Nausea and vomiting

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9 Nausea and vomiting

Nick Talley

Case

A 21-year-old university student consults because of episodic nausea and vomiting. In between attacks, he is well. However, approximately every 2 months he will experience worsening nausea preceding violent vomiting episodes that can last for 3–5 days. The vomiting has been so severe that he has presented to casualty where intravenous injections of antiemetics have been given. There is mild abdominal pain associated with the nausea and vomiting at times. His bowel habit has been normal. He denies any neurological symptoms. He has had a history of occasional migraine-type headaches, but has otherwise been in excellent health. He has not been taking any regular medications. He has already seen a gastroenterologist who performed an upper endoscopy that was normal and a small bowel x-ray that was normal. Screening blood tests (including electrolytes, liver function tests and a blood count) have all been normal.

You ask him two specific questions. First, you ask whether he feels the compulsion to take a hot bath or shower during an episode; while the patient is surprised by the question he acknowledges this is true and this seems to help. You also ask him whether he has ever used marijuana. The patient admits he has from time to time smoked marijuana to try to prevent his symptoms.

Physical examination is completely unremarkably, including a full neurological examination and fundoscopy.

You make an astute diagnosis of cyclic vomiting syndrome secondary to cannabis use. You explain to the patient that in some cases vomiting can be precipitated by use of marijuana. You strongly encourage him to cease all marijuana use. A prescription for a tricyclic antidepressant (desipramine) is subsequently given because the attacks do continue off cannabis. The dose is slowly titrated up, and the patient has an excellent response with a substantial reduction in the number of vomiting episodes over the subsequent 6 months.

Definition

Nausea and vomiting are common symptoms. Nausea is best considered a painless, unpleasant, subjective feeling of wanting to vomit. Vomiting, on the other hand, is the forceful expulsion of gastric or intestinal contents through the mouth, secondary to a pre-programmed series of motor and autonomic responses. Vomiting is not retching; ‘retching’ describes contractions of the abdominal muscles that typically precede vomiting, associated with laboured, rhythmic respiration, not the expulsion of the contents through the mouth. Vomiting must be distinguished from regurgitation, which is an effortless movement of gastric material into the mouth. Clinically, it is key to distinguish vomiting from rumination, as management is totally different. In the rumination syndrome, there is effortless regurgitation of recently ingested food into the mouth that is not preceded by nausea or abdominal muscular contractions. The food tastes like it has not been eaten. Often the patient will re-chew or spit the food out, but this does not always occur. Rumination typically occurs within minutes of a meal and is almost always repetitive.

Physiology of Vomiting

With the onset of nausea, there will be accompanying autonomic discharge of variable severity. This results in intense salivation, bradycardia, sweating, pallor and hypotension. The normal electrical activity of the stomach may become slow, fast or fluctuate wildly with nausea. It is unclear whether the same neural pathways that mediate vomiting also mediate nausea.

Just prior to vomiting, a large amplitude contraction in the small bowel is propagated retrogradely. Moderate amplitude phasic contractions may also occur in the small intestine, with these motor activities probably being mediated by the vagus nerve. These motor changes result in the small bowel contents entering the relaxed stomach where closure of the pylorus then occurs with contraction of the abdominal muscles, causing respiration to be suspended. Gastric contents are then forced against a contracted diaphragm, the lower oesophageal sphincter relaxes and the cardia elevates. Gastric contents are forced into the oesophagus, which dilates. Protection of the airway occurs via the glottis closing and the soft palate rising, and then the vomitus is forcibly ejected from the mouth.

The vomiting centre is located in the dorsal portion of the medulla. The vomiting centre has afferent inputs via vagal fibres, which are rich in 5-hydroxytryptamine type 3 (5-HT3) receptors. There is afferent input from sympathetic nerves. There is also input from the vestibular system, which is rich in histamine H1 and muscarinic cholinergic fibres. The chemoreceptor trigger zone is in the area postrema in the floor of the fourth ventricle. This area, when stimulated, will activate the vomiting centre, and is responsive to drugs, hypoxia, toxins and acidosis; it is rich in dopamine D2 and 5-HT3 receptors. The presence of these receptor subtypes forms the rationale for drugs used to treat nausea and vomiting. Other trigger areas include the pharynx, coronary vessels, peritoneum and bile ducts, cortex, thalamus and hypothalamus, and the vestibular apparatus (motion sickness).

