Mnemonic: “A nectarine Sucks in a coal line"
Pronunciation:
suks in il KOE leen / an EK teen
Class: Depolarizing neuromuscular blocking agent (DNBA)
Year of approval: 1951
FDA-approved for:
Neuromuscular blockade induction / maintenance
Used for:
Rapid sequence intubation,
Electroconvulsive therapy (ECT)
Succinylcholine, also called suxamethonium and referred to as “sux”, is a depolarizing skeletal muscle relaxant administered intravenously. Succinylcholine takes effect within 1 minute of administration and lasts about 5 minutes, which is the ideal duration of paralysis for electroconvulsive therapy (ECT).
The succinylcholine molecule consists of two molecules of acetylcholine linked by their acetyl groups. Think “sux-cessive acetylcholines” or two acetylcholine molecules having “sux”.
The role of acetylcholine in normal muscle contraction is to bind to postsynaptic nicotinic cholinergic receptors on the neuromuscular end plate, causing depolarization leading to muscle contraction. Acetylcholine, in normal physiology, quickly unbinds from the receptor.
Succinylcholine binds the same receptors but does not unbind. Within seconds of succinylcholine infusion, muscle twitching begins around the eyes and progresses down the body. Fasciculations can look like worms moving under the skin, easily observable in the calf muscles. When fasciculations cease, the patient is paralyzed, including muscles of respiration. With ECT, the electroencephalogram (EEG) will provide evidence of induced seizure while motor seizure is imperceptible or barely perceptible due to paralysis by succinylcholine. The purpose of paralysis during ECT to minimize strain on the cardiovascular system and prevent injury from convulsions.
Paralysis continues until succinylcholine is metabolized by pseudocholinesterase, within about 5 minutes. If the patient has pseudocholinesterase deficiency, neuromuscular blockade by succinylcholine will be prolonged (discussed below).
Neuromuscular blocking agents (NMBAs) come in two forms: depolarizing (e.g., succinylcholine) and nondepolarizing (drugs ending in -curonium or -curium). Nondepolarizing NMBAs (e.g., rocuronium) bind to nicotinic cholinergic receptors without causing depolarization while preventing acetylcholine from binding.
Succinylcholine does not act upon the central nervous system because it does not cross the blood-brain barrier. The patient must be anesthetized prior to receiving succinylcholine because awake paralysis would cause considerable psychological distress while making it impossible to communicate.
Succinylcholine binds muscarinic acetylcholine receptors in the heart, initially producing bradycardia (cholinergic effect) followed by tachycardia (anticholinergic effect) after 15–30 seconds. Succinylcholine has the potential to cause cardiac arrhythmias, asystole, or cardiac arrest.
Succinylcholine is used in rapid sequence intubation (RSI) performed in the emergency department to a critically ill or injured patient presumed to have a full stomach, to prevent aspiration. With succinylcholine the duration of paralysis is brief, allowing the patient to breathe within a few minutes if intubation fails.
While succinylcholine is useful for ECT and RSI, rocuronium is preferred for facilitating intubation in the ICU due to risks and side effects of succinylcholine (Booij, 2001). In the ICU, rapid return of spontaneous ventilation is not necessary because artificial ventilation is reliably established.
The mechanism of succinylcholine (depolarization of muscle cell membrane) results in the release of intracellular potassium which can lead to hyperkalemia, potentially leading to cardiac arrest. Succinylcholine is contraindicated in medical conditions associated with hyperkalemia such as extensive burns, muscle crush injury, and neuroleptic malignant syndrome. Patients at increased risk for succinylcholine-induced hyperkalemia include those with myopathy, stroke, brain tumors, head injury, or encephalitis.
Succinylcholine has one boxed warning, regarding risk of cardiac arrest in pediatric patients subsequently found to have undiagnosed muscular dystrophy, usually males under 8 years old. Infants or children experiencing seemingly idiopathic cardiac arrest soon after the administration of succinylcholine should be treated immediately for hyperkalemia.
Myalgia (muscle aching) is a common post-ECT side effect, reported by about 50% of patients. Post-ECT myalgia can be prominent if vigorous muscle contractions occur upon infusion of succinylcholine. A wide variety of regimens has been tried to reduce incidence and severity of succinylcholine-induced myalgia. The most common practice is to administer a sub-paralyzing dose of a nondepolarizing neuromuscular blocker a few minutes before succinylcholine, to abolish visible fasciculations (Wong & Chung, 2002). For example, 0.05 mg/kg rocuronium can be infused about 2 minutes before succinylcholine.
