Poster Presentation ESA-SRB 2023 in conjunction with ENSA

A peculiar presentation of paralysis (#315)

Sneha Krishna 1 , Liza Phillips 1 , Stephanie Teasdale 1
  1. Mater Hospital Brisbane, South Brisbane, QLD, Australia

Introduction

Thyrotoxic periodic paralysis (TPP) is a rare cause of acute quadriparesis affecting 0.1-0.2% of thyrotoxic patients. It is a sporadic cause of hypokalaemic periodic paralysis, which has an incidence of 1 in 100,000.1 We present a case of TPP in an Italian gentleman.

 

Case

A 43-year-old man of Italian descent presents with severe hypokalaemia of 1.7 mmol/L and acute proximal quadriparesis several hours post ingestion of a large carbohydrate-heavy meal. There were no sensory, speech, or visual deficits on examination. There were three prior episodes with resolution of symptoms within 48 hours without medical intervention. Investigations revealed a new diagnosis of T3 thyrotoxicosis secondary to Graves’ disease (TSH <0.01 mU/L, free T4 18.5 pmol/L, free T3 7.7 pmol/L, TSH receptor antibodies 1.4 IU/L). He was appropriately treated with intravenous potassium, carbimazole 10mg daily, and propranolol PRN.

 

Discussion

TPP is a rare neuromuscular disorder affecting 1-2% of thyrotoxic East Asian men between age 20 to 40 and is much less common in Western populations.1 It is characterised by intermittent painless proximal muscle paralysis and hypokalaemia, often triggered after carbohydrate-rich meals or strenuous exercise. Whilst many cases of hypokalaemic periodic paralysis are hereditary, TPP is sporadic and can be triggered by any cause of hyperthyroidism including levothyroxine excess.2

The pathogenesis is not well understood, as many have mildly elevated serum thyroid hormone levels. Thyroid hormone increases sodium-potassium ATPase pump activity, causing a rapid shift of potassium intracellularly and hyperpolarisation of skeletal muscle membrane.3 Insulin can act synergistically with thyroid hormone as it also activates the sodium-potassium ATPase pump. Pre-existing insulin resistance combined with a carbohydrate-heavy meal can trigger a TPP attack. Rapid intravenous potassium replacement during acute attack is warranted to prevent arrhythmia. Non-selective beta-blockade can prevent recurrence until euthyroidism is achieved.3

  1. Kung, A. W. (2006). Thyrotoxic periodic paralysis: A diagnostic challenge. The Journal of Clinical Endocrinology & Metabolism, 91(7), 2490–2495. https://doi.org/10.1210/jc.2006-0356
  2. Chaudhry, M. A., & Wayangankar, S. (2016). Thyrotoxic Periodic Paralysis: A Concise Review of the Literature. Current rheumatology reviews, 12(3), 190–194. https://doi.org/10.2174/1573397112666160404124822
  3. Kung, A. W. (2006). Thyrotoxic periodic paralysis. A diagnostic challenge. The Journal of Clinical Endocrinology & Metabolism, 91(7), 2490-2495. https://doi.org/10.1210/jc.2006-0356