Overview of Digestive System
The digestive tract includes the oral cavity and associated organs (lips, teeth, tongue, and salivary glands), the esophagus, the forestomachs (reticulum, rumen, omasum) of ruminants and the true stomach in all species, the small intestine, the liver, the exocrine pancreas, the large intestine, and the rectum and anus. Gut-associated lymphoid tissue (tonsils, Peyer’s patches, diffuse lymphoid tissue) is distributed along the GI tract. The peritoneum covers the abdominal viscera and is involved in many GI diseases. Fundamental efforts to manage GI disorders should always be directed toward localizing disease to a particular segment and determining a cause. A rational therapeutic plan can then be formulated.
The primary functions of the GI tract include prehension of feed and water; mastication, ensalivation, and swallowing of feed; digestion of feed and absorption of nutrients; maintenance of fluid and electrolyte balance; and evacuation of waste products. There are four primary functions—digestion, absorption, motility, and evacuation—and, correspondingly, four primary modes of dysfunction.
Normal GI tract motility involves peristalsis, muscle activity that moves ingesta from the esophagus to the rectum; segmentation movements, which churn and mix the ingesta; and segmental resistance and sphincter tone, which retard aboral progression of gut contents. In ruminants, these movements are of major importance in normal forestomach function.
Abnormal motor function usually manifests as decreased motility. Segmental resistance is usually reduced, and transit rate increases. Motility depends on stimulation via the sympathetic and parasympathetic nervous systems (and thus on the activity of the central and peripheral parts of these systems) and on the GI musculature and its intrinsic nerve plexuses. Debility, accompanied by weakness of the musculature, acute peritonitis, and hypokalemia, produces atony of the gut wall (paralytic ileus). The intestines distend with fluid and gas, and fecal output is reduced. In addition, chronic stasis of the small intestine may predispose to abnormal proliferation of microflora. Such bacterial overgrowth may cause malabsorption by injuring mucosal cells, by competing for nutrients, and by deconjugating bile salts and hydroxylating fatty acids.
Vomiting is a neural reflex act that results in ejection of food and fluid from the stomach through the oral cavity. It is always associated with antecedent events such as premonition, nausea, salivation, or shivering and is accompanied by repeated contractions of the abdominal muscles.
Regurgitation is characterized by passive, retrograde reflux of previously swallowed material from the esophagus, stomach, or rumen. In diseases of the esophagus, swallowed material may not reach the stomach.
One of the major consequences of subnormal motility is distention with fluid and gas. Much of the accumulated fluid is saliva and gastric and intestinal juices secreted during normal digestion. Distention causes pain and reflex spasm of adjoining gut segments. It also stimulates further secretion of fluid into the lumen of the gut, which exacerbates the condition. When the distention exceeds a critical point, the ability of the musculature of the wall to respond diminishes, the initial pain disappears, and paralytic ileus develops in which all GI muscle tone is lost.
Dehydration, acid-base and electrolyte imbalance, and circulatory failure are major consequences of GI distention. Accumulation of gut fluids stimulates additional secretion of fluids and electrolytes in the anterior segments of the intestine, which can worsen the abnormalities and lead to shock.
Abdominal pain associated with GI disease usually is caused by stretching of the intestinal wall. Contraction of the gut causes pain by direct and reflex distention of neighboring segments. Spasm, an exaggerated segmenting contraction of one section of intestine, results in distention of the immediately anterior segment when a peristaltic wave arrives. Other factors that may cause abdominal pain include edema and failure of local blood supply, eg, in local embolism or twisting of the mesentery.
Specific diseases cause diarrhea by varied and characteristic mechanisms, the recognition of which is useful in understanding, diagnosing, and managing GI diseases. The major mechanisms of diarrhea are increased permeability, hypersecretion, and osmosis. Disorders of motility are often secondary. In healthy animals, water and electrolytes continuously transfer across the intestinal mucosa. Secretions (from blood to gut) and absorptions (from gut to blood) occur simultaneously. In clinically healthy animals, absorption exceeds secretion, ie, there is net absorption. Inflammation in the intestines can be accompanied by an increase in “pore size” in the mucosa, permitting increased flow through the membrane (“leak”) down the pressure gradient from blood to the intestinal lumen. If the amount exuded exceeds the absorptive capacity of the intestines, diarrhea results. The size of the material that leaks through the mucosa varies, depending on the magnitude of the increase in pore size. Large increases in pore size permit exudation of plasma protein, resulting in protein-losing enteropathies (eg, lymphangiectasia in dogs, paratuberculosis in cattle, nematode infections). Greater increases in pore size result in the loss of RBCs, producing hemorrhagic diarrhea (eg, hemorrhagic gastroenteritis, parvovirus infection, severe hookworm infection).
