Adverse effects of suxamethonium
- Especially in patient who is ambulant soon after surgery, such as the day-case patient.
- Caused by the initial fasciculations, are more common in young, healthy patients with a large muscle mass.
- Occur in unusual sites, such as the diaphragm and between the scapulae, and are not relieved easily by conventional analgesics.
- The incidence and severity may be reduced by the use of a small dose of a non- depolarising NMBA given immediately before administration of suxamethonium (e.g. atracurium 0.05 mg/kg). However, this technique, termed precurarisation or pretreatment, reduces the potency of suxamethonium, necessitating the administration of a larger dose to produce the same effect.
Increased intraocular pressure
- Caused by the initial contraction of the external ocular muscles and internal ocular muscles after administration of suxamethonium.
- It is not reduced by precurarisation.
- The effect lasts for as long as the neuromuscular block
- Concern has been expressed that it may be sufficient to cause expulsion of the vitreal contents in the patient with an open eye injury. This is unlikely.
- Protection of the airway from gastric contents must take priority in the patient with a full stomach in addition to an eye injury.
Increased intragastric pressure
In the patient with the incompetence of the lower oesophageal sphincter from, for example, hiatus hernia, regurgitation may occur.
- Muscle fasciculations stimulate muscle stretch receptors, which subsequently increase cerebral activity.
- The increase in intracranial pressure can be attenuated by maintaining good airway control and instituting hyperventilation.
- It can also be prevented by pretreating with a nondepolarizing muscle relaxant and administering intravenous lidocaine (1.5–2.0 mg/kg) 2 to 3 min prior to intubation.
- It is not contraindicated for rapid sequence induction of patients with intracranial mass lesions or other causes of increased intracranial pressure.
- During halothane anesthesia increases serum potassium concentration by 0.5 mmol/L. This is thought to be caused by muscle fasciculation. The effect is less marked with the newer potent inhalational agents.
- A similar increase occurs in patients with renal failure, but as these patients may already have an elevated serum potassium concentration, such an increase may precipitate cardiac irregularities and even cardiac arrest.
- In some conditions in which the muscle cells are swollen or damaged, or in which there is the proliferation of extra-junctional receptors [the immature isoform of the ACh receptor may be expressed inside and outside the neuromuscular junction (upregulation)], this release of potassium may be exaggerated. This is most marked in the burned patient.
- In diseases of the muscle cell or its nerve supply, hyperkalemia after suxamethonium may also be exaggerated. These include muscular dystrophies, dystrophia myotonica and paraplegia. Hyperkalemia has been reported to cause death in such patients.
- Suxamethonium may also precipitate prolonged contracture of the masseter muscles in patients with these disorders, making tracheal intubation impossible. The drug should be avoided in any patient with a neuromuscular disorder, including the patient with malignant hyperthermia, in whom the drug is a recognised trigger factor.
- Hyperkalemia after suxamethonium has also been reported in patients with widespread intra- abdominal infection, severe trauma and closed head injury.
- The risk of hyperkalemia usually seems to peak in 7 to 10 days following the injury, but the exact time of onset and the duration of the risk period varies. The risk of hyperkalemia from suxamethonium is minimal in the first 2 days after spinal cord or burn injury.
- Hyperkalemic cardiac arrest can prove to be quite refractory to routine cardiopulmonary resuscitation, requiring calcium, insulin, glucose, bicarbonate, and even cardiopulmonary bypass to support the circulation while reducing serum potassium levels.
- Conditions associated with hyperkalemia with Suxamethonium -
- Burn injury
- Massive trauma
- Spinal cord injury
- Closed head injury
- Ruptured cerebral aneurysm
- Prolonged total body immobilisation
- Guillain–Barré syndrome
- Severe Parkinson disease
- Myopathies (eg, Duchenne dystrophy)
- Severe intraabdominal infection
- Hemorrhagic shock with metabolic acidosis
- Suxamethonium has muscarinic, in addition to nicotinic effects.
- Stimulation of nicotinic receptors in parasympathetic and sympathetic ganglia, and muscarinic receptors in the sinoatrial node of the heart, can increase or decrease blood pressure and heart rate.
- Low doses of succinylcholine can produce negative chronotropic and inotropic effects, but higher doses usually increase heart rate and contractility and elevate circulating catecholamine levels.
- The direct vagal effect (muscarinic) produces sinus bradycardia, especially in patients with a high vagal tone, such as children and the physically fit.
- It is also more common in the patient who has not received an anticholinergic agent (such as glycopyrronium bromide) or who is given repeated increments of suxamethonium (if administered 3 - 8 minutes after the first bolus dose).
- It is advisable to use an anticholinergic routinely if it is planned to administer more than one dose of suxamethonium.
- Nodal or ventricular escape beats may develop in extreme circumstances.
- Immunoglobulin E (IgE)–mediated allergic reactions to suxamethonium are rare but may occur, especially after repeated exposure to the drug.
- They are more common after suxamethonium than any other neuromuscular blocking agent.
- A blood test is available to measure plasma suxamethonium IgE concentrations to aid in the diagnosis of allergic anaphylaxis to this agent. No such test is available commercially for the other NMBAs.
Masseter Muscle Rigidity
- Succinylcholine transiently increases muscle tone in the masseter muscles. Some difficulty may initially be encountered in opening the mouth because of incomplete relaxation of the jaw.
- A marked increase in tone preventing laryngoscopy is abnormal and can be a premonitory sign of malignant hyperthermia.
Succinylcholine is a potent triggering agent in patients susceptible to malignant hyperthermia
Patients afflicted with myotonia may develop myoclonus after the administration of succinylcholine.
- Reduced levels of normal pseudocholinesterase may have a longer than normal duration of action.
- Atypical pseudocholinesterase will experience markedly prolonged paralysis.
Causes of reduced plasma cholinesterase activity include the following:
- Liver disease.
- Renal disease.
- Carcinomatosis and starvation
- Pregnancy, for two reasons: an increased circulating volume (dilutional effect) and decreased enzyme synthesis.
- Anticholinesterases: inhibit plasma cholinesterase in addition to acetylcholinesterase. The organophosphorus compound ecothiopate, once used topically as a miotic in ophthalmology, is also an anticholinesterase.
- Drugs which are metabolised by plasma cholinesterase and which therefore decrease its availability, including etomidate, ester local anaesthetics, anticancer drugs such as methotrexate, monoamine oxidase inhibitors and esmolol.
- Cardiopulmonary bypass, plasmapheresis.
- Smith and Aitkenhead's Textbook of Anaesthesia, 7th Edition
Morgan & Mikhail's Clinical Anesthesiology, 6e