Factors increasing the risk (to either the woman, the fetus/es, or both) of pregnancy complications beyond the normal level of risk may be present in a woman's medical profile either before she becomes pregnant or during the pregnancy. These pre-existing factors may relate to physical and/or mental health, and/or to social issues, or a combination.

Some common risk factors include:

- Age of either parent

- Adolescent parents

- Older parents

- Exposure to environmental toxins in pregnancy

- Exposure to recreational drugs in pregnancy:

- Ethanol during pregnancy can cause fetal alcohol syndrome and fetal alcohol spectrum disorder.

- Tobacco smoking and pregnancy, when combined, causes twice the risk of premature rupture of membranes, placental abruption and placenta previa. Also, it causes 30% higher odds of the baby being born prematurely.

- Prenatal cocaine exposure is associated with, for example, premature birth, birth defects and attention deficit disorder.

- Prenatal methamphetamine exposure can cause premature birth and congenital abnormalities. Other investigations have revealed short-term neonatal outcomes to include small deficits in infant neurobehavioral function and growth restriction when compared to control infants. Also, prenatal methamphetamine use is believed to have long-term effects in terms of brain development, which may last for many years.

- Cannabis in pregnancy is possibly associated with adverse effects on the child later in life.

- Exposure to Pharmaceutical drugs in pregnancy. Anti-depressants, for example, may increase risks of such outcomes as preterm delivery.

- Ionizing radiation

- Risks arising from previous pregnancies:

- Complications experienced during a previous pregnancy are more likely to recur.

- Many previous pregnancies. Women who have had five previous pregnancies face increased risks of very rapid labor and excessive bleeding after delivery.

- Multiple previous fetuses. Women who have had more than one fetus in a previous pregnancy face increased risk of mislocated placenta.

- Multiple pregnancy, that is, having more than one fetus in a single pregnancy.

- Social and socioeconomic factors. Generally speaking, unmarried women and those in lower socioeconomic groups experience an increased level of risk in pregnancy, due at least in part to lack of access to appropriate prenatal care.

- Unintended pregnancy. Unintended pregnancies preclude preconception care and delays prenatal care. They preclude other preventive care, may disrupt life plans and on average have worse health and psychological outcomes for the mother and, if birth occurs, the child.

- Height. Pregnancy in women whose height is less than 1.5 meters (5 feet) correlates with higher incidences of preterm birth and underweight babies. Also, these women are more likely to have a small pelvis, which can result in such complications during childbirth as shoulder dystocia.

- Weight

- Low weight: Women whose pre-pregnancy weight is less than 45.5 kilograms (100 pounds) are more likely to have underweight babies.

- Obese women are more likely to have very large babies, potentially increasing difficulties in childbirth. Obesity also increases the chances of developing gestational diabetes, high blood pressure, preeclampsia, experiencing postterm pregnancy and/or requiring a cesarean delivery.

- Intercurrent disease in pregnancy, that is, a disease and condition not necessarily directly caused by the pregnancy, such as diabetes mellitus in pregnancy, SLE in pregnancy or thyroid disease in pregnancy.

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.

Some disorders and conditions can mean that pregnancy is considered high-risk (about 6-8% of pregnancies in the USA) and in extreme cases may be contraindicated. High-risk pregnancies are the main focus of doctors specialising in maternal-fetal medicine.

Serious pre-existing disorders which can reduce a woman's physical ability to survive pregnancy include a range of congenital defects (that is, conditions with which the woman herself was born, for example, those of the heart or , some of which are listed above) and diseases acquired at any time during the woman's life.

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.

Methods of measuring blood loss associated with childbirth vary, complicating comparison of prevalence rates. A systematic review reported the highest rates of PPH in Africa (27.5%), and the lowest in Oceania (7.2%), with an overall rate globally of 10.8%. The rate in both Europe and North America was around 13%. The rate is higher for multiple pregnancies (32.4% compared with 10.6% for singletons), and for first-time mothers (12.9% compared with 10.0% for women in subsequent pregnancies). The overall rate of severe PPH (>1000 ml) was much lower at an overall rate of 2.8%, again with the highest rate in Africa (5.1%).

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.

