Successful treatment of adult cerebral salt wasting with fludrocortisone.

Report of a Case. A 75-year-old man presented with a 3-week history of worsening ataxia following blunt head trauma in a motor vehicle crash 1 month earlier. His history included uncomplicated type 2 diabetes mellitus and hypertension, managed with rosiglitazone, 4 mg/d, and ramipril, 2.5 mg/d. The patient was confused and had marked truncal ataxia. Central venous pressure was low at 3 mm Hg, indicating volume depletion. Euglycemia and normotension were maintained following the discontinuation of both rosiglitazone and ramipril therapies. A computed tomographic scan of the brain demonstrated acute and chronic bilateral frontoparietal subdural hematomas measuring up to 22 mm in the maximum dimension, with shift of the septum pellucidum to the right by 5 mm and subfalcine herniation. Findings from serum biochemical analysis demonstrated a serum sodium level of 123 mEq/L (137-146 mEq/L) (milliequivalents per liter to millimoles per liter is a 1-to-1 conversion); an osmolality of 259 mOsm/kg (275-295 mOsm/kg) (milliosmoles per kilogram to millimoles per kilogram is a 1-to-1 conversion), a uric acid level of 0.34 mg/dL (4.2-8.4 mg/dL) (to convert to micromoles per liter, multiply by 59.485), a urinary sodium level of 236 mEq/L; and a urinary osmolality of 825 mOsm/kg. Hypothyroidism, hypoadrenalism, and liver and renal failure were excluded from serum biochemical analysis. Findings from serum biochemical analysis performed 1 month prior immediately following the motor vehicle crash were normal. Bilateral burr holes were made for drainage, with subsequent reduction in size of bilateral hematomas. Hyponatremia was corrected with 3% hypertonic saline. Withdrawal of hypertonic saline 3 days later led to a decrease in serum sodium level to 120 mEq/L (Figure). Hypertonic saline was reintroduced to maintain a serum sodium level above 125 mEq/L. A repeated attempt to withdraw hypertonic saline 3 days later again led to a fall in serum sodium level with persistent inappropriate natriuresis (Figure). N-terminal pro-brain natriuretic peptide level was not elevated. Plasma renin activity and aldosterone concentration measured on day 6 were undetectable. Treatment with fludrocortisone was commenced initially at 0.2 mg/d and later reduced to 0.1 mg/d, and a rapid reduction in natriuresis and restoration of serum sodium level to the normal range was observed (Figure).