(oks A ze pam)
Management of anxiety disorders, including anxiety associated with depression; management of ethanol withdrawal
Hypersensitivity to oxazepam or any component of the formulation (cross-sensitivity with other benzodiazepines may exist)
Anxiety, mild-to-moderate: Oral: 10-15 mg 3-4 times daily
Anxiety, severe or associated with depression: Oral: 15-30 mg 3-4 times daily
Ethanol withdrawal: Oral: 15-30 mg 3-4 times daily
Anxiety: Oral: Initial: 10 mg 3 times daily. If necessary, increase cautiously to 15 mg 3-4 times daily. Dose titration should be slow to evaluate sensitivity.
Children >12 years and Adolescents: Refer to adult dosing.
No dosage adjustment provided in manufacturers labeling
Hemodialysis: Not dialyzable (0% to 5%) (Greenblatt, 1981; Mokhlesi, 2003)
No dosage adjustment provided in manufacturers labeling; however, pharmacokinetic studies have shown that hepatic dysfunction is not expected to significantly decrease clearance (Furlan, 1999; Greenblatt, 1981).
Administer orally in divided doses.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, Oral:
Generic: 10 mg, 15 mg, 30 mg
Alcohol (Ethyl): CNS Depressants may enhance the CNS depressant effect of Alcohol (Ethyl). Monitor therapy
Azelastine (Nasal): CNS Depressants may enhance the CNS depressant effect of Azelastine (Nasal). Avoid combination
Blonanserin: CNS Depressants may enhance the CNS depressant effect of Blonanserin. Consider therapy modification
Brimonidine (Topical): May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Buprenorphine: CNS Depressants may enhance the CNS depressant effect of Buprenorphine. Management: Consider reduced doses of other CNS depressants, and avoiding such drugs in patients at high risk of buprenorphine overuse/self-injection. Initiate buprenorphine patches (Butrans brand) at 5 mcg/hr in adults when used with other CNS depressants. Consider therapy modification
Cannabis: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
CloZAPine: Benzodiazepines may enhance the adverse/toxic effect of CloZAPine. Management: Consider decreasing the dose of (or possibly discontinuing) benzodiazepines prior to initiating clozapine. Consider therapy modification
CNS Depressants: May enhance the adverse/toxic effect of other CNS Depressants. Monitor therapy
Dimethindene: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Doxylamine: May enhance the CNS depressant effect of CNS Depressants. Management: The manufacturer of Diclegis (doxylamine/pyridoxine), intended for use in pregnancy, specifically states that use with other CNS depressants is not recommended. Monitor therapy
Dronabinol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Droperidol: May enhance the CNS depressant effect of CNS Depressants. Management: Consider dose reductions of droperidol or of other CNS agents (e.g., opioids, barbiturates) with concomitant use. Consider therapy modification
Flunitrazepam: CNS Depressants may enhance the CNS depressant effect of Flunitrazepam. Consider therapy modification
Fosphenytoin: Benzodiazepines may increase the serum concentration of Fosphenytoin. Short-term exposure to benzodiazepines may not present as much risk as chronic therapy. Monitor therapy
HYDROcodone: CNS Depressants may enhance the CNS depressant effect of HYDROcodone. Management: Consider starting with a 20% to 30% lower hydrocodone dose when using together with any other CNS depressant. Dose reductions in the other CNS depressant may also be warranted. Consider therapy modification
HydrOXYzine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Kava Kava: May enhance the adverse/toxic effect of CNS Depressants. Monitor therapy
Magnesium Sulfate: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Methadone: Benzodiazepines may enhance the CNS depressant effect of Methadone. Avoid combination
Methotrimeprazine: CNS Depressants may enhance the CNS depressant effect of Methotrimeprazine. Methotrimeprazine may enhance the CNS depressant effect of CNS Depressants. Management: Reduce adult dose of CNS depressant agents by 50% with initiation of concomitant methotrimeprazine therapy. Further CNS depressant dosage adjustments should be initiated only after clinically effective methotrimeprazine dose is established. Consider therapy modification
MetyroSINE: CNS Depressants may enhance the sedative effect of MetyroSINE. Monitor therapy
Minocycline: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Mirtazapine: CNS Depressants may enhance the CNS depressant effect of Mirtazapine. Monitor therapy
Nabilone: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
OLANZapine: May enhance the adverse/toxic effect of Benzodiazepines. Management: Avoid concomitant use of parenteral benzodiazepines and IM olanzapine due to risks of additive adverse events (e.g., cardiorespiratory depression). Olanzapine prescribing information provides no specific recommendations regarding oral administration. Avoid combination
Orphenadrine: CNS Depressants may enhance the CNS depressant effect of Orphenadrine. Avoid combination
