With early intervention, morbidity and mortality of cases of intestinal obstruction is low. The outcome is in part dependent upon congenital comorbidities and delays in diagnosis and management.

The most common cause of non-duodenal intestinal atresia is a vascular accident in utero that leads to decreased intestinal perfusion and ischemia of the respective segment of bowel. This leads to narrowing, or in the most severe cases, complete obliteration of the intestinal lumen.

In the case that the superior mesenteric artery, or another major intestinal artery, is occluded, large segments of bowel can be entirely underdeveloped. Classically, the affected area of bowel assumes a spiral configuration and is described to have an "apple peel" like appearance; this is accompanied by lack of a dorsal mesentery.

Ileal atresia can also result as a complication of meconium ileus.

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

The different types of intestinal atresia are named after their location:

- Duodenal atresia – malformation of the duodenum, part of the intestine that empties from the stomach

- Jejunal atresia – malformation of the jejunum, the second part of the intestine extending from the duodenum to the ileum

- Ileal atresia – malformation of the ileum, the lower part of the small intestine

- Colon atresia – malformation of the colon

Duodenal atresia has a strong association with Down syndrome. It is the most common type, followed by ileal atresia.

An inherited form – familial multiple intestinal atresia – has also been described. This disorder was first reported in 1971. It is due to a mutation in the gene TTC7A on short arm of chromosome 2 (2p16). It is inherited as an autosomal recessive gene and is usually fatal in infancy.

If left untreated, gastroschisis is fatal to the infant; however, in adequate settings the survival rate for treated infants is 90%.

Most risks of gastroschisis are related to decreased bowel function. Sometimes blood flow to the exposed organs is impaired or there may be less than the normal amount of intestine. This may put infants at risk for other dangerous conditions such as necrotizing enterocolitis. Also, because their intestines are exposed, infants with gastroschisis are at increased risk for infection, and must be closely monitored.

Prognosis is usually very good, although complications are more likely to occur when there are serious congenital anomalies. Late complications may occur in about 12 percent of patients with duodenal atresia, and the mortality rate for these complications is 6 percent.

Neonates with TEF or esophageal atresia are unable to feed properly. Once diagnosed, prompt surgery is required to allow the food intake. Some children do experience problems following TEF surgery; they can develop dysphagia and thoracic problems. Children with TEF can also be born with other abnormalities, most commonly those described in VACTERL association - a group of anomalies which often occur together, including heart, kidney and limb deformities. 6% of babies with TEF also have a laryngeal cleft.

The prognosis for non-ischemic cases of SBO is good with mortality rates of 3–5%, while prognosis for SBO with ischemia is fair with mortality rates as high as 30%.

Cases of SBO related to cancer are more complicated and require additional intervention to address the malignancy, recurrence, and metastasis, and thus are associated with poorer prognosis.

All cases of abdominal surgical intervention are associated with increased risk of future small-bowel obstructions. Statistics from U.S. healthcare report 18.1% re-admittance rate within 30 days for patients who undergo SBO surgery. More than 90% of patients also form adhesions after major abdominal surgery.

Common consequences of these adhesions include small-bowel obstruction, chronic abdominal pain, pelvic pain, and infertility.

As of 2015 the worldwide incidence was about 2 to 5 per 10 000 live births, and this number seemed to be increasing.

As of 2017 the CDC estimates that about 1,871 babies are born each year in the United States with gastroschisis.

Biliary atresia seems to affect females slightly more often than males, and Asians and African Americans more often than Caucasians. It is common for only one child in a pair of twins or within the same family to have the condition. There seems to be no link to medications or immunizations given immediately before or during pregnancy. Diabetes during pregnancy particularly during the first trimester seems to predispose to a number of distinct congenital abnormalities in the infant such as sacral agenesis and the syndromic form of biliary atresia.

Fetal and neonatal bowel obstructions are often caused by an intestinal atresia, where there is a narrowing or absence of a part of the intestine. These atresias are often discovered before birth via an ultrasound, and treated with using laparotomy after birth. If the area affected is small, then the surgeon may be able to remove the damaged portion and join the intestine back together. In instances where the narrowing is longer, or the area is damaged and cannot be used for a period of time, a temporary stoma may be placed.

