BACKGROUND: Historically, hyponatremia in patients with varying brain diseases was termed cerebral salt wasting. Hyponatremia secondary to CSW was reported to be a distinct entity from SIADH, with the distinguishing feature of decreased extracellular fluid volume. Brain natriuretic peptide, a peptide with natriuretic, vasorelaxant, and aldosterone-inhibiting properties, was recently implicated in aneurysmal SAH patients with CSW. Here, we describe 2 cases of CSW in TBI patients with elevated BNP levels. This phenomenon has not been previously described. CASE DESCRIPTION: Two patients with TBI and hyponatremia were subject to analysis. Central lines were placed to assess volume status. Levels of BNP were measured at the onset of hypertonic saline infusion. Electrocardiogram and cardiac enzyme studies were performed to assess cardiac function. Serial imaging was performed to assess the extent of brain injury. CONCLUSIONS: These patients with TBI had findings consistent with CSW with elevated BNP levels in the setting of normal cardiac function. In both cases, a high BNP level was observed after declining plasma Na levels despite aggressive hypertonic saline infusion. High BNP levels may be associated with CSW. Further studies are necessary to establish a causative role for BNP in TBI-induced CSW.
BACKGROUND: Historically, hyponatremia in patients with varying brain diseases was termed cerebral salt wasting. Hyponatremia secondary to CSW was reported to be a distinct entity from SIADH, with the distinguishing feature of decreased extracellular fluid volume. Brain natriuretic peptide, a peptide with natriuretic, vasorelaxant, and aldosterone-inhibiting properties, was recently implicated in aneurysmal SAH patients with CSW. Here, we describe 2 cases of CSW in TBIpatients with elevated BNP levels. This phenomenon has not been previously described. CASE DESCRIPTION: Two patients with TBI and hyponatremia were subject to analysis. Central lines were placed to assess volume status. Levels of BNP were measured at the onset of hypertonicsaline infusion. Electrocardiogram and cardiac enzyme studies were performed to assess cardiac function. Serial imaging was performed to assess the extent of brain injury. CONCLUSIONS: These patients with TBI had findings consistent with CSW with elevated BNP levels in the setting of normal cardiac function. In both cases, a high BNP level was observed after declining plasma Na levels despite aggressive hypertonicsaline infusion. High BNP levels may be associated with CSW. Further studies are necessary to establish a causative role for BNP in TBI-induced CSW.
Authors: Mendel Castle-Kirszbaum; Mervyn Kyi; Christopher Wright; Tony Goldschlager; R Andrew Danks; W Geoffrey Parkin Journal: Neurosurg Rev Date: 2021-01-03 Impact factor: 3.042
Authors: Jan Leonard; Raymond E Garrett; Kristin Salottolo; Denetta S Slone; Charles W Mains; Matthew M Carrick; David Bar-Or Journal: Scand J Trauma Resusc Emerg Med Date: 2015-11-11 Impact factor: 2.953
Authors: Hikmet Memmedov; Ebubekir Bakan; Nurinnisa Ozturk; Nurcan Kılıc Baygutalp; Omer Kaynar; Mehmet Ali Gul; Abdulsamed Kaya; Fatih Kıyıcı; Ahmet Gokhan Yazıcı Journal: Pan Afr Med J Date: 2022-02-03