Hypersecretion is a net intestinal loss of fluid and electrolytes that is independent of changes in permeability, absorptive capacity, or exogenously generated osmotic gradients. Enterotoxic colibacillosis is an example of diarrheal disease due to intestinal hypersecretion; enterotoxigenic Escherichia coli produce enterotoxin that stimulates the crypt epithelium to secrete fluid beyond the absorptive capacity of the intestines. The villi, along with their digestive and absorptive capabilities, remain intact. The fluid secreted is isotonic, alkaline, and free of exudates. The intact villi are beneficial because a fluid (administered PO) that contains glucose, amino acids, and sodium is absorbed, even with hypersecretion.
Osmotic diarrhea is seen when inadequate absorption results in a collection of solutes in the gut lumen, which cause water to be retained by their osmotic activity. It develops in any condition that results in nutrient malabsorption or maldigestion or when an animal ingests a large amount of osmotically active substances that are not absorbed, eg, an overeating puppy.
Malabsorption (see Malassimilation Syndromes in Large Animals and see Diseases of the Stomach and Intestines in Small Animals) is failure of digestion and absorption due to some defect in the villous digestive and absorptive cells, which are mature cells that cover the villi. Several epitheliotropic viruses directly infect and destroy the villous absorptive epithelial cells or their precursors, eg, coronavirus, transmissible gastroenteritis virus of piglets, and rotavirus of calves. Feline panleukopenia virus and canine parvovirus destroy the crypt epithelium, which results in failure of renewal of villous absorptive cells and collapse of the villi; regeneration is a longer process after parvoviral infection than after viral infections of villous tip epithelium (eg, coronavirus, rotavirus). Intestinal malabsorption also may be caused by any defect that impairs absorptive capacity, such as diffuse inflammatory disorders (eg, lymphocytic-plasmacytic enteritis, eosinophilic enteritis) or neoplasia (eg, lymphosarcoma).
Other examples of malabsorption include defects of pancreatic secretion that result in maldigestion. Rarely, because of failure to digest lactose (which, in large amounts, has a hyperosmotic effect), neonatal farm animals or pups may have diarrhea while they are being fed milk. Reduced secretion of digestive enzymes at the surface of villous tip cells is characteristic of epitheliotropic viral infections recognized in farm animals.
The ability of the GI tract to digest food depends on its motor and secretory functions and, in herbivores, on the activity of the microflora of the forestomachs of ruminants, or of the cecum and colon of horses and pigs. The flora of ruminants can digest cellulose; ferment carbohydrates to volatile fatty acids; and convert nitrogenous substances to ammonia, amino acids, and protein. In certain circumstances, the activity of the flora can be suppressed to the point that digestion becomes abnormal or ceases. Incorrect diet, prolonged starvation or inappetence, and hyperacidity (as occurs in engorgement on grain) all impair microbial digestion. The bacteria, yeasts, and protozoa also may be adversely affected by the oral administration of drugs that are antimicrobial or that drastically alter the pH of rumen contents.
Signs of GI disease include excessive salivation, diarrhea, constipation or scant feces, vomiting, regurgitation, GI tract hemorrhage, abdominal pain and distention, tenesmus, shock and dehydration, and suboptimal performance. The location and nature of the lesions that cause malfunction often can be determined by recognition and analysis of the clinical findings. In addition, abnormalities of prehension, mastication, and swallowing usually are associated with diseases of the oral mucosa, teeth, mandible or other bony structures of the head, pharynx, or esophagus. Vomiting is most common in single-stomached animals and usually is due to gastroenteritis or nonalimentary disease (eg, uremia, pyometra, endocrine disease). The vomitus in a dog or cat with a bleeding lesion (gastric ulcer or neoplasm) may contain frank blood or have the appearance of coffee grounds. Horses and rabbits do not vomit. Regurgitation may signify disease of the oropharynx or esophagus and is not accompanied by the premonitory signs seen with vomiting.
Large-volume, fluid diarrhea usually is associated with hypersecretion (eg, in enterotoxigenic colibacillosis in newborn calves) or with malabsorptive (osmotic) effects. Blood and fibrinous casts in the feces indicate a hemorrhagic, fibrinonecrotic enteritis of the small or large intestine, eg, bovine viral diarrhea, coccidiosis, salmonellosis, or swine dysentery. Black, tarry feces (melena) indicate hemorrhage in the stomach or upper part of the small intestine. Tenesmus of GI origin usually is associated with inflammatory disease of the rectum and anus.
