Potency and Metabolism of Prilocaine as a local anesthetics

Pharmacologically, prilocaine is similar to both lidocaine and mepivacaine. Chemically, prilocaine is a toluidine derivative, and lidocaine and mepivacaine are xylidine derivatives.

Prilocaine is equal in potency to lidocaine and mepivacaine, and two-thirds as potent as articaine and one-fourth as potent as bupivacaine. Prilocaine is much less toxic (approximately half) than lidocaine and articaine and slightly less toxic than mepivacaine. It is much less toxic than bupivacaine, approximately one-fifth as toxic. It is the least toxic anesthetic currently available, and minimally affects the CNS and cardiovascular system (CVS). When compared with lidocaine with a similar intravenous (IV) dose, CNS toxicity following the administration of prilocaine is shorter and less severe.4 Like mepivacaine, prilocaine produces very little vasodilation and is an effective plain anesthetic. In fact, when 4% prilocaine is administered as a nerve block it increases its duration from short to intermediate action providing pulpal anesthesia for approximately 40 to 60 minutes and soft tissue anesthesia for approximately 2 to 4 hours.

Prilocaine is especially effective when slightly longer duration of action is needed than that of mepivacaine and lidocaine. Prilocaine plain has a slightly longer duration than mepivacaine plain, and prilocaine with 1:200,000 epinephrine has a slightly longer duration than lidocaine 1:100,000 epinephrine. Prilocaine 1:200,000 is also useful when a lower concentration of epinephrine is needed for patients with cardiovascular disease (such as ASA III) who are epinephrine-sensitive. The epinephrine dilution of 1:200,000 is half the potency of the 1:100,000 dilution; therefore patients with cardiovascular disease can receive twice as many cartridges (4.4) of prilocaine with epinephrine as they can cartridges (2.2) of lidocaine 1:100,000 epinephrine.
Lidocaine

Prilocaine is metabolized more easily by the liver than lidocaine and mepivacaine, because much of the drug is already metabolized by alternate sites in the lungs and kidneys before it reaches the liver.6 Prilocaine differs significantly from lidocaine and mepivacaine because it is a secondary amine, and it is metabolized by hepatic amidases directly into orthotoluidine and N-propylalanine with the major end product being carbon dioxide. The primary limiting factor for clinical use of prilocaine is methemoglobinemia, which can occur when prilocaine is metabolized to orthotoluidine. Methemoglobinemia is characterized by the presence of a higher than normal level of methemoglobin in the blood that does not bind to oxygen. In large doses of prilocaine (more than the MRD), clinical cyanosis of the lips and mucous membranes can be observed. This is a relative contraindication to the use of prilocaine, and minimal doses should be administered to patients at risk for methemoglobinemia or patients with oxygenation difficulties.

Topical uses of prilocaine can be found in combination with lidocaine in products such as Oraqix (Dentsply Pharmaceutical) and EMLA (AstraZeneca, see Chapter 6). Table 5-15 lists the main properties of prilocaine, and Tables 5-16 and 5-17 give helpful tips for anesthetic selection and precautions for prilocaine formulations (also see Chapter 7 for specific guidelines related to the precautions for local anesthetics and vasoconstrictors).

The MRD for prilocaine is 4.0 mg/lb or 8.8 mg/kg, and the absolute MRD is 600 mg (see Table 5-18 for prilocaine MRDs and Chapter 8 for calculation guidelines).

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