Succinyl Choline

Generic Name: Succinyl Choline
Brand Name: -
Dosage Form: Injection 500mg/10ml
Pharmacological Category: Neuromuscular Blocking Agents
Therapeutic Category: Antimyasthenic, Muscle Relaxant
Pregnancy Category: category C

Pharmacology

Succinylcholine is a depolarizing skeletal muscle relaxant. As does acetylcholine, it combines with the cholinergic receptors of the motor end plate to produce depolarization. This depolarization may be observed as fasciculations. Subsequent neuromuscular transmission is inhibited so long as adequate concentration of succinylcholine remains at the receptor site. Onset of flaccid paralysis is rapid (less than 1 minute after IV administration), and with single administration lasts approximately 4 to 6 minutes.

Pharmacokinetics:

Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg.

Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes.

The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds.

Indications:

• Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal intubation, endoscopic examinations, electrically or pharmacologically induced convulsive therapy) after general anesthesia.
• Drug of choice for skeletal muscle relaxation during orthopedic manipulations.
• Treatment to increase pulmonary compliance during assisted or controlled respiration.

Contraindications:

Personal or familial history of malignant hyperthermia.
• Myopathies associated with elevated serum creatine kinase (CK, CPK) values.
• Upper motor neuron injury, multiple trauma, extensive or severe burns, extensive denervation of skeletal muscle because of CNS disease or injury. (See Hyperkalemia under Cautions.)
• Known hypersensitivity to succinylcholine or any ingredient in the formulation.

Precautions:

Succinylcholine should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma.
Succinylcholine may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of succinylcholine will minimize this effect.

Succinylcholine may increase intragastric pressure, which could result in regurgitation and possible aspiration of stomach contents.
Neuromuscular blockade may be prolonged in patients with hypokalemia or hypocalcemia.

Since allergic cross-reactivity has been reported in this class, request information from your patients about previous anaphylactic reactions to other neuromuscular blocking agents. In addition, inform your patients that severe anaphylactic reactions to neuromuscular blocking agents.

Drug Interactions:

β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

Side Effects:

Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast breathing; fast, slow, or irregular heartbeat; flushing; high body temperature; increased pressure in the eye; pauses in breathing; pounding in the chest; severe muscle pain with or without decreased urination; severe or persistent dizziness or headache; slowed or shallow breathing; tightening of the jaw or other muscles.

Storage:

• Store between 2-8 C°
• Protect from light and freezing

Packing:

• Injection 500mg/10ml:Box of 5 Ampoules

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Image: 
Brand Name: 

-

Dosage Form: 

Injection 500mg/10ml

Pharmacological Category: 

Neuromuscular Blocking Agents

Therapeutic Category: 

Antimyasthenic, Muscle Relaxant

Pregnancy Category: 

category C

Succinylcholine is a depolarizing skeletal muscle relaxant. As does acetylcholine, it combines with the cholinergic receptors of the motor end plate to produce depolarization. This depolarization may be observed as fasciculations. Subsequent neuromuscular transmission is inhibited so long as adequate concentration of succinylcholine remains at the receptor site. Onset of flaccid paralysis is rapid (less than 1 minute after IV administration), and with single administration lasts approximately 4 to 6 minutes.

Pharmacokinetics: 

Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg.

Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes.

The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds.

Indications: 

• Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal intubation, endoscopic examinations, electrically or pharmacologically induced convulsive therapy) after general anesthesia.
• Drug of choice for skeletal muscle relaxation during orthopedic manipulations.
• Treatment to increase pulmonary compliance during assisted or controlled respiration.

Contraindications: 

Personal or familial history of malignant hyperthermia.
• Myopathies associated with elevated serum creatine kinase (CK, CPK) values.
• Upper motor neuron injury, multiple trauma, extensive or severe burns, extensive denervation of skeletal muscle because of CNS disease or injury. (See Hyperkalemia under Cautions.)
• Known hypersensitivity to succinylcholine or any ingredient in the formulation.

Precautions: 

Succinylcholine should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma.
Succinylcholine may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of succinylcholine will minimize this effect.

