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not be corrected unless the patient’s serum potassium falls in a critically low range
(less than 2 mEq/L), significant muscular weakness develops, or if hypokalemia is
associated with EKG changes. Hypocalcemia should remain uncorrected as well,
unless clinical signs or symptoms develop. Supplemental calcium may increase the
risk of formation of calcium phosphate precipitates in the kidney.
Renal tubular dysfunction is common in oncology patients. Patients may waste
electrolytes such as sodium, potassium, calcium, magnesium, and phosphorus
through their kidneys as a result of specific treatment exposures or prior renal injury.
Antifungal agents such as amphotericin and ambisome cause potassium wasting,
which may have clinical significance. Calcineurin inhibitors, such as tacrolimus or
cyclosporine, which may be used after stem cell transplantation, can cause
significant magnesium wasting. Patients with hypomagnesemia are more likely to
experience seizures when on calcineurin inhibitors so the magnesium should be kept
more than 1.8 mEq/L in these patients. In addition, patients with tumors of the CNS
may renally waste sodium so monitoring of serum sodium is crucial, especially in
the postoperative period.
Patients receiving drugs that cause salt wasting are often prescribed oral
electrolyte replacement. However, inability to tolerate oral medications or
nonadherence may allow electrolyte abnormalities to develop. Most of these
derangements are clinically asymptomatic with the notable exceptions of
hypocalcemia, which can cause tetany or cardiac arrhythmias and hyponatremia
resulting in refractory seizures. For the most part, management and replacement
strategies for these electrolyte abnormalities do not differ from children who do not
have cancer (see Chapter 100 Renal and Electrolyte Emergencies ). However, when
replacing calcium in pediatric oncology patients, the clinician should remember that
hypomagnesemia, a common side effect of cancer therapies, could complicate
efforts to address hypocalcemia.
Elevated blood sugar can be a transient side effect of corticosteroids as well as
asparaginase therapy. Asparaginase affects the body’s ability to make many proteins,
including insulin. In ALL treatment, steroids and asparaginase may be used together
and hyperglycemia may result. Treatment need not include insulin if dietary


measures alone are sufficient to control the serum blood sugar. If blood glucose is
greater than 250 mg/dL or is significant enough to cause glycosuria or ketonuria,
treatment with small doses of insulin may be considered. However, the approach to
insulin use in this setting should be conservative so as to limit the risks of
hypoglycemia. Diabetic ketoacidosis is rare in this situation.
High serum calcium levels are observed commonly in the setting of adult
malignancy but are rare in children with cancer. Hypercalcemia is usually related to
the tumor destroying bone or to ectopic production of parathyroid hormone by the



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