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  1. Pharmacology. Phenobarbital is a barbiturate commonly used as an anticonvulsant. Because of the delay in onset of the therapeutic effect of phenobarbital, diazepam (See Benzodiazepines (Diazepam, Lorazepam, and Midazolam)) is usually the initial agent for parenteral anticonvulsant therapy. After an oral dose of phenobarbital, peak brain concentrations are achieved within 10–15 hours. Onset of effect after intravenous administration usually occurs within 5 minutes, although peak effects may take up to 30 minutes. Therapeutic plasma levels are 15–35 mg/L. The drug is eliminated by metabolism and renal excretion, and the elimination half-life is 48–100 hours.

  2. Indications

    1. Control of tonic-clonic seizures and status epilepticus, generally as a second- or third-line agent after diazepam or phenytoin has been tried. Note: For treatment of drug-induced seizures, especially seizures caused by theophylline, phenobarbital often is tried before phenytoin.

    2. Management of withdrawal from ethanol and other sedative-hypnotic drugs.

  3. Contraindications

    1. Known sensitivity to barbiturates.

    2. Manifest or latent porphyria.

  4. Adverse effects

    1. Central nervous system depression, coma, and respiratory arrest may result, especially with rapid bolus or excessive doses.

    2. Hypotension may result from rapid intravenous administration. This can be prevented by limiting the rate of administration to less than 50 mg/min (children: 1 mg/kg/min). Hypotension may be due to the drug itself or to the diluent propylene glycol.

    3. Parenteral solutions are highly alkaline, and precautions need to be taken to avoid extravasation. Intra-arterial infusions may cause vasospasms and gangrene. Subcutaneous administration may cause necrosis and is not recommended.

    4. Use in pregnancy. FDA Category D (possible fetal risk). Phenobarbital readily crosses the placenta, and chronic use may cause hemorrhagic disease of the newborn (owing to vitamin K deficiency) or neonatal dependency and withdrawal syndrome. However, these potential effects do not preclude its acute, short-term use in a seriously symptomatic patient (See Introduction in Section III).

  5. Drug or laboratory interactions

    1. Phenobarbital has additive CNS and respiratory depression effects with other sedative drugs.

    2. Hepatic enzyme induction with chronic use, although this is not encountered with acute phenobarbital dosing.

    3. Extracorporeal removal techniques (eg, hemodialysis, hemoperfusion, and repeat-dose activated charcoal [See Repeat-dose activated charcoal]) may enhance the clearance of phenobarbital, so that supplemental dosing may be required to maintain therapeutic levels.

  6. Dosage and method of administration

    1. Parenteral. Administer slowly intravenously (rate: ≤50 mg/min; children: ≤1 mg/kg/min) until seizures are controlled or the loading dose of 10–15 mg/kg is achieved. For status epilepticus, give 15–20 mg/kg IV over 10–15 minutes, not to exceed 100 mg/min (as much as 30 mg/kg has been required in the first 24 hours to treat status epilepticus in children). Slow the infusion rate if hypotension develops. Intermittent infusions of 2 mg/kg every 5–15 minutes may diminish the risk for respiratory depression or hypotension. For alcohol withdrawal seizures, initial dose of 260 mg, then 130 mg every 30 minutes until signs of mild intoxication (see below). For sedation, the average dose is 100–320 mg up to a maximum of 600 mg/d.

      1. If intravenous access is not immediately available, phenobarbital may be given intramuscularly; the initial dose ...

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