Hyperkalemia in Emergency Medicine

Practice Essentials

Hyperkalemia is defined as a potassium level greater than 5.5 mEq/L. [1] It can be difficult to diagnose clinically because symptoms may be vague or absent. However, the fact that hyperkalemia can lead to sudden death from cardiac arrhythmias requires that physicians be quick to consider hyperkalemia in patients who are at risk for it. [2, 3] Initial emergency department care includes assessment of the ABCs and prompt evaluation of the patient's cardiac status with an electrocardiogram (ECG). In patients in whom hyperkalemia is severe (potassium >7.0 mEq/L) or symptomatic, treatment should commence before diagnostic investigation of the underlying cause. See the ECG below.

Widened QRS complexes in hyperkalemia. Signs and symptoms of hyperkalemia Patients with hyperkalemia may be asymptomatic, or they may report the following symptoms (cardiac and neurologic symptoms predominate):

• Generalized fatigue

• Weakness

• Paresthesias

• Paralysis

• Palpitations

Evaluation of vital signs is essential for determining the patient’s hemodynamic stability and the presence of cardiac arrhythmias related to hyperkalemia. [1] Additional important components of the physical exam may include the following:

• Cardiac examination may reveal extrasystoles, pauses, or bradycardia

• Neurologic examination may reveal diminished deep tendon reflexes or decreased motor strength

• In rare cases, muscular paralysis and hypoventilation may be observed

• Signs of renal failure, such as edema, skin changes, and dialysis sites, may be present

• Signs of trauma may indicate that the patient has rhabdomyolysis, which is one cause of hyperkalemia

Diagnosis of hyperkalemia Laboratory studies The following lab studies can be used in the diagnosis of hyperkalemia:

• Potassium level: The relationship between serum potassium level and symptoms is not consistent; for example, patients with a chronically elevated potassium level may be asymptomatic at much higher levels than other patients; the rapidity of change in the potassium level influences the symptoms observed at various potassium levels

• Blood urea nitrogen (BUN) and creatinine levels: For evaluation of renal status

• Calcium level: If the patient has renal failure (because hypocalcemia can exacerbate cardiac rhythm disturbances)

• Glucose level: In patients with diabetes mellitus

• Digoxin level: If the patient is on a digitalis medication

• Arterial or venous blood gas: If acidosis is suspected

• Urinalysis: To look for evidence of glomerulonephritis if signs of renal insufficiency without a known cause are present

• Cortisol and aldosterone levels: To check for mineralocorticoid deficiency when other causes are eliminated

Electrocardiography Electrocardiography is essential and may be instrumental in diagnosing hyperkalemia in the appropriate clinical setting. Electrocardiographic changes have a sequential progression that roughly correlates with the patient’s potassium level. Potentially life-threatening arrhythmias, however, can occur without distinct electrocardiographic changes at almost any level of hyperkalemia. Management of hyperkalemia Prehospital care Prior to reaching the emergency department, treatment of a patient with hyperkalemia includes the following:

• A patient with known hyperkalemia or a patient with renal failure with suspected hyperkalemia should have intravenous access established and should be placed on a cardiac monitor [4]

• In the presence of hypotension or marked QRS widening, intravenous bicarbonate, calcium, and insulin given together with 50% dextrose may be appropriate

• Avoid calcium if digoxin toxicity is suspected; magnesium sulfate (2 g over 5 min) may be used alternatively in the face of digoxin-toxic cardiac arrhythmias

Inhospital care Once the patient reaches the emergency department, assessment and treatment include the following:

• Continuous ECG monitoring with frequent vital sign checks: When hyperkalemia is suspected or when laboratory values indicative of hyperkalemia are received

• Assessment of the ABCs and prompt evaluation of the patient's cardiac status with an electrocardiogram (ECG)