History

Nausea and vomiting are non-specific symptoms and may occur in many diseases. Box 9.1 lists the important causes of nausea and vomiting. When taking the targeted history, it is key to differentiate between vomiting, regurgitation and rumination.

Box 9.1 Common causes of nausea and vomiting

Intestinal obstruction

• Anatomic:

– small bowel obstruction, e.g. adhesions;
– gastric outlet obstruction, e.g. pyloric ulcer.

• Functional:

– diabetic gastroparesis;
– idiopathic gastroparesis;
– chronic intestinal pseudo-obstruction.

Infections

• Food poisoning
• Viral or bacterial diarrhoea
• Acute viral hepatitis

Central nervous system disorders

• Migraine
• Meningitis
• Increased intracranial pressure
• Ménière’s disease
• Motion sickness

Metabolic disorders

• Renal failure
• Diabetic ketoacidosis
• Adrenal insufficiency (Addison’s disease)
• Hyperthyroidism

Visceral pain

• Peritonitis
• Cholecystitis
• Pancreatitis

Drugs

Psychiatric disorders

• Anorexia or bulimia nervosa
• Panic attacks

Other

• Pregnancy
• Conditioned reflexes
• Cyclical vomiting
• Functional vomiting

It is very helpful to determine the duration, frequency and intensity of nausea and vomiting, and its relationship to eating. Self-limiting symptoms will often occur with an acute infectious gastroenteritis, with inflammatory disease such as cholecystitis or pancreatitis, or from drugs. Gastroenteritis is usually associated with headache, myalgias and diarrhoea and will settle within 5 days, so a longer duration of symptoms should raise the suspicion of another cause. An insidious onset of nausea without vomiting can occur with functional dyspepsia, gastroparesis, medication use, gastro-oesophageal reflux disease, pregnancy and metabolic disorders. Vomiting on waking in the morning may occur from excess alcohol use the night before. Early morning vomiting can also occur with pregnancy, renal failure and raised intracranial pressure.

The character of the vomit is useful to document. Undigested food in the vomit may occur from oesophageal disorders (e.g. achalasia or Zenker’s diverticulum). Gastric outlet obstruction may result in partially digested food, free of bile. In small bowel obstruction, the vomitus is usually bile stained. Faecal vomiting indicates distal small bowel obstruction or a gastrocolonic fistula.

The presence of other gastrointestinal symptoms such as abdominal pain or diarrhoea suggests a primary gastrointestinal disease. In the presence of significant weight loss with nausea and vomiting, consideration needs to be given to a gastrointestinal tract malignancy, intestinal obstruction or an eating disorder. An adolescent female with a history of repeated bouts of vomiting immediately after meals, particularly after binge eating, may have anorexia nervosa or bulimia nervosa; accompanying weight loss, fear of gaining weight, impaired body image, amenorrhoea and binge eating should be asked about. The vomiting is generally self-induced; laxatives, diuretics and vigorous exercise may also be used to prevent weight gain (Ch 17).

Diseases of the central nervous system can present with vomiting. This may manifest as sudden projectile vomiting without nausea. Emesis may also be triggered by an abrupt change in body position. It is unusual for a patient with a brain tumour to present with vomiting in the absence of other neurological symptoms such as headache, vertigo, deafness, tinnitus or visual impairment.

If the patient describes acute episodes of nausea and vomiting separated by intervening totally asymptomatic periods, this is suggestive of cyclical vomiting, which can occur in adults but is much more common in children; a history of migraine may be present.

Symptoms of systemic diseases that may cause nausea and vomiting, including diabetes mellitus, renal failure, hypercalcaemia and hyperthyroidism, should be actively sought.

Gastro-oesophageal reflux disease can present with recurrent vomiting in the absence of heartburn and acid regurgitation.

