Succinylcholine Chloride (succinylcholine chloride in sodium chloride,iso-osmotic/PF)

Dosage of succinylcholine chloride is expressed in terms of the salt. The dosage must be carefully adjusted according to individual requirements and response. The use of a peripheral nerve stimulator is recommended during continuous IV infusion of the drug to avoid overdose, detect development of Phase II block, follow rate of recovery, and assess the effects of reversing agents.

Succinylcholine chloride usually is administered IV. For patients in whom a suitable vein is not accessible, the drug may be administered by IM injection.

Succinylcholine chloride is supplied in multiple-dose vials and single-dose prefilled syringes containing a 20 mg/mL solution. Unopened vials and prefilled syringes should be stored under refrigeration at 2-8degreesC, but may be kept at room temperature for up to 14 days without significant loss of potency.

Dilution of the 20 mg/mL solution is not required prior to IV or IM injection.

For prolonged procedures, the manufacturer states that succinylcholine chloride may be given by continuous IV infusion or intermittent IV injection. For continuous IV infusion, succinylcholine chloride usually is diluted to a concentration of 1-2 mg/mL with a compatible IV solution such as 5% dextrose injection or 0.9% sodium chloride injection. The 1-mg/mL concentration is usually preferred for optimum rate control. Diluted solutions of succinylcholine chloride may be stored under refrigeration at 2-8degreesC for up to 24 hours. Succinylcholine injections should not be admixed with alkaline (pH exceeding 8.5) solutions (e.g., barbiturates).

No dosing information is available for this tab.

No dosing information is available for this tab.

There is no enhanced messaging for this drug.

There are no contraindication interactions for this drug.

Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

Neuromuscular Blocking Agents/General Anesthetics (Inhl)

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: General anesthetics enhance the pharmacologic effects of nondepolarizing muscle relaxants.

CLINICAL EFFECTS: May see an increase in the neuromuscular blocking effects of the nondepolarizing muscle relaxant including respiratory depression, bradycardia, hypotension, flushing, or muscle weakness.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: It may be necessary to decrease the dose of the nondepolarizing muscle relaxant. Monitor neuromuscular function and adjust the dose of the nondepolarizing muscle relaxant accordingly.

DISCUSSION: Concomitant administration of general anesthetics and nondepolarizing muscle relaxants has been shown to produce synergistic neuromuscular blocking effects of nondepolarizing muscle relaxants.

Neuromuscular Blocking Agents/Misc Antibiotics

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Aminoglycosides, bacitracin, clindamycin, lincomycin, and polymyxins may enhance the pharmacologic effects of neuromuscular blocking agents.

CLINICAL EFFECTS: May see an increase in the pharmacologic effects of neuromuscular blocking agents, including prolonged respiratory depression and apnea.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: If it is necessary to administer these drugs concurrently, do so with extreme caution. Monitor neuromuscular function and adjust the dose of the neuromuscular blocking agent accordingly.

DISCUSSION: Concomitant administration of aminoglycosides, bacitracin, clindamycin, lincomycin, and polymixins with neuromuscular blocking agents has been shown to produce synergism of the effects on skeletal muscles. Concurrent administration of these drugs has been associated with prolonged respiratory depression, respiratory paralysis, and fatal apnea. The interaction usually occurs when the antibiotic is given prior to or concurrently with the neuromuscular blocking drug, but it may also occur when given after administration. Any antibiotic dosage or route of administration may produce respiratory depression.

Neuromuscular Blocking Agents/Quinine Derivatives

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Synergistic or additive pharmacologic activity.

CLINICAL EFFECTS: May see an increase in the neuromuscular blocking effects, including profound sedation, respiratory depression, coma, and/or death.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Avoid concurrent administration of neuromuscular blocking agents and quinine derivatives during the first several hours of postoperative period. If administered, respiratory support may be needed. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.

DISCUSSION: Administration of quinidine during the immediate postoperative period has been associated with respiratory paralysis and apnea.

Neuromuscular Blocking Agents/Verapamil

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Unknown.

