General Administration Information
For storage information, see the specific product information within the How Supplied section.
-Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.
-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.
-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.
-To avoid distress to the patient, administer succinylcholine after unconsciousness has been induced; in emergent life-threatening situations, it may be necessary to administer succinylcholine before unconsciousness. Adequate amnesia, sedation, and analgesia should accompany neuromuscular blockade.
-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 (both of which have been reported in pediatric patients who received succinylcholine).
-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. 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 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.
-Pretreatment with anticholinergic agents (e.g., atropine) may reduce the occurrence of bradyarrhythmias.
-Do not mix succinylcholine with alkaline solutions with a pH more than 8.5 (e.g., barbiturate solutions); succinylcholine has an acidic pH of 3.5.
-Due to the risk for rhabdomyolysis and life-threatening hyperkalemia that has occurred in pediatric patients with unidentified myopathies, reserve succinylcholine use for emergent situations when immediate securing of the airway is needed; intermittent IV infusions and continuous IV infusions are generally not recommended in pediatric patients.
-No dilution necessary. For small doses, may dilute 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).
-Administer via IV push over 10 to 30 seconds. Monitor heart rate and blood pressure.
-Storage: Use diluted solution within 24 hours of preparation. Discard unused portion.
-If necessary, succinylcholine may be administered intramuscularly to infants and older pediatric patients when intravenous access cannot be secured.-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 or deltoid ). Some experts recommend administration into the deltoid because the time to onset is typically more rapid than with administration into the quadriceps.
There have been rare reports of acute rhabdomyolysis with hyperkalemia followed by ventricular dysrhythmias, cardiac arrest, and death after the administration of succinylcholine to apparently healthy pediatric patients who were subsequently found to have undiagnosed skeletal muscle myopathy, most frequently Duchenne's muscular dystrophy. This syndrome often presents as peaked T-waves and sudden cardiac arrest within minutes after the administration of succinylcholine in healthy appearing pediatric patients (usually, but not exclusively, males, and most frequently 8 years or younger). There have also been reports in adolescents. Therefore, when a healthy appearing infant or child develops cardiac arrest soon after administration of succinylcholine, not felt to be due to inadequate ventilation, oxygenation, or anesthetic overdose, institute immediate treatment for hyperkalemia, including intravenous calcium, bicarbonate, glucose with insulin, and hyperventilation. Due to the abrupt onset of this syndrome, routine resuscitative measures are likely to be unsuccessful. However, extraordinary and prolonged resuscitative efforts have resulted in successful resuscitation in some reported cases. Arrhythmias as well as rhabdomyolysis with possible acute renal failure (unspecified) associated with myoglobinuria have been reported with succinylcholine use.
Bradycardia has been reported with succinylcholine use. In both adults and pediatric patients, the incidence of bradycardia, which may progress to asystole, is higher after a second dose of succinylcholine. The incidence and severity of bradycardia are higher in pediatric patients than adults. Whereas bradycardia is common in pediatric patients after an initial dose of 1.5 mg/kg, bradycardia is seen in adults only after repeated exposure. Pretreatment with anticholinergic agents (e.g., atropine) may reduce the occurrence of bradyarrhythmias. Hypertension has also been reported with succinylcholine use.
Although rare, severe anaphylactic or anaphylactoid reactions to neuromuscular blocker agents (NMBAs), including succinylcholine, have been reported; some cases have been fatal. Immediate availability of appropriate emergency treatment for anaphylaxis is advised because of the potential life-threatening severity of a reaction. The potential for histamine-release is present after succinylcholine administration; however, signs and symptoms of histamine-mediated release such as flushing, hypotension, and bronchospasm are uncommon in normal clinical usage. Rare hypersensitivity reactions (e.g., angioedema, bronchospasm, wheezing, flushing, rash, erythema, urticaria, pruritus, hypotension, sinus tachycardia) related to histamine release have been reported after succinylcholine administration.
