Hypokalemia Diagnostic Approach

FIGURE 3-7

Overview of diagnostic approach to hypokalemia: hypokalemia without total body potassium depletion. Hypokalemia can result from transcellular shifts of potassium into cells without total body potassium depletion or from decreases in total body potassium. Perhaps the most dramatic examples occur in catecholamine excess states, as after administration of l^adreneric receptor (P2AR) agonists or during "stress." It is important to note that, during some conditions (eg, ketoaci-dosis), transcellular shifts and potassium depletion exist simultaneously. Spurious hypokalemia results when blood specimens from leukemia patients are allowed to stand at room temperature; this results in leukocyte uptake of potassium from serum and artifactual hypokalemia. Patients with spurious hypokalemia do not have clinical manifestations of hypo-kalemia, as their in vivo serum potassium values are normal. Theophylline poisoning prevents cAMP breakdown (see Fig. 3-3). Barium poisoning from the ingestion of soluble barium salts results in severe hypokalemia by blocking channels for exit of potassium from cells. Episodes of hypokalemic periodic paralysis can be precipitated by rest after exercise, carbohydrate meal, stress, or administration of insulin. Hypokalemic periodic paralysis can be inherited as an autosomal-dominant disease or acquired by patients with thyrotoxicosis, especially Chinese males. Therapy of megaloblastic anemia is associated with potassium uptake by newly formed cells, which is occasionally of sufficient magnitude to cause hypokalemia [13].

Approach Hypokalemia
FIGURE 3-8

Diagnostic approach to hypokalemia: hypokalemia with total body potassium depletion secondary to extrarenal losses. In the absence of redistribution, measurement of urinary potassium is helpful in determining whether hypokalemia is due to renal or to extrarenal potassium losses. The normal kidney responds to several (3 to 5) days of potassium depletion with appropriate renal potassium conservation. In the absence of severe polyuria, a "spot" urinary potassium concentration of less than 20 mEq/L indicates renal potassium conservation. In certain circumstances (eg, diuretics abuse), renal potassium losses may not be evident once the stimulus for renal potassium wasting is removed. In this circumstance, urinary potassium concentrations may be deceptively low despite renal potassium losses. Hypokalemia due to colonic villous adenoma or laxative abuse may be associated with metabolic acidosis, alkalosis, or no acid-base disturbance. Stool has a relatively high potassium content, and fecal potassium losses could exceed 100 mEq per day with severe diarrhea. Habitual ingestion of clay (pica), encountered in some parts of the rural southeastern United States, can result in potassium depletion by binding potassium in the gut, much as a cation exchange resin does. Inadequate dietary intake of potassium, like that associated ith anorexia or a "tea and toast" diet, can lead to hypokalemia, owing to delayed renal conservation of potassium; however, progressive potassium depletion does not occur unless intake is well below 15 mEq of potassium per day.

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