Fluid and electrolyte disturbances in critically ill patients

Jay Wook Lee, Jay Wook Lee

Abstract

Disturbances in fluid and electrolytes are among the most common clinical problems encountered in the intensive care unit (ICU). Recent studies have reported that fluid and electrolyte imbalances are associated with increased morbidity and mortality among critically ill patients. To provide optimal care, health care providers should be familiar with the principles and practice of fluid and electrolyte physiology and pathophysiology. Fluid resuscitation should be aimed at restoration of normal hemodynamics and tissue perfusion. Early goal-directed therapy has been shown to be effective in patients with severe sepsis or septic shock. On the other hand, liberal fluid administration is associated with adverse outcomes such as prolonged stay in the ICU, higher cost of care, and increased mortality. Development of hyponatremia in critically ill patients is associated with disturbances in the renal mechanism of urinary dilution. Removal of nonosmotic stimuli for vasopressin secretion, judicious use of hypertonic saline, and close monitoring of plasma and urine electrolytes are essential components of therapy. Hypernatremia is associated with cellular dehydration and central nervous system damage. Water deficit should be corrected with hypotonic fluid, and ongoing water loss should be taken into account. Cardiac manifestations should be identified and treated before initiating stepwise diagnostic evaluation of dyskalemias. Divalent ion deficiencies such as hypocalcemia, hypomagnesemia and hypophosphatemia should be identified and corrected, since they are associated with increased adverse events among critically ill patients.

Keywords: hyperkalemia; hypernatremia; hypocalcemia; hypokalemia; hyponatremia; hypophosphatemia; intensive care.

References

    1. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368–1377.
    1. Sakr Y, Vincent JL, Reinhart K, et al. High tidal volume and positive fluid balance are associated with worse outcome in acute lung injury. Chest. 2005;128:3098–3108.
    1. Bouchard J, Soroko SB, Chertow GM, et al. Fluid accumulation, survival and recovery of kidney function in critically ill patients with acute kidney injury. Kidney Int. 2009;76:422–427.
    1. Payen D, de Pont AC, Sakr Y, Spies C, Reinhart K, Vincent JL. A positive fluid balance is associated with a worse outcome in patients with acute renal failure. Crit Care. 2008;12:R74.
    1. Bouchard J, Mehta RL. Fluid balance issues in the critically ill patient. Contrib Nephrol. 2010;164:69–78.
    1. Schetz M. Critical Care Nephrology. 2nd ed. Philadelphia: Saunders; 2009. Assessment of volume status; pp. 499–504.
    1. Funk GC, Lindner G, Druml W, et al. Incidence and prognosis of dysnatremias present on ICU admission. Intensive Care Med. 2010;36:304–311.
    1. Stelfox HT, Ahmed SB, Khandwala F, Zygun D, Shahpori R, Laupland K. The epidemiology of intensive care unit-acquired hyponatraemia and hypernatraemia in medical-surgical intensive care units. Crit Care. 2008;12:R162.
    1. Buckley MS, Leblanc JM, Cawley MJ. Electrolyte disturbances associated with commonly prescribed medications in the intensive care unit. Crit Care Med. 2010;38(6 Suppl):S253–S264.
    1. Thurman JM, Berl T. Therapy in Nephrology and Hypertension, a Companion to Brenner & Rector's The Kidney. 3rd ed. Philadelphia: Saunders; 2008. Therapy of dysnatremic disorders; pp. 337–352.
    1. Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med. 2000;342:1581–1589.
    1. Liamis G, Kalogirou M, Saugos V, Elisaf M. Therapeutic approach in patients with dysnatraemias. Nephrol Dial Transplant. 2006;21:1564–1569.
    1. Costanzo MR, Ronco C. Extracorporeal fluid removal in heart failure patients. Contrib Nephrol. 2010;165:236–243.
    1. Bondanelli M, Ambrosio MR, Zatelli MC, De Marinis L, degli Uberti EC. Hypopituitarism after traumatic brain injury. Eur J Endocrinol. 2005;152:679–691.
    1. Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. Anesthesiology. 2006;104:158–169.
    1. Blumberg A, Weidmann P, Shaw S, Gnadinger M. Effect of various therapeutic approaches on plasma potassium and major regulating factors in terminal renal failure. Am J Med. 1988;85:507–512.
    1. von Landenberg P, Shoenfeld Y. New approaches in the diagnosis of sepsis. Isr Med Assoc J. 2001;3:439–442.
    1. Shor R, Halabe A, Rishver S, et al. Severe hypophosphatemia in sepsis as a mortality predictor. Ann Clin Lab Sci. 2006;36:67–72.
    1. Cohen J, Kogan A, Sahar G, Lev S, Vidne B, Singer P. Hypophosphatemia following open heart surgery: incidence and consequences. Eur J Cardiothorac Surg. 2004;26:306–310.
    1. Bugg NC, Jones JA. Hypophosphataemia. Pathophysiology, effects and management on the intensive care unit. Anaesthesia. 1998;53:895–902.
    1. Cross HS, Debiec H, Peterlik M. Mechanism and regulation of intestinal phosphate absorption. Miner Electrolyte Metab. 1990;16:115–124.
    1. Nouri P, Llach F. Therapy in Nephrology and Hypertension, a Companion to Brenner & Rector's The Kidney. 3rd ed. Philadelphia: Saunders; 2008. Hypercalcemia, Hypocalcemia, and Other Divalent Cation Disorders; pp. 412–425.
    1. Zaloga GP. Hypocalcemia in critically ill patients. Crit Care Med. 1992;20:251–262.
    1. Zivin JR, Gooley T, Zager RA, Ryan MJ. Hypocalcemia: a pervasive metabolic abnormality in the critically ill. Am J Kidney Dis. 2001;37:689–698.
    1. Spahn DR. Hypocalcemia in trauma: frequent but frequently undetected and underestimated. Crit Care Med. 2005;33:2124–2125.
    1. Williams SF, Meek SE, Moraghan TJ. Spurious hypocalcemia after gadodiamide administration. Mayo Clin Proc. 2005;80:1655–1657.
    1. Besunder JB, Smith PG. Toxic effects of electrolyte and trace mineral administration in the intensive care unit. Crit Care Clin. 1991;7:659–693.

Source: PubMed

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