Chapter 16. Local Anesthetics

Local anesthesia is the condition that results when sensory transmission from a local area of the body to the central nervous system (CNS) is blocked. The local anesthetics constitute a group of chemically similar agents that block the sodium channels of excitable membranes. Because these drugs can be administered by topical application or by injection in the target area, the anesthetic effect can be restricted to a localized area (e.g., cornea, arm, foot). Even when these drugs are given in the vicinity of the spinal cord, it is still considered a form of local anesthesia because only a specific level of cord impulse transmission is blocked. When given intravenously, however, these drugs can have effects on other tissues.

Local anesthetics are used for a variety of purposes, including localized surgical procedures, labor and delivery, and joint manipulations. They can also be used for short-term pain relief in conditions such as tendonitis or in long-term situations such as pain associated with cancer. Table 16–1 presents some of the methods of delivery of local anesthetics and the common clinical uses of each method.

Most local anesthetics in current use are esters or amides. In addition, they are amines with the ability to bind a proton (H+ ion) and become charged under acidic conditions. They differ in potency, duration of action, and surface activity (Figure 16–1). Many short-acting local anesthetics are readily absorbed into the bloodstream from the injection site after administration. Therefore, the duration of local action is limited unless blood flow to the area is reduced. This can be accomplished by coadministration of a vasoconstrictor (usually an alpha [α] agonistsympathomimetic such as epinephrine or phenylephrine) with the local anesthetic agent. The vasoconstrictor retards the removal of the drug from the injection site and may reduce the potential for CNS toxicity. Cocaine is an important exception because it has intrinsic sympathomimetic action (Chapter 6). The longer-acting agents (e.g., tetracaine and bupivacaine) are also less dependent on the coadministration of vasoconstrictors. Surface activity (ability to reach superficial nerves when applied to the surface of the skin or mucous membranes) is a property of only a few local anesthetics (e.g., cocaine and benzocaine).

Metabolism of ester local anesthetics is carried out by plasma cholinesterases and occurs rapidly. Procaine, the prototypic ester local anesthetic, has a half-life of 1 to 2 minutes. The amides are metabolized in the liver with half-lives of 2 to 6 hours.

Local anesthetics block voltage-dependent sodium channels and reduce the influx of sodium ions, thereby preventing depolarization of the membrane and blocking conduction of the action potential. Local anesthetics gain access to their receptors on the channels from the cytoplasm or the membrane (Figure 16–2). Because the drug molecule must cross the lipid membrane to reach the cytoplasm, the more lipid-soluble (nonionized, uncharged) form reaches effective intracellular concentrations more rapidly than does the ionized form. On the other hand, once inside the axon, the ionized (charged) form of the drug is the more effective blocking entity. Thus, both the nonionized and the ionized forms of the drug play important roles, the first in reaching the receptor site and the second in causing the effect. The affinity of the receptor site within the sodium channel for the local anesthetic is a function of the state of the channel, whether it is resting, open, or inactivated, and therefore is both voltage- and time-dependent, following the same rules of sodium channel blocking as antiarrhythmic drugs (Chapter 10). More rapidly firing nerve fibers (e.g., sensory fibers) are usually blocked before more slowly firing fibers (e.g., motor fibers).

When the local anesthetic is bound to the receptor site on the sodium channel, the channel is maintained in a blocked condition. By blocking a sufficient number of channels, the anesthetic prevents action potential propagation along the affected portion of the nerve axon. Other ions can influence local anesthetic action. For example, high concentrations of extracellular K+ enhance local anesthetic activity, whereas elevated extracellular Ca2+ antagonizes blockade.

The differences in sensitivity of various types of nerve fibers to local anesthetics depend on fiber diameter, myelination, physiologic firing rate, and anatomic location (Table 16–2). In general, smaller fibers are blocked more easily than larger fibers, and myelinated fibers are blocked more easily than unmyelinated fibers. Activated pain fibers fire rapidly; therefore, pain sensation appears to be blocked by lower concentrations of local anesthetics. Fibers located in the periphery of a thick nerve bundle are blocked sooner than those in the core because they are exposed earlier to higher concentrations of the anesthetic.

The local anesthetics are commonly used for minor skin injuries or irritations and various surgical procedures. Local anesthetics are also used in spinal anesthesia by injection of the drug into the epidural or subarachnoid space surrounding the spinal cord (Figure 16–3). They can be used to produce temporary autonomic blockade in ischemic conditions in the limbs. Slow epidural infusion at low concentrations has been used successfully for postoperative analgesia (in the same way as postoperative epidural opioid infusion; i.e., patient-controlled analgesia [PCA], refer to Chapter 20). However, repeated epidural injection in anesthetic doses may lead to tachyphylaxis. See Table 16–1 for a list of clinical uses of local anesthetics.

