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    Muscle Relaxants, Peripherally Acting

    BOXED WARNING

    Bradycardia, children, Guillain-Barre syndrome, hyperkalemia, infants, malignant hyperthermia, myopathy, neonates, rhabdomyolysis

    Safe and effective use of succinylcholine has been established in neonates, infants, children, and adolescents; however, there are rare reports of ventricular dysrhythmias and cardiac arrest secondary to acute rhabdomyolysis with hyperkalemia in apparently healthy pediatric patients who receive succinylcholine. Many of these pediatric patients were subsequently found to have undiagnosed skeletal muscle myopathy such as Duchenne's muscular dystrophy. The syndrome often presents as sudden cardiac arrest within minutes after the administration of succinylcholine. These pediatric patients are usually, but not exclusively, males, and most frequently 8 years of age or younger. There have also been reports in adolescents. There may be no signs or symptoms to alert the practitioner to which pediatric patients are at risk. A careful history and physical may identify developmental delays suggestive of a myopathy. A preoperative creatine kinase could identify some but not all pediatric patients at risk. Due to the abrupt onset of this syndrome, routine resuscitative measures are likely to be unsuccessful. Careful monitoring of the electrocardiogram may alert the practitioner to peaked T-waves (an early sign). Administration of intravenous calcium, bicarbonate, and glucose with insulin, with hyperventilation have resulted in successful resuscitation in some of the reported cases. Extraordinary and prolonged resuscitative efforts have been effective in some cases. Chronic abdominal infections, subarachnoid hemorrhage, tetanus, disuse atrophy, Guillain-Barre syndrome, and degenerative nervous system disorders may also increase the risk for hyperkalemia. In addition, in the presence of signs of malignant hyperthermia, appropriate treatment should be initiated concurrently. Since it is difficult to identify which pediatric patients are at risk, it is recommended that the use of succinylcholine in pediatric patients should be reserved for emergency intubation or instances where immediate securing of the airway is necessary, e.g., laryngospasm, difficult airway, full stomach, or for intramuscular use when a suitable vein is inaccessible. The incidence and severity of bradycardia is higher in pediatric patients than adults; the incidence of bradycardia is higher following the second dose of succinylcholine. Pre-treatment with anticholinergic agents, e.g., atropine, may reduce the occurrence of bradyarrhythmias. For routine elective surgery, children and adolescents should receive non-depolarizing neuromuscular agents. Succinylcholine is contraindicated for patients with a personal or familial history of malignant hyperthermia, skeletal muscle myopathy, or hypersensitivity to the drug. Acute rhabdomyolysis can occur when used in individuals with a known skeletal muscle myopathy.

    DEA CLASS

    Rx

    DESCRIPTION

    Ultra short-acting, depolarizing-type, skeletal muscle relaxant; fastest onset of neuromuscular blockers; reserved for emergency use only in children due to rare, severe arrhythmias.

    COMMON BRAND NAMES

    Anectine, Quelicin

    HOW SUPPLIED

    Anectine/Quelicin/Succinylcholine/Succinylcholine Chloride Intravenous Inj Sol: 1mL, 20mg
    Quelicin Intramuscular Inj Sol: 1mL, 20mg

    DOSAGE & INDICATIONS

    For neuromuscular blockade.
    For neuromuscular blockade during short surgical procedures.
    Intravenous dosage
    Adults

    Average dose is 0.6 mg/kg IV (range 0.3—1.1 mg/kg) given over 10—30 seconds. Additional doses, if necessary, are administered in accordance with the patient's response. A test dose of 0.1 mg/kg IV may be given initially to assess individual patient response and recovery time.

    Intramuscular dosage
    Adults, Older Children, and Infants

    A dose of up to 3—4 mg/kg IM may be given, but the total dose must not exceed 150 mg. NOTE: In pediatric patients, the use of a nondepolarizing neuromuscular blocker is preferred to avoid the rare risk of succinylcholine-induced acute rhabdomyolysis with hyperkalemia and asystole. In pediatric patients, succinylcholine should be reserved for emergency procedures or when IV access is not available.

    For neuromuscular blockade during long surgical procedures.
    Continuous Intravenous Infusion dosage
    Adults

    Solutions containing 0.1% to 0.2% succinylcholine in D5W or NS (or other appropriate diluent) are usually infused IV at rate of 2.5 mg/minute for up to one hour, but the rate requirements may range from 0.5 to 10 mg/minute depending on the individual patient characteristics and response.

    Neonates, Infants, and Children

    Not recommended. NOTE: In pediatric patients, the use of a nondepolarizing neuromuscular blocker is preferred to avoid the rare risk of succinylcholine-induced acute rhabdomyolysis with hyperkalemia and asystole. In pediatric patients, succinylcholine should be reserved for emergency procedures or when IV access is not available.

    Intermittent Intravenous Injection dosage
    Adults

    Initial dose is 0.3—1.1 mg/kg intermittent IV injection, followed by additional doses of 0.04-0.07 mg/kg as needed to maintain adequate relaxation.

    Neonates, Infants, and Children

    1—2 mg/kg intermittent IV injection; additional doses may be administered as needed based upon patient response. NOTE: In pediatric patients, the use of a nondepolarizing neuromuscular blocker is preferred to avoid the rare risk of succinylcholine-induced acute rhabdomyolysis with hyperkalemia and asystole. In pediatric patients, succinylcholine should be reserved for emergency procedures or when IV access is not available.

    For the facilitation of endotracheal intubation.
    NOTE: In pediatric patients, the use of a nondepolarizing neuromuscular blocker is preferred to avoid the rare risk of succinylcholine-induced acute rhabdomyolysis with hyperkalemia and asystole. In pediatric patients, succinylcholine should be reserved for emergency procedures or when IV access is not available.
    Intravenous dosage
    Adults

    0.6 mg/kg IV (range: 0.3—1.1 mg/kg).

    Older Children and Adolescents

    1 mg/kg IV.

    Infants and Small Children

    2 mg/kg IV.

    Intramuscular dosage
    Adults, Children, and Infants

    A dose of up to 3—4 mg/kg IM may be given, but the total dose must not exceed 150 mg. The onset of effect is usually observed about 2—3 minutes after the dose.

    For control of muscle contractions during electroconvulsive therapy (ECT)†.
    Intravenous dosage
    Adults

    10—30 mg IV given about 1 minute before ECT. Dosage for the individual patient must be determined based on his/her size and physical condition.

    Intramuscular dosage
    Adults

    A dose of up to 3—4 mg/kg IM may be given, but the total dose must not exceed 150 mg.

    †Indicates off-label use

    MAXIMUM DOSAGE

    Adults

    Short procedures: 1.1 mg/kg IV over 10—30 seconds; 150 mg IM. Long procedures: 10 mg/min continuous IV infusion (0.1—0.2% succinylcholine IV solution) or 1.1 mg/kg intermittent IV infusion followed by additional doses of 0.04—0.07 mg/kg as needed to maintain adequate relaxation. Maximum dose is always dependent upon patient response.