• Discontinuation of any potassium-sparing drugs or dietary potassium

If the hyperkalemia is known to be severe (potassium >7.0 mEq/L) or if the patient is symptomatic, begin treatment before diagnostic investigation of the underlying cause. Individualize treatment based upon the patient's presentation, potassium level, and ECG. Dialysis is the definitive therapy in patients with renal failure or in whom pharmacologic therapy is not sufficient. Any patient with significantly elevated potassium levels should undergo dialysis, as pharmacologic therapy alone is not likely to adequately bring down the potassium levels in a timely fashion. Medications Drugs used in the treatment of hyperkalemia include the following:

• Calcium (either gluconate or chloride): Reduces the risk of ventricular fibrillation caused by hyperkalemia

• Insulin administered with glucose: Facilitates the uptake of glucose into the cell, which results in an intracellular shift of potassium

• Alkalinizing agents: Increases the pH, which results in a temporary potassium shift from the extracellular to the intracellular environment; these agents enhance the effectiveness of insulin in patients with acidemia

• Beta2-adrenergic agonists: Promote cellular reuptake of potassium

• Diuretics: Cause potassium loss through the kidney

• Binding resins: Promote the exchange of potassium for sodium in the gastrointestinal (GI) system

• Magnesium sulfate: Has been successfully used to treat acute overdose of slow-release oral potassium
  

Background

Hyperkalemia is a potentially life-threatening illness that can be difficult to diagnose because of a paucity of distinctive signs and symptoms. The physician must be quick to consider hyperkalemia in patients who are at risk for this disease process. Because hyperkalemia can lead to sudden death from cardiac arrhythmias, any suggestion of hyperkalemia requires an immediate ECG to ascertain whether electrocardiographic signs of electrolyte imbalance are present.

Pathophysiology

Potassium is a major ion of the body. Nearly 98% of potassium is intracellular, with the concentration gradient maintained by the sodium- and potassium-activated adenosine triphosphatase (Na+/K+ –ATPase) pump. The ratio of intracellular to extracellular potassium is important in determining the cellular membrane potential. Small changes in the extracellular potassium level can have profound effects on the function of the cardiovascular and neuromuscular systems. The normal potassium level is 3.5-5.0 mEq/L, and total body potassium stores are approximately 50 mEq/kg (3500 mEq in a 70-kg person). Minute-to-minute levels of potassium are controlled by intracellular to extracellular exchange, mostly by the sodium-potassium pump that is controlled by insulin and beta-2 receptors. A balance of GI intake and renal potassium excretion achieves long-term potassium balance. Hyperkalemia is defined as a potassium level greater than 5.5 mEq/L. [1] Ranges are as follows:

• 5.5-6.0 mEq/L - Mild

• 6.1-7.0 mEq/L - Moderate

• 7.0 mEq/L and greater - Severe

Hyperkalemia results from the following:

• Decreased or impaired potassium excretion - As observed with acute or chronic renal failure [5] (most common), potassium-sparing diuretics, urinary obstruction, sickle cell disease, Addison disease, and systemic lupus erythematosus (SLE)

• Additions of potassium into extracellular space - As observed with potassium supplements (eg, PO/IV potassium, salt substitutes), rhabdomyolysis, and hemolysis (eg, blood transfusions, burns, tumor lysis)

• Transmembrane shifts (ie, shifting potassium from the intracellular to extracellular space) - As observed with acidosis and medication effects (eg, acute digitalis toxicity, beta-blockers, succinylcholine)

• Fictitious or pseudohyperkalemia - As observed with improper blood collection (eg, ischemic blood draw from venipuncture technique), laboratory error, leukocytosis, and thrombocytosis

Epidemiology

In a study from Taiwan of inpatients, outpatients, and patients in the emergency department, with serum potassium levels of 6 mmol/L or greater, Kuo et al found the highest incidence to be in the emergency department (0.92%), but determined that the worst outcomes were among inpatients, with a 51% mortality rate. [7] Sex The male-to-female ratio is 1:1.

