section epub:type=”chapter” id=”c0026″ role=”doc-chapter”> Gastrointestinal diseases encompass the esophagus (e.g., esophagitis, esophageal stricture), stomach (e.g., gastritis, foreign body), pancreas (e.g., pancreatitis, exocrine pancreatic insufficiency), liver (e.g., hepatic lipidosis, cholangitis syndrome), and intestinal tract (e.g., inflammatory bowel disease, lymphoma) and are very common in cats. This chapter details a rational and logical approach to diagnosis and management of gastrointestinal diseases in cats. Cat; feline; vomiting; regurgitation; gastrointestinal disease; inflammatory bowel disease; antiemetic drugs; prokinetic drugs; gastroesophageal reflux; esophageal disease; esophageal stricture; dysphagia; odynophagia; gastritis; gastrointestinal foreign body; gastrointestinal neoplasia; gastrointestinal lymphoma; diarrhea; gastrointestinal eosinophilic sclerosing fibroplasia; intussusception; constipation; anal sac disease; gastrointestinal parasites; pancreatitis; exocrine pancreatic insufficiency; hepatic lipidosis; cholangitis syndrome; triaditis; portosystemic shunts; extrahepatic bile duct obstruction; peritonitis; ascites. Randolph M. Baral Vomiting begins with retching, a series of brief negative intrathoracic pressure pulses that coincide with positive abdominal contractions. These pressure changes occur because of repeated herniations of the abdominal esophagus and cardiac portion of the stomach into the esophagus. During retching, food freely moves back and forth in the esophagus, which is now dilated because of the ingesta. Ultimately, the diaphragm rapidly moves cranially, resulting in positive intrathoracic pressure that leads to expulsion of these contents.1 Vomiting is such an active process that it seems to involve the whole cat, and so it is little wonder that it concerns owners so much. Since vomiting is mediated by the CNS with input and influence from just about anywhere in the body, it is important to summarize this physiology so it can be appreciated when managing clinical cases. Vomiting results from stimulation of the “vomiting center,” which is in the brainstem; there are four main pathways that stimulate the vomiting center,1 and these are summarized below and in Fig. 26.1. These complex pathways highlight the need to consider the whole cat and not just the cat’s GI tract when assessing a cat presenting for vomiting. The approach to managing a cat with vomiting must follow logical steps. When the underlying cause is GI disease, a precise diagnosis can only be reached after obtaining biopsy samples. A summary of diagnostic steps and possible underlying causes is shown in Fig. 26.2. The decision to proceed to steps 4 and 5 assumes that the prior steps have narrowed the underlying cause as GI, pancreatic, or hepatic in origin. The important aspects of the clinical history are given in Table 26.1. Signalment is important, because younger cats are more likely to have ingested foreign bodies (though not all older cats have grown out of this habit). Some extra-GI problems, such as hyperthyroidism and renal disease, are more likely to occur in older cats. Table 26.1 Adapted from Hall JE. Clinical approach to chronic vomiting. In: August JR, ed. Consultations in Feline Internal Medicine, 3rd ed. Philadelphia: Saunders; 1997: 63. Most texts and references instruct clinicians to distinguish between vomiting and regurgitation, with the latter noted as being quite passive.1–3 In practice, it can be hard to make this distinction, because it is the author’s experience that cats with esophageal disease can have quite forceful, spasmodic movements when ejecting ingesta by regurgitation—although it is also possible for regurgitation to be a passive process. Given that the physiology of vomiting, as described earlier, results in ingesta being forced into and then evacuated from the esophagus, it is hardly surprising that it can resemble regurgitation. Fortunately, regurgitation and esophageal disease do vary from vomiting in other ways! Vomiting is usually preceded by the cat licking its lips, salivating, or making attempts to swallow. Regurgitated ingesta is often in a tube-like structure and if undigested can be covered with frothy saliva. Partially digested food suggests vomitus, and the presence of bile or digested blood confirms this. It is important to determine if the cat vomits regularly. Many owners have seen their cat vomit on a regular basis with no evidence of the cat being unwell, and this is