MONOGRAPH FOR UKPID
HALOPERIDOL
HY Allen
ZM Everitt
AT Judd
National Poisons Information Service (Leeds Centre)
Leeds Poisons Information Centre
Leeds General Infirmary
Leeds
LS1 3EX
UK
This monograph has been produced by staff of a National Poisons
Information Service Centre in the United Kingdom. The work was
commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.
Peer review group: Directors of the UK National Poisons Information
Service.
MONOGRAPH FOR UKPID
Drug name
Haloperidol
Chemical group
Butyrophenone
Origin
Synthetic
Name
Brand name(s)
Dozic(R), Haldol(R), Serenace(R)
Synonyms
Common names
Product licence number
Haldol(R) 5 mg 0242/0031R
Haldol(R) 10mg 0242/0039R
Haldol(R) 5mg/ml injectable solution 0242/0036R
Haldol(R) 10mg/2ml injectable solution 0242/0036R
Haldol(R) 2mg/ml oral liquid 0242/0035R
Serenace(R) 5mg ampoules 0530/0368
Serenace(R) 20 mg ampoules 0530/0369
Serenace(R) 1.5mg tablets 0530/0370
Serenace(R) 5 mg tablets 0530/0371
Serenace(R) 10 mg tablets 0530/0372
Serenace(R) 20 mg tablets 0530/0373
Serenace(R) 2mg/ml liquid 0530/0374
Serenace(R) 500 microgram capsules 0530/0375
CAS number
Haloperidol: 52-86-8
Manufacturer
of Dozic(R):
Rosemont Pharmaceuticals Limited, Rosemont House, Yorkdale
Industrial Park, Braithwaite Street, Leeds LS11 9XE
Tel no. 0113244 1999
of Haldol(R):
Janssen-Cilag Limited, PO Box 79, Saunderton, High Wycombe, Bucks
HP14 4HJ
Tel no. 01494 567567
of Serenace(R):
Baker Norton, H. N.Norton & Co Limited, Gemini House, Flex
Meadow, Harlow, Essex CM19 5TJ
Tel no. 01279 426666
Form
Oral tablets
Oral capsules
Oral liquid
Injection for intramuscular or intravenous use
NOTE: a separate entry exists for depot injections - see under
'Haloperidol Decanoate'.
Formulation details
Tablets of 1.5mg, 5mg, 10mg, 20mg
Capsules of 500 micrograms
Oral liquid of 1mg/ml, 2mg/ml
Injection of 5mg/ml, 10mg/2ml, 20mg/2ml
Pack size
Dozic(R) oral liquid 1mg/ml and 2mg/ml: 100ml pack
Haldol(R) tablets 5mg, 10mg: pack of 100
Haldol(R) oral liquid 2mg/ml: 100ml pack
Haldol(R) injection 5 mg/ml: 5x1ml ampoules
Haldol(R) injection 10mg/2ml: 5x2ml ampoules
Serenace(R) capsules 500 micrograms: various pack sizes, in bottles
starting at 7 to 250 capsules and blister packs in sizes from 7 to 120
capsules, also dispensing packs of 1,000 and 5,000 capsules.
Serenace(R) tablets 1.5mg, 5mg, 10mg, 20mg: various pack sizes, in
bottles starting at 7 to 250 tablets and blister packs in sizes from 7
to 120 tablets, also dispensing packs of 1,000 and 5,000 capsules.
Serenace(R) oral liquid 2mg/ml: 100ml and 500ml
Serenace(R) 5mg ampoules: 6x1ml and 10x1ml
Serenace(R) 20mg ampoules: 10x2ml
Packaging
Haldol(R) 5mg : blue cross-scored tablets and marked JANSSEN
Haldol(R) 10 mg: yellow scored tablets marked JANSSEN and H/10
Serenace(R) 1.5mg: white tablets marked NORTON 1.5 and SERENACE
Serenace(R) 5 mg: bright pink tablets marked NORTON 5 and SERENACE
Serenace(R) 10mg: pale pink tablets marked NORTON 10 and SERENACE
Serenace(R) 20 mg: dark pink tablets marked NORTON 20 and SERENACE
Serenace(R) 500 micrograms: two-tone green capsules marked NORTON 500
and SERENACE
Chemical structure
Haloperidol: C21H23ClFNO2 Molecular weight = 375.9
Chemical name
4-[4-(4-Chlorophenyl)-4-hydroxypiperidino]-4-fluorobutyrophenone
Indication
Schizophrenia and other psychoses, especially paranoid, mania,
short-term adjunctive management of psychomotor agitation, excitement,
violent or dangerously impulsive behaviour, mental or behavioural
disorders especially when associated with hyperactivity and
aggression, short-term adjunctive management of severe anxiety,
restlessness and agitation in the elderly, intractable hiccup, nausea
and vomiting, Gilles de la Tourette syndrome and severe tics.
