AUTHOR INFORMATION

Section 1 of 12

Authored by Eric D Harry, MD, Pediatric Critical Care Fellow, Children's Hospital and Regional Medical Center

Coauthored by Jerry Zimmerman, MD, Professor, Department of Pediatrics/Anesthesia, University of Washington School of Medicine; Director, Division of Pediatric Critical Care Medicine, Children's Hospital of Seattle

Edited by G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, Miller School of Medicine, University of Miami; Director of Pediatric Critical Care Medicine, Jackson Children's Hospital; Robert Konop, PharmD, Director, Clinical Account Management, Ancillary Care Management, Inc; Barry 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; Associate Professor, Department of Clinical Pediatrics, State University of New York at Stony Brook; and Maureen Strafford, MD, Arnold P Gold Foundation Associate Professor, Departments of Anesthesiology and Pediatrics, Tufts University and Tufts-New England Medical Center

Author's Email:	Eric D Harry, MD
Editor's Email:	G Patricia Cantwell, MD

eMedicine Journal, March 8 2005, VOLUME 6, Number 3

INTRODUCTION

Section 2 of 12

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, with more than 98% of the total body potassium existing 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 is dependent upon adequate luminal sodium delivery to the distal convoluted tubule (DCT) and CCD.

Hyperkalemia in children is commonly fictitious. Fictitious hyperkalemia, or pseudohyperkalemia, can easily occur because of hemolysis during phlebotomy, especially with heel-poke or finger-stick phlebotomy as commonly performed on children. Hemolysis can be caused by fist clenching during phlebotomy; it can also be caused by prolonged tourniquet application. Thrombocytosis, also, can lead to 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 commonly caused by one of 3 basic mechanisms, though 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 red blood cells (pRBCs) also carry potentially high concentrations of potassium that can lead to hyperkalemia during pRBC transfusion.

• 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 a 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 resting action potential and by preventing repolarization, leading to muscle paralysis. ECG findings are classic and begin with tenting of the T wave (see Image 1), followed by lengthening and eventual disappearance of the P wave and widening of the QRS complex. Just before the heart stops, the QRS and T wave merge to form a sine wave (see Image 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

*See Image 3 for a printer-friendly version of the table.

Frequency:

• In the US: Hyperkalemia is a manifestation of a disease and 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.

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 exists.

Sex: No sex-related predilection exists.

Age: No age-related predilection exists.

CLINICAL

Section 3 of 12

History:

• History for a previously well child with acute hyperkalemia should focus on how the blood sample was drawn, potassium intake or recent blood product transfusion, risk factors for transcellular shift of potassium 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: Though 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

  • Intravenous (IV) or oral potassium
  
  
  
• 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
  
  
  
• 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)

DIFFERENTIALS

Section 4 of 12

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

WORKUP

Section 5 of 12

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 arterial blood gas 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) 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 (such as 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 Image 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 Image 2)
  
  
  

TREATMENT

Section 6 of 12

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
  
  
  
  • Shifting potassium intracellularly
    • 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 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 obtained 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:

• Nephrologist - Hyperkalemia associated with renal failure



• Hematologist/oncologist - Hyperkalemia resulting from tumor lysis syndrome



• Social services specialist - For children who develop hyperkalemia following accidental 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.

MEDICATION

Section 7 of 12

Hyperkalemia is defined as a serum potassium level more than 5.5 mEq/L. Severe hyperkalemia, defined as is an elevated serum potassium level with associated ECG changes (initially peaked T waves progressing to widening of the QRS then sine wave pattern) (see Images 1-2) is a life-threatening medical emergency and requires immediate therapy.

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 -- 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.
Adult Dose	Calcium gluconate (10%): 1 g/dose slow IV Calcium chloride (10%): 250-500 mg/dose slow IV
Pediatric Dose	Calcium gluconate (10%): 100 mg/kg/dose slow IV Calcium chloride (10%): 20 mg/kg/dose slow IV
Contraindications	Ventricular fibrillation not associated with hyperkalemia; digitalis toxicity; hypercalcemia; renal insufficiency; cardiac disease
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
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure

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 -- 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).
Adult Dose	10 U of regular insulin in 500 mL of 20% dextrose solution, infuse IV over 1-2 h
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
Contraindications	Documented hypersensitivity
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
Pregnancy	B - Usually safe but benefits must outweigh the risks.
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

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) -- 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.
Adult Dose	44-88 mEq/dose IV
Pediatric Dose	1-2 mEq/kg/dose IV
Contraindications	Alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema; abdominal pain from unknown cause
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
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Do not mix with calcium in same IV line (results in precipitation); correct hypocalcemia before administration because hypocalcemia may worsen; use extravasation precautions

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) -- 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.
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
Pediatric Dose	Oral: 0.5-1 g/kg PO Retention enema: 0.5-1 g/kg in 3-5 mL of 25% sorbitol
Contraindications	Documented hypersensitivity; hypernatremia; bowel obstruction (avoid PO); contraindicated rectal manipulation (eg, patients with neutropenia)
Interactions	Systemic alkalosis may occur if administered concurrently with magnesium hydroxide, aluminum carbonate or similar antacids, and laxatives
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	May cause constipation by itself; sorbitol can cause diarrhea

FOLLOW-UP

Section 8 of 12

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 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 upon the etiology.

