See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/283960542

Diagnosis and management of gastrointestinal motility disorders in dogs and

cats

Article · June 1997

CITATIONS READS

20 1,894

2 authors, including:

Jean Hall
Oregon State University
111 PUBLICATIONS 2,180 CITATIONS

SEE PROFILE

All content following this page was uploaded by Jean Hall on 23 November 2015.

The user has requested enhancement of the downloaded file.

 Vol. 19, No.6 June 1997 t,.
Continuing Education Article #4
Refereed Peer Review
Successfully complete the quizzes at the end of each CE article in this series,
and receive a certificate indicating completion of a course of study in
Gastrointestinal Prokinetic Therapy. This is the fifth of five articles.

Diagnosis and
Disorders of gastrointestinal
motility are a common cause of
Management of
gastroenterologic disease in dogs
and cats.
Gastrointestinal
Motility disorders can be
Motility Disorders
mechanical or functional in
origin, p. 721 .
in Dogs and Cats
Examples of functional
motility disorders of the
esophagus include idiopathic University of Pennsylvania Oregon State University
megaesophagus, dysautonomia,
Robert J. Washabau, VMD , PhD Jean A. Hall, DVM, PhD
hiatal hernia, esophagitis, and
gastroesophageal reflux, p. 722.

The following are functional

motility disorders of the stomach:
infection, inflammation, postgastric
dilatation-volvulus, ulcer, and
T he firs t four articles in this five-part series on gastrointestinal prokinetic
therapy discussed dopaminergic antagonist drugs, motilin-like drugs,
serotonergic drugs, and acetylcholinesterase inhibitors or parasympathet-
ic potentiating drugs, respectively. T his article considers the diagnosis and man-

..
agement of esophageal, gastric, small intestinal, and colonic motility disorders.
idiopathic disease, p. 728 .
ESOPHAGEAL MOTILITY DISORDERS
Functional motility disorders of Mechanical Obstruction
the intestine include infection,
Anatomic lesions of the esophagus (e.g., tumor, foreign body, stricture, vas-
inflammation, postoperative ileus,
cular ring anomaly, fis tula, and gastroesophageal intussusception) impede
and idiopathic and inflammatory esophageal peristalsis because of mechanical obstruction. Diagnosis of mechan-
bowel disease, p. 730. ical obstruction of the esophagus is usually straightforward and involves the use
of survey and contrast rad iography, endoscopy, and occasionally ultrasonogra-
Examples of functional motility phy. Mechanical obstruction should be treated as a primary disorder, which
disorders of the colon are feline
m ight require chemotherapy, surgical resection, endoscopic or surgical removal
idiopathic megacolon and
of foreign bodies, endoscopic or surgical reduction of intussusception, or bal-
inflammatory bowel disease,
loon dilation or bougienage (Figure 1).
p. 730.
Functional Obstruction
Cricopharyngeal Achalasia
C ricopharyngeal achalasia, a disorder of the cricopharyngeal sphincter, is
722 Small Animal The Compendium June 1997

,. ESOPHAGEAL MOTILITY DISORDER .

Gastroesophageal Idiopathic
reflux megaesophagus

1. Chemotherapy 1. Elevated oral

2. Surgical feedings

•
resection . 2. Gastrostomy
tube feedings
. 3. Antibiotics
(pneumonia)

Key
Finding
Therapy

Figure 1-Management of esophageal motility disorders.

characterized by cricopharyngeal hypertension and in- is questionable, electromyography of the oropharyngeal

adequate relaxation during swallowing. Affected pup- musculature should be performed to exclude the pos-
pies develop progressive dysphagia, and regurgitation is sibility of a more proximal oropharyngeal motility dis-
observed shortly after weaning. Patients make repeated, order.
no ~roductive attempts to swallow that culminate in Cricopharyngeal achalasia is best treated by cricopha-
regurgitation of undigested food. Coughing develops as ryngeal myotomy. Most patients experience immediate
a consequence of food aspiration; pulmonary crackles relief after surgery. 3 Effective medical management of
may be detected in patients with aspiration pneumonia. the disorder has not been reported.
Diagnosis of cricopharyngeal achalasia is technically
difficult and requires videofluoroscopy and esophageal Idiopathic Megaesophagus
manometry. Because of the inability to evaluate the Congenital megaesophagus in puppies is usually
rapid, complex series of events that occurs during swal- diagnosed by a history of regurgitation, weight loss,
lowing, survey and static barium-contrast radiographs and/or coughing associated with aspiration pneumonia
are not useful in diagnosing the disorder. The videoflu- as well as by the radiographic finding of generalized
oroscopic finding of multiple, nonproductive attempts esophageal dilation. An increased incidence has been
at swallowing barium liquid or paste only suggests a di- reported in Irish setters, Great Danes, German shep-
agnosis of cricopharyngeal achalasia. Definitive diagno- herds, Labrador retrievers, Chinese shar-peis, and New-
sis requires the manometric demonstration of elevated foundlands; heritability has been demonstrated in
basal pressures and inadequate relaxation during swal- miniature schnauzers and wirehaired fox terriers. Al-
lowing. '·2 If manometry is unavailable and the diagnosis though the pathogenesis of the congenital form is not

