emDocs Cases: Updates in Management of Hyperkalemia

Authors: Brit Long, MD (@long_brit, SAUSHEC EM Attending Physician) and Justin R. Warix, DO, FAAEM (EM Attending Physician, Central Peninsula Hospital, Soldotna, AK) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) 

Welcome back to emDocs Cases! Today we have case-based discussion on a core EM topic, with a look at some controversy and cutting edge treatments.

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A 62-year-old female with history of renal disease on dialysis, hypertension, and CAD presents with nausea and weakness. She missed today’s dialysis session. Her VS are normal, and her exam is also normal. What’s your first test you obtain?

The ECG!

You see large, peaked T waves with absence of P waves. The VBG returns with potassium of 7.3 mmol/L, with sodium 140 mmol/L and normal lactate.  You ask for your standard hyperkalemia regimen, or C BIG K DROP – see more from https://canadiem.org/tiny-tip-hyperkalemia-management/

This regimen classically consists of Calcium (gluconate or chloride salt), Beta agonist (10-20 mg albuterol nebulized) and/or Bicarbonate (1 amp), Insulin (10 units regular/Glucose D50 1 amp), Kayexalate (15-30 g oral or rectal), Diuretics (Furosemide 40 mg), and Renal unit for dialysis Of Patient.

 

What’s the literature behind this regimen? Is there anything better?

Before we start, let’s cover some basics.

– Most potassium is intracellular (98%), with 75% found in skeletal muscle. A significant gradient between the intracellular and extracellular environment plays a vital role in generation of cellular action potentials.1-5

– The renal system plays the most important role in regulation of potassium (90% of excretion). Normal levels are 3.5-5.0 mEq/L or mmol/L.1,2

– Changes in these levels affect cell membrane potentials and result in cardiac and neuromuscular symptoms. The Na-K-ATPase pump plays a large role in the cell membrane gradient.

– Mild hyperkalemia: 5.5-6.5 mEq/L (close to 10% of admitted patients).4-7

– Moderate levels are 6.5-7.5 mEq/L, and severe > 7.5 mEq/L.4-7

Etiology: Causes of elevated potassium include: excessive exogenous potassium, excessive endogenous potassium (hemolysis, rhabdomyolysis, burns, tumor lysis syndrome, trauma), redistribution (acidemia, medications (succinylcholine, beta-blockers), and insulin deficiency), decrease in excretion (renal failure/injury, decreased mineral corticoids, medications), factitious (hemolysis, thrombocytosis, venipuncture issue, leukocytosis).5-8

Clinical Manifestations: Since potassium plays an important role in Na-K-ATPase physiology, hyperkalemia can result in several important effects, primarily cardiac and neuromuscular. However, clinical features are nonspecific and include general weakness, lethargy, or confusion. Deep tendon reflexes may be depressed or absent, though cranial nerves, diaphragm function, and sensation are typically normal. GI effects include nausea, vomiting, and diarrhea.

– The ECG is one of the most important diagnostic tests in hyperkalemia. Predicted changes are classically thought to follow 1) Peaked T waves, 2) PR interval prolongation with loss of p wave, 3) QRS widening, 4) Sine wave pattern, and 6) Asystole.  Peaked T waves are a result of resting membrane potential changes.9-12

– These changes do not appear in order though. Dodge et al. found patients may progress from sinus rhythm to V fib.13 ECG demonstrates sensitivity of 34-43% in predicting hyperkalemia, with specificity 85-86%.12,14

– Slow change in serum potassium may result in no ECG changes, and levels above 9.0 mEq/L may not demonstrate expected findings.12,15

 

Our patient presented with weakness and ECG changes. You have asked for several medications, and let’s begin our deep dive into hyperkalemia treatment.

 

Management

– Treatment is not dependent on the cause of hyperkalemia but must focus on reversing or avoiding dysrhythmic effects and complications.

– Establish your safety net of IV access, continuous monitoring, and O2.

– Management focuses on cardiac stabilization, transcellular shift, and potassium excretion.  This must begin immediately once hyperkalemia is suspected, either by ECG changes (including peaked T waves) or by potassium > 6.5 mmol/L. 4,5,10,11,16

 

1) Cardiac Membrane Stabilization

Calcium decreases hyperkalemia’s depolarization effect and reduces the threshold potential of cardiac myocytes within minutes.4,5,17-19 This stabilizes the cardiac cellular membrane, but it does not result in transcellular shift or excretion of potassium, which requires other medications.