Malignant hyperthermia can be precipitated by many drugs used in anesthetic practice, including halogenated anesthetics and succinylcholine. The risk of developing malignant hyperthermia after succinylcholine administration increases with the concomitant administration of volatile anesthetics. Malignant hyperthermia frequently presents as intractable spasm of the jaw muscles (masseter spasm) which may progress to generalized rigidity, increased oxygen demand, tachycardia, tachypnea, and profound hyperpyrexia. Successful outcome depends on recognition of early signs, such as jaw muscle spasm, acidosis, or generalized rigidity to initial administration of succinylcholine for tracheal intubation, or failure of tachycardia to respond to deepening anesthesia. Skin mottling, rising temperature, and coagulopathies may occur later in the course of the hypermetabolic process. Recognition of the syndrome is a signal for discontinuance of anesthesia, attention to increased oxygen consumption, correction of acidosis, support of circulation, assurance of adequate urinary output, and institution of measures to control rising temperature. Intravenous dantrolene sodium is recommended as an adjunct to supportive measures in the management of malignant hyperthermia.
Succinylcholine is used for the purpose of inducing temporary paralysis; however, some of its most serious adverse effects are extensions of its therapeutic use. Careful monitoring of physiologic parameters and response to a peripheral nerve stimulator are recommended during continuous infusions and repeated dosing. Though paralysis may be used to facilitate mechanical ventilation, hypoxia may result from inadequate ventilation and/or a deterioration in pulmonary mechanics associated with prolonged paralysis. Excessive doses or prolonged exposure to neuromuscular blocking agents (NMBAs) can cause skeletal muscle weakness, and patients may consequentially experience prolonged apnea, dyspnea, respiratory depression, and/or profound muscular weakness (muscle paralysis). Muscle weakness in critically ill patients is multifactorial; however, prolonged recovery is most often related to excessive dosing of neuromuscular blockers or use of these agents in patients with hepatic or renal dysfunction. These patients may take hours to days to recover due to long-term accumulation of the drug. Perhaps the most devastating complication of neuromuscular blockade, acute quadriplegic myopathy syndrome (AQMS), presents as acute paresis, myonecrosis with increased creatine phosphokinase (CPK), and abnormal electromyography (EMG). After drug discontinuation, patients present with flaccid paralysis, decreased deep tendon reflexes, and respiratory insufficiency. Sensory function and extraocular movement are preserved, and there are no abnormal cerebrospinal fluid findings. Prolonged rehabilitation as well as chronic ventilatory support are often needed in patients with AQMS. Recovery may take weeks to months. To reduce the risk of prolonged recovery and AQMS, periodic screening of CPK during ongoing neuromuscular blockage may be helpful. Though periodic interruption of therapy is often not feasible and there is no direct evidence showing that it reduces the incidence of AQMS, daily 'drug holidays' may be considered for patients who will tolerate an interruption in therapy.
Patients receiving succinylcholine are at risk for developing xerophthalmia, leading to keratitis, conjunctivitis, and corneal abrasion because muscle paralysis inhibits eyelid movement and complete closure. Prophylactic eye care is essential; use artificial tears or ophthalmic ointment at regular intervals during neuromuscular blockade. Additionally, paralyzed patients with prolonged immobility are at risk for skin erosion, skin ulcer (pressure sore), and deep vein thrombosis (DVT). Frequent repositioning, physical therapy, and sequential compression devices (if age appropriate) are indicated. The use of special mattresses may be considered.
Awake, paralyzed patient-anxiety and panic may be the most bothersome adverse effect associated with neuromuscular blockade. Neuromuscular blockers, such as succinylcholine, do not provide sedation or analgesia and should be administered only after unconsciousness has been induced. In emergent life-threatening situations, it may be necessary to administer succinylcholine before unconsciousness. It is essential that amnesia, sedation, and analgesia are adequately maintained throughout paralyzation. Depth of sedation is difficult to monitor due to lack of movement with paralyzation. Physiologic parameters such as heart rate or blood pressure may be of use; however, there are many confounding influences on these parameters in critically ill patients.
