Nausea, vomiting and gastric outlet symptoms

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Vomiting is the coordinated expulsion of gastric contents, whereas regurgitation is passive return to the mouth and rumination is repeated effortless postprandial return followed by rechewing or expulsion. This distinction prevents inappropriate antiemetic escalation. Establish onset, frequency, relation to meals, content, abdominal distension, bowel function, pain, headache, vertigo, fever and weight. Review opioids, antibiotics, digoxin, metformin, GLP-1 receptor agonists, chemotherapy and other emetogenic medicines, and ask sensitively about cannabis. Pregnancy, migraine, vestibular disease, intracranial pathology, adrenal crisis, uraemia, hypercalcaemia, ketoacidosis and infection may present without a primary gastric disorder.

Gastric outlet obstruction produces early satiation, postprandial fullness, epigastric distension, weight loss and vomiting of food eaten hours earlier. Causes include gastric or pancreatic malignancy, peptic scarring, inflammatory narrowing, bezoar and external compression. A succussion splash several hours after eating is supportive but insensitive. Gastroparesis produces similar retention without mechanical obstruction, often related to diabetes, surgery or medicines. Functional dyspepsia and chronic nausea-vomiting syndromes can overlap but should not be diagnosed around progressive weight loss, persistent obstruction or uninvestigated metabolic disease.

Management begins with airway and volume. Record orthostatic symptoms, urine output, weight and nutritional intake; correct sodium, potassium, chloride, magnesium and glucose abnormalities deliberately. Imaging depends on the question: abdominal radiography has limited sensitivity, contrast CT assesses obstruction and complications, ultrasound answers biliary and pregnancy questions, and endoscopy visualises outlet lesions and permits biopsy. A gastric-emptying study is meaningful only after structural obstruction is excluded and medicines or glycaemia that alter emptying are considered. Chronic unexplained symptoms require nutrition, dietetic, motility and psychological assessment rather than repeated emergency antiemetics alone.

Key points

Clarify whether material is gastric, bilious, bloody, coffee-ground or faeculent and whether nausea precedes it; effortless regurgitation and rumination have different mechanisms from forceful vomiting.
Early morning headache or neurological change, chest pain, pregnancy, drugs, cannabis, alcohol withdrawal, sepsis and metabolic disease must remain in the differential even when abdominal symptoms dominate.
Postprandial fullness, early satiation and late vomiting of recognisable food suggest impaired gastric emptying or outlet obstruction, but structural narrowing must be excluded before diagnosing gastroparesis.
Repeated vomiting commonly causes volume depletion, hypochloraemic metabolic alkalosis, hypokalaemia and kidney injury; diarrhoea or ketoacidosis may alter the acid-base pattern.
Check capillary glucose, ketones, renal function, electrolytes, magnesium and an ECG when illness is severe or QT-prolonging antiemetics are being considered.
Pregnancy testing belongs early in any relevant presentation. Hyperemesis is a diagnosis after assessing severity and excluding other obstetric, medical and surgical causes.
Nasogastric decompression can reduce vomiting and aspiration in significant obstruction, but insertion requires an indication, safe position confirmation and ongoing loss replacement.
Give thiamine before carbohydrate loading to a severely malnourished or prolonged-vomiting patient at risk of deficiency, using the local refeeding protocol.
Antiemetics should be selected by likely mechanism, comorbidity, interactions, pregnancy and QT or extrapyramidal risk, then reviewed for response rather than stacked automatically.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Gastrointestinal obstruction or inflammation

Gastric outlet or bowel obstruction, gastroenteritis, pancreatitis, cholecystitis and peritonitis activate visceral and vagal emetic pathways.

Central, metabolic and pregnancy-related

Raised intracranial pressure, migraine, pregnancy, sepsis, ketoacidosis, uraemia and electrolyte disturbance stimulate central chemoreceptor or vestibular circuits.

