Suxamethonium Cl

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Suxamethonium Cl uses


WARNING

RISK OF CARDIAC ARREST FROM HYPERKALEMIC RHABDOMYOLYSIS

There have been rare reports of acute rhabdomyolysis with hyperkalemia followed by ventricular dysrhythmias, cardiac arrest, and death after the administration of Suxamethonium Cl to apparently healthy children who were subsequently found to have undiagnosed skeletal muscle myopathy, most frequently Duchenne's muscular dystrophy.

This syndrome often presents as peaked T-waves and sudden cardiac arrest within minutes after the administration of the drug in healthy appearing children (usually, but not exclusively, males, and most frequently 8 years of age or younger). There have also been reports in adolescents.

Therefore, when a healthy appearing infant or child develops cardiac arrest soon after administration of Suxamethonium Cl not felt to be due to inadequate ventilation, oxygenation, or anesthetic overdose, immediate treatment for hyperkalemia should be instituted. This should include administration of intravenous calcium, bicarbonate, and glucose with insulin, with hyperventilation. Due to the abrupt onset of this syndrome, routine resuscitative measures are likely to be unsuccessful. However, extraordinary and prolonged resuscitative efforts have resulted in successful resuscitation in some reported cases. In addition, in the presence of signs of malignant hyperthermia, appropriate treatment should be instituted concurrently.

Since there may be no signs or symptoms to alert the practitioner to which patients are at risk, it is recommended that the use of Suxamethonium Cl in children should be reserved for emergency intubation or instances where immediate securing of the airway is necessary, e.g. laryngospasm, difficult airway, full stomach, or for intramuscular use when a suitable vein is inaccessible (see PRECAUTIONS: Pediatric Use and DOSAGE AND ADMINISTRATION ).

This drug should be used only by individuals familiar with its actions, characteristics, and hazards.

DESCRIPTION

Suxamethonium Cl (succinylcholine chloride) is an ultra short-acting depolarizing-type, skeletal muscle relaxant for intravenous (IV) administration.

Suxamethonium Cl chloride is a white, odorless, slightly bitter powder and very soluble in water. The drug is unstable in alkaline solutions but relatively stable in acid solutions, depending upon the concentration of the solution and the storage temperature. Solutions of Suxamethonium Cl chloride should be stored under refrigeration to preserve potency. Suxamethonium Cl Injection is a sterile nonpyrogenic solution for IV injection, containing 20 mg Suxamethonium Cl chloride in each mL and made isotonic with sodium chloride. The pH is adjusted to 3.5 with hydrochloric acid. Methylparaben (0.1%) is added as a preservative.

The chemical name for Suxamethonium Cl chloride is 2,2'-[(1,4-dioxo-1,4-butanediyl)bis(oxy)]bis[N,N,N-trimethylethanaminium] dichloride, and the structural formula is:

Suxamethonium Cl Suxamethonium Cl Chloride Chemical Structure

CLINICAL PHARMACOLOGY

Suxamethonium Cl 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 Suxamethonium Cl 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.

Suxamethonium Cl is rapidly hydrolyzed by plasma cholinesterase to succinylmonocholine (which possesses clinically insignificant depolarizing muscle relaxant properties) and then more slowly to succinic acid and choline (see PRECAUTIONS ). About 10% of the drug is excreted unchanged in the urine. The paralysis following administration of Suxamethonium Cl is progressive, with differing sensitivities of different muscles. This initially involves consecutively the levator muscles of the face, muscles of the glottis, and finally, the intercostals and the diaphragm and all other skeletal muscles.

Suxamethonium Cl has no direct action on the uterus or other smooth muscle structures. Because it is highly ionized and has low fat solubility, it does not readily cross the placenta.

Tachyphylaxis occurs with repeated administration (see PRECAUTIONS ).

Depending on the dose and duration of Suxamethonium Cl administration, the characteristic depolarizing neuromuscular block (Phase I block) may change to a block with characteristics superficially resembling a nondepolarizing block (Phase II block). This may be associated with prolonged respiratory muscle paralysis or weakness in patients who manifest the transition to Phase II block. When this diagnosis is confirmed by peripheral nerve stimulation, it may sometimes be reversed with anticholinesterase drugs such as neostigmine (see PRECAUTIONS ). Anticholinesterase drugs may not always be effective. If given before Suxamethonium Cl is metabolized by cholinesterase, anticholinesterase drugs may prolong rather than shorten paralysis.