PROGRESSIVE DYSPHAGIA • ELEVATED BASAL PRESSURES • REGURGITATION

 The Compendium June 1997 Small Animal 723

completely understood, recent studies suggest a defect response of the cricopharyngeal and gastroesophageal
in vagal afferent innervation to the esophagus.4-6 Treat- sphincters to intraluminal stimuli suggests a defect in
ment consists of dietary management and supportive the afferent neural pathway, 12 like the disturbance that
care for aspiration pneumonia. Some patients exhibit has been characterized in congenital canine megaesoph-
improvement or resolution of clinical signs with matu- agus. 5·6
ration. Because the gastroesophageal sphincter is normoten-
Congenital idiopathic megaesophagus has also been sive and relaxes appropriately with swallowing in dogs
reported in several cats. 7•8 Megaesophagus may have affected with idiopathic megaesophagus, gastroesoph-
been secondary to pyloric dysfunction in one group of ageal sphincter myotomy cannot be recommended in
cats. 8 treating this disorder. Instead, current therapeutic rec-
Acquired megaesophagus is a common cause of re- ommendations include elevated feedings, treatment for
gurgitation in adult dogs. Like the congenital form, the reflux esophagitis in cases in which ir can be demon-
disorder is characterized by ineffective esophageal peri- strated, and antibiotic therapy for documented aspira-
stalsis and esophageal dilation. Acquired megaesoph- tion pneumonia (Figure 1).
agus may develop as a consequence of an underlying Affected animals should be fed a high-calo rie diet, in
disease process (e.g., myasthenia gravis, myositis or my- small, frequent feedings, from an elevated or upright
opathy, esophagitis, adrenocortical insufficiency, lead position to take advantage of gravity drainage through
poisoning, distemper, brain stem disease, or dysautono- a nonperistaltic esophagus. Dietary consistency should
mia).9 In most cases, there is no known cause and the be formulated to produce the fe west clinical signs.
condition is referred to as idiopathic megaesophagus. Some patients handle liquid diets well; others do better
The morbidity and mortality of the disorder are un- with solids. Patients that cannot maintain adequate
acceptably high. Many patients eventually succumb to nutritional balance with oral intake should be fed by
the effects of chronic malnutrition and repeated temporary or permanent tube gastrostomy. Gastrosto-
episodes of aspiration pneumonia. my tubes can be placed surgically or percutaneo usly
The minimal diagnostic investigation of acquired with endoscopic guidance.
megaesophagus should include complete blood count, Esophagitis, if present, should be treated with oral
serum chemistry analysis, urinalysis, serology for nico- sucralfate suspensions (0.5 to 1.0 g three times daily)
tinic acetylcholine receptor antibodies, serum anti- and gastric acid secretory inhibitors (e.g., oral or intra-
nuclear antibody titer, survey thoracic radiographs, and venous cimetidine at 5 to 10 mg/kg three to four times
esophageal videofluoroscopy. Additional tests that daily; oral or intravenous ranitidine at 1.0 to 2. 0 mg/kg
might be considered are fecal examination for Spirocer- two to three times daily; or oral omeprazole at 0. 7
ca lupi ova, serum lead concentration, thyroid function mg/kg once daily). Pulmonary infections should be
assays, esophageal endoscopy, and electrophysiologic identified by culture and sensitivity, and an appropriate
~eal evaluation (nerve conduction velocity and electromyog- antibiotic should be selected for the offending organ-
5- raphy). The additional medical investigation depends isms. This may be accomplished by transtracheal wash
:lis- on the individual case presentation. 9·10 or by bronchoalveolar lavage at the time of endoscopy.
The pathogenesis of idiopathic megaesophagus is not It has been suggested that cisapride, a 5-HT4 seroron-
ha- completely understood. The disorder has been com- ergic agonist, might improve esophageal peristalsis in
are pared with esophageal achalasia in humans. Achalasia is dogs with idiopathic megaesophagus. This would not
:of a failure of relaxation of the gastroesophageal sphincter seem to be a rational clinical application of the drug be-
with secondary dilation of the esophageal body. A sim- cause a smooth muscle prokinetic agent would nor be
ilar disorder has not been rigorously documented in expected to have much effect on striated muscle fu nc-
dogs. 11 Recent studies suggest several important differ- tion. Indeed, the prokinetic effect of cisapride in the
tlly ences between canine idiopathic megaesophagus and esophagus of humans or cats is confined to the lower
)55, human achalasia. esophageal body at the transition zone from striated
•nia In dogs with idiopathic megaesophagus, (1) the re- muscle to smooth muscle. Cisapride has no effect on
zed sponse of the cricopharyngeal sphincter and gastro- upper esophageal peristalsis in these species. Further-
een esophageal sphincter to swallowing is intact and nor- more, 5-hydroxytryptamine (serotonin) stimulates con-
ep- mal, (2) balloon distention in the proximal esophageal traction of the smooth muscle of the canine gas tro-
~w­ body induces minimal increases in cricopharyngeal esophageal sphincter but does not affect the striated
In sphincter pressure, and (3) balloon distention of the muscle of the canine esophageal body. 13 Cisapride rhus
.-\1- distal esophageal body induces minimal relaxation of cannot be recommended in treating idiopathic m ega-
nor the gastroesophageal sphincter. The diminished motor esophagus in dogs. 14 ·15 A cisapride-induced increase in

DIETARY MANAGEMENT • THYROID FUNCTION ASSAYS • REFLUX ESOPHAGITIS

724 Small Animal The Compendium June 1997

gasuoeso phageal sphincter pressure could diminish ed feedings, expressing the urinary bladder, and antibi-
esophageal clearance and worsen clinical signs in dogs otics) is the basis of therapy for this disorder, some cats
with idiopathic megaesophagus. A preliminary report reportedly demonstrate improvement with parasym-
sugges ts that cisapride actually decreases esophageal pathomimetic drugs (e.g., bethanechol or meroclo-
transit rate in normal dogs. 16 pramide). Gastrostomy tube feeding or total parenteral
T here are no other clinically useful drugs for improv- nutrition may sustain some patients until they regain
ing esophageal peristalsis in dogs with acquired idio- neurologic function. In general, dysautonomia is associ-
pathic megaesophagus. Bethanechol chloride, a cho- ated with a guarded to poor prognosis for long-term
linomimetic drug, reportedly increased esophageal survival in dogs and cats. Although 20% to 40% of
contraction amplitude in dogs with idiopathic mega- affected cats are likely to recover, recovery may take 2
esophagus bur did not affect the frequency of motor to 12 months. Complete recovery is uncommon; many
response to swallowing. 17 cats are left with residual impairment (e.g., intermittent
regurgitation, dilated pupils, and fecal or urinary in-
Dysautonomia continence).
Dysautonomia is a generalized autonomic neurop-
athy originally reponed (as the Key-Gaskell syndrome) Esophagitis
in cats in the United Kingdom. The condition has now Esophagitis is an acute or chronic inflammatory dis-
been reported in dogs and cats from Western Europe order of the esophageal mucosa that may involve the
and the United States. The clinical signs reflect gen- underlying submucosa and muscularis. Regurgitation
eralized autonomic dysfunction; megaesophagus, is the most important sign in cats and dogs with
esophageal hypomotility, and regurgitation are con- esophagitis. Severely affected patients may manifest ex-
sistent findings. 18 Pathologically, degenerative lesions cessive salivation, dysphagia, and painful swallowing
are found in autonomic ganglia, intermediate gray (odynophagia) with severe inflammation of the esopha-
columns of the spinal cord, and some sympathetic ax- gus.
ons. Despite an intensive search for genetic, roxie, nu- Esophagitis most often results from chronic gastritis
tritional, and infectious causative agents, a definitive with persistent vomiting or, less frequently, from reflux
cause has not been established. of gastric juice during anesthetic episodes. Esophagitis
The most frequently reported clinical signs are de- is more likely to develop after repeated episodes of gas-
pression, anorexia, constipation, and regurgitation or tric reflux than after a single, long episode of acid expo-
vomiting. Fecal and urinary incontinence are reponed sure. 19 Esophageal endoscopy is the preferred method
less commonly. Physical examination findings that are of diagnosing esophagitis. After predisposing condi-
consistent with dysautonomia include dry mucous tions are corrected, therapy for the disorder is based on
membranes, pupillary dilation, prolapsed nictitating drugs that form diffusion barriers (oral sucralfate at 0.5
membranes, reduced or absent pupillary light reflex, to 1.0 g three times daily) and H 2-recepror antagonists
bradycardia, and areflexic anus. Paresis and conscious (e.g., oral or intravenous cimetidine at 5 to 10 mg/kg
proprioceptive deficits have been reponed in a few pa- three to four times daily). Oral cisapride (0.1 to 0.5
tients.1 8 mg/kg two to three times daily) or metoclopramide
In most cases, a clinical diagnosis is based on the his- (0.2 to 0.5 mg/kg three times daily) can be adminis-
tory and physical examination findings. Additional tered to increase gastroesophageal sphincter tone and
findings that are consistent with the diagnosis include reduce reflux (Figure 1).
esophageal dilation and hypomotility on survey and
barium-contrast radiographs, delayed gastric emptying Hiatal Hernia
on barium-contrast radiographs, reduced tear produc- Hiatal hernias may occur as congenital or acquired
tion in Schirmer's tear tests, atropine-insensitive brady- lesions. Congenital hiatal hernias have been reponed in
cardia, and bladder and colonic distention on survey Chinese shar-peis, English bulldogs, and chow chows
radiographs. There are few diagnostic differentials to and apparently result from incomplete closure of the
consider in a cat with the myriad of manifestations diaphragmatic hiatus during embryologic devel-
characteristic of this syndrome. Early in the course of opment. 20 Clinical signs include regurgitation, vomit-
the illness, however, other diagnostic differentials to ing, and dyspnea. Clinical signs result from mechanical
consider are colonic or intestinal obstruction, other obstruction or the deleterious effects of gastric and in-
causes of megaesophagus, and feline lower urinary tract testinal juice (e.g., hydrogen ions, pepsins, and bile
disease. salts) on esophageal mucosa. A clinical diagnosis may
Although supportive care (e.g., artificial tears, elevat- be made if a gas-filled, soft tissue opacity is radiograph-

