Veterinary Medicine

Canine Parvovirus

1. What are the common clinical signs in dogs with canine parvovirus (CPV)?

• Lethargy

• Vomiting

• Inappetence

• Fever

• Acute-onset diarrhea

• Profound neutropenia (white blood cells < 1000/mm3)

Puppies between the ages of 6 weeks to 6 months are most commonly affected. In a Canadian study, sexually intact dogs had a 4-fold greater risk than spayed or neutered dogs, and the months of July, August, and September had a 3-fold increase in cases of canine parvovirus.

2. What systems other than the GI tract are involved with canine parvovirus?

In a study of dogs with the GI form of canine parvovirus, arrhythmia was diagnosed in 21 of 148 cases, including supraventricular arrhythmias and conduction disturbances. Some dogs developed significant enlargement of the cardiac silhouette and other radiographic cardiac abnormalities. CPV can replicate in bone marrow, heart, and endothelial cells; replication in endothelial cells of the brain produces neurologic disease.

3. What other infectious diseases may be mistaken for canine parvovirus infection?

Infection with Salmonella sp., Campylobacter sp., or Escherichia coli may mimic canine parvovirus symptoms and also cause the shift in white blood cells. CPV infection also may be confused with hemorrhagic gastroenteritis (HGE), although HGE is seen most commonly in smaller breeds and usually resolves in 24 hours. Coronavirus often presents with GI signs, but neutropenia tends to resolve more rapidly than with canine parvovirus infection. Clinical signs of infection with coronavirus are usually seen only in dogs also infected with parvovirus.

4. What is the primary mode of transmission of canine parvovirus?

The number of viral particles in the feces is quite high; the fecal-oral route is the most likely means of transmission. No studies of vomitus have been done, but it probably contains viral particles.

5. How does canine parvovirus infect the intestines?

Viral replication occurs in the oropharynx during the first 2 days of infection, spreading to other organ systems via the blood. By the third to fifth day a marked viremia develops. The virus reaches the intestinal mucosa from the blood rather than from the intestinal lumen. Clinical signs are seen 4-5 days after exposure, and the incubation period ranges from 3-8 days, with shedding of the virus on day 3.

6. Where does canine parvovirus replicate in the body?

The virus replicates in rapidly dividing cells, which include lymph nodes, spleen, bone marrow, and intestines. In the intestines, viral replication kills the germinal epithelium of the intestinal crypts, leading to epithelial loss, shortening of the intestinal villi, vomiting, and diarrhea. Lymphoid necrosis and destruction of myeloproliferative cells result in lymphopenia and, in severe cases, panleukopenia. Only about one-third of canine parvovirus cases have defined neutropenia or lymphopenia.

7. How has the clinical presentation of CPV infection changed since the 1970s?

There are several strains of canine parvovirus, including the original strain, CPV-1; the minute virus; and the most severe strain, CPV-2 (with subtypes 2a and 2b). CPV-2b is now the most common strain in the United States. CPV-1, which dominated in the 1970s, caused a milder disease associated with fever and a larger window for treatment. CPV-2b causes a more explosive acute syndrome that affects young dogs 6-12 weeks of age, making the window between the first signs of GI upset and treatment much narrower and more critical. There have been no major changes in presentation in the past 6 years; lethargy, listlessness, and bloody diarrhea are the most common presenting signs. Other diseases associated with or mistaken for canine parvovirus are canine distemper virus, coccidial or giardial infection, hookworms, roundworms, or a combination of these.

8. When and how does one diagnose canine parvovirus?

CPV is most easily diagnosed with a fecal enzyme-linked immunosorbent assay (ELIS A). If the test is negative but canine parvovirus is still suspected, isolate the animal and run the test again in 48 hours. The virus is not usually shed until day 3, and conscientious clients may bring the animal to the hospital at the first sign of illness. The period during which canine parvovirus is shed in the feces is brief, and the virus is not usually detectable until day 10-12 after infection. Usually the acute phase of illness has passed by this time. Modified live canine parvovirus vaccines shed in the feces may give a false-positive ELISA result 4-10 days after vaccination.

One also may use a combination of ELISA, complete blood count, and radiographs to diagnose canine parvovirus. Radiographs may help to rule out the possibility of an intestinal foreign body, and detection of generalized ileus with fluid-filled loops of intestines supports the diagnosis of canine parvovirus. Be sure to have enough antigen in the fecal sample when running the ELISA; watery stools may dilute the antigen and give a false-negative result.

Conclusive proof of canine parvovirus infection is made with electron microscope identification of the virus.

9. What are the recommendations for inpatient care of dogs with CPV?

1. Aggressive fluid therapy. Correct dehydration and provide intravenous maintenance fluid volumes of a balanced crystalloid solution. Make every attempt to replace continuing losses (vomitus and diarrhea) with equal volumes of crystalloid fluids. The easiest method is simply to estimate the volume lost and double your estimate. Continuing losses need to be replaced at the time that they occur. Use Normosol with at least 20 mEq/L of potassium chloride supplementation. Monitor glucose level. If necessary, add 2.5-5% dextrose to intravenous fluids. A 5% dextrose solution creates an osmotic diuresis, but it also allows assessment of progress in dealing with a septic case (glucose increases when the animal receives 5% dextrose if the sepsis is resolving). Low levels of magnesium chloride may be added to fluids to help correct unresponsive hypokalemia.

2. Antibiotic therapy. Broad-spectrum parenteral antibiotics are recommended because of disruption of the mucosal barrier and potential sepsis. Bacteremia is identified in 25% of dogs infected with parvovirus. A combination of ampicillin and gentamicin is recommended. Most veterinarians use only a first-generation cephalosporin in dogs without neutropenia or fever and reserve ampicillin and gentamicin or amikacin for dogs with signs of sepsis. One should be cautious about using an aminoglycoside because of renal toxicity.

3. Endotoxin-neutralizing products. Endotoxin-neutralizing products may be administered along with antibiotic therapy. The rationale for their use is based on the large population of gram-negative bacteria; by killing the bacteria, antibiotic therapy may shower the body with en-dotoxin, thus exacerbating the canine parvovirus condition. Studies have shown that endotoxin-neutralizing products decrease the incidence of septic shock. They may be diluted (4 ml/kg) with an equal volume of saline and administered intravenously over 30-60 minutes. Dogs who have recovered from parvovirus infections can be a good source for serum. Serum should be collected within 4 months of infection.

4. Antiemetics. Metoclopramide is the drug of choice. Phenothiazine derivatives should be used with caution and only after adequate volume replacement is initiated to avoid severe hypotension. Antiemetics are especially useful when continued vomiting makes it difficult to maintain hydration or electrolyte balance.

5. Motility modifiers. The use of motility modifiers is controversial. Anticholinergic anti-diarrheal medications may suppress segmental contractions and actually hasten transit time. Narcotic analgesics and synthetic opiates are better choices but should be reserved for severe or prolonged cases because slowing the flow through the intestine may increase toxin absorption.

6. Nothing per os (NPO). Begin a slow return to water 24 hours after the animal stops vomiting, and slowly progress to gruel made from a bland diet.

10. What is granulocyte colony-stimulating factor (GCSF)? What role does it have in treating dogs with CPV?

Granulocyte colony-stimulating factor selectively stimulates release of granulocytes form the bone marrow. Preliminary studies have shown that it reduces morbidity and mortality due to canine parvovirus. Unfortunately, it is available only as a human drug and is expensive, but when the positive benefits are considered, its use may be justified.

11. Does interferon benefit a dog with parvovirus infection?

Interferon given parenterally has been shown to be beneficial. The suggested dosage of human recombinant interferon is 1.3 million units/m2 subcutaneously 3 times/week.

12. How is a dog with canine parvovirus monitored?

Monitor respiration and central venous pressure (CVP) to prevent overhydration. With osmotic diarrhea the animal loses protein. If abdominal or extremity swelling is observed or if the total solids drop by 50% from admission values or go below 2.0 gm/dl, the animal should be supplemented with either 6% hetastarch or plasma to maintain colloid oncotic pressures. Blood glucose should be monitored at least 4 times/day on the first two days. Glucose level may drop precipitously and suddenly. Most importantly, weigh the dog at least twice each day. If adequate crystalloid replacement is provided, body weight does not decrease from initial values. Ideally body weight should increase at a rate comparable to the degree of dehydration originally assessed. Dogs that can hold down water for 12 hours may be offered a gruel made from bland foods. Most dogs force-fed by hand will vomit. This response may be physical or psychological (association of food with vomiting). Nasogastric tubes seem to help this problem. Metoclopramide speeds gastric emptying, acts as an antiemetic, and decreases gastric distention when added to the liquid diet. Dogs that are not vomiting should be offered food even if the diarrhea has not totally stopped. A low-fat, high-fiber diet is a good choice to stimulate intestinal motility.

13. How do you know when to send a dog home?

The dog should stay in the hospital for 12 hours after it has ingested solid food with no vomiting. Clients should report immediately any vomiting in the next 7 days or refusal to eat for 24 hours. A high-fiber diet is recommended for reducing diarrhea. A recheck appointment in 1 week with a stool sample helps the clinician to assess progress.

14. What recommendations do you offer to clients who have had a CPV-infected animal in their household and now want a new pet?

Prevention involves a proper vaccination regimen, limited exposure to other animals (especially in puppies less than 12 weeks of age), cleaning contaminated areas with bleach (allowing prolonged contact time), and vacuuming all surfaces with which the previous pet came into contact (rugs, carpet, walls, furniture). Newer higher-titer vaccines (some of which may be started as early as 4 weeks) are helpful. Generally, one should wait at least 1 month before bringing the new pet into the home. It is doubtful that the environment (especially outdoors) will ever be completely free of the virus. Canine parvovirus is a hardy and ubiquitous organism.

15. How long can a dog with CPV be expected to retain immunity?

A dog that has recovered from canine parvovirus can maintain life-long immunity.

16. What is the recommended vaccination schedule for dogs? Is it the same for every breed?

Some breeds are more susceptible to canine parvovirus than others. Rottweilers, American pitbull terriers, Doberman pinschers, and German shepherds are the most susceptible, whereas toy poodles and Cocker spaniels are less susceptible. The new higher-titer vaccines have a higher antigen level and a more virulent vaccine strain that can overcome maternal antibodies, unlike the older lower-titer vaccines. These vaccines narrow the window of infection, especially for susceptible breeds. The vaccination protocol for the new high-titer vaccines is 6, 9, and 12 weeks. Susceptible breeds should be vaccinated only with the high-titer canine parvovirus vaccine and then with a combination vaccine at 6-8, 12, and 16 weeks. For less susceptible breeds, the combination vaccines at 6-8, 12, and 16 weeks should be adequate. Some parvovirus vaccines are approved for use as early as 4 weeks of age.

17. How do you manage a sick puppy when the client is unwilling to pursue hospital treatment for CPV?

Canine parvovirus can be treated on an outpatient basis. A combination of dietary restriction, subcutaneous fluids, and, in some cases, GI medications may be used with a follow-up appointment in 1-3 days. Outpatient recommendations include the following:

• Small, frequent amounts of fluid

• Bland food

• Oral antibiotics

• Strong recommendation to have the pet reexamined and admitted for therapy if vomiting returns or anorexia persists

Nine of ten clients bring the dog back for inpatient care shortly after taking it home. Before treating an outpatient, remember that mildly depressed dogs may have a rectal temperature of 106° F and a blood glucose of 30 mg/dl in 12 hours or less.

18. Should a dog with suspected CPV be hospitalized and placed in isolation?

Undoubtedly hospitalization provides the best chance for survival. Isolation is more controversial. In most veterinary hospitals, isolation means that the animal is housed in a section of the hospital that is not staffed at all times. The adage “out of sight, out of mind” has led to the demise of many CPV-infected dogs. Experience with housing dogs with canine parvovirus in the critical care unit at the Veterinary Teaching Hospital of Colorado State University has shown that nosocomial infections can be avoided with a common-sense approach to patient management. The animal is placed in the least traveled area and has its own cleaning supplies; gowns and gloves are worn each time the animal is handled; and the animal’s cage is kept as clean as humanly possible. These procedures are no different from those in an isolation area. By being housed in an area where constant attention can be given, the animal receives adequate fluid replacement therapy and is monitored for changes, which occur rapidly.

19. How is nutrition provided for vomiting dogs?

Tough question! Dogs that have not eaten for 3-5 days are probably in a negative nitrogen balance, and certainly intestinal villi have undergone atrophy if not already destroyed by the canine parvovirus. The sooner patients begin receiving oral nutrition, the more rapidly they will recover. In addition, micronutrient therapy for the intestinal mucosa is required for maintenance of the mucosal barrier. Without this barrier, sepsis and bacteremia are more likely. Unfortunately, the only means to provide micronutrients is the oral route.

Glucose therapy does not provide nutritional support. It is best to think of dextrose as simply a source of water. One liter of 5% dextrose solution contains a mere 170 kcal. Increasing dextrose concentrations beyond 5% usually results in glycosuria and osmotic diuresis.

Patients that have not eaten for several days are primed for fat metabolism; thus, Intralipid (20%) may be added to fluids. It should be administered through a central IV catheter and requires strict aseptic management, which may be difficult if the patient is in an isolation area of the hospital.

For dogs that retain water without vomiting, glutamine may be added directly to the water bowl. Often placing electrolyte solutions in the water bowl is a good way to start the animal drinking. Placing dextrose in these fluids or even using commercial solutions such as Ensure-Plus in the bowl helps to provide intestinal nutrients.

20. Should parvovirus antibody levels be measured to check the immune status of the puppy?

Although antibodies to parvovirus can be measured, a negative titer does not necessarily mean that the dog is susceptible to canine parvovirus. Repeated revaccination of antibody-negative dogs usually does not result in significant titers.

Veterinary Medicine

Esophageal Disorders

1. What is the most common clinical sign of an esophageal disorder?


2. What is the difference between regurgitation and reflux?

Regurgitation refers to passive, retrograde movement of ingested material to a level proximal to the upper esophageal sphincter; usually this material has not reached the stomach. In most cases, regurgitation results from abnormal esophageal peristalsis, esophageal obstruction, or asynchronous function of the gastroesophageal junction.

Reflux refers to the movement of gastric and duodenal contents into the esophagus without associated eructation or vomiting.

3. List the causes of regurgitation.

1. Megaesophagus

• Idiopathic

• Secondary

  • Myasthenia gravis
  • Polyneuropathy
  • Systemic lupus erythematosus
  • Polymyositis
  • Toxicosis (lead, thallium)
  • Hypothyroidism
  • Hypoadrenocorticism

2. Esophageal foreign body

3. Esophageal stricture

• Intraluminal stricture

• Extraluminal stricture due to compression

  • Abscess
  • Cranial mediastinal mass
  • Thoracic hilar lymphadenopathy

4. Vascular ring anomaly

5. Neoplasia (primary or metastatic)

6. Granuloma (e.g., Spirocerca lupi)

7. Hiatal hernia

8. Esophageal diverticula

4. What is megaesophagus?

Megaesophagus is a specific syndrome characterized by a dilated, hypoperistaltic esophagus.

5. What is the most common complication of megaesophagus?

Aspiration pneumonitis.

6. Does esophageal dilatation on thoracic radiographs confirm an esophageal disorder?

No. The following conditions often produce transient dilatation of the esophagus:

• Aerophagia

• Anxiety

• Respiratory distress (dyspnea)

• Anesthesia

• Vomiting

7. How is esophageal motility evaluated?

Thoracic radiography initially evaluates for evidence of an esophageal foreign body, esophageal dilatation, or thoracic mass. Ideally a barium esophagogram with fluoroscopy should be performed. It is best to mix food with the barium to observe for decreased contractility.

