Neurocritical Care

, Volume 18, Issue 1, pp 5–12 | Cite as

Randomized, Double-Blind Trial of the Effect of Fluid Composition on Electrolyte, Acid–Base, and Fluid Homeostasis in Patients Early After Subarachnoid Hemorrhage

  • Laura Lehmann
  • Stepani Bendel
  • Dominik E. Uehlinger
  • Jukka Takala
  • Margaret Schafer
  • Michael Reinert
  • Stephan M. Jakob
Original Article

Abstract

Background

Hyper- and hyponatremia are frequently observed in patients after subarachnoidal hemorrhage, and are potentially related to worse outcome. We hypothesized that the fluid regimen in these patients is associated with distinct changes in serum electrolytes, acid–base disturbances, and fluid balance.

Methods

Thirty-six consecutive patients with SAH were randomized double-blinded to either normal saline and hydroxyethyl starch dissolved in normal saline (Voluven®; saline) or balanced crystalloid and colloid solutions (Ringerfundin® and Tetraspan®; balanced, n = 18, each) for 48 h. Laboratory samples and fluid balance were evaluated at baseline and at 24 and 48 h.

Results

Age [57 ± 13 years (mean ± SD; saline) vs. 56 ± 12 years (balanced)], SAPS II (38 ± 16 vs. 34 ± 17), Hunt and Hess [3 (1–4) (median, range) vs. 2 (1–4)], and Fischer scores [3.5 (1–4) vs. 3.5 (1–4)] were similar. Serum sodium, chloride, and osmolality increased in saline only (p ≤ 0.010, time–group interaction). More patients in saline had Cl >108 mmol/L [16 (89 %) vs. 8 (44 %); p = 0.006], serum osmolality >300 mosmol/L [10 (56 %) vs. 2 (11 %); p = 0.012], a base excess <−2 [12 (67 %) vs. 2 (11 %); p = 0.001], and fluid balance >1,500 mL during the first 24 h [11 (61 %) vs. 5 (28 %); p = 0.046]. Hyponatremia and hypo-osmolality were not more frequent in the balanced group.

Conclusions

Treatment with saline-based fluids resulted in a greater number of patients with hyperchloremia, hyperosmolality, and positive fluid balance >1,500 mL early after SAH, while administration of balanced solutions did not cause more frequent hyponatremia or hypo-osmolality. These results should be confirmed in larger studies.

Keywords

Subarachnoid hemorrhage Fluid therapy Osmolality Acid–base balance 

Supplementary material

12028_2012_9764_MOESM1_ESM.docx (15 kb)
Supplementary material 1 (DOCX 14 kb)

