- Email: [email protected]
Recognition and Treatment of Hyperkalemia
PHARMACY COLUMN
Barbara J. Zarowitz
Recognition and Treatment of Hyperkalemia Barbara J. Zarowitz, PharmD, FCCP, BCPS, CGP, FASCP, and Allen Lefkovitz, PharmD, CGP, FASCP Hyperkalemia is a common condition defined as an abnormally high concentration of potassium in the blood.1 Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart.1-3 Both hypokalemia and hyperkalemia can lead to arrhythmias. Serum potassium is important for normal transmission of electrical signals throughout the nervous system. The concentration of potassium in the body is regulated by the kidneys, and balance is maintained through excretion in urine.1,4 Most (80%90%) of potassium is excreted by the kidneys, and the remainder is eliminated through the gastrointestinal tract.2,3 Chemical and hormonal influences also help regulate the internal potassium balance. Normally, 98% of the potassium in the body is found inside the cells of various tissues, whereas only about 2% is circulating in the blood.2,3 Hyperkalemia can be asymptomatic, but patients with hyperkalemia may report vague symptoms including nausea, fatigue, muscle weakness, or tingling sensations.2 Serious symptoms of hyperkalemia include bradycardia, a weak pulse, and potentially fatal cardiac standstill. Typically, the normal potassium concentration in the blood is 3.5–5.0 mEq/L. Potassium concentrations between 5.1 mEq/L and 6.0 mEq/ L reflect mild hyperkalemia. Potassium concentrations of 6.1 mEq/L to 7.0 mEq/L are moderate hyperkalemia, and concentrations above 7 mEq/ L are severe hyperkalemia.1 The major causes of hyperkalemia include kidney dysfunction, diseases of the adrenal gland, and certain medications.1-5
Geriatric Nursing, Volume 29, Number 5
Elderly patients are particularly prone to developing hyperkalemia due to aging-associated reductions in glomerular filtration rate, renal tubular functions, and renin-angiotensin-aldosterone system activity.4 Additionally, serum potassium can be elevated because of shifts of potassium from extracellular fluid into the vasculature, such as occurs with acidosis and in the presence of insulin deficiency.2 In trauma, crush injuries, burns, chemotherapy (tumor lysis syndrome), or rhabdomyolysis the release of potassium from ischemic or injured cells can result in significant hyperkalemia.2 Lastly, drugs may cause hyperkalemia through several mechanisms as depicted in Table 1. Hyperkalemia due to excessive total body potassium occurs when the body fails to excrete potassium, ingestion is excessive, or both. Ageassociated changes in renal function coupled with frequent administration of potassium supplements or potassium-sparing diuretics and other drugs (Table 1) that contribute to or cause hyperkalemia exacerbate the underlying tendency toward hyperkalemia.4 In the elderly, the most common cause of hyperkalemia is medications.4 The Boston Collaborative Drug Surveillance Program found that 3.6% of 4921 patients prescribed potassium supplements developed hyperkalemia with the incidence highest in the elderly and those with azotemia.6 Salt substitutes, consistently primarily of potassium chloride, represent an unintended source of exogenous potassium and are often recommended in older persons with hypertension or heart disease to decrease sodium intake. One shake of Morton Lite Salt contains 5.7 mEq of potassium. Hyperkalemia has been reported with an incidence of 10%-19% in patients who receive potassium-sparing diuretics. For
333
Table 1. Causes of Hyperkalemia Mechanism
Cause of Hyperkalemia
Factitious Hyperkalemia Increased Intake
Hemolysis upon venupuncture Potassium supplements Penicillin G potassium Nutritional supplements (enteral feedings) Cell destruction Increased Shift from Massive hemolysis Intracellular Space Tumor lysis syndrome Rhabdomyolysis Burns Trauma Normal anion gap acidosis Lack of insulin Diabetic ketoacidosis Starvation Somatostatin Hyperosmolality Hyperkalemic periodic paralysis Succinylcholine Beta-blockers Digoxin intoxication Dried toad skin (Chan Su/Senso) Intravenous amino acids (hyperalimentation) Impaired Renal Excretion Decreased distal blood flow Decreased effective circulating blood volume Chronic or acute renal failure Nonsteroidal antiinflammatory drugs Hyperaldosteronism Primary adrenal insufficiency Medications and herbals Potassium-sparing diuretics (spironolactone, triamterene, amiloride) angiotensin-converting enzyme inhibitors/angiotensin receptor blockers Trimethoprim/pentamidine Cyclosporine/tacrolimus Heparin Primary rennin insufficiency Pseudohypoaldosteronism Distal renal tubular acidosis Congenital adrenal hyperplasia Interstitial renal disease Alfalfa Unknown Mechanism Dandelion Noni juice Adopted from Sood MM, Sood AR, Richardson R2 with permission.
