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Vomiting
Other namesEmesis, throwing up, puking, barfing, spewing, upchucking, heaving, hurling, ralphing, being sick
A Renaissance drawing with vivid colours depicting a woman holding the head of a man, who is bent over and expelling a brownish-red material from his mouth. A second woman stands at the left of the image in the doorway to the room, and appears to offer support. A crude representation of vomiting.
14th-century illustration of vomiting from the Casanatense Tacuinum Sanitatis
SpecialtyGastroenterology
SymptomsNausea
ComplicationsAspiration, electrolyte and water loss, damage to the enamel of the teeth, tear of the esophageal mucosa
Risk factorsHistory of migraine, history of PONV or motion sickness in a child's parent or sibling, better ASA physical status, intense preoperative anxiety, certain ethnicities or surgery types, decreased perioperative fluids, crystalloid versus colloid administration

Vomiting (also known as emesis, puking, barfing, and throwing up)[a] is the forceful expulsion of the contents of one's stomach through the mouth and sometimes the nose.[1]

Vomiting can be the result of ailments like food poisoning, gastroenteritis, pregnancy, motion sickness, or hangover; or it can be an after effect of diseases such as brain tumors, elevated intracranial pressure, or overexposure to ionizing radiation.[2] The feeling that one is about to vomit is called nausea; it often precedes, but does not always lead to vomiting. Impairment due to alcohol or anesthesia can cause inhalation of vomit. In severe cases, where dehydration develops, intravenous fluid may be required. Antiemetics are sometimes necessary to suppress nausea and vomiting. Self-induced vomiting can be a component of an eating disorder such as bulimia nervosa, and is itself now classified as an eating disorder on its own, purging disorder.

Complications

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Vomiting

Aspiration

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Vomiting is dangerous if gastric content enters the respiratory tract. Under normal circumstances, the gag reflex and coughing prevent this from occurring; however, these protective reflexes are compromised in persons who are under the influence of certain substances (including alcohol) or even mildly anesthetized. The individual may choke and asphyxiate[3] or develop aspiration pneumonia.[4]

Dehydration and electrolyte imbalance

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Prolonged and excessive vomiting depletes the body of water (dehydration), and may alter the electrolyte status. Gastric vomiting leads to the loss of acid and chloride directly. Combined with the resulting alkaline tide, this leads to hypochloremic metabolic alkalosis (low chloride levels together with high HCO−
3 and CO
2 and increased blood pH) and often hypokalemia (potassium depletion). The hypokalemia is an indirect result of the kidney compensating for the loss of acid. With the loss of intake of food the individual may eventually become cachectic. A less frequent occurrence results from a vomiting of intestinal contents, including bile acids and HCO−
3.

Mallory–Weiss tear

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See also: Mallory–Weiss syndrome

Repeated or profuse vomiting may cause erosions to the esophagus or small tears in the esophageal mucosa (Mallory–Weiss tear). This may become apparent if fresh red blood is mixed with vomit after several episodes.

Dentistry

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Recurrent vomiting, such as observed in bulimia nervosa or more rarely anorexia nervosa, may lead to the destruction of the tooth enamel due to the acidity of the vomit. Digestive enzymes can also have a negative effect on oral health, by degrading the tissue of the gums.

Pathophysiology

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Receptors on the floor of the fourth ventricle of the brain represent a chemoreceptor trigger zone, known as the area postrema, stimulation of which can lead to vomiting.[2] The area postrema is a circumventricular organ and as such lies outside the blood–brain barrier; it can therefore be stimulated by blood-borne drugs that can stimulate vomiting or inhibit it.[5]

There are various sources of input to the vomiting center:

The vomiting act encompasses three types of outputs initiated by the chemoreceptor trigger zone: Motor, parasympathetic nervous system (PNS), and sympathetic nervous system (SNS). They are as follows:

Phases

[edit]

The vomiting act has two phases. In the retching phase, the abdominal muscles undergo a few rounds of coordinated contractions together with the diaphragm and the muscles used in respiratory inspiration. For this reason, an individual may confuse this phase with an episode of violent hiccups. In this retching phase, nothing has yet been expelled. In the next phase, also termed the expulsive phase, intense pressure is formed in the stomach brought about by enormous shifts in both the diaphragm and the abdomen. These shifts are, in essence, vigorous contractions of these muscles that last for extended periods of time—much longer than a normal period of muscular contraction. The pressure is then suddenly released when the upper esophageal sphincter relaxes resulting in the expulsion of gastric contents. As the mouth and nasal cavity are connected via the back of the throat, particularly forceful vomiting, or producing large quantities of vomit may result in material being ejected through the nostrils in addition to the mouth. Individuals who do not regularly exercise their abdominal muscles may experience pain in those muscles for a few days. The decrease in pressure and the release of endorphins into the bloodstream after the expulsion causes the vomiter to feel relief almost immediately after vomiting.[15]

Contents

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Partially digested food, with a rubber glove for scale

Gastric secretions and likewise vomit are highly acidic. Recent food intake appears in the gastric vomit. Irrespective of the content, vomit tends to be malodorous.

The content of the vomitus (vomit) may be of medical interest. Fresh blood in the vomit is termed hematemesis ("blood vomiting"). Altered blood bears resemblance to coffee grounds (as the iron in the blood is oxidized) and, when this matter is identified, the term coffee-ground vomiting is used. Bile can enter the vomit during subsequent heaves due to duodenal contraction if the vomiting is severe. Fecal vomiting is often a consequence of intestinal obstruction or a gastrocolic fistula and is treated as a warning sign of this potentially serious problem (signum mali ominis).

If the vomiting reflex continues for an extended period with no appreciable vomitus, the condition is known as non-productive emesis or "dry heaves", which can be painful and debilitating.