8. What is myasthenia gravis?

Myasthenia gravis is an immune-mediated disorder, either acquired or congenital (familial), resulting from the action of autoantibodies against nicotinic acetylcholine receptors at the neuro-muscular junctions.

9. What are the most common clinical signs of myasthenia gravis?

• Premature fatigue with exercise

• Spastic pelvic limb gait

• Tetraparesis

• Collapse

• Tachypnea

• Respiratory distress

• Sialosis

• Regurgitation

• Dysphagia

• Weakness of facial muscles

• Decreased palpebral reflex

10. What is the test of choice for myasthenia gravis?

Acetylcholine receptor antibody titers (> 0/6 nM/L) in dogs. Antibodies are detectable in 80-90% of dogs with acquired disease.

11. What other tests can be used for myasthenia gravis?

• Edrophonium response test. Edrophonium (0.1-0.2 mg/kg IV) results in dramatic improvement in gait for 1-2 minutes in many but not all animals. Pretreatment with atropine (0.02 mg/kg IV) decreases salivation, defecation, urination, bronchosecretion, and bronchoconstriction. Oxygen and an endotracheal tube should be readily available.

• Ten percent or greater decremental response to the fourth or fifth compound action potential recorded from the interosseous muscle after repetitive stimulation of the tibia or ulnar nerve at 3 Hz.

• Increase in jitter on single-fiber electromyography.

• Intercostal muscle biopsy identifying acetylcholine receptor antibodies at the neuromuscular junction.

12. Describe the typical profile of a dog with myasthenia gravis.

• Breeds most commonly affected: golden retriever, German shepherd

• Bimodal age of onset: 2-4 years and 9-13 years

13. How is myasthenia gravis treated?

1. Anticholinesterase drugs — neostigmine

• Injectable (Prostigmin [Roche]): 0.02 mg/lb IM every 6 hr

• Oral (Mestinon [Roche]): 0.25-0.45 mg/lb every 8-12 hr

2. Corticosteroids

14. Describe the principles for management of megaesophagus.

1. Remove the cause if possible.

2. Minimize chances for aspiration of esophageal contents. (Feed the animal in an upright position so that the upper body is elevated to at least 45° above the lower body. Maintain this position for at least 10 minutes after eating and before bedtime.)

3. Maximize nutrient intake to the GI tract (if possible, feed 2-4 times/day).

15. What is an alternative means of feeding dogs with megaesophagus?

Gastrostomy tube.

16. What is the prognosis for a dog with megaesophagus?

Guarded to poor.

17. List causes of esophageal stricture in dogs.

• Esophagitis

• Reflux of gastric acid during general anesthesia (on a tilted operating table)

• Ingestion of a strong acid or alkali material

• Esophageal foreign bodies

• Thermal burns

• Hairballs (cats)

18. How is esophageal stricture diagnosed?

Esophageal stricture is diagnosed by barium esophagogram and esophageal endoscopy.

19. List the treatment options for esophageal stricture and the success rate for each.

• Surgery (esophagotomy, patch grafting, resection and anastomosis): < 50% success

• Esophageal bougienage: 50-70% success

• Balloon catheter dilatation: > 50-70% success (treatment of choice, ideally done under fluoroscopy)

20. What are the most common areas of the esophagus in which foreign bodies lodge?

• Thoracic inlet

• Hiatus of the diaphragm

• Base of the heart

21. How do you manage dogs with an esophageal foreign body?

Esophageal foreign bodies are considered an emergency. The following steps are recommended:

1. Endoscopic removal of the foreign body is usually successful. Either extract the foreign body or carefully push it into the stomach. If the foreign body is a bone, it is often best to push it into the stomach. Gastrostomy is not usually required for removal of the bone, but serial radiography should be done to ensure digestion or passage of the bone.

2. If esophagoscopy is unsuccessful, surgical removal is required.

3. Assess the esophageal mucosa for hemorrhage, erosions, lacerations, or perforations.

4. Withhold food and water for 24-48 hours, and give crystalloid fluids and parenteral antibiotics.

22. What treatments are available for esophageal reflux?

Metoclopramide (Reglan) increases gastroesophageal sphincter tone and decreases gastric reflux into the stomach.

H2 receptor-blocking agents (e.g., cimetidine or ranitidine) reduce the acidity of refluxed gastric contents.

Sucralfate suspension is an aluminum salt that selectively binds to injured gastroesophageal mucosa and acts as an effective barrier against the damaging actions of gastric acid, pepsin, and bile acids associated with reflux esophagitis.

Veterinary Medicine

Canine Hemorrhagic Gastroenteritis

1. What is canine hemorrhagic gastroenteritis (HGE)?

Canine hemorrhagic gastroenteritis is a syndrome characterized by the acute onset of profuse vomiting and bloody diarrhea with significant hemoconcentration.

2. What is the cause3 of hemorrhagic gastroenteritis?

The cause is unknown. Although the term hemorrhagic gastroenteritis implies an inflammatory condition, the disease is more likely due to altered intestinal mucosal permeability and perhaps mucosal hypersecretion. Cultures of GI contents from HGE-affected dogs have yielded large numbers of Clostridium perfringens, leading to speculation that this organism or its exotoxins are the cause.

3. Which dogs are most likely to be affected with HGE?

Toy and miniature breeds seem particularly prone to HE (hemorrhagic gastroenteritis), especially toy and miniature poodles and schnauzers, but the syndrome may affect any breed.

4. What are the clinical signs of hemorrhagic gastroenteritis?

• Acute onset of vomiting

• Profuse, bloody, fetid diarrhea

• Severe depression

• Shock

5. How is the diagnosis of HGE made?

• Extreme hemoconcentration (packed cell volume > 50-60%)

• Bloody, fetid diarrhea

• No leukopenia

• Fecal cytology with increased numbers of clostridial organisms

6. Describe the treatment for hemorrhagic gastroenteritis.

• Intensive fluid therapy until the packed cell volume is in the normal range and then continued intravenous crystalloid fluids (Normosol-R + potassium chloride) until vomiting is controlled.

• Antibiotics to control C. perfringens (ampicillin or amoxicillin)

• Restriction of food and water

• Antiemetic drugs (metoclopramide)

7. What is the prognosis of hemorrhagic gastroenteritis?

• Early, aggressive fluid therapy consistently results in significant improvement within 24 hours.

• If vomiting and diarrhea are not resolved in 48 hours, a search for other causes mimicking hemorrhagic gastroenteritis should be conducted (parvovirus, coronavirus, GI foreign bodies, intussusception, intestinal volvulus, clostridial enteritis, lymphocytic-plasmocytic enteritis).

Veterinary Drugs



An ethanolamine derivative antihistamine, dimenhydrinate contains approximately 54% diphenhydramine and 46% 8-chlorotheophylline. It occurs as an odorless, bitter and numbing-tasting, white crystalline powder with a melting range of 102°-107°C. Dimenhydrinate is slightly soluble in water and is freely soluble in propylene glycol or alcohol. The pH of the commercially available injection ranges from 6.4 to 7.2.

Storage – Stability – Compatibility

Dimenhydrinate products should be stored at room temperature; avoid freezing the oral solution and injectable products. The oral solution should be stored in tight containers and tablets stored in well-closed containers.

Dimenhydrinate injection is reportedly compatible with all commonly used intravenous replenishment solutions and the following drugs: amikacin sulfate, atropine sulfate, calcium gluconate, chloramphenicol sodium succinate, corticotropin, ditrizoate meglumine and sodium, diphenhydramine HCl, droperidol, fentanyl citrate, heparin sodium, iothalamate meglumine and sodium, meperidine HCl, methicillin sodium, metoclopramide, morphine sulfate, norepinephrine bitartrate, oxytetracycline HCl, penicillin G potassium, pentazocine lactate, perphenazine, phenobarbital sodium, potassium chloride, scopolamine HBr, vancomycin HCl and vitamin B-complex w/ vitamin C.

The following drugs are either incompatible or compatible only in certain concentrations with dimenhydrinate: aminophylline, ammonium chloride, amobarbital sodium, butorphanol tartrate, glycopyrrolate, hydrocortisone sodium succinate, hydroxyzine, iodipamide meglumine, pentobarbital sodium, prochlorperazine edisylate, promazine HCl, promethazine HCl, tetracycline HCl, and thiopental sodium. Compatibility is dependent upon factors such as pH, concentration, temperature, and diluents used and it is suggested to consult specialized references for more specific information.

Dimenhydrinate: Pharmacology

Dimenhydrinate has antihistaminic, antiemetic, anticholinergic, CNS depressant and local anesthetic effects. These principle pharmacologic actions are thought to be a result of only the diphenhydramine moiety. Used most commonly for its antiemetic/motion sickness effects, dimenhydrinate’s exact mechanism of action for this indication is unknown, but the drug does inhibit vestibular stimulation. The anticholinergic actions of dimenhydrinate may play a role in blocking acetylcholine stimulation of the vestibular and reticular systems. Tolerance to the CNS depressant effects can ensue after a few days of therapy and antiemetic effectiveness also may diminish with prolonged use.

Dimenhydrinate: Uses – Indications

In veterinary medicine, dimenhydrinate is used primarily for its antiemetic effects in the prophylactic treatment of motion sickness in dogs and cats.


The pharmacokinetics of this agent have apparently not been studied in veterinary species. In humans, the drug is well absorbed after oral administration with antiemetic effects occurring within 30 minutes of administration. Antiemetic effects occur almost immediately after IV injection. The duration of effect is usually 3-6 hours.

Diphenhydramine is metabolized in the liver, and the majority of the drug is excreted as metabolites into the urine. The terminal elimination half-life in adult humans ranges from 2.4 – 9.3 hours.


Dimenhydrinate is contraindicated in patients who are hypersensitive to it or to other antihistamines in its class. Because of their anticholinergic activity, an-tihistamines should be used with caution in patients with angle closure glaucoma, prostatic hypertrophy, pyloroduodenal or bladder neck obstruction, and COPD if mucosal secretions are a problem. Additionally, they should be used with caution in patients with hyperthyroidism, seizure disorders, cardiovascular disease or hypertension. It may mask the symptoms of ototoxicity and should therefore be used with this knowledge when concomitantly administering with ototoxic drugs.

Dimenhydrinate: Adverse Effects – Warnings

Most common adverse reactions seen are CNS depression (lethargy, somnolence) and anticholinergic effects (dry mouth, urinary retention). GI effects (diarrhea, vomiting, anorexia) are less common, but have been noted.

The sedative effects of antihistamines, may adversely affect the performance of working dogs. The sedative effects of antihistamines may diminish with time.

Dimenhydrinate: Overdosage

Overdosage may cause CNS stimulation (excitement to seizures) or depression (lethargy to coma), anticholinergic effects, respiratory depression and death. Treatment consists of emptying the gut if the ingestion was oral. Induce emesis if the patient is alert and CNS status is stable. Administration of a saline cathartic and/or activated charcoal may be given after emesis or gastric lavage. Treatment of other symptoms should be performed using symptomatic and supportive therapies. Phenytoin (IV) is recommended in the treatment of seizures caused by antihistamine overdose in humans; use of barbiturates and diazepam are avoided.

Dimenhydrinate: Drug Interactions

Increased sedation can occur if dimenhydrinate (diphenhydramine) is combined with other CNS depressant drugs. Antihistamines may partially counteract the anticoagulation effects of heparin or warfarin. Diphenhydramine may enhance the effects of epinephrine. Dimenhydrinate may potentiate the anticholinergic effects of other anticholinergic drugs. Dimenhydrinate has been demonstrated to induce hepatic microsomal enzymes in animals (species not specified); the clinical implications of this effect are unclear.

Laboratory Interactions – Antihistamines can decrease the wheal and flare response to antigen skin testing. In humans, it is suggested that antihistamines be discontinued at least 4 days before testing.

Dimenhydrinate: Doses

Doses for dogs:

For prevention and treatment of motion sickness:

a) 8 mg/kg PO q8h

b) 25 – 50 mg PO once to 3 times a day

c) 4 – 8 mg/kg PO q8h

Doses for cats:

For prevention and treatment of motion sickness:

a) 12.5 mg (total dose) PO q8h

b) 12.5 mg PO once to 3 times a day

c) 8 mg/kg PO q8h

d) 4 – 8 mg/kg PO q8h

Monitoring Parameters

1) Clinical efficacy and adverse effects (sedation, anticholinergic signs, etc.)

Dosage Forms – Preparations – FDA Approval Status – Withholding Times

Veterinary-Approved Products:


Human-Approved Products:

Dimenhydrinate Tablets or capsules 50 mg; Commonly known as Dramamine® (Upjohn) (OTC); Many other OTC products also available

Dimenhydrinate Oral Liquid 12.5 mg/4 ml, 12.5 mg/5 ml and 15.62 mg/5 ml; in pints and gallons and in 90 ml, 120 ml and 480 ml bottles Children’s Dramamine® (Upjohn) (OTC); generic (OTC)

Dimenhydrinate Injection 50 mg/ml; in 1 ml amps and vials, 5 & 10 ml vials; Dramamine® (Upjohn); Generic; (Rx)



Constipation; Cause

The etiopathogenesis of idiopathic megacolon is still incompletely understood. Several reviews have emphasized the importance of considering an extensive list of differential diagnoses (e. g., neuromuscular, mechanical, inflammatory, metabolic and endocrine, pharmacologic, environmental, and behavioral causes) for the obstipated cat (Box Differential Diagnosis of Constipation in the Cat). A review of published cases suggests that 96% of cases of obstipation are accounted for by idiopathic megacolon (62%), pelvic canal stenosis (23%), nerve injury (6%), or Manx sacral spinal cord deformity (5%). A smaller number of cases are accounted for by complications of colopexy (1%) and colonic neoplasia (1%); colonic hypo- or aganglionosis was suspected, but not proved, in another 2% of cases. Inflammatory, pharmacologic, and environmental and behavioral causes were not cited as predisposing factors in any of the original case reports. Endocrine factors (e. g., obesity, hypothyroidism) were cited in several cases, but were not necessarily impugned as part of the pathogenesis of megacolon. It is important to consider an extensive list of differential diagnoses in an individual animal, but it should be kept in mind that most cases are idiopathic, orthopedic, or neurologic in origin. Behavioral (e. g., stress) or environmental (e. g., competition for the litter box) factors, or both, may play an important role in the development of this lesion, but they have not been very well characterized in retrospective or prospective studies.

Differential Diagnosis of Constipation in the Cat

Neuromuscular Dysfunction

Colonic smooth muscle: idiopathic megacolon, aging

Spinal cord disease: lumbosacral disease, cauda equine syndrome, sacral spinal cord deformities (Manx cat)

Hypogastric or pelvic nerve disorders: traumatic injury, malignancy, dysautonomia

Submucosal or myenteric plexus neuropathy: dysautonomia, aging

Mechanical Obstruction

Intraluminal: foreign material (bones, plant material, hair), neoplasia, rectal diverticula, perineal hernia, anorectal strictures

Intramural: neoplasia

Extraluminal: pelvic fractures, neoplasia


Perianal fistula, proctitis, anal sac abscess, anorectal foreign bodies, perianal bite wounds

Metabolic and Endocrine

Metabolic: dehydration, hypokalemia, hypercalcemia Endocrine: hypothyroidism, obesity, nutritional secondary hyperparathyroidism


Opioid agonists, cholinergic antagonists, diuretics, barium sulfate, phenothiazines

Environmental and Behavioral

Soiled litter box, inactivity, hospitalization, change in environment

Constipation: PaThophysiology

Megacolon develops through two pathologic mechanisms: (1) dilation and (2) hypertrophy. Dilated megacolon is the end stage of colonic dysfunction in idiopathic cases. Cats affected with idiopathic dilated megacolon have permanent loss of colonic structure and function. Medical therapy may be attempted in such cases, but most affected cats eventually require colectomy. Hypertrophic megacolon, on the other hand, develops as a consequence of obstructive lesions (e. g., malunion of pelvic fractures, tumors, foreign bodies).

