Title : Diagnostic and Management Challenge in Torsades de Pointes with Thyrotoxic Periodic Paralysis
Abstract:
Background:
Thyrotoxic periodic paralysis (TPP) is a rare but potentially fatal manifestation of hyperthyroidism characterized by sudden hypokalemic paralysis. Excess thyroid hormone stimulates the Na?/K?-ATPase pump, causing rapid intracellular potassium shifts and severe hypokalemia. These shifts markedly increase the risk of cardiac electrical instability, QTc prolongation, and torsades de pointes (TdP). Young men, particularly of Asian or Hispanic descent, are most commonly affected, and clinical thyroid signs may be subtle, delaying recognition.
Objective:
To describe the diagnostic considerations and treatment strategies for torsades de pointes occurring in the setting of thyrotoxic periodic paralysis.
Methods:
A detailed case review was conducted, examining clinical presentation, laboratory and ECG findings, arrhythmia progression, and resuscitative interventions. Findings were compared with existing literature on the pathophysiology and management of TPP-associated arrhythmias.
Results:
A 21-year-old male with autism presented with sudden generalized paralysis overnight after exercise. Prehospital monitoring revealed diffuse ST depression, and upon arrival, he exhibited intermittent ventricular tachycardia. ECG showed sinus tachycardia with diffuse ST depressions. He shortly developed torsades de pointes. Magnesium, calcium, and bicarbonate were administered; however, his rhythm deteriorated into ventricular flutter and ultimately asystole despite defibrillation, epinephrine, amiodarone, lidocaine, and fluid resuscitation. Laboratory studies revealed profound hypokalemia (<1.0 mmol/L), hypomagnesemia, metabolic acidosis with normal anion gap, and severe thyrotoxicosis (TSH <0.00 μIU/mL). The constellation of hypokalemia, paralysis, and ventricular arrhythmias was consistent with TPP complicated by TdP.
Conclusion:
This case illustrates the high risk of malignant arrhythmias in TPP due to severe potassium shifts and QTc prolongation. Management hinges on early recognition, cautious potassium supplementation, and magnesium administration with continuous cardiac monitoring. Nonselective beta-blockers can mitigate thyroid-driven potassium shifts, whereas amiodarone should be avoided due to its QT-prolonging effects. Lidocaine may be considered in refractory cases, but it is not a first-line therapy for QT-prolongation–related arrhythmias.
Beta-blockers are an important adjunct for immediate and short-term prevention, but rapid and sustained euthyroidism is the cornerstone of long-term recurrence prevention in TPP. Failure to promptly identify TPP may lead to refractory arrhythmias and fatal outcomes, highlighting the need to consider this diagnosis in young patients presenting with sudden paralysis and