Oxytocin is typically used right after the delivery of the baby to prevent PPH. Misoprostol may be used in areas where oxytocin is not available. Early clamping of the umbilical cord does not decrease risks and may cause anemia in the baby, thus is usually not recommended.

Active management of the third stage is a method of shortening the stage between when the baby is born and when the placenta is delivered. This stage is when the mother is at risk of having a PPH. Active management involves giving a drug which helps the uterus contract before delivering the placenta by a gentle but sustained pull on the umbilical cord whilst exerting upward pressure on the lower abdomen to support the uterus.

Another method of active management which is not recommended now is fundal pressure. A review into this method found no research and advises controlled cord traction because fundal pressure can cause the mother unnecessary pain. Allowing the cord to drain appears to shorten the third stage and reduce blood loss but evidence around this subject is not strong enough to draw solid conclusions.

Nipple stimulation and breastfeeding triggers the release of natural oxytocin in the body, therefore it is thought that encouraging the baby to suckle soon after birth may reduce the risk of PPH for the mother. A review looking into this did not find enough good research to say whether or not nipple stimulation did reduce PPH. More research is needed to answer this question.

Hypercoagulability in pregnancy, particularly due to inheritable thrombophilia, can lead to placental vascular thrombosis. This can in turn lead to complications like early-onset hypertensive disorders of pregnancy, pre-eclampsia and small for gestational age infants (SGA). Among other causes of hypercoagulability, Antiphospholipid syndrome has been associated with adverse pregnancy outcomes including recurrent miscarriage. Deep vein thrombosis has an incidence of one in 1,000 to 2,000 pregnancies in the United States, and is the second most common cause of maternal death in developed countries after bleeding.

Many factors can contribute to the loss of uterine muscle tone, including:

- overdistention of the uterus

- multiple gestations

- polyhydramnios

- fetal macrosomia

- prolonged labor

- oxytocin augmentation of labor

- grand multiparity (having given birth 5 or more times)

- precipitous labor (labor lasting less than 3 hours)

- magnesium sulfate treatment of preeclampsia

- chorioamnionitis

- halogenated anesthetics

- uterine leiomyomata

- full bladder

- retained colyledon, placental fragments

- placenta previa

- placental abruption

- constriction ring

- incomplete separation of the placenta

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.

Unfractionated heparin, low molecular weight heparin, warfarin (not to be used during pregnancy) and aspirin remain the basis of antithrombotic treatment and prophylaxis both before and during pregnancy.

While the consensus among physicians is the safety of the mother supersedes the safety of the developing fetus, changes in the anticoagulation regimen during pregnancy can be performed to minimize the risks to the developing fetus while maintaining therapeutic levels of anticoagulants in the mother.

The main issue with anticoagulation in pregnancy is that warfarin, the most commonly used anticoagulant in chronic administration, is known to have teratogenic effects on the fetus if administered in early pregnancy. Still, there seems to be no teratogenic effect of warfarin before six weeks of gestation. However, unfractionated heparin and low molecular weight heparin do not cross the placenta.

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.

There is no effective pharmacological treatment for retained placenta. It is useful ensuring the bladder is empty. However, ergometrine should not be given as it causes tonic uterine contractions which may delay placental expulsion. Controlled cord traction has been recommended as a second alternative after more than 30 minutes have passed after stimulation of uterine contractions, provided the uterus is contracted. Manual extraction may be required if cord traction also fails, or if heavy ongoing bleeding occurs. Very rarely a curettage is necessary to ensure that no remnants of the placenta remain (in rare conditions with very adherent placenta such as a placenta accreta).

However, in birth centers and attended home birth environments, it is common for licensed care providers to wait for the placenta's birth up to 2 hours in some instances.

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.

Women with a bleeding disorder may be prone to more excessive bleeding. A hematologic work-up should discover the cause.

On occasion an ovarian cyst can rupture and give rise to internal hemorrhage. This may occur during ovulation or as a result of endometriosis.

If the pregnancy test is positive, consider pregnancy related bleeding (see obstetrical hemorrhage), including miscarriage and ectopic pregnancy.