Suxamethonium Cl has no direct effect on the myocardium. Suxamethonium Cl stimulates both autonomic ganglia and muscarinic receptors which may cause changes in cardiac rhythm, including cardiac arrest. Changes in rhythm, including cardiac arrest, may also result from vagal stimulation, which may occur during surgical procedures, or from hyperkalemia, particularly in children (see PRECAUTIONS: Pediatric Use ). These effects are enhanced by halogenated anesthetics.

Suxamethonium Cl causes an increase in intraocular pressure immediately after its injection and during the fasciculation phase, and slight increases which may persist after onset of complete paralysis (see WARNINGS ).

Suxamethonium Cl may cause slight increases in intracranial pressure immediately after its injection and during the fasciculation phase (see PRECAUTIONS ).

As with other neuromuscular blocking agents, the potential for releasing histamine is present following Suxamethonium Cl administration. Signs and symptoms of histamine-mediated release such as flushing, hypotension, and bronchoconstriction are, however, uncommon in normal clinical usage.

Suxamethonium Cl has no effect on consciousness, pain threshold, or cerebration. It should be used only with adequate anesthesia (see WARNINGS ).

INDICATIONS AND USAGE

Suxamethonium Cl chloride is indicated as an adjunct to general anesthesia, to facilitate tracheal intubation, and to provide skeletal muscle relaxation during surgery or mechanical ventilation.

CONTRAINDICATIONS

Suxamethonium Cl is contraindicated in persons with personal or familial history of malignant hyperthermia, skeletal muscle myopathies, and known hypersensitivity to the drug. It is also contraindicated in patients after the acute phase of injury following major burns, multiple trauma, extensive denervation of skeletal muscle, or upper motor neuron injury, because Suxamethonium Cl administered to such individuals may result in severe hyperkalemia which may result in cardiac arrest (see WARNINGS ). The risk of hyperkalemia in these patients increases over time and usually peaks at 7 to 10 days after the injury. The risk is dependent on the extent and location of the injury. The precise time of onset and the duration of the risk period are not known.

WARNINGS

Suxamethonium Cl SHOULD BE USED ONLY BY THOSE SKILLED IN THE MANAGEMENT OF ARTIFICIAL RESPIRATION AND ONLY WHEN FACILITIES ARE INSTANTLY AVAILABLE FOR TRACHEAL INTUBATION AND FOR PROVIDING ADEQUATE VENTILATION OF THE PATIENT, INCLUDING THE ADMINISTRATION OF OXYGEN UNDER POSITIVE PRESSURE AND THE ELIMINATION OF CARBON DIOXIDE. THE CLINICIAN MUST BE PREPARED TO ASSIST OR CONTROL RESPIRATION.

TO AVOID DISTRESS TO THE PATIENT, Suxamethonium Cl SHOULD NOT BE ADMINISTERED BEFORE UNCONSCIOUSNESS HAS BEEN INDUCED. IN EMERGENCY SITUATIONS, HOWEVER, IT MAY BE NECESSARY TO ADMINISTER Suxamethonium Cl BEFORE UNCONSCIOUSNESS IS INDUCED.

Suxamethonium Cl IS METABOLIZED BY PLASMA CHOLINESTERASE AND SHOULD BE USED WITH CAUTION, IF AT ALL, IN PATIENTS KNOWN TO BE OR SUSPECTED OF BEING HOMOZYGOUS FOR THE ATYPICAL PLASMA CHOLINESTERASE GENE.

Anaphylaxis

Severe anaphylactic reactions to neuromuscular blocking agents, including Suxamethonium Cl, have been reported. These reactions have in some cases been life-threatening and fatal. Due to the potential severity of these reactions, the necessary precautions, such as the immediate availability of appropriate emergency treatment, should be taken. Precautions should also be taken in those individuals who have had previous anaphylactic reactions to other neuromuscular blocking agents since cross-reactivity between neuromuscular blocking agents, both depolarizing and non-depolarizing, has been reported in this class of drugs.

Hyperkalemia

Suxamethonium Cl should be administered with GREAT CAUTION to patients suffering from electrolyte abnormalities and those who may have massive digitalis toxicity, because in these circumstances Suxamethonium Cl may induce serious cardiac arrhythmias or cardiac arrest due to hyperkalemia.

