Endocrine Abstracts

Background: Cranial diabetes inspidus (DI) may be familial or acquired. Traumatic brain injury is an important cause of acquired cranial DI, occurring in up to 22% of patients with moderate or severe head injuries¹.

Case 1: A 20-year-old male was admitted following a road traffic accident (RTA) with polytrauma including several skull fractures, subdural haematoma, and pneumocephalus. The following day, he developed polyuria and polydipsia. Biochemistry was suggestive of DI (serum osmolality-301 mOsm/kg, Serum Na 141, urine osmolality 86 mOsm/kg, urine Na- <10 mmol/l). He was managed conservatively for his neurosurgical injuries, but underwent intervention for a comminuted mandibular fracture. He was started on oral desmopressin 100 μg mane and 200 μg nocte with good clinical response. Anterior pituitary function was normal. At 6 months, he is well and off desmopressin.

Case 2: A 23-year-old male presented with a 4 week history of polydipsia and polyuria which started within 24 h of RTA. He had a small intracranial bleed but required no surgical intervention. He had mild hypernatraemia(147 mmol/l) with an elevated serum osmolality (303 mOsm/kg) and inappropriately low urine osmolality (70 mOsm/kg). Calcium, potassium, glucose, and anterior pituitary function tests were normal. His symptoms and biochemistry normalised rapidly after a dose of Desmopressin. MRI pituitary showed loss of the posterior pituitary bright spot. He was started on desmopressin nasal spray 10 μg morning and 20 μg night time. He remains asymptomatic on same dose of Desmopressin at 18 months post head injury.

Discussion: Both syndrome of inappropriate ADH and DI are common immediately post head injury. Most of these patients recover, however a small but significant number (6.9%) are left with permanent DI¹. Water intake may be inadequate in the early post head injury period due to impaired cognition, physical disability, or coexisting hypodipsia with potentially serious consequences¹. In contrast to DI, anterior pituitary hormone deficiencies may develop many years after head injury^2.

Reference: A Agha et al. Posterior pituitary dysfunction after traumatic brain injury. The Journal of Clinical Endocrinology & Metabolism 89(12) 5987–5992.

S Benvenga et al. 2000 Hypopituitarism secondary to head trauma. The Journal of Clinical Endocrinology & Metabolism.