Emetic agents: complete clinical overview
Emetics are substances that provoke emesis (vomiting). They were once used after poisoning to empty the stomach. Current toxicology practice has moved away from induced emesis because it rarely improves outcome, can delay definitive care and may cause aspiration or further injury. This lesson preserves the historical pharmacology and doses for examination purposes, while making the modern emergency approach explicit.
Learning objectives
- Describe the neural and gastrointestinal pathways that produce vomiting.
- Classify emetics as central or reflex/peripheral agents.
- Explain the historical mechanisms, doses and limitations of apomorphine and ipecac.
- Recognise when vomiting must never be induced after an ingestion.
- Apply a modern, airway-first approach to the poisoned patient.
Why uncontrolled vomiting matters
Repeated vomiting can cause dehydration, potassium and chloride loss, metabolic alkalosis, malnutrition, aspiration and tears at the gastro-oesophageal junction. In a patient with poisoning, the greatest immediate danger may be loss of airway reflexes and aspiration rather than the poison remaining in the stomach. These facts explain why a treatment intended to cause vomiting must have a very high safety threshold.
Physiology of emesis
Coordinating centres
- Vomiting centre: a functional network in the dorsolateral medulla/lateral reticular formation. It organises salivation, retching, closure of the glottis, reverse peristalsis, abdominal contraction and expulsion.
- Nucleus tractus solitarius (NTS): integrates vagal visceral afferents, pharyngeal input and brainstem signalling.
- Chemoreceptor trigger zone (CTZ): in the area postrema on the floor of the fourth ventricle. It lies outside the blood-brain barrier, so it can detect emetogenic substances in blood and cerebrospinal fluid.
Afferent inputs that can trigger vomiting
| Input | Typical stimulus | Important receptors/signals |
|---|---|---|
| Gastrointestinal tract and pharynx | Irritants, distension, infection, chemotherapy | Vagal/spinal afferents; 5-HT3, NK1, cholinergic pathways |
| CTZ/area postrema | Drugs, toxins, uraemia, metabolic disturbance | D2, 5-HT3, opioid and other receptors |
| Vestibular apparatus | Motion sickness | H1, M1 |
| Higher cortex/limbic system | Fear, pain, sights, smells, anticipatory nausea | Multiple pathways |
Chemotherapy and gut serotonin pathway
Cytotoxic drugs, radiation and luminal irritants can stimulate enterochromaffin cells in the intestinal mucosa to release serotonin (5-hydroxytryptamine, 5-HT). Serotonin activates 5-HT3 receptors on enteric extrinsic primary afferent neurones. Signals then travel through vagal and spinal visceral afferents to the NTS and CTZ. Circulating 5-HT may also stimulate the CTZ directly. This pathway is why 5-HT3-receptor antagonists are major antiemetics.
Classification of emetic agents
Central emetic
Apomorphine stimulates dopamine D2 receptors in the CTZ. It historically produced rapid vomiting after parenteral administration.
Reflex/peripheral emetic
Ipecacuanha (ipecac) irritates gastric mucosa and its alkaloids also stimulate the CTZ.
Historical gastric irritants
Mustard preparations and concentrated salt solutions were used historically. They have no role in safe contemporary care.
Apomorphine
Apomorphine is a semi-synthetic derivative of morphine but its key pharmacological action is dopamine agonism. In the CTZ it stimulates D2 receptors and produces vomiting. It was historically given by injection because oral administration was slow and unreliable for the emetic purpose.
| Feature | Key point |
|---|---|
| Historical emetic dose | 6 mg IM or SC, with vomiting historically expected within about 5 minutes. |
| Current status | Not a current human-poisoning emetic. There is no recommended modern emetic dose for home or routine emergency use. |
| Major danger | Central nervous system and respiratory depression, hypotension, reduced airway protection and aspiration. |
| Current therapeutic role | Used in selected patients for Parkinson disease “off” episodes under specialist prescribing; nausea and vomiting are adverse effects. |
Ipecacuanha (ipecac)
Ipecac was prepared from the dried root of Cephaelis ipecacuanha. Important alkaloids include emetine and cephaeline. It acts in two ways: local irritation of gastric mucosa evokes a reflex response, while absorbed alkaloids can stimulate the CTZ. Vomiting often occurred only after 15 minutes or longer, which limited usefulness in urgent poisoning.
| Historical teaching dose from the supplied slide deck | Modern interpretation |
|---|---|
| Adults: 15–30 mL syrup of ipecac | For historical/exam recognition only. Ipecac is not recommended for routine poisoning management in adults or children; it should not be kept or administered as household poisoning first aid. |
| Children: 10–15 mL | |
| Infants: 5 mL |
Historic dose lists do not establish a safe practice. Evidence showed that ipecac removes only a variable amount of stomach contents, becomes less effective as time passes, may lead to prolonged vomiting and can delay activated charcoal, antidotes and transport. Modern toxicology position statements therefore advise against routine use at the scene or in the emergency department.
