HY Allen
    ZM Everitt
    AT Judd

    National Poisons Information Service (Leeds Centre)
    Leeds Poisons Information Centre
    Leeds General Infirmary
    LS1 3EX

    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


    Drug name

    Chlorpromazine hydrochloride

    Chemical group





    UK Brand name(s)
    Largactil(R), Chloractil(R)


    Common names

    Product licence number

    Largactil(R) 10mg: 0012/5108R
    Largactil(R) 25mg: 0012/5109R
    Largactil(R) 50mg: 0012/5110R
    Largactil(R) 100mg: 0012/5111R
    Largactil(R) injection solution 2.5%: 0012/5308R
    Largactil(R) syrup: 0012/5083R
    Largactil(R) Forte Suspension: 0012/5001R

    CAS number



    Rhône-Poulenc Rorer Ltd, RPR House, 50 Kings Hill Ave., Kings Hill,
    West Malling, Kent, ME19 4AH.
    Tel. no. 01732 584000
    Fax. no. 01732 584086

    Available as Largactil(R) from Rhône-Poulenc Rorer, and as generics or
    branded generics from Antigen, APS, DDSA (Chloractil(R)), Hillcross,
    Rosemont and Norton.


    Oral liquids

    Formulation details

    Tablets of 10 mg, 25 mg, 50 mg, and 100 mg
    Syrup containing 25 mg / 5 ml
    Forte suspension equivalent to 100 mg/5 ml (as chlorpromazine
    Injection of 25 mg / ml.
    Suppositories of 100 mg (unlicensed product)

    Pack size

    Largactil tabs 10 mg, 25 mg, 50 mg, and 100 mg - blister packs of 56
    Largactil syrup - 100ml pack
    Largactil forte suspension - 100ml pack
    Largactil injection - ampoules of 1 ml and 2 ml

    Pack sizes may differ for generics and branded generics.


    Largactil(R) tabs 10mg - white tablets marked LG10
    Largactil(R) tabs 25mg - white tablets marked LG25
    Largactil(R) tabs 50mg - white tablets marked LG50
    Largactil(R) tabs 100mg - white tablets marked LG100

    Chemical structure


    Chemical name

    3-(2-Chlorophenothiazin-10-yl)propyldimethylamine hydrochloride


    Schizophrenia and other psychoses, (especially paranoid and
    hypomania); short-term adjunctive management of anxiety, psychomotor
    agitation, excitement, and violent or dangerously impulsive behaviour;
    intractable hiccup; nausea and vomiting of terminal illness (where
    other drugs have failed or are not available); induction of
    hypothermia; childhood schizophrenia and autism.

    Therapeutic dosage - adults

    BY MOUTH: 75-300 mg daily in divided doses (doses up to 1 g used in
    BY DEEP IM INJECTION: 25-50 mg every 6-8 hours.
    BY RECTUM (unlicensed route): 100 mg every 6-8 hours.

    For equivalent therapeutic effect:

    100 mg by rectum ° 20-25 mg by IM injection ° 40-50 mg by mouth

    Therapeutic dosage - children

    BY MOUTH: 1-5 years:     500 micrograms/kg 4-6 hourly (maximum 40 mg
              6-12 years:    _ to ´ adult dose (maximum 75 mg daily).

              500 micrograms/kg 6-8 hourly with maximum daily dose as for
    oral dose.

    BY RECTUM (unlicensed route):
              1-4 years:          12.5 mg 3-4 hourly.
              5-12 years:         25 mg 3-4 hourly.
              over 12 years:      50-100 mg 3-4 hourly.


    Coma caused by CNS depressants, bone marrow depression,



    Although the phenothiazines show similar toxic properties to the
    tricyclic antidepressants, overdoses tend to be less serious, with
    severe hypotension and cardiotoxicity being less common. (Ellenhorn


    There are a large number of adverse effects associated with
    therapeutic use including changes in hepatic, cardiovascular,
    respiratory, haematologic, ocular and endocrine functions, besides
    extrapyramidal reactions and the risk of neuroleptic malignant
    Postural hypotension commonly occurs, especially after intramuscular



    1.   Chlorpromazine enhances the central nervous system depression
         produced by other CNS DEPRESSANT drugs.

    2.   The hypotensive effect of ANTIHYPERTENSIVE AGENTS is likely to be
         enhanced, the exception being GUANETHIDINE where chlorpromazine
         may antagonise its hypotensive effect (Fruncillo 1985, Janowsky
    3.   There is an increased risk of ventricular arrhythmias when
         chlorpromazine is taken with drugs that increase the QT interval

    4.   Combination with other antidopaminergic agents such as
         METOCLOPRAMIDE or PROCHLORPERAZINE increases the risk of
         extrapyramidal effects.


