The influence of renal impairment on the pharmacokinetics of haloperidol has not been evaluated. About one-third of a haloperidol dose is excreted in urine, mostly as metabolites. Less than 3% of administered haloperidol is eliminated unchanged in the urine. Haloperidol metabolites are not considered to make a significant contribution to its activity, although for the reduced metabolite of haloperidol, back-conversion to haloperidol cannot be fully ruled out. Even though impairment of renal function is not expected to affect haloperidol elimination to a clinically relevant extent, caution is advised in patients with renal impairment, and especially those with severe impairment, due to the long half-life of haloperidol and its reduced metabolite, and the possibility of accumulation (see section ).
-Initial dose: to 10 mg orally in divided doses every 6 to 8 hours
-Maintenance dose: 1 to 5 mg/day
-Maximum dose: Up to 40 mg/day
-Maintenance doses may be given as single daily doses.
-Many patients achieve therapeutic effect with doses of less than 20 mg. Patients who are severely disturbed or inadequately controlled may require a dose of up to 40 mg/day.
Fluphenazine Decanoate for Injection:
-Initial dose: to 25 mg deep IM injection into the gluteal region
-Maintenance dose: to 100 mg IM, usually every 3 to 4 weeks
-Maximum dose: 100 mg/injection
Fluphenazine HCl for Injection:
-Initial dose: to 10 mg IM, given as divided doses every 6 to 8 hours
-Maximum dose: Up to 10 mg/day
-Patients may switch from Fluphenazine HCl for Injection to oral formulations when symptoms are controlled. The dose of an oral formulation is approximately 2 to 3 times the dose of fluphenazine HCl for injection.
-Fluphenazine decanoate for injection may be given subcutaneously.
-Management of manifestations of schizophrenia
-Management of patients requiring prolonged parenteral neuroleptic therapy (., patients with chronic schizophrenia)
Neuroleptic drugs elevate prolactin levels; the elevation persists during chronic administration. Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin dependent in vitro , a factor of potential importance if the prescription of these drugs is contemplated in a patient with a previously detected breast cancer . Although disturbances such as galactorrhea , amenorrhea , gynecomastia , and impotence have been reported, the clinical significance of elevated serum prolactin levels is unknown for most patients. An increase in mammary neoplasms has been found in rodents after chronic administration of neuroleptic drugs. Neither clinical studies nor epidemiologic studies conducted to date, however, have shown an association between chronic administration of these drugs and mammary tumorigenesis; the available evidence is considered too limited to be conclusive at this time.