PDR MEMBER LOGIN:
  • PDR Search

    Required field
  • Advertisement
  • CLASSES

    Muscle Relaxants, Peripherally Acting

    BOXED WARNING

    Burns, digitalis toxicity, Guillain-Barre syndrome, hyperkalemia, trauma

    Succinylcholine is contraindicated in patients after the acute phase of injury after 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. Risk for hyperkalemia in such patients increases over time and usually peaks 7 to 10 days after the injury; however, the precise onset and duration of the risk period are unknown. Risk is dependent on extent and location of injury. Additionally, succinylcholine should be administered with great caution in patients with electrolyte imbalances and those who take digoxin and may have digitalis toxicity, as succinylcholine-induced hyperkalemia may cause serious cardiac arrhythmias and cardiac arrest. Succinylcholine should not be used in any patient with a serum potassium more than 5.5 mEq/L. Chronic abdominal infections, subarachnoid hemorrhage, tetanus, disuse atrophy, Guillain-Barre syndrome, and degenerative nervous system disorders may also increase the risk for hyperkalemia.

    Bradycardia, children, infants, malignant hyperthermia, myopathy, neonates, rhabdomyolysis

    Succinylcholine is contraindicated in patients with a personal or familial history of malignant hyperthermia and/or skeletal muscle myopathy. Malignant hyperthermia may be precipitated by succinylcholine; concomitant use of volatile anesthetics may further increase the risk of developing this hypermetabolic state. Use succinylcholine with caution in neonates, infants, children, and adolescents; in general, the use of succinylcholine should be limited to very urgent clinical situations. There have been rare reports of ventricular dysrhythmias and fatal cardiac arrest secondary to rhabdomyolysis with hyperkalemia, primarily in healthy appearing pediatric patients who were subsequently found to have undiagnosed skeletal muscle myopathy, most frequently Duchenne's muscular dystrophy. Although some patients will have no identifiable risk factors, a careful history and physical exam may identify developmental delays suggestive of myopathy, and a preoperative creatinine kinase could identify some patients at risk. When succinylcholine is used in pediatric patients, closely monitor body temperature, expired CO2, heart rate, blood pressure, and electrocardiogram; careful monitoring may help detect early signs of malignant hyperthermia and/or hyperkalemia. The rhabdomyolysis syndrome often presents as peaked T-waves and sudden cardiac arrest within minutes after succinylcholine administration. Many affected patients are males and 8 years of age or younger; however, cases have also been reported in females and adolescents. Bradycardia, which may progress to asystole, has also been reported more commonly in infants and children, as well as in patients receiving repeated doses, intravenous administration (compared to intramuscular administration), or concurrent agents that have negative chronotropic effects (e.g., halothane, propofol, fentanyl). Pretreatment with anticholinergic agents (e.g., atropine) may reduce the occurrence of bradyarrhythmias. If cardiac arrest occurs immediately after the administration of succinylcholine, hyperkalemia should be suspected and managed accordingly (e.g., intravenous calcium, bicarbonate, glucose with insulin, hyperventilation). In the presence of signs of malignant hyperthermia, appropriate treatment (e.g., dantrolene, supportive care) should be initiated concurrently. Because it is difficult to identify which patients are at risk, it is recommended that succinylcholine use 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 lack of intravenous access); for routine elective surgery, pediatric patients should receive nondepolarizing neuromuscular agents.

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

    DOSAGE & INDICATIONS

    For neuromuscular blockade.
    NOTE: In pediatric patients, the use of succinylcholine should be limited to emergent intubations or when immediate securing of the airway is needed. In general, nondepolarizing neuromuscular blocking agents are preferred for routine elective surgery or prolonged paralysis.
    For neuromuscular blockade during short surgical procedures.
    Intravenous dosage
    Adults

    Average dose is 0.6 mg/kg IV (range 0.3 to 1.1 mg/kg) given over 10 to 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

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

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

    Solutions containing 0.1% to 0.2% succinylcholine in 5% Dextrose Injection or 0.9% Sodium Chloride Injection (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.