Hypertrophic megacolon may be reversible with early pelvic osteotomy, or it may progress to irreversible dilated megacolon if appropriate therapy is not instituted.

Constipation and obstipation are earlier manifestations of the same problem. Constipation is defined as infrequent or difficult evacuation of feces but does not necessarily imply a permanent loss of function. Many cats suffer from one or two episodes of constipation without further progression. Intractible constipation that has become refractory to cure or control is referred to as obstipation. The term obstipation implies a permanent loss of function. A cat is assumed to be obstipated only after several consecutive treatment failures. Recurring episodes of constipation or obstipation may culminate in the syndrome of megacolon.

The pathogenesis of idiopathic dilated megacolon appears to involve functional disturbances in colonic smooth muscle. In vitro isometric stress measurements have been performed on colonic smooth muscle obtained from cats suffering from idiopathic dilated megacolon. Megacolonic smooth muscle develops less isometric stress in response to neurotransmitter (acetylcholine, substance P, cholecystokinin), membrane depolarization (potassium chloride), or electrical field stimulation, when compared with healthy controls. Differences have been observed in longitudinal and circular smooth muscle from the descending and ascending colon. No significant abnormalities of smooth muscle cells or of myenteric neurons were observed on histologic evaluation. These studies initially suggested that the disorder of feline idiopathic megacolon is a generalized dysfunction of colonic smooth muscle and that treatments aimed at stimulating colonic smooth muscle contraction might improve colonic motility. More recent studies suggest that the lesion may begin in the descending colon and progress to involve the ascending colon over time.

Clinical Examination

History Constipation, obstipation, and megacolon mav in observed in cats ol any age, sex, or breed; however, most cases are observed in middle-aged (mean: 5.8 vears) male cats (70% male, 30% female) of domestic shorthair (DSH) (46%), domestic longhair (15%), or Siamese (12%) breeding. Affected cats are usually presented for reduced, absent, or painful defecation for a period of time ranging from days to weeks or months. Some cats are observed making multiple, unproductive attempts to defecate in the litter box, whereas other cats may sit in the litter box for prolonged periods of time without assuming a defecation posture. Dry, hardened feces are observed inside and outside of the litter box. Occasionally, chronically constipated cats have intermittent episodes of hematochezia or diarrhea due to the mucosal irritant effect of fecal concretions. This may give the pet owner the erroneous impression that diarrhea is the primary problem. Prolonged inability to defecate may result in other systemic signs, including anorexia, lethargy, weight loss, and vomiting.

Physical examination

Colonic impaction is a consistent physical examination finding in affected cats. Other findings will depend upon the severity and pathogenesis of constipation. Dehydration, weight loss, debilitation, abdominal pain, and mild to moderate mesenteric lymphadenopathy may be observed in cats with severe idiopathic megacolon. Colonic impaction may be so severe in such cases as to render it difficult to differentiate impaction from colonic, mesenteric, or other abdominal neoplasia. Cats with constipation due to dysautonomia may have other signs of autonomic nervous system failure, such as urinary and fecal incontinence, regurgitation due to megaesophagus, mydriasis, decreased lacrimation, prolapse of the nictitating membrane, and bradycardia. Digital rectal examination should be carefully performed with sedation or anesthesia in all cats. Pelvic fracture malunion may be detected on rectal examination in cats with pelvic trauma. Rectal examination might also identify other unusual causes of constipation, such as foreign bodies, rectal diverticula, stricture, inflammation, or neoplasia. Chronic tenesmus may be associated with perineal herniation in some cases. A complete neurologic examination, with special emphasis on caudal spinal cord function, should be performed to identify neurologic causes of constipation (e. g., spinal cord injury, pelvic nerve trauma, Manx sacral spinal cord deformity).

Diagnosis of Constipation

Although most cases of obstipation and megacolon are unlikely to have significant changes in laboratory data (e. g., complete blood count, serum chemistry, urinalysis), these tests should nonetheless be performed in all cats presented for constipation. Metabolic causes of constipation, such as dehydration, hypokalemia, and hypercalcemia may be detected in some cases. Basal serum T4 concentration and other thyroid function tests should also be considered in cats with recurrent constipation and other signs consistent with hypothyroidism. Although hypothyroidism was documented in only one case of obstipation and megacolon, obstipation is a frequent clinical sign in kittens affected with congenital or juvenile-onset hypothyroidism. Constipation could also theoretically develop after successful treatment of feline hyperthyroidism.

Abdominal radiography should be performed in all constipated cats to characterize the severity of colonic impaction and to identify predisposing factors such as intraluminal radioopaque foreign material (e. g., bone chips), intraluminal or extraluminal mass lesions, pelvic fractures, and spinal cord abnormalities. The radiographic findings of colonic impaction cannot be used to distinguish between constipation, obstipation, and megacolon in idiopathic cases. First or second episodes of constipation in some cats may be severe and generalized but may still resolve with appropriate treatment.

Ancillary studies may be indicated in some cases. Extraluminal mass lesions may be further evaluated by abdominal uhrasonography and guided biopsy, whereas intraluminal mass lesions are best evaluated by endoscopy. Colonoscopy mav also be used to evaluate the colon and anorecuim for suspected inflammatory lesions, strictures, sacculations, and diverticula. Barium enema contrast radiography may be used if colonoscopy is not possible. Both colonoscopy and barium enema contrast radiography will require general anesthesia and evacuation of impacted feces. Cerebrospinal fluid analysis, CT or MRI, and electrophysiologic studies should be considered in animals with evidence of neurologic impairment. Finally, colonic biopsy or anorectal manometry will be necessary to diagnose suspected cases of aganglionic megacolon.

Treatment of Constipation

The specific therapeutic plan will depend upon the severity of constipation and the underlying cause (Table Drug Index — Constipation). Medical therapy may not be necessary with first episodes of constipation. First episodes are often transient and resolve without therapy. Mild to moderate or recurrent episodes of constipation, on the other hand, usually require some medical intervention. These cases may be managed, often on an outpatient basis, with dietary modification, water enemas, oral or suppository laxatives, colonic prokinetic agents, or a combination of these therapies. Severe cases of constipation usually require brief periods of hospitalization to correct metabolic abnormalities and to evacuate impacted feces using water enemas, manual extraction of retained feces, or both. Follow-up therapy in such cases is directed at correcting predisposing factors and preventing recurrence. Subtotal colectomy will become necessary in cats suffering from obstipation or idiopathic dilated megacolon. These cats, by definition, are unresponsive to medical therapy. Although pelvic osteotomy is described for cats with pelvic canal stenosis, subtotal colectomy is an effective treatment and is considered the standard of surgical care.

Drug Index — Constipation

Drug Classification And Example Dose
Rectal Suppositories
Dioctyl sodium sulfosuccinate (Colace, Mead Johnson) 1-2 pediatric suppositories
Glycerin 1-2 pediatric suppositories
Bisacodyl (Dulcolox; Boehringer Ingelheim) 1-2 pediatric suppositories
Warm tap water 5-10 mL / kg
Warm isotonic saline 5-10 mL / kg
Dioctyl sodium sulfosuccinate (Colace, Mead Johnson) 5-10 mL / cat
Dioctyl sodium sulfosuccinate (Disposaject, PittmanMoore) 250 mg (12 ml) given pre rectum
Mineral oil 5-10 mL / cat
Lactulose (Cephulac. Merrell Dow; Duphalac, Reid Rowell) 5-10 mL / cat
Oral Laxatives
Bulk laxatives
Psyllium (Metamucil, Searle) 1-4 tsp mixed with food, every 24 or 12 hours
Canned pumpkin 1-4 tsp mixed with food, every 24 hours
Coarse wheat bran 1-4 tblsp mixed with food, every 24 hours
Emollient laxatives
Dioctyl sodium sulfosuccinate (Colace, Mead Johnson) 50 mg orally, every 24 hours
Dioctyl calcium sulfosuccinate (Surfax, Hoechst) 50 mg orally, every 24 or 12 hours as needed
Lubricant laxatives
Mineral oil 10-25 ml orally, every 24 hours
Petrolatum (Laxatone, Evsco) 1-5 ml orally, every 24 hours
Hyperosmotic laxatives
Lactulose (Cephulac, Merrell Dow, Duphalac, Reid Rowell) 0.5 ml / kg orally, every 12 to 8 hours as needed
Stimulant laxatives
Bisacodyl (Dulcolax, Boehringer Ingelheim) 5 mg orally, every 24 hours
Prokinetic Agents
Cisapride (compounding pharmacies) 0.1-1.0 mg / kg orally every 12 to 8 hours
Tegaserod (Zelnorm, Novartis) – dogs 0.05-0.10 mg / kg orally, twice a day
Ranitidine (Zantac, Claxo SmithKline) 1.0-2.0 mg / kg orally, every 12 to 8 hours
Nizatidine (Axid, Eli Lilly) 2.5-5.0 mg / kg orally, every 24 hours


Removal of Impacted Feces

Removal of impacted feces may be accomplished through the use of rectal suppositories, enemas, or manual extraction.

Rectal suppositories

A number of pediatric rectal suppositories are available for the management of mild constipation. These include dioctyl sodium sulfosuccinate (emollient laxative), glycerin (lubricant laxative), and bisacodyl (stimulant laxative). The use of rectal suppositories requires a compliant pet and pet owner. Suppositories can be used alone or in conjunction with oral laxative therapy.


Mild to moderate or recurrent episodes of constipation may require administration of enemas, manual extraction of impacted feces, or both. Several types of enema solutions may be administered, such as warm tap water (5 to 10 mL / kg), warm isotonic saline (5 to 10 mL / kg), dioctyl sodium sulfosuccinate (5 to 10 mL / cat), mineral oil (5 to 10 mL / cat), or lactulose (5 to 10 mL / cat). Enema solutions should be administered slowly with a well-lubricated 10 to 12F rubber catheter or feeding tube. Enemas containing sodium phosphate are contraindicated in cats because of their propensity for inducing severe hypernatremia, hyperphos-phatemia, and hypocalcemia in this species.

Manual extraction

Cases unresponsive to enemas may require manual extraction of impacted feces. Cats should be adequately rchydrated and then anesthetized with an endotracheal tube in place to prevent aspiration should colonic manipulation induce vomiting. Water or saline is infused into the colon while the fecal mass is manually reduced by abdominal palpation. Sponge forceps may also be introduced rectally (with caution) to break down the fecal mass. It may be advisable to evacuate the fecal mass over a period of several days to reduce the risks of prolonged anesthesia and perforation of a devitalized colon. If this approach fails, colotomy may be necessary to remove the fecal mass. Laxative or prokinetic therapy (or both) may then be instituted once the fecal mass has been removed.

Laxative Therapy

Laxatives promote evacuation of the bowel through stimulation of fluid and electrolyte transport or increases in propulsive motility. They are classified as bulk-forming, emollient, lubricant, hyperosmotic, or stimulant laxatives according to their mechanism of action. Hundreds of products are available for the treatment of constipation. Table Drug IndexConstipation summarizes those products that have been used with some success in cats.

Bulk-forming laxatives

Most of the available bulk-forming laxatives are dietary fiber supplements of poorly digestible polysaccharides and celluloses derived principally from cereal grains, wheat bran, and psyllium. Some constipated cats will respond to supplementation of the diet with one of these products, but many require adjunctive therapy (e. g., other types of laxatives or colonic prokinetic agents). Dietary fiber is preferable because it is well tolerated, more effective, and more physiologic than other laxatives. Fiber is classified as a bulk-forming laxative, although it has many other properties. The beneficial effects of fiber in constipation include increased fecal water content, decreaseo intestinal transit time, and increased frequency of defecation. Fiber supplemented diets are available commercially, or the pet owner may wish to add psyllium (1 to 4 teaspoon per meal), wheat bran (1 to 2 tablespoon per meal), or pumpkin (1 to 4 tablespoon per meal) to canned cat food. Cats should be well hydrated before commencing fiber supplementation to maximize the therapeutic effect. Fiber supplementation is most beneficial in mildly constipated cats, prior to the development of obstipation and megacolon. In obstipated and megacolon cats, fiber may in fact be detrimental. Low-residue diets may be more beneficial in obstipated and megacolonic cats.

Emollient laxatives

Emollient laxatives are anionic detergents that increase the miscibility of water and lipid in digesta, thereby enhancing lipid absorption and impairing water absorption. Dioctyl sodium sulfosuccinate and dioctyl calcium sulfosuccinate are examples of emollient laxatives available in oral and enema form. Anecdotal experience suggests that dioctyl sodium sulfosuccinate therapy may be most useful in animals with acute but not chronic constipation. As with bulk-forming laxatives, animals should be well hydrated before emollient laxatives are administered. It should be noted that clincial efficacy has not been definitively established for the emollient laxatives. Dioctyl sodium sulfosuccinate, for example, inhibits water absorption in isolated colonic segments in vitro, but it may be impossible to achieve tissue concentrations great enough to inhibit colonic water absorption in vivo. Dioctyl sodium sulfosuccinate at a dose of 30 mg / kg / day had no effect on fecal consistency in beagle dogs. Further studies are required to determine the clinical efficacy and therapeutic role of dioctyl sodium sulfosuccinate in the management of the constipated cat.

Lubricant laxatives

Mineral oil and white petrolatum are the two major lubricant laxatives available for the treatment of constipation. The lubricating properties of these agents impede colonic water absorption and permit greater ease of fecal passage. These effects are usually moderate, however, and, in general, lubricants are beneficial only in mild cases of constipation. Mineral oil use should probably be limited to rectal administration because of the risk of aspiration pneumonia with oral administration, especially in depressed or debilitated cats.

Hyperosmotic laxatives

This group of laxatives consists of the poorly absorbed polysaccharides (e. g., lactose, lactulose), the magnesium salts (e. g., magnesium citrate, magnesium hydroxide, magnesium sulfate), and the polyethylene glycols. Lactose is not effective as a laxative agent in all cats. Lactulose is the most effective agent in this group. The organic acids produced from lactulose fermentation stimulate colonic fluid secretion and propulsive motility. Lactulose administered at a dose of 0.5 mL / kg body weight every 8 to 12 hours fairly consistently produces soft feces in the cat. Many cats with recurrent or chronic constipation have been well managed with this regimen of lactulose. The dose may have to be tapered in individual cases if flatulence and diarrhea become excessive. Magnesium salts are not currently recommended in the treatment of feline constipation and idiopathic megacolon. Some veterinarians have reported anecdotal successes with the polyethylene glycols.

Stimulant laxatives

The stimulant laxatives (bisacodyl, phenolphthalein, castor oil, cascara, senna) are a diverse group of agents that have been classified according to their ability to stimulate propulsive motility. Bisacodyl, for example, stimulates NO-mediated epithelial cell secretion and myenteric neuronal depolarization. Diarrhea results from the combined effect of increased mucosal secretion and colonic propulsion. Bisacodyl (at a dose of 5 mg orally, every 24 hours) is the most effective stimulant laxative in the cat. It may be given individually or in combination with fiber supplementation for long-term management of constipation. Daily administration of bisacodyl should probably be avoided, however, because of injury to myenteric neurons with chronic use.

