Why this poison is interesting

Every other pharmaceutical page in this library takes a class and finds the property its members share. This page does the opposite. Olanzapine, quetiapine and haloperidol are prescribed for the same indications and share one receptor target, and their three UK overdose sections describe three genuinely different poisonings.¹²³ Haloperidol's most prominent features are severe extrapyramidal reactions, hypotension and sedation.³ Olanzapine's are tachycardia, agitation and aggressiveness, dysarthria, extrapyramidal symptoms and reduced consciousness, each in over 10% of overdose cases.¹ Quetiapine's are drowsiness, tachycardia, hypotension and anticholinergic effects, escalating to QT prolongation, seizures, status epilepticus and rhabdomyolysis.²

The one thing they do share is a warning, and it is printed on all three labels in three different forms. Adrenaline is contraindicated. Quetiapine's label: epinephrine and dopamine should be avoided, since beta stimulation may worsen hypotension in the setting of quetiapine-induced alpha blockade.² Olanzapine's: do not use epinephrine, dopamine, or other sympathomimetic agents with beta-agonist activity since beta stimulation may worsen hypotension.¹ Haloperidol's: adrenaline must not be used because it might cause profound hypotension in the presence of haloperidol.³ Three independent regulator-approved documents, one instruction.

The third reason is a pharmaceutical one. Quetiapine's extended-release tablets form a bezoar. The label states that in extended-release overdose gastric bezoar formation has been reported and appropriate diagnostic imaging is recommended, that routine gastric lavage may not be effective in the removal of the bezoar due to gum like sticky consistency of the mass, and that endoscopic pharmacobezoar removal has been performed successfully in some cases.⁴ A label recommending imaging and endoscopy for a tablet is describing a poisoning whose timeline is set by a physical object.

A poison is a drug whose kinetics have escaped its pharmacology.

The toxic principle

An antipsychotic is defined by dopamine D2 antagonism and characterised, in overdose, by everything else it binds. The five receptor families that matter are D2, alpha-1 adrenergic, muscarinic, histamine H1, and — as a channel rather than a receptor — the cardiac potassium current that determines the QT interval.

The adrenaline paradox, explained by the labels themselves

Adrenaline acts at alpha-1 receptors, where it causes vasoconstriction, and at beta-2 receptors, where it causes vasodilatation. In a normal patient the alpha effect dominates and the net result is a rise in blood pressure. In a patient whose alpha-1 receptors are blocked by an antipsychotic, only the beta-2 effect remains — so adrenaline vasodilates. Quetiapine's label puts it in exactly those terms: beta stimulation may worsen hypotension in the setting of quetiapine-induced alpha blockade.² Olanzapine's extends the warning to other sympathomimetic agents with beta-agonist activity¹, and haloperidol's states adrenaline might cause profound hypotension in the presence of haloperidol.³ This is the same argument as the cocaine page's unopposed-alpha phenomenon, running in the opposite direction — and unlike that one, it is stated on three labels rather than inferred from case reports. Established

The corollary is what to give instead. Both quetiapine's and haloperidol's labels direct treatment of hypotension with fluids and sympathomimetics — quetiapine's says intravenous fluids and/or sympathomimetic agents while excluding adrenaline and dopamine², and haloperidol's names dopamine or noradrenaline while excluding adrenaline.³ The three labels disagree about dopamine, and that disagreement is real: olanzapine's and quetiapine's exclude it because of its beta activity¹², haloperidol's includes it.³ A predominantly alpha-1 agonist is the mechanistically consistent choice across all three, which is what noradrenaline is.

Two further mechanisms deserve naming because they produce the most severe presentations. Quetiapine lowers the seizure threshold — its label lists seizures, status epilepticus and rhabdomyolysis among overdose effects² — and all three prolong the QT interval, with haloperidol's label warning that the risk of ventricular arrhythmias, possibly associated with QTc prolongation, must be considered.³

Toxicokinetics

The three drugs' kinetics diverge as much as their clinical pictures do, and the divergences are the reason the observation periods differ. The table takes each label in turn where they differ.