Therapeutic dosage - adults
By mouth:
1-15mg daily in divided doses (up to 100mg in resistant
schizophrenia)
Reduced doses in elderly.
By IM (or IV) injection:
2-10 mg repeated (as frequently as every 30-60 minutes if
required) to a maximum of 60mg.
Therapeutic dosage - children
By mouth:
25-50 micrograms/kg daily in two divided doses to a maximum of
10mg, or 30 mg in adolescents (exceptionally 60mg).
By injection:
Not recommended.
Contra-indications
Comatose states, CNS depression, Parkinson's disease, known
hypersensitivity to haloperidol, lesions of the basal ganglia, and
during lactation.
Abuses
Abuse of haloperidol has been reported.
Doses between 10 mg and 60 mg taken by a number of young people
resulted in a variety of extrapyramidal symptoms, cold sweats, and
insomnia. The extrapyramidal effects included opisthotonus, protruding
tongue, torticollis, and dystonia of the jaw, neck and mouth. The
adverse effects were generally noticed within a few hours, although
one patient reported a delay of 48 hours before first noticing any ill
effect (Doenecke & Heuermann 1980, Kenyon-David 1981).
Epidemiology
Although widely used as an antipsychotic, acute poisoning with
haloperidol is rare.
Adverse effects
Extrapyramidal effects such as acute dystonia, Parkinsonian rigidity,
tremor, and akathisia. Also sedation, agitation, drowsiness, insomnia,
headache, nausea, blurring of vision, urinary retention, hypotension,
depression, confusional states, impairment of sexual function, skin
reactions, epileptic fits, hyperprolactinaemia, ventricular
arrhythmias, and abnormalities of liver function tests.
Tardive dyskinesia, and neuroleptic malignant syndrome have both been
associated with haloperidol therapy.
Interactions
PHARMACODYNAMIC
1. Enhancement of central nervous system depression produced by
other CNS DEPRESSANT drugs.
2. Combination with other antidopaminergic agents, such as
METOCLOPRAMIDE or PROCHLORPERAZINE increases the risk of
extrapyramidal effects (Dollery 1991).
PHARMACOKINETIC
1. The metabolism of TRICYCLIC ANTIDEPRESSANTS is impaired by
haloperidol resulting in higher serum tricyclic levels (Stockley
1996).
OTHER
1. There is limited evidence to suggest that profound drowsiness and
confusion may be associated with combined use of haloperidol and
INDOMETHACIN (Stockley 1996).
2. Combination with high doses of LITHIUM have produced
encephalopathic syndromes and severe extrapyramidal
reactions(Cohen & Cohen 1974, Stockley 1996).
ETHANOL
Possible enhancement of central nervous system depression, and
precipitation of extrapyramidal side effects by ALCOHOL (Stockley
1996).
Mechanism of action
The precise mechanism of antipsychotic action is unclear, but is
considered to be associated with the potent dopamine D2 receptor
blocking activity of haloperidol and the resulting adaptive changes in
the brain.
It is also a potent antagonist of opiate receptors, and has weak
antagonist activity at muscarinic, histamine H1, alpha-adrenergic, and
serotonin receptors (Dollery 1991).
Mechanism of toxicity
Toxicity is due to an extension of the pharmacological actions. The
various receptor antagonist actions of haloperidol result in
extrapyramidal reactions, a reduction in seizure threshold,
hypothermia, orthostatic hypotension, QT prolongation on the ECG,
sedation, and antimuscarinic effects.
Pharmacokinetics
ABSORPTION
Following oral administration peak plasma concentrations usually occur
within 3-6 hours (Kunka & Perel 1989). Oral bioavailability is about
65% after first-pass metabolism (Holley et al. 1983).
Following intramuscular administration peak plasma haloperidol
concentrations occur within 15-60 minutes, and the systemic
bioavailability is approximately 75% (Adam & Fernandez 1987, Javaid
1994).
