Vomiting: Introduction - The Merck Veterinary Manual

Vomiting: Introduction

Etiology, Pathophysiology, and Clinical Findings

Vomiting is the forceful ejection of the contents of the stomach and proximal small intestine. It is a vigorously active motion signaled by hypersalivation, retching, and forceful contractions of the abdominal muscles and the diaphragm. Vomiting must be differentiated from regurgitation, which is a passive motion facilitated by gravity and body position of the animal. With regurgitation, the expelled food and fluid tends to be undigested, has a neutral pH depending on the composition of the diet, and may have a cylindrical shape reflecting the shape of the esophagus. Dyspnea or cough is more often associated with regurgitation, which indicates a lesion of the oral cavity, pharynx, or esophagus.

Etiology, Pathophysiology, and Clinical Findings:

Vomiting represents a coordinated effort of the GI, musculoskeletal, and nervous systems to expel food, fluid, or debris from the GI tract. It is initiated by direct stimulation of the vomiting center in the brain stem or indirectly via the chemoreceptor trigger zone (CTZ) or abdominal afferent nerves. Stimulation of receptors in the semicircular canals of the vestibular system, or inflammation within the CNS and increases in intracranial pressure, can also promote vomiting. The CTZ responds to substances in the blood, eg, drugs, ketones, or uremic or bacterial toxins. Most of the receptors involved in the vomiting reflex are found in the abdominal viscera, especially in the duodenum. Abdominal afferent neural stimulation may arise from GI tract inflammation; stretching or distention of the bowel; or irritation or inflammation of the liver, pancreas, kidneys, spleen, genitourinary tract, or peritoneum. Motor efferent innervation of the vomiting reflex is mediated from the spinal and phrenic nerves, which innervate muscles of the abdominal wall and diaphragm.

Vomiting can be due to primary GI disease, renal or hepatic failure, electrolyte abnormalities (eg, hypoadrenocorticism), pancreatitis, or CNS disorders (including toxin ingestion).

Anxiety, depression, hypersalivation, and repeated swallowing accompanied by relaxation of the gastroesophageal sphincter are followed by retching. The proximal small intestine and gastric antrum contract, propelling their contents into the body of the stomach where movement is inhibited. The gastroesophageal sphincter moves into the thoracic cavity, rendering it incompetent and facilitating gastroesophageal reflux. Esophageal and pharyngoesophageal sphincter motility is repressed, and the nasopharynx closes to prevent nasal regurgitation. Forceful contractions of the abdominal muscles and diaphragm against a closed glottis and increases in intra-abdominal pressure force expulsion of food, fluid, or debris.

Diagnosis:

The diagnostic approach to vomiting varies depending on whether the vomiting is acute or chronic. Acute or even sporadic vomiting is generally not associated with other abnormalities. Chronic vomiting may be associated with weakness, lethargy, weight loss, dehydration, electrolyte imbalance, and acid-base disorders.

When vomiting has been of a short duration, ie, <3-4 days, and without associated adverse clinical signs, the diagnostic approach may be limited to a detailed history (including questions related to possible ingestion of garbage or toxins), a physical examination (including abdominal palpation), examination of the oropharynx, and a rectal examination (checking for evidence of dietary indiscretion). If nothing of significance is found, symptomatic therapy may be administered.

Chronic vomiting, vomiting that occurs more often than once or twice daily, and vomiting accompanied by hematemesis, abdominal pain, depression, dehydration, weakness, fever, or other adverse clinical signs should be approached more vigorously. In addition to a detailed history and physical examination, an initial database should include a CBC, biochemical profile (including serum electrolytes), urinalysis, and abdominal radiographs (and abdominal ultrasonography if available). A more detailed database will be dictated by any identified abnormalities. In many cases, endoscopic evaluation and biopsy of the stomach and small intestine is the only test that can determine the nature of the disease.

Treatment and Control:

Control of vomiting should be directed to identifying the inciting cause and (if possible) eliminating it and to controlling accompanying secondary changes.