Mustard and concentrated salt solutions
Powdered mustard and strong salt water were formerly used as gastric irritants. They are not medicines for poisoning and there is no safe recommended dose. Salt loading can cause dangerous hypernatraemia, seizures and brain injury; forced fluids and vomiting also create aspiration risk. Mustard can injure or irritate the gastrointestinal tract and does not provide reliable decontamination.
When emesis must never be induced
| Situation | Why vomiting is dangerous or ineffective |
|---|---|
| Corrosives: strong acids or alkalis | Vomiting re-exposes the oesophagus and mouth to the corrosive substance and can worsen burns, bleeding or perforation. |
| Hydrocarbons: kerosene, petrol, diesel and many solvents | Even a small aspiration can cause severe chemical pneumonitis. |
| Reduced consciousness, seizures, absent gag/cough reflexes | The patient cannot protect the airway; aspiration is likely. |
| Convulsant or CNS-stimulant poisoning | Seizures can occur suddenly during vomiting; airway loss and trauma are major risks. |
| Opioid, sedative or phenothiazine poisoning | Emetics may be ineffective and sedation further increases aspiration risk. |
| Ingestion of sharp objects or a substance with a specific antidote plan | Vomiting may cause mechanical injury or delay the appropriate antidote and specialist pathway. |
Complications of induced emesis
- Aspiration: gastric content entering the lungs may cause obstruction, aspiration pneumonia or chemical pneumonitis.
- Airway loss: especially with alcohol, opioids, head injury, post-ictal states or sedatives.
- Caustic re-injury: repeated oesophageal exposure after acid or alkali ingestion.
- Electrolyte and fluid disturbance: prolonged vomiting can cause dehydration, hypokalaemia and metabolic alkalosis.
- Delayed definitive care: emesis may delay charcoal, antidotes, resuscitation, transfer and expert toxicology advice.
- Trauma: retching can cause mucosal tears and rarely rupture in susceptible patients.
Modern emergency approach to a poisoned patient
1. Start with ABCDE, not gastric emptying
Assess and support airway, breathing, circulation, disability and exposure. Give oxygen and ventilatory support when indicated. Check glucose, vital signs, mental state and ECG where relevant. A drowsy or seizing patient requires airway-centred resuscitation.
2. Obtain the exposure history
Identify the substance, formulation, estimated amount, time of ingestion, co-ingestants, symptoms, patient weight, medical conditions and medicines. Preserve the container, blister pack or label if safe to do so.
3. Contact expert help early
Follow local emergency and poison-centre advice. Do not delay transport to attempt a home remedy. In Uganda or any setting without immediate toxicology support, stabilise and refer urgently using local emergency pathways.
4. Use gastrointestinal decontamination selectively
Activated charcoal may be considered only after clinical assessment for a toxin that binds charcoal, with a protected airway and an appropriate time window. A commonly taught clinician-directed single dose is 1 g/kg orally or by nasogastric tube (usual maximum 50 g). It is not routine first aid and is not useful for every poison.
5. Escalate to specific treatment
Use the appropriate antidote, enhanced elimination method, monitoring and critical-care support when indicated. Gastric lavage is exceptional, restricted to selected life-threatening ingestions, and must be performed by an experienced team with airway protection; there is no home lavage dose or technique.
Clinical applications and cases
Case 1: kerosene ingestion in a child
A toddler is brought after drinking an unknown amount of kerosene. The key danger is aspiration pneumonitis. Do not give an emetic, milk, oil, salt water or a large drink. Assess breathing, oxygen saturation and mental state, keep the child upright if conscious, and refer urgently for clinical assessment.
Case 2: suspected caustic ingestion
A patient has painful swallowing and drooling after a cleaning liquid. Do not induce vomiting or attempt chemical neutralisation. Protect the airway, keep the patient nil by mouth until assessed when appropriate, identify the product and arrange urgent specialist evaluation.
Case 3: sedative overdose with drowsiness
A drowsy patient cannot safely swallow and may aspirate. The priority is airway positioning, oxygenation, monitoring, glucose testing and urgent emergency transfer—not ipecac or any oral home treatment.
Dose and prescribing examination table
| Agent/intervention | Dose | Clinical status |
|---|---|---|
| Apomorphine | Historical emetic teaching: 6 mg IM/SC | Not recommended for modern poisoning; no self-administered emetic dose. |
| Syrup of ipecac | Historical slide doses: adult 15–30 mL; child 10–15 mL; infant 5 mL | Not recommended; no current routine emetic dose. |
| Mustard or concentrated salt water | No safe dose | Never use to induce vomiting. |
| Activated charcoal | Common clinician-directed single dose: 1 g/kg PO/NG; usual maximum 50 g | Only after professional toxicology/clinical assessment and with a protected airway. |
High-yield revision points
- The CTZ is in the area postrema and is outside the blood-brain barrier.
- Apomorphine causes emesis by D2-receptor stimulation in the CTZ.
- Ipecac acts both by gastric irritation and CTZ stimulation, but is obsolete for routine poisoning care.
- Never induce vomiting after corrosive or hydrocarbon ingestion or when consciousness is impaired.
- Modern poisoning management prioritises ABCDE resuscitation, early expert advice and selected—not automatic—decontamination.
- Historical doses are examination facts, not instructions for patient use.
