Dermatologic Surgical Procedures

Punch biopsy, shave biopsy, electrodesiccation and curettage (ED&C), blunt dissection, and simple excision and suture closure are the basic techniques that should be learned by physicians who treat skin disease. One should be familiar with the more sophisticated techniques, such as Mohs micrographic surgery, so that referral to physicians who perform these techniques can be made at the proper time. The instruments used for most basic dermatologic surgical procedures are shown in Fig. 27.1 .

Antibiotic Prophylaxis

Antibiotics are not helpful in treating cutaneous abscesses, inflamed epidermal cysts, uninfected atopic eczema, and cutaneous ulcers caused by venous insufficiency or diabetes in the absence of significant contiguous soft tissue inflammation.
Prophylactic antibiotics are rarely appropriate for routine dermatologic surgery and are not indicated for patients who have prosthetic joints or vascular grafts.
Topical antibiotics are no better than white petrolatum in covering sutured wounds, and with moist occlusive dressings, no ointment is necessary.

The Division of Dermatologic Surgery at the Mayo Clinic has designed a chart that summarizes the recommendations in the advisory statement (2008) for antibiotic prophylaxis in dermatologic surgery ( Fig. 27.2 ). The advisory statement provides an update on the indications for antibiotic prophylaxis in dermatologic surgery for the prevention of infective endocarditis, hematogenous total joint infection, and surgical site infection.

FIG 27.2, Recommendations for antibiotic prophylaxis in dermatologic surgery.

For patients with high-risk cardiac conditions, and a defined group of patients with prosthetic joints at high risk for hematogenous total joint infection, prophylactic antibiotics are recommended when the surgical site is infected or when the procedure involves breach of the oral mucosa. For the prevention of surgical site infections, antibiotics may be indicated for procedures on the lower extremities or groin, for wedge excisions of the lip and ear, for construction of skin flaps on the nose or skin grafts, and for use in patients with extensive inflammatory skin disease.

The first step in determining the need for antibiotic prophylaxis in dermatologic surgery is assessment of the risk of surgical site infection and aggressive treatment of any cutaneous infection in patients with joint or valve replacements.
Perforating dermatologic surgery involves invasion of or immediate destruction of the epidermis or mucosa and includes excision, Mohs micrographic surgery, biopsy, ablative laser, incision and drainage, and ED&C. Nonperforating dermatologic surgical procedures, such as cryotherapy and nonablative laser, are not an indication for prophylaxis.
Oral mucosa is defined as portions of the nonglabrous oral tissue posterior to the junction where closed lips meet.
Patients with low-risk cardiac indications do not receive antibiotic prophylaxis for oral procedures but receive therapeutic antibiotics for an infected site. Examples of patients who would not routinely receive antibiotic prophylaxis for infective endocarditis include those with pacemakers, defibrillators, peripheral vascular stents, vascular grafts, coronary artery stents, breast implants, penile prostheses, and central nervous system shunts.
Antibiotics are not indicated in patients with orthopedic pins, plates, or screws and not in the majority of healthy patients with a total joint prosthesis.

Mohs Micrographic Surgery – Indications for Antibiotics

The routine administration of prophylactic antibiotics for Mohs micrographic surgery is not recommended. With the low rate of bacteremia during Mohs surgery, prophylaxis against infective endocarditis and hematogenous total joint infection is usually not indicated. For patients who are at high risk for surgical site infection based on the site or technique used, antibiotic prophylaxis should be given. For patients at high risk for infective endocarditis or hematogenous total joint infection, if the surgical site includes oral mucosa, antibiotic prophylaxis is indicated. If the site is infected before the procedure , aggressive treatment should be initiated, cultures ascertained, and prophylaxis for infective endocarditis or hematogenous total joint infection also given. Mohs surgical cases are heterogeneous, and some may involve breach of nasal mucosa or may extend over many hours; each patient's clinical scenario should be considered individually and prophylaxis decisions should be made after taking into account all relevant factors. As the risk of surgical site infection increases and the potential morbidity following an infection increases, the threshold for antibiotic prophylaxis should decrease.

Local Anesthesia

Lidocaine (Xylocaine) 1% or 2%, with or without epinephrine, is used for most surgical procedures. The onset of anesthesia is almost instantaneous, and the duration is adequate for most minor procedures. A 27-gauge or, preferably, a 30-gauge needle is used.

