Hyperkalemia in Emergency Medicine Clinical Presentation
- Author: David Garth, MD; Chief Editor: Erik D Schraga, MD more...
History
Hyperkalemia can be difficult to diagnose clinically because complaints may be vague. 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:
- Generalized fatigue
- Weakness
- Paresthesias
- Paralysis
- Palpitations
Hyperkalemia is suggested in any patient with a predisposition toward elevated potassium level. Potential potassium level elevation is observed in the following:
- Acute or chronic renal failure, especially in patients who are on dialysis
- Trauma, including crush injuries (rhabdomyolysis), or burns
- 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.
- Medications - Potassium supplements, potassium-sparing diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), beta-blockers, digoxin, succinylcholine, and digitalis glycoside
- Medication combinations (ie, spironolactone, ACE inhibitors)[5]
- 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
- Hemolysis (in laboratory tube) most common
- Thrombocytosis
- Leukocytosis
- Venipuncture technique (ie, ischemic blood draw from prolonged tourniquet application)
Redistribution
- Acidosis
- Insulin deficiency
- Beta-blocker drugs
- Acute digoxin intoxication or overdose
- Succinylcholine[6]
- Arginine hydrochloride
- Hyperkalemic familial periodic paralysis
Excessive endogenous potassium load
- Hemolysis
- Rhabdomyolysis
- Internal hemorrhage
Excessive exogenous potassium load
- Parenteral administration
- Excess in diet
- Potassium supplements
- Salt substitutes
Diminished potassium excretion
- Decreased glomerular filtration rate (eg, acute or end-stage chronic renal failure)
- Decreased mineral corticoid activity
- Defect in tubular secretion (eg, renal tubular acidosis II and IV)
- Drugs (eg, NSAIDs, cyclosporine, potassium-sparing diuretics)
Laboratory error [7]
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