Chapter 1. The History of Local Anesthesia

The history of local anesthesia suffers, if it suffers from anything, from the lack of a distinct Eureka moment. It is arguable that we do not have in our history a pivotal day that signified the wholesale change from an era before local anesthesia to the dawn of a new and wonderful age that included parts of the body being rendered insensate for therapeutic reasons. We do not have the equivalent of 16 October 1846 and the trembling hands of William Thomas Green Morton. What we have is a remarkably slow concatenation of the three elements necessary for the administration of the vast majority of local anesthetics: a syringe, a needle, and a local anesthetic drug. Many, however, would argue that to these three need be added several other factors: a detailed knowledge of anatomy and an appreciation of the body's pain mechanisms and more objective methods to localize peripheral nerves and monitor administration of local anesthetics. The authors make no excuse for concentrating in this chapter on the early history of local anesthesia in order to dissect the development of these three vital components.

The origins of the first attempts at some form of local analgesia or anesthesia are lost in the mists of time. Direct nerve compression and the direct application of ice to peripheries before surgery have distant origins but were certainly in regular use from the latter half of the eighteenth century. The first detailed appreciation of the benefits of local anesthesia was written by James Young Simpson and published in 1848, decades before local anesthesia became a practical possibility (Figure 1–1). In this paper, he also described his own unsuccessful experiments with the topical application of a variety of liquids and vapors in an attempt to produce local anesthesia. The paper was published less than 2 years after Oliver Wendell Holmes had coined the term anesthesia, and it therefore almost certainly represents the first use of the term local anesthesia, although Simpson would have used the (arguably more correct) English spelling anaesthesia. However, Simpson was well aware that his were far from being the first attempts to produce peripheral insensibility, for he refers to some ancient methods, which he considered `apocryphal,' and also to Moore's method of nerve compression (Figure 1–2).1

Another distinguished British physician and president of the Medical Society of London in 1868 was Sir Benjamin Ward Richardson. He spent many years in the attempt to alleviate pain by modifying substances capable of producing general or local anesthesia. He brought into use no fewer than 14 anesthetics and invented the first double-valved mouthpiece for the administration of chloroform. He initially experimented with electricity before turning to the effects of cold as an anesthetic. Cold was known to produce a numbing effect and was used as far back as Napoleon's time when his surgeon, Baron Larrey, used its effects to alleviate pain. He introduced a method of producing local insensibility by freezing the part with an ether spray, which became the most practical method of using local anesthesia until cocaine's actions became apparent. The ether spray was utilized as a local agent until it was replaced by ethyl chloride in 18802 (Figure 1–3).

The Origins

If local anesthesia has a Eureka moment, then it may have happened in the forests of South America. Centuries ago, an unnamed inhabitant of these climates may have been experimenting by putting leaves of various plants into his mouth and giving them a good chew. We can imagine that this would be a largely unrewarding hobby, but let us focus on the moment when he first placed a coca leaf into his mouth and masticated vigorously. Did he fall to his knees and shout in wonderment: “My lips have gone numb—surely this is the dawn of a new age of painless surgery!". Almost certainly not—although he might have later told his friends that he felt somewhat excited, energetic, and euphoric while he chewed the leaves.

For thousands of years, South American peoples have chewed the coca leaf. It is a remarkable plant in that it contains vital nutrients as well as numerous alkaloids, most notably cocaine. The coca leaves are taken from a shrub of the genus Erythroxylon coca, named by Patrico Browne because of the reddish hue of the wood of the main species.3 Many species of this genus have been grown in Nicaragua, Venezuela, Bolivia, and Peru since pre-Columbian times. Erythroxylon coca contains the highest concentration of the alkaloid known as cocaine in its leaves3,4 (Figure 1–4).

Traditionally, the leaves were chewed for social, mystical, medicinal, and religious purposes. The Florentine cartographer Amerigo Vespucci (1451–1512) was arguably the first European to document the human use of the coca leaf.5,6 In his account of his voyage to America on the second expedition of Alonso de Ojeda and Juan de la Cosa from 1499 to 1500, he reported that the inhabitants of the Island of Margarita chewed certain herbs containing a white powder.7 Among sixteenth-century Spanish chroniclers, the appearance of coca is associated with Francisco Pizarro's (1475–1541) conquest of the Inca or Tawantinsuyo Empire in 1532. Pedro Pizarro (1515–1571), Francisco Pizarro's cousin who played a leading role in the capture of the last king of the Incas, described coca consumption by the nobles and high officials of the Inca Empire.8 After the fall of the Inca Empire in the early 1500s, coca consumption spread to the population at large, creating a drastic change in the entire social system.

When the Spaniards conquered South America, they initially ignored the aboriginal claims that the leaf gave them vigor and liveliness. They self-righteously declared the practice of chewing the leaf the “work of the Devil."5 But once they found that the claims of the natives were true, they not only legalized the leaf, but they taxed it—taking 10% of the value of each crop! The taxes were then used to support the Roman Catholic Church—the main source of revenue for the church to thrive. In 1609, Padre Blas Valera wrote: “Coca protects the body from many ailments, and our doctors use it in powdered form to reduce the swelling of wounds, to strengthen broken bones, to expel cold from the body or prevent it from entering, and to cure rotten wounds or sores that are full of maggots. And if it does so much for outward ailments, will not its singular virtue have even great effect in the entrails of those who eat it?"9 If the padre was blessed with the ability to foresee the future, perhaps his enthusiasm would have been redirected toward limiting the use of the leaf, and the field of anesthesia might have taken a different turn.

Another member of the clergy, Bernabé Cobo, who spent his life bringing Christianity to the Incas, is the first to describe the anesthetic effects of coca. In a 1653 manuscript, he mentioned that toothaches could be alleviated by chewing the coca leaves. In 1859, an Italian physician by the name of Paolo Mantegazza had witnessed the use of coca by the natives in Peru. He wrote a paper describing the medicinal use in the treatment of “a furred tongue in the morning, flatulence and whitening of the teeth."10

Needles & Syringes

If local anesthetic drugs are the bullets used when fighting pain, the gun needed to fire it is made up of a syringe and a needle. Without the bullets, the gun is useless and, just as certainly, without the gun, the bullets will have little effect. The development of the hypodermic syringe and needle was therefore an important prerequisite for the use of cocaine for anything but topical application. A thorough sifting of the available historical evidence and independent reexamination of the sources support the following outline of the facts. In 1845, Francis Rynd described the idea of introducing a solution of morphine hypodermically in the neighborhood of a peripheral nerve to alleviate neuralgic pain.11 He introduced the solution by means of gravity, passively through a cannula once the trocar had been removed.

