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Hypokalemia

EKG: low or inverted T, decreased ST segment; increased PR interval & U waves, prominent R, atrial or vent. arrhythmia.

SX:

In most circumstances, mild hypokalemia (plasma [K+] 3.0 to 3.5 mEq/L) causes no symptoms. The major disturbances seen with more severe potassium deficiency result from changes in cardiovascular, neuromuscular, and renal function. Cardiac toxicity may be manifested by serious arrhythmias, which occur because hyperpolarization of the myocardial cell membrane leads to a prolonged refractory period and increased susceptibility to reentrant arrhythmias. Other electrocardiographic changes of hypokalemia include T wave depression and prominent U waves.

Diff.Dx:
A. Inadequate dietary potassium intake

B. GI losses: vomiting, diarrhea, chronic laxative abuse

C. Skin losses: profuse sweating; extensive burns

D. Renal losses

1. * Diuretics
2. * Hypomagnesemia (Ref: Arch IM 1992/01;152:40)
3. Mineralocorticoid excess
   a. Primary aldosteronism: (1) adrenal adenoma. (2) bilateral adrenal hyperplasia
   b. Cushing's syndrome: (1) Primary adrenal disease. (2) Secondary to non endocrine tumor
   c. Accelerated hypertension
   d. Renal vascular hypertension
   e. Renin producing tumor
   f. Adrenogenital syndrome
   g. Licorice excess
4. Bartter's syndrome
   A rare condition usually found in children, & is characterized by increased renin & aldosterone production without hypertension. Hyperplasia of the juxtaglomerular apparatus is found on renal biopsy. Metab. alkalosis is usually present due to increased aldosterone production.
5. Liddle's syndrome
   An extremely rare disorder in a family with hypokalemia, hypertension & low aldosterone secretion & plasma renin activity. Renal potassium wasting was present & could be blocked by triamterene but not by spironolactone.
6. Misc:
   Renal tubular acidosis
   Metabolic alkalosis
   Acute hyperventilation
   Starvation
   Ureterosigmoidostomy
   Antibiotics: Carbenecillin, Gentamicin, Amphotericin B
   Diabetic ketoacidosis
   Acute leukemia

E. Cellular shift of K+
1. Metabolic Alkalosis, to a lesser degree, acute respiratory alkalosis
2. Hypokalemic Periodic paralysis
3. Barium or theophylline poisoning
4. Insulin administration (or glucose administration in a nondiabetic)

RX:   Correct underlying causes.
1. KCl 50 meq in 250 cc D5W or saline IV over 3- 5h (in emergency), or IV KCl up to
    60 meq/l of D5NS or D5W IV infusion over a few hours.

2. KCl 30-40 meq PO 1-3x/d as indicated.

3. If hypomagnesemia, give MgSO4 1-2 g IV over 15 min, or 1 g IM q4-6h.

     
                                                                                                                                                 
REF: ACP Medicine 2006

Treatment of Hypokalemia

For each 1 mEq/L fall in the plasma [K+], potassium stores fall by 200 to 400 mEq, until the plasma [K+] drops below 2.0 mEq/L. At that point, the total deficit may exceed 1,000 mEq. With both oral and parenteral replacement, potassium enters the plasma before it is transferred into cells. Consequently, potassium supplementation, particularly when given intravenously, carries the risk of hyperkalemia if the dose is too large or if it is administered too rapidly. Therefore, potassium should be administered orally whenever possible.

Potassium replacement using potassium-rich foods can be effective when metabolic acidosis or renal failure is present. However, dietary potassium is not effective in correcting the potassium deficit that occurs with metabolic alkalosis. In most foods, potassium is bound to poorly reabsorbable anions such as phosphate. Therefore, chloride salts (e.g., potassium chloride, which is used when metabolic alkalosis is caused by diuretics) are usually required to restore potassium losses. An exception to this may be in the preventive treatment of renal calculi with thiazide diuretics, where potassium citrate can maintain a normal serum potassium level.35

Potassium can be administered intravenously into a peripheral vein in concentrations as high as 40 mEq/L; higher concentrations can cause phlebitis and thus should be infused only into a large vein. Except in unusual settings, the rate of administration should probably not exceed 20 to 40 mEq/hr, although dosages as high as 100 mEq/hr have been infused in selected patients with paralysis or life-threatening arrhythmias.  Glucose-containing solutions should be avoided because insulin stimulation can drive potassium into cells, thereby exacerbating the hypokalemia.

For patients taking diuretics for high blood pressure, several alternatives are available to correct hypokalemia without use of potassium chloride supplementation. Because patient compliance decreases as the number of medications (including potassium supplements) increases, reducing the diuretic dose (e.g., to 12.5 mg of hydrochlorothiazide) or substituting an alternative agent should be considered first.

Edematous individuals or patients with primary aldosteron ism who also experience hypokalemia can be treated with potassium-sparing diuretics (amiloride or spironolactone) until more definitive therapy can be performed (e.g., the surgical removal of an adrenal adenoma in primary aldosteronism).

In patients with hypokalemic periodic paralysis , administration of potassium chloride can abort acute attacks within minutes; however, long-term potassium chloride supplementation does not usually prevent attacks. Hyperthyroidism should be treated when present, and the administration of a nonselective beta-adrenergic blocker (e.g., propranolol) may prevent episodes in patients with the familial form of the disorder.

2006