SHILPA GURNURKAR, MD
Associate Professor of Pediatrics, UCF COM
Nemours Children's Hospital
Orlando, Florida, United States
Disclosure information not submitted.
Title: Hyperthyroidism Presenting as Thyrotoxic Periodic Paralysis
Introduction: Thyrotoxic periodic paralysis (TPP) is characterized by abrupt onset of paralysis and hypokalemia in the setting of uncontrolled hyperthyroidism. While mostly reported in Asian males aged 20-40, here we report TPP as the initial presentation of hyperthyroidism in a previously healthy African American adolescent male.
Description: A 15-year-old previously healthy African American male presented with complaints of sudden onset bilateral lower extremity weakness. The child reported he woke up in the morning and was unable to bear weight or ambulate, repeatedly falling to the ground. In the ER, the child had normal mentation, appropriate strength and tone of the upper extremities, but flaccid bilateral lower extremities with a strength recorded of 0/5, absent deep tendon reflexes. Laboratory studies were remarkable for a serum potassium of < 2.0 mmol/L (3.5-5.1), serum phosphorus level of 0.9 mg/dL (2.5-4.9), a TSH< 0.01mcIUnit/mL and an elevated Free T4 of 7.4ng/dL. The patient was given IV potassium replacements and then transferred to our children’s hospital. Additional history was gathered of chronic fatigue, weakness, intermittent palpitations, anxiety, weight loss, loss of appetite and difficulty sleeping for about one month. Physical exam remained consistent with bilateral lower extremity weakness. Deep tendon reflexes present, sensation and mental status intact. He was noted to be tachycardic (HR 80-130 bpm) and hypertensive (SBP 140-160 mmHg). The child was diagnosed with TPP and new onset hyperthyroidism. He was managed with electrolyte replacements and methimazole. With improvement of his hyperthyroidism, the child’s electrolyte derangements and lower extremity paralysis resolved.
Discussion: The mechanism for electrolyte derangements and sudden onset lower extremity paralysis in TPP is not yet well understood. It is hypothesized to be related to increased Na+/K+-ATPase activity leading to increased intracellular shift of potassium ions in the hyperthyroid state, thus causing hypokalemia due to intracellular shift. Recognition of this rare presentation can be lifesaving. Treatment is focused on correction of the electrolyte derangements and thyrotoxicosis. TPP should be considered with any presentation of sudden onset lower extremity paralysis with hypokalemia.