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.

Fetal and neonatal intestinal atresia are treated using laparotomy after birth. If the area affected is small, 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 period of time, a temporary stoma may be placed.

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.

Gastroschisis requires surgical treatment to return the exposed intestines to the abdominal cavity and close the hole in the abdomen. Sometimes this is done immediately but more often the exposed organs are covered with sterile drapings, and only later is the surgery done. Affected newborns frequently require more than one surgery, as only about 10% of cases can be closed in a single surgery.

Given the urgent need for surgery after birth, it is recommended that delivery occur at a facility equipped for caring for these high-risk neonates, as transfers to other facilities may increase risk of adverse outcomes. There is no evidence that cesarean deliveries lead to better outcomes for babies with gastroschisis, so cesarean delivery is only considered if there are other indications.

The main cause for lengthy recovery periods is the time taken for the infant's bowel function to return to normal. After surgery infants are fed through IV fluids and gradually introduced to normal feeding.

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.

Intestinal atresia is a malformation where there is a narrowing or absence of a portion of the intestine. This defect can either occur in the small or large intestine.

Duodenal atresia, also known as duodenojejunal atresia, is the congenital absence or complete closure of a portion of the lumen of the duodenum. It causes increased levels of amniotic fluid during pregnancy (polyhydramnios) and intestinal obstruction in newborn babies. Radiography shows a distended stomach and distended duodenum, which are separated by the pyloric valve, a finding described as the double-bubble sign.

Treatment includes suctioning out any fluid that is trapped in the stomach, providing fluids intravenously, and surgical repair of the intestinal closure.

Some causes of bowel obstruction may resolve spontaneously; many require operative treatment. In adults, frequently the surgical intervention and the treatment of the causative lesion are required. In malignant large bowel obstruction, endoscopically placed self-expanding metal stents may be used to temporarily relieve the obstruction as a bridge to surgery, or as palliation. Diagnosis of the type of bowel obstruction is normally conducted through initial plain radiograph of the abdomen, luminal contrast studies, computed tomography scan, or ultrasonography prior to determining the best type of treatment.

In the management of small bowel obstructions, a commonly quoted surgical aphorism is: "never let the sun rise or set on small-bowel obstruction" because about 5.5% of small bowel obstructions are ultimately fatal if treatment is delayed. However improvements in radiological imaging of small bowel obstructions allow for confident distinction between simple obstructions, that can be treated conservatively, and obstructions that are surgical emergencies (volvulus, closed-loop obstructions, ischemic bowel, incarcerated hernias, etc.).

A small flexible tube (nasogastric tube) may be inserted through the nose into the stomach to help decompress the dilated bowel. This tube is uncomfortable but does relieve the abdominal cramps, distention, and vomiting. Intravenous therapy is utilized and the urine output is monitored with a catheter in the bladder.

Most people with SBO are initially managed conservatively because in many cases, the bowel will open up. Some adhesions loosen up and the obstruction resolves. However, when conservative management is undertaken, the patient is examined several times a day, and X-ray images are obtained to ensure that the individual is not getting clinically worse.

Conservative treatment involves insertion of a nasogastric tube, correction of dehydration and electrolyte abnormalities. Opioid pain relievers may be used for patients with severe pain. Antiemetics may be administered if the patient is vomiting. Adhesive obstructions often settle without surgery. If the obstruction is complete a surgery is usually required.

Most patients do improve with conservative care in 2–5 days. However, on some occasions, the cause of obstruction may be a cancer and in such cases, surgery is the only treatment. These individuals undergo surgery where the cause of SBO is removed. Individuals who have bowel resection or lysis of adhesions usually stay in the hospital a few more days until they are able to eat and walk.

Small bowel obstruction caused by Crohn's disease, peritoneal carcinomatosis, sclerosing peritonitis, radiation enteritis, and postpartum bowel obstruction are typically treated conservatively, i.e. without surgery.

Treatment is surgical, potentially with a laparoscopic resection. In patients with bleeding, strangulation of bowel, bowel perforation or bowel obstruction, treatment involves surgical resection of both the Meckel's diverticulum itself along with the adjacent bowel segment, and this procedure is called a "small bowel resection". In patients without any of the aforementioned complications, treatment involves surgical resection of the Meckel's diverticulum only, and this procedure is called a simple diverticulectomy.

With regards to asymptomatic Meckel's diverticulum, some recommend that a search for Meckel's diverticulum should be conducted in every case of appendectomy/laparotomy done for acute abdomen, and if found, Meckel's diverticulectomy or resection should be performed to avoid secondary complications arising from it.

