Succinylcholine chloride is a short-acting depolarizing neuromuscular blockade that is approved by the United States Food and Drug Administration (FDA) as a provision to other sedatives or hypnotics. It is a correlate of acetylcholine (ACh); hence, it disrupts all cholinergic receptors of the parasympathetic and sympathetic nervous systems. Its use can expedite rapid endotracheal intubation, facilitate surgical procedures, and aid in mechanical ventilation by relaxation of skeletal muscles. Due to its rapid onset and short mechanism of action, it is the drug of choice in emergency situations where immediate airway management is required. The drug's rapid onset allows for quick intervention and control of the airway, and its short duration is advantageous when endotracheal intubation can not be achieved. The skeletal muscle relaxation provided by succinylcholine is beneficial during certain surgical procedures, more specifically, when abdominal wall muscle disruption is necessary, mechanical ventilation is difficult or defied, or in surgical cases where spontaneous respiration of the patient is counterproductive to the procedure.
Succinylcholine is often used as an adjunct therapy in patients undergoing electroconvulsive shock therapy (ETC) to control muscle contractions induced as a result of the electrical impulses delivered during the procedure. However, this is an off-label use that is not currently approved by the FDA.
A depolarizing neuromuscular blocking agent, succinylcholine adheres with post-synaptic cholinergic receptors of the motor end plate, inducing continuous disruption that results in transient fasciculations or involuntary muscle contractions, and subsequent skeletal muscle paralysis. Following pharmacological onset, further neuromuscular transmittance across the neuromuscular junction is interrupted, given the medication dosage is sufficient and remains bound to the cholinergic receptor sites of the motor end plate. Depolarization of the postjunctional membrane deactivates sodium avenues resulting in inhibited responses to acetylcholine normally released. The mechanism of action is apparent within 60 seconds of intravenous administration and continues up to 360 seconds or 6 minutes. Succinylcholine's pharmacological and chemical composition makes it neuromuscular receptor site-specific, thus succinylcholine is ineffective on smooth and cardiac muscles of the body. Plasma pseudocholinesterase is responsible for the rapid hydrolyzation and metabolism of the drug in the bloodstream. A very minimal percentage of succinylcholine encompasses the neuromuscular motor end-plates post administration. Skeletal muscle paralysis will continue pending sufficient disassociation of succinylcholine from the acetylcholine neuromuscular receptor sites and consequential pseudocholinesterase hydrolyzation permitting baseline neuromuscular receptor function and thus normal motor end-plate activity.
Succinylcholine doses should be calculated following a thorough patient assessment and evaluation. Dosing is patient specific and calculated based on current total body weight in conjunction with the overall physical condition; calculations hold true even in obese and obstetrical patients. The FDA-approved intravenous dose for rapid sequence intubation is 1.5 mg/kg. However, if estimating the dose higher succinylcholine dosing for rapid sequence intubation is far better than underdosing. A reasonably higher dose of the drug produces the same paralysis as an appropriate weight-based dose with little to no known dose associated increased risk for the patient. A deficient dose of succinylcholine can result in inadequate paralysis, thus creating unforeseen challenges while attempting to perform intubation or other procedures in which the depolarizing neuromuscular blockade is utilized. Intravenous injection is the most common form of administration. However, it can be safely administered intramuscularly or via continuous intravenous infusion in surgical cases of prolonged duration. Special precautions should be taken in conjunction with the use of a peripheral nerve stimulator when administering a continuous infusion of succinylcholine to avoid toxicity or overdose. Succinylcholine should never be administered without assuring adequate sedation prior to administration.
Hyperkalemia is the most common adverse effect of succinylcholine administration and is attributed to the drugs stimulatory effect on skeletal muscles. Serum potassium levels may increase as much as 0.5 mEq/L which is clinically insignificant unless predisposition to hyperkalemia exists as a result of disease pathophysiology that induces upregulation of postjunctional acetylcholine receptors. If such disease pathology is present, succinylcholine use is contraindicated. If hyperkalemia is sufficient to create electrocardiography changes, succinylcholine should be avoided in such circumstances. Special considerations should also be taken with those who have chronically elevated potassium levels such as renal failure patients, so as to not induce acute on chronic hyperkalemia. Succinylcholine should be avoided in patients with significant burn or traumatic injuries that are 24 to 72 hours post-injury due to the high probability of acute hyperkalemia that may be exacerbated as a result. Marked and/or untreated hyperkalemia may result in dysrhythmias or even death
Masseter muscle spasms, otherwise known as trismus, may follow the administration of succinylcholine in a small percentage of the population and can be an isolated adverse effect, or rarely, seen in conjunction with malignant hyperthermia. The presence of hyperthermia, trismus, and metabolic derangements consequent to succinylcholine administration should precipitate a differential diagnosis and interventional plan appropriate for malignant hyperthermia. If trismus occurs subsequent to succinylcholine administration, an appropriate dose of non-depolarizing neuromuscular blocking agents such as rocuronium or vecuronium should be administered and have proven to be highly effective in such circumstances.
