30 An Overview of Anesthetic Modalities Used in Hair Restoration Surgery

Carlos J. Puig

Summary

This chapter reviews the history, dosing, pharmacology, and toxicology of scalp anesthesia for hair restoration surgery. This chapter also describes various methodologies for administering local anesthesia to the scalp and face, using safe and comfortable techniques.

Cocaine, the only naturally occurring local anesthetic, is indigenous to the Andes Mountains, West Indies, and Java, and was introduced in Europe in the mid-1800s following its isolation from the coca leaf.1 All other anesthetics are synthetically derived.

In the 1880s, Koller introduced cocaine into the field of ophthalmology, and Hall introduced it to dentistry. Halsted was the first to report the use of cocaine for nerve blocks in the United States in 1885 but became addicted to the drug through self-experimentation.²

In 1904, procaine, the first synthetic derivative of cocaine, was added to the pharmacopeia. The need in World War II for a safer, longer acting, local anesthetic encouraged Swedish chemist Nils Lofgren to develop lidocaine, the most widely used cocaine derivative.

30.2 Local Anesthetics

30.2.1 Pharmacology

Local anesthetics are weak bases that contain a hydrophilic amine residue separated from a lipophilic aromatic ring by an intermediate alkyl chain. They function by blocking sodium channels within nerve axons, thereby preventing the depolarization of nerve fibers. In general, the effectiveness of anesthesia is related to the diameter, myelination, and conduction velocity of the affected nerve fibers.³

There are two classes of local anesthetics, amino esters and amino amides (Fig. 30.1). Amino esters are unstable in solution, whereas amino amides are very stable. It is easy to remember that all the amino amides contain the letter “i” twice, as does the term “amino amides” (Table 30.1). The ester anesthetics include procaine, tetracaine, and chloroprocaine. These are rapidly metabolized by plasma pseudocholinesterase, and consequently people with pseudocholinesterase deficiency are prone to toxicity at normal therapeutic doses.⁴ The amide class of anesthetics are lidocaine, mepivacaine, bupivacaine, and prilocaine. In contrast to ester anesthetics, the amides are less allergenic and have greater potency, a rapid onset, and longer duration of action. Since they are primarily cleared by hepatic metabolism, patients with liver disease are more prone to toxicity. The two pharmacologic classes have no cross-reactivity, so amide anesthetics can be safely administered to patients with an ester anesthetic allergy.

Table 30.1 Mnemonic: There are 2- i’s as in amino amides

Local anesthetics exist in ionized and nonionized forms, the proportions of which vary with the pH of the environment. Only the nonionized portion is capable of diffusing across nerve membranes; therefore, anesthetics with a larger nonionized portion have a faster onset of action. Local anesthetics also differ in respect to the pH at which the ionized and nonionized forms are present at equilibrium; generally in the pH range of 7.6 to 8.9, more ionization occurs.

The more closely the equilibrium pH for a given anesthetic approximates the physiologic pH of tissues (i.e., 7.35–7.45), the more rapid the onset of action (Video 30.1).

A decrease in pH shifts equilibrium toward the ionized form, delaying onset of action. This explains why local anesthetics are slower in onset of action and less effective in the presence of inflammation, which creates a more acidic environment. Contrastingly, the addition of sodium bicarbonate is used clinically to increase the pH of local anesthetic solutions, thereby enhancing onset of action. However, overzealous alkalization can cause the local anesthetic molecules to precipitate from solution.

All local anesthetics, except cocaine, are vasodilators, which occur via direct relaxation of peripheral arteriolar smooth muscle fibers. Greater vasodilator activity of a local anesthetic leads to faster absorption and, thus, shorter duration of action. To counteract this, epinephrine is used both in combination with commercially available local anesthetics and alone, to increase the duration of the anesthesia and for surgical hemostasis.5

30.2.2 Lidocaine

Lidocaine is the most common short-acting local anesthetic used in hair transplantation surgery (Table 30.2). Though the literature says the onset of action is 2 to 4 minutes, practical experience suggests that the onset of action is only 10 to 15 seconds, and the duration of action is 30 to 60 minutes when used alone, or 120 minutes when combined with epinephrine.⁶

