The differential diagnosis list for the vomiting patient is exhaustive and includes both gastrointestinal and non-gastrointestinal disorders. Therefore the nutritional management of the vomiting patient will depend on the ultimate diagnosis. For example patients that are vomiting secondary to a systemic disease such as renal failure are most appropriately managed by nutrient alterations designed to minimize uremic toxins. This lecture will confine the discussion of nutritional considerations for the vomiting patient to those patients whose vomiting is due to a gastric cause.
Gastric causes of vomiting can be broadly classified into gastric outflow obstruction and disruption of the mucosal barrier (gastritis). Causes of gastric outflow obstruction can be divided into functional (i.e., motility disorders) and physiological obstruction. Most disturbances of gastric motor activity delay gastric emptying.
Delayed Gastric Emptying
A brief review of gastric motility will help understand the nutritional effects that can be employed to facilitate gastric emptying. The proximal stomach receives and stores boluses of food from the esophagus. Contractions of the proximal stomach are regulated by neural, hormonal (stimulated by motilin; inhibited by CCK, gastrin, secretin, GIP, glucagon, and somatostatin) and paracrine (histamine, serotonin) inputs. The proximal stomach is responsible for facilitating receptive relaxation, so that with the onset of deglutition and before the arrival of the bolus of food from the esophagus, the pressure within the lumen of the proximal stomach decreases to allow the stomach to fill without large increases in intra-gastric pressure. Accommodation allows the stomach to be distended to a large size with little or no change in intragastric pressure.
The slow sustained contractions of the proximal stomach gradually press the ingested contents toward the distal stomach and duodenum. The steady pressure exerted on the gastric content by the sustained contractions of the proximal stomach has a major role in controlling gastric emptying of liquids. Increasing the strength of the contractions increase intragastric pressure and speed gastric emptying of liquids.
The distal stomach refers to the distal two thirds of corpus, antrum, and gastroduodenal junction. The primary role of the distal stomach is retention and trituration (grinding) of solids and prevention of duodenogastric reflux. Contractions in the distal stomach are triggered by distension and involve neural, hormonal (stimulated by gastrin, CCK, motilin; inhibited by secretin, VIP, glucagon, GIP, somatostatin) and paracrine (histamine, serotonin, substance P) effects. The peristaltic waves of the distal stomach aid in the aboral propulsion of the contents and mix it with gastric juice. The liquids in chyme are permitted to pass readily through into the duodenum, but solids are retained by the terminal antrum and gastroduodenal junction. Powerful terminal antral contractions grind the solids into particles about 0.1mm in size, which then become suspended in the liquid phase of the gastric chime and are then emptied from the stomach with the liquids. Once gastric content has been emptied into the duodenum, the gastroduodenal junction prevents its reflux back into the stomach. The rate of gastric emptying is carefully controlled by feedback from small intestinal receptors so that the rate is commensurate with digestion and absorption in the small intestine. In contrast to the liquids and digestible solids in chyme, indigestible solids larger than about 1 mm are held in the stomach throughout the postprandial period, after which they are emptied by cyclically recurring bursts of interdigestive gastric contractions.
The rate of emptying of solutions that are colder or warmer than body temperature is slower than that of fluids at body temperature. The rate of emptying of liquids is faster when larger volumes are ingested, however the rate of emptying of gastric solids does not vary greatly with the volume ingested. Carbohydrates generally empty faster than proteins, which in turn empty faster than fats, however, isocaloric amounts of fat, protein, and carbohydrate empty at similar rates. Gastric contents at pH 7.0 empty more rapidly than those that are more acidic. The viscosity of gastric chyme has little influence on its rate of emptying. As the osmolality of a solution increased the rate of its emptying is decreased.
Acidic solutions empty more slowly form the stomach than neutral solutions because of the presence of small intestinal receptors sensitive to acid. The receptors detect the acids and activate mechanisms which in turn slow gastric emptying. Intestinal receptors sensitive to osmolarity of the just emptied gastric chyme also influence gastric emptying. The osmoreceptors are postulated to act in response to a change in their volume brought about by the osmotically active particles. In general, the more hyperosmolar the solution, the slower is gastric emptying. A model postulates that when chyme is hyperosmolar, the osmoreceptors shrink in size and thereby activate mechanisms designed to slow gastric emptying. In contrast, with hypoosmolar chyme the receptor increases in size which speeds gastric emptying. Small intestinal receptors sensitive to fatty acids as well as to mono and diglycerides are also present. Unsaturated fats slow emptying more than saturated fats. The fatty acid chain length is also important. The greatest slowing of gastric emptying is brought about by fatty acids with chain lengths of 14 carbon atoms. Receptors sensitive to L-tryptophan are able to detect physiologic concentrations of this amino acid in chyme and activate an inhibitory feedback mechanism that slows gastric emptying.
Studies on the nutritional management of delayed gastric empting are lacking in dogs, however, by reviewing the physiology, it seems logical to consider frequent feedings of small volumes of highly digestible, isocaloric, liquid, low fat foods that are low in soluble fiber. Small frequent feedings attempt to compensate for conditions of impaired ability of the stomach to distend in response to a meal. The food should be fed at body temperature. The osmolality can be decreased by diluting or blending the food with water. Feeding liquid diets will facilitate gastric emptying.
Accelerated Gastric Emptying
Accelerated gastric empting is rarely diagnosed in dogs. In humans, accelerated gastric emptying is termed the dumping syndrome. Accelerated gastric emptying overloads the neutralizing, digestive and absorptive capacities of the intestinal and causes duodenal ulceration. Management techniques include frequent feeding of low osmolality meals that are high in soluble fiber. Soluble fiber such as psyllium husks attract water and for gels which slows gastric emptying. Ideally, patients should be fed dry food, and water with the meal should be avoided.
Acute gastritis is typically managed by NPO for 12-36 hours as food increases the release of HCL which in turn, may increase mucosal damage. Although NPO has been the traditional management technique for patients that are vomiting, recent evidence suggests that the presence of food in the GIT provides trophic signals in addition to direct nutrition to the enterocytes. The trophic signals increase mesenteric blood flow, stimulate the release of digestive enzymes and enterohormones which influence intestinal cell proliferation, differentiation, and the rate of mucosal cell turnover. Studies in piglets have suggested that small bowel atrophy begins within days of nil per os. The signs of atrophy that have been noted include decreased villus height, decreased absorption and a reduction in brush border enzymes. These changes ultimately compromise the intestinal barrier. Enteral feeding has been shown to be a powerful mechanism to prevent gastrointestinal atrophy in piglets.
A recent randomized controlled clinical trial investigated the effect of enteral nutrition on intestinal permeability, intestinal protein loss and outcome in dogs with parvo-viral enteritis, compared to nil per os. Enteral nutrition was associated with a shorter time to recovery, increased body weight gain, and improved gut barrier function. This study suggests that feeding, rather than dietary rest should be considered for some patients with gastrointestinal disease.
When feeding the patient with gastritis, small frequent quantities of highly digestible, low fat, moderate protein, isocaloric diets are appropriate. Frequent small quantities are imperative as distension of an acutely inflamed stomach can trigger the vomiting reflex. High digestibility decreases the production of HCl, and increases the rate at which the gastric contents are emptied from the stomach. Low dietary fat concentration is important to increase the rate of gastric emptying. Amino acids are the most potent stimulators of gastrin and HCl secretion hence the protein content of the diet should be adequate, but not excessive. Compared to protein and fat, CHO provides the least stimulation of HCl, hence an easily digestible starch such as rice is appropriate for the patient with gastritis.