To the Editor:
We read with interest the recent article by Sala-Blanch et al. 1, in which the authors prospectively evaluated the frequency of subclinical neurologic injury following nerve-stimulator-guided low-pressure intraneural injection of local anesthetic and radio-opaque contrast for a single-shot sciatic popliteal bock in 16 patients undergoing hallux valgus repair. Intraneural injection was confirmed by ultrasound and computed tomography scan imaging. Patients underwent physical examination and conventional electrophysiologic studies both preoperatively and postoperatively at weeks 1 and 4 to detect clinical and subclinical nerve injury, respectively. None of the 16 patients demonstrated evidence of clinical or subclinical nerve injury. Based on these results, the authors cautiously concluded that low-pressure intraneural injection within the sciatic nerve at the popliteal level may not result in clinical or subclinical nerve injury. Despite material differences in methodology, Sala-Blanch et al. 's findings are in stark contrast to a recent publication that reported the frequency of subclinical nerve injury after nerve-stimulator-guided continuous femoral nerve block in young adults undergoing anterior cruciate ligament repair to be 24% at 4 weeks, based on clinical examination and conventional electrophysiologic study2; all patients recovered at 6 months.
Therefore, we believe that some additional information is necessary in order for the readership, ourselves included, to meaningfully interpret the clinical relevance of the present results. First, the authors defined electrophysiologic nerve injury as “a change in latency (more than 120%) or in amplitude and conduction velocity (less than 80%) compared with baseline data obtained in the same individual.” However their table 3 summarizes the mean electrophysiologic records for all the patients at the three time-points. Averaging theses values may mask potential electrophysiologic variations, which may occur following nerve injury. We believe the raw electrophysiologic data for each patient both at baseline and at 4 weeks postoperatively should also be reported, as the evolution over time may further inform our understanding of nerve injury. Indeed, the value of electrodiagnostic data at 1 week postoperatively may be questionable, as motor and sensory axons can remain excitable for a period of 7 and 11 days, respectively, following an insult.3Nonetheless, the results of Sala-Blanch et al. 's study do seem to lend support to the growing body of important literature suggesting that intraneural injection may not always lead to nerve injury, and for this, we are sincerely grateful.