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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Nausea and vomiting in advanced illness

Palliative and end-of-life care · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Vomiting with acute instability

Haematemesis, faeculent vomit, peritonism, severe distension, shock, aspiration, neurological deficit or reduced consciousness may indicate bleeding, obstruction, perforation, sepsis or raised intracranial pressure.

Action: Use ABCDE care, protect the airway, stop unsafe oral intake and medicines, obtain intravenous or subcutaneous access and call urgent medical or surgical help within the agreed ceiling. Treat hypoglycaemia and fluid or electrolyte compromise while providing antiemetic relief that does not delay imaging or definitive treatment.

Overview

Identify the dominant nausea mechanism and reversible emergencies, restore a reliable medicine route, choose one mechanism-matched antiemetic with explicit safety checks, and review symptom relief, hydration, nutrition and adverse effects against the person's goals.

Nausea is a subjective urge to vomit and can be more disabling than vomiting itself. Ask the patient to describe pattern rather than selecting a drug from the diagnosis. Early satiety and food retained for hours suggests stasis; colic and obstipation suggests obstruction; vertigo suggests vestibular drive; morning headache suggests intracranial pressure; new opioid or renal decline suggests chemical stimulation. Several mechanisms may coexist.

Assessment must establish urgency and route. Record observations, hydration, urine, oral intake and aspiration risk. Examine the abdomen for distension, tenderness, hernia, mass, ascites and bowel sounds, but recognise that sounds do not reliably exclude obstruction. Perform rectal examination with consent when impaction could change management, avoiding unnecessary trauma in severe neutropenia or thrombocytopenia.

Practice

Two practice questions

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Palliative and end-of-life careOriginal SBA

Mechanism-led antiemetic choice

A patient has early satiety, epigastric fullness and vomiting of food eaten many hours earlier, with no colic or complete obstruction. Which initial antiemetic best matches the likely mechanism?

Choose one answer, then submit
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • NICE NG31 care of dying adultsIndividual nausea assessment, reversible causes, route and antiemetic selection in the last days.
  • Scottish palliative nausea guidelineMechanism-led antiemetic selection, subcutaneous doses and safety cautions.
  • BNF antiemetics summaryUK antiemetic dosing, contraindications, interactions and adverse effects.
  • Scottish bowel obstruction guidelineProkinetic contraindications and medical management of malignant obstruction.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
Mechanism-led prescribing makes response interpretable. Metoclopramide promotes gastric and proximal intestinal motility and blocks dopamine; it suits stasis but may intensify colic against a complete blockage. Haloperidol blocks central dopamine and can help drug or metabolic nausea. Cyclizine has antihistamine and antimuscarinic action for vestibular and pressure-related nausea but can worsen dry mouth, retention, delirium and constipation.

Serotonin antagonists such as ondansetron are valuable for chemotherapy, radiotherapy and selected refractory nausea. They commonly cause constipation and prolong QT, making them a poor uncritical addition during bowel obstruction. Levomepromazine affects several receptor systems and can rescue refractory mixed-mechanism nausea, but sedation and hypotension mean that a low specialist dose and early review are important.

Route failure is a clinical event. If vomiting prevents oral absorption, identify which analgesic, antiseizure, steroid, Parkinson or withdrawal-prevention medicines need urgent replacement. Use a single subcutaneous antiemetic test and build a continuous infusion only after response and compatibility review. Do not put every possible antiemetic into one pump or combine a prokinetic with a strong antimuscarinic without explaining the intended balance.

Hydration and nutrition require separate decisions. Offer mouth care, small sips and preferred bland or cool food when safe. A time-limited parenteral-fluid trial may improve thirst, delirium or renal clearance, but can worsen oedema, ascites and secretion. In the last days, reduced intake is expected; explaining this can reduce family pressure while nausea and dry mouth continue to receive active treatment.

