Concomitant use of benzodiazepines and opioids may result in profound sedation, respiratory depression, coma, and death. Reserve concomitant prescribing of these drugs for use in patients for whom alternative treatment options are inadequate. Limit dosages and durations to the minimum required. Follow patients for signs and symptoms of respiratory depression and sedation.
The use of benzodiazepines, including oxazepam, exposes users to risks of abuse, misuse, and addiction, which can lead to overdose or death. Abuse and misuse of benzodiazepines commonly involve concomitant use of other medications, alcohol, and/or illicit substances, which is associated with an increased frequency of serious adverse outcomes. Before prescribing oxazepam and throughout treatment, assess each patient's risk for abuse, misuse, and addiction.
The continued use of benzodiazepines, including oxazepam, may lead to clinically significant physical dependence. The risks of dependence and withdrawal increase with longer treatment duration and higher daily dose. Abrupt discontinuation or rapid dosage reduction of oxazepam after continued use may precipitate acute withdrawal reactions, which can be life-threatening. To reduce the risk of withdrawal reactions, use a gradual taper to discontinue oxazepam or reduce the dosage.
Note: Reduce dose or avoid use in patients receiving opioids or with significant chronic disease (eg, respiratory compromise). Avoid use in patients with a history of substance use, misuse of medications, or depression (Craske 2022).
Alcohol withdrawal syndrome, mild to moderate (alternative agent):
Note : Symptom-triggered regimens may be preferred in settings that can provide frequent clinical reassessment. Although longer-acting benzodiazepines are preferred in general, shorter-acting benzodiazepines, including oxazepam, may be preferable in patients with impaired liver function to decrease risk of accumulation and oversedation (ASAM 2020; WFSBP [Soyka 2017]). Safety: If usual total daily doses are insufficient, reassess patient and reconsider withdrawal management strategies. Dosage and frequency may vary; refer to institutional-specific protocols.
Symptom-triggered regimen, mild to moderate withdrawal (eg, CIWA-Ar score ≤20): Oral: 15 to 30 mg as needed per institution-specific protocol until symptoms resolve (eg, 15 mg for CIWA-Ar 8 to 15; 30 mg for CIWA-Ar 16 to 20); dose, frequency, taper, and patient reassessment are determined by withdrawal symptom severity using a validated severity assessment scale score (eg, CIWA-Ar). Usual total daily dose: 120 mg/day (ASAM 2020; Daeppen 2002; Hoffman 2021; WFSBP [Soyka 2017]; manufacturer’s labeling). Alternatively, some experts use the following for very mild withdrawal symptoms (CIWA-Ar <10) in supervised ambulatory settings: 30 mg every 6 hours as needed on day 1, followed by 5 to 15 mg every 6 hours as needed on days 2 to 5 (Holt 2021).
Fixed-dose regimen, mild withdrawal (eg, CIWA-Ar score ≤15): Oral: 30 mg every 6 hours for 1 day, then 15 mg every 6 hours for 2 days; additional doses may be considered based on withdrawal symptoms and validated assessment scale score (eg, CIWA-Ar) (Daeppen 2002; Hoffman 2021; WFSBP [Soyka 2017]; manufacturer’s labeling). Alternatively, some experts use the following higher dose regimen: 30 mg every 6 hours on day 1, followed by 30 mg every 8 hours on day 2, then 30 mg every 12 hours on day 3; then 30 mg at night or as needed (Holt 2021).
Anxiety disorders (adjunctive therapy or monotherapy) (alternative agent):
Note: Generally used short term for symptom relief until preferred therapy (eg, serotonin reuptake inhibitor) is effective (eg, 4 to 6 weeks, followed by tapering). Long-term, low-dose therapy (eg, 7.5 mg/day) may be considered in select patients when other treatments are ineffective or poorly tolerated (Craske 2022; Katzman 2014; WFSBP [Bandelow 2012]). Use with caution in patients with comorbid posttraumatic stress disorder; benzodiazepines may worsen symptoms (VA/DoD 2017).
Oral: Initial: 10 to 15 mg 3 times daily (Ansseau 1990; Rimòn 1991; manufacturer's labeling); although most patients will experience relief with this dose, may increase daily dose based on response and tolerability in increments of 15 to 30 mg every 2 to 3 days to a total daily dose of 30 to 120 mg/day in 3 to 4 divided doses (Craske 2022; manufacturer's labeling). Usual dosage: 45 to 60 mg/day in divided doses (Ansseau 1990; Rimòn 1991).
