winterweek ra and neurologic complications

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  • 8/12/2019 Winterweek RA and Neurologic Complications

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    All local anesthetics are potentially neurotoxic, and the neural blockade can be seen as a

    reversible expression of this. Commercial local anesthetics are supplied in concentration

    that under normal conditions do not cause nerve damage; however, the use of higher

    concentrations and intraneural injections, especially when epinephrine has been added,

    can result in severe damage with persistent dysfunction and pain (6,13).

    Under normal conditions, the injected local anesthetic is rapidly diluted and buffered by

    the interstitial fluid, absorption into the blood commences within a very short time. This

    means that after injection the concentration of the local anesthetic at the site of injection

    decreases relatively quickly.

    Nerve ischemia may be complete for a limited time only, and can be caused by extra-

    neural or intraneural factors. Extraneural ischemia can be due to local interference with

    circulation (e.g., iatrogenic interference with blood circulation, arteriosclerosis, or global

    hypoperfusion. Intraneural ischemia can be caused by intraneural angiopathy, as in di-

    abetic neuropathy or systemic lupus erythematosus, or by an increase in endoneural

    pressure due to endoneural edema or an intraneural injection.

    Experimentally, it was found that intrafascicular injections in rabbit sciatic nerve in vivo

    could produce endoneurial pressures of more than 700 mmHg, and after such injections

    the endoneurial pressure could exceed the estimated capillary perfusion pressure for

    about 15 minutes. During this period the nerve fascicle is ischemic and is thus vulnerable

    to otherwise toxicologically neutral local anesthetic solutions (14). Similar condition canalso occur in humans, and admixture of epinephrine with the local anesthetic can en-

    hance ischemia and thus increase the risk of neurotoxic injury.

    Conclusions

    Different factors may be involved in neurological complications after peripheral nerve

    blocks

    - the tourniquet

    - the surgeon. Surgery is implicated in neural damage secondary to traction and/or com-

    pression. Experimental studies have shown that stretch and compression act synergic-

    ally for nerve damage.

    - the anesthetist. The following rules should be applied to avoid anesthetist induced

    neural damage

    do not touch the nerve

    do not go into the nerve

    do not inject local anesthetics into the nerve (15)

    use the lowest local anesthetic concentration possible

    use the most friendly local anesthetic

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    The best treatment of neurologic deficit after regional anesthesia is prevention. A careful

    and well documented technique in an awake patient should prevent any nerve damage

    due to the needle or an intraneural injection. Awareness of the problems associated with

    operative positions and careful positioning of the patient with adequate padding belong to

    the appropriate precautions. Once damage has occurred, it can take several forms, rang-

    ing from a mild, reversible neurapraxia to a permanent sensoritmotor deficit.

    References

    1. Selander D. Nerve toxicity of local anaesthetics. In Lfstrm JB, Sjstrand U (eds):Local anaesthesia and Regional Blockade. Amsterdam: Elsevier Science PublisherB.V., 1988, p 77-97

    2. Bonica JJ, Moore DC, Orlov M. Brachial plexus block anesthesia. Am J Surg 1949;

    78: 65,3. Hamelberg W, Dysart R, Bosomworth P. Perivascular axillary versus supraclavicular

    brachial plexus block and general anesthesia. Anesth Analg 1962; 41: 85,

    4. Mogensen BA, Mattsson HS. Posttraumatic instability of the metacarpophalangealjoint of the thumb. Hand 1980; 12: 85,

    5. Kroll DA, Caplan RA, Posner K, et al. Nerve injury associated with anesthesia. Anes-thesiology 1990; 73: 202,

    6. Selander D, Edshage S, Wolff T. Parasthesiae or no parasthesiae? Nerve lesionsafter axillary blocks. Acta Anaesth Scand 1979; 23: 27,

    7. Gillespie JK, Menk EJ, Middaugh RE. Refelx sympathetic dystrophy: A complication ofinterscalene block. Anesth Analg 1987; 66:1316,

    8. Stark RH. Neurologic injury from axillary block anesthesia. J Hand Surg 1996; 21A:391,

    9. Selander D. Neurotoxicity of local anesthetics: Animal data. Reg Anesth 1993; 18:461,

    10. Plevak DJ, Linstromberg JW, Danielsson DR. Paresthesia vs. non paresthesia - theaxillary block. Anesthesiology 1983; 59: A216

    11. Selander D. Peripheral nerve damage and regional anesthesia (Letter). Br J Anaesth1995; 75: 116,

    12. Selander D, Dhunr KG, Lundborg G. Peripheral nerve injury due to injection needlesused for regional anesthesia. Acta Anaesthesiol Scand 1977; 21: 182,

    13. Selander D, Brattsand R, Lundborg G, et al. Local anesthetics: Importance of mode ofapplication, concentration and adrenaline for the appearance of nerve lesions. ActaAnaesth Scand 1979; 23: 127,

    14. Selander D, Sjstrand J. Longitudal spread of intraneurally injected local anesthetics.Acta Anaesth Scan 1978; 22: 622,

    15. Hadzic A, Dilberovic F, Shah S et al. Combination of intraneural injection and highinjection pressure leads to fascicular injury and neurologic deficits in dogs. RegAnesth Pain Med 2004;29:417-23.

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