"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.

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.

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.

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.

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.

Several aspects of maternal adaptation to pregnancy are affected by dysfunction of placenta. Maternal arteries fail to transform into low-resistance vessels (expected by 22–24 weeks of gestation). This increases vascular resistance in fetoplacental vascular bed eventually leading to reduction in metabolically active mass of placenta like a vicious cycle.

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.

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.

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.

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.

Despite these risks for gestational hypertension, the hemochorial placenta has been favored because of its advantages in the way that it aids in diffusion from mother to fetus later in pregnancy. The bipedal posture that has allowed humans to walk upright has also led to a reduced cardiac output, and it has been suggested that this is what necessitated humans’ aggressive early placental structures. Increased maternal blood pressure can attempt to make up for lower cardiac output, ensuring that the fetus’s growing brain receives enough oxygen and nutrients. The benefits of being able to walk upright and run on land have outweighed the disadvantages that come from bipedalism, including the placental diseases of pregnancy, such as gestational hypertension. Similarly, the advantages of having a large brain size have outweighed the deleterious effects of having a placenta that does not always convert the spiral arteries effectively, leaving humans vulnerable to contracting gestational hypertension. It is speculated that this was not the case with Neanderthals, and that they died out because their cranial capacity increased too much, and their placentae were not equipped to handle the fetal brain development, leading to widespread preeclampsia and maternal and fetal death.

Gestational hypertension in the early stages of pregnancy (trimester 1) has been shown to improve the health of the child both in its first year of life, and its later life. However, when the disease develops later in the pregnancy (subsequent trimesters), or turns into preeclampsia, there begin to be detrimental health effects for the fetus, including low birth-weight. It has been proposed that fetal genes designed to increase the mother’s blood pressure are so beneficial that they outweigh the potential negative effects that can come from preeclampsia. It has also been suggested that gestational hypertension and preeclampsia have remained active traits due to the cultural capacity of humans, and the tendency for midwives or helpers to aid in delivering babies.

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 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).

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

Major risk factors for cerebral infarction are generally the same as for atherosclerosis: high blood pressure, Diabetes mellitus, tobacco smoking, obesity, and dyslipidemia. The American Heart Association/American Stroke Association (AHA/ASA) recommends controlling these risk factors in order to prevent stroke. The AHA/ASA guidelines also provide information on how to prevent stroke if someone has more specific concerns, such as Sickle-cell disease or pregnancy. It is also possible to calculate the risk of stroke in the next decade based on information gathered through the Framingham Heart Study.

Some evidence suggests that magnesium sulfate administered to mothers prior to early preterm birth reduces the risk of cerebral palsy in surviving neonates. Due to the risk of adverse effects treatments may have, it is unlikely that treatments to prevent neonatal strokes or other hypoxic events would be given routinely to pregnant women without evidence that their fetus was at extreme risk or has already suffered an injury or stroke. This approach might be more acceptable if the pharmacologic agents were endogenously occurring substances (those that occur naturally in an organism), such as creatine or melatonin, with no adverse side-effects.

Because of the period of high neuronal plasticity in the months after birth, it may be possible to improve the neuronal environment immediately after birth in neonates considered to be at risk of neonatal stroke. This may be done by enhancing the growth of axons and dendrites, synaptogenesis and myelination of axons with systemic injections of neurotrophins or growth factors which can cross the blood–brain barrier.

It is diagnosed by a microscopic examination of the placenta.

Commonly used criteria from Altshuler are: "a minimum of 10 villi, each with 10 or more vascular channels, in 10 or more areas of 3 or more random, non-infarcted placental areas when using a ×10 ocular." The Altshuler criteria are not theoretically rigorous, as they do not define the area. Normal villi have up to five vascular channels.

Of the infants that survive, there may be as many as 1 million a year that develop cerebral palsy, learning difficulties or other disabilities. Cerebral palsy is the most common physical disability in childhood, and it is characterized by a lack of control of movement. Other neurological defects that can occur after a neonatal stroke include hemiparesis and hemi-sensory impairments Some studies suggest that when tested as toddlers and preschoolers, children who previously had neonatal strokes fall within normal ranges of cognitive development. Less is known about longer-term cognitive outcome, but there has been evidence that cognitive deficits may emerge later in childhood when more complex cognitive processes are expected to develop.

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.

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.

It is a rare disease, with an incidence of 1 in 1200 placentas. Women with cardiac problems, disorders of circulation, monosomy, hypertension and diabetes are predisposed to Breus' mole. The mole is formed as a sub-chorionic hematoma, formed out of the intervillous blood, causing progressive accumulation of the clotting substance called fibrin with increasing gestational age. Evidence from Southern blot test reveals that 85 percent of the clotted material is maternal blood. Breus mole is reported to be found in the placetae of macerated stillborn foetuses, indicating that massive subchorionic hematoma could have been the cause of their demise. A massive Breus' mole can cause disturbances in blood flow in the spiral arteries and might result in intrauterine growth restriction of the foetus.

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.