noted frequently in the veterinary literature.1,2 Hairballs can cause gastric irritation, and it may be that eating quickly also stimulates the peripheral sensory receptors that contribute to vomiting. If a cat does vomit regularly, it is important to assess if the cat is presenting for a change in the vomiting pattern (e.g., frequency or timing in relation to eating) and if the cat is unwell in any way, such as anorexia or weight loss. The pattern of vomiting is important in all cases, because cats presenting with acute gastritis usually have a sudden onset of frequent vomiting compared to those with chronic disease processes that may vomit every few days. The timing in relation to eating can be helpful because the stomach should empty by 6 to 8 hours after a meal; vomiting longer than 8 hours after a meal can suggest motility or retention disorders. The description of the vomitus can be helpful. If bile is present, the pylorus is not obstructed; the presence of blood (digested or fresh) indicates ulceration. Hair in the vomitus can indicate hairball gastritis, and the possibility of trichobezoar obstruction should be considered. Access to foreign bodies or toxins is an important aspect of the clinical history. Has the cat been seen playing with an insect, mouse, or other prey? Are there any medications unaccounted for (e.g., a medication tablet dropped on the floor)? Are lilies present in the house? Vomiting is the major sign of gastric disease but given the number of potential organ systems that can be involved, a thorough physical examination should be undertaken. Because linear foreign bodies are a common cause of vomiting, all cats presenting for anorexia or vomiting should have the underside of the tongue evaluated for the presence of string caught there. Applying gentle pressure with a thumb in the intermandibular space to elevate the tongue is an effective way to visualize lesions or foreign bodies in the sublingual area (see Chapter 3: Deciphering the Cat: The Medical History and Physical Examination, Fig. 3.9). A thorough examination may reveal specific signs, such as a palpable thyroid nodule and tachycardia in the case of hyperthyroidism or palpably small kidneys with chronic kidney disease. The author has found that some cats with dental disease can gorge their food, resulting in vomiting; paying attention to the state of the teeth and gums is important. Of course, some cats have multiple problems, and correction of dental disease may not resolve vomiting if there is a concurrent disease. In the examination, it is also important to note consequences of both the underlying process and the vomiting itself; these include the demeanor of the cat, hydration status, and whether abdominal pain is present. The physical examination findings, together with the clinical history, help determine the next appropriate steps. Well cats that are not continually vomiting and are appropriately hydrated, with no other specific signs, may be treated as outpatients by fasting for 24 hours, then returning to food with a bland diet, such as plain cooked chicken or commercial, low-residue prescription diets designed for this purpose. Follow-up is important to ensure signs do not progress. Cats with nonspecific signs may require supportive care with subcutaneous or intravenous fluids and perhaps analgesia (with an opioid). If clinical signs do not resolve, the pursuit of a specific diagnosis should be attempted. The practitioner must ask the following important questions: Routine serum/plasma biochemistries, hematology, urinalysis, and total thyroxine (T4) (for older cats) testing is not only important to distinguish primary from secondary GI disease but to look for consequences of vomiting that may need to be addressed, such as dehydration and electrolyte abnormalities. Careful interpretations should be made. Severe azotemia, even with hyperphosphatemia, can occur because of primary GI disease, and the distinction from renal disease usually requires an assessment of urine specific gravity. Cobalamin, folate, feline trypsin-like immunoreactivity (fTLI), and feline pancreatic lipase immunoreactivity (fPLI) tests are useful markers of intestinal and pancreatic disease,4–7 but it is important to note that they typically do not give a precise diagnosis. More detail about the utility of these tests is noted later in the section Approach to the Cat with Diarrhea. Radiography is most useful for identifying foreign bodies or signs of intestinal obstruction