Rational Diagnostic and Therapeutic Approach to the Vomiting Cat
World Small Animal Veterinary Association World Congress Proceedings, 2013
Stanley L. Marks, BVSc, PhD, DACVIM (Internal Medicine, Oncology), DACVN
School of Veterinary Medicine, University of California-Davis, Davis, CA, USA

Vomiting is the forceful expulsion of contents of the stomach and often, the proximal small intestine. It is a manifestation of a large number of conditions, many of which are not primary disorders of the gastrointestinal tract. Vomiting is a common problem seen by veterinarians and there are many reasons behind it. Vomiting is often associated with inflammation or obstruction of the stomach, but may also be associated with diseases of other parts of the gastrointestinal tract or other abdominal organs. Within the gastrointestinal tract, vomiting may also occur due to inflammation, infection, obstruction, motility disorders, or neoplasia affecting the small intestine or, less commonly, colon. Other disorders that may be associated with vomiting include liver, kidney, and pancreatic disease, peritonitis, Addison's disease, hyperthyroidism, diabetic ketoacidosis, pyometra, neoplasia, toxicoses, and central nervous system disorders.

Pathophysiology of the Vomiting Reflex and Mechanisms of Action of Antiemetics

The 4 essential components of the emetic reflex (vomiting reflex) are

1.  Visceral receptors (located in the gastrointestinal tract, peritoneum, bile ducts, etc.)

2.  Vagal and sympathetic afferent neurons

3.  Chemoreceptor trigger zone (CRTZ or CTZ) located within the area postrema of the fourth ventricle that is sensitive to blood-borne substances, and

4.  Emetic (vomiting) center within the reticular formation of the medulla oblongata, receiving input from vagal and sympathetic neurons, CRTZ, vestibular apparatus, and cerebral cortex (Table 1).

There are two main pathways associated with the vomiting reflex: a humoral pathway influenced by blood-borne substances that affect the CRTZ, and a neural pathway influenced by inflammation, infection, malignancy or toxicity of the GI tract that result in activation of the emetic center by vago-sympathetic, CRTZ, vestibular, or cerebrocortical neurons.

Table 1
Table 1

 

Vomiting associated with primary gastrointestinal tract disease results from activation of visceral receptors, afferent neurons, and the emetic center. Efferent information transmitted back to the gastrointestinal tract stimulates the motor correlates of vomiting (retrograde duodenal and gastric contractions, relaxation of the caudal esophageal sphincter, gastroesophageal reflux, opening of the proximal esophageal sphincter, and evacuation of gastrointestinal contents). A neural pathway can also be involved in vomiting associated with motion sickness. Motion within the semicircular canals is transduced to vestibulo-cochlear neurons that ultimately synapse in the CRTZ or emetic center. Cats and dogs experience motion sickness, although the neuroanatomy and pharmacology appear to be somewhat different between the two species. Histaminergic neurons and the CRTZ are involved in motion sickness in the dog, whereas their involvement has not yet been conclusively demonstrated in the cat. This is why H1-receptor antagonists work well in the dog for preventing or managing motion sickness, but not in the cat. Motion sickness in cats is thought to be influenced by one or more receptors in the emetic center, which is why α2-receptor antagonists would be a better choice.

Some neurotransmitter-receptor systems are probably more important than others. For example, apomorphine, a D2 dopamine receptor agonist, is a potent emetic agent in the dog, but it does not readily induce emesis in the cat. This finding has two important implications:

1.  CRTZ D2 dopamine receptors are not as important in mediating humoral emesis in the cat, and

2.  D2 dopamine receptor antagonists [e.g., metoclopramide (Reglan)] are not very effective anti-emetic agents in the cat.