Olanzapine, quetiapine and haloperidol — three labels, three answers
Parameter	Therapeutic	In overdose	Why it changes
Absorption	Olanzapine: peak plasma concentrations within 5 to 8 hours, unaffected by food¹. Haloperidol: peak within 2 to 6 hours, bioavailability 60 to 70%³	Correspondingly late peaks	Olanzapine's five-to-eight-hour peak is the longer of the two the labels quantify, and is a plain argument against short observation. Quetiapine's label gives no time to peak at all. A patient assessed at four hours has not been assessed at the peak.
Extended-release absorption	Quetiapine XL: same drug, formulation-controlled release⁴	Delayed peak sedation, delayed peak pulse and prolonged recovery compared with immediate-release quetiapine overdose⁴	The label states the difference in overdose terms rather than in pharmacokinetic ones, which is unusually direct. It is the same trap as the modified-release calcium-channel blockers, with the additional bezoar problem below.
The pharmacobezoar	—	Gastric bezoar formation has been reported ... appropriate diagnostic imaging is recommended; routine gastric lavage may not be effective ... due to gum like sticky consistency of the mass; endoscopic pharmacobezoar removal has been performed successfully in some cases⁴	A physical object inside the stomach, releasing drug on its own schedule. Nothing else in this library has a kinetics row that is answered by an endoscope. The clinical consequence is that the exposure has no predictable end until the mass is dealt with.
Protein binding	Olanzapine about 93% (albumin and alpha-1-acid glycoprotein)¹; quetiapine approximately 83%²; haloperidol 88 to 92%, with high inter-subject variability³	Unchanged	All three are highly bound, and all three therefore fail the first test for dialysability. Haloperidol's label draws the conclusion explicitly — see the final row.
Volume of distribution	Haloperidol: 8 to 21 L/kg after intravenous dosing; crosses the blood–brain barrier easily³	Unchanged	Eight to twenty-one litres per kilogram is enormous — of the same order as the argument that defeats extracorporeal removal on the digoxin page. Haloperidol's label cites both this and the protein binding as its reasons.
Metabolism	Olanzapine: conjugative and oxidative; the major circulating metabolite, the 10-N-glucuronide, does not pass the blood–brain barrier, and the predominant pharmacological activity is the parent's¹. Quetiapine: CYP3A4 primarily, to the active norquetiapine². Haloperidol: CYP3A4 and CYP2D6; metabolites not considered to contribute significantly³	Pathways unchanged	Only quetiapine has a clinically active metabolite, and norquetiapine's half-life is longer than the parent's². Olanzapine's label makes the pharmacologically decisive point about its own metabolite: it cannot reach the brain.
Half-life	Olanzapine 33.8 h in non-elderly, 51.8 h in the elderly¹. Quetiapine about 7 h, norquetiapine about 12 h². Haloperidol on average 24 h (range of means 15 to 37)³	Prolonged in the elderly and in hepatic impairment	A threefold spread across three drugs of the same class. Olanzapine's elderly figure is the outlier that matters: a half-life of over two days in the population most likely to be prescribed it and most likely to fall.
Elimination	Olanzapine: about 57% of radiolabelled drug in urine, principally as metabolites; no significant difference in half-life with creatinine clearance below 10 mL/min¹. Quetiapine: 73% urine, 21% faeces, under 5% as free drug². Haloperidol: 33% urine, 21% faeces, under 3% unchanged³	Little changed by renal impairment	All three are eliminated as metabolites rather than as parent drug, so renal failure changes surprisingly little. Olanzapine's label states this directly, comparing severe renal impairment with health and finding no significant difference.¹
Clearance modifiers	Olanzapine clearance is lower in the elderly, in females and in non-smokers — half-life 38.6 h non-smoking versus 30.4 h smoking¹	Unchanged	Smoking status altering a drug's half-life by a quarter is a genuine and under-appreciated modifier, mediated by CYP1A2 induction. The label notes the effect is small relative to overall between-individual variability.¹
Dialysability	—	No. Haloperidol's label: dialysis is not recommended in the treatment of overdose because it removes only very small amounts of haloperidol, and separately because of the high haloperidol distribution volume and its high protein binding, only very small amounts are removed by dialysis³. EXTRIP has published no recommendation covering any antipsychotic⁵	Haloperidol's label states both the conclusion and its two premises, and both premises are checkable on the same document: 8–21 L/kg³ and 88–92% binding.³ The argument generalises to olanzapine (93% bound¹) and quetiapine (83%²). This is an EXTRIP absence that costs nothing.

