Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2009) 19 P253

SFEBES2009 Poster Presentations Pituitary (56 abstracts)

A case of headache and severe hyponatraemia – SIADH or pituitary apoplexy?

R Merriman , A Eggins , A Nasruddin , M Cummings & P Kar


Queen Alexandra Hospital, Portsmouth,UK.


History: A 62-year-old female presented to casualty with headache and hyponatraemia (Na 113 mmol/l) on the background of nausea and vomiting, preceded by sudden onset occipital headache 10 days previously. Other routine blood results were unremarkable apart from K 3.4 mmol/l.

Biochemical investigations were consistent with SIADH. (Serum osmolality 233 mos/kg, urine 641 mos/kg, urinary Na 43 mmol/l). Early morning cortisol on admission was 828 nmol/l.

Examination on admission was unremarkable with no focal neurology. There was suggestion of coarse facial features. Patient was euvolaemic with a BP of 140/90 mmHg. CT head was initially reported as completely normal.

Hormonal profile suggested hypogonadotrophic hypogonadism (LH 4.0 iu/l, FSH 24.1 iu/l, prolactin 120 miu/l, TSH 1.82 mU/l, free-T4 9.4 pmol/l, oestradiol <50 pmol/l).

Her biochemistry was suggestive of SIADH and/or pituitary pathology. The differential diagnosis included subarachnoid haemorrhage and pituitary apoplexy. An MRI showed recent haemorrhage into a pituitary macroadenoma (15 mm×14 mm×13 mm). Hyponatraemia improved but remained abnormal with fluid restriction (120 mmol/l). Repeat 0900 a.m. cortisol 3 days post admission dropped to 295 nmol/l. Hydrocortisone replacement therapy was commenced. Following 24 h of steroid replacement her Na improved to 128 mmol/l and she felt clinically better.

On closer questioning she revealed her feet had enlarged by two shoe sizes in 4 years, she had noticed teeth irregularity and thought her nose had increased in size suggesting the possibility of acromegaly.

Discussion: Acute headache is a common presentation and it is important to keep in mind the differential diagnosis of pituitary apoplexy, especially on the background of a clinical suspicion of pituitary disease.

An additional learning point is that a ‘normal’ random cortisol does not rule out acute pituitary pathology. It is interesting to note the drop in 0900 a.m. cortisol levels, possibly indicative of a developing adrenal insufficiency. One should also bear in mind that biochemistry indicative of SIADH can be mimicked by cortisol deficiency.

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