Refractory hyponatremia post-TBI unmasks secondary adrenal insufficiency from remote steroid use

Post-traumatic brain injury (TBI) is frequently complicated by hyponatremia, often attributed to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). However, differentiating SIADH from other causes, such as adrenal insufficiency, can be challenging, especially when standard treatments fail. Secondary adrenal insufficiency, particularly from prior exogenous corticosteroid use, can lead to prolonged suppression of the hypothalamic-pituitary-adrenal (HPA) axis, making diagnosis difficult years after cessation.

A male patient in his early 60s developed persistent hyponatremia following lumbar spine surgery complicated by TBI with subarachnoid hemorrhage. Initial evaluation indicated hypotonic hyponatremia with inappropriately concentrated urine, consistent with SIADH. Standard therapy, including hypertonic saline and oral sodium supplementation, provided only transient improvement. Given a history of secondary adrenal insufficiency due to long-term topical corticosteroid use, adrenal function was reassessed via an adrenocorticotropic hormone (ACTH) stimulation test.

The ACTH stimulation test definitively confirmed secondary adrenal insufficiency in the patient. This diagnosis clarified the underlying cause of the previously refractory hyponatremia. The patient's serum sodium levels, which had been persistently low despite conventional SIADH management, showed a dramatic and sustained improvement following the new therapeutic approach. This highlights a critical diagnostic pathway often overlooked in complex neurological cases. The resolution of hyponatremia was directly attributable to the targeted hormonal replacement.

Initiation of hydrocortisone therapy led to sustained normalization of serum sodium.