    1.   The metabolism of TRICYCLIC ANTIDEPRESSANTS is impaired by
         chlorpromazine, increasing the risk of toxicity (Balant-Gorgia &
         Balant 1987).


    An interaction between phenothiazine drugs and 'caffeinated' beverages
    has been reported. A precipitation occurs when these drugs are diluted
    in tea or coffee (including decaffeinated varieties) which is
    considered to be a nonspecific reaction between the
    nitrogen-containing organic bases and tannic acid. The reaction is
    reversible in the acid environment of the stomach (Curry et al. 1991).


    The administration of ethanol with chlorpromazine results in
    potentiated sedative effects and impaired co-ordination (Lieber 1994,
    Milner & Landauer 1971, Zirkle 1959).


    Chlorpromazine blocks post-synaptic D2 dopamine receptors. It is
    considered that dopamine receptor blockade in the mesolimbic area
    accounts for the antipsychotic effect, whilst blockade in the
    nigrostriatal system produces the extrapyramidal effects associated
    with chlorpromazine use. The anti-emetic effect results from dopamine
    antagonism in the chemoreceptor trigger zone. Chlorpromazine also
    possesses antimuscarinic properties. It is an antagonist at histamine
    (H1), serotonin and alpha-1-adrenergic receptors (Dollery 1991).


    The extrapyramidal, anticholinergic, sedative, and hypotensive
    features of toxicity result from the blockade of dopaminergic,
    muscarinic, histaminic, and alpha adrenergic receptors respectively.
    The cardiotoxic effects of phenothiazines in overdose are similar to
    that of the tricyclic antidepressants. (Ellenhorn 1997). Cardiac
    arrhythmia and apparent 'sudden death' have been associated with
    therapeutic doses of chlorpromazine, the sudden cardiovascular
    collapse being attributed to ventricular dysrhythmia (Fowler et al.
    1976, Hollister & Kosec 1965).



    Peak plasma concentrations occur on average 2-3 hours (range 1.5-8
    hours) after an oral dose (Midha et al. 1989, Yeung et al. 1993).
    After intramuscular injection chlorpromazine is slowly absorbed from
    the injection site, with the peak plasma concentration occurring 6-24
    hours after administration (Dahl & Strandjord 1977).
    The oral bioavailability of chlorpromazine is about 30% that of
    intramuscular doses (Dahl & Strandjord 1977) and about 10% that of
    intravenous doses (Yeung et al. 1993) as a result of pre-systemic


    Chlorpromazine is highly lipid soluble and is 98% bound to plasma
    proteins (Dollery 1991). It is extensively distributed throughout the
    body and has a mean volume of distribution of 17 L/kg (Yeung et al.


    Chlorpromazine is subject to significant pre-systemic metabolism
    attributed to first passage through the gut wall, liver and lung
    (Yeung et al. 1993).
    It is extensively metabolised involving cytochrome P450 microsomal
    pathways (Lieber 1994) with more than 100 metabolites being
    theoretically possible (Javaid 1994). The major routes of metabolism
    include hydroxylation, N-oxidation, sulphoxidation, demethylation,
    deamination and conjugation (Dollery 1991). A number of the
    metabolites may contribute to the pharmacological effects of
    chlorpromazine including 7-hydroxychlorpromazine,
    chlorpromazine-N-oxide, 3-hydroxychlorpromazine and
    desmethylchlorpromazine (Chetty et al. 1994). Although the metabolite
    chlorpromazine-N-oxide does not possess activity in vitro, it exerts
    an indirect pharmacological effect in vivo by reverting to
    chlorpromazine (Cheng & Jusko 1993). It is considered that one of the
    metabolites produced (chlorpromazine-sulphoxide) may oppose the
    alpha-adrenergic blocking action of chlorpromazine (Chetty et al.
    There is limited evidence to suggest that following multiple doses,
    the metabolism of chlorpromazine may be increased due to induction of
    microsomal liver enzymes (Dahl & Strandjord 1977).


