148
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Injection nerve palsy: What's to blame?

      letter

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Sir, We read with interest the article “Injection nerve palsy” by Kakati et al.[1] and appreciate their meticulous study on nerve injection injuries (NII). Critically, several mechanisms of NII that may play a role in the nerve damage were not fully explored in their article. It has previously been shown that injection pressure is a factor in the degree of NII with high pressures (>11 psi) causing more damage than those with low pressures (<11 psi).[2] This measurement is affected both by the gauge of the needle used and the size of the barrel used, with a smaller gauge and larger barrel leading to a higher pressure of drug delivery. Additionally, the needle tip can play a role in the degree of damage.[3] While tapered needles generally do not cause as much damage, in the case of beveled needles it is critical to insert the needle parallel to the nerve fibers as this leads to reduced chances of nerve damage. Also, the authors have only briefly described the importance of chemical injury in the pathogenesis of NII. It is worthwhile to mention here that in many instances the peripheral neuritis and nerve damage have been seen to occur even with the use of correct technique of injection. Chemical neurotoxicity of the agent injected has been blamed in such cases, as has also been suggested by a number of animal studies. This concept was explored by Gentili et al.[4] who injected different compounds into nerve fascicles of rats and found that penicillin G, diazepam, and chlorpromazine were the most neurotoxic, damaging even the extrafascicular nerve fibers, while minimal damage was caused by injections of iron–dextran, meperidine and cephalothin. Also, the quantity of drug injected dictated the degree of injury. In a recent study by Senes et al.[5] the authors created a list of drugs and their comparative neurotoxicities. They found that hydroxybenzoate, alcohol and diacetin were the most neurotoxic, sodium cefuroxime and phenobarbital were moderately neurotoxic, while naloxone (with hydroxybenzoate), vitamin K (with glycocholic acid and lecithin), and glycocholic acid and lecithin when used individually were comparatively least neurotoxic. Others have gone to show the various mechanisms by which nerves can be damaged by the agent. Steroids cause direct toxicity on peripheral nerve fibers and cause ischemic changes in the nerve.[6] Penicillin has been shown to cause granuloma formation when given into sciatic nerves in dogs.[7] Lidocaine, procaine and tetracaine split the myelin lamellae and cause more severe damage than bupivacaine.[8] It is not unreasonable to think that the differing neurotoxicities of drugs as well as how these drugs are delivered could have effects on patient recovery both, in cases that resolve on their own and those that do or not improve with surgery. Though Kakati et al.[1] have mentioned that there were no data available regarding the nature of drugs their patients received or the precise way in which they received them, it would be interesting to know what role these factors play if at all.

          Related collections

          Most cited references8

          • Record: found
          • Abstract: found
          • Article: not found

          Ropivacaine-induced peripheral nerve injection injury in the rodent model.

          Intraneural administration of local anesthetics has been associated with nerve damage. We undertook the present study to investigate histological changes induced by ropivacaine injection into rat sciatic nerve. Fifty-four adult male Lewis rats were randomly distributed into 9 groups, 6 animals per group. Fifty microliters of normal saline, 10% phenol, or 0.75% ropivacaine were administered by intrafascicular injection, extrafascicular injection, or extraneural (topical) placement. At 2 weeks, animals were killed and the sciatic nerve at the injection site was evaluated with light microscopy, quantitative histomorphometry, and electron microscopy. On cross-sectional evaluation, extrafascicular ropivacaine injection and extraneural placement of ropivacaine were both associated with damage to the perineurium, with focal demyelination surrounded by edematous endoneurium. Intrafascicular injection of ropivacaine resulted in a wedge-shaped region of demyelination and focal axonal loss with some regeneration, bordered by a region of normally myelinated axons in a background of edematous endoneurium. Extrafascicular injection resulted in more significant damage than extraneural placement of ropivacaine, but less than intrafascicular injection as shown with quantitative histomorphometry. Quantitatively, ropivacaine-injured specimens had significantly lower nerve density than saline-injured specimens. Wallerian degeneration and perineural edema were also demonstrated qualitatively with electron microscopy. This study demonstrates that, in the rat model, ropivacaine is associated with marked histological abnormality, including edema of the perineurium and axonal destruction with wallerian degeneration, when injected into or extraneurally placed onto a nerve. Extrafascicular injection and extraneural placement were associated with similar, although milder, histological damage than intrafascicular injection. Further work is needed to investigate the functional implications, if any, of the histological abnormalities observed in this study.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Peripheral nerve injection injury with steroid agents.

            The possible neurotoxic effects of five commonly used steroid agents were examined. Using histologic studies and studies of the microneural circulation, it was found the steroids can indeed cause neurotoxicity. The injection site was critical in effecting injury. Only intrafascicular injection caused damage. The damage produced varied with the agent used. Dexamethasone (Decadron) caused minimal damage, while hydrocortisone (Solu-Cortef) and triamcinolone hexacetonide (Aristospan) caused widespread axonal and myelin degeneration. Disturbance in the blood-nerve barrier correlated with the changes noted on light and electron microscopy, but is thought to be coincidentally and not causally related. In conclusion, it was shown that the intrafascicular injection of commonly used steroid agents had a direct toxic effect on peripheral nerve-fibers and caused a disruption of the blood-nerve barrier. Use of the more toxic agents in the vicinity of peripheral nerves should probably be avoided.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Complications of regional anesthesia.

              The use of regional anesthesia, either alone or as an adjunct to general anesthesia, is at an all-time high. Demonstrated benefits include reduced side effects, more efficient use of facilities and enhanced patient satisfaction with the improved postoperative pain relief. New advances in equipment, techniques and medications have been incorporated over the past 10 years, and especially over the last 2 years. As the number of practitioners and procedures increase, the number of complications may rise as well. The specific issues of nerve damage, treatment of local anesthetic toxicity with lipid solutions and prevention of wrong-sided procedures are examined with special reference to recent publications. Specific needle shapes, appropriate pharmacologic resuscitation from intravascular injection of local anesthetics and institutional procedures to positively identify patients and the correct block location are all part of a strategy to minimize the occurrence of adverse outcomes and to mitigate the consequences of those adverse events when they do occur. More importantly, these are changes that can be instituted immediately with minimal expense to the institution and great benefit to the patient.
                Bookmark

                Author and article information

                Journal
                J Neurosci Rural Pract
                J Neurosci Rural Pract
                JNRP
                Journal of Neurosciences in Rural Practice
                Medknow Publications & Media Pvt Ltd (India )
                0976-3147
                0976-3155
                Oct-Dec 2013
                : 4
                : 4
                : 481
                Affiliations
                [1] Department of Neurosurgery, Baylor College of Medicine, Houston, Texas, USA
                [1 ] Department of Neurosurgery, Rajendra Institute of Medical Sciences, Ranchi, Jharkhand, India
                Author notes
                Address for correspondence: Dr. Shashikant Patil, Department of Neurosurgery, Baylor College of Medicine, 1709 Dryden Street, Suite 1750, Houston, TX 77030, USA. E-mail: spatil@ 123456bcm.edu
                Article
                JNRP-4-481
                10.4103/0976-3147.120202
                3858783
                24347971
                bd1f8c0e-b1a3-42b2-87a6-6c7fbaa888c4
                Copyright: © Journal of Neurosciences in Rural Practice

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Letters to the Editor

                Neurosciences
                Neurosciences

                Comments

                Comment on this article