Hyperkalemia

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Hyperkalemia

Hyperkalemia is defined as a higher than normal concentration of potassium ions in the circulating blood.

Physiology: Potassium is the primary or intracellular cation and plays a key role in intracellular volume regulation. Total body potassium is approximately 53-55 mEq/kg body weight, as determined by evaluating gamma emissions of radionuclide-tagged potassium. Almost 100% of body potassium is contained in the intracellular fluid space, most in skeletal muscle. Both animal and vegetable food sources contain significant amounts of potassium; therefore, moderate to large amounts of potassium are consumed every day, regardless of the type of diet. Despite the level of consumption, however, a balance between intake and excretion maintains plasma potassium levels within a narrow range (3.5-4.5 mEq/L). Less than 10% of potassium is excreted through sweat and stools, while more than 90% is excreted by the kidneys.

Within the kidneys, a large amount of filtered potassium is reabsorbed (along with sodium) at the proximal convoluted tubule, thus regulating potassium excretion. Normally, considerable amounts of potassium are secreted into the distal tubules and some into the collecting tubules and ducts. Significant reabsorption occurs in the descending loop of Henle, so that only 10% of the potassium remains by the time the filtrates reach the distal convoluted tubule.

Aldosterone affects potassium secretion in the distal nephron by its action on the Na-K-ATPase pump. Elevated levels of aldosterone stimulate potassium secretion, while low levels inhibit potassium secretion by the cortical collecting duct. Increased sodium reabsorption and potassium secretion is due to its effects on the transport system. In addition, potassium levels are partly responsible for a negative feedback to the adrenal cortex such that high levels of potassium decrease aldosterone production, while low levels depress the secretion of aldosterone.

Pathophysiology: Plasma potassium levels generally are maintained between 3.5-4.5 mEq/L. Levels of 7.0 mEq/L can lead to significant hemodynamic and neurologic consequences. Levels exceeding 8.5 mEq/L cause respiratory paralysis and cardiac arrest and quickly can be fatal. High levels of potassium cause abnormal heart and skeletal muscle function by lowering resting action potential and by preventing repolarization and muscle paralysis. ECG findings are classic and begin with tenting of the T wave (see Picture 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 Picture 2).

Frequency:

In the US: Hyperkalemia is a manifestation of a disease and not a disease itself, so incidence is unknown. Hyperkalemia most commonly is 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 excretion of potassium increasing by as much as 5-10 times normal.

Race: No racial predilection exists.

Sex: No sex-related predilection exists.

Age: No age-related predilection exists.

History:

History for a previously well child should include the following:

Presence of drugs in the household, such as potassium preparations, digitalis, and diuretics

History of trauma (crush injuries)

Decreased intravascular volume with metabolic acidosis (acute gastroenteritis)

History for a child with chronic illness should include the following:

Acute or chronic renal failure

Adrenogenital syndromes

Malignancy (tumor lysis syndrome)

Family history (hyperkalemic episodic paralysis)

Physical: Hyperkalemia's signs and symptoms relate to abnormalities of membrane polarization. High serum levels disturb the ratio of potassium between the intracellular and extracellular space, which interferes with repolarization following completion of the action potential. Findings depend on the degree of hyperkalemia and primarily relate to the deleterious effects on the heart. Children with serum potassium levels more than 8 mEq/L can present with circulatory failure and wide-complex tachycardia or ventricular fibrillation. Other symptoms include weakness that progresses to paralysis and respiratory failure. Patients may complain of nausea, vomiting, and paresthesias (eg, tingling).

