Therapeutic Effects: Short-acting depolarizing neuromuscular blockade

Anesthesia Implications

Use – the rapid onset along with rapid metabolism makes this drug ideal in situations of questionable airways and situations requiring rapid intubation (trauma).

Sedation First – always ensure adequate sedation prior to administration of succinylcholine.

Hyperkalemia – this is the most common adverse affect of succinylcholine administration. Anticipate an increase of 0.5 mEq/L. Conditions that result in upregulation of postjunctional acetylcholine receptors (eg. burn victims) may exhibit an exaggerated increase. Other conditions to be mindful of are those that result in chronically high potassium levels (eg. renal failure). There is a black-box warning on succinylcholine that hyperkalemia may result in patients less than 8 years old with undiagnosed muscular dystrophy. If cardiac arrest follows administration, hyperkalemia should be one of the top differential diagnosis.

Malignant Hyperthermia – succinylcholine is on the list of drugs that can induce malignant hyperthermia. In rare circumstances, a masseter spasm at induction may queue an impending malignant hyperthermic reaction. The accompanying symptoms of trismus, hyperthermia, rising end-tidal CO2, etc. should trigger differential diagnosis of malignant hyperthermia.

Bradycardia – this is a side effect that is most prominent in the pediatric population. Acetylcholine interacts with nicotinic receptors which results in an increased muscarinic tone (bradycardia). Atropine (0.02 mg/kg), if not contraindicated, is a good countermeasure.

increased Intraocular pressure (IOP) – Succinylcholine in isolation increases IOP. However, the sedative drugs typically given prior to administration of succinylcholine make this affect negligible.

Prolonged duration – cholinesterase inhibitors, timolol, cyclophosphamide, bambuterol, aminoglycoside antibiotics, neostigmine can all prolong the duration of succinylcholine. In general, a prolonged response to succinylcholine suggests a pseudocholinesterase deficiency. Chronic cocaine users can have low levels of pseudocholinesterase. With acute cocaine intoxication, cocaine competes with succinylcholine for metabolism by pseudocholinesterase, decreasing the metabolism of both drugs.

Toxicity – Doses above 1.5 mg/kg or utilizing a continuous infusion of succinylcholine may lead to toxicity. This is manifest as general muscle weakness, decreased respiratory reserve, low tidal volumes, or apnea. The treatment for toxicity is respiratory support until the drug has been adequately metabolized.

Contraindications

Patients inadequately sedated
Burn victims greater than or equal to 24 hours after injury
Acute trauma resulting in hyperkalemic rhabdomyolysis (eg. crush injuries)
Muscular Myopathies (eg. Duchenne muscular dystrophy)
Chronic hyperkalemic patients
Patient or family history of malignant hyperthermia
closed-angle glaucoma
severe liver and/or renal impairment or failure
cerebrovascular accident longer than 72 hours

IV push dose

Intubation:
Adults – 1.5 mg/kg TOTAL body weight (even in the obese).
Neonates – require a larger IV dose (2 mg/kg). Remember that pediatric patients may exhibit bradycardia. Atropine (0.02 mg/kg) is a good countermeasure.

Pediatric Laryngospasm:
1 – 2 mg/kg. Succinylcholine is given along with atropine (0.02 mg/kg) to prevent bradycardia.

IM dose: Adult: 4 mg/kg
PEDs: 4 mg/kg. Neonate: 5 mg/kg

Laryngospasm:
PEDs: 4 mg/kg. Onset time of 3 to 4 minutes for maximal twitch depression. Relaxation of airway tissue MAY occur within 1 minute. This route of administration may last upward of 20 minutes. Atropine (0.02 mg/kg) should be given along with the succinylcholine to prevent bradycardia.

Classification: Short-acting depolarizing neuromuscular blocker

Time to Onset: 60 seconds

Duration: up to 6 minutes

Method of Action: Succinylcholine is a correlate of acetylcholine. As such, it interacts with all cholinergic receptors in both the parasympathetic and sympathetic systems. At the motor endplate, continuous binding to the cholinergic receptors initially manifests as involuntary muscle twitches (fasciculations) and, after a short period of time, blocks sodium channels which inhibits binding of natural acetylcholine. This results in skeletal muscle paralysis. Composition of this drug makes it specific to skeletal muscle, so cardiac and smooth muscle remain unaffected.

Metabolism: Rapid hydrolyzation by plasma pseudocholinesterase