References

  1. 1.
    Berendes E, Walter M, Cullen P, et al. Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage. Lancet. 1997;349:245–9.PubMedCrossRefGoogle Scholar
  2. 2.
    Espiner EA, Leikis R, Ferch RD, et al. The neuro–cardio–endocrine response to acute subarachnoid haemorrhage. Clin Endocrinol (Oxf). 2002;56:629–35.CrossRefGoogle Scholar
  3. 3.
    Wartenberg KE, Schmidt JM, Claassen J, et al. Impact of medical complications on outcome after subarachnoid hemorrhage. Crit Care Med. 2006;34:617–23.PubMedCrossRefGoogle Scholar
  4. 4.
    Hasan D, Wijdicks EF, Vermeulen M. Hyponatremia is associated with cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage. Ann Neurol. 1990;27:106–8.PubMedCrossRefGoogle Scholar
  5. 5.
    Qureshi AI, Suri MF, Sung GY, et al. Prognostic significance of hypernatremia and hyponatremia among patients with aneurysmal subarachnoid hemorrhage. Neurosurgery. 2002;50:749–55.PubMedCrossRefGoogle Scholar
  6. 6.
    Mandal AK, Saklayen MG, Hillman NM, Markert RJ. Predictive factors for high mortality in hypernatremic patients. Am J Emerg Med. 1997;15:130–2.PubMedCrossRefGoogle Scholar
  7. 7.
    Bennani SL, Abouqal R, Zeggwagh AA, et al. Incidence, causes and prognostic factors of hyponatremia in intensive care. Rev Med Interne. 2003;24:224–9.PubMedCrossRefGoogle Scholar
  8. 8.
    Lee CT, Guo HR, Chen JB. Hyponatremia in the emergency department. Am J Emerg Med. 2000;18:264–8.PubMedCrossRefGoogle Scholar
  9. 9.
    Tommasino C, Moore S, Todd MM. Cerebral effects of isovolemic hemodilution with crystalloid or colloid solutions. Crit Care Med. 1988;16:862–8.PubMedCrossRefGoogle Scholar
  10. 10.
    Zornow MH, McQuitty C, Prough DS. Perioperative fluid management of the neurosurgical patient. In: Albin MS, editor. Textbook of neuroanesthesia with neurosurgical and neuroscience perspectives. New York: McGraw-Hill; 1997. p. 117–48.Google Scholar
  11. 11.
    Williams EL, Hildebrand KL, McCormick SA, Bedel MJ. The effect of intravenous lactated Ringer’s solution versus 0.9 % sodium chloride solution on serum osmolality in human volunteers. Anesth Analg. 1999;88:999–1003.PubMedGoogle Scholar
  12. 12.
    O’Malley CM, Frumento RJ, Hardy MA, et al. A randomized, double-blind comparison of lactated Ringer’s solution and 0.9 % NaCl during renal transplantation. Anesth Analg. 2005;100:1518–24.PubMedCrossRefGoogle Scholar
  13. 13.
    Wilkes NJ, Woolf R, Mutch M, et al. The effects of balanced versus saline-based hetastarch and crystalloid solutions on acid–base and electrolyte status and gastric mucosal perfusion in elderly surgical patients. Anesth Analg. 2001;93:811–6.PubMedCrossRefGoogle Scholar
  14. 14.
    Van Swieten JC, Koudstaal PJ, Visser MC, Schouten HJ, van Gijn J. Interobserver agreement for the assessment of handicap in stroke patients. Stroke. 1988;19:604–7.PubMedCrossRefGoogle Scholar
  15. 15.
    Sayama T, Inamura T, Matsushima T, Inoha S, Inoue T, Fukui M. High incidence of hyponatremia in patients with ruptured anterior communicating artery aneurysms. Neurol Res. 2000;22:151–5.PubMedGoogle Scholar
  16. 16.
    Wijdicks EF, Vermeulen M, ten Haaf JA, Hijdra A, Bakker WH, van Gijn J. Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm. Ann Neurol. 1985;18:211–6.PubMedCrossRefGoogle Scholar
  17. 17.
    Diringer MN, Wu KC, Verbalis JG, Hanley DF. Hypervolemic therapy prevents volume contraction but not hyponatremia following subarachnoid hemorrhage. Ann Neurol. 1992;31:543–50.PubMedCrossRefGoogle Scholar
  18. 18.
    Solomon RA, Post KD, McMurtry JG 3rd. Depression of circulating blood volume in patients after subarachnoid hemorrhage: implications for the management of symptomatic vasospasm. Neurosurgery. 1984;15:354–61.PubMedCrossRefGoogle Scholar
  19. 19.
    Hasan D, Lindsay KW, Wijdicks EF, et al. Effect of fludrocortisone acetate in patients with subarachnoid hemorrhage. Stroke. 1989;20:1156–61.PubMedCrossRefGoogle Scholar
  20. 20.
    Audibert G, Steinmann G, de Talancé N, et al. Endocrine response after severe subarachnoid hemorrhage related to sodium and blood volume regulation. Anesth Analg. 2009;108:1922–8.PubMedCrossRefGoogle Scholar
  21. 21.
    Bederson JB, Connolly ES Jr, Batjer HH, American Heart Association, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke. 2009;40:994–1025.PubMedCrossRefGoogle Scholar
  22. 22.
    Diringer M, Bleck T, Claude Hemphill J, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s multidisciplinary consensus conference. Neurocrit Care. 2011;15:211–40.PubMedCrossRefGoogle Scholar
  23. 23.
    Isotani E, Suzuki R, Tomita K, et al. Alterations in plasma concentrations of natriuretic peptides and antidiuretic hormone after subarachnoid hemorrhage. Stroke. 1994;25:2198–203.PubMedCrossRefGoogle Scholar
  24. 24.
    Kurokawa Y, Uede T, Ishiguro M, et al. Pathogenesis of hyponatremia following subarachnoid hemorrhage due to ruptured cerebral aneurysm. Surg Neurol. 1996;46:500–7.PubMedCrossRefGoogle Scholar
  25. 25.
    Wijdicks EF, Schievink WI, Burnett JC Jr. Natriuretic peptide system and endothelin in aneurysmal subarachnoid hemorrhage. J Neurosurg. 1997;87:275–80.PubMedCrossRefGoogle Scholar
  26. 26.
    Moro N, Katayama Y, Kojima J, Mori T, Kawamata T. Prophylactic management of excessive natriuresis with hydrocortisone for efficient hypervolemic therapy after subarachnoid hemorrhage. Stroke. 2003;34:2807–11.PubMedCrossRefGoogle Scholar
  27. 27.
    Katayama Y, Haraoka J, Hirabayashi H, et al. A randomized controlled trial of hydrocortisone against hyponatremia in patients with aneurysmal subarachnoid hemorrhage. Stroke. 2007;38:2373–5.PubMedCrossRefGoogle Scholar
  28. 28.
    Fukui S, Otani N, Katoh H, et al. Female gender as a risk factor for hypokalemia and QT prolongation after subarachnoid hemorrhage. Neurology. 2002;59:134–6.PubMedCrossRefGoogle Scholar
  29. 29.
    Fukui S, Katoh H, Tsuzuki N, et al. Multivariate analysis of risk factors for QT prolongation following subarachnoid hemorrhage. Crit Care. 2003;7:R7–12.PubMedCrossRefGoogle Scholar
  30. 30.
    Brown MJ, Brown DC, Murphy MB. Hypokalemia from beta2-receptor stimulation by circulating epinephrine. N Engl J Med. 1983;309:1414–9.PubMedCrossRefGoogle Scholar
  31. 31.
    Mayer SA, Lin J, Homma S, et al. Myocardial injury and left ventricular performance after subarachnoid hemorrhage. Stroke. 1999;30:780–6.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Laura Lehmann
    • 1
  • Stepani Bendel
    • 1
  • Dominik E. Uehlinger
    • 2
  • Jukka Takala
    • 1
  • Margaret Schafer
    • 1
  • Michael Reinert
    • 3
  • Stephan M. Jakob
    • 1
  1. 1.Department of Intensive Care MedicineBern University Hospital (Inselspital) and University of BernBernSwitzerland
  2. 2.Department of Nephrology and HypertensionBern University Hospital (Inselspital) and University of BernBernSwitzerland
  3. 3.Department of NeurosurgeryBern University Hospital (Inselspital) and University of BernBernSwitzerland

Personalised recommendations