Causes:

Pseudohyperkalemia (release of potassium from cell lysis)

Leucocytosis
Thrombocytosis
Hemolysis (improper collection)

True hyperkalemia

Decreased renal excretion - Renal insufficiency or failure, drugs that block potassium excretion, hypoaldosteronism, congenital renal defects

Transcellular shift or increased cellular release - Metabolic acidosis, acute tumor lysis syndrome, crush injuries, use of depolarizing neuromuscular blocking agents such as succinylcholine, ACE inhibitors, acute digoxin toxicity, familial hyperkalemic paralysis

High potassium intake - Toxic ingestion of potassium preparations, intravenous potassium administration, rapid infusion of “old” blood

Other Problems to be Considered:

Acute renal failure
Drug overdose/poisoning

Lab Studies:

Laboratory studies depend on etiology but may include the following:

Serum electrolytes

An ECG is essential in all children suspected of having hyperkalemia. ECG reveals the sequence of changes as follows:

Serum potassium levels more than 6.0 mEq/L - T waves tall and tented

Serum potassium levels more than 7.0 mEq/L - P-R interval lengthens, P wave may disappear, R wave amplifies

Serum potassium levels more than 8.0 mEq/L - QRS widens; just before the heart stops, the wide QRS merges with the T wave, thus forming a sinusoidal wave

BUN, creatinine

Uric acid

Urinalysis

Digoxin levels (if toxicity suspected)

Urine electrolytes, including potassium

Imaging Studies:

Imaging studies generally are not indicated except to assess the primary disease state.

Procedures:

Emergent hemodialysis sometimes is necessary to treat severe symptomatic hyperkalemia, which is resistant to drug therapy. Depending on the potassium gradient, removal of potassium with hemodialysis approaches 70 to 150 mEq.

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 is almost equal to the removal rate effected by Kayexalate.

Continuous arteriovenous (CAVHD) or veno-venous (CVVHD) hemofiltration with dialysis also has been used to remove potassium. However, potassium removal with these methods are similar to that of peritoneal dialysis and Kayexalate. CVVHD or CAVHD may be used for chronic removal of potassium, but in acute, severe life-threatening hyperkalemia unresponsive to medical therapy, hemodialysis remains the procedure of choice.

Medical Care:

Goals of management include the following:

Counteract the deleterious electrophysiologic effects of hyperkalemia.

Shift potassium intracellularly.

Remove excess potassium.
If indicated, treat tumor lysis syndrome or rhabdomyolysis induced by crush or severe traumatic injury.

Inhaled beta-adrenergic agents (eg, albuterol) have been used to manage hyperkalemia with variable results.

Consider further workup to determine etiology of hyperkalemia.
Supportive care may include adequate intravascular volume expansion, if indicated.

Consultations: Consultations may be necessary in cases of hyperkalemia that result from conditions or disease states as follows:

Nephrology - Hyperkalemia associated with renal failure

Hematology/oncology - Hyperkalemia resulting from tumor lysis syndrome

Social services - For children who develop hyperkalemia following accidental ingestions or poisonings

Nutritional support - Particularly for patients whose hyperkalemia is caused by renal failure, which requires close regulation of potassium and sodium intake

Endocrinology - 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.

Adobe Acrobat Reader (stand-alone) or Viewer (browser-integrated JAVA plug-in) is required to view this document. To obtain these free products, please visit Hyperkalemia is defined as a serum potassium level of >5.5 mEq/L. Serum potassium level of >7 mEq/L with EKG changes such as tall, peaked T waves with widening of the QRS or a sine wave pattern (see EKG's) is considered severe hyperkalemia, is life-threatening, and requires immediate therapy (outlined below) consisting of intravenous calcium to stabilize the myocardium; and rapid means of decreasing serum levels by alkalinization with sodium bicarbonate, and a continuous intravenous infusion of dextrose and insulin. Occasionally emergent dialysis may be required.Kayexalate is not indicated as the first line of therapy in severe hyperkalemia.

Drug Category: Stabilization of the myocardium -- The use of calcium does not lower serum potassium levels. It is used primarily to protect the myocardium from the deleterious effects of hyperkalemia by antagonizing the membrane actions of potassium.