Bradycardia may manifest following succinylcholine administration in a select population, especially pediatrics, as a result of the nicotinic activation that manifests as muscarinic stimulation and lower heart rate. Pre-treatment with an age-appropriate dose of atropine has shown to be beneficial in preventing or minimalizing bradycardia that may occur as a result of succinylcholine administration. Bradycardia may also be seen in patients that require a continuous infusion of the depolarizing neuromuscular blocking agent and can also be corrected with atropine in such situations.
Increases in intraocular pressure have been associated with succinylcholine administration. However sufficient research to support the theory and its associated risk is currently unavailable. Any increase in intraocular pressure can be counteracted or prevented with the use of an appropriate sedative in conjunction with the depolarizing neuromuscular blockade.
Succinylcholine administration without assurance of adequate sedation can result in paralysis in a conscious to semi-conscious patient. This can be avoided by making sure the patient is adequately sedated prior to administration of succinylcholine.
The administration of succinylcholine chloride is contraindicated in patients with known decreased plasma cholinesterase activity, recent burns or trauma within 24 to 72 hours, and muscle myopathies. In patients with decreased plasma cholinesterase activity, drug metabolism is prolonged thus prolonging the duration of its paralytic and other effects. Patients with recent burns or acute trauma are susceptible to have hyperkalemic rhabdomyolysis which is exacerbated by the administration of succinylcholine chloride and can result in ventricular dysrhythmias or even death. Those with muscle myopathies may be undiagnosed, the most frequent is Duchenne muscular dystrophy, in which succinylcholine chloride administration is contraindicated. Other conditions that pose a potential contraindication to the administration of the deplarizing neuromuscular blockade or use with caution are mastocytosis, myxedema, myasthenia gravis, muscular dystrophy, closed angle glaucoma, severe liver and/or renal impairment or failure, cerebrovascular accident longer than 72 hours, and malignant hyperthermia. Those on aminoglycoside antibiotics or cholinesterase inhibitors should not be given succinylcholine chloride due to their ability to exacerbate paralysis or reduce the metabolism of the depolarizing neuromuscular blockade. If neuromuscular blockade is needed in patients with these high risk conditions consideration can be given to using a non-depolarizing neuromuscular blocking agent.
Use of neuromuscular blockade, i.e. paralytics, is also contraindicated in patients who are not adequately sedated. While the agent will remain effective in producing neuromuscular blockage without adequate sedation the patient may be conscious or semi-conscious while paralyzed. For obvious reasons this should be avoided.
The therapeutic index is the measurement range of drug safety among the average age groups. The range for adults is 0.3 to 1 mg/kg with a recommended dose of 0.6 mg/kg administered intravenously. Patients who have been given succinylcholine chloride should be placed on continuous cardiac monitoring in conjunction with end-tidal carbon dioxide monitoring. Pulse oximetry should also be monitored. If a continuous infusion of succinylcholine chloride is required, a nerve stimulator should be used to monitor the effects of the neuromuscular blockage to a train of 4 in conjunction with continuous cardiac monitoring and end-tidal carbon dioxide measurements. The use of a nerve stimulator will indicate whether the patient is exhibiting a phase-I neuromuscular block or it has converted to a phase-II neuromuscular block.
Administered doses of succinylcholine higher than those recommended based on patient's actual body weight may result in neuromuscular blockade toxicity, which may result in neuromuscular paralysis beyond the time required for procedures, surgical interventions, and anesthesia. Succinylcholine toxicity may manifest via generalized muscle weakness, decreased or absent respiratory reserve, low inspiratory or tidal volumes, or apnea. Taking the dose of succinylcholine administered above the recommended dose and the duration of administration into consideration, depolarizing neuromuscular blockade toxicity which is a phase-I blockade may convert to a phase-II blockade with patient assessment characteristics resembling those of a non-depolarizing neuromuscular blockade. Primary treatment and intervention for succinylcholine toxicity is airway maintenance and respiratory support sufficient for the patient to maintain adequate oxygenation until the drug is metabolized and the patient can maintain adequate oxygenation and ventilation without mechanical support.