Suxamethonium Cl Martindale

Suxamethonium Cl Martindale





International Med
Full Prescribing Info
Suxamethonium chloride.
Each 2ml ampoule contains 100mg of Suxamethonium Chloride.
Excipients/Inactive Ingredients: Hydrochloric Acid, Water for Injections, Nitrogen.
Pharmacology: Pharmacodynamics: Suxamethonium is closely related in structure to acetylcholine. Suxamethonium is quickly hydrolysed by plasma cholinesterase. Suxamethonium acts on the skeletal muscle motor endplate just like acetylcholine as an agonist, to cause flaccid paralysis of muscle (phase 1 block). Suxamethonium diffuses slowly to the endplate and the concentration at the endplate persists for long enough to cause loss of electrical excitability. The depolarization of the muscle endplate establishes a voltage gradient and this causes opening of voltage-dependent ion channels of the muscle leading to transient contraction of the muscle. Although the end-plate stays depolarised, the muscle membrane accounts for this depolarization and remains flaccid. If suxamethonium is kept continuously present during infusion, the junctional membrane slowly regains its resting potential with the return of neuromuscular transmission; to maintain the effect, a higher infusion rate is required (tachyphylaxis). With continued infusion, neuromuscular transmission will fail again (phase 2 block) even though the membrane potential of the end-plate stays unchanged and normal or near normal. A phase 2 block has clinical characteristics of a non-depolarizing block. A phase 2 block may be associated with prolonged neuromuscular blockade and apnoea. The mechanism of this block is not known but channel blocking by penetration of suxamethonium into the sub-end plate cytoplasm, intracellular accumulation of calcium and sodium, the loss of intracellular potassium, and activation of Na,K-ATPase all contribute.
Pharmacokinetics: Neuromuscular-blocking drugs are used mainly in anaesthesia to produce muscle relaxation. Although complete relaxation can be produced by anaesthetic drugs alone, the concentrations needed to obliterate spinal reflexes are high and it is much more satisfactory to produce paralysis by blocking neuromuscular transmission. The drugs are given intravenously, and act within about 30 to 60 seconds. Suxamethonium acts for about 2 to 6 minutes, being hydrolysed by plasma cholinesterase (pseudocholinesterase). One molecule of choline is split off rapidly to form succinylmonocholine (a weak muscle relaxant), which is then slowly hydrolysed to succinic acid and choline. Only a small proportion of suxamethonium is excreted unchanged in the urine.
Toxicology: Preclinical safety data: There is no pre-clinical data of relevance to the prescriber which is additional to that already included in other sections of the monograph.
Used in anaesthesia as a muscle relaxant to facilitate endotracheal intubation, mechanical ventilation and a wide range of surgical and obstetrics procedures.
It is also used to reduce the intensity of muscular contractions associated with pharmacologically or electrically - induced convulsions.
Dosage/Direction for Use
Usually by bolus injection.
Adults and Children over 12 years: The dose is dependent on body weight, the degree of muscular relaxation required, the route of administration, and the response of individual patients.
To achieve endotracheal intubation Suxamethonium Chloride is usually administered intravenously in a dose of 1mg/kg. This dose will usually produce muscular relaxation in about 30 to 60 seconds and has a duration of action of about 2 to 6 minutes. Larger doses will produce more prolonged muscular relaxation, but doubling the dose does not necessarily double the duration of relaxation. Supplementary doses of Suxamethonium Chloride of 50% to 100% of the initial dose administered at 5 to 10 minute intervals will maintain muscle relaxation during short surgical procedures performed under general anaesthesia.
For prolonged surgical procedures Suxamethonium Chloride may be given by intravenous infusion as a 0.1% to 0.2% solution, diluted in 5% glucose solution or sterile isotonic saline solution, at a rate of 2.5 to 4mg per minute. The infusion rate should be adjusted according to the response of individual patients.
The total dose of Suxamethonium Chloride given by repeated intravenous injection or continuous infusion should not exceed 500mg per hour.