Succinylcholine may increase intragastric pressure, which could result in regurgitation and possible aspiration of stomach contents.
Neuromuscular blockade may be prolonged in patients with hypokalemia or hypocalcemia.

Since allergic cross-reactivity has been reported in this class, request information from your patients about previous anaphylactic reactions to other neuromuscular blocking agents. In addition, inform your patients that severe anaphylactic reactions to neuromuscular blocking agents.

Drug Interactions: 

β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

Side Effects: 

Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast breathing; fast, slow, or irregular heartbeat; flushing; high body temperature; increased pressure in the eye; pauses in breathing; pounding in the chest; severe muscle pain with or without decreased urination; severe or persistent dizziness or headache; slowed or shallow breathing; tightening of the jaw or other muscles.

Storage: 

• Store between 2-8 C°
• Protect from light and freezing

Packing: 

• Injection 500mg/10ml:Box of 5 Ampoules

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) ) [field_contraindications] => Array ( [0] => Array ( [value] => Personal or familial history of malignant hyperthermia. • Myopathies associated with elevated serum creatine kinase (CK, CPK) values. • Upper motor neuron injury, multiple trauma, extensive or severe burns, extensive denervation of skeletal muscle because of CNS disease or injury. (See Hyperkalemia under Cautions.) • Known hypersensitivity to succinylcholine or any ingredient in the formulation. [format] => 1 [safe] =>

Personal or familial history of malignant hyperthermia.
• Myopathies associated with elevated serum creatine kinase (CK, CPK) values.
• Upper motor neuron injury, multiple trauma, extensive or severe burns, extensive denervation of skeletal muscle because of CNS disease or injury. (See Hyperkalemia under Cautions.)
• Known hypersensitivity to succinylcholine or any ingredient in the formulation.

[view] =>

Personal or familial history of malignant hyperthermia.
• Myopathies associated with elevated serum creatine kinase (CK, CPK) values.
• Upper motor neuron injury, multiple trauma, extensive or severe burns, extensive denervation of skeletal muscle because of CNS disease or injury. (See Hyperkalemia under Cautions.)
• Known hypersensitivity to succinylcholine or any ingredient in the formulation.

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Injection 500mg/10ml

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Injection 500mg/10ml

) ) [field_drug_interactions] => Array ( [0] => Array ( [value] =>

β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

[format] => 1 [safe] =>

β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

[view] =>

β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

) ) [field_indications] => Array ( [0] => Array ( [value] => • Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal intubation, endoscopic examinations, electrically or pharmacologically induced convulsive therapy) after general anesthesia. • Drug of choice for skeletal muscle relaxation during orthopedic manipulations. • Treatment to increase pulmonary compliance during assisted or controlled respiration. [format] => 1 [safe] =>

• Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal intubation, endoscopic examinations, electrically or pharmacologically induced convulsive therapy) after general anesthesia.
• Drug of choice for skeletal muscle relaxation during orthopedic manipulations.
• Treatment to increase pulmonary compliance during assisted or controlled respiration.

[view] =>

• Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal intubation, endoscopic examinations, electrically or pharmacologically induced convulsive therapy) after general anesthesia.
• Drug of choice for skeletal muscle relaxation during orthopedic manipulations.
• Treatment to increase pulmonary compliance during assisted or controlled respiration.

) ) [field_packing] => Array ( [0] => Array ( [value] => • Injection 500mg/10ml:Box of 5 Ampoules [format] => 1 [safe] =>

• Injection 500mg/10ml:Box of 5 Ampoules

[view] =>

• Injection 500mg/10ml:Box of 5 Ampoules

) ) [field_pdf] => Array ( [0] => Array ( [fid] => 179 [uid] => 1 [filename] => succinylcholine.pdf [filepath] => sites/default/files/pdf/succinylcholine.pdf [filemime] => application/pdf [filesize] => 135676 [status] => 1 [timestamp] => 1329487795 [list] => 1 [data] => [i18nsync] => 1 [nid] => 275 [view] => ) ) [field_pharmacokinetics] => Array ( [0] => Array ( [value] => Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg. Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes. The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds. [format] => 1 [safe] =>

Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg.

Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes.

The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds.