    Elderly

    For short procedures: 1.1 mg/kg IV over 10—30 seconds. For long procedures: 10 mg/min continuous IV infusion (0.1—0.2% succinylcholine IV solution) or 1.1 mg/kg intermittent IV infusion followed by additional doses of 0.04—0.07 mg/kg as needed to maintain adequate relaxation. Maximum dose is always dependent upon patient response.

    Adolescents

    Short procedures: 150 mg deep IM injection. Long procedures: 2 mg/kg intermittent IV injection. Rapid IV injection may result in profound bradycardia or asystole. Continuous IV infusion is not recommended in pediatric patients due to risk of malignant hyperthermia.

    Children

    Short procedures: 150 mg deep IM injection. Long procedures: 2 mg/kg intermittent IV injection. Rapid IV injection may result in profound bradycardia or asystole. Continuous IV infusion is not recommended in pediatric patients due to risk of malignant hyperthermia.

    Infants

    Short procedures: 150 mg deep IM injection. Long procedures: 2 mg/kg intermittent IV injection. Rapid IV injection may result in profound bradycardia or asystole. Continuous IV infusion is not recommended in pediatric patients due to risk of malignant hyperthermia.

    DOSING CONSIDERATIONS

    Hepatic Impairment

    Specific guidelines for dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed.

    Renal Impairment

    Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.

    ADMINISTRATION

    Injectable Administration

    Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.
    Only experienced clinicians familiar with the use of neuromuscular blocking drugs should administer or supervise the use of succinylcholine. Adequacy of respiration must be assured through assisted or controlled ventilation.
    Succinylcholine does not provide sedation or analgesia and should be administered only after unconsciousness has been induced; however, in emergent life-threatening situations, it may be necessary to administer succinylcholine prior to unconsciousness. Every effort should be made to avoid patient distress; amnesia and analgesia should be adequately maintained throughout paralyzation.
    Monitor heart rate, blood pressure, and oxygen saturation during neuromuscular blockade. Continuously monitor temperature and expired carbon dioxide to aid in early recognition of malignant hyperthermia. Monitor ECG; peaked T-waves are an early sign of cardiac arrest secondary to rhabdomyolysis and hyperkalemia.
    Storage of unopened vials:
    Manufacturer recommendations: Store in refrigerator at 2—8 degrees C (36 to 46 degrees F) until vial expiration date. Multi-dose vials are stable for up to 14 days at room temperature without significant loss of potency.
    Independent stability studies: Independent studies have produced inconsistent results, but generally, the drug appears to be stable in unopened vials for 2 months or more at room temperature. Succinylcholine 20 mg/ml and 50 mg/ml products from various manufacturers have been shown to retain at least 90% potency when stored unopened at room temperature for time periods ranging from 2—8.3 months, depending on the specific product. The degradation rate appears to be faster for the 50 mg/ml than the 20 mg/ml concentration.  These results should not be extrapolated to environments with variable temperatures (e.g., emergency transport vehicles), where 10% degradation times have been reported to be shorter (1—3 months).
    Storage of undiluted succinylcholine chloride (20 mg/ml) in polypropylene syringes: Undiluted succinylcholine chloride (20 mg/ml) was stable for 45 days at room temperature (25 degrees C) and 90 days refrigerated (4 degrees C) in 12 ml polypropylene syringes.

    Intravenous Administration

    The incidence of bradycardia is higher with repeated doses of succinylcholine. Pretreatment with anticholinergic agents (e.g., atropine) may reduce the occurrence of bradyarrhythmias.
    Succinylcholine has an acidic pH of 3.5 and should not be mixed with alkaline solutions with a pH > 8.5 (e.g., barbiturate solutions).
    Due to the risk for rhabdomyolysis and life-threatening hyperkalemia that has occurred in pediatric patients with unidentified myopathies, succinylcholine should be limited to emergent situations when immediate securing of the airway is needed; therefore, intermittent IV infusions and continuous IV infusions are generally not recommended in pediatric patients.
     
    IV Push
    No dilution necessary. For small doses, may dilute to a concentration of 1—2 mg/ml in a compatible intravenous solution (e.g., 5% dextrose or 0.9% NaCl).
    Administer via IV push over 10—30 seconds. Monitor heart rate and blood pressure carefully during administration.
    Storage: Use diluted solution within 24 hours of preparation. Discard unused portion.
     
    Continuous IV Infusion
    This route is preferred for long surgical procedures due to possible tachyphylaxis and prolonged apnea associated with administration of repeated fractional doses.
    Dilute succinylcholine to a concentration of 1—2 mg/ml in a compatible intravenous solution (e.g., 5% dextrose or 0.9% NaCl).
    Infuse IV at a rate of 2.5 mg/minute (range = 0.5—10 mg/minute). Adjust rate based on patient response and requirements.
    Storage: Use diluted solution within 24 hours of preparation. Discard unused portion.

    Intramuscular Administration

    If necessary, succinylcholine may be administered intramuscularly to infants, older pediatric patients, or adults when intravenous access cannot be secured. Onset of intubating conditions occurs in 2—3 minutes.
    In patients with laryngospasm, relief of the spasm sufficient for effective bag-valve-mask ventilation should occur within 30 seconds of administration to allow for adequate ventilation until intubating conditions are achieved.
    Inject deeply into a large muscle mass (e.g., anterolateral thigh [preferred in children < 2 years] or deltoid). Aspirate prior to injection to avoid injection into a blood vessel. Some experts recommend administration into the deltoid because the time to onset is typically more rapid than with administration in to the quadriceps.

    STORAGE

    Anectine:
    - Discard product if it contains particulate matter, is cloudy, or discolored
    - May be stored at room temperature for up to 2 weeks
    - Store between 36 to 46 degrees F
    Quelicin:
    - Discard product if it contains particulate matter, is cloudy, or discolored
    - Product is stable for up to 14 days at 68 to 77 degrees F following multiple uses
    - Refrigerate (between 36 and 46 degrees F)

    CONTRAINDICATIONS / PRECAUTIONS

    General Information

    Succinylcholine has no effect on consciousness, pain threshold, or cerebration. To avoid distress to the patient, it should not be administered before unconsciousness has been induced.
     
    With prolonged administration of succinylcholine, the characteristic depolarization block (Phase I block) can change to a nondepolarizing block (Phase II block). Prolonged respiratory depression or apnea may be observed in patients experiencing this transition to Phase II block.

