sukkinyylikoliini

Sukkinyylikoliini, known in English as succinylcholine (also suxamethonium), is a short-acting depolarizing neuromuscular blocker used to induce rapid muscle relaxation during anesthesia and airway management. It is a quaternary ammonium compound and a choline ester that acts at the neuromuscular junction.

Mechanism of action: Sukkinyylikoliini binds to nicotinic acetylcholine receptors on the motor endplate, causing initial fasciculations followed by sustained depolarization and inability to transmit further impulses. This results in flaccid paralysis. Its effect is brief because it is rapidly hydrolyzed by plasma cholinesterase (pseudocholinesterase) in the blood.

Pharmacokinetics and administration: The onset of action after intravenous administration is typically 30 to 60 seconds, with a duration of about 5 to 10 minutes, depending on individual cholinesterase activity. Because of its rapid onset and short duration, it is commonly used for rapid sequence induction and tracheal intubation. It is generally given IV; IM use is uncommon due to slower and less predictable onset.

Indications, contraindications, and safety: Sukkinyylikoliini is indicated for rapid onset muscle relaxation in anesthesia, especially during rapid sequence intubation, when quick airway control is essential. Contraindications and cautions include known or suspected pseudocholinesterase deficiency, hyperkalemia risk (particularly in patients with burns, extensive trauma, denervation injuries, or neuromuscular disorders), conditions associated with increased intracranial, intraocular, or intragastric pressure, and a history of malignant hyperthermia. It can cause bradycardia, arrhythmias, malignant hyperthermia in susceptible individuals, and post-twitch fasciculation-related myalgias.

Usage context: Although still employed in some settings for its speed, succinylcholine is increasingly replaced by non-depolarizing neuromuscular blockers with reversal agents, owing to a more favorable safety profile. No reliable antagonist reverses its effect; its duration ends with metabolic breakdown.