Nausea is the subjective feeling of a need to vomit. Vomiting (emesis) is the oral expulsion of gastrointestinal contents resulting from contractions of gut and thoracoabdominal wall musculature. Vomiting is contrasted with regurgitation, the effortless passage of gastric contents into the mouth. Rumination is the repeated regurgitation of stomach contents, which may be rechewed and reswallowed. In contrast to vomiting, these phenomena often exhibit volitional control. Indigestion is a nonspecific term that encompasses a variety of upper abdominal complaints including nausea, vomiting, heartburn, regurgitation, and dyspepsia (the presence of symptoms thought to originate in the gastroduodenal region). Some individuals with dyspepsia report predominantly epigastric burning, gnawing discomfort, or pain. Others with dyspepsia experience a constellation of symptoms including postprandial fullness, early satiety (an inability to complete a meal due to premature fullness), bloating, eructation (belching), and anorexia.
Vomiting is coordinated by the brainstem and is effected by responses in the gut, pharynx, and thoracoabdominal wall. The mechanisms underlying nausea are poorly understood but likely involve the cerebral cortex, because nausea requires conscious perception. This is supported by electroencephalographic studies showing activation of temporofrontal regions during nausea.
Brain stem nuclei—including the nucleus tractus solitarius; dorsal vagal and phrenic nuclei; medullary nuclei that regulate respiration; and nuclei that control pharyngeal, facial, and tongue movements—coordinate the initiation of emesis. Neurotransmitters involved in this coordination are uncertain, but neurokinin NK1, serotonin 5-HT3, and vasopressin pathways may participate.
Somatic and visceral muscles exhibit stereotypic responses during emesis. Inspiratory thoracic and abdominal wall muscles contract, producing high intrathoracic and intraabdominal pressures that facilitate expulsion of gastric contents. The gastric cardia herniates across the diaphragm and the larynx moves upward to promote oral propulsion of the vomitus. Under normal conditions, distally migrating gut contractions are regulated by an electrical phenomenon, the slow wave, which cycles at 3 cycles/min in the stomach and 11 cycles/min in the duodenum. With emesis, there is slow-wave abolition and initiation of orally propagating spikes that evoke retrograde contractions that assist in oral expulsion of intestinal contents.
Emetic stimuli act at several sites. Emesis provoked by unpleasant thoughts or smells originates in the cerebral cortex, whereas cranial nerves mediate vomiting after gag reflex activation. Motion sickness and inner ear disorders act on the labyrinthine apparatus, whereas gastric irritants and cytotoxic agents such as cisplatin stimulate gastroduodenal vagal afferent nerves. Nongastric visceral afferents are activated by intestinal and colonic obstruction and mesenteric ischemia. The area postrema, a medullary nucleus, responds to bloodborne emetic stimuli and is termed the chemoreceptor trigger zone. Many emetogenic drugs act on the area postrema, as do bacterial toxins and metabolic factors produced during uremia, hypoxia, and ketoacidosis.
Neurotransmitters that mediate induction of vomiting are selective for these anatomic sites. Labyrinthine disorders stimulate vestibular muscarinic M1 and histaminergic H1 receptors, whereas vagal afferent stimuli activate serotonin 5-HT3 receptors. The area postrema is richly served by nerves acting on 5-HT3, M1, H1, and dopamine D2 subtypes. Transmitters in the cerebral cortex are poorly understood, although cannabinoid CB1 pathways may participate. Optimal pharmacologic therapy of vomiting requires understanding of these pathways.
Nausea and vomiting are caused by conditions within and outside the gut as well as by drugs and circulating toxins (Table 39–1).
Table 39–1 Causes of Nausea and Vomiting
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Table 39–1 Causes of Nausea and Vomiting
Small bowel obstruction
Superior mesenteric artery syndrome
Altered sensorimotor function
Cyclic vomiting syndrome
Anorexia and bulimia nervosa
Thyroid and parathyroid disease
Visceral obstruction and inflammation of hollow and solid viscera may produce vomiting. Gastric obstruction results from ulcer disease and malignancy, while small-bowel and colonic obstruction occur because of adhesions, benign or malignant tumors, volvulus, intussusception, or inflammatory diseases such as Crohn's disease. The superior mesenteric artery syndrome, occurring after weight loss or prolonged bed rest, results when the duodenum is compressed by the overlying superior mesenteric artery. Abdominal irradiation impairs intestinal motor function and induces strictures. Biliary colic causes nausea via action on visceral afferent nerves. Vomiting with pancreatitis, cholecystitis, and appendicitis is due to visceral irritation and induction of ileus. Enteric infections with viruses or bacteria such as Staphylococcus aureus and Bacillus cereus commonly cause vomiting, especially in children. Opportunistic infections such as cytomegalovirus or herpes simplex virus induce emesis in immunocompromised individuals.
Disordered gut sensorimotor function commonly causes nausea and vomiting. Gastroparesis is defined as a delay in gastric emptying of food and occurs after vagotomy, with pancreatic adenocarcinoma, with mesenteric vascular insufficiency, or in systemic diseases such as diabetes, scleroderma, and amyloidosis. The most common form of disease, idiopathic gastroparesis, occurs in the absence of systemic illness and may follow a viral prodrome, suggesting an infectious etiology. Intestinal pseudoobstruction is characterized by disrupted intestinal and colonic motor activity and leads to retention of food residue and secretions; bacterial overgrowth; nutrient malabsorption; and symptoms of nausea, vomiting, bloating, pain, and altered defecation. Intestinal pseudoobstruction may be idiopathic or inherited as a familial visceral myopathy or neuropathy, or it may result from systemic disease or as a paraneoplastic complication ...