Principles and Practices: Navigating Local Anesthesia in Dentistry

The advent of local anesthesia has revolutionized the field of dentistry, transforming what were once painful procedures into routine practices. However, the application of local anesthesia is not without challenges and requires an extensive understanding of various principles, methodologies, and recent advancements. This article delves into these aspects, exploring the selection of anesthetic agents, injection sites, procedural techniques, armamentarium, and necessary precautions to ensure patient safety. It underscores the crucial roles of all dental team members in this process, from preventing and managing toxicity to addressing medical emergencies and providing patient-centered care. This article seeks to build a foundational understanding for the safe treatment of patients, emphasizing the importance of continuous learning and skill enhancement in achieving optimal patient outcomes and driving the field of dentistry forward.

Pain is characterized as an adverse sensory and psychological response, induced by genuine or potential tissue injury, often connected with dental therapy.¹ Local anesthesia refers to the process of injecting an anesthetic agent in the vicinity of the nerves that transmit sensory information to a particular part of the oral cavity that is earmarked for treatment. This anesthetic agent temporarily obstructs the transmission of nociceptive nerve impulses, hence enabling the provision of dental treatment without inducing pain.¹

Local anesthetics hold a notable record of reliability and safety in the realms of medicine and dentistry. Their application is so regular, and the occurrence of adverse reactions so uncommon, that it is understandable if healthcare providers sometimes disregard many of their pharmacotherapeutic tenets.² All local anesthetics function similarly, by temporarily interacting with sodium channels, stopping sodium from penetrating the cells and thus preventing the transmission of nerve impulses.³ This means that nociceptive signals related to painful sensations don't make it to the brain, so the patient doesn't experience pain.¹

Types of Local Anesthetics

All local anesthetics, as part of the broader category of anesthetic compounds, work in a similar manner.³ They bind temporarily to sodium channels within cells, thereby blocking the entry of sodium into the cells.^1,3 This action inhibits cell depolarization and stops the transmission of nerve impulses, including nociceptive signals related to pain.^1,3 Consequently, these pain signals do not reach the brain, resulting in the patient not experiencing pain. This process effectively halts the previously ongoing action potential.^1,3

Local anesthetics are classified into two subclasses based on where their metabolism takes place.^2,4,5 Amino amides undergo hydrolysis in the liver.^4,5 On the other hand, amino esters are metabolized by plasma cholinesterases.⁴ Ester local anesthetics-apart from benzocaine, which is used in various topical anesthetic formulations-are rarely utilized and are no longer available in dental cartridges.²

The five amide-based, injectable local anesthetics currently utilized in the United States are lidocaine, mepivacaine, prilocaine, articaine, and bupivacaine.⁶ These agents obstruct the conduction of impulses to the central nervous system, exhibiting marginal clinical differences beyond the onset and duration of action.⁶ Each has proven efficacy: Lidocaine, the initial synthesized amide, serves as the benchmark; mepivacaine exhibits minimal vasodilation; prilocaine's effect duration fluctuates based on injection type;
articaine represents the most recent addition; bupivacaine provides the longest duration of action.⁶ Articaine stands out due to its dual characteristics of both amide and ester properties.^5,7 Articaine was formulated with the aim of providing deep anesthesia while also ensuring relatively quick detoxification.^5,7

The use of a local anesthetic (LA) agent is contraindicated in the event of a known allergy to the agent itself or any constituent of the anesthetic solution.¹ Allergy stands as the sole absolute contraindication to local anesthesia, although certain agents or techniques should be used judiciously or avoided altogether in particular individuals.¹ Documentation of true allergic reactions to amide-type local anesthetics is exceptionally uncommon.^3,8 Despite the rarity of allergies to local anesthetics or cartridge components, practitioners must be ready to diagnose and treat allergic reactions. Anaphylactic symptoms can range from dermatological, respiratory, and gastrointestinal in conscious patients to cardiovascular collapse or respiratory compromise in sedated patients.³ Anaphylaxis management includes activating emergency services, discontinuing the allergenic agent, ensuring airway patency, and administering oxygen and epinephrine.³ Additional steps, given adequate training and availability of medications, may include administering an H1 and H2 blocker, a corticosteroid like hydrocortisone, and an intravenous fluid bolus, provided intravenous access is established.³