Medicines, substances and gut-brain disorders

Opioids, chemotherapy, alcohol withdrawal, cannabis, gastroparesis, rumination and functional vomiting cause distinct temporal patterns and management needs.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Emetic network activation
Vagal, vestibular, cortical and blood-borne signals converge on brainstem circuits coordinating nausea, retching and forceful expulsion.
2
Gastric retention or retrograde propulsion
Obstruction or dysmotility distends the stomach, while coordinated diaphragmatic and abdominal contraction drives contents upwards through the oesophagus.
3
Fluid and acid loss
Repeated gastric loss depletes water, hydrogen, chloride and potassium, causing alkalosis, renal hypoperfusion and progressive weakness.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Gastric outlet obstructionRed flag

Progressive early satiation, epigastric fullness, weight loss, dehydration and large-volume late postprandial vomiting suggest retention proximal to the pylorus or duodenum. Malignancy must be excluded promptly, particularly with short progressive history.

Small-bowel obstructionRed flag

Colicky abdominal pain, distension, vomiting and reduced stool or flatus, especially after surgery or with a hernia, support mechanical obstruction. Constant pain, guarding, fever or acidosis raises strangulation.

Diabetic ketoacidosisRed flag

Vomiting with thirst, polyuria, dehydration, deep breathing, abdominal pain, hyperglycaemia and ketonaemia indicates a metabolic emergency. Abdominal tenderness can improve with correction and should not conceal coexisting surgical disease.

Hyperemesis gravidarum

Severe nausea and vomiting beginning in early pregnancy with dehydration, weight loss or electrolyte disturbance supports hyperemesis after excluding molar or multiple pregnancy and non-obstetric causes. Later onset requires wider reconsideration.

Gastroparesis phenotype

Chronic nausea, early satiation, postprandial fullness, upper pain and vomiting with diabetes, surgery or motility-altering medicines supports delayed gastric emptying only after mechanical obstruction is excluded objectively.

Cannabinoid hyperemesis pattern

Recurrent severe vomiting in a long-term frequent cannabis user, often with temporary relief from hot bathing, raises cannabinoid hyperemesis. Sustained cessation is diagnostic and therapeutic, while acute red flags still require exclusion.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Capillary glucose, ketones and blood gasFirst step
Why
Identify diabetic ketoacidosis, starvation ketosis, hypoglycaemia and acid-base consequences of vomiting.
Interpretation and limitations
Ketoacidosis requires the current emergency protocol. Metabolic alkalosis supports gastric hydrogen and chloride loss, but mixed disorders are common and must be interpreted with chloride, lactate and renal function.
02
Renal profile, magnesium and corrected calcium
Why
Quantify dehydration, kidney injury and electrolyte triggers or consequences of vomiting before replacement and antiemetic treatment.
Interpretation and limitations
Replace deficits with monitored therapy and repeat testing. Hypokalaemia and hypomagnesaemia increase arrhythmia risk, while hypercalcaemia can itself cause nausea and ileus.
03
Pregnancy test and obstetric ultrasound
Why
Identify pregnancy and investigate gestation, viability, multiple pregnancy or trophoblastic disease when clinically indicated.
Interpretation and limitations
Pregnancy changes differential, imaging and medicines. Hyperemesis should not be used to explain focal peritonism, fever, neurological signs or later-onset vomiting without further assessment.
04
ECG
Why
Detect electrolyte-related arrhythmia and establish QT interval before or during medicines that can prolong repolarisation.
Interpretation and limitations
Correct potassium and magnesium and rationalise QT-prolonging combinations when abnormal. A normal baseline trace does not remove the need for review after physiology or medication changes.
05
Contrast CT abdomen and pelvis
Why
Identify level and cause of obstruction, gastric distension, transition point, malignancy, inflammation, perforation or ischaemia.
Interpretation and limitations
Discuss protocol and oral-contrast need with radiology. Closed-loop features, compromised enhancement, free gas or progressive physiology require urgent surgical action rather than serial antiemetics.
06
Upper gastrointestinal endoscopy
Why
Visualise and biopsy gastric, pyloric or duodenal narrowing and assess retained contents or mucosal disease.
Interpretation and limitations
A heavily retained stomach increases aspiration risk and needs procedural planning and often decompression. Negative mucosal assessment does not prove normal motility.
07
Standardised gastric-emptying assessment
Why
Confirm delayed emptying when gastroparesis remains suspected after structural obstruction is excluded.
Interpretation and limitations
Ensure the laboratory protocol, relevant medicine withholding and glucose context are documented. Delayed emptying must be correlated with symptoms; normal emptying redirects towards other gastric sensorimotor or gut-brain disorders.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Mechanical outlet or bowel obstruction

Distension, obstipation, late food or faeculent vomit and a transition point on imaging require decompression and surgical or endoscopic planning.