Key points

  • First-line history defines nausea versus retching or vomiting, volume and content, relation to food, movement, medicines, bowels, headache and abdominal pain.
  • Examine hydration, mouth, abdomen, bowel sounds, rectum when indicated, neurology, vestibular signs and current patches, pumps and medicines.
  • Treat the cause when useful: constipation, obstruction, infection, hypercalcaemia, uraemia, gastric stasis, raised intracranial pressure and medicine toxicity need different interventions.
  • Choose the first antiemetic by dominant mechanism rather than prescribing several empirically: prokinetic, dopamine antagonist, antihistamine-antimuscarinic or serotonin antagonist each has a different role.
  • Metoclopramide is first-line for gastric stasis or partial obstruction without colic, but avoid it in complete mechanical obstruction, perforation, Parkinson's disease and previous dystonia.
  • Haloperidol can help chemically mediated nausea from opioids or organ failure; use low doses and review Parkinson, Lewy-body, QT and extrapyramidal risk.
  • Cyclizine can help vestibular or raised-pressure nausea and complete obstruction but adds anticholinergic effects and can oppose a prokinetic when combined without rationale.
  • Switch to subcutaneous, buccal, rectal or transdermal routes when vomiting makes oral absorption unreliable and reconcile essential medicines at the same time.
  • The gold-standard plan states the presumed mechanism, first medicine, rescue, route, response time, adverse-effect checks and a second-line strategy if the formulation is wrong.

Aetiology

01

Chemical and medication causes

Opioids, antibiotics, anticancer treatment, uraemia, hypercalcaemia, hepatic failure, sepsis and toxins stimulate the chemoreceptor trigger zone.

02

Gastric stasis and dysmotility

Autonomic dysfunction, opioids, diabetes, ascites, gastric infiltration and severe illness delay emptying and produce early satiety, reflux and large-volume vomiting.

03

Mechanical obstruction and constipation

Luminal tumour, adhesions, carcinomatosis, faecal impaction and extrinsic compression cause partial or complete interruption of gastrointestinal transit.

04

Central and vestibular causes

Raised intracranial pressure, brainstem disease, motion sensitivity, migraine, anxiety and conditioned treatment responses activate central vomiting pathways.

Pathophysiology

  1. 1
    Chemoreceptor trigger activation

    Circulating medicines and metabolites stimulate dopamine, serotonin and neurokinin receptors in the area postrema outside the blood-brain barrier.

  2. 2
    Vagal afferent signalling

    Gastric or intestinal distension, inflammation and chemotherapy release serotonin and activate vagal pathways to the medullary vomiting network.

  3. 3
    Vestibular signalling

    Histamine and muscarinic pathways carry motion and labyrinthine disturbance to the vomiting centre, producing nausea with vertigo or movement.

  4. 4
    Pressure-mediated vomiting

    Intracranial mass, oedema or hydrocephalus activates central pathways and may produce vomiting with little preceding nausea.

  5. 5
    Motor evacuation response

    Coordinated diaphragmatic, abdominal, gastric and oesophageal activity expels contents but risks aspiration, dehydration and mucosal injury when recurrent.

Clinical features and red flags

Chemical nausea

Persistent nausea with little relation to meals after opioid, chemotherapy, renal, calcium or hepatic change suggests chemoreceptor stimulation.

Gastric stasis

Early satiety, reflux, epigastric fullness and large vomits containing old food points to delayed gastric emptying.

Mechanical obstruction

Colic, distension, reduced stool or flatus and bilious or faeculent vomiting supports partial or complete bowel obstruction.

Vestibular pattern

Vertigo, movement provocation, nystagmus and nausea out of proportion to abdominal findings suggests labyrinthine or central vestibular input.

Raised-pressure pattern

Progressive morning headache, vomiting, focal neurology, seizure or cognitive change requires urgent brain assessment.

Aspiration riskRed flag

Drowsiness, bulbar dysfunction, cough failure or active large-volume vomiting threatens airway contamination and requires immediate positioning and support.

