A 66 year old male was diagnosed with thyrotoxicosis in July 2012 on a background of chronic atrial fibrillation and no previous thyroid disease. Atrial fibrillation was managed with amiodarone for five years however it was ceased twelve months prior to the diagnosis of amiodarone-induced thyrotoxicosis. A thyroid nuclear uptake scan showed reduced uptake in the thyroid gland. Despite two months of Carbimazole which initially showed improvement in T4 and T3 levels, in September 2012 the patient presented with sweating, palpitations and weight loss. Free T4 level was above 100 pmol/L (10-22 pmol/L) with free T3 level 24.1 pmol/L (3.2-6.3pmol/L) and suppressed TSH <0.04 mIU/L. Burch and Wartofsky score was supportive of thyroid storm (35 / 140).
A thyroidectomy was organised however persistent tachycardia ranging between 140 to 180 beats per minute and an episode of pulseless electrical activity requiring cardiopulmonary resuscitation caused concern for safety of anaesthesia. Thyroid function remained persistently elevated despite maximal thionamide therapy (Propylthiouracil 150mg QID) and steroid treatment (Dexamethasone 4mg bd IV). Therapeutic plasma exchange (TPE) was initiated to optimise cardiac effects of thyrotoxicosis prior to surgery. There was symptomatic improvement after the first TPE with improved energy, limb strength and appetite however heart rate reached a minimum of only 130 beats per minute (ranging between 130-160/min). The patient underwent three further treatments with TPE. Following each TPE free T4 and free T3 hormone levels decreased, however there was no sustained improvement in clinical status and urgent total thyroidectomy proceeded.
TPE removes plasma from the blood which is replaced with albumin. By this extra-corporeal process, protein-bound thyroid hormones within plasma are removed as a temporary measure before definitive thyroidectomy. TPE has a transitory effect and thus should be associated with medications to block thyroid hormone release.