Key result
IV potassium plus antithyroid therapy and beta-blockers prompt rapid neurological recovery in thyrotoxic periodic paralysis.
Case Report (n=1)
Thyrotoxic periodic paralysis is a rare presentation of Graves' disease that can manifest with acute paralysis and transient ventricular arrhythmia, which resolves with cautious potassium replacement and antithyroid therapy.
May inform acute management of thyrotoxic periodic paralysis; hypothesis-generating pending controlled trials.
Thyrotoxic periodic paralysis (TPP) is a rare variant presentation associated with thyrotoxicosis. It is characterised by acute hypokalaemic paralysis due to intracellular potassium shift. We describe a man in his early 30s who presented with sudden-onset flaccid quadriparesis and transient self-reverted broad-complex tachycardia. Arterial blood gas analysis revealed severe hypokalaemia (1.2 mmol/L; reference range 3.5-5.1 mmol/L). Thyroid function tests demonstrated suppressed thyroid-stimulating hormone (<0.01 mIU/L; reference range 0.4-4.0 mIU/L) with markedly elevated free triiodothyronine and thyroxine levels, consistent with thyrotoxicosis due to Graves' disease. He was treated with cautious intravenous potassium replacement and initiation of antithyroid therapy with beta-blockade, resulting in rapid and complete neurological recovery. This case underscores the importance of recognising TPP as a distinct clinical presentation of thyrotoxicosis in young men presenting with acute paralysis and cardiac arrhythmia.
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Makashir et al. (2026) conducted a case report in Thyrotoxic periodic paralysis (n=1). Intravenous potassium replacement and antithyroid therapy with beta-blockade was evaluated. Intravenous potassium replacement and antithyroid therapy with beta-blockade resulted in rapid and complete neurological recovery in a man with thyrotoxic periodic paralysis.
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