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.

Once a child is born prematurely, thought must be given to decreasing the risk for developing NEC. Toward that aim, the methods of providing hyperalimentation and oral feeds are both important. In a 2012 policy statement, the American Academy of Pediatrics recommended feeding preterm infants human milk, finding "significant short- and long-term beneficial effects," including reducing the rate of NEC by a factor of two or more.

A study by researchers in Peoria, IL, published in "Pediatrics" in 2008, demonstrated that using a higher rate of lipid (fats and/or oils) infusion for very low birth weight infants in the first week of life resulted in zero infants developing NEC in the experimental group, compared with 14% with NEC in the control group. (They started the experimental group at 2 g/kg/d of 20% IVFE and increased within two days to 3 g/kg/d; amino acids were started at 3 g/kg/d and increased to 3.5.)

Neonatologists at the University of Iowa reported on the importance of providing small amounts of trophic oral feeds of human milk starting as soon as possible, while the infant is being primarily fed intravenously, in order to prime the immature gut to mature and become ready to receive greater oral intake. Human milk from a milk bank or donor can be used if mother's milk is unavailable. The gut mucosal cells do not get enough nourishment from arterial blood supply to stay healthy, especially in very premature infants, where the blood supply is limited due to immature development of the capillaries, so nutrients from the lumen of the gut are needed.

A Cochrane review published in April 2014 has established that supplementation of probiotics enterally "prevents severe NEC as well as all-cause mortality in preterm infants."

Increasing amounts of milk by 30 to 40 ml/kg is safe in infant who are born weighing very little. Not beginning feeding an infant by mouth for more than 4 days does not appear to have protective benefits.

Data from the NICHD Neonatal Research Network's Glutamine Trial showed that the incidence of NEC among extremely low birthweight (ELBW, <1000 g) infants fed with more than 98% human milk from their mothers was 1.3%, compared with 11.1% among infants fed only preterm formula, and 8.2% among infants fed a mixed diet, suggesting that infant deaths could be reduced by efforts to support production of milk by mothers of ELBW newborns.

Research from the University of California, San Diego found that higher levels of one specific human milk oligosaccharide, disialyllacto-N-tetraose, may be protective against the development of NEC.

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.

Specific types of enterocolitis include:

- necrotizing enterocolitis (most common in premature infants)

- pseudomembranous enterocolitis (also called "Pseudomembranous colitis")

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.

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.

In Germany, 90% of cases of infectious enteritis are caused by four pathogens, Norovirus, Rotavirus, "Campylobacter" and "Salmonella". Other common causes of infectious enteritis include bacteria such as "Shigella" and "E. coli," as well as viruses such as adenovirus, astrovirus and calicivirus. Other less common pathogens include "Bacillus cereus, Clostridium perfringens, Clostridium difficile" and "Staphylococcus aureus".

"Campylobacter jejuni" is one of the most common sources of infectious enteritis, and the most common bacterial pathogen found in 2 year old and smaller children with diarrhoea. It has been linked to consumption of contaminated water and food, most commonly poultry and milk. The disease tends to be less severe in developing countries, due to the constant exposure which people have with the antigen in the environment, leading to early development of antibodies.

Rotavirus is responsible for infecting 140 million people and causing 1 million deaths each year, mostly in children younger than 5 years. This makes it the most common cause of severe childhood diarrhoea and diarrhea-related deaths in the world. It selectively targets mature enterocytes in the small intestine, causing malabsorption, as well as inducing secretion of water. It has also been observed to cause villus ischemia, and increase intestinal motility. The net result of these changes is induced diarrhoea.

Enteritis necroticans is an often fatal illness, caused by β-toxin of "Clostridium perfringens". This causes inflammation and segments of necrosis throughout the gastrointestinal tract. It is most common in developing countries, however has also been documented in post-World War II Germany. Risk factors for enteritis necroticans include decreased trypsin activity, which prevent intestinal degradation of the toxin, and reduced intestinal motility, which increases likelihood of toxin accumulation.

