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AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Eric D Harry, MD, Pediatric Intensivist, Department of Pediatric Critical Care, Mary Bridge Children's Hospital
Eric D Harry is a member of the following medical societies: American Academy of Pediatrics and Society of Critical Care Medicine
Coauthor(s):
Jerry Zimmerman, MD, PhD, Professor, Department of Pediatrics/Anesthesia, University of Washington School of Medicine; Director, Division of Pediatric Critical Care Medicine, Children's Hospital of Seattle
Editors: G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine; Barry J Evans, MD, Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center; Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital; Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Author and Editor Disclosure
Synonyms and related keywords:
hyperkaliemia, hyperpotassemia, potassium, potassium level, serum potassium level, K+, potassium excretion, potassium intake, hemolysis, phlebotomy, fictitious hyperkalemia, pseudohyperkalemia, true hyperkalemia, renal insufficiency, transcellular potassium shift, thrombocytosis, aldosterone, acute hyperkalemia, severe hyperkalemia, hemodialysis, total body potassium, laboratory hyperkalemia, acidosis, tumor lysis syndrome, rhabdomyolysis, insulin deficiency, malignant hyperkalemia, hyperkalemic periodic paralysis, primary adrenal disease, Addison disease, 21-hydroxylase deficiency, hyporeninemic hypoaldosteronism, renal tubular disease, gastroenteritis, acute glomerulonephritis, hemolytic-uremic syndrome, HUS, hypertension, diabetes, respiratory failure, metabolic acidosis, congenital adrenal hyperplasia, head trauma, thermal burns, electrical burns
Background
Hyperkalemia is defined as a higher than normal concentration of potassium (K+) ions in the circulating blood (serum potassium >5.5 mEq/L). Because hyperkalemia can cause lethal cardiac arrhythmia, it is one of the most serious electrolyte disturbances.
Pathophysiology
Potassium is the primary intracellular cation; more than 98% of the total body potassium is found in the intracellular space, primarily in muscle. Normal homeostatic mechanisms serve to precisely maintain the serum potassium level within a narrow range (3.5-5.0 mEq/L). The primary mechanisms for maintaining this balance are the buffering of extracellular potassium against a large intracellular potassium pool (via the sodium-potassium pump) and urinary excretion of potassium. Ninety percent of potassium excretion occurs in the urine; less than 10% of potassium excretion occurs through sweat or stool. Within the kidneys, potassium excretion occurs mostly in the principal cells of the cortical collecting duct (CCD). Potassium excretion depends on adequate luminal sodium delivery to the distal convoluted tubule (DCT) and CCD. Laboratory hyperkalemia (fictitious or pseudohyperkalemia) can easily occur because of hemolysis during phlebotomy, especially with heel-poke and finger-stick phlebotomy, which are commonly performed in children. Hemolysis can also be caused by fist clenching during phlebotomy or during prolonged tourniquet application. Thrombocytosis can also lead to false elevations of serum potassium levels. The normal serum potassium level is 0.4 mEq/L higher than the plasma level because of potassium release during clot formation. For every 100,000/mL elevation in the platelet count, the serum potassium increases by approximately 0.15 mEq/L. This can easily be corrected based on a measurement of whole blood potassium level. A similar effect on serum but not plasma potassium can also be seen with leukocytosis. True hyperkalemia is caused by one of 3 basic mechanisms, although the root cause for any individual patient is often multifactorial.
- Increased K+ intake: Increased K+ intake is most commonly caused by intravenous or oral potassium supplementation. Packed RBCs (PRBCs) also carry potentially high concentrations of potassium that can lead to hyperkalemia during PRBC transfusion.1
- Transcellular K+ shifts: In a transcellular potassium shift, a hydrogen ion enters a cell and leads to decreased K+ uptake by the cell in order to maintain electro-neutrality. Acidosis is the most common cause of hyperkalemia due to transcellular potassium shift, but any process that leads to cellular injury or death (eg, tumor lysis syndrome, rhabdomyolysis, crush injury, massive hemolysis) can cause hyperkalemia, as intracellular potassium is released by disruption of the cell membrane. Other causes of hyperkalemia due to transcellular shift of potassium include toxins (digitalis intoxication or fluoride intoxication), succinylcholine, beta-adrenergic blockade, exercise, insulin deficiency, malignant hyperkalemia, and hyperkalemic periodic paralysis.
