It is important to review the child’s diet, history of gastrointestinal losses, and medications. Emesis and diuretic use can be surreptitious. The presence of hypertension suggestsexcess mineralocorticoids. Concomitant electrolyte abnormalities are useful clues. The combination of hypokalemiaand metabolic acidosis is characteristic of diarrhea, distal renal tubular acidosis, and proximal renal tubular acidosis.A concurrent metabolic alkalosis is characteristic of gastriclosses, aldosterone excess, diuretics, Bartter syndrome, orGitelman syndrome.
Factors that influence the therapy of hypokalemia include the potassium level, clinical symptoms, renal function, presence of transcellular shifts of potassium, ongoing losses, and the patient’s ability to tolerate oral potassium. Severe, symptomatic hypokalemia requires aggressive treatment. Supplementation
Causes of Hypokalemia
Transcellular shifts Alkalemia Insulin β-Adrenergic agonists Drugs/toxins (theophylline, barium, toluene) Hypokalemic periodic paralysis Refeeding syndrome
Without specific acid-base disturbance Tubular toxins (amphotericin, cisplatin, aminoglycosides) Interstitial nephritis Diuretic phase of acute tubular necrosis Postobstructive diuresis Hypomagnesemia High urine anions (e.g., penicillin or penicillin derivatives) With metabolic alkalosis
RTA, renal tubular acidosis.
is more cautious if renal function is decreased because of the kidney’s limited ability to excrete excessive potassium. The plasma potassium level does not always provide an accurate estimation of the total body potassium deficit because there may be shifts of potassium from the intracellular space to the plasma. Clinically, this shift occurs most commonly with metabolic acidosis and as a result of the insulin deficiency of diabetic ketoacidosis; the plasma potassium underestimates the degree of total body potassium depletion. When these problems are corrected, potassium moves into the intracellular space, and these patients require more potassium supplementation to correct the hypokalemia. Patients who have ongoing losses of potassium need correction of the deficit and replacement of the ongoing losses.
Because of the risk of hyperkalemia, intravenous (IV) potassium should be used cautiously. Oral potassium is safer in nonurgent situations. The dose of IV potassium is 0.5 to 1 mEq/kg, usually given over 1 hour. The adult maximum dose is 40 mEq. Conservative dosing is generally preferred. For patients with excessive urinary losses, potassium-sparing diuretics are effective. When hypokalemia, metabolic alkalosis, and volume depletion are present, restoration of intravascular volume decreases urinary potassium losses.
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Three basic mechanisms cause hyperkalemia (Table 36-2). Inthe individual patient, the etiology is sometimes multifactorial.Factitious hyperkalemia is usually due to hemolysis during phlebotomy, but it can be the result of prolonged tourniquetapplication or fist clenching, which causes local potassiumrelease from muscle. Falsely elevated serum potassium levels can occur when serum levels are measured in patients withmarkedly elevated white blood cell or platelet counts; a promptlyanalyzed plasma sample usually provides an accurate result.
Because of the kidney’s ability to excrete potassium, it is unusual for excessive intake, by itself, to cause hyperkalemia. This mechanism can occur in a patient who is receiving large quantities of IV or oral potassium for excessive losses that are no longer present. Frequent or rapid blood transfusions can increase the potassium level acutely secondary to the high
Causes of Hyperkalemia