To date, the precise causative factor has not been verified, and the disease has been attributed by various sources to viruses, parasites, bacteria, use of antibiotics and sulfonamides, and heavy metal poisoning. Other possible causes include peracute salmonellosis, clostridial enterocolitis, and endotoxemia. "Clostridium difficile" toxins isolated in the horse have a genotype like the current human "epidemic strain", which is associated with human "C. difficile"-associated disease of greater than historical severity. "C. difficile" can cause pseudomembranous colitis in humans, and in hospitalized patients who develop it, fulminant "C. difficile" colitis is a significant and increasing cause of death.

Horses under stress appear to be more susceptible to developing colitis X. Disease onset is often closely associated with surgery or transport. Excess protein and lack of cellulose content in the diet (a diet heavy on grain and lacking adequate hay or similar roughage) is thought to be the trigger for the multiplication of clostridial organisms. A similar condition may be seen after administration of tetracycline or lincomycin to horses. These factors may be one reason the condition often develops in race horses, having been responsible for the deaths of the Thoroughbred filly Landaluce,

the Quarter Horse stallion Lightning Bar,

and is one theory for the sudden death of Kentucky Derby winner Swale.

The link to stress suggests the condition may be brought on by changes in the microflora of the cecum and colon that lower the number of anaerobic bacteria, increase the number of Gram-negative enteric bacteria, and decrease anaerobic fermentation of soluble carbohydrates, resulting in damage to the cecal and colonic mucosa and allowing increased absorption of endotoxins from the lumen of the gut.

The causative agent may be "Clostridium perfringens", type A, but the bacteria are recoverable only in the preliminary stages of the disease.

The suspect toxin could also be a form of "Clostridium difficile". In a 2009 study at the University of Arizona, "C. difficile" toxins A and B were detected, large numbers of "C. difficile" were isolated, and genetic characterization revealed them to be North American pulsed-field gel electrophoresis type 1, polymerase chain reaction ribotype 027, and toxinotype III. Genes for the binary toxin were present, and toxin negative-regulator tcdC contained an 18-bp deletion. The individual animal studied in this case was diagnosed as having peracute typhlocolitis, with lesions and history typical of those attributed to colitis X.

Use of antibiotics may also be associated with some forms of colitis-X. In humans, "C. difficile" is the most serious cause of antibiotic-associated diarrhea, often a result of eradication of the normal gut flora by antibiotics. In one equine study, colitis was induced after pretreatment with clindamycin and lincomycin, followed by intestinal content from horses which had died from naturally occurring idiopathic colitis. (A classic adverse effect of clindamycin in humans is "C. difficile"-associated diarrhea.) In the experiment, the treated horses died. After necropsy, "Clostridium cadaveris" was present, and is proposed as another possible causative agent in some cases of fatal colitis.

Toxic megacolon is mainly seen in ulcerative colitis and pseudomembranous colitis, two chronic inflammations of the colon (and occasionally, in the other type of inflammatory bowel disease, Crohn's disease). Its mechanism is incompletely understood. It is probably due to an excessive production of nitric oxide, at least in ulcerative colitis. The prevalence is about the same for both sexes.

In patients with HIV/AIDS, cytomegalovirus (CMV) colitis is the leading cause of toxic megacolon and emergency laparotomy. CMV may also increase the risk of toxic megacolon in non-HIV/AIDS patients with IBD.

Risperidone, an anti-psychotic medication, can result in megacolon.

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.

Short bowel syndrome in adults and children is usually caused by surgery. This surgery may be done for:

- Crohn's disease, an inflammatory disorder of the digestive tract

- Volvulus, a spontaneous twisting of the small intestine that cuts off the blood supply and leads to tissue death

- Tumors of the small intestine

- Injury or trauma to the small intestine

- Necrotizing enterocolitis (premature newborn)

- Bypass surgery to treat obesity

- Surgery to remove diseases or damaged portion of the small intestine

Some children are also born with an abnormally short small intestine, known as congenital short bowel.

