Nausea and Vomiting

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Chapter 29

Nausea and Vomiting

Leslie S. Zun

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.

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.

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.

Figure 29-1 Pathophysiology of nausea and vomiting. GI, gastrointestinal.

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.

Figure 29-2 Vomiting process. GI, gastrointestinal.

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:

Table 29-1

Differential Diagnosis of Nausea and Vomiting

CNS, central nervous system; DKA, diabetic ketoacidosis; ICP, intracranial pressure.

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).

Figure 29-3 Approach to the patient with nausea and vomiting. CNS, central nervous system; ECG, electrocardiogram; IV, intravenous; MI, myocardial infarction; Psych, psychogenic; Rx, treatment.

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, including over-the-counter drugs and supplements, should be elicited in the history.

Physical Examination

The important physical examination findings are outlined in Table 29-2. During evaluation, findings of jaundice, lymphadenopathy, nystagmus, fever, and goiter can help determine the cause of the disease. Oral examination may reveal loss of dental enamel commonly seen with bulimia. Abdominal examination may reveal ascites, distention, hernias, abdominal tenderness and masses, organomegaly, or hyperactive or hypoactive bowel sounds, with appropriate laboratory testing for occult blood in the stool. Orthostatic vital signs often are obtained but are of limited value in determination of the extent of dehydration, and results should not alter clinical decision-making. It also is important to evaluate neurologic status (including cranial nerve evaluation, funduscopic examination, and gait observation) to rule out a central cause of a patient’s symptoms. Provocative testing for vertigo such as with the Nylen-Barany test may elicit nausea and vomiting. Attentive physicians may elicit evidence of depression or anxiety that may lead to a psychiatric diagnosis.

Table 29-2

Physical Examination of the Patient with Nausea and Vomiting

CNS, central nervous system; CPA, cerebellopontine angle; HEENT, head, eyes, ears, nose, throat; ICP, intracranial pressure.

In children the examination should search for other additional diagnostic clues. A bulging fontanelle (meningitis), projective vomiting (pyloric stenosis), unusual odors (metabolic cause), visible bowel loops (obstruction), enlarged parotid, and loss of dental enamel (bulimia) point to specific causative disorders. Most of these disorders are age dependent.

Ancillary Studies

Because of the broad differential diagnosis for nausea and vomiting, there is no standard panel of laboratory tests. Appropriate testing is determined by the specifics of the history and physical examination. The following general guidelines regarding specific tests are useful.

Complete blood count: Most patients do not require a complete blood count for the diagnosis and management of nausea and vomiting. Elevated hemoglobin may suggest dehydration, but other tests are better for this purpose. An elevated white blood count is entirely nonspecific and of no discriminatory value.

Serum electrolytes: Measurement of serum electrolytes is not indicated in most cases of vomiting. Severe, protracted vomiting can cause a hypochloremic, hypokalemic metabolic alkalosis. Patients with this history or with clinical evidence of dehydration should undergo electrolyte testing. In general, serum electrolyte testing is indicated only in patients with symptoms lasting longer than 3 days or signs of significant dehydration who require intravenous fluid to replenish vascular volume.

Blood urea nitrogen and creatinine: A blood urea nitrogen–to-creatinine ratio greater than 20:1 implies significant dehydration.

Serum lipase: Lipase determination is indicated in cases of suspected pancreatitis.

Urine tests: A urine pregnancy test should be performed in all women of childbearing age with nausea and vomiting. A urine analysis that shows nitrites, leukocyte esterase, white blood cells, and bacteria suggests a urinary tract infection. Ketones may support a diagnosis of diabetic ketoacidosis or prolonged starvation state. Hematuria indicates a possible renal calculus.

Cultures: Blood cultures may be indicated in the febrile patient with nausea and vomiting who requires admission to hospital. Urine cultures may be necessary to determine an underlying cause of fever, and stool cultures looking for enteric pathogens, parasites, or leukocytes may be valuable.

Liver function and ammonia tests: Liver function tests are indicated in cases of suspected hepatitis or biliary disease. Ammonia testing is useful if liver failure is suspected.

Serum drug levels: Serum drug levels may be important in determining the cause of nausea and vomiting in patients on theophylline, digoxin, or salicylates, especially in elders who are taking medication without supervision.