The diagnosis is suspected based on polyhydramnios in uteru, bilious vomiting, failure to pass meconium in the first day of life, and abdominal distension. The presentations of NBO may vary. It may be subtle and easily overlooked on physical examination or can involve massive abdominal distension, respiratory distress and cardiovascular collapse. Unlike older children, neonates with unrecognized intestinal obstruction deteriorate rapidly.

A method for repairing long-gap esophageal atresia using magnets has been developed, that does not require replacing the missing section with grafts of the intestine or other body parts. Using electromagnetic force to attract the upper and lower ends of the esophagus together was first tried in the 1970s by using steel pellets attracted to each other by applying external electromagnets to the patient. In the 2000s a further refinement was developed by Mario Zaritzky's group and others. The newer method uses permanent magnets and a balloon.

1. The magnets are inserted into the upper pouch via the baby's mouth or nose, and the lower via the gastrotomy feeding tube hole (which would have had to be made anyway to feed the baby, therefore not requiring any additional surgery).

2. The distance between the magnets is controlled by a balloon in the upper pouch, between the end of the pouch and the magnet. This also controls the force between the magnets so it is not strong enough to cause damage.

3. After the ends of the esophagus have stretched enough to touch, the upper magnet is replaced by one without a balloon and the stronger magnetic attraction causes the ends to fuse (anastomosis).

In April 2015 Annalise Dapo became the first patient in the United States to have their esophageal atresia corrected using magnets.

Imperforate anus has an estimated incidence of 1 in 5000 births. It affects boys and girls with similar frequency. However, imperforate anus will present as the low version 90% of the time in females and 50% of the time in males.

Imperforate anus is an occasional complication of sacrococcygeal teratoma.

It occurs in approximately 1 in 2500 live births.

Congenital esophageal atresia (EA) represents a failure of the esophagus to develop as a continuous passage. Instead, it ends as a blind pouch. Tracheoesophageal fistula (TEF) represents an abnormal opening between the trachea and esophagus. EA and TEF can occur separately or together. EA and TEF are diagnosed in the ICU at birth and treated immediately.

The presence of EA is suspected in an infant with excessive salivation (drooling) and in a newborn with drooling that is frequently accompanied by choking, coughing and sneezing. When fed, these infants swallow normally but begin to cough and struggle as the fluid returns through the nose and mouth. The infant may become cyanotic (turn bluish due to lack of oxygen) and may stop breathing as the overflow of fluid from the blind pouch is aspirated (sucked into) the trachea. The cyanosis is a result of laryngospasm (a protective mechanism that the body has to prevent aspiration into the trachea). Over time respiratory distress will develop.

If any of the above signs/symptoms are noticed, a catheter is gently passed into the esophagus to check for resistance. If resistance is noted, other studies will be done to confirm the diagnosis. A catheter can be inserted and will show up as white on a regular x-ray film to demonstrate the blind pouch ending. Sometimes a small amount of barium (chalk-like liquid) is placed through the mouth to diagnose the problems.

Treatment of EA and TEF is surgery to repair the defect. If EA or TEF is suspected, all oral feedings are stopped and intravenous fluids are started. The infant will be positioned to help drain secretions and decrease the likelihood of aspiration. Babies with EA may sometimes have other problems. Studies will be done to look at the heart, spine and kidneys.

Surgery to repair EA is essential as the baby will not be able to feed and is highly likely to develop pneumonia. Once the baby is in condition for surgery, an incision is made on the side of the chest. The esophagus can usually be sewn together. Following surgery, the baby may be hospitalized for a variable length of time. Care for each infant is individualized.

Its very commonly seen in a newborn with imperforate anus.

