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Hyperkalemia
Merima Bucaj, DO
Roselyn Jan Wuthrich Clemente-Fuentes, MD
image BASICS
DESCRIPTION
  • Hyperkalemia is a common electrolyte disorder that may be defined as a plasma potassium (K) concentration >5.5 mEq/L (>5 mmol/L).
  • Hyperkalemia depresses cardiac conduction and can lead to fatal arrhythmias.
  • Normal K regulation
    • Ingested K enters portal circulation; pancreas releases insulin in response. Insulin facilitates K entry into cells.
    • K in renal circulation causes renin release from juxtaglomerular cells, leading to activation of angiotensin I, which is converted to angiotensin II in lungs. Angiotensin II acts in adrenal zona glomerulosa to stimulate aldosterone secretion. Aldosterone, at the renal collecting ducts, causes K to be excreted and sodium to be retained.
  • Four major causes
    • Increased load: either endogenous from tissue release or exogenous from a high intake, usually in association with impaired excretion
    • Decreased excretion: due to decreased glomerular filtration rate
    • Cellular redistribution: shifts from intracellular space (majority of K is intracellular) to extracellular space
    • Pseudohyperkalemia: related to red cell lysis during collection or transport of blood sample, thrombocytosis, or leukocytosis
Geriatric Considerations
Increased risk for hyperkalemia because of decreases in renin and aldosterone as well as comorbid conditions
EPIDEMIOLOGY
Prevalence
  • 1-10% of hospitalized patients
  • 2-3% in general population but as high as 50% in patients with chronic kidney disease (1)
  • Predominant sex: male = female
  • No age-related predilection
ETIOLOGY AND PATHOPHYSIOLOGY
  • Pseudohyperkalemia
    • Hemolysis of red cells in phlebotomy tube (spurious result is most common)
    • Thrombolysis
    • Leukocytosis
    • Thrombocytosis
    • Hereditary spherocytosis
    • Infectious mononucleosis
    • Traumatic venipuncture or fist clenching during phlebotomy (spurious result)
  • Transcellular shift (redistribution)
    • Metabolic acidosis
    • Insulin deficiency
    • Hyperglycemia (diabetic ketoacidosis or hyperosmolar hyperglycemic state)
    • Tissue damage (rhabdomyolysis, burns, trauma) (2)
    • Tumor lysis syndrome (3)
    • Cocaine abuse
    • Exercise with heavy sweating
    • Mannitol
  • Impaired K excretion
    • Renal insufficiency/failure
    • Addison disease
    • Mineralocorticoid deficiency
    • Primary hyporeninemia, primary hypoaldosteronism
    • Type IV renal tubular acidosis (hyporeninemic hypoaldosteronism)
  • Medication-induced
    • Excess K supplementation
    • Statins
    • ACE inhibitors
    • Angiotensin receptor blockers
    • &bgr;-Blockers
    • Cyclosporine
    • Digoxin toxicity
    • Ethinyl estradiol/drospirenone
    • Heparin
    • NSAIDs
    • Penicillin G potassium
    • Pentamidine
    • Spironolactone
    • Succinylcholine
    • Tacrolimus
    • Trimethoprim, particularly with other medications associated with hyperkalemia (4,5)
Genetics
Associated with some inherited diseases and conditions
  • Familial hyperkalemic periodic paralysis
  • Congenital adrenal hyperplasia
RISK FACTORS
  • Impaired renal excretion of K
  • Acidemia
  • Massive cell breakdown (rhabdomyolysis, burns, trauma)
  • Use of K-sparing diuretics.
