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Product Name
:
LIDOCAINE-ELSaad (amp)
Chemical Name
:
Lidocaine HCl
Therapeutic Category
:
Analgesic & Anesthetic
Pharmacologic Category
:
Antiarrhythmic Agent, Class Ib - Local Anesthetic
Pharmaceutical Form
:
Ampoule
Composition
:
Lidocaine HCl 20mg / 40mg / 50mg
Monitoring Parameters
Dosing
 
Dosing: Adult
Antiarrhythmic (ACLS, 2010):
VF or pulseless VT (after defibrillation attempts, CPR, and vasopressor administration) if amiodarone is not available: I.V., intraosseous (I.O.): Initial: 1-1.5 mg/kg. If refractory VF or pulseless VT, repeat 0.5-0.75 mg/kg bolus every 5-10 minutes (maximum cumulative dose: 3 mg/kg). Follow with continuous infusion (1-4 mg/minute) after return of perfusion. Reappearance of arrhythmia during constant infusion: 0.5 mg/kg bolus and reassessment of infusion (Zipes, 2000)
Intratracheal (loading dose only): 2-3.75 mg/kg (2-2.5 times the recommended I.V. dose); dilute in 5-10 mL NS or sterile water. Note: Absorption is greater with sterile water and results in less impairment of PaO2.
Hemodynamically stable monomorphic VT: I.V.: 1-1.5 mg/kg; repeat with 0.5-0.75 mg/kg every 5-10 minutes as necessary (maximum cumulative dose: 3 mg/kg). Follow with continuous infusion of 1-4 mg/minute (or 14-57 mcg/kg/minute).
Note: Reduce maintenance infusion in patients with CHF, shock, or hepatic disease; initiate infusion at 10 mcg/kg/minute (maximum dose: 1.5 mg/minute or 20 mcg/kg/minute).
Anesthesia, local injectable: Varies with procedure, degree of anesthesia needed, vascularity of tissue, duration of anesthesia required, and physical condition of patient; maximum: 4.5 mg/kg/dose not to exceed 300 mg; do not repeat within 2 hours.

Dosing: Pediatric

Antiarrhythmic:
I.V., intraosseous (I.O.): Note: For use in VF or pulseless VT if amiodarone is not available; give after defibrillation attempts, CPR, and epinephrine:
Loading dose: 1 mg/kg (maximum: 100 mg); follow with continuous infusion; may administer second bolus of 0.5-1 mg/kg if delay between bolus and start of infusion is >15 minutes (PALS, 2000; PALS, 2010)
Continuous infusion: 20-50 mcg/kg/minute (PALS, 2010). Per the manufacturer, do not exceed 20 mcg/kg/minute in patients with shock, hepatic disease, cardiac arrest, or CHF.
Intratracheal: 2-3 mg/kg; flush with 5 mL of NS and follow with 5 assisted manual ventilations (PALS, 2010)
Anesthesia, local injectable: Refer to adult dosing.

Dosing: Geriatric

Refer to adult dosing.

Dosing: Renal Impairment

Not dialyzable (0% to 5%) by hemo- or peritoneal dialysis; supplemental dose is not necessary.

Dosing: Hepatic Impairment

Reduce maintenance infusion. Initial: 0.75 mg/minute or 10 mcg/kg/minute; maximum dose: 1.5 mg/minute or 20 mcg/kg/minute. Monitor lidocaine concentrations closely and adjust infusion rate as necessary; consider alternative therapy.
Use
 
Local and regional anesthesia by infiltration, nerve block, epidural, or spinal techniques; acute treatment of ventricular arrhythmias from myocardial infarction or cardiac manipulation
Use - Unlabeled/Investigational
ACLS guidelines: Hemodynamically stable monomorphic ventricular tachycardia (VT) (preserved ventricular function); polymorphic VT (preserved ventricular function); drug-induced monomorphic VT; when amiodarone is not available, pulseless VT or ventricular fibrillation (VF) (unresponsive to defibrillation, CPR, and vasopressor administration)
PALS guidelines: When amiodarone is not available, pulseless VT or VF (unresponsive to defibrillation, CPR, and epinephrine administration); consider in patients with cocaine overdose to prevent arrhythmias secondary to MI
I.V. infusion for chronic pain syndrome
Adverse Reactions
 