Metabolism and the metabolites

Only one of the three has a metabolite that matters, and one has a metabolite whose irrelevance is itself instructive.

Three antipsychotics — and the one active metabolite between them

Olanzapine, quetiapine or haloperidolAll three are already fully active. No bioactivation anywhere in this class
Olanzapine — conjugation and oxidation¹10-N-glucuronideThe major circulating metabolite, and it does not pass the blood–brain barrier¹. A metabolite that cannot reach the target organ
Quetiapine — CYP3A4²NorquetiapineActive. Steady-state peak molar concentrations 35% of quetiapine's; half-life about 12 h against the parent's 7 h²
Haloperidol — CYP3A4, CYP2D6, glucuronidation, ketone reduction³Reduced haloperidol and othersNot considered to make a significant contribution, though the reduction pathway accounts for about 23% of biotransformation and back-conversion cannot be fully ruled out³
The overdose syndromeWhich features dominate depends on which affinities the particular drug has¹²³

Elimination and accumulation

The three drugs are eliminated slowly, by metabolism, and largely as metabolites — so renal failure matters little and hepatic function matters more. What accumulates in a clinically important way is drug in the stomach, not drug in the blood.

The quetiapine XL bezoar is the most unusual elimination problem in the library

The extended-release label describes it in three sentences that between them define a management problem: gastric bezoar formation has been reported after extended-release quetiapine overdose; appropriate diagnostic imaging is recommended to further guide patient management; routine gastric lavage may not be effective in the removal of the bezoar due to gum like sticky consistency of the mass; and endoscopic pharmacobezoar removal has been performed successfully in some cases.⁴ This is not delayed absorption in the ordinary sense. A modified-release tablet dissolves on a schedule the manufacturer designed. A bezoar is an unplanned physical object of unknown size releasing drug at an unknown rate, and the label's own answer to it is imaging and endoscopy rather than pharmacology. The extended-release label adds that in extended-release overdose there is delayed peak sedation, delayed peak pulse and prolonged recovery.⁴ The immediate-release label carries no such sentence.

Olanzapine's accumulation problem is demographic rather than mechanical. Its half-life is 51.8 hours in healthy subjects aged 65 and over against 33.8 hours in non-elderly¹, and clearance is additionally lower in females and in non-smokers.¹ The label is careful to note that the magnitude of these effects is small compared with overall between-individual variability¹ — but a drug with a two-day half-life in the elderly, prescribed heavily to the elderly, is a drug whose steady state is reached slowly and departed from slowly.

Target organs — and why those

Basal ganglia

TargetD2 receptors in the nigrostriatal pathway

Why hereThe mechanism the drugs were designed for, appearing as toxicity. Dopaminergic transmission in the nigrostriatal pathway opposes cholinergic tone; blocking D2 receptors there releases the cholinergic system, producing the extrapyramidal syndrome. Haloperidol dominates this card because it is the most D2-selective of the three and the least anticholinergic — it has no muscarinic blockade of its own to offset what it creates. Its label names severe extrapyramidal reactions as the most prominent overdose symptom, manifest by muscular rigidity and a generalised or localised tremor.³ Established

At the bedsideAcute dystonia, oculogyric crisis, trismus, torticollis, rigidity and tremor. Haloperidol's label recommends parenteral administration of an antiparkinson medicinal product for severe reactions³ — an anticholinergic, restoring the balance the D2 blockade upset.

