Advanced Education In General Dentistry

Module 01: Advanced Pain Control and Sedation

Advanced Techniques and Local Anesthesia

Local Anesthetics

Local anesthetics function by altering the resting potential of the nerve, altering the threshold potential at which the nerve will fire, decreasing the rate of depolarization and prolonging the repolarization phase. Local anesthetics bind to receptors on the sodium channel, displacing calcium. By blocking the sodium channel, they decrease sodium conductance, thereby decreasing the rate of depolarization. If sodium cannot flow, the nerve will not fire, and threshold potential cannot be achieved, thus blocking conduction.

See Mechanism of Action in "Local Anesthetic Review."

There are two different types of local anesthetics, defined by the chemical linkages between the groups.

More Information
LINK: See Classification of Local Anesthetics and Properties of Local Anesthetics in "Local Anesthetic Review."

Those with ester linkages include drugs such as procaine, chloroprocaine and tetracaine. These are readily hydrolyzed by pseudocholinesterase, and patients may exhibit an allergy to esters, but are in fact allergic to PABA, which is a metabolite of the ester. Those with amides linkages, which are more popular and in wider use because of the problem with allergies, include prilocaine, articaine, mepivicaine, lidocaine, bupivacaine, etidocaine.

An easy way to remember which local anesthetics are amides is to keep in mind that all of the amide agents have an "I" in their names, besides the "I" in the 'caine ending.

Local anesthetics tend to be basic compounds, with pKa's ranging from 7.6 to 8.9, and are poorly soluble in water. (See "Clinical Pharmacology" in Local Anesthetic Review*). They are combined with acids to form salts, and are dispensed as the hydrochloric acid salt dissolved in either saline or water; therefore the extracellular pH is critical to the action of the local anesthetic.

Like all agents, local anesthetics can dissociate into its base and its acid, and as the pH drops, more anesthetic will exist in a cationic form. The cationic form is not hydrophobic, and therefore will not diffuse readily through the cell membrane; this forms the chemical reasoning for why injecting into an infected area does not provide an excellent level of local anesthesia. The action on the nerve membrane, of course, is dependant upon the pKa and the pH of the extracellular fluid, and the intracellular fluid in infection is stable. The extracellular pH, rather, is unstable in an area of infection. It is the extracellular pH that changes.

More Information
LINK: For a table of See Clinical Pharmacology in "Local Anesthetic Review."

Clinical cautions:

Vaso Constrictors in Local Anesthetics

Many of these agents have vaso-constrictors within them, which offset the vasso-dilating properties that are inherent in the local anesthetic agent. Keep in mind that vaso-constrictors have three different types of adronergic receptors:

Epinephrine, a vasoconstrictor in local anesthetics, acts at the a½, Β1, and Β2 receptors causing vasoconstriction, cardiac stimulation, and bronchodilation. Generally epinephrine 1/1,000 is used in an emergency situation in either IM or subcutaneously.

Doses may vary depending upon the patient:

For example, a patient with asthma who does not have an albuturol nebulizer, may be given 0.3 or 0.4 CCs of 1/1,000 epinephrine subcutaneously in an emergency situation to act as a broncho-dilator. For cardiac arrest, a 1/10,000 dilution is generally used.

Vaso-constrictors should be used with caution or not at all in patients with uncontrolled hypertension, patients who have had a recent M.I. or a stroke, or patients who have had a recent coronary artery bypass. Patients with dysrythmias or unstable angina are also not good candidates to receive a vasoconstrictor. In the operating room, patients who are being administered a halogenated inhalational agent such as a halothane should not be administered exogenous epinephrine locally because it can predispose the patient to ventricular dysrythmias. Patients on non-specific beta blockers, MAO inhibitors, tricyclic antidepressants should also not receive vasoconstrictor in their local anesthetic. Another vasoconstrictor that's used besides epinephrine is levonordephrine or neocobephrine It's potency as a vasopressor is 15% that of epinephrine.

Common Local Anesthetics

Lidocaine has an anesthetic half-life of about 1.6 hours. Its advantages include a very rapid onset.

Mepivicaine comes as 3% carbocaine. It too has very rapid onset, and a recommended dosage similar to lidocaine; however, carbocaine does not contain a vasoconstrictor.

Prilocaine is generally available as 4%, and may or may not contain 1/200,000 epinephrine. Prilocaine can induce metheboglobinemia, especially in predisposed patients at high dosages. It is also believed to be less toxic than lidocaine, and it is good for prolonged anesthesia.

Articaine must be used with care in patients with methemoglobinemia. Patients who are allergic to sulphur drugs cannot receive articaine, and it is also contraindicated in ASA III and IV patients.

Bupivicaine or marcaine is a long-acting agent. The maximimum recommended dose is 1.3 mg/kg, and its onset of action 6-10 minutes, which is longer than that of lidocaine.

Etidocaine is another long-acting local that has an onset of action in 3 minutes.

Post-Operative Pain Management

Post-Operative Pain Management

Third molar pain has certainly served as a pain model for many, many years, and the method that works best for controlling pain includes three main components:

  1. use of a long-acting local anesthetic
  2. administration of an I.V. steroid to minimize swelling and inflammation
  3. administration of a non-steroidal anti-inflammatory drug on a regular basis.

All of these actions will minimize the need for post-operative opiods, and this works very well in ASA I and II patients.

Drug/drug interactions to be concerned about: