Note: Enlon is no longer available in the US.
Diagnosis of myasthenia gravis: Limited data available: Note: Usually administered IV; if not possible, IM or SubQ may be used; however, the results are variable and it may take longer for reaction (Kliegman 2015). Atropine should be available at bedside during the testing for the rare case in which severe bradycardia, cardiac arrhythmia, or hypotension develops. Edrophonium is not the ideal agent in neonates due to its brief effects which make objective assessment difficult; there is also an increased incidence of cardiac arrhythmias associated with this drug when given to neonates (Kliegman 2015).
Test dose: Some experts suggest an initial test dose to assess for hypersensitivity or sensitivity to muscarinic effects: IV: 0.01 mg/kg (Kliegman 2015; Swaiman 2012)
Diagnostic dose:
IV: 0.1 mg/kg (Avery 1994; Papazian 1992)
IM, SubQ: 0.15 mg/kg, may repeat at doses of 0.15 mg/kg. Maximum total dose: 0.6 mg (Papazian 1992; Schara 2012)
Note: Enlon is no longer available in the US.
Diagnosis of myasthenia gravis: Note: Usually administered IV; if not possible, IM or SubQ may be used; however, the results are variable and it may take longer for reaction (Kliegman 2015). Atropine should be available at bedside during the testing for the rare case in which severe bradycardia, cardiac arrhythmia, or hypotension develops.
Test dose: Limited data available: Some experts suggest an initial test dose to assess for hypersensitivity or sensitivity to muscarinic effects: IV: 0.01 mg/kg (Kliegman 2015; Swainman 2012)
Diagnostic dose:
Manufacturer's labeling:
Infants: IV: 0.5 mg
Children and Adolescents:
≤34 kg:
IV: 1 mg; if no response after 45 seconds, it may be repeated in 1 mg increments every 30 to 45 seconds to a total of 5 mg
IM: 2 mg
>34 kg:
IV: 2 mg; if no response after 45 seconds, it may be repeated in 1 mg increments every 30 to 45 seconds to a total of 10 mg
IM: 5 mg
Alternate dosing: Weight-directed dosing: Limited data available: Children and Adolescents:
IV, IM, SubQ: Initial: 0.01 to 0.02 mg/kg every 30 to 45 seconds up to the maximum dose (Kliegman 2015; Swaiman 2012). Note: Typical cumulative dose for a 3 to 5 year old is 5 mg/dose (Kliegman 2011)
Maximum total dose (Kliegman 2015; Swaiman 2012):
Children and Adolescents: <30 kg: 0.1 mg/kg
Children and Adolescents ≥30 kg: 0.2 mg/kg or 10 mg; whichever is less
Reversal of nondepolarizing neuromuscular blocking agents: Limited data available: Infants, Children, and Adolescents: IV: Usual dose: 0.5 to 1 mg/kg/dose; minimum dose: 0.3 mg/kg/dose (Cote 2013); doses studied range from 0.1 mg/kg to 1.43 mg/kg/dose (Bevan 1996; Fisher 1984; Kirkegaard-Nielsen 1995; Meakin 1983; Abdulatif 1996)
There are no dosage adjustments provided in the manufacturer's labeling.
There are no dosage adjustments provided in the manufacturer's labeling.
(For additional information see "Edrophonium (United States: Not available): Drug information")
Note: Enlon is no longer available in the United States.
Diagnosis of myasthenia gravis:
Note: Methods vary in regards to the initial and repeat doses. However, all regimens utilize a maximum cumulative dose of 10 mg and emphasize that the incremental administration is to help avoid excessive muscarinic side effects. Atropine should be available at the bedside during the testing for the rare case in which severe bradycardia, cardiac arrhythmia, or hypotension develops. The following edrophonium dosing strategies have been described: IV:
2 mg; if after 90 seconds there is definite improvement, then test is considered positive and may be terminated. If symptoms recur, then may administer another 2 mg dose. If there is no definite improvement with the initial dose, then may administer 3 mg and observe patient for an additional 90 seconds; if test not positive, then may administer the remaining 5 mg and observe patient for 3 to 5 more minutes (Seybold 1986).
Or
1 mg (test dose); if after 60 seconds there are no adverse effects, then administer 3 mg. If after 60 seconds there is no improvement, then administer an additional 3 mg; after an additional 60 seconds, repeat a 3 mg dose if necessary for a total dose of 10 mg (Pascuzzi 2003).
