Some recent research has suggested that a proportion of cases of migraine may be caused by PFO. While the exact mechanism remains unclear, closure of a PFO can reduce symptoms in certain cases. This remains controversial; 20% of the general population has a PFO, which for the most part, is asymptomatic. About 20% of the female population has migraines, and the placebo effect in migraine typically averages around 40%. The high frequency of these facts finding statistically significant relationships between PFO and migraine difficult (i.e., the relationship may just be chance or coincidence). In a large randomized controlled trial, the higher prevalence of PFO in migraine patients was confirmed, but migraine headache cessation was not more prevalent in the group of migraine patients who underwent closure of their PFOs.

A PDA is sometimes idiopathic. Known risk factors include:

- Preterm birth

- Congenital rubella syndrome

- Chromosomal abnormalities (e.g., Down syndrome)

- Genetic conditions such as Loeys-Dietz syndrome (would also present with other heart defects), Wiedemann-Steiner syndrome, and CHAR syndrome.

Since PDA is usually identified in infants, it is less common in adults, but it can have serious consequences, and is usually corrected surgically upon diagnosis.

Venous thrombus (clots in the veins) are quite common. Embolizations (dislodgement of thrombi) normally go to the lung and cause pulmonary emboli. In an individual with ASD, these emboli can potentially enter the arterial system, which can cause any phenomenon attributed to acute loss of blood to a portion of the body, including cerebrovascular accident (stroke), infarction of the spleen or intestines, or even a distal extremity (i.e., finger or toe).

This is known as a paradoxical embolus because the clot material paradoxically enters the arterial system instead of going to the lungs.

VSDs are the most common congenital cardiac abnormalities. They are found in 30-60% of all newborns with a congenital heart defect, or about 2-6 per 1000 births. During heart formation, when the heart begins life as a hollow tube, it begins to partition, forming septa. If this does not occur properly it can lead to an opening being left within the ventricular septum. It is debatable whether all those defects are true heart defects, or if some of them are normal phenomena, since most of the trabecular VSDs close spontaneously. Prospective studies give a prevalence of 2-5 per 100 births of trabecular VSDs that close shortly after birth in 80-90% of the cases.

Congenital VSDs are frequently associated with other congenital conditions, such as Down syndrome.

A VSD can also form a few days after a myocardial infarction (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead heart tissue.

The causes of congenital VSD (ventricular septal defect) include the

incomplete looping of the heart during days 24-28 of development. Faults with NKX2.5 gene are usually associated with isolated (non syndromic) ASD in humans when one copy is missing.

Risk factors for thromboembolism, the major cause of arterial embolism, include disturbed blood flow (such as in atrial fibrillation and mitral stenosis), injury or damage to an artery wall, and hypercoagulability (such as increased platelet count). Mitral stenosis poses a high risk of forming emboli which may travel to the brain and cause stroke. Endocarditis increases the risk for thromboembolism, by a mixture of the factors above.

Atherosclerosis in the aorta and other large blood vessels is a common risk factor, both for thromboembolism and cholesterol embolism. The legs and feet are major impact sites for these types. Thus, risk factors for atherosclerosis are risk factors for arterial embolisation as well:

- advanced age

- cigarette smoking

- hypertension (high blood pressure)

- obesity

- hyperlipidemia, e.g. hypercholesterolemia, hypertriglyceridemia, elevated lipoprotein (a) or apolipoprotein B, or decreased levels of HDL cholesterol)

- diabetes mellitus

- Sedentary lifestyle

- stress

Other important risk factors for arterial embolism include:

- recent surgery (both for thromboembolism and air embolism)

- previous stroke or cardiovascular disease

- a history of long-term intravenous therapy (for air embolism)

- Bone fracture (for fat embolism)

A septal defect of the heart makes it possible for paradoxical embolization, which happens when a clot in a vein enters the right side of the heart and passes through a hole into the left side. The clot can then move to an artery and cause arterial embolisation.

In the United States, approximately 550,000 people die each year from heart-related arterial embolism and thrombosis. Approximately 250,000 of these individuals are female, and approximately 100,000 of all these deaths are considered premature, that is, prior to the age of average life expectancy.

Carotid cavernous fistulae may form following closed or penetrating head trauma, surgical damage, rupture of an intracavernous aneurysm, or in association with connective tissue disorders, vascular diseases and dural fistulas.

