The Silent Threat of Hypokalemia after High Voltage Electrical Injuries: A Case Study and Review of the Literature

Abstract

High-voltage electrical injuries, especially from lightning strikes, can cause life-threatening complications due to extreme temperature and voltage exposure. While burns and cardiac complications have been widely described, the documentation of metabolic imbalances, particularly hypokalemia, has not been as prevalent. This report focuses on a patient with profound transient hypokalemia following a lightning strike, alongside a review of three similar cases of transient hypokalemia from the literature. Our patient, a previously healthy young man, was struck by lightning and subsequently suffered transient hypokalemia with lower extremity sensory changes, which resolved after the normalization of serum potassium levels. While the exact underlying mechanisms of transient hypokalemia following high-voltage electrical injuries are unknown, we propose a multifactorial mechanism, which includes massive intracellular shifts of potassium due to elevated epinephrine levels and the prevention of potassium efflux through the electrical disruption of voltage-gated potassium channels. Our report underscores the importance of recognizing hypokalemia in patients with high-voltage electrical injuries and contributes to the understanding of the complex mechanisms involved. Further research is necessary to understand the connection between cellular changes induced by high-voltage exposure and their effects on metabolism, particularly in relation to hypokalemia.

Keywords: electrical injuries; hypokalemia; lightning strikes; literature review; metabolic disturbances; potassium channels.

Figure 1

Initial ECG demonstrating a mild intraventricular conduction delay, characterized by a prolonged QTc of 461 milliseconds, merging of the T and U waves (most prominent in lead II), and distinct U wave most visible in V3. ECG, electrocardiogram.

Figure 2

Physical, metabolic, and cellular manifestations of high-voltage electrical injuries. Na⁺, sodium, K⁺, potassium.

Figure 3

(A) Normal K⁺ channel and Na⁺/K⁺-ATPase function: K⁺ enters the cell via the Na⁺/K⁺-ATPase while Na⁺ exits the cell through the Na⁺/K⁺-ATPase. K⁺ exits the cell through voltage-gated K⁺ channels embedded in the cell membrane. (B) Following high-voltage shock, increased β2-adrenergic signaling causes heightened Na⁺/K⁺-ATPase activity, reduced K⁺ conductance through voltage-gated K⁺ channels, and reduced selectivity against Na⁺ by 50% [35]. K⁺, potassium; Na⁺/K⁺-ATPase, sodium–potassium pump; Na⁺, sodium.