Several centuries past before the development of a syringe to deliver medicine was described by Alexander Wood (Figure 1–5). Wood, a contemporary of James Young Simpson, was, in 1855, the first to combine needle and syringe for hypodermic medication. He used the equipment manufactured by a gentleman by the name of Ferguson who had developed the graduated glass syringe and hollow needle for the purpose of treating aneurysms by injecting ferric perchloride into the aneurysm to form a coagulated mass. Wood, a physician interested in the treatment of neuralgia, reasoned that morphine might be more effective if it were injected close to the nerve supplying the affected area. Although morphine may have some peripheral actions, and the effect of Wood's morphine was almost certainly central, he was nevertheless the first to think of the possibility of producing nerve blockade by direct drug injection. Thus he has been called the “father-in-law” of local anesthesia—all he lacked was an agent that worked locally. Wood's contribution was therefore his procedure of subcutaneous injection. This technique was subsequently adopted by C. Hunter and renamed hypodermic injection presumably because Hunter's purpose was to provide systemic absorption of medications injected.12,13

The Introduction of Cocaine

The growth in Western science and technology exploded during the nineteenth century. Six years after Charles Darwin's controversial book, On the Origin of Species by Means of Natural Selection, Joseph Lister was an important figure in changing the face of surgery. He applied Pasteur's principles of bacterial growth in eliminating sepsis in the operating theatre. Other prominent figures contributed to the understanding of human physiology, eg, Sydney Ringer's discovery of the need for calcium and potassium to maintain cardiac excitability, significantly advancing medical care. And then there was cocaine.

Although the stimulant and hunger-suppressant effects of coca had been known for years, the isolation of the cocaine alkaloid was not achieved until 1855. Scientists attempted to isolate cocaine, but none were successful for two reasons: coca did not grow in the colder environment of Europe, and the chemistry involved was unknown at that time. Finally in 1855, the German chemist Friedrich Gaedcke was able to isolate the cocaine alkaloid and publish the description in the journal Archieves de Pharmacie. In 1856, Friedrich Wöhler asked a colleague to bring him a large amount of coca leaves from South America. Wöhler then gave the leaves to Albert Niemann, a PhD student at the University of Göttingen in Germany, who then developed an improved purification process. His dissertation, On a New Organic Base in the Coca Leaves, published in 1860, earned him his doctoral degree. Of interest, he described cocaine as having “a bitter taste, promotes the flow of saliva, and leaves a peculiar numbness, followed by a sense of cold when applied to the tongue."14,15 Following Niemann, the first experimental study on cocaine was conducted by a former naval surgeon from Peru, Thomas Moreno y Maiz. He discovered that the injection of cocaine solutions caused insensitivity in rats, guinea pigs, and frogs. But it wasn't until 1880 when Basil Von Anrep experimented on himself, that the application of cocaine for surgery was appreciated. Von Anrep injected a small amount of cocaine under the skin on his arm and noted that the area became insensitive to pinpricks. He did the same to his tongue with the same effect. He published his findings with the caveat “the animal experiments have no practical application; nevertheless I would recommend trying cocaine as a local anesthetic in persons of melancholy disposition."16

The groundwork was in place, but the final step toward the clinical use of cocaine had yet to be taken. Viennese ophthalmologist Karl Koller (1857–1944) rose to the challenge (Figure 1–6). Koller was an intern working in the Viennese General Hospital, where he was befriended by Sigmund Freud17 (Figure 1–7). Freud wanted to know more about the stimulating action of cocaine, which he hoped might prove useful in curing one of his close friends of morphine addiction. This friend was a pathologist and had developed an agonizingly painful thenar neuroma secondarily to cutting himself during the performance of an autopsy. Freud was able to obtain a supply of cocaine from the pharmaceutical firm, Merck. He shared it with Koller, who helped him investigate its effects on the nervous system during the spring of 1884.18

Koller had dreams of achieving an appointment to assistant, and knew his chances would be greatly enhanced by the creation of a respectable piece of research. The research he produced proved worthy enough, but interpersonal animosity intervened, and he was not awarded the position. Deeply disappointed, he moved first to the Netherlands, then to the United States.19 In July 1884, Freud published a review of cocaine and his experiments with the drug, again noting, but without lending any particular attention to, the alkaloid's anesthetic effect on mucous membranes.20 It was Koller who grasped the importance of this observation. His discovery was no accident, for he was keenly aware of the limitations of general anesthesia in ophthalmic surgery. Koller understood what others had failed to recognize because of his past experience in the field of ophthalmology. Many eye surgeries at that time were still being performed without anesthesia. Almost four decades after the discovery of ether, general anesthesia by mask had a number of limitations for ophthalmic surgery, eg, the anesthetized patient could not cooperate with his surgeon, the anesthesiologist's apparatus interfered with surgical access. At that time, many surgical incisions in the eye were not closed, as fine sutures were not yet available. Vomiting from chloroform or ether threatened to cause extrusion of the internal contents of the globe, markedly increasing the risk of permanent blindness. As a medical student, Koller had worked in a laboratory searching for a topical ophthalmic anesthetic to overcome the restrictions posed by general anesthesia. The medications available at that time had proved to be ineffective.

One day, Freud gave Koller a small sample of cocaine in an envelope, which he slipped into his pocket (an everyday occurrence in many American and European cities to this day). When the envelope leaked, a few grains of cocaine stuck to Koller's finger, which he casually licked with his tongue. His tongue became numb—if he had been able to mouth the word Eureka with a numb tongue, he may well have done so at this precise instant. At that moment, Koller realized that he had found what he had been searching for. He immediately created a suspension of cocaine crystals in his laboratory.2 Koller realized that this had been noted by all who had worked with cocaine and that “in the moment it flashed upon me that I was carrying in my pocket the local anesthetic for which I had searched some years earlier".1 In Freud's absence, he and another colleague, Joseph Gartner, dissolved a trace of the white powder in distilled water and instilled the solution into the conjunctival sac of a frog. After a minute or so, “the frog allowed his cornea to be touched and he also bore injury to the cornea without a trace of reflex action or defense.” Koller wrote: “One more step had yet to be taken. We trickled the solution under each other's lifted eyelids. Then we placed a mirror before us, took pins, and with the head tried to touch the cornea. Almost simultaneously we were able to state `I can't feel anything'".21,22 Then, he experimented with dog and guinea pig corneas with 2 to 5% cocaine solutions.23

Koller soon achieved the extraordinary notoriety he had longed for when in September of 1884 he performed the first ophthalmologic surgical procedure on a patient with glaucoma using local anesthesia. The German Ophthalmologist Society Congress was to meet in Heidelberg in September of 1884 where Koller was going to present his findings. Unfortunately, he was unable to attend. He asked Dr. Joseph Brettauer, an ophthalmologist from Trieste, to present his paper at the Congress. The effect of his work was immediate. Koller was able to present his findings in October of that year to the Viennese Medical Society. He published his findings in late 1884.21

Physicians in the United States soon heard about Koller's amazing work. Dr. Henry Noyes of New York, an attendee of the Heidelberg Congress, published a summary of Koller's work in the New York Medical Record.24 Another American physician, Dr. Bloom, translated Koller's article into English and published it in The Lancet in December of that same year. Koller's work was the trigger for the development of regional/local anesthesia. In the subsequent year, more than 60 publications on local anesthesia with cocaine appeared in the United States and Canada.