Symptomatic therapy for acute vomiting includes fasting and withholding water for 24 hr to rest the GI tract. (Water can be provided in the form of ice.) Animals predisposed to hypovolemia, eg, animals with concurrent renal insufficiency or cardiac disease, should receive parenteral fluid therapy. If the vomiting has stopped after 24 hr, the animal may be offered small amounts of water initially. If no further vomiting occurs, small amounts of a commercial low-fat diet can be fed 4-6 times the first day or so, after which the animal can be fed its standard diet.

Therapy for chronic vomiting is also directed to elimination of the primary cause and, in addition, to correction of dehydration, electrolyte imbalances, and acid-base disorders. The vomiting reflex should be suppressed. (Specific treatment regimens are detailed under respective disease headings.) If untreated, persistent vomiting may result in prerenal azotemia. Vomiting associated with GI obstruction ( Gastrointestinal Obstruction) commonly results in hypokalemia, hypochloremia, metabolic alkalosis, and paradoxical aciduria due to losses of secretions rich in potassium, chloride, and hydrogen. However, continued vomiting, lack of water intake, insensible water losses, and catabolism of body energy stores contribute to dehydration, poor tissue perfusion, hypoxia, and lactic acidosis. In the absence of gastric obstruction, the loss of bicarbonate from duodenal secretions may predispose to metabolic acidosis. It is therefore difficult to accurately predict the acid-base status of a vomiting animal, especially when the cause or duration of vomiting is unknown.

Antiemetic therapy is indicated in animals with intractable vomiting, dehydration, and weakness. (See also Drugs to Control or Stimulate Vomiting.) Commonly used antiemetics include antispasmodic medication, agents that depress the CTZ, drugs that suppress the emetic center, drugs that have peripheral activity, and the newer serotonin-antagonist agents. Drugs that act directly on the emetic center are very effective but tend to be less effective in the control of vomiting associated with severe GI disease. Drugs that act on the emetic center as well as the CTZ are more efficacious.

Antispasmodic agents (eg, scopolamine, 0.03 mg/kg, SC or IM, qid) inhibit cholinergic activity from visceral receptors. Consequently, they may inhibit vomiting associated with excessive contraction of GI smooth muscle. These drugs are rarely effective in small animals.

Drugs that depress the CTZ are used primarily to control motion sickness in people and may be useful to prevent nausea caused by drugs. They include dimenhydrinate (8 mg/kg, PO, tid) and trimethobenzamide (3 mg/kg, bid-tid). Trimethobenzamide is not as consistently effective as the phenothiazine antiemetic agents.

Diphenhydramine (2-4 mg/kg, PO, tid), an antihistamine, works by blocking H₁ receptors in the vestibular apparatus and, to a lesser extent, the CTZ. It may be useful in management of motion sickness.

Drugs acting directly on the emetic center include the phenothiazine tranquilizers such as prochlorperazine (0.3 mg/kg, tid, PO; 0.1 mg/kg, IM, qid; or 0.1-0.5 mg/kg, SC, tid) and chlorpromazine (0.5 mg/kg, PO, qid; 0.5 mg/kg, IM, tid; or 1 mg/kg, rectally, tid). Phenothiazine agents also inhibit activity of the CTZ and have weak anticholinergic effects. The antiemetic effects are seen at dosages lower than those required to cause tranquilization.

Dopaminergic antagonists such as metoclopramide (0.2-0.5 mg/kg, PO or SC, qid, or 1-2 mg/kg/day, slow IV or 1.3 µg/kg/min) and domperidone (0.05-0.1 mg/kg, PO, sid-bid) act at the level of the CTZ and peripheral receptors and are useful in the management of vomiting associated with toxins in the blood. Ondansetron (0.5-1 mg/kg, PO, sid-bid, or 30 min before chemotherapy, PO) is a potent antiemetic agent. It is a selective serotonin-receptor antagonist with both central and peripheral activity. It should be considered in cases unresponsive to other antiemetic agents. Dolasetron (0.6-1.0 mg/kg, IV, PO) is a serotonin type III antagonist used to reduce nausea and vomiting secondary to anesthesia, chemotherapy, enteritis, and renal and hepatic disease. To date, no side effects have been reported in pets.