Crohn's disease – also known as regional enteritis, it can occur along any surface of the gastrointestinal tract. In 40% of cases it is limited to the small intestine.

Coeliac disease – caused by an autoimmune reaction to gluten by genetically predisposed individuals.

Eosinophilic enteropathy – a condition where eosinophils build up in the gastrointestinal tract and blood vessels, leading to polyp formation, necrosis, inflammation and ulcers. It is most commonly seen in patients with a history of atopy, however is overall relatively uncommon.

The incidence of colic can be reduced by restricted access to simple carbohydrates including sugars from feeds with excessive molasses, providing clean feed and drinking water, preventing the ingestion of dirt or sand by using an elevated feeding surface, a regular feeding schedule, regular deworming, regular dental care, a regular diet that does not change substantially in content or proportion and prevention of heatstroke. Horses that bolt their feed are at risk of colic, and several management techniques may be used to slow down the rate of feed consumption.

Supplementing with previously mentioned form of pysllium fiber may reduce risk of sand colic if in a high-risk area. Most supplement forms are given one week per month and available wherever equine feed is purchased.

Turnout is thought to reduce the likelihood of colic, although this has not been proven. It is recommended that a horse receive ideally 18 hours of grazing time each day, as in the wild. However, many times this is difficult to manage with competition horses and those that are boarded, as well as for animals that are easy keepers with access to lush pasture and hence at risk of laminitis. Turnout on a dry lot with lower-quality fodder may have similar beneficial effects.

Enterocolitis or coloenteritis is an inflammation of the digestive tract, involving enteritis of the small intestine and colitis of the colon. It may be caused by various infections, with bacteria, viruses, fungi, parasites, or other causes. Common clinical manifestations of enterocolitis are frequent diarrheal defecations, with or without nausea, vomiting, abdominal pain, fever, chills, alteration of general condition. General manifestations are given by the dissemination of the infectious agent or its toxins throughout the body, or – most frequently – by significant losses of water and minerals, the consequence of diarrhea and vomiting.

Among the causal agents of acute enterocolitis are:

- bacteria: "Salmonella", "Shigella", "Escherichia coli", "Campylobacter" etc.;

- viruses: enteroviruses, rotaviruses, Norwalk virus, adenoviruses;

- fungi: candidiasis, especially in immunosuppressed patients or who have previously received prolonged antibiotic treatment;

- parasites: "Giardia lamblia" (with high frequency of infestation in the population, but not always with clinical manifestations), "Balantidium coli", "Blastocystis homnis", "Cryptosporidium" (diarrhea in people with immunosuppression), "Entamoeba histolytica" (produces the amebian dysentery, common in tropical areas).

Laparotomy for other forms of volvulus, especially anal volvulus.

Pneumatosis intestinalis (also called intestinal pneumatosis, pneumatosis cystoides intestinalis, or pneumatosis coli) is of an intestine, that is, gas cysts in the bowel wall. As a radiological sign it is highly suggestive for necrotizing enterocolitis. This is in contrast to gas in the intestinal lumen (which is relieved by flatulence). In newborns, pneumatosis intestinalis is considered diagnostic for necrotizing enterocolitis, and the air is produced by bacteria in the bowel wall. The pathogenesis of pneumatosis intestinalis is poorly understood and is likely multifactorial. PI itself is not a disease, but rather a clinical sign. In some cases, PI is an incidental finding, whereas in others, it portends a life-threatening intra-abdominal condition.

Inflammation can spread to other parts of the gut in patients with typhlitis. The condition can also cause the cecum to become distended and can cut off its blood supply. This and other factors can result in necrosis and perforation of the bowel, which can cause peritonitis and sepsis.