GREAT CAUTION should be observed if Suxamethonium Cl is administered to patients during the acute phase of injury following major burns, multiple trauma, extensive denervation of skeletal muscle, or upper motor neuron injury (see CONTRAINDICATIONS ). The risk of hyperkalemia in these patients increases over time and usually peaks at 7 to 10 days after the injury. The risk is dependent on the extent and location of the injury. The precise time of onset and the duration of the risk period are undetermined. Patients with chronic abdominal infection, subarachnoid hemorrhage, or conditions causing degeneration of central and peripheral nervous systems should receive Suxamethonium Cl with GREAT CAUTION because of the potential for developing severe hyperkalemia.

Malignant Hyperthermia

Suxamethonium Cl administration has been associated with acute onset of malignant hyperthermia, a potentially fatal hypermetabolic state of skeletal muscle. The risk of developing malignant hyperthermia following Suxamethonium Cl administration increases with the concomitant administration of volatile anesthetics. Malignant hyperthermia frequently presents as intractable spasm of the jaw muscles (masseter spasm) which may progress to generalized rigidity, increased oxygen demand, tachycardia, tachypnea, and profound hyperpyrexia. Successful outcome depends on recognition of early signs, such as jaw muscle spasm, acidosis, or generalized rigidity to initial administration of Suxamethonium Cl for tracheal intubation, or failure of tachycardia to respond to deepening anesthesia. Skin mottling, rising temperature, and coagulopathies may occur later in the course of the hypermetabolic process. Recognition of the syndrome is a signal for discontinuance of anesthesia, attention to increased oxygen consumption, correction of acidosis, support of circulation, assurance of adequate urinary output, and institution of measures to control rising temperature. Intravenous dantrolene sodium is recommended as an adjunct to supportive measures in the management of this problem. Consult literature references and the dantrolene prescribing information for additional information about the management of malignant hyperthermic crisis. Continuous monitoring of temperature and expired CO2 is recommended as an aid to early recognition of malignant hyperthermia.

Other

In both adults and children, the incidence of bradycardia, which may progress to asystole, is higher following a second dose of Suxamethonium Cl. The incidence and severity of bradycardia is higher in children than in adults. Pretreatment with anticholinergic agents (e.g., atropine) may reduce the occurrence of bradyarrhythmias.

Suxamethonium Cl causes an increase in intraocular pressure. It should not be used in instances in which an increase in intraocular pressure is undesirable (e.g., narrow angle glaucoma, penetrating eye injury) unless the potential benefit of its use outweighs the potential risk.

Suxamethonium Cl is acidic (pH = 3.5) and should not be mixed with alkaline solutions having a pH greater than 8.5 (e.g., barbiturate solutions).

PRECAUTIONS


General

When Suxamethonium Cl is given over a prolonged period of time, the characteristic depolarization block of the myoneural junction (Phase I block) may change to a block with characteristics superficially resembling a nondepolarizing block (Phase II block). Prolonged respiratory muscle paralysis or weakness may be observed in patients manifesting this transition to Phase II block. The transition from Phase I to Phase II block has been reported in seven of seven patients studied under halothane anesthesia after an accumulated dose of 2 to 4 mg/kg Suxamethonium Cl (administered in repeated, divided doses). The onset of Phase II block coincided with the onset of tachyphylaxis and prolongation of spontaneous recovery. In another study, using balanced anesthesia (N2O/O2/narcotic-thiopental) and Suxamethonium Cl infusion, the transition was less abrupt, with great individual variability in the dose of Suxamethonium Cl required to produce Phase II block. Of 32 patients studied, 24 developed Phase II block. Tachyphylaxis was not associated with the transition to Phase II block, and 50% of the patients who developed Phase II block experienced prolonged recovery.

When Phase II block is suspected in cases of prolonged neuromuscular blockade, positive diagnosis should be made by peripheral nerve stimulation prior to administration of any anticholinesterase drug. Reversal of Phase II block is a medical decision which must be made upon the basis of the individual, clinical pharmacology, and the experience and judgment of the physician. The presence of Phase II block is indicated by fade of responses to successive stimuli (preferably “train-of-four”). The use of an anticholinesterase drug to reverse Phase II block should be accompanied by appropriate doses of an anticholinergic drug to prevent disturbances of cardiac rhythm. After adequate reversal of Phase II block with an anticholinesterase agent, the patient should be continually observed for at least 1 hour for signs of return of muscle relaxation. Reversal should not be attempted unless: (1) a peripheral nerve stimulator is used to determine the presence of Phase II block (since anticholinesterase agents will potentiate succinylcholine-induced Phase I block), and (2) spontaneous recovery of muscle twitch has been observed for at least 20 minutes and has reached a plateau with further recovery proceeding slowly; this delay is to ensure complete hydrolysis of Suxamethonium Cl by plasma cholinesterase prior to administration of the anticholinesterase agent. Should the type of block be misdiagnosed, depolarization of the type initially induced by Suxamethonium Cl (i.e., Phase I block) will be prolonged by an anticholinesterase agent.

