Nausea and vomiting accompany a variety of illnesses. Symptoms may be due to primary GI disorders such as bowel obstruction or gastroenteritis. However, symptoms may also represent pathology of the central nervous system (increased intracranial pressure, tumor), psychiatric conditions (bulimia nervosa, anxiety), endocrine or metabolic abnormalities (diabetic ketoacidosis, hyponatremia), or iatrogenic causes (medications, toxins). Also, nausea and vomiting may be the result of severe pain, myocardial infarction, sepsis, or other systemic illnesses. A comprehensive history and physical examination, as well as the use of various diagnostic modalities, are needed to determine the cause and its complications.
In the United States, the most common cause of acute nausea and vomiting is viral gastroenteritis. Other important considerations are side effects from medication and, in young women, pregnancy.1
Multiple neurons in the medulla oblongata are activated in a sequential fashion to induce vomiting. The vomiting center is the chemoreceptor trigger zone, located in the area postrema of the fourth ventricle. Chemoreceptors in this area are outside the blood–brain barrier and are stimulated by circulating medications and toxins, including dopaminergic antagonists (levodopa, bromocriptine), nicotine, digoxin, and opiate analgesics. Another important peripheral pathway for emesis is mediated through vagal afferents. Vagal activation is triggered by direct gastric mucosal irritants (such as nonsteroidal inflammatory agents) or increased luminal distention (gastric outlet obstruction, gastroparesis). Vagus activation stimulates neurons in the area postrema and nucleus tractus solitarius. These areas are rich in serotonin receptors and are a major site of action of antiemetic drugs, such as granisetron and odansetron.2 Similar receptors are found throughout the gastrointestinal tract, as well as the cortex and limbic system, vestibular system, heart, and genitalia. The anatomic locations and receptor-mediated triggering factors in emesis are shown in Table 69-1.
Table 69-1 Anatomic Locations of Receptor-Mediated Triggering Factors in Emesis |Favorite Table|Download (.pdf)
Table 69-1 Anatomic Locations of Receptor-Mediated Triggering Factors in Emesis
Chemoreceptor trigger (area postrema)
Medications (dopamine agonists, digoxin, opiates, nicotine, chemotherapeutic drugs)
Metabolic (uremia, diabetic ketoacidosis, hypercalcemia)
Neuroendocrine (hyperemesis gravidum)
Peripheral vagal afferents
Gastric irritants (salicylate, erythromycin, copper, ipecac)
Bacterial toxins (Staphylococcus enterotoxin)
Gastrointestinal distention (biliary colic, small bowel obstruction)
Inflammation (peritonitis, cholecystitis)
Labyrinth tumors or infections
Benign position vertigo or Ménière’s disease
Cerebral cortex and limbic system
Psychogenic (fear, anxiety)
Efferent pathways in the vagal, phrenic, and spinal nerves control the physiologic event of vomiting through coordinated muscle activity. Three stages of vomiting have been described: nausea, retching, and actual vomiting. Nausea is the unpleasant feeling that precedes vomiting. During nausea, there may be autonomic symptoms of hypersalivation, repetitive swallowing, and tachycardia. The exact physiologic pathway is ...