One of the most significant publications was that of N. J. Hepburn, an ophthalmologist from New York.15 Self-experimentation was the standard for drug trials in those days. To determine whether a drug was safe or effective, the researcher or physician commonly tried the drug on himself. It takes courage to try a new drug on a patient, but it takes a particular and much greater form of courage to try that drug on yourself. Hepburn was no different from his colleagues. He gave himself a succession of subcutaneous injections of 0.4 mL (8 mg) of cocaine at 5-min intervals. By the eighth injection, the stimulating effects of the drug were strong enough that he decided it was best to stop. Unfortunately, Hepburn didn't stop with those initial injections. He repeated the “experiment” 2 days later and 4 days after that, each time increasing the total amount of cocaine injected. Most likely by this time he was hopelessly addicted.

By November of 1884, the ophthalmologist C. S. Bull reported that he had been able to use cocaine to produce anesthesia of the cornea and conjunctiva in more than 150 cases.25 He was enthusiastic about the advantages of the drug in that he saved time required for complete anesthesia with ether; patients were less nauseated, the engorgement of the ocular blood vessels (caused by ether) was eliminated, and he was less hampered by the anesthesia equipment required for inhalation anesthesia. Cocaine revolutionized eye, nose, and mouth surgery. Operations that had been exceedingly difficult or painful became routine when topical or injectable cocaine was used. Koller didn't forget the contribution of his friend, Freud. He gave him the credit as his muse. Despite his disillusionment at not being foremost with the discovery, Freud is considered by many to be the founder of psychopharmacology because of his initial use of cocaine. He is considered the predecessor in the discovery and experimentation with mescaline, LSD, and amphetamines to modify behavior and to attempt to cure mental illness.20

Dangers of Cocaine

The “wonder drug” cocaine was soon sold everywhere and in almost everything. Following its isolation from the coca leaf, cocaine emerged as an ingredient in wine both in the United States and in Europe in amounts up to 7 mg/oz. In the original recipe for Coca-Cola (1866), coca leaves were included in the ingredients. It wasn't until 1906 when the Pure Food and Drug Act was passed that the Coca-Cola company began using decocainized leaves.14 Until 1916, cocaine could be purchased over the counter at Harrods in London. It was found in tonics, toothache cures, and medicines (Figure 1–8). Coca cigarettes were sold with the promise of lifting depression. Those who purchased cocaine were promised in ads by the pharmaceutical firm Parke-Davis, that it could “make the coward brave, the silent eloquent, and render the sufferer insensitive to pain.” In the operatic world, it became commonplace to use cocaine to ease the pain of sore throats and to shrink nasal mucous membranes to enable the singers to improve the resonation of their voices.

Had cocaine's use been restricted to enhancing opera singing and local anesthesia, it would have become the achievement of nineteenth-century medicine. As had happened earlier with brandy, tobacco, morphine, and other drugs, cocaine was administered in too high concentrations and with too few precautions. In 1886 William Hammond, a former US Army Surgeon General, assured an audience of physicians that cocaine addiction did not exist. Based on self-experimentation, he concluded that regular use of cocaine was as easy to stop as quitting coffee. It did not have the addictive qualities of drugs like opium. But when Hammond finished his lecture, an addiction specialist named Jansen Mattison offered a rebuttal. He related incidences of fierce addictions in patients under his care. He described cocaine's damaging effect on nerves and its ability to produce hallucinations, delusions, and emaciation. Many other practitioners began to encounter serious side effects.26,27

Mattison knew what he was talking about. Over the next several years, medical journals published hundreds of case reports of “cocainism.” Unfortunately, many of the addicts were medical practitioners who had experimented on themselves, most notably Freud and William Stewart Halsted.28,29 The opiate addicts, promised a cure for their addiction, switched to cocaine, but continued to use both drugs, further compromising their health.

Several researchers deserve the credit for making the infiltration of cocaine safer. Maximillian Oberst, Ludwig Pernice, and Carl Ludwig Schleich, all from Germany, described the use of low concentrations of cocaine as effective means of local anesthetic.30 The Parisian surgeon Paul Reclus described the use of very low concentrations of cocaine as effective anesthesia without harmful side effects for tooth extractions and pulpotomies.31

About the same time, Halsted was experimenting with low concentrations of cocaine applied by compression devices. Unfortunately, he too became addicted to both cocaine and morphine and could not publish his results.12,17,29 Over time, the maximum “safe” cocaine dosage for infiltration anesthesia was established at 50 mg.

Niemann, in his pioneer work, had hydrolyzed benzoic acid from cocaine. In the search for other benzoic acid esters with local anesthetic properties, amylocaine (stovaine) was introduced in 1903. It became popular for spinal anesthesia until it was shown to be an irritant. But it was the development of procaine in 1904 by the German chemist Alfred Einhorn that revolutionized local anesthetics.33 On November 27 1904, Einhorn (1856–1917) patented 18 para-aminobenzoic acid derivatives that had been developed in the Meister Lucius and Brüning plants at Höchst, in Hesse, Germany. His compound Number Two was to bring about a radical change in local anesthetic practice. He named the new anesthetic, Novocain.11

Procaine (Novocain) was introduced into clinical practice by Professor Heinrich Braun in 1905. Braun published a study comparing this new anesthetic to stovaine and alypine, two other promising local anesthestics.34 Procaine was found to be safe and quickly became the standard local anesthetic drug. Within a short time, procaine completely replaced cocaine as the most commonly used local anesthetic. But because of the short duration of action and prominent allergic potential limiting its clinical effectiveness, the search for longer lasting compounds continued.11,18,26,35

In the years that followed, several local anesthetics were synthesized and used in clinical practice until side effects or other unfavorable characteristics were noted. In 1925 Karl Meischer synthesized dibucaine and in 1928 Otto Eisleb synthesized tetracaine. Both were effective local anesthetics and had the desirable qualities of longer duration and potency, but systemic toxic effects limited their usefulness for regional techniques other than for spinal anesthesia. Most of the compounds developed during this time were amino ester derivatives, similar to cocaine, with similar allergic potential.