Discontinuation of therapy: Unless safety concerns require a more rapid withdrawal, gradually taper to detect reemerging symptoms and minimize rebound and withdrawal symptoms (Lader 2011; VA/DoD 2021).
Low or moderate dose, no concerns for benzodiazepine use disorder: Taper total daily dose by 20% to 25% every week based on response and tolerability (taper increments will be limited by available dosage forms) (Craske 2022; VA/DoD 2021).
Extended or high-dose therapy, or suspected benzodiazepine use disorder: Taper total daily dose by approximately 25% every 1 to 2 weeks based on response, tolerability, and individual patient factors (taper increments will be limited by available dosage forms) (Park 2022; VA/DoD 2021). Reduce dose more rapidly in the beginning and slow the dose reduction as the taper progresses because earlier stages of withdrawal are easier to tolerate (Lader 2011; VA/DoD 2021). The optimal duration and taper increment will vary; up to 6 months may be necessary for some patients on higher doses, and a taper rate of 50% every week may be tolerated in some patients (Park 2022; VA/DoD 2021). For benzodiazepines with half-lives significantly <24 hours, including oxazepam, consider substituting an equivalent dose of a long-acting benzodiazepine to allow for a more gradual reduction in drug serum concentrations (Lader 2011; VA/DoD 2021).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling
Hemodialysis: Not dialyzable (0% to 5%) (Greenblatt 1981; Mokhlesi 2003)
There are no dosage adjustment provided in the manufacturer's labeling; however, pharmacokinetic studies have shown that hepatic dysfunction is not expected to significantly decrease clearance (Furlan 1999; Greenblatt 1981).
Children >12 years and Adolescents: Refer to adult dosing.
There are no dosage adjustments provided in the manufacturer's labeling.
Hemodialysis: Not dialyzable (0% to 5%) (Greenblatt 1981; Mokhlesi 2003)
There are no dosage adjustments provided in the manufacturer's labeling; however, pharmacokinetic studies have shown that hepatic dysfunction is not expected to significantly decrease clearance (Furlan 1999; Greenblatt 1981).
Anxiety disorders (adjunctive therapy or monotherapy): Oral: Initial: 10 mg 3 times daily. If necessary, increase cautiously to 15 mg 3 to 4 times daily.
Discontinuation of therapy: Refer to adult dosing.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, Oral:
Generic: 10 mg, 15 mg, 30 mg
Yes
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Generic: 10 mg, 15 mg, 30 mg
C-IV
Oral: Administer without regard to meals.
Alcohol withdrawal syndrome: Management of the symptoms associated with alcohol withdrawal, including tremor and anxiety.
Anxiety disorders: Treatment of anxiety disorders or short-term relief of the symptoms of anxiety, including anxiety associated with depression and anxiety, tension, agitation, and irritability in older patients.
Oxazepam may be confused with oxcarbazepine, oxaprozin, quazepam
Serax may be confused with Eurax, Urex, ZyrTEC
Beers Criteria: Oxazepam is identified in the Beers Criteria as a potentially inappropriate medication to be avoided in patients 65 years and older (independent of diagnosis or condition) due to increased risk of impaired cognition, delirium, falls, fractures, and motor vehicle accidents with benzodiazepine use. However, use may be appropriate in the elderly when used for seizure disorders, rapid eye movement sleep behavior disorders, benzodiazepine or ethanol withdrawal, severe generalized anxiety disorder, or periprocedural anesthesia (Beers Criteria [AGS 2019]).
Murelax [Australia] may be confused with MiraLax brand name for polyethylene glycol 3350 [US]
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. 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
Hypersensitivity to oxazepam or any component of the formulation.
Canadian labeling: Additional contraindications (not in US labeling): Glaucoma (history of); myasthenia gravis; use in infants.
Documentation of allergenic cross-reactivity for drugs in this class is limited. However, because of similarities in chemical structure and/or pharmacologic actions, the possibility of cross-sensitivity cannot be ruled out with certainty.
