R Kogawa1, K Kinoshita2, K Tanjoh1. 1. Division of Emergency and Critical Care Medicine, Department of Acute Medicine, Nihon University School of Medicine, 30-1 Oyaguchi Kamimachi, Itabashi-ku, Tokyo, 173-8610, Japan. 2. Division of Emergency and Critical Care Medicine, Department of Acute Medicine, Nihon University School of Medicine, 30-1 Oyaguchi Kamimachi, Itabashi-ku, Tokyo, 173-8610, Japan. kinoshita.kosaku@nihon-u.ac.jp.
Abstract
OBJECTIVE: Spinal cord injury (SCI) is a pathological condition known to produce hyponatremia. The aim of this study was to elucidate the dynamics of urinary sodium excretion in patients with spinal cord injury. METHODS: SCI patients undergoing intensive care management were enrolled in this study. These patients were divided into two groups: those with Frankel Grade A spinal cord injury manifesting complete, severe motor disorders (FA group) and those with incomplete spinal cord injury (non-FA group). The occurrence of episode of hyponatremia (serum sodium <135 mmol/L), hypotension, and bradycardia during the first 14 hospital days was counted and fractional excretion of sodium (FENa) was calculated on the 1st, 7th, and 14th hospital days. RESULTS: Thirty-four patients (FA group, n = 9; non-FA group, n = 25) were included. Eight patients (88.9 %) in the FA group and three patients (12 %) in the non-FA group experienced at least one episode of hyponatremia during the first 14 hospital days. In the FA group, the FENa was significantly increased on the 7th and 14th hospital days compared to the 1st hospital day. FENa on the 14th hospital day was a significant independent predictor of hyponatremic episodes. Hypotension and bradycardia as the symptoms of sympathetic blockade differed significantly as independent predictors of increased FENa on the 14th hospital day. CONCLUSION: Urinary sodium excretion calculated by FENa increased in patients with severe spinal cord injury. Sympathetic blockade due to SCI may increase urine sodium excretion and lead to hyponatremia.
OBJECTIVE:Spinal cord injury (SCI) is a pathological condition known to produce hyponatremia. The aim of this study was to elucidate the dynamics of urinary sodium excretion in patients with spinal cord injury. METHODS: SCI patients undergoing intensive care management were enrolled in this study. These patients were divided into two groups: those with Frankel Grade A spinal cord injury manifesting complete, severe motor disorders (FA group) and those with incomplete spinal cord injury (non-FA group). The occurrence of episode of hyponatremia (serum sodium <135 mmol/L), hypotension, and bradycardia during the first 14 hospital days was counted and fractional excretion of sodium (FENa) was calculated on the 1st, 7th, and 14th hospital days. RESULTS: Thirty-four patients (FA group, n = 9; non-FA group, n = 25) were included. Eight patients (88.9 %) in the FA group and three patients (12 %) in the non-FA group experienced at least one episode of hyponatremia during the first 14 hospital days. In the FA group, the FENa was significantly increased on the 7th and 14th hospital days compared to the 1st hospital day. FENa on the 14th hospital day was a significant independent predictor of hyponatremic episodes. Hypotension and bradycardia as the symptoms of sympathetic blockade differed significantly as independent predictors of increased FENa on the 14th hospital day. CONCLUSION: Urinary sodium excretion calculated by FENa increased in patients with severe spinal cord injury. Sympathetic blockade due to SCI may increase urine sodium excretion and lead to hyponatremia.
Authors: D Hasan; K W Lindsay; E F Wijdicks; G D Murray; P J Brouwers; W H Bakker; J van Gijn; M Vermeulen Journal: Stroke Date: 1989-09 Impact factor: 7.914
Authors: M B Bracken; M J Shepard; W F Collins; T R Holford; W Young; D S Baskin; H M Eisenberg; E Flamm; L Leo-Summers; J Maroon Journal: N Engl J Med Date: 1990-05-17 Impact factor: 91.245