Color of vomit[16]
  • Bright red in the vomit suggests bleeding from the esophagus
  • Dark red vomit with liver-like clots suggests profuse bleeding in the stomach, such as from a perforated ulcer
  • Coffee-ground-like vomit suggests less severe bleeding in the stomach because the gastric acid has had time to change the composition of the blood
  • Yellow or green vomit suggests bile, indicating that the pyloric valve is open and bile is flowing into the stomach from the duodenum. This may occur during successive episodes of vomiting after the stomach contents have been completely expelled.[17]

Causes

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Vomiting may be due to a large number of causes, and protracted vomiting has a long differential diagnosis.[citation needed]

Digestive tract

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Causes in the digestive tract

Sensory system and brain

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Causes in the sensory system:[citation needed]

Causes in the brain:[citation needed]

Metabolic disturbances (these may irritate both the stomach and the parts of the brain that coordinate vomiting):[citation needed]

Pregnancy:[21]

Drug reaction (vomiting may occur as an acute somatic response to):[citation needed]

High altitude:

Illness (sometimes colloquially known as "stomach flu"—a broad name that refers to gastric inflammation caused by a range of viruses and bacteria):[citation needed]

Psychiatric/behavioral:

Emetics

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An emetic, such as syrup of ipecac, is a substance that induces vomiting when administered orally or by injection. An emetic is used medically when a substance has been ingested and must be expelled from the body immediately. For this reason, many toxic and easily digestible products such as rat poison contain an emetic.[24] This presents no problem for the effectiveness of the rodenticide as rodents are unable to vomit.[25] Inducing vomiting can remove the substance before it is absorbed into the body. Emetics can be divided into two categories: those which produce their effect by acting on the vomiting center in the medulla, and those which act directly on the stomach itself. Some emetics, such as ipecac, fall into both categories: they initially act directly on the stomach, while their further and more vigorous effect occurs by stimulation of the medullary center.[24]

Salt water and mustard water, which act directly on the stomach, have been used since ancient times as emetics.[26] Care must be taken with salt, as excessive intake can potentially be harmful.[27][28] Copper sulfate was also used in the past as an emetic.[29][30] It is now considered too toxic for this use.[31]

Hydrogen peroxide is used as an emetic in veterinary practice.[32][33]

Self-induced

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  • Eating disorders (anorexia nervosa or bulimia nervosa)
  • To eliminate an ingested poison (some poisons should not be vomited as they may be more toxic when inhaled or aspirated; it is better to ask for help before inducing vomiting)
  • Some people who engage in binge drinking induce vomiting to make room in their stomachs for more alcohol consumption.
  • Participants in milk chugging typically end up vomiting most of the milk they consume, as proteins in the ingested milk (such as casein) rapidly denature and unravel on contact with gastric acid and protease enzymes, rapidly filling the stomach. Once the stomach becomes full, stretch receptors in the stomach wall trigger signals to vomit to expel any further liquid the participant ingests.
  • People suffering from nausea may induce vomiting in hopes of feeling better.

Miscellaneous

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Other types

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  • Projectile vomiting is vomiting that ejects the gastric contents with great force.[34] It is a classic symptom of infantile hypertrophic pyloric stenosis, in which it typically follows feeding and can be so forceful that some material exits through the nose.[35]

Treatment

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An antiemetic is a drug that is effective against vomiting and nausea. Antiemetics are typically used to treat motion sickness and the side effects of medications such as opioids and chemotherapy.

Antiemetics act by inhibiting the receptor sites associated with emesis. Hence, anticholinergics, antihistamines, dopamine antagonists, serotonin antagonists, and cannabinoids are used as antiemetics.[36]

Evidence to support the use of antiemetics for nausea and vomiting among adults in the emergency department is poor.[37] It is unclear if any medication is better than another or better than no active treatment.[37]

Epidemiology

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Nausea and/or vomiting are the main complaints in 1.6% of visits to family physicians in Australia.[38]

Society and culture

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Herodotus, writing on the culture of the ancient Persians and highlighting the differences with those of the Greeks, notes that to vomit in the presence of others is prohibited among Persians.[39][40]

Social cues

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A drunk man vomiting, while a young slave is holding his forehead. Brygos Painter, 500–470 BC

It is quite common that, when one person vomits, others nearby become nauseated, particularly when smelling the vomit of others, and often to the point of vomiting themselves.[citation needed] This tendency in human populations has been observed at drinking parties, where excessive consumption of alcoholic beverages may cause a number of party members to vomit nearly simultaneously, triggered by the initial vomiting of a single member of the party.[citation needed]

Intense vomiting in ayahuasca ceremonies is a common phenomenon. However, people who experience "la purga" after drinking ayahuasca, in general, regard the practise as both a physical and spiritual cleanse and often come to welcome it.[41] It has been suggested that the consistent emetic effects of ayahuasca—in addition to its many other therapeutic properties—was of medicinal benefit to indigenous peoples of the Amazon, in helping to clear parasites from the gastrointestinal system.[42]

There have also been documented cases of a single ill and vomiting individual inadvertently causing others to vomit, when they are especially fearful of also becoming ill, through a form of mass hysteria.

Special bags are often supplied on boats for sick passengers to vomit into.

Most people try to contain their vomit by vomiting into a sink, toilet, or trash can, as vomit is difficult and unpleasant to clean. On airplanes and boats, special bags are supplied for sick passengers to vomit into. A special disposable bag (leakproof, puncture-resistant, odorless) containing absorbent material that solidifies the vomit quickly is also available, making it convenient and safe to store until there is an opportunity to dispose of it conveniently.

People who vomit chronically (e.g., as part of an eating disorder such as bulimia nervosa) may devise various ways to hide this disorder.

An online study of people's responses to "horrible sounds" found vomiting "the most disgusting". Professor Trevor Cox of the University of Salford's Acoustic Research Centre said, "We are pre-programmed to be repulsed by horrible things such as vomiting, as it is fundamental to staying alive to avoid nasty stuff." It is thought that disgust is triggered by the sound of vomiting to protect those nearby from possibly diseased food.[43]

Psychology

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Emetophilia is sexual arousal from vomiting, or watching others vomit.[44] Emetophobia is a phobia that causes overwhelming, intense anxiety pertaining to vomiting.

