Abstract
Severe or acute hyponatremia carries high risk for cerebral edema, seizure and brain death, and requires intensive care unit (ICU) admission and urgent correction. A small immediate correction is sufficient for preventing neurologic sequelae of hyponatremia. Severe chronic hyponatremia should be evaluated with attention to volume status and treated accordingly. The volume status of an ICU patient can be difficult to assess, and hyponatremia may be multifactorial. A small volume trial of isotonic fluids can be informative in these cases. In all cases of hyponatremia, correction should progress slowly with frequent monitoring of serum sodium. Osmotic demyelination syndrome (ODS) results from overly rapid correction of serum sodium. It can cause devastating paralysis, but meaningful recovery is possible. Vasopressin type 2 (V2) receptor antagonists are promising for management of the syndrome of inappropriate antidiuretic hormone activity (SIADH), but the potential for hypovolemia and overly rapid correction of serum sodium in critically ill patients is concerning, and there are no trials specific to ICU settings to guide use. Based on case reports and animal models, urea is an intriguing therapeutic option for correcting serum sodium with reduced risk of ODS, and for preventing ODS in high-risk patients.
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References
Sterns RH, Hix JK, Silver SM. Management of hyponatremia in the ICU. Chest. 2013;144:672–9.
Ellison DH, Berl T. The syndrome of inappropriate antidiuresis. N Engl J Med. 2007;356:2064–72.
Verbalis JG, Goldsmith SR, Greenberg A, Schrier RW, Sterns RH. Hyponatremia treatment guidelines 2007: expert panel recommendations. Am J Med. 2007;120:S1–S21.
Sterns RH, Nigwekar SU, Hix JK. The treatment of hyponatremia. Semin Nephrol. 2009;29:196–215.
Verbalis JG, Goldsmith SR, Greenberg A, Korzelius C, Schrier R, Sterns RH, Thompson CJ. Diagnosis, evaluation and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013;126:S1–S42.
Fenske W, Störk S, Koschker A, Blechschmidt A, Lorenz D, Wortmann S, Allolio B. Value of fractional uric acid excretion in differential diagnosis of hyponatremic patients on diuretics. J Clin Endocrinol Metab. 2008;93:2991–7.
Hato T, Ng R. Diagnostic value of urine sodium concentration in hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion versus hypovolemia. Hawaii Med J. 2010;69:264–7.
Schrier RW, Gross P, Gheorghiade M, Berl T, Verbalis JG, Czerwiec F, Orlandi C. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. N Engl J Med. 2006;355:2099–112.
Ghali JK, Koren MJ, Taylor JR, Brooks-Asplund E, Fan K, Long WA, Smith N. Efficacy and safety of oral conivaptan: a V1/V2a vasopressin receptor antagonist, assessed in a randomized, placebo-controlled trial in patients with euvolemic or hypervolemic hyponatremia. J Clin Endocrinol Metab. 2006;91:2145–52.
Annane D, Decaux G, Smith N, Conivaptan Study Group. Efficacy and safety of oral conivaptan, a vasopressin-receptor antagonist, evaluated in a randomized, controlled trial in patients with euvolemic or hypervolemic hyponatremia. Am J Med Sci. 2009;337:28–36.
Decaux G, Andres C, Kengge FG, Soupart A. Treatment of euvolemic hyponatremia in the intensive care unit by urea. Crit Care. 2010;14:R184.
Decaux G, Brimioulle S, Genette F, Mockel J. Treatment of the syndrome of inappropriate secretion of antidiuretic hormone by urea. Am J Nephrol. 1980;69:99–106.
Coussement J, Danguy C, Zouaoui-Boudjeltia K, Defrance P, Bankir L, Biston P, Piagnerelli M. Treatment of the syndrome of inappropriate secretion of antidiuretic hormone with urea in critically Ill patients. Am J Nephrol. 2012;35:265–70.
Louis G, Megarbane B, Lavoué S, Lassalle V, Argaud L, Poussel JF, Georges H, Bollaert P. Long-term outcome of patients hospitalized in intensive care units with central or extrapontine myelinolysis. Crit Care Med. 2012;40:970–2.
Gankam KF, Soupart A, Pochet R, et al. Re-induction of hyponatremia after rapid overcorrection of hyponatremia reduces mortality in rats. Kidney Int. 2009;76:614–21.
Soupart A, Ngassa M, Decaux G. Therapeutic relowering of the serum sodium in a patient after excessive correction of hyponatremia. Clin Nephrol. 1999;51:383–6.
Oya S, Tsutsumi K, Ueki K, Kirino T. Reinduction of hyponatremia to treat central pontine myelinolysis. Neurology. 2001;57:1931–2.
Sterns RH, Silver SM. Hemodialysis in hyponatremia: is there a risk? Semin Dial Transplant. 1990;3:3–4.
Dhrolia MF, Akhtar SF, Ahmed E, Naqvi A, Rizvi A. Azotemia protects the brain from osmotic demyelination on rapid correction of hyponatremia. Saudi J Kidney Dis Transpl. 2014;25(3):558–66.
Soupart A, Silver S, Schröeder B, Sterns R, Decaux G. Rapid (24-hour) reaccumulation of brain organic osmolytes (particularly myo-inositol) in azotemic rats after correction of chronic hyponatremia. J Am Soc Nephrol. 2002;13:1433–41.
Soupart A, Stenuit A, Perier O, Decaux G. Limits of brain tolerance to daily increment in serum sodium in chronically hyponatremic rats treated by hypertonic saline or urea: advantage of urea. Clin Sci. 1991;80:77–84.
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Scatena, R. (2020). Management of Severe Hyponatremia and SIADH. In: Hyzy, R.C., McSparron, J. (eds) Evidence-Based Critical Care. Springer, Cham. https://doi.org/10.1007/978-3-030-26710-0_51
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