Definition

Persistent vomiting lasting longer than 5–7 days or vomiting that occurs intermittently several days/week. This condition is usually non-responsive to symptomatic treatment.

Pathophysiology

• Vomiting occurs when the vomiting center, located within the medulla oblongata, is activated by the humoral or neural pathway.
• There are four main components to the vomiting reflex: (1) visceral receptors within the GI tract; (2) vagal and sympathetic afferent neurons; (3) CRTZ; and (4) vomiting center.
• The humoral pathway is mediated via activation of the CRTZ and is affected by uremic toxins, liver disease, digoxin toxicity, endotoxemia, apomorphine, and other bloodborne triggers.
• The neural pathway is mediated via activation of the vomiting center and is affected by disorders associated with obstruction, distension, or inflammation of the gastrointestinal tract.
• All causes of vomiting (including the vestibular apparatus and cerebrum) are ultimately mediated via the vomiting center.

Systems Affected

• Endocrine/Metabolic-dehydration, electrolyte and acid-base imbalances.
• Cardiovascular-hypovolemia or electrolyte and acid-base imbalances can cause arrhythmias.
• Gastrointestinal-gastroesophageal reflux, esophagitis, and subsequent esophageal stricture.
• Respiratory-aspiration pneumonia.
• Neurologic-altered mentation.

Signalment

• Dog and cat.
• Young animals are more likely to ingest foreign bodies; linear foreign bodies are more common in cats.
• Confirmed or suspected breed predispositions-brachycephalic breeds are prone to pyloric outflow obstruction secondary to mucosal hypertrophy; Basenji, German shepherd, and Shar-Pei are prone to inflammatory bowel disease; rottweiler are prone to eosinophilic IBD; Airedale terrier prone to pancreatic carcinoma; beagle, Bedlington terrier, cocker spaniel, Doberman pinscher, Labrador retriever, Skye terrier, and standard poodle are prone to chronic hepatitis. Yorkshire terrier predisposed to intestinal lymphangiectasia.

Signs

Causes

Risk Factors

Breed-associated disease (see “Signalment”)

Differential Diagnosis

• Vomiting must first be differentiated from regurgitation.
• Regurgitation is a passive retrograde movement of fluid or undigested food into the oronasal cavity that has not yet reached the stomach and occurs without an abdominal component, thus localizing disease to the esophagus.
• Vomiting is a centrally mediated reflex often preceded by prodromal signs of restlessness, nausea, salivation, and repeated swallowing.
• Vomiting patients may also regurgitate because of secondary esophagitis.
• Vomitus of food or partially digested food is more common with primary gastric disease, while vomitus of bile is more likely intestinal in origin.

CBC/Biochemistry/Urinalysis

• CBCs are often unremarkable with primary gastric disease.
• Chronic GI bleeding can cause a nonregenerative anemia, often with characteristics of iron deficiency (microcytosis, hypochromasia, thrombocytosis).
• Acute GI bleeding can cause either regenerative or nonregenerative anemia, depending on severity and duration.
• Nonregenerative anemia may also occur secondary to chronic metabolic or inflammatory diseases.
• IBD, chronic pancreatitis, cholangiohepatitis, and cholecystitis may cause neutrophilic leukocytosis and monocytosis.
• Eosinophilia can occur from eosinophilic gastroenteritis, adrenocortical insufficiency, and GI parasitism.
• Thrombocytopenia has been reported with IBD.
• Dehydration increases the packed cell volume and total protein.
• Biochemistry provides diagnostic and therapeutic information; normal results rule-out metabolic disease as the underlying etiology with the exception of hypoadrenocorticism that can have normal electrolytes.
• Electrolyte and acid-base imbalances reflect severity of losses and can help to localize disease.
• Hypochloremic metabolic alkalosis, often with hypokalemia, indicates substantial loss of gastric content, most consistent with a gastric outflow obstruction.
• Hyperkalemia in the vomiting patient suggests hypoadrenocorticism or oliguric/anuric renal failure; occasionally, enteritis caused by trichuriasis or bacterial infection (salmonellosis) mimics hypoadrenocorticism.
• Metabolic acidosis is common in patients with dehydration, renal failure, DKA, and severe gastroenteritis with diarrhea.
• Increased liver enzyme activity, hypoalbuminemia, hyperbilirubinemia, hypoglycemia, or low urea nitrogen concentration indicates hepatic disease.
• Persistent hyperglycemia and glucosuria is consistent with diabetes mellitus.
• Hyperglobulinemia may indicate chronic inflammation or infection.
• Hypoalbuminemia, lymphopenia, and hypomagnesemia occur secondary to a protein-losing enteropathy caused by infiltrative intestinal diseases such as lymphocytic plasmacytic gastroenteritis, neoplasia, histoplasmosis, or primary intestinal lymphangiectasia.
• Hypocholesterolemia may also be seen with lymphangiectasia.
• Urinalysis is used to rule out non-GI causes of chronic vomiting such as renal failure and DKA.
• Acidic urine in the hypokalemic, hypochloremic, alkalotic patient indicates substantial loss of gastric content as would occur with gastric outflow obstruction.