Chronic nausea with little or no vomiting, and not accompanied by other symptoms or signs, presents a diagnostic challenge. Organic diseases rarely cause chronic persistent nausea alone.

In the first trimester of pregnancy, nausea and vomiting are common. All women of childbearing age should have pregnancy excluded as a cause.

Physical Examination

An abdominal examination may reveal evidence of obstruction, malignancy or peritoneal signs, but is usually negative in the patient with chronic symptoms. Scars from previous surgery should be noted. Assessment of hydration status (skin turgor, mucous membranes, pulse, and blood pressure lying and standing) is important in terms of management decisions. The pigmentation of Addison’s disease should be looked for. Evidence of fever should be sought. Chronic vomiting can also cause dental erosions and caries. Self-induced vomiting can cause calluses or ulcers on the dorsum of the hand and dental erosions (from acid) and hypertrophied salivary glands. Pinhead-sized red macules on the face and upper neck may occur with recurrent vomiting.

A careful neurological examination should be conducted. Evidence of nystagmus may occur in labyrinthitis. Focal neurological signs are usually present if there is a central nervous system cause for the nausea and vomiting, although the changes may be relatively subtle. Look in the fundi for evidence of raised intracranial pressure.

Investigation

Investigation is undertaken to:

1. define any derangements that may result from the loss of fluid and electrolytes during vomiting; and
2. determine the diagnosis of the underlying cause.

The investigations need to be guided by the initial history and physical examination. Serum electrolytes will exclude hypokalaemia, renal failure and metabolic alkalosis due to chronic loss of gastric contents. Serum albumin levels, if low, would suggest a chronic disease or malnutrition. Anaemia would suggest colonic or small bowel disease, whereas leucocytosis would suggest an inflammatory process. If there is upper abdominal pain, pancreatic and liver enzymes can be useful. Peripherally, eosinophilia can occur in eosinophilic gastroenteritis, which can present with recurrent vomiting. Pregnancy testing is mandatory before radiographic testing in any woman of reproductive age with new-onset nausea and vomiting.

A suggested management algorithm for chronic nausea and vomiting is shown in Figure 9.1. Supine and upright abdominal x-rays will document small bowel obstruction, although in 20% of cases partial small bowel obstruction can be missed with plain films. Upper endoscopy will exclude gastric outlet obstruction and significant gastroduodenal disease, such as peptic ulcer. If small-bowel follow-through fails to reveal evidence of obstruction, which can occur with a partial lesion, an enteroclysis (where barium and methylcellulose are infused into the proximal intestine via a nasojejunal tube in order to provide double-contrast pictures) or computed tomography enterography can be useful. If there is any suggestion of lower bowel obstruction, barium enema or colonoscopy should be undertaken.

image

Figure 9.1 Diagnostic algorithm for nausea and vomiting.

Endocrine disease may present with chronic vomiting and, therefore, testing should be done to exclude diabetes mellitus, hypothyroidism and, in particular, Addison’s disease.

If the patient has normal structural evaluations and continues to be symptomatic, gastric emptying testing can be undertaken. An alternative is 13C octanoic acid breath testing, which is non-radioactive and can be used in children or pregnant women. However, symptom improvement on prokinetics correlates poorly with changes in gastric emptying, and abnormal emptying is not a reliable way to direct management of nausea and vomiting. Another controversial test is electrogastrography. Cutaneous electrodes can measure the gastric slow wave activity. In the setting of vomiting, there may be slow (bradygastria) or fast (tachygastria) myoelectric rhythms, but this has not been established to be useful for directing treatment of chronic nausea or vomiting. Antroduodenal manometry is valuable in specialised centres. Approximately 40% of patients with unexplained nausea and vomiting have normal results, and the test alters management in only about 10% of cases. It is useful to consider this test when symptoms continue to be very troublesome; normal results of antroduodenal manometry should direct evaluation outside the gastrointestinal tract, which is of value.

Consequences of Nausea and Vomiting

The main complications with acute vomiting include trauma to the distal oesophagus as well as severe fluid and electrolyte disturbances.