A major breakthrough came in the mid 1940s when the Swedish chemists, Nils Löfgren and Bengt Lundquist, developed a new local anesthetic they called lidocaine. Lidocaine was an amino amide derivative, a stable compound not influenced by exposure to high temperatures, and, most importantly, one that did not have the allergic potential of the ester-type local anesthetics. With the development of this amide-type anesthetic drug, a whole new class of new local anesthetics were synthesized. In 1957 Af Ekenstam developed mepivacaine and bupivacaine, and in 1969 Löfgren and Claes Tegnér developed prilocaine. Prilocaine's synthesis began because of a desire to produce a local anesthetic with a potency similar to that of lidocaine but without lidocaine's systemic toxic effects. Unfortunately, it was soon discovered that large doses of prilocaine produced a metabolite that caused methemoglobinemia. Although probably not clinically significant, this discovery severely limited its use in clinical practice.36 In 1972 etidocaine was introduced to the clinical scene, but was soon discovered to lack a differential sensory–motor blockade. Its clinical usefulness was therefore limited.

The only new ester local anesthetic developed in more recent times was chloroprocaine. Its rapid hydrolysis reduced the possibility of systemic toxicity, but its usefulness was restricted to procedures of short duration that did not produce a high degree of postoperative pain. In modern regional practices it has been used both in spinal anesthesia and in nerve blocks for short, relatively painless procedures.

After the development of etidocaine, a pause in the development of newer local anesthetics occurred. One of the goals of modern pharmaceutical research is modification in the delivery of the most commonly used local anesthetics rather than the development of completely new drugs. For example, liposomal delivery systems that allow slow release of commonly used local anesthetics deposited at specific sites may make the practice of indwelling peripheral nerve block catheters obsolete in the foreseeable future.

Infiltration Anesthesia

In 1895, a then novel approach, termed infiltration anesthesia, had been promoted by Karl Ludwig Schleich (1859–1922).35 Schleich applied the principle that pure water has a weak anesthetic effect but is painful on injection, whereas physiologic saline is not. In 1869, Pierre Carl Edouard Potain first observed that the subcutaneous injection of water produced local anesthesia. Halsted, a surgeon at Roosevelt hospital in New York City, in a frank letter to the editor of the New York Medical Journal in 1885, declared that the “skin can be completely anesthetized to any extent by cutaneous injections of water."37 In his own practice, Halsted had begun using water instead of cocaine in skin incisions, noting that the anesthesia did not subside completely when hyperemia reappeared.

In the belief that there was a solution capable of performing as a useful anesthetic that would not cause pain on injection, Schleich mixed 0.2% sodium chloride with 0.02% cocaine. He used the mixture to produce cutaneous anesthesia for sebaceous cystectomy, hemorrhoidectomies, and small abscesses. Although Braun dismissed Schleich's solutions as “nonphysiologic,” Schleich's work was important in advancing the application of small quantities of local anesthetics for surgical procedures. Because of the reported serious toxic reactions and fatalities reported with cocaine, enthusiasm for the utilization of local anesthesia had waned considerably. Paul Reclus undoubtedly understood that the cause of death from local anesthetics was related to overdose from excessively high doses. He was able to demonstrate that absorption could be limited with lower concentrations of cocaine, a fact that Schleich obviously supported and implemented.31 Schleich's approach still seems to be relevant, particularly with the recent European enthusiasm for tumescent anesthesia, in which sometimes huge volumes of very dilute local anesthetic are used for surface surgery.

Conduction Anesthesia

With the excitement generated by Koller's report of cocaine anesthesia in 1884, several US surgeons concurrently entertained the idea of injecting cocaine directly into tissues to render them insensitive. William Burke injected five drops of 2% cocaine solution close to a metacarpal branch of the ulnar nerve and then painlessly removed a bullet from the base of his patient's little finger.38 However, it was William Stewart Halsted (1852–1922; Figure 1–9) and his associate John Hall at Roosevelt Hospital in New York City, who most clearly saw the great possibilities of conduction block.39 Hall experimented on himself by blocking a cutaneous branch of the ulnar nerve in his own forearm.40 He and Halsted did not stop with upper extremity injections; they also successfully injected the musculocutaneous (superficial peroneal) nerve of the leg. Hall described the manifestation of systemic symptoms such as giddiness, severe nausea, cold perspiration, and dilated pupils, but these symptoms did not stop these daring scientists from further self-experimentation. Halsted blocked Hall's supratroclear nerve to remove a congenital cystic tumor. One can assume that both Halsted and Hall had run out of minor surgical ailments in themselves and therefore had to look to others on whom they could experiment. In the days long before ethics committees and informed consent, one is tempted to speculate about the true “volunteer” status of the poor, and most likely, unsuspecting, medical students. Hall's report was unequivocal in predicting that this mode of administration of cocaine would find wide application in outpatient surgery once the limits of safety had been determined—remarkably prescient of him!40

Although the conduction blocks were successful, unfortunately, several members of their group became addicted to cocaine. No further publications about the usefulness of cocaine anesthesia for surgical procedures were presented. It is one of the great sadnesses of the development of analgesic drugs in the history of humankind that two of the most effective agents, morphine and cocaine, are wickedly addictive. They deprived medicine of many of the potential discoveries of its most gifted sons and daughters. However, that Hall and Halsted were the true progenitors of conduction anesthesia can scarcely be doubted.17,26

In 1891, François-Franck was the first to apply the term blocking to the infiltration of a nerve trunk in any part.41 He correctly discovered that the effect of the blocking drug was not limited to sensory fibers, but provided blockade of all nerves, both motor and sensory. He noted that sensory anesthesia became apparent more rapidly than the motor paralysis, a fact confirmed by von Anrep's observations in 1880.16 François-Frank described the action of cocaine as transitory and noninjurious, “physiologic and segmental” anesthesia. He may well have borrowed part of it from J. Leonard Corning, who in 1886 wrote that “the thought of producing anaesthesia by abolishing conduction in sensory nerves, by suitable means, should have been rife in the minds of progressive physicians".42 Corning most likely got the idea from Halsted, because he had frequently observed Halsted and Hall's work at Roosevelt Hospital in New York.

