A Rare Case of Hyponatremia Due to Cerebral Salt Wasting After Transsphenoidal Pituitary Surgery

Friday, May 13, 2022

12:35 PM – 12:50 PM

Location: Station 2, Sapphire West Foyer

Submitter(s)

KH
Katherine Hu, DO
Endocrinology Fellow
Hackensack Meridian Jersey Shore University Medical Center
Asbury Park, New Jersey, United States

Primary Author(s)

KH
Katherine Hu, DO
Endocrinology Fellow
Hackensack Meridian Jersey Shore University Medical Center
Asbury Park, New Jersey, United States

Co-Author(s)

JF
Jonathan Figueroa
KZ
Khin Zin
NP
Nikunjkumar Patel, MD, FACP
Endocrinology Fellow
Jersey Shore University Medical Center
Woodbridge, New Jersey, United States
RO
Raquel Ong
SH
Soemiwati Holland
KC
Krishna Chalasani
JC
Jennifer Cheng, DO
Endocrinology Program Director
JSUMC

Introduction : Hyponatremia is a known complication after transsphenoidal pituitary surgery (TSS), most commonly caused by syndrome of inappropriate antidiuretic hormone secretion (SIADH) and rarely caused by cerebral salt-wasting (CSW). Differentiating between these two etiologies remains a clinical challenge but is important as they have opposing treatments. We present a case of a man who underwent TSS for nonfunctional pituitary macroadenoma and subsequently developed CSW.

Case Description : A 67 year-old man with no significant past medical history presented to the emergency department with sudden-onset headaches. CT head showed a 3.3 cm sellar mass. Dedicated MRI pituitary imaging showed a 3.6 x 2.3 x 2.2 cm sellar mass with superior displacement of the optic chiasm, invasion into the cavernous sinus, and features suggesting pituitary apoplexy. Preoperative biochemical evaluation showed no pituitary hormonal abnormalities. The patient was given dexamethasone to decrease cerebral edema and underwent emergent transsphenoidal pituitary tumor resection. Final pathology showed pituitary adenoma with extensive necrosis and negative staining for ACTH, GH, TSH, and prolactin. Postoperative course was complicated by hyponatremia, central adrenal insufficiency requiring hydrocortisone, and bacterial meningitis requiring IV antibiotics. Serum sodium was 129 mEq/L with corresponding serum osmolality 280 mOsm/kg, urine sodium 117 mEq/L, and urine osmolarity 755 mOsm/kg, suggesting SIADH or CSW. The patient was treated with 1 liter fluid restriction and sodium chloride tablets up to 4 grams three times daily for presumed SIADH. On re-evaluation for refractory hyponatremia, he had orthostatic hypotension with adequate urine output which distinguishes CSW from SIADH. The patient was taken off fluid restriction and received volume repletion with isotonic saline. Serum sodium levels improved with appropriate rate of correction. The patient was discharged home on physiologic dose hydrocortisone and sodium chloride tablets 1 gram three times daily to maintain adequate serum sodium levels.

Discussion : This rare case of a patient with CSW after TSS, complicated by postoperative central adrenal insufficiency and bacterial meningitis, highlights the difficulty in diagnosing the etiology of hyponatremia and the importance of distinguishing CSW from the more common SIADH as the treatments are opposing. When evaluating hyponatremia, we should assess serum osmolality, urine sodium, and urine osmolality. SIADH and CSW can both cause inappropriately concentrated urine, so we must assess volume status to distinguish between the two. SIADH causes euvolemic hyponatremia, whereas CSW causes hypovolemic hyponatremia with positive orthostatics, hypotension, poor skin turgor, decreased central venous pressure, or elevated hematocrit. SIADH is treated with fluid restriction, whereas CWS is treated with volume repletion with either isotonic saline for mild to moderate cases or 3% hypertonic saline for severe cases. Outpatient management with sodium chloride tablets may be necessary as CSW may not resolve until weeks to months from onset.