#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

Diagnosis of hyponatraemia in neurointensive care: the role of renal function parameters


Authors: V. Špatenková 1;  A. Kazda 2;  P. Barsa 1;  V. .beneš 1;  P. Škrabálek 3;  D. Králová 4;  P. Suchomel 1
Authors‘ workplace: Neurocentrum, Krajská nemocnice Liberec, a. s. 1;  Katedra klinické biochemie IPVZ, Praha 2;  Oddělení klinické biochemie, Krajská nemocnice Liberec, a. s. 3;  Institut biostatistiky a analýz, LF a PřF MU, Brno 4
Published in: Cesk Slov Neurol N 2008; 71/104(2): 156-162
Category: Original Paper

Overview

Introduction:
Hyponatraemia with hypoosmolality in acute brain diseases can be associated with two syndromes:  the cerebral salt wasting syndrome (CSW) and the syndrome of inappropriate secretion of the antidiuretic hormone (CSW). Distinguishing between the two is essential as each of the syndromes requires a different therapy and is done with the use of renal function parameters. The objective of the study was to evaluate hyponatraemia after introducing the above parameters in clinical practice at our neurologic-neurosurgical care unit (NNICU). 

Methods:
We retrospectively analysed all hyponatraemia (SNa+ < 135 mmol/l) in patients (pts) with acute brain diseases admitted to our NNICU over a period of five years. First we divided them according to measured serum osmolality, and then we diagnosed the group with hypoosmolality (SOsm < 275 mmol/kg) using renal function parameters (p-value related to normal levels).

Results:
There were 251 pts with a total of 736 days of hyponatraemia over the period under observation. The majority of pts had normal serum osmolality (155 pts, 297 days), some had hyperosmolality (38 pts, 41 days), and only 50 pts (169 days) had low plasma osmolality. Serum osmolality was not measured for the rest of hyponatraemias. In the hypoosmolal group renal function parameters were examined in 31 patients (62%). 25 patients of the above patients were diagnosed for the CSW syndrome (dUNa+ 546.6 + 383.7 mmol/day, p < 0,001; CEl 0.065 ± 0.036 ml/s, p < 0.001; CNa+ 0.061 ± 0.036 ml/s, p < 0.001; EWC -0.015 ± 0.032 ml/s, p = 0.030; FENa+ 0.029 ± 0.016, p < 0.001), 6 patients had other causes of hyponatraemia. None of the patients had SIADH.

Conclusion:
Renal function parameters represent a very easy and available method of differential diagnosis of hyponatraemias in patients receiving neurointensive care.

Key words:
hyponatraemia – hypoosmolality – CSW – SIADH – renal function parameters


Sources

1. Sivakumar V, Rajshekhar V, Chandy MJ. Management of neurosurgical patients with hyponatremia and natriuresis. Neurosurgery 1994; 34: 269–274.

2. Betjes MG. Hyponatremia in acute brain disease: the cerebral salt wasting syndrome. Eur J Intern Med 2002; 13: 9–14.

3. Fraser JF, Stieg PE. Hyponatremia in the neurosurgical patient: epidemiology, pathophysiology, diagnosis, and management. Neurosurgery 2006; 59: 222–229.

4. Naval NS, Stevens RD, Mirski MA, Bhardwaj A. Controversies in the management of aneurysmal subarachnoid hemorrhage. Crit Care Med 2006; 34: 511–524.

5. Harrigan MR. Cerebral salt wasting syndrome: a review. Neurosurgery 1996; 38: 152–160.

6. Qureshi AI, Suri MF, Sung GY, Straw RN, Yahia AM, Saad M et al. Prognostic significance of hypernatremia and hyponatremia among patients with aneurysmal subarachnoid hemorrhage. Neurosurgery 2002; 50: 749–755.

7. Ke C, Poon WS, Ng HK, Tang NL, Chan Y, Wang JY et al. The impact of acute hyponatraemia on severe traumatic brain injury in rats. Acta Neurochir Suppl 2000; 76: 405–408.

8. Unterberg A, Kiening K, Schmiedek P, Lanksch W. Long-term observations of intracranial pressure after severe head injury. The phenomenon of secondary rise of intracranial pressure. Neurosurgery 1993; 32: 17–23.

9. Wijdicks EF, Ropper AH, Hunnicutt EJ, Richardson GS, Nathanson JA. Atrial natriuretic factor and salt wasting after aneurysmal subarachnoid hemorrhage. Stroke 1991; 22: 1519–1524.

10. Kazda A, Balík M. Osmolální dysbalance v intenzivní péči a jejich monitorování. Klin Biochem Metab 1996; 4: 223–227.

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. Cort JH. Cerebral salt wasting. Lancet 1954; 266: 752–754.

13. 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: 529–542.

14. Kazda A, Špatenková V, Škrabálek P. Akutní onemocnění mozku – poruchy vodního a natriového hospodářství, natriuretické peptidy. Klin Biochem Metab 2003; 11: 74–82.

15. Lolin Y, Jackowski A. Hyponatraemia in neurosurgical patients: diagnosis using derived parameters of sodium and water homeostasis. Br J Neurosurg 1992; 6: 457–466.

16. Shoker AS. Application of the clearance concept to hyponatremic and hypernatremic disorders: a phenomenological analysis. Clin Chem 1994; 40: 1220–1227.

17. Jabor A. Clearance bezelektrolytové vody u selhávajících ledvin, při hypernatremii a hyponatremii. Klin Biochem Metab 1997; 5: 248–250.

18. Kröll M, Juhler M, Lindholm J. Hyponatraemia in acute brain disease. J Intern Med 1992; 232: 291–297.

19. Berendes E, Walter M, Cullen P, Prien T, Van Aken H, Horsthemke J et al. Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage. Lancet 1997; 349: 245–249.

20. Jabor A. Hodnocení poruch osmolality s využitím efektivní osmolální clearance, clearance sodíku, clearance bezelektrolytové vody a modelu extracelulárního a intracelulárního prostoru. Klin Biochem Metab 1997; 5: 241–247.

21. Fall PJ. Hyponatremia and hypernatremia. A systematic approach to causes and their correction. Postgrad Med 2000; 107: 75–82.

22. Singh S, Bohn D, Carlotti AP , Cusimano M, Rutka JT, Halperin ML. Cerebral salt wasting: truths, fallacies, theories, and challenges. Crit Care Med 2002; 30: 2575–2579.

23. 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: 154–172.

24. Tomlinson S, Hendy GN, O'Riordan JL. A in vivo experimental model for the study of resistance to the renal action of parathyroid hormone in man. Calcif Tissue Res 1976; 21(Suppl): 267–271.

25. Norenberg MD, Leslie KO, Robertson AS. Association between rise in serum sodium and central pontine myelinolysis. Ann Neurol 1982; 11: 128–135.

26. Sterns RH, Cappuccio JD, Silver SM, Cohen EP. Neurologic sequelae after treatment of severe hyponatremia: a multicenter perspective. J Am Soc Nephrol 1994; 4: 1522–1530.

Labels
Paediatric neurology Neurosurgery Neurology
Login
Forgotten password

Enter the email address that you registered with. We will send you instructions on how to set a new password.

Login

Don‘t have an account?  Create new account

#ADS_BOTTOM_SCRIPTS#