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Management. When hypercalcemia is mild, no specific therapy is
warranted and efforts should focus on identifying the underlying condition.
Chronic moderate hypercalcemia (12 to 14 mg/dL) may be well tolerated
and not require immediate intervention, though thorough evaluation should
be pursued. If hypercalcemia is severe (greater than 14 mg/dL) or
associated with clinically significant symptoms, prompt intervention is
warranted. Given the gastrointestinal and renal manifestations associated
with hypercalcemia, patients may present with hypovolemia. Initial efforts
should focus on restoring adequate intravascular volume with isotonic IV
fluids, which will increase GFR and increase renal excretion of calcium.
Agents that inhibit osteoclasts, such as calcitonin and bisphosphonates, may
be used to treat hypercalcemia secondary to increased bone resorption.
Calcitonin has rapid onset of action but resistance develops rapidly;
bisphosphonates such as pamidronate and zoledronic acid have delayed
onset but long duration of action, so may be useful when combined with
calcitonin. Loop diuretics such as furosemide are no longer routinely
recommended due to risk of hypovolemia and electrolyte imbalance, but
may be used judiciously if necessary to prevent fluid overload in patients
with renal failure or CHF. If the patient is in renal failure or efforts with
saline diuresis and first-line agents are not sufficient, renal replacement
therapy (RRT) may be necessary. Consultation with a pediatric nephrologist
or endocrinologist is advised.
DISORDERS OF ACID–BASE HOMEOSTASIS
Goals of Treatment
Maintenance of normal acid–base balance involves expiration of carbon
dioxide, metabolism of organic acids, and buffering and renal excretion of
nonvolatile acids. Severe uncompensated acid–base disorders are associated
with a variety of cardiovascular, metabolic, neurologic, and respiratory
consequences. General goals include treatment of the underlying etiology
and maintenance of normal pH in order to prevent potentially fatal