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 places where a Caesarean section could not be performed due to the lack of a surgeon or equipment, infant could be delivered vaginally. There were two ways of doing this with a placenta previa:

- The baby's head can be brought down to the placental site (if necessary with Willet's forceps or a vulsellum) and a weight attached to its scalp

- A leg can be brought down and the baby's buttocks used to compress the placental site

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".

An initial assessment to determine the status of the mother and fetus is required. Although mothers used to be treated in the hospital from the first bleeding episode until birth, it is now considered safe to treat placenta previa on an outpatient basis if the fetus is at less than 30 weeks of gestation, and neither the mother nor the fetus are in distress. Immediate delivery of the fetus may be indicated if the fetus is mature or if the fetus or mother are in distress. Blood volume replacement (to maintain blood pressure) and blood plasma replacement (to maintain fibrinogen levels) may be necessary.

Corticosteroids are indicated at 24–34 weeks gestation, given the higher risk of premature birth.

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.

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.

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.

Obstetrical bleeding also known as obstetrical hemorrhage and maternal hemorrhage, refers to heavy bleeding during pregnancy, labor, or the postpartum period. Bleeding may be vaginal or less commonly but more dangerously, internal, into the abdominal cavity. Typically bleeding is related to the pregnancy itself, but some forms of bleeding are caused by other events.

The most frequent cause of maternal mortality worldwide is severe hemorrhage with 8.7 million cases occurring in 2015 and 83,000 of those events resulting in maternal death. Between 2003 and 2009, hemorrhage accounted for 27.1% of all maternal deaths globally

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.

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 Dutch 2010 research showed that "low-risk" pregnancy in the Netherlands may actually carry a higher risk of perinatal death than a "high-risk" pregnancy.

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.

A method to treat ejaculatory duct obstruction is transurethral resection of the ejaculatory ducts (TURED). This operative procedure is relatively invasive, has some severe complications, and has led to natural pregnancies of their partners in approximately 20% of affected men. A disadvantage is the destruction of the valves at the openings of the ejaculatory ducts into the urethra such that urine may flow backwards into the seminal vesicles. Another, experimental approach is the recanalization of the ejaculatory ducts by transrectal or transurethral inserted balloon catheter. Though much less invasive and preserving the anatomy of the ejaculatory ducts, this procedure is probably not completely free of complications either and success rates are unknown. There is a clinical study currently ongoing to examine the success rate of recanalization of the ejaculatory ducts by means of balloon dilation.

Usually, affected men have a normal production of spermatozoa in their testicles, so that after spermatozoa were harvested directly from the testes e.g. by TESE, or the seminal vesicles (by needle aspiration) they and their partners are potentially candidates for some treatment options of assisted reproduction e.g. in-vitro fertilisation. Note that in this case, most of the treatment (e.g. ovarian stimulation and transvaginal oocyte retrieval) is transferred to the female partner.

Surgery (orchiopexy) to retrieve the testes and position them in the scrotum is the primary treatment. Occasionally they are unsalvageable if located high in the retroperitoneum. During this surgery, the uterus is usually removed and attempts made to dissect away Müllerian tissue from the vas deferens and epididymis to improve the chance of fertility. If the person has male gender identity himself and the testes cannot be retrieved, testosterone replacement will be usually necessary at puberty should the affected individual choose to pursue medical attention. Lately, laparoscopic hysterectomy is offered to patients as a solution to both improve the chances of fertility and to prevent the occurrences of neoplastic tissue formation.

Currently, there is controversy over whether or not inheritance truly plays a role in FAD, and if so which gene it acts upon. FAD does not come from strictly one predisposing factor, such as hypertension. It is suggested that the combination of environmental factors along with genetics may contribute to causing FAD. Before newer and more effective cures and therapies can be developed, first the specific gene mutation must be identified. Until such a gene is determined, scientists say patient education, and physician awareness is vital. Currently scientists have found animal models to be beneficial in understanding the pathology behind FAD. In the future there is hope to develop drugs that will better support and strengthen the aortic wall. Endovascular methods of treatment are becoming increasingly popular, and scientists hope to use this technique in both acute and chronic cases.