Identifying the optimal LA agent requires a thorough analysis of several factors, inclusive of determining the maximum recommended doses for each administered agent.⁶ Clinicians bear a legal and ethical responsibility to identify and administer the most suitable anesthetic and dosage for each patient, as deviations from this standard constitute substandard care.⁶

Onset and Duration

In every instance of local anesthesia administration, clinicians must consider the projected duration of the procedure and the patient's physical and mental health status.⁵ The choice of anesthetic and injection technique should correspond with the specifics of the procedure and the patient's condition, factoring in elements like medical history and the patient's treatment plan.^5,9

Anesthesia onset is dictated by anesthetic lipid solubility and pKa (a number that shows how weak or strong an acid is).^3,10Greater lipid solubility equals higher potency. Anesthetics, as hydrochloride salts, transition from water to lipid-soluble to penetrate neurons.^3,10 This rate, steered by pKa and physiological pH, impacts anesthesia speed.^3,10 Higher pKa values slow onset. This underlines the difficulty in anesthetizing infected patients due to lower pH. Bupivacaine, highly lipid-soluble, requires less drug for nerve blockade than mepivacaine. Thus, lower pKa anesthetics induce quicker effects.^3,10 Local anesthetic duration depends on protein binding and redistribution.^3,11 Higher binding signifies extended action.^3,11 Anesthetic diffusion governs effects on dental pulp/soft tissues.^3,11 Quicker absorption in vascular areas reduces target tissue presence.^3,11 Understanding this, anesthetic cartridges to be enhanced with additional elements to extend their effect. Incorporating a vasoconstrictor like epinephrine or levonordefrin can cause vascular beds around the action site to constrict upon solution deposition, which slows down the drug's absorption into the bloodstream, thereby prolonging the anesthetic's effect.¹² However, it is advised to exercise caution while administering anesthetics with vasoconstrictors in hypertensive patients or those with cardiac irregularities, due to the potential risk of escalating blood pressure or inducing cardiac dysrhythmias.¹³

Toxicity and Potential Interactions

Toxicity and potential interactions also warrant consideration. While drug interactions with local anesthetics are infrequent, reportable interactions of vasoconstrictors with beta-blockers, tricyclic antidepressants, amphetamines, and volatile anesthetics can induce hypertension and cardiac arrhythmias.^1,3 Toxicity may ensue from surpassing the maximum recommended anesthetic dose or from concurrent use of the anesthetic agent by the patient, precipitating significant neurologic and cardiac implications.^5,14,15 The initial manifestation of toxicity includes sensory disruptions and convulsions, escalating to a diminished level of consciousness, with potential progression to coma or respiratory failure.^14,15 An augmented plasma concentration of the drug can disrupt cardiac conduction, leading to arrhythmias or even cardiac arrest.^3,14,15 Unfortunately, the use of anesthetic cartridges has led to a lack of understanding about the actual dosage administered. These cartridges often contain two drugs: a local anesthetic and a vasopressor, each with a separate dose.² To circumvent systemic toxicity, it is incumbent upon clinicians to administer the least effective dose of anesthetic. The maximum recommended dose (MRD) is dictated by both the anesthetic and vasoconstrictor constituents, with the MRD being established by whichever component reaches its limit first.^5,9 It's crucial to factor in the patient's weight in dosage calculations, ensuring precision to avert potential cellular membrane disruption.^3,5,9,14,15 To quantify the local anesthetic in a cartridge, one must multiply the solution's concentration (expressed in mg/mL) by the volume of the cartridge, which typically approximates 1.8 mL in North America or 2.2 mL in many other countries.^3,14,15

Dosage

Lidocaine with epinephrine at a ratio of 1:100,000 is the prevalent dental anesthetic in the United States, proving efficacious for individuals with good health. Lidocaine with epinephrine at a concentration of 1:50,000 may be utilized for hemostasis, although it heightens the risk of cardiovascular reactions. Mepivacaine at a 2% concentration with a 1:20,000 levonordefrin vasoconstrictor provides anesthesia on par with lidocaine. Anesthetics devoid of vasoconstrictors, such as mepivacaine 3% plain, have reduced durations, making them suitable for brief procedures or patients with sensitivity to vasoconstrictors.

