NP12 Nephrology

Electrolyte Disorders

Essential Med Notes 2015

Approach to Hypokalemia
1. emergency measures: obtain ECG; if potentially life threatening, begin treatment immediately
2. rule out transcellular shifts of K+ as cause of hypokalemia
3. assess contribution of dietary K+ intake
4. spot urine K:Cr (should be less than 1 in setting of hypokalemia)
if <1 consider GI loss
if >1 consider a renal loss
5. consider 24 h K+ excretion
6. if renal K+ loss, check BP and acid-base status
7. may also assess plasma renin and aldosterone levels, serum [Mg2+]
Hypokalemia

Decreased Intake
Limited dietary intake
Clay ingestion

Increased Loss

Spot urine K:Cr

Spot urine K:Cr <1

Spot urine K:Cr >1

GI Losses
Diarrhea
Laxatives
Villous adenoma

Renal losses

Hypo- or normotensive
Check acid base status

Acidemic
DKA
RTA

Variable
HypoMg
Vomiting/NG

Redistribution into Cells

Metabolic alkalosis (K+/H+ exchange across cell membrane)
Insulin (stimulates Na+/K+ ATPase)
Catecholamines, 2-agonists (Ventolin), theophylline
(stimulates Na+/K+ ATPase)
Tocolytic agents
Uptake into newly forming cells
Vitamin B12 injections in pernicious anemia
Colony stimulating factors h WBC production

Check BP

Hypertensive
1 hyperaldosteronism (e.g. Conns syndrome)
2 hyperaldosteronism (renovascular disease, renin tumor)
Non-aldosterone mineralocorticoid (Cushings, exogenous)

Alkalemic
Diuretics (furosemide, HCTZ) manifest as renal losses due to
hyperaldosteronism and metabolic alkalosis
Inherited renal tubular lesions
Bartters (loop of Henle dysfunction: furosemide-like effect)
Gitelmans (DCT dysfunction: thiazide-like)

Figure 7. Approach to hypokalemia

Treatment
treat underlying cause
if true K+ deficit, potassium repletion (decrease in serum [K+] of 1 mEq is roughly
100-200 mEq of total body loss)
oral sources food, tablets (K-Tab), KCl liquid solutions; preferable route if the patient
tolerates PO medications
IV usually KCl in saline solutions, avoid dextrose solutions (may exacerbate hypokalemia
via insulin release)
max 40 mEq/L via peripheral vein, 60 mEq/L via central vein, max infusion 20 mEq/h
K+-sparing diuretics (triamterene, spironolactone, amiloride) can prevent renal K+ loss
restore Mg2+ if necessary
if urine output and renal function are impaired, correct with extreme caution
risk of hyperkalemia with potassium replacement especially high in elderly, diabetics, and
patients with decreased renal function
beware of excessive potassium repletion, especially if transcellular shift caused hypokalemia

Hyperkalemia
serum [K+] >5.0 mEq/L
Signs and Symptoms
usually asymptomatic but may develop nausea, palpitations, muscle weakness, muscle stiffness,
paresthesias, areflexia, ascending paralysis, and hypoventilation
impaired renal ammoniagenesis and metabolic acidosis

Hypokalemia often accompanied by

metabolic alkalosis
Potassium leaves cells, replaced by H+
Kidney tubular cells see high H+, think
acidosis and increase ammonium
synthesis and excretion
Increase in bicarbonate generation