Nausea and Vomiting - Clinical Tree

Key Concepts

Nausea and vomiting can result from a primary problem in the gastrointestinal (GI) tract but can also result from problems in the neurological, vestibular, urogenital, cardiac, or other systems.
In the acutely vomiting patient, associated symptoms and medication history are most helpful in narrowing the differential diagnosis.
Laboratory studies are not necessary for all patients with vomiting. In patients with severe or protracted vomiting, consider checking electrolytes and renal function, particularly when intravenous (IV) rehydration is initiated.
In patients with undifferentiated nausea or vomiting or vomiting due to non-obstructive GI disease, ondansetron is the first-line antiemetic due to its low side effect profile. However, no definitive evidence exists for the superiority of one antiemetic agent over others.
Although evidence is limited, metoclopramide is the antiemetic of choice in hyperemesis gravidarum and vomiting associated with headache, and ondansetron is the drug of choice in chemotherapy-induced vomiting.
Ondansetron is the first-line agent for children with vomiting due to acute gastroenteritis.
Consider cannabinoid hyperemesis syndrome (CHS) in all patients with protracted vomiting. Emergency department (ED) treatment of CHS includes the use of capsaicin cream as well as haloperidol or lorazepam.

Foundations

Epidemiology

The most common causes of nausea and vomiting are GI disorders. Nausea and vomiting may also represent disorders outside the GI tract, such as hyperemesis gravidarum, intracranial lesions and infections, myocardial infarction, diabetic ketoacidosis, and drug toxicities. With heightened access to marijuana, there has been an increased prevalence of cannabinoid hyperemesis syndrome (CHS). A cross-sectional study in the United States noted a near doubling of presentations for cyclical vomiting associated with marijuana use after legalization in one state.

Pathophysiology

The act of vomiting occurs in three phases: nausea, retching, and actual vomiting. Nausea may occur without retching or vomiting, and retching may occur without vomiting. Similar pathways mediate them. In the nausea phase, increased tone in the musculature of the duodenum and jejunum, combined with a concomitant decrease in gastric tone, leads to the reflux of intestinal contents into the stomach. There is often associated hypersalivation, repetitive swallowing, and tachycardia.

Retching is the rhythmic, synchronous contraction of the diaphragm, abdominal muscles, and intercostal muscles against a closed glottis without the expulsion of gastric contents.

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

Rumination may be confused with vomiting. Ruminating is when stomach contents dribble out of the mouth non-forcefully, which may be voluntary and is not associated with muscle contraction. Patients may swallow ruminated contents.

The complex act of vomiting is coordinated by the vomiting center located in the medulla. The vomiting center contains muscarinic receptors, which, when stimulated, trigger the vomiting reflex. The efferent pathways from the vomiting center are mainly through the vagus, phrenic, and spinal nerves ( Fig. 25.1 ). 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 (1) visceral afferent impulses directly from the GI tract; (2) visceral afferent impulses from outside the GI tract, including the biliary system, peritoneum, pharynx, genitalia, and heart; (3) extramedullary central nervous system (CNS) afferents, including the vestibular system, thalamus, and cerebral cortex; and (4) the chemoreceptor trigger zone (CTZ) ( Fig. 25.2 ), which is located in the area postrema in the floor of the fourth ventricle. Part of the CTZ is located outside of the blood-brain barrier, enabling it to respond to endogenous and exogenous substances that activate vomiting (see Fig. 25.2 ).

Fig. 25.2, Pathophysiology of Nausea and Vomiting.

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 D ₂ and serotonin receptors, and the lateral vestibular nucleus is rich with cholinergic and histamine receptors. Serotonin receptors are also widely found in the GI tract. These receptor sites are targets for the various medications used to treat nausea and vomiting.

The pathophysiology of cannabinoid hyperemesis syndrome remains unknown, although downregulation of the cannabinoid receptor CB1 is speculated. While cannabinoid receptors typically inhibit vomiting, chronic cannabis use downregulates the receptors, predisposing to CHS. Other purported mechanisms include the pro-emetic properties of cannabis at higher and more sustained doses, as well as decreased gastric motility induced by cannabis.

Diagnostic Approach

Differential Diagnosis Considerations

The differential diagnosis for nausea and vomiting is broad in scope; almost any organ system can be involved. Acute vomiting begins abruptly, generally lasts less than 1 week before presentation, and is frequently associated with acute conditions. Chronic vomiting generally occurs longer than 1 month, is frequently associated with motility disorders, effects of systemic treatments (such as for cancer), neuropsychiatric conditions (e.g., bulimia), or neurologic conditions. Persistent vomiting has varying definitions and is not well defined in the literature. Cyclic vomiting occurs in discrete episodes with intervening asymptomatic periods. Common causes of nausea and vomiting are outlined in Table 25.1 , and a differential diagnosis is presented in Tables 25.2 and 25.3 .

