Intestinal failure is decreased intestinal function such that nutrients, water, and electrolytes are not sufficiently absorbed. Short bowel syndrome is when there is less than of working bowel and is the most common cause of intestinal failure.

The symptoms of short bowel syndrome can include:

- Abdominal pain

- Diarrhea and steatorrhea (oily, bulky stool, which can be malodorous)

- Fluid depletion

- Weight loss and malnutrition

- Fatigue

Persons with short bowel syndrome may have complications caused by malabsorption of vitamins and minerals, such as deficiencies in vitamins A, D, E, K, B (folic acid), and B, calcium, magnesium, iron, and zinc. These may appear as anemia, hyperkeratosis (scaling of the skin), easy bruising, muscle spasms, poor blood clotting, and bone pain.

Clinical features of intestinal pseudo-obstruction can include abdominal pain, nausea, severe distension, vomiting, dysphagia, diarrhea and constipation, depending upon the part of the gastrointestinal tract involved. In addition, in the moments in which abdominal colic occurs, an abdominal x-ray shows intestinal air fluid level. All of these features are also similar in true mechanical obstruction of the bowel.

Intestinal pseudo-obstruction is a clinical syndrome caused by severe impairment in the ability of the intestines to push food through. It is characterized by the signs and symptoms of intestinal obstruction without any lesion in the intestinal lumen. Clinical features can include abdominal pain, nausea, severe distension, vomiting, dysphagia, diarrhea and constipation, depending upon the part of the gastrointestinal tract involved. The condition can begin at any age and it can be a primary condition (idiopathic or inherited) or caused by another disease (secondary).

It can be chronic or acute.

Depending on the nature of the disease process causing malabsorption and its extent, gastrointestinal symptoms may range from severe to subtle or may even be totally absent. Diarrhea, weight loss, flatulence, abdominal bloating, abdominal cramps, and pain may be present. Although diarrhea is a common complaint, the character and frequency of stools may vary considerably ranging from over 10 watery stools per day to less than one voluminous putty-like stool, the latter causing some patients to complain of constipation. On the other hand, stool mass is invariably increased in patients with steatorrhea and generalized malabsorption above the normal with 150–200 g/day. Not only do unabsorbed nutrients contribute to stool mass but mucosal fluid and electrolyte secretion is also increased in diseases associated with mucosal inflammation such as coeliac disease. In addition, unabsorbed fatty acids, converted to hydroxy-fatty acids by colonic flora, as well as unabsorbed bile acids both impair absorption and induce secretion of water and electrolytes by the colon adding to stool mass. Weight loss is common among patients with significant intestinal malabsorption but must be evaluated in the context of caloric intake. Some patients compensate for fecal wastage of unabsorbed nutrients by significantly increasing their oral intake. Eliciting a careful dietary history from patients with suspected malabsorption is therefore crucial. Excessive flatus and abdominal bloating may reflect excessive gas production due to fermentation of unabsorbed carbohydrate, especially among patients with primary or secondary disaccharidase deficiency. Malabsorption of dietary nutrients and excessive fluid secretion by inflamed small intestine also contribute to abdominal distention and bloating. Prevalence, severity, and character of abdominal pain vary considerably among the various disease processes associated with intestinal malabsorption. For example, pain is common in patients with chronic pancreatitis or pancreatic cancer and Crohn disease, but it is absent in many patients with coeliac disease or postgastrectomy malabsorption.

Substantial numbers of patients with intestinal malabsorption present initially with symptoms or laboratory abnormalities that point to other organ systems in the absence of or overshadowing symptoms referable to the gastrointestinal tract. For example, there is increasing epidemiologic evidence that more patients with coeliac disease present with anemia and osteopenia in the absence of significant classic gastrointestinal symptoms. Microcytic, macrocytic, or dimorphic anemia may reflect impaired iron, folate, or vitamin B12 absorption. Purpura, subconjunctival hemorrhage, or even frank bleeding may reflect hypoprothrombinemia secondary to vitamin K malabsorption. Osteopenia is common, especially in the presence of steatorrhea. Impaired calcium and vitamin D absorption and chelation of calcium by unabsorbed fatty acids resulting in fecal loss of calcium may all contribute. If calcium deficiency is prolonged, secondary hyperparathyroidism may develop. Prolonged malnutrition may induce amenorrhea, infertility, and impotence. Edema and even ascites may reflect hypoproteinemia associated with protein losing enteropathy caused by lymphatic obstruction or extensive mucosal inflammation. Dermatitis and peripheral neuropathy may be caused by malabsorption of specific vitamins or micronutrients and essential fatty acids.

