Red flags
- Nausea + severe headache + visual change - raised ICP (brain metastases)
- Nausea + absolute constipation + distension - bowel obstruction
- Nausea + polyuria/polydipsia/confusion - hypercalcaemia
- Nausea after opioid dose increase with drowsiness/pinpoint pupils - opioid toxicity, not a primary GI problem
- Persistent vomiting preventing oral intake of essential medications (esp. anti-seizure, cardiac) - needs an urgent alternate route
Differential by mechanism
By mechanism -> maps directly to receptor and drug choice
| Mechanism | Trigger | Key receptor | Example causes |
|---|---|---|---|
| Chemical/metabolic (CTZ) | Drugs, opioids, uraemia, hypercalcaemia, sepsis | D2, 5-HT3 | Opioids, chemotherapy, renal/hepatic failure |
| Gastric stasis/outlet | Delayed gastric emptying | D2 (gut) | Opioids, ascites, hepatomegaly, autonomic failure |
| Bowel obstruction | Mechanical or pseudo-obstruction | Multiple | Peritoneal disease, faecal impaction, tumour |
| Vestibular | Movement, base-of-skull disease | H1, ACh | Opioids (some), vestibular pathology |
| Cortical/anxiety | Anticipatory, raised ICP | GABA, H1 | Anxiety, brain metastases, meningeal disease |
- Many patients have more than one mechanism active simultaneously
Focused history
- Timing relative to meals, movement, medication dosing
- Volume and content of vomit - undigested food (gastric stasis), faeculent (obstruction)
- Associated headache, vertigo, abdominal pain/distension, bowel habit
- Full medication review - opioids are the commonest reversible cause, also chemotherapy, antibiotics, iron
- Anticipatory nausea (conditioned response, esp. with chemotherapy) vs a new organic cause
Focused examination
- Abdominal distension, bowel sounds (absent/tinkling -> obstruction), succussion splash (gastric stasis)
- Signs of dehydration
- Neurological exam if headache or any suggestion of raised ICP
- Assess hydration/oral intake tolerance to decide route of antiemetic delivery
Investigation strategy
- Directed by suspected mechanism, and only if the result will change management
- Calcium, renal function - readily reversible metabolic causes
- Abdominal X-ray/CT if obstruction suspected
- Medication review is itself the most useful "test" - trial withdrawal/substitution of a likely culprit drug
Management
Match the antiemetic to the mechanism
| Mechanism | First-line antiemetic |
|---|---|
| Chemical/metabolic (opioid, drug, metabolic) | Haloperidol (low dose) - potent D2 antagonist at the CTZ |
| Gastric stasis | Metoclopramide (prokinetic) - avoid if complete mechanical obstruction/colic - risk of worsening cramping |
| Bowel obstruction | See obstruction-specific management - avoid prokinetics; hyoscine butylbromide for colic, consider octreotide to reduce secretions |
| Vestibular | Cyclizine or other antihistamine |
| Cortical/raised ICP | Dexamethasone + treat the cause; cyclizine as adjunct |
| Chemotherapy-induced | 5-HT3 antagonist (ondansetron) +/- dexamethasone +/- NK1 antagonist (aprepitant) per emetogenicity |
General principles
- Broad-spectrum agents (levomepromazine/methotrimeprazine) - useful when mechanism unclear or multiple mechanisms active, or first-line agent fails
- Regular dosing, not just PRN, once a cause is identified and ongoing
- Non-oral route (subcutaneous, buccal) if vomiting prevents reliable oral absorption
- Reassess response within 24h and switch class rather than simply escalating the dose of an ineffective agent
- Address reversible contributors alongside drug therapy - laxatives for constipation, treat hypercalcaemia, review/reduce causative drugs
Traps
- Escalating the dose of an antiemetic that targets the wrong receptor instead of switching class to match the mechanism
- Using metoclopramide in complete/suspected mechanical bowel obstruction - worsens colic
- Attributing all nausea to "the cancer" without checking calcium and reviewing the drug chart - opioids and hypercalcaemia are both readily addressed
- Relying on oral antiemetics in a patient who is vomiting them back up - switch route
- Stopping an effective antiemetic too early - opioid-induced nausea settles over days, but disease-related nausea usually needs ongoing regular dosing
Talk track
1. Find the mechanism before choosing the drug
- "Nausea has five common mechanisms, each with a different best-fit antiemetic - I don't reach for ondansetron by default."
2. Check the reversible causes first
- "Calcium, renal function, and the drug chart - opioids and hypercalcaemia are both fixable."
3. Match drug to mechanism, and know the exception
- "Haloperidol for chemical causes, metoclopramide for stasis - but never a prokinetic if obstruction is on the table."
4. Reassess and switch class, not just dose
- "If it's not working in 24 hours, I change the mechanism I'm targeting, not just the dose."
5. Protect the oral route
- "If they can't keep it down, the antiemetic goes subcutaneous too."
8 of 8 sections written · drafted 2026-09-13