AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Cardiac glycosides are found in a diverse group of plants including Digitalis purpurea and Digitalis lanata (foxgloves), Nerium oleander (common oleander), Thevetia peruviana (yellow oleander), Convallaria majalis (lily of the valley), Urginea maritima and Urginea indica (squill), Strophanthus gratus (ouabain), Apocynum cannabinum (dogbane), and Cheiranthus cheiri (wallflower). In addition, the venom gland of cane toad (Bufo marinus) contains large quantities of a purported aphrodisiac substance that has resulted in cardiac glycoside poisoning.

Ancient Egyptians and Romans first used plants containing cardiac glycosides medicinally as emetics and for heart ailments. Toxicity from herbal cardiac glycosides was well recognized by 1785, when William Withering published his classic work describing therapeutic uses and toxicity of foxglove, D purpurea.

Therapeutic use of herbal cardiac glycosides continues to be a source of toxicity today. Recently, D lanata was mistakenly substituted for plantain in herbal products marketed to cleanse the bowel; human toxicity resulted. Cardiac glycosides have been also found in Asian herbal products and have been a source of human toxicity.

Toxicity may occur after consuming teas brewed from plant parts or after consuming leaves, flowers, or seeds from plants containing cardiac glycosides. Significant toxicity usually is a result of suicide attempt or inappropriate self-administration for the therapeutic purposes.

Pathophysiology

More than 200 naturally occurring cardiac glycosides have been identified. These bind to a site on the cell membrane, producing reversible inhibition of the sodium (Na⁺)-potassium (K⁺)-adenosine triphosphatase (ATPase) pump, which causes increased intracellular sodium and decreased intracellular potassium. In myocytes, elevated intracellular sodium concentrations produce increased intracellular calcium concentrations via a Na⁺-calcium (Ca⁺⁺)-exchanger. In response to the increased intracellular calcium, the sarcoplasmic reticulum releases additional calcium intracellularly resulting in depolarization of the cell.

As a result of this excessive intracellular calcium, enhanced cardiac contractions, which are delayed after depolarizations, occur. These clinically manifest as aftercontractions, such as premature ventricular contractions (PVCs). Cardiac glycosides also have vagotonic effects, resulting in bradycardia and heart blocks. Inhibition of Na⁺-K⁺-ATPase in skeletal muscle results in increased extracellular potassium and contributes to hyperkalemia.

Cardiac glycosides primarily affect cardiovascular, neurologic, and gastrointestinal systems. Of these, effects on the cardiac system are most significant. The pathophysiology that produces cardiotoxicity involves prolonging refractory period in atrioventricular (AV) node, shortening refractory periods in atria and ventricles, and decreasing resting membrane potential (increased excitability). At therapeutic doses, cardiac glycosides also may increase inotropy. Any dysrhythmia characterized by both increased automaticity and depressed conduction is suggestive of cardiac glycoside toxicity.

Sinus rhythm with PVCs is the most common rhythm associated with digitalis toxicity. Other dysrhythmias often associated with cardiac glycoside toxicity include bradydysrhythmias, sinus bradycardia with all types of AV nodal block, junctional rhythms, and sinus arrest. Dysrhythmias characterized by increased automaticity and conduction blockade, when combined, are highly suggestive of cardiac toxicity. These dysrhythmias include the following:

• Tachydysrhythmias, such as atrial tachycardia with block

• Junctional tachycardia

• Ventricular tachycardia

• Ventricular fibrillation

• Paroxysmal atrial tachycardia with block

• Bidirectional ventricular tachycardia

More than a single dysrhythmia may be present and progression into a rapidly life-threatening rhythm, such as ventricular tachycardia, may abruptly occur.

Frequency

United States

Toxic exposure to plants containing cardiac glycosides is rare. Of 1.39 million exposures to toxic, nonpharmaceutical substances reported by the American Association of Poison Control Centers (AAPCC) in 2003, only 1,471 were due to exposure to plants containing cardiac glycosides. Cardiac glycoside exposure from plants accounts for only 1.0% of plant exposures and 0.1% of exposures in the 2003 report.