Drug Name
Calcium chloride or calcium gluconate -- Intravenous calcium in indicated all in cases of severe hyperkalemia (>7 meQ/L), especially when accompanied by EKG changes. Calcium chloride contains 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.
The administration of calcium should be accompanied by the use of other therapies that actually help lower the serum levels of potassium.
Other forms of calcium such as calcium glubionate or gluceptate have even less elemental calcium than calcium gluconate, and are generally not recommended for the therapy of hyperkalemia.
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; 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
-- Insulin/glucose infusion: causes a transcellular shift of potassium into muscle cells, thereby lowering (temporarily) serum levels of potassium.

Drug Name
Insulin and glucose infusion -- The presence of insulin results in the intracellular movement of glucose, followed by entry of potassium into muscle cells. The effect is almost immediate, but temporary, and should therefore be followed by therapy which actually enhances potassium clearance, such as Kayexalate.
Adult Dose 10 units of regular insulin in 500 mL of 20% dextrose solution; infuse over 1-2 hrs
Pediatric Dose 5 units insulin in 100 mL of 25% dextrose solution, and infuse to provide 0.1 unit of insulin/kg/hr or
Regular insulin 0.1 U/kg IV with 25% glucose as 0.5 mg/kg (2 mL/kg) over 30 minutes. May repeat this dose in 30-60 minutes or begin infusion of 25% Dextrose 1-2 mL/hour with 0.1 U/kg/hour of regular insulin
Contraindications Documented hypersensitivity
Interactions Medications that may decrease hypoglycemic effects of insulin include acetazolamide,
AIDS antivirals, asparaginase, phenytoin, nicotine isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, oral 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, MAO inhibitors, 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 insulin and may need more insulin to treat hyperkalemia; hypothyroidism may delay insulin turnover, requiring less insulin to treat hyperkalemia; monitor glucose carefully; dose adjustments of insulin may be necessary in patients diagnosed with renal and hepatic dysfunction
-- Alkali

Drug Name
Sodium bicarbonate -- The intravenous infusion of sodium bicarbonate helps shift potassium into the cells, further lowering serum potassium levels. Sodium bicarbonate can be considered in the treatment of hyperkalemia even in the absence of metabolic acidosis.
Adult Dose 44-88 mEq IV per dose
Pediatric Dose 1-2 mEq/kg/dose IV
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Do not mix sodium bicarbonate and calcium in-line. This will result in precipitation.
Correct hypocalcemia before administration of sodium bicarbonate, as hypocalcemia may worsen.
-- Beta-agonist agents

Drug Name
Albuterol nebulization -- Albuterol and other beta-adrenergic agents induce the intracellular movement of potassium via the stimulation of the Na-K ATP pump. Studies have shown that intravenous salbutamol (not available in the US) is highly effective in lowering serum potassium. Some studies in adults and children using nebulized albuterol indicate that this method of therapy is effective in lowering serum potassium. However, peak response is unclear, and therefore, it has not been established as the first line of therapy in severe hyperkalemia.
Drug Category: Exchange resin -- Kayexalate 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) -- Do not use as a first-line therapy for severe life-threatening hyperkalemia; use in the second stage of therapy to reduce total body potassium.
Adult Dose 15-30 g PO bid/qid; may mix with 50 mL of 25% sorbitol to prevent constipation
To administer as a retention enema, use 50 g of resin in 200 mL of 25% sorbitol
Pediatric Dose 0.5-1.0 g/kg PO, or as retention enema in 3-5 mL of 25% sorbitol
Contraindications Documented hypersensitivity and hypernatremia; avoid oral intake in cases of bowel obstruction; rectal manipulation is contraindicated (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

