A 32-year-old man was admitted to The Alfred Hospital, Melbourne, Australia in December 2010 following a high-speed motorcycle accident with an initial Glasgow coma score (GCS) of 14. In addition to a TBI, he sustained C4 to C7 ligamentous damage, multiple fractures of the pelvis, ribs, sternum and facial bones, and significant soft-tissue trauma. By day 2 of admission, his GCS had normalised. Despite a mild TBI and the absence of structural damage on CT and MRI brain imaging, he developed post-traumatic amnesia and subjective long-term cognitive deficits preventing him from returning to work. Formal neuropsychiatric evaluation and functional imaging was not performed, so there was no objective evidence of permanent brain damage. The GCS was introduced as a method for determining the severity of brain dysfunction 6 h after head trauma and cannot predict long-term cognitive function, so it likely underestimated the impact of this injury on our patient's long-term cognitive function. On day 3 of his admission, he developed hyponatremia consistent with SIADH: serum sodium 117 mmol/l (reference range: 135-143), serum osmolality 247 mmol/kg (280-300), urine sodium 112 mmol/l (>30) and urine osmolality 920 mmol/kg. He was symptomatic with nausea, but cognition remained intact with a GCS of 15. He was clinically euvolemic with a urine output of 100 ml/h and an overall minor positive net external fluid balance (total daily fluid input 2600 ml, total daily fluid output 2450 ml). His thyroid function was normal: fT4 15.5 pmol/l (9.1-19.6), TSH 2.29 mU/l (0.3-5), and repeated cortisol levels were robust: day 4 admission 0820 h cortisol 357 nmol/l (100-540), day 6 admission 0910 h cortisol 583 nmol/l. An MRI pituitary was also performed, which was normal. An insulin tolerance test was not performed as repeated cortisol levels were considered sufficient especially a value >550 nmol/l. Furthermore, it might be unsafe to perform in a head-injured patient at least in the acute setting. He was not taking any medications at the time of presentation and denied a history of illicit drug use. Temporary 1.5 l fluid restriction normalized sodium levels. Following discharge to a rehabilitation unit he experienced recurrence of moderate hyponatremia, again consistent with SIADH, requiring long-term fluid restriction. Over the subsequent 3 years, he was advised to adhere to 1.2 l fluid restriction, which only maintained serum sodium levels of 128-130 mmol/l. Adherence was difficult, resulting in nine hospital admissions due to worsening hyponatremia with symptoms including nausea and malaise. On each occasion biochemistry remained consistent with SIADH and serum sodium improved with tight fluid restriction as low as 500 ml daily. Psychogenic polydipsia is an important consideration in those presenting with recurrent euvolaemic hyponatraemia, but the fluid restriction required in this case to achieve normonatraemia was severe and inconsistent with a diagnosis of psychogenic polydipsia. There was no evidence of hypopituitarism, malignancy, intercurrent pulmonary disease or nervous system disorders during this time, and pain was well controlled on paracetamol and buprenorphine. The etiology of his chronic SIADH was considered to be most likely secondary to prior TBI. He was most recently admitted in September 2014, presenting with several hours of nausea, malaise and anorexia in the context of not adhering to his fluid restriction. He was clinically euvolaemic. Biochemistry was consistent with SIADH: serum sodium 119 mmol/l, serum osmolality 253 mmol/kg, urine sodium 119 mmol/l, urine osmolality 764 mmol/kg, TSH 0.55 mU/l (0.3-5), fT4 12.6 pmol/l (9.1-19.6), cortisol at 0600 h 347 nmol/l (100-540). Serum sodium improved with a daily 500 ml fluid restriction. 
Please refer to the preceding case description.