Version May 2024
Note: Adjust dose based on patient's age, weight, and condition.
Sedative/preanesthesia:
IM: 150 to 200 mg, as a single dose.
IV: Initial: 100 mg; if needed, may administer additional increments after at least 1 minute, up to a total dose of 200 to 500 mg.
Seizures: IV: Note: Mechanical ventilation and cardiovascular monitoring required; titrate dose to cessation of electrographic seizures or burst suppression (NCS [Brophy 2012]).
Neurocritical Care Society recommendations (NCS [Brophy 2012]):
Loading dose: 5 to 15 mg/kg administered at a rate of ≤50 mg/minute, may give additional 5 to 10 mg/kg; follow with a continuous infusion.
Continuous infusion: 0.5 to 5 mg/kg/hour. If the patient experiences breakthrough status epilepticus while on continuous infusion, administer an additional 5 mg/kg bolus and increase infusion rate by 0.5 to 1 mg/kg/hour every 12 hours. Note: A period of at least 24 to 48 hours of electrographic control is recommended prior to withdrawing the continuous infusion; withdraw gradually to prevent recurrent status epilepticus.
Barbiturate coma in severe brain injury patients/elevated intracranial pressure (off-label use): IV: Loading dose: 10 mg/kg given over 30 minutes (or ≤25 mg/minute), followed by 5 mg/kg every hour for 3 doses; monitor blood pressure and respiratory rate. Maintenance infusion: Initial: 1 mg/kg/hour; may increase to 2 to 4 mg/kg/hour; maintain burst suppression on EEG (Censullo 2003; Eisenberg 1988).
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. However, a reduced dosage is recommended.
Note: A risk of propylene glycol toxicity exists in patients receiving pentobarbital, especially in patients with renal impairment; monitor closely (eg, osmolal gap) if using for prolonged periods of time or at high doses (Miller 2008; Pillai 2014).
There are no dosage adjustments provided in the manufacturer’s labeling. However, a reduced dosage is recommended.
Avoid use (Ref).
(For additional information see "Pentobarbital: Pediatric drug information")
Note: Adjust dose based on patient's age, weight, kidney and liver function, and medical condition. Consider the potential for delayed metabolism or elimination in infants <6 months of age (Krauss 2006).
Hypnotic: Note: Use has generally been replaced by other agents.
Infants, Children, and Adolescents: IM: 2 to 6 mg/kg/dose; maximum dose: 100 mg/dose.
Preoperative sedation: Note: Use has generally been replaced by other agents.
Infants, Children, and Adolescents:
IM: 2 to 6 mg/kg/dose; maximum dose: 100 mg/dose (Krauss 2006; manufacturer's labeling).
IV: 1 to 3 mg/kg/dose every 10 minutes up to a maximum total dose of 6 mg/kg, not to exceed total dose of 100 mg (Coté 2013; Coté 2019; manufacturer's labeling).
Procedural sedation: Note: Use has generally been replaced by other agents.
IM: Infants, Children, and Adolescents: IM: 2 to 6 mg/kg; maximum dose: 100 mg/dose (Krauss 2006).
IV: Infants, Children, and Adolescents: IV: Initial: 1 to 2 mg/kg/dose; additional doses of 1 to 2 mg/kg every 3 to 5 minutes to desired effect; usual effective total dose: 1 to 6 mg/kg; maximum total dose: 100 mg (Krauss 2006; Mason 2004). Note: Patients receiving concurrent barbiturate therapy may require higher total mg/kg doses (up to 9 mg/kg) (Mason 2004).
Oral: Limited data available:
Infants: Oral: Initial: 4 mg/kg/dose; if needed, may administer supplemental doses of 2 to 4 mg/kg/dose every 30 minutes; maximum total dose: 8 mg/kg (Mason 2004).
Children <4 years: Oral: 3 to 6 mg/kg/dose; maximum dose: 100 mg/dose (Krauss 2006).
Children ≥4 years and Adolescents: Oral: 1.5 to 3 mg/kg/dose; maximum dose: 100 mg/dose (Krauss 2006).
Rectal: Limited data available:
Children <4 years: Rectal: 3 to 6 mg/kg/dose; maximum dose: 100 mg/dose (Krauss 2006).
Children ≥4 years and Adolescents: Rectal: 1.5 to 3 mg/kg/dose; maximum dose: 100 mg/dose (Krauss 2006).
Reduction of elevated intracranial pressure (ICP): Limited data available: Note: Intubation is required; adjust dose based on hemodynamics, ICP, cerebral perfusion pressure, and EEG; continuous arterial blood pressure monitoring and cardiovascular support are recommended (BTF [Kochanek 2019]).