– Calcium can be given as two forms: chloride or gluconate salt. Ca chloride salt contains 13.6 meq in 10 mL, while Ca gluconate salt contains 4.6 meq in 10 mL.4,5,18,19  Ca gluconate can be given through a peripheral IV line. Ca chloride extravasation can cause tissue necrosis, and central line is recommended if possible (unless code situation.)4,5

CaCl 1 g contains approximately 270 mg Ca2+, while 3 ampules calcium gluconate contains the equivalent amount (approximately 90 mg Ca2+ per ampule).18,19

– Literature suggests Ca gluconate has similar time of onset as Ca chloride and may not require hepatic activity. Several studies conducted in patients undergoing liver transplant demonstrate similar increase in Ca after either formulation.19-21  A study conducted in dogs and pediatric patients demonstrates similar findings.21

– Onset of action is less than 3 minutes, with duration 20-60 minutes.4,5

Bottom Line: 1g (10 mL) Ca gluconate IV should be provided to patients with ECG findings (peaked T waves or worse), with reassessment within 5 minutes. More calcium should be provided if no change or worsening in ECG is observed. A patient in cardiac arrest or with central access should be given 1 g Ca chloride IV.

Is there another option for cardiac stabilization? Hypertonic saline (3%) can be used in 100 ml boluses, though this has been predominantly studied in patients with hyponatremia and hyperkalemia.22

 

2) Transcellular Shift 

This should occur with or immediately after calcium in order to redistribute potassium.4,5,23-25

 

A) Insulin and Glucose – These measures lower serum potassium in a dose dependent fashion.4,5,23-26 Activation of Na-K-ATPase and intracellular pump recruitment (GLUT4 receptors) to the cellular membrane are responsible for K transport intracellularly.27

– Classically, regular insulin 10-20 units is provided, with dextrose 25 g (one amp of D50) if blood glucose levels are less than 250 mg/dL.4,5,28,29

– Insulin and glucose decreases potassium by 0.45-0.61 mmol/L within 15 minutes,30-32 0.87 mmol/L at 30 minutes,33,34 and 0.47 mmol/L at one hour.23,24,33,34 Other studies suggest it may result in a decrease up to 1.2 mmol/L.23,24

– Insulin/glucose has onset of action less than 15 minutes (more commonly 5-10 minutes), and time of maximal action 25-30 minutes.23,24  Duration of action is 2 hours.

– Risks include hypoglycemia, which is often underestimated. This rate reaches 8.7% with 10 units of regular insulin.35  A rate of 13% was suggested in a study of patients with end stage renal disease,36 which reaches 75% at 60 minutes in patients undergoing hemodialysis.26 A systematic review suggests 18%.26

– The amount of glucose to provide can be difficult to determine, and Table 1 below offers an easy to follow means of determining what should be provided.

– Factors include absence of prior diabetes, absence of diabetic medications, and lower glucose before treatment. Renal injury or disease is a potential factor, as insulin is renally metabolized.4,5,36

– A potential change includes using short-acting insulin, such as lispro or aspart, which possess shorter half-lives, are more rapidly absorbed, and are not prolonged in renal failure/injury. This can be provided as short-acting insulin bolus of 10 units only, or 6 unit bolus followed by 20 unit per hour infusion of lispro or aspart. These regimens provide similar decreases in serum potassium while resulting in less hypoglycemia.4,5

– Glucose only is not recommended, which may result in hypertonicity and hyperkalemia.37,38

Bottom Line: Short acting insulin 10 units IV, with glucose infusion as above.

 

B) Beta agonistsCatecholamines increase activity of Na-K-ATPase pump and the Na-K-2Cl cotransporter.1-5,39,40

– Nebulized albuterol is given in doses of 10-20 mg, rather than the normal 5 mg for obstructive disease.

– Levalbuterol and albuterol demonstrate equal ability to decrease potassium.4,5,23,24

-Albuterol can be given IV in doses of 0.50 mg, and terbutaline can be given IM in doses of 0.25 mg. 4,5,23,24,31,41-43

– Potassium decreases by 0.6 mmol/L with 10 mg, and 1.0 mmol/L with 20 mg at one hour.31,41-43

– Onset is 20-30 minutes, with duration over two hours.31,41-43

– IV formulations include epinephrine, albuterol 0.5 mg, or salbutamol 2.5 mg, though side effects are more common.23,24,34

– Side effects include tremor, palpitations, and anxiety. IV forms have greater risk of increased blood pressure and headache.

– Combination treatment with insulin and glucose results in even greater decrease in potassium, 1.2-1.5 mmol/L at one hour after medication administration.31,41-43

Bottom Line: Albuterol 20 mg in 4 mL normal saline solution nebulized over 10 minutes.

