Prevention of radiation injury to the small bowel is a key aim of techniques such as brachytherapy, field size, multiple field arrangements, conformal radiotherapy techniques and intensity-modulated radiotherapy. Medications including ACE inhibitors, statins and probiotics have also been studied and reviewed.

In people presenting with symptoms compatible with radiation enteropathy, the initial step is to identify what is responsible for causing the symptoms. Management is best with a multidisciplinary team including gastroenterologists, nurses, dietitians, surgeons and others.

Medical treatments include the use of hyperbaric oxygen which has beneficial effects in radiation proctitis or anal damage. Nutritional therapies include treatments directed at specific malabsorptive disorders such as low fat diets and vitamin B12 or vitamin D supplements, together with bile acid sequestrants for bile acid diarrhea and possibly antibiotics for small intestinal bacterial overgrowth. Probiotics have all been suggested as another therapeutic avenue.

Endoscopic therapies including argon plasma coagulation have been used for bleeding telangiectasia in radiation proctitis and at other intestinal sites, although there is a rick of perforation. Sucralfate enemas look promising in proctitis.

Surgical treatment may be needed for intestinal obstruction, fistulae, or perforation, which can happen in more severe cases. These can be fatal if patients present as an emergency, but with improved radiotherapy techniques are now less common.

Optimal treatment usually produces significant improvements in quality of life.

Symptoms such as diarrhea and painful defecation need to be systematically investigated and the underlying causes each carefully treated. Complications such as obstruction and fistulae may require surgery. Several other methods have been studied in attempts to lessen the effects of radiation proctitis. These include sucralfate, hyperbaric oxygen therapy, corticosteroids, metronidazole, argon plasma coagulation, radiofrequency ablation and formalin irrigation.

Radiation proctitis (and the related radiation colitis) is inflammation and damage to the lower parts of the colon after exposure to x-rays or other ionizing radiation as a part of radiation therapy. Radiation proctitis most commonly occurs after treatment for cancers such as cervical cancer, prostate cancer, and colon cancer. Radiation proctitis involves the lower intestine, primarily the sigmoid colon and the rectum and is part of the conditions known as pelvic radiation disease and radiation enteropathy.

Mild cases usually do not require treatment and will go away after a few days in healthy people. In cases where symptoms persist or when it is more severe, specific treatments based on the initial cause may be required.

In cases where diarrhoea is present, replenishing fluids lost is recommended, and in cases with prolonged or severe diarrhoea which persists, intravenous rehydration therapy or antibiotics may be required. A simple oral rehydration therapy (ORS) can be made by dissolving one teaspoon of salt, eight teaspoons of sugar and the juice of an orange into one litre of clean water. Studies have shown the efficacy of antibiotics in reducing the duration of the symptoms of infectious enteritis of bacterial origin, however antibiotic treatments are usually not required due to the self-limiting duration of infectious enteritis.

Enteropathy refers to any pathology of the intestine. Although enteritis specifically refers to an inflammation of the intestine, and is thus a more specific term than "enteropathy", the two phrases are sometimes used interchangeably.

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.

Proximal enteritis usually is managed medically. This includes nasogastric intubation every 1–2 hours to relieve gastric pressure secondary to reflux, which often produces to 2–10 L, as well as aggressive fluid support to maintain hydration and correct electrolyte imbalances. Maintaining hydration in these patients can be very challenging. In some cases, fluid support may actually increase reflux production, due to the decreased intravascular oncotic pressure from low total protein and albumin levels, leading to loss of much of these IV fluids into the intestinal lumen. These horses will often display dependent edema (edema that collects in locations based on gravity). Colloids such as plasma or Hetastarch may be needed to improve intravascular oncotic pressure, although they can be cost prohibitive for many owners. Reflux levels are monitored closely to help evaluate fluid losses, and horses recovering from DPJ show improved hydration with decreased reflux production and improved attitude.

Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used for pain relief, reduction of inflammation, and for their anti-endotoxin effects, but care must be taken since they may produce gastrointestinal ulceration and damage the kidneys. Due to a suspected link to "Clostridial" infection, anti-microbials are often administered, usually penicillin or metronidazole. Aminoglycosides should be used with extreme caution due to the risk of nephrotoxicosis (damage to the kidney). The mucosa of the intestines is damaged with DPJ, often resulting in absorption of endotoxin and risking laminitis, so therapy to combat and treat endotoxemia is often employed. This includes treatment with drugs that counteract endotoxin such as Polymyxin B and Bio-Sponge, fluid support, and laminitis prevention such as icing of the feet. Prokinetic drugs such as lidocaine, erythromycin, metoclopramide, and bethanechol are often used to treat the ileus associated with the disease.

Horses are withheld food until reflux returns to less than 1–2 L of production every 4 hours, and gut sounds return, often requiring 3–7 days of therapy. Parenteral nutrition is often provided to horses that are withheld feed for greater than 3–4 days. It is suspected to improve healing and shorten the duration of the illness, since horses often become cachexic due to the protein losing enteropathy associated with this disease.

Surgery may need to be performed to rule out colic with similar presenting signs such as obstruction or strangulation, and in cases that are long-standing (> 7 days) to perform a resection and anastomosis of the diseased bowel. However, some horses have recovered with long-term medical support (up to 20 days).