Concerns related to adverse effects:
• Anterograde amnesia: Benzodiazepines have been associated with anterograde amnesia (Nelson 1999).
• 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 (Mancuso 2004).
• Sleep-related activities: Hazardous sleep-related activities such as sleep-driving, cooking and eating food, and making phone calls while asleep have been noted with benzodiazepines (Dolder 2008).
Disease-related concerns:
• Depression: Avoid use in patients with depression because of concerns about worsening mood symptoms, particularly if suicidal risk may be present, except for acute or emergency situations (eg, acute agitation, status epilepticus) (Craske 2022).
• 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).
• Respiratory disease: Reduce dose or avoid use in patients with respiratory disease, including chronic obstructive pulmonary disease or sleep apnea. Benzodiazepines may cause significant respiratory depression.
Concurrent drug therapy issues:
• Concomitant use with opioids: [US Boxed warning]: Concomitant use of benzodiazepines and opioids may result in profound sedation, respiratory depression, coma, and death. Reserve concomitant prescribing of these drugs for use in patients for whom alternative treatment options are inadequate. Limit dosages and durations to the minimum required. Follow patients for signs and symptoms of respiratory depression and sedation.
Special populations:
• Older adult: Relative to other benzodiazepines, oxazepam possesses a short half-life and lacks an active metabolite which may be preferable in older adults 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. Older adult patients may be at an increased risk of death with use; risk has been found highest within the first 4 months of use in older adult dementia patients (Jennum 2015; Saarelainen 2018).
• Fall risk: Use with extreme caution in patients who are at risk of falls; benzodiazepines have been associated with falls and traumatic injury (Nelson 1999).
Other warnings/precautions:
• Abuse, misuse, and addiction: [US Boxed warning]: The use of benzodiazepines, including oxazepam, exposes users to risks of abuse, misuse, and addiction, which can lead to overdose or death. Abuse and misuse of benzodiazepines commonly involve concomitant use of other medications, alcohol, and/or illicit substances, which is associated with an increased frequency of serious adverse outcomes. Assess each patient's risk for abuse, misuse, and addiction prior to and throughout treatment; counsel patients at increased risk on proper use and monitoring for signs and symptoms of abuse, misuse, and addiction. Institute early treatment or refer patients in whom substance use disorder is suspected. Limit dosages and durations to the minimum required.
• Appropriate use: Does not have analgesic, antidepressant, or antipsychotic properties; not indicated for use in the treatment of psychosis.
• Dependence and withdrawal reactions: [US Boxed warning]: The continued use of benzodiazepines, including oxazepam, may lead to clinically significant physical dependence. The risks of dependence and withdrawal increase with longer treatment duration and higher daily dose. Abrupt discontinuation or rapid dosage reduction of oxazepam after continued use may precipitate acute withdrawal reactions, which can be life-threatening. To reduce the risk of withdrawal reactions, use a gradual taper to discontinue oxazepam or reduce the dosage. Some patients may develop a protracted withdrawal syndrome lasting >12 months; may be difficult to differentiate withdrawal symptoms from reemergence or continuation of symptoms for which benzodiazepines were prescribed. Flumazenil may cause withdrawal in patients receiving long-term benzodiazepine therapy.
• 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.