 

 

C) Sodium BicarbonateBolus sodium bicarbonate has been recommended for acute treatment of hyperkalemia, based on studies evaluating prolonged bicarbonate infusion (over hours).23,24,31,32,44-46

– However, the literature in patients with normal pH does not support bicarbonate for hyperkalemia.4,5,23,24

– When compared with other agents, bicarbonate does not result in significant decrease in potassium at 30 and 60 minutes.23,24,32 Several controlled studies indicate sodium bicarbonate does not decrease potassium within 60 minutes.4,5,23,24 Studies that do suggest a decrease utilized bicarbonate infused over hours (rather than bolus) and in patients with acidemia.47,48

 

Combination Treatment

– Use of multiple agents provides the best means of potassium redistribution, with Cochrane review recommending combined insulin, glucose, and beta agonists.4,5,23-26

– Allon et al. finds maximum decrease in potassium by 1.21 mmol/L with IV insulin glucose with nebulized albuterol.31

– Bicarbonate should not be used unless the patient is acidemic.4,5

Bottom Line: Sodium bicarbonate can be used in patients with acidemia and hyperkalemia, but is not useful in other patients.  Combination therapy is efficacious with beta agonist and insulin/glucose in shifting potassium.

 

The patient’s glucose is 153. You give calcium gluconate 10% 10 mL IV, followed by 10 units short-acting insulin with one amp D50 and 20 mg albuterol nebulized. What’s your next step?

 

3) Potassium Excretion 

Means of excretion include urine, GI system, and blood.1-5 Kidneys are the predominant route of excretion. Physicians should assess patient volume status and ability to produce urine. If the patient can produce urine, a diuretic is a valid option.4,5  However, hemodialysis is the best means of definitive potassium removal.

A) Urinary DiuresisThis can be used while preparing the patient for hemodialysis. Urinary diuresis is not helpful if the patient cannot produce urine, though it may be helpful in patients with moderately compromised renal function.4,5

– Loop diuretics such as furosemide provide the greatest urinary excretion of potassium.

– Combination with acetazolamide can increase potassium excretion further, though this agent alone is not recommended.49

– These agents are best in patients with hypervolemia or euvolemia.  If provided, physicians should carefully monitor urinary output and electrolytes.

– If hypovolemic, IV fluids should be provided. This post will not evaluate which is best, but literature suggests Lactated Ringers or plasmalyte is better than Normal Saline. See this post from Josh Farkas at PulmCrit for more: https://emcrit.org/pulmcrit/myth-busting-lactated-ringers-is-safe-in-hyperkalemia-and-is-superior-to-ns/.

 

B) GISeveral options are available, with several new agents offering better options than Kayexalate.

– Sodium polystyrene sulfonate (SPS), or Kayexalate, is an ion-exchange resin that exchanges sodium for ammonium, calcium, magnesium, and potassium to allow potassium elimination through feces.4,5,23-26 Unfortunately, the literature behind SPS is extremely weak, with recent studies and Cochrane reviews recommending against its use.50,51  This medication provides a sodium load while placing the patient at risk for constipation, obstruction, and even worse, intestinal ischemia and necrosis. The medication even possesses a black box warning from the FDA.4,5,23,24,52  For more, see http://www.emdocs.net/skeptical-em-myths-evidence/ and http://rebelem.com/kayexalate-useful-treatment-hyperkalemia-emergency-department/

Patiromer is a synthetic polymer consisting of nonabsorbable spherical beads.52,53  The medication’s onset of action is 7-48 hours, with duration of effect 12-24 hours. 52-54  Healthy volunteers demonstrate a dose-related decrease in potassium by 15-20 mmol.55-57  Doses of 15-30g/day seem effective. The most common side effect includes hypomagnesemia (8.6%), though no cardiac dysrhythmias were found in those patients. Of note, the medication possesses a black box warning for separation of at least six hours from other oral medications.4

Sodium zirconium cyclosilicate (ZS-9) is a synthetic polymer consisting of nonabsorbable spherical beads.53,54 The medication binds greater than nine times the amount of potassium when compared with SPS, as one binding pore within the crystal structure binds to potassium specifically.143,149  ZS-9’s onset of action is 1-6 hours, with duration of effect 4-12 hours. Several studies support its use, with 10g/day decreasing potassium by 0.4 mmol/L at one hour and 0.7 mmol/L at 4 hours.58-60

– A meta-analysis compared patiromer and ZS-9, finding patiromer decreases potassium by 0.36 mEq/L by day 3 of treatment.61 ZS-9 demonstrates a decrease by 0.17 mEq/L at one hour and 0.67 mEq/L at 2 days.61

 

C) DialysisThis is the most efficacious way to remove potassium, with potassium decreasing by 1 mmol/L at 1 hour and 2 mmol/L by 2-3 hours. Lower potassium dialysate and increased blood flow can result in faster serum potassium decreases.4,5

– Increases in machine blood pump speed and plasma-to-dialysate concentration can decrease potassium within minutes; thus the importance of dialysis (especially in cardiac arrest).4,5,41

– Rebound hyperkalemia may be seen after dialysis, likely related to predialysis potassium levels.4,5

– Hemodialysis should be considered early in patient with diagnosed renal failure, inability to produce urine, hyperkalemia resistant to other treatment, cardiac arrest, and marked tissue destruction.62-64

 Bottom Line: Dialysis is most efficacious in definitive potassium removal. SPS is not effective and should be avoided due to its risk of colonic necrosis.