Patients who receive neuromuscular blocking agents for a prolonged period may develop tachyphylaxis (i.e., tolerance). Prolonged neuromuscular blockade leads to proliferation of acetylcholine receptors at the neuromuscular junction resulting in increased drug requirements. Switch patients who develop tachyphylaxis to succinylcholine and still require neuromuscular blockade to another agent. Continuous monitoring of neuromuscular transmission with a peripheral nerve stimulator is strongly recommended during continuous infusion or repeated dosing. Target response is typically 1 to 2 twitches. Incorrect electrode placement, direct stimulation of muscle due to large electrode size, acute illness, capillary leak, and edema may affect an appropriate assessment. Monitor visual and tactile stimulation on muscle movement as well as heart rate, blood pressure, and mechanical ventilator status during administration. Depending on the dose and duration of succinylcholine administration, the characteristic depolarizing neuromuscular block (Phase I block) may change to a block with characteristics superficially resembling a non-depolarizing block (Phase II block). This may be associated with prolonged respiratory muscle paralysis or weakness in patients who manifest the transition to Phase II block. When this diagnosis is confirmed by peripheral nerve stimulation, it may sometimes be reversed with anticholinesterase drugs such as neostigmine. Anticholinesterase drugs may not always be effective. If given before succinylcholine is metabolized by cholinesterase, anticholinesterase drugs may prolong rather than shorten paralysis.
Muscle fasciculation, jaw rigidity, and postoperative muscle pain (myalgia) have been reported with succinylcholine use. Although some clinicians use defasciculating doses of nondepolarizing agents before succinylcholine use in older patients to reduce the severity of fasciculations, these are not commonly used in pediatric patients for several reasons: 1) patients under the age of 6 do not fasciculate, 2) the use of a defasciculating dose delays the onset of paralysis and increases the succinylcholine dose requirement, 3) defasciculating doses may lead to a significant degree of neuromuscular blockade in patients with severe respiratory or hemodynamic compromise leading to respiratory insufficiency or laryngeal incompetency, and 4) full efficacy may take up to 3 minutes, making the technique less optimal when emergency intubation is required.
Succinylcholine may cause transient increased intraocular pressure (ocular hypertension), increased intracranial pressure, and increased intragastric pressure (resulting in regurgitation and aspiration of the stomach contents) immediately after administration and during the fasciculation phase. Slight increases in pressure may persist after the onset of paralysis. Induction of adequate anesthesia before succinylcholine administration may minimize the drug's effect on intracranial pressure.
Hypersalivation has been reported with succinylcholine use.
In emergent life-threatening situations, it may be necessary to administer succinylcholine before unconsciousness. Otherwise, administer succinylcholine only after unconsciousness has been induced; maintain adequate amnesia and analgesia throughout paralyzation. Neuromuscular blocking agents do not cause sedation or analgesia. Individualize succinylcholine doses. Use of a peripheral nerve stimulator will permit the most advantageous use of succinylcholine, minimize the possibility of overdosage or underdosage, and assist in the evaluation of recovery.
Succinylcholine administration requires an experienced clinician who is familiar with its actions and the possible complications that may occur after its use as well as requires a specialized care setting where facilities for intubation, artificial respiration, oxygen therapy, and reversal agents are immediately available. Accidental exposure to a neuromuscular blocking agent may be fatal in a patient for whom it is not intended. Store succinylcholine with cap and ferrule intact and in a manner that minimizes the possibility of selecting the wrong product. Confirm proper medication selection and clearly communicate the intended dose.
Succinylcholine is contraindicated in patients known to have a hypersensitivity to the drug. Use succinylcholine with caution in patients with neuromuscular blocking agent hypersensitivity since cross-reactivity between neuromuscular blocking agents, both depolarizing and non-depolarizing, has been reported. Severe anaphylactic reactions to neuromuscular blocking agents, including succinylcholine, have been reported. These reactions have been life-threatening and fatal in some cases. Due to the potential severity of these reactions, ensure the necessary precautions, such as the immediate availability of appropriate emergency treatment.
