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Disulfiram Toxicity Treatment & Management

  • Author: Samara Soghoian, MD, MA; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Jan 06, 2016
 

Prehospital Care

For patients with possible disulfiram-ethanol reaction, the following should be performed:

  • Provide supplemental oxygen, obtain intravenous access, and place all patients on a monitor. Administer thiamine, glucose, and naloxone to patients with altered mental status, as needed.
  • Intravenous fluids should be instituted if hypotension, tachycardia, or severe vomiting is present.
  • Patients with coma or a severely altered mental status should be intubated for airway protection. The frequent occurrence of vomiting secondary to DER places these patients at high risk for aspiration.
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Emergency Department Care

ED treatment of disulfiram-ethanol reaction (DER) is primarily supportive. No specific antidote has been tested for efficacy in the treatment of DER or acute disulfiram overdose, though fomepizole has the theoretical benefit of blocking ethanol metabolism to acetaldehyde and may be a useful therapy in patients presenting with DER. Patients with a severely altered mental status or coma should be intubated for airway protection. The risk of aspiration in patients with DER is high.

  • Mild sedation with benzodiazepines may be useful in the agitated patient, and benzodiazepines may be used to treat seizures. However, sedation of patients with intractable vomiting increases the risk of aspiration and its sequelae and should be approached with caution. Benzodiazepines also have the potential to exacerbate hypotension.
  • In cases of intractable vomiting, phenothiazine use must be considered cautiously because their alpha-blockade effect may worsen or induce hypotension. Metoclopramide, ondansetron, or granisetron are considered the antiemetics of choice in these cases.
  • Intravenous fluids should be given to patients experiencing a DER to replace volume losses from emesis and third spacing of intravascular fluid.
  • Intravenous fluids and vasopressors are indicated to support blood pressure and treat patients who are in shock.
  • Decontamination procedures are not likely to be beneficial once the reaction begins. Consider gastric emptying only in the hospital setting with cases of massive ethanol ingestion in which a patent and protected airway can be maintained.
  • Inducing emesis with ipecac syrup is not recommended. Ipecac syrup contains ethanol, which could precipitate DER. Emesis may delay administration of activated charcoal, worsen the nausea and vomiting associated with disulfiram toxicity, and increase the likelihood of pulmonary aspiration if seizures and coma suddenly occur.
  • In acute disulfiram overdose, consider the use of activated charcoal, if available and if the patient is alert and able to drink it safely. Use of multiple dose activated charcoal (MDAC) may be beneficial.
    • Multiple dose activated charcoal can increase the rate of elimination of disulfiram and its metabolites that undergo enterohepatic recirculation. Activated charcoal is not indicated for disulfiramlike syndromes, and it is not indicated for the treatment of DER.
    • The risk-benefit of administering charcoal to a patient with altered mental status and a high likelihood of vomiting and potential aspiration must be carefully weighed.
  • In severe DER, hemodialysis may be indicated to enhance the elimination of ethanol and acetaldehyde. Neither hemodialysis nor hemoperfusion has been beneficial for treatment of acute disulfiram overdose.
  • Some authors have suggested that fomepizole (Antizol) may be beneficial in cases of severe DER. Fomepizole is a potent inhibitor of alcohol dehydrogenase that may limit the metabolism of ethanol by this enzyme and thereby prevent further accumulation of acetaldehyde. No studies have examined the utility of fomepizole in this context; however, a theoretical benefit exists in patients taking disulfiram who present with DER after a large ethanol ingestion.
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Consultations

Consult with the local poison control center or a medical toxicologist.

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Contributor Information and Disclosures
Author

Samara Soghoian, MD, MA Clinical Assistant Professor of Emergency Medicine, New York University School of Medicine, Bellevue Hospital Center

Samara Soghoian, MD, MA is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

José Eric Díaz-Alcalá, MD, FAAEM, FACMT Medical and Executive Co-Director, Medical Toxicology Consultant, Administración de Servicios Médicos de Puerto Rico, ASEM Poison Control Center; Chief, Emergency Medicine Unit, Medical Toxicology Consultant, VA Caribbean Healthcare System

José Eric Díaz-Alcalá, MD, FAAEM, FACMT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Medical Toxicology

Disclosure: Nothing to disclose.

Sage W Wiener, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Undersea and Hyperbaric Medical Society, Wilderness Medical Society, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

David C Lee, MD Research Director, Department of Emergency Medicine, Associate Professor, North Shore University Hospital and New York University Medical School

David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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The pathway of ethanol metabolism. Disulfiram reduces the rate of oxidation of acetaldehyde by competing with the cofactor nicotinamide adenine dinucleotide (NAD) for binding sites on aldehyde dehydrogenase (ALDH).
Disulfiram, prodrug for active metabolites.
 
 
 
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