Neonatal bowel obstruction (NBO) or neonatal intestinal obstruction is the most common surgical emergency in the neonatal period. It may occur due to a variety of conditions and has an excellent outcome based on timely diagnosis and appropriate intervention.

In some communities mothers routinely push the small bulge back in and tape a coin over the palpable hernia hole until closure occurs. This practice is not medically recommended as there is a small risk of trapping a loop of bowel under part of the coin resulting in a small area of ischemic bowel. This "fix" does not help and germs may accumulate under the tape, causing infection. The use of bandages or other articles to continuously reduce the hernia is not evidence-based.

An umbilical hernia can be fixed in two different ways. The surgeon can opt to stitch the walls of the abdominal or he/she can place mesh over the opening and stitch it to the abdominal walls. The latter is of a stronger hold and is commonly used for larger defects in the abdominal wall. Most surgeons will not repair the hernia until 5–6 years after the baby is born. Most umbilical hernias in infants and children close spontaneously and rarely have complications of gastrointestinal-content incarcerations.

How far the projection of the swelling extends from the surface of the abdomen (the belly) varies from child to child. In some, it may be just a small protrusion; in others it may be a large rounded swelling that bulges out when the baby cries. It may hardly be visible when the child is quiet and or sleeping.

Normally, the abdominal muscles converge and fuse at the umbilicus during the formation stage, however, in some cases, there remains a gap where the muscles do not close and through this gap the inner intestines come up and bulge under the skin, giving rise to an umbilical hernia. The bulge and its contents can easily be pushed back and reduced into the abdominal cavity.

In contrast to an inguinal hernia, the complication incidence is very low, and in addition, the gap in the muscles usually closes with time and the hernia disappears on its own. The treatment of this condition is essentially conservative: observation allowing the child to grow up and see if it disappears. Operation and closure of the defect is required only if the hernia persists after the age of 3 years or if the child has an episode of complication during the period of observation like irreducibility, intestinal obstruction, abdominal distension with vomiting, or red shiny painful skin over the swelling. Surgery is always done under anesthesia. The defect in the muscles is defined and the edges of the muscles are brought together with sutures to close the defect. In general, the child needs to stay in the hospital for 2 days and the healing is complete within 8 days.

At times, there may be a fleshy red swelling seen in the hollow of the umbilicus that persists after the cord has fallen off. It may bleed on touch, or may stain the clothes that come in contact with it. This needs to be shown to a pediatric surgeon. This is most likely to be an umbilical polyp and the therapy is to tie it at the base with a stitch so that it falls off and there is no bleeding. Alternatively, it may be an umbilical granuloma that responds well to local application of dry salt or silver nitrate but may take a few weeks to heal and dry.

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.

Many people are managed through day surgery centers, and are able to return to work within a week or two, while intense activities are prohibited for a longer period. People who have their hernias repaired with mesh often recover within a month, though pain can last longer. Surgical complications include pain that lasts more than three months, surgical site infections, nerve and blood vessel injuries, injury to nearby organs, and hernia recurrence. Pain that lasts more than three months occurs in about 10% of people following hernia repair.

Meckel's diverticulum occurs in about 2% of the population. Prevalence in males is 3–5 times higher than in females. Only 2% of cases are symptomatic, which usually presents among children at the age of 2.

Most cases of Meckel's diverticulum are diagnosed when complications manifest or incidentally in unrelated conditions such as laparotomy, laparoscopy or contrast study of the small intestine. Classic presentation in adults includes intestinal obstruction and inflammation of the diverticulum (diverticulitis). Painless rectal bleeding most commonly occurs in toddlers.

Inflammation in the ileal diverticulum has symptoms that mimic appendicitis, therefore its diagnosis is of clinical importance. Detailed knowledge of the pathophysiological properties is essential in dealing with the life-threatening complications of Meckel's diverticulum.

An acquired umbilical hernia directly results from increased intra-abdominal pressure caused by obesity, heavy lifting, a long history of coughing, or multiple pregnancies.

The benefits of the use of an external device to maintain reduction of the hernia without repairing the underlying defect (such as hernia trusses, trunks, belts, etc.) are unclear.

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.

The primary concern with umbilical cord prolapse is inadequate blood supply, and thus oxygen, to the fetus if the cord becomes compressed. The cord can become compressed either due to mechanical pressure (usually from the presenting fetal part) or from sudden contraction of the vessels due to decreased temperatures in the vagina in comparison to the uterus. This can lead to death of the fetus or other complications.