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Alcohol (Ethyl): CNS Depressants may enhance the CNS depressant effect of Alcohol (Ethyl). Risk C: Monitor therapy
Alizapride: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Azelastine (Nasal): May enhance the CNS depressant effect of CNS Depressants. Risk X: Avoid combination
Blonanserin: CNS Depressants may enhance the CNS depressant effect of Blonanserin. Management: Use caution if coadministering blonanserin and CNS depressants; dose reduction of the other CNS depressant may be required. Strong CNS depressants should not be coadministered with blonanserin. Risk D: Consider therapy modification
Brexanolone: CNS Depressants may enhance the CNS depressant effect of Brexanolone. Risk C: Monitor therapy
Brimonidine (Topical): May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Bromopride: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Bromperidol: May enhance the CNS depressant effect of CNS Depressants. Risk X: Avoid combination
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 at lower doses in patients already receiving CNS depressants. Risk D: Consider therapy modification
Cannabinoid-Containing Products: CNS Depressants may enhance the CNS depressant effect of Cannabinoid-Containing Products. Risk C: Monitor therapy
Chlormethiazole: May enhance the CNS depressant effect of CNS Depressants. Management: Monitor closely for evidence of excessive CNS depression. The chlormethiazole labeling states that an appropriately reduced dose should be used if such a combination must be used. Risk D: Consider therapy modification
Chlorphenesin Carbamate: May enhance the adverse/toxic effect of CNS Depressants. Risk C: 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. Monitor for respiratory depression, hypotension, and other toxicities if these agents are combined. Risk D: Consider therapy modification
CNS Depressants: May enhance the adverse/toxic effect of other CNS Depressants. Risk C: Monitor therapy
Daridorexant: May enhance the CNS depressant effect of CNS Depressants. Management: Dose reduction of daridorexant and/or any other CNS depressant may be necessary. Use of daridorexant with alcohol is not recommended, and the use of daridorexant with any other drug to treat insomnia is not recommended. Risk D: Consider therapy modification
DexmedeTOMIDine: CNS Depressants may enhance the CNS depressant effect of DexmedeTOMIDine. Management: Monitor for increased CNS depression during coadministration of dexmedetomidine and CNS depressants, and consider dose reductions of either agent to avoid excessive CNS depression. Risk D: Consider therapy modification
Difelikefalin: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Dimethindene (Topical): May enhance the CNS depressant effect of CNS Depressants. Risk C: 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. Risk C: Monitor therapy
Droperidol: May enhance the CNS depressant effect of CNS Depressants. Management: Consider dose reductions of droperidol or of other CNS agents (eg, opioids, barbiturates) with concomitant use. Risk D: Consider therapy modification
Esketamine: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Flunarizine: CNS Depressants may enhance the CNS depressant effect of Flunarizine. Risk X: Avoid combination
Flunitrazepam: CNS Depressants may enhance the CNS depressant effect of Flunitrazepam. Management: Reduce the dose of CNS depressants when combined with flunitrazepam and monitor patients for evidence of CNS depression (eg, sedation, respiratory depression). Use non-CNS depressant alternatives when available. Risk D: Consider therapy modification
HydrOXYzine: May enhance the CNS depressant effect of CNS Depressants. Management: Consider a decrease in the CNS depressant dose, as appropriate, when used together with hydroxyzine. Increase monitoring of signs/symptoms of CNS depression in any patient receiving hydroxyzine together with another CNS depressant. Risk D: Consider therapy modification
Kava Kava: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Kratom: May enhance the CNS depressant effect of CNS Depressants. Risk X: Avoid combination
Lemborexant: May enhance the CNS depressant effect of CNS Depressants. Management: Dosage adjustments of lemborexant and of concomitant CNS depressants may be necessary when administered together because of potentially additive CNS depressant effects. Close monitoring for CNS depressant effects is necessary. Risk D: Consider therapy modification
Lisuride: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Lofexidine: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Magnesium Sulfate: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Melatonin: May enhance the sedative effect of Benzodiazepines. Risk C: Monitor therapy
Methadone: Benzodiazepines may enhance the CNS depressant effect of Methadone. Management: Clinicians should generally avoid concurrent use of methadone and benzodiazepines when possible; any combined use should be undertaken with extra caution. Risk D: Consider therapy modification
Methotrimeprazine: CNS Depressants may enhance the CNS depressant effect of Methotrimeprazine. Methotrimeprazine may enhance the CNS depressant effect of CNS Depressants. Management: Reduce the usual dose of CNS depressants by 50% if starting methotrimeprazine until the dose of methotrimeprazine is stable. Monitor patient closely for evidence of CNS depression. Risk D: Consider therapy modification
