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Orthostatic Hypotension

Fluid and Salt Intake for Management of OH

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 2004Davidson et al. 1976).

Author Year; Country
Research Design
Total Sample Size
Methods Outcome
Frisbie 2004; USA

Population: Chronic cervical complete tetraplegia; AIS A
Treatment: Evaluation of urinary salt and water output in relation to prescribed dosage of ephedrine (doses range from 0 to 100 mg daily)
Outcome Measures: Severity of OH, urinary output.

  1. With decreasing ephedrine dose (and OH severity), there was a mean increase in daily output of urine sodium (from 50 to 181 mEq), water (from 1.5 to 5.3 L), rate of creatinine secretion sodium concentrations, and rates of water excretion, and a decrease in urine osmolality.
Frisbie & Steele 1997; USA

Population: SCI; Ephedrine (medically treated for OH) group: mean(SD) age 57(15) yrs, mean(SD) duration of paralysis 26(15) yrs; No ephedrine group: mean(SD) age 51(15.2) yrs, mean(SD) YPI 22(13.5).
Treatment: Retrospective chart review of use of ephedrine (n=30), sodium/salt supplementation (n=6), fludrocortisone (n=3) or physical therapy.
Outcome Measures: OH symptoms, serum sodium and urine osmolality.

  1. 3/4 patients on ephedrine who started sodium/salt supplementation with meals became independent of ephedrine use.
  2. Symptoms of OH were reduced consciousness (100% of subjects), strength (75%), vision (56%) and breathe (53%). Precipitating factors were hot weather (77%) bowel care (33%) and meals (30%).
  3. Low blood sodium found in 54% of the ephedrine (OH) patients and 16% of those without.
Muneta et al. 1992; Japan
Case report

Population: 72-year old woman with non-traumatic SCI and paroxysmal hypotension.
Treatment: Several weeks of salt/sodium supplement (7 then 15 g/day) was followed by L-threo-3,4-dihydroxyphenylserine (100 mg up to 600 mg/day).
Outcome Measures: Blood pressure, catecholamines (epinephrine & non-epinephrine), plasma renin activity.

  1. After sodium supplement, a marked increase in BP and norepinephrine were observed in response to sitting, along with a decrease in basal plasma renin activity.
  2. Addition of L-threo-3,4-dihydroxyphenylserine for 2 weeks, showed elevation in catecholamines about 5 and 10 times without an apparent increase in resting BP level.
  3. Significant improvement in the symptoms of the paroxysmal hypotension and patient able to participate in rehabilitation program.


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 1997Muneta 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.

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