Red flags requiring action

  • Colicky pain, distension, constipation or obstipation and faeculent vomiting suggests mechanical bowel obstruction and makes routine prokinetic treatment unsafe in complete obstruction.
  • Rigid abdomen, rebound, fever, lactate rise or haemodynamic instability suggests perforation, ischaemia or peritonitis and requires urgent surgical assessment.
  • Haematemesis, coffee-ground material, melaena, syncope or anticoagulant exposure requires acute gastrointestinal-bleeding management.
  • Progressive morning headache, projectile vomiting, focal neurology, seizure or altered consciousness suggests raised intracranial pressure.
  • Polyuria, dehydration, constipation, confusion or arrhythmia may indicate hypercalcaemia and needs urgent calcium and renal assessment.
  • Repeated vomiting with poor urine output, postural hypotension or marked electrolyte disturbance threatens renal injury, delirium and arrhythmia.
  • New dystonia, akathisia, rigidity, QT symptoms or profound sedation after antiemetic therapy requires immediate medicine review.

Investigations

  1. 01
    First-line mechanism historyFirst stepFirst line
    Why
    Link symptoms with meals, bowel function, movement, medicines, headache, pain, treatment and vomiting content and timing.
    Interpretation and limitations
    Select the most likely receptor and motility mechanism while identifying bleeding, obstruction and neurological emergency features.
  2. 02
    Hydration and abdominal examination
    Why
    Assess pressure, pulse, mucosa, urine, distension, tenderness, hernia, mass, ascites, bowel sounds and peritoneal signs.
    Interpretation and limitations
    Instability or peritonism accelerates emergency imaging and surgical review; benign examination does not fully exclude partial obstruction.
  3. 03
    Rectal examination when indicated
    Why
    Detect rectal loading, tumour, bleeding or an empty rectum when constipation or distal obstruction may change treatment.
    Interpretation and limitations
    Findings guide suppository, enema or obstruction work-up; obtain consent and consider neutropenia, thrombocytopenia, pain and trauma risk.
  4. 04
    Targeted blood tests
    Why
    Check glucose, renal and liver function, calcium, sodium, potassium, inflammation and full blood count where correction is plausible.
    Interpretation and limitations
    Results identify metabolic mechanism and determine antiemetic, hydration, steroid and opioid safety in renal or hepatic impairment.
  5. 05
    Abdominal or brain imaging
    Why
    Use CT abdomen for suspected obstruction or complication and urgent CT or MRI brain for pressure or focal neurological features.
    Interpretation and limitations
    Imaging should answer a treatment-changing question and should not be delayed by repeated empirical antiemetic trials when red flags are present.
  6. 06
    Observed antiemetic trial
    Why
    Give one mechanism-matched medicine by a reliable route and assess nausea, vomiting, oral intake, alertness and adverse effects.
    Interpretation and limitations
    Meaningful response supports the formulation; failure prompts mechanism review before adding another agent and is the practical clinical benchmark.

Differential diagnosis

01

Complete bowel obstruction

Obstipation, colic, marked distension and high-volume or faeculent vomit favour a mechanical block and contraindicate routine metoclopramide.

02

Gastric outlet delay

Early satiety, epigastric fullness, succussion and large food-containing vomit hours after eating suggests impaired gastric emptying or outlet obstruction.

03

Raised intracranial pressure

Progressive headache, focal deficit, seizure, papilloedema and morning or projectile vomiting requires urgent brain imaging and specialist assessment.

04

Metabolic nausea

Confusion, thirst, oliguria, jaundice or systemic decline points to calcium, renal, hepatic, glucose, infection or medicine-related chemical stimulation.

05

Vestibular or cortical nausea

Vertigo, movement trigger, anticipatory pattern, odour sensitivity or anxiety without abdominal signs suggests vestibular or higher-centre contribution.

