- 0.1 Signs
- 0.2 Diarrhea
- 0.2.1 Classifications of Diarrhea
- 0.2.2 Causes of Secretory Diarrhea
- 0.2.3 Malabsorption
- 0.2.4 Pathophysiologic Mechanisms of Malabsorption
- 0.2.5 Melena
- 0.2.6 Causes of Melena
- 0.2.7 Borborygmi and Flatulence
- 0.2.8 Weight Loss or Failure to Thrive
- 0.2.9 Protein-Losing Enteropalhy
- 0.2.10 Protein-Losing Enteropathies
- 0.2.11 Relative Advantages of Endoscopic and Surgical Intestinal Biopsy
- 0.3 Diagnosis of Small Intestinal Disease
- 0.4 Occult blood
- 0.5 Small Intestine: Imaging
- 0.6 Small Intestine: Special Tests
- 0.7 Endoscopy
- 0.8 Small Intestine: Intestinal Biopsy
- 0.9 Acute Small Intestinal Disease
- 1 Viral Enteritides
- 2 Bacterial Enteritides
- 3 Rickettsial Diarrhea (Salmon Poisoning)
- 4 Algal Infections
- 5 Fungal Infections
- 6 Helminths
- 7 Protozoa
- 8 Chronic Idiopathic Enteropathies
- 9 Adverse Reactions To Food
- 10 Small Intestinal Bacterial Overgrowth
- 11 Inflammatory Bowel Disease
- 12 Lymphangiectasia
- 13 Miscellaneous Causes Of Protein-Losing Enteropathy
- 14 Intestinal Neoplasia
- 15 Adynamic Ileus And Intestinal Pseudo-Obstruction
- 16 Intestinal Obstruction
- 17 Short Bowel Syndrome
- 18 Irritable Bowel Syndrome
Diarrhea is an increase in fecal mass caused by an increase in fecal water and / or solid content. It is accompanied by an increase in frequency and / or fluidity and / or volume of feces. Yet it must be remembered that the absence of recognizable diarrhea does not preclude the possibility of significant small intestine disease.
Classifications of Diarrhea
- Permeability (exudative)
- Small intestinal
- Large intestinal
- Diet; bacterial, viral, parasitic causes; other
- Exocrine pancreatic insufficiency, salmonellosis, lymphoma, other
- Acute, nonfatal, self-limiting
- Acute potentially fatal
- Acute systemic disease
Diarrhea can be classified in several ways (Box Classifications of Diarrhea). These categories are not mutually exclusive, and they allow the problem to be viewed from different perspectives, facilitating diagnosis and the choice of appropriate treatment. A mechanistic approach is simple, and many small intestine diseases have a component of osmotic diarrhea, but even in a situation as simple as lactase deficiency, other mechanisms become involved. Osmotic diarrhea in lactose malabsorption causes intestinal distension, which induces peristalsis and rapid transit, and bacterial fermentation products in the colon cause secretion. Bacterial fermentation of unabsorbed solutes is often a complicating factor in malabsorption. The fecal pH is often low because of the production of volatile fatty acids, and some products of fermentation (e. g., hydroxylated fatty acids, unconjugated bile acids) can cause colonic inflammation and secretion, and therefore signs of large intestinal diarrhea frequently accompany prolonged small intestine disease.
Osmotic diarrhea Excess water-soluble molecules in the intestinal lumen retain water osmotically and overwhelm the absorptive capacity of the small intestine and colon (e. g., sudden diet change, overeating, and malabsorption). The diarrhea typically resolves when food or laxatives are withheld.
Secretory diarrhea Stimulation of small intestine secretion such that the reserve absorptive capacity is overwhelmed results in diarrhea even though the absorptive ability of the small intestine and colon may not actually be impaired. Treatment with oral rehydration fluids containing glucose and amino acids (e. g., glycine) to increase water absorption is appropriate.
Typically secretory diarrhea does not resolve with fasting but does not cause weight loss unless anorexia, vomiting, or additional small intestine damage is a factor. Morbidity and even mortality are associated with the dehydration that results from excessive fluid loss. Secretory diarrhea typically is caused by chemical toxins and toxins elaborated by enteric bacteria (Box Causes of Secretory Diarrhea).
