Soft Tissue Workshop Local Anesthetics and Regional Anesthesia of the Head and Neck

Local Anesthetics

Local Anesthetic  A local anesthetic is an agent that interrupts pain impulses in a specific region of the body without a loss of patient consciousness. Normally, the process is completely reversible--the agent does not produce any residual effect on the nerve fiber.

Advantages of Local Anesthesia  The patient is conscious during surgery.  Smooth postoperative course.  Patient awake and maintains his own airway.  Less pain needs less narcotics, lighter anesthesia in general cases.  Less nursing care after procedures, less admissions.  Less expensive

Disadvantages of Local Anesthesia  The patient may prefer to be asleep  Specialized skill necessary.  Some blocks require up to 30 minutes to be fully effective.  Analgesia may not always be totally effective, and general anesthesia may be required anyway.

Disadvantages of Local Anesthesia  Generalized toxicity may occur if local anesthetic drugs are given intravenously by mistake or an overdose is given.  Widespread sympathetic blockade can result in hypotension.  There is a small but definite incidence of prolonged nerve damage.

Characteristics of the Ideal Local Anesthetic  Effective when injected or applied topically  Short onset of action  Duration long enough for procedure  Non-Irritating to tissues  Non-damaging to nerve structures  High margin of safety  Soluble in water, stable in solution  Inexpensive and available

History  First local anesthetic - Cocaine which was isolated from coca leaves by Albert Niemann in Germany in the 1860s.  Very first clinical use of Cocaine was in 1884 by Sigmund Freud who used it to wean a patient from morphine addiction.  Very first clinical use of Cocaine was in 1884 by Sigmund Freud who used it to wean a patient from morphine addiction.  It was Freud and his colleague Karl Kollar who first noticed its anesthetic effect. Kollar first introduced it to clinical ophthalmology as a topical ocular anesthetic.  It was Freud and his colleague Karl Kollar who first noticed its anesthetic effect. Kollar first introduced it to clinical ophthalmology as a topical ocular anesthetic.  Also in 1884, Dr. William Stewart Halsted was the first to describe the injection of cocaine into a sensory nerve trunk to create surgical anesthesia.

Chemistry All local anesthetics are weak bases, classified as tertiary amines.

Esters  These include cocaine, procaine, tetracaine, and chloroprocaine.  They are hydrolyzed in plasma by pseudo- cholinesterase. One of the by-products of metabolism is paraaminobenzoic acid, the common cause of allergic reactions seen with these agents

Amides  These include lidocaine, mepivicaine, prilocaine, bupivacaine, and etidocaine.  They are metabolized in the liver to inactive agents. True allergic reactions are rare (especially with lidocaine)

Mechanism of Action  Local anesthetics are weak bases that work to block nerve conduction by reducing the influx of sodium ions into the nerve cytoplasm.  Sodium ions cannot flow into the neuron, thus the potassium ions cannot flow out, thereby inhibiting the depolarization of the nerve.  Sodium ions cannot flow into the neuron, thus the potassium ions cannot flow out, thereby inhibiting the depolarization of the nerve.  If this process can be inhibited for just a few Nodes of Ranvier along the way, then nerve impulses generated downstream from the blocked nodes cannot propagate to the ganglion.

Mechanism of action  local anesthetics bind directly to the intracellular voltage-dependent sodium channels  Block primarily open and inactive sodium channels, at specific sites within the channel

Mechanism of action  1) slow rate of depolarization  2) reduce height of action potential  3) reduce rate of rise of action potential  4) slow axonal conduction  5) ultimately prevent propagation of action potential  6) do not alter resting membrane potential  7) increase threshold potential

Factors affecting local anesthetic action Effect of pH  charged (cationic) form binds to receptor site and does not readily cross the cell membrane, thus, tissue acidosis (abscesses and cellulitis) renders local anesthetic agents ineffective  uncharged form penetrates membrane  efficacy of drug can be changed by altering extracellular or intracellular pH

Susceptibility to block by local anesthetics of types of nerve fibers  In general, small nerve fibers are more susceptible than large fibers; however,  the type of fiber  degree of myelination  fiber length and  frequency- dependence are also important in determining susceptibility

Order of sensory function block  1. pain  2. cold  3. warmth  4. touch  5. deep pressure  6. motor Recovery in reverse order

Recovery from local anesthesia  After injection, the drug is absorbed into the blood and removed from the area  Absorption varies with the vascularity of the area injected  Epinephrine is potent vasoconstrictor and results in decreased blood flow…slower absorption…decreased likelihood of systemic reaction and prolonged anesthetic effect

TOXICITIES OF LOCAL ANESTHETICS  Essentially all systemic toxic reactions associated with local anesthetics are the result of over-dosage leading to high blood levels of the agent given. Therefore, to avoid a systemic toxic reaction to a local anesthetic, the smallest amount of the most dilute solution that effectively blocks pain should be administered.

