Since antiquity, man has searched for the ability to provide local and/or regional anesthesia. Numerous methods have been described in historical texts, including the application of cold/ice, compression, rubbing, and acupuncture to painful areas. In the mid-1880s, cocaine was being studied in Peru. Soon after, it began to be used in medicine as a local and regional anesthetic in the United States and Europe for minor surgeries and dental procedures. Since that time, our understanding of macro and micro neuroanatomy, cellular biology, and pharmacology, has vastly expanded. This has allowed for entire medical subspecialties, such as regional anesthesia, pain medicine, and the like, to have developed and serve a vast array of patients.
Local or regional anesthesia is indicated for a diversity of clinical circumstances ( Table 23-1 ). It is easy to provide when one understands the regional anatomy, block technique, and pharmacology of the agents injected. These nerve blocks can provide anesthesia for procedures, as well as rapid diagnostic, prognostic, and therapeutic data when applied in the appropriate clinical setting. The result, either temporary or permanent, allows for pain relief, increased functionality, and independence, especially within the context of a well-designed, multidisciplinary pain treatment program. However, these positive outcomes may only occur when provided to the appropriate patient. The clinician must understand when providing a regional anesthetic may be contraindicated ( Table 23-2 ).
| With Local Anesthetics |
| Provides anesthesia for procedures |
| Differentiates pain problems and helps better understand nociceptive pathways |
| Serves as a treatment for inflammatory compression neuropathies in combination with corticosteroids |
| Provides treatment for sympathetic mediated pain syndromes |
| Differentiates spasticity from joint contractures |
| Helps predict the effect of a neurolytic procedure |
| Allows selective recording in nerve conduction studies |
| Promotes functional activities in an occupational or physical therapy program |
| Assists in serial or inhibitory casting |
| With Normal Saline |
| Provides placebo response |
| With Neurolytic Agents (Chemical Neurolysis) |
| Facilitates functional goals in the spastic patient: positioning, ambulation, bracing, transfers |
| Improves caregiver tasks (such as hygiene) in the spastic patient: perineal, axillary, elbow, or hand regions |
| Improves self-image of the spastic patient by reducing joint deformities and improving cosmesis |
| May improve residual voluntary muscle control by eliminating unwanted hypertonia in the spastic patient |
| Reduces pain caused by hypertonia |
| Provides treatment for specific, intractable pain disorders |
| Prevents nerve compression injuries in hyperflexed joints (i.e., median nerve at the wrist from wrist flexor spasticity) |
| Prevents skin breakdown by promoting proper seating and positioning |
| Patient Selection Factors | Relative Contraindication | Absolute Contraindication |
|---|---|---|
| Patient cooperation | Psychiatric disorder (e.g., needle phobia, anxiety) | Patient refusal |
| Movement disorder (e.g., essential tremor, tics) | ||
| Language barrier, pediatric patient | ||
| Acutely intoxicated | ||
| Anatomic and physiologic | Anatomic abnormalities | |
| factors | Technical challenges (e.g., obesity, arthritis) | |
| Anesthetic considerations |
| |
| Coexisting diseases | Neurological disease (e.g., multiple sclerosis) | Infection at injection site |
| Comatose state | Allergy to anesthetic | |
| Sepsis | Coagulopathy/systemic anticoagulation | |
| Coagulopathy (e.g., hemophilia) | ||
| Trauma (especially neurological trauma) | ||
| Perioperative issues | Surgical duration to outlast regional anesthetic | Block will hinder the procedure |
| Surgical positioning discomfort | ||
| Prolonged surgical time |
The American Society of Anesthesiologists (ASA) sets standards for the safe practice of anesthesia, including that for neural blockade. This includes appropriate monitoring of the patient and immediate access to supplemental oxygen and resuscitation equipment, in the rare occurrence of a catastrophic event. However, the ASA standards were written for perioperative patients, and not those presenting to the pain clinic. There is no official standard for monitoring within the realm of pain medicine. However, a recent survey of various pain centers within the United States demonstrated that for peripheral nerve blocks, 56% place a noninvasive blood pressure cuff and 52% place a pulse oximeter during the procedure. This is despite the fact that 72% of pain clinics had treated an average of 7.3 vasovagal reactions within the 12-month study period. Periprocedure nothing by mouth (NPO) status is another area in which the ASA has clear guidelines, yet these too are lacking for patients undergoing office-based neural blockade.
The Joint Commission on the Accreditation of Healthcare Organizations (JCAHO) expects that universal protocols, such as preprocedure patient and site verification, as well as procedural time-outs, occur, before an anesthetic or invasive intervention is instituted. These standards also apply for neural blockade.