Suxamethonium Cl should be employed with caution in patients with fractures or muscle spasm because the initial muscle fasciculations may cause additional trauma.

Suxamethonium Cl may cause a transient increase in intracranial pressure; however, adequate anesthetic induction prior to administration of Suxamethonium Cl will minimize this effect.

Suxamethonium Cl 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, including Suxamethonium Cl have been reported.

Reduced Plasma Cholinesterase Activity

Suxamethonium Cl should be used carefully in patients with reduced plasma cholinesterase activity. The likelihood of prolonged neuromuscular block following administration of Suxamethonium Cl must be considered in such patients (see DOSAGE AND ADMINISTRATION ).

Plasma cholinesterase activity may be diminished in the presence of genetic abnormalities of plasma cholinesterase (e.g., patients heterozygous or homozygous for atypical plasma cholinesterase gene), pregnancy, severe liver or kidney disease, malignant tumors, infections, burns, anemia, decompensated heart disease, peptic ulcer, or myxedema. Plasma cholinesterase activity may also be diminished by chronic administration of oral contraceptives, glucocorticoids, or certain monoamine oxidase inhibitors, and by irreversible inhibitors of plasma cholinesterase (e.g., organophosphate insecticides, echothiophate, and certain antineoplastic drugs).

Patients homozygous for atypical plasma cholinesterase gene (1 in 2500 patients) are extremely sensitive to the neuromuscular blocking effect of Suxamethonium Cl. In these patients, a 5- to 10-mg test dose of Suxamethonium Cl may be administered to evaluate sensitivity to Suxamethonium Cl, or neuromuscular blockade may be produced by the cautious administration of a 1-mg/mL solution of Suxamethonium Cl by slow IV infusion. Apnea or prolonged muscle paralysis should be treated with controlled respiration.

Drug Interactions

Drugs which may enhance the neuromuscular blocking action of Suxamethonium Cl include: promazine, oxytocin, aprotinin, certain non-penicillin antibiotics, quinidine, β-adrenergic blockers, procainamide, lidocaine, trimethaphan, lithium carbonate, magnesium salts, quinine, chloroquine, diethylether, isoflurane, desflurane, metoclopramide, and terbutaline. The neuromuscular blocking effect of Suxamethonium Cl may be enhanced by drugs that reduce plasma cholinesterase activity (e.g., chronically administered oral contraceptives, glucocorticoids, or certain monoamine oxidase inhibitors) or by drugs that irreversibly inhibit plasma cholinesterase (see PRECAUTIONS ).

If other neuromuscular blocking agents are to be used during the same procedure, the possibility of a synergistic or antagonistic effect should be considered.

Carcinogenesis, Mutagenesis, Impairment of Fertility

There have been no long-term studies performed in animals to evaluate carcinogenic potential.

Pregnancy

Teratogenic Effects

Pregnancy Category C

Animal reproduction studies have not been conducted with Suxamethonium Cl chloride. It is also not known whether Suxamethonium Cl can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Suxamethonium Cl should be given to a pregnant woman only if clearly needed.

Nonteratogenic Effects

Plasma cholinesterase levels are decreased by approximately 24% during pregnancy and for several days postpartum. Therefore, a higher proportion of patients may be expected to show increased sensitivity to Suxamethonium Cl when pregnant than when nonpregnant.

Labor and Delivery

Suxamethonium Cl is commonly used to provide muscle relaxation during delivery by cesarean section. While small amounts of Suxamethonium Cl are known to cross the placental barrier, under normal conditions the quantity of drug that enters fetal circulation after a single dose of 1 mg/kg to the mother should not endanger the fetus. However, since the amount of drug that crosses the placental barrier is dependent on the concentration gradient between the maternal and fetal circulations, residual neuromuscular blockade (apnea and flaccidity) may occur in the neonate after repeated high doses to, or in the presence of atypical plasma cholinesterase in, the mother.

Nursing Mothers

It is not known whether Suxamethonium Cl is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised following Suxamethonium Cl administration to a nursing woman.