Drug Name	Calcium chloride or calcium gluconate -- Intravenous calcium in indicated all in cases of severe hyperkalemia (>7 meQ/L), especially when accompanied by EKG changes. Calcium chloride contains 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. The administration of calcium should be accompanied by the use of other therapies that actually help lower the serum levels of potassium. Other forms of calcium such as calcium glubionate or gluceptate have even less elemental calcium than calcium gluconate, and are generally not recommended for the therapy of hyperkalemia.
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; 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 Name	Insulin and glucose infusion -- The presence of insulin results in the intracellular movement of glucose, followed by entry of potassium into muscle cells. The effect is almost immediate, but temporary, and should therefore be followed by therapy which actually enhances potassium clearance, such as Kayexalate.
Adult Dose	10 units of regular insulin in 500 mL of 20% dextrose solution; infuse over 1-2 hrs
Pediatric Dose	5 units insulin in 100 mL of 25% dextrose solution, and infuse to provide 0.1 unit of insulin/kg/hr or Regular insulin 0.1 U/kg IV with 25% glucose as 0.5 mg/kg (2 mL/kg) over 30 minutes. May repeat this dose in 30-60 minutes or begin infusion of 25% Dextrose 1-2 mL/hour with 0.1 U/kg/hour of regular insulin
Contraindications	Documented hypersensitivity
Interactions	Medications that may decrease hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, oral 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, MAO inhibitors, 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 insulin and may need more insulin to treat hyperkalemia; hypothyroidism may delay insulin turnover, requiring less insulin to treat hyperkalemia; monitor glucose carefully; dose adjustments of insulin may be necessary in patients diagnosed with renal and hepatic dysfunction

Drug Name	Sodium bicarbonate -- The intravenous infusion of sodium bicarbonate helps shift potassium into the cells, further lowering serum potassium levels. Sodium bicarbonate can be considered in the treatment of hyperkalemia even in the absence of metabolic acidosis.
Adult Dose	44-88 mEq IV per dose
Pediatric Dose	1-2 mEq/kg/dose IV
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Do not mix sodium bicarbonate and calcium in-line. This will result in precipitation. Correct hypocalcemia before administration of sodium bicarbonate, as hypocalcemia may worsen.

Drug Name	Albuterol nebulization -- Albuterol and other beta-adrenergic agents induce the intracellular movement of potassium via the stimulation of the Na-K ATP pump. Studies have shown that intravenous salbutamol (not available in the US) is highly effective in lowering serum potassium. Some studies in adults and children using nebulized albuterol indicate that this method of therapy is effective in lowering serum potassium. However, peak response is unclear, and therefore, it has not been established as the first line of therapy in severe hyperkalemia.

Drug Name	Sodium polystyrene sulfonate (Kayexalate) -- Do not use as a first-line therapy for severe life-threatening hyperkalemia; use in the second stage of therapy to reduce total body potassium.
Adult Dose	15-30 g PO bid/qid; may mix with 50 mL of 25% sorbitol to prevent constipation To administer as a retention enema, use 50 g of resin in 200 mL of 25% sorbitol
Pediatric Dose	0.5-1.0 g/kg PO, or as retention enema in 3-5 mL of 25% sorbitol
Contraindications	Documented hypersensitivity and hypernatremia; avoid oral intake in cases of bowel obstruction; rectal manipulation is contraindicated (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

Further Inpatient Care:

Hyperkalemia, by itself, is not a disease and generally is the result of other diseases such as congenital adrenal hyperplasia, acute renal failure, rhabdomyolysis, and tumor lysis syndrome. Following emergent management and stabilization of hyperkalemia, hospitalize the patient and initiate further workup to determine the inciting cause.

Further Outpatient Care:

Continuing care relates to the basic disease process that led to hyperkalemia.

In patients with congenital adrenal hyperplasia, corticosteroid supplementation is necessary.

Continued renal replacement therapy may be needed for patients with acute renal failure.

Transfer:

Patients with acute life-threatening hyperkalemia should receive care in an appropriately monitored bed, preferably in an ICU.

Transfer any patient who develops hyperkalemia as a result of renal failure to a renal unit for continuing care.

Complications:

If untreated, severe hyperkalemia can kill.

Possible complications include arrhythmias.

Prognosis:

Prognosis depends upon the etiology of the hyperkalemia.

Patient Education:

Teach patients with hyperkalemia that is expected to recur to avoid foods that are high in potassium. Education to avoid salt substitutes is especially important, as these generally consist of potassium salts.

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, 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 frequently is 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 key to appropriate management 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 the patient's serum potassium may be elevated. Failure to obtain an ECG or 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.

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