Antihistamine Toxicity Treatment & Management

  • Author: Loren Keith French, MD; Chief Editor: Asim Tarabar, MD   more...
 
Updated: May 5, 2010
 

Prehospital Care

Paramedics should follow set protocols for gastric decontamination, hypotension, and seizures; symptomatic patients should be transported rapidly with intravenous access and cardiac monitoring. Benzodiazepines may be used for agitation or seizures.

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Emergency Department Care

Basic tenets of emergency care should dictate therapy. Perform bedside determinations of glucose for patients with altered levels of conscious and treat with intravenous dextrose, if appropriate. For hypotensive patients, administer 0.9% sodium chloride solution or lactated Ringer solution as boluses. Dopamine, or other cardiac pressor, may be titrated to achieve an acceptable blood pressure.

  • Administer activated charcoal to patients who are cooperative, can retain a good gag reflex, and can take liquids by mouth safely. Perform endotracheal intubation before instillation of activated charcoal for patients with significant CNS depression and unprotected airway. The clinician should be aware that a severely toxic patient can experience seizures and aspirate charcoal.
  • Gastric emptying has not proven beneficial if the patient presents more than one hour postingestion, although case reports involving anticholinergic agents have demonstrated erratic absorption and repeated worsening of anticholinergic symptoms over 9 days. Ipecac syrup is not recommended in the ED because it may delay the administration of activated charcoal and seizures may occur at any time, with the possibility of aspiration. Repeated doses of activated charcoal may prevent continued absorption, although the development of ileus generally limits its use.
  • Agitation
    • Anticholinergic-induced delirium ranges from mild confusion to severe agitation with associated hyperthermia and rhabdomyolysis. The administration of chemical and physical restraints often is necessary to prevent patients from harming themselves or others. Controlling muscular activity is crucial in severely agitated patients, because agitation may exacerbate muscle injury, acidosis, rhabdomyolysis, and hyperthermia. Although benzodiazepines often are considered first-line, physostigmine is safe and effective for the treatment of antihistamine-induced agitated delirium, provided that the ECG does not demonstrate conduction disturbances (ie, PR and QRS prolongation); one study suggests that physostigmine is more effective and just as safe as benzodiazepines to control antihistamine-induced agitated delirium.[46]
    • Neuroleptic agents, such as haloperidol, have been used but have anticholinergic effects and may exacerbate hyperthermia or provoke a dystonic reaction and their use should be discouraged.
    • Physostigmine, a naturally occurring alkaloid obtained from the Ordeal bean Physostigma venenosum, is the only reversible acetylcholinesterase inhibitor lacking a charged quaternary amine moiety. As a tertiary amine, physostigmine traverses the blood-brain barrier and binds to central acetylcholinesterase, increasing acetylcholine levels and, thus, reversing central anticholinergic delirium. Peripheral signs and symptom also are reversed. Considering that patients with anticholinergic symptoms usually fare well with supportive therapy alone, physostigmine is indicated only in the following limited circumstances:
      • Single-drug (anticholinergic) exposure[46]
      • Pronounced hallucinations, delirium, or agitation (suggesting a CNS effect) unresponsive to benzodiazepines
      • Intractable seizures resistant to all other treatments
      • Absence of QRS prolongation on ECG
    • Physostigmine should not be used in known antidepressant overdoses. Case series of patients taking maprotiline indicated that seizures developed in 6 out of 7 patients treated with physostigmine. Other reports describe development of asystole for the administration of physostigmine after cyclic antidepressant poisoning. In a series of 21 patients receiving physostigmine, 2 patients experienced seizures and 2 experienced cholinergic reactions (hypersalivation in one patient, bradycardia and hypotension in the other). Thus, use physostigmine cautiously.
    • Always have atropine at bedside when using physostigmine in order to reverse excessive cholinergic activity (eg, bradycardia, salivation)
  • Manage hyperthermia, especially when severe agitation is present, with neuromuscular paralysis, evaporative cooling, and ice-bath immersion if temperature is higher than 105°F. Use of dantrolene or bromocriptine is controversial.
  • Cardiovascular toxicity
    • Sinus tachycardia usually does not require treatment. Sedation with a benzodiazepine may be helpful when agitation is also present. Intravenous sodium bicarbonate improves widening of QRS that may result from antihistamines with sodium channel blocking properties (eg, diphenhydramine, pyrilamine).
    • Provide support for patients with profound cardiovascular toxicity. In rare cases of refractory shock, placement of an intra-aortic balloon pump for several hours may bridge the patient through a period of cardiovascular collapse.
  • Case reports suggest that physostigmine ends seizures, but clinical experience is limited and no proof of its efficacy for seizure control exists. Treat antihistamine-induced seizures with benzodiazepines and barbiturates. Reserve physostigmine for refractory seizures. One case of using flumazenil for successful reversal of antihistamine-induced depressed mental status in a 7-month-old infant was reported in 2003.[47] Evidence to recommend this therapy is insufficient.

The American Association of Poison Control Centers has issued evidence-based consensus guidelines on the out-of-hospital management of diphenhydramine and dimenhydrinate poisoning.[48]

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Consultations

  • Regional poison control center or a medical toxicologist as soon as possible
  • Intensivist for invasive monitoring and hemodynamic support in complicated cases
  • Nephrology service in the case of rhabdomyolysis and acute renal failure
  • Psychiatry for intentional overdoses
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Contributor Information and Disclosures
Author

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

Disclosure: Nothing to disclose.

Coauthor(s)

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

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.

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