Epinephrine

The vasoconstriction induced by epinephrine prevents absorption of lidocaine, prolongs anesthesia, and controls bleeding. Lidocaine with epinephrine is safe for distal digits, penis, ears, and toes, but should not be administered for digital blocks, where complete blood flow to the digit could be compromised.

Lidocaine Allergy

Allergy to lidocaine is very rare. Most patients who claim to be allergic have had a vasovagal response. Bacteriostatic saline is an alternative for patients who are allergic to lidocaine (see the following discussion).

Pain Reduction

Anesthetics produce a sharp pain during skin infiltration. Pain is greater with rapid injections and can be minimized with slow injections through a 30-gauge needle. The needle should be inserted slowly but firmly into the dermis. A needlestick at 90 degrees to the skin surface causes less pain because fewer nerves are transversed by the needle. The skin is rapidly pinched between the thumb and forefinger and shaken just before and during the injection. Pinching the skin in the area to be injected either distracts the patient or blocks the transmission of pain impulses caused by the injections. Placing the needle distal to the area of pinched skin is more effective. Anesthesia is initiated by injecting a tiny amount of fluid; after a few seconds, infiltration is continued slowly until the skin surrounding the lesion blanches. A wheal can be raised by inserting the needle almost vertically. Penetration of the thick palm and sole skin is very painful. The area about the nostrils is very sensitive. Intrafollicular injection into the large follicles of the nose and cheeks minimizes pain. Superficial injections into the penis and vulva are well tolerated.

Painless Anesthesia

Icing the lesion for 1 minute numbs the skin and minimizes needle-penetration pain. Adequate anesthesia with little or no infiltration pain can be induced with the following preparations. Bacteriostatic saline and lidocaine diluted with bacteriostatic saline solution injections are less painful than 1% lidocaine with sodium bicarbonate. It is unlikely that the pain of infiltration is a simple function of the pH of the anesthetic solution.

Bacteriostatic Saline

Commercially available bacteriostatic saline contains benzyl alcohol, which acts as a painless anesthetic. The anesthetic effect dissipates rapidly when injected subcutaneously. The volume of saline required to achieve anesthesia is at least two to three times that required when using 1% lidocaine and is of brief duration.

Saline and Epinephrine

The addition of 3 mL of epinephrine 1 mg/mL (1 : 100,000 diluted) to 30 mL of bacteriostatic saline extends the duration of anesthesia from 4 minutes to 120 minutes. Bacteriostatic saline should not be used as an anesthetic for newborns.

Saline Diluted With Lidocaine

A mixture of saline (27 mL) and lidocaine 1% with or without epinephrine (3 mL) is also effective.

Buffered Lidocaine

The addition of sodium bicarbonate (NaHCO ₃ ) reduces the pain produced by infiltration of lidocaine with or without epinephrine. One milliliter of NeutraCaine, a 7.5% sodium bicarbonate buffer solution, is added to 5 mL of lidocaine or bupivacaine. Buffered lidocaine and epinephrine maintain greater than a 90% concentration 2 weeks after buffering when stored at 0 to 4° C. This permits batch buffering and storage for up to 2 weeks when properly refrigerated. NaHCO ₃ enhances the killing effect that has been described for lidocaine alone. The inability to recover common pathogenic bacteria from biopsy specimens could be the result of exposure to lidocaine buffered with NaHCO ₃ . Warming the local mixture to 40° C reduces the discomfort of injection even further.

The Ice–Saline–Lidocaine Technique

This is a simple method of minimizing pain when obtaining local anesthesia. Cryo-Gel packs are applied before the local anesthetic injection to minimize the pain of piercing the skin with the injection needle. The surgical field is then infiltrated with benzyl alcohol–containing normal saline. Subsequently, lidocaine with epinephrine can be infiltrated without discomfort.

EMLA, ELA-Max

EMLA is a mixture of 2.5% lidocaine and 2.5% prilocaine in an oil and water emulsion. ELA-Max is a topical anesthetic cream with 4% lidocaine at pH 7.4. These agents should be applied to the desired area for approximately 1 hour under an occlusive dressing. They provide effective analgesia, making them useful for superficial surgery, split-thickness skin grafts, venipuncture, argon laser treatment, epilation, and debridement of infected ulcers. Other indications have included use in postherpetic neuralgia, hyperhidrosis, painful ulcers, and inhibition of itching and burning. A single application of ELA-Max in children weighing less than 10 kg or between 10 and 20 kg should not be applied over an area larger than 100 cm ² .

