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Basics ⬇

Basics

Definition

Gastric motility disorders result from conditions that directly or indirectly disrupt normal gastric emptying, which in turn may cause abnormal gastric retention, gastric distention, and subsequent gastric signs associated with anorexia, nausea, and vomiting.

Pathophysiology

The stomach has two distinct motor regions. The proximal stomach relaxes to accommodate food and regulates the expulsion of liquids. Intrinsic slow contractions of this region push liquids through the pylorus. The distal stomach mechanically breaks down and expels solids through strong peristaltic contractions. The gastric pacemaker, an area of intrinsic electrical activity, located in the greater curvature of the stomach regulates distal gastric motility and emptying. Gastric electrical activity, dietary composition, and extrinsic factors all influence emptying. During fasting, indigestible solids are expelled from the stomach by migrating myoelectric complexes (MMC). These complexes produce strong “digestive housekeeper” contractions that sweep through the stomach and small intestine to mid-jejunum every 2 hours in the fasted state preparing the GI tract for the next meal. MMC motility is under the regulation of the hormone motilin. Dysrhythmias in normal gastric electrical activity may be fundamental in the pathophysiology of disorders affecting gastric motility.

Systems Affected

Gastrointestinal

Incidence/Prevalence

Unknown. Many factors can alter gastric emptying although they may not result in clinical disease.

Signalment

Species

Dog and cat

Breed Predilections

Unknown

Mean Age and Range

Signs occur at any age though it is uncommon to observe primary motility disorders in young animals.

Signs

General Comments

Clinical signs are often secondary to the primary etiology causing the gastric motility disorder.

Historical Findings

  • The major clinical sign is chronic post-prandial vomiting of food. The stomach should normally be empty after an average-sized meal in approximately 6–8 hours in dogs and 4–6 hours in cats (note: normal emptying times vary greatly from animal to animal and are influenced by meal volume, caloric density, fiber content, and environmental factors). Vomiting of undigested food >12 hours following the meal suggests abnormal gastric motility or possibly outflow obstruction. Vomiting can occur, however, any time following eating.
  • Other signs include gastric distention, nausea, anorexia, belching, pica, and weight loss.
  • The distal esophageal sphincter may also be incompetent with gastric hypomotility and signs associated with reflux esophagitis may be present.

Physical Examination Findings

  • Normal or findings associated with the underlying cause of the disorder.
  • Palpation of a large, distended stomach.
  • Decreased gastric sounds on abdominal auscultation.

Causes

  • Primary idiopathic gastric motility disorders may arise from defects in normal myoelectric activity. Most motility disorders occur secondary to other primary conditions.
  • Metabolic disorders include hypokalemia, uremia, hepatic encephalopathy, and hypothyroidism.
  • Nervous inhibition as the result of stress, fear, pain, or trauma.
  • Drugs such as the anticholinergics, -adrenergic agonists, narcotics, and chemotherapeutics.
  • Primary gastric disease such as outflow obstructions, gastritis, gastric ulcers, parvovirus, and gastric surgery.
  • Gastric dilatation volvulus (GDV) syndrome is suspected to be in part the result of abnormal gastric motility associated with changes in myoelectric and mechanical activity. Some dogs with GDV may also continue to have signs of gastric hypomotility following surgical gastropexy.
  • Gastroesophageal reflux and enterogastric reflux (see Bilious Vomiting Syndrome) may result from primary gastric hypomotility.
  • Dysautonomia is associated with abnormal esophageal, gastric and intestinal motility.

Risk Factors

Any potential gastric disease may result in secondary hypomotility.

Diagnosis ⬆ ⬇

Diagnosis

Differential Diagnosis

The differential diagnosis is extensive and should include any condition causing vomiting. Gastric outflow obstructions must always be ruled out.

CBC/Biochemistry/Urinalysis

Routine hemogram, serum chemistry profile, urinalysis, and fecal flotation must be performed to rule out the potential cause of gastric hypomotility. Continued vomiting may result in dehydration, electrolyte abnormalities, or acid–base imbalance.

Other Laboratory Tests

Specialized testing may be required to determine a specific cause of gastric hypomotility, and is individualized for each patient.