Children, 1 to under 12 years: 1-2mg/kg by intravenous injection.
Suxamethonium Chloride may be given intramuscularly to children at doses up to 4mg per kg. A total dose of 150mg should not be exceeded.
Infants, under 1 year: 2mg/kg by intravenous injection.
Suxamethonium Chloride may be given intramuscularly to infants at doses of up to 4 to 5mg per kg. A total dose of 150mg should not be exceeded.
Elderly: As for adults.
The elderly may be more susceptible to cardiac arrhythmias, especially if digitalis-like drugs are also being taken. See also Precautions.
Profound, prolonged muscle paralysis with respiratory depression are manifestations of a suxamethonium overdose. Ventilatory support is required.
The decision to use neostigmine to reverse a Phase II suxamethonium-induced block depends on the judgement of the clinician in the individual case. Valuable information in regard to this decision will be gained by monitoring neuromuscular function. If neostigmine is used, its administration should be accompanied by appropriate doses of an anticholinergic agent such as atropine.
Suxamethonium has no effect on the level of consciousness and therefore should not be administered to a patient who is not fully anaesthetised.
Suxamethonium should not be administered to patients who are known to be hypersensitive to the drug.
Suxamethonium is contraindicated in patients with a personal or family history of malignant hyperthermia and if the condition occurs unexpectedly, all anaesthetic agents known to be associated with its development including Suxamethonium must be discontinued straight away. Full supportive measures must be employed immediately. Intravenous dantrolene sodium is indicated in the treatment of malignant hyperthermia.
Suxamethonium is contraindicated in patients with an inherited atypical cholinesterase activity.
An acute transient rise in serum potassium often occurs following the administration of Suxamethonium in normal individuals; the magnitude of this rise is of the order of 0.5 mmol/litre. In certain pathological states or conditions, this increase in serum potassium following suxamethonium administration may be excessive and cause serious cardiac arrhythmias and cardiac arrest. For this reason the use of suxamethonium is contraindicated in: Patients recovering from major trauma, or severe burns; the period of greatest risk of hyperkalaemia is from about 5 to 70 days after injury and may be further prolonged if there is delayed healing due to persistent infection.
Patients with neurological deficits involving spinal cord injury, peripheral nerve injury or acute muscle wasting (upper and/or lower motor neurone lesions); the potential for potassium release occurs within the first 6 months after the acute onset of the neurological deficit and correlates with the degree and extent of muscle paralysis. Patients who have been immobilised for prolonged periods of time may be at similar risk.
Patients with pre-existing hyperkalaemia. If there is no hyperkalaemia or neuropathy then renal failure is not a contraindication to the administration of a normal single dose of Suxamethonium Injection, but multiple or large doses may cause clinically significant rises in serum potassium and should not be used.
Suxamethonium causes a slight transient rise in intra-ocular pressure and is therefore contraindicated in the presence of open eye injuries unless the potential benefit outweighs the potential risk to the eye.
Suxamethonium is contraindicated in patients with congenital myotonic diseases such as myotonia congenita and dystrophia myotonica as it is associated with rigidity and severe spasms.
Suxamethonium is contraindicated in patients with Duchenne muscular dystrophy since its administration may be associated with cardiac arrest, hyperkalaemia, hyperthermia, myoglobinaemia, post-operative respiratory depression and rigidity.
Special Precautions
Suxamethonium should be administered under the supervision of an anaesthetist familiar with it and who is skilled in the management of artificial respiration and only where there are adequate facilities for immediate endotracheal intubation with administration of oxygen by intermittent positive pressure ventilation.
The patient must be monitored fully with a peripheral nerve stimulator during prolonged administration of suxamethonium in order to avoid overdosage.
