Vomiting is one of the most common medical presentations to the emergency room. It is not uncommon for the dog or cat to eat
grass or their food and vomit – and subsequently go about their lives unaffected. So – when is vomiting an emergency? While
there are no simple, nor clear cut answers, the simple guidelines in the box can guide the triage nurse or doctor.
Vomiting is an emergency when the cause of vomiting can be associated with
- a potentially life-threatening etiology (eg. toxins, GDV, foreign body, sepsis)
- possible decompensation of a chronic serious disease (eg. renal failure, diabetes);
OR the effect of vomiting causes compromise of
The gastrointestinal (GI) signs can be caused by pathology initiated within the GI tract (primary) or caused by systremic
problems (secondary). Catastrophic problems related to vomiting can include: cardiac arrest (vasovagal reflex bradycardia),
upper airway obstruction, aspiration pneumonia, profound hemorrhage, severe hypovolemic, distributive and/or septic shock,
and ischemia of GI organs. The animal must be rapidly stabilized and causes requiring surgical correction rapidly investigated.
Vomiting is a reflex expulsion of gastric contents. Vomiting can be active with GI contractions or passive. It is important
to understand the mechanisms of vomiting center stimulation to identify the cause and best therapeutic approach (see Figure
Figure 1. Mechanisms of vomiting and site of antiemetic action.
The color of the vomitus will locate the origin. Clear vomitus is swallowed saliva from stomach;. yellow reflects refluxed
digested bile from stomach;. green suggests undigested bile from the upper duodenum due to obstruction or ileus; and brown
fluid with a fetid odor is from the small intestines suggesting total obstruction or generalized ileus. Blood in the vomitus
from primary GI causes typically appears as red colored fluid or as "coffee grounds". This "hematemesis" suggests a serious
underlying pathology. Streaks of blood within the clear or yellow vomitus is from gastric irritation due to vomiting and is
not indicative of specific pathology.
The timing and force of vomiting can suggest the location : shortly after eating indicates gastric inflammation or obstruction;
large amounts of undigested food up to 6 hours post prandial suggests pyloric obstruction or gastric atony; projectile vomiting
indicates pyloric or upper duodenal outflow obstruction or ileus; and non-productive vomiting or retching may indicate the
presence of gastric dilatation-volvulus.
There are four mechanisms of diarrhea that can occur in any combination: osmotic diarrhea; secretory diarrhea; increased intestinal
permeability; and abnormal gastrointestinal motility. Bacterial endotoxins can inhibit the ion pumps in GI epithelium resulting
in secretory diarrhea. Any cause of GI mucosal erosions (eg severe shock, toxins, hyperthermia, foreign body) or blunting
of GI epithelium (e.g. viral or baterial agents) can cause diarrhea by any or all mechanisms listed above: osmotic due to
cellular debris in the intestinal lumen; secretory due to bacterial endotoxins or other pump inhibitors; motility due to ileus;
and increased permeability. The presence of blood [melena (digested) or hematochezia(fresh)] indicates that the intestinal
barrier is damaged and increased protein loss and bacterial translocation anticipated. Small intestinal diarrhea typically
results in greater fluid, electrolyte, protein, and acid-base abnormalities than large intestinal diarrhea and is characterized
by liquid projectile feces. Large bowel diarrhea generally has a "pudding" consistency with mucous or fresh blood.
The systemic inflammatory response syndrome (SIRS) can be associated any cause of vomiting and/or diarrhea..The increase in
capillary permeability can lead to third spacing of fluid and electrolytes into the intestinal tract. Vomiting associated
with gastric outflow or upper duodenal obstruction (mechanical or physiologic) can cause hypochloremic metabolic alkalosis.
Other causes usually result in metabolic acidosis depending upon the perfusion status of the animal.
Resuscitation: Hypovolemia should be rapidly resuscitated with a combination of isotonic replacement crystalloids and synthetic
colloids. Isotonic balanced buffered crystalloids (0.9% saline if metabolic acidosis) (10-20mls/kg IV) are administered with
hetastarch or dextran-70 (5-20 ml/kg dogs; 5 ml/kg cats) titrated to supranormal end-points. When abdominal hemorrhage or
brain pathology is suspected, fluids are titrated using small volume resuscitation techniques to hypotensive resuscitation
end-points. Analgesia is provided using narcotic injections: 0.4mg/kg butorphanol, 0.2mg/kg hydromorphone IV, 0.05-0.1mg/kg
, or oxymorphone IV, with or without a sedative.
Measures necessary to prevent vomiting and aspiration are used to include antiemetic (see Figure 1) and/or promotility agents
and nasogastric tube suctioning. When vomiting is associated with an unobstructive ileus or stimulation of the vomiting center
or CRTZ zone, antiemetics are indicated alone or in combination: metoclopramide 0.2-0.4 mg/kg SQ q6-8h or followed by a 1.0-2.0
mg/kg/24h IV by constant rate infusion; ondansetron 0.1-0.2 mg SQ q 8h, or 0.5 mg IV load followed by 0.5 mg/kg/h IV by constant
rate infusion; chlorpromazine 0.05 mg/kg IV, 0.01-0.025 mg/kg IV (cats) q 4-6h if cardiovascularly stable; ranitidine 2 mg/kg
IV q 12 h. When an unobstructive ileus is occurring, administration of promotility agents is indicated, such as metoclopramide
or cisapride (dog: 0.1-0.5 mg/kg PO q8-12h, cat: 0.5-1 mg/kg PO q 8h). When esophageal or gastric ulceration is suspected,
sucralfate (0.5-1 gram q 4-8h) and one of the H2-antagonsits or hydrogen pump inhibitors are indicated: ranitidine (2-2.5mg/kg
q 12 h); or cimetadine (4mg/kg IV q 6-8h); or omperazole (0.7 mg/kg, up to 20mg PO q 24h). Intestinal motility suppressants
are not recommended for routine use. Most anti-diarrheal medications decrease peristalsis which may lead to severe intestinal
bacterial overgrowth and translocation.