example, triamterene/hydrochlorothiazide results in hyperkalemia in 26% of patients in a small study.7 The risk is further compounded in those with preexisting renal impairment or diabetes, patients taking potassium supplements, and
334
those taking another medication that impairs potassium secretion.8 Additional drug classes commonly associated with hyperkalemia are nonsteroidal antiinflammatory drugs (NSAIDs), such as ibuprofen and
Geriatric Nursing, Volume 29, Number 5
meloxicam, and angiotensin-converting enzyme inhibitors (ACEIs, e.g., lisinopril, captopril, ramipril) or angiotensin receptor blockers (ARBs; e.g., valsartan, losartan). NSAIDs disrupt potassium homeostasis by inhibiting renal prostaglandin synthesis and can also induce prerenal azotemia by causing preglomerular arteriolar vasodilation and postglomerular arteriolar vasoconstriction. The changes within the glomerulus precipitate an abrupt decrease in glomerular filtration rate and decrease potassium excretion.4 ACEIs and ARBs, which decrease angiotensin II, can increase serum potassium by decreasing glomerular filtration rate and by creating a persistent hypoaldosteronemia. When postglomerular arteriolar vasoconstriction is blocked by ACEI/ARB via effects on angiotensin II, glomerular filtration is reduced and hyperkalemia can occur.9,10 Given the high utility of medications that can affect potassium homeostasis in older adults, clinicians must be vigilant when prescribing new medications for a patients with underlying conditions and accompanying medications that can increase the risk of hyperkalemia. Regimens should be tailored to minimize the risk through recognition of kidney function, choice of medication, and initial dose selected to avoid serious sequelae.
Recognition of Hyperkalemia Prompt recognition of hyperkalemia is crucial to avoid potentially fatal consequences. Lifethreatening cardiac arrhythmias can lead to sudden cardiac arrest. Mechanistically, potassium is important to maintenance of myocyte contraction and generation of a resting membrane potential. When potassium moves across the cellular membrane into the intracellular space via the sodium-potassium adenosine triphosphatase pump, a negative (–90 mV) resting membrane potential is created. As potassium begins to move extracellularly, the concentration gradient across the myocyte cell membrane decreases, which leads to a slowing of myocardial functioning.2 Figure 1 demonstrates the electrocardiographic manifestations typically associated with hyperkalemia.2 While there is patient-to-patient variability, in general the electrocardiogram (ECG) changes correlate with hyperkalemia. In a retrospective study, ECG changes correlated with hyperkalemia in approximately 43% of patients with serum potassium concentrations of 6-6.8 mEq/L and 55% of those with serum potassium concentrations of greater than 6.8 mEq/L.5
Figure 1. Electrocardiographic Manifestations of Hyperkalemia. Reprinted with permission from Mayo Clinic Proceedings.