Neurological or metabolic emergency

Headache, focal signs, altered consciousness, pregnancy, hyperglycaemia, uraemia or sepsis redirects immediate testing beyond the abdomen.

Rumination or cannabinoid hyperemesis

Effortless immediate postprandial return suggests rumination, while prolonged cannabis exposure and stereotyped episodes support cannabinoid-related vomiting after exclusion of danger.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Initial stabilisationCorrect threats before symptomsFirst stepVomiting is persistent, severe or associated with physiological abnormality.

1Assess airway and aspiration risk, breathing, circulation, mental state and abdominal signs; obtain venous access, bedside glucose and ketones and relevant bloods.
2Provide monitored crystalloid and electrolyte replacement based on losses and comorbidity, keep nil by mouth when obstruction or procedure is plausible, and measure urine output.
3Select one mechanism-appropriate antiemetic after ECG and interaction review where indicated, rather than giving several QT-prolonging agents simultaneously.
4EscalationEscalate haematemesis, peritonism, DKA, neurological signs, pregnancy instability or obstruction to the relevant acute specialty while resuscitation continues.

02Suspected obstructionDecompress and define anatomyDistension, obstipation, late food vomiting or persistent gastric retention suggests a mechanical blockage.

1Obtain early surgical or upper gastrointestinal review, assess hernias and peritonism, institute fasting and consider nasogastric decompression when vomiting or distension is significant.
2Arrange contrast CT for level and complications, and upper endoscopy with biopsy when gastric or duodenal outlet pathology is likely.
3Replace measured gastric losses and monitor chloride, potassium, renal function and acid-base state; nutrition planning should begin if obstruction will not resolve promptly.
4Move to endoscopic, oncological or operative treatment according to anatomy and physiology rather than labelling delayed emptying before the lumen is assessed.

03PregnancyGrade severity and preserve nutritionNausea and vomiting occurs with confirmed or possible pregnancy.

1Confirm pregnancy and gestational context, assess dehydration, weight loss, ketones and electrolytes, and exclude abdominal, urinary, endocrine and neurological alternatives.
2Use RCOG-aligned antiemetic treatment and rehydration appropriate to severity, adding thiamine before dextrose in prolonged vomiting.
3Arrange ambulatory or inpatient obstetric care when oral intake fails, comorbidity is present or physiology is abnormal, and assess thrombosis and nutrition risks under local policy.
4Review mental health, social impact and recurrence; symptoms should not be trivialised as ordinary morning sickness.

04Chronic retentionSeparate structure from motilityEarly satiation, postprandial fullness and recurrent vomiting continue beyond an acute illness.

1Review weight, nutrition, glucose control, surgery and medicines that slow gastric emptying, and identify cancer or obstruction warnings.
2Exclude structural disease through endoscopy and appropriate cross-sectional imaging before requesting a standardised emptying study.
3Use dietetic strategies, glycaemic optimisation and specialist-selected prokinetic or antiemetic treatment only after the mechanism and medicine risks are reviewed.
4For normal emptying with persistent symptoms, consider functional dyspepsia, chronic nausea-vomiting syndrome, rumination and eating disorder through multidisciplinary assessment.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Reduces nausea and vomiting enough to permit hydration and definitive investigation while the underlying cause is treated.

Mechanism-selected antiemetic

Choose one current BNF and locally approved agent and route, adjusting for pregnancy, renal or hepatic impairment, QT interval and likely central or gastric mechanism.

