Q. Patient presents with a large, swollen laceration above right eyebrow. After administering a local anesthetic, irrigating the cut with saline, cleaning the site of injury with betadine, and setting up the sterile field, a medical student began suturing. As the tip of the needle entered the skin, the patient jerked and complained that they felt sharp pain. More local anesthetic was administered. Minutes before, however, the medical student tested the area by lightly tapping the skin with the tip of the needle and the patient had even confirmed that he could only feel dull pressure. Why might the local anesthetic not have worked as expected?
A. Local anesthetics depress the central nervous system in a dose-dependent manner. The time for onset of these local anesthetics depends on a complex equilibrium between a water-soluble state and a lipid-soluble state. Greater lipid solubility is ideal because it enhances diffusion through nerve sheaths, meaning a greater portion of the administered dose can enter neurons. All local anesthetics have a pKA, or physiologic pH, of >7.4 and exist in a water-soluble form in solution as opposed to a lipid soluble form. Even when injected into tissue having a normal pH of 7.4, a greater proportion of the anesthetic molecules exist in the water-soluble form. The acidic environment associated with inflamed tissues favors the water-soluble configuration even more, and accounts for difficulty when attempting to anesthetize inflamed or infected tissues. In these cases, fewer molecules exist in lipid-soluble forms that can penetrate nerves. This could have been what had happened with the patient I saw – the patient may have needed a higher dose or anesthetic, or the anesthetic may have needed more time to spread throughout the tissue due to the highly inflamed nature of the laceration site. Resources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1693664/