Prilocaine at a 4% concentration offers satisfactory local anesthesia and exhibits efficient hepatic metabolism, although its efficacy can fluctuate depending on the injection site. It is not recommended for patients with diminished oxygen-carrying capacity. Bupivacaine at a 0.5% concentration is the most potent amide anesthetic, recommended for prolonged procedures and post-operative pain management. However, it is not advised for pediatric patients or those with special needs due to an elevated risk of injury.

Articaine, a 4% solution incorporating either 1:100,000 or 1:200,000 epinephrine, exhibits higher potency than lidocaine, necessitating a lower dosage. It is safer for patients with hepatic disease due to fewer required injections and enhanced diffusability, but it does present a risk for paresthesia. Despite the availability of various anesthetic options, lidocaine remains the most frequently used, with bupivacaine being the preferred choice for extensive procedures. For long procedures, a combination approach may be employed, initially using a less irritating agent, such as lidocaine or prilocaine, followed by bupivacaine. In restating this crucial point, the choice of anesthetic should be determined by both the expected duration of the procedure and any potential complications related to the concentrations of vasopressors in the anesthetic.

Technique

Nerve blocks and local infiltrations differ in insertion depth and anesthetization coverage.⁵ The type of injection that a dental hygienist is authorized to administer is stipulated by state practice acts.⁵ The majority of states grant dental hygienists the license to administer both types of injections.⁵ Articaine is useful when blocks aren't allowed, as it can spread to lingual surfaces from buccal infiltrations, offering deeper anesthesia.⁵

Buccal infiltration anesthesia, involving a 2 mm to 3 mm needle insertion into the buccal sulcus, is typically used for maxilla due to its porous structure.^1,16,17 Palatal infiltrations anesthetize the nasopalatine or greater palatine nerve endings but can be painful due to the hard palate bone.^1,18 Techniques like topical anesthesia, cooling, pressure application, or needle retraction can alleviate discomfort.^1,7 Intrapapillary infiltration, often used for primary teeth, bypasses the need for palatal infiltration by anesthetizing the palatal interdental papilla and free gingiva after a buccal infiltration.^1,18 Maxillary blocks include the posterior superior alveolar block for maxillary molars and adjacent tissues excluding the first molar's mesiobuccal root, middle superior alveolar block for maxillary premolars, first molar's mesiobuccal root, and surrounding tissues, and anterior superior alveolar block for incisor and canine teeth and related tissues.^1,7 The infraorbital block anesthetizes ipsilateral maxillary teeth, periodontium, buccal soft tissues, maxillary tuberosity, and skin of the lower eyelid, nose, cheek, and upper lip. It can be administered intraorally or extraorally.¹⁹ The greater palatine block anesthetizes the hard palate posterior to the canine tooth, while the nasopalatine block anesthetizes the bilateral palatal premaxilla and, in some cases, maxillary incisors.^7,19 The nasopalatine block, through buccal and intrapapillary infiltrations, anesthetizes the palatal premaxilla and possibly maxillary incisors, using a needle inserted into the incisive papilla until bone contact. Typically, 0.25 mL of anesthetic suffices.¹

The inferior alveolar nerve block (IANB) anesthetizes mandibular teeth and surrounding tissues, requiring a patient's mouth fully open for needle insertion into the pterygotemporal depression.^1,7 The Gow-Gates technique blocks the mandibular nerve at its division point, providing widespread anesthesia but requiring a fully open mouth for needle insertion at the condylar neck.^20,21It has a higher success rate but slower onset than IANB.^1,21 The Vazirani-Akinosi technique, suitable for patients with trismus, anesthetizes several nerves with the patient's mouth closed and needle insertion parallel to the maxillary occlusal plane.²¹ Mental and incisive blocks are useful for bilateral anesthesia on or anterior to the mandibular premolars, requiring needle insertion next to the mental foramen.¹ The buccal nerve block, used for buccal mucosa or gingiva anesthesia of mandibular molars, requires needle insertion into the buccal vestibule.¹ The introduction of articaine has enhanced the efficacy of mandibular buccal infiltrations, due to its high lipid solubility.^22,23 This allows it to be used effectively for buccal infiltrations in the posterior mandible, serving as a viable alternative or supplement to an IANB. Studies have documented success rates between 84% and 94% for articaine buccal infiltrations in anesthetizing mandibular molars.^22,23

