A 19-year-old Caucasian man, with no past medical history presented to ER with acute onset generalized muscle weakness, more pronounced in both legs, which started upon awakening in the morning. He reported 40 lbs weight loss over 2 months in spite of increased appetite. Patient denied palpitations, heat intolerance, dysphagia or change in bowel movements. Review of systems was otherwise negative. He never smoked or used alcohol and recreational drugs. Family history was unremarkable.
Physical exam revealed cachectic male with normal vitals except pulse of 110 b/m. Head exam showed temporal muscle wasting bilaterally, lid lag, orbital lag, and mild exophthalmos. Neck exam revealed diffuse symmetric thyroid enlargement with firm consistency. Neurologic exam was positive for brisk and symmetric patellar reflexes and fine tremors in bilateral hands. Strength was 4/5 in all muscle groups of both lower extremities. Rest of exam was unremarkable.
Serum potassium (K) on presentation was 1.9 mEq/L (3.5–5.1). Previous serum K less than a month prior was 4.9. Serum phosphorus and magnesium were normal. EKG showed sinus tachycardia.
An initial clinical diagnosis of periodic hypokalemic paralysis was made. Treatment began with K replacement. His serum K was checked 4 hours later and was 3.4 and reexamination showed complete resolution of lower extremity weakness with no change in the rest of his physical exam. Initial TSH was <0.02 mU/L (0.47–4.68), free T4 level: 5.5 ng/dL (0.8–2.2) and total T3: 539 ng/dL (80-206 ). His thyroid-stimulating immunoglobulin level was elevated at 382% (<140%). Ultrasonography of the neck showed prominent thyroid gland with increased vascularity.
Thyrotoxicosis was diagnosed and he was given propranolol 10 mg PO TID and methimazole 10 mg PO TID. Patient was discharged home with the diagnosis of thyrotoxic periodic paralysis (TPP) secondary to new onset Graves’ disease. At 6 week follow-up, his weight had returned to normal and there had been no more episodes of muscle weakness. His head and neck exam showed improvement of the initial findings. Repeat blood work showed TSH: < 0.02, free T4: 1.8, and TT3: 209.
Discussion:
Hyperthyroidism is associated with some muscular disorders, including thyrotoxic myopathies and periodic paralysis. As it is the most frequent cause of hyperthyroidism, Graves’ disease is the most common disorder associated with TPP. Despite the higher incidence of hyperthyroidism in females, about 95 % of TPP occurs in males.
Acute hypokalemic paralysis is a rare cause of acute weakness. Morbidity and mortality associated with unrecognized disease can occur including respiratory failure and possibly death. Common causes of hypokalemic paralysis include TPP that is frequently seen in Asian males. TTP is characterized by sudden onset of hypokalemia and paralysis that mainly affects the lower extremities. Treatment of TPP includes replacing K rapidly, using nonselective beta-blockade and correcting the underlying hyperthyroidism. TPP is curable once a euthyroid state is achieved.
Conclusions:
TPP can be the initial presentation of thyrotoxicosis. This condition is very rare in Caucasian populations. TPP is commonly misdiagnosed in western countries due to its similarities to familial periodic paralysis. Diagnosis of TPP is often delayed likely because of the subtle presentation of thyrotoxicosis and lack of awareness about it. Increased awareness among physicians will result in early diagnosis, appropriate treatment, and prevention of rebound hyperkalemia.