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.

Horses form ulcers in the stomach fairly commonly, a disease called equine gastric ulcer syndrome. Risk factors include confinement, infrequent feedings, a high proportion of concentrate feeds, such as grains, excessive non-steroidal anti-inflammatory drug use, and the stress of shipping and showing. Gastric ulceration has also been associated with the consumption of cantharidin beetles in alfalfa hay which are very caustic when chewed and ingested. Most ulcers are treatable with medications that inhibit the acid producing cells of the stomach. Antacids are less effective in horses than in humans, because horses produce stomach acid almost constantly, while humans produce acid mainly when eating. Dietary management is critical. Bleeding ulcers leading to stomach rupture are rare.

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.

Ileus is a cause of colic in horses due to functional obstruction of the intestines. It most commonly seen in horses postoperatively, especially following colic surgery. Horses experiencing ileus are at risk for gastric rupture due to rapid reflux build-up, and require intense medical management with frequent nasogastric intubation. Ileus may increase adhesion formation, because intestinal segments have more prolonged contact and intestinal distention causes serosal injury and ischemia. It is usually treated with aggressive fluid support, prokinetics, and anti-inflammatories.

DPJ is most commonly seen in the Southeastern US, although cases have been reported throughout the United States and Canada, as well as sporadically in the United Kingdom and Europe. Horses in the Southeastern US tend to have a more severe form of the disease relative to other locations. Age, breed, and gender appear to have no effect on disease prevalence.

Cholesterol gallstone formation risk factors include age, female sex, family history, race, pregnancy, parity, obesity, birth control, diabetes mellitus, cirrhosis, prolonged fasting, rapid weight loss, total parenteral nutrition, ileal disease and impaired gallbladder emptying.

Patients that have gallstones and biliary colic are at increased risk for complications, including cholecystitis. Complications from gallstone disease is 0.3% per year and therefore prophylactic cholecystectomy are rarely indicated unless part of a special population that includes porcelain gallbladder, individuals eligible for organ transplant, diabetics and those with sickle cell anemia.

The differential diagnoses of acute abdomen include but are not limited to:

1. Acute appendicitis

2. Acute peptic ulcer and its complications

3. Acute cholecystitis

4. Acute pancreatitis

5. Acute intestinal ischemia (see section below)

6. Acute diverticulitis

7. Ectopic pregnancy with tubal rupture

8. Ovarian torsion

9. Acute peritonitis (including hollow viscus perforation)

10. Acute ureteric colic

11. Bowel volvulus

12. Bowel obstruction

13. Acute pyelonephritis

14. Adrenal crisis

15. Biliary colic

16. Abdominal aortic aneurysm

17. Familial Mediterranean fever

18. Hemoperitoneum

19. Ruptured spleen

20. Kidney stone

21. Sickle cell anaemia

Paralysis of the intestine is often termed paralytic ileus, in which the intestinal paralysis need not be complete, but it must be sufficient to prohibit the passage of food through the intestine and lead to intestinal blockage. Paralytic ileus is a common side effect of some types of surgery, commonly called postsurgical ileus. It can also result from certain drugs and from various injuries and illnesses, such as acute pancreatitis. Paralytic ileus causes constipation and bloating. On listening to the abdomen with a stethoscope, no bowel sounds are heard because the bowel is inactive.

A temporary paralysis of a portion of the intestines occurs typically after abdominal surgery. Since the intestinal content of this portion is unable to move forward, food or drink should be avoided until peristaltic sound is heard, by auscultation (use of a stethoscope) of the area where this portion lies. Intestinal atony or paralysis may be caused by inhibitory neural reflexes, inflammation or other implication of neurohumoral peptides.

The cause of colic is generally unknown. Fewer than 5% of infants who cry excessively turn out to have an underlying organic disease, such as constipation, gastroesophageal reflux disease, lactose intolerance, anal fissures, subdural hematomas, or infantile migraine. Babies fed cow's milk have been shown to develop antibody responses to the bovine protein, causing colic. Studies performed showed conflicting evidence about the role of cow's milk allergy. While previously believed to be related to gas pains, this does not appear to be the case. Another theory holds that colic is related to hyperperistalsis of the digestive tube (increased level of activity of contraction and relaxation). The evidence that the use of anticholinergic agents improve colic symptoms supports this hypothesis.