Armamentarium

The administration of local anesthetics necessitates a specialized armamentarium. Among these, numerous types of syringes are available. It is incumbent upon the clinician to select a syringe that ensures optimal comfort during usage. Selection considerations should account for anthropometric factors, such as the clinican's hand size, as well as ergonomic preferences, such as a proclivity for a thumb ring or half-moon handle design.^5,7 The needle's size, both in terms of gauge and length, is determined by the injection location and the depth of penetration.^5,7 The clinician's personal preferences may influence the choice if there are multiple suitable options for the type of injection. Pre-sterilized, stainless-steel needles of varying lengths-extra short (12 mm), short (20 mm), or long (32 mm)-form a key part of the dental armamentarium. The gauge of the needle, indicating its diameter, varies too, with larger numbers denoting smaller diameters and lumens.⁵ Dental procedures typically employ needles with gauges of 25, 27, or 30.^9.5,7,9 Patients usually cannot perceive any discomfort difference with smaller gauge needles, but larger ones are often preferred due to less deflection in deeper tissues and improved aspiration reliability, aided by the larger lumen.²⁴

Advances

At the present time, the market offers a plethora of electronic devices engineered to assist in the dispensation of local anesthesia. These devices are distinctively equipped with digital controls that can be adjusted to facilitate aspiration and ensure uninterrupted delivery of the local anesthetic solution, like the Calaject.^3,25Other similar devices include EZFLOW and the Wand. Several of these devices are enhanced by microprocessor assistance, enabling them to monitor the counterpressure imposed by the tissues receiving the local anesthetic injection and adjust the rate of injectate deposition in response.²⁶  These computer-controlled devices present a notable advantage over the traditional syringe and needle armamentarium due to their less foreboding appearance.³ Moreover, they guarantee precise aspiration and controlled duration of local anesthesia delivery, which may contribute to a reduction in injection-associated discomfort.³

Complications

The delivery of local anesthesia harbors potential complications, such as anesthetic failure, which can arise from anatomical variations, poor technique, patient anxiety, and infection.^3,5 This failure is more prevalent with the conventional IANB method, though it can be mitigated through other techniques, such as Gow-Gates and Vazirani-Akinosi.³ Anesthetic success can also be impacted by conditions like retrognathic mandibles and infection, which may necessitate changes in injection points or anesthetic solution preparation.³ Hematomas, a complication that can arise from puncturing a blood vessel during the procedure, can cause discomfort and, in rare instances, sensory disturbances from maxillary artery puncture.^3,5 Intravascular injection can lead to palpitations and visual disturbances, while overdosing on certain anesthetics can result in methemoglobinemia, a serious condition.³ Other potential complications include needle fracture, nerve injury due to various causes, ocular complications from maxillary artery injection, psychogenic reactions from patient anxiety, and post-treatment soft tissue trauma from biting numb areas.^3,5,7 Transient facial palsy is a rare occurrence that can be immediate or delayed, resulting from direct anesthesia of the facial nerve or other complex mechanisms.³ Management includes eye protection, artificial tears, and sunglasses.^3,7Trismus, another possible complication, can result from muscle spasticity or hematoma and is usually managed conservatively with a soft diet, analgesia, and physiotherapy.^3,5

Conclusion

The inception and implementation of local anesthesia have significantly transformed clinical dentistry by converting previously painful procedures into routine practices. As delineated in this article, the secure and efficacious use of local anesthesia necessitates meticulous consideration of a variety of factors, ranging from the selection of anesthetic agent to the technique and precautions employed. Every member of the dental team has a pivotal role in ensuring patient safety, managing potential toxicity, and addressing any emergent medical situations. It is imperative for clinicians to continually enhance their theoretical knowledge and practical skills through advanced literature review, dialogue with colleagues, continuing education courses, and direct patient care. This persistent commitment to learning and development is crucial to securing optimal patient outcomes and propelling the field of dentistry forward.

About the Author

Joy D. Void-Holmes, RDH, BSDH, DHSc
Founder
Dr. Joy, RDH™

Co-Founder
JELL-ED™

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