Concomitant use of benzodiazepines and opioids may result in profound sedation, respiratory depression, coma, and death. Reserve concomitant prescribing of these drugs 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 triazolam, 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 triazolam and throughout treatment, assess each patient's risk for abuse, misuse, and addiction.
The continued use of benzodiazepines, including triazolam, 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 triazolam 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 triazolam or reduce the dosage.
Note: Reduce dose or avoid use in patients receiving opioids, with significant chronic disease (eg, respiratory compromise), or at increased risk for accumulation (eg, advanced cirrhosis). Avoid use in patients with a history of substance use, misuse of medications, or depression (Craske 2022).
Dental preprocedure oral sedation (off-label use): 0.25 mg 1 hour before procedure; 0.125 mg used for elderly patients or patients sensitive to sedative effects (Dionne 2006).
Insomnia, sleep onset (alternative agent):
Note: Due to risk of next day impairment, dependence, and habituation, benzodiazepines should be reserved for patients in whom alternative, safer therapies for insomnia have failed (Neubauer 2021). When used, limit long-term use (>4 weeks) to cases for which nonpharmacologic treatments are not available or not effective and benefits are felt to outweigh risks (ACP [Qaseem 2016]; ESRS [Riemann 2017]).
Oral: Initial: 0.125 to 0.25 mg once daily at bedtime, as needed; may increase daily dose to 0.5 mg at bedtime, if needed, based on response and tolerability.
Discontinuation of therapy: Reduce by 0.125 mg every 1 to 2 weeks until lowest available dose is reached, then discontinue. Patients on long-term therapy or in whom discontinuation has previously failed may benefit from a slower taper in conjunction with cognitive behavioral therapy for insomnia (Bélanger 2009).
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; use with caution.
There are no dosage adjustments provided in the manufacturer's labeling; use with caution.
(For additional information see "Triazolam: Pediatric drug information")
Insomnia (short-term use): Adolescents ≥18 years: Oral: 0.125 to 0.25 mg at bedtime; the lower dose of 0.125 mg at bedtime may be sufficient in some patients, such as those with low body weight; maximum daily dose: 0.5 mg/day
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; use with caution.
There are no dosage adjustments provided in the manufacturer's labeling; use with caution.
Insomnia, sleep onset (alternative agent): Oral: Initial: 0.125 mg once daily, as needed, at bedtime; maximum dose: 0.25 mg/day. Avoid use (Beers Criteria [AGS 2019]).
Discontinuation of therapy: Refer to adult dosing.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Halcion: 0.25 mg [scored]
Generic: 0.125 mg, 0.25 mg
Yes
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Generic: 0.25 mg
C-IV
An FDA-approved patient medication guide, which is available with the product information and at https://www.accessdata.fda.gov/drugsatfda_docs/label/2021/017892s055lbl.pdf#page=20, must be dispensed with this medication.
Oral: Administer on an empty stomach; do not take with a meal or immediately after a meal. Onset of action is rapid; patient should take immediately before bedtime.
Oral: Administer dose in bed, since onset of hypnotic effect is rapid; tablet may be crushed or swallowed whole
Insomnia, sleep onset: Short-term (generally 7 to 10 days) treatment of insomnia.
Oral sedation prior to outpatient dental procedures
Triazolam may be confused with alPRAZolam
Halcion may be confused with halcinonide, Haldol
Beers Criteria: Triazolam 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]).