- Decreased K+ excretion: The most common cause of decreased potassium excretion leading to hyperkalemia is renal failure. Other causes include primary adrenal disease (eg, Addison disease, 21-hydroxylase deficiency), hyporeninemic hypoaldosteronism, renal tubular disease (pseudohypoaldosteronism I or II), or medications (eg, ACE inhibitors, angiotensin II blockers, spironolactone or other potassium-sparing diuretics).
Plasma potassium levels are generally maintained at 3.5-5 mEq/L. Levels greater than 7 mEq/L can lead to significant hemodynamic and neurologic consequences. Levels exceeding 8.5 mEq/L can cause respiratory paralysis or cardiac arrest and can quickly be fatal. High levels of potassium cause abnormal heart and skeletal muscle function by lowering cell-resting action potential and preventing repolarization, leading to muscle paralysis. ECG findings are classic and begin with tenting of the T wave (see Media file 1), followed by lengthening and eventual disappearance of the P wave and widening of the QRS complex.2 Just before the heart stops, the QRS and T wave merge to form a sine wave (see Media file 2). Select Factors Affecting Plasma Potassium | Factor | Effect on Plasma K+ | Mechanism | | Aldosterone | Decrease | Increases sodium resorption, which increases filtrate load to kidneys, leading to increased K+ excretion | | Insulin | Decrease | Stimulates K+ entry into cells by increasing sodium efflux (energy-dependent process) | | Beta-adrenergic agents | Decrease | Increases skeletal muscle uptake of K+ | | Alpha-adrenergic agents | Increase | Impairs cellular K+ uptake | | Acidosis (decreased pH) | Increase | Impairs cellular K+ uptake | | Alkalosis (increased pH) | Decrease | Enhances cellular K+ uptake | | Cell damage | Increase | Intracellular K+ release | | Succinylcholine | Increase | Cell membrane depolarization |
Frequency
United States
Hyperkalemia is a manifestation of a disease and is not a disease by itself. The incidence of hyperkalemia in the pediatric population is unknown. Hyperkalemia is most commonly associated with renal insufficiency and with diseases that involve defects in mineralocorticoid, aldosterone, and insulin function and causes of acidosis.
Mortality/Morbidity
Sudden and rapid onset of hyperkalemia can be fatal. With slow or chronic increase in potassium levels, adaptation occurs via renal excretion, with fractional potassium excretion increasing by as much as 5-10 times the reference range.
Race
No racial predilection is observed.
Sex
No sex-related predilection is observed.
Age
No age-related predilection is observed.
History
- History for a previously well child with acute hyperkalemia should focus on how the blood sample was obtained, potassium intake or recent blood product transfusion, risk factors for transcellular shift of potassium (acidosis) or tissue death/necrosis, medication use associated with hyperkalemia, and presence or signs of renal insufficiency.
- Specific questions may be focused on the following:
- Urine output (last void or number of wet diapers) and fluid intake
- History of vomiting or diarrhea (which may indicate acute gastroenteritis)
- Cola-colored urine (which may indicate acute glomerulonephritis)
- Bloody stool (which may indicate indicating hemolytic-uremic syndrome [HUS])
- Recent enema use
- Presence of drugs in the household, such as potassium preparations, digoxin, and diuretics
- Any history of trauma (crush injuries) or thermal injury (burns)
- Medical history, family history, and review of systems should be explored for any of the following:
- Acute or chronic renal failure
- Hypertension
- Diabetes
- Adrenogenital syndromes
- Malignancy (tumor lysis syndrome)
- Family history (hyperkalemic periodic paralysis)
- Neuromuscular disorder
- Malignant hyperthermia
Physical
High serum levels interfere with repolarization of the cellular membrane following completion of the action potential. Findings depend on the degree of hyperkalemia and primarily relate to the deleterious effects of elevated plasma potassium levels on cardiac conduction. Children with hyperkalemia can present with cardiac arrest due to wide-complex tachycardia or ventricular fibrillation.
