Hypopituitarism secondary to pituitary apoplexy is a rare but recognised complication following cardiac surgery but not cardiac arrest.
We present a case report of acute pituitary apoplexy following a cardiac arrest on a background of sepsis. A 65-year-old gentleman presented with 3-day history of abdominal pain and vomiting. Of note, he underwent an appendicectomy 2 months earlier. He was septic and investigations revealed bowel perforation with faecal peritonitis. He underwent a hemicolectomy within 24 h of admission, but unfortunately suffered a cardiac arrest intra-operatively. Two cycles of CPR were administered after which his rhythm switched from PEA to pulseless ventricular fibrillation. He was cardioverted successfully to sinus rhythm and admitted to ITU. His blood pressure remained low and he required inotropic support. His serum sodium fell to 130 mmol/l over the next couple of days post his cardiac arrest. Hypo-cortisolaemia was suspected and a short Synacthen test performed. This showed an inadequate response with baseline morning cortisol of 69 nmol/l and a peak cortisol of 286 nmol/l at 60 min. ACTH was undetectable.
Pituitary profile suggested pan-hypopituitarism: TSH 0.18 mIU/l, free T4 <5.2 pmol/l, free 3 <1.5 pmol/l, LH 1.0 IU/l (NR 212 IU/l), FSH 1.5 IU/l (NR 1.78.0 IU/l), testosterone <0.3 nmol/l, prolactin 75 mU/l, GH <0.05 μg/l, and IGF1 5.8 nmol/l (NR 636 nmol/l). Pituitary MRI findings were suggestive of an infarct within an existing right sided pituitary tumour. He has since been started on hydrocortisone, thyroxine and testosterone replacement therapy.
Given the clinical presentation, we felt that a period of systemic hypo-perfusion during the cardiac arrest led to ischaemia and infarction of the existing pituitary tumour causing pan-hypopituitarism.
The prevalence of pituitary tumours is estimated at 17% and therefore it is important to consider the possibility of pituitary apoplexy in patients post cardiac arrest especially in the presence of hyponatraemia and hypotension.