International

Deliberate ingestion of yellow oleander seeds (Thevetia peruviana), known as "lucky nuts," has recently become a popular method of self-harm in northern Sri Lanka. Thousands of cases are reported yearly, with a case-fatality rate of untreated patients ranging between 5 and 10%.

Exposure rates may be higher in countries or communities that rely heavily on folk or herbal medicines including plants containing cardiac glycosides.

Mortality/Morbidity

• Factors increasing morbidity and mortality and similar to those affecting digoxin-poisoned patients and may be divided into host-specific and plant-specific categories.
  • Host-specific factors include advanced age, renal impairment, myocardial ischemia, hypothyroidism, hypoxia, and electrolyte abnormalities (eg, hypokalemia, hyperkalemia, hypomagnesemia, hypercalcemia).

  • Plant-specific factors include species, part ingested, specific type of cardiac glycosides contained in the plant, and concentration of cardiac glycosides.
• Mortality is rare, but case reports documenting fatalities from oleander, foxglove, squill, and other related plants do exist. In 2003, although the AAPCC reported no deaths in 1,471 exposures to cardiac glycoside-containing plants, during the same period, 16 fatalities were reported from 2,820 exposures to pharmaceutical cardiac glycosides. The AAPCC noted moderate to major morbidity in only 2% of cardiac glycoside-containing plant exposures. In contrast, moderate-to-major morbidity occurred in 23% of pharmaceutical cardiac glycoside exposures.
• Morbidity associated with exposure to cardiac glycoside-containing plants tends to be less severe than that associated with pharmaceutical cardiac glycosides. This may reflect age differences, lower concentrations of bioactive cardiac glycosides, and intentional versus unintentional exposure ratios. Pharmaceutical exposures generally occur in an older population (>60 y) and more often are due to intentional acute or chronic ingestion. Most plant exposures occur in children younger than 6 years and are usually unintentional and without associated significant toxicity. More serious toxicity occurs with intentional ingestions by adolescents and adults.

Age

AAPCC data from 2003 show the following age breakdowns for plant cardiac glycoside exposure:

• Infants and children younger than 6 years - 57%
• Children aged 6-19 years - 19%
• Adults older than 19 years - 23%

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• As with all toxic exposures, history should focus on answering the following 6 key questions:
• • Who was exposed and are there other victims?

  • To what were they exposed?

  • When were they exposed?

  • Where were they exposed?

  • Why were they exposed (unintentional vs intentional)?

  • To how much were they exposed (eg, amount, concentration)?

• Although acute and chronic toxicity are treated in similar manners, their noncardiac clinical manifestations differ. In acute toxicity, the following may be present:
• • GI symptoms, usually evolve within minutes to hours, are nonspecific, and include nausea, vomiting, and abdominal pain.

  • Neurological symptoms often are nonspecific and include weakness and altered mental status (eg, disorientation, confusion, lethargy).

• In chronic toxicity, signs and symptoms are insidious, which make diagnose difficult at times.
• • GI symptoms are nonspecific and include anorexia, nausea, vomiting, diarrhea, abdominal pain, and weight loss.

  • Neurological symptoms include confusion, drowsiness, disorientation, delirium, headache, hallucinations, and seizures.

  • Visual disturbances manifest as photophobia, blurry vision, scotomas, decreased visual acuity, and color vision aberrations (eg, chromatopsia, xanthopsia [ie, yellow halos around lights]).

• Cardiac symptoms are similar in both acute and chronic toxicity and include palpitations, chest pressure or shortness of breath, lightheadedness, dizziness, and faintness.

Physical

Focus is on cardiovascular, neurologic, and GI systems.

• Vital signs
• • Bradycardia or tachycardia may be seen.

