Barbiturate Toxicity Treatment & Management

• Ensuring adequate airway, breathing, and circulation is essential.

  • Secure the airway and make sure the patient has good breath sounds bilaterally and is not hypotensive.
  • Perform an emergent endotracheal (ET) intubation if the patient has a significantly depressed level of consciousness and is not able to maintain the airway or has signs of increased intracranial pressure, ventilatory failure, or hypoxia.
  • Administer supplemental oxygen and obtain venous access.
  • In cases of hypotension, 2 large-bore intravenous lines are necessary for the administration of intravenous fluids and medications. Measure blood glucose level, and administer naloxone 2 mg IV to all patients with an altered mental status.

Treatment of the patient with barbiturate toxicity is predominantly supportive. The mainstay of treatment underscores the importance of preventing hypoxemia and hypotension. Management strategies generally fall into 3 major areas: supportive care, decontamination, and enhancement of elimination.

• Assess the airway and adequacy of respiration, and perform ET intubation if necessary. Check ET tube placement if the patient has been intubated. If the patient has not been intubated, provide supplemental oxygen and continue to monitor his or her airway status. Obtain intravenous access and an initial pulse oximeter reading, and place the patient on a cardiac monitor. Measure blood glucose, and administer naloxone 2 mg IV to all patients with altered mental status.
• Obtain a rectal temperature to check for hypothermia. If the patient is hypothermic, immediately initiate a careful rewarming (to avoid precipitating a fall in blood pressure).
• Aggressively initiate fluid therapy if the patient has a low blood pressure or appears to be in hypovolemic shock.
• Initiate treatment with pressors (eg, norepinephrine, dopamine) if shock persists or worsens. In general, initiate pressors after aggressive and adequate fluid resuscitation has been attempted and the patient is determined to be euvolemic.
• GI decontamination

  • Since barbiturates are well adsorbed by activated charcoal, an initial dose of 1 g/kg should be administered. A cathartic is often administered to prevent constipation and to facilitate more rapid passage of the charcoal because barbiturates slow intestinal motility. Only perform GI decontamination after the airway is protected and hemodynamic stabilization has been addressed. Large-bore orogastric tube placement and gastric lavage have not been proven beneficial. They may increase risk of aspiration and have the added deleterious effect of delaying activated charcoal delivery. Activated charcoal orally or by nasogastric tube is recommended for all patients with potential barbiturate toxicity.
  • Multiple doses of activated charcoal (MDAC) have been shown to enhance elimination of phenobarbital and to reduce the serum half-life. The recommended adult dose is 15-20 g given orally every 6 hours. Note that a definite improvement in clinical outcome has not been shown in any studies using MDAC and that patients with barbiturate toxicity are at increased risk of impaction and gut perforation with the use of MDAC due to decreased GI motility.
  • Induction of emesis with ipecac syrup is contraindicated in these patients because their depressed neurologic response increases the risk of aspiration.
• Alkalinization of the urine enhances the elimination of phenobarbital and, likely, other long-acting barbiturates by ion trapping. Urinary alkalinization is not recommended for short-acting barbiturate toxicity.

  • Enhanced urinary elimination has been well established as a treatment for phenobarbital and butalbital. Phenobarbital's low pKa (7.2), higher water solubility, and slow hepatic metabolism with a subsequently long half-life allow a larger proportion of drug to be renally excreted.
  • Enhancement of urinary elimination may be accomplished with an initial sodium bicarbonate bolus of 1 mEq/kg followed by a constant infusion. This infusion may be made by adding 100-150 mEq of sodium bicarbonate to 850 mL of D5 and titrating to maintain a urine pH of greater than 7.5 with an arterial pH of less than 7.50. The goal should be a urine output of 150-250 mL/h.
  • Risks include hypokalemia, fluid overload, tetany, and the possibility of excessive elevations in arterial pH.
• Extracorporeal elimination is rarely advised. Even though plasma clearance and elimination half-life has been shown to be decreased, no controlled studies demonstrating a patient benefit are available. Current literature suggests hemoperfusion is preferable to hemodialysis in terms of absolute clearance rates. Because the majority of patients do well with supportive care alone and blood levels do not correlate with duration of coma/ventilatory time, routine extracorporeal drug removal is not recommended. An argument can be made for this procedure in a patient who remains unstable despite aggressive supportive care, especially in a patient with rising drug blood levels.

• Consider consulting a toxicology service if available.
• Patients requiring admission are generally admitted to the ICU after consultation with an intensivist.
• If a patient is considered for hemodialysis or hemoperfusion, a nephrologist should be consulted.