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Hyperkalemia

Last updated: December 3, 2020

Summary

Hyperkalemia (high serum potassium) is a common and potentially life-threatening disorder of potassium balance. The most common cause is decreased kidney function. It can also be caused by acidosis, cell breakdown, endocrinological disturbances (e.g., hypoaldosteronism, hypocortisolism), and drugs such as potassium-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitors, nonsteroidal antiinflammatory drugs (NSAIDs), and digoxin. Serum potassium (K+) is often falsely elevated due to the method of sampling and levels should be confirmed with repeat testing. To determine the underlying cause of hyperkalemia, it is essential to review the patient's medications, check kidney and endocrine function, and screen for cell lysis (e.g., hemolysis, rhabdomyolysis) and acid-base disorders. Acute increases in serum K+ are very dangerous, as they influence the resting membrane potential and thus the electrical excitability of cells. These changes can lead to life-threatening cardiac arrhythmias. It is, therefore, essential to obtain an ECG to determine the level of cardiotoxicity. Management depends on the severity of the hyperkalemia and includes restriction of dietary K+, as well as medications to bind, shift, or eliminate K+, or to stabilize the cardiac membrane (e.g., calcium gluconate) if necessary. In refractory cases, dialysis may be required. Serum K+ should be monitored closely until it is corrected.

See also “Hypokalemia.”

Definition

  • Hyperkalemia: Serum potassium level > 5 mEq/L
  • Acute hyperkalemia: Abnormal ↑ K+ not known to be chronic
  • Chronic hyperkalemia: Recurrent episodic ↑ K+ that require ongoing treatment

References: [1][2]

Etiology

  1. Potassium excess
  2. Extracellular shift
  3. Pseudohyperkalemia: due to the release of potassium from red blood cell lysis
    • Blood drawn from the side of IV infusion or a central line without previous flushing
    • Prolonged use of a tourniquet
    • Fist clenching during blood withdrawal
    • Delayed sample analysis

Errors in blood-drawing technique may lead to red blood cell lysis and a falsely elevated serum potassium concentration (pseudohyperkalemia)!

When K+ shifts out of the cell, it's a BAD LOSS! – Beta-blockers, Acidosis, Digoxin, Lysis, hyperOsmolality, high Sugar, Succinylcholine

References:[1][3][4][5][6]

Pathophysiology

  • Potassium is an important factor in maintaining the resting membrane potential
  • ↑ Extracellular K+concentration → ↓ resting membrane potential (less negative than -90 mV) → ↑ excitability

Particularly acute extracellular changes in concentration influence excitability! Chronic changes lead to intracellular compensation!

Clinical features

Symptoms usually occur if serum potassium levels are > 7.0 mEq/L or they change rapidly.

Hyperkalemia (and hypokalemia) can cause cardiac arrhythmia and lead to ventricular fibrillation!

References:[1][7][8][9]

Diagnostics

All patients require an ECG and routine laboratory studies to confirm the diagnosis and assess the need for urgent treatment. Further diagnostic testing depends on the suspected underlying etiology. Inquire about last renal replacement therapy for patients with ESRD (e.g., screen for missed hemodialysis appointments, adherence to peritoneal dialysis)

Laboratory studies [10][11]

Routine studies

An inverse relationship between serum K+ and pH (e.g., ↓ pH → ↑ K+) has previously been observed in specific types of metabolic acidosis. However, the underlying mechanisms are complex and this association is inconsistent in clinical practice. [10][14]

Investigation of underlying causes [15][16][17]

Depending on symptoms and risk factors, further testing may be appropriate, particularly if renal function is normal.

ECG findings in hyperkalemia [19][20][21]

The correlation between serum K+ levels and the severity of ECG changes is loose. Findings are more likely to occur with rapid-onset hyperkalemia.