Manufacturer’s labeling: Dosing in the prescribing information may not reflect current clinical practice.
IV: 2 mg test dose administered over 15 to 30 seconds; if no cholinergic reaction occurs after 45 seconds then administer 8 mg. If cholinergic reaction occurs after initial test dose, stop testing; test dose may be repeated after 30 minutes
IM: 10 mg; if cholinergic reaction occurs, administer 2 mg 30 minutes later to rule out false-negative reaction.
Evaluation of treatment requirements in myasthenia gravis: IV: 1 to 2 mg given 1 hour after oral dose of anticholinesterase; response will be myasthenic in undertreated patients, adequate in the controlled patient, and cholinergic in the overtreated patient; adjust as appropriate.
Differentiation of cholinergic from myasthenic crisis: IV: 1 mg; may repeat after 1 minute. Note: Intubation and controlled ventilation may be required if patient has cholinergic crisis.
Reversal of nondepolarizing neuromuscular blocking agents: Note: Atropine should be administered with edrophonium (or glycopyrrolate administered several minutes prior to edrophonium) to diminish the cholinergic effects, especially bradycardia (Barash 2009; Morgan 2013).
IV: Usual dose: 0.5 to 1 mg/kg (Engbaek 1985; Miller 2010; Morgan 2013).
Manufacturer’s labeling: IV: Dosing in the prescribing information may not reflect current clinical practice. 10 mg over 30 to 45 seconds; may repeat as necessary up to a maximum cumulative dose of 40 mg.
There are no dosage adjustments provided in manufacturer's labeling.
There are no dosage adjustments provided in the manufacturer's labeling.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Frequency not defined. Some reactions listed are based on reports for other agents in this same pharmacologic class and may not be specifically reported for edrophonium.
Cardiovascular: Atrioventricular block, cardiac arrhythmia (especially bradycardia), cardiac arrest, ECG changes (nonspecific), flushing, hypotension, syncope, tachycardia, thrombophlebitis (IV)
Central nervous system: Convulsions, dizziness, drowsiness, dysarthria, headache, loss of consciousness, voice disorder
Dermatologic: Diaphoresis, skin rash, urticaria
Gastrointestinal: Diarrhea, dysphagia, flatulence, hypersecretory conditions (gastric and intestinal), increased peristalsis, nausea, salivation, stomach cramps, vomiting
Genitourinary: Urinary frequency, urinary urgency
Hypersensitivity: Anaphylaxis, hypersensitivity reaction
Neuromuscular & skeletal: Fasciculations, laryngospasm, weakness
Ophthalmic: Conjunctival hyperemia, diplopia, lacrimation, miosis, accommodation disturbance (spasm)
Respiratory: Bronchoconstriction, increased bronchial secretions, respiratory arrest, respiratory paralysis
Hypersensitivity to edrophonium, sulfites, or any component of the formulation; GI or GU obstruction
Concerns related to adverse effects:
• Cholinergic crisis: Overdosage can cause cholinergic crisis, which may be fatal. Atropine should always be readily available as an antagonist and for treatment of cholinergic reactions.
Disease-related concerns:
• Arrhythmias: Use with caution in patients with cardiac arrhythmias (eg, bradyarrhythmias) due to cholinergic effects.
• Asthma: Use with caution in patients with bronchial asthma due to potential bronchoconstriction and/or increased secretions.
• Myasthenia gravis: Avoid use as an agent to reverse non-depolarizing neuromuscular blockade in patients with myasthenia gravis; may exacerbate muscular weakness.
Concurrent drug therapy issues:
• Drug/drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult Drug Interactions database for more detailed information.
Dosage form specific issues:
• Sodium sulfite: Products may contain sodium sulfite.
Edrophonium is not recommended for use in infants; its effect is too brief for objective assessment and may have an increased risk of acute cardiac arrhythmias in infants, especially neonates (Kliegman 2015).
Enlon is no longer available in the US.
Yes
Solution (Enlon Injection)
10 mg/mL (per mL): $6.40
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Parenteral: Edrophonium is administered by direct IV or IM injection; if not possible, SubQ may be used.
Diagnosis of myasthenia gravis: Administer as IV Push; in adults, doses have been administered over 15 to 30 seconds and follow with a saline flush (Pascuzzi 2003)
Injection: May administer undiluted by IV, IM, or SubQ injection; refer to individual indications in dosing for detailed recommendations.