[view] =>

Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg.

Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes.

The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds.

) ) [field_pharmacological_category] => Array ( [0] => Array ( [value] => Neuromuscular Blocking Agents [format] => 1 [safe] =>

Neuromuscular Blocking Agents

[view] =>

Neuromuscular Blocking Agents

) ) [field_precautions] => Array ( [0] => Array ( [value] => Succinylcholine should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma. Succinylcholine may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of succinylcholine will minimize this effect. Succinylcholine may increase intragastric pressure, which could result in regurgitation and possible aspiration of stomach contents. Neuromuscular blockade may be prolonged in patients with hypokalemia or hypocalcemia. Since allergic cross-reactivity has been reported in this class, request information from your patients about previous anaphylactic reactions to other neuromuscular blocking agents. In addition, inform your patients that severe anaphylactic reactions to neuromuscular blocking agents. [format] => 1 [safe] =>

Succinylcholine should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma.
Succinylcholine may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of succinylcholine will minimize this effect.

Succinylcholine may increase intragastric pressure, which could result in regurgitation and possible aspiration of stomach contents.
Neuromuscular blockade may be prolonged in patients with hypokalemia or hypocalcemia.

Since allergic cross-reactivity has been reported in this class, request information from your patients about previous anaphylactic reactions to other neuromuscular blocking agents. In addition, inform your patients that severe anaphylactic reactions to neuromuscular blocking agents.

[view] =>

Succinylcholine should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma.
Succinylcholine may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of succinylcholine will minimize this effect.

Succinylcholine may increase intragastric pressure, which could result in regurgitation and possible aspiration of stomach contents.
Neuromuscular blockade may be prolonged in patients with hypokalemia or hypocalcemia.

Since allergic cross-reactivity has been reported in this class, request information from your patients about previous anaphylactic reactions to other neuromuscular blocking agents. In addition, inform your patients that severe anaphylactic reactions to neuromuscular blocking agents.

) ) [field_pregnancy_category] => Array ( [0] => Array ( [value] => category C [format] => 1 [safe] =>

category C

[view] =>

category C

) ) [field_references] => Array ( [0] => Array ( [value] => [format] => [safe] => [view] => ) ) [field_side_effects] => Array ( [0] => Array ( [value] => Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast breathing; fast, slow, or irregular heartbeat; flushing; high body temperature; increased pressure in the eye; pauses in breathing; pounding in the chest; severe muscle pain with or without decreased urination; severe or persistent dizziness or headache; slowed or shallow breathing; tightening of the jaw or other muscles. [format] => 1 [safe] =>

Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast breathing; fast, slow, or irregular heartbeat; flushing; high body temperature; increased pressure in the eye; pauses in breathing; pounding in the chest; severe muscle pain with or without decreased urination; severe or persistent dizziness or headache; slowed or shallow breathing; tightening of the jaw or other muscles.

[view] =>

Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast breathing; fast, slow, or irregular heartbeat; flushing; high body temperature; increased pressure in the eye; pauses in breathing; pounding in the chest; severe muscle pain with or without decreased urination; severe or persistent dizziness or headache; slowed or shallow breathing; tightening of the jaw or other muscles.

) ) [field_storage] => Array ( [0] => Array ( [value] => • Store between 2-8 C° • Protect from light and freezing [format] => 1 [safe] =>

• Store between 2-8 C°
• Protect from light and freezing

[view] =>

• Store between 2-8 C°
• Protect from light and freezing

) ) [field_therapeutic_category] => Array ( [0] => Array ( [value] => Antimyasthenic, Muscle Relaxant [format] => 1 [safe] =>

Antimyasthenic, Muscle Relaxant

[view] =>

Antimyasthenic, Muscle Relaxant

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Injection 500mg/10ml

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Injection 500mg/10ml

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Neuromuscular Blocking Agents

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Neuromuscular Blocking Agents

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Antimyasthenic, Muscle Relaxant

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Antimyasthenic, Muscle Relaxant

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Antimyasthenic, Muscle Relaxant

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Antimyasthenic, Muscle Relaxant

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Therapeutic Category: 

Antimyasthenic, Muscle Relaxant

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Succinylcholine is a depolarizing skeletal muscle relaxant. As does acetylcholine, it combines with the cholinergic receptors of the motor end plate to produce depolarization. This depolarization may be observed as fasciculations. Subsequent neuromuscular transmission is inhibited so long as adequate concentration of succinylcholine remains at the receptor site. Onset of flaccid paralysis is rapid (less than 1 minute after IV administration), and with single administration lasts approximately 4 to 6 minutes.