The advantage of utilizing cocaine as a local anesthetic was that it anesthetized only the section of the body where surgery was to be performed, the goal of because regional techniques in modern practice. But the price to be paid was in the duration of action and toxicity, not to mention the more commonly recognized problem of addiction. The dose of cocaine was limited to 30 mg because of rapid absorption. Unfortunately, the duration of anesthesia was therefore to no more than 15 min. Corning, in 1885, began researching means of prolonging the local anesthetic action of cocaine for surgery. He believed that once cocaine was injected beneath the skin, capillary circulation was responsible for distributing, diluting, and removing the anesthetic substance. In one experiment, he injected 0.3 mL of a 4% solution of cocaine into a cutaneous nerve of the arm and produced immediate anesthesia of the skin of the forearm. By compressing the extremity proximal to the site of injection with an Esmarch bandage, he was able to intensify and prolong the anesthesia to the forearm.43

Corning's successes with prolonging the action of local anesthetic with a physical tourniquet inspired Heinrich F. W. Braun to substitute epinephrine, a “chemical tourniquet,” for the Esmarch tourniquet.44 John Jacob Abel had isolated the pure form from the suprarenal medulla in 1897, and it had been subsequently used in ophthalmology to limit hemorrhage and in the treatment of glaucoma.45

During its use in ophthalmology and subsequently in ear, nose, and throat surgeries, it was discovered that epinephrine prolonged the effect of cocaine, thereby allowing a reduction in dose and limiting side effects. Braun determined the optimal solution of epinephrine with cocaine by once again experimenting on himself. He discovered that the maximal dose that he could tolerate without side effects was 0.5 mg (0.5 mL of a 1:1000 solution of epinephrine). He coined the term conduction anesthesia when publishing the results of his experimentation.46

Intravenous Regional Anesthesia

The first reported use of intravenous regional anesthesia can be traced back to August Karl Gustav Bier (Figure 1–10), the originator of the infamous Bier block. Bier, a German surgeon (1861–1949), influenced surgery, anesthesia, and general medicine with his contributions through the decades. Intravenous regional anesthesia (IVRA) was first described by Bier in 1908. His method consisted of occluding the circulation in a segment of the arm with two tourniquets. He then injected a solution of dilute procaine through a venous cut-down in the isolated segment. The injected solution diffused through the entire section of the limb quickly producing direct vein anesthesia in just a few minutes.47 The anesthesia lasted as long as the upper tourniquet was in place. Recovery of sensation was rapid after the tourniquet was removed.48 Despite his successes, IVRA was not widely used until the technique was reintroduced by C. M. Holmes in the 1960s.49

Spinal Anesthesia

Soon after its introduction in 1884, local anesthesia became very popular with surgeons, particularly those in France, Germany, and the United States.18 This was in large part due to concerns about the safety of inhalational anesthesia which, increased by the introduction of chloroform, had given rise to significant worries about toxicity. General anesthetic mortality was high at this time, and there was a distinct shortage of personnel trained to administer general anesthesia.50 In a bizarre twist, the first spinal anesthetic was given some 5 years before the first lumbar puncture. The term spinal anesthesia was introduced by Corning, a neurologist, in his famous paper of 1885 entitled “Spinal Anaesthesia and Local Medication of the Cord with Cocaine."42 He theorized that interspinal blood vessels would carry the local anesthetic (cocaine) to communicating vessels into the spinal cord. He did not mention anything about cerebrospinal fluid or the depth of the needle insertion into the spinal space. It is speculated that he was aiming directly at the spinal cord as he introduced a needle between the eleventh and twelfth vertebrae. In his paper he wrote: “I reasoned that it was highly probably that, if the anesthetic was placed between the spinous processes of the vertebrae, it would be rapidly transported by the blood to the substance of the cord and would give rise to anaesthesia of the sensory and perhaps also of the motor tracts of the same. To be more explicit, I hoped to produce artificially a temporary condition of things analogous in its physiological consequences to the effects observed in transverse myelitis or after total section of the cord."42

Corning's report was based on a series of two injections: one human and one animal (a dog). After first assessing its action in a dog, producing a blockade of rapid onset that was confined to the animal's rear legs, he administered cocaine to a man who was “addicted to masturbation.” It may be that many anesthesiologists have spent much time wondering whether masturbation played any role in local anesthesia—this question can now be answered in the affirmative. Corning administered one dose without effect and then, after a second dose had been given, the patient's legs “felt sleepy.” The man had impaired sensibility in his lower extremity after about 20 minutes. He left Corning's office “none the worse for the experience"—although this experience itself may well have put him off his penchant for onanism. Corning had injected a total of 120 mg of cocaine, about four times the potentially lethal dose, in a period of 8 min. What he achieved in this patient was probably what is now called epidural, or extradural, anesthesia. The dog probably received a spinal anesthetic with approximately 13 mg of cocaine as a spinal anesthetic, as judged by the rate of onset described.

Although Corning most assuredly had an innovative idea, his results were not more than a lucky accident because he injected a fatal dose of cocaine into the man. A direct communication between the extradural capillaries and the spinal cord does not exist. Based on the education that Corning received at the time, he was probably unaware of the existence of the subarachnoid space and cerebrospinal fluid.

Lumbar Puncture/Spinal Anesthesia

Heinrich Irenaeus Quincke (Figure 1–11) is credited with the introduction and popularization for the lumbar puncture. It was developed as a treatment for hydrocephalus in children with tubercular meningitis, then later as a diagnostic method for certain central nervous system diseases.51 He based his approach on sound anatomic knowledge of the subarachnoid space and spinal cord. He used needles with an internal diameter of 0.5 to 1.2 mm and entered the subarachnoid space via a paravertebral approach. Interestingly, he prescribed bedrest for 24 h following the puncture.

Despite the strides made by Quincke, utilizing his technique for spinal anesthesia did not occur for 8 years after Quincke's first publication. Bier published his renowned paper on spinal anesthesia in 1899. Bier had the good fortune to work at the same institution as Quincke and was most likely familiar with his work. His intention was to use spinal anesthesia with cocaine for major operations. He realized that he could produce a profound block with a minimum amount of the drug, thereby eliminating the majority of the adverse side effects noted by his colleagues. In his experiments, he noted that the extent of anesthesia produced was not always predictable. As was popular with his colleagues, he experimented on himself. He had his assistant, August Hildebrandt, perform lumbar punctures on him. In the first attempt, Hildebrandt was unable to administer an appreciable amount of cocaine before a large volume of cerebrospinal fluid leaked out of Bier. Because of the poor response, they were close to abandoning the experiment. Hildebrandt then offered to be the next “guinea pig” instead. Bier successfully placed the spinal anesthetic and proceeded to “punish” Hildebrandt with blows to the tibia, pulling on his testicle, and even putting out a cigar on Hildebrandt's thigh.52,53

Unfortunately, both men developed violent headaches that lasted for days, leading Bier to recommend the following practices that are still being followed today: preventing the excessive loss of cerebrospinal fluid, using very fine (small) needles, and strict bedrest if significant loss of CSF cannot be avoided.54

Intelligent prescience was at work again.