Geriatric Nursing, Volume 29, Number 5
335
Basic Principles in Approaching Hyperkalemia Figure 2 summarizes an algorithmic approach to the management of hyperkalemia. If life-threat-
ening hyperkalemia is not present, older persons can likely be managed safely in the nursing facility or as outpatients with resin exchange and a laxative. Additional fluid may help to stimulate renal elimination of excess potassium when
Figure 2. Algorithm for the Management of Hyperkalemia. Reprinted with permission from Mayo Clinic Proceedings.
336
Geriatric Nursing, Volume 29, Number 5
Geriatric Nursing, Volume 29, Number 5
Table 2. Treatment Options for Management of Hyperkalemia Medication Calcium chloride
Dose 1 g (13.5 mEq)
Route of Administration IV over 5-10 min
Dextrose 50% 50 mL (25 g) Dextrose 10% 1000 mL(100 g) Sodium bicarbonate 50-100 mEq
IV over 5 min IV over 1 – 2 h IV over 2-5 min
Insulin (regular)
IV with 10% dextrose
1 unit per 3-5 g dextrose Sodium polystyrene 15 g (or 60 mL) 1 to 4 sulfonate times daily by mouth 30-50 g in normal saline per rectum every 2 h Hemodialysis 2-4 h Adapted from references 1 and 11.
Orally with 70% sorbitol Rectally as a retention enema Intravascular
Mechanism of Action Raises threshold potential and reestablishes cardiac excitability Increases insulin release Increases serum pH Increases potassium intracellular uptake Exchanges resin Na+ for K+
Removal from plasma
Expected Result
Onset/ Duration
Reverses ECG effects 1-2 min/10-30 min
Redistribution of K+ into the cell Redistribution of K+ into the cell Redistribution of K+ into the cell Increase in resin-bound K+ elimination Increase in K+ elimination
30 min/2-6 h 30 min/2-6 h 1 h/variable 1 h/variable
Immediate/ variable
337
volume status is low or when urine output is absent unless contraindicated by end-stage renal disease. Potassium that cannot be eliminated renally or through the gastrointestinal tract through resin exchange may increase the need for the hyperkalemic patient to undergo hemodialysis. As was reviewed earlier, potassium can be eliminated from the body renally or through the gastrointestinal tract; therefore, augmentation of one or both mechanisms is attempted in the management of hyperkalemia. If life-threatening hyperkalemia is present, emergent intervention is needed to stabilize the myocardium, shift potassium intracellular, and then enhance potassium elimination as described earlier. Patients with severe hyperkalemia (serum potassium $8 mEq/L), with ECG changes other than peaked T waves, or acute worsening of renal function and supervening medical function are candidates for hospitalized treatment of hyperkalemia following immediate myocardial stabilization. Serum potassium .8 mEq/L typically involves hospitalization and treatment with calcium chloride 1 g given intravenously (IV) over 5-10 min followed immediately with an ampule of 50% dextrose IV over 5 min with or without insulin, depending on the blood sugar. Immediate interventions to push potassium intracellularly (i.e., calcium/glucose/ insulin) must be followed by potassium removal through dialysis, sodium polystyrene sulfonate, or both to rid the body of the excess potassium. Close follow-up and monitoring are required. Table 2 summarizes treatment options for hyperkalemia.
Summary
For non-life-threatening hyperkalemia (serum potassium \8 mEq/L), removal of excess potassium can occur with an exchange resin such as Kayexalate (sodium polystyrene sulfonate) or hemodialysis. Each gram of sodium polystyrene sulfonate may bind as much as 1 mEq of potassium and release 1-2 mEq of sodium. The dose of sodium polystyrene sulfonate is typically 15 g (4 level teaspoons) or 60 mL of the commercial suspension given 1 to 4 times daily. It should be administered in 70% sorbitol orally. Sodium polystyrene sulfonate can be administered rectally as 30-50 g in normal saline as a retention enema, every 2 hours until symptoms abate or serum potassium is less than 6.5 mEq/L and then every 6 hours thereafter. Exchange resins must be administered with sorbitol to eliminate the bound potassium and prevent constipation. Sorbitol is generally too irritating for rectal administration. Exchange resins should not be administered to patients with ileus or bowel obstruction. Serum potassium should be repeated 2 hours following treatment and additional therapy guided by the repeat value. Prompt recognition of hyperkalemia and its causes is important to prevent life-threatening situations. Given the predilection of older persons to hyperkalemia, clinicians should be alert to conditions that may give rise to hyperkalemia. In particular, a careful examination of the ongoing risk versus benefit of medications that can contribute to or cause hyperkalemia with progression of renal impairment, altered intake, and changes in underlying medical conditions is crucial.
