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Cocaine was the first agent used for topical anesthesia. It was isolated from the coca leaves that native peoples of the Andes Mountains chew for multiple effects including local anesthesia and stimulant properties to ward off fatigue. Chemists working with the coca alkaloids noticed that the crystals could numb their tongues. In 1884, a German surgeon demonstrated the successful use of cocaine to anesthetize the cornea during eye surgery. One of the most prominent surgeons at Johns Hopkins University, Dr. William Halsted, read about this account and began investigations with cocaine for general surgery. They successfully used cocaine during surgery, but unfortunately Dr. Halsted and several colleagues became addicted.79 Today, cocaine is used for topical anesthesia of mucous membranes using a 4% to 10% solution. If the solution remains on the membrane for 5 minutes, anesthesia and vasoconstriction of the area will occur. Cocaine has inherent vasoconstrictor properties thus requires no additional epinephrine. The toxicity of cocaine is a result of its vasoconstrictor properties and ability to inhibit catecholamine, including norepinephrine reuptake. Toxic manifestations include excitation, dysphoria, tremor, seizure activity, hypertension, tachycardia, myocardial ischemia, and infarction. Cocaine is used primarily for nasal surgeries, although its abuse potential has resulted in a decrease in use and a search for alternate anesthetics. When cocaine was compared with li-docaine/phenylephrine for nasal intubations, the results were the same with less toxicity in the lidocaine/phenyle-phrine group.80

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