Delayed Gastric Emptying And Motility Disorders
Disorders of gastric motility can disrupt the storage and mixing of food and its expulsion into the duodenum. Normal gastric motility is the result of the organized interaction of smooth muscle with neural and hormonal stimuli. Delayed gastric emptying is the most commonly recognized manifestation of gastric motility disorders. Rapid gastric emptying and motility disorders associated with retrograde transit of bile or ingesta are less well defined.
Delayed gastric emptying is caused by outflow obstruction or defective propulsion (Table Causes of Delayed Gastric Emptying) and is usually suspected by the vomiting of food at least 8 and often 10 tol6 hours after a meal.
Causes of Delayed Gastric Emptying
|Hypertrophy of pyloric mucosa|
|Metabolic (hypokalemia, hypocaIcemia, hypoadrenocorticism)|
|Nervous inhibition (trauma, pain, stress?)|
|Gilatation and volvulus|
Vomiting of food some time after ingestion (more than 8 hours) is the most common sign. Vomiting may be projectile with pyloric stenosis. Abdominal distension, weight loss, melena, abdominal discomfort, distention, bloating, and anorexia are more variably present.
The signalment and history may be helpful narrowing down the cause. Development of vomiting at weaning raises the possibility of pyloric stenosis. Access to foreign bodies, bones, and medications is of obvious relevance to outflow obstruction. Brachycephalic, middle-aged, small breed dogs, such as shih tzus, seem predisposed to the syndrome of hypertrophic pylorogastropathy, where vomiting is secondary to pyloric outflow obstruction caused by hypertrophy of the pyloric mucosa and / or muscularis. Gastric neoplasia is usually detected in older animals, and weight loss, hematemesis, and pallor may be present. Gastric pythiosis is more prevalent in young large breed dogs in the Gulf states of the United States. Large breed, deep-chested dogs are more prone to dilatation and volvulus that may have an underlying problem with gastric emptying (see gastric dilatation / dilatation and volvulus above).
A thorough physical examination is performed to detect causes of vomiting such as string foreign bodies, or intestinal masses or thickenings, non-gastrointestinal (GI) causes, including thyroid (nodules-cats), liver (jaundice, hepatomegaly) or kidney disease (renomegaly, lumpy or small), and the systemic effects of vomiting, such as dehydration and weakness.
The diagnostic approach is to confirm delayed gastric emptying and to detect causes of gastric outflow obstruction that may require surgery, and non-gastric disorders associated with defective propulsion. Historical and physical findings are combined with clinicopathologic testing, plain radiographs, and ultrasonography.
Hematology, serum biochemistry, urinalysis, fecal analysis (e. g., parasites, parvo), and serology (e. g., FelV) are employed to detect non-GI causes of vomiting or delayed gastric emptying and to determine the consequences of vomiting. Laboratory findings vary depending on the severity of vomiting and completeness of pyloric obstruction and the presence of disorders associated with blood loss or inflammation. The complete blood count is often normal, but anemia may accompany gastric ulcers or neoplasia. Hyperglobulinemia may be present where outflow obstruction is secondary to fugal granuloma. The presence of hypochloremia, hypokalemia, and metabolic alkalosis, with or without aciduria, should increase suspicion of an upper gastrointestinal obstruction or potential hypersecretion of gastric acid.
Radiographs are essential to confirm the retention of food or fluid in the stomach longer than 8 hours, and often 12 to 16 hours, after a meal, and to detect extra gastric disorders such as peritonitis. Ultrasound may detect mural thickening or irregularity of the stomach suggestive of neoplasia, granuloma, or hypertrophy. Ultrasound may also reveal radiolucent foreign objects and detect non-gastric causes of delayed emptying, such as pancreatitis. Contrast radiography can be used to detect mural abnormalities and to confirm a suspicion of gastric obstruction where plain radiographs are inconclusive. However, endoscopy is usually favored over radiographic procedures for confirming gastric outflow obstruction and gastric and duodenal causes of decreased propulsion (e. g., ulcers, gastritis). Measurement of gastric pH and scrum gastrin can help to differentiate idiopathic hypertrophic pylorogastropathy from hypertrophy associated with hypergastrinemia. Pancreatic polypeptide-producing tumors may also be associated with mucosal hypertrophy. Endoscopy is hampered by the recent administration of barium so it is often performed first. Endoscopic biopsy is limited to the superficial mucosa and surgical biopsy is frequently required to achieve a definitive diagnosis of granulomatous, neoplastic, or hypertrophic conditions.
