Location
Philadelphia, PA
Start Date
3-5-2023 1:00 PM
End Date
3-5-2023 4:00 PM
Description
Background:
Hypokalemic Periodic Paralysis (HPP) is a rare neuromuscular disorder characterized by acute, transient muscle weakness and paralysis secondary to hypokalemia and can be complicated by cardiac arrhythmias. Thyrotoxic Periodic Paralysis (TPP) is an acquired type of HPP seen in the setting of thyrotoxicosis. Most TPP patients present with subtle signs and symptoms of thyrotoxicosis prior to an acute muscle paralysis event. Therefore, recognizing TPP in the emergency setting is critical in preventing life-threatening cardiac, respiratory, renal, or other systemic complications induced by a hypokalemic state.
Case Report:
An 18-year-old Hispanic male presented to the emergency department, with no past medical history, complaining of complete weakness and sudden onset lower extremity paralysis upon waking. He stated that he had less severe episodes of this muscle paralysis twice in the past. His physical exam was significant for tachycardia, thyroid goiter, thyroid bruit, decreased muscle strength in his lower extremities bilaterally with allodynia. His initial EKG showed sinus tachycardia, prolonged QT interval, U-waves, and 2nd-degree Mobitz atrioventricular nodal block which normalized after potassium repletion. He was admitted to the ICU for continued management of hypokalemic periodic paralysis secondary to severe thyrotoxicosis.
Conclusion:
The signs of thyrotoxicosis are subtle, if not absent, prior to an acute episode of muscle paralysis secondary to TPP. Additionally, precipitating factors such as high-carbohydrate meals or strenuous exercise may be subtle or absent prior to a paralytic episode. The classic triad of tachycardia, high-voltage QRS, and first-degree AV block are commonly seen in patients with TPP. Uniquely, this patient’s EKG revealed a newly diagnosed 2nd-degree Mobitz AV nodal block which is rare and important to recognize. The prevalence and pathogenesis behind the cardiac arrhythmias concurrent with TPP episodes remain unknown.
Embargo Period
1-4-2024
Hypokalemic Periodic Paralysis Secondary to Thyrotoxicosis
Philadelphia, PA
Background:
Hypokalemic Periodic Paralysis (HPP) is a rare neuromuscular disorder characterized by acute, transient muscle weakness and paralysis secondary to hypokalemia and can be complicated by cardiac arrhythmias. Thyrotoxic Periodic Paralysis (TPP) is an acquired type of HPP seen in the setting of thyrotoxicosis. Most TPP patients present with subtle signs and symptoms of thyrotoxicosis prior to an acute muscle paralysis event. Therefore, recognizing TPP in the emergency setting is critical in preventing life-threatening cardiac, respiratory, renal, or other systemic complications induced by a hypokalemic state.
Case Report:
An 18-year-old Hispanic male presented to the emergency department, with no past medical history, complaining of complete weakness and sudden onset lower extremity paralysis upon waking. He stated that he had less severe episodes of this muscle paralysis twice in the past. His physical exam was significant for tachycardia, thyroid goiter, thyroid bruit, decreased muscle strength in his lower extremities bilaterally with allodynia. His initial EKG showed sinus tachycardia, prolonged QT interval, U-waves, and 2nd-degree Mobitz atrioventricular nodal block which normalized after potassium repletion. He was admitted to the ICU for continued management of hypokalemic periodic paralysis secondary to severe thyrotoxicosis.
Conclusion:
The signs of thyrotoxicosis are subtle, if not absent, prior to an acute episode of muscle paralysis secondary to TPP. Additionally, precipitating factors such as high-carbohydrate meals or strenuous exercise may be subtle or absent prior to a paralytic episode. The classic triad of tachycardia, high-voltage QRS, and first-degree AV block are commonly seen in patients with TPP. Uniquely, this patient’s EKG revealed a newly diagnosed 2nd-degree Mobitz AV nodal block which is rare and important to recognize. The prevalence and pathogenesis behind the cardiac arrhythmias concurrent with TPP episodes remain unknown.