Neurovascular Bundle Anatomy
The neurovascular bundle consists of peripheral nerve fibers wrapped in connective tissue, intermingled by a capillary plexus ( Fig. 23-1 ). Three types of connective tissue are present within the peripheral nerve: endoneurium, perineurium, and epineurium. The endoneurium is a delicate, supporting structure located adjacent to individual axons within a fascicle. This layer covers the entire individual nerve fiber. Individual fascicles are bound by the perineurium. The perineurial barrier is formed by adjacent perineurial cells via tight junctions, which help manage the axonal microenvironment, in addition to the blood-nerve barrier and nerve-cerebrospinal fluid (CSF) barrier. The fascicles are bound in groups by the outermost layer, the epineurium ( Fig. 23-2 ), which encloses the nerve as a whole. This layer contains the vasa nervorum, which divides into arterioles that penetrate the perineurium ( Fig. 23-3 ). Ultimately, a network of capillaries reaches each fascicle to supply individual axons. More specifically, the vasa nervorum forms the endoneurial capillaries. The endoneurial capillary endothelium contains tight junctional connections, which create the blood-nerve barrier. Cells that compose the distal layer of the arachnoid membrane are connected by tight junctions as well, which form the boundary of the nerve-CSF barrier. As nerve roots leave the subarachnoid space, the perineurium fuses with the cells of the distal layer of the arachnoid membrane. Anterior and posterior nerve roots, which are motor and sensory, respectively, initially leave the spinal cord separately, but merge via the connective tissue architecture, to become mixed sensorimotor nerves exiting the spinal canal.
The neurovascular bundle usually lies well protected between muscle or bone. At its most proximal location—the spinal root level—the neurovascular bundle contains motor, sensory, and autonomic fibers. These roots divide into dorsal and ventral rami, the latter of which reconnect to form a plexus of nerves. Ultimately, terminal nerve branches of isolated fiber types—sensory or motor branches—are formed.
Local Anesthetic Pharmacology
Local anesthetic agents are categorized by their chemical composition—esters and amides ( Table 23-3 ). Ester and amide anesthetics are weak bases—their pKa is near physiologic pH. Each is comprised of a lipophilic group, such as a benzene ring, and a hydrophilic group, such as a tertiary amine. These groups are either connected by an ester or amide linkage. This linkage is what imparts their categorization as an ester or amide. Esters are readily metabolized by plasma cholinesterase, thus their half-life is very short, on the order of minutes. Para-aminobenzoic acid (PABA) is one of the break-down products of this reaction. Amides undergo hepatic metabolism through N -dealkylation and hydrolysis. This is a slower process, imparting a longer half-life (2 to 3 hours), assuming the patient has normal liver function. Some patients with local anesthetic allergy may be sensitive to PABA, and a detailed history and chart review may be necessary to delineate if a ester local anesthetic was really the causative agent responsible for an earlier allergic reaction. Some local anesthetics, esters and amides alike, are stored in multi-use vials with the preservative methylparaben. Methylparaben may also cause an allergic reaction in patients with a PABA allergy.
| Esters | Amides |
| Procaine | Lidocaine |
| Cocaine | Mepivacaine |
| Chloroprocaine | Bupivacaine |
| Tetracaine | Etidocaine |
| Ropivacaine |
All local anesthetics are weak bases, and their pKa is near physiologic pH. This allows for these agents to be present in both the ionized (charged) and nonionized (uncharged) forms when administered. The lower the agent’s pKa and higher the pH, the more that will be uncharged in-vivo. The uncharged local anesthetics are lipophilic and readily cross cell membranes, namely neuronal axons. Thus, the more uncharged local anesthetic that exists in vivo for a given agent, the more potent and faster onset that agent is rendered. For this reason, clinicians will elect to add sodium bicarbonate to their local anesthetics, to raise the pH and thereby increase the amount of nonionic local anesthetic.
Local anesthetics act on neuronal axons. These agents, when uncharged, passively diffuse to the sodium channels of axons. These sodium channels allow Na + to enter the axon, depolarize, and propagate an action potential to allow for communication between neurons. Local anesthetics inhibit this process by binding to these sodium channels, ceasing depolarization as well as action potential propagation, and thus neuronal signaling and transmission of pain signals ( Tables 23-4 and 23-5 ).
| Letter Class | Numeral Class | Diameter (μm) | Conduction (msec) | Myelin | Drug Sensitivity | Function |
|---|---|---|---|---|---|---|
| — | Ia | 12-20 | 70-120 | ++ | ++ | Muscle spindle primary endings |
| — | Ib | 12-20 | 70-120 | ++ | ++ | Golgi tendon organs |
| A-α | — | 6-22 | 70-120 | ++ | ++ | Motor efferent, proprioception afferent |
| A-β | II | 6-22 | 30-70 | ++ | ++ | Motor efferent, proprioception afferent, encapsulated an accessory structured nerve endings (e.g., Meissner corpuscles) |
| A-γ | — | 3-6 | 10-50 | ++ | ++ | Muscle spindle efferent |
| A-δ | III | 1-4 | 5-30 | ++ | +++ | Pain, temperature (cold), touch, afferent, hair receptors |
| B | — | <3 | 3-15 | + | ++++ | Preganglionic autonomic |
| C | IV | 0.3-1.3 | 0.5-2 | — | ++++ | Pain, temperature (warm), afferent, itch, postganglionic autonomic |
| Class | Relative Axonal Diameter | Afferent Function | Efferent Function |
|---|---|---|---|
| Ia | ++++ | Muscle spindle | |
| Ib | ++++ | Golgi tendon organ | |
| A-α | ++++ | Lower motor neuron | |
| A-β | +++ | Meissner and pacinian corpuscles, Merkel endings | |
| A-γ | +++ | Axons to intrafusal fibers | |
| A-δ | ++ | Sharp pain, cold, some touch | Preganglionic autonomic |
| C | + (No Myelin) | Dull pain, heat, itch | Postganglionic autonomic |
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