Mortality/Morbidity The primary cause of morbidity and death is potassium's effect on cardiac function. [8, 9, 10] The mortality rate can be as high as 67% if severe hyperkalemia is not treated rapidly. [11] In a study of almost 21,800 inpatients with hyperkalemia, Davis et al found that death and readmission were fairly common whether the hyperkalemia was mild, moderate, or severe. (In this report, mild, moderate, and severe were designated as >5.0-5.5 mEq/L, >5.5-6.0 mEq/L, and >6.0 mEq/L, respectively.) During their inpatient stay, normalization of potassium levels occurred in 87.7%, 86.8%, and 81.9% of the mild, moderate, and severe patients, respectively. Nonetheless, inpatient mortality rates in the mild, moderate, and severe groups were 12.3%, 15.5%, and 19.5%, respectively. Moreover, the all-cause inpatient readmission rates for the three groups at 30-90 days post discharge were 19.7-31.2%, 21.5-32.1%, and 19.6-31.4%, respectively. [12] A study by Krogager et al indicated that in patients who need diuretic treatment following a myocardial infarction, a potassium level above or below the 3.9-4.5 mmol/L range significantly increases the mortality risk, with the highest risk (38.3% mortality rate at 90-day follow-up) found in patients with severe hyperkalemia (>5.5 mmol/L). [13] A study by Norring-Agerskov indicated that hyperkalemia is associated with increased 30-day mortality in hip-fracture patients, with a hazard ratio of 1.93. The study included 7293 patients with hip fracture, aged 60 years or older. [14]

Medicine Clinical Presentation

History Hyperkalemia can be difficult to diagnose clinically because symptoms may be vague or absent. The history is most valuable in identifying conditions that may predispose to hyperkalemia. Hyperkalemia frequently is discovered as an incidental laboratory finding. Cardiac and neurologic symptoms predominate. Patients may be asymptomatic or report the following:

• Generalized fatigue

• Weakness

• Paresthesias

• Paralysis

• Palpitations

Hyperkalemia is suggested in any patient with a predisposition toward elevated potassium level. Potential potassium level elevation is observed in the following:

• Acute or chronic renal failure, especially in patients who are on dialysis

• Trauma, including crush injuries (rhabdomyolysis), or burns

• Ingestion of foods high in potassium (eg, bananas, oranges, high-protein diets, tomatoes, salt substitutes). This alone is not likely to cause clinically significant hyperkalemia in most people; it is often a contributing factor to an acute potassium elevation.

• Medications - Potassium supplements, potassium-sparing diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), beta-blockers, digoxin, succinylcholine, and digitalis glycoside

• Medication combinations (ie, spironolactone, ACE inhibitors) [15]

• Redistribution - Metabolic acidosis (diabetic ketoacidosis [DKA]), catabolic states

Physical Evaluation of vital signs is essential to determine hemodynamic stability and presence of cardiac arrhythmias related to the hyperkalemia. [1] Cardiac examination may reveal extrasystoles, pauses, or bradycardia. Neurologic examination may reveal diminished deep tendon reflexes or decreased motor strength. In rare cases, muscular paralysis and hypoventilation may be observed. Search for the stigmata of renal failure, such as edema, skin changes, and dialysis sites. Look for signs of trauma that could put the patient at risk for rhabdomyolysis.

