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.

The causes are divided into benign or malignant.

- Benign

- Peptic ulcer disease

- Infections, such as tuberculosis; and infiltrative diseases, such as amyloidosis.

- A rare cause of gastric outlet obstruction is blockage with a gallstone, also termed "Bouveret's syndrome".

- In children congenital pyloric stenosis / congenital hypertrophic pyloric stenosis may be a cause.

- A pancreatic pseudocyst can cause gastric compression.

- Pyloric mucosal diaphragm could be a rare cause.

- Malignant

- Tumours of the stomach, including adenocarcinoma (and its linitis plastica variant), lymphoma, and gastrointestinal stromal tumours

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.

In a peptic ulcer it is believed to be a result of edema and scarring of the ulcer, followed by healing and fibrosis, which leads to obstruction of the gastroduodenal junction (usually an ulcer in the first part of the duodenum).

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.

Gastric volvulus of unknown cause comprises two thirds of cases and is presumably due to abnormal laxity of the gastrosplenic, gastroduodenal, gastrophrenic, and gastrohepatic ligaments. Type 1 gastric volvulus is more common in adults but has been reported in children.

Type 2 gastric volvulus is found in one third of patients and is usually associated with congenital or acquired abnormalities that result in abnormal mobility of the stomach.

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.

Pancreaticobiliary maljunction is a congenital malformation, in which the pancreatic and bile ducts join anatomically outside the duodenal wall, forming a markedly long common channel. This anomaly prevents normal control by the sphincter of Oddi located in the duodenal wall, allowing regurgitation of pancreatic juices into the biliary tract and possibly leading to a higher probability of pancreaticobiliary cancers.

Anorectal anomalies are medical problems affecting the structure of the anus and rectum. A person with an anorectal problem would have some sort of deformative feature of the anus or rectum, collectively known as an anorectal malformation.

Examples of anorectal anomalies include:

- Anal stenosis

- Imperforate anus

- Proctitis

- Anal bleeding

- Anal fistula

- Anal cancer

- Anal itching

- Hemorrhoid (piles)

Among those in the intensive care unit, ulceration resulting in bleeding is very rare.

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.

Evidence does not support a role for specific foods including spicy foods and coffee in the development of peptic ulcers. People are usually advised to avoid foods that bother them.

There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. Heightened mast cell activation has been proposed to be a common factor among FGIDs, contributing to visceral hypersensitivity as well as epithelial, neuromuscular, and motility dysfunction.

Acute erosive gastritis typically involves discrete foci of surface necrosis due to damage to mucosal defenses. NSAIDs inhibit cyclooxygenase-1, or COX-1, an enzyme responsible for the biosynthesis of eicosanoids in the stomach, which increases the possibility of peptic ulcers forming. Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach called prostaglandin. These drugs used in a short period are not typically dangerous. However, regular use can lead to gastritis. Additionally, severe physiologic stress ("stress ulcers") from sepsis, hypoxia, trauma, or surgery, is also a common etiology for acute erosive gastritis. This form of gastritis can occur in more than 5% of hospitalized patients.

Also, note that alcohol consumption does not cause chronic gastritis. It does, however, erode the mucosal lining of the stomach; low doses of alcohol stimulate hydrochloric acid secretion. High doses of alcohol do not stimulate secretion of acid.

The estimated detection rate of AVM in the US general population is 1.4/100,000 per year. This is approximately one fifth to one seventh the incidence of intracranial aneurysms. An estimated 300,000 Americans have AVMs, of whom 12% (approximately 36,000) will exhibit symptoms of greatly varying severity.

Risk factors for stress ulcer formation that have been identified are numerous and varied. However, two landmark studies and one position paper exist that addresses the topic of risk factors for stress ulcer formation:

- Non-critically ill medical patients with 2 or more of the following: respiratory failure, sepsis, heart failure, hepatic encephalopathy, jaundice, kidney failure, stroke, hypertension, previous gastrointestinal disease and treatment with corticosteroids, NSAIDS, heparin, or warfarin.

- In surgical critically ill patients, only those patients who are on a mechanical ventilator for more than 48 hours and/or those with a coagulopathy.

- The American Society of Health-System Pharmacists guideline recommends against the practice of stress ulcer prophylaxis in non-critically ill patients.

Can occur due to autosomal dominant diseases, such as hereditary hemorrhagic telangiectasia.