Review sedation, extrapyramidal effects, anticholinergic burden, constipation and QT-prolonging combinations. Avoid automatic polypharmacy and stop ineffective agents after a defined reassessment.

Prevents or treats neurological injury from thiamine deficiency during nutritional and intravenous fluid restoration.

Parenteral thiamine for deficiency risk

Give the local high-risk thiamine regimen before carbohydrate or dextrose administration in prolonged vomiting, severe restriction, alcohol dependence or refeeding risk.

Do not delay urgent glucose for hypoglycaemia, but give thiamine promptly. Parenteral administration needs local anaphylaxis readiness, and wider refeeding electrolytes require active monitoring.

May improve gastric emptying and selected symptoms in objectively supported gastroparesis alongside dietary and metabolic management.

Specialist prokinetic therapy

Use a time-limited current BNF regimen only after obstruction is excluded, with agent choice and duration determined by motility expertise and patient risk.

Metoclopramide can cause acute and tardive movement disorders, domperidone carries cardiac risk and macrolides have interactions and tachyphylaxis. Review rather than continue indefinitely.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Dehydration, alkalosis and kidney injury

Ongoing losses cause hypochloraemia, hypokalaemia, contraction alkalosis, hypotension and impaired renal filtration during sustained or recurrent vomiting.

Aspiration and oesophageal injury

Reduced consciousness or gastric retention increases aspiration risk, while forceful retching can cause Mallory-Weiss tears or full-thickness rupture.

Malnutrition and thiamine deficiency

Persistent vomiting depletes energy, protein and vitamins; carbohydrate given after prolonged poor intake can precipitate neurological or refeeding complications.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Measure fluid balance, urine output, daily or serial weight, postural symptoms and oral tolerance, replacing ongoing gastric losses rather than only the initial deficit.
Repeat sodium, potassium, chloride, bicarbonate, magnesium, glucose, ketones and renal function at a frequency matched to severity and replacement.
Review ECG and adverse effects when QT-prolonging or dopamine-blocking antiemetics are combined or physiology changes.
Monitor nasogastric output, tube position and aspiration risk and document the continuing indication for decompression each day.
For chronic symptoms, track weight, micronutrient risk, food restriction, glycaemic control and functional impact with dietetic and specialist follow-up.
Escalate new focal pain, faeculent or bloody content, fever, neurological signs or failure to respond because the original diagnosis may be wrong.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Content localises imperfectly

Bilious material indicates duodenogastric reflux and makes a purely proximal gastric blockage less likely, but repeated vomiting can alter contents. Faeculent odour with distension strongly raises distal obstruction or fistula.

Alkalosis can perpetuate

Chloride and potassium depletion sustain renal bicarbonate retention, so replacing only water may not correct vomiting-related alkalosis. Urine chloride and clinical context can help in complex cases.

Hot bathing is a clue

Compulsive hot showers can temporarily relieve cannabinoid hyperemesis but are not pathognomonic. The essential therapeutic test is sustained cannabis cessation with follow-up.

Retained food has hazards

A stomach full of retained contents increases aspiration risk during sedation and endoscopy. Communicating this concern changes fasting, decompression, anaesthetic support and procedure timing.

Rumination is not vomiting

Effortless return of recently eaten food without preceding nausea may reflect rumination syndrome. Recognising it opens behavioural breathing treatment and avoids repeated escalation of antiemetics.

11Common pitfallsFrequent interpretation and management errors.

01
Calling persistent vomiting gastroenteritis without checking pregnancy, glucose, ketones, electrolytes and obstruction features.
02
Diagnosing gastroparesis before mechanical gastric or duodenal obstruction has been excluded.
03
Stacking several QT-prolonging antiemetics without ECG, potassium, magnesium or interaction review.
04
Giving carbohydrate loading to a severely malnourished patient without prompt thiamine and refeeding-risk management.
05
Leaving a nasogastric tube without position checks, loss replacement or a daily indication review.
06
Trivialising hyperemesis in pregnancy and overlooking weight, thrombosis, mental-health and nutrition consequences.