The vomiting patient is a diagnostic challenge because of the wide variety of gastric, intestinal, and non-GI disorders (metabolic, neurologic, paraneoplastic) that cause this clinical sign.
The vomiting patient is a diagnostic challenge because of the wide variety of gastric, intestinal, and non-GI disorders (metabolic, neurologic, paraneoplastic) that cause this clinical sign. The clinician must remember that not all animals with gastric disease will present with vomiting, and not all animals that vomit have gastric disease. Although vomiting does not always indicate a serious disorder, it is frequently the first sign of parvovirus infection, hemorrhagic gastroenteritis, pancreatitis, intestinal obstruction, Addison's disease, renal failure, and many other life-threatening diseases. For that reason, collecting a detailed history and performing a thorough physical examination is essential to determine a diagnostic and therapeutic plan. It is VITAL to rule out dysphagia and regurgitation as causes of ‘vomtiing'.
Physical examination findings of animals with primary gastric disease are often nonspecific. Cranial abdominal pain, distension or mass, or the presence of melena on digital rectal examination, are findings most consistent with gastric disease. Anorexia may be the only clinical sign of gastric disease. Thorough physical examination is important to assess the overall condition of the patient and to rule-out non-gastric causes of vomiting.
Vomiting, hematemesis, melena, anorexia, abdominal pain and/or abdominal distension are predominant signs of gastric disease. Diarrhea and weight loss occur less frequently. Acute onset of vomiting associated with hemorrhagic diarrhea is often indicative infectious gastroenteritis (parvovirus, Salmonella). Chronic intermittent vomiting associated with other signs such as polydipsia and polyuria could be caused by metabolic disease (renal failure, diabetic ketoacidosis, Addison's disease).
Hematemesis and melena are signs of disease that usually indicate gastric bleeding. Digested blood in vomitus, often described as resembling coffee grounds, is typical of gastric bleeding. Fresh blood is more likely to be of oral or esophageal origin. Melena can be caused by bleeding anywhere in the upper gastrointestinal tract and usually indicates significant hemorrhage. It manifests are dark, tarry stool. Gastric bleeding is the most common cause of melena. Low-grade, chronic GI bleeding can cause severe anemia without obvious melena. Clotting disorders must be ruled-out as a cause for hematemesis or melena.
Abdominal distension is a less common, yet important, sign of gastric disease. When accompanied by unproductive retching in a large breed dog, gastric dilatation or volvulus must be ruled in/out. In this instance, distension is primarily caused by air in the stomach. Post-prandial abdominal distension can occur due to gastric retention disorders. Non-gastric causes of abdominal distension include ascites, peritonitis, organomegaly, neoplasia, Cushing's disease, pregnancy and obesity.
Laboratory Evaluation: Initial diagnostic testing is done to distinguish primary gastrointestinal causes from non-GI causes. Most metabolic causes are ruled out by a CBC, biochemical profile, and urinalysis.
Usually normal with primary gastric diseases; however a CBC can provide clues to the cause of vomiting.
· Chronic gastric bleeding causes a non-regenerative anemia, often with characteristics of iron-deficiency (microcytosis, hypochromasia, thrombocytosis).
· Parvovirus causes neutropenia..
· Acute pancreatitis and bacterial gastroenteritis often cause a neutrophilic leukocytosis.
· Eosinophilia can be associated with eosinophilic gastroenteritis, GI parasites, and Addison's disease.
Biochemistry panel provides useful information in the vomiting patient both from diagnostic and therapeutic perspectives. Normal biochemical tests eliminate most metabolic causes of vomiting. Atypical hypoadrenocorticism (cortisol deficiency only, in which electrolytes are typically normal), cannot be ruled out until an ACTH-stimulation test has been done
Electrolyte and acid-base disorders are common if vomiting has been severe or chronic; however they do not reliably indicate the cause of the problem.
Fecal floatation is indicated in every dog or cat with vomiting. Gastric parasites, giardiasis and heavy intestinal worm burden may cause vomiting.