Recurrent vomiting may result in laceration of the oesophageal mucosa at the gastro-oesophageal junction, and a small amount of blood may streak the vomitus, typically following repeated vomiting. Haemorrhaging may occur as a consequence of a laceration to the mucosa into the submucosa, termed a Mallory-Weiss tear. If the laceration extends through the submucosa and the serosa to result in an oesophageal perforation, this is called Boerhaave’s syndrome. This perforation typically enters the left chest cavity, producing intense pain. Acute severe vomiting, particularly in patients with neurological defects or impaired consciousness from alcohol intoxication, may result in aspiration of vomitus into the lungs.

Recurrent vomiting in young and elderly people, particularly, may result in severe fluid and electrolyte disturbances. Most of these losses occur from the vomited secretions of the stomach and upper small intestine. As hydrogen, sodium, potassium and chloride irons are lost from gastric secretions, prolonged vomiting results in metabolic alkalosis, hypokalaemia and dehydration.

Occasionally, a patient who is vomiting will conceal it and present with unexplained hypochloraemic hypokalaemic metabolic alkalosis. Here, the differential diagnosis includes surreptitious diuretic use, primary hyperaldosteronism and Bartter’s syndrome. The urine chloride is typically low with vomiting (or diuretics).

Chronic nausea and vomiting significantly impair quality of life, and warrants appropriate therapy.

Important Diseases that may cause Nausea and Vomiting

Gastric and intestinal obstruction

The nature of vomiting and associated symptoms caused by intestinal obstruction depends on the level of the gut involved as well as the rapidity with which the obstruction occurs (Ch 4). Acute small bowel obstruction is more likely to be associated with severe pain compared with obstruction of a more insidious onset. Bile is almost always present in the vomitus when the obstruction is below the duodenal ampulla. The vomiting of partially digested food one to several hours after eating would suggest obstruction at the pylorus. Malignant obstruction of any form is usually accompanied by anorexia and weight loss. Complete obstruction of the stomach or duodenum usually results in the loss of large volumes of fluid in the vomitus (Ch 4).

Functional obstruction, as seen in diabetic gastroparesis or postvagotomy, differs from mechanical gastric obstruction in that intense nausea and anorexia are more common; signs of peripheral and autonomic neuropathy are usually present if diabetes mellitus is the cause. Postprandial fullness and early satiety are common symptoms with diabetic gastroparesis.

Physical examination of the abdomen varies depending upon the cause of the obstruction. In pyloric obstruction, upper abdominal distension and a succussion splash may be observed. Generalised abdominal discomfort may be noted. Distended loops of bowel are observed with peristaltic rushes early in intestinal obstruction, but absent bowel sounds are noted later.

Infection

Acute viral gastroenteritis may result in vomiting. Bacterial gastroenteritis induces vomiting usually accompanied by fever and diarrhoea (see Ch 13). Nausea and vomiting, which occasionally may be prolonged and result in dehydration, may be prominent characteristics of acute viral hepatitis (Ch 24).

Central nervous system disorders

Space-occupying lesions with increased intracranial pressure are a cause of vomiting often without associated anorexia or nausea. The vomiting may be sudden and projectile in nature, and may occur early in the morning or with a sudden change in body position. Signs of raised intracranial pressure such as papilloedema on fundoscopy may not always be present. Radiological investigations, including magnetic resonance imaging of the brain, are important to perform if persistent or recurrent vomiting of unknown cause is being investigated.

Nausea and vomiting due to diseases of the vestibular apparatus are accompanied by vertigo and nystagmus. Tinnitus also accompanies Ménière’s disease. Migraine headaches that are often unilateral and may be accompanied by a prodrome of visual disturbances are characteristically associated with nausea and vomiting.

Metabolic disorders

In certain metabolic disorders, vomiting is invariably present, such as in untreated renal failure and in diabetic ketoacidosis. Nausea and sometimes vomiting may accompany hypoadrenalism (Addison’s disease) and less commonly hyperthyroidism.