Surgical repair can sometimes result in complications, including:

- Stricture, due to gastric acid erosion of the shortened esophagus

- Leak of contents at the point of anastomosis

- Recurrence of fistula

- Gastro-esophageal reflux disease

- Dysphagia

- Asthma-like symptoms, such as persistent coughing/wheezing

- Recurrent chest infections

- Tracheomalacia

With a high lesion, many children have problems controlling bowel function and most also become constipated. With a low lesion, children generally have good bowel control, but they may still become constipated.

For children who have a poor outcome for continence and constipation from the initial surgery, further surgery to better establish the angle between the anus and the rectum may improve continence and, for those with a large rectum, surgery to remove that dilated segment may significantly improve the bowel control for the patient. An antegrade enema mechanism can be established by joining the appendix to the skin (Malone stoma); however, establishing more normal anatomy is the priority.

Esophageal diseases can derive from congenital conditions, or they can be acquired later in life.

Many people experience a burning sensation in their chest occasionally, caused by stomach acids refluxing into the esophagus, normally called heartburn. Extended exposure to heartburn may erode the lining of the esophagus, leading potentially to Barrett's esophagus which is associated with an increased risk of adenocarcinoma most commonly found in the distal one-third of the esophagus.

Some people also experience a sensation known as globus esophagus, where it feels as if a ball is lodged in the lower part of the esophagus.

The following are additional diseases and conditions that affect the esophagus:

- Achalasia

- Acute esophageal necrosis

- Barrett's esophagus

- Boerhaave syndrome

- Caustic injury to the esophagus

- Chagas disease

- Diffuse esophageal spasm

- Esophageal atresia and Tracheoesophageal fistula

- Esophageal cancer

- Esophageal dysphagia

- Esophageal varices

- Esophageal web

- Esophagitis

- GERD

- Hiatus hernia

- Jackhammer esophagus (hypercontractile peristalsis)

- Killian–Jamieson diverticulum

- Mallory-Weiss syndrome

- Neurogenic dysphagia

- Nutcracker esophagus

- Schatzki's ring

- Zenker's Diverticulum

Atresia is a condition in which an orifice or passage in the body is (usually abnormally) closed or absent.

Examples of atresia include:

- Biliary atresia, a condition in newborns in which the common bile duct between the liver and the small intestine is blocked or absent.

- Choanal atresia, blockage of the back of the nasal passage, usually by abnormal bony or soft tissue.

- Esophageal atresia, which affects the alimentary tract and causes the esophagus to end before connecting normally to the stomach.

- Imperforate anus, malformation of the opening between the rectum and anus.

- Intestinal atresia, malformation of the intestine, usually resulting from a vascular accident in utero.

- Microtia, absence of the ear canal or failure of the canal to be tubular or fully formed (can be related to Microtia, a congenital deformity of the pinna, or outer ear).

- Ovarian follicle atresia, the degeneration and subsequent resorption of one or more immature ovarian follicles.

- Potter sequence, congenital decreased size of the kidney leading to absolutely no functionality of the kidney, usually related to a single kidney.

- Pulmonary atresia, malformation of the pulmonary valve in which the valve orifice fails to develop.

- Renal agenesis, only having one kidney.

- Tricuspid atresia, a form of congenital heart disease whereby there is a complete absence of the tricuspid valve, and consequently an absence of the right atrioventricular connection.

- Vaginal atresia, a congenital occlusion of the vagina or subsequent adhesion of the walls of the vagina, resulting in its occlusion.

Very few risk factors for choanal atresia have been identified. While causes are unknown, both genetic and environmental triggers are suspected. One study suggests that chemicals that act as endocrine disrupters may put an unborn infant at risk. A 2012 epidemiological study looked at atrazine, a commonly used herbicide in the U.S., and found that women who lived in counties in Texas with the highest levels of this chemical being used to treat agricultural crops were 80 times more likely to give birth to infants with choanal atresia or stenosis compared to women who lived in the counties with the lowest levels. Another epidemiological report in 2010 found even higher associations between increased incidents of choanal atresia and exposure to second-hand-smoke, coffee consumption, high maternal zinc and B-12 intake and exposure to anti-infective urinary tract medications.