Various classifications have been proposed for CCF. They may be divided into low-flow or high-flow, traumatic or spontaneous and direct or indirect. The traumatic CCF typically occurs after a basal skull fracture. The spontaneous dural cavernous fistula which is more common usually results from a degenerative process in older patients with systemic hypertension

and atherosclerosis. Direct fistulas occur when the Internal Carotid artery (ICA) itself fistulizes into the Cavernous sinus whereas indirect is when a branch of the ICA or External Carotid artery (ECA) communicates with the cavernous sinus.

A popular classification divides CCF into four varieties depending on the type of arterial supply.

Occurring at a rate between 1 in 10,000 to 1 in 50,000 with a male-to-female ratio of 2.3-6:1, bladder exstrophy is relatively rare. For those individuals with bladder exstrophy who maintain their ability to reproduce, the risk of bladder exstrophy in their children is approximately 500-fold greater than the general population.

Environmental factors refer for example to maternal smoking and the maternal exposure to amine-containing drugs. Several research groups have found evidence that these environmental factors are responsible for an increase in the risk of craniosynostosis, likely through effects on fibroblast growth factor receptor genes.

On the other hand, a recent evaluation of valproic acid (an anti-epilepticum), which has been implicated as a causative agent, has shown no association with craniosynostosis.

Certain medication (like amine-containing drugs) can increase the risk of craniosynostosis when taken during pregnancy, these are so-called teratogenic factors.

Biomechanical factors include fetal head constraint during pregnancy. It has been found by Jacob et al. that constraint inside the womb is associated with decreased expression of Indian Hedgehog protein and noggin. These last two are both important factors influencing bone development.

Omphalomesenteric duct cysts (ODC, also known as an omphalomesenteric duct remnant or vitelline cyst) are developmental defects relating to the closure of the omphalomesenteric duct. It usually disintegrates within six weeks of gestation, but remnants of the cyst can sometimes be found along the intestines or umbilicus. Any remnants can be removed via surgical means.

A nasal septum perforation is a medical condition in which the nasal septum, the cartilaginous membrane dividing the nostrils, develops a hole or fissure.

This may be brought on directly, as in the case of nasal piercings, or indirectly, as by long-term topical drug application, including intranasal ethylphenidate, methamphetamine, cocaine, crushed prescription pills, or decongestant nasal sprays, chronic epistaxis, excessive nose picking and as a complication of nasal surgery like septoplasty or rhinoplasty. Much less common causes for perforated nasal septums include rare granulomatous inflammatory conditions like granulomatosis with polyangiitis. It has been reported as a side effect of anti-angiogenesis drugs like bevacizumab.

Approximately 20–40 percent of all infants with duodenal atresia have Down syndrome. . Approximately 8% of infants with Down syndrome have duodenal atresia.

Early treatment includes removing fluids from the stomach via a nasogastric tube, and providing fluids intravenously. The definitive treatment for duodenal atresia is surgery (duodenoduodenostomy), which may be performed openly or laparoscopically. The surgery is not urgent. The initial repair has a 5 percent morbidity and mortality rate.

There are many causes of "fetal distress" including:

- Breathing problems

- Abnormal position and presentation of the fetus

- Multiple births

- Shoulder dystocia

- Umbilical cord prolapse

- Nuchal cord

- Placental abruption

- Premature closure of the fetal ductus arteriosus

- Uterine rupture

- Intrahepatic cholestasis of pregnancy, a liver disorder during pregnancy

The most important criterion for improving long-term prognosis is success of the initial closure. If a patient requires more than one closure their chance of continence drops off precipitously with each additional closure - at just two closures the chance of voiding continence is just 17%.

Even with successful surgery, people may have long-term complications. Some of the most common include:

- Vesicoureteral reflux

- Bladder spasm

- Bladder calculus

- Urinary tract infections

Septal perforations are managed with a multitude of options. The treatment often depends on the severity of symptoms and the size of the perforations. Generally speaking anterior septal perforations are more bothersome and symptomatic. Posterior septal perforations, which mainly occur iatrogenically, are often managed with simple observation and are at times intended portions of skull base surgery. Septal perforations that are not bothersome can be managed with simple observation. While no septal perforation will spontaneously close, for the majority of septal perforations that are unlikely to get larger observation is an appropriate form of management. For perforations that bleed or are painful, initial management should include humidification and application of salves to the perforation edges to promote healing. Mucosalization of the perforation edges will help prevent pain and recurrent epistaxis and majority of septal perforations can be managed without surgery.