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
>10%: Nervous system: Drowsiness (14%)
1% to 10%:
Gastrointestinal: Nausea and vomiting (5%)
Nervous system: Ataxia (5%), dizziness (5% to 8%), headache (10%)
<1%:
Cardiovascular: Tachycardia
Dermatologic: Dermatitis
Gastrointestinal: Constipation, diarrhea, dysgeusia, xerostomia
Nervous system: Abnormal dreams, confusion, depression, dysesthesia, euphoria, insomnia, memory impairment, nightmares, pain, paresthesia
Neuromuscular & skeletal: Asthenia, muscle cramps
Ophthalmic: Visual disturbance
Otic: Tinnitus
Respiratory: Paranasal sinus congestion
Postmarketing:
Cardiovascular: Chest pain, syncope
Dermatologic: Pruritus
Endocrine & metabolic: Change in libido, menstrual disease
Gastrointestinal: Anorexia, glossalgia, glossitis, stomatitis
Genitourinary: Urinary incontinence, urinary retention
Hepatic: Jaundice
Nervous system: Abnormal behavior, aggressive behavior, agitation, anterograde amnesia, anxiety, central nervous system depression, complex sleep-related disorder, delusion, depersonalization, drug habituation, dysarthria, dystonia, falling, fatigue, hallucination, impaired consciousness, irritability, mania, rebound insomnia, restlessness, sedated state, somnambulism, withdrawal syndrome
Neuromuscular & skeletal: Muscle spasticity
Miscellaneous: Paradoxical reaction
Hypersensitivity to triazolam, other benzodiazepines, or any component of the formulation; concurrent therapy with strong cytochrome P450 3A (CYP 3A) inhibitors (eg, itraconazole, ketoconazole, nefazodone, lopinavir, ritonavir).
Canadian labeling: Additional contraindications (not in the US labeling): History of paradoxical reactions to alcohol and/or sedative medications; history of substance or alcohol abuse; myasthenia gravis; narrow-angle glaucoma; pregnancy.
Concerns related to adverse effects:
• Amnesia: Benzodiazepines have been associated with anterograde amnesia (Nelson 1999). Traveler's amnesia (if taken to induce sleep while traveling) due to insufficient time for sleep prior to awakening and initiating activity has also been reported.
• 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).
• Hypersensitivity reactions: Reports of hypersensitivity reactions, including anaphylaxis and angioedema, have been reported with triazolam. Patients who develop angioedema should not be rechallenged with triazolam.
• Paradoxical reactions: Paradoxical reactions, including hyperactive or aggressive behavior, have been reported with benzodiazepines; risk may be increased in adolescent/pediatric patients, geriatric patients, or patients with a history of alcohol use disorder or psychiatric/personality disorders (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; undergoes extensive hepatic metabolism.
• Renal impairment: Use with caution in patients with renal impairment.
• 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.
• Sleep apnea: Benzodiazepines can suppress respiratory drive in patients with obstructive sleep apnea; use caution when prescribing for insomnia in this population (Webster 2020).
Special populations:
• Debilitated patients: Use with caution in debilitated patients; potential for oversedation, impaired coordination, and dizziness with use.
• Older adult: Older adult patients experience greater sedation and increased psychomotor impairment (Greenblatt 1991). 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: 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. Should be used only after evaluation of potential causes of sleep disturbance. Failure of sleep disturbance to resolve after 7 to 10 days may indicate psychiatric or medical illness. Use for >21 days requires complete reevaluation of patient. A worsening of insomnia or the emergence of new abnormalities of thought or behavior may represent unrecognized psychiatric or medical illness and requires immediate and careful evaluation. Prescription should be written for a maximum of 7 to 10 days and should not be prescribed in quantities exceeding a 1-month supply. Use lowest effective dose; adverse reactions of triazolam are dose related.
• Dependence and withdrawal reactions: 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.
• Rebound insomnia: Following withdrawal of therapy, transient insomnia may recur accompanied by other reactions including restlessness, anxiety, and mood changes (Bélanger 2009).
• Tolerance: Triazolam is a short half-life benzodiazepine. Duration of action after a single dose is determined by redistribution rather than metabolism. Tolerance develops to the hypnotic effects (Vinkers 2012). Chronic use of this agent may increase the perioperative benzodiazepine dose needed to achieve desired effect.
• Withdrawal: A longer sleep-onset latency and increased awakenings during sleep may occur for 1 to 2 days following the discontinuation of GABA-mediated (GABAergic) medications. A more severe withdrawal syndrome may rarely occur following abrupt discontinuation or large decreases in dose after sustained use (>10 days), and is characterized by new-onset agitation, ataxia, depersonalization, dizziness, dysphoria, fatigue, headache, hypersensitivity to stimuli, irritability, muscle cramps or pain, nausea, sweating, twitching, vomiting, and weakness. This withdrawal syndrome generally resolves within weeks or upon re-initiation of the GABAergic medication. Intermittent dosing may reduce the risk of withdrawal symptoms (BAP [Wilson 2019]). Use caution when reducing dose or withdrawing therapy; decrease slowly and monitor for withdrawal symptoms.
