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:
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Generalized fatigue
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Weakness
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Paresthesias
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Paralysis
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Palpitations
Hyperkalemia is suggested in any patient with a predisposition toward elevated potassium level. Potential potassium level elevation is observed in the following:
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Acute or chronic renal failure, especially in patients who are on dialysis
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Trauma, including crush injuries (rhabdomyolysis), or burns
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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.
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Medications - Potassium supplements, potassium-sparing diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), beta-blockers, digoxin, succinylcholine, and digitalis glycoside
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Medication combinations (ie, spironolactone, ACE inhibitors) [15]
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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:
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Hemolysis (in laboratory tube) most common
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Severe thrombocytosis
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Severe leukocytosis
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Venipuncture technique (ie, ischemic blood draw from prolonged tourniquet application)
Redistribution may result from the following:
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Acidosis
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Beta-blocker drugs
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Acute digoxin intoxication or overdose
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Succinylcholine [16]
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Arginine hydrochloride
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Hyperkalemic familial periodic paralysis
Excessive endogenous potassium load may result from the following:
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Hemolysis
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Rhabdomyolysis
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Internal hemorrhage
Excessive exogenous potassium load may result from the following:
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Parenteral administration
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Excess in diet
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Potassium supplements
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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:
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Decreased glomerular filtration rate (eg, acute or end-stage chronic renal failure)
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Decreased mineral corticoid activity
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Defect in tubular secretion (eg, renal tubular acidosis II and IV)
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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]
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Widened QRS complexes in hyperkalemia.
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Widened QRS complexes in a patient whose serum potassium level was 7.8 mEq/L.
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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.