Bier was able to demonstrate that small amounts of local anesthetic (cocaine) injected into the subarachnoid space could provide surgical anesthesia for over 67% of the body. The anesthetic condition lasted approximately 45 min, an adequate time for many surgical procedures. His work provided the basis of spinal anesthesia as we practice it in modern medicine. Coincidentally, the practice of wearing rubber gloves emerged as a part of aseptic technique prior to Bier's work on spinal anesthesia, thus preventing many of the serious complications that could have occurred without this prophylactic measure.55

So who deserves the laurels for the first spinal anesthetic? The history of anesthesiology is similar to that of other medical branches in that it has had its share of quarrels concerning priority. International disputes between the surgeon August Bier and his former colleague, August Hildebrandt regarding the question of who was the actual inventor of spinal anesthesia are well-documented. Although Hildebrandt and other colleagues frequently give credit to Corning, Bier insisted that he administered and described the technique of spinal anesthesia. In an extensive review (in the original language) of Corning's publication and those of Bier of Germany, the author compared key factors, ie, the mention of cerebrospinal fluid, dose of injected cocaine, onset of action, and height of sensory analgesia. He noted that Corning's dose of local anesthetic was eight times higher than the dose given by Bier, yet the onset of analgesia was slower with a lower sensory block. Cerebrospinal fluid was not mentioned in Corning's paper. Bier concluded that Corning's injection was extradural, and that he (Bier) deserved to be acknowledgement for introducing spinal anesthesia.53,56–58

After Bier's work in spinal anesthesia (published in 1899), interest in spinal anesthesia spread rapidly. Within 2 years of Bier's work, it has been estimated that more than 1000 papers were published relating to spinal anesthesia. Frederick Dudley Tait and Guido Caglieri in San Francisco were the first Americans to use true spinal anesthesia clinically.59 Rudoph Matas, head of the Department of Surgery at the University of Louisiana (later known as Tulane University), was the first American to report on spinal anesthesia. In his description of spinal anesthesia, Matas initially dissolved cocaine in water, creating a hypobaric solution. Later he changed his “standard” mixture to cocaine with morphine, making him a pioneer in the use of spinal opioids to enhance central neuraxial anesthesia.59

With the vast interest in spinal anesthesia, serious complications from its application were soon observed. F. Gumprecht published a report of 15 cases of sudden death after spinal anesthesia.60 Multiple cases of respiratory arrest and hypotension, following Harvey Cushing's introduction of blood pressure measurement, were also reported leading to spinal anesthesia falling into disfavor.61,62 Several pioneers sought to determine the causes of the variations in blood pressure from spinal anesthesia. Several theories emerged that have shaped our understanding of physiology today. L. G. Gray and H. T. Parsons of England did an extensive study to evaluate the causes for the changes in blood pressure after spinal anesthesia. They concluded that the decrease in arterial blood pressure was attributed to the diminished negative intrathoracic pressure during inspiration. High spinal anesthesia paralyzed the abdominal and thoracic muscles necessary to maintain that negative pressure.63 With the understanding that hypotension was a primary danger with spinal anesthesia, G. Smith and W. Porter determined in 1915 that the fall in blood pressure was related to paralysis of the vasomotor fibers in the splanchnic area that regulated the tone of the blood vessels. They concluded that for spinal anesthesia to be effective without serious drops in blood pressure, cephalad diffusion of the local anesthetic should be avoided.64 Gastan Labat contended that the serious adverse effects of spinal anesthesia were related to cerebral ischemia, not hypotension. He recommended that the patient should be placed in the Trendelenburg position after the spinal injection to keep the brain supplied with blood, therefore avoiding respiratory embarrassment.65 Rather than looking at the position of the patient during injection, Arthur E. Barker promoted the idea that the baricity of the solution was instrumental in determining the cephalad spread. He made the injected solution stovaine, less toxic than cocaine but more irritating, hyperbaric with 5% glucose.66 Barker was also a strong advocate for using sterile equipment and medication for spinal techniques. In 1934, Pitkin and Etherington-Wilson experimented with hypobaric solutions and changes in patient position to maintain control of the spread of the anesthetic.32 Although there were other proponents of hypobaric spinal anesthesia, most had to deal with serious adverse effects, such as respiratory impairment and profound blood pressure changes requiring resuscitative maneuvers. It was not until 1920 that W. G. Hepburn and Lincoln Sise revived Barker's methods. Sise, an anesthesiologist at the Lahey Clinic in Boston, used hyperbaric tetracaine, rather than stovaine.

Because of the irritating qualities of stovaine, Sise was interested in finding other local anesthetics that would provide sufficient length of anesthesia with limited side effects—something modern anesthesiologists can relate to in our daily practice. He was frustrated by the short duration of action of Novocaine, “the ending of a spinal anesthesia in the midst of an operation is always disturbing and annoying, but when this takes place in the midst of an abdominal operation, with the belly open, it may be dangerous as well."67 He began using tetracaine because of its longer duration of action, but was concerned about controlling the height of the block. Following Barker's recommendations regarding hyperbaric solutions, he added 10% glucose with success. He applied the same technique to tetracaine in 1935.67,68

The most negative consequence of spinal anesthesia came from a trial in 1953. Two healthy young men had received spinal anesthesia on the same day in a hospital in England. Both developed permanent painful spastic paresis. Although the exact cause of the neurologic injury was never proven, it was suspected to be caused by contamination of the local anesthetic solution.69,70 Several other cases of paralysis after spinal anesthesia followed, casting a dark shadow on the future application of this anesthetic technique. Fortunately, a follow-up analysis of over 10,000 spinal anesthetics was published by L. D. Vandam and R. D. Dripps. “The most gratifying result was the failure to discover persistent, progressive major neurological disease,” providing the way for spinal anesthesia to again emerge as a safe, effective means of providing anesthesia.71

The recurring problem of the inadequate duration of single-injection spinal anesthesia led a Philadelphia surgeon, William Lemmon, to report the development of an apparatus for continuous spinal anesthesia in 1940.72 Lemmon began with the patient in the lateral position. The spinal tap was performed with a malleable silver needle that was left in position. As the patient was turned supine, the needle was positioned through a hole in the mattress and table. Additional injections of local anesthetic could be administered as required. Malleable silver needles also found a less cumbersome and more common application in 1942 when Waldo Edwards and Robert Hingson encouraged the use of Lemmon's needles for continuous caudal anesthesia in obstetrics. In 1944, Edward Tuohy of the Mayo Clinic introduced important modifications of the continuous spinal techniques. He developed the now-familiar Tuohy needle as a means of improving the ease of passage of lacquered silk ureteral catheters through which he injected incremental doses of local anesthetic.73

