creation date: 2025-09-25 16:30
tags: Pathologies
Hyperkalemia
Background
Definitions
Hypokalemia refers to a serum potassium level above normal limits.
Pseudohyperkalemia refers to a false elevation in measured potassium due to collection methods and is the most common cause of an elevated potassium level.
Etiology
Pseudohyperkalemia may be due to:
- Hemolysis of sample (causing intracellular potassium to be added to serum levels)
- Leukocytosis or thrombocytosis may also result in elevation of potassium falsely
True hyperkalemia etiology can be categorize as:
Increased potassium intake
- Uncommon but can occur with patients with renal disease or medication predisposing hyperkalemia
- Foods include dried fruits, avocados, many vegetables, red meats, fruits such as bananas, mangoes, and kiwis.
Intracellular potassium shifts
- Cellular injury can shift potassium from intracellular to extracellular space
- Rhabdomyolysis (eg. from trauma, exercise, hemolysis)
- Metabolic acidosis (often by decreased, effective circulating arterial blood volume)
- Insulin deficiency and diabetic ketoacidosis
- Medications (eg. succinylcholine)
Impaired potassium excretion
- Acute or chronic kidney disease (typically not seen until GFR <30 mL/min)
- Tubular dysfunction due to aldosterone deficiency (hypocortisolism and hypoaldsteronism) or insensitivity
Pathogenesis
The exact pathophysiology of hyperkalemia depends on the etiology. Potassium is primarily an intracellular ion and thus serum potassium makes up a small percent of total body potassium.
Potassium is integral to many physiological processes within the body and disruption to its levels result in the myriad of symptoms which present.
Briefly, potassium is involved in maintaining cell membrane potentials, nerve impulse conduction, muscle functions, and acid-base balance.
Elevated levels of potassium alter membrane potentials (raises resting potential close to threshold) which results in initial hyperexcitability of muscles but is followed by inactivation of voltage-gated sodium channels resulting in impairing conduction of cardiac electrical signals and neuromuscular signals.
Clinical Presentation
Signs & Symptoms
Hyperkalemia is often asymptomatic at mild levels. Symptoms typically occur when serum potassium is ≥7.0 mmol/L or if the rise in serum potassium was rapid.
Muscle weakness or paralysis
- Ascending muscle weakness beginning at the legs
- Can progress to flaccid paralysis with sphincter tone and cranial nerve function intact
- Respiratory muscle weakness is rare
Cardiac manifestations
ECG abnormalities manifest as:
- Initial: tall peaked T waves and shortened QT interval
- Progression:
- Elongating PR and QRS duration
- P wave disappears
- QRS widens to sine pattern
- Flatline
Conduction and arrhythmic abnormalities include:
- RBBB, LBBB, bifascicular block, advanced AV block
- Sinus bradycardia, sinus arrest, slow idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, asystole
Urinary
- Reduces renal ammonium excretion which can lead to metabolic acidosis
History & Physical Exam
As hyperkalemia is most typically found incidentally on laboratory testing, history may elicit an inciting cause and/or predisposing factors.
History should also include urine output. Anuria would guide treatment, possibly indicating dialysis.
Findings may include complaints of symptoms. Additionally, concurrent findings relating to renal disease may be likely due to their cooccurence.
Diagnosis
Criteria
The upper limit of normal serum potassium levels of 5.0 mmol/L.
The urgency of hyperkalemia is based on:
- Presence/absence of symptoms and signs
- Severity of potassium elevation
- Etiology
An emergency is generally if:
- Signs and symptoms such as muscle weakness and cardiac abnormalities are present
- Concurrent tissue breakdown/GI bleed
- Concurrent severe kidney function impairment
Work-up
The most important aspect of the workup is to exclude pseudohyperkalemia, especially in cases where no cause of hyperkalemia is evident. A sample collection without tourniquet, repeated fist clenching, or trauma will demonstrate true serum potassium. In most cases, labs will rule out hemolysis internally.
Laboratory testing beyond serum potassium include:
- Serum blood urea nitrogen, creatinine, eGFR for renal function
- Urinalysis for renal disease
- Serum calcium (hypocalcemia can exacerbate hyperkalemia manifestations as it worsens the hyperdepolarization effect)
- Serum glucose and blood gases if diabetic
- Creatine kinase and urine myoglobin if suspected rhabdomyolysis
An ECG is used for hyperkalemia findings, especially if serum potassium is elevated.
Differential
The primary differential is pseudohyperkalemia. Other differential diagnoses reflect the underlying causes of hyperkalemia.
Red Flags / Complications
Severe hyperkalemia can result in:
- Cardiac arrest
- Paralysis
Management
Hyperkalemic emergency
In emergencies, rapid treatment consist of stabilizing, shifting potassium, then elimination.
If ECG changes are seen or potassium levels are >6.5 or 7 mmol/L, stabilize:
- Intravenous calcium (antagonize membrane action of hyperkalemia by raising threshold potential following RMP increase caused by extracellular potassium)
- Calcium gluconate or calcium chloride
Following stabilization, serum potassium can be transiently lowered by shifting potassium:
- Sodium bicarbonate (rapid)
- Intravenous insulin (drives potassium intracellularly) after glucose (prevent hypoglycemia) - slower due to rate of glucose administration
- Beta-agonists
Removal of excess potassium should be initiated which can include:
- Loop or thiazide diuretics
- Gastrointestinal cation exchanger (requires confirm bowel activity; else risk necrosis)
- Dialysis
Assessment of kidney during elimination can be done using Foley catheter to track volume status.
Continuous cardiac monitoring and serial ECGs should be checked. Serum potassium should be monitored 1-2 hours post-treatment and as needed beyond that. Patients who receive insulin with or without dextrose should undergo hourly glucose measurements for hypoglycemia.
Non-emergency hyperkalemia
In cases of non-emergency hyperkalemia, a rapid response it not required. In patients with severe kidney impairment, dialysis with or without a gastrointestinal cation exchanger is typically recommended.
Patients with normal kidney function or mild kidney impairment will generally improve with treatment of underlying cause. Additionally, saline infusions and loop diuretics can be used.