TABLE 25.1

Disorders Commonly Associated With Vomiting.

Disorder	Class	History	Prevalence	Physical Examination	Useful Tests	Comments
Nausea and vomiting of pregnancy (NVP)	Acute	Vomiting may occur in the morning or throughout the day. Associated breast tenderness. NVP typically starts in weeks 4–7, peaks in weeks 10–16, and disappears by week 20. Vomiting that begins after week 12 or continues past week 20 should prompt a search for another cause.	Very common Affects 75% of all pregnancies	Benign abdomen	Urine pregnancy test Serum electrolytes, urine ketones to exclude hyperemesis gravidarum	Consider NVP in all females of childbearing capacity. Prognosis for mother and infant is excellent. NVP is associated with a decreased risk of miscarriage, fetal growth retardation, and fetal mortality.
Hyperemesis gravidarum	Acute	Severe, protracted form of NVP. No universally accepted definition of the disease. Generally accepted hallmarks include 5% weight loss, ketonuria, and electrolyte disturbance. Hyperemesis is associated with multiple gestation, molar pregnancy.	Affects 0.3%–3% of pregnancies	Signs of dehydration Benign abdomen	β-hCG Urinalysis for ketones (65% of patients) Serum electrolytes Ultrasound examination to exclude molar pregnancy or multiple gestations (if not already performed in current pregnancy)	Studies are conflicting on fetal outcomes. There may be an association with low fetal birth weight and maternal weight loss.
Gastroenteritis	Acute	Fever, diarrhea, and crampy abdominal pain. Vomiting and pain occur early, usually followed by diarrhea within 24 h.	Very common	Benign abdomen	Usually not necessary	Early gastroenteritis, when only vomiting and periumbilical pain are present, may be confused with early appendicitis. Diarrhea is usually in the diagnosis of gastroenteritis.
Gastritis	Acute	Epigastric pain, belching, bloating, fullness, heartburn, and food intolerance. Use of NSAIDs or alcohol is common.	Very common	Mild epigastric tenderness may be present.	Lipase, LFTs, and pregnancy test may be necessary to exclude other diagnoses	Removal of inciting agent along with antacid therapy will resolve symptoms in majority of patients.
Peptic ulcer disease (PUD)	Acute Chronic	Epigastric pain present in 90% of cases. Presence of severe pain should raise suspicion of perforation.	Very common	Mild epigastric tenderness	Hemoglobin and hemoccult testing if bleeding is suspected Upright chest film or CT scan if perforation is suspected	Three major causes of PUD are NSAIDs, Helicobacter pylori infection, and hypersecretory states.
Biliary disease		Abdominal pain may be midepigastric or RUQ. Onset frequently after a fatty meal. May have history of similar episodes in the past.	Very common	RUQ tenderness present in most cases. If instructed to breathe deeply during alpation in the RUQ, the patient experiences heightened tenderness and inspiratory arrest (Murphy sign).	WBCs Lipase Serum bilirubin LFTs RUQ ultrasound examination	Normal temperature, WBCs, and spontaneous resolution of symptoms suggest biliary colic. Fever, Murphy sign, elevated WBCs, and suggestive ultrasound indicate cholecystitis.
Myocardial infarction (MI)	Acute	Patients typically have substernal chest pain. Vomiting may be an associated symptom.	Common	Patients often are anxious and in distress from pain. No diagnostic examination findings.	ECG (new Q waves, ST segment changes, or T wave inversions) troponin	Not all patients have chest pain. Some patients, particularly women and diabetic patients, may not have chest pain. Consider an ECG and troponins for this subset of patients and patients with cardiac risk factors and isolated vomiting or vomiting with epigastric pain.
Diabetic ketoacidosis (DKA)	Acute	Polydipsia and polyuria occur early. Without treatment, altered mental status and coma may develop. .	Common	“Fruity” breath odor results from serum acetone. Tachypnea Signs of dehydration may be present. Severe cases often manifest with altered mental status or coma.	Serum glucose Electrolytes serum beta hydroxybutyrate VBG	Any protracted vomiting, especially in children, should prompt measurement of a fingerstick glucose test.
Pancreatitis	Acute Chronic	Presenting symptom is epigastric pain, which often radiates to the back. Most cases are caused by gallstones or alcoholism.	Common	Epigastric tenderness is present. Associated paralytic ileus may cause abdominal distention and decreased bowel sounds. Frank shock may be present in severe cases.	Lipase WBC Serum glucose LDH AST Hematocrit BUN Calcium VBG	Early aggressive intravenous hydration is especially important in pancreatitis patients with severe vomiting.
Appendicitis	Acute	Abdominal pain classically begins in periumbilical region and later moves to right lower quadrant. Anorexia is common.	Common	Localized tenderness over right lower quadrant. Low-grade fever may be present.	WBC Ultrasound Abdominal CT	Early appendicitis can be a difficult diagnosis to make.
Bowel obstruction	Acute Chronic	Abdominal pain, vomiting, obstipation and constipation. Typically, patients will have a surgical history.	Common	Abdominal distention, mild diffuse tenderness, and high-pitched “tinkling” bowel sounds may be present. Thorough search for hernias should be performed.	Electrolytes Lactate POCUS Abdominal CT	Adhesions, hernias, and tumors account for 90% of bowel obstructions. NG tube placement can relieve the vomiting of obstructed gastrointestinal contents.
Carbon monoxide (CO) poisoning	Acute	Headache is usually present. CO poisoning often occurs during winter months when furnaces are turned on. Family members (or pets) may have similar symptoms if they also have been exposed.	Uncommon	No reliable signs of early CO poisoning.	CO level	Because CO is a tasteless, odorless gas, patients may not realize they have been exposed.
Boerhaave syndrome	Acute	Patients may have neck, chest, or epigastric pain. Forceful, protracted vomiting usually causes the tear. Most cases follow a bout of heavy eating and drinking. Other reported causes include childbirth, defecation, seizures, and heavy lifting.	Uncommon	Tachypnea, tachycardia, and hypotension may be present. Escaped air from the esophagus may produce subcutaneous emphysema. Air in the mediastinum produces a “crunching” sound as the heart beats (Hamman sign).	CXR showing mediastinal air is suggestive but CT is more sensitive. Esophagogram with water-soluble contrast is definitive.	The classic presentation includes forceful vomiting, severe chest pain, subcutaneous emphysema, and multiple CXR findings. There is a growing body of evidence that most cases do not have this “classic” picture. In more subtle presentations, the diagnosis can be difficult to make.
Cannabinoid hyperemesis syndrome	Cyclic	Severe retching and vomiting in the context of daily marijuana use. Relieved with hot showers.	Increasing	Severe distress from vomiting, dehydration. Occasional epigastric tenderness.	Electrolytes and renal function	Ask about marijuana use in all patients with intractable, recurrent, or episodic vomiting.