Table 30.2 Commonly used local anesthetics in hair transplantation

For infiltrative anesthesia, the recommended maximum total daily dose (TDD) of lidocaine is 4.5 mg/kg (maximum: 300 mg) when used alone, or 7 mg/kg (maximum: 500 mg) when combined with epinephrine.⁶ In humans, there is no clinical basis for these dosage guidelines, and experience in dermatologic surgery suggests that they may be too conservative,⁷ which is especially true in procedures that employ tumescent anesthetic techniques.⁸ The American Academy of Dermatology has published guidelines for liposuction,⁹ which indicate a maximum safe of lidocaine of 55 mg/kg; however, some experts note that 35 mg/kg is a more reasonable limit, citing that the hepatic metabolism of lidocaine is limited. Once saturation occurs, and absorption exceeds elimination, plasma lidocaine concentrations increase precipitously.¹⁰

In hair transplantation, the TDD is routinely exceeded without toxicity probably because of the staged administration (see Chapter 31). However, physicians must take into account multiple factors when determining the maximum lidocaine dosage, including the general health status and daily medication use of the patient, their body weight, the dosing interval, the length of the surgery, the epinephrine concentration and volume used, the concomitant use of other local anesthetics, the administration of neuroprotective medications such as benzodiazepines, and the anesthetic technique.

As with all local anesthetics, adverse reactions may occur following administration of lidocaine. Usually, these result from administration of too much drug or accidental direct intravascular injection of the drug. Adverse reactions occur primarily in the central nervous system (CNS; neurotoxicity) and the cardiovascular system (myotoxicity) because these tissues function because of excitable membranes, the target of local anesthetic action.

The hair restoration surgeon must be alert to identify the progression of signs and symptoms of toxicity that may be observed in the patient. These include lightheadedness, tinnitus, circumoral numbness, a metallic taste (copper penny taste), or double vision. Upon examination, the patient may become drowsy or slur speech and may develop nystagmus. At higher levels of anesthetics, the patient may become anxious and develop fine tremors of the muscles of the hands and/or face. These tremors may worsen and coalesce into a grand mal seizure. Ultimately, the patient may experience generalized CNS depression leading to hypoxia, acidosis, and respiratory arrest.

Lidocaine decreases the rate of depolarization of cardiac tissue, which is the rationale behind the use of lidocaine in the treatment of ventricular arrhythmias. At higher concentrations, amplitude of the cardiac action potential is also decreased, as is the velocity of conduction. At toxic doses, the negative inotropic effects of local anesthetics may lead to chronotropic effects such as bradycardia, ventricular fibrillation, or asystole. Other cardiovascular effects include hypotension, which occurs via the direct vasodilating effects of local anesthetics on peripheral arteriolar smooth muscle.

30.2.3 Bupivacaine

Bupivacaine is the most commonly used long-acting local anesthetic in hair transplantation. The onset of action is slower than lidocaine. When used alone, the duration of action is 120 to 240 minutes, and when combined with epinephrine it is 180 to 240 minutes.³ For infiltrative anesthesia, the TDD is 175 mg without epinephrine and 200 mg with epinephrine.⁴

Most practitioners use 0.25% bupivacaine for field blocks, and 0.5% bupivacaine for peripheral nerve blocks. Commonly, bupivacaine is combined with lidocaine in an attempt to achieve anesthesia that has both a rapid onset and a prolonged duration. However, a study comparing 1% lidocaine, 1:1 mixture of lidocaine and bupivacaine, and bupivacaine alone found no significant difference in the time of onset or the duration of the different combinations.¹¹ The author’s own experience is substantially different. The author performs a ring block with a 50/50 mixture of 2% lidocaine with epinephrine 1:100,000 and 0.25% bupivacaine, and tumescence of the region with 20 to 40 mL of a modified Klein liposuction solution (see Chapter 31), and usually achieves 8 to 9 hours of anesthesia and hemostasis seldom needing reinforcement (Table 30.3).

Table 30.3 Comparison of Puig’s modified Klein solution and Klein solution

30.3 Injection Techniques

Fear of pain and poor results are the two greatest deterrents to patients consenting to cosmetic surgery. Pain is a perception, an interpretation of physical stimuli mediated by numerous factors, including emotional variables, in multiple regions of the CNS.12

Therefore, limiting the pain of infiltrative anesthesia demands that both physical and emotional factors be addressed.