[#title] => [#description] => [#printed] => 1 ) [field_pharmacokinetics] => Array ( [#type_name] => product [#context] => full [#field_name] => field_pharmacokinetics [#post_render] => Array ( [0] => content_field_wrapper_post_render ) [#weight] => 4 [field] => Array ( [#description] => [items] => Array ( [0] => Array ( [#formatter] => default [#node] => stdClass Object *RECURSION* [#type_name] => product [#field_name] => field_pharmacokinetics [#weight] => 0 [#theme] => text_formatter_default [#item] => Array ( [value] => Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg. Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes. The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds. [format] => 1 [safe] =>

Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg.

Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes.

The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds.

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Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg.

Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes.

The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds.

) [#title] => [#description] => [#children] =>

Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg.

Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes.

The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds.

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Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg.

Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes.

The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds.

[#printed] => 1 ) [#title] => [#description] => [#children] =>
Pharmacokinetics: 

Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg.

Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes.

The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds.

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• Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal intubation, endoscopic examinations, electrically or pharmacologically induced convulsive therapy) after general anesthesia.
• Drug of choice for skeletal muscle relaxation during orthopedic manipulations.
• Treatment to increase pulmonary compliance during assisted or controlled respiration.

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• Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal intubation, endoscopic examinations, electrically or pharmacologically induced convulsive therapy) after general anesthesia.
• Drug of choice for skeletal muscle relaxation during orthopedic manipulations.
• Treatment to increase pulmonary compliance during assisted or controlled respiration.

) [#title] => [#description] => [#children] =>

• Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal intubation, endoscopic examinations, electrically or pharmacologically induced convulsive therapy) after general anesthesia.
• Drug of choice for skeletal muscle relaxation during orthopedic manipulations.
• Treatment to increase pulmonary compliance during assisted or controlled respiration.

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• Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal intubation, endoscopic examinations, electrically or pharmacologically induced convulsive therapy) after general anesthesia.
• Drug of choice for skeletal muscle relaxation during orthopedic manipulations.
• Treatment to increase pulmonary compliance during assisted or controlled respiration.

[#printed] => 1 ) [#title] => [#description] => [#children] =>
Indications: 

• Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal intubation, endoscopic examinations, electrically or pharmacologically induced convulsive therapy) after general anesthesia.
• Drug of choice for skeletal muscle relaxation during orthopedic manipulations.
• Treatment to increase pulmonary compliance during assisted or controlled respiration.

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Personal or familial history of malignant hyperthermia.
• Myopathies associated with elevated serum creatine kinase (CK, CPK) values.
• Upper motor neuron injury, multiple trauma, extensive or severe burns, extensive denervation of skeletal muscle because of CNS disease or injury. (See Hyperkalemia under Cautions.)
• Known hypersensitivity to succinylcholine or any ingredient in the formulation.

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Personal or familial history of malignant hyperthermia.
• Myopathies associated with elevated serum creatine kinase (CK, CPK) values.
• Upper motor neuron injury, multiple trauma, extensive or severe burns, extensive denervation of skeletal muscle because of CNS disease or injury. (See Hyperkalemia under Cautions.)
• Known hypersensitivity to succinylcholine or any ingredient in the formulation.

) [#title] => [#description] => [#children] =>

Personal or familial history of malignant hyperthermia.
• Myopathies associated with elevated serum creatine kinase (CK, CPK) values.
• Upper motor neuron injury, multiple trauma, extensive or severe burns, extensive denervation of skeletal muscle because of CNS disease or injury. (See Hyperkalemia under Cautions.)
• Known hypersensitivity to succinylcholine or any ingredient in the formulation.