Survey radiographs may identify foreign bodies, gastric distension with fluid or gas, and displacement or malposition of the stomach. Frequently normal.
Gastric distension with air is common in the excited, dyspneic or struggling patient due to aerophagia, but can occur secondary to gastric dilatation/volvulus syndrome.
A fluid-distended stomach can be caused by gastric outflow obstruction, but also occurs after drinking.
Gastric wall thickness, gastric ulcers and gastric masses are difficult to identify with survey radiographs unless outlined by intraluminal air.
Pneumoperitoneum indicates rupture of a hollow viscous such as a penetrating gastric or intestinal ulcer, abdominal infection with gas-forming bacteria, or less commonly from perforation of the vagina or uterus.
Contrast radiographs of the stomach and duodenum are indicated when laboratory data and survey radiographs have not revealed the cause of persistent vomiting. Contrast radiographs help to identify gastric or proximal duodenal foreign bodies, gastric wall masses or infiltrative disease, mucosal ulceration, delayed gastric emptying or gastroparesis.
Ultrasonography has limited use in evaluating the stomach wall for masses or infiltrative lesions as sensitivity is closely dependent on the skills of the ultrasonographer. Air in the lumen interferes with evaluation of the gastric wall.
Endoscopy is one of the most useful methods of diagnosis of gastric disease because it allows direct visualization and biopsy of the surface of the stomach and duodenum. Always biopsy the pyloric antrum, incisura angularis, fundus and cardia. Small lesions not detected by radiographs or ultrasound are easily seen with an endoscope and foreign bodies can be removed. Histologic lesions can be present in a normal appearing stomach or duodenum; multiple biopsies should always be obtained from the stomach and duodenum, even if the gross appearance is normal.
Exploratory laparotomy is a very appropriate diagnostic tool in both cases of acute and chronic vomiting. Be sure to rule out metabolic disease, prior to surgery. ALWAYS biopsy organs, even if they appear grossly normal.
Small and large intestinal disease and diarrhea
Although the most common clinical sign of small or large intestinal disease is diarrhea, it is very important to remember that diseases of these organs may primarily manifest as vomiting (particularly in cats), anorexia, weight loss, hematochezia, melena, dyschezia, borborygmus, flatulence or even ascites. Never rule out intestinal disease solely because of the lack of diarrhea. Because the main function of the colon is water reabsorption, small intestinal disease is frequently quite severe before diarrhea occurs.
Pathophysiology of diarrhea
Diarrhea is defined as an increase in one or more of the characteristics of the bowel movement: frequency, fluid content, and/or volume. Diseases affecting either the small or large intestine can result in diarrhea AND diarrhea may be a manifestation of disease in a non-GI organ. Abnormalities in motility, secretion, digestion and absorption, and/or permeability changes of the intestine can result in diarrhea, resulting in increased fecal water content.
Normal Structure and Function of the Small Intestines
One of the normal functions of the intestine is to mix and transport luminal contents at a controlled rate, allowing optimal digestion and absorption of nutrients. There are two basic types of motility in the small intestine. Segmentation is caused by rhythmic contractions of circular muscle. Segmentation mixes the digestive enzymes and nutrients and increases resistance to the passage of nutrients through the intestine, allowing adequate time for digestion and absorption. Peristalsis is a longitudinal wave of constriction that moves ingesta in the aborad direction.
In most diseases that cause diarrhea, the strength of segmentation is decreased and the intestine acts as a flaccid tube, offering little resistance to flow through its lumen. Inadequate or absent propulsive motor activity is known as ileus and results in bowel distention with gas and fluid. When segmentation and resistance are reduced, very little peristaltic activity is needed to propel liquid contents over a long span of the intestine. Hypomotility allows abnormal bacterial overgrowth in the small intestine.
Fluid and electrolytes, as well as a variety of hormones and enzymes, are continuously secreted by cells at the base of the intestinal villi. They are rapidly reabsorbed by the mucosal cells at the tips of the villi. Normally the absorptive capacity exceeds secretion so that a net absorption and conservation of fluid and electrolytes occur. The secretory process is mediated by cyclic AMP.