  • Mild hyperkalemia: 5.5–6.4 mEq/L
  • Moderate hyperkalemia: 6.5–8.0 mEq/L
    • Lengthening of QRS interval (QRS complex widening)
    • Widening and flattening of P wave, which eventually disappears
  • Severe hyperkalemia: > 8.0 mEq/L

Urgent K+-lowering treatment may be necessary even in the absence of ECG changes.

Treatment

Approach [2][10][15][22]

  • Risk stratification [23]
    • The risk of hyperkalemic emergency (acute severe elevation requiring urgent lowering) is elevated if any of the following are present:
    • Less urgent hyperkalemia (typically chronic elevations that can be lowered more slowly) is more likely in the following cases:
      • Asymptomatic patient
      • Serum K+ = 5.5–6.0 mEq/L
      • No high-risk comorbidities
Therapeutic approach to hyperkalemia [2][10][15][22]
Treatment strategy Acute hyperkalemia [25] Chronic hyperkalemia
Cardiac membrane stabilization
  • Not routinely required
Intracellular K+ shifting
Enhanced K+ elimination
Reduced K+ intake
  • Low-potassium diet [11][26]
  • Consider dietitian consult.
Treatment of underlying cause
  • Medication review: Adjust medications that affect K+ metabolism.
    • Decrease dose (or consider discontinuation) of drugs required to treat underlying conditions, e.g., RAAS inhibitors.
    • Recommend avoiding nonessential drugs associated with hyperkalemia (e.g., NSAIDs, OTC supplements).
  • Identify and treat other reversible conditions: e.g., primary adrenal insufficiency, AKI, tumor lysis syndrome.
Monitoring and disposition
  • Continuous cardiac monitoring if cardiotoxicity is present
  • Repeat serum K+ every 2 hours
  • In refractory or severe hyperkalemia: Consider critical care consult.
  • Serum K+ prior to and after initiating drugs that affect K+ metabolism
  • The frequency of serum K+ monitoring should be tailored to the patient's comorbidities and prescribed medications.
  • Typically can be managed as outpatients

Cardiac arrhythmias due to hyperkalemia can cause sudden death.

To remember K+-lowering treatments, think C BIG K Die (if you see a big serum K+, your patient may die!): Calcium salts, Beta-agonists/Bicarbonate, Insulin + Glucose, Kation exchange medication, Dialysis/Diuretics.

Cardiac membrane stabilization [22]

Calcium salts reduce cardiac irritability.

Calcium salts have no influence on serum K+ levels and therefore should be paired with another K+-lowering agent.

Intracellular potassium shifting [10][23][25]

These drugs should be given in tandem with calcium salts (if calcium is indicated).

  • Insulin and glucose: preferred acute noninvasive K+-lowering treatment; short-acting insulin combined with 50% dextrose
    • Patients with glucose levels > 250 mg/dL should not receive D50W.
    • Monitor all patients for hypoglycemia hourly for at least 2 hours after administration.
  • Inhaled SABAs: e.g., nebulized albuterol (off-label) ; to consider as an adjunct to insulin (not effective as a monotherapy) [22][27]

Enhanced potassium elimination [2][22]

Hemodialysis is the most effective definitive therapy for refractory hyperkalemia. However, it is not a first-line option because of its invasive nature and adverse effects. It is the treatment of choice for patients already receiving regular renal replacement therapy.

Cation-exchange medications [23][28]

  • Mechanism of action: These drugs release Na+ or Ca2+ ions in the gut, which are exchanged for K+, thereby enhancing enteral K+ elimination.
  • Clinical applications: nonurgent lowering of K+ [10]
  • Options
  • Considerations
    • Avoid simultaneous administration with other oral medications, as resins may bind them, reducing absorption.
    • Give with a laxative (avoid sorbitol). [30]

Sodium polystyrene sulfonate carries a risk of intestinal necrosis (especially if combined with the laxative sorbitol) and should be avoided in patients with abnormal bowel function. [30]

Additional medications [10][25]

The following medications are typically reserved to treat refractory hyperkalemia and only in specific circumstances.

References

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