Local anesthetic nerve block

Sonography guided femoral nerve block.

Local anesthetic nerve block (local anesthetic regional nerve blockade, or often simply nerve block) is a short-term nerve block, usually lasting hours or days, involving the injection of an anesthetic, a corticosteroid and other agents onto or near a nerve, usually for pain relief or anesthesia.

A combination of local anesthetic (such as lidocaine), epinephrine, a steroid (corticosteroid) and an opioid is often used. Epinephrine produces constriction of the blood vessels which delays the diffusion of the anesthetic. Steroids can help to reduce inflammation. Opioids are painkillers. These blocks can be either single treatments, multiple injections over a period of time, or continuous infusions. A continuous peripheral nerve block can be introduced into a limb undergoing surgery, for example, a femoral nerve block to prevent pain in knee replacement.[1]

Local anesthetic nerve blocks are sterile procedures that are usually performed in an outpatient facility or hospital. The procedure can be performed with the help of ultrasound, fluoroscopy (a live X-ray) or CT. Use of any one of these imaging modalities enables the physician to view the placement of the needle. A probe positioning system can be used to hold the ultrasound transducer steady. Electrical stimulation can provide feedback on the proximity of the needle to the target nerve.

Mechanism of Action

Main article: Mechanism of Action

Voltage-gated sodium channels conduct electrical impulses and mediate fast depolarization along nerves.[2] These channels are the target of local anesthetics (LA). LA target open channels, bind on the inner side of the nerve membrane, and prevent ion flow. LA often contain a tertiary amine group. Both the protonated and neutral forms lessen the membrane permeability of the nerve to sodium.[3] Recently, studies have implicated that multiple S6 segments form the LA binding site within the channel.[4] S6 segments are transmembrane helices within the channel protein. There are four homologous repeats in the channel protein with segments labeled S1-S6 indicating the 6 transmembrane α-helices. Thus, in total, there are four S6 segments. S6 segments in particular are implicated in formation of the inner pore. Additionally, open or inactivated sodium channels produce a higher binding affinity than resting states due to conformational change during gating.[5] Dissociation of LA occurs only from open channels.[3]

Common Nerve Blockers & Adjuvants

Local anesthetics, class I antiarrhythmic drugs, and some anticonvulsants target voltage-gated sodium channels. Drugs commonly used for peripheral nerve blocks include lidocaine, ropivacaine, bupivacaine, and mepivacaine.[6] These drugs are often combined with adjuvants with the end goal of increasing the duration of the analgesia or shortening time of onset. Additives may include epinephrine, clonidine, and dexmedetomide. Epinephrine is the most widely used additive. It increases the length of analgesic duration and decreases blood flow by acting as an agonist at the α1-adrenoceptor. Vasoconstriction caused by LA may be further enhanced synergistically with the addition of epinephrine. Epinephrine use is controversial due to its potential neurotoxicity but is a valuable biomarker for intravascular injection. It is recommended that epinephrine be used only with nerve blocks performed without ultrasound guidance. Clonidine is an α2-adrenoceptor agonist. Its addition to LA provides approximately an additional 100 minutes of analgesia. Dexmedetomidine is not as widely used as epinephrine and clonidine and is not currently approved in the US. Studies in humans indicate improved onset time and increased duration of analgesia.[7]

Toxicity and Nerve Injury

Local anesthetic toxicity is indicated by numbness and tingling around the mouth, metallic taste, or ringing in the ears. Additionally, this may lead to seizures, arrhythmias, and may progress to cardiac arrest. This reaction may stem from an allergy, excessive dose, or intravasucular injection.[6] Other complications include nerve injury. Nerve injury is thought to affect 0.5-1.0% of patients receiving nerve blocks, although some studies suggest as many as 10-15%.[8] Permanent nerve injury, however, only affects 1.5 in every 10,000 patients. The use of ultrasound and nerve stimulation has greatly improved practitioners’ ability to safely administer nerve blocks. Nerve injury most often occurs from ischaemia, direct neurotoxicity, or needle misplacement. Ropivacaine is less toxic than lidocaine, however, ropivacaine is correlated with histological damage such as axonal destruction and Wallerian degeneration in rodents. Needle choice studies have also found that nerve injury was more likely with short-bevel needles compared to long-bevel needles. Finally, preexisting pathology also determines whether a patient is more likely to suffer nerve injury.[8]

See also

References

  1. ↑ UCSD. Regional anesthesia
  2. ↑ Marban E, Yamagishi T, Tomaselli GF (1998). "Structure and function of voltage-gated sodium channels". The Journal of Physiology 508 (3): 647–57. doi:10.1111/j.1469-7793.1998.647bp.x. PMC 2230911. PMID 9518722.
  3. 1 2 Strichartz G (1976). "Molecular mechanisms of nerve block by local anesthetics". Anesthesiology 45 (4): 421–41. PMID 9844.
  4. ↑ Nau C, Wang GK (2004). "Interactions of local anesthetics with voltage-gated Na+ channels". The Journal of Membrane Biology 201 (1): 1–8. PMID 15635807.
  5. ↑ Catterall WA (2000). "From ionic currents to molecular mechanisms: the structure and function of voltage-gated sodium channels". Neuron 26 (1): 13–25. doi:10.1016/S0896-6273(00)81133-2. PMID 10798388.
  6. 1 2 http://prc.coh.org/ComRegNB.pdf[]
  7. ↑ Brummett CM, Williams BA (2011). "Additives to local anesthetics for peripheral nerve blockade". International Anesthesiology Clinics 49 (4): 104–16. doi:10.1097/AIA.0b013e31820e4a49. PMC 3427651. PMID 21956081.
  8. 1 2 Jeng CL, Torrillo TM, Rosenblatt MA (2010). "Complications of peripheral nerve blocks". British Journal of Anaesthesia 105 (Suppl 1): i97–107. doi:10.1093/bja/aeq273. PMID 21148659.
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