ESOPHAGEAL PERISTALSIS • DEPRESS I ON • CHRONIC GASTRITIS

 726 Small Animal The Compendium June 1997

ically evident in the caudodorsal thorax. Affected pa- consistent with reflux esophagitis. Definitive diagnosis
tients often fail to respond to medical treatment and requires determinations of gastroesophageal sphincter
ubsequendy require surgery (e.g., crural apposition, pressure and 24-hour intraluminal pH measurement;
gastropexy, and possibly esophagopexy). 20 these techniques are available only in major referral
Although the pathogenesis of acquired hiatal hernia centers.
is not completely understood, recent reports suggest Because dietary fat delays gastric emptying and re-
that hiatal hernia is likely to occur secondary to in- duces gastroesophageal sphincter pressure, patients
creased intraabdominal pressure with chronic vomiting should be fed fat-restricted diets. Owners should avoid
disorders. 21 Regurgitation is the most important clinical late-night feedings , which tend to reduce gastroesoph-
sign observed in cats and dogs with acquired hiatal her- ageal sphincter pressure during sleep. In addition to nu-
nia.20·22 Patients with acquired hiatal hernia usually re- tritional considerations, rational medical therapy for
spond to acid neutralization therapy (e.g., H 2-receptor this disorder includes drugs that form diffusion barriers
antagonists and/or application of diffusion barriers) (e.g., sucralfate), gastric acid secretory inhibitors (e.g.,
and occasionally require restorative surgerf 2 (Figure 1). cimetidine, ranitidine, or omeprazole), and pro-
kinetic agents (e.g., cisapride or metoclopramide).
Gastroesophageal Reflux Drugs that form diffusion barriers may be the most
Gastroesophageal reflux has been poorly documented important medical therapy in patients with gastro-
in veterinary species but is more common than was esophageal reflux. Oral sucralfate (0.5 to 1.0 g three
previously believed. Reflux is a disorder of the gastro- times daily) protects against mucosal damage from gas-
esophageal sphincter that permits retrograde movement troesophageal reflux and promotes healing of existing
of gastrointestinal fluids or ingesta into the esophagus. esophagitis. 28 Dogs with refractory cases of gastro-
Chronic vomiting, disorders of gastric emptying, hiatal esophageal reflux should be medicated with acid secre-
hernia, and anesthesia-induced decreases in gastro- tory inhibitors and/or prokinetic agents. The H 2-his-
esophageal sphincter pressure are the major causes of tamine receptor antagonists (e.g., oral or intravenous
gastroesophageal reflux in dogs and cats. The normal cimetidine at 5 to 10 mg/kg three to four times daily
esophagus rapidly clears acid by secondary peristalsis; and ranitidine at 1.0 to 2.0 mg/kg two to three times
remaining acid is neutralized by swallowed saliva. 23 daily) inhibit gastric acid secretion and reduce the
Anesthetic drugs can decrease gastroesophageal sphinc- amount of acid reflux. Omeprazole (0.7 mg/kg once
ter pressure/ 4 reduce peristalsis, and decrease salivation. daily) , an H+,K+-ATPase inhibitor, could also be used to
The frequency of reflux, the length of contact time, inhibit gastric acid secretion. Oral cisapride (0.1 to 1.0
and the composition of the refluxed material (gastric mg/kg two to three times daily) and metoclopramide
acid, pepsin, trypsin, bile salts, and duodenal bicarbo- (0.2 to 0.5 mg/kg three to four times daily) are useful
nate) determine the severity of the esophagitis. Gastric in treating gastroesophageal reflux because they pro-
acid alone produces mild esophagitis; combinations of mote gastric emptying and increase gastroesophageal
acid and pepsin or trypsin, bicarbonate, and bile salts sphincter pressure (Figure 1 and Table 1).
produce severe esophagitis. 25 The risk of reflux esoph-
agitis is greater with multiple episodes of acid exposure GASTRIC MOTiliTY DISORDERS
than with a single, long episode. 19 Mechanical Obstruction
The clinical signs of gastroesophageal reflux are simi- Anatomic lesions of the pylorus and adjacent duode-
lar to those of esophagitis. In severe cases, patients may nal segment (e.g., infiltrative pyloric neoplasia, chronic ca
exhibit regurgitation, salivation, odynophagia, exten- hypertrophic pyloric gastropathy, chronic hypertrophic
sion of the head and neck during swallowing, and total gastritis, eosinophilic gastritis, gastric foreign bodies, F
avoidance of food . In milder cases, patients may have antral polyps, hepatic or pancreatic abscesses, and in-
occasional episodes of regurgitation in the early morn- traabdominal neoplasia) impede gastric emptying be- as
ing. Such cases probably result from transient relax- cause of mechanical obstruction. 29 ·30 Diagnosis of me- ab
ation of the gastroesophageal sphincter during sleep. 26 chanical obstruction is usually straightforward and m
The history may suggest a diagnosis of gastroesoph- involves survey and contrast radiography, ultrasono- d
ageal reflux. Survey thoracic radiographs are often nor- graphy, and/or gastroscopy. Mechanical obstruction n
mal. Videofluoroscopy may demonstrate intermittent should be treated as a primary disorder (e.g., with en-
gastroesophageal reflux, but this finding may also be doscopic polypectomy, surgical pylorectomy, and gas-
observed in normal animals without esophagitis. 27 En- troduodenostomy) (Figure 2). Surgical removal of the
doscopy is currently the best means of documenting foreign object or the affected area is the preferred thera- an
mucosal inflammation in the distal esophagus, which is py.29 Gastrointestinal prokinetic agents are contraindi- tn

CRURAL APPOSITION • ACQUIRED HIATAL HERNIA • CHRONIC VOMITING

I
 The Compendium June 1997 Small Animal 727

TABLE I
Mechanisms, Sites of Activity, and Indications for Gastrointestinal Prokinetic Agents

Agent Mechanism ofAction Sites ofActivity Indications

Metoclopramide D 2 dopaminergic antagonist LES, stomach, intestine, CRTZ Vomiting disorders,

re-
0.2-adrenergic antagonist Stomach gastroesophageal
~ 2 -adrenergic antagonist Stomach reflux, delayed
5-HT4 serotonergic agonist LES, stomach, intestine gastric emptying,
5-HT3 serotonergic antagonist Stomach, intestine postoperative ileus,
nu- intestinal pseudo-
for obstruction
Domperidone D 2 dopaminergic antagonist Stomach, CRTZ Vomiting disorders
a 2-adrenergic antagonist Stomach
~ 2 -adrenergic antagonist Stomach
Cisapride 5-HT4 serotonergic agonist LES, stomach, intestine Gastroesophageal reflux,
5-HT 1 serotonergic antagonist Stomach, intestine, emetic center delayed gastric
5-HT3 serotonergic antagonist Stomach, intestine, CRTZ emptying,
5-HT2 serotonergic agonist Colon postoperative ileus,
Nonserotonergic mechanism Canine antrum intestinal pseudo-
obstruction,
constipation,
chemotherapy-induced
emesis
Erythromycin Motilin agonist (in cats) Stomach, intestine Delayed gastric emptying
5-HT3 serotonergic agonist Stomach, intestine (liquids more than
(in dogs) solids)
Ranitidine Acetylcholinesterase inhibitor Stomach, intestine, colon Delayed gastric
Possibly M 3 muscarinic agonist Stomach emptying, intestinal
pseudo-obstruction,
constipation
Nizatidine Acetylcholinesterase inhibitor Stomach, intestine, colon Delayed gastric
Possibly M 3 muscarinic agonist Stomach emptying, intestinal
pseudo-obstruction,
constipation

