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Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e

Chapter 72: Nausea and Vomiting Bophal Sarha Hang; Susan Bork; Je� Ditko�; Britt Long; Alex Koyfman

Content Update

See discussion at end of chapter on GASTROPARESIS.

INTRODUCTION AND EPIDEMIOLOGY

Nausea and vomiting accompany a variety of illnesses. Symptoms may be due to primary GI disorders suchas bowel obstruction or gastroenteritis. However, symptoms may also represent pathology of the centralnervous 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 ofvarious 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 e�ects from medication and, in young women, pregnancy.1

PATHOPHYSIOLOGY

Multiple neurons in the medulla oblongata are activated in a sequential fashion to induce vomiting. Thevomiting 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 circulatingmedications and toxins, including dopaminergic antagonists (levodopa, bromocriptine), nicotine, digoxin,and opiate analgesics. Another important peripheral pathway for emesis is mediated through vagal a�erents.Vagal activation is triggered by direct gastric mucosal irritants (such as nonsteroidal inflammatory agents) orincreased luminal distention (gastric outlet obstruction, gastroparesis). Vagus activation stimulates neuronsin 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 foundthroughout the gastrointestinal tract, as well as the cortex and limbic system, vestibular system, heart, andgenitalia. The anatomic locations and receptor-mediated triggering factors in emesis are shown in Table 72–1.

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Abbreviations: 5-HT3 = serotonin; H1 = histamine; M1 = muscarine.

Table 72–1

Anatomic Locations of Receptor-Mediated Triggering Factors in Emesis

Anatomic Site Chemoreceptors Triggering Factor

Chemoreceptor trigger

(area postrema)

Dopamine

5-HT3

H1

M1

Vasopressin

Medications (dopamine agonists, digoxin, opiates,

nicotine, chemotherapeutic drugs)

Metabolic (uremia, diabetic ketoacidosis, hypercalcemia)

Neuroendocrine (hyperemesis gravidum)

Toxins

Peripheral vagal a�erents 5-HT3 Gastric irritants (salicylate, erythromycin, copper, ipecac)

Bacterial toxins (Staphylococcus enterotoxin)

Gastrointestinal distention (biliary colic, small bowel

obstruction)

Inflammation (peritonitis, cholecystitis)

Chemotherapy

Radiation

Vestibular system H1

M1

Motion

Labyrinth tumors or infections

Benign position vertigo or Ménière's disease

Cerebral cortex and limbic

system

Poorly

characterized

Psychogenic (fear, anxiety)

Noxious odors

Visual stimuli

E�erent pathways in the vagal, phrenic, and spinal nerves control the physiologic event of vomiting throughcoordinated muscle activity. Three stages of vomiting have been described: nausea, retching, and actualvomiting. Nausea is the unpleasant feeling that precedes vomiting. During nausea, there may be autonomicsymptoms of hypersalivation, repetitive swallowing, and tachycardia. The exact physiologic pathway is notwell understood but may be related to a�erent abdominal vagal stimulation. During retching, there is gastricrelaxation and repetitive simultaneous contraction of the diaphragm and abdominal muscles that allow forthe development of a pressure gradient. Vomiting is the retrograde expulsion of gastric contents, and it is aresponse to changes in intra-abdominal and intrathoracic pressure generated by the contraction of the

abdominal and respiratory muscles.3

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CLINICAL FEATURES

The di�erential diagnosis of nausea and vomiting is exhaustive, as pathology of almost every organ systemmay lead to nausea and vomiting (Table 72–2). A thorough history and physical examination will help guidethe diagnostic approach to the patient presenting with nausea and vomiting.

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Table 72–2

Di�erential Diagnosis of Nausea and Vomiting

Gastrointestinal Neurologic Infectious Drugs/Toxins Endocrine Miscellaneous

Functional

disorders

Head injury Bacterial

toxins

Digoxin Pregnancy Myocardial

infarction

Psychogenic Stroke Pneumonia Aspirin Adrenal

insu�iciency

Acute

glaucoma

Irritable bowel

syndrome

Pseudotumor Spontaneous

bacterial

peritonitis

NSAIDs Diabetic

ketoacidosis

Nephrolithiasis

Obstruction Hydrocephalus Urinary tract

infection

Acetaminophen Parathyroid

disorders

Pain

Adhesions Mass lesion Viruses Opiates Thyroid

disorders

Psychiatric

disorders

Esophageal

disorders

Meningitis Adenovirus Alcohol Uremia Anorexia

nervosa

Achalasia Migraines Norwalk

virus

Theophylline Electrolyte

disorders,

especially

hyponatremia

Bulimia

Intussusception Labyrinthitis Rotavirus Chemotherapeutics Conversion

disorder

Tumor Ménière's

disease

Anticonvulsants Depression

Pyloric stenosis Motion

sickness

Antibiotics

Strangulated

hernia

Antiarrhythmics

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Abbreviation: NSAIDs = nonsteroidal anti-inflammatory drugs.

