(265) Thyrotoxic Periodic Paralysis: A Breathless Presentation of Graves Disease in a Young Hispanic Male

Introduction: Thyrotoxic periodic paralysis (TPP), a hypokalemia-mediated temporary paresis or paralysis, is an unusual presentation of hyperthyroidism. It is classically described in males of Asian descent, and usually presents with paresthesia and non-life-threatening arrhythmia. TPP can be fatal in cases with respiratory muscle involvement. We report a case of severe TPP with unstable ventricular tachycardia (VT) and respiratory failure in an unusual demographic.

Description: A 31-year-old Hispanic male was evaluated in the ER for acute on chronic back pain and lower extremity paresthesia. On exam he had bilateral patellar areflexia and ankle clonus. Magnetic resonance imaging of his spine was normal and his symptoms resolved with ketorolac, dexamethasone, and diazepam. He was discharged but returned a few hours later with recurrent symptoms. He was in mild distress with sinus tachycardia in the 90-100s, then rapidly became obtunded and hypoxic. During preparation for intubation, he had two episodes of sustained unstable VT requiring cardioversion.

Lab workup revealed severe hypokalemia (1.9 mmol/L) and thyroid stimulating hormone (TSH) < 0.005 uIU/mL, raising suspicion for TPP. He was given a total of 60mEq intravenous potassium chloride which resulted in rebound hyperkalemia to 6.3 mmol/L. Further studies were consistent with acute thyrotoxicosis and he was started on propranolol, methimazole, and hydrocortisone. He sustained no further arrhythmias and rapidly began to generate spontaneous breaths. He was extubated within 12 hours and discharged home the following day with endocrinology follow-up.

Discussion: TPP is an important differential in patients with severe hypokalemia, rapid onset paralysis, arrhythmia, and respiratory failure. Common EKG changes include interval prolongation or T-wave changes but wide-complex tachycardia has not previously been reported. Hypokalemia is a result of massive intracellular potassium shifts rather than total body deficit. Aggressive repletion can lead to rebound hyperkalemia and should be avoided. Due to the classic association of TPP with male gender and Asian descent, it is likely underrecognized and underreported in other demographics. High index of suspicion is needed, as with appropriate treatment the clinical course is very favorable.