CRTZ = chemorecepror trigger zone; 5-HT = 5-hydroxytryptamine; LES = lower esophageal sphincter.

cared in treating patients with mechanical obstruction. Delayed gastric emptying has also been associated
with several secondary conditions, including electrolyte
Functional Obstruction disturbances, metabolic disorders, concurrent drug us-
Functional disorders of gastric emptying (referred to age (anticholinergics, ~-adrenergic agonists. and opi-
as delayed gastric emptying or gastroparesis) result from ates), acute stress, and acute abdom inal inflammation Y
abnormalities in myenteric neuronal or gastric smooth Gastric emptying disorders are usually diagnosed after
muscle function or from abnormalities in antropyloro- mechanical obstruction has been ruled our.
duodenal coordination. Delayed gastric emptying is A gastric motility disorder should be considered
now recognized as an important cause of upper gastro- when there is a history of chronic vomiting. Vomiting
intestinal tract signs (e.g., anorexia and vomiting). 31 of undigested to partially digested food usually occurs
Delayed gastric emptying has been reported in animals more than 10 hours after a m eal, at a time when the
recovering from gastric dilatation-volvulus, 32 infectious stomach should be empty. Other signs of a gas tric
and inflammatory gastric diseases, 33 experimental gas- motility disorder include gastric distentio n, nausea,
tric ulcer/ 4 and radiation gastritis. 35 anorexia, belching, polydipsia, pica, and weight loss.

FREQUENCY OF REFLUX • VIDEOFLUOROSCOPY • FAT-RESTRICTED DIETS

728 Small Animal The Compendium June 1997

GASTRIC MOTILITY DISORDER

\ Polypectomy
\1. Chemotherapy
2. Partial
I1&#.1.1§§.1.
!
Antiinflammatory
drugs (e.g.,
,. ,.
Antibiotics r
gastrectomy prednisone) a
e

Resolution

Key
Finding

Figure 2-Management of gastric motility disorders.

The physical examination may be normal or reveal abnormalities of gastric emptying in routine upper
findings associated with the underlying cause. There gastrointestinal radiographic studies. However, such
may be increased bowel sounds with abdominal auscul- studies provide inadequate information for assessing
tation or nonspecific pain on abdominal palpation. emptying of the typical heterogeneous meal because
Laboratory findings depend on the underlying cause. solids and liquids empty differently, as do large and
Dogs with persistent vomiting may exhibit dehydra- small particles, and lipids and carbohydrate solutions.
tion, electrolyte abnormalities, or acid-base imbalances. Barium mixed with food is believed to be better than
Hypokalemia is the most common electrolyte abnor- liquid barium for testing distal gastric motor function.
mality. Paradoxic aciduria is observed in some dogs Small radiopaque particles mixed with food are also
when vomiting occurs secondary to pyloric outflow used to assess gastric emptying. If available, radio-
obstruction. isotopic methods are the most tolerable and clinically
Methods that are available for evaluating gastric emp- accurate means of evaluating gastric emptying.
tying include oral administration of radioisotopes cou- Because surgical procedures are often unsuccessful,
pled with external scanning, serial sampling of gastric dietary management and gastric prokinetic agents are
contents by intubation, ultrasonography, computed to- used to treat patients with delayed gastric emptying dis-
mography, electrophysiology, and manometry. Radio- orders (Figure 2). Dietary management is based on the
graphic techniques are the most definitive means that knowledge that liquids are emptied from the stomach
are generally available to practitioners for diagnosing more rapidly than solids, carbohydrates are emptied
gastric motility disorders. more rapidly than proteins, and proteins are emptied
Liquid barium sulfate can be used to detect gross more rapidly than lipids. A low-fat, low-protein diet of

GASTRIC EMPTYING . ELECTROLYTE DISTURBANCES • PARADOXIC ACIDURIA

 The Compendium June 1997 Small Animal 729

liquid or semiliquid consistency thus should be fed at tussusception) (Figure 3). Gastrointestinal prokin etic
frequent intervals to facilitate gastric emptying. Diets agents are contraindicated in treating patients with
should be selected for low acidity and low osmolality these disorders.
and should be fed at warm temperatures (22° to 38oC
[72° to 100"F]). Functional Obstruction
Gastric prokinetic agents should be considered in pa- Functional disorders of small intestinal transit (in-
tients that fail to respond to dietary management alone. testinal pseudo-obstruction) have been associated with
The 5-HT4 serotonergic agonists (e.g., cisapride and parvoviral enteritis, postoperative ileus, nematode infes-

• metoclopramide), motilin-like drugs (e.g., erythro-

mycin), and acetylcholinesterase inhibitors (e.g., raniti-
dine and nizatidine) have been used to treat delayed gas-
tric emptying (Figure 2 and Table I). We currently
tation, intestinal sclerosis, and radiation enteritis. 40 .4·H>
The clinical signs vary depending on the cause, the lo-
cation in the small intestine, and the duration. Chronic
diarrhea and weight loss are common. Vomiting is
recommend cisapride as the initial gastric prokinetic common with more proximal obstructions. Over-
agent. Doses of cisapride from 0.05 to 0.20 mg/kg growth of small intestinal bacteria, a common compli-
enhance gastric emptying in dogs with normal empty- cation of disordered motility, contributes to the patho-
ing.1 4·36 However, doses of 0.5 to 1.0 mg/kg are required physiology and clinical signs.
to enhance gastric emptying in dogs with delayed gastric The medical investigation should be directed at iden-
emptying induced by a 2-adrenergic agonists, dopamine, tifying the underlying cause. In some cases, a primary
disopyramide, or antral tachygastria. 14 ·15 entity may not be obvious. Gastrointestinal prokinetic
Cisapride accelerates gastric emptying in dogs by therapy should be used to promote intestinal transit in
stimulating pyloric and duodenal motor activity, by such cases (Figure 3). 5-HT4 serotonergic agonists (e.g.,
enhancing antropyloroduodenal coordination, and by cisapride or metoclopramide) and motilin-like drugs
increasing the mean propagation distance of duodenal (e.g., erythromycin) have been recommended in the
contractions. 36 In this regard, cisapride is apparently su- therapy of patients with these disorders. 15 ·37·38
perior to metoclopramide and domperidone in stimu- In the treatment of small intestinal motility disor-
lating gastric emptying. 15 ·36·37 If oral cisapride (0.1 to ders, the 5-HT4 serotonergic agonists apparently have
1.0 mg/kg two to three times daily) fails to improve distinct advantages over other gastrointestinal prokinet-
gastric emptying, we recommend the use of oral ic agents. Cisapride, for example, stimulates jejunal
erythromycin (0.5 to 1.0 mg/kg three times daily) or spike burst migration, 46 jejunal propulsive motility, 47
one of the acetylcholinesterase inhibitors (e.g., oral ran- and antropyloroduodenal coordination 48 after intestinal
itidine at 1.0 to 2.0 mg/kg twice daily or nizatidine at lipid infusion in dogs. Cisapride thus apparently has a
2.5 to 5.0 mg/kg once daily) in place of cisapride. 10.3 8·39 rational place in the treatment of patients with post-
operative ileus and intestinal pseudo-obstruction. Well-
1pper SMALL INTESTINAL MOTILITY DISORDERS designed clinical trials are required to determine the
uch Mechanical Obstruction effectiveness of cisapride compared with that of other
~ss mg Mechanical obstruction of the small intestine may be prokinetic agents in treating patients with these die-
cause associated with foreign body ingestion, neoplasia, stric- orders.
e and tures, hematomas, or intussusceptions. 40 Acute obstruc-
· ·ons . tion of the intestine is characterized by distention, Inflammatory Bowel Disease
than increased intraluminal pressure, and increased motor ac- Inflammatory bowel disease is a common disorder
~Lion . tivity in the segment of bowel proximal to the occlusion. of dogs and cats. The disorder may involve se,·eral
, also Distention of the bowel proximal to the obstruction re- anatomic sites (e.g., the stomach, small intestine, an
d io- sults from fluid and gas accumulation. Intestinal secre- colon). Clinical signs associated with inflamma;:or)'
cally tion is stimulated, absorption of fluid is decreased, and bowel disease include vomiting, diarrhea. weight los.;,
aerophagia causes gas accumulation. As the small bowel tenesmus, urgent defecation, hematochezia. and exces-
~ss ful, distends, neuromuscular activity increases. 41 Distally, the sive mucus in feces. The diarrhea of inflam matorY bow-
~a re bowel becomes quiescent; nearly all motor activity el disease is associated with excessive secretion and mal-
~~ ceases. 42 .4 3 The increased motor activity of the proximal absorption. Inflammation disrupts the tight junction
n ~ segment tends to subside with chronic obstruction. between epithelial cells, which reduces absorption and
m~h The diagnosis of obstruction can be confirmed via promotes loss of nutrients , electrol ytes. and water.
pried radiography. Mechanical obstruction of the small intes- Inflammatory mediators may also stimulate abnormal
~~ tine should be treated as a primary disorder (e.g., by motor activity. Inflammati on produced by 95%
~ d enterectomy, foreign body removal, or reduction of in- ethanol-20% acetic acid perfusion in the canine ileum.