DISTRIBUTION
Haloperidol is about 92% bound to plasma proteins (Forsman & Ohman
1977b). It is widely distributed in the body, with an apparent volume
of distribution of about 18 L/kg (Holley et al. 1983).
METABOLISM
The pharmacokinetic profile of haloperidol varies widely between
individuals, largely resulting from metabolic differences.
It is metabolised in the liver via three major pathways. Oxidative
dealkylation forms inactive metabolites, reduction produces the active
metabolite reduced haloperidol, and conjugation of both haloperidol
and reduced haloperidol forms inactive metabolites (Forsman et al.
1977, Forsman & Larsson 1978). Reduced haloperidol is much less active
than haloperidol, but the conversion is reversible and re-oxidation to
haloperidol occurs (Chakraborty et al. 1989, Cheng & Jusko 1993).
The cytochrome P452D6 has been shown to be involved in the oxidative
metabolic pathway (Llerena et al 1992).
ELIMINATION
Haloperidol is excreted slowly in the urine and faeces. About 30% of a
dose is excreted in urine and about 20% of a dose in faeces via
biliary elimination (Beresford & Ward 1987). Only 1% of a dose is
excreted as unchanged drug in the urine (Forsman et al. 1977). It
takes 28 days to fully eliminate a single oral dose (Dollery 1991).
There is evidence of enterohepatic recycling (Chakraborty et al.
1989).
Half-life - substance
About 20 hours but widely variable (range 10-36 hours)
(Forsman & Ohman 1976, Holley et al 1983).
Half-life - metabolites
NA
Special populations
ELDERLY
Haloperidol plasma concentrations in the elderly tend to be higher
than in younger patients on equivalent doses but the difference is not
significant (Forsman & Ohman 1977a).
RENAL IMPAIRMENT
It is not anticipated that renal impairment would alter the
pharmacokinetic profile of haloperidol.
HEPATIC IMPAIRMENT
The clearance of haloperidol may be reduced in severe liver
impairment.
GENDER
Gender has been found not to influence haloperidol plasma
concentrations (Forsman & Ohman 1977a).
BREAST MILK
Haloperidol is excreted into breast milk.
In one patient, levels of haloperidol in the breast milk were 0.005
mg/L following an average dose of 30mg daily. Using these data and
assuming a milk intake of 1.5L daily, an infant could receive up to
0.0075 mg haloperidol daily, or 0.02% of the maternal dose (Stewart et
al. 1980).
In a second patient receiving 10 mg haloperidol daily, milk levels up
to 0.0235 mg/L were measured. The milk to plasma ratio for haloperidol
in this patient was 0.6 (Whalley et al. 1981).
Toxicokinetics
Absorption
Distribution
Metabolism
Elimination
Half-life - substance
Half-life - metabolites
Special populations
CHILDREN: elimination half-lives between 9 and 39 hours (average 19
hours) have been reported following accidental ingestions in children
(Yoshida et al. 1993).
Breast milk
Summary
TYPE OF PRODUCT
Antipsychotic
INGREDIENTS
Capsules of 500 micrograms
Tablets of 1.5 mg, 5 mg, 10 mg, and 20 mg
Oral liquid of 1 mg/ml, 2 mg/ml, 10mg/ml
Ampoules of 5 mg/ml, 10 mg/2ml, and 20 mg/2ml for IM or IV use.
NOTE: a separate entry exists for depot injections - see under
'Haloperidol Decanoate'.
SUMMARY OF TOXICITY
Features of toxicity generally become evident within 2-12 hours of an
ingestion, and may last for several days. Ingestions of up to 50 mg
have resulted in rigidity, dystonic reactions, drowsiness, and tremor.
Larger amounts have been associated with hypotension, prolongation of
the QT interval, and the development of torsade de pointes.
Antimuscarinic effects are rare.
Children appear particularly susceptible to dystonic reactions and
disturbances of temperature and blood pressure.
FEATURES
Acute dystonic reactions, drowsiness, hypotension or hypertension,
cardiac arrhythmias, and hypothermia.
SUMMARY OF MANAGEMENT: SUPPORTIVE
1. Maintain a clear airway and adequate ventilation if consciousness
is impaired.
2. If within 1 hour of the ingestion and more than 30 mg has been
ingested by an adult or more than 100 microgram/kg by a child,
give oral activated charcoal.
3. Acute dystonic reactions can be managed with IV procyclidine or
benztropine.