References Hold or discontinue medications that may have caused or contributed to hyperkalemia (NSAIDs, potassium supplements, ACEIs/ARBs, aldosterone antagonists, potassium-sparing diuretics, betablockers, heparin, digoxin toxicity, trimethoprimsulfamethoxazole). Determine and validate the serum potassium to determine the most appropriate intervention (improper handling of blood samples can result in elevated serum potassium). Everyone with serum potassium .8 mEq/L or those with symptoms and a serum potassium of 6.5-8 mEq/L should be treated. Treatment should be determined based upon the emergent nature of the need to lower serum potassium.
338
1. Schultz N. Body electrolyte homeostasis. In: DiPiro JT, Talbert RL, Hayes PE, Yee GC, editors. Pharmacotherapy: a pathophysiologic approach. 2nd ed. East Norwalk, CT: Appleton & Lange; 1993. p. 771-8. 2. Sood MM, Sood AR, Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia. Mayo Clin Proc 2007;82:1553-61. 3. Stoppler, M. Hyperkalemia.MedicineNet.com. Available: www.medicinenet.com/hyperkalemia/article.htm. Cited July 14, 2008. 4. Perazella MA, Mahnensmith RL. Hyperkalemia in the elderly: drugs exacerbate impaired potassium homeostasis. J Gen Intern Med 1997;12:646-56. 5. Acker CG, Johnson JP, Pavelsky PM, et al. Hyperkalemia in hospitalized patients: causes, adequacy of treatment, and results of an attempt to improve physician
Geriatric Nursing, Volume 29, Number 5
6. 7. 8. 9.
10.
compliance with published therapy guidelines. Arch Intern Med 1998;158:917-24. Lawson DH. Adverse reactions to potassium chloride. Q J Med 1971;43:433-40. McDonald CJ. Dyazide and hyperkalemia. Ann Intern Med 1976;84:612-3. Ponce SP, Jennings AE, Madias NE, et al. Drug-induced hyperkalemia. Med 1985;64:357-70. Textor SC, Bravo EL, Fouad FM, et al. Hyperkalemia in azotemic patients during angiotensin-converting enzyme inhibition and aldosterone reduction with captopril. Am J Med 1982;73:719-25. Altlas SA, Case DB, Sealey JE, et al. Interruption of the rennin-angiotensin system in hypertensive patients by captopril induced sustained reduction in aldosterone secretion, potassium retention and natriuresis. Hypertension 1979;1:274-80.