Gastrointestinal Neurologic Infectious Drugs/Toxins Endocrine Miscellaneous

Volvulus Hormones

Organic

disorders

Illicit drugs

Appendicitis Radiation therapy

Cholecystitis Toxins

Cholangitis Arsenic

Hepatitis Organophosphates

Irritable bowel

disease

Carbon monoxide

Mesenteric

ischemia

Ricin

Pancreatitis

Peptic ulcer

disease

Peritonitis

HISTORY

Identify the onset and duration of the symptoms. The evaluation for acute symptoms is quite di�erent fromthe evaluation of a chronic problem. If the problem is chronic, asking the patient the results of any tests thathave already been performed will help narrow the diagnostic possibilities. Chronic symptoms are defined asthose symptoms present for >1 month.

Frequency of the episodes is helpful to gauge the severity of illness. Ask how many times vomiting occurredand the interval between episodes. Timing of the episodes, such as increased number of episodes in themorning, may suggest pregnancy or a central nervous system cause, whereas postprandial vomiting suggestsgastroparesis or gastric outlet obstruction.

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The content of the vomitus may be helpful to determine whether an obstruction is present and its location.Esophageal disorders produce vomitus with undigested food particles. Bile is o�en associated with a smallbowel obstruction, whereas vomitus composed of food particles and devoid of bile o�en represents a gastricoutlet obstruction. Large bowel obstruction o�en is composed of feculent material and has a foul odor.

Because of the number of organ systems that are the potential cause of pathology, it is important to ask thepatient about associated symptoms. The presence or absence of abdominal pain is a focal starting point. Ifpain is present, elicit its location and quality. Pain preceding the nausea and vomiting is most particularly

associated with an obstructive process.2 Fever or, possibly, diarrhea suggests gastroenteritis. Ask about sickcontacts or ingestion of food suspicious for a foodborne illness. A history of recent weight loss is associatedwith a malignancy or psychiatric component. Any central nervous system sign, such as headache, visualchanges, vertigo, or neurologic deficits, may suggest a central cause for the nausea and vomiting. Obtain athorough past medical history. Always ask about prior abdominal surgeries because the patient is at risk forbowel obstruction from adhesions. Review the patient's medication list to identify a medication with acommon side e�ect of nausea and vomiting, such as nonsteroidal anti-inflammatory agents, cancerchemotherapeutic agents, various antibiotics, various antihypertensives and antiarrhythmics, and oralcontraceptives. Other medications at toxic levels are known to cause nausea and vomiting. Examples includeacetaminophen, salicylates, and digoxin.

PHYSICAL EXAMINATION

Assess vital signs for hypotension and tachycardia. Observe skin turgor, mucous membrane hydration, andcapillary refill to assess for dehydration. In children, the most useful predictors of significant dehydration(>5% loss of body weight) are abnormal capillary refill, abnormal skin turgor, absent tears, and abnormal

respiratory pattern.4 The abdominal examination is particularly important to assess for an emergent

problem, as well as to help narrow the di�erential diagnosis to a possible gastrointestinal cause.5 Inspect,auscultate, and palpate the abdomen. (For further discussion of abdominal evaluation, see chapter 71, AcuteAbdominal Pain.)

Investigate any other important examination findings particular to various organ systems, as findings mayprovide valuable information regarding the cause of the nausea and vomiting (Table 72–3).