More sophisticated procedures to directly evaluate gastric emptying and motility are usually employed to determine if vomiting is due to an undefined gastric motility disorder and to optimize prokinetic therapy (Table A Review of Methods for Assessment of the Rate of Gastric Emptying in the Dog and Cat). Radiographic contrast procedures are readily available but are hampered by the wide variability in emptying times for barium in liquid or meal form. The administration of barium impregnanted polyspheres (BIPS) is a simplified contrast procedure suited to routine clinical practice as it requires many fewer radiographs than traditional barium series and is standardized in terms of test performance and interpretation but its utility in clinical patients remains to be determined. Scintigraphic techniques are generally considered the most accurate way to evaluate emptying but are restricted to referral institutions. Ultrasound can be useful for detecting gastric wall abnormalities and measuring contractile activity. A test employing the labeled C-octanoic acid has been evaluated in people and dogs and found to reflect gastric emptying (the values are longer than scintigraphy as C-octanoate has to be absorbed and metabolized before CO2 is liberated).
A Review of Methods for Assessment of the Rate of Gastric Emptying in the Dog and Cat
|Method||Species||Test Meal||n||Gastric Half Emptying Time (t ½)|
|Radioscintigraphy||Dog||Eggs, starch + glucose||27||66 min (median), 45-227 min (95% Cl)|
|Beef baby food + kibble||6||4.9±1.96 hours (mean ±sd)|
|Liver||4||About 2 hours|
|Canned dog food + egg||6 (18 tests)||172 ±17 min (mean ±sd)|
|Canned dog food + egg||7 (14 tests)||285 ± 34 min (mean ± sd); 294 ± 39 min (mean ± sd)|
|Canned dog food||6||77 min (mean)|
|Cat||Dry cat food||10||2.47 ±0.71 hours (mean ±sd)|
|Liver + cream||6 (15 tests)||163 ±11 min (mean ±se)|
|Canned cat food||20||2.69 ±0.25 hours (mean ±sd)|
|Dry cat food||20||3.86 ± 0.24 hours (mean ± sd)|
|Eggs||10||330 min (median), 210—769 min (range)|
|Radiography||Dog||Dry dog food + radio-opaque solids||10||3.5 hours (median), 1—6 hours (range)|
|Canned dog food + egg + barium impregnanted polyspheres||6 (18 tests)||Small barium impregnanted polyspheres 416±81 min (mean±se)|
|Canned dog food + barium impregnanted polyspheres||20||Small barium impregnanted polyspheres 6.05±2.99 hr (mean ±sd)
Large barium impregnanted polyspheres 7.11 ± 3.60 hr (mean ± sd)
|Kibble + barium impregnanted polyspheres||8||Small barium impregnanted polyspheres = 8.29 ±1.62 hr (70% of dogs ± se)
Large barium impregnanted polyspheres = 29.21 ±18.31 hr (70% of dogs + se)
|Kibble + liquid barium||9 (27 tests)||Total gastric emptying time = 7—15 hr (range)|
|Kibble + liquid barium||4||Total gastric emptying time = 7.6 ±1.98 hr (mean±se)|
|Cat||Canned cat food + barium impregnanted polyspheres||10||Small barium impregnanted polyspheres 6.43 + 2.59 hr (mean ±sd)
Large barium impregnanted polyspheres 7.49 + 4.09 hr (mean±sd)
|Canned cat food + barium impregnanted polyspheres||6||Small barium impregnanted polyspheres – 7.7 hr (median), 3.5-10.9 hr (range)
Large barium impregnanted polyspheres – 8.1 hr (median), 5-19.6 hr (range)
|Canned cat food + barium impregnanted polyspheres||10||Small barium impregnanted polyspheres-5.36 hr (median)
Large barium impregnanted polyspheres – 6.31 hr (median)
|Cat food + liquid barium||8||Gastric emptying time = 11.6 ± 0.9 hr (mean ± sd)|
|Gastric Emptying||Cat||Canned cat food||6||Peak C-excretion = 56.7 ±9.8 min (mean ± sd)|
|Breath Test||Dog||Bread, egg + margarine||6 (18 tests)||3.43 ± 0.50 hr (mean ± sd)|