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. In such individuals, succinylcholine can cause severe hyperkalemia, which can result in serious cardiac arrhythmias and cardiac arrest. Risk of hyperkalemia increases over time and usually peaks 7 to 10 days after the injury; however, risk is dependent on the extent and location of injury, and the precise onset and duration of the risk period are unknown. Use succinylcholine with caution in patients with electrolyte abnormalities, digitalis toxicity, chronic abdominal infections, subarachnoid hemorrhage, tetanus, disuse atrophy, Guillain-Barre syndrome, and degenerative nervous system disorders because of the potential for developing severe hyperkalemia. Do not use succinylcholine in any patient with a serum potassium of more than 5.5 mEq/L.
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 (NMBAs). Electrolyte imbalance can alter a patient's sensitivity to 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.
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, use succinylcholine with caution in patients with any condition in which a significant release of histamine may be contraindicated. Also, 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). Carefully monitor respiratory status and adequacy of ventilation after drug recovery until the patient is clearly stabilized.
Use succinylcholine with caution in patients with neuromuscular disease (e.g., myasthenia gravis, myasthenic syndrome ); prolonged or exaggerated neuromuscular blockade may occur after neuromuscular blocking agent use. 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). Additionally, patients with weak muscle tone or severe obesity are at an increased risk for airway and ventilation complications. Monitor patients carefully until recovery is fully complete.
Use succinylcholine carefully in patients with reduced plasma cholinesterase activity (pseudocholinesterase deficiency). Consider the likelihood of prolonged neuromuscular block after administration of succinylcholine in such patients. Plasma cholinesterase activity may be diminished in the presence of genetic abnormalities of plasma cholinesterase (e.g., patients heterozygous or homozygous for atypical plasma cholinesterase gene), severe hepatic disease, severe renal disease, malignant tumors, infection, burns, anemia, decompensated cardiac disease, peptic ulcer disease, or myxedema. Plasma cholinesterase activity may also be diminished by chronic administration of oral contraceptives, corticosteroid therapy, or certain monoamine oxidase inhibitors and by cholinesterase inhibitor toxicity due to irreversible inhibitors of plasma cholinesterase (e.g., organophosphate insecticides, echothiophate, and certain antineoplastic drugs).
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 this risk. In neonates, infants, children, and adolescents, reserve the use of succinylcholine 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). 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. Affected pediatric patients are typically, but not exclusively, males 8 years or younger. Although some patients 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 patients at risk. Closely monitor body temperature, expired CO2, heart rate, blood pressure, and electrocardiogram in pediatric patients to 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 of succinylcholine administration. If cardiac arrest occurs immediately after succinylcholine administration, institute treatment for hyperkalemia (e.g., intravenous calcium, bicarbonate, glucose with insulin, hyperventilation). If malignant hyperthermia is suspected, initiate appropriate treatment (e.g., dantrolene, supportive care) concurrently.
Do not use succinylcholine in patients in whom an increase in intraocular pressure is undesirable (e.g., narrow-angle glaucoma, penetrating ocular trauma) unless the potential benefit of its use outweighs the potential risk. Succinylcholine causes an increase in intraocular pressure.
Use succinylcholine with caution in patients with bone fractures or muscle spasm as initial muscle fasciculations can cause additional injury.
Description: Succinylcholine is a parenteral, short-acting, depolarizing neuromuscular blocking agent (NMBA) indicated 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 in pediatric patients. Succinylcholine has the fastest onset time of any NMBA, typically allowing intubation within 60 seconds. In addition to its rapid onset and short duration, advantages of succinylcholine include its organ-independent metabolism and ability to be administered intramuscularly in patients without venous access. Succinylcholine induces histamine release and vagal stimulation. Bradycardia is more common in infants and children compared to adults; repeated dosing also increases the risk of bradycardia. Succinylcholine-induced muscle contraction and fasciculation can cause sudden, large releases of potassium, which may induce cardiac dysrhythmias. There have been rare reports of ventricular dysrhythmias and fatal cardiac arrest after the administration of succinylcholine in pediatric patients with undiagnosed skeletal muscle myopathies. Due to these risks, when prolonged paralysis is necessary, the use of a nondepolarizing NMBA is recommended. Succinylcholine is FDA-approved in patients as young as neonates.