Symptoms short of circulatory collapse/cardiac arrest include respiratory failure and weakness that progresses to paralysis. Patients may report nausea, vomiting, and paresthesias (eg, tingling). Most often, patients with hyperkalemia are asymptomatic, with the first clinical manifestation of the condition either ECG changes (peaked T waves) or sudden cardiac arrest.
Causes
Although the etiology of hyperkalemia can be multifactorial, differential diagnoses include fictitious hyperkalemia and hyperkalemia due to increased potassium intake, transcellular potassium shift, or decreased potassium excretion.
- Fictitious hyperkalemia
- Hemolysis or tissue ischemia during phlebotomy
- Thrombocytosis or leukocytosis (affects serum K+ but not plasma K+)
- Hyperkalemia due to increased K+ intake
- Blood transfusion (increasing risk with duration of cell storage)
- Intravenous (IV) or oral potassium
- Maintenance K+ in IVF or oral solutions combined with decreased renal function
- Hyperkalemia due to transcellular K+ shift
- Metabolic acidosis
- Acute tubular necrosis
- Electrical burns
- Thermal burns
- Cell depolarization
- Congenital adrenal hyperplasia
- Head trauma
- Rhabdomyolysis
- Digitalis toxicity
- Tumor lysis syndrome
- Succinylcholine use in a child with neuromuscular disease, prolonged bedrest (including patients in ICUs), or more than 24 hours after crush or burn injury3
- Hyperkalemia due to decreased K +excretion
- Acute renal failure
- Primary adrenal disease
- Hyporeninemic hypoaldosteronism
- Renal tubular disease
- Medications (eg, potassium sparing diuretics, ACE inhibitors, angiotensin II blockers)
Acidosis, Metabolic
Acute Tubular Necrosis
Burns, Electrical
Burns, Thermal
Congenital Adrenal Hyperplasia
Head Trauma
Rhabdomyolysis
Toxicity, Digitalis
Tumor Lysis Syndrome
Other Problems to be Considered
Acute renal failure
Drug overdose or poisoning
Lab Studies
- Laboratory studies depend on etiology but may include the following:
- Serum electrolyte tests
- Serum BUN and creatinine tests
- Urinalysis (UA)
- Depending on the etiology or on clinical suspicion, other studies to consider include the following:
- Venous, capillary, or ABG measurements (for acid-base disorders)
- Serum uric acid and phosphorous tests (for tumor lysis syndrome)
- Serum creatinine phosphokinase (CPK) and calcium measurements (for rhabdomyolysis)
- Urine myoglobin test (for crush injury or rhabdomyolysis; suspect if UA reveals blood in the urine but no RBCs are seen on urine microscopy)
- Specific drug level tests for suspected toxicity (digoxin)
- CBC count (for thrombocytosis, leukocytosis, or malignancy)
- Urine electrolyte tests, including potassium and osmolality (osm) tests
- Plasma osm test
- When the etiology of hyperkalemia remains unclear, calculation of the transtubular potassium gradient (TTKG) using the following formula may be useful:
TTKG = (K+ urine X Osm plasma)/(K+ plasma X Osm urine)
- The normal TTKG varies from 5-15. In the setting of hyperkalemia with normal renal excretion of potassium, the TTKG should be greater than 10. A TTKG of less than 8 in the setting of hyperkalemia implies inadequate potassium excretion, which is usually secondary to aldosterone deficiency or unresponsiveness. Checking a serum aldosterone level may be helpful.
Imaging Studies
- Imaging studies are not generally indicated, except to assess the primary disease state (eg, excluding obstructive uropathy as a cause for acute renal failure).
