Pituitary infarction: a potentially fatal cause of postoperative hyponatraemia and ocular palsy

Abstract

PRACTICEThe patient presented to his general practitioner nine days after surgery with his right eye completely closed and a mild intermittent headache. On examination he was clinically normovolaemic and had no features of hypopituitarism. He had right sided ptosis and a sluggishly reactive and slightly dilated right pupil. He had normal abduction but moderate restriction of right eye movements in all other directions, consistent with an isolated partial right oculomotor nerve palsy. His visual acuity and visual fields were normal. He was admitted under neurosurgery and a diagnosis of posterior communicating artery aneurysm was considered.He was hyponatraemic, with a sodium value of 128 mmol/L (reference range 136-146), and fluids were immediately restricted to 1 L per 24 hours. Magnetic resonance imaging and magnetic resonance angiography of the head incidentally showed an enlarged pituitary gland, with diffuse high T1 signal consistent with a sub acute pituitary haemorrhage. He showed no evidence of a posterior communicating artery aneurysm. Pituitary magnetic resonance imaging two days later ( fig 1A) showed a bilobed haemorrhagic intrasellar/suprasellar mass measuring 14×13×12 mm, consistent with haemorrhage into a pituitary macroadenoma. The mass extended into the roof of the right cavernous sinus, where it abutted the right oculomotor nerve at its peripheral aspect.Despite fluid restriction, the next day (postoperative day 10) plasma sodium was 129 mmol/L, urine sodium was 55 mmol/L, and urine osmolality was inappropriately high (626 mmol/kg). Plasma cortisol at 9 am was low (51 nmol/L; 250-800), free thyroxine was also low (7 pmol/L; 10-24), and thyroid stimulating hormone was normal (0.49 mIU/L; 0.4-4.0), consistent with secondary hypoadrenalism and hypothyroidism. The cortisol result was not available until a day later (postoperative day 11), and at that stage intravenous (50 mg eight hourly) and later oral hydrocortisone supplementation was started, after which the hyponatraemia promptly resolved (fig 2). He was maintained on oral hydrocortisone (15 mg at 8 am, 5 mg at 3 pm) and daily thyroxine (50 μg).Further pituitary function tests showed luteinising hormone and follicle stimulating hormone values of 0.4 IU/L (2-8) and 1.9 IU/L (2-14), respectively, and total testosterone was also low at 1.1 nmol/L (9-38), confirming secondary hypogonadism. Prolactin and insulin-like growth factor 1 were within normal limits. Two days after the markedly low cortisol measurement, plasma adrenocorticotrophin was normal at 9.2 pmol/L (1-12). During admission his right eye symptoms gradually resolved and he was discharged 14 days after surgery.The initial non-suppressed plasma adrenocorticotrophin concentration raised the possibility of recovery of pituitary function and prompted repeat measurement of morning cortisol and adrenocorticotrophin on postoperative day 20Postsurgical hyponatraemia with ocular palsy suggests hypopituitarism from haemorrhagic infarction of an unsuspected pituitary adenoma Hyponatraemia is the mo...

Isolated Third Cranial Nerve Palsy Associated with Sudden Worsening of Hypotonic Hyponatremia Secondary to Ischemic Pituitary Apoplexy

“…In particular, while the phenomenon of apoplexy seems to be datable well before entry into ED, the acute neurological deficit was simultaneous with hypotonic hyponatremia, which was further aggravated after medical intervention in the ED. Furthermore, the clinical evolution of the picture was very rapid, with the occurrence and disappearance of the palsy in just about one week, a timing which is much lower than the data available in the literature (median time to disappearance or improvement of neurological symptoms during conservative therapy of about 90 days) [5,14]. Of note, anti-edema treatment with a potent steroid such as dexamethasone, started right upon ED admission, was not sufficient to prevent this complication.…”