Management

01Initial nauseaFormulate mechanism and secure the routeFirst stepNausea or vomiting is new, changed or inadequately controlled.+
  1. 1Identify emergency features, assess hydration and aspiration, examine abdomen and neurology and reconcile bowel pattern, medicines and essential oral treatment.
  2. 2Treat reversible contributors and choose one antiemetic whose receptor and motility action fits the dominant mechanism and organ-function risks.
  3. 3Use a reliable route, prescribe rescue and review within the drug's onset window, documenting response, toxicity and the next branch if symptoms persist.
02Suspected obstructionAvoid prokinetic harm in complete blockageVomiting accompanies colic, distension and reduced stool or flatus.+
  1. 1Stop unsafe oral intake and stimulant or bulk laxatives, assess peritonism and hydration and obtain CT and surgical or oncology review according to goals.
  2. 2Use metoclopramide only when obstruction is partial and there is no colic, while complete obstruction requires non-prokinetic antiemetic and antisecretory treatment.
  3. 3Provide non-oral analgesia, decompression or intervention as appropriate and review fluid, mouth care and nutrition separately.
03Refractory symptomsReassess before combining antiemeticsA correctly delivered first antiemetic does not achieve acceptable relief or causes limiting harm.+
  1. 1Check adherence, pump and site, route, obstruction status, constipation, pressure, metabolic change and whether the presumed mechanism remains credible.
  2. 2Switch to or add a pharmacologically complementary agent such as levomepromazine under specialist guidance, avoiding opposing or duplicative adverse effects.
  3. 3Set a new response time, monitor sedation, QT, movement disorder, bowel and bladder effects and simplify once control is achieved.
04Last-days careRelieve nausea without burdensome investigationThe person is recognised to be dying and invasive diagnosis cannot improve an agreed outcome.+
  1. 1Check comfort-relevant causes such as retention, impaction, medicine toxicity and pump failure and explain reduced intake to family.
  2. 2Use a patient-specific subcutaneous antiemetic and rescue, mouth care, positioning and small sips if safe, avoiding routine fluid without a symptom goal.
  3. 3Review comfort and adverse effects at least daily and after every rescue and adjust the pump only from actual response and compatibility evidence.
Key medicines and prescribing safety5 treatments · regimens, roles and cautions+
Promotes gastric emptying and blocks dopamine for nausea caused by stasis, gastroparesis or selected partial obstruction without colic.

Metoclopramide for gastric stasis

Give 10 mg orally or subcutaneously up to three times daily for a reviewed trial, reducing dose and extending interval in renal impairment according to the BNF and local palliative protocol.

Avoid in complete mechanical obstruction, perforation, Parkinson's disease or previous dystonia; monitor akathisia, extrapyramidal effects, diarrhoea and opposing antimuscarinic treatment.

Blocks central dopamine and can relieve nausea driven by opioids, uraemia, hypercalcaemia or other circulating chemical stimuli.

Haloperidol for chemical nausea

Start 500 micrograms to 1.5 mg orally or subcutaneously once daily or as a protocol-defined dose in a frail palliative adult, using the lowest effective total and reducing with hepatic impairment.

Avoid routine use in Parkinson's disease or Lewy-body dementia; review QT, electrolytes, akathisia, rigidity, swallowing and interacting antipsychotics.

Provides antihistamine and antimuscarinic treatment for vestibular nausea, raised intracranial pressure and selected complete-obstruction symptoms.

Cyclizine for vestibular or pressure-related nausea

Give 50 mg orally or subcutaneously up to three times daily under the local protocol, with lower or less frequent dosing considered in frailty or hepatic impairment.

Dry mouth, retention, blurred vision, constipation, delirium and injection-site irritation occur; avoid unreasoned combination with prokinetic metoclopramide.

Complications

01

Aspiration

Reduced consciousness, dysphagia or repeated vomiting can contaminate the airway, causing obstruction, chemical pneumonitis, infection and respiratory failure.

02

Fluid and electrolyte loss

Vomiting causes dehydration, potassium and chloride depletion, alkalosis, kidney injury, weakness, delirium and potentially dangerous cardiac arrhythmia.

