Barbiturate Toxicity Medication

  • Author: Keith A Lafferty, MD; Chief Editor: Asim Tarabar, MD   more...
 
Updated: Jun 15, 2010
 

Medication Summary

GI decontamination with activated charcoal and urinary alkalinization may be beneficial in patient management. Also, pharmacologic support may be required in hypotensive patients with the use of pressor agents.

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GI decontaminants

Class Summary

These agents are used to minimize the amount of toxin absorbed from the GI tract into systemic circulation. Depending upon the amount of drug ingested and time from ingestion to treatment, gastric lavage may be used. Activated charcoal is beneficial in adsorbing the ingested agent and is considered safer than emetics.

Activated charcoal (Liqui-Char)

 

Prevents absorption by adsorbing drug in the intestine. Multidose charcoal may interrupt enterohepatic recirculation and enhance elimination by enterocapillary exsorption. Theoretically, by constantly bathing the GI tract with charcoal, the intestinal lumen serves as a dialysis membrane for reverse-absorption of drug from intestinal villous capillary blood back into the intestine.

Supplied as an aqueous mixture or in combination with a cathartic (usually sorbitol 70%).

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Alkalinizing agent

Class Summary

Sodium bicarbonate is the primary agent used clinically to enhance elimination. The goal of use is to alkalinize the urine to promote renal excretion and decrease elimination half-life of the barbiturate.

Sodium bicarbonate (Neut)

 

Goal is to maintain a urinary pH >7.5 and urine output >2 mL/kg/h. Monitor arterial or venous pH; a blood pH >7.55 may increase patient morbidity.

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Adrenergic Agonist Agents

Class Summary

These agents improve the hemodynamic status by increasing myocardial contractility and heart rate. This results in an increase in cardiac output. They also increase peripheral resistance by inducing vasoconstriction. Increased cardiac output and increased peripheral resistance lead to increased blood pressure.

Norepinephrine (Levophed)

 

Stimulates beta1-adrenergic and alpha-adrenergic receptors, which, in turn, increases cardiac muscle contractility, heart rate, and vasoconstriction. As a result, systemic blood pressure and coronary blood flow increase.

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Contributor Information and Disclosures
Author

Keith A Lafferty, MD  Adjunct Assistant Professor of Emergency Medicine, Temple University; Consulting Staff, Department of Emergency Medicine, South West Regional Medical Center

Keith A Lafferty, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Rehab Abdel-Kariem, MD  Resident Physician, Department of Emergency Medicine, Temple University Hospital

Rehab Abdel-Kariem, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physicians, American Medical Student Association/Foundation, Physicians for Human Rights, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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.

Michael J Burns, MD  Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency 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.

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