Hyperkalemia

Etiology
Pseudohyperkalemia
Intake
Shift
Renal excretion
Pseudohyperkalemia (Release of K+ just prior to sampling)

Hemolysis from making fist or prolonged tournique use

Leukocytosis
Thrombocytosis
Mononucleosis (RBCs are leaky)

Increased Intake
Rarely the sole cause.
Shift Out of Cells
via Na/K pump
Acidosis
Insulin deficiency
B-blockade may exacerbate
Digoxin Toxicity
From cell destruction:
Rhabdomyolysis
Tumor lysis
Massive transfusion of stored RBCs
Hyperkalemic Periodic Paralysis. Autosomal dominant Na-channel Defect. Episodic limb
weakness with normal or elevated K+.
Decresed Renal Elimination
Potassium excretion is regulated largely in the distal tubule. There is an negative
electrochemical gradient in the tubule lumen. This draws K+ & H+ into the lumen for
excretion. The gradient is increased by the activity of aldosterone, which increases Na+
resorption there.
1) Aldosterone deficiency
i) Addison's
ii) Congenital Adrenal Hyperplasia
iii) Heparin inhibits aldosterone production which can result in hyperkalemia in renally
compromised patients
iv) NSAIDS decrease renin production & GFR
v) ACE-Inhibitors block the production of angiotension II which usually stimulates
aldosterone production. It also can decrease GFR
2) Aldosterone receptor antagonists (spironolactone)
3) Renal aldosterone resistance

i) Type IV RTA
ii) Familial Pseudohypoaldosteronism
4) Decreased Na+ delivery to the distal tubule, so the electrochemical gradient cannot be
sufficiently generated
i) Renal failure
ii) ACE-I
iii) NSAIDs
5) Increased Distal Resorption of Cli) Gordon's syndrome
ii) Cyclosporine
History & Physical
Usually asymptomatic
Weakness-->ascending paralysis
Parethesias
Areflexia
Ventricular fibrillation and/or asystole
Labs
1) Lytes including bicarb (repeat if hemolysed)
2) urine lytes
3) urine & plasma osmolality
4) BUN, Cr, albumin (to calculate GFR)
5) ECG: Peaked T-waves ---> flattening of p-wave & widening QRS ---> Sine-wave
Diagnostic Approach

1) Rule out pseudohyperkalemia & redistribution from clinical history & repeat lytes if
hemolysed.
2) Use lytes & osmolality to calculate transtubular potassium gradient (TTKG).

TTKG= ([K+]u pOSM)

([K+]p uOSM)
3) If TTKG <10, this suggests lack of drive to excrete K+ in tubule.
4) Give fluorinef (mineralocorticoid) & remeasure to check if this is due to lack of
aldosterone or inhibited response.
5) If responds to fluorinef, determine renin & aldosterone levels to see if primary or
secondary hypoadrenalism
Treatment
1) If ECG changes, put on monitor. If more than just peaked T's, & give 10cc of 10%
Calcium gluconate IV q30-60 minutes. Stabilizes cardiac membranes. If no change in
ECG is seen after 10 minutes, give a repeat dose.
2) Give 50cc of D50, followed by 10U of Insulin R IV push (15-30 min onset, 2-3h
duration).
3) If DKA, this should be enough (unless pH <7.0, then give bicarb as below)
4) Except in chronic renal failure (due to salt load & ineffectiveness), give 3 50meq amps
of Na Bicarbonate in 1L of D5W IV
5) If no IV access, give ventolin 1cc in 2cc N/S by nebulizer or 4 puffs via aerochamber
(onset 30 minutes, lasts 2-4h)
Theses measures will give you a transient shift in K+.
6) Give K-binder resin, like Kayexalate 30g po or pr q4-6h
7) If kidney's working & volume status is good, can use some furosemide or thiazide
diuretic to promote K+ elimination.
8) Repeat lytes in 1 hour, then q2h
9) Refractory or very severe hyperkalemia is an indication for emergent dialysis.
References
Schwab, T., 1998. Mayo Internal Medicine Board Review 1998-99. Nephrology Chapter.
Udaya, B.S. (Ed.). Lippincott-Raven: Philadelphia.
Singer, G & B. Brenner, 1998. Fluid and electrolyte disturbances in Harrison's Principles
of Internal Medicine, 14th ed. Fauci et al. (Ed.). McGraw-Hill Pub., USA.
Mendell, J.R., R.C. Griggs, & L.J Ptacek. Diseases of Muscle in Harrison's Principles of
Internal Medicine, 14th ed. Fauci et al. (Ed.). McGraw-Hill Pub., USA.

Singer, G.G., 1998. Fluid and electrolyte management. in Washington Manual of Medical
Therapeutics, 29th ed. Carey et al., Ed. Lippincott-Raven: Pennsylvania.