Psychological and social factors have been proposed as a cause, but there is no evidence. Studies performed don't support the theory that maternal (or paternal) personality or anxiety causes colic, nor that it is a consequence of a difficult temperament of the baby, but families with colicky children may eventually develop anxiety, fatigue and problems with family functioning as a result. There is some evidence that cigarette smoke may increase the risk. It seems unrelated to breast or bottle feeding with rates similar in both groups. Reflux does not appear to be related to colic.

Infants who are colicky do just as well as their non colicky peers with respect to temperament at one year of age.

The presence of gallstones can lead to inflammation of the gall bladder (cholecystitis) or the biliary tree (cholangitis) or acute inflammation of the pancreas (pancreatitis). Rarely, a gallstone can become impacted in the ileocecal valve that joins the caecum and the ileum, causing gallstone ileus (mechanical ileus).

Complications from delayed surgery include pancreatitis, empyema, and perforation of the gallbladder, cholecystitis, cholangitis, and obstructive jaundice.

Biliary pain in the absence of gallstones, known as postcholecystectomy syndrome, may severely impact the patient's quality of life, even in the absence of disease progression.

Colic (from Greek κολικός "kolikos", "relative to the colon") or cholic is a form of pain that starts and stops abruptly. It occurs due to muscular contractions of a hollow tube (colon, ureter, gall bladder, etc.) in an attempt to relieve an obstruction by forcing content out. It may be accompanied by vomiting and sweating. Types include:

- Baby colic, a condition, usually in infants, characterized by incessant crying

- Renal colic, a pain in the flank, characteristic of kidney stones

- Biliary colic, blockage by a gallstone of the common bile duct or cystic duct

- Horse colic, a potentially fatal condition experienced by horses, caused by intestinal displacement or blockage

- Devon colic, an affliction caused by lead poisoning

- Painter's colic or lead poisoning

Acute abdomen is occasionally used synonymously with peritonitis. While this is not entirely incorrect, peritonitis is the more specific term, referring to inflammation of the peritoneum. It manifests on physical examination as rebound tenderness, or pain upon "removal" of pressure more than on "application" of pressure to the abdomen. Peritonitis may result from several of the above diseases, notably appendicitis and pancreatitis. While rebound tenderness is commonly associated with peritonitis, the most specific finding is rigidity.

After the material has passed, a veterinarian may try to prevent the onset of aspiration pneumonia by placing the horse on broad-spectrum antibiotics. The animal should be monitored for several days to ensure that it does not develop pneumonia, caused by inhalation of bacteria-rich food material into the lungs.

The material caught in a horse's throat usually causes inflammation, which may later lead to scarring. Scarring reduces the diameter of the esophagus (a stenosis or stricture), which increases the chance that the horse may choke again. The veterinarian may therefore place the horse on a course of NSAIDs, to help to control the inflammation of the esophagus.

Often the horse will only be fed softened food for a few days, allowing the esophagus to heal, before it is allowed to gradually resume its normal diet (e.g. hay and unsoaked grain). Horses with re-occurring chokes may require their diet to be changed.

Cholecystitis occurs when the gallbladder becomes inflamed. Gallstones are the most common cause of gallbladder inflammation but it can also occur due to blockage from a tumor or scarring of the bile duct. The greatest risk factor for cholecystitis is gallstones. Risk factors for gallstones include female sex, increasing age, pregnancy, oral contraceptives, obesity, diabetes mellitus, ethnicity (Native North American), rapid weight loss.

The inflammation of cholecystitis can lead to adhesions between the gallbladder and other parts of the gastrointestinal tract, most commonly the duodenum. These adhesions can lead to the formation of direct connections between the gallbladder and gastrointestinal tract, called fistulas. With these direct connections, gallstones can pass from the gallbladder to the intestines. Gallstones can get trapped in the gastrointestinal tract, most commonly at the connection between the small and large intestines (ileocecal valve). When a gallstone gets trapped, it can lead to an intestinal obstruction, called gallstone ileus, leading to abdominal pain, vomiting, constipation, and abdominal distension.

Choking horses should be deprived of food and drink pending veterinary attention, so as not to increase the obstructive load within the esophagus. The veterinarian will often sedate the horse and administer spasmolytics, such as butylscopolamine, to help the esophagus to relax. Once the muscles of the esophagus no longer force the food down the throat (active peristalsis), it may slip down on its own accord. If spasmolytics do not solve the problem, the veterinarian will usually pass a stomach tube through one of the nostrils and direct it into the esophagus until the material is reached, at which point "gentle" pressure is applied to manually push the material down. Gentle warm water lavage (water sent through the stomach tube, to soften the food material) may be required to help the obstructing matter pass more easily, but caution should be exercised to prevent further aspiration of fluid into the trachea.