03

Medicine-route failure

Oral analgesic, antiseizure, corticosteroid and antiemetic absorption becomes unreliable, precipitating pain, withdrawal or recurrent neurological symptoms.

04

Malnutrition and distress

Persistent nausea suppresses intake, worsens cachexia and transforms food, smell and medication into feared triggers for patients and families.

05

Antiemetic toxicity

Dopamine blockade, anticholinergic burden, QT prolongation, sedation, constipation and extrapyramidal effects can create new symptoms or worsen obstruction.

Monitoring and follow-up

  • Record nausea severity, vomit frequency and content, oral intake and the patient-selected function after each treatment change.
  • Monitor hydration, urine, weight, sodium, potassium and renal function during persistent losses or fluid trials.
  • Review bowel movement, flatus, distension and colic daily when obstruction or constipating antiemetics are possible.
  • Check alertness, postural pressure, akathisia, dystonia, rigidity, QT symptoms, dry mouth and retention during antiemetic therapy.
  • Inspect subcutaneous sites and pump delivery and count rescue response before increasing a continuous infusion.
  • Reconcile essential oral medicines whenever vomiting worsens and confirm an alternative route where omission risks pain, seizure or withdrawal.
  • Review renal and hepatic function after acute illness and adjust metoclopramide, opioid, ondansetron and sedating agents accordingly.

Special situations

Pattern predicts receptor

Meal delay, movement, chemical exposure, colic and headache often identify a more rational first antiemetic than the diagnosis label.

One trial teaches more

Starting several agents together hides which mechanism responded and compounds sedation, QT and anticholinergic harm.

Prokinetic can increase colic

Driving contractions against a complete mechanical block may intensify pain and vomiting rather than restore transit.

Antiemetics can oppose

Cyclizine's antimuscarinic action can counter a prokinetic strategy, so combination needs a deliberate reason.

Oral failure extends beyond antiemetic

Vomiting can remove analgesic, steroid, antiseizure and Parkinson treatment and trigger a second clinical crisis.

Intake pressure worsens nausea

Small wanted portions and family reassurance are often kinder than urging calories into a nauseated person.

Common pitfalls

  1. 01

    Selecting an antiemetic without asking about bowels, meals, movement and headache.

  2. 02

    Giving metoclopramide in complete mechanical obstruction or perforation.

  3. 03

    Using haloperidol in Parkinson's disease without specialist advice.

  4. 04

    Combining prokinetic and antimuscarinic medicines without a mechanism rationale.

  5. 05

    Adding ondansetron while ignoring severe constipation and QT risk.

  6. 06

    Continuing oral medicines despite repeated unabsorbed vomiting.

  7. 07

    Putting several untested antiemetics into a syringe pump.

  8. 08

    Attributing every episode to cancer and missing hypercalcaemia or raised intracranial pressure.

  9. 09

    Giving routine parenteral fluid without a symptom target and stop rule.

  10. 10

    Measuring success by absence of vomit while persistent nausea remains severe.

Treats chemotherapy, radiotherapy, postoperative and some refractory serotonin-mediated nausea when a 5-HT3 antagonist fits the mechanism.

Ondansetron for serotonin-mediated nausea

Use 4 mg orally, sublingually or intravenously twice daily initially for a selected indication, increasing only under the BNF or oncology protocol with renal, hepatic and QT review.

Constipation, headache and QT prolongation are important; severe hepatic impairment limits the daily dose and complete obstruction requires particular bowel caution.

Blocks several dopamine, histamine, muscarinic and serotonin pathways and can relieve refractory nausea with overlapping mechanisms.

Levomepromazine for refractory mixed nausea

A specialist palliative regimen may start 6.25 mg orally at night or 6.25 mg subcutaneously as needed, using a low reviewed 24-hour infusion only when repeated benefit and compatibility support it.

Marked sedation, hypotension, anticholinergic effects, QT prolongation and extrapyramidal reactions occur; use lower exposure in frailty and hepatic impairment.