    Excretion is primarily via the kidneys with less than 1% of a dose
    excreted as unchanged drug in the urine, and 20-70% as conjugated or
    unconjugated metabolites (Dollery 1991). 5-6% of a dose is excreted in
    faeces via biliary elimination (Dollery 1991).
    Some metabolites can still be detected up to 18 months after
    discontinuation of long-term therapy (Dollery 1991).


    The half-life of chlorpromazine is usually within the range 8-35 hours
    (Dollery 1991), although it is as short as 2 hours or as long as 60
    hours in some individuals (Midha et al. 1989). The half-lives of the
    primary metabolites are generally within the same range (Yeung et al.

    Special populations

    ELDERLY: it has been suggested that the elderly metabolise
    antipsychotic drugs more slowly than do the non-elderly adult
    population (Balant-Gorgia & Balant 1987).

    RENAL IMPAIRMENT: the effects of renal disease on chlorpromazine
    pharmacokinetics are not known, but since it is extensively
    metabolised in the liver, they are not anticipated to be great.

    HEPATIC IMPAIRMENT: it is considered that hepatic dysfunction will
    increase the bioavailability of chlorpromazine and delay its
    elimination (Dollery 1991).


    Breast milk

    Chlorpromazine has been identified in the milk of nursing mothers
    receiving the drug.
    In one study (Blacker et al. 1962) the peak milk concentration of
    chlorpromazine (0.29 mg/L) occurred 2 hours after a single oral dose
    of 1200 mg, although in this report the assay design was relatively
    nonspecific and no account was taken of active metabolites.
    In a later study chlorpromazine and several metabolites were
    identified in the breast milk of four nursing mothers receiving the
    drug (doses not specified). The milk concentrations ranged from
    0.007-0.098 mg/L, with maternal serum levels ranging from 0.016-0.052
    mg/L. In two of the four patients the milk concentrations of
    chlorpromazine were higher than the maternal plasma concentrations.
    One of the babies was reported to be drowsy and lethargic (the milk
    chlorpromazine level in this case was 0.092 mg/L) (Wiles et al. 1978).








    Special populations





    Breast milk



    A phenothiazine antipsychotic.


    Tablets of 10 mg, 25 mg, 50 mg, and 100 mg.
    Oral liquids containing 25 mg / 5 ml, and 100 mg / 5 ml.
    Injection of 25 mg / ml.
    Suppositories of 100 mg (unlicensed product).


    Central nervous system depression is the most common feature of
    toxicity and usually begins 1-2 hours after ingestion. Hypotension and
    anticholinergic symptoms are also common. Acute dystonic reactions and
    cardiac arrhythmias may occur. Chlorpromazine lowers the seizure
    threshold (a dose-related effect) so convulsions may occur in patients
    not previously known to be epileptic.

    Individual response to chlorpromazine overdose is variable - an
    ingestion of 20 g has been survived, whilst 2 g has proved fatal.

    In children, hypotension and drowsiness can follow doses ranging from
    100-375 mg, with severe central nervous system depression resulting
    from higher doses. Fatalities have been reported in children, the
    doses ingested ranging from 20-74 mg/kg.

    In mixed drug ingestions chlorpromazine enhances the sedation produced
    by other central nervous system depressants including ethanol.


    Drowsiness, hypotension, anticholinergic symptoms (e.g. dry mouth,
    dilated pupils, urinary retention, visual disturbances), acute
    dystonic reactions, and cardiac arrhythmias.


    Acute pulmonary oedema, and neuroleptic malignant syndrome.


    1.   Maintain a clear airway and adequate ventilation if consciousness
         is impaired.

    2.   If within 1 hour of the ingestion and more than 500mg has been
         ingested by an adult, or more than 4mg/kg by a child, give oral
         activated charcoal.

    3.   Monitor the cardiac rhythm.

    4.   Manage hypotension with IV fluids.

    5.   Treat acute dystonic reactions with IV procyclidine or

    Clinical Features

    Features - acute


    Hypotension, sinus tachycardia, varying degrees of CNS depression,
    blurred vision, dry mouth, urinary retention, acute dystonic
    reactions, akathisia, parkinsonism, ECG changes including prolonged PR
    and QT intervals, ventricular tachyarrhythmias, convulsions,
    hypothermia (or occasionally hyperthermia), pulmonary oedema, and
    respiratory depression (Allen et al. 1980, Barry et al. 1973,
    Ellenhorn 1997, Li & Gefter 1992, Reid & Harrower 1984).



