Cardiac Glycoside Plant Poisoning Treatment & Management

  • Author: Raffi Kapitanyan, MD; Chief Editor: Asim Tarabar, MD   more...
 
Updated: May 10, 2011
 

Prehospital Care

  • Advanced life support (ALS) should transport patients who have ingested herbal cardiac glycosides or significant amounts of plants known to contain cardiac glycosides.
  • Prehospital care should focus on ABCs, with special emphasis on supporting respiratory and cardiac function.
  • During transport, the patient should receive supplemental oxygen and an IV line. Cardiac and pulse oximeter monitoring should be continuous.
  • In patients with protected airway and normal mental status, activated charcoal can be administered.
  • Atropine should be given to patients with clinically significant bradycardia (eg, hypotension, change of mental status).
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Emergency Department Care

Address principles of care for toxicologic emergencies, including providing general supportive care, preventing further exposure and absorption, administering antidote (eg, fragment antigen binding [Fab] fragments), and treating complications. Management is very similar to that for digoxin/digitoxin poisoning.

General supportive care: Attention to ABCs is paramount. Treat life-threatening conditions in accordance with advanced cardiac life support (ACLS) principles, except as outlined below.

Administer oxygen and start an IV line. Place patient on continuous cardiac monitoring and pulse oximeter. Treat patients with altered mental status in accordance with standard protocols based on a fingerstick glucose determination and primary survey.

Prevent further exposure. Remove plant parts or any medications brought with patient from treatment area, particularly if patient is suicidal.

Prevent further absorption. Oral administration of activated charcoal is recommended if no contraindications exist.

Administer antidote. Sheep-derived digoxin antibody Fab fragments reportedly are effective for some plant cardiac glycosides. Consider use in life-threatening complications, such as ventricular dysrhythmias, hyperkalemia, high degree heart block, and cardiac arrest that do not respond rapidly to conventional treatment. Indications for digoxin antibody Fab fragments are the same for both pharmaceutical as well as nonpharmaceutical cardiac glycoside toxicity and include the following:

  • Hyperkalemia (>5.0 mEq/L) in acute toxicity
  • Life-threatening supraventricular and ventricular dysrhythmias
  • Hemodynamically significant bradycardia unresponsive to atropine
  • Chronic digoxin toxicity with dysrhythmias, significant GI symptoms, acute altered mental status, or renal insufficiency
  • Serum digoxin level >15 ng/mL at any time
  • Ingestion of 10 mg in an adult or 4 mg in a child
  • Poisoning by nondigoxin cardiac glycoside
  • To aid in treatment of suspected cardiac glycoside poisoning without a confirmatory level

Digoxin levels are not meaningful after administration of digoxin-specific Fab fragments. The levels may not change or may be falsely elevated if a "free digoxin assay" is not used. Because onset of action of Fab fragments may take 30-60 minutes, intervening treatment of significant complications should occur.

Bradydysrhythmias

Atropine and cardiac pacing may be tried. If atropine is not rapidly successful, consider administration of Fab fragments. Patients requiring transcutaneous cardiac pacing should receive Fab fragments prior to it. Transvenous pacing and use of isoproterenol have resulted in degeneration of cardiac rhythms and both of these should be avoided. Do not delay administration of Fab fragments because of pacemaker placement. Do not use overdrive pacing for the control of ventricular dysrhythmias.

Phenytoin and lidocaine may be used as antidysrhythmics if Fab fragments are not immediately available. However, it should be remembered that Fab fragments are the definitive antidote to cardiac glycoside poisoning.

Tachydysrhythmias

Phenytoin and lidocaine (which decrease automaticity without slowing AV nodal conduction and increase fibrillation threshold) may be used to treat ventricular dysrhythmias.

Magnesium has been reported to reverse digoxin-induced dysrhythmias and may be useful as long as anuric renal failure is not present.

Use cardioversion only as a last resort, since it may induce intractable ventricular fibrillation. Fab fragments should be given with cardioversion.

If time permits, cardioversion should be attempted after a loading dose of phenytoin and at a significantly reduced initial power setting of 5-10 J.

Quinidine and procainamide may enhance cardiac glycoside toxicity by slowing conduction across AV node; both should be avoided.

Beta-blockers and calcium channel blockers have questionable value.

Hyperkalemia

Life-threatening hyperkalemia (>6.5 mEq/L) may be seen with acute toxicity and results from a redistribution phenomenon rather than increased body stores.

Glucose, insulin, sodium bicarbonate, and albuterol may be used to facilitate redistribution of potassium intracellularly. However, albuterol may precipitate cardiac dysrhythmias.

Calcium should be avoided to prevent overloading myocytes with calcium, which is associated with development of a "stone heart," increased dysrhythmias, and a higher rate of death. A recent pilot study in a porcine model shows that, in contrast to earlier studies, IV calcium administration to treat hyperkalemia secondary to cardiac glycoside toxicity resulted in no benefit or harm. However, the authors do not recommend its use in the clinical setting at this time until more definitive studies are undertaken.[5] Theoretically calcium can be used after administration of Fab fragments and reversal of cardiac-glycosides toxicity.

Life-threatening hyperkalemia should be treated with Fab fragments.

Forced diuresis, hemoperfusion, and hemodialysis are ineffective in enhancing the elimination of digoxin because of its large volume of distribution. Hemodialysis will efficiently remove potassium from extracellular fluid.

Cardiac arrest

Give 10-20 vials of Fab and continue to treat with standard ACLS protocols. Prolonged efforts at resuscitation may be warranted until Fab fragments begin to work. Phenytoin and lidocaine are antidysrhythmics of choice in patients poisoned with cardiac glycosides.

