Is There Still a Role for Succinylcholine in Contemporary Clinical Practice? Christian Bohringer, Hana Moua and Hong Liu*
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Translational Perioperative and Pain Medicine ISSN: 2330-4871 Review Article | Open Access Volume 6 | Issue 4 Is There Still a Role for Succinylcholine in Contemporary Clinical Practice? Christian Bohringer, Hana Moua and Hong Liu* Department of Anesthesiology and Pain Medicine, University of California Davis Health, Sacramento, California, USA ease which explains why pre-pubertal boys were at an Abstract especially increased risk of sudden hyperkalemic cardiac Succinylcholine is a depolarizing muscle relaxant that has arrest following the administration of succinylcholine. been used for rapid sequence induction and for procedures requiring only a brief duration of muscle relaxation since the In 1993 the package insert was revised to the following: late 1950s. The drug, however, has serious side effects and “Except when used for emergency tracheal intubation a significant number of contraindications. With the recent or in instances where immediate securing of the airway introduction of sugammadex in the United States, a drug is necessary, succinylcholine is contraindicated in chil- that can rapidly reverse even large amounts of rocuronium, succinylcholine should no longer be used for endotracheal dren and adolescent patients…”. There were objections intubation and its use should be limited to treating acute la- to this package insert by some anesthesiologists and ryngospasm during episodes of airway obstruction. Given in late 1993 it was revised to “In infants and children, the numerous risks with this drug, and the excellent ablation especially in boys under eight years of age, the rare of airway reflexes with dexmedetomidine, propofol, lido- possibility of inducing life-threatening hyperkalemia in caine and the larger amounts of rocuronium that can now be administered even for an anesthesia of short duration. The undiagnosed myopathies by the use of succinylcholine use of succinylcholine for endotracheal intubation should must be balanced against the risk of alternative means disappear from clinical practice. of securing the airway” [5,6]. These hyperkalemic car- diac arrests are not very common due to the relatively Keywords low incidence of undiagnosed Duchenne’s and other Succinylcholine, Depolarizing muscle relaxant, Rapid se- muscular dystrophies. They are, however, especial- quence induction ly traumatic because they occur in apparently healthy children whose myopathy was previously undiagnosed Introduction and they frequently end in death of the child or a child The depolarizing muscle relaxant drug succinylcho- with significant brain damage. If a hyperkalemic arrest line was introduced in the United Sates in 1952 and occurs, calcium as well as insulin and glucose need to be has been widely used in clinical medicine since the late administered [7]. Only about half the patients will sur- 1950s [1,2]. It was initially widely accepted as an intu- vive this type of hyperkalemic cardiac arrest with appro- bation drug due to its rapid onset and its short dura- priate treatment and the risk of hyperkalemia should, tion of action. A significant advantage of this drug over therefore, not be taken lightly. other muscle relaxants was the short duration of action Cardiac arrests following succinylcholine occur in in most patients as long as the patient did not have a both children and adults. There are many cases of hy- pseudocholinesterase deficiency. Since the introduction perkalemic cardiac arrest in patients with stroke, spinal of the rapid acting reversal agent sugammadex that is cord injury, burns and immobilization. These conditions specific for rocuronium this advantage is no longer pres- are associated with an extra-junctional proliferation of ent [3]. acetylcholine receptors in skeletal muscle which causes an exaggerated release of potassium from skeletal mus- Disadvantages of Succinylcholine cle cells following the administration of succinylcholine. In 1993 the Food and Drug Administration (FDA) is- It takes some time for this extra-junctional proliferation sued a “Black Box Warning” in response to a series of to occur but hyperkalemia has been observed as early intractable cardiac arrests that occurred in children with as four days after the injury [8]. Given the high preva- previously undiagnosed muscular dystrophy [4]. This lence rate of contraindication to succinylcholine its use warning significantly reduced its use in children and ad- in the intensive care unit has been discouraged [9]. In olescents. Duchenne’s muscular dystrophy was the con- the emergency department, its use is also problematic dition most commonly involved. This is an x-linked dis- because there is often only a limited amount of infor- Transl