DELAYED GASTRIC EMPTYING AND GASTRIC MOTILITY DISORDERS

Delayed gastric emptying can be caused by mechanical obstruction of gastric outflow, by functional gastric motility disorders, or by a com­bination of both. Causes of mechanical outflow obstruction include gastric foreign bodies, pyloric mucosal hyperplasia or muscular hypertrophy, antral polyps, neoplasia, eosinophilic granuloma, or fungal granuloma.

Functional gastric motility disorders occur secondary to inflammatory, infiltrative, or ulcera­tive disease of the upper GI tract, electrolyte imbalances (hypokalemia), metabolic diseases (hypoadrenocorticism, diabetes mellitus, ure­mia, hypergastrinemia), drugs (anticholinergics, β-adrenergic agonists, opiates), and peritonitis. Gastric hypomotility often occurs postoperatively, particularly following GDV or spinal injury. If delayed gastric emptying is observed in a patient with chronic vomiting and an underlying cause such as mechanical or metabolic disease is not found, a functional motility disorder should be considered as the cause of the clinical signs. Several types of motility disorders occur in the dog, including retrograde transit (duodenogastric reflux), delayed gastric emptying, and accelerated gastric emptying that infrequently occurs second­ary to gastroduodenal surgery. Similar functional motility disorders have not been described in cats. Delayed gastric emptying and retrograde transit are probably caused by a functional abnormality of the gastric myenteric plexus or gastric smooth muscle and are referred to as primary or idiopathic delayed gastric emptying. Specific causes of delayed gastric emptying are listed in Box 5-7.

Clinical signs of mechanical gastric-outlet obstruction and functional gastric motility disor­ders are similar but vary according to the underly­ing cause.

Diagnosis of delayed gastric emptying is made on the basis of history, physical examination, exclusion of metabolic diseases that cause chronic vomiting, and radiographic studies (Table 5-7). In general, lab­oratory changes caused by delayed gastric emptying are minimal and nonspecific. Anemia, often with iron deficiency, may occur with ulcerative malig­nancy such as gastric carcinoma. Electrolyte and acid-base imbalances are uncommon unless signifi­cant obstruction to gastric outflow has occurred, in

which instance hypochloremic alkalosis might develop. Hypokalemia can result from chronic vom­iting; however,it can also be a cause of gastric hypo­motility.

Survey abdominal radiographs can be normal or might reveal an enlarged stomach, depending on the cause, duration, and severity of delayed emptying.

ium more accurately estimates gastric emptying time of solids. Interpretation of both types of con­trast studies is subjective, and results of both can vary significantly in normal animals. Fluoroscopic exam­ination improves accuracy of interpretation by allowing visualization of sequential changes in the shape of the stomach and pylorus and of movement of contrast through the pylorus. Liquid barium should begin to enter the duodenum within 15 minutes after administration, and gastric empty­ing of liquid should be complete within 1 to 4 hours. Complete gastric emptying of a barium meal should occur within 8 hours but might not be com­plete in some normal dogs until 15 hours after feed­ing. If most of the liquid barium is retained in the stomach after 4 hours, if liquid barium is present in the stomach longer than 12 hours, or if a large amount of a barium meal is retained longer than 8 to 10 hours, delayed gastric emptying is present.

An alternative method to barium studies for evaluation of gastric emptying is the use of radiopaque BIPS. BIPS are given with a canned- food meal consisting of approximately 25% of the daily caloric intake. Abdominal radiographs should then be taken at 4- to 6-hour intervals over the next 12 to 24 hours. The percentage of BIPS that have left the patient's stomach is compared with a standard curve for normal gastric emptying that is provided by the manufacturer. When radiographic gastric-emptying studies are done, it is important to remember that fear and anxiety from physical restraint often cause a transient delay of gastric emptying.

More accurate techniques to evaluate gastric motility are limited to hospitals with nuclear med­icine and GI motility laboratory facilities. Scintigraphic studies using radioactive tracers mixed with food is the method of choice for measuring gastric emptying time. Electrogastro- grams can also be done and are useful to detect abnormal patterns of gastric motility such as tachygastria and bradygastria.