See also

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Notes

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Vomiting

View on Grokipedia
from Grokipedia
Vomiting, also known as emesis, is the forceful, involuntary expulsion of the stomach's contents through the , often involving reverse and coordinated contractions of the diaphragm and abdominal muscles. It is typically preceded by , an unpleasant subjective sensation signaling the urge to vomit, and serves as a protective reflex to eliminate potentially harmful substances from the or respond to systemic disturbances. This process distinguishes vomiting from simpler acts like regurgitation, as it requires active neural coordination and can occur in response to diverse stimuli ranging from peripheral to central origins. The physiology of vomiting is orchestrated by the vomiting center located in the of the , which integrates emetic signals from multiple pathways. Key inputs include the (CTZ) in the , a circumventricular organ that lacks a blood-brain barrier and detects blood-borne toxins, drugs, or metabolic byproducts. Additional triggers arise from vagal afferents in the sensing irritation or distension, the during motion imbalance, and higher cerebral centers processing psychological or visual cues. Once activated, the response involves relaxation of the gastric fundus, closure of the , and forceful abdominal thrusting to propel contents upward, often accompanied by —ineffective expulsive efforts without emission. Vomiting arises from a broad spectrum of causes, including benign triggers like , excessive alcohol intake, or viral , as well as more serious conditions such as chemotherapy-induced effects, (), migraines, or obstructions in the digestive tract. In clinical contexts, it may signal underlying pathologies like , , or metabolic derangements such as . Management focuses on hydration to prevent , especially in vulnerable populations like children and the elderly, and pharmacological interventions with antiemetics targeting specific pathways—such as 5-HT3 antagonists like for chemotherapy-related vomiting or dopamine antagonists like metoclopramide for postoperative cases. Prompt medical evaluation is essential if vomiting lasts more than 24-48 hours, contains blood or bile, or is accompanied by severe , confusion, or signs of like reduced urine output.

Basics and Pathophysiology

Definition

Vomiting, also known as emesis, is defined as the forceful, involuntary expulsion of the contents of the through the mouth, typically resulting from coordinated contractions of the abdominal muscles and diaphragm. This process is mediated by the vomiting center located in the of the , which integrates sensory inputs to trigger the reflex. Vomiting must be distinguished from related phenomena such as regurgitation, which involves the passive, nonforceful of undigested gastric contents into the or mouth without associated or abdominal effort. In contrast, represents the subjective, unpleasant sensation often preceding vomiting, serving as a prodromal warning but not always culminating in expulsion. Expectoration, meanwhile, refers to the coughing up of or from the , originating from the lungs or airways rather than the gastrointestinal system. Anatomically, vomiting involves the , where gastric contents accumulate, the as the conduit for retrograde propulsion, and the diaphragm, which contracts to increase intra-abdominal pressure and facilitate expulsion. The lower esophageal sphincter relaxes to allow passage, while reverse in the directs material upward toward the mouth. From an evolutionary standpoint, vomiting functions as a protective reflex to expel potentially harmful toxins or pathogens from the before they can be absorbed into the bloodstream, a mechanism conserved across many including , amphibians, reptiles, birds, and mammals. This adaptive response enhances survival by mitigating the effects of ingested poisons, as observed in various animal models where emetic reflexes prevent intoxication from tainted food sources.

Mechanisms and Phases

Vomiting is coordinated by a central vomiting center located in the of the , specifically within the dorsal vagal complex, which integrates emetic signals and orchestrates the motor responses. This center receives inputs from multiple sources, including the (CTZ) in the , which lacks a blood-brain barrier and detects circulating emetic stimuli; vagal and splanchnic afferents from the conveying visceral sensations; the via cranial nerve VIII for balance-related signals; and higher brain centers such as the and for cognitive or emotional inputs. The nucleus tractus solitarius within the dorsal vagal complex serves as the primary integration site for these afferent signals, relaying them to the dorsal motor nucleus of the vagus for efferent output to the viscera. A key component of this neural control is the (CPG), a network of neurons primarily in the medullary , including the Bötzinger complex, that produces the rhythmic, coordinated motor patterns essential for vomiting without requiring ongoing external sensory input. This CPG synchronizes activity across respiratory, abdominal, and gastrointestinal muscles, involving neurotransmitters such as serotonin (via 5-HT3 receptors), (via NK1 receptors), and (via D2/D3 receptors) to modulate the reflex. Key nerves involved include: the (cranial nerve X) transmits gastrointestinal afferent signals and efferent commands to the gut and lower esophageal sphincter, while the innervates the diaphragm for its contractions; the (IX) contributes to pharyngeal coordination, and the (XII) aids in suprahyoid muscle movements. The vomiting process unfolds in three sequential phases: prodromal, , and expulsion, each marked by distinct physiological changes. The prodromal phase involves the onset of accompanied by autonomic alterations, including increased salivation via the (VII), sweating, and , alongside gastrointestinal adjustments such as relaxation of the gastric fundus and lower esophageal sphincter, increased tone in the , and initiation of antiperistaltic waves in the proximal to propel contents upward. These changes, lasting throughout the episode, prepare the digestive tract by reversing normal motility patterns under vagal control. During the retching phase, rhythmic contractions of the diaphragm and abdominal muscles occur without expulsion of contents, driven by the CPG to generate intra-abdominal pressure. The closes to protect the airway, the elevates, and the rises, while antiperistaltic waves—manifesting as retrograde giant contractions propagating from the mid-jejunum to the gastric antrum at 10-15 cm/s—mix and move gastric contents into the without passage through the upper esophageal . This phase features alternating relaxation and contraction of diaphragmatic and cricopharyngeus muscles, coordinated by the vagus and phrenic nerves, resulting in spasmodic respiratory efforts against a closed . The expulsion phase culminates in the forceful ejection of gastric contents through the , involving a deep inspiration followed by closure of the and elevation of the to isolate the airway. Coordinated contraction of the diaphragm (via the ) and abdominal muscles compresses the , while relaxation of the cardia and , combined with longitudinal stretching of the , facilitates rapid bolus propulsion via sustained antiperistaltic waves and pharyngeal contractions mediated by IX, X, and XII. The upper esophageal sphincter briefly relaxes, allowing expulsion, after which clears residual material from the oral cavity.