Vascular smooth muscle

TargetAlpha-1 adrenergic receptors

Why hereThe organ that makes adrenaline dangerous. Alpha-1 blockade produces vasodilatation and hypotension directly, and — because it removes the receptor adrenaline relies on — converts adrenaline from a vasopressor into a vasodilator. All three labels state the warning independently¹²³, which is as close to unanimity as this library gets. Established

At the bedsideHypotension, orthostatic hypotension, and in severe cases circulatory collapse.³ Fluids first; if a vasopressor is needed, a predominantly alpha-1 agonist is the mechanistically consistent choice. Quetiapine's and olanzapine's labels exclude both adrenaline and dopamine¹²; haloperidol's excludes adrenaline but names dopamine and noradrenaline.³

Heart — repolarisation

TargetCardiac potassium currents

Why hereBlockade of the delayed rectifier potassium current prolongs repolarisation and therefore the QT interval, creating the substrate for torsade de pointes. All three labels carry it: quetiapine's lists QT-prolongation among overdose effects², and haloperidol's states that the risk of ventricular arrhythmias, possibly associated with QTc prolongation, must be considered³, directing that ECG monitoring continue until the ECG is normal.³ Established

At the bedsideQT prolongation and torsade. Haloperidol's label sets the endpoint of monitoring as a normal ECG rather than a fixed number of hours³ — a rare and useful piece of label-specified guidance, and one that fits a drug with a 24-hour half-life.

Brain — arousal and the seizure threshold

TargetH1 receptors for the sedation; the seizure threshold by an unstated mechanism

Why hereH1 antagonism accounts for the sedation that dominates olanzapine and quetiapine overdose, and it is why the two drugs used most for their sedative properties are the two whose overdose looks most like coma. The seizure threshold is a separate matter and neither label explains it. Quetiapine's lists seizures, status epilepticus²; olanzapine's lists convulsion¹. Both state the finding and neither offers a mechanism, which is the same position tramadol's labels take. Inferred

At the bedsideSedation from drowsiness to coma¹², respiratory depression, aspiration.¹ Seizures, including status epilepticus with quetiapine.² Olanzapine's label reports reduced level of consciousness ranging from sedation to coma in over 10% of overdose cases.¹

Muscarinic receptors — the anticholinergic organ system

TargetPeripheral and central muscarinic receptors

Why hereQuetiapine's card, and the one that generated the strangest advice on any label in this band. Quetiapine's label names anti-cholinergic effects among overdose features and lists urinary retention, confusion, delirium and/or agitation.² It then discusses physostigmine — and the discussion is examined below, because it is the clearest instance in the library of a label recommending a treatment while listing the conditions under which it must not be given. Established

At the bedsideTachycardia, dry mouth, urinary retention, delirium, agitation, hyperthermia. The tachycardia has two causes at once — anticholinergic, and reflex from alpha-blockade-induced hypotension — which is why it is so consistent a finding.

Skeletal muscle and thermoregulation

TargetNeuroleptic malignant syndrome, and rhabdomyolysis from any cause

Why hereTwo overlapping problems. Rhabdomyolysis is listed directly on quetiapine's overdose section² and follows from seizures, agitation and prolonged immobility. Neuroleptic malignant syndrome is named on olanzapine's overdose section as a possible sequela¹ — the label's own hedge — and is conventionally attributed to central D2 blockade producing rigidity, hyperthermia and autonomic instability. The syndrome is real and well described; its distinction from severe extrapyramidal toxicity with hyperthermia is less clean at the bedside than the textbooks suggest. That separability claim is unproven rather than refuted, and no source contesting it is cited here — so this card is marked as inference. Note what clonus does and does not do: it separates serotonin toxicity from this syndrome, and it does not separate this syndrome from severe extrapyramidal toxicity with fever. Inferred

At the bedsideRigidity, hyperthermia, raised creatine kinase, autonomic instability, altered consciousness. Check creatine kinase and temperature in any antipsychotic overdose with rigidity. For the bedside differentiation from serotonin toxicity, see the SSRI page — clonus is the discriminating finding, and it belongs to serotonin toxicity.

Stomach — quetiapine XL only

TargetA physical mass of coalesced tablets

Why hereNot a receptor and not an organ toxicity — a mechanical event, and it belongs on this list because it changes management more than anything else on the page. The label reports gastric bezoar formation after extended-release quetiapine overdose, recommends diagnostic imaging, warns that routine lavage may fail due to gum like sticky consistency of the mass, and records successful endoscopic removal in some cases.⁴ Established

At the bedsideProlonged and unpredictable absorption, delayed peak sedation and pulse, prolonged recovery.⁴ Consider imaging in a large extended-release quetiapine ingestion, on the label's own recommendation.