Geriatric Nursing, Volume 29, Number 5
11. Clinical Pharmacology On-line. Gold Standard, Inc. 2008. Available: www.clinicalpharmacology-ip.com. Cited July 14, 2008. BARBARA J. ZAROWITZ, PharmD, FCCP, BCPS, CGP, FASCP, is chief clinical officer and vice president in the professional services group, Omnicare, Inc., Livonia, MI, and Adjunct Professor of Pharmacy Practice, College of Pharmacy and Health Sciences, Wayne State University, Detroit, MI. ALLEN LEFKOVITZ, PharmD, CGP, FASCP, is a clinical pharmacist in the professional services group at Omnicare, Inc., Dayton, OH, and a consultant pharmacist at Beeber Pharmacies, Dayton, Ohio. 0197-4572/08/$ - see front matter Ó 2008 Mosby, Inc. All rights reserved. doi:10.1016/j.gerinurse.2008.08.002
339
Barbara J. Zarowitz
Recognition and Treatment of Hyperkalemia Barbara J. Zarowitz, PharmD, FCCP, BCPS, CGP, FASCP, and Allen Lefkovitz, PharmD, CGP, FASCP Hyperkalemia is a common condition defined as an abnormally high concentration of potassium in the blood.1 Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart.1-3 Both hypokalemia and hyperkalemia can lead to arrhythmias. Serum potassium is important for normal transmission of electrical signals throughout the nervous system. The concentration of potassium in the body is regulated by the kidneys, and balance is maintained through excretion in urine.1,4 Most (80%90%) of potassium is excreted by the kidneys, and the remainder is eliminated through the gastrointestinal tract.2,3 Chemical and hormonal influences also help regulate the internal potassium balance. Normally, 98% of the potassium in the body is found inside the cells of various tissues, whereas only about 2% is circulating in the blood.2,3 Hyperkalemia can be asymptomatic, but patients with hyperkalemia may report vague symptoms including nausea, fatigue, muscle weakness, or tingling sensations.2 Serious symptoms of hyperkalemia include bradycardia, a weak pulse, and potentially fatal cardiac standstill. Typically, the normal potassium concentration in the blood is 3.5–5.0 mEq/L. Potassium concentrations between 5.1 mEq/L and 6.0 mEq/ L reflect mild hyperkalemia. Potassium concentrations of 6.1 mEq/L to 7.0 mEq/L are moderate hyperkalemia, and concentrations above 7 mEq/ L are severe hyperkalemia.1 The major causes of hyperkalemia include kidney dysfunction, diseases of the adrenal gland, and certain medications.1-5
Geriatric Nursing, Volume 29, Number 5
Elderly patients are particularly prone to developing hyperkalemia due to aging-associated reductions in glomerular filtration rate, renal tubular functions, and renin-angiotensin-aldosterone system activity.4 Additionally, serum potassium can be elevated because of shifts of potassium from extracellular fluid into the vasculature, such as occurs with acidosis and in the presence of insulin deficiency.2 In trauma, crush injuries, burns, chemotherapy (tumor lysis syndrome), or rhabdomyolysis the release of potassium from ischemic or injured cells can result in significant hyperkalemia.2 Lastly, drugs may cause hyperkalemia through several mechanisms as depicted in Table 1. Hyperkalemia due to excessive total body potassium occurs when the body fails to excrete potassium, ingestion is excessive, or both. Ageassociated changes in renal function coupled with frequent administration of potassium supplements or potassium-sparing diuretics and other drugs (Table 1) that contribute to or cause hyperkalemia exacerbate the underlying tendency toward hyperkalemia.4 In the elderly, the most common cause of hyperkalemia is medications.4 The Boston Collaborative Drug Surveillance Program found that 3.6% of 4921 patients prescribed potassium supplements developed hyperkalemia with the incidence highest in the elderly and those with azotemia.6 Salt substitutes, consistently primarily of potassium chloride, represent an unintended source of exogenous potassium and are often recommended in older persons with hypertension or heart disease to decrease sodium intake. One shake of Morton Lite Salt contains 5.7 mEq of potassium. Hyperkalemia has been reported with an incidence of 10%-19% in patients who receive potassium-sparing diuretics. For
333
Table 1. Causes of Hyperkalemia Mechanism
Cause of Hyperkalemia
Factitious Hyperkalemia Increased Intake
Hemolysis upon venupuncture Potassium supplements Penicillin G potassium Nutritional supplements (enteral feedings) Cell destruction Increased Shift from Massive hemolysis Intracellular Space Tumor lysis syndrome Rhabdomyolysis Burns Trauma Normal anion gap acidosis Lack of insulin Diabetic ketoacidosis Starvation Somatostatin Hyperosmolality Hyperkalemic periodic paralysis Succinylcholine Beta-blockers Digoxin intoxication Dried toad skin (Chan Su/Senso) Intravenous amino acids (hyperalimentation) Impaired Renal Excretion Decreased distal blood flow Decreased effective circulating blood volume Chronic or acute renal failure Nonsteroidal antiinflammatory drugs Hyperaldosteronism Primary adrenal insufficiency Medications and herbals Potassium-sparing diuretics (spironolactone, triamterene, amiloride) angiotensin-converting enzyme inhibitors/angiotensin receptor blockers Trimethoprim/pentamidine Cyclosporine/tacrolimus Heparin Primary rennin insufficiency Pseudohypoaldosteronism Distal renal tubular acidosis Congenital adrenal hyperplasia Interstitial renal disease Alfalfa Unknown Mechanism Dandelion Noni juice Adopted from Sood MM, Sood AR, Richardson R2 with permission.