    Contact dermatitis.


    Other routes

    BY INJECTION: as for acute ingestion.

    Features - chronic


    As for acute ingestion, but with the additional risks of the
    development of neuroleptic malignant syndrome (characterised by muscle
    rigidity, hyperthermia, altered consciousness, and autonomic
    instability), and tardive dyskinesia (involuntary movements of the
    tongue, face, jaw, or mouth) (Rosenberg & Green 1989).



    Contact dermatitis.


    Other routes

    BY INJECTION: as for chronic ingestion.

    At risk groups


    Elderly and volume depleted subjects are particularly susceptible to
    postural hypotension.


    The administration of chlorpromazine near term has been associated
    with unpredictable falls in maternal blood pressure which could be
    dangerous to the mother and the foetus. Administration near term has
    also resulted in an extrapyramidal syndrome in some infants,
    characterised by tremors, increased muscle tone, and hyperactive deep
    tendon reflexes persisting some months (Briggs 1994).

    One psychiatric patient who ingested 8 g of chlorpromazine in the last
    ten days of pregnancy, delivered a hypotonic, lethargic infant with
    depressed reflexes and jaundice (Hammond & Toseland 1970).





    Pharmacists, nurses, and other health workers should avoid direct
    contact with chlorpromazine due to a risk of contact sensitisation.
    Tablets should not be crushed and solutions handled with care (BNF


    RENAL IMPAIRMENT: renal impairment is unlikely to increase the risk of
    HEPATIC IMPAIRMENT: increased risk of toxicity due to impaired
    metabolism and hepatotoxic potential.
    CARDIAC DISEASE: increased risk of cardiotoxicity due to underlying
    EPILEPSY: increased risk of seizures due to lowered seizure threshold.



    If within one hour of the ingestion, and more than 500mg has been
    ingested by an adult, or 100mg by a child, oral activated charcoal may
    be given to reduce drug absorption.
         ADULT DOSE: 50g; CHILD DOSE; 1g/kg.
    If the patient is drowsy this should be administered via a nasogastric
    tube, and if there is no gag reflex present, using an endotracheal
    tube to protect the airway.

    Supportive care


    Clear and maintain airway, and give cardiopulmonary resuscitation if
    Evaluate the patient's condition and provide support for vital
    functions. The aim is to maintain vital bodily functions with minimal
    intervention whilst the elimination of chlorpromazine takes place.
    Particular care should be given to the prevention of hypoxia and
    acidosis, and the correction of any electrolyte imbalance.



    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) 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: vasopressors with mixed alpha and beta adrenergic effects (e.g.
    adrenaline, dopamine) should not be used as hypotension may be

    2.  COMA
    Good supportive care is essential.


    In practice it is seldom necessary or advisable to use specific drug
    treatment for arrhythmias. If hypoxia and acidosis are reversed, and
    adequate serum potassium levels maintained, then the majority of
    patients will show improvement with supportive measures. Where these
    measures fail and life-threatening arrhythmias persist, intravenous
    sodium bicarbonate should be given (even in the absence of acidosis)
    before considering antiarrhythmic drug therapy.
    Where an antiarrhythmic is considered necessary, lignocaine is the
    preferred drug.
         ADULT DOSE: 50-100 mg lignocaine by IV bolus given over a few
    minutes, followed by an infusion of 4 mg/minute for 30 minutes, 2
    mg/minute for 2 hours, then 1 mg/minute (BNF 1998).
    NOTE: the use of quinidine, procainamide, flecainide, or disopyramide,
    is contraindicated as these agents further depress cardiac conduction
    and contractility. The use of beta-blockers and calcium channel
    blockers should also be avoided as they decrease cardiac output and
    exacerbate hypotension.