OxyCODONE: CNS Depressants may enhance the CNS depressant effect of OxyCODONE. Management: When oxycodone is combined with another CNS depressant, a dose reduction of one or both agents should be considered. The extended release oxycodone starting dose should be reduced 50% to 67% when initiated in patients already receiving CNS depressants. Consider therapy modification
Paraldehyde: CNS Depressants may enhance the CNS depressant effect of Paraldehyde. Avoid combination
Perampanel: May enhance the CNS depressant effect of CNS Depressants. Management: Patients taking perampanel with any other drug that has CNS depressant activities should avoid complex and high-risk activities, particularly those such as driving that require alertness and coordination, until they have experience using the combination. Consider therapy modification
Phenytoin: Benzodiazepines may increase the serum concentration of Phenytoin. Short-term exposure to benzodiazepines may not present as much risk as chronic therapy. Monitor therapy
Piribedil [INT]: CNS Depressants may enhance the CNS depressant effect of Piribedil [INT]. Monitor therapy
Pramipexole: CNS Depressants may enhance the sedative effect of Pramipexole. Monitor therapy
ROPINIRole: CNS Depressants may enhance the sedative effect of ROPINIRole. Monitor therapy
Rotigotine: CNS Depressants may enhance the sedative effect of Rotigotine. Monitor therapy
Rufinamide: May enhance the adverse/toxic effect of CNS Depressants. Specifically, sleepiness and dizziness may be enhanced. Monitor therapy
Selective Serotonin Reuptake Inhibitors: CNS Depressants may enhance the adverse/toxic effect of Selective Serotonin Reuptake Inhibitors. Specifically, the risk of psychomotor impairment may be enhanced. Monitor therapy
Sodium Oxybate: Benzodiazepines may enhance the CNS depressant effect of Sodium Oxybate. Avoid combination
Suvorexant: CNS Depressants may enhance the CNS depressant effect of Suvorexant. Management: Dose reduction of suvorexant and/or any other CNS depressant may be necessary. Use of suvorexant with alcohol is not recommended, and the use of suvorexant with any other drug to treat insomnia is not recommended. Consider therapy modification
Tapentadol: May enhance the CNS depressant effect of CNS Depressants. Management: Start tapentadol at a dose of one-third to one-half of the normal dose if being initiated in a patient who is taking another drug with CNS depressant effects. Monitor closely for evidence of excessive CNS depression. Consider therapy modification
Teduglutide: May increase the serum concentration of Benzodiazepines. Monitor therapy
Tetrahydrocannabinol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Thalidomide: CNS Depressants may enhance the CNS depressant effect of Thalidomide. Avoid combination
Theophylline Derivatives: May diminish the therapeutic effect of Benzodiazepines. Consider therapy modification
Trimeprazine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Yohimbine: May diminish the therapeutic effect of Antianxiety Agents. Monitor therapy
Zolpidem: CNS Depressants may enhance the CNS depressant effect of Zolpidem. Management: Reduce the Intermezzo brand sublingual zolpidem adult dose to 1.75 mg for men who are also receiving other CNS depressants. No such dose change is recommended for women. Avoid use with other CNS depressants at bedtime; avoid use with alcohol. Consider therapy modification
Respiratory and cardiovascular status; periodic CBC and liver function tests
Frequency not defined.
Cardiovascular: Edema, hypotension, syncope
Central nervous system: Amnesia, ataxia, dizziness, drowsiness, drug dependence, dysarthria, euphoria, headache, lethargy, memory impairment, slurred speech, vertigo
Dermatologic: Maculopapular rash, morbilliform rash, urticaria
Endocrine & metabolic: Decreased libido, menstrual disease
Gastrointestinal: Nausea
Genitourinary: Urinary incontinence
Hematologic & oncologic: Hematologic disease, leukopenia
Hepatic: Jaundice
Hypersensitivity: Fixed drug eruption
Neuromuscular & skeletal: Hyporeflexia, tremor
Ophthalmic: Blurred vision, diplopia
Miscellaneous: Paradoxical central nervous system stimulation, paradoxical excitation
In patients with severe renal insufficiency, the elimination half-life of oxazepam was prolonged to a mean of 48 hours (range: 24 to 91); however, clearance of total drug was relatively normal suggesting that a large increase in volume of distribution accounts for the prolongation in half-life (Greenblatt, 1981).
A statistically significant increase in elimination half-life in patients >80 years of age has been reported, due to a 30% increase in volume of distribution and a 50% reduction in unbound clearance of oxazepam.
A small but statistically significant prolongation of half-life elimination (9.7 hours versus 7.8 hours) and reduction of total clearance (0.82 mL/minute/kg versus 1.15 mL/minute/kg) has been reported in females in comparison to males, respectively (Greenblatt, 1981).
