Treatment with cautious potassium replacement, propranolol, and antithyroid therapy led to complete resolution of paralysis within 24 hours without rebound hyperkalaemia.
Case Report (n=1)
This case highlights the importance of recognizing thyrotoxic periodic paralysis in individuals of any ethnic background and emphasizes cautious potassium replacement to prevent rebound hyperkalemia.
A Caucasian man in his 20s with no known medical history presented to the emergency department with acute flaccid quadriparesis following a high-carbohydrate meal and strenuous physical activity. Initial evaluation revealed profound hypokalaemia (1.7 mmol/L; reference 3.5–5 mmol/L), marked QTc prolongation (594 ms), and mild troponin I elevation (51 ng/L; reference <40 ng/L). He reported two similar episodes over the preceding year that had been attributed to dehydration. Thyroid function testing demonstrated severe hyperthyroidism with suppressed thyroid-stimulating hormone (<0.003 mIU/L; reference 0.4–4 mIU/L), with positive thyroid-stimulating immunoglobulin confirming Graves’ disease as the underlying cause. Thyrotoxic periodic paralysis (TPP) was diagnosed. Treatment included cautious potassium replacement, propranolol and antithyroid therapy. Paralysis resolved completely within 24 hours without rebound hyperkalaemia. He remained clinically well without recurrence after achieving euthyroid state. This case highlights the importance of recognising TPP in individuals of any ethnic background and emphasises key management principles to prevent serious complications.
Kothia et al. (Mon,) conducted a case report in Thyrotoxic periodic paralysis (n=1). Potassium replacement, propranolol and antithyroid therapy was evaluated on Resolution of paralysis. Treatment with cautious potassium replacement, propranolol, and antithyroid therapy led to complete resolution of paralysis within 24 hours without rebound hyperkalaemia.