example, triamterene/hydrochlorothiazide results in hyperkalemia in 26% of patients in a small study.7 The risk is further compounded in those with preexisting renal impairment or diabetes, patients taking potassium supplements, and
334
those taking another medication that impairs potassium secretion.8 Additional drug classes commonly associated with hyperkalemia are nonsteroidal antiinflammatory drugs (NSAIDs), such as ibuprofen and
Geriatric Nursing, Volume 29, Number 5
meloxicam, and angiotensin-converting enzyme inhibitors (ACEIs, e.g., lisinopril, captopril, ramipril) or angiotensin receptor blockers (ARBs; e.g., valsartan, losartan). NSAIDs disrupt potassium homeostasis by inhibiting renal prostaglandin synthesis and can also induce prerenal azotemia by causing preglomerular arteriolar vasodilation and postglomerular arteriolar vasoconstriction. The changes within the glomerulus precipitate an abrupt decrease in glomerular filtration rate and decrease potassium excretion.4 ACEIs and ARBs, which decrease angiotensin II, can increase serum potassium by decreasing glomerular filtration rate and by creating a persistent hypoaldosteronemia. When postglomerular arteriolar vasoconstriction is blocked by ACEI/ARB via effects on angiotensin II, glomerular filtration is reduced and hyperkalemia can occur.9,10 Given the high utility of medications that can affect potassium homeostasis in older adults, clinicians must be vigilant when prescribing new medications for a patients with underlying conditions and accompanying medications that can increase the risk of hyperkalemia. Regimens should be tailored to minimize the risk through recognition of kidney function, choice of medication, and initial dose selected to avoid serious sequelae.
Recognition of Hyperkalemia Prompt recognition of hyperkalemia is crucial to avoid potentially fatal consequences. Lifethreatening cardiac arrhythmias can lead to sudden cardiac arrest. Mechanistically, potassium is important to maintenance of myocyte contraction and generation of a resting membrane potential. When potassium moves across the cellular membrane into the intracellular space via the sodium-potassium adenosine triphosphatase pump, a negative (–90 mV) resting membrane potential is created. As potassium begins to move extracellularly, the concentration gradient across the myocyte cell membrane decreases, which leads to a slowing of myocardial functioning.2 Figure 1 demonstrates the electrocardiographic manifestations typically associated with hyperkalemia.2 While there is patient-to-patient variability, in general the electrocardiogram (ECG) changes correlate with hyperkalemia. In a retrospective study, ECG changes correlated with hyperkalemia in approximately 43% of patients with serum potassium concentrations of 6-6.8 mEq/L and 55% of those with serum potassium concentrations of greater than 6.8 mEq/L.5
Figure 1. Electrocardiographic Manifestations of Hyperkalemia. Reprinted with permission from Mayo Clinic Proceedings.
Geriatric Nursing, Volume 29, Number 5
335
Basic Principles in Approaching Hyperkalemia Figure 2 summarizes an algorithmic approach to the management of hyperkalemia. If life-threat-
ening hyperkalemia is not present, older persons can likely be managed safely in the nursing facility or as outpatients with resin exchange and a laxative. Additional fluid may help to stimulate renal elimination of excess potassium when
Figure 2. Algorithm for the Management of Hyperkalemia. Reprinted with permission from Mayo Clinic Proceedings.
