Hyperkalemia is defined as a high serum concentration of potassium (>5 mEq/L). It may be classified as mild (5.1-6 mEq/L), moderate (6.1-7 mEq/L) or severe (>7 mEq/L).
It is a dangerous condition because it can cause severe neuromuscular and cardiovascular complications.
It may occur due to impaired renal excretion or by extracellular shift / cell release.
Impaired Renal Excretion
Acute or chronic kidney disease
Acquired hyporeninemic hypoaldosteronism
Congenital adrenal hyperplasia (recesssive or autosomal dominant)
Primary hypoaldosteronism or hyporeninemia
Systemic lupus erythematosus
Type IV renal tubular acidosis
Extracellular shift / Cell release
Damage to tissue from rhabdomyolysis, burns, or trauma
Familial hyperkalemic periodic paralysis
Hyperosmolar states, (e.g., uncontrolled diabetes, glucose infusions)
Insulin deficiency or resistance
Tumor lysis syndrome
Drugs (beta-blockers, digitalis overdose, succinylcholine, cyclosporine, tacrolimus, diazoxide, minoxidil, isoflurane)
SIGNS AND SYMPTOMS:
Muscle weakness (ascending muscle weakness)
Dyspnea and palpitations may be present
ECG changes: The ECG changes will depend on how high the potassium levels are and how quick they increased. Changes observed include tall peaked T waves, shortened QT interval, widening of PR interval and QRS, P wave flattening or disappearance, conduction abnormalities (RBBB, LBBB, AVB) and arrhythmias (bradycardia or ventricular tachycardia or fibrillation)
Nausea and vomiting
Metabolic acidosis (K+ interferes with renal ammonium (acid) excretion)
In addition to history, physical examination and potassium levels other tests are important. An ECG should be obtained. Urinary potassium, sodium, osmolality, CBC and metabolic profile may be obtained. Pseudohyperkalemia should be ruled out (repeat the potassium measurement).
The most common causes of acute hyperkalemia are related to cellular release, whereas chronic hyperkalemia is usually due to reduced kidney excretion or impaired response to aldosterone.
Treatment of Acute Hyperkalemia (symptomatic and/or ECG changes):
Stabilize the membrane
Calcium gluconate 1000 mg (10 mL of 10% solution) IV over two to three minutes should be given to reduce cardiac cell membrane excitability.
Shift the potassium to the cells
Insulin and glucose should be used to reduce the potassium levels. Preparation is as follows: 10 units of regular insulin, followed immediately by 50 mL of 50% dextrose (25 g of glucose). We subsequently infuse 10% dextrose at 50 to 75 mL/hour and closely monitor blood glucose levels every hour for five to six hours.
Diuretics (40 mg of furosemide every 12 hours) for patients without oliguria or severe kidney impairment.
If the patient cannot receive diuretics or does not respond to the previously mentioned treatments, hemodialysis should be considered.
If dialysis is not available, gastrointestinal cation exchange substances can be used (eg, patiromer – VELTASSA, 8.4g-25.2g orally once daily OR sodium polystyrene sulfonate – KAYEXALATE 15g PO 1-4 times a day or rectal 30-50g q6h).
Other therapies that may be used include beta-adrenergic agonists (e.g. albuterol 10 to 20mg in 4mL saline by nebulization over 10 minutes). Sodium bicarbonate – 1.4% 500 mL IV over 2 hours may be considered only in very selected patients (e.g. severe acidosis).
Treating the cause of hyperkalemia is, obviously, important.
Treatment of Chronic Hyperkalemia:
Chronic hyperkalemia (e.g. CKD patients) should be managed with avoidance of medications that may increase the potassium, low potassium diet, diuretics (loop or thiazides), cation exchange resins (patiromer – VELTASSA 8.4g to 25.2g oral, packets) and dialysis when needed.
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