Drugs

The potent emetic agent Ipecac is given as a therapeutic agent to induce vomiting. Morphine and opiate derivatives produce nausea and vomiting in some people when given in therapeutic doses, and in most patients when given in large doses.

Non-steroidal anti-inflammatory drugs may be associated with nausea and sometimes vomiting in susceptible individuals with or without accompanying peptic ulcer disease. Other gastric irritants such as iron preparations can also cause nausea. Erythromycin, despite its prokinetic actions, often induces nausea. Both digitalis and theophylline preparations may cause insidious nausea and occasionally vomiting; they may have been taken for months or years before symptoms occur because of a narrow margin between toxic and therapeutic levels.

Visceral pain

Vigorous stimulation of visceral afferent fibres either due to direct external pressure on certain organs such as the kidney and the testis or via unusual distension, as in obstruction of the intestine, ureter, cystic duct or common bile duct, results in nausea and vomiting. In addition, local inflammation in any of the above organs is frequently accompanied by nausea and vomiting (e.g. with mumps, orchitis, cholecystitis or ascending cholangitis). Nausea and vomiting also occur with acute pancreatitis.

Infiltration of the gastrointestinal tract (e.g. eosinophils in eosinophilic gastroenteritis, amyloid in amyloidosis or malignant cells in carcinoma or lymphoma) may be associated with vomiting. Severe pain in other areas outside the abdomen may also be accompanied by nausea and vomiting (e.g. acute myocardial infarction).

Psychiatric disease

Nausea and vomiting are prominent symptoms in eating disorders, including anorexia nervosa and bulimia nervosa (Ch 17). Panic attacks can also cause nausea. If nausea is not accompanied by anorexia or is associated with weight gain, an organic cause is rarely observed.

Pregnancy

In any woman of childbearing age who describes nausea of recent onset, a pregnancy test should be considered. Morning sickness may also occur in susceptible women who use oral contraceptives. Morning nausea during the first 12 weeks of pregnancy is common and occurs in up to 90% of normal pregnancies. Accompanying vomiting, however, occurs in only 25–50%. The nausea usually resolves spontaneously as the day progresses, with the appetite returning to normal in the afternoon and evening. In the majority of pregnant subjects, nausea and vomiting is self-limiting and disappears spontaneously in the first trimester. If vomiting is severe and is associated with dehydration or electrolyte disturbances, it is termed ‘hyperemesis gravidarum’. The cause is unknown. This state can potentially threaten the fetus and mother because of electrolyte disturbances and nutritional deficiencies.

Conditioned reflexes

An offensive sight (e.g. blood) or unpleasant smell may result in immediate nausea and sometimes vomiting in susceptible people. Conditioning may occur in response to such sights or smells, so that nausea and vomiting is more easily precipitated by the same circumstances in the future. Such conditioning also applies to motion sickness and the vomiting induced by chemotherapy.

Principles of Treatment

Treatment involves successfully correcting any dehydration and electrolyte abnormalities. Malnutrition should also be corrected, if present. If clinically necessary, intravenous fluids (normal saline with potassium) should be given and a nasogastric tube put in place; the output, which should be replaced intravenously, should be measured.

Dietary modification is particularly important if there is evidence of gastroparesis. Frequent small meals (six per day), a low-fat diet, avoidance of indigestible material to reduce the chance of bezoar formation and reduced fibre intake can all be useful. Splitting the ingestion of liquids and solids may reduce symptoms. Liquids are generally tolerated better than solids in this setting, and so the use of a blender or liquid formulas can be helpful. Medical therapy (Table 9.1) may be necessary.

Table 9.1 Examples of drugs to control nausea and vomiting

image

Medical therapy

Antiemetics

Neuroleptic agents such as prochlorperazine, chlorpromazine or haloperidol have both anticholinergic and antihistamine effects as well as blocking dopamine D2 receptors in the chemoreceptor trigger zone. Sedation, blood dyscrasias, dystonia and jaundice are potential side effects. Prochlorperazine (5–10 mg three times a day) is most widely used and can be given orally, rectally or parenterally.