CLINICAL EFFECTS: The neuromuscular blocking effect of nondepolarizing muscle relaxants may be extended, producing profound sedation, respiratory depression, coma, and/or death.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: If possible, avoid administration of nondepolarizing neuromuscular blocking agents to patients receiving verapamil. When both drugs must be given, carefully monitor respiratory function to avoid prolonged neuromuscular blockade. If needed, blockade may be reversed by giving edrophonium. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.

DISCUSSION: Patients receiving verapamil have experienced prolonged skeletal muscle paralysis after administration of usual therapeutic doses of a nondepolarizing neuromuscular blocking agent. While muscle paralysis was unresponsive to treatment with neostigmine, reversal of blockade has been achieved by administration of edrophonium.

Succinylcholine/Cyclophosphamide

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Cyclophosphamide may reduce plasma concentrations of the enzyme that metabolizes succinylcholine, pseudocholinesterase.

CLINICAL EFFECTS: The neuromuscular blocking activity of succinylcholine may be prolonged producing profound sedation, respiratory depression, coma, and/or death.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: If possible, avoid administration of succinylcholine to patients receiving cyclophosphamide. When both drugs must be given, carefully monitor neuromuscular function to avoid overdosage of succinylcholine and prolonged apnea. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.

DISCUSSION: Case reports and in vitro investigations support that concurrent administration of cyclophosphamide and succinylcholine can produce prolonged neuromuscular blockade. The effect may be greatest when large dosages of cyclophosphamide are given.

Succinylcholine/Echothiophate Iodide

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Decreased pseudocholinesterase activity.

CLINICAL EFFECTS: Succinylcholine administered to patients receiving echothiophate are at risk of developing respiratory depression and prolonged periods of apnea, with death a possibility. Effects may be seen for several weeks after stopping the echothiophate.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Avoid concomitant use of these agents or use with caution. It is recommended that plasma pseudocholinesterase measurements be taken before succinylcholine is given.

DISCUSSION: This interaction is well documented.

Succinylcholine/Trimethaphan

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Unknown. Trimethaphan is believed to inhibit plasma cholinesterase.

CLINICAL EFFECTS: May see an increase in the neuromuscular blocking effects of succinylcholine, producing prolonged respiratory depression and apnea.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Avoid concurrent administration of succinylcholine and trimethaphan. If both agents are given concomitantly, prior measurement of plasma cholinesterase activity is advisable.

DISCUSSION: Concurrent administration of succinylcholine and trimethaphan has been reported to produce prolonged apnea. In addition, trimethaphan has been reported to produce nondepolarizing neuromuscular blockade and increase the activity of both depolarizing and nondepolarizing muscle relaxants.

Moderate Interaction: Assess the risk to the patient and take action as needed.

Anesthesia Agents/Glp-1 Receptor Agonists

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: GLP-1 receptor agonists can cause delayed gastric emptying.(1,2)

CLINICAL EFFECTS: Gastric contents may remain in the stomach after preoperative fasting, which could increase the risk of regurgitation and aspiration.(1,2)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: The American Society of Anesthesiologists (ASA) recommends the following for patients receiving elective procedures: - For patients on daily dosing, consider holding GLP-1 agonists on the day of the procedure. For patients on weekly dosing, consider holding GLP-1 agonists a week prior to the procedure. - Consult an endocrinologist for patients taking GLP-1 agonists for diabetes management if the GLP-1 agonist is held longer than the dosing schedule to avoid hyperglycemia. - For patients requiring urgent or emergent procedures, proceed and treat the patient as 'full stomach.'(3)

DISCUSSION: In one case report, a 31-year-old patient taking semaglutide followed preoperative fasting guidelines but food residue was discovered upon endoscopy, leading to cancellation of the surgical procedure.(4) In a case report, a semaglutide-treated patient experienced regurgitation upon induction of general anesthesia despite a 20 hour preoperative fasting period. The patient received semaglutide two days before the scheduled procedure.(5) A case report of a 42-year-old patient after fasting for 18 hours showed substantial gastric content upon endoscopy. The patient experienced intraoperative pulmonary aspiration of gastric contents which were suctioned from the trachea and bronchi using bronchoscopy.(6)

Neuromuscular Blocking Agents/Lincosamides

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Lincosamides appear to augment the neuromuscular blocking effects of nondepolarizing muscle relaxants.

