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.

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.

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.

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.

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.

Vasa previa is seen more commonly with velamentous insertion of the umbilical cord, accessory placental lobes (succenturiate or bilobate placenta), multiple gestation, IVF pregnancy. In IVF pregnancies incidences as high as one in 300 have been reported. The reasons for this association are not clear, but disturbed orientation of the blastocyst at implantation, vanishing embryos and the increased frequency of placental morphological variations in in vitro fertilisation pregnancies have all been postulated.

Research shows that symptoms of Posttraumatic stress disorder are common following childbirth, with prevalence of 24-30.1% at 6 weeks, dropping to 13.6% at 6 months. PTSD is rarer; a review found that following normal childbirth (excluding stillbirth and some other complications) rates of PTSD ranged from 2.8-5.6% after 6 weeks, dropping to 1.5% at 6 months.

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.

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.

Although the risk of placental abruption cannot be eliminated, it can be reduced. Avoiding tobacco, alcohol and cocaine during pregnancy decreases the risk. Staying away from activities which have a high risk of physical trauma is also important. Women who have high blood pressure or who have had a previous placental abruption and want to conceive must be closely supervised by a doctor.

The risk of placental abruption can be reduced by maintaining a good diet including taking folic acid, regular sleep patterns and correction of pregnancy-induced hypertension.

It is crucial for women to be made aware of the signs of placental abruption, such as vaginal bleeding, and that if they experience such symptoms they must get into contact with their health care provider/the hospital "without any delay".

Velamentous cord insertion is an abnormal condition during pregnancy. Normally, the umbilical cord inserts into the middle of the placenta as it develops. In velamentous cord insertion, the umbilical cord inserts into the fetal membranes (choriamniotic membranes), then travels within the membranes to the placenta (between the amnion and the chorion). The exposed vessels are not protected by Wharton's jelly and hence are vulnerable to rupture. Rupture is especially likely if the vessels are near the cervix, in which case they may rupture in early labor, likely resulting in a stillbirth. This is a serious condition called vasa previa. Not every pregnancy with a velamentous cord insertion results in vasa previa, only those in which the blood vessels are near the cervix.

When a velamentous cord insertion is discovered, the obstetrician will monitor the pregnancy closely for the presence of vasa previa. If the blood vessels are near the cervix, the baby will be delivered via cesarean section as early as 35 weeks to prevent the mother from going into labor, which is associated with a high infant mortality. Early detection can reduce the need for emergency cesarean sections.

A sperm granuloma is a lump of extravasated sperm that appears along the vasa deferentia or epididymides in vasectomized men. Sperm granulomas are rounded or irregular in shape, one millimeter to one centimeter or more, with a central mass of degenerating sperm surrounded by tissue containing blood vessels and immune system cells. Sperm granulomas can be either asymptomatic or symptomatic (i.e., either not painful or painful, respectively) (see post-vasectomy pain syndrome).

The vast majority of sperm granulomas in vasectomized men are present as a result of the pressure-induced changes of vasectomy.

Spontaneous cases are considered to be caused by intrinsic factors that weaken the arterial wall. Only a very small proportion (1–4%) have a clear underlying connective tissue disorder, such as Ehlers–Danlos syndrome type 4 and more rarely Marfan's syndrome. Ehlers-Danlos syndrome type 4, caused by mutations of the "COL3A" gene, leads to defective production of the collagen, type III, alpha 1 protein and causes skin fragility as well as weakness of the walls of arteries and internal organs. Marfan's syndrome results from mutations in the "FBN1" gene, defective production of the protein fibrillin-1, and a number of physical abnormalities including aneurysm of the aortic root.

There have also been reports in other genetic conditions, such as osteogenesis imperfecta type 1, autosomal dominant polycystic kidney disease and pseudoxanthoma elasticum, α antitrypsin deficiency and hereditary hemochromatosis, but evidence for these associations is weaker. Genetic studies in other connective tissue-related genes have mostly yielded negative results. Other abnormalities to the blood vessels, such as fibromuscular dysplasia, have been reported in a proportion of cases. Atherosclerosis does not appear to increase the risk.

