You receive a call from the lab for a critical result; your patient has a potassium of 6.0. You order an ECG and then look around for an attending for help. Should you just give the patient sodium zirconium cyclosilicate (commercially known as Lokelma), or should you throw the kitchen sink at the patient? Are those T waves peaked? Panic no longer - let’s talk hyperkalemia.
This patient has never had hyperkalemia before, he has well functioning kidneys, and he isn’t even taking any meds. What’s going on?
Remember one of the top EM rules: Trust but verify. The first thing to consider is a pseudohyperkalemia. Upwards of 98% of potassium in the human body is stored intracellularly, so the first thought for elevated values is lysis, starting with hemolysis. Venous blood gases (VBGs) are run on whole blood, so they cannot tell you if the sample is hemolyzed or not - best to wait for the Basic Metabolic Panel (BMP). If the BMP is hemolyzed, you can always resend a VBG. Long tourniquet times, delays in blood processing, blood drawn through J loops or narrow-gauge needles, and fist clenching can cause hemolysis. Also, remember that any cell that lyses can elevate the potassium, so consider lysis as the etiology of hyperkalemia in patients with polycythemia, leukocytosis (eg. leukemias), and thrombocytosis, as well (1).
After double checking, you note that the hyperkalemia is real. What’s on the differential?
Other than renal failure, we have a few things to consider. Toxicologic etiologies should always be on the differential: Consider ACE inhibitors, ARBs, beta blockers, NSAIDs, digoxin, and sulfamethoxazole-trimethoprim (commercially known as Bactrim) as the culprit. If the patient has experienced a traumatic mechanism, consider that crush injuries and burns can elevate the potassium level. Additionally, massive transfusions may be the culprit, as potassium leaks out of packed red blood cells (pRBCs) into the supernatant while awaiting use (2). Rhabdomyolysis, in which muscle cell breakdown occurs, is another common etiology. Lastly, acidosis can elevate the potassium as the body tries to regulate protons via the K+/H+ pump.
The ECG looks normal. Is treatment really necessary?
While ECG changes are specific at detecting elevated potassium levels that can be lethal, they are not sensitive. Generally, ECG changes in hyperkalemia follow an expected course: peaked T’s, flat P waves with prolonged PR, widened QRS, and ultimately the sine wave. However, be aware that ECG changes do not always follow a predictable pattern, and patients can decompensate quickly at a wide range of potassium levels (2,3). If you see a wide QRS, junctional rhythm, or bradycardia, get your cardiac pads and IV calcium ready (3). Review the FOAMed links at the end of this page to review what these changes look like on an ECG.
Is the potassium even that high? When should we be giving certain treatments?
Per the Kidney Disease: Improving Global Outcomes conference, a potassium level of <6.0 with no ECG changes may be classified as mild (4). Recommendations for treatment of a potassium level of <6.0 are variable and depend on the underlying cause. If your patient has poor renal function and a potassium level of 5.9, you might be able to stick to excreters (e.g. furosemide if the patient still makes urine, Lokelma) and hold off on rapid-acting agents. Any potassium level over 6.0 should prompt an ECG, and treatment at this level is typically recommended with potassium shifters (e.g. short-acting insulin and albuterol), excreters (e.g. furosemide, Lokelma), and possibly hemodialysis.
The T waves appear slightly peaked; should we consider giving IV calcium?
There is an unclear role in giving calcium for repolarization changes. Peaked T waves have not definitively been shown to lead to short-term adverse cardiac events in the setting of hyperkalemia, but they are early signs of hyperkalemia (3,4). Use of calcium for peaked T waves in potassium levels of <6.5 is controversial, though it is generally accepted and is part of the hyperkalemia protocol in the Cook County Emergency Department (5). That said, if your patient’s ECG demonstrates atrioventricular (AV) blocks, wide QRS complexes, or bradycardia, you should give calcium. If the potassium level is >6.5 or the patient has experienced cardiac arrest, you should give calcium. Recognize that calcium is also a short-acting medication, with its effects lasting only 30 minutes to one hour, so we need to consider ways to shift and eliminate calcium, as well.
Albuterol is relatively benign, right? What role does it play in hyperkalemia management?
While albuterol is generally well tolerated, make sure to order the correct dosing. If you want to use albuterol to shift potassium levels, you must use large doses, such as 10 mg over 15 minutes. As a point of comparison, neb treatments that are typically used for asthma or COPD are 2.5 mg over 15 minutes.
If considering giving insulin to shift potassium, how should we manage a patient with a normal glucose?
If the patient is insulin-naive, has renal failure, or already has a low glucose level, you should start with 5 units of short-acting IV insulin. Though some studies have found that 10 units of short-acting IV insulin may provide increased potassium reduction, it is not a consistent finding across studies, has unclear clinical relevance, and may worsen rates of hypoglycemia; thus, it should be avoided (6). Check out the EM Docs summary in the FOAMed resources below for further information on this.
