Introduction: The triphasic response to pituitary stalk injury encompasses an initial phase of diabetes insipidus (DI), followed by anti-diuretic hormone (ADH) mediated hyponatremia and a subsequent phase of diabetes insipidus. It is uncommonly seen post-pituitary surgery and its occurrence after traumatic brain injury (TBI) is even less recognized. We present a case of classic triphasic response post TBI.
Case Description: A 24-year-old Female presented to the Emergency Department after a road traffic accident where she had been flung from a motorcycle. She sustained bilateral maxillary and facial fractures, dental injuries, mild lung contusions and lacerations. She was adjudged to have mild traumatic brain injury based on computed tomography findings of small subarachnoid hemorrhage.
She had initial hypernatremia with peak serum sodium of 160 mmol/L, serum osmolality of 340 mmol/kg and urine osmolality of 225 mmol/kg. This suggests partial DI, which improved with hypotonic fluid administration and did not require desmopressin therapy. Serum cortisol and thyroid function tests were normal. No features of pituitary apoplexy were seen on the computed tomography scan. Magnetic resonance imaging was contraindicated post-facial fracture fixation.
On day 7 post injury, she developed severe hyponatremia with serum sodium nadir of 118 mmol/L. The serum osmolality was 256 mmol/kg and the urine osmolality was 864 mmol/kg, which suggests severe ADH mediated hyponatremia. She was managed aggressively with fluid restriction, nutritional supplementation and high dose oral salt loading with good effect. After 7 days of hyponatremic phase, she developed polyuria with mild hypernatremia and dilute urine. She responded well to a trial of oral desmopressin and was discharged to a rehabilitation facility.
Discussion: Diabetes insipidus is an uncommon sequela of TBI. It has been attributed to pituitary vascular injury, diffuse axonal injury to the hypothalamus or direct pituitary stalk damage from trauma. It can occur in the absence of anterior pituitary failure. While severity of brain injury does correlate to likelihood of DI, permanent DI has been described even in mild TBI.
As symptoms of hyponatremia or hypernatremia may be non-specific and may be masked by depressed consciousness post-injury, careful laboratory and urine output monitoring coupled with clinical vigilance is required to make the diagnosis. To avoid significant morbidity and mortality, careful use of desmopressin, sodium supplementation and fluid restriction is required. Knowledge of the expected time course and expectant titration of intervention can help to avoid rapid fluctuations in serum sodium levels.
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