For perforations in which anosmia, or the loss of smell, and a persistent whistling are a concern the use of a sillicone septal button is a treatment option. These can be placed while the patient is awake and usually in the clinic setting. While complications of button insertion are minimal, the presence of the button can be bothersome to most patients.

For patients who desire definitive close, surgery is the only option. Prior to determining candidacy for surgical closure, the etiology of the perforation must be determined. Often this requires a biopsy of the perforation to rule out autoimmune causes. If a known cause such as cocaine is the offending agent, it must be ensured that the patient is not still using the irritant.

For those that are determined to be medically cleared for surgery, the anatomical location and size of the perforation must be determined. This is often done with a combination of a CT scan of the sinuses without contrast and an endoscopic evaluation by an Ear Nose and Throat doctor. Once dimensions are obtained the surgeon will decide if it is possible to close the perforation. Multiple approaches to access the septum have been described in the literature. While sublabial and midfacial degloving approaches have been described, the most popular today is the rhinoplasty approach. This can include both open and closed methods. The open method results in a scar on the columella, however, it allows for more visibility to the surgeon. The closed method utilizes an incision all on the inside of the nose. The concept behind closure includes bringing together the edges of mucosa on each side of the perforation with minimal tension. An interposition graft is also often used. The interposition graft provides extended stability and also structure to the area of the perforation. Classically, a graft from the scalp utilizing temporalis fascia was used. Kridel, et al., first described the usage of acellular dermis so that no further incisions are required; they reported an excellent closure rate of over 90%. Overall perforation closure rates are variable and often determined by the skill of the surgeon and technique used. Often surgeons who claim a high rate of closure choose perforations that are easier to close. An open rhinoplasty approach also allows for better access to the nose to repair any concurrent nasal deformities, such as saddle nose deformity, that occur with a septal perforation.

Germinal matrix hemorrhage is a bleeding into the subependymal germinal matrix with or without subsequent rupture into the lateral ventricle. Such intraventricular hemorrhage can occur due to perinatal asphyxia in preterm neonates.

Treatment is symptomatic, often addressing indicators associated with peripheral pulmonary artery stenosis. Laryngotracheal calcification resulting in dyspnea and forceful breathing can be treated with bronchodilators including the short and long-acting β2-agonists, and various anticholinergics. Prognosis is good, yet life expectancy depends on the severity and extent of diffuse pulmonary and arterial calcification.

Typical recovery from NEC if medical, non-surgical treatment succeeds, includes 10–14 days or more without oral intake and then demonstrated ability to resume feedings and gain weight. Recovery from NEC alone may be compromised by co-morbid conditions that frequently accompany prematurity. Long-term complications of medical NEC include bowel obstruction and anemia.

In the United States it caused 355 deaths per 100,000 live births in 2013, down from 484 per 100,000 live births in 2009. Rates of death were almost three times higher for the black populations than for the white populations.

Overall, about 70-80% of infants who develop NEC survive. Medical management of NEC shows an increased chance of survival compared to surgical management. Despite a significant mortality risk, long-term prognosis for infants undergoing NEC surgery is improving, with survival rates of 70–80%. "Surgical NEC" survivors are at risk for complications including short bowel syndrome and neurodevelopmental disability.

Involutional stenosis is probably the most common cause of NLD obstruction in older persons. It affects women twice as frequently as men. Although the inciting event in this process is unknown, clinicopathologic study suggests that compression of the lumen of the NLD is caused by inflammatory infiltrates and edema. This may be the result of an unidentified infection or possibly an autoimmune disease.

Pancreas divisum in individuals with no symptoms does not require treatment. Treatment of those with symptoms varies and has not been well established. A surgeon may attempt a sphincterotomy by cutting the minor papilla to enlarge the opening and allow pancreatic enzymes to flow normally. During surgery, a stent may be inserted into the duct to ensure that the duct will not close causing a blockage. This surgery can cause pancreatitis in patients, or in rare cases, kidney failure and death.

An association with adenoma of the minor papilla has been reported.