Introduction: Thyrotoxic Periodic Paralysis (TPP) is complication of hyperthyroidism, characterized by recurrent episodes of flaccid paralysis associated with hypokalemia. This unusual but serious complication of hyperthyroidism can lead to paralysis, cardiac arrhythmias and respiratory failure.
Case Presentation: A 30 year old male with no significant past medical or surgical history presented to the Emergency Department with severe lower extremity weakness. Associated symptoms included nausea, flushing and palpitations. He denied any fever, chills, recent infections, bowel changes, bowel/bladder incontinence or numbness/tingling. Vital signs included blood pressure of 117/59, Pulse of 129, Temperature of 36.7C (98F) and SPO2 of 96%. On physical exam, the patient appeared flushed. Thyroid, cardiac, and abdominal exam were within normal limits. However, neurological exam showed proximal lower extremity muscle strength of 2/5 and distal lower extremity muscle strength of 4/5 with hypoactive deep tendon reflexes and no sensory loss. Laboratory testing revealed Potassium of 1.8 mmol/l, Glucose of 152 mg/dl, Thyroid Stimulating Hormone (TSH) of <0.005 (Normal 0.358-3.740 mclU/ml), Free Thyroxine (T4) of 3.80 (Normal 0.76-1.46 ng/dl), Thyroid Stimulating Immunoglobulin (TSI) of 1.6 (Normal <1.3 TSI Index). Electrocardiogram revealed U waves and high voltage QRS in leads II, V2-V6. Magnetic resonance imaging of the lumbar spine was negative for acute abnormalities. The patient was diagnosed with Thyrotoxic Periodic Paralysis and subsequently started on potassium replacement and anti-thyroid medications.
Discussion: TPP is an uncommon but life-threatening complication of hyperthyroidism. Patients often present with flaccid muscle paralysis, hypokalemia, low TSH levels and elevated T4 levels. It is hypothesized that elevated thyroid hormones alter the plasma membrane permeability to potassium by increasing the Na/K ATPase activity on the skeletal muscle membrane. The shift of potassium into cells, leads to hyperpolarization of muscle membrane and decreased muscle fiber excitability. Patients are predisposed to episodes of paralysis by increased susceptibility to hypokalemia by epinephrine or insulin. The inciting event is commonly at rest after strenuous physical activity, stress, or after a high-carbohydrate diet. Treatment is focused on cautiously replacing potassium as to prevent fatal cardiac arrhythmias, as well as restoring the patient to a euthyroid state.
Conclusions: Attention must be paid to signs and symptoms of possible underlying active thyroid disease in patients with hypokalemia induced paralysis. Early diagnosis and treatment can prevent future paralytic attacks and cardiopulmonary complications.
To cite this abstract:Rizvi N, Jaffari F, Rajput F. A Case of Lower Extremity Paralysis. Abstract published at Hospital Medicine 2015, March 29-April 1, National Harbor, Md. Abstract 667. Journal of Hospital Medicine. 2015; 10 (suppl 2). https://www.shmabstracts.com/abstract/a-case-of-lower-extremity-paralysis/. Accessed April 9, 2020.