Haldol Decanoas 50Mg/ml 1AHALDOL Decanoate proviron while on cycle indicated for the maintenance treatment of schizophrenia and schizoaffective disorder in adult patients currently stabilised with oral haloperidol see section 5. The haldol decanoas 50 mg / 1 ml dose will depend on both the severity of the symptoms and mh current oral haloperidol dose. Patients must always be maintained on the lowest effective dose. As the initial dose of haloperidol decanoate is based on a multiple of the daily oral haloperidol dose, specific guidance on switching from other antipsychotics cannot be provided mt section 5. Haloperidol decanoate dose recommendations for adults aged 18 years and above. Transition from oral haloperidol. Supplementation with non-decanoate haloperidol.
Haldol Decanoate - Summary of Product Characteristics (SmPC) - (eMC)
HALDOL Decanoate is indicated for the maintenance treatment of schizophrenia and schizoaffective disorder in adult patients currently stabilised with oral haloperidol see section 5. The individual dose will depend on both the severity of the symptoms and the current oral haloperidol dose.
Patients must always be maintained on the lowest effective dose. As the initial dose of haloperidol decanoate is based on a multiple of the daily oral haloperidol dose, specific guidance on switching from other antipsychotics cannot be provided see section 5. Haloperidol decanoate dose recommendations for adults aged 18 years and above. Transition from oral haloperidol.
Supplementation with non-decanoate haloperidol. The influence of renal impairment on the pharmacokinetics of haloperidol has not been evaluated. No dose adjustment is recommended, but caution is advised when treating patients with renal impairment. However, patients with severe renal impairment may require a lower initial dose, with subsequent adjustments at smaller increments and at longer intervals than in patients without renal impairment see section 5.
The influence of hepatic impairment on the pharmacokinetics of haloperidol has not been evaluated. Since haloperidol is extensively metabolised in the liver, it is recommended to halve the initial dose, and adjust the dose with smaller increments and at longer intervals than in patients without hepatic impairment see sections 4. No data are available. It is administered as a deep intramuscular injection in the gluteal region.
It is recommended to alternate between the two gluteal muscles. As the administration of volumes greater than 3 ml is uncomfortable for the patient, such large volumes are not recommended. Rare cases of sudden death have been reported in psychiatric patients receiving antipsychotics, including haloperidol see section 4.
Elderly patients with dementia-related psychosis treated with antipsychotics are at an increased risk of death. Analyses of seventeen placebo-controlled studies modal duration of 10 weeks , largely in patients taking atypical antipsychotics, revealed a risk of death in treated patients of between 1. Over the course of a typical 10 week controlled study, the rate of death in patients treated with antipsychotics was about 4.
Although the causes of death were varied, most of the deaths appeared to be either cardiovascular e. Observational studies suggest that treatment of elderly patients with haloperidol is also associated with increased mortality. This association may be stronger for haloperidol than for atypical antipsychotic medicinal products, is most pronounced in the first 30 days after the start of treatment, and persists for at least 6 months. The extent to which this association is attributable to the medicinal product, as opposed to being confounded by patient characteristics, has not yet been elucidated.
The risk of these events appears to increase with high doses, high plasma concentrations, in predisposed patients or with parenteral use, particularly intravenous administration.
Caution is advised in patients with bradycardia, cardiac disease, family history of QTc prolongation or history of heavy alcohol exposure. Caution is also required in patients with potentially high plasma concentrations see section 4. A baseline ECG is recommended before treatment. During therapy, the need for ECG monitoring for QTc interval prolongation and for ventricular arrhythmias must be assessed in all patients.
Whilst on therapy, it is recommended to reduce the dose if QTc is prolonged, but haloperidol must be discontinued if the QTc exceeds ms. Electrolyte disturbances such as hypokalaemia and hypomagnesaemia increase the risk for ventricular arrhythmias and must be corrected before treatment with haloperidol is started. Therefore, baseline and periodic electrolyte monitoring is recommended. Tachycardia and hypotension including orthostatic hypotension have also been reported see section 4.
Caution is recommended when haloperidol is administered to patients manifesting hypotension or orthostatic hypotension. In randomised, placebo-controlled clinical studies in the dementia population, there was an approximately 3-fold increased risk of cerebrovascular adverse events with some atypical antipsychotics. Observational studies comparing the stroke rate in elderly patients exposed to any antipsychotic to the stroke rate in those not exposed to such medicinal products found an increased stroke rate among exposed patients.
This increase may be higher with all butyrophenones, including haloperidol. The mechanism for this increased risk is not known.
An increased risk cannot be excluded for other patient populations. Haloperidol has been associated with neuroleptic malignant syndrome: Hyperthermia is often an early sign of this syndrome. Antipsychotic treatment must be withdrawn immediately and appropriate supportive therapy and careful monitoring instituted.
Tardive dyskinesia may appear in some patients on long-term therapy or after discontinuation of the medicinal product. The syndrome is mainly characterized by rhythmic involuntary movements of the tongue, face, mouth or jaw.
The manifestations may be permanent in some patients. The syndrome may be masked when treatment is reinstituted, when the dose is increased or when a switch is made to a different antipsychotic. If signs and symptoms of tardive dyskinesia appear, the discontinuation of all antipsychotics, including HALDOL Decanoate, must be considered. Extrapyramidal symptoms may occur e. The use of haloperidol has been associated with the development of akathisia, characterised by a subjectively unpleasant or distressing restlessness and need to move, often accompanied by an inability to sit or stand still.