from other causes. The major findings are noted later in the section on Intestinal Obstruction. Contrast radiography can aid in the diagnosis for both discrete and linear foreign bodies but should be used with caution, because intestinal perforation may be present. Nonionic iodinated agents that are typically used for myelography (such as iopamidol or iohexol) should be used because barium irritates the peritoneum and oral iodine compounds are hypertonic. Hypertonic compounds may draw fluid into the stomach and intestines after oral administration, with the potential of creating further fluid and electrolyte imbalances in an already compromised patient.8 Ultrasonography is a useful diagnostic adjunct and helps to detect and characterize localized thickening of the stomach or intestinal wall, lymphadenopathy, radiolucent foreign bodies, and changes in the size and echogenicity of the pancreas, liver, kidneys, or spleen. Abdominal effusions can be assessed and sampled. Ultrasound-guided fine needle aspirates (FNAs) can be used to sample masses, bile, or peritoneal fluid. It should be recognized that in most cases of GI disease, imaging will not give a definitive diagnosis and biopsy will be required using endoscopy, laparoscopy, or laparotomy. It is also important to recognize that a significant proportion (as much as 30%) of cats may have a histologic diagnosis of GI disease but ultrasonographically normal small intestines.9 Ultrasonography can be a considered a way to “survey the field,” assessing: These factors may be used to assess the appropriateness of endoscopy versus laparotomy or laparoscopy to obtain diagnostic samples. Histologic evaluation of affected tissue is usually needed for diagnosis of most chronic GI diseases. Intestinal biopsy samples can be obtained by of endoscopy, laparotomy, or laparoscopy, each of which has advantages and disadvantages. Laparotomy allows gross examination of and access to the entire intestinal tract as well as other abdominal organs. Laparotomy is the most invasive alternative, but with careful anesthesia and analgesia, most cats recover uneventfully. One survey found that 83% of cats undergoing exploratory laparotomy survived the hospitalization, and although complications occurred in 26% of cats, these were more likely to be associated with the underlying disease process and not surgery or anesthesia.10 Laparoscopy is becoming more common but still is not readily available in most veterinary clinics. This alternative is less invasive and allows exploration of the abdomen but not as thoroughly as with laparotomy. Full thickness intestinal biopsies require exteriorization, although this is not necessarily required for other abdominal organs. There is the possibility of anesthetic complications associated with insufflating the abdomen. Endoscopy is the least invasive procedure and is the only alternative that allows examination of the intestinal lumen. Equipment is available that allows access to all areas of the GI tract. However, available equipment and operator expertise may limit which areas of the feline GI tract can be examined and biopsied in many veterinary practices. In addition, endoscopy does not allow examination or sampling of any other part of the GI tract and does not enable full-thickness biopsy samples. One study found that, of cats investigated for GI disease, 9 of 33 cats (27%) had no pathology recognized proximal to the jejunum (i.e., the effective length of some endoscopes would have precluded diagnosis), and other organs were affected in 9 of 10 cats with inflammatory bowel disease (IBD) and 7 of 8 cats with intestinal small cell lymphoma.11 Additionally, hypocobalaminemia, an important marker of GI disease, reflects distal small intestinal disease which would require, in many cases, ileal biopsies to diagnose (beyond the reach of some endoscopes). Careful case selection for endoscopy from survey ultrasonography can reduce the number of missed diagnoses from endoscopy, but the possibility remains depending on the available equipment. The quality of endoscopically obtained biopsy samples varies greatly with the skill of the endoscopist. It has been stated that “it is exceedingly easy to take inadequate tissue samples with a flexible endoscope.”12 In an assessment of endoscopically obtained biopsy samples, two laboratories were compared, one that received samples from any practitioner and the other that received samples only from practitioners trained to take, mount, and