Although the incidence and extent of fasciculation after succinylcholine can be decreased by pretreatment with a 10 mg dose succinylcholine, this “self-taming” technique seems to offer no advantage in decreasing the severity of post-procedure myalgia (Brodsky & Brock-Utne, 1979).
Muscle pain is more severe when succinylcholine is administered at a dose of 1.5 mg/kg compared with 0.5 mg/kg (Stewart et al, 1991).
Although succinylcholine is the standard neuromuscular blocker for ECT, it is not necessarily the best choice. Vahap et al (2014) concluded that rocuronium, reversed with sugammadex, resulted in quicker awakening time and less myalgia and headache after ECT compared to succinylcholine.
Succinylcholine is contraindicated in pseudocholinesterase deficiency (1 in 500, autosomal recessive). A patient with pseudocholinesterase deficiency will experience prolonged paralysis for up to 8 hours, requiring mechanical ventilation. It is important to recognize the reaction and continue anaesthesia because awake paralysis may lead to post-traumatic stress disorder. In pseudocholinesterase deficiency, the intermediately long-acting nondepolarizing relaxant rocuronium can be used instead of succinylcholine. Mivacurium is also contraindicated in pseudocholinesterase deficiency.
Other risks of succinylcholine include anaphylaxis and malignant hyperthermia. Succinylcholine increases saliva production as a cholinergic effect. It does not appear to markedly affect seizure threshold.
Dosing: For ECT, the initial dose will be defined by the anesthesiologist. The traditional dose for intubation is 1 mg/kg. 0.67 mg/kg may be a suitable dose for ECT. Lean or muscular patients may need more than 0.67 mg/kg. Obese patients may need less than 0.67 mg/kg. El-Orbany et al (2004) concluded that 0.5–0.6 mg/kg of succinylcholine is as effective as 1.0 mg/kg with regard to intubating conditions, with a more rapid recovery from neuromuscular blockade and apnea time.
Dynamic interactions:
❖ Hyperkalemia
❖ Neuromuscular blockade
❖ Cholinergic effects
– bradycardia
– salivation
Kinetic interactions:
❖ Cholinesterase inhibitors may prolong neuromuscular blockade by interfering with breakdown of succinylcholine:
– donepezil (Aricept)
– rivastigmine (Exelon)
– galantamine (Razadyne)
❖ Other drugs that decrease cholinesterase activity:
– corticosteroids
– estrogens
– ketamine
– chlorpromazine (Thorazine)
– metoclopramide (Reglan)
– memantine (Namenda)
– ginkgo biloba
❖ The effect of succinylcholine is potentiated by:
– lithium
– quinidine
– cyclophosphamide
– aminoglycoside (tobra/genta/neo-mycin)
Here is a sneak preview of some other medication mascots for drugs used in electroconvulsive therapy. Stay tuned for future posts.
Rocuronium (ZEMURON)
Pronounced: ROK ur OH nee um
Mnemonic: “Zemur on Rocker”
Mascot: A Zemur (Zebra Lemur) on a Rocker
Rocuronium—"Rock"—is a nondepolarizing neuromuscular blocker that can be used in stead of succinylcholine for ECT—"Let's use Rock, not Sux". Duration of action is longer than with succinylcholine.
Sugammadex (BRIDION)
Pronounced: soo GAM ma dex
Mnemonic: "Mad Sugar"
Mascot: Mad sugar cube encapsulating rocuronium.
Sugammadex (Bridion) is a selective relaxant binding agent (SRBA) used to reverse neuromuscular blockade induced by rocuronium and vecuronium.
Methohexital (BREVITAL)
Pronounced:
METH oh HEX i tal / BREV i tal
Mnemonic: “Briefly vital Metal hexapod”
Methohexital is a rapid, ultra-short-acting barbiturate used to induce deep sedation for ECT.
Etomidate (AMIDATE)
Pronounced:
e TOM i date / AM i date
Mnemonic: “Am I dating eTom?”
Etomidate is a non-barbiturate GABA-A receptor modulator that can be used to induce deep sedation for ECT. If it is difficult to induce a seizure with methohexital, etomidate can be used because it lowers seizure threshold.