Causes Pseudohyperkalemia may result from the following:

• Hemolysis (in laboratory tube) most common

• Severe thrombocytosis

• Severe leukocytosis

• Venipuncture technique (ie, ischemic blood draw from prolonged tourniquet application)

Redistribution may result from the following:

• Acidosis

• Beta-blocker drugs

• Acute digoxin intoxication or overdose

• Succinylcholine [16]

• Arginine hydrochloride

• Hyperkalemic familial periodic paralysis

Excessive endogenous potassium load may result from the following:

• Hemolysis

• Rhabdomyolysis

• Internal hemorrhage

Excessive exogenous potassium load may result from the following:

• Parenteral administration

• Excess in diet

• Potassium supplements

• Salt substitutes

A study by Te Dorsthorst et al indicated that dietary hyperkalemia may not be a condition of renal impairment. In an analysis of 35 case reports that included 44 incidences of hyperkalemia arising from oral intake, the investigators found no kidney dysfunction in 17 patients. Salt substitutes and supplements were the primary causes of hyperkalemia in patients with normal renal function. [17] Diminished potassium excretion may result from the following:

• Decreased glomerular filtration rate (eg, acute or end-stage chronic renal failure)

• Decreased mineral corticoid activity

• Defect in tubular secretion (eg, renal tubular acidosis II and IV)

• Drugs (eg, NSAIDs, cyclosporine, potassium-sparing diuretics)

Laboratory error may be the cause of reported hyperkalemia, so if not consistent with the clinical picture, repeat laboratory studies. [18]

Differential Diagnoses

• Hypocalcemia

Workup

Laboratory Studies

Potassium level The relationship between the serum potassium level and symptoms is not consistent. For example, patients with a chronically elevated potassium level may be asymptomatic at much higher levels than other patients. The rapidity of change in the potassium level influences the symptoms observed at various potassium levels. BUN and creatinine level For evaluation of renal status Calcium level If patient has renal failure (because hypocalcemia can exacerbate cardiac rhythm disturbances) Glucose level In patients with diabetes mellitus Digoxin level If patient is on a digitalis medication Arterial or venous blood gas If acidosis is suspected Urinalysis If signs of renal insufficiency without an already known cause are present (to look for evidence of glomerulonephritis)

Other Tests Continuous cardiac monitoring Indicated for evaluation of rhythm disturbances ECG ECG is essential and may be instrumental in diagnosing hyperkalemia in the appropriate clinical setting. ECG changes have a sequential progression of effects, which roughly correlate with the potassium level. ECG findings may be observed as follows:

• Early changes of hyperkalemia include peaked T waves, shortened QT interval, and ST-segment depression.

• These changes are followed by bundle-branch blocks causing a widening of the QRS complex, increases in the PR interval, and decreased amplitude of the P wave (see the images below).

Widened QRS complexes in hyperkalemia.

Widened QRS complexes in a patient whose serum potassium level was 7.8 mEq/L

• These changes reverse with appropriate treatment (see the image below).

ECG of a patient with pretreatment potassium level of 7.8 mEq/L and widened QRS complexes after receiving 1 ampule of calcium chloride. Notice narrowing of QRS complexes and reduction of T waves.

• Without treatment, the P wave eventually disappears and the QRS morphology widens to resemble a sine wave. Ventricular fibrillation or asystole follows.

• ECG findings generally correlate with the potassium level, but potentially life-threatening arrhythmias can occur without distinct ECG changes at almost any level of hyperkalemia.

Cortisol and aldosterone levels To check for mineralocorticoid deficiency when other causes are eliminated

Treatment & Management

Prehospital Care A patient with known hyperkalemia or a patient with renal failure with suspected hyperkalemia should have intravenous access established and should be placed on a cardiac monitor. [4] In the presence of hypotension or marked QRS widening, intravenous bicarbonate, calcium, and insulin, given together with 50% dextrose, may be appropriate, as discussed in Medication. Avoid calcium if digoxin toxicity is suspected. Magnesium sulfate (2 g over 5 min) may be used alternatively in the face of digoxin-toxic cardiac arrhythmias.