    Bradycardia, children, Guillain-Barre syndrome, hyperkalemia, infants, malignant hyperthermia, myopathy, neonates, rhabdomyolysis

    Safe and effective use of succinylcholine has been established in neonates, infants, children, and adolescents; however, there are rare reports of ventricular dysrhythmias and cardiac arrest secondary to acute rhabdomyolysis with hyperkalemia in apparently healthy pediatric patients who receive succinylcholine. Many of these pediatric patients were subsequently found to have undiagnosed skeletal muscle myopathy such as Duchenne's muscular dystrophy. The syndrome often presents as sudden cardiac arrest within minutes after the administration of succinylcholine. These pediatric patients are usually, but not exclusively, males, and most frequently 8 years of age or younger. There have also been reports in adolescents. There may be no signs or symptoms to alert the practitioner to which pediatric patients are at risk. A careful history and physical may identify developmental delays suggestive of a myopathy. A preoperative creatine kinase could identify some but not all pediatric patients at risk. Due to the abrupt onset of this syndrome, routine resuscitative measures are likely to be unsuccessful. Careful monitoring of the electrocardiogram may alert the practitioner to peaked T-waves (an early sign). Administration of intravenous calcium, bicarbonate, and glucose with insulin, with hyperventilation have resulted in successful resuscitation in some of the reported cases. Extraordinary and prolonged resuscitative efforts have been effective in some cases. Chronic abdominal infections, subarachnoid hemorrhage, tetanus, disuse atrophy, Guillain-Barre syndrome, and degenerative nervous system disorders may also increase the risk for hyperkalemia. In addition, in the presence of signs of malignant hyperthermia, appropriate treatment should be initiated concurrently. Since it is difficult to identify which pediatric patients are at risk, it is recommended that the use of succinylcholine in pediatric patients should be reserved for emergency intubation or instances where immediate securing of the airway is necessary, e.g., laryngospasm, difficult airway, full stomach, or for intramuscular use when a suitable vein is inaccessible. The incidence and severity of bradycardia is higher in pediatric patients than adults; the incidence of bradycardia is higher following the second dose of succinylcholine. Pre-treatment with anticholinergic agents, e.g., atropine, may reduce the occurrence of bradyarrhythmias. For routine elective surgery, children and adolescents should receive non-depolarizing neuromuscular agents. Succinylcholine is contraindicated for patients with a personal or familial history of malignant hyperthermia, skeletal muscle myopathy, or hypersensitivity to the drug. Acute rhabdomyolysis can occur when used in individuals with a known skeletal muscle myopathy.

    Burns, digitalis toxicity, trauma

    Succinylcholine is contraindicated in patients after the acute phase of injury following a major burns, multiple trauma, extensive denervation of skeletal muscle, or upper motor neuron injury. Succinylcholine administration to such patients can cause severe hyperkalemia, which can result in cardiac arrest. The risk in these patients increases over time and usually peaks at 7 to 10 days after the injury. The precise time of onset and the duration of the risk period are not known. Additionally, succinylcholine should be administered with great caution in cases of quinidine therapy, digitalis therapy, digitalis toxicity, preexisting hyperkalemia, or other electrolyte imbalance. Such patients tend to become severely hyperkalemic after succinylcholine administration, and cardiac arrhythmias or cardiac arrest can occur.

    Glaucoma, ocular surgery, ocular trauma

    Succinylcholine increases intraocular pressure and should be used cautiously when increased intraocular pressure is undesirable such as in patients with narrow angle glaucoma, ocular surgery, or penetrating ocular trauma.

    Labor, obstetric delivery, pregnancy

    Succinylcholine is classified as FDA pregnancy risk category C. It should be given to a pregnant woman only if clearly needed. During pregnancy, reduced plasma cholinesterase activity may occur; a higher proportion of patients may experience prolonged apnea to succinylcholine when pregnant compared to nonpregnant females. Succinylcholine is used during labor and obstetric delivery by cesarean section. After a single dose of 1 mg/kg to the mother, small amounts of the drug do enter the fetal circulation but not in an amount that would endanger the fetus. However, the amount of drug that enters the fetal circulation is dependent on the concentration gradient between maternal and fetal circulations. Therefore, residual neuromuscular blockage (i.e., apnea and flaccidity) may occur in the neonate after repeated high doses or in the presence of atypical plasma cholinesterase in the mother.

    Breast-feeding

    According to the manufacturer, it is not known if succinylcholine is excreted in human breast milk. However, the drug is rapidly eliminated and has poor oral absorption, so it is not likely to reach the circulation or cause adverse effects in breast-fed infants. In a comparison study of the neonatal effects of epidural and general anesthesia for cesarean section, the regimen that included succinylcholine caused a delay in the time to the first breast-feeding but how succinylcholine contributed to this difference in outcome was not known by the authors. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally administered drug, healthcare providers are encouraged to report the adverse effect to the FDA.

    Anemia, cardiac disease, cholinesterase inhibitor toxicity, edema, hepatic disease, infection, malnutrition, myxedema, peptic ulcer disease, pseudocholinesterase deficiency, renal disease

    Succinylcholine should be used cautiously in cases of reduced plasma cholinesterase activity including genetic disorders of plasma pseudocholinesterase deficiency, anemia, dehydration, neurotoxic insecticide exposure, cholinesterase inhibitor toxicity, malnutrition, pregnancy, hepatic disease, renal disease, malignant tumor, infection, burns, decompensated cardiac disease, peptic ulcer disease, or myxedema. It is important to note that onset of neuromuscular blockade may be delayed in patients with cardiac disease or other conditions associated with poor circulation and edema. Subsequent doses should be administered with caution in any patient with a predisposition to delayed onset or prolonged duration of paralysis.

    Myasthenia gravis, neuromuscular disease, obesity

    Patients with conditions that impair neuromuscular function can experience prolonged or exaggerated neuromuscular blockade after receiving neuromuscular blocking agents. These conditions include myasthenia gravis, myasthenic syndrome (Eaton Lambert syndrome), myopathy, or any other neuromuscular disease. Because myasthenia gravis involves destruction of acetylcholine receptors instead of receptor upregulation, as seen in other neuromuscular diseases, these patients tend to be less sensitive to the effects of succinylcholine compared to nondepolarizing agents (e.g., rocuronium, vecuronium). In addition to neuromuscular disease, patients with weak muscle tone and those who suffer from severe obesity are at an increased risk for airway and ventilation complications. Use succinylcholine with caution in patients with these conditions, and continue to monitor patients carefully until recovery is fully complete.

    Requires a specialized care setting, requires an experienced clinician, respiratory insufficiency

    Administration of succinylcholine requires an experienced clinician familiar with the actions, characteristics, and hazards of neuromuscular blockade. Neuromuscular blocking agents cause respiratory insufficiency by paralyzing respiratory muscles; administration requires a specialized care setting. Succinylcholine should be used only when necessary equipment and personnel skilled in airway management are immediately available. Adequacy of respiration must be assured through assisted or controlled ventilation. Reversal agents should also be available.

    Neuromuscular blocking agent hypersensitivity

    Although rare, severe anaphylactic or anaphylactoid reactions to neuromuscular blockers, including succinylcholine, have been reported; some cases have been life-threatening and fatal. Precautions should be taken in patients who have experienced anaphylaxis from any neuromuscular blocking agent (i.e., neuromuscular blocking agent hypersensitivity), as cross-reactivity has been reported with this class. Immediate availability of appropriate emergency treatment for anaphylaxis is advised because of the potential for a life-threatening reaction.

    Asthma, chronic obstructive pulmonary disease (COPD), pulmonary disease, respiratory depression

    Use neuromuscular blocking agents (NMBAs), including succinylcholine, with caution in patients with asthma or other pulmonary conditions. NMBAs stimulate histamine release, which could exacerbate asthma. Histamine-mediated effects (e.g., flushing, hypotension, bronchoconstriction) are uncommon in normal clinical usage of succinylcholine, however any NMBA should be used with caution in those with any condition in which a release of histamine may be contraindicated. In addition, NMBAs cause respiratory muscle paralysis; residual muscle weakness and decreased respiratory function (respiratory depression) can persist even after drug discontinuation. Use NMBAs with caution in patients with pulmonary disease and conditions associated with low pulmonary function reserve, such as chronic obstructive pulmonary disease (COPD). Carefully monitor respiratory status and adequacy of ventilation after drug recovery until the patient is clearly stabilized.

    Acid/base imbalance, adrenal insufficiency, dehydration, electrolyte imbalance, hypercalcemia, hypermagnesemia, hypocalcemia, hypokalemia, hypothermia, metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis

    Various physiologic states can alter the expected effects of succinylcholine; carefully consider each patient's clinical condition when dosing succinylcholine and monitoring the patient. Cachectic and debilitated patients are more sensitive to neuromuscular blocking agents. Electrolyte imbalance can alter a patient's sensitivity to neuromuscular blocking agents (NMBAs). Hypercalcemia can decrease sensitivity to NMBAs, while most other electrolyte disturbances increase sensitivity (e.g., hypokalemia, hypocalcemia, hypermagnesemia). Use succinylcholine cautiously in patients with conditions that may lead to electrolyte imbalances, such as adrenal insufficiency. Severe acid/base imbalance may alter a patient's sensitivity to NMBAs: metabolic acidosis and respiratory acidosis may enhance neuromuscular blockade and prolong recovery time, while metabolic alkalosis and respiratory alkalosis can reduce the potency of the drug. Dehydration and hypothermia can also increase a patient's sensitivity to NMBAs.

    Increased intracranial pressure

    Succinylcholine may cause a transient increased intracranial pressure; adequate anesthetic induction prior to administration will minimize this effect. Additionally, intragastric pressure may increase with succinylcholine administration, possibly resulting in regurgitation and aspiration of stomach contents.

    Bone fractures

    Initial muscle fasciculations associated with succinylcholine administration can cause additional injury in patients with bone fractures or muscle spasms.

    ADVERSE REACTIONS

    Severe

    acute quadriplegic myopathy syndrome / Delayed / Incidence not known
    apnea / Delayed / Incidence not known
    muscle paralysis / Delayed / Incidence not known
    asystole / Rapid / Incidence not known
    rhabdomyolysis / Delayed / Incidence not known
    cardiac arrest / Early / Incidence not known
    hyperkalemia / Delayed / Incidence not known
    bradycardia / Rapid / Incidence not known
    arrhythmia exacerbation / Early / Incidence not known
    renal tubular obstruction / Delayed / Incidence not known
    bronchospasm / Rapid / Incidence not known
    angioedema / Rapid / Incidence not known
    anaphylactoid reactions / Rapid / Incidence not known
    disseminated intravascular coagulation (DIC) / Delayed / Incidence not known
    malignant hyperthermia / Rapid / Incidence not known
    lactic acidosis / Delayed / Incidence not known
    increased intracranial pressure / Early / Incidence not known
    ocular hypertension / Delayed / Incidence not known
    thrombosis / Delayed / Incidence not known
    keratitis / Delayed / Incidence not known

    Moderate

    hypoxia / Early / Incidence not known
    myopathy / Delayed / Incidence not known
    dyspnea / Early / Incidence not known
    respiratory depression / Rapid / Incidence not known
    hypotension / Rapid / Incidence not known
    premature ventricular contractions (PVCs) / Early / Incidence not known
    sinus tachycardia / Rapid / Incidence not known
    hypertension / Early / Incidence not known
    edema / Delayed / Incidence not known
    wheezing / Rapid / Incidence not known
    skin ulcer / Delayed / Incidence not known
    conjunctivitis / Delayed / Incidence not known
    skin erosion / Delayed / Incidence not known
    tolerance / Delayed / Incidence not known

    Mild

    anxiety / Delayed / Incidence not known
    weakness / Early / Incidence not known
    myalgia / Early / Incidence not known
    premature atrial contractions (PACs) / Early / Incidence not known
    urticaria / Rapid / Incidence not known
    rash (unspecified) / Early / Incidence not known
    hypersalivation / Early / Incidence not known
    pruritus / Rapid / Incidence not known
    flushing / Rapid / Incidence not known
    fever / Early / Incidence not known
    xerophthalmia / Early / Incidence not known