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Personal or familial history of malignant hyperthermia.
• Myopathies associated with elevated serum creatine kinase (CK, CPK) values.
• Upper motor neuron injury, multiple trauma, extensive or severe burns, extensive denervation of skeletal muscle because of CNS disease or injury. (See Hyperkalemia under Cautions.)
• Known hypersensitivity to succinylcholine or any ingredient in the formulation.

[#printed] => 1 ) [#title] => [#description] => [#children] =>
Contraindications: 

Personal or familial history of malignant hyperthermia.
• Myopathies associated with elevated serum creatine kinase (CK, CPK) values.
• Upper motor neuron injury, multiple trauma, extensive or severe burns, extensive denervation of skeletal muscle because of CNS disease or injury. (See Hyperkalemia under Cautions.)
• Known hypersensitivity to succinylcholine or any ingredient in the formulation.

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Succinylcholine should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma.
Succinylcholine may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of succinylcholine will minimize this effect.

Succinylcholine may increase intragastric pressure, which could result in regurgitation and possible aspiration of stomach contents.
Neuromuscular blockade may be prolonged in patients with hypokalemia or hypocalcemia.

Since allergic cross-reactivity has been reported in this class, request information from your patients about previous anaphylactic reactions to other neuromuscular blocking agents. In addition, inform your patients that severe anaphylactic reactions to neuromuscular blocking agents.

[#delta] => 0 ) [#title] => [#description] => [#theme_used] => 1 [#printed] => 1 [#type] => [#value] => [#prefix] => [#suffix] => [#children] =>

Succinylcholine should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma.
Succinylcholine may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of succinylcholine will minimize this effect.

Succinylcholine may increase intragastric pressure, which could result in regurgitation and possible aspiration of stomach contents.
Neuromuscular blockade may be prolonged in patients with hypokalemia or hypocalcemia.

Since allergic cross-reactivity has been reported in this class, request information from your patients about previous anaphylactic reactions to other neuromuscular blocking agents. In addition, inform your patients that severe anaphylactic reactions to neuromuscular blocking agents.

) [#title] => [#description] => [#children] =>

Succinylcholine should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma.
Succinylcholine may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of succinylcholine will minimize this effect.

Succinylcholine may increase intragastric pressure, which could result in regurgitation and possible aspiration of stomach contents.
Neuromuscular blockade may be prolonged in patients with hypokalemia or hypocalcemia.

Since allergic cross-reactivity has been reported in this class, request information from your patients about previous anaphylactic reactions to other neuromuscular blocking agents. In addition, inform your patients that severe anaphylactic reactions to neuromuscular blocking agents.

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Succinylcholine should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma.
Succinylcholine may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of succinylcholine will minimize this effect.

Succinylcholine may increase intragastric pressure, which could result in regurgitation and possible aspiration of stomach contents.
Neuromuscular blockade may be prolonged in patients with hypokalemia or hypocalcemia.

Since allergic cross-reactivity has been reported in this class, request information from your patients about previous anaphylactic reactions to other neuromuscular blocking agents. In addition, inform your patients that severe anaphylactic reactions to neuromuscular blocking agents.

[#printed] => 1 ) [#title] => [#description] => [#children] =>
Precautions: 

Succinylcholine should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma.
Succinylcholine may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of succinylcholine will minimize this effect.

Succinylcholine may increase intragastric pressure, which could result in regurgitation and possible aspiration of stomach contents.
Neuromuscular blockade may be prolonged in patients with hypokalemia or hypocalcemia.

Since allergic cross-reactivity has been reported in this class, request information from your patients about previous anaphylactic reactions to other neuromuscular blocking agents. In addition, inform your patients that severe anaphylactic reactions to neuromuscular blocking agents.

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β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

[format] => 1 [safe] =>

β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

[#delta] => 0 ) [#title] => [#description] => [#theme_used] => 1 [#printed] => 1 [#type] => [#value] => [#prefix] => [#suffix] => [#children] =>

β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

) [#title] => [#description] => [#children] =>

β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

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β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

[#printed] => 1 ) [#title] => [#description] => [#children] =>
Drug Interactions: 

β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

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Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast breathing; fast, slow, or irregular heartbeat; flushing; high body temperature; increased pressure in the eye; pauses in breathing; pounding in the chest; severe muscle pain with or without decreased urination; severe or persistent dizziness or headache; slowed or shallow breathing; tightening of the jaw or other muscles.