    Intermittent Intravenous Injection dosage
    Adults

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

    For muscular relaxation during non-emergent endotracheal intubation.
    NOTE: In pediatric patients, the use of succinylcholine should be limited to emergent intubations or when immediate securing of the airway is needed (e.g., laryngospasm, difficult airway, full stomach). In general, the use of a nondepolarizing neuromuscular blocking agent is preferred to avoid the rare risk of succinylcholine-induced acute rhabdomyolysis with hyperkalemia and asystole.
    Intravenous dosage
    Adults

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

    Infants, Children, and Adolescents 6 months to 17 years

    1 to 2 mg/kg IV. In general, younger patients require larger doses; some experts recommend 2 mg/kg IV for infants and toddlers, 1.5 mg/kg IV for older children, and 1 mg/kg IV for adolescents. Onset of intubating conditions usually occurs 30 to 60 seconds and persists 3 to 12 minutes after a single dose.

    Neonates and Infants younger than 6 months

    2 mg/kg IV; range 1 to 3 mg/kg/dose IV. May repeat 1 mg/kg/dose IV if intubating conditions are not attained within an adequate time period (1 to 5 minutes). Max: 4 mg/kg per intubation attempt. Onset of intubating conditions usually occurs 30 to 60 seconds and persists 3 to 12 minutes after a single dose.

    Intramuscular dosage
    Adults

    3 to 4 mg/kg IM (Max: 150 mg); this route should be used only if the IV route is not accessible. Onset of intubating conditions usually occurs in 5 to 6 minutes, but may be seen in 2 to 3 minutes.

    Infants, Children, and Adolescents

    3 to 4 mg/kg IM; doses up to 5 mg/kg IM may be necessary in infants younger than 6 months. Max: 150 mg/dose. This route should only be used if the IV route is not accessible. Onset of intubating conditions usually occurs 2 to 5 minutes and persists 10 to 30 minutes after a single dose.

    Neonates

    2 to 4 mg/kg IM; this route should only be used if the IV route is not accessible. Onset of intubating conditions usually occurs 2 to 5 minutes and persists 10 to 30 minutes after a single 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.

    For muscular relaxation during rapid-sequence intubation†.
    NOTE: In pediatric patients, the use of succinylcholine should be limited to emergent intubations or when immediate securing of the airway is needed. In general, the use of a nondepolarizing neuromuscular blocking agent is preferred to avoid the rare risk of succinylcholine-induced acute rhabdomyolysis with hyperkalemia and asystole. 
    Intravenous dosage
    Adults

    1.5 mg/kg IV. Onset of intubating conditions usually occurs within 30 to 60 seconds and persists 5 to 15 minutes after a single dose.

    Infants, Children, and Adolescents 6 months to 17 years

    1 to 2 mg/kg IV. In general, younger patients require larger doses; some experts recommend 2 mg/kg IV for infants and toddlers, 1.5 mg/kg IV for older children, and 1 mg/kg IV for adolescents. Onset of intubating conditions usually occurs within 30 to 60 seconds and persists 3 to 12 minutes after a single dose.

    Neonates and Infants younger than 6 months

    2 mg/kg/dose IV; range 1 to 3 mg/kg/dose IV. May repeat 1 mg/kg/dose IV if intubating conditions are not attained within an adequate time period (1 to 5 minutes). Max: 4 mg/kg per intubation attempt. Onset of intubating conditions usually occurs within 30 to 60 seconds and persists 3 to 12 minutes after a single dose.

    Intramuscular dosage
    Adults

    4 mg/kg IM (Max: 150 mg); use only if IV route not accessible. Onset of intubating conditions usually occurs within 5 to 6 minutes, but may be seen within 2 to 3 minutes.

