database updatedHaloperidol is an antipsychotic drug that has similar actions to the antipsychotic medicine phenothiazine. The drug works as an inverse agonist of dopamine, a chemical haldol moa the brain involved in thinking, feeling and behavior. Haloperidol is classified as a highly potent neuroleptic, meaning it relieves nervous tension through the depression of nerve function. Haloperidol haldol moa around fifty times stronger than chlorpromazine, the first antipsychotic drug that was haldol moa in Haloperidol has shown beneficial effects in the treatment of delusions and hallucinations. These effects are mainly achieved proviron arimidex cycle blockage of dopamine receptors in the mesocortex and limbic system.
Haloperidol | C21H23ClFNO2 - PubChem
Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death. Analyses of seventeen placebo-controlled trials modal duration of 10 weeks , largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1. Over the course of a typical 10 week controlled trial, the rate of death in drug-treated patients was about 4. Although the causes of death were varied, most of the deaths appeared to be either cardiovascular e.
Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality. The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic s of the patients is not clear.
It has a markedly extended duration of effect. It is available in sesame oil in sterile form for intramuscular IM injection. The structural formula of haloperidol decanoate, 4- 4-chlorophenyl [4- 4-fluorophenyl oxobutyl]-4 piperidinyl decanoate, is:. Haloperidol decanoate is almost insoluble in water 0.
Before using haloperidol, tell your doctor or pharmacist if you are allergic to it; or if you have any other allergies. This product may contain inactive ingredients such as sesame oil , which can cause allergic reactions or other problems. Talk to your pharmacist for more details. This medication should not be used if you have certain medical conditions. Before using this medicine, consult your doctor or pharmacist if you have: Before using this medication, tell your doctor or pharmacist your medical history, especially of: A 21 gauge needle is recommended.
The maximum volume per injection site should not exceed 3 mL. Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.
These patients should be previously stabilized on antipsychotic medication before considering a conversion to haloperidol decanoate. Furthermore, it is recommended that patients being considered for haloperidol decanoate therapy have been treated with, and tolerate well, short-acting HALDOL haloperidol in order to reduce the possibility of an unexpected adverse sensitivity to haloperidol. Close clinical supervision is required during the initial period of dose adjustment in order to minimize the risk of overdosage or reappearance of psychotic symptoms before the next injection.
During dose adjustment or episodes of exacerbation of symptoms of schizophrenia , haloperidol decanoate therapy can be supplemented with short-acting forms of haloperidol. The starting dose of haloperidol decanoate should be based on the patient's age, clinical history, physical condition, and response to previous antipsychotic therapy.
The preferred approach to determining the minimum effective dose is to begin with lower initial doses and to adjust the dose upward as needed. For patients previously maintained on low doses of antipsychotics e. Conversion from oral haloperidol to haloperidol decanoate can be achieved by using an initial dose of haloperidol decanoate that is 10 to 20 times the previous daily dose in oral haloperidol equivalents. In patients who are elderly, debilitated, or stable on low doses of oral haloperidol e.
In patients previously maintained on higher doses of antipsychotics for whom a low dose approach risks recurrence of psychiatric decompensation and in patients whose long-term use of haloperidol has resulted in a tolerance to the drug, 20 times the previous daily dose in oral haloperidol equivalents should be considered for initial conversion, with downward titration on succeeding injections.
The initial dose of haloperidol decanoate should not exceed mg regardless of previous antipsychotic dose requirements. If, therefore, conversion requires more than mg of haloperidol decanoate as an initial dose, that dose should be administered in two injections, i. The maintenance dosage of haloperidol decanoate must be individualized with titration upward or downward based on therapeutic response. The usual maintenance range is 10 to 15 times the previous daily dose in oral haloperidol equivalents dependent on the clinical response of the patient.
Close clinical supervision is required during initiation and stabilization of haloperidol decanoate therapy. Haloperidol decanoate is usually administered monthly or every 4 weeks. Clinical experience with haloperidol decanoate at doses greater than mg per month has been limited.