Intensified and prolonged neuromuscular blockade following Suxamethonium Injection may occur secondary to reduced plasma cholinesterase activity in the following states: pregnancy, abnormal plasma cholinesterase, tetanus, tuberculosis, burns, debilitating disease, malignancy, chronic anaemia and malnutrition, hepatic failure, renal failure, autoimmune diseases such as myxoedema and collagen diseases, following plasma exchange, plasmapheresis, cardiopulmonary bypass and as a result of drug interactions.
If Suxamethonium Chloride is given over a prolonged period, the characteristic depolarising neuromuscular (or Phase I) block may change to one with characteristics of a non-depolarising (or Phase II) block. Although the characteristics of a developing Phase II block resemble those of a true non-depolarising block, the former cannot always be fully or permanently reversed by anticholinesterase agents. When a Phase II block is fully established, its effects will then usually be fully reversible with standard doses of neostigmine accompanied by an anticholinergic agent.
In healthy adults, suxamethonium occasionally causes a mild transient slowing of the heart rate on initial administration. Bradycardias are more commonly observed in children and on repeated administration of suxamethonium in both children and adults. Pre-treatment with intravenous atropine or glycopyrrolate significantly reduces the incidence and severity of suxamethonium-related bradycardia.
In the absence of pre-existing or evoked hyperkalaemia, ventricular arrhythmias are rarely seen following suxamethonium administration. Patients taking digitalis-like drugs are however more susceptible to such arrhythmias. The action of suxamethonium on the heart may cause changes in cardiac rhythm including cardiac arrest.
Suxamethonium must not be administered to patients with advanced myasthenia gravis as the patients may develop Phase 2 block which can result in delayed recovery. Patients with myasthenic Eaton Lambert syndrome are more sensitive than normal to suxamethonium which demands a reduction in dose.
Tachyphylaxis occurs after repeated administration of suxamethonium. Some authorities advocate routine premedication of paediatric patients with intravenous atropine. Intramuscular atropine is not effective. Pretreatment with intravenous atropine or glycopyrrolate significantly reduces the incidence and severity of suxamethonium-related bradycardia. Extra care or monitoring must be carried out on infants and children being given suxamethonium, due to the increased risks of undiagnosed muscular disorders or unknown predisposition to malignant hyperthermia.
Suxamethonium Chloride should not be mixed in the same syringe with any other agent, especially thiopental.
Suxamethonium Chloride is acidic and should not be mixed with highly alkaline solutions, e.g. barbiturates.
In patients with severe sepsis, the potential for hyperkalaemia seems to be related to the severity and duration of infection.
Effects on ability to drive and use machines: Do not attempt to drive or operate machinery.
Use In Pregnancy & Lactation
Suxamethonium should not be administered to a pregnant or lactating woman.
Suxamethonium has no direct action on the uterus or other smooth muscle structures. In normal therapeutic doses it does not cross the placental barrier in sufficient amounts to affect the respiration of the infant. The benefits of the use of suxamethonium as part of a rapid sequence induction for general anaesthesia normally outweighs the possible risk to the foetus. Plasma cholinesterase levels fall during the first trimester of pregnancy to about 70 to 80% of their pre-pregnancy values; a further fall to about 60 to 70% of the pre-pregnancy levels occurs within 2 to 4 days after delivery. Plasma cholinesterase levels then increase to reach normal over the next 6 weeks. Consequently, a high proportion of pregnant and puerperal patients may exhibit mildly prolonged neuromuscular blockade following Suxamethonium Injection.
It is not known whether suxamethonium or its metabolites are excreted in human milk.
Adverse Reactions
Muscle pains are frequently experienced after administration of suxamethonium and most commonly occur in ambulatory patients undergoing short surgical procedures under general anaesthesia. There appears to be no direct connection between the degree of visible muscle fasciculation after suxamethonium administration and the incidence or severity of pain. The use of small doses of non-depolarising muscle relaxants given minutes before suxamethonium administration has been advocated for the reduction of incidence and severity of suxamethonium-associated muscle pains. This technique may require the use of doses of suxamethonium in excess of 1mg/kg to achieve satisfactory conditions for endotracheal intubation.
