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Cerebral salt wasting syndrome

VACCA, VINCENT M. JR. RN, CCRN, MSN

ACTION STAT

Act fast to manage life-threatening fluid volume depletion.

Clinical Nurse Educator, Neuroscience Intensive Care Unit, Brigham and Women's Hospital, Boston, Mass.

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EARLIER TODAY, Sam Pappageno, 60, was clinically stable. But now when you assess him, you find that he can't follow simple commands, has orthostatic hypotension, and is oliguric with dry mucous membranes. You take his vital signs: BP, 100/60; heart rate, 120 beats/minute; respirations, 16; temperature, 98.6° F (37° C); and SpO2, 95% on room air.

You notify the health care provider, then administer supplemental oxygen by nasal cannula at 2 liters/minute and perform a focused neurologic assessment. Start an I.V. infusion of 0.9% sodium chloride solution, insert an indwelling urinary catheter, obtain a stat 12-lead ECG, and send blood and urine samples for testing as ordered.

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What's the situation?

Three days ago, Mr. Pappageno had a resection of a benign noninvasive pituitary adenoma. His recovery seemed to be going well, but now he's exhibiting signs and symptoms of intravascular volume depletion and deterioration in level of consciousness. Lab tests reveal serum sodium of 119 mEq/liter (normal range, 134 to 146 mEq/liter), blood urea nitrogen of 75 mg/dl (normal range, 8 to 25 mg/dl), and serum osmolality of 270 mOsm/kg (normal range, 274 to 296 mOsm/kg). His urine sodium level and urine osmolality are both elevated, and the other results are within normal limits.

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What's your assessment?

Based on Mr. Pappageno's recent brain injury, hyponatremia, and dehydration, as well as his other signs and symptoms, you suspect one of two similar central nervous system complications—either cerebral salt wasting syndrome (CSWS) or syndrome of inappropriate antidiuretic hormone secretion (SIADH).

Patients with CSWS have decreased plasma volume, decreased extracellular fluid, and primary hyponatremia. In contrast, those with SIADH have increased plasma volume, increased extracellular fluid, and dilutional hyponatremia. Differentiating the two disorders is critical because fluid restriction, the treatment for SIADH, would place the patient with CSWS at high risk for vasospasm and cerebral ischemia, increasing the risk of secondary brain injury. The patient with CSWS needs fluid volume and sodium replacement.

In a patient with a traumatic brain injury, CSWS usually appears within the first week after injury. It may also develop in a patient with other acute central nervous system disorders, such as stroke or intracranial surgery.

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What must you do immediately?

The infusion you started earlier of 0.9% sodium chloride solution will begin to treat Mr. Pappageno's hyponatremia and hypovolemia. The health care provider inserts a pulmonary artery catheter to administer hypertonic saline and monitor central venous pressure and fluid balance.

The health care provider may also prescribe fludrocortisone, a mineralocorticoid, to enhance sodium reabsorption in the distal renal tubules.

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What should be done later?

Mr. Pappageno's intravascular volume depletion and hyponatremia were corrected, and his ongoing sodium loss replaced via I.V. infusion of saline solutions. Cerebral salt wasting syndrome usually resolves spontaneously in 2 to 4 weeks.

The rest of Mr. Pappageno's recovery is uneventful and he's discharged home 1 week later, with detailed instructions about his medications, symptoms to report to the health care provider, fluids, and activity. He'll get follow-up home visits from the visiting nurse association.

© 2005 Lippincott Williams & Wilkins, Inc.