336
Geriatric Nursing, Volume 29, Number 5
Geriatric Nursing, Volume 29, Number 5
Table 2. Treatment Options for Management of Hyperkalemia Medication Calcium chloride
Dose 1 g (13.5 mEq)
Route of Administration IV over 5-10 min
Dextrose 50% 50 mL (25 g) Dextrose 10% 1000 mL(100 g) Sodium bicarbonate 50-100 mEq
IV over 5 min IV over 1 – 2 h IV over 2-5 min
Insulin (regular)
IV with 10% dextrose
1 unit per 3-5 g dextrose Sodium polystyrene 15 g (or 60 mL) 1 to 4 sulfonate times daily by mouth 30-50 g in normal saline per rectum every 2 h Hemodialysis 2-4 h Adapted from references 1 and 11.
Orally with 70% sorbitol Rectally as a retention enema Intravascular
Mechanism of Action Raises threshold potential and reestablishes cardiac excitability Increases insulin release Increases serum pH Increases potassium intracellular uptake Exchanges resin Na+ for K+
Removal from plasma
Expected Result
Onset/ Duration
Reverses ECG effects 1-2 min/10-30 min
Redistribution of K+ into the cell Redistribution of K+ into the cell Redistribution of K+ into the cell Increase in resin-bound K+ elimination Increase in K+ elimination
30 min/2-6 h 30 min/2-6 h 1 h/variable 1 h/variable
Immediate/ variable
337
volume status is low or when urine output is absent unless contraindicated by end-stage renal disease. Potassium that cannot be eliminated renally or through the gastrointestinal tract through resin exchange may increase the need for the hyperkalemic patient to undergo hemodialysis. As was reviewed earlier, potassium can be eliminated from the body renally or through the gastrointestinal tract; therefore, augmentation of one or both mechanisms is attempted in the management of hyperkalemia. If life-threatening hyperkalemia is present, emergent intervention is needed to stabilize the myocardium, shift potassium intracellular, and then enhance potassium elimination as described earlier. Patients with severe hyperkalemia (serum potassium $8 mEq/L), with ECG changes other than peaked T waves, or acute worsening of renal function and supervening medical function are candidates for hospitalized treatment of hyperkalemia following immediate myocardial stabilization. Serum potassium .8 mEq/L typically involves hospitalization and treatment with calcium chloride 1 g given intravenously (IV) over 5-10 min followed immediately with an ampule of 50% dextrose IV over 5 min with or without insulin, depending on the blood sugar. Immediate interventions to push potassium intracellularly (i.e., calcium/glucose/ insulin) must be followed by potassium removal through dialysis, sodium polystyrene sulfonate, or both to rid the body of the excess potassium. Close follow-up and monitoring are required. Table 2 summarizes treatment options for hyperkalemia.
Summary
For non-life-threatening hyperkalemia (serum potassium \8 mEq/L), removal of excess potassium can occur with an exchange resin such as Kayexalate (sodium polystyrene sulfonate) or hemodialysis. Each gram of sodium polystyrene sulfonate may bind as much as 1 mEq of potassium and release 1-2 mEq of sodium. The dose of sodium polystyrene sulfonate is typically 15 g (4 level teaspoons) or 60 mL of the commercial suspension given 1 to 4 times daily. It should be administered in 70% sorbitol orally. Sodium polystyrene sulfonate can be administered rectally as 30-50 g in normal saline as a retention enema, every 2 hours until symptoms abate or serum potassium is less than 6.5 mEq/L and then every 6 hours thereafter. Exchange resins must be administered with sorbitol to eliminate the bound potassium and prevent constipation. Sorbitol is generally too irritating for rectal administration. Exchange resins should not be administered to patients with ileus or bowel obstruction. Serum potassium should be repeated 2 hours following treatment and additional therapy guided by the repeat value. Prompt recognition of hyperkalemia and its causes is important to prevent life-threatening situations. Given the predilection of older persons to hyperkalemia, clinicians should be alert to conditions that may give rise to hyperkalemia. In particular, a careful examination of the ongoing risk versus benefit of medications that can contribute to or cause hyperkalemia with progression of renal impairment, altered intake, and changes in underlying medical conditions is crucial.