    DRUG INTERACTIONS

    Acetaminophen; Butalbital; Caffeine; Codeine: (Moderate) Concomitant use of codeine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Acetaminophen; Caffeine; Dihydrocodeine: (Moderate) Additive CNS depression may occur if dihydrocodeine is used concomitantly with other CNS depressants, including neuromuscular blockers.
    Acetaminophen; Codeine: (Moderate) Concomitant use of codeine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Acetaminophen; Hydrocodone: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Acetaminophen; Oxycodone: (Moderate) Concomitant use of oxycodone with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Acetaminophen; Propoxyphene: (Moderate) Concomitant use of propoxyphene with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Acetazolamide: (Moderate) Nondepolarizing neuromuscular blockers when combined with carbonic anhydrase inhibitors may lead to prolonged respiratory depression. This action is due to enhanced neural blockade as a result of potential hypokalemia from the carbonic anhydrase inhibitor. Serum potassium concentrations should be checked and adjusted prior to the administration of nondepolarizing neuromuscular blockers.
    Alfentanil: (Moderate) Concomitant use of alfentanil with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Aliskiren; Amlodipine: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Aliskiren; Amlodipine; Hydrochlorothiazide, HCTZ: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Ambenonium Chloride: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    Amide local anesthetics: (Moderate) Local anesthetics can prolong and enhance the effects of neuromuscular blockers. Monitoring of neuromuscular function is recommended.
    Aminoglycosides: (Moderate) Aminoglycosides traditionally have been associated with neuromuscular blockade, but this event is most likely to occur when aminoglycoside solutions are used to irrigate wounds intraoperatively. Neuromuscular blockers should be used cautiously in patients receiving aminoglycosides.
    Amlodipine: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Amlodipine; Atorvastatin: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Amlodipine; Benazepril: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Amlodipine; Hydrochlorothiazide, HCTZ; Olmesartan: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Amlodipine; Hydrochlorothiazide, HCTZ; Valsartan: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Amlodipine; Olmesartan: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Amlodipine; Telmisartan: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Amlodipine; Valsartan: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Amphotericin B cholesteryl sulfate complex (ABCD): (Moderate) Amphoterecin B may cause hypokalemia, which potentiates neuromuscular blockade with nondepolarizing neuromuscular blockers.
    Amphotericin B lipid complex (ABLC): (Moderate) Amphoterecin B may cause hypokalemia, which potentiates neuromuscular blockade with nondepolarizing neuromuscular blockers.
    Amphotericin B liposomal (LAmB): (Moderate) Amphoterecin B may cause hypokalemia, which potentiates neuromuscular blockade with nondepolarizing neuromuscular blockers.
    Amphotericin B: (Moderate) Amphoterecin B may cause hypokalemia, which potentiates neuromuscular blockade with nondepolarizing neuromuscular blockers.
    Apomorphine: (Moderate) Apomorphine causes significant somnolence. Concomitant administration of apomorphine and CNS depressants could result in additive depressant effects.
    Aspirin, ASA; Butalbital; Caffeine; Codeine: (Moderate) Concomitant use of codeine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Aspirin, ASA; Caffeine; Dihydrocodeine: (Moderate) Additive CNS depression may occur if dihydrocodeine is used concomitantly with other CNS depressants, including neuromuscular blockers.
    Aspirin, ASA; Carisoprodol; Codeine: (Moderate) Concomitant use of codeine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Aspirin, ASA; Oxycodone: (Moderate) Concomitant use of oxycodone with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Atropine; Difenoxin: (Moderate) Concurrent administration of diphenoxylate/difenoxin with neuromuscular blockers can potentiate the CNS-depressant effects of diphenoxylate/difenoxin. Use caution during coadministration.
    Atropine; Diphenoxylate: (Moderate) Concurrent administration of diphenoxylate/difenoxin with neuromuscular blockers can potentiate the CNS-depressant effects of diphenoxylate/difenoxin. Use caution during coadministration.
    Atropine; Edrophonium: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    Bacitracin: (Moderate) Systemic bacitracin may act synergistcally to increase or prolong skeletal muscle relaxation produced by neuromuscular blocking agents and/or general anesthetics. Use of topically administrated preparations containing bacitracin, especially when applied to large surface areas, may have additive nephrotoxic potential.
    Belladonna; Opium: (Moderate) Additive CNS depression may occur if opiate agonists are used concomitantly with other CNS depressants, including neuromuscular blockers.
    Benzodiazepines: (Moderate) Concurrent use of benzodiazepines and other CNS active medications including neuromuscular blockers, can potentiate the CNS effects of either agent. Lower doses of one or both agents may be required. The severity of this interaction may be increased when additional CNS depressants are given.
    Benzonatate: (Moderate) Benzonatate may enhance the neuromuscular blocking action of nondepolarizing agents.
    Beta-blockers: (Moderate) Beta-blockers can enhance the neuromuscular blocking activity of succinylcholine.
    Bismuth Subcitrate Potassium; Metronidazole; Tetracycline: (Moderate) Tetracyclines may potentiate the neuromuscular effects of nondepolarizing neuromuscular blockers.
    Bismuth Subsalicylate; Metronidazole; Tetracycline: (Moderate) Tetracyclines may potentiate the neuromuscular effects of nondepolarizing neuromuscular blockers.
    Botulinum Toxins: (Major) The effects of botulinum toxins can be potentiated by neuromuscular blockers, or other drugs that interfere with neuromuscular transmission. Monitor for symptoms of unintended or prolonged neuromuscular blockade, including respiratory rate and muscle movements.
    Brompheniramine; Guaifenesin; Hydrocodone: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Brompheniramine; Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Calcium Carbonate: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Calcium Carbonate; Magnesium Hydroxide: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Calcium Carbonate; Risedronate: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Calcium Salts: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Calcium: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Calcium; Vitamin D: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Capreomycin: (Moderate) Partial neuromuscular blockade has been reported with capreomycin after the administration of large intravenous doses or rapid intravenous infusion. Depolarizing neuromuscular blockers and non-depolarizing neuromuscular blockers could potentiate the neuromuscular blocking effect of capreomycin. If these drugs are used in combination, monitor patients for increased adverse effects.
    Carbamazepine: (Moderate) If neuromuscular blockers are administered to patients chronically receiving anticonvulsant agents such as carbamazepine, shorter durations of neuromuscular block may occur and infusion rates may be higher due to the development of resistance to muscle relaxants.
    Carbinoxamine; Hydrocodone; Phenylephrine: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Carbinoxamine; Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Carbonic anhydrase inhibitors: (Moderate) Nondepolarizing neuromuscular blockers when combined with carbonic anhydrase inhibitors may lead to prolonged respiratory depression. This action is due to enhanced neural blockade as a result of potential hypokalemia from the carbonic anhydrase inhibitor. Serum potassium concentrations should be checked and adjusted prior to the administration of nondepolarizing neuromuscular blockers.
    Cardiac glycosides: (Major) Concomitant use of digoxin with succinylcholine can cause arrhythmias because succinylcholine causes extrusion of potassium from the muscle cells.
    Chloroquine: (Moderate) Chloroquine may affect presynaptic and postsynaptic myoneural function and potentiate the neuromuscular blocking action of neuromuscular blockers.
    Chlorpheniramine; Codeine: (Moderate) Concomitant use of codeine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Chlorpheniramine; Dihydrocodeine; Phenylephrine: (Moderate) Additive CNS depression may occur if dihydrocodeine is used concomitantly with other CNS depressants, including neuromuscular blockers.
    Chlorpheniramine; Dihydrocodeine; Pseudoephedrine: (Moderate) Additive CNS depression may occur if dihydrocodeine is used concomitantly with other CNS depressants, including neuromuscular blockers.
    Chlorpheniramine; Guaifenesin; Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Chlorpheniramine; Hydrocodone: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Chlorpheniramine; Hydrocodone; Phenylephrine: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Chlorpheniramine; Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Cholinesterase inhibitors: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    Chromium: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Cisplatin: (Moderate) Hypokalemia potentiates the neuromuscular blockade from nondepolarizing neuromuscular blockers. Drugs such as cisplatin are associated with a significant risk of hypokalemia and should be monitored closely when used with neuromuscular blockers.
    Clozapine: (Moderate) Skeletal muscle relaxants should be combined cautiously with clozapine because they could cause additive depressant effects and possible respiratory depression or hypotension.
