The purpose of peripheral nerve blocks is to inhibit impulse transmission distally in a nerve terminal, thus terminating the pain signal perceived by the cortex. Nerve blocks can be used to treat acute pain (e.g., procedural anesthesia and perioperative analgesia), as well as for diagnosis and treatment of chronic pain. Impulse blockade can be brief (hours) or prolonged (months), depending on the medication used in the block and the technique (e.g., single shot block versus catheter). Nerve blocks are also used in the emergency department for the following indications:
Many nerves can be blocked depending on the injury. These include the following upper or lower extremities:
Peripheral nerve blocks have gained widespread acceptance as technological advancements have improved accuracy, efficacy, and safety. Nonetheless, in-depth knowledge of peripheral nerve anatomy remains an essential component of successful and safe peripheral nerve blockade. Peripheral nerve blocks were originally performed by eliciting paresthesias to localize peripheral nerves, followed years later by nerve stimulation techniques. More recently, ultrasound-guidance has improved anesthesiologists’ and emergency physicians' abilities to visualize nerve structures and other surrounding structures (e.g., vasculature and pleura).
Peripheral nerve blocks offer many advantages to traditional anesthetic and analgesic techniques. Patients who would otherwise have excessive risks with general anesthesia can safely undergo surgery painlessly with regional anesthesia. Additionally, the adverse effects of perioperative opioid analgesia can be minimized or avoided completely while still providing superior pain control. If a prolonged blockade is desired, peripheral nerve catheters can remain for several days to provide more extended analgesia than a single-shot block alone.
Although peripheral nerve blocks are overall very safe when performed correctly, there are rare but serious risks associated with them. Risks include block failure, bleeding, infection, damage to surrounding structures, permanent nerve injury, and intravascular uptake of local anesthetic resulting in systemic toxicity. Contraindications include an inability to cooperate with placement (sometimes seen in pediatric patients, combative patients, or those with severe dementia), systemic or local infection at the site of the block, and the presence of coagulopathy or systemic anticoagulation.
Local anesthetics have a significant risk of systemic toxicity when administered intravascularly. Symptoms usually manifest in the central nervous system first (metallic taste, auditory changes, circumoral numbness, blurred vision, agitation, seizures), followed by cardiovascular effects (hypotension, decreased cardiac contractility, dysrhythmias, complete heart block, cardiovascular collapse). Bupivacaine is particularly cardiotoxic, and cardiovascular collapse has been reported in the absence of antecedent neurologic symptoms. Neurolytic blocks with alcohol and phenol are used in chronic pain, usually as a last resort in cancer pain. They cause a semi-permanent destruction of the nerve, which blocks impulse transmission and improves pain. Risks with a neurolytic destruction of a nerve include the development of central or deafferentation pain syndromes, which are very difficult to treat.
Contraindications include an allergy to aminoesters (procaine, cocaine, tetracaine).
Amides-lidocaine/bupivacaine/mepivacaine/ropivacaine (usually preservative).
Before performing a peripheral nerve block, a complete history and physical exam are essential. The emphasis in the history should be placed on the existence of underlying severe cardiac or pulmonary disease, opioid intolerance, pre-existing neurologic deficit, easy bleeding or bruising, and anticoagulation medications. The physical exam should be directed to sensory and motor function of the extremity to be blocked, evidence of coagulopathy (widespread bruising), evidence of systemic infection (fever or elevated white blood cell count), and infection at the site of the block (redness, swelling, warmth).
When evaluating a patient for peripheral nerve blockade, thorough risk/benefit analysis and informed consent are necessary. Discussion with the surgeon can help direct block location and local anesthetic selection, or preference toward a catheter if longer block duration is preferable. Each patient’s maximum local anesthetic dose must be calculated before performing of the block and should never be exceeded.
Emergency airway equipment, resuscitation drugs (including lipid emulsion 20%), supplemental oxygen, and hemodynamic monitoring must be immediately available where blocks are performed. Blocks should be performed with strict sterile technique. Anxiolytic medications may be used to facilitate patient comfort. Awake patients reduce the risk of nerve injury by reporting paresthesias so the needle can be redirected before injection of local anesthetic. Additionally, an awake patient can report early symptoms of local anesthetic systemic toxicity (i.e., tinnitus, circumoral numbness, and tachycardia with epinephrine), to avoid more serious complications with large volume local anesthetic injection (seizures, coma, and cardiac collapse). Recommended maximum dosages for local anesthetics are widely available, but practitioners should always use the lowest dose necessary to achieve the desired result due to the significant risk of systemic toxicity.
Point of care, bedside ultrasound can be used to locate and visualize the nerve.
If a complication occurs, early recognition and treatment are essential to reduce long-term morbidity to the patient. Intravenous lipid emulsion 20% must immediately be available in locations that perform peripheral nerve blocks. Patients with suspected local anesthetic overdose should be treated immediately with intravenous lipid emulsion 20% (Intralipid) 1.5 mL/kg (lean body mass) given over one minute, followed by a 0.25 mL/kg/min infusion. Refractory cases of local anesthetic systemic toxicity may require cardiopulmonary bypass/extracorporeal membrane oxygenation until the drug has been metabolized.