    The ventricular arrhythmia, TORSADE DE POINTES, may prove difficult to
    manage. The preferred treatment is cardiac overdrive pacing, but in
    cases where cardiac pacemaker insertion is not readily available,
    intravenous magnesium sulphate has been shown to be effective (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).
    Torsade de pointes has also been successfully managed in adults by the
    intravenous administration of 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). However it should be used with
    caution as its beta-2-adrenergic agonist effects exacerbate


    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, and oral:
         ADULT DOSE:    5-10 mg (use lower end of dose range in elderly),
         CHILD DOSE under 2 years: 500 micrograms-2 mg (unlicensed
                   2-10 years:    2-5 mg (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).


    Diazepam by slow intravenous injection preferably in emulsion form,
    may be given to control muscle spasms and convulsions not remitting
         ADULT DOSE: 10 mg repeated as required depending upon clinical
         CHILD DOSE: 200 - 300 micrograms/kg.


    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.


    The development of neuroleptic malignant syndrome 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: 1 mg/kg body weight by rapid IV injection repeated as
    required to a cumulative maximum of 10 mg/kg (BNF 1998).


    Pulmonary oedema typically resolves with conventional supportive
    management within 18-40 hours of ingestion (Li & Gefter 1992).


    Monitor the heart rate and rhythm, blood pressure, arterial blood
    gases, serum electrolytes, body temperature, respiratory rate and
    depth, and urinary output.

    Observe for a minimum of 4 hours post-ingestion where:
         i) more than 4 mg/kg has been ingested by a child (or more than
    the child's normal therapeutic dose, if this is greater),
         ii) more than 500 mg is known to have been ingested by an adult
    (or more than the patients's normal therapeutic dose, if this is
         iii) the patient is symptomatic.
    Where symptoms develop following overdose, they may persist for 24
    hours. Complications following severe toxicity may require the patient
    to be hospitalised for several days.


    None available.

    Elimination techniques

    Haemodialysis and diuresis are ineffective as ways of increasing drug
    elimination due to the large volume of distribution and high lipid
    solubility of chlorpromazine. It is not considered that haemoperfusion
    will be of benefit (Ellenhorn 1997).


    Where there is evidence of severe toxicity a chest radiograph should
    be performed within 24 hours of the ingestion to exclude pulmonary

    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


    A 27 year old woman was admitted 12 hours after ingesting 8 g
    chlorpromazine and 150 mg flurazepam. After 18 hours she was fully
    alert and normotensive. Six hours later she sustained a cardiac arrest
    and was successfully resuscitated. Subsequent ventricular tachycardia
    responded to intravenous lignocaine, and a prolonged QT interval
    shortened progressively to normal over the next three days (Reid &
    Harrower 1984).



    Several studies to determine the relationship between plasma
    concentration and therapeutic response have been performed. The
    majority of studies showed large individual variations in
    chlorpromazine concentration relative to dose, and no clear
    association between plasma concentration and therapeutic response has
    been made (Dahl & Strandjord 1977).
    As a consequence the measurement of plasma chlorpromazine
    concentrations following overdose is not routinely advised.

    Sample container

    Storage conditions


    Interpretation of data

    Although no clear relationship exists between plasma concentration and
    therapeutic effect,
    it has been suggested that therapeutic response may be associated with
    the plasma concentration range 0.05-0.30 mg/L (Rivera-Calimlim et al.
    In a study of unexplained deaths in patients receiving multiple
    antipsychotic therapy, five cases had concentrations of antipsychotic
    drugs which were considered 'probably' toxic and were implicated in
    the development of ventricular fibrillation. The plasma chlorpromazine
    concentrations in these cases were in the range 0.5-7.0 mg/L (Jusic &
    Lader 1994).

    Conversion factors

    1 mg/L = 2.817 micromoles/L
    1 micromole/L = 0.355 mg/L

    The molecular weight of chlorpromazine hydrochloride is 355.3


    Toxicological data






    Chlorpromazine readily crosses the placenta. Although one study found
    an increased incidence of malformations in first trimester
    phenothiazine-exposed infants compared to non-exposed controls
    (3.5%compared to 1.6%), most reports describing the use of
    phenothiazines in pregnancy (during all stages of gestation) conclude
    that they do not adversely affect the foetus or newborn (Briggs 1994).

    Relevant animal data

    Relevant in vitro data


    HY Allen
    ZM Everitt
    AT Judd

    National Poisons Information Service (Leeds Centre)
    Leeds Poisons Information Centre
    Leeds General Infirmary
    LS1 3EX

    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 November 1996
    Updated May 1998


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