A 45-year-old male is admitted to the ICU following a severe traumatic brain injury (TBI) with subarachnoid hemorrhage. To manage cerebral edema, he is receiving intermittent doses of mannitol and a continuous 3% hypertonic saline infusion. By day 3 post-injury, he develops polyuria and a rising serum sodium level that has now reached 164 mmol/L. Despite aggressive fluid replacement, his serum sodium continues to climb, and he develops hypotension, necessitating further fluid resuscitation. Laboratory results reveal a creatinine of 1.6 mg/dL (baseline 0.9 mg/dL), low urine sodium concentration, serum hypernatremia, and high plasma osmolality.
The ICU team is now facing a diagnostic and therapeutic dilemma: Is this Diabetes Insipidus (DI), Cerebral Salt Wasting (CSW), or a combination influenced by hyperosmolar therapies and mild renal impairment?