 

You call the nephrologist concerning dialysis and repeat an ECG, which demonstrates normal sinus rhythm with rate 72 bpm. The nephrologist states she will be right down to see the patient.

 

What happens in cardiac arrest due to hyperkalemia?

Hyperkalemia alters the cardiomyocyte resting potential, resulting in inactivation of sodium channels and blocking conduction. Patients in arrest due to hyperkalemia require immediate compressions and ACLS measures.28,29

– Patients with cardiac arrest with history of known renal failure, critical illness, or on hemodialysis warrant rapid blood gas assessment measuring potassium.

– Suspicion of hyperkalemia as etiology requires calcium chloride 10% (1 amp or 10 mL), with repeat dosing until QRS < 100 ms, through peripheral IV or central line.28,29

– Epinephrine should be provided to follow, as well as insulin and glucose.

– Sodium Bicarbonate can be provided as 1 amp.

– Once hyperkalemia is confirmed on VBG or other lab testing, hemodialysis is essential.

– ROSC may occur after calcium chloride membrane stabilization, which lasts 20-30 minutes. At this point, intracellular shift and elimination are goals.4,5,28,29,65

 

Key Points

Potassium plays a key role in physiology and is predominantly found intracellularly. Hyperkalemia results in change in cell membrane potentials, primarily in cardiac and neuromuscular cells.

– ECG is the first essential test, but absence of findings cannot be relied on to exclude hyperkalemia.

– Management includes cardiac membrane stabilization, transcellular shift, and excretion.

Calcium gluconate 10% can be given for membrane stabilization unless the patient is in cardiac arrest, in which 10 mL calcium chloride should be given.

Beta agonists and short acting insulin with glucose are efficacious in shifting potassium intracellularly. Dextrose infusion should be provided based on serum glucose.

– Sodium bicarbonate is not recommended unless the patient is acidemic.

– Excretion includes urinary diuresis, GI elimination, and hemodialysis.

– SPS or kayexalate is not recommended. New medications including patiromer and sodium zirconium cyclosilicate hold promise for GI excretion.

Dialysis is the ultimate means of removing potassium. Lactated Ringers and Plasmalyte may be safer for fluid rehydration if needed.

 

References/Further Reading:

  1. Faridi AB, Weisberg LS. Acid-base, electrolyte and metabolic abnormalities. In: Critical Care Medicine: Principles of Diagnosis and Management in Adults. Parrillo JE, Dellinger RP (Eds). Third Edition. Philadelphia, Elsevier, 2008;1203–1243.
  2. Mount DB, Zandi-Nejad K. Disorders of potassium balance. In: Brenner and Rector’s The Kidney, 9th Ed, WB Saunders & Company, Philadelphia 2011. p.640.
  3. Brown RS. Potassium homeostasis and clinical implications. Am J Med.1984 Nov 5;77(5A):3-10.
  4. Kidney International 2016;89:546–554.
  5. Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008;36(12):3246-51.
  6. Gennari FJ: Disorders of potassium homeostasis. Hypokalemia and hyperkalemia. Crit Care Clin 2002;18:273–288
  7. Stevens MS, Dunlay RW. Hyperkalemia in hospitalized patients. Int Urol Nephrol 2000; 32:177–180.
  8. Mandal AK. Hypokalemia and hyperkalemia. Med Clin North Am. 1997;81(3):611-639.
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  10. Surawicz B. Electrolytes and the electrocardiogram. Postgrad Med 1974; 55:123–129.
  11. Freeman K,Feldman JA, Mitchell P, et al. Effects of presentation and electrocardiogram on time to treatment of hyperkalemia. Acad Emerg Med. 2008 Mar;15(3):239-49.
  12. Mattu A, Brady WJ, Robinson D. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med. 2000; 18: 721–729.
  13. Dodge HT, Grant RP, Seavey PW. The effect of induced hyperkalemia on the normal and abnormal electrocardiogram. Am Heart J.1953 May;45(5):725-40.
  14. Wrenn KD,Slovis CM, Slovis BS. The ability of physicians to predict hyperkalemia from the ECG. Ann Emerg Med. 1991 Nov;20(11):1229-32.
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