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Table 72–3

Di�erential Diagnosis Based on Physical Examination Findings

Physical

ExaminationAbnormal Signs or Symptoms Some Diagnostic Considerations

General Toxic appearing

Generalized weakness

Weight loss

Dehydration

Chronic malnutrition

Malignancy

Vital signs Fever

Tachycardia

Hypotension

Hypertension

Infection (gastroenteritis, appendicitis, cholecystitis)

Bowel perforation secondary peritonitis

Severe volume depletion

Intracranial hemorrhage or stroke

Head, eyes,

ears, nose,

throat

Nystagmus

Exophthalmos

Pin-point pupils

Fixed-dilated pupil, eye pain

Dry mucous membranes

Poor dental enamel, parotid

gland enlargement

Peripheral vs. central causes (benign positional vertigo,

cerebellar infarct)

Graves' disease

opiate abuse

Acute glaucoma

Dehydration

Bulimia

Bulimia

Abdomen Distention, decreased bowel

sounds, surgical scars

Hernias or palpable masses

Abdominal rigidity

Small bowel obstruction, gastroparesis, gastric outlet

obstruction, ileus

Incarcerated hernia, tumors

Peritonitis

Neurologic Mental status

Cranial nerve findings or

neurologic deficits

Papilledema

Dehydration, intracranial lesion or pathology, brainstem

tumor, elevated intracranial pressure

Extremities Scarring on dorsal surface of

the hands

Bulimia

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Physical

ExaminationAbnormal Signs or Symptoms Some Diagnostic Considerations

Skin Jaundice

Poor skin turgor

Hyperpigmentation

Decreased elasticity

Skin track marks

Hepatobiliary disease (hepatitis, choledocholithiasis)

Dehydration

Addison's disease

Scleroderma

Drug abuse/withdrawal

DIAGNOSTIC TESTING

LABORATORY

A�er completing a proper history and physical examination, obtain serum and urine studies to helpdetermine the cause of the symptoms and to evaluate for complications. Most o�en, a CBC as well aselectrolyte testing is part of the basic evaluation. Obtain a pregnancy test in a woman in childbearing yearswho has not had a hysterectomy. Obtain liver function tests and a serum lipase in patients with upperabdominal pain or jaundice. Check thyroid function tests if thyrotoxicosis is suspected. Obtain specific druglevels for possible ingestions or suspected toxicity in patients taking acetaminophen, salicylates, digoxin, ortheophylline. Also, obtain ethanol levels and narcotic drug screening tests in patients with suspectedintoxication or withdrawal states. A urinalysis may be beneficial in several ways. The specific gravity may beused to help determine the degree of dehydration. The presence of ketones may suggest not onlydehydration, but also diabetic ketoacidosis or hyperemesis gravidarum in a pregnant patient. The presenceof bilirubinuria may suggest a biliary tract obstruction. Nitrites, leukocyte-esterase, bacteria, and white bloodcells may indicate an upper or lower urinary tract infection. Also, red blood cells, in the proper clinicalpicture, may support a diagnosis of kidney stones. Lastly, an erythrocyte sedimentation rate may beevaluated to search for an inflammatory cause.

IMAGING

Flat and upright abdominal films are useful screening tests for bowel obstruction. Plain radiography is lesssensitive than CT scanning, but the radiation dose is <1 mSv, about one tenth the radiation dose of an

abdominal CT scan.6,7 Abdominal CT with PO and IV contrast can diagnose a mechanical obstruction,identify the cause, and visualize visceral and vascular pathology. A noncontrast abdominopelvic CT or renalUS are tests of choice if kidney stones are suspected. If the history or physical examination suggest a CNScause, a CT of the head or MRI of the brain is ordered to evaluate for an intracranial mass or lesion. Otherradiographic tests are available but are o�en ordered for a patient who requires admission to the hospital, orupon consultation with a gastroenterologist. These tests include esophagogastroduodenoscopy, upper GI

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radiography with barium contrast, small bowel follow-through, enteroclysis, gastric emptying scintigraphy,antroduodenal manometry, and cutaneous electrogastrography.

ANCILLARY TESTING

An abdominal US is helpful to evaluate a patient with associated right upper quadrant or epigastric pain todiagnose possible gallbladder, hepatic, or pancreatic pathology. Hepatobiliary iminodiacetic acid scans aresometimes performed in suspected cases of biliary dysfunction and/or cholecystitis. Suspected testiculartorsion would also be diagnosed by US. Obtain an electrocardiogram for suspected myocardial infarction.Measure intraocular eye pressures if glaucoma is a part of the di�erential diagnosis.

