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Traumatic needle damage to nerves during regional anesthesia: presentation of a novel mechanotransduction hypothesis

Abstract

Despite advances in needle positioning techniques, nerve damage still occurs after regional anesthesia. Recognized causes include local anesthetic toxicity, subperineural injection, high subepineural fluid injection pressures and subepineural hematoma after forceful needle-–nerve contact.

We hypothesize that subperineural injection is still possible, but less likely to be the cause of nerve damage because needle penetration of fascicles and mechanical damage is difficult to achieve. High-resolution (75 µm) 40 MHz micro-ultrasound images of pig axillae show short-bevelled 22 g, 0.7 mm wide block needles that are three times larger than the average fascicle. Fascicular bundles are extremely difficult to puncture because they spin away on needle contact. Histology from fresh cadavers after supposed intrafascicular injection shows fluid spread within perineurium and intrafascicular perineural septae, but no breach of endoneurium or axons.

We propose that mechanotransduction, the cellular changes that occur in response to force, contributes to nerve damage. Piezo ion channel proteins transduce force into electrical activity by rapid entry of cations into cells. Excessive Ca2+ influx into cells has the potential to inhibit nerve regeneration. Cellular changes include regulation of gene expression. The forces associated with purposeful needle insertion are generally unknown. Our experiments in the soft embalmed Thiel cadaver showed a lognormal range of forces between 0.6 N and 16.8 N on epineural penetration.

We hypothesize that forceful needle injury may cause nerve damage by activation of Piezo receptors and release of intracellular Ca2+.

  • nerve block
  • peripheral nerve injuries
  • neurologic manifestations

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