Timeline of effects

Antipsychotic overdose — three drugs, and one formulation that rewrites the clock

Time

What you seeWhat is happening

0–2 hEarly
What you seeDrowsiness, tachycardia, dry mouth. Acute dystonia may appear early and is disproportionately alarming.
What is happeningAbsorption under way. Nothing has peaked: olanzapine's peak is at 5 to 8 hours¹ and haloperidol's at 2 to 6³.
1 hThe decontamination window
What you see—
What is happeningConcomitant activated charcoal reduced olanzapine oral bioavailability by 50 to 60%.¹ Quetiapine's label notes that prevention of absorption in overdose has not been investigated, and that lavage can be indicated in severe poisoning within one hour.²
2–8 hPeak — immediate release
What you seeSedation to coma, tachycardia, hypotension, extrapyramidal features, dysarthria, agitation or aggressiveness.¹ In over 10% of olanzapine overdoses.¹
What is happeningPeak plasma concentrations: olanzapine 5 to 8 h¹, haloperidol 2 to 6 h³. Which features dominate is determined by the drug's affinity profile rather than by the dose.
4–24 hThe cardiac and seizure window
What you seeQT prolongation, torsade, seizures and status epilepticus.²³
What is happeningPotassium-channel blockade at peak concentrations. Haloperidol's label sets the endpoint of ECG monitoring as a normal ECG, not a fixed interval.³
8 h onwardsExtended-release quetiapine
What you seeThe gap drawn here is a bezoar releasing drug on no schedule anyone can predict. Delayed peak sedation, delayed peak pulse, prolonged recovery.⁴
What is happeningGastric bezoar formation has been reported ... routine gastric lavage may not be effective ... due to gum like sticky consistency of the mass⁴. This is a latent phase produced by a physical object, and it is the only one of its kind in the library — the nearest relative is tablet dissolution on the calcium-channel blocker page, but a designed release schedule is at least predictable.
24–72 hThe long tail
What you seeProlonged sedation, particularly in older patients.
What is happeningOlanzapine half-life 33.8 h, rising to 51.8 h in the elderly¹; haloperidol on average 24 h, range of means 15 to 37³. Quetiapine is the short one at about 7 h, with norquetiapine at 12² — unless there is a bezoar.
DaysNeuroleptic malignant syndrome, if it happens
What you seeRigidity, hyperthermia, autonomic instability, raised creatine kinase.
What is happeningNamed as a possible sequela of olanzapine overdose on its label.¹ It does not belong to a point on the dose–time curve and is more often a therapeutic-dose event than an overdose one.

What the mechanism predicts at the bedside

Which antipsychotic, and which formulation. Half-lives run from about 7 hours to 51.8¹², and extended-release quetiapine can form a bezoar.⁴ The class name predicts almost nothing.
Do not give adrenaline for hypotension. All three labels warn against it¹²³; alpha blockade leaves only its beta-2 vasodilator effect. This is about a drug interaction, not about cardiac arrest, where resuscitation guidelines govern.
Note that the three labels disagree about dopamine — excluded on olanzapine's and quetiapine's for its beta activity¹², named as an option on haloperidol's.³ A predominantly alpha-1 agonist is consistent with all three.
ECG, and repeat it. Haloperidol's label sets a normal ECG as the endpoint of monitoring rather than a number of hours.³
Rigidity plus fever needs a creatine kinase and a temperature, and the question of neuroleptic malignant syndrome.¹
Clonus points away from this class and towards serotonin toxicity — see the SSRI page. It is the single most useful discriminator between two syndromes that otherwise overlap heavily.
Consider imaging in a large extended-release quetiapine ingestion, on the label's own recommendation, and know that lavage may not retrieve a bezoar.⁴
Charcoal is worth more here than on most pages: it reduced olanzapine bioavailability by 50 to 60%.¹
An olanzapine patient assessed at four hours has not been assessed at the peak, which is at five to eight.¹
Do not request dialysis. Haloperidol's label states dialysis removes only very small amounts and gives its two reasons — high volume of distribution and high protein binding.³ EXTRIP has addressed no antipsychotic.⁵

The antidote, from the poison's side

All three labels state that there is no specific antidote.¹²³ What exists is one treatment aimed at a receptor — the anticholinergic for extrapyramidal reactions — and one much-discussed treatment that quetiapine's label offers and then substantially withdraws.

