Endocrine Abstracts

There have been several case reports over the years of hypopituitarism occurring after cerebral oedema caused by diabetic ketoacidosis (DKA). The case reports have ranged from a single hormone defect to a more extensive loss of hormone production. What is not reported in the literature so far is what happens to these patients and their hormone deficiencies in the longer term.

This is a case report of a young man who presented with DKA aged twelve who rapidly developed cerebral oedema. He was given mannitol then intubated and ventilated overnight because he became increasingly drowsy and developed a dilated right pupil. Afterwards he had a right hemi-paresis and behavioural abnormalities that required special schooling. He was followed up in the paediatric endocrine clinic where it was noted at the age of 15 that he had failed to grow as expected. The resulting investigations showed a deficiency of GH, TSH, LH and FSH. He was treated with GH and TSH and responded appropriately. GH and TSH were withdrawn at 18 years because his TSH normalised. An MRI scan at 18 years showed that his anterior pituitary and pituitary stalk appeared normal, absent signal from the posterior pituitary and an abnormal density in the right temporal lobe. Now aged 21 he continues to be deficient in LH, FSH and GH. His TSH is now at the upper limit of normal and is suggestive of early primary hypothyroidism. His steroid reserve is normal. He has been commenced on testosterone replacement.

This suggests that there is a degree of reversibility to the partial hypopituitarism after cerebral oedema but it is unclear to what extent this recovery can occur.