Other Tests
An ECG is essential in all children in whom hyperkalemia is suspected. ECG reveals the sequence of changes as follows:
- Serum K+ 5.5-6.5 mEq/L - Tall, peaked T waves with narrow base, best seen in precordial leads (see Media file 1)
- Serum K+ 6.5-8.0 mEq/L - Peaked T waves, prolonged PR interval, decreased or disappearing P wave, widening of QRS, amplified R wave
- Serum K+ greater than 8.0 mEq/L - Absence of P wave; progressive QRS widening, intraventricular/fascicular/bundle branch blocks; progressive widening of QRS, eventually merging with the T wave just before cardiac arrest, forming the sine wave pattern (see Media file 2)
Medical Care
- Hyperkalemia is a true medical emergency, with 3 primary goals of immediate management:
- Stabilizing the myocardial cell membrane to prevent lethal cardiac arrhythmia (and to gain time to shift potassium intracellularly and enhance potassium elimination)
- Calcium chloride IV
- Calcium gluconate IV
- Intracellularly shifting potassium
- Sodium bicarbonate IV
- Regular insulin and glucose IV
- Inhaled beta-adrenergic agents, such as albuterol (used to manage hyperkalemia with variable results)
- Enhancing total body potassium elimination
- Sodium polystyrene sulfonate (Kayexalate) PO/PR
- Furosemide (only if renal function is maintained)
- Emergent hemodialysis
- Arrhythmias due to hyperkalemia are very difficult to treat with defibrillation, epinephrine, or antiarrhythmic drugs without emergently lowering the serum potassium level.
- After initial stabilization, further workup should be performed to diagnose the etiology of the hyperkalemia. Children with acquired Addison disease or other primary adrenal disease require stress-dose steroid supplementation and children with hypoaldosteronism require mineralocorticoid supplementation. Supportive care may include adequate intravascular volume expansion, if indicated.
- Emergent hemodialysis is sometimes necessary to treat severe symptomatic hyperkalemia that is resistant to drug therapy.
- Even in patients with severe hyperkalemia and a high gradient, peritoneal dialysis (PD) is not as efficient as hemodialysis in the removal of potassium. Rates of removal with PD are almost equal to the removal rate using sodium polystyrene sulfonate (Kayexalate).
- Continuous arteriovenous hemofiltration with dialysis (CAVHD) or continuous veno-venous hemofiltration with dialysis (CVVHD) have also been used to remove potassium. However, potassium removal with these methods is similar to that of PD and sodium polystyrene sulfonate (Kayexalate). CVVHD or CAVHD may be used for long-term removal of potassium, but in acute, severe, life-threatening hyperkalemia unresponsive to medical therapy, hemodialysis remains the procedure of choice.
Consultations
Consultations with the following specialists may be necessary in cases of hyperkalemia that result from certain conditions or disease states:
- Pediatric intensivist or neonatologist - Management of life-threatening hyperkalemia (hyperkalemia with ECG changes)
- Nephrologist - Hyperkalemia associated with renal failure
- Hematologist/oncologist - Hyperkalemia resulting from tumor lysis syndrome
- Social services specialist - Children who develop hyperkalemia following unintentional ingestions or poisonings
- Nutritional support specialist - Particularly for patients whose hyperkalemia is caused by renal failure, which requires close regulation of potassium and sodium intake
- Endocrinologist - Patients with suspected mineralocorticoid abnormalities such as congenital adrenal hyperplasia
Diet
Potassium intake must be closely monitored (and possibly restricted) in patients with renal failure.
Hyperkalemia is defined as a serum potassium level more than 5.5 mEq/L. Severe hyperkalemia, defined as an elevated serum potassium level with associated ECG changes (peaked T waves that progress to widening of the QRS and then to a sine wave pattern), is a life-threatening medical emergency and requires immediate therapy (see Media files 1-2). Treatment for severe hyperkalemia consists of 3 steps: (1) immediate stabilization of the myocardial cell membrane, (2) rapidly shifting potassium intracellularly, and (3) enhancing total body potassium elimination (see Medical Care). In addition, all sources of exogenous potassium should be immediately discontinued, including IV and oral potassium supplementation, total parenteral nutrition, and any blood product transfusion. Drugs associated with hyperkalemia should also be discontinued. Albuterol and other beta-adrenergic agents induce the intracellular movement of potassium via the stimulation of the sodium/potassium–adenosine triphosphate (Na+/K+-ATP) pump. Studies have shown that IV salbutamol (not available in the United States) is highly effective in lowering serum potassium levels. Some studies in adults and children using nebulized albuterol indicate that this method of therapy is effective in lowering serum potassium levels. However, peak response is unclear; therefore, it has not been established as the first line of therapy in severe hyperkalemia.