General dosing information:
-Limit the use of succinylcholine in pediatric patients for emergency intubation or when immediate securing of the airway is necessary (e.g., laryngospasm, difficult airway, full stomach) or for intramuscular use when a suitable vein is inaccessible. In general, nondepolarizing neuromuscular blocking agents are preferred for routine elective surgery or prolonged paralysis.
-Monitor heart rate, blood pressure, and oxygen saturation. 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.
-Pretreatment with anticholinergic agents (e.g., atropine) may reduce the occurrence of bradyarrhythmias.
For neuromuscular blockade during rapid-sequence intubation (RSI) and for non-emergent endotracheal intubation when immediate securing of the airway is necessary (e.g., laryngospasm, difficult airway, full stomach):
Neonates: 2 mg/kg/dose IV. Dosage range: 1 to 3 mg/kg/dose. Onset of intubating conditions is 30 to 60 seconds. May repeat 1 mg/kg/dose IV if intubating conditions are not attained within an adequate period (1 to 5 minutes). Max: 4 mg/kg per intubation attempt.
Infants 1 to 5 months: 2 mg/kg/dose IV. Dosage range: 1 to 3 mg/kg/dose. Onset of intubating conditions is 30 to 60 seconds. May repeat 1 mg/kg/dose IV if intubating conditions are not attained within an adequate period (1 to 5 minutes). Max: 4 mg/kg per intubation attempt.
Infants and Children 6 to 23 months: 1 to 2 mg/kg/dose IV. Onset of intubating conditions is 30 to 60 seconds.
Children and Adolescents 2 to 17 years: 1 to 1.5 mg/kg/dose IV. Onset of intubating conditions is 30 to 60 seconds.
Neonates: 2 to 4 mg/kg/dose IM. Onset of intubating conditions is 2 to 5 minutes.
Infants 1 to 5 months: 4 to 5 mg/kg/dose IM. Onset of intubating conditions is 2 to 5 minutes.
Infants and Children 6 months to 12 years: 4 mg/kg/dose (Max: 150 mg/dose) IM. Onset of intubating conditions is 2 to 5 minutes.
Adolescents: 3 to 4 mg/kg/dose (Max: 150 mg/dose) IM. Onset of intubating conditions is 2 to 5 minutes.
Maximum Dosage Limits:
3 mg/kg/dose IV (Max: 4 mg/kg IV per intubation attempt); 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.
6 to 11 months: 2 mg/kg/dose IV; 4 mg/kg/dose IM.
1 year: 2 mg/kg/dose IV; 4 mg/kg/dose IM.
2 to 12 years: 1.5 mg/kg/dose IV; 4 mg/kg/dose (Max: 150 mg/dose) IM.
1.5 mg/kg/dose IV; 4 mg/kg/dose (Max: 150 mg/dose) IM.
Patients with Hepatic Impairment Dosing
Specific guidelines for dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed.
Patients with Renal Impairment Dosing
Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.
