J Neurol Surg A Cent Eur Neurosurg 2015; 76(04): 279-290
DOI: 10.1055/s-0034-1393927
Original Article
Georg Thieme Verlag KG Stuttgart · New York

The Impact of a Standardized Sodium Protocol on Incidence and Outcome of Dysnatremias in Neurocritical Care

Vera Spatenkova
1   Neurocenter, Regional Hospital, Liberec, Czech Republic
,
Ondrej Bradac
2   Department of Neurosurgery, Military University Hospital and First Medical School, Charles University, Prague, Czech Republic
,
Pavel Skrabalek
3   Department of Clinical Biochemistry, Regional Hospital, Liberec, Czech Republic
› Author Affiliations
Further Information

Publication History

01 November 2013

20 May 2014

Publication Date:
24 December 2014 (online)

Abstract

Background Dysnatremias are common and prognostically serious in neurocritical care. We studied whether a standardized sodium protocol would improve our neurocritical care of dysnatremias.

Methods A 5-year prospective study of a standardized sodium protocol for 1,560 patients admitted with various brain diseases in an adult neurologic-neurosurgical intensive care unit (NNICU) was compared with a 5-year retrospective analysis of 1,440 patients without the sodium protocol. Hyponatremia was defined as serum sodium (SNa+) < 135 mmol/L and hypernatremia SNa+ > 150 mmol/L. The sodium protocol involved measuring SNa+, serum, and urine osmolality, measured and calculated renal function parameters, fluid intake 40 mL/kg weight/day without hypotonic saline, thiazide, and desmopressin acetate in all normonatremic NNICU patients.

Results In the protocol study, hyponatremia occurred slightly less often (15.7 versus 16.3% of patients; p = 0.684), hypernatremia was significantly higher (respectively 8.5% versus 5.2% of patients; p < 0.001), and no differences were noted in hypo/hypernatremia (p = 0.483). There were no differences in the incidence of hypo-osmolal hyponatremia (respectively 3.5% versus 3.5% of patients; p = 0.987), cerebral salt wasting (CSW; respectively 1.7% versus 1.7% of patients; p = 0.883), syndrome of inappropriate secretion of antidiuretic hormone (SIADH; respectively 0.1% versus 0.3% of patients; p = 0.152), central diabetes insipidus (CDI; respectively 1.0% versus 0.6% of patients; p = 0.149). In hyponatremia there were no differences in the Glasgow Coma Scale (GCS) score upon onset of hyponatremia (p = 0.294), NNICU mortality (respectively 1.0% versus 0.4% patients; p = 0.074), and bad outcome upon discharge from NNICU (respectively 5.1% versus 6.5% of patients; p = 0.101), but in hypernatremia GCS score upon onset (p < 0.001), mortality (respectively 2.8% versus 1.0%; p < 0.001), and bad outcome from NNICU (respectively 6.7% versus 2.7% patients; p < 0.001) were significantly higher. Multivariate logistic regression analysis showed that hypernatremia, compared with hyponatremia, was a significant predictor of mortality during NNICU stay (respectively odds ratio [OR]: 1.14; p = 0.003 versus OR; 5.3; p = 0.002).

Conclusions The standard sodium protocol lowered the frequency of SIADH, which was encountered in only one patient over 5 years. However, it did not significantly reduce the incidence and improve the outcome of hyponatremia. Hypernatremia occurred more often and had a higher mortality and worse outcome than hyponatremia, but these patients were neurologically worse upon its onset. The prospective study confirmed that CSW, SIADH, and CDI were not common in our neurocritical care.