The intended effect of any administered local anesthetic is to produce a regional response by affecting specifically targeted nerves. However, these drugs can be absorbed into the general circulation and have effects on other tissues and organs. Systemic effects are most likely to occur if an excess of drug is used, if there is greater absorption of the drug than anticipated, or if the drug is unintentionally injected directly into the systemic circulation.

The most important toxic effects of most local anesthetics are in the CNS. All local anesthetics are capable of producing a spectrum of central effects, including lightheadedness, sedation, restlessness, confusion, agitation, nystagmus, and, at very high doses, tonic-clonic convulsions. Convulsions may be followed by coma with respiratory and cardiovascular depression. Thus, CNS excitation may be followed by CNS depression. This depression may impair respiratory function and death from respiratory failure may occur.

With the exception of cocaine, all local anesthetics are vasodilators. Patients with preexisting cardiovascular disease may develop heart block and other disturbances of cardiac electrical function at high plasma levels of local anesthetics. The direct cardiovascular effects associated with local anesthetics (except cocaine) include vasodilation, decreased heart rate, decreased force of contraction, and decreased cardiac excitability and conduction. These depressant effects on the heart can occur if sufficient amounts of the local anesthetic reach the systemic circulation. They may be opposed by baroreceptor reflex responses evoked by hypotension. Bupivacaine may produce severe cardiovascular toxicity, including arrhythmias and hypotension, if given intravenously.

The ability of cocaine to block norepinephrine reuptake at sympathetic neuroeffector junctions and the vasoconstricting actions of the drug contribute to cardiovascular toxicity. When used as a drug of abuse, the cardiovascular toxicity of cocaine includes severe hypertension with cerebral hemorrhage, cardiac arrhythmias, and myocardial infarction.

Severe local anesthetic toxicity is treated symptomatically; there are no specific antidotes. Convulsions are usually managed with intravenous diazepam or a short-acting barbiturate such as thiopental. Hyperventilation with oxygen is helpful. Occasionally, a neuromuscular-blocking drug may be used to control violent convulsive activity. The cardiovascular toxicity of bupivacaine overdose is difficult to treat and has caused fatalities in healthy young adults.

Local anesthetics have applications in many different clinical conditions. For this reason, there are multiple patient situations where physical therapists may encounter their use both directly and indirectly. Patients suffering from minor skin injuries or irritations may be using a topical anesthetic. Therapists may be involved in administering the local anesthetic either topically or transdermally for the treatment of hypertonicity (i.e., increased resistance to passive stretch secondary to an upper motor neuron lesion) or musculoskeletal disorders (tendonitis, bursitis), respectively. Some patients involved in rehabilitation programs may have received central nerve blocks for severe and chronic pain and have been referred for comprehensive therapy programs to improve their overall functional status. Patients who have received autonomic blocks may need intervention to reestablish normal sympathetic function and blood flow. Finally, the physical therapist should be aware of patients with indwelling catheters which deliver sustained spinal analgesia following surgery or other medical procedures and the possible effects on motor and sensory loss in the affected extremities. Motor and sensory assessment is vital before attempting to implement any therapeutic procedure to ensure proper outcomes.

Because of the seriousness of systemic side effects associated with local anesthetics, physical therapists should always be alert for signs and symptoms of the systemic adverse effects of local anesthetics in patients receiving these drugs.

Adverse Drug Reactions

CNS effects

• Confusion
• Agitation
• Restlessness

Cardiovascular effects

• Hypotension
• Bradycardia
• Decreased cardiac output

Effects Interfering with Rehabilitation

• Inability to feel sensations such as pain, deep pressure, light touch, heat, and cold
• Possible motor impairment
• Impairment due to systemic distribution (light-headedness, sedation, restlessness, confusion, agitation, convulsions, decreased heart rate, and hypotension)

Possible Therapy Solutions

• Time: If effects are not life-threatening, they will diminish with time.
• Advise physician if effects are prolonged.

Potentiation of Functional Outcomes Secondary to Drug Therapy

• Local anesthetic relief of pain may allow increased function without sedation.

