggets), overfeeding during pregnancy can also cause intrauterine growth restriction, by altering nutrient partitioning between dam and conceptus. Fetal growth restriction in adolescent ewes overnourished during early to mid pregnancy is not avoided by switching to lower nutrient intake after day 90 of gestation; whereas such switching at day 50 does result in greater placental growth and enhanced pregnancy outcome. Practical implications include the importance of estimating a threshold for "overnutrition" in management of pregnant ewe hoggets. In a study of Romney and Coopworth ewe hoggets bred to Perendale rams, feeding to approximate a conceptus-free live mass gain of 0.15 kg/day (i.e. in addition to conceptus mass), commencing 13 days after the midpoint of a synchronized breeding period, yielded no reduction in lamb birth mass, where compared with feeding treatments yielding conceptus-free live mass gains of about 0 and 0.075 kg/day.

In both of the above models of IUGR in sheep, the absolute magnitude of uterine blood flow is reduced. Evidence of substantial reduction of placental glucose transport capacity has been observed in pregnant ewes that had been heat-stressed during placental development.

Eclampsia, like pre-eclampsia, tends to occur more commonly in first pregnancies. Women who have long term high blood pressure before becoming pregnant have a greater risk of pre-eclampsia. Furthermore, women with other pre-existing vascular diseases (diabetes or nephropathy) or thrombophilic diseases such as the antiphospholipid syndrome are at higher risk to develop pre-eclampsia and eclampsia. Having a large placenta (multiple gestation, hydatidiform mole) also predisposes women to eclampsia. In addition, there is a genetic component: a woman whose mother or sister had the condition is at higher risk than otherwise. Women who have experienced eclampsia are at increased risk for pre-eclampsia/eclampsia in a later pregnancy.

of fetal membranes (afterbirth) is observed more frequently in cattle than in other animals. In a normal condition, a cow’s placenta is expelled within a 12-hour period after calving.

An important risk factor for placenta accreta is placenta previa in the presence of a uterine scar. Placenta previa is an independent risk factor for placenta accreta. Additional reported risk factors for placenta accreta include maternal age and multiparity, other prior uterine surgery, prior uterine curettage, uterine irradiation, endometrial ablation, Asherman syndrome, uterine leiomyomata, uterine anomalies, hypertensive disorders of pregnancy, and smoking.

The condition is increased in incidence by the presence of scar tissue i.e. Asherman's syndrome usually from past uterine surgery, especially from a past dilation and curettage, (which is used for many indications including miscarriage, termination, and postpartum hemorrhage), myomectomy, or caesarean section. A thin decidua can also be a contributing factor to such trophoblastic invasion. Some studies suggest that the rate of incidence is higher when the fetus is female. Other risk factors include low-lying placenta, anterior placenta, congenital or acquired uterine defects (such as uterine septa), leiomyoma, ectopic implantation of placenta (including cornual pregnancy).

Pregnant women above 35 years of age who have had a Caesarian section and now have a placenta previa overlying the uterine scar have a 40% chance of placenta accreta.

In humans, retained placenta is generally defined as a placenta that has not undergone placental expulsion within 30 minutes of the baby’s birth where the third stage of labor has been managed actively.

Risks of retained placenta include hemorrhage and infection. After the placenta is delivered, the uterus should contract down to close off all the blood vessels inside the uterus. If the placenta only partially separates, the uterus cannot contract properly, so the blood vessels inside will continue to bleed. A retained placenta thereby leads to hemorrhage.

The reported incidence of placenta accreta has increased from approximately 0.8 per 1000 deliveries in the 1980s to 3 per 1000 deliveries in the past decade.

Incidence has been increasing with increased rates of Caesarean deliveries, with rates of 1 in 4,027 pregnancies in the 1970s, 1 in 2,510 in the 1980s, and 1 in 533 for 1982–2002. In 2002, ACOG estimated that incidence has increased 10-fold over the past 50 years. The risk of placenta accreta in future deliveries after Caesarian section is 0.4-0.8%. For patients with placenta previa, risk increases with number of previous Caesarean sections, with rates of 3%, 11%, 40%, 61%, and 67% for the first, second, third, fourth, and fifth or greater number of Caesarean sections.

Overall, GTD is a rare disease. Nevertheless, the incidence of GTD varies greatly between different parts of the world. The reported incidence of hydatidiform mole ranges from 23 to 1299 cases per 100,000 pregnancies. The incidence of the malignant forms of GTD is much lower, only about 10% of the incidence of hydatidiform mole. The reported incidence of GTD from Europe and North America is significantly lower than the reported incidence of GTD from Asia and South America. One proposed reason for this great geographical variation is differences in healthy diet in the different parts of the world (e.g., carotene deficiency).

However, the incidence of rare diseases (such as GTD) is difficult to measure, because epidemiologic data on rare diseases is limited. Not all cases will be reported, and some cases will not be recognised. In addition, in GTD, this is especially difficult, because one would need to know all gestational events in the total population. Yet, it seems very likely that the estimated number of births that occur at home or outside of a hospital has been inflated in some reports.