Physostigmine — a label that gives a dose and then explains when not to use it

Quetiapine's label states: based on public literature, patients with delirium and agitation and a clear anti-cholinergic syndrome may be treated with physostigmine, 1–2 mg (under continuous ECG monitoring). This is not recommended as standard treatment, because of potential negative effect of physostigmine on cardiac conductance. Physostigmine may be used if there are no ECG aberrations. Do not use physostigmine in case of dysrhythmias, any degree of heart block or QRS-widening.² Read the whole passage and the treatment nearly disappears: it is sourced to public literature rather than to trial data, is explicitly not standard treatment, requires continuous ECG monitoring, and is contraindicated by exactly the abnormalities a severe quetiapine overdose produces. A drug whose contraindications are the poisoning's own features is not an antidote to that poisoning. Traditional teaching

Supportive care and the airway: The treatment. All three labels describe symptomatic treatment, monitoring of vital organ function and support of respiration.¹²³ Olanzapine's overdose section lists respiratory depression and aspiration among significant sequelae¹ — the airway is the first organ at risk.
Fluids, and a vasopressor if needed: For hypotension. Not adrenaline¹²³; olanzapine's and quetiapine's also exclude dopamine¹² while haloperidol's names it.³ A predominantly alpha-1 agonist satisfies all three.
Anticholinergic antiparkinsonian agents: Haloperidol's label: in cases of severe extrapyramidal reactions, parenteral administration of an antiparkinson medicinal product is recommended.³ The only receptor-directed treatment on the page that all parties agree on, and it works by restoring the dopamine–acetylcholine balance that D2 blockade upset.
Activated charcoal: Reduced olanzapine oral bioavailability by 50 to 60%¹ — one of the larger quantified charcoal effects in the library. Quetiapine's label notes that prevention of absorption in overdose has not been investigated, and that charcoal should be considered.² Haloperidol's label states the efficacy of charcoal has not been established.³
Sodium bicarbonate: For QRS widening, which quetiapine's label names as a contraindication to physostigmine² and which places such a patient with the sodium-channel blockade page. Not named as a treatment on any of the three labels.
Magnesium: For torsade, the consequence of the QT prolongation all three labels describe.¹²³ Again not named on the labels — this is the standard treatment of the rhythm rather than of the poisoning.
Physostigmine: See above. Offered on quetiapine's label with a dose and then hedged almost out of existence.²
Endoscopy: An intervention no other page in this library lists. Endoscopic pharmacobezoar removal has been performed successfully in some cases⁴ — for a mass that lavage cannot retrieve.
Extracorporeal removal: No. Dialysis is not recommended ... because it removes only very small amounts of haloperidol³; EXTRIP has published nothing on the class.⁵