Other Laboratory Tests

• ACTH stimulation test is used to confirm hypoadrenocorticism. A resting cortisol test <2 µg/dL should be followed with an ACTH stimulation test to confirm hypoadrenocorticism.
• Pancreatic lipase immunoreactivity assay may help confirm pancreatitis together with supportive history and physical exam findings and ultrasound.
• Bile acid concentration (pre- and postprandial) is used to help confirm hepatobiliary dysfunction.
• Fecal testing for gastrointestinal parasitism.

Imaging

• Survey radiographs of the abdomen help identify foreign bodies, GI distension with fluid or gas, and displacement, malposition, shape, and/or size changes of abdominal organs.
• Survey radiographs of the thorax are used to evaluate for pulmonary metastases, gross esophageal abnormalities, or infectious disease.
• A gastrogram or upper GI series can be used to identify foreign bodies, GI wall masses or infiltrative disease, mucosal ulceration, delayed gastric emptying, and motility disorders; however, the procedure is relatively insensitive for detection of mucosal ulceration.
• Abdominal ultrasonography helps identify parenchymal abnormalities of the liver, gallbladder, kidneys, pancreas, GI tract, and mesenteric lymph nodes.
• CT and MRI further evaluate for parenchymal abnormalities of abdominal organs.

Diagnostic Procedures

• Gastroduodenoscopy-allows direct inspection of the gastric and intestinal lumen to identify gross mucosal lesions and foreign bodies and provides a minimally invasive method of biopsy to evaluate for microscopic disease. Limitations of endoscopy include the working length of the endoscope (unable to access the jejunum in large-breed dogs) and depth of the biopsies.
• Laparoscopy or exploratory laparotomy is used for more extensive diagnostic and therapeutic procedures.

Drug(s)