Cancer chemotherapy induced-emesis is usually mediated by activation of 5-hydroxytryptamine 3 (5-HT3) receptors in the CRTZ of the cat, while visceral and vagal afferent 5-HT3 receptors may be more importantly involved in the dog. Antagonists of the 5-HT3 receptor are effective for the prevention of emesis associated with chemotherapy in cats and dogs. Dolasetron (Anzemet) and ondansetron (Zofran) are potent inhibitors of the 5-HT3 receptors, which is why these drugs are such effective antiemetics for patients receiving chemotherapy, or patients that are refractory to conventional antiemetics. Cisapride (Propulsid) is a potent 5-HT4 agonist, ensuring its potent prokinetic activity; however, its 5-HT3 inhibitory activity is very low precluding its use as a direct antiemetic. Lastly, metoclopramide exhibits 5-HT4 agonistic activity, D2-dopaminergic antagonistic activity, and weak 5-HT3 antagonistic activity. Metoclopramide is a relatively effective antiemetic agent when given as a constant rate infusion to dogs; however, it is not as effective in the cat for the reasons mentioned above. Dolasetron and ondansetron are much more potent 5-HT3 antagonists than metoclopramide and appear to be more effective antiemetics. Note that metoclopramide has prokinetic effects, as well as antiemetic effects, whereas dolasetron and ondansetron do not have any prokinetic activity.

A relatively new antiemetic, Cerenia (maropitant citrate) has been approved for use in dog and cats. This drug is a potent neurokinin-1 (NK-1) receptor antagonist, and prevents the binding of substance P with this receptor. The NK-1 receptor has been shown to play an important role in vomiting mediated via the CRTZ and vomiting center, and the drug has shown promise for the prevention of motion sickness, chemotherapy-induced nauseousness and vomiting, as well as the management of vomiting from a variety of other causes. Cerenia is available in injectable and tablet form, and was recently approved for use in the dog and cat as an antiemetic, and in dogs for the prevention of motion sickness.

Diagnostic Approach to the Vomiting Cat

1. The most critical step during initial evaluation of cats presenting for vomiting is to differentiate between true vomiting and regurgitation

In contrast to regurgitation, which is a passive process, vomiting is an active neurologically mediated reflex that is usually associated with antecedent events, such as retching and salivation, and is followed by abdominal contractions. Expulsion of yellow material suggests bile-stained duodenal contents and is more consistent with vomiting. Be cautious in overinterpreting the timing of the event in relation to the consumption of the meal. Regurgitating cats can passively expel their esophageal or gastric contents hours after ingestion of a meal in some cases.

Important questions to consider when differentiating vomiting from regurgitating include the following:

1.  Did you observe active abdominal contractions when your cat was "throwing up" or were the events passive?

2.  How long after eating do the episodes occur?

3.  What is the appearance of the material?

4.  Have you noticed any concurrent diarrhea in your cat?

5.  Do the episodes occur at any particular time of the day or night?

6.  How often do you feed your cat?

7.  Does your cat have access to chew toys or linear foreign bodies (dental floss, etc.)?

8.  Has there been recent administration of any medications, including NSAIDs?

9.  Do you have any other pets in the house, and how are they doing?

2. The second important step is to determine if the animal has either a self-limiting or possible life-threatening problem

This decision is based on a comprehensive history and thorough physical examination, clinical experience, and understanding of the differential diagnosis of vomiting. The age and breed of the animal help rank the probability for possible causes. Pancreatitis, IBD, and cholangitis can be associated with intermittent episodes of vomiting in cats. Siamese cats are predisposed to IBD and consideration of the breed is always important in helping to formulate a list of differentials for the animal. Aggravation of the vomiting by a certain diet raises the possibility of dietary intolerance or food allergy. Persistent vomiting of large volumes of liquid vomitus in spite of food restriction is highly suggestive of pyloric or upper intestinal obstruction. Vomiting of food greater than 12 hours after ingestion is consistent with delayed gastric emptying. The physical examination may reveal the cause of the vomiting (e.g., foreign body wrapped around the base of the tongue) or yield findings that narrow the differential list (e.g., lymphadenopathy secondary to intestinal lymphoma, icterus secondary to liver disease, abdominal discomfort secondary to pancreatitis).

