Rebound Hyperkalemia in Hypokalemic Thyrotoxic Periodic Paralysis

Figure 1.. Electrolyte and treatment timeline: Potassium levels and therapies administered during the first 40 hours after patient presentation to medical care is shown. The blue shading represents normal laboratory potassium range. Therapies and the time they were administered relative to time from presentation are shown. Abbreviations: D50: 50% IV dextrose; IV: intravenous; PO: oral; PTU: propylthiouracil.

Figure 2.. Thyrotoxic periodic paralysis physiology and acute treatment. (A) Schematic depiction of physiologic processes that result in hypokalemia leading to muscle weakness. Black arrows depict processes that can worsen hypokalemia-related weakness. Red items depict treatments that can lead to improvement in hypokalemia-related weakness. Purple items depict external factors that can worsen hypokalemia-related weakness. Right center depicts an EKG with a red box around a U-wave which can be in hypokalemia. (B) Treatment algorithm for acute thyrotoxic periodic paralysis and possible rebound hyperkalemia. Abbreviation: TPP: thyrotoxic periodic paralysis.

Figure 3.. Electrocardiogram changes reflective of abnormal potassium levels. (A) EKG obtained with a potassium level of 2.2 mEq/L (normal, 3.6-5.1 mEq/L) showing the presence of U waves. (B) EKG obtained with potassium levels at 6.8 mEq/L showing the presence of peaked T waves. (C) EKG for comparison while potassium levels were normal at 4.1 mEq/L. The blue boxes to the right of (A-C) show magnified V2 leads for the same voltage and time windows.