  • In absence of concomitant ingestion, environmental exposure, thyroid disorder, or underlying infection, patient generally is normothermic.

• Lungs: Examination findings typically are normal in the absence of preexisting disease, but rales have been reported.
• Heart
• • Bradydysrhythmias or tachydysrhythmias can occur, typically with increased automaticity and depressed conduction.

  • Pulses may be weak, thready, and irregular.

• Abdomen
• • Abdomen is generally soft.

  • Vomiting and diarrhea may be noted.

  • Emesis may contain plant material.

• Neurologic
• • Findings may include an altered level of consciousness, hypotonia, hyporeflexia, dysarthria, ataxia, horizontal nystagmus, and generalized seizures.

  • The patient typically has a nonfocal neurologic examination with pupillary reflexes intact.

• Skin: Skin may be pale, diaphoretic, and cool.

Causes

Exposure to plants containing glycosides can occur through ingestion of sap, berries, leaves, blossoms, seeds, or ingestion of teas brewed from plant parts; plant extracts also have been intentionally injected.

Other implicated routes of exposures, perhaps more folkloric than well documented, include drinking lily-of-the-valley vase water, eating food prepared with or stirred by poisonous plant parts, and inhaling smoke from burning plants.

• While there are many plant sources of cardiac glycosides, common ones include the following:
• • Purple foxglove (Digitalis purpurea)

  • Woolly foxglove (Digitalis lanata)

  • Ouabain (Strophanthus gratus)

  • Lily-of-the-valley (Convallaria majalis)

  • Common oleander (Nerium oleander)

  • Yellow oleander (Thevetia peruviana)

  • Squill or sea onion (Urginea maritima)

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Baclofen toxicity

Consider in the differential diagnosis entities in which GI upset is associated with hypotension, dysrhythmias (eg, bradycardias, tachycardias), or altered mental status (think TIPS AEIOU; trauma, infection, psychogenic causes, seizure/syncope, alcohol, encephalopathy/endocrinopathy/electrolytes, insulin, opiates, uremia). Consider co-ingestants. Address the possibility of intentional ingestion as a suicide attempt.

Other plants that may produce similar cardiac effects include Aconitum napellus (Monkshood) and other Aconitum species, Veratrum album (and other veratridine alkaloids), yew (Taxus brevifolia), and grayanotoxins (rhododendron). The cane toad (Bufo marinus) contains the cardioactive compound bufadienolide in its dried secretions that also has resulted in cardiac glycoside toxicity. Dried toad venom is used in China as a traditional medicine known as chan su and is a major component of kyushin, another popular herbal medication used in Asia.

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Fingerstick glucose determination: Assess for hypoglycemia as a possible cause of altered mental status.
• Complete blood count (CBC): Determine if anemia is a cause or potential complicating factor of dysrhythmia or hypotension.
• Electrolytes
• • Hyperkalemia is a primary manifestation of acute cardiac glycoside toxicity and an early predictor of need for antidotal therapy.

  • Hypokalemia exacerbates cardiac glycoside toxicity, and it is more typical in chronic toxicity. It is usually secondary to the use of loop diuretics, poor dietary intake, diarrhea, and administration of potassium-binding resins.

  • Hypercalcemia and hypomagnesemia exacerbate cardiac glycoside toxicity. Magnesium and ionized calcium levels may be helpful, but serum magnesium levels do not reflect total body load of magnesium.

• BUN and creatinine
• • Renal impairment negatively impairs elimination of glycosides and may exacerbate hyperkalemia.

  • In addition to certain medical conditions (eg, pregnancy, liver disease, subarachnoid hemorrhage, CHF, IDDM, stress, hypothermia), renal insufficiency is associated with elevated endogenous digoxinlike immunoreactive factors that can give false-positive digoxin assay results.

• Cardiac glycoside level
• • Some plant glycosides cross-react with commonly used digoxin radioimmunoassays (RIAs) and digoxin fluorescence polarization immunoassays. Detectable levels of cardiac glycosides have been associated with ingestion of foxglove and oleander; however, levels do not correlate with severity of illness.

