Unappreciated aspects of fluid and electrolyte physiology and implications to patient recovery

Abstract

Fluid and electrolyte management of the critically ill patient is a ‘‘core skill’’ for the anesthesiologist and intensivist. Critically ill patients often present with any of a number of insults that result in fluid and electrolyte derangements, and an important part of resuscitative therapy is aggressive fluid and electrolyte management. Once the initiating insult has been stabilized, electrolyte and fluid management often continues to occupy a central component of therapy, and is usually directed at trying to reestablish physiologically appropriate interstitial and vascular compartment volumes. Despite 30 years of research, basic questions are still debated concerning the type of fluid to administer (blood products, artificial colloids, or crystalloids), the amount of fluid to administer (the choice and measurement of appropriate physiological indices), and the clinical scenario wherein fluids should be administered (acute trauma, head injury, sepsis, major surgery, or heartrenalor hepatic failure, etc.). Indeed, the challenge of fluid and electrolyte management in the critically ill patient is somewhat analogous to the question of whether a regional or general anesthetic is best for hip replacement in a frail 92-yr-old woman with poor heart function and tenuous kidneys. While there are many components to the question, the answer is often reduced to ‘‘a good anesthetic is better than a bad one’’. By extension, proper fluid and electrolyte management is better than inappropriate management. While the answer may be unsatisfying to residents, they can be re-assured that the answer(s) becomes clearer after they gain a thorough understanding of the physiology of fluid and electrolytes and once they acquire several years of experience. In their paper in the current issue of the Journal, Stelfox et al. retrospectively examine the incidence of intensive care unit (ICU) acquired disturbances in plasma sodium concentration [Na] in a large population of post cardiac surgical patients. The authors found that the incidence of ICU acquired hypoand hypernatremia was 12% and 4%, respectively. More importantly, they demonstrated that hospital mortality in patients with acquired disturbances in [Na], whether hypoor hypernatremia, was significantly higher than hospital mortality in patients without acquired disturbances in [Na]. While the authors correctly pointed out that their study was limited by its retrospective nature, the fact that association was identified rather than causality, and the association was restricted to a large unselected population of patients undergoing heart surgery, the study begs the question – What is the nature of the link between changes in [Na] acquired after ICU admission and increased hospital mortality? The answer cannot be unravelled easily because: 1) apart from acute severe hyperkalemia, severe hyponatremia, fulminant pulmonary or cerebral edema, alterations in electrolyte concentrations and/or volume status are not lethal in themselves; and 2) changes in [Na] and volume compartments have ramifications throughout the physiological arena. The answer as to why acutely ill patients develop changes in fluid and electrolyte status is partly a function of: 1) the effects of the initial insult on control mechanisms; 2) the unavoidable consequences of therapy in P. Wilkes, MD, PhD (&) Division of Cardiac Anesthesia, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, ON K1Y 4W7, Canada e-mail: pwilkes@ottawaheart.ca