Abdominal imaging: Flat and upright plain radiographs are indicated only for patients with suspected bowel obstruction or ileus in whom computed tomography (CT) scanning is not planned. CT scan of the abdomen has supplanted plain radiography for the evaluation of many patients with suspected obstruction because of the improved ability to discern the cause of the problem in addition to the presence of obstruction. An abdominal ultrasound study is indicated in cases of suspected choledocholithiasis or cholecystitis in adults and suspected pyloric stenosis and intussusception in children. Imaging studies such as cranial CT scan or magnetic resonance imaging (MRI) may be needed for evaluation for possible CNS trauma, tumor, or infectious causes of nausea and vomiting.

Electrocardiogram: An electrocardiogram (ECG) is indicated in cases of suspected coronary artery ischemia.

Thyroid function tests: Although not usually available during the patient’s stay in the ED, thyroid function tests may indicate a thyroid cause for the vomiting.

Differential Diagnosis

Clinical and diagnostic findings are helpful in differentiating among the common and catastrophic causes of nausea and vomiting (Table 29-3). The differential diagnosis in adults is extensive; etiologic categories include medication-induced causes, infectious and toxic causes, disorders of the GI tract, CNS causes, pregnancy-related nausea and vomiting, endocrine and metabolic disorders, radiation-induced nausea and vomiting, postoperative nausea and vomiting (PONV), unknown (as in cyclic vomiting), psychogenic causes, and other causes such as acute myocardial infarction and acute graft-versus-host disease.

Table 29-3

Disorders Commonly Associated with Vomiting

ABGs, arterial blood gases; AST, aspartate aminotransferase; β-hCG, β-human chorionic gonadotropin; BUN, blood urea nitrogen; CT, computed tomography; CXR, chest radiography; ECG, electrocardiogram; ERCP, endoscopic retrograde cholangiopancreatography; ETOH, ethyl alcohol; Hct, hematocrit; LDH, lactate dehydrogenase; NSAID, nonsteroidal anti-inflammatory drug; PO₂, partial pressure of oxygen; WBC, white blood cell.

Pediatric Considerations

The evaluation and management of pediatric patients with nausea and vomiting depend on age and likely causative disorders (Table 29-4). Mild degrees of reflux and associated regurgitation are common in the first few months of life, but vomiting in infancy can be associated with life-threatening illness. In the first week of life, obstructive lesions of the alimentary tract, inborn errors of metabolism, and serious infectious processes are associated with vomiting. After the first week of life, pyloric stenosis needs to be considered. The diagnosis of “feeding problems” should be considered a diagnosis of exclusion. After the first month of life, infections, metabolic diseases, cow’s milk intolerance, failure to thrive, and subdural hematoma from abuse should be prime considerations. Thereafter, various disorders are associated with vomiting, including recurrent cyclic vomiting, acute surgical emergencies, food poisoning, toxic ingestion, Henoch-Schönlein purpura, pneumonia, and diabetic ketoacidosis. Anorexia nervosa and bulimia should be considered in teenagers with recurrent vomiting.

Table 29-4

Etiology of Nausea and Vomiting in Pediatric Age Groups

PUD, peptic ulcer disease; URI, upper respiratory infection; UTI, urinary tract infection.

Adapted from Li HK, Sunku BK: Vomiting and nausea. In Wyllie R, Hyams JS, eds: Pediatric Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. Philadelphia: WB Saunders; 2005:127-149.

Management

Symptomatic relief of nausea and vomiting should not await identification of the underlying cause. Decreased oral intake is a major cause of dehydration and malnutrition. If the patient is able to take oral liquids, a solution containing sodium, carbohydrate, and water is recommended. Many sports drinks contain the proper balance of these elements.¹ Patients who are dehydrated and in whom intake of oral fluids is not possible or is contraindicated should be given intravenous fluids. Hypokalemia is rarely of clinical significance but may be found with profound vomiting secondary to contraction metabolic alkalosis. Treatment of the underlying condition with administration of intravenous fluids is indicated. Placement of a nasogastric tube is an option in some cases of refractory vomiting in patients with gastroparesis, pancreatitis, or bowel obstruction.

Pharmacologic management of patients with nausea and vomiting is outlined in Table 29-5. To allow the physician to make an appropriate choice for each patient, the pharmacologic therapies available may be classified into histamine antagonists, muscarinic antagonists, dopamine antagonists, and serotonin antagonists.

