Abstract
In recent decades, the use of energy-based devices has substantially increased the incidence of iatrogenic thermal injury to nerves (cauterization, etc.). While recovery of the nerve after thermal injury is important, the changes in neural structure, function, and peripheral inflammatory reactions postinjury remain unclear. This study is aimed at demonstrating the changes mentioned above during the acute, subacute, and chronic stages of nerve reinnervation after thermal injury. Spontaneous reinnervation was evaluated, including the neural structures, nerve conduction abilities, and muscle regeneration. These effects vary depending on the severity of thermal injury (slight, moderate, and severe). Peripheral inflammatory reactions, as impediments to reinnervation, were found in significant numbers 3 days after thermal injury, exhibiting high expression of IL-1β and TNF-α, but low expression of IL-10. Our findings reveal the pathogenesis of peripheral nerve reinnervation after thermal injury, which will assist in selecting appropriate treatments in further research.
Highlights
Energy-based devices (EBDs) have been widely adopted for hemostasis in recent decades due to the easy application and effective reduction in blood loss [1, 2]
The nerve conduction velocity (NCV) index was measured in each time point after thermal injury to assess spontaneous nerve reinnervation recovery
The NCV index was recorded at 30 days after thermal injury to evaluate the recovery of spontaneous nerve reinnervation, presenting as 0:97 ± 0:05, 0:45 ± 0:04, and 0:06 ± 0:08 in slight, moderate, and severe groups, respectively, with significant difference
Summary
Energy-based devices (EBDs) have been widely adopted for hemostasis in recent decades due to the easy application and effective reduction in blood loss [1, 2]. As a less reversible type, was associated with obvious histologic damage [4,5,6]. It has been revealed that the peripheral nerves manifest as a reversible conduction block when exposed to lower-grade thermal injury but manifest with axonal degeneration at higher temperatures [7]. There is a decrease in the manifestation of electromyographic (EMG) changes in amplitude with a concomitant increase in latency during acute thermal nerve damage [8]. It is unclear whether peripheral nerves could develop spontaneous reinnervation after thermal injury. It is unclear how the functional recovery differs when considering the severity or the time of recovery after thermal injury
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
