Endocrine Abstracts

Introduction: Pituitary apoplexy is essentially bleeding into a necrotic area of the pituitary tumour, which has presumably outgrown its blood supply and caused infarction. Usually this is a haemorrhagic infarction but rarely a non-haemorrhagic infarction can cause marked pituitary swelling and presents as pituitary apoplexy. Our case represents a typical case of pituitary apoplexy with rapid evolving neurological deficit due to pituitary necrosis rather than haemorrhage.

Case: A 66-year-old taxi driver who was previously fit and well presented with seven days history of severe frontal headache associated with vomiting and photophobia. He also reported blurred vision around ‘edges’ of vision and dizziness on standing. Urgent CT head was done in pursuit of subarachnoid haemorrhage showed a large iso-dense pituitary mass with supra-sellar extension and bony erosion of the sella. There was no evidence pituitary haemorrhage. Visual field testing by 120 point Humphrey fields revealed bitemporal hemianopia. Next day MRI pituitary showed a 3.6 cm pituitary mass extending superiorly to indent and displace the inferior surface of the frontal lobe. The optic chiasm was compressed by the tumour, which was also extending laterally and abutting both internal carotid arteries. Again there was no evidence of bleed within the tumour. On the second day of admission he developed right third nerve palsy with diplopia and ptosis of the right eye. Later on during the same day his visual acuity deteriorated to fingers counting. He was operated urgently by transphenoidal debulking of pituitary tumour. The tumour capsule was tough (unusual for an apoplexy) and difficult to remove. Preoperative hormonal profile: random cortisol 80 nmol/l, FT₄ 8.6 pmol/l, TSH 0.39 mu/l, prolactin 203 mu/l, FSH 1.6 iu/l, LH 0.3 iu/l and testosterone 0.6 nmol/l. Necrotic and barely viable pituitary tissue was seen on pituitary histopathology. Reticlin stain showed expanded effaced retculin and hormonal stains were negative for all hormones. He made an excellent recovery with complete resolution of his visual acuity and field defect. His 3rd nerve palsy had almost recovered with only subtle mild medial rectus weakness. He was started on hormonal replacement therapy with hydrocortisol, thyroxine and testosterone and he is back to his normal life, driving his car without any problem. Two follow up MRIs showed small remnant tumour with no evidence of change in size or compression of adjacent tissue.