  • Negative digoxin RIA does not rule out a plant glycoside exposure.

  • Consider other tests, such as cardiac enzymes, thyroid function tests (TFTs), arterial blood gasses (ABGs), or urine drug screens, depending on the patient's presentation.

  • Consider checking acetaminophen (APAP), salicylate (ASA), and ethanol (ETOH) levels, especially if overdose is suspected.

• Consider a pregnancy test for women with intentional ingestions or suicidal ideation.

Imaging Studies

• Chest x-ray (CXR) may be indicated for patients with severely toxic reactions or patients with pulmonary findings on physical examination.

Other Tests

• Electrocardiogram (ECG) and continuous cardiac monitoring
• • Assess cardiac rhythm and look for signs of ischemia or infarction.

  • Nonspecific ST segment and T wave abnormalities, consistent with "dig effect," (ST "scooping" or "strain"-like pattern) may be noted. This does not signify toxicity merely the presence of cardiac glycoside.

  • Peaked T waves may occur in hyperkalemia.

• Pulse oximetry to monitor oxygen saturation and heart rate

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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).

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

• Since 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. 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.

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.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Categories of drugs used to manage cardiac glycoside plant toxicity include drugs to minimize absorption and increase excretion, drugs that lower extracellular potassium, antidysrhythmics, and antidotes (eg, digoxin Fab fragments).

Drug Category: GI decontaminants

Activated charcoal is used to bind toxin within the GI tract. Due to enterohepatic/enteroenteric recirculation of cardiac glycosides, multiple doses can be given to help enhance elimination.

Drug Category: Antihyperkalemics

Hyperkalemia usually results from acute overdose and represents redistribution of potassium from intracellular to extracellular compartment; therefore, drugs of choice include agents that promote potassium redistribution from extracellular to intracellular compartments. Avoid calcium, as it may exacerbate effects of cardiac glycosides and may promote rhythm deterioration when used in this context.

Drug Category: Antiarrhythmic agents

Used to treat variety of bradydysrhythmias and tachydysrhythmias occurring with cardiac glycoside toxicity.

Drug Category: Antidote

Sheep-derived IgG antibodies to digoxin have been used successfully in patients with oleander toxicity. They cross-react with other cardiac glycosides and may be helpful in certain situations, including hyperkalemia not quickly responsive to standard treatments, life-threatening dysrhythmias not quickly responsive to standard treatments, and cardiac arrest.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Admit patients who show any signs of cardiac glycoside toxicity to a monitored setting for observation and further care.
• Admit to ICU/CCU patients with severe signs of toxicity or in whom Fab fragments were used without resolution of symptoms.
• Patients treated with Fab fragments and with complete resolution of symptoms may be admitted to a monitored setting. Clinicians should be aware of possibility of delayed toxicity if GI decontamination was not completed (especially for the leaves in the GI tract).

Further Outpatient Care

• Patients meeting the following criteria (measured serially over time) may be discharged:
• • Asymptomatic throughout the course of an ED observation period (12 h postingestion)

  • Normal vital signs

  • Baseline mental status

  • Baseline cardiac rate and rhythm; unchanged ECG

  • Electrolytes within reference range

  • Negative cardiac glycoside assay for any patient not regularly taking a digoxin preparation

  • Unintentional ingestion or clearance by psychiatry in a case of intentional ingestion

• Follow-up with primary care provider should be arranged within 1-2 days following unintentional ingestions.
• Close follow-up is mandatory if psychiatry recommends discharge of a patient after intentional ingestion or for any patient with underlying cardiac disease.

Transfer

• Arrange transfer to another facility with sufficient resources and expertise to care for patient under the following circumstances:
• • Lack of Fab fragments or lack of expertise in their use. However, with the assistance of local poison control center, toxicologist, or cardiologist, administration of Fab fragments should be performed prior to the transfer of symptomatic patient.

