⚠️ Warnings
If suxamethonium is administered intravenously too rapidly, uncoordinated muscle contractions may occur. As these contractions are painful, use without anesthesia is undesirable.
Administration of suxamethonium may cause bradycardia and/or cardiac arrest due to hyperkalemia.
Due to the risk of prolonged apnea, the use of adequate ventilatory equipment and the presence of an anesthesiologist are strongly recommended.
A high rate of cross-sensitivity (more than 50%) has been reported between neuromuscular blocking agents.
Therefore, before administering suxamethonium, hypersensitivity to other neuromuscular blocking agents should be excluded where possible. In sensitive patients, suxamethonium should only be used when absolutely necessary. Patients who experience a hypersensitivity reaction during general anesthesia should subsequently be tested for hypersensitivity to other neuromuscular blocking agents.
During prolonged administration of suxamethonium, the patient should be carefully monitored using a peripheral nerve stimulator to prevent overdose.
The effect of suxamethonium may be enhanced during hypothermic surgery.
In hereditary atypical plasma cholinesterase activity and abnormal plasma pseudocholinesterase activity, markedly prolonged apnea and respiratory distress may occur, or the effect at usual doses may be insufficient, making intubation difficult. This must be taken into account, the patient should be monitored, appropriate ventilatory equipment should be available, and the dose should be adjusted as necessary. Genetic testing of the patient is recommended if esterase enzyme mutations are suspected.
Prolonged and more intense neuromuscular blockade following suxamethonium injection may occur due to decreased plasma cholinesterase activity in the following situations or pathological conditions:
physiological changes, e.g., during pregnancy and the puerperium (see section 4.6);
genetically determined abnormalities of plasma cholinesterase (see section 4.3);
severe generalized tetanus, tuberculosis, other severe or chronic infections;
following severe burns;
chronic debilitating conditions, malignant disease, chronic anemia, and malnutrition;
end-stage hepatic failure, acute or chronic renal failure;
autoimmune disorders: myxedema, collagen disorders;
iatrogenic conditions: following plasma exchange, plasmapheresis, cardiopulmonary bypass, and due to concomitant pharmacotherapy (see section 4.5).
Hyperkalemia
In healthy individuals, an acute transient increase in serum potassium concentration commonly occurs following administration of suxamethonium; the magnitude of this increase is in the order of 0.5 mmol/L. In certain pathological situations or conditions, excessive increases in serum potassium may occur following suxamethonium administration, which may cause serious cardiac arrhythmias and cardiac arrest in:
patients recovering from severe trauma; the period of greatest risk of hyperkalemia is approximately 5 to 70 days after injury and may be longer if healing is delayed due to persistent infection;
patients with neurological disorders involving spinal cord injury, peripheral nerve injury, or acute muscle atrophy (upper and/or lower motor neuron lesions); the risk of potassium release occurs in the first 6 months after the onset of the acute neurological disorder and is related to the degree and extent of muscle paralysis. Patients who have been immobile for a prolonged period may be at similar risk;
patients with pre-existing hyperkalemia (see section 4.3). In the absence of hyperkalemia or neuropathy, renal failure is not a contraindication for a normal single dose of suxamethonium injection solution, but repeated or high doses may lead to clinically significant increases in serum potassium and should not be used;
patients with severe sepsis; the risk of hyperkalemia appears to be related to the severity and duration of the infection.
Phase II block
If suxamethonium chloride is administered over a prolonged period, the characteristic effect of a depolarizing neuromuscular blocking agent (Phase I) may change to a non-depolarizing block (Phase II). Although the features of a developing Phase II block resemble a non-depolarizing block, Phase II block cannot always be fully and definitively reversed with anticholinesterase agents. Once Phase II block is fully established, its effects can usually be completely reversed with standard doses of neostigmine in combination with an anticholinergic agent. Neonates and patients with myasthenia gravis develop immediate Phase II block.
Bradycardia
In healthy adults, suxamethonium occasionally causes mild transient slowing of heart rate after the first dose. Bradycardia is more frequently observed in children and with repeated administration of suxamethonium in both children and adults.
Premedication with intravenous atropine or glycopyrrolate significantly reduces the incidence and severity of suxamethonium-related bradycardia.
Ventricular arrhythmias
In the absence of pre-existing or induced hyperkalemia, ventricular arrhythmias are rarely observed after suxamethonium administration. However, patients receiving digitalis-like drugs are more susceptible to these arrhythmias (see section 4.5). The effect of suxamethonium on the heart may lead to changes in cardiac rhythm, including cardiac arrest.
Myasthenia gravis
Administration of suxamethonium injection is not recommended in patients with advanced myasthenia gravis. Although these patients are resistant to suxamethonium, they develop Phase II block, which may result in slower recovery. Patients with myasthenic Eaton-Lambert syndrome are more sensitive than usual to suxamethonium injection, requiring dose reduction.
Open eye injuries/glaucoma
Suxamethonium causes a mild, transient increase in intraocular pressure and is therefore not recommended in cases of open eye injury or when an increase in intraocular pressure is undesirable, unless the potential benefit of treatment outweighs the potential risk to the eye.
Tachyphylaxis
Tachyphylaxis occurs with repeated administration of suxamethonium.
Pediatric patients
Bradycardia is more frequently observed in children and with repeated administration of suxamethonium. Some experts recommend routine premedication with intravenous atropine in pediatric patients. Intramuscular administration of atropine is not effective. Pretreatment with intravenous atropine or glycopyrrolate significantly reduces the incidence and severity of suxamethonium-induced bradycardia. Neonates develop immediate Phase II block.
Intractable cases of cardiac arrest have been described in pediatric patients with undiagnosed neuromuscular disorders. Increased caution or additional monitoring should be exercised with infants and children receiving suxamethonium due to the increased risk of undiagnosed muscle disorders or predisposition to malignant hyperthermia (see sections 4.3 and 4.8).
Suxamethonium chloride must not be mixed with other medicinal products in the same syringe, particularly with thiopental.
Suxamethonium should be used with caution in:
respiratory disorders and electrolyte abnormalities.
This product contains less than 1 mmol sodium (23 mg) per ampoule, which means it is essentially 'sodium-free'.