submit endoscopy samples. All slides were reviewed by three pathologists who found that, of samples from the first laboratory, 15% of the slides were considered inadequate for diagnosis, 71% were considered questionable, and only 14% were adequate. By comparison, in the second laboratory (with samples from experienced practitioners) 0% of slides were inadequate, 21% were questionable, and 79% were considered adequate for diagnosis.13 In the case of distinguishing between lymphocytic intestinal infiltrates (commonly known as IBD) and lymphocytic neoplasia (small cell lymphoma), endoscopically obtained samples can give an incorrect diagnosis.14 Many of these problems can be minimized with experienced operators and careful case selection from survey ultrasonography. Although often due to a GI stimulus, vomiting is mediated by the vomiting center in the brainstem. Thus, investigations should initially distinguish between GI and extra-GI causes. If extra-GI causes of vomiting have been ruled out, definitive diagnosis typically requires biopsy samples for definitive diagnosis to enable successful therapy. Katrina R. Viviano Therapeutic strategies used in the treatment of feline GI diseases include nonspecific supportive therapies and specific, targeted therapies based on the primary underlying disease process. The most effective therapies for treating vomiting and diarrhea in cats are those directed at treating the primary underlying disease process. However, symptomatic and supportive care may be the primary therapeutic recommendations in some cases (e.g., acute gastroenteritis), necessary prior to arriving at a definitive diagnosis, at the onset of targeted therapy, or during periods of clinical relapse. Antiemetics and prokinetics are used to control or prevent vomiting through specific receptor interactions mediated either centrally or peripherally (Fig. 26.3). The five most common antiemetics control vomiting by different mechanisms. They include dolasetron and ondansetron, maropitant, mirtazapine, metoclopramide, and the phenothiazines (Table 26.2). In cats, metoclopramide functions both as an antiemetic and prokinetic, and mirtazapine has antiemetic properties but also is used as an appetite stimulant. In addition, the prokinetic cisapride is used to control vomiting in some cats when intestinal dysmotility is the cause of emesis. Table 26.2 Dolasetron and ondansetron are selective serotonin antagonists that inhibit central and peripheral 5-HT3 receptors. Their main antiemetic effect is through antagonism of the peripheral 5-HT3 receptors in the GI tract. In cats, 5-HT3 antagonism of the chemoreceptor trigger zone is also likely important in the antiemetic effect of dolasetron and ondansetron. Dolasetron and ondansetron were originally introduced to prevent vomiting secondary to chemotherapy because of their superior clinical efficacy. The clinical use of dolasetron and ondansetron in cats has not been associated with reported side effects, and experimental studies report minimal toxicity in animals at doses 30 times the antiemetic dose.1 Side effects reported in humans include headaches, elevated liver enzymes, rare hypersensitivity reactions, prolongation of the QT interval, and arrhythmias.2,3 Dolasetron is commonly used for parenteral administration and ondansetron for oral administration, dictated primarily based on the tablet sizes available and cost; however, as new pharmacokinetic and pharmacodynamics data become available in cats, alternative dosing strategies may be utilized. For example, ondansetron (2 mg/cat) when administered subcutaneously (SC) in healthy cats has increased bioavailability and prolonged drug exposure (significantly longer elimination half-life) compared to intravenous (IV) or oral (PO, per os) dosing.4 Cats with liver disease experience delayed ondansetron clearance and drug exposure compared to age-matched healthy geriatric cats.5 A study in healthy cats treated with dolasetron (0.8 and 1 mg/kg, IV) has raised questions about 24 hour dosing intervals and efficacy to control vomiting in cats.6 Additional studies are need to determine optimal dosages of dolasetron and ondansetron in cats. In the absence of additional data in healthy or ill cats, an empirical dosing recommendation for dolasetron is 0.5 to 1 mg/kg, IV, every 24 hours, and for ondansetron, 0.5 mg/kg, PO, every 12 hours. Transdermal administration of ondansetron is not recommended due to poor drug absorption. A study in healthy cats treated