Motion sickness is treated with anticholinergic agents such as scopolamine. This can be given as a transdermal patch. Sometimes this will also help gastrointestinal causes of nausea and vomiting. H1-receptor antagonists such as promethazine (25 mg four times a day) or diphenhydramine (25–50 mg three to four times a day) can be helpful in vestibular disturbances and motion sickness, and sometimes improve gastrointestinal-related nausea.

5-HT3 antagonists (e.g. ondansetron, granisetron and dolasetron) are useful in postoperative vomiting, in prevention of chemotherapy-induced emesis and after radiation therapy, but appear to produce relatively little improvement in other forms of vomiting. Tetrahydrocannabinol and nabilone have proven useful in chemotherapy-induced emesis. These cannabinoids can produce drowsiness, orthostatic hypotension, dry mouth and tachycardia, as well as anxiety, depression and visual hallucinations.

The neurokinin-1 antagonist aprepitant is indicated for chemotherapy-induced nausea and vomiting. It is given orally (80–125 mg) and side effects include somnolence, fatigue and hiccups. Talnetant and osanetant are other neurokinin antagonists. Any benefit in gastrointestinal disease is uncertain.

Prokinetic agents

Metoclopramide (5–20 mg four times a day) is a substituted benzamide, and is a dopamine D2-receptor antagonist. It has central antidopaminergic effects and stimulates cholinergic actions locally in the gut. It is associated with side effects including drowsiness, dystonia, parkinsonism and, rarely, cardiac arrhythmias or tardive dyskinesia (which can be irreversible despite ceasing the medication, particularly in the elderly). Metoclopramide is available both orally and parenterally. Domperidone is another substituted benzamide that poorly penetrates the central nervous system and so has fewer central side effects. It can cause cardiac arrhythmias and gynaecomastia (5%).

Erythromycin is a macrolide antibiotic that, through motilin receptors, accelerates gastric emptying. However, it has a very narrow therapeutic window and high doses induce nausea. While the drug may accelerate emptying, it usually does not relieve symptoms when taken orally for nausea and vomiting. Other motilin agonists have proven disappointing in clinical studies of functional dyspepsia.

Benzodiazepines

Lorazepam and other benzodiazepines can reduce anticipatory nausea and vomiting prior to chemotherapy, although any benefit in other causes of nausea and vomiting is unclear. They may be a useful adjunctive treatment in combination with other therapy.

Tricyclic antidepressants

Limited data from primarily retrospective analyses suggest that low-dose tricyclics will reduce chronic nausea and vomiting in up to 80% of patients with functional bowel disease.

Botulinum toxin injection

Patients with gastroparesis may have temporary symptom reduction after injection of botulinum toxin into the pylorus, although data are limited.

Gastric electrical stimulation

Gastric electrical stimulation is emerging as a potentially useful therapy for refractory gastroparesis with nausea and vomiting. Applying stimulation parameters at four times the basal rate (12 cycles per minute), symptoms, but not gastric emptying, have been reported to improve. The neurostimulators are placed in the subcutaneous pouch and the electrodes are placed along the greater gastric curvature at laparotomy or laparoscopy. High-frequency gastric electrical stimulation is approved for patients with chronic intractable nausea and vomiting due to idiopathic or diabetic gastroparesis.

Alternative treatments

Acupressure or acupuncture, ginger, hypnosis, transcutaneous electrical nerve stimulation, behaviour modification treatments and psychological therapies are of some efficacy in selected clinical settings, but data remain limited, particularly in terms of idiopathic nausea and vomiting.

Specific Clinical Scenarios

Gastroparesis

Start with an antiemetic and prokinetic agent in combination. Combination therapy tends to be more useful than in the clinical setting. If maximal medical therapy fails, options include gastric electrical stimulation, endoscopic placement of a percutaneous endoscopic gastrostomy, jejunostomy or a subtotal gastrectomy in extreme cases. Gastric bypass procedures and less extensive gastric resection should be avoided as they give much poorer results.

