Epithelial and vascular reactions may be due to dosage-related cytotoxic nature of LAs or they may be vasopressor-induced.14,20 Clinical manifestations may include edema, desquamation, and ischemic necrosis (Figure 5). These ADEs are usually transient in nature. Injection into muscles may result in LA-associated myotoxicity and vasoconstrictor-associated necrosis. Clinical manifestations include acute pain and trismus. Healing with fibrosis may lead to chronic trismus.14,20
Figure 5. Edema and Desquamation Secondary to the Repeated Topical Application 10% Lidocaine Stray.
Neurologic deficit may be LA-induced neurotoxicity related to the total dose of the LA administered, the particular LA used, and the technique employed (e.g., infiltration versus nerve block).14,20,49-52 Most cases of neurologic deficit involve the lingual nerve. Signs and symptoms include transient anesthesia or paresthesia characterized as sensation of pricking or tingling of the lip, tongue, and other oral tissues and may take 2 to 6 months to resolve.
In rare instances, the neurologic deficit may be permanent. Based on LA usage by U.S. dentists, the reported incidence of permanent paresthesia following mandibular nerve block with prilocaine 4% and articaine 4% is 7.3 and 3.6 times greater, respectively, than expected.49 These findings are consistent with those reported from other countries.50,51 Clinicians should consider this evidence when assessing the risks and benefits of administering 4% LA formulations for mandibular nerve block anesthesia.
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