Imaging

Survey Radiographs

Abdominal radiographs may reveal a gas-, fluid-, or ingesta-distended stomach. (Note: it is important to determine when the patient was last fed in relationship to when radiographs were taken.)

Liquid Barium Contrast Study

May be evidence of delayed gastric emptying and decreased gastric contractions if evaluated using fluoroscopy. Some cases may have normal emptying of liquids but abnormal emptying of solids. (Note: the stress of radiographs may decrease gastric emptying even in the normal animal.)

Food Barium Contrast Study

Barium mixed with a standard meal may demonstrate delayed gastric emptying of solids. Normal dogs should empty their stomachs by approximately 6–8 hours. Abnormal gastric retention is associated with significantly longer gastric emptying times.

Food-Marker Contrast Study

Barium-impregnated small markers (BIPS) or other radiopaque markers mixed with a standard meal will have delayed passage similar to the food barium contrast study.

Radionuclide Emission IMAGING

Radionuclide markers mixed with a meal give the most clinically accurate measurement of emptying. Gastric emptying times (time for a standard meal to leave the stomach) range from 4 to 8 hours.

Ultrasonography

Ultrasound can be used to evaluate antral and pyloric motility.

Smartpill

This is a non-invasive wireless sensor capsule that is given orally and transmits data on pressures, transit time, luminal pH and temperature as it passes through the stomach and small and large bowel. It has been validated for use in the healthy dog but as yet there are limited reports evaluating clinical conditions.

Diagnostic Procedures

Endoscopy

Endoscopic findings are frequently normal in idiopathic conditions. Food may be found in the stomach when it should be empty following a 12-hour pre-endoscopic fasting period. Endoscopy will detect obstructive or inflammatory diseases of the stomach.

Pathologic Findings

  • Idiopathic conditions have normal gastric mucosa.
  • Gastric histology may identify inflammatory or neoplastic causes to explain the gastric hypomotility.

Treatment ⬆ ⬇

Treatment

Appropriate Health Care

  • Most patients are treated as outpatients.
  • With severe vomiting or dehydration and electrolyte imbalance, hospitalization and specific therapy are required.

Nursing Care

Dehydration with fluid and electrolyte imbalance requires appropriate fluid replacement.

Activity

Restrictions are based on the underlying disease.

Diet

  • Dietary manipulation is important in the management of primary gastric motility disorders.
  • Diets should be formulated that are liquid or a semi-liquid consistency and low in fat and fiber content.
  • Small-volume meals with frequent feeding should be given.
  • Often dietary manipulation alone is successful in managing patients with delayed gastric emptying from a motility disorder.

Client Education

Discuss possible underlying etiologies of altered gastric motility and that the response to therapy varies with individual cases.

Surgical Considerations

  • Large-breed dogs with chronic GDV syndrome and gastric retention should have a prophylactic surgical gastropexy.
  • Following any gastric surgery it generally takes several days but up to 14 days for motility to return to normal.
  • Patients with mechanical gastric outflow obstructions require surgical correction.