Vein of Galen malformations are devastating complications. Studies have shown that 77% of untreated cases result in mortality. Even after surgical treatment, the mortality rate remains as high as 39.4%. Most cases occur during infancy when the mortality rates are at their highest. Vein of Galen malformations are a relatively unknown affliction, attributed to the rareness of the malformations. Therefore, when a child is diagnosed with a faulty Great Cerebral Vein of Galen, most parents know little to nothing about what they are dealing with. To counteract this, support sites have been created which offer information, advice, and a community of support to the afflicted (, ).

The prevalence of congenital Chiari I malformation, defined as tonsilar herniations of 3 to 5 mm or greater, was previously believed to be in the range of one per 1000 births, but is likely much higher. Women are three times more likely than men to have a congenital Chiari malformation. Type II malformations are more prevalent in people of Celtic descent. A study using upright MRI found cerebellar tonsillar ectopia in 23% of adults with headache from motor-vehicle-accident head trauma. Upright MRI was more than twice as sensitive as standard MRI, likely because gravity affects cerebellar position.

Cases of congenital Chiari malformation may be explained by evolutionary and genetic factors. Typically, an infant's brain weighs around 400g at birth and triples to 1100-1400g by age 11. At the same time the cranium triples in volume from 500 cm to 1500 cm to accommodate the growing brain. During human evolution, the skull underwent numerous changes to accommodate the growing brain. The evolutionary changes included increased size and shape of the skull, decreased basal angle and basicranial length. These modifications resulted in significant reduction of the size of the posterior fossa in modern humans. In normal adults, the posterior fossa comprises 27% of the total intracranial space, while in adults with Chiari Type I, it is only 21%. If a modern brain is paired with a less modern skull, the posterior fossa may be too small, so that the only place where the cerebellum can expand is the foramen magnum, leading to development of Chiari Type I. H. neanderthalensis had platycephalic (flattened) skull. Some cases of Chiari are associated with platybasia (flattening of the skull base).

Venous malformation is a subtype of vascular malformation affecting the venous vasculature. They are usually congenital and found at birth and are treated by Schlerotherapy or Laser Therapy.

In most cases, a fetus with CPAM is closely monitored during pregnancy and the CPAM is removed via surgery after birth. Most babies with a CPAM are born without complication and are monitored during the first few months. Many patients have surgery, typically before their first birthday, because of the risk of recurrent lung infections associated with CPAMs. Some pediatric surgeons can safely remove these lesions using very tiny incisions using minimally invasive surgical techniques (thoracoscopy). However, some CPAM patients live a full life without any complication or incident. It is hypothesized that there are thousands of people living with an undetected CPAM. Through ultrasound testing employed in recent years, many more patients are aware that they live with this condition. Rarely, long standing CPAMs have been reported to become cancerous.

Very large cystic masses might pose a danger during birth because of the airway compression. In this situation, a special surgical type of delivery called the EXIT procedure may be used.

In rare extreme cases, where fetus's heart is in danger, fetal surgery can be performed to remove the CPAM. If non-immune hydrops fetalis develop, there is a near universal mortality of the fetus without intervention. Fetal surgery can improve the chances of survival to 50-60%. Recently, several studies found that a single course of prenatal steroids (betamethasone) may increase survival in hydropic fetuses with microcystic CPAMs to 75-100%. These studies indicate that large microcystic lesions may be treated prenatally without surgical intervention. Large macrocyst lesions may require in utero placement of a Harrison thoracoamniotic shunt.

The complications that are usually associated with vein of Galen malformations are usually intracranial hemorrhages. Over half the patients with VGAM have a malformation that cannot be corrected. Patients frequently die in the neonatal period or in early infancy.

The most widely accepted pathophysiological mechanism by which Chiari type I malformations occur is by a reduction or lack of development of the posterior fossa as a result of congenital or acquired disorders. Congenital causes include hydrocephalus, craniosynostosis (especially of the lambdoid suture), hyperostosis (such as craniometaphyseal dysplasia, osteopetrosis, erythroid hyperplasia), X-linked vitamin D-resistant rickets, and neurofibromatosis type I. Acquired disorders include space occupying lesions due to one of several potential causes ranging from brain tumors to hematomas.

Head trauma may cause cerebellar tonsillar ectopia, possibly because of dural strain. Additionally, ectopia may be present but asymptomatic until whiplash causes it to become symptomatic. Posterior fossa hypoplasia causes reduced cerebral and spinal compliance.

Functional gastrointestinal disorders are very common. Globally, irritable bowel syndrome and functional dyspepsia alone may affect 16–26% of the population.