Brief History: The patient is a 48-year-old female who sought rehabilitation therapy to improve her overall physical conditioning and reduce intermittent back pain caused by strenuous activities. She stated that several years ago a physician had prescribed a skeletal muscle relaxant but she felt this really did not help her problem and made her sleepy. She stated her back pain was always associated with activities demanding flexion of her trunk such as yard work and vacuuming. She also noted that it was increasingly hard to stay seated at her desk at work for long periods of time. Most recently, some of her exercise routines at a local fitness center have resulted in back pain.

Current Medical Status and Drug Therapy: The patient’s current medical status was unremarkable. The only medication she was currently taking was an over-the-counter analgesic such as ibuprofen or acetaminophen as needed for pain.

Rehabilitation Setting: Initial evaluation revealed no remarkable abnormalities in postural alignment of her spine or sacroiliac joints. The patient pointed to her lower lumbar spine and sacral region as the site of her back pain and denied any radiation of symptoms into her lower extremities. On physical examination, the patient had minimal weakness in her core trunk stabilizing musculature and palpable protective guarding of her lower lumbar paraspinal musculature. The physical therapist suggested that the patient see her physician to rule out spinal pathology.

Problem/Clinical Options: Her physician ordered a magnetic resonance image (MRI), and it was found that the patient had significant lumbar stenosis. Owing to her relatively young age and her high degree of physical activity, her physician suggested a conservative program of physical therapy and postural education. The physician also prescribed lidocainetransdermal patches to be worn over the site of pain as needed for pain control. The patient was instructed to wear the transdermal patch for no more than 12 hours per 24-hour period. The patient now reports that most of her pain occurred in the late afternoon and early evenings so she began applying the patch when she first noticed the pain in the afternoon and would wear it through the evening until bedtime. She also began a rehabilitative program consisting of therapeutic exercise, deep tissue massage, and patient education about proper posture and positioning in the work place.

Ultimately, the patient was able to discontinue use of lidocainetransdermal patches and maintain an active lifestyle without recurrence of low back pain.

Articaine (Septocaine)

Parenteral: 4% with 1:100,000 epinephrine

Benzocaine (generic, others)

Topical: 5, 6% creams; 15, 20% gels; 5, 20% ointments; 0.8% lotion; 20% liquid; 20% spray

Bupivacaine (generic, Marcaine, Sensorcaine)

Parenteral: 0.25, 0.5, 0.75% for injection; 0.25, 0.5, 0.75% with 1:200,000 epinephrine

Butamben Picrate (Butesin Picrate)

Topical: 1% ointment

Chloroprocaine (generic, Nesacaine)

Parenteral: 1, 2, 3% for injection

Cocaine (generic)

Topical: 40, 100 mg/mL solutions; 5-, 25-g powder

Dibucaine (generic, Nupercainal)

Topical: 0.5% cream; 1% ointment

Dyclonine (Dyclone)

Topical: 0.5, 1% solution

Levobupivacaine (Chirocaine)

Parenteral: 2.5, 5, 7.5 mg/mL

Lidocaine (generic, Xylocaine, others)

Parenteral: 0.5, 1, 1.5, 2, 4% for injection; 0.5, 1, 1.5, 2% with 1:200,000 epinephrine; 1, 2% with 1:100,000 epinephrine, 2% with 1:50,000 epinephrine

Topical: 2.5, 5% ointments; 0.5, 4% cream; 0.5, 2.5% gel; 2, 2.5, 4% solutions; 23, 46 mg/2 cm2 patch

Lidocaine and etidocaine eutectic mixture (EMLA cream)

Topical: lidocaine 2.5% plus etidocaine 2.5%

Mepivacaine (generic, Carbocaine, others)

Parenteral: 1, 1.5, 2, 3% for injection; 2% with 1:20,000 levonordefrin

Pramoxine (Tronothane, others)

Topical: 1% cream, lotion, spray, and gel

Prilocaine (Citanest)

Parenteral: 4% for injection; 4% with 1:200,000 epinephrine

Procaine (generic, Novocain)

Parenteral: 1, 2, 10% for injection

Proparacaine (generic, Alcain, others)

0.5% solution for ophthalmic use

Ropivacaine (Naropin)

Parenteral: 0.2, 0.5, 0.75, 1% solution for injection

Tetracaine (Pontocaine)

Parenteral: 1% for injection; 0.2, 0.3% with 6% dextrose for spinal anesthesia

Topical: 1% ointment; 0.5% solution (ophthalmic); 1, 2% cream; 2% solution for nose and throat; 2% gel