    Infants, Children, and Adolescents

    3 to 4 mg/kg IM; doses up to 5 mg/kg IM may be necessary in infants younger than 6 months. Max: 150 mg/dose. This route should only be used if the IV route is not accessible. Onset of intubating conditions usually occurs within 2 to 5 minutes and persists 10 to 30 minutes after a single dose.

    Neonates

    2 to 4 mg/kg IM; this route should only be used if the IV route is not accessible. Onset of intubating conditions usually occurs within 2 to 5 minutes and persists 10 to 30 minutes after a single dose.

    †Indicates off-label use

    MAXIMUM DOSAGE

    Adults

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

    Geriatric

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

    Adolescents

    2 mg/kg/dose IV; 4 mg/kg/dose IM (Max: 150 mg/dose IM).

    Children

    2 mg/kg/dose IV; 4 mg/kg/dose IM (Max: 150 mg/dose IM).

    Infants

    6 to 11 months: 2 mg/kg/dose IV; 4 mg/kg/dose IM.
    1 to 5 months: 3 mg/kg/dose IV (Max: 4 mg/kg IV per intubation attempt); 5 mg/kg/dose IM.

    Neonates

    3 mg/kg/dose IV (Max: 4 mg/kg IV per intubation attempt); 4 mg/kg/dose IM.

    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.
    Accidental administration of neuromuscular blocking agents can be fatal. Store succinylcholine with the cap and ferrule intact, in a manner that minimizes the possibility of selecting the wrong product.
    Storage of unopened vials:
    Manufacturer recommendations: Store in refrigerator at 2 to 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 to 8.3 months, depending on the specific product. 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 to 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 more than 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 to 2 mg/mL in a compatible intravenous solution (5% Dextrose Injection or 0.9% Sodium Chloride Injection).
    Administer via IV push over 10 to 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 to 2 mg/mL in a compatible intravenous solution (e.g., 5% Dextrose Injection or 0.9% Sodium Chloride Injection).
    Infuse IV at a rate of 2.5 mg/minute (range = 0.5 to 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 to 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 younger than 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
    - See package insert for detailed storage information
    - Store between 36 to 46 degrees F
    Quelicin:
    - Discard product if it contains particulate matter, is cloudy, or discolored
    - See package insert for detailed storage information
    - Store between 36 to 46 degrees F

    CONTRAINDICATIONS / PRECAUTIONS

    General Information

    Succinylcholine does not cause sedation or analgesia and ideally 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. Doses of succinylcholine should be individualized. With prolonged administration of succinylcholine, the characteristic depolarization block (Phase I block) can change to a nondepolarizing block (Phase II block). Prolonged respiratory muscle paralysis or weakness may be observed in patients experiencing this transition to Phase II block. Anticholinesterase agents (e.g., neostigmine) will potentiate succinylcholine-induced Phase I block and, if Phase II block is suspected, diagnosis with a peripheral nerve stimulator should precede the administration of a reversal agent. In general, use of a peripheral nerve stimulator will permit the most advantageous use of a neuromuscular blocking agent, minimize the possibility of overdosage or underdosage, and assist in the evaluation of recovery.

    Burns, digitalis toxicity, Guillain-Barre syndrome, hyperkalemia, trauma

    Succinylcholine is contraindicated in patients after the acute phase of injury after 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. Risk for hyperkalemia in such patients increases over time and usually peaks 7 to 10 days after the injury; however, the precise onset and duration of the risk period are unknown. Risk is dependent on extent and location of injury. Additionally, succinylcholine should be administered with great caution in patients with electrolyte imbalances and those who take digoxin and may have digitalis toxicity, as succinylcholine-induced hyperkalemia may cause serious cardiac arrhythmias and cardiac arrest. Succinylcholine should not be used in any patient with a serum potassium more than 5.5 mEq/L. Chronic abdominal infections, subarachnoid hemorrhage, tetanus, disuse atrophy, Guillain-Barre syndrome, and degenerative nervous system disorders may also increase the risk for hyperkalemia.

