Format

Send to

Choose Destination
See comment in PubMed Commons below
Semin Oncol. 2000 Jun;27(3):322-34.

Metabolic emergencies in the cancer patient.

Author information

  • 1Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.

Abstract

The acute tumor lysis syndrome (ATLS) is characterized by the rapid development of hyperuricemia, hyperkalemia, hyperphosphatemia, and acute renal failure (ARF). Hematologic malignancies are responsible for most cases of ATLS. Control of hyperuricemia and the achievement of a high urine flow are the mainstays of prevention. Urinary alkalinization should be performed only when hyperuricemia is present. Hypercalcemia occurs in 10% to 20% of patients with cancer at some time during the disease course. Parathyroid hormone-related protein (PTHrP) is the most common mediator of humoral hypercalcemia of malignancy (HHM), while local osteolysis is the principal mechanism in patients with bone metastasis. Hydration with saline and administration of pamidronate control hypercalcemia in most patients. Hyponatremia with an increase in total-body salt and water content, manifested as edema and/or ascites, is the most common electrolyte abnormality in cancer patients. Hyponatremia due to salt depletion may occur in patients who receive cisplatin. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) may occur in association with cancer of the lung, after high-dose cyclophosphamide, and during vigorous fluid administration in patients with chemotherapy-associated emesis. Lactic acidosis without tissue hypoperfusion may be seen in patients with extensive liver metastasis or with certain hematologic malignancies. In the latter cases, lactate levels parallel disease activity and chemotherapy often leads to resolution of the lactic acidosis. Idiopathic hyperammonemia has been described after intensive chemotherapy for hematological malignancies and following bone marrow transplantation.

PMID:
10864220
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center