Gastric and Intestinal Motility Disorders

Gastric and Intestinal Motility Disorders

Frédéric P. Gaschen, Baton Rouge, Louisiana

The prevalence of canine and feline nonobstructive gastrointestinal (GI) motility disorders cannot be documented precisely. They may go unnoticed by the animal’s owner because of subtle clinical signs that are difficult to recognize until the problem is severe. However, these disorders likely are of significant clinical importance. They may result from primary segmental or diffuse inflammatory or neoplastic infiltration of the GI wall. GI motility also may be influenced by a variety of diseases affecting other organs, such as abdominal inflammation (e.g., pancreatitis, postoperative ileus) or diseases such as endocrinopathies, electrolyte abnormalities (e.g., hypokalemia, hypocalcemia), and uremic syndrome. Moreover, diseases affecting the autonomous nervous system (e.g., dysautonomia) often significantly affect GI motility.

Most available information on canine and feline GI motility has been obtained from studies using dogs and cats as animal models; only a few studies focus on spontaneous canine and feline GI motility disorders.

In dogs and cats, motility disorders resulting from obstruction of gastric outflow, of the small intestine or colon by foreign bodies, or by space-occupying lesions are a common occurrence. Their diagnosis generally is straightforward, and their treatment is surgical. Therefore they will not be further discussed in this chapter.

Disorders of Gastric Emptying

Physiology

After ingestion of solid food, the gastric antrum acts as a pump from which peristaltic waves originate, while the gastric body acts as a high compliance reservoir. The mechanical action of the antral pump is divided into three phases: (1) propulsion, (2) emptying of fine particles and mixing, and (3) retropulsion of particles larger than 1 mm for continued grinding. In healthy animals, the rate of gastric emptying is modulated by the composition of the diet (e.g., moisture and fat, protein and carbohydrate content) and is under the influence of neural and endocrine factors. Complete emptying of the stomach is followed by synchronized housekeeping contractions (migratory motor complexes [MMC] phase III).

Clinical Signs

Signs associated with disorders of gastric motility in dogs and cats are listed in Box 125-1. However, the signs may be difficult to recognize before the problem becomes severe.

Etiology

Primary Disorders of Gastric Motility

Primary functional disorders appear to be rare in small animals. Slower gastric emptying occurs in dogs following circumcostal gastropexy performed after gastric dilation-volvulus (GDV). Gastric motility is impaired in the fasting and postprandial phases in these dogs (Hall et al, 1992). However, it has not been established whether this abnormal motility is involved in the etiology of GDV or simply a consequence of surgical treatment. The exact role of gastric dysmotility in canine GDV has not been elucidated to date.

Dysautonomia is discussed in further detail later; it also may influence gastric emptying. The diagnosis of duodenogastric reflux (DGR) in dogs has been the subject of controversy because this reflux may occur as a physiologic event. Moreover, most instances of vomiting are accompanied by some degree of DGR. However, a syndrome characterized by bilious vomiting, often before the morning meal, has been observed in apparently healthy dogs and attributed to DGR. Initial treatment consists of a late evening meal and may require addition of drugs lowering gastric acidity (H₂-receptor antagonist, proton-pump inhibitor) and/or prokinetics.

Secondary Disorders of Gastric Motility

Inflammation of the GI tract or other abdominal organs, abdominal surgery, or metabolic disorders may cause secondary gastric motility abnormalities.

Gastric or Intestinal Inflammation.

GI inflammation is a common cause of gastric motility changes. Therefore it is hardly surprising that GI parasites, gastric ulcers, parvovirosis, adverse food reactions, dysbiosis, and inflammatory bowel disease (IBD) often are accompanied by abnormal gastrointestinal motility.

Acute canine pancreatitis also is associated commonly with decreased gastric and intestinal motility. This can complicate treatment significantly and probably is caused by extension of the inflammatory process to stomach and duodenum, which are in close proximity of the pancreas. In a similar manner peritonitis also affects gastric motility, and postoperative ileus is a frequent occurrence (see later).

Diseases Affecting Multiple Organ Systems.

Systemic disorders also may affect GI motility. Hypoadrenocorticism often is accompanied by decreased gastric motility. Furthermore, abnormal small intestinal and colonic motility have been shown in dogs with ablation of 66% of renal mass and chronic renal disease, whereas gastric emptying seemed normal. However, it is not known if a larger reduction of functional renal mass, as is observed in clinical cases (>75%), may have negative effects on gastric motility. Finally, delayed gastric emptying may be induced by various medications; opioid analgesics and anticholinergics may interfere with GI neurotransmitters and cause impaired smooth muscle function. Vincristine, a frequently used chemotherapy agent, recently has been shown to decrease gastric antral motility transiently (Tsukamoto et al, 2011).

Diagnostic Approach

A detailed history and physical exam may help identify subtle changes suggestive of GI dysmotility. However, the initial approach of the dog or cat with suspected GI motility disorder consists of first ruling out obstructive GI disease with abdominal radiographs. Presence of food in the stomach after prolonged fasting (i.e., more than 10 to 12 hours) suggests delayed gastric emptying. In addition, an abdominal ultrasound exam may reveal severely decreased gastric and duodenal motility. Once GI obstruction has been ruled out, CBC, chemistry panel, and urinalysis are necessary to look for underlying disorders that may secondarily influence motility.

Evaluation of Gastrointestinal Motility

The various methods available to investigate gastric emptying have been reviewed in detail (Wyse et al, 2003). They aim at evaluating the gastric emptying or intestinal transit time of solid food and include radionuclide scintigraphy, radiographic contrast studies (barium meals and barium impregnated polyethylene spheres, or BIPS), and abdominal ultrasound. Gastric emptying also can be measured using indirect techniques relying on duodenal absorption of compounds that subsequently can be detected in the breath (e.g., ¹³C-octanoid acid) or in the blood (e.g., acetaminophen). Recently, a wireless motility capsule (SmartPill) has been validated for use in dogs (Boillat et al, 2010) (Figure 125-1).

Figure 125-1 Wireless motility capsule recording in a young healthy male mixbreed dog. The top line reflects the temperature (in degrees Celsius), the line below represents the pH, while the bottom line shows the pressure profile (in mm Hg). Time is shown on the X axis (in hours [h] and minutes [min]). The massive rise in pH at 6 h 42 min indicates exit of the capsule from the stomach. The slight decline in pH at 9 h 20 min indicates entry into the large bowel. Gastric emptying time was 6 h 38 min, small bowel transit time was 2 h 38 min, and large bowel transit time was 36 h 57 min.

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Jul 18, 2016 | Posted by admin in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off

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