Children and Adolescents: Note: Reserve higher doses for use in patients with refractory intracranial hypertension (BTF [Kochanek 2019]).
Bolus dose: IV: 5 to 10 mg/kg over 20 to 30 minutes; may repeat 5 mg/kg as needed based on clinical response and clinical target (Adelson 2003; Mazzola 2002; Rangel-Castilla 2008; Shein 2016).
Continuous IV infusion: Initial: 1 mg/kg/hour; adjust to maintain burst suppression on EEG; maintenance dose range: 1 to 2 mg/kg/hour (Adelson 2003; Rangel-Castilla 2008).
Sedation of mechanically ventilated ICU patient (alternative agent): Limited data available:
Infants, Children, and Adolescents: IV: Loading dose: 1 mg/kg followed by a continuous IV infusion of 1 mg/kg/hour. Additional boluses at a dose equal to hourly rate may be given every 2 hours as needed. If ≥4 to 6 boluses are administered within 24 hours, then increase maintenance rate by 1 mg/kg/hour; reported required range: 1 to 6 mg/kg/hour (median: 2 mg/kg/hour). Tapering of dose and/or conversion to oral phenobarbital has been reported for therapy ≥5 days (Tobias 1995; Tobias 2000a; Tobias 2000b). Note: Higher rates of adverse effects were observed in a small report that used higher loading and initial maintenance doses (Yanay 2004).
Status epilepticus refractory to standard therapy: Note: Mechanical ventilation and cardiovascular monitoring required; monitor blood pressure and respiratory rate; titrate dose to cessation of electrographic seizures or burst suppression (AES [Glauser 2016]; NCS [Brophy 2012]).
Infants, Children, and Adolescents:
Loading dose: IV: Usual dose: 5 mg/kg; doses up to 15 mg/kg have been described; administration >50 mg/minute is not recommended (NCS [Brophy 2012]).
Continuous IV infusion: Initial: 0.5 to 1 mg/kg/hour; may increase up to 5 mg/kg/hour; maintain burst suppression on EEG for 24 to 48 hours (no seizure activity); if the patient experiences breakthrough status epilepticus while on continuous infusion, administer an additional 5 mg/kg bolus and increase infusion rate by 0.5 to 1 mg/kg/hour every 12 hours until burst suppression (Abend 2008; Holmes 1999; Kim 2001; NCS [Brophy 2012]). Note: Withdraw gradually to prevent withdrawal seizures (Holmes 1999; Kim 2001; NCS [Brophy 2012]).
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. However, a reduced dosage is recommended.
Note: A risk of propylene glycol toxicity exists in patients receiving pentobarbital, especially in patients with renal impairment; monitor closely (eg, osmolar gap) if using for prolonged periods of time or at high doses (Miller 2008; Pillai 2014).
There are no dosage adjustments provided in the manufacturer's labeling. However, a reduced dosage is recommended.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
Frequency not defined.
Cardiovascular: Bradycardia, hypotension, syncope
Central nervous system: Abnormality in thinking, agitation, anxiety, ataxia, central nervous system stimulation, confusion, depression, dizziness, drowsiness, hallucination, headache, insomnia, nervousness, nightmares, psychiatric disturbance
Dermatologic: Exfoliative dermatitis, skin rash
Gastrointestinal: Constipation, nausea, vomiting
Hematologic & oncologic: Megaloblastic anemia
Hepatic: Hepatotoxicity
Hypersensitivity: Angioedema, hypersensitivity reaction
Local: Injection site reaction
Neuromuscular & skeletal: Hyperkinesia, laryngospasm
Respiratory: Apnea (especially with rapid IV use), hypoventilation, respiratory depression
Miscellaneous: Fever
Hypersensitivity to barbiturates or any component of the formulation; porphyria.
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).
• Respiratory depression: May cause respiratory depression particularly when administered intravenously; use with caution in patients with respiratory disease. Intubation is typically required prior to treatment for seizures or traumatic brain injury (NCS [Brophy 2012]).
Disease-related concerns:
• Depression: Use with caution in patients with depression or suicidal tendencies.
• Hepatic impairment: Use with caution in patients with hepatic impairment; reduce dose as appropriate. Do not use in patients showing premonitory signs of hepatic coma.
• Renal impairment: Use with caution in patients with renal impairment; reduce dose as appropriate.
• Substance abuse: Use with caution in patients with a history of drug abuse; potential for drug dependency exists. Tolerance, psychological and physical dependence may occur with prolonged use.
