Differential diagnosis of vomiting

Roland Psáder, DVM, PhD

Head of the Clinical Diagnostic Unit
Department of Internal Medicine
Animal is „vomiting”
Vomiting
• Expulsion of material from the stomach and/or
intestines
Regurgitation
• Expulsion of material from the mouth, pharynx,
or oesophagus
Expectoration
• Expulsion of material from the respiratory tract
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Regurgitation vs. Vomiting vs. Expectoration

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 Regurgitation vs. vomiting
• Spontaneous • Nausea
• Passive backflow • Active muscle
contractions, retching
• Undigested food, no bile • Undigested or digested
food, gastric chyme,
• Eating the regurgitated bile
content (no nausea)
• Cervical oesophagus can
be distended
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Distinguishing regurgitation from vomiting
History
– V: nausea, retching, bile
– R: stretching or flexing the neck during swallowing, aspiration
of water/liquid and coughing, eating the content
Physical examination
– Palpation of distended cervical oesophagus, cervical mass,
injury or foreign body
Thoracic radiography
– Obvious megaoesophagus, foreign body, perforation and
pleuritis or PTX, retention of contrast material
Endoscopy: oesophagitis, hiatal hernia, stricture
Fluoroscopy: motility disorders, hiatal hernia, stricture 5
Physiology of vomiting: humoral
and neural pathways

Washabau: https://veteriankey.com/vomiting 6
Causes of vomiting
 Dogs: 370<
 Cats: 280<

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 Causes of vomiting
• Diet (Acute=A/Chronic=Chr)
• Emetogenic substances (A)
• Gastrointestinal (GI) tract obstruction (A/Chr)
• GI/Abdominal inflammation/irritation (A/Chr)
• Extraalimentary tract diseases (A/Chr)
• Motion sickness (A)
• Central nervous system (CNS) (A/Chr)
• Miscellaneous (A/Chr)
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 Common causes of vomiting
• Metabolic diseases
– Renal d.
– Hepatobiliary d.
– Electrolyte or acid-base
derangements
• Endocrine diseases
– Hypoadrenocorticism
– Hyperthyroidism
– DKA
• Toxins/Drugs
– Heavy metals, ethylene glycol
– NSAIDs, antibiotics, chemotherapy
agents
• Dietary causes
– Spoiled food, allergy, intolerance
• Abdominal diseases
– Pancreatitis
– Peritonitis
– Neoplasia
• Gastric diseases
– Gastritis
– GDV, foreign body
– Delayed gastric emptying
– Neoplasia
• Small intestinal diseases
– IBD/CCE, obstruction, parasites,
neoplasma, infections
• Large intestinal diseases
– Constipation, colitis 9
Diagnostic approach of vomiting

History and
physical
examination

Obvious Inapparent

Chronic
Treatment Acute Hematemesis
(1-2 weeks)
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History of vomiting patient
• Regurgitation / vomiting / expectoration?
• Duration
– Food more than 8 hours after ingestion -> delayed gastric
emptying
– Acute or chronic (>1-2 weeks)?
• Hematemesis?

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Diagnostic approach of
acute vomiting

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 Causes of acute vomiting

• Non-life-threatening: acute gastritis, Ascaris infection

(puppies), Giardia, motion sickness

• Potentially life-threatening: foreign body, ulcer,

intussusception, parvo, distemper, infectious canine hepatitis,
leptospirosis, AHDS (acute haemorrhagic diarrhoea syndrome), GDV
(gastric dilatation and volvulus), acute pancreatitis, acute renal failure,
acute hepatic failure, hypoadrenocorticism, pyometra,
peritonitis, sepsis, DKA (diabetic ketoacidosis)

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 Acute
vomiting

History and
physical
examination

Mild signs, Severe or life-

likely self- threatening
resolving signs

Minimal CBC, biochemistry,

diagnostics (fecal urinalysis, fecal ex.,
exam., +/-
radiographs) radiography, +/-
ultrasound

Parasites Nonspecific
(anthelmintic gastroenteritis Systemic or
therapy) Positive No significant
supportive therapy metabolic
imaging findings
disease

Treatment Treatment Specific Supportive

success failure Surgery
therapy therapy
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Diagnostic approach of
chronic vomiting

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 Causes of chronic vomiting
• Metabolic disease: renal disease, pancreatitis, hepatic disease,
biliary disease, hypoadrenocorticism, Ca↑, feline
hyperthyreoidism, K↓
• Gastric disease: foreign body, mucosal hypertrophy, gastritis,
neoplasia, polyps, hypomotility, enterogastric reflux, parasites
• Small intestinal disease: Giardia, nematodes, IBD, subileus,
neoplasia, fungal disease
• Large intestinal disease: obstipation,chronic colitis
• Neurologic disease: vestibular disease, autonomic epilepsy,
neoplasia
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 Chronic
vomiting

CBC, biochemistry, urinalysis, T4

(cats), cortizol (ca), fecal exam,
radiographs

Parasites
Systemic or Mass
anthelmintic No specific findings
metabolic disease Obstruction
therapy

Additional diagnostics
Specific +/- Ultrasonography Ultrasonography, heartworm test,
therapy Laparotomy
Bile acids profile, ACTH stimulation