Colonic Prokinetic Agents

Previous studies of feline colonic smooth muscle function have suggested that stimulation of colonic smooth muscle contraction might improve colonic motility in cats affected with idiopathic dilated megacolon. Unfortunately, many of the currently available gastrointestinal prokinetic agents have not proved useful in the therapy of feline constipation, either because of significant side effects (e. g., bethanechol) or because the prokinetic effect is limited to the proximal gastrointestinal tract (e. g., metoclopramide, domperidone, erythromycin). The 5-HT4 serotonergic agonists (e. g., cisapride, prucalopride, tegaserod, mosapride) appear to have the advantage of stimulating motility from the gastroesophageal sphincter to the descending colon with relatively few side effects. Cisapride, for example, increases gastroesophageal sphincter pressure, promotes gastric emptying, and enhances small intestinal and colonic propulsive motility. Cisapride enhances colonic propulsive motility through activation of colonic neuronal or smooth muscle 5-HT receptors in a number of animal species. In vitro studies have shown that cisapride stimulates feline colonic smooth muscle contraction, although it has not yet been conclusively shown that cisapride stimulates feline colonic propulsive motility in vivo. A large body of anecdotal experience suggests that cisapride is effective in stimulating colonic propulsive motility in cats affected with mild to moderate idiopathic constipation; cats with long-standing obstipation and megacolon are not likely to show much improvement with cisapride therapy. Cisapride was widely used in the management of canine and feline gastric emptying, intestinal transit, and colonic motility disorders throughout most of the 1990s. Cisapride was withdrawn from the American, Canadian, and certain Western European countries in July 2000 after reports of untoward cardiac side effects in human patients. Cisapride causes QT interval prolongation and slowing of cardiac repolarization via blockade of the rapid component of the delayed rectifier potassium channel (IKr). This effect may result in a fatal ventricular arrhythmia referred to as torsades de pointes. Similar effects have been characterized in canine cardiac Purkinje fibers, but in vivo effects have not yet been reported in dogs or cats. The withdrawal of cisapride has created a clear need for new gastrointestinal prokinetic agents, although cisapride continues to be available from compounding pharmacies throughout the United States. Two new prokinetic agents, tegaserod and prucalopride, are in differing stages of drug development and may prove useful in the therapy of gastrointestinal motility disorders of several animal species.

Tegaserod is a potent partial nonbenzamide agonist at 5-HT4 receptors and a weak agonist at 5-HT1D receptors. Tegaserod has definite prokinetic effects in the canine colon, but it has not yet been studied in the feline colon. Intravenous doses of tegaserod (0.03 to 0.3 mg / kg) accelerate colonic transit in dogs during the first hour after intravenous administration. Tegaserod at doses of 3 to 6 mg / kg orally has also been shown to normalize intestinal transit in opioid-induced bowel dysfunction in dogs, and it may prove useful in other disorders of intestinal ileus or pseudo-obstruction. Gastric effects of tegaserod have not been reported in the dog, so this drug may not prove as useful as cisapride in the treatment of delayed gastric emptying disorders. In vitro studies suggest that tegaserod does not prolong the QT interval or delay cardiac repolarization as has been occasionally reported with cisapride. Tegaserod was marketed under the trade name of Zelnorm in the United States in September 2002 for the treatment of constipation-predominant IBS in women. As with many other drugs in companion animal medicine, tegaserod has not been licensed for the treatment of canine or feline gastrointestinal motility disorders.

Prucalopride is a potent 5-HT4 receptor agonist that stimulates giant migrating contractions and defecation in the dog and cat. Prucalopride also appears to stimulate gastric emptying in the dog. In lidamidine-induced delayed gastric emptying in dogs, prucalopride (0.01 to 0.16 mg / kg) dose-dependendy accelerates gastric emptying of dextrose solutions. Prucalopride has not yet been marketed in the United States or elsewhere.

Misoprostol is a prostaglandin E, analogue that reduces the incidence of nonsteroidal anti-inflammatory drug (NSAID)-induced gastric injury. The main side effects of misoprostol therapy are abdominal discomfort, cramping, and diarrhea. Studies in dogs suggest that prostaglandins may initiate a giant migrating complex pattern and increase colonic propulsive activity. In vitro studies of misoprostol show that it stimulates feline and canine colonic smooth muscle contraction. Given its limited toxicity, misoprostol may be useful in cats (and dogs) with severe refractory constipation.

Ranitidine and nizatidine, classic histamine H2 receptor antagonists, may also stimulate canine and feline colonic motility. These drugs stimulate contraction apparently through inhibition of tissue acetylcholinesterase and accumulation of acetylcholine at the motor endplate. It is not yet clear how effective these drugs are in vivo, although both drugs stimulate feline colonic smooth muscle contraction in vitro. Cimetidine and famotidine, members of the same classification of drug, are without this effect.

Constipation; Surgery

Colectomy should be considered in cats that are refractory to medical therapy. Cats have a generally favorable prognosis for recovery after colectomy, although mild to moderate diarrhea may persist for weeks to months postoperatively in some cases. Although pathologic hypertrophy may be reversible with early pelvic osteotomy in some cases, subtotal colectomy is an effective treatment for this condition regardless of duration, and pelvic osteotomy is not required.

Prognosis of Constipation

Many cats have one or two episodes of constipation without further recurrence, although others may progress to complete colonic failure. Cats with mild to moderate constipation generally respond to conservative medical management (e. g., dietary modification, emollient or hyperosmotic laxatives, colonic prokinetic agents). Early use of colonic prokinetic agents (in addition to one or more laxative agents) is likely to prevent the progression of constipation to obstipation and dilated megacolon in these cats. Some cats may become refractory to these therapies, however, as they progress through moderate or recurrent constipation to obstipation and dilated megacolon. These cats eventually require colectomy. Cats have a generally favorable prognosis for recovery after colectomy, although mild to moderate diarrhea may persist for 4 to 6 weeks postoperatively in some cases.


Small Intestinal Disease



Diarrhea is an increase in fecal mass caused by an increase in fecal water and / or solid content. It is accompanied by an increase in frequency and / or fluidity and / or volume of feces. Yet it must be remembered that the absence of recognizable diarrhea does not preclude the possibility of significant small intestine disease.

Classifications of Diarrhea


  • Osmotic
  • Secretory
  • Permeability (exudative)
  • Dysmotility
  • Mixed


  • Acute
  • Chronic


  • Extraintestinal
  • Small intestinal
  • Large intestinal
  • Diffuse


  • Biochemical
  • Allergic
  • Inflammatory
  • Neoplastic


  • Diet; bacterial, viral, parasitic causes; other


  • Exocrine pancreatic insufficiency, salmonellosis, lymphoma, other


  • Acute, nonfatal, self-limiting
  • Acute potentially fatal
  • Acute systemic disease
  • Chronic

Diarrhea can be classified in several ways (Box Classifications of Diarrhea). These categories are not mutually exclusive, and they allow the problem to be viewed from different perspectives, facilitating diagnosis and the choice of appropriate treatment. A mechanistic approach is simple, and many small intestine diseases have a component of osmotic diarrhea, but even in a situation as simple as lactase deficiency, other mechanisms become involved. Osmotic diarrhea in lactose malabsorption causes intestinal distension, which induces peristalsis and rapid transit, and bacterial fermentation products in the colon cause secretion. Bacterial fermentation of unabsorbed solutes is often a complicating factor in malabsorption. The fecal pH is often low because of the production of volatile fatty acids, and some products of fermentation (e. g., hydroxylated fatty acids, unconjugated bile acids) can cause colonic inflammation and secretion, and therefore signs of large intestinal diarrhea frequently accompany prolonged small intestine disease.

Osmotic diarrhea Excess water-soluble molecules in the intestinal lumen retain water osmotically and overwhelm the absorptive capacity of the small intestine and colon (e. g., sudden diet change, overeating, and malabsorption). The diarrhea typically resolves when food or laxatives are withheld.

Secretory diarrhea Stimulation of small intestine secretion such that the reserve absorptive capacity is overwhelmed results in diarrhea even though the absorptive ability of the small intestine and colon may not actually be impaired. Treatment with oral rehydration fluids containing glucose and amino acids (e. g., glycine) to increase water absorption is appropriate.

Typically secretory diarrhea does not resolve with fasting but does not cause weight loss unless anorexia, vomiting, or additional small intestine damage is a factor. Morbidity and even mortality are associated with the dehydration that results from excessive fluid loss. Secretory diarrhea typically is caused by chemical toxins and toxins elaborated by enteric bacteria (Box Causes of Secretory Diarrhea).

Causes of Secretory Diarrhea
  • Bacterial enterotoxins and endotoxins (e. g., Clostridium perfringens, Escherichia coli. Salmonella spp., Shigella spp., Yersinia enterocolitica)
  • Unconjugated bile acids from bacterial fermentation
  • Hydroxylated fatty acids from bacterial fermentation
  • Ciardia infection
  • Possibly hyperthyroidism
  • Laxatives (castor oil, dioctyl sodium sulfosuccinate, bisacodyl)
  • Cardiac glycosides
  • Amine precursor uptake and decarboxylation (APUD) neoplasms (excess vasoactive intestinal polypeptide, serotonin, prostaglandins, substance P)
  • Intestinal inflammation

Permeability (exudative) diarrhea Intestinal inflammation can stimulate increased fluid and electrolyte secretion and impair absorption. Leakage of tissue fluid, serum proteins, blood, and mucus may occur from sites of inflammation, ulceration, or infiltration or if portal hypertension or lymphatic obstruction is present. Increased permeability severe enough to cause loss of plasma proteins in excess of their rate of synthesis results in a protein-losing enteropathy.


Failure of food assimilation is sometimes classified as primary failure to digest (maldigestion) or primary failure to absorb (malabsorption). However, such a classification is misleading, because failure of absorption is an inevitable consequence of failure to digest. The preferred use of the term malabsorption is to describe defective absorption of dietary constituent resulting from interference with the digestive and / or absorptive phases in the processing of that molecule.

Within this broad definition, the site of the primary abnormality may be found in the luminal, mucosal, or transport phase (Table Pathophysiologic Mechanisms of Malabsorption). Also, the reserve capacity of the distal small intestine and colon may prevent overt diarrhea despite significant malabsorption and weight loss. The clinical manifestations of malabsorption, namely diarrhea, weight loss, and altered appetite (polyphagia, coprophagia, pica), are largely a result of the lack of nutrient uptake and the losses in feces. Animals are often systemically healthy and have an increased appetite unless an underlying neoplastic or a severe inflammatory condition is present. Only when the patient is quite malnourished or develops hypoproteinemia does it become ill.

Pathophysiologic Mechanisms of Malabsorption
Mechanism Example
Luminal Phase
Rapid intestinal transit Hyperthyroidism
Defective substrate hydrolysis
Enzyme inactivation Gastric hypersecretion
Lack of pancreatic enzymes Exocrine pancreatic insufficiency
Fat maldigestion
Decreased bile salt delivery Cholestatic liver disease, biliary obstruction
Increased bile salt loss Heal disease
Bile salt deconjugation Bacterial overgrowth
Fatty acid hydroxylation Bacterial overgrowth
Impaired release of CCK, secretin Impairment of pancreatic secretion due to severe small intestine disease
Cobalamin malabsorption
Intrinsic factor deficiency Exocrine pancreatic insufficiency Giant schnauzer defect
Competition for cobalamin Bacterial overgrowth
Mucosal Phase
Brush border enzyme deficiency
Congenital Trehalase (cats)
Acquired Relative lactose deficiency
Brush border transport protein deficiency
Congenital Intrinsic factor receptor
Acquired Secondary to diffuse small intestine disease
Enterocyte defects
Enterocyte processing defects Abetalipoproteinemia
Reduction in surface area Villus atrophy
Immature enterocytes Increased enterocyte turnover
Mucosal inflammation Inflammatory bowel disease
Transport Phase
Lymphatic obstruction
Primary Lymphangiectasia
Secondary Obstruction caused by neoplasia, infection, or inflammation
Vascular compromise
Vasculitis Infection, immune mediated
Portal hypertension Hepatopathy, right heart failure, cardiac tamponade

The presence of dark, tarry, oxidized blood in feces, a condition called melena, reflects either swallowed blood or generalized or localized gastrointestinal bleeding, which usually occurs proximal to the large intestine (Table Causes of Melena). Medication with ferrous sulfate or bismuth subsalicylate (Pepto-Bismol) also can impart a black color to the feces. It has been estimated that the loss of 350 to 500 mg / kg of hemoglobin into the gastrointestinal tract is required for melena to be visible. The presence of microcytosis with or without thrombocytosis is suggestive of iron deficiency secondary to chronic blood loss. An increased blood urea nitrogen (BUN) to creatinine ratio (from bacterial digestion of blood) provides supporting evidence. Hypoproteinemia may indicate significant blood loss or the presence of a protein-losing enteropathy.

Causes of Melena
Mechanism Source
Ingestion of blood Oral, nasal, pharyngeal, or pulmonary bleeding
Coagulopothies Thrombocytopenia, factor deficiencies, DIC
Gastrointestinal erosion / ulceration
Metabolic Uremia, liver disease
Inflammatory Gastritis, enteritis, hemorrhagic gastroenteritis
Neoplastic Leiomyoma, adenocarcinoma, lymphosarcoma
Paraneoplastic Mastocytosis, hypergastrinemia and other APUDomas
Vascular A-V fistula, aneurysms, angiodysplasia
Ischemia Hypovolemic shock, hypoadrenocorticism, thrombosis / infarction, reperfusion
Drug induced Nonsteroidal and steroidal anti-inflammatory agents
Foreign objects

APUD, amine precursor uptake and decarboxylation tumor; A-V, arteriovenous; DIC, disseminated intravascular coagulation

The general approach to melena is to rule out bleeding diatheses, ingestion of blood, and underlying metabolic disorders before pursuing primary gastrointestinal causes. Ultrasonography is particularly useful for detecting gastrointestinal masses and thickening. The next step for investigating upper gastrointestinal blood loss is endoscopy. If the source of gastrointestinal bleeding is still undetermined, lagged red cell scintigraphy, exploratory laparotomy, angiog-raphy. and enteroscopy may be used to localize the site.

Borborygmi and Flatulence

Borborygmus is a rumbling noise caused by the propulsion of gas through the intestines. Swallowed air and bacterial fermentation of ingesta are the main causes of borborygmi and flatulence. Feeding a diet that is highly digestible, with a low fiber content (e. g., cottage cheese and rice in a 1:2 ratio) leaves little material present in the intestine for bacterial fermentation and can effect a cure in some cases. If borborygmi or flatulence continues despite dietary modification, the animal may be excessively aerophagic or may have malabsorption, especially if diarrhea or weight loss are also present.

Weight Loss or Failure to Thrive

General causes of weight loss are reduced nutrient intake, increased nutrient loss, and increased catabolism or ineffective metabolism. The history should reveal whether the type and amount of diet fed is adequate and whether anorexia, dysphagia, or vomiting is a potential cause. Weight loss or failure to thrive accompanied by diarrhea often is a feature of mal-absorption, and the diagnostic approach is the same as for chronic diarrhea. However, diarrhea does not invariably accompany malabsorption that causes weight loss.

Protein-Losing Enteropalhy

When small intestine disease is severe enough for protein leakage into the gut lumen to exceed protein synthesis, hypoproteinemia develops. Chronic diarrhea associated with hypoproteinemia usually requires intestinal biopsy to define the cause of the protein-losing enteropathy (Table Protein-Losing Enteropathies). Nonintestinal diseases, which may potentially be associated with intestinal protein loss (e. g., portal hypertension), usually present with ascites before diarrhea. Hypoproteinemia associated with gastrointestinal disease is much less common in cats than in dogs and most often accompanies gastrointestinal lymphoma.