You should give at least 25 g of dextrose with insulin, such as 50 ml (one amp) of D50 or 250 ml of D10. Effects of insulin can linger in patients with impaired renal function, and hypoglycemia can occur 2-3 hours after insulin administration, so make sure you are obtaining hourly blood glucose checks (6,7). You can initiate a D10 drip at 50ml/hr to avoid hypoglycemia. Effects after albuterol and short-acting insulin should start at approximately 15 minutes and peak around an hour, so recheck your potassium around that time, too. After 2-3 hours, potassium will start to shift back, so remember to decide on a way to eliminate potassium, as well.
If the QRS is widening, what calcium options are available?
Unless the patient is getting CPR, use IV calcium gluconate as the standard agent for treatment. Calcium chloride is the other IV agent, but it is toxic when it extravasates, so we reserve it for code scenarios only. One confusing point here is that calcium chloride has 3x the availability of elemental calcium compared to calcium gluconate, so while we give 1 g (amp) of calcium chloride in a code, you may need to redose calcium gluconate a few times to get the same effect. Start with calcium gluconate 1 gm via IV piggyback over 5-15 minutes and redose if needed to get the QRS complex narrowed again.
PHEW! The patient made it. Good job!
A whirlwind, but just remember, recheck the potassium if you are in doubt. Order calcium if that ECG demonstrates an signs of hyperkalemia. Use potassium shifting medications, but strictly monitor your patient’s glucose levels. And ultimately, come up with a plan to get calcium excreted. If you have not gotten enough, check out the FOAMed links below for more information!
Authored by Samson Frendo, MD and Eric Leser, MD.
FOAMed Resources:
Emergency Medicine Cases Overview: https://emergencymedicinecases.com/emergency-management-hyperkalemia/
LITFL ECGs: https://litfl.com/hyperkalaemia-ecg-library/
Emergency Medicine Cases more ECGs: https://emergencymedicinecases.com/ecg-cases-10-hyperkalemia-the-great-imitator/
Rebel EM - contains a good chart of tx options with time to onset and duration of action: https://rebelem.com/ecg-changes-hyperkalemia/
EM Docs Insulin Dosing in Hyperkalemia: https://www.emdocs.net/insulin-dosing-in-hyperkalemia-is-it-a-one-size-fits-all/
References:
Okpara, H. , Izuchukwu, E. & Ilechukwu, E. (2023). Pseudohyperkalemia Revisited: An Updated Review of a Foremost Preanalytical Error of Serum or Plasma Potassium Measurement in the Clinical Laboratory. Nigerian Journal of Medicine, 32 (6), 567-579. doi: 10.4103/NJM.NJM_49_23.
Ashurst, J., Sergent, S., & Wagner, B. (2016). Evidence-Based Management Of Potassium Disorders In The Emergency Department [Review of Evidence-Based Management Of Potassium Disorders In The Emergency Department]. EB Medicine, 18(11), 1–24. https://www.ebmedicine.net/topics/hepatic-renal-genitourinary/hyperkalemia-hypokalemia
Durfey N, Lehnhof B, Bergeson A, Durfey SNM, Leytin V, McAteer K, Schwam E, Valiquet J. Severe Hyperkalemia: Can the Electrocardiogram Risk Stratify for Short-term Adverse Events? West J Emerg Med. 2017 Aug;18(5):963-971. doi: 10.5811/westjem.2017.6.33033. Epub 2017 Jul 10. PMID: 28874951; PMCID: PMC5576635.
Lindner, G. , Burdmann, E. , Clase, C. , Hemmelgarn, B. , Herzog, C. , Małyszko, J. , Nagahama, M. , Pecoits-Filho, R. , Rafique, Z. , Rossignol, P. & Singer, A. (2020). Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. European Journal of Emergency Medicine, 27 (5), 329-337. doi: 10.1097/MEJ.0000000000000691.
Gupta AA, Self M, Mueller M, Wardi G, Tainter C. Dispelling myths and misconceptions about the treatment of acute hyperkalemia. Am J Emerg Med. 2022 Feb;52:85-91. doi: 10.1016/j.ajem.2021.11.030. Epub 2021 Nov 27. PMID: 34890894.
Moussavi, K. , Nguyen, L. , Hua, H. & Fitter, S. (2020). Comparison of IV Insulin Dosing Strategies for Hyperkalemia in the Emergency Department. Critical Care Explorations, 2 (4), e0092. doi: 10.1097/CCE.0000000000000092.
Rafique Z, Peacock F, Armstead T, Bischof JJ, Hudson J, Weir MR, Neuenschwander J. Hyperkalemia management in the emergency department: An expert panel consensus. J Am Coll Emerg Physicians Open. 2021 Oct 1;2(5):e12572. doi: 10.1002/emp2.12572. PMID: 34632453; PMCID: PMC8485984.