CLINICAL EFFECTS: The effects of nondepolarizing neuromuscular relaxants may be prolonged leading to profound sedation, respiratory depression, coma, and/or death.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Monitor respiratory function of the patient and provide the necessary support. In patients who have received nondepolarizing muscle relaxants, avoid use of lincosamides in the recovery room. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.

DISCUSSION: Lincomycin has been reported to augment the neuromuscular blocking effect of pancuronium in seven anesthetized patients. The effect was readily antagonized by neostigmine administration. In a case report, clindamycin produced prolonged neuromuscular blockade in a patient who had received pancuronium. Neostigmine was ineffective in antagonizing the blockade.

Neuromuscular Blocking Agents/Polypeptide Antibiotics

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Synergistic pharmacologic activity. Polymyxin B affects neuromuscular transmission by blocking acetylcholine receptors. Its action is thus post-synaptic and the neuromuscular block has no antagonists. Polymyxin B causes neostigmine resistance to d-tubocurarine blockade and calcium resistance to the blockade evoked by aminoglycoside antibiotics (1,2,3,4). A pre-synaptic mechanism may also be involved with decreased release of acetylcholine.

CLINICAL EFFECTS: May see an increase in the neuromuscular blocking effects, including profound sedation, respiratory depression, coma, and/or death.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: If it is necessary to administer these drugs concurrently, do so with extreme caution. Monitor neuromuscular function and adjust the dose of the neuromuscular blocking agent accordingly. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.

DISCUSSION: Concomitant administration of polypeptide antibiotics and neuromuscular blocking agents has been shown to produce synergism of the effects on skeletal muscles. Concurrent administration of these drugs has been associated with prolonged respiratory depression, respiratory paralysis, and apnea. This interaction has been documented with colistimethate, polymyxin B, bacitracin, and vancomycin.

Succinylcholine/Anticholinesterases

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Anticholinesterases inhibit plasma cholinesterases, delaying succinylcholine hydrolysis and prolonging its duration of action.

CLINICAL EFFECTS: May see an increase in the neuromuscular blocking effects of succinylcholine, producing profound sedation, respiratory depression, coma, and/or death.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Avoid concurrent administration of anticholinesterases and succinylcholine in patients with depolarizing type (phase I) neuromuscular blockade. In addition, use with caution in the presence of a nondepolarizing type (phase II) blockade. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.

DISCUSSION: Concomitant administration of anticholinesterases and succinylcholine has been associated with prolonged respiratory depression and apnea.

Succinylcholine/Lidocaine; Procaine

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Since both succinylcholine and procaine are metabolized by plasma pseudocholinesterase, competitive inhibition of succinylcholine metabolism by procaine is believed to be responsible. The mechanism between succinylcholine and lidocaine is not well understood.

CLINICAL EFFECTS: The neuromuscular blocking activity of succinylcholine may be increased, producing profound sedation, respiratory depression, coma, and/or death.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: If it is necessary to administer these drugs concurrently, do so with extreme caution. Monitor neuromuscular function and adjust the dose of the neuromuscular blocking agent accordingly. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.

DISCUSSION: Available data indicate that intravenous administration of high doses of procaine prolonged the neuromuscular activity of succinylcholine.

Succinylcholine/Metoclopramide

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Metoclopramide inhibits plasma cholinesterase, decreasing the inactivation of succinylcholine.

CLINICAL EFFECTS: The pharmacologic effects of succinylcholine may be increased, resulting in profound sedation, respiratory depression, coma, and/or death.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Monitor neuromuscular function and supply mechanical respiratory support if prolonged respiratory depression occurs. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.

DISCUSSION: In controlled studies, administration of metoclopramide to patients receiving intubating doses of succinylcholine prolonged the neuromuscular blockade produced by succinylcholine by 23% to 228%.

*Skeletal muscle myopathies.

*Known hypersensitivity to succinylcholine.

*After the acute phase of injury following major burns, multiple trauma, extensive denervation of skeletal muscle, or upper motor neuron injury.

*Known or suspected genetic susceptibility to malignant hyperthermia.