Patient Education:

• Teach patients to recognize the symptoms of hyperkalemia, such as palpitations, dizziness, and weakness.

MISCELLANEOUS

Section 9 of 12

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, for example. 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.

TEST QUESTIONS

Section 10 of 12

CME Question 1: A child has ingested his grandmother’s potassium tablets and presents in the emergency department (ED) with a serum potassium level of 12 mEq/L. The ECG tracing on the monitor shows peaked T waves and a wide QRS. After the ABCs, which of the following is the most appropriate management strategy?

A: IV calcium chloride (CaCl), followed by IV sodium bicarbonate and glucose/regular insulin infusion
B: Immediate peritoneal dialysis
C: Sodium polystyrene sulfonate through a nasogastric (NG) tube
D: Administration of activated charcoal
E: IV calcium gluconate, 25% dextrose 2 mL/kg IV push

The correct answer is A: The patient has life-threatening and acute hyperkalemia after ingesting potassium tablets. Immediately administer calcium to stabilize the myocardium. Following this, administer sodium bicarbonate IV and glucose/regular insulin solution to shift potassium intracellularly. Sodium polystyrene sulfonate may be administered following stabilization of the patient.

CME Question 2: What is the role of calcium in the treatment of hyperkalemia?

A: To lower intracellular potassium levels
B: To augment therapeutic effects of other agents used in the treatment of hyperkalemia
C: To stabilize the myocardium
D: To increase renal excretion of potassium
E: To increase binding of potassium to chloride to form salts, which are excreted

The correct answer is C: Calcium administration stabilizes the myocardium and protects the heart from adverse arrhythmogenic effects of hyperkalemia.

Pearl Question 1 (T/F): Thrombocytosis results in true hyperkalemia because the high numbers of platelets compete with potassium entry into the cells.

The correct answer is False: Thrombocytosis causes pseudohyperkalemia and is an in vitro phenomenon caused by the release of intracellular potassium when platelets are left standing.

Pearl Question 2 (T/F): The effects of aldosterone on the maintenance of serum potassium levels are related to the influence of the hormone on the sodium shift into the extracellular space.

The correct answer is False: Aldosterone regulates potassium excretion and the maintenance of serum potassium levels by varying distal tubular intracellular concentration and, therefore, its resorption.

Pearl Question 3 (T/F): Emergency hemodialysis must be initiated for a serum potassium level of 7 mEq/L before providing any other therapy.

The correct answer is False: Emergency hemodialysis is indicated only in severe hyperkalemia that is resistant to treatment with calcium, sodium bicarbonate, and insulin/glucose solution, especially in the presence of acute renal failure.

Pearl Question 4 (T/F): The sinusoidal ECG pattern observed in severe hyperkalemia is due to merging of the widened QRS with the T wave.

The correct answer is True: ECG findings are classic and begin with tenting of the T wave, followed by lengthening and eventual disappearance of the P wave and widening of the QRS complex. Just before the heart stops, the QRS and T wave merge to form a sine wave.

PICTURES

Section 11 of 12

Caption: Picture 1. Peaked T waves.
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Caption: Picture 2. Sinusoidal wave.
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Caption: Picture 3. Printer-friendly version of table (PDF).
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Caption: Picture 4. Hyperkalemia diagnosis and treatment flow chart.
Picture Type: Image

BIBLIOGRAPHY

Section 12 of 12

• Behrman R, Kliegman R, Jenson H: Nelson Textbook of Pediatrics, 17th Ed. Philadelphia, PA: WB Saunders; 2004.
• Brenner B: Brenner & Rector’s The Kidney, 7th Ed. St Louis, MO: WB Saunders; 2004.
• Finberg L, Kravath R, Hellerstein S: Potassium. In: Water and Electrolytes in Pediatrics: Physiology, Pathophysiology, and Treatment. Philadelphia, PA: WB Saunders; 1993:70-1.
• Goldfrank LR, ed: Goldfrank's Toxicologic Emergencies, 6th Ed. Stanford, CT: Appleton & Lange; 1998.
• Kokko, JP, Tannen RL: Potassium Disorders. In: Fluids and Electrolytes. Philadelphia, PA: WB Saunders; 1990: 195-300.
• Lieh-Lai, M, Asi-Bautista, M, Ling-McGeorge, K: Hyperkalemia. In: Pediatric Acute Care Handbook. Philadelphia, PA: Lippincott, Williams, & Wilkins; 1995.
• Mattu A, Brady WJ, Robinson DA: Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med 2000 Oct; 18(6): 721-9[Medline].
• Maxwell MH, Kleeman CR: Maxwell and Kleeman's Clinical Disorders of Fluid and Electrolyte Metabolism, 5th Ed. New York, NY: McGraw-Hill; 1994.

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