 
  • References

  • 1 Diringer MN. Management of sodium abnormalities in patients with CNS disease. Clin Neuropharmacol 1992; 15 (6) 427-447
  • 2 Tisdall M, Crocker M, Watkiss J, Smith M. Disturbances of sodium in critically ill adult neurologic patients: a clinical review. J Neurosurg Anesthesiol 2006; 18 (1) 57-63
  • 3 Qureshi AI, Suri MF, Sung GY , et al. Prognostic significance of hypernatremia and hyponatremia among patients with aneurysmal subarachnoid hemorrhage. Neurosurgery 2002; 50 (4) 749-755 ; discussion 755–756
  • 4 Aiyagari V, Deibert E, Diringer MN. Hypernatremia in the neurologic intensive care unit: how high is too high?. J Crit Care 2006; 21 (2) 163-172
  • 5 Diringer MN, Zazulia AR. Hyponatremia in neurologic patients: consequences and approaches to treatment. Neurologist 2006; 12 (3) 117-126
  • 6 Fisher LA, Ko N, Miss J , et al. Hypernatremia predicts adverse cardiovascular and neurological outcomes after SAH. Neurocrit Care 2006; 5 (3) 180-185
  • 7 Fraser JF, Stieg PE. Hyponatremia in the neurosurgical patient: epidemiology, pathophysiology, diagnosis, and management. Neurosurgery 2006; 59 (2) 222-229 ; discussion 222–229
  • 8 Nathan BR. Cerebral correlates of hyponatremia. Neurocrit Care 2007; 6 (1) 72-78
  • 9 Dvir D, Beigel R, Hoffmann C, Tsarfati G, Farfel Z, Pauzner R. Hyponatremic brain edema: correlation with serial computed tomography scans. Isr Med Assoc J 2009; 11 (7) 442-443
  • 10 Schrier RW, Bansal S. Diagnosis and management of hyponatremia in acute illness. Curr Opin Crit Care 2008; 14 (6) 627-634
  • 11 Peters JP, Welt LG, Sims EA, Orloff J, Needham J. A salt-wasting syndrome associated with cerebral disease. Trans Assoc Am Physicians 1950; 63: 57-64
  • 12 Schwartz WB, Bennett W, Curelop S, Bartter FC. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. Am J Med 1957; 23 (4) 529-542
  • 13 Sherlock M, O'Sullivan E, Agha A , et al. Incidence and pathophysiology of severe hyponatraemia in neurosurgical patients. Postgrad Med J 2009; 85 (1002) 171-175
  • 14 Murphy-Human T, Diringer MN. Sodium disturbances commonly encountered in the neurologic intensive care unit. J Pharm Pract 2010; 23 (5) 470-482
  • 15 Rabinstein AA, Wijdicks EF. Hyponatremia in critically ill neurological patients. Neurologist 2003; 9 (6) 290-300
  • 16 Shoker AS. Application of the clearance concept to hyponatremic and hypernatremic disorders: a phenomenological analysis. Clin Chem 1994; 40 (7 Pt 1) 1220-1227
  • 17 Lolin Y, Jackowski A. Hyponatraemia in neurosurgical patients: diagnosis using derived parameters of sodium and water homeostasis. Br J Neurosurg 1992; 6 (5) 457-466
  • 18 Overgaard-Steensen C. Initial approach to the hyponatremic patient. Acta Anaesthesiol Scand 2011; 55 (2) 139-148
  • 19 Wong MF, Chin NM, Lew TW. Diabetes insipidus in neurosurgical patients. Ann Acad Med Singapore 1998; 27 (3) 340-343
  • 20 Spatenkova V, Bradac O, Kazda A, Suchomel P. Central diabetes insipidus is not a common and prognostically worse type of hypernatremia in neurointensive care. Neuroendocrinol Lett 2011; 32 (6) 879-884
  • 21 Betjes MG. Hyponatremia in acute brain disease: the cerebral salt wasting syndrome. Eur J Intern Med 2002; 13 (1) 9-14
  • 22 Naval NS, Stevens RD, Mirski MA, Bhardwaj A. Controversies in the management of aneurysmal subarachnoid hemorrhage. Crit Care Med 2006; 34 (2) 511-524
  • 23 Spatenkova V, Bradac O, Skrabalek P. Outcome and frequency of sodium disturbances in neurocritically ill patients. Acta Neurol Belg 2013; 113 (2) 139-145
  • 24 Vaidya C, Ho W, Freda BJ. Management of hyponatremia: providing treatment and avoiding harm. Cleve Clin J Med 2010; 77 (10) 715-726
  • 25 Funk GC, Lindner G, Druml W , et al. Incidence and prognosis of dysnatremias present on ICU admission. Intensive Care Med 2010; 36 (2) 304-311
  • 26 Polderman KH, Schreuder WO, Strack van Schijndel RJ, Thijs LG. Hypernatremia in the intensive care unit: an indicator of quality of care?. Crit Care Med 1999; 27 (6) 1105-1108
  • 27 Sam R, Feizi I. Understanding hypernatremia. Am J Nephrol 2012; 36 (1) 97-104
  • 28 Sterns RH, Riggs JE, Schochet Jr SS. Osmotic demyelination syndrome following correction of hyponatremia. N Engl J Med 1986; 314 (24) 1535-1542
  • 29 Norenberg MD, Leslie KO, Robertson AS. Association between rise in serum sodium and central pontine myelinolysis. Ann Neurol 1982; 11 (2) 128-135
  • 30 Adams RD, Victor M, Mancall EL. Central pontine myelinolysis: a hitherto undescribed disease occurring in alcoholic and malnourished patients. AMA Arch Neurol Psychiatry 1959; 81 (2) 154-172