Hyperkalemia
Hyperkalemia (plasma K+>5 mEq/L) causes increased extracellular potassium that leads to depolarization of the cell membrane and resulting cardiac arrhythmias, ventricular fibrillation, or asystole. Net K+,absorption or excretion is determined by the actions of aldosterone and the effective plasma K+
level on the collecting duct. Normally, potassium is excreted almost exclusively (90%) by the kidney, with some excretion by the colon.
Differential Diagnosis
Decreased renal excretion of potassium
- Acute or chronic renal insufficiency: Due to a decrease in distal solute (NaCl) delivery and a decrease in overall renal mass
- Impaired Na+reabsorption (common): Aldosterone deficit results in decreased K+ excretion
–Resistance to aldosterone: Drugs (e.g., potassium-sparing diuretics, trimethoprim, pentamidine), tubulointerstitial disease
–Secondary hypoaldosteronism: Drugs (e.g., ACE inhibitors, NSAIDs, heparin), hyporeninemia, AIDS
–Renal tubular acidosis, type 4
–Primary hypoaldosteronemia
–Gordon's syndrome
–Postuterojejunostomy
Increased potassium release from cells
- Pseudohyperkalemia
–Prolonged use of a tourniquet with or without repeated fist clenching
–Hemolysis after blood is drawn
–Marked leukocytosis and thrombocytosis:
Cells release K+
into the serum in the process of clotting; measure plasma K+ rather than serum K+
in these cases
-
Tissue breakdown: Intravascular hemolysis, tumor lysis syndrome, excessive exercise, trauma, and rhabdomyolysis
-
- Metabolic acidosis: K+is shifted out of cells to buffer the increased H+
-
Hyperosmolar states (e.g., hyperglycemia): K+ diffuses out of cells along with water
-
Insulin deficiency
-
Medications
–α-adrenergic agonists
–β2 antagonists
–Excessive supplementation in a patient with impaired renal function
–Severe digitalis toxicity (paralyzes Na+/K+ ATPase)
–Succinylcholine
-
Hyperkalemic periodic paralysis
-
Depolarizing muscle paralysis
Excess intake of potassium
-
Oral or IV potassium replacement
-
Dietary excess
Workup and Diagnosis
- History and physical examination
–May be completely asymptomatic
–May present with numbness, weakness (possibly leading to paralysis), decreased reflexes, or irritability
–Hypoventilation is a late finding
–Cardiac toxicity most likely will only be detected with
ECG, unless the patient is hemodynamically unstable
-
Rule out pseudohyperkalemia (e.g., hemolysis) by repeat measurement
-
Initial laboratory tests may include electrolytes, calcium, magnesium, phosphate, and BUN/creatinine, cortisol, renin, and aldosterone levels
-
ECG shows classic progressive changes, including peaked T-waves, prolonged PR and QT intervals, flattening of the P waves, and ST depression; QRS widening to a sine-wave pattern; Vfib may follow
- Assess K+secretion and calculate TTKG as follows: Urine
K+
concentration divided by ratio of urine to plasma
osmolality (Uosm/Posm); the ratio is finally divided by
plasma K+
–TTKG >10 suggests hypovolemia or low protein intake
–If TTKG <5, assess response to mineralocorticoids: An increase in TTKG to >10 suggests primary or secondary hypoaldosteronism; if TTKG is <10, assess the clinical picture; hypertension with low renin and aldosterone suggests chloride shunt (e.g., cyclosporine, RTA, Gordon's syndrome), whereas hypotension with high renin and aldosterone suggests aldosterone-resistant states (e.g.,
K+sparing diuretics)
Treatment
- Emergency intervention is necessary if K+exceeds 7.5 mEq/L, rise is sudden (e.g., less concern if patient has CRI, because these patients often live with K+levels of 5 to 5.5), or ECG changes are present
–IV calcium to decrease cell membrane excitability
–Sodium bicarbonate, insulin (add glucose to prevent hypoglycemia), and/or β2 agonists (e.g., albuterol) are used to shift K+back into cells
- Removal of K+may be accomplished by ion exchange resins (e.g., sodium polystyrene sulfonate, retention enema), diuretics (loop and/or thiazide diuretics may be used if renal function is adequate), or dialysis (reserved for life-threatening hyperkalemia or renal failure)
- Treat underlying causes
–Discontinue causative medications (e.g., NSAIDs, ACE inhibitors, K+
supplements)
–IV fluid administration if hypovolemic
–Correct metabolic acidosis
–Correct renal obstruction
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Book Source Details
- Book Title: In a Page: Signs and Symptoms
- Author(s): Scott Kahan, Ellen G. Smith
- Year of Publication: 2004
- Copyright Details: In a Page: Signs and Symptoms, Copyright © 2004 Lippincott Williams & Wilkins.
Other Book Chapters Related to Hyperkalemia
Read excerpts from these other book chapters related to Hyperkalemia:
Medical Books Excerpts
- Hyperkalemia
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
Copyright Details: In a Page: Signs and Symptoms, Copyright © 2008 Williams & Wilkins.
More About Causes of Hyperkalemia
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More About This Book:
Title: In a Page: Signs and Symptoms
Authors: Scott Kahan, Ellen G. Smith
Publisher: Lippincott Williams & Wilkins
Copyright: 2004
ISBN: 1-4051-0368-X
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» Next page: Hyperkalemia (In A Page: Pediatric Signs and Symptoms)
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