Small amounts of soft feces may indicate a partial obstruction of the intestines. Abdominal distention can result from accumulation of gas, fluid, or ingesta, usually due to hypomotility (functional obstruction, adynamic paralytic ileus) or to a physical obstruction (eg, foreign body or intussusception). Distention may, of course, result from something as direct as overeating. A “ping” heard during auscultation and percussion of the abdomen indicates a gas-filled viscus. A sudden onset of severe abdominal distention in an adult ruminant usually is due to ruminal tympany. Ballottement and succussion may reveal fluid-splashing sounds when the rumen or bowel is filled with fluid. Varying degrees of dehydration and acid-base and electrolyte imbalance, which may lead to shock, are seen when large quantities of fluid are lost (eg, in diarrhea or sequestered in intestinal obstruction) or in gastric or abomasal volvulus.
Abdominal pain is due to stretching or inflammation of the serosal surfaces of abdominal viscera or the peritoneum; it may be acute or subacute, and its manifestation varies among species. In horses, acute abdominal pain is common (see Colic in Horses). Subacute pain is more common in cattle and is characterized by reluctance to move and by grunting with each respiration or deep palpation of the abdomen. Abdominal pain in dogs and cats may be acute or subacute and is characterized by whining, meowing, and abnormal postures (eg, outstretched forelimbs, the sternum on the floor, and the hindlimbs raised). Abdominal pain may be difficult to localize to a particular viscus or organ within the abdomen.
A complete, accurate history and routine clinical examination can often determine the diagnosis. In outbreaks of GI tract disease in farm animals, the history and epidemiologic findings are of prime importance. In small animals, travel history or other details such as recent adoption from a shelter or recent kenneling or exposure to other animals in dog parks might give clinical suspicion to certain infectious diseases. If the history and epidemiologic and clinical findings are consistent with GI disease, the lesion should be localized within the system, and the type of lesion and its cause determined.
The abnormality may sometimes be localized to the large or small intestine by history, physical examination, and fecal characteristics (see Table: Differentiation of Small-Intestinal from Large-Intestinal Diarrhea). The distinction is important because it narrows the differential diagnoses and determines the direction of further investigation. However, the clinician should appreciate that in some instances the disorder can involve the entire bowel, with one set of localizing signs overshadowing the other.
Differentiation of Small-Intestinal from Large-Intestinal Diarrhea
The clinical and laboratory techniques and their applications include the following: 1) visual inspection of the oral cavity and of the contour of the abdomen for distention or contraction; 2) palpation through the abdominal wall or per rectum to evaluate shape, size, and position of abdominal viscera; 3) abdominal percussion to detect “pings,” which suggest gas-filled viscera; 4) auscultation to determine the intensity, frequency, and duration of GI movements, as well as fluid-splashing sounds associated with fluid-filled stomachs and intestines and fluid-rushing sounds associated with diarrheal disease; 5) succussion to reveal fluid-splashing sounds; 6) ballottement to evaluate density and size of abdominal organs by their movement away from and back to the abdominal wall; and 7) gross examination of feces to assess bulk, consistency, color, and presence of mucus, blood, or undigested food particles.
Microscopic studies include examination for parasites. Cytology of a rectal or colonic mucosal smear stained with new methylene blue or Wright stain for fecal leukocytes is useful to detect inflammatory bowel disease or the presence of intracellular fungal organisms in the case of infection with Histoplasma capsulatum. The following may be useful (or necessary): 1) bacterial culture and virus isolation; 2) endoscopy to visualize the mucosal surface of the esophagus, stomach, duodenum, colon, and rectum; 3) abdominocentesis to collect fluid from distended viscera or from the peritoneal cavity for examination; 4) radiography (contrast) to diagnose obstructive disease; 5) abdominal ultrasonography to evaluate the wall thickness of the stomach and intestines and to detect abdominal masses, intussusceptions, and mesenteric lymphadenopathy in small animals, and to investigate abdominal disorders in horses and cows; 6) biopsy (endoscopic, laparoscopic, ultrasound-guided, surgical) to obtain samples for microscopic examination (samples of intestines and liver are useful to diagnose chronic enteritis and liver disease); and 7) tests for digestion and absorption to estimate and differentiate malabsorption and maldigestion. Common absorption tests include the measurement of the serum concentrations of cobalamin (vitamin B12) and folate. In addition, in small animals, an increased serum folate concentration in conjunction with a decreased cobalamin is consistent with antibiotic-responsive diarrhea. Exocrine pancreatic function can be evaluated by the determination of serum trypsin-like immunoreactivity and by measurement of serum canine and feline pancreas-specific lipase, which are sensitive and specific markers for the diagnosis of pancreatitis; laparotomy and biopsy may be indicated in cases in which the diagnosis is not clear or in which surgical correction may be required.