Each mL contains: Atracurium besilate 10 mg.
Pharmacology: Competitive neuromuscular blockers act by competing with acetylcholine for receptors on the motor end plate of the neuromuscular junction to produce blockade. The muscles that produce fine rapid movements such as those of the face are the first to be affected followed by those of the limbs and torso; the last to be affected are those of the diaphragm. The paralysis is reversible with recovery occurring in reverse order. Restoration of normal neuromuscular function can be hastened by increasing the concentration of acetylcholine at the motor end plate by giving an anticholinesterase such as neostigmine.
Pharmacodynamics: Atracurium is a highly selective competitive (non-depolarizing) neuromuscular blocking agent with an intermediate duration of action.
Non-depolarizing agents antagonize the neurotransmitter action of acetylcholine by binding with receptor sites on the motor-end plate.
Atracurium can be used in a wide range of surgical procedures and to facilitate controlled ventilation.
Pediatric population: The limited data in neonates from literature reports suggest variability in the time to onset and duration of action of Atracurium in this population as compared to children.
Pharmacokinetics: Following intravenous injection, Atracurium undergo spontaneous degradation via Hofman elimination (a non-enzymatic breakdown process occurring at physiological pH and temperature) to produce laudanoside and other metabolites. There is also hydrolysis by non-specific plasma esterases. The metabolites have no neuromuscular blocking activity.
About 80% of atracurium is bound to plasma proteins. Atracurium and its metabolites cross the placenta in clinically insignificant amounts.
Excretion of Atracurium is in urine and bile, mostly as metabolites. The elimination half-life has been reported to be approximately 20 minutes for atracurium.
Atracurium besilate is used as an adjunct to general anesthesia or sedation in the intensive care unit (ICU) to relax skeletal muscles and to facilitate tracheal intubation and mechanical ventilation.
The usual initial dose of atracurium besilate for adults and children over one month of age is 300 to 600 μg per kg body weight by intravenous injection. Subsequent doses of 100 to 200 mcg per kg may be given as necessary, typically after 15 to 25 minutes. It is recommended that in patients with cardiovascular disease that initial dose should be administered over a period of 60 seconds.
Atracurium besilate may also be given by continuous intravenous infusion at a rate of 5 to 10 mcg per kg per minute to maintain neuromuscular block during prolonged procedures. Somewhat higher infusion rates may be used in patients undergoing controlled ventilation in intensive care.
Or as prescribed by the physician.
Symptoms: Prolonged muscle paralysis and its consequences are the main signs of overdosage.
Management: It is essential to maintain a patient airway together with assisted positive pressure ventilation until spontaneous respiration is adequate. Full sedation will be required since consciousness is not impaired. Recovery may be hastened by the administration of anticholinesterase agents accompanied by atropine or glycopyrrolate, once evidence of spontaneous recovery is present.
Atracurium is contraindicated in patients known to be hypertensive to atracurium, cisatracurium or benzenesulfonic acid.
In common with all the other neuromuscular blocking agents, atracurium paralyses the respiratory muscles as well as other skeletal muscles but has no effect on consciousness. Atracurium should be administered only with adequate general anesthesia and only by or under the close supervision of an experienced anesthetist with adequate facilities for endotracheal intubation and artificial ventilation.
The potential for histamine release exists in susceptible patients during atracurium administration. Caution should be exercised in administering atracurium to patients with history suggestive of an increased sensitivity to the effects of histamine. In particular, bronchospasm may occur in patients with a history of allergy and asthma.
High rates of cross-sensitivity between neuromuscular blocking agents have been reported. Therefore, where possible, before administering atracurium, hypersensitivity to other neuromuscular blocking agents should be excluded. Atracurium should only be used when absolutely essential in susceptible patients. Patients who experience a hypersensitivity reaction under general anesthesia should be tested subsequently for hypersensitivity to other neuromuscular blockers.
Monitoring of serial creatinine phosphate (CPK) values should be considered in asthmatic patients receiving high dose corticosteroids and neuromuscular blocking agents in ICU.
Atracurium does not have significant vagal or ganglionic blocking properties in the recommended dosage range. Consequently, atracurium has no clinically significant effects on heart rate in the recommended dosage range and it will not counteract the bradycardia produced by many anesthetic agents or by vagal stimulation during surgery.
In common with other non-depolarizing neuromuscular blocking agents, increased sensitivity to atracurium may be expected in patients with myasthenia gravis and other forms of neuromuscular disease.