LOW ACIDITY • CISAPRIDE • ACETYLCHOLINESTERASE INHIBIT ORS

 Th
730 Small Animal The Compendium June 1997

INTESTINAL MOTILITY DISORDER

\
Intussusception ~

I ,. .,.
1. Chemotherapy
2. Partial
gastrectomy
-- . I
.
•
Antiinflammatory
drugs (e.g.,
prednisone)
Antibiotics Low-fat diet,
antibiotics

01
ski!

Resolution

Key
Prokinetic therapy:
cisapride or
'
metoclopramide
Finding
Therapy

Figure 3-Management of intestinal motility disorders.

for example, significantly increases the frequency of gi- COLONIC MOTILITY DISORDERS
ant migrating contractions and decreases the frequency Feline Idiopath ic Megacolon
of migrating motor complexes. 49 Colonic dilatation results in disruption of the coordi-
In this canine model, diarrhea, urgent defecation, nated motility patterns of the distal colon and rectum
hematochezia, and apparent abdominal discomfort are that permit receptive relaxation for fecal storage as well
related to the increased frequency of giant migrating con- as the giant migrating contractions associated with the
tractions.49 Inhibition of giant migrating contractions defecation reflex. This eventually leads to constipation,
by specific antagonists during inflammation thus may obstipation, and idiopathic megacolon. Many cats pre-
minimize clinical signs and may alter the course of the sent with chronic histories of tenesmus and inability to
disease. Platelet-activating factor (PAF) is believed to be pass feces. Diagnosis is usually based on a history of ob-
one of the inflammatory cytokines that mediates the stipation (dyschezia, depression , anorexia, and vomit-
increased frequency of giant migrating contractions. 50 ing) and abdominal palpation (colonic impaction). Ra-
The PAF antagonist BN 50727 inhibits the contractile diography is often necessary to rule out obstructive
response to PAF in the experimentally inflamed canine causes.
ileum. 5° Motor abnormalities (i.e., giant migrating con- Several researchers have emphasized the importance of
tractions) thus may be the major cause of clinical signs considering an extensive list of diagnostic differentials
in experimental inflammatory bowel disease. It remains (e.g., neuromuscular, mechanica l, inflammatory,
to be determined whether the same motor abnormali- metabolic- endocrine, pharmacologic, environmental,
ties and inflammatory cytokines are involved in sponta- and behavioral causes) for an obstipated cat. A recent re-
neo us canine inflammatory bowel disease. view, however, suggests that 96% of cases of obstipation

INCREASED INTRALUMINAL PRESSURE • INTESTINAL TRANSIT • DIARRHEA

732 Small Animal The Compendium June 1997

Resolution
Dietary fiber Recurrence Dioctyl sodium
sulfosuccinate or petrolatum
and/or cisapride

Resolution
Dietary fiber,
lactulose,
bisacodyl

Pelvic osteotomy or colectomy

Colectomy

Colectomy
Key
Finding
Therapy
Time period

Figure 4-Managemenr of feline idiopathic megacolon. (From Washabau RJ, Hasler AH: Constipation, obstipation, and
megacolon, in August JR [ed]: Consultations in Feline Internal Medicine. Philadelphia, WB Saunders Co, 1996, p 108.
Modified with permission.)

are accounted for by idiopathic megacolon (62%), pelvic cases (more than 60%) have no evidence of neurologic
canal stenosis (23%), nerve injury (6%), or Manx sacral disease. 51 These idiopathic cases may involve distur-
spinal cord deformity (5%)? Fewer cases are accounted bances of colonic smooth muscle.
for by complications of colopexy (1 %) and colonic neo- Recent studies suggest that colonic smooth muscle
plasia (1 %). In another 2% of cases, colonic hypogan- function is impaired in cats with idiopathic mega-
glionosis or aganglionosis was suspected but not proven. colon. 52 In vitro isometric stress measurements were
Inflammatory, pharmacologic, and environmental- performed on colonic smooth muscle segments ob-
behavioral causes were not cited as predisposing factors tained from cats with idiopathic dilated megacolon.
in any of the original case reports. Endocrine factors Compared with that of healthy controls, megacolonic
(obesity in five cases and hypothyroidism in one case) smooth muscle developed less isometric stress in re-
were cited but were not necessarily implicated as part of sponse to neurotransmitters (acetylcholine, substance P,
the pathogenesis of megacolon. Although it is important and cholecystokinin), membrane depolarization (potas-
to consider an extensive list of diagnostic differentials in sium chloride), and electrical field stimulation. These
an individual animal, most cases are idiopathic, orthope- differences were observed in longitudinal and circular
dic, or neurologic in origin. 51 smooth muscle from the ascending and descending
The pathogenesis of idiopathic megacolon has been colon. No significant abnormalities of smooth muscle
variably attributed to a primary neurogenic or degener- cells or myenteric neurons were observed on histologic
ative neuromuscular disorder. Although few cases evaluation. These studies suggest that feline idiopathic
(1 1%) evidently result from neurologic disease, most megacolon is a generalized dysfunction of colonic