Do not refrigerate or freeze. Since vast experience has accumulated with HALDOL, the adverse reactions are reported for that compound as well as for haloperidol decanoate. As with all injectable medications, local tissue reactions have been reported with haloperidol decanoate. Tachycardia , hypotension , and hypertension have been reported. The nature of the evidence makes it impossible to determine definitively what role, if any, HALDOL played in the outcome of the reported cases.
The possibility that HALDOL caused death cannot, of course, be excluded, but it is to be kept in mind that sudden and unexpected death may occur in psychotic patients when they go untreated or when they are treated with other antipsychotic drugs.
EPS can be categorized generally as Parkinson-like symptoms, akathisia , or dystonia including opisthotonos and oculogyric crisis. While all can occur at relatively low doses, they occur more frequently and with greater severity at higher doses.
The symptoms may be controlled with dose reductions or administration of antiparkinson drugs such as benztropine mesylate USP or trihexyphenidyl hydrochloride USP. It should be noted that persistent EPS have been reported; the drug may have to be discontinued in such cases.
Symptoms of dystonia, prolonged abnormal contractions of muscle groups, may occur in susceptible individuals during the first few days of treatment. While these symptoms can occur at low doses, they occur more frequently and with greater severity with high potency and at higher doses of first generation antipsychotic drugs.
An elevated risk of acute dystonia is observed in males and younger age groups. Generally, patients receiving short-term therapy experience no problems with abrupt discontinuation of antipsychotic drugs. However, some patients on maintenance treatment experience transient dyskinetic signs after abrupt withdrawal.
In certain of these cases the dyskinetic movements are indistinguishable from the syndrome described below under " Tardive Dyskinesia " except for duration. Although the long- acting properties of haloperidol decanoate provide gradual withdrawal, it is not known whether gradual withdrawal of antipsychotic drugs will reduce the rate of occurrence of withdrawal emergent neurological signs.
Tardive dyskinesia, a syndrome consisting of potentially irreversible, involuntary, dyskinetic movements, may appear in some patients on long-term therapy with haloperidol decanoate or may occur after drug therapy has been discontinued.
The risk appears to be greater in elderly patients on high-dose therapy, especially females. The symptoms are persistent and in some patients appear irreversible.
The syndrome is characterized by rhythmical involuntary movements of tongue, face, mouth or jaw e. Sometimes these may be accompanied by involuntary movements of extremities and the trunk.
There is no known effective treatment for tardive dyskinesia; antiparkinson agents usually do not alleviate the symptoms of this syndrome.
It is suggested that all antipsychotic agents be discontinued if these symptoms appear. Should it be necessary to reinstitute treatment, or increase the dosage of the agent, or switch to a different antipsychotic agent, this syndrome may be masked. It has been reported that fine vermicular movement of the tongue may be an early sign of tardive dyskinesia and if the medication is stopped at that time the full syndrome may not develop.
Tardive dystonia, not associated with the above syndrome, has also been reported. Tardive dystonia is characterized by delayed onset of choreic or dystonic movements, is often persistent, and has the potential of becoming irreversible.
Reports have appeared citing the occurrence of mild and usually transient leukopenia and leukocytosis , minimal decreases in red blood cell counts, anemia , or a tendency toward lymphomonocytosis.
Agranulocytosis has rarely been reported to have occurred with the use of HALDOL, and then only in association with other medication. Maculopapular and acneiform skin reactions and isolated cases of photosensitivity and loss of hair.
Lactation , breast engorgement, mastalgia , menstrual irregularities, gynecomastia , impotence , increased libido , hyperglycemia , hypoglycemia and hyponatremia. Anorexia , constipation, diarrhea , hypersalivation, dyspepsia , nausea and vomiting. Dry mouth , blurred vision , urinary retention, diaphoresis and priapism. Cataracts, retinopathy and visual disturbances. An encephalopathic syndrome characterized by weakness, lethargy, fever , tremulousness and confusion, extrapyramidal symptoms, leukocytosis, elevated serum enzymes, BUN , and FBS followed by irreversible brain damage has occurred in a few patients treated with lithium plus HALDOL.
