Nausea and Vomiting

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Chapter 29

Nausea and Vomiting

Perspective

Nausea and vomiting may constitute the primary presentation of many gastrointestinal (GI) disorders (e.g., bowel obstruction, gastroenteritis) or the secondary presentation of numerous systemic conditions (1) caused by severe pain, especially visceral pain; (2) caused by or related to severe systemic illness, such as myocardial infarction, sepsis, or shock; or (3) related to definitive conditions by specific mechanisms, such as pregnancy (hormones), increased intracranial pressure (central mechanism), toxins (homeostatic response), motion sickness (neuroendocrine), and chemotherapy (chemoreceptor trigger zone [CTZ]). In addition, vomiting may cause serious sequelae, such as aspiration pneumonia, Mallory-Weiss syndrome, esophageal rupture, volume depletion, and metabolic derangement. Classification by duration and frequency of the vomiting (acute, recurrent, chronic, or cyclic) may assist in determination of the underlying cause.

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.

Diagnostic Approach

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:

Hypovolemia is caused by loss of water and sodium chloride in the vomitus. The contraction of the extracellular fluid space leads to activation of the renin-angiotensin-aldosterone system.

Metabolic alkalosis is produced by loss of hydrogen ions in the vomitus. Many factors serve to maintain the alkalosis, including volume contractions, hypokalemia, chloride depletion, shift of extracellular hydrogen ions into cells, and increased aldosterone.

Hypokalemia is produced primarily by loss of potassium in the urine. The metabolic alkalosis leads to large amounts of sodium bicarbonate being delivered to the distal tubule. Secondary hyperaldosteronism from volume depletion causes reabsorption of sodium and excretion of large amounts of potassium in the urine.

Mallory-Weiss tears typically result from a forceful bout of retching and vomiting. The lesion itself is a 1- to 4-cm tear through the mucosa and submucosa; 75% of cases occur in the stomach, with the remainder near the gastroesophageal junction. Bleeding usually is mild and self-limited; however, 3% of deaths from upper GI bleeds are a result of Mallory-Weiss tears.

Boerhaave’s syndrome refers to a perforation of all layers of the esophagus occurring as a result of forceful retching or vomiting. The overlying pleura is torn so that there is free passage of esophageal contents into the mediastinum and thorax; 80% of cases involve the posterolateral aspect of the distal esophagus. Boerhaave’s syndrome constitutes a surgical emergency. The mortality rate has been reported as 50% if surgical repair is not performed within 24 hours.

Aspiration of gastric contents is a concern in patients who have altered mental status or pulmonary findings after an episode of vomiting. Patients with pulmonary findings after vomiting need further evaluation for aspiration.

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

History

Duration of the vomiting can lead to a diagnosis. Acute vomiting is episodic vomiting that occurs for less than 1 week and is associated with obstructive, ischemic, toxic, metabolic, infectious, neurologic, and postoperative causes. Chronic vomiting occurs with partial obstructions, motility disorders, and neurologic conditions or may be related to pregnancy or psychogenic in origin.

Timing of the vomiting may be important. An acute onset of nausea and vomiting suggests gastroenteritis, pancreatitis, cholecystitis, or a drug-related side effect. Symptoms occurring primarily in the morning suggest pregnancy, although this pattern also may be seen with uremia, alcohol ingestion, or increased intracranial pressure. Delayed vomiting more than 1 hour after eating suggests gastric outlet obstruction or gastroparesis. Vomiting of material eaten more than 12 hours previously is pathognomonic for outlet obstruction. Episodic nausea and vomiting occurring for more than 1 month are considered chronic. Discrete episodes of intractable vomiting with intervening asymptomatic periods are considered cyclic.

Content of the vomitus may provide clues to its cause. The presence of bile indicates a patent connection between the duodenum and the stomach and essentially rules out a gastric outlet obstruction. Regurgitation of undigested food can suggest achalasia, esophageal stricture, or Zenker’s diverticulum. Feculent material usually suggests a distal bowel obstruction but also may be seen with gastrocolic fistula or bacterial overgrowth of stomach contents in long-standing outlet obstruction.

Associated symptoms and signs may be helpful. Chronic headaches with nausea and vomiting should raise suspicion of elevated intracranial pressure. Vomiting without preceding nausea is typical of central nervous system (CNS) pathology. The social history should include inquiries about alcohol or other substance use. The past medical history will reveal the presence of any GI disease or previous surgeries. Nutritional history is valuable in the consideration of failure to thrive in infancy. Finally, a thorough medication list,