Table 29-5

Commonly Used Medications for the Treatment of Nausea and Vomiting

MEDICATION	DOSE	COMMENTS
Promethazine (Phenergan)	Adult: 12.5-25 mg IV, IM, PO, or by rectum Pediatric: 0.25-1 mg/kg/dose q4-6h prn IV, IM, PO, or by rectum; max 25 mg/dose	May be repeated every 4-6 hr until cessation of vomiting. May cause dry mouth, dizziness, blurred vision. Boxed warning for use under 2 yr old.
Prochlorperazine (Compazine)	Adult: 5-10 mg IM or PO; 2.5-10 mg IV; 25 mg by rectum Pediatric: 0.4 mg/kg/24 hr tid-qid PO or by rectum; 0.1-0.15 mg/kg/dose tid-qid IM; max 40 mg/24 hr	May be repeated every 4 hr IV or IM or every 12 hr by rectum until cessation of vomiting. May cause lethargy, hypotension, extrapyramidal effects.
Metoclopramide (Reglan)	Adult: 10 mg IM or IV, may repeat q6h Pediatric: 1-2 mg/kg/dose q2-6h IV q2-3h	May cause dystonic reactions, tardive dyskinesia, neuroleptic malignant syndrome.
Ondansetron (Zofran)	Adult: 4 mg IV single dose Pediatric: up to 40 kg: 0.1 mg/kg; >40 kg: 4 mg/dose IV single dose	May cause headache, dizziness, and musculoskeletal pain.

IM, intramuscularly; IV, intravenously; PO, orally; prn, as needed.

The phenothiazines are widely used as general-purpose antiemetics. These agents have multiple complex mechanisms of action. The antiemetic effect is apparently through blockade of the dopamine D₂ receptor in the CTZ. Prochlorperazine (Compazine), droperidol (Inapsine), haloperidol (Haldol), and promethazine (Phenergan) are commonly used medications in this class. Mild to moderate side effects are fairly common and include dystonic reactions, sedation, and feelings of restlessness. These side effects may be treated with diphenhydramine (Benadryl) or benztropine (Cogentin). Although prochlorperazine was found to be more effective in reducing vomiting than promethazine, use of prochlorperazine has been reported to be associated with a 16% incidence of akathisia and a 4% incidence of dystonia, so patients should be advised about this potential and its mitigation with diphenhydramine or benztropine. Neuroleptic malignant syndrome, blood dyscrasias, and cholestatic jaundice have been documented with use of phenothiazines but are extremely rare.

The serotonin receptor antagonists, such as ondansetron, granisetron, and tropisetron, have generated much interest because of their beneficial effect in chemotherapy-induced emesis. Their principal site of action is the area postrema, although they also affect receptors in the GI tract. The antiserotonin agents have been used with success for vomiting related to various drug ingestions.

The side effects of the serotonin receptor antagonists are mild and include headache and constipation.

The prokinetic agents are useful in patients with gastroparesis, gastroesophageal reflux disease, and other putative dysmotility syndromes. Metoclopramide (Reglan) has the most applicability in the ED. It has dopamine antagonist activity at the CTZ and exerts anticholinergic and antiserotonin effects. The primary effect is increased gastric emptying; the exact mechanism for this is not understood. Metoclopramide has multiple antiemetic actions and may be used as a general-purpose agent. Metoclopramide has been associated with tardive dyskinesia, prompting the Food and Drug Administration to issue a black box warning.² The most common side effects of metoclopramide are restlessness, drowsiness, and diarrhea. These effects are usually mild and transient.

Antihistamines are useful in nausea and vomiting associated with motion sickness and vertigo. Agents such as dimenhydrinate (Gravol, Dramamine) and meclizine (Antivert) directly inhibit vestibular stimulation and vestibular-cerebellar pathways. Their anticholinergic effect also may contribute to their effectiveness in vertigo and motion sickness. Antihistamines have some role as general antiemetics but are better used in the prevention of motion sickness; for nausea and vomiting, they are less effective than the phenothiazines. The most common side effects of antihistamines are drowsiness, blurred vision, dry mouth, and hypotension. The newer, less-sedating antihistamines, such as cetirizine and fexofenadine, are thought to be less effective as antiemetics.

