The pathophysiology for the hypokalemia in TPP is thought to involve the sodium/potassium–adenosine triphosphatase (Na+/K+–ATPase) pump. This pump activity is increased in skeletal muscle and platelets in patients with TPP vs patients with thyrotoxicosis alone.3,5
The role of Hashimoto thyrotoxicosis. Most acquired cases of TPP are mainly secondary to Graves disease with elevated levels of TSI and mildly elevated or normal levels of TPO. In this case, the patient was in the acute phase of Hashimoto thyrotoxicosis (“hashitoxicosis”) with elevated levels of TPO and only mildly elevated TSI.Imaging studies to support the diagnosis, such as a thyroid uptake scan or ultrasonography, are not necessary to determine the cause of thyrotoxicosis. In the absence of test results for TPO and TSI antibodies, however, a scan can be helpful.6,7
Treatment of TPP consists of early recognition and supportive management by correcting the potassium deficit; failure to do so could cause severe complications, such as respiratory failure and psychosis.8 Because of the risk for rebound hyperkalemia, serial potassium levels must be measured until a stable potassium level in the normal range is achieved.
Nonselective beta-blockers, such as propranolol (3 mg/kg) 4 times per day, have been reported to ameliorate the periodic paralysis and prevent rebound hyperkalemia.9 Finally, restoring a euthyroid state will prevent the patient from experiencing future attacks.
THE TAKEAWAY
Few medical conditions result in complete muscle paralysis in a matter of hours. Clinicians should consider the possibility of TPP in any patient who presents with acute onset of paralysis.
CORRESPONDENCE
Jorge Luis Chavez, MD; 8405 E. San Pedro Drive, Scottsdale, AZ 85258; jorgeluischavezmd@yahoo.com.