Effects vary with route of administration. Many effects are dose related.
Frequency not defined.
Cardiovascular: Arrhythmia, bradycardia, arterial spasms, cardiovascular collapse, defibrillator threshold increased, edema, flushing, heart block, hypotension, sinus node supression, vascular insufficiency (periarticular injections)
Central nervous system: Agitation, anxiety, apprehension, coma, confusion, disorientation, dizziness, drowsiness, euphoria, hallucinations, headache, hyperesthesia, hypoesthesia, lethargy, lightheadedness, nervousness, psychosis, seizure, slurred speech, somnolence, unconsciousness
Gastrointestinal: Metallic taste, nausea, vomiting
Local: Thrombophlebitis
Neuromuscular & skeletal: Paresthesia, transient radicular pain (subarachnoid administration; up to 1.9%), tremor, twitching, weakness
Otic: Tinnitus
Respiratory: Bronchospasm, dyspnea, respiratory depression or arrest
Miscellaneous: Allergic reactions, anaphylactoid reaction, sensitivity to temperature extremes
Following spinal anesthesia: Positional headache (3%), shivering (2%) nausea, peripheral nerve symptoms, respiratory inadequacy and double vision (<1%), hypotension, cauda equina syndrome
Postmarketing and/or case reports: Asystole, disorientation, methemoglobinemia, skin reaction
Contraindications
 
Hypersensitivity to lidocaine or any component of the formulation; hypersensitivity to another local anesthetic of the amide type; Adam-Stokes syndrome; severe degrees of SA, AV, or intraventricular heart block (except in patients with a functioning artificial pacemaker); premixed injection may contain corn-derived dextrose and its use is contraindicated in patients with allergy to corn-related products
Warnings / Precautions Drug
 
Concerns related to adverse effects:
• Intra-articular infusion related chondrolysis: Continuous intra-articular infusion of local anesthetics after arthroscopic or other surgical procedures is not an approved use; chondrolysis (primarily in the shoulder joint) has occurred following infusion, with some cases requiring arthroplasty or shoulder replacement.
Disease-related concerns:
• Hepatic dysfunction: Use extreme caution in patients with severe hepatic dysfunction; may have increased risk of lidocaine toxicity.
• Pseudocholinesterase deficiency: Use caution in patients with pseudocholinesterase deficiency; may have increased risk of lidocaine toxicity
Dosage form specific issues:
• Injectable anesthetic: Follow appropriate administration techniques so as not to administer any intravascularly. Solutions containing antimicrobial preservatives should not be used for epidural or spinal anesthesia. Some solutions contain a bisulfite; avoid in patients who are allergic to bisulfite. Resuscitative equipment, medicine and oxygen should be available in case of emergency. Use products containing epinephrine cautiously in patients with significant vascular disease, compromised blood flow, or during or following general anesthesia (increased risk of arrhythmias). Adjust the dose for the elderly, pediatric, acutely ill, and debilitated patients.
• Intravenous: Constant ECG monitoring is necessary during I.V. administration. Use cautiously in hepatic impairment, any degree of heart block, Wolff-Parkinson-White syndrome, HF, marked hypoxia, severe respiratory depression, hypovolemia, history of malignant hyperthermia, or shock. Increased ventricular rate may be seen when administered to a patient with atrial fibrillation. Correct electrolyte disturbances, especially hypokalemia or hypomagnesemia, prior to use and throughout therapy. Correct any underlying causes of ventricular arrhythmias. Monitor closely for signs and symptoms of CNS toxicity. The elderly may be prone to increased CNS and cardiovascular side effects. Reduce dose in hepatic dysfunction and CHF.
Other warnings/precautions:
• CAST trial: In the Cardiac Arrhythmia Suppression Trial (CAST), recent (>6 days but <2 years ago) myocardial infarction patients with asymptomatic, non-life-threatening ventricular arrhythmias did not benefit and may have been harmed by attempts to suppress the arrhythmia with flecainide or encainide. An increased mortality or nonfatal cardiac arrest rate (7.7%) was seen in the active treatment group compared with patients in the placebo group (3%). The applicability of the CAST results to other populations is unknown. Antiarrhythmic agents should be reserved for patients with life-threatening ventricular arrhythmias.
Metabolism/Transport Effects
Substrate of CYP1A2 (minor), CYP2A6 (minor), CYP2B6 (minor), CYP2C9 (minor), CYP2D6 (major), CYP3A4 (major), P-glycoprotein; Inhibits CYP1A2 (strong), 2D6 (moderate), 3A4 (moderate.
Interactions
 