A causal relationship between these events and the concomitant administration of lithium and HALDOL has not been established; however, patients receiving such combined therapy should be monitored closely for early evidence of neurological toxicity and treatment discontinued promptly if such signs appear.
In 5 other schizophrenic patients treated with oral haloperidol and rifampin, discontinuation of rifampin produced a mean 3. Thus, careful monitoring of clinical status is warranted when rifampin is administered or discontinued in haloperidol-treated patients. Cases of sudden death, QT-prolongation, and Torsades de Pointes have been reported in patients receiving haloperidol. Higher than recommended doses of any formulation and intravenous administration of haloperidol appear to be associated with a higher risk of QT-prolongation and Torsades de Pointes.
Although cases have been reported even in the absence of predisposing factors, particular caution is advised in treating patients with other QT-prolonging conditions including electrolyte imbalance [particularly hypokalemia and hypomagnesemia ], drugs known to prolong QT, underlying cardiac abnormalities, hypothyroidism , and familial long QT-syndrome.
A syndrome consisting of potentially irreversible, involuntary , dyskinetic movements may develop in patients treated with antipsychotic drugs. Although the prevalence of the syndrome appears to be highest among the elderly, especially elderly women, it is impossible to rely upon prevalence estimates to predict, at the inception of antipsychotic treatment, which patients are likely to develop the syndrome. Whether antipsychotic drug products differ in their potential to cause tardive dyskinesia is unknown.
Both the risk of developing tardive dyskinesia and the likelihood that it will become irreversible are believed to increase as the duration of treatment and the total cumulative dose of antipsychotic drugs administered to the patient increase. However, the syndrome can develop, although much less commonly, after relatively brief treatment periods at low doses. There is no known treatment for established cases of tardive dyskinesia, although the syndrome may remit, partially or completely, if antipsychotic treatment is withdrawn.
Antipsychotic treatment, itself, however, may suppress or partially suppress the signs and symptoms of the syndrome and thereby may possibly mask the underlying process. The effect that symptomatic suppression has upon the long-term course of the syndrome is unknown. Given these considerations, antipsychotic drugs should be prescribed in a manner that is most likely to minimize the occurrence of tardive dyskinesia.
Chronic antipsychotic treatment should generally be reserved for patients who suffer from a chronic illness that 1 is known to respond to antipsychotic drugs, and 2 for whom alternative, equally effective, but potentially less harmful treatments are not available or appropriate.
In patients who do require chronic treatment, the smallest dose and the shortest duration of treatment producing a satisfactory clinical response should be sought. The need for continued treatment should be reassessed periodically. If signs and symptoms of tardive dyskinesia appear in a patient on antipsychotics, drug discontinuation should be considered. However, some patients may require treatment despite the presence of the syndrome.
A potentially fatal symptom complex sometimes referred to as Neuroleptic Malignant Syndrome NMS has been reported in association with antipsychotic drugs. Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status including catatonic signs and evidence of autonomic instability irregular pulse or blood pressure , tachycardia , diaphoresis, and cardiac dysrhythmias.
Additional signs may include elevated creatine phosphokinase, myoglobinuria rhabdomyolysis and acute renal failure. The diagnostic evaluation of patients with this syndrome is complicated.
In arriving at a diagnosis , it is important to identify cases where the clinical presentation includes both serious medical illness e. Other important considerations in the differential diagnosis include central anticholinergic toxicity, heat stroke , drug fever and primary central nervous system CNS pathology.
The management of NMS should include 1 immediate discontinuation of antipsychotic drugs and other drugs not essential to concurrent therapy, 2 intensive symptomatic treatment and medical monitoring, and 3 treatment of any concomitant serious medical problems for which specific treatments are available.