Non-islet cell tumour induced-hypoglycaemia as a cause of delirium

An 84-year-old gentleman presented to the Emergency Department following a fall. He was hypoxic and was diagnosed with a community acquired pneumonia, confirmed on chest radiograph and had an Enterococcus faecalis urinary infection. A Mini Mental State Examination of 15/30 confirmed cognitive impairment. He had treatment resistant prostate cancer with rising prostate specific antigen and metastases of the spine and lung, despite being on third-line antiandrogen therapy. His presentation involved many potential causes of delirium. However, he displayed widely fluctuating behaviour throughout each day with episodes of aggression with which he became diaphoretic, followed by lucid periods. He also intermittently agreed and then refused investigations. Computer tomography (CT) of the brain showed extensive small vessel disease but no cause for this new confusion. As part of the investigations of confusion capillary blood glucose (CBG) monitoring was initiated and hypoglycaemia (1.9 mmol/L) was noted during an episode of aggression and confusion which improved with correction of hypoglycaemia. He fulfilled Whipples’ Triad; low blood glucose concentration with symptoms of hypoglycaemia, resolving when the blood glucose is raised. A further episode of hypoglycaemia was recorded and confirmed on serum glucose (1.5 mmol/L; normal 3.9–6.0 mmol/L). We investigated for endogenous causes of hypoglycaemia; there was no history of diabetes mellitus; therefore, he had not been taking blood glucose lowering medications. An adrenal CTscan with contrast washout suggested some abnormality of the adrenals with likely metastasis but adrenal function was normal on short synacthen test, renal and liver functions were normal. He did not have cardiac failure or overwhelming sepsis. He had normal thyroid function. During a further hypoglycaemic episode, C-peptide was reduced at 36 pmol/L (normal range 298–2350 pmol/L) and insulin unrecordable (<2 mIU/L).The ratio of insulin-like growth factor-II: insulin-like growth factor-I was at the higher end of normal (IGF-II 36.7 μmol/L, IGF-I 4.4 μmol/L, ratio 8.3 [normal <10]). Insulin-like growth factor binding protein 3 (IGFBP-3) was suppressed 0.8 mg/L (2.20– 4.5 mg/L). This was consistent with a non-islet cell tumour induced hypoglycaemia. The patient was commenced on prednisolone. Initially, CBG and delirium showed significant improvement. However, severe hypoglycaemia (serum glucose 1.1 mmol/L) soon returned, associated with hypothermia (temp 33.1). High dose growth hormone (4 mg per day) was added to the treatment, which maintained normoglycaemia.