Treatment of gastric emptying disorders is directed at the underlying cause. Gastric ulcers, erosions, and inflammation should be investigated and managed medically as described above. Foreign bodies are removed either endoscopically or surgically. Pyloric stenosis, polyps, and hypertrophic gastropathy that is not associated with hypergastrinemia are managed surgically. When hypertrophic gastropathy, ulcers or erosions, or excessive gastric juice is encountered at endoscopy, intravenous H2-antagonists can be given during the endoscopic procedure to try to prevent postoperative perforation or esophagitis. Neoplasia, polyps, and granulomas may require extensive gastric resection and Billroth procedures.
Dietary modification to facilitate gastric emptying may be beneficial irrespective of cause.
Small amounts of semi-liquid, protein- and fat-restricted diets fed at frequent intervals may facilitate emptying, such as an “intestinal disease diet” blended with water and mixed with an equal volume of boiled rice.
In nonobstructive situations gastric emptying can be enhanced and duodenogastric reflux inhibited by prokinetic agents such as metoclopramide, cisapride, erythromycin, or ranitidine. “- The choice of prokinetic deper is if a central antiemetic effect is required (e. g., metoclopramide), if a combined antacid prokinetic is indicated (e. g., ranitidine), or if treatment with one agent has been ineffective or caused adverse effects (e. g., behavioral changes with metoclopramide). Metoclopramide (0.2 to 0.5 mg / kg PO SC TID) has central antiemetic properties in addition to its prokinetic activity in the stomach and upper gastrointestinal tract and is frequently an initial choice in patients with underlying metabolic diseases associated with vomiting and delayed gastric emptying.
However, metoclopramide may only facilitate the emptying of liquids and is less effective in promoting organized gastro-duodcnal and intestinal moulity than cisapride. Cisapride (0.1 to 0.5 mg / kg PO TID) has no central antiemetic effects but is generally more potent in promotion of the gastric emptying of solids than metoclopramide, but it does have more drug interactions and its availability is limited. Erythromycin (dog: 0.5 to 1.0 mg / kg PO TID, between meals) releases motilin and acts at motilin receptors and mimics phase III of the interdigestive migrating myoelectric complex (MMC) promoting the emptying of solids. Niaztidine and ranitidine (0.25 to 0.5 mg / lb PO TID) have prokinetic activity attributed to an organophosphate-like effect.
No controlled trials in dogs and cats have evaluated the efficacy of different prokinetics in different disease states, and treatment is usually based on a best guess / least harmful basis. Where true prokinetic activity is required, cisapride and erythromycin appear to be the most efficacious. Treatment trials with prokinetics should probably be structured to last between 5 and 10 days to determine benefit. A diary of clinical signs and the objective assessment of gastric emptying using the tests described above, before and after therapy helps to optimize treatment. Combination therapy, such as erythromycin and cisapride, is not recommended due to the potential for adverse drug interactions. The prognosis for patients with delayed gastric emptying depends on the cause.
A suspected motility disorder characterized by duodenogastric reflux is thought to account for a syndrome known as the bilious vomiting syndrome. Affected dogs usually vomit early in the morning. Remission may be achieved by feeding the animal late at night. Prokinetic agents may also be employed.