Primary GI disease Non-GI

suspected disease

Stable Unstable Specific

disease disease therapy

Diet trial Gastroduodenoscopyor

Hypoallergenic surgerywith biopsy
Highly digestible

Treatmentfailure
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 Physical examination of vomiting patient
• Oral examination
– Uraemia (halitosis), ulcers, linear foreign body (tongue)
• Mucous membranes
– Icterus, ulcers
• Cardiac arrhythmia
– Metabolic derangements/toxins
• Abdominal palpation
– Pain (pancreatitis, obstruction), effusion (peritonitis), gas
distention (GDV, ileus), abdominal mass (neoplasia, foreign body)
• Rectal examination
– Melena, constipation, undigested foreign substances 18
Laboratory evaluation of vomiting patient
Primary GI diseases from metabolic diseases?
Complete blood counts (CBCs):
Often normal with primary gastric disease
Anemia: acute (regenerative/nonregenerative) / chronic gastric
bleeding (nonregenerative, microcytosis, hypochromasia,
thrombocytosis)
Neutropenia: parvo
Neutrophilic leukocytosis: acute pancreatitis, IBD, bacterial
enterocolitis
Eosinophilia: parasitism, eosinophilic gastroenteritis,
hypoadrenocorticism
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 Laboratory evaluation of vomiting patient
• Biochemical tests: most metabolic causes
(one exception: hypoadrenocorticism→ ACTH s mula on test)
• Hypoproteinemia: frequently in PLE (IBD, lymphoma), chronic
renal failure, chronic hepatic disease; infrequently in gastric
lymphoma, gastric carcinoma
• Hypokalemia: loss of K+ both in vomitus and urine, lack of
dietary intake
• Hyperkalemia: most likely renal failure or hypoadrenocorticism
• Acid-base status in vomiting:
– Hypochloremic metabolic alkalosis (acute gastritis, outflow
obstruction)
– Normal (simultaneous loss of gastric HCl and duodenal HCO3-)
– Metabolic acidosis (caused by dehydration, prerenal azotemia, lactic
acidosis) 20
 Radiography of vomiting patient
• Survey radiographs: identify foreign bodies, gastric distension
(aerophagia with dyspnea!, GDV), displacement, malposition,
delayed gastric emptying (overnight fasted patient with fluid and
ingesta in the stomach), penetrating gastric or intestinal ulcer
(pneumoperitoneum)

Location of the pylorus is essential: displacement dorsally and to

the left: GDV (↔gastric distension)

• Contrast radiography: foreign bodies, masses, deep

ulceration, gastric motility disorder (atropine, ketamine, xylazine
slow gastric emptying!), pylorus obstruction
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 US, Endoscopy, other methods
• Ultrasonography:
– dilated stomach with fluid (pylorus obstruction, motility disorder)
– thickening of the gastric and intestinal wall
(chronic inflammation, neoplasia)
– abdominal organs
– ileus
• Gastroduodenoscopy
– most useful method for gastric diseases
– direct visualization, biopsy, histopathology
• bleeding ulcer? infiltrative disease? IBD? neoplasma?
foreign body removal?
• Fluoroscopy, nuclear scintigraphy, BIPS (Barium-impregnated
polyethylene spheres)
– oesophageal motility, gastric emtying 23
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 Symptomatic-supportive therapy
Antiemetics:
• Maropitant-citrate ( Cerenia inj.) (inhibition of NK-1 receptor;
1mg/kg SID SQ/IV)
• Phenotiazines (CRTZ, vomiting center): hypotension, sedation;
chlorpromazine (0,15-0,25 mg/lb TID SQ,IM), prochlorpromazine
(0,25mg/lb TID SQ,IM after rehydration! for 24-36 hours)
• Metoclopramide (CRTZ, GI smooth muscle): 0,15-0,2 mg/lb
q6h PO,SQ,IM, 0,5-1mg/lb/day continuous infusion
(extrapyramidal signs, GI obstrucion!)
• Ondansetron (CRTZ, blocks vagal afferent neurons): 0,05-0,15
mg/lb slow SID-TID IV or 30 minutes before chemotherapy PO
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 Symptomatic-supportive therapy 2.
Fluid:
• 0,9% saline infusion:
deficits: dehydration(%)x10xBW(kg)= ml
maintenance: 50ml/kg/day
• K+ supplementation: max. 0,5mmol/kg/hour iv.
Serum level (mmol/l) K+ added (mmol/l)
<2 80
2,0-2,5 60
2,5-3,0 40
3,0-3,5 30
If serum level is not known, 20mmol/l
Dietary: NPO for 24 hours, if vomiting resolves low-fat,
single protein-source diet or GI diet in case of GI diseases
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Symptomatic-supportive therapy 2.
Antacids:
• H2-receptor antagonists (competitively and reversibly bind H2
receptors): suppress but not eliminate gastric secretion! famotidine(once daily
0,25mg/lb PO,IV)> ranitidine(1,0mg/lb PO,IV,SQ,IM BID,TID, prokinetic effect! )>
cimetidine for 7 to 10 days, particularly if hematemesis or melena is present
• Proton-pump inhibitors: much more potent! If GEU or esophagitis is
suspected or H2-receptor antagonists are not effective! Omeprazole,
pantoprazole and lansoprazole are safe (0,7-1 mg/kg SID/BID)

Protectives:
• Sucralfate (aluminium hydroxide complex): provides a barrier to acid
penetration, inactivates pepsin, absorbs bile acids, stimulates PG synthesis. It
should not be given within 2 hours of other oral medications!
• Misoprostol (synthetic prostaglandin analogue): is indicated for patients
with suspected NSAID induced gastritis! It should not be used in pregnant
patients! 27
Thank you for your attention!
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