    Codeine: (Moderate) Concomitant use of codeine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Codeine; Guaifenesin: (Moderate) Concomitant use of codeine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Codeine; Phenylephrine; Promethazine: (Moderate) Because promethazine causes pronounced sedation, an enhanced CNS depressant effect or additive drowsiness may occur when it is combined with other CNS depressants. (Moderate) Concomitant use of codeine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Codeine; Promethazine: (Moderate) Because promethazine causes pronounced sedation, an enhanced CNS depressant effect or additive drowsiness may occur when it is combined with other CNS depressants. (Moderate) Concomitant use of codeine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Colistimethate, Colistin, Polymyxin E: (Moderate) Depolarizing neuromuscular blockers and non-depolarizing neuromuscular blockers can potentiate the neuromuscular blocking effect of colistimethate sodium. If these drugs are used in combination, monitor patients for increased adverse effects. Neuromuscular blockade may be associated with colistimethate sodium, and is more likely to occur in patients with renal dysfunction.
    Collagenase: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Corticosteroids: (Moderate) Caution and close monitoring are advised if corticosteroids and neuromuscular blockers are used together, particularly for long periods, due to enhanced neuromuscular blocking effects. In such patients, a peripheral nerve stimulator may be of value in monitoring the response. Concurrent use may increase the risk of acute myopathy. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
    Cyanocobalamin, Vitamin B12: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Cyclophosphamide: (Major) Cyclophosphamide treatment, which causes a marked and persistent inhibition of cholinesterase activity, potentiates the effect of depolarizing neuromuscular blockers, such as succinylcholine, and may cause prolonged apnea. If a patient has been treated with cyclophosphamide within 10 days of general anesthesia, the anesthesiologist should be alerted.
    Cyclosporine: (Moderate) Cyclosporine may potentiate the action of nondepolarizing neuromuscular blockers. Prolonged neuromuscular blockade has been reported in patients receiving cyclosporine who receive neuromuscular blockers as part of surgical anesthesia. Monitor patients for recurrent neuromuscular blockade and respiratory depression; extended ventilatory support may be required.
    Demeclocycline: (Moderate) Tetracyclines may potentiate the neuromuscular effects of nondepolarizing neuromuscular blockers.
    Dexpanthenol: (Minor) The effects of succinylcholine may be prolonged with dexpanthenol administration. It is recommended to separate doses of dexpanthenol and succinylcholine by at least 1 hour to decrease the potential for this effect.
    Dextromethorphan; Promethazine: (Moderate) Because promethazine causes pronounced sedation, an enhanced CNS depressant effect or additive drowsiness may occur when it is combined with other CNS depressants.
    Dextromethorphan; Quinidine: (Major) Quinidine can potentiate the effects of neuromuscular blockers. Neostigmine will not reverse these effects. Respiratory support may be necessary if quinidine is given concomitantly or shortly after a neuromuscular blocking agent.
    Digitoxin: (Major) Concomitant use of digoxin with succinylcholine can cause arrhythmias because succinylcholine causes extrusion of potassium from the muscle cells.
    Digoxin: (Major) Concomitant use of digoxin with succinylcholine can cause arrhythmias because succinylcholine causes extrusion of potassium from the muscle cells.
    Dihydrocodeine; Guaifenesin; Pseudoephedrine: (Moderate) Additive CNS depression may occur if dihydrocodeine is used concomitantly with other CNS depressants, including neuromuscular blockers.
    Diltiazem: (Moderate) Prolongation of the effects of neuromuscular blockers is possible when they are given in combination with calcium-channel blockers, particularly diltiazem.
    Diphenhydramine; Hydrocodone; Phenylephrine: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Donepezil: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    Donepezil; Memantine: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    Doxycycline: (Moderate) Tetracyclines may potentiate the neuromuscular effects of nondepolarizing neuromuscular blockers.
    Edrophonium: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    Enalapril; Felodipine: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Ester local anesthetics: (Moderate) Local anesthetics can prolong and enhance the effects of neuromuscular blockers. Local anesthetics interfere with the release of acetylcholine and thus, can produce neuromuscular blockade. Potentiation of neuromuscular blockade by a local anesthetic can occur with either depolarizing or nondepolarizing neuromuscular blockers. Monitoring of neuromuscular function is recommended.
    Estrogens: (Minor) Estrogens have been associated in rare cases with pseudocholinesterase deficiency. Since non-depolarizing neuromuscular blockers are metabolized by cholinesterase, prolonged neuromuscular blockade may occur in individuals on concurrent therapy with estrogens.
    Felodipine: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Fentanyl: (Major) Although adequate sedation and analgesia must accompany the use of neuromscular blockers, coadministration of opioids such as fentanyl may enhance neuromuscular blockade and produce an increased degree of respiratory depresssion. Monitor patients for signs of respiratory depression that may be greater than otherwise expected. A dose reduction of one or both drugs may be warranted.
    Fosphenytoin: (Moderate) Chronic antiepileptic drug therapy with phenytoin may antagonize the effects of nondepolarizing neuromuscular blockers. This interaction lengthens the onset and shortens the duration of neuromuscular blockade. The exact mechanism for this interaction is unknown, but could involve neuromuscular and hepatic enzyme induction effects of phenytoin.
    Galantamine: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    General anesthetics: (Major) Increased neuromuscular blockade may occur if general anesthetics are used with nondepolarizing neuromuscular blockers.
    Guaifenesin; Hydrocodone: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Guaifenesin; Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Hetastarch; Dextrose; Electrolytes: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Homatropine; Hydrocodone: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Hydrocodone: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Hydrocodone; Ibuprofen: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Hydrocodone; Phenylephrine: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Hydrocodone; Potassium Guaiacolsulfonate: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Hydrocodone; Potassium Guaiacolsulfonate; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with other CNS depressants, such as neuromuscular blockers, can potentiate CNS and respiratory depression. A dose reduction of one or both drugs may be warranted.
    Hydromorphone: (Moderate) Concomitant use of hydromorphone with other central nervous system (CNS) depressants, such as skeletal muscle relaxants, can potentiate the effects of hydromorphone and may lead to additive CNS or respiratory depression, profound sedation, or coma. Furthermore, opioid analgesics such as hydromorphone may enhance the action of neuromuscular blockers and produce an excessive degree of respiratory depression. Careful monitoring of a patient's respiratory rate and oxygenation is imperative. Prior to concurrent use of hydromorphone in patients taking a CNS depressant, assess the level of tolerance to CNS depression that has developed, the duration of use, and the patient's overall response to treatment. Consider the patient's use of alcohol or illicit drugs. If hydromorphone is used concurrently with a CNS depressant, a reduced dosage of hydromorphone and/or the CNS depressant is recommended. Carefully monitor the patient for hypotension, CNS depression, and respiratory depression. Carbon dioxide retention from opioid-induced respiratory depression can exacerbate the sedating effects of opioids.
    Ibuprofen; Oxycodone: (Moderate) Concomitant use of oxycodone with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Indapamide: (Moderate) Concomitant administration of indapamide to patients receiving nondepolarizing neuromuscular blockers can cause prolonged neuromuscular blockade due to indapamide-induced hypokalemia. Serum potassium concentrations should be determined and adjusted prior to initiation of neuromuscular blockade therapy.
    Irinotecan: (Moderate) Irinotecan has anticholinesterase activity, which may antagonize the neuromuscular blockade of non-depolarizing drugs such as atracurium. Although an interaction has not been proven, use caution if these drugs are used concomitantly.
    Isocarboxazid: (Major) Limited data suggest that the neuromuscular blocking effect of succinylcholine may be enhanced by drugs that reduce plasma pseudocholinesterase, such as monoamine oxidase inhibitors (MAOIs). These drugs should be used together with caution.
    Isradipine: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Ketorolac: (Moderate) Ketorolac may enhance the muscle-relaxant effect of nondepolarizing neuromuscular blockers. Caution should be exercised during concomitant administration of ketorolac with these agents.
    Levomethadyl: (Moderate) Concomitant use of levomethadyl with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Levorphanol: (Moderate) Additive CNS depression may occur if opiate agonists are used concomitantly with other CNS depressants, including neuromuscular blockers.
    Lincosamides: (Moderate) Lincosamides can potentiate the action of neuromuscular blockers, leading to skeletal muscle weakness, respiratory depression, or paralysis. Concurrent use during surgery or during the postoperative period requires close monitoring.
    Lithium: (Moderate) Lithium may potentiate the effects of nondepolarizing neuromuscular blockers. Monitor for prolonged paralysis or toxicity.
    Loop diuretics: (Moderate) Furosemide-induced hypokalemia can potentiate neuromuscular blockade with nondepolarizing neuromuscular blockers. In addition, furosemide may antagonize the skeletal muscle relaxing effect of tubocurarine and can potentiate neuromuscular blockade following succinylcholine administration.
    Magnesium: (Moderate) Parenteral magnesium salts can enhance the neuromuscular blocking effects of neuromuscular blockers. Caution should be exercised when using these agents concurrently.
    Mepenzolate: (Moderate) CNS depression can be increased when mepenzolate is combined with other CNS depressants such as neuromuscular blockers.