Store at 20°C to 25°C (68°F to 77°F).
Differential diagnosis of myasthenia gravis (FDA approved in pediatric patients [age not specified] and adults); evaluation of treatment in myasthenia gravis (FDA approved in adults); evaluating emergency treatment in myasthenic crises (FDA approved in adults); reversal of nondepolarizing neuromuscular blockers (FDA approved in adults)
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Amifampridine: Acetylcholinesterase Inhibitors may enhance the therapeutic effect of Amifampridine. Amifampridine side effects may also be increased. Amifampridine may enhance the therapeutic effect of Acetylcholinesterase Inhibitors. Acetylcholinesterase inhibitor side effects may also be increased. Risk C: Monitor therapy
Anticholinergic Agents: Acetylcholinesterase Inhibitors may diminish the therapeutic effect of Anticholinergic Agents. Anticholinergic Agents may diminish the therapeutic effect of Acetylcholinesterase Inhibitors. Risk C: Monitor therapy
Benoxinate: Acetylcholinesterase Inhibitors may enhance the therapeutic effect of Benoxinate. Specifically, the effects of benoxinate may be prolonged. Risk C: Monitor therapy
Beta-Blockers: Acetylcholinesterase Inhibitors may enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy
Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Risk C: Monitor therapy
Cardiac Glycosides: Edrophonium may enhance the AV-blocking effect of Cardiac Glycosides. Risk C: Monitor therapy
Ceritinib: Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Risk D: Consider therapy modification
Chlorprothixene: Acetylcholinesterase Inhibitors may enhance the adverse/toxic effect of Chlorprothixene. Acetylcholinesterase Inhibitors may enhance the therapeutic effect of Chlorprothixene. Risk C: Monitor therapy
Cholinergic Agonists: Acetylcholinesterase Inhibitors may enhance the adverse/toxic effect of Cholinergic Agonists. Specifically, cholinergic effects may be enhanced or increased. Risk C: Monitor therapy
Corticosteroids (Systemic): May enhance the adverse/toxic effect of Acetylcholinesterase Inhibitors. Increased muscular weakness may occur. Risk C: Monitor therapy
Dipyridamole: May diminish the therapeutic effect of Acetylcholinesterase Inhibitors. Risk C: Monitor therapy
Etrasimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Fexinidazole: Bradycardia-Causing Agents may enhance the arrhythmogenic effect of Fexinidazole. Risk X: Avoid combination
Fingolimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider therapy modification
Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Risk C: Monitor therapy
Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Risk C: Monitor therapy
Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Neuromuscular-Blocking Agents (Nondepolarizing): Acetylcholinesterase Inhibitors may diminish the neuromuscular-blocking effect of Neuromuscular-Blocking Agents (Nondepolarizing). Risk C: Monitor therapy
Ozanimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Ponesimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider therapy modification
Siponimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider therapy modification
Succinylcholine: Acetylcholinesterase Inhibitors may enhance the neuromuscular-blocking effect of Succinylcholine. Risk C: Monitor therapy
Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Due to the theoretical potential for complications, consider a lower initial dose when using edrophonium for the diagnosis of myasthenia gravis during pregnancy (Varner, 2013).
Pre- and postinjection strength (cranial musculature is most useful); heart rate, respiratory rate, blood pressure, changes in fasciculations
Inhibits destruction of acetylcholine by acetylcholinesterase. This facilitates transmission of impulses across myoneural junction and results in increased cholinergic responses such as miosis, increased tonus of intestinal and skeletal muscles, bronchial and ureteral constriction, bradycardia, and increased salivary and sweat gland secretions.
Onset of action: IM: 2 to 10 minutes; IV: 30 to 60 seconds
Duration: IM: 5 to 30 minutes: IV: 10 minutes
Distribution: Vd: Infants: 1.18 ± 0.2 L/kg; Children: 1.22 ± 0.74 L/kg; Adults: 0.9 ± 0.13 L/kg
Half-life elimination: Infants: 73 ± 30 minutes; Children: 99 ± 31 minutes; Adults: 126 ± 59 minutes; Anephric patients: 2.4 to 4.4 hours
Excretion: Adults: Primarily urine (67%)
Clearance: Infants: 17.8 mL/kg/minute; Children: 14.2 mL/kg/minute; Adults: 8.3 ± 2.9 mL/kg/minute
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