The Art of Patient Comfort — Dr. Feck Breaks Down The Importance of Local Anesthesia & Sedation

By Genni Burkhart

Perhaps no other discovery has contributed more to the modernization of dentistry than the introduction of local anesthetics. While it's easy to take for granted something used regularly, local anesthesia is arguably the greatest advancement in the history of dentistry.

But why is it important to discuss local anesthesia, especially when dealing with more systemic forms of anesthesia such as sedation? The answer lies in potential interactions with medications patients are taking. As such, it's essential to take time and fully consider these interactions carefully.

Additionally, sedation appointments can be lengthy, increasing the potential for toxicity during the procedure. This means there's an increased risk of reaching near-toxic levels of anesthesia. Patients often present with multiple medical conditions, all of which local anesthesia could impact. The sedation candidate frequently has "special needs," and these patients are often difficult to get profoundly numb.

For all these reasons—and to meet course accreditation requirements—a thorough discussion of local anesthetics is necessary. Understanding the complexities of local anesthesia, especially in the context of sedation and patient-specific factors, is crucial for safe and effective dentistry.

Relationship to Sedation Dentistry: Rationale For This Subject

• Drug interaction potential with existing drugs
• Increased toxicity potential
• More local anesthetic/vasoconstrictor
• Medical conditions
• Special needs of the sedation patient
• Local anesthetic resistant
• Course accreditation requirements

History of Anesthetics

The history of anesthetics in dentistry began with the introduction of cocaine as the first local anesthetic in the late 19th century, which revolutionized pain management in dental procedures. This was followed by safer and more effective agents like procaine (Novocain) in the early 20th century and later lidocaine in the 1940s, allowing dentists to perform complex procedures with minimal patient discomfort.

The development of these anesthetics transformed dentistry by making treatments more accessible and less painful for patients.

Highlights:

• Cocaine: 1860 isolated by Albert Neimann
• Introduced as an ophthalmic anesthetic by Carl Koller in 1884
• Chronic use associated with addiction, studied by Sigmund Freud and William Halstead
• The only local anesthetic available for the next 30 years
• Procaine 1898
• Lidocaine 1943
• Bupivacaine 1957
• Articaine 1976

Differences and Similarities in Anesthetics

The most commonly used anesthetics are lidocaine, prilocaine, mepivacaine, bupivacaine, and articaine. While all of these are chemically very similar, understanding the differences among them helps you choose the proper anesthetic for each patient.

Here are a few highlights of these commonly used anesthetics:

Lidocaine

• First amino amide local anesthetic
• Xylocaine, Octocaine
• Available in 1% and 2% concentrations
• 2% with 1:200,000 epinephrine
• 1% and 2% with 1:100:000 epinephrine
• 2% with 1:50,000 epinephrine
• Pregnancy Category A
• Half-Life 1.5-2 hours
• Metabolism 90% Hepatic (CYP1A2)
• Elimination - Renal

Prilocaine

• Less pain upon injection than other local anesthetics, possibly due to higher pH
• Rare side effect of methemoglobinemia
• Available in 3% and 4% concentrations
• 4% with 1:200:000 epinephrine (Citanest Forte)
• Metabolism is hepatic and renal
• Pregnancy Category B
• Half-life 10-150 minutes

Mepivacaine

• Carbocaine, Polocaine
• Available in 1%, 1.5%, 2%, and 3% concentrations
• 3% without epinephrine
• Surgical anesthesia of Mepivacaine without vasoconstrictor is 20-25 minutes
• 2% with 1:20,000 levonordephrin
• Chemically related to bupivacaine
• Pregnancy Category C
• Less pronounced vasodilator activity than lidocaine

Bupivacaine

• Marcaine, Sensorcaine, Vivacaine
• Available in 0.25, 0.5, and 0.75 concentrations
• Pregnancy Category A, greater cardiotoxicity
• Periods of analgesia that persist after the return of sensation, during which time the need for strong analgesics is reduced

Articaine

• Considered "controversial"
• Contains both ester and amide groups
• Available in 4% concentration with 1:100,000 epinephrine
• Higher relative lipid solubility

pKa of the Agent

An important characteristic of local anesthetics is the pKa of the drug. The pKa is the hydrogen ion concentration in which the drug exists in the tissues at equilibrium. (protonated and unprotonated forms) For most anesthetics, the pKa is 8-9 making them weak bases.