Medications ⬆ ⬇

Medications

Drug(s) Of Choice

Gastric Prokinetic Agents

  • Metoclopramide increases the amplitude of antral contractions, inhibits fundic receptive relaxation, and coordinates duodenal and gastric motility. It is a dopamine receptor antagonist in the proximal GI tract resulting in increased release of acetylcholine from enteric neurons. At higher concentrations it has serotonin (5HT4) agonist effects. It also has antiemetic effects, blocking the chemoreceptor trigger zone in the brainstem in dogs but not cats. Oral dosage is 0.2–0.5 mg/kg q8h given 30 minutes before meals (use lower dose in cats) or as a CRI at 1–2 mg/kg q24h. Metoclopramide is generally considered to be a weak prokinetic agent in dogs and recent studies suggest it has little effect at increasing the lower esophageal sphincter pressure.
  • Cisapride works directly by cholinergic neurotransmission (5HT4 agonist) of gastrointestinal smooth muscle, stimulating motility. The proposed mechanism of action is that it enhances the release of acetylcholine at the myenteric plexus, but does not induce nicotinic or muscarinic receptor stimulation. Cisapride increases lower esophageal sphincter pressure, improves gastric emptying, and promotes increased motility of both the small and large intestine. A suggested dose is 0.2–0.5 mg/kg PO q8–12h given before meals. Cisapride is currently available through compounding pharmacies because the human product has been removed from the market because of associated cardiac arrhythmias not identified to occur in dogs or cats. Mosapride (0.5–2 mg/kg PO q12-24h) and Prucalopride (0.02–0.6 mg/kg PO q12–24h) are also serotoninergic (5HT4 agonist) prokinetic agents not yet available in the United States.
  • Macrolide antibiotics, including erythromycin and clarithromycin, are motilin receptor agonists and increase gastrointestinal motility. Motilin is a GI hormone that promotes MMC associated motility. Erythromycin given at low (sub-microbiologic) doses binds on motilin receptors promoting acetylcholine release, which in turn promotes gastric emptying. The suggested dose of erythromycin for specific motility effects is 0.5–1 mg/kg PO q8–12h, given 30 minutes before meals.
  • Other drugs: Domperidone is a peripheral dopamine receptor antagonist that has been marketed outside the United States. It regulates the motility of gastric and small-intestinal smooth muscle similar to that of metoclopramide. Mirtazapine is a noradrenergic and specific serotonergic antidepressant and has reported gastric prokinetic effects in dogs.
  • The H2 receptor antagonists ranitidine (1–2 mg/kg q8h) and nizatidine (2.5–5 mg/kg q24h) have reported prokinetic effects on gastric motility due to acetylcholinesterase inhibition. They are considered as poor prokinetic drugs and recent studies question ranitidine's prokinetic activity in dogs. Neither cimetidine nor famotidine affect gastric emptying.

Contraindications

  • Gastric prokinetic agents should not be administered in patients with a gastric outflow obstruction.
  • Metoclopramide is contraindicated with concurrent phenothiazine and narcotic administration or in animals with epilepsy.

Precautions

  • Metoclopramide may cause nervousness, anxiety, or depression.
  • Cisapride may cause depression, vomiting, diarrhea, or abdominal cramping.
  • Erythromycin may cause vomiting.

Follow-Up ⬆ ⬇

Follow-Up

Patient Monitoring

  • Response to therapy varies according to the underlying cause.
  • Failure to respond medically necessitates further investigation for mechanical obstruction.

Expected Course and Prognosis

  • The length of treatment depends on the ability to resolve the underlying disorder or on the response to therapy.
  • It may take gastric surgery or parvovirus cases several days to up to 2 weeks to regain normal gastric function.
  • Generalized dysautonomia has a grave prognosis.

Miscellaneous ⬆

Miscellaneous

Associated Conditions

Gastric hypomotility may be associated with both reflux esophagitis and reflux gastritis (see bilious vomiting syndrome).

Pregnancy/Fertility/Breeding

Avoid gastric prokinetic agents in pregnant animals.

Synonyms

  • Gastric atony
  • Gastric hypomotility

Abbreviation

  • GDV = gastric dilation and volvulus syndrome

Suggested Reading

Gaschen FP. Gastric and intestinal motility disorders. In: Bonagura JB, Twedt DC, eds Current Veterinary Therapy XV. St. Louis, MO: Elsevier, 2014, pp. 513–518.

Simpson KW: Stomach. In: Washabau RJ, Day MJ, eds. Canine and Feline Gastroenterology, 1st ed. St. Louis, MO: Elsevier, 2013, pp. 606–650.

Washabau RJ. Prokinetic agents. In: Washabau RJ, Day MJ, eds. Canine and Feline Gastroenterology, 1st ed. St. Louis, MO: Elsevier, 2013, pp. 530–536.

Wyse CA, McLellan AM, Dickie DGM, et al. A review of methods for the assessment of the rate of gastric emptying in the dog and cat: 1898–2002. J Vet Intern Med 2003, 17:609–621.

Author David C. Twedt

Consulting Editor Stanley L. Marks

Client Education Handout Available Online