[#delta] => 0 ) [#title] => [#description] => [#theme_used] => 1 [#printed] => 1 [#type] => [#value] => [#prefix] => [#suffix] => [#children] =>

Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast breathing; fast, slow, or irregular heartbeat; flushing; high body temperature; increased pressure in the eye; pauses in breathing; pounding in the chest; severe muscle pain with or without decreased urination; severe or persistent dizziness or headache; slowed or shallow breathing; tightening of the jaw or other muscles.

) [#title] => [#description] => [#children] =>

Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast breathing; fast, slow, or irregular heartbeat; flushing; high body temperature; increased pressure in the eye; pauses in breathing; pounding in the chest; severe muscle pain with or without decreased urination; severe or persistent dizziness or headache; slowed or shallow breathing; tightening of the jaw or other muscles.

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Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast breathing; fast, slow, or irregular heartbeat; flushing; high body temperature; increased pressure in the eye; pauses in breathing; pounding in the chest; severe muscle pain with or without decreased urination; severe or persistent dizziness or headache; slowed or shallow breathing; tightening of the jaw or other muscles.

[#printed] => 1 ) [#title] => [#description] => [#children] =>
Side Effects: 

Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast breathing; fast, slow, or irregular heartbeat; flushing; high body temperature; increased pressure in the eye; pauses in breathing; pounding in the chest; severe muscle pain with or without decreased urination; severe or persistent dizziness or headache; slowed or shallow breathing; tightening of the jaw or other muscles.

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• Store between 2-8 C°
• Protect from light and freezing

[#delta] => 0 ) [#title] => [#description] => [#theme_used] => 1 [#printed] => 1 [#type] => [#value] => [#prefix] => [#suffix] => [#children] =>

• Store between 2-8 C°
• Protect from light and freezing

) [#title] => [#description] => [#children] =>

• Store between 2-8 C°
• Protect from light and freezing

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• Store between 2-8 C°
• Protect from light and freezing

[#printed] => 1 ) [#title] => [#description] => [#children] =>
Storage: 

• Store between 2-8 C°
• Protect from light and freezing

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• Injection 500mg/10ml:Box of 5 Ampoules

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• Injection 500mg/10ml:Box of 5 Ampoules

) [#title] => [#description] => [#children] =>

• Injection 500mg/10ml:Box of 5 Ampoules

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• Injection 500mg/10ml:Box of 5 Ampoules

[#printed] => 1 ) [#title] => [#description] => [#children] =>
Packing: 

• Injection 500mg/10ml:Box of 5 Ampoules

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Image: 
Brand Name: 

-

Dosage Form: 

Injection 500mg/10ml

Pharmacological Category: 

Neuromuscular Blocking Agents

Therapeutic Category: 

Antimyasthenic, Muscle Relaxant

Pregnancy Category: 

category C

Succinylcholine is a depolarizing skeletal muscle relaxant. As does acetylcholine, it combines with the cholinergic receptors of the motor end plate to produce depolarization. This depolarization may be observed as fasciculations. Subsequent neuromuscular transmission is inhibited so long as adequate concentration of succinylcholine remains at the receptor site. Onset of flaccid paralysis is rapid (less than 1 minute after IV administration), and with single administration lasts approximately 4 to 6 minutes.

Pharmacokinetics: 

Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action. The ED95 of succinylcholine (the dose causing on average 95% suppression of neuromuscular response) is 0.51 to 0.63 mg/kg. Using cumulative dose-response techniques, Kopman and coworkers estimated that its potency is far greater, with an ED95 of less than 0.3 mg/kg.

Administration of 1 mg/kg of succinylcholine results in complete suppression of response to neuromuscular stimulation in approximately 60 seconds. In patients with genotypically normal butyrylcholinesterase (also known as plasma cholinesterase or pseudocholinesterase) activity, recovery to 90% muscle strength after the administration of 1 mg/kg succinylcholine requires 9 to 13 minutes.

