Endocrine Abstracts

Introduction: The incidence of hospitalised and fatal traumatic brain injury(TBI) is 235/100 000 with an average mortality rate of 15/100 000. A meta-analysis from 19 studies showed a prevalence of hypopituitarism after TBI of 27.5%.

Case report: We report case of 72-year-old man, who suffered traumatic brain injury in October 2021, sustaining multiple skull fractures, with traumatic subarachnoid haemorrhage and subsequent pneumocephalus. He underwent burr-hole surgery with an extended stay on the neurosurgery ITU. After returning to ward, he started vomiting, became tachypnoeic, hypotensive and suffered a PEA cardiac arrest. ROSC was achieved and he was taken to ICU. During ITU stay he required adrenaline boluses followed by noradrenaline infusion to maintain his blood pressure. He was given stress dose of steroids during his subsequent ITU stay. He developed hyponatraemia that was attributed to SIADH, cortisol was not checked on admission. He was stepped down from ITU to ward and was noted to have postural hypotension and continuing hyponatraemia. He received a long acting steroid injection in knee for pseudogout and was manged with intravenous fluid and slow sodium tablets. He was discharged in February 2022 but developed ongoing symptoms-persistent tiredness and weight loss. His symptoms worsened in April 2022 when he presented to his GP with dizzy spells and was found to have postural hypotension and ongoing hyponatraemia. He was prescribed slow sodium tablets and fludrocortisone. He had a syncopal episode while on holiday and was admitted to hospital. He had hyponatraemia and was confused on admission. He subsequently underwent short Synacthen test and was diagnosed as having secondary adrenal insufficiency. He was then commenced on replacement hydrocortisone.A full pituitary hormone profile was completed. This showed evidence of secondary hypothyroidism and secondary hypogonadism. He was subsequently started on Levothyroxine and testosterone replacement, MRI pituitary showed partial pituitary damage with residual intact normal tissue.

Discussion: Pituitary dysfunction after TBI is a common complication. Postulated mechanisms of pathophysiology include primary injury caused by direct trauma and secondary involvement due to illness, hypotension and infarction. Unrecognised hypocotisolism related to pituitary dysfunction after TBI can be life threatening. In our patient, while he was inpatient had a long-acting steroid injection and stress-doses of steroid that may have temporarily protected him from symptoms of secondary adrenal insufficiency. His low sodium during admission was attributed to SIADH but secondary adrenal insufficiency should always be suspected in patients of TBI having hyponatraemia or/and hypotension.