Special populations:
• Debilitated patients: Use with caution in patients who are debilitated; marked excitement, depression, and confusion may occur.
• Older adult: Use with caution in older adult patients; marked excitement, depression, and confusion may occur.
• Pediatric neurotoxicity: In pediatric and neonatal patients <3 years of age and patients in third trimester of pregnancy (ie, times of rapid brain growth and synaptogenesis), the repeated or lengthy exposure to sedatives or anesthetics during surgery/procedures may have detrimental effects on child or fetal brain development and may contribute to various cognitive and behavioral problems. Epidemiological studies in humans have reported various cognitive and behavioral problems, including neurodevelopmental delay (and related diagnoses), learning disabilities, and ADHD. Human clinical data suggest that single, relatively short exposures are not likely to have similar negative effects. No specific anesthetic/sedative has been found to be safer. For elective procedures, risk vs benefits should be evaluated and discussed with parents/caregivers/patients; critical surgeries should not be delayed (FDA 2016).
Dosage form specific issues:
• Propylene glycol: Some dosage forms may contain propylene glycol; large amounts are potentially toxic and have been associated with hyperosmolality, lactic acidosis, seizures, and respiratory depression; use caution (AAP 1997; Zar 2007). See manufacturer’s labeling.
Other warnings/precautions:
• Acute or chronic pain: Use caution when administering to patients with acute or chronic pain; paradoxical excitement could be induced or important symptoms could be masked.
• Appropriate use: IV administration: Too rapid IV administration may cause respiratory depression, apnea, laryngospasm, or vasodilation with hypotension.
• Withdrawal: Antiseizure medications should not be discontinued abruptly because of the possibility of increasing seizure frequency; therapy should be withdrawn gradually to minimize the potential of increased seizure frequency, unless safety concerns require a more rapid withdrawal.
In pediatric and neonatal patients <3 years of age and patients in third trimester of pregnancy (ie, times of rapid brain growth and synaptogenesis), the repeated or lengthy exposure to sedatives or anesthetics during surgery/procedures may have detrimental effects on the child's or fetus' brain development and may contribute to various cognitive and behavioral problems; the FDA is requiring warnings be included in the manufacturer's labeling for all general anesthetic/sedative drugs. Multiple animal species studies have shown adverse effects on brain maturation; in juvenile animals, drugs that potentiate GABA activity and/or block NMDA receptors for >3 hours demonstrated widespread neuronal and oligodendrocyte cell loss along with alteration in synaptic morphology and neurogenesis. Epidemiological studies in humans have reported various cognitive and behavioral problems including neurodevelopmental delay (and related diagnoses), learning disabilities, and attention deficit hyperactivity disorder (ADHD). Human clinical data suggest that single, relatively short exposures are not likely to have similar negative effects. Further studies are needed to fully characterize findings and ensure that these findings are not related to underlying conditions or the procedure itself. No specific anesthetic/sedative has been found to be safer. For elective procedures, risk vs benefits should be evaluated and discussed with parents/caregivers/patients; critical surgeries should not be delayed (FDA 2016).
Some dosage forms may contain propylene glycol; in neonates, large amounts of propylene glycol delivered orally, intravenously (eg, >3,000 mg/day), or topically have been associated with potentially fatal toxicities which can include metabolic acidosis, seizures, renal failure, and CNS depression; toxicities have also been reported in children and adults including hyperosmolality, lactic acidosis, seizures, and respiratory depression; use caution (AAP 1997; Shehab 2009).
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Solution, Injection, as sodium:
Nembutal: 50 mg/mL (20 mL [DSC], 50 mL [DSC]) [latex free; contains alcohol, usp, propylene glycol]
Generic: 50 mg/mL (20 mL, 50 mL)
Solution, Injection, as sodium [preservative free]:
Generic: 50 mg/mL (20 mL, 50 mL)
Yes
Solution (PENTObarbital Sodium Injection)
50 mg/mL (per mL): $72.62 - $84.00
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C-II
Administer by deep IM or slow IV injection.
IM: Inject into a large muscle. No more than 5 mL (250 mg) should be injected at any one site because of possible tissue irritation.
IV: Do not exceed 50 mg/minute; IV push doses may be given undiluted. Parenteral solutions are highly alkaline; may be an irritant; avoid extravasation. Avoid intra-arterial injection. Discontinue administration of injection if patient complains of limb pain.
Parenteral:
IM: May be administered by deep IM; inject into a large muscle. No more than 5 mL should be injected at any one site because of possible tissue irritation.