Warning Signs of Serious Disease

The presence of one or more of the following historical features or physical exam findings warrants hospitalization and a more comprehensive work-up of the animal:

 Fever

 Melena

 Weakness

 Anorexia > 48 hrs

 Abdominal pain

 Vomiting of "coffee grounds" or frank blood

 Pale, congested, or muddy mucous membranes

 Abdominal organomegaly (enlargement of liver, spleen, kidneys, or lymph nodes; thickened intestinal loops)

The history may uncover the administration of NSAIDs (aspirin, ibuprofen) that may be the cause of the acute vomiting. The presence of concurrent diarrhea may indicate a food-responsive enteropathy, IBD, or gastrointestinal parasites (ascarids in kittens, Giardia infection). Physical examination is often normal, although cats with acute vomiting may present with mild lethargy and mild to moderate dehydration. Abdominal palpation is often normal, although evidence of mild abdominal pain may be found.

A complete blood count (CBC) should be obtained if the animal is febrile on physical exam. Abdominal radiographs should be obtained in ANY animal with an acute history of vomiting to rule out gastric or intestinal foreign bodies. The diagnostic work-up of animals with one or more of the warning signs mentioned above should include more comprehensive testing, including a complete blood count, serum biochemical profile, urinalysis, zinc sulfate fecal flotation, SPEC fPL (for pancreatitis) and abdominal imaging with survey abdominal radiographs followed by abdominal ultrasound if warranted. A parvo SNAP test should be considered on any kitten with vomiting or diarrhea, irrespective of the patient's vaccination history. Abdominal radiographs are especially helpful in animals suspected of ingesting foreign bodies, or in animals with gaseous distention of the stomach or intestinal tract. Abdominal radiographs are of lower diagnostic yield in animals with abdominal effusions or in severely emaciated animals. A serum T4 is warranted in cats > 5 years old with a history of vomiting or diarrhea. The decision for performing more in-depth diagnostic tests such as endoscopy is based on ongoing clinical signs, response to therapy, and initial test results.

Therapy for the Acutely Vomiting Cat

In general, goals of therapy include (1) removing the underlying cause, (2) controlling the vomiting episodes, and (3) correcting the fluid, electrolyte, and acid-base abnormalities that are a frequent consequence of chronic vomiting.

Diet

Cats with intractable vomiting should be kept NPO until the vomiting ceases for 12 to 24 hours. This is predominantly to decrease the risk of aspiration. If vomiting does not recur after 24 hours, a small volume of a digestible intestinal formula or elimination diet (containing a novel, single protein source) should be fed. Dietary fat content appears to play a smaller role in gastric emptying in the cat. Cats do not need a carbohydrate source and are best managed with a single-protein source such as cooked chicken breast. Feeding small meals frequently will minimize gastric distention and gastric acid secretion. Commercially available intestinal diets are suitable for managing cats with acute gastritis.

Cytoprotective Agents

1. Histamine H2-Receptor Antagonists

Histamine H2-receptor antagonists are the most commonly used drugs to manage gastric ulceration or severe gastritis. These agents competitively block the H2 receptor on the parietal cell, reducing gastric acid secretion. The H2 receptor antagonists currently available include cimetidine, ranitidine, famotidine, and nizatidine. Cimetidine (Tagamet) is the least potent of the H2-receptor antagonists, and also inhibits the cytochrome P-450 enzyme system, potentially resulting in altered metabolism of co-administered drugs that are metabolized by the same enzyme system. Ranitidine (Zantac) is approximately 5–12 times more potent than cimetidine on a molar basis in inhibiting gastric acid secretion in humans. Ranitidine also inhibits the cytochrome P-450 enzyme system, but much less than cimetidine. In addition, ranitidine stimulates gastrointestinal motility in vitro by inhibition of acetylcholinesterase activity. Famotidine (Pepsid) and nizatidine (Axid) are more potent than cimetidine and famotidine, and these agents do not inhibit the cytochrome P-450 enzyme system. Nizatidine also stimulates gastrointestinal motility in vitro via inhibition of acetylcholinesterase activity.

2. Sucralfate (Carafate)

Sucralfate (Carafate) is a basic aluminum salt of a sulfated disaccharide that has selective binding to proteins at the ulcer site by way of electrostatic interactions. At low pH, sucralfate dissociates into aluminum and sucrose sulfate. The drug has a sustained local protective effect against acid, pepsin and bile at the ulcer site, forming a protective barrier. In addition, sucralfate increases the luminal concentration of prostaglandin E2, which is also protective against ulcerogenic factors. Because sucralfate is not absorbed from the gastrointestinal tract, it has virtually no systemic toxicity. The only side effect that may be seen in rare instances is constipation (due to the aluminum moiety). Sucralfate may also inhibit the absorption of other drugs, including tetracycline, phenytoin, and potentially the H2-receptor antagonists.