with both single-dose and multi-dose applications of ondansetron formulated in a transdermal gel reported inadequate serum concentrations of ondansetron for clinical use.7 Maropitant, a neurokinin-1 (NK-1) receptor antagonist, blocks the binding of substance P to the NK-1 receptors located in the emetic center, the CRTZ, and the enteric plexus.8 In cats, maropitant has been reported to be efficacious in treating xylazine-induced vomiting and motion sickness.9 The label dosage in cats is 1 mg/kg, IV, SC, or PO, every 24 hours for up to 5 days.9 Anecdotally, it has been used for longer than 5 days in cats with chronic vomiting, such as those with chronic kidney disease (CKD). Maropitant is well-tolerated in cats. In a randomized, placebo-controlled, blinded clinical study in 33 cats with stable CKD (International Renal Interest Society [IRIS] stage II–III), maropitant (4 mg/cat, PO, every 24 hours) significantly decreased the incidence of chronic vomiting during the 2-week trial compared to placebo. Maropitant did not clinically impact appetite, activity, weight, or serum creatinine in these cats and no adverse effects, including unusual behavior, were reported by owners in the maropitant treated group.10 Mirtazapine, a piperazinoazepine, antagonizes the presynaptic alpha2-adrenergic receptor, increasing noradrenergic and serotonergic neurotransmission; the primary mechanism targeted for its use is as an antidepressant in humans. Mirtazapine is also a potent antagonist of the postsynaptic serotonergic receptors (5-HT2 and 5-HT3) and histamine H1 receptors. The effect on neurotransmission is complex but the overall increase in serotonin and norepinephrine results in appetite simulation. The effects on the histamine and 5-HT3 receptors contribute to its antinausea and antiemetic properties. Clinically, mirtazapine is commonly used as an appetite stimulant in cats. Anorexia is a common clinical problem in ill cats, and in some anorexic or partially anorexic cats the use of an appetite stimulant as adjunctive therapy to nutritional support (e.g., feeding tubes) may be of clinical benefit. Prior to the development of mirtazapine, cyproheptadine was the most commonly used appetite stimulant in cats, with variable clinical results.11 Mirtazapine is an effective appetite stimulant in cats, with a shorter half-life than that reported in humans.12 The oral dosage of 1.88 mg/cat, every 24 hours, in healthy cats and every 48 hours in cats with CKD is recommended based on the pharmacokinetics and pharmacodynamics of mirtazapine in cats.12,13 A licensed transdermal formulation is available in some countries (Mirataz, Dechra) and offers an alternative route of administration in cats. Mirtazapine delivered as a transdermal formulation (2 mg/cat) is reported to be well-tolerated and effective in achieving weight gain in cats with a variety of systemic disorders contributing to unintentional weight loss.14 In people, age and kidney and liver dysfunction affect mirtazapine metabolism (hepatic CYP 450 enzymes) and clearance (excreted in urine and feces), suggesting that dosage adjustment may be necessary in patients with suboptimal renal or hepatic function.15 The pharmacokinetics of oral mirtazapine was investigated in cats with liver disease compared to age-matched control cats.16 Cats with liver disease reached maximum serum concentrations in significantly shorter times and had a prolonged half-life compared to age-matched control cats. The results of this study suggest cats with liver disease may require altered dosing regimens to avoid side effects. Side effects reported in cats treated with mirtazapine include behavior changes (vocalization and interaction), tremors, muscle twitching, and hyperactivity.12,17,18 In a retrospective study in 84 cats, adverse effects of mirtazapine toxicity (i.e., serotonin syndrome) were reported more frequently in association with accidental ingestions (n = 59) and in cats treated with high doses (3.75 mg and 15.0 mg; n = 65).18 Treatment recommendations for a cat with clinical signs of serotonin syndrome (e.g., vocalization, agitation, vomiting, ataxia, restlessness, tremors, hypersalivation, or tachypnea) include the discontinuation of mirtazapine and the administration of cyproheptadine (2–4 mg/cat, PO or per rectum, every 4–8 hours until resolution of clinical signs). Metoclopramide is both an antiemetic and prokinetic drug that acts peripherally on the GI tract and centrally within the CNS. At low doses, metoclopramide