Certain bacterial toxins (Salmonella, E. coli, Shigella, Clostridium spp) stimulate cyclic AMP and induce hypersecretion of sodium, chloride, and bicarbonate, resulting in severe fluid and electrolyte secretion into the intestinal lumen. Secretory diarrhea develops because the absorptive capacity of the small intestine and colon is overwhelmed by the large quantity of water and electrolytes presented to it. Dehydration, electrolyte depletion, and acidosis from loss of bicarbonate can be particularly severe in secretory diarrhea.
Abnormal secretion of gastrointestinal hormones such as gastrin, vasoactive intestinal peptide, and others can also cause hypersecretion in the small intestine.
The mucosal barrier is formed by the intestinal epithelium. Tight junctions encircle the lateral aspects of enterocytes, excluding antigens and bacteria. Enterocytes are shed from the villus tip, but the integrity of the tight junctions is probably loosest in the crypts, where fluid secretion occurs.
Altered permeability of this barrier will cause diarrhea. Structural damage to the gut wall from inflammatory or infiltrative diseases can result in an exudative diarrhea from increased mucosal permeability. Serum proteins, blood, and mucus are subsequently lost to the intestinal lumen. The presence of blood in the feces strongly suggests that the gut defense barrier has been significantly compromised.
This is important clinically because of the increased risk of bacterial translocation and sepsis.
Lymphangiectasia is another example of altered gut permeability. Intestinal lymphatics and lacteals become dilated and eventually rupture, with loss of protein rich fluid into the intestine, causing a protein-losing enteropathy syndrome.
Digestion and absorption
Approximately 80% of all absorptive functions of the GI tract occur in the small intestine. All fat, carbohydrate, and protein is absorbed by this organ. Reabsorption of bile salts occurs in the ileum to maintain an adequate bile acid pool for digestion of fat.
Carbohydrate is hydrolyzed to monosaccharides by pancreatic amylase and brush boarder enzymes. Specific transport proteins in the brush boarder transport these into cytosol. Protein is degraded by gastric pepsin and pancreatic proteolytic enzymes (trypsin, chymotrypsin) to amino acids, oligo- and dipeptides. Brush boarder peptidases hydrolyze peptides to amino acids, which are transported into cytosol via specific transport proteins. Lipid is emulsified in the stomach and degraded by pancreatic lipase to monoglycerides and free fatty acids (FFA). These mix with conjugated bile salts which enhance passive diffusion of monoglycerides and FFA. Bile salts remain in the intestinal lumen until reabsorbed in the ileum. Short-chain FA are absorbed directly into portal blood.
Malabsorption and maldigestion cause diarrhea and occur when nutrients are not absorbed and/or digested. This results in osmotic diarrhea. Fat malabsorption and maldigestion result in steatorrhea. Unabsorbed fatty acids have a significant osmotic effect, holding water in the gut lumen and inhibiting the normal absorption of water and electrolytes in the colon. Unabsorbed fats that reach the colon are converted by bacteria to hydroxy fatty acids that stimulate further secretion of water and electrolytes
Carbohydrate maldigestion occurs when deficiencies of proteases (pancreatic exocrine insufficiency) or disaccharidases exist and may cause diarrhea. Lactase deficiency occurs in people and lactose intolerance is known to occur in small animals. Undigested carbohydrates undergo bacterial fermentation in the colon. The fermentation products add to the osmotic load in the colon and decrease colonic pH, stimulating secretion of water and electrolytes.
Malabsorption results from decreased mucosal absorptive surface secondary to diffuse inflammation and/or cellular infiltration, biochemical defects of brush boarder enzymes, decreased transport of nutrients. Malabsorptive disease results in similar clinical and laboratory features, regardless of the underlying cause:
Continuous or intermittent small bowel diarrhea
· Substantial weight loss
· Polyphagia >> hyporexia
· Ascites, peripheral edema
· Panhypoproteinemia (low serum albumin and globulin)