The first step in management of uterine atony is uterine massage. The next step is pharmacological therapies, the first of which is oxytocin, used because it initiates rhythmic contractions of the uterus, compressing the spiral arteries which should reduce bleeding. The next step in the pharmacological management is the use of methylergometrine, which is an ergot derivative, much like that use in the abortive treatment of migraines. Its side effect of hypertension means its use should not be used in those with hypertension or pre-eclampsia. In those with hypertension, the use of prostaglandin F is indicated (but beware of its use in patients with asthma).

Another option Carbetocin and Carboprost where Oxytocin and ergometrin is inappropriate.

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.

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.

IUGR affects 3-10% of pregnancies. 20% of stillborn infants have IUGR. Perinatal mortality rates are 4-8 times higher for infants with IUGR, and morbidity is present in 50% of surviving infants.

According to the theory of thrifty phenotype, intrauterine growth restriction 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.

Its incidence is reported as 0.5-0.9% of all pregnancies, and 10-20% of women with severe pre-eclampsia. HELLP usually occurs in Caucasian women over the age of 25.

There are risks to both the mother and the unborn child (fetus) when eclampsia occurs. The fetus may grow more slowly than normal within the womb (uterus) of a woman with eclampsia, which is termed intrauterine growth restriction and may result in the child appearing small for gestational age or being born with low birth weight. Eclampsia may cause problems with the placenta to occur. The placenta may bleed (hemorrhage) or it may begin to separate from the wall of the uterus. It is normal for the placenta to separate from the uterine wall during delivery, but it is abnormal for it to separate prior to delivery; this condition is called placental abruption and can be dangerous for the fetus. Placental insufficiency may also occur, a state in which the placenta fails to support appropriate fetal development because it cannot deliver the necessary amount of oxygen or nutrients to the fetus. During an eclamptic seizure, the beating of the fetal heart may become slower than normal (bradycardia). If any of these complications occurs, fetal distress may develop. If the risk to the health of the fetus or the mother is high, the definitive treatment for eclampsia is delivery of the baby. It may be safer to deliver the infant preterm than to wait for the full 40 weeks of fetal development to finish, and as a result prematurity is also a potential complication of eclampsia.

In the mother, changes in vision may occur as a result of eclampsia, and these changes may include blurry vision, one-sided blindness (either temporary due to amaurosis fugax or potentially permanent due to retinal detachment), or cortical blindness, which affects the vision from both eyes. There are also potential complications in the lungs. The woman may have fluid slowly collecting in the lungs in a process known as pulmonary edema. During an eclamptic seizure, it is possible for a person to vomit the contents of the stomach and to inhale some of this material in a process known as aspiration. If aspiration occurs, the woman may experience difficulty breathing immediately or could develop an infection in the lungs later, called aspiration pneumonia. It is also possible that during a seizure breathing will stop temporarily or become inefficient, and the amount of oxygen reaching the woman's body and brain will be decreased (in a state known as hypoxia). If it becomes difficult for the woman to breathe, she may need to have her breathing temporarily supported by an assistive device in a process called mechanical ventilation. In some severe eclampsia cases, the mother may become weak and sluggish (lethargy) or even comatose. These may be signs that the brain is swelling (cerebral edema) or bleeding (intracerebral hemorrhage).

The pathogenesis of RLP is varied. Although very common during pregnancy, non-gestating women can also experience RLP. The most common causes of RLP are as follows:

- RLP may be caused by a spasm or cramp when the ligament contracts involuntarily. The ligament pulls on nerve fibers and sensitive structures of the female reproductive system. Since the uterus tends to be oriented towards the right side of the body, the pain is also often felt on the right side. This leads to frequent confusion with appendicitis.

- During pregnancy, the uterus expands to accommodate the growing fetus. This increase in size and weight of the uterus puts stress on the ligament that holds it, causing it to stretch. During physical exertion or sudden movements, the ligament is overly stretched, causing pain.

- Varicosities, e.g. enlargement of the blood vessels of the round ligament can occur during pregnancy, causing pain and swelling. The varicocoele starts at the veins draining the round ligament and the inguinal canal and is associated with engorgement of the veins of the ovaries and the pelvis during pregnancy.

- Endometriosis that infiltrates or borders the uterine round ligament can cause RLP in fertile, non-gestating women.

- Other pathologies that involve the uterine round ligament can cause RLP.