Bile acid malabsorption, known also as bile acid diarrhea, is a cause of several gut-related problems, the main one being chronic diarrhea. It has also been called bile acid-induced diarrhea, cholerheic or choleretic enteropathy and bile salt malabsorption. It can result from malabsorption secondary to gastrointestinal disease, or be a primary disorder, associated with excessive bile acid production. Treatment with bile acid sequestrants is often effective.

External signs and symptoms are constipation of very long duration, abdominal bloating, abdominal tenderness and tympany, abdominal pain, palpation of hard fecal masses and, in toxic megacolon, fever, low blood potassium, tachycardia and shock. Stercoral ulcers are sometimes observed in chronic megacolon, which may lead to perforation of the intestinal wall in approximately 3% of the cases, leading to sepsis and risk of death.

Symptoms of ileus include, but are not limited to:

- moderate, diffuse abdominal discomfort

- constipation

- abdominal distension

- nausea/vomiting, especially after meals

- vomiting of bilious fluid

- lack of bowel movement and/or flatulence

- excessive belching

Proximal enteritis, also known as anterior enteritis or duodenitis-proximal jejunitis (DPJ), is inflammation of the duodenum and upper jejunum. It produces a functional stasis of the affected intestine (ileus) and hypersecretion of fluid into the lumen of that intestine. This leads to large volumes of gastric reflux, dehydration, low blood pressure, and potentially shock. Although the exact cause is not yet definitively known, proximal enteritis requires considerable supportive care.

Megacolon is an abnormal dilation of the colon (also called the large intestine). The dilation is often accompanied by a paralysis of the peristaltic movements of the bowel. In more extreme cases, the feces consolidate into hard masses inside the colon, called fecalomas (literally, "fecal tumor"), which can require surgery to be removed.

A human colon is considered abnormally enlarged if it has a diameter greater than 12 cm in the cecum (it is usually less than 9 cm), greater than 6.5 cm in the rectosigmoid region and greater than 8 cm for the ascending colon. The transverse colon is usually less than 6 cm in diameter.

A megacolon can be either acute or chronic. It can also be classified according to cause.

Bile acid malabsorption was first recognized in patients with ileal disease. When other causes were recognized, and an idiopathic, primary form described, a classification into three types was proposed:

- Type 1: Bile acid malabsorption, secondary to ileal resection, or ileal inflammation (e.g. in Crohn's disease)

- Type 2: Idiopathic bile acid malabsorption, Primary bile acid diarrhea

- Type 3: Secondary to various gastrointestinal diseases including cholecystectomy, vagotomy, small intestinal bacterial overgrowth, radiation enteropathy, celiac disease, chronic pancreatitis, etc.

Signs include acute onset of moderate to severe pain, large volumes of gastric reflux (4–20 L per decompression) which is usually orange-brown and fetid, distended small intestine (up to 5–7 cm in diameter) palpable on rectal examination, fever, depression, increased heart rate (>60 bpm), increased respiratory rate, prolonged CRT, and darkened mucous membranes. After gastric decompression, the horse may show signs of malaise and act lethargic, but pain level usually improves.

Abdominocentesis usually reveals a yellow, turbid fluid with an increased white blood cell count (usually 5,000–10,000 cells/microliter) and protein level (>3.5 g/dl), although the fluid may be serosanginous in severe cases. A chemistry panel will often show electrolyte abnormalities (hypokalemia, hyponatremia, hypochloremia) due to electrolyte loss into the lumen of the intestine. Leukocytes may be normal, increased, or decreased. PCV and total protein are usually both increased due to fluid loss, and the horse displays a prerenal azotemia. On the chemistry panel, liver enzymes such as GGT, ALP, AST are increased, likely due to ascending infection from the common bile duct, endotoxin absorption, and hypoperfusion. A metabolic acidosis with a high anion gap is often seen due to loss of bicarbonate in gastric reflux and an increase in lactic acid in the blood, secondary to hypovolemia and decreased tissue perfusion.

Usually the patient has abdominal distention, pain and altered bowel movements. There may also be nausea and vomiting.

Decreased propulsive ability may be broadly classified as caused either by bowel obstruction or intestinal atony or paralysis. However, instances with symptoms and signs of a bowel obstruction occur, but with the absence of a mechanical obstruction, mainly in acute colonic pseudo-obstruction, Ogilvie's syndrome.

The main symptoms of AIE include:

- Diarrhea (frequent loss of fluids)

- Intestinal inflammation

- Vomiting

- Intestinal bleeding

- Difficulty or inability to gain weight

- Rapid weight loss

- Decreased urine output from dehydration

EE is rarely symptomatic and is considered a subclinical condition. However, adults may have mild symptoms or malabsorption such as altered stool consistency, increased stool frequency and weight loss.

DIOS is sometimes classified by the degree of obstruction as incomplete or complete DIOS.

Regardless of cause, volvulus causes symptoms by two mechanisms:

- Bowel obstruction manifested as abdominal distension and bilious vomiting.