    Meperidine: (Moderate) Concomitant use of meperidine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Meperidine; Promethazine: (Moderate) Because promethazine causes pronounced sedation, an enhanced CNS depressant effect or additive drowsiness may occur when it is combined with other CNS depressants. (Moderate) Concomitant use of meperidine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Methadone: (Moderate) Concomitant use of methadone with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of methadone on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Methazolamide: (Moderate) Nondepolarizing neuromuscular blockers when combined with carbonic anhydrase inhibitors may lead to prolonged respiratory depression. This action is due to enhanced neural blockade as a result of potential hypokalemia from the carbonic anhydrase inhibitor. Serum potassium concentrations should be checked and adjusted prior to the administration of nondepolarizing neuromuscular blockers.
    Methohexital: (Moderate) Methohexital may enhance the neuromuscular activity of neuromuscular blocking agents, prolonging neuromuscular blockade.
    Metoclopramide: (Moderate) Metoclopramide has been implicated in prolonging neuromuscular blockade from succinylcholine. Patients receiving metoclopramide and succinylcholine should be monitored for this effect. Succinylcholine doses may need to be reduced.
    Minocycline: (Moderate) Tetracyclines, such as minocycline, may potentiate the neuromuscular effects of nondepolarizing neuromuscular blockers. Additionally, injectable minocycline contains magnesium sulfate heptahydrate, which can also enhance the neuromuscular blocking effects of neuromuscular blockers. Caution should be exercised when using these agents concurrently.
    Monoamine oxidase inhibitors: (Major) Limited data suggest that the neuromuscular blocking effect of succinylcholine may be enhanced by drugs that reduce plasma pseudocholinesterase, such as monoamine oxidase inhibitors (MAOIs). These drugs should be used together with caution.
    Morphine: (Moderate) Concomitant use of morphine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of morphine on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Morphine; Naltrexone: (Moderate) Concomitant use of morphine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of morphine on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Nabilone: (Moderate) Concomitant use of nabilone with other CNS depressants like neuromuscular blockers can potentiate the effects of nabilone on respiratory depression.
    Nalbuphine: (Minor) Concomitant use of nalbuphine with other CNS depressants like neuromuscular blockers can potentiate the effects of nalbuphine on respiratory depression, CNS depression, and sedation.
    Neostigmine: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    Nicardipine: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Nimodipine: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Nisoldipine: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Oxycodone: (Moderate) Concomitant use of oxycodone with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Oxymorphone: (Moderate) Additive CNS depression may occur if opiate agonists are used concomitantly with other CNS depressants, including neuromuscular blockers.
    Pantothenic Acid, Vitamin B5: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Perindopril; Amlodipine: (Minor) Calcium-channel blockers may prolong neuromuscular blockade.
    Phenelzine: (Major) Limited data suggest that the neuromuscular blocking effect of succinylcholine may be enhanced by drugs that reduce plasma pseudocholinesterase, such as monoamine oxidase inhibitors (MAOIs). These drugs should be used together with caution.
    Phenylephrine; Promethazine: (Moderate) Because promethazine causes pronounced sedation, an enhanced CNS depressant effect or additive drowsiness may occur when it is combined with other CNS depressants.
    Phenytoin: (Moderate) Chronic antiepileptic drug therapy with phenytoin may antagonize the effects of nondepolarizing neuromuscular blockers. This interaction lengthens the onset and shortens the duration of neuromuscular blockade. The exact mechanism for this interaction is unknown, but could involve neuromuscular and hepatic enzyme induction effects of phenytoin.
    Physostigmine: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    Polymyxin B: (Moderate) Systemic Polymyxin B can increase the neuromuscular blockade effects of neuromuscular blockers. Polymyxin B affects both pre- and post-synaptic myoneural areas by inhibiting release of acetylcholine pre-synaptically and/or blocking acetylcholine activity post-synaptically. Thus, polymyxin B acts synergistically with these agents, increasing or prolonging the skeletal muscle relaxation of neuromuscular blockers. If polymyxin B is used postoperatively, neuromuscular blockade may recur and may cause respiratory paralysis. Concomitant use should be avoided if possible.
    Polymyxins: (Moderate) Depolarizing neuromuscular blockers and non-depolarizing neuromuscular blockers can potentiate the neuromuscular blocking effect of colistimethate sodium. If these drugs are used in combination, monitor patients for increased adverse effects. Neuromuscular blockade may be associated with colistimethate sodium, and is more likely to occur in patients with renal dysfunction.
    Procainamide: (Moderate) Patients taking procainamide who require depolarizing neuromuscular blocking agents may require less than usual doses, due to procainamide effects of reducing acetylcholine release. In addition, procainamide appears to potentiate or prolong the effects of nondepolarizing neuromuscular blockers. Patients receiving procainamide following surgery should be monitored for potential prolongation of neuromuscular blockade.
    Promethazine: (Moderate) Because promethazine causes pronounced sedation, an enhanced CNS depressant effect or additive drowsiness may occur when it is combined with other CNS depressants.
    Propoxyphene: (Moderate) Concomitant use of propoxyphene with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Pyridostigmine: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    Pyridoxine, Vitamin B6: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Quinidine: (Major) Quinidine can potentiate the effects of neuromuscular blockers. Neostigmine will not reverse these effects. Respiratory support may be necessary if quinidine is given concomitantly or shortly after a neuromuscular blocking agent.
    Quinine: (Moderate) Quinine can potentiate the pharmacologic effects of neuromuscular blockers.
    Remifentanil: (Moderate) Concomitant use of remifentanil with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of alfentanil on respiration, alertness, and blood pressure. A dose reduction of one or both drugs may be warranted.
    Rivastigmine: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    Sedating H1-blockers: (Moderate) An enhanced CNS depressant effect may occur when sedating H1-blockers are combined with other CNS depressants including neuromuscular blockers.
    Selegiline: (Major) Limited data suggest that the neuromuscular blocking effect of succinylcholine may be enhanced by drugs that reduce plasma pseudocholinesterase, such as monoamine oxidase inhibitors (MAOIs). These drugs should be used together with caution.
    Skeletal Muscle Relaxants: (Moderate) Concomitant use of skeletal muscle relaxants with other CNS depressants can result in additive CNS depression. Also, dantrolene may potentiate neuromuscular block.
    Sufentanil: (Major) High doses of neuromuscular blockers may produce increases in heart rate during sufentanil-oxygen anesthesia. Bradycardia and hypotension has also been reported with concomitant use of neuromuscular blockers during sufentanil-oxygen anesthesia; this effect may be more pronounced in the presence of beta-blockers and/or calcium-channel blockers. Additive CNS depression will also be noted with concurrent use and the doses of sufentanil and the neuromuscular blocker should be adjusted accordingly.
    Tacrine: (Major) Cholinesterase inhibitors may be used to reverse the actions of nondepolarizing neuromuscular blockers; however, cholinesterase inhibitors may also prolong the neuromuscular blocking effects if given with depolarizing neuromuscular blockers, as these drugs are metabolized by acetylcholinesterase. In addition, neuromuscular blocking agents can antagonize the effects of the cholinesterase inhibitors; temporary dosage adjustment following surgery may be necessary.
    Tapentadol: (Moderate) Additive CNS depressive effects are expected if tapentadol is used in conjunction with other CNS depressants including neuromuscular blockers. When such combined therapy is contemplated, a dose reduction of one or both agents should be considered.
    Tetracycline: (Moderate) Tetracyclines may potentiate the neuromuscular effects of nondepolarizing neuromuscular blockers.
    Thalidomide: (Moderate) Thalidomide and other agents that slow cardiac conduction such as neuromuscular blockers should be used cautiously due to the potential for additive bradycardia.
    Thiazide diuretics: (Moderate) Concomitant administration of hydrochlorothiazide to patients receiving nondepolarizing neuromuscular blockers (e.g., tubocurarine) can cause prolonged neuromuscular blockade due to hydrochlorothiazide-induced hypokalemia. Serum potassium concentrations should be determined and corrected (if necessary) prior to initiation of neuromuscular blockade therapy.
    Thiopental: (Moderate) Thiopental may enhance the neuromuscular activity of neuromuscular blocking agents, prolonging neuromuscular blockade.
    Trandolapril; Verapamil: (Moderate) Prolongation of the effects of neuromuscular blockers is possible when they are given in combination with calcium-channel blockers, particularly verapamil and diltiazem. It may be necessary to decrease the dosage of verapamil when it is administered to patients receiving non-depolarizing or polarizing neuromuscular blockers.
    Tranylcypromine: (Major) Limited data suggest that the neuromuscular blocking effect of succinylcholine may be enhanced by drugs that reduce plasma pseudocholinesterase, such as monoamine oxidase inhibitors (MAOIs). These drugs should be used together with caution.
    Vancomycin: (Moderate) Vancomycin may potentiate the neuromuscular effects of neuromuscular blockers.
    Verapamil: (Moderate) Prolongation of the effects of neuromuscular blockers is possible when they are given in combination with calcium-channel blockers, particularly verapamil and diltiazem. It may be necessary to decrease the dosage of verapamil when it is administered to patients receiving non-depolarizing or polarizing neuromuscular blockers.
    Zinc Salts: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.