inhibits dopaminergic (D2) transmission, and at higher doses it inhibits serotonergic 5-HT3 receptors in the CRTZ.1,19 Metoclopramide also acts peripherally as a prokinetic at the level of the smooth muscle of the stomach and duodenum, triggering gastric emptying and duodenal contractions. Multiple suggested mechanisms mediate metoclopramide’s prokinetic activity, including augmentation of acetylcholine release, increased smooth muscle sensitivity to cholinergic neurotransmission, antagonism of dopamine, and/or serotonergic 5HT4 receptor activation.19,20 Metoclopramide increases the lower esophageal sphincter tone in humans,21 although in cats, the impact of metoclopramide on the lower esophageal sphincter is considered weak.22 Adverse CNS extrapyramidal signs occur secondary to dopamine (D2) antagonism, including excitement and behavior changes. Extrapyramidal signs are most often seen at the higher doses needed to block 5-HT3 receptors. Because of metoclopramide’s prokinetic properties, an intestinal obstruction should be ruled out prior to use. Dopamine is a less important neurotransmitter in the CRTZ of cats than alpha2-adrenergic and 5-HT3-serotonergic receptors, suggesting that D2-dopaminergic antagonist may be a less effective antiemetic in cats. Clinically, metoclopramide is commonly used to control vomiting in cats, although this clinical response may be secondary to 5-HT3 antagonism and/or its prokinetic effects.22,23 Extrapolated from the short elimination half-life of metoclopramide in dogs (90 minutes), frequent intermittent dosing or delivery by a constant rate infusion (CRI) is necessary. Empirical dosing in cats is 0.2–0.4 mg/kg, SC or PO, every 8 hours or 1–2 mg/kg/day as a CRI. Dose reduction by 50%–75% is recommended in cats with underlying renal azotemia; approximately 25% of metoclopramide is excreted in the urine.24,25 Cisapride is a serotonergic 5-HT4 agonist that increases propulsive GI motility from the lower esophageal sphincter to the colon. Cisapride binds serotonergic 5-HT4 receptors in the myenteric plexus, increasing the release of acetylcholine in GI smooth muscle. Stimulatory effects on the GI tract include smooth muscle peristalsis in the distal esophagus (in humans and cats), increased gastroesophageal sphincter pressure, improved gastric emptying, (in dogs, cisapride has greater prokinetic activity in the stomach relative to metoclopramide,26,27 similar data is not available for cats), and motility of the small intestine as well as the colon.28,29 In cats, cisapride induces colonic smooth muscle contractions, which are dependent on the influx of extracellular calcium and is only partially cholinergic dependent.30 Cisapride has no direct antiemetic effect, although it is indicated for vomiting cats with colonic dysmotility secondary to megacolon.31 Colonic disease (e.g., colonic distention or colitis) can trigger the vomiting reflex. Other potential indications include refractory generalized ileus or gastroesophageal reflux (GER). The dosage recommendation based on pharmacokinetics in healthy cats is 2.5–5 mg/cat, PO, every 12 hours.32 Prior to starting cisapride, an intestinal obstruction should be ruled out because of the drug’s strong prokinetic effects. Side effects reported in humans are cramping and diarrhea. Potentially life-threatening side effects include QT prolongation and ventricular arrhythmias; this is the primary concern that resulted in the removal of cisapride from the market in the United States, although it is still available from compounding pharmacies.33 In cats, QT prolongation requires 20 times the therapeutic dose of cisapride.34 The concurrent use of cisapride and dolasetron is not recommended due to the risk of prolongation of the QT interval and ventricular arrhythmias.2 Other potential drug interactions include the azole antifungals (e.g., ketoconazole, itraconazole) secondary to the inhibition of hepatic isoenzyme (CYP3A) reducing cisapride metabolism.33 The mechanisms of action of the broad spectrum antiemetics prochlorperazine and chlorpromazine include antagonism of D2-dopaminergic, histaminergic (H1 and H2), and cholinergic (muscarinic) receptors within the CRTZ and, at high doses, the alpha-adrenergic receptors (alpha1 and alpha2) within the vomiting center. In cats, alpha2-receptors play a key role in emesis, suggesting cats may be more sensitive to the antiemetic effects of the phenothiazines. Prochlorperazine and chlorpromazine produce an antiemetic