Card
OBSTIPATION • ENDOCRINE FACTORS • IDIOPATHIC MEGACOLON
Cardh
734 Small Animal The Compendium June 1997

smooth muscle and that treatments aimed at stimulat- weeks to months after surgery; constipation may recur
ing colonic smooth muscle contraction might improve m some cats.
colonic motility. 52
Traditional therapy for constipation and idiopathic Inflammatory Bowel Disease
megacolon has been aimed at improving fecal hydra- Experimental canine colitis is associated with an in-
tion and bulk (Figure 4). Cat owners thus are advised creased incidence of giant migrating contractions that is
to encourage water consumption and to increase the highly correlated with the clinical signs of tenesmus, di-
fiber content of the diet with bulk laxatives (e.g., psylli- arrhea, hematochezia, and excessive mucus in feces. 55 •56
um). Warm-water enemas can be given intermittently These findings are similar to those reported in experi-
as needed. Thereafter, patients may be treated with mental canine ileitis 49 •50 and suggest that the diarrhea
emollient laxatives (e.g., dioctyl sodium sulfosuccinate), produced in inflammatory bowel disease may be largely
stimulant laxatives (e.g., bisacodyl), lubricant laxatives attributable to the numerous giant migrating contrac-
(e.g., mineral oil or petrolatum), saline laxatives (e.g., tions that emerge during acute inflammation. Therapy
magnesium citrate), hyperosmotic agents (e.g., lactu- and resolution of disease may be facilitated by charac-
lose), or motility agents. 51 Hyperosmotic agents that terizing the mechanisms that are involved in the regula-
contain sodium phosphate are contraindicated in cats tion of this abnormal motor pattern.
because these agents tend to induce severe hyperna-
tremia, hyperphosphatemia, and hypocalcemia in this
species. 53
In several species, cisapride enhances colonic propul-
About the Authors
Dr. Washabau is affiliated with the Department of Clinical
sive motility via activation of colonic smooth muscle 5-
Studies, School of Veterinary Medicine, University of
HT2a receptors. 14 ' 15 Although in vitro studies demon-
Pennsylvania, Philadelphia, Pennsylvania. Dr. Hall is affil-
strate that cisapride stimulates feline colonic smooth
iated with the college of Veterinary Medicine, Oregon
muscle contraction, 54 it has not yet been proven that
State University, Corvallis, Oregon. Drs. Washabau and
cisapride stimulates feline colonic propulsive motility in
Hall are Diplomates of the American College of Veterinary
vivo. Current anecdotal reports suggest that cisapride is
Internal Medicine.
effective in stimulating colonic propulsive motility in
cats with mild to moderate idiopathic constipation; cats
with longstanding obstipation and megacolon are not
likely to demonstrate much improvement with cis- REFERENCES
apride therapy. The recommended dosage of oral cis- 1. Rosin ER: Quantitation of the pharyngoesophageal sphinc-
apride for cats with mild to moderate idiopathic consti- ter in the dog. Am] Vet Res 47:660-662, 1986.
2. Lang IM, Dantas RO, Cook IJ, et a!: Videoradiographic,
pation has been 0.1 to 0.5 mg/kg two to three times
manometric, and electromyographic analysis of canine upper
daily. Higher doses (0.5 to 1.0 mg/kg) may be neces- esophageal sphincter. Am j Physiol260:G911-G919, 1991.
sary in cats with moderate to severe constipation. No 3. Goring RL, Kagan KG: Cricopharyngeal achalasia in the
significant side effects have yet been observed or report- dog: Radiographi ~ evaluation and surgical management.
ed in cats medicated with oral cisapride at dosages of Compend Contin Educ Pract Vet4(5):438-444, 1982.
0.1 to 1.0 mg/kg two to three times daily. 4. Tan BJK, Diamant N: Assessment of the neural defect in a
dog with idiopathic megaesophagus. Dig Dis Sci 32:76-85,
Colectomy should be considered in cats that are re-
1987.
fractory to medical therapy (Figure 4). Cats have a gen- 5. Holland CT, Satchell PM, Farrow BRH: Vagal afferent dys-
erally favorable prognosis for recovery after colectomy. function in naturally occurring canine esophageal motility
Mild to moderate diarrhea occasionally persists for disorder. Dig Dis Sci 39:2090-2098, 1994.

Gastrointestinal Health

To improve intestinal health by including fiber in the diet, choose fibers that
1) Support the growth of beneficial intestinal bacteria, and 2) Result in
sufficient production of short chain fatty acids to stimulate intestinal cell
•••
·~
""
proliferation and differentiation. lAMS
For more information calll-800-535-(VETS)8387 COMPANY

Reference: Kerley MS, Sunvold GO. Physiological response to short chain fatty acid production in the intestine. In: Recent Advances in Canine and
r, Feline Nutritional Research: Proceedings of the 19961ams International Nutrition Symposium, Wilmington OH: Orange Frazier Press; 1996:33-39 ~
 The Compendium June 1997 Small Animal 735

