Local and regional anesthesia techniques, Part 1: Overview and five simple techniques


Local and regional anesthesia techniques, Part 1: Overview and five simple techniques

In this first article in a four-part series, these clinicians describe five easy-to-perform anesthetic techniques to improve patient care: infiltration anesthesia, splash blocks, digital nerve blocks, intravenous regional anesthesia, and soaker-type catheters.
Jan 01, 2009

Illustration by Elaine Kurie
Local and regional anesthesia techniques in veterinary practice have many advantages. These techniques

  • Provide effective preemptive and multimodal analgesia
  • Reduce the amount of inhalational agent needed to maintain anesthesia, resulting in improved cardiopulmonary stability during anesthesia
  • Modulate the sympathetically driven stress response to surgical trauma
  • Reduce the development of central sensitization.

Multimodal analgesia can be provided with combinations of local anesthetics, opioids, and alpha2 agonists.

In this article, we give an overview of drugs used for local and regional anesthesia and then discuss five anesthetic techniques—infiltration anesthesia, splash blocks, digital nerve blocks, intravenous regional anesthesia, and soaker-type catheters. We will discuss additional techniques—intra-articular stifle blocks, brachial plexus nerve blocks, intercostal nerve blocks, intrapleural nerve blocks, maxillary and mandibular nerve blocks, and epidural anesthesia and analgesia—in subsequent articles throughout this year. All of these techniques are easy to perform, do not require special equipment, and can greatly enhance the analgesic management of veterinary patients.


Three general drug groups are used to produce regional anesthesia and analgesia in veterinary patients—local anesthetics, opioids, and alpha2 agonists.

Local anesthetic drugs

TABLE 1: Characteristics of Amide-linked and Ester-linked Local Anesthetics
Local anesthetics are weak bases that are poorly soluble in water. Commercially available preparations are formulated as acidic hydrochloride salts to improve stability and water solubility. The pH of commercial preparations of local anesthetics ranges from 3.9 to 6.6. Most local anesthetics are marketed as racemic mixtures of left and right enantiomers. The enantiomers vary in pharmacokinetic, pharmacodynamic, and toxic properties.1,2

Structure and effects. Local anesthetic molecules consist of a lipophilic unsaturated aromatic ring and hydrophilic portion, usually a tertiary amine, separated by a connecting hydrocarbon chain. The lipophilic portion is essential for the anesthetic activity. Local anesthetics are categorized as amino esters or amino amides based on the chemical bond between the aromatic ring and the hydrocarbon chain of the molecule (Table 1). Although lidocaine (known as lignocaine in the United Kingdom) and bupivacaine are most commonly used in small-animal practice, a variety of local anesthetics are available, varying in their chemical structures, potency, onset of action, and duration of effect (Table 2).1,2

TABLE 2: Local Anesthetics and Their Physical, Chemical, and Pharmacodynamic Properties
Local anesthetics block nerve conduction in all types of neurons, including all pain (A delta and C fibers), sensory, motor, proprioceptive, and sympathetic nerve fibers (Table 3). The minimum concentration of local anesthetic necessary to block conduction is higher for motor nerve fibers than for sensory fibers, so sensory anesthesia can occur without muscle blockade. Typically, autonomic preganglionic B fibers are blocked first. A delta and C sensory fibers are blocked before and at lower concentrations than larger sensory A beta, motor A alpha, and proprioceptive A gamma fibers. The order of blockade varies with anatomical location, the specific nerve, and the local anesthetic used.1,2

TABLE 3: Types of Neurons Blocked with Local Anesthetics
The active form of local anesthetics, the nonionized base, diffuses across the axonal nerve membrane where it blocks the generation and conduction of nerve impulses by inhibiting voltage-gated sodium channels. The degree of drug ionization depends on the local anesthetic's dissociation constant (pKa) and the surrounding tissue's pH. When the pKa and pH are identical, 50% of the drug is ionized and 50% is nonionized. The dissociation constants of local anesthetics vary from 7.6 to 9.1, which means that less than 50% of local anesthetic exists in the active, nonionized form at the normal tissue pH of 7.4. The potency, speed of onset of nerve blockade, and duration of anesthesia are related to the degree of ionization of the local anesthetic molecule and, thus, lipid solubility. Alkalizing the local anesthetic by adding sodium bicarbonate increases the percentage that exists in the nonionized, lipid-soluble form and also reduces pain on injection. Thus, buffering the local anesthetic solution with sodium bicarbonate before administration may increase efficacy as well as decrease pain on injection. Acidosis at the injection site, as occurs with tissue infection, increases the ionized portion of the drug, decreasing the local anesthetic's efficacy.1,2