Case Presentation:
A 51‐year‐old woman with a history of glioblastoma multiforme resection and meningitis presented with mental status changes. Ventriculostomy was performed for hydrocephalus, and CSF revealed recurrent staph meningitis. Antibiotics were started. The RNs then noticed the patient heavily salting all her food. Her urine output was 300‐500 cc/hour. Serum sodium was 135. The neurosurgical team sent labs, started ½ NS, and gave desmopressin for presumed DI. A hospitalist consult was called. Lab studies prior to desmopressin revealed serum Na of 135, urine osmolarity of 425, urine Na of 193, and serum osmolarity of 288. Physical exam and labs showed dehydration with I/Os of 2600/5000 cc, tachycardia, and BUN/CR of 19/.6. Given the patient's polyuria, high urine Na, and dehydration, the diagnosis of cerebral salt wasting (CSW) was made. The relatively normal serum sodium was felt to be a result of the patient's high salt intake. She was placed on normal saline. Because the patient had received desmopressin, we expected SIADH to develop with hyponatremia. The following morning her volume status and polyuria had normalized, but serum sodium had dropped to 128. Serum osmolarity was now 269, and urine osmolarity was 998. Urine Na was 219. Free water restriction was started for SIADH, and her serum Na was corrected to 135 over the next few days.
Discussion:
Polyuria and hyponatremia in neurosurgical patients are common and often present a diagnostic and therapeutic challenge. CSW occurs in patients with subarachnoid hemorrhage but rarely in patients with meningitis. SIADH is common in many forms of CNS disease. Identifying the correct cause of high urine output and hyponatremia is critical for initiating correct therapy, especially because choosing the wrong diagnosis and therapy can significantly worsen the patient's condition. DI presents with hypernatremia and low urine osmolarity and was quickly ruled out in this case. Both SIADH and cerebral salt wasting present with low serum osmolarity, high urine osmolarity, and high urine Na, but CSW presents with polyuria and dehydration. Our patient fit the clinical profile of CSW, which is treated with volume and salt replacement. Because hyponatremia persisted after urine volume normalized and hydration status was corrected, we reevaluated our patient. The persistently low serum osmolarity and Na with elevated urine Na then suggested SIADH. The treatment of SIADH is free‐water restriction, so the treatment plan was altered. After receiving the 2 very different therapeutic approaches, the patient had correction of her polyuria and hyponatremia with a good clinical outcome.
Conclusions:
It is very unusual for a patient to develop both CSW and SIADH during the same hospitalization. This case illustrates a patient with initial CSW that then progressed to SIADH at first due to desmopressin then to her multiple CNS insults. Hospitalists should repeatedly evaluate hydration status and urine volume in the hyponatremic neurosurgical patient in order to make the correct diagnosis and choose the appropriate therapy.
Author Disclosure:
T. Tassava, none; P. Almalouf, none.