Substrate of CYP3A4 (major); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential
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
Clofazimine: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). 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
CYP3A4 Inducers (Moderate): May decrease the serum concentration of Triazolam. Risk C: Monitor therapy
CYP3A4 Inducers (Strong): May decrease the serum concentration of Triazolam. Management: Consider alternatives to this combination when possible. If combined, monitor for reduced triazolam efficacy. Substantial triazolam dose increases will likely be required. Risk D: Consider therapy modification
CYP3A4 Inhibitors (Moderate): May increase the serum concentration of Triazolam. Management: Consider triazolam dose reduction in patients receiving concomitant moderate CYP3A4 inhibitors. Risk D: Consider therapy modification
CYP3A4 Inhibitors (Strong): May increase the serum concentration of Triazolam. Risk X: Avoid combination
CYP3A4 Inhibitors (Weak): May increase the serum concentration of Triazolam. 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
Delavirdine: May increase the serum concentration of Triazolam. Risk X: Avoid combination
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
Erdafitinib: May increase the serum concentration of CYP3A4 Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk X: Avoid combination
Esketamine: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Fexinidazole: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk X: Avoid combination
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
Fusidic Acid (Systemic): May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk X: Avoid combination
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
Itraconazole: May increase the serum concentration of Triazolam. Risk X: Avoid combination
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
Pacritinib: May increase the serum concentration of CYP3A4 Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk X: Avoid combination
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
RaNITIdine (Withdrawn from US Market): May increase the serum concentration of Triazolam. 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
Spironolactone: May increase the serum concentration of CYP3A4 Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). 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
Tipranavir: May increase the serum concentration of Triazolam. Risk X: Avoid combination
Treosulfan: May increase the serum concentration of CYP3A4 Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk X: Avoid combination
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
Benzodiazepine serum concentrations may be increased by grapefruit juice. Management: Limit or avoid grapefruit juice (Sugimoto 2006).
A case report describes placental transfer of triazolam following a maternal overdose (Sakai 1996).
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; Wikner 2007). Infants exposed to triazolam during pregnancy should be monitored for respiratory depression, sedation, withdrawal, or feeding problems.
Data collection to monitor pregnancy and infant outcomes following exposure to triazolam is ongoing. Health care providers are encouraged to enroll females exposed to triazolam during pregnancy in the National Pregnancy Registry for Other Psychiatric Medications (866-961-2388 or https://womensmentalhealth.org/research/pregnancyregistry/othermedications/).
It is not known if triazolam is present in breast milk.
Although information specific to triazolam has not been located, all benzodiazepines are expected to be present in breast milk. Drowsiness, lethargy, or weight loss in breastfed infants have been observed in case reports following maternal use of some benzodiazepines (Iqbal 2002). According to the manufacturer, the decision to continue or discontinue breastfeeding 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 triazolam via breast milk should be monitored for respiratory depression, sedation, withdrawal, or feeding problems. Breastfeeding women may express and discard milk during therapy and for 28 hours after the last triazolam dose to minimize possible exposure to the infant.
Respiratory rate.
Binds to stereospecific benzodiazepine receptors on the postsynaptic GABA neuron at several sites within the central nervous system, including the limbic system and 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).
Onset of action: Hypnotic: 15 to 30 minutes (Pakes 1981)
Duration of action: Hypnotic: 6 to 7 hours
Distribution: Vd: 0.6 to 1.7 L/kg (Pakes 1981)
Protein binding: 89% (Pakes 1981)
Metabolism: Extensively hepatic; hydroxylation via CYP3A4 (initial step in metabolism) with subsequent glucuronide conjugation to 6 metabolites, including a short-acting active metabolite, alpha-hydroxytriazolam (Pakes 1981)
Half-life elimination: 1.5 to 5.5 hours
Time to peak: Oral: Within 2 hours
Excretion: Urine (~80% as metabolites; small amounts as unchanged drug)
Older adult: Cmax and AUC are increased; clearance is decreased (Greenblatt 1991)
Tablets (Halcion Oral)
0.25 mg (per each): $6.80
Tablets (Triazolam Oral)
0.125 mg (per each): $3.67 - $6.04
0.25 mg (per each): $3.67 - $6.04
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