Abstract: PO1471
Thyrotoxic Periodic Paralysis: A Stunning Diagnosis
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 1
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Starakiewicz, Piotr, Columbia University Irving Medical Center, New York, New York, United States
- Husain, Syed Ali, Columbia University Irving Medical Center, New York, New York, United States
Introduction
Thyrotoxic periodic paralysis (TPP), acute hypokalemia and proximal muscle weakness in the setting of thyrotoxicosis, is primarily seen in Asian men with undiagnosed hyperthyroidism in the 2nd-4th decade, often with family history of paralysis and thyroid disease. We describe a case of a young male presenting with acute TPP.
Case Description
A 28year-old white male with no medical history presented with acute onset diffuse weakness with inability to get out of bed, preceded the night prior by leg stiffness. He exercised 2 days prior. He reported marijuana use and a balanced diet. He denied recent travel, medication or supplements. His father had Hashimoto’s thyroiditis.
Exam showed tachcyardia (106 bpm) and hypertension (132/74 mmHg), and EKG revealed sinus tachycardia with QTc 629. Labs showed: K+ 1.7 mEq/L, HCO3- 22 mmol/L, Cr 0.7 mg/dL, TSH <0.01, fT4 >6ng/dL, and T3 320ng/dL. Fractional excretion of K+ was 3.2%. He was treated with 120mEq KCl with repeat K+ 5.6 mEq/L in 4 hours and symptom resolution. Elevated TSH receptor, anti-thyroglobulin, and thyroid stimulating antibodies with a homogenous radioactive iodine uptake scan [Fig 1] confirmed Grave’s disease. He was started on metoprolol and methimazole and discharged home without further episodes.
Discussion
TPP results from acute intracellular K+ shift due to Na/K-ATPase activation in myocytes from a hyperadrenergic state (increased number and sensitivity of β-receptors) and thyroid hormone stimulation. Muscle hyperpolarization and loss of excitability required for contraction results. Body K+ stores remain unchanged. Episodes are associated with high insulin or epinephrine states (eg. mornings, exercise, high-carbohydrate meal). Paralysis, lasting minutes to days, is ascending, symmetrical, and proximal, chiefly affecting legs (bulbar or respiratory involvement is rare). Usually painless, it can be preceded by muscle aches or cramps. Sinus tachycardia is common and life-threatening arrhythmias can occur. Labs demonstrate normal acid-base status and low urinary K. CPK can be elevated. Low TSH, elevated free T4 and T3 confirm the diagnosis. Treatment involves cautious K replacement (due to risk of rebound hyperkalemia), non-selective β-blockers, and therapy for hyperthyroid state