Composition of Vomit

Vomit primarily consists of gastric contents, which include partially digested food, (HCl), , and a high proportion of (approximately 97-99%). These components arise from the stomach's secretory activity, where parietal cells produce HCl and chief cells secrete pepsinogen, which is activated to in the acidic environment. , secreted by goblet cells in the , is also present, providing a protective layer but appearing in variable amounts depending on or . In cases of duodenal reflux, vomit may incorporate bile from the , resulting in a yellow or green coloration due to the presence of and salts. , produced by the liver and stored in the , contains water, acids, , enzymes, and electrolytes, and its into the often occurs during prolonged vomiting or pyloric incompetence. Intestinal fluids, including those from the proximal , can contribute additional electrolytes and digestive residues if the retrograde propulsion extends beyond the . The composition varies based on the timing relative to meals and the underlying cause. For instance, vomit shortly after eating may contain recognizable food particles, whereas prolonged or obstruction leads to expulsion of more fluid gastric secretions without solid . In gastrointestinal obstructions, such as , the material may develop a fecal from bacterial overgrowth and stagnant intestinal contents, though true fecal is rare. can appear in vomit as , presenting as bright red streaks if fresh or a coffee-ground consistency if partially digested by , indicating upper from sources like ulcers or . Vomit is characteristically acidic, with a pH typically ranging from 1 to 3, reflecting the dominance of gastric (pH around 1.5-3.5). The volume per vomiting episode can reach 1 to 2 liters when the is full, comprising secretions rich in , and sodium ions (up to 150 mEq/L each), though this can be influenced by hydration status, recent intake, and the extent of intestinal involvement. may reduce output, while distended states increase it. These characteristics—odor, color, and consistency—offer diagnostic clues; for example, the coffee-ground appearance suggests slower upper hemorrhage, bilious tint points to distal obstruction or , and fecal-like smell signals severe or blockage, guiding further clinical evaluation without confirming etiology alone.

Causes

Gastrointestinal Causes

Gastrointestinal causes of vomiting primarily involve disruptions in the digestive tract's structure, , or inflammatory processes, leading to the accumulation of gastric contents and activation of emetic reflexes. These conditions often present with vomiting as a prominent symptom due to mechanical blockage, irritation, or impaired emptying of the and intestines. Unlike systemic or neurological triggers, these originate directly from the gastrointestinal mucosa, lumen, or surrounding tissues. Mechanical obstructions in the prevent the normal passage of contents, resulting in distension and forceful vomiting. In infants, is a leading cause, characterized by thickening of the pyloric muscle that obstructs gastric outlet, typically manifesting as non-bilious, projectile vomiting starting around 3-6 weeks of age. Intestinal blockages, such as —a twisting of the bowel—can lead to complete or partial obstruction, often producing bilious vomiting due to upstream accumulation of intestinal fluids and . These obstructions require prompt intervention to prevent complications like from ongoing fluid loss. Inflammatory and infectious conditions irritate the gastrointestinal lining, triggering vomiting through local and release. , the most common such cause, is frequently viral (e.g., , the leading pathogen in developed countries) or bacterial (e.g., species), causing acute and vomiting alongside . In children, vomiting occurs in approximately 70-90% of acute cases, particularly with infections, which account for a significant portion of pediatric emergency visits for . involves of the appendix, often presenting with vomiting in up to 75% of cases, especially as pain migrates to the right lower quadrant. Peptic ulcers, erosions in the stomach or duodenal lining, can cause vomiting, sometimes with blood (), due to irritation or partial obstruction from . Functional disorders impair gastric motility without structural blockage, leading to recurrent or persistent vomiting. , a condition of delayed gastric emptying often linked to (affecting up to 50% of patients with long-standing and poor glycemic control) or idiopathic factors, commonly results in and vomiting of undigested food. involves episodic, intense vomiting attacks lasting hours to days, with no identifiable obstruction, and is more prevalent in children with a family history of migraines. Postoperative gastrointestinal issues, such as or adhesions, commonly induce vomiting following . Postoperative , a temporary of bowel motility, affects nearly all patients after major procedures and manifests with and vomiting due to gas and fluid accumulation, typically resolving within 2-5 days. Adhesions, scar tissues forming between organs, can cause chronic or acute small , leading to bilious vomiting in recurrent episodes. These conditions highlight the role of surgical trauma in disrupting normal .

Neurological and Sensory Causes

Vomiting can arise from central nervous system disorders that directly stimulate or irritate the vomiting center in the medulla oblongata. Increased intracranial pressure, often due to brain tumors or meningitis, elevates pressure within the cranial vault, leading to nausea and vomiting as prominent symptoms. In cases of brain tumors, particularly those in the posterior fossa, projectile vomiting occurs due to direct mechanical pressure on the vomiting center, distinguishing it from other forms of emesis by its forceful, unheralded nature. Clinical examples include an infant presenting with intermittent projectile vomiting, often upon waking or position changes, without preceding nausea, accompanied by progressive drowsiness, diagnosed via head CT or MRI as brain tumor or hydrocephalus causing elevated intracranial pressure. In adults, sudden projectile vomiting with headache and ataxia may indicate brain metastasis, as seen in cases involving solitary metastatic lesions affecting emetic pathways. Strokes affecting the medulla, such as lateral medullary syndrome (Wallenberg syndrome), frequently manifest with acute vertigo, ataxia, and intractable vomiting resulting from ischemia in the brainstem's emetic pathways. Migraines, especially those with , commonly involve and vomiting as accompanying features, affecting up to 90% of patients during attacks due to activation of central trigeminovascular pathways and associated autonomic responses. These symptoms often precede or coincide with and can persist even after resolution, highlighting the migraine's impact on emetic centers. Vestibular disorders contribute to vomiting through disruption of balance signals to the . Motion sickness results from conflicting sensory inputs—such as visual and vestibular cues—to the , provoking and vomiting in susceptible individuals during exposure to real or apparent motion. , an inflammation of the often viral in origin, causes severe vertigo accompanied by and vomiting due to acute unilateral vestibular hypofunction. Similarly, Meniere's disease features recurrent episodes of vertigo with associated and vomiting, stemming from endolymphatic hydrops that distorts vestibular function. Sensory-related causes include post-traumatic effects following . Vomiting after signals potential intracranial pathology, increasing the risk of or more severe brain injury by up to fourfold, as it reflects irritation of central emetic pathways from trauma-induced pressure changes. to the head or neck region induces nausea and vomiting in a significant proportion of patients, attributed to direct irradiation of structures like the , with incidence rates as high as 48% in affected cohorts. Distinguishing central from peripheral vertigo-associated vomiting is crucial for diagnosis; central causes, such as brainstem lesions, produce more severe, persistent vomiting with multidirectional nystagmus and additional neurological deficits, whereas peripheral etiologies like labyrinthitis yield episodic symptoms that improve with repositioning.