The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase to succinylmonocholine and choline. Butyrylcholinesterase has an enormous capacity to hydrolyze succinylcholine, and only 10% of the administered drug reaches the neuromuscular junction. The initial metabolite, succinylmonocholine, is a much weaker neuromuscular blocking agent than succinylcholine and is metabolized much more slowly to succinic acid and choline. The elimination half-life of succinylcholine is estimated to be 47 seconds.

Indications: 

• Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal intubation, endoscopic examinations, electrically or pharmacologically induced convulsive therapy) after general anesthesia.
• Drug of choice for skeletal muscle relaxation during orthopedic manipulations.
• Treatment to increase pulmonary compliance during assisted or controlled respiration.

Contraindications: 

Personal or familial history of malignant hyperthermia.
• Myopathies associated with elevated serum creatine kinase (CK, CPK) values.
• Upper motor neuron injury, multiple trauma, extensive or severe burns, extensive denervation of skeletal muscle because of CNS disease or injury. (See Hyperkalemia under Cautions.)
• Known hypersensitivity to succinylcholine or any ingredient in the formulation.

Precautions: 

Succinylcholine should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma.
Succinylcholine may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of succinylcholine will minimize this effect.

Succinylcholine may increase intragastric pressure, which could result in regurgitation and possible aspiration of stomach contents.
Neuromuscular blockade may be prolonged in patients with hypokalemia or hypocalcemia.

Since allergic cross-reactivity has been reported in this class, request information from your patients about previous anaphylactic reactions to other neuromuscular blocking agents. In addition, inform your patients that severe anaphylactic reactions to neuromuscular blocking agents.

Drug Interactions: 

β-Adrenergic blocking agents

Possible increased neuromuscular blockade

 

Anesthetics, inhalation (e.g., desflurane, isoflurane)

Possible increased neuromuscular blockade

 

Antiarrhythmic agents (lidocaine, procainamide, quinidine)

Possible increased neuromuscular blockade

 

Anti-infective agents (aminoglycosides, bacitracin, clindamycin, lincomycin, polymyxins, tetracyclines)

Possible increased neuromuscular blockade

 

Antimalarials (chloroquine, quinine)

Possible increased neuromuscular blockade

 

Aprotinin

Possible increased neuromuscular blockade

 

Cholinesterase inhibitors (demecarium, isofluorophate, organophosphate insecticides)

Decreased activity of plasma pseudocholinesterase

 

Contraceptives, oral

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Corticosteroids

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Cyclophosphamide

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Lithium

Possible increased neuromuscular blockade

 

Magnesium salts

Possible increased neuromuscular blockade

 

MAO inhibitors

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Metoclopramide

Possible increased neuromuscular blockade

 

Neostigmine

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Oxytocin

Possible increased neuromuscular blocking effect

 

Phenothiazines

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Procaine

Potential decreased metabolism of succinylcholine

Concurrent IV administration not recommended

Skeletal muscle relaxants (pancuronium)

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

Terbutaline

Possible increased neuromuscular blockade

 

Thiotepa

Possible decreased plasma cholinesterase activity and increased neuromuscular blockade

 

 

Side Effects: 

Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast breathing; fast, slow, or irregular heartbeat; flushing; high body temperature; increased pressure in the eye; pauses in breathing; pounding in the chest; severe muscle pain with or without decreased urination; severe or persistent dizziness or headache; slowed or shallow breathing; tightening of the jaw or other muscles.

Storage: 

• Store between 2-8 C°
• Protect from light and freezing

Packing: 

• Injection 500mg/10ml:Box of 5 Ampoules

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CONTACT US:

Head Office:
Address: No.1, Beastoon Ave., Dr. Fatemi Sq., Tehran1431663135 Iran
Tel: (+98 21)-889 65323
Fax: (+98 21)-889 57056
Factory:
Address: Caspian tamin Pharmaceutical Co., Entrance 1, Rasht Industrial Zone, Rasht, Guilan, Iran
Tel: (+98 131) 338-2511- 8
Fax: (+98 131) 338 – 2517