The anticholinergic agent scopolamine in a transdermal patch (Transderm Scop) or hyoscine (Buscopan) in an oral form may be used for prophylaxis and treatment of motion sickness. These agents also have mild efficacy in preventing cytotoxic chemotherapy-related nausea and vomiting but are not useful in the emergency department (ED).

Benzodiazepine medications have been used for nausea and vomiting with variable results. Limited studies have evaluated the efficacy of benzodiazepines in the treatment of hyperemesis gravidarum, in prophylaxis for emetogenic chemotherapy, and preoperatively for minor gynecologic surgery. Although this aspect was not directly measured in these studies, the researchers inferred that part of the response may be related to the anxiolytic component.3–5 No studies have addressed the use of benzodiazepines to treat nonspecific nausea and vomiting in an ED population.

An oral neurokinin-1 antagonist, aprepitant (Emend), has been found to be an effective adjunctive agent for use in patients undergoing cancer chemotherapy.⁶ Aprepitant blocks the effects of substance P in the brain. Currently, it is not indicated for use in patients with established nausea and vomiting.

Adjuncts to pharmacologic agents have been investigated with limited results. Increased inhaled oxygen as well as ginger and ginger extract have not been found to be effective. Investigations of intravenous fluids have not been definitive in the treatment of nausea and vomiting. The use of acupressure point P6 on the wrist has been found to be effective as compared with placebo.⁷

The medication choice is directed at the underlying cause of the nausea and vomiting, if known, such as motion sickness, PONV, or nausea and vomiting related to cancer chemotherapy. For all other patients, the choice of antiemetic agent has not been well studied in emergency medicine. One study found droperidol to be more effective than prochlorperazine or metoclopramide as compared with placebo for moderate to severe nausea of any cause.⁸ There also has been limited research regarding the preferred agents for the treatment of nausea and vomiting in the field. One study found that ondansetron was moderately effective in the treatment of nausea and vomiting in this setting.⁹ The need for antiemetics and the response to therapy may be measured with scales similar to those used for pain assessment, such as the visual analog scale and the verbal categorical scale.¹⁰

As with adults, the underlying cause of nausea and vomiting in children is first addressed in determining treatment choices. Most agents used in adults are recommended for children in a weight-based dosing regimen. Ondansetron and metoclopramide have value for antiemetic treatment to reduce nausea and vomiting in pediatric patients. These agents are particularly effective in improving the ability of patients with gastroenteritis to maintain oral hydration.¹¹

Special Situations

Medications such as antihistamines are frequently used in the mistaken belief that they reduce the incidence of nausea and vomiting when opioid analgesics are administered in the ED for pain control. Studies have demonstrated that the incidence of nausea and vomiting related to opioid administration in the ED is low and that these medications have little efficacy in reducing nausea and vomiting.12,13

Many agents have been advocated for the treatment of nausea and vomiting of pregnancy (NVP). The treatments include nonpharmacologic methods—avoiding triggers, making dietary changes, using acupuncture or acupressure, taking ginger, and undergoing behavioral therapy—and pharmacologic therapies—pyridoxine, antihistamines, metoclopramide, ondansetron, or prochlorperazine. Hyperemesis gravidarum is treated essentially the same as NVP. For mild symptoms, pyridoxine (vitamin B₆), acupressure, ginger, and administration of antiemetics including antihistamines, metoclopramide, ondansetron, prochlorperazine, and phenothiazines may be used. Pyridoxine, acupressure, and ginger are thought to be of benefit but are not commonly used in the ED. For severe symptoms, hospitalization, fluids, corticosteroids, and electrolyte replacement may be needed. No specific medication has been shown to be superior to others in the treatment of hyperemesis gravidarum.¹¹

Chemotherapy-related nausea and vomiting may be seen in ED patients. The chemotherapy-induced nausea and vomiting may be acute (up to 24 hours) or delayed (after 24 hours).¹³ The incidence of nausea and vomiting is correlated with the emetic potential of the chemotherapeutic agents, the patient’s risk factors and other comorbid disorders, and antiemetic treatment. Patients commonly are given the serotonin antagonists dexamethasone and aprepitant for both immediate and delayed prophylaxis. Cannabinoids also have been used to control chemotherapy-induced nausea and vomiting. Choice of agents for the ED treatment of chemotherapy-induced vomiting has not been studied, but the serotonin antagonists and aprepitant are often used.