Obstetric & Epidural Anesthesia

The origin of epidural analgesia began with Jean Enthuse Sicard, a neurologist, who introduced cocaine through the sacral hiatus for the treatment of sciatica and tabes. Independently, Fernand Cathelin used the same technique for surgical anesthesia.74,75 In 1921, the Spanish surgeon Fidel Pagés-Miravé used a lumbar approach to the epidural space for surgical patients. His greatest contribution to the field of anesthesia was the introduction of segmental anesthesia, thereby eliminating some of the serious side effects of complete neuraxial blocks. Unfortunately, he died in an automobile accident before his methods could be shared by the students he worked with at the time. In 1931, Achille Dogliotti published a report on epidural injection of local anesthetics without knowledge of Pagés-Miravé's work. One of the most important features of Dogliotti's work was his identification of the epidural space. He produced a textbook of his technique that was both reproducible and easy to learn.76 The limitation of epidural anesthesia was similar to that of spinal anesthesia—the duration of anesthesia provided. In 1947, Manuel Martinez Curbelo of Cuba is credited with using the Tuohy needle and a small ureteral catheter to provide continuous lumbar epidural analgesia.77

In the practice of obstetrics, religious beliefs obstructed the progress of pain relief for women in labor. It was commonly believed that providing anesthesia for the woman in labor went against God's will. James Young Simpson is credited with providing the first ether anesthetic for a complex obstetric delivery in 1847. He was severely criticized by both his peers and the clergy, but many women, most conspicuously Queen Victoria, began requesting anesthesia for the delivery of their children. There wasn't much progress in the field of obstetric analgesia/anesthesia from 1860 to 1940 until John Bonica, chief of anesthesia at the University of Washington, took over the management of his wife's anesthesia (and probably saved her life) during labor in 1943. She had a near fatal complication during open drop ether anesthesia. From the time that he intervened in his wife's care, he devoted his career to the advancement of anesthetic care of the mother and fetus.78

When Bonica was chief of anesthesia, caudal anesthesia was the primary means used for providing labor analgesia. This followed a report by W. B. Edwards and R. A. Hingson that analgesia for labor and delivery could be satisfactorily achieved with caudal injections of tetracaine through a needle left in place within the sacral canal.79 When commercially available catheters became available in the 1970s, continuous epidural analgesia gained popularity. In the years following Bonica's contributions, epidural anesthesia for obstetrics has become the norm. Modifications of the techniques and the introduction of either spinal or epidural opioids have made labor and delivery a most pleasant experience for expecting mothers.

Fundamental to modern neural blockade is the concept that pain is a sensory warning conveyed by specific nerve fibers, amenable, at least in principle, to modulation or interruption anywhere in the nerve's pathway. This outlook may be traced back to developments in the study of physiology that finally supplanted the view, first expressed by Plato and Aristotle, that pain, like pleasure, is a passion of the soul, ie, an emotion and not one of the senses. Philosophical changes growing out of the great revolutions of the eighteenth century and the birth of biology as a science gradually, although not entirely, effaced the religious connotations of pain in Western civilization. The doctrine of specific energies of the senses was first promulgated by Johannes P. Müller (1801–1858) in 1826.80 This doctrine, although not specific for the conduction of pain, initiated the movement of scientific thought toward analysis and classification of the specific characters of different nerves. The theory that pain was a separate and distinct sense was first definitively developed by Moritz S. Schiff (1823–1896) in 1858. By examining the effect of incisions in the spinal cord, Schiff was able to demonstrate that touch and pain were independent sensations. On animals, he demonstrated that injury to specific sections of the spinal cord resulted in loss of one modality without affecting the other.81

Müller's theories led Erasmus Darwin (grandfather of Charles Darwin) to suggest the intensive theory of pain. Darwin felt that the sensation of pain was not a separate modality, but resulted from “whenever the sensorial motions are stronger than usual.” Basically it is a theory of sensory overload leading to pain.82 The theories of pain remained controversial throughout the early twentieth century, but by the midtwentieth century, the specificity theory (each sensory modality is transmitted along an independent pathway), became universally accepted as the most credible.

Applying drugs to transmitting nerves to alleviate neuralgic pain was first introduced by Francis Rynd in the early 1800s. Rynd's ideas possibly influenced the later development of both nerve blocks and opioid regional anesthesia.81 When Carl Koller discovered the utility of cocaine as a surgical local anesthetic, a vast new world of local and regional analgesic therapy began. Corning is credited with the concept of direct application of an analgesic to the spinal cord for alleviation of pain, but it was not until the mechanism of pain was more fully understood that pain therapy could be focused on interrupting pain pathways. Unfortunately, by believing that pain pathway interruption was the complete answer to blocking pain, researchers focused only on that aspect, closing their minds to other related aspects of pain development. When Jean Joseph Emile Letievant described specific neurectomy techniques in the late nineteenth century, a myriad of surgical interventions, such as, rhizotomy, cordotomy and, tractotomy emerged to treat pain.83

Unfortunately, most of these techniques were atrocious failures that often created more intense pain than was present prior to the procedure. Ronald Melzack and Patrick Wall's hypothesis that a spinal gate controls the cephalad transmission of nociception led to the modern introduction of electrical stimulation as a method of treating chronic pain. The concept proposed in the theory, that pain perception could be lessened by increasing activity in neural structures not associated with pain, led to chronic stimulation of the deep brain and spinal cord as a modality for the management of chronic pain. Consequently, both the brain and spinal structures emerged as targets for neuroaugmentation.84,85 Although great strides have been made in our understanding of pain development and treatment, it is only through continued research that our understanding of preemptive pain control, such as those methods used in regional anesthesia, can be complete.

Orthopedic surgery has always lent itself to regional anesthesia techniques because of the ability to isolate anesthesia to the extremity being operated on. Initially, general anesthesia and nerve blocks were combined (still a somewhat common practice today). Harvey Cushing is credited with coining the name regional anesthesia for his method of blocking a nerve plexus under direct vision during general anesthesia. His goal was to decrease the anesthetic requirements and to provide postoperative pain relief. It's amazing to consider that he developed this technique in 1902, more than 100 years ago. A similar approach had been proposed by George Crile, 15 years earlier, to decrease the stress of surgery. Upper extremity anesthesia by blocking the brachial plexus percutaneously was achieved by many of our early colleagues. G. Hirschel is credited with developing the “blind” axillary brachial plexus block and D. Kulenkampff the supraclavicular technique, both in 1911. Because the risk of pneumothorax was high with the technique described by Kulenkampff, it was subsequently modified by A. Mulley using a lateral paravertebral approach. Mulley's approach is most likely the precursor of what is now commonly referred to as the “Winnie block” for the brachial plexus.

