I. History Taking

A complete and detailed history is the first step in establishing a correct diagnosis of a vomiting disorder. The patient's signalment will usually establish some level of probability for many of the differential diagnoses. For example, adrenocortical insufficiency would be an important differential diagnosis for a two year old dog presented with an acute history of vomiting and muscular weakness, with or without diarrhea. Similarly, the acute onset of vomiting in an unvaccinated puppy should alert the veterinarian to the possibility of an infectious disease, for example, parvoviral or distemper viral gastroenteritis. Chronic vomiting in an eleven year old dog, on the other hand, would elicit a different set of differential diagnoses.

Following consideration of the patient's signalment, the history taking should ascertain vaccination status, travel history, and any recent dietary changes. Previous medical problems, medication history, and the possible ingestion of toxic substances or foreign bodies should also be ascertained. These pieces of information can be quite useful in formulating a list of differential diagnoses. Next, the veterinarian should be convinced that the pet owner is describing vomiting, and not some other sign. For example, the coughing associated with inflammatory disorders of the upper airway will often be described as vomiting by many pet owners. Gagging is also occasionally confused with vomiting. A careful history taking will usually discriminate coughing and gagging from vomiting. Pet owners will also often confuse regurgitation and dysphagia with vomiting. Regurgitation is the passive evacuation of ingested food from the pharynx and/or esophagus; the premonitory signs of retching and abdominal contractions seen with vomiting are not observed with regurgitation. The description of regurgitation by a pet owner would suggest a more proximal disorder of the pharynx or esophagus. Dysphagia or difficulty in swallowing would also suggest a more proximal disorder of the pharynx.

The history taking should then elicit the duration, frequency, and time of vomiting episodes, as well as the relationship of vomiting to food and water consumption. Disorders of vomiting that are of short duration are usually self-limiting and not worthy of extensive investigation; chronic vomiting histories, on the other hand, are more serious and certainly require a more detailed investigation. Frequent vomiting usually occurs as result of systemic, metabolic, or endocrine disorders or severe inflammatory disorders of the primary gastrointestinal tract. Vomiting that occurs in the immediate post-prandial period is usually suggestive of overeating, excitement, or disorders of the esophageal body or esophageal hiatus (e.g., hiatal hernia). Conversely, vomiting of undigested or partially digested food 8 or more hours post-prandially would suggest a distal gastric (corpus, antrum, and pylorus) motility disorder or obstruction. Vomiting of water would be more suggestive of a proximal gastric (cardia, fundus) motility disorder. Vomiting during the early morning hours often may result from gastroesophageal reflux.

Finally, the physical characteristics of the vomitus, including the color, amount, odor, consistency, and the presence or absence of blood or bile should be ascertained. Undigested food in the vomitus implies a gastric etiology, while digested food (chyme) implies an intestinal etiology for the vomiting. The presence of blood in the vomitus implies disruption of the gastrointestinal mucosa; blood may appear as frank red clots or as a dark brown "coffee-grounds" material resulting from acid proteolysis. Bile in the vomitus usually suggests only that the pylorus has permitted bile reflux. However, bile salts are known to increase the permeability of the gastric mucosal barrier resulting in a syndrome of bile reflux gastritis. Bilious vomiting, therefore, might provide a clue to the pathogenesis of the disorder. A fecal odor has been described with lower intestinal (jejuno-ileal) obstruction.

II. Physical Examination

Examination of the mouth and pharyngeal structures often provide important clues to the pathogenesis of vomiting, e.g., uremic breath or ulcers, icteric mucous membranes, severe pharyngitis or pharyngeal string foreign bodies. The physical examination finding of generalized lymphadenopathy would suggest neoplasia or a systemic inflammatory disease as the pathogenesis of the vomiting. Hence, all lymph nodes should be carefully palpated to determine if they are enlarged and/or painful. The presence of fever on physical examination would likewise suggest an inflammatory pathogenesis for the vomiting disorder. Extreme bradycardia or other rhythm disturbance detected upon cardiac auscultation might be an important sign of a metabolic disturbance such as adrenocortical insufficiency or septic shock. The abdomen should then be carefully palpated for effusion (e.g., peritonitis), masses (e.g., carcinomatosis or other malignancy), pain (e.g., peritonitis, pancreatitis, or nephritis), gaseous or fluid distension of the intestine (e.g., obstruction), kidney size and shape (e.g., end-stage fibrotic kidneys or nephritis), liver size (e.g., hepatitis), uterine distension (e.g., pyometra), and urinary bladder size (e.g., bladder obstruction). Rectal examination might also provide some evidence of pain or hematochezia (e.g., colitis), worms (e.g., hook or whipworms), or painful prostatomegaly (e.g., prostatitis or prostatic neoplasia). Finally, examination of the central nervous system should be considered, especially in the animal in which the cause of vomiting is not so obvious. Some animals with intervertebral disc disease will vomit because of pain.

III. Diagnostic Workup

If a definitive diagnosis is not established from the history and physical examination, then the following "initial tests" are warranted: complete blood count, serum chemistry, urinalysis, fecal parasitological examination, and abdominal radiographs.

Peripheral eosinophilia in a complete blood count would suggest the possibilities of systemic mast cell disease, intestinal parasitism, or adrenocortical insufficiency. Leukopenia and neutropenia might be observed in the acute phase of a viral gastroenteritis. Leukocytosis, on the other hand, might suggest an inflammatory disorder like acute pancreatitis. The serum chemistry will often help identify systemic, metabolic, and endocrine causes of vomiting. For example: 1) azotemia and hyperphosphatemia suggest that the vomiting has resulted from chronic renal failure; 2) hyperglycemia, acidosis, glucosuria, and ketonuria suggest diabetic ketoacidosis as the cause of vomiting; 3) hyponatremia and hyperkalemia suggest adrenocortical insufficiency; 4) amylasemia and lipasemia suggest acute pancreatitis; 5) increases in serum liver enzyme activities (ALT, AST, ALP) suggest primary liver disease; and, 6) hypercalcemia suggests parathyroid or other malignancy. Urinalysis will be useful in differentiating pre-renal and primary renal azotemia, while fecal examination may provide evidence of intestinal helminth infestation.

Survey radiographs of the abdomen are certainly indicated in the initial workup of a vomiting disorder. The abdominal radiographs will provide useful information about the abdominal alimentary and extra-alimentary structures. The decision to perform additional tests is based on response to empirical therapies and initial test results. Further tests might include: thoracic radiography, abdominal ultrasonography, contrast radiography, ACTH stimulation, liver function tests, gastrointestinal endoscopy, and laparotomy.

IV. Differential Diagnosis

After identifying problems from the history and physical examination, a reasonable list of differential diagnoses may then be considered based upon pathogenetic mechanism.

 Abdominal alimentary disorders--Infection, inflammation, toxicity, cancer, obstruction

 Abdominal extra-alimentary disorders--Peritonitis, urinary tract rupture, splenitis, pyometra

 Metabolic disorders--Uremia, liver failure, hypercalcemia

 Endocrine disorders--Diabetic ketoacidosis, hyperthyroidism, hypoadrenocorticism

 Systemic disorders--Septicemia, endotoxemia, multiple organ failure

 Neurologic disorders--Encephalitis, hydrocephalus, brainstem disorders

 Exogenous medication--Digitalis glycosides, macrolide antibiotics, metronidazole

 Physiology alterations--Pregnancy, motion sickness, stress and anxiety