Describe Suxamethonium in detail.

Pharmacology

Suxamethonium (succinylcholine) is the only depolarising relaxant in common use. It is structurally two ACh molecules joined together, and it acts as an agonist at the nicotinic receptor, depolarising the end-plate. Its great advantages are a very rapid onset (~30–60 s) and a very short duration (~3–5 min) — because it is rapidly hydrolysed by plasma (pseudo)cholinesterase. The intubating dose is 1–1.5 mg/kg.

Uses

Its speed and brevity make it the classic relaxant for rapid sequence induction (securing the airway fast in the aspiration-risk patient) and for brief procedures requiring relaxation, and it is invaluable for the rapid relief of laryngospasm.

Complications

• Suxamethonium has a long list of adverse effects.
• Hyperkalaemia — it raises serum potassium (~0.5 mmol/L normally), but causes dangerous, potentially fatal hyperkalaemia in burns, major trauma/crush, spinal cord injury/denervation, and prolonged immobility (from up-regulation of extrajunctional receptors).
• Muscle pains (myalgia) after fasciculations.
• Bradycardia (especially with a repeat dose, and in children) — prevented by atropine. It is a trigger for malignant hyperthermia. It raises intra-ocular, intragastric and intracranial pressure. Rarely, anaphylaxis. In those with abnormal cholinesterase it causes prolonged apnoea (suxamethonium apnoea).

Phase II Block

With a large or repeated dose (or an infusion), the character of the block changes from the normal depolarising phase I to a phase II (‘dual’) block that resembles a non-depolarising block (with fade), reflecting desensitisation of the receptor. This prolongs recovery.

WHY It Persists Despite its Hazards

Given its formidable list of complications, it is reasonable to ask why suxamethonium remains in use at all, and the answer lies in the two properties that no non-depolarising agent has traditionally matched: an onset within thirty to sixty seconds and an offset within a few minutes from spontaneous breakdown by plasma cholinesterase. This combination makes it uniquely suited to securing the airway quickly in the aspiration-risk patient and to situations where paralysis may need to be short-lived — and it is the reason the search for a replacement has centred on the rocuronium–sugammadex combination, which can reproduce the rapid onset and now, with sugammadex, a rapid offset.

Fasciculations & Their Consequences

The brief, visible fasciculations that precede paralysis are the outward sign of the initial depolarisation, and several of suxamethonium’s adverse effects flow directly from them. The disorganised muscle contraction releases potassium into the circulation and produces the postoperative muscle pains (myalgia) that patients often notice a day or two later, while the same generalised contraction contributes to transient rises in intra-ocular, intragastric and intracranial pressure. Understanding that these effects share a single origin — the depolarising fasciculation — helps make sense of an otherwise disparate list of complications, and explains why techniques such as a small pre-dose of a non-depolarising agent have been used to attenuate them.

Rapid onset and offset — hence its role in rapid sequence induction.

• Suxamethonium: only common depolarising relaxant; agonist; very fast onset, very short (hydrolysed by plasma cholinesterase); 1–1.5 mg/kg.
• Uses: rapid sequence induction, brief relaxation, relief of laryngospasm.
• Complications: dangerous hyperkalaemia (burns/crush/spinal injury/denervation), myalgia, bradycardia (atropine), MH trigger, ↑IOP/ICP/intragastric pressure.
• Suxamethonium apnoea in abnormal cholinesterase; anaphylaxis (rare).
• Large/repeated doses → phase II (dual) block resembling non-depolarising.