TREATMENT

Stabilize the patient, paying attention to the ABCs: airway, breathing, and circulation. A�er stabilization,provide symptomatic relief (Table 72–4). Definitive management will o�en require disease-specifictreatment. If no clear cause is noted at the outset, an H1 histaminergic such as promethazine or a serotonin

receptor antagonist such as ondansetron may be helpful for initial treatment, pending further workup.8

However, promethazine is more sedating, with the potential side e�ect of vascular damage during IVadministration. Recent studies have also compared the e�icacy of selective serotonin receptor antagonist(tropisetron, ondansetron) versus other agents in treating nausea and vomiting for undi�erentiated EDpatients. Serotonin receptor blockers significantly lower the rates of vomiting when compared with

metoclopramide.9 Both ondansetron and prochlorperazine are equally e�ective.10 Patients given either drugmust be monitored for akathisia that may develop up to 48 hours a�er administration. Based on overallsafety and e�icacy, serotonin receptor antagonists such as ondansetron should be used as first-line therapyfor undi�erentiated nausea and vomiting in all age groups. For patients in the ED who have no response toondansetron in 30 minutes, administration of another drug with activity at a di�erent receptor site is more

likely to be successful than repeat dosing of ondansetron.11

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Table 72–4

Antiemetic Agents for the Treatment of Nausea and Vomiting

Medication Class RouteCommon Side

E�ectsComments

Antihistamines

Dimenhydrinate

(Dramamine®)

Diphenhydramine

(Benadryl®)*

Meclizine (Antivert®)

PO

IV, IM,

PO

PO

Drowsiness Also show e�icacy in prevention of motion

sickness. Useful for migraines and vertigo.

Used in migraines and vertigo, which are

vestibular in origin.

Benzodiazepines

Alprazolam (Xanax®)

Diazepam (Valium®)

Lorazepam (Ativan®)

PO

PO, IV,

PR

PO, IV,

IM

Sedation Adjunct for chemotherapy-induced nausea

and vomiting.

Butyrophenones

Haloperidol

(Haldol®)*

PO, IM Agitation,

restlessness,

sedation

Treatment of acute chemotherapy-induced

symptoms.

Corticosteroids

Dexamethasone

PO, IV,

IM

Insomnia Used as an adjunct in severe cases of

chemotherapy-induced nausea and vomiting;

reduces prostaglandin formation.

Serotonin antagonists

Ondansetron

(Zofran®)*

Granisetron (Kytril®)*

Dolasetron (Anzemet®)*

PO, IV,

SL

PO, IV

PO, IV

Constipation,

dizziness

Well tolerated; uncommon side e�ects include

headache, rare case report of anaphylaxis.

Phenothiazines

Prochlorperazine

(Compazine®)†

Promethazine

(Phenergan®)†

PO, IV,

IM

PO, IV,

IM, PR

Extrapyramidal

symptoms,‡

sedation,

orthostatic

hypotension

Treatment in migraines, vertigo, and motion

sickness; rare side e�ects include neuroleptic

malignant syndrome, blood dyscrasias, and

cholestatic jaundice.

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*QT-interval prolongation reported.

†Nonspecific Q or T distortions reported.

‡Extrapyramidal symptoms: dystonia, tardive dyskinesia, oculogyric crisis, parkinsonism.

Medication Class RouteCommon Side

E�ectsComments

Benzamides

Metoclopramide

(Reglan®)

Trimethobenzamide

(Tigan®)

PO, IV,

IM

PO

Extrapyramidal

symptoms,‡

hyperprolactinemia

Used in treatment of gastroparesis and

children with reflux.

CYCLIC VOMITING SYNDROME

PATHOPHYSIOLOGY

Cyclic vomiting syndrome (CVS) usually presents in childhood with more than half of cases resolving by theteenage years. The condition is rare in adults. Predisposing mitochondrial DNA mutations (15519T and3010A) have been found in many patients with CVS. It is more common in females than males. In adults,there is a higher incidence of opiate and tobacco use.

The cause is unknown, but it is thought to be related to dysregulation of the neuroendocrine system.Accompanying symptoms of lethargy, anorexia, pallor, abdominal pain, or autonomic symptoms such assweating and salivation implicate abnormal vagal tone. It has also been suggested that CVS is a functionaldisorder associated with migraines. Patients commonly have a history of migraines and report a prodrome

with nausea and photophobia prior to attacks.12

DIAGNOSIS

CVS is characterized by recurrent nausea and vomiting separated by symptom-free periods. Since there is nospecific confirmatory test for CVS, diagnosis is clinical and involves excluding other common causes ofsymptoms. The diagnosis is o�en delayed for years a�er multiple ED visits and hospitalizations. Patients maybe given the label of  "drug-seeking."  Co-morbid conditions may also include anxiety, depression, andirritable bowel.