Metabolic, Drug-Induced, and Other Causes

Vomiting can arise from metabolic disturbances that disrupt systemic homeostasis, such as uremia in chronic kidney disease, where accumulated toxins stimulate the chemoreceptor trigger zone (CTZ) in the brainstem. In diabetic ketoacidosis (DKA), severe hyperglycemia and acidosis lead to frequent vomiting, often producing acidic vomit due to gastric acid and ketone accumulation, exacerbating dehydration and electrolyte imbalances. Hypercalcemia, commonly from hyperparathyroidism or malignancy, induces nausea and vomiting by altering gastrointestinal motility and central emetic pathways. Adrenal insufficiency, including Addison's disease, presents with intractable vomiting alongside fatigue and hypotension, resulting from cortisol deficiency that impairs stress response and fluid balance. Drug-induced vomiting is a frequent of various medications, often mediated through the CTZ via serotonin activation. Emetogenic agents like trigger acute and delayed vomiting by releasing serotonin from enterochromaffin cells in the gut, stimulating vagal afferents and the CTZ; is classified as highly emetogenic, affecting up to 90% of untreated patients. Opioids, such as , cause and vomiting in 25-40% of patients by direct CTZ stimulation and delayed gastric emptying. Certain antibiotics, including erythromycin, can induce vomiting through its motilin receptor agonism, which promotes abnormal gastrointestinal contractions mimicking . GLP-1 receptor agonists, such as and , used for and weight management, cause vomiting in approximately 15-20% of patients through delayed gastric emptying and central emetic activation. Toxic exposures represent another key category, where ingested substances directly irritate the gut or activate central emetic centers. Food poisoning from , caused by , often begins with and vomiting before progressing to neurological symptoms like . Scombroid , resulting from in spoiled fish, produces rapid-onset vomiting, flushing, and due to mast cell degranulation. induces vomiting through multiple mechanisms, including gastric irritation leading to and central effects on the CTZ, with blood alcohol concentrations of 0.2-0.4% commonly precipitating emesis. In , —a severe form of and vomiting—affects 0.3-3.6% of pregnancies, causing significant and metabolic derangements like . Other causes encompass systemic conditions beyond primary metabolic or toxic origins. Cardiovascular events, particularly inferior , are associated with vomiting in up to 50% of cases due to vagal stimulation from ischemic pain and Bezold-Jarisch reflex activation. (PONV) occurs in 20-40% of patients after general , driven by volatile anesthetics and opioids that sensitize emetic pathways. Psychogenic vomiting involves recurrent episodes without organic pathology, often linked to , though detailed elsewhere. Evidence indicates can trigger vomiting as a metabolic disturbance via , where excessive inflammatory cytokines like IL-6 disrupt gastrointestinal and systemic .

Clinical Presentation and Diagnosis

Signs and Symptoms

Vomiting is characterized by the forceful expulsion of gastric contents through the , typically preceded by , an unpleasant queasy sensation in the often accompanied by the urge to vomit. , the labored and ineffectual attempt at vomiting without expulsion, frequently occurs alongside or prior to the act itself. Common associated symptoms include or cramping, diaphoresis (profuse sweating), (pallor of the skin), and (elevated ), reflecting activation. In some instances, particularly with intense emetic stimuli, (slowed ) may arise due to vagal nerve stimulation. Prodromal signs often signal an impending episode, including yawning, increased salivation, , and a subjective feeling of discomfort or impending doom. Following the emetic event, individuals commonly experience relief from but may feel profound exhaustion or . These features align briefly with the integrated phases of the vomiting reflex, where autonomic changes precede and accompany the expulsion. Vomiting patterns vary in frequency, distinguishing acute episodes (sudden onset lasting hours to days) from chronic recurrent forms (persisting or recurring over weeks to months). Volume can range from small amounts to large projectile ejections, with timing often postprandial (shortly after meals) or cyclical, sometimes linked to associated features like in migraine-related cases. In infants, vomiting manifests with fussiness, poor feeding, excessive crying, and signs of such as reduced urine output or a sunken , potentially leading to if recurrent. Among the elderly, episodes frequently result in rapid , presenting with confusion, weakness, and altered mental status due to fluid and shifts.

Diagnostic Approaches

The diagnostic evaluation of vomiting commences with a detailed and to ascertain the onset, pattern, and potential precipitants of symptoms, as well as to identify alarm features warranting urgent investigation. Key historical elements include the temporal profile (acute versus chronic), frequency and volume of emetic episodes, associated manifestations such as , , , or vertigo, and exacerbating factors like specific foods, medications, or motion. Red flags in the history encompass unintentional exceeding 5% of body weight, progressive , recurrent vomiting after meals suggesting obstruction, or neurological symptoms including severe , focal deficits, or altered , which may indicate pathology. The complements the history by assessing for through indicators like dry , sunken eyes, reduced skin turgor, and , alongside evaluation of , tenderness, or masses that could signal or obstruction. Neurological assessment is critical to detect deficits such as , , or meningismus, while may reveal or fever pointing to systemic involvement. Presence of , , or feculent odor in vomitus further heightens concern for hepatobiliary or proximal gastrointestinal complications. Laboratory investigations form the of initial diagnostic testing, tailored to the clinical context. Serum electrolytes and renal function tests are routinely obtained to identify hypokalemic hypochloremic from gastric losses or prerenal from volume depletion. A pregnancy test is mandatory in females of reproductive age to exclude , while a screen is indicated if of toxins or substances is suspected. Additional tests, such as complete blood count for or , liver enzymes for hepatobiliary involvement, and serum or for pancreatic , are pursued based on suggestive history or examination findings. Radiographic and advanced imaging modalities are selected to investigate structural or neurological etiologies. Plain abdominal can reveal air-fluid levels or dilated bowel loops indicative of obstruction, while abdominal ultrasound evaluates for gallstones, , or . Computed tomography (CT) of the abdomen is reserved for suspected perforation, ischemia, or in refractory cases, and CT of the head is essential for patients with neurological red flags to rule out , mass lesions, or infection. Upper gastrointestinal allows direct visualization and for suspected mucosal lesions, bleeding sources, or in chronic presentations. Specialized physiologic studies are employed for suspected functional disorders. Scintigraphy-based gastric emptying studies quantify delayed emptying in , with delayed retention of more than 60% at 2 hours or 10% at 4 hours confirming the . Esophageal manometry or antroduodenal manometry assesses motility abnormalities in cases of suspected achalasia or pseudo-obstruction, measuring parameters like lower esophageal sphincter pressure or duodenal contraction waves. In acute settings, particularly emergency departments, point-of-care ultrasound (POCUS) enhances rapid assessment of severity by evaluating (IVC) dimensions and respiratory variability. A subcostal view showing IVC diameter less than 2.1 cm with greater than 50% collapsibility during inspiration correlates with low right atrial pressure and intravascular volume depletion, guiding rehydration strategies; however, interpretation requires caution in patients with cardiac arrhythmias, , or , where accuracy diminishes.