Drug Category: Myocardium stabilizers
Calcium does not lower serum potassium levels. It is primarily used to protect the myocardium from the deleterious effects of hyperkalemia (ie, arrhythmias) by antagonizing the membrane actions of potassium.
| Drug Name | Calcium chloride or calcium gluconate |
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| Description | IV calcium is indicated in all cases of severe hyperkalemia (ie, >7 mEq/L), especially when accompanied by ECG changes. Calcium chloride contains about 3 times more elemental calcium than an equal volume of calcium gluconate. Therefore, when hyperkalemia is accompanied by hemodynamic compromise, calcium chloride is preferred over calcium gluconate.
Administration of calcium should be accompanied by the use of other therapies that actually help lower the K+ serum levels.
Other calcium salts (eg, glubionate, gluceptate) have even less elemental calcium than calcium gluconate and are generally not recommended for therapy of hyperkalemia. Calcium chloride 1 g = 270 mg (13.5 mEq) of elemental calcium.
Calcium gluconate 1 g = 90 mg (4.5 mEq) of elemental calcium. |
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| Adult Dose | Calcium gluconate (10%): 1 g/dose slow IV
Calcium chloride (10%): 250-500 mg/dose slow IV |
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| Pediatric Dose | Calcium gluconate (10%): 100 mg/kg/dose slow IV, up to the adult dose
Calcium chloride (10%): 20 mg/kg/dose slow IV, up to the adult dose
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| Contraindications | Ventricular fibrillation not associated with hyperkalemia; digitalis toxicity; hypercalcemia; renal insufficiency; cardiac disease |
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| Interactions | Coadministration with digoxin may cause arrhythmias; coadministration with thiazides may induce hypercalcemia; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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| Precautions | Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure |
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Drug Category: Intracellular transporters
Regular insulin and glucose cause a transcellular shift of potassium into muscle cells, thereby temporarily lowering K+ serum levels.
| Drug Name | Insulin and dextrose, IV |
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| Description | Regular insulin presence results in intracellular movement of glucose, followed by K+ entry into muscle cells. Although effect is almost immediate, it is temporary, and, therefore, should be followed by therapy that actually enhances potassium clearance (eg, sodium polystyrene sulfonate). |
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| Adult Dose | 10 U of regular insulin in 500 mL of 20% dextrose solution, infuse IV over 1-2 h |
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| Pediatric Dose | 5 U regular insulin in 100 mL of 25% dextrose solution, infuse IV to provide 0.1 U (regular insulin)/kg/h
Alternatively, regular insulin 0.1 U/kg IV administered concurrently with 25% dextrose as 0.5 mg/kg (2 mL/kg) IV over 30 min; may repeat this dose in 30-60 min or begin infusion of 25% dextrose 1-2 mL/h with 0.1 U/kg/h of regular insulin |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Medications that may decrease hypoglycemic effects of regular insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine, isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, PO contraceptives, diazoxide, dobutamine, phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin
Medications that may increase hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta-blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Hyperthyroidism may increase renal clearance of regular insulin and more regular insulin may be needed to treat hyperkalemia; hypothyroidism may delay regular insulin turnover, requiring less regular insulin to treat hyperkalemia; monitor glucose carefully; dose adjustments of regular insulin may be necessary in patients with renal and hepatic dysfunction |
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Drug Category: Alkalinizing agents
Sodium bicarbonate IV is used as a buffer that breaks down to water and carbon dioxide after binding free hydrogen ions.
| Drug Name | Sodium bicarbonate (Brioschi) |
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| Description | IV infusion helps shift K+ into cells, further lowering serum K+ levels. Can be considered in treatment of hyperkalemia even in absence of metabolic acidosis. |
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| Adult Dose | 44-88 mEq/dose IV |
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| Pediatric Dose | 1-2 mEq/kg/dose IV |
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| Contraindications | Documented hypersensitivity; hypernatremia, (exchanges Na for K, care must be considered in patients at risk for CHF); bowel obstruction (avoid PO); contraindicated rectal manipulation (eg, patients with neutropenia) |
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| Interactions | Urinary alkalinization, induced by increased concentrations, may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases levels of amphetamines, pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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| Precautions | Do not mix with calcium in same IV line (results in precipitation); correct hypocalcemia before administration because hypocalcemia may worsen; use extravasation precautions |
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Drug Category: Exchange resins
Sodium polystyrene sulfonate is an exchange resin that can be used to treat mild-to-moderate hyperkalemia. Each mEq of potassium is exchanged for 1 mEq of sodium.
| Drug Name | Sodium polystyrene sulfonate (Kayexalate) |
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| Description | Exchanges sodium for potassium and binds it in the gut, primarily in large intestine, and decreases total body potassium. Onset of action after PO administration ranges from 2-12 hours and is longer when administered PR.
