A 67-Year-Old Woman With Orthostatic Hypotension and Edema

Catherine Anastasopoulou, MD, PhD; Kimberly Lessard, DO


March 08, 2018

The patient in this case required treatment with both hydrocortisone and fludrocortisone. Because her morning cortisol confirmed deficient glucocorticoid levels, replacement with hydrocortisone was absolutely necessary. Hydrocortisone is most often initiated twice daily to match the diurnal pattern of cortisol release. Certain elements of this patient's presentation, including hypotension and hyponatremia, are reflective of a significant mineralocorticoid deficiency. As a result, mineralocorticoid replacement therapy with fludrocortisone was also indicated. Fludrocortisone acetate, a prodrug to fludrocortisone, is a synthetic oral adrenocortical steroid with potent mineralocorticoid properties and also moderate-high glucocorticoid effect.

In primary adrenal insufficiency, both mineralocorticoid and glucocorticoid deficiency can lead to the development of adrenal crisis. Hypotension can be seen in all forms of adrenal insufficiency; however, primary adrenal insufficiency may also cause significant intravascular volume depletion related to the degree of mineralocorticoid involvement. Mineralocorticoid (ie, aldosterone) deficiency leads to decreased sodium retention and subsequent volume depletion. Insufficient aldosterone also leads to suppressed vasoconstrictive response, causing decreased blood pressure and orthostatic changes. Glucocorticoid deficiency alone can also potentiate hypotension due to decreased vascular response to the effects of angiotensin II and norepinephrine, as well as decreased renin and increased prostacyclin production. In primary adrenal insufficiency, dual therapy with both an oral glucocorticoid (hydrocortisone) and an oral mineralocorticoid (fludrocortisone) is required to achieve adequate and balanced adrenocortical replacement.

No male or female hormone replacement, such as dehydroepiandrosterone (DHEA), is required in similar patients because those hormones are not affected by the adrenal dysfunction. Furthermore, replacement with salt tablets is inappropriate in patients such as the one in this case. IV normal saline should be used in the initial treatment of hyponatremia related to primary adrenal insufficiency if signs of significant volume depletion are present. Initiation of fludrocortisone should be performed immediately to improve sodium retention. Patients can be encouraged to liberalize their sodium intake but are unlikely to require sodium tablets to normalize blood sodium levels or blood pressure.

Along with IV fluids, the patient in this case was started on twice-daily hydrocortisone (20-mg morning dose, 10-mg evening dose) as well as fludrocortisone (0.05 mg orally daily). Furosemide was discontinued. At the time of discharge, the patient's sodium had improved to 138 mmol/L, and her blood pressure averaged 115/71 mm Hg. At follow-up, she was found to have stable blood pressure (118/73 mm Hg) without orthostasis and was noted to have improvement in her mentation and fatigue. She had no further falls and also had marginal improvement in her lower extremities. Repeat chemistry from this visit revealed a sodium level of 143 mmol/L, a potassium level of 4.1 mmol/L, and a glucose level of 138 mg/dL. At this point, her hydrocortisone was reduced to a once-daily morning dose of 20 mg.

The patient will have repeat chemistry as well as a cortisol levels obtained in the upcoming weeks to assess for the potential return of adrenal function. Given the etiology of her primary adrenal failure, significant gain in adrenal function is not expected, and long-term glucocorticoid and mineralocorticoid replacement therapy is likely required.


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