Tricia Tan

Pituitary macroadenomas: are combination antiplatelet and anticoagulant therapy contraindicated? A case report.

BackgroundPituitary apoplexy is a life-threatening endocrine emergency that is caused by haemorrhage or infarction of the pituitary gland, commonly within a pituitary adenoma. Patients classically present with headache, ophthalmoplegia, visual field defects and altered mental state, but may present with a typical symptoms such as fever and altered conscious level.Case presentationA 57-year-old female with a known pituitary macroadenoma was treated for suspected acute coronary syndrome with aspirin, clopidogrel and full dose enoxaparin. She developed a severe and sudden headache, nausea and vomiting and visual deterioration. A CT scan showed haemorrhage into the pituitary macroadenoma. She underwent neurosurgical decompression. Post-operatively her visual fields and acuity returned to baseline. She was continued on hydrocortisone and thyroxine replacement on discharge.ConclusionThis case illustrates the risks of anticoagulation in a patient with a known pituitary macroadenoma, and raises the issue of whether these tumours present a relative contraindication to the use of dual antiplatelet and anticoagulation in acute coronary syndrome.

A man with anxiety, confusion, and red eyes

A 31 year old man presented with a four day history of anxiety, insomnia, and confusion. Over the past few months he had intermittently noticed red eyes and a “tummy ache.” A concomitant history from his parents revealed a previous episode of confusion and concern about excessive alcohol intake—he had been drinking 10 units of vodka a day for the past six years. He denied any medical history or current drugs. On examination, he was agitated, tachycardic (heart rate 110 beats/min), and he had bilateral conjunctivitis. Initial investigations showed a calcium concentration of 3.54 mmol/L (reference range 2.15-2.6) and metabolic alkalosis (table⇓). He was treated for acute hypercalcaemia with fluids and discharged when levels normalised. nnView this table:nnThe patient’s biochemistry results at different time points nnnnBefore further outpatient investigations were performed, he was readmitted two weeks later with confusion and a witnessed seizure. Investigations again showed a raised calcium (3.80 mmol/L), metabolic alkalosis, and new onset acute renal failure (table). Plasma glucose was normal. He was once again treated for acute hypercalcaemia and stabilised. On day three of admission, calcium carbonate tablets were discovered on his bedside table. He reported regularly ingesting up to three packets a day to treat symptoms of indigestion.nnnn### 1 How do you explain this patient’s ocular symptoms?nn#### Short answernnBilateral conjunctivitis is a rare complication of severe hypercalcaemia.nn#### Long answernnAlthough rare, hypercalcaemia can cause ocular complications, …

A case of severe hyponatraemia

A 32 year old woman was admitted with a two day history of extreme fatigue, severe headache, vomiting, postural dizziness, and blurring of peripheral vision on her left lateral gaze. Two days earlier she had had an emergency caesarean section for an anterior uterine rupture at 29 weeks’ gestation. During the operation she lost 1.5 litres of blood and became hypotensive with a blood pressure of 87/54 mm Hg. She could not lactate post partum. nnOn examination, she was confused and slow to respond. Her blood pressure was 98/60 mm Hg, pulse rate 80 beats per minute, and respiratory rate 14 breaths per minute. Neurological examination showed a left VIth cranial nerve palsy. Her visual fields were full to confrontation, and dilated fundoscopy was unremarkable. Initial investigations showed a serum sodium of 116 mmol/l (138 mmol/l immediately postoperatively) and potassium of 3.7 mmol/l. Her serum osmolality was 240 mOsm/kg (normal 275-95) with a urine osmolality of 535 mOsm/kg and her urine sodium concentration was 91 mmol/l.nnnn### Short answers