Mechanism of Action

Local anesthetics work by interrupting the signals that nerves send to your brain, stopping pain in a specific area. Normally, when a nerve is triggered, sodium (Na+) ions rush into the nerve cell, disrupting the balance, or equilibrium, between sodium and potassium (K+) ions.

This imbalance creates an electrical charge, which travels down the nerve as a signal to your brain, letting you know something hurts. Local anesthetics prevent this by binding to sodium channels, stopping sodium from entering the cell.

Without sodium, the nerve can’t create that charge or send the signal, so you don’t feel pain. Potassium still plays its role, trying to maintain equilibrium, but without the sodium influx, the nerve can't depolarize and pass on the message. Once the anesthetic wears off, the sodium channels reopen, and the nerves return to their normal function, allowing sensations to come through again.

Abnormal Anatomy

While normal nerve anatomy is well understood in dentistry, not all patients present with textbook anatomy. For patients who don't achieve numbness easily due to altered or atypical nerve pathways, it's essential to have a working knowledge of supplementary anesthesia techniques such as periodontal ligament injections and intraosseous injections. These techniques can be invaluable in providing effective anesthesia when conventional methods are insufficient.

Nerve Morphology

In general, the profession of anesthesia is related to the diameter, myelination, and conduction velocity of affected nerve fibers. Clinically, the order of loss of nerve function is as follows:

1. Pain
2. Temperature
3. Touch
4. Proprioception
5. Skeletal Muscle Tone

Patients who are difficult to anesthetize often have variations in nerve morphology, making standard anesthesia techniques less effective.

Onset of Action

The onset of action for local anesthetics is primarily determined by how quickly the drug reaches the nerve site, the specific characteristics of the nerve fibers involved, and the anesthetic's ability to penetrate nerve membranes due to its lipid solubility. In essence, closer proximity to the nerve, thinner pain fibers, and higher lipid solubility all contribute to a faster onset of anesthesia.

Highlights:

• Diffusion to the site: The closer to the nerve, the faster the action. As a result, infiltration often works faster than blocks.
• Nerve morphology: Pain fibers are relatively thin compared to motor fibers.
• Lipid Solubility: Lipophilic agents penetrate the nerve sheath more readily.

In Conclusion

Understanding the complexities of local anesthesia is paramount for safe and effective dental practice—especially given that more emergencies occur in dental offices related to the administration of local anesthetics than those accompanying oral or IV sedation.

The course "Local Anesthesia and Sedation," taught by Dr. Anthony Feck, DMD, delves deeply into the different types of local anesthetics and the critical drug interactions between local anesthetics, vasoconstrictors, and sedative drugs. This comprehensive course, worth 1 Continuing Education (CE) credit, provides a top-down look at what you must consider and account for to treat patients safely.

By taking this course, you'll learn more about potential drug interactions with existing medications, the potential for increased toxicity due to prolonged procedures, and the special needs of sedation patients who may be resistant to local anesthetics. The course also covers the timeline of local anesthetic development, the chemical characteristics and properties of agents, and explains essential concepts like pKa and its importance. By studying the mechanism of action and recognizing the signs of overdose and toxicity, you'll be better equipped to navigate the complexities of modern and safe sedation dentistry.

Author: With 14 years as a published journalist, editor, and writer, Genni Burkhart's career has spanned politics, healthcare, law, business finance, technology, and news. She resides in Northern Colorado, where she works as the editor-in-chief of the Incisor at DOCS Education.