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

Most of the symptoms of BLS are non specific but nevertheless warrant the utmost attention. These include:

- Loss of appetite

- Nausea

- Flatulence

- Diarrhea

- Fullness after a meal

- Fatty stools (steatorrhea)

- Unintentional weight loss

- Generalised weakness

As a result of the concomitant vitamin and mineral deficiencies that occur as a result of the malabsorption associated with BLS patients with advanced cases should be investigated for:

- Vitamin B12 deficiency

- Folate deficiency

- Iron deficiency

- Vitamin E deficiency

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.

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.

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.

Blind loop syndrome (BLS), commonly referred to in the literature as small intestinal bacterial overgrowth (SIBO) or bacterial overgrowth syndrome (BOS), is a state that occurs when the normal bacterial flora of the small intestine proliferates to numbers that cause significant derangement to the normal physiological processes of digestion and absorption. In some cases of blind loop syndrome, overgrowth of pathogenic non-commensal bacteria has also been noted. It has long been understood that from birth, and throughout life, large amounts of bacteria reside symbiotically within animal gastrointestinal tracts such as the human gastrointestinal tract. The understanding of this gut flora has even led to novel treatments for bowel irregularity that utilize so called "probiotics" or good bacteria that aid in normal digestion.

The problem of BLS arises when the bacterial colonies residing in the upper gastrointestinal tract begin to grow out of control or are altered in their makeup thereby creating a burden on the normal physiological processes occurring in the small intestine. This results in problems inclusive of but not restricted to vitamin B12 deficiency, fat malabsorption and steatorrhea, fat-soluble vitamin deficiencies and intestinal wall injury.

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.

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 Connective tissue abnormality may cause Intestinal Desmosis The absence of the tendinous plexus layer was first described in 1998 by Meier-Ruge. Desmosis is implicated in disturbed gut motility.

Normal peristalsis depends upon the interaction between muscles, nerve cells and tendinous connective tissue. A malfunction of any of these leads to intestinal motility disorders.

Desmosis may be congenital (aplastic form) or acquired (atrophic form).

The "aplastic" form is rare. Typical clinical findings are hypoperistalsis, and pseudo-obstruction. These are found in premature infants, associated with low birth weight. The "atrophic" form is more frequent. Inflammation of the muscularis propria releases enzymes including collagenases which destroy the connective tissue of the bowel wall. Primarily newborns and small children are affected, although this manifestation can also be found in adults. The most common location is the colon with a necrotizing enterocolitis as well as Crohn Disease and diverticulitis. If the taenia are also affected, the disease is defined as complete atrophic desmosis, all other forms without involvement of the taenia are referred to as incomplete. Clinically, patients demonstrate chronic constipation.

As proposed by Giuseppe Martucciello, microscopic diagnosis requires laparoscopic intestinal full-thickness biopsies from colon. Histological findings are absence of the tendinous plexus layer and connective tissue fibers in longitudinal and circular muscle layer.

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.

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.

Hereditary folate malabsorption (HFM - OMIM #229050) is a rare autosomal recessive disorder caused by loss-of-function mutations in the proton-coupled folate transporter (PCFT) gene, resulting in systemic folate deficiency and impaired delivery of folate to the brain.

Affected infants present within a few months after birth with failure to thrive and severe folate deficiency manifested as macrocytic anemia and developmental delays. There can be (i) pancytopenia, (ii) diarrhea and/or mucositis and/or (iii) immune deficiency due to T-cell dysfunction and hypoimmunoglobulinemia resulting in pneumonia usually due to Pneumocystis jirovecii. Recently, several infants with the immune deficiency syndrome were described. Untreated, or with inadequate treatment, there are progressive systemic and neurological signs with a spectrum of manifestations including seizures that are often intractable. Females with HFM are fertile and, if folate sufficient during pregnancy, have normal offspring. Subjects that carry one mutated PCFT allele are normal. The genomic and clinical features of HFM were recently reviewed.

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.

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.

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.

Neonatal bowel obstruction (NBO) or neonatal intestinal obstruction is the most common surgical emergency in the neonatal period. It may occur due to a variety of conditions and has an excellent outcome based on timely diagnosis and appropriate intervention.

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.

Diverticular disease can present with painless rectal bleeding as bright red blood per rectum. Diverticular bleeding is the most common cause of acute lower gastrointestinal bleeding. However, it is estimated that 80% of these cases are self-limiting and require no specific therapy.

Depending on the level of obstruction, bowel obstruction can present with abdominal pain, swollen abdomen, abdominal distension, vomiting, fecal vomiting, and constipation.

Bowel obstruction may be complicated by dehydration and electrolyte abnormalities due to vomiting; respiratory compromise from pressure on the diaphragm by a distended abdomen, or aspiration of vomitus; bowel ischemia or perforation from prolonged distension or pressure from a foreign body.

In small bowel obstruction, the pain tends to be colicky (cramping and intermittent) in nature, with spasms lasting a few minutes. The pain tends to be central and mid-abdominal. Vomiting may occur before constipation.

In large bowel obstruction, the pain is felt lower in the abdomen and the spasms last longer. Constipation occurs earlier and vomiting may be less prominent. Proximal obstruction of the large bowel may present as small bowel obstruction.

Infection of a diverticulum can result in diverticulitis. This occurs in 10–25% of people with diverticulosis. Tears in the colon leading to bleeding or perforations may occur; intestinal obstruction may occur (constipation or diarrhea does not rule this possibility out); and peritonitis, abscess formation, retroperitoneal fibrosis, sepsis, and fistula formation are also possible occurrences. Rarely, an enterolith may form. Infection of a diverticulum often occurs as a result of stool collecting in a diverticulum.

It is defined as diverticular disease with signs and symptoms of diverticular inflammation. Clinical features of acute diverticulitis include constant abdominal pain, localized abdominal tenderness in the left lower quadrant of the abdomen, nausea, vomiting, constipation or diarrhea, fever and leukocytosis.

Most people with colonic diverticulosis are unaware of this structural change. When symptoms do appear in a person over 40 years of age it is important to obtain medical advice and exclude more dangerous conditions such as cancer of the colon or rectum.

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

Patients (often infants) present acutely with midgut volvulus, manifested by bilious vomiting, crampy abdominal pain, abdominal distention, and the passage of blood and mucus in their stools. Patients with chronic, uncorrected malrotation can have recurrent abdominal pain and vomiting.

Malrotation can also be asymptomatic.

Strictly speaking, colic refers only to signs originating from the gastrointestinal tract of the horse. Signs of colic may be caused by problems other than the GI-tract e.g. problems in the liver, ovaries, spleen, urogenital system, testicular torsion, pleuritis, and pleuropneumonia. Diseases which sometimes cause symptoms which appear similar to colic include uterine contractions, laminitis, and exertional rhabdomyolysis. Colic pain secondary to kidney disease is rare.

Uterine tears often occur a few days post parturition. They can lead to peritonitis and require surgical intervention to fix. Uterine torsions can occur in the third trimester, and while some cases may be corrected if the horse in anesthetized and rolled, others require surgical correction.