Functional gastric motility disorders are charac­terized by delayed gastric emptying in the absence of morphologic lesions. Partial obstruction caused by restrictive or infiltrating mural diseases of the pylorus, such as muscular hypertrophy, neoplasia, or granulomatous diseases, produces annular nar­rowing of the pyloric canal. Barium may only fill the narrow entrance to the pylorus, resulting in a thin stream of barium often referred to as having a “beaklike” appearance (see Figure 5-3, C); this is a common finding with antral pyloric hypertro­phy. Polyplike filling defects can be caused by mucosal hypertrophy, inflammatory granuloma, neoplasia, or foreign body.

Once delayed gastric emptying has been con­firmed, additional diagnostic procedures such as ultrasonography, endoscopy, or exploratory sur­gery are necessary to determine if an obstructive lesion is present. Ultrasonography is useful to detect foreign bodies, mural thickening, and masses not detected by radiographs. Endoscopy and mucosal biopsies are useful in diagnosing chronic gastritis, IBD, neoplasia, or foreign body. Surgical examination and biopsy should be con­sidered if the cause of delayed gastric emptying is uncertain. Full-thickness gastric biopsy allows examination of muscle and nerve plexuses not included in endoscopic pinch biopsy specimens that usually extend only into the submucosa.

Specific Syndromes of Delayed Gastric Emptying

Antral pyloric hypertrophy syndrome, also referred to as pyloric stenosis and chronic hypertrophic pyloric gastropathy (CHPG), occurs either as a congenital condition or more frequently as an acquired disorder (Table 5-8).Young to middle­age male brachycephalic breeds, particularly box­ers, Boston terriers, Lhasa apsos, and Maltese, Pekingese, and shih tzu dogs, are most commonly affected. Clinical and radiographic signs of delayed gastric emptying with intermittent gastric dilata­tion and episodes of projectile vomiting are often observed. Physical examination and laboratory find­ings are usually normal. Contrast radiographs often reveal a distended stomach with delayed gastric emp­tying of contrast material and an abrupt narrow­ing of the pyloric canal with only a narrow stream of barium passing through (see Figure 5-3, C). Endoscopic examination usually reveals a thick­ened pyloric mucosa that sometimes appears as a protuberant mass, often with mucosal erosions (see Figure 5-3, D). Histologically the mucosa is thick­ened with edema and hyperplasia, and the muscu- laris is usually hypertrophied.

Treatment requires pyloroplasty with submu­cosal resection to remove thickened mucosal folds to reestablish gastric outflow. Y-U antral advance­ment flap pyloroplasty is the most effective method of reestablishing gastric outflow while preserving normal pyloric function. Prognosis is generally good following pyloroplasty, although some patients require a feeding schedule of small frequent meals and treatment with metoclo­pramide to enhance gastric emptying.

Primary Gastric Motility Disorders

Delayed gastric emptying can be caused by abnor­mally slow gastric contraction (bradygastria), rapid rhythm (tachygastria), or irregular rhythm (dysrhythmia), conditions thought to be caused by abnormal gastric pacemaker activity.

Treatment relies on a combination of dietary changes and prokinetic drugs to improve gastric emptying (Box 5-8). Surgical procedures are gen­erally not successful to improve gastric emptying for patients with primary functional gastric motil­ity disorders. Liquified or blenderized diets are useful to try because liquids empty from the stom­ach more rapidly than solids. Because fats and pro­teins delay gastric emptying, diets low in fat and protein and high in carbohydrates should be tried

Figure 5-8 Gastric retention of food particles and bile-colored fluid in a 12-year-old miniature poodle with clinical signs of intermittent vomiting, regurgitation, inappetence, and bloating. The dog had no food or water for 14 hours before endoscopy. Results of gastric mucosal biopsies were normal, and the dog was diagnosed with primary (idiopathic) gastric motility disorder. Clinical signs improved, but did not resolve, when the dog was treated with cisapride and dietary management (small meals, fat- restricted food). (See color plate.)

initially for patients with suspected functionally delayed gastric emptying. If dietary changes are unsuccessful, gastric prokinetic drugs should be added to the therapeutic plan.