Protein-Losing Enteropathies
Causes Examples
Lymphangiectasia Primary lymphatic disorder, venous hypertension (e. g., right heart failure, hepatic cirrhosis)
Infectious Parvovirus, salmonellosis, histoplasmosis, phycomycosis
Structural Intussusception
Neoplasia Lymphosarcoma
Inflammation Lymphocytic-plasmacytic, eosinophilic, granulomatous
Endoparasites Ciardia, Ancylostoma spp.
Gastrointestinal hemorrhage hemorrhagic gastroenteritis, neoplasia, ulceration


Clinical presentation Breeds that appear to be predisposed to protein-losing enteropathy are the basenji, lundehund, soft-coated wheaten terrier, Yorkshire terrier, and Shar Pei. Clinical signs associated with protein-losing enteropathy include weight loss, diarrhea, vomiting, edema, ascites, and pleural effusion. Weight loss frequently is the predominant feature, and diarrhea is not invariably present, particularly with lymphangiectasia and focal intestinal neoplasia. Physical findings may include edema, ascites, emaciation, thickened intestines, and melena. Thromboembolism is a feature of some cases of protein-losing enteropathy.

Diagnosis The serum concentrations of both albumin and globulin are reduced in most patients with protein-losing enteropathy. Exceptions are raised hyperglobulinemia with hypoalbuminemia found in histoplasmosis and immunoproliferative small intestine disease in the basenji. Renal and hepatic causes of hypoalbuminemia are eliminated by assay of serum bile acids and urinary protein loss respectively. Hypocholesterolemia and lymphopenia are common in protein-losing enteropathy. Hypocalcemia and hypomagnesemia are also reported. Measurement of fecal loss of alpha, -protease inhibitor may be a sensitive test for protein-losing enteropathy.

Survey abdominal radiographs often are normal in patients with protein-losing enteropathy, but ultrasound scans may reveal intestinal thickening, mesenteric lymphadenopathy, or abdominal effusion. Thoracic radiographs may show pleural effusion, metastatic neoplasia, or evidence of histoplasmosis. Although intestinal function tests may confirm the presence of malabsorption, they rarely provide a definitive diagnosis, and intestinal biopsy is more appropriate. Because many intestinal causes of protein-losing enteropathy are diffuse, endoscopy is the safer way to obtain biopsies, but surgical biopsy may be required to obtain a definitive diagnosis for lymphoma and for diseases that cause secondary lymphangiectasia (Box Relative Advantages of Endoscopic and Surgical Intestinal Biopsy).

Relative Advantages of Endoscopic and Surgical Intestinal Biopsy



  • Minimally invasive
  • Allows visualization and biopsy of focal lesions
  • Permits multiple biopsies
  • Minimal adverse reactions
  • Allows steroids to be started early


  • Requires general anesthesia
  • Permits access only to duodenum (and distal ileum?)
  • Allows only small, superficial (and crushed) biopsies
  • Requires expensive equipment
  • Technically demanding



  • Allows biopsy of multiple sites
  • Permits large, full-thickness biopsies
  • Allows inspection of other organs
  • Offers potential for corrective surgery


  • Requires general anesthesia
  • Poses a surgical risk
  • Requires convalescence
  • Requires delay before steroids can be started

Treatment Plasma transfusion may be indicated during the perioperative period when collecting biopsy specimens, and diuretics may reduce ascites. Spironolactone (1 to 2 mg / kg given orally twice daily) may be more effective than furosemide for treating ascites. Thromboembolism is a feature of some cases of protein-losing enteropathy. Specific treatments are discussed later.

Diagnosis of Small Intestinal Disease

Occult blood

These tests are used to search for intestinal bleeding from ulcerated mucosa and benign or malignant tumors. Unfortunately, all versions nonspecifically test for hemoglobin and are very sensitive, reacting with any meat diet and not just patient blood. Therefore the patient must be fed a meat-free diet for at last 72 hours for a positive result to have any reliability.

Alpha1-protease inhibitor This test assays the presence in feces of a naturally occurring endogenous serum protein that is resistant to bacterial degradation if it is lost into the intestinal lumen. To improve diagnostic accuracy, three fresh fecal samples should be sampled. The assay is valid only if used on fecal samples collected after voluntary evacuation, because abrasion of the colonic wall during manual evacuation is enough to elevate alpha1-protease inhibitor (alpha1-PI) concentrations. It appears to be of value for the diagnosis of protein-losing enteropathy and may prove to be more a sensitive marker than measurement of serum albumin for the detection of early disease.

Rectal cytology At the end of the rectal examination, the recta] wall is mildly abraded, the gloved finger rolled on a microscope slide, and the smear stained. Although the result is often negative and, when positive, probably more representative of large intestinal disease, an increased number of neutrophils may be suggestive of a bacterial problem, indicating the need for fecal culture. Clostridial endospore elements (Histoplasma, Aspergillus, Pythium, and Candida spp. ) may be identified. The test is fast and simple but in all cases confirmatory tests are indicated.

Small Intestine: Imaging

Small Intestine: Special Tests


Flexible endoscopy allows gross examination of the small intestine mucosa and collection of tissue samples without the need for invasive surgery. The proximal small intestine can be viewed during gastroduodenoscopy, and the distal small intestine often can be visualized by passing the endoscope retrograde through the ileocolic valve. Therefore only the midjejunum cannot be satisfactorily examined by routine endoscopy. However, given that most cases of malabsorption involve diffuse disease, this limitation may not be significant. Enteroscopy, which was developed in humans and which uses a much narrower, thinner endoscope, may allow examination of most of the jejunum.

Abnormal findings on gross endoscopic examination include mucosal granularity and friability, erosions / ulcers, retained food, mass lesions, and hyperemia / erythema. However, none of these characteristics is pathognomonic for particular disease conditions, and gross findings frequendy do not correlate with those of the histopathologic examination. A milky white appearance or a milky exudate is suggestive of lymphangiectasia, and the presence of intraluminal parasites may be diagnostic in some cases.

Small Intestine: Intestinal Biopsy

Acute Small Intestinal Disease

Viral Enteritides

Bacterial Enteritides

Rickettsial Diarrhea (Salmon Poisoning)

Neorickettsia helminthoeca and Neorickettsia elokominica are found in the metacercariae of the fluke Nanophyetus salmonicola, which is present in salmon in the western regions of the Cascade Mountains from northern California to central Washington. About a week after ingestion of infected salmon by dogs, the rickettsiae emerge from the mature fluke and cause a disease characterized by high fever, hemorrhagic gastroenteritis, vomiting, lethargy, anorexia, polydipsia, nasal-ocular discharge, and peripheral lymphadenopathy. Mortality is extremely high in untreated patients.

The diagnosis is based on a history of ingestion of raw fish in an endemic area, the detection of operculated fluke eggs in feces, and the presence of intracytoplasmic inclusion bodies in macrophages from lymph node aspirates. Oxytetracycline (7 mg / kg given intravenously three times a day) is the treatment of choice and should be continued for at least 5 days. The trematode vector is eradicated with praziquantel.

Algal Infections

Toxic algal blooms can lead to acute gastroenteritis and death in animals that drink contaminated water. Blue-green algae can synthesize an anticholinesterase that induces vomiting, diarrhea, ataxia, and rapid death in dogs. Prototheca spp. are achlorophyllous algae that cause protothecosis. Typically a cutaneous infection in cats, in dogs it can involve the intestine. Large intestinal disease is more common, but fatal disseminated disease affecting the small intestine has been reported.

Fungal Infections



Chronic Idiopathic Enteropathies

Adverse Reactions To Food

Small Intestinal Bacterial Overgrowth

Inflammatory Bowel Disease


Miscellaneous Causes Of Protein-Losing Enteropathy

Common causes of protein-losing enteropathy include lymphoma and IBD. However, there have also been recent reports of protein-losing enteropathy associated with intestinal crypt lesions without evidence of lymphangiectasia or inflammation in most cases. The underlying etiology of such lesions is not known. Response to therapy with antibacterials and immunosuppressive medication is variable; some dogs deteriorate suddenly and can die from thromboembolic disease

Intestinal Neoplasia

Adynamic Ileus And Intestinal Pseudo-Obstruction

Adynamic ileus is a common sequel to parvoviral enteritis, abdominal surgery, pancreatitis, peritonitis, endotoxemia, hypokalemia, and dysautonomia. The term intestinal pseudo-obstruction describes a condition in which patients show clinical evidence consistent with an obstruction, but no mechanical cause can be found. The condition has been associated with both visceral neuropathies and myopathies in humans, and such causes may occur in small animals. Most canine cases are associated with idiopathic sclerosing enteropathy, with fibrosis and a mononuclear cell infiltrate of the tunica muscularis. A case of feline intestinal pseudo-obstruction occurred secondary to intestinal lymphoma. After the possibility of a mechanical obstruction has been eliminated, management of both adynamic ileus and intestinal pseudo-obstruction is aimed at identifying any underlying cause and providing specific treatment. Symptomatic therapy to stimulate intestinal motility is also indicated. Suitable prokinetic agents include the 5-HT4 receptor agonist cisapride, the D2 dopaminergic antagonist metoclopramide, and motilin-like drugs such as erythromycin. In dogs and cats cisapride appears to be the most effective agent, but it is no longer marketed in many countries. Antibacterials may also be appropriate, given the probability of secondary SIBO, and immunosuppressive medication may be appropriate if an underlying inflammatory bowel disease is suspected. Feeding is beneficial in humans, and nutritional support can be continued indefinitely, although vomiting, constipation, and diarrhea usually continue. Unfortunately, most cases reported in the veterinary literature responded poorly to therapy, and the prognosis is grave.

Intestinal Obstruction

Intestinal obstruction can be classified as acute or chronic, partial or complete, and simple or strangulated. Obstruction can be the result of extraluminal, intramural, or intraluminal mass lesions. The most common extraluminal cause of obstruction is intussusception. Younger animals are more likely to develop intussusception after a case of gastroenteritis or after having intestinal surgery, although an increased risk in postparturient queens has also been reported. Intestinal neoplasia is the more frequent cause of intussusception in middle-aged and older animals. Intramural causes include intestinal neoplasia (most common), hematomas, granulomas (e. g., focal FIP), inflammatory bowel disease, stricture, and phycomycosis. Most intraluminal obstructions are caused by foreign objects, such as stones, fruit pits, and toys in dogs and linear foreign objects in cats. Intestinal volvulus describes a condition in which the intestines rotate around the mesenteric axis, compromising the cranial mesenteric artery, and complete vascular obstruction may lead to strangulation. Reports are sporadic, but a predisposition in German shepherds has been reported.

The prognosis depends on the cause of the obstruction and the severity of associated abnormalities. The outcome is likely to be favorable with simple foreign bodies, but it is grave for animals with volvulus or metastatic intestinal neoplasia. The patient may be at risk of developing short bowel syndrome if a significant length of intestine must be removed.

Short Bowel Syndrome

Irritable Bowel Syndrome

Irritable bowel syndrome (IBS) is characterized by recurrent, usually acute, episodes of abdominal pain, borborygmi, and diarrhea. In the absence of morphologic changes, a functional disorder is considered the cause of this enigmatic problem. Disordered intestinal motility may be of primary importance, and a number of mechanisms have been proposed for irritable bowel syndrome in humans (Box Causes of Irritable Bowel Syndrome). However, it is not known whether any are responsible in dogs and cats. A variety of treatments, including antispasmodics (anticholinergics and also smooth muscle relaxants, such as mebeverine), anxiolytics (e. g., diazepam, chlordiazepoxide) and dietary modification (low-fat diet, increased fiber) have been tried with no consistent results. IBS probably will remain a frustrating condition to diagnose and treat successfully until its etiology is better understood.

Causes of Irritable Bowel Syndrome

  • Primary motility disorders
  • Visceral hyperalgesia
  • Psychosomatic disorders
  • Food intolerance
  • Undiagnosed inflammatory disease

Viral Enteritides

Most viral enteritides of dogs and cats, especially the parvovirus infections, cause an acute and usually self-limiting diarrhea, although severe cases in young or immunocompromised patients may be fatal. Canine parvovirus infection is described here as the index case for viral enteritides.

Canine Parvovirus

Canine parvovirus type 2 (CPV-2) is a highly contagious cause of acute enteritis. It emerged as a pathogen in the late 1970s, perhaps from a mutation of a feline vaccine as it is related to feline panleukopenia and mink enteritis viruses. CPV-2b has emerged as the most prevalent antigenic variant. There have been reports of cats being infected with canine parvovirus type 2, but the severity of signs is much reduced.

Infected dogs shed massive quantities of virus particles in feces during the acute illness and then for about 8 to 10 days afterward. Parvovirus is extremely stable and can remain infectious in the environment for many months. Infection is acquired via the fecal-oral route and is more common in the summer months. The virus has an affinity for rapidly dividing cells and localizes to the intestine (crypt cells), bone marrow, and lymphoid tissues. It causes apoptotic cell death, leading to intestinal crypt necrosis and severe diarrhea, leukopenia, and lymphoid depletion.

Clinical Findings

Clinical signs of diarrhea typically occur 4 to 7 days after infection. Anorexia, depression, fever, vomiting, diarrhea (often profuse and hemorrhagic), and dehydration are common. Hypothermia and disseminated intravascular coagulation (DIC) are associated with terminal bacterial sepsis or endotoxemia. Dogs of any age can be affected, but the incidence of clinical disease is highest in puppies between weaning and 6 months. Puppies younger than 6 weeks usually are protected by maternal antibody. In dogs older than 6 months, males are more likely to become infected than females. Overcrowding, intestinal parasitism, concurrent infection with distemper virus, coronavirus, Giardia, Salmonella, or Campylobacter spp. can increase the severity of illness.

Puppies infected in utero or shortly after birth may develop myocarditis and either die suddenly or develop cardiomyopathy if maternal antibody is absent. This situation rarely arises nowadays because widespread vaccination and infection have left few seronegative dams. Yet death still occurs, especially in young puppies, and particularly in susceptible breeds such as rottweilers, Dobermans, English springer spaniels, and American pit bull terriers. Death is usually attributed to dehydration, electrolyte imbalances, hypercoagulability, endotoxic shock, or overwhelming bacterial sepsis related to mucosal barrier disruption and leukopenia. Infected dogs are immunosuppressed and susceptible to catheter infections. Endotoxemia, TNF activity, coliform septicemia, and proliferation of enteric C. perfringens determine morbidity and mortality.


Parvovirus should be suspected in young dogs with sudden onset of vomiting and diarrhea, especially if they are also depressed, febrile, or leukopenic or if they have been in contact with infected dogs. Leukopenia (often 500 to 2000 white blood cells per microliter) may be detected in up to 85% of field cases and is very suggestive of parvovirus infection. It reflects neutropenia and lymphopenia. Neutropenia results from impaired bone marrow production with concurrent r. eutrophil loss through the damaged gastrointestinal tract, and severe neutropenia crudely correlates with a poor prognosis.

In the absence of leukopenia, clinical signs are indistinguishable from those of other bacterial or viral enteritides, gastrointestinal foreign bodies with peritonitis, or intussusception. Abdominal radiographs may reveal non-specific gas and fluid accumulation, and ileus. Biochemical abnormalities often include hypokalemia, hypoglycemia, prerenal azotemia, and increased bilirubin or liver enzymes.