The following adverse reactions have been reported after administration of suxamethonium: Cardiovascular: bradycardia, tachycardia, hypertension, hypotension, arrhythmias.
Respiratory: bronchospasm, prolonged respiratory depression and apnoea.
Musculoskeletal: muscle fasciculation, post-operative muscle pains, myoglobinaemia, myoglobinuria.
Other: anaphylactic reactions, hyperthermia, increased intra-ocular pressure, increased intragastric pressure, rash, skin flushing, excessive salivation.
There are case reports of hyperkalaemia-related cardiac arrests following the administration of suxamethonium to patients with congenital cerebral palsy, tetanus, Duchenne muscular dystrophy, and closed head injury.
Drug Interactions
Suxamethonium, a depolarising muscle relaxant of short duration, may interact with the following: Anti-arrhythmics: Lidocaine, procaine, procainamide, chloroprocaine, cocaine, quinidine and verapamil enhance muscle relaxant effect.
Antibacterials: effect of muscle relaxants is enhanced by aminoglycosides such as dibekacin, kanamycin, neomycin, ribostamycin and streptomycin, the effect of suxamethonium is also enhanced by vancomycin, azlocillin, clindamycin, colistin, piperacillin and polymyxin B.
Anticholinesterases: Cholinesterase and pseudocholinesterase both degrade suxamethonium. Therefore anticholinesterases will enhance suxamethonium. Examples of anticholinesterases include aprotinin, cyclophosphamide, dexpanthenol, ecothiopate, metoclopramide (non-selective drug), neostigmine, phenelzine (MAOI), promazine, quinine and chloroquine (antimalarials), tacrine and trimetaphan (ganglion blocking drug), oestrogen and testosterone. Exposure to pesticides may also reduce pseudocholinesterase activity such as diazinon, malathion and sheep dips.
Antiepileptics: effect of muscle relaxants antagonised by carbamazepine and phenytoin (recovery from neuromuscular blockade accelerated).
Antihypertensives: trimetaphan can increase the effects of suxamethonium.
Antineoplastics (anticancer drugs): cyclophosphamide, chlormethine, thiotepa and tretamine all reduce pseudocholinesterase activity.
Beta-blockers: propranolol enhances muscle relaxant effect.
Benzodiazepines: diazepam and midazolam may alter the depth/duration of suxamethonium.
Calcium-channel Blockers: nifedipine and verapamil enhance effect of non-depolarising muscle relaxants; hypotension, myocardial depression, and hyperkalaemia reported with intravenous dantrolene and verapamil.
Cardiac Glycosides: increased risk of arrhythmias if suxamethonium is given with digoxin.
Cytotoxics: cyclophosphamide and thiotepa enhance effect of suxamethonium.
General Anaesthetics: propofol can cause serious bradycardia if given with suxamethonium and fentanyl citrate-droperidol (Innovar) enhances the effects of suxamethonium. Suxamethonium also interacts with halothane, isoflurane, enflurane, cyclopropane, propanidid and ether.
Histamine Antagonists: high concentrations of cimetidine may inhibit pseudocholinesterase.
Lithium: lithium enhances muscle relaxant effect.
Magnesium Salts: parenteral magnesium enhances effect of suxamethonium.
Parasympathomimetics: demecarium and ecothiopate eye-drops, neostigmine and pyridostigmine, and possibly donepezil enhance effect of suxamethonium but antagonise effect of non-depolarising muscle relaxants.
Sympathomimetics: bambuterol enhances effect of suxamethonium.
Caution For Usage
Special precaution for disposal and other handling: Use once and discard any remaining solution.
Not for dilution.
Incompatibilities: None Known.
Store at 2°C - 8°C. Do not freeze.
Shelf life: 18 months
ATC Classification
M03AB01 - suxamethonium ; Belongs to the class of choline derivative agents used as peripherally-acting muscle relaxants.
Soln for inj (amp) (clear, colourless solution) 50 mg/mL x 2 mL x 10's.
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