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Review
, 9 (1), 32

Management of Hyperkalemia in the Acutely Ill Patient

Affiliations
Review

Management of Hyperkalemia in the Acutely Ill Patient

François Dépret et al. Ann Intensive Care.

Abstract

Purpose: To review the mechanisms of action, expected efficacy and side effects of strategies to control hyperkalemia in acutely ill patients.

Methods: We searched MEDLINE and EMBASE for relevant papers published in English between Jan 1, 1938, and July 1, 2018, in accordance with the PRISMA Statement using the following terms: "hyperkalemia," "intensive care," "acute kidney injury," "acute kidney failure," "hyperkalemia treatment," "renal replacement therapy," "dialysis," "sodium bicarbonate," "emergency," "acute." Reports from within the past 10 years were selected preferentially, together with highly relevant older publications.

Results: Hyperkalemia is a potentially life-threatening electrolyte abnormality and may cause cardiac electrophysiological disturbances in the acutely ill patient. Frequently used therapies for hyperkalemia may, however, also be associated with morbidity. Therapeutics may include the simultaneous administration of insulin and glucose (associated with frequent dysglycemic complications), β-2 agonists (associated with potential cardiac ischemia and arrhythmias), hypertonic sodium bicarbonate infusion in the acidotic patient (representing a large hypertonic sodium load) and renal replacement therapy (effective but invasive). Potassium-lowering drugs can cause rapid decrease in serum potassium level leading to cardiac hyperexcitability and rhythm disorders.

Conclusions: Treatment of hyperkalemia should not only focus on the ability of specific therapies to lower serum potassium level but also on their potential side effects. Tailoring treatment to the patient condition and situation may limit the risks.

Keywords: Acute kidney injury; Emergency; Hyperkalemia; Intensive care; Renal replacement therapy.

Conflict of interest statement

Dr. Dépret has nothing to disclose. Dr. Peacock reports grants and personal fees from Astra Zeneca, grants and personal fees from Relypsa, outside the submitted work. Dr. Liu reports grants from NIH: National Heart, Lung and Blood Institute, grants from NIH: National Institute of Diabetes and Digestive and Kidney Disease, personal fees from Achaogen, personal fees from Durect, personal fees from Z S Pharma, personal fees from Theravance, personal fees from Quark, personal fees from Potrero Med, other from Amgen, grants from American Society of Nephrology, grants from National Kidney Foundation, grants from National Policy Forum on Critical Care and Acute Renal Failure, personal fees from Baxter, outside the submitted work. Dr. Rafique reports personal fees and other from AstraZeneca, grants and personal fees from Vifor, outside the submitted work. Dr. Rossignol reports personal fees from French National Research Agency Fighting Heart Failure (ANR-15-RHU-0004), personal fees from French PIA project «Lorraine Université d’Excellence» GEENAGE (ANR-15-IDEX-04-LUE) programs, outside the submitted work. Dr. Legrand reports grants from French ministry of health, grants and nonfinancial support from Sphingotec, personal fees from Fresenius, personal fees from Baxter-Hospal, and personal fees from Novartis, outside the submitted work.

Figures

Fig. 1
Fig. 1
Suggested algorithm for hyperkalemia treatment in the acutely ill. *In case of Digitalis intoxication or hypercalcemia. **Sodium zirconium cyclosilicate and patiromer when available, kayexalate if not available. ESKD end-stage kidney disease, AKI acute kidney injury, CKD chronic kidney disease, RRT renal replacement therapy
Fig. 2
Fig. 2
Cardiac effect of hypertonic sodium and calcium salt during hyperkalemia. During hyperkalemia, resting membrane potential increases, derecruiting the sodium voltage gate channel Nav1.5 (left panel). Calcium salts bind to calcium-dependent calmodulin and protein kinase II (CaMKII) and activates the sodium voltage gate channel leading to an intracellular sodium entrance (right panel). Calcium salt restores the channel activity though the calcium-dependent calmodulin (CaM), recruiting the voltage-gated channel Nav1.5, increasing the intracellular sodium entrance, restore dV/dt phase 0 action potential and increase in the resting membrane potential. Hypertonic sodium increases extracellular sodium concentration and “forces” intracellular sodium entrance (right panel). The bottom panel represents on the left the decrease of dV/dt phase 0 action potential due to hyperkalemia (Bottom left panel), restored by either calcium or hypertonic sodium (Bottom right panel)(Adapted from [40, 41] with authorization)
Fig. 3
Fig. 3
Action mechanisms of plasma lowering treatments by intracellular transfer. β-2 agonist (i.e., salbutamol) binds the β-2 receptor, insulin binds insulin receptors and sodium bicarbonate (NaHCO3) induces an intracellular entrance of sodium through the Na+/H+ exchanger (NHE), all activate the sodium–potassium adenosine triphosphatase (NaK+ ATPase) leading to a potassium transfer from the extracellular space to the intracellular space
Fig. 4
Fig. 4
Action mechanisms of hypokalemic treatments by intracellular transfer. a Potassium dialysance, flux and plasma kinetic under short high efficient hemodilaysis. b Potassium dialysance, flux and plasma kinetic under long low efficient hemodilaysis. c Potassium clearance, flux and plasma kinetic under hemofiltration. K potassium, CVVHD continuous venovenous hemodialysis, CVVHF continuous venovenous hemofiltration
Fig. 5
Fig. 5
First-line treatment of hyperkalemia. During hyperkalemia with ECG modifications, first-line therapy should consist on cardiomyocyte stabilization using calcium salt or hypertonic sodium (red panel), second line therapy on treatment leading to a fast transfer of potassium from extracellular to intracellular space using either insulin–glucose i.v, aerosol of β2 agonist and/or sodium bicarbonate (in case of metabolic acidosis and hypovolemic patient) depending of the patient’s comorbidities and clinical status. Insulin–glucose is recommended as the first-line treatment in severe hyperkalemia (i.e., above 6.5 mmol/L) but close glucose monitoring is mandatory. β2 agonists can be used in spontaneously breathing patients but with safety concerns in patients with unstable angina or cardiac failure. Hypertonic sodium bicarbonate should probably be restricted to hypovolemic patients with metabolic acidosis (blue panel). Strategies increasing potassium renal excretion decreases the total potassium pool (i.e., hemodynamic optimization and correction of acute kidney injury or loop Henle diuretics in patients with fluid overload) (green panel). Indications of renal replacement therapy are patients with severe acute kidney injury associated to severe hyperkalemia or persistent hyperkalemia despite first-line medical treatment

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