Endocrine Abstracts

A 52 year old lady was admitted with collapse in May 2001 with h/o being nauseous, generally unwell, off her feet and food for several weeks. GP consultation five weeks before, for similar complaints, resulted in thyroid function tests confirming hypothyroidism. Thyroxine 25 mcg was commenced by the GP and uptitrated to 50 mcg. She however deteriorated despite this treatment becoming increasingly lethargic and sleepy. On admission she appeared tanned, BP was 93/50 she was dysarthric and plantars were extensor. Investigations showed blood sugar 5.8 mmol, serum Na 93, K 4.6, urea 4.6 and creatinine 66, random cortisol 43 nmol/l, plasma osmolality 201, urinary Na 63 mmol/l. A clinical diagnosis of Addisonian crisis was made and she was treated with IV hydrocortisone, IV liotyronine and normal saline infusion. The serum sodium was corrected slowly over five days as shown:

With this management she showed slight initial improvement but on the 23rd there was general deterioration, she became increasingly dysarthric, dysphagic, hypertonic, cogwheeling & subsequently choreaform movements of the arms and head. CT brain and initial MR scans were unremarkable but subsequent MR scan showed subtle high signal changes consistent with myelinolysis in the pons and also in both thalami and basal ganglia. CSF was normal. The Parkinsonian syndrome was treated with Madopar. She needed PEG feeding and was transferred to a Neurology unit. Thyroid autoantibodies and ACTH (359 ng/l) remained elevated, but thyroid functions improved and she was completely weaned off Thyroxine. Hydrocortisone and Madopar were continued. She made good recovery and by March 2002 was able to feed orally and the PEG was removed. Severe untreated hyponatremia may cause encephalopathy and treatment is fraught with danger of Myelinolysis. This can occur after relatively rapid correction of hyponatremia. Though initially called ‘central pontine myelinolysis,’ it is now known to affect extrapontine areas as well. The manifestations usually evolve several days after correction of hyponatremia. As illustrated by this case the treatment of hypothyroidism without recognition of concomitant hypoadrenalism can precipitate Addisonian crisis. The thyroxine replacement increases cortisol clearance and also increases metabolism, thus decreasing circulating cortisol availability and increasing need that cannot be provided by the failing adrenals.