CVS has been well described with four phases: 1) Asymptomatic periods of several or many months; 2)Prodrome phase lasting minutes to hours, with lethargy, photophobia, anorexia, sweating, or salivation; 3)

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Hyperemesis phase, which usually starts in the morning with severe nausea and vomiting, lasting for days toa week with the mean duration being 3.4 days; 4) Finally, recovery phase with improvement in symptoms andenergy levels.

The ROME III diagnosis criteria include recurrent episodes of intractable vomiting that is self-limiting, lastingless than 7 days, and without an organic cause. Typically, patients have more than two episodes of vomitingin the past year with symptom-free intervals in between.

ED TREATMENT

Management in the ED is symptomatic, with antiemetics (ondansetron), sedatives (lorazepam), analgesics,and intravenous fluids. For prophylaxis, patients can try to avoid  triggers such as sleep deprivation, diet, andphysical or emotional stress. Amitriptyline is the standard for medical prophylaxis and has shown responserates as high as 86%. Other therapies include migraine prophylaxis drugs such as sumatriptan, propranolol,and topiramate. Mitochondrial-targeted therapies such as L-carnitine, coenzyme Q-10, and riboflavin have

shown excellent e�icacy in combination with amitriptyline and alone.13

GASTROPARESIS

Britt Long and Alex Koyfman

Gastroparesis is delayed gastric emptying in the absence of an obstructing lesion. This condition, which istypically chronic, is associated with decreased quality of life and increased healthcare utilization, though it is

not typically associated with significant mortality.14–16 The most common cause is ‘idiopathic’ but othercauses include diabetes, bariatric and gastric surgery, viral illness, gastroesophageal reflux disease, and non-

ulcer dyspepsia.14–17 Connective tissue or neurologic disease, and even pregnancy, can also be associated

with gastroparesis. The incidence appears to be increasing, especially in diabetics.17–19 Symptoms ofgastroparesis typically include early satiety, bloating, postprandial nausea, gastroesophageal reflux,

vomiting, and abdominal pain.14–16 If severe and chronic, patients may develop weight loss, electrolyteabnormalities, and nutritional or vitamin deficiencies. 

Physical examination may reveal a succussion splash, which indicates excessive gastric fluid from delayed

emptying or mechanical outlet obstruction.14–16,20 Significant abdominal tenderness and peritoneal

findings should be absent.14–16,20 Initial investigations include serum electrolytes, liver function studies,serum lipase, and pregnancy test. If concern for mechanical obstruction is present, image withabdominal/pelvic CT. Ultrasonography has been used to diagnose gastroparesis and determine e�ectiveness

of treatment.21 Outpatient diagnostics include endoscopy, scintigraphy, electrogastrography, or assessment

with the wireless motility capsule.14–16

Management includes volume resuscitation with electrolyte repletion. Several medications may be used forsymptomatic treatment. Prokinetic agents include metoclopramide (dopamine antagonist, 5-20 mg) and

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1. 

2. 

3. 

4. 

5. 

6. 

7. 

erythromycin (motilin receptor agonist, 40-250 mg). Both agents may decrease symptoms and increasegastric emptying. Metoclopramide can decrease nausea, provide analgesia, and act as a prokinetic and is afirst line agent. Erythromycin may demonstrate tachyphylaxis and should be a second line medication. Othermedications include domperidone (a peripherally selective dopamine D2 receptor antagonist - approved inCanada but as of this writing, not in the U.S.), diphenhydramine, prochlorperazine, and ondansetron.Opioids can treat pain; however, they may result in delayed gastric emptying and are not recommended for

first line therapy.14–16 Haloperidol can treat symptoms of nausea, vomiting, and pain. Haloperidol may beadministered IV or IM. One study demonstrated a significant decrease in ED and hospital length of stay,

hospital admission, and opioid administration, with no adverse events.21 A randomized controlled trial

reported haloperidol 5 mg IV significantly reduces pain and nausea.22 Patients whose symptoms improve areappropriate for discharge and follow up with a primary care provider or gastroenterologist for furthermanagement.

Acknowledgments: The authors gratefully acknowledge the contributions of Annie T. Sadosty and Jennifer J.Hess, the authors of this subject in the previous edition.

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