Key result
Intravenous amiodarone and potassium replacement successfully reversed ventricular tachycardia and acute paraparesis in a patient with profound hypokalemia induced by thyrotoxic periodic paralysis.
Case Report (n=1)
No
Severe hypokalemia in thyrotoxic periodic paralysis can precipitate lethal ventricular tachycardia, requiring prompt recognition and potassium replacement.
Prompt potassium repletion may be lifesaving in thyrotoxic VT; single case leaves open amiodarone's added benefit.
Thyrotoxic periodic paralysis (TPP) is a potentially fatal complication of hyperthyroidism, characterized by recurrent muscle paralysis and hypokalemia. We present a case of a 32-year-old apparently healthy male patient, who presented with acute paraparesis associated with hypokalemia (K: 1.6 mmol/L), complicated by ventricular tachycardia (VT). Advanced cardiac life support was initiated with an amiodarone infusion, and eventually QRS complex narrowed and wide complex tachycardia resolved. Intravenous potassium chloride (KCl) 40 mEq over 2-3 h and oral KCL 40 mEq were administered to treat the electrolyte imbalance. Patient paralysis was quickly reversed; motor function was regained with movement of the lower extremities. This case highlights the importance of early recognition and prompt treatment of TPP as a differential diagnosis for muscle weakness, especially in the setting of severe hypokalemia. It is important to pay attention to the possibility of the development of lethal VT associated with hypokalemia in the setting of hyperthyroidism and thyrotoxic paralysis.
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Shaaban et al. (2019) conducted a case report in Thyrotoxic periodic paralysis with hypokalemic ventricular tachycardia (n=1). Potassium chloride and amiodarone was evaluated on Resolution of ventricular tachycardia and muscle paralysis. Intravenous amiodarone and potassium replacement successfully reversed ventricular tachycardia and acute paraparesis in a patient with profound hypokalemia induced by thyrotoxic periodic paralysis.
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