| |
Jakarta, 29 May 2009
Fluid and Electrolytes in Cancer Patients
Fluid and electrolyte abnormalities are common in patients with cancer. The etiology may be common to all patient populations or be specific to cancer patients. Hyponatremia is frequently hypovolemic due to renal loss of sodium from diuretics or salt-wasting nephropathy as seen with some chemotherapeutic agents such as cisplatin. Cerebral salt wasting also can occur in patients with intra- cerebral lesions. Normovolemic hyponatremia may occur in association with SIADH from cervical cancer, lymphoma, and leukemia, or from certain chemotherapeutic agents. Hypernatremia in cancer patients is most often due to poor oral intake or gastrointestinal volume loss (ileus, obstruction). Central DI can also lead to hypernatremia in patients with central nervous system lesions.
Hypokalemia can develop from gastrointestinal losses associated with diarrhea due to radiation enteritis or chemotherapy, or directly from tumors such as villous adenomas of the colon. Tumor lysis syndrome can precipitate severe hyperkalemia from massive cell destruction.
Hypocalcemia can be seen following removal of a thyroid or parathyroid tumor or following a central neck dissection by damage to the parathyroid glands. Hungry bone syndrome produces acute and profound hypocalcemia following parathyroid surgery for secondary or tertiary hyperparathyroidism when calcium is rapidly taken up by bones. Prostate and breast cancer can result in increased osteoblastic activity that increases bone formation thereby decreasing serum calcium. Acute hypocalcemia also can occur with hyperphosphatemia as phosphorus complexes with calcium. Hypomagnesemia is a side effect of ifosfamide and cisplatin therapy. Hypophosphatemia can be seen with hyperparathyroidism as phosphorus reabsorption is decreased, while oncogenic osteomalacia increases urinary excretion of phosphorus. Other causes of hypophosphatemia in cancer patients include renal tubular dysfunction from multiple myeloma, Bence Jones proteins, and certain chemotherapeutic agents. Acute hypophosphatemia can occur as rapidly proliferating malignant cells take up phosphorus in acute leukemia or from hungry bone syndrome following parathyroidectomy. Tumor lysis syndrome or bisphosphonates (used in the treatment of increased calcium) can also cause hyperphosphatemia.
Malignancy is the most common etiology of hypercalcemia in hospitalized patients and is due to increased bone resorption or decreased renal excretion. Bone destruction occurs from bony metastasis as seen with breast or renal cell cancer, but also can occur with multiple myeloma. With Hodgkin's and non-Hodgkin's lymphoma, hypercalcemia results from increased calcitriol formation, which in turn increases absorption of calcium from both the gastrointestinal tract and bone. Humoral hypercalcemia of malignancy is a common cause of hypercalcemia in cancer patients. As parathyroid-related protein is secreted, it binds to parathyroid receptors, stimulating calcium resorption from bone and decreasing renal excretion of calcium. The treatment of hypercalcemia of malignancy should begin with saline volume expansion. This alone will decrease renal reabsorption of calcium as the associated volume deficit is corrected. Once an adequate volume status has been achieved, a loop diuretic may be added. Unfortunately, these measures are only temporary and additional measures need to be taken. A variety of drugs are available with varying times of onset, duration of action, and side effects. Bisphosphonates (etidronate and pamidronate) inhibit bone resorption and osteoclastic activity. They act slowly (within 48 hours) but last for up to 15 days. Calcitonin also is effective by inhibiting bone resorption and increasing renal excretion of calcium. It acts quickly (within 2 to 4 hours), but its use is limited by the development of tachyphylaxis. Corticosteroids may decrease tachyphylaxis and can be used alone to treat hypercalcemia. Gallium nitrates are potent inhibitors of bone resorption. They display a long duration of action but can cause nephrotoxicity. Mithramycin is an antibiotic that blocks osteoclastic activity but can be associated with liver, renal, and hematologic abnormalities, and therefore its use is limited to the treatment of Paget's disease of the bone. For patients in whom hypercalcemia is severe and refractory, or who are unable to tolerate volume expansion (due to pulmonary edema or congestive heart failure), dialysis is an option.
Tumor lysis syndrome results when the release of intracellular metabolites is greater than the kidneys' excretory capacity. A rapid release of uric acid, potassium, and phosphorus occurs and is associated with marked hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and acute renal failure. It is typically seen with poorly differentiated lymphomas and leukemias, but also can be seen with a number of solid tumor malignancies. Tumor lysis syndrome most commonly develops following treatment with chemotherapy or radiotherapy. Once it develops, volume expansion should be undertaken, as should correction of electrolyte abnormalities. Associated hypocalcemia should not be treated unless it is symptomatic, to avoid metastatic calcifications. Dialysis may be required for impaired renal function or for correction of electrolyte abnormalities.
Reference:
Brunicardi FC et al. Schwartz's Principles of Surgery, 8th Edition
Iyan Darmawan, MD
Medical Director
iyan@ho.otsuka.co.id
|
|