    Bradycardia, children, infants, malignant hyperthermia, myopathy, neonates, rhabdomyolysis

    Succinylcholine is contraindicated in patients with a personal or familial history of malignant hyperthermia and/or skeletal muscle myopathy. Malignant hyperthermia may be precipitated by succinylcholine; concomitant use of volatile anesthetics may further increase the risk of developing this hypermetabolic state. Use succinylcholine with caution in neonates, infants, children, and adolescents; in general, the use of succinylcholine should be limited to very urgent clinical situations. There have been rare reports of ventricular dysrhythmias and fatal cardiac arrest secondary to rhabdomyolysis with hyperkalemia, primarily in healthy appearing pediatric patients who were subsequently found to have undiagnosed skeletal muscle myopathy, most frequently Duchenne's muscular dystrophy. Although some patients will have no identifiable risk factors, a careful history and physical exam may identify developmental delays suggestive of myopathy, and a preoperative creatinine kinase could identify some patients at risk. When succinylcholine is used in pediatric patients, closely monitor body temperature, expired CO2, heart rate, blood pressure, and electrocardiogram; careful monitoring may help detect early signs of malignant hyperthermia and/or hyperkalemia. The rhabdomyolysis syndrome often presents as peaked T-waves and sudden cardiac arrest within minutes after succinylcholine administration. Many affected patients are males and 8 years of age or younger; however, cases have also been reported in females and adolescents. Bradycardia, which may progress to asystole, has also been reported more commonly in infants and children, as well as in patients receiving repeated doses, intravenous administration (compared to intramuscular administration), or concurrent agents that have negative chronotropic effects (e.g., halothane, propofol, fentanyl). Pretreatment with anticholinergic agents (e.g., atropine) may reduce the occurrence of bradyarrhythmias. If cardiac arrest occurs immediately after the administration of succinylcholine, hyperkalemia should be suspected and managed accordingly (e.g., intravenous calcium, bicarbonate, glucose with insulin, hyperventilation). In the presence of signs of malignant hyperthermia, appropriate treatment (e.g., dantrolene, supportive care) should be initiated concurrently. Because it is difficult to identify which patients are at risk, it is recommended that succinylcholine use 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 lack of intravenous access); for routine elective surgery, pediatric patients should receive nondepolarizing neuromuscular agents.

    Glaucoma, ocular surgery, ocular trauma

    Succinylcholine increases intraocular pressure and should be used cautiously when increased intraocular pressure is undesirable, (e.g., narrow angle glaucoma, penetrating ocular trauma, ocular surgery).

    Labor, obstetric delivery, pregnancy

    Use succinylcholine during pregnancy only if clearly needed. Reduced plasma cholinesterase activity may occur in pregnancy; 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

    It is not known if succinylcholine is excreted in human breast milk. Because many drugs are excreted in human milk, use caution after administering succinylcholine to a breast-feeding woman. 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.

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

    Succinylcholine is metabolized by plasma cholinesterase and should be used with great caution in patients with reduced plasma cholinesterase activity because prolonged neuromuscular blockade may occur. Plasma cholinesterase activity may be diminished in pseudocholinesterase deficiency (e.g., patients heterozygous or homozygous for atypical plasma cholinesterase gene), anemia, dehydration, malnutrition, pregnancy, severe hepatic disease, severe renal disease, malignant tumors, infection, burns, decompensated cardiac disease, peptic ulcer disease, myxedema, or recent plasmapheresis therapy. In addition, irreversible inhibitors of plasma cholinesterase (e.g., organophosphate insecticides [cholinesterase inhibitor toxicity], cyclophosphamide) and chronic administration of certain drugs (e.g., oral contraceptives, glucocorticoids) may reduce plasma cholinesterase activity. 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.