Causes of Secretory Diarrhea
- Bacterial enterotoxins and endotoxins (e. g., Clostridium perfringens, Escherichia coli. Salmonella spp., Shigella spp., Yersinia enterocolitica)
- Unconjugated bile acids from bacterial fermentation
- Hydroxylated fatty acids from bacterial fermentation
- Ciardia infection
- Possibly hyperthyroidism
- Laxatives (castor oil, dioctyl sodium sulfosuccinate, bisacodyl)
- Cardiac glycosides
- Amine precursor uptake and decarboxylation (APUD) neoplasms (excess vasoactive intestinal polypeptide, serotonin, prostaglandins, substance P)
- Intestinal inflammation
Permeability (exudative) diarrhea Intestinal inflammation can stimulate increased fluid and electrolyte secretion and impair absorption. Leakage of tissue fluid, serum proteins, blood, and mucus may occur from sites of inflammation, ulceration, or infiltration or if portal hypertension or lymphatic obstruction is present. Increased permeability severe enough to cause loss of plasma proteins in excess of their rate of synthesis results in a protein-losing enteropathy.
Failure of food assimilation is sometimes classified as primary failure to digest (maldigestion) or primary failure to absorb (malabsorption). However, such a classification is misleading, because failure of absorption is an inevitable consequence of failure to digest. The preferred use of the term malabsorption is to describe defective absorption of dietary constituent resulting from interference with the digestive and / or absorptive phases in the processing of that molecule.
Within this broad definition, the site of the primary abnormality may be found in the luminal, mucosal, or transport phase (Table Pathophysiologic Mechanisms of Malabsorption). Also, the reserve capacity of the distal small intestine and colon may prevent overt diarrhea despite significant malabsorption and weight loss. The clinical manifestations of malabsorption, namely diarrhea, weight loss, and altered appetite (polyphagia, coprophagia, pica), are largely a result of the lack of nutrient uptake and the losses in feces. Animals are often systemically healthy and have an increased appetite unless an underlying neoplastic or a severe inflammatory condition is present. Only when the patient is quite malnourished or develops hypoproteinemia does it become ill.
Pathophysiologic Mechanisms of Malabsorption
|Rapid intestinal transit||Hyperthyroidism|
|Defective substrate hydrolysis|
|Enzyme inactivation||Gastric hypersecretion|
|Lack of pancreatic enzymes||Exocrine pancreatic insufficiency|
|Decreased bile salt delivery||Cholestatic liver disease, biliary obstruction|
|Increased bile salt loss||Heal disease|
|Bile salt deconjugation||Bacterial overgrowth|
|Fatty acid hydroxylation||Bacterial overgrowth|
|Impaired release of CCK, secretin||Impairment of pancreatic secretion due to severe small intestine disease|
|Intrinsic factor deficiency||Exocrine pancreatic insufficiency Giant schnauzer defect|
|Competition for cobalamin||Bacterial overgrowth|
|Brush border enzyme deficiency|
|Acquired||Relative lactose deficiency|
|Brush border transport protein deficiency|
|Congenital||Intrinsic factor receptor|
|Acquired||Secondary to diffuse small intestine disease|
|Enterocyte processing defects||Abetalipoproteinemia|
|Reduction in surface area||Villus atrophy|
|Immature enterocytes||Increased enterocyte turnover|
|Mucosal inflammation||Inflammatory bowel disease|
|Secondary||Obstruction caused by neoplasia, infection, or inflammation|
|Vasculitis||Infection, immune mediated|
|Portal hypertension||Hepatopathy, right heart failure, cardiac tamponade|
The presence of dark, tarry, oxidized blood in feces, a condition called melena, reflects either swallowed blood or generalized or localized gastrointestinal bleeding, which usually occurs proximal to the large intestine (Table Causes of Melena). Medication with ferrous sulfate or bismuth subsalicylate (Pepto-Bismol) also can impart a black color to the feces. It has been estimated that the loss of 350 to 500 mg / kg of hemoglobin into the gastrointestinal tract is required for melena to be visible. The presence of microcytosis with or without thrombocytosis is suggestive of iron deficiency secondary to chronic blood loss. An increased blood urea nitrogen (BUN) to creatinine ratio (from bacterial digestion of blood) provides supporting evidence. Hypoproteinemia may indicate significant blood loss or the presence of a protein-losing enteropathy.