Emergency Department Care Perform continuous ECG monitoring with frequent vital sign checks when hyperkalemia is suspected or when laboratory values indicative of hyperkalemia are received. Initial management includes assessment of the ABCs and prompt evaluation of the patient's cardiac status with an ECG. Discontinue any potassium-sparing drugs or dietary potassium. If the hyperkalemia is known to be severe (potassium >7.0 mEq/L) or if the patient is symptomatic, begin treatment before diagnostic investigation of the underlying cause. Individualize treatment based upon the patient's presentation, potassium level, and ECG. Not all patients should receive every medication listed in Medication. Patients with mild hyperkalemia, for example, may need only excretion enhancement. Some studies are emerging that suggest sodium polystyrene sulfonate (SPS), also known as Kayexalate, may be unhelpful in hyperkalemia and may increase the chance of colonic necrosis (especially when used with sorbitol). [19, 20, 21, 22] A retrospective study by Lee and Moffett, however, found SPS to be a safe and effective treatment for hyperkalemia in most pediatric patients. However, the investigators suggested that the drug may not be an appropriate first single-line agent when patients with severe acute hyperkalemia need their serum potassium level reduced by over 25% or when patients have a high cardiac arrhythmia risk. [23] Generally, SPS is considered safe orally but is not recommended as a retention enema, which has a higher rate of colonic necrosis. Effects are expected to be minor and not adequate to reduce potassium levels to normal levels. Phase II and III clinical trials have indicated that patiromer and sodium zirconium cyclosilicate (ZS-9) have a dose-dependent ability to lower potassium levels. In 2015, patiromer (Veltassa) was approved by the US Food and Drug Administration (FDA) for the treatment of hyperkalemia in adults, although its labeling specified that, owing to its delayed onset of action, it "should not be used as an emergency treatment for life-threatening hyperkalemia." In 2018, ZS-9 (Lokelma) became FDA approved for adults with hyperkalemia as well, but like patiromer, it is also not to be used for the emergency treatment of life-threatening hyperkalemia. [24, 25, 26, 27] A study by Jacob et al of adult patients who received intravenous regular insulin during emergency department treatment for hyperkalemia found the incidence of hypoglycemia and severe hypoglycemia to be 19.8% and 5.2%, respectively. The median blood glucose level at baseline was significantly lower in patients who developed hypoglycemia than in those who did not. The investigators suggested that standard insulin doses may not be suitable for hyperkalemic patients with low baseline glucose. [28]

Medication

Medication Summary Direct treatment is aimed at stabilizing the myocardium, shifting potassium from the extracellular environment to the intracellular compartment, and promoting the renal excretion and GI loss of potassium.

Electrolyte supplements Class Summary These agents are used to treat hyperkalemia and to reduce the risk of ventricular fibrillation caused by hyperkalemia. They act quickly and can be lifesaving, thus they are the first-line treatment for severe hyperkalemia when the ECG shows significant abnormalities (eg, widening of QRS interval, loss of P wave, cardiac arrhythmias). Calcium usually is not indicated when the ECG shows only peaked T waves. Calcium chloride (Kalcinate) Calcium increases threshold potential, thus restoring normal gradient between threshold potential and resting membrane potential, which is elevated abnormally in hyperkalemia. One ampule of calcium chloride has approximately 3 times more calcium than calcium gluconate. The onset of action is less than 5 min and lasts about 30-60 minutes. Doses should be titrated with constant monitoring of ECG changes during administration; repeat the dose if ECG changes do not normalize within 3-5 minutes.

Antidotes Class Summary Insulin is administered with glucose to facilitate the uptake of glucose into the cell, which results in an intracellular shift of potassium. Dextrose (D-Glucose)

Glucose and insulin temporarily shift K+ into cells; effects occur within first 30 minutes of administration. Insulin (Humulin, Humalog, Novolin)

Insulin stimulates cellular uptake of K+ within 20-30 minutes; administer glucose along with insulin to prevent hypoglycemia (monitor blood glucose levels closely).

