Original Articles

Chronic Severe Hyponatremia and Cardiopulmonary Bypass: Avoiding Osmotic Demyelination Syndrome

^* Department of Cardiothoracic Surgery, Confluence Health: Central Washington Hospital, Wenatchee, Washington
^† Staff Anesthesiologist, Portland VA Medical Center, Department of Anesthesia and Perioperative Medicine, Oregon State University, Portland, Oregon
^‡ Cardiac Surgeon, Chairman Department of Surgery, Confluence Health: Central Washington Hospital, Wenatchee, Washington
^§ Program Director, Clinical Perfusion Education, School of Allied Health Professions, University of Nebraska Medical Center, Omaha, Nebraska

Address correspondence to: Susan Canaday, BS, CCP, Department of Perfusion, Confluence Health: Central Washington Hospital, 1201 South Miller Street, Wenatchee, WA 98801. E-mail: canada_s_2010@msn.com

Received: 5 October 2015
Accepted: 9 December 2015

Abstract

Serum sodium concentration affects every cell in the body with respect to cellular tonicity. Hyponatremia is the most frequent electrolyte abnormality encountered, occurring at clinical admission in 22% of elderly patients. Any rapid correction of chronic severe hyponatremia can result in rapid cellular shrinking due to loss of intracellular free water. This is commonly associated with paralysis and severe brain damage due to osmotic demyelination syndrome (ODS). ODS occurs because the body has the ability to compensate for cellular fluid shifts due to chronic hyponatremia (by a decrease in brain concentration of several ions, amino acids, and organic osmolytes). Thus, the neurons are often at a functional state of fluid balance despite the sodium imbalance. The initiation of cardiopulmonary bypass (CPB) can introduce between 1 and 2 L of priming solution containing a normal sodium concentration creating a rapid rise in sodium concentration within the extracellular fluid. This abrupt change establishes a situation where intracellular free water can be lost resulting in cellular shrinking and ODS. In presenting this case study, we hope to add to the current literature with a specific isotonic approach to treating the chronically severe hyponatremic patient pre-CPB, during CPB, and post-CPB.