Management

Initial Treatment

The initial management of acute vomiting prioritizes stabilization by addressing , imbalances, and symptom control to prevent complications such as . is the cornerstone for mild to moderate cases, utilizing World Health Organization-recommended low-osmolarity oral rehydration solutions containing glucose 13.5 g/L, 2.6 g/L, 1.5 g/L, and dihydrate 2.9 g/L to facilitate sodium and water absorption in the intestines. These solutions, along with other fluids such as water, herbal teas (chamomile, fennel, ginger, peppermint), and vegetable broths, should be consumed in small, frequent sips to replace lost fluids and prevent dehydration while minimizing the risk of triggering further vomiting; pharmacy-provided rehydration solutions are also recommended. In young children and toddlers, particularly in cases of vomiting without diarrhea, it is generally safe to allow the child to sleep for a few hours without immediate fluid intake if the stomach remains upset, as sleep can facilitate gastric emptying and reduce further vomiting episodes. Fluid repletion should resume with small sips of oral rehydration solution or clear fluids upon awakening, with close monitoring for dehydration signs including no urine output for more than 8 hours. In severe cases with significant fluid loss or inability to tolerate oral intake, intravenous isotonic fluids like 0.9% normal saline are administered at rates adjusted to the degree of , typically 20 mL/kg bolus initially followed by maintenance. Antiemetic therapy is initiated promptly to interrupt the vomiting cycle. , a selective , serves as a first-line agent with a typical adult dose of 4-8 mg intravenously, effective for various etiologies including postoperative and chemotherapy-induced vomiting. For vomiting linked to , metoclopramide is preferred at 10 mg intravenously or orally to enhance gastric motility and reduce , though its use is limited to short-term due to potential extrapyramidal side effects. Supportive measures include placing the patient on nil per os (NPO) status to allow gastrointestinal rest, implementing aspiration precautions such as lateral positioning during episodes, and continuous monitoring of , urine output, and mental status to gauge hydration status and response to treatment. In specific scenarios like , the combination of (pyridoxine 10-25 mg) and doxylamine (12.5-25 mg) is recommended as a first-line , taken orally up to three times daily, due to its established safety profile in reducing without adverse fetal effects. Electrolyte correction is essential, particularly for resulting from gastric losses, with intravenous replacement at 10-20 mEq per hour in monitored settings, titrated to maintain serum levels above 3.5 mEq/L while avoiding overcorrection. Post-2020 guidelines endorse adjunctive non-pharmacologic interventions, such as at the P6 (Neiguan) acupoint on the inner , applied via bands or manual for 5-10 minutes several times daily, to alleviate with minimal risk. For mild nausea and vomiting, several home remedies are commonly used to relieve symptoms and prevent dehydration. These include consuming ginger (tea or candied), peppermint (tea or aromatherapy), sipping small amounts of clear fluids (water, ginger ale, broths), eating bland foods (crackers, toast, bananas, rice), using wrist acupressure, and getting fresh air/rest. These help soothe the stomach and prevent dehydration. Individuals should seek medical help for severe/persistent symptoms, dehydration signs, or blood in vomit.

Supportive and Specific Therapies

Supportive therapies for vomiting address underlying etiologies to alleviate symptoms and prevent recurrence, while specific therapies target chronic or refractory cases. For gastrointestinal obstructions causing persistent vomiting, such as , surgical intervention via is the definitive treatment, performed laparoscopically or openly to incise the hypertrophied pyloric muscle and restore gastric emptying. This procedure achieves near-complete resolution of vomiting in over 95% of cases when performed timely. Infectious causes of vomiting, particularly bacterial from pathogens like , warrant targeted antibiotic therapy in severe or high-risk cases to eradicate the infection and halt emesis. Recommended agents include or third-generation cephalosporins, which reduce symptom duration and prevent complications like . For leading to vomiting due to gastric irritation or bleeding, proton pump inhibitors (PPIs) such as form the cornerstone of therapy, suppressing acid production to promote mucosal healing and symptom relief. Chronic management of recurrent vomiting, such as in gastroparesis or cyclic vomiting syndrome (CVS), often involves prokinetic agents like domperidone, which enhance gastric motility and reduce nausea and vomiting frequency by up to 82% in responsive patients. The 2024 American Gastroenterological Association (AGA) Clinical Practice Update recommends prophylactic therapy for moderate-to-severe CVS (≥4 episodes/year lasting >2 days with emergency visits or hospitalizations), with tricyclic antidepressants (e.g., amitriptyline 75–150 mg at bedtime) as first-line, and topiramate, aprepitant, zonisamide, or levetiracetam as second-line options; abortive therapy emphasizes early intervention with sumatriptan (20 mg intranasally or 6 mg subcutaneously) plus ondansetron (8 mg sublingual). Behavioral therapies, including cognitive behavioral therapy (CBT) combined with biofeedback, are effective for CVS by addressing triggers and improving coping mechanisms, leading to decreased episode severity in pediatric and adult cases. In severe, refractory vomiting where oral intake is impossible, advanced nutritional support through total parenteral nutrition (TPN) bypasses the to maintain hydration and nutrition, particularly in conditions like protracted or severe . Neuromodulators, such as tricyclic antidepressants (e.g., amitriptyline), provide benefit for central or functional causes of chronic vomiting by modulating visceral hypersensitivity, achieving symptom reduction in 68-76% of CVS patients. Tailored approaches in specific populations enhance outcomes; for instance, enteral tube feeding via is utilized in children with severe vomiting disorders to ensure caloric intake while minimizing aspiration risk, though monitoring for tolerance is essential. In endocrine disorders like contributing to vomiting, thyroid resolves gastrointestinal symptoms by normalizing metabolic function. Emerging biologics, including neurokinin-1 (NK1) receptor antagonists , offer promise for refractory vomiting unresponsive to standard antiemetics, with clinical trials demonstrating complete response rates of 68-80% in CVS and chemotherapy-induced cases.