Pediatric Use

There are rare reports of ventricular dysrhythmias and cardiac arrest secondary to acute rhabdomyolysis with hyperkalemia in apparently healthy children who receive Suxamethonium Cl (see BOX WARNING ). Many of these children were subsequently found to have a skeletal muscle myopathy such as Duchenne’s muscular dystrophy whose clinical signs were not obvious. The syndrome often presents as sudden cardiac arrest within minutes after the administration of Suxamethonium Cl. These children are usually, but not exclusively, males, and most frequently 8 years of age or younger. There have also been reports in adolescents. There may be no signs or symptoms to alert the practitioner to which patients are at risk. A careful history and physical may identify developmental delays suggestive of a myopathy. A preoperative creatine kinase could identify some but not all patients at risk. Due to the abrupt onset of this syndrome, routine resuscitative measures are likely to be unsuccessful. Careful monitoring of the electrocardiogram may alert the practitioner to peaked T-waves (an early sign). Administration of IV calcium, bicarbonate, and glucose with insulin, with hyperventilation have resulted in successful resuscitation in some of the reported cases. Extraordinary and prolonged resuscitative efforts have been effective in some cases. In addition, in the presence of signs of malignant hyperthermia, appropriate treatment should be initiated concurrently (see WARNINGS ). Since it is difficult to identify which patients are at risk, it is recommended that the use of Suxamethonium Cl in children should be reserved for emergency intubation or instances where immediate securing of the airway is necessary, e.g., laryngospasm, difficult airway, full stomach, or for intramuscular use when a suitable vein is inaccessible.

As in adults, the incidence of bradycardia in children is higher following the second dose of Suxamethonium Cl. The incidence and severity of bradycardia is higher in children than in adults. Pretreatment with anticholinergic agents, e.g., atropine, may reduce the occurrence of bradyarrhythmias.

ADVERSE REACTIONS

Adverse reactions to Suxamethonium Cl consist primarily of an extension of its pharmacological actions. Suxamethonium Cl causes profound muscle relaxation resulting in respiratory depression to the point of apnea; this effect may be prolonged. Hypersensitivity reactions, including anaphylaxis, may occur in rare instances. The following additional adverse reactions have been reported: cardiac arrest, malignant hyperthermia, arrhythmias, bradycardia, tachycardia, hypertension, hypotension, hyperkalemia, prolonged respiratory depression or apnea, increased intraocular pressure, muscle fasciculation, jaw rigidity, postoperative muscle pain, rhabdomyolysis with possible myoglobinuric acute renal failure, excessive salivation, and rash.

There have been post-marketing reports of severe allergic reactions (anaphylactic and anaphylactoid reactions) associated with use of neuromuscular blocking agents, including Suxamethonium Cl. These reactions, in some cases, have been life-threatening and fatal. Because these reactions were reported voluntarily from a population of uncertain size, it is not possible to reliably estimate their frequency (see WARNINGS and PRECAUTIONS ).

OVERDOSAGE

Overdosage with Suxamethonium Cl may result in neuromuscular block beyond the time needed for surgery and anesthesia. This may be manifested by skeletal muscle weakness, decreased respiratory reserve, low tidal volume, or apnea. The primary treatment is maintenance of a patent airway and respiratory support until recovery of normal respiration is assured. Depending on the dose and duration of Suxamethonium Cl administration, the characteristic depolarizing neuromuscular block (Phase I) may change to a block with characteristics superficially resembling a nondepolarizing block (Phase II) (see PRECAUTIONS ).

DOSAGE AND ADMINISTRATION

The dosage of Suxamethonium Cl should be individualized and should always be determined by the clinician after careful assessment of the patient.

Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration whenever solution and container permit. Solutions which are not clear and colorless should not be used.

Adults

For Short Surgical Procedures

The average dose required to produce neuromuscular blockade and to facilitate tracheal intubation is 0.6 mg/kg Suxamethonium Cl Injection given intravenously. The optimum dose will vary among individuals and may be from 0.3 to 1.1 mg/kg for adults. Following administration of doses in this range, neuromuscular blockade develops in about 1 minute; maximum blockade may persist for about 2 minutes, after which recovery takes place within 4 to 6 minutes. However, very large doses may result in more prolonged blockade. A 5- to 10-mg test dose may be used to determine the sensitivity of the patient and the individual recovery time.

For Long Surgical Procedures

The dose of Suxamethonium Cl administered by infusion depends upon the duration of the surgical procedure and the need for muscle relaxation. The average rate for an adult ranges between 2.5 and 4.3 mg per minute.