There have been numerous reports of associated risk factors for vertebral artery dissection; many of these reports suffer from methodological weaknesses, such as selection bias. Elevated homocysteine levels, often due to mutations in the "MTHFR" gene, appear to increase the risk of vertebral artery dissection. People with an aneurysm of the aortic root and people with a history of migraine may be predisposed to vertebral artery dissection.

Thrombosis prevention is initiated with assessing the risk for its development. Some people have a higher risk of developing thrombosis and its possible development into thromboembolism. Some of these risk factors are related to inflammation. "Virchow's triad" has been suggested to describe the three factors necessary for the formation of thrombosis: stasis of blood, vessel wall injury, and altered blood coagulation. Some risk factors predispose for venous thrombosis while others increase the risk of arterial thrombosis.

Individuals with CAVD can reproduce with the assistance of modern technology with a combination of testicular sperm extraction and intracytoplasmic sperm injection (ICSI). However, as the risk of either cystic fibrosis or renal agenesis is likely to be higher in the children, genetic counseling is generally recommended.

Prognosis of spontaneous cervical arterial dissection involves neurological and arterial results. The overall functional prognosis of individuals with stroke due to cervical artery dissection does not appear to vary from that of young people with stroke due to other causes. The rate of survival with good outcome (a modified Rankin score of 0–2) is generally about 75%, or possibly slightly better (85.7%) if antiplatelet drugs are used. In studies of anticoagulants and aspirin, the combined mortality with either treatment is 1.8–2.1%.

After the initial episode, 2% may experience a further episode within the first month. After this, there is a 1% annual risk of recurrence. Those with high blood pressure and dissections in multiple arteries may have a higher risk of recurrence. Further episodes of cervical artery dissection are more common in those who are younger, have a family history of cervical artery dissection, or have a diagnosis of Ehlers-Danlos syndrome or fibromuscular dysplasia.

There are two main populations of CAVD; the larger group is associated with

cystic fibrosis and occurs because of a mutation in the CFTR gene, while the smaller group (estimated between 10 and 40%) is associated with Unilateral Renal agenesis (URA). The genetic basis of this second group is not well understood.

Mutation of the CFTR gene is found to result in obstructive azoospermia in postpubertal males with cystic fibrosis. Strikingly, CAVD is one of the most consistent features of cystic fibrosis as it affects 98-99% of individuals in this CF patient population. In contrast, acute or persistent respiratory symptoms present in only 51% of total CF patients.

In the subset of males with both CBAVD and URA, the CFTR mutation has been shown to occur at a rate only slightly higher than the overall population. Thus, McCallum, et al. have suggested another mutation may be responsible for this condition.

The main causes of thrombosis are given in Virchow's triad which lists thrombophilia, endothelial cell injury, and disturbed blood flow.

Persistent Müllerian duct syndrome (PMDS) is the presence of Müllerian duct derivatives (fallopian tubes, uterus, and/or the upper part of the vagina) in what would be considered a genetically and otherwise physically normal male animal by typical human based standards. In humans, PMDS typically is due to an autosomal recessive congenital disorder and is considered by some to be a form of pseudohermaphroditism due to the presence of Müllerian derivatives.

Typical features include undescended testes (cryptorchidism) and the presence of a small, underdeveloped uterus in an XY infant or adult. This condition is usually caused by deficiency of fetal anti-Müllerian hormone (AMH) effect due to mutations of the gene for AMH or the anti-Müllerian hormone receptor, but may also be as a result of insensitivity to AMH of the target organ.

Ejaculatory duct obstruction (EDO) is a congenital or acquired pathological condition which is characterized by the obstruction of one or both ejaculatory ducts. Thus, the efflux of (most constituents of) semen is not possible.

It is a cause of male infertility and / or pelvic pain. Ejaculatory duct obstruction must not be confused with an obstruction of the vas deferens.

If both ejaculatory ducts are completely obstructed, affected men will demonstrate male infertility due to aspermia/azoospermia. They will suffer from a very low volume of semen which lacks the gel-like fluid of the seminal vesicles or from no semen at all while they are able to have the sensation of an orgasm during which they will have involuntary contractions of the pelvic musculature. This is contrary to some other forms of anejaculation.

Ejaculatory duct obstruction is the underlying cause for 1–5% of male infertility.

In addition, it is reported to be a cause for pelvic pain, especially shortly after ejaculation. In case of proven fertility but unresolved pelvic pain, even one or both partially obstructed ejaculatory ducts may be the origin of pelvic pain and oligospermia.

