suxamethonium

the SAS brand of suxamethonium uses the hydrochloride salt and thus contains 10% more suxamethonium base than the Astra Zeneca product which uses a chloride salt.

the only depolarising neuromuscular blocking agent (NBMA) in use
also known as succinylcholine, sux, and Scoline
It has been in use since the pharmacological properties of succinylcholine were discovered around 1950 by K.H. Ginzel, H Klupp, and Gerhard Werner in Vienna, Austria.

dose: 1.5 mg/kg iv
- it is far better to over-estimate the dose than under-estimate the dose as inadequate doses can leave the patient partially paralysed and difficult to intubate.
dosing is based on total body weight - this holds true in both morbidly obese and pregnant patients
myasthenia gravis patients:
- can be used safely in patients with myasthenia gravis without risk of precipitating severe hyperkalemia
- patients with myasthenia gravis are relatively resistant to suxamethonium, and when undergoing RSI should receive 2 mg/kg in order to stimulate sufficiently the remaining acetylcholine receptors unaffected by the disease.

onset: intubation-level paralysis occurring 45 to 60 seconds after dosing
duration of action: 6 to 10 minutes
stability of solution:
- slowly degrades at room temperature, but retains 90 percent of its activity for up to three months when so stored
- if it is stored at room temperature, a quality management system is necessary to ensure removal of stock before it becomes outdated.
consists of two acetylcholine molecules that are linked by their acetyl groups.
It imitates the action of acetylcholine at the neuromuscular junction, acting on muscle type nicotinic receptors, but it is degraded not by acetylcholinesterase but by butyrylcholinesterase, a plasma cholinesterase. This hydrolysis by butyrylcholinesterase is much slower than that of acetylcholine by acetylcholinesterase.

Binding of suxamethonium to the nicotinic acetylcholine receptor results in opening of the receptor's nicotinic sodium channel; sodium moves into the cell, a disorganised depolarisation of the motor end plate occurs and calcium is released from the sarcoplasmic reticulum. This results in fasciculation.
In the normal muscle, following depolarisation, acetylcholine is rapidly hydrolysed by acetylcholinesterase and the muscle cell is able to 'reset' ready for the next signal.
Suxamethonium has a longer duration of effect than acetylcholine and is not hydrolysed by acetylcholinesterase. It does not allow the muscle cell to 'reset' and keeps the 'new' resting membrane potential below threshold. When acetylcholine binds to an already depolarised receptor it cannot cause further depolarisation.
Calcium is removed from the muscle cell cytosol independent of repolarisation (depolarization signalling and muscle contraction are independent processes). As the calcium is taken up by the sarcoplasmic reticulum, the muscle relaxes. This explains muscle flaccidity rather than tetany following fasciculation.

Following infusion or repeated doses of suxamethonium, phase 2 block may occur.
The receptor blockade takes on characteristics of a non-depolarising neuromuscular block (ie. fade in response to nerve stimulation, however unlike non-depolarizing neuromuscular blocking agents it cannot be reversed).

muscle pains
mild hyperkalaemia - typical dose results in rise of serum potassium of 0.5mM in normal patients as the acetylcholine receptor is activated and allows potassium to flow from intracellular to extracellular fluid.
acute rhabdomyolysis with hyperkalaemia
transient ocular hypertension - but usually safe to use in open globe injuries, particularly if pre-treatment with a non-depolarising agent¹⁾
trismus or masseter muscle spasm occurs after suxamethonium administration in 0.001 to 0.1% of patients
changes in cardiac rhythm including bradycardia, cardiac arrest, and ventricular dysrhythmias.
- in patients with neuromuscular disease or extensive burns, a single injection of suxamethonium can lead to massive release of potassium from skeletal muscles with resultant cardiac arrest.
- bradycardia — succinylmonocholine, the initial metabolite of suxamethonium, sensitizes the cardiac muscarinic receptors in the sinus node, and repeat doses may cause bradycardia
malignant hyperthermia, is a rare (0.0004 to 0.00625% of pts) and potentially fatal reaction.

¹⁾