Hemostasis

Monsel's solution (ferric subsulfate) is a valuable agent for providing rapid hemostasis. It is particularly effective in controlling bleeding after curettage of seborrheic keratosis and basal cell carcinoma (BCC). Immediate hemostasis is most efficiently achieved if the solution is applied when the wound is not bleeding. To exert tension and stop bleeding, the thumb and index finger are placed at the opposite edges of the wound, and the skin is stretched. The blood is then wiped with gauze, the Monsel's solution is applied with a cotton-tipped applicator, and the tension is maintained for approximately 15 seconds. The lack of blood flow apparently allows more complete coagulation.

Monsel's Artifact

When a biopsy is repeated, an area of skin that has been treated with Monsel's solution has a pigmented artifact that can interfere with histologic interpretation. The use of Monsel's solution should be avoided after biopsies of pigmented lesions or tumors that may prove to be diagnostic problems. The pathologist should be informed if Monsel's solution has been used.

Wound Healing

Types of Cutaneous Wounds

Full-Thickness Wounds

In full-thickness wounds, the epidermis and the full thickness of the dermis are lost. The defect is deeper than the adnexa (hair follicles, eccrine sweat ducts). These wounds heal by contraction (associated with myofibroblast development), granulation tissue formation (with fibroplasia and neovascularization), and reepithelialization. Contraction causes a 40% decrease in the size of the wound. Epithelialization occurs from the wound edges.

Partial-Thickness Wounds

In partial-thickness wounds, the epidermis and some portion of the dermis with parts of the adnexa remain in the wound bed. Such wounds are produced by shave excisions, ED&C, dermabrasion, chemical peels, and carbon dioxide (CO ₂ ) laser surgery. These wounds heal quickly through reepithelialization from the wound edges and adnexal structures in the base of the wound. Wound contraction is minimal when only the most superficial portion of the dermis has been lost.

Physiology of Wound Healing

The acute phase of wound healing takes 3 to 14 days and has three phases: inflammation, proliferation, and remodeling with wound contraction ( Fig. 27.3 ). The inflammatory phase begins as neutrophils and macrophages appear. The proliferative phase involves the formation of a collagen matrix and granulation tissue and then epidermal cell migration over the matrix. The remodeling phase sees fibroblasts evolve to compact and contract the wound. Wounds gain about 20% of their final strength in the first 3 weeks. Protein or vitamin deficiencies may impair collagen production, and necrotic tissue in the wound bed may impede reepithelialization.

Inflammatory Phase

Neutrophils appear in a wound 6 hours after the event, reach their greatest number after 24 to 48 hours, and start to disappear after 72 hours. Aggregated platelets and damaged cells secrete chemical mediators to attract and activate inflammatory cells and fibroblasts. Vasodilation and increased permeability of local capillaries permit neutrophils to move into the wound site to phagocytize bacteria and debris.

Proliferative Phase

Activated macrophages release vascular endothelial growth factor (VEGF) to stimulate granulation tissue formation. Fibroblasts populate the wound after 48 to 72 hours. Fibroblasts produce a collagen matrix, new blood vessels invade the forming granulation tissue, and epidermal cells migrate across the wound surface to close the wound. Keratinocytes initially migrate over a matrix of fibrin, collagen, and elastin. This matrix acts as a structural support for cell migration. Epidermal migration and proliferation occur from the epithelial cells at the edge of the wound and from appendageal structures remaining in the wound bed. The rate of reepithelialization is directly related to the moistness of the wound. Open, dry wounds reepithelialize slower than occluded, moist wounds. The migration of keratinocytes beneath a dry crust is slower than the migration over an occluded, moist wound, where the plane of epithelial cell migration lies near the wound surface ( Fig. 27.4 ). Protein or vitamin deficiencies may impair collagen production, and necrotic tissue in the wound bed may impede reepithelialization.

FIG 27.4, Occlusive dressing. The effects of tissue humidity on reepithelialization are shown. Occlusive dressings allow epithelialization to occur at the wound surface. In open wounds the epithelium migrates beneath a desiccated crust and devitalized dermis.