IV:
Intermittent IV injection: Administer undiluted (50 mg/mL) by slow IV injection; infuse over 10 to 30 minutes not to exceed 50 mg/minute; rapid IV injection may cause respiratory depression, apnea, laryngospasm, bronchospasm, and hypotension; loading doses have been infused over 30 to 160 minutes in traumatic brain injury patients to decrease the risk of hypotension and decrease cerebral perfusion pressure (Schaible 1982; Wermeling 1987).
Continuous IV infusion: Administer at a concentration ≤50 mg/mL via infusion pump; if administering diluted solution monitor for precipitation (Gupta 2001; Sugai 1998). Solution highly alkaline (pH=9.5); care should be taken to avoid extravasation; consider administration using large bore vein (not hand or wrist) or via a running IV line at port farthest from patient's vein.
Oral: Parenteral solution may be mixed with flavored (eg, cherry) syrup prior to administration to improve palatability (Chung 2000; Mason 2004).
Sedative/preanesthesia: Short-term (<2 weeks) treatment of insomnia or as preanesthesia.
Limitations of use: Note: The manufacturer labeling includes indications as a hypnotic for short-term treatment of insomnia; however, pentobarbital is no longer recommended to be used this way (Schutte-Rodin 2008).
Seizures: Emergency control of certain anticonvulsive episodes (eg, status epilepticus, cholera, eclampsia, meningitis, tetanus, toxic reactions to strychnine or local anesthetics).
Barbiturate coma in severe brain injury patients/elevated intracranial pressure
PENTobarbital may be confused with PHENobarbital
Nembutal may be confused with Myambutol
Beers Criteria: Pentobarbital 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 its high rate of physical dependence, tolerance to sleep benefits, and increased risk of overdose at low dosages (Beers Criteria [AGS 2023]).
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
Blood Pressure Lowering Agents: Barbiturates may enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
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
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
Desmopressin: Hyponatremia-Associated Agents may enhance the hyponatremic effect of Desmopressin. Risk C: Monitor therapy
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
Doxycycline: Barbiturates may decrease the serum concentration of Doxycycline. Risk C: Monitor therapy
Doxylamine: CNS Depressants may enhance the CNS depressant effect of Doxylamine. 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
Griseofulvin: Barbiturates may decrease the serum concentration of Griseofulvin. Risk C: Monitor therapy
Hemin: Barbiturates may diminish the therapeutic effect of Hemin. 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
Ixabepilone: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
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
Mefloquine: May diminish the therapeutic effect of Antiseizure Agents. Mefloquine may decrease the serum concentration of Antiseizure Agents. Management: Mefloquine is contraindicated for malaria prophylaxis in persons with a history of seizures. If antiseizure drugs are being used for another indication, monitor antiseizure drug concentrations and treatment response closely with concurrent use. 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
Methoxyflurane: Barbiturates may enhance the nephrotoxic effect of Methoxyflurane. Barbiturates may increase the metabolism of Methoxyflurane. Risk X: Avoid combination
Metoclopramide: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Metoprolol: PENTobarbital may enhance the hypotensive effect of Metoprolol. PENTobarbital may decrease the serum concentration of Metoprolol. Risk C: Monitor therapy
MetroNIDAZOLE (Systemic): May enhance the adverse/toxic effect of Products Containing Propylene Glycol. A disulfiram-like reaction may occur. Risk X: Avoid combination
MetyraPONE: Antiseizure Agents may diminish the diagnostic effect of MetyraPONE. Management: Consider alternatives to the use of the metyrapone test in patients taking antiseizure agents. Risk D: Consider therapy modification
MetyroSINE: CNS Depressants may enhance the sedative effect of MetyroSINE. Risk C: Monitor therapy
Mianserin: May enhance the CNS depressant effect of Barbiturates. Mianserin may diminish the therapeutic effect of Barbiturates. Barbiturates may decrease the serum concentration of Mianserin. Risk X: Avoid combination
Minocycline (Systemic): May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Multivitamins/Minerals (with ADEK, Folate, Iron): May decrease the serum concentration of Barbiturates. Risk C: Monitor therapy
Nabilone: May enhance the CNS depressant effect of CNS Depressants. Risk X: Avoid combination
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
Ornidazole: May enhance the adverse/toxic effect of Products Containing Propylene Glycol. Specifically, a disulfiram-like reaction may occur. Risk X: Avoid combination