6. Holland CT, Satchell PM, Farow BRH: Vagal esophagomo- lower esophageal sphincter relaxation ro postprandial gas-
ror nerve function and esophageal moror performance in troesophageal reflux and belching in dogs. Gastroenterology
dogs with congenital idiopathic megaesophagus. Am J Vet 90:545-551, 1986.
Res 57:906-911, 1996. 27. Watrous B, Suter PF: Normal swallowing in rhe dog: A
Hoenig M, Mahaffey MB, Parnell PG, er al: Megaesophagus cineradiographic study. Vet Radiol20:99-109, 1979.
in rwo cars.jAVMA 196:763-765, 1990. 28. Katz PO, Geisinger KR, Hassan M, et al: Acid-induced
Pearson H, Gaskell CJ, Gibbs C, er al: Pyloric and esoph- esophagitis in cats is prevented by sucralfate bur not synthet-
ageal dysfunction in rhe cat. J Small Anim Pract 15:487- ic prostaglandin E. Dig Dis Sci 33:217-224, 1988.
501, 1974. 29. Gualtieri M, Monzeglio MG: Gastrointestinal polyps in
Washabau RJ: Swallowing disorders, in Simpson JW, Hall small animals. Eur j Comp Gastroenterol1:5-11, 1996.
EJ (eds): Manual of Canine and Feline Gastroenterology. 30. Matthiesen DT, Walter MC: Surgical treatment of chronic
Cheltenham, England, British Small Animal Veterinary hypertrophic pyloric gasrropathy in 45 dogs. JMHA 22:
241-247, 1986.
Association, 1996, pp 67-89.
31. Burrows CF: Gastric disease, in Simpson JW, Hall EJ (eds):
10. Washabau RJ, Hall JA: Gastrointestinal motility disorders of Manual of Canine and Feline Gastroenterology. Cheltenham,
dogs and cats. Eur J Comp Gastroenterol2:9-19, 1997. England, British Small Animal Veterinary Association, 1996,
11. Diamant N, Szczepanski M, Mui H: Manometric character- pp 90-113.
a- istics of idiopathic megaesophagus in the dog: An unsuitable 32. Hall JA, Solie TN, Seim HB, et al: Gastric myoelectric and
model for achalasia in man. Gastroenterology 65:216-223, motor activity in dogs with gastric dilation-volvulus. Am j
1973. Physiol265:G646-G653, 1993.
12. Washabau RJ, Gaynor A: Pathogenesis of canine mega- 33. Hall JA: Diagnosis and management of gastric motility dis-
esophagus: Neuropathy. Proc ACVIM:581-582, 1996. orders. ProcACVIM:180-183, 1994.
13. Cohen ML, Susemichel AD, Bloomquist W, et al: 5-HT, re- 34. Fioramonti J, Bueno L: Gastrointestinal myoelectric activity
ceptors in rat but not guinea pig, rabbit or dog esophageal disturbances in gastric ulcer disease in rats and dogs. Dig Dis
muscle. Gen Pharmacol25: 1143-1148, 1994. Sci 25:575-580, 1980.
14. Washabau RJ, Hall JA: Clinical pharmacology of cisapride. 35. DuBois A, Jacobus JP, Grissom MP, et al: Altered gastric
JAVMA 207:1285-1288, 1995. emptying and prevention of radiation-induced vomiting in
15. Washabau RJ, Hall JA: Gastrointestinal prokinetic therapy: dogs. Gastroenterology 86:444-448, 1984.
Serotonergic drugs. Compend Contin Educ Pract Vet 19(4): 36. Orihata M, Sarna SK: Contractile mechanisms of action of
473-480, 1997. gastroprokinetic agents: Cisapride, meroclopramide, and
16. Mears EA, Jenkins C, Mays L, et al: The effect of metoclo- domperidone. Am j Physiol266:G665-G676, 1994.
pramide and cisapride on esophageal motility in normal bea- 37. Hall JA, Washabau RJ: Gastrointestinal prokineric therapy:
gles. j Vet Intern Med 10:156, 1996. Dopaminergic antagonist drugs. Compend Contin Educ Pract
17. Diamant N, Szczepanski M, Mui H: Idiopathic megaesoph- Vet 19(2):214-221, 1997.
agus in the dog: Reasons for spontaneous improvement and 38. Hall JA, Washabau RJ: Gastrointestinal prokinetic therapy:
a possible method of medical therapy. Can Vet j 15:66-71, Motilin-like drugs. Compend Contin Educ Pract Vet 19(3):
1974. 281-288, 1997.
18. Sharp NJH: Feline dysauronomia. Semin Vet Med Surg 39. Hall JA, Washabau RJ: Gastrointestinal prokinetic therapy:
5:67-71, 1990. Acetylcholinesterase inhibitors. Compend Contin Educ Pract
19. Cassidy Y, Geisinger KT, Kraus BB, et al: Continuous versus Vet 19(5):615-621, 1997.
intermittent acid exposure in the production of esophagitis 40. Guilford WG, Strombeck DR: Intestinal obstruction, pseu-
in a feline model. Dig Dis Sci 37:1206-1211, 1992. do-obstruction, and foreign bodies, in Strombeck's Small An-
20. Callan MB, Washabau RJ, Saunders HM, et al: Congenital imal Gastroenterology, ed 3. Davis, CA, Sronegate Publish-
esophageal hiatal hernia in the Chinese shar-pei dog. j Vet ing, 1996, pp 487-502.
Intern Med7:210-215, 1993. 41. Ellison GW: Intestinal obstruction, in Bojrab MJ (ed): Dis-
21. Twedt DC: Diseases of the esophagus, in Ettinger SJ, Feld- ease Mechanisms in Small Animal Surgery. Philadelphia, Lea
man EC (eds): Textbook of Veterinary Internal Medicine, ed & Febiger, 1993, pp 252-257.
4. Philadelphia, WB Saunders Co, 1995, pp 1124-1142. 42. Summers RW, Yanda R, Prihoda M, et al: Acute intestinal
22. Ptymak C, Saunders HM, Washabau RJ: Hiatal hernia re- obstruction: An electromyographic study in dogs. Gastroen-
pair by restoration and stabilization of normal anatomy. Vet terology 85:1301-1306, 1983.
Surg 18:386-391, 1989. 43. Prihoda M, Flatt A, Summers RW: Mechanisms of motility
23. Johnson SE, Zeiner H, Sherding RG: Esophageal acid clear- changes during acute intestinal obstruction in the dog. Am J
ance test in healthy dogs. Can] Vet Res 53:244-247, 1989. Physiol247:G37-G42, 1984.
24. Hall JA, Magne M, Twedt DC: Effect of acepromazine, di- 44. Moore R, Carpenter J: Intestinal sclerosis with pseudo-
azepam, fentanyl-droperidol, and oxymorphone on gastro- obstruction in three dogs.jAVMA 184:830-833, 1984.
esophageal sphincter pressure in healthy dogs. Am j Vet Res 45. Otterson MF, Sarna SK, Moulder JE: Effects of fractionated
48:556-558, 1987. doses of ionizing radiation on small intestinal moror activity.
25. Evander A, Little AG, Riddell RH, et al: Composition of the Gastroenterology 95:1249-1257, 1988.
refluxed material determines the degree of reflux esophagitis 46. Summers RW, Flatt AJ: A comparative study of the effects
~
19 in the dog. Gastroenterology 93:280-286, 1987. of four moror-stimulating agents on canine jejunal spike
26. Patrikios J, Marrin CJ, Dent J: Relationship of transient bursts. Scandj Gastroenterol23:1173-ll81, 1988.
736 Small Animal The Compendium June 1997

4 - . Schemann M, Ehrlein HJ: 5-hydroxytryprophan and cis- d. prokinetic agents (e.g., cisapride or metoclopramide).
apri de stimulate propulsive jejunal motility and transit of e. all of the above
chyme in dogs. Digestion 34:229-235, 1986.
48. Edelbroek M, Schuurkes JAJ, de Ridder WJE, et al: Effect of
3. The preferred colonic prokinetic agent for treating
cisapride on myoelectrical and motor responses of antropy-
loroduodenal region during inrraduodenal lipid and antral patients with idiopathic megacolon is
tachygastria in conscious dogs. Dig Dis Sci 40:901-911, a. metoclopramide.
1995. b. domperidone.
49. Jouet P, Sarna SK, Singaram C, et al: Immunocytes and ab- c. cisapride.
normal gastrointestinal motor activity during ileitis in dogs. d. erythromycin.
Am j Physiol269:G913-G924, 1995. e. sucralfate.
50. Jouet P, Sarna SK: Platelet-activating factor stimulates giant
migrating contractions during ileal inflammation. J Pharma- 4. Which of the following groups of laxatives should be
col Exp Ther 279:207-213, 1996. avoided in treating constipated cats?
51. Washabau RJ, Hasler AH: Constipation, obstipation, and
a. hyperosmotic laxatives (e.g., sodium phosphate)
megacolon, in August JR (ed): Consultations in Feline Inter-
nal Medicine. Philadelphia, WB Saunders Co, 1996, pp
b. emollient laxatives (e.g., dioctyl sodium sulfosucci-
104-113. nate)
52. Washabau RJ, Stalis I: Alterations in colonic smooth muscle c. lubricant laxatives (e.g., mineral oil)
function in cats with idiopathic megacolon. Am J Vet Res d. bulk laxatives (e.g., psyllium)
57:580-587, 1996. e. stimulant laxatives (e.g., bisacodyl)
53. Atkins CE, Tyler R, Greenlee P: Clinical, biochemical,
acid-base, and electrolyte abnormalities in cats after hyper- 5. Patients with gastric emptying disorders usually bene-
tonic sodium phosphate enema administration. Am J Vet Res fit from diets that are
46:980-986, 1985.
a. enriched in lipids over carbohydrates.
54. Washabau RJ, Sammarco J: Effects of cisapride on feline
b. fed at cold temperatures.
colonic smooth muscle function. Am] Vet Res 57:541-546,
c. fed in a solid (not a liquid) consistency.
1996.
d. high in acidity.
55. Sethi AK, Sarna SK: Colonic motor activity in acute colitis
in conscious dogs. Gastroenterology 100:954-962, 1991.
e. low in osmolality.
56. Sethi AK, Sarna SK: Colonic motor response to a meal in
acure colitis. Gastroenterology 101:1537-1546, 1991. 6. The best prokinetic agents for treating patients with
delayed gastric emptying disorders are the
a. 5-HT4 serotonergic receptor agonists (e.g., cis-
apride), motilin agonists (e.g., erythromycin), and
acetylcholinesterase inhibitors (e.g., ranitidine).
ARTICLE #4 REVIEW QUESTIONS b. D 2 dopaminergic receptor antagonists (e.g., dom-
The article you have read qualifies for ltz hour of peridone) and acetylcholinesterase inhibitors (e.g.,
Continuing Education Credit from the Auburn cimetidine).
University College of Veterinary Medicine. Choose c. M 1 muscarinic cholinergic receptor antagonists
only the one best answer to each of the following (e.g., aminopentamide) and 5-HT 3 serotonergic
questions; then mark your answers on the test receptor antagonists (e.g., ondansetron).
form inserted in The Compendium. d. 11,0-opioid receptor agonists (e.g., loperamide) and
motilin agonists (e.g., erythromycin).
e. 5-HT3 serotonergic receptor antagonists (e.g., on-
1. The most important cause of acquired-onset mega- dansetron) and acetylcholinesterase inhibitors (e.g.,
esophagus is nizatidine).
a. hypoadrenocorticism.
b. lead poisoning. 7. Mechanical obstruction of the small intestine cannot
c. myasthenia gravis. be treated by
d. idiopathic, probably neuropathy. a. surgical reduction of intussusception.
e. polymyositis. b. retrieval of foreign bodies.
c. gastrointestinal prokinetic therapy.
2. The treatment of gastroesophageal reflux and reflux d. chemotherapy.
esophagitis could include e. partial enterectomy.
a. low-fat diets.
b. chemical diffusion barriers (e.g., sucralfate). 8. The preferred prokinetic agent for treating patients
c. H 2 histaminergic receptor antagonists (e.g., cimeti- with intestinal pseudo-obstruction is
dine or ranitidine). a. cisapride.
 View publication stats