AST, Aspartate aminotransferase; β-hCG, beta-human chorionic gonadotropin; BUN, blood urea nitrogen; CT, computed tomography; CXR, chest radiography; ECG, electrocardiogram; ETOH, ethyl alcohol; Hct, hematocrit; LDH, lactate dehydrogenase; LFT, liver function test; NSAID, nonsteroidal anti-inflammatory drug; Po2, partial pressure of oxygen; POCUS , Point of Care Ultrasound; RUQ, right upper quadrant; VBG, venous blood gases; WBC, white blood cell.

TABLE 25.2

Causes of Nausea and Vomiting

Acute	Chronic	Episodic	Cyclical
Ischemic bowel	Chronic pancreatitis	Cholelithiasis	Cyclical vomiting syndrome
Ruptured viscus	Gastroparesis	IBD	Cannabinoid hyperemesis syndrome
Cholangitis	PUD	IBS
Cholecystitis/cholelithiasis	Gastritis	Gastritis
Bowel obstruction	Gastric outlet obstruction	BPPV
Appendicitis	CNS tumor	Motion sickness
Peritonitis	Raised ICP	Chemotherapy
Acute pancreatitis	Migraine	DKA
PUD	Drug toxicity	Uremia
Gastroenteritis	Bulimia	Pregnancy
Hepatitis	Carbon monoxide
Food poisoning	Pregnancy
Intracerebral bleed
Meningitis
Cerebellar infarct
Drug toxicity
Drug withdrawal
Renal colic
Gonadal torsion
Pyelonephritis
Myocardial infarction
Sepsis
Carbon monoxide
Alcohol intoxication
Alcohol withdrawal

BPPV, Benign paroxysmal peripheral vertigo; CNS, central nervous system; DKA, diabetic ketoacidosis; IBD, inflammatory bowel disease; IBS, inflammatory bowel syndrome; ICP, intracranial pressure; PUD, peptic ulcer disease.