Solutions containing from 1 to 2 mg per mL Suxamethonium Cl have commonly been used for continuous infusion. The more dilute solution (1 mg per mL) is probably preferable from the standpoint of ease of control of the rate of administration of the drug and, hence, of relaxation. This IV solution containing 1 mg per mL may be administered at a rate of 0.5 mg (0.5 mL) to 10 mg (10 mL) per minute to obtain the required amount of relaxation. The amount required per minute will depend upon the individual response as well as the degree of relaxation required. Avoid overburdening the circulation with a large volume of fluid. It is recommended that neuromuscular function be carefully monitored with a peripheral nerve stimulator when using Suxamethonium Cl by infusion in order to avoid overdose, detect development of Phase II block, follow its rate of recovery, and assess the effects of reversing agents (see PRECAUTIONS ).

Intermittent IV injections of Suxamethonium Cl may also be used to provide muscle relaxation for long procedures. An IV injection of 0.3 to 1.1 mg/kg may be given initially, followed, at appropriate intervals, by further injections of 0.04 to 0.07 mg/kg to maintain the degree of relaxation required.

Pediatrics

For emergency tracheal intubation or in instances where immediate securing of the airway is necessary, the IV dose of Suxamethonium Cl is 2 mg/kg for infants and small children; for older children and adolescents the dose is 1 mg/kg.

Rarely, IV bolus administration of Suxamethonium Cl in infants and children may result in malignant ventricular arrhythmias and cardiac arrest secondary to acute rhabdomyolysis with hyperkalemia. In such situations, an underlying myopathy should be suspected.

Intravenous bolus administration of Suxamethonium Cl in infants or children may result in profound bradycardia or, rarely, asystole. As in adults, the incidence of bradycardia in children is higher following a second dose of Suxamethonium Cl. The occurrence of bradyarrhythmias may be reduced by pretreatment with atropine (see PRECAUTIONS: Pediatric Use ).

Intramuscular Use

If necessary, Suxamethonium Cl may be given intramuscularly to infants, older children, or adults when a suitable vein is inaccessible. A dose of up to 3 to 4 mg/kg may be given, but not more than 150 mg total dose should be administered by this route. The onset of effect of Suxamethonium Cl given intramuscularly is usually observed in about 2 to 3 minutes.

Compatibility and Admixtures

Suxamethonium Cl is acidic (pH 3.5) and should not be mixed with alkaline solutions having a pH greater than 8.5 (e.g., barbiturate solutions). Suxamethonium Cl Injection is stable for 24 hours after dilution to a final concentration of 1 to 2 mg/mL in 5% Dextrose Injection, USP or 0.9% Sodium Chloride Injection, USP. Aseptic techniques should be used to prepare the diluted product. Admixtures of Suxamethonium Cl should be prepared for single patient use only. The unused portion of diluted Suxamethonium Cl should be discarded.

HOW SUPPLIED

For immediate injection of single doses for short procedures: Suxamethonium Cl (succinylcholine chloride) Injection, 20 mg in each mL.

Multiple-dose vials of 10 mL, box of 10 vials (NDC 0781-3009-95).

Store in refrigerator at 2° to 8°C (36° to 46°F). The multi-dose vials are stable for up to 14 days at room temperature without significant loss of potency.

Manufactured by

Agila Specialties Pvt. Ltd.

(Specialty Formulation Facility)

Bangalore – 560 105, India for

Sandoz Inc.

Princeton, NJ 08540

04-2011

1016206

Manufactured by

Agila Specialties Pvt. Ltd.

(Sterile Product Division)

Bangalore – 560 076, India for

Sandoz Inc.

Princeton, NJ 08540

04-2011

1016227

NDC 0781-3009-70

Anectine®

(succinylcholine

chloride injection, USP)

200 mg/10 mL

(20 mg/mL)

WARNING: Paralyzing Agent.

Causes Respiratory Arrest.

Multiple-Dose Vial

SANDOZ

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References

  1. Dailymed."ANECTINE (SUCCINYLCHOLINE CHLORIDE) INJECTION, SOLUTION [SANDOZ INC]". https://dailymed.nlm.nih.gov/dailym... (accessed August 28, 2018).
  2. "succinylcholine". https://pubchem.ncbi.nlm.nih.gov/co... (accessed August 28, 2018).
  3. "succinylcholine". http://www.drugbank.ca/drugs/DB0020... (accessed August 28, 2018).

Frequently asked Questions

Can i drive or operate heavy machine after consuming Suxamethonium Cl?

Depending on the reaction of the Suxamethonium Cl after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Suxamethonium Cl not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.

Is Suxamethonium Cl addictive or habit forming?

Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.

Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.

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