In three cases of hypokalemic periodic paralysis with varying etiologies, timely recognition and correction of hypokalemia resulted in complete resolution of muscle weakness and paralysis.
Case Report (n=3)
Timely recognition and correction of severe hypokalemia in hypokalemic periodic paralysis leads to rapid resolution of life-threatening paralysis.
Abstract Introduction Hypokalemic periodic paralysis (HPP) is a rare neuromuscular disorder caused by mutations in skeletal muscle calcium or sodium ion channels. It manifests as recurrent episodes of flaccid paralysis or profound muscle weakness, often triggered by exercise, stress, high-carbohydrate intake, alcohol, thyrotoxicosis, or potassium loss. We present three cases of HPP with varying etiologies and presentations. Case Presentation Case 1: A 38-year-old woman with alcoholic liver cirrhosis, hypertension, and chronic electrolyte abnormalities (hypokalemia, hypomagnesemia, and hypophosphatemia) presented with diarrhea and inability to move her extremities. Labs revealed potassium (K) 1.2 mmol/L, magnesium (Mg) 1.5 mg/dL, phosphorus (P) 0.7 mg/dL, creatinine 1.4 mg/dL, and lactic acid 3.9 mmol/L. Urinalysis showed bilirubinuria and proteinuria. Her hypokalemia and acute kidney injury were attributed to gastrointestinal volume loss. She was treated with IV fluids, potassium at 10 mEq/h until K 2.5, and magnesium and phosphorus replacement. Her K improved to 3.2 mmol/L with complete resolution of weakness. Case 2 A 26-year-old woman with no prior medical history awoke with diffuse pain, numbness, and inability to stand or walk. Exam revealed flaccid paralysis of all extremities. Labs showed K 1.2 mmol/L, Mg 1.5 mg/dL, and P 1.0 mg/dL. After IV fluid resuscitation and electrolyte repletion, her K improved to 4.3 mmol/L within six hours and symptoms resolved. Thyroid studies revealed TSH 0.0025 µIU/mL and free T4 3.12 ng/dL, consistent with thyrotoxic periodic paralysis. She was started on propranolol 10 mg TID and methimazole 10 mg TID with outpatient endocrinology follow-up. Case 3 A 27-year-old man with Graves’ disease presented with sudden generalized paralysis sparing the head. Labs showed K 1.3 mmol/L, Mg 1.9 mg/dL, and P 2.0 mg/dL. ECG demonstrated sinus bradycardia, first-degree AV block, and prolonged QT interval. He received oral potassium and IV fluids with 20 mEq K. Repeat K levels four hours later revealed K 1.5 mmol/L, but his paralysis resolved. He continued to receive aggressive potassium replacement. Thyroid studies revealed TSH 0.0025 µIU/mL and free T4 1.56 ng/dL. Methimazole was increased from 5 mg TID to 10 mg BID, and propranolol 10 mg BID was continued. Discussion Although uncommon, HPP can be life-threatening due to cardiac arrhythmias or respiratory failure. Timely recognition and correction of hypokalemia are critical for favorable outcomes. This abstract is funded by: None
Xiong et al. (Fri,) conducted a case report in Hypokalemic periodic paralysis (n=3). Potassium replacement and supportive care was evaluated on Resolution of paralysis or muscle weakness. In three cases of hypokalemic periodic paralysis with varying etiologies, timely recognition and correction of hypokalemia resulted in complete resolution of muscle weakness and paralysis.