Amiodarone: May decrease the metabolism of Lidocaine (Systemic). Risk C: Monitor therapy
Bendamustine: CYP1A2 Inhibitors (Strong) may increase the serum concentration of Bendamustine. Concentrations of the active metabolites of bendamustine may be decreased. Risk C: Monitor therapy
Beta-Blockers: May decrease the metabolism of Lidocaine (Systemic). Risk C: Monitor therapy
Budesonide (Systemic, Oral Inhalation): CYP3A4 Inhibitors (Moderate) may increase the serum concentration of Budesonide (Systemic, Oral Inhalation). Management: Consider reducing the oral budesonide dose when used together with a CYP3A4 inhibitor. This interaction is likely less severe with orally inhaled budesonide. Monitor patients closely for signs/symptoms of corticosteroid excess. Risk D: Consider therapy modification
Colchicine: CYP3A4 Inhibitors (Moderate) may increase the serum concentration of Colchicine. Management: Reduce colchicine dose as directed when using with a moderate CYP3A4 inhibitor, and increase monitoring for colchicine-related toxicity. Use extra caution in patients with impaired renal and/or hepatic function. Risk D: Consider therapy modification
Conivaptan: May increase the serum concentration of CYP3A4 Substrates. Risk X: Avoid combination
CYP1A2 Substrates: CYP1A2 Inhibitors (Strong) may decrease the metabolism of CYP1A2 Substrates. Risk D: Consider therapy modification
CYP2D6 Inhibitors (Moderate): May decrease the metabolism of CYP2D6 Substrates. Risk C: Monitor therapy
CYP2D6 Inhibitors (Strong): May decrease the metabolism of CYP2D6 Substrates. Risk D: Consider therapy modification
CYP2D6 Substrates: CYP2D6 Inhibitors (Moderate) may decrease the metabolism of CYP2D6 Substrates. Exceptions: Tamoxifen. Risk C: Monitor therapy
CYP3A4 Inducers (Strong): May increase the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
CYP3A4 Inhibitors (Moderate): May decrease the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
CYP3A4 Inhibitors (Strong): May decrease the metabolism of CYP3A4 Substrates. Risk D: Consider therapy modification
CYP3A4 Substrates: CYP3A4 Inhibitors (Moderate) may decrease the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
Cyproterone: May decrease the serum concentration of CYP1A2 Substrates. Risk C: Monitor therapy
Darunavir: May increase the serum concentration of Lidocaine (Systemic). Risk C: Monitor therapy
Dasatinib: May increase the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Deferasirox: May decrease the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Disopyramide: May enhance the arrhythmogenic effect of Lidocaine (Systemic). Disopyramide may increase the serum concentration of Lidocaine (Systemic). Specifically, the unbound/free fraction of lidocaine. Risk C: Monitor therapy
Eplerenone: CYP3A4 Inhibitors (Moderate) may increase the serum concentration of Eplerenone. Management: A lower starting dose of eplerenone (25 mg once daily for adults) is recommended in patients with hypertension who are also taking drugs that are moderate inhibitors of CYP3A4. Risk D: Consider therapy modification
Etravirine: May decrease the serum concentration of Lidocaine (Systemic). Risk C: Monitor therapy
Everolimus: CYP3A4 Inhibitors (Moderate) may increase the serum concentration of Everolimus. Management: Everolimus dose reductions are required for patients being treated for subependymal giant cell astrocytoma or renal cell carcinoma. See prescribing information for specific dose adjustment and monitoring recommendations. Risk D: Consider therapy modification
Fesoterodine: CYP2D6 Inhibitors may increase serum concentrations of the active metabolite(s) of Fesoterodine. Risk C: Monitor therapy
Halofantrine: CYP3A4 Inhibitors (Moderate) may increase the serum concentration of Halofantrine. Risk D: Consider therapy modification
Lurasidone: CYP3A4 Inhibitors (Moderate) may increase the serum concentration of Lurasidone. Risk D: Consider therapy modification
Peginterferon Alfa-2b: May decrease the serum concentration of CYP2D6 Substrates. Risk C: Monitor therapy
P-glycoprotein/ABCB1 Inducers: May decrease the serum concentration of P-glycoprotein/ABCB1 Substrates. P-glycoprotein inducers may also further limit the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy
P-glycoprotein/ABCB1 Inhibitors: P-glycoprotein/ABCB1 Substrates may increase the serum concentration of P-glycoprotein/ABCB1 Inhibitors. P-glycoprotein inhibitors may also enhance the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy
Pimecrolimus: CYP3A4 Inhibitors (Moderate) may decrease the metabolism of Pimecrolimus. Risk C: Monitor therapy
Salmeterol: CYP3A4 Inhibitors (Moderate) may increase the serum concentration of Salmeterol. Risk C: Monitor therapy
Saquinavir: May enhance the arrhythmogenic effect of Lidocaine (Systemic). Saquinavir may increase the serum concentration of Lidocaine (Systemic). Risk X: Avoid combination
Saxagliptin: CYP3A4 Inhibitors (Moderate) may increase the serum concentration of Saxagliptin. Risk C: Monitor therapy
Telaprevir: May enhance the adverse/toxic effect of Lidocaine (Systemic). Telaprevir may increase the serum concentration of Lidocaine (Systemic). Risk C: Monitor therapy
Thioridazine: CYP2D6 Inhibitors may decrease the metabolism of Thioridazine. Risk X: Avoid combination
Tocilizumab: May decrease the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Tolvaptan: CYP3A4 Inhibitors (Moderate) may increase the serum concentration of Tolvaptan. Risk X: Avoid combination
Vilazodone: CYP3A4 Inhibitors (Moderate) may increase the serum concentration of Vilazodone. Risk C: Monitor therapy
Pregnancy
 
