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Heparin-Induced Hyponatremia

at time of writing, Pharmacy Practice Resident, Department of Pharmacy, The Regional Medical Center at Memphis, Memphis, TN; now, Medication Safety Pharmacist, Department of Pharmacy, The Regional Medical Center at Memphis

Angela M Sneed, PharmD

at time of writing, Pharmacy Practice Resident, Department of Pharmacy, The Regional Medical Center at Memphis; now, Clinical Staff Pharmacist, Department of Pharmacy, Baptist Memorial Hospital, Memphis

Christine Brown, RN

Nutrition Support Nurse, Department of Nursing, Methodist University of Tennessee (UT) Bowld Hospital, Memphis

Cecilia A Ellis, RD

Nutrition Support Dietitian, Department of Food and Nutrition Services, Methodist UT Bowld Hospital

Gayle Minard, MD

Associate Professor of Surgery, Department of Surgery, University of Tennessee Health Sciences Center; Director, Nutrition Support Service, The Regional Medical Center at Memphis, Methodist UT Bowld Hospital

Rex O Brown, PharmD FCCP BCNSP

Professor and Vice Chair, Department of Pharmacy, University of Tennessee Health Sciences Center; Nutrition Support Pharmacist, The Regional Medical Center at Memphis, Methodist UT Bowld Hospital

Reprints: N Elizabeth Norman PharmD, Department of Pharmacy, The Regional Medical Center at Memphis, 877 Jefferson Ave., Memphis, TN 38103-2807, fax 901/545-7351, enorman{at}the-med.org

OBJECTIVE: To report a case of hyponatremia in a patient receiving systemic unfractionated heparin (UFH) therapy and parenteral nutrition.

CASE SUMMARY: A 70-year-old African American woman was started on parenteral nutrition for postoperative ileus following an elective surgical procedure. Three days later, she was diagnosed with a pulmonary embolism and intravenous UFH therapy was initiated. During the 7-day course of UFH therapy, the patient's serum sodium concentration steadily declined and urine sodium concentration progressively increased. Physical examination revealed no signs or symptoms of hypo- or hypervolemia. The patient's serum potassium concentration increased modestly, although significant hyperkalemia was not observed. After discontinuation of UFH, serum concentrations of both sodium and potassium returned to baseline levels.

DISCUSSION: Although heparin-induced hyperkalemia is well documented, cases associated with substantial hyponatremia have been reported less frequently. An objective causality assessment revealed that the adverse drug reaction was probable in this case. Hyponatremia and hyperkalemia result from the antagonism of aldosterone by UFH within the zona glomerulosa of the adrenal glands.

CONCLUSIONS: The use of UFH may result in significant hyponatremia as well as hyperkalemia. Reversal of these electrolyte disturbances occurs after discontinuation of heparin.

Key Words: heparin, hyperkalemia, hyponatremia, parenteral nutrition

Published Online, January 12, 2004. www.theannals.com, DOI 10.1345/aph.1C442