Monograph content under development
Mechanism of Action: Muscle contraction is initiated by an action potential traveling from the central nervous system to the nerve terminal. At the nerve terminal, the action potential causes an influx of calcium, initiating release of acetylcholine (ACh) into the synaptic cleft. ACh binds to ACh receptors on the muscle fiber's motor end-plate causing a conformational change that briefly opens sodium ion channels. When an adequate number of ACh receptors are activated, membrane potential decreases and voltage-dependent sodium ion channels of adjacent muscle membranes activate, transmitting the action potential throughout the muscle fiber and resulting in muscle contraction. Succinylcholine, a depolarizing neuromuscular blocking agent, produces skeletal muscle paralysis by competing with ACh for cholinergic receptor sites at the motor end-plate. Like ACh, it activates the receptor and causes membrane depolarization. Because succinylcholine is resistant to degradation by acetylcholinesterase, it remains bound to the receptor and thereby inhibits repolarization, resulting in an extended duration of neuromuscular blockade. Depolarization results in fasciculation of the skeletal muscles and muscle paralysis. Neuromuscular transmission is inhibited until succinylcholine is degraded by pseudocholinesterase. The paralysis after 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. Muscle tone generally returns in the reverse order. Succinylcholine has no direct effect on the uterus, myocardium, or other smooth muscle structures. Succinylcholine does, however, stimulate both autonomic ganglia and muscarinic receptors, which may affect cardiac rhythm.
Pharmacokinetics: Succinylcholine can be administered intravenously or intramuscularly. Succinylcholine is highly ionized and has low lipid solubility; it is rapidly distributed into the extracellular space. Succinylcholine is rapidly hydrolyzed by plasma cholinesterase to succinylmonocholine, a metabolite which possesses clinically insignificant depolarizing neuromuscular blocking properties. Succinylmonocholine is further hydrolyzed to succinic acid and choline. Up to 10% of a succinylcholine dose is excreted unchanged in the urine.
Plasma cholinesterase activity may be diminished in patients with genetic abnormalities of plasma cholinesterase, malignant tumors, infections, burns, anemia, decompensated heart disease, peptic ulcer, severe hepatic or renal dysfunction, or myxedema. In addition, chronic administration of drugs that antagonize plasma cholinesterase (e.g., oral contraceptives, glucocorticoids, monoamine oxidase inhibitors, cyclophosphamide) may decrease cholinesterase activity and increase duration of neuromuscular blockade.
Affected cytochrome P450 isoenzymes and drug transporters: none
Onset of paralysis occurs less than 1 minute after intravenous administration and persists approximately 3 to 12 minutes after administration of a single dose. When used for paralysis before intubation, intubating conditions are typically present in children 45 to 60 seconds after administration. Patients with reduced plasma cholinesterase activity may experience longer durations of action. After a single dose of succinylcholine 1 to 2 mg/kg in adult anesthetized patients, concentrations were below the limit of detection (2 mcg/mL) within 2.5 minutes.
Onset of paralysis occurs in approximately 2 to 5 minutes after intramuscular administration and persists for 5 to 30 minutes, with the upper end of the range typically limited to neonates and those with reduced plasma cholinesterase activity.
Neonates and Infants
Neonates and infants have a larger extracellular fluid compartment resulting in a larger Vd compared to other populations; extracellular fluid constitutes approximately 45%, 30%, 20%, and 16% of body weight at birth, 2 months, 6 years, and adulthood, respectively. Because of their larger Vd, neonates and young infants often require larger doses on a mg/kg basis. Developmental differences in the neuromuscular junction during the first 2 months of life may also influence the pharmacokinetics of succinylcholine in this population. In general, immature acetylcholine receptors result in greater variability of neuromuscular blockade response. In addition, the immature receptor has a smaller single-channel conductance that opens for a longer time than the mature receptor, allowing the immature muscle to be more easily depolarized. Though neonates and infants have fewer acetylcholine receptors compared to other populations, the immature receptor has a greater affinity for succinylcholine.
Children have a larger extracellular fluid compartment resulting in a larger Vd compared to adults; extracellular fluid constitutes approximately 20% of body weight at 6 years compared to 16% of body weight in adulthood. Because of differences in Vd, children often require more succinylcholine on a mg/kg basis than adolescents and adults (but less than neonates and infants).
Plasma cholinesterase activity may be reduced in patients with severe hepatic disease, which may result in prolonged neuromuscular blockade.
Plasma cholinesterase activity may be reduced in patients with severe renal disease, which may result in prolonged neuromuscular blockade.