    Accidental exposure, 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 (NMBAs) cause respiratory insufficiency by paralyzing respiratory muscles; administration requires a specialized care setting. Use succinylcholine only when necessary equipment and personnel skilled in airway management are immediately available. Adequacy of respiration must be assured through assisted or controlled ventilation. Accidental exposure to a NMBA in a patient for whom it is not intended can be fatal. Confirm proper medication selection and store NMBAs with the cap and ferrule intact, in a manner that minimizes the possibility of selecting the wrong product. Ensure that the intended dose is clearly labeled and communicated.

    Neuromuscular blocking agent hypersensitivity

    Succinylcholine is contraindicated in patients known to have a succinylcholine chloride hypersensitivity. Although rare, severe anaphylactic or anaphylactoid reactions to neuromuscular blockers, including succinylcholine, have been reported; some cases have been life-threatening and fatal. Succinylcholine should be used with caution in patients with a neuromuscular blocking agent hypersensitivity, as cross-reactivity has been reported with both depolarizing and nondepolarizing agents in this class. Immediate availability of appropriate emergency treatment for anaphylaxis is advised.

    Asthma, chronic lung disease (CLD), 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 neonatal chronic lung disease (CLD) or 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 alkalosis, metabolic acidosis, and respiratory acidosis may enhance neuromuscular blockade and/or prolong recovery time, while respiratory alkalosis reduces 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
    hyperkalemia / Delayed / Incidence not known
    rhabdomyolysis / Delayed / Incidence not known
    arrhythmia exacerbation / Early / Incidence not known
    cardiac arrest / Early / Incidence not known
    asystole / Rapid / Incidence not known
    bradycardia / Rapid / 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
    hypertension / Early / Incidence not known
    sinus tachycardia / Rapid / Incidence not known
    hypotension / Rapid / Incidence not known
    premature ventricular contractions (PVCs) / 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 / 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 Acetate: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    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 Chloride: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Calcium Citrate: (Moderate) Calcium salts may antagonize the effects of nondepolarizing neuromuscular blockers.
    Calcium Gluconate: (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.
    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: (Moderate) Although adequate sedation and analgesia must accompany the use of neuromuscular blockers, coadministration of opioids such as fentanyl, may enhance neuromuscular blockade and produce an increased degree of respiratory depression, hypotension, or sedation. Monitor patients for signs of respiratory depression or sedation that may be greater than otherwise expected. Use the lowest effective doses and minimum treatment durations needed to achieve the desired clinical effect.
    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 Liposomal: (Moderate) Monitor for altered clinical response to neuromuscular blockers if coadministration with irinotecan is necessary. Irinotecan has anticholinesterase activity, which may prolong the neuromuscular blocking effects of suxamethonium and antagonize the neuromuscular blockade of non-depolarizing drugs. According to the manufacturer of irinotecan, an interaction with neuromuscular blocking agents cannot be ruled out.
    Irinotecan: (Moderate) Monitor for altered clinical response to neuromuscular blockers if coadministration with irinotecan is necessary. Irinotecan has anticholinesterase activity, which may prolong the neuromuscular blocking effects of suxamethonium and antagonize the neuromuscular blockade of non-depolarizing drugs. According to the manufacturer of irinotecan, an interaction with neuromuscular blocking agents cannot be ruled out.
    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.
    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: (Moderate) High doses of neuromuscular blockers may produce increases in heart rate during sufentanil-oxygen anesthesia. Bradycardia and hypotension have 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.
    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.

    PREGNANCY AND LACTATION

    Pregnancy

    Use succinylcholine during pregnancy only if clearly needed. Reduced plasma cholinesterase activity may occur in pregnancy; 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.

    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.
     
    Affected cytochrome P450 isoenzymes: none

    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 to 30 mg to healthy adults, complete muscle relaxation occurs in 0.5 to 1 minute. This effect persists for 2 to 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 (less than 2 mcg/mL) after 2.5 minutes.

    Intramuscular Route

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