References Hold or discontinue medications that may have caused or contributed to hyperkalemia (NSAIDs, potassium supplements, ACEIs/ARBs, aldosterone antagonists, potassium-sparing diuretics, betablockers, heparin, digoxin toxicity, trimethoprimsulfamethoxazole). Determine and validate the serum potassium to determine the most appropriate intervention (improper handling of blood samples can result in elevated serum potassium). Everyone with serum potassium .8 mEq/L or those with symptoms and a serum potassium of 6.5-8 mEq/L should be treated. Treatment should be determined based upon the emergent nature of the need to lower serum potassium.
338
1. Schultz N. Body electrolyte homeostasis. In: DiPiro JT, Talbert RL, Hayes PE, Yee GC, editors. Pharmacotherapy: a pathophysiologic approach. 2nd ed. East Norwalk, CT: Appleton & Lange; 1993. p. 771-8. 2. Sood MM, Sood AR, Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia. Mayo Clin Proc 2007;82:1553-61. 3. Stoppler, M. Hyperkalemia.MedicineNet.com. Available: www.medicinenet.com/hyperkalemia/article.htm. Cited July 14, 2008. 4. Perazella MA, Mahnensmith RL. Hyperkalemia in the elderly: drugs exacerbate impaired potassium homeostasis. J Gen Intern Med 1997;12:646-56. 5. Acker CG, Johnson JP, Pavelsky PM, et al. Hyperkalemia in hospitalized patients: causes, adequacy of treatment, and results of an attempt to improve physician
Geriatric Nursing, Volume 29, Number 5
6. 7. 8. 9.
10.
compliance with published therapy guidelines. Arch Intern Med 1998;158:917-24. Lawson DH. Adverse reactions to potassium chloride. Q J Med 1971;43:433-40. McDonald CJ. Dyazide and hyperkalemia. Ann Intern Med 1976;84:612-3. Ponce SP, Jennings AE, Madias NE, et al. Drug-induced hyperkalemia. Med 1985;64:357-70. Textor SC, Bravo EL, Fouad FM, et al. Hyperkalemia in azotemic patients during angiotensin-converting enzyme inhibition and aldosterone reduction with captopril. Am J Med 1982;73:719-25. Altlas SA, Case DB, Sealey JE, et al. Interruption of the rennin-angiotensin system in hypertensive patients by captopril induced sustained reduction in aldosterone secretion, potassium retention and natriuresis. Hypertension 1979;1:274-80.
Geriatric Nursing, Volume 29, Number 5
11. Clinical Pharmacology On-line. Gold Standard, Inc. 2008. Available: www.clinicalpharmacology-ip.com. Cited July 14, 2008. BARBARA J. ZAROWITZ, PharmD, FCCP, BCPS, CGP, FASCP, is chief clinical officer and vice president in the professional services group, Omnicare, Inc., Livonia, MI, and Adjunct Professor of Pharmacy Practice, College of Pharmacy and Health Sciences, Wayne State University, Detroit, MI. ALLEN LEFKOVITZ, PharmD, CGP, FASCP, is a clinical pharmacist in the professional services group at Omnicare, Inc., Dayton, OH, and a consultant pharmacist at Beeber Pharmacies, Dayton, Ohio. 0197-4572/08/$ - see front matter Ó 2008 Mosby, Inc. All rights reserved. doi:10.1016/j.gerinurse.2008.08.002
339