Definitive diagnosis requires demonstration of canine parvovirus type 2 virus (orviral antigens) in the feces. Fecal enzyme-linked immunosorbent assay is regarded as an accurate and specific diagnostic test but is most sensitive in the first 7 to 10 days when virus excretion is greatest. Single anti-CPV antibody determination in serum (by hemagglutination inhibition) is not useful for diagnosis except in the presence of typical clinical signs in an unvaccinated animal. A rising IgG titer by paired serology provides only a retrospective diagnosis. Serum IgM analysis may provide evidence of recent infection.


Treatment is supportive and is similar to regimens used in most animals with severe gastroenteritis. Intravenous fluid therapy usually is indicated and is continued until vomiting stops and oral intake resumes. A balanced electrolyte solution (e. g., lactated Ringer’s solution) supplemented with potassium and 2.5% glucose is often used. Plasma or whole blood infusions are given to treat severe hypoproteinemia or anemia. Antibiotics are used to control potentially fatal sepsis (see above).

Traditionally, oral intake is withheld until vomiting has stopped for at least 24 hours; this may take 3 to 5 days in severe cases. Rather than avoid the oral route completely, it may be better to trickle feed small amounts of glutamine-containing solutions to reduce bacterial translocation. Once vomiting has been controlled, small amounts of a bland diet are fed initially. Frequent or persistent vomiting can be managed with intermittent injections or constant-rate infusion of metoclopramide, once intestinal obstruction has been ruled out. Phenothiazines (e. g., chlorpromazine) can be used if metoclopramide is ineffective and the animal has been rehydrated.

Administration of corticosteroids is of unproven benefit and is probably best limited to dogs with severe endotoxic shock. Flunixin meglumine is best avoided because of its adverse effects on the gastrointestinal tract and kidneys. Antiendotoxin therapy has been useful in some patients, but the timing of antiendotoxins in relation to antibiotic therapy may be important. Because antibiotics may increase endotoxin liberation, it may be preferable to administer antiendotoxin serum before antibiotics. However, one study showed that the use of the antiendotoxin rBPI21 had no beneficial effect on survival, and in another study, use of antiendotoxin was correlated with decreased suvival. Administration of recombinant human granulocyte colony-stimulating factor (G-CSF) to neutropenic parvoviral enteritis patients may raise neutrophil counts but is of no clinical benefit, because the endogenous granulocyte colony-stimulating factor concentration is already elevated. In contrast, administration of feline interferon-omega was found to improve clinical signs and reduce mortality.


Severe infection and leukopenia are associated with a high mortality rate, but most dogs with parvovirus recover if dehydration and sepsis are treated appropriately. Complications include hypoglycemia, hypoproteinemia, anemia, intussusception, and secondary bacterial or viral infections.


Prevention is achieved by limiting exposure to the virus, adequate disinfection (1:32 dilution of sodium hypochlorite bleach), and vaccination. Vaccination is an effective means of preventing and controlling canine parvovirus type 2, but maternal antibody interference is a problem. Maternally derived antibodies (MDAs) can persist for up to 18 weeks and can interfere with vaccination, although most modern vaccines can overcome maternally derived antibodies by 10 to 12 weeks of age. Modified live canine parvovirus type 2 vaccines are most commonly used; killed vaccines provide less duration of immunity but may be recommended in pregnant dogs and puppies younger than 5 weeks. Vaccines may differ in efficacy; low-passage, high-titer vaccines are considered most effective, and only one injection at or after 12 weeks may be needed. In susceptible breeds and dogs in high-risk areas, vaccination may begin at 6 to 8 weeks of age and be repeated every 3 to 4 weeks until 18 weeks of age. There is good correlation between the antibody titer and resistance to infection with canine parvovirus. Annual revaccination is currendy recommended.

Feline Parvovirus (Feline Panleukopenia)

Feline panleukopenia is a highly contagious infection of cats that causes severe acute diarrhea and death, similar to canine parvovirus. Mortality in young kittens is high (50% to 90%), therefore the prognosis is guarded until the vomiting and diarrhea stop and the leukopenia resolves.

Canine Coronavirus

Canine coronavirus (CCV) can cause diarrhea of variable severity in dogs. Transmission is by the fecal-oral route. The incubation period is 1 to 4 days, and infected dogs may shed virus intermittently for months after clinical recovery. However, the significance of coronavirus as a primary pathogen is unclear. Experimental inoculation is associated with only mild disease and canine coronavirus infection, and antibodies against canine coronavirus are present in many healthy and diarrheic dogs. Infection is very prevalent, particularly in animal shelter and laboratory dogs. Most canine coronavirus infections are probably subclinical, although severe enteritis may occur in dense populations or with concurrent infections. In such situations, vaccination may be helpful.

Feline Enteric Coronavirus

Feline enteric coronavirus (FECV) is ubiquitous in the cat population. Mild to moderately severe diarrhea, which may be associated with weight loss, is seen in kittens infected with feline enteric coronavirus. Inapparent infection is common in normal cats, many of which shed FECV in feces and are seropositive. Feline enteric coronavirus infection is important, because enteric coronaviruses may mutate to feline infectious peritonitis virus (FIPV).

Intestinal Feline Infectious Peritonitis

An unusual manifestation of feline infectious peritonitis (FIP) of isolated mural intestinal lesions has been reported. Predominant clinical signs were diarrhea and vomiting, and all cats had a palpable mass in the colon or ileocecocolic junction. Affected intestine was markedly thickened and nodular, with multifocal pyogranulomas extending through the intestinal wall.

Feline Immunodeficiency Virus

Infection with feline immunodeficiency virus (FIV) is associated with a 10% to 20% incidence of chronic enteritis. Although secondary and opportunistic infections may be responsible for signs, sometimes no other etiologic agent can be identified. Anorexia, chronic diarrhea, and emaciation are typical. Palpably thickened bowel loops reflect chronic enteritis with transmural granulomatous inflammation.

Feline Leukemia Virus

Among its many manifestations, feline leukemia virus (FeLV) infection can be associated with fatal peracute enterocolitis and lymphocytic ileitis.


A torovirus-like agent has been isolated from the feces of cats afflicted with a characteristic syndrome of chronic diarrhea and protruding nictitating membrane. However, a clear association with clinical signs was not demonstrated.



Gastric Erosion And Ulceration

Gastric erosions and ulcers are associated with a number of primary gastric and non-gastric disorders (Table Association of Gastric Ulceration and Erosion with Specific Diseases). Clinical signs range in duration and severity, from acute to chronic and mild to life threatening. The pathomechanisms underlying gastric damage can be broadly attributed to impairment of the gastric mucosal barrier (defined above) through direct injury, interference with gastroprotective prostaglandins (PGE2), mucous or bicarbonate, decreased blood flow, and hypersecretion or gastric acid.

Association of Gastric Ulceration and Erosion with Specific Diseases

Gastric Problem Related Diseases
Metabolic / Endocrine Hypoadrenocorticism, uremia, liver disease, mastocytosis, d. i. c.
Hypergastrinemia and other APUDomas
Inflammatory Gastritis
Neoplastic Leiomyoma, adenocarcinoma, lymphosarcoma
Drug-induced Nonsteroidal and steroidal anti-inflammatories
Hypotension Shock, sepsis
Idiopathic Stress, spinal surgery, exercise induced (sled dogs)


Perhaps the most predictable recipe for gastric erosion is the combination of a non-steroidal anti-inflammatory and a glucocorticoid, either alone, or in combination with interver-tebral disk disease.

Nonsteroidal anti-inflammatory drugs cause direct mucosal damage and interfere with prostaglandin synthesis. Flunixin mcglumine, aspirin, and ibuprofen have all been associated with erosions in healthy dogs. To circumvent toxicity caused by the inhibition of “friendly prostaglandins” (PGE2), drugs that preferentially block “inducible” cyclooxygenase (COX-2) have been developed. These COX-2 selective agents, such as carprofen, meloxicam, derccoxib, and potentially etodolac, are less ulcerogenic in normal dogs. However, even COX-2 selective drugs such as meloxicam are ulcerogenic in combination with dexamethasone, and their safety in sick animals remains to be determined.

High doses of glucocorticoids alone, such as dexamethasone and methylprednisolone, have also been associated with gastric erosions but the mechanisms by which they induce damage are not clear. Unlike NSAIDs, their effects are not ameliorated by PGE2 analogs.

Hypersecretion of gastric acid in response to histamine release from mast cell tumors, and gastrin from gastrinomas has also been clearly implicated as a cause of gastroduodenal ulceration and esophagitis in dogs and cats.

Renal failure, hepatic failure, hypoadrenocorticism, and hypotension are frequently proposed as risk factors for gastric erosion or ulceration, although few details have been published on the pathogenesis, frequency, or severity of gastric damage in these conditions. In a recent study of dogs with renal failure, ulceration was present in only 1 of 28 dogs. The predominant findings in these dogs were mucosal edema, vasculopathy, and mineralization that correlated to the degree of azotemia and calcium phosphorous product.

Sled dogs in the Iditarod are prone to develop gastric erosions and / or ulcers. This finding is similar to exercising humans and horses in whom the pathogensis is not understood hut is responsive to acid suppression.

Erosions and ulcers are aJso a sequela of gastric cancer and gastritis and are discussed elsewhere in this chapter.

Clinical Findings

Vomiting, hematemesis, and melena may be present in patients with gastric erosions or ulcers. Pale mucous membranes, abdominal pain, weakness, inappetance, hypcrsalivation (potentially associated with esophagitis as a consequence of gastric acid hypersecretion), and evidence of circulatory compromise are more variably present. Access to toxins and drugs, particularly NSAlDs, should be determined.

Clinicopathologic testing is directed at identifying diseases associated with gastric erosions and ulcers (see Table Association of Gastric Ulceration and Erosion with Specific Diseases) and the consequences of erosion / ulceration. The complete blood count may reveal anemia that is initially regenerative but can progress to become microcytic, hypochromic, and minimally regenerative. When accompanied by thromhocytosis and decreased iron saturation or low serum ferritin, these findings are characteristic of chronic bleeding and iron deficiency. Lack of a stress leukogram and eosiniphilia in dogs is supportive of hypoadrenocorticism. Eosinophilia could also be consistent with dietary allergy, eosinophilic gastroenteritis, mastocytosis, or a hyperseosinophilic syndrome. A neutrophilic leukocytosis and a left shift may indicate inflammation or possible gastric perforation. Examination of a buffy coat smear may help to detect mastocytosis.

Biochemistry and urinalysis may reveal findings consistent with dehydration (azotemia and hypersthcnuria), renal failure (e. g., azotemia and isosthenuria), hepatic disease (e. g., increased liver enzymes or bilirubin; decreased cholesterol, albumin, BUN], or hypoadrenocorticism (i. e., Na+:K+ ratio <27:1). It will also identify electrolyte and acid base abnormalities associated with vomiting and gastrointestinal ulceration. The presence of a metabolic alkalosis, hypochloremia, hypokalemia, and acid urine is consistent with upper gastrointestinal obstruction (physical or functional) or a hypersecretory state. Testing should be performed to detect abnormalities in primary and secondary hemostasis that may be associated with gastrointestinal bleeding. Serum gastrin and potentially histamine concentrations can be evaluated where acid hypersecretion is suspected as a cause of ulceration.


Diagnostic imaging

Plain radiographs are not usually helpful in diagnosing gastric erosions or ulcers but may help to rule out other causes of vomiting, such as foreign bodies, peritonitis, and gastric perforation. Contrast radiographs may reveal filling defects but do not allow detailed mucosal evaluation or sampling.

Ultrasonography can be performed to evaluate the gastric wall for thickening associated with ulcers and masses and also helps to rule out non-gastric causes of vomiting. The information provided by radiography and ultrasound is complementary to endoscopic evaluation, which is the diagnostic test of choice.

Endoscopy allows the direct evaluation of gastric damage and mucosal sampling. NSAID-associated ulcers tend to be found in the antxum and are not usually associated with marked mucosal thickening or irregular edges. This contrasts with ulcerated tumors that frequently have thickened edges and surrounding mucosa. Ulcers should be biopsied at the periphery to avoid perforation. Endoscopic biopsies are not ideal for diagnosing infiltrative gastric tumors and several biopsies from the same site are usually taken to enable sampling of deeper tissue. Endoscopic guided fine-needle aspirates, with use of a needle and tubing in the biopsy channel, can also be used to sample deep lesions. Even with this approach the diagnosis may be missed, and surgical biopsy required for a definitive diagnosis.

The combination of mucosal erosion or ulceration, antral mucosal hypertrophy, copious gastric juice, and esophagitis is highly suggestive of a gastric hypersecretory state. It is prudent to measure gastric pH and serum gastrin in patients with gastric erosion / ulceration that is not associated with drugs or gastric tumors. Dogs with mast cell tumors and hyperhistaminemia-induced acid hypersecretion have low serum gastrin concentrations. Finding a combination of gastric pH less than 3 and a high serum gastrin concentration prompts further investigation of gastrinoma by secretin stimulation test, ultrasonography (liver and pancreas), and pentertreotide scintigraphy.


Treatment of gastric erosions and ulcers is directed at the underlying cause, which ensures adequate hydration and perfusion, including blood transfusion if needed, and restoring electrolyte and acid base disturbances. Additional support is directed at shoring up the gastric mucosal barrier by enhancing mucosal protection and cytoprotection, and decreasing gastric acid secretion. Where vomiting is persistent, antiemetics may help to reduce fluid loss, discomfort, and the risk of esophagitis.

Fluid Therapy

The rate of fluid administration depends on the presence or absence of shock, the degree of dehydration, and the presence of diseases (e. g., cardiac or renal), which predispose to volume overload. Patients with a history of vomiting who are mildly dehydrated are usually responsive to crystalloids (e. g., LRS or 0.9% NaCl) at a rate that will provide maintenance and replace both deficits and ongoing losses over a 24-hour period. Potassium depletion is often a consequence of prolonged vomiting or anorexia, and most polyionic replacement fluids contain only small amounts of potassium. Therefore KC1 is added to parenteral fluids on the basis of serum levels.

Patients with signs of shock require more aggressive support. The volume deficit can be replaced with crystalloids at an initial rate of 60 to 90 mLAg / h, then tailored to maintain tissue perfusion and hydration. Colloid solutions can also be used to treat animals in shock to reduce the amount of crystalloid required (e. g., Hetastarch, hemaccel at 10 to 20 mL / kg IV over 4 to 6 hours). Plasma, colloids, packed cells, or whole blood is occasionally required to treat severe hypoproteinemia or anemia, which can develop in vomiting animals with severe ulceration or HGE.

Central venous pressure monitoring and evaluation of urine output are necessary in patients with severe gastrointestinal disease, particularly those complicated by third space losses of fluid into the gut or peritoneum.

The effect of vomiting on acid-base balance is hard to predict and therapeutic intenention to correct acid-base imbalances should be based on blood gas determination. Where severe metabolic acidosis is present (pH <7.1, HCO3- <10 mmol / L), sodium bicarbonate (l mmolAg) can be given under careful supervision for the development of worsening hypokalemia, and hypocalcemia, and CSF acidosis. Further bicarbonate supplementation is based on repeated blood gas analysis. Metabolic alkalosis usually responds to replacing volume deficit, chloride, and potassium with IV 0.9% NaCl + KG. Diagnostic investigations should initially center on ruling out upper gastrointestinal obstruction. The administration of antisecretory drugs such as H2 antagonists may help to limit Cl–efflux into gastric juice.

Reducing Acid Secretion and Providing Mucosal Protection

Pharmacologic inhibition of acid secretion can be effected by blocking H2 (cimeridine, ranitidine, famotidine), gastrin (proglumide), and acetylcholine (atropine, pirenzipine) receptors, and by inhibiting adenyl cyclase (PGE analogs) and H+/K+ ATPase (e. g., omeprazole). H Long-acting somatostatin analogs such as octreotide directly decrease the secretion of gastrin and gastric acid.

