Hyperkalemia in Adults: Review of a Common Electrolyte Imbalance

Pseudohyperkalemia

Pseudohyperkalemia is a transiently elevated serum potassium level that erroneously represents the true serum potassium level. It results from hemolysis due to mechanical trauma during the blood draw (eg, a tourniquet tied too tightly or use of a small-bore needle) or during specimen handling afterwards.²⁵ Furthermore, leukocytosis, thrombocytosis, and polycythemia make red blood cells more fragile, increasing the chance of hemolysis and potassium leakage.²⁶ Blood transfusion also can lead to pseudohyperkalemia. When blood is stored, potassium leakage from the cells and cell lysis, along with diminished Na-K-ATPase activity, lead to a buildup of potassium in the medium surrounding the stored red blood cells.^27,28 The rise in serum potassium levels post-transfusion is usually transient, as the blood cells redistribute the potassium load once they become metabolically active.^27,29

CLINICAL MANIFESTATIONS

Clinical manifestations of mild to moderate hyperkalemia (serum potassium > 5.5 mEq/L but < 6.5 mEq/L) include fatigue, generalized weakness, nausea, vomiting, constipation, and diarrhea.¹⁵ In many patients, mild to moderate hyperkalemia may not be associated with any acute symptoms and vital signs may be normal.¹³ Severe hyperkalemia (serum potassium > 6.5 mEq/L) may present clinically with acute extremity paresthesias, muscle weakness and paralysis, heart palpitations, dyspnea, altered mental status, cardiac arrhythmias, and cardiac arrest.^30,31 Irregular heart rhythm, decreased deep tendon reflexes, or decreased strength may be revealed on physical exam.³ Individuals with ESRD on hemodialysis seem to tolerate higher levels of potassium than the general population without displaying clinical symptoms. However, these individuals are still susceptible to the cardiac effects of hyperkalemia.³²

INITIAL ASSESSMENT

In assessing hyperkalemia, the clinician must perform a focused history and physical exam and review the patient’s medication list, including supplements and dietary habits that impact potassium intake. Potassium-rich foods include meat, fish, milk, almonds, spinach, cantaloupe, bananas, oranges, mushrooms, and potatoes.³³ Hyperkalemia may present in association with various medical emergencies. The clinician should have an index of suspicion, depending on the patient’s overall medical profile and presentation, for emergencies such as cardiac ischemia, sepsis, adrenal crisis, DKA, TLS, and digoxin overdose.

The clinician must identify whether an elevated potassium level requires emergent therapy; assessment of vital signs is paramount in determining this. Orthostatic hypotension and tachycardia may hint that the patient is volume depleted. The patient should be examined for signs of hemodynamic shock with the CAB sequence: circulation, airway, breathing.³⁴ Symptoms such as chest pain, shortness of breath, muscle weakness, paralysis, and altered mental status suggest that an expedited evaluation is warranted.

With a serum potassium level > 5.5 mEq/L, urgent electrocardiography should be performed.²⁶ ECG findings observed with serum potassium levels of 5.5-6.5 mEq/L usually include peaked T-waves and prolonged PR intervals (see Figure 2). With potassium levels > 6.5 mEq/L consistent with further cardiac destabilization, the P-wave flattens then disappears, the QRS complex broadens, and sinus bradycardia or ectopic beats may occur.^12,26 ST depression, T-wave inversion, or ST elevation also may be seen.¹² With serum potassium levels > 7.5 mEq/L, progressive widening of the QRS complex to a sine-wave with bundle branch blocks or fascicular blocks may occur (see Figure 3).²⁶ Without prompt intervention, ventricular fibrillation may ensue.²⁶

An extensive laboratory workup may be necessary to investigate the etiology; this includes a complete blood count, metabolic panel, liver function tests, cardiac enzymes, blood gas analysis, serum/urine osmolality, urinalysis, urine electrolytes, and toxicology screen.^13,26 Arterial blood gas (ABG) analysis may show metabolic acidosis with AKI or DKA, or an elevated lactate may occur with sepsis. In patients with hyperglycemia, besides checking for acidosis, obtaining blood/urine ketone levels and a metabolic panel with anion gap to evaluate for DKA is useful.³⁵

When assessing a patient with an elevated creatinine, the GFR at the time of evaluation should be compared with the patient’s baseline GFR to determine chronicity and duration of his/her kidney disease.³⁶ Obtaining a urinalysis and urine electrolytes in addition to the basic metabolic panel can help narrow the etiology.³⁶ A Foley catheter should be placed in cases of urinary retention because without intervention, urinary obstruction may lead to AKI and hyperkalemia. Myoglobinuria on urinalysis and an elevated creatine kinase are diagnostic markers of rhabdomyolysis.¹⁸

TLS should be considered in patients who recently received chemotherapy, especially those with proliferative hematologic malignancies, such as acute lymphoblastic leukemia, acute myeloid leukemia, and Burkitt lymphoma.²⁴ In TLS, bloodwork often reveals hyperkalemia along with AKI, an elevated uric acid level, hyperphosphatemia, and hypocalcemia.²⁴

Patients presenting with hyperkalemia, hypotension, hypoglycemia, and hyponatremia may have adrenal insufficiency.²⁰ If insufficiency is suspected, a cortisol level may be checked during morning hours; a low level is often suggestive of this diagnosis.³⁷ Treatment includes daily doses of steroids, and consultation with an endocrinologist is recommended.³⁷

If an elevated potassium level is not accompanied by renal dysfunction, electrolyte imbalances, ECG changes, or inciting medications, pseudohyperkalemia should be considered.³⁸ A repeat lab sample should be checked. Consider obtaining an ABG analysis, as the shorter time interval between drawing the blood sample and the sample analysis reportedly increases the reliability of the resulting potassium level.³⁸