OH is common among patients with higher levels of SCI, may be present without symptoms, and often coexists with abnormal sodium and fluid metabolism. Increases in fluid intake and a diet high in salt/sodium can expand extracellular fluid volume and improve orthostatic responses. This simple dietary intervention appears to be effective in patients with idiopathic OH without SCI (Claydon & Hainsworth 2004; Davidson et al. 1976).
Three out of 4 subjects taking sodium/salt supplementation with meals in Frisbie and Steele’s (1997) study became independent of their use of Ephedrine. In 4 patients with OH, Frisbie (2004) demonstrated that the estimated daily intake of sodium and water was inversely related to their Ephedrine requirements and suggested that greater sodium and water intake may lead to a more balanced renal action. Thus, level 5 evidence from two observation studies (Frisbie & Steele 1997; Muneta et al. 1992) suggest that sodium and fluid regulation in conjunction with other pharmacological interventions may reduce symptoms of OH. However, as no evidence exists on the effect of sodium/salt or fluid regulation alone for OH management in SCI, these conclusions should be interpreted with caution. As of now, there are no guidelines suggesting appropriate water and sodium intake specific to individuals with SCI.
There is no evidence on the effect of sodium or fluid regulation alone for OH management in SCI. Sodium and fluid regulation was evaluated in combination with other pharmacological interventions and thus, the effects of sodium and fluid regulation cannot be determined.
- The benefits of salt loading have not been sufficiently proven effective in individuals with SCI.