• Amyotrophic lateral sclerosis
• Angle-closure glaucoma
• Major traumatic injury
• Malignant hyperthermia
• Myopathy
• Rhabdomyolysis
• Severe burns

• Bradycardia
• Digitalis toxicity
• Duchenne muscular dystrophy
• Fever
• Hyperkalemia
• Hypocalcemia
• Hypokalemia
• Muscular dystrophy
• Myasthenia gravis
• Ocular hypertension
• Ocular injury
• Surgical procedure on eye proper
• Systemic mastocytosis

• Anemia
• Burns
• Butyrylcholinesterase deficiency
• Cardiac decompensation
• Fracture
• Glaucoma
• Infection
• Kidney disease with reduction in glomerular filtration rate (GFr)
• Malignancy
• Muscle spasm
• Myxedema
• Predisposition to aspiration
• Severe hepatic disease

Adverse reactions reported with succinylcholine include cardiac arrest, malignant hyperthermia, arrhythmias, bradycardia, tachycardia, hypertension, hypotension, hyperkalemia, prolonged respiratory depression, and apnea.

More Frequent

• Ocular hypertension

Less Frequent

• Bradycardia
• Cardiac arrhythmia
• Hypotension
• Tachycardia

Rare or Very Rare

• Allergic dermatitis
• Anaphylaxis
• Apnea
• Bronchospastic pulmonary disease
• Cardiac arrest
• Cardiogenic shock
• Edema
• Erythema
• Flushing
• Hyperkalemia
• Hypertension
• Malignant hyperthermia
• Muscle fasciculation
• Myoglobinuria
• Pruritus of skin
• Respiratory depression
• Rhabdomyolysis
• Skin rash

More Frequent

• Muscle rigidity
• Myalgia

Less Frequent

• Sialorrhea

Rare or Very Rare

• Trismus

No enhanced messaging available.

Safety and effectiveness of succinylcholine have been established in pediatric patients from neonates to adolescents. However, because of the risk of ventricular dysrhythmias, cardiac arrest, and death from hyperkalemic rhabdomyolysis in pediatric patients, use of succinylcholine should be reserved for emergency intubation or instances where immediate securing of the airway is necessary (e.g., laryngospasm, difficult airway, full stomach, or for IM use when a suitable vein is inaccessible).

IV bolus administration of succinylcholine in pediatric patients may result in profound bradycardia or, rarely, asystole; this occurs more commonly among pediatric patients than adult patients.

The effective dose of succinylcholine in pediatric patients may be higher than predicted based on body weight dosing alone.

Available data from published case reports and case series over decades of use have not identified a drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes with the use of succinylcholine during pregnancy.

Succinylcholine is commonly used during caesarean section to provide muscle relaxation. It is known to cross the placental barrier in an amount that is dependent on the concentration gradient between the maternal and fetal circulation. Apnea and flaccidity can occur in the newborn after repeated high doses of succinylcholine are administered to the mother, or in the presence of atypical plasma cholinesterase in the mother.

Plasma cholinesterase levels are decreased by approximately 24% during pregnancy and for several days postpartum; this can prolong the effect of succinylcholine. If succinylcholine is used during labor and delivery, there is a risk for prolonged apnea.

There are no data regarding the presence of succinylcholine or its metabolite in human or animal milk; the effects on the breast-fed child and effects on milk production are not known.

Consider the developmental and health benefits of breast-feeding along with the mother's clinical need for succinylcholine and any potential adverse effects on the breast-fed infant from the drug or underlying maternal condition.

The manufacturer recommends cautious dose selection, usually starting at the low end of the dosage range, for geriatric patients, reflecting the greater frequency of decreased hepatic, renal, or cardiac function in this patient population.

Clinical studies of succinylcholine did not include sufficient numbers of patients >=65 years of age to determine whether they respond differently from younger patients. Other reported clinical experience has not identified differences in responses between geriatric and younger patients.

In general, select dosages cautiously in geriatric patients, usually starting at the low end of the dosage range because of the greater frequency of decreased hepatic, renal, or cardiac function and of concomitant disease or other drug therapy in this patient population.