Alkalinizing agents Class Summary These agents increase the pH, which results in a temporary potassium shift from the extracellular to the intracellular environment. These agents enhance the effectiveness of insulin in patients with acidemia. Sodium bicarbonate (Neut)

Bicarbonate ions neutralize hydrogen ions and raise urinary and blood pH. The onset of action is within minutes and lasts approximately 15-30 minutes. It is only likely to be efficacious if underlying acidosis is present. Monitor blood pH to avoid excess alkalosis. Use 8.4% solution in adults and children and 4.2% solution in infants.

Beta2-adrenergic agonists Class Summary These agents promote cellular reuptake of potassium, possibly via the cyclic gAMP receptor cascade. Albuterol (Ventolin, Proventil) Albuterol is an adrenergic agonist that increases the plasma insulin concentration, which may, in turn, help shift K+ into the intracellular space. It lowers K+ levels by 0.5-1.5 mEq/L. Albuterol can be very beneficial in patients with renal failure when fluid overload is a concern. The onset of action is 30 minutes; the duration of action is 2-3 hours.

Diuretics Class Summary These agents cause the loss of potassium through the kidney. Furosemide (Lasix)

Effects are slow and frequently take an hour to begin. Furosemide lowers the potassium level by an inconsistent amount. Large doses may be needed in renal failure. Ethacrynic acid (Edecrin)

Ethacrynic acid increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule.

Binding resins Class Summary These agents promote exchange of potassium for sodium in GI system. Sodium polystyrene sulfonate (Kayexalate)

Sodium polystyrene sulfonate exchanges Na+ for K+ and binds it in the gut, primarily in the large intestine, decreasing total body potassium. The onset of action after oral administration ranges from 2-12 hours (longer when administered rectally). It lowers K+ over 1-2 hours, with a duration of action of 4-6 hours. The potassium level drops by approximately 0.5-1 mEq/L. Multiple doses are usually necessary.

Electrolytes Class Summary These agents have been successfully used in the treatment of acute SLOW released oral potassium overdose. Magnesium sulfate

Magnesium sulfate is a nutritional supplement in hyperalimentation; it is a cofactor in enzyme systems involved in neurochemical transmission and muscular excitability. In adults, 60-180 mEq of potassium, 10-30 mEq of magnesium, and 10-40 mmol of phosphate per day may be necessary for an optimum metabolic response. Give intravenously for acute suppression of torsade. Repeat doses are dependent upon continuing the presence of a patellar reflex and adequate respiratory function.

Consultations

Consult a nephrologist or the dialysis team for patients with either severe symptomatic hyperkalemia or renal failure. Admit these patients to an ICU.

Follow-up

Further Outpatient Care Adjust diet to decrease potassium dietary load. Adjust medications that predispose to or exacerbate hyperkalemia. Repeat potassium level tests in 2-3 days. Reevaluate renal function if signs of renal insufficiency are present.

Further Inpatient Care Order continuous cardiac monitoring for patients who are hyperkalemic. Definitive therapy is dialysis in patients with renal failure or when pharmacologic therapy is not sufficient. Any patient with significantly elevated potassium levels should undergo dialysis, as pharmacologic therapy alone is not likely to adequately bring down the potassium levels in a timely fashion. Monitor serial potassium levels. Resolve acid-base problems. Correct coexistent electrolyte disturbances. Treat digoxin toxicity, if present.

Transfer If unable to correct hyperkalemia with pharmacologic therapy and dialysis is unavailable, stabilize the patient and transfer to a center where dialysis can be performed.

Deterrence/Prevention Avoid foods high in potassium. Avoid medications that predispose to hyperkalemia.

Complications Life-threatening cardiac arrhythmias may ensue. Hypokalemia may result from the treatment of hyperkalemia.

Prognosis Expect full resolution with correction of the underlying etiology. Reduction of plasma potassium should begin within the first hour of initiation of treatment.

Patient Education Pursue diet modification. Discontinue use of medications that may worsen hyperkalemia. Encourage adherence to dialysis schedule if patient is noncompliant.

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