A 57-year lady with a history of hypertension for which she was taking bendroflumethiazide and ramipril presented with a 1 week history of worsening frontal headache and vomiting. Twenty-four hours prior to admission she became confused, had photophobia, slurred speech and was unsteady. On examination she had a Glasgow coma score of 12, was apyrexial, normotensive, tachycardic and confused. Fundoscopy was normal. There was no neck stiffness and no cranial nerve palsies. Initial CT scan of the brain was normal. Blood tests showed Na 104 mmol/l, K 2.6 mmol/l, urea 2.2 mmol/l, creat 47 umol/l. Serum osmolality was 229 mOsm/kg, urine osmolality 36 mOsm/kg and urinary Na 14 mmol/l.
In view of the severe hyponatraemia, the possibility of coexisting cerebral oedema was considered and hence a lumbar puncture was not carried out on admission. Acyclovir along with ceftriaxone were given empirically but subsequent CSF was normal. Twelve hours later she developed polyuria, passing around 500 ml of urine per hour. This responded to DDAVP. An MRI scan showed a pituitary haemorrhage and no pituitary tumour. Her free T4 was 19.2 pmol/l, TSH 0.94 μ/l, random serum cortisol 730 nmol/l, ACTH 42 ng/l and prolactin 407 μ/l.
The diabetes insipidus was transient, lasting for 3 days. She made a very gradual recovery, had some cognitive deficit and 2 months later was transferred to a neuro-rehab unit.
This is an unusual presentation of a patient with pituitary apoplexy with a gradual onset of symptoms. Initially she was severely hyponatraemic due to a combination of bendroflumethiazide and vomiting. Her paired serum and urine osmolalities did not fit with an SIADH. She developed an isolated diabetes insipidus which was transient and had no other anterior pituitary hormone deficiency.