Cyclical vomiting syndrome

This is a condition characterised by discrete acute episodes of nausea and vomiting with completely asymptomatic intervening periods. Migraine headaches, motion sickness and atopy may be positive on history taking. While primarily a condition of childhood, there are reports in adults. Typically in adults, the episodes of nausea and vomiting last for 3–6 days. Cyclical vomiting is often associated with abdominal pain (in two-thirds of patients) and psychiatric diagnoses are uncommon (in one-fifth). In children, an association with mitochondrial DNA mutations has been described. Tricyclic antidepressants appear to be useful for this syndrome. Antimigraine therapy (e.g. beta-blockers or sumatriptan) may also be of some value, particularly if there is a family history of migraine. Cannabis hyperemesis can mimic cyclic vomiting syndrome; compulsive bathing to relieve symptoms is a characteristic feature.

Functional vomiting

This is a rare condition that has been defined by the Rome Foundation Committee (Box 9.2). If gastric emptying is delayed, it is important to exclude chronic intestinal pseudo-obstruction as well as mechanical intestinal obstruction. No medications have established efficacy in this group, but anecdotally, tricyclic antidepressants seem to be of value and can be tried at a low dose, but may require full dose to be efficacious.

Box 9.2 Functional vomiting diagnostic criteria

• Frequent episodes of vomiting, occurring on at least 1 separate day in a week over 3 months
• Absence of criteria for an eating disorder, rumination or significant psychiatric disease
• Absence of self-induced and medication-induced vomiting
• Absence of abnormalities in the gut or central nervous system, and metabolic diseases to explain the recurrent vomiting

From Rome III. The functional gastrointestinal disorders. 3rd edn. 2006:331, with permission. http://www.romecriteria.org

Key Points

• Nausea is a painless, unpleasant, subjective feeling of wanting to vomit, while vomiting is the forceful expulsion of gastric or intestinal contents through the mouth.
• ‘Retching’ describes contractions of the abdominal muscles that typically precede vomiting.
• Regurgitation is an effortless movement of gastric material into the mouth. Rumination syndrome is the effortless regurgitation of recently ingested food back into the mouth and is not preceded by nausea; patients may say they are ‘vomiting’.
• All women of childbearing age must have pregnancy excluded as a cause of nausea or vomiting.
• Chronic nausea without vomiting can be caused by functional dyspepsia, gastroparesis, medication use, gastro-oesophageal reflux disease, pregnancy and metabolic disorders.
• Early morning vomiting occurs in pregnancy, in renal failure and with raised intracranial pressure.
• Self-induced vomiting (bulimia) can cause calluses or ulcers on the dorsum of the hand and dental erosions (from acid).
• Haemorrhaging may occur as a consequence of vomiting from a laceration to the mucosa into the submucosa—a Mallory-Weiss tear.
• If there is vomiting, any dehydration and electrolyte abnormalities must always be checked and corrected.
• Dietary modification is important if there is evidence of gastroparesis. Antiemetic and prokinetic therapy is helpful in combination for this syndrome.

Further reading

Abell T.L., Bernstein R.K., Cutts T., et al. Treatment of gastroparesis: a multidisciplinary clinical review. Neurogastroenterol Motil. 2006;18:263-283.

Bai Y., Xu M.J., Yang X., et al. A systematic review on intrapyloric botulinum toxin injection for gastroparesis. Digestion. 2010;81(1):27-34.

Ma J., Rayner C.K., Jones K.L., et al. Diabetic gastroparesis: diagnosis and management. Drugs. 2009;69(8):971-986.

Parkman H.P., Camilleri M., Farrugia G., et al. Gastroparesis and functional dyspepsia: excerpts from the AGA/ANMS meeting. Neurogastroenterol Motil. 2010;22(2):113-133.

Quigley E.M.M., Hasler W.L., Parkman H.P. AGA technical review on nausea and vomiting. Gastroenterology. 2001;120:263-286.

Soffer E., Abell T., Lin Z., et al. Review article: gastric electrical stimulation for gastroparesis—physiological foundations, technical aspects and clinical implications. Aliment Pharmacol Ther. 2009;30(7):681-694.

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