4. Check the cardiac rhythm and blood pressure.
5. Manage hypotension with IV fluids.
6. Cardiac overdrive pacing is the preferred management for torsade
de pointes.
7. Other measures as indicated by the patients clinical condition.
Features - acute
Ingestion
Acute dystonic reactions and other extrapyramidal signs (such as
rigidity, and tremor), drowsiness, hypotension (or rarely
hypertension), hypothermia, hypokalaemia, and cardiac arrhythmias
particularly prolongation of the QT interval and torsade de pointes
(Aunsholt 1989, Cummingham & Challapalli 1979, Henderson et al. 1991,
Scialli & Thornton 1978, Sinaniotis et al. 1978, Yoshida et al. 1993,
Zee-Cheng et al. 1985).
Inhalation
NA
Dermal
NA
Ocular
Other routes
BY INJECTION: as for acute ingestion.
Features - chronic
Ingestion
As for acute ingestion, but with the additional risks of the
development of neuroleptic malignant syndrome (characterised by
hyperthermia, muscle rigidity, autonomic instability, altered
consciousness, and coma), and tardive dyskinesia (involuntary
movements of the tongue, face, jaw, or mouth).
Inhalation
NA
Dermal
NA
Ocular
Other routes
BY INJECTION: as for chronic ingestion.
At risk groups
ELDERLY
Increased risk of toxic events.
PREGNANCY
The safety of haloperidol in human pregnancy has not been established.
There are two reports of limb defects in infants after first trimester
use of haloperidol given with other potentially teratogenic drugs
(AHFS 1998, Briggs 1994, Kopelman et al. 1975). Other investigators
have not found an association between haloperidol and birth defects.
CHILDREN
There appears to be a high incidence of dystonic reactions reported in
children (Yoshida et al. 1993).
ENZYME DEFICIENCIES
The metabolism of haloperidol is subject to genetic polymorphism.
Subjects deficient in the isoenzyme P4502D6 are poor metabolisers of
haloperidol and will be at risk from high haloperidol plasma
concentrations due to a reduced metabolic capacity (Llerena et al.
1992). Approximately 7% of the caucasian population is deficient in
this enzyme.
ENZYME INDUCED
Reduced risk of toxicity from haloperidol.
Therapeutic administration with enzyme inducing drugs for a period of
1-3 weeks results in lower haloperidol plasma concentrations (Forsman
& Ohman 1977a, Jann et al. 1985).
Occupations
Others
RENAL IMPAIRMENT: renal impairment is unlikely to increase the risk of
toxicity.
HEPATIC IMPAIRMENT: increased risk of toxicity due to impaired
metabolism.
CARDIAC DISEASE: increased risk of cardiotoxicity due to underlying
disease.
EPILEPSY: increased risk of seizures due to lowered seizure threshold.
Management
Decontamination
If within one hour of ingestion, and more than 30 mg has been taken by
an adult or more than 100 microgram/kg by a child, oral activated
charcoal should be given to reduce the absorption.
ADULT DOSE; 50 g,
CHILD DOSE; 1 g/kg.
If the patient is drowsy this should be administered via a nasogastric
tube, and if there is no gag reflex present, using a cuffed
endotracheal tube to protect the airway.
Supportive care
MANAGEMENT OF THE SYMPTOMATIC PATIENT: SUPPORTIVE
Clear and maintain the airway, and give cardiopulmonary resuscitation
if necessary.
Evaluate the patient's condition and provide support for vital
functions.
1. ACUTE DYSTONIC AND OTHER EXTRAPYRAMIDAL REACTIONS
Severe dystonic reactions can be controlled within a few minutes by
giving procyclidine or benztropine by the intravenous (or
intramuscular) route. Subsequent oral doses may be required for 2-3
days to prevent recurrence. Less severe extrapyramidal symptoms can be
controlled by oral doses of procyclidine, benztropine, or other
similar anticholinergic drug (Corre et al. 1984, Guy's, Lewisham & St.
Thomas Paediatric Formulary 1997, BNF 1998).
Procyclidine IV, IM:
Adult dose: 5-10 mg (use lower end of dose
range in elderly),
Child dose under 2 years: 500 micrograms-2 mg (unlicensed
indication)
Child dose 2-10 years: 2-5 mg (unlicensed indication).
