Melissa M J Chua1, Alejandro Enríquez-Marulanda2, Santiago Gomez-Paz3, Yosuke Akamatsu4, Mohamed M Salem5, Georgios A Maragkos6, Luis C Ascanio7, Khalid A Hanafy8, Corey R Fehnel9, Christopher S Ogilvy10, Justin Moore11, Ajith J Thomas12. 1. Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States; Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, 60 Fenwood Road, BTM 4th floor, Boston, MA 02215, United States. Electronic address: mchua@bwh.harvard.edu. 2. Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: alejandroe185@gmail.com. 3. Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: sggomezp@gmail.com. 4. Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: redpine7219@gmail.com. 5. Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: msalem_123@yahoo.com. 6. Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States; Department of Neurosurgery, Mount Sinai Hospital, New York, NY, United States. Electronic address: geomaragkos91@gmail.com. 7. Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States; Department of Neurosurgery, Mount Sinai Hospital, New York, NY, United States. Electronic address: luisascanio29@gmail.com. 8. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: khalid.a.hanafy@gmail.com. 9. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: cfehnel@bidmc.harvard.edu. 10. Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: cogilvy@bidmc.harvard.edu. 11. Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: jmoore4@bidmc.harvard.edu. 12. Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: athomas6@bidmc.harvard.edu.
Abstract
OBJECTIVES: Vasospasm is a well-known complication of aneurysmal subarachnoid hemorrhage (aSAH) that generally occurs 4-14 days post-hemorrhage. Based on American Heart Association guidelines, the current understanding is that hyponatremic episodes may lead to vasospasm. Therefore, we sought to determine the association between repeated serum sodium levels of aSAH patients and its relationship to radiographic vasospasm. MATERIALS AND METHODS: A single-center retrospective analysis from 2007-2016 was conducted of aSAH patients. Daily serum sodium levels were recorded up to day 14 post-admission. Hyponatremia was defined as a serum sodium value of < 135 mEq/L. We evaluated the relationship to radiologic vasospasm, neurologic deterioration, functional status at discharge, and mortality. A repeated measures analysis using a mixed-effect regression model was performed to assess the interindividual relationship between serum sodium trends and outcomes. RESULTS: A total of 271 aSAH patients were included. There were no significant differences in interindividual serum sodium values over time and occurrence of radiographic vasospasm, neurologic deterioration, functional, or mortality outcomes (p = .59, p = .42, p = .94, p = .99, respectively) using the mixed-effect regression model. However, overall mean serum sodium levels were significantly higher in patients who had neurologic deterioration, poor functional outcome (mRS 3-6), and mortality. CONCLUSIONS: Serum sodium level variations are not associated with subsequent development of cerebral vasospasm in aSAH patients. These findings indicate that serum sodium may not have an impact on vasospasm, and avoiding hypernatremia may provide a neurologic, functional and survival benefit.
OBJECTIVES: Vasospasm is a well-known complication of aneurysmal subarachnoid hemorrhage (aSAH) that generally occurs 4-14 days post-hemorrhage. Based on American Heart Association guidelines, the current understanding is that hyponatremic episodes may lead to vasospasm. Therefore, we sought to determine the association between repeated serum sodium levels of aSAH patients and its relationship to radiographic vasospasm. MATERIALS AND METHODS: A single-center retrospective analysis from 2007-2016 was conducted of aSAH patients. Daily serum sodium levels were recorded up to day 14 post-admission. Hyponatremia was defined as a serum sodium value of < 135 mEq/L. We evaluated the relationship to radiologic vasospasm, neurologic deterioration, functional status at discharge, and mortality. A repeated measures analysis using a mixed-effect regression model was performed to assess the interindividual relationship between serum sodium trends and outcomes. RESULTS: A total of 271 aSAH patients were included. There were no significant differences in interindividual serum sodium values over time and occurrence of radiographic vasospasm, neurologic deterioration, functional, or mortality outcomes (p = .59, p = .42, p = .94, p = .99, respectively) using the mixed-effect regression model. However, overall mean serum sodium levels were significantly higher in patients who had neurologic deterioration, poor functional outcome (mRS 3-6), and mortality. CONCLUSIONS: Serum sodium level variations are not associated with subsequent development of cerebral vasospasm in aSAH patients. These findings indicate that serum sodium may not have an impact on vasospasm, and avoiding hypernatremia may provide a neurologic, functional and survival benefit.
Authors: E Sander Connolly; Alejandro A Rabinstein; J Ricardo Carhuapoma; Colin P Derdeyn; Jacques Dion; Randall T Higashida; Brian L Hoh; Catherine J Kirkness; Andrew M Naidech; Christopher S Ogilvy; Aman B Patel; B Gregory Thompson; Paul Vespa Journal: Stroke Date: 2012-05-03 Impact factor: 7.914