Umbilical cord ulceration and intestinal atresia is a rare congenital disease that leads to intestinal atresia, umbilical cord ulceration and severe intrauterine haemorrhage. Only 15 cases have so far been reported, though newer studies are beginning to conclude that this disease has a higher incidence rate than has been previously reported. A particular study has given intestinal atresia and umbilical cord ulceration a clear link after 5 such cases were reported at the time of publication.

There is no cure for short bowel syndrome except transplant. In newborn infants, the 4-year survival rate on parenteral nutrition is approximately 70%. In newborn infants with less than 10% of expected intestinal length, 5 year survival is approximately 20%. Some studies suggest that much of the mortality is due to a complication of the total parenteral nutrition (TPN), especially chronic liver disease. Much hope is vested in Omegaven, a type of lipid TPN feed, in which recent case reports suggest the risk of liver disease is much lower.

Although promising, small intestine transplant has a mixed success rate, with postoperative mortality rate of up to 30%. One-year and 4-year survival rate are 90% and 60%, respectively.

Some cases of biliary atresia may result from exposure to aflatoxin B1, and to a lesser extent aflatoxin B2 during late pregnancy. Intact maternal detoxification protects baby during intrauterine life, yet after delivery the baby struggles with the aflatoxin in its blood and liver. Moreover, the baby feeds aflatoxin M1 from its mom, as aflatoxin M1 is the detoxification product of aflatoxin B1. It is a milder toxin that causes cholangitis in the baby.

There are isolated examples of biliary atresia in animals. For instance, lambs born to sheep grazing on land contaminated with a weed (Red Crumbweed) developed biliary atresia at certain times. The plants were later found to contain a toxin, now called biliatresone Studies are ongoing to determine whether there is a link between human cases of biliary atresia and toxins such as biliatresone. There are some indications that a metabolite of certain human gut bacteria may be similar to biliatresone.

Colitis is inflammation of the colon. Acute cases are medical emergencies as the horse rapidly loses fluid, protein, and electrolytes into the gut, leading to severe dehydration which can result in hypovolemic shock and death. Horses generally present with signs of colic before developing profuse, watery, fetid diarrhea.

Both infectious and non-infectious causes for colitis exist. In the adult horse, "Salmonella", "Clostridium difficile", and "Neorickettsia risticii" (the causative agent of Potomac Horse Fever) are common causes of colitis. Antibiotics, which may lead to an altered and unhealthy microbiota, sand, grain overload, and toxins such as arsenic and cantharidin can also lead to colitis. Unfortunately, only 20–30% of acute colitis cases are able to be definitively diagnosed. NSAIDs can cause slower-onset of colitis, usually in the right dorsal colon (see Right dorsal colitis).

Treatment involves administration of large volumes of intravenous fluids, which can become very costly. Antibiotics are often given if deemed appropriate based on the presumed underlying cause and the horse's CBC results. Therapy to help prevent endotoxemia and improve blood protein levels (plasma or synthetic colloid administration) may also be used if budgetary constraints allow. Other therapies include probiotics and anti-inflammatory medication. Horses that are not eating well may also require parenteral nutrition. Horses usually require 3–6 days of treatment before clinical signs improve.

Due to the risk of endotoxemia, laminitis is a potential complication for horses suffering from colitis, and may become the primary cause for euthanasia. Horses are also at increased risk of thrombophlebitis.

Specific causes of colic are best managed with certain drugs. These include:

- Spasmolytic agents, most commonly Buscopan, especially in the case of gas colic.

- Pro-motility agents: metoclopramide, lidocaine, bethanechol, and erythromycin are used in cases of ileus.

- Anti-inflammatories are often used in the case of enteritis or colitis.

- Anti-microbials may be administered if an infectious agent is suspected to be the underlying cause of colic.

- Phenylephrine: used in cases of nephrosplenic entrapment to contract the spleen, and is followed by light exercise to try to shift the displaced colon back into its normal position.

- Psyllium may be given via nasogastric tube to treat sand colic.

- Anthelminthics for parasitic causes of colic.