Different prokinetic drugs have different modes of action and therefore have different effects on gastric, pyloric, and duodenal contractions. For that reason, whether a particular drug is effective in improving motility depends on both the spe­cific effects of that drug and how the underlying abnormality is affecting gastric motility. In general, cisapride has been considered to be the most effec­tive prokinetic drug because it accelerates gastric emptying in dogs by stimulating both pyloric and duodenal motor activity, by improving coordina­tion among antral, pyloric, and duodenal contrac­tions, and by increasing propagation distance of duodenal contractions. The result is a predictable promotility effect, particularly in the upper GI tract, with no significant adverse effects being reported in dogs or cats. Because of the uncertain availability of cisapride, other drugs, including metoclopramide, erythromycin, and ranitidine, are alternatives to consider for treatment of delayed gastric emptying. Metoclopramide is not as effec­tive as cisapride in accelerating gastric emptying. However, it does enhance coordination of gastro- pyloroduodenal contractions to improve gastric emptying of liquids and to prevent gastric stasis and enterogastric reflux. Metoclopramide also inhibits dopaminergic D₂ receptors in the CRTZ to diminish central stimulation of nausea and vomiting that can occur from delayed gastric emp­tying. Another alternative is erythromycin, which at low dosages will induce antral contractions and accelerate gastric emptying of solids. The contrac­tions stimulated by erythromycin are similar to those that normally occur in the fasting state to empty the stomach of nondigestible solids. As a result, treatment with erythromycin might result in larger than normal and less-digested food parti­cles being expelled into the duodenum, which could possibly cause worsening of the GI signs. The H₂-receptor antagonists ranitidine and nizatidine are

CRTZ, Chemoreceptor trigger zone; CNS, central nervous system; PO, orally; SQ, subcutaneously; IM, intramuscularly.

[*]Contraindicated in gastric outlet obstruction.

1"May be more effective than metoclopramide to enhance gastric emptying of solids.

used primarily to inhibit gastric acid secretion. These drugs also stimulate GI motility by inhibiting acetylcholinesterase activity, thereby increasing the amount of acetylcholine available to bind to smooth muscle muscarinic receptors. The result is primarily stimulation of gastric emptying, with some increase in small intestinal and colonic motility.

The choice of which prokinetic drug to use first depends in part on whether an underlying cause has been identified. For example, ranitidine and nizatidine are useful in the treatment of gastric motility disorders associated with gastric ulcerative or inflammatory diseases where both acid sup­pression and stimulation of gastric emptying are beneficial. Metabolic causes of delayed gastric emptying such as uremia or diabetic ketoacidosis, where central stimulation of vomiting might also occur, and gastric hypomotility following surgery for GDV tend to respond well to treatment with metoclopramide. If an underlying abnormality cannot be identified, the choice of treatment is trial and error. In general, cisapride (if available) should be tried initially, with erythromycin being a second choice. Metoclopramide and ranitidine or nizatidine are considered if inadequate response is achieved with the initial treatment.

Clinical experience indicates that several days of treatment are often required before a clinical response is observed. Some patients with functional dysrhythmias that respond to prokinetic drugs may require treatment indefinitely, perhaps at lower or less frequent dosing than the standard recommen­dations, whereas other patients might eventually be weaned off therapy. To determine if a lower drug dose is adequate requires individualized treatment for each patient. A suggested protocol is to first decrease the frequency of dosing (e.g., if a drug is being given three times a day, decrease to two times a day; if being given two times a day, decrease to every day). If clinical signs are adequately controlled for several days, alternate-day treatment can then be tried. If signs are still controlled, discontinuing the drug should be considered. If the signs reoccur, treatment must be resumed, and the lowest possible effective dose is used on a longer-term basis.