This is most likely to occur within the first few weeks of treatment. In patients who develop these symptoms, increasing the dose may be detrimental. Acute dystonia may occur during the first few days of treatment with haloperidol, but later onset as well as onset after dose increases has been reported. Dystonic symptoms can include, but are not limited to, torticollis, facial grimacing, trismus, tongue protrusion, and abnormal eye movements, including oculogyric crisis.
Males and younger age groups are at higher risk of experiencing such reactions. Acute dystonia may necessitate stopping the medicinal product. Antiparkinson medicinal products of the anticholinergic type may be prescribed as required to manage extrapyramidal symptoms, but it is recommended that they are not prescribed routinely as a preventive measure. If concomitant treatment with an antiparkinson medicinal product is required, it may have to be continued after stopping HALDOL Decanoate if its excretion is faster than that of haloperidol in order to avoid the development or aggravation of extrapyramidal symptoms.
The possible increase in intraocular pressure must be considered when anticholinergic medicinal products, including antiparkinson medicinal products, are administered concomitantly with HALDOL Decanoate.
It has been reported that seizures can be triggered by haloperidol. Caution is advised in patients suffering from epilepsy and in conditions predisposing to seizures e. As haloperidol is metabolised by the liver, dose adjustment and caution is advised in patients with hepatic impairment see sections 4. Isolated cases of liver function abnormalities or hepatitis, most often cholestatic, have been reported see section 4.
Thyroxin may facilitate haloperidol toxicity. Antipsychotic therapy in patients with hyperthyroidism must be used only with caution and must always be accompanied by therapy to achieve a euthyroid state.
Hormonal effects of antipsychotics include hyperprolactinaemia, which may cause galactorrhoea, gynaecomastia and oligomenorrhea or amenorrhoea see section 4. Tissue culture studies suggest that cell growth in human breast tumours may be stimulated by prolactin. Although no clear association with the administration of antipsychotics and human breast tumours has been demonstrated in clinical and epidemiological studies, caution is recommended in patients with relevant medical history.
HALDOL Decanoate must be used with caution in patients with pre-existing hyperprolactinaemia and in patients with possible prolactin-dependent tumours see section 5. Hypoglycaemia and syndrome of inappropriate antidiuretic hormone secretion have been reported with haloperidol see section 4.
Cases of venous thromboembolism VTE have been reported with antipsychotics. Patients being considered for HALDOL Decanoate therapy must be initially treated with oral haloperidol to reduce the possibility of an unexpected adverse sensitivity to haloperidol. It may be combined with antidepressants to treat those conditions in which depression and psychosis coexist see section 4. Caution is advised when HALDOL Decanoate is used in combination with medicinal products known to cause electrolyte imbalance see section 4.
Haloperidol is metabolised by several routes see section 5. The major pathways are glucuronidation and ketone reduction. Inhibition of these routes of metabolism by another medicinal product or a decrease in CYP2D6 enzyme activity may result in increased haloperidol concentrations.
Examples of medicinal products that may increase haloperidol plasma concentrations based on clinical experience or drug interaction mechanism include:. Increased haloperidol plasma concentrations may result in an increased risk of adverse events, including QTc-prolongation see section 4. It is recommended that patients who take haloperidol concomitantly with such medicinal products be monitored for signs or symptoms of increased or prolonged pharmacologic effects of haloperidol, and the HALDOL Decanoate dose be decreased as deemed necessary.
Coadministration of haloperidol with potent enzyme inducers of CYP3A4 may gradually decrease the plasma concentrations of haloperidol to such an extent that efficacy may be reduced. Enzyme induction may be observed after a few days of treatment. Maximal enzyme induction is generally seen in about 2 weeks and may then be sustained for the same period of time after the cessation of therapy with the medicinal product.
Sodium valproate is known to inhibit glucuronidation, but does not affect haloperidol plasma concentrations. Haloperidol can increase the CNS depression produced by alcohol or CNS-depressant medicinal products, including hypnotics, sedatives or strong analgesics.
An enhanced CNS effect, when combined with methyldopa, has also been reported. Haloperidol may antagonise the action of adrenaline and other sympathomimetic medicinal products e. Haloperidol is an inhibitor of CYP2D6. Haloperidol inhibits the metabolism of tricyclic antidepressants e. In rare cases the following symptoms were reported during the concomitant use of lithium and haloperidol: Most of these symptoms were reversible. It remains unclear whether this represents a distinct clinical entity.
Nonetheless, it is advised that in patients who are treated concomitantly with lithium and HALDOL Decanoate, therapy must be stopped immediately if such symptoms occur. However, there have been isolated case reports of birth defects following foetal exposure to haloperidol in combination with other medicinal products.
Animal studies have shown reproductive toxicity see section 5. There have been reports of agitation, hypertonia, hypotonia, tremor, somnolence, respiratory distress, or feeding disorder. Consequently, it is recommended that newborn infants be monitored carefully.
Haloperidol is excreted in human milk. Small amounts of haloperidol have been detected in plasma and urine of breast-fed newborns of mothers treated with haloperidol.
There is insufficient information on the effects of haloperidol in breast-fed infants.