  • Excess K supplementation
GENERAL PREVENTION
Diet and oral supplement compliance in those at risk
image DIAGNOSIS
PHYSICAL EXAM
  • Decreased deep tendon reflexes
  • Flaccid paralysis of extremities
DIAGNOSTIC TESTS & INTERPRETATION
  • Serum electrolytes
  • Renal function: BUN, creatinine
  • Urinalysis: K, creatinine, osmoles (to calculate fractional excretion of K and transtubular K gradient; both assess renal handling of K)
  • Disorders that may alter lab results
    • Acidemia: K shifts from the intracellular to extracellular space
    • Insulin deficiency
    • Hemolysis of sample
  • Cortisol and aldosterone levels to check for mineralocorticoid deficiency when other causes are ruled out
Diagnostic Procedures/Other
EKG abnormalities usually occur when K ≥7 mEq/L
  • Peaked T wave with shortened QT interval in precordial leads (most common, usually earliest EKG change) (6)
  • Lengthening of PR interval
  • Loss of P wave
  • Widened QRS
  • Sine wave at very high K
  • Can eventually lead to arrhythmias including ventricular fibrillation and asystole
image TREATMENT
MEDICATION
  • Stabilize myocardial membranes. Initial treatment with calcium gluconate IV 1,000 mg (10 mL of 10% solution) over 2 to 3 minutes
    • With constant cardiac monitoring
    • Can repeat after 5 minutes if needed
    • Effect begins within minutes, but only lasts 30 to 60 minutes and should be used in conjunction with definitive therapies
    • Can also use calcium chloride (3 times as concentrated; however, it needs central or deep vein to avoid tissue necrosis)
  • Drive extracellular potassium into cells
    • Nebulized albuterol (at 10 to 20 mg/4 mL saline over 10 minutes—4 to 8 times bronchodilation dose) and other &bgr;-agonists have an additive effect with insulin and glucose
    • Dextrose 50% 1 amp (if plasma glucose <250 mg/dL) and insulin 10 U IV may drive K intracellularly but does not decrease total body K and may result in hypoglycemia (close monitoring advised, especially 1 to 2 hours postinjection).
    • Sodium bicarbonate not routinely recommended but some possible benefits in severe metabolic acidosis (7)[C]
  • P.509

  • Remove excess potassium from body.
    • Cation exchange resins definitive treatment but require several doses and best used with rapidly acting transient therapies above and when dialysis not readily available (8)[A]
    • Sodium polystyrene sulfonate (Kayexalate): 15 g PO or 30 g rectally
      • This requires 1 to 4 hours to lower K. This may be repeated q6h, if necessary.
      • Enema has faster effect than PO.
    • Hemodialysis is the definitive therapy when other measures are not effective. This may be required particularly when conditions such as digitalis toxicity, rhabdomyolysis, end-stage renal disease, severe chronic kidney disease, or acute kidney injury, are present. Should watch for postdialysis rebound
    • Little clinical evidence for the use of diuretics (loop and thiazides), however, can consider for control of chronic hyperkalemia (2)[B].
    • Zirconium cyclosilicate and patiromer calcium are promising therapies in development which bind potassium in intestinal tract (9)[C].
INPATIENT CONSIDERATIONS
Admission Criteria/Initial Stabilization
  • If hyperkalemia is severe, treat first, and then do diagnostic investigations.
  • IV calcium to stabilize myocardium (caution in setting of digoxin toxicity, when calcium may worsen effects of toxicity)
  • Insulin (usually 10 U IV, given with 50 mL of 50% glucose (if serum glucose <250 mg/dL) to avoid hypoglycemia; consider repeating if elevation persists.
  • Inhaled &bgr;2-agonist (nebulized albuterol)
  • Discontinue any medications that may increase K (e.g., K-sparing diuretics, exogenous K).
  • Admit for cardiac monitoring if EKG changes are present or if K is >6 mEq/L (6 mmol/L).
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
  • Reduction of plasma K should begin within the first hour of treatment initiation.
  • Serum K levels should be rechecked every 2 to 4 hours until the patient has stabilized, and recurrent hyperkalemia is no longer a threat.
  • Identification and elimination of possible causes and risk factors for hyperkalemia are essential.
DIET
≤80 mEq (≤80 mmol) of K/24 hours. Many foods contain K. Those that are particularly high in K (>6.4 mEq/serving) include bananas, orange juice, other citrus fruits and their juices, tomatoes, tomato juice, cantaloupe, honeydew melon, peaches, potatoes, and salt substitutes. Multiple herbal medications can also increase K levels, including alfalfa, dandelion, horsetail nettle, milkweed, hawthorn berries, toad skin, oleander, foxglove, and ginseng.