The Compendium June 1997 Small Animal 737 Droncir

(praziquantel)
Injectable Cestocide For Dogs And Cats
And Canine Cestocide Tablets
b. domperidone. PRODUCT DESCRIPTION
c. sucralfate. Droncit Injectable Cestocide is a clear solution containing 56.8
milligrams of praziquantel per ml.
d. omeprazole. Each DronciF Canine Cestocide Tablet contains 34mg of
praziquantel.
mg I I I e. ranitidine.
INDICATIONS
Droncit (praziquantel) Injectable Cestocide is indicated for th e
removal of the following canine and/or feline cestodes. Dogs:
9. The pathogenesis of most cases of feline idiopathic Dipylidium caninum, Taenia pisiformis, Echinococcus granulosus
and for the removal and control of Echinococcus multilocularis. Cats:
megacolon is believed to involve Taenia taeniaeformis and Dipylidium caninum.
DronciF (praziquantel) Canine Cestocide Tab lets are indicated
a. endocrinopathy. for the removal of the following canine cestodes: Dipylidium can·
b. colonic inflammation. inurn, Taenia pisiformis, Echinococcus granulosus and for the
removal and control of Echinococcus multilocularis.
c. enteric neuronal abnormalities. PRECAUTIONS
be d. colonic smooth muscle abnormalities. Strict hygienic precautions should be taken when handling dogs
or feces suspected of harboring E. multilocularis. Infected dogs
e. pharmacologic side effects. treated for the first time with Droncit Injectable solution and dogs
treated at intervals greater than 28 days may shed eggs in the feces
after treatment. The animal should be held in the clinic during this
Cl- interval and all feces should be incinerated or autoclaved. If these
10. Which of the following is an esophageal motility dis- procedures are not possible, the eggs can be destroyed by soak·
order rhat might cause both mechanical and function- ing the feces in a sodium hypochlorite (bleach) solution of 3.75%
or greater'. All areas where the animal was maintained or in con-
al obstruction? tact with should be thoroughly cleaned with sodium hypochlorite
and allowed to dry completely before reuse.
a. hiatal hernia
ADVERSE REACTIONS
b. esophagitis Mild side effects were observed in 18 of 189 dogs (9.5%) and
c. idiopathic megaesophagus 8 of 85 cats (9.4%) administered Droncit Injectable in field trials.
ne- For dogs the majority of these were described as brief pain
d. gasrroesophageal reflux responses following injections to larger dogs (weighing over 50
lbs.). Two dogs exhibited a brief period of mild vomiting and/or
e. dysautonomia drowsy or staggering gait. The eight cats exhibited either diarrhea,
weakness, vomition , salivation , sleepiness, burning on injection
and/or a temporary lack of appetite. Local irritatio n or swelling at
the site of subcutaneous injections have been reported for cats.
Seven instances (3.2%) of either vomiting, anorexia. lethargy or
diarrhea were reported dunng the field trials in which 218 dogs were
administered DronciF Canine Cestocide Tablets. The investigators
rated these as non-significant.
Advances (continued from page 671) WARNING
Keep out of the reach of children. Not for human use.
CAUTION
Federal (U.S.A.) law restricts this drug to use by or on the order
role of critical care technicians age the formation of more 24- of a licensed veterinarian.
and nurses. These individuals hour full-service facilities. REFERENCES
1 Craig, P.S. and McPharson C.N.L. , 1988 Sodium Hypochlonte as
have become very important to an Ovicide for Echinococcus. Ann Trap Med and Parasit 82(2)
the emergency/ critical care 211-213.
Injectable NADA 111-607, Approved by FDA Canme Tablets NADA
teams. The role and number of 111-798, Approved by FDA
advanced-trained, AVECCT-cer-
ABOUT THE AUTHOR Droncir
tified technicians will continue
Colonel Stamp is currently (praziquantel}
to expand. Feline Cestocide Tablets
the Commander, Head-
Each tablet contains 23 mg praziquante..
quarters, U.S. Army Veteri-
Summary INDICATIONS
nary Command, Fort Sam DronciF Feline Cestocide Tablets are mdicated for the removal
n-
Emergency/critical care Houston , San Antonio , of the follo wing feline cestodes: Dipylidium camnum and Taenia
g., medicine is unique in that it relies
taeniaeformis.
Texas and is the Executive ADVERSE REACTIONS
heavily on a blend of technology Secretary of the Veterinary One instance of diarrhea and one of sal vat1on (1. 5%) were
reported during the field trials in wh1ch 135 cats were administered
and effective nursing care. There Emergency and Critical DronciF Feline Cestocide.
Ot
will continue to be significant ad- Care Society. He has Doc- WARNING:
Keep out of the reach of children. Not for human use.
vances in specialist and techni- tor of Medicine and Master CAUTION:
cian training as interest grows of Science degrees. He is a Federal (U.S.A.) law restncts th1s drug to use by or on the order
of a licensed veterinarian.
exponentially in this discipline. Diplomate of the American
User-friendly, economical but College of Veterinary
sophisticated technology made Emergency and Critical Bayerffi
increasingly available to an en- Care and a Diplomate of
rs larging pool of progressive the American Board of Vet-
Bayer Corporation, Agnculture Division
emergency/critical care practi- erinary Practitioners. Animal Health, Shawnee Mission, Kansas 66201
tioners will undoubtedly encour- ©1997, Bayer Corporation