    PREGNANCY AND LACTATION

    Pregnancy

    According to the manufacturer, it is not known if succinylcholine is excreted in human breast milk. However, the drug is rapidly eliminated and has poor oral absorption, so it is not likely to reach the circulation or cause adverse effects in breast-fed infants. In a comparison study of the neonatal effects of epidural and general anesthesia for cesarean section, the regimen that included succinylcholine caused a delay in the time to the first breast-feeding but how succinylcholine contributed to this difference in outcome was not known by the authors. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally administered drug, healthcare providers are encouraged to report the adverse effect to the FDA.

    MECHANISM OF ACTION

    Mechanism of Action: Succinylcholine (suxamethonium) is a depolarizing skeletal muscle relaxant. It competes with acetylcholine for the cholinergic receptors of the motor endplate, and, like acetylcholine, it combines with these receptors to produce depolarization. Succinylcholine, however, causes a more prolonged depolarization than acetylcholine because it has a high affinity for the cholinergic receptor and a strong resistance to acetylcholinesterase. Depolarization results in fasciculation of the skeletal muscles followed by muscle paralysis. Neuromuscular transmission is inhibited as long as an adequate concentration of succinylcholine remains at the receptor site.The paralysis following succinylcholine administration is selective. Initially, paralysis involves the levator muscles of the face and muscles of the glottis. Paralysis consecutively involves the intercostals, the diaphragm, and all other skeletal muscles. Recovery of muscles generally occurs in the reverse order.

    PHARMACOKINETICS

    Succinylcholine is administered intravenously or intramuscularly.  Succinylcholine does not readily cross the placenta because it is highly ionized and has low fat solubility. Up to 10% of a succinylcholine dose is excreted unchanged in the urine. The remainder of a dose is rapidly hydrolyzed by plasma pseudocholinesterase to succinlymonocholine and choline. Succinylmonocholine possesses nondepolarizing muscle-relaxant properties. Succinylmonocholine is excreted partly in urine; the remainder is broken down by alkaline hydrolysis to the inactive metabolites succinate and choline. Hydrolysis of succinylmonocholine occurs relatively slowly, so succinylmonocholine can accumulate and cause prolonged apnea, especially in patients with impaired renal function.

    Intravenous Route

    Succinylcholine is poorly absorbed from the gastrointestinal tract, but when administered intravenously, it has a rapid onset and a short duration of action. Following IV administration of 10—30 mg to healthy adults, complete muscle relaxation occurs in 0.5—1 minute. This effect persists for 2—3 minutes and gradually dissipates within 10 minutes. Patients with low pseudocholinesterase concentrations may experience longer durations of action.
     
    After IV administration, succinylcholine is distributed in the extracellular fluid and rapidly reaches its site of action at the motor endplate of the myoneural junction. Following an intravenous bolus dose of 1 or 2 mg/kg, succinylcholine serum concentrations are below the detection limit (<2 ug/mL) after 2.5 minutes.

    Intramuscular Route

    After IM injection of succinylcholine, muscle relaxation occurs in 2—3 minutes and persists for 10—30 minutes. Patients with low pseudocholinesterase concentrations may experience longer durations of action.