Critical appraisal

The neuroleptic malignant syndrome claim was badged traditional teaching and was downgraded to inferred at audit. Two independent reviewers judged the citation insufficient and both were right. What was being downgraded is not the existence of the syndrome but the clean clinical separation of NMS from severe extrapyramidal toxicity with hyperthermia. The citation offered was olanzapine's label listing possible neuroleptic malignant syndrome among overdose sequelae¹ — a regulator hedging on causal attribution in individual overdose reports does not speak to bedside separability at all, so it was an absence dressed as doubt, the same shape as the calcium-channel-blocker badge the Band B audit removed. The consensus diagnostic-criteria literature would contest the separability claim properly; none is cited here, and until one is the claim is inference.
The physostigmine badge is on much firmer ground. Quetiapine's label offers it based on public literature, states it is not recommended as standard treatment, and contraindicates it in dysrhythmias, any degree of heart block or QRS widening.² A label that supplies a dose and then withdraws the indication is a citation for the doubt in the strongest form this project accepts — the same shape as the lithium precedent. The independent evidence against physostigmine as a reversal agent in a different poisoning is set out on the GHB page.
The three labels genuinely disagree about dopamine, and this page reports the disagreement rather than resolving it. Olanzapine's and quetiapine's exclude sympathomimetics with beta-agonist activity¹²; haloperidol's names dopamine and noradrenaline as options.³ The 'sources disagree' finding is the one this library is most prone to manufacturing, so the check was made explicitly: all three statements sit in the treatment paragraph of the overdose section of their respective labels, addressing the same clinical question. The disagreement is real.
The adrenaline warning is the strongest claim on the page and is supported three times over from independent documents.¹²³ It is deliberately not badged down. The mechanism — unopposed beta-2 vasodilatation in the presence of alpha-1 blockade — is stated in those terms on quetiapine's label itself.²
The seizure-threshold mechanism is not explained on any of the labels, which list seizures and status epilepticus² and convulsion¹ without attributing a cause. This page marks it as inference rather than printing a receptor account, in the same way the tramadol page does.
The haloperidol back-conversion caveat is quoted exactly and is not built upon. The label says the reduction pathway accounts for about 23% of biotransformation and that back-conversion cannot be fully ruled out.³ Nothing on this page treats that as an established accumulation mechanism; it is recorded because a label admitting an unresolved question is worth preserving.
Olanzapine's 'over 10%' figure describes the frequency of symptoms in overdose cases, which is a passive-surveillance figure from a label rather than a cohort study.¹ It is quoted as the label states it and no rate is derived from it.
Neither the bezoar's frequency nor its size is known. The label reports that it has occurred and gives management advice⁴; nothing quantifies the risk, and this page attaches no threshold to it.
No lethality figure appears on this page. Olanzapine's label carries one and it is deliberately not reproduced, in line with this site's permanent boundary — as on the digoxin and lithium pages, where the same decision was taken.
EXTRIP has addressed no antipsychotic.⁵ The absence is uninformative: haloperidol's label answers the question directly and gives both premises.³

References

1
ZYPREXA 10 mg coated tablets (olanzapine) — Summary of Product Characteristics. electronic medicines compendium, product 15471. Sections 4.9 (Overdose) and 5.2 (Pharmacokinetic properties). Source of the over-10% overdose symptom frequencies, the charcoal 50–60% bioavailability reduction, the epinephrine/dopamine warning, the 33.8 h and 51.8 h half-lives, the smoking and sex effects, the renal impairment comparison, and the statement that the major circulating metabolite does not pass the blood–brain barrier. medicines.org.uk/emc/product/15471
2
SEROQUEL 25 mg film-coated tablets (quetiapine) — Summary of Product Characteristics. electronic medicines compendium, product 5495. Sections 4.9 (Overdose) and 5.2 (Pharmacokinetic properties). Source of the QT, seizure, status epilepticus and rhabdomyolysis overdose features, the physostigmine passage in full with its contraindications, the epinephrine/dopamine warning and its alpha-blockade explanation, the 83% protein binding, and the 7 h and 12 h half-lives of quetiapine and norquetiapine. medicines.org.uk/emc/product/5495
3
HALDOL 2 mg/ml oral solution (haloperidol) — Summary of Product Characteristics. electronic medicines compendium, product 15252. Sections 4.9 (Overdose) and 5.2 (Pharmacokinetic properties). Source of the extrapyramidal-dominant overdose picture, the adrenaline contraindication, the recommendation of an antiparkinson agent, the instruction that ECG monitoring continue until the ECG is normal, the 8–21 L/kg volume of distribution, 88–92% protein binding, the 24 h mean half-life, the dialysis statements, and the 23% reduction-pathway back-conversion caveat. medicines.org.uk/emc/product/15252
4
Seroquel XL 300 mg prolonged-release tablets (quetiapine) — Summary of Product Characteristics. electronic medicines compendium, product 7603. Section 4.9 (Overdose). Source of the delayed peak sedation and pulse and prolonged recovery in extended-release overdose, and of the gastric bezoar passage — imaging recommended, routine lavage may not be effective due to the gum-like sticky consistency of the mass, and endoscopic pharmacobezoar removal performed successfully in some cases. medicines.org.uk/emc/product/7603
5
EXTRIP Workgroup — published recommendations index. Extracorporeal Treatments in Poisoning Workgroup. Cited for the absence of any recommendation covering the antipsychotics. extrip-workgroup.org/recommendations

Antipsychotics

At a glance