• Antisecretory drugs such as H₂-receptor blockers (e.g., famotidine, ranitidine) or proton-pump inhibitors such as omeprazole (more potent)-famotidine 0.5–1 mg/kg PO, IV, or SC q12h; ranitidine 1–2 mg/kg PO, IV q12h; omeprazole 0.7–1.5 mg/kg PO q12–24h.
• Protectants such as sucralfate (0.5–1 g/dog PO q8–12h; 0.25 g/cat PO q8–12h) to accelerate gastric mucosal healing; can be used with antisecretory drugs for patients with evidence of upper GI bleeding (e.g., hematemesis or melena).
• Antibiotics-indicated for treatment of Helicobacter-associated gastritis, SIBO, and as an adjunct to corticosteroids in the treatment of IBD.
• Suggested treatment of Helicobacter-associated gastritis-amoxicillin 20 mg/kg PO q8h plus omeprazole 0.7–1.5 mg/kg PO q24h and metronidazole 10 mg/kg PO q12h for 21 days; clarithromycin 7.5 mg/kg PO q12h can be used with amoxicillin and metronidazole (as above) as an alternative therapy for cats.
• Metronidazole-may be used at 10 mg/kg PO q12h in conjunction with corticosteroids to treat IBD, although evidence of direct benefit of this approach is currently lacking.
• Antibiotic-responsive enteropathy (tylosin-responsive enteropathy)-tylosin is the drug of choice administered at 5–10 mg/kg q24h for 8–12 weeks. Alternative option is metronidazole (10 mg/kg q12h for 8–12 weeks) although tylosin is felt to be superior for this disorder.
• Use corticosteroids in conjunction with dietary changes to treat biopsy-confirmed IBD; azathioprine, chlorambucil, or cyclosporine can also be used in patients with poor response to corticosteroids alone or to decrease the dosage of steroids required to control symptoms. Avoid the use of more than 2 immunomodulatory drugs given concurrently.
• Prokinetic drugs (e.g., metoclopramide, cisapride or erythromycin) are used to treat delayed gastric emptying not associated with obstructive disease.
• Pyrantel pamoate is effective for Physaloptera; fenbendazole is effective for Ollulanus.
• Iron supplementation for animals with chronic GI bleeding that develop microcytic hypochromic anemia.
• Surgery and/or chemotherapy for neoplasia, depending on the tumor type and location.
• Paraneoplastic hypersecretion of gastric acid, as occurs with mastocytosis and gastrin-secreting pancreatic tumors, is best treated with antisecretory drugs (e.g., omeprazole) to diminish gastritis, gastric ulcer, and chronic vomiting.
• Reserve antiemetics for patients with persistent vomiting unresponsive to treatment of the underlying disease. Maropitant is a neurokinin-1 receptor antagonist suppressing vomiting at the CRTZ, vomiting center, and vagal afferents; maropitant 1 mg/kg SC q24h, 2 mg/kg PO q24h. Phenothiazines (e.g., chlorpromazine) work at both the CRTZ and vomiting center; chlorpromazine 0.5 mg/kg SC, IM q6–8h.
• Prokinetic drugs (e.g., metoclopramide)-metoclopramide also blocks the dopaminergic 2 receptors at the CRTZ, but this effect is far weaker in cats compared to dogs; metoclopramide 0.2–0.5 mg/kg IV, IM, PO q6–8h; metoclopramide can also be administered as a continuous rate infusion of 1–2 mg/kg/24h in hospitalized patients.
• Vomiting caused by chemotherapy is best treated with ondansetron 0.5–1 mg/kg IV, PO given 30 minutes before chemotherapy.

Precautions

• Do not give -adrenergic blockers such as chlorpromazine to dehydrated patients as they can cause hypotension.
• Use antiemetics with caution, as they can mask the underlying problem.
• Metoclopramide can cause lethargy, restlessness, agitation, and other behavioral changes, particularly in cats.
• Corticosteroids are immunosuppressive and are a risk factor for development of GI ulceration; use caution when treating IBD with corticosteroids at high dosages or for long periods.
• Azathioprine and chlorambucil are myelotoxic; monitor CBCs for neutropenia and thrombocytopenia every 2 weeks for the first month of treatment and monthly thereafter.
• Cyclosporine can exacerbate vomiting and diarrhea when used at high dosages; use with caution in patients with renal disease.
• Do not use anticholinergics as antiemetics, as they can exacerbate vomiting by causing gastric atony and gastric retention.
• Metoclopramide and cisapride are contraindicated in patients with GI obstruction.

Possible Interactions

Ranitidine interferes with hepatic metabolism of theophylline, phenytoin, and warfarin, and should not be used concurrently with these drugs. Avoid use of cimetidine because it is a weak H₂-receptor antagonist and is a potent inhibitor of the cytochrome P450 enzyme pathway.

Zoonotic Potential

Helicobacter heilmanii and H. felis may have zoonotic potential; they have been isolated from humans with chronic gastritis, most of whom have had close contact with dogs or cats.

Abbreviations

• ACTH = adrenocorticotropic hormone
• CNS = central nervous system
• CRTZ = chemoreceptor trigger zone
• CT = computed tomography
• DKA = diabetic ketoacidosis
• GI = gastrointestinal
• IBD = inflammatory bowel disease
• MRI = magnetic resonance imaging
• NSAID = nonsteroidal anti-inflammatory drug
• SIBO = small intestinal bacterial overgrowth

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