Perioper & Pain Med 2019; 6 (4) DOI: 10.31480/2330-4871/100 • Page 129 • DOI: 10.31480/2330-4871/100 Acetylcholine Succinylcholine Figure 1: Parasympathomimetic action because it is essentially two molecules of acetylcholine combined with each other. mation available about a patient’s health status when is not fatal as long as the persistent weakness is rec- an unconscious patient needs to be urgently intubated. ognized and appropriately treated prior to extubation. Rocuronium is also increasingly replacing succinylcho- Clinical signs of persistent neuromuscular block are: a line in the prehospital environment [10] Succinylcholine lag of the eye lids when trying to open the eyes and lack is also associated with the risk of severe bradycardia of antigravity power with the classic “fish out of water” and asystolic cardiac arrest. This is due to its parasym- appearance need to be recognized before extubation. If pathomimetic action because it is essentially two mol- the patient is extubated before the succinylcholine has ecules of acetylcholine combined with each other (Fig- worn off this will lead to hypoxia that is followed by an ure 1). This is more likely to occur with large and repeat emergency re-intubation. The pupils are usually dilated doses, and succinylcholine infusions. When large doses and the patient is tachycardic and hypertensive because or an infusion are administered the patient should be being awake with persistent neuromuscular weakness pre-treated with a prophylactic dose of atropine prior leads to a potent activation of the sympathetic nervous to administering the succinylcholine. Infusions of suc- system. It is important to check the pupil diameter be- cinylcholine in particular are an outdated anesthesia cause persistent neuromuscular block is often misdiag- technique that should no longer be employed because nosed as delayed emergence from general anesthesia of the risk of bradycardia and prolonged duration of drugs. If excessive amounts of general anesthesia drugs neuromuscular block. are postulated to be the cause for a patient’s non-re- sponsiveness after an anesthesia, then the pupils should Prolonged neuromuscular block: Recovery from neu- be constricted. A nerve stimulator can be used to dis- romuscular blockade is unpredictable after succinyl- tinguish a depolarizing block without fade on train of choline. The prevalence of pseudocholinesterase de- four (TOF) and without post-tetanic facilitation due to ficiency is much higher than that of undiagnosed my- succinylcholine from a non-depolarizing block with fade opathies. Significantly prolonged apnea following suc- on TOF and post-tetanic facilitation due to residual ro- cinylcholine occurs in around one in three thousand curonium, vecuronium or cis-atracurium. It is, however, administrations [11]. The cause is usually a congenital very important in this circumstance to administer some deficiency of the pseudocholinesterase enzyme but se- propofol to the patient prior to the use of the nerve vere liver disease and malnutrition may also lead to stimulator to prevent recall of the tetanic stimulus. It is prolonged paralysis [12,13]. Patients who experience already stressful enough for a patient to be awake and a prolonged block after succinylcholine will also have a feeling weak. An awake patient with persistent neuro- prolonged block after mivacurium because this drug is muscular block should never be subjected to the painful also eliminated by the same plasma enzyme [14]. Bu- stimuli of a nerve stimulator without proper sedation tyryl-cholinesterase deficiency is a condition charac- [16]. The patient should be reassured that the weak- terized by autosomal recessive inheritance and novel ness that he/she feels is a side effect of a medication mutations in the butyryl-cholinesterase gene continue and will get better. Many patients with a persistent neu- to be identified [15]. romuscular block after anesthesia think that they had Unlike the cardiac arrests that occur with myopa- a stroke during their surgery and an explanation and thies and immobilization, the prolonged neuromuscular reassurance to them while they are still intubated is of block in patients with pseudocholinesterase deficiency utmost importance. If there is fade and post-tetanic fa- Transl Perioper & Pain Med 2019; 6 (4) • Page 130 • DOI: 10.31480/2330-4871/100 cilitation the residual neuromuscular block may be due should be used [23,24]. to rocuronium, then, more sugammadex should be ad- Masseter spasm after succinylcholine makes endo- ministered to reverse it. A non-depolarizing block may tracheal intubation difficult or impossible and may her- also be due to a phase two block in patients that have a ald the development of a malignant hyperthermia reac- butyryl-cholinesterase deficiency or have been adminis- tion. If masseter spasm occurs the patient needs