Why We Do What We Do: Succinylcholine-Induced Hyperkalemia

Home / Lectures / Why We Do What We Do: Succinylcholine-Induced Hyperkalemia

potassium cartoon

Succinylcholine has proven to be one of the best paralytic agents used for rapid sequence intubation. In a recent Cochrane Review, Succinylcholine was compared to Rocuronium and demonstrated consistent improved intubation conditions. (Granted the review does not address intubation coupled with common dissociative agents, only noting no difference when paired with Propofol.)(1) Most would agree that succinylcholine is their “go-to” medication because of how truly effective it is. It is armed with a rapid-onset within one minute as well as short duration of action (7-8 minutes) (2). Despite it’s benefits, Succinylcholine has some attributes that make clinicians pause when using it. Most prevalent on that list is Hyperkalemia. So what does the evidence say?

Succinylcholine causes for a transient elevation in potassium by 0.5 – 1.0 mEq in the first 3-5 minutes following administration. This is not of grave concern for most patients as their potassium level is likely normal with hopefully normal kidney function. A recent study has addressed the hyperkalemia concern by publishing a retrospective look on anesthesia data. The study noted a lack of poor outcomes, including dysrhythmias and death when coupled with elevated potassium pre-operatively (3). So what is the big concern if anesthesiologists are saying its not a big deal? Should ER doctors be concerned about succinylcholine-induced hyperkalemia?

Understanding why hyperkalemia happens in the presence of succinylcholine is helpful…so let’s discuss that first. As succinylcholine replaces acetylcholine, there is a transient release of potassium by nicotinic receptors. Those patients who have been immobilized either due to casting, paralysis, muscle disorders or nerve injuries have an up-regulation of their nicotinic receptors (4). Just like insulin receptors increase in Type-2 diabetes, muscle cells produce more nicotinic receptors when they aren’t getting the stimulus they expect. As a result, the administration of succinylcholine leads to depolarization and a large efflux of intracellular potassium into the plasma. Further, it is theorized that succinylcholine is metabolized much more slowly than acetylcholine and thus causes a sustained depolarization exaggerating the potassium release.

How does this apply to Emergency medicine? Do we need to consider this physiology in the acutely burned patient? To answer the burn question, the answer is no in cases of acute second and third degree burns. (If they largely enter the muscle, it would give me pause.) The literature and father of Succinylcholine induced Hyperkalemia research, Dr. Gerald Gronert, says that “after thermal injury, the onset seems to be approximately a week to 10 days and persists until skin is covered, good overall healing, decent appetite, and weight gain.” The reason why there is a delay in succinylcholine potentiating hyperkalemia is that there is a delay in the time it takes to up-regulate the nicotinic receptors. His conclusions are drawn from research in a burn unit during Vietnam as well as porcine studies(5). So we don’t need to worry about acute burns, only those patients that have bounced back to the Emergency Department after leaving the burn unit.

What about patients with muscle injury particularly crush injury in trauma? We have to worry about these patients as they likely have rhabdomyolysis. In rhabdo, there may be a large amount of K+ hanging around in the plasma milieu due to cell death. A slight tip in the scale from 7.6 to 8.1 may mean the difference in cardiac dysrhythmia.

We know that we have to be particularly concerned with those patients who have up-regulation in their nictonic receptors. A recent study noted patient that had been in the ICU for 16 days are at increased risk (6). Other patients to consider at risk include paraplegics, quadriplegics, as well as patients with muscular dystrophy as they have up-regulation in their nicotinic receptors. Neuropathy and cerebral injury are other situations where there is up-regulation (5,6). When considering your acutely ill and septic patients there has been no correlation seen with succinylcholine-induced hyperkalemia and sepsis unless paired with rhabdo, nerve injury (especially cerebral injury), patients confined to bed or thermal injury.

The last group of patients you may consider poor candidates for succinylcholine are renal failure patients. However, based on a review article published in 2000, there is evidence to support the safe use of Succinylcholine in patients with renal insufficiency. The authors did suggest in their article that a level above 6.0 mEq may warrant treatment before succinylcholine’s use. It is, however, absolutely contraindicated in patients with rhabdo/trauma, nerve injury/disorder, or thermal injury coupled with kidney injury(2). I would advise caution in the Emergency Department as we don’t know the potassium of the renal patient you are treating upon arrival.

So what do we walk away with?:

• Anybody with rhabdo/trauma/muscle disorder, nerve injury/disorder, been lying in bed for a really long time or thermal injury (outside of the initial burn) does not get succinylcholine
• Most patients will be fine because it is rare to cause hyper-K with succinylcholine
• Hyperkalemia seems to be induced by higher concentration/up-regulation of nicotinic receptors
• If you don’t know if you should use succinylcholine, use Rocuronium knowing that you may be sacrificing rapid onset and short duration of succinylcholine but you are maintaining your piece of mind

Reference:
1. Lee, PJ & Wells, G, Rocuronium versus succinylcholine for rapid sequence induction intubation, Cochrane Database of Systematic Reviews 2003. Issue 2 No.: CD002788. DOI: 10.1002/14651858.CD002788
2. Thapa, S, Brull, S, Succinylcholine-Induced Hyperkalemia in Patients with Renal Failure: An Old Question Revisited, Anesthesia & Analgesia, July 2000 Vol. 91(1):237-241.
3. Schow, AJ et al., Can Succinylcholine Be Used Safely in Hyperkalemic Patients?, Anesth Analg 2002; 95:119-122.
4. Jeevndra Martyn, JA, Richtsfeld, M, Succinylcholine-induced Hyperkalemia in Acquired Pathologic States: Etiologic Factors and Molecular Mechanisms, Anesthesiology 2006; 104:158-169.
5. Gronert, GA, Succinylcholine-Induced Hyperkalemia and Beyond, Anesthesiology, 2009; 111 (6): 1372-1377
6. Blanie, A et al., The Limits of Succinylcholine for Critically Ill Patients, Anesth Analg 2012; 115:873-9.

4 Comments

  • jacobidoc

    great post! there was no mention of avoiding succinylcholine in the pediatric population (kids younger than 5). anesthesiologists avoid succ’s in this population because of the potential of hyperK leading to cardiac arrest in undiagnosed muscular dystrophy pt’s. the thought being that by the age of 5, they will have been diagnosed. the data stems from a few case reports (most recent one published in the 1980’s) were ped’s pt’s were paralyzed with succ’s and subsequently suffered mortal outcomes. it’s easy to avoid succ’s in the OR because you have time to think ahead and plan for the case, plus there are so many different options for induction and paralytic agents. however, this is never the case in the ED. does anyone know if this is avoided in pediatric ED’s?

    • Ismael

      In the Montefiore Peds ED, succinylcholine is avoided in kids less than 3yrs old (more or less). The case reports referred to above have guided their practice. The thought is that once a child is 3ys old they are walking and any significant muscular disorder should be diagnosed. They prefer to use the non-depolarizing neuromuscular blockers

  • Awesome post, Mike.

    Can you tell us how the authors concluded that “a K level above 6 may warrant treatment before succinylcholine’s use?” This is a hard topic to study, but was there any study that made ROC curves that showed the most effective cutoff value is really 6.0?

Leave a Reply