Do not use as a first-line therapy for severe life-threatening hyperkalemia. Use in second stage of therapy to reduce total body potassium. |
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| Adult Dose | Oral: 15-30 g PO bid/qid; may mix with 50 mL of 25% sorbitol to prevent constipation
Retention enema: 50 g of resin in 200 mL of 25% sorbitol |
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| Pediatric Dose | Oral: 0.5-1 g/kg PO
Retention enema: 0.5-1 g/kg in 3-5 mL of 25% sorbitol |
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| Contraindications | Documented hypersensitivity; hypernatremia, (exchanges Na for K, care must be considered in patients at risk for CHF); bowel obstruction (avoid PO); contraindicated rectal manipulation (eg, patients with neutropenia) |
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| Interactions | Systemic alkalosis may occur if administered concurrently with magnesium hydroxide, aluminum carbonate or similar antacids, and laxatives |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | May cause constipation by itself; sorbitol can cause diarrhea |
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Further Inpatient Care
- Hyperkalemia, by itself, is not a disease and is generally the result of diseases such as congenital adrenal hyperplasia, acute renal failure, rhabdomyolysis, or tumor lysis syndrome.
- Following emergent management and stabilization of hyperkalemia, the patient should be hospitalized, and further workup should be initiated to determine the inciting cause and to prevent recurrence.
Further Outpatient Care
- Continuing care relates to the basic disease process that led to the hyperkalemia.
- In patients with congenital adrenal hyperplasia, corticosteroid supplementation is necessary.
- Continued renal replacement therapy may be needed for patients with acute renal failure.
- Patients with chronic mineralocorticoid deficiency require fludrocortisone.
Transfer
- Patients with acute life-threatening hyperkalemia should receive care in a pediatric or neonatal ICU capable of providing emergent hemodialysis.
- Any child who develops hyperkalemia as a result of renal failure should be referred to a pediatric nephrologist for continuing care.
Complications
- If untreated, severe hyperkalemia can result in cardiac arrhythmia or death.
Prognosis
- Prognosis depends on the etiology.
Patient Education
- Teach patients to recognize the symptoms of hyperkalemia, such as palpitations, dizziness, and weakness.
Medical/Legal Pitfalls
- Failure to obtain historical data that may lead to the diagnosis of hyperkalemia is a potential pitfall, as in the case of a previously healthy toddler who presents with hyperkalemia and arrhythmias after ingesting potassium tablets. Failure to suspect hyperkalemia may prevent the physician from eliciting historical information about medications at home. If the practitioner does not suspect hyperkalemia, no appropriate treatment can be administered.
- With congenital adrenal hyperplasia, hyperkalemia is frequently observed with hyponatremia in an infant who presents with circulatory collapse. Failure to recognize this disease entity prevents the physician from administering corticosteroids, which are essential to appropriate treatment of these children.
- Failure to recognize ECG patterns of hyperkalemia (eg, tall, peaked T waves; tall, peaked sine waves) also leads to inappropriate treatment. For example, a child with chronic renal failure or congenital adrenal hyperplasia may present with nonspecific symptoms of nausea and vomiting yet have an elevated serum potassium level. Failure to obtain an ECG or the inability to recognize the classic ECG signs of hyperkalemia prevents the physician from obtaining appropriate serum electrolyte measurements and, more importantly, prevents the physician from instituting appropriate life-saving measures.
Special Concerns
- Patients with burns, crush injuries, and myopathies are at high risk of developing hyperkalemia, which is aggravated by the administration of succinylcholine. This drug should be avoided in such patients.
| Media file 3:
Hyperkalemia diagnosis and treatment flow chart. |
 |  View Full Size Image | |
Media type: Chart
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Hyperkalemia excerpt Article Last Updated: Feb 13, 2008
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