A Cochrane review on antidotes for acute cardiac glycoside poisoning that specifically looked at yellow oleander suggests that some evidence supports multiple-dose activated charcoal (MDAC) and anti-digoxin Fab antitoxin.[6] Pharmokinetic differences between individual cardiac glycosides may limit treatment options that proved effective for yellow oleander. The authors conclude that considering the cost limits in developing countries where most poisonings take place, more research is required to develop cheap antidotes that may be effective.

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Consultations

Poison center and toxicology

Consider consultation for any question regarding management (strongly recommended if use of Fab fragments is considered or if symptoms and signs of toxicity are severe).

Cardiology

Consider consultation for advice regarding treatment of cardiac manifestations of toxicity, as needed.

Consider consultation if use of Fab fragments is contemplated and a toxicologist is unavailable.

Psychiatry

Consultation is recommended for any patients with suspected intentional ingestions.

Primary care physician

Consult for admission or for information regarding patient's medical histories.

Botanist

Consultation with a botanist may facilitate plant identification.

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Contributor Information and Disclosures
Author

Raffi Kapitanyan, MD  Assistant Professor of Emergency Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School

Raffi Kapitanyan, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Mark Su, MD, FACEP, FACMT  Consulting Staff and Director of Fellowship in Medical Toxicology, Department of Emergency Medicine, North Shore University Hospital; Consulting Staff, North Shore University Hospital

Mark Su, MD, FACEP, FACMT 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.

Douglas R Landry, MD  Consulting Staff, Department of Emergency Medicine, Sentara Bayside Hospital

Douglas R Landry, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

B Zane Horowitz, MD, FACMT  Professor, Department of Emergency Medicine, Oregon Health and Sciences University; Medical Director, Oregon Poison Center; Medical Director, Alaska Poison Control System

B Zane Horowitz, MD, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Medical Toxicology

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 Hodgman, MD  Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare

Michael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society

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.

References
  1. Bessen HA. Therapeutic and toxic effects of digitalis: William Withering, 1785. J Emerg Med. 1986;4(3):243-8. [Medline].

  2. Bronstein, AC, Spyker, DA, Cantilena Jr., LR, et al. 2006 annual report of the American Association of Poison Control Centers National Poison Data System. Clinical Toxicology. Dec 2007;45(8):815-917.

  3. Eddleston M, Ariaratnam CA, Sjostrom L, Jayalath S, Rajakanthan K, Rajapakse S. Acute yellow oleander (Thevetia peruviana) poisoning: cardiac arrhythmias, electrolyte disturbances, and serum cardiac glycoside concentrations on presentation to hospital. Heart. Mar 2000;83(3):301-6. [Medline].

  4. Gowda RM, Cohen RA, Khan IA. Toad venom poisoning: resemblance to digoxin toxicity and therapeutic implications. Heart. Apr 2003;89(4):e14. [Medline].

  5. Hack JB, Woody JH, Lewis DE, et al. The effect of calcium chloride in treating hyperkalemia due to acute digoxin toxicity in a porcine model. J Toxicol Clin Toxicol. 2004;42(4):337-42. [Medline].

  6. Roberts DM, Buckley NA. Antidotes for acute cardenolide (cardiac glycoside) poisoning. Cochrane Database Syst Rev. Oct 18 2006;CD005490. [Medline].

  7. Bain RJ. Accidental digitalis poisoning due to drinking herbal tea. Br Med J (Clin Res Ed). Jun 1 1985;290(6482):1624. [Medline].

  8. Cheung K, Urech R, Taylor L. Plant cardiac glycosides and digoxin Fab antibody. J Paediatr Child Health. Oct 1991;27(5):312-3. [Medline].

  9. Dickstein ES, Kunkel FW. Foxglove tea poisoning. Am J Med. Jul 1980;69(1):167-9. [Medline].

  10. Eddleston M, Rajapakse S, Rajakanthan, Jayalath S, Sjostrom L, Santharaj W. Anti-digoxin Fab fragments in cardiotoxicity induced by ingestion of yellow oleander: a randomised controlled trial. Lancet. Mar 18 2000;355(9208):967-72. [Medline].

  11. el Bahri L, Djegham M, Makhlouf M. Urginea maritima L (Squill): a poisonous plant of North Africa. Vet Hum Toxicol. Apr 2000;42(2):108-10. [Medline].

  12. Furbee B, Wermuth M. Life-threatening plant poisoning. Crit Care Clin. Oct 1997;13(4):849-88. [Medline].

  13. Goldfrank, Flomenbaum, Lewin, et al. Cardiac glycosides. In: Goldfrank's Toxicologic Emergencies. 7th ed. 2002:724-734.

  14. Rich SA, Libera JM, Locke RJ. Treatment of foxglove extract poisoning with digoxin-specific Fab fragments. Ann Emerg Med. Dec 1993;22(12):1904-7. [Medline].

  15. Plants - cardiac glycosides. In: Rumack BH, ed. Poisondex. 1997:94.

  16. Slifman NR, Obermeyer WR, Aloi BK, Musser SM, Correll WA Jr, Cichowicz SM. Contamination of botanical dietary supplements by Digitalis lanata. N Engl J Med. Sep 17 1998;339(12):806-11. [Medline].

  17. Van Deusen SK, Birkhahn RH, Gaeta TJ. Treatment of hyperkalemia in a patient with unrecognized digitalis toxicity. J Toxicol Clin Toxicol. 2003;41(4):373-6. [Medline].

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The plant shown is foxglove (Digitalis purpura), which contains cardiac glycosides, not tropane alkaloids. © 2000 Richard Wagner
 
 
 
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