ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2012) 28 P269

A case report of hypopituitarism following recovery from cardiac arrest - a poorly recognised sequelae?

Stonny Joseph1, Mark Fenton2 & Edward Kearney3

1Department of Diabetes and Endocrinology, Queen Elizabeth the Queen Mother Hospital, Margate, United Kingdom; 2Department of Cardiology, Kent and Canterbury Hospital, Canterbury, United Kingdom; 3Department of Clinical Biochemistry, Queen Elizabeth the Queen Mother Hospital, Margate, United Kingdom.

Hypopituitarism is a recognised complication of pituitary and hypothalamic pathology. It can also be a consequence, less commonly, of traumatic brain injury. It has never been described in patients following recovery from a cardiac arrest. We present a case history of hypopituitarism following successful cardiopulmonary resuscitation for a ventricular tachycardia (VT) cardiac arrest. A 51 year old patient with known prolonged QT (Romano ward) syndrome and chronic obstructive airways disease was admitted into ITU with Type 2 respiratory failure. During his in patient stay he had a VT cardiac arrest and after 10 mins of CPR he was resuscitated and temporary paced. He eventually required an intra-cardiac defibrillator (ICD) and maintained on propanolol. In the ensuing 4 months post discharge, he noticed loss of secondary sexual characteristics, lethargy, reduced libido, and dizzy spells. Routine investigations did not show any abnormality although he was noted to be hyponatraemic with sodium of 131 mmol/L. His symptoms were attributed to his medication. He re-presented 2 years later with worsening lethargy and further weight gain. Baseline Pituitary function tests done after referral to the endocrine clinic, revealed a TSH 1.5 mIU/L, T4 6 pmol/lL, Cortisol <30 nmol/l, FSH <0.5 IU/L, LH <0.5 IU/L, Testosterone <0.5 nmol/l, Prolactin 35 mU/L and IGF-1 3.9 nmol/l (NR 9–40 nmol/l). He had a flat growth hormone response to dynamic testing. An enhanced CT scan (MRI scan contraindicated) revealed a very small pituitary parenchyma with appearances suggestive of empty sella syndrome. He was commenced on hydrocortisone, thyroxine and growth hormone replacement therapy with significant symptomatic improvement. Our case report suggests that hypopituitarism could be a sequelae following recovery from a cardiac arrest. A postulated mechanism could be pituitary hypoperfusion and hypoxaemia resulting in pituitary infarction. This case study highlights the need to consider pituitary pathology and investigations in patients who present with persistent non-specific symptoms post recovery from a cardiac arrest.

Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.

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