Pediatric Autonomic-Mediated Orthostatic Intolerance
Fludrocortisone is a synthetic steroid with potent mineralocorticoid properties and high glucocorticoid activity. Mineralocorticoids increase reabsorption of sodium in the distal tubule of the nephron, resulting in fluid retention and an increase in blood pressure. Fludrocortisone may also increase peripheral alpha-adrenergic sensitivity, facilitating vasoconstriction. Low-dose fludrocortisone therapy, along with increased salt intake, has been used in the management of orthostatic intolerance for several decades.
In adolescents and adults, the usual fludrocortisone dose is 0.1–0.2 mg/day. Doses of 0.05–0.1 mg/day have been used for younger children. Fludrocortisone is available in 0.1 mg scored tablets. As a result of its long biologic half-life, 18 to 36 hours in adults, it can be given once daily. Full effects may not be seen for 2 to 3 weeks after beginning treatment. As with any long-term steroid use, fludrocortisone should be gradually tapered prior to discontinuation. The dose should be increased during periods of severe illness, trauma, or surgery to prevent drug-induced adrenal insufficiency. Patients receiving fludrocortisone should be monitored for steroid-related adverse effects as well as hypokalemia and encouraged to increase dietary potassium intake if necessary.
The utility of fludrocortisone in preventing recurrent syncope continues to be debated. While many clinicians have found it beneficial, there is little research to support its use. In 2005, Salim and Di Sessa randomized 33 children with a history of syncope and a positive tilt test to receive either fludrocortisone 0.1 mg/day and table salt 1 gram/day or placebo for one year. The average number of syncopal episodes prior to the study was 4.4 ± 4.8. Thirty-two children (mean age 13.9 ± 2.5 years, 20 females) were available at follow-up. Therapy was continued for an average of 176 ± 117 days. Syncopal episodes continued to occur in 10 of 18 children (55%) in the treatment group and 5 of 14 (36%) of the controls (p < 0.05). Patients in both groups experienced an increase in their symptoms after treatment was discontinued, suggesting a significant placebo response.
The impact of fludrocortisone on nausea associated with orthostatic intolerance was evaluated in 17 adolescents (11–17 years of age). All patients had a history of nausea, dizziness, or syncope and a confirmed diagnosis of orthostatic hypotension by tilt table testing. Fludrocortisone was given at a dose of 0.1–0.2 mg/day for a minimum of 4 weeks prior to assessment. The median duration of treatment was 11 weeks (range 4–54 weeks). At 4-week follow-up, 11 patients (65%) had significant improvement, defined as a reduction in nausea severity of more than 50%. One patient (6%) had moderate improvement, one (6%) had mild improvement, and the remaining four patients (24%) had no improvement. The effect of treatment on syncope was not reported. The authors concluded that fludrocortisone treatment appears to improve nausea associated with autonomic-mediated orthostatic intolerance.
Fludrocortisone
Fludrocortisone is a synthetic steroid with potent mineralocorticoid properties and high glucocorticoid activity. Mineralocorticoids increase reabsorption of sodium in the distal tubule of the nephron, resulting in fluid retention and an increase in blood pressure. Fludrocortisone may also increase peripheral alpha-adrenergic sensitivity, facilitating vasoconstriction. Low-dose fludrocortisone therapy, along with increased salt intake, has been used in the management of orthostatic intolerance for several decades.
In adolescents and adults, the usual fludrocortisone dose is 0.1–0.2 mg/day. Doses of 0.05–0.1 mg/day have been used for younger children. Fludrocortisone is available in 0.1 mg scored tablets. As a result of its long biologic half-life, 18 to 36 hours in adults, it can be given once daily. Full effects may not be seen for 2 to 3 weeks after beginning treatment. As with any long-term steroid use, fludrocortisone should be gradually tapered prior to discontinuation. The dose should be increased during periods of severe illness, trauma, or surgery to prevent drug-induced adrenal insufficiency. Patients receiving fludrocortisone should be monitored for steroid-related adverse effects as well as hypokalemia and encouraged to increase dietary potassium intake if necessary.
The utility of fludrocortisone in preventing recurrent syncope continues to be debated. While many clinicians have found it beneficial, there is little research to support its use. In 2005, Salim and Di Sessa randomized 33 children with a history of syncope and a positive tilt test to receive either fludrocortisone 0.1 mg/day and table salt 1 gram/day or placebo for one year. The average number of syncopal episodes prior to the study was 4.4 ± 4.8. Thirty-two children (mean age 13.9 ± 2.5 years, 20 females) were available at follow-up. Therapy was continued for an average of 176 ± 117 days. Syncopal episodes continued to occur in 10 of 18 children (55%) in the treatment group and 5 of 14 (36%) of the controls (p < 0.05). Patients in both groups experienced an increase in their symptoms after treatment was discontinued, suggesting a significant placebo response.
The impact of fludrocortisone on nausea associated with orthostatic intolerance was evaluated in 17 adolescents (11–17 years of age). All patients had a history of nausea, dizziness, or syncope and a confirmed diagnosis of orthostatic hypotension by tilt table testing. Fludrocortisone was given at a dose of 0.1–0.2 mg/day for a minimum of 4 weeks prior to assessment. The median duration of treatment was 11 weeks (range 4–54 weeks). At 4-week follow-up, 11 patients (65%) had significant improvement, defined as a reduction in nausea severity of more than 50%. One patient (6%) had moderate improvement, one (6%) had mild improvement, and the remaining four patients (24%) had no improvement. The effect of treatment on syncope was not reported. The authors concluded that fludrocortisone treatment appears to improve nausea associated with autonomic-mediated orthostatic intolerance.
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