Basic Principles of Neural Blockade

23 Basic Principles of Neural Blockade



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).1


Table 23-1 Indications for Percutaneous Nerve Blocks













































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 studies7
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

Table 23-2 Relative and Absolute Contraindications for Regional Anesthesia1



































































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  

Adapted from Tsui, BCH, Finucane, BT: Managing adverse outcomes during regional anesthesia. In Longnecker DE, Brown DL, Newman MF, Zapol WM (eds): Anesthesiology. New York, McGraw Hill, 2008, p 1054.


The American Society of Anesthesiologists (ASA) sets standards for the safe practice of anesthesia, including that for neural blockade.2 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.3 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.3 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.3a



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.4,5 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.6 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.6





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.8


Table 23-3 Categorization of Local Anesthetic Agents





















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).




Local anesthetics block in a sequential order, which is related to the diameter of the axon (see Tables 23-4 and Table 23-5). C-fibers, which carry pain and temperature information, are blocked first, as their diameter is small. A-α and A-β fibers have the largest axonal diameter, and are the last to become blocked. These fibers are primarily motor and proprioceptive. However, nerves with myelin may only require pharmacologic sodium channel blockade at the nodes of Ranvier, leaving these nerves susceptible to local anesthetic action.8


Mechanical or chemical vasoconstriction is sometimes beneficial for local anesthesia. It allows for a block of longer duration and stronger intensity by decreasing systemic uptake. This also imparts protection against systemic local anesthetic toxicity. Dilute epinephrine is the most common agent added to local anesthetics for this purpose, although phenylephrine and norepinephrine may also suffice, with lesser results.9 Epinephrine dilutions of 1:200,000 (5 mcg/mL) and 1:400,000 (2.5 mcg/mL) are typically prepared with the local anesthetic. An added benefit of adding epinephrine is that it may serve as an early indicator of unintentional vascular injection. This is sometimes referred to as a “test dose”, whereby a small dose of local anesthetic with epinephrine is injected while the patient’s heart rate is monitored. An increase in heart rate above 20% of the baseline heart rate would confer a positive test dose, indicating an intravascular injection may have occurred. There are potential contraindications to the addition of a chemical vasoconstrictor to local anesthetics, although the evidence for these may be weak10 (Table 23-6). Furthermore, chemical tourniquets should not be used when anesthetizing digits, ears, noses, genitals, or other areas with a poor collateral blood supply because this could lead to tissue necrosis. However, several recent large trials and literature reviews failed to demonstrate consistent tissue injury from the use of chemical vasoconstriction in some of these areas.1214


Table 23-6 Relative Contradictions to the Addition of Chemical Vasoconstrictors to Local Anesthetics











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Jun 19, 2016 | Posted by in PAIN MEDICINE | Comments Off on Basic Principles of Neural Blockade

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