Causes of Melena
|Ingestion of blood||Oral, nasal, pharyngeal, or pulmonary bleeding|
|Coagulopothies||Thrombocytopenia, factor deficiencies, DIC|
|Gastrointestinal erosion / ulceration|
|Metabolic||Uremia, liver disease|
|Inflammatory||Gastritis, enteritis, hemorrhagic gastroenteritis|
|Neoplastic||Leiomyoma, adenocarcinoma, lymphosarcoma|
|Paraneoplastic||Mastocytosis, hypergastrinemia and other APUDomas|
|Vascular||A-V fistula, aneurysms, angiodysplasia|
|Ischemia||Hypovolemic shock, hypoadrenocorticism, thrombosis / infarction, reperfusion|
|Drug induced||Nonsteroidal and steroidal anti-inflammatory agents|
APUD, amine precursor uptake and decarboxylation tumor; A-V, arteriovenous; DIC, disseminated intravascular coagulation
The general approach to melena is to rule out bleeding diatheses, ingestion of blood, and underlying metabolic disorders before pursuing primary gastrointestinal causes. Ultrasonography is particularly useful for detecting gastrointestinal masses and thickening. The next step for investigating upper gastrointestinal blood loss is endoscopy. If the source of gastrointestinal bleeding is still undetermined, lagged red cell scintigraphy, exploratory laparotomy, angiog-raphy. and enteroscopy may be used to localize the site.
Borborygmi and Flatulence
Borborygmus is a rumbling noise caused by the propulsion of gas through the intestines. Swallowed air and bacterial fermentation of ingesta are the main causes of borborygmi and flatulence. Feeding a diet that is highly digestible, with a low fiber content (e. g., cottage cheese and rice in a 1:2 ratio) leaves little material present in the intestine for bacterial fermentation and can effect a cure in some cases. If borborygmi or flatulence continues despite dietary modification, the animal may be excessively aerophagic or may have malabsorption, especially if diarrhea or weight loss are also present.
Weight Loss or Failure to Thrive
General causes of weight loss are reduced nutrient intake, increased nutrient loss, and increased catabolism or ineffective metabolism. The history should reveal whether the type and amount of diet fed is adequate and whether anorexia, dysphagia, or vomiting is a potential cause. Weight loss or failure to thrive accompanied by diarrhea often is a feature of mal-absorption, and the diagnostic approach is the same as for chronic diarrhea. However, diarrhea does not invariably accompany malabsorption that causes weight loss.
When small intestine disease is severe enough for protein leakage into the gut lumen to exceed protein synthesis, hypoproteinemia develops. Chronic diarrhea associated with hypoproteinemia usually requires intestinal biopsy to define the cause of the protein-losing enteropathy (Table Protein-Losing Enteropathies). Nonintestinal diseases, which may potentially be associated with intestinal protein loss (e. g., portal hypertension), usually present with ascites before diarrhea. Hypoproteinemia associated with gastrointestinal disease is much less common in cats than in dogs and most often accompanies gastrointestinal lymphoma.
|Lymphangiectasia||Primary lymphatic disorder, venous hypertension (e. g., right heart failure, hepatic cirrhosis)|
|Infectious||Parvovirus, salmonellosis, histoplasmosis, phycomycosis|
|Inflammation||Lymphocytic-plasmacytic, eosinophilic, granulomatous|
|Endoparasites||Ciardia, Ancylostoma spp.|
|Gastrointestinal hemorrhage||hemorrhagic gastroenteritis, neoplasia, ulceration|
Clinical presentation Breeds that appear to be predisposed to protein-losing enteropathy are the basenji, lundehund, soft-coated wheaten terrier, Yorkshire terrier, and Shar Pei. Clinical signs associated with protein-losing enteropathy include weight loss, diarrhea, vomiting, edema, ascites, and pleural effusion. Weight loss frequently is the predominant feature, and diarrhea is not invariably present, particularly with lymphangiectasia and focal intestinal neoplasia. Physical findings may include edema, ascites, emaciation, thickened intestines, and melena. Thromboembolism is a feature of some cases of protein-losing enteropathy.
Diagnosis The serum concentrations of both albumin and globulin are reduced in most patients with protein-losing enteropathy. Exceptions are raised hyperglobulinemia with hypoalbuminemia found in histoplasmosis and immunoproliferative small intestine disease in the basenji. Renal and hepatic causes of hypoalbuminemia are eliminated by assay of serum bile acids and urinary protein loss respectively. Hypocholesterolemia and lymphopenia are common in protein-losing enteropathy. Hypocalcemia and hypomagnesemia are also reported. Measurement of fecal loss of alpha, -protease inhibitor may be a sensitive test for protein-losing enteropathy.
Survey abdominal radiographs often are normal in patients with protein-losing enteropathy, but ultrasound scans may reveal intestinal thickening, mesenteric lymphadenopathy, or abdominal effusion. Thoracic radiographs may show pleural effusion, metastatic neoplasia, or evidence of histoplasmosis. Although intestinal function tests may confirm the presence of malabsorption, they rarely provide a definitive diagnosis, and intestinal biopsy is more appropriate. Because many intestinal causes of protein-losing enteropathy are diffuse, endoscopy is the safer way to obtain biopsies, but surgical biopsy may be required to obtain a definitive diagnosis for lymphoma and for diseases that cause secondary lymphangiectasia (Box Relative Advantages of Endoscopic and Surgical Intestinal Biopsy).
