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Cough, Cold, and Allergy Preparation Toxicity Medication

  • Author: Laleh Gharahbaghian, MD; Chief Editor: Timothy E Corden, MD  more...
Updated: Dec 29, 2015

Medication Summary

Most patients with toxicity from cold, cough, or allergy preparations have good outcomes with simple observation and meticulous attention to supportive care. Activated charcoal can reduce absorption of the medication in patients who present early after ingestion. Benzodiazepines can be used for control of anxiety, agitation, and seizures. Limit treatment with physostigmine to severe cases.


Antidotes, Other

Class Summary

GI decontamination with oral activated charcoal is selectively used in the emergency treatment of poisoning caused by some drugs and chemicals.

Activated charcoal (Actidose-Aqua, EZ-Char, Kerr Insta-Char)


Activated charcoal is used in emergency treatment for poisoning caused by drugs and chemicals. A network of pores adsorbs 100-1000 mg of drug per gram. 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 into intestine.

Activated charcoal achieves its maximum effect when administered within 30 minutes after ingestion of a drug or toxin. However, decontamination with activated charcoal may be considered in any patient who presents within 4 hours after the ingestion. Repeated doses may help to lower systemic levels of ingested compounds, especially sustained-release preparations. Activated charcoal does not dissolve in water. Supply it as an aqueous mixture or in combination with a cathartic (usually sorbitol 70%).


Anxiolytics, Benzodiazepines

Class Summary

Diazepam is indicated for the control of anxiety and agitation.

Diazepam (Valium, Diastat)


Diazepam is indicated for treatment of acute dystonic reactions caused by antihistamines, as well as for muscle activity and agitation associated with serotonin syndrome. Diazepam depresses all levels of the CNS (eg, limbic system and reticular formation), possibly by increasing the activity of gamma-aminobutyric acid (GABA). It is a third-line agent for agitation or seizures because of its shorter duration of anticonvulsive effects and accumulation of active metabolites that may prolong sedation.

Lorazepam (Ativan)


A sedative hypnotic with short onset of effects and relatively long half-life, lorazepam is used to treat seizures. By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, lorazepam may depress all levels of the CNS, including the limbic system and reticular formation. It is the drug of choice for seizure control because of a more prolonged anticonvulsant effects than diazepam or midazolam (4-6 h vs 1-3 h). It has an excellent safety profile, but the patient's blood pressure should be monitored after administration of this agent.



Midazolam is an alternative agent for termination of refractory status epilepticus. Compared with diazepam, midazolam has twice the affinity for benzodiazepine receptors; however, because it is water soluble, midazolam takes approximately 3 times longer than diazepam to achieve peak electroencephalographic effects. Thus, the clinician must wait 2-3 minutes to fully evaluate sedative effects before initiating a procedure or repeating the dose. This agent may be administered intramuscularly if vascular access cannot be obtained.

Clonazepam (Klonopin)


Clonazepam is a long-acting benzodiazepine that increases presynaptic GABA inhibition and reduces the monosynaptic and polysynaptic reflexes. It suppresses muscle contractions by facilitating inhibitory GABA neurotransmission and the action of other inhibitory transmitters.


Anticholinergic Toxicity Antidotes

Class Summary

Acetylcholinesterase inhibitors are indicated to reverse central and peripheral toxicity of anticholinergic substances.



Physostigmine is a reversible cholinesterase inhibitor that increases the concentration of acetylcholinesterase in the myoneural junction. It readily crosses the blood-brain barrier to produce desired CNS effects. This agent should not be given unless recommended by a regional poison control center or in direct consultation with a toxicologist.


Electrolyte Supplements, Parenteral

Class Summary

These agents alter the electrophysiologic mechanisms responsible for arrhythmia in patients with toxicity from cold, cough, or allergy medications.

Sodium Bicarbonate (Neut)


Intravenous sodium bicarbonate, 100 mEq over 5 minutes, followed by continuous infusion used for its alkalization properties to maintain a serum pH of 7.5-7.55, has reversed hypotension and resulted in narrowing of the QRS complex in isolated case reports. Sodium bicarbonate is the first-line agent for patients with prolongation of QRS interval after an overdose of an antihistamine with quinidinelike effects.

Magnesium sulfate


Magnesium acts as an antiarrhythmic agent and diminishes the frequency of premature ventricular contractions (PVCs), particularly those resulting from acute ischemia. Deficiency in this electrolyte can precipitate refractory ventricular fibrillation (VF) and is associated with sudden cardiac death. Magnesium sulfate is the first-line agent in the treatment of antihistamine-associated torsade de pointes.

Contributor Information and Disclosures

Laleh Gharahbaghian, MD Director, Emergency Ultrasound Program and Fellowship, Clinical Associate Professor, Department of Surgery, Division of Emergency Medicine, Stanford University Medical Center

Laleh Gharahbaghian, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


Nicholas Lopez, MD Attending Physician, Department of Emergency Medicine, Queen of the Valley Medical Center, Sutter Solano Medical Center

Nicholas Lopez, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

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.

Loren Keith French, MD Attending Physician of Toxicology, Department of Emergency Medicine, Oregon Health and Sciences University and Oregon Poison Center

Disclosure: Nothing to disclose.

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.

Annette M Lopez, MD Toxicology Fellow, Oregon Health and Science University School of Medicine

Disclosure: Nothing to disclose.

David J McCann, MD Resident Physician, Department of Emergency Medicine, Harvard University Affiliated Emergency Medicine Residency Program, Harvard Medical School

Disclosure: Nothing to disclose.

Nathanael J McKeown, DO Assistant Professor, Department of Emergency Medicine, Oregon Health and Science University School of Medicine; Medical Toxicologist, Oregon Poison Center; Attending Physician, Emergency Medicine, Portland Veteran Affairs Medical Center

Nathanael J McKeown, DO is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Jennifer A Oman, MD Associate Clinical Professor, Department of Emergency Medicine, University of California, Irvine, School of Medicine

Jennifer A Oman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Brett Roth, MD  Assistant Professor, Department of Emergency Medicine, Division of Clinical Toxicology, University of Texas Southwestern Medical Center at Dallas, Southwestern Medical School

Disclosure: Nothing to disclose.

Anne Rutkowski, MD Resident Physician, Department of Emergency Medicine, Harbor-University of California at Los Angeles Medical Center

Disclosure: Nothing to disclose.

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.

Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center

Disclosure: Merck Salary Employment

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.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Terfenadine is the antihistamine most commonly associated with torsade de pointes in both acute overdose and therapeutic administration.
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