Historically, the rate of fetal death in the setting of cord prolapse has been as high 40%. However, these estimates occurred in the context of home or births outside of the hospital. When considering cord prolapses that have occurred in inpatient labor and delivery settings, the rate drops to as low as 0-3%, though the mortality rate remains higher than for fetuses without cord prolapse. The reduction in mortality for hospital births is likely due to the ready availability of immediate cesarean section.

Many other fetal outcomes have been studied, including Apgar score (a quick assessment of a newborn's health status) at 5 minutes and length of hospitalization after delivery. While both measures are worse for newborns delivered after cord prolapse, it is unclear what effect this has in the long-term. Relatively large studies that have tried to quantify long-term effects of cord prolapse on children found that less than 1% (1 in 120 studied) suffered a major neurologic handicap, and less than 1% (110 in 16,675) had diagnosed cerebral palsy.

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.

International Omphalocele Awareness Day is celebrated annually on January 31, as part of Birth Defect Awareness Month. Several U.S. states have passed resolutions to officially recognize the date.

The gold standard for treatment of umbilical cord prolapse in the setting of a viable pregnancy typically involves immediate delivery by the quickest and safest route possible. This usually requires cesarean section, especially if the woman is in early labor. Occasionally, vaginal delivery will be attempted if clinical judgment determines that is a safer or quicker method.

Other interventions during management of cord prolapse are typically used to decrease the chance of complications while preparations for delivery are being made. These interventions are focused on reducing pressure on the cord to prevent fetal complications from cord compression. The following maneuvers are among those used in clinical practice:

- manual elevation of the presenting fetal part

- repositioning of the mother to be head down with feet elevated

- filling of the bladder with a foley catheter, or tube through the urethra to elevate the presenting fetal part

- use of tocolytics (medications to suppress labor) have been proposed, usually in addition to bladder filling rather than a standalone intervention

If the mother is far from delivery, funic reduction (manually placing the cord back into the uterine cavity) has been attempted, with successful cases reported.

Endotoxemia is a serious complication of colic and warrants aggressive treatment. Endotoxin (lipopolysaccharide) is released from the cell wall of gram-negative bacteria when they die. Normally, endotoxin is prevented from entering systemic circulation by the barrier function of the intestinal mucosa, antibodies and enzymes which bind and neutralize it and, for the small amount that manages to enter the blood stream, removal by Kupffer cells in the liver. Endotoxemia occurs when there is an overgrowth and secondary die-off of gram negative bacteria, releasing mass quantities of endotoxin. This is especially common when the mucosal barrier is damaged, as with ischemia of the GI tract secondary to a strangulating lesion or displacement. Endotoxemia produces systemic effects such as cardiovascular shock, insulin resistance, and coagulation abnormalities.

Fluid support is essential to maintain blood pressure, often with the help of colloids or hypertonic saline. NSAIDs are commonly given to reduce systemic inflammation. However, they decrease the levels of certain prostaglandins that normally promote healing of the intestinal mucosa, which subsequently increases the amount of endotoxin absorbed. To counteract this, NSAIDs are sometimes administered with a lidocaine drip, which appears to reduce this particular negative effect. Flunixin may be used for this purpose at a dose lower than that used for analgesia, so can be safely given to a colicky horse without risking masking signs that the horse requires surgery. Other drugs that bind endotoxin, such as polymyxin B and Bio-Sponge, are also often used. Polymixin B prevents endotoxin from binding to inflammatory cells, but is potentially nephrotoxic, so should be used with caution in horses with azotemia, especially neonatal foals. Plasma may also be given with the intent of neutralizing endotoxin.

Laminitis is a major concern in horses suffering from endotoxemia. Ideally, prophylactic treatment should be provided to endotoxic horses, which includes the use of NSAIDs, DMSO, icing of the feet, and frog support. Horses are also sometimes administered heparin, which is thought to reduce the risk of laminitis by decreasing blood coagulability and thus blood clot formation in the capillaries of the foot.

Gastroschisis is a similar birth defect, but in gastroschisis the umbilical cord is not involved and the lesion is usually to the right of midline. Parts of organs may be free in the amniotic fluid, and not enclosed in a membranous (peritoneal) sac. Gastroschisis is less frequently associated with other defects than omphalocele.

Omphaloceles occurs more frequently with increased maternal age.

Other related syndromes are Pentalogy of Cantrell, Beckwith-Wiedemann, and OEIS complex (omphalocele, exstrophy of the cloaca, imperforate anus, spinal defects).

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.