Prevention Strategies

Lifestyle modifications play a key role in preventing vomiting, particularly through dietary adjustments that minimize gastric irritation. Consuming small, frequent meals throughout the day rather than large portions helps maintain stable stomach acid levels and reduces the likelihood of triggered by an empty or overly full stomach. Avoiding trigger foods such as fatty, greasy, spicy, or overly sweet items is recommended, as these can slow gastric emptying and exacerbate symptoms. Bland, dry foods like crackers, toast, bananas, rice are preferable in at-risk situations to promote tolerance and prevent episodes. Additionally, maintaining consistent hydration habits, such as taking small sips of clear fluids frequently, prevents that could otherwise intensify and lead to vomiting. Pharmacologic prophylaxis targets specific high-risk scenarios to avert vomiting onset. For patients undergoing , guidelines endorse a combination of dexamethasone (typically 12-20 mg) and a antagonist such as as first-line preventive therapy, which significantly reduces both acute and delayed emesis. This regimen is particularly effective for highly emetogenic agents, with network meta-analyses confirming its superior control over monotherapy options. In , transdermal patches applied behind the ear 4-6 hours prior to exposure prevent and vomiting by blocking muscarinic receptors, offering protection for up to 72 hours. Clinical trials demonstrate this approach reduces symptom incidence and severity by 60-80% compared to . Public health measures emphasize and education to curb infectious causes of vomiting. The , administered orally to infants in a two- or three-dose series, reduces severe pediatric by 85%, thereby preventing associated vomiting and hospitalization. education, including practices like thorough handwashing, separating raw and cooked foods, cooking to safe internal temperatures, and prompt refrigeration, mitigates foodborne pathogens that trigger vomiting. These interventions, promoted by agencies such as the FDA and USDA, lower outbreak risks in communities. Context-specific strategies address procedural and physiological vulnerabilities. Preoperative fasting guidelines recommend withholding solids for at least 6 hours and clear liquids for 2 hours before to minimize aspiration risk and postoperative vomiting, while allowing carbohydrate-rich fluids closer to in enhanced recovery protocols. For , counseling on early dietary modifications—such as small, frequent bland meals and ginger supplementation—helps prevent progression to , with preemptive use of and showing efficacy in reducing symptom severity. Psychological approaches, including and (CBT), offer prevention for psychogenic vomiting by addressing underlying anxiety or phobic responses. Recent randomized trials indicate that CBT targeting of vomiting achieves clinically significant reductions in episode frequency for 50% of participants, through techniques like exposure and . -based interventions complement this by promoting stress reduction and body awareness, further decreasing psychogenic triggers in susceptible individuals.

Complications

Acute Complications

One of the most serious acute complications of vomiting is aspiration, where gastric contents are inhaled into the lungs, potentially leading to aspiration pneumonia or chemical pneumonitis. This risk is heightened in patients who are supine during vomiting episodes, as the position facilitates the passage of vomit into the airway. Chemical pneumonitis arises specifically from the acidic nature of vomited material irritating lung tissue, causing inflammation and acute respiratory distress. Elderly individuals and those who are intoxicated face an elevated risk of aspiration due to impaired swallowing reflexes and reduced consciousness, respectively. Vomiting can rapidly induce through substantial fluid loss, with each episode potentially expelling several hundred milliliters of fluid, leading to symptoms such as , dry mucous membranes, and . This fluid depletion is compounded by the loss of electrolytes, including sodium and , resulting in imbalances like and that can exacerbate cardiovascular instability and . Forceful or repeated retching during vomiting may cause a Mallory-Weiss tear, a longitudinal mucosal laceration at the gastroesophageal junction that presents with hematemesis. This complication accounts for 5% to 15% of cases of acute upper gastrointestinal bleeding. The acidic gastric contents in vomit can also erode tooth enamel upon contact, leading to dental erosion that increases susceptibility to caries and tooth sensitivity. This enamel demineralization occurs due to the low pH of vomited material, which dissolves the protective surface layer of teeth.

Chronic and Systemic Complications

Chronic vomiting, especially when associated with purging behaviors in eating disorders such as and , frequently results in and substantial . The repeated expulsion of contents deprives the body of vital nutrients, proteins, and calories, leading to deficiencies in vitamins, minerals, and electrolytes that impair overall metabolic function. This nutritional depletion exacerbates muscle wasting and weakens , creating a cycle of further health deterioration. Gastrointestinal damage from prolonged vomiting includes , where the esophageal lining becomes inflamed due to repeated exposure to and mechanical trauma. In extreme instances, forceful vomiting can precipitate Boerhaave syndrome, a spontaneous full-thickness rupture of the , which carries a of approximately 35-40% even with intervention. This perforation often stems from increased intraluminal pressure during , leading to mediastinal contamination and if not promptly addressed. Systemically, the loss of hydrogen ions and chloride through vomiting induces , shifting the body's acid-base balance and potentially causing or . imbalances, particularly low and magnesium levels, heighten the risk of cardiac arrhythmias, including potentially fatal ventricular rhythms. In conditions like , persistent vomiting contributes to renal strain through and , which can progress to in severe cases. Among vulnerable populations, children experiencing recurrent vomiting, as seen in , often face growth delays due to chronic , poor nutrient absorption, and disrupted feeding patterns. Similarly, individuals with purging-type eating disorders develop from sustained , which suppresses production and bone mineralization, increasing fracture risk over time.

Epidemiology

Prevalence and Distribution

Vomiting is a widespread symptom, primarily occurring as part of acute gastrointestinal illnesses that affect a significant portion of the global population annually. alone causes approximately 685 million cases of acute worldwide each year, leading to and vomiting in about one in five instances. Overall, diarrheal diseases, which frequently include vomiting, result in nearly 1.7 billion cases among children under five globally per year, according to estimates as of 2024. Recent estimates as of 2024 show a continued decline, with among under-5s at approximately 10.9% globally, reflecting improvements in and . Chronic vomiting, defined as recurrent episodes lasting weeks or more without identifiable , has a of 1-2% in adults, often linked to conditions like (CVS), which affects 0.3-2% of the population depending on the region. Demographic patterns show vomiting is particularly prevalent among certain groups. In children, acute episodes from viral are common, with most experiencing at least one episode by age five due to pathogens like . Among pregnant women, nausea and vomiting of pregnancy (NVP) impacts 70-80% to varying degrees, with mild cases predominant and severe affecting 0.3-3% of pregnancies. Travelers to developing regions face elevated risks, with occurring in 30-70% of short-term visitors and vomiting as an accompanying symptom in approximately 10-30% of cases. Geographically, infectious causes of vomiting are more prevalent in low- and middle-income countries, where limited contributes to higher rates of ; for instance, the burden is disproportionately borne by children in these regions, accounting for the majority of the 1.7 billion annual childhood cases. In contrast, high-income settings see lower infectious rates but higher recognition of non-infectious chronic forms. Post-2020 trends indicate a resurgence in viral etiologies, such as , with outbreaks and cases spiking above pre-pandemic levels in 2023-2025 due to reduced population immunity during restrictions. Additionally, vomiting related to contexts, particularly eating disorders like (prevalence 0.3%), remains underreported, though 2024 data show a 73% rise in program admissions, many involving purging behaviors.