Relative Advantages of Endoscopic and Surgical Intestinal Biopsy
- Minimally invasive
- Allows visualization and biopsy of focal lesions
- Permits multiple biopsies
- Minimal adverse reactions
- Allows steroids to be started early
- Requires general anesthesia
- Permits access only to duodenum (and distal ileum?)
- Allows only small, superficial (and crushed) biopsies
- Requires expensive equipment
- Technically demanding
- Allows biopsy of multiple sites
- Permits large, full-thickness biopsies
- Allows inspection of other organs
- Offers potential for corrective surgery
- Requires general anesthesia
- Poses a surgical risk
- Requires convalescence
- Requires delay before steroids can be started
Treatment Plasma transfusion may be indicated during the perioperative period when collecting biopsy specimens, and diuretics may reduce ascites. Spironolactone (1 to 2 mg / kg given orally twice daily) may be more effective than furosemide for treating ascites. Thromboembolism is a feature of some cases of protein-losing enteropathy. Specific treatments are discussed later.
These tests are used to search for intestinal bleeding from ulcerated mucosa and benign or malignant tumors. Unfortunately, all versions nonspecifically test for hemoglobin and are very sensitive, reacting with any meat diet and not just patient blood. Therefore the patient must be fed a meat-free diet for at last 72 hours for a positive result to have any reliability.
Alpha1-protease inhibitor This test assays the presence in feces of a naturally occurring endogenous serum protein that is resistant to bacterial degradation if it is lost into the intestinal lumen. To improve diagnostic accuracy, three fresh fecal samples should be sampled. The assay is valid only if used on fecal samples collected after voluntary evacuation, because abrasion of the colonic wall during manual evacuation is enough to elevate alpha1-protease inhibitor (alpha1-PI) concentrations. It appears to be of value for the diagnosis of protein-losing enteropathy and may prove to be more a sensitive marker than measurement of serum albumin for the detection of early disease.
Rectal cytology At the end of the rectal examination, the recta] wall is mildly abraded, the gloved finger rolled on a microscope slide, and the smear stained. Although the result is often negative and, when positive, probably more representative of large intestinal disease, an increased number of neutrophils may be suggestive of a bacterial problem, indicating the need for fecal culture. Clostridial endospore elements (Histoplasma, Aspergillus, Pythium, and Candida spp. ) may be identified. The test is fast and simple but in all cases confirmatory tests are indicated.
Flexible endoscopy allows gross examination of the small intestine mucosa and collection of tissue samples without the need for invasive surgery. The proximal small intestine can be viewed during gastroduodenoscopy, and the distal small intestine often can be visualized by passing the endoscope retrograde through the ileocolic valve. Therefore only the midjejunum cannot be satisfactorily examined by routine endoscopy. However, given that most cases of malabsorption involve diffuse disease, this limitation may not be significant. Enteroscopy, which was developed in humans and which uses a much narrower, thinner endoscope, may allow examination of most of the jejunum.
Abnormal findings on gross endoscopic examination include mucosal granularity and friability, erosions / ulcers, retained food, mass lesions, and hyperemia / erythema. However, none of these characteristics is pathognomonic for particular disease conditions, and gross findings frequendy do not correlate with those of the histopathologic examination. A milky white appearance or a milky exudate is suggestive of lymphangiectasia, and the presence of intraluminal parasites may be diagnostic in some cases.
Rickettsial Diarrhea (Salmon Poisoning)
Neorickettsia helminthoeca and Neorickettsia elokominica are found in the metacercariae of the fluke Nanophyetus salmonicola, which is present in salmon in the western regions of the Cascade Mountains from northern California to central Washington. About a week after ingestion of infected salmon by dogs, the rickettsiae emerge from the mature fluke and cause a disease characterized by high fever, hemorrhagic gastroenteritis, vomiting, lethargy, anorexia, polydipsia, nasal-ocular discharge, and peripheral lymphadenopathy. Mortality is extremely high in untreated patients.
The diagnosis is based on a history of ingestion of raw fish in an endemic area, the detection of operculated fluke eggs in feces, and the presence of intracytoplasmic inclusion bodies in macrophages from lymph node aspirates. Oxytetracycline (7 mg / kg given intravenously three times a day) is the treatment of choice and should be continued for at least 5 days. The trematode vector is eradicated with praziquantel.
