Endocrine Abstracts

Case history: A 28 year old male presented following his first generalised tonic clonic seizure in the context of a headache with mild photophobia, nausea and vomiting. He was haemodynamically stable, euvolaemic and had no focal neurological deficit, but was mildly disoriented. He had reported cannabis and MDMA use 8 days prior to his presentation. The patient was profoundly hyponatraemic with a serum sodium of 108.

Investigations: Serum osmolality was 223, urinary osmolality 676 and urinary sodium 55. Bloods revealed hypopituitarism, with hypocortisolaemia (8am cortisol 64), hypothyroidism (TSH 0.33, T4 7.1), and hypogonadtrophic hypogonadism (LH 0.4, FSH 2.2, testosterone 0.6). ACTH was less than 1, and IGF-1 and prolactin were normal. An MR pituitary revealed a large sella mass, with an expanded sella turcica and compressed optic chiasm. Visual acuity and fields were intact. Pituitary antibodies were negative and serum ACE normal.

Results and treatment: The patient was managed conservatively for hypopituitarism secondary to a non-haemorrhagic pituitary apoplexy (PA) complicating a pre-existing pituitary lesion of unknown aetiology. He received fluid therapy, including hypertonic 1.8% saline, intravenous hydrocortisone, levothyroxine replacement and empirical IV ceftriaxone. Due to a rapid rise in serum sodium, desmopressin was introduced to control the serum sodium. Once stabilised, the patient was discharged on oral hydrocortisone, thyroxine and desmopressin. Subsequent MR pituitary scans revealed a reduction in the size of the pituitary lesion, with resolution of the chiasmal compression. Minor high T1 signal was noted, suggestive of a resolving intralesional haemorrhage.

Conclusions and points for discussion: Numerous pathologies from neoplasia and infiltrative conditions to granulomatous disease may be implicated in the aetiology of hypopituitarism. The expanded sella turcica suggested an element of chronicity, consistent with a longstanding pituitary lesion. The patient was clinically well-androgenised, however, highlighting that an acute decompensating insult, such as an apoplexy, precipitated the presentation. MDMA use may have contributed to the clinical picture: it can produce hyponatraemia by stimulating the secretion of antidiuretic hormone, by acting on aquaporin 2 channels in the collecting duct to increase fluid retention and by producing neurogenic primary polydipsia.

PA, defined as infarction or haemorrhage typically into an underlying pituitary adenoma, has a wide spectrum of manifestations. It classically presents with a sudden onset severe headache with nausea, vomiting, impaired consciousness, ophthalmoplegia and haemodynamic instability. It can, however, present subacutely or remain clinically silent. Initial management is supportive with intravenous fluids, corticosteroids and replacement of deficient hormones. After initial stabilisation, patients with severely impaired visual acuity, persistent visual field deficits or impaired consciousness may be considered for neurosurgical decompression.