Metoclopramide: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
MetyroSINE: CNS Depressants may enhance the sedative effect of MetyroSINE. Risk C: Monitor therapy
Minocycline (Systemic): May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
OLANZapine: Benzodiazepines may enhance the adverse/toxic effect of OLANZapine. Management: Monitor closely for hypotension, respiratory or central nervous system depression, and bradycardia if olanzapine is combined with benzodiazepines. Use of parenteral benzodiazepines with IM olanzapine is not recommended. Risk C: Monitor therapy
Olopatadine (Nasal): May enhance the CNS depressant effect of CNS Depressants. Risk X: Avoid combination
Opioid Agonists: CNS Depressants may enhance the CNS depressant effect of Opioid Agonists. Management: Avoid concomitant use of opioid agonists and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Risk D: Consider therapy modification
Orphenadrine: CNS Depressants may enhance the CNS depressant effect of Orphenadrine. Risk X: Avoid combination
Oxomemazine: May enhance the CNS depressant effect of CNS Depressants. Risk X: Avoid combination
Oxybate Salt Products: Benzodiazepines may enhance the CNS depressant effect of Oxybate Salt Products. Risk X: Avoid combination
OxyCODONE: CNS Depressants may enhance the CNS depressant effect of OxyCODONE. Management: Avoid concomitant use of oxycodone and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Risk D: Consider therapy modification
Paraldehyde: CNS Depressants may enhance the CNS depressant effect of Paraldehyde. Risk X: Avoid combination
Perampanel: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Piribedil: CNS Depressants may enhance the CNS depressant effect of Piribedil. Risk C: Monitor therapy
Pramipexole: CNS Depressants may enhance the sedative effect of Pramipexole. Risk C: Monitor therapy
Procarbazine: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Ropeginterferon Alfa-2b: CNS Depressants may enhance the adverse/toxic effect of Ropeginterferon Alfa-2b. Specifically, the risk of neuropsychiatric adverse effects may be increased. Management: Avoid coadministration of ropeginterferon alfa-2b and other CNS depressants. If this combination cannot be avoided, monitor patients for neuropsychiatric adverse effects (eg, depression, suicidal ideation, aggression, mania). Risk D: Consider therapy modification
ROPINIRole: CNS Depressants may enhance the sedative effect of ROPINIRole. Risk C: Monitor therapy
Rotigotine: CNS Depressants may enhance the sedative effect of Rotigotine. Risk C: Monitor therapy
Rufinamide: May enhance the adverse/toxic effect of CNS Depressants. Specifically, sleepiness and dizziness may be enhanced. Risk C: Monitor therapy
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. Risk D: Consider therapy modification
Teduglutide: May increase the serum concentration of Benzodiazepines. Risk C: Monitor therapy
Thalidomide: CNS Depressants may enhance the CNS depressant effect of Thalidomide. Risk X: Avoid combination
Theophylline Derivatives: May diminish the therapeutic effect of Benzodiazepines. Risk C: Monitor therapy
Trimeprazine: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Valerian: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Yohimbine: May diminish the therapeutic effect of Antianxiety Agents. Risk C: 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. Risk D: Consider therapy modification
Oxazepam crosses the placenta (Kangas 1980).
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; Shyken 2019; Tinker 2019; Wikner 2007). Newborns exposed to oxazepam in utero should be monitored for feeding problems, respiratory depression, sedation, and withdrawal.
Data collection to monitor pregnancy and infant outcomes following exposure to oxazepam is ongoing. Health care providers are encouraged to enroll patients exposed to oxazepam during pregnancy in the National Pregnancy Registry for Psychiatric Medications (866-961-2388).
Oxazepam is present in breast milk (Wretlind 1987).
Drowsiness, lethargy, or weight loss in breastfeeding infants have been observed in case reports following maternal use of some benzodiazepines (Iqbal 2002). According to the manufacturer, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and the benefits of treatment to the mother. Infants exposed to oxazepam via breastmilk should be monitored for feeding problems, respiratory depression, and poor weight gain.
Respiratory and cardiovascular status (as clinically indicated); CBC (periodic); liver function tests (periodic)
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 (Vinkers 2012).
Absorption: Slowly absorbed from the GI tract (Greenblatt 1981)
Distribution: Vd: 0.6 to 2 L/kg (Greenblatt 1981)
Protein binding: 96% to 98% (Greenblatt 1981)
Metabolism: Hepatic glucuronide conjugation to produce a single, major inactive metabolite (benzophenone) (Greenblatt 1981)
Half-life elimination: ~8 hours (range: 6 to 11 hours)
Time to peak, serum: ~3 hours
Excretion: Urine (as inactive glucuronide conjugate)
Altered kidney function: 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).
Older adult: 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.
Sex: 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).
Capsules (Oxazepam Oral)
10 mg (per each): $1.15
15 mg (per each): $1.45
30 mg (per each): $2.10
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