Concerns related to adverse effects:
- CNS depression: May cause CNS depression, which may impair physical or mental abilities; patients must be cautioned about performing tasks which require mental alertness (eg, operating machinery or driving).
- Hypotension: May cause hypotension (rare); use with caution in patients with cardiovascular or cerebrovascular disease, or in patients who would not tolerate transient decreases in blood pressure.
- Paradoxical reactions: Paradoxical reactions, including hyperactive or aggressive behavior, have been reported with benzodiazepines, particularly in adolescent/pediatric or psychiatric patients.
- Transient amnesia: Benzodiazepines have been associated with transient amnesia.
Disease-related concerns:
- Depression: Use benzodiazepines with caution in patients with depression, particularly if suicidal risk may be present.
- Drug abuse: Use with caution in patients with a history of drug abuse or acute alcoholism; potential for drug dependency exists. Tolerance, psychological and physical dependence may occur with prolonged use.
- Hepatic impairment: Use with caution in patients with hepatic impairment; however, oxazepam has been shown to be less affected by hepatic dysfunction due to its relative slow extraction by the liver and phase II metabolic pathway (glucuronidation) (Furlan, 1999; Greenblatt, 1981).
- Impaired gag reflex: Use with caution in patients with an impaired gag reflex.
- Respiratory disease: Use with caution in patients with respiratory disease.
Concurrent drug therapy issues:
- CNS depressants/psychoactive medications: Use with caution in patients receiving other CNS depressants or psychoactive medication; effects with other sedative drugs or ethanol may be potentiated.
Special populations:
- Debilitated patients: Use with caution in debilitated patients.
- Elderly: Relative to other benzodiazepines, oxazepam possesses a short half-life and lacks an active metabolite which may be preferable in the elderly if benzodiazepine use is required for anxiety (Flint, 2005). Kinetics were not altered in patients of advanced age compared to younger patients, except in patients >80 years of age where an increased half-life was observed due to an increased volume of distribution and a decrease in unbound clearance.
- Fall risk: Use with extreme caution in patients who are at risk of falls; benzodiazepines have been associated with falls and traumatic injury.
Other warnings/precautions:
- Appropriate use: Does not have analgesic, antidepressant, or antipsychotic properties; not indicated for use in the treatment of psychosis.
- Tolerance: Oxazepam is a short half-life benzodiazepine. Duration of action after a single dose is determined by redistribution rather than metabolism. Tolerance does not develop to the anxiolytic effects (Vinkers, 2012). Chronic use of this agent may increase the perioperative benzodiazepine dose needed to achieve desired effect.
- Withdrawal: Rebound or withdrawal symptoms may occur following abrupt discontinuation or large decreases in dose. Use caution when reducing dose or withdrawing therapy; decrease slowly and monitor for withdrawal symptoms. Flumazenil may cause withdrawal in patients receiving long-term benzodiazepine therapy.
Oxazepam crosses the placenta. Teratogenic effects have been observed with some benzodiazepines; however, additional studies are needed. The incidence of premature birth and low birth weights may be increased following maternal use of benzodiazepines; hypoglycemia and respiratory problems in the neonate may occur following exposure late in pregnancy. Neonatal withdrawal symptoms may occur within days to weeks after birth and "floppy infant syndrome " � (which also includes withdrawal symptoms) have been reported with some benzodiazepines (Bergman, 1992; Iqbal, 2002; Kangas, 1980; Wikner, 2007).
Binds to stereospecific benzodiazepine receptors on the postsynaptic GABA neuron at several sites within the central nervous system, including the limbic system, reticular formation. Enhancement of the inhibitory effect of GABA on neuronal excitability results by increased neuronal membrane permeability to chloride ions. This shift in chloride ions results in hyperpolarization (a less excitable state) and stabilization. Benzodiazepine receptors and effects appear to be linked to the GABA-A receptors. Benzodiazepines do not bind to GABA-B receptors.
Slowly absorbed from the GI tract (Greenblatt, 1981)
Vd: 0.6 to 2 L/kg (Greenblatt, 1981)
Hepatic glucuronide conjugation to produce a single, major inactive metabolite (benzophenone) (Greenblatt, 1981)
Urine (as inactive glucuronide conjugate)
Serum: ~3 hours
~8 hours (range: 6 to 11 hours)
96% to 98%
- Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)
- Patient may experience fatigue or headache. Have patient report immediately to prescriber signs of liver problems (dark urine, feeling tired, lack of appetite, nausea, abdominal pain, light-colored stools, vomiting, or yellow skin or eyes), severe dizziness, passing out, change in balance, edema, slurred speech, tremors, decreased libido, chills, pharyngitis, or memory impairment (HCAHPS).
- Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.
Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for healthcare professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience, and judgment in diagnosing, treating, and advising patients.