gms | German Medical Science

63rd Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Japanese Neurosurgical Society (JNS)

German Society of Neurosurgery (DGNC)

13 - 16 June 2012, Leipzig

The course of hyper- and hyponatremia in patients suffering from aneurysmal subarachnoid hemorrhage

Meeting Abstract

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  • K. Beseoglu - Neurochirurgische Klinik, Heinrich-Heine-Universität Düsseldorf
  • H.J. Steiger - Neurochirurgische Klinik, Heinrich-Heine-Universität Düsseldorf
  • D. Hänggi - Neurochirurgische Klinik, Heinrich-Heine-Universität Düsseldorf

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS). Leipzig, 13.-16.06.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. DocFR.09.06

doi: 10.3205/12dgnc240, urn:nbn:de:0183-12dgnc2407

Published: June 4, 2012

© 2012 Beseoglu et al.
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Outline

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Objective: Hyper- as well as hyponatremia are known complications after aneurysmal subarachnoid hemorrhage (SAH) causing a higher morbidity and mortality probably due to hypothalamic dysregulation. The goal of the present retrospective analysis is to determine the course and pathological patterns of hypo- and hypernatremia in a large patient population after aneurysmal SAH.

Methods: A retrospective analysis including 152 consecutive patients suffering from severe aneurysmal SAH was performed. 105 (69.1%) females and 47 (30.9%) males with a mean age of 53.9 ± 14.6 years were included. Serum sodium levels (SSL) in mmol/l were recorded every eight hours starting from admission for a maximum of 16 days. The initial value was obtained within the first 12 hours after hemorrhage. Hypernatremia was defined as sodium level above 145 mmol/l and hyponatremia was defined as sodium level below 135 mmol/l. Serum sodium levels were correlated to time after aneurysmal SAH.

Results: 73 (48.0%) patients showed hypernatremia, 27 (17.8%) of them as severe hypernatremia with sodium level above 150 mmol/l. The majority of patients developed hypernatremia after 48 h to 80 h after SAH with a maximum of patients at 72 h (n = 38) after ictus. Poor grade Patients (WFNS grade 4 and 5) show a significantly higher number of initial hypernatremia (32.8% vs. 17.2%, p = 0.046) with maximum sodium level being determined by SAH severity (WFNS 1 vs. WFNS 5, p < 0.01). 63 (41.4%) patients experienced hyponatremia with a maximum number of patients between day 10 and 12 (n = 24). Onset of hyponatremia was around day 7 after ictus. Aneurysm in close proximity to hypothalamic structures showed a higher incidence of hyponatremia (anterior communicating artery 43.8% and posterior communicating artery 44.8% vs. middle cerebral artery 34.3%). 26 (17.1%) Patients showed episodes of hyper- and hyponatremia, 8 of these with episodes of severe hypernatremia.

Conclusions: Sodium imbalance after SAH follows a uniform pattern with hypernatremia occurring early after ictus and hyponatremia following later on. SAH severity and aneurysm location are determinants for the incidence and severity of hyper- and hyponatremia. Clinicians should be aware of this characteristic pattern to adjust therapy accordingly.