Risk Factors and Outcomes

Risk factors for vomiting can be categorized as modifiable or non-modifiable, influencing the likelihood of episodes across various etiologies such as infections, treatments, and underlying conditions. Modifiable risks include poor personal , which facilitates the transmission of pathogens like , a leading cause of acute and vomiting. Travel to endemic areas heightens exposure to infectious agents such as or other enteropathogens that provoke severe vomiting. Exposure to is a significant modifiable risk in patients, with up to 70-80% experiencing depending on the regimen's emetogenic potential. Non-modifiable risks encompass demographic and inherent factors that cannot be altered. Infants and the elderly are particularly susceptible due to immature or declining physiological reserves, increasing vulnerability to dehydration from even mild episodes. Genetic predispositions, such as family history of migraines, elevate the risk of cyclic vomiting syndrome, characterized by recurrent severe episodes. Comorbidities like diabetes mellitus contribute through mechanisms such as gastroparesis or diabetic ketoacidosis, both of which frequently manifest with persistent vomiting. Most acute vomiting cases, often due to viral gastroenteritis, resolve spontaneously within 24-48 hours in approximately 95% of instances, with supportive care addressing hydration and symptom relief. In contrast, chronic conditions like untreated carry a poorer , with many cases requiring hospitalization for and nutritional support (estimated in 0.5-2% of pregnancies). Mortality from vomiting itself is rare, occurring in less than 0.1% of cases, primarily as a result of complications such as severe in infants and the elderly or in vulnerable groups with impaired swallowing. Recent 2025 projections indicate that will exacerbate foodborne risks leading to vomiting, with models forecasting a 10-20% rise in Salmonella-related illnesses due to warmer temperatures and altered precipitation patterns favoring pathogen growth in produce. Additionally, expanded vector-borne diseases like dengue, which often present with vomiting, are expected to increase by up to 15% in endemic regions due to shifting habitats.

Society and Culture

Historical and Cultural Views

In , and his followers viewed vomiting as a key mechanism for restoring humoral balance, prescribing emetics to purge excess or and treat conditions like fevers and digestive disorders. This approach stemmed from the theory of four humors—blood, , yellow , and black bile—where imbalance caused illness, and induced vomiting served as a therapeutic purgation to expel morbid matter. Similarly, ancient Egyptian healers documented the use of emetic substances in medical papyri, such as mustard seeds and onions, to induce vomiting for relieving chest pains, treating snakebites, and facilitating bodily detoxification as part of purification practices. From the medieval period through the , emetics remained central to Western medical practice, particularly for cases, with ipecacuanha root gaining prominence as a reliable vomitive after its introduction to in the and widespread adoption by the 1800s for evacuating toxins from the . By the mid-20th century, this paradigm shifted toward antiemetic therapies; the synthesis of in 1950 and its clinical introduction in 1952 marked a breakthrough, initially employed to control before its broader applications. This transition reflected growing recognition of vomiting's physiological triggers, moving away from routine purgation toward targeted suppression. Cross-culturally, vomiting has carried diverse symbolic meanings beyond . In ancient Indian Ayurvedic traditions, part of broader Asian healing systems, therapeutic emesis () forms a of panchakarma , inducing vomiting with preparations to cleanse the body of toxins (ama) and promote spiritual purification by balancing doshas. Conversely, Western cultural norms have historically stigmatized public vomiting as a breach of and bodily control, associating it with intemperance or weakness, particularly from the onward when etiquette emphasized restraint in bodily functions. Certain taboos have further shaped perceptions, notably the 19th- and early 20th-century of pregnancy-related vomiting () as a manifestation of , attributing severe to psychological instability rather than physiological causes, which delayed recognition of it as a distinct medical condition. Indigenous North American practices offer another perspective, with tribes like the Zuni employing over a dozen emetic plants—such as decoctions of bark or roots—to induce vomiting for treating ailments, fevers, and as part of holistic rituals that integrate physical and spiritual wellness.

Psychological and Social Dimensions

Vomiting is frequently linked to psychological conditions, where acute emotional distress can trigger physiological responses. Anxiety disorders, including panic attacks, often precipitate episodes of vomiting through heightened activation, as seen in where emotional stress serves as a key trigger. In (PTSD), conditioned associations with trauma can lead to vomiting as a somatic manifestation of re-experiencing symptoms, with studies identifying PTSD as a precipitant in adult cases of recurrent vomiting. Self-induced vomiting plays a central role in , an characterized by recurrent followed by compensatory purging behaviors, such as self-induced vomiting, which occurs in the majority of diagnosed individuals and contributes to severe medical complications. Socially, vomiting evokes widespread aversion, particularly in public settings, where the of drives avoidance behaviors and is a core feature of , a affecting daily functioning and social interactions. Media representations amplify these dynamics, frequently depicting vomiting as comedic relief in films during party or intoxication scenes or as a horrific element in horror genres to evoke and tension. This portrayal reinforces cultural taboos, heightening individual distress. Stigma surrounding profoundly impacts health-seeking behavior, with often leading to delayed medical care, especially among those with eating disorders where purging is involved and exacerbates secrecy. differences further influence experiences, as women report greater sensitivity to and are more prone to vomiting in response to stressors like motion or postoperative recovery compared to men. Post-pandemic surges have intensified these issues, with 2023-2024 studies documenting a 11-44% rise in gut-brain interaction disorders involving and vomiting, attributed to elevated stress levels. A 2025 European guideline on chronic and vomiting underscores the roles of biological, psychological, and social factors in these conditions. Effective interventions for psychogenic vomiting include (CBT), which targets underlying anxiety and avoidance patterns, achieving symptom reduction in cases linked to social phobia or specific vomiting fears. Support groups, such as those facilitated by the National Eating Disorders Association, offer peer-based emotional relief and coping strategies for individuals managing vomiting-related psychological burdens.

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