  • Lack of personnel experienced in management of cardiac glycoside toxicity

  • Lack of facilities or equipment to manage severe glycoside poisoning

• Transfer is usually to a tertiary care center with a toxicologist. In the US, follow all applicable COBRA transfer regulations.

Complications

• Complications of herbal cardiac glycoside toxicity are secondary to inadequate tissue perfusion caused by dysrhythmia-induced hypotension and include the following:
• • Hypoxic seizures

  • Encephalopathy or ischemic stroke

  • Myocardial ischemia

  • Acute tubular necrosis

Prognosis

• Unintentional ingestion of plants containing cardiac glycosides rarely results in death. However, other plants capable of inducing a similar syndrome of cardiac toxicity (eg, aconite) have been responsible for deaths after ingestion. When death occurs, it generally is due to lethal dysrhythmias and refractory hyperkalemia.
• Severity of hyperkalemia is predictive of outcome.

Patient Education

• For excellent patient education resources, visit eMedicine's Drug Overdose Center and Poisoning - First Aid and Emergency Center. Also, see eMedicine's patient education articles Poisoning, Drug Overdose, and Activated Charcoal.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to consider diagnosis because presentation was soon after ingestion when only nonspecific GI symptoms exist
• Failure to consider diagnosis because incomplete history was obtained (eg, use of alternative medications, plants)
• Failure to diagnose or correct electrolyte abnormalities, especially hypokalemia or hyperkalemia
• Using calcium to treat hyperkalemia induced by cardiac glycoside exposure
• Failure or delay to give digoxin Fab fragments to treat life-threatening dysrhythmias or hyperkalemia after other methods have failed to quickly correct the abnormality
• Failure to use reduced power settings for cardioversion of ventricular tachycardia or other tachydysrhythmias
• Failure to consult psychiatry for all intentional ingestions
• Failure to appreciate that a negative cardiac glycoside assay result does not exclude severe herbal cardiac glycoside toxicity
• Use of overdrive pacing for the control of ventricular dysrhythmias
• Use of transvenous pacer for the control of bradycardia prior to administration of Fab fragments resulting in cardiac excitation and consequent ventricular dysrhythmias

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Bain RJ. Accidental digitalis poisoning due to drinking herbal tea. Br Med J (Clin Res Ed). Jun 1 1985;290(6482):1624. [Medline].
• Bessen HA. Therapeutic and toxic effects of digitalis: William Withering, 1785. J Emerg Med. 1986;4(3):243-8. [Medline].
• Cheung K, Urech R, Taylor L. Plant cardiac glycosides and digoxin Fab antibody. J Paediatr Child Health. Oct 1991;27(5):312-3. [Medline].
• Dickstein ES, Kunkel FW. Foxglove tea poisoning. Am J Med. Jul 1980;69(1):167-9. [Medline].
• Eddleston M, Ariaratnam CA, Sjöström 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].
• Eddleston M, Rajapakse S, Rajakanthan, Jayalath S, Sjöström 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].
• Furbee B, Wermuth M. Life-threatening plant poisoning. Crit Care Clin. Oct 1997;13(4):849-88. [Medline].
• Goldfrank, Flomenbaum, Lewin, et al. Cardiac glycosides. In: 7th ed. Goldfrank's Toxicologic Emergencies. 2002:724-734.
• Gowda RM, Cohen RA, Khan IA. Toad venom poisoning: resemblance to digoxin toxicity and therapeutic implications. Heart. Apr 2003;89(4):e14. [Medline].
• 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].
• Litovitz TL, Klein-Schwartz W, Caravati EM. 2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2004;22(5):335-404. [Medline].
• 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].
• Plants - cardiac glycosides. In: Rumack BH, ed. Poisondex. 1997:94.
• 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].
• 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].
• 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].

Article Last Updated: Sep 13, 2006