Endocrine Abstracts

Case history: 48-years old man, with no comorbidities, presented to A&E due to global headache of 20 days duration, with associated intermittent vomiting, but no photophobia, cranial nerve impairment, neck pain or visual disturbance. The first head-scan (CT, computed tomography) was unremarkable, hence was discharged with safety advises. One week later, he represented to A&E with similar complaints. On enquiries, he mentioned to be reviewed by an optician 6 months ago, and was advised to use glasses. Detailed clinical assessment highlighted features of acromegaly, with acral enlargement, prognathism, fleshy nose, macroglossia and prominent eyebrows.

Investigations: The routine biochemistry showed profound hyponatremia 115 mmol/l (normal 135-145), from a baseline of 137 mmol/l previously. Further biochemistry showed serum osmolality 242 mOsm/Kg (normal 275-295), Urine Osmolality 476 mOsm/Kg (normal 50-1400); Urine Na 106 mmol/l. Hormone results were as follows: random early morning cortisol of 65 nmol/l, FT4 15.5 pmol/l (normal 12.0-22.0), TSH 0.13 munit/l (normal 0.3 – 4.2). A repeat head-CT revealed no pathology.

Results and treatment: Given the results, he was started on intravenous hydrocortisone replacement. He received IV Hydrocortisone of 100mg STAT followed by 50 mg QDS. Hypertonic saline as per trust”s protocol was co-administered. A total of 5 doses of 150 ml 2.7% NaCl boluses was given in ITU, with minor improvement of Na to 117 mmol/l. Subsequently, he received 30% NaCl infusion at 5 ml/hour with close hourly monitoring of serum sodium. After achieving a level of 125 mmol/l of serum sodium, he was stepped down to medical ward. His 9AM Pituitary profile showed ACTH <1.5ng/l (normal 2.7 – 63.3); Prolactin 375nU/l (normal 86-324); FSH 5.3 IU/l (1.5-12.4), LH 3.2 (1.7-8.6); Testosterone 3.9 nmol/l (8.6-29.0) with IGF-1 of 47.3 nmol/l (8.5-31) and GH 3.43 mg/l. Urgent MRI Pituitary was done, which showed pituitary macroadenoma, with supra-sellar extension and hyperintense signal keeping with possible haemorrhage. Formal visual field assessment showed bilateral temporal field defects. Glucocorticoid replacement resulted in normalization of electrolytes. The case was discussed in the pituitary MDT and was deemed suitable for routine surgery. He was discharged with plan of outpatient oral glucose tolerance test for formal assessment of GH.

Conclusions: The spectrum of clinical presentation of pituitary apoplexy can be highly variable. Acute hyponatremia is an unusual presentation, especially in context of absent ocular manifestations. Severe glucocorticoid deficiency should be considered as differential in acute hyponatremia.