Epidemiology

The most common causes of nausea and vomiting are acute gastroenteritis, febrile systemic illnesses, and drug effects. Acute viral gastroenteritis is the most common GI disease in the United States. Emesis associated with pregnancy is common, especially in the first trimester, and sometimes represents hyperemesis gravidarum. Nausea and vomiting are most commonly caused by medications in the adult population. Although the scope of the differential diagnosis in the pediatric population is broad, acute vomiting is commonly seen with infectious disorders affecting the GI tract as well as with infections in other areas of the body.

Pathophysiology

The act of vomiting can be divided into three distinct phases: nausea, retching, and actual vomiting (Fig. 29-1). Nausea may occur without retching or vomiting, and retching may occur without vomiting. Nausea is defined as a vague and extremely unpleasant feeling that often precedes vomiting. The exact neural pathways mediating nausea are not clear, but they are likely to be the same pathways that mediate vomiting. Mild activation of the pathways may result in nausea, whereas more intense stimulation results in vomiting. During nausea there is an increase in tone in the musculature in the duodenum and jejunum, with a concomitant decrease in gastric tone; this leads to reflux of intestinal contents into the stomach. There is often associated hypersalivation, repetitive swallowing, and tachycardia.

Retching is characterized as rhythmic, synchronous contractions of the diaphragm, abdominal muscles, and intercostal muscles that occur against a closed glottis. There is a resultant increase in abdominal pressure with a concurrent decrease in intrathoracic pressure. This pressure gradient causes gastric contents to move up into the esophagus. The mouth is usually closed.

Vomiting is the forceful expulsion of gastric contents through the mouth. There is contraction of the external oblique and abdominal rectus muscles, and the hiatal portion of the diaphragm relaxes; this increases the pressure in the abdominal and the thoracic compartments. There is contraction of the pyloric portion of the stomach. Simultaneously, there is relaxation of the gastric fundus, cardia, and upper esophageal sphincter as the vomitus is brought up and out the mouth. The glottis closes to prevent aspiration.

The complex act of vomiting is not completely understood but is thought to be coordinated by a vomiting center located in the lateral reticular formation of the medulla (Fig. 29-2). The efferent pathways from the vomiting center are mainly through the vagus, phrenic, and spinal nerves. These pathways are responsible for the integrated response of the diaphragm, intercostal muscles, abdominal muscles, stomach, and esophagus. The vomiting center is activated by afferent stimuli from a variety of sources. These include vagal and sympathetic impulses directly from the GI tract. Direct irritation of the stomach lining causes vomiting in this way. Other GI sources of afferent impulses include the pharynx, small bowel, colon, biliary system, and peritoneum. Receptors also are found outside the GI tract in the vestibular system, heart, and genitalia.

The other major source of impulses to the vomiting center is the CTZ. The CTZ is located in the area postrema, the floor of the fourth ventricle. Part of this area is located outside of the blood-brain barrier, enabling it to respond to endogenous and exogenous substances that activate vomiting. It is activated by hormones, peptides, medications, or toxins in the circulation, including opiates, digitalis, chemotherapy agents, salicylate, syrup of ipecac, and dopamine neurotransmitters.

The discovery of various neurotransmitters and their receptor sites within the medulla has improved the understanding and development of therapeutic agents. The CTZ area is rich in dopamine D₂ receptors, which are antagonized by drugs such as prochlorperazine, metoclopramide, and droperidol. The serotonin receptor has been found widely in the area postrema and the GI tract. It may act directly and through the release of dopamine. The serotonin receptor antagonists ondansetron and granisetron have been shown to be effective in preventing chemotherapy-induced nausea and vomiting. Concentrations of cholinergic and histamine receptors are found in the lateral vestibular nucleus and are important in motion sickness. Meclizine, diphenhydramine, and scopolamine act by antagonizing these receptors. Activation of cannabinoid receptors has been found to inhibit the emetic reflex.

Differential Considerations

The differential diagnosis for nausea and vomiting is particularly broad in scope; almost any organ system can be involved (Table 29-1). Vomiting also can result in complications, which must be considered in addition to the causes. The sequelae of vomiting may include the following:

Rapid Assessment and Stabilization

The initial assessment is directed toward the patient’s hemodynamic status and identification of the critical causes or sequelae of vomiting (see Table 29-1). Data gathered include duration of vomiting, whether blood is in the vomitus, symptoms of volume depletion, and associated symptoms pointing to serious underlying disease. Physical findings include level of consciousness, abdominal examination, rapid neurologic screen, and serial vital signs. Initial stabilization may include establishing intravenous access and fluid resuscitation in patients with signs of volume depletion, cardiac monitoring, and therapeutic measures directed toward specific underlying diseases (e.g., nasogastric tube for intractable vomiting in the setting of a small bowel obstruction) (Fig. 29-3).

Pivotal Findings