The spread of regional anesthesia in the United States was greatly facilitated by the work of Gaston Labat (Figure 1–12). Recruited to work at the Mayo Clinic in Rochester, Minnesota, Labat published his influential textbook, Regional Anesthesia, in which he described his techniques to the next generation of physicians, most notably Hippolite Wertheim, John Lundy, Ralph Waters, and Emery Rovenstine. Labat worked at the Mayo Clinic, then moved to Bellevue Hospital in New York City where he worked with Wertheim. Together, they formed the first American Society of Regional Anesthesia. Labat's successor, Emery A Rovenstine, was recruited to Bellevue to continue Labat's work. It was Rovenstine who was responsible for creating the specialty of anesthesiology in the 1920s and 1930s. He also is responsible for the creation of the first American clinic for the treatment of chronic pain, where he and his associates refined techniques of both lytic and therapeutic injections. Rovenstine and his successors used the American Society of Regional Anesthesia to educate physicians about pain management throughout the United States.86

The development of the multidisciplinary pain clinic was one of many contributions to anesthesiology made by John J. Bonica, a renowned teacher of regional techniques. During his periods of military, civilian, and university service at the University of Washington, John Bonica formulated a series of improvements in the management of chronic pain. His text, The Management of Pain, is regarded as a classic of the literature.87,88

Ever since Koller's original work, the popularity of local anaesthesia has waxed and waned, like that of many other medical developments. The announcement of his work produced a massive wave of enthusiasm, which was tempered as the problems of cocaine became increasingly appreciated. The first resurgence of interest came with the introduction of safer drugs at the beginning of the twentieth century, and the second as a result of the efforts of Labat, Lundy, Maxson, Odom, and Pitkin in the United States in the years between the two World Wars.

In Britain, general anesthesia has traditionally been administered by qualified doctors (though not always by specialists who practiced anesthesia exclusively). Standards have usually been high because the conduct of general anesthesia has been their entire responsibility. By contrast, local and regional techniques, if they were used at all, were performed by the surgeon, whose interest and attention were divided between anesthetic and operation. Regional anesthesia was not seen always to be to the patient's best advantage under such circumstances. Nevertheless, when the examination for the Diploma in Anaesthesia was instituted in 1935, the curriculum included local anesthesia. This, together with the establishment of anesthesia as an independent specialty within the UK National Health Service in 1948, did much to encourage local anesthetic techniques. Unfortunately, the years between 1950 and 1955 saw a sharp decrease in the use of local, and particularly spinal, anesthesia in the UK and in the United States. The many advances in general anesthesia then taking place were partly responsible, since they encouraged the belief that a local technique was unnecessary. More important though was the fear of severe neurologic damage. The report entitled “The Grave Spinal Cord Paralyses Caused by Spinal Anesthesia” written in 1950 in New York by a British-trained neurologist, Foster Kennedy, was followed by the Woolley and Roe case and lead to a virtual extinction of the use of regional techniques (see discussion in the section on Spinal Anesthesia).70 After a number of reports of the safe use of local anesthetics for surgical procedures emerged, regional anesthesia techniques once again began to slowly emerge.

Local anesthetic techniques are of value in blocking afferent stimuli even in major surgery because of the reduction in the pain and stress suffered by the patient. This approach is now extending even to cardiac surgery, but the concept is far from new. As early as 1902, Harvey Cushing was advocating the combination of local with general anesthesia to decrease “surgical shock,” a concept that was further developed by Crile. The term balanced anaesthesia is very common today and implies a triad of sleep produced by either inhalational or intravenous route, profound analgesia with opioid drugs, and muscle relaxation by neuromuscular block. But interestingly, when Lundy first used the term in 1926, he intended that the second and third parts of the triad would be produced by a local anesthetic block, something proponents of regional anesthesia are implementing in modern anesthesia practice.

Other advances, although more difficult to quantify, have directly or indirectly helped the cause of local anesthesia. For example, developments in the field of medical plastics have resulted in safe and reliable syringes, catheters, and filters, and the anesthesiologist can select from a wide variety of sedative and anxiolytic drugs that, when carefully used, can greatly improve the patient's acceptance of a nerve block. Of great importance has been the understanding of the effects and treatment of sympathetic block. Ephedrine became available in 1924 and was first used to treat hypotension during spinal anesthesia in 1927, but readily available intravenous fluids and equipment for their administration are more recent developments.

Most currently used techniques of regional anesthesia were devised during that first decade of the twentieth century: brachial plexus block, axillary and supraclavicular approaches; intravenous regional anesthesia; celiac plexus block; caudal anesthesia; hyperbaric and hypobaric techniques of spinal anesthesia, and all the presently employed nerve blocks for the head and neck as applied in dentistry and plastic surgery. Thereafter, aside from technical innovation and understanding of some of the physiologic and toxicologic responses to local anesthetics, the great impetus to regional anesthesia came from the synthesis of the amide local anesthetics and an understanding of their pharmacodynamic and especially pharmacokinetic properties.32

In present-day practice, more advanced techniques of regional anesthesia (eg, continuous catheters, combination blocks, deep plexus blocks) have evolved because of the groundwork put in place by those earlier pioneers. With the advent of the Internet providing easier access to current medical practice, patients are better educated and are becoming advocates for regional anesthetic techniques.

It is appropriate to conclude by mentioning the organizations that seek to promote education and training in the use of regional anesthetic techniques. The American Society of Regional Anesthesia was reborn in 1975 and became firmly established. Its European counterpart (the European Society of Regional Anaesthesia and Pain Medicine) is younger, but is now equally well established, and similar societies are flourishing in many other parts of the world. Other important educational entities, such as the New York Society of Regional Anesthesia (founded in 1994, by Drs. Hadzic and Vloka), have been developed to continue to promote the safe and effective practice of regional anesthesia.

The history of local and regional anesthesia did not end in the first half of the twentieth century. In fact, it is often said, “we are making history every day.” For instance, important techniques developed in the last few decades have refined our ability to identify peripheral nerves accurately. With the increasingly enthusiastic introduction of the use of ultrasound for nerve location, the rate of development in this area of regional anesthetic practice will increase at a greater pace. Perhaps the most important role for the regional anesthesiologists who will make history in the next few decades will be to document the clinical advantages and benefits of local and regional anesthesia. This endeavor will not just manifest itself as enthusiasm and skill, but will be based on the generation of convincing data through careful clinical research and academic cooperation within the regional anesthesia community. Books such as this are a vital part of building the future of regional anesthesia and in themselves will form a part of the history of local and regional anesthesia.