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.

Newer clinical trial results (2007), e.g. the COURAGE trial, have demonstrated that aggressively treating some of the physiologic behavioral factors that promote atheromas with "optimal medical therapy" (not opening narrowing(s), a.k.a. stenoses, per se) produced the most effective results in terms of improving human survival and quality of life for those identified as having already developed advanced cardiovascular disease with many vulnerable plaques.

Treatment is focused on reducing stroke episodes and damage from a distending artery. Four treatment modalities have been reported in the treatment of vertebral artery dissection. The two main treatments involve medication: anticoagulation (using heparin and warfarin) and antiplatelet drugs (usually aspirin). More rarely, thrombolysis (medication that dissolves blood clots) may be administered, and occasionally obstruction may be treated with angioplasty and stenting. No randomized controlled trials have been performed to compare the different treatment modalities. Surgery is only used in exceptional cases.

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.

From analysis of the existing small treatment trials of cervical artery dissection (carotid and vertebral) it appears that aspirin and anticoagulation (heparin followed by warfarin) are equally effective in reducing the risk of further stroke or death. Anticoagulation is regarded as more powerful than antiplatelet therapy, but anticoagulants may increase the size of the hematoma and worsen obstruction of the affected artery. Anticoagulation may be relatively unsafe if a large stroke has already occurred, as hemorrhagic transformation is relatively common, and if the dissection extends into V4 (carrying a risk of subarachnoid hemorrhage). Anticoagulation may be appropriate if there is rapid blood flow (through a severely narrowed vessel) on transcranial doppler despite the use of aspirin, if there is a completely occluded vessel, if there are recurrent stroke-like episodes, or if free-floating blood clot is visible on scans. Warfarin is typically continued for 3–6 months, as during this time the flow through the artery usually improves, and most strokes happen within the first 6 months after the development of the dissection. Some regard 3 months as sufficient.

Professional guidelines in the UK recommend that patients with VA dissection should be enrolled in a clinical trial comparing aspirin and anticoagulation if possible. American guidelines state that the benefit of anticoagulation is not currently established.

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.

Conservative management is indicated in people where repair carries a high risk of mortality and in patients where repair is unlikely to improve life expectancy. The mainstay of the conservative treatment is smoking cessation.

Surveillance is indicated in small asymptomatic aneurysms (less than 5.5 cm) where the risk of repair exceeds the risk of rupture. As an AAA grows in diameter, the risk of rupture increases. Surveillance until an aneurysm has reached a diameter of 5.5 cm has not been shown to have a higher risk as compared to early intervention.

Many surgical procedures have been developed to create a neovagina, as none of them is ideal. Surgical intervention should only be considered after non-surgical pressure dilation methods have failed to produce a satisfactory result. Neovaginoplasty can be performed using skin grafts, a segment of bowel, ileum, peritoneum, Interceed, buccal mucosa, amnion, or dura mater. Success of such methods should be determined by sexual function, and not just by vaginal length, as has been done in the past. Ileal or cecal segments may be problematic because of a shorter mesentery, which may produce tension on the neovagina, leading to stenosis. The sigmoid neovagina is thought to be self-lubricating, without the excess mucus production associated with segments of small bowel. Vaginoplasty may create scarring at the introitus (the vaginal opening), which requires additional surgery to correct. Vaginal dilators are required postoperatively to prevent vaginal stenosis from scarring. Other complications include bladder and bowel injuries. Yearly exams are required as neovaginoplasty carries a risk of carcinoma, although carcinoma of the neovagina is uncommon. Neither neovaginoplasty nor vaginal dilation should be performed before puberty.

Arterial thrombosis is platelet-rich, and inhibition of platelet aggregation with antiplatelet drugs such as aspirin may reduce the risk of recurrence or progression.

The treatment for thrombosis depends on whether it is in a vein or an artery, the impact on the person, and the risk of complications from treatment.