John A. Yagiela

Anesthetic Efficacy of Different Ropivacaine Concentrations for Inferior Alveolar Nerve Block

This study was conducted on 72 American Society of Anesthesiologists class 1 patients scheduled for extraction of a mandibular third molar after inferior alveolar nerve block. Each patient was randomly administered one of the following ropivacaine concentrations: 0.75%, 0.5%, 0.375%, or 0.25% (18 patients per group). Onset of block (mean +/- SD) was rapid for both 0.75% (1.4 +/- 0.4 minutes) and 0.5% (1.7 +/- 0.5 minutes) ropivacaine but significantly slower for the 0.375% (4.2 +/- 2.5 minutes) and 0.25% (10.7 +/- 3.0 minutes) concentrations. Tooth extraction was performed successfully with the 0.5% and 0.75% concentrations, and supplemental injections were not required. Second injections, however, were required with 0.375% ropivacaine. Anesthesia was unsuccessful in 13 patients given 0.25% ropivacaine even after 3 injections. The mean durations of soft tissue anesthesia were 3.3 +/- 0.3 hours and 3.0 +/- 0.3 hours for the 0.75% and 0.5% concentrations, but significantly shorter with more dilute concentrations. The duration of analgesia showed a similar pattern, with the 0.75% and 0.5% concentrations producing prolonged analgesia of 6.0 +/- 0.4 hours and 5.6 +/- 0.4 hours. These results indicate that 0.5% and 0.75% concentrations were effective for intraoral nerve blockade, with both a rapid onset and prolonged duration of pain control.

Pharmacokinetics of lidocaine with epinephrine following local anesthesia reversal with phentolamine mesylate.

Phentolamine mesylate accelerates recovery from oral soft tissue anesthesia in patients who have received local anesthetic injections containing a vasoconstrictor. The proposed mechanism is that phentolamine, an alpha-adrenergic antagonist, blocks the vasoconstriction associated with the epinephrine used in dental anesthetic formulations, thus enhancing the systemic absorption of the local anesthetic from the injection site. Assessments of the pharmacokinetics of lidocaine and phentolamine, and the impact of phentolamine on the pharmacokinetics of lidocaine with epinephrine were performed to characterize this potentially valuable strategy. The blood levels of phentolamine were determined following its administration intraorally and intravenously. Additionally, the effects of phentolamine mesylate on the pharmacokinetics of intraoral injections of lidocaine with epinephrine were evaluated. Sixteen subjects were enrolled in this phase 1 trial, each receiving 4 drug treatments: 1 cartridge lidocaine/epinephrine followed after 30 minutes by 1 cartridge phentolamine (1L1P), 1 cartridge phentolamine administered intravenously (1Piv), 4 cartridges lidocaine/epinephrine followed after 30 minutes by 2 cartridges phentolamine (4L2P), and 4 cartridges lidocaine/epinephrine followed by no phentolamine (4L). Pharmacokinetic parameters estimated for phentolamine, lidocaine, and epinephrine included peak plasma concentration (Cmax), time to peak plasma concentration (Tmax), area under the plasma concentration-time curve from 0 to the last time point (AUClast) or from time 0 to infinity (AUCinf), elimination half-life (t1/2), clearance (CL), and volume of distribution (Vd). The phentolamine Tmax occurred earlier following the intravenous administration of 1Piv (7 minutes than following its submucosal administration in treatment 1L1P (15 minutes) or 4L2P (11 minutes). The phentolamine t1/2, CL, and Vd values were similar for 1L1P, 1Piv, and 4L2P. The Tmax for lidocaine occurred later and the Cmax for lidocaine was slightly higher when comparing the 4L2P treatment and the 4L treatment. The phentolamine-induced delay of the lidocaine Tmax likely represents phentolamines ability to accelerate the systemic absorption of lidocaine from oral tissues into the systemic circulation.

Effect of midazolam pretreatment on the intravenous toxicity of lidocaine with and without epinephrine in rats

The effect of the benzodiazepine midazolam on the intravenous toxicity of lidocaine with and without epinephrine was studied in male Sprague-Dawley rats. Test rats with and control rats without midazolam premedication (2.5 mg/kg intraperitoneally, 10% of the median dose that caused loss of the righting reflex in a third group of rats) were given 2% lidocaine with and without 10 μg/ml epinephrine intravenously in doses sufficient to construct log-dose response curves for both convulsant and lethal responses. In control rats the median convulsant dose (CD50) of lidocaine was 15.2 mg/kg given alone and 10.9 mg/kg with epinephrine (a statistically significant difference); respective values for the median lethal dose (LD50) were 26.4 and 18.5 mg/kg (also statistically significant). While epinephrine enhanced lidocaine seizure activity and lethality by approximately 50%, midazolam almost completely prevented lidocaine-induced convulsions but had no significant effect on mortality.

Advanced Techniques and Armamentarium for Dental Local Anesthesia

Computer-controlled local anesthetic delivery (C-CLAD) devices and systems for intraosseous (IO) injection are important additions to the dental anesthesia armamentarium. C-CLAD using slow infusion rates can significantly reduce the discomfort of local anesthetic infusion, especially in palatal tissues, and facilitate palatal approaches to pulpal nerve block that find special use in cosmetic dentistry, periodontal therapy, and pediatric dentistry. Anesthesia of single teeth can be obtained using either C-CLAD intraligamentary injections or IO injections. Supplementary IO anesthesia is particularly suited for providing effective pain control of teeth diagnosed with irreversible pulpitis.

The use of amide local anesthetics in patients susceptible to malignant hyperthermia

The use of amide local anesthetics in dental patients presumed to be susceptible to malignant hyperthermia (MH) is controversial. A literature review of 17 recent dental publications and their reference citations revealed that the recommendation to avoid local anesthetics of the amide type in dental treatment of MH-susceptible (MHS) patients is based on in vitro muscle investigations, unpublished communications, and a single case report suggestive of MH. Therefore, a survey of members of the Malignant Hyperthermia Association of the United States designed to determine what, if any, MH-like reactions have occurred in patients with MHS receiving dental treatment was conducted. Of a total of 307 MHS respondents, 36 (12%) reported adverse reactions to dental care. Only one respondent, however, reported symptoms suspicious of MH (fever, muscle pain) in which the administration of amide local anesthetics appeared to be closely linked. Fifty-six (18%) of the respondents have had difficulty obtaining routine dental care since being identified as MHS; this includes 27 who have been refused dental treatment or have had to undergo operative procedures without the benefit of local anesthesia. These results support the conclusions that amide local anesthetics may be administered to MHS patients without significant risk and that currently the diagnosis of MH susceptibility can adversely affect the quality of dental care.

ANESTHESIA AND PAIN MANAGEMENT

Acute orofacial pain is usually managed by the administration of local anesthetics, systemic analgesics, or a combination of the two methods. In an emergency, intraoral maxillary nerve blockade is helpful for controlling pain in the midface, although infiltrations may be more suitable for discomfort originating from individual teeth or portions of the alveolar process. Mandibular anesthesia can be achieved by open or closed-mouth techniques for inferioral alveolar-lingual nerve blockade. Systemic pain relief is optimized by using full analgesic doses of NSAIDs, with opioids serving to increase the degree of analgesia if required, or to be used, often with acetaminophen, in patients intolerant to NSAIDs.