Hypersensitivity of Local Anesthetics Some patients are hypersensitive (allergic) to some local anesthetics. Although such allergies are very rare, a careful patient history should be taken in an attempt to identify the presence of an allergy. There are two basic types of local anesthetics (the amide type and the ester type). A patient who is allergic to one type may or may not be allergic to the other type.

Central Nervous System Toxicities Local anesthetics, if absorbed systematically in excessive amounts, can cause central nervous system (CNS) excitement or, if absorbed in even higher amounts, can cause CNS depression.

CNS toxicity continued  Excitement. Tremors, shivering, and convulsions characterize the CNS excitement.  Depression. The CNS depression is characterized by respiratory depression and, if enough drug is absorbed, respiratory arrest.

Cardiovascular Toxicities  Local anesthetics if absorbed systematically in excessive amounts can cause depression of the cardiovascular system.  Peripheral vascular action arteriolar dilation (except cocaine which is vasoconstrictive)  Hypotension and atrioventricular block characterize such depression. These may ultimately result in both cardiac and respiratory arrest.

Signs of toxicity  Signs of toxicity occur on a continuum. From early to late stages of toxicity, these signs are: circum-oral and tongue numbness, lightheadedness, tinnitus, visual disturbances, muscular twitching, convulsions, unconsciousness, coma, respiratory arrest, then cardiovascular collapse.

Treatment of Toxicity  Oxygen by face mask or intubation  Anticonvulsants such as benzodiazepines and barbiturates (diazepam 5-10 mg, thiopental mg) are the drugs of choice for seizure control.  Phenytoin is not effective and should be avoided.  Succinylcholine is sometimes also used to terminate the neuromuscular effects of seizures. Because succinylcholine paralyzes all muscles, the patient requires intubation.  In severe reactions, monitor the cardiovascular system (CVS) and support the patient with intravenous fluids and vasopressors as required.  Metabolic acidosis may develop, and the use of sodium bicarbonate can be considered, although, as in other instances of acute metabolic acidosis, this is controversial.

Lidocaine  Amide, vasodilator (use epinephrine)  4% solution for topical use  0.5%-1% solution for injection into soft tissues  Maximum dose 5mg/kg without epinephrine; 7mg/kg with epinephrine  10mg/ml in 1% lidocaine  20mg/ml in 2% lidocaine

Mepivacaine (Carbocaine)  Efficacy and toxicity similar to lidocaine but diffuses more readily through tissues and has a longer half-life

Bupivacaine (Marcaine)  Long duration of action, used for nerve blocks or infiltrated into wound closure for postoperative pain relief  Total dose 3mg/kg alone; 4mg/kg with epi

Ropivacaine  Newer agent, efficacy similar to bupivacaine but is less toxic and less moor block for he same degree of sensory block  S stereoisomer of bupivacaine and has the substitution of a propyl for a butyl  Slightly less potent and has safer cardiotoxicity profile

Cocaine  Unique among topical anesthetics because it is a potent vasoconstrictor  Can be used alone in upper aerodigestive tract for both anesthesia and control of hemorrhage  Limited to mucous membranes of the head and neck  4% solution for direct application to mucous membranes  Quick onset of action (5-10 minutes) and duration of action as long as 6 hours  Blocks uptake of epinephrine and norepinephrine by adrenergic nerve endings – potentiates the effects of catecholamines  Total dose limited to 1.5 mg/kg

Benzocaine  Topical spray before endoscopic procedures  Can cause methemoglobinemia if used in large doses

Local Anesthetics Drug Chemical Characteristic Metabolism Max dose (mg/kg) Onset/Duration CocaineEsterCholinesterase min 6 hours LidocaineAmideLiver min 1-3 hrs BenzocaineEsterCholinesterase3 BupivicaineAmideLiver3-4

Regional Blocks in Head and Neck

Scalp Blocks

Trigeminal Nerve Blocks

Mandibular Nerve Blocks

Inferior Alveolar Nerve Block