Refractory cases are sometimes anesthetised, with an orotracheal tube placed to prevent further aspiration and to allow for more vigorous lavage. Disruption of the impacted material can sometimes be achieved via endoscopy. If these methods still do not lead to results, the horse may require surgery to remove the material.

Some workers have advocated the use of oxytocin in choke, on the grounds that it decreases the esophageal muscular tone. However, this technique is not suitable in pregnant mares, as it may lead to abortion.

The clinical course of biliary sludge can do one of three things: (1) it can resolve completely, (2) wax and wane, or (3) progress to gallstones. If the biliary sludge has a cause (e.g. pregnancy), it oftentimes is resolved when the underlying cause is removed.

The prevalence of biliary sludge is low in the general population. It has been reported that the prevalence ranges from 0-0.20% in men and 0.18-0.27% in women. However, in patients with certain conditions, the prevalence may be higher.

Equine enteroliths are found by walking pastures or turning over manure compost piles to find small enteroliths, during necroscopy, and increasingly, during surgery for colic. Therefore, the incidence of asymptomatic enteroliths is unknown.

Equine enteroliths typically are smoothly spherical or tetrahedral, consist mostly of the mineral struvite (ammonium magnesium phosphate), and have concentric rings of mineral precipitated around a nidus.

Enteroliths in horses were reported widely in the 19th century, infrequently in the early 20th century, and now increasingly. They have also been reported in zebras: five in a zoo in California and one in a zoo in Wisconsin. Struvite enteroliths are associated with elevated pH and mineral concentrations in the lumen. In California, struvite enteroliths are associated also with a high proportion of alfalfa in the feed and less access to grass pasture. This association has been attributed to the cultivation of alfalfa on serpentine soils, resulting in high concentrations of magnesium in the alfalfa.

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.

An enterolith is a mineral concretion or calculus formed anywhere in the gastrointestinal system. Enteroliths are uncommon and usually incidental findings but, once found, they require at a minimum watchful waiting. If there is evidence of complications, they must be removed.

An enterolith may form around a "nidus", a small foreign object such as a seed, pebble, or piece of twine, that serves as an irritant. In this respect, an enterolith forms by a process similar to the creation of a pearl.

An enterolith is not to be confused with a gastrolith, which helps digestion.

Treatment for colitis-X usually does not save the horse. The prognosis is average to poor, and mortality is 90% to 100%. However, treatments are available, and one famous horse that survived colitis-X was U.S. Triple Crown winner Seattle Slew, that survived colitis-X in 1978 and went on to race as a four-year-old.

Large amounts of intravenous fluids are needed to counter the severe dehydration, and electrolyte replacement is often necessary. Flunixin meglumine (Banamine) may help block the effects of toxemia. Mortality rate has been theorized to fall to 75% if treatment is prompt and aggressive, including administration of not only fluids and electrolytes, but also blood plasma, anti-inflammatory and analgesic drugs, and antibiotics. Preventing dehydration is extremely important. Nutrition is also important. Either parenteral or normal feeding can be used to support the stressed metabolism of the sick horse. Finally, the use of probiotics is considered beneficial in the restoration of the normal intestinal flora. The probiotics most often used for this purpose contain "Lactobacillus" and "Bifidobacterium".

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.

In RPC the gallstones found within the biliary system are calcium bilirubinate stones or pigmented calcium stones. Calcium bilirubinate stones are prevalent in Asia and very rare in Europe and the United States. In addition to the presence of these friable concretions of various shapes and sizes within the biliary tree, the bile is often muddy in consistency and contains numerous fine particles of calcium bilirubinate. This differs greatly from cholesterol stones, which are common in Europe and the United States. Pure cholesterol stones contain >96% cholesterol whereas mixed cholesterol stones contain 71.3% cholesterol. The formation of calcium bilirubinate stones in RPC has been attributed to the high incidence of infection with "Escherichia coli" in the bile. In humans, the majority of bilirubin is excreted in the bile as bilirubin glucuronide.

Hepatolithiasis is associated with Clonorchis sinensis and Ascaris lumbricoides infestation of the liver. This theory is based on high incidence of dead parasites or ova within stone in autopsy findings.