Historically, the mortality rate for typhlitis was as high as 50%, mostly because it is frequently associated with bowel perforation. More recent studies have demonstrated better outcomes with prompt medical management, generally with resolution of symptoms with neutrophil recovery without death

In adults, most common causes are hemorrhoids and diverticulosis, both of which are relatively benign; however, it can also be caused by colorectal cancer, which is potentially fatal. In a newborn infant, haematochezia may be the result of swallowed maternal blood at the time of delivery, but can also be an initial symptom of necrotizing enterocolitis, a serious condition affecting premature infants. In babies, haematochezia in conjunction with abdominal pain is associated with intussusception. In adolescents and young adults, inflammatory bowel disease, particularly ulcerative colitis, is a serious cause of haematochezia that must be considered and excluded.

Hematochezia can be due to upper gastrointestinal bleeding. However, as the blood from such a bleed is usually chemically modified by action of acid and enzymes, it presents more commonly as black "tarry" feces known as melena. Haematochezia from an upper gastrointestinal source is an ominous sign, as it suggests a very significant bleed which is more likely to be life-threatening.

Beeturia can cause red colored feces after eating beets because of insufficient metabolism of a red pigment, and is a differential sign that may be mistaken as hematochezia.

Consumption of dragon fruit or pitaya may also cause red discoloration of the stool and sometimes the urine (pseudohematuria). This too, is a differential sign that is sometimes mistaken for hematochezia.

In infants, the Apt test can be used to distinguish fetal hemoglobin from maternal blood.

Other common causes of blood in the stool include:

- Colorectal cancer

- Crohns disease

- Ulcerative colitis

- Other types of inflammatory bowel disease, inflammatory bowel syndrome, or ulceration

- Rectal or anal hemorrhoids or anal fissures, particularly if they rupture or are otherwise irritated

- "Shigella" or shiga toxin producing "E. coli" food poisoning

- Necrotizing enterocolitis

- Diverticulosis

- Salmonellosis

- Upper gastrointestinal bleeding

- Peptic ulcer disease

- Esophageal varices

- Gastric cancer

- Intense exercise, especially a high-impact activity like running in hot weather.

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.

In a cecal volvulus, the cecum may be returned to a normal position and sutured in place, a procedure known as cecopexy. If identified early, before presumed intestinal wall ischemia has resulted in tissue breakdown and necrosis, the cecal volvulus can be detorsed laparoscopically.

PROM occurring before 37 weeks (PPROM) is one of the leading causes of preterm birth. 30-35% of all preterm births are caused by PPROM. This puts the fetus at risk for the many complications associated with prematurity such as respiratory distress, brain bleeds, infection, necrotizing enterocolitis (death of the fetal bowels), brain injury, muscle dysfunction, and death. Prematurity from any cause leads to 75% of perinatal mortality and about 50% of all long-term morbidity. PROM is responsible for 20% of all fetal deaths between 24 and 34 weeks gestation.

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.

The condition is usually caused by Gram-positive enteric commensal bacteria of the gut (gut flora). "Clostridium difficile" is a species of Gram-positive bacteria that commonly causes severe diarrhea and other intestinal diseases when competing bacteria are wiped out by antibiotics, causing pseudomembranous colitis, whereas Clostridium septicum is responsible for most cases of neutropenic enterocolitis.

Typhlitis most commonly occurs in immunocompromised patients, such as those undergoing chemotherapy, patients with AIDS, kidney transplant patients, or the elderly.

Before 24 weeks the fetus is still developing its organs, and the amniotic fluid is important for protecting the fetus against infection, physical impact, and for preventing the umbilical cord from becoming compressed. It also allows for fetal movement and breathing that is necessary for the development of the lungs, chest, and bones. Low levels of amniotic fluid due to mid-trimester or previable PPROM (before 24 weeks) can result in fetal deformity (ex: Potter-like facies), limb contractures, pulmonary hypoplasia (underdeveloped lungs), infection (especially if the mother is colonized by group B streptococcus or bacterial vaginosis), prolapsed umbilical cord or compression, and placental abruption.