Succinylcholine

Definition

For 50 years, the rapid onset and short duration of succinylcholine has afforded distinct advantages over other neuromuscular blocking drugs. Unfortunately succinylcholine also has numerous well-described complications that are related to its mechanism of action or pharmacokinetics or that occur as an idiosyncratic effect ( Box 98.1 ). The most serious reactions are hyperkalemia, unanticipated prolonged muscle relaxation, and malignant hyperthermia (see Chapter 195 ). Hyperkalemia-induced cardiac arrest may develop soon after succinylcholine administration to patients with conditions that predispose to acetylcholine receptor upregulation ( Box 98.2 ) or rhabdomyolysis.

Prolonged relaxation may occur after succinylcholine administration with the development of a phase II block or with decreased metabolism. After a single large dose, repeated doses, or a prolonged continuous infusion of succinylcholine, the postjunctional receptor may not respond normally to acetylcholine, even after the receptor-nicotinic channel has repolarized. This is termed a phase II block .

Under normal circumstances, the short duration of the effect of succinylcholine is the result of rapid hydrolysis by butyrylcholinesterase (BChE), also known as pseudocholinesterase or plasma cholinesterase. Ninety percent of an intravenous dose of succinylcholine is rapidly hydrolyzed to a nearly inactive metabolite in the plasma and liver by BChE. Neuromuscular block terminates by the diffusion of succinylcholine from the end plate into the extracellular fluid, where BChE influences the onset and duration of action by controlling the rate of hydrolysis. A prolonged duration of succinylcholine may occur when quantities of normal BChE are significantly decreased or when an abnormal variant of BChE is present.

Recognition

T-wave elevation, QRS complex prolongation and a sinusoidal QRS waveform (see Chapter 87 ), and asystole or ventricular fibrillation occurring shortly after succinylcholine administration are the characteristic alterations observed on the electrocardiogram (ECG) in patients with exaggerated potassium (K ⁺ ) release and hyperkalemia. Measurement of serum K ⁺ concentrations confirms hyperkalemia. However, if the ECG is abnormal, treatment should precede confirmation of serum K ⁺ concentrations.

The presence of abnormal BChE is frequently recognized only after failure to emerge from general anesthesia and prolonged muscle weakness occurs in an otherwise healthy patient who received a normal dose of succinylcholine. The presence of very low levels of a normal BChE or abnormal forms of BChE leads to variable prolongation of neuromuscular block ( Table 98.1 ). These abnormalities are not uncommon. In a recent observational study in Switzerland, 16% of patients having rapid-sequence induction with 1 mg/kg succinylcholine had duration of block greater than 10 minutes. The diagnosis is confirmed by characteristic findings on peripheral nerve stimulation, including a train-of-four ratio (T ₄ /T ₁ ) of less than 0.3 and the presence of fade and posttetanic facilitation typical of a phase II block caused by the elevated concentration of unmetabolized succinylcholine at the neuromuscular junction.