TABLE 25.3

Differential Diagnosis of Nausea and Vomiting

Etiologic Category	Critical Diagnoses	Emergent Diagnoses	Nonemergent Diagnoses
Gastrointestinal (GI)	Boerhaave syndrome	Gastric outlet obstruction	Gastritis
	Ischemic bowel	Pancreatitis	Gastroparesis
	GI bleeding	Cholecystitis	Peptic ulcer disease
	Ruptured viscus	Bowel obstruction or ileus	Inflammatory bowel disease
	Cholangitis		Biliary colic
	Peritonitis	Appendicitis	Hepatitis
			Gastroenteritis Food poisoning Inflammatory bowel syndrome
		Spontaneous bacterial peritonitis
Neurologic	Intracerebral bleed	Meningitis	Migraine
Neurologic	Meningitis	CNS tumor
Vestibular	Cerebellar infarct	Raised ICP Suppurative labyrinthitis	BPPV
Endocrine	DKA	Adrenal insufficiency	Thyroid disorder
Endocrine		Uremia
Pregnancy		Hyperemesis gravidarum	Nausea and vomiting of pregnancy
Drug toxicity	Acetaminophen
	Aspirin	Digoxin
		Theophylline
		Barbiturates
		Carbamazepine
		Valproic acid
Therapeutic drug use			Aspirin
			Antibiotics
			cannabis
			Ibuprofen
			Chemotherapy
Drugs of abuse		Alcohol withdrawal	Opioid
			Opioid withdrawal
			Alcohol
			Cannabis
Genitourinary	Gonadal torsion		Urinary tract infection
Genitourinary			Nephrolithiasis
Miscellaneous	Myocardial infarction	Carbon monoxide	Motion sickness
	Sepsis	Electrolyte disorders	Labyrinthitis
	Organophosphate poisoning

BPPV, Benign paroxysmal peripheral vertigo; CNS, central nervous system; DKA, diabetic ketoacidosis; ICP, intracranial pressure.

Pivotal Findings

Symptoms

A thorough history, including past medical history, medications, and drug use, will generally elicit suspected etiologies of vomiting. The content and color of the vomitus may help determine its cause ( Table 25.4 ). Although coffee ground emesis suggests a slower bleeding rate than bright red blood, this distinction is variable. The history is directed at assessing for both the causes of vomiting and its sequelae.

TABLE 25.4

Differential Diagnosis Based on Content of Vomitus.

Color/Content of Vomitus	Diagnoses
Bright red blood	Peptic ulcer Gastritis Esophageal varices Aortoenteric fistula Esophageal rupture Duodenal or gastric tumors Mallory-Weiss syndrome Dieulafoy lesion Foreign body
Coffee grounds	Peptic ulcer Gastritis Esophageal varices Duodenal or gastric tumors Mallory-Weiss syndrome
Undigested food	Gastric outlet obstruction Achalasia Esophageal stricture Foreign body
Feces	Small bowel obstruction Large bowel obstruction
Bilious (adults)	Small bowel obstruction Large bowel obstruction

The timing and duration of the vomiting may be important. Symptoms occurring primarily in the morning may suggest increased intracranial pressure. Vomiting occurring 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.

Associated symptoms are helpful: Vomiting with diarrhea is generally due to infectious gastroenteritis but may also be present in mesenteric ischemia or other GI surgical emergencies. Vomiting associated with abdominal pain is generally caused by diseases of the GI system. Chronic headaches with nausea and vomiting should raise suspicion of elevated intracranial pressure. Vomiting without preceding nausea is also suspicious for CNS pathology.

The social history should include alcohol or other substance use. The past medical history should include GI diseases or prior surgery. Finally, a thorough medication list, including over-the-counter drugs and supplements, should be elicited.

A history of similar episodes should be elicited. A history of severe episodes of nausea and vomiting lasting hours to days with symptom-free intervals may lead to a diagnosis of cyclical vomiting syndrome (CVS). In patients with a history of cyclical vomiting, chronic use of cannabis is essential to elicit, as it may lead to a diagnosis of cannabis hyperemesis syndrome. Symptoms are similar to CVS, though patients will often note temporary relief with a hot shower. The onset of the syndrome may occur following years of chronic marijuana use but can also occur with daily marijuana use of less than 1-year duration. The Rome IV diagnostic criteria for CHS can be found in Box 25.1 .

BOX 25.1

Rome IV Criteria for Cannabinoid Hyperemesis Syndrome.

Rome IV criteria

Must include all of the following:

1.
Stereotypical episodic vomiting resembling cyclical vomiting syndrome in terms of onset, duration, and frequency
2.
Presentation after prolonged, excessive cannabis use
3.
Relief of vomiting episodes by sustained cessation of cannabis use

Criteria fulfilled for the last 3 months, with symptom onset at least 6 months before diagnosis

Supportive remarks:

May be associated with pathologic bathing behaviors (prolonged hot baths or showers)

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