30.3.1 Concomitant Physical Stimulation

Melzack and Wall formalized the phenomenon of the Gate Control theory, which states that the ascending transmission of nociceptive information by slowly conducting A-delta and C-nerve fibers can be modified by afferent signals relaying the sensation of touch, pressure, and vibration, which are carried out by rapidly conducting A-alpha and A-beta nerve fibers.¹³ So one can distract the patient’s attention from the site of injection using this theory by either pinching or shaking the skin, or by using a small handheld vibrator near the site of anesthesia.^14,15

30.3.2 Buffering

Local anesthetics are weak bases that are commercially available as hydrochloride salts in an acidic form. The acidity is higher in solutions containing premixed epinephrine. A low pH chemically stabilizes anesthetics and extends medication shelf life, but it causes a burning sensation when injected. Moreover, it increases the percentage of charged anesthetic molecules, thereby hindering local anesthetic diffusion across nerve cell membranes, and consequently slowing down the onset of anesthesia and reducing its effectiveness.⁴

Buffering solutions can diminish pain and increase efficacy. Lidocaine is buffered with 8.4% sodium bicarbonate in a volume ratio of 9:1, whereas bupivacaine is buffered in a volume ratio of 50:1. However, when Straub studied postoperative edema in hair transplantation, he found that the incidence of postoperative facial edema was increased by nearly 400% in patients who received buffered lidocaine.¹⁶ Other surgeons report that buffering is associated with more bleeding. Another solution, to reducing the pain associated with the low pH associated with premixed lidocaine/epinephrine solutions, is to use a plain lidocaine stock solution and add the epinephrine in the desired concentration just prior to injecting.

30.3.3 Warming

Harris reviewed the literature and found that the combination of warming and buffering had the greatest effect on reducing patient discomfort.^17,19 Buffering had a greater impact than warming, but warming the solution using dry heat or warm water baths to a temperature of 37°C always reduced pain on injection.¹⁷

30.3.4 Needle Caliber

Smaller caliber needles such as 30 gauge have the potential to cause less pain than larger ones when injecting local anesthetics.¹⁸ A number of needle-free instruments have been developed to administer local anesthetics, but all are more painful than fine needle injection.

30.3.5 Rate of Injection

In a large study assessing the impact of this variable, researchers found that reducing the speed of administration had a greater impact on pain than buffering.¹⁹ The Wand, an instrument supplied by Milestone Scientific, mechanically injects anesthetic solutions at a slow and steady rate, but is not widely used.

30.3.6 Depth of Injection

Superficial injections into the upper dermis result in a more rapid onset and a longer duration of anesthesia, but more infiltrative pain. For this reason, many practitioners perform initial injections into deeper tissue, and then move into more superficial planes.

30.3.7 Topical Anesthetics

The application of topical anesthetics such as EMLA cream, or 4% lidocaine/prilocaine compounded, is of little practical use for hair restoration surgery as they take 1 to 2 hours to take effect, and often still do not prevent the pain of deep injection.²⁰

30.3.8 The Office Environment

There is a strong emotional component to the patient’s perception of pain and discomfort. A relaxed, confident office staff, in a pleasant, comfortable physical environment, is critical to allaying the patient’s fears and anxiety.

Surgical trays, instruments, needles, and syringes should be kept covered and out of the patient’s view. Lighting should be subtle and relaxing during the administration of the anesthetic. A television program or movie is an excellent distractor during the slow gentle administration of the local anesthetic. An anxiolytic agent may also reduce the patient’s perception of pain.

Field blocks are the most common means of administering local anesthesia, be it to anesthetize a wound for repair, an area for excisional biopsy for disease, or performing a hair transplant. In hair restoration surgery, the donor and recipient areas are generally anesthetized by creation of an anesthetized perimeter of the treatment area, a “field block” surrounding the treatment area (Fig. 30.2). In the donor region, the nerve supply approaches from the cervical spine via the greater occipital, postauricular, and auricular temporal nerves. Indeed these nerves innervate the posterior half to two-thirds of the scalp. In the frontal recipient area, the innervation for the middle one-third of the hairline originates from the supratrochlear and supraorbital nerves just above the eyes, and the lateral hairline innervates from the zygomaticotemporal and auricular temporal nerves. Hairline field blocks are infused about 1 cm below the proposed hairline, and posteriorly on the same line to overlap with the donor area block.

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