B
Pregnancy Implications
Animal studies with lidocaine have not shown teratogenic effects. Lidocaine and the MEGX metabolite cross the placenta. Use is not contraindicated during labor and delivery. Topical lidocaine is used locally to provide analgesia prior to episiotomy and during repair of obstetric lacerations. Administration by the perineal route may result in greater absorption than administration by the epidural route. Adverse events have been reported in the infant following maternal administration, however, when used in appropriate doses, the risk to the fetus is low. Cumulative exposure from all routes of administration should be considered.
Lactation
 
Enters breast milk/use caution (AAP rates “compatible”; AAP 2001 update pending)
Breast-Feeding Considerations
Small amounts of lidocaine and the MEGX metabolite are found in breast milk. The actual amount may depend on route and duration of administration. When administered topically at recommended doses, the amount of lidocaine available to the nursing infant would not be expected to cause adverse events. Cumulative exposure from all routes of administration should be considered.
Mechanism of Action
 
Class Ib antiarrhythmic; suppresses automaticity of conduction tissue, by increasing electrical stimulation threshold of ventricle, His-Purkinje system, and spontaneous depolarization of the ventricles during diastole by a direct action on the tissues; blocks both the initiation and conduction of nerve impulses by decreasing the neuronal membrane's permeability to sodium ions, which results in inhibition of depolarization with resultant blockade of conduction
Pharmacodynamics / Kinetics
 
Onset of action: Single bolus dose: 45-90 seconds
Duration: 10-20 minutes
Distribution: Vd: 1.1-2.1 L/kg; alterable by many patient factors; decreased in CHF and liver disease; crosses blood-brain barrier
Protein binding: 60% to 80% to alpha1 acid glycoprotein
Metabolism: 90% hepatic; active metabolites monoethylglycinexylidide (MEGX) and glycinexylidide (GX) can accumulate and may cause CNS toxicity
Half-life elimination: Biphasic: Prolonged with congestive heart failure, liver disease, shock, severe renal disease; Initial: 7-30 minutes; Terminal: Infants, premature: 3.2 hours, Adults: 1.5-2 hours
Excretion: Urine (<10% as unchanged drug, ~90% as metabolites)
 
   
 
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