PATIENT EDUCATION
Consult with a dietitian about a low-K diet.
PROGNOSIS
  • Associated with poor prognosis in patients with heart failure and chronic kidney disease
  • Associated with poor prognosis in disaster medicine, with trauma, tissue necrosis, K+ supplementation, metabolic acidosis, if calcium gluconate administered for treatment of hyperkalemia, if AKI, or if prolonged duration of hyperkalemia (2,7)
REFERENCES
1. Palmer BF, Clegg DJ. Hyperkalemia. JAMA. 2015;314(22):2405-2406.
2. Zimmerman JL, Shen MC. Rhabdomyolysis. Chest. 2013;144(3):1058-1065.
3. Howard SC, Jones DP, Pui CH. The tumor lysis syndrome. N Engl J Med. 2011;364(19):1844-1854.
4. Antoniou T, Gomes T, Juurlink DN, et al. Trimethoprim-sulfamethoxazole-induced hyperkalemia in patients receiving inhibitors of the renin-angiotensin system: a population-based study. Arch Intern Med. 2010;170(12):1045-1049.
5. Weir MA, Juurlink DN, Gomes T, et al. Beta-blockers, trimethoprim-sulfamethoxazole, and the risk of hyperkalemia requiring hospitalization in the elderly: a nested case-control study. Clin J Am Soc Nephrol. 2010;5(9):1544-1551.
6. Wong R, Banker R, Aronowitz P. Electrocardiographic changes of severe hyperkalemia. J Hosp Med. 2011;6(4):240.
7. Khanagavi J, Gupta T, Aronow WS, et al. Hyperkalemia among hospitalized patients and association between duration of hyperkalemia and outcomes. Arch Med Sci. 2014;10(2):251-257.
8. Sterns RH, Rojas M, Bernstein P, et al. Ionexchange resins for the treatment of hyperkalemia: are they safe and effective? J Am Soc Nephrol. 2010;21(5):733-735.
9. Ingelfinger JR. A new era for the treatment of hyperkalemia? N Engl J Med. 2015;372(3):275-277.
Additional Reading
&NA;
  • Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med. 2009;361(1):62-72.
  • Hall AB, Salazar M, Larison DJ. The sequencing of medication administration in the management of hyperkalemia. J Emerg Nurs. 2009;35(4):339-342.
  • Hollander-Rodriguez JC, Calvert JF Jr. Hyperkalemia. Am Fam Physician. 2006;73(2):283-290.
  • Jain N, Kotla S, Little BB, et al. Predictors of hyperkalemia and death in patients with cardiac and renal disease. Am J Cardiol. 2012;109(10):1510-1513.
  • Noori N, Kalantar-Zadeh K, Kovesdy CP, et al. Dietary potassium intake and mortality in longterm hemodialysis patients. Am J Kidney Dis. 2010;56(2):338-347.
  • Pepin J, Shields C. Advances in diagnosis and management of hypokalemic and hyperkalemic emergencies. Emerg Med Pract. 2012;14(2):1-17.
  • Riccardi A, Tasso F, Corti L, et al. The emergency physician and the prompt management of severe hyperkalemia. Intern Emerg Med. 2012;7(Suppl 2):S131-S133.
See Also
&NA;
  • Addison Disease; Hypokalemia
  • Algorithm: Hyperkalemia
Codes
&NA;
ICD10
E87.5 Hyperkalemia
Clinical Pearls
&NA;
  • Emergency and urgent management of hyperkalemia takes precedent to a thorough diagnostic workup. Urgent treatment includes stabilization of the myocardium with calcium gluconate to protect against arrhythmias and pharmacologic strategies to move K from the extracellular (vascular) space into cells.
  • Calcium and dextrose/insulin are only temporizing measures and do not actually lower total body K levels. Definitive treatment with either dialysis or cation exchange resin (sodium polystyrene sulfonate) necessary.
  • To lower a patient's risk of developing hyperkalemia, have the patient follow a low-K diet, use selective &bgr;1-blockers, such as metoprolol or atenolol, instead of nonselective &bgr;-blockers such as carvedilol. Avoid NSAIDs. Concomitant use of kaliuretic loop diuretics may be useful.