Toxic algal blooms can lead to acute gastroenteritis and death in animals that drink contaminated water. Blue-green algae can synthesize an anticholinesterase that induces vomiting, diarrhea, ataxia, and rapid death in dogs. Prototheca spp. are achlorophyllous algae that cause protothecosis. Typically a cutaneous infection in cats, in dogs it can involve the intestine. Large intestinal disease is more common, but fatal disseminated disease affecting the small intestine has been reported.
Miscellaneous Causes Of Protein-Losing Enteropathy
Common causes of protein-losing enteropathy include lymphoma and IBD. However, there have also been recent reports of protein-losing enteropathy associated with intestinal crypt lesions without evidence of lymphangiectasia or inflammation in most cases. The underlying etiology of such lesions is not known. Response to therapy with antibacterials and immunosuppressive medication is variable; some dogs deteriorate suddenly and can die from thromboembolic disease
Adynamic Ileus And Intestinal Pseudo-Obstruction
Adynamic ileus is a common sequel to parvoviral enteritis, abdominal surgery, pancreatitis, peritonitis, endotoxemia, hypokalemia, and dysautonomia. The term intestinal pseudo-obstruction describes a condition in which patients show clinical evidence consistent with an obstruction, but no mechanical cause can be found. The condition has been associated with both visceral neuropathies and myopathies in humans, and such causes may occur in small animals. Most canine cases are associated with idiopathic sclerosing enteropathy, with fibrosis and a mononuclear cell infiltrate of the tunica muscularis. A case of feline intestinal pseudo-obstruction occurred secondary to intestinal lymphoma. After the possibility of a mechanical obstruction has been eliminated, management of both adynamic ileus and intestinal pseudo-obstruction is aimed at identifying any underlying cause and providing specific treatment. Symptomatic therapy to stimulate intestinal motility is also indicated. Suitable prokinetic agents include the 5-HT4 receptor agonist cisapride, the D2 dopaminergic antagonist metoclopramide, and motilin-like drugs such as erythromycin. In dogs and cats cisapride appears to be the most effective agent, but it is no longer marketed in many countries. Antibacterials may also be appropriate, given the probability of secondary SIBO, and immunosuppressive medication may be appropriate if an underlying inflammatory bowel disease is suspected. Feeding is beneficial in humans, and nutritional support can be continued indefinitely, although vomiting, constipation, and diarrhea usually continue. Unfortunately, most cases reported in the veterinary literature responded poorly to therapy, and the prognosis is grave.
Intestinal obstruction can be classified as acute or chronic, partial or complete, and simple or strangulated. Obstruction can be the result of extraluminal, intramural, or intraluminal mass lesions. The most common extraluminal cause of obstruction is intussusception. Younger animals are more likely to develop intussusception after a case of gastroenteritis or after having intestinal surgery, although an increased risk in postparturient queens has also been reported. Intestinal neoplasia is the more frequent cause of intussusception in middle-aged and older animals. Intramural causes include intestinal neoplasia (most common), hematomas, granulomas (e. g., focal FIP), inflammatory bowel disease, stricture, and phycomycosis. Most intraluminal obstructions are caused by foreign objects, such as stones, fruit pits, and toys in dogs and linear foreign objects in cats. Intestinal volvulus describes a condition in which the intestines rotate around the mesenteric axis, compromising the cranial mesenteric artery, and complete vascular obstruction may lead to strangulation. Reports are sporadic, but a predisposition in German shepherds has been reported.
The prognosis depends on the cause of the obstruction and the severity of associated abnormalities. The outcome is likely to be favorable with simple foreign bodies, but it is grave for animals with volvulus or metastatic intestinal neoplasia. The patient may be at risk of developing short bowel syndrome if a significant length of intestine must be removed.
Irritable Bowel Syndrome
Irritable bowel syndrome (IBS) is characterized by recurrent, usually acute, episodes of abdominal pain, borborygmi, and diarrhea. In the absence of morphologic changes, a functional disorder is considered the cause of this enigmatic problem. Disordered intestinal motility may be of primary importance, and a number of mechanisms have been proposed for irritable bowel syndrome in humans (Box Causes of Irritable Bowel Syndrome). However, it is not known whether any are responsible in dogs and cats. A variety of treatments, including antispasmodics (anticholinergics and also smooth muscle relaxants, such as mebeverine), anxiolytics (e. g., diazepam, chlordiazepoxide) and dietary modification (low-fat diet, increased fiber) have been tried with no consistent results. IBS probably will remain a frustrating condition to diagnose and treat successfully until its etiology is better understood.
Causes of Irritable Bowel Syndrome
- Primary motility disorders
- Visceral hyperalgesia
- Psychosomatic disorders
- Food intolerance
- Undiagnosed inflammatory disease