Gastrointestinal diseases refer to diseases involving the gastrointestinal tract, namely the esophagus, stomach, small intestine, large intestine and rectum, and the accessory organs of digestion, the liver, gallbladder, and pancreas.

Diseases of the hepatobiliary system affect the biliary tract (also known as the "biliary tree"), which secretes bile in order to aid digestion of fats. Diseases of the gallbladder and bile ducts are commonly diet-related, and may include the formation of gallstones that impact in the gallbladder (cholecystolithiasis) or in the common bile duct (choledocholithiasis).

Gallstones are a common cause of inflammation of the gallbladder, called cholecystitis. Inflammation of the biliary duct is called cholangitis, which may be associated with autoimmune disease, such as primary sclerosing cholangitis, or a result of bacterial infection, such as ascending cholangitis.

Disease of the biliary tree may cause pain in the upper right abdomen, particularly when pressed. Disease might be investigated using ultrasound or ERCP, and might be treated with drugs such as antibiotics or UDCA, or by the surgical removal of the gallbladder.

Horses may develop pharyngitis, laryngitis, or esophagitis secondary to indwelling nasogastric tube. Other complications include thrombophlebitis, laminitis (which subsequently reduces survival rate), and weight loss. Horses are also at increased risk of hepatic injury.

Survival rates for DPJ are 25–94%. Horses that survive the incident rarely have reoccurrence.

Specific types of enteropathy include:

- Enteropathy-associated T-cell lymphoma

- Environmental enteropathy

- Eosinophilic enteropathy

- Gluten-sensitive enteropathy (which can progress to coeliac disease)

- Coeliac disease

- Human immunodeficiency virus (HIV) HIV Enteropathy

- Immunodysregulation polyendocrinopathy and enteropathy, X-linked (see FOXP3)

- Protein-losing enteropathy

- Radiation enteropathy

- Tropical enteropathy

If the condition also involves the stomach, it is known as "gastroenteropathy".

In pigs, porcine proliferative enteropathy is a diarrheal disease.

All the factors collectively causing CNE are generally only present in the hinterlands of New Guinea and parts of Africa, Latin America, and Asia. These factors include protein deprivation (causing inadequate synthesis of trypsin protease (an enzyme), to which the toxin is very sensitive), poor food hygiene, episodic meat feasting, staple diets containing trypsin inhibitors (sweet potatoes), and infection by "Ascaris" parasites which secrete a trypsin inhibitor. In New Guinea (origin of the term "pigbel"), the disease is usually spread through contaminated meat (especially pork) and perhaps by peanuts. (CNE was also diagnosed in post World War II Germany, where it was known as "Darmbrand" or "fire bowels").

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.

One study suggests that on very long trips in the wilderness, taking multivitamins may reduce the incidence of diarrhea.

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.

CNE is a necrotizing inflammation of the small bowel (especially the jejunum but also the ileum). Clinical results may vary from mild diarrhea to a life-threatening sequence of severe abdominal pain, vomiting, bloody stool, ulceration of the small intestine with leakage (perforation) into the peritoneal cavity and possible death within a single day due to peritonitis. Many patients exhibit meteorism. Treatment involves suppressing the toxin-producing organisms with antibiotics such as penicillin G or metronidazole. About half of seriously ill patients require surgery for perforation, persistent intestinal obstruction, or failure to respond to the antibiotics. An investigational toxoid vaccine has been used successfully in some developing countries but is not available outside of research.

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.

The risk of fecal-oral transmission of pathogens that cause diarrhea can be significantly reduced by good hygiene, including washing hands with soap and water after urination and defecation, and washing eating utensils with warm soapy water. Additionally a three-bowl system can be used for washing eating utensils.

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.

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).

Specific types of enterocolitis include:

- necrotizing enterocolitis (most common in premature infants)

- pseudomembranous enterocolitis (also called "Pseudomembranous colitis")

Since many, if not most, anal cancers derive from HPV infections, and since the HPV vaccine before exposure to HPV prevents infection by some strains of the virus and has been shown to reduce the incidence of potentially precancerous lesions, scientists surmise that HPV vaccination may reduce the incidence of anal cancer.

On 22 December 2010, the U.S. Food and Drug Administration approved Gardasil vaccine to prevent anal cancer and pre-cancerous lesions in males and females aged 9 to 26 years. The vaccine has been used before to help prevent cervical, vulvar, and vaginal cancer, and associated lesions caused by HPV types 6, 11, 16, and 18 in women.

10 to 20% of patients treated for anal cancer will develop distant metastatic disease following treatment. Metastatic or recurrent anal cancer is difficult to treat, and usually requires chemotherapy. Radiation is also employed to palliate specific locations of disease that may be causing symptoms. Chemotherapy commonly used is similar to other squamous cell epithelial neoplasms, such as platinum analogues, anthracyclines such as doxorubicin, and antimetabolites such as 5-FU and capecitabine. JD Hainsworth developed a protocol that includes Taxol and Carboplatinum along with 5-FU. Median survival rates for patients with distant metastases ranges from 8 to 34 months.

The treatment of choice is a large resection or amputation of the affected limb. Radiation therapy can precede or follow surgical treatment. Tumors that have advanced locally or have metastasized can be treated with mono or polychemotherapy, systemically or locally. However, chemotherapy and radiation therapy have not been shown to improve survivorship significantly.