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: CNS Depressants may enhance the CNS depressant effect of Oxybate Salt Products. Management: Consider alternatives to this combination when possible. If combined, dose reduction or discontinuation of one or more CNS depressants (including the oxybate salt product) should be considered. Interrupt oxybate salt treatment during short-term opioid use Risk D: Consider therapy modification
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
Secnidazole: Products Containing Propylene Glycol may enhance the adverse/toxic effect of Secnidazole. Risk X: 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. Risk D: Consider therapy modification
Thalidomide: CNS Depressants may enhance the CNS depressant effect of Thalidomide. Risk X: Avoid combination
Theophylline Derivatives: Barbiturates may decrease the serum concentration of Theophylline Derivatives. Risk C: Monitor therapy
Tricyclic Antidepressants: Barbiturates may increase the metabolism of Tricyclic Antidepressants. Management: Monitor for decreased efficacy of tricyclic antidepressants if a barbiturate is initiated/dose increased, or increased effects if a barbiturate is discontinued/dose decreased. Tricyclic antidepressant dose adjustments are likely required. Risk D: Consider therapy modification
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
Valproate Products: May increase the serum concentration of Barbiturates. Barbiturates may decrease the serum concentration of Valproate Products. Risk C: Monitor therapy
Vitamin K Antagonists (eg, warfarin): Barbiturates may increase the metabolism of Vitamin K Antagonists. Management: Monitor INR more closely. Anticoagulant dose increases of 30% to 60% may be needed after a barbiturate is initiated or given at an increased dose. Anticoagulant dose decreases may be needed following barbiturate discontinuation or dose reduction. Risk D: Consider therapy modification
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
Zuranolone: May enhance the CNS depressant effect of CNS Depressants. Management: Consider alternatives to the use of zuranolone with other CNS depressants or alcohol. If combined, consider a zuranolone dose reduction and monitor patients closely for increased CNS depressant effects. Risk D: Consider therapy modification
Barbiturates can be detected in the placenta, fetal liver and fetal brain. Fetal and maternal blood concentrations may be similar following parenteral administration. An increased incidence of fetal abnormalities may occur following maternal use. When used during the third trimester of pregnancy, withdrawal symptoms may occur in the neonate including seizures and hyperirritability; symptoms may be delayed up to 14 days. Use of hypnotic doses during labor does not impair uterine activity; however, use of full anesthetic doses decrease the force and frequency of uterine contractions. Respiratory depression may occur in the newborn when sedative-hypnotic barbiturates are administered to the mother during labor; resuscitation equipment should be available, especially for premature infants.
Barbiturates are present in breast milk. The manufacturer recommends that caution be exercised when administering pentobarbital to breastfeeding women.
Respiratory status (for conscious sedation, includes pulse oximetry), cardiovascular status, CNS status; cardiac monitor and blood pressure monitor required; clinical signs of propylene glycol toxicity (for continuous high-dose and/or long duration IV use), including serum creatinine, BUN, serum lactate, and osmolal gap (Miller 2008; Pillai 2014). Monitor infusion site.
Barbiturate coma: Monitor oxygenation as well as arterial and central venous pressures to guide fluid and vasoactive therapy for maintenance of blood pressure; temperature
Elevated ICP: Monitor ICP, CPP, EEG
Therapeutic:
Sedation: 1 to 5 mcg/mL (SI: 4 to 22 micromole/L)
Coma or intracranial pressure therapy: Target: 30 to 40 mcg/mL (SI: 132 to 176 micromole/L) (Eisenberg 1988)
Potentially toxic: >10 mcg/mL (SI: >44 micromole/L); dependent on reason for use and patient condition
Barbiturate with sedative, hypnotic, and antiseizure properties. Barbiturates depress the sensory cortex, decrease motor activity, alter cerebellar function, and produce drowsiness, sedation, and hypnosis. In high doses, barbiturates exhibit antiseizure activity; barbiturates produce dose-dependent respiratory depression; reduce brain metabolism and cerebral blood flow in order to decrease intracranial pressure
Onset of action (Krauss 2006): Children and Adults: Sedation: IM: 10 to 15 minutes; IV: Almost immediate, within 3 to 5 minutes; Oral, Rectal: 15 to 60 minutes
Duration (Krauss 2006): Children and Adults: Sedation: IM: 1 to 2 hours; IV: 15 to 45 minutes; Oral, Rectal: 1 to 4 hours
Distribution: Vd: Children: 0.8 L/kg (Schaible 1982); Adults: 1 L/kg (Ehrnebo 1974)
Protein binding: 45% to 70%
Metabolism: Hepatic via hydroxylation and glucuronidation (Wermeling 1985)
Half-life elimination: Terminal: Children: 26 ± 16 hours (Schaible 1982); Adults: Healthy: 22 hours (average) (Ehrnebo 1974); Range: 15 to 50 hours; dose dependent
Excretion: Urine (<1%, as unchanged drug)
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