Ejaculatory duct obstruction may result in a complete lack of semen (aspermia) or a very low-volume semen (oligospermia) which may contain only the secretion of accessory prostate glands downstream to the orifice of the ejaculatory ducts.

In addition to the congenital form which is often caused by cysts of the müllerian duct the obstruction can be acquired due to an inflammation caused by chlamydia, prostatitis, tuberculosis of the prostate and other pathogens. In Addition, calculus was reported to mechanically block the ejaculatory duct, leading to infertility. However, in many patients, there is no history of an inflammation and the underlying cause simply remains unknown.

Incidence rates of cranial aneurysms are estimated at between 0.4% and 3.6%. Those without risk factors have expected prevalence of 2–3%. In adults, females are more likely to have aneurysms. They are most prevalent in people ages 35 – 60, but can occur in children as well. Aneurysms are rare in children with a reported prevalence of .5% to 4.6%. The most common incidence are among 50-year-olds, and there are typically no warning signs. Most aneurysms develop after the age of 40.

Because both the Wolffian ducts and Müllerian ducts begin to develop, the tissues are often intertwined, resulting in obstruction or nonpatency of the vas deferens or other parts of the reproductive excretory ducts. This can result in infertility, the most serious potential problem caused by this condition. Sometimes, transverse testicular ectopia is evident.

Cryptorchidism in AMH deficiency suggests that AMH may play a role in transabdominal testicular descent, perhaps by facilitating contraction of the gubernaculum.

Other Müllerian derivatives which may be present in at least a rudimentary form are the cervix, upper part of the vagina, and fallopian tubes.

The condition can come to attention because of a bulge in the inguinal canal of an XY infant due to herniation of the uterus. The presence of a uterus may be noticed if an ultrasound or MRI of the pelvis is performed to locate the testes or for other reasons. Occasionally the uterus is discovered during abdominal surgery for some other purpose in later childhood or adult life.

Although persistent Müllerian duct syndrome is classified as an intersex condition, it does not involve ambiguity or malformation of the external genitalia, which appear typical (apart from cryptorchidism if present). Sometimes the uterus enters a hernia. Sometimes the Müllerian structures get entangled with the spermatic ducts and interfere with the descent of the testes.

Apart from humans, this syndrome has been reported in dogs.

The exact causes of the degenerative process remain unclear. There are, however, some hypotheses and well-defined risk factors.

- Tobacco smoking: More than 90% of people who develop an AAA have smoked at some point in their lives.

- Alcohol and hypertension: The inflammation caused by prolonged use of alcohol and hypertensive effects from abdominal edema which leads to hemorrhoids, esophageal varices, and other conditions, is also considered a long-term cause of AAA.

- Genetic influences: The influence of genetic factors is high. AAA is four to six times more common in male siblings of known patients, with a risk of 20-30%. The high familial prevalence rate is most notable in male individuals. There are many hypotheses about the exact genetic disorder that could cause higher incidence of AAA among male members of the affected families. Some presumed that the influence of alpha 1-antitrypsin deficiency could be crucial, while other experimental works favored the hypothesis of X-linked mutation, which would explain the lower incidence in heterozygous females. Other hypotheses of genetic causes have also been formulated. Connective tissue disorders, such as Marfan syndrome and Ehlers-Danlos syndrome, have also been strongly associated with AAA. Both relapsing polychondritis and pseudoxanthoma elasticum may cause abdominal aortic aneurysm.

- Atherosclerosis: The AAA was long considered to be caused by atherosclerosis, because the walls of the AAA frequently carry an atherosclerotic burden. However, this hypothesis cannot be used to explain the initial defect and the development of occlusion, which is observed in the process.

- Other causes of the development of AAA include: infection, trauma, arteritis, and cystic medial necrosis.

Incidence rates are two to three times higher in males, while there are more large and giant aneurysms and fewer multiple aneurysms. Intracranial hemorrhages are 1.6 times more likely to be due to aneurysms than cerebral arteriovenous malformations in whites, but four times less in certain Asian populations.

Most patients, particularly infants, present with subarachnoid hemorrhage and corresponding headaches or neurological deficits. The mortality rate for pediatric aneurysms is lower than in adults.