Nausea and vomiting

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9 Nausea and vomiting


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.

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).


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.

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

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