Procyclidine oral:
Adult dose: 2.5-10mg three times a day
Child 7-14 years 1.25mg three times a day
(unlicensed indication)
Child over 14 years 2.5mg three times a day (unlicensed
indication)
Benztropine dose IV, IM, and oral:
Adult dose: 1-2 mg (use lower end of dose range in elderly),
Child dose: 20 micrograms/kg (unlicensed indication).
2. HYPOTENSION
Hypotension should be managed by the administration of intravenous
fluids and by physical means. Where these measures fail, consideration
may be given to the use of a direct acting sympathomimetic such as
noradrenaline with appropriate haemodynamic monitoring (e.g. insertion
of Swan-Ganz catheter).
ADULT DOSE: IV infusion of noradrenaline acid tartrate 80
micrograms/ml (equivalent to noradrenaline base 40 micrograms/ml) in
dextrose 5% via a central venous catheter at an initial rate of 0.16
to 0.33 ml/minute adjusted according to response (BNF 1998).
CHILD DOSE (unlicensed indication): IV infusion of noradrenaline
acid tartrate 0.04-0.2 microgram/kg/minute (equivalent to 0.02-0.1
microgram/kg/minute of noradrenaline base) in glucose 5% or
glucose/saline via a central venous catheter (Guy's, Lewisham & St
Thomas Paediatric Formulary 1997).
NOTE: sympathomimetics with mixed alpha and beta adrenergic effects
(e.g. adrenaline and dopamine) should not be used as hypotension may
be exacerbated.
3. CARDIAC ARRHYTHMIAS
The ventricular arrhythmia, torsade de pointes, may prove difficult to
manage. Treatment is aimed at shortening the QT interval by
accelerating the heart rate. The preferred method is by CARDIAC
OVERDRIVE PACING (Henderson et al. 1991).
Alternatively isoprenaline may be used to increase the heart rate, but
with caution, as the unopposed beta2-adrenergic agonist effects will
exacerbate hypotension.
ADULT DOSE: intravenous isoprenaline infused at a starting dose
of 0.2 micrograms/minute and titrated to maintain a heart rate of 100
beats per minute (Kemper et al. 1983).
Intravenous magnesium sulphate has also been shown to be effective in
the management of torsade de pointes (Tzivoni et al. 1988).
ADULT DOSE; 8 mmol of magnesium sulphate (4 ml of 50% solution)
by intravenous injection over 10-15 minutes, repeated once if
necessary (BNF 1998). CHILD DOSE: clinical experience in children is
lacking, but based on the above recommendations for management in
adults, doses of 0.08-0.2 mmol/kg (0.04-0.1 ml/kg of 50% solution) may
be considered appropriate (based on Guy's, Lewisham & St Thomas
Paediatric Formulary, 1997).
4. TEMPERATURE DISTURBANCES
Where the patient is hypothermic the body temperature should be
allowed to recover naturally by wrapping the patient in blankets to
conserve body heat.
Conventional external cooling procedures should be used in patients
who are hyperthermic.
5. NEUROLEPTIC MALIGNANT SYNDROME
The development of NMS with a high central temperature (over 39°C) is
best treated by paralysing and mechanically ventilating the patient.
This usually controls the muscle spasm and allows the temperature to
fall. If the body temperature is 40°C or over, administer intravenous
dantrolene.
ADULT DOSE: dantrolene 1 mg/kg body weight by rapid IV injection
repeated as required to a cumulative maximum of 10 mg/kg (BNF 1998).
Monitoring
Monitor the heart rate and rhythm, blood pressure, and body
temperature. Correct any electrolyte abnormalities.
OBSERVE for a minimum of 12 hours post-ingestion where:
i) more than 15 mg has been ingested by an adult (or more than
the patients' normal therapeutic dose, if this is greater),
ii) more than 50 microgram/kg has been ingested by a child,
iii) the patient is symptomatic.
Antidotes
There is no specific antidote.
Elimination techniques
Forced diuresis, peritoneal dialysis, haemodialysis, and charcoal
haemoperfusion are ineffective (Dollery 1991).
Investigations
Management controversies
Gastric lavage is not recommended as the procedure may be associated
with significant morbidity, and there is no evidence that it is of any
greater benefit than activated charcoal used alone.
If the procedure is used (i.e. in cases where activated charcoal
cannot be administered), a cuffed endotracheal tube should be used to
protect the airway if the patient is drowsy, and activated charcoal
left in the stomach following the lavage.
Case data
CASE REPORT 1 - Hypokalaemia and prolonged QT interval after 300 mg
haloperidol in an adult.
