Barbiturate Toxicity Treatment & Management

Updated: Jan 14, 2017
  • Author: Keith A Lafferty, MD; Chief Editor: Asim Tarabar, MD  more...
  • Print
Treatment

Prehospital Care

Ensuring adequate airway, breathing, and circulation is essential. Emergency medical personnel should do the following:

  • 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.
Next:

Emergency Department Care

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.

Supportive care

Assess the airway and adequacy of respiration and perform ET intubation if necessary. If the patient has not been intubated, provide supplemental oxygen and continue to monitor the 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) 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.

Gastrointestinal decontamination

Despite the fact that barbiturates are well adsorbed by activated charcoal and a study in which volunteers given 50 g of activated charcoal showed a mean reduction in absorption of 47.3%, 40.07%, and 16.5% when it was administered at 30 minutes, 60 minutes, and 120 minutes, respectively, current guidelines in overdose management question its benefit. There is no evidence that the administration of activated charcoal improves clinical outcome. Indeed, its use has decreased to less than 5% of all reported ingestions in recent years. [18]

A single dose of activated charcoal may be given within an hour of overdose if the clinician estimates that a clinically significant fraction of the ingested substance remains in the GI tract, the toxin is adsorbed by charcoal, further absorption may result in clinical deterioration, and the patient has no depression of his or her mental status. Activated charcoal is a hydrocarbon with a high aspiration ratio; hence, the administration of charcoal is contraindicated in any patient who does not have an intact or protected airway.

Of note, giving this noninnocuous substance to any patient with any ingestion must be weighed against the fact that general supportive care and the use of a few specific antidotes has decreased the mortality rate in unselected overdose patients to less than 1% if the patient arrives at the hospital in time for the clinician to intervene. [18]

Although multiple doses of activated charcoal (MDAC) have been shown to enhance elimination of phenobarbital and to reduce the serum half-life, a definite improvement in clinical outcome has not been shown in any studies using MDAC.

Induction of emesis with ipecac syrup is contraindicated in these patients because their depressed neurologic response increases the risk of aspiration.

Enhancement of elimination

The goal of enhanced elimination is to decrease the duration of ventilatory support, mitigate hypotension, and decrease morbidity/mortality. Since barbiturates are weak acids, enhanced renal elimination occurs through alkalinization of the urine. The presence of more protons and less additional substituents on the C-5 position decreases the pKa, thus increasing the acidity of the barbiturate structure. In this way, phenobarbital and, likely, other long-acting barbiturates, can be converted to water-soluble salts with the appropriate base and eliminated through ion trapping by decreasing tubular reabsorption, analogous to that of salicylate poisoning treatment.

Enhanced urinary elimination has been well established as a treatment for phenobarbital and butalbital. Phenobarbital's low pKa (4.2), higher water solubility, and slow hepatic metabolism with a subsequently long half-life allow a larger proportion of drug to be renally excreted. Urinary alkalinization is not recommended for short-acting barbiturates.

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 up to 30%, no controlled studies demonstrating a patient benefit are available. [8] Current literature suggests hemoperfusion is marginally preferable to hemodialysis in terms of absolute clearance rates (clearance decreases when the duration of treatment exceeds 2-3 h). 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.

While there remains no specific antidote for barbiturate toxicity, numerous publications have outlined the possible clinical use of intravenous lipid emulsion (ILE) as an antidote. The suggested mechanism of ILE in lipophilic drug toxidrome is the formation of a lipid sink that acts to sequester lipophilic toxins (such as local anesthetics), thereby decreasing the targeted drug concentration and toxicity. [19] However, although ILE continues to be a therapy of interest, its role at this time is limited. A review of approximately 42 case reports with ILE use showed a possible benefit. It has been used in patients with negative hemodynamics whose condition remains unresponsive to conventional supportive therapy.

Previous
Next:

Consultations

See the list below:

  • 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.
Previous