BACKGROUND: Hyponatremia is a frequently observed electrolyte abnormality in patients with central nervous system disease. Several mechanisms, such as SIADH, hypopituitarism, and CSWS, have been proposed with varied incidences among several studies. We attempted to clarify the incidence and mechanism of hyponatremia for each type of TBI. We also assessed the efficacy of sodium supplementation and retention therapy. For sodium retention therapy, hydrocortisone was administered, expecting its mineralocorticoid effect, when the hyponatremia was associated with excess natriuresis. METHODS: Retrospective analysis of 298 patients with TBI between January 2003 and December 2004 was performed. The incidence, background, clinical data, and outcome were evaluated. RESULTS: Of the 298 patients, 50 (16.8%) presented hyponatremia during the time course. Hyponatremia was associated with longer hospital stay (P < .001) and bad outcome (P = .02). Among these 50 patients, 37 recovered from the hyponatremia with simple sodium supplementation. The remaining 13 patients presented massive natriuresis and required additional sodium retention therapy. Hydrocortisone statistically reduced the amount of sodium excretion (P = .002) and returned the serum sodium level to a normal value. CONCLUSIONS: A high rate of hyponatremia after TBI was observed. Further studies are required to establish the precise mechanism of hyponatremia after TBI. Clear definition of CSWS is required to avoid confusion of the pathophysiology that causes hyponatremia. Hydrocortisone was useful to prevent excess natriuresis.
BACKGROUND:Hyponatremia is a frequently observed electrolyte abnormality in patients with central nervous system disease. Several mechanisms, such as SIADH, hypopituitarism, and CSWS, have been proposed with varied incidences among several studies. We attempted to clarify the incidence and mechanism of hyponatremia for each type of TBI. We also assessed the efficacy of sodium supplementation and retention therapy. For sodium retention therapy, hydrocortisone was administered, expecting its mineralocorticoid effect, when the hyponatremia was associated with excess natriuresis. METHODS: Retrospective analysis of 298 patients with TBI between January 2003 and December 2004 was performed. The incidence, background, clinical data, and outcome were evaluated. RESULTS: Of the 298 patients, 50 (16.8%) presented hyponatremia during the time course. Hyponatremia was associated with longer hospital stay (P < .001) and bad outcome (P = .02). Among these 50 patients, 37 recovered from the hyponatremia with simple sodium supplementation. The remaining 13 patients presented massive natriuresis and required additional sodium retention therapy. Hydrocortisone statistically reduced the amount of sodium excretion (P = .002) and returned the serum sodium level to a normal value. CONCLUSIONS: A high rate of hyponatremia after TBI was observed. Further studies are required to establish the precise mechanism of hyponatremia after TBI. Clear definition of CSWS is required to avoid confusion of the pathophysiology that causes hyponatremia. Hydrocortisone was useful to prevent excess natriuresis.
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