As with other neuromuscular blocking agents, severe acid-base and/or serum electrolyte abnormalities may increase or decrease the sensitivity of patients to atracurium.
As with other non-depolarizing neuromuscular blockers, hypophosphatemia may prolong recovery. Recovery may be hastened by correcting this condition.
Atracurium should be administered over a period of 60 seconds to patients who may be unusually sensitive to falls in arterial blood pressure, for example those who are hypovolemic.
Atracurium is inactivated by high pH and so must not be mixed in the same syringe with thiopental or any alkaline agent.
When a small vein is selected as the injection site, atracurium should be flushed through the vein with physiological saline after injection.
When other anesthetic drugs are administered through the same in-dwelling needle or cannula as atracurium, it is important that each drug is flushed through with an adequate volume of physiological saline. Atracurium besilate is hypotonic and must not be administered into the infusion line of a blood transfusion.
Studies in malignant hyperthermia in susceptible animals (swine), and clinical studies in patients susceptible to malignant hypothermia indicate that atracurium does not trigger this syndrome.
In common with other non-depolarizing neuromuscular blocking agents, resistance may develop in patients suffering from burns.
Such patients may require increased doses, dependent on the time elapsed since the burn injury and the extent of the burn.
Intensive Care Unit (ICU) patients: When administered to laboratory animals in high doses, Laudanosine, a metabolite of atracurium has been associated with transient hypotension and in some species, cerebral excitatory effects. Although seizures have been seen in ICU patients receiving atracurium, a causal relationship to laudanosine has not been established.
The adverse effects of competitive neuromuscular blockers are generally similar although they differ in their propensity to cause histamine release and cardiovascular effects. Histamine release and associated cardiovascular effects appear to be rare with the aminosteroidal blockers.
Competitive neuromuscular blockers with vagolytic activity may produce tachycardia and a rise in blood pressure. The use of blockers which lack an effect on the vagus may result in bradycardia during anaesthesia due to the effects of other drugs employed or as a result of vagal stimulation. Reduction in blood pressure with compensatory tachycardia may occur with some competitive neuromuscular blockers due in part to sympathetic ganglion blockade or the release of histamine.
Reduction in gastrointestinal motility and tone may occur as a result of ganglionic blockade.
Histamine release may also lead to wheal-and-flare effects at the site of injection, flushing, occasionally bronchospasm, and rarely anaphylactoid reactions.
Malignant hyperthermia has been associated rarely with competitive neuromuscular blockers.
In overdosage, there is prolonged apnoea due to paralysis of the intercostal muscles and diaphragm, with cardiovascular collapse and the effects of histamine release.
A number of drugs may influence neuromuscular transmission and thus interfere with the action of both competitive and depolarizing neuromuscular blockers, resulting in potentiation or antagonism of neuromuscular block. Some interactions may be advantageous, such as the reversal of competitive neuromuscular block by anticholinesterases. In general, adverse reactions are potentially more serious in patients with impaired neuromuscular function.
Drug interactions affecting neuromuscular blockers of either type (competitive and depolarising) as well as those specific for competitive neuromuscular blockers.
Lidocaine, procainamide, quinidine and verapamil all have same neuromuscular blocking activity and may enhance the block produced by neuromuscular blockers. Large doses of lidocaine may reduce the release of acetylcholine and act directly on the muscle membrane.
Quinidine has a curare-like action at the neuromuscular junction and depresses the muscle action potential. If given during recovery from neuromuscular block, it can result in muscle weakness and apnoea and it should be avoided, if possible, in the immediate postoperative period.
Some antibacterials in very high concentration can produce a muscle paralysis that may be additive to or synergistic with that produced by neuromuscular blockers. The neuromuscular block produced by antibacterials may be enhanced in patients with intracellular potassium deficiency, low plasma-calcium concentration, neuromuscular disease, or a tendency to a high plasma-antibacterial concentration, for example after large doses or in renal impairment. The interaction appears to be more important for competitive neuromuscular blockers.
The antibacterials most commonly implicated are aminoglycosides, lincosamides, polymyxins and more rarely, tetracyclines.
Store at temperatures between 2-8°C.
M03AC04 - atracurium ; Belongs to the class of other quaternary ammonium-containing agents used as peripherally-acting muscle relaxants.
Atracor soln for inj 10 mg/mL
2.5 mL x 10 × 1's
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