Written by Nicole McCoin
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A large observational series with over 4,000 intubations compared succinylcholine vs. rocuronium in rapid sequence intubation (RSI) and found no association between these two paralytics and first-pass intubation success or peri-intubation adverse effects.
Why does this matter?…. Because I am not a clairvoyant.
As much as I would love to know if my 65 year-old who is not protecting his airway has hyperkalemia, I usually don’t. I want to be able to turn to rocuronium as my beacon in the dark…a drug that will lead to an uneventful RSI. The anesthesia literature notes advantages to succinylcholine: faster onset, offset, and superior intubating conditions. However, this literature draws from RCTs in the OR and uses the Goldberg scale. This study is more applicable to the ED setting.
Succinycholine vs rocuronium? Not a “polarizing” issue in this article!
Alright, enough with the puns. Here is a quick synopsis of this article while you drink your morning coffee. This was a large observational series in which the authors analyzed prospectively collected data from 4,275 intubations in the National Emergency Airway Registry, which includes 22 emergency departments. First-pass intubation success was 87.0% among succinylcholine encounters and 87.5% among rocuronium encounters (adjusted OR 0.9; 95% confidence interval of 0.6 to 1.3). The incidence of adverse events was also comparable between the two paralytic agents, with a rate of 14.7% for succinylcholine and 14.8% for rocuronium (adjusted OR 1.1; 95% confidence interval of 0.9 to 1.3). Adverse events included issues ranging from mechanical (e.g. esophageal intubation or airway injury) to systemic (e.g. hypotension and cardiac arrest). The analyses performed in this paper show a lack of association between the choice of paralytic and first-pass success and adverse events, which suggests either agent is equally effective and safe.
Source
Emergency Department Intubation Success With Succinylcholine Versus Rocuronium: A National Emergency Airway Registry Study. Ann Emerg Med. 2018 Dec;72(6):645-653. doi: 10.1016/j.annemergmed.2018.03.042. Epub 2018 May 7.
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Reviewed by Clay Smith and Thomas Davis
Do we worry too much about hyperkalemia with succinylcholine? I haven’t looked into the literature and my attendings have not been able to answer the question with regards to what Rosen’s (8th edition) states below. It seems that we should be more worried about a mechanism of having upregulated ACh receptors such as genetic neuromuscular diseases, burns…. than ESRD.
“The mechanism by which severe hyperkalemia occurs is related to receptor upregulation on the postsynaptic muscle membrane. When a muscle is deprived of ACh stimulation for several days, receptor upregulation occurs, causing an increase in receptor density and a change of receptor subtypes on the muscle surface. ACh receptors are primarily K+ ion channels, and at-risk patients can have immediate, massive efflux of potassium as these newly recruited receptors are depolarized by succinylcholine. This occurs predominantly at the site of injury but may occur also in tissue remote from original insult. Although the hyperkalemia occurs within minutes after administration of succinylcholine and may be severe or fatal, the patient’s vulnerability to succinylcholine induced hyperkalemia does not become significant until 5 days after the inciting injury or burn as receptor upregulation production of protein subunits. Succinylcholine remains the agent of choice for RSI in acute burn, trauma, stroke, and spinal cord injury if intubation occurs less than 5 days after onset of the condition."
Great point and excellent question. Both hyperkalemia and up-regulation of ACh should be considered. Succinylcholine will increase serum potassium levels (0.5-1 mEq/L is classic teaching), but the effect is larger in patients with conditions that lead to up-regulation of the ACh receptor. So, if you have a dialysis patient with hyperkalemia and EKG changes, the potassium release from depolarization may be enough to push their serum level high enough to be problematic, even in the absence of ACh receptor up-regulation. Conversely, if you have a patient with a normal serum K but they are 7 days out from a burn injury, succinylcholine can cause a larger increase in serum K during depolarization than would typically be expected, which can be enough to cause symptomatic hyperkalemia.
Great points all and really helpful discussion. The risk of an unrecognized myopathy with unregulated post-synaptic receptors and resultant hyperkaemia is why we switched from succinylcholine to rocuronium in our children’s hospital.