A 56 year old woman reportedly ingested 300 mg of haloperidol in a
suicide attempt. Her plasma electrolytes had been assessed three weeks
before the attempt when her serum potassium was 4.4 mmol/L. All other
tests including her ECG were normal at this assessment. On admission
she complained of dry mouth and blurred vision, was pale and drowsy,
with a blood pressure of 120/60 mm Hg. An ECG revealed a sinus rhythm
of 80 beats per minute with a prolonged QT interval of 0.6s (corrected
QT of 0.71s). The corrected serum calcium was 2.47 mmol/L and the
serum potassium was 2.7 mmol/L. The potassium depletion was corrected
by intravenous infusion. The QT interval returned to normal after 12
hours and at no time were ventricular arrhythmias observed. The
patient was discharged 32 hours after admission (Aunsholt 1989).
CASE REPORT 2 - Delayed hypertension following haloperidol ingestion
in an infant.
A 22-month-old presented with profound lethargy, urticaria, dystonia,
rigidity, and fine tremor 26 hours after an accidental ingestion of 15
or 20 mg haloperidol. Her blood pressure was 136/66 mm Hg rising to
164/134 mm Hg over the next 10 hours. She was given IV hydralazine,
and required antihypertensive therapy for five days. Subsequent
recovery was complete with no other cause for the hypertension being
found (Cummingham & Challapalli 1979).
CASE REPORT 3 - Torsade de pointes after haloperidol and orphenadrine
ingestion in an adult.
A 48 year old woman was admitted to hospital shortly after ingesting
up to 210mg haloperidol and 1400 mg orphenadrine. She was
semi-conscious and pulseless. ECG monitoring revealed a broad complex
polymorphous tachycardia. Once in sinus rhythm after resuscitative
measures her blood pressure was 110/60 mg Hg. gastric lavage was
performed followed by activated charcoal administration. A mild
hypokalaemia was corrected. Further ECG monitoring revealed frequent
multiform ventricular extrasystoles, with episodes of polymorphous
ventricular tachycardia. An IV injection of 100 mg lignocaine followed
by a lignocaine infusion did not prevent recurrent episodes of
polymorphous ventricular tachycardia. A diagnosis of torsade de
pointes was made, the lignocaine discontinued, and atrial overdrive
pacing started at a rate of 85 per minute. The QT interval became
normal 2 days after admission and the patient returned to sinus rhythm
when atrial pacing was discontinued (Henderson et al. 1991).
Analysis
Agent/toxin/metabolite
The measurement of plasma haloperidol is of little benefit as no
correlation has been established between plasma haloperidol
concentration and therapeutic or toxic effect.
Sample container
NA
Storage conditions
NA
Transport
NA
Interpretation of data
It has been suggested that a plasma haloperidol concentration of
0.005-0.012 mg/L may be associated with a clinical response, but this
range should only be viewed as a rough guide (Van Putten et al. 1992).
Conversion factors
1 micromole/L = 0.376 mg/L
1mg/L = 2.659 micromoles/L
Others
NA
Toxicological data
Carcinogenicity
An increase in mammary neoplasms has been observed in rodents
following long term administration of prolactin-stimulating
antipsychotic agents. Although no association between human breast
cancer and long term administration of these drugs has been shown,
current evidence is too limited to be conclusive (AHFS 1998).
Genotoxicity
Mutagenicity
Reprotoxicity
Hyperprolactinaemia resulting from haloperidol therapy may lead to
infertility in women and impotence in men.
Teratogenicity
Haloperidol has been shown to be teratogenic and fetotoxic in animals
at dosages 2-20 times the usual maximum human dosage (AHFS 1998).
In human pregnancy, haloperidol has not been associated with
teratogenic effects when used alone, but there are two reports of limb
defects following the first trimester administration of haloperidol
with other drugs (Briggs 1994, Kopelman et al. 1975).
Relevant animal data
Relevant in vitro data
Authors
HY Allen
ZM Everitt
AT Judd
National Poisons Information Service (Leeds Centre)
Leeds Poisons Information Centre
Leeds General Infirmary
Leeds
LS1 3EX
UK
This monograph was produced by the staff of the Leeds Centre of the
National Poisons Information Service in the United Kingdom. The work
was commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.
Peer review was undertaken by the Directors of the UK National Poisons
Information Service.
Prepared October 1996
Updated May 1998
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