Remodeling

Wounds gain about 20% of their final strength in the first 3 weeks of normal wound healing through collagen deposition, remodeling, and wound contraction. Fibroblasts remodel the collagen matrix. Wound contraction begins at 1 week after the wound occurs. Myofibroblasts are modified fibroblasts that resemble smooth muscle cells. They contain large amounts of contractile proteins and are responsible for wound contraction.

Tensile strength in a wound increases progressively up to 1 year after the wound occurs. Tensile strength in a healed wound is always less than 80% of normal. Healing time is related to the logarithm of the area. The width of the wound is a better predictor of healing time than is the area in which the wound occurred. Wounds created by destructive techniques (e.g., cryosurgery, electrosurgery, laser surgery, and chemical cautery) heal more slowly than clean wounds created by scalpel or curette surgery.

Normal Wound Healing

Wound management guidelines are listed in Box 27.1 .

Box 27.1

Wound Management Guidelines

1
Use antiseptics for disinfection of intact skin only.
2
Select a method of wounding that minimizes tissue necrosis.
3
Use pinpoint electrocoagulation, pressure, topical thrombin, collagen, or gelatin rather than caustic agents to establish hemostasis.
4
To prevent wound infection and to accelerate healing, apply topical antibiotics to the wound instead of antiseptics.
5
Substitute tap water for hydrogen peroxide to cleanse wounds.
6
Use nonadherent occlusive dressing on wounds to accelerate healing.

Impairment of Wound Healing

Topical Therapy

Topical steroids may interfere with healing because of their antiinflammatory action ( Table 27.1 ).

TABLE 27.1

Topical Agents That Affect Epidermal Migration

Agents	Relative Rate of Healing (%) *
Triamcinolone acetonide ointment (0.1%)	−34
Furacin	−30
USP petrolatum	−8
Eucerin	+5
Benoxyl lotion base (benzoyl peroxide preparation)	+14
Silvadene cream	+28
Neosporin ointment	+28
Telfa dressing	+14

USP, United States pharmacopeia.

* Compared with untreated.

Antiseptic Solutions

One percent povidone–iodine, 3% hydrogen peroxide, and 0.5% chlorhexidine solutions are toxic for fibroblasts and keratinocytes and may delay the formation of granulation tissue.

Hemostatic Solutions

Monsel's solution (ferric subsulfate), 30% aluminum chloride, and silver nitrate produce tissue necrosis and delay reepithelialization. The effect on small wounds is minimal.

Contact Dermatitis

Contact allergic reactions may occur with tapes and antibiotic ointments. Neomycin is a common sensitizer. Polysporin and bacitracin are not common sensitizers.

Systemic Factors

Malnutrition interferes with healing. Vitamin C and zinc deficiencies lead to poor healing. Systemic steroids in a dosage greater than 10 mg a day interfere with healing. Clinical experience suggests no impairment of wound healing for patients taking chemotherapeutic drugs.

Wound Dressings

Wound Dressings – Mechanism of Action

Occlusion of wounds leads to faster healing. The process of neovascularization within granulation tissue is stimulated by hypoxic conditions such as those that occur beneath occlusive, oxygen-impermeable dressings. Occlusive dressings prevent crust formation and drying of the wound bed. The rate of epithelialization is faster under occlusive dressings. Wound fluid under occlusive dressings is favorable to fibroblast proliferation. Adhesive occlusive dressings may remove newly formed epithelium. Hydrocolloid adhesive occlusive dressings prevent entry of bacteria into the wound. The use of occlusive dressings in chronic wounds leads to less pain, better granulation tissue, and painless wound debridement. In acute wounds, occlusive dressings promote bacterial growth but result in faster reepithelialization. There are numerous dressings available. These are routinely used in wound care clinics where complicated venous and arterial ulcers are treated.

Function

Protection with dressings exerts pressure and maintains a moist wound environment. Dressings reduce pain when applied to partial-thickness wounds. Topical antimicrobial agents that may enhance reepithelialization include neomycin, polymyxin B, Neosporin ointment, silver sulfadiazine, and 20% benzoyl peroxide lotion. Hexachlorophene, chlorhexidine, and alcohol may retard reepithelialization.

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