pathophysiology OF ACUTE SMALL INTESTINAL DISEASE
Normal physiologic functions of the small intestine include motility (propulsion and mixing of food), secretion (fluids of differing electrolyte concentrations added to intestinal contents), digestion (physicochemical reactions breaking down ingesta into simpler compounds that can be absorbed), and absorption (selective uptake of products of digestion along with water and electrolytes).
Very large quantities of water and electrolytes, relative to total body stores, are cycled through the gastrointestinal (Gi) tract daily. For example, nearly half the total volume of extracellular fluid is secreted into the upper Gi tract each day, an amount greatly exceeding oral intake. under normal conditions fecal losses of water and electrolytes amount to only approximately 0.1% of the total amount cycled through the Gi tract. However, when normal small intestinal absorptive or secretory function is disrupted acutely, massive fluid and electrolyte losses may ensue.Absorption of most important nutrients occurs by active mechanisms that require specific mucosal carriers. Mucosal villi are the primary site of absorption, whereas intestinal crypts are largely responsible for secretion. Passive transport of ions is determined largely by relative transmucosal concentration and electrical potential differences. Absorption may also be modified by incorporation of solute into bulk flow of water (solvent drag). Absorption of sodium, mediated by energyrequiring active transport processes in both the large and the small intestine, is crucial to the absorption of water, electrolytes, and certain nutrients.
Within the jejunum, glucose, other actively absorbed monosaccharides, amino acids, and bicarbonate all enhance sodium absorption. sodium resorption in turn enhances absorption of glucose and amino acids. Therefore fluids administered for purposes of oral rehydration should contain both glucose and sodium, because absorption of sodium is necessary for passive absorption of water.
Potassium moves inward across the intestinal mucosa along its concentration gradient. Chloride follows passively inward along an electrical gradient established by inward sodium transport. Bicarbonate is rapidly absorbed in the jejunum by active transport or is neutralized by hydrogen ions, generating water and carbon dioxide. In the ileum, chloride absorption and bicarbonate absorption are coupled, such that bicarbonate moves out in exchange for inward transport of chloride. As a result, pH and bicarbonate concentration increase in the distal small bowel; fluid losses originating there are more likely to cause metabolic acidosis than are losses from the proximal small intestine.Intestinal secretion involves the net efflux of an isotonic solution of water and electrolytes. This is an important mechanism of fluid loss and may induce severe diarrhea. Intestinal secretion can be triggered by a number of stimuli, including bacterial enterotoxins, malabsorbed substances such as unconjugated bile acids and fatty acids, certain drugs, and mechanical obstruction of the small bowel.
Abnormal intestinal motility also may induce diarrhea and fluid losses, although the relationships between intestinal motility, secretion, and absorption are generally poorly understood.
Diarrhea results from either impaired absorption or excessive solute (including exudation) secretion. Increased osmolality within the intestinal lumen results in net water loss as well. Diarrhea usually results in loss of fluids isotonic to plasma. The major solutes in diarrhea fluid are sodium, chloride, organic anions, and potassium. In most instances the primary body deficits due to diarrhea are in sodium and water. Loss of isotonic fluid decreases circulating plasma volume and may in severe instances (e.g., parvoviral enteritis) precipitate hypovolemic shock. Because isotonic fluids are lost, serum electrolyte concentrations usually remain normal initially. During diarrheal diseases the most important source of potassium loss is via urine, mediated by aldosterone released in response to extracellular fluid volume depletion.
When diarrhea is severe and/or prolonged, significant amounts of potassium also may be lost via feces. Mild metabolic acidosis and hypokalemia are the most common acid-base and electrolyte alterations observed in patients with acute small intestinal disease and diarrhea.Causes of Diarrhea
Acute diarrheas can be grouped by mechanism or disease. The most common mechanisms include abnormal fluid secretion (primarily sodium), malabsorption, and abnormal intestinal motility. The best understood stimuli in humans are bacterial enterotoxins resulting in secretory diarrhea. Bacteria such as Escherichia coli and Vibrio, Clostridium, and Staphylococcus spp. induce intestinal secretion by increasing intracellular concentrations of cyclic adenosine nucleotides. Acute diarrhea in patients that eat spoiled food (garbage enteritis) may be from ingestion of preformed enterotoxins. Dietary fatty acids and bile acids also stimulate intestinal secretion, as do certain GI hormones and intestinal obstruction.
Malabsorptive diarrhea results from mucosal or submucosal diseases that impair absorption by either the small or the large intestine. Diseases of the intestinal mucosa may directly impair sodium resorption, thereby inhibiting water resorption and inducing diarrhea. Poorly absorbed dietary substances (e.g., complex carbohydrates such as sucralfate) also may interfere with water resorption by altering osmotic gradients. Some products of maldigestion, such as bile acids, may directly inhibit sodium transport in the colon and also induce diarrhea.
Intestinal mucosal damage results in generalized transudation of water and electrolytes, as well as plasma proteins and blood, when injury is severe. Normal mechanisms for sodium transport also are disrupted. These mechanisms (combined secretory and malabsorptive diarrhea) are thought to be largely responsible for diarrhea that develops in acute small intestinal diseases characterized by severe, bloody diarrhea. Examples include acute viral enteritis and canine hemorrhagic gastroenteritis.
It is likely that altered intestinal motility plays a role in the pathogenesis of acute diarrhea, although the mechanisms and prevalence in animals are poorly understood. Segmental contractions of the intestines are reduced with most causes of diarrhea, leading to hypomotile gut. For this reason, drugs that reduce intestinal motility, such as anticholinergic agents, are not recommended for symptomatic treatment of acute diarrhea.
Diseases resulting in acute diarrhea can be grouped into primary (diseases of the intestine) or secondary (diseases outside the intestine with diarrhea as a sequela) causes (Box 6-1). The most common primary diseases are parasites, infectious diseases, ingestion of toxins, and obstruction. Secondary diarrheas are less common causes of acute diarrhea and are discussed in other chapters.
BOX 6-1
Differential Diagnoses for Vomiting and Diarrhea in Dogs and Cats
Primary GI Diseases
Obstruction: masses, foreign body, intussusception, hiatal hernia
Dietary intolerance
Drugs/toxins
Inflammatory gastric and bowel diseases Neoplasia
Infectious diseases (viral, bacterial, fungal) Parasites
Secondary GI Diseases
Renal disease
Hepatic disease
Pancreatitis
Hypoadrenocorticism (rare in cats)
Diabetes mellitus with ketoacidosis
Peritonitis
Central nervous system/vestibular disease
Pancreatic exocrine insufficiency (diarrhea only; rare in cats)