Abstract: TH-PO358
Unraveling an Uncommon Encounter: Hypokalemic Periodic Paralysis with Brugada Phenocopy Amidst Hypokalemia
Session Information
- Sodium, Potassium, and Volume Disorders: Clinical
October 24, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- El-Charabaty, Elie, Staten Island University Hospital, Staten Island, New York, United States
- Hashmi, Syed Salman Hamid, Staten Island University Hospital, Staten Island, New York, United States
- El Sayegh, Suzanne E., Staten Island University Hospital, Staten Island, New York, United States
Introduction
Hypokalemic Periodic Paralysis (HPP) presents a diagnostic challenge due to its painless muscle weakness, often linked to ion channel dysregulation. This paper discusses Brugada Phenocopies (BrP), showcasing Electrocardiography (ECG) patterns resembling Brugada Syndrome without the genetic condition. The case contributes to understanding BrP induced by hypokalemia alongside HPP, possibly the seventh documented instance.
Case Description
A 43-year-old man with a medical history significant for hypertension and coronary artery disease presented to the emergency department with lower limb weakness. He reported normal muscular strength the day prior but experienced weakness upon waking the next morning. He attributed his symptoms to a substantial meal consumed after breaking his Ramadhan fast, recalling a similar episode following heavy meals in the past. He had a family history of early cardiac-related deaths. The patient was alert and oriented but demonstrated reduced strength in both upper (3/5) and lower (0/5 bilaterally) limbs. ECG revealed a Brugada type 1 pattern. Laboratory analysis revealed hypokalemia (2.5 mmol/L), elevated creatine kinase (326 U/L), and normal thyroid function. Following potassium supplementation, his symptoms resolved, ECG normalized and subsequent tests demonstrated improvement in potassium levels. A neurology evaluation yielded no significant findings. The patient was discharged with plans for outpatient follow-up.
Discussion
HPP occurs in the context of increased carbohydrate intake, potentially leading to rapid insulin release and activation of Na-K ATPase, enhancing cellular potassium absorption and lowering serum potassium levels. Symptoms range from weakness and fatigue to severe neuromuscular weakness and cardiac arrhythmias. Investigating hypokalemia requires excluding hypomagnesemia, thyroid function tests, and metabolic acidosis/alkalosis before considering HPP. Management involves gradual oral potassium repletion to avoid the risk of hyperkalemia associated with intravenous administration. Clinicians should consider including HPP in differential diagnoses of patients presenting with weakness. An electrophysiological evaluation suggested Brugada pattern induced by hypokalemia, which resolved during the hospitalization. In this case, the association with Brugada phenocopies is intriguing.