3. Misoprostol (Cytotec)

Misoprostol (Cytotec) is another gastric mucosal protectant that represents the first synthetic analogue of prostaglandin E1 to become commercially available. Misoprostol exerts both a local cytoprotective effect on the mucosa and also decreases acid secretion by a direct effect on the gastric parietal cells. Parietal cells contain prostaglandin receptors in proximity to histamine H2-receptors. Misoprostol exerts multiple cytoprotective effects, including:

 Increasing bicarbonate and mucus secretion

 Inhibiting back diffusion of hydrogen ions

 Enhancing mucosal blood flow

 Preserving mucosal regenerative capacity

4. Omeprazole (Prilosec)

Omeprazole (Prilosec) is currently the most potent inhibitor of gastric acid secretion available. Omeprazole irreversibly blocks the gastric proton pump (hydrogen-potassium ATPase), causing a marked decrease in gastric acid secretion. Omeprazole is now available OTC, markedly reducing its cost and increasing its availability and usage in small animals. Omeprazole should be considered in small animals diagnosed with severe reflux esophagitis, or gastric ulceration secondary to systemic mastocytosis or gastrinoma.

Prokinetic Agents

Agents which enhance gastrointestinal motility, such as metoclopramide (Reglan) and cisapride (Propulsid), may be indicated if the gastritis is associated with delayed gastric emptying, and there is no evidence of gastrointestinal obstruction.

Crystalloid Fluids

In mild dehydration, subcutaneous fluids are useful. Isotonic fluids should be used and no more than 10 to 20 ml/kg should be given at each injection site. The rate of subcutaneous fluid flow usually is governed by patient comfort. These fluids are aseptically administered and multiple sites are required to provide adequate fluid volume. Generally, all subcutaneous fluids are resorbed within 6 to 8 hours. If fluids are still noted subcutaneously after this time, the use of intravenous fluids to reestablish peripheral perfusion should be considered. The % dehydration can easily be determined by assessing the patient during the physical examination. Animals with a history of fluid loss, but no findings of dehydration on physical examination, are considered to be < 5% dehydrated; animals with dry oral mucous membranes but no panting or pathological tachycardia are considered to be 5% dehydrated; animals with mild to moderate decreased skin turgor, dry oral mucous membranes, slight tachycardia, and normal pulse pressure are considered to be 7% dehydrated, and animals with moderate to marked degree of decreased skin turgor, dry oral mucous membranes, tachycardia, and decreased pulse pressure are considered to be 10% dehydrated. Animals with marked loss of skin turgor, dry oral mucous membranes, and significant signs of shock are considered to be 12% dehydrated.

The volume of fluid administered during the dehydration phase is based on an assessment of fluid needs for the following:

 Returning the patient's status to normal (deficit volume)

 Replacing normal ongoing losses (maintenance volume)

 Replacing continuing abnormal losses (continuing losses volume)

The deficit volume is an estimate based on findings from the physical examination (see estimates for % dehydration above) or on known changes in body weight. To make the calculation of deficit volume, the estimated dehydration is multiplied by the body weight, and this is replaced during the first 24 hrs. Don't forget that you must also add "daily maintenance volumes" to your calculated deficit volume if the animal is not eating nor drinking.

Example

A 22-lb (10 kg) dog is assessed to be 7% dehydrated. What volume of fluid deficit should be given during the first 24 hours?

Total deficit replacement volume = deficit volume + maintenance volume

Deficit replacement volume (ml) = % dehydration x body weight (kg) = 7% (0.07) x 10 X 1000 = 700 mL

Maintenance volume = 50 mL/kg/day for dogs and 40 mL/kg/day for cats.

Fluid requirement is determined by adding the dog's deficit volume (700 mL) to the dog's maintenance volume [(50 mL x 10) = 500 mL] = 1,200 mL. Continuing losses such as vomiting or diarrhea should be estimated and added to the patient's fluid volume.