effect at relatively low doses, but because of antagonism of the alpha-receptors, vasodilation and hypotension can be clinically significant side effects. In addition, antagonism of the histaminergic receptors carries the risk of sedation. Phenothiazines have the potential to lower the seizure threshold, limiting use in patients with a known seizure history. Other CNS-associated side effects linked to D2 antagonism occur at higher doses and produce extrapyramidal signs, including rigidity, tremors, weakness, and restlessness. The need for frequent dosing (0.2–0.4 mg/kg, SC, every 8 hours) and the risk of hypotension and sedation limit the clinical use of phenothiazine antiemetics to hospitalized patients suffering from refractory vomiting. Their use is not recommended in dehydrated or hypotensive patients. Diet trials are commonly used in cats with idiopathic GI signs and in cats with suspected or known food hypersensitivities. Dietary strategies used to control vomiting in cats focus on feeding either a highly digestible or an elimination (novel protein/carbohydrate or hydrolyzed protein) diet.35 The empirical use of elimination diets in cats is relatively successful. While traditional diet trials are recommended for a minimum of 8 to 12 weeks, approximately 50% of cats with idiopathic GI signs are responsive to a novel protein/carbohydrate diet within 2 to 3 days36 and the remainder will likely experience clinical improvement within the first 1 to 2 weeks of the diet trial. Highly digestible diets improve absorption and assimilation of nutrients in the face of a compromised digestive tract. These diets contain highly digestible proteins and carbohydrates, moderate to low fat, low concentrations of soluble and insoluble fiber, and are supplemented with omega-3 fatty acids. Novel protein/carbohydrate or elimination diets are recommended when a food allergy or intolerance is suspected. These diets contain novel highly digestible carbohydrate and protein sources. Diets formulated with hydrolyzed proteins can be used as an alternative to novel protein/carbohydrate diets. Additional information is summarized in Table 26.3 for the common drugs used in the treatment of gastric ulcers in cats. Table 26.3
Digestive System, Liver, and Abdominal Cavity
Abstract
Keywords
Approach to the Vomiting cat
INTRODUCTION
STEP 1: SIGNALMENT AND CLINICAL HISTORY
Question
Interpretation
Signalment
Younger cats more likely to ingest foreign bodies and hunt prey; older cats are more likely to have systemic or chronic diseases.
Diet
Regular diet, any dietary change; potential for food intolerance, food hypersensitivity, food sensitivity.
Environment
Plants and foreign bodies, was cat seen with prey, access to toxins; health status of other cats in the household.
Duration and frequency
Regular vomiter? Acute versus chronic, and severity.
Relationship to eating
Describe vomiting process
Vomiting (licking lips, salivation, multiple swallowing) versus regurgitation (can be passive but not always); nature of ingesta also helps distinguish vomiting from regurgitation.
Appearance of vomitus
Deworming history
Rule GI parasites in/out.
Previous illnesses
Organ system affected, recurrence.
Current medications
Drug reaction or toxicity.
Behavioral changes
Co-existing systemic signs
STEP 2: PHYSICAL EXAMINATION
STEP 3: BLOOD AND URINE TESTING
Routine Tests
Blood Tests for Gastrointestinal Disease
STEP 4: IMAGING
STEP 5: BIOPSIES
SUMMARY
For the References and other additional features, please visit eBooks.Health.Elsevier.com.
Therapeutics for Vomiting and Diarrhea
NONSPECIFIC SUPPORTIVE THERAPIES FOR VOMITING
Antiemetics and Prokinetics
Drug/Dosage
Mechanism of Action
Precautions
Drug Interactions
Dosage Adjustments
Antiemetics
5-HT3 antagonism
Adverse Effects:
Cisapride:
NK-1 antagonist
Antiemetic/Appetite stimulant
5-HT2, 5-HT3 antagonismH1 antagonism
Adverse Effects:
MAO inhibitors:
Prokinetics
5-HT4 agonist
Adverse Effects:
Dolasetron:
Prokinetic/Antiemetic
Adverse Effects:
Phenothiazines:
Dolasetron and Ondansetron
Maropitant
Mirtazapine
Metoclopramide
Cisapride
Phenothiazines
Dietary Modification
Highly Digestible Diets
Novel Protein/Carbohydrate or Elimination Diets
TARGETED THERAPIES WITH SPECIFIC INDICatIONS FOR VOMITING
Treatment of Gastrointestinal Ulcers
Drug
Dosages
Mechanism of Action
Adverse Effects
Drug Interactions
Dosage Adjustments
Omeprazole
1 mg/kg, PO, every 12 hours
H+/K+ ATPase inhibitor
Diarrhea
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