- Ischemia (loss of blood flow) to the affected portion of intestine.

Depending on the location of the volvulus, symptoms may vary. For example, in patients with a cecal volvulus, the predominant symptoms may be those of a small bowel obstruction (nausea, vomiting and lack of stool or flatus), because the obstructing point is close to the ileocecal valve and small intestine. In patients with a sigmoid volvulus, although abdominal pain may be present, symptoms of constipation may be more prominent.

Volvulus causes severe pain and progressive injury to the intestinal wall, with accumulation of gas and fluid in the portion of the bowel obstructed. Ultimately, this can result in necrosis of the affected intestinal wall, acidosis, and death. This is known as a closed loop obstruction because there exists an isolated ("closed") loop of bowel. Acute volvulus often requires immediate surgical intervention to untwist the affected segment of bowel and possibly resect any unsalvageable portion.

Volvulus occurs most frequently in middle-aged and elderly men. Volvulus can also arise as a rare complication in persons with redundant colon, a normal anatomic variation resulting in extra colonic loops.

Sigmoid volvulus is the most-common form of volvulus of the gastrointestinal tract. and is responsible for 8% of all intestinal obstructions. Sigmoid volvulus is particularly common in elderly persons and constipated patients. Patients experience abdominal pain, distension, and absolute constipation.

Cecal volvulus is slightly less common than sigmoid volvulus and is associated with symptoms of abdominal pain and small bowel obstruction.

Volvulus can also occur in patients with Duchenne muscular dystrophy due to the smooth muscle dysfunction.

Signs and symptoms of DIOS include a sudden onset of crampy abdominal pain, vomiting, and a palpable mass (often in the right lower quadrant) in the abdomen. The characteristic abdominal pain is typically located in the center or right lower quadrant of the abdomen. X-rays of the abdomen may reveal stool in the colon and air-fluid levels in the small intestines.

People who have been treated with radiotherapy for pelvic and other abdominal cancers frequently develop gastrointestinal symptoms. These include:

- rectal bleeding

- diarrhea and steatorrhea

- other defecation disorders including fecal urgency and incontinence.

- nutritional deficiencies and weight loss

- abdominal pain and bloating

- nausea, vomiting and fatigue

Gastrointestinal symptoms are often found together with those in other systems including genitourinary disorders and sexual dysfunction. The burden of symptoms substantially impairs the patients' quality of life.

Nausea, vomiting, fatigue and diarrhea may happen early during the course of radiotherapy. Radiation enteropathy represents the longer-term, chronic effects which may be found after a latent period most commonly of 6 months to 3 years after the end of treatment. In some cases, it does not become a problem for 20-30 years after successful curative therapy.

Ogilvie syndrome is the acute dilation of the colon in the absence of any mechanical obstruction in severely ill patients.

Colonic pseudo-obstruction is characterized by massive dilatation of the cecum (diameter > 10 cm) and right colon on abdominal X-ray. It is a type of megacolon, sometimes referred to as "acute megacolon", to distinguish it from toxic megacolon.

The condition carries the name of the British surgeon Sir (1887–1971), who first reported it in 1948.

Cancers (neoplasia) other than lipoma are relatively rare causes of colic. Cases have been reported with intestinal cancers including intestinal lymphosarcoma, leiomyoma, and adenocarcinoma, stomach cancers such as squamous cell carcinoma, and splenic lymphosarcoma.

Gastric squamous cell carcinoma is most often found in the non-glandular region of the stomach of horses greater than 5 years of age, and horses often present with weight loss, anorexia, anemia, and ptyalism. Gastric carcinoma is usually diagnosed via gastroscopy, but may sometimes be felt on rectal if they have metastasized to the peritoneal cavity. Additionally, laparoscopy can also diagnose metastasized cancer, as can presence of neoplastic cells on abdominocentesis. Often the signs of intestinal neoplasia are non-specific, and include weight loss and colic, usually only if obstruction of the intestinal lumen occurs.

Long-term use of NSAIDs can lead to mucosal damage of the colon, secondary to decreased levels of homeostatic prostaglandins. Mucosal injury is usually limited to the right dorsal colon, but can be more generalized. Horses may display acute or chronic intermittent colic, peripheral edema secondary to protein losing enteropathy, decreased appetite, and diarrhea. Treatment involves decreasing the fiber levels of the horse's diet by reducing grass and hay, and placing the horse on an easily digestible pelleted feed until the colon can heal. Additionally, the horse may be given misoprostol, sucralfate, and psyllium to try to improve mucosal healing, as well as metronidazole to reduce inflammation of the colon.

Environmental enteropathy is believed to result in chronic malnutrition and subsequent growth stunting (low height-for-age measurement) as well as other child development deficits.