Animals that are deemed to be 7% dehydrated should be administered fluids intravenously.

Lactated Ringer's solution and 0.9% saline are the fluids of choice. Acetated polyionic solutions such as Normosol-R and Plasmalyte should not be given SQ due to the discomfort associated with administration. Potassium supplementation to replace that lost in vomitus is usually necessary, since whole body depletion of potassium can cause hypomotility of the gastrointestinal tract. Metabolic acidosis is often present, but will usually be corrected by appropriate fluid therapy.

Antibiotics

Antibiotics are generally avoided unless the animal is febrile, has evidence of vomiting blood or bloody stools, or has an abnormal CBC that suggests systemic infection. Broad-spectrum coverage with antibiotics, such as amoxicillin together with enrofloxacin, provides excellent coverage against most bacteria that are associated with infection following breakdown of the gastrointestinal mucosal barrier.

Antiemetics

Antiemetic therapy is warranted: (1) when the vomiting is frequent or severe enough to make the animal feel uncomfortable; (2) persistent vomiting places the animal at risk for aspiration pneumonia or acid-base and electrolyte disturbances; and (3) the animal is not suffering from gastrointestinal obstruction or toxicity.

There are a number of important differences between the neurotransmitter-receptor systems associated with vomiting in dogs and cats. For example, apomorphine is a potent agent that can be used to induce vomiting in the dog, but is somewhat ineffective in the cat. Metoclopramide (Reglan) is a somewhat ineffective drug to resolve vomiting in cats, but is a lot more effective in dogs. Metoclopramide also has prokinetic activity (promote intestinal peristalsis and motility to move food down the GI tract), but should NEVER be given to vomiting animals until abdominal radiographs have been taken to rule out an intestinal foreign body or obstruction. Animals with GI foreign bodies or obstruction can perforate their bowel if metoclopramide is inadvertently given. Finally, antihistamine drugs are effective in the dog to prevent motion sickness, but are relatively ineffective in cats.

Prevention of Motion Sickness

Dogs: H1-receptor antagonists (e.g., diphenhydramine, dimenhydrinate) or NK-1 receptor antagonists (Cerenia).

Cats: Chlorpromazine (an α2-adrenergic antagonist) or Cerenia.

Management of Vomiting Associated with Kidney Disease

Metoclopramide, Cerenia, and ondansetron or dolasetron. Gastric antacids, such as famotidine, should also be used to manage the gastritis and gastric ulceration associated with uremia.

Prevention and Management of Vomiting Associated with Cancer Chemotherapy

Ondansetron or dolasetron, and Cerenia

Management of Delayed Gastric Emptying

Cisapride or metoclopramide. Metoclopramide has a short half-life (60–90 minutes) in dogs, and is best given as a constant rate infusion for maximal effect. Remember that the prokinetic drugs should not be given to dogs unless a foreign body or gastric obstruction has been ruled out.

Dosages of commonly used antiemetics in dogs and cats

 Prochlorperazine, (Compazine) - 0.5 mg/kg q 8h, SC, IM

 Metoclopramide, (Reglan) - 0.2–0.4 mg/kg q6h PO, SC, IM; or 1–2 mg/kg/24h as CRI

 Diphenhydramine, (Benadryl) - 2–4 mg/kg q8h PO, IM

 Ondansetron, (Zofran) - 0.5–1.0 mg/kg q12–24h, or 0.5–1.0 mg/kg 30 min before chemo

 Maropitant citrate (Cerenia)

 Dogs:

 1 mg/kg SC (prevent vomiting)

 2 mg/kg SC (treat vomiting)

 8 mg/kg PO or SC (motion sickness)

 Cats:

 1 mg/kg SC, PO (prevent vomiting & motion sickness)

Deworming Medication

Intestinal parasites such as ascarids are a well-documented cause of vomiting in pups and animals > 6 weeks and can be treated with a broad-spectrum anthelminthic, such as Panacur at 50 mg/kg q 24 hrs for 5 consecutive days.

  

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Stanley L. Marks, BVSc, PhD, DACVIM (Internal Medicine, Oncology), DACVN
School of Veterinary Medicine
University of California-Davis
Davis, CA, USA


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