Decreasing gastric acid secretion with an H2 receptor antagonist has been shown to promote mucosal healing in dogs with a variety ot experimentally induced ulcers and erosions. Famotidine is an attractive choice as it does not inhibit P450 enzymes and can be given once daily. The additional prokinetic activity of ranitidine or nizatidine (mediated by anticholinesterase activity) may make them good choices in the face of delayed gastric emptying associated with defective propulsion. In patients with severe or persistent gastric ulceration that is refractory to H2 antagonists, more complete inhibition of gastric acid secretion can be achieved with a H+/K+-ATPase inhibitor such as omeprazole (0.2 to 0.7 mg / kg SID PO—dogs). Omeprazole is the initial drug of choice in patients with acid hypersecretion secondary to r. ast cell tumors and gastrinoma (Zollinger-Ellison syndrome). Omeprazole has been shown to have few long-term side effects in dogs, but it should be used with caution in patients with liver disease and reviewed for interactions with drugs such as cisapride.

In sled dogs with exercise-associated gastric hemorrhage treatment with omeprazole significantly reduced mean gastric severity score compared to placebo but also was associated with increased frequency of diarrhea (omeprazole 54%, placebo 21%). The authors recommended further investigation of diarrhea associated with omeprazole treatment hefore omeprazole can be recommended for routine prophylactic treatment in these athletes.

The combination of omeprazole and the long acting somatostatin analog Octreotide effectively reduced vomiting in a dog with gastrinoma (Octreotide 2 to 20 μg / kg SC TID). Octreotide can also be employed to rapidly decrease gastric acid secretion in patients discovered to have large ulcers at endoscopy and may also be useful for controlling gastric bleeding (see human studies).

Mucosal Protectants

The PGE2 analog, misoprostol, protects against NSA1D-induced erosions in dogs at doses that do not inhibit acid secretion (3 to 5 μg / kg PO TID in dogs) and may be given to dogs receiving chronic NSAIDs for arthritis. The main side effect of misoprostol is diarrhea and it should not be given to pregnant animals.

The mucosal protectant polyaluminum sucrose sulfate (sucralfate) binds to areas denuded of mucosal epithelium regardless of the underlying cause and is useful lor treating gastric erosions and ulcers and esophagitis. Sucralfate can be given to patients receiving injectable antacids, but it may compromise absorption of other oral medications and is probably best separated from these by 2 hours or so.

In contrast to the efficacy of misoprostol and H2 antagonists in preventing NSAID-induced erosions, the prophylactic administration of various combinations of misoprostol, cimetidine, and omeprazole has not been shown to prevent gastric erosions in dogs with or without intervertebral disk disease receiving high-dose glucocorticoids. However, these drugs may speed healing of gastric lesions in these patients. Sucralfate is probably the drug of choice for treating gastrointestinal ulceration in patients receiving high doses of corticosteroids because it is not dependent on the premise that acid is causing or delaying healing.

Mast cell tumors are also worth considering separately as gastric ulceration is a frequent and severe complication. Mast cell tumors are thought to cause vomiting via the central effects of histamine on the CRTZ and the peripheral effects of histamine on gastric acid secretion (with resultant hyperacidity and ulceration). Treatment of mastocyosis with H1 and H2 histamine antagonists (e. g., diphenhydramine and famotidine) should reduce the central and peripheral effects of histamine. Corticosteroids are used to decrease tumor burden. Where acid hypersecretion is present, or is suspected, it is likely best managed with proton pump inhibitors (e. g., omeprazole 0.2 to 0.7 mg / kg SID). Somatostatin analogs may also be useful for controlling refractory gastric acid hypersecretion (Octreotide 2 to 20 μg / kg SC TID).


Antiemetics can be used where vomiting is severe or compromising fluid and electrolyte balance, or causing discomfort. The initial agent used in dogs is usually metoclopramide, which antagonizes D2-dopaminergic and 5HT3-serotonergic receptors and has cholinergic effects on smooth muscle (1 mg / kg / 24h CRI IV). Phenothiazine derivatives such as chlorpromazine and prochlorperazine are antagons of alpha1 and alpha2-adrenergic, H1 -and H2-histaminergic, and D2-dopaminergic receptors in the vomiting center and CRTZ and are used if metoclopramide is ineffective and the patient is normotensive. Nonselective cholinergic receptor antagonists (other than the M1 specific antagonist- pirenzipine) such as atropine, scopolamine, aminopentamide, and isopropamide are generally avoided as they may cause ileus, delayed gastric emptying, and dry mouth.

Antibiotics and Analgesia

Prophylactic antibiotic cover (e. g., cephalosporins, ampicillin) may be warranted in animals with shock and major gastrointestinal barrier dysfunction. Leukopenia, neutrophilia, fever, and bloody stools are additional indications for prophylactic antibiotics in animals with vomiting or diarrhea. Initial choices in these situations include ampicillin or a cephalosporin (effective against gram-positive and some gram-negative and anaerobic bacteria), which can be combined with an aminoglycoside (effective against gram-negative aerobes) when sepsis is present and hydration status is adequate, Enrofloxacin is a suitable alternative to an aminoglycoside in skeletally mature patients at risk of nephrotoxicity from an aminoglycoside.

Analgesia can be provided using opioids like buprenor-phine (0.0075 to 0.01 mg / kg IM).

Surgery may be required when the cause of ulceration is unclear or to resect large non-healing ulcers or those about to perforate.


Chronic Gastritis

Gastritis is a common finding in dogs, with 35% of dogs investigated for chronic vomiting and 26% to 48% of asymptomatic dogs affected. The prevalence in cats has not been determined. The diagnosis of chronic gastritis is based on the histologic examination of gastric biopsies and it is usually subclassified according to histopathological changes and etiology.

Histopathologic Features of Gastritis

Gastritis in dogs and cats is usually classified according to the nature of the predominant cellular infiltrate (eosinophilic, lymphocytic, plasmacytic, granulomatous, lymphoid follicular), the presence of architectural abnormalities (atrophy, hypertrophy, fibrosis, edema, ulceration, metaplasia), and their subjective severity (mild, moderate, severe). A standardized visual grading scheme has been proposed by Happonen et al and has been adapted for pathologists.

The most common form of gastritis in dogs and cats is mild to moderate superficial lymphoplasmacytic gastritis with concomitant lymphoid follicle hyperplasia. Eosinophilic, granulomatous, atrophic, and hyperplastic gastritis are less common.


Despite the high prevalence of gastritis an underlying cause is rarely identified, and in the absence of systemic disease, ulcerogenic or irritant drugs, gastric foreign objects, parasites (Physalloptera and Ollulanus spp. ), and in rare instances fungal infections (Pythium insidiosum, Histoplasma spp. ), it is usually attributed to dietary allergy or intolerance, occult parasitism, or a reaction to bacterial antigens, or unknown pathogens. Treatment is often empirical but can serve to define the cause of gastritis, such as diet responsive, antibiotic responsive, steroid responsive, or parasitic.

Although the basis of the immunologic response in canine and feline gastritis is unknown, recent studies in experimental animals have shed light on the immunologic environment in the gastrointestinal tract and reveal a complex interplay between the gastrointestinal microflora, the epithelium, immune effector cells such as lymphocytes and macrophages, and soluble mediators such as chemokines and cytokines. In health, this system avoids active inflammation by antigen exclusion and the induction of immune tolerance. The development of intestinal inflammation in mice lacking the cytokines IL-10, TGFP, or IL-2 indicates the central importance of cytokines in damping down mucosal inflammation. In many of these murine models gastrointestinal inflammation only develops in the presence of indigenous intestinal microflora, leading to the hypothesis that spontaneous mucosal inflammation may be the result of a loss of tolerance to the indigenous gastrointestinal microflora. The role of these mechanisms in outbred species such as the dog and cat remains to be determined, but clearly loss of tolerance to bacterial of dietary antigens should be considered.

The epithelial cell is also emerging as a “general” in the inflammatory response, with gram-negative or pathogenic bacteria inducing proinflammatory cytokine (e. g., IL-8, ILI-p) secretion from epithelial cells, whereas commensal or bacteria such as S. fecium or Lactobacillus spp. induce the production of the immunomodulatory cytokines TGFB or IL-10.The pro-inflammatory cytokines produced by epithelial cells are modulated by the production of IL-10 from macrophages and potentially by the epithelial cells themselves. In this context, dogs with lymphoplasmacytic gastritis of undetermined etiology showed a correlation between the expression of the immunomodulatory cytokine IL-10 and proinflammatory cytokines (IFN-γ, IL-1β, IL-8). Simultaneous expression of IL-10 and IFN-y mRNA has also been observed in the intestines of beagle dogs (lamina propria cells and the intestinal epithelium) in the face of a Iuminal bacterial flora that was more numerous than that of control dogs. Thus it is tempting to visualize a “homeostatic loop” consisting of proinflammatory stimuli and responses, countered by immunomodulation and repair, with an imbalance in either of these arms manifested as gastritis.

The importance of unknown pathogens in the development of mucosal inflammation is best demonstrated by the gastric bacterium Helicobacter pylori, a gram-negative bacterium, which chronically infects more than half of all people worldwide. Chronic infection of human adults with H. pylori is characterized by the infiltration of polymorphonuclear and mononuclear cells and the up-regulation of pro-inflammatory cytokines and the chemokine IL-8.Mucosal T cells in infected individuals are polarized toward the production of gamma interferon (IFN-γ), rather than IL-4 or IL-5 indicating a strong bias toward a TH-1 type response). This sustained gastric inflammatory and immune response to infection appears to be pivotal for the development of peptic ulcers and gastric cancer in people.

There is also a high prevalence of gastric Helicobacter spp. infection in dogs (67% to 100% of healthy pet dogs, 74% to 90% of vomiting dogs, 100% of laboratory beagles) and cats (40% to 100% of healthy and sick cats). In contrast to people, in whom Helicobacter pylori infection predominates, dogs and cats are colonized by a variety of large spiral organisms (5 to 12 n). In cats from Switzerland, United States, and Germany, Helicobacter heilmannii is the predominant species, with Helicobacter bizzozeronii and Helicobacter felis much less frequent. In dogs from Finland, Switzerland, the United States, and Denmark Helicobacter bizzozeronii and Helicobacter salomonis are most common followed by Helicobacter heilmanni and Helicobacter felis. Helicobacter bilis and Flexispira rappini have also been described. Cats can also be colonized by Helicobacter pylori (2 to 5 p) but infection has been limited to a closed colony of laboratory cats.

Ownership of dogs and cats has been correlated with an increased risk of infection of Helicobacter heilmannii in people. Case reports have also suggested the transmission of Helicobacter spp. from pets to man. Recent studies clearly confirm that dogs and cats harbor H. heilmannii, but the subtypes of H. heilmannii present in dogs and cats (types 2 and 4) are of minor importance (approximately 15% of cases) to humans, who are predominantly colonized by H. heilmannii type 1 (the predominant Helicobacter sp. in pigs).

The effect of eradicating Helicobacter spp. on gastritis and clinical signs, the main form of evidence supporting the pathogenic role of H. pylori in human gastritis, has not been thoroughly investigated to date in dogs and cats. An uncontrolled treatment trial of dogs and cats with gastritis and Helicobacter spp. infection showed that clinical signs in 90% of 63 dogs and cats responded to treatment with a combination of metronidazole, amoxicillin, and famotidine, and that 14 of the 19 animals re-endoscoped had resolution of gastritis and no evidence of Helicobacter spp. in gastric biopsies.

Controlled clinical trials are required to confirm these observations but have been hampered by a much higher apparent recrudescence or re-infection rate than the 1 % to 2% per year observed after treatment of H. pylori-infected people. With such limited information from eradication trials, most current knowledge about the pathogenicity of Helicobacter spp. for dogs and cats comes from the evaluation of animals with and without infections and clinical signs, and a small number of experimental infections.

The large Helicobacter species found in dogs an cats do not attach to the epithelium but colonize the superficial mucus and gastric glands, particularly of the fundus and cardia, and may also be observed intracellularly. Degeneration of gastric glands, with vacuolation, pyknosis, and necrosis of parietal cells is more common in infected than uninfected animals. Inflammation is generally mononuclear in nature and ranges from mild to moderate in severity. Gastric lymphoid hyperplasia is common and can be extensive in dogs and cats infected with Helicobaaer spp. (particularly when full thickness gastric biopsies are evaluated). In addition to this local gastric immune response, a systemic response characterized by increased circulating anti-Helicobacter IgG has been detected in sera from naturally infected dogs and cats. However, the gastritis observed in cats and dogs infected with large HLOs is generally less severe than that observed in Helicobacter pylori infected humans (where neutrophilic aggregates, and moderate to severe gastritis, are commonly encountered), and gastro-intestinal ulcers, gastric neoplasia, or changes in serum gastrin or acid secretion have not been associated with Helicobacter spp. infection in dogs and cats.

These differences between people, dogs, and cats may be attributed to differences in the virulence of the infecting Helicobacter spp., or the host response. Studies that address this issue indicate that Helicobacter pylori evokes a more severe pro-inflammatory cytokine and cellular response in dogs and cats than natural or experimental infection with large Helicobacter spp. The limited mucosal inflammatory response and absence of clinical signs in the vast majority of dogs and cats infected with non-H. pylori Helicobaaer spp., despite significant antigenic stimulation (evidenced by seroconversion and lymphoid follicle hyperplasia) suggest that large gastric Helicobacter spp. are more commensal than pathogenic. With this in mind, it is interesting to speculate that it is the loss of tolerance to gastric Helicobacter spp., rather than the innate pathogenicity of these bacteria, that explains the development of gastritis and clinical signs in some dogs and cats. However, much still remains to be learned about the role of Helicobacter spp. in canine and feline gastritis.

Clinical Findings

The major clinical sign of chronic gastritis is vomiting of food or bile. Decreased appetite, weight loss, melena, or hematemesis is variably encountered. The concurrent presence of dermatoIogic and gastrointestinal signs raises the likelihood of dietary sensitivity. Access to toxins, medications, foreign bodies, and dietary practices should be thoroughly reviewed. The signalment should not be overlooked as it may increase the probability that chronic gastritis is the cause of vomiting. Hypertrophy of the fundic mucosa is frequendy associated with a severe enteropathy in basenjis and stomatocytosis, hemolytic anemia, icterus, and polyneuropathy in Drentse Patrijshond. Hypertrophy of the pyloric mucosa is observed in small brachycephalic dogs such as Lhasa apso and is associated with gastric outflow obstruction (see Delayed Gastric Emptying and Motility Disorders). Atrophy of the gastric mucosa that may progress to adenocarcinoma has been reported in Lundehunds with protein-losing gastroenteropathy.

Young, large breed, male dogs in the Gulf states of the United States may have granulomatous gastritis caused by Pythium spp. with infection more prevalent in fall, winter, and spring. Physical examination is often unremarkable. Abdominal distension may be related to delayed gastric emptying caused by obstruction or defective propulsion. Abdominal masses, lymphadenopathy, or ocular changes may be encountered in dogs with gastric fungal infections.


A biochemical profile, complete blood count, urinalysis, and T4 (cats) should be performed as a basic screen for metabolic, endocrine, infectious, and other non-GI causes of vomiting, as well as the acid base and electrolyte changes associated with vomiting, outflow obstruction, or acid hypersecretion. Clinicopathologic tests are often normal in patients with chronic gastritis.

Eosinophilia may prompt the consideration of gastritis associated with dietary hypersensitivity, endoparasites, or mast cell tumors. Hyperglobulinemia and hypoalbuninemia may be present in basenjis with gastropathy / enteropathy, or dogs with gastric pythisosis. Panhypoproteinemia is a feature of gastroenteropathy in Lundehunds, moderate to severe generalized inflammatory bowel disease, gastrointestinal lymphoma, and gastrointestinal histoplasmosis. More specific testing, such as an adrenocorticotropic hormone stimulation test, or serology for Pythium isnsidiosum, is performed based on the results of these initial tests. Determination of food specific IgE has not been shown to be useful in the diagnosis of dietary sensitivity in dogs or cats. The utility of noninvasive tests, such as serum pepsinogen and gastric permeability to sucrose, used to diagnose gastritis in people has not been determined in dogs and cats.

Abdominal radiographs are frequently normal in dogs and cats with gastritis but may show gastric distention or delayed gastric emptying (food retained more than 12 hours after a meal). Contrast radiography may reveal ulcers or thickening of the gastric rugae or wall but has largely been supersceded by the combination of ultrasonography to detect mural abnormalities and endoscopy to observe and sample the gastric mucosa.

Endoscopic examination enables the visualization of foreign bodies, erosions, ulceration, hemorrhage, rugal thickening, lymphoid follicle hyperplasia (evident as mucosal pock marks), increased mucus or fluid (dear or bile stained), and increased or decreased mucosal friability. Discrete focal or multifocal mucosal nodules may be observed with Ollulanus spp. infection.

Gastric phycomycosis can be associated with irregular masses in the pyloric outflow tract and may prompt serologic testing by ELISA, Western blotting, and culture of fresh gastric biopsies. Parasites such as Physalloptera spp. may be observed as 1- to 4-cm worms. Large amounts of bile stained fluid is suggestive of duodenogastric reflux-associated gastritis, whereas lots of clear fluid my indicate hypersecretion of gastric acid. Gastric fluid can be aspirated for cytology (Helicobacter spp., parasite ova or larvae) and pH measurement. Impression smears of gastric biopsies are an effective way of looking for Helicobacter spp. (5 to 12 u spirals) and are more sensitive than the biopsy urease test (Helicobacter spp. produce urease). Serum gastrin should be measured in the face of unexplained gastric erosions, ulcers, fluid accumulation, or mucosal hypertrophy.

The endoscopic procedure of dribbling dietary antigens onto the gastric mucosa to ascertain the presence of food allergy has not been useful in dogs or cats: it is highly subjective, detects only immediate hypersensitivity, and does not correlate with the results of dietary elimination trials. The stomach should be biopsied even when it looks grossly normal (usually three biopsies from each region- pylorus, fundus, and cardia). Thickened rugae may require multiple biopsies, and a full-thickness biopsy is often required to differentiate gastritis from neoplasia or fungal infection and to diagnose submucosal or muscular hypertrophy. The results of gastric ultrasonography can help to forewarn the clinician of these possibilities and are complement to the endoscopic findings.

Gastric sections should be stained with H&E for evaluation of cellularity and architecture, and modified Steiner stain for gastric spiral bacteria. Further special stains, such as Gomori’s methenamine silver, are indicated if pyogranulomatous inflammation is present to detect fungi. Masson’s trichrome can be used to highlight gastric fibrosis, whereas sirius red and alcian blue help to reveal eosinophils and mast cells, respectively. Immunocytochemistry can be employed to help distinguish lymphoma from severe lymphocytic gastritis. Mucin staining has been performed in Lundchunds with gastric atrophy and showed an abnormal presence of mucus neck cells and pseudo-pyloric metaplasia.

The interpretation of gastric biopsies has important implications for patient care because biopsy findings are often used to guide treatment. For example, moderate lymphoplasmacytic gastritis without Helicobacter spp. infection is often treated with corticosteroids, whereas mild lymphoplasmacytic gastritis may be treated with a change in diet. As the histopathologic evaluation of gastric biopsies has not been standardized, the prudent clinician should carefully review histologic sections to get a feel for the pathologist’s interpretation. Even with optimum evaluation similar histologic changes can be observed in patients with different underlying etiologies, so well-structured treatment trials often form the basis of an etiologic diagnosis.


Treatment of gastritis initially centers on the detection and treatment of underlying metabolic disorders and the removal of drugs, toxins, foreign bodies, parasites, and fungal infections.

Parasitic Gastritis

Ollulanus tricuspis is a microscopic worm (0.7 to 1 mm long, 0.04 mm wide) that infects the feline stomach. Its predominant cat-to-cat transmisison is through ingestion of vomitus. It can also undergo internal autoinfection with worm burdens reaching up to 11, 000 per stomach. Mucosal abnormalities range from none, to rugal hyperplasia, and nodular (2 to 3 mm) gastritis.

Histologic findings include lymphoplasmacytic infiltrates, lymphoid follicular hyperplasia, fibrosis, and up to 100 / hpf globular leukocytes. Ollulanus spp. are not detected by fecal examination and require evaluation of gastric juice, vomitus, or histologic sections for larvae or worms. Gastric lavage and xylazine-induced emesis have been described to aid diagnosis. Treatment with fenbendazole 10 mg / kg PO SID 2d may be effective.

Physalloptera spp. are about 2 to 6 cm long worms that are sporadically detected in the stomachs of dogs and cats. Physalloptera rara are most commonly described and appear to be primarily a parasite of coyotes. Diagnosis is difficult as worm burden is often low and the eggs are transparent and difficult to see in sugar floatation. Treatment with pyrantel pamoate (5 mg / kg PO:dogs single dose; cats two doses 14 days apart) may be effective. Control of infection may be difficult due to the ingestion of intermediate hosts, such as cockroaches and beedes, and paratenic hosts, such as lizards and hedgehogs.

Given the difficult diagnosis of Ollulanus and Physalloptera spp., empirical therapy with an anthelminthic such as fenbendazole may be warranted in dogs and cats with unexplained gastritis.

Gastric infection with Gnathostoma spp. (cats), Spirocerca spp. (dogs), and Aonchotheca spp. (cats) has been associated with gastric nodules that have been treated by surgical resection of affected gastric tissue.

Gastric Pythiosis

The presence of transmural thickening of the gastric outflow tract and histology that indicates pyogranulomatous inflammation raise the possibility of infection with fungi such as Pythium insidiosum. Special staining (Gomoris methenamine silver), culture, serology, and PCR of infected tissues can be used to help confirm the diagnosis. Treatment consists of aggressive surgical resection combined with itraconazole (10 mg / kg PO SID) and terbinafine (5 to 10 mg / kg PO SID) for 2 to 3 months post-surgery. ELISA titers of pre- and post-treatment samples may show a marked drop during successful treatment and drugs can be stopped. Medical therapy is continued for another 2 to 3 months if titers remain elevated. The prognosis is poor and fewer than 25% of afflicted animals are cured with medical therapy alone.

Helicobacter-Associated Gastritis

The general lack of knowledge of the pathogenicity of gastric Helicobacter spp. has meant that veterinarians are faced with the dilemma of either treating or ignoring spiral bacteria observed in biopsies from patients with chronic vomiting and gastritis. In light of their pathogenicity in man, ferrets, cheetahs, and mice, it would seem prudent that eradication of gastric Helicobacter spp. is attempted prior to initiating treatment with immunosuppressive agents to control gastritis. However, this must be decided on an individual basis. For example, in the patient with a lvmphoplasmacytic infiltrate of the stomach and small intestine with a concomitant gastric Helicobacter spp. infection, should one treat for inflammatory bowel disease, Helicobacter, or both?

The author recommends treating only symptomatic patients that have biopsy-confirmed Helicobacter spp. infection and gastritis. Current treatment protocols are based on those found to be effective in humans infected with Helicobacter pylori. An uncontrolled treatment trial of dogs and cats with gastritis and Helicobacter spp. infection showed that clinical signs in 90% of 63 dogs and cats responded to treatment with a combination of metronidazole, amoxicillin, and famotidine, and that 74% of 19 animals re-endoscoped had no evidence of Helicobacter spp. in gastric biopsies.

Unfortunately these promising results regarding the eradication of Helicobacter spp. have not been borne out by more controlled studies in asymptomatic Helicobacter-infected dogs and cats. Treatment combinations that have been critically evaluated are (1) amoxicillin (20 mg / kg PO BID 14d), metronidazole (20 mg / kg PO BID 14d), and famotidine (0.5 mg / kg PO BID 14d) in dogs; (2) clarithromycin (30 mg PO BID 4d), metronidazole (30 mg PO BID 4d), ranitidine (10 mg PO BID 4d), and bismuth (20 mg PO BID 4d) (CMRB) in H. heilmannii infected cats and (3) azithromycin (30 mg PO SID 4d), tinidazole (100 mg PO SID 4d), ranitidine (20 mg PO SID 4d) and bismuth (40 mg PO SID 4d)(ATRB) in H. heilmannii-infecled cats. Re-evaluation of infection status at 3 days (dogs) or 10 days (cats) after treatment revealed six of eight dogs and 11 of 11 CMRB and four of six ATRB-treated cats to be Helicobacter spp. free on the basis of histology and urease testing (dogs) or C-urea breath test (dogs and cats). However, at 28 days (dogs) or 42 days (cats) after completing antimicrobial therapy, eight of eight dogs and four of eleven cats that received CMRB, five of six cats that received ATRB were found to be re-infected. A transient effect of combination therapy (amoxicillin 20 mg / kg PO TID 2Id, metronidazole 20 mg / kg PO TID 21d, and omeprazole 0.7 mg PO SID 2Id) on bacterial colonization has also been observed in six cats with H. pylori infection.

Further analysis of gastric biopsies from infected dogs and H. pylori infected cats using PCR and Helicobacter-specific primers revealed persistence of Helicobacter DNA in gastric biopsies that appeared negative on histology and urease testing. These studies suggest that antibiotic regimens that are effective against H. pylori in people may only cause transient suppression, rather than eradication, of gastric Helicobacter spp. in dogs and cats.

The author has recendy employed the combination of amoxicillin (20 mg / kg PO BID), clarithromycin (7.5 mg / kg PO BID) and metronidazole (10 mg / kg PO BID) for 14 days to eradicate Helicobacter pylori infection in cats. Further controlled trials of antibiotic therapy in infected dogs and cats, particularly symptomatic patients with gastritis and Helicobacter spp. infection, are clearly required before guidelines regarding the treatment of gastric Helicobacter spp. in dogs and cats can be made.

Chronic Gastritis of Unknown Cause

Lymphocytic plasmacytic gastritis of unknown cause is common in dogs and cats. It may be associated with similar infiltrates in the intestines, particularly in cats (who should also be evaluated for the presence of pancreatic and biliary disease). The cellular infiltrate varies widely in severity and it may be accompanied by mucosal atrophy or fibrosis, and less commonly hyperplasia.

Patients with mild Iymphoplasmacytic gastritis are initially treated with diet. The diet is usually restricted in antigens to which the patient has been previously exposed, such as a lamb-based diet if the patient has previously been fed chicken and beef, or contains hydrolyzed proteins (usually chicken or soy) that may be less allergenic than intact proteins. Many of these diets are also high in carbohydrate and restricted in fat, which facilitates gastric emptying, and may contain other substances such as menhaden fish oil or antioxidants that may alter inflammation.

The test diet is fed exclusively for a period of about 2 weeks while vomiting episodes are recorded. If vomiting is improved a challenge with the original diet is required to confirm a diagnosis of food intolerance. The introduction of a specific dietary component to the test diet, such as beef, is required to confirm dietary sensitivity. If vomiting is unresponsive the patient may be placed on a different diet for another 2 weeks, usually the limit of client tolerance, or started on prednisolone (1 to 2 mg / kg / day PO, tapered to every other day at the lowest dose that maintains remission over 8 to 12 weeks).

Patients with moderate to severe Iymphoplasmacytic gastritis are usually started on a combination of a test diet and prednisolone. If the patient goes into remission they are maintained on the test diet while prednisolone is tapered and potentially discontinued. Antacids and mucosal protectants are added to the therapeutic regimen if ulcers or erosion are detected at endoscopy or if hematemesis or melena is noted.

If gastritis is unresponsive to diet, prednisolone, and antacids, additional immunosuppression may be indicated. Gastric biopsies should be carefully re-evaluated for evidence of lymphoma. In dogs immunosuppression is usually increased with azathioprine (PO 2 mg / kg SID for 5d then EOD, on alternating days with prednisolone). Chlorambucil may be a safer alternative to azathioprine in cats (PO) and has been successfully employed in the management of inflammatory bowel disease and small cell lymphoma. Prokinetic agents such as metoclopramide, cisapride, and erythromycin can be used as an adjunct where delayed gastric emptying is present. These are discussed below.

Diffuse eosinophillic gastritis of undefined etiology is usually approached in a similar fashion to Iymphoplasmacytic gastritis. The presence of eosinphilia, dermatologic changes, and eosinophilic infiltrates may be even more suggestive of dietary sensitivity. In cats it should be determined if it is part of a hypereosinophilic syndrome. Treatment for occult parasites, dietary trials, and immunosuppression can be carried out as described above. Focal eosinophilic granulomas can be associated with parasites or fungal infection that should be excluded prior to immunosuppression with corticosteroids.

Atrophic Gastritis

Atrophic gastritis in dogs and cats is often associated with a marked cellular infiltrate. In people atrophy is associated with Helicobacter spp. infection and inflammation, and immune-mediated destruction. Gastric disease is often not discovered until the patient presents with pernicious anemia secondary to cobalamin deficiency caused by a lack of gastric intrinsic factor. In people, atrophic gastritis, intestinal metaplasia of the gastric mucosa, and hypochlorhydia are thought to precede the development of gastric cancer. The host inflammatory response is also thought to contribute to the development of atrophy and pro-inflammatory IL-1β and IL-10 gene polymorphisms in people are associated with increased inflammation, gastric atrophy, hypochlorhydria, and gastric cancer.

Atrophic gastritis has been infrequently described in dogs and cats but does share some similarities with people. Atrophy has been associated with gastric adenocarcinoma in Lundehunds and in dogs with Iymphoplasmacytic gastritis of undetermined cause atrophy correlates with the expression of mRNA for IL-1 B and IL-10 and the presence of neutrophils. However, there is no clear evidence that Iymphoplasmacytic gastritis progresses to atrophy and gastric cancer in dogs or cats, and the role of Helicobacter spp. or antigastric antibodies in the development of atrophy in dogs and cats remains to be determined.

In contrast to humans, dogs and cats with atrophic gastritis have not been reported to develop cobalamin deficiency. This is probably because the pancreas, rather than the stomach, is the main source of intrinsic factor in these species. Achlorhydria has been described in dogs and may enable the proliferation of bacteria in the stomach and upper small intestine, although this has not been proven. The treatment of atrophic gastritis has received limited attention, but Helkobacter spp. eradication and immunosuppression have been effective in people.

Hypertrophic Gastritis

Hypertrophy in the fundic mucosa is uncommon and is often part ol the breed-specific gastropathies or gastroenteropathies mentioned above. Concurrent hypergastrinemia should prompt consideration of underlying hepatic or renal disease, achlorhydria, or gastrin-producing tumors, which should be pursued appropriately. Basenji gastoenteropathy is variably associated with fasting hypergastrinemia and exaggerated secretin stimulated gastrin, and anecdotal reports suggest that affected basenjis may respond to antimicrobial therapy. Antral hypertrophy